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"bradycardia" Definitions
  1. relatively slow heart action— compare TACHYCARDIA
"bradycardia" Synonyms
"bradycardia" Antonyms

355 Sentences With "bradycardia"

How to use bradycardia in a sentence? Find typical usage patterns (collocations)/phrases/context for "bradycardia" and check conjugation/comparative form for "bradycardia". Mastering all the usages of "bradycardia" from sentence examples published by news publications.

Bradycardia is when your resting heart rate is slower than normal.
She learned she had bradycardia, or a slow heartbeat, and arrhythmia, and was given a pacemaker.
But if you have chronic or persistent bradycardia, she says your doctor may treat it in a few ways.
It's intended for patients with atrial fibrillation (an irregular or rapid heart rate) and other dangerous arrhythmias, including bradycardia-tachycardia syndrome.
"We had a trifecta of concerning findings—cerebellar lesions in rats, seizures in monkeys, and bradycardia in dogs," Vocci told me.
Ibogaine also appeared to affect the heart, causing bradycardia and increasing the risk of a life-threatening arrhythmia called torsades de pointes.
Steinbaum says borderline or occasional bradycardia may not require medical intervention, and if there are no symptoms, it can be generally monitored.
Defibrillators help patients with bradycardia -- a slow heartbeat -- by pacing the heartbeat and those with tachycardia -- a fast heartbeat -- by delivering shocks that reset heartbeats to normal.
Bradycardia, or a heart rate that is too slow, can be a serious condition, especially if the heart is not pumping enough oxygen-rich blood throughout the body.
These devices can help track your heart rate 24/7 over many months and years, so it&aposs easier to detect if and when you have bouts of bradycardia.
But if nothing comes up during your visit — possibly because you have a minor case of bradycardia that only occurs occasionally — the doctor may give you a portable EKG to take with you.
If bradycardia is not caused by exercise, a low heart rate means that your heart — which isn&apost as efficient as a highly-trained athlete — is not pumping enough oxygen-rich blood in the body.
Mr. Voinovich had a pacemaker installed in 2003 because his heart rate had slowed down over several years as a result of a condition called progressive sinus bradycardia, and he had experienced other health problems in recent years.
Newman told doctors that her daughter had a nervous system dysfunction that manifested as "hypothermia, hyperthermia, bradycardia, tachycardia, and 'turning purple,'" and the hospital decided to proceed with a surgery to install a pacemaker, despite the normal evaluation, based on "the medical history provided by the defendant, combined with a single report of the primary pediatrician" that the child had a low heart rate.
Ictal bradycardia is when people with temporal lobe epilepsy experience bradycardia with their seizures (epileptic discharges). Bradycardia is defined by a slower than normal heart rate, less than 60 bpm. (Normal range is 60-100 bpm). Ictal epileptic discharges can effect changes in cardiac rhythm.
Levobetaxolol should not be used by people who have sinus bradycardia, atrioventricular block, cardiogenic shock, or overt cardiac failure. The drug has been associated with bradycardia and hypertension.
Anticholinergic drugs increase heart rate and are used to treat bradycardia.
Side effects of aceclidine include increased salivation and bradycardia (in excessive doses).
Pathological causes include sinus bradycardia, sinus arrest, sinus exit block, or AV block.
Transient episodes of bradycardia, decreased oxygen saturation, hypotension, or endotracheal tube blockage may occur.
Arrhythmias such as tachycardia, bradycardia, atrioventricular block, and premature ventricular beats have also been reported.
The symptomatic patient may present with dyspnea, cyanosis, chest pain, pulsus paradoxus, bradycardia or tachycardia.
Caution should be used in administrating propafenone in individuals with hepatic dysfunction, asthma, CHF, or bradycardia.
Junctional rhythms (if a bradycardia) can cause decreased cardiac output. Therefore, the person may exhibit signs and symptoms similar to other bradycardia such as lightheadedness, dizziness, low blood pressure, and fainting. This rhythm can usually be tolerated if the rate is above 50 beats per minute.
Sinus bradycardia is a sinus node dysfunction with a rate that is lower than normal. In humans, bradycardia is generally defined to be a rate of under 60 beats per minute. A normal heartbeat in human is usually at a rate of 60 to 100 beats per minute.
Bradycardia is a condition typically defined wherein an individual has a resting heart rate of under 60 beats per minute (BPM) in adults, although some studies use a heart rate of less than 50 BPM. Bradycardia typically does not cause symptoms until the rate drops below 50 BPM. When symptomatic, it may cause fatigue, weakness, dizziness, sweating, and at very low rates, fainting.Sinus Bradycardia – eMedicine During sleep, a slow heartbeat with rates around 40–50 BPM is common, and is considered normal.
If the decrease during exhalation drops the heart rate below 60 BPM on each breath, this type of bradycardia is usually deemed benign and a sign of good autonomic tone. The second, sinus bradycardia, is a sinus rhythm of less than 60 BPM. It is a common condition found in both healthy individuals and those considered well-conditioned athletes. Studies have found that 50–85% of conditioned athletes have benign sinus bradycardia, as compared to 23% of the general population studied.
The diving bradycardia was first described by Edmund Goodwyn in 1786 and later by Paul Bert in 1870.
Ictal bradycardia is a potential cause or reason for ictal asystole to occur and is believed to help explain the phenomenon of sudden unexpected death in epilepsy (SUDEP).Through the simultaneous use of electroencephalograph (EEG) and electrocardiograms (ECG), researchers can monitor and record a patient going through ictal bradycardia seizures. And most importantly provide treatment with both antiepileptic drugs and cardiac pace as deemed necessary for the patient. Although there is limited amount of information about ictal bradycardia, as it is a relatively new discovery and is considered to be rare condition, researchers suggest that early diagnosis and treatment of ictal bradycardia can eliminate the chances of sudden unexpected death in epilepsy.
Other symptoms of alarm bradycardia, such as salivation, urination, and defecation, can also cause the predator to lose interest.
STS-135 produces bradycardia and hypothermia in rats at doses of 1–10 mg/kg, suggesting cannabinoid-like activity.
The heart muscle of athletes has become conditioned to have a higher stroke volume, so requires fewer contractions to circulate the same volume of blood. The third, sick sinus syndrome, covers conditions that include severe sinus bradycardia, sinoatrial block, sinus arrest, and bradycardia-tachycardia syndrome (atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia).
The most common cause of cardiac syncope is cardiac arrhythmia (abnormal heart rhythm) wherein the heart beats too slowly, too rapidly, or too irregularly to pump enough blood to the brain. Some arrhythmias can be life-threatening. Two major groups of arrhythmias are bradycardia and tachycardia. Bradycardia can be caused by heart blocks.
Knockdown of desmcollin-2 caused malformations in desmosomal plaques and bradycardia, dilation of the ventricular chamber and reduced fractional shortening.
Common side effects of one ChEI include insomnia, nausea and vomiting, accidental injury, headache, dizziness, bradycardia, hypotension, ecchymosis, and sleep disturbance.
By convention, a heart rate of less than 60 beats per minute in the adult patient is called bradycardia. Not all instances of bradycardia require medical treatment. Normal heart rate varies substantially between individuals, and many athletes in particular have a relatively slow resting heart rate. In addition, the heart rate is known to naturally slow with age.
Defibrillation or cardioversion may be accomplished by an implantable cardioverter-defibrillator (ICD). Electrical treatment of arrhythmias also includes cardiac pacing. Temporary pacing may be necessary for reversible causes of very slow heartbeats, or bradycardia (for example, from drug overdose or myocardial infarction). A permanent pacemaker may be placed in situations where the bradycardia is not expected to recover.
People with third-degree AV block typically experience severe bradycardia (an abnormally low measured heart rate), hypotension, and at times, hemodynamic instability.
Cardiovascular effects include hypotension, bradycardia, arrhythmias, and/or cardiac arrest – some of which may be due to hypoxemia secondary to respiratory depression.
Hubert Von Luschka at whonamedit.com Gross total resection of tumours that extend through foramen of Lushka is sometimes not possible due to bradycardia.
Phenylephrine may cause side effects such as headache, reflex bradycardia, excitability, restlessness and cardiac arrhythmias. Phenylephrine is not suggested for use in patients with hypertension.
Possible side effects include cardiac effects such as bradycardia and QT interval prolongation. Also, possible central nervous system toxicity has been shown in animal studies.
An overdose of Prajmaline is possible. The range of symptoms seen during a Prajmaline overdose include: no symptoms, nausea/vomiting, bradycardia, tachycardia, hypotension, and death.
They can be used to treat hearts that are classified as either a tachycardia that beats too fast, or a bradycardia that beats too slow.
The decreased heart rate can cause a decreased cardiac output resulting in symptoms such as lightheadedness, dizziness, hypotension, vertigo, and syncope. The slow heart rate may also lead to atrial, junctional, or ventricular ectopic rhythms. Bradycardia is not necessarily problematic. People who regularly practice sports may have sinus bradycardia, because their trained hearts can pump enough blood in each contraction to allow a low resting heart rate.
Glycopyrronium was first used in 1961 to treat peptic ulcers. Since 1975, intravenous glycopyrronium has been used before surgery to reduce salivary, tracheobronchial, and pharyngeal secretions. It is also used in conjunction with neostigmine, a neuromuscular blocking reversal agent, to prevent neostigmine's muscarinic effects such as bradycardia. It can be administered to raise the heart rate in bradycardia, which often will also increase the blood pressure.
Also Beta-receptor antagonists should be avoided in patients with AV node dysfunction and/or patients on other medications which might cause bradycardia (i.e. calcium channel blockers). The potential for these contraindications and drug-drug interaction could lead to asystole and cardiac arrest. Certain calcium channel blocker should be avoided with some beta-receptor blockers since they may cause severe bradycardia and other potential side effects.
The treatment of bradycardia is dependent on whether or not the person is stable or unstable. If oxygen saturations are low, supplemental oxygen should be provided.
Retrieved on February 6, 2007. In the case of epidural hematoma in the posterior cranial fossa, tonsillar herniation causes Cushing's triad: hypertension, bradycardia, and irregular breathing.
It is characterized by an abrupt decrease in cardiac output and loss of consciousness due to a transient arrhythmia; for example, bradycardia due to complete heart block.
Highly trained athletes may also have athletic heart syndrome, a very slow resting heart rate that occurs as a sport adaptation and helps prevent tachycardia during training. The term "relative bradycardia" is used to refer to a heart rate that, although not actually below 60 BPM, is still considered too slow for the individual's current medical condition. The word "bradycardia" is from the Greek βραδύς bradys "slow", and καρδία kardia "heart".
A small fetomaternal hemorrhage could cause an increase in maternal antigens, while a large fetomaternal hemorrhage could cause fetal anemia and death. Fetal bradycardia, low heart rate, is another complication that may occur. Most cases of fetal bradycardia are self-resolved within five minutes. The complication of infection has a low incidence rate, and preventative measures are implemented against the risk of infection, such as antibiotic usage and the aseptic technique.
If untreated, arrhythmias may present as bradycardia, tachycardia, or progress to atrial/ventricular fibrillation.Katzung, Bertram G.; Masters, Susan B.; Trevor, Anthony J. (2009). Basic and Clinical Pharmacology. 11th ed.
Illustration comparing the EKGs of a healthy person (top) and a person with bradycardia (bottom): The points on the heart where the EKG signals are measured are also shown.
AM-2201 produces bradycardia and hypothermia in rats at doses of 0.3–3 mg/kg, comparable to the potency of JWH-018 in rats, suggesting potent cannabinoid-like activity.
Mild symptoms include nausea, flushing, tiredness. Neurologic symptoms are seen most commonly including decreased deep tendon reflexes. Severe symptoms include paralysis, respiratory failure, and bradycardia progressing to cardiac arrest.
There is very little formal, modern published information on the pharmacological actions of cerberin. One primary source reports that its ingestion results in electrocardiogram (ECG) changes, such as various types of bradycardia (e.g., sinus bradycardia), AV dissociation, and junctional rhythms; second-degree sinoatrial block and nodal rhythm are also described. In the case of digitalis administration, ST depression or T wave inversion may occur without indicating toxicity; however, PR interval prolongation indicate toxicity.
This ECG from the same patient shows atrial fibrillation at around 126 beats per minute. Sick sinus syndrome (SSS), is a group of abnormal heart rhythms (arrhythmias) presumably caused by a malfunction of the sinus node, the heart's primary pacemaker. Tachycardia-bradycardia syndrome is a variant of sick sinus syndrome in which the arrhythmia alternates between slow and fast heart rates. Tachycardia-bradycardia syndrome is often associated with ischemic heart disease and heart valve disease.
As stated above, overdosage of tacrine may give rise to severe side effects such as nausea, vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Atropine is a popular treatment for overdose.
It can result in many abnormal heart rhythms (arrhythmias), including sinus arrest, sinus node exit block, sinus bradycardia, and other types of bradycardia (slow heart rate). Sick sinus syndrome may also be associated with tachycardias (fast heart rate) such as atrial tachycardia (PAT) and atrial fibrillation. Tachycardias that occur with sick sinus syndrome are characterized by a long pause after the tachycardia. Sick sinus syndrome is also associated with azygos continuation of interrupted inferior vena cava.
The US Centers for Disease Control and Prevention reported in 2011 that 15.2% of adult males and 6.9% of adult females had clinically-defined bradycardia (a resting pulse rate below 60 BPM).
A common side effect during IV administration is reflex bradycardia. The low concentration eye drops do not cause blood pressure changes and the changes with the higher dose drops do not last long.
Cardiovascular effects include hypotension, bradycardia, arrhythmias, and/or cardiac arrest – some of which may be due to hypoxemia secondary to respiratory depression.Rossi S, editor. Australian Medicines Handbook 2006. Adelaide: Australian Medicines Handbook; 2006.
Heart related causes may include an abnormal heart rhythm, problems with the heart valves or heart muscle and blockages of blood vessels from a pulmonary embolism or aortic dissection among others.Syncope from bradycardia.
Typically, tachycardic-generated syncope is caused by a cessation of beats following a tachycardic episode. This condition, called tachycardia-bradycardia syndrome, is usually caused by sinoatrial node dysfunction or block or atrioventricular block.
For infants, bradycardia is defined as a heart rate less than 100 BPM (normal is around 120–160 BPM) . Premature babies are more likely than full-term babies to have apnea and bradycardia spells; their cause is not clearly understood. The spells may be related to centers inside the brain that regulate breathing which may not be fully developed. Touching the baby gently or rocking the incubator slightly will almost always get the baby to start breathing again, which increases the heart rate.
The dose of local anesthesia is often reduced when a patient has any systemic health implications or habits which may cause an interference. From time to time the local anaesthetic itself should be reduced (therefore reducing the maximum dose). This is particularly done when alcoholism, anaemia (if using Prilocaine), anorexia, bradycardia or GORD is concerned. On other occasions the vasoconstrictor used (often adrenaline) must be reduced when an individual suffers from angina, bradycardia, chronic bronchitis, cardia disarrhythmia, COPD or glaucoma.
Bradycardia was defined as a heart rate less than 60 beats per minute when textbooks asserted that the normal range for heart rates was 60–100 bpm. The normal range has since been revised in textbooks to 50–90 bpm for a human at total rest. Setting a lower threshold for bradycardia prevents misclassification of fit individuals as having a pathologic heart rate. The normal heart rate number can vary as children and adolescents tend to have faster heart rates than average adults.
The spleen contracts in response to lowered levels of oxygen and increased levels of carbon dioxide, releasing red blood cells and increasing the oxygen capacity of the blood. This may start before the bradycardia.
Side effects of ergotamine include nausea and vomiting. At higher doses, it can cause raised arterial blood pressure, vasoconstriction (including coronary vasospasm) and bradycardia or tachycardia. Severe vasoconstriction may cause symptoms of intermittent claudication.
2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 1730 The toxic effects to humans following on amitraz-uptake include loss of consciousness, vomiting, respiratory failure, miosis, hypothermia, bradycardia, hyperglycemia and central nervous system depression.
Sinus bradycardia can also be an adaptive advantage; for example, diving seals may have a heart rate as low as 12 beats per minute, helping them to conserve oxygen during long dives. Sinus bradycardia is a common condition found in both healthy individuals and those who are considered well conditioned athletes. Heart rates considered bradycardic vary by species; for example, in the common housecat, a rate of under 120 beats per minute is abnormal. Generally, smaller species have higher heart rates while larger species have lower rates.
Contraindications to ticagrelor are active bleeding, increased risk of bradycardia, concomitant therapy of ticagrelor and strong cytochrome P-450 3A (CYP3A4) inhibitors and moderate or severe hepatic impairment due to the risk of increased exposure to ticagrelor.
Isoprenaline, or isoproterenol, is a medication used for the treatment of bradycardia (slow heart rate), heart block, and rarely for asthma. It is a non-selective β adrenoreceptor agonist that is the isopropylamine analog of epinephrine (adrenaline).
Symptoms typically occur between thirty minutes and four hours after ingestion and include nausea and vomiting, abdominal pain, numbness, headache, sweating, muscle weakness, bradycardia, hypotension, cardiac arrhythmia, and seizures. Treatment for poisoning includes gastrointestinal decontamination with activated charcoal followed by supportive care including antiemetics for persistent nausea and vomiting, along with atropine for treatment of bradycardia and fluid replacement and vasopressors for the treatment of hypotension. The toxins are only produced during active growth. In the winter months, the plant degrades and metabolizes most of its toxic alkaloids.
Hypotension is corrected with fluid replacement, although catecholamines such as norepinephrine or dopamine may be required to increase blood pressure. Bradycardia is treated with atropine or an infusion of norepinephrine to increase coronary blood flow and heart rate.
Labetalol is contraindicated in people with overt cardiac failure, greater-than-first-degree heart block, severe bradycardia, cardiogenic shock, severe hypotension, anyone with a history of obstructive airway disease including asthma, and those with hypersensitivity to the drug.
In June 2003, doctors implanted a pacemaker into Voinovich's heart because his heart rate had slowed down due to progressive sinus bradycardia. Voinovich died in his sleep in Cleveland on June 12, 2016, at the age of 79.
The symptoms of a cholinergic toxidrome include bronchorrhea, confusion, defecation, diaphoresis, diarrhea, emesis, lacrimation, miosis, muscle fasciculations, salivation, seizures, urination, and weakness. Complications include bradycardia, hypothermia, and tachypnea. Substances that may cause this toxidrome include carbamates, mushrooms, and organophosphates.
Hayes D. L. "Advances in pacing therapy for bradycardia". International Journal of Cardiology. 32 (1991) 183-196 Future pacemakers that adaptively respond to physiological requirements are being developed in order to negate the limitations observed with their current use.
Symptoms of overdose are due to excessive pharmacodynamic actions on β1 and also β2-receptors. These include bradycardia (slow heartbeat), severe hypotension with shock, acute heart failure, hypoglycemia and bronchospastic reactions. Treatment is largely symptomatic. Hospitalization and intensive monitoring is indicated.
Huperzine A may have additive effects if taken with drugs causing bradycardia, such as beta-blockers. which may decrease heart rate. Theoretically, there may be possible additive cholinergic effects if huperzine A is taken with other acetylcholinesterase inhibitors or cholinergic agents.
Athlete's heart most often does not have any physical symptoms, although an indicator would be a consistently low resting heart rate. Athletes with AHS often do not realize they have the condition unless they undergo specific medical tests, because athlete's heart is a normal, physiological adaptation of the body to the stresses of physical conditioning and aerobic exercise. People diagnosed with athlete's heart commonly display three signs that would usually indicate a heart condition when seen in a regular person: bradycardia, cardiomegaly, and cardiac hypertrophy. Bradycardia is a slower than normal heartbeat, at around 40–60 beats per minute.
Bradycardia may be associated with medical conditions such as hypothyroidism. Trained athletes tend to have slow resting heart rates, and resting bradycardia in athletes should not be considered abnormal if the individual has no symptoms associated with it. For example, Miguel Indurain, a Spanish cyclist and five time Tour de France winner, had a resting heart rate of 28 beats per minute, one of the lowest ever recorded in a healthy human. Daniel Green achieved the world record for the slowest heartbeat in a healthy human with a heart rate of just 26 bpm in 2014.
The symptoms of an opiate toxidrome include the classic triad of coma, pinpoint pupils, and respiratory depression as well as altered mental states, shock, pulmonary edema and unresponsiveness. Complications include bradycardia, hypotension, and hypothermia. Substances that may cause this toxidrome are opioids.
J. Hay. Bradycardia and cardiac arrhythmia produced by depression of certain of the functions of the heart. The Lancet 1906, 1: 139–143. In 1907 he was appointed Assistant Physician and set up the first specialised heart department in the north of England.
Clonidine has some role in the treatment of spasticity, acting principally by inhibiting excessive sensory transmission below the level of injury. Its use however is mainly as a second or third line agent, due to side effects such as hypotension, bradycardia and drowsiness.
However, those with CPVT may develop a less serious heart rhythm disturbance called atrial fibrillation, which can be detected on examination as an irregular pulse. Furthermore, approximately 20% of those with CPVT have a slow resting heart rate known as a sinus bradycardia.
Exercise training may decrease cardiovascular mortality and sudden cardiac death. Regular exercise training is also thought to modify cardiac autonomic control. Individuals who exercise regularly have a 'training bradycardia' (i.e., low resting heart rate) and generally have higher HRV than sedentary individuals.
Side effects are similar to other angiotensin II receptor antagonists and include tachycardia and bradycardia (fast or slow heartbeat), hypotension (low blood pressure) and edema (swelling of arms, legs, lips, tongue, or throat, the latter leading to breathing problems). Allergic reactions may also occur.
Theoretical treatment with lipid emulsion therapy has been considered in severe cases, but is not yet standard of care. Caution should be taken when using verapamil with a beta blocker due to the risk of severe bradycardia. If unsuccessful, ventricular pacing should be used.
Treatment of poisoning is mainly supportive. All patients require close monitoring of blood pressure and cardiac rhythm. Gastrointestinal decontamination with activated charcoal can be used if given within one hour of ingestion. The major physiological antidote is atropine, which is used to treat bradycardia.
Much can be learned by observing the QRS morphology (named for the respective portions of the polarization/repolarization waveform of the wave, P,Q,R,S,T wave). Rhythm abnormalities can also be visualized as in slow heart rate bradycardia, or fast heart rate tachycardia.
Treatment of poisoning is mainly supportive. All patients require close monitoring of blood pressure and cardiac rhythm. Gastrointestinal decontamination with activated charcoal can be used if given within one hour of ingestion. The major physiological antidote is atropine, which is used to treat bradycardia.
It is only when bradycardia presents with signs and symptoms of shock that it requires emergency treatment with transcutaneous pacing. False capture with visible phantom beats Some common causes of hemodynamically significant bradycardia include myocardial infarction, sinus node dysfunction and complete heart block. Transcutaneous pacing is no longer indicated for the treatment of asystole (cardiac arrest associated with a "flat line" on the ECG), with the possible exception of witnessed asystole (as in the case of bifascicular block that progresses to complete heart block without an escape rhythm). During transcutaneous pacing, pads are placed on the patient's chest, either in the anterior/lateral position or the anterior/posterior position.
The increased respiratory and cardiac workload causes increased blood flow to the cardiac and respiratory muscles. Stroke volume is not greatly affected by immersion or variation in ambient pressure, but bradycardia reduces the overall cardiac output, particularly due to the diving reflex in breath-hold diving.
The side effects of nicergoline are usually limited to nausea, hot flushes, mild gastric upset, hypotension and dizziness. At high drug dosages, bradycardia, increased appetite, agitation, diarrhea and perspiration were reported. Most of the available literature suggests that the side effects of nicergoline are mild and transient.
A resting heart that beats slower than 60 beats per minute, or faster than 100 beats per minute, is regarded as having an arrhythmia. A heartbeat slower than 60 beats per minute is known as bradycardia, and a heartbeat faster than 100 is known as a tachycardia.
Contraindications of Combigan include the following: reactive airway disease including bronchial asthma, a history of bronchial asthma, severe chronic obstructive pulmonary disease, sinus bradycardia, secondary or third degree atrioventricular block, overt cardiac failure, cardiogenic shock, age less than 2 years, and hypersensitivity to any component of Combigan.
On land, the American mink moves by a bounding gait, with speeds of up to . It also climbs trees and swims well. During swimming, the mink propels itself primarily through undulating movements of the trunk. When diving, it undergoes bradycardia, which is likely an adaptation to conserve oxygen.
Hampton, J. P. (2011). Rapid- sequence intubation and the role of the emergency department pharmacist. American Journal of Health-System Pharmacy, 68(14), 1320–1330. doi:10.2146/ajhp100437 Atropine may also be used as a premedication agent in pediatrics to prevent bradycardia caused by hypoxia, laryngoscopy, and succinylcholine.
Cardiovascular features include hypotension, sinus bradycardia, and ventricular arrhythmias. Other features may include sweating, dizziness, difficulty in breathing, headache, and confusion. The main causes of death are ventricular arrhythmias and asystole, paralysis of the heart or of the respiratory center. The only post-mortem signs are those of asphyxia.
The sensation of palpitations can arise from extra-systoles or tachyarrhythmia. It is very rarely noted due to bradycardia. Palpitations can be described in many ways. The most common descriptions include a flip-flopping in the chest, a rapid fluttering in the chest, or pounding in the neck.
It is contraindicated if there has been a past history of angioedema; heart conduction disorders (e.g. sick sinus syndrome, second- or third-degree heart block); bradycardia; severe heart failure or coronary artery disease. Also: Raynaud's syndrome, intermittent claudication, epilepsy, depression, Parkinson's disease, glaucoma. Use in pregnancy is discouraged.
Cardiovascular features include hypotension, sinus bradycardia, and ventricular arrhythmias. Other features may include sweating, dizziness, difficulty in breathing, headache, and confusion. The main causes of death are ventricular arrhythmias and asystole, paralysis of the heart or of the respiratory center. The only post-mortem signs are those of asphyxia.
Drawing of an inverted uterus Uterine inversion is often associated with significant postpartum bleeding. Traditionally it was thought that it presented with haemodynamic shock "out of proportion" with blood loss, however blood loss has often been underestimated. The parasympathetic effect of traction on the uterine ligaments may cause bradycardia.
Observations on seals diving unrestricted in open water indicate that bradycardia is not as common as laboratory work suggested. It appears that the animals respond differently to voluntary immersion compared to forced immersion, and when forced underwater and unable to predict the length of a dive, the seal would go into emergency response against asphyxia with a strong bradycardia response. When the dive was at the option of the seal, the response was proportional to the time the seal intended to dive, and would generally remain in aerobic metabolism, which would require a far shorter recovery time and allow repeat dives after a short surface interval. Anticipatory tachycardia shortly before surfacing was also reported on voluntary dives.
The syndrome clinically presents as acute refractory bradycardia that leads to asystole, in the presence of one or more of the following conditions; metabolic acidosis, rhabdomyolysis, hyperlipidemia, and enlarged liver. The association between PRIS and Propofol infusions is generally noted at infusions higher than 4 mg.kg for greater than 48 hours.
The decrease in heart rate directly impacts aortic flow. Bradycardia caused by xylazine administration is effectively prevented by administration of atropine or glycopyrrolate. Arrhythmias associated with xylazine includes other symptoms such as sinoatrial block, atrioventricular block, A-V dissociation, and sinus arrhythmia. Xylazine administration can lead to diabetes mellitus and hyperglycemia.
Unfortunately, this immobilization technique is potentially life-threatening for mammals (but not for reptiles). Mammals would undergo states of bradycardia or hypoxia as an over-activation of parasympathetic vagus system. The organs of the oxygen- hungry mammal are deprived of oxygen due to lack of blood flow, and the animal dies.
The most common side effects are drowsiness, incoherence, hallucinations, convulsions, slow heart rate (reflex bradycardia). Fear, anxiety, restlessness, tremor, insomnia, confusion, irritability, and psychosis. Nausea, vomiting, reduced appetite, urinary retention, dyspnea, weakness. Potentially fatal reactions are due to atrioventricular block, central nervous system stimulation, cerebral hemorrhage, pulmonary edema, and ventricular arrhythmias.
During clinical trials fingolimod gave rise to side effects such as hypertension and bradycardia, macular edema, elevated liver enzymes or reduction in lymphocite levels. Teriflunomide is considered a very safe drug. Nevertheless, there have been reports of liver failure, and PML. Teriflunomide is also known to be dangerous for fetal development.
This test requires the intravenous administration of edrophonium chloride or neostigmine, drugs that block the breakdown of acetylcholine by cholinesterase (acetylcholinesterase inhibitors). This test is no longer typically performed, as its use can lead to life-threatening bradycardia (slow heart rate) which requires immediate emergency attention. Production of edrophonium was discontinued in 2008.
A diagnosis of bradycardia in adults is based on a heart rate less than 60 BPM, although some studies use a heart rate of less than 50 BPM. This is determined usually either by palpation or EKG. If symptoms occur, a determination of electrolytes may be helpful in determining the underlying cause.
All patients require close monitoring of blood pressure and cardiac rhythm. Gastrointestinal decontamination with activated charcoal can be used if given within one hour of ingestion. The major physiological antidote is atropine, which is used to treat bradycardia. Other drugs used for ventricular arrhythmia include lidocaine, amiodarone, bretylium, flecainide, procainamide, and mexiletine.
While epinephrine is often used to treat cardiac arrest, it has not been shown to improve long-term survival or mental function after recovery. It does, however, improve return of spontaneous circulation. When used intravenously, epinephrine is typically given every three to five minutes. Epinephrine infusions may also be used for symptomatic bradycardia.
The vasoconstriction causes a large increase in resistance to flow, and is compensated by a proportional reduction of heart rate to maintain a suitable blood pressure sufficient to provide the reduced circulation. A bulbous enlargement of the ascending aorta in seals has elastic walls and contributes to maintaining a sufficient diastolic pressure during bradycardia. The heart rate in seals may drop as low as 4 to 6 beats per minute to balance central arterial blood pressure with the large increase in peripheral vascular resistance. The bradycardia also contributes to a major reduction of cardiac workload, so that the reduced myocardial blood flow in diving seals is tolerable, and allows the heart to function in anaerobic metabolism without evidence of myocardial dysfunction.
Perfusion of organs during bradycardia and peripheral vasoconstriction in forced submersions of ducks has shown similar findings to seals, confirming redistribution of blood flow to essentially the brain, heart, and andadrenal glands. Heart rate during a free dive decreases from the pre-dive level, but does not usually drop below the resting heart rate. In free-diving cormorants, heart rate dropped at the start of the dive, and usually stabilized at depth, but increased again at the start of ascent, with average heart rates during the dive much the same as at rest, but the variation in heart rate and vasoconstriction varies considerably between species, and true bradycardia occurs in emperor penguins on long duration dives. Birds display complex cardiovascular responses during free dives.
Common adverse effects in studies were temporary bradycardia (slow heartbeat), usually at the beginning of the treatment, dyspnoea (breathing difficulties), and increased liver enzymes (without symptoms). No significant increase of infections was observed under ponesimod therapy. QT prolongation is detectable but was considered to be too low to be of clinical importance in a study.
In C. Stein, A. Stracciolini, & K. Ackerman (Eds.), The young female athlete (p. 64). Switzerland, Springer International Publishing. Affected athletes may also struggle with low self-esteem and depression. Upon physical examination, a physician may also note the following symptoms: elevated carotene in the blood, anemia, orthostatic hypotension, electrolyte irregularities, hypoestrogenism, vaginal atrophy, and bradycardia.
The scorpion is venomous, but much less toxic than others of its genus. Its venom is neurotoxic and cardiotoxic, causing the release of catecholamines. Local effects from the sting can include pain, redness, itching, and swelling. The venom can produce cardiac effects such as arrhythmia, pulmonary edema, tachycardia or bradycardia, and hyper- or hypotension.
Adequate iodine intake is necessary for the production of thyroid hormone. According to Payton R. G. et al., a common disorder of the thyroid gland is hypothyroidism, which is more prevalent in women than in men. Symptoms of hypothyroidism include cold intolerance, weight gain, fatigue, anemia, difficulty concentrating, amenorrhea, bradycardia (low heart rate) and goiter.
Treatment for autonomic dysfunction varies greatly on the severity of the dysfunction and the type. Many patients with ROHHAD experience strabismus, which is a weakness in eye muscle causing a "cross- eyed" effect. This can be treated with glasses, eye muscle exercises, or even surgery. ROHHAD patients also often experience bradycardia, or low heart rate.
Use of pilocarpine may result in a range of adverse effects, most of them related to its non-selective action as a muscarinic receptor agonist. Pilocarpine has been known to cause excessive salivation, sweating, bronchial mucus secretion, bronchospasm, bradycardia, vasodilation, and diarrhea. Eye drops can result in brow ache and chronic use in miosis.
The N/OFQ-NOP system has also been implicated in control of the cardiovascular system, as nociceptin administration has led to high blood pressure and bradycardia. Nociceptin has significant effects on cardiovascular parameters such as blood pressure and heart rate that vary by species, as it is excitatory for rodents yet inhibitory for sheep.
Overdosing of up to 80 times the usual therapeutic dose has been described. Expected symptoms include severe hypotension (low blood pressure) and reflex tachycardia. Bradycardia (slow heartbeat) can also occur due to blockage of calcium channels in the atrioventricular node of the heart. There is no treatment besides monitoring blood pressure and heart function.
Leaf or flower consumption of R. arborescens results in drooling and a blazing sensation in the mouth. This is supplemented with emesis, diarrhea, muscular weakness and weak vision. Other lethal cardiovascular effects include bradycardia, hypotension, and atrioventricular block. Dyspnea, and prostration may develop and someone may die in the span of one to two days.
If a person is unstable, the initial recommended treatment is intravenous atropine. Doses less than 0.5 mg should not be used, as this may further decrease the rate. If this is not effective, intravenous inotrope infusion (dopamine, epinephrine) or transcutaneous pacing should be used. Transvenous pacing may be required if the cause of the bradycardia is not rapidly reversible.
The initial signs are gastrointestinal, including nausea, vomiting, and diarrhea. This is followed by a sensation of burning, tingling, and numbness in the mouth and face, and of burning in the abdomen. In severe poisonings, pronounced motor weakness occurs and cutaneous sensations of tingling and numbness spread to the limbs. Cardiovascular features include hypotension, sinus bradycardia, and ventricular arrhythmias.
Potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel 4 is a protein that in humans is encoded by the HCN4 gene. There are four HCN channels. HCN4 is prominently expressed in the pace maker region of the mammalian heart. Some humans with bradycardia and Sick sinus syndrome have been shown to have mutations in their HCN4 gene.
There is no absolute contraindication to the use of dexmedetomidine. It has a biphasic effect on blood pressure with lower readings at lower drug concentrations and higher readings at higher concentrations. Rapid IV administration or bolus has been associated with hypertension due to peripheral α2-receptor stimulation. Bradycardia can be a limiting factor with infusions especially in higher doses.
Heart block comes in varying degrees and severity. It may be caused by reversible poisoning of the AV node (with drugs that impair conduction) or by irreversible damage to the node. Bradycardias may also be present in the normally functioning heart of endurance athletes or other well- conditioned persons. Bradycardia may also occur in some types of seizures.
An arrhythmia can present itself as either bradycardia or tachycardia. Untreated arrhythmias may progress to atrial fibrillation or ventricular fibrillation. Treatment is aimed at normalizing cardiac rhythm by altering ion flow across the membrane. Antiarrhythmic agents can reduce arrhythmia related symptoms such as palpitations or syncope; however, they often have a narrow therapeutic index and can also be proarrhythmic.
OT can modify heart rates and cause excessive fluid intake (antidiuretic effect). Intravenous infusion (IV) of oxytocin is often used to induce labor and enhance milk lactation during postpartum care. IV use can cause side-effects such as cardiovascular manifestations in the form of tachycardia and bradycardia. In addition, nausea, vomiting, and headaches can occur with IV application.
Sick sinus syndrome, a sinus node dysfunction, causing alternating bradycardia and tachycardia. Often there is a long pause (asystole) between heartbeats. Adams-Stokes syndrome is a cardiac syncope that occurs with seizures caused by complete or incomplete heart block. Symptoms include deep and fast respiration, weak and slow pulse and respiratory pauses that may last for 60 seconds.
These most often occur years after the development of ptosis and ophthalmoplegia. Atrioventricular (abbreviated "AV") block is the most common cardiac conduction deficit. This often progresses to a Third-degree atrioventricular block, which is a complete blockage of the electrical conduction from the atrium to the ventricle. Symptoms of heart block include syncope, exercise intolerance, and bradycardia.
Combination products are also available with paracetamol (acetaminophen), ibuprofen, naloxone, and aspirin. Common side effects include euphoria, constipation, nausea, vomiting, loss of appetite, drowsiness, dizziness, itching, dry mouth, and sweating. Severe side effects may include addiction, dependence, hallucinations, respiratory depression (a reduction in breathing), bradycardia, and low blood pressure. Those allergic to codeine may also be allergic to oxycodone.
Severely high hypernatremia may lead to fibrillation, which may cause CO to cease. Severe hyponatremia leads to both bradycardia and other arrhythmias. Hypokalemia (low potassium levels) also leads to arrhythmias, whereas hyperkalemia (high potassium levels) causes the heart to become weak and flaccid, and ultimately to fail. Heart muscle relies exclusively on aerobic metabolism for energy.
Pilsicainide is a drug used clinically in Japan to treat cardiac arrhythmias. A cardiac arrhythmia includes any abnormal heartbeat and can be manifested as tachycardia, bradycardia, or other irregular rhythms. Pilsicainide has been proven successful in treating both ventricular and supraventricular arrhythmias with few adverse effects. It is especially effective in the treatment of atrial fibrillation.
The U.S. Food and Drug Administration (FDA) and international health authorities have published an alert of galantamine based on data from two studies during the treatment for mild cognitive impairment (MCI); higher mortality rates were seen in drug-treated patients. On April 27, 2006, FDA approved labeling changes concerning all form of galantamine preparations (liquid, regular tablets, and extended release tablets) warning of the risk of bradycardia (slow resting heart rate), and sometimes atrioventricular block, especially in predisposed persons. At the same time, the risk of syncope (fainting) seems to be increased relative to placebo. "In randomized controlled trials, bradycardia was reported more frequently in galantamine-treated patients than in placebo-treated patients, but was rarely severe and rarely led to treatment discontinuation" These side effects have not been reported in Alzheimer's Disease related studies.
The large difference in oxygen affinity between hemoglobin and myoglobin does not allow transfer of oxygen from muscle stores to blood for uses in other tissues, so for a dive to be fully aerobic, the blood flow to working muscles must be restricted so the oxygen on the myoglobin can be used locally, keeping the hemoglobin supplies for the vital organs, particularly the brain. this requires peripheral vasoconstriction which necessitates some degree of bradycardia. On an intentionally long dive, circulation will be shut off to the muscles and viscera from the start of the dive, with profound bradycardia, and the blood oxygen is effectively reserved for the brain. The muscles use the oxygen from myoglobin, then switch to anaerobic metabolism, the same system used by seals on forced dives.
Normal sinus rhythm, with solid black arrows pointing to normal P waves representative of normal sinus node function, followed by a pause in sinus node activity (resulting in a transient loss of heart beats). Note that the P wave that disrupts the pause (indicated by the dashed arrow) does not look like the previous (normal) P waves -- this last P wave is arising from a different part of the atrium, representing an escape rhythm. A slow rhythm (less than 60 beats/min) is labelled bradycardia. This may be caused by a slowed signal from the sinus node (sinus bradycardia), by a pause in the normal activity of the sinus node (sinus arrest), or by blocking of the electrical impulse on its way from the atria to the ventricles (AV block or heart block).
When the face is submerged and water fills the nostrils, sensory receptors sensitive to wetness within the nasal cavity and other areas of the face supplied by the fifth (V) cranial nerve (the trigeminal nerve) relay the information to the brain. The tenth (X) cranial nerve, (the vagus nerve) - part of the autonomic nervous system - then produces bradycardia and other neural pathways elicit peripheral vasoconstriction, restricting blood from limbs and all organs to preserve blood and oxygen for the heart and the brain (and lungs), concentrating flow in a heart–brain circuit and allowing the animal to conserve oxygen. In humans, the diving reflex is not induced when limbs are introduced to cold water. Mild bradycardia is caused by subjects holding their breath without submerging the face in water.
In tests, minor cardiac arrhythmias occurred slightly more often in cooled infants, however the effect was not unexpected because mild sinus bradycardia is known to be associated with hypothermia. In tests, all cases were resolved with appropriate therapy. The cold cap system also increased the incidence of scalp edema; however, all cases were resolved prior to or after completion of treatment.
The reflex can be blocked by intravenous injection of an anti-muscarinic acetylcholine (ACh) antagonist, such as atropine or glycopyrrolate. If bradycardia does occur, removal of the stimulus is immediately indicated. This often results in the restoration of normal sinus rhythm of the heart. If not, the use of atropine or glycopyrrolate will usually be successful and permit continuation of the surgical procedure.
In humans, the symptoms of poisoning normally appear between 30 minutes and three hours after exposure. Initial symptoms typically include nausea, vomiting, and abdominal pain; sweating, confusion, and agitation follow. In significant poisoning, cardiac abnormalities including tachycardia or bradycardia, hypotension, and ECG changes develop. Neurological effects include muscle twitching and seizures; consciousness becomes progressively impaired after a few hours leading to coma.
Celivarone is an experimental drug being tested for use in pharmacological antiarrhythmic therapy. Cardiac arrhythmia is any abnormality in the electrical activity of the heart. Arrhythmias range from mild to severe, sometimes causing symptoms like palpitations, dizziness, fainting, and even death. They can manifest as slow (bradycardia) or fast (tachycardia) heart rate, and may have a regular or irregular rhythm.
Usually the seals use an intermediate process, where the most active muscles are shut off from circulation and use locally stored oxygen to avoid compromising the blood oxygen stores, which requires a limited degree of bradycardia to compensate for the increased peripheral vascular restriction, which makes attempts to calculate ADL impracticable, even if the available oxygen stores are accurately assessed.
They were large, streamlined, flightless birds with teeth for grasping slippery prey. Today, cormorants, loons, and grebes are the major groups of foot propelled diving birds. Other diving birds are wing-propelled, most notably the penguins, dippers and auks. A rapid onset bradycardia has been observed in diving birds during forced submersion,including penguins, cormorants, guillemots, puffins, and rhinoceros auklets.
The observed toxic dose in about 50% of these patients has been 0.3 g to 1.25 g of 12.5% amitraz formulations and 0.5 to 2 g of 20% formulations. The remaining patients took doses up to 10 g. Other frequently occurring symptoms after massive amitraz intoxication are CNS depression, respiratory depression, miosis, hypothermia, hyperglycemia, loss of consciousness, vomiting and bradycardia.
Vagotonia is the state of the autonomic nervous system in which the equilibrium between the sympathetic and parasympathetic nervous system is biased towards the parasympathetic, the opposite phenomenon being sympatheticotonia. There is an associated clinical syndrome with low blood pressure (hypotension), low heart rate (bradycardia), miosis, often cold hands and feet, a cold and clammy diaphoresis, severe fatigue, and sometimes vasovagal syncope.
When breathing with the face submerged, the diving response increases proportionally to decreasing water temperature. However, the greatest bradycardia effect is induced when the subject is holding their breath with their face wetted. Apnea with nostril and facial cooling are triggers of this reflex. The diving response in animals, such as the dolphin, varies considerably depending on level of exertion during foraging.
Possible side effects include nausea, vomiting, abdominal pain, diarrhea, headache, dizziness, tinnitus, chest pain, palpitation, bradycardia, transient hypertension and other cardiac arrhythmias, dyspnea, rashes, and shock.Ergometrine drug information An overdose produces a characteristic poisoning, ergotism or "St. Anthony's fire": prolonged vasospasm resulting in gangrene and amputations; hallucinations and dementia; and abortions. Gastrointestinal disturbances such as diarrhea, nausea, and vomiting, are common.
According to the FDA, carvedilol should not be used in people with bronchial asthma or bronchospastic conditions. It should not be used in people with second- or third-degree AV block, sick sinus syndrome, severe bradycardia (unless a permanent pacemaker is in place), or a decompensated heart condition. People with severe hepatic impairment are also advised to not take carvedilol.
There is also a risk of anemia via lack of red blood cells. The drug can also damage nerves, causing peripheral neuropathy that may be irreversible. Thalidomide has several cardiovascular adverse effects, including risk of heart attacks, pulmonary hypertension, and changes in heart rhythm including syncope, bradycardia, and atrioventricular block. It can cause liver damage and severe skin reactions like Stevens–Johnson syndrome.
The resting 12-lead ECG is a useful test to differentiate CPVT from other electrical diseases of the heart that can cause similar abnormal heart rhythms. Unlike conditions such as long QT syndrome and Brugada syndrome, the resting 12-lead ECG in those with CPVT is generally normal. However, approximately 20% of those affected have a slow resting heart rate or sinus bradycardia.
Tachycardia is a high heart rate, defined as above 100 bpm at rest. Bradycardia is a low heart rate, defined as below 60 bpm at rest. During sleep a slow heartbeat with rates around 40–50 bpm is common and is considered normal. When the heart is not beating in a regular pattern, this is referred to as an arrhythmia.
There is no antidote for zygacine poisoning so only the symptoms arising from poisoning in humans are usually treated, of which bradycardia and hypotension are prioritized. These symptoms are initially treated with atropine, a muscarinic receptor agonist. In a case study in which atropine was not sufficient, hypotension and bradcycardia were successfully treated using dopamine.West, Patrick, and B. Zane Horowitz.
More than half of the patients had some reported adverse event and the rate was higher in patients who received a single 800 mg dose over patients who received 3 400 mg doses. The most common effect was asymptomatic bradycardia where patients heart rates fell below 60 Beats Per Minute. Other reported events include hypokalemia, elevated liver enzymes as well as anemia.
Neostigmine can induce generic ocular side effects including: headache, brow pain, blurred vision, phacodonesis, pericorneal injection, congestive iritis, various allergic reactions, and rarely, retinal detachment. Neostigmine will cause slowing of the heart rate (bradycardia); for this reason it is usually given along with a parasympatholytic drug such as atropine or glycopyrrolate. Gastrointestinal symptoms occur earliest after ingestion and include anorexia, nausea, vomiting, abdominal cramps, and diarrhea.
Widened pulse pressure (systolic - diastolic blood pressure), bradycardia, and irregular respiration would be alarming for Cushing's reflex, a sign of acutely elevated intracranial pressure. Photophobia is due to meningeal irritation. In severe cases, people may experience concomitant encephalitis (meningoencephalitis), which is suggested by symptoms such as altered mental status, seizures or focal neurologic deficits. Babies with viral meningitis may only appear irritable, sleepy or have trouble eating.
Conversely, parasympathetic activation leads to decreased cardiac output via decrease in heart rate, resulting in a tendency to lower blood pressure. By coupling sympathetic inhibition and parasympathetic activation, the baroreflex maximizes blood pressure reduction. Sympathetic inhibition leads to a drop in peripheral resistance, while parasympathetic activation leads to a depressed heart rate (reflex bradycardia) and contractility. The combined effects will dramatically decrease blood pressure.
These pauses in breathing may be accompanied by minor oxygen desaturation and bradycardia. It usually occurs when the infant is sleeping deeply, but may occur with light sleep or even when awake. Studies have shown that 78% of healthy full-term infants experience episodes of periodic breathing in the first two weeks of life, which typically resolves in the first six months of life.
Overdose of bisoprolol leads to fatigue, hypotension, low blood sugar, bronchospasms, and bradycardia. Bronchospasms and low blood sugar because at high doses drug can be an antagonist for β2 adrenergic receptors located in lung and in liver. Bronchospasm is due to blockage in lungs of β2 receptor and low blood sugar because of decreased stimulation of glycogenolysis and gluconeogenesis in the liver via β2 receptor.
Typically, acute hypoxia causes hyperventilation, bradycardia and an elevation in gill vascular resistance in teleosts. However, the benefit of these changes in blood pressure to oxygen uptake has not been supported in a recent study of the rainbow trout. It is possible that the acute hypoxia response is simply a stress response, and the advantages found in early studies may only result after acclimatization to the environment.
Clonidine also may cause bradycardia, probably by increasing signaling through the vagus nerve. When given intravenously, clonidine can temporarily increase blood pressure by stimulating α1 receptors in smooth muscles in blood vessels. This hypertensive effect is not usual when clonidine is given by mouth or by the transdermal route. Plasma concentration of clonidine exceeding 2.0 ng/mL does not provide further blood pressure reduction.
Excessive doses of metoprolol can cause severe hypotension, bradycardia, metabolic acidosis, seizures, and cardiorespiratory arrest. Blood or plasma concentrations may be measured to confirm a diagnosis of overdose or poisoning in hospitalized patients or to assist in a medicolegal death investigation. Plasma levels are usually less than 200 μg/l during therapeutic administration, but can range from 1–20 mg/l in overdose victims.
Hiroshi K, Makoto S, Kazuhide O, et al. On the ionic mechanism of cyproheptadine-induced bradycardia in a rabbit sinoatrial node preparation. European Journal of Pharmacology 1987; vol 139:307-313 The IUPAC name of AH-1058 is: 4-(5H-dibenzo[a,d]cyclohepten-5-ylidene)-1-[E-3-(3-methoxy-2-nitro) phenyl-2-propenyl]piperidine hydrochloride.Takahara A, Sugiyama A, Dohmoto H, et al.
Calls to US poison control centers related to e-cigarette exposures involved inhalations, eye exposures, skin exposures, and ingestion, in both adults and young children. Minor, moderate, and serious adverse effects involved adults and young children. Minor effects correlated with e-cigarette liquid poisoning were tachycardia, tremor, chest pain and hypertension. More serious effects were bradycardia, hypotension, nausea, respiratory paralysis, atrial fibrillation and dyspnea.
Symptoms of hypoestrogenism, whose severity will positively correlate with the duration of hypoestrogenism, will be present in FHA patients; these can can include lack of cervical mucus, pale areola and nipples, thinned, reddened vaginal and vestibular epithelium, and uterine hyperplasia, though FHA is not typically associated with hot flashes. FHA may present with weight loss, bradycardia, mottled, cool extremities, and/or yellowing of the skin.
Methacholine is primarily used to diagnose bronchial hyperreactivity, which is the hallmark of asthma and also occurs in chronic obstructive pulmonary disease. This is accomplished through the bronchial challenge test, or methacholine challenge, in which a subject inhales aerosolized methacholine, leading to bronchoconstriction. Other therapeutic uses are limited by its adverse cardiovascular effects, such as bradycardia and hypotension, which arise from its function as a cholinomimetic.
Oral or intravenous harmine doses ranging from 30–300 mg may cause agitation, bradycardia or tachycardia, blurred vision, hypotension, paresthesias. Serum or plasma harmine concentrations may be measured as a confirmation of diagnosis. The plasma elimination half-life is on the order of 1–3 hours.R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 727-728.
CardiacSense Ltd is a private limited company founded in 2009 as Sportracker. The company formerly developed a device for tracking heart rate readings during sports activities. In 2015 the company changed its name to CardiacSense and refocused activities on medical devices. CardiacSense’s devices monitor heart rate for the purpose of detecting heart disorders such as atrial fibrillation tachycardia, bradycardia, PVCs, PACs, Pause, LQT and cardiac arrest.
It is the snake responsible for more bites in the state of Bahia, the venom contains high fibrinolytic, proteolytic, hemorrhagic and edematogenic activity, and low coagulant activity, which can cause myonecrosis in humans. Symptoms include local pain, edema, erythema and ecchymosis (local symptoms) , hemorrhagic and coagulation symptoms, digestive disorders (nausea, vomiting and diarrhea), urinary disorders (oliguria, anuria, hematuria) with headaches, dizziness, hypotension, bradycardia, visual disturbances and tremors.
Chemical structure of atropine Patients with bradycardia are treated with atropine. Atropine is a muscarinic antagonist, which can obstruct the muscarinic receptor and acetylcholine cannot bind to the receptor for sustaining transmission of nerve signals to the heart through the parasympathetic nervous system. This allows an increase in heart rate. Hyperthermia, dilated pupils and dry mouth are side effects associated with the use of atropine.
An ECG showing digoxin toxicity with the classic "scooped out" ST segment In digoxin toxicity, the finding of frequent premature ventricular beats (PVCs) is the most common and the earliest dysrhythmia. Sinus bradycardia is also very common. In addition, depressed conduction is a predominant feature of digoxin toxicity. Other ECG changes that suggest digoxin toxicity include bigeminal and trigeminal rhythms, ventricular bigeminy, and bidirectional ventricular tachycardia.
However, other sinus rhythms can be entirely normal in particular patient groups and clinical contexts, so the term is sometimes considered a misnomer and its use is sometimes discouraged. Example of a sinus rhythm with bifascicular block. Other types of sinus rhythm that can be normal include sinus tachycardia, sinus bradycardia, and sinus arrhythmia. Sinus rhythms may be present together with various other cardiac arrhythmias on the same ECG.
The time depends on pulse rate, pulmonary function, RBC count, and other metabolic factors. Lidocaine can be given in 1.5 mg/kg IV a few minutes before sedation and paralysis. The purpose of administering lidocaine is to blunt the sympathetic response of an increased heart rate, blood pressure, and intracranial pressure caused by laryngoscopy. Atropine can be given when children produce a vagal response, evidenced by bradycardia, in response to intubation.
Romifidine is a drug that is used in veterinary medicine as a sedative mainly in large animals such as horses, although it may be used in a wide variety of species. It is not used in humans, but is closely related in structure to the commonly used drug clonidine. Romifidine acts as an agonist at the α2 adrenergic receptor subtype. Side effects can include bradycardia and respiratory depression.
An increase in heart rhythm is common during seizures. This type of epileptic seizure is known as ictal tachycardia, in which the subject's heart rate increase of more than 10 beats per minute of above the baseline. In comparison, ictal bradycardia causes epileptic discharges that disrupt the normal cardiac rhythm in a negative fashion. Slowing the heart beat down by more than 10 beats per minute below the average baseline.
Rose spots on abdomen of a person with typhoid fever Paratyphoid fever resembles typhoid fever. Infection is characterized by a sustained fever, headache, abdominal pain, malaise, anorexia, a nonproductive cough (in early stage of illness), a relative bradycardia (slow heart rate), and hepatosplenomegaly (an enlargement of the liver and spleen). About 30% of Caucasians develop rosy spots on the central body. In adults, constipation is more common than diarrhea.
Alinidine (ST567) is a negative chronotrope that was developed in the 1970s and 1980s. It causes bradycardia by inhibiting the pacemaker current by altering the maximal channel conductance and alter the voltage threshold.Snyders DJ, Van Bogaert P-P: Alinidine modifies the pacemaker current in sheep Purkinje fibers. Pflügers Arch 1987, 410:83-91 The development of alinidine was halted because it was not sufficiently specific for its target.
The efferent portion is carried by the vagus nerve from the cardiovascular center of the medulla to the heart, of which increased stimulation leads to decreased output of the sinoatrial node. This reflex is especially sensitive in neonates and children, particularly during strabismus correction surgery. However, this reflex may also occur with adults. Bradycardia, junctional rhythm and asystole, all of which may be life- threatening, can be induced through this reflex.
In a third-degree heart block, about 61% take place at the bundle branch-Purkinje system, 21% at the AV node, and 15% at the bundle of His. AV block may be ruled out with an EKG indicating "a 1:1 relationship between P waves and QRS complexes." Ventricular bradycardias occurs with sinus bradycardia, sinus arrest, and AV block. Treatment often consists of the administration of atropine and cardiac pacing.
A reflex sympathetic response, caused by the peripheral dilation of vessels and the resulting drop in blood pressure, works to counteract the negative inotropic, chronotropic and dromotropic effects of diltiazem. Undesirable effects include hypotension, bradycardia, dizziness, flushing, fatigue, headaches and edema. Rare side effects are congestive heart failure, myocardial infarction, and hepatotoxicity. Diltiazem is one of the most common drugs that cause drug- induced lupus, along with hydralazine, procainamide, isoniazid, minocycline.
However, if it's caused by problems with development in the heart – if Gata5 did not express properly in the embryo- then this can lead to constant ectopic foci problems. These problems include tachycardia (the heart beating too fast), bradycardia (the heart beating too slow), or ventricular fibrillation which is a serious condition where the ventricles of the heart aren't pumping consistently and can't get blood out to the body.
Propafenone works by slowing the influx of sodium ions into the cardiac muscle cells, causing a decrease in excitability of the cells. Propafenone is more selective for cells with a high rate, but also blocks normal cells more than class Ia or Ib. Propafenone differs from the prototypical class Ic antiarrhythmic in that it has additional activity as a beta-adrenergic blocker which can cause bradycardia and bronchospasm.
The headache is worse on coughing, sneezing or bending and progressively worsens over time. There may also be personality or behavioral changes. In addition to the above, if mass effect is present with resulting displacement of brain tissue, additional signs may include pupillary dilatation, abducens palsies, and the Cushing's triad. Cushing's triad involves an increased systolic blood pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory pattern.
The Symplicity HTN-1, HTN-2 and HTN-3 trials have demonstrated acceptable safety profiles for catheter based renal denervation. Patients may experience pain during application of radiofrequency pulses and intraprocedural bradycardia requiring atropine has also been reported. Other documented procedure related complications include femoral artery pseudoaneurysm and renal artery dissection. Of particular concern is the theoretical risk of damage to renal arteries during delivery of radiofrequency energy.
Funeral of Kenan Evren held on 12 May 2015 Evren was hospitalized for massive gastrointestinal bleeding on 3 August 2009, in Yalıkavak, Bodrum, where his summer house is located. A temporary artificial pacemaker was applied to Evren while in intensive care due to bradycardia. His large intestine was removed a week later at GATA in Istanbul (Gülhane Military Medicine Academy) where he was transferred. He was discharged on 24 September 2009.
The of lofexidine is above 77 mg/kg in animals. Studies of high-dose, single administrations of lofexidine proved tolerable for animals, but repeat administration induced symptoms consistent with toxicity. In studies on mice, rats, and dogs, these included ataxia, somnolence, and tremors. It is expected that an overdose of lofexidine would result in symptoms akin to its pharmacological side effects in humans, such as bradycardia and hypotension.
JWH-018 is a full agonist of both the CB1 and CB2 cannabinoid receptors, with a reported binding affinity of 9.00 ± 5.00 nM at CB1 and 2.94 ± 2.65 nM at CB2. JWH-018 has an EC50 of 102 nM for human CB1 receptors, and 133 nM for human CB2 receptors. JWH-018 produces bradycardia and hypothermia in rats at doses of 0.3–3 mg/kg, suggesting potent cannabinoid-like activity.
Chronic use is reported to be associated with physical deterioration, dependence, abscesses, and skin ulceration, which can be physically debilitating and painful. Hypertension followed by hypotension, bradycardia, and respiratory depression lower tissue oxygenation in the skin. Thus, chronic use of xylazine can progress the skin oxygenation deficit, leading to severe skin ulceration. Lower skin oxygenation is associated with impaired healing of wounds and a higher chance of infection.
Besipirdine is reported to be well tolerated. More severe adverse effects, such as bradycardia and postural hypotension, may have been a result of a high ratio of adrenergic to cholinergic potency caused by the metabolite P86-7480, which has direct vasoconstrictor effects. Some studies suggest that the effects of besipirdine on cognition are reversible after withdrawal from treatment, indicating that the efficacy of the drug is primarily symptomatic and not neuroprotective.
While adrenergic antagonists have been used for years, there are multiple issues with using this class of drug. When overused, adrenergic antagonists can result in bradycardia, hypotension, hyperglycemia and even hypodynamic shock. This is because adrenergic stimulation by agonists results in normal calcium channel regulation. If these adrenergic receptors are blocked too often, there will be an excess in calcium channel inhibition, which causes most of these problems.
Liebermeister's rule concerns the increment ratio between an adult individual's cardiac frequency and temperature when in fever. Each Celsius grade of body temperature increment corresponds to an 8 beats per minute increase in cardiac frequency. An exception to this rule by creating a relative bradycardia is known as Faget sign (pulse-temperature dissociation) common in some diseases, especially yellow fever, tularaemia and salmonella typhi. It is named for Carl von Liebermeister.
In another case, a two-year-old boy was admitted to the hospital after ingestion of of demeton-S- methyl. Symptoms included excessive salivation, vomiting, bronchial hypersecretion, muscarinic effects on pulse rate and pupil size, and slight bradycardia. In this case, too, serum-cholinesterase levels were significantly lowered, but returned to baseline after admission to the hospital. Lastly, one case of lethal suicide intoxication with demeton-S-methyl has been reported.
In children, clonidine premedication is at least as effective as benzodiazepines and has less serious side effects. However, oral clonidine can take up to 45 minutes to take full effect, and drawbacks include hypotension and bradycardia. Midazolam, a benzodiazepine characterized by a rapid onset and short duration, is effective in reducing preoperative anxiety, including separation anxiety in children. Dexmedetomidine and certain atypical antipsychotic agents may be used in uncooperative children.
This draws on the simplifying claims of the Triune brain theory which are no longer considered accurate due to the many exceptions to this rule (please see Triune brain - Status of the model for more). The DVC provides primary control of subdiaphragmatic visceral organs, such as the digestive tract. Under normal conditions, the DVC maintains regulation of these digestive processes. However, prolonged disinhibition can be lethal for mammals, as it results in apnea and bradycardia.
Numerous secondary medical problems are associated with catastrophic spinal cord injury. These include cardiovascular complications, such as deep vein thrombosis, pulmonary embolism, orthostatic hypotension, bradycardia, autonomic dysreflexia, altered thermoregulation, and changes to cardiac function as a result of injury to the sympathetic nervous system. Other problems may include pulmonary and gastrointestinal problems, heterotopic ossification, osteoporosis, and other pathologic fractures. Pneumonia is a common cause of death among patients with spinal cord injuries.
Neurokinin has been shown to contribute to both bradycardia and myocardial infarctions through the activation of NK2 receptors. The dual sensory-motor function of neurokinin A containing afferent neurons is a component of the intracardiac nervous system. Varicose processes of tachykinin-containing nerves are abundant in coronary arteries and in the cardiac ganglia. The diverse responses that are triggered by locally released tachykinins produce beneficial effects such as modulation of ganglion transmission.
Cardiovascular symptoms include bradycardia, tachycardia, hypotension, hypertension, orthostatic tachycardia, exercise intolerance, and rhythm disorders. Death from the condition can occur, but is very rare. Dyspareunia and other ciguatera symptoms have developed in otherwise healthy males and females following sexual intercourse with partners suffering ciguatera poisoning, signifying that the toxin may be sexually transmitted. Diarrhea and facial rashes have been reported in breastfed infants of poisoned mothers, suggesting that ciguatera toxins migrate into breast milk.
There was a significant reduction in the rate of cardiovascular death, but not in the rate of death from any cause. Later post- hoc analysis of the ATHENA-results showed a significant reduction in the rate of stroke. Patients randomized to dronedarone were more likely to develop bradycardia and QT-interval prolongation (but only 1 case of Torsades). Nausea, diarrhea, rash, and creatinine elevation also were more common in the dronedarone arm.
Bufadienolide is a chemical compound with steroid structure. Its derivatives are collectively known as bufadienolides, including many in the form of bufadienolide glycosides (bufadienolides that contain structural groups derived from sugars). These are a type of cardiac glycoside, the other being the cardenolide glycosides. Both bufadienolides and their glycosides are toxic; specifically, they can cause an atrioventricular block, bradycardia (slow heartbeat), ventricular tachycardia (a type of rapid heartbeat), and possibly lethal cardiac arrest.
At doses of less than 0.2 mg/day, reserpine has few adverse effects, the most common of which is nasal congestion. Reserpine can cause: nasal congestion, nausea, vomiting, weight gain, gastric intolerance, gastric ulceration (due to increased cholinergic activity in gastric tissue and impaired mucosal quality), stomach cramps and diarrhea are noted. The drug causes hypotension and bradycardia and may worsen asthma. Congested nose and erectile dysfunction are other consequences of alpha-blockade.
He tells Warrick the pie is "low fat, low sugar, low carb." Warrick, with a grimaced expression on his face and a mouthful of pie, replies "low taste". In "The Theory of Everything", he mentions that he suffers from bradycardia and subsequently wears a pacemaker. In the season 12 episode "Genetic Disorder" his wife Judy reports a murder that happened at their house, which suggests to Jim Brass that she had an affair.
The neuroregulation of bradycardia and vasoconstriction of the dive response in both mammals and diving ducks can be triggered by facial immersion, wetting of the nostrils and glottis, or stimulation of trigeminal and glossopharyngeal nerves. Animals cannot convert fats to glucose, and in many diving animals carbohydrates are not readily available from the diet, nor stored in large quantities, so as they are essential for anaerobic metabolism, they could be a limiting factor.
ICP is very likely to cause severe harm if it rises too high. Very high intracranial pressures are usually fatal if prolonged, but children can tolerate higher pressures for longer periods. An increase in pressure, most commonly due to head injury leading to intracranial hematoma or cerebral edema, can crush brain tissue, shift brain structures, contribute to hydrocephalus, cause brain herniation, and restrict blood supply to the brain. It is a cause of reflex bradycardia.
Fatal opioid overdose typically occurs due to bradypnea, hypoxemia, and decreased cardiac output (hypotension occurs due to vasodilation, & bradycardia further contributes to decreased cardiac output). A potentiation effect occurs when opioids are combined with ethanol, benzodiazepines, or barbiturates, which results in an increased risk for overdose to occur. Substantial tolerance to respiratory depression develops quickly, and tolerant individuals can withstand larger doses. However, tolerance to respiratory depression is lost just as quickly during withdrawal.
Xylazine overdose is usually fatal in humans. Because it is used as a drug adulterant, the symptoms caused by the drugs accompanying xylazine administration vary between individuals. The most common side effects in humans associated with xylazine administration include bradycardia, respiratory depression, hypotension, transient hypertension secondary to vagus nerve stimulation, and other changes in cardiac output. Xylazine significantly decreases heart rate in animals that are not premedicated with medications that have anticholinergic effects.
As the condition persists, papillary and vital signs may result including bradycardia and widened pulse pressure. The cells in the brain may swell to the point where blood flow is interrupted resulting in cerebral edema. Swollen brain cells may also apply pressure to the brain stem causing central nervous system dysfunction. Both cerebral edema and interference with the central nervous system are dangerous and could result in seizures, brain damage, coma or death.
Women who are pregnant or may become pregnant are strongly advised to not take amiodarone. Since amiodarone can be expressed in breast milk, women taking amiodarone are advised to stop nursing. It is contraindicated in individuals with sinus nodal bradycardia, atrioventricular block, and second or third degree heart block who do not have an artificial pacemaker. Individuals with baseline depressed lung function should be monitored closely if amiodarone therapy is to be initiated.
Atrial premature complexes (APCs) do not have a compensatory pause since they reset the sinus node but atrial or supraventricular bigeminy can occur. If the APCs are very premature, the wavefront can encounter a refractory AV node and not be conducted. This can be mistaken for sinus bradycardia if the APC is buried in the T wave since the APC will reset the SA node and lead to a long P-P interval.
When one strains to increase the flow of urine, it stimulates the vagus nerve (usually more pronounced in elderly men with large prostates). The vagus nerve stimulus causes slowing down of the heart (bradycardia) and a drop in blood pressure. The heart cannot perform effectively as a pump because insufficient blood comes to it. It can be associated with a very rare tumor known as a paraprostatic pheochromocytoma within the urinary bladder.
Antibiotics, such as ampicillin, chloramphenicol, trimethoprim-sulfamethoxazole, amoxicillin, and ciprofloxacin, have been commonly used to treat typhoid fever.Baron S et al. Treatment of the disease with antibiotics reduces the case-fatality rate to about 1%.. World Health Organization Without treatment, some patients develop sustained fever, bradycardia, hepatosplenomegaly, abdominal symptoms, and occasionally, pneumonia. In white-skinned patients, pink spots, which fade on pressure, appear on the skin of the trunk in up to 20% of cases.
Vernakalant is contraindicated in a number of heart conditions: severe aortic stenosis, low blood pressure (systolic pressure under 100 mmHg), heart failure (NYHA class III–IV), prolonged QT time, severe bradycardia (slow heart rate), sinus node dysfunction, second or third-degree atrioventricular block, and acute coronary syndrome including heart attack. Vernakalant and other intravenous rhythm control drugs (class I and class III antiarrhythmics) must not be given within four hours of each other.
Muscarine poisoning is characterized by miosis, blurred vision, increased salivation, excessive sweating, lacrimation, bronchial secretions, bronchoconstriction, bradycardia, abdominal cramping, increased gastric acid secretion, diarrhea and polyuria. If muscarine reaches the brain it can cause tremor, convulsions and hypothermia. Cardiac ventricles contain muscarinic receptors that mediate a decrease in the force of contractions leading to a lower blood pressure. If muscarine is administered intravenously, muscarine can trigger acute circulatory failure with cardiac arrest.
Each of the many different synthetic cannabinoids can have different effects at different dosages. The CDC described synthetic cannabinoid overdoses between 2010 and 2015 and of 277 drug overdose patients who reported synthetic cannabinoid as the sole agent, 66.1% reported problems in the central nervous system (e.g., agitation, coma, toxic psychosis), 17% reported cardiovascular problems (e.g., tachycardia, bradycardia), 7.6% reported pulmonary problems (5.4% of which had respiratory depression), and 4% reported acute kidney injury.
A profound lethargy and characteristic lowering of the head with reduced sensitivity to environmental stimuli (sound, pain, etc.) are seen with detomidine. A short period of reduced coordination is characteristically followed by immobility and a firm stance with front legs spread. Following administration there is an initial increase in blood pressure, followed by bradycardia and second degree atrioventricular block (this is not pathologic in horses). The horse commonly sweats to excess, especially on the flanks and neck.
An acute anticholinergic syndrome is reversible and subsides once all of the causative agents have been excreted. Reversible Acetylcholinesterase inhibitor agents such as physostigmine can be used as an antidote in life-threatening cases. Wider use is discouraged due to the significant side effects related to cholinergic excess including seizures, muscle weakness, bradycardia, bronchoconstriction, lacrimation, salivation, bronchorrhea, vomiting, and diarrhea. Even in documented cases of anticholinergic toxicity, seizures have been reported after the rapid administration of physostigmine.
Apnea in seals is induced by stimulation of trigeminal and glossopharyngeal nerve receptors in the mouth. The consequent asphyxia stimulates peripheral chemoreceptors which induce an increasing peripheral vasoconstriction and bradycardia. Conversely, if the peripheral chemoreceptors are stimulated by hypoxia while the animal is breathing, the ventilation, heart rate and vasodilation of skeletal muscles is increased. Oxygen consumption during a dive can be reduced by about 70%, attributed to anaerobic metabolism and probably also cooling of the body.
Arrhythmia, also known as cardiac arrhythmia or heart arrhythmia, is a group of conditions in which the heartbeat is irregular, too fast, or too slow. The heart rate that is too fast – above 100 beats per minute in adults – is called tachycardia, and a heart rate that is too slow – below 60 beats per minute – is called bradycardia. Some types of arrhythmias have no symptoms. Symptoms when present may include palpitations or feeling a pause between heartbeats.
Subclavian steal syndrome arises from retrograde (reversed) flow of blood in the vertebral artery or the internal thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the subclavian artery. Symptoms such as syncope, lightheadedness, and paresthesias occur while exercising the arm on the affected side (most commonly the left). Aortic dissection (a tear in the aorta) and cardiomyopathy can also result in syncope. Various medications, such as beta blockers, may cause bradycardia induced syncope.
Masters tries to convince the patient to amputate the arm but Kendall refuses, and her parents refuse to overrule her. Unable to accept the patient's decision, Masters goes to House for advice. House suggests that she break the rules if it is so important to her, but she refuses. After talking once more with the patient, Masters causes Kendall to experience bradycardia and convinces the parents that the cancer has caused a clot to lodge in her heart.
Most side effects are direct consequences of the vasodilation and the following low blood pressure. They include headache ("nitrate headache") resulting from the widening of blood vessels in the brain, reflex tachycardia (fast heart rate), flush, dizziness, nausea and vomiting. These effects usually subside after a few days if the treatment is continued. Occasionally, severe hypotension occurs shortly after beginning of treatment, possibly resulting in intensified angina symptoms or syncope, sometimes with bradycardia (slow heart rate).
Vincent died on February 10, 2019 at the age of 74 in Asheville, North Carolina due to cardiac arrest while hospitalized at Mission Hospital Memorial Campus. Bradycardia, a decreased heart rate, was listed as an underlying cause of death. His death was not publicly announced until March 8, when TMZ broke the news and showed a slightly redacted copy of Vincent's death certificate. He is survived by his third wife, Patricia Ann Christ, and his daughter from his first marriage, Amber Vincent.
Overdose of GHB can sometimes be difficult to treat because of its multiple effects on the body. GHB tends to cause rapid unconsciousness at doses above 3500 mg, with single doses over 7000 mg often causing life-threatening respiratory depression, and higher doses still inducing bradycardia and cardiac arrest. Other side-effects include convulsions (especially when combined with stimulants), and nausea/vomiting (especially when combined with alcohol). The greatest life threat due to GHB overdose (with or without other substances) is respiratory arrest.
An ectopic pacemaker is an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the heart. It is thus a cardiac pacemaker that is ectopic, producing an ectopic beat. Acute occurrence is usually non-life-threatening, but chronic occurrence can progress into tachycardia, bradycardia or ventricular fibrillation. In a normal heart beat rhythm, the SA node usually suppresses the ectopic pacemaker activity due to the higher impulse rate of the SA node.
A number of persons have developed toxicity due to acute overdosage with nifedipine, either accidentally or intentionally, and via either oral or parenteral administration. The adverse effects include lethargy, bradycardia, marked hypotension and loss of consciousness. The drug may be quantified in blood or plasma to confirm a diagnosis of poisoning, or to assist in a medicolegal investigation following death. Analytical methods usually involve gas or liquid chromatography and specimen concentrations are usually in the 100-1000 μg/L range.
Cardiac arrhythmia Cardiac arrhythmia, also known as "cardiac dysrhythmia" or "irregular heartbeat", is a group of conditions in which the heartbeat is irregular, too fast, or too slow. A heart rate that is too fast – above 100 beats per minute in adults – is called tachycardia and a heart rate that is too slow – below 60 beats per minute – is called bradycardia. Many types of arrhythmia have no symptoms. When symptoms are present these may include palpitations or feeling a pause between heartbeats.
The largest known case of ingestion with a known outcome involved a 1260 mg of oral aripiprazole, 42 times the recommended dose. The patient survived and fully recovered. Common adverse reactions, reported in at least 5% of overdose cases, included vomiting, somnolence, and tremor. Other clinically important signs and symptoms of overdoses include acidosis, aggression, atrial fibrillation, bradycardia, coma, confusion, convulsion, depressed level of consciousness, hypertension, hypokalemia, hypotension, lethargy, loss of consciousness, pneumonia aspiration, respiratory arrest, status epilepticus, and tachycardia.
Decreased cardiac output despite normal blood volume, due to severe congestive heart failure, large myocardial infarction, heart valve problems, or extremely low heart rate (bradycardia), often produces hypotension and can rapidly progress to cardiogenic shock. Arrhythmias often result in hypotension by this mechanism. Excessive vasodilation, or insufficient constriction of the blood vessels (mostly arterioles), causes hypotension. This can be due to decreased sympathetic nervous system output or to increased parasympathetic activity occurring as a consequence of injury to the brain or spinal cord.
Apnea of prematurity is defined as cessation of breathing by a premature infant that lasts for more than 20 seconds and/or is accompanied by hypoxia or bradycardia. Apnea is traditionally classified as either obstructive, central, or mixed. Obstructive apnea may occur when the infant's neck is hyperflexed or conversely, hyperextended. It may also occur due to low pharyngeal muscle tone or to inflammation of the soft tissues, which can block the flow of air though the pharynx and vocal cords.
No drug has been shown to be able to arrest or slow down the process of this condition. There is promise that two drugs, tafamidis and diflunisal, may improve the outlook, since they were demonstrated in randomized clinical trials to benefit patient affected by the related condition FAP-1 otherwise known as transthyretin-related hereditary amyloidosis. Permanent pacing can be employed in cases of symptomatic slow heart rate (bradycardia). Heart failure medications can be used to treat symptoms of difficulty breathing and congestion.
Seventy-one serious adverse events, including 42 acute intoxications and 29 deaths (Germany (5), Hungary (3), Poland (1), Sweden (9), United Kingdom (10), Norway (1)) that occurred in nine European countries between 2014 and 2016 have been associated with MDMB-CHMICA. Side effects such as unconsciousness or coma, hyperemesis, nausea, seizures, convulsions, tachycardia, bradycardia, mydriasis, syncope, spontaneous urinating and defecating, shortness of breath, somnolence, respiratory acidosis, metabolic acidosis, collapse, lower limbs paralysis, chest pain, aggression and severe disturbance of behaviour were reported.
The most common clinical manifestations are related to mental status and gastrointestinal function; they include lethargy, anorexia, vomiting, weight loss, and weakness. Additional findings may include dehydration, bradycardia, weak femoral pulses, abdominal pain, lack of appetite, tremors or shaking, muscle weakness, low body temperature, collapse, and pain in the hindquarters. Polyuria and polydipsia, diarrhea, and shivering are occasionally reported. Hypoglycemia can also be present, and initially may be confused with a seizure disorder or an insulin-secreting pancreatic tumor (insulinoma).
Serious side effects that are advised to be reported immediately include symptoms of bradycardia (resting heart rate slower than 60 beats per minute), persistent symptoms of dizziness, fainting and unusual fatigue, bluish discoloration of the fingers and toes and/or lips, numbness/tingling/swelling of the hands or feet, sexual dysfunction, erectile dysfunction, hair loss, mental/mood changes, depression, breathing difficulty, cough, dyslipidemia and increased thirst. Consuming alcohol while taking metoprolol may cause mild body rashes and is not advised.
ANK2 mutations have also been identified in patients with sinus node dysfunction. Mechanistic studies on effects of these mutations in mice showed severe bradycardia and variability in heart rate, as well as dysfunction in ankyrin-B-based trafficking pathways in primary and subsidiary pacemaker cells. In a large genotype-phenotype study of 874 patients with hypertrophic cardiomyopathy, patients with ANK2 variants exhibited greater maximum left ventricular wall thickness. In patients with both ischemic and non-ischemic heart failure, ankyrin-B levels are altered.
The plant is toxic to animals, including all classes of livestock and poultry, as well as felines and canines. Digitalis poisoning can cause heart block and either bradycardia (decreased heart rate) or tachycardia (increased heart rate), depending on the dose and the condition of one's heart. Notably, the electric cardioversion (to "shock" the heart) is generally not indicated in ventricular fibrillation in digitalis toxicity, as it can increase the dysrhythmia.Robert Alan Lewis, Lewis' Dictionary of Toxicology, 1998, page 387, 1566702232.
Some also have muscle aches, headache, tiredness, loss of appetite, loss of coordination (ataxia), chest pain, or diarrhea and vomiting. Up to half of those with Legionnaires' disease have gastrointestinal symptoms, and almost half have neurological symptoms, including confusion and impaired cognition. "Relative bradycardia" may also be present, which is low to normal heart rate despite the presence of a fever. Laboratory tests may show that kidney functions, liver functions, and electrolyte levels are abnormal, which may include low sodium in the blood.
The venom produces mainly cardiopulmonary abnormalities like circulatory derangements, myocarditis and changes in cardiac sarcolemmal ATPase and by these abnormalities it can finally cause death. In rural India the scorpion and its venom is a commonly known factor of children's death. The venom initially causes transient cholinergic stimulation (vomiting, profuse sweating, bradycardia, priapism, hypersalivation, and hypotension) which is followed by sustained adrenergic hyperactivity (hypertension, tachycardia, and myocardial failure). The adrenergic phase but not the cholinergic phase is a dose-dependent phenomenon.
The initial treatment of nicotine poisoning may include the administration of activated charcoal to try to reduce gastrointestinal absorption. Treatment is mainly supportive and further care can include control of seizures with the administration of a benzodiazepine, intravenous fluids for hypotension, and administration of atropine for bradycardia. Respiratory failure may necessitate respiratory support with rapid sequence induction and mechanical ventilation. Hemodialysis, hemoperfusion or other extracorporeal techniques do not remove nicotine from the blood and are therefore not useful in enhancing elimination.
Baroreceptors are integral to the body's function: Pressure changes in the blood vessels would not be detected as quickly in the absence of baroreceptors. When baroreceptors are not working, blood pressure continues to increase, but, within an hour, the blood pressure returns to normal as other blood pressure regulatory systems take over. Baroreceptors can also become oversensitive in some people (usually the carotid baroreceptors in older males). This can lead to bradycardia, dizziness and fainting (syncope) from touching the neck (often whilst shaving).
The resulting influx of Na+ also leads to the increase of intracellular Ca2+ concentrations, causing the overproduction of reactive oxygen species responsible for neuronal damage. Veratridine is readily absorbed through the skin and mucous membranes and through ingestion. The tissues most affected are the heart, nerves, and skeletal muscles: main symptoms of veratridine toxicity include severe nausea, bradycardia, hypotension, difficulty breathing, salivation, and muscle weakness. Treatment involves the administration of activated charcoal, atropine, and benzodiazepines (if the affected individual is seizing).
The three most prevalent clinical analeptic uses of caffeine are in the treatment of asthma, apnea of prematurity, and bronchopulmonary dysplasia in newborn infants. Caffeine is a weak bronchodilator, which explains the relief of the effects of asthma. There is preliminary research that indicates that caffeine reduces the incidence of cerebral palsy and cognitive delay, but additional research is needed here. Apnea of prematurity is officially described as a cessation of breathing for more than 15–20 seconds, usually accompanied by bradycardia and hypoxia.
In children, the most common cause of cardiopulmonary arrest is shock or respiratory failure that has not been treated, rather than a heart arrhythmia. When there is a cardiac arrhythmia, it is most often asystole or bradycardia, in contrast to ventricular fibrillation or tachycardia as seen in adults. Other causes can include drugs such as cocaine, methamphetamine, or overdose of medications such as antidepressants in a child who was previously healthy but is now presenting with a dysrhythmia that has progressed to cardiac arrest.
Serious adverse effects include gastrointestinal toxicity, hepatotoxicity, interstitial lung disease, prolonged QT syndrome, hyperglycemia, bradycardia, and pancreatitis. The most commonly reported side effects were diarrhea, nausea, elevated liver enzymes, vomiting, abdominal pain, fatigue, decreased appetite, and constipation. Due to the risk of elevated liver enzymes, liver function tests should be performed every two weeks for the first 9 weeks of treatment. Finally, ceritinib is both a substrate and potent inhibitor of the enzyme CYP3A4, so medications should be monitored carefully that may interact with ceritinib.
It is not recommended for diabetics, it is contraindicated in patients with cardiac disease. Due to its potent sedative effects it is commonly used in more aggressive animals, where a drug combination with a lesser effect (such as acepromazine plus an opioid, or an opioid plus a benzodiazepine) would not allow the administration of the inductive agent without risk to the veterinarian. As such the use of alpha-two agonists is only recommended in healthy animals. Following administration, marked peripheral vasoconstriction and bradycardia are noted.
An AV-junctional rhythm, or atrioventricular nodal bradycardia, is usually caused by the absence of the electrical impulse from the sinus node. This usually appears on an electrocardiogram (EKG) with a normal QRS complex accompanied with an inverted P wave either before, during, or after the QRS complex. An AV-junctional escape beat is a delayed heartbeat originating from an ectopic focus somewhere in the AV junction. It occurs when the rate of depolarization of the SA node falls below the rate of the AV node.
Idioventricular rhythm, also known as atrioventricular bradycardia or ventricular escape rhythm, is a heart rate of less than 50 BPM. This is a safety mechanism when a lack of electrical impulse or stimuli from the atrium occurs. Impulses originating within or below the bundle of His in the AV node will produce a wide QRS complex with heart rates between 20 and 40 BPM. Those above the bundle of His, also known as junctional, will typically range between 40 and 60 BPM with a narrow QRS complex.
Marine mammals are able to dive for long periods. Both pinnipeds and cetaceans have large and complex blood vessel systems which serve to store oxygen to support deep diving. Other important reservoirs include muscles, blood, and the spleen which all have the capacity to hold a high concentration of oxygen. They are also capable of bradycardia (reduced heart rate), and vasoconstriction (shunting most of the oxygen to vital organs such as the brain and heart) to allow extended diving times and cope with oxygen deprivation.
Bradycardia, junctional rhythms and QRS widening are particularly associated with increased risk of adverse outcomes The serum potassium concentration at which electrocardiographic changes develop is somewhat variable. Although the factors influencing the effect of serum potassium levels on cardiac electrophysiology are not entirely understood, the concentrations of other electrolytes, as well as levels of catecholamines, play a major role. ECG findings are not a reliable finding in hyperkalemia. In a retrospective review, blinded cardiologists documented peaked T-waves in only 3 of 90 ECGs with hyperkalemia.
So details of the canonical text may be legend. Experiment by Oliver und Schäfer: an adrenal extract increases the blood pressure and contracts the spleen. On March 10, 1894, Oliver and Schäfer presented their findings to the Physiological Society in London. A 47-pages account followed a year later, in the style of the time without statistics, but with precise description of many individual experiments and 25 recordings on kymograph smoked drums, showing, besides the blood pressure increase, reflex bradycardia and contraction of the spleen.
Activated charcoal is useful to absorb the drug. Atropine will counteract bradycardia, glucagon helps with hypoglycemia, dobutamine can be given against hypotension and the inhalation of a β2-mimetic as hexoprenalin or salbutamol will terminate bronchospasms. Blood or plasma atenolol concentrations may be measured to confirm a diagnosis of poisoning in hospitalized patients or to assist in a medicolegal death investigation. Plasma levels are usually less than 3 mg/L during therapeutic administration, but can range from 3–30 mg/L in overdose victims.
Phenobarbital causes a depression of the body's systems, mainly the central and peripheral nervous systems. Thus, the main characteristic of phenobarbital overdose is a "slowing" of bodily functions, including decreased consciousness (even coma), bradycardia, bradypnea, hypothermia, and hypotension (in massive overdoses). Overdose may also lead to pulmonary edema and acute renal failure as a result of shock, and can result in death. The electroencephalogram (EEG) of a person with phenobarbital overdose may show a marked decrease in electrical activity, to the point of mimicking brain death.
The most noticeable effects are on the cardiovascular system, which displays peripheral vasoconstriction, slowed heart rate, redirection of blood to the vital organs to conserve oxygen, release of red blood cells stored in the spleen, and, in humans, heart rhythm irregularities. Although aquatic animals have evolved profound physiological adaptations to conserve oxygen during submersion, the apnea and its duration, bradycardia, vasoconstriction, and redistribution of cardiac output occur also in terrestrial animals as a neural response, but the effects are more profound in natural divers.
Due to hazardous side effects, including hypotension and bradycardia, xylazine was not approved by the Food and Drug Administration (FDA) for human use. As a result, xylazine's mechanism of action in humans remains unknown. Xylazine was approved by the FDA for veterinary use and is now used as an animal tranquilizer. In the United States, xylazine was only approved by the FDA for veterinary use as a sedative, analgesic, and muscle relaxant in dogs, cats, horses, elk, fallow deer, mule deer, sika deer, and white-tailed deer.
He is also remembered for studying the physiological effects of pharmacological substances such as curare, atropine and veratrum on the body's muscles, heart, nerves and circulatory system. The eponymous "Bezold-Jarisch reflex" is a triad of responses (apnea, bradycardia, and hypotension) resulting from an intravenous injection of veratrum alkaloids. This medical sign is named along with pharmacologist Adolf Jarisch Jr. (1891–1965), who in 1937 re-confirmed Bezold's earlier experiments. Bezold died at the age of 32 due to a mitral stenosis caused by rheumatic endocarditis.
Compounds such as levetiracetam, lamotrigine, and carbamazepine are known to block the P-type channels, which have helped to decrease the occurrence of seizures. Overall, there are various non-selective calcium channel blockers that help alleviate symptoms of hypertension, schizophrenia, cardiac arrhythmia, epilepsy, pain, asthma, bradycardia, angina pectoris and Alzheimer's disease. Although many of the therapeutic compounds' main target is not P-type channels, further research needs to determine if the clinical effects of these compounds are also influenced by the P-type channel blockage.
Bowen at the 25th Annual "A Time for Heroes" Celebration in October 2014 Bowen suffers from the cardiovascular condition bradycardia in which her regular heartbeat is below normal. As a result, she has worn a pacemaker since her early twenties. Bowen married Scott Phillips, a real estate investor and software developer, on September 9, 2004. The couple has three sons, the first born in April 2007, and twins born in May 2009, with whom she was visibly pregnant when shooting the pilot for Modern Family.
These patients often respond well to atropine, but make require temporary transcutaneous pacing or transvenous pacing until they are not longer symptomatic. Patients with second-degree Mobitz II and third-degree heart block are much more likely to have symptomatic bradycardia and hemodynamic instability, such as hypotension. Additionally, there is an increased risk of patients with Mobitz II heart block developing third-degree heart block. Therefore, these patients often require temporary pacing with transcutaneous or transvenous pacing wires, and many will ultimately require a permanent implanted pacemaker.
Since animals are potentially suffering from severe metabolic derangements at the time of initial presentation, animals need to be stabilized prior to surgery. Common physiologic derangements noted on bloodwork are elevated kidneys values (azotemia) and elevated potassium levels (hyperkalemia). The presence of profound sedation, low body temperature, and/or a slow heart rate (bradycardia) are usually associated with more severe blood derangements. Ideally, the urethral obstruction is removed or temporarily bypassed with urethral flushing (urohydropulsion) and the placement of an in-dwelling urinary catheter prior to surgery.
Most stable patients have persistent bradycardia-related symptoms and require identification and treatment of any reversible cause or permanent implantable pacemaker. Reversible causes of complete AV block should be ruled out before the insertion of a permanent pacemaker, such as drugs that slows heart rate and which induce hyperkalemia. Complete atrioventricular block in acute myocardial infarction should be treated with temporary pacing and revascularization. Complete atrioventricular block caused by hyperkalemia should be treated to lower serum potassium levels and patients with hypothyroidism should also receive thyroid hormone.
Gelsemine is a highly toxic and therefore possibly fatal substance for which there is no antidote, but the symptoms can be managed in low dose intoxications. In the case of an oral exposure a gastric lavage is performed, which must be done within approximately one hour of ingestion. Activated charcoal is then administered to bind the free toxin in the gastrointestinal tract to prevent absorption. Benzodiazepine or phenobarbital is also generally administered to help control seizing, and atropine can be used to treat bradycardia.
Seizures may occur, and the autonomic nervous system may also be affected. Tetanospasmin appears to prevent the release of neurotransmitters by selectively cleaving a component of synaptic vesicles called synaptobrevin II. Loss of inhibition also affects preganglionic sympathetic neurons in the lateral gray matter of the spinal cord and produces sympathetic hyperactivity and high circulating catecholamine levels. Hypertension and tachycardia alternating with hypotension and bradycardia may develop. Tetanic spasms can occur in a distinctive form called opisthotonos and be sufficiently severe to fracture long bones.
The symptoms of intoxication with mushrooms rich in muscarine, especially Inocybe, are very typical: The symptoms start early, after one-quarter to two hours, with headache, nausea, vomiting, and constriction of the pharynx. Then salivation, lacrimation, and diffuse perspiration set in, combined with miosis, disturbed accommodation, and reduced vision. Gastric and small bowel colic leads to diarrhea, and there is a painful urge for urination. Bronchoconstriction leads to asthmatic attacks and severe dyspnea, and bradycardia combined with marked hypotension and vasodilation results in circulatory shock.
Lou (Christine Woods) is a thirty-seven-year-old woman who works as the assistant to a high-profile feminist activist and travels around the world at her boss's side. In the middle of a meeting, Lou suddenly began to hallucinate ants crawling all over her body. She is admitted to House's treatment for what at first appear to be psychiatric symptoms. While House is in the midst of disregarding the patient, Foreman states that she was also found to have abdominal pain, anemia, and bradycardia.
Less common secondary effects include muscle cramps, decreased heart rate (bradycardia), decreased appetite and weight, and increased gastric acid production. Glutamate is an excitatory neurotransmitter of the nervous system, although excessive amounts in the brain can lead to cell death through a process called excitotoxicity which consists of the overstimulation of glutamate receptors. Excitotoxicity occurs not only in Alzheimer's disease, but also in other neurological diseases such as Parkinson's disease and multiple sclerosis. Memantine is a noncompetitive NMDA receptor antagonist first used as an anti-influenza agent.
Healthy human fetuses have a high variability in heart rate, which is mediated by the vagus. On the other hand, heart rate decelerations, which are also mediated by the vagus, are a sign of fetal distress. More specifically, prolonged withdrawal of vagal influence on the heart creates a physiological vulnerability to the influence of the Dorsal Vagal Control, which in turn produces bradycardia (very low heart rate). However, the onset of this deceleration is commonly preceded by transitory tachycardia, which is reflective of the immediate effects of Ventral Vagal Control withdrawal.
These factors include activation of stretch receptors due to increased ventilation and the release of circulating catecholamines. However, if respiratory activity is arrested (e.g. in a patient with a high cervical spinal cord injury), then the primary cardiac reflex to transient hypercapnia and hypoxia is a profound bradycardia and coronary vasodilation through vagal stimulation and systemic vasoconstriction by sympathetic stimulation. In normal cases, if there is reflexive increase in respiratory activity in response to chemoreceptor activation, the increased sympathetic activity on the cardiovascular system would act to increase heart rate and contractility.
While a few exceptionally trained aerobic athletes demonstrate resting heart rates in the range of 30–40 beats per minute (the lowest recorded figure is 28 beats per minute for Miguel Indurain, a cyclist)–for most individuals, rates lower than 50 beats per minute would indicate a condition called bradycardia. Depending upon the specific individual, as rates fall much below this level, the heart would be unable to maintain adequate flow of blood to vital tissues, initially resulting in decreasing loss of function across the systems, unconsciousness, and ultimately death.
N-Methylphenylethanolamine also caused a decrease in heart rate which was inversely related to the dose (i.e. progressively larger doses caused less bradycardia), and which was quantitatively less than that produced by the same doses of phenylethanolamine. The drug produced a fall in body temperature which was also inversely correlated with the dose, and which was smaller than that produced by the same doses of phenylethanolamine. Additional symptoms that were observed included profuse salivation and piloerection, although, in contrast to phenylethanolamine, N-methylphenylethanolamine did not produce any stereotyped or rapid eye movements.
Sea lion releasing air underwater In order to be able to dive for a long period of time, Steller sea lions exhibit apnea, bradycardia, and peripheral vasoconstriction. This allows them to maximize their oxygen stores and efficiently forage during their dives. In addition to those adaptations, their thick blubber layer and outer fur layer keep their body insulated during dives. Trained Steller sea lions from Vancouver Aquarium were placed in the open ocean at the University of British Columbia's Open Water Research Station to study their diving metabolism and behavior.
Paradoxical reactions such as anxiety, delirium, combativeness, hallucinations, and aggression can also occur following benzodiazepine overdose. Gastrointestinal symptoms such as nausea and vomiting have also been occasionally reported. Cases of severe overdose have been reported and symptoms displayed might include prolonged deep coma or deep cyclic coma, apnea, respiratory depression, hypoxemia, hypothermia, hypotension, bradycardia, cardiac arrest, and pulmonary aspiration, with the possibility of death. Severe consequences are rare following overdose of benzodiazepines alone but the severity of overdose is increased significantly if benzodiazepines are taken in overdose in combination with other medications.
Fetal blood sampling from the umbilical cord and intrauterine platelet transfusion was the first antenatal treatment for NAIT to prevent intracerebral hemorrhage. However, this is no longer recommended routinely because of the serious risk of harms. Cordocentesis in the presence of a low platelet count may lead to serious complications, these included slowing of the baby's heart (fetal bradycardia), tamponade of the cord, and bleeding complications in the baby, including exsanguination. Fetal blood sampling is estimated to cause death of the baby in 1.3% of procedures, however the incidence varies significantly from center to center.
Aquatic mammals are also less sensitive to low alveolar oxygen concentrations and high carbon dioxide concentrations than purely terrestrial mammals. Seals, whales and porpoises have slower respiratory rates and larger tidal volume to total lung capacity ratio than land animals which gives them a large exchange of gas during each breath and compensates for low respiratory rate. This allows greater utilisation of available oxygen and reduced energy expenditure. In seals, bradycardia of the diving reflex reduces heart rate to about 10% of resting level at the start of a dive.
Most infected cats have been healthy before a very sudden onset of severe disease. The course of clinical disease is often swift with clinical signs of lethargy and inappetence within 5 to 20 days after the tick bite. Cats develop a high fever, but the temperature may become low before death. Other clinical findings can be: dehydration, icterus (jaundice), enlarged liver and spleen, lymphadenopathy, pale mucus membranes, respiratory distress, tachycardia or bradycardia, and tick infestation (although ticks are not often found on infected cats since cats typically groom ticks off their fur).
This response, referred to as "alarm bradycardia", causes the fawn's heart rate to drop from 155 to 38 beats per minute within one beat of the heart. This drop in heart rate can last up to two minutes, causing the fawn to experience a depressed breathing rate and decrease in movement, called tonic immobility. Tonic immobility is a reflex response that causes the fawn to enter a low body position that simulates the position of a dead corpse. Upon discovery of the fawn, the predator loses interest in the "dead" prey.
Infrequent adverse reactions in patients taking opioids for pain relief include: dose-related respiratory depression (especially with more potent opioids), confusion, hallucinations, delirium, urticaria, hypothermia, bradycardia/tachycardia, orthostatic hypotension, dizziness, headache, urinary retention, ureteric or biliary spasm, muscle rigidity, myoclonus (with high doses), and flushing (due to histamine release, except fentanyl and remifentanil). Both therapeutic and chronic use of opioids can compromise the function of the immune system. Opioids decrease the proliferation of macrophage progenitor cells and lymphocytes, and affect cell differentiation (Roy & Loh, 1996). Opioids may also inhibit leukocyte migration.
Bradycardia is the response to facial contact with cold water: the human heart rate slows down ten to twenty-five percent. Seals experience changes that are even more dramatic, going from about 125 beats per minute to as low as 10 on an extended dive. During breath-holding, humans also display reduced left ventricular contractility and diminished cardiac output, effects that may be more severe during submersion due to hydrostatic pressure. Slowing the heart rate reduces the cardiac oxygen consumption, and compensates for the hypertension due to vasoconstriction.
The most common side effects of fingolimod have been head colds, headache, increased gamma-glutamyl transfer (≤15%), diarrhea (13%), nausea (13%), abdominal pain (11%) and fatigue. A few cases of skin cancer have been reported, which has also been reported in patients taking natalizumab (Tysabri), an approved MS drug. Fingolimod has also been associated with potentially fatal infections, bradycardia and, in 2009, a case of hemorrhaging focal encephalitis, an inflammation of the brain with bleeding. Two people died: one due to brain herpes infection, and a second one due to herpes zoster.
On the other hand, cardiac arrhythmia are changes in heart rate, whether faster (tachycardia) or slower (bradycardia). Medicinal treatments for this condition work primarily to counteract tachycardia or atrial fibrillation by slowing down heart rate, as done by cardiac glycosides. Nevertheless, due to questions of toxicity and dosage, cardiac glycosides have been replaced with synthetic drugs such as ACE inhibitors and beta blockers and are no longer used as the primary medical treatment for such conditions. Depending on the severity of the condition, though, they may still be used in conjunction with other treatments.
The Bezold–Jarisch reflex (also called the Bezold reflex, the Jarisch-Bezold reflex or Von Bezold–Jarisch reflex) involves a variety of cardiovascular and neurological processes which cause hypopnea (excessively shallow breathing or an abnormally low respiratory rate), hypotension (abnormally low blood pressure) and bradycardia (abnormally low resting heart rate) in response to noxious stimuli detected in the cardiac ventricles. The reflex is named after Albert von Bezold and Adolf Jarisch Junior. The significance of the discovery is that it was the first recognition of a chemical (non-mechanical) reflex.
There are no expected pharmacokinetic interactions between thalidomide and other medicines due to its neutral effects on P-glycoprotein and the cytochrome P450 family. It may interact with sedatives due to its sedative action and bradycardic agents, like beta-blockers, due to its bradycardia-inducing effects. The risk of peripheral neuropathy may be increased by concomitant treatment with other agents known to cause peripheral neuropathy. The risk of venous thromboembolisms with thalidomide seems to be increased when patients are treated with oral contraceptives or other cytotoxic agents (including doxorubicin and melphalan) concurrently.
Other causes of acquired LQTS include abnormally low levels of potassium (hypokalaemia) or magnesium (hypomagnesaemia) within the blood. This is can be exacerbated following a sudden reduction in the blood supply to the heart (myocardial infarction), low levels of thyroid hormone (hypothyroidism), and a slow heart rate (bradycardia). Anorexia nervosa has been associated with sudden death, possibly due to QT prolongation. The malnutrition seen in this condition can sometimes affect the blood concentration of salts such as potassium, potentially leading to acquired long QT syndrome, in turn causing sudden cardiac death.
Management is dependent upon the severity, or degree, of the blockage, the consistency of symptoms, as well as the cause of the AV block. Patients with first-degree AV block do not have any resulting severe or life-threatening symptoms, such as symptomatic bradycardia or hypotension, and, thus, do not require treatment. Similarly, patients with second-degree Mobitz I AV block rarely develop life-threatening symptoms, and patients who are asymptomatic do not require treatment. However, in some cases, patients with Mobtz I block can develop life-threatening symptoms that requires intervention.
Dent, M. R., Singal, T., Tappia, P. S., Sethi, R., Dhall, N. S. (2008). β-Adrenoceptor-Linked Signal Transduction Mechanisms in Congestive Heart Failure. Chapter 2, pp 27-49 in Signal transduction in the cardiovascular system in health and disease, Eds Srivastava, Ashok K., Anand-Srivastava, Madhu B. Springer Science & Business Media, 2008 The ability of penbutolol to act as a partial agonist proves useful in the prevention of bradycardia as a result of decreasing the heart rate excessively. Penbutolol binding β1 adrenergic receptors also alters kidney functions.
Diving birds, such as penguins, have a similar diving reflex. The diving reflex is triggered specifically by chilling the face and breath-hold. The most noticeable effects are on the cardiovascular system, which displays peripheral vasoconstriction, slowed pulse rate, redirection of blood to the vital organs to conserve oxygen, release of red blood cells stored in the spleen, and, in humans, heart rhythm irregularities. Aquatic mammals have evolved physiological adaptations to conserve oxygen during submersion, but the apnea, bradycardia, and vasoconstriction are shared with terrestrial mammals as a neural response.
The toxic effects of accumulation of acetylcholine can be divided into three categories, based upon its actions in different parts of the nervous system. Muscarinic receptors that respond to acetylcholine are found in smooth muscles, the heart and exocrine glands. The muscarinic symptoms of cholinergic poisoning are therefore tightness in the chest, wheezing due to bronchoconstriction, bradycardia, miosis, increased salivation, lacrimation and sweating and increased peristalsis, which leads to nausea, vomiting and diarrhea. Nicotinic receptors responding to acetylcholine can be found in skeletal muscle and the autonomic ganglia.
Bainbridge Reflex is involved in Respiratory Sinus Arrhythmia. During inhalation intrathoracic pressure decreases. It triggers increased venous return which is registered by stretch receptors, which via Bainbridge Reflex increases the heart rate momentarily during inspiration. This is not to be confused with stage 4 of the Valsalva maneuver, in which the release of high intrathoracic pressure previously generated by forced expiration against a closed glottis, now restores venous return and cardiac output into a vasoconstricted circulation, stimulating the vagus nerve and leading to a slowing of the heart, or bradycardia.
The myelin sheath is therefore less likely to break down and stays intact for a longer time. The binding to receptor S1P1 is the one that contributes to the mechanism of action, while the others are thought to produce the unwanted side effects of the drugs. The aim in the future for these drugs is therefore to find chemicals/drugs that can bind more selectively to the S1P1 subtype. Adverse side effect of the drugs at first dose can be bradycardia, influenza, back pain, hypertension, headache, cough, dyspnea and diarrhea.
The symptoms are usually not subtle, although asymptomatic events have been documented. Autonomic dysreflexia differs from autonomic instability, the various modest cardiac and neurological changes that accompany a spinal cord injury, including bradycardia, orthostatic hypotension, and ambient temperature intolerance. In autonomic dysreflexia, patients will experience hypertension, sweating, spasms (sometimes severe spasms) and erythema (more likely in upper extremities) and may suffer from headaches and blurred vision. Mortality is rare with AD, but morbidity such as stroke, retinal hemorrhage and pulmonary edema if left untreated can be quite severe.
Other physical exam findings suggestive of cardiac chest pain may include hypertension, tachycardia, bradycardia, and new heart murmurs. Chest pain that is reproducible during the physical exam with contact of the chest wall is more indicative of non-cardiac chest pain, but still cannot completely rule out acute coronary syndrome. For this reason, in general, additional tests are required to establish the diagnosis. In the emergency department the typical approach to chest pain involves ruling out the most dangerous causes: heart attack, pulmonary embolism, thoracic aortic dissection, esophageal rupture, tension pneumothorax, and cardiac tamponade.
In type I hypersensitivity allergic reactions, an allergen (a type of antigen) interacts with and cross-links surface IgE antibodies on mast cells and basophils. Once the allergen cross-links Immunoglobulin E, tyrosine kinases rapidly signal into the cell, leading to cell degranulation and the release of histamine (and other chemical mediators) from the mast cell or basophil. Once released, the histamine can react with local or widespread tissues through histamine receptors. Histamine, acting on H1-receptors, produces pruritus, vasodilation, hypotension, flushing, headache, bradycardia, bronchoconstriction, increase in vascular permeability and potentiation of pain.
While in the healthy heart, waves of electrical impulses originate in the sinus node before spreading to the rest of the atria, the atrioventricular node, and finally the ventricles (referred to as a normal sinus rhythm), this normal rhythm can be disrupted. Abnormal heart rhythms or arrhythmias may be asymptomatic or may cause palpitations, blackouts, or breathlessness. Some types of arrhythmia such as atrial fibrillation increase the long term risk of stroke. Some arrhythmias cause the heart to beat abnormally slowly, referred to as a bradycardia or bradyarrhythmia.
Apocrine gland anal sac adenocarcinomas first appear as small lumps associated with one of the anal sacs (rarely bilateral), but they can grow to a large size. Smaller tumors are undetectable without a rectal examination, while larger tumors can cause pain and straining to defecate. Between 25 and 40 percent of dogs with these tumors will also develop hypercalcaemia through secretion of parathyroid hormone-related protein by the tumor. Symptoms of hypercalcaemia include increased drinking and urination, vomiting, loss of appetite, weight loss, and bradycardia (slow heart rate).
The T (and occasionally U) waves are chiefly influenced by the parasympathetic nervous system guided by integrated brainstem control from the vagus nerve and the thoracic spinal accessory ganglia. An impulse (action potential) that originates from the SA node at a relative rate of 60-100bpm is known as normal sinus rhythm. If SA nodal impulses occur at a rate less than 60bpm, the heart rhythm is known as sinus bradycardia. If SA nodal impulses occur at a rate exceeding 100bpm, the consequent rapid heart rate is sinus tachycardia.
Adverse drug reactions (ADRs) associated with the use of beta blockers include: nausea, diarrhea, bronchospasm, dyspnea, cold extremities, exacerbation of Raynaud's syndrome, bradycardia, hypotension, heart failure, heart block, fatigue, dizziness, alopecia (hair loss), abnormal vision, hallucinations, insomnia, nightmares, sexual dysfunction, erectile dysfunction and/or alteration of glucose and lipid metabolism. Due to the high penetration across the blood–brain barrier, lipophilic beta blockers, such as propranolol and metoprolol, are more likely than other, less lipophilic, beta blockers to cause sleep disturbances, such as insomnia and vivid dreams and nightmares.
64, XXV.21 It is also toxic, causing tinnitus, vertigo, stupor, thirst, a feeling of suffocation, swelling of the tongue and throat, emesis and catharsis, bradycardia (slowing of the pulse), and finally collapse and death from cardiac arrest. Research in the 1970s, however, showed that the roots of H. niger do not contain the cardiotoxic compounds helleborin, hellebrin, and helleborein that are responsible for the lethal reputation of black hellebore. It seems that earlier studies may have used a commercial preparation containing a mixture of material from other species such as Helleborus viridis, green hellebore.
Elephant seals are able to slow down their heartbeat (bradycardia) and divert blood flow from the external areas of the body to important core organs. They can also slow down their metabolism while performing deep dives. Elephant seals have a helpful feature in their bodies known as the countercurrent heat exchanger to help conserve energy and prevent heat loss. In this system, arteries and veins are organized in a way to maintain a constant body temperature by having the cool blood flowing to the heart warmed by blood going to external areas of the animal.
This means that even at a therapeutic dose (5 µg/kg), some epibatidine might bind to the muscarinic acetylcholine receptors and cause adverse effects, such as hypertension, bradycardia and muscular paresis. Compared to the gold standard in pain management, morphine, epibatidine needed only 2.5 μg/kg to initiate a pain-relieving effect whilst the same effect required approximately 10 mg/kg of morphine (4,000 times the efficacy.) Currently, only rudimentary research into epibatidine's effects has yet been performed; the drug has been administered only to rodents for analysis at this time.
Absorption of small volumes of irrigating fluid via the prostatic venous sinuses will inevitably occur in most TURP operations. The average rate of absorption is 20ml/min, and therefore length of surgery may have an effect on the total volume absorbed. Fluid absorption leads to rapid volume expansion, which causes hypertension and reflex bradycardia. The oncotic pressure of blood will decrease as a result of the dilution of serum proteins, and this coupled with hypertension will push fluid from the intra-vascular to the interstitial compartment causing pulmonary and cerebral edema.
Until recently (within the last 20 years), β-blockers were contraindicated in CHF, owing to their negative inotropic effect and ability to produce bradycardia – effects which worsen heart failure. However, current guidelines recommend β-blocker therapy for patients with systolic heart failure due to left ventricular systolic dysfunction after stabilization with diuretic and ACEI therapy, irrespective of symptomatic severity or blood pressure. As with ACEI therapy, the addition of a β-blocker can decrease mortality and improve left ventricular function. Several β-blockers are specifically indicated for CHF including: bisoprolol, carvedilol, nebivolol and extended-release metoprolol.
By reducing heart rate to well below surface rates, oxygen is saved by reducing gas exchange as well as reducing the energy required for a high heart rate. Bradycardia is a control mechanism to allow a switch from pulmonary oxygen to oxygen stored in the muscles which is needed when the sea lions are diving to depth. Another way sea lions mitigate the oxygen obtained at the surface in dives is to reduce digestion rate. Digestion requires metabolic activity and therefore energy and oxygen are consumed during this process; however, sea lions can limit digestion rate and decrease it by at least 54%.
Side effects when used as drugs may include loss of appetite, nausea, vomiting, loose stools, vivid dreams at night, dehydration, rash, bradycardia, peptic ulcer disease, seizures, weight loss, rhinorrhea, salivation, muscle cramps, and fasciculations. ChEIs are indirect-acting parasympathomimetic drugs. It came to light during the Berlin Charité hospital treatment for poisoning of Russian dissident Alexei Navalny that a nerve agent known as belonging to the Novichok agents is a ChEI. On October 6, 2020, OPCW published an official statement stating than substance found in the body of Navalny is not in the list of prohibit substances.
Schematic diagram of normal sinus rhythm for a human heart as seen on an electrocardiogram. Ajmaline was first discovered to lengthen the refractory period of the heart by blocking sodium ion channels, but it has also been noted that it is also able to interfere with the hERG (human Ether-a-go-go-Related Gene) potassium ion channel. In both cases, Ajmaline causes the action potential to become longer and ultimately leads to bradycardia. When ajmaline reversibly blocks hERG, repolarization occurs more slowly because it is harder for potassium to get out due to less unblocked channels, therefore making the RS interval longer.
There are 6 different sinus arrhythmia. A normal heart should have a normal sinus rhythm, this rhythm can be identified by a ventricular rate of 60-100 bpm, at a regular rate, with a normal PR interval (0.12 to 0.20 second) and a normal QRS complex (0.12 second and less). Sinus bradycardia is another regular rhythm however the ventricular rate is only between 40-60 bpm, with a normal PR interval and a normal QRS complex. Sinus tachycardia is another regular rhythm however the ventricular rate is quicker, between 100 - 160 bpm, with a normal PR interval and normal QRS complex.
From 1890 to 1914 Dehio was editor of St. Petersburger Medizinischen Wochenschrift for Dorpat. He was the president of the Naturalists' Society at the University of Dorpat in 1899–1901, and for a period of time was vice- president of the society to combat leprosy in Livonia. An atropine test known as "Dehio's test" is attributed to him, which states: "If an injection of atropine relieves bradycardia, the condition is due to action of the vagus; if it does not, the condition may be due to an affection of the heart itself". One of Dehio's daughters was the writer Else Hueck-Dehio.
Toxicology and Applied Pharmacology. Vol. 44, Pg. 1, 1978. At sufficiently high doses, it is associated with nicotine poisoning, which, while common in children (in whom poisonous and lethal levels occur at lower doses per kilogram of body weight) rarely results in significant morbidity or death. The initial symptoms of a nicotine overdose typically include nausea, vomiting, diarrhea, hypersalivation, abdominal pain, tachycardia (rapid heart rate), hypertension (high blood pressure), tachypnea (rapid breathing), headache, dizziness, pallor (pale skin), auditory or visual disturbances, and perspiration, followed shortly after by marked bradycardia (slow heart rate), bradypnea (slow breathing), and hypotension (low blood pressure).
There is a serious risk of bradycardia when daclatasvir is used with sofosbuvir and amiodarone Because it has not been extensively studied as a single agent, it is unknown what specific side effects are linked to this medication alone. Adverse events on daclatasvir have only been reported on combination therapy with sofusbivir or triple therapy with sofusbivir/ribavirin. Common adverse events occurring in >5% of people on combination therapy (sofusbivir + daclatasvir) include headache and fatigue; in triple therapy (daclatasvir + sofusbivir + ribavirin) the most common adverse events (>10%) include headache, fatigue, nausea and hemolytic anemia. Daclatasvir could cause hepatitis B re-activation in people co-infected with hepatitis B and C viruses.
In general, two types of problems result in bradycardias: disorders of the SA node, and disorders of the AV node. With SA node dysfunction (sometimes called sick sinus syndrome), there may be disordered automaticity or impaired conduction of the impulse from the SA node into the surrounding atrial tissue (an "exit block"). Second- degree sinoatrial blocks can be detected only by use of a 12-lead EKG. It is difficult and sometimes impossible to assign a mechanism to any particular bradycardia, but the underlying mechanism is not clinically relevant to treatment, which is the same in both cases of sick sinus syndrome: a permanent pacemaker.
Neonatal withdrawal syndrome associated with benzodiazepines include hypertonia, hyperreflexia, restlessness, irritability, abnormal sleep patterns, inconsolable crying, tremors, or jerking of the extremities, bradycardia, cyanosis, suckling difficulties, apnea, risk of aspiration of feeds, diarrhea and vomiting, and growth retardation. This syndrome can develop between three days to three weeks after birth and can have a duration of up to several months. The pathway by which clonazepam is metabolized is usually impaired in newborns. If clonazepam is used during pregnancy or breastfeeding, it is recommended that serum levels of clonazepam are monitored and that signs of central nervous system depression and apnea are also checked for.
This is due to profound depression of the central nervous system, and is usually reversible. Treatment of phenobarbital overdose is supportive, and mainly consists of the maintenance of airway patency (through endotracheal intubation and mechanical ventilation), correction of bradycardia and hypotension (with intravenous fluids and vasopressors, if necessary), and removal of as much drug as possible from the body. Depending on how much time has elapsed since ingestion of the drug, this may be accomplished through gastric lavage (stomach pumping) or use of activated charcoal. Hemodialysis is effective in removing phenobarbital from the body, and may reduce its half-life by up to 90%.
Cullen had a style that very much centred round his left jab. He had problems with his right hand during his early amateur days and this made him depend more on his left hand. He had large reserves of stamina due to an abnormally slow heart rate, known as bradycardia, and he would use his left jab to score points whilst using his mobility to keep away from his opponent’s punches. This did not always lead to an attractive contest earning him the nickname the one armed bandit, and Cullen was not as popular outside his native North-East as his talent would seem to merit.
The cranium dysfunction mechanical changes in the gut can compress the vagus nerve at any number of locations along the vagus, slowing the heart. As the heart slows, autonomic reflexes are triggered to increase blood pressure and heart rate. This is complemented by gastro-coronary reflexes whereby the coronary arteries constrict with "functional cardiovascular symptoms" similar to chest-pain on the left side and radiation to the left shoulder, dyspnea, sweating, up to angina pectoris -like attacks with extrasystoles, drop of blood pressure, and tachycardia (high heart beat) or sinus bradycardia (heart beat below 60). Typically, there are no changes / abnormalities related in the EKG detected.
This can affect exocrine glands (increased salivation, perspiration, lacrimation), the respiratory system (excessive bronchial secretions, tightness of the chest, and wheezing), the gastrointestinal tract (nausea, vomiting, diarrhea), the eyes (miosis, blurred vision) and the cardiovascular system (decrease in blood pressure, and bradycardia). Overstimulation of the nicotinic receptors in the para- or sympathic nervous system may also cause adverse effects on the cardiovascular system, such as pallor, tachycardia and increased blood pressure. In the somatic nervous system, accumulation of acetylcholine may cause muscle fasciculation, paralysis, cramps, and flaccid or rigid tone. Overstimulation of the nerves in the central nervous system, specifically in the brain, may result in drowsiness, mental confusion and lethargy.
Health care providers should also monitor vital signs (blood pressure, heart rate, etc.) before the infusion starts, periodically during infusion and post-infusion in a health care setting. Health care providers should perform electrocardiogram (ECG) monitoring during infusion in patients with a history of slow heart rate (bradycardia), conduction disorder (impaired progression of electrical impulses through the heart) or structural heart disease (defect or abnormality of the heart), as some patients with CLN2 disease can develop conduction disorders or heart disease. Hypersensitivity reactions have also been reported in Brineura- treated patients. Due to the potential for anaphylaxis, appropriate medical support should be readily available when Brineura is administered.
Autonomic dysreflexia (AD), also previously known as mass reflex, is a potential medical emergency classically characterized by uncontrolled hypertension and bradycardia, although tachycardia is known to commonly occur. AD occurs most often in individuals with spinal cord injuries with lesions at or above the T6 spinal cord level, although it has been reported in patients with lesions as low as T10. Guillain–Barré syndrome may also cause Autonomic Dysreflexia. The uncontrolled hypertension in AD may result in mild symptoms, such as sweating above the lesion level, goosebumps, blurred vision, or headache; However, severe hypertension may result in potentially life- threatening complications including seizure, intracranial bleed, or retinal detachment.
Mutations in emerin cause X-linked recessive Emery–Dreifuss muscular dystrophy, which is characterized by early contractures in the Achilles tendons, elbows and post-cervical muscles; muscle weakness proximal in the upper limbs and distal in lower limbs; along with cardiac conduction defects that range from sinus bradycardia, PR prolongation to complete heart block. In these patients, immunostaining of emerin is lost in various tissues, including muscle, skin fibroblasts, and leukocytes, however diagnostic protocols involve mutational analysis rather than protein staining. In nearly all cases, mutations result in a complete deletion, or undetectable levels, of emerin protein. Approximately 20% of cases have X chromosomes with an inversion within the Xq28 region.
Kashima Operation should be avoided in cases when a tumour is diffused throughout the thyroid cartilage, because operating in such cases may damage the tumour which may lead to its metastasis. The procedure should be avoided in patients with history of bradycardia, aneurysms or recent infarcts where general anesthesia may become a threat to patient’s life. In patients with fractured cervical spine it is not possible to perform this laser surgery because proper positioning of the patient would not be possible. Similarly in cases of severe ankylosing spondylitis, due to complete fusion and rigidity of the spine, movements are not possible which again hampers the proper positioning of the patient.
The lead usually lodges in the apex or septum of the right ventricle. Just like pacemakers, ICDs can have a single wire or lead in the heart (in the right ventricle, single chamber ICD), two leads (in the right atrium and right ventricle, dual chamber ICD) or three leads (biventricular ICD, one in the right atrium, one in the right ventricle and one on the outer wall of the left ventricle). The difference between pacemakers and ICDs is that pacemakers are also available as temporary units and are generally designed to correct slow heart rates, i.e. bradycardia, while ICDs are often permanent safeguards against sudden life-threatening arrhythmias.
The most common complication is a hemorrhage, or bleeding, of the puncture site and can be especially dangerous when the fetus is younger than 21 weeks. The risk of hemorrhage is greater if the fetus has a defect that affects its platelets. A transfusion of donor platelets is usually done in such cases to reduce the risk of bleeding. If the bleeding is severe, immediate delivery is an option as long as the fetus is old enough to survive, or fetal blood volume restoration may be considered. Another possible complication is cord hematoma, which doesn’t have any characteristic symptoms but can be indicated by sudden bradycardia.
About 75 percent of individuals with Holt–Oram syndrome also have congenital heart problems, with the most common being defects in the tissue wall between the upper chambers of the heart (atrial septal defect) or the lower chambers of the heart (ventricular septal defect). People with Holt–Oram syndrome may also have cardiac conduction disease, or abnormalities in the electrical system that coordinates contractions of the heart chambers. Cardiac conduction disease can lead to slow heart rate (bradycardia); rapid, ineffective contraction of the heart muscles (fibrillation); and heart block. People with Holt-Oram syndrome may have only congenital heart defects, only cardiac conduction disease, both or neither.
Transvenous cardiac pacing, also called endocardial pacing, is a potentially life-saving intervention used primarily to correct profound bradycardia. It can be used to treat symptomatic bradycardias that do not respond to transcutaneous pacing or to drug therapy. Transvenous pacing is achieved by threading a pacing electrode through a vein into the right atrium, right ventricle, or both. This means of pacing the heart is not as popular as other means of pacing (see transcutaneous pacing, implanted pacemaker, epicardial pacing) because it is a temporary solution to pace the heart and yet involves a similar level of risk of bleeding as a more permanent solution like placing an implanted pacemaker.
For patients who present in an emergency setting with symptomatic bradycardias, usually drugs like atropine or sympathomimetic drugs (epinephrine or dopamine) can be used to increase the heart rate to an adequate level until the underlying cause of the bradycardia can be isolated and then, possibly, a permanent pacemaker can be placed. For patients for whom transvenous pacing is chosen, the procedure is done at the bedside with a local anesthetic alone or in conjunction with conscious sedation. The pacing electrode is advanced through the vein under fluoroscopic and electrocardiographic guidance. An x-ray after the procedure is always obtained to confirm placement of the pacing electrode.
Over 10% of oral sotalol users experience fatigue, dizziness, lightheadedness, headache, weakness, nausea, shortness of breath, bradycardia (slow heart rate), a sensation of the heart beating too hard, fast, or irregularly, or chest pain. Higher doses of sotalol increase the risk for all of these possible side effects. In rare cases, the QT prolongation caused by sotalol can lead to the development of life-threatening torsade de pointes (TdP) polymorphic ventricular tachycardia. Across several clinical trials, 0.6% of oral sotalol patients with supraventricular abnormal heart rhythms (such as atrial fibrillation) developed TdP. For patients who had a history of sustained ventricular tachycardia (abnormal rhythm lasting more than 30 seconds), 4% developed TdP.
The name of this drug is also given as 3,6-dipropanoylmorphine and its 6-mono-acetylated homologue is also a longer-acting heroin-like drug, as are 3,6-diformylmorphine and 6-formylmorphine. Dipropanoylmorphine, though rarely used, is considered to be a safer and less addictive alternative to morphine. Studies and clinical trials comparing dipropanoylmorphine to morphine have produced results that indicate the incidence of side-effects are far more common with morphine. Respiratory depression, euphoria, excessive sedation and somnolence (so-called 'nodding' by recreational opioid users), constipation, miosis (pinpoint pupils), nausea, bradycardia, behavioral disturbances, and severe physical and psychological dependence on morphine is more likely with the use of morphine versus dipropanoylmorphine.
Overall, 14.5% of patients taking ivabradine experience luminous phenomena (by patients described as sensations of enhanced brightness in a fully maintained visual field). This is probably due to blockage of Ih ion channels in the retina, which are very similar to cardiac If. These symptoms are mild, transient, and fully reversible. In clinical studies, about 1% of all patients had to discontinue the drug because of these sensations, which occurred on average 40 days after the drug was started. In a large clinical trial, bradycardia (unusually slow heart rate) occurred in 2% and 5% of patients taking ivabradine at doses of 7.5 and 10 mg respectively (compared to 4.3% in those taking atenolol).
PB-22 (QUPIC, SGT-21 or 1-pentyl-1H-indole-3-carboxylic acid 8-quinolinyl ester) is a designer drug offered by online vendors as a cannabimimetic agent, and detected being sold in synthetic cannabis products in Japan in 2013. PB-22 represents a structurally unique synthetic cannabinoid chemotype, since it contains an ester linker at the indole 3-position, rather than the precedented ketone of JWH-018 and its analogs, or the amide of APICA and its analogs. PB-22 has an EC50 of 5.1 nM for human CB1 receptors, and 37 nM for human CB2 receptors. PB-22 produces bradycardia and hypothermia in rats at doses of 0.3–3 mg/kg, suggesting potent cannabinoid-like activity.
Blood-injection-injury (BII) type phobia is a type of specific phobia characterized by the display of excessive, irrational fear in response to the sight of blood, injury, or injection, or in anticipation of an injection, injury, or exposure to blood. Blood-like stimuli (paint, ketchup) may also cause a reaction. This is a common phobia with an estimated 3-4% prevalence in the general population, though it has been found to occur more often in younger and less educated groups. When exposed to phobic triggers, those with the phobia often experience a two-phase response: an initial increase in heart rate and blood pressure, followed quickly by bradycardia (decreased heart rate) and hypotension (decreased blood pressure).
Deliberate ingestion of Roundup ranging from 85 to 200 ml (of 41% solution) has resulted in death within hours of ingestion, although it has also been ingested in quantities as large as 500 ml with only mild or moderate symptoms. Consumption of over 85 ml of concentrated product is likely to cause serious symptoms in adults, including burns due to corrosive effects as well as kidney and liver damage. More severe cases lead to "respiratory distress, impaired consciousness, pulmonary edema, infiltration on chest X-ray, shock, arrhythmias, kidney failure requiring haemodialysis, metabolic acidosis, and hyperkalaemia" and death is often preceded by bradycardia and ventricular arrhythmias. Skin exposure can cause irritation, and photocontact dermatitis has been occasionally reported.
The usage of succinylcholine, the depolarizing neuromuscular agent, can lead to hyperkalemia, malignant hyperthermia, myalgia, increased intragastric pressure, increased intraocular pressure, increased intracranial pressure, cardiac dysrhythmias (bradycardia is the most common type) and allergic reactions. As a result, it is contraindicated for patients with susceptibility to malignant hyperthermia, denervating conditions, major burns after 48 hours, and severe hyperkalemia. For nondepolarizing NMBAs except vecuronium, pipecuronium, doxacurium, cisatracurium, rocuronium and rapacuronium, they produce certain extent of cardiovascular effect.Moreover, Tubocurarine can produce hypotension effect while Pancuronium can lead to moderate increase in heart rate and small increase in cardiac output with little or no increase in systemic vascular resistance, which is unique in nondeploarizing NMBAs.
In the case of inhalation, aerosolized toxins carried onshore in sea spray can cause respiratory irritation that can escalate, in more extreme cases, to more severe airway constriction, an effect observed at pM concentrations. More significant are the cases of ingestion, whether by direct swallowing of seawater during blooms of K. brevis or digestion of contaminated filter- feeding animals. After feeding upon K. brevis, aquatic invertebrates and shellfish in particular can accumulate brevetoxins, resulting in neurotoxic shellfish poisoning (NSP). In humans, the characteristic symptoms of NSP include Paresthesia (tingling), reversal of hot-cold temperature sensation, myalgia (muscle pain), vertigo, ataxia (loss of coordination), abdominal pain, nausea, diarrhea, headache, bradycardia (slow heart rate), dilated pupils and as respiratory distress, as previously mentioned.
In sufficient amounts, the theobromine found in chocolate is toxic to animals such as cats, dogs, horses, parrots, and small rodents because they are unable to metabolise the chemical effectively. If animals are fed chocolate, the theobromine may remain in the circulation for up to 20 hours, possibly causing epileptic seizures, heart attacks, internal bleeding, and eventually death. Medical treatment performed by a veterinarian involves inducing vomiting within two hours of ingestion and administration of benzodiazepines or barbiturates for seizures, antiarrhythmics for heart arrhythmias, and fluid diuresis. A typical dog will normally experience great intestinal distress after eating less than of dark chocolate, but will not necessarily experience bradycardia or tachycardia unless it eats at least a half a kilogram (1.1 lb) of milk chocolate.
Cardiovascular diseases represent a major cause of worldwide mortality, and the relevance of the genetic component in these diseases has recently become more apparent. Genetic alterations of HCN4 channels (the molecular correlate of sinoatrial f-channels) coupled to rhythm disturbances have been reported in humans. For example, an inherited mutation of a highly conserved residue in the CNBD of the HCN4 protein (S672R) is associated with inherited sinus bradycardia. In vitro studies indicate that the S672R mutation causes a hyperpolarizing shift of the HCN4 channel open probability curve of about 5 mV in heterozygosis, an effect similar to the hyperpolarizing shift caused by parasympathetic stimulation and able to explain a reduction of inward current during diastole and the resulting slower spontaneous rate.
Blood shift is a term used when blood flow to the extremities is redistributed to the head and torso during a breath-hold dive. Peripheral vasoconstriction occurs during submersion by resistance vessels limiting blood flow to muscles, skin, and viscera, regions which are "hypoxia-tolerant", thereby preserving oxygenated blood for the heart, lungs, and brain. The increased resistance to peripheral blood flow raises the blood pressure, which is compensated by bradycardia, conditions which are accentuated by cold water. Aquatic mammals have blood volume that is some three times larger per mass than in humans, a difference augmented by considerably more oxygen bound to hemoglobin and myoglobin of diving mammals, enabling prolongation of submersion after capillary blood flow in peripheral organs is minimized.
Cardiac arrhythmias are a common characteristic of the human diving response. As part of the diving reflex, increased activity of the cardiac parasympathetic nervous system not only regulates the bradycardia, but also is associated with ectopic beats which are characteristic of human heart function during breath-hold dives. Arrhythmias may be accentuated by neural responses to face immersion in cold water, distension of the heart due to central blood shift, and the increasing resistance to left ventricular ejection (afterload) by rising blood pressure. Other changes commonly measured in the electrocardiogram during human breath- hold dives include ST depression, heightened T wave, and a positive U wave following the QRS complex, measurements associated with reduced left ventricular contractility and overall depressed cardiac function during a dive.
51 (1975) 244-250 For example, certain situations of excessive or reduced heart rate (tachycardia or bradycardia, respectively) can cause a BBB known as a rate-dependent bundle branch block (RDBBB). This manifests in a similar fashion to a regular bundle branch block, but occurs only under conditions that affect contractile rate. Tachycardia- dependent bundle branch block (TDBBB) can affect either ventricle in the heart, and occurs when the heart's rate of contraction reaches an elevated level and becomes uncoupled from the heart's refractory period (the time it takes for a cardiac cell to "reset" for future contraction). Thus the cell is unable to contract by the time the next electrical stimuli is present, and a blocking of this signal occurs.
Another study published in February 2011 in Arts in Psychotherapy by Jayne M. Standley of the National Institute for Infant and Child Medical Music Therapy at Florida State University suggests that babies who receive this kind of therapy leave the hospital sooner. Additional research by Jayne M. Standley has demonstrated that the physiological responses of prematurely delivered infants undergoing intensive care can be regulated by listening to gentle lullabies through headphones. In addition to slowing heart and respiration rates, lullabies have been associated with increased oxygen saturation levels and the possible prevention of potentially life-threatening episodes of apnea and bradycardia. Gentle music can also provide stimulation for premature infants to behave in ways that boost their development and keep them alive.
The toxicity of the yew plant is due to some substances that are found in it, the principal ones are: toxic alkaloids (taxine B, paclitaxel, isotaxine B, taxine A), glycosides (taxicatine) and taxane derivates (taxol A, taxol B). There have been many studies about the toxicity of the taxine alkaloids and they have shown that their mechanism of action is interfering with the sodium and calcium channels of the myocardial cells, increasing the cytoplasmic calcium concentrations. Their mechanism is similar to drugs such as verapamil, although taxines are more cardioselective. They also reduce the rate of the depolarization of the action potential in a dose-dependent manner. This produces bradycardia, hypotension, depressed myocardial contractility, conduction delay, arrhythmias, and other complications.
Franz Köhler Digitalis toxicity (also known as digitalis intoxication and digitalism) results from an overdose of digitalis and causes nausea, vomiting and diarrhea, as well as sometimes resulting in xanthopsia (jaundiced or yellow vision) and the appearance of blurred outlines (halos), drooling, abnormal heart rate, cardiac arrhythmias, weakness, collapse, dilated pupils, tremors, seizures, and even death. Bradycardia also occurs. Because a frequent side effect of digitalis is reduction of appetite, some individuals have used the drug as a weight-loss aid. Digitalis is an example of a drug derived from a plant that was formerly used by folklorists and herbalists; herbalists have largely abandoned its use because of its narrow therapeutic index and the difficulty of determining the amount of active drug in herbal preparations.
The NICHD nomenclature defines baseline fetal heart rate as: The baseline FHR is determined by approximating the mean FHR rounded to increments of 5 beats per minute (bpm) during a 10-minute window, excluding accelerations and decelerations and periods of marked FHR variability (greater than 25 bpm). There must be at least 2 minutes of identifiable baseline segments (not necessarily contiguous) in any 10-minute window, or the baseline for that period is indeterminate. In such cases, it may be necessary to refer to the previous 10-minute window for determination of the baseline. Abnormal baseline is termed bradycardia when the baseline FHR is less than 110 bpm; it is termed tachycardia when the baseline FHR is greater than 160 bpm.
This results in bradycardia, vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion, while there's piloerection, pale and cool skin below the lesion due to the prevailing sympathetic outflow. Initial treatment involves sitting the patient upright, removing any constrictive clothing (including abdominal binders and support stockings), rechecking blood pressure frequently, and then checking for and removing the inciting issue, which may require urinary catheterization or bowel disimpaction. If systolic blood pressure remains elevated (over 150 mm Hg) after initial steps, fast-acting short-duration antihypertensives are considered, while other inciting causes must be investigated for the symptoms to resolve. Prevention of AD involves educating the patient, family and caregivers of the precipitating cause, if known, and how to avoid it, as well as other triggers.
When not breathing for long and dangerous periods of time in cold water, a person's body undergoes great temporary changes to try to prevent death. It achieves this through the activation of the mammalian diving reflex, which has 3 main properties. Other than Bradycardia and Peripheral vasoconstriction, there is a blood shift which occurs only during very deep dives that affects the thoracic cavity (a chamber of the body protected by the thoracic wall.) When this happens, organ and circulatory walls allow plasma/water to pass freely throughout the thoracic cavity, so its pressure stays constant and the organs aren't crushed. In this stage, the lungs' alveoli fill up with blood plasma, which is reabsorbed when the organism leaves the pressurized environment.
UR-144 has high affinity for the CB2 receptor with a Ki of 1.8 nM but 83x lower affinity for the CB1 receptor with a Ki of 150 nM. UR-144 was found to possess an EC50 of 421 nM for human CB1 receptors, and 72 nM for human CB2 receptors. UR-144 produces bradycardia and hypothermia in rats at a dose of 10 mg/kg, suggesting weak cannabinoid-like activity. Chemically it is closely related to other 2,2,3,3-tetramethylcyclopropyl synthetic cannabinoids like A-796,260 and A-834,735 but with a different substitution on the 1-position of the indole core, in these compounds its 1-pentyl group is replaced with alkylheterocycles like 1-(2-morpholinoethyl) and 1-(tetrahydropyran-4-ylmethyl).
Deliberate ingestion of Roundup ranging from 85 to 200 ml (of 41% solution) has resulted in death within hours of ingestion, although it has also been ingested in quantities as large as 500 ml with only mild or moderate symptoms. Consumption of over 85 ml of concentrated product is likely to cause serious symptoms in adults, including burns due to corrosive effects as well as kidney and liver damage. More severe cases lead to "respiratory distress, impaired consciousness, pulmonary edema, infiltration on chest X-ray, shock, arrhythmias, renal failure requiring haemodialysis, metabolic acidosis, and hyperkalaemia" and death is often preceded by bradycardia and ventricular arrhythmias. Skin exposure to ready-to-use concentrated glyphosate formulations can cause irritation, and photocontact dermatitis has been occasionally reported.
There is also a superficial venous system by which excess heat can be dissipated to the surroundings. The ascending aorta of pinnipeds is dilated to form an elastic aortic bulb which can hold the stroke volume of the heart and is thought to function as a hydraulic accumulator, to maintain blood pressure and flow during the long diastole of bradycardia, which is critical to the perfusion of the brain and heart, and compensates for the high resistance of the circulatory system due to vasoconstriction. Retia mirabilia are networks of anastomosing arteries and veins and are found in cetaceans and sirenians. Their function is not altogether clear, and may involve windkessel functions, intrathoracic vascular engorgement to prevent lung squeeze, thermoregulation, and the trapping of gas bubbles in the blood.
For instance, the arterial blood pressure in mammals is homeostatically controlled, and measured by stretch receptors in the walls of the aortic arch and carotid sinuses at beginnings of the internal carotid arteries. The sensors send messages via sensory nerves to the medulla oblongata of the brain indicating whether the blood pressure has fallen or risen, and by how much. The medulla oblongata then distributes messages along motor or efferent nerves belonging to the autonomic nervous system to a wide variety of effector organs, whose activity is consequently changed to reverse the error in the blood pressure. One of the effector organs is the heart whose rate is stimulated to rise (tachycardia) when the arterial blood pressure falls, or to slow down (bradycardia) when the pressure rises above set point.
When the arterial blood pressure rises the arterioles are stimulated to dilate making it easier for blood to leave the arteries, thus deflating them, and bringing the blood pressure down, back to normal. At the same time the heart is stimulated via cholinergic parasympathetic nerves to beat more slowly (called bradycardia), ensuring that the inflow of blood into the arteries is reduced, thus adding to the reduction in pressure, and correction of the original error. Low pressure in the arteries, causes the opposite reflex of constriction of the arterioles, and a speeding up of the heart rate (called tachycardia). If the drop in blood pressure is very rapid or excessive, the medulla oblongata stimulates the adrenal medulla, via "preganglionic" sympathetic nerves, to secrete epinephrine (adrenaline) into the blood.
Mutations in the ANK2 gene have been associated with a dominantly-inherited, cardiac arrhythmia syndrome known as ankyrin-B syndrome, previously referred to as long QT syndrome, type 4, which can be described as an atypical arrhythmia syndrome with bradycardia, atrial fibrillation, conduction block, arrhythmia and risk of sudden cardiac death. Intense investigation is currently ongoing regarding linking ANK2 mutations to the range of severity of cardiac phenotypes, and initial evidence suggests that the varying degrees of loss of function of ankyrin-B protein may explain the effect of any particular mutation. Initially, a Glu1425Gly mutation in ANK2 was found to cause dominantly-inherited long QT syndrome, type 4, cardiac arrhythmia. The mechanistic underpinnings of this mutation include abnormal expression and targeting of the sodium pump, the sodium-calcium exchanger, and inositol-1,4,5-trisphosphate receptors to transverse tubules, as well as calcium handling resulting in extrasystoles.
Dermal exposure resulted in nausea, dizziness, vomiting, headache, or tachycardia. Nicotine poisoning tends to produce symptoms that follow a biphasic pattern. The initial symptoms are mainly due to stimulatory effects and include nausea and vomiting, excessive salivation, abdominal pain, pallor, sweating, hypertension, tachycardia, ataxia, tremor, headache, dizziness, muscle fasciculations, and seizures. After the initial stimulatory phase, a later period of depressor effects can occur and may include symptoms of hypotension and bradycardia, central nervous system depression, coma, muscular weakness and/or paralysis, with difficulty breathing or respiratory failure. From September 1, 2010 to December 31, 2014, there were at least 21,106 traditional cigarette calls to US poison control centers. During the same period, the ten most frequent adverse effects to traditional cigarettes reported to US poison control centers were vomiting (80.0%), nausea (9.2%), drowsiness (7.8%), cough (7.2%), agitation (6.6%), pallor (3.0%), tachycardia (2.5%), diaphoresis (1.5%), dizziness (1.5%), and diarrhea (1.4%).
Symptoms of exposure to this type of compound include cholinesterase inhibition, miosis, frontal headache, increased bronchial secretion, nausea, vomiting, sweating, abdominal cramps, diarrhea, lacrimation, increased salivation, bradycardia, cyanosis and muscular twitching of the eyelids, tongue, face and neck, possibly progressing to convulsions. Other symptoms include hyperemia of the conjunctiva, dimness of vision, rhinorrhea, bronchoconstriction, cough, fasciculation, anorexia, incontinence, eye changes, weakness, dyspnea, bronchospasm, hypotension or hypertension due to asphyxia, restlessness, anxiety, dizziness, drowsiness, tremor, ataxia, depression, confusion, neuropathy (rare), coma and death from depression of respiratory or cardiovascular systems. Exposure to this type of compound may result in giddiness, nervousness, blurred vision, discomfort (tightness) in chest, papilledema, muscular weakness, loss of reflexes, loss of sphincter control, cardiac arrhythmias, various degrees of heart block and cardiac arrest. It may also result in spasm of accommodation, aching pain in and about the eye, nystagmus, delayed distal axonopathy and paresthesias and paralysis of limbs.
Effects on ryanodine receptors specifically were also rescued by a potent Ca2+/calmodulin-dependent protein kinase II inhibitor, suggesting that inhibition of Ca2+/calmodulin- dependent protein kinase II may also be a potential treatment strategy. These mice also display several electrophysiological abnormalities, including bradycardia, variable heart rate, long QT intervals, catecholaminergic polymorphic ventricular tachycardia, syncope, and sudden cardiac death. Mechanistic explanations underlying these effects were explained in a later study conducted in the ankyrin-B (-/+) mice, which showed that reduction of ankyrin-B alters the transport of sodium and calcium and enhances the coupled openings of ryanodine receptors, which results in a higher frequency of calcium sparks and waves of calcium. It is now becoming clear that ankyrin-B exists in a biomolecular complex with the sodium potassium ATPase, sodium calcium exchanger and inositol triphosphate receptor which is localized in T-tubules within discrete microdomains of cardiomyocytes that are distinct from dyads formed by dihydropyridine receptors complexed to ryanodine receptors.
Seizures rarely occur. Because atracurium undergoes Hofmann elimination as a primary route of chemodegradation, one of the major metabolites from this process is laudanosine, a tertiary amino alkaloid reported to be a modest CNS stimulant with epileptogenic activity and cardiovascular effects such a hypotension and bradycardia. As part of the then fierce marketing battle between the competing pharmaceutical companies (Burroughs Wellcome Co. and Organon, Inc.) with their respective products, erroneous information was quickly and subtly disseminated very shortly after the clinical introduction of atracurium that the clinical use of atracurium was likely to result in a terrible tragedy because of the significant clinical hazard by way of frank seizures induced by the laudanosine by-product \- the posited hypothesis being that the laudanosine produced from the chemodegradation of parent atracurium would cross the blood–brain barrier in sufficiently high enough concentrations that lead to epileptogenic foci. Fortunately, both for the public and for atracurium, rapid initial investigations irrefutably failed to find any overt or EEG evidence for a connection between atracurium administration and epileptogenic activity.
"Black hellebore" was used by the Greek and Romans to treat paralysis, gout and other diseases, more particularly insanity. "Black hellebore" is also toxic, causing tinnitus, vertigo, stupor, thirst, anaphylaxis, emesis (vomiting), catharsis, bradycardia (slowing of the heart rate), and finally, collapse and death from cardiac arrest. Although Helleborus niger (black hellebore) contains protoanemonin,Olson, Kent R., Poisoning & Drug Overdose, p312 at Google Book Search, accessed 12 January 2009 or ranunculin,Smolinske, Susan C., Toxicity of Houseplants, pp38, 153 at Google Book Search, accessed 12 January 2009 which has an acrid taste and can cause burning of the eyes, mouth, and throat, oral ulceration, gastroenteritis, and hematemesis,Olson, Kent R, Poisoning & Drug Overdose, p309 at Google Book Search, accessed 12 January 2009 research in the 1970s showed that the roots of H. niger do not contain the cardiotoxic compounds helleborin, hellebrin, and helleborein that are responsible for the lethal reputation of "black hellebore". It seems that earlier studies may have used a commercial preparation containing a mixture of material from other species such as Helleborus viridis, green hellebore.

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