Reduced cerebral blood flow with orthostasis precedes hypocapnic hyperpnea, sympathetic activation, and postural tachycardia syndrome.
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The word hyperpnea uses combining forms of hyper- + -pnea, yielding "excessive breathing". See pronunciation information at dyspnea.
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Respiratory apnea followed the hyperpnea and lasted approximately 2 min when the animal was returned to the respirator.
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Common features include ataxia, hypotonia, episodic hyperpnea, newborn apnea, developmental delay, oculomotor apraxia, nystagmus, dysmorphic facies and polydactyly.
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Catecholamines by the adrenal glands and postganglionic nerve terminals and Ach by ganglions and postganglionic nerve terminals are released when the poison strikes. Also other neurotransmitters are released by the whole venom and isolated toxins. In rats, the Tityustoxin caused dramatic effects on the circulatory and respiratory systems, consisting of hypotension, tachypnea, hyperpnea, ataxic and gasping breathing. Following these initial effects, 5 or 10 µg of TsTX induced hypertension and hyperpnea.
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Severe overdosage may cause tachypnea or hyperpnea, hallucinations, hypertensive crisis, convulsions or delirium, but in some individuals there may be CNS depression with somnolence, stupor or respiratory depression.
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The human body can adapt to high altitude through both immediate and long-term acclimatization. At high altitude, in the short term, the lack of oxygen is sensed by the carotid bodies, which causes an increase in the breathing depth and rate (hyperpnea). However, hyperpnea also causes the adverse effect of respiratory alkalosis, inhibiting the respiratory center from enhancing the respiratory rate as much as would be required. Inability to increase the breathing rate can be caused by inadequate carotid body response or pulmonary or renal disease.
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A doubling or more of these small pressure differences could be achieved only by very major changes in the breathing effort at high altitudes. All of the above influences of low atmospheric pressures on breathing are accommodated primarily by breathing deeper and faster (hyperpnea). The exact degree of hyperpnea is determined by the blood gas homeostat, which regulates the partial pressures of oxygen and carbon dioxide in the arterial blood. This homeostat prioritizes the regulation of the arterial partial pressure of carbon dioxide over that of oxygen at sea level.
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Brain control of exhalation can be broken down into voluntary control and involuntary control. During voluntary exhalation, air is held in the lungs and released at a fixed rate. Examples of voluntary expiration include: singing, speaking, exercising, playing an instrument, and voluntary hyperpnea. Involuntary breathing includes metabolic and behavioral breathing.
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The partial pressure of carbon dioxide has been noted by Yushi et al. to drop as low as 6.7 mmHg, while oxygen saturation remains at 99-100%. Respiratory alkalosis is induced in people affected with CNH, which stimulates the hyperpnea to attempt to compensate the rise of the blood’s pH. Some of the reported cases of CNH claim alkaline cerebral spinal fluid (CSF).
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Abnormal breathing patterns include Kussmaul breathing, Biot's respiration and Cheyne–Stokes respiration. Other breathing disorders include shortness of breath (dyspnea), stridor, apnea, sleep apnea (most commonly obstructive sleep apnea), mouth breathing, and snoring. Many conditions are associated with obstructed airways. Hypopnea refers to overly shallow breathing; hyperpnea refers to fast and deep breathing brought on by a demand for more oxygen, as for example by exercise.
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The terms hypoventilation and hyperventilation also refer to shallow breathing and fast and deep breathing respectively, but under inappropriate circumstances or disease. However, this distinction (between, for instance, hyperpnea and hyperventilation) is not always adhered to, so that these terms are frequently used interchangeably. A range of breath tests can be used to diagnose diseases such as dietary intolerances. A rhinomanometer uses acoustic technology to examine the air flow through the nasal passages.
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Diagnosing adipsia can be difficult as there is no set of concrete physical signs that are adipsia specific. Changes in the brain that are indicative of adipsia include those of hyperpnea, muscle weakness, insomnia, lethargy, and convulsions (although uncommon except in extreme cases of incredibly rapid rehydration). Patients with a history of brain tumors, or congenital malformations, may have hypothalamic lesions, which could be indicative of adipsia. Some adults with Type A adipsia are anorexic in addition to the other symptoms.
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This rise in respiration rate however is not necessarily associated with a greater rate of oxygen consumption. Therefore, unlike most other birds, the common ostrich is able to dissipate heat through panting without experiencing respiratory alkalosis by modifying ventilation of the respiratory medium. During hyperpnea ostriches pant at a respiratory rate of 40–60 cycles per minute, versus their resting rate of 6–12 cycles per minute. Hot, dry and moisture lacking properties of the common ostrich respiratory medium affects oxygen's diffusion rate (Henry's Law).
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Cheyne–Stokes respiration is an abnormal pattern of breathing characterized by progressively deeper, and sometimes faster, breathing followed by a gradual decrease that results in a temporary stop in breathing called an apnea. The pattern repeats, with each cycle usually taking 30 seconds to 2 minutes. It is an oscillation of ventilation between apnea and hyperpnea with a crescendo- diminuendo pattern, and is associated with changing serum partial pressures of oxygen and carbon dioxide. Cheyne–Stokes respiration and periodic breathing are the two regions on a spectrum of severity of oscillatory tidal volume.
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Since the composition of the atmospheric air is almost constant below 80 km, as a result of the continuous mixing effect of the weather, the concentration of oxygen in the air (mmols O2 per liter of ambient air) decreases at the same rate as the fall in air pressure with altitude. Therefore, in order to breathe in the same amount of oxygen per minute, the person has to inhale a proportionately greater volume of air per minute at altitude than at sea level. This is achieved by breathing deeper and faster (i.e. hyperpnea) than at sea level (see below). Fig.
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High levels of lactic acid in the blood are observed in all people with GSD I, due to impaired gluconeogenesis. Baseline elevations generally range from 4 to 10 mol/mL, which will not cause any clinical impact. However, during and after an episode of low blood sugar, lactate levels will abruptly rise to exceed 15 mol/mL, the threshold for lactic acidosis. Symptoms of lactic acidosis include vomiting and hyperpnea, both of which can exacerbate hypoglycemia in the setting of GSD I. In cases of acute lactic acidosis, patients need emergency care to stabilize blood oxygen, and restore blood glucose.
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Most of the signs and symptoms of the Joubert syndrome appear very early in infancy with most children showing delays in gross motor milestones. Although other signs and symptoms vary widely from individual to individual, they generally fall under the hallmark of cerebellum involvement or in this case, lack thereof. Consequently, the most common features include ataxia (lack of muscle control), hyperpnea (abnormal breathing patterns), sleep apnea, abnormal eye and tongue movements, and hypotonia in early childhood. Other malformations such as polydactyly (extra fingers and toes), cleft lip or palate, tongue abnormalities, and seizures may also occur.
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At this point the lungs contain the functional residual capacity of air, which, in the adult human, has a volume of about 2.5–3.0 liters. During heavy breathing (hyperpnea) as, for instance, during exercise, exhalation is brought about by relaxation of all the muscles of inhalation, (in the same way as at rest), but, in addition, the abdominal muscles, instead of being passive, now contract strongly causing the rib cage to be pulled downwards (front and sides). This not only decreases the size of the rib cage but also pushes the abdominal organs upwards against the diaphragm which consequently bulges deeply into the thorax. The end-exhalatory lung volume is now less air than the resting "functional residual capacity".
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There is no effort made to breathe during the pause in breathing: there are no chest movements and no muscular struggling, although when awakening occurs in the middle of a pause, the inability to immediately operate the breathing muscles often results in cognitive struggle accompanied by a feeling of panic exacerbated by the feeling associated with excessive blood CO2 levels. Even in severe cases of central sleep apnea, however, the effects almost always result in pauses that make breathing irregular rather than cause the total cessation of breathing over the medium term. After the episode of apnea, breathing may be faster and/or more intense (hyperpnea) for a period of time, a compensatory mechanism to blow off retained waste gases, absorb more oxygen, and, when voluntary, enable a return to normal instinctive breathing patterns by restoring oxygen to the breathing muscles themselves.
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That is to say, at sea level the arterial partial pressure of CO2 is maintained at very close to 5.3 kPa (or 40 mmHg) under a wide range of circumstances, at the expense of the arterial partial pressure of O2, which is allowed to vary within a very wide range of values, before eliciting a corrective ventilatory response. However, when the atmospheric pressure (and therefore the partial pressure of O2 in the ambient air) falls to below 50-75% of its value at sea level, oxygen homeostasis is given priority over carbon dioxide homeostasis. This switch-over occurs at an elevation of about 2500 m (or about 8000 ft). If this switch occurs relatively abruptly, the hyperpnea at high altitude will cause a severe fall in the arterial partial pressure of carbon dioxide, with a consequent rise in the pH of the arterial plasma.
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In the absence of central apnea, any sudden drop in oxygen or excess of carbon dioxide, even if small, strongly stimulates the brain's respiratory centers to breathe; the respiratory drive is so strong that even conscious efforts to hold one's breath do not overcome it. In pure central sleep apnea, the brain's respiratory control centers, located in the region of the human brain known as the pre-Botzinger complex, are imbalanced during sleep and fail to give the signal to inhale, causing the individual to miss one or more cycles of breathing. The neurological feedback mechanism that monitors blood levels of carbon dioxide and in turn stimulates respiration fails to react quickly enough to maintain an even respiratory rate, allowing the entire respiratory system to cycle between apnea and hyperpnea, even for a brief time following an awakening during a breathing pause. The sleeper stops breathing for up to two minutes and then starts again.
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