Human Physiology - William F. Ganong 2002

Respiration
Adaptive respiratory changes in health and disease
Other respiratory anomalies

Asphyxia

Asphyxia caused by airway occlusion results in the simultaneous onset of acute asphyxia and Hypoxia. This stimulates the respiratory drive, leading to immense breathing efforts. Blood pressure and Heart rate increase sharply. Catecholamine secretion rises, while blood pH drops. Over time, respiratory efforts cease, blood pressure falls, and The Heart rate slows down. Animals subjected to asphyxia can still be revived via Artificial ventilation, although they remain prone to ventricular fibrillation, likely due to a combination of hypoxic myocardial damage and high blood catecholamine levels. If artificial ventilation is not initiated, cardiac arrest ensues within 4–5 minutes.

Drowning

Drowning is suffocation resulting from submersion, most commonly in Water. In 10% of drowning victims, after all attempts to inhale cease, the initial gulp of water triggers laryngospasm, leading to death from asphyxia without any water actually reaching the Lungs. In other cases, the vocal cord Muscles relax, and fluid enters the lungs. Fresh water is rapidly absorbed, dissolving into the plasma and causing intravascular hemolysis. Ocean water is significantly hypertonic and draws fluid from The Vascular System into the lungs, reducing plasma volume. The primary objective in treating near-drowning victims is resuscitation, though long-term management must account for the circulatory impacts of residual lung fluid.

Periodic Breathing

Acute episodes of voluntary mechanical hyperventilation reflect an interaction with chemical Respiratory Control mechanisms. If a normal individual hyperventilates for 2–3 minutes and then stops, normal breathing can resume without any conscious effort; however, a period of apnea ensues. This occurs when a few shallow breaths are followed by another apneic period, which repeats after the next few breaths (periodic breathing). These cycles can persist for some time until normal breathing pattern is restored (Fig. 37-11). Apnea clearly results from a CO₂ deficit, as it does not occur when hyperventilation is performed with a gas mixture containing 5% CO₂. During apnea, alveolar P_O2 decreases while P_CO2 increases. Respiration resumes due to hypoxic stimulation of the carotid and aortic chemoreceptors before CO₂ levels return to normal. A few breaths eliminate the hypoxic stimulus, and breathing stops once again before alveolar P_O2 drops further. Gradually, P_CO2 returns to normal, and regular breathing continues.

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Fig. 37-11. Changes in respiration and alveolar gas composition following 2 minutes of forced hyperventilation.

Cheyne-Stokes Respiration

Periodic breathing is observed in various pathological conditions and is frequently referred to as Cheyne-Stokes respiration. This breathing pattern is most characteristic of patients with decompensated Heart Failure and uremia, but it also occurs in those with Brain lesions and, under normal conditions, in some individuals during Sleep (Fig. 37-12). Occasionally, patients exhibiting Cheyne-Stokes respiration show an increased sensitivity to CO₂. This heightened response is undoubtedly the result of damage to Neural Pathways that normally inhibit respiration. In some individuals, CO₂ triggers relative hyperventilation, lowering arterial P_CO2, which is then followed by apnea; arterial P_CO2 subsequently rises back toward normal, but the respiratory mechanism becomes once again hyper-reactive to CO₂. Breathing stops, and the cycle repeats.

Another cause of periodic breathing in cardiac patients is an prolonged Circulation time from the lungs to the brain, which delays changes in arterial gas tensions and their subsequent effect on the respiratory centers in the Medulla Oblongata. If an individual with sluggish circulation experiences hyperventilation, the P_CO2 in their pulmonary blood drops, and it takes longer than normal for this low-P_CO2 blood to reach the brain. During this interval, pulmonary capillary P_CO2 continues to fall, and once this blood reaches the brain, the low P_CO2 inhibits the respiratory center, inducing apnea. In other words, the regulatory respiratory loops fluctuate abnormally because the negative feedback loop from the lungs to the brain is abnormally delayed.

Sleep Apnea

Sleep apnea episodes may be of central origin—such as impaired neural drive to the Respiratory Muscles—or due to upper airway obstruction (obstructive sleep apnea). This condition can occur at any age and happens when the pharyngeal muscles relax during sleep. In some cases, a reduced capacity of the genioglossus Muscle to contract during sleep is responsible for the blockage. These muscles normally pull the Tongue forward; when they fail to contract, the tongue falls backward, causing airway obstruction. After several strenuous respiratory efforts, the patient wakes up, takes a few normal breaths, and falls back asleep. Unsurprisingly, apnea episodes are most frequent during REM sleep, when muscle tone is at its lowest (see Chapter 11). Symptoms of sleep apnea include loud snoring, morning headaches, fatigue, and excessive daytime sleepiness. When severe and prolonged, it serves as an indicator of pulmonary Hypertension, heart failure, myocardial infarction, and stroke. Furthermore, traffic accidents among drivers with sleep apnea occur up to seven times more frequently than among other drivers.

Fig. 37-12. Cheyne-Stokes respiration during sleep. Two periods of apnea are separated by an increase followed by a decrease in tidal volume V_T (reprinted with permission from Cherniack NS: Respiratory dysrhythmias during sleep. N J Med 1981;305:325).

Sudden Infant Death Syndrome

Evidence suggests that sudden infant death syndrome (SIDS) may represent a form of sleep apnea. This tragic disorder, in which seemingly healthy infants are found dead in their cribs, has drawn considerable attention. Periods of apnea are common in premature infants. However, episodes of prolonged apnea do not reliably correlate with subsequent mortality, and none of the previously established chemosensitivity tests are reliable predictors of which infants are predisposed to SIDS. Some cases are linked to Cardiac Arrhythmias complicated by congenital long QT syndrome (see Chapter 28). Additionally, evidence shows that the risk of SIDS increases if the mother smokes. Another major risk factor is prone sleeping (sleeping on The Stomach). Educating mothers to place infants on their backs to sleep has significantly reduced the incidence of SIDS.