Chapter 035. Hypoxia and Cyanosis (Part 3)

Adaptation to Hypoxia An important component of the respiratory response to hypoxia originates in special chemosensitive cells in the carotid and aortic bodies and in the respiratory center in the brainstem. The stimulation of these cells by hypoxia increases ventilation, with a loss of CO2, and can lead to respiratory alkalosis. When combined with the metabolic acidosis resulting from the production of lactic acid, the serum bicarbonate level declines (Chap. 48).With the reduction of PaO2, cerebrovascular resistance decreases and cerebral blood flow increases in an attempt to maintain O 2 delivery to the brain. However, when the reduction of...
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Chapter 035. Hypoxia and Cyanosis (Part 3) Chapter 035. Hypoxia and Cyanosis (Part 3) Adaptation to Hypoxia An important component of the respiratory response to hypoxia originatesin special chemosensitive cells in the carotid and aortic bodies and in therespiratory center in the brainstem. The stimulation of these cells by hypoxiaincreases ventilation, with a loss of CO2, and can lead to respiratory alkalosis.When combined with the metabolic acidosis resulting from the production oflactic acid, the serum bicarbonate level declines (Chap. 48). With the reduction of PaO2, cerebrovascular resistance decreases andcerebral blood flow increases in an attempt to maintain O 2 delivery to the brain.However, when the reduction of PaO2 is accompanied by hyperventilation and areduction of Pa CO2, cerebrovascular resistance rises, cerebral blood flow falls, andhypoxia is intensified. The diffuse, systemic vasodilation that occurs in generalized hypoxia raisesthe cardiac output. In patients with underlying heart disease, the requirements ofperipheral tissues for an increase of cardiac output with hypoxia may precipitatecongestive heart failure. In patients with ischemic heart disease, a reduced Pa O2may intensify myocardial ischemia and further impair left ventricular function. One of the important mechanisms of compensation for chronic hypoxia isan increase in the hemoglobin concentration and in the number of red blood cellsin the circulating blood, i.e., the development of polycythemia secondary toerythropoietin production (Chap. 103). In persons with chronic hypoxemiasecondary to prolonged residence at a high altitude (>13,000 ft, 4200 m), acondition termed chronic mountain sickness develops. It is characterized by ablunted respiratory drive, reduced ventilation, erythrocytosis, cyanosis, weakness,right ventricular enlargement secondary to pulmonary hypertension, and evenstupor. CYANOSIS Cyanosis refers to a bluish color of the skin and mucous membranesresulting from an increased quantity of reduced hemoglobin, or of hemoglobinderivatives, in the small blood vessels of those areas. It is usually most marked inthe lips, nail beds, ears, and malar eminences. Cyanosis, especially if developedrecently, is more commonly detected by a family member than the patient. Theflorid skin characteristic of polycythemia vera (Chap. 103) must be distinguishedfrom the true cyanosis discussed here. A cherry-colored flush, rather thancyanosis, is caused by COHb (Chap. e35). The degree of cyanosis is modified by the color of the cutaneous pigmentand the thickness of the skin, as well as by the state of the cutaneous capillaries.The accurate clinical detection of the presence and degree of cyanosis is difficult,as proved by oximetric studies. In some instances, central cyanosis can be detectedreliably when the SaO2 has fallen to 85%; in others, particularly in dark-skinnedpersons, it may not be detected until it has declined to 75%. In the latter case,examination of the mucous membranes in the oral cavity and the conjunctivaerather than examination of the skin is more helpful in the detection of cyanosis. The increase in the quantity of reduced hemoglobin in the mucocutaneousvessels that produces cyanosis may be brought about either by an increase in thequantity of venous blood as a result of dilation of the venules and venous ends ofthe capillaries or by a reduction in the SaO2 in the capillary blood. In general,cyanosis becomes apparent when the concentration of reduced hemoglobin incapillary blood exceeds 40 g/L (4 g/dL). It is the absolute, rather than the relative, quantity of reduced hemoglobinthat is important in producing cyanosis. Thus, in a patient with severe anemia, therelative quantity of reduced hemoglobin in the venous blood may be very largewhen considered in relation to the total quantity of hemoglobin in the blood.However, since the concentration of the latter is markedly reduced, the absolutequantity of reduced hemoglobin may still be small, and, therefore, patients withsevere anemia and even marked arterial desaturation may not display cyanosis.Conversely, the higher the total hemoglobin content, the greater is the tendencytoward cyanosis; thus, patients with marked polycythemia tend to be cyanotic athigher levels of SaO2 than patients with normal hematocrit values. Likewise, localpassive congestion, which causes an increase in the total quantity of reducedhemoglobin in the vessels in a given area, may cause cyanosis. Cyanosis is alsoobserved when nonfunctional hemoglobin, such as methemoglobin orsulfhemoglobin (Chap. 99), is present in blood. Cyanosis may be subdivided into central and peripheral types. ...