Following this the hypercapnic blood arrives the respiratorycenter respiratory stimulation

and 2 to 3 mm Hg rise of PaC02 Level is common in normal sleep. In less severe cases, symptoms of CO2 retention include drowsiness, tremor and altered personality but the cyanosis is not necessarily present (as O2 lack, usually, is of insufficient degree). In fulminant cases there may be stupor and death. Most modern inhalation anesthetics excepting ether produce some hypercapnea. In conclusion, hypercapnia is seen in normal sleep, drug or disease induced hypoventilation, Pickwickian syndrome and anesthesia ASPHYXIA Officially speaking, this means a combination of CO2 retention and O2 lack, although this term (asphyxia) is used somewhat indiscriminately. Causes. (i) Strangulation, acute tracheal obstruction (say, due to 'choking', during swallowing of food), diaphragmatic paralysis etc. are well known causes of acute asphyxia, (ii) In the disease cor pulmonale (right ventricular failure due to disease of the lungs), a state of chronic asphyxia (characterized by low PaO2 and high PaCO2) persists. [The usual pathogenesis in cor pulmonale is, emphysema causing hypoxia (which powerfully causes vasoconstriction of pulmonary vessels) pulmonary hypertension right ventricular hypertrophy right ventricular failure]. Acute asphyxia The features of acute asphyxia are shown in table 4.6.3. There are three stages and death occurs within, usually five minutes In Maria Puzo's famous novel'God father' (publisher, Signet Book) a pen picture of a murder by strangulation has been described. The reader may recall that the victim, on being strangulated, struggled violently, convulsed, defecated, collapsed and then died, and the whole episode lasted only a few minutes. CYANOSIS It is a condition characterized by bluish or violet discoloration of the skin and the mucous membrane. The skin dis- coloration is obvious in fair complexioned persons but not so in dark or frankly black persons. Therefore, it is advisable always to look for cyanosis in the mucous membrane (undersurface of the tongue) in dark persons. The discoloration is due to the presence of excessive amounts of reduced Hb. Well known examples of cyanosis are (i) hypoxic hypoxia and (ii) stagnant hypoxia. The explanation of cyanosis in these two conditions should be obvious to the student. For cyanosis to appear, at least 5 gm of reduced Hb must be present/100 ml of blood. Therefore, in anemic hypoxia, where Hb concentration is already below 5 gm/100 ml, O2 lack may be present but the cyanosis will be absent. On the other hand, in polycythemia, there may be cyanosis, because the resulting increase in viscosity slows down the velocity of blood in the capillaries, and the blood becomes excessively reduced because of the long stay in the capillaries of the peripheral tissues. Central cyanosis occurs in lung diseases and are associated with hyperkmetic circulation but peripheral vasodilatation The pulse therefore is full bounding and the extremities remain warm. (ii) Peripheral cyanosis occurs typically in circulatory failure; blood in the capillaries of the periphery stays a longer time and thus becomes cyanosed. Pulse is thready and the extremities become cold. In short, in central cyanosis, the central oxygenating machine of the body (= the lungs) is at fault whereas in peripheral cyanosis, there is fault of the 02 transport, from lung to the periphery. In the infants and very youngs, exposure to cold may produce mild cyanosis, which is not abnormal. PERIODIC BREATHING Two types of periodic breathing are commonly seen: (1) Cheyne-Stokes breathing and (n) Blot's breathing Fig. 4.6.2. Cheyne-Stokes breathing In Cheyne Stokes breathing (fig 4.6.2), the respiration shows a 'hunting' behavior (when an animal, say a tiger, is hunting a prey, say a deer, in the forest, it has to occasionally, advance stealthily with a dead slow speed and after some time, it has to advance very fast to the same deer. This is hunting behavior). At times the depth of the respiration is hardly perceptible. This period is followed by ex-aggerated respiratory movements. These exaggerated movements progressively wane and the period of apnea returns. Thus, periods of apnea and hyperapnea go on cyclically. Explanation As it occurs commonly in left ventricular failure, the oc-curance of Cheyne-Stoke's respiration in left ventricular failure (LVF) will be discussed : LVF pulmonary edema hampering of gaseous exchange in the lungs elevation of C02 tension in arterial blood ( PaCO2) however, as there is LVF this CO2 rich blood reaches the respiratory center slowly and during this period the respiratory center is exposed to a blood which is deficient in CO2 (hypocapnic blood) respiratory inhibition. Following this the hypercapnic blood arrives the respiratorycenter respiratory stimulation washing out of CO2 from the body return of hypocapnia and loss of respiratory drive. Apart from LVF, Cheyne-Stokes respiration may be seen in head injury, cerebral haemorrhage and in high altitude sickness specially when the subject is sleeping. Appearance of Cheyne-Stokes respiration in the new born while asleep is normal. Blot's breathing In this condition, which is seen in cases of severe brain damage, the periods of apnea are interrupted by a few deep breathings VOLUNTARY HYPERBREATHING In this condition, the sequence of events will be as follows: Very severe voluntary hyperbreathing washing out O2 alveolar C02 and increase of alveolar 02, i.e , PaCO2 falls (see also fig 4.3.7). but Pa02 rises hypocapnia (low PaCO2) respiratory drive is lost a period of apnea, dul