transient hyperpnea correction of blood gas abnormalities due to the phase of apnea normal respiratory rhythm

ring which PaC02 and PaC02 begin lo rise and return to normal or rise above normal values a transient hyperpnea correction of blood gas abnormalities due to the phase of apnea normal respiratory rhythm. Therefore, after a bout of severe" voluntary hyperventilation, apnea follows then comes slight hyperpnic phase and then the respiration is back to normal. The appearance of apnea in conscious hyperventilating subjects, is, however, nol regularly seen. Explanation of symptomatology 1. During voluntary hyperbreathing stage, the PaC02, falls and Pa02 rises. (A similar sort of things happen in high altiludes and Ihe reader is referred to the 'alveolar equation' in high altitude sickness, earlier in this chapter). 2. In normal persons and in normal environment O2 has practically no influence on Ihe frequency and amplitude of respiration. It is only Ihe C02, amongst the gases, which has a strong influence. Therefore low PaC02 withdrawal of the slimutation from the C02 sensitive chemoreceptors (fig 43.8) of medulla apnea. 3. During the voluntary hyperpnea, the subject may feel dizziness and visual blackouts. This is due to low PaC02 When PaC02 of cerebral arteries fall they undergo vasospasm. This may be called, therefore, hypocapnic cerebral vasospasm. 4. Afterwards, urine may become strongly alkaline. This is because the hypocapnia produces alkalosis, called, respiralory alkalosis. The kidneys now excrete the excess alkali ions and the" homeostasis of pH is maintained. BREATH HOLDING Healthy persons, at the end of respiration can hold up his breath for about 50 seconds or so. After 50 seconds, the subject feels distressed and develops a strong desire lo breathe. Al this point," (called the 'breaking point') he is forced to breathe once again. At the 'breaking point', typically the Pa02 and PaC02 are both about 50 mm Hg (normal, about 95 and 40 mm Hg respectively). The breaking point depends mainly on the PaC02. Thus, if the PaC02 of 50 mm Hg is reached quickly, as in breath holding following muscular exercise, the duration of breath" holding will be short. On the other hand, if one holds up breath after a voluntary hyperventilation, the duration may be substantially prolonged. This is because the hyperventilation causes, washing out of C02 so that building up of PaC02" requires more time. Professional divers in the rivers, who have to stay under water for sometime, often make severe voluntary hyperventilation before diving so that underwater stay can be lengthened. This, however, is dangerous, because the attainment of the value of 50 mm Hg for PaC02 is delayed no doubt but by this time the Pa02 might become dangerously low and Ihe subject may become unconscious due lo hypoxia under water. Although PaC02 value is the most, important influencing factor for determining the breaking point, other factors are also important. Such factors are (i) Ihe concomitant hypoxemia, (ii) neural factors like the role of vagus and the glossopharyngeal nerves. They however will not be discussed here. OXYGEN THERAPY The classical indications of oxygen therapy are such conditions like hypoxic hypoxia, CO poisoning etc. In the typical hypoxic hypoxia, everything is normal but the availability of 02is poor. Whereas in CO poisoning, 02, particularly when given under pressure, replaces CO from the Hb molecule by mass action. (iii) In Imonary edema, 02 therapy often improves the picture sharply. This is because, in this condition, there is difficulty in diffusion through thealveolo capillary membrane. Inhalation of 100% 02 increases the PI02 resulting in elevation of PA02 and so,the alveolo capillary gradient of 02 greatly increases and the diffusion of 02 improves (recall Ihe Fick's Law, p.164). On the other hand,, in anemia, the amount of Hb or RBC is poor, but Ihe Pa02 is normal. Inhalation of 100% 02 and Ihe following rise of PI02 and Pa02 therefore can increase only Ihe 02in physical solution (normally about 0.3 ml/ 100 ml) but not the 02 bound with the Hb, as Hb is practically saturated with the 02. Therefore in anemia, the improvment by 02 therapy is only marginal. In advanced cases of chronic bronchitis and corpulmonale 02 therapy must be given with caution. In these conditions, there is chronic hypoxia as well as hypercapnia. The medullary C02 sensilive cells (central chemoreceptors, fig. 4.3.8), owing to chronic exposure lo the excess C02, lose their sensitivity to C02, and 02lack remains Ihe only drive left to the patient for the breathing. 02 therapy, therefore, might kill Ihe patient by withdrawing the only drive left to Ihe patient . In CO poisoning and. with surgeries on heart or lung, greatly hyperbaric 02 (i.e. 02 under high pressure) therapy is done where such facilities exist. Its dangers are given beow: 1. When the PI02 is very high, the Pa02 also becomes high and the amount of dissolved
02 (in physical solution) may rise greatly (say to values like 4 or 5 ml/100 ml from a normal value of 0.3 ml/100 ml); when this occurs, for oxygenation of the tissues, this dissolved 02 alone is sufficient and the Hb02 is not called for so that it remains mtact. This meeans, that the carbamino Hb compounds cannot be formed and C02 accumulates in Ihe tissues. (Recall, the carbamino Hb compounds, as shown in p. 172 play a very crucial part in transfer of C02). Accumulation of C02 can lead to, rather paradoxically, exaggerated respiration (panling for air due to excess O2!!) 2. High Pa02 produces cerebral vasospasm. This is lo some extent beneficial as the brain tissues are proteced from the mjurl