The phase of apnea normal respiratory rhylhrn Therefore, afler a bout of severe" voluntary hypervenMahOn. apnea follows then comes slighl

ring twelfth PaCO2 aid P*C02 begin (0 snub and return in normal or ri«» above normal values a trsn&ionl hyperpnp* correction of blood gas abnormalities due lo The phase of apnea normal respiratory rhylhrn Therefore, afler a bout of severe" voluntary hypervenMahOn. apnea follows then comes slighl hyperpmc phase and then Ihe respiration 15 back 10 normal The appearance of apnea in conscious hyperventilating subjects, is. however, nol regularly seen Enplanafton of symptom it ology
1 During voluntary hyperbrtathmg stage, the PaC02, falU and PaO2 uses (A similar sort of ihings happen in high attitude; and lh& reader is referred to (h* 'alveolai equal ion1 in high altitude sickness earlier in this chapter) 2 In normal persons and in non-nal environment 02 has practically no influence on Ihe frequency and amplitude of respiration H is only the C02. amongst Ihe gases, which has a strong influence Therefore law PaC02 withdrawal of the stimufation from ihe C02 sensitive chemoreceptoTS (fig 4 36) of medulla epnea 3 During the voluntary tiyperpnea. ihe subject may feel a:zness and visual biat kouT. This 15 due to low PeC02 When PiCO2 of ctmbril anenes fall they undergo vasospism This may b* called, msre'ore. hypocapmc cerebral vasospasm 1 Aflprwar-H unne may become slrongly alkaline This is because tht hfpoeapnis produces atkalosis. called, respiratory alkalosis The kidneys now eicrete the e'cess alhah ions and th*" homaostasrs of pH is maintained BREATH HOLDING Healthy persons, at Iht and of respiration can hold up his breath for •bout 50 seconds or so After 50 seconds ihe subject (a els distressed and develops a strong desire to breathe A] [his point,, (called ihe breaking point") ha is forced to breathe once again ae the 'breaking point1. typicaHy the PaO2 and PaCQJ are both about 60 mm Kg [normal, about 95 arid 4Q mm Hg respectively) The breaking paint depends mainly on ihe PaC02 Thus r lithe PaCO2 of 50 mm Hg i* reached quickly, as in breath holding Following muacular exercise, Ihe durihDn of breath holding will be short On the other hand if one holds up breath after a voluntary hyperventilation. Ihe duration may b* substantially prolonged This is because Ihe hyperventjlalion causes, washing out of CO2 so that buridmg up of PaC02" requires more lima Professional divers in the rive/is, who hive to stay under wstsi for sometime, often mike seven voluntary hypefvenl rial ten before diving so thai undarwater slay can be lengthened Thiv however, is dangerous, bacaus* the attainment of Ihe value of 60 mm Hg tor PaC02 it delayed no doubi but by this time the Pa02 mighi become dangerously \o*t and the subject may become unconscious due to hyprj*ia under waisr AHhough PaC02 value is Ihe mosii important influencing laclor for deiermming tr>e breaking point, oiher factors are also important Such (actors are (0 the concomitant hypoiemia. (n) neural factors like the role of vagus and the glosSOpharyngeal nerves They however will nol be drccusied hvre OXYGEN THERAPY The daiiical indcaTions of oirygtn therapy arB such condrtions like hypouc hypoxil. CO poisoning flic ip Ihe typical hypoiic hypoma, *verylhmg is normal bul The availably of O2n poor Whereas in CO poisoning, 02, particularly wtien given underpressure, replaces CO from ihe Hb molecule by mass action (in) In imonai-. edema. 02 therapy oflen trnpcoves the picture sharply/. This is because, inlhis condilion, there is ditlicully. m diffusion through thealveolo capillary membrane Inhalation of 1CK% 02 increases lh« PI02 lesulting in elevation of PAO2 and so .the alveolo capillary gradiBril of 02 greatly increases and the diffusion ofO2 improves (recall ihe Pick's Law. p 1EW) On ihe other hand., m anemia. The amounl of Hb or PBC fc poor, but the PaO2 is nomial Inhalation of 100% 02 and the following rse o( PIO2 and Pa02 therefore can increase only the 02m physical solution (normally about 0 3 ml/ 100 ml) but not Ihe 02 bound with the Kb, as Hb is praclicilly saturated wilh the 02 Therefore m anemia, the improvement by O2 therapy is only marginal In advanced cases of chronic bronchitis and corpulmcinale O2 therapy must be given with caution In these conrttionsr there Js chrome hypona as well as hypercapma The medullary CO2 sensitive celfs (central chemoreceplors, fig4 38), owing to chronic eicposura to the excess CO?, lose their sensitivity lo CO?, and O2tack remains the only dnve lefl to the patient for [h* breaihing 02 therapy, therefore, might kill ihe patient by withdrawing the only drive laftia ihe patient In CO poisoning and, with surgenes on hearl or lung, grealfy hyperbaTC 02 (i e 02 under high pressure) therapy is done where Such fec*lles e^isl Us dangers are given beow 1 When the PLO2 is very high, Ihe PaO2 ai*o becomes high and the amount of dissolved
02 (m physical solution) may rise greatly [say to values like 4 or 5 ml/100 ml from a normal value ofO 3 ml/IX ml), when Ihn occurs, for onygenatron of the tissues, this dissoked 02 alone is sufficient tnd tht HbO2 is not called for so that il remains imact This maeans, that Ihe carbamino Hb compounds cannot be formed and CO2 accumulates in the tissues (Retati. tht carbamioo Hb compounds, as shown m p 172 play a very crucial parr in transfer of CQ2) Accumulation of CO? can lead to. rather paradoxically, exaggerated respiration (panting for air due in excess O2'i) 2 High PaU2 produces cerebral vavot0*im Tins is id tame e'leni btntficial »s ihe hi »in ii»«uet ara protaciid from ihe mjur