56 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



during cooling, as in alligators, or fall as in hibernators. The current favoring of 

 hyperventilation is based largely on the incidence of ventricular fibrillation in animals 

 cooled without assisted respiration. On the other hand, vigorous hyperventilation 

 may deprive tissue of oxygen by two factors: (1 ) the rising pH further shifts the 

 oxygen dissociation curve to low tensions, and (2) cardiac filling and output is 

 reduced. 



A further complication arises when an attempt is made to relate ventilation, as 

 measured by tidal volume and respiratory rate, to the resultant pH and Pco^- At 

 2)7° these relationships are conveniently obtained from diagrams. During hypo- 

 thermia, the metabolic production of COo falls, solubilities change, and the lung may 

 behave differently. Reports have suggested that during hypothermia, COj elimina- 

 tion from the lung may somehow be blocked (Osborn^). We have therefore done 

 the following experiments to establish some of the relationships between ventilation 

 and blood gases during hypothermia. 



Dogs were curarized. anesthetized and ventilated at known rates with known 

 volumes of air, and cooled in ice packs. Determinations included lung compliance, 

 arterial blood pH and Pco.,, end-expiratory Poo,, expired air COj concentrations, 

 anatomic and physiologic dead space and alveolar ventilation. Results are as 

 follows : 



(1) The anatomic or airway dead space at 25° was increased by 70-90 per cent. 

 A similar increase in the warm animal is obtained with atropine. Bronchoconstric- 

 tion resulting from vagal stimulation, easily observed as a decreasing anatomic dead 

 space, is blocked at 2S° . The cardiodepressor effect of vagal stimulation is greatly 

 depressed or absent at 25°. 



(2) Physiologic dead space, calculated from the Bohr formula using arterial 

 Pco.,. is also increased during hypothermia, again due to bronchodilatation. 



(3) Alveolar dead space, a portion of the physiologic dead space due to uneven 

 distribution within the lung, is unchanged or reduced during hypothermia. If there 

 were any block in C():. excretion, from any cause, it would be expected to enlarge 

 this value. 



(4) The difference between arterial and alveolar (end-expiratory) CO2 tensions 

 is a further measure of uneven distribution, primarily of blood flow. This differ- 

 ence was not altered, or often reduced during hypothermia, again suggesting no 

 impairment in COj excretion. 



(5) The slope of the alveolar nitrogen plateau after a single breath of oxygen is 

 a measure of uneven ventilation. No significant change was observed in this slope. 



(6) As temperature falls, provided tidal volume and rate are held constant, the 

 arterial Pco., at 25° falls to about ^ the control value. This fall reflects a comparable 

 decrease in metabolism. The arterial pH usually rises 0.1 unit. 



(7) Metabolic acidosis occurs to a variable extent, both at Ci7° and during cool- 

 ing, depending on the depth of anesthesia, and the agent used. Acidosis was less 

 severe with iientobarbital than with chloralose. 



(8) Compliance tends to decrease during hypothermia, ])ut not significantlv more 

 than during a sinn'lar s])an of time at Z7° . This progressive fall is proI)abl\- due to 

 such lung changes as atelectasis, congestion and rarely edema. 



In summary, hypothermia leads to an increased anatomic dead space through 



