476 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



RESPIRATION- 

 CATHETER TIP: 



PRESSURE 

 mm. Hg 



SATURATION: 



EGG- 

 Signal Marker- 



milMOlNAPY 

 JO 



5tait W 



ARTERY 



9!)% 



ithdrawal 



WEDGf: 



".■VVv'^vw^.- 



nap Fri e F rorr Wadg 



VE 



MTRIC 



-Y') 



IV. 



A 



'A 



/' 



RESPIRATION- 

 PRESSURE 

 mm. Hg 

 SATURATION: 



ECG- 



f:t. 

 ;;o 



1-0 



PUi.MON/RY 



ARTE 



Stirt /Vitlidra 



RY 



wal 



. V' ' A'V^ ^^V ^.y\ ^^, -..^ 



6b7c 



T ip Post 



OUTFLOW FT. VE^TRIGLE-♦ 



■v,?,^ 



Pu 



6! 



1. Vdlve 



RESPIRATION- 



PRESSURE 

 mm. Hg 



SATURATION: 

 EGG- 



SO 



l-Ci 



^ yf> -^ 



St(trt yi/ittidra 



RT 

 6 



vol 



Tip 



VENTRICLE 



% 



PO! t Ticu 



RT. /JR 



>piq Ar 



lUM 



•.r^ 



.r 



FIG. 43. Photokymographic record obtained during cardiac catheterization showing pressure re- 

 lationships and other physiologic variables in a 30-year-old man who had Ebstein's malformation of 

 tricuspid valve with severe regurgitation (functional absence) of this valve and a patent foramen 

 ovale. Top panel: Withdrawal of catheter tip was begun (at signal mark) from pulmonary-artery 

 wedge position where blood thai was 99% saturated had been obtained. Catheter tip suddenly 

 snapped free frcm wedge position (at signal) and passed rapidly back to outllow tract of right ven- 

 tricle, at which position blood that wzis 61% saturated was obtained. Middle panel: Withdrawal of 

 catheter tip from right pulmonary artery to outflow tract of right ventricle. Pressure levels are low 

 for both positions and blood o.xygen saturations are not significantly different. Bottom panel : with- 

 drawal of catheter tip from outflow tract of right ventricle through region of tricuspid valve (as 

 seen roentgenoscopically) to high right atrium. Note /) that there is no significant difference in 

 pressure or in contour of pressure pulses in right ventricle and atrium, indicating absence of func- 

 tioning tricuspid valve, and 2) that right atrial pressure exceeds pulmonary-artery wedge (left 

 atrial) pressure so that flow through defect in atrial septum would be chiefly in right-lo-left direction. 



Right-to-Left Shunts 



In the presence of venoarterial .shunts, venous blood 

 that is low in o.xygen saturation mixes with blood of 

 high oxygen saturation that has traversed the pul- 

 monary circulation, has returned to the left side of the 

 heart and is destined for the systemic circulation. As a 

 consequence, the amount of oxygen in the blood enter- 

 ing the systemic circulation is decreased. 



The clinical consequence of hypoxia is commonly 

 the occurrence of cyanosis. Cyanosis is usually appar- 

 ent to most observers when saturation of capillary 

 blood is reduced to 80 to 90 per cent of normal (64, 

 115). .Several considerations, however, make it haz- 

 ardous to assume either that arterial unsaturation is 

 the cause of slis;ht peripheral cyanosis or that normal 



arterial saturation is present in the absence of cyanosis. 

 Cyanosis usually becomes evident when the concen- 

 tration of unsaturated hemoglobin in capillary blood 

 is increased to approximately 5 g per 100 ml. In 

 patients with severe anemia, therefore, cyanosis may 

 not be evident in spite of severe arterial hyperemia. 



Visible cyanosis may occur in the presence of normal 

 arterial oxygen saturation if tissue extraction of oxy- 

 gen per unit of blood flow is increased sufficiently to 

 cause capillary unsaturation of this degree. Slowing of 

 superficial blood flow due to cold with consequent 

 increase in tissue extraction of oxygen and a widened 

 arteriovenous oxygen diflercnce (stagnant hypox- 

 emia) provides an example of this \ariety of cyanosis. 

 Another import. int cause of stagnant hypoxemia with 



