ABNORMALITIES IN ORGAN BLOOD-FLOW AND ITS DISTRIBUTION DURING POSITIVE END-EXPIRATORY PRESSURE

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  • 1 January 1979
    • journal article
    • research article
    • Vol. 85  (4) , 425-432
Abstract
Current evidence is inconclusive regarding the possibility that positive end-expiratory pressure (PEEP) redistributes flow and may be directly responsible for systemic organ dysfunction. The hypothesis that PEEP may induce abnormalities in the distribution of cardiac output (CO) is tested. Anesthetized dogs [8] were studied during 0 cm H2O PEEP (Z1); 15 cm H2O PEEP (P); Z2; and bleeding (B) to reduce the CO to the same level as P. At each of the 4 periods, a different 15 .mu. radiolabelled microsphere was injected into the left atrium. Another 4 dogs were used to verify that each type of microsphere had the same flow distribution. CO fell from 3.1 liters/min to 1.9 during P (P < 0.01) and to 2.0 during B (P < 0.01). Mean arterial pressure (MAP) declined from 102-83 mm Hg (P < 0.01) and 86 mm Hg (P < 0.01), respectively. Left atrial pressure (LAP) rose from 5.0-7.9 mm Hg during P (P < 0.01) and fell during B to 2.7 mm Hg. CO and its distribution were the same during Z1 and Z2. P caused selective reductions in hepatic (52%), adrenal (25%) and bronchial (24%) blood flows (P < 0.01). Total flow to these organs during B was the same as during Z. Total renal flow was unchanged by P or B, but the cortical:medullary flow ratio increased during P from 24-49 (P < 0.01) and was unchanged by B. P induced a decrease in fundal mucosal flow as compared with Z (P < 0.01). Total coronary flow fell from 100-64 ml/min during both P and B (P < 0.01). P led to a selective fall in subendocardial flow (67 ml/min .times. 100 gm) as compared with B (82.5 ml/min .times. 100 gm, P < 0.01) as well as in the subendocardial:subepicardial flow ratio (1.069 vs. 1.112 ml/min .times. 100 gm, P < 0.05). The higher left ventricular filling pressure (LAP) during P as compared with during B apparently compressed the endocardium and induced relative ischemia. Similarly the high airway pressure during P may have impeded bronchial mucosal flow. The causes and consequences of the other P-induced variations in flow are speculative.