John W. Hyland

THE PULMONARY BLOOD VOLUME IN MAN

The measurement of blood volume in the pulmonary vascular bed during life became theoretically feasible with the introduction of indicator dilution methods by Stewart (1) and Hamilton, Moore, Kinsman and Spurling (2). The principles and formulas set forth by these investigators have since undergone extensive scrutiny by theoretical analysis, in circulation models, and in vivo. As a result of these studies, there exists now general agreement that the introduction of an indicator substance into the central circulation, either directly or by peripheral venous injection, and downstream recording of its concentration change with time during the first transit permits the determination of three important circulatory parameters: 1) the cardiac output, 2) the mean transit time from injection to sampling site, and 3) by multiplication of cardiac output and mean transit time, the circulating volume of blood between injection and sampling sites, including all temporally equidistant points in the vascular bed. Practically speaking, then, the measurement of pulmonary blood volume in vivo requires determination of the mean transit time of an indicator from the pulmonary artery to the left atrium together with cardiac output. The development of right and left heart catheterization has made the pulmonary artery and left atrium accessible as injection and sampling sites in man. Injection of an indicator through a

Dopamine-Induced Alterations in Coronary Hemodynamics in Dogs

The effect of intravenous infusions of dopamine on left circumflex coronary blood flow and myocardial oxygen consumption in doses ranging from 5 to 100 μg/kg/min was studied in 17 open-chest dogs anesthetized with chloralose. Flow was measured with an electromagnetic flowmeter. Dopamine caused a progressive and linear increase of coronary flow that was proportional to increases in myocardial oxygen consumption up to a dose of 80 μg/kg/min; at this dose, the increase over control was 365% (28 to 129 ml/min). These changes accompanied marked increases in stroke volume, left ventricular dP/dt, and mean systolic ejection rate. Mean aortic pressure and heart rate changed little at doses below 10 μg/kg/min, but increased steadily with doses over the range of 15 to 40 μg/kg/min. Dopamine is a potent stimulator of coronary blood flow and myocardial contractility. The fact that the increased coronary flow was proportional to increases in myocardial oxygen consumption indicates that the induced coronary vasodilation is secondary to increased myocardial oxygen demands, rather than the result of primary coronary vasodilation.

Right coronary blood flow in acute pulmonary embolism

Abstract Right coronary arterial blood flow was measured by means of an electromagnetic flowmeter during acute pulmonary embolism in open-chest anesthetized pigs. This study was undertaken in order to determine whether or not acute pulmonary embolism causes an impediment of right coronary flow which may be responsible for myocardial ischemia. Pulmonary embolism was induced with autologous blood clots in amounts sufficient to produce pulmonary hypertension, but not sufficient to produce shock. No reduction of right coronary blood flow after pulmonary embolization was observed. To the contrary, average right coronary mean flow increased from 27 to 61 ml. per minute (P

Thoracic Outlet Syndrome Masquerading as Coronary Artery Disease (Pseudoangina)

Abstract Forty-four patients presenting with chest pain suggesting coronary artery disease had normal exercise stress tests and selective coronary angiography and subsequently were found to have an unsuspected thoracic outlet syndrome. Thirteen additional patients had both significant coronary artery disease and thoracic outlet syndrome. Esophageal and pulmonary disease were ruled out and the diagnosis of brachial plexus compression in the thoracic outlet established by a reduction of the ulnar nerve conduction velocity (UNCV) below normal, the normal value being 72 meters per second. Clinical improvement from thoracic outlet compression resulted either from physical therapy if the UNCVs were above 55 m./sec, or from transaxillary surgical extirpation of the first rib if the UNCVs were below 55 m./sec. Thirteen patients with coronary artery disease and thoracic outlet syndrome required therapy for both problems before improvement ensued. Although the usual symptomatology for thoracic outlet syndrome involves pain and paresthesias of the shoulder, arm, and hand, the chest wall is frequently involved. If the chest pain is predominant with minimal shoulder-hand symptoms, the diagnosis is not suggested clinically and can only be established by the high index of suspicion, positive UNCV reduction, and a normal coronary angiogram. Pathways of pain in angina pectoris and afferent stimuli originating from brachial plexus compression at the thoracic outlet stimulate the same autonomic and somatic spinal centers that induce referred pain to the chest wall and arm.