Ralph Shabetai

The hemodynamics of cardiac tamponade and constrictive pericarditis

Abstract This review of the hemodynamic alterations that accompany cardiac tamponade and constrictive pericarditis describes studies carried out in man and in experimental animals. Both constrictive pericarditis and cardiac tamponade increase pulmonary and systemic venous pressure and decrease cardiac output and stroke volume. In cardiac tamponade, the superior and inferior vena caval pressure record shows a single nadir, the x descent; this pressure event is accompanied by an increase in velocity of blood flow and, by inference, in quantity of blood flow. The y descent is absent from the vena caval and right atrial pressure curves, and no early diastolic dip appears in the right ventricular pressure tracing. During inspiration, blood flow velocity and, by inference, forward flow increase in the superior and inferior venae cavae and in the pulmonary artery. Pulsus paradoxus is almost invariably present. The major factors causing pulsus paradoxus are related to inspiratory augmentation of systemic venous return. The ensuing expansion of right-sided heart volume increases intrapericardial pressure, but does not increase systemic arterial pressure and flow until the subsequent expiration. In constrictive pericarditis a peak of blood flow velocity accompanies the x descent of superior vena caval pressure. A second flow velocity peak accompanies the y descent. Respiration fails to alter superior vena caval pressure or blood flow velocity, but during inspiration the velocity of pulmonary arterial blood flow increases. Pulsus paradoxus occurs much less often than in cardiac tamponade, and its mechanism is not well understood. Atrial fibrillation is common, and myocardial contractility is impaired.

Electrophysiologic and hemodynamic effects of verapamin. Correlation with plasma drug concentrations.

Verapamil was administered intravenously to 30 open-chest dogs and the electrophysiologic and hemodynamic effects of the drug were correlated with the corresponding plasma concentrations. At concentrations below 152 ng/ml, verapamil prolonged the A-H interval, abolished ventriculoatrial conduction, but did not significantly change sinus rate, cardiac output, left ventricular dp/dt, or systemic vascular resistance. Concentrations above 200 ng/ml were associated with slowing of the sinus rate, high degree atrioventricular block during atrial pacing, 24% decrease in mean aortic pressure, and decreased cardiac output and left ventricular dp/dt. Sinus arrest, high degree atrioventricular block during sinus rhythm, decreased systemic vascular resistance and increased left ventricular end-diastolic pressure occurred when plasma verapamil concentrations exceeded 400 ng/ml. These results show that plasma verapamil concentrations reliably reflect the electrophysiologic and hemodynamic actions of the drug, and that “therapeutic” drug effects can be achieved at plasma concentrations at which myocardial depressant effects are unlikel

Cardiac amyloidosis, constrictive pericarditis and restrictive cardiomyopathy

Cardiac amyloidosis is not characterized by a single hemodynamic pattern. Some of the cases present the clinical findings of restrictive cardiomyopathy and in these differentiation from constrictive pericarditis remains difficult in spite of the introduction of techniques designed to assess myocardial contractility and ventricular diastolic compliance. The clinical features and the demonstration of left ventricular diastolic pressure greater than right remain the most useful means of distinguishing restrictive cardiomyopathy from constrictive pericarditis. In other cases of cardiac amyloidosis the diastolic pressure is elevated throughout diastole and ventricular ejectile ability is lost. These cases do not simulate constrictive pericarditis and should not be classified as restrictive cardiomyopathy.

Reversal of the cardiovascular effects of verapamil by calcium and sodium: differences between electrophysiologic and hemodynamic responses.

The reversibility of verapamil-induced hemodynamic and electrophysiologic changes by intravenously administered CaCI2 and NaCI was tested in 34 anesthetized open-chest dogs during verapamil infusions which produced plasma verapamil concentrations of 70-2042 ng/ml. An increase of serum calcium concentration (Ca). to an average 6.5 mEq/l abolished the depressive effects of verapamil on cardiac output and left ventricular dp/dt and diminished drug-related hypotension by an average of 52%, but did not affect verapamil-induced prolongation of AH interval and slowing of sinus rate. Further increase of (Ca). to an average of 8.2 mEq/l decreased AH prolongation caused by verapamil from an average of 95% to 45% of control value, but had no effect on verapamil-induced slowing of sinus rate or second-degree atrioventricular (AV) block during atrial pacing. Rapid intravenous injection of 40 ml 2 M NaCI, transiently raised serum Na+ concentration to 162 mE/l, decreased AH prolongation caused by verapamil to an average of 22% of control value, decreased slowing of sinus rate from an average of 34% to an average of 19% of control value, and decreased the severity of second-degree AV block, but had no effect on verapamil-induced complete AV block or sinus arrest. Hypernatremia had no effect on AH interval and sinus rate without prior CaCl2 infusion. In the absence of verapamil, neither increase of (Ca). to 8.2 mEq/l, nor NaCl injection following CaCl2 had any effect on AH interval or sinus rate. This study suggests 1) that both Ca+ and Na+ compete with verapamil, but Na+ acts only in the presence of hypercalcemia; 2) different verapamil effects differ in their reversibility; and 3) treatment with calcium may be useful in counteracting the negative inotropic effect of verapamil

Monophasic Action Potentials in Man

Monophasic action potentials with an amplitude of up to 70 mv were recorded with suction electrodes from the endocardial surface of the right atrium and both ventricles during diagnostic cardiac catheterization. The method was simple and safe. The monophasic action potential of human beings had the same shape and the same relation to the electrocardiogram as the transmembrane action potential of animals has. Also changes in heart rate and administration of calcium and digitalis had the same effect on the monophasic action potential of man as on the transmembrane action potential of animals.When injections of contrast material into the coronary arteries produced T-wave changes, the monophasic action potential from the ventricle perfused by the contrast medium lengthened, but the monophasic action potential from the other ventricle did not change.Our study suggests that the monophasic action potential may be helpful in estimating the refractory period at the site of recording and in explaining the pathogenesis of abnormal repolarization in the electrocardiogram.

DIGITAL BOUNDARY DETECTION, VOLUMETRIC AND WALL MOTION ANALYSIS OF LEFT VENTRICULAR CINE ANGIOGRAMS.

Abstract A set of algorithms have been developed to automate the analysis of cine ventriculographic data by digital methods. The visual data in the form of a cine ventriculogram is converted to digital data and stored in packed form on magnetic tape. The analysis procedure then (1) detects the ventricular boundary, (2) smooths the rough ventricular outline, (3) detects the aortic valve position and (4) translates and rotates each ventricular outline to a common set of internal axes. The program calculates on a frame by frame basis ventricular volume, projected ventricular area and constructs an instantaneous polar analysis of wall position. It currently takes 27 sec of computer time to digitize and analyze one frame of data.

Asymmetrical Hypertrophic Cardiomyopathy Simulating Mitral Stenosis

Hypertrophic cardiomyopathy usually involves the left ventricle more severely than the right, and when asymmetrical may produce the syndrome of idiopathic subaortic stenosis. Less commonly, clinical manifestations of inflow-tract obstruction predominate and produce a syndrome that may be mistaken for mitral stenosis, principally because of an apical diastolic rumbling murmur. The probability of this diagnostic error and the risk of a consequent unnecessary operation can be reduced by appreciating the significance of the clues to left ventricular disease revealed by the electrocardiogram and the chest roentgenogram. Furthermore, proper timing of the heart sounds differentiates the protodiastolic filling sound of cardiomyopathy from the opening snap of mitral stenosis. The correct diagnosis is established following ventriculographic and hemodynamic studies.

Nature of the conduction disturbance in selective coronary arteriography and left heart catheterization

Abstract The electrocardiographic changes associated with coronary arteriography were compared with those occurring during left ventricular catheterization in 16 patients. In 1 patient, a 36 year old man, transient left anterior divisional block was documented when the catheter tip was in the outflow tract of the left ventricle. The ÂQRS shifted from +90 to −50°, the initial 0.02 second QRS forces shifted interiorly and to the right, and the QRS interval increased from 0.07 to 0.09 second, fulfilling previously described criteria for the diagnosis of left anterior divisional block. This was attributed to transient injury of the anterior division of the left bundle branch. During recovery, several progressively decreasing degrees of left anterior divisional block were recorded. In the same patient and in the other 15, selective opacification of the coronary arteries shifted the main QRS forces, without change in the direction of the initial QRS forces. The axis shifts occurring during coronary arteriography are attributed to parietal block. Selective opacification of the coronary arteries does not affect the intraventricular conducting fascicles and Purkinje fibers.

A new syndrome in hypovolemic shock: Systolic murmur and intraventricular pressure gradient☆

Abstract A grade 5 6 systolic murmur appeared in a patient with severe shock produced by gram-negative bacteremia. Cardiac catheterization demonstrated a systolic pressure difference of 70 mm. Hg between the left ventricle and the aorta. “Infundibular” pressure was recorded while the catheter was withdrawn from the left ventricle into the aorta. Left ventricular systolic pressure increased, and arterial systolic pressure fell in postextrasystolic beats. Immediately after the administration of propranolol, blood and phenylephrine, the systolic pressure difference between the left ventricle and the aorta and the systolic murmur disappeared. Autopsy revealed a normal heart. We believe this is the first reported case with clinical and hemodynamic evidence of an intracavitary left ventricular systolic pressure difference in a man with shock and without severe left ventricular hypertrophy. The sudden occurrence of a loud murmur when left ventricular systolic pressure greatly exceeded aortic systolic pressure and the disappearance of the murmur when these two pressures were equal suggests that outflow tract obstruction may develop in shock. However, the severity of the patients clinical condition prevented us from obtaining measurements crucial to the determination of the mechanism of the systolic pressure difference.

Automated Scanning And Analysis Of Ventricular Cine Angiograms

Automated computer analysis of cine ventriculograms provides a rapid, reproducible means of analyzing visual data obtained at cardiac catheterization. At the present time several laboratories routinely do semiautomated volumetric analysis of cine ventriculograms. However, their method requires the cardiologist or a trained technician to manually trace the outline of the ventricle on each frame. (Ref. 1 and 2) This technique is time-consuming and prone to errors.