Stephen J. Leshin

Dimensional changes of the left ventricle during acute pulmonary arterial hypertension in dogs

Abstract Left ventricular dimensions and volumes were measured by an endocardial marker technique in eight closed chest dogs during progressive increases of 10 mm Hg in mean pulmonary arterial pressure. Right ventricular volumes were measured by biplane cineanglography. Increasing mean pulmonary arterial pressure caused a progressive increase in right ventricular volume; at a mean pulmonary arterial pressure of 60 mm Hg, right ventricular end-diastolic volume increased by 48 percent and end-systolic volume by 50 percent. Left ventricular volumes began to decrease significantly at a mean pulmonary arterial pressure of 30 mm Hg, and when a mean pulmonary arterial pressure of 60 mm Hg was reached, left ventricular end-diastolic volume had decreased by 30 percent and left ventricular end-systolic volume by 19 percent. Changes in ventricular filling pressure dlrectionally followed the volume changes of the respective ventricle. Left ventricular stroke volume decreased 45 percent at a mean pulmonary arterial pressure of 60 mm Hg but increasing heart rate prevented a decrease in cardiac output. The decrease in left ventricular volume as pulmonary arterial pressure was Increased was associated with a disproportionate reduction in the left ventricular septal-lateral axis. At end-diastole, this dimension decreased by 22 percent at a mean pulmonary arterial pressure of 60 mm Hg, the anterior-posterior axis decreased by 8 percent and the base-apex axis by 4 percent. A similar disproportionate decrease of the septal-lateral axis occurred at end-systole. Even at the modest increase in mean pulmonary arterial pressure to 20 mm Hg, only the septal-lateral dimension was significantly shortened, and the right ventricular end-diastolic volume had increased by 17 percent but left ventricular end-diastolic volume was not significantly changed. Thus, during acute pulmonary hypertension, the right ventricle progressively dilates resulting in a distinctive change in the shape of the left ventricle that suggests septal buiging and that may impair left ventricular function.

Intraaortic balloon counterpulsation in patients in cardiogenic shock, medically refractory left ventricular failure and/or recurrent ventricular tachycardia

Of the 27 patients described, 23 were in cardiogenic shock, 2 had severe left ventricular failure, and 2 had medically refractory ventricular tachycardia. Utilizing intraaortic counterpulsation, adequate systemic blood pressure was initially restored in 19 patients. Nine of these were subsequently weaned from circulatory assistance, but only three were discharged from the hospital and are currently alive. The remaining 10 patients who derived initial benefit from circulatory assistance were balloon-dependent in that they could not be weaned from circulatory assistance. Eight of these patients subsequently underwent cardiac catheterization; four had inoperable disease. The remaining four patients underwent surgery for either resection of the area of infarction and/or for myocardial revascularization; only one survived to subsequently leave the hospital. Ventricular volumes were abnormal and ejection fractions were below 30 per cent in all the patients in cardiogenic shock except one who underwent cardiac catheterization and ultimately died. Ejection fractions were greater than 30 per cent in the two patients with cardiogenic shock who were weaned from balloon support and survived to leave the hospital without surgery. Both of these patients had inferior myocardial infarction. The data obtained from this experience suggest that intraaortic counterpulsation is a very useful adjunct to currently existing medical measures to treat both cardiogenic shock and medically refractory left ventricular failure but that most patients have such extensive disease that they can neither be weaned from balloon support nor undergo successful infarctectomy or myocardial revascularization.

Ventricular conduction blocks and sudden death in acute myocardial infarction. Potential indications for pacing.

Abstract Of 425 patients with acute myocardial infarction admitted to a coronary-care unit 77 (18 per cent) had ventricular conduction blocks. Complete heart block developed in 43 per cent with right-bundle-branch block and left-axis deviation, in 17 per cent with left-bundle-branch block, and in 6 per cent without ventricular conduction blocks. In-hospital mortality was 30 per cent in patients with and 14 per cent without ventricular conduction block. Late sudden death occurred in five of six patients with right-bundle-branch block and left-axis deviation who had transient complete heart blocks during myocardial infarction, whereas eight similar patients with complete heart block with permanent pacing were alive. These findings suggest that patients with this form of block with an acute myocardial infarction should have temporary standby pacemakers inserted. If complete heart block develops in such cases in association with an acute myocardial infarction, even though transient, permanent pacing should be...

Changes in left ventricular function produced by the injection of contrast media

Abstract The effect of radiopaque contrast media on left ventricular volume and function was analyzed during and after selective left ventricular injection of 1 c.c. per kilogram of contrast medium (76 per cent meglumine diatrizoate) or physiological saline. Radiopaque markers were implanted near the endocardium of the left ventricle in open-chest dog preparations. Biplane cinefluorography films were taken while monitoring left ventricular pressure and its derivative ( dp dt ), aortic pressure, and the ECG. End-systolic and diastolic volumes were calculated from the biplane cine films and matched with the simultaneous pressures. Systolic and diastolic volumes, stroke volume, peak left ventricular pressure, left ventricular end-diastolic pressure, and maximal rate of left ventricular pressure rise (max. dp dt ) were compared for 16 beats and for 15 minutes after injection of physiological saline or contrast medium. In 7 paired studies the injection of either contrast medium or saline produced an immediate increase in left ventricular end-diastolic pressure and volume, stroke volume, ejection fraction, max. dp dt , and peak left ventricular pressure, indicating a Frank-Starling effect. Thirteen to 16 beats after the injection of saline, all values returned toward control levels; whereas, after contrast medium injection, left ventricular end-diastolic pressure and volume increased further with a fall in max. dp dt , indicating a decrease in contractility. Subsequently, at 1 minute after the injection of contrast media, left ventricular contractility increased, as evidenced by a rise in max. dp dt and a fall in left ventricular end-diastolic volume. All values returned to control values after 15 minutes. Thus, the injection of either saline or contrast medium results in an immediate alteration in left ventricular function secondary to an increased volume load (the Frank-Starling mechanism). Left ventricular function returns rapidly to control level after the saline injection. After the contrast medium injection, however, the volume effect is followed first by a transient deterioration in function and subsequently bya transient increase in left ventricular function, an effect possibly resulting from changes in osmolality.

Role of the Frank-Starling Mechanism In Exercise

The mechanisms which determine the response of stroke volume to mild, moderate, and severe exercise were compared in nine dogs running on a level treadmill. The dogs ran for 3-minute periods at 3–4 mph (mild exercise), 6–8 mph (moderate exercise), and 10–14 mph (severe exercise). Heart rate increased from a standing control value of 107 ± 6 beats/min to 191 ± 10 beats/min in mild, 221 ± 8 beats/min in moderate, and 263 ± 9 beats/min in severe exercise. Stroke volume increased 14%, 19%, and 15% for mild, moderate, and severe exercise, respectively. During mild exercise, left ventricular internal diameter decreased at end-systole but was unchanged at end-diastole. During moderate and severe exercise, end-diastolic diameter increased consistently as did left ventricular end-diastolic pressure. It was concluded that, despite extremely high heart rates, stroke volume increased during exercise. The augmentation in stroke volume was due to the combined effects of an increase in contractility, caused by increased sympathetic nervous system activity, and the operation of the Frank-Starling mechanism.

Clinical Physiology: Skeletal Muscle Metabolites in Patients with Cardiogenic Shock or Severe Congestive Heart Failure

Skeletal muscle metabolite concentrations were determined in 19 patients in either cardiogenic shock or severe left ventricular failure by obtaining a needle biopsy specimen of lateral thigh muscle. Evidence of anaerobic skeletal muscle metabolism was found in both patient groups with the greatest lactate accumulation and most severe high-energy phosphate depletion present in the patients in cardiogenic shock. The skeletal muscle lactate accumulation was most pronounced in the patients that died. Blood lactate values did not absolutely predict skeletal muscle lactate concentrations in those patients in whom skeletal muscle lactate concentrations were the highest. The patients in cardiogenic shock and severe left ventricular failure who survived demonstrated a reduction in skeletal muscle lactate levels and a restoration of high-energy phosphates over several days which correlated with clinical and hemodynamic improvement.

Routine fogarty thrombectomy in arterial catheterization.

Abstract Routine use of the Fogarty embolectomy catheter after cardiac catheterization through a brachial arteriotomy in 25 patients was associated with a decline in major and minor complications f...