Dwight Davis

Delayed reversal of impaired vasodilation in congestive heart failure after heart transplantation.

The effects of changes in central cardiovascular function on peripheral vasodilation were investigated. Strain gauge plethysmography was used to measure the maximal blood flow response following release of forearm arterial occlusion and the peak reactive hyperemic blood flow response (ml/min.100 ml) before and twice after orthotopic heart transplantation in 10 subjects with severe congestive heart failure. The 2 posttransplantation studies were done before hospital discharge (mean 18 days after transplantation) and again after discharge (mean 114 days after transplantation). Transplantation led to a significant but delayed increase in maximal vasodilation (reactive hyperemic blood flow: pretransplant 21 +/- 3; predischarge 25 +/- 2; postdischarge 43 +/- 5) and a concurrent significant reduction in minimal forearm resistance. Although the improvement in peripheral vasodilator function may be linked to improvement in cardiac function, this linkage is not direct, nor is it immediate. If the normalization of maximal metabolic blood flow is related to resumption of normal physical activity postdischarge, then much of the basic abnormality in vasodilator capacity in congestive heart failure may be related to physical deconditioning.

Enhanced metabolic vasodilation secondary to diuretic therapy in decompensated congestive heart failure secondary to coronary artery disease

Since sodium and water retention have been implicated as major factors limiting maximal metabolic vasodilation in congestive heart failure (CHF), the effect of rigorous diuresis on maximal vasodilatory capacity was studied systematically in 9 subjects hospitalized with decompensated CHF. Peak reactive hyperemic blood flow, measured by strain-gauge plethysmography, was used as an index of maximal vasodilatory capacity. After 24 hours of diuresis and a 2.2-kg weight loss, maximal flow increased from 19.9 to 26.1 ml/min X 100 ml (p less than 0.05). Despite a further 1.4-kg weight loss between 24 and 48 hours, maximal blood flow increased no more (26.1 to 25.8 ml/min X 100 ml). Since blood pressure did not change significantly, minimal forearm resistance and maximal conductance showed similar improvements. It is unlikely that vasoconstrictor hormone changes could account for this effect since a marked decrease in plasma norepinephrine occurred in only 2 of 8 subjects and plasma renin activity decreased in only 1 subject. As a group there was no significant change in norepinephrine level, which remained substantially above normal (1,525 to 1,148 pg/ml), or in plasma renin activity (12.3 to 18.9 ng/ml/hour). Because the improvement in vasodilator capacity reached a plateau by 24 hours despite continued diuresis, and because peak reactive hyperemic blood flow was still 32% below normal, it is suggested that a second mechanism besides sodium and water retention is responsible for a significant portion of the impaired peripheral vasodilation in CHF.

Regional blood flow in congestive heart failure: Concept of compensatory mechanisms with short and long time constants

With physiologic stress to the cardiovascular system, some circulatory compensatory mechanisms are designed to restore homeostasis quickly (e.g., sympathetic nervous system activation and the Frank-Starling mechanism). These compensatory mechanisms are not nearly as effective when there is a chronic pathologic stress such as congestive heart failure (CHF). In this circumstance, other mechanisms that operate with longer time constants come into play (e.g., activation of the renin-angiotensin-aldosterone system, myocardial hypertrophy and deconditioning). The most successful chronic drug therapies of CHF are those that are designed to reverse the latter group of compensatory mechanisms, a process that is slow. It takes especially long to reverse those CHF-induced changes in blood vessels and skeletal muscle metabolism that are activated to cope with inadequate delivery of oxygenated blood to working muscles. The concept that compensatory mechanisms have either short or long time constants for activation, effectiveness and reversal may help explain why the improvement in exercise tolerance with effective heart failure therapy lags behind hemodynamic improvement.

Heart transplantation for tumor

Unresectable cardiac tumors, although unusual, are often rapidly fatal. A 31-year-old woman presented with a large tumor arising from the left ventricle and causing symptoms of a constrictive cardiomyopathy. After evaluation with echocardiography, angiography, and computed tomography, an exploration was carried out to confirm the extent of disease. Orthotopic heart transplantation was subsequently performed when a donor organ became available. She is now alive and disease-free 12 months after transplantation.

Effects of nadolol and propranolol on plasma lidocaine clearance

Nadolol and propranolol effects on lidocaine elimination were followed in six healthy men and women. Each received three separate 30‐hr infusions of lidocaine (2 mg/min): one alone, one after 3 days pretreatment with nadolol (160 mg daily), and one after 3 days pretreatment with propranolol (80 mg every 8 hr). Liver blood flow was determined by the systemic clearance of indocyanine green. Steady‐state plasma lidocaine levels were increased by nadolol (2.1 ± 0.2 to 2.7 ± 0.3 μg/ml) and by propranolol (2.1 ± 0.2 to 2.5 ± 0.3 μg/ml). Lidocaine plasma clearance was decreased by nadolol (1030 ± 81 to 850 ± 82 ml/min) and by propranolol (1030 ± 81 to 866 ± 75 ml/min). Hepatic blood flow was decreased by nadolol (1275 ± 77 to 902 ± 102 ml/min) and propranolol (1275 ± 77 to 957 ± 119 ml/min). The hepatic extraction ratio for lidocaine was increased by nadolol (0.86 ± 0.06 to 0.91 ± 0.05) and by propranolol (0.86 ± 0.06 to 0.90 ± 0.06). Lidocaine intrinsic clearance was not changed by nadolol (8.19 ± 1.87 to 9.52 ± 2.36 l/min) or propranolol (8.19 ± 1.87 to 9.50 ± 3.13 l/min). Our data indicate that both nadolol and propranolol reduce lidocaine clearance by their effects on hepatic blood flow and not by inhibition of lidocaine metabolism.

Bridging to transplant. Equal extended survival for patients undergoing LVAD support when compared with long-term medical management.

Implantation of ventricular assist devices (VADs) to support patients awaiting cardiac transplant has become an effective means of assuring that these critically ill patients survive to transplant. The authors undertook a retrospective analysis of 115 consecutive patients listed for cardiac transplant from January 1992 through June 1995. A VAD was implanted in 19 of these patients. Survival was calculated by intent to treat from the time of transplant listing through heart transplant, if it occurred. The analysis demonstrates that the patients who underwent implantation of a VAD as bridge to transplant had survival times similar to those of patients with medical management. These survival statistics demonstrate the utility of VADs as an effective means to bridge critically ill patients until a suitable donor organ becomes available. In addition, as previous studies have suggested for acute results, earlier implementation and better patient selection may lead to improved long-term survival.

Termination Of Sustained Tachycardia By External Noninvasive Pacing

Invasive cardiac pacing has proved useful in the induction and termination of reentrant sustained tachycardias. In one of our two cases, programmed ventricular extrastimulation was used to induce sustained ventricular tachycardia from the endocardial surface of the right ventricle. Induced ventricular tachycardia was terminoted by burst ventricular pacing with an external cardiac pacemaker. In our second patient, external pacing was effective at inducing and terminating sustained supraventricular tachycardia. These patients illustrate that the principles of terminating sustained reentrant tachycardia with invasive pacing may also apply to noninvasive external pacing. The usefulness of this approach in treating reentrant tachycardias needs further evaluation.

Diagnosis and Management of Cardiac Arrhythmias in the Postoperative Period

Various rhythm disturbances occur in the postoperative patient. Proper management requires an awareness of clinical circumstances in which they are most likely to happen. Often, the appearance of new arrhythmias in the postoperative period is a manifestation of underlying remediable medical problems. Direct antiarrhythmic therapy is unnecessary in many patients when these precipitating conditions are properly treated.

Normalization of the norepinephrine kinetic response to orthostatic stress after cardiac transplantation

Abstract In summary, we have demonstrated through the use of forearm venous NE kinetic methodology that plasma NE and NE spillover increase normally in response to orthostatic stress after cardiac transplantation. These findings suggest that, in the absence of ventricular afferents, systemic arterial baroreflexes respond in a compensatory manner to activate the sympathetic nervous system.

Pacemakers in Noncardiac Surgery

The authors look at the use of pacemakers in three groups of patients: one with previously implanted cardiac pacemakers, one requiring temporary pacing systems for reasons related to their heart, and one in whom indications exist for permanent pacemaker implantation, but because of a surgical emergency, cannot have a permanent unit implanted before the noncardiac operation.