Modern Treatment of Coronary Occlusion and Insufficiency

Goblin, Richard

doi:10.1016/s0025-7125(16)33655-0

Cited by 8 publications

(2 citation statements)

References 49 publications

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“…Early clinical trials consisting of the administration of digitalis to alternate patients after myocardial infarction with and without complica tions suggested that digitalis could be tolerated in this setting [4,9] and was considered clinically useful [25], More recently, in a group of patients with cardiogenic shock, acute digitalization was found not to alter cardiac output, mean arterial pressure, central venous pressure, or peripheral systemic resistance [27]. Rapid administration of digitalis in man may cause peripheral arteriolar constriction, thus increasing afterload.…”

Section: Hemodynamic and Clinical Trialsmentioning

confidence: 99%

Digitalis: Reappraisal of its Use after Acute Myocardial Infarction

Kones¹

1974

Cardiology

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Digitalis is a potent inhibitor of sarcolemmal sodium (Na⁺), potassium (K⁺)-ATPase, and, through this property, effects net movement of calcium (Ca⁺⁺) into the myocardial cell. Augmented contractility probably directly results from increased concentrations of activator Ca⁺⁺ available to the contractile elements. The clinical manifestations of digitalis toxicity are due to intracellular K⁺ depletion, which is an obligatory consequence of Na⁺, K⁺-ATPase inhibition.Digitalis, as a positive inotropic agent, also augments myocardial energy consumption in the nonfailing heart. However, when digitalis is employed in the enlarged, failing heart, a simultaneous reduction in the intramyocardial tension leaves net myocardial oxygen balance unchanged or improved. Digitalis has no unique effect on myocardial energy metabolism. Digitalis acutely increases peripheral vascular resistance in man. Through sympathetically mediated responses, digitalis dilates peripheral blood vessels in patients with heart failure. The direct action of digitalis on the coronary vascular bed is uncertain. In ischemic heart muscle, digitalis can improve contractility, but at a metabolic price. The extent to which myocardial energy balance is affected depends on the simultaneous effect of digitalis on all determinants of myocardial oxygen consumption. Similarly, the hemodynamic changes effected by digitalis are not completely predictable because of many variables changing simultaneously, but generally reflect improved ventricular function. Studies in the dog indicate that the cardiovascular response to digitalis after myocardial infarction is a function of the particular time it is administered during recovery. Initial insensitivity is regained within one weeks’ time. Acute intravenous injections of digitalis in patients with myocardial infarctions may increase after load, thus offsetting the anticipated increase in stroke volume due to the change in contractility alone.The use of digitalis after uncomplicated myocardial infarctions is not recommended. Patients with clinical evidence of heart failure are likely to benefit from digitalis. The larger the heart size and the greater the time passed after the acute infarction when digitalis is administered, the better will be the response. No data presently available clearly demonstrate the efficacy of digitalis in patients with cardiogenic shock.

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Section: Hemodynamic and Clinical Trialsmentioning

confidence: 99%

Digitalis: Reappraisal of its Use after Acute Myocardial Infarction

Kones¹

1974

Cardiology

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“…Gorlin measured cardiac output in two patients before and after rapid digitalization and found increases in both patients. 53 In an experimental model of cardiogenic shock Cronin and Zsoter showed that digitalis causes an increase in blood pressure, a slight increase in cardiac output, and a very significant increase in stroke volume with a fall in LVEDP. 54 The increase in blood pressure preceded the increase in cardiac output and they suggested that the direct vasoconstrictor effects of digitalis preceded the inotropic action.…”

Section: Digitalismentioning

confidence: 99%

Use of Drugs in Cardiogenic Shock due to Acute Myocardial Infarction

Loeb

1972

Circulation

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As a plan of therapy for shock associated with acute myocardial infarction in a general hospital and assuming that septic and hemorrhagic shock has been eliminated as diagnostic possibilities we would suggest the following: (1) Pain should be relieved using morphine or pentazocine, and atropine if brady-cardia is present. Oxygen by mask should be administered to bring the arterial oxygen tension to about 100 mm Hg. The airway must be examined and, if air exchange is poor and the arterial oxygen very low or carbon dioxide high, respiratory assistance and occasionally intubation may be required. (2) Blood pressure must be stabilized at an adequate level for perfusion of vital organs, or progression may be so rapid that death will occur before proper evaluation can be made and more rational therapy started. For this purpose we would start a norepinephrine infusion at a rate just sufficient to keep the systolic blood pressure near 100 mm Hg. If the shock syndrome is present but arterial pressure is normal or only slightly reduced, we would eliminate this step in therapy. (3) Arrhythmias or heart block should be corrected by methods discussed elsewhere in this symposium. (4) A venous catheter should be inserted so that the catheter tip is just within the thorax. If the central venous pressure (CVP) is below 10 cm H 2 O we would begin a regimen of plasma volume expansion giving 100 cc of 40 dextran over a period of 10 min, waiting 10 min, and if the CVP has not risen 1 cm H 2 O repeat the process until shock is relieved, the CVP continues to increase or is above 15 cm H 2 O, or 1000 cc of 40 dextran has been given. If the patient accepts more than 1000 cc of fluid in this manner without elevating the CVP it is most likely that some other major process causing fluid loss is complicating the myocardial infarction. (5) If or when CVP is above 10 cm H 2 O, and if the patient remains in shock and is hypotensive, we would add norepinephrine infusion at a rate just sufficient to bring the systolic pressure between 100 and 110 mm Hg. If this cannot be accomplished with small amounts of norepinephrine then intraarterial pressure must be measured since the discrepancy between the cuff pressure and actual pressure may be increasing with further pressor infusion. (6) If the patient is normotensive and has a CVP above 10 cm H 2 O but manifests the shock syndrome, an isoproterenol infusion should be instituted, but to use this regimen one must be able to measure intraarterial pressure. If CVP falls, simultaneous plasma volume expansion may be necessary. If arterial pressure begins to fall, norepinephrine should be substituted. We would use dopamine first in this particular situation, but this agent is not as yet generally available. (7) With the CVP elevated and blood pressure stable, arterial oxygenation established, and arrhythmias corrected, if the patient is still in a low cardiac output state with continued oliguria and poor tissue perfusion, digitalization with about half to two thirds the normal digitalizing dose should be undertaken. (8) If a further inotropic response is needed glucagon may be added at this point. With an initial bolus injection efficacy should be established and if found helpful a constant infusion should follow. Aminophylline should be given simultaneously to potentiate the action of glucagon. (9) The patient who at this point remains oliguric and with a small pulse pressure may be benefited by cautious vasodilation with chlorpromazine or phentolamine and simultaneous further plasma volume expansion. (10) A patient who remains pressor-dependent or responds poorly to pressors will probably need circulatory assistance. However, unless some definitive measure can be undertaken to restore or replace nonfunctioning myocardium this too will be of little benefit. (11) A patient who stabilizes well but experiences a fall in blood pressure as the pressor infusion is being discontinued should have plasma volume expansion as the pressor infusion is decreased. The physician must resist the temptation to restart the infusion as the pressure falls, unless the shock syndrome accompanies the hypotension.

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Must cardiology lose its heart?

Gorlin

1992

Journal of the American College of Cardiology

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Regulations and restrictions imposed by external agencies are forcing cardiologists into an unnatural self-protective and defensive posture against their patients. The key to breaking the pattern of mutual skepticism and mistrust lies in returning the focus to its rightful place: the patients' needs. Thus, payment systems must be devised that reward cognitive skills, time spent with patients and continuity of care as they reward technologic interventions and procedures. In advocating necessary changes in the system, only physicians themselves can provide a convincing voice in the political arena. They must look beyond their own self-interest to recapture the moral and ethical high ground where the best care of their patients and their own professional satisfaction stand side by side.

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Modern Treatment of Coronary Occlusion and Insufficiency

Cited by 8 publications

References 49 publications

Digitalis: Reappraisal of its Use after Acute Myocardial Infarction

Digitalis: Reappraisal of its Use after Acute Myocardial Infarction

Use of Drugs in Cardiogenic Shock due to Acute Myocardial Infarction

Must cardiology lose its heart?

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