HIGH CARDIAC OUTPUT HYPERTENSIONS EDWARD D. FROHLICH, M.D.

discussing the role of high cardiac output (or a hyperkinetic circulation) systemic arterial hypertension, we must first define what is meant by a hyperdynamic circulation. In general, these terms refer to a hypertensive state In

in

that is associated with an increased cardiac output, increased heart rate, and increased state of ventricular contractility.’, ’2 It is unusual to determine cardiac function in patients with uncomplicated systemic hypertensive diseases because very few of these patients undergo hemodynamic studies as part of their clinical evaluation. Moreover, unless the hypertensive disease is associated with atherosclerosis of the coronary arteries, the investigation of these patients with uncomplicated or mild to moderately severe hypertension does not involve direct cardiac catheterization techniques. Nevertheless, it is still possible, with indicator-dilution techniques, to measure cardiac output,3, and, using rapid recording of arterial pressure, to measure left ventricular ejection time and to calculate a variety of indices of left ventricular performance.’ Further, using echocardiographic techniques, we can augment our information about the heart in hypertension. Thus, it is now possible to characterize, by invasive as well as by noninvasive means, the systemic circulation in a fashion similar to the means by which the hyperdynamic or hyperkinetic heart syndromes were characterized as having 7 an increased heart rate, cardiac output, and left ventricular ejection rate.2, Therefore, we have used these same criteria to characterize the hemodynamic indices of the hypertensive diseases. It is clear from our studies that we are suggesting that the hypertensive diseases characterized by a hyperkinetic circulation do not have as severely elevated cardiac output as in patients with beriberi, arteriovenous fistulae, or even fever. The cardiac output, however, in these hypertensive diseases is significantly greater than in the normal individual or in other hypertensive patients who are characterized as having a normal circulation and cardiac output.44 PHYSIOLOGICAL CONCEPTS

There are a variety of physiological factors that.can increase cardiac output and the inotropic and chronotropic function of the myocardium. For example, peripheral venoconstriction may serve to redistribute a normal circulating intravascular volume from the peripheral to the central circulation, thereby George Lynn Cross Research Professor of Medicine and Director, Hypertension Section, Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma. Presently, Vice President, Research and Education, Alton Ochsner Medical Foundation, New Orleans, Louisiana 70121.

Supported, RR-62).

in part,

Presented at the

by grants-in-aid

Annual 1976.

Twenty-Second

Springs, California, January 4-11,

from the National Institutes of Health

Meeting,

American

College

475

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of

(HL

17478 and

Angiology,

Palm

476

increasing the venous return to the heart and hence the cardiac output (provided the ventricular function is not impaired). A net increase in adrenergic activity, either through inhibition of parasympathetic function or through stimulation of adrenergic mechanisms (e.g., increased nerve activity, increased release of norepinephrine from nerve endings, decreased nerve ending reuptake of norepinephrine, increased adrenergic receptor reactivity) will also serve to increase ventricular function. This augmented adrenergic input to the myocardium will result in increased heart rate, stroke volume, cardiac output, and myocardial contractility. A number of humoral agents (e.g., catecholamines, dopamine, angiotensin II, calcium ion), and hormonal substances (e.g., glucagon, thyroid hormone, vasopressin, and probably adrenal steroids) will increase inotropic or chronotropic effects upon the myocardium and, thus, cardiac output. Finally, many therapeutic agents (including digitalis, isoproterenol, and synthetic sympathomimetic agents having beta-adrenergic receptor agonistic effects) will also increase cardiac output and have been used to clinical advantage in patients with low cardiac output and impaired ventricular function. NORMOTENSIVE HYPERKINETIC CIRCULATORY STATES

Several hemodynamic circulatory conditions are frequently encountered in the normal individual and under pathological circumstances (Table 1). They are characterized hemodynamically by an increased heart rate, cardiac output, and ventricular contractility. For example, in the normal individual the best examples of a hyperkinetic circulation may be demonstrated by exercise and acute anxiety; in both conditions the increased cardiac output is associated with an increased peripheral oxygen demand by the tissues. In disease , thyrotoxicosis, fever, arteriovenous fistulae, Paget’s disease, beriberi, TABLE 1 Common

(Adapted

from

hyperdynamic circulatory states Frohlich Pathophysiology, Reference 8)

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477 TABLE 2

Idiopathic high

cardiac output

syndromes

and certain

malignancies have been associated with a hyperkinetic or hyperdynamic circulation. In addition, a variety of names have been ascribed to idiopathic hyperkinetic circulatory states (Table 2); all have been characterized clinically. (The suggested physiological mechanism for the increased cardiac output in each of these examples had been investigated and is outlined in Table 1 [8].) With respect to the idiopathic hyperkinetic circulatory states, these have been documented ever since the days of Avicenna when he reported the association of fear, increased heart rate, widely dilated pupils, diaphoresis, tremors, and a bounding pulse.9 This description is very similar indeed to a variety of hyperkinetic heart syndromes whose popularity and publication seem

to be associated with several

wars:

the soldier’s heart

or

Da Costa’s

syndrome, described during the Civil War; 10 neurocirculatory asthenia, described by Sir Thomas Lewis&dquo; and by Paul Dudley White 12 during World War I; essential cirulatory kinesis 13 and the hyperkinetic heart syndrome, 1, 7, reported during and after World War II. By the 1960’s, with the use of betaadrenergic receptor blocking drugs, we described the hyperdynamic betaadrenergic circulatory state involving both normotensive and hypertensive patients.15, 16 In these latter patients, the symptoms of cardiac awareness were mimicked by the intravenous infusion of the beta-adrenergic receptor agonist isoproterenol, and were inhibited or prevented with prolonged treatment using the beta-adrenergic receptor blocking drugs. 14

HYPERTENSIVE HYPERKINETIC CIRCULATORY STATES

Hyperkinetic Heart Syndrome: Hyperdynamic Beta-Adrenergic Circulatory State. Presented in Table 3 are the various forms of primary and secondary hypertensive diseases which may be associated with a hyperkinetic circulation. The hyperkinetic heart syndrome was described by Gorlin and his associates; 2, ’ and this clinical problem was found primarily in normotensive individuals or patients with systolic hypertension. The hyperdynamic betaadrenergic circulatory state, described in 1966, involved patients with rapid heart action, palpitations, and disabling tachycardia in the upright posture or following even the slightest exertion. 15, 16 As indicated, these symptoms were

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478

provoked under controlled laboratory conditions with intravenous infusion of specific beta-adrenergic receptor agonist isoproterenol. When these patients were treated with beta-adrenergic receptor blocking drugs the symptoms could be either totally prevented or markedly attenuated and arterial pressure was controlled. It is important to point out that the patients with increased arterial pressure should not be considered a specific etiological group of patients with hypertension; some had labile or borderline hyperten-

the

sion,

some

had renal arterial disease, and

some were

without

a cause

(essential

hypertension) . Systolic Hypertension. We have recently subdivided patients with systolic pressure elevation (> 150 mm Hg systolic pressure but with diastolic pressure

High cardiac output hypertensions.

HIGH CARDIAC OUTPUT HYPERTENSIONS EDWARD D. FROHLICH, M.D. discussing the role of high cardiac output (or a hyperkinetic circulation) systemic arteri...
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