Hemodynamic Response to Exercise after Beta-Adrenergic Blockade in Normal and Labile Hypertensive Patients

The effect of sustained beta-adrenergic blockade (BB) on the hemodynamic response to graded exercise has been studied in 31 patients with high blood pressure. Hemodynamic investigations were conducted during a control period and were repeated after 1 mo of BB. Similar readjustments were observed at rest and during submaximal and maximal exercise. No significant change occurred in maximal physical working capacity during beta blockade. This resulted from hemodynamic readjustments. Maximal exercise heart rate was reduced by 34%, and this was compensated for by a 31% enhancement in stroke index. Consequently cardiac index decreased by only 14%. In the Fick equation the decrease in cardiac index was further compensated by an increase of the total arteriovenous O2 difference of 8%, thereby maintaining O2 delivery to the tissues. At maximal exercise mean brachial artery pressure dropped 14.5%, while mean pulmonary artery pressure increased by 20%. It is concluded that the compensatory action of the stroke volume, resulting from the interaction of an increased preload and a decreased impedance, played a major role in the hemodynamic readjustments following chronic BB to maintain maximal working capacity.

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HEMODYNAMIC RESPONSE TO EXERCISE AFTER PROPRANOLOL IN NORMAL SUBJECTS

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y66-055 ◽

1966 ◽

Vol 44 (3) ◽

pp. 465-474 ◽

Cited By ~ 33

Author(s):

Gordon R. Cumming ◽

W. Carr

Keyword(s):

Cardiac Output ◽

Adrenergic Receptors ◽

Systolic Pressure ◽

Normal Subjects ◽

Cardiac Response ◽

Adrenergic Blockade ◽

Beta Adrenergic ◽

Arterial Systolic Pressure ◽

Consistent Change ◽

Response To Exercise

Supine exercise after beta-adrenergic blockade with propranolol in six normal subjects caused (a) a mean decrease of 13% in resting heart rate; (b) a mean decrease of 20% in resting cardiac output; (c) a mean reduction of 17% in exercise cardiac output and a mean reduction of 21% in exercise pulse rate; (d) a decrease in the elevation of arterial systolic pressure produced by exercise; (e) an increase in exercise end-diastolic pressures in the left ventricle and in exercise pulmonary artery pressures; (f) more rapid recovery of circulatory function after exercise. There was no consistent change in pulmonary vascular resistance. Even though the normal cardiac response to exercise would seem to be dependent on intact beta-adrenergic receptors, the exercise loads chosen were completed just as easily after the blockade as before.

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The Effect of Beta Adrenergic Blockade on the Exaggerated Natriuresis and Diuresis of Hypertensive Patients.

Annals of Internal Medicine ◽

10.7326/0003-4819-74-5-832_1 ◽

1971 ◽

Vol 74 (5) ◽

pp. 832

Author(s):

William J. Mroczek

Keyword(s):

Adrenergic Blockade ◽

Beta Adrenergic ◽

Hypertensive Patients

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Effects of Chronic Beta-Adrenergic Blockade on Systemic and Renal Haemodynamic Responses to Hyperosmotic Saline in Hypertensive Patients

Clinical Science ◽

10.1042/cs0430385 ◽

1972 ◽

Vol 43 (3) ◽

pp. 385-391 ◽

Cited By ~ 45

Author(s):

X. H. Krauss ◽

M. A. D. H. Schalekamp ◽

G. Kolsters ◽

G. A. Zaal ◽

W. H. Birkenhäger

Keyword(s):

Venous Return ◽

Venous Pressure ◽

Control Period ◽

Adrenergic Blockade ◽

Central Blood Volume ◽

Myocardial Depression ◽

Central Venous ◽

Sharp Rise ◽

Beta Adrenergic ◽

Hypertensive Patients

1. Ten patients with essential hypertension received an intravenous load of hyperosmotic saline before and during treatment with propranolol. In seven patients blood pressure was lowered by the drug. 2. In the control period saline infusion induced a sharp rise in cardiac output due to an increase in stroke volume. This pattern was absent during beta-adrenergic blockade. Renal blood flow showed a moderate rise in the control studies; this rise was not reduced during treatment. Natriuresis was reduced by propranolol. 3. Measurements of central blood volume and central venous pressure in five patients revealed that modified responses during beta-adrenergic blockade may be due to a reduced venous return rather than to myocardial depression.

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