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Does the Decrease in Heart Rate Prevent a Detrimental Decrease of the End-Systolic Volume during Central Hypovolemia in Man?

Department of Medical Physiology C Panum Institute, University of Copenhagen

Jens Marving

Department of Clinical Physiology, University of Copenhagen

Niels H. Secher

Department of Anesthesiology, Glostrup Hospital, University of Copenhagen, Copenhagen, Denmark

Inge-Lis K. Hansen

Department of Clinical Physiology, University of Copenhagen

Jørn Giese

Department of Clinical Physiology, University of Copenhagen

Jørgen Warberg

Department of Medical Physiology C Panum Institute, University of Copenhagen

Peter Bie

Department of Medical Physiology C Panum Institute, University of Copenhagen

Central hypovolemia occurring with epidural anesthesia was investigated by measurement of hemodynamic and endocrine variables in 10 patients. Responses fell into two categories. Four patients experienced a hypotensive bradycardic episode after seventeen ± four minutes. In this group epidural anesthesia initially induced a tendency toward an increase in heart rate from 65 ± 4 to 73 ± 5 beats/min concomitantly with decreases in end-diastolic (172 ± 22 to 138 ± 16 mL), end-systolic (67 ± 12 to 51 ± 9 mL), and stroke (105 ± 10 to 85 ± 7 mL) volumes (radionuclide cardiography). A subsequent decrease in mean arterial pressure from 76 ± 3 to 67 ± 4 mmHg was associated with a decrease in venous return as reflected by the decrease in cardiac output from 6.1 ± 0.4 to 4.7 ± 0.7 L/min. In this situation when the venous return was critically reduced, the heart rate was 49 ± 4 beats/min and no further reduction in end-diastolic and end-systolic volumes was observed. The observed endocrine changes were compatible with a response to central hypovolemia. In the other 6 patients the reaction to epidural anesthesia did not induce statistically signif icant changes in hemodynamic and endocrine variables.

It is concluded (1) that the decrease in heart rate associated with central hypovolemia during epidural anesthesia seems to be elicited when the left ven tricular end-systolic volume is decreased by about 25% and (2) that a further decrease in end-systolic volume during progressive central hypovolemia is avoided possibly as a direct consequence of the slowing of the heart.

Angiology, Vol. 41, No. 9, 687-695 (1990)
DOI: 10.1177/000331979004100903


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