SPINAL ANAESTHESIA AND LEFT VENTRICULAR EJECTION FRACTION

Ladjevic N, Risovic M, Filimonovic J, Vucovic D, Cosic O, Andjelic N.

Institute of Anaesthesia, Belgrade University Clinical Centre, Yugoslavia

Extremely important physiological responses to spinal anaesthesia occur in the cardiovascular system (1). It is determinated by combined effects of:

A. Sympathetic denervation

B. Level of neural block

C. vagal reaction

Higer level of neural block will induce more significant changes in the cardiovascular system.

After pharmacological sympathetic denervation the total peripheral vascular resistance (TPVR) decreases insignificantly for about 15 - 18 %. The mean arterial pressure decreases for 15 - 18 % in the presence of normal cardiac output.

Veins and venules have small amount of smooth muscle cells, so after acute pharmacological sympathetic denervation no basic tone of these vessels remain. As a result - maximal vasodilation occurs. The intraluminal hydrostatic pressure in veins depends on the gravitational force. If the position of the denervated veins is above the level of the right atrium, gravitation will promote return of blood from these veins into the heart. Preload, and consequently, return of venous blood into the heart depends on the positioning of the patient during spinal anaesthesia, and particularly during high spinal anaesthesia.

Preload determines cardiac output and it is most important to know that during spinal anaesthesia (which induces total sympathetic denervation) the cardiac output remains normal in normovolemic patients if the legs are elevated above the level of the heart. In the head - up position the cardiac output will be significantly decreased.

The main determinant of the coronary blood flow (CBF) as well as the myocardial oxygenation, is the perfusion pressure of the coronary vessels. The decrease of the mean arterial blood pressure in spinal anaesthesia is correlated to the decrease of the CBF. Hackel and soll (2) found that in a healthy cardiovascular system the mean arterial pressure (MAP) decreases from 119.5 mmHg to 67.2 mmHg during spinal anaesthesia, and that CBF decreases from 153.2 ml/min to 73.6 ml/min per 100 g. A decrease of oxygen delivery of 48 % is accompanied by a decrease of the oxygen demand of the myocardial muscles by 58 %.

An average oxygen consumption of 16.1 ml/min/100g before spinal anaesthesia decreases to 7.5 ml/min/100g after it. Almost identical results are obtained in animal experiments (3,4).

The oxygenation of the two most important organs, the heart and the brain, was studied in detail, and it remains within the normal range in cases of moderate hypotension during spinal anaesthesia in healthy patients.

The question is at what level of hypotension the reflexed decrease of cerebrovascular resistance and myocardial oxygen demand are insufficient to compensate for the decrease in the cerebral and coronary perfusion pressures. It is impossible to determine exactly this critical value of arterial blood pressure. Some data suggest that a decrease in systolic blood pressure up to 33 % of the normal values (measured at the morning before rising up from bed) does not require treatment during spinal anaesthesia in healthy patients. In hypertensive patients this limit is about 25 %.

Spinal anaesthesia can be used also in patients with coronary artery disease (stable angina pectoris). However, adequate preload is necessary following the administration of spinal anaesthesia, which can be done by placing the patient in the lithotomy position.

Methods:

Our study included 65 patients undergoing transurethral prostatic electroresection (TURP) in spinal anaesthesia, at L2 - L3 level with 3 ml of Bupivacaine 0,5 %. The patients were divided into three groups: according to position (head - up or lithotomy), presence of coronary artery disease (stable angina pectoris) and into two subgroups (SG): SG 1 = patients with great changes in mean arterial presure (MAP); MAP decreases by 20 % and heart rate (HR) increases by 20 - 30 % or over 110 beats/ min-1; SG 2: slight changes of MAP and HR. All patients were examined prior to and 5 min after induction of spinal anaesthesia for measurement of left ventricular ejection frection (LVEF) with 2D echocardiography, and MAP and HR changes were noted.

Group I included 15 patients, average age of 65.3 years. They had no cardiac dysfunction, and after induction of spinal anaesthesia were positioned in the head - up position.

Group II included 30 patients, average age of 66.1 years, all with stable angina pectoris, and all were positioned in the head - up position after the induction of the spinal anaesthesia

Group III consisted of 20 patients with stable angina pectoris. All were positioned in the lithotomy position after the induction of the spinal anaesthesia

Results:

In the first group there were no LVEF differences prior to and after the spinal anaesthesia (p > 0,05) and only 3 patients had considerable MAP changes and /or HR changes, but without LVEF changes.

In the second group, there were 12 patients in the SG1 and 18 patients in the SG2. The LVEF difference prior to and after the spinal anaesthesia was statistically higher in group II vs group I. In the SG1 it was 0.0658 +/- 0.013 and 0.0056 +/- 0.009 in SG2. The decrease of the LVEF was more significant in the SG1 of the second group (t = 14.82; p < 0.01), than in the SG2. There were notable MAP and HR changes in 40 % of the patients in the SG2.

Data was analysed by the Student t test, and the conclusion was that the changes in the ejection fraction of the left ventricle were most significant in the subgroup 1 (p < 0,01).

The third group had no major MAP and HR changes and had no statistically significant LVEF differences after spinal anaesthesia (LVEF average prior to spinal anaesthesia was 0.4385 +/- 0.037; LVEF average after spinal anaesthesia was 0.4305 +/- 0.034; t = 3.39; p > 0.05).

Conclusion:

Spinal anaesthesia induces very little changes in the LV ejection fraction, arterial blood pressure and heart rate in patients that do not suffer from angina pectoris. In patients with stable angina pectoris if positioned after spinal anaesthesia induction in the lithotomy position, the changes of the LV ejectin fraction were also statistically insignificant. Statistically significant changes of LV ejection fraction occured in patients suffering from stable angina pectoris that were positioned in the head - up position after the induction of the spinal anaesthesia.

Spinal anaesthesia can be applied in patients with coronary artery disease (stable angina pectoris). However, adequate left ventricular preload is necessary following the administration of the spinal anaesthesia, which is possible by placing the patient in the lithotomy position.

References:

1. Green, N.M.: Physiology of spinal anaesthesia. Williams & Wilkins, Baltimore, 1981.

2. Hackel, D.B.: Effects of hypotension due to spinal anaesthesia on coronary blood flow and myocardial metabolism in man. Circulation 13 : 92, 1956.

3. Eckenhoff, J.E.: Influence of hypotension on coronary blood flow, cardiac work and cardiac efficiancy. Am. J. Physiol. 152 : 545, 1948.

4. Sivarajan, M., Amory, D.W., Lindbloom, L.E. and Schwettman, R.S.: Systemic and regional blood flow changes during spinal anaesthesia in the Rhesus monkey. Anesthesiology 43 : 78, 1975.