Anesth Analg 2000;91:766-767
© 2000 International Anesthesia Research Society
LETTERS TO THE EDITOR
Heparin-Mediated Hypotension Associated with Cardiac Surgery
Thomas F. Slaughter, MD, and
Jonathan B. Mark, MD
Department of Anesthesiology Duke University and the Durham Veterans Affairs Medical Centers Durham, NC 27710
To the Editor: We read with great interest the article by Jacka and Clark (1) describing an association among heparin administration, hyperkalemia, and hypotension/bradycardia during cardiac surgery. We recently observed a similarly severe hypotensive episode in a cardiac surgical patient in response to heparin administration; however, absence of hyperkalemia in our case necessitates an alternative pathophysiologic explanation.
The patient, a 58-yr-old man with unstable angina and an otherwise unremarkable medical history, was admitted for coronary artery bypass graft surgery. Preoperative medications included ranitidine and metoprolol. After an uneventful anesthetic induction with midazolam and fentanyl and surgical isolation of the internal mammary artery, administration of 300 U/kg of porcine heparin through the central venous catheter resulted, within 90 s, in a 35% reduction in arterial blood pressure (123/59 to 80/40 mm Hg). Heart rate remained unchanged at 70 bpm. Intraoperative transesophageal echocardiography revealed no abnormalities in left ventricular function, and no acute changes in the electrocardiogram were noted. Administration of phenylephrine in two 100-µg doses corrected the arterial pressure. Laboratory findings before the hypotensive episode and 10 min after were unremarkable with no change in serum potassium concentration (K = 4.3 mmol/L).
Several reports have described an association between hypotension and heparin administration preceding cardiopulmonary bypass (1–3). In a prospective investigation, Urban et al. (3) reported hypotension in 17 of 20 patients in response to 300 U/kg heparin. Although generally less dramatic than the hypotension observed in our case, a 13% decrease in arterial pressure occurred within 76 ± 26 s of heparin administration. The authors further demonstrated a correlation between serum ionized calcium concentrations and the hypotensive response. Administration of small doses of calcium chloride before heparin administration increased serum ionized calcium concentration and abolished the hypotensive response. In a subsequent prospective investigation, Casthely et al. (4) demonstrated an association between heparin-mediated hypotension and histamine release. H1-receptor blockade significantly attenuated the hypotensive response to heparin; in contrast, patients receiving only H2-receptor blockade experienced an exaggerated hypotensive response.
Although a hyperkalemic response to heparin, as described by Jacka and Clark (1), may be associated with hemodynamic instability, it is unlikely to be the primary cause. Instead, vasodilation secondary to heparin-mediated hypocalcemia and/or histamine release appear more likely mechanisms. Clinically significant episodes of heparin-mediated hypotension are uncommon. However, in those few cases of prolonged and/or exaggerated hypotension, administration of calcium chloride or a specific vasoconstrictor is reasonable. In patients with a history of a clinically significant hypotensive response to heparin, preoperative administration of an H1-receptor blocker may be prudent.
References
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Jacka MJ, Clark AG. Cardiovascular instability requiring treatment after intravenous heparin for cardiopulmonary bypass. Anesth Analg 2000; 90: 42–4.[Free Full Text]
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Seltzer JI, Gerson JI. Decrease in arterial pressure following heparin injection prior to cardiopulmonary bypass. Acta Anaesthesiol Scand 1979; 23: 575–8.[Web of Science][Medline]
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Urban P, Scheidegger D, Buchmann B, Skarvan K. The hemodynamic effects of heparin and their relation to ionized calcium levels. J Thorac Cardiovasc Surg 1986; 91: 303–6.[Abstract]
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Casthely PA, Yoganathan D, Karyanis B, et al. Histamine blockade and cardiovascular changes following heparin administration during cardiac surgery. J Cardiothorac Anesth 1990; 4: 711–4.[Medline]
Response
Michael J. Jacka, MD, FRCPC, MSc, and
Andrew Clark, MD, FRCPC
Department of Anesthesia University of Toronto Sudbury, Ontario, Canada
Department of Anesthesia Dalhousie University Saint John, NB, Canada
In Response: We thank Drs. Slaughter and Mark for their interest in this topic, their case description, and their subsequent discussion.
Clearly, an association between administration of IV heparin for cardiopulmonary bypass and subsequent hemodynamic instability exists (1–4). The factors which are causal, versus confounding, remain unclear. Our study (1), by its case-control nature, was hypothesis-generating, and we found an association among change in serum potassium, heparin administration, and hemodynamic change. Regarding the observed mean increase of 1.94 mmol/L in serum potassium in the treated group in our review, the range was from 1.14 to 3.04 mmol/L. The lack of any observed change in serum potassium in Slaughter and Mark’s patient would have been unusual in our review, although statistical comparisons would not be possible based on one patient. However, it is noted that Slaughter and Mark administered 300 IU/kg of porcine heparin, whereas our patients received 400 IU/kg. The dose-response effect, if any, of heparin on serum electrolyte levels is unknown and may explain part of the difference in these observations.
The other mechanisms suggested by Slaughter and Mark, including hypocalcemia (2) and histamine release (3) merit further investigation. Although not reported in our earlier work (1), we observed a nonsignificant increase in serum ionized calcium in the treated group of 0.01 mmol/L (range: -0.32 to +0.62) and a nonsignificant decrease in the nontreated group of 0.02 mmol/L (range: -0.34 to +0.41).
Further investigation might also include, in addition to the dose-response relationship (if any), determination of the frequency and intensity of the hemodynamic effect associated with heparin, its complete hemodynamic characterization (i.e., effect on systemic and pulmonary vascular resistances, cardiac output, and filling pressures), the decay curve of this hemodynamic effect, the association with any patient- or procedure-descriptors, and impact of preventive maneuvers.
References
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Jacka MJ, Clark AG. Cardiovascular instability requiring treatment after intravenous heparin for cardiopulmonary bypass. Anesth Analg 2000; 90: 42–4.
-
Seltzer JL, Gerson JI. Decrease in arterial pressure following heparin injection prior to cardiopulmonary bypass. Acta Anaesthesiol Scand 1979; 23: 575–8.
-
Urban P, Scheidegger D, Buchmann B, Skarvan K. The hemodynamic effects of heparin and their relation to ionized calcium levels. J Thorac Cardiovasc Surg 1986; 91: 303–6.
-
Casthely PA, Yoganathan D, Karyanis B, et al. Histamine blockade and cardiovascular changes following heparin administration during cardiac surgery. J Cardiothorac Anesth 1990; 4: 711–4.
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