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Canadian Journal of Anesthesia 51:850-851 (2004)
© Canadian Anesthesiologists' Society, 2004

Correspondence

Coronary spasm in a 59-yr-old woman with hyperventilation

Pascal Fangio, MD, Bernard De Jonghe, MD, Jean-Claude Lachérade, MD, Jean-Pierre Terville, MD and Hervé Outin, MD

Poissy, France

To the Editor:

Severe alkalemia can compromise myocardial perfusion by causing coronary arteriolar constriction, an effect that is more pronounced in respiratory than in metabolic alkalosis. Alkalemia reduces the anginal threshold and predisposes to myocardial ischemia.1 We describe a case of acute coronary syndrome provoked by severe respiratory alkalosis.

A 59-yr-old schizophrenic woman was admitted to our intensive care unit (ICU) because of symptomatic acute hyponatremia after massive oral intake of water. Initial arterial blood gas determination showed pH, 7.69; PaCO2, 21 mmHg; PaO2, 73 mmHg on room air; HCO3, 25 mmol·L–1. The initial electrocardiogram showed sinus rhythm and marked ST-segment elevation in leads V2-V4 and concurrent ST-segment depression in leads II, III, aVF (FigureGo). The patient did not complain of chest pain, discomfort, or dyspnea but breathed deeply at a rate of 24 breaths·min–1. On admission, troponin I levels were 0.13 ng·mL–1 and peaked at 3.08 ng·mL–1 nine hours later (normal value < 0.1 ng·mL–1). ST-segment elevation subsided on the subsequent electrocardiogram obtained four hours after admission, ruling out the initial diagnosis of acute myocardial infarction. Concomitantly, arterial blood gases showed the complete resolution of alkalemia (pH, 7.42; PaO2, 96 mmHg; PaCO2, 25.3 mmHg; HCO3, 16.2 mmol·L –1). The suspicion of acute coronary syndrome was treated with low-molecular-weight heparin, aspirin, clopidogrel and diltiazem. Cardiac catheterization performed 36 hr after ICU-admission revealed stenoses of 50 to 70% in the left anterior descending and circumflex coronary arteries, and stenosis of 70 to 90% in the right coronary artery, with thrombolysis in myocardial infarction grade III blood flow. A final diagnosis of hyperventilation-induced transient coronary-artery spasm with underlying chronic ischemic cardiopathy was made.



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  		FIGURE Electrocardiogram on admission, reflecting ST-segment elevation in leads V2, V3, V4; and ST-segment depression in leads II, III, aVF.

 
Severe hyperventilation and alkalemia can provoke chest pain and ST-segment elevation, thereby mimicking acute myocardial infarction.2 Alkalemia-induced coronary spasm is usually considered responsible for this acute coronary syndrome, all the more that cardiologists use hyperventilation to induce coronary arterial spasm during cardiac catheterization in patients with suspected Prinzmetal’s angina.3 In this patient, ischemic changes were likely favoured by a three-vessel coronary artery disease. Severe hyperventilation can be observed in psychiatric conditions, as in this patient, as well as in patients with central nervous system lesions, or with inappropriate ventilator setting in the ICU or the operating room.1 Although prolonged hyperventilation-induced coronary spasm can lead to myocardial infarction even in the absence of underlying coronary disease,4 resolution of vasospasm usually occurs rapidly after correction of alkalemia. Calcium-antagonists might prove effective in cases of prolonged spasm.5

Footnotes

There was no financial support for this study.

References

1 Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders. Second of two parts. N Engl J Med 1998; 338: 107–11.[Free Full Text]

2 Heckerling PS, Hanashiro PK. ST segment elevation in hyperventilation syndrome (Letter). Ann Emerg Med 1985; 14: 1122–3.[Medline]

3 Chen HS, Pinto DS. Images in clinical medicine. Prinzmetal’s angina. N Engl J Med 2003; 349: e1.[Free Full Text]

4 Chelmowski MK, Keelan MH Jr. Hyperventilation and myocardial infarction. Chest 1988; 93: 1095–6.[Abstract/Free Full Text]

5 Abernethy DR, Schwartz JB. Calcium-antagonist drugs. N Engl J Med 1999; 341: 1447–57.[Free Full Text]





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