1 Medical Intensive Care Unit, University Hospital Henri-Mondor and Medical Faculty (Paris XII), Créteil, France. 2 Department of Cardiology, University Hospital Henri-Mondor and Medical Faculty (Paris XII), Créteil, France
* Corresponding author: E-mail: francois.lemaire{at}hmn.ap-hop-paris.fr
Accepted for publication February 5, 2004.
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Abstract |
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Keywords: complications, myocardial ischaemia ; heart, left ventricular dysfunction ; heart, mitral insufficiency ; surgery, coronary angioplasty ; ventilation, mechanical ; ventilation, weaning
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Introduction |
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Case report |
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After admission, the patient was intubated and mechanically ventilated (Evita 2, Drägerwerk, Lübeck, Germany). Fluid administration failed to restore the arterial pressure, so an infusion of epinephrine (0.4 mg kg1 min1) was started. Appropriate antibiotics were given. The ECG showed signs of myocardial ischaemia and troponin Ic blood level was increased (35 ng ml1). Echocardiography was unchanged.
On the third day of treatment, the patient was afebrile and the circulation was stable so the epinephrine dose was reduced to 0.1 mg kg1 min1, and weaning from mechanical ventilation was started. The ventilator was switched from assist-control to a pressure support of 16 cm H2O, and 5 cm H2O positive end-expiratory pressure. On day 5, these values were unchanged, and the ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen () was 300 mm Hg. Right atrial pressure was 6 cm H2O, the circulation was stable, systolic arterial pressure 110 mm Hg, epinephrine infusion at 0.1 mg kg1 min1, and troponin was decreasing (9.5 ng ml1). As the level of pressure support was progressively decreased from 16 to 10 cm H2O (PEEP being constant), hypotension developed (systolic arterial pressure: 85 mm Hg) and the epinephrine dose had to be increased to 0.4 mg kg1 min1. The respiratory state worsened, as respiratory frequency increased from 24 to 36 bpm and
ratio decreased from 300 to 150, so we re-started controlled ventilation. Clinical and radiographic signs of acute pulmonary oedema developed and right atrial pressure increased from 6 to 13 cm H2O. Ischaemic changes were seen on the ECG (Fig. 1A), and troponin Ic increased to 13.6 ng ml1. These features suggested ischaemic cardiac failure. Echocardiography showed severe antero-lateral-basal hypokinesia and massive mitral regurgitation without left ventricular (LV) dilatation. At coronary angiography, three marked stenoses were shown on the left anterior descending vessel and one on the left circumflex (Fig. 2A). With the Cardiovascular Angiography Analysis System (CAAS), stenosis was greater than 70%, and dilation was recommended. Transluminal angioplasty was done and stents were inserted (four stents on the anterior descending and one on the circumflex; Fig. 2B).
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Discussion |
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Cardiac ischaemia results from an imbalance between oxygen supply and demand.1 Oxygen supply is reduced by hypoxaemia, which is common during weaning, because of tachypnoea and worsening of ventilation-perfusion matching,2 and can be made worse by pulmonary oedema. Myocardial oxygen delivery is also reduced by catecholamine-induced tachycardia, which limits the diastolic perfusion time. In addition, increased LV end-diastolic pressure may reduce diastolic sub-endocardial blood flow, and coronary narrowing could also limit coronary blood flow, reducing oxygen supply to the myocardium. An increase in cardiac afterload, caused by changing from positive pressure mechanical ventilation to negative pressure spontaneous breathing,3 can also impair myocardial function. Mitral regurgitation has been described during weaning4 and may have worsened the cardiac failure. The sequence of events suggests an ischaemic cause.
However, during weaning, pleural pressure decreases in inspiration, and diastolic transmyocardial pressure and systemic venous return will increase. This will increase the volume of the left ventricle and dilate the mitral valve ring. If the efficiency of apposition of the valve leaflets was impaired, this would contribute to the mitral regurgitation we observed.
Several studies have reported cardiac ischaemia during weaning, and greater risk of weaning failure (Table 1). Räsänen and colleagues5 observed angina and electrocardiographic evidence of myocardial ischaemia in six of 12 patients during weaning from the ventilator after acute myocardial infarction. These changes were concomitant with increased pulmonary artery occlusion pressure. Lemaire and colleagues6 described patients with ischaemic heart disease who had scintigraphic evidence of abnormal left ventricular wall motion during mechanical ventilation (MV), which worsened during spontaneous ventilation. Treatment of the cardiac failure allowed weaning. Hurford and colleagues7 reported abnormal scintigraphic perfusion images suggesting ischaemia in five out of 15 patients. During weaning, ECG changes suggesting ischaemia were found in six of 17 ventilated patients8 and silent myocardial ischaemia, shown by S-T segment analysis, was noted in 914% of patients during weaning after non-cardiac surgery.9 Others have reported similar findings.10 11
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We suggest that coronary angioplasty should be considered when cardiac ischaemia and left ventricular failure occur during weaning. Ischemic myocardial dysfunction during weaning may be associated with acute ischaemic mitral insufficiency and may contribute to weaning failure. If ischaemic heart failure can be demonstrated, then appropriate treatment can allow successful weaning and reduce the possibility of cardiac damage during weaning attempts.
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Acknowledgments |
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References |
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