Title
Intravenous fluid therapy to treat acute pulmonary oedema: the case of left ventricular outflow tract obstruction following acute myocardial infarction
Introduction
A low cardiac output state following a large anterior territory myocardial infarction (MI) is well recognised in the cardiac ICU and often leads to systemic hypoperfusion due to myocardial ischaemia induced ventricular dysfunction (1). Echocardiography has pioneered early bedside diagnosis of left ventricular (LV) predominant cardiogenic shock following MI, and feasibly allowed identification of rarer time critical mechanical complications. We report a case of left ventricular outflow tract obstruction following an acute myocardial infarction whereby early echocardiographic recognition and subsequent reversal of interventions was paramount.
Clinical Case
A 72-year-old woman presented with anterior ST elevation myocardial infarction (STEMI). Angiography showed an occluded previously stented left anterior descending (LAD) coronary artery. During primary percutaneous coronary intervention and stent deployment to the LAD, she was found to be in cardiogenic shock (lactate of 6.0 mmol/l). Inotropic support was commenced and an intra-aortic balloon pump (IABP) was implanted. On admission to the ICU, the patient had significant cardiovascular support (Epinephrine 0.11 mcg/kg/min, Norepinephrine 0.11 mcg/kg/min) with a cardiac index (CI) of 1.6 l/min/m
2. The patient required intubation and mechanical ventilation due to pulmonary oedema. Milrinone was commenced to further escalate inotropic support, but her lactate continued to rise (7.3 mmol/l). A bedside echocardiogram was performed demonstrating an impaired LV (EF 35-40%), apical akinesia with hyperdynamic basal segments, thickened septum and a narrowed LVOT with turbulent flow due to systolic anterior motion (SAM) of the anterior mitral valve leaflet. Following recognition of LVOTO, fluid resuscitation was commenced and in the next 12 hours inotropic support was weaned. This resulted in consistent improvement in CI (3.1 l/min/mm2). In the next 24 hours, the endotracheal tube was removed, and the patient was discharged from critical care.
Discussion
The mainstay of treatment for shock following large territory ischaemia is inotropic support with identification of other mechanical and non mechanical factors. LVOT obstruction is bespoke from other commonly encountered complications, in that escalating doses of inotropes and decreased intravascular filling have profound detrimental effects (2). A dynamic LVOT obstruction after an MI can result from a compensatory hyperdynamic segment of normal myocardium after infarction and stunning of a distal segment (3). Additional factors that coexist following cardiopulmonary resuscitation, arterial puncture, and concurrent illness such as hypovolaemia, vasodilation, and excess catecholamine administration worsen the haemodynamic compromise (4). Physiologically, judicious intravenous fluid administration in this case improved the preload, increased the LVEDV, decreased the LVOT obstruction, decreased the afterload, and improved cardiac output. Interrogation of the LVOT using 2D echo will often identify pathological features, including turbulent blood flow on colour doppler, asymmetrical septal hypertrophy, systolic anterior motion of the mitral valve, and compensatory distal hypercontractility (5). Despite reliable diagnosis being dependent on skill level of intensive care clinicians in 2D echo, LVOT velocity measurements have a low intra and interobserver variability (3-4%) (6). This case highlights the role of focused echo in identification of LVOTO in patients in shock following acute MI.