At the completion of the lung implantations, an attempt at weaning from CPB resulted in severe pulmonary hypertension and systemic hypotension. Epinephrine, dopamine, nitroglycerine, and inhaled NO were administered. After a further failed attempt at separation, an initial loading dose of milrinone 50 μg/kg was administered and an infusion commenced with no improvement (Table 1, F).
TEE revealed mild hypocontractility of the right ventricle with a hypercontractile left ventricle. Marked systolic anterior motion (SAM) of the anterior mitral valve leaflet was present (Fig. 1) with DLVOTO and severe mitral regurgitation (MR), which persisted throughout systole. Left ventricular hypertrophy (LVH) with wall thickness of 16 mm was present without evidence of asymmetric septal hypertrophy.
Norepinephrine and subsequently phenylephrine were substituted (for milrinone), and packed red cells and pentastarch were administered. SAM improved, MR was reduced to moderate, and it was possible to wean from CPB (Table 1, G). Two and a half hours after separation from CPB vasopressors were discontinued (Table 1, H). Hypotension later recurred and vasopressin 6 U/h was commenced. Repeat TEE at this time confirmed the presence of SAM with a left ventricular outflow tract (LVOT) gradient of 31 mm Hg associated with severe MR.
DLVOTO is a cause of sudden death in hypertrophic cardiomyopathy. It has been described complicating myocardial infarction (1), cardiac tamponade (2), atrial fibrillation (3), mitral valve repair (4), and during dobutamine stress echocardiography (5). Flow acceleration in the LVOT causing a local reduction in pressure from the Venturi effect has been considered to be the cause of SAM, although recent work (6) demonstrates that SAM can develop early in systole when LVOT velocities are relatively low and emphasizes the role of flow drag. Contributing factors to development of SAM probably include reduced end-diastolic left ventricular (LV) dimensions because of hypovolemia or LVH and increased ejection velocities resulting from enhanced contractile state or peripheral vasodilation. Variations in mitral valve anatomy may play a role with anterior displacement of the coaptation line, redundant valvular tissue, and lax chordae possibly contributing (6).
The spectrum of abnormalities ranges from mild chordal SAM without significant outflow gradient to high-grade obstruction resulting in shock. The associated MR may range from minimal and/or transient to severe.
The initial interpretation of events in this patient was that pulmonary arterial hypertension with lung deflation was because of a further increase in resistance in a pathologic pulmonary vasculature and systemic hypotension as a result of acute right ventricular failure. There was no response to measures aimed at supporting right ventricular function and pharmacologically relieving pulmonary hypertension. The same situation persisted at initial attempts at separation from CPB.
Assessment with TEE demonstrated that the pulmonary hypertension was secondary to severe mitral regurgitation and hypotension resulting from DLVOTO. Although the right ventricle appeared mildly hypocontractile, it was not dilated and septal shift was not present. No unusual features of mitral valve anatomy were present.
Maneuvers that may reduce DLVOTO include intravascular volume expansion and heart rate reduction which increase LV end diastolic volume as well as vasoconstriction and reduction of inotropic state to reduce LVOT ejection velocities. The substitution of vasoconstrictor drugs for inotropes and volume expansion greatly reduced the hemodynamic impact of the obstruction. Inhaled NO appeared to produce no measurable benefit. The subsequent addition of β blockers in the intensive care unit was considered beneficial although we did not observe a clear relationship between timing of administration and hemodynamic changes.
TEE was invaluable in resolving the cause of hemodynamic instability and resulted in a major change in management and successful outcome.
1. Armstrong WF, Marcovitz PA. Dynamic left ventricular outflow tract obstruction as a complication of acute myocardial infarction. Am Heart J 1996; 131: 827–30.
2. Deligonul U, Uppstrom E, Penick D. Dynamic left ventricular outflow tract obstruction induced by pericardial tamponade during acute anterior myocardial infarction. Am Heart J 1991; 121: 190–4.
3. Vaughan-Whitley K, Mooss A. Dynamic left ventricular outflow tract obstruction related to atrial fibrillation. Chest 1992; 102: 1618–9.
4. Lee KS, Stewart WJ, Lever HM. Mechanism of outflow tract obstruction causing failed mitral valve repair: anterior displacement of leaflet coaptation. Circulation 1993; 88: 1124–9.
5. Pellikka PA, Oh JK, Bailey KR, et al. Dynamic intraventricular obstruction during dobutamine stress echocardiography: a new observation. Circulation 1992; 86: 1429–32.
© 2002 International Anesthesia Research Society
6. Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G. Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy. J Am Coll Cardiol 2000; 36: 1344–54.