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ST depression, hypertension, pulmonary edema -- what was the inciting factor?

Posted Nov 07 2009 9:46am
This patient, with a history of CVA and hypertension, presented with a two hour onset of pulmonary edema and chest pressure, severely elevated blood pressure, and very tachycardic. His prehospital BP was 280/150, and it was 230/150 in the ED. He had not been taking his antihypertensives He was speaking in 1-2 word sentences and had diffuse rales. Chest xray confirmed pulmonary edema. The initial EKG follows:

This shows horizontal ST depression in V4-V6 diagnostic of ischemia. There is no LVH. The ST depression is not secondary to LVH, but due to ischemia. There is also ST elevation in aVR, which may be a sign of severe acute left main ischemia.

The important diagnostic question is: what initiated this ischemia? There are two primary possibilities. First, the patient has hypertension which worsened, increasing afterload, leading to some pulmonary edema and demand ischemia and worsening in a vicious cycle. Second, he had an acute coronary syndrome which initiated the increase in end diastolic pressure, leading to pulmonary edema, increased catecholamine output, increased BP and HR, with a different kind of vicious cycle.

The first possibility is made significantly less likely by the absence of LVH. Patients with this syndrome of demand ischemia almost always have LVH on the ECG. If this was all initiated by hypertension, then managing the demand by treating the blood pressure and other physiologic variables such as pulmonary edema, hypoxia, etc. would result in resolution of the ischemia, and could be measured by resolving ST depression on the ECG.

Either way, it is necessary to manage the airway, ventilation and oxygenation, treat the hypertension (high dose intravenous nitrates are a fine method), and normalize other important physiologic variables such as anemia and electrolytes.

However, in the second case, aggressive antiplatelet and antithrombotic therapy is essential. If there is no resolution of ischemia with these aggressive medical measures, then urgent cardiac catheterization is indicated and an interventionalist should be consulted immediately.

In this case, the physiologic derangements were well managed and the patient stabilized without endotracheal intubation, the BP came down with 160 mcg/min of IV nitroglycerine, and 1.25 mg of IV enalapril, but there was no followup ECG before admission.

Very soon after admission, the patient's chest pain increased and the following ECG was recorded 2 hours after the first ECG:

This ECG shows new Right Bundle Branch Block and marked ischemic ST elevation in leads V1-V5, I, and aVL, diagnostic of a proximal LAD occlusion. Emergent angiogram confirmed proximal LAD occlusion proximal to two large diagonal vessels, and severe circumflex disease also, but the left main was widely open. The LAD was opened as the patient was prepared for subsequent CABG. The patient survived but does have a severely decreased ejection fraction. The patient had no LVH on echo.

Learning points:

1) Flash pulmonary edema may be from demand ischemia, especially with hypertension, but it may be due to severe acute coronary syndrome.
2) When due to hypertension, there is almost always LVH on the ECG
3) Ischemic ST depression is associated with very high risk.
4) If ischemic ST depression is refractory to management of hemodynamic variables, hemoglobin, oxygenation (i.e., refractory to management of those variables that contribute to demand ischemia), aggressive medical treatment for ACS must be started.
5) If the ischemia is refractory to maximal medical management, angiogram with possible PCI is indicated.
6) Always repeat the ECG to assess management of ST depression.
7) In ACS, thrombus may be partially occlusive and result in ST depression. It may be fully occlusive, without collaterals, resulting in ST elevation. Or it may start as partly occlusive and extend to complete occlusion, as in this case.
8) New Right Bundle Branch block in the presence of STEMI has a very high mortality.

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