Physical exam of the patient should include assessment of volume status, pulmonary auscultation, abdominal exam, inspection of the wound, and extremity exam. There is no substitute for bedside ultrasound in rapid assessment of this patient's shock. This should include ultrasound views of the heart (pump function/contractility, pericardial effusion, right ventricle dilation or strain), inferior vena cava (volume status), lungs (sliding signs to rule out pneumothorax and presence or absence of A or B lines), abdomen (free fluid, cholecystitis, abdominal aortic aneurysm), soft tissue exam of the wound, and limited compression ultrasound of lower extremity veins, which increase the probability of pulmonary embolism. This rapid ultrasound exam of the patient takes approximately two minutes, and allows diagnosis of the type of shock and possible source.
A chest radiograph (Figure 2) was concerning for pulmonary edema and showed no evidence of focal pneumonia. This was confirmed by bedside thoracic ultrasound, which demonstrated numerous B lines. (Figure 3.) Given her increased work of breathing, she was placed on noninvasive positive pressure ventilation. Initial cardiac troponin I was 2.1 ng/mL. Bedside cardiac ultrasound showed poor contractility. There was regional wall motion abnormality in the inferior myocardium and lateral regions. The IVC was dilated and the right ventricle was not enlarged. The ultrasound of the abdomen, surgical wound, and lower extremity veins were unremarkable.
With no evidence of lower extremity DVT or right ventricular strain, pulmonary embolism is less likely in this patient. A D-dimer would be elevated post-operatively, and would not be useful to further risk-stratify this patient. She has a Wells' score of 3 (for tachycardia and recent surgery), giving her an intermediate risk. It is far from the most likely diagnosis, though. Given the pulmonary congestion and poor systolic function, along with clinical features such as cool extremities, this is consistent with cardiogenic shock. The ECG with diffuse ST depression leads us to identify this as a high-risk NSTEMI with pump failure.
Risk scoring for NSTEMI patients can be done. One score is Fillip, which classifies the degree of heart failure. It has a direct correlation with in-hospital mortality. Our patient would be Fillip class IV. The Grace and TIMI scores can provide estimates of mortality for patients with NSTEMI.
She was loaded with heparin and given aspirin. Nitroglycerin was contraindicated given her cardiogenic shock. Given her ongoing chest pain and hemodynamic stability, she was taken immediately for coronary angiography. Dual-antiplatelet therapy is important (with clopidogrel, ticagrelor, or prasugrel), but this can be deferred in the ED for patients proceeding immediately to angiography and given by the cardiac interventionist after the coronary anatomy has been defined.
The coronary angiogram revealed severe three-vessel coronary artery disease and a proximal left anterior descending artery stenosis culprit lesion that was stented. (Figure 4.) A mid-left circumflex chronic total occlusion was also identified but not treated.
The cardiogenic shock persisted despite reperfusion. LVEDP was 24. She was placed on an intra-aortic balloon pump, which improved her cardiac index to 1.5. Aortic balloon pumps inflate during diastole and increase the coronary perfusion. When the balloon deflates during systole, a reduction in the afterload is seen, which increases cardiac output.
After the procedure, she reported that she had been having some exertional chest pain for two weeks but had believed it was her asthma, which she had not reported to her physician or surgeon. This may have represented episodes of stable or unstable angina pointing toward the severity of her coronary artery disease. Repeat ECG (not shown) showed improved but still persistent anterolateral ST depression. Over the first 12 hours, when IABP augmentation was weaned from 1:1 to 1:3, she experienced chest pain and wedge pressure increased. This indicated that her cardiac function had not yet recovered. But by the second day, this had improved, and she was able to be weaned from the balloon pump. Peak cardiac troponin I was 105 ng/mL.
Remember that the risk period for preoperative myocardial infarction is up to 30 days and is highest within the first week. This is because the vulnerable plaque is not only subject to the catecholamine stress response during and immediately after surgery, but also the circulating inflammatory mediators that are generated during the healing process. This inflation can weaken the cap, leading to a rupture or erosion and thrombus formation.
And dual antiplatelet therapy (DAPT) is critical in treatment of STEMI and high-risk NSTEMI, but it is not always required to begin in the emergency department. Upstream DAPT can be deferred until after the coronary anatomy has been defined (coronary angiography) if the patient is going immediately to the cardiac catheterization lab. If it is determined that the patient has multi-vessel disease requiring coronary bypass surgery, then DAPT causes a higher risk of bleeding morbidity. This outweighs the reperfusion benefits of DAPT if there is no delay between the ED and angiography.
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