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Spontaneous Circulation: Just When Things Appear to be Going Well

Bruen, Charles MD

doi: 10.1097/01.EEM.0000472676.17405.ad
Spontaneous Circulation

Dr. Bruenis a fellow in critical care medicine and emergency cardiology at Hennepin County Medical Center in Minneapolis. He has special interest in stabilization, resuscitation, hemodynamic evaluation, and emergency cardiovascular care. Visit his website, http://resusreview.com, follow him @resusreview, and read his past columns athttp://bit.ly/SponCirc.

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Figure 2

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Figure

It had eventually become a choice of evils. Despite her age — 79 — she prided herself on never needing hospitalization or surgery. Secretly, she knew this wasn't because of the universe's gift of perfect health but because of stupefying panic and fear. She did love her doctor, though, because he had her obstructive lung disease and high cholesterol under control. He had been recommending knee replacement surgery for years to deal with her pain, and she repeatedly demurred.

This changed one day at the grocery store when the pain was so great she couldn't continue to walk the aisles and a stranger had to get her one of those motorized carts so she could finish her shopping. The embarrassment allowed her to muster the courage to undergo the procedure.

The surgery was uncomplicated. Postoperative pain was minimal, and rehab was progressing nicely. She had gone home on the fourth day and was only using half of her prescribed pain medications.

When she woke up the next morning, however, things took a turn for the worse. She felt nauseated and lightheaded. Her husband, a retired internist, found her clammy, diaphoretic, and with cool extremities. He was unable to palpate a pulse. Sure that she was developing an infection, he called EMS to bring her to the hospital. She began to have chest pain and experience difficulty breathing during the ambulance ride. This continued in the emergency department. Her blood pressure was 60/30 mm Hg, and her heart rate was 128.

An ECG was obtained (Figure 1). This was a very concerning tracing. It showed sinus tachycardia with marked left axis deviation. The QRS was wide and the pattern was consistent with left bundle branch block. No leads demonstrated ST-segment elevation, but the widespread ST depression was highly concerning for subendocardial ischemia.

She presented with severe hypotension and the hallmarks. The goal in the emergency department is to quickly sort out the type of shock and begin appropriate treatment. Septic shock and pulmonary embolism or hypovolemia should be high on the differential for a postoperative patient with immobilization. Typical sources in this patient that may have developed into sepsis include pneumonia and abdominal, genitourinary, or skin soft tissue infections. Cold, clammy extremities are usually associated with cardiac etiologies, and primary pump failure is a consideration in a patient with chest pain.

Figure 1

Figure 1

Figure 3

Figure 3

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.

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Table

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.

Figure 4

Figure 4

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