"Lose Yourself" in Cardiogenic Shock

The physician's palms are sweaty, while his patient endorses that his knees are weak and that his arms are heavy. Upon palpation the physician notices that the extremities are swelling and that there is pitting edema already. The doctor is nervous, but on the surface, he looks calm and ready. Because he read this blog post on cardiogenic shock that references Tintinalli's.

Now that I am done paying homage to Eminem, let’s talk about cardiogenic shock and how to prevent you from losing yourself the next time you come across this diagnosis in your emergency department.

The most common precipitant of cardiogenic shock is myocardial infarction, which significantly reduces the heart's contractility and, subsequently, the ejection fraction (EF). However, there are many ways a patient may find themselves in cardiogenic shock and it's best discussed by grouping the causes into the following three categories:

1) Mechanical complications (e.g. free wall rupture, aortic dissection)

2) Severely depressed EF (e.g. sepsis, medication toxicity)

3) Hinderance to forward flow (e.g. pericardial tamponade, aortic stenosis, atrial fibrillation with a rapid ventricular rate).

Ultimately, "pump failure" results in hypo-perfusion to vital organs, including the heart (via the coronaries), resulting in decompensation. The definitive management relies on figuring out the primary cause of the patients current presentation.

Depending on the etiology, the history may vary; however, patients usually complain of generalized weakness, chest pain, and shortness of breath. A thorough history and physical is necessary to uncover the underlying etiology.

Patients are less likely to be deemed to be in any form of shock by providers unless the systolic blood pressure is less than 90 mmHg, but keep in mind that this may not be the case if a patient has pre-existing hypertension. If possible, compare to previously documented vitals from a prior visit. A patient with a blood pressure that is typically 160/90 may be considered to be relatively hypotensive even with a BP of 120/80. Vitals will also usually show tachycardia (unless the shock is secondary to medication toxicity), tachypnea, and a low oxygen saturation due to pulmonary edema.

After ensuring the patient is on the monitor with intravenous access established, perform the physical exam. You may find the following: cool skin and/or mottled extremities (which represents hypoperfusion), pulmonary edema, jugular venous distension, and peripheral swelling (if the left ventricle is compromised). Keep in mind, acute myocardial infarction may result in mechanical complications, so one should also listen carefully for murmurs which may represent acute mitral or aortic regurgitation or an acute ventral septal defect.

Although laboratory markers are not specific for the diagnosis, one should order the following: complete blood count, basic metabolic profile, troponin, serum B-type natriuretic peptide, liver function test, venous blood gas. The history and physical exam will guide the physician in ordering additional blood tests, like blood cultures if the patient is febrile, or pre-op labs if you suspect the patient will be going to cath lab or another emergent procedure.

Immediately obtain an electrocardiogram to assess for ischemia, electrolyte abnormalities, or medication toxicity (e.g. digoxin, tricyclic antidepressants). A chest x-ray is useful to assess for pulmonary edema, although if acute, the results may lag. Most importantly, utilize a point of care ultrasound to assess the EF, visualize significant wall motion abnormalities, valvular defects, pulmonary edema by visualizing B-lines, and measuring the inferior vena cava.

And now for what we all signed up to do, treat and stabilize!

Provide supplemental oxygen and maintain an oxygen saturation greater than 91%. If additional support is necessary, you may need to place the patient on bilevel positive airway pressure or perform endotracheal intubation; this may decrease the preload and cardiac output due to the increase in intrathoracic pressure, which will worsen the hypotension. Consider giving a fluid bolus or utilize push dose pressors to combat this adverse effect.

Yes, you read that correctly! Contrary to popular belief, you can give fluids to a patient in cardiogenic shock. If the patient is hypotensive and pulmonary congestion is absent (auscultation reveals clear lungs, POCUS shows minimal B-lines), give 250 - 500 mL, and reassess after completion. If no improvement or patient worsens (e.g. develops congestion, worsening dyspnea), initiate pressor support for hypotension or inotropes if congestion without profound hypotension.

The vasopressor you choose will depend on your blood pressure. If systolic blood pressure is less than 90 mmHg, use dobutamine with a vasoconstrictor (norepinephrine or dopamine). If the systolic blood pressure is less than 70 mmHg, use norepinephrine alone, as dobutamine has vasodilatory potential. Epinephrine is associated with higher rates of tachycardia, dysrhythmias and acidosis.

Now that you have stabilized the patient, disposition them accordingly by either sending them to the catherization laboratory, the operating room, or to the cardiac critical care unit.

And that just about wraps up cardiogenic shock. Thank you for reading my blog post!

Manthey, David E, and Bret A Nicks. “Cardiogenic Shock.” Tintinalli's Emergency Medicine , 9th ed., McGraw Hill, 2019, pp. 352–357.

Reyentovich, Alex. “Clinical Manifestations and Diagnosis of Cardiogenic Shock in Acute Myocardial Infarction.” UpToDate, 6 Jan. 2020, www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-cardiogenic-shock-in-acute-myocardial-infarction?search=cardiogenic+shock&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2.