Diagnosing Cardiogenic Shock in the ED

Authors: Madison Daly, MD (EM Resident Physician, University of Vermont Medical Center Emergency Medicine Residency Program) and Skyler Lentz, MD (@skylerlentz, Assistant Professor of Surgery (EM) and Medicine (Critical Care), University of Vermont Medical Center) // Reviewed by: Tim Montrief, MD (@EMinMiami); Alex Koyfman, MD (@EMHighAK); and Brit Long, MD (@long_brit)

Case: A 73-year-old male with a history of hypertension, coronary artery disease, and previous myocardial infarction (MI) presents to the emergency department (ED) with fatigue, shortness of breath, decreased urine output, and ankle swelling. Upon arrival, his vital signs include BP 87/58 mm Hg, HR 102, RR 24, T saturation 86% on room air, and temperature 98.2 F, and he has crackles on auscultation. How would you manage this patient?

What is cardiogenic shock?

Although definitions vary, cardiogenic shock (CS) is a clinical diagnosis broadly defined as a state of low cardiac output with associated inadequate end-organ perfusion, or tissue hypoperfusion secondary to cardiac damage. ¹ Commonly used criteria derived from the SHOCK trial consists of hypotension (SBP <90mmHg or >90mmHg with supportive care), evidence of end-organ hypoperfusion, and cardiac index (CI) <2.2 L/min/m² or pulmonary capillary wedge pressure ≥ 15 mmHg ^2,3 Although this definition is useful to standardize inclusion criteria for clinical trials, it is less valuable for diagnosing CS in the emergency department (ED). On shift in a busy ED, CS can be challenging to diagnose because of the diverse presentations, overlap with other shock states (i.e. sepsis), poorly understood pathophysiology, complex and multifactorial causes and varied hemodynamic parameters.⁴ In the absence of invasive cardiac output (CO) and PCWP values, CS can be inferred using evidence of elevated filling pressures (i.e. pulmonary congestion or elevated JVP), clinical signs of hypoperfusion and a history and echo suggestive of cardiac failure. Mortality secondary to CS is high (~25-70%), but early recognition and intervention improves survival.^4,5 Emergency physicians have the opportunity to diagnose CS on admission and must maintain a high clinical suspicion when seeing any critically ill patient. This review will focus on recognition and tips on how to not miss the diagnosis of CS through physical exam, labs, bedside ultrasound and imaging.

What are the causes of cardiogenic shock?

Most studies of CS focus on patients with CS secondary to myocardial infarctions (MIs) involving the left ventricle. Although MIs are the primary cause of CS (~70%), any cause of ventricular dysfunction and reduced CO or cardiac index (CO/body surface area) as a potential cause must be considered.⁶ This includes, but is not limited to, nonischemic causes of right heart failure, myocarditis, takotsubo cardiomyopathy, hypertrophic cardiomyopathy, or valvular heart disease (Table 1). To make things more challenging, CS is a continuum rather than a static state, ranging from worsening heart failure to refractory shock with irreversible end organ damage (Figure 1). CS becomes even more variable with the occurrence of secondary insults such as arrhythmias or progressive ischemia and acidosis.³ It should be noted that in 2/3 of cases, CS is not present on admission but later develops within 48 hours of hospitalization as the patient progresses down the continuum of shock.⁷ It is important to frequently reevaluate patients’ vital signs, symptoms, physical exam, and bedside echo.

Table 1: Causes of CS, adapted from Parrillo & Dellinger (2013).⁸ 70% of CS cases are caused by acute MIs.⁶ Effects of acute MI with associated percentages taken from the results of the SHOCK trial registry.^9.10 

Figure 1: Continuum of CS, adapted from Bellumkonda et al. (2018).³ This spectrum may deviate with secondary insults (ex. new arrhythmias).

Mortality in cardiogenic shock

Although mortality secondary to CS remains high,⁴ early recognition and intervention improves survival.⁵ Using data which included the SHOCK trial registry, 30-day in-hospital mortality of 1,217 patients that were diagnosed with CS secondary to left ventricle (LV) or right ventricle (RV) failure due to an acute MI was 57%. If you take several risk factors into account, specifically shock on admission, age, previous coronary artery bypass grafting (CABG), noninferior MI, creatinine >1.9 mg/dL, decreased SBP, anoxic brain injury, and clinical evidence of end-organ hypoperfusion, patients could be subdivided with mortality ranging from 12% to 88%.¹¹ In the GRACE trial, CS weakly but significantly decreased between 1999 and 2006, likely due to the increased use of percutaneous coronary intervention (PCI), an important form of early intervention for patients with MI complicated by CS.¹² Even when stratifying patients based on risk factors, PCI and CABG benefited both low and high risk patients.¹¹ Early diagnosis and appropriate treatment remains, particularly in the case of myocardial ischemia, an important modifiable contributor to outcomes for patients with CS.

Additionally, the longer CS progresses, the more likely there will be a maladaptive inflammatory response secondary to an increase in cytokines like TNF-alpha and IL-6, which inhibit cardiac activity. ^4,13 There is also an increase of vasopressin and angiotensin II, which increases afterload, worsens CO, and increases water and salt retention, thereby causing pulmonary edema. Nitric oxide (NO) is also increased through the activation of NO synthase, leading to vasodilation and myocardial depression. All these maladaptive responses to low CO and myocardial ischemia lead to worsening cardiac tissue damage, depressed CO, and distributive shock. It should be noted that some cases of CS are iatrogenic, when patients on the verge of heart failure are treated with aggressive diuretics, nitrates, beta blockers, ACEI, and morphine. ¹⁴ Therefore, as the first physician to evaluate patients, emergency physicians need to identify and treat CS in a time-sensitive and clinically appropriate way.

Clinical Evaluation

Classically, patients with CS present with complaints of dyspnea, chest pain, fatigue, and/or ankle swelling.¹⁵ Physical exam may reveal signs of congestion including peripheral edema, jugular venous distension (JVD), crackles/rales on auscultation, and signs of hypoperfusion such as cool, poorly perfused extremities (Table 2). In a small retrospective review of 30 patients in undifferentiated shock, those with CS were more likely to have JVD (80% compared to 0% and 20%), cold skin (57.1% compared to 14.3% and. 28.5%), and pulmonary rales (75% vs 16.7% and 8.3%) compared to patients with distributive and hypovolemic shock, respectively.¹⁶ In another prospective study with 68 patients, residents used specific clinical exam findings to differentiate categories of shock. CS was categorized by SBP less than 90, signs of low output (cold hands, poor capillary refill, and weak pulse), elevated jugular venous pressure (JVP)> 7 cmH₂O, S3 gallop, and crackles to 1/3 of the lungs. Of 68 patients, 11 met criteria for CS. In patients with echocardiographic evidence of low cardiac output, elevated JVP predicted CS with an accuracy of 80%, which was unchanged when adding the presence of crackles.¹⁷

Table 2: Physical exam components seen in acute heart failure and subsequent cardiogenic shock.¹⁸

Although JVP is a useful proxy for elevated wedge pressures,¹⁹ it may be difficult to assess due to body habitus and positioning of the patient (head of the bed should be elevated 45 degrees which can be difficult in patients with severe orthopnea).²⁰ JVP is measured by calculating the highest pulsation point in cm above the sternal angle and then add 5 (as the right atrium is 5 cm below the sternal angle), which correlates to distension in cmH₂0 (Figure 2). Elevated values are often considered greater than 6-8 cmH₂0.¹⁸ Of note, elevated JVP is associated with increased risk of mortality, with a relative risk (RR) of 1.52.¹⁸

Figure 2: Measuring JVP, adapted from Shah & Cowger (2014).¹⁸

Labs may show a metabolic acidosis (as lactate increases due to peripheral ischemia), renal hypoperfusion with resulting acute kidney injury, and possible evidence of cardiac ischemia with elevated troponin and EKG changes.¹⁵ In the CardShock study, a multicenter, prospective, observational study of 219 CS patients, lactate levels were significantly associated with increased mortality (adjusted odds ratio of 1.4).⁶ It is important to note that lactate elevation is not specific to sepsis and can be seen in any hypoperfused state such as CS.

On the other hand, these physical exam findings and hemodynamic parameters do not always hold true. In a study using the SHOCK Trial registry, 5.2% of CS patients did not have overt hypotension although did have signs of peripheral hypoperfusion and low CI.²¹ This is likely due to an adaptive catecholamine release in early CS, which increases systemic vascular resistance (SVR) and transiently maintains blood pressure, though generally with a narrow pulse pressure.²² Even patients with clinically significant pulmonary edema on imaging can present with wheezing or even clear lung sounds rather than rales.²³ In one study, pulmonary congestion was only seen in approximately 2/3 cases of CS secondary to MI.²¹ Furthermore, even with decreased LV contractility, CS patients may not have a severe reduction in LVEF. ^14,24 In fact, the mean EF in a cohort of CS patients is about 30%, which is reduced but higher than expected.²

Though the exam is not perfect, a detailed physical exam looking for signs of congestion and peripheral hypoperfusion along with a careful review of vital signs and labs may be the first hint your patient has cardiogenic shock.

Point-of-care ECHO for evaluating cardiogenic shock

When patients present to the ED hypotensive or hypoperfused, the RUSH exam is a quick way to differentiate shock by looking at the “the pump, the tank, and the pipes.”^25,26 For CS, transthoracic echocardiogram classically demonstrates a hypodynamic, dilated LV, with poor LV squeeze and associated inadequate motion of the anterior leaflet of the mitral valve during systole and diastole (i.e. poor contractility). Estimation of ejection fraction (EF) and CO (as CO=stroke volume (SV) x heart rate (HR)) through simply “eyeballing” LV squeeze is an adequate assessment by physicians in the acute setting.²⁷ In CS, the inferior vena cava (IVC), which is an indirect measurement of effective intravascular volume, should have a diameter of >2 cm diameter and collapses less than 50% with inspiration. These findings correlate with an elevated central venous pressure.²⁸ However, the IVC assessment may be inaccurate if the patient has already received vasodilators, diuretics, and/or is ventilated.²⁹ Thoracic windows are likely to show pulmonary edema in the form of excessive B lines (“lung rockets”) which are the result of septal thickening from water accumulation in the interstitium.³⁰ Along with pulmonary congestion, there may be pleural and peritoneal fluid on RUSH exam.²⁵ In a meta-analysis that used data from three original papers and two case reports, the RUSH protocol was shown to be both sensitive and specific (0.89 and 0.97, respectively) in the diagnosis of CS.³¹ Despite a high resulting positive likelihood ratio (LR) of 22.29, there was only a moderate negative LR of 0.17, suggesting the RUSH exam is not the perfect test to rule out CS. Therefore, the RUSH exam should be used in the context of a careful history and physical exam rather than used alone to diagnose cardiogenic shock.

Figure 3: RUSH bedside US exam for the evaluation of undifferentiated hypotension with associated findings suggestive of CS.^25,26,29,30

Rather than just estimating CO through “eyeballing,” one way to measure CO with ultrasound is to first determine SV using left ventricular outflow tract velocity time interval (LVOT VTI, or the velocities of blood flow at the aortic outflow tract) and LVOT diameter. Specifically, SV, or the amount of blood ejected through the left ventricle per beat, is calculated by LVOT VTI × cross sectional area of the LVOT [VTI (cm) x D² x0.785 (cm²)].³² To measure LVOT diameter, place the phased array probe in the parasternal long axis view and measure the distance of the LVOT just above the aortic valve while in mid-systole. VTI is measured in the apical-5-chamber view. Using the pulsed-wave doppler mode, the doppler wave is placed just above the aortic valve and doppler waveforms are recorded. Be sure to line up the axis with the outflow tract as best as possible to avoid over/under estimations. After selecting “LVOT VTI” measurement tool, measure the waveform of one ejection period.^33,34 Normal LVOT VTI ranges from 18-22 cm, although possibly lower with HRs >95 bpm.³⁵ In patients with atrial fibrillation, VTI measurements will likely be an underestimate of true value, and therefore averaging 3-5 consecutive waveforms is suggested. As one would expect, there is a correlation between low LVOT VTI and adverse outcomes.³²

Figure 4: A) Parasternal long axis view with LVOT diameter of 2.13 cm. B). Apical-5-chamber view using PW doppler to measure VTI of 20 cm. Using the equations SV=VTIxD²x0.785 and CO=SVxHR, with a HR of 85, SV=71 ml and CO= 5 L/min. Using the equation CI = CO/BSA, CI = 3.1 L/min/m² (not indicative of CS).

Recommended evaluation pathway

As discussed above, there is not a single exam finding or lab test that can diagnose CS. Therefore, when there is a high suspicion of CS in the setting of hypotension or signs of hypoperfusion, we suggest using history, a detailed physical exam, bedside US, labs (specifically creatinine, lactate, troponin, BNP and other markers of hypoperfusion/end-organ-damage), and EKG (as acute MI is the primary cause of CS and signs of ischemia and may require emergent revascularization) to aid in diagnosis (See Figure 5). Consider an arterial catheter monitor to BP and guide treatment. Beyond a focused cardiac and pulmonary examination, physical exam should focus on JVD and extremity perfusion. The RUSH exam and calculation of EF/CO/CI through LVOT VTI measurements discussed above are valuable adjuncts to the evaluation. Using a comprehensive approach to evaluate for CS will create a better understanding of this heterogeneous disease and help guide management.

Case Conclusion: On further evaluation, the patient’s jugular venous pressure is elevated to 10 cmH₂0, and his feet are cool with delayed capillary refill. Bedside RUSH exam shows bilateral diffuse pulmonary edema and an estimated low EF. LVOT VTI is measured at only 10 cm. EKG shows ST elevations in the precordial leads. Lactate and troponin are mildly elevated. The patient is stabilized with a short trial of dobutamine, IV furosemide, and CPAP with moderate improvement in vitals and respiratory status, and subsequently sent to the cath lab for emergent PCI.

Take home points:

• CS is primarily caused by an acute MI (~70%) and is the focus of most studies but other causes should also be considered (see full list in Figure 1).
• Mortality secondary to CS remains high (~60%), although early identification and intervention improves survival.
• Perform a careful physical exam looking for hypoperfusion and congestion. JVP is an important physical exam component for the diagnosis of CS and is associated with increased mortality (RR = 1.52).
• The RUSH exam is both sensitive and specific (0.89 and 0.97, respectively) in the diagnosis of CS. Bedside ultrasound should be repeated frequently as most patients do not initially present in CS.
• Using LVOT VTI is a simple and noninvasive method for evaluating CO with low measurements associated with adverse outcomes.
• A suggested approach for evaluating patients with suspected CS with focus on its heterogeneous pathology and presentation is summarized in Figure 5.

FOAMed Resources:

• EM in 5: Shock
• emDocs: Cardiogenic Shock
• emDocs: ED Management of Heart Failure- Pearls and Pitfalls
• emDocs: RUSH (“Rapid Ultrasound for Shock”) Protocol
• emDocs: The Hypotensive ED Patient: A Sequential Systematic Approach
• First 10 EM: Undifferentiated Hypotension

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