The clinical presentation of this case is consistent with a ST-segment elevation myocardial infarction (STEMI) complicated by cardiogenic shock (CS). Cardiogenic shock is defined as end-organ hypoperfusion due to cardiac failure. Hemodynamically, this manifests as persistent hypotension (systolic blood pressure < 90 mm Hg), severe reduction in cardiac index (< 1.8 L/min/m²), and adequate or elevated filling pressure (pulmonary capillary wedge pressure [PCWP] > 18 mm Hg). It is clinically diagnosed by the constellation of signs of hypoperfusion (decreased urine output, altered sensorium, and/or lactic acidosis), low cardiac output (CO; tachycardia, cool extremities), and congestion (jugular venous distention, pulmonary edema, and/or peripheral edema).¹

The initial approach to the patient in cardiogenic shock should include fluid resuscitation unless pulmonary edema is present. Oxygenation and airway protection are critical; intubation and mechanical ventilation are often required, as was evident in this case. A 12-lead ECG and cardiac enzymes were appropriately and promptly obtained to identify the cause of chest pain and low blood pressure and initiate appropriate therapy for STEMI complicated by CS. The patient should be emergently taken to cardiac catheterization laboratory, and antithrombotic therapy in the form of aspirin and heparin should be administered, with possible withholding of clopidogrel until after angiography as these patients may require emergent coronary artery bypass graft (CABG) surgery based on angiography findings.² An arterial catheter should be placed to continuously monitor the blood pressure. In addition, a central venous catheter should be placed to monitor central venous pressure and administer inotropic (dobutamine or milrinone) and/or vasopressor therapy. A transthoracic ECG should be obtained expeditiously to evaluate for etiologies of ventricular dysfunction and detect possible early mechanical complications of myocardial infarction. Lastly, patient monitoring in a cardiac intensive care unit (CICU) is essential given the high rates of morbidity and mortality associated with CS.¹

The predominant cause of CS is anterior myocardial infarction (MI) complicated by left ventricular (LV) dysfunction; however, it can also occur from mechanical complications (ventricular septal rupture, free wall rupture, and papillary muscle rupture) following an MI and should be strongly considered in patients with CS secondary to a non–anterior wall MI. Other causes of CS include acute myopericarditis, stress-induced (or “tako-tsubo”) cardiomyopathy, pulmonary embolism, large right ventricular infarction or acute valvular dysfunction.² Of particular interest to the neurology setting are acute neurologic events such as cerebrovascular accidents, which can initiate a sympathetic storm leading to a catecholamine surge, and subsequently causing “tako-tsubo” cardiomyopathy leading to CS.³ Although the incidence of CS associated with MI has declined with increased rates of revascularization, it still continues to complicate 3% to 8% of acute MI cases. Moreover, in these select cases, the mortality is substantially elevated (40%-60%).^2,4

Pathophysically, a cascade of events is initiated in response to myocardial injury or ischemia (Figure 38-2). In addition to myocardial dysfunction, a systemic inflammatory response syndrome (SIRS) is often seen in response to an MI due to the release of interleukin-6, TNF-α, and other cytokines. Furthermore, excess nitric oxide synthesis induced by MI causes vasodilation, contributing to low blood pressure. These inflammatory mediators have a negative inotropic effect, causing further cardiac depression. The combination of decreased contractility and a resultant surge in catecholamine leads to reflex vasoconstriction, hence increasing systemic vascular resistance (SVR).² In an effort to maintain perfusion, the renin-angiotensin system is activated as well, promoting salt and water retention, and as a consequence, increases the propensity for pulmonary edema to develop. This increases stress on the heart, increasing oxygen demand, and worsening ischemia perpetuates the vicious cycle and ultimately causes multiorgan dysfunction syndrome (MODS) due to systemic hypoperfusion and microcirculatory dysfunction. Timely revascularization leads to relief of ischemia and interruption of this sequence of events. However, if revascularization is delayed and MODS develop, it is difficult to improve prognosis even if the hemodynamics have improved.²

When CS is due to MI, time to reperfusion is a critical factor in limiting the extent of myocardial injury and maximizing potential recovery of LV dysfunction, and hence survival. It is often said “time is muscle,” because the longer the blockage persists, the more myocardial tissue is in jeopardy and is irreversibly damaged.⁵ Restoration of coronary flow of an infarct-related artery can abort the infarction and potentiate myocardial salvage; however, the greatest benefits are observed within the first 2 hours from symptom onset. This benefit is seen regardless of the modality of reperfusion (fibrinolysis or percutaneous coronary intervention [PCI]) used; however, PCI has a greater mortality benefit and is therefore strongly recommended as the initial management strategy.^5,6 Whenever possible, the goal of achieving a “door-to-balloon” time of 90 minutes or “door-to-needle” of 30 minutes (if delay of more than 120 minutes to a PCI-capable facility) from first medical contact should be attained.⁴

The landmark SHOCK trial by Hochman et al studied the impact of early revascularization (percutaneous coronary intervention or bypass surgery) vs optimal medical therapy (IABP and thrombolytic therapy) in 302 patients who had CS due to LV dysfunction after acute infarction on all-cause mortality at 30 days.⁷ In this randomized control trial, overall mortality at 30 days was not significantly reduced by early revascularization or medical therapy (P = 0.11) highlighting the poor prognosis of CS. However, a significant survival benefit (absolute risk reduction of 13%) was seen at 6 months of follow-up,⁷ as well as at 3- and 6-year follow-up in patients with early revascularization.^{8, 9} Thus, early revascularization in suitable CS patients is recommended, irrespective of time delay.

The diagnosis and management of CS is traditionally aided by the use of a PAC (Figure 38-4). First developed in 1969 by Dr. H. J. C. Swan, the PAC, also known as a Swan-Ganz, has evolved over time into a useful tool to measure hemodynamics as well as to guide therapy.¹⁰ Typical hemodynamic parameters consistent with cardiogenic shock are low cardiac output (CI < 2.2 L/min/m²), elevated pulmonary capillary wedge pressure (> 18 mm Hg), hypotension, and elevated SVR (> 1200 dyne/s/cm^-5). Cardiac output (L/min) can be calculated by the Fick equation (Figure 38-5) or with the PAC by thermodilution. The Fick equation and thermodilution operate on a basic assumption that flow across the pulmonary circulation is equal to the cardiac output from the left ventricle, which holds true in the absence of an intracardiac shunt or severe valvular regurgitation.¹⁰

The Fick equation states that cardiac output is equal to the amount of oxygen consumed divided by the difference between the oxygen content of the arterial system and that of the pulmonary venous system. The oxygen consumption at rest is assumed to be 250 mL/min based on physiologic experiments. Oxygen content in blood is determined primarily by hemoglobin, as it is the principal source by which oxygen is delivered; each gram of hemoglobin can carry 1.36 mL of O². Under physiologic circumstances, arterial oxygen saturation is near 100%, and mixed venous oxygen saturation (drawn from the PA port) is approximately 75%. Taking this into account, and using the Fick equation, this patient’s cardiac output is calculated to be 2.57 L/min, with a cardiac index (adjusted for body surface area) of 1.29 L/min/m², which is low.¹⁰

Thermodilution measures cardiac output by detecting the temperature change (measured by a thermistor at the tip of the catheter) of a known quantity of a cold injectate (10 mL of normal saline at room temperature) delivered into the right atrium (RA) as it circulates through the pulmonary artery. The change in temperature vs time is graphed, and the cardiac output is inversely related to the area under a thermodilution curve, with a smaller area under the curve indicating higher cardiac output (Figure 38-6). Errors in interpretation of cardiac output derived from thermodilution may arise in the setting of severe tricuspid regurgitation or pulmonic regurgitation as these allow the injectate to recirculate, thereby exaggerating the low-output curve. Similarly, in the setting of intracardiac shunts, the opposite is observed where a falsely high CO might be obtained.¹⁰

Although the PA catheter is considered by many to be the gold standard in continuous hemodynamic monitoring, it came under much scrutiny with its increasing use across critical care units in the 1990s. An observational trial by Connors et al of PA catheter use in critically ill patients found an association of its use with an increased utilization of resources, mortality, and lack of benefit; however, excess risk was not seen in patients with heart failure.¹¹ A randomized controlled study, the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial,¹² sought to investigate whether PA catheter use is safe and improves clinical outcomes in patients hospitalized with severe symptomatic heart failure. The patients were randomized to therapy guided by clinical assessment only or PA catheter plus clinical assessment. The primary endpoint was the number of days alive out of the hospital during the first 6 months. The study was terminated early because of the lack of a significant difference in the primary endpoint and an early risk of adverse events in the PA catheter group.¹² Of note, this trial only comprised stable patients where urgent management requiring a PA catheter would be unnecessary, and furthermore, the use of inotropic agents was discouraged; thus, a selection bias was present where patients with severe CS were likely excluded. In a retrospective analysis of two large multicenter, international randomized controlled clinical trials (GUSTO IIb and GUSTO III) of ACS patients, the use of a PA catheter was also associated with an increase in mortality, except in patients with CS.¹³ The lack of an increased risk of mortality with PA catheter use in patients with CS was further corroborated in a study using data from the Global Registry of Acute Coronary Events (GRACE).¹⁴ Although no randomized controlled trial has established a benefit with the PA catheter, it is still recommended in the appropriate clinical setting. It is a valuable diagnostic tool in identifying CS, as well as for tailoring therapy, when used by a clinician who can utilize the data effectively to make informed decisions.¹⁵ The fact is that the PAC, which is essentially a diagnostic tool, has been judged by clinical outcomes—standards that are meant to determine the efficacy of therapeutics. Indeed, few other diagnostic tools have been subject to such rigorous and perhaps misdirected scrutiny.¹⁰