Contemporary Management of Concomitant Cardiac Arrest and Cardiogenic Shock Complicating Myocardial Infarction

Cardiac arrest is a major risk factor for mortality among patients with CS, and likewise CS is a major risk factor for mortality among patients with CA.^,, In-hospital and long-term outcomes are exponentially complicated with the combination of both CA+CS in patients with AMI. Patients with AMICS-CA have the highest in-hospital mortality, frequently exceeding 40% to 50%, and those who survive to hospital discharge continue to experience an increased mortality after discharge due to the residual risk associated with their underlying heart disease.^, Patients with AMICS-CA have higher rates of cardiac and noncardiac organ failure, organ support therapies, longer in-hospital stay, higher long-term mortality, higher health care resource use, readmissions, and higher post-acute care use compared to AMI with CS or CA alone.^,,, In patients with STEMI and NSTEMI alike, the in-hospital mortality is highest in those with CS+CA (Table 3).^,,,, In patients with AMICS-CA, the neurological injury, need for mechanical ventilation, prolonged duration of immobilization, trauma secondary to resuscitation, end-organ damage, heart failure, and long-term medications lead to a much higher use of post-acute care resources.

Cardiac arrest complicates one of three CS hospitalizations, and the prevalence of CA increases significantly with the increasing stage of CS.^,, Furthermore, CA is associated with an increased mortality at each level of CS severity within the SCAI shock classification and should be considered as a risk modifier at every stage.^,,, Importantly, patients who develop CA as a complication of CS (ie, in-hospital CA) and CA patients who develop CS after ROSC are similarly high-risk groups whose prognosis is determined both by the severity of CS and the circumstances surrounding CA.^, A 12-year study assessing CA complicating CS observed improved outcomes in isolated CS patients but not in those CS admissions complicated by CA over the study period. Although in-hospital survival was lower for CS patients complicated with CA, the 1-year post-discharge survival rate, analyzed for hospital survivors, was similar in both groups, showing the high upfront risk without an increase in subsequent mortality when CA complicates CS. Clinical trials of mechanical circulatory support (MCS) devices in CS have included mostly patients with CA, and the presence of anoxic brain injury in enrolled patients with CA could have attenuated the benefit of MCS and masked a potentially beneficial impact of the MCS; future trials in CS populations should stratify randomization by the presence of CA.^,

Hypotension occurs in up to 66% of patients with CA and can be secondary to transient myocardial stunning, use of sedative medications in comatose patients, as well as CS secondary to myocardial ischemia and myocardial dysfunction. The true incidence and outcomes of CS in patients with CA post-ROSC is heterogenous due to varying definitions and inconsistent cardiac functional assessment in published studies, although most studies have shown worse outcomes in patients with shock after CA.^,,,, Low MAP, elevated blood lactate, and higher requirements of vasopressors after CA is associated with worse short- and long-term outcomes and increased mortality.^, Shock with persistently low cardiac index at 24 hours after ROSC is associated with a higher early mortality from multiorgan dysfunction.

Supportive management of CS includes optimization of fluid status, restoration of adequate hemodynamics and organ perfusion using vasopressors and inotropes, and support of organ failure. A similar approach is taken for patients with CA, and should be taken for patients with CA+CS. One particular challenge in caring for patients with CA+CS is the exacerbation of hemodynamic instability and shock severity caused by PAMD and the systemic inflammatory response syndrome resulting from CA, which can further aggravate organ failure, lower vascular resistance, and worsen shock, necessitating higher vasopressor doses. Capillary leak and other factors developing after CA can lower filling pressures, requiring fluid resuscitation even in patients with CS. Most crucially, shock after CA can evolve from an early cardiogenic phenotype with PAMD and stunning into a mixed or predominantly vasodilatory pathophysiology over the first 8 to 24 hours. Emphasis should be placed on continuous clinical assessment of the patient’s perfusion status, with frequent serial biomarker monitoring to complement clinical judgement. Apart from direct evidence of end-organ dysfunction, the most commonly monitored biomarkers for assessing the severity of perfusion deficits are lactate and mixed venous oxygen saturation. As described above, in patients with AMICS-CA, shock is often due to a combination of vasoplegia and CS. Guidelines recommend pulmonary artery catheter (PAC) monitoring in patients with an uncertain mechanism of shock and patients with CS who do not respond to initial therapy. The use of a PAC provides continuous hemodynamic profiling, facilitating optimization of volume status, differentiation of right-sided, left-sided, and biventricular dysfunction, as well as aids in the selection, titration, and weaning of pharmacological and MCS support to restore CO. A large multicenter registry noted lower in-hospital mortality across all SCAI stages in patients who received comprehensive hemodynamic profiling with a PAC. To continually optimize hemodynamics and titrate therapies effectively, invasive hemodynamic monitoring with a PAC is valuable in our estimation and, despite the use of several minimally invasive devices for monitoring of CO, the PAC remains the gold standard for complete hemodynamic assessment (Figure 2). Although the use of PAC is controversial for many patients, recent studies have highlighted its importance in patients with CS, and this applies to patients with AMICS-CA as well. Based on available published evidence, we prefer an approach which titrates norepinephrine as the first-line vasopressor to target an adequate MAP (typically greater than 65 to 70 mm Hg) and independently titrates dobutamine as the first-line inotrope to target an adequate cardiac index (typically >2.2 L/min per m²) and cardiac power output (ideally >0.6 W) with normal and systemic oxygen delivery (evidenced by mixed venous oxygen saturation ≥60% to 65%) and normalization of lactate and urine output (Figure 2).^,, Although normalization of the cardiac index using inotropes is logical, we believe that it is more important to normalize systemic oxygen delivery and restore perfusion. In post-arrest patients, a higher MAP goal of 80 to 100 mm Hg has been proposed to mitigate secondary brain injury due to impaired cerebral blood flow autoregulation; however, this approach has not been shown to improve neurological outcomes, and the potential adverse effects of higher vasoactive drug doses in patients with CS should be considered. Most patients with CA+CS are intubated and mechanically ventilated, and a lung-protective ventilation strategy targeting a low tidal volume of 6 to 8 mL/kg predictive body weight with moderate positive end expiratory pressure of 5 to 15 cm H₂O and goal plateau pressure of less than 30 cm H₂O is prudent; either high or low levels of oxygen and CO₂ in the blood have been associated with poor outcomes after CA, so maintaining normal levels is ideal. Hyperventilation can be used to correct severe acidosis, but this may cause cerebral vasoconstriction that could exacerbate ABI; untreated acidosis may compromise cardiovascular function, so administering alkali therapy may be necessary.

Targeted temperature management (TTM) has been shown to be associated with improved survival and neurological function in CA patients and remains the standard-of-care for those who are persistently comatose after resuscitation from CA, although the temperature goals during TTM have changed recently.^{,  ,  ,}  The early trials of TTM after CA did not include patients with concomitant CS.^, In the subsequent TTM trials, hypothermia (33 °C in both TTM and TTM-2) was not found to be superior to normothermia (36 °C in TTM and 37.5 °C in TTM-2); these studies excluded patients with severe or refractory CS.^, However, in the TTM trial, temperatures were achieved with a suite of targeted interventions in similar percentage of subjects in both the groups and, in the TTM-2 trial, 46% of the patients in the normothermia groups received cooling with a temperature management device.^, Furthermore approximately 15% of patients in both groups in the TTM-2 trial had recorded temperatures above 37.7 °C. Moderate hypothermia of 31 °C was not superior when compared with a mild hypothermia of 34 °C in the (CAPITAL CHILL) trial.^,, The key crucial message from these trials is the need for close temperature monitoring with pharmacotherapy, device cooling, and a targeted temperature management protocol for comatose patients after ROSC. The goal temperature during TTM can be personalized to the individual patient based on the discretion of the treating physician. There are known adverse hemodynamic effects of lower targeted temperatures during TTM, making a higher target temperature of (36 °C to 37.5 °C) reasonable for patients with concomitant CS, in our opinion.^,

The American Heart Association and the European Resuscitation Council guidelines recommend TTM for patients with in-hospital and OHCA and with any arrest rhythm.^{,,,  ,}  More specific to the AMICS-CA population, the German-Austrian S3 guidelines recommend cooling of body temperature for at least 24 hours for all resuscitated comatose patients with AMI-CS. Targeted temperature management, particularly at lower target temperatures, causes a reduction in CO associated with a reduction in heart rate and an increased vascular resistance, which may lead to increased vasopressor requirements and impaired lactate clearance. Targeted temperature management is not beneficial per se among patients with AMI-CS without CA, but presumably can still be of benefit for patients with CA despite its adverse hemodynamic effects. In patients with AMICS-CA, TTM should be initiated as early as possible, but this can be challenging for patients with AMI-CS as they often require percutaneous coronary intervention (PCI) and MCS device placement. We emphasize the importance of close temperature monitoring in patients with AMICS-CA with a strict goal to prevent fever and suggest a higher goal temperature (36 °C to 37.5 °C) recognizing that the set goal for a targeted temperature management protocol should be personalized to the individual patient.

Given the dynamic and complex nature of patients with AMICS-CA, management should be focused with an emphasis on the overall prognosis, probability of meaningful neurological recovery, and candidacy for revascularization. Patients with persistent shock after ROSC and a Glasgow Coma Scale of greater than or equal to 8 should be immediately triaged to the catheterization laboratory. However, neurologic prognostication for comatose CA patients is notoriously difficult during the very early post-ROSC period when decisions regarding coronary angiography and revascularization must be made (Figure 3).^, Although the presence of a multitude of high-risk clinical features, listed in a recent American College of Cardiology (ACC) consensus statement, can identify patients with CA who are unlikely to survive, declaring futility in such cases is extremely controversial. Guidelines recommend short door-to-balloon time and early PCI in cases of STEMI and high-risk NSTEMI; patients with AMICS-CA clearly qualify. There appears to be a higher survival benefit from early reperfusion in the cohort of AMICS-CA compared with hemodynamically stable patients. This emphasizes the need for immediate PCI in patients with AMICS-CA. Use of invasive hemodynamic monitoring with a PAC, MCS, and TTM should be performed with the goal to achieve revascularization at the earliest and safest manner possible (Figure 3). Although this approach remains controversial, there are proponents of performing hemodynamic stabilization, potentially including PAC and temporary MCS placement, before coronary angiography in patients with AMICS. However, caution must be taken when diagnosing STEMI based on an electrocardiogram performed immediately after ROSC due to the potential for metabolic disturbances resulting from CA to create transient ST-segment changes.