Introduction
Cardiogenic shock (CS) is a state of insufficient cardiac output and end-organ perfusion that can be the terminal phase of many different cardiac conditions, including acute coronary syndromes, arrhythmias, progression of chronic cardiomyopathy, and acute cardiac dysfunction in the setting of idiopathic, traumatic, or inflammatory cardiomyopathies. This shock state is characterized by pathologic systemic vasoconstriction, impairment of tissue microcirculation, release of proinflammatory cytokines, and alterations in nitric oxide synthase activity. Subsequently, even with restoration of normal cardiac output, microcirculatory dysfunction can ensue, leading to loss of peripheral vasomotor tone, coagulopathy, and multisystem organ failure.
According to data from the Nationwide Inpatient Sample (NIS), the number of hospital discharges of patients with a complication of CS has doubled over a decade (from 55,123 in 2004 to 126,555 in 2014). Acute myocardial infarction is the most common precipitant of CS in the United States, and the incidence of CS complicating ST elevation myocardial infarction (STEMI) has increased from 6.5% in 2003 to 10% in 2010. In patients enrolled into the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS), fewer patients undergoing durable left ventricular assist device (LVAD) implantation in 2012–2014 were classified as INTERMACS Profile 1 (“critical CS”; 14%) or 2 (“decompensating on inotropes”; 36%) compared with those undergoing implantation between 2008 and 2011 (16% and 43%, respectively). The decrement in shock phenotype is likely due to changes in patient selection. Nonetheless, CS or progressive decompensation (INTERMACS Profile 1–2 status) is present preoperatively in 50% of patients, and ~ 26% of ventricular assist device (VAD) patients are on some sort of temporary circulatory support prior to durable VAD intervention.
Patients with CS have other high-risk factors for mortality upon presentation. While patients presenting with STEMI are getting younger (mean age has dropped from 70 years in 2004 to 68 years in 2010), they have higher burdens of comorbidities, including diabetes, obesity, peripheral vascular disease, and chronic kidney disease. While both sexes have had an increase in CS frequency over the past decade, the incidence of CS complicating STEMI is overall higher in women (11%) than in men (9.7%). In INTERMACS, patients requiring temporary mechanical circulatory support (TCS) for CS stabilization prior to durable VAD support are older, with greater evidence of malnutrition and renal dysfunction, and they are more likely to have suffered a preoperative cardiac arrest, with greater requirements for preoperative vasopressor and ventilator support than those who are more stable.
Survival in patients with CS, regardless of management strategy, remains universally poor, and complication burdens are high. In patients with a global discharge diagnosis of CS, inpatient mortality ranges from 32% to 58%. Those patients presenting with STEMI as the etiology for CS have demonstrated an improvement in survival with time, but inpatient mortality is still approximately 34%. Durable LVAD patients with preoperative CS have a 1-year survival of 69%–80% compared with 83%–84% in those who are more stable, and 1-year mortality after durable VAD is highest (29%–43%) in those patients who need TCS in the form of extracorporeal membrane oxygenation (ECMO) or percutaneous circulatory support ( Fig. 5.1 ). Patients with preoperative CS also have longer lengths of stay and greater needs for postoperative right ventricular (RV) support, inotropes, and hemodialysis after durable VAD implantation.
The advent of percutaneous TCS technologies and the creation of multidisciplinary teams trained in the management of CS have contributed to small gains in patient outcomes. However, as outlined in this chapter, survival is largely driven by the severity of shock at presentation, the ability to reverse the instigator of CS, the complication burdens encountered during CS resuscitation, and the opportunity for durable VAD support in those with ongoing cardiac failure.
The spectrum of cardiogenic shock
CS is best identified using both hemodynamic criteria and clinical signs/symptoms. While various definitions are used in the literature, evidences of persistent hypotension (systolic blood pressure < 80–90 mm Hg or a mean arterial pressure 30 mm Hg below baseline) with a low cardiac index (< 1.8 L/min/m 2 without support or < 2.0–2.2 L/min/m 2 with support), reduced cardiac power output (< 0.6 W), and elevated filling pressures (left ventricular end-diastolic pressure > 18 mm Hg or right atrial pressure > 10–15 mm Hg), along with cool extremities, lactic acidosis, and/or evidence of end-organ dysfunction, are signs of CS. CS presents on a wide continuum, and patient phenotypes can vary based on underlying cardiac etiology and the presence or absence of preexisting systolic dysfunction ( Fig. 5.2 ). Compared to patients presenting with acute myocardial infarction and previously normal hearts, CS patients with longstanding HF, for example, tend to have worse hypochloremia, lower oxygen delivery and lower oxygen carrying capacity due to chronic anemia, greater peripheral extraction from chronically low cardiac output (lower mixed venous pulmonary artery saturations), greater degrees of anaerobic metabolism, and greater degrees of biventricular volume overload. In a study of 64 patients undergoing ECMO for management of CS, recovery of cardiac function allowing support wean was achieved in 49% of those with acute primary CS compared with 0% of patients with chronic heart failure due to ischemic or nonischemic etiologies.
Many risk factors for mortality in CS have been identified. In patients with acute coronary syndromes, the speed and success of reperfusion and the number of vessels requiring percutaneous intervention are correlated with mortality. Other markers of mortality in CS of any etiology include advanced age, preoperative cardiac arrest, higher Acute Physiology and Chronic Health Evaluation II (APACHE II) score, higher serum lactate and creatinine, altered mentation, need for ventilator support, and the number of inotropes/vasopressors required for support. Because many of these risk factors are also markers of risk for RV failure and/or death after durable VAD, fewer patients with critical CS are undergoing VAD implant in the United States.
The management of CS has evolved greatly over the last two decades. Options for temporary support devices have expanded beyond the intraaortic balloon pump (IABP) and ECMO to include percutaneously placed continuous-flow support devices and surgically placed paracorporeal pumps (discussed in detail later in this chapter). The clinical impact of CS and advanced heart failure has spurred the growth of the Advanced Heart Failure surgical and medical specialties and the development of institutional CS protocols dedicated to rapid patient resuscitation. In an analysis of 287 consecutive CS patients with acute coronary syndromes enrolled into the national cVAD registry, early initiation of Impella (Abiomed Inc., Danvers, MA) TCS before escalation of inotropes was associated with improved survival. In the cohort, overall survival to discharge was 44%. While survivors had similar hemodynamics prior to the initiation of mechanical circulation support (MCS), survivors of CS were more likely to have received TCS prior to percutaneous intervention and had shorter times from the onset of CS to TCS initiation. Patients who received TCS within 1.3 hours of CS presentation had a 66% survival to discharge, compared with 37% and 26% in those who received TCS at 1.3–4.3 and > 4.3 hours after CS presentation, respectively. The frequency of survival was also inversely proportional to the number of inotropes required prior to the initiation of MCS. Results from the latter trial and others led to the development of CS teams across the United States. The Detroit CS Initiative, for example, is a multicenter consortium examining outcomes in patients presenting with acute myocardial infarctions and evidence of CS at four Detroit, MI, medical centers. Using a protocolized management plan, survival to TCS explant improved from 51% prior to initiation of the shock protocol to 85% after. In a similar analysis by the Inova Heart and Vascular Institute, survival improved from 47% prior to the initiation of a formal shock team to 81% within 2 years of shock protocol implementation.
Short-term mechanical circulatory support devices
Temporary circulatory support is increasingly being utilized in the management of CS and is best categorized by the method of device placement (surgical vs. percutaneous). Presently available percutaneous TCS devices include the IABP, ECMO, the Impella system, and the TandemHeart (TH) system (LivaNova, London, England) ( Tables 5.1 and 5.2 , Fig. 5.3 ). The CentriMag (Abbott, St. Paul, MN) and the CardioHelp (Maquet, Rasttat, Germany) are the main devices used for surgical paracorporeal support alone or as a driver during central or peripherally cannulated ECMO. These devices can be used in various configurations, in isolation or in conjunction with other devices, providing right and/or left ventricular support. For patients on ECMO, left ventricular TH, Impella, or IABP may be applied to assist in venting the left ventricle (LV). A comprehensive characterization of available TCS devices is depicted in Table 5.2 , and clinical trial outcomes are summarized in Table 5.1 . Patient support requirements, anatomy and size of available vasculature access, and institutional preference and expertise are all integral to selecting the optimal support for the patient in shock. A detailed discussion of each device is outlined in the following.
| Author | Year | Population | TCS Randomization | Primary Endpoint | Mortality |
|---|---|---|---|---|---|
| Thiele et al. | 2005 | Acute MI/CS | IABP vs. TH | Cardiac power index | 30 day: 45% IABP vs. 43% TH |
| Ohman et al. | 2005 | Acute MI/CS | IABP vs. fibrinolytic medical therapy | 30-day mortality | 6 month: 39% IABP vs. 80% medical |
| Burkhoff et al. | 2006 | Acute MI/CS or ADHF | IABP vs. TH | Improvement in hemodynamics | 30 day: 36% IABP vs. 47% TH |
| Seyfarth et al. | 2008 | Acute MI/CS | IABP vs. Impella 2.5 | Cardiac index | 30 day: 46% in both groups |
| Prodzinksky et al. | 2010 | Acute MI/CS | IABP vs. medical therapy | APACHE II score | N/A |
| Thiele et al. | 2012 | Acute MI/CS | IABP vs. medical therapy | 30-day mortality | 30 day: 40% IABP vs. 41% medical |
| Ouweneel et al. | 2017 | Acute MI/CS | IABP vs. Impella CP | 30-day mortality | 6 month: 50% both groups |
| Left Ventricular Temporary Mechanical Support | Right Ventricular Support | Biventricular Support | |||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| IABP | Impella 2.5 | Impella CP | Impella 5.0 | Impella LD | TandemHeart | CentriMag | ProTek DUO | Impella RP | CentriMag | Veno-Arterial ECMO | |
| Pump mechanism | Pneumatic | Axial flow | Axial flow | Axial flow | Axial flow | Centrifugal flow | Centrifugal flow | Centrifugal flow | Axial flow | Centrifugal flow | Centrifugal flow |
| Pump location | Extracorporeal | Intracorporeal | Intracorporeal | Intracorporeal | Intracorporeal | Paracorporeal | Paracorporeal | Paracorporeal | Intracorporeal | Paracorporeal | Paracorporeal |
| Cannula size | 8 Fr | 13 Fr | 14 Fr | 22 Fr | 22 Fr | 21 Fr inflow/var. outflow | Variable | 21 Fr Inflow | 23 Fr | Variable | Var inflow/outflow |
| Placement | Perc | Perc | Perc | Perc | Sternotomy | Perc | Perc/Sternotomy | Perc | Perc | Perc/sternotomy | Perc/sternotomy |
| Inflow | N/A | LV | LV | LV | LV | LA | LA or LV | RA | IVC | RA | RA |
| Outflow | N/A | Aorta | Aorta | Aorta | Aorta | FA | Aorta | PA | PA | PA | FA or aorta |
| Effect on LV afterload | Reduce | Reduce | Reduce | Reduce | Reduce | Increase | Increase | None | None | None | Increase |
| Max flow (L/min) | 1 | 2.5 | 3.5 | 5 | 5 | 4 | > 5 | 4 | 4.5 | > 5 | > 5 |
| Intensity of anticoagulation | Low | Low | Low | Low | Low | High | Moderate | High | Low | Moderate | High |
| Duration of support | Hours to days | Hours to days | Days | Days to weeks | Days to weeks | Days to weeks | Days to weeks | Days to weeks | Days | Days to weeks | Days to weeks |
| Hemolysis | Rare | Low–mod | Low–mod | Low | Low | Low | Low | Low | Low–mod | Low | Low |
| Risk of limb ischemia | Low | Low | Low | Low | None | High | Low–high a | None | None | None | Low–high a |
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