Cardiogenic Shock Treatment & Management

Cardiogenic shock is an emergency involving acute hemodynamic instability that necessitates immediate resuscitative therapy before shock irreversibly damages vital organs. The key to a good outcome in patients with cardiogenic shock is an organized approach, with rapid diagnosis and prompt initiation of pharmacologic therapy to maintain blood pressure and cardiac output and respiratory support, as well as reversal of the underlying cause. ^{[1, 24]}

All patients require admission to an intensive care setting, which may involve emergency transfer to the cardiac catheterization suite, critical care transport to a tertiary care center, or internal transfer to the intensive care unit (ICU).

Early and definitive restoration of coronary blood flow (ie, early revascularization) is the most important intervention for achieving an improved survival rate. ^{[1, 24]} At present, it represents standard therapy for patients with cardiogenic shock due to myocardial ischemia.

Correction of electrolyte and acid-base abnormalities, such as hypokalemia, hypomagnesemia, and acidosis, is essential in cardiogenic shock.

Cardiogenic shock may be prevented with early revascularization in patients with myocardial infarction (MI) and with required intervention in patients with structural heart disease.

Procedures

Placement of a central line may facilitate volume resuscitation, provide vascular access for multiple infusions, and allow invasive monitoring of central venous pressure. Central venous pressure may also be used to guide fluid resuscitation.

Although not necessary for the diagnosis of cardiogenic shock, invasive monitoring with a pulmonary artery catheter may be helpful in guiding fluid resuscitation in situations in which left ventricular (LV) preload is difficult to determine.

Pulmonary artery catheter pressure measurements may also be useful in prognosis. Retrospective evaluation of these measurements from the SHOCK trial demonstrated that stroke volume index (SVI) and stroke work index (SWI) vary inversely with mortality. ^[23]

An arterial line may be placed to provide continuous blood pressure monitoring. This is particularly useful if the patient requires inotropic medications.

When immediate stabilization is necessary for recovery cardiac and other organ systems, consider placing a temporary over durable mechanical circulatory support device (MCS) as the first-line device. ^{[1, 24]}  Temporary MCS options include the following ^[1] :

• Intra-aortic balloon pump (IABP)
• Percutaneous MCS
• Extracorporeal membrane oxygenation (ECMO)

An IABP may be placed in the emergency department (ED) as a bridge to percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG), to decrease myocardial workload, and to improve end-organ perfusion. ^[12]  Consider placing an IABP in patients with cardiogenic shock who have acute mitral regurgitation or a ventricular septal defect, as well as select patients with severe cardiogenic shock when other MCS devices are unavailable. ^{[1, 24]}  In the setting of poor oxygenation not expected to quickly improve with an alternative temporary MCS device or during cardiopulmonary resuscitation, the preferred temporary MCS option may be veno-arterial (VA) ECMO. ^{[1, 24]}

However, consider long-term durable MCS devices in the following patients with cardiogenic shock ^{[1, 24]} :

• Those unlikely to recover without long-term MCS support
• Those can have a meaningful recovery
• Those without irreversible end-organ dysfunction, systemic infections, or relative contraindications to implantation of durable MCS devices

In addition, patients undergoing evaluation for MCS implantation should also concurrently be assessed for transplantation. ^{[1, 24]}

PCI and coronary artery bypass

An early revascularization strategy with either PCI or CABG, in collaboration between cardiologists and surgeons, is recommended for appropriate patients with suspected cardiogenic shock related to acute coronary syndrome (eg, those with uncertain neurologic status, those who received previous fibrinolysis), regardless of the time delay from MI onset. ^{[1, 24]}  Radial arterial access is preferred for angiography and PCI, when feasible. When it is not possible to promptly complete an early invasive approach, consider fibrinolysis in STEMI-associated cardiogenic shock. ^{[1, 24]}

The SHOCK trial demonstrated that either PCI or CABG is the treatment of choice for cardiogenic shock and that each has been shown to markedly decrease mortality rates at 1 year. PCI should be initiated within 90 minutes of presentation; however, it remains helpful, as an acute intervention, within 12 hours of presentation.

If such a facility is not immediately available, thrombolytics should be considered. However, this treatment is second-best. An increased mortality is seen in situations where thrombolytics are used instead of PCI. This is due to the relative ineffectiveness of the thrombolytic medications to lyse clots in low-blood-pressure situations. ^{[26, 3]}

The 2019 American Heart Association (AHA) scientific statement on contemporary management of cardiogenic shock suggests that all patients with cardiogenic shock without serious bleeding complications continue post-PCI dual antiplatelet therapy without interruption. ^[1] Consider using an IV glycoprotein IIb/IIIa inhibitor or cangrelor, a P2Y₁₂ inhibitor, when oral agents cannot be administered or absorption concerns exist. For patients requiring post-PCI anticoagulation, the AHA suggests preferential use of IV unfractionated heparin.

Acute kidney injury

Consider continuous renal replacement therapy in patients with stage 2 acute kidney injury (a rise in in serum creatinine level ≥2.0 times baseline and urine output < 0.5 mL/kg/hr for ≥12 hours, or when “life threatening changes in fluid, electrolyte, and acid-base balance” exist). ^[1]

Prehospital care is aimed at minimizing any further ischemia and shock. All patients require intravenous (IV) access, high-flow oxygen administered by mask, and cardiac monitoring.

Twelve-lead electrocardiography (ECG) performed in the field by appropriately trained paramedics may be useful in decreasing door-to-PCI times and/or time to the administration of thrombolytics because acute ST-segment elevation MI (STEMI) can be identified earlier. The ED can thus be alerted and may mobilize the appropriate resources.

Inotropic medications should be considered in systems with appropriately trained paramedical personnel.

When clinically necessary, positive pressure ventilation and endotracheal intubation should be performed. Continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) support can be considered in appropriately equipped systems. Note that there is a potential for hemodynamic deterioration in association with induction therapies, such as sedatives and analgesics; vagal stimulation association with endotracheal tube placement; the transition from spontaneous breathing to positive-pressure ventilation; and inappropriate ventilation settings. ^[1]  

Initial management includes fluid resuscitation to correct hypovolemia and hypotension, unless pulmonary edema is present. Central venous and arterial lines are often required. Swan-Ganz catheterization and continuous percutaneous oximetry are routine.

Oxygenation and airway protection are critical; intubation and mechanical ventilation are commonly required. However, although positive-pressure ventilation (PPV) may improve oxygenation, it may also compromise venous return, preload, to the heart. In any event, the patient should be treated with high-flow oxygen. Studies in patients with acute cardiogenic pulmonary edema have shown noninvasive ventilation to improve hemodynamics and reduce the intubation rate. Mortality, however, is unaffected.

A study by Shin et al suggested that patients who receive extracorporeal cardiopulmonary resuscitation (CPR) versus conventional CPR for longer than 10 minutes following in-hospital arrest have a greater chance of survival. ^[27]

Venoarterial (VA) extracorporeal membrane oxygenation (ECMO) aids in increasing tissue perfusion by increasing arterial blood flow and is used to treat medically refractory cardiogenic shock or cardiac arrest ^[28]  and, potentially, postcardiotomy cardiogenic shock. ^[29] However, complications can include left ventricular distention and pulmonary edema, distal limb ischemia, hemorrhage, and thromboembolism, ^{[28, 29]} as well as hemolysis, infection, acute kidney injury, and upper body hypoxia. ^[29]

All patients with cardiogenic shock require close hemodynamic monitoring, volume support to ensure adequate sufficient preload, and ventilatory support.

Pharmacologic therapy

Patients with MI or acute coronary syndrome (ACS) are given aspirin and heparin. Both of these medications have been shown to be effective in reducing mortality in separate studies. Before initiating therapy, however, care should be taken to ensure that the patient does not have a myocardial wall rupture that is amenable to surgery.

There is no need to start clopidogrel until after angiography, because angiography may demonstrate that there is a need for urgent CABG. ^[3]

The glycoprotein IIb/IIIa inhibitors improve the outcome of patients with non–ST-segment elevation ACS (NSTACS). They have been found to reduce recurrent MI following PCI and in cardiogenic shock.

Avoid beta-blockers in patients with signs of heart failure or low-output states, and avoid renin-angiotensin-aldosterone system (RAAS) antagonists in hypotensive patients. ^[1] However, initiating beta-blockers may be reasonable for patients who are euvolemic and off inotropes and vasopressors for a minimum of 24 hours. Consider initiating RAAS inhibitor therapy in patients off vasopressors for 24 hours who have nearly baseline renal function and a low risk of RAAS-associated hyperkalemia or hypotension. ^[1]

Initiating statins is reasonable in patients with cardiogenic shock associated with myocardial infarction. ^[1]

Dopamine, norepinephrine, and epinephrine are vasoconstricting drugs that help to maintain adequate blood pressure during life-threatening hypotension and help to preserve perfusion pressure for optimizing flow in various organs. ^[25] The mean blood pressure required for adequate splanchnic and renal perfusion (mean arterial pressure [MAP] of 60 or 65 mm Hg) is based on clinical indices of organ function.

In patients with inadequate tissue perfusion and adequate intravascular volume, initiation of inotropic and/or vasopressor drug therapy may be necessary. Dopamine increases myocardial contractility and supports the blood pressure; however, it may increase myocardial oxygen demand. Dobutamine may be preferable if the systolic blood pressure is higher than 80 mm Hg; it has the advantage of not affecting myocardial oxygen demand as much as dopamine does. However, the resulting tachycardia may preclude the use of this inotropic agent in some patients. Dopamine will cause more tachycardia than dobutamine for any corresponding increase in cardiac output.

Dopamine is usually initiated at a dosage of 5-10 mcg/kg/min IV, and the infusion rate is adjusted according to the blood pressure and other hemodynamic parameters. Often, patients may require high dosages of dopamine (as much as 20 mcg/kg/min).

If the patient remains hypotensive despite moderate doses of dopamine, a direct vasoconstrictor (eg, norepinephrine) should be started at a dosage of 0.5 mcg/kg/min and titrated to maintain an MAP of 60 mm Hg. The potent vasoconstrictors (eg, norepinephrine) are best reserved for situations of refractory hypotension and organ hypoperfusion because of their unfavorable role in increasing afterload and cardiac filling pressure and, consequently, impairing cardiac output. However, one study of patients with shock found no difference in outcome between treatment with norepinephrine and treatment with dopamine. ^[30]  

Vasopressor supportive therapy

There is no consensus regarding the first-line choice of vasopressor in cardiogenic shock. However, because norepinephrine is associated with few arrhythmias than other vasopressors, it may be the vasopressor of choice to use for many patients with cardiogenic shock. ^{[1, 24]}

The following is a brief review of the mechanism of action and indications for drugs used for hemodynamic support of cardiogenic shock. ^{[31, 32]}

There is little in the way of randomized clinical trial data to guide the use of inotropic or pressor therapy in patients with cardiogenic shock. The use of these agents is indicated in patients with cardiogenic shock, but it is important to note that a survival benefit has not been established. Indeed, routine use of these agents in patients with hemodynamically stable, decompensated heart failure was associated with greater morbidity and no clinical benefit (Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure [OPTIME-CHF]). ^{[33, 34]}

Dopamine

Dopamine is a precursor of norepinephrine and epinephrine and has varying effects according to the doses infused. A dosage of less than 5 mcg/kg/min causes vasodilation of renal, mesenteric, and coronary beds. At a dosage of 5-10 mcg/kg/min, beta1-adrenergic effects induce an increase in cardiac contractility and heart rate.

At dosages higher than 10 mcg/kg/min, predominant alpha-adrenergic effects lead to arterial vasoconstriction and an elevation in blood pressure. The blood pressure increases primarily as a result of its inotropic effect. The undesirable effects are tachycardia and increased pulmonary shunting, as well as the potential for decreased splanchnic perfusion and increased pulmonary arterial wedge pressure.

Norepinephrine

Norepinephrine is a potent alpha-adrenergic agonist with only minor beta1-adrenergic agonist effects. Norepinephrine can increase blood pressure successfully in patients who remain hypotensive following dopamine. The dosage of norepinephrine may vary from 0.2 to 1.5 mcg/kg/min, and high dosages (up to 3.3 mcg/kg/min) have been used because of the alpha-receptor down-regulation in persons with sepsis.

Epinephrine

Epinephrine is an agonist of alpha1, beta1, and beta2 receptors. It can increase the MAP by increasing the cardiac index and stroke volume, as well as systemic vascular resistance (SVR) and heart rate. Epinephrine decreases the splanchnic blood flow and may increase oxygen delivery and consumption.

Administration of this agent may be associated with an increase in systemic and regional lactate concentrations. The use of epinephrine is recommended only in patients who are unresponsive to traditional agents. Other undesirable effects include an increase in lactate concentration, a potential to produce myocardial ischemia, the development of arrhythmias, and a reduction in splanchnic flow.

Levosimendan

Levosimendan, widely used in Europe but not approved for use in the United States, can be considered for use in conjunction with vasopressors to improve coronary blood flow. ^{[35, 36]}  This agent acts by increasing the sensitivity of the cardiac myofilament to calcium, rather than increasing intracellular concentrations of free calcium. Levosimendan stabilises troponin C and the kinetics of actin-myosin cross-bridges without increasing myocardial consumption of adenosine triphosphate (ATP).  Levosimendan is a potent inotrope and also a vasodilator of the arterial, venous, and coronary circulation. It should be used with caution, however, in that it can cause hypotension. 

Inotropic supportive therapy

Dobutamine

Dobutamine (sympathomimetic agent) is a beta1-receptor agonist, though it has some beta2-receptor and minimal alpha-receptor activity. It is used in a dosage range of 2 to 20 mcg/kg/min and has a half-life of approximately 2 minutes. IV dobutamine induces significant positive inotropic effects, with mild chronotropic effects through activation of adenyl cyclase, an increase in intracellular cyclic adenosine monophosphate (cAMP) and, therefore, calcium levels. It also induces mild peripheral vasodilation (decrease in afterload). The combined effect of increased inotropy and decreased afterload induces a significant increase in cardiac output.

In the setting of acute MI, dobutamine use could increase the size of the infarct because of the increase in myocardial oxygen consumption that may ensue. In general, caution should be exercised when administering dobutamine in patients with moderate or severe hypotension (eg, systolic blood pressure < 80 mm Hg), because the peripheral vasodilation, in some cases, may cause a further fall in blood pressure.

Phosphodiesterase III inhibitors

Phosphodiesterase III inhibitors (PDIs), which include inamrinone (formerly amrinone) and milrinone, are inotropic agents with vasodilating properties and long half-lives. Milrinone is used in a dosage range of 0.3 to 0.75 mcg/kg/min and has a long half-life of 1.5 to 3 hours, with the longer half-life in patients with renal impairment.

The mechanism of action of PDIs is distinct from dobutamine in that they prevent breakdown of cAMP, thereby increasing intracellular cAMP levels. The hemodynamic properties of PDIs are (1) a positive inotropic effect on the myocardium and peripheral vasodilation (decreased afterload) and (2) a reduction in pulmonary vascular resistance (decreased preload).

PDIs may be beneficial in persons with cardiac pump failure who require more concomitant pulmonary and systemic vasodilation than is typically achieved by dobutamine. Unlike catecholamine inotropes, these drugs are not dependent on adrenoreceptor activity; therefore, patients are less likely to develop tolerance to these medications.

PDIs are less likely than catecholamines to cause adverse effects known to be associated with adrenoreceptor activity (eg, increased myocardial oxygen demand, myocardial ischemia). They are also associated with less tachycardia and myocardial oxygen consumption. However, the incidence of tachyarrhythmias is greater with PDIs than with dobutamine.

Although thrombolytic therapy (TT) reduces mortality rates in patients with acute MI, its benefits for patients with cardiogenic shock secondary to MI are disappointing. When used early in the course of MI, TT reduces the likelihood of subsequent development of cardiogenic shock after the initial event.

In the Gruppo Italiano Per lo Studio Della Streptokinase Nell'Infarto Miocardio trial, 30-day mortality rates were 69.9% in patients with cardiogenic shock who received streptokinase, compared to 70.1% in patients who received a placebo. ^{[37, 38]}

Similarly, other studies employing a tissue plasminogen activator did not show reductions in mortality rates from cardiogenic shock. Lower rates of reperfusion of the infarct-related artery in patients with cardiogenic shock may help to explain the disappointing results from TT. Other reasons for the decreased efficacy of TT are the existence of hemodynamic, mechanical, and metabolic causes of cardiogenic shock that are unaffected by TT.

Thrombolytic therapy plus IABP

A prospective cohort study demonstrated the potential survival benefit of combining TT with IABP counterpulsation in patients with MI complicated by cardiogenic shock. ^[39]  Of the 1190 patients enrolled, the treatments were (1) no TT and no IABP counterpulsation (33%, n = 285), (2) IABP counterpulsation only (33%, n = 279), (3) TT only (15%, n = 132), and (4) TT and IABP counterpulsation (19%, n = 160).

Patients in cardiogenic shock who were treated with TT had lower in-hospital mortality rates than did those who did not receive TT (54% vs 64%), and patients selected for IABP counterpulsation had lower in-hospital mortality rates than did those who did not receive IABP counterpulsation (50% vs 72%). ^[39]  Furthermore, a significant difference was noted for inhospital mortality rates among the four treatment groups; that is, TT plus IABP counterpulsation (47%), IABP counterpulsation only (52%), TT only (63%), no TT and no IABP counterpulsation (77%). Revascularization influenced in-hospital mortality rates significantly (39% with revascularization vs 78% without revascularization). ^[39]

The use of the IABP reduces systolic LV afterload and augments diastolic coronary perfusion pressure, thereby increasing cardiac output and improving coronary artery blood flow. The IABP is effective for the initial stabilization of patients with cardiogenic shock. However, an IABP is not definitive therapy; the IABP stabilizes patients so that definitive diagnostic and therapeutic interventions can be performed. ^{[40, 41]}

The IABP also may be a useful adjunct to thrombolysis in acute MI for initial stabilization and transfer of patients to a tertiary care facility. Some studies have shown lower mortality rates in patients with MI and cardiogenic shock treated with an IABP and subsequent revascularization. ^{[39, 42]}

Complications may be documented in up to 30% of patients who undergo IABP therapy; these relate primarily to local vascular problems, embolism, infection, and hemolysis.

The impact of treatment with an IABP on long-term survival is controversial and depends on the patient’s hemodynamic status and the etiology of the cardiogenic shock. Patient selection is the key issue; inserting the IABP early, rather than waiting until full-blown cardiogenic shock has developed, may result in clinical benefit.

Ramanathan et al found that rapid and complete reversal of systemic hypoperfusion with IABP counterpulsation in the SHOCK trial and SHOCK registry was independently associated with improved inhospital, 30-day, and 1-year survival, regardless of early revascularization. This suggests that complete reversal of systemic hypoperfusion with IABP counterpulsation is an important early prognostic feature. ^[43]

In the IABP-SHOCK II study, 600 patients with cardiogenic shock complicating acute MI were randomized to IABP counterpulsation or no IABP counterpulsation. All patients were expected to undergo early revascularization. Use of IABP counterpulsation did not significantly reduce 30-day mortality in these patients. ^[44]

Various LV assist devices (LVADs) capable of providing complete short-term hemodynamic support have been developed. ^{[45, 46]} The application of LVAD during reperfusion, after acute coronary occlusion, causes reduction of the LV preload, increases regional myocardial blood flow and lactate extraction, and improves general cardiac function. The LVAD makes it possible to maintain the collateral blood flow as a result of maintaining the cardiac output and aortic pressure, keeping wall tension low and reducing the extent of microvascular reperfusion injury. ^{[40, 41, 47]}

A pooled analysis from 17 studies showed that the mean age of this group of patients with LVADs was 59.5 ± 4.5 years and that mean support duration was 146.2 ± 60.2 hours. In 78.5% of patients (range, 53.8-100%), adjunctive reperfusion therapy, mainly percutaneous transluminal coronary angioplasty (PTCA), was used. Mean weaning and survival rates were 58.5% (range, 46-75%) and 40% (range, 29-58%), respectively. ^[40]

In any case, comparing studies is difficult because important data are usually missing, mean age of patients were different, and time to treatment is not standardized. Hemodynamic presentation seems to be worse compared with data reported in the SHOCK trial, with lower cardiac index, lower systolic aortic pressure, and higher serum lactates. Taking these considerations into account, LVAD support seems to give no survival improvement in patients with cardiogenic shock complicating acute MI, compared with early reperfusion alone or in combination with IABP.

In a randomized, controlled trial in which 129 patients with end-stage heart failure who were ineligible for cardiac transplantation were assigned either to receive an LVAD (68 patients) or to undergo optimal medical management, survival rates were higher in the LVAD group. The rates of survival at 1 year were 52% in the device group and 25% in the medical therapy group, whereas the rates at 2 years were 23% and 8%, respectively. In addition, the quality of life was significantly improved at 1 year in the device group. ^[48]

Implantable LVADs are being used as a bridge to heart transplantation for patients with acute MI and cardiogenic shock. ^[49] According to the HeartMate Data Registry ^[50] , from 1986-1998, 41 patients (5% of the total number of HeartMate IP patients) were supported with this implantable pneumatic device for acute MI, and 25 (61%) were successfully bridged to heart transplantation. (See an example of an LVAD below.)

However, LVADs as a bridging option for patients with cardiogenic shock must be considered cautiously and must be avoided in patients who are unlikely to survive or are not likely to be transplant candidates. Further investigations are required to better define indications, support modalities, and outcomes.

The indications for insertion of a ventricular assist device are controversial. Such an aggressive approach to support the circulatory system in cardiogenic shock is appropriate (1) after the failure of medical treatment and an IABP, (2) when the cause of cardiogenic shock is potentially reversible, or (3) if the device can be used as a bridging option.

The retrospective and prospective data favor aggressive mechanical revascularization in patients with cardiogenic shock secondary to MI.

Reestablishing blood flow in the infarct-related artery may improve left ventricular function and survival following MI. In acute MI, studies show that PTCA can achieve adequate flow in 80-90% of patients, compared with 50-60% of patients after TT.

Several retrospective clinical trials have shown that patients with cardiogenic shock due to myocardial ischemia benefitted (reduction in 30-day mortality rates) when treated with angioplasty. A study of direct (primary) PTCA in patients with cardiogenic shock reported lower mortality rates in patients treated with angioplasty combined with the use of stents than in patients treat with medical therapy. ^[51]

A study by Antoniucci et al found that mortality increases in relation to the length of time to treatment in patients with acute MI who are not considered to be at low risk. ^[52] To study the relation of time to treatment and mortality in patients with acute MI, a series of 1336 patients who underwent successful primary PTCA were stratified into low-risk and not–low-risk patient groups. The 6-month mortality rate was 9.3% for not–low risk patients and 1.3% for the low-risk patients. An increase in the mortality rate from 4.8% to 12.9% with increasing time to reperfusion was observed in the not–low-risk group. A delay from symptom onset to treatment resulted in higher mortality rates for the not–low-risk patients. ^[52]

Using prospective data from the British Cardiovascular Intervention Society (BCIS) PCI database that evaluated data from 6489 English and Welsh patients undergoing PCI for ACS in the setting of cardiogenic shock, Kunadian et al reported mortality rates of 37.3% at 30 days, 40.0% at 90 days, and 44.3% at 1 year. ^[18]

Critical left main artery disease and three-vessel coronary artery disease (CAD) are common findings in patients who develop cardiogenic shock. The potential contribution of ischemia in the noninfarcted zone contributes to the deterioration of already compromised myocardial function.

CABG in the setting of cardiogenic shock is generally associated with high surgical morbidity and mortality rates. Because the results of PCI can be favorable, routine bypass surgery is often discouraged for these patients.

Results from the SHOCK (SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK) trial supported the superiority of a strategy that combines early revascularization with medical management in patients with cardiogenic shock. ^{[26, 51, 53]} In the study, patients were assigned to receive either optimal medical management, including an IABP and TT, or cardiac catheterization followed by revascularization using PTCA or CABG.

The mortality rates at 30 days were 46.7% in the early intervention group and 56% in patients treated with optimal medical management. Although these 30-day results did not reach statistical significance, the mortality rate at 6 months was significantly lower in the early intervention group (50.3% vs 63.1%). ^[51]

The 1-year survival rates were also reported from the SHOCK trial. ^[26] The survival rate at 1-year was 46.7% for patients in the early revascularization group and 33.6% in the conservative management group. The treatment benefit was apparent only for patients younger than 75 years (51.6% survival rate in early revascularization group vs 33.3% in patients treated with optimal medical management).

Based on the outcome of this study, the recommendation is that patients with acute MI complicated by cardiogenic shock, particularly those younger than 75 years, should be rapidly transferred to a center with personnel capable of performing early angiography and revascularization procedures. ^[54] Long-term follow-up was conducted annually until 2005. A strategy of early revascularization resulted in a 13.2% absolute and 67% relative improvement in 6-year survival compared with initial medical therapy. ^[55]

Immediately transfer a patient who develops cardiogenic shock to an institution at which invasive monitoring, coronary revascularization, and skilled personnel are available to provide expert care.

Patients with cardiogenic shock who are admitted to a hospital without facilities for revascularization should be immediately transferred to a tertiary care center with such facilities. If time to PCI is more than 1 hour and onset of symptoms has been within 3 hours, rapid administration of TT is recommended.

It should be kept in mind, however, that attempts to transfer a patient with cardiogenic shock must be made only when everything possible has been done to stabilize his or her condition and when the level of care during the transfer will not significantly decrease.

Although cardiogenic shock is not entirely preventable, measures can be taken to minimize the risk of occurrence, recognize it at earlier stages, and begin corrective therapy more expeditiously. Deterrence and prevention require a high degree of suspicion and heightened awareness.

Care is required in treating patients with ACS who are not yet in cardiogenic shock. Careful use of beta blockers and angiotensin-converting enzyme (ACE) inhibitors in these patients is essential to avoid hypotension leading to cardiogenic shock. ^[3]

Consult a cardiologist at the earliest opportunity because their insight and expertise may be invaluable for facilitating echocardiographic support, placement of an IABP, and transfer to more definitive care (eg, cardiac catheterization suite, ICU, operating room). In severe cases, also consider discussing the case with a cardiothoracic surgeon.