Cardiogenic shock (CS) is defined as an inability of the heart to provide adequate blood flow to maintain the metabolic demands of tissue despite adequate intravascular volume. This definition, and similar variants, has been used for decades in numerous textbooks despite its inherent vagaries. For practical purposes, most would agree that CS exists when a patient exhibits sustained hypotension with evidence of impaired cardiac function. With few exceptions, CS is an emergency that requires prompt diagnosis and appropriate therapy. This chapter reviews how to best diagnose and manage CS in the intensive care unit (ICU).
Epidemiology and Etiology
Although there are a plethora of theoretical causes of CS in the ICU ( Table 51-1 ), the most frequent cause of CS in the ICU is acute coronary syndrome (ACS) resulting in acute left ventricular dysfunction. Autopsy studies have shown that more than 40% of left ventricular myocardium must be sacrificed for CS to ensue. Other relatively common causes, usually as a result of acute myocardial infarction (AMI), include acute mitral regurgitation, cardiac tamponade (from ventricular free-wall rupture), and ventricular septal rupture. Finally, a rare though increasingly recognized cause of CS in the ICU (particularly in the postoperative setting) is a stress-induced (so-called Takotsubo) cardiomyopathy. CS occurs in 8.6% of patients sustaining ST-elevation myocardial infarction (STEMI) and in roughly 2.5% of patients with sustained non-ST-elevation myocardial infarction (NSTEMI). Rarely, drugs have been shown to incite CS. In the Clopidogrel and Metoprolol in Myocardial Infarction Trial (COMMIT), the incidence of CS was 5% in patients receiving early metoprolol (roughly 30% greater than those who did not receive metoprolol). Finally, all of these scenarios incite an acute inflammatory response that augments the initial insult and results in a vicious cycle that, if left untreated, culminates in death ( Fig. 51-1 ). Mortality rates for patients who sustain STEMI with CS are approximately 68% over 30 days compared with approximately 10% in those patients who did not have CS. Evaluation of mortality trends within the United States reveals that a changing management scheme has decreased the mortality of this disease significantly (60.3% in 1995 vs. 47.9% in 2004). Although this change in mortality is undoubtedly multifactorial, few would argue that an increased rate of cardiac catheterization (51.5% in 1995 vs. 74.4% in 2004) and of percutaneous cardiac intervention (27.4% in 1995 vs. 54.4% in 2004) had a major impact. Of note, during this registry period (that included more than 250,000 patients in more than 750 U.S. hospitals), there was no change in the use of intraaortic balloon pumps (IABPs) (39%) or in immediate coronary artery bypass graft (CABG) surgery (3%). Although prognostication can be difficult in this population, recent evidence suggests that hemodynamic variables in the first 24 hours may be useful.
Acute myocardial infarction
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Other conditions
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Diagnosis
What is evident from almost all studies is that rapid diagnosis of CS is imperative. Hemodynamic criteria consistent with a diagnosis of CS include sustained (≥30 minutes) hypotension with systolic blood pressure less than 90 mm Hg, depressed cardiac index (CI) (<2.2 L/min/m 2 ), and elevated pulmonary artery occlusion pressure (PAOP) (>15 mm Hg). From the aforementioned indices, it would appear that one should be able to rapidly identify this entity if CI is known. Many patients with CS have a distributive shock, though, which lowers their systemic vascular resistance (SVR) and normalizes their CI. Thus it is necessary that the clinician have a systematic method of diagnosing CS.
In the absence of more objective data, a critically ill patient in shock usually has hypovolemia, sepsis, pulmonary embolism, or myocardial ischemia. As with most ailments, diagnosis begins with the physical examination. Often, the diagnosis can be made simply by placing one’s hands on the patient’s extremities. Frequently, CS manifests with cold and clammy extremities as the body attempts to maintain adequate perfusion to vital organs by peripheral vasoconstriction. With impaired myocardial contraction, auscultation of the lungs frequently reveals crackles due to an elevated left ventricular end-diastolic pressure (LVEDP) with exudate filling the pulmonary interstitium. Obviously, however, most physical examination findings, although supportive of a diagnosis, are nonspecific. Therefore additional information is frequently needed. A chest radiograph should be ordered in any patient presenting with symptoms of shock. Signs of interstitial edema (often in the absence of physical examination findings) are suggestive of CS. An electrocardiogram should be ordered and examined for signs of myocardial ischemia. If CS remains a consideration, cardiac enzymes should be sent.
Echocardiography is the test of choice to diagnose CS and should be ordered promptly. The sensitivity of this modality approaches 100%, whereas the specificity is roughly 95%. If transesophageal imaging is unavailable, contraindicated, or too cumbersome, transthoracic echocardiography should be ordered. A quick examination should allow rapid assessment of any left or right ventricular dysfunction, new valvular regurgitation, pericardial effusion, and ventricular septal rupture. Rapid availability of this imaging modality may preclude the need for further invasive monitors because pulmonary artery systolic pressure and PAOP can be estimated by Doppler echocardiography. Precise physiologic parameters are frequently necessary both to diagnose and to manage patients with CS. Invasive monitoring is probably warranted if there are persistent signs of hypoperfusion despite adequate volume therapy. The American College of Cardiology and American Heart Association (ACC/AHA) gives a class IIa (weight of evidence and opinion is in favor of usefulness and efficacy) recommendation for placement of a pulmonary artery catheter (PAC) in patients with CS. PACs can aid in diagnosis and can be helpful with subsequent management, although data showing a mortality benefit are equivocal. There are data to suggest that certain calculated indices, such as cardiac power and stroke work index, may have short-term prognostic value. Interpretation of PAC data requires a detailed knowledge of pathophysiology. A quick look at the numbers will rarely yield the diagnosis. Most causes of cardiogenic shock result in elevated central venous and pulmonary arterial pressures (the exception being isolated right ventricular ischemia). For the various causes to be differentiated, a detailed understanding of the various waveforms is necessary.
The central venous pressure (CVP) is probably the most underused physiologic parameter. A plethora of information can be obtained with proper analysis. For the interpretation of the various waves, the scale must be set so that all portions of the wave can be seen (usually a scale with 20 to 30 mm Hg maximum is optimal). The various components of the CVP can be seen in Fig. 51-2 . By breaking the waveform into various cardiac events, it becomes apparent that not all elevated venous pressures are equal. Cardiac tamponade will cause a monophasic CVP with a very small x -descent and often complete loss of the y -descent, whereas right ventricular ischemia with tricuspid regurgitation will yield a very large, fused c-v wave. The c-v wave is a fused c and v wave resulting from severe tricuspid regurgitation. Because of the regurgitant flow, there is an inability to differentiate the slight increased atrial pressure generated from closure of the tricuspid valve and atrial filling during atrial diastole. A complete analysis of CVP waveform is beyond the scope of this chapter, and the reader is referred to other texts.
The equivalent CVP for the left side of the heart is the PAOP. Similarly, with correct identification of the waves and translation of the waves into a portion of the cardiac cycle, various diseases become unmasked. Acute mitral regurgitation is associated with very large v waves on PAOP. Acute cardiac ischemia often first manifests as left ventricular diastolic dysfunction. This, in turn, leads to a higher left ventricular end-diastolic volume (LVEDV) that causes an elevated LVEDP. Although this culminates in an elevated PAOP, through evaluation of the waveform, an exaggerated a wave is consistent with diastolic dysfunction.
Management: An Evidence-Based Approach
Management of CS should focus on augmentation of oxygen delivery and blood pressure to restore microcirculatory function and maximize tissue perfusion. A delay in diagnosis or therapy will have a direct impact on mortality. Management of CS can be pharmacologic therapy, mechanical therapy, or revascularization.
Pharmacologic Therapy
It should be stated at the outset that there have been very few large controlled trials evaluating the efficacy of different vasopressor or inotrope therapies in CS, none of which have confirmed any outcome difference with any particular agent.
Initial treatment for patients with CS should focus on restoration of normal hemodynamics, oxygenation, and avoidance of arrhythmia. In patients without significant pulmonary edema, it is reasonable to administer a fluid challenge before vasopressor therapy. If pulmonary edema is present or there is no response to a fluid challenge, pharmacologic therapy should be initiated. Pharmacologic therapy for CS initially should focus on those compounds that have both inotropic and vasopressor activity. Drugs to consider as first-line treatment include norepinephrine, dopamine, dobutamine, and epinephrine. There is some evidence, however, that dopamine administration for CS may in fact increase mortality ; however, this has not been validated in randomized controlled studies. In addition, in patients with heart failure, a 2002 meta-analysis showed a trend (not statistically significant) with increased mortality in patients given adrenergic inotropic agents. Part of the reason for these observations may be that the improved hemodynamics seen with these agents come at a cost of increased myocardial oxygen consumption. More recently, vasopressin was used in place of norepinephrine and showed similar hemodynamic effects. Although phosphodiesterase inhibitors (e.g., milrinone) may be considered (particularly with right ventricular dysfunction), the resultant decrease in SVR is often not well tolerated by the hemodynamically unstable patient. Finally, levosimendan, an investigational calcium sensitizer that also promotes coronary vasodilation, continues to show promise as a novel treatment for CS. These studies highlight the need for randomized controlled trials to confirm the efficacy of one therapy over another. In general, maintenance of normal physiologic parameters (e.g., mean arterial pressure, CI) should be the goal. Although high-dose vasopressors have been associated with poorer survival, this finding may be an epiphenomenon representing only those patients who have greater hemodynamic instability.
Mechanical Therapy
In patients who are unresponsive to conventional pharmacologic therapy, mechanical augmentation of flow may be of benefit. The ACCF/AHA guidelines have recently downgraded the recommendation of an IABP for CS from a class I (“is recommended”) to a class IIa (“can be useful”). The only randomized trial to evaluate the efficacy of IABP (with or without thrombolysis) in patients with CS was able to show a dramatic decrease in 6-month mortality rate (39% vs. 80%; P <.05) in patients with severe shock who received an IABP. Nonrandomized trials also have shown decreased mortality. More recent observational studies, however, have been fraught with greater equipoise. The use of this device, though, is frequently associated with more aggressive therapies such as revascularization. One of the inherent benefits of IABP counterpulsation devices is that they can be placed at the bedside to augment diastolic pressure and reduce left ventricular afterload (without increasing myocardial oxygen demand). The incidence of major complications (e.g., arterial injury and perforation, limb ischemia, visceral ischemia) with IABP insertion is 2.5% to 3.0%. If an IABP is contraindicated (e.g., severe aortic insufficiency, severe peripheral vascular disease, aortic aneurysm, and dissection) or unavailable or the patient is unresponsive to its effects, ventricular assist device (VAD) placement may be considered. A variety of other devices, including institution of extracorporeal membrane oxygenation and placement of the CardioWest total artificial heart, also have been tried with varying success. Newer percutaneous VADs are making this option more feasible in smaller centers. A 2005 investigation randomized patients with CS to IABP or TandemHeart (a percutaneous left ventricular assist device [LVAD]). Although there were no significant differences in 30-day mortality between the two groups, patients in the LVAD subgroup had a significant improvement in hemodynamics, renal function, and clearance of serum lactate compared with the IABP cohort. A more recent multicenter randomized trial comparing TandemHeart with IABP in 42 patients with CS revealed similar improvements in hemodynamics with the LVAD without a statistically significant difference in 30-day mortality. Although many of these newer devices appear promising, there will clearly be a limited number of centers that will have access to such technology. Experience with device placement and hemodynamic management is necessary for optimal benefit. In the National Registry of Myocardial Infarction, IABP use was independently associated with survival in those centers with experience in their use. Finally, many of these devices are placed as a bridge to cardiac transplantation, and resources must be available to continue this often lengthy, workup.
Revascularization Therapy
Although management of AMI is beyond the scope of this chapter, a brief synopsis is provided here. Because AMI is frequently the inciting event culminating in CS, reestablishing blood flow to the affected myocardial territory is of utmost importance. It has become evident that prompt revascularization reduces the mortality of this disease. One method of reestablishing coronary arterial flow is by the administration of thrombolytic agents. In a randomized trial involving more than 40,000 patients with AMI, the GUSTO-I (Global Utilization of Tissue Plasminogen Activator and Streptokinase for Occluded Coronary Arteries) trial demonstrated a survival advantage with the use of tissue plasminogen activator (tPA) over streptokinase. Since these results have been published, a number of other thrombolytics have been developed; however, randomized trials have been unable to show a difference with respect to CS progression between the tPA and these newer agents. Moreover, once CS has been established, no studies have shown an improvement in mortality with the administration of thrombolytic agents. The preferred modality of revascularization remains either percutaneous coronary intervention (PCI) or CABG. Although a facilitated PCI strategy (i.e., planned immediate PCI after fibrinolytic administration) has not been shown to be effective, fibrinolytics may still be considered in those situations in which PCI is not attainable for more than 90 minutes, the patient is within 3 hours of his or her infarction, and there are no contraindications. The Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial emphasized this aspect, showing that early revascularization reduced mortality by 22% in those patients who presented with CS and by 16% in those who had CS subsequent to admission. The question of how and when it is best to achieve reperfusion has been evaluated. The SHOCK trial prospectively randomized 302 patients with CS due to AMI to either emergency revascularization (either CABG or PCI) or medical stabilization. Although 30-day mortality was similar for both groups, there was a significant survival advantage in the early revascularization group at 6 months, 1 year, and 6 years. This trial did not demonstrate an advantage of one revascularization therapy over another. Given these results and others, early revascularization (either with PCI or CABG surgery) therapy is a class I recommendation by the ACC/AHA for patients younger than 75 years with CS complicated by ACS. Although there are few data to support revascularization in the non–ST-segment elevation CS population, the SHOCK registry did find a nonsignificant decrease in mortality among those patients who underwent early revascularization.
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