Hemodynamic criteria
Systolic blood pressure (SBP) below 90 mmHg (or more than 30 mmHg below basal in hypertensive patients) for more than 30 min
Use of vasopressors and inotropes to keep SBP above 90 mmHg
Cardiac index of less than 2.2 L/min/m2
Pulmonary artery occlusion pressure of above 15 mmHg
Signs of tissue hypoperfusion
Pale, cool, and clammy peripheries
Prolonged capillary refill times
Altered sensorium
Oliguria/anuria (less than 0.5 mL/kg/h)
Signs of pulmonary congestion
Tachycardia
Lactic acidosis
Mixed venous saturation below 65 %
Other causes of shock (distributive, hypovolemic, and obstructive) must be ruled out and contributing factors – such as hypovolemia, hypoxia, and acidosis – must be corrected in order to determine the etiology of shock.
Echocardiography represents a fundamental tool in the diagnostic workup of CS. Nonischemic causes of CS can be investigated: pericardial effusions, valvular abnormalities, and acute overload signs such as in massive pulmonary embolism and volemic status but also mechanical complications of MI. It also allows quantification of the severity of cardiac involvement and evaluation of systolic and diastolic function and regional abnormalities.
Echocardiography should nowadays be applied as a first-line diagnostic technique together with traditional hemodynamic tools in a so-called echodynamic approach to CS and to any cause of hemodynamic instability.
The presence of current myocardial ischemia must be assessed and appropriate investigations must be performed. In this regard, coronary angiography should be performed in all patients with cardiogenic shock in whom acute myocardial infarction is suspected and who are candidates for revascularization with either percutaneous coronary intervention or coronary artery bypass graft surgery. In addition, all patients who have undergone reperfusion therapy should be evaluated for failure of reperfusion.
9.4 Management
Prompt restoration of adequate blood flow to the affected myocardium is the key management measure in all patients with ongoing ischemia.
Systemic thrombolysis, percutaneous coronary revascularization (PCI), and surgical revascularization represent the available alternatives.
Thrombolysis should be restricted to patients who would have otherwise no chance of timely reperfusion, as in CS its likelihood of success is reduced by both the low coronary blood flow and the hostile biochemical environment [13].
PCI represents the optimal treatment for patients in whom CS developed early after myocardial infarction and the coronary anatomy makes it feasible.
Surgery may allow a more complete revascularization, but it is more invasive and requires longer times to reperfusion. It is better reserved to patients in whom PCI is impossible for any technical or clinical reason [14].
Of course, the need for a prompt myocardial reperfusion should not de-emphasize the concurrent necessity to sustain the patient’s hemodynamics, restore an adequate tissue perfusion, and reverse metabolic derangements.
Fluid replacement and supplemental oxygen when needed are the basic measures. If respiratory failure is severe, ventilatory support (either noninvasive or invasive) should be provided.
Optimization of myocardial performance is generally sought with the use of catecholamines. Although they are frequently needed to increase tissue perfusion, this can be seen as a “palliative” therapy, as no evidence of survival benefit exists with the use of such drugs, which might on the contrary worsen myocardial dysfunction by increasing myocardial oxygen consumption [15, 16]. The dosage of inotropic agents should be continuously titrated to the minimum necessary dosage needed to achieve the therapeutic goals, in order to minimize oxygen consumption and arrhythmogenic effects. An interesting alternative with regard to myocardial oxygen consumption is represented by the class of calcium sensitizers, levosimendan being the only compound currently available on the market. Since its positive inotropic effect is based on a reversible increase of the affinity of the myocardial contractile apparatus to calcium and not on the increased influx of calcium, it does not increase myocardial oxygen consumption nor has an arrhythmogenic effect. Moreover, both its peripheral vasodilatory and anti-inflammatory effects might also be useful in the setting of CS [17–19].
In many patients, fluids and inotropes alone are unable to stabilize hemodynamics. In such cases, a mechanical support device is needed.
The simplest form of mechanical support is represented by intra-aortic balloon counterpulsation (IABP). The rationale for aortic counterpulsation is particularly strong in the setting of myocardial ischemia and infarction and in postischemic acute mitral regurgitation, for its positive effects on coronary perfusion and afterload reduction.
The benefit of IABP on early mortality in patients with CS has been recently questioned by the results of the IABP-SHOCK II Trial [4]. These results were quite surprising, but the trial raised many criticisms, and a change in the current guidelines based on this evidence seems unjustified at the moment.
IABP may be unable to adequately support a patient with severe CS, especially when a large portion of the myocardium (more than 40 % on average) is affected. It is generally accepted that a cardiac output of at least 2.5 L/min is needed for the patient to take advantage of counterpulsation.
In such a condition, a full mechanical circulatory support (MCS) must be considered and, if indicated, implanted as early as possible.
MCS is required to rapidly improve the coronary perfusion, unload both ventricles, decrease the oxygen myocardial demand, and maintain end-organ perfusion. Currently, there are several MCS devices available, such as extracorporeal membrane oxygenation (ECMO), paracorporeal or extracorporeal ventricular assist devices (VADs), percutaneous VADs, and total artificial heart (TAH). Most of them are particularly expensive and need time and a surgical approach for implantation. ECMO represents an ideal choice for these patients because of the quick and easy insertion of this device even during fatal arrhythmia or cardiac arrest. With respect to surgically implanted VADs, ECMO offers some unique advantages in that it is readily available to provide circulatory support, with the ability to resolve organ injury in patients who present with cardiac arrest or with severe hemodynamic instability associated with multiorgan failure.
9.5 Role of ECLS
Whenever ECLS is deemed necessary to support a patient in CS, this should be set up without delay, as the early introduction of ECMO has been related with better clinical outcome and hospital survival [20]. MCS can interrupt the inflammatory cascade initiated by the onset of shock and prevent progression to irreversible end-organ damage and subsequent death; however, a window of opportunity remains during which rescue is possible.
Each patient should be considered as a candidate for ECMO; however, not all patients affected by refractory CS meet the criteria for ECMO institution (Table 9.2).
Table 9.2
Contraindications to ECMO institution
Advanced age (more than 75–80 years old) |
Disseminated malignancy |
Severe degenerative brain disease |
Unwitnessed cardiac arrest |
Prolonged CPR time (more than 45–60 min) |
Aortic dissection |
Severe peripheral vasculopathy |
Irreversible renal disease (dialyzed patients) |
Severe aortic regurgitation |
Ungraftable coronary arteries |
Non-eligibility to heart transplant or VAD |
Several considerations must be taken into account in order to determine a patient’s eligibility for ECLS. Candidates should be selected only if significant organ recovery is expected or there is no contraindication to long-term mechanical support or transplant.
Up to 60 % of survivors cannot be weaned and require a ventricular assist device (VAD) or transplantation [21, 22]. ECMO may therefore provide a bridge to decision; it is less costly than VADs, can be initiated quickly, and offers biventricular and respiratory support, thereby stabilizing patients while their suitability for a VAD or transplant is evaluated. Institutions that do not provide this therapy should consider referring patients to an experienced center once IABP support has been initiated. In these situations, expert retrieval teams from the specialist center should provide transport [23, 24].
The ideal indication for ECMO institution is isolated severe heart failure in the absence of signs and symptoms of multiorgan failure.
Factors such as age, comorbidities, and neurological, renal, and hepatic status could preclude ECMO institution. The most common contraindications to ECMO are based on irreversible multiorgan failure, severity of cerebral damage, and absence of chances for recovery in patients who are not candidates for heart transplantation or long-term VAD implantation.
ECLS is able to stabilize the majority of patients, prevent organ dysfunction, and revert metabolic derangements, provided it is implanted in a timely fashion. Its positive effect on mid- to long-term outcome appears reasonable, with reported survival rates of 20–43 % among patients who received ECLS for cardiac arrest, severe cardiogenic shock, or failure to wean from cardiopulmonary bypass following cardiac surgery. The evidence is however quite weak due to the small numbers of observational studies and case series and the lack of RCTs.
Our group, as well as Combes and coworkers, demonstrated a 28–31 % survival to discharge in patients supported with ECMO for postcardiotomic or post-AMI shock refractory to conventional management including IABP [21, 25].
The pooled data from the ELSO (Extracorporeal Life Support Organization) Registry report an average survival rate of 39 % for adult patients with cardiogenic shock [26]. These results are consistent with the recent report from Sakamoto and colleagues. In a population of patients with acute coronary syndromes complicated by cardiogenic shock or cardiac arrest, they demonstrated a 32.7 % survival to hospital discharge. The extrapolation of data on the circulatory status at the onset of ECMO reveals a 41 % survival to discharge in patients with CS, with the circulatory status being one of the independent predictors of in-hospital mortality at multivariate analysis, together with failed angioplasty and ECLS-related complications. Interestingly, univariate analysis showed a significant negative impact of the time from collapse to ECMO on mortality [27]. This was lately confirmed by Kim and colleagues, who also noted an association between pre-ECMO lactate levels and mortality [28].
Moreover, Bermudez and colleagues recently reported what is common gut feeling: patients presenting for an acutely decompensated chronic heart failure do much worst on ECMO than patients with acute cardiogenic shock, with 2-year survival rates of 11 and 48 %, respectively [29].
Similar results have been reported in a number of small studies and case series.
The available evidence and clinical current practice suggest a careful selection of potential candidates to ECLS and the prompt institution of the extracorporeal support in order to prevent progression of distal organ failure and avoid the progression to an irreversible degree of multiple organ dysfunction [30].
9.6 Patient Care During ECLS
As stated before, extracorporeal support should be commenced as soon as it becomes necessary, avoiding unnecessary and deleterious delays.
Cannulation techniques are described elsewhere in this book.
Once implanted, ECMO management should follow a standardized protocol, though individualized on each patient’s needs.