Management of Cardiogenic Shock Complicating ACS
Management of Cardiogenic Shock Complicating ACS
Cardiogenic shock (CS) remains the leading cause of mortality in patients hospitalised with acute myocardial infarction (AMI). Recent guidelines supporting a strategy of early revascularisation (ERV) have led to some improvements in the outcomes of this patient subset. However, despite significant improvements in treatment, the mortality rate associated with CS in the context of AMI remains high, especially in those patients who present to hospital late or have delayed coronary reperfusion. This article aims to review the available data relating to this important condition, and provide guidelines for current best practice in the management of CS.
CS is a condition characterised by inadequate tissue perfusion, usually in the setting of AMI. There have been many definitions applied to the diagnosis of CS, but the most uniformly accepted clinical definition of CS is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. Haemodynamic criteria are also important in the diagnosis of CS. The most important are sustained hypotension (systolic blood pressure (BP) <90 mm Hg for at least 1 h) and a reduced cardiac index (<2.2 l/min/m) in the presence of elevated pulmonary capillary wedge pressure (PCWP) >18 mm Hg.
There are inconsistencies in the reported incidence of CS. These inconsistencies may be largely related to the varying definitions that have been adopted to describe this clinical entity. Additionally, the true incidence of CS complicating AMI may be underestimated since a proportion of patients will die before arrival at hospital. Given these limitations, the historically reported incidence of CS complicating AMI is between 5–8%. There is contemporary evidence that the rate of CS complicating ST elevation myocardial infarction (STEMI) has seen a small decrease in incidence, which in part may be due to the more rapid diagnosis and better hospital based treatment of STEMI.
The Swiss AMIS Plus registry data found that percutaneous coronary intervention (PCI) was independently associated with lower risk of CS development during hospitalisation in acute coronary syndrome (ACS) patients who were not already in CS upon admission (odds ratio (OR) 0.59, 95% confidence interval (CI) 0.39 to 0.89; p=0.012). This study also highlighted that while rates of CS developing during hospitalisation have decreased (between 1997 and 2006) from 10.6% to 2.7% (p<0.001), the admission CS rates have remained essentially unchanged at approximately 2%. In a US study examining the outcomes of over 10 000 patients with STEMI over a 20 year period, the incidence of CS decreased in elderly patients (>75 years) but did not significantly change among younger patients. In women the incidence of new onset CS complicating STEMI decreased in all age groups over time. The improvement in outcomes in elderly patients with STEMI may be due to the more frequent and widespread use of cardiac catheterisation and PCI in elderly patients, which will be discussed later in this article.
The diagnosis of CS should be made when other mechanisms of hypotension, such as hypovolaemia, vasovagal reactions, anaphylaxis, electrolyte disturbances, pharmacological side effects, sepsis or arrhythmias, have been excluded. It is usually associated with extensive left ventricular damage, but may occur with predominant right ventricular infarction in the context of occlusion of the right coronary artery. A list of possible aetiological mechanisms is detailed in Table 1. Although extensive myocardial infarction with significant left and/or right ventricular dysfunction is the most common mechanism of CS, less extensive STEMI, or non-ST elevation myocardial infarction (NSTEMI), may also result in CS in patients with pre-existing cardiac dysfunction. Other causes of CS include mechanical complications which occur as a result of myocardial infarction. These include acute severe mitral regurgitation (MR) (figure 1), interventricular septal rupture resulting in ventricular septal defect, and left ventricular free wall rupture. In the SHOCK (SHould we emergently revascularise Occluded Coronary arteries for shocK) registry of 1160 patients, 74.5% had predominantly left ventricular failure, 8.3% had MR, 4.6% had ventricular septal rupture, 3.4% had isolated right ventricular shock, 1.7% had tamponade or cardiac rupture, and 8% had shock that was the result of other causes. In patients with suspected CS, ventricular function and associated mechanical complications should be evaluated urgently by two dimensional echocardiography. Haemodynamic assessment of pulmonary filling pressure ('wedge pressure') with a balloon flotation catheter should be considered if there is any doubt relating to volume or haemodynamic status.
(Enlarge Image)
Figure 1.
Transthoracic echocardiogram apical two chamber view demonstrating acute severe mitral regurgitation (MR).
Intrinsic myocardial disease such as myocarditis and cardiomyopathies, or even dynamic outflow tract obstruction, may result in CS. Shock may be part of the presenting syndrome, but may also develop over the subsequent hours after hospital admission. Patients in the SHOCK registry developed signs of CS at a median of 7 h after myocardial infarction, and 75% developed CS within 24 h. Similar results were found in the GUSTO-1 study (Global Utilisation of Streptokinase and Tissue plasminogen activator for Occluded coronary arteries).
Factors that increase the risk of developing CS in the context of STEMI include older age, female sex, anterior STEMI, hypertension, type II diabetes mellitus, multivessel coronary artery disease (CAD), prior STEMI or angina, STEMI with new left bundle branch block, and prior diagnosis of heart failure (table 2).
Early recognition of the signs of CS is paramount to allow the initiation of interventions that may influence outcome. There is a wide spectrum of clinical symptoms, signs and haemodynamic findings, and variability in the severity of CS. The physician must be alert to the signs of inadequate tissue perfusion as it is possible for patients with significant anterior infarction to develop clinical signs, and biochemical markers of tissue hypoperfusion, while they maintain a systolic BP >90 mm Hg.
Many patients with CS progress to multiorgan failure. A systemic inflammatory response syndrome (SIRS)-like pathophysiological process is described to occur in CS patients, similar to patients with septic shock. This is characterised by raised concentrations of inflammatory markers (white blood cells, interleukins, C reactive protein) and pyrexia (which is often seen in patients with extensive myocardial infarction). It has previously been shown in studies of septic shock patients with multiorgan failure that serial APACHE (Acute Physiology and Chronic Health Outcomes Evaluation) II scores can predict prognosis, whereby survivors show significant improvement in APACHE II score (≥4 point drop) from admission to day 4 compared with non-survivors. The physiological parameters assessed in the APACHE II score are detailed in Table 3. A more recent study of serial APACHE II scores in CS patients has found that a similar reduction in scores by day 4 can distinguish survivors from non-survivors. This non-invasive tool may also provide a means to predict the effect of therapeutic interventions on the outcome of patients in CS. In the same study the investigators found that changes in cardiac index and interleukin 6 were less reliable than APACHE II score at predicting survivors of CS.
A CS severity scoring system has been developed from analysis of the original SHOCK trial and registry patient data. Mortality ranged from 22–88%, depending on score category. ERV was of greatest benefit in moderate-to-high risk patients. End organ hypoperfusion and anoxic brain injury were both independent predictors of death. However, these CS patients were all treated between 1993 and 1999, when CS management may not have been reflective of current practice and technology. Further work is needed in this area of prognostication for CS.
Abstract and Introduction
Abstract
Cardiogenic shock (CS) remains the leading cause of mortality in patients hospitalised with acute myocardial infarction (AMI). Recent guidelines supporting a strategy of early revascularisation (ERV) have led to some improvements in the outcomes of this patient subset. However, despite significant improvements in treatment, the mortality rate associated with CS in the context of AMI remains high, especially in those patients who present to hospital late or have delayed coronary reperfusion. This article aims to review the available data relating to this important condition, and provide guidelines for current best practice in the management of CS.
Definition
CS is a condition characterised by inadequate tissue perfusion, usually in the setting of AMI. There have been many definitions applied to the diagnosis of CS, but the most uniformly accepted clinical definition of CS is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. Haemodynamic criteria are also important in the diagnosis of CS. The most important are sustained hypotension (systolic blood pressure (BP) <90 mm Hg for at least 1 h) and a reduced cardiac index (<2.2 l/min/m) in the presence of elevated pulmonary capillary wedge pressure (PCWP) >18 mm Hg.
Incidence
There are inconsistencies in the reported incidence of CS. These inconsistencies may be largely related to the varying definitions that have been adopted to describe this clinical entity. Additionally, the true incidence of CS complicating AMI may be underestimated since a proportion of patients will die before arrival at hospital. Given these limitations, the historically reported incidence of CS complicating AMI is between 5–8%. There is contemporary evidence that the rate of CS complicating ST elevation myocardial infarction (STEMI) has seen a small decrease in incidence, which in part may be due to the more rapid diagnosis and better hospital based treatment of STEMI.
The Swiss AMIS Plus registry data found that percutaneous coronary intervention (PCI) was independently associated with lower risk of CS development during hospitalisation in acute coronary syndrome (ACS) patients who were not already in CS upon admission (odds ratio (OR) 0.59, 95% confidence interval (CI) 0.39 to 0.89; p=0.012). This study also highlighted that while rates of CS developing during hospitalisation have decreased (between 1997 and 2006) from 10.6% to 2.7% (p<0.001), the admission CS rates have remained essentially unchanged at approximately 2%. In a US study examining the outcomes of over 10 000 patients with STEMI over a 20 year period, the incidence of CS decreased in elderly patients (>75 years) but did not significantly change among younger patients. In women the incidence of new onset CS complicating STEMI decreased in all age groups over time. The improvement in outcomes in elderly patients with STEMI may be due to the more frequent and widespread use of cardiac catheterisation and PCI in elderly patients, which will be discussed later in this article.
Aetiology
The diagnosis of CS should be made when other mechanisms of hypotension, such as hypovolaemia, vasovagal reactions, anaphylaxis, electrolyte disturbances, pharmacological side effects, sepsis or arrhythmias, have been excluded. It is usually associated with extensive left ventricular damage, but may occur with predominant right ventricular infarction in the context of occlusion of the right coronary artery. A list of possible aetiological mechanisms is detailed in Table 1. Although extensive myocardial infarction with significant left and/or right ventricular dysfunction is the most common mechanism of CS, less extensive STEMI, or non-ST elevation myocardial infarction (NSTEMI), may also result in CS in patients with pre-existing cardiac dysfunction. Other causes of CS include mechanical complications which occur as a result of myocardial infarction. These include acute severe mitral regurgitation (MR) (figure 1), interventricular septal rupture resulting in ventricular septal defect, and left ventricular free wall rupture. In the SHOCK (SHould we emergently revascularise Occluded Coronary arteries for shocK) registry of 1160 patients, 74.5% had predominantly left ventricular failure, 8.3% had MR, 4.6% had ventricular septal rupture, 3.4% had isolated right ventricular shock, 1.7% had tamponade or cardiac rupture, and 8% had shock that was the result of other causes. In patients with suspected CS, ventricular function and associated mechanical complications should be evaluated urgently by two dimensional echocardiography. Haemodynamic assessment of pulmonary filling pressure ('wedge pressure') with a balloon flotation catheter should be considered if there is any doubt relating to volume or haemodynamic status.
(Enlarge Image)
Figure 1.
Transthoracic echocardiogram apical two chamber view demonstrating acute severe mitral regurgitation (MR).
Intrinsic myocardial disease such as myocarditis and cardiomyopathies, or even dynamic outflow tract obstruction, may result in CS. Shock may be part of the presenting syndrome, but may also develop over the subsequent hours after hospital admission. Patients in the SHOCK registry developed signs of CS at a median of 7 h after myocardial infarction, and 75% developed CS within 24 h. Similar results were found in the GUSTO-1 study (Global Utilisation of Streptokinase and Tissue plasminogen activator for Occluded coronary arteries).
Factors that increase the risk of developing CS in the context of STEMI include older age, female sex, anterior STEMI, hypertension, type II diabetes mellitus, multivessel coronary artery disease (CAD), prior STEMI or angina, STEMI with new left bundle branch block, and prior diagnosis of heart failure (table 2).
Identification of Patients at Risk
Early recognition of the signs of CS is paramount to allow the initiation of interventions that may influence outcome. There is a wide spectrum of clinical symptoms, signs and haemodynamic findings, and variability in the severity of CS. The physician must be alert to the signs of inadequate tissue perfusion as it is possible for patients with significant anterior infarction to develop clinical signs, and biochemical markers of tissue hypoperfusion, while they maintain a systolic BP >90 mm Hg.
Risk Scoring Models
Many patients with CS progress to multiorgan failure. A systemic inflammatory response syndrome (SIRS)-like pathophysiological process is described to occur in CS patients, similar to patients with septic shock. This is characterised by raised concentrations of inflammatory markers (white blood cells, interleukins, C reactive protein) and pyrexia (which is often seen in patients with extensive myocardial infarction). It has previously been shown in studies of septic shock patients with multiorgan failure that serial APACHE (Acute Physiology and Chronic Health Outcomes Evaluation) II scores can predict prognosis, whereby survivors show significant improvement in APACHE II score (≥4 point drop) from admission to day 4 compared with non-survivors. The physiological parameters assessed in the APACHE II score are detailed in Table 3. A more recent study of serial APACHE II scores in CS patients has found that a similar reduction in scores by day 4 can distinguish survivors from non-survivors. This non-invasive tool may also provide a means to predict the effect of therapeutic interventions on the outcome of patients in CS. In the same study the investigators found that changes in cardiac index and interleukin 6 were less reliable than APACHE II score at predicting survivors of CS.
A CS severity scoring system has been developed from analysis of the original SHOCK trial and registry patient data. Mortality ranged from 22–88%, depending on score category. ERV was of greatest benefit in moderate-to-high risk patients. End organ hypoperfusion and anoxic brain injury were both independent predictors of death. However, these CS patients were all treated between 1993 and 1999, when CS management may not have been reflective of current practice and technology. Further work is needed in this area of prognostication for CS.
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