Cardiogenic shock overview: Difference between revisions
| Line 3: | Line 3: | ||
{{CMG}}; {{AE}} {{JS}} {{sali}} | {{CMG}}; {{AE}} {{JS}} {{sali}} | ||
==Overview== | ==Overview== | ||
Before the routine use of early revascularization, MI-associated CS had an in-hospital mortality exceeding 80%. A registry trial of 250 patients with acute MI described the association between bedside physical examination (Killip classification) for the assessment of heart failure (HF) and the risk of mortality. Patients with Killip class IV (CS) had a mortality of 81%. Subsequently, the Diamond and Forrester classification using right-sided heart catheterization described the role of cardiac hemodynamics in stratifying risk after acute MI in the prereperfusion era. Patients in Diamond and Forrester subgroup IV with a pulmonary capillary wedge pressure (PCWP) >18 mm Hg and a cardiac index (CI) <2.2 L·min−1·m−2, indicative of CS, had a mortality of 51%. Treatment efforts to reduce mortality initially focused on improvement of hemodynamic parameters by mechanical devices. The intra-aortic balloon pump (IABP), introduced in a registry cooperative trial, decreased systolic blood pressure (SBP), increased diastolic blood pressure, and modestly but significantly increased CI. Nevertheless, mortality remained virtually unchanged, with only 15 survivors among 87 patients (83% mortality). The early reperfusion era did not affect outcomes for shock complicating acute MI. Fibrinolysis was effective for patients with ST-segment–elevation MI (STEMI) in general, but it is less clear if fibrinolysis reduces mortality in those with CS.The first major breakthrough in CS treatment was achieved by the randomized SHOCK trial. Although an early invasive strategy coupled with percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) did not reduce 30-day mortality (the primary outcome of the trial), a significant mortality reduction emerged at 6 and 12 months that persisted at longer-term follow-up. Subsequent registries confirmed the survival advantage of early revascularization. Further efforts to reduce CS mortality have been directed toward improvements in MCS devices. The largest randomized trial in patients with acute MI complicated by CS did not show a benefit with routine IABP placement in addition to revascularization. As a result, there has been a decrease in the use of IABPs in clinical practice and a downgrading in guideline recommendations. Recently, other percutaneous MCS devices have shown promise in the treatment of CS, but more data from randomized clinical trials are needed. | Acute cardiac hemodynamic instability may result from disorders that impair function of the myocardium, valves, conduction system, or pericardium, either in isolation or in combination. CS is pragmatically defined as a state in which ineffective cardiac output caused by a primary cardiac disorder results in both clinical and biochemical manifestations of inadequate tissue perfusion. The clinical presentation is typically characterized by persistent hypotension unresponsive to volume replacement and is accompanied by clinical features of end-organ hypoperfusion requiring intervention with pharmacological or mechanical support. Although not mandated, objective hemodynamic parameters for CS can help confirm the diagnosis and enable comparison across cohorts and clinical trials. Definitions in clinical practice guidelines and operationalized definitions used in the SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) and IABP-SHOCK II (Intraaortic Balloon Pump in Cardiogenic Shock II) trials.Before the routine use of early revascularization, MI-associated CS had an in-hospital mortality exceeding 80%. A registry trial of 250 patients with acute MI described the association between bedside physical examination (Killip classification) for the assessment of heart failure (HF) and the risk of mortality. Patients with Killip class IV (CS) had a mortality of 81%. Subsequently, the Diamond and Forrester classification using right-sided heart catheterization described the role of cardiac hemodynamics in stratifying risk after acute MI in the prereperfusion era. Patients in Diamond and Forrester subgroup IV with a pulmonary capillary wedge pressure (PCWP) >18 mm Hg and a cardiac index (CI) <2.2 L·min−1·m−2, indicative of CS, had a mortality of 51%. Treatment efforts to reduce mortality initially focused on improvement of hemodynamic parameters by mechanical devices. The intra-aortic balloon pump (IABP), introduced in a registry cooperative trial, decreased systolic blood pressure (SBP), increased diastolic blood pressure, and modestly but significantly increased CI. Nevertheless, mortality remained virtually unchanged, with only 15 survivors among 87 patients (83% mortality). The early reperfusion era did not affect outcomes for shock complicating acute MI. Fibrinolysis was effective for patients with ST-segment–elevation MI (STEMI) in general, but it is less clear if fibrinolysis reduces mortality in those with CS.The first major breakthrough in CS treatment was achieved by the randomized SHOCK trial. Although an early invasive strategy coupled with percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) did not reduce 30-day mortality (the primary outcome of the trial), a significant mortality reduction emerged at 6 and 12 months that persisted at longer-term follow-up. Subsequent registries confirmed the survival advantage of early revascularization. Further efforts to reduce CS mortality have been directed toward improvements in MCS devices. The largest randomized trial in patients with acute MI complicated by CS did not show a benefit with routine IABP placement in addition to revascularization. As a result, there has been a decrease in the use of IABPs in clinical practice and a downgrading in guideline recommendations. Recently, other percutaneous MCS devices have shown promise in the treatment of CS, but more data from randomized clinical trials are needed. | ||
==Historical Perspective== | ==Historical Perspective== | ||
Revision as of 15:52, 31 December 2019
|
Cardiogenic Shock Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Cardiogenic shock overview On the Web |
|
American Roentgen Ray Society Images of Cardiogenic shock overview |
|
Risk calculators and risk factors for Cardiogenic shock overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3]
Overview
Acute cardiac hemodynamic instability may result from disorders that impair function of the myocardium, valves, conduction system, or pericardium, either in isolation or in combination. CS is pragmatically defined as a state in which ineffective cardiac output caused by a primary cardiac disorder results in both clinical and biochemical manifestations of inadequate tissue perfusion. The clinical presentation is typically characterized by persistent hypotension unresponsive to volume replacement and is accompanied by clinical features of end-organ hypoperfusion requiring intervention with pharmacological or mechanical support. Although not mandated, objective hemodynamic parameters for CS can help confirm the diagnosis and enable comparison across cohorts and clinical trials. Definitions in clinical practice guidelines and operationalized definitions used in the SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) and IABP-SHOCK II (Intraaortic Balloon Pump in Cardiogenic Shock II) trials.Before the routine use of early revascularization, MI-associated CS had an in-hospital mortality exceeding 80%. A registry trial of 250 patients with acute MI described the association between bedside physical examination (Killip classification) for the assessment of heart failure (HF) and the risk of mortality. Patients with Killip class IV (CS) had a mortality of 81%. Subsequently, the Diamond and Forrester classification using right-sided heart catheterization described the role of cardiac hemodynamics in stratifying risk after acute MI in the prereperfusion era. Patients in Diamond and Forrester subgroup IV with a pulmonary capillary wedge pressure (PCWP) >18 mm Hg and a cardiac index (CI) <2.2 L·min−1·m−2, indicative of CS, had a mortality of 51%. Treatment efforts to reduce mortality initially focused on improvement of hemodynamic parameters by mechanical devices. The intra-aortic balloon pump (IABP), introduced in a registry cooperative trial, decreased systolic blood pressure (SBP), increased diastolic blood pressure, and modestly but significantly increased CI. Nevertheless, mortality remained virtually unchanged, with only 15 survivors among 87 patients (83% mortality). The early reperfusion era did not affect outcomes for shock complicating acute MI. Fibrinolysis was effective for patients with ST-segment–elevation MI (STEMI) in general, but it is less clear if fibrinolysis reduces mortality in those with CS.The first major breakthrough in CS treatment was achieved by the randomized SHOCK trial. Although an early invasive strategy coupled with percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) did not reduce 30-day mortality (the primary outcome of the trial), a significant mortality reduction emerged at 6 and 12 months that persisted at longer-term follow-up. Subsequent registries confirmed the survival advantage of early revascularization. Further efforts to reduce CS mortality have been directed toward improvements in MCS devices. The largest randomized trial in patients with acute MI complicated by CS did not show a benefit with routine IABP placement in addition to revascularization. As a result, there has been a decrease in the use of IABPs in clinical practice and a downgrading in guideline recommendations. Recently, other percutaneous MCS devices have shown promise in the treatment of CS, but more data from randomized clinical trials are needed.
Historical Perspective
The term "cardiogenic shock" is thought to have first arisen in 1942 with Stead who, after studying a series of two patients, described them as having a "shock of cardiac origin". This designation would later be rephrased as "cardiogenic shock". However, the clinical features of cardiogenic shock had first been described by Herrick, in 1912, who noticed in severe coronary artery disease patients a profound weakness, a rapid pulse, pulmonary rales, faint cardiac tones, cyanosis and dyspnea. Despite its still high incidence and mortality nowadays, cardiogenic shock has seen its impact decreased throughout the years. Particularly since the 1970's, when the mortality rate for this condition was about 80-90%, these values have been decreasing since then, particularly due to the earlier diagnosis and better management of CS, with more effective reperfusion techniques. Today the its mortality rate is about 50%.
Classification
The Society for Cardiovascular Angiography and Intervention (SCAI) developed an expert consensus statement, endorsed by multiple relevant societies, proposing a novel CS classification scheme, which categorizes patients with or at risk of CS into worsening stages of hemodynamic compromise for the purposes of facilitating patient care and research. The SCAI CS classification consensus statement describes 5 stages of CS, each of which may have an “A” modifier signifying the occurrence of cardiac arrest (CA). This classification schema was developed based on expert consensus opinion and its ability to discriminate among levels of mortality risk in critically ill patients remains to be established. The goal of this study was to examine the construct validity of the SCAI CS staging schema by demonstrating the ability of a simple functional classification of SCAI shock stages at the time of cardiac intensive care unit (CICU) admission to predict mortality in CICU patients.The purpose of the classification schema is to assist in clear communication among clinicians and researchers regarding the patient’s current clinical status, recognizing that CS encompasses a spectrum, including those at high risk of developing shock from myocardial dysfunction to those who develop hemodynamic collapse and cardiac arrest. The CS classification schema includes five stages of shock labeled A through E. The authors categorized patients in three domains, including laboratory findings, physical exams findings, and hemodynamics. When cardiac arrest has occurred the modifier (A) is added to stage classification (i.e. stage CA).
Pathophysiology
The pathophysiology of cardiogenic shock is complex and not fully understood. Ischemia to the myocardium causes derangement to both systolic and diastolic left ventricular function, resulting in a profound depression of myocardial contractility. This, in turn, leads to a potentially catastrophic and vicious spiral of reduced cardiac output and low blood pressure, perpetuating further coronary ischemia and impairment of contractility. Several physiologic compensatory processes ensue. These include:The activation of the sympathetic system leading to peripheral vasoconstriction which may improve coronary perfusion at the cost of increased afterload, and Tachycardia which increases myocardial oxygen demand and subsequently worsens myocardial ischemia.These compensatory mechanisms are subsequently counteracted by pathologic vasodilation that occurs from the release of potent systemic inflammatory markers such as interleukin-1, tumor necrosis factor a, and interleukin-6. Additionally, higher levels of nitric oxide and peroxynitrite are released, which also contribute to pathologic vasodilation and are known to be cardiotoxic. Unless interrupted by adequate treatment measures, this self-perpetuating cycle leads to global hypoperfusion and the inability to effectively meet the metabolic demands of the tissues, progressing to multiorgan failure and eventually death.
Causes
The most common cause of cardiogenic shock is acute myocardial infarction with left ventricular dysfunction. Less commonly, right ventricular myocardial infarction can lead to cardiogenic shock. Other causes of cardiogenic shock include mechanical injuries such as acute valvular regurgitation or rupture, free wall rupture, and ventricular septum rupture.
Epidemiology and Demographics
In defiance of the historic numbers of mortality from cardiogenic shock of 80% to 90%, in the modern era, this type of shock comprises a mortality risk of around 50%, in the face of the diagnostic and treatment techniques, which have greatly been developed in recent years. Depending on the demographic and clinical factors, this risk can range from 10% to 80%. The incidence of cardiogenic shock among patients with acute MI is approximately 5% to 10%. Because atherosclerosis and myocardial infarction are both more frequent among males, cardiogenic shock is more common in this gender. However, because women tend to present with acute myocardial infarction at a later age, along with the fact that they have a greater chance of having multivessel coronary artery disease when they first develop symptoms, a greater proportion of women with acute MI develop cardiogenic shock.
Risk Factors
The identification of high-risk groups for developing cardiogenic shock and its promoting factors is mandatory for the improvement of the survival rate of these patients. This will facilitate the providing of adequate therapeutic measures and the avoidance of others which would otherwise lead to iatrogenic shock. Considering that the most common cause of cardiogenic shock is acute coronary syndrome, either with or without persistent ST-segment elevation, these patients are at higher risk and will benefit highly from these measures.
Natural history, Complications and Prognosis
Cardiogenic shock (CS) is a clinical condition, defined as a state of systemic hypoperfusion originated in cardiac failure, in the presence of adequate intravascular volume, typically followed by hypotension, which leads to insufficient ability to meet oxygen and nutrient demands of organs and other peripheral tissues.It may range from mild to severe hypoperfusion and may be defined in terms of hemodynamic parameters, which according to most studies, means a state in which systolic blood pressure is persistently < 90 mm Hg or < 80 mm Hg, for longer than 1 hour, with adequate or elevated left and right ventricular filling pressures that does not respond to isolated fluid administration, is secondary to cardiac failure and occurs with signs of hypoperfusion (oliguria, cool extremities, cyanosis and altered mental status) or a cardiac index of < 2.2 L/min/m² (on inotropic, vasopressor or circulatory device support) or < 1.8-2.2 L/min/m² (off support) and pulmonary artery wedge pressure > 18 mm Hg. In the presence of CS, a pathological cycle develops in which ischemia, the initial aggression, leads to myocardial dysfunction. This will affect parameters like the cardiac output, stroke volume and myocardial perfusion thereby worsening the ischemia. The body will then initiate a series of compensatory mechanisms, such as sympathetic stimulation of the heart and activation of the renin/angiotensin/aldosterone system, trying to overcome the cardiac aggression, however, this will ultimately lead to a downward spiral worsening of the ischemia. Inflammatory mediators, originated in the infarcted area, will also intervene at some point causing myocardial depression, decreasing contractility and worsening hypotension. Lactic acidosis will also develop, resulting from the poor tissue perfusion, that is responsible for a shift in metabolism to glycolysis, which will further depress the myocardium, thereby worsening the clinical scenario. CS has several risk factors which will contribute to the progression of the condition. Depending on these underlying factors and in concordance to the pathological mechanism responsible for the development of CS, the patient will have higher or lower probability of developing complications, of which the most common are cardiac, renal and pulmonary. The presence of certain risk factors and the etiology behind the shock will dictate the outcome of the condition. Despite the decreasing incidence and mortality rate seen throughout recent years, CS is still associated with a poor prognosis, particularly in elderly patients.
Diagnosis
Attending to the catastrophic outcome of cardiogenic shock in a very short time span, its diagnosis must be reached as early as possible in order for proper therapy to be started. This period until diagnosis and treatment initiation is particularly important in the case of cardiogenic shock since the mortality rate of this condition complicating acute-MI is very high, along with the fact that the ability to revert the damage caused, through reperfusion techniques, declines considerably with diagnostic delays. Therefore and due to the unstable state of these patients, the diagnostic evaluations are usually performed as supportive measures are initiated. The diagnostic measures should start with the proper history and physical examination, including blood pressure measurement, followed by an EKG, echocardiography, chest x-ray and collection of blood samples for evaluation. The physician should keep in mind the common features of shock, irrespective of the type of shock, in order to avoid delays in the diagnosis. Although not all shock patients present in the same way, these features include: abnormal mental status, cool extremities, clammy skin, manifestations of hypoperfusion, such as hypotension and oliguria, as well as evidence of metabolic acidosis on the blood results.
History and Symptoms
Attending to the catastrophic outcome of cardiogenic shock in a very short time span, its diagnosis must be reached as early as possible in order for proper therapy to be started. This period until diagnosis and treatment initiation is particularly important in the case of cardiogenic shock since the mortality rate of this condition complicating acute-MI is very high, along with the fact that the ability to revert the damage caused, through reperfusion techniques, declines considerably with diagnostic delays. Therefore and due to the unstable state of these patients, the diagnostic evaluations are usually performed as supportive measures are initiated. The diagnostic measures should start with the proper history and physical examination, including blood pressure measurement, followed by an EKG, echocardiography, chest x-ray and collection of blood samples for evaluation. The physician should keep in mind the common features of shock, irrespective of the type of shock, in order to avoid delays in the diagnosis. Although not all shock patients present in the same way, these features include: abnormal mental status, cool extremities, clammy skin, manifestations of hypoperfusion, such as hypotension and oliguria, as well as evidence of metabolic acidosis on the blood results.
Physical Examination
Physical examination findings in patients with cardiogenic shock include the following: Altered mental status, cyanosis, cold and clammy skin, mottled extremities Peripheral pulses are faint, rapid and sometimes irregular if there is an underlying arrhythmia, Jugular venous distension, Diminished heart sounds, S3 or S4, may be present, murmurs in the presence of valvular disorders such as mitral regurgitation or aortic stenosis, Pulmonary vascular congestion may be associated with rales Peripheral edema may be present in the setting of fluid overload.
Laboratory Finding
Attending to the catastrophic outcome of cardiogenic shock in a very short time span, its diagnosis must be reached as early as possible in order for proper therapy to be started. This period until diagnosis and treatment initiation is particularly important in the case of cardiogenic shock since the mortality rate of this condition complicating acute-MI is very high, along with the fact that the ability to revert the damage caused, through reperfusion techniques, declines considerably with diagnostic delays. Therefore and due to the unstable state of these patients, the diagnostic evaluations are usually performed as supportive measures are initiated. The diagnostic measures should start with the proper history and physical examination, including blood pressure measurement, followed by an EKG, echocardiography, chest x-ray and collection of blood samples for evaluation. The physician should keep in mind the common features of shock, irrespective of the type of shock, in order to avoid delays in the diagnosis. Although not all shock patients present in the same way, these features include: abnormal mental status, cool extremities, clammy skin, manifestations of hypoperfusion, such as hypotension and oliguria, as well as evidence of metabolic acidosis on the blood results.
Electrocardiogram
An electrocardiogram may be useful in distinguishing cardiogenic shock from septic shock or neurogenic shock. A diagnosis of cardiogenic shock is suggested by the presence of ST segment changes, new left bundle branch block or signs of a cardiomyopathy. Cardiac arrhythmias may also be present.
Chest X-ray
The chest x ray will show pulmonary edema, pulmonary vascular redistribution, enlarged hila, kerley's B lines, and bilateral pleural effusions in patients with left ventricular failure. In contrast, a pneumonia may be present in the patient with septic shock.
Echocardiography
Echocardiography is an important imaging modality for the evaluation of the patient with cardiogenic shock. This test will allow the identification of certain characteristics that, when complemented by a proper medical history and physical examination, will likely prompt to the diagnosis. These may include: poor wall motion, papillary muscle rupture, pseudoaneurysms, ventricular septal defects, among others. The echocardiographic findings may also suggest or rule out a different diagnosis. The test will provide information about the overall hemodynamic status of the heart as well, which may reveal to be vital in order to plan further measures and predict the outcome.
Treatment
Cardiogenic shock is considered an emergency and irrespectively to the therapeutic approach, the target goal of any therapy is prompt revascularization of ischemic myocardium. This should be achieved in the shortest timespan possible. There are two major categories of treatment for cardiogenic shock, the medical/conservative approach and the interventional approach. The ideal treatment combines both mechanisms, in which medical therapy, after restored filling pressures, allows hemodynamical stabilization of the patient, until interventional methods, that contribute to the reversal of the process leading to the shock state, may performed. The interventional approach may include PCI or coronary artery bypass graft surgery (CABG) and in both techniques the goal is not only reperfusion of the occluded coronary artery, but also prevention of vessel reoclusion. If there is no access to a cardiac catheterization facility, nor the possibility of transferring the patient to one within 90 minutes, then immediately thrombolytic therapy should be considered. Other important factors to increase the chances of a better outcome are: mechanical ventilation, in order to improve tissue oxygenation, and close monitoring of the therapeutic dosages, particularly of vasoactive drugs, since these have been associated with excess mortality due to toxicity effects.Also, it is recommended invasive hemodynamic monitoring, in order to monitor and guide the effects of the therapy as well as the overall status of the patient. The success of reperfusion is usually suggested by the relief of symptoms, restoration of hemodynamic parameters and electrical stability, as well as the reduction of at least 50% in the ST-segment on the EKG, in the case of a STEMI.