Cardiogenic shock overview: Difference between revisions
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==History and Symptoms== | ==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 [[therapy|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 [[medical history|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. | 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 [[therapy|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 [[medical history|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== | ==Laboratory Finding== | ||
Revision as of 14:52, 31 December 2019
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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
Cardiogenic shock is defined as a state of systemic hypoperfusion, originated in cadiac failure in the presence of adequate intravascular volume, typically followed by hypotension, which results in the 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. It is secondary to cardiac failure. it occurs with signs of hypoperfusion (oliguria, cool extremities, cyanosis and altered mental status) or a cardiac index of < 2.2 L/min/m², if on inotropic, vasopressor or circulatory device support, or < 1.8-2.2 L/min/m², if off support, and pulmonary artery wedge pressure > 18 mm Hg. Despite the importance of these values, the diagnosis of shock is primarily based on the clinical findings and only then, supported by the measurement of hemodynamic values, which may be obtained through pulmonary artery catheterization or doppler echocardiography. The level of hemodynamic derangement will directly dictate the short-term outcome of the patient. Although there are several possible causes for cardiogenic shock, the most common remain the myocardial infarction and the left ventricular failure. Nevertheless, it is important to exclude possible mechanical complications, which in the presence of myocardial infarction might be responsible for the shock. Despite the improvements made in the earlier diagnosis, prompt and adequate treatment and resources for patients presenting with myocardial infarction, cardiogenic shock remains as the most common cause of death in patients following MI. However, evidence shows that patients in cardiogenic shock may benefit greatly from an invasive early approach, increasing their chances of short and long-term survival and quality of life.
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
Cardiogenic shock 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.[1] 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.
Pathophysiology
Cardiogenic shock 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 cardiogenic shock 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.
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.