Cardiogenic shock overview: Difference between revisions
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==Natural history, Complications and Prognosis== | ==Natural history, Complications and Prognosis== | ||
Cardiogenic shock (CS) is a clinical condition, defined as a state of systemic [[hypoperfusion]] originated in [[heart failure|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 [[heart failure|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 [[RAAS|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 [[MI|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. | 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 [[RAAS|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 [[MI|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. | 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. | ||
Revision as of 16:14, 16 January 2020
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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
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 hypotensionunresponsive 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%. .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.
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
The presenting symptoms of cardiogenic shock are variable. The most common clinical manifestations of shock, such as hypotension, altered mental status, oliguria, and cold, clammy skin, can be seen in patients with cardiogenic shock. History plays a very important role in understanding the etiology of the shock and thus helps in the management of cardiogenic shock.The patient should also be assessed for cardiac risk factors: Diabetes mellitus, Tobacco smoking, Hypertension, Hyperlipidemia, A family history of premature coronary artery disease, Age older than 45 in men and older than 55 in women, Physical inactivity.
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
Biomarkers of cardiac myonecrosis are useful to gauge the severity of acute underlying myocardial injury in conditions such as fulminant myocarditis. In ACS, cardiac troponin is noted to be elevated and has a rise-and-fall pattern consistent with acute ischemic injury. A mismatch between the degree of segmental dysfunction on imaging and troponin release may be noted in the setting of stunned/hibernating myocardium or when presentation is significantly delayed after the ischemic insult. Myocardial necrosis biomarker levels may provide an idea of the extent of myocardial injury, whereas serial measurements are useful in assessing early washout after successful reperfusion and in estimating the amount of cardiac necrosis. Natriuretic peptides are significantly elevated in the setting of acute HF culminating in CS and are associated with mortality in MI-associated CS. Oxygen-carrying capacity is the product of cardiac output and the oxygen content of blood. Thus, an ineffective CI will result in inadequate peripheral tissue oxygen delivery. Elevated arterial lactic acid levels are nonspecifically indicative of tissue hypoxia but are associated with mortality in CS.The pathogenesis of lactate production in CS is uncertain, although impaired oxygen delivery, stress-induced hyperlactatemia, and impaired clearance are likely contributors. A peripheral oxygen demand-delivery mismatch will result in low central venous oxygen measurements. A mixed venous oxygen saturation sample is ideally obtained from the distal port of a pulmonary artery catheter (PAC) and is a reflection of oxygen saturation from blood returning to the heart via the superior and inferior vena cava, as well as the coronary sinus. Serial measurements of arterial lactate and mixed venous oxygen saturation levels may be helpful to temporally monitor responses to therapeutic interventions. Arterial blood gas measurements also permit the assessment of [[arterial] oxygenation and ventilation, as well as metabolic and respiratory acid-base disorders. Acute kidney injury, which is reflected by a rise in serum creatinine and a potential reduction in urinary output, in the setting of CS may indicate renal hypoperfusion and is associated with poor outcomes. It should be noted that novel renal biomarkers such as neutrophil gelatinase–associated lipocalcin, kidney injury molecule 1, and cystatin C were not more effective than standard evaluation with serum creatinine for assessing risk. Acute ischemic or congestive liver injury can occur in the setting of CS and manifests as a marked elevation in serum aspartate aminotransferase, alanine aminotransferase, serum bilirubin, and lactate dehydrogenase levels, often accompanied by an increase in prothrombin time with a peak at 24 to 72 hours that subsequently recovers to baseline within 5 to 10 days, and a ratio of alanine aminotransferase to lactate dehydrogenase of <1.5. This should be differentiated from chronic to subacute elevation of liver function abnormalities in the setting of venous congestion resulting from right-sided HF.
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.Chest x-ray provides information on cardiac size and pulmonary congestion and may suggest alternative pathogeneses such as aortic dissection, pericardial effusion, pneumothorax, esophageal perforation, or pulmonary embolism. The test enables clinicians to confirm the position of the endotracheal tube and the position of supportive devices, including temporary pacing wires.
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. Transthoracic and transesophageal (in the case of inadequate visibility) echocardiography is increasingly used for non-invasive hemodynamic assessment and monitoring in the ICU setting. Using echocardiography, it is possible to assess preload, fluid responsiveness, systolic and diastolic cardiac function, and calculate cardiac output, intravascular and intra-cardiac pressures. It is the golden standard in the initial hemodynamic assessment and should be used as complementary tool in invasively monitored patients in the case of new circulatory or respiratory failure. Echocardiography is indispensable in the management of shock patients and is extremely powerful diagnostic role for the cardiac abnormalities (pericardial effusion and tamponade, acute cor pulmonale and acute or chronic valvular disorders) as a cause for hemodynamic instability. It is the most important and suitable method for assessment of right ventricular function, for diagnosis of septic cardiomyopathy and cardiac causes of weaning failure.
CT Scan
The CT scan is usually not recommended as an initial imaging study, when evaluating patients with cardiogenic shock. However, it may be helpful in certain situations, such as: aortic dissection, pulmonary emboli and internal hemorrhage, this last one more related to hypovolemic shock.
MRI
New non-invasive imaging techniques such as cardiovascular magnetic resonance (CMR) imaging promise the non-invasive diagnosis of myocarditis which can be the cause of cardiogenic shock. Considering the hallmarks of acute and chronic myocarditis (accumulation of inflammatory cells; swelling, necrosis and/or apoptosis of cardiomyocytes; increase in extracellular space and water content; myocardial remodelling with fibrotic tissue replacement), an imaging modality such as CMR that enables non-invasive detection of changes in myocardial tissue composition is highly valuable and welcome.
Other Diagnostic Studies
The Swan-ganz catheter, right heart catheter or pulmonary artery catheter has been gradually replaced by echocardiography with color Doppler throughout the years, however, it is still common practice in some centers. It may be used for different situations, such as: confirming the diagnosis of cardiogenic shock following clinical evaluation, ensuring adequacy of filling pressures, establishing the relationship between these filling pressures and cardiac output as well as helping in possible adjustments in therapy. It is still a very important tool for the assessment of hemodynamic parameters, such as cardiac power and stroke work index, which are important data for short-term prognosis.It may also be helpful in distinguishing cardiogenic shock from septic shock and in optimizing the patient's left ventricular filling pressures. The presence of significant V waves (greatly exceeding the pulmonary capillary wedge pressure) on the pulmonary artery tracing suggests either acute mitral regurgitation or a ventricular septal defect. The revascularization procedure may consist of percutaneous coronary intervention procedure or coronary artery bypass graft surgery. Patients who have undergone reperfusion procedures with either percutaneous coronary intervention or fibrinolytic therapy, experiencing new symptoms, should also be evaluated for failure of the initial treatment.
Medical Therapy
Cardiogenic shock is a medical emergency, rescusitive measures should be initiated immediately while the underlying etiology of the cardiogenic shock is promptly investigated. Myocardial infarction (MI) is the most common cause of cardiogenic shock, and when present, prompt revascularization should be performed. Other causes, such as free wall rupture, acute valvular abnormality, or left ventricular septum rupture, may require more invasive interventions. The management plan of cardiogenic shock includes the initiation of resuscitation and general measures, optimization of the blood pressure (pharmacological therapy or mechanical therapy when hypotension is refractory to inotrope and vasopressors), reperfusion or revascularization, and hemodynamic monitoring and stabilization. Urgent revascularization is a priority over hemodynamic monitoring in MI patients with cardiogenic shock and should not be delayed. The first line strategy for reperfusion is percutaneous coronary intervention which is preffered over coronary artery bypass graft (CABG), when PCI or CABG can not be perfomed, fibrinolytic therapy is indicated in the absence of any contraindications.
Surgery
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.
Primary Prevention
The most common causes of cardiogenic shock remain MI. The American College of Cardiology and American Heart Association, in collaboration with the Canadian Cardiovascular Society, have issued an update of the 2004 guideline for the management of patients with ST-segment elevation myocardial infarction. The American Academy of Family Physicians endorses and accepts this guideline as its policy. Early recognition and prompt initiation of reperfusion therapy remains the cornerstone of management of ST-segment elevation myocardial infarction. Aspirin should be given to symptomatic patients. Beta blockers should be used cautiously in the acute setting because they may increase the risk of cardiogenic shock and death. The combination of clopidogrel and aspirin is indicated in patients who have had ST-segment elevation myocardial infarction. A stepped care approach to analgesia for musculoskeletal pain in patients with coronary heart disease is provided. Cyclooxygenase inhibitors and nonsteroidal anti-inflammatory drugs increase mortality risk and should be avoided. Primary prevention is important to reduce the burden of heart disease.
Secondary Prevention
Secondary prevention includes early detection and halting the progression of established but asymptomatic disease. For CAD, this includes taking measures to prevent cardiovascular symptoms (e.g., dyspnea), damage (e.g., ventricular dysfunction), and events (e.g., acute coronary syndromes). However, once such symptoms, damage, or events occur, it is too late for secondary prevention.