Cardiogenic shock

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammad Salih, MD. João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

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.

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.

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).

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.

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.

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.

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.

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.

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.

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 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.

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.

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.

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 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.

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.

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.

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.

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.

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.

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 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.

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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]

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%.

• Posttraumatic syndrome was first decribed by the Greek physicians, Hippocrates and Galen.
• The term shock would only be introduced in 1743 by the English physician Clarke, after the mistranslation of the work of French surgeon Henri Fraçois Le Dran, who in 1737 had written “A Treatise of of Reflections Drawn from Experience with Gunshot Wounds”, in which he had described the term “choc” as a result of a severe impact or jolt.
• Clarke defined it as a sudden deterioration of a patient’s condition following a severe trauma.
• The concept would then be spread by Edwin A. Moses, who in 1867 used it in his “A Practical Treatise on Shock after Operations and Injuries”, defining it as an “effect on the animal system, produced by violent injuries from any cause, or from violent mental emotions”.^[1]
• 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”.^[2] 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.^[3]
• In 1967, after studying a series of 250 patients with acute MI, Killip and Kimball proposed a clinical classification of hemodynamic status, which included 4 classes and that is still in widespread use:^[4]
  • I – no clinical signs of heart failure
  • II – S3 gallop and/or basilar rales on lung auscultation and/or elevated JVP
  • III – Pulmonary edema
  • IV – Cardiogenic shock
• Throughout the years the outcome of cardiogenic shock has been improving, with a decrease in mortality seen particularly during the 1990’s.
• According to the studies, from 1975 to 1990, the in-hospital mortality from this condition averaged 77%. Between 1993 and 1995 this percentage declined to 61%, reaching about 59% in 1997.
• For this decrease, revascularization techniques along with an aggressive approach to shock have contributed greatly.^[5][6]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammad Salih, MD. João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

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).

• Here is a brief description of each stage, including the domains of patient characteristics that you can expect to find when your patient is each stage.^[1][2]

• Patient identified at risk of developing, but is not yet displaying signs or symptoms of CS
• Diagnoses such as non-ST elevated myocardial infarction, ST elevated myocardial infarction (especially in the anterior wall distribution or large infarcts), and decompensated heart failure (both systolic and diastolic)
• Physical exam, laboratory, and hemodynamics are within normal limits.

• Also referred to as pre-shock or compensated shock
• Patient with relative hypotension (SBP < 90 mm Hg or mean arterial pressure [MAP] < 60 mm Hg or drop in MAP of > 30 mm Hg from baseline) or tachycardia (pulse > 100 bpm) without hypoperfusion
• Physical exam findings may include elevated jugular vein distension (JVP), rales in lung fields, warm skin with strong distal pulses, normal mentation
• Laboratory findings may include normal lactate, minimal renal function impairment, and elevated brain natriuretic peptide (BNP)
• Hemodynamic findings include relative hypotension, tachycardia, normal cardiac index (≥ 2.2 L/min/m2) and pulmonary arterial (PA) oxygen saturation ≥ 65%.

• Patient with hypotension and signs of hypoperfusion that require various interventions (inotropes, pressor, mechanical support, or extracorporeal membrane oxygenation [ECMO])
• Physical exam findings may include distressed/panicked appearance, ashen/mottled/ dusky skin color, extensive rales in lung fields, cold/clammy skin temperature, altered mentation, decreased urine output (< 30 mL/h)
• Laboratory findings may include lactate ≥ 2 mmol/L, decreased renal function (creatinine doubling or > 50% drop in glomerular filtration rate [GFR])
• Hemodynamic findings may include SBP <90 mm Hg or MAP < 60 mm Hg or drop in MAP > 30 mm Hg from baseline and devices/medications utilized to maintain adequate SBP, *cardiac index < 2.2 L/min/m2, pulmonary artery capillary wedge pressure (PCWP) > 15 mm Hg, cardiac power output ≤ 0.6 W/m2.

• Patient who fail to stabilize after at least 30 minutes of initial treatment methods
• Treatment efforts are escalated, including the addition of multiple pressors; mechanical circulatory support may be initiated
• Physical exam, laboratory, and hemodynamic findings are similar to those found in stage C, but deteriorating.

• Patient with circulatory collapse, possibly with cardiac arrest with ongoing cardiopulmonary resuscitation (CPR) and/or ECMO
• Patient requires multiple interventions (mechanical ventilation, defibrillation) and assistance from multiple clinicians
• Physical exam findings may include near pulselessness, severe hypotension, lethal cardiac disturbances (pulseless electrical activity [PEA], ventricular tachycardia, ventricular fibrillation)
• Laboratory findings may include lactate ≥ 5 mmol/L and pH ≤ 7
• Hemodynamic findings include no SBP without resuscitation, PEA or ventricular arrythmias, hypotension despite maximum medical interventions.

In cardiogenic shock, the root abnormality is the inability of the heart to pump out enough blood to maintain normal organ perfusion and blood pressure. However, this failure may be due to different factors, which allow us to classify cardiogenic shock into two categories:^[3][4][5]

• Intrinsic – this includes the conditions affecting the heart or the structures that allow it to function properly. In this category, the affected structures may be: the myocardial muscle, responsible to pump out the blood; the heart valves allowing the blood in and out of the heart chambers; the conduction system, responsible for the transmission of the electrical signals that allow the myocardium to contract in a coordinated fashion or, a combination of the previous. Examples of such factors are: myocardial infarction, mitral regurgitation and electrolyte imbalances.
• Compressive – this includes the conditions in which an otherwise “healthy heart” is prevented from working properly and pumping the blood through the vascular system, by a mechanism not related to it. The degree of impact that an extrinsic factor must have on the heart will depend on the overall “health status” of this last one. An “healthy heart” might take a more aggressive outside influence without compromising its function, while a heart already weakened by another disease, such as atherosclerosis, might fail more promptly. An example of such factor is cardiac tamponade.

Often times both factors are affecting the heart‘s ability to perform its function, at which times it might be hard to identify clearly the underlying mechanism of the cardiogenic shock.^[6]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammad Salih, MD. João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

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.

• The most common insult for cardiogenic shock is left ventricular pump failure in the setting of acute myocardial infarction.
• It usually takes a considerable area of infarcted myocardium (around 40%) to lead to cardiogenic shock.
• A smaller infarct may also originate this condition in a patient with a previously compromised ventricle function.
• There may also be other etiologies, other parts of the circulatory system may contribute, either alone or in combination, with inadequate compensation, or additional defects for this shock of cardiac origin, such as:^[1]
• Systolic Left Ventricular Dysfunction – acute myocardial infarction, CHF, Cardiomyopathy, Coronary artery bypass grafting, Myocarditis, Myocardial contusion and Hypophosphatemia
• Diastolic Left Ventricular Dysfunction – Ischemia
• Obstruction of Left Ventricular Outflow, with Increased Afterload – Aortic stenosis, Hypertrophic Cardiomyopathy, Coarctation of the Aorta and Malignant Hypertension
• Reversal of flow into the left ventricle – Acute aortic insufficiency and endocarditis
• Inadequate left ventricular filling due to mechanical causes – Tamponade and pulmonary embolism
• Inadequate left ventricular filling due to inadequate filling time – Tachycardia and tachycardia-mediated cardiomyopathy
• Conduction abnormalities – Atrioventricular block and sinus bradycardia
• Mechanical defect – VSD and left ventricle free wall rupture
• Right ventricular failure – Pulmonary embolism and hypoxic pulmonary vasoconstriction^[1]

• Cardiac dysfunction in patients with cardiogenic shock is usually initiated by myocardial infarction or ischemia.
• The myocardial dysfunction resulting from ischemia worsens that ischemia, creating a downward spiral.
• When a critical mass of left ventricular myocardium is ischemic or necrotic and fails to pump, stroke volume and cardiac output decrease.
• Myocardial perfusion, which depends on the pressure gradient between the coronary arterial system and the left ventricle.
• The duration of diastole, is compromised by hypotension and tachycardia. Which in turn, exacerbates ischemia.
• The increased ventricular diastolic pressures caused by pump failure further reduce coronary perfusion pressure, and the additional wall stress elevates myocardial oxygen requirements, further worsening ischemia.
• Decreased cardiac output also compromises systemic perfusion, which can lead to lactic acidosis and further compromise of systolic performance.
• The pathologic process begins with myocardial ischemia leading to an abnormal function of the cardiac muscle.
• This abnormality worsens the initial ischemia, which then deteriorates even further the ventricular function, creating the so called “downward spiral”.^[2]
• When ischemia reaches a point that the left ventricular myocardium fails to pump properly, parameters like stroke volume and cardiac output will therefore decrease.
• The pressure gradient produced between the pressure within the coronary arteries and the left ventricle, along with the duration of the diastole, dictate myocardial perfusion.
• This will be compromised by the hypotension and the tachycardia, worsening the myocardial ischemia and the perfusion of other vital organs.
• The fact that the heart is the only organ that benefits from a low blood pressure, as afterload decreases, makes these hemodynamical changes both beneficial and detrimental.
• The pump failure will then decrease the ability to push the blood out of the ventricle, thereby increasing the ventricular diastolic pressures.
• This will not only reduce the coronary perfusion pressure, as it will also increase the ventricle wall stress, so that the myocardial oxygen requirements will also raise, consequently propagating the ischemia.^[2][1][3]
• cardiac pump failure and hypoperfusion of the peripheral tissues is that this last one, leads to the release of catecholamines.
• Catecholamines such as norepinephrine, will increase the heart‘s contractility and peripheral blood flow, by causing constriction of arterioles, together with angiotensin II, to maintain perfusion, however, this will also increase the heart‘s oxygen demand and have proarrhythmic and myocardiotoxic consequences.
• The increased SVR coupled with the low cardiac output will lead to an even more pronounced reduction of tissue perfusion.^[1]
• The ischemia generated by all these processes increases the diastolic stiffness of the ventricle wall and this, along with the left ventricular dysfunction, will increase the left atrial pressure. The increased left atrial pressure will propagate through the pulmonary veins, generating pulmonary congestion, which by decreasing oxygen exchanges, leads to hypoxia.
• The hypoxia will further worsen the ischemia of the myocardium and the pulmonary congestion will propagate its effect through the pulmonary arteries to the right ventricle, hence jeopardizing its performance.
• Once myocardial function is affected, the body will put in motion compensatory mechanisms to try to increase the cardiac output. These include:^[4]
• Tachycardia and increased contractility through sympathetic stimulation
• Activation of the renin/angiotensin/aldosterone system, leading to fluid retention and consequently increased preload
• These compensatory mechanisms eventually become maladaptive seeing that:^[1][5]
• Tachycardia and increased contractility will increase cardiac muscle oxygen demand, thereby exacerbating the initial ischemia;
• Vasoconstriction, as a response to impaired cardiac output, in order to try to maintain coronary artery perfusion and systemic blood pressure (SVR) increases myocardial afterload, leading to an impairment in myocardial performance and an increase in its oxygen demand, worsening ischemia;
• The activation of the neurohormonal cascade will promote retention of water and sodium, in order to compensate for the hypotension and improve perfusion, yet this will also exacerbate pulmonary edema.
• The prolonged systemic hypoperfusion and hypoxia will cause a shift in cellular metabolism, prioritizing glycolysis, leading to a state of lactic acidosis, which jeopardizes contractility and systolic performance, thereby affecting the previously described system.
• All these factors affecting oxygen demand and cardiac performance create a vicious cycle that if not interrupted, may eventually lead to death.
• The therapeutic approach to cardiogenic shock focuses in disrupting this cycle.^[6]
• The area of original infarct, remote territories may also exhibit some kind of myocardial damage, called myocardial stunning.
• Myocardial stunning is the name given the myocardium which remains dysfunctional even though the restoration to normal perfusion.
• The pathophysiology of myocardial stunning is multifactorial and involves calcium overload in the sarcolemma and diastolic dysfunction, as well as the release of myocardial depressant substances.
• This calcium overload is responsible for the activation of proteases called calpains. These and other proteases will be responsible for the degradation of myofilaments, which will decrease the response to calcium, thereby explaining the temporary myocardial dysfunction after reperfusion.
• Areas of stunned myocardium may remain stunned after revascularization due to the need to resynthetize new myofilaments.^[7]
• These regions retain contractile reserve and usually respond to inotropic stimulation.
• Stunned myocardium, hibernating myocardium does respond earlier to revascularization since myocardial cells remain viable and when reperfused, calcium levels normalize.^[8][9][10]

• 5% of the cases but represents as high mortality rate as left ventricular shock.
• The right ventricular regions more commonly affected by infarction are the inferior and inferior-posterior walls.
• The coronary arteries frequently occluded in this setting are the right coronary artery, or the left circumflex coronary artery, in a left dominant system.^[11][12] Patients with right coronary artery occlusion, in a right dominant system, are at higher risk of developing papillary muscle rupture and therefore undergoing valvular heart disease, such as mitral regurgitation.^[12][13][14]
• Right ventricle failure may affect left ventricular performance by several means:^[15][16]
• Decrease in right ventricular output leading to a decrease in left ventricular filling thereby affecting overall cardiac output;
• Increased right ventricular telediastolic pressure, leading to a shifting of the interventricular septum into the left ventricle, therefore jeopardizing left ventricular filling and systolic function.

• Ventricular septal rupture and free wall rupture, which constitute two entities of cardiac rupture, represent the second most common cause of death in patients with acute myocardial infarction, during hospital stay.^[17][18][19]
• Ventricular septal rupture in the SHOCK registry, it accounted for 4.6% of the cases of cardiogenic shock.^[20]
• The most recent registries show that ventricular septal rupture generally develops within the first 16 to 24 hours post-MI and has the following characteristics:^{[21][22][23][24][25][12][26][12][27][28]}
• According to the SHOCK trial data, this type of rupture had 55% of mortality rate within the first 30 days.^[28] Free wall rupture may also be classified as simple or complex. It may occur either on the anterior or the lateral and posterior left ventricular walls.^[28][17] These last two are thought to rupture easier, however, because of the higher proportion of anterior MIs, they are seen less frequently.^[12]
• The rupture may present with different types of courses:
  • Acute – the patient generally feels acute onset of chest pain, developing cardiac tamponade, hemodynamical collapse and sudden death. Because of the rapid course of this type, it is usually not controlled with current therapies.^[29][30]
  • Subacute – this type generally results in smaller and contained ruptures. These may be stabilized by the formation of a clot or fibrinous pericardial adhesions for a short period of time. Therapeutical measures must be applied urgently.^[31][24]
  • Chronic – less frequently associated with cardiogenic shock.

• Studies like the SHOCK trial show that not all patients follow this classic paradigm, since:^[32][33][34]
• The range of elevation of systemic vascular resistance in this trial was wide, suggesting that the compensatory vasoconstriction wasn’t a rule in every patient;
• The mean ejection fraction was also moderately decreased in this trial, showing that other mechanisms besides cardiac failure were present;
• Some of the patients had leukocytosis and fever, which along with the decreased systemic vascular resistance suggested SIRS.
• These facts have introduced the concept that myocardial infarction may cause SIRS and that inflammation plays an important part in the development and persistence of cardiogenic shock, contributing to myocardial dysfunction and vasodilation.
• The possibility of developing SIRS raises with the increasing permanence in cardiogenic shock.^[1][35][36]
• At the time of the cardiac injury, the myocardium releases into circulation cytokines, particularly during the first 24 to 72 hours after the MI. *These will induce the enzyme nitric oxide synthase, thereby increasing the level of nitric oxide, which will be responsible for vasodilation and worsening of hypotension, further jeopardizing left ventricle performance.^{[37][38][39][40][41][42]} NO may also form a toxic radical, called peroxynitrite, when combined with superoxide, affecting myocardial contractility.^[43]
• Among these released cytokines during cardiogenic shock, are interleukin-6 and tumor necrosis factor.
• IL-6,is specific cytokine is correlated with the degree of organ failure and therefore mortality.^[44]
• These inflammatory mediators, among other actions, are responsible for the release of BNP, which makes the levels of BNP good markers, not only for the level of inflammation, but also to evaluate hemodynamic decompensation.^[45]
• Other circulatory factors, such as procalcitonin, complement and CRP, have been reported in some studies to contribute to the development of SIRS in cardiogenic shock.^[46][47]
• Besides the aforementioned macrocirculatory changes in cardiogenic shock, which may also be seen in septic shock, it is important to mention that microcirculatory abnormalities, caused in part by the inflammatory cascades, play an important part in the pathogenesis of organ failure as well.^[48][49][50]

• An important number of patients in cardiogenic shock complicating myocardial infarction (around 3/4), develop it after hospital admission.^[51][52]
• In some of these patients, it is reported that the development of shock, particularly in high risk patients, is related to the use of certain classes of medications, used to treat the MI. These include:^{[53][54][55][56]}
• Beta-blockers
• ACE inhibitors
• Morphine
• Diuretics (As a cause or aggravating factor. This is due to the fact that pulmonary edema is a common complication of cardiogenic shock, leading to a decrease of circulating plasma volume, particularly in patients with prior heart failure.
• After the administration of high-dose diuretics, the plasma volume will further decline)
• Excess fluid administration (In the case of right ventricular myocardial infarction, the excess volume loading in these patients may also contribute to the development of shock)

http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]

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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]

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.

Cardiogenic Shock is a life-threatening condition and must be treated as such irrespective of the causes. Life-threatening conditions may result in death or permanent disability within 24 hours if left untreated.

The most common causes of cardiogenic shock remain:^[1]

• Myocardial infarction^[2]
• Left ventricular failure^[3]

However, other likewise important causes must be identified. These may be classified according to their nature into:

• Arrhythmic

• Atrioventricular block^[4]
• Sinoatrial block
• Supraventricular tachycardia
• Ventricular tachycardia^[5]

• Mechanical

• Acute mitral regurgitation (papillary muscle rupture, chordae tendinae rupture)^[6]
• Free wall rupture
• Hypertrophic cardiomyopathy^[7]
• Obstruction to left ventricular filling (mitral stenosis, left atrial myxoma)
• Obstruction to left ventricular outflow tract (aortic stenosis, hypertrophic obstructive cardiomyopathy)
• Ventricular septal defect

• Myopathic

• Cardiomyopathy
• Myocardial contusion
• Myocardial infarction
• Myocarditis
• Myxedema coma^[8]
• Postischemic myocardial stunning
• Septic myocardial depression

• Pharmacologic

• Anthracyclines^[9]
• Beta-blockers
• Calcium channel blockers

• Acute MI

• Congestive heart failure (CHF)

• Cardiomyopathy

• Coronary artery bypass grafting

• Myocarditis

• Myocardial contusion

• Hypophosphatemia as can be seen in the refeeding syndrome)

• Septic shock with myocardial depression

• Subendocardial ischemia

• Excess wall stress

• Valvular heart disease

• Hypertensive crisis

• Aortic stenosis

• Coarctation of the aorta

• Hypertrophic obstructive cardiomyopathy (HOCM)

• Malignant hypertension

• Aortic insufficiency
• Endocarditis
• Aortic dissection
• Chordal rupture, from degenerative disease or trauma^[13]

• Tamponade
• Mitral stenosis
• Atrial myxoma

• Tachycardia

• Tachycardia mediated cardiomyopathy

• Atrioventricular block

• Sinus bradycardia

• Ventricular septal defect (VSD)
• Ruptured chordae
• Myocardial rupture of the left ventricular free wall

• Pulmonary embolism

• Hypoxic pulmonary vasoconstriction

• Excess administration of vasodilators and venodilators
• Apical balloon syndrome or Takotsubo cardiomyopathy^[14]

• Bezold-Jarisch reflex

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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] Ramyar Ghandriz MD[4]

Shock is a clinical syndrome resulting from the hypoperfusion of the tissues. Regardless of the underlying cause, this hypoperfusion leads to the failure to meet tissues’ nutritional and oxygen needs, causing cellular dysfunction. The affected tissues lead to the production and release of inflammatory mediators that will further jeopardize perfusion through changes in the vasculature. The results of these changes are organ failure and death if treatment in not timely applied. According to the underlying cause, there will be different types of shock, which will have similar presentations. It is mandatory to determine the underlying cause of the condition so that proper treatment may be started. 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.

Depending on the author and the source used there will be different ways of organizing the types of shock. Sometimes it might be difficult to differentiate, from the clinical standpoint, two types of shock since components of each type may combine in a single patient. The clinical presentation of shock is usually the result of a complexity of processes, such as the sympathetic and endocrine responses to hypoperfusion, along with manifestations of organ failure. Patients who present with signs and symptoms of hypoperfusion following a diagnosed or suspected myocardial infarction, are commonly suffering a cardiogenic shock as a complication of the MI. However, other clinical scenarios, not related to acute MI, may present similarly:^[1][2]

• Hypovolemic shock

• More than a simple loss of intravascular volume, hypovolemic shock is a dynamic process in which the responses to the initial insult, and the period of time during which they are in practice, will dictate the response to treatment and therefore the outcome. Several causes may be in the origin of this type of shock, including: hemorrhage, dehydration, GI or urinary losses and severe venodilation (in the setting of other conditions). There is a relationship between the clinical status of the patient and the amount of circulating blood volume, the signs may include pallor, cool extremities, tachycardia and tachypnea, oliguria and decreased consciousness. Compensatory mechanisms are responsible for tolerating initial blood loss, however they begin to fail after about 20-25% of blood has been lost. This tolerance will be dictated mostly by the previous cardiac reserve of the patient, along with the velocity of loss of intravascular volume^[3][4].
• When comparing hypovolemic and cardiogenic shock (most commonly complicating acute-MI) some specific clinical signs of shock will be similar, however, others will be different, particularly signs of CHF, such as the presence of distended jugular and peripheral veins, presence of an S3 sound and pulmonary edema on the cardiogenic type.
• When comparing hemodynamic data, similarities include: decreased cardiac index, stroke volume index, cardiac output, mixed venous oxygen saturation and increased difference in arteriovenous O₂ saturation and SVR.

Differences to be noted include:

<math>\mbox{Shock index} = \frac{heart\ rate}{systolic\ blood\ pressure}</math>

Other measures include: decreased ventricular preload, ventricular diastolic volumes and pressures, pulmonary wedge pressure and central venous pressure.

• When treating hypovolemic shock it’s mandatory to rule out cardiogenic cause because part of the treatment for hypovolemic shock, urgent intravascular volume replacement, may further jeopardize the cardiac condition in the cardiogenic form.

• Obstructive shock

• This form of shock results from an obstruction to the flow of blood through the cardiovascular system, including the vessels and the heart. Therefore, different causes may give rise to this condition, such as: tension pneumothorax, pulmonary emboli, pericardial tamponade and constrictive pericarditis.^[5] As in other types of shock, the clinical response will be heavily dictated by the timespan during which the insult develops and urgent therapy must be applied^[6][7].
• To evaluate the hemodynamics of obstructive shock it is important to know the underlying etiology of the shock, since different causes will present with different hemodynamic values. One example of cause of obstructive shock is cardiac tamponade, which, similarly to the cardiogenic form, will likely present with: decreased cardiac index, stroke volume, stroke work, mixed venous oxygen saturation and increased difference in arteriovenous O₂ saturation, right and left ventricular diastolic pressures, pulmonary artery diastolic pressure, serum lactate and CVP. Other causes may be observed on the table below.

• Distributive shock

• The hallmark of this form of shock is the decrease of peripheral resistance. This may be present in a series of conditions that may lead to distributive shock, such as: sepsis, anaphylaxis, toxic shock syndrome and adrenal crisis.
• When compared to cardiogenic shock it presents with similarities, such as: decreased cardiac index, left and right ventricular stroke work and increased serum lactate. The differences reside in: overall decreased of SVR, which after fluid resuscitation may become elevated, ventricular filling pressure, difference in arteriovenous O₂ saturation and increase of mixed venous oxygen saturation. It is important to note that, unlike cardiogenic and other types of shock, in the distributive kind there is an increase in venous oxygen saturation which, despite the increased O₂ demand, might be due to the increased total body perfusion, that is responsible for diminishing the effectiveness of individual tissue perfusion^[8][9][10].

The following table outlines the major differential diagnoses of Shock on the basis of clinical manifestations..^{[13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48]}

Abbreviations: ABG (arterial blood gas); ACE (angiotensin converting enzyme); BMI (body mass index); CBC (complete blood count); CSF (cerebrospinal fluid); CXR (chest X-ray); ECG (electrocardiogram); FEF (forced expiratory flow rate); FEV1 (forced expiratory volume); FVC (forced vital capacity); JVD (jugular vein distention); MCV (mean corpuscular volume); Plt (platelet); RV (residual volume); SIADH (syndrome of inappropriate antidiuretic hormone); TSH (thyroid stimulating hormone); Vt (tidal volume); WBC (white blood cell); Coronary CT angiography (CCTA); multidetector row scanners (MDCT); Cardiovascular magnetic resonance — CMRI; Myocardial perfusion imaging (MPI); single-photon emission CT (SPECT); Positron emission tomography (PET) scanning; Magnetic resonance (MR) angiography, Computed tomographic (CT) angiography, and Transesophageal echocardiography (TEE), late gadolinium enhancement (LGE); right ventricular hypertrophy (RVH), right atrial enlargement (RAE), functional tricuspid regurgitation (TR), Pulmonary artery systolic pressure (PASP; adenosine deaminase (ADA); Serum amyloid A (SAA), soluble interleukin-2 receptor (sIL2R); High-resolution CT (HRCT) scanning

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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]

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.

• Higher incidence of CS are observed in women, Asian/Pacific Islanders, and patients aged >75 years^[1].
• The incidence of CS has increased in recent years, while the reason for increasing incidence is unclear, improved diagnosis and better access to care are both likely contributory.
• The in‐hospital mortality has improved^[2].
• The 6‐ to 12‐month mortality in cardiogenic shock has remained unchanged at ≈50% over the past 2 decades^[3].
• Survivors of MI‐associated CS have an 18.6% risk of 30‐day readmission after discharge, with a median time of 10 days.
• The risk of readmission is slightly lower among patients with STEMI versus NSTEMI. The most common causes of readmission are congestive heart failure and new myocardial infarction.

• prevalence of CS between 1997 and 2012, was 600 per 100,000. Over the 15‐year study period, the prevalence of CS increased to 700 per 100,000.
• Female sex, low socioeconomic status, mechanical circulatory support (MCS) device placement, atrial fibrillation, and ventricular tachycardia are predictors of readmission^[4].
• With the improvements made in the time for diagnosis and therapeutic measures offered for acute myocardial infarction, in which increasing rates of use of primary PCI in recent years have a major role, the once very stable incidence of cardiogenic shock in this group of patients is finally declining.^[5]
• Cardiogenic shock is still an important complication in 5-8% of patients presenting with ST elevation myocardial infarction^[6][7] and 2.5% of those with non ST elevation myocardial infarction.^[8][9]
• The high incidence of left ventricular dysfunction following myocardial infarction, cardiogenic shock due to right ventricle failure (incidence of 2.8%) has as high mortality risk as shock following left ventricle failure.^[10]
• According to the SHOCK registry, both groups of patients benefit equally from revascularization procedures.^[11]

• Multicentre hospital‐based registries and surveys in the USA and Europe have shown the typical patient with CS to be >70 years of age.
• CS patients to the ICU has increased over time in patients aged ≤65 years (from 44% to 51%), but remained relatively unchanged above this age (from 52% to 51%).
• Also according to this registry, the 3 and 6 year survival rates of the group who underwent early revascularization were 41.4% and 32.8% respectively.^[12]

• There is no racial predilection to CS.

• Female sex, although initially classified as an independent predictor of outcome,^[13] studies have revealed that this assumption wasn’t true.^[14][15][16]

• The time course evaluated by the GUSTO-I trial showed that, of the 41.000 patients with acute MI treated with fibrinolytic therapy, 0.8% were in shock on admission, an additional 5.3% developed shock after admission as a sudden event or as a gradual fall in blood pressure, and approximately 50% of the patients who developed shock after admission.^[17]
• The increase in the use of primary PCI, as the main reperfusion strategy for MI, over thrombolysis, has also contributed to the decrease in the incidence of CHF.^[18][19] Back in the prereperfusion era, the 30-day mortality for acute MI complicated by cardiogenic shock was about 80%. This number went down to 58%, according to the GUSTO I registry, in patients who were treated with thrombolysis.^[20]
• Recently, improvements in mortality have been shown and confirmed, as by the GRACE registry, which studied a group of patients from 1999 to 2006, and that demonstrated a 24% decline in cardiogenic shock complicating acute MI, with the use of PCI reperfusion.^[21]

• Elderly^[22][14][3]
• Diabetic patients^[23]
• Larger extent of left ventricular injury^[8][24][25]

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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]

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.

According to several studies and considering that left ventricular dysfunction is the most common cause of developing cardiogenic shock following myocardial infarction, the most common risk factors for this condition include:

• Older age (> 65 years)^[1] For every 10 years of age, the risk is 47% greater.^[2]
• Female sex, although some studies do not consider female sex as an independent predictor of poor outcome^[3]
• Prior myocardial infarction (MI)^[3]
• Prior angina^[3]
• Peripheral vascular disease^[3]
• Left ventricular ejection fraction < 35%^[1]
• Moderate to severe mitral regurgitation^[4]
• Larger infarct area (estimated by serial cardiac markers)^[1]
• Diabetes mellitus^[1]
• Impaired fasting glucose^[5]
• ST elevation^[6]
• ST depression^[6]
• Q waves (EKG evidence of prior myocardial infarction)^[6]
• According to the analysis of PURSUIT trial database^[7] in Non-ST-segment elevation myocardial infarction patients who received eptifibatide saw their 30-day mortality risk reduced by 50%. In this trial, risk factors for development of cardiogenic shock like age and presence of ST depression in the initial EKG, in patients with Non-ST-segment elevation myocardial infarction, was also noted.
• Left bundle branch block^[8]
• History of hypertension^[9][10]
• Heart failure on admission^[9][10]
• Multivessel coronary artery disease^[9][10]
• Early use of beta blockers in large infarcts^[9][10]
• In certain cases, excessive use of diuretics causing depletion of intravascular volume^[11]
• Systolic blood pressure < 120 mm Hg^[9][10]
• Sinus tachycardia^[9][10]
• Heart rate < 60 bpm^[12]
• Physical findings of hypoperfusion at time of diagnosis, such as altered state of consciousness or cold and clammy skin^[13]
• Oliguria^[13]
• Cardiogenic shock on admission^[14]
• Timespan between symptom onset and when reperfusion is restored^[15]