The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. Cardiogenic shock is the leading cause of death in acute myocardial infarction (MI), with mortality rates as high as 70-90% in the absence of aggressive, highly experienced technical care. See the image below.
Patient with an acute anterolateral myocardial infarction who developed cardiogenic shock. Coronary angiography images showed severe stenosis of the l....
The diagnosis of cardiogenic shock can sometimes be made at the bedside by observing the following:
Findings on physical examination include the following:
See Clinical Presentation for more detail.
Invasive hemodynamic monitoring
See Workup for more detail.
Cardiogenic shock is an emergency requiring the following:
Invasive procedures include the following:
Features of dopamine are as follows:
Features of dobutamine are as follows:
If the patient remains hypotensive despite moderate doses of dopamine, a direct vasoconstrictor may be administered, as follows:
Phosphodiesterase inhibitors (eg, inamrinone [formerly amrinone], milrinone) are inotropic agents with vasodilating properties and long half-lives that are beneficial in patients with cardiac pump failure, but they may require concomitant vasopressor administration
PCI and CABG
See Treatment and Medication for more detail.
Cardiogenic shock is a physiologic state in which inadequate tissue perfusion results from cardiac dysfunction, most often systolic. It is a major, and frequently fatal, complication of a variety of acute and chronic disorders, occurring most commonly following acute myocardial infarction (MI). (See Pathophysiology, Etiology, and Prognosis.)
Although ST-segment elevation MI (STEMI, previously termed Q-wave MI) is encountered in most patients, cardiogenic shock may also develop in patients with non ̶ ST-segment elevation acute coronary syndrome (NSTEMI, NSTACS, or unstable angina). (See the image below.)
Patient with an acute anterolateral myocardial infarction who developed cardiogenic shock. Coronary angiography images showed severe stenosis of the l....
The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. Hemodynamic criteria for cardiogenic shock are sustained hypotension (systolic blood pressure <90 mm Hg for ≥30 min) and a reduced cardiac index (<2.2 L/min/m2) in the presence of normal or elevated pulmonary capillary wedge pressure (>15 mm Hg) or right ventricular end-diastolic pressure (RVEDP) (>10 mm Hg). (See DDx, Workup.)
Cardiogenic shock continues to be a difficult clinical problem; the management of this condition requires a rapid and well-organized approach. (See Prognosis, Treatment, and Medication.)
The diagnosis of cardiogenic shock may be made at the bedside by observing hypotension, absence of hypovolemia, and clinical signs of poor tissue perfusion, which include oliguria, cyanosis, cool extremities, and altered mentation. These signs usually persist after attempts have been made to correct hypovolemia, arrhythmia, hypoxia, and acidosis. (See Presentation, DDx.)
Shock is identified in most patients on the basis of findings of hypotension and inadequate organ perfusion, which may be caused by either low cardiac output or low systemic vascular resistance (SVR). Circulatory shock can be subdivided into four distinct classes according to the underlying mechanism and characteristic hemodynamic findings. In all patients, before a definite diagnosis of septic shock is established, the following four classes of shock should be considered and systematically differentiated. (See Pathophysiology, Etiology, Presentation and Workup.)
Cardiogenic shock characterized by primary myocardial dysfunction renders the heart to be unable to maintain adequate cardiac output. These patients demonstrate clinical signs of low cardiac output, with adequate intravascular volume. The patients have cool and clammy extremities, poor capillary refill, tachycardia, narrow pulse pressure, and low urine output.
Hypovolemic shock results from loss of blood volume, the possible reasons for which include gastrointestinal bleeding, extravasation of plasma, major surgery, trauma, and severe burns.
Obstructive shock results from impedance of circulation by an intrinsic or extrinsic obstruction. Pulmonary embolism, dissecting aneurysm, and pericardial tamponade all result in obstructive shock.
Distributive shock is caused by conditions producing direct arteriovenous shunting and is characterized by decreased SVR or increased venous capacitance because of the vasomotor dysfunction. These patients have high cardiac output, hypotension, high pulse pressure, low diastolic pressure, and warm extremities with good capillary refill. Such findings upon physical examination strongly suggest a working diagnosis of septic shock.
Patients should receive instruction regarding the early warning signs of acute MI and how to access the emergency medical system (eg, calling 911).
Patients must also be instructed on cardiac risk factors, particularly those that are reversible and subject to change (eg, smoking, diet, exercise).
For patient education information, see the First Aid and Injuries Center and the Healthy Living Center, as well as Shock and Cardiopulmonary Resuscitation (CPR).
Cardiogenic shock is recognized as a low-cardiac-output state secondary to extensive left ventricular (LV) infarction, development of a mechanical defect (eg, ventricular septal defect or papillary muscle rupture), or right ventricular (RV) infarction.
Autopsy studies show that cardiogenic shock is generally associated with the loss of more than 40% of the LV myocardial muscle. The pathophysiology of cardiogenic shock in the setting of coronary artery disease, is described below.
Cardiogenic shock is characterized by systolic and diastolic dysfunction leading to end organ hypoperfusion. The interruption of blood flow in an epicardial coronary artery causes the zone of myocardium supplied by that vessel to lose the ability to shorten and perform contractile work. If a sufficient area of myocardium undergoes ischemic injury, LV pump function become depressed and systemic hypotension develops.
Patients who develop cardiogenic shock from acute MI consistently have evidence of progressive myocardial necrosis with infarct extension. Decreased coronary perfusion pressure and cardiac output as well as increased myocardial oxygen demand play a role in the vicious cycle that leads to cardiogenic shock and potentially death.
Patients suffering from cardiogenic shock often have multivessel coronary artery disease with limited coronary blood flow reserve. Ischemia remote from the infarcted zone is an important contributor to shock. Myocardial diastolic function is also impaired, because ischemia decreases myocardial compliance and impairs filling, thereby increasing LV filling pressure and leading to pulmonary edema and hypoxemia.
Tissue hypoperfusion, with consequent cellular hypoxia, causes anaerobic glycolysis, the accumulation of lactic acid, and intracellular acidosis. Also, myocyte membrane transport pumps fail, which decreases transmembrane potential and causes intracellular accumulation of sodium and calcium, resulting in myocyte swelling.
If ischemia is severe and prolonged, myocardial cellular injury becomes irreversible and leads to myonecrosis, which includes mitochondrial swelling, the accumulation of denatured proteins and chromatin, and lysosomal breakdown. These events induce fracture of the mitochondria, nuclear envelopes, and plasma membranes.
Additionally, apoptosis (programmed cell death) may occur in peri-infarcted areas and may contribute to myocyte loss. Activation of inflammatory cascades, oxidative stress, and stretching of the myocytes produces mediators that overpower inhibitors of apoptosis, thus activating the apoptosis.
Large areas of myocardium that are dysfunctional but still viable can contribute to the development of cardiogenic shock in patients with MI. This potentially reversible dysfunction is often described as myocardial stunning or as hibernating myocardium. Although hibernation is considered a different physiologic process than myocardial stunning, the conditions are difficult to distinguish in the clinical setting and they often coexist.
Myocardial stunning represents postischemic dysfunction that persists despite restoration of normal blood flow. By definition, myocardial dysfunction from stunning eventually resolves completely. The mechanism of myocardial stunning involves a combination of oxidative stress, abnormalities of calcium homeostasis, and circulating myocardial depressant substances.
Hibernating myocardium is a state of persistently impaired myocardial function at rest, which occurs because of the severely reduced coronary blood flow. Hibernation appears to be an adaptive response to hypoperfusion that may minimize the potential for further ischemia or necrosis. Revascularization of the hibernating (and/or stunned) myocardium generally leads to improved myocardial function.
Consideration of the presence of myocardial stunning and hibernation is vital in patients with cardiogenic shock because of the therapeutic implications of these conditions. Hibernating myocardium improves with revascularization, whereas the stunned myocardium retains inotropic reserve and can respond to inotropic stimulation.
Cardiogenic shock is the most severe clinical expression of LV failure. The primary mechanical defect in cardiogenic shock is a shift to the right for the LV end-systolic pressure-volume curve, because of a marked reduction in contractility. As a result, at a similar or even lower systolic pressure, the ventricle is able to eject less blood volume per beat. Therefore, the end-systolic volume is usually greatly increased in persons with cardiogenic shock. The degree to which LV end systolic volume increases is a powerful hemodynamic predictor of mortality following STEMI.
To compensate for the diminished stroke volume, the curvilinear diastolic pressure-volume curve also shifts to the right, with a decrease in diastolic compliance. This leads to increased diastolic filling and increased LV end-diastolic pressure. The attempt to enhance cardiac output by this mechanism comes at the cost of having a higher LV diastolic filling pressure, which ultimately increases myocardial oxygen demand and can lead to pulmonary edema.
As a result of decreased contractility, the patient develops elevated LV and RV filling pressures and low cardiac output. Mixed venous oxygen saturation falls because of the increased tissue oxygen extraction, which is due to the low cardiac output. This, combined with the intrapulmonary shunting that is often present, contributes to substantial arterial oxygen desaturation.
When a critical mass of LV myocardium becomes ischemic and fails to pump effectively, stroke volume and cardiac output are curtailed. The LV pump function becomes depressed; cardiac output, stroke volume, and blood pressure decline while end-systolic volume increases. Myocardial ischemia is further exacerbated by impaired myocardial perfusion due to hypotension and tachycardia.
The LV pump failure increases ventricular diastolic pressures concomitantly, causing additional wall stress and thereby elevating myocardial oxygen requirements. Systemic perfusion is compromised by decreased cardiac output, with tissue hypoperfusion intensifying anaerobic metabolism and instigating the formation of lactic acid (lactic acidosis), which further deteriorates the systolic performance of the myocardium.
Depressed myocardial function also leads to the activation of several physiologic compensatory mechanisms. These include sympathetic stimulation, which increases the heart rate and cardiac contractility and causes renal salt and fluid retention, hence augmenting the LV preload. The elevated heart rate and contractility increases myocardial oxygen demand, further worsening myocardial ischemia.
Fluid retention and impaired LV diastolic filling triggered by tachycardia and ischemia worsen pulmonary venous congestion and hypoxemia. Sympathetically mediated vasoconstriction to maintain systemic blood pressure amplifies myocardial afterload, which additionally impairs cardiac performance.
Finally, excessive myocardial oxygen demand with simultaneous inadequate myocardial perfusion worsens myocardial ischemia, initiating a vicious cycle that ultimately ends in death, if uninterrupted.
Usually, a combination of systolic and diastolic myocardial dysfunction is present in patients with cardiogenic shock. Metabolic derangements that impair myocardial contractility further compromise systolic ventricular function. Myocardial ischemia decreases myocardial compliance, thereby elevating LV filling pressure at a given end-diastolic volume (diastolic dysfunction), which leads to pulmonary congestion and congestive heart failure.
Shock state, irrespective of the etiology, is described as a syndrome initiated by acute systemic hypoperfusion that leads to tissue hypoxia and vital organ dysfunction. All forms of shock are characterized by inadequate perfusion to meet the metabolic demands of the tissues. A maldistribution of blood flow to end organs begets cellular hypoxia and end organ damage, the well-described multisystem organ dysfunction syndrome. The organs of vital importance are the brain, heart, and kidneys.
A decline in higher cortical function may indicate diminished perfusion of the brain, which leads to an altered mental status ranging from confusion and agitation to flaccid coma. The heart plays a central role in propagating shock. Depressed coronary perfusion leads to worsening cardiac dysfunction and a cycle of self-perpetuating progression of global hypoperfusion. Renal compensation for reduced perfusion results in diminished glomerular filtration, causing oliguria and subsequent renal failure.
Cardiogenic shock can result from the following types of cardiac dysfunction:
The vast majority of cases of cardiogenic shock in adults are due to acute myocardial ischemia. Indeed, cardiogenic shock is generally associated with the loss of more than 40% of the LV myocardium, although in patients with previously compromised LV function, even a small infarction may precipitate shock. Cardiogenic shock is more likely to develop in people who are elderly or diabetic or in persons who have had a previous inferior MI.
Complications of acute MI, such as acute mitral regurgitation, large RV infarction, rupture of the interventricular septum or LV free wall, and tamponade can result in cardiogenic shock. Conduction abnormalities (eg, atrioventricular blocks, sinus bradycardia) are also risk factors.
Many cases of cardiogenic shock occurring after acute coronary syndromes may be due to medication administration. The use of beta blockers and angiotensin-converting enzyme (ACE) inhibitors in acute coronary syndromes must be carefully timed and monitored.[2, 6, 7]
In children, preceding viral infection may cause myocarditis. In addition, children and infants may have unrecognized congenital structural heart defects that are well compensated until there is a stressor. These etiologies plus toxic ingestions make up the three primary causes of cardiogenic shock in children.
A systemic inflammatory response syndrome–type mechanism has also been implicated in the etiology of cardiogenic shock. Elevated levels of white blood cells, body temperature, complement, interleukins, and C-reactive protein are often seen in large myocardial infarctions. Similarly, inflammatory nitric oxide synthetase (iNOS) is also released in high levels during myocardial stress. Nitric oxide production induced by iNOS may uncouple calcium metabolism in the myocardium resulting in a stunned myocardium. Additionally, iNOS leads to the expression of interleukins, which may themselves cause hypotension.
The primary abnormality in systolic dysfunction is abated myocardial contractility. Acute MI or ischemia is the most common cause; cardiogenic shock is more likely to be associated with anterior MI. The causes of systolic dysfunction leading to cardiogenic shock can be summarized as follows:
Increased LV diastolic chamber stiffness contributes to cardiogenic shock during cardiac ischemia, as well as in the late stages of hypovolemic shock and septic shock. Increased diastolic dysfunction is particularly detrimental when systolic contractility is also depressed. The causes of cardiogenic shock due primarily to diastolic dysfunction can be summarized as follows:
Greatly increased afterload
Increased afterload, which can impair cardiac function, can be caused by the following:
Valvular and structural abnormality
Valvular dysfunction may immediately lead to cardiogenic shock, or it may aggravate other etiologies of shock. Acute mitral regurgitation secondary to papillary muscle rupture or dysfunction is caused by ischemic injury. Rarely, acute obstruction of the mitral valve by a left atrial thrombus may result in cardiogenic shock by means of severely decreased cardiac output. Aortic and mitral regurgitation reduce forward flow, raise end-diastolic pressure, and aggravate shock associated with other etiologies.
Valvular and structural abnormalities associated with cardiogenic shock include the following:
Reduced myocardial contractility can result from the following:
Greatly increased afterload
Afterload increase associated with RV failure can result from the following:
Ventricular tachyarrhythmias are often associated with cardiogenic shock. Furthermore, bradyarrhythmias may cause or aggravate shock due to another etiology. Sinus tachycardia and atrial tachyarrhythmias contribute to hypoperfusion and aggravate shock.
The incidence rate of cardiogenic shock ranges from 5% to 10% in patients with acute MI. In the Worcester Heart Attack Study, a community-wide analysis, the reported incidence rate was 7.5%. The literature contains few data on cardiogenic shock in patients without ischemia.
A 2014 review of the 2003-2010 Nationwide Inpatient Sample (NIS) databases revealed a 7.9% incidence in patients with STEMI. Overall, of cases with cardiogenic shock and STEMI, 42.3% were located in the anterior wall, 38.6% in the inferior wall, and 19.1% at other sites.
As many as 3% of patients with NSTACS develop cardiogenic shock.
Several multicenter thrombolytic trials in Europe reported a prevalence rate of cardiogenic shock following MI of approximately 7%.
Asian/Pacific Islanders have a higher incidence of cardiogenic shock (11.4%) than white (8%), black (6.9%), and Hispanic (8.6%) patients.
Although the overall incidence of cardiogenic shock has traditionally been higher in men than in women, a difference resulting from the increased prevalence of coronary artery disease in males, the 2003-2010 NIS data revealed women had a higher overall incidence of cardiogenic shock (8.5%) than men (76%) during this period. Moreover, a higher percentage of female patients with MI developed cardiogenic shock than did males with MI.
Median age for cardiogenic shock mirrors the bimodal distribution of disease. For adults, the median age ranges from 65-66 years. For children, cardiogenic shock presents as a consequence of fulminant myocarditis or congenital heart disease.
Overall, the 2003-2010 NIS data revealed patients aged 75 years and older suffered cardiogenic shock more often than those younger than 75 years.
Cardiogenic shock is the leading cause of death in acute MI. In the absence of aggressive, highly experienced technical care, mortality rates among patients with cardiogenic shock are exceedingly high (up to 70-90%). The key to achieving a good outcome is rapid diagnosis, prompt supportive therapy, and expeditious coronary artery revascularization in patients with myocardial ischemia and infarction.[12, 13, 14] Thus, with the implementation of prompt revascularization, improved interventional procedures, and better medical therapies and mechanical support devices, the mortality rates from cardiogenic shock may continue to decline.
The overall in-hospital mortality rate for patients with cardiogenic shock is 39%. For persons 75 years and older, the mortality rate is 55%; for those younger than 75 years, it is 29.8%. For women, it is 44.4% compared to 35.5% in men.
Race-stratified inpatient mortality rates from cardiogenic shock are as follows (race-based mortality differences persisted even after adjustment for early mechanical revascularization status) :
Mortality rates are similar for patients with cardiogenic shock secondary to STEMI or NSTACS.[15, 16]
Evidence of RV dilatation on an echocardiogram may indicate a worse outcome in patients with cardiogenic shock, as may RV infarction on a right-side electrocardiogram. The prognosis for patients who survive cardiogenic shock is not well studied but may be favorable if the underlying cause of shock is expeditiously corrected.
Complications of cardiogenic shock may include the following:
The following predictors of mortality were identified from the Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial :
Echocardiographic findings such as LV ejection fraction (LVEF) and mitral regurgitation are independent predictors of mortality. An ejection fraction of less than 28% has been associated with a survival rate of 24% at 1 year, compared to a survival rate of 56% with a higher ejection fraction. Moderate or severe mitral regurgitation was found to be associated with a 1-year survival rate of 31%, compared to a survival rate of 58% in patients with no regurgitation. The time to reperfusion is an important predictor of mortality in acute MI complicated by cardiogenic shock. In patients with shock, the in-hospital mortality rate increased progressively with increasing time-to-reperfusion.
Outcomes in cardiogenic shock significantly improve only when rapid revascularization can be achieved. The SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock?) trial demonstrated that overall mortality when revascularization occurs is 38%. When rapid revascularization is not attempted, mortality rates approach 70%. Rates vary depending on the procedure (eg, percutaneous transluminal coronary angioplasty, stent placement, thrombolytic therapy).
Cardiogenic shock is a medical emergency. A complete clinical assessment is critical to understanding the cause of the shock and to targeting therapy for correcting the cause. The presenting history will vary depending on the underlying etiology of cardiogenic shock.
Cardiogenic shock following acute myocardial infarction (MI) generally develops after admission to the hospital, though a small number of patients are in shock at presentation. Patients demonstrate clinical evidence of hypoperfusion (low cardiac output), which is manifested by sinus tachycardia, low urine output, and cool extremities. Systemic hypotension, defined as systolic blood pressure below 90 mm Hg or a decrease of 30 mm Hg in mean blood pressure, ultimately develops and further propagates tissue hypoperfusion.
Most patients who develop acute MI present with an abrupt onset of squeezing or heavy substernal chest pain; the pain may radiate to the left arm or the neck. The chest pain may be atypical, the location being epigastric or only in the neck or arm. The pain quality may be burning, sharp, or stabbing. Pain may be absent in persons with diabetes or in elderly individuals.
Patients also may report associated autonomic symptoms, including nausea, vomiting, and sweating.
A history of previous cardiac disease, use of cocaine, previous MI, or previous cardiac surgery should be obtained. A patient thought to have myocardial ischemia should be assessed for cardiac risk factors. The evaluation should reveal a history of hyperlipidemia, left ventricular (LV) hypertrophy, hypertension, or cigarette smoking or a family history of premature coronary artery disease (CAD). The presence of two or more risk factors increases the likelihood of acute MI.
Other associated symptoms are diaphoresis, exertional dyspnea, or dyspnea at rest. Presyncope or syncope, palpitations, generalized anxiety, and depression are other features indicative of poor cardiac function.
Cardiogenic shock is diagnosed after documentation of myocardial dysfunction and exclusion of alternative causes of hypotension, such as hypovolemia, hemorrhage, sepsis, pulmonary embolism, pericardial tamponade, aortic dissection, or preexisting valvular disease.
Shock is present if evidence of multisystem organ hypoperfusion in the presence of hypotension is detected upon physical examination (systolic blood pressure <90 mm Hg, cardiac index <2.2 L/min/m2, and the presence of normal or elevated pulmonary capillary occlusion pressure [>15 mm Hg], or right ventricular [RV] end-diastolic pressure [RVEDP; >10 mm Hg]).
Characteristics of patients with cardiogenic shock include the following:
A systolic murmur is generally heard in patients with acute mitral regurgitation or ventricular septal rupture. The associated parasternal thrill indicates the presence of a ventricular septal defect, whereas the murmur of mitral regurgitation may be limited to early systole. Approximately two thirds of patients will develop pulmonary congestion manifested as rales on pulmonary examination.
The systolic murmur, which becomes louder upon Valsalva and prompt standing, suggests hypertrophic obstructive cardiomyopathy (idiopathic hypertropic subaortic stenosis).
As previously discussed, the keys to achieving a good outcome in patients with cardiogenic shock are rapid diagnosis, prompt supportive therapy, and expeditious coronary artery revascularization in patients with myocardial ischemia and infarction.
Any patient presenting with shock must receive an early working diagnosis, urgent resuscitation, and subsequent confirmation of the working diagnosis.
In addition to laboratory studies, workup in cardiogenic shock can include imaging studies such as echocardiography, chest radiography, and angiography; electrocardiography (ECG); and invasive hemodynamic monitoring.
Measurement of routine biochemical parameters, such as electrolytes, renal function (eg, urea and creatinine levels), and liver function tests (eg, bilirubin, aspartate aminotransferase [AST], alanine aminotransferase [ALT], and lactate dehydrogenase [LDH]), are useful for assessing proper functioning of vital organs.
A complete blood count (CBC) is generally helpful to exclude anemia. A high white blood cell (WBC) count may indicate an underlying infection, and the platelet count may be low because of coagulopathy related to sepsis.
The diagnosis of acute myocardial infarction (MI) is aided by a variety of serum markers, which include creatine kinase (CK) and its subclasses, troponin, myoglobin, and LDH. The value for the isoenzyme of creatine kinase with muscle and blood subunits is most specific, but it may be falsely elevated in persons with myopathy, hypothyroidism, renal failure, or skeletal muscle injury.
The rapid release and metabolism of myoglobin occurs in persons with MI. A fourfold rise of myoglobin over 2 hours appears to be a test result that is sensitive for MI. The serum LDH value increases approximately 10 hours after the onset of MI, peaks at 24-48 hours, and gradually returns to normal in 6-8 days. The LDH fraction 1 isoenzyme is primarily released by the heart, but it also may come from the kidneys, stomach, pancreas, and red blood cells.
Cardiac troponins T and I are widely used for the diagnosis of myocardial injury. Troponin elevation in the absence of clinical evidence of ischemia should prompt a search for other causes of cardiac damage, such as myocarditis.
Troponin T and I can be detected in serum within the first few hours after onset of acute MI. Troponin levels peak at 14 hours after acute MI, peak again several days later (biphasic peak), and remain abnormal for 10 days. This characteristic could make troponin T (in combination with CK-MB) useful for retrospective diagnosis of acute MI in patients who seek care very late.
Troponin T is an independent prognostic indicator of adverse outcomes and can be used as a patient risk-stratifying tool in patients with unstable angina or non–Q-wave MI.
Arterial blood gas values indicate overall acid-base homeostasis and the level of arterial blood oxygenation. (Acidosis can have a particularly deleterious effect on myocardial function.) A base deficit elevation (reference range, +3 to –3 mmol/L) correlates with the occurrence and severity of shock. A base deficit is also an important marker to follow during resuscitation of a patient from shock.
An elevated serum lactate level is an indicator of shock. Serial lactate measurements are useful markers of hypoperfusion and are also used as indicators of prognosis. Elevated lactate values in a patient with signs of hypoperfusion indicate a poor prognosis; rising lactate values during resuscitation portend a very high mortality rate.
Brain natriuretic peptide (BNP) may be useful as an indicator of congestive heart failure (CHF) and as an independent prognostic indicator of survival. A low BNP level may effectively rule out cardiogenic shock in the setting of hypotension; however, an elevated BNP level does not rule in the disease.
Echocardiography should be performed early to establish the cause of cardiogenic shock. Echocardiography provides information on global and regional systolic function and on diastolic dysfunction. Echocardiography findings can also lead to a rapid diagnosis of mechanical causes of shock, such as acute ventricular septal defect, free myocardial wall rupture, pericardial tamponade, and papillary muscle rupture causing acute myocardial regurgitation.
In addition, an echocardiogram may reveal akinetic or dyskinetic areas of ventricular wall motion or may demonstrate valvular dysfunction. Ejection fraction may be estimated as well (although results from the SHOCK trial indicated that left ventricular [LV] ejection fraction [LVEF] is not always depressed in the setting of cardiogenic shock). If a hyperdynamic LV is found, the echocardiogram may suggest other causes of shock such as sepsis or anemia. (See the images below.)
Short-axis view of the left ventricle demonstrating small pericardial effusion, low ejection fraction, and segmental wall motion abnormalities. Courtesy of Michael Stone, MD, RDMS.
Pleural sliding in an intercostal space demonstrating increased lung comet artifacts suggestive of pulmonary edema. Courtesy of Michael Stone, MD, RDMS.
Chest radiographic findings are useful for excluding other causes of shock or chest pain. The presence of a widened mediastinum may indicate aortic dissection. Tension pneumothorax or pneumomediastinum that are readily detected on radiographic films may manifest as low-output shock.
Most patients with established cardiogenic shock exhibit findings of LV failure, the radiologic features of which include pulmonary vascular redistribution, interstitial pulmonary edema, enlarged hilar shadows, the presence of Kerley B lines, cardiomegaly, and bilateral pleural effusions. Alveolar edema manifests as bilateral perihilar opacities in a so-called butterfly distribution.
Ultrasonography can be used to guide fluid management. In the spontaneously breathing patient, inferior vena cava (IVC) collapse with respiration suggests dehydration, whereas a lack of IVC collapse suggests intravascular euvolemia.
Coronary angiography is urgently indicated in patients with myocardial ischemia or MI who also develop cardiogenic shock. Angiography is required to help assess the anatomy of the coronary arteries as well as evaluate the need for urgent revascularization.
Coronary angiography findings often demonstrate multivessel coronary artery disease (CAD) in persons with cardiogenic shock. In these patients, a compensatory hyperkinesis cannot occur in the noninfarct territory because of the severe coronary artery atherosclerosis.
The most common cause of cardiogenic shock is extensive MI, though a smaller infarction in a previously compromised LV also may precipitate shock. After MI, large areas of nonfunctional, but viable, myocardium (hibernating myocardium) can also cause or contribute to cardiogenic shock. (See the images below.)
Patient with an acute anterolateral myocardial infarction who developed cardiogenic shock. Coronary angiography images showed severe stenosis of the l....
A coronary angiogram image of a patient with cardiogenic shock demonstrates severe stenosis of the left anterior descending coronary artery.
A coronary angiogram image of a patient with cardiogenic shock demonstrates severe stenosis of the left anterior descending coronary artery. Following....
Acute myocardial ischemia is diagnosed on the basis of the presence of ST-segment elevation, ST-segment depression, or Q waves. T-wave inversion, though a less sensitive finding, may also be seen in persons with myocardial ischemia. An ECG with right-side chest leads may document right ventricular (RV) infarction and may be prognostically, as well as diagnostically, useful.[17, 21]
Perform electrocardiography immediately to help diagnose MI and/or myocardial ischemia. A normal ECG, however, does not rule out the possibility of acute MI. (See the images below.)
This ECG shows evidence of an extensive anterolateral myocardial infarction; this patient subsequently developed cardiogenic shock.
ECG tracing shows further evolutionary changes in a patient with cardiogenic shock.
ECG tracing in a patient who developed cardiogenic shock secondary to pericarditis and pericardial tamponade.
A 63-year-old man admitted to the emergency department with clinical features of cardiogenic shock. The ECG revealed findings indicative of wide-compl....
Invasive hemodynamic monitoring (Swan-Ganz catheterization) is very useful for helping to exclude other causes and types of shock (eg, volume depletion, obstructive shock, and septic shock).
The hemodynamic measurements of cardiogenic shock are a pulmonary capillary wedge pressure (PCWP) higher than 15 mm Hg and a cardiac index lower than 2.2 L/min/m2.
The presence of large V waves on the PCWP tracing suggests severe mitral regurgitation, whereas a step-up in oxygen saturation between the right atrium (RA) and the RV is diagnostic of ventricular septal rupture.
High right-side filling pressures in the absence of an elevated PCWP, when accompanied by ECG criteria, indicate RV infarction.
Cardiogenic shock is an emergency necessitating immediate resuscitative therapy before shock irreversibly damages vital organs. The key to a good outcome in patients with cardiogenic shock is an organized approach, with rapid diagnosis and prompt initiation of pharmacologic therapy to maintain blood pressure and cardiac output and respiratory support, as well as reversal of the underlying cause.
All patients require admission to an intensive care setting, which may involve emergency transfer to the cardiac catheterization suite, critical care transport to a tertiary care center, or internal transfer to the intensive care unit (ICU).
Early and definitive restoration of coronary blood flow is the most important intervention for achieving an improved survival rate. At present, it represents standard therapy for patients with cardiogenic shock due to myocardial ischemia.
Correction of electrolyte and acid-base abnormalities, such as hypokalemia, hypomagnesemia, and acidosis, is essential in cardiogenic shock.
Cardiogenic shock may be prevented with early revascularization in patients with myocardial infarction (MI) and with required intervention in patients with structural heart disease.
Placement of a central line may facilitate volume resuscitation, provide vascular access for multiple infusions, and allow invasive monitoring of central venous pressure. Central venous pressure may also be used to guide fluid resuscitation.
Although not necessary for the diagnosis of cardiogenic shock, invasive monitoring with a pulmonary artery catheter may be helpful in guiding fluid resuscitation in situations in which left ventricular (LV) preload is difficult to determine.
Pulmonary artery catheter pressure measurements may also be useful in prognosis. Retrospective evaluation of these measurements from the SHOCK trial demonstrated that stroke volume index (SVI) and stroke work index (SWI) vary inversely with mortality.
An arterial line may be placed to provide continuous blood pressure monitoring. This is particularly useful if the patient requires inotropic medications.
An intra-aortic balloon pump (IABP) may be placed in the emergency department (ED) as a bridge to percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG), to decrease myocardial workload and to improve end-organ perfusion.
Clinicians should be alert to the fact that the SHOCK trial demonstrated that either PCI or CABG is the treatment of choice for cardiogenic shock and that each has been shown to markedly decrease mortality rates at 1 year. PCI should be initiated within 90 minutes of presentation; however, it remains helpful, as an acute intervention, within 12 hours of presentation.
If such a facility is not immediately available, thrombolytics should be considered. However, this treatment is second-best. An increased mortality is seen in situations where thrombolytics are used instead of PCI. This is due to the relative ineffectiveness of the thrombolytic medications to lyse clots in low-blood-pressure situations.[22, 2]
Prehospital care is aimed at minimizing any further ischemia and shock. All patients require intravenous (IV) access, high-flow oxygen administered by mask, and cardiac monitoring.
Twelve-lead electrocardiography (ECG) performed in the field by appropriately trained paramedics may be useful in decreasing door-to-PCI times and/or time to the administration of thrombolytics because acute ST-segment elevation MI (STEMI) can be identified earlier. The ED can thus be alerted and may mobilize the appropriate resources.
Inotropic medications should be considered in systems with appropriately trained paramedical personnel.
When clinically necessary, positive pressure ventilation and endotracheal intubation should be performed. Continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) support can be considered in appropriately equipped systems.
Initial management includes fluid resuscitation to correct hypovolemia and hypotension, unless pulmonary edema is present. Central venous and arterial lines are often required. Swan-Ganz catheterization and continuous percutaneous oximetry are routine.
Oxygenation and airway protection are critical; intubation and mechanical ventilation are commonly required. However, although positive-pressure ventilation (PPV) may improve oxygenation, it may also compromise venous return, preload, to the heart. In any event, the patient should be treated with high-flow oxygen. Studies in patients with acute cardiogenic pulmonary edema have shown noninvasive ventilation to improve hemodynamics and reduce the intubation rate. Mortality, however, is unaffected.
A study by Shin et al suggested that patients who receive extracorporeal cardiopulmonary resuscitation (CPR) versus conventional CPR for longer than 10 minutes following in-hospital arrest have a greater chance of survival.
All patients with cardiogenic shock require close hemodynamic monitoring, volume support to ensure adequate sufficient preload, and ventilatory support.
Patients with MI or acute coronary syndrome (ACS) are given aspirin and heparin. Both of these medications have been shown to be effective in reducing mortality in separate studies. Before initiating therapy, however, care should be taken to ensure that the patient does not have a myocardial wall rupture that is amenable to surgery.
There is no need to start clopidogrel until after angiography, because angiography may demonstrate that there is a need for urgent CABG.
The glycoprotein IIb/IIIa inhibitors improve the outcome of patients with non–ST-segment elevation ACS (NSTACS). They have been found to reduce recurrent MI following PCI and in cardiogenic shock.
Dopamine, norepinephrine, and epinephrine are vasoconstricting drugs that help to maintain adequate blood pressure during life-threatening hypotension and help to preserve perfusion pressure for optimizing flow in various organs. The mean blood pressure required for adequate splanchnic and renal perfusion (mean arterial pressure [MAP] of 60 or 65 mm Hg) is based on clinical indices of organ function.
In patients with inadequate tissue perfusion and adequate intravascular volume, initiation of inotropic and/or vasopressor drug therapy may be necessary. Dopamine increases myocardial contractility and supports the blood pressure; however, it may increase myocardial oxygen demand. Dobutamine may be preferable if the systolic blood pressure is higher than 80 mm Hg; it has the advantage of not affecting myocardial oxygen demand as much as dopamine does. However, the resulting tachycardia may preclude the use of this inotropic agent in some patients. Dopamine will cause more tachycardia than dobutamine for any corresponding increase in cardiac output.
Dopamine is usually initiated at a dosage of 5-10 mcg/kg/min IV, and the infusion rate is adjusted according to the blood pressure and other hemodynamic parameters. Often, patients may require high dosages of dopamine (as much as 20 mcg/kg/min).
If the patient remains hypotensive despite moderate doses of dopamine, a direct vasoconstrictor (eg, norepinephrine) should be started at a dosage of 0.5 mcg/kg/min and titrated to maintain an MAP of 60 mm Hg. The potent vasoconstrictors (eg, norepinephrine) are best reserved for situations of refractory hypotension and organ hypoperfusion because of their unfavorable role in increasing afterload and cardiac filling pressure and, consequently, impairing cardiac output. However, one study of patients with shock found no difference in outcome between treatment with norepinephrine and treatment with dopamine. There is no consensus regarding the first-line choice of vasopressor in cardiogenic shock.
The following is a brief review of the mechanism of action and indications for drugs used for hemodynamic support of cardiogenic shock.[25, 26]
There is little in the way of randomized clinical trial data to guide the use of inotropic or pressor therapy in patients with cardiogenic shock. The use of these agents is indicated in patients with cardiogenic shock, but it is important to note that a survival benefit has not been established. Indeed, routine use of these agents in patients with hemodynamically stable, decompensated heart failure was associated with greater morbidity and no clinical benefit (Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure [OPTIME-CHF]).[27, 28]
Dopamine is a precursor of norepinephrine and epinephrine and has varying effects according to the doses infused. A dosage of less than 5 mcg/kg/min causes vasodilation of renal, mesenteric, and coronary beds. At a dosage of 5-10 mcg/kg/min, beta1-adrenergic effects induce an increase in cardiac contractility and heart rate.
At dosages higher than 10 mcg/kg/min, predominant alpha-adrenergic effects lead to arterial vasoconstriction and an elevation in blood pressure. The blood pressure increases primarily as a result of its inotropic effect. The undesirable effects are tachycardia and increased pulmonary shunting, as well as the potential for decreased splanchnic perfusion and increased pulmonary arterial wedge pressure.
Norepinephrine is a potent alpha-adrenergic agonist with only minor beta1-adrenergic agonist effects. Norepinephrine can increase blood pressure successfully in patients who remain hypotensive following dopamine. The dosage of norepinephrine may vary from 0.2 to 1.5 mcg/kg/min, and high dosages (up to 3.3 mcg/kg/min) have been used because of the alpha-receptor down-regulation in persons with sepsis.
Epinephrine is an agonist of alpha1, beta1, and beta2 receptors. It can increase the MAP by increasing the cardiac index and stroke volume, as well as systemic vascular resistance (SVR) and heart rate. Epinephrine decreases the splanchnic blood flow and may increase oxygen delivery and consumption.
Administration of this agent may be associated with an increase in systemic and regional lactate concentrations. The use of epinephrine is recommended only in patients who are unresponsive to traditional agents. Other undesirable effects include an increase in lactate concentration, a potential to produce myocardial ischemia, the development of arrhythmias, and a reduction in splanchnic flow.
Levosimendan, widely used in Europe but not approved for use in the United States, can be considered for use in conjunction with vasopressors to improve coronary blood flow.[29, 30] This agent acts by increasing the sensitivity of the cardiac myofilament to calcium, rather than increasing intracellular concentrations of free calcium. Levosimendan stabilises troponin C and the kinetics of actin-myosin cross-bridges without increasing myocardial consumption of adenosine triphosphate (ATP). Levosimendan is a potent inotrope and also a vasodilator of the arterial, venous, and coronary circulation. It should be used with caution, however, in that it can cause hypotension.
Dobutamine (sympathomimetic agent) is a beta1-receptor agonist, though it has some beta2-receptor and minimal alpha-receptor activity. It is used in a dosage range of 2 to 20 mcg/kg/min and has a half-life of approximately 2 minutes. IV dobutamine induces significant positive inotropic effects, with mild chronotropic effects through activation of adenyl cyclase, an increase in intracellular cyclic adenosine monophosphate (cAMP) and, therefore, calcium levels. It also induces mild peripheral vasodilation (decrease in afterload). The combined effect of increased inotropy and decreased afterload induces a significant increase in cardiac output.
In the setting of acute MI, dobutamine use could increase the size of the infarct because of the increase in myocardial oxygen consumption that may ensue. In general, caution should be exercised when administering dobutamine in patients with moderate or severe hypotension (eg, systolic blood pressure <80 mm Hg), because the peripheral vasodilation, in some cases, may cause a further fall in blood pressure.
Phosphodiesterase III inhibitors
Phosphodiesterase III inhibitors (PDIs), which include inamrinone (formerly amrinone) and milrinone, are inotropic agents with vasodilating properties and long half-lives. Milrinone is used in a dosage range of 0.3 to 0.75 mcg/kg/min and has a long half-life of 1.5 to 3 hours, with the longer half-life in patients with renal impairment.
The mechanism of action of PDIs is distinct from dobutamine in that they prevent breakdown of cAMP, thereby increasing intracellular cAMP levels. The hemodynamic properties of PDIs are (1) a positive inotropic effect on the myocardium and peripheral vasodilation (decreased afterload) and (2) a reduction in pulmonary vascular resistance (decreased preload).
PDIs may be beneficial in persons with cardiac pump failure who require more concomitant pulmonary and systemic vasodilation than is typically achieved by dobutamine. Unlike catecholamine inotropes, these drugs are not dependent on adrenoreceptor activity; therefore, patients are less likely to develop tolerance to these medications.
PDIs are less likely than catecholamines to cause adverse effects known to be associated with adrenoreceptor activity (eg, increased myocardial oxygen demand, myocardial ischemia). They are also associated with less tachycardia and myocardial oxygen consumption. However, the incidence of tachyarrhythmias is greater with PDIs than with dobutamine.
Although thrombolytic therapy (TT) reduces mortality rates in patients with acute MI, its benefits for patients with cardiogenic shock secondary to MI are disappointing. When used early in the course of MI, TT reduces the likelihood of subsequent development of cardiogenic shock after the initial event.
In the Gruppo Italiano Per lo Studio Della Streptokinase Nell'Infarto Miocardio trial, 30-day mortality rates were 69.9% in patients with cardiogenic shock who received streptokinase, compared to 70.1% in patients who received a placebo.[31, 32]
Similarly, other studies employing a tissue plasminogen activator did not show reductions in mortality rates from cardiogenic shock. Lower rates of reperfusion of the infarct-related artery in patients with cardiogenic shock may help to explain the disappointing results from TT. Other reasons for the decreased efficacy of TT are the existence of hemodynamic, mechanical, and metabolic causes of cardiogenic shock that are unaffected by TT.
A prospective cohort study demonstrated the potential survival benefit of combining TT with IABP counterpulsation in patients with MI complicated by cardiogenic shock. Of the 1190 patients enrolled, the treatments were (1) no TT and no IABP counterpulsation (33%, n = 285), (2) IABP counterpulsation only (33%, n = 279), (3) TT only (15%, n = 132), and (4) TT and IABP counterpulsation (19%, n = 160).
Patients in cardiogenic shock who were treated with TT had lower in-hospital mortality rates than did those who did not receive TT (54% vs 64%), and patients selected for IABP counterpulsation had lower in-hospital mortality rates than did those who did not receive IABP counterpulsation (50% vs 72%). Furthermore, a significant difference was noted for inhospital mortality rates among the four treatment groups; that is, TT plus IABP counterpulsation (47%), IABP counterpulsation only (52%), TT only (63%), no TT and no IABP counterpulsation (77%). Revascularization influenced in-hospital mortality rates significantly (39% with revascularization vs 78% without revascularization).
The use of the IABP reduces systolic LV afterload and augments diastolic coronary perfusion pressure, thereby increasing cardiac output and improving coronary artery blood flow. The IABP is effective for the initial stabilization of patients with cardiogenic shock. However, an IABP is not definitive therapy; the IABP stabilizes patients so that definitive diagnostic and therapeutic interventions can be performed.[34, 35]
The IABP also may be a useful adjunct to thrombolysis in acute MI for initial stabilization and transfer of patients to a tertiary care facility. Some studies have shown lower mortality rates in patients with MI and cardiogenic shock treated with an IABP and subsequent revascularization.[33, 36]
Complications may be documented in up to 30% of patients who undergo IABP therapy; these relate primarily to local vascular problems, embolism, infection, and hemolysis.
The impact of treatment with an IABP on long-term survival is controversial and depends on the patient’s hemodynamic status and the etiology of the cardiogenic shock. Patient selection is the key issue; inserting the IABP early, rather than waiting until full-blown cardiogenic shock has developed, may result in clinical benefit.
Ramanathan et al found that rapid and complete reversal of systemic hypoperfusion with IABP counterpulsation in the SHOCK trial and SHOCK registry was independently associated with improved inhospital, 30-day, and 1-year survival, regardless of early revascularization. This suggests that complete reversal of systemic hypoperfusion with IABP counterpulsation is an important early prognostic feature.
In the IABP-SHOCK II study, 600 patients with cardiogenic shock complicating acute MI were randomized to IABP counterpulsation or no IABP counterpulsation. All patients were expected to undergo early revascularization. Use of IABP counterpulsation did not significantly reduce 30-day mortality in these patients.
Various LV assist devices (LVADs) capable of providing complete short-term hemodynamic support have been developed. The application of LVAD during reperfusion, after acute coronary occlusion, causes reduction of the LV preload, increases regional myocardial blood flow and lactate extraction, and improves general cardiac function. The LVAD makes it possible to maintain the collateral blood flow as a result of maintaining the cardiac output and aortic pressure, keeping wall tension low and reducing the extent of microvascular reperfusion injury.[34, 35, 39]
A pooled analysis from 17 studies showed that the mean age of this group of patients with LVADs was 59.5 ± 4.5 years and that mean support duration was 146.2 ± 60.2 hours. In 78.5% of patients (range, 53.8-100%), adjunctive reperfusion therapy, mainly percutaneous transluminal coronary angioplasty (PTCA), was used. Mean weaning and survival rates were 58.5% (range, 46-75%) and 40% (range, 29-58%), respectively.
In any case, comparing studies is difficult because important data are usually missing, mean age of patients were different, and time to treatment is not standardized. Hemodynamic presentation seems to be worse compared with data reported in the SHOCK trial, with lower cardiac index, lower systolic aortic pressure, and higher serum lactates. Taking these considerations into account, LVAD support seems to give no survival improvement in patients with cardiogenic shock complicating acute MI, compared with early reperfusion alone or in combination with IABP.
In a randomized, controlled trial in which 129 patients with end-stage heart failure who were ineligible for cardiac transplantation were assigned either to receive an LVAD (68 patients) or to undergo optimal medical management, survival rates were higher in the LVAD group. The rates of survival at 1 year were 52% in the device group and 25% in the medical therapy group, whereas the rates at 2 years were 23% and 8%, respectively. In addition, the quality of life was significantly improved at 1 year in the device group.
Implantable LVADs are being used as a bridge to heart transplantation for patients with acute MI and cardiogenic shock. According to the HeartMate Data Registry , from 1986-1998, 41 patients (5% of the total number of HeartMate IP patients) were supported with this implantable pneumatic device for acute MI, and 25 (61%) were successfully bridged to heart transplantation. (See an example of an LVAD below.)
HeartMate II Left Ventricular Assist Device. Reprinted with the permission of Thoratec Corporation.
However, LVADs as a bridging option for patients with cardiogenic shock must be considered cautiously and must be avoided in patients who are unlikely to survive or are not likely to be transplant candidates. Further investigations are required to better define indications, support modalities, and outcomes.
The indications for insertion of a ventricular assist device are controversial. Such an aggressive approach to support the circulatory system in cardiogenic shock is appropriate (1) after the failure of medical treatment and an IABP, (2) when the cause of cardiogenic shock is potentially reversible, or (3) if the device can be used as a bridging option.
The retrospective and prospective data favor aggressive mechanical revascularization in patients with cardiogenic shock secondary to MI.
Reestablishing blood flow in the infarct-related artery may improve left ventricular function and survival following MI. In acute MI, studies show that PTCA can achieve adequate flow in 80-90% of patients, compared with 50-60% of patients after TT.
Several retrospective clinical trials have shown that patients with cardiogenic shock due to myocardial ischemia benefitted (reduction in 30-day mortality rates) when treated with angioplasty. A study of direct (primary) PTCA in patients with cardiogenic shock reported lower mortality rates in patients treated with angioplasty combined with the use of stents than in patients treat with medical therapy.
A study by Antoniucci et al found that mortality increases in relation to the length of time to treatment in patients with acute MI who are not considered to be at low risk. To study the relation of time to treatment and mortality in patients with acute MI, a series of 1336 patients who underwent successful primary PTCA were stratified into low-risk and not–low-risk patient groups. The 6-month mortality rate was 9.3% for not–low risk patients and 1.3% for the low-risk patients. An increase in the mortality rate from 4.8% to 12.9% with increasing time to reperfusion was observed in the not–low-risk group. A delay from symptom onset to treatment resulted in higher mortality rates for the not–low-risk patients.
Using prospective data from the British Cardiovascular Intervention Society (BCIS) PCI database that evaluated data from 6489 English and Welsh patients undergoing PCI for ACS in the setting of cardiogenic shock, Kunadian et al reported mortality rates of 37.3% at 30 days, 40.0% at 90 days, and 44.3% at 1 year.
Critical left main artery disease and three-vessel coronary artery disease (CAD) are common findings in patients who develop cardiogenic shock. The potential contribution of ischemia in the noninfarcted zone contributes to the deterioration of already compromised myocardial function.
CABG in the setting of cardiogenic shock is generally associated with high surgical morbidity and mortality rates. Because the results of PCI can be favorable, routine bypass surgery is often discouraged for these patients.
Results from the SHOCK (SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK) trial supported the superiority of a strategy that combines early revascularization with medical management in patients with cardiogenic shock.[22, 43, 45] In the study, patients were assigned to receive either optimal medical management, including an IABP and TT, or cardiac catheterization followed by revascularization using PTCA or CABG.
The mortality rates at 30 days were 46.7% in the early intervention group and 56% in patients treated with optimal medical management. Although these 30-day results did not reach statistical significance, the mortality rate at 6 months was significantly lower in the early intervention group (50.3% vs 63.1%).
The 1-year survival rates were also reported from the SHOCK trial. The survival rate at 1-year was 46.7% for patients in the early revascularization group and 33.6% in the conservative management group. The treatment benefit was apparent only for patients younger than 75 years (51.6% survival rate in early revascularization group vs 33.3% in patients treated with optimal medical management).
Based on the outcome of this study, the recommendation is that patients with acute MI complicated by cardiogenic shock, particularly those younger than 75 years, should be rapidly transferred to a center with personnel capable of performing early angiography and revascularization procedures. Long-term follow-up was conducted annually until 2005. A strategy of early revascularization resulted in a 13.2% absolute and 67% relative improvement in 6-year survival compared with initial medical therapy.
Immediately transfer a patient who develops cardiogenic shock to an institution at which invasive monitoring, coronary revascularization, and skilled personnel are available to provide expert care.
Patients with cardiogenic shock who are admitted to a hospital without facilities for revascularization should be immediately transferred to a tertiary care center with such facilities. If time to PCI is more than 1 hour and onset of symptoms has been within 3 hours, rapid administration of TT is recommended.
It should be kept in mind, however, that attempts to transfer a patient with cardiogenic shock must be made only when everything possible has been done to stabilize his or her condition and when the level of care during the transfer will not significantly decrease.
Although cardiogenic shock is not entirely preventable, measures can be taken to minimize the risk of occurrence, recognize it at earlier stages, and begin corrective therapy more expeditiously. Deterrence and prevention require a high degree of suspicion and heightened awareness.
Care is required in treating patients with ACS who are not yet in cardiogenic shock. Careful use of beta blockers and angiotensin-converting enzyme (ACE) inhibitors in these patients is essential to avoid hypotension leading to cardiogenic shock.
Consult a cardiologist at the earliest opportunity because his or her insight and expertise may be invaluable for facilitating echocardiographic support, placement of an IABP, and transfer to more definitive care (eg, cardiac catheterization suite, ICU, operating room). In severe cases, also consider discussing the case with a cardiothoracic surgeon.
The following organizations have released guidelines that include recommendations for the management of cardiogenic shock:
According to the 2013 ACCF/AHA guidelines for the management of ST-elevation myocardial infarction (STEMI), the greater the number of the following risk factors present, the higher the risk of developing cardiogenic shock :
The 2013 ACCF/AHA guidelines for the management patients with STEMI who develop cardiogenic shock include the following :
The 2015 ESC guidelines for the management of acute coronary syndromes (ACSs) concur with ACCF/AHA guidelines for STEMI. However, the 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure recommend against the routine use of IABP in the management of cardiogenic shock (class III; level of evidence, B), but short-term mechanical circulatory support (MCS) may be considered for managment of refractory cardiogenic shock in selected patients (class IIb; level of evidence, C). Additional recommendations for the management of cardiogenic shock include the following :
The 2014 AHA/American College of Cardiology (ACC) guideline for the management of patients with non–ST-elevation ACS (NSTE-ACS) includes the following recommendations for the management of cardiogenic shock :
The following organizations have released guidelines for the utilization of MCS:
A 2015 clinical expert consensus statement from the SCAI/ACC/HFSA/STS noted that historically, the IABP and extracorporeal membrane oxygenation (ECMO) devices were the only MCS devices available to clinicians, but axial-flow pumps such as Impella and left atrium–to–femoral artery bypass pumps such as the TandemHeart subsequently entered clinical practice. The consensus-based recommendations included the following :
In its 2013 guidelines for mechanical circulatory support, the ISHLT recommended long-term MCS for acute cardiogenic shock in the following groups (class IIa; level of evidence, C) :
Vasopressors augment the coronary and cerebral blood flow during the low-flow state associated with shock. Sympathomimetic amines with both alpha- and beta-adrenergic effects are indicated for persons with cardiogenic shock. Dopamine and dobutamine are the drugs of choice to improve cardiac contractility, with dopamine the preferred agent in patients with hypotension.
Vasodilators relax vascular smooth muscle and reduce the SVR, allowing for improved forward flow, which improves cardiac output.
Diuretics are used to decrease plasma volume and peripheral edema. The reduction in extracellular fluid and plasma volume associated with diuresis may initially decrease cardiac output and, consequently, blood pressure, with a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, the plasma volume and peripheral vascular resistance usually return to pretreatment values.
Clinical Context: Dopamine stimulates adrenergic and dopaminergic receptors. Its hemodynamic effect depends on the dose. Lower doses primarily stimulate dopaminergic receptors that produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and vasoconstriction.
Clinical Context: Dobutamine is a sympathomimetic amine with stronger beta effects than alpha effects. It produces systemic vasodilation and increases the inotropic state. Higher doses may cause an increase in heart rate, exacerbating myocardial ischemia.
Clinical Context: Norepinephrine is a naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. It stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction. Norepinephrine increases blood pressure and afterload. Increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia.
Norepinephrine is generally reserved for use in patients with severe hypotension (eg, systolic blood pressure < 70 mm Hg) or hypotension unresponsive to other medication.
Clinical Context: Milrinone is a selective phosphodiesterase inhibitor in cardiac and vascular tissue with positive inotropic and vasodilator effects; it has little chronotropic activity. This agent's mode of action differs from that of either digitalis glycosides or catecholamines.
Clinical Context: Formerly known as amrinone, inamrinone is a phosphodiesterase inhibitor with positive inotropic and vasodilator activity. It produces vasodilation and increases the inotropic state. Inamrinone is more likely to cause tachycardia than is dobutamine, and it may exacerbate myocardial ischemia.
These agents augment coronary and cerebral blood flow during the low-flow state associated with cardiogenic shock. They also improve cardiac output in refractory hypotension and shock.
Clinical Context: This agent causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. The result is a decrease in preload and blood pressure (ie, afterload).
Vasodilators decrease preload and/or afterload.
Clinical Context: Aspirin is an odorless, white, powdery substance available in 81 mg, 325 mg, and 500 mg, for oral use. When exposed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids. It is a stronger inhibitor of prostaglandin synthesis and platelet aggregation than are other salicylic acid derivatives. The acetyl group is responsible for inactivation of cyclo-oxygenase via acetylation. Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero order pharmacokinetics.
Aspirin irreversibly inhibits platelet aggregation by inhibiting platelet cyclo-oxygenase. This, in turn, inhibits the conversion of arachidonic acid to prostaglandin 12 (a potent vasodilator and inhibitor of platelet activation) and thromboxane A2 (a potent vasoconstrictor and platelet aggregate). Platelet-inhibition lasts for the life of the cell (approximately 10 d).
Aspirin may be used at a low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis. It reduces the likelihood of myocardial infarction (MI) and is also very effective in reducing the risk of stroke. Early administration of aspirin in patients with acute MI may reduce cardiac mortality in the first month.
Agents that irreversibly inhibit platelet aggregation may improve morbidity.
Clinical Context: Morphine sulfate is the drug of choice for narcotic analgesia due to its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Various intravenous doses are used; the drug is commonly titrated until the desired effect is achieved.
Analgesics reduce pain, which decreases sympathetic stress and provides some preload reduction.
Clinical Context: Furosemide increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule.
Individualize the dose to the patient. Depending on the response, administer furosemide at increments of 20-40mg no sooner than 6-8 hours after the previous dose, until the desired diuresis occurs. When treating infants, titrate the drug in increments of 1mg/kg/dose until a satisfactory effect is achieved.
These drugs cause diuresis to decrease plasma volume and edema and thereby decrease cardiac output and, consequently, blood pressure. The initial decrease in cardiac output causes a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, extracellular fluid and plasma volumes return almost to pretreatment levels. Peripheral vascular resistance decreases below that of the pretreatment baseline.
Clinical Context: Nesiritide is a recombinant deoxyribonucleic acid (DNA) form of human B-type natriuretic peptide (hBNP), which dilates veins and arteries.
Human BNP binds to the particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells. Binding to the receptor causes an increase in cyclic GMP, which serves as a second messenger to dilate veins and arteries. Pulmonary capillary wedge pressure is reduced and dyspnea is improved in patients with acutely decompensated congestive heart failure.
Nesiritide may be considered in the treatment of patients with cardiogenic shock. Although nesiritide has been shown to increase mortality and renal dysfunction, it continues to be studied as a treatment for acute congestive heart failure and currently retains US Food and Drug Administration (FDA) approval. However, it should be used with caution in the setting of cardiogenic shock because it has been shown to cause hypotension.
These drugs cause arterial and venous dilation by binding to the cyclic guanosine monophosphate (GMP) receptors on vascular smooth muscle, causing smooth muscle relaxation. Natriuretic peptides produce dose-dependent decreases in pulmonary capillary wedge pressure and systemic arterial pressure.
A 63-year-old man admitted to the emergency department with clinical features of cardiogenic shock. The ECG revealed findings indicative of wide-complex tachycardia, likely ventricular tachycardia. Following cardioversion, his shock state improved. The cause of ventricular tachycardia was myocardial ischemia.
A 63-year-old man admitted to the emergency department with clinical features of cardiogenic shock. The ECG revealed findings indicative of wide-complex tachycardia, likely ventricular tachycardia. Following cardioversion, his shock state improved. The cause of ventricular tachycardia was myocardial ischemia.