Cardiogenic shock Definition 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). Cardiogenic shock is a condition in which your heart suddenly can't pump enough blood to meet your body's needs. Cardiogenic shock is most often caused by a severe heart attack. Cardiogenic shock is rare, but it's often fatal if not treated immediately. If treated immediately, about half the people who develop cardiogenic shock survive. 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 at least 30 min) and a reduced cardiac index (< 2.2 L/min/m2) in the presence of elevated pulmonary capillary wedge pressure (>15 mm Hg). Pathophysiology Cardiogenic shock is recognized as a low cardiac output state secondary to extensive left ventricular infarction, development of a mechanical defect (eg, ventricular septal defect or papillary muscle rupture), or right ventricular infarction. Disorders that can result in the acute deterioration of cardiac function and lead to cardiogenic shock include myocardial infarction (MI) or myocardial ischemia, acute myocarditis, sustained arrhythmia, severe valvular dysfunction, and decompensation of end-stage cardiomyopathy from multiple etiologies. Autopsy studies show that cardiogenic shock is generally associated with the loss of more than 40% of the left ventricular myocardial muscle. Myocardial pathology Cardiogenic shock is characterized by systolic and diastolic dysfunction. Patients who develop cardiogenic shock from acute MI consistently have evidence of progressive myocardial necrosis with infarct extension. Decreased coronary perfusion pressure and increased myocardial oxygen demand play a role in the vicious cycle that leads to cardiogenic shock. 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 causes decreased myocardial compliance, thereby increasing left ventricular filling pressure, which may lead to pulmonary edema and hypoxemia.

Cellular pathology 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. Reversible myocardial dysfunction 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. Cardiovascular mechanics of cardiogenic shock The main mechanical defect in cardiogenic shock is a shift to the right for the left ventricular 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 stroke volume is decreased, and to compensate for this, the curvilinear diastolic pressure-volume curve also shifts to the right, with a decrease in diastolic compliance. This leads to increased diastolic filling, which is associated with an increase in enddiastolic pressure. The attempt to enhance cardiac output by this mechanism comes at the cost of having a higher left ventricular diastolic filling pressure, which ultimately increases myocardial oxygen demand and causes pulmonary edema. As a result of decreased contractility, the patient develops elevated left and right ventricular 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. Systemic effects When a critical mass of left ventricular myocardium becomes ischemic and fails to pump effectively, stroke volume and cardiac output are curtailed. Myocardial ischemia is further exacerbated by compromised myocardial perfusion due to hypotension and tachycardia. The 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, 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 fluid retention, hence augmenting the left ventricular preload. The raised heart rate and contractility increases myocardial oxygen demand, further worsening myocardial ischemia. Fluid retention and impaired left ventricular diastolic filling triggered by tachycardia and ischemia contribute to 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 left ventricular filling pressure at a

given end-diastolic volume (diastolic dysfunction), which leads to pulmonary congestion and congestive heart failure. Shock state 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. Etiology Cardiogenic shock can result from the following types of cardiac dysfunction: Systolic dysfunction Diastolic dysfunction Valvular dysfunction Cardiac arrhythmias Coronary artery disease Mechanical complications 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 left ventricular myocardium, although in patients with previously compromised left ventricular 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 myocardial infarction (MI). Complications of acute MI, such as acute mitral regurgitation, large right ventricular infarction, and rupture of the interventricular septum or left ventricular free wall, 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.[1, 2, 3] 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 3 primary causes of cardiogenic shock in children. A systemic inflammatory response syndrometype 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. Left ventricular failure Systolic dysfunction 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: Ischemia/MI Global hypoxemia Valvular disease Myocardial depressant drugs - Eg, beta blockers, calcium channel blockers, and antiarrhythmics Myocardial contusion Respiratory acidosis Metabolic derangements - Eg, acidosis, hypophosphatemia, and hypocalcemia Severe myocarditis End-stage cardiomyopathy - Including valvular causes Prolonged cardiopulmonary bypass. Cardiotoxic drugs - Eg, doxorubicin (Adriamycin) Diastolic dysfunction Increased left ventricular 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: Ischemia Ventricular hypertrophy Restrictive cardiomyopathy Prolonged hypovolemic or septic shock Ventricular interdependence External compression by pericardial tamponade

Greatly increased afterload Increased afterload, which can impair cardiac function, can be caused by the following: Aortic stenosis Hypertrophic cardiomyopathy Dynamic aortic outflow tract obstruction Coarctation of the aorta Malignant hypertension Valvular and structural abnormality Valvular dysfunction may immediately lead to cardiogenic shock or 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: Mitral stenosis Endocarditis Mitral aortic regurgitation Obstruction due to atrial myxoma or thrombus Papillary muscle dysfunction or rupture Ruptured septum or free wall arrhythmias Tamponade Decreased contractility Reduced myocardial contractility can result from the following: Right ventricular infarction Ischemia Hypoxia Acidosis Right ventricular failure Greatly increased afterload Afterload increase associated with right ventricular failure can result from the following: Pulmonary embolism Pulmonary vascular disease - Eg, pulmonary arterial hypertension and veno-occlusive disease Hypoxic pulmonary vasoconstriction Peak end-expiratory pressure

High alveolar pressure Acute respiratory distress syndrome Pulmonary fibrosis Sleep disordered breathing Chronic obstructive pulmonary disease Arrhythmias 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. Clinical presentation 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. Cardiogenic shock following acute MI generally develops after admission to the hospital, although 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 in mean blood pressure by 30 mm Hg, 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 myocardial infarction (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 hypertrophy, hypertension, or cigarette smoking or a family history of premature coronary artery disease. The presence of 2 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. Physical Examination 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 is detected upon physical examination. Characteristics of patients with cardiogenic shock include the following: Patients in shock usually appear ashen or cyanotic and have cool skin and mottled extremities Peripheral pulses are rapid and faint and may be irregular if arrhythmias are present Jugular venous distention and crackles in the lungs are usually (but not always) present; peripheral edema also may be present. Heart sounds are usually distant, and third and fourth heart sounds may be present The pulse pressure may be low, and patients are usually tachycardic Patients show signs of hypoperfusion, such as altered mental status and decreased urine output 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. The systolic murmur, which becomes louder upon Valsalva and prompt standing, suggests hypertrophic obstructive cardiomyopathy (idiopathic hypertropic subaortic stenosis). Laboratory Studies Biochemical profile Measurement of routine biochemical parameters, such as electrolytes, renal function (eg, urea and creatinine), and liver function tests (eg, bilirubin, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase [LDH]), are useful for assessing proper functioning of vital organs. CBC count 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. Cardiac enzymes The diagnosis of acute myocardial infarction (MI) is aided by a variety of serum markers, which include creatine kinase and its subclasses, troponin, myoglobin, and LDH. The value for the isoenzyme of creatine kinase with muscle and blood subunits is most specific but 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 4-fold 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 also may come from the kidneys, stomach, pancreas, and red blood cells. Troponins 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 I and T 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 nonQ-wave MI. Arterial blood gases 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 is +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. Lactate 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 Brain natriuretic peptide (BNP) may be useful as an indicator of congestive heart failure 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. Imaging Studies Echocardiography 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 ejection fraction is not always depressed in the setting of cardiogenic shock). If a hyperdynamic left ventricle is found, the echocardiogram may suggest other causes of shock such as sepsis or anemia Chest radiography Chest radiographic findings are useful for excluding other causes of shock or chest pain. A widened mediastinum may indicate aortic dissection. Tension pneumothorax or pneumomediastinum readily detected on radiographic films may manifest as low-output shock. Most patients with established cardiogenic shock exhibit findings of left ventricular 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 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 artery angiography Coronary angiography is urgently indicated in patients with myocardial ischemia or myocardial infarction (MI) who also develop cardiogenic shock. Angiography is required to help assess the anatomy of the coronary arteries and the need for urgent revascularization. Coronary angiography findings often demonstrate multivessel coronary artery disease 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, although a smaller infarction in a previously compromised left ventricle also may precipitate shock. Following MI, large areas of nonfunctional, but viable, myocardium (hibernating myocardium) can also cause or contribute to cardiogenic shock. ECG Acute myocardial ischemia is diagnosed based on the presence of ST-segment elevation, ST-segment depression, or Q waves. T-wave inversion, although a less sensitive finding, may also be seen in persons with myocardial ischemia. An ECG with right-sided chest leads may document right ventricular infarction and may be prognostically, as well as diagnostically, useful.

Perform electrocardiography immediately to help diagnose myocardial infarction (MI) and/or myocardial ischemia. A normal ECG, however, does not rule out the possibility of acute MI Invasive Hemodynamic Monitoring Invasive hemodynamic monitoring (Swan-Ganz catheterization) is very useful for helping 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) of greater than 15 mm Hg and a cardiac index of less than 2.2 L/min/m2. The presence of large V waves on the PCWP tracing suggests severe mitral regurgitation, while a step-up in oxygen saturation between the right atrium and the right ventricle is diagnostic of ventricular septal rupture. High right-sided filling pressures in the absence of an elevated PCWP, when accompanied by electrocardiographic criteria, indicate right ventricular infarction. Treatments and drugs Cardiogenic shock treatment focuses on repairing the damage to your heart muscle and other organs caused by lack of oxygen. Emergency life support Emergency life support is a necessary treatment for most people who have cardiogenic shock. During emergency life support, you're given extra oxygen to breathe to minimize damage to your muscles and organs. If necessary, you'll be connected to a breathing machine (ventilator). You'll receive medications and fluid through an intravenous (IV) line in your arm. Medications Medications to treat cardiogenic shock work to improve blood flow through your heart and increase your heart's pumping ability. Aspirin. You may be given aspirin by emergency medical personnel soon after they arrive on the scene or as soon as you get to the hospital. Aspirin reduces blood clotting and helps keep your blood flowing through a narrowed artery. Take an aspirin yourself while waiting for help to arrive only if your doctor has previously told you to do so if symptoms of a heart attack occur. Thrombolytics. These drugs, also called clot busters, help dissolve a blood clot that's blocking blood flow to your heart. The earlier you receive a thrombolytic drug after a heart attack, the greater the chance you'll survive and lessen the damage to your heart.

You'll usually receive thrombolytics only if emergency cardiac catheterization isn't available. Superaspirins. Doctors in the emergency room may give you other drugs that are similar to aspirin to help prevent new clots from forming. These include medications, such as clopidogrel (Plavix) and others called platelet glycoprotein IIb/IIIa receptor blockers. Other blood-thinning medications. You'll likely be given other medications, such as heparin, to make your blood less likely to form more dangerous clots. Heparin is given intravenously or by an injection under your skin and is usually used during the first few days after a heart attack. Inotropic agents. You may be given medications, such as dopamine or epinephrine, to improve and support your heart function until other treatments start to work. Medical procedures Medical procedures to treat cardiogenic shock usually focus on restoring blood flow through your heart. They include: Angioplasty and stenting. Usually, once blood flow is restored through a blocked artery, the signs and symptoms of cardiogenic shock improve. Emergency angioplasty opens blocked coronary arteries, letting blood flow more freely to your heart. Doctors insert a long, thin tube (catheter) that's passed through an artery, usually in your leg, to a blocked artery in your heart. This catheter is equipped with a special balloon. Once in position, the balloon is briefly inflated to open up a blocked coronary artery. At the same time, a metal mesh stent may be inserted into the artery to keep it open long term, restoring blood flow to the heart. In most cases, you doctor will place a stent coated with a slowreleasing medication to help keep your artery open. Balloon pump. Depending on your condition, your doctors may choose to insert a balloon pump in the main artery of your heart (aorta). The balloon pump inflates and deflates to mimic the pumping action of your heart, helping blood flow through. Surgery If medications and medical procedures don't work to treat cardiogenic shock, your doctor may recommend surgery. Coronary artery bypass surgery. Bypass surgery involves sewing veins or arteries in place at a site beyond a blocked or narrowed coronary artery. This restores blood flow to the heart. Your doctor may suggest that you have this procedure after your heart has had time to recover from your heart attack. Surgery to repair an injury to your heart. Sometimes an injury in your heart, such as a tear in one of your heart's chambers or a damaged heart valve, can cause cardiogenic shock. If an injury causes your cardiogenic shock, your doctor may recommend surgery to correct the problem.

Heart pumps. These mechanical devices, called ventricular assist devices (VADs), are implanted into the abdomen and attached to a weakened heart to help it pump. Implanted heart pumps can extend and improve the lives of some people with end-stage heart failure who aren't eligible for or able to undergo heart transplantation or are waiting for a new heart. Heart transplant. If your heart is so damaged that no other treatments work, a heart transplant may be a last resort for treating cardiogenic shock.

Septic shock Septic shock is a serious condition that occurs when an overwhelming infection leads to life-threatening low blood pressure. Acute respiratory distress syndrome Disseminated intravascular coagulation Meningococcemia Waterhouse-Friderichsen syndrome Causes Septic shock occurs most often in the very old and the very young. It also occurs in people who have other illnesses. Any type of bacteria can cause septic shock. Fungi and (rarely) viruses may also cause the condition. Toxins released by the bacteria or fungi may cause tissue damage, and may lead to low blood pressure and poor organ function. Some researchers think that blood clots in small arteries cause the lack of blood flow and poor organ function. The body also produces a strong inflammatory response to the toxins. This inflammation may contribute to organ damage. Risk factors for septic shock include: Diabetes Diseases of the genitourinary system, biliary system, or intestinal system Diseases that weaken the immune system such as AIDS Indwelling catheters (those that remain in place for extended periods, especially intravenous lines and urinary catheters and plastic and metal stents used for drainage) Leukemia Long-term use of antibiotics Lymphoma Recent infection Recent surgery or medical procedure Recent use of steroid medications Symptoms Septic shock can affect any part of the body, including the heart, brain, kidneys, liver, and intestines. Symptoms may include: Cool, pale extremities High or very low temperature, chills Lightheadedness Low blood pressure, especially when standing Low or absent urine output Palpitations Rapid heart rate

Restlessness, agitation, lethargy, or confusion Shortness of breath Skin rash or discoloration Exams and Tests Blood tests may be done to check for infection, low blood oxygen level, disturbances in the body's acid-base balance, or poor organ function or organ failure. A chest x-ray may show pneumonia or fluid in the lungs (pulmonary edema). A urine sample may show infection. Additional studies, such as blood cultures, may not become positive for several days after the blood has been taken, or for several days after the shock has developed. Tests and diagnosis Diagnosing sepsis can be difficult because its signs and symptoms can be caused by other disorders. Doctors often order a battery of tests to try to pinpoint the underlying infection. Blood tests A sample of your blood can be tested for: Evidence of infection Clotting problems Abnormal liver or kidney function Impaired oxygen availability Electrolyte imbalances Other laboratory tests Depending on your symptoms, your doctor may also want to run tests on one or more of the following bodily fluids: Urine. If your doctor suspects that you have a urinary tract infection, he or she may want your urine checked for signs of bacteria. Wound secretions. If you have a wound that appears infected, testing a sample of the wound's secretions can help show what type of antibiotic might work best. Respiratory secretions. If you are coughing up mucus (sputum), it may be tested to determine what type of germ is causing the infection. Imaging scans If the site of infection is not obvious, your doctor may order one or more of the following imaging tests: X-ray. Using low levels of radiation, X-rays are a good tool to visualize problems in the lungs. X-rays are painless and take only a few minutes to complete. Computerized tomography (CT). Infections in the appendix, pancreas or bowels are easier to see on CT scans. This technology takes X-rays from a variety of angles and combines them to depict cross-sectional slices of your body's internal structures. The test is painless and usually takes less than 20 minutes.

Ultrasound. This technology uses sound waves to produce real-time images on a video monitor. Ultrasound may be particularly useful to check for infections in your gallbladder or ovaries. Magnetic resonance imaging (MRI). MRIs may be helpful in identifying soft tissue infections, such as abscesses within the spine. This technology uses radio waves and a strong magnet to produce cross-sectional images of your internal structures. Treatment Septic shock is a medical emergency. Patients are usually admitted to the intensive care unit of the hospital. Treatment may include: Breathing machine (mechanical ventilation) Drugs to treat low blood pressure, infection, or blood clotting Fluids given directly into a vein (intravenously) Oxygen Surgery There are new drugs that act against the extreme inflammatory response seen in septic shock. These may help limit organ damage. Hemodynamic monitoring -- the evaluation of the pressures in the heart and lungs -- may be required. This can only be done with special equipment and intensive care nursing. Treatments and drugs Early, aggressive treatment boosts your chances of surviving sepsis. People with severe sepsis require close monitoring and treatment in a hospital intensive care unit. If you have severe sepsis or septic shock, lifesaving measures may be needed to stabilize breathing and heart function. Medications A number of different types of medications are used in treating sepsis. They include: Antibiotics. Treatment with antibiotics begins immediately even before the infectious agent is identified. Initially you'll receive broad-spectrum antibiotics, which are effective against a variety of bacteria. The antibiotics are administered intravenously (IV). After learning the results of blood tests, your doctor may switch to a different antibiotic that's more appropriate against the particular bacteria causing the infection. Vasopressors. If your blood pressure remains too low even after receiving intravenous fluids, you may be given a vasopressor medication, which constricts blood vessels and helps to increase blood pressure. Others. Other medications you may receive include low doses of corticosteroids, insulin to help maintain stable blood sugar levels, drugs that modify the immune system responses, and painkillers or sedatives. Therapy

People with severe sepsis usually receive supportive care including oxygen and large amounts of intravenous fluids. Depending on your condition, you may need to have a machine help you breathe or dialysis for kidney failure. Surgery Surgery may be needed to remove sources of infection, such as collections of pus (abscesses). Outlook (Prognosis) Septic shock has a high death rate. The death rate depends on the patient's age and overall health, the cause of the infection, how many organs have failed, and how quickly and aggressively medical therapy is started. Possible Complications Respiratory failure, cardiac failure, or any other organ failure can occur. Gangrene may occur, possibly leading to amputation. When to Contact a Medical Professional Go directly to an emergency department if you develop symptoms of septic shock. Prevention Prompt treatment of bacterial infections is helpful. However, many cases of septic shock cannot be prevented. Alternative Names Bacteremic shock; Endotoxic shock; Septicemic shock; Warm shock

Anaphylactic shock Definition Anaphylaxis is a severe, potentially life-threatening allergic reaction. It can occur within seconds or minutes of exposure to something you're allergic to, such as a peanut or the venom from a bee sting. The flood of chemicals released by your immune system during anaphylaxis can cause you to go into shock; your blood pressure drops suddenly and your airways narrow, blocking normal breathing. Signs and symptoms of anaphylaxis include a rapid, weak pulse, a skin rash, and nausea and vomiting. Common triggers of anaphylaxis include certain foods, some medications, insect venom and latex. Anaphylaxis requires an immediate trip to the emergency department and an injection of epinephrine. If anaphylaxis isn't treated right away, it can lead to unconsciousness or even death. Symptoms Anaphylaxis symptoms usually occur within minutes of exposure to an allergen. Sometimes, however, anaphylaxis can occur a half-hour or longer after exposure. Anaphylaxis symptoms include: Skin reactions, including hives along with itching, and flushed or pale skin (almost always present with anaphylaxis) A feeling of warmth The sensation of a lump in your throat Constriction of the airways and a swollen tongue or throat, which can cause wheezing and trouble breathing A weak and rapid pulse Nausea, vomiting or diarrhea Dizziness or fainting When to see a doctor Seek emergency medical help if you, your child or someone else you're with has a severe allergic reaction. If the person having the attack carries an epinephrine autoinjector (such as an EpiPen or EpiPen Jr), give him or her a shot right away. Even if symptoms improve after an emergency epinephrine injection, a visit to the emergency department is still necessary to make sure symptoms don't return. Make an appointment to see your doctor if you or your child has had a severe allergy attack or any signs and symptoms of anaphylaxis in the past. The diagnosis and long-term management of anaphylaxis are complicated, so you'll probably need to see a doctor who specializes in allergies and immunology.

Causes Your immune system produces antibodies that defend against foreign substances. This is good when a foreign substance is harmful (such as certain bacteria or viruses). But some people's immune systems overreact to substances that shouldn't cause an allergic reaction. When this occurs, the immune system sets off a chemical chain reaction, leading to allergy symptoms. Normally, allergy symptoms aren't life-threatening. But some people have a severe allergic reaction that can lead to anaphylaxis. Even if you or your child has had only a mild anaphylactic reaction in the past, there's still a risk of more severe anaphylaxis. A number of allergens can trigger anaphylaxis, depending on what you're allergic to. Common anaphylaxis triggers include: Certain medications, especially penicillin Foods, such as peanuts, tree nuts (walnuts, pecans, almonds, cashews), wheat (in children), fish, shellfish, milk and eggs Insect stings from bees, yellow jackets, wasps, hornets and fire ants Less common causes of anaphylaxis include: Latex Medications used in anesthesia Exercise Anaphylaxis symptoms are sometimes caused by aspirin and other drugs such as ibuprofen (Advil, Motrin, others) and naproxen (Aleve, Midol Extended Relief) and the intravenous (IV) contrast used in some X-ray imaging tests. Although similar to allergy-induced anaphylaxis, this type of reaction isn't triggered by allergy antibodies. Anaphylaxis triggered by exercise is not common and varies from person to person. In some people, aerobic activity, such as jogging, triggers anaphylaxis. In others, less intense physical activity, such as walking, can trigger a reaction. Eating certain foods before exercise or exercising when the weather is hot, cold or humid also has been linked to anaphylaxis in some people. Talk with your doctor about any precautions you should take when exercising. If you don't know what triggers your allergy attack, your doctor may do tests to try to identify the offending allergen. In some cases, the cause of anaphylaxis is never identified. This is known as idiopathic anaphylaxis. Risk factors There aren't many known risk factors for anaphylaxis, but some things that may increase your risk include: A personal history of anaphylaxis. If you've experienced anaphylaxis once, your risk of having this serious reaction increases. Future reactions may be more severe than the first reaction.

Allergies or asthma. People who have either condition are at increased risk of having anaphylaxis. A family history. If you have family members who've experienced exercise-induced anaphylaxis, your risk of developing this type of anaphylaxis is higher than it is for someone without a family history. Complications An anaphylactic reaction can be life-threatening when a severe attack occurs; it can stop breathing or stop your heartbeat. In this case, you'll need cardiopulmonary resuscitation (CPR) and other emergency treatment right away. Tests and diagnosis Your doctor will ask you questions about your allergies or any previous allergic reactions you've had. This evaluation will include questions about: Whether any particular foods seem to cause a reaction Any medications you take, and if certain medications seem linked to your symptoms Whether you've had allergy symptoms when your skin has been exposed to latex Whether stings from any particular type of insect seem to cause your symptoms To help confirm the diagnosis: You may be tested for allergies with skin tests or blood tests You may also be asked to keep a detailed list of what you eat or to stop eating certain foods for a time Your doctor will want to rule out other conditions as a possible cause of your symptoms, including: Seizure disorders A condition other than allergies that causes flushing or other skin symptoms Mastocytosis, an immune system disorder Psychological issues, such as panic attacks Heart or lung problems Treatments and drugs During an anaphylactic attack, an emergency medical team may perform cardiopulmonary resuscitation (CPR) if you stop breathing or your heart stops beating. You may be given medications including: Epinephrine (adrenaline) to reduce your body's allergic response Oxygen, to help compensate for restricted breathing Intravenous (IV) antihistamines and cortisone to reduce inflammation of your air passages and improve breathing A beta-agonist (such as albuterol) to relieve breathing symptoms What to do in an emergency If you're with someone who is having an allergic reaction and shows signs of shock caused by anaphylaxis, act fast. Signs and symptoms of shock caused by anaphylaxis

include pale, cool and clammy skin, weak and rapid pulse, trouble breathing, confusion, and loss of consciousness. Even if you're not sure symptoms are caused by anaphylaxis, take the following steps immediately: Call 911 or emergency medical help. Get the person in a comfortable position and elevate his or her legs. Check the person's pulse and breathing and, if necessary, administer CPR or other firstaid measures. Give medications to treat an allergy attack, such as an epinephrine autoinjector or antihistamines, if the person has them. Using an autoinjector Many people at risk of anaphylaxis carry an autoinjector. This device is a combined syringe and concealed needle that injects a single dose of medication when pressed against your thigh. Always be sure to replace epinephrine before its expiration date, or it may not work properly. Be sure you know how to use the autoinjector. Also, make sure the people closest to you know how to administer the drug if they're with you during an anaphylactic emergency, one of them could save your life. Medical personnel called in to respond to a severe anaphylactic reaction also may give you an epinephrine injection or another medication to treat your symptoms. Long-term treatment If your anaphylactic reaction is triggered by insect stings, you may be able to get a series of allergy shots (immunotherapy) to reduce your body's allergic response and prevent a severe reaction in the future. Unfortunately, in most other cases there's no way to treat the underlying immune system condition that can lead to anaphylaxis. But you can take steps to prevent a future attack and be prepared in the event one does occur. Avoid your known allergy triggers as much as you can. You may need to carry self-administered epinephrine. During an anaphylactic attack, you can give yourself the drug using an autoinjector (EpiPen, EpiPen Jr or Twinject). Your doctor may recommend taking prednisone or antihistamines. Neurogenic Shock Hypotension secondary to a nervous system disfunction made by a severe trauma or a poor loco-regional anesthesia with an accidental rising up of the level of anesthesia. Physiology Main mechanism acute disfunction of the sympathetic nervous system.

Hypotension is caused by central simpaticolisis or medullary simpaticolisis. Under these conditions, it disappears sympathetic tonus, resulting vasodilation, decreased systemic vascular resistance, accompanied by nervous response by increased venous return capacity decrease vascular, decreased preload and cardiac output, followed by severe hypotension. Diagnosis Is established based on historical data, suggesting etiology, traumatic accident or spinal anesthesia, and clinical data - hypotension with warm extremities. Principles of treatment Sympathetic restoration by giving sympathomimetic vasoconstrictors drugs (ephedrine, neosinefrina, norepinephrine), maintaining adequate intravascular volume with fluid volume management solutions. Extracardiac obstructive shock Is produced by> extrinsic vascular compression, mediastinal tumors, complex diseases that induce increased intrathoracic pressure (pneumothorax pressure mechanical ventilation with PEEP), intrinsic vascular obstruction (pulmonary embolism, gas embolism, tumors, aortic dissection, aortic coartaction, acute lung hypertension), pericardial disease (tamponade secondary to trauma, myocardial rupture, Dressler syndrome, inflammatory, autoimmune, infectious, malignant, in uremia or during anticoagulant therapy, constrictive pericarditis) miscelanee (hyperviscosity syndromes, sickle cell crisis, polycythemia vera) Distributive shock Occurs in the systemic inflammatory response syndrome (SIRS) after > sepsis, septic shock (bacteria, fungi, viruses, rickets), pancreatitis, polytrauma, burns anaphylaxis (venoms, drugs) neurogenic shock (spinal trauma, spinal anesthesia High) given toxic shock / drugs (vasodilators, benzodiazepines) shock endocrine (thyroid in myxedema, medulosupra-renalian failure)