| Cardiogenic shock | |
|---|---|
| Ultrasound image after cardiogenic shock due tomyocarditis[1] | |
| Specialty | Cardiology |
| Symptoms | Fatigue,rapid heartbeat,shortness of breath,hypotension,sweating,chest pain,dizziness orlightheadedness,nausea,decreased level of consciousness[2] |
| Complications | Worsening of or causingheart failure and/orheart block, seriousarrhythmias such asventricular fibrillation,cor pulmonale, respiratory or kidney or liver dysfunction or failure,multiple organ dysfunction syndrome,cardiac arrest, death |
| Causes | Heart attack, myocarditis,endocarditis, certain medications and substances[2] |
| Risk factors | Heart failure, old age,hypertension[2] |
| Prognosis | 60% mortality in cardiogenic shock not related to heart attack[3] 30-day mortality 40% for cardiogenic shock due to heart attack[4] |
Cardiogenic shock is a medical emergency resulting from inadequate blood flow to the body's organs due to the dysfunction of theheart. Signs of inadequate blood flow include low urine production (<30 mL/hour), cool arms and legs, and decreased level of consciousness. People may also have a severely low blood pressure.
Causes of cardiogenic shock includecardiomyopathic, arrhythmic, and mechanical. Cardiogenic shock is most commonly precipitated bya heart attack. Cardiogenic shock is estimated to complicate 5-10% of all heart attacks.[5]
Treatment of cardiogenic shock depends on the cause with the initial goals to improve blood flow to the body. If cardiogenic shock is due to a heart attack, attempts toopen the heart's arteries may help.[4] Certain medications, such as dobutamine and milrinone, improve the heart's ability to contract and can also be used.[4] When these measures fail, more advanced options such as mechanical support devices (such as anintra-aortic balloon pump orleft ventricular assist device).[4]
Cardiogenic shock is a condition that is difficult to fully reverse even with an early diagnosis.[5] However, early initiation of treatment may improve outcomes. Care should also be directed to any other organs that are affected by this lack of blood flow (e.g.,dialysis for the kidneys, mechanical ventilation for lung dysfunction).
Mortality rates for cardiogenic shock are high but have been decreasing in the United States. This is likely due to its rapid identification and treatment in recent decades. Some studies have suggested that this is possibly related to new treatment advances. The 30-day mortality rate for cardiogenic shock after a heart attack is 40% with a 1-year mortality rate of 50%.[4] Nonetheless, the mortality rates remain high and multi-organ failure in addition to cardiogenic shock is associated with higher rates of mortality.[6]
Cardiogenic shock may present as shortness of breath (respiratory distress) due to fluid buildup in the lungs (pulmonary edema).[4] Reduced perfusion to the brain can cause drowsiness, withanoxic brain injury causing coma and death.Low blood pressure due to decrease incardiac output may causecirculatory shock with symptoms of a rapid, weak pulse due to decreased circulation, cool, clammy, and mottled skin (cutis marmorata) due to vasoconstriction and subsequent hypoperfusion of the skin,low urine output, confusion.[4] Increased heart filling pressures can causeorthopnea and distendedjugular veins due to increasedjugular venous pressure.[4]
Cardiogenic shock is caused by the failure of the heart to pump effectively. It is due to damage to theheart muscle, most often from a heart attack.[7] Other causes includeabnormal heart rhythms,cardiomyopathy,heart valve problems, ventricular outflow obstruction (i.e. systolic anterior motion inhypertrophic cardiomyopathy),myocardial contusion or ventriculoseptal defects. It can also be caused by a sudden depressurization (e.g. in an aircraft), where air bubbles are released into the bloodstream (Henry's law), causingheart failure.[8][9][10][11][12][13][14]
In cardiogenic shock due to a heart attack, shock can develop at the time of the heart attack or after. The median time from heart attack to developing shock was about 5.5-6 hours.[4] In a registry study, 74% of people developed shock within 24 hours of the heart attack, with 46.6% developing shock within 6 hours of the heart attack.[4] Theleft anterior descending artery and theleft main coronary artery are the two most commonly blocked arteries in heart attacks that lead to cardiogenic shock.[4]
An electrocardiogram is recommended for those with cardiogenic shock and can assess for heart muscle damage or abnormal heart rhythms or rate.[4]
Anechocardiogram can assess for structural heart disease or complications due to cardiogenic shock. Some structural complications include ventricular free wall rupture,interventricular septum rupture,papillary muscle rupture with acutemitral valve regurgitation. These structural complications are associated with a high mortality and can severely worsen cardiogenic shock.[4]
Apulmonary artery catheter which can provide invasive hemodynamic monitoring (such as thepulmonary capillary wedge pressure,pulmonary artery pressure and other markers of heart function) can provide valuable information regarding disease severity and response to treatment. Invasive hemodynamic monitoring was associated with lower mortality in those with cardiogenic shock due to heart attack based on observational data, but randomized trials are lacking.[4]
When cardiomyopathy of an unknown cause is suspected as the cause of cardiogenic shock, abiopsy of heart muscle may be needed to make a definitediagnosis.[15]
If thecardiac index falls acutely below 2.2 L/min/m2, the person may be in cardiogenic shock, but a consensus value is not established.[16]
Initial management of cardiogenic shock involves medications to augment the heart's function. Certain medications, such asdobutamine ormilrinone, enhance the heart's pumping function and are often used first-line to improve the low blood pressure and delivery of blood to the rest of the body.[5]
Patients who have cardiogenic shock unresponsive to medication therapy may be candidates for more advanced options such as a mechanical circulatory support device. There are several types of mechanical circulatory support devices, the most common being intra-aortic balloon pumps, left ventricular assist devices, and venous-arterial extra-corporeal membrane oxygenation. It is important to note, however, that none of these devices are permanent solutions but rather are a bridge to a more definitive therapy such as aheart transplantion, surgical correction of heart, or coronary revascularization.
In cardiogenic shock due to heart attack, revascularization of the occluded coronary artery is shown to reduce mortality. Early revascularization is associated with better outcomes.[4] It is unclear if multi-vessel revascularization (revascularizing other coronary arteries that are not occluded, in addition to the culprit coronary artery) has additional benefit.[4]
An intra-aortic balloon pump is a device placed by a cardiac surgeon into thedescending aorta. It consists of a small balloon filled with helium that helps the heart to pump blood by inflating duringdiastole (the resting phase of the cardiac cycle) and deflating duringsystole (the contracting phase of the cardiac cycle).[17] Intra-aortic balloon pumps do not directly increase cardiac output, but importantly, they decrease the amount of pressure that the heart has to pump against, thereby allowing for more blood flow and oxygen to be delivered to the heart muscles.[18]
Intra-aortic balloon pumps have been around for several decades and are most commonly used first-line of the mechanical circulatory support devices.[5] However, it is not without its potential complications. Potential complications include injury upon insertion of the device to arteries supplying the spinal cord as well as risks with any procedure such as bleeding and infection.[18] Contraindications to intra-aortic balloon pumps include aortic dissection, an abdominal aortic aneurysm, and irregularly fast heart beats.[17]
There are several types of left ventricular assist devices, with the Impella devices being some of the most common. This device is placed by a cardiac surgeon into theleft ventricle of the heart and essentially acts as a pump, drawing blood from the left ventricle and pushing it out into the aorta so that it could be delivered to the rest of the body.[5] Unlike intra-aortic balloon pumps, the Impella acts independently from the cardiac cycle.[18] It can be adjusted to pump at faster rates to take blood out of the left ventricle and into the aorta more quickly, thereby decreasing the amount of work that the left ventricle has to do.[5] While the Impella is commonly used in settings of cardiogenic shock, some evidence suggests that it placing an Impella device in an acute cardiogenic shock setting, where the heart fails to pump suddenly, may not necessarily guarantee increased survival.[19]
Potential complications specific to an Impella device includehemolysis (shearing of the blood cells) as well as the formation of lesions on the heart valve, namely themitral oraortic valves.[18] Contraindications to an Impella device insertion include aortic dissection, the presence of a mechanical aortic valve, and the presence of a blood clot in the left ventricle.[17]
Venous-arterial extra-corporeal membrane oxygenation is a circuit support system that is meant to replace the function of the heart as it heals or awaits a more definitive treatment.[18] It consists of a circuit that essentially drains blood from a patient's venous system, runs that blood through a circulator which adds oxygen and removes carbon dioxide, and ultimately returns blood back into the patient's arterial system where the newly oxygenated blood can be delivered to the person's organs. Some evidence suggests that the combination of both an Impella device and Venous-arterial extra-corporeal membrane oxygenation may decrease the heart'spulmonary capillary wedge pressure, thereby decreasing the amount of stress on the cardiac muscles.[20]
Because venous-arterial extra-corporeal membrane oxygenation is an invasive procedure, it is not usually a first-line option in cardiogenic shock and is often reserved only for people who have cardiogenic shock refractory to other treatments or devices or concomitantcardiac arrest.[18]
Complications of venous-arterial extra-corporeal membrane oxygenation include anair embolism,pulmonary edema, and blood clotting in the circuit machine.[18] It may also increase left ventricle afterload (causing the heart to pump against higher pressures) or cause pulmonary edema.[4]