Redirect circulatory shock
|Classification and external resources|
As this is a type of circulatory shock there is insufficient perfusion of tissue (i.e. the heart) to meet the required demands for oxygen and nutrients. Cardiogenic shock is a largely irreversible condition and as such is more often fatal than not. The condition involves increasingly more pervasive cell death from oxygen starvation (hypoxia) and nutrient starvation (e.g. hypoglycemia). Because of this it may lead to cardiac arrest (or circulatory arrest) which is an acute cessation of cardiac pump function.
Cardiogenic shock is defined by sustained hypotension with tissue hypoperfusion despite adequate left ventricular filling pressure. Signs of tissue hypoperfusion include oliguria (<30 mL/h), cool extremities, and altered level of consciousness.
Signs and symptoms
- Anxiety, restlessness, altered mental state due to decreased cerebral perfusion and subsequent hypoxia.
- Hypotension due to decrease in cardiac output.
- A rapid, weak, thready pulse due to decreased circulation combined with tachycardia.
- Cool, clammy, and mottled skin (cutis marmorata), due to vasoconstriction and subsequent hypoperfusion of the skin.
- Distended jugular veins due to increased jugular venous pressure.
- Oliguria (low urine output) due to insufficient renal perfusion if condition persists.
- Rapid and deeper respirations (hyperventilation) due to sympathetic nervous system stimulation and acidosis.
- Fatigue due to hyperventilation and hypoxia.
- Absent pulse in tachyarrhythmia.
- Pulmonary edema, involving fluid back-up in the lungs due to insufficient pumping of the heart.
Cardiogenic shock is caused by the failure of the heart to pump effectively. It can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes include arrhythmia, cardiomyopathy, cardiac valve problems, ventricular outflow obstruction (i.e. aortic valve stenosis, aortic dissection, cardiac temponade, constrictive pericaditis systolic anterior motion (SAM) in hypertrophic cardiomyopathy) or ventriculoseptal defects. It can also be caused by a sudden decompressurization (e.g. in an aircraft), where air bubbles are released into the bloodstream (Henry's Law), causing heartfailure.
An electrocardiogram helps establishing the exact diagnosis and guides treatment, it may reveal:
In cardiogenic shock, depending on the type of myocardial infarction, treatment involves infusion of fluids, or in shock refractory to fluids, inotropic medications. In case of cardiac arrhythmia several anti-arrhythmic agents may be administered, i.e. adenosine, verapamil (source is outdated - verapamil and β-blocker are contraindicated in cardiogenic shock), amiodarone, β-blocker or glucagon. Positive inotropic agents, which enhance the heart's pumping capabilities, are used to improve the contractility and correct the hypotension. Should that not suffice an intra-aortic balloon pump (which reduces workload for the heart, and improves perfusion of the coronary arteries) can be considered or a left ventricular assist device (which augments the pump-function of the heart). Finally, as a last resort, if the patient can be made stable enough and otherwise qualifies, cardiac transplantation can be performed. These invasive measures are important tools- more than 50% of patients who do not die immediately due to cardiac arrest from a lethal arrthythmia and live to reach the hospital (who have usually suffered a severe acute myocardial infarction, which in itself still has a relatively high mortality rate), die within the first 24 hours. The mortality rate for those still living at time of admission who suffer complications (among others, cardiac arrest or further arrhythmias, heart failure, cardiac tamponade, a ruptured or dissecting aneurysm, or another heart attack) from cardiogenic shock is even worse around 85%, especially without drastic measures such as ventricular assist devices or transplantation.
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