Patho physiology: Cardiogenic shock is a condition in which your heart suddenly can't pump enough blood to meet your body's needs. The condition 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 the condition survive.
Treatment: During this treatment, which most people who have cardiogenic shock need, 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 to treat cardiogenic shock work to improve blood flow through your heart and increase your heart's pumping ability such as Aspirin, Thrombolytics, Superaspirins, Other blood-thinning medications, Inotropic agents. Medical procedures to treat cardiogenic shock usually focus on restoring blood flow through your heart. They include: Angioplasty and stenting, Balloon pump. If medications and medical procedures don't work to treat cardiogenic shock, your doctor may recommend surgeries are Coronary artery bypass surgery, Surgery to repair an injury to your heart, Heart pumps, Heart transplant.
Research: The administration of an experimental agent known as TRO40303 to patients who have had a heart attack, with the hope of preventing tissue damage when impaired blood flow is corrected (reperfusion), was disappointingly ineffective according to results of a European study of patients with acute ST-elevation myocardial infarction (STEMI). Results for TRO40303 are a surprising contrast to promising earlier studies that had generated high hopes for the agent. "Negative studies rarely lead to phenomenal breakthroughs and monumental change-of-practice, but it is important to be aware that negative studies increase our understanding of disease and of therapeutic options," he said. The study's finding of lack of benefit of TRO40303, "provides important information on current state-of-the-art STEMI treatment, and may reflect the fact that the high quality of modern care leaves little room for improvement." TRO40303 has been shown in animals and laboratory models to block mitochondrial permeability that leads to reperfusion injury. When blocked vessels that cause a heart attack (infarct) are cleared, allowing reperfusion, cardiac muscle may be injured causing what is known as an infarct expansion. Mitochondrial permeability has been shown to play an important role in this process
Statistics: Deaths (n = 180) occurred < or =30 days in 86% and >30 days in 14%. Known causes of death < or =30 days were cardiac in 88% (37% arrhythmic) and non-cardiac in 12% (29% septic). Non-cardiac deaths < or =30 days occurred later (206 [91,394] versus 41 [15,156] h, P<0.01) and were more frequently associated with signs of inflammation (43 versus 12%, P = 0.01) than cardiac deaths < or =30 days. Known causes of in-hospital death >30 days (n = 19) were cardiac in 58% and non-cardiac in 42%. Among deaths < or =30 days systemic vascular resistance index was higher (2,666+/-1,063 versus 2,090+/-731 dynes.sec.cm(-5) m(2), P = 0.05) than among deaths >30 days. Among the 116 survivors of the initial hospitalization with data available, 52 (45%) were readmitted, most of which due to heart failure (n = 22, 42%) and myocardial ischemia (n = 16, 31%).