Should that not suffice an intra-aortic balloon pump (which reduces workload for the heart, and improves perfusion of the coronary arteries) or a left ventricular assist device (which augments the pump-function of the heart) can be considered. Mechanical ventilation or ECMO may be used to help stabilize people with severe or refractory cardiogenic shock until they can be given some type of definitive treatment, such as a ventricular assist device. Finally, as a last resort, if the person is stable enough and otherwise qualifies, heart transplantation, or if not eligible an artificial heart, can be placed. These invasive measures are important tools—more than 50% of patients who do not die immediately due to cardiac arrest from a lethal abnormal heart rhythm and live to reach the hospital (who have usually experienced 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 develop complications (among others, cardiac arrest or further abnormal heart rhythms, 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.Cardiogenic shock may be treated with intravenous dobutamine, which acts on β1 receptors of the heart leading to increased contractility and heart rate. References
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Cardiogenic Shock by eMedicine
The gene is located on the short arm of chromosome 2 (2p24.1–2p24.3) The gene lies on the Crick (minus) strand and is 79,745 bases in length. The encoded protein is 1181 amino acids in length and its predicted molecular weight is 133.547 kiloDaltons.The gene IFT43 lies on the Watson (plus) strand of the long arm of chromosome 14 (14q24.3). A mouse model for IFT122 has been created. Mutants deficient in IFT122 show multiple developmental defects (many are lethal), including exencephaly, situs viscerum inversus, delay in turning, hemorrhage and defects in limb development. In the node, primary cilia were absent or malformed in homozygous mutant and heterozygous embryos, respectively. Impairment of the Sonic hedgehog pathway was apparent in both neural tube patterning (expansion of motoneurons and rostrocaudal level-dependent contraction or expansion of the dorsolateral interneurons) and limb patterning (ectrosyndactyly). Pathophysiology
The IFT machinery is organized in two structural complexes — A and B. These complexes are involved in the coordinated movement of macromolecular cargo from the basal body along axonemal microtubules to the cilium tip and back again. The anterograde movement of IFT particles out to the distal tip of cilia and flagella is driven by kinesin-2 while the retrograde movement of particles back to the cell body is driven by cytoplasmic dynein 1b/2The IFT-A protein complex is involved in retrograde ciliary transport. Disruption of IFT43 disturbs transport from the ciliary tip to the base. Anterograde transport in the opposite direction remains normal resulting in accumulation of the IFT complex B proteins in the ciliary tip.