الفهرس 
Etiology and Pathophysiology of Cardiogenic ShockOnly 14 pages are availabe for public view
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Abstract
The clinical definition of cardiogenic shock (C. Shock) is decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume. Hemodynamic criteria are sustained hypotension (systolic blood pressure < 90 mm Hg for at least 30 minutes) and a reduced cardiac index (CI < 2.2 L/min/m2) in the presence of elevated pulmonary artery occlusion pressure (PAOP > 15 mm Hg).
Cardiogenic shock (C. shock) as a complication of AMI continues to be an unfortunately far too common clinical problem that carries a high mortality rate. Before the advent and widespread use of thrombolytic therapy, up to 20% of patients with AMI developed C. shock.
It is important to emphasize that the mechanical complications secondary tomyocardial rupture (free wall, septum, or papillary muscle rupture) account for the minority of the cases. In the majority of the patients, the cause of death is low cardiac output secondary to predominantly LV failure, which in turn leads to organ failure, arrhythmias, and irreversible shock.
The hallmark feature of C. shock is hypotension with systemic hypoperfusion. Persistent hypotension is defined as a systolic blood pressure of less than 90 mm Hg for more than 30 minutes despite vasopressor infusion and volume administration. Systemic hypoperfusion results in decreased urine output (<20 ml/h) and altered mental status. As a compensatory response to cardiogenic shock, plasma levels of norepinephrine increase, leading to sinus tachycardia with a thready pulse and arteriolar vasoconstriction (cool clammy skin)
Early and definitive restoration of coronary blood flow is the most important intervention for achieving an improved survival rate. At present, it represents standard therapy for patients with cardiogenic shock due to myocardial ischemia.
Inotropic and vasopressor drugs are considered the principal initial interventions for reversing hypotension and improving vital organ perfusion. However, those drugs should be used at the lowest possible doses as higher doses have been associated with poor survival. The most commonly used agents in CS include dopamine, dobutamine, epinephrine and norepinephrine.
Newer classes of inotropes and vasopressors have been introduced; some of them are being used in clinical practice and others are still under investigations (i.e., Amrinone, milrinone, Levosimendan, Vasopressin, Nitric Oxide (NO) inhibitors, Complement blocking agents, and Sodium/hydrogen-exchange inhibitors).
Levosimendan represents a new calcium sensitizer with positive inotropic properties. It causes conformational changes in cardiac troponin C during systole, leading to sensitization of the contractile apparatus to calcium ions without increasing intracellular calcium [in contrast to other positive inotropic drugs].
Intravenous vasopressin therapy was associated with increased MAP with no adverse effect on other hemodynamic parameters
Although low levels of NO are cardioprotective, excess levels of NO have further detrimental effects on the myocardium and vascular tone, so NO inhibitors have benefit in improving C. shock.
Pexelizumab is a unique antibody fragment that blocks activation of complement C5, which is involved in inflammation, vasoconstriction, leukocyte activation, and apoptosis.
Although early reperfusion of the coronary system is the corner-stone of management of C. shock, this will not always provide full resolution for such a grave situation. Additional time may be needed after restoration of blood flow for the injured myocardium to recover from stunning or hibernation. This time delay is critical because persistent hypoperfusion may worsen cardiac function and cause multiple organ failure. Thus, methods for mechanical support of the myocardium that maintain normal systemic perfusion may improve the outcome of patients with C. shock complicating acute MI which include the following;
1. Intra aortic balloon counterpulsation can be considered as a short term VAD. It is effective in stabilization of patients, decreasing afterload and increasing coronary perfusion pressure through the principle of diastolic inflation and systolic deflation.
2. Percutaneous Ventricular Assist Devices, in contrast to IABP, can compensate for the loss of myocardial pump function, normalizing cardiac output and thus allowing physiologic perfusion of vital organs.
• The Tandem heart is a percutaneous left atrial-to-femoral artery ventricular assist device. This device is placed via the femoral vein and then crosses the interatrial septum. Blood from the left atrium will be directed to an extracorporeal pump and then redirected to the abdominal aorta.
• The impella recover is a percutaneous transvalvular LVAD (axial flow pump), which is placed via the femoral artery, retrograde across the aortic valve into the left ventricle
3. Extracorporeal membrane oxygenation (ECMO) provides temporary circulatory support in patients who present with severe hemodynamic instability associated with multiorgan failure.
Finaly, Despite the fast advances in the pathophysiology understanding and management technology, ischemic CS remains the most serious complication of acute MI. ischemic CS is associated with high mortality rate both in the acute and long-term setting. Further randomized trials and guidelines are needed to save resources and lives.