Documentation Guidelines

• Physical findings of cardiovascular and neurological systems

• Adequacy of airway, breathing, and circulation; mental status; skin color; vital signs; moisture of mucous membranes; capillary refill; heart sounds; presence of pulsus paradoxus or jugular venous distension; hemodynamic parameters; intake and output

• Response to interventions

• Fluid resuscitation, inotropic agents, pericardiocentesis, surgery

• Presence of complications

• Asystole, ventricular tachycardia, ventricular fibrillation; recurrence of tamponade; infection; ongoing hemorrhage

MEDICATIONS. Be sure the patient understands all medications, including dosage, route, side effects, and any routine laboratory testing. The patient needs to understand to avoid over-the-counter medications that include aspirin or ibuprofen.

COMPLICATIONS. The patient needs to understand the possibility of recurrence and the symptoms to report to the physician. The patient and significant other(s) also need to understand that symptoms of inadequate tissue perfusion (change in mental status; cool, clammy, cyanotic skin; dyspnea; chest pain) warrant activation of the Emergency Medical System.

Cardiogenic shock occurs when cardiac output is insufficient to meet the metabolic demands of the body, resulting in inadequate tissue perfusion. There are four stages of cardiogenic shock: initial, compensatory, progressive, and refractory.

During the initial stage, there is diminished cardiac output without any clinical symptoms. In the compensatory stage, the baroreceptors respond to the decreased cardiac output by stimulating the sympathetic nervous system to release catecholamines to improve myocardial contractility and vasoconstriction, leading to increased venous return and arterial blood pressure. Impaired renal perfusion activates the renin-angiotensin system, whose end-product, angiotensin II, causes sodium and water retention as well as vasoconstriction. The progressive stage follows the compensatory stage if there is no intervention or if the intervention fails to reverse the inadequate tissue perfusion. Compensatory mechanisms, aimed at improving cardiac output and tissue perfusion, place an increased demand on an already compromised myocardium. As tissue perfusion remains inadequate, the cells begin anaerobic metabolism, leading to metabolic acidosis and fluid leakage out of the capillaries and into the interstitial spaces. A decrease in circulating volume and an increase in blood viscosity may cause clotting in the capillaries and tissue death.

As the body releases fibrinolytic agents to break down the clots, disseminated intravascular coagulation (DIC) may ensue. Lactic acidosis causes depression of the myocardium and a decrease in the vascular responsiveness to catecholamines, further reducing cardiac output. Blood pools and stagnates in the capillaries, and the continued increase in hydrostatic pressure causes fluid to leak into the interstitium. Severe cerebral ischemia causes depression of the vasomotor center and loss of sympathetic stimulation, resulting in blood pooling in the periphery, a decrease in preload, and further reduction in cardiac output. If there is no effective intervention at this point, the shock will progress to the refractory stage, when the chance of survival is

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