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 extremely limited. Most experts acknowledge that Cardiogenic shock is often unresponsive to treatment and has a mortality rate ranging from 50% to 80%.
The most common cause of Cardiogenic shock is acute myocardial infarction (MI) resulting in a loss of more than 40% of the functional myocardium. Cardiogenic shock occurs with 10% to 20% of all hospital admissions for acute MI and carries an 80% mortality rate. Other causes include papillary muscle rupture, left ventricular free wall rupture, acute ventricular septal defect, severe congestive heart failure, end-stage cardiomyopathy, severe valvular dysfunction, acute cardiac tamponade, cardiac contusion, massive pulmonary embolus, or overdose of drugs such as beta blockers or calcium channel blockers.
Nursing care plan assessment and physical examination
The patient is likely to have a history of symptoms of an acute MI, including crushing, viselike chest pain or heaviness that radiates to the arms, neck, or jaw, lasting more than 20 minutes and unrelieved by nitroglycerin and rest. Other MI symptoms include shortness of breath, nausea, anxiety, and a sense of impending doom. The patient may also have a history of symptoms of any of the other etiologies mentioned above.
During the initial stage of shock, there are no clinical findings unless the cardiac output can be measured. When the patient has entered the compensatory stage, symptoms may include an altered level of consciousness; sinus tachycardia; the presence of an S3 or S4 gallop rhythm; jugular venous distension; hypotension; rapid, deep respirations; pulmonary crackles; venous oxygen saturation (SvO2) less than 60%; cyanosis; urine output less than 20 mL/hr; decreased urinary sodium; increased urinary osmolarity; peripheral edema; hyperglycemia; hypernatremia; cold, clammy skin; and decreased bowel sounds. As the patient enters the progressive stage, the symptoms become more pronounced and resistant to treatment. The patient becomes mentally unresponsive; hypotension becomes worse, requiring high doses of positive inotropic agents; metabolic and respiratory acidosis become apparent; oliguria or anuria and anasarca may ensue; and symptoms of DIC may be present. When the shock reaches the refractory stage, multisystem organ failure is apparent, with the above symptoms unresponsive to treatment.
The patient in Cardiogenic shock is in a life-threatening situation. The chances for survival are small, and the patient may experience a sense of impending doom. The impaired tissue perfusion may lead to anxiety and fear. The patient and his or her family or significant other may be in crisis. Both the patient and the family may be experiencing grief in response to the potential loss of life.
Nursing care plan primary nursing diagnosis: Altered tissue perfusion (peripheral, cerebral, renal, and cardiopulmonary) related to inadequate cardiac output.
Nursing care plan intervention and treatment
The primary goal in treating Cardiogenic shock is improvement in tissue perfusion and oxygenation. To limit the infarct size and treat the dyspnea, pulmonary congestion, hypoxemia, and acidosis, the physician is likely to prescribe oxygen. If a previously normocapnic patient’s PaCO2 decreases below 50 mm Hg, then the patient may require endotracheal intubation and mechanical ventilation. Although the patient needs an adequate blood pressure, afterload may also need to be decreased, which may be accomplished with the intra-aortic balloon pump (IABP). A left ventricular assist device (LVAD) may be used to replace the function of the patient’s heart for several days to provide total rest for the heart. An LVAD diverts blood from the left atrium or left ventricle by means of a pressure gradient and moves it to the external pump, after which the blood is returned to the aorta during diastole. An LVAD can reduce the patient’s right ventricular contraction. Monitor the patient’s central venous pressure carefully.
Limiting myocardial oxygen consumption is a primary concern. Decreasing oxygen demand may limit ischemia, injury, and infarction. Restrict the patient’s activity, and maintain the patient on bedrest. Address the patient’s anxiety by explaining all procedures. Permit the family or significant others to remain with the patient as long as their presence does not cause added stress. Maintaining a calm and peaceful environment provides reassurance and reduces anxiety, which, in turn, will reduce myocardial oxygen consumption. Restricted activity could lead to impaired skin integrity, necessitating frequent assessment and care of the skin. Adequate protein and calories are essential for the prevention or healing of impaired skin integrity and should be provided by oral, enteral, or parenteral means.
Nursing care plan discharge and home health care guidelines
Teach the patient how to reduce controllable risk factors for heart disease. If the physician has referred the patient to a cardiac rehabilitation program, encourage attendance. Be sure the patient understands the medication prescribed.
Teach the patient to restrict fluids to 2 to 2.5 L per day, or as prescribed by the physician, and observe sodium restrictions. The patient should report a weight gain of greater than 4 pounds in 2 days to the physician. Finally, teach the patient to monitor for increasing shortness of breath and edema and to report either of those signs or symptoms to the physician. If the patient experiences acute shortness of breath, she or he should call 911 or go to the emergency department immediately.