cardiogenic shock(redirected from Shock, cardiogenic)
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Shock, which is associated with a dangerously low blood pressure, can be produced by factors that attack the strength of the heart as a pump, decrease the volume of the blood in the system, or permit the blood vessels to increase in diameter.
cardiogenic shockCardiac shock Cardiology The inability of the heart to deliver sufficient blood–O2 to the tissues to meet resting metabolic demands due to pump failure Epidemiology CS complicates 7–10% cases of acute MI and is the leading cause of death in Pts hospitalized with acute MI; when hemodynamic monitoring is available, CS is defined by a systolic BP < 30 mm Hg–or < 80 mm Hg in absence of hypovolemia, ↑ arteriovenous O2 difference–> 5.5 ml/dL, and ↓ cardiac index–< 2.2 L/min/m2 body surface, with an ↑ pulmonary capillary wedge pressure–>15 mm Hg Etiology MI, cardiomyopathy, overwhelming infection, heart attack or disease, hormonal insufficiency, hypoglycemia, hypothermia, allergic reaction, drugs, spinal cord injury Clinical Cold extremities, cyanosis, persistent oliguria, CHF Mortality > 80% Managememt Emergency revascularization–CABG or angioplasty, fluid restriction, diuretics, vasopressors–eg, dopamine to maintain BP; IV agents–eg, dobutamine, to ↑ inotropism
cardiogenic shockSurgical SHOCK due to inadequate blood circulation as a result of HEART FAILURE or PULMONARY EMBOLISM.
|Mean LOS:||4.6 days|
|Description:||MEDICAL: Heart Failure and Shock With CC|
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 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.
While several genetic factors may contribute to susceptibility to cardiogenic shock, no direct genetic link has been documented. Tumor necrosis factor (TNF)-alpha variants have been associated with severe heart failure. Polymorphisms in several genes may be predictors of survival: TNF-alpha, interleukin (IL)-6, IL-10, transforming growth factor (TGF)-beta, and interferon (IFN)-gamma cytokine. Persons who carry the TNF-2 allele appear to have better outcomes than persons with other variants of this gene.
Gender, ethnic/racial, and life span considerations
Cardiogenic shock can occur at any age but is more common in the middle-aged and older adult. Anyone at risk for coronary artery disease, either male or female, is also at risk for cardiogenic shock as a result of an acute MI. The elderly are at greater risk because of their diminished ability to compensate for an inadequate cardiac output and tissue perfusion. While the overall incidence of cardiogenic shock is higher in men than in women, the percentage of female patients with MI who develop cardiogenic shock is higher than that of male patients with MI. Ethnicity and race have no known effect on the risk of cardiogenic shock.
Global health considerations
European countries have a prevalence of cardiogenic shock similar to that of the United States. No data are available for developing nations.
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; lasts more than 20 minutes; and is 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.
Most common symptoms are hypotension in the absence of hypovolemia, oliguria, cyanosis, cool extremities, and reduced mental status. 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 distention; hypotension; rapid, deep respirations; pulmonary crackles; venous oxygen saturation (SvO2) less than 60%; cyanosis; urine output less than 20 mL/hour; 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.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Hemodynamic monitoring||Right atrial pressure (RA): 1–8 mm Hg; pulmonary artery occlusion pressure (PAOP): 4–12 mm Hg; cardiac output (CO): 4–7 L/min; systemic vascular resistance (SVR): 800–1,200 dynes/sec per cm−5||RA: 6 mm Hg; PAOP: > 18 mm Hg; CO: < 5 L/min; SVR: > 1,200 dynes/sec per cm−5||Elevated filling pressures in heart and low systolic blood pressure occur in the setting of low cardiac output; arterial constriction occurs as a compensatory mechanism. Hemodynamic monitoring with serial measures of cardiac output is important in the diagnosis of cardiogenic shock.|
Other Tests: Serum laboratory tests, urinalysis, hematological and coagulation studies
Primary nursing diagnosis
DiagnosisAltered tissue perfusion (peripheral, cerebral, renal, and cardiopulmonary) related to inadequate cardiac output
OutcomesCirculation status; Cardiac pump effectiveness; Tissue perfusion: Cardiopulmonary, Cerebral, Renal, Peripheral; Vital sign status
InterventionsCirculatory care; Emergency care; Vital signs monitoring; Cardiac care; Cardiac precautions; Oxygen therapy; Fluid/electrolyte management; Fluid monitoring; Shock management: Volume, Medication administration, Resuscitation, Surveillance
Planning and implementation
The SHOCK trial (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) demonstrated that either percutaneous coronary intervention (PCI) within 90 minutes of presentation or coronary artery bypass is the treatment of choice for cardiogenic shock. Both procedures decreased mortality rates at 1 year. 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 an 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.
General Comments: Improving cardiac output, which is necessary to improve tissue perfusion, can be accomplished in several ways. If the patient is able to maintain hemodynamic stability, the physician prescribes medications, namely diuretics and nitrates, to reduce preload. During the later phases of shock, the patient may be too hypotensive to tolerate the vasodilative effects of both diuretics and nitrates. The patient needs improvement in myocardial contractility without adding significant workload on the heart. Dopamine may also be used in an attempt to improve contractility and cardiac output. Other vasoactive drugs, such as amrinone, may also be used. Vasopressors may be used in an attempt to increase the mean arterial blood pressure to a level that provides adequate tissue perfusion (>70 mm Hg). Several agents that may be administered include dopamine, epinephrine, norepinephrine, and phenylephrine hydrochloride.
|Medication or Drug Class||Dosage||Description||Rationale|
|Dobutamine (dopamine is the drug of choice for hypotensive patients)||2–40 μg/kg per min (but usually in the range of 2–20 μg/kg per min); milrinone may be added if patients are not responding or are developing tachycardia in response to dobutamine||Sympathomimetic||Dobutamine improves heart contractility without much effect on heart rate; renal function may also improve through increased cardiac output and renal perfusion|
|Nitroglycerine||Begin at 5 mcg/min and increase by 5 mcg/min every 3–5 min||Vasodilator||Relax vascular smooth muscle and reduce systemic vascular resistance, thereby increasing cardiac output|
|Diuretics||Varies by drug||Loop diuretics, (preload) diuretics||Reduces venous return|
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 reduces 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.
Evidence-Based Practice and Health Policy
Cheng, R., Hachamovitch, R., Kittleson, M., Patel, J., Arabia, F., Moriguchi, J., …Azarbal, B. (2013). Complications of extracorporeal membrane oxygenation for treatment of cardiogenic shock and cardiac arrest: A meta-analysis of 1,866 adult patients. The Annals of Thoracic Surgery. Advanced online publication. doi 10.1016/j.athoracsur.2013.09.008
- Treatment for cardiogenic shock with extracorporeal membrane oxygenation (ECMO) is associated with improved survival but significant complications and morbidity risks.
- A systematic review of 17 data-based studies among patients who received ECMO for treatment of cardiogenic shock revealed a cumulative survival rate of 534 of 1,529 patients, which ranged in individual studies from 20.8% to 65.4%.
- Lower extremity ischemia was reported in 112 of 667 patients (16.9%), compartment syndrome and fasciotomy was reported in 33 of 335 patients (10.3%), and lower extremity amputation was reported in 7 of 192 patients (4.7%).
- Neurologic complications were reported in 151 of 1,019 patients (13.3%), and stroke was reported in 36 of 630 patients (5.9%). Thoracotomy for bleeding or tamponade was reported in 409 of 828 patients (41.9%).
- Acute kidney injury was reported in 197 of 380 patients (55.6%), and renal replacement therapy was initiated in 758 of 1,452 patients (46%) after ECMO. Infection was reported in 321 of 922 patients (30.4%).
- Physical findings: Cardiopulmonary, renal, neurological, and integumentary systems; skin integrity
- Hemodynamic response to inotropic medications, diuretics, nitrates, IABP, and oxygen
- Presence of complications: Pulmonary congestion, respiratory distress, unrelieved chest pain, and skin breakdown
- Reaction to the crisis and prognosis
Discharge and home healthcare 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.