cardiogenic shock

(redirected from Shock, cardiogenic)
Also found in: Dictionary, Thesaurus, Encyclopedia.

shock

 [shok]
1. a sudden disturbance of mental equilibrium.
2. a condition of acute peripheral circulatory failure due to derangement of circulatory control or loss of circulating fluid. It is marked by hypotension and coldness of the skin, and often by tachycardia and anxiety. Untreated shock can be fatal. Called also circulatory collapse.

Mechanisms of Circulatory Shock. The essentials of shock are easier to understand if the circulatory system is thought of as a four-part mechanical device made up of a pump (the heart), a complex system of flexible tubes (the blood vessels), a circulating fluid (the blood), and a fine regulating system or “computer” (the nervous system) designed to control fluid flow and pressure. The diameter of the blood vessels is controlled by impulses from the nervous system which cause the muscular walls to contract. The nervous system also affects the rapidity and strength of the heartbeat, and thereby the blood pressure as well.



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.
Types of Circulatory Shock. There are five main types: Hypovolemic (low-volume) shock occurs whenever there is insufficient blood to fill the circulatory system. Neurogenic shock is due to disorders of the nervous system. Anaphylactic (allergic) shock and septic shock are both due to reactions that impair the muscular functioning of the blood vessels. And cardiogenic shock is caused by impaired function of the heart.
Hypovolemic (Low-Volume) Shock. This is a common type that happens when blood or plasma is lost in such quantities that the remaining blood cannot fill the circulatory system despite constriction of the blood vessels. The blood loss may be external, as when a vessel is severed by an injury, or the blood may be “lost” into spaces inside the body where it is no longer accessible to the circulatory system, as in severe gastrointestinal bleeding from ulcers, fractures of large bones with hemorrhage into surrounding tissues, or major burns that attract large quantities of blood fluids to the burn site outside blood vessels and capillaries. The treatment of hypovolemic shock requires replacement of the lost volume.
Neurogenic Shock. This type, often accompanied by fainting, may be brought on by severe pain, fright, unpleasant sights, or other strong stimuli that overwhelm the usual regulatory capacity of the nervous system. The diameter of the blood vessels increases, the heart slows, and the blood pressure falls to the point where the supply of oxygen carried by the blood to the brain is insufficient, which can bring on fainting. Placing the head lower than the body is usually sufficient to relieve this form of shock.
Anaphylactic (Allergic) Shock. This type (see also anaphylaxis) is a rare phenomenon that occurs when a person receives an injection of a foreign protein but is highly sensitive to it. The blood vessels and other tissues are affected directly by the allergic reaction. Within a few minutes, the blood pressure falls and severe dyspnea develops. The sudden deaths that in rare cases follow bee stings or injection of certain medicines are due to anaphylactic reactions.
Septic Shock. This type, resulting from bacterial infection, is being recognized with increasing frequency. Certain organisms contain a toxin that seems to act on the blood vessels when it is released into the bloodstream. The blood eventually pools within parts of the circulatory system that expand easily, causing the blood pressure to drop sharply. Gram-negative shock is a form of septic shock due to infection with gram-negative bacteria.
Cardiogenic Shock. This type may be caused by conditions that interfere with the function of the heart as a pump, such as severe myocardial infarction, severe heart failure, and certain disorders of rate and rhythm.
Pathogenesis of shock. (ARDS = adult respiratory distress syndrome, GI = gastrointestinal, IL = interleukin, TNF = tumor necrosis factor.) From Damjanov, 2000.
anaphylactic shock see anaphylactic shock.
cardiogenic shock shock resulting from primary failure of the heart in its pumping function, as in myocardial infarction, severe cardiomyopathy, or mechanical obstruction or compression of the heart; clinical characteristics are similar to those of hypovolemic shock.
colloidoclastic shock colloidoclasia.
cultural shock feelings of helplessness and discomfort experienced by an outsider attempting to comprehend or effectively adapt to a different cultural group or unfamiliar cultural context.
electric shock see electric shock.
hypovolemic shock shock resulting from insufficient blood volume for the maintenance of adequate cardiac output, blood pressure, and tissue perfusion. Without modification the term refers to absolute hypovolemic shock caused by acute hemorrhage or excessive fluid loss. Relative hypovolemic shock refers to a situation in which the blood volume is normal but insufficient because of widespread vasodilation as in neurogenic shock or septic shock. Clinical characteristics include hypotension; hyperventilation; cold, clammy, cyanotic skin; a weak and rapid pulse; oliguria; and mental confusion, combativeness, or anxiety.
insulin shock a hypoglycemic reaction to overdosage of insulin, a skipped meal, or strenuous exercise in an insulin-dependent diabetic, with tremor, dizziness, cool moist skin, hunger, and tachycardia; if untreated it may progress to coma and convulsions.
respirator shock circulatory shock due to interference with the flow of blood through the great vessels and chambers of the heart, causing pooling of blood in the veins and the abdominal organs and a resultant vascular collapse. The condition sometimes occurs as a result of increased intrathoracic pressure in patients who are being maintained on a mechanical ventilator.
septic shock shock associated with overwhelming infection, usually by gram-negative bacteria, although it may be produced by other bacteria, viruses, fungi, and protozoa. It is thought to result from the action of endotoxins or other products of the infectious agent on the vascular system causing large volumes of blood to be sequestered in the capillaries and veins; activation of the complement and kinin systems and the release of histamine, cytokines, prostaglandins, and other mediators may be involved. Clinical characteristics include initial chills and fever, warm flushed skin, increased cardiac output, and a lesser degree of hypotension than with hypovolemic shock; if therapy is ineffective, it may progress to the clinical picture associated with hypovolemic shock.
shell shock old term for posttraumatic stress disorder.
spinal shock the loss of spinal reflexes after injury of the spinal cord that appears in the muscles innervated by the cord segments situated below the site of the lesion.

car·di·o·gen·ic shock

shock resulting from decline in cardiac output secondary to serious heart disease, usually myocardial infarction.
Synonym(s): cardiac shock

cardiogenic shock

Etymology: Gk, kardia + genein, to produce; Fr, choc
an abnormal condition often but not always characterized by a low cardiac output associated with acute myocardial infarction and congestive heart failure. Cardiogenic shock is fatal in about 80% of cases, and immediate therapy is necessary. Depending on the signs, therapy may include diuretics, vasoactive drugs, and the application of various devices. Compare hypovolemic shock. See also electric shock, septic shock, shock.

cardiogenic shock

Cardiac 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

car·di·o·gen·ic shock

(kahr'dē-ō-jen'ikshok)
Condition resulting from decline in cardiac output secondary to serious heart disease, usually myocardial infarction.

cardiogenic shock

Surgical SHOCK due to inadequate blood circulation as a result of HEART FAILURE or PULMONARY EMBOLISM.

Cardiogenic Shock

DRG Category:292
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%.

Causes

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.

Genetic considerations

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.

Assessment

History

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.

Physical examination

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.

Psychosocial

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.

Diagnostic highlights

TestNormal ResultAbnormality With ConditionExplanation
Hemodynamic monitoringRight 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−5RA: 6 mm Hg; PAOP: > 18 mm Hg; CO: < 5 L/min; SVR: > 1,200 dynes/sec per cm−5Elevated 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

Diagnosis

Altered tissue perfusion (peripheral, cerebral, renal, and cardiopulmonary) related to inadequate cardiac output

Outcomes

Circulation status; Cardiac pump effectiveness; Tissue perfusion: Cardiopulmonary, Cerebral, Renal, Peripheral; Vital sign status

Interventions

Circulatory 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

Collaborative

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.

Pharmacologic highlights

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 ClassDosageDescriptionRationale
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 dobutamineSympathomimeticDobutamine improves heart contractility without much effect on heart rate; renal function may also improve through increased cardiac output and renal perfusion
NitroglycerineBegin at 5 mcg/min and increase by 5 mcg/min every 3–5 minVasodilatorRelax vascular smooth muscle and reduce systemic vascular resistance, thereby increasing cardiac output
DiureticsVaries by drugLoop diuretics, (preload) diureticsReduces venous return

Independent

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%).

Documentation guidelines

  • 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.

recurrence of chest pain.
Teach the patient to call 911 for any chest pain that is not relieved by rest and/or nitroglycerin. Instruct the patient not to ignore the pain or wait to call for assistance.

recurrence of heart failure.
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.

shock

a condition of acute peripheral circulatory failure due to derangement of circulatory control or loss of circulating fluid. It is marked by hypotension, coldness of the skin and tachycardia.

allergic shock
see anaphylactic shock.
shock bodies
hyaline globules composed of fibrin degradation products which act as microthrombi and cause hemorrhage and necrosis.
burn shock
the loss and redistribution of fluid, electrolytes and plasma protein, increased blood viscosity and increased peripheral resistance that follow a severe burn contribute to shock.
cardiogenic shock
classically associated with acute myocardial infarction in humans; in animals may be caused by intrinsic congestive heart failure, cardiac depression caused by anesthetic overdosage or other drugs with negative inotropism, rarely, thromboembolism.
colloidoclastic shock
shock due to breakdown of the physical equilibrium of the body colloids. Thought to cause anaphylactic shock due to the absorption of the colloids into the bloodstream.
distributive shock
see vasogenic shock (below).
electric shock
see electrical injuries.
electroplectic shock
electric shock. See also electrical stunning.
endotoxic shock
caused by endotoxins, especially Escherichia coli. See also toxemic shock.
shock gut
animals in shock develop changes in the gut including congestion and hemorrhage into the lumen.
hypovolemic shock
shock due to reduced blood volume as a result of water deprivation, fluid loss due to diarrhea, vomiting, extensive burns, intestinal obstruction, whole blood loss.
insulin shock
a condition of circulatory insufficiency resulting from overdosage with insulin, which causes too sudden reduction of blood sugar. It is marked by tremor, weakness, convulsions and collapse.
irreversible shock
shock which has reached the stage where irreparable damage has been done to tissues, e.g. liver, kidneys and treatment will not salvage the patient although it might prolong life for a long time.
shock lung
animals in shock due to massive burns, septicemia, disseminated intravascular coagulation (DIC), acute viral or bacterial pneumonias or trauma develop an acute respiratory distress syndrome. The pulmonary lesion is a nonspecific acute or subacute interstitial pneumonia.
nervous shock
a temporary cessation of function in nervous tissue caused by an acute insult such as trauma without the part having been directly or detectably damaged. The loss of function is only temporary, usually for a few minutes but it may last for several hours. There may be residual signs due to direct damage when the shock passes. Stunning by a lightning stroke is an example.
shock organs
those organs, specific to each animal species, which respond to allergens circulating in the blood.
septic shock
see toxemic shock.
spinal shock
flaccid paralysis up and down the body from the site of the spinal cord lesion. Accompanied by a fall in skin temperature, vasodilatation and sweating. Signs disappear within an hour or two. There may be residual signs due to physical injury to tissue.
toxic shock
see toxemic shock.
vasogenic shock, vasculogenic shock
shock exists because of the severe reduction in effective circulating blood volume caused by sequestration of blood and other fluids in the vascular system and their withdrawal from the circulating blood. Is the classical shock of traumatic injury, burns, uterine prolapse, extensive surgery.