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Chapter: Medical Surgical Nursing: Shock and Multisystem Failure

Cardiogenic Shock

Cardiogenic Shock
Cardiogenic shock occurs when the heart’s ability to contract and to pump blood is impaired and the supply of oxygen is inade-quate for the heart and tissues.

Cardiogenic Shock

Cardiogenic shock occurs when the heart’s ability to contract and to pump blood is impaired and the supply of oxygen is inade-quate for the heart and tissues. The causes of cardiogenic shock are known as either coronary or noncoronary. Coronary cardio-genic shock is more common than noncoronary cardiogenic shock and is seen most often in patients with myocardial in-farction. Coronary cardiogenic shock occurs when a significant amount of the left ventricular myocardium has been destroyed (Price et al., 1999). Patients experiencing an anterior wall my-ocardial infarction are at the greatest risk for developing cardio-genic shock because of the potentially extensive damage to the left ventricle caused by occlusion of the left anterior descending coro-nary artery (Chart 15-4). Non-coronary causes can be related to severe metabolic problems (severe hypoxemia, acidosis, hypo-glycemia, and hypocalcemia) and tension pneumothorax.


In cardiogenic shock, cardiac output, which is a function of both stroke volume and heart rate, is compromised. When stroke vol-ume and heart rate decrease or become erratic, blood pressure drops and tissue perfusion is compromised. Along with other tis-sues and organs being deprived of adequate blood supply, the heart muscle itself receives inadequate blood. The result is im-paired tissue perfusion. Because impaired tissue perfusion weak-ens the heart and impairs its ability to pump blood forward, the ventricle does not fully eject its volume of blood at systole. As a result, fluid accumulates in the lungs. This sequence of events can occur rapidly or over a period of days (Fig. 15-5).

Clinical Manifestations

Patients in cardiogenic shock may experience angina pain and develop dysrhythmias and hemodynamic instability.

Medical Management

The goals of medical management are to (1) limit further myo-cardial damage and preserve the healthy myocardium and (2) im-prove the cardiac function by increasing cardiac contractility, decreasing ventricular afterload, or both (Price et al., 1999). In general, these goals are achieved by increasing oxygen supply to the heart muscle while reducing oxygen demands.



As with all forms of shock, the underlying cause of cardiogenic shock must be corrected. It is necessary first to treat the oxygena-tion needs of the heart muscle to ensure its continued ability to pump blood to other organs. In the case of coronary cardiogenic shock, the patient may require thrombolytic therapy, angioplasty, or coronary artery bypass graft surgery. In the case of noncoro-nary cardiogenic shock, the patient may require a cardiac valve replacement or correction of a dysrhythmia.



First-line treatment of cardiogenic shock involves the following actions:

·      Supplying supplemental oxygen


·       Controlling chest pain


·       Providing selected fluid support


·       Administering vasoactive medications


·       Controlling heart rate with medication or by implementa-tion of a transthoracic or intravenous pacemaker


·      Implementing mechanical cardiac support (intra-aortic bal-loon counterpulsation therapy, ventricular assist systems, or extracorporeal cardiopulmonary bypass)



In the early stages of shock, supplemental oxygen isadministered by nasal cannula at a rate of 2 to 6 L/min to achieve an oxygen saturation exceeding 90%. Monitoring arterial blood gas values and pulse oximetry values helps to indicate whether the patient requires a more aggressive method of oxygen delivery.


Pain Control.

If the patient experiences chest pain, morphine sul-fate is administered intravenously for pain relief. In addition to relieving pain, morphine dilates the blood vessels. This reduces the workload of the heart by both decreasing the cardiac filling pressure (preload) and reducing the pressure against which the heart muscle has to eject blood (afterload). Morphine also relieves the patient’s anxiety. Cardiac enzyme (CPK-MB and cTn-I) lev-els are measured, and serial 12-lead electrocardiograms are ob-tained to assess the degree of myocardial damage.


Hemodynamic Monitoring.

Hemodynamic monitoring is initi-ated to assess the patient’s response to treatment. In many insti-tutions, this is performed in the intensive care unit, where an arterial line can be inserted. The arterial line enables accurate and continuous monitoring of blood pressure and provides a port from which to obtain frequent arterial blood samples without having to perform repeated arterial punctures. A multilumen pul-monary artery catheter is inserted to allow measurement of the pulmonary artery pressures, myocardial filling pressures, cardiac output, and pulmonary and systemic resistance.


Vasoactive medication therapy consists of multiple pharmaco-logic strategies to restore and maintain adequate cardiac output. In coronary cardiogenic shock, the aims of vasoactive medication therapy are improved cardiac contractility, decreased preload and afterload, or stable heart rate.

Because improving contractility and decreasing cardiac work-load are opposing pharmacologic actions, two classifications of medications may be administered in combination: sympath-omimetic agents and vasodilators. Sympathomimetic medications increase cardiac output by mimicking the action of the sympa-thetic nervous system through vasoconstriction, resulting in in-creased preload, and by increasing myocardial contractility (inotropic action) or increasing the heart rate (chronotropic ac-tion). Vasodilators are used to decrease preload and afterload, thus reducing the workload of the heart and the oxygen demand. Med-ications commonly combined to treat cardiogenic shock include dobutamine, dopamine, and nitroglycerin (see Table 15-1).


Dobutamine (Dobutrex) produces inotropic effectsby stimulating myocardial beta receptors, increasing the strengthof myocardial activity and improving cardiac output. Myocar-dial alpha-adrenergic receptors are also stimulated, resulting in decreased pulmonary and systemic vascular resistance (decreased afterload). Dobutamine enhances the strength of cardiac con-traction, improving stroke volume ejection and overall cardiac output (Jindal et al., 2000; Price et al., 1999).


Intravenous nitroglycerin (Tridil) in low dosesacts as a venous vasodilator and therefore reduces preload. At higher doses, nitroglycerin causes arterial vasodilation and there-fore reduces afterload as well. These actions, in combination with medium-dose dopamine, increase cardiac output while minimiz-ing cardiac workload. Additionally, vasodilation enhances blood flow to the myocardium, improving oxygen delivery to the weak-ened heart muscle (Price et al., 1999).


Dopamine (Intropin) is a sympathomimetic agentthat has varying vasoactive effects depending on the dosage. It may be used with dobutamine and nitroglycerine to improve tissue per-fusion. Low-dose dopamine (0.5 to 3.0 μg/kg/min) increases renal and mesenteric blood flow, thereby preventing ischemia of these organs because shock causes blood to be shunted away from the kidneys and the mesentery. This dosage, however, does not im-prove cardiac output. Medium-dose dopamine (4 to 8 μg/kg/min) has sympathomimetic properties and improves contractility (ino-tropic action) and slightly increases the heart rate (chronotropic action). At this dosage, dopamine increases cardiac output and therefore is desirable. High-dose dopamine (8 to 10 μg/kg/min) predominantly causes vasoconstriction, which increases afterload and thus increases cardiac workload. Because this effect is unde-sirable in patients with cardiogenic shock, dopamine dosages must be carefully titrated. Once the patient’s blood pressure stabilizes, low-dose dopamine may be continued for its effect of promoting renal perfusion in particular. In severe metabolic acidosis, which occurs in the later stages of shock, dopamine’s effectiveness is di-minished. To maximize the effectiveness of any vasoactive agent, metabolic acidosis must first be corrected. The physician may pre-scribe intravenous sodium bicarbonate to treat the acidosis (Jindal et al., 2000).


Other Vasoactive Medications.

Additional vasoactive agents thatmay be used in managing cardiogenic shock include norepineph-rine (Levophed), epinephrine (Adrenalin), milrinone (Primacor), amrinone (Inocor), vasopressin (Pitressin), and phenylephrine (Neo-Synephrine). Each of these medications stimulates differ-ent receptors of the sympathetic nervous system. A combination of these medications may be prescribed, depending on the pa-tient’s response to treatment. All vasoactive medications have ad-verse effects, making specific medications more useful than others at different stages of shock. Diuretics such as furosemide (Lasix) may be administered to reduce the workload of the heart by re-ducing fluid accumulation (see Table 15-1).


Antiarrhythmic Medications.

Antiarrhythmic medication is alsopart of the medication regimen in cardiogenic shock. Multiple factors, such as hypoxemia, electrolyte imbalances, and acid–base imbalances, contribute to serious cardiac dysrhythmias in all pa-tients with shock. Additionally, as a compensatory response to de-creased cardiac output and blood pressure, the heart rate increases beyond normal limits. This impedes cardiac output further by shortening diastole and thereby decreasing the time for ventricu-lar filling. Consequently, antiarrhythmic medications are re-quired to stabilize the heart rate. For a full discussion of cardiac dysrhythmias as well as commonly prescribed medications.


Fluid Therapy.

In addition to medications, appropriate fluid isnecessary in treating cardiogenic shock. Administration of fluids must be monitored closely to detect signs of fluid overload. In-cremental intravenous fluid boluses are cautiously administered to determine optimal filling pressures for improving cardiac out-put. A fluid bolus should never be given quickly because rapid fluid administration in patients with cardiac failure may result in acute pulmonary edema.




If cardiac output does not improve despite supplemental oxygen, vasoactive medications, and fluid boluses, mechanical assistive de-vices are used temporarily to improve the heart’s ability to pump. Intra-aortic balloon counterpulsation is one means of providing temporary circulatory assistance. A polyurethane balloon catheter is inserted percutaneously through the common femoral artery and advanced into the descending thoracic aorta. The balloon catheter is connected to a console containing a gas-filled pump. The timing of the balloon inflation is synchronized electrocardiographically with the beginning of diastole, and the balloon deflation occurs just before systole. The goals of intra-aortic balloon counterpulsation include the following:


·        Increased stroke volume


·         Improved coronary artery perfusion


·         Decreased preload


·         Decreased cardiac workload


·         Decreased myocardial oxygen demand (Kumar et al., 2000)


Other means of mechanical assistance include left and right ventricular assist devices and total artificial hearts. These devices are electrical pumps or pumps driven by air. They assist or replace the ventricular pumping action of the heart. Human heart trans-plantation may be the only option remaining for a patient who has cardiogenic shock and who cannot be weaned from mechan-ical assistive devices.


Another short-term means of providing cardiac or pulmonary support to the patient in cardiogenic shock is through an extra-corporeal device similar to the cardiopulmonary bypass (CPB) used in open-heart surgery. The CPB system requires systemic anticoagulation, arterial and venous cannulation of the femoral artery and vein, and connection to a centrifugal, oxygenated pump. The catheter tip is advanced into the right atrium. This system lowers left and right ventricular pressures, reducing the workload and oxygen needs of the heart. Complications of CPB include coagulopathies, myocardial ischemia, infection, and thromboembolism. CPB is used only in emergency situations until definitive treatment, such as heart transplantation, can be initiated.


Nursing Management




In some circumstances, identifying patients at risk early and pro-moting adequate oxygenation of the heart muscle and decreasing cardiac workload can prevent cardiogenic shock. This can be ac-complished by conserving the patient’s energy, promptly reliev-ing angina, and administering supplemental oxygen. Often, however, cardiogenic shock cannot be prevented. In such instances, nursing management includes working with other mem-bers of the health care team to prevent shock from progressing and to restore adequate cardiac function and tissue perfusion.



A major role of the nurse is monitoring the patient’s hemo-dynamic and cardiac status. Arterial lines and electrocardiographic monitoring equipment must be maintained and functioning properly. The nurse anticipates the medications, intravenous flu-ids, and equipment that might be used and is ready to assist in implementing these measures. Changes in hemodynamic, cardiac, and pulmonary status are documented and reported promptly. Additionally, adventitious breath sounds, changes in cardiac rhythm, and other abnormal physical assessment findings are re-ported immediately.


The nurse has a critical role in safe and accurate administration of intravenous fluids and medications. Fluid overload and pul-monary edema are risks because of ineffective cardiac function and accumulation of blood and fluid in the pulmonary tissues. The nurse documents and records medications and treatments that are administered as well as the patient’s response to treatment.


The nurse needs to be knowledgeable about the desired effects as well as the side effects of medications. For example, it is im-portant to monitor the patient for decreased blood pressure after administering morphine or nitroglycerin. The patient receiving thrombolytic therapy must be monitored for bleeding. Arterial and venous puncture sites must be observed for bleeding and pressure must be applied at the sites if bleeding occurs. Neuro-logic assessment is essential after the administration of throm-bolytic therapy to assess for the potential complication of cerebral hemorrhage associated with the therapy. Intravenous infusions must be observed closely because tissue necrosis and sloughing may occur if vasopressor medications infiltrate the tissues. Urine output, BUN, and serum creatinine levels are monitored to de-tect decreased renal function secondary to the effects of cardio-genic shock or its treatment.


The nurse plays a critical role in caring for the patient receiving intra-aortic balloon counterpulsation. The nurse makes ongoing timing adjustments of the balloon pump to max-imize its effectiveness by synchronizing it with the cardiac cycle. The patient is at great risk for circulatory compromise to the leg on the side where the catheter for the balloon has been placed; therefore, the nurse must frequently check the neurovascular sta-tus of the lower extremities.



Throughout care, the nurse must take an active role in safe-guarding the patient, enhancing comfort, and reducing anxiety. This includes administering medication to relieve chest pain, pre-venting infection at the multiple arterial and venous line insertion sites, protecting the skin, and monitoring respiratory function. Proper positioning of the patient promotes effective breathing without decreasing blood pressure and may also increase the pa-tient’s comfort while reducing anxiety.


Brief explanations about procedures that are being performed and the use of comforting touch often provide reassurance to the patient and family. Families are usually anxious and benefit from opportunities to see and talk to the patient. Explanations of treat-ments and the patient’s response to them are often comforting to family members.

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