Cardiogenic Shock

Dr. Belal Hijji, RN, PhD

October 12 & 15, 2011

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Learning Outcomes

At the end of this lecture, students will be able to:

• Provide a brief description of the cardiogenic shock, its etiology, and its pathophysiology.

• Identify the clinical manifestations of cardiogenic shock.

• Discuss the medical and nursing management of a patient with cardiogenic shock.

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Description of Cardiogenic Shock

• Cardiogenic shock results from failure of the heart (Rt. ventricle, or left ventricle, or both) to effectively pump blood forward.

• The outcome of pump failure is decreased tissue perfusion and circulatory failure.

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Etiology and Pathophysiology of Cardiogenic Shock

• Etiology: Cardiogenic shock can result from primary ventricular ischemia most commonly caused by acute MI and structural problems such as congestive heart failure, intracardiac tumor, acute myocarditits, Hemorrhage, and prolonged septic shock. Other conditions that may cause cardiogenic shock are bradydysrhytmias and tachydysrhythmias.

• Pathophysiology: Impaired ability of the ventricle to pump blood forward, leads to decreased stroke volume (SV) and an increase in the blood in the left ventricle at the end of the systole. A decrease in the SV results in a decrease in cardiac output (CO) which is responsible for decreased oxygen supply and ineffective tissue perfusion.

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Clinical Manifestations of Cardiogenic Shock

• SBP <90 mm Hg.

• Acute drop in blood pressure > 30 mm Hg.

• HR > 100 bpm.

• Weak, thready pulse.

• Diminished heart sounds.

• Change in sensorium.

• Cool, pale , moist skin.

• Urine output < 30 mL/hr.

• Chest pain.

• Dysrhythmias and tachypneas.

• Decreased cardiac output.

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Medical Management of a Patient With Cardiogenic Shock

• Treatment requires aggressive approach where its goals are to treat the underlying cause, enhance the effectiveness of the pumping function, and improve tissue perfusion.

• Inotropic agents increase myocardial contractility and maintain adequate blood pressure and improve tissue perfusion.

• Inotropic agents include cardiac glycosides (digoxin), sympathomimetic agents (epinephrine, dopamine, norepinephrine, dobutamine), and phosphodiesterase inhibitors (amrinone, milrinone).

• Diuretics (lasix) to decrease preload (volume of blood in the left ventricle at the end of diastole).

• Vasodilators are used after stabilising blood pressure to reduce preload and afterload which is the ventricular wall tension during systolic ejection. Afterload means an increase in the work of heart.

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Medical Management of a Patient With Cardiogenic Shock (Continued…)

• Antidysrhythmic agents (lidocaine, propranolol) to suppress dysrhythmias (disturbance in the normal cardiac conduction pathway). Regular and irregular heart rate calculations are presented on next two slides.

• Intubation and mechanical ventilation may be indicated to support oxygenation.

• If drug therapy is unsuccessful, intraaortic balloon pump (IABP) (Slide 9) support should be instituted. IABP is a temporary measure to decrease myocardial workload by improving myocardial supply and decreasing myocardial demand. IABP inflates during diastole and deflates just before systole.

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Nursing management of Patient With Cardiogenic Shock

• Limit myocardial oxygen demand by:– Administering analgesics, sedatives, and other agents as

prescribed.

– Positioning the patient for comfort.

– Limiting activities.

– Providing calm and quiet environment

– Offering support to reduce anxiety.

– Teaching the patient about his condition.

• Enhancing myocardial oxygen supply by:– Administering oxygen.

– Monitoring the patient’s respiratory status.

– Administering prescribed medications.

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Nursing management of Patient With Cardiogenic Shock (Continued…)

• Providing comfort and psychological support.

• Moving the patient Q2H to prevent pressure ulcers.

• Observing for IABP-related complications such as:– Embolus formation: Assess peripheral pulses.

– Infection.

– Thrombocytopenia.

– Bleeding.

– Balloon rupture due to repeated contact with calcified plaque in the aorta as the balloon inflates and deflates.

– Circulatory compromise of the cannulated extremity.