Download Etiology

Cardiogenic Shock
Dr. Belal Hijji, RN, PhD
October 12 & 15, 2011
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
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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
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work of heart.
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.
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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:
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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.
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