Cardiogenic shock

Submitted to:
Prof. Janeirah Q. Manalundong - Mamowalas, MANc, MN, RN

Submitted by:
Shereen D. Al-Obinay
Section A
OVERVIEW
Cardiogenic shock is also sometimes called“pump failure”.
Cardiogenic shock is a condition of diminished cardiac output that severely impairs cardiac
perfusion. It reflects severe left-sided heart failure.
Statistics and Incidences
Cardiogenic shock occurs as a serious complication in 5% to 10% of patients hospitalized with
acute myocardial infarction.
Historically, mortality for cardiogenic shock had been 80% to 90%, but recent studies indicate
that the rate has dropped to 56% to 67% due to the advent of thrombolytics, improved
interventional procedures, and better therapies.
Incidence of cardiogenic shock is more common in men than in women because of their higher
incidence of coronary artery disease.
Pathophysiology
This is what happens in cardiogenic shock:
1. Inability to contract. When the myocardium can’t contract sufficiently to maintain adequate
cardiac output, stroke volume decreases and the heart can’t eject an adequate volume of blood
with each contraction.
2. Pulmonary congestion. The blood backs up behind the weakened left ventricle, increasing
preload and causing pulmonary congestion.
3. Compensation. In addition, to compensate for the drop in stroke volume, the heart rate
increases in an attempt to maintain cardiac output.
4. Diminished stroke volume .As a result of the diminished stroke volume, coronary artery
perfusion and collateral blood flow is decreased.
5. Increased workload. All of these mechanisms increase the heart’s workload and enhance left-
sided heart failure.
6. End result. The result is myocardial hypoxia, further decreased cardiac output, and a triggering
of compensatory mechanisms to prevent decompensation and death.
Classification
The causes of cardiogenic shock are known as either coronary or non-coronary.
o Coronary - Coronary cardiogenic shock is more common than noncoronary cardiogenic
shock and is seen most often in patients with acute myocardial infarction.
o Noncoronary - Noncoronary cardiogenic shock is related to conditions that stress the
myocardium as well as conditions that result in an ineffective myocardial function.
Causes
 Myocardial infarction (MI). Regardless of the underlying cause, left ventricular
dysfunction sets in motion a series of compensatory mechanisms that attempt to increase
cardiac output, but later on leads to deterioration.
 Myocardial ischemia. Compensatory mechanisms may initially stabilize the patient but
later on would cause deterioration with the rising demands of oxygen of the already
compromised myocardium.
PRESENTING SIGNS AND SYMPTOMS
 Cardiogenic shock produces symptoms of poor tissue perfusion.
 Clammy skin. The patient experiences cool, clammy skin as the blood could not circulate
properly to the peripheries.
 Decreased systolic blood pressure. The systolic blood pressure decreases to 30 mmHg
below baseline.
 Tachycardia. Tachycardia occurs because the heart pumps faster than normal to compensate
for the decreased output all over the body.
 Rapid respirations. The patient experiences rapid, shallow respirations because there is not
enough oxygen circulating in the body.
 Oliguria.
 Mental confusion. Insufficient oxygenated blood in the brain could gradually cause mental
confusion and obtundation.
 Cyanosis.

PHYSICAL EXAMINATION FINDINGS

Diagnosis of cardiogenic shock may include the following diagnostic tests:
Auscultation
- Gallop rhythm, faint heart sounds and, possibly, if the shock results from rupture of
the ventricular septum or papillary muscles, a holosystolic murmur.
DIAGNOSTIC FINDINGS
Pulmonary artery pressure (PAP). may show increase in PAP, reflecting a rise in left
ventricular end- diastolic pressure and increased resistance to the afterload.
Arterial pressure monitoring. Invasive arterial pressure monitoring may indicate
hypotension due to impaired ventricular ejection.
ABG analysis. Arterial blood gas analysis may show metabolic acidosis and hypoxia.
Electrocardiography. may show possible evidence of acute MI, ischemia, or ventricular
aneurysm.
Echocardiography. Echocardiography can determine left ventricular function and reveal
valvular abnormalities.
Enzyme levels. Enzyme levels such as lactic dehydrogenase, creatine kinase. Aspartate
aminotransferase and alanine aminotransferase may confirm MI.
Laboratory markers for ventricular dysfunction (eg, BNP) and cardiac enzyme levels
(CK-MB and cTn-I) are measured, and serial 12-lead ECGs are obtained to assess the
degree of myocardial damage. Continuous ECG and ST-segment monitoring is also used
to closely monitor the patient for ischemic changes.
GOAL OF TREATMENT
The major goals for the patient are:
Prevent recurrence of cardiogenic shock.
Monitor hemodynamic status.
Administer medications and intravenous fluids.
Maintain intra-aortic balloon counterpulsation.
Medical Management
The aim of treatment is to enhance cardiovascular status by:
 Oxygen. Oxygen is prescribed to minimize damage to muscles and organs.
 Angioplasty and stenting. A catheter is inserted into the blocked artery to open it up.
 Balloon pump. A balloon pump is inserted into the aorta to help blood flow and reduce
workload of the heart.
 Pain control. In a patient that experiences chest pain, IV morphine is administered for
pain relief.
 Hemodynamic monitoring
 Fluid therapy.
Pharmacologic Therapy:
 IV dopamine. Dopamine, a vasopressor, increases cardiac output, blood pressure, and
renal blood flow.
 IV dobutamine. Dobutamine is an inotropic agent that increase myocardial contractility.
 Norepinephrine. Norepinephrine is a more potent vasoconstrictor that is taken when
necessary.
 IV nitroprusside. Nitroprusside is a vasodilator that may be used with a vasopressor to
further improve cardiac output by decreasing peripheral vascular resistance and reducing
preload.
Surgical Management
 Intra-aortic balloon pump (IABP). The IABP is a mechanical-assist device that attempts
to improve the coronary artery perfusion and decrease cardiac workload through an
inflatable balloon pump which is percutaneously or surgically inserted through the
femoral artery into the descending thoracic aorta.

ACUTE CARE PATIENT MANAGEMENT AND MONITORING (Critical care)

 Hemodynamic status. Arterial lines and ECG monitoring equipment must be well
maintained and functioning; changes in hemodynamic, cardiac, and pulmonary status and
laboratory values are documented and reported; and adventitious breath sounds, changes
in cardiac rhythm, and other abnormal physical assessment findings are reported
immediately.
 Fluids. IV infusions must be observed closely because tissue necrosis and sloughing may
occur if vasopressor medications infiltrate the tissues, and it is also necessary to monitor
the intake and output.
  Intra-aortic balloon counter pulsation. The nurse makes ongoing timing adjustments of
the balloon pump to maximize its effectiveness by synchronizing it with the cardiac
cycle.
 Enhance safety and comfort. Administering of medication to relieve chest pain,
preventing infection at the multiple arterial and venous line insertion sites, protecting the
skin, and monitoring respiratory and renal functions help in safeguarding and enhancing
the comfort of the patient.
 Arterial blood gas. Monitor ABG values to measure oxygenation and detect acidosis from
poor tissue perfusion.
 Positioning. If the patient is on the IABP, reposition him often and perform passive range
of motion exercises to prevent skin breakdown, but don’t flex the patient’s “ballooned”
leg at the hip because this may displace or fracture the catheter.
 Laboratory Marker Monitoring.

NURSING DIAGNOSIS
 Decreased cardiac output related to changes in myocardial contractility/ inotropic
changes
 Impaired gas exchange related to changes in alveolar-capillary membrane.
 Excess fluid volume related to a decrease in renal organ perfusion, increased sodium and
water, hydrostatic pressure increase, or decrease plasma protein.
 Ineffective tissue perfusion related to reduction/cessation of blood flow.
 Acute pain related to ischemic tissues secondary to blockage or narrowing of coronary
arteries.

References:
o Brunner and Suddarth's Textbook of Medical-Surgical Nursing 12th edition
o Essentials of Human Anatomy Physiology - Marieb, Elaine N. [SRG] 11th edition
o Medical-Surgical nursing: CONCEPTS AND CLINICAL APPLICATION. Josie
Quiambao-Udan 2nd edition 2009
o www.nurseslabs.com