Cardiogenic shock is characterized by decreased tissue perfusion and impaired cellular metabolism. It progresses through four stages as the body attempts compensation. The compensatory stage involves nervous, hormonal and chemical responses to shunt blood to vital organs. In the progressive stage, compensatory mechanisms begin to cause problems by failing to maintain cardiac output. Cardiogenic shock is divided into coronary and non-coronary types. Clinical signs include pale skin, tachycardia, weak pulses and decreased urine output. Treatment goals are to improve tissue perfusion, decrease myocardial oxygen demand, improve contractility and decrease infarct size using fluids, inotropes, vasopressors and IABP as needed.

1. QAISAR IQBAL
SHIFA COLLEGE OF NURSING
SHOCK
(CARIOGENIC SHOCK)

2. Objectives
o Define the cardiogenic shock
o Discus the stages of shock
o Describe the Pathophysiology of shock
o List out the clinical sign of shock
o Discus the common test
o Describe the treatment of cardiogenic shock

3. INTRODUCTION
Shock is a complex clinical syndrome initiated by
a variety of factors. It is characterized by
DECREASE TISSUE PERFUSION and leads to
IMMPAURD CELLULAR METABOLISM.
Survival varies with early recognition and
treatment.

4. INTRODUCTION..cont..

5. STAGES OF SHOCKS
A body specific responses to shock are influenced by:
1. The severity and duration of the shock state
2.The specific tissue needs
3.The state of the health, underlying condition and age
of pt
4.There are 4 primary stages
INITIAL STAGECOMPENSATORYPROGRESSIVEREFACTORY

6. STAGE I: THE INITIAL STAGE
During this stage, the cardiac output may be
decreased, but no signs and symptoms are
evident. Early, non specific changes may be
occurring at the cellular level, but no clinical
manifestations characterize the stage.

7. STAGE II: THE COMPENSATORY STAGE
During this stage, the body’s compensatory mechanisms
immediately kick in to try and prevent any damage to
organs. In other words, the mechanisms shunt the blood
to vital organs to try and preserve them. However, these
mechanisms are short lived, and only server to buy time
so that the underlying problem can be resolved. The
prognosis varies with the severity and duration of shock
the degree of inadequacy in Sa02, degree of deficit in
Cellular oxygenation, and cellular ability to utilize 02.

8. THE COMPENSATORY STAGE…Continue
There are three levels of compensation:
Nervous system
Hormonal
Chemical

10. STAGE III: PROGRESSIVE STAGE
In the progressive stage, the underlying problem
still exist but the compensatory mechanism progress
past being helpful and begin to cause problem
themselves. The prolonged vasoconstriction fails to
maintain an adequate cardiac output and begins to
work against the patient.

11. PROGRESSIVE STAGE..Cont…
It affects the body at many levels:
Systemic Circulation
Specific Organ system

12. CARDIOGENIC SHOCK (PUMP FAILURE)
This type of shock is divided into two category:
ETIOLOGY
CORONARY CARDIOGENIC SHOCK NON CORONARY CARDIOGENIC
SHOCK
1) More common
2) Occurs after an acute MI,
especially if there is left ventricular
involvement.
3) Coronary artery diseases.
1) With this type, the problem seems
to be in the mycardium itself, rather
then a diseases of the coronary
arteries.
2) Contractility is impaired, although
coronary perfusion may be normal.
3) May be caused by viral infection,
mycarditis, cardiomyopathies.

13. PATHOPHYSIOLOGY

14. IMPAIRED DIASTOLIC FUNCTION

15. CLINICAL FINDINGS
Lethargy, decrease LOC.
Skin is pale, cool, clammy, may have peripheral
cyanosis.
Tachycardia (compensatory mechanism).
Pulses weak.
Neck vein distended.
Decrease urine output.
Tachypnea, increase work of breathing with
pulmonary edema, crackles.

16. HEMODYNAMICS
Increase heart rate.
Decrease blood pressure.
Increase SVR.
Increase respiratory rate.
Decrease cardiac output.
Decrease urine output.

17. COMMON TESTS
ABGS.
Electrolytes.
BUN creatine.
CBC.
Twelve lead ECG.
Coronary Angiogram.

18. TREATMENT
Goals:
Improve tissue perfusion.
Decrease myocardial oxygen consumption.
Improve ventricular contractility.
Decrease infarct size.

19. TREATMENT
Intervention
ABC
Restore blood pressure first then optimize cardiac
out put – fluid, inotropes, vasopressors, IABP.
Morphine-sedative, pain relief, decrease preload.

20. TREATMENT
Intervention
ABC
Restore blood pressure first then optimize cardiac
out put – fluid, inotropes, vasopressors, IABP

21. NURSING DIAGNOSIS
In effective cardio pulmonary tissue perfusion
related to acute myocardial ischemia.
Decrease cardiac output related to alteration in
contractility.
Alter nutrition less then body requirement related to
increase metabolic demand.

22. THE END