Cardiogenic shock

1. CARDIOGENIC
SHOCK
Reshma R
CRRI

2. DEFINITION
 Cardiogenic shock (CS) is defined as persistent
hypotension and tissue hypoperfusion due to cardiac
dysfunction in the presence of adequate intravascular
volume and left ventricular filling pressure.
 Hemodynamically : persistent hypotension (systolic blood
pressure <80 to 90 mm Hg or mean arterial pressure 30
mm Hg lower than baseline) with severe reduction in
cardiac index (<1.8 L · min−1 · m−2 without support or <2.0
to 2.2 L · min−1 · m−2 with support) and adequate or
elevated filling pressure (eg, left ventricular [LV] end-
diastolic pressure >18 mm Hg or right ventricular [RV]
end-diastolic pressure >10 to 15 mm Hg

3. ETIOLOGY
 COMMON- left ventricular failure due to extensive acute
myocardial infarction
 ACCORDING TO SHOCK TRIAL REGISTRY

4. GENERAL ETIOLOGIC FACTORS
Acute myocardial infarction
 Pump failure
 Large infarction
 Smaller infarction with preexisting left ventricular dysfunction
 Infarction extension
 Severe recurrent ischemia
 Infarction expansion
Mechanical complications
 Acute mitral regurgitation caused by papillary muscle rupture
 Ventricular septal defect
 Free-wall rupture
 Pericardial tamponade
 Right ventricular infarction

5. Otherconditions
 End-stage cardiomyopathy
 Myocarditis
 Myocardial contusion
 Prolonged cardiopulmonary bypass
 Septic shock with severe myocardial depression
 Left ventricular outflow tract obstruction
 Aortic stenosis
 Hypertropic obstructive cardiomyopathy
 Obstruction to left ventricular filling
 Mitral stenosis
 Left atrial myxoma
 Acute mitral regurgitation (chordal rupture)

6. PATHOPHYSIOLOGY

7. CLINICALPRESENTATION
 Evidence of hypoperfusion (low cardiac output)
manifested by
sinus tachycardia,
low urine output, and cool extremities
patients who develop acute MI present with
an abrupt onset of squeezing or heavy substernal chest
pain; the pain may radiate to the left arm or the neck.
The chest pain may be atypical, the location be in
epigastric or only in the neck or arm.
The pain quality may be burning, sharp, or stabbing.

8. PhysicalExamination
 ashen or cyanotic ,cool skin and mottled extremities
 Peripheral pulses are rapid and faint and irregular if arrhythmias are
present
 Jugular venous distention and crackles
 peripheral edema also may be present.
 third and fourth heart sounds may be present
 The pulse pressure may be low, and patients are usually tachycardic
 signs of hypoperfusion, such as altered mental status and decreased
urine output
 systolic murmer
 paradoxical thrill

9. DIAGNOSIS
Laboratory Studies
 RFT, LFT, serum electrolytes to assess the functiong of vital organs
 (CBC) is helpful to exclude anemia
Cardiac enzymes to diagnose MI
creatine kinase- elevate within 10hrs, peaks at 24-48 hours
troponin-Troponin levels peak at 14 hours after acute MI
myoglobin- 4-fold rise of myoglobin over 2 hours
LDH
ABG

10. LDH- Elevated lactate values in a patient with signs of hypoperfusion
BNP- indicator for heart failure
IMAGING STUDIES
echocardiography
helps to deteremine mechanical causes of shock, such as acute
ventricular septal defect, free myocardial wall rupture, pericardial
tamponade, and papillary muscle rupture causing acute mitral
regurgitation
 Assess the valvular and left ventricle function

11. CHESTXRAY
 HELP TO exclude other causes of chest pain tension pneumothorax
,pneumomediastinum etc
Manifest signs of LVF
 pulmonary vascular redistribution,
 interstitial pulmonary edema,
 enlarged hilar shadows
 the presence of Kerley B lines,
 cardiomegaly, and bilateral pleural effusions.

12. Ultrasonography
Ultrasonography can be used to guide fluid management
Coronary artery angiography
Assess the anatomy of the coronary arteries and need for
revascularisation
ECG
Assesss ST-segment elevation, ST-segment depression, or Q waves. T-
wave inversion

13. MANAGEMENT

14. PHARMACOLOGIC MANAGEMENT
Inotropic Agents
augments the coronary blood flow
Dopamine
Dopamine stimulates adrenergic and dopaminergic receptors
Action depend upon the dose
 (low dose): 1-5 mcg/kg/min IV- increase urine output and renal blood
flow
 (medium dose): 5-15 mcg/kg/min IV ; increase renal blood flow, cardiac
output, heart rate, and cardiac contractitlity
 (high dose): 20-50 mcg/kg/min IV ; increase blood pressure and
stimulate vasoconstriction; may not have a beneficial effect in blood
pressure; may increase risk of tachyarrhythmias

15. Dobutamine
 a sympathomimetic amine with stronger beta effects than alpha effects
 produces systemic vasodilation and increases the inotropic state
 DOSAGE; 2-20 mcg/kg/min IV or IO
 not to exceed 40 mcg/kg/min
 Higher doses may cause an increase in heart rate, exacerbating
myocardial ischemia

16. Norepinephrine
 is a naturally occurring catecholamine with potent alpha-receptor and
mild beta-receptor activity
 It stimulates beta1- and alpha-adrenergic receptors, resulting in
increased cardiac muscle contractility, heart rate, and vasoconstriction
 There by increase bp and afterload
 Increased afterload may result in decreased cardiac output, increased
myocardial oxygen demand, and cardiac ischemia
 DOSAGE
Initial: 8-12 mcg/min IV infusion; titrate to effect
Maintenance: 2-4 mcg/min IV infusion

17. Vasodilators
 Vasodilators decrease preload and/or afterload.
Nitroglycerin IV
causes relaxation of vascular smooth muscle by stimulating
intracellular cyclic guanosine monophosphate production
 intolerant of or unresponsive to SL NTG 5 mcg/min
 Increase by 5 mcg/min q3-5min up to 20 mcg/min, THEN
Increase by 10 mcg/min

18. DIURETICS
 to decrease plasma volume and edema and thereby decrease cardiac
output and, consequently, blood pressure
 Furosemide (Lasix)
inhibits sodium and chloride reabsorption in the ascending loop of
Henle and the distal renal tubule.
DOSAGE; Alternative: 20-40 mg IV/IM once

19. Complications
Bleeding
Thrombocytopenia
hemolysis,
leg ischemia,
aortic dissection,
femoral artery injury,
thromboembolism, and sepsis

20.  Thank you