Cardiogenic shock

1. Prepared by
SALMAN HABEEB
*CARDIOGENIC
SHOCK

2. *
*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. *
*COMMON- left ventricular failure due to extensive
acute myocardial infarction
*ACCORDING TO SHOCK TRIAL REGISTRY

4. *
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. *
*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. *

7. *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. *
*history of previous cardiac disease,
*use of cocaine,
*previous myocardial infarction (MI), or previous
cardiac surgery
* A patient thought to have MI should be assessed for
cardiac risk factors.
*associated symptoms are
* diaphoresis,
*exertional dyspnea,
*Presyncope or syncope,
*palpitations, generalized anxiety, and are other
features indicative of poor cardiac function.

9. *
*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

10. *
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

11. 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

12. *
*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.

13. 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

14. *Help to precise measurement of volume status,
left and right ventricular filling pressures, and
cardiac output
* Help guide fluid management and the use of
inotropic agents and vasopressors
*Hemodynamic measurements can help guide
fluid management and the use of inotropic
agents and vasopressors

15. *
*class I - patients with hypotension not responding to fluid
administration or when mechanical complications of
myocardial infarction are suspected and echocardiography is
not available.
*class II recommendation for patients in CS who have
persistent signs of hypoperfusion and in patients receiving
inotropic and vasopressor drugs.
(PCWP) of greater than 15 mm Hg and a cardiac index of less
than 2.2 L/min/m2

17. *

18. 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

19. 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

20. *Norepinephrine
(Levophed)
*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

21. *Milrinone
*It is a selective phosphodiesterase inhibitor in cardiac and
vascular tissue with positive inotropic and vasodilator
effects; it has little chronotropic activity
*DOSAGE
50 mcg/kg loading dose by IV push over 10 minutes, then
0.375-0.75 mcg/kg/min IV
Maintenance: 1.13 mg/kg/day

22. *Inamrinone
*Formerly known as amrinone, inamrinone is a
phosphodiesterase inhibitor with positive inotropic and
vasodilator activity
*DOSAGE
*Load: 0.75 mg/kg IV bolus over 2-3 minutes, THEN
*5-10 mcg/kg/min IV
*should not exceed 10 mg/kg/day
*likely to cause tachycardia than is dobutamine, and it may
exacerbate myocardial ischemia

24. *
*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

25. *
*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

31. IABP

34. *
*Bleeding
*Thrombocytopenia
*hemolysis,
*leg ischemia,
*aortic dissection,
*femoral artery injury,
*thromboembolism, and sepsis

36. * many patients develop CS IN HSPITAL results from
infarction extension, reocclusion of a previously patent
coronary artery, recurrent ischemia, or decompensation
of left ventricular function in the noninfarcted zone
because of metabolic derangements
*FIBRINOLYTIC therapy as not much effective as primary
coronary intervention

37. *
*Used for patients with CS refractory to IABP
and reperfusion strategies
* very low cardiac output, less than 1.2
L/min/m2

38. *
Mechanical circulatory device that is used to
replace the pumping action of a failing
human heart.
Left ventricular failure is primarily treated
using a VAD.

40. *Almost all VADs are made up of 3 parts:
*A pump that is implanted inside the body
(an implantable VAD) or that is placed
outside the body (an external
or paracorporeal VAD)
*A system controller that stays outside the
body and is used to program the settings of
the VAD
*An outside energy source to power the
pump—either a console or a battery pack.

41. *Pic