Cardiogenic_Shock.ppt

5/19/2018 Cardiogenic_Shock.ppt

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Cardiogenic Shock andHemodynamics


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Outline

Overview of shock

Hemodynamic Parameters

PA catheter, complications

Differentiating Types of Shock

Cardiogenic Shock

Etiologies

Pathophysiology

Clinical Findings

Treatment


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SHOCK= Inadequate Tissue Perfusion

Mechanisms: Inadequate oxygen delivery

Release of inflammatory mediators

Further microvascular changes, compromisedblood flow and further cellular hypoperfusion

Clinical Manifestations: Multiple organ failure

Hypotension


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Hemodynamic Parameters

Systemic Vascular Resistance (SVR)

Cardiac Output (CO) Mixed Venous Oxygen Saturation (SvO2)

Pulmonary Capillary Wedge Pressure

(PCWP)

Central Venous Pressure (CVP)


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Normal Values

Right Atrial

Pressure, CVP

Mean 0-6mmHg

Pulmonary

Artery Pressure

Systolic

End-diastolic

mean

15-30mmHg

4-12mmHg

9-19mmHg

PCWP Mean 4-12mmHgCardiac Output 4-8 L/min

Mixed Venous

O2 Sat

>70%

SVR 800-1200


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Differentiating Types of Shock


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PA Catheter Complications

Path of PAC: central venous circulation R

heart pulmonary artery. The proximal port is in

R atrium, distal port in pulm artery

Arrhythmias

RBBB

PA rupture

PAC related infection

Pulmonary infarction


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Cardiogenic Shock

Systemic hypoperfusion secondary to

severe depression of cardiac output andsustained systolic arterial hypotension

despite elevated filling pressures.


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Cardiogenic Shock

Etiologies

Pathophysiology Clinical/Hemodynamic Characteristics

Treatment Options


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Etiologies

Acute myocardialinfarction/ischemia

LV failure

VSR

Papillary muscle/chordalrupture- severe MR

Ventricular free wallrupture with subacute

tamponade

Other conditions complicating largeMIs

Hemorrhage

Infection

Excess negative inotropic orvasodilator medications

Prior valvular heart disease

Hyperglycemia/ketoacidosis

Post-cardiac arrest

Post-cardiotomy

Refractory sustainedtachyarrhythmias

Acute fulminant myocarditis

End-stagecardiomyopathyHypertrophiccardiomyopathy with severeoutflow obstruction

Aortic dissection with aorticinsufficiency or tamponade

Pulmonary embolu

Severe valvular heart disease -Critical aortic or mitral stenosis,Acute severe aortic or MR


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Pathophysiology


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Clinical Findings

Physical Exam: elevated JVP, +S3, rales,oliguria, acute pulmonary edema

Hemodynamics: dec CO, inc SVR, decSvO2

Initial evaluation: hemodynamics (PAcatheter), echocardiography, angiography


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4 Potential Therapies

Pressors

Intra-aortic Balloon Pump (IABP) Fibrinolytics

Revascularization: CABG/PCI

Refractory shock: ventricular assist device,

cardiac transplantation


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Pressors do not change outcome

Dopamine


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IABP is a temporizing measure

Augments coronary blood flow in diastole

Balloon collapse in systole creates a vacuum

effectdecreases afterload

Decrease myocardial oxygen demand


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Indication for IABP


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Contraindications to IABP

Significant aortic regurgitation or significant

arteriovenous shunting

Abdominal aortic aneurysm or aortic dissection

Uncontrolled sepsis

Uncontrolled bleeding disorder

Severe bilateral peripheral vascular disease Bilateral femoral popliteal bypass grafts for severe

peripheral vascular disease.


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Complications of IABP

Cholesterol Embolization

CVA Sepsis

Balloon rupture

Thrombocytopenia Hemolysis

Groin Infection

Peripheral Neuropathy


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Revascularization

SHOCK trial

Overall 30-Day Survival in the Study

Hochman J et al. N Engl J Med 1999;341:625-634


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SHOCK trial

Hochman J et al. N Engl J Med 1999;341:625-634


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Copyright restrictions may apply.

Hochman, J. S. et al. JAMA 2006;295:2511-2515.

Kaplan-Meier Long-term Survival of All Patients and Those Discharged Alive FollowingHospitalization

SHOCK 6 years later


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Question 1


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Answer


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Question 2


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Answer


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Question 3


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Answer

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Cardiogenic_Shock.ppt

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