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Cardiogenic_Shock.ppt
- 1. Cardiogenic Shock and Hemodynamics DRDODIYI-MANUEL ST
- 2. Outline • Overview ofshock • Hemodynamic Parameters • PA catheter, complications • Differentiating Types of Shock • Cardiogenic Shock • Etiologies • Pathophysiology • Clinical Findings • Treatment
- 3. introduction • Cardiogenic shockis a life threatening emergency • characterized by systemic hypoperfusion due to severe • depression of the cardiac index(<2.2L/min/m2 and sustained • systolic arterial hypotension(<90mmHg) despite an elevated • filling pressure( pulmonary cappilary wedge pressure PCWP) (> 18mmHg)
- 4. SHOCK=InadequateTissuePerfusion • Mechanisms: • Inadequateoxygen delivery • Release of inflammatory mediators • Further microvascular changes, compromised blood flow and further cellular hypoperfusion • Clinical Manifestations: • Multiple organ failure • Hypotension
- 5. Hemodynamic Parameters • SystemicVascular Resistance (SVR) • Cardiac Output (CO) • Mixed Venous Oxygen Saturation (SvO2) • Pulmonary Capillary Wedge Pressure (PCWP) • Central Venous Pressure (CVP)
- 6. pathophysiolgy • CS ischaracterized by a vicious cycle which ↓ myocardial contractility due to ischemia → ↓CO, & ↓BP →SV& diastolic LV end diastolic pressure & progressive myocardial dysfxn. • Inflammatory cytokines, inducible nitric oxide synthase, perryoxynitrite. Lactic acidosis from poor perfussionand hypoxemia from pulmonary edema → pump failure, myocardial ischemia. • Severe acidosis <7.25 reduces efficacy of endogenous & exogenously administered catecholamines. • Refractory ventricular / atrial tachyarrythmias exacerbate CS.
- 7. Clinical features • Chestpain •Dyspnoea • Pallor • diaphoretic • Altered sensorium • Somnolence • Cold extremeties • Confusion, agitation • Weak, rapid or absent pulse. • PR 90-110bpm, severe bradycardia • Oliguria (UO < 30ml/hr)
- 8. Cfxs • Soft S1, S3 gallop • Systolic murmur MR, VSD. • Crepitation if there is pulm oedema. • Laboratory Investigations • Increased WBC ± left shift • ↑ Urea & creatinine , ↓ HCO3 • ↑ transaminases • ↑CKMB, troponin I & T • CXR – fxs of acute pulmonary edema. • Normal heart size - !st MI, Enlarged – previous MI • Echo – left → Right shunt (VSD) AR, Tamponade, MR
- 9. Treatment • Medications • Aorticcounterpulsation • Reperfussion, revascularization • RVI- caution IV fluid • IABD • Repair of septal rupture.
- 10. Normal Values Right Atrial Pressure,CVP Mean 0-6mmHg Pulmonary Artery Pressure Systolic End-diastolic mean 15-30mmHg 4-12mmHg 9-19mmHg PCWP Mean 4-12mmHg Cardiac Output 4-8 L/min Mixed Venous O2 Sat >70% SVR 800-1200
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- 12. 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
- 13. Cardiogenic Shock • Systemichypoperfusion secondary to severe depression of cardiac output and sustained systolic arterial hypotension despite elevated filling pressures.
- 14. Cardiogenic Shock • Etiologies •Pathophysiology • Clinical/Hemodynamic Characteristics • Treatment Options
- 15. Etiologies • Acute myocardial infarction/ischemia •LV failure • VSR • Papillary muscle/chordal rupture- severe MR • Ventricular free wall rupture with subacute tamponade • Other conditions complicating large MIs • Hemorrhage • Infection • Excess negative inotropic or vasodilator medications • Prior valvular heart disease • Hyperglycemia/ketoacidosis • Post-cardiac arrest • Post-cardiotomy • Refractory sustained tachyarrhythmias • Acute fulminant myocarditis • End-stage cardiomyopathyHypertrophic cardiomyopathy with severe outflow obstruction • Aortic dissection with aortic insufficiency or tamponade • Pulmonary embolu • Severe valvular heart disease -Critical aortic or mitral stenosis, Acute severe aortic or MR
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- 17. Clinical Findings • PhysicalExam: elevated JVP, +S3, rales, oliguria, acute pulmonary edema • Hemodynamics: dec CO, inc SVR, dec SvO2 • Initial evaluation: hemodynamics (PA catheter), echocardiography, angiography
- 18. 4 Potential Therapies •Pressors • Intra-aortic Balloon Pump (IABP) • Fibrinolytics • Revascularization: CABG/PCI • Refractory shock: ventricular assist device, cardiac transplantation
- 19. Pressors do notchange outcome • Dopamine • <2 renal vascular dilation • <2-10 +chronotropic/inotropic (beta effects) • >10 vasoconstriction (alpha effects) • Dobutamine – positive inotrope, vasodilates, arrhythmogenic at higher doses • Norepinephrine (Levophed): vasoconstriction, inotropic stimulant. Should only be used for refractory hypotension with dec SVR. • Vasopression – vasoconstriction • VASO and LEVO should only be used as a last resort
- 20. IABP is atemporizing measure • Augments coronary blood flow in diastole • Balloon collapse in systole creates a vacuum effect decreases afterload • Decrease myocardial oxygen demand
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- 22. 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.
- 23. Complications of IABP •Cholesterol Embolization • CVA • Sepsis • Balloon rupture • Thrombocytopenia • Hemolysis • Groin Infection • Peripheral Neuropathy
- 24. Revascularization – SHOCK trial Overall30-Day Survival in the Study Hochman J et al. N Engl J Med 1999;341:625-634
- 25. SHOCK trial Hochman Jet al. N Engl J Med 1999;341:625-634
- 26. Copyright restrictions mayapply. Hochman, J. S. et al. JAMA 2006;295:2511-2515. Kaplan-Meier Long-term Survival of All Patients and Those Discharged Alive Following Hospitalization SHOCK – 6 years later
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