Cardiogenic shock lecture note

1. Cardiogenic Shock and
Hemodynamics
DR DODIYI-MANUEL ST

2. Outline
• Overview of shock
• Hemodynamic Parameters
• PA catheter, complications
• Differentiating Types of Shock
• Cardiogenic Shock
• Etiologies
• Pathophysiology
• Clinical Findings
• Treatment

3. introduction
• Cardiogenic shock is 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:
• Inadequate oxygen delivery
• Release of inflammatory mediators
• Further microvascular changes, compromised blood flow and
further cellular hypoperfusion
• Clinical Manifestations:
• Multiple organ failure
• Hypotension

5. Hemodynamic Parameters
• Systemic Vascular Resistance (SVR)
• Cardiac Output (CO)
• Mixed Venous Oxygen Saturation (SvO2)
• Pulmonary Capillary Wedge Pressure (PCWP)
• Central Venous Pressure (CVP)

6. pathophysiolgy
• CS is characterized 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
• Aortic counterpulsation
• 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

11. Differentiating Types of Shock

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
• Systemic hypoperfusion 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

16. Pathophysiology

17. Clinical Findings
• Physical Exam: 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 not change
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 a temporizing measure
• Augments coronary blood flow in diastole
• Balloon collapse in systole creates a vacuum effect 
decreases afterload
• Decrease myocardial oxygen demand

21. Indication for IABP

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
Overall 30-Day Survival in the Study
Hochman J et al. N Engl J Med 1999;341:625-634

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

26. 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 Following
Hospitalization
SHOCK – 6 years later

27. Question 1

28. Answer

29. Question 2

30. Answer

31. Question 3

32. Answer