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SYOK KARDIOGENIK

Dr.Suhaemi, SpPD, Finasim


History
• 1700s: Shock first defined as a sequelae of severe trauma

• 1935, 1940: Harrison and Blalock classified types of shock

• 1950: Treatment of CS with O2, phlebotomy, morphine. Also in favor was


ethyl alcohol vapor, digitalis, quinidine

• 1960: Introduction of CCUs; improvement in mortality from arrhythmia,


but not CS

• 1962: First IABP designed

• 1968: IABP placed by Dr. Kantrowitz in 5 patients with CS

2
EKG

3
Phone a friend
a. Call your attending
b. Call the cardiologist
c. Call the cardiothoracic surgeon
d. Call your mother

4
Hemodynamic Parameters
 Systemic Vascular Resistance (SVR)
 Cardiac Output (CO)
 Mixed Venous Oxygen Saturation (SvO2)
 Pulmonary Capillary Wedge Pressure (PCWP)
 Central Venous Pressure (CVP)
Normal Values

Right Atrial Mean 0-6mmHg


Pressure, CVP
Pulmonary Systolic 15-30mmHg
Artery Pressure End-diastolic 4-12mmHg
mean 9-19mmHg
PCWP Mean 4-12mmHg
Cardiac Output 4-8 L/min
Mixed Venous >70%
O2 Sat
SVR 800-1200
Differentiating Types of Shock
Cardiogenic Shock
 Systemic hypoperfusion secondary to severe
depression of cardiac output and sustained
systolic arterial hypotension despite elevated
filling pressures.
CARDIOGENIC SHOCK — IDENTIFICATION

PATIENT PRESENTATION

 Appear ashen or cyanotic and


have cool skin and mottled
extremities
 Peripheral pulses are rapid and
faint and may be irregular if
arrhythmias are present
 Jugular venous distention and
crackles in the lungs are usually
(but not always) present
 Patients show signs of
hypoperfusion, such as altered
mental status and decreased
urine output

Source: Andrew Lenneman, MD. Cardiogenic Shock. Medscape Reference February 2011
CARDIOGENIC SHOCK — IDENTIFICATION

CARDIOGENIC SHOCK HEMODYNAMIC PARAMETERS

 Systolic B/P <90 mmHg or a


MAP 30 mmHg lower than
baseline
 Cardiac Index <1.8 L/m/M2
without support and adequate
filling pressures
 Cardiac Index <2.0-2.2
L/m/M2 with support and
adequate filling pressures
 PCWP >15–18 mmHg

Source: Reynolds H, Hochman J; Circulation 2008;117(5):686-697


Cardiogenic Shock
• 5-15% of ACS cases
• Small percentage with NSTEMI have CS
(GUSTO II-B, PURSUIT trials)
• Loss of 40% of ventricular muscle mass
• Myocytes adjacent to infarct are susceptible to
expanding ischemia

11
CARDIOGENIC SHOCK — IDENTIFICATION

CARDIOGENIC SHOCK RISK FACTORS

 Four risk factors account for >85% of


the predictive information needed to
determine if a patient is at high risk
to develop cardiogenic shock:
 Age
 Single greatest risk factor
 For every ten year increase in age, the risk
of developing shock increases by 47%
 Systolic Blood Pressure
 HR
 Killip Class

Source: Hasdai D, et al. American Heart Journal. 1999;138 (1 Pt 1):21-31


Classic Criteria for Diagnosis of
Cardiogenic Shock

1. Systemic Hypotension
systolic arterial pressure < 80 mmHg
2. Persistent Hypotension
at least 30 minutes
3. Reduced Systolic Cardiac Function
Cardiac index < 1.8 x m²/min
4. Tissue Hypoperfusion
Oliguria, cold extremities, confusion
5. Increased Left Ventricular Filling
Pulmonary capillary wedge pressure > 18 mmHg
Etiologies
 Acute myocardial  Other conditions complicating large
MIs  
infarction/ischemia   Hemorrhage
 LV failure    Infection  
 Excess negative inotropic or
 VSR  vasodilator medications  
 Papillary muscle/chordal  Prior valvular heart disease  
 Hyperglycemia/ketoacidosis
rupture- severe MR  Post-cardiac arrest
 Ventricular free wall  Post-cardiotomy
rupture with subacute  Refractory sustained
tamponade  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
Pathophysiology
Cardiogenic Shock
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
4 Potential Therapies
 Pressors
 Intra-aortic Balloon Pump (IABP)
 Fibrinolytics
 Revascularization: CABG/PCI

 Refractory shock: ventricular assist device,


cardiac transplantation
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
Pharmacologic Treatment of
Cardiogenic Shock
• SBP <70 mm Hg + shock
→ Norepinephrine
• SBP 70-100 mm Hg + shock
→ Dopamine
• SBP 70-100 mm Hg – shock
→ Dobutamine
• Refractory hypotension + shock
→ Amrinone or milrinone may improve cardiac output

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


Indication for IABP
Revascularization – SHOCK trial

Overall 30-Day Survival in the Study

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


Cardiogenic Shock Outcome

P=0.04

Antman et al. JACC 2004; 44: 671


CARDIOGENIC SHOCK — CASE STUDY
CARDIOGENIC SHOCK — CASE STUDY

CARDIOGENIC SHOCK CALCULATION TABLE (EXAMPLE)

Points
 70-year-old, 60 kg female
Age 37
from the US with a history
Systolic B/P 49
of hypertension, no prior Weight 17
PCTA, diagnosed with HR 17
acute anterior MI. On Diastolic B/P 5
admission, HR=123, Killip Class 9
B/P=112/70 and a few MI Location 8

crackles in lungs Thrombolytics 0


Misc [6+3+2+5] 16
Total 155
40% probability of shock

Source: Hasdai, D, et al; J Am Coll Cardiol 2000; 35:136-43


CARDIOGENIC SHOCK — CASE STUDY

PATIENT CONDITION WHEN SHE LEFT THE CATH LAB AFTER SUCCESSFUL STENTING OF LAD

 HR=105,
B/P=102/65
 Few crackles in
lungs when she
left CCL
CARDIOGENIC SHOCK — CASE STUDY

NOW LET’S TAKE A LOOK AT THIS PATIENT 4 HOURS LATER IN THE CCU

 BP 80/40, HR – 135
 Skin cool and clammy; becoming agitated
 Saturating 90% on 2L per N/C
 Crackles more prominent
 Short of breath with minimal activity
 Pulses weak and thready
 Has not urinated since admission
 12 Lead EKG shows no changes

3/2/2010 V
CARDIOGENIC SHOCK — CASE STUDY

INTERVENTIONS

 2D Echo at bedside
 No mechanical complications i.e. VSD or MR
 Shows wall motion abnormality
 100% non-rebreather oxygen mask
 Fluid bolus 250cc NS
 Dopamine 10 mcg/kg/min
 Dobutrex 5 mcg/kg/min
 Lasix 40 mg IV
 Foley catheter placed
 Swan-Ganz Catheter inserted at bedside
CARDIOGENIC SHOCK — CASE STUDY

PATIENT CONDITION AFTER INTERVENTIONS

 BP 88/48; HR – 145; CI – 1.8 L;


PCWP – 22
 Skin remains cool and clammy
 Patient is lethargic
 Saturating 94% on 100% NRB
 Patient complains of difficulty
breathing
 Pulses remain weak and thready
 Response from diuretic minimal
100 cc urine from catheter total
CARDIOGENIC SHOCK — CASE STUDY

FURTHER INTERVENTIONS AFTER NO IMPROVEMENT IN PATIENT CONDITION

 Considering intubation
 Dopamine increased to 20
mcg/kg/min
 Dobutrex 10 mcg/kg/min
 Bumex (diuretic) 4 mg IV
given
 Preparing patient for
IABP placement

3/2/2010 V
CARDIOGENIC SHOCK — TREATMENT

CARDIOGENIC SHOCK PHARMACOLOGICAL TREATMENT

 Negative inotropes and vasodilators should be


used in the lowest doses possible
 Higher doses results in poorer survival rates
 Positive inotropes increase myocardial ATP
consumption resulting in a short term
hemodynamic improvement
 The cost is an increased oxygen demand on the
failing heart

Reynolds H, Hochman J; Circulation 2008;117(5):686-697


CARDIOGENIC SHOCK — TREATMENT

CARDIOGENIC SHOCK GENERAL SUPPORT MEASURES

 Arterial oxygenation and near-


normal pH should be maintained to
minimize ischemia
 There should be a low threshold to
institute mechanical ventilation via
mask or ET tube
 Positive end-expiratory pressure
decreases preload and afterload
 Mechanical ventilation also
decreases the work of breathing

Reynolds H, Hochman J; Circulation 2008;117(5):686-697


CARDIOGENIC SHOCK — TREATMENT

INDEPENDENT RISK FACTORS FOR LOWER SURVIVAL RATES

 Older age (p=0.0007)


 Shock on admission (p=0.012)
 Hx of hypertension (p=0.032)
 Creatinine > 1.9 (p<0.0001)
 Noninferior MI location (p=0.022)

Reynolds H, Hochman J; Circulation 2008;117(5):686-697


CARDIOGENIC SHOCK — TREATMENT

KEY TO TREATMENT

“Effective therapy for cardiogenic shock


must include a prevention strategy. This
requires identification of patients at high risk
for shock development and selection patients
who are candidates for aggressive
intervention.”

Source: Barry WL, et al. Clinical Cardiology 1998;21(2):72-80


CARDIOGENIC SHOCK — TREATMENT

MECHANICAL SUPPORT WITH IABC IAB INFLATION:


INCREASES SUPPLY OF OXYGEN TO MYOCARDIUM

How it works
 Balloon inflates at onset of diastole

(when aortic valve closes)


 Displaces blood, causing an increase

in aortic pressure

Benefits
 Increases coronary artery perfusion

 Increases mean arterial pressure


CARDIOGENIC SHOCK — TREATMENT

MECHANICAL SUPPORT WITH IABC IAB DEFLATION:


DECREASES DEMAND FOR OXYGEN BY LEFT VENTRICLE

How it works
 Balloon deflates just prior to systolic ejection
(before aortic valve opens)
 Results in a rapid decrease in aortic pressure

Benefits
 Decreases afterload
 Decreases cardiac workload
 Increases cardiac output

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