Transcript Cardiogenic Shock

INTRA-AORTIC BALLOON COUNTERPULSATION
CARDIOGENIC SHOCK: LOOK, LISTEN AND TREAT
Class Code: 220
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LEARNING OBJECTIVES
At the conclusion of this program, the participants will be able to:
 Identify the signs and symptoms of cardiogenic
shock
 Identify two factors that place a patient at risk for
developing cardiogenic shock
 Discuss what is currently being stated in the
literature regarding the usefulness of IABC in the
setting of cardiogenic shock
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CARDIOGENIC SHOCK — BACKGROUND
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CARDIOGENIC SHOCK — BACKGROUND
CARDIOGENIC SHOCK – NRMI DATABASE 1995 - 2004
 CS developed in 8.6% of patients with acute myocardial infarction
(ST-segment elevation or left bundle branch block) hospitalized in
775 U.S. hospitals with revascularization capability
 Overall in-hospital mortality decreased from 60.3% in 1995 to
47.9% in 2004
 29% of patients with CS were in shock as they presented to hospital
 71% developed CS after admission
 CS patients were more likely to have a history of hypertension,
dyslipidemia, and prior coronary angioplasty
Source: Crit Care Med 2008 Vol. 36, No. 1 (Suppl.)
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CARDIOGENIC SHOCK — BACKGROUND
CARDIOGENIC SHOCK — BACKGROUND
Definition of Cardiogenic Shock
 State of inadequate tissue perfusion due to cardiac dysfunction or a
state of end-organ hypo-perfusion due to cardiac failure
Mortality rate for Cardiogenic Shock
 50% - 80%
Incidence of Cardiogenic Shock
 5% - 8%
Cardiogenic shock is the leading cause of death
for patients hospitalized with acute MI
Source: Reynolds H, Hochman J; Circulation 2008;117(5):686-697
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CARDIOGENIC SHOCK — BACKGROUND
THE PATHOPHYSIOLOGY OF CARDIOGENIC SHOCK
 Myocardial injury causes systolic and
diastolic dysfunction
 A decrease in cardiac output leads to a
decrease in systemic and coronary
perfusion
 This reduction in systemic and coronary
perfusion worsens ischemia and causes
cell death in the infarct border zone and
the remote zone of myocardium
Source: Reynolds H, Hochman J; Circulation 2008;117(5):686-697
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CARDIOGENIC SHOCK — BACKGROUND
ACUTE MYOCARDIAL INFARCTION AND CARDIOGENIC SHOCK
 The most common cause of cardiogenic shock is
extensive acute myocardial infarction
 Patients with previous impairment of ventricular function
may also experience shock with the occurrence of a
small infarction
 The cardiovascular system fails to maintain sufficient
perfusion resulting in inadequate cellular metabolism and
eventually cell death
 The consequence is irreversible cell damage
Source: Reynolds H, Hochman J; Circulation 2008;117(5):686-697
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CARDIOGENIC SHOCK — BACKGROUND
TIMEFRAME FOR DEVELOPMENT OF CARDIOGENIC SHOCK
 Median time frame for development of cardiogenic
shock is 12 hours into AMI
 39.6% develop cardiogenic shock within 6 hours
 63.2% develop cardiogenic shock within 24 hours
 The majority of patients develop shock after
arrival to the hospital
Source: Hasdai D, et al. American Heart Journal. 1999;138 (1 Pt 1):21-31
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CARDIOGENIC SHOCK — BACKGROUND
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CARDIOGENIC SHOCK — IDENTIFICATION
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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
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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
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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
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CARDIOGENIC SHOCK — CASE STUDY
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CARDIOGENIC SHOCK — CASE STUDY
CARDIOGENIC SHOCK CALCULATION TABLE (EXAMPLE)
 70-year-old, 60 kg female from the US with a
history of hypertension, no prior PCTA,
diagnosed with acute anterior MI. On
admission, HR=123, B/P=112/70 and a few
crackles in lungs
Points
Age
37
Systolic B/P
49
Weight
17
HR
17
Diastolic B/P
5
Killip Class
9
MI Location
8
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
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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
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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
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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
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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
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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
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CARDIOGENIC SHOCK — TREATMENT
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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
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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
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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
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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
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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
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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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CARDIOGENIC SHOCK — TREATMENT
INDICATIONS — CARDIOGENIC SHOCK
Source: Abdel-Wahab, et al; Am J Cardiol 2010;105:967-971
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CARDIOGENIC SHOCK — TREATMENT
CONCLUSION
 CS is a treatable illness with a reasonable chance
for full recovery.
 It is important to realize that although patients with
CS are at very high risk for early death, great
potential exists for salvage.
 Clinicians and researchers must focus on the
potential for full recovery if we are truly to make an
impact on the burden of this disease.
 Prevention with very early reperfusion therapy
remains the major goal.
Source: Reynolds H, Hochman J; Circulation 2008;117(5):686-697
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QUESTIONS?
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