Cardiogenic Shock in Acute MI: Mechanical Circulatory Support€¦ · Critical cardiogenic shock...
Transcript of Cardiogenic Shock in Acute MI: Mechanical Circulatory Support€¦ · Critical cardiogenic shock...
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Cardiogenic Shock in Acute MI:Role for Mechanical Circulatory Support
Craig S Smith, M.D.4/5/19
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No Disclosures
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Coronary Syndromes: Improvement in Treatment
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Prevalence of Cardiogenic Shock in Primary PCI
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Timing is Everything...• After acute MI with Primary PCI
Vfib: 94.7% before or during PCI6.3% AV Block (86% before/during PCI: 90+% resolve)4.5% “impeding shock” coming into PCI4.2% Shock- most prehospital1% develop post PCI Can J Cardiol 2006 Oct; 22(12):1047-52.
•Shock trial: median 6.2 hours after symptom onset (74% within 1 day)LM: 1.7 hrsRCA: 3.5 hrsLCx: 3.9 hrsLAD: 11hrs Late shock (>24hours): recurrent ischemia, Q waves, LAD
JACC 2000 Sep; 36 (3 Suppl A): 1084-90.
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EVOLUTION OF THE CARDIAC CARE UNIT“..times they are a changin’ ” B Dylan
1980s
Resuscitation
1990s
Intervention
TodayComprehensive
CriticalCare
Rapid Defibrillation
Post MI Care
Gen ICU RN
STEMIs
Antiarrhytmics
All ACS
Specialized RN
CHF
IABP
Rapid Defibrillation
TTM
MCS
Advanced CHF
Pul HTN
Multidisciplinary
Performance Tracked
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Cardiogenic Shock
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• Not “just” decreased CI (def ≤ 1.8, or 2.2 with pressors, SBP ≤ 90mmHg )
• Multiorgan dysfunction syndrome due to peripheral hypoperfusion with microcirculatory dysfunction
• Complicated by SIRS (~25%)
• Once multiple systems involved, difficult to improve prognosis by merely fixing CO.
• Most due to decompensated CHF
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1010
Exam !?
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ECG in Cardiogenic Shock
The ST pattern in Cardiogenic shock:
70-85% ST elevations MI/ New LBBB• Mortality: 53-63%
15-30 % Non-ST elevation MI• Older• Mortality: 77%
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¨ BP¡ Pulse pressure : large (elderly/AI), narrow (pre-shock)
¡ Proportional pulse pressure = SBP-DBP/ SBP¡ No BETA BLOCKERS¡ Does pulse disappear with respiration? (tamponade)¡ Pulse equal in both arms? (dissection)¡ Fistula in the arm? (Effusion)
¡ Murmur¡ New ?¡ Upper right sternal border : AS (elderly) HOCM (young)¡ Listen for the MR murmur in the back if Q waves!
¡ Neck Veins¡ TR with elevated INR think Pul HTN and RV failure¡ PRELOAD ASSESSMENT IS KEY!
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Mortality by Clinical Presentation
Mortality RespiratoryDistress Hypotension
Hypo perfusion
21%
22%
70%
60%
5.6%
28%
65%
1.4%
SHOCK Registry JACC Sept. 2000, Supp. A
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Intermacs 1
Critical cardiogenic shock describes a patient who is “crashing and burning”, in which a patient has life threatening hypotension and rapidly escalating inotropic pressor support, with critical organ hypoperfusion often confirmed by worsening acidosis and lactate levels.
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CS Level 1SBP <90 30 min pre-ionotropes
Pulmonary congestionor
Impaired end-organ perfusion:AMS
Cold/ClammyOliguria
Lactate >2
CS Level 2 (Profound)CS Level 1
CI <2.2 L/min/m or
Lactate > 3Despite
2 Ionotropes/Pressors
CS Level 3 (Deep)CS Level 2
Two of the following:Lactate > 8mmol/l
AnuriaRHF
Escalating PressorsRespiratory Failure
Courtesy of Eddie Rame MDUPENN
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Three HighDose
2% 3% 7.5%21%
42%
80%
Pre-Shock Profound ShockShock
No HemodynamicSupport
Needs Partial Hemodynamic Support
Needs Full Hemodynamic Support
Mortality Risk with Inotrope Dosing
Samuels LE et al , J Card Surg. 1999 Jul-Aug;14(4):288-93
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IABP SHOCK-2 Trial: Predictors of Mortality
Thiele et al, Lancet 2013
Univariate Multivariate
The two strongest predictors (age and prior stroke) cannot be modified by any acute intervention
The next three predictors (lactate, oliguria, and pH) suggest that the amount of LV support is important
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(Was) Controversial
Gusto 1/Shock benefit
Objective Data
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P=NS, .02@ 6mo.
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The Challenge of Age…
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Clinical Intuition in the Information Age:Shock in the Elderly
41%
75%
57%53%
0%
10%
20%
30%
40%
50%
60%
70%
80%
<75 years (n=246) >75 years (n=56)
30-d
ay M
orta
lity
(%)
ERVIMS
p=0.01 p=0.01
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Elderly - SHOCK & other registry dataClinicians Needed!
48% 47% 46%
81%
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
SHOCK Registry Mayo Clinic Northern NewEngland
30-d
ay M
orta
lity
(%)
ERVIMS
n=44 n=233 n=61 n=74
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PA Cath: Resistance is not futile! Importance of SVR
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42 yo/ trop 7038.5 at hour 36 then
SVR 400Mechanical Support
LOS 12 days
64 yo/ trop 70No fever
SVR mildly upJust meds
Walked out in 3 days
55 yo diabetic/ trop 70No feverSVR high
IABPMonomorphic VT
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With RBCs and O2, Comes WBCs….
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Inflammation / NOS : Local & Systemic EffectsFever, leukocytosis, Big temp (38.5+) typically hour 24-30 Nitric Oxide (neuronal, endothelial, inducible)
•Low levels (eNOS) is cardioprotective, increases contractility
•High levels (iNOS) in inflammatory conditions particularly MI and reperfusion
– ↓ Contractility– Suppression of mitochondrial respiration in nonischemic myocardium– Alters substrate metabolism (glucose)– Reduced efficacy of catechols– Vasodilation– Interaction at high levels with free radicals causes cell death/toxicity
vs.
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Hockman. Circ 2003; 107:2998-3002
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CS Survivors…
Average EF only ~ 30%
Huge variability in SVR , may not be elevated despite vasopressors
SIRS (~20% of CS, 2 days post)
Most survivors of CS have NYHA Class I Inconsistent with >40% myonecrosis
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Hemodynamic Phenotype
Tailored Support and Decongestion Strategies
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48 yo male with 2 hours CP:
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Stormy Course
• Day 1: CVP 16, SVR 1800, CI 2.2 (MCS), MAPs OK
• Day 2: Fever to 39 C, CVP 12, SVR 600, CI 2.4 (MCS), Levophed
• Day 4: CVP 20, suction alarms on MCS, SVR 1600, CI 1.9 (MCS), Milrinone
• Day 9: antibiotics CVP 6, SVR 600, CI 3, Neo and fluids
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Shock mortality predictor ≠ CI, CO, SVR, PCWP but rather reserve pumping capacity.
Heart pump dependent on preload and resistance circuit,function can be variable(i.e. what do you want the EF to be?)
Cardiac Power (or reserve) = pressure x flowMAP x CO/451 (Left Ventricle)
Finke JACC 2004 44:340
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CS Level 1SBP <90 30 min pre-ionotropes
Pulmonary congestionor
Impaired end-organ perfusion:AMS
Cold/ClammyOliguria
Lactate >2
CS Level 2 (Profound)CS Level 1
CI <2.2 L/min/m or
Lactate > 3Despite
2 Ionotropes/Pressors
CS Level 3 (Deep)CS Level 2
Two of the following:Lactate > 8mmol/l
AnuriaRHF
Escalating PressorsRespiratory Failure
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CS: Hemo-Metabolic Problem (aka “Post-ICEBERG SYNDROME”)
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“More Horsepower”
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Cardiogenic Shock Line : Triggers
CS Level 1SBP <90 30 min pre-ionotropes
tachyPP = 20
PPP (PP/SBP) = 0.2
Pulmonary congestionor
Impaired end-organ perfusion:AMS
Cold/ClammyOliguria (<30cc/hr )
Lactate >2
Make the Call
2x4 RuleLactate 2 = ICU
Lactate 4 = Meds No More
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Changes in Sublingual Microcirculation
IMPROVED END ORGAN PERFUSION WITH PVAD
MCS OFF MCS ON
Lam, et. al., Clin Res Cardiol, 2009,
Baseline prior to Impella support After 48hrs of Impella support
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Percutaneous Left Ventricular Support Devices- Which one?
Werdan et al, EHJ 2014
$ $$ $$
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International Journal of Cardiology, Volume 201, 2015, 684–691
Normal
Drugs
CHF
Impella
ECMO
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Stagnant areas of blood in LV and Ao Root thrombus
LV distention and pulmonary hemorrhageNo recovery of LV
ECMO: No LV decompression
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Important of maintaining residual LV flow
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Timing is Everything
Only 15% with IABP pre PCI
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15%13%
15%
35%
30%
35%
0%
5%
10%
15%
20%
25%
30%
35%
40%
CPR VF/VT arrest Any event
Even
t rat
e (%
)
IABP pre (n=62)IABP post/none (n=57)
Single center registry Primary PCI for shock
Brodie AJC 1999;84:18
Timing is Everything
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Impella 2.5 initiated prior to unprotected left main PCI in acute myocardial infarction complicated by cardiogenic shock improves early survival
Journal of Interventional Cardiology17 APR 2017 DOI: 10.1111/joic.12377http://onlinelibrary.wiley.com/doi/10.1111/joic.12377/full#joic12377-fig-0002
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1.0
0.8
0.6
0.4
0.2
0 5 10 15 20 25 30
Surv
ival
Rat
e
IABP/Inotropes Pre-PCI
Impella Pre - PCI
Days from initiation of Impella
Log-Rank, p=0.004
O’Neill, et. al, J Interven Cardiol, 2014
Timing of Support Impacts Outcomes30 Day Survival
cVAD Registry*N= 154
Door to Balloon Metric - Cardiogenic Shock & hemodynamic support are excluded from Door to Balloon (DTB) metrics Source: CMS, SCAI & ACC *The catheter based VAD Registry is a worldwide, multicenter, IRB approved, monitored clinical registry of all patients at participating sites; registry data is used for FDA PMA submissions
cVAD Registry
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RV
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LVPhysically Larger
One jobGets most of the attentionReplaceable with machine
Simple algorithmEasy to understand
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LVPhysically Larger
One jobGets most of the attentionReplaceable with machine
Simple algorithmEasy to understand
RVPhysically Smaller
Multiple jobsUnderappreciated
When fails, all hell breaks looseCan’t put a number on it
Understanding is Nuanced
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• RV empties when relaxing
• Very sensitive to afterload
• Prolongs isovolumetric timeincreases O2 cost
1 Ejection (opened PV)2 Relaxation3 Close of pulmonic/aortic valve
end of ejection
RV Physiology
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RV: Lots of Ways to Fail!
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When to pull the trigger ?
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Impella : Left “Bipella” : Left & Right
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(a few) Predictors of RV failure
CVP / PCWP
MAP/CVP
PAPi (Pulmonary artery pulsatility index) =
RVSWI =
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PASP-PADPRA
(mPAP-CVP) x Stroke Volume Index
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National Shock Initiative: CS with Acute MI
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National Shock Initiative
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Importance of Escalation and Recovery strategies
No RecoveryEscalate (& Ambulate) or Transfer
Guidance by RHC Is Critical
Worsening / not improvingclinical, echocardiographic & hemodynamic parameters (concordant):• ↓ Cardiac output• ↓ CPO• ↓ Urine output• ↑ Lactate, ↓ MVO2• Inotrope dependent• Absent pulsatilityCPO remains < 0.6
After 24 hours
PAPi ≤ 0.9 (RV Failure)
Biventricular supportwith Impella RP® on the right side
(transfer if not available)
RV Failure as defined by Recover Right1:
• CI < 2.2 L/min/m2 (despite continuous infusion of ≥ 1 high dose inotrope, ie, da/dobutamine≥ 10 µg/kg/min or equivalent) and any of the following:1. CVP > 15 mmHg, or 2. CVP/PCWP or LAP ratio >0.63, or3. RV dysfunction on TTE
(TAPSE score ≤14 mm)
0.9 < PAPi ≤ 1.5 (RV dysfunction)
Consider supporting theright side with Impella RP (transfer if not available)
IMP-127-16
CPO = (MAP × CO)/451.PAPi = sPAP - dPAP/RA.Anderson MB, et al. J Heart Lung Transplant. 2015;34(12):1549-1560.
PAPi > 1.5 (acceptable RV function)
Consider left-side escalationwith Impella 5.0™
(transfer if not available)
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Should you pull the trigger ?
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What ICEBERG?