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Key elements of a cardiogenic shock team
Associate Professor of Medicine
Medical Director, Cardiac Intensive Care Unit
Director, Interventional Cardiology Fellowship Program
Co-Director, Cardiac Catheterization Laboratory
University of Chicago Medicine | Chicago, IL
Sandeep Nathan, MD, MSc, FACC, FSCAI
Getinge symposium | SCAI 2019 | Las Vegas
Disclosures
Affiliation/Financial Relationship Company
• Grant / Research Support None relevant
• Consulting / Advisory Panel / Honoraria Abiomed
Cardiovascular Systems, Inc
Getinge
Terumo Interventional Systems
• Major Stock Shareholder/Equity None
• Royalty Income None
• Ownership / Founder None
• Intellectual Property Rights None
• Other Financial Benefit None
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Therapeutic targets in the
management of cardiogenic shock
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Progression of cardiogenic shock from a
hemodynamic problem to a cardiometabolic syndrome
Reyentovich, A., et al. Nature Reviews Cardiology 2016.
Myocardial ischemia
Hemodynamic
instability
Volume overload &
systemic hypoperfusion
Coronary perfusion
End-organ
dysfunction
Clinical stability
Death
Culprit PCI
Vasoactives → LV/RV
unloading w/pMCS
Escalation of pMCS /
devices in combo?
Complete revasc?
Renal & hepatic unloading, renal replacement Rx
ECG ’s, sxs, cardiac
biomarkers
MAP,
LV-ESP & EDP
Aortic pulse
pressure
Pulmonary
edema, BNP,
Neuro ’s,
lactate
ECG ’s,
biomarkers,
ventricular
arrhythmias
Creatinine,
LFTs, lactate,
coagulopathy
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Right ventricular failure (RVF) / RV shock
• Right ventricular failure (RVF) results from any structural or functional
process(es) that decrease the RV’s ability to pump blood into the
pulmonary circulation
• RVF and/or RV shock are rarely seen in isolation in the critically ill patient
outside of pure RV infarction
• RVF is increasingly being recognized as a key contributing factor to critical
illness across a variety of medical and cardiac illnesses
• The addition of RVF to critical illness portends poorer outcomes although the
magnitude of this negative impact remains poorly characterized
• The pathophysiology of RVF, as with LVF, is complex and varied but
remains less studied than LV failure
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Is it really as distinct as LV- vs. RV-shock?
• Hemodynamically defined RV dysfunction is common in AMI-CS and is largely undetected in
the absence of invasive hemodynamic assessment
Esposito M., and Kapur, N. F1000Research. 2017.
Lala A, et al. J Cardiac Fail 2018;24:148–156.
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Goals of care in cardiogenic shock
Early recognition & triage
Standardized diagnostic criteria Defined classes & stages
Multimodality assessment of cardiac and end-organ function
Early & continuous multidisciplinary input
Clear delineation of the initial careplan & escalation strategy
Early revascularization (when
appropriate)
Appropriate selection &
early use of MCS
Rapid escalation (or de-escalation) of care, as required
Involvement of consultants & ancillary service providers
Improved survival to discharge and beyond
Emergency medical
providers & primary
service (CCU / CVICU)
Multidisciplinary
Cardiogenic Shock
Team:
• Interventional
Cardiology
• Advanced Heart
Failure & Transplant
• CV Surgery
• Cardiac Critical
Care
Primary service
provider
1
2 3
4
5
6
7 8
9
10
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Goals of percutaneous circulatory support
• Decrease preload
• Decrease afterload
• Augment cardiac
output / power
Provide adequate
organ perfusion
and O2 delivery
Bridge patients to
• Recovery
• Decision
• Durable VAD
• Transplant
Support patients
through high-risk
procedures
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Establishing care pathways for cardiogenic shock
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What therapies can your center deliver 24/7?
Level 1
Level 2
Level 3
• Multiple percutaneous and surgical
support devices
• VAD and transplant programs
• Cardiac arrest & ECLS protocols
• Percutaneous devices and surgical
support options
• STEMI program
• No or limited percutaneous support
devicesSmaller community hospitals
Larger community hospitals
Some teaching hospitals
Quaternary centers / large
academic medical centers
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Level 1 or “Full-service” program
• Primary management:
– Advanced heart failure specialist
– Interventional cardiologist / Cardiac intensivist
• Device deployment / management / escalation:
– Interventional cardiologist
– Cardiac surgeon
• Core team members:
– ICU pharmacist
– Perfusionist
– Advanced cardiac fellows
– APN / RN
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Level 2 or “Mid-level” program
• Primary management:
– Heart failure specialist / Interventional cardiologist
– (Cardiac) intensivist
• Device deployment / management:
– Interventional cardiologist
– +/- Cardiac surgeon
• Core team members:
– Pharmacist
– Perfusionist
– APN/RN
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Level 1 care for cardiogenic shockPathway for instituting a shock program
Clear agreement
between all key
stakeholders
regarding
indications,
contraindications
and
programmatic
goals.
Assembly of a
24/7/365
multidisciplinary
cardiogenic
shock team
INSTITUTIONAL & SPECIALTY-
SPECIFIC “BUY-IN”
SHOCK TEAM
APPROACH
Key issues: • Implanting MDs
& location, • Explanting
MDs, location & timing
• Bed geography
OPERATOR
TRAINING,
COORDINATION
OF CARE
DELIVERY,
THROUGHPUT &
LOGISTICS
NURSING,
TECH,
PERFUSION
SUPPORT &
ICU CARE
• Establish initial & repeating training for nurses & techs.
• Have a clear understanding with perfusionists.
• Train ICU nurses & designate receiving units
EQUIPMENT &
INVENTORY
ISSUES
Key issues:
• Hardware
ownership, ratios
& location
• Disposables
• Cath lab vs.
OR/C-arm vs.
procedure room
vs. HOR?
• ECLS cart
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Level 1 care for cardiogenic shockKey members of the shock team
Assembly of a
24/7/365
multidisciplinary
cardiogenic
shock team
SHOCK TEAM
APPROACH
SUPPORTING STAFF
1. Vascular Surgery
2. Cath Lab: Nurses,
Technologists (ideally
with 1 “super-user”
each)
3. ICU: Nursing
leadership support
4. Perfusionists
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Interventional Cardiology
Cardiac Critical Care Specialists
Cardiovascular Surgery
Advanced Heart Failure
ED & IC
EMS
Level 1 care for cardiogenic shockChain of communication within the center
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Level 1 care for cardiogenic shockChain of communication within the center
Shock team
decision
HF, ICU & CV
surgeryICED
Key issues to resolve:
• Initial care plan including MCS, vasoactive support, ICU care
• Identifying NOK / POA
• Identifying goals of care / limitations to care
• Chart out escalation plan
• Decide on timing of next clinical / hemodynamic “snapshot”
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Protocolizing cardiogenic shock care
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Activate Cardiac Cath Lab
Yes
No
Access
Assess
Hemodynamics
pMCS
Reassess
Hemodynamics
Acute MI?
Coronary Angiogram
with PCI
Begin Weaning
Catecholamines*
PCI: Coronary angiography
and PCI with goal of complete
revascularization.
Access:
1. Femoral arterial access using micropuncture with
image guidance (ultrasound and/or fluoroscopy)1
2. Angiography via 4F micropuncture dilator to
confirm puncture site & vessel size
3. Place appropriately sized (5 or 6 Fr) arterial
sheath
4. Obtain venous access (femoral or internal
jugular)
Assess Hemodynamics: LVEDP or PAC
• If sustained hypotension (SBP < 90 mmHg) for > 30 min
Or
• CI < 2.2 with LVEDP or PCWP >15 mmHg,
consider mechanical circulatory support If femoral arterial anatomy suitable and no
contraindications, place, or escalate to
(if IABP already in place), Impella 2.5 or Impella CP
BEST PRACTICESBEST PRACTICES
* If consistent with overall hemodynamic management
CO, cardiac output; CPO, cardiac power output; dPAP, diastolic pulmonary arterial pressure; MAP, mean arterial pressure; PAC, pulmonary
arterial catheter; PAPi, pulmonary artery pulsatility index; RA, right arterial pressure; sPAP, systolic pulmonary arterial pressure.
Soverow J, Lee MS. J Invasive Cardiol. 2014;26(12):659-667
Step 1: Objectively assess, stabilize &
perform complete revascularization
Reassess Hemodynamics: PAC (if not done
initially)
1. CPO = (CO MAP)/451
2. PAPi = (sPAP-dPAP)/CVP
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CPO < 0.6 CPO > 0.6
PAPI
< 1 ≥1
RV Preserved: Escalate
MCS or consider transfer
to LVAD/Transplant Center
RV Dysfunction:
Right-sided MCS
(T/C Impella RP)
Reassess Hemodynamics via PAC prior to Discharge from the Cath Lab:1. Cardiac Power Output (CPO) = (CO MAP) / 451
2. Pulmonary Artery Pulsatility Index (PAPI) = (sPAP-dPAP) / CVP
Admit to ICU to maximizesupportive care and to actively
assess for myocardial recovery
Yes
No
Persistent Hypoxemia?
PaO2 < 55 on 100% FiO2
Consider higher power
support device
Anderson MB, et al. J Heart Lung Transplant. 2015;34(12):1549-1560.
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, or
3. RV dysfunction on TTE
(TAPSE score ≤14 mm)
Step 2: Reassessment prior to discharge
from cardiac cath lab
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Step 3: Consideration for escalation,
weaning and transfer for higher level care
Assess for Myocardial Recovery(At least every 12 hours)
Continue MCS support &
frequent clinical reassessment
Failure to recover within 48-72 h,
consider escalation or durable
VAD/transplant
Improving
Clinical, Echocardiographic &
Hemodynamic parameters
(concordant):
• ↑ Cardiac output
• ↑ CPO
• ↑ Urine output
• ↓ Lactate
• Inotropes low dose/discontinued
• Adequate Ramp test
Wean & Explant MCS (After a
clinically-determined duration
of support)
Worsening
Clinical, Echocardiographic &
Hemodynamic parameters
(concordant):
• ↓ Cardiac output
• ↓ CPO
• ↓ Urine output
• ↑ Lactate
• Inotrope dependent
• Absent pulsatility
Mixed picture
Clinical, Echocardiographic &
Hemodynamic parameters
(discordant):
• Some parameters are improving
• Pressors lowered but not
discontinued
• Fails “ramp test”
No RecoveryEscalate or Transfer
Refer to institutional protocol
for escalation or transfer
Inadequate RecoveryMyocardial Recovery
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Tehrani, B.N. et al. J Am Coll Cardiol. 2019;73(13):1659–69.
INOVA H&V Institute protocol for CS
Compared with 30-day survival of 47% in 2016, 30-day survival in 2017 and 2018 increased to 57.9% and 76.6%, respectively (p < 0.01)
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INOVA risk prediction model for mortality in CS
• Independent predictors of 30-day mortality were age >71 years, diabetes mellitus, dialysis, >36 h of
vasopressor use at time of diagnosis, lactate levels >3.0 mg/dl, CPO <0.6 W, and PAPi <1.0 at 24 h after
diagnosis and implementation of therapies.
• Either 1 or 2 points were assigned to each variable, and a 3-category risk score was determined: 0 to 1
(low), 2 to 4 (moderate), and >5 (high).
Tehrani, B.N. et al. J Am Coll Cardiol. 2019;73(13):1659–69.
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The Shock Team in action:
Clinical profile of a cardiogenic shock patient
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Profile of an IHCA/CS patient
57 yo male presenting off-hours w inferior STEMI , sx to door: 60-90 min,
hemodynamically stable in ED; door to cath lab transport: 27 min
As patient brought to CCL, PMVT → VF arrest.
25+ minutes of intermittent cardiac arrest with LUCAS-assisted CPR;
IABP considered but Impella CP used 2/2 lack of organized rhythm.
PCI performed of large RCA with heavy thrombus burden.
ROSC regained after RCA opened; patient transferred to CCU
intubated, on low-dose epinephrine gtt and Impella CP with
intravascular cooling started but terminated early because of
meaningful neurologic activity 1-2 hrs after completion of PCI
Patient discharged alive 1 week later with no neurologic deficits &
normal LVEF; Alive & well 6+ mo. later, back to working full time
EMS→
ED→ IC
IC/CICU
IC+HF+ CV Surg
IC+HF+ CICU
IC/Gen Card
Ideal profile of the IHCA/CS patient
* Images used with the patient’s permission.
Summary
• Cardiogenic shock represents a dynamic set of conditions, presentation
profiles and pathophysiologic mechanisms. Thus, CS care requires
continuous monitoring and willingness to adjust the treatment plan.
• Biventricular dysfunction is more common than recognized therefore
assessment of both RV and LV function is critical.
• Time, team and treatment choices are all equally important in
combating shock.
• Given the lack of clear superiority of any one device, protocols and
standardization are keys to success.
• Integration of device therapy with system of cares is likely to offer the
greatest impact on outcomes.
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Thank you!
Email: [email protected] | Twitter: @SandeepNathanMDML-0801 Rev A/MCV00091529 REV A26