Hypotension is common after cardiac arrest due to factors like stunned myocardium. Post-cardiac arrest patients are vulnerable to hypoperfusion which can worsen outcomes. Hemodynamic support is critical to support neurological recovery, especially in the initial 6-24 hours, but vasopressors can paradoxically worsen cerebral blood flow. Characterizing the cause of shock, such as through echocardiogram or CT, helps determine optimal hemodynamic management including temperature targets, vasopressors, and consideration of mechanical support like ECMO if cardiac output is failing. A multidisciplinary discussion is important for complex post-cardiac arrest patients in shock.

1. Hemodynamic management
after cardiac arrest: Optimizing
care and outcomes
Dave Seder, MD

2. Hypotension after cardiac arrest
is common and multifactorial
• Stunned myocardium due to
hypoperfusion, defibrillation, and
catecholamine storm
– Frequently reverses by 24-48h
• Consider MI, other cardiac processes
(tamponade, valves), PE, tension
pneumothorax d/t rib fractures
• Vasodilation due to ischemia-
reperfusion and/or aspiration varies
from mild to quite severe
Kern. J Am Coll Cardiol 1996;28:232-40
Laurent. J Am Coll Cardiol 2002;40:2110-6

3. Post-CA brain is highly
vulnerable to hypoperfusion
• Impaired cerebral
autoregulation
• Thrombosed microcapillary
beds and increased blood
viscosity
• 20-30% incidence of elevated
ICP, and 50% incidence
inadequate CPP
• Low BP associated with
worse outcomes overall
Intensive Care Med 1991;17:392
National Inpatient Sample
•1+ episodes of SBP<90 within 60
minutes ICU arrival independently
associated with death – OR 2.69
Crit Care Med 2009;37:2895-903

4. Blood pressure = blood flow
• Hemodynamic support after CA is therefore
critical for neurological recovery
– This is especially true during the initial 6-24 hours
after resuscitation
• But, vasopressor administration in a
failing heart can sometimes paradoxically
worsen cerebral blood flow, or increase
cardiac strain

5. Temperature Target in patients
with shock
• TTM trial subgroup of
patients with shock at
admission had higher lactate
levels, higher vasopressor
requirements, and (non-
significantly) worse outcomes
at 33C than at 36C
• ICU mortality (61 vs. 44 %, p
= 0.06; relative risk 1.37, 95 %
CI 0.99-1.91)
Intensive Care Med 2014;40:1210-19.
Crit Care Med 2015;43:318-27

6. Patients with shock on admission
after cardiac arrest
• If SBP<90 mmHg, or vasopressors needed to
maintain a SBP>90 mmHg, and/or clinical signs
of end-organ hypoperfusion. Then:
– 36ºC is preferred to 33ºC
– Must characterize shock further and consider
hemodynamic optimization
– Rapid rewarming is detrimental – avoid warming
quickly!
• If not in shock, please target MAP >80mmHg!

7. Characterizing shock after CA
• Echo (everyone)
• Left heart cath +/- PCI (STEMI, arrhythmias)
• CT pulmonary angiogram (suspected PE)
• CXR (suspected PTX)
• Right heart catheter (underutilized)
• FloTrac (pulse contour analysis CO/CI)

8. Vasopressors after cardiac arrest
• If predominant process is vasodilation, OK to use
constrictors like norepinephrine and vasopressin
• If LV is failing, then increasing afterload will only
result in worse brain perfusion and increased strain on
the heart - the “death spiral”
• Inotropes may be preferable, or a mix of pressors and
inotropes
• ECMO or IABP may be appropriate if cardiac output
failing despite inotropes

9. Glucose, CO2, O2, and BP
• After correction for
severity, each persistent
physiologic derangement
was associated with 0.71
OR of a good functional
outcome.
• Correct physiologic
derangements!

10. Who may be appropriate for
ECMO after cardiac arrest?
• Mild or moderate brain
injury
– Low SR6, higher BIS6 on
moderate sedation and NMB
• Otherwise viable
• Progressive cardiogenic
shock without
overwhelming MOSF
DECILES NUMBER OF
PATIENTS (N=353)
RISK OF NED SR6
1 31 (8,8%) 3% 0%
2 43 (12,2%) 2% 1-3%
3 32 (9,1%) 6% 4-13%
4 35 (9,9%) 11% 14-36%
5 35 (9,9%) 23% 37-63%
6 38 (10,8%) 60% 64-82%
7 33 (9,3%) 88% 83-90%
8 35 (9,9%) 71% 91-96%
9 22 (6,2%) 82% 97-99%
10 49 (13,9%) 84% 100%
Patients with SR6<60% are at much lower risk of
neurological-etiology death

11. Assess relative risks before ECMO

12. The huddle…
• Progressive shock after resuscitation:
– Etiology w/u, hemodynamic monitoring and
thoughtful use of vasopressors, inotropes, and TTM
• Lower MAP target and higher temperature target may be
appropriate if the LV is failing and/or worsening shock
– Early assessment of neurological risk, premorbid
status, and overall viability in terms of organ failure
• Interdisciplinary conversation between
providers at bedside is necessary in post-
resuscitation shock, and must occur 24/7

13. Summary
• Hypotension is common after CA, and should be
treated aggressively but thoughtfully to maximize
cerebral blood flow and minimize cardiac work.
• Shock etiology should be determined, and
hemodynamic monitoring initiated to guide therapy
• Mechanical circulatory support for progressive
cardiogenic shock should be considered, if
neurological risk category is low or moderate, and
other exclusions are absent
• A multidisciplinary “huddle” should be used to clarify
management goals in patient with shock after CA