Transcript perioperativeCardiacTamponade

 68 y/o female undergoing
RFA for paroxysmal
ventricular tachycarida
 PMH: DM, HTN, COPD
 All: erythromycin –
nausea
 Soc: quit smoking 20 yrs
ago, no EtOH or drugs
 5 hours into RFA, decreased
responsiveness, hypotensive
 Patient in SVT, paced out by
cardiologists
 Remained hypotensive,
pressors started, intubated
 Marked JVD noted
 TTE emergently preformed
 1.1-1.3cm effusion over right
heart
 RV collaspe
 Tamponade physiology
 Effusion drained under
ultrasound
 35cc frank bloody fluid
removed
 Patient immediately stabilized
 Extubated at end of case, taken
to CICU
 Discharged 2 days later
 Continues medical
management of SVT
 A condition where fluid
accumulates around the great
vessels or chambers of the
heart and decreases stroke
volume to clinically significant
levels
 2 layers
 Parietal pericardium
 Fibrous
 ~2mm
 Visceral pericardium
 Thin mesothelial layer
 Typically contains 25 –
50cc serous fluid.
 Pericardial space can be
considered a potential
space
 Slowly accumulating
effusion
 Allows for pericardial
distension
 May have effusion up to
1500cc before symptoms
arise
 Typically ‘medical’
causes’
 Uremia
 Malignancy
 Hypothyroidism
 Rapidly accumulating
effusion
 Usually see in
perioperative setting
 As little as 200cc fluid
for symptoms
 Beck’s Triad
 Hypotension
 Jugular venous
distension
(Kussmal’s sign)
 Distant heart
sounds
 Commonly sited
changes:
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Low voltage QRS
T wave inversions
PR depression
ST changes
 Not supported by
data
 Combination of low
voltage QRS and PR
depression has
weak association
with effusion
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Alteration in
configuration of
electrocardiographic
complexes arising
from the same
pacemaker and
independent of
periodic extracardiac
phenomenon
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Caused by swinging
of the heart in
pericardial fluid
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Rare phenomenon
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Resolves with
drainage of effusion
 Decline in arterial pulse with
negative pressure inspiration
 Not a paradox, but
exaggeration of normal
respiratory decrease in arterial
BP assoc. with effusion
 Not an all-or none
phenomonon
 Systolic pressure
change greater than 10
accepted as significant
 Respiratory variation
switched with positive
pressure ventilation
 Curtiss et al:
 SBP change greater
than 12mm HG or 9%
92% and 97%
accurate respectively
 May be found in other conditions:
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Tracheal compression
Tension pneumothorax
Pleural effusion
RV infarct
PE
Hemorrhageic shock
 May be absent in:
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Extreme hypotension
Aortic regurgitation
Atrial septal defect
Increased LVEDP
Cardiac adhesions
 All CVP values elevated
 Obliteration of Y descent
 PCWP and CVP
equalize
 PA systolic pressure
 Decreases with
inspiration with
mild or moderate
tamponade
 May increase with
severe tamponade
 Very sensitive (64-100%)
 Very specific (80-100%)
 Free wall diastolic inversion
that persists 1/3 into systole
 Affected by:
 Tricuspid regurgitation
 Plerual effusion
 Ventricular rhythm
 Pulmonary HTN
 RVH
 Not as well described
 May be tethered to
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pulmonary veins
Found more often with
loculated and smaller
effusions
Seen after CT surgery
Optimal views with TEE
Decreased chamber size
rather than collapse
 Early to mid-diastolic
inward motion of the
right ventricle
 Sensitivity 60 to 81%
 Specificity 90 to 94%
 Increased sensitivity
and specificity with
concurrent RA
collapse
 Affected by same
confounding factors as
RA collapse
 Tethering to anterior
chest wall may affect
sensitivity after open
heart surgery
 Most resistant to
circumferential
tamponade
 Most often seen
with regional
tamponade
 May be associated
with SAM
 Smaller effusion for
tamponade with LV
dysfunction
 Normal VTI ~10%
 First inspiratory beat:
 Increase in Tricuspid
VTI 80%
 Increase in Pulmonic
VTI 90%
 Decrease in Mitral VTI
35%
 Decrease in Aortic VTI
30%
 May identify subclinical
tamponade
 Useful in identifying
low=pressure tamponade
 Seen in hypovolemia
 JVD, pulsus paradoxus absent
 May be resistant to volume
loading
 Effect of transmural pressure
 Low CVP and modestly elevated
intrapericardial pressure result in
tamponade physiology
 May not have typical 2D echo
findings
 Doppler may be diagnostic
 Evidence indicates rate of
tamponade increasing
 Tamponade associated
with ~0.1 – 0.2% of
interventional procedures
 Minimal risk with
diagnostic procedures
 Analysis of 14,972
diagnostic caths showed
no tamponade
Risk factors include
 Elderly
 Female sex
 Multi-vessel
disease
 Complex
coronary lesions
 Immediate presentation
 Associated with direct coronary
perforation
 Hypotension, chest pain, shortness
of breath
 94% patients require ventilatory
support
 82% of patients require CPR
 Delayed presentation
 45-60% of all cases
 Usually 2 to 36 hours
 Mortality
 Unclear but may be up to 42%
 Probably related to site of
perforation and rate of fluid
accumulation
 Increasing frequency
as rate of implanted
devices increases
 Several methods of
extraction
 Manual
 Constant tension
 Excitimer laser
 Wires may fibrose
over time
 ICD wires more likely
to tenaciously fibrose
 1.4% experience cardiac tamponade
 Associated with 20% mortality
 Tamponade most common major problem
 Risk Factors
 Female
 ICD
 Multiple leads
 Leads greater than 8 years old
 North American Society of Pacing and
Electrophyiology Policy Statement
 Large bore peripheral IV
 Arterial Line
 “Adequate” anesthesia
 MHMC
 Endotracheal intubation/GA
 Large bore IV
 Arterial line
 No longer have OR and surgeon ready
 ASA Closed Claims Database
Analysis 2004
 16 cases of cardiac tamponade in
6449 claims
 Significantly (p<0.05) higher
association with mortality
compared to other
complications
 78-95% rate of mortality
 Right atrium most common site
of perforation, right ventricle
second
 Presentation may be
from minutes to days
 Many reports of
finding previously
healthy patients
expired at bedside
 Several reports of
pericardiocentesis
removing TPN
 Increased incidence of
tamponade with left
internal jugular
placement
 Tip position important
 Vessel wall erosion plays
a major role in delayed
presentations
 More vessel wall contact
increases change of erosion
 Right atrial placement
increases risk of
perforation
 Don’t be the ‘I’ in iatrogenic
 NOT necessary to ‘bury’
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guidewire or elicit
dysrhythmia
Check line with CXR
Don’t place lines too deep
Consider contrast injection
Observe PA catheter
waveforms after transport
to the ICU
 Two main categories:
 Penetrating Trauma
 Blunt Trauma
 Tamponade in 80-90% of all
penetrating wounds
 Wounds of axilla, neck, back,
mediastinum, epigastrium,
and upper abdomen
 Typically caused by knives and
guns.
 Reports of embolized bullets,
nails, knitting needles, lawn
mower projectiles , and ice
picks permeate literature
 Review of 1802 penetrating cardiac
injuries found
 Right ventricle 43%
 Left ventricle 33%
 Right atrium 14%
 Left atrium 5%
 Intrapericardial vessels 5%
 Associated with area each structure
occupies in the anterior chest
 Left ventricle often
spontaneously seals due to
thick myocardium
 Right ventricle unlikely to
spontaneously seal
 Atria may seal due to low
pressure and tethering to
pericardium but thin walls
make this unlikely
 *Remember myocardial wall
stress inversely related to
thickness
 Smaller wounds (>2.5cm)
are associated more
commonly with
tamponade
 Larger wounds are
associated with
exsangiunation into chest
 Larger wounds less likely
to spontaneously seal
 Only 20% present with tamponade
 Remainder result in exsanguination
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into chest
Higher velocity associated with
exsanguination
Lower velocity associated with
tamponade
Knife wounds more likely to result
in tamponade because pericardium
will spontaneously close
Stab and gunshot wounds usually
affect more than one cardiac
structure
 Penetrating injury usually
declares itself immediately
 Can have delayed presentation
up to four weeks
 Re-bleed usually in non-
surgically repaired wounds
 Pericardial effusion seen in 22%
of all penetrating injuries but
rarely a problem
 10% of all blunt chest
trauma sustain cardiac or
aortic injuries
 Very few patients require
operative treatment
 Most patients expire before
they reach the hospital
 Chirillo et al TEE study of
83 patients with chest
trauma
 40 with pericardial effusion
 One with pericardial
tamponade
 History of airbag
deployment associated with
tamponade
 1st and 2nd rib fractures
often associated with
tamponade
 COPD patients at risk of pneumopericardium
 Effusion found in 50 to 85% of
patients
 Tamponade estimated at 0.75 to
0.8% from two recent large
reviews (range Zero to 8.8%)
 Higher rate in valve replacement
vs CABG
 More common in females
 Early tamponade
 Active re-bleed
 Signs/symptoms of low CO
 Acute decrease in chest tube
output
 Late tamponade
 Post-pericardotomy
syndrome
 Presents 15-20 days post-op
 Very inconsistent
presentation
 Anterior effusion more common with CABG
 Typical TEE
findings
 Loculated effusion
 Posterior location
 Small volume
 Left atrial collapse
common
 Paradoxical LV
motion possible
 effusions with
valves
Recognize Condition
 Medical management
 “Tight” - increase SVR,
minimize chamber
collapse
 “Tachy”– fixed CO,
increase HR
 “Tank full” –volume
load
 Surgical Decompression
 Open chest
 Subxiphoid incision
 Pericardiocentesis
 w/wo drain
 w/wo echo guidance
 Mayo Clinic Study (1999)
 97% successful in most cases
 96% successful with loculated
effusions
 Major complication 2%
 Coronary chamber laceration
 Pneumothorax w/ chest tube
 Minor complications 1.2%
 Small pneumothorax
 Pleural-pericardial fistula
 Optimize patient pre-op
 Avoid positive pressure
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ventilation
Anesthetic depends on
etiology
Consider relief of
tamponade under local
Consider pre-induction
arterial line
Central line in EJ if time
Consider double set-up
 Most agents cause
hypotension
 Anesthetic requirements
increase after relief of
tamponade
 Have epinephrine and
atropine available
 Consider ketamine
 May be sympathetically
depleted
 Theoretical concern?
 Described in several case
reports