Mortalità in anestesia

Mortalità in anestesia
Claudio Melloni
Anestesia e Rianimazione
Ospedale di Faenza(RA)

What lessons have the
ASA closed claims
teached to us?

What is a claim?
l Claim is a demand for
financial compensation by
an individual who has
sustained an injury from
medical care.
l Once a claim is resolved
the file is closed

Che cosa sono gli ASA
Closed claims?
l Collection of 35 USA insurance
companies
l 14500 anesthesiologists covered
l 50-55% of all USA practicing
anesthesiologists

Closed claim
l Medical records
l Narrative statement by the
involved health care personnel
l Deposition summaries
l Outcome and follow up reports
l Cost of the settlement or jury award

Utilità dei closed claims
Collection of “ sentinel”
events
Identification of areas of
risk(and litigation….)
Provides direction for
further analysis

Demography and general
characteristics
Adults(91%>16 years)
Generally healthy:asa 1 & 2 69%
Non emergency surgery 75%
GA 67%
The database is not a collection of medically or
surgically compromised patients in whom the
underlying disease plays a major role in the
outcome;for this reason the closed claim
database offers the unique opportunity to discern
how the process of care contributes to the genesis
of adverse outcomes…..

Problemi nella
interpretazione dei dati
Data collected to resolve claims
Not collected for outcome research
Total number of anesthesia and patients unknown
Unknown denominator for risk calculation
Retrospective
Lag time in
publication;closure,availability,study,calculations…pu
blication
Geographic imbalance ?
Interrater reliability;bias…
Claims selectivity;only 30-33% of claims available are
evaluated….

Definizioni
Complication;adverse outcome or
injury sustained by the patient
Damaging event:the specific
incident or mechanism that led to
the adverse outcome(e.g.airway
obstruction)

Risarcimenti (*1000 $)
Outcome median range
Death(1725) 216 260-14700
Brain damage adults(676)
673 2750-23200
Brain damage newborns(129)
499 3333-6800

Relationships associated
with payment
Appropriateness /
unappropriateness
of care gravity of injury standard of care
Frequency of paymentmagnitude of payment
Better
monitoring

Relationships emerged form studies of
closed claims:
Frequency of payment linked to appropriateness of
care,but not to severity of injury
magnitude of payment linked to both severity of injury
and to standard of care
adverse outcome judged preventable with better
monitoring were far costlier than those which were
not considered preventable with better monitoring.
Cheney FW et al. Standard of care and anesthesia liability. JAMA
1989;261:1599-1603 Tinker JH et al. Role of monitoring devices in prevention of
anesthetic mishaps: a closed claims analysis. 1999;71:535-540.

Effect of outcome on
physician judgements
Examination of the Closed Claims database
suggests the presence of a recurrent
association between the severity of an
adverse outcome and accompanying
judgments of appropriateness of care.
Caplan RA.Effect of outcome on physician judgement of appropriateness of care.
JAMA 1991;265:1957-1960.

Severity of
adverse outcome
judgments of
appropriateness
of care.

physician judgements:2
Specifically, non disabling iniuries are
more often associated with ratings of
appropriate care, while disabling
injuries and death are more often
associated with ratings of less than
appropriate care.

physician judgements:3
This raises the possibility that highly
unfavorable outcomes may predispose (bias)
peer reviewers towards harsher
judgments,while minor injuries may elicit less
critical responses.

Study of peer review:1
cases from the Closed Claims database
study of peer review with 112 practicing anesthesiologists
volunteered to judge appropriateness of care involving adverse
anesthetic outcomes.
The original outcome in each case was either temporary or
permanent.
For each original case, a matching alternate case was devised.
The alternate case was identical to the original in every respect,
except that a plausible outcome of opposite severity was
substituted.
The original and alternate cases were randomly divided into two
sets and assigned to reviewers.
The reviewers were blind to the intent of the study.

Study of peer review:2
The care in each case was independently rated by the
reviewers
based upon the conventional criterion of reasonable
and prudent practice at the time of the event.
Knowledge of the severity of injury produced a
significant inverse effect on judgments of
appropriateness of care.
the proportion of ratings for appropriate care by 31
percentage points when the outcome was changed
from temporary to permanent, and increased by 28
percentage points when the outcome was changed
from permanent to temporary.

Effect of outcome on judgements of
appropriate care
0
10
20
30
40
50
60
70
actually
temporary
changed to
permanent
actually
permanent
changed to
temporary
% of
appro
priate
ness
of
care

Schroeder SA et al. Do bad outcomes
mean bad care? JAMA 199 1; 265:1995.
non disabling iniuries = appropriate
care
disabling injuries and death = less
than appropriate care.

Concern about peer review
and bias
obstacle to objective
evaluation of major
medical risks….
Frequency and size of
payments!!
Foster practices
which result in minor
but avoidable
injuries….
If such injuries are
pervasive…
» Aggregate cost

Incidence % of claims related to the
most common adverse outcomes
0
5
10
15
20
25
30
death
nerve damage
brain damage
airway trauma
pnx
eye injury
fetal/newborn injury
headache
stroke
awareness
aspiration
bckpain
myocardial infarction
burns

Most common damaging
events:%
resp
cardiovasc
equipment
reg block techn.
surg.techn.
wrong drug dose
1382
717
591
372
278
209

Conclusioni
Damaging events and adverse outcome show tight
clustering in a small number of specific categories;
Damaging events:3 categories account for almost half
of claims;resp, equipment & cardiovascular
account for 46% of claims:
Adverse outcome:death,nerve damage,brain
damage account for almost 65% of claims
This clustering of damaging events and adverse
outcome is of fundamental importance since suggests
that research and risk management strategies
directed at just a few areas of clinical practice could
result in large improvements in professional liability.

Most common adverse outcomes Range
of payments($*1000)
0
5000
10000
15000
20000
25000
death
nerve
dam
age
brain
dam
age
airw
ay
traum
a
eye
in.
pnx
fetal/new
born
in,.
stroke
aspirationback
painheadacheM
I
burns
aw
areness
min
med
max

Most common adverse outcomes
Median Payment:$*1000
0
100
200
300
400
500
600
700
median payment
death
nerve damage
brain damage
airway trauma
eye injury
pnx
fetal7newborn injury
stroke
aspiration
back pain
headache
MI
burns
awareness

Claims differ in different
populations;
»FOR INCIDENCE
»FOR SERIOUSNESS

Morray J, Geiduschek J, Caplan R, Posner K, Gild W,
Cheney FW: A comparison of pediatric and adult
anesthesia malpractice claims. ANESTHESIOLOGY
78:461-7, 1993

Chadwick,HS,Posner,K,Kaplan,RA,Ward,RJ,Cheney
FW.A comparison of obstetric and nonobstetric
anesthesia malpractice claims.Anesthesiology
1991;74:242-249.
ob vs non ob:190 vs 1351
» ob cases 67% CS,33% vaginal
» 65% associati a anest reg,33% con
GA
» 2 claims per non disponibilità
dell’anestesista!

ASA closed claims project
Malpractice claims against anesthesiologists:
OB VS NON OB
0
5
10
15
20
25
30
35
40
%
ob nonob
morte (materna)
danno cerebrale neonatale
cefalea
morte neonatale
dolore dur.anest
danno neurale
danno cerebrale paz.
distress emotivo
dolore dorso

Claims ostetrici:regionale vs GA.
0
5
10
15
20
25
30
35
40
45
%
reg GA
morte materna
cefalea
morte neonatale
dolore dur.anest
danno neurale
danno cerebrale paz
distress emoz
dolore dorso
*
*
*
*

Patogenesi del danno neonatale
45% attribuiti a
cause
anestetiche:
GA:4
» 1 broncospasmo
» 1 intub esofagea
» 1 aspir polm
» 1 ritardo anest.
» Regionale:13
» 9 convuls da iniez
intravasc
» 1 eclampsia
» 1 ritardo disponibilità
» 3 spinali alte
37% a probl ostetrici
o congeniti,
13% con probl di
rianimaz.

Dati relativi ai pagamenti:OB VS
NON OB
claims non ob claims ob Claims ob
regionale generale
non pagati(%) 32 38 43 27
pagati(%) 59 53 48 63
pagamento mediano($) 85000 203000 91000 225000
range di pagamento($) 15000-6 milioni 675000-5.4 milioni 675-2.5 mil750-5.4 mil
GA pagata il 63% vs 48% delle reg.

Conclusioni dai closed
claims obs
Danno cerebrale neonatale è il claim più
frequente,anche se solo il 50% è LEGATO
ALL’ANESTESIA!.
Pagamento mediano per il danno cerebr.
Neonatale:500.000 $ ,vs 120.000 $ dei danni
ob;
Cefalea è il III problema: e risulta in pagamento
il 56% delle volte……...

Characteristics of
respiratory related claims
high frequency of severe
outcomes:85% death or brain
damage
Costly payments($ 200.000 and +)
72% judged preventable by
monitoring (pulse oximetry and
etCO2)
Monitoring helpful in reducing
inadequate ventilation and
inadeq.oxygenation

Classification of the most common
respiratory system damaging
events:% of 1382 cases.
diff intub
inadeq vent/O2
esoph intub
airway obstruct
aspiration
premat extub
bronchospasm

Trends in death and brain damage
according to the basic damaging event
0
5
10
15
20
25
30
35
40
45
50
%
1980 1990
Resp event
cardiovasc event
equipment probl

Most common respiratory events
associated with death and brain damage
inadequate ventilation
esophag intub
difficult intub
other resp events
adv resp events
inadequate ventilation
esophag intub
difficult intub
other resp events
1980
1990
Adv resp events

Other respiratory damaging events
associated with death or brain damage
0
2
4
6
8
10
12
%
1980 1990
air obs
bronchospasm
premat extub
aspir

Which is the impact of pulse
oxymetry and end tidal CO2
monitoring in death and
brain damage?

Respiratory damaging events associated
with death or brain damage by
monitoring group
0
5
10
15
20
25
30
35
%
inadeq ventil esophag intub diff.intub
none
SpO2 only
SpO2+etCO2
102
167

Cardiovascular damaging events
0
10
20
30
40
50
60
unexp./other
cv event
neurax
cardiac arrest
inadeq fluid blood loss
1980
1990

Unexplained/other damaging
cardiovascular events in the
90’s(137)(death and brain damage)
arrhyth
MI
pulm emb
stroke
path abnorm
multifactorial

How do end tidal CO2 and
SpO2 monitoring affect the
occurrence of cardiovascular
damaging events as the
mechanism of brain damage
or death?

Cardiovascular damaging events
by monitoring group
0
10
20
30
40
50
60
unexpect/othercvevent
neuraxcardiacarrest
inadeqfluids
bloodloss
none
SpO2 only
SpO2+etCO2
72
194
192??

Conclusions from the
data about the future
role of monitoring in
the prevention of
severe anesthesia
related injury?

Better monitoring
would have prevented
death or brain damage

Better monitoring would have prevented
death or brain damage in the 90’s
no
yes
Resp events:221

Cardiovascular events judged
preventable by better monitoring
no
yes

Respiratory and cardiovascular events contribution to
deaths and brain damage(Cheney,FW Anesthesiology
1999;91:552-6)
0
10
20
30
40
50
60
70
80
%
'70 '80 '90
resp
cardiovasc
inadeq vent
esoph.intub
<standard of care
plaintiff payment

Trends in death and brain
damage
0
10
20
30
40
50
60
70
80
%
'70-79 '80-89 '90-94
nerve injury
brain damage
death
“The fact that professional
liability premiums for anesthesiologi
have decreased significantly since th
mid-1980s would imply an overall
reduction in severe injuries.”

Emerging trends
Claims fro death and permanent brain damage
are decreasing
injuries attributed to inadequate ventilation and
oxygenation are decreasing;SpO2 and etCO2
monitoring are the most likely causes
relative increase in the proportion of
cardiovascular damaging events and
respiratory events not prevented by monitoring
better monitoring would not lead to further
reductions in death and brain damage

Death associated with Regional
anesthesia in the 90’s(97 cases):etiology
pain management
neuraxial block
notblock related
intravasc
injection
other block
related

Neuraxial cardiac arrest
Sudden and unexpected
severe bradycardia and /or
asystole
occurring during neuraxial
block
with relatively stable
haemodynamics preceding
the event.

Cardiac arrest associated
with neuraxial block
900 cases in claims 1988;
14 cases of neuraxial cardiac arrest…..,all pts
were resuscitated,8 survived but only 1
regained a sufficient neurologic function…..
Hypothesis:
poor cerebral perfusion pressures
engendered by closed chest cardiac
massage in the presence of high
sympathetic blockade.

Sudden cardiac arrest during
regional anesthesia

Cardiac arrest during
spinal anesthesia
Closed claim database:14/1000 (1978-86)
Features consistent with a sentinel event:
» Young healthy adults for relatively minor surgery
» Standard anesthetic techniques and monitoring
» Arrest followed by prompt & brief CPR
» All resuscitation successful
» Death/severe brain damage;13/14 !!
» Up tp the year 2000 other 41 cases were reported in the
literature(26 spi + 15 epid);but outcome much better…..

Risk factors for cardiac arrest
during spinal anesthesia
Advanced age & high ASA physical status(Auroy)
baseline HR < 60 (Carpenter et al).
ASA physical status I patients(ASA closed claims)
Current therapy with b-blockers
block height >T6
patients who are <50 years old (Tarkkila)
patients with first-degree heart block (Liu)

Conclusions from cases of sudden bradycardia or
asystole associated with spinal anesthesia:
Cases do occur
There are no clear clinical
predictors…
Prompt recognition and treatment
keys to injury prevention.

Incidence of anesthesia related cardiac
arrest/per 10.000 anesthetics
0
1
2
3
4
5
6
7
incidence mortality
Biboulet
Olsson
Auroy
Newland:direct
Newland: related
Newland anesth.attrib
Aubas
Aubas reg only
Tarkkila
Geffin
spinal
*10 !!
GA
GA

Caplan RA, Ward RJ, Posner K, Cheney FW. Unexpected
cardiac arrest during spinal anesthesia: Anesthesiology 1988;
68:5–11.
2: Joshi GP, Shearer VE, Racz T. Ruptured aortic aneurysm
and cardiac arrest associated with spinal anesthesia.
Anesthesiology 1997; 86:244–7.
3: Geffin B, Shapiro L. Sinus bradycardia and asystole during
spinal and epidural anesthesia: J Clin Anesth 1998; 10:278–85.
4: Tarkkila PJ, Kaukinen S. Complications during spinal
anesthesia: Reg Anesth 1991; 16:101–6.
5: Auroy Y, Narchi P, Messiah A. Serious complications
related to regional anesthesia. Anesthesiology 1997; 87:479–
86.
6: Chopra V, Bovill JG, Spierdijk J. Accidents, near accidents
and complications during anaesthesia: Anaesthesia 1990;
45:3–6.

Newland MC,Ellis SJ,Lydiatt CA, Peters KR,Tinker
JH,Romberger DJ,Ullrich FA Anderson J.Anesthestic-related
Cardiac Arrest and Its Mortality: A Report Covering 72,959
Anesthetics over 10 Years from a US Teaching Hospital.
August 15, 1989 to August 14,
1999,
72,959 anesthetics
University of Nebraska Hospital
A total of 144 cardiac arrest (within
24-h periop.)
19.7/ 10,000 anesthetics (95%
confidence interval [CI], 16.52-
22.96)

Newland MC,Ellis SJ,Lydiatt CA, Peters KR,Tinker
JH,Romberger DJ,Ullrich FA Anderson J.Anesthestic-related
Cardiac Arrest and Its Mortality: A Report Covering 72,959
Anesthetics over 10 Years from a US Teaching Hospital.
: A prospective and retrospective case analysis study
of all perioperative cardiac arrests occurring during a
10-yr period from 1989 to 1999 was done to determine
the incidence, cause, and outcome of cardiac arrests
attributable to anesthesia.
Methods: One hundred forty-four cases of cardiac
arrest within 24 h of surgery were identified over a 10-
yr period from an anesthesia database of 72,959
anesthetics. Case abstracts were reviewed by a Study
Commission composed of external and internal
members in order to judge which cardiac arrests were
anesthesia-attributable and which were anesthesia-
contributory. The rates of anesthesia-attributable and

Newland et al.Anesthestic-related Cardiac Arrest and Its
Mortality: A Report Covering 72,959 Anesthetics over 10 Years
from a US Teaching Hospital.
Results: Fifteen cardiac arrests out of a total number of 144 were judged to
be related to anesthesia. Five cardiac arrests were anesthesia-attributable,
resulting in an anesthesia-attributable cardiac arrest rate of 0.69 per 10,000
anesthetics (95% confidence interval, 0.085-1.29). Ten cardiac arrests were
found to be anesthesia-contributory, resulting in an anesthesia-contributory
rate of 1.37 per 10,000 anesthetics (95% confidence interval, 0.52-2.22).
Causes of the cardiac arrests included medication-related events (40%),
complications associated with central venous access (20%), problems in
airway management (20%), unknown or possible vagal reaction in (13%),
and one perioperative myocardial infarction. The risk of death related to
anesthesia-attributable perioperative cardiac arrest was 0.55 per 10,000
anesthetics (95% confidence interval, 0.011-1.09).
Conclusions: Most perioperative cardiac arrests were related to medication
administration, airway management, and technical problems of central
venous access. Improvements focused on these three areas may result in
better outcomes.

Risk factors for cardiac arrest
(Newland et al.Anesthestic-related Cardiac Arrest and Its Mortality: A Report
Covering 72,959 Anesthetics over 10 Years from a US Teaching Hospital.)
As compared to controls, patients experiencing
cardiac arrest were:
more likely male (OR 0.71; 95% CI, 0.49-1.02;P = 0.07)
» more likely to have a greater ASA physical status (P <
0.0001; 68% ASA IV or V vs. 14% for controls)
» more likely to have emergency surgery (OR, 5.14; 95% CI,
3.49-7.56;P < 0.0001)
– thoracic (including cardiac)-spine or upper abdominal surgery
(P < 0.0001),
» longer operations (OR, 1.00; 95% CI, 1.003-1.00;P =
0002)
» and surgery after 3 pm (OR, 0.45; 95% CI, 0.30-0.66;P <
0.0001).

Auroy et al.Serious Complications Related to Regional
Anesthesia: Results of a Prospective Survey in
France.Anesthesiology 87:479-86, 1997
Self reporting by participating anesthesiologists
(736 /4,927 :14.9%)
103,730 regional anesthetics during the 5-
month study period:40,640 spinal anesthetics,
30,413 epidural anesthetics, 21,278 peripheral
nerve blocks, 11,229 intravenous regional
anesthetics.

Auroy et al;summary of results
103,730 regional anesthetic procedures:sufficient prospective
data for investigators??
32 Cardiac arrest,28 radicular deficits,23 seizures,5
cauda equina,1 paraplegia,7 deaths
More Ko following spinal;
» cardiac arrest 6,4/10.000,(6/26 deaths)
» neurol Ko 6/10.000
» permanent cauda equina assoc with lidocaine 5%
All 26 reported seizures were preceded by minor
auditory symptoms and complaints of metallic
taste;more frequent occurrence of seizures after
peripheral block than after epidural anesthesia

Cardiac Arrest(da Auroy et al.Serious Complications Related to
Regional Anesthesia: Results of a Prospective Survey in France.Anesthesiology 87:479-
86, 1997
incidence of cardiac arrest was significantly
greater with spinal anesthesia (6.4 ± 1.2 per
10,000 patients) than with epidural
anesthesia and peripheral nerve blocks
combined (1.0 ± 0.4 per 10,000 patients; P <
0.05
During the 26 cardiac arrests occurring with spinal anesthesia,
15 patients were treated only with closed-chest cardiac
massage and ephedrine; one patient was treated only with
epinephrine (0.5 mg); and 10 patients were treated with closed
chest cardiac massage and epinephrine (3.4 ± 3.6 mg).

Cardiac Arrest(da Auroy et al.Serious
Complications Related to Regional Anesthesia: Results of a
Prospective Survey in France.Anesthesiology 87:479-86, 1997
Fatal outcome from cardiac arrest:6/26
Risk of death after cardiac arrest was significantly
associated with age and American Society of
Anesthesiologists' (ASA) physical status class. The
average age of survivors was 57 ± 20 yr, whereas the average
age of nonsurvivors was 82 ± 7 yr. The difference in average
ages was statistically significant (P < 0.05). Similarly, the
breakdown of ASA physical status for survivors versus
nonsurvivors was n = 13 versus n = 0 for ASA I; n = 5 versus n
= 2 for ASA II; n = 2 versus n = 3 for ASA III; and n = 1 versus n
= 0 for ASA IV.

Auroy et al.Serious Complications Related to
Regional Anesthesia: Results of a Prospective
Survey in France.Anesthesiology 87:479-86, 1997
0
1
2
3
4
5
6
7
8
1/10.000
spinal epidural periph.reg i.v.reg Total
cardiac arrest
death
seizures
neurol.injury
radiculopathy
cauda equina
paraplegia

Cardiac Arrest(da Auroy et al.Serious Complications Related to
Regional Anesthesia: Results of a Prospective Survey in France.Anesthesiology 87:479-
86, 1997
Two variables were statistically different regarding
cardiac arrest in patients undergoing spinal
anesthesia: (1) the time between onset of spinal
blockade and occurrence of cardiac arrest was
longer in nonsurvivors than in survivors (42 ± 19
min versus 17 ± 16 min, respectively; P < 0.05);
and (2) total hip arthroplasty (THA) more
frequently was the type of surgery in nonsurvivors
than in survivors (5 of 6 THA among nonsurvivors
compared with 2 of 20 non-THA surgeries in
survivors; P < 0.05). During THA, three cardiac arrests
happened at the time of cement insertion and were fatal. Blood
loss at the time of cardiac arrest was 700 ml in nine cardiac
arrest patients, with four arrests being fatal. Sedation was not

Cardiac Arrest:epidural & peripheral nerve block(da
Auroy et al.Serious Complications Related to Regional Anesthesia: Results of a
Prospective Survey in France.Anesthesiology 87:479-86, 1997
3 reversible cardiac arrest were reported with
epidural anesthesia.
3 cardiac arrest were reported during peripheral
nerve blocks. In each case, these appeared to
be associated with inadequate analgesia. In
two of the three cases, cardiac arrest also was
associated with vasovagal responses, treated,
and reversed. One fatal cardiac arrest resulted
from a myocardial infarction. No neurologic
sequelae were observed in the 25 patients who
recovered from cardiac arrest.

Biboulet et al.Fatal and non fatal cardiac arrests related
to anesthesia.General Anesthesia*Can J Anesth 2001 /
48 / 326-332
0
0,1
0,2
0,3
0,4
0,5
0,6
0,7
1/10.000
AG epid spinl caudal ivra plexus nerve
cardiac arrest
death
71826
4145
7656
2081
3308
9222
3231

Treatment of
bradycardia/hypotension associated
Treat aggressively
HR <60 ,>50:atropine 0.5-1 mg
HR <50,>30;atropine 0.5-1
mg+ephedrine 10-20 mg
HR<30 epinephrine 0.1 mg
Asystole:epi 1 mg + chest
compressions

P waves without QRS;O2 + Atropine 1,2 mg
Repetitive chest thumping

After 30 sec of
precordial thumping
;high grade AV block
with occasional
supraventricular beat
Precordial thumping
resumed at arrows
again resulting in QR
and patient awakenin
Thumping
stopped :pt
awaken
and asks why he
is beaten!
Resuscitation lasted 3 min..sinus bradycardia
…NSR..ok.
Operation performed,no sequelae,
pt discharged 24 hr later in good health.

asystole following spinal
anesthesia
Cerebral deoxygenation?see article from
reg anesth & turp…..univ of cairo….
Reflex;decreased venosu return..empty
atrium..empty ventricle….bradycardia
…. fall in CO?
Vasovagal reflex?
Organize a study….Somanetics ,CO
impedance
,FC,NIBP,consciousneess,level of
blockade…

Caplan RA, Ward R, Posner K, et al.
Unexpected cardiac arrest during spinal
anesthesia: a closed claims analysis of
the predisposing factors. Anesthesiology
1988; 68:5-11.
13 Caplan RA. The ASA closed claims
project: lessons learned. Annual
refresher course lectures, 1997. 242.
14 Auroy Y, Narchi P, Messiah A, et al.
Serious complications related to regional
anesthesia. Anesthesiology 1999; 87:47-
86.

Krisner AC, Hogan QH, Wenzel W, et al. The efficacy
of epinephrine or vasopressin for resuscitation during
epidural analgesia. Anesth Analg 2001; 93:734-742
Cardiopulmonary resuscitation (CPR) during epidural
anesthesia is considered difficult because of diminished
coronary perfusion pressure. The efficacy of epinephrine and
vasopressin in this setting is unknown. Therefore, we designed
this study to assess the effects of epinephrine versus
vasopressin on coronary perfusion pressure in a porcine model
with and without epidural anesthesia and subsequent cardiac
arrest. Thirty minutes before induction of cardiac arrest, 16 pigs
received epidural anesthesia with bupivacaine while another 12
pigs received only saline administration epidurally. After 1 min
of untreated ventricular fibrillation, followed by 3 min of basic
life-support CPR, Epidural Animals and Control Animals
randomly received every 5 min either epinephrine (45, 45, and
200 mg/kg) or vasopressin (0.4, 0.4, and 0.8 U/kg). During
basic life-support CPR, mean ± SEM coronary perfusion
pressure was significantly lower after epidural bupivacaine than

epinephrine(+) or vasopressin(triangle)
Krisner AC, Hogan QH, Wenzel W, et al. The efficacy of
epinephrine or vasopressin for resuscitation during
epidural analgesia. Anesth Analg 2001; 93:734-742

and CPR with epinephrine Krisner AC, Hogan
QH, Wenzel W, et al. The efficacy of epinephrine or
vasopressin for resuscitation during epidural analgesia.
Anesth Analg 2001; 93:734-742

and CPR with vasopressin and epidural
bupivacaine Krisner AC, Hogan QH, Wenzel W, et al.
The efficacy of epinephrine or vasopressin for resuscitation
during epidural analgesia. Anesth Analg 2001; 93:734-742

KrisnerKrisner AC, Hogan QH, Wenzel W, et al.
The efficacy of epinephrine or vasopressin for resuscitation
during epidural analgesia. Anesth Analg 2001; 93:734-742
our results demonstrate that CPR during epidural
anesthesia is possible, although the underlying
pathophysiology has to be carefully considered.
Epidural blockade profoundly decreases ventricular
fibrillation mean frequency during basic life-support
CPR and is reversed by both epinephrine and
vasopressin. If our findings can be extrapolated to a
clinical setting, advanced cardiac life support should
be started immediately, and vasopressor drugs should
not be withheld. In the context of epidural anesthesia,
both epinephrine and vasopressin increase coronary
perfusion pressure sufficiently during CPR. During
epidural block, muscarinic blockade may be needed

Hogan QH, Stadnicka A, Stekiel TA.
Effects of epidural and systemic
lidocaine on sympathetic activity and
mesenteric circulation in rabbits.
Anesthesiology 1993; 79:1250–
60.<ldn>!
2: Jacobsen J, Sofelt S, Brocks V.
Reduced left ventricle diameters at
onset of bradycardia during epidural
anesthesia. Acta Anaesthiolol Scand
1992; 36:831–6.
3: Caplan RA, Ward RJ, Posner K,

13: Schultz CH, Rivers EP, Feldkamp
CS. A characterization of hypothalamic-
pituitary-adrenal axis function during and
after human cardiac arrest. Crit Care
Med 1993; 21:1339–47.<ldn>!
14: Vallotton MB. At the cutting edge:
Mol Cell Endocrinol 1991; 78:C73–6.
15: Lindner KH, Prengel AW,
Pfenninger EG. Vasopressin improves
vital organ blood flow during closed-
chest cardiopulmonary resuscitation in

Guidelines 2000 for cardiopulmonary
resuscitation and emergency
cardiovascular care. Resuscitation 2000;
46:1–447.
26: Lindner KH, Ahnefeld FW, Bowdler
IM. Comparison of different doses of
epinephrine on myocardial perfusion and
resuscitation success during
cardiopulmonary resuscitation in a pig
model. Am J Emerg Med 1991; 9:27–
31.<ldn>!
27: Brown CG, Werman HA, Davis EA.

Leclercq JF, Rosengarten MD, Kural S.
Effects of intrinsic sympathetic activity of
beta-blockers on SA and AV nodes in
man. Eur J Cardiol 1981; 12:367–
75.<ldn>!
38: Noc M, Weil MH, Gazmuri RJ.
Ventricular fibrillation voltage as a
monitor of the effectiveness of
cardiopulmonary resuscitation. J Lab
Clin Med 1994; 124:421

5 Aromaa U, Lahdensuu M, Cozanitis DA. Severe
complications associated with epidural and spinal
anaesthesia in Finland 1987-1993: a study based on
patient insurance claims. Acta Anaesthesiol Scand
1997; 41:445-452.
6 Caplan RA, Ward RJ, Posner K, Cheney FW.
Unexpected cardiac arrest during spinal anesthesia: a
closed claims analysis of predisposing factors.
Anesthesiology 1988; 68:5-11.
7 Carpenter RL, Caplan RA, Brown DL, et al.
Incidence and risk factors for side effects of spinal
anesthesia. Anesthesiology 1992; 76:906-916.

Anesth Analg 2001; 92:252-
256
Cardiac arrests during spinal anesthesia
are described as “very rare,” “unusual,”
and “unexpected,” but are actually
relatively common . The two largest
prospective studies designed to evaluate
the incidence of complications during
spinal anesthesia reported two arrests in
1881 patients and 26 arrests in 40,640
patients for an overall incidence of
seven arrests for every 10,000 (0.07%)
spinal anesthetics. A review of
approximately 4000 regional anesthetics

4: Tarkkila PJ, Kaukinen S.
Complications during spinal anesthesia:
Reg Anesth 1991; 16:101–6.<ldn>!
MEDLINEÒ RECORD:
AB - Complications during spinal
anesthesia were studied prospectively in
1881 patients. Twenty-six percent of the
patients suffered from one or more
complications. The most common

et cause des arrets cardiaques peroperatoires et en salle
de reveil.A prpopos de 102468
anesthesies.Ann.Fr.Anesth.Reanim. 1991;10:436-442.
102468 anesthetics
189 CA
29 linked totally or partially to
anesth.;11 survived:mortality
1.1/10.000
8/29 during regional 7 pd &1 only
under spinal:8/12981=6/10.000

BODILY MN. Bradycardia and asystole during spinal
anesthesia : a report of three cases without morbidity.
Anesthesiology, 70 : 866-868, 1989.
3 cases
not associted with hypoxemia
full recovery

The most common serious
cardiovascular side-effects from spinal
anesthesia are hypotension and
bradycardia, with an incidence of cardiac
arrest said to range from 0.4 to 1.0 per
10 000 spinal anesthetics . Risk factors
for hypotension include block height T5
or greater, age older than 40 years,
baseline systolic blood pressure less
than 120 mmHg, and spinal puncture
performed above L3-L4. Hypotension
occurs as a result of reductions in

Interestingly, the first publication from
the American Society of
Anesthesiologists Closed Claims Project
database in 1988 reported sudden
cardiac arrest in 14 healthy patients
undergoing spinal anesthesia. Six
patients died, and of the eight survivors,
seven had serious neurological damage.
That initial report emphasized the
suddenness of the bradycardia and
asystole that can develop with spinal
anesthesia, despite seemingly

Prospective studies by Carpenter and
colleagues as well as by Auroy et al.
found no link between sedation and
cardiac arrest during spinal anesthesia.
Clearly, a circulatory etiology seems
much more probable than a respiratory
etiology, given the blockade of
sympathetic efferents and the profound
decrease in venous return associated
with higher levels of spinal blockade.
The reduced preload triggers
bradycardia by three possible reflexes

Another fascinating area in which our
understanding of physiology has
expanded recently is the appreciation of
convergence in mechanisms of general
and spinal anesthesia. For example,
minimum alveolar concentration, a
traditional measure of inhalational agent
potency, appears to have a primary
mechanism in the spinal cord .
Alternatively, central neuraxial
anesthesia may have direct effects on
the suppression of consciousness, and

Conclusions from closed claims
analysis
90’sClaims for death and brain damage are
decreasing compared to 80’s
Claims Inadeq ventilation/oxygenation and
esophageal intubation decreased from 90’s to 80’s….
That happened thanks to the widespread use of
Oxygenation and end tidal CO2 monitoring (and
LMA????….)
Cardiovascular causes of death and brain damage
increased;is this real or is because the relative
reduction in the respiratory causes?
Could better monitoring decrease deaths and brain
damage?

Recurrent patterns in the analysis of
sudden cardiac arrest during spinal
anesthesia
Healthy adult patients
Conventionally managed spinal(but often epi
i.t,fent & midaz i.v…..)
Relatively minor surgery
Block at T4 or higher
Onset within 30 min from start of spinal
Presence of apparent normal haemodynamics
and respiration in about 50% of cases

Although resuscitation was promptly
initiated,epinephrine was nor
administered until a median of 7 min had
elapsed;bad outcomes(1989) suggest
that insufficient restoration of peripheral
tone in the setting of high sympathetic
blockade may contribute to the severity
of cardiac and neurologic outcome
.Rosenberg 1996 & 1998)and
colleagues have provided experimental
results consistent with this
hypothesis.:Using a canine

Conclusions from
Rosenberg
These studies support the
potential importance of
exogenous earlier
epinephrine administration
when cardiac arrest occurs in
the setting of central
neuraxial blockade.

Third Degree Heart Block and Asystole
Associated with Spinal Anesthesia
1998 ; 89:257-260
We present a case of spinal anesthesia-
induced asystole in which onset and
recovery could be recorded by means of
Holter monitoring. Holter monitoring
revealed that shortly after subarachnoid
injection, a first degree heart block
developed that, without any previous
change in heart rate, progressed to a
complete heart block. After successful
resuscitation, a first degree heart block
that persisted until 6 h after
subarachnoid injection partly outlasted

68-yr-old patient was scheduled for
elective total hip arthroplasty. Apart from
arterial hypertension, treated with
nifedipine, he had no history of
cardiovascular disease. Physical
examination and preoperative 12-lead
electrocardiograph (ECG) revealed no
abnormal condition. Premedication
consisted of 7.5 mg oral midazolam
administered 1 h before surgery.
Intraoperative monitoring included pulse
oximetry, noninvasive blood pressure

Our case suggests that a new first
degree heart block during spinal
anesthesia may be a warning sign of
impending complete heart block or
asystole. Moreover, a spinal anesthesia-
induced first degree heart block may
persist for a prolonged period of time
after the level of spinal anesthesia has
receded below the thoracic dermatomes
associated with sympathetic innervation
of the heart. However, the present case
illustrates that the value of first degree

Our case reemphasizes that in a
witnessed cardiac arrest, prompt
treatment is crucial. This implies strict
adherence to established safety
standards, i.e., the presence of qualified
anesthesia personnel throughout the
procedure and the continuous
monitoring of the electrocardiogram. The
initial treatment of asystole consists in
precordial chest thumping and the
administration of vagolytic and

It is noteworthy that previous reports
indicate that acute bradycardia or
asystole may occur at any time during
neuraxial anesthesia. In our case, first
degree heart block persisted longer than
the sensory blockade of the upper
thoracic dermatomes. Liguori and
Sharrock reported a case of severe
bradycardia 210 min after epidural
injection, when sensory and motor
modalities had considerably receded.
Both their observation and our case

Anesthesia: A Randomized, Double-blind, Cross-over
Comparison of Phenylephrine and
Epinephrine.Anesthesiology 1997; 86:797-805
Background: Despite many advantages,
spinal anesthesia often is followed by
undesirable decreases in blood
pressure, for which the ideal treatment
remains controversial. Because spinal
anesthesia-induced sympathectomy and
management with a pure alpha-
adrenergic agonist can separately lead
to bradycardia, the authors hypothesized
that epinephrine, a mixed alpha- and
beta-adrenergic agonist, would more
effectively restore arterial blood pressure

Epinephrine
Sedative medications before spinal
anesthesia were limited to 2 mg of
midazolam and 100 mg of fentanyl
intravenously. Fluid administration
was limited to 3 ml/kg before spinal
anesthesia.

Epinephrine
After spinal anesthesia, when a 15%
reduction in systolic arterial pressure
was observed, treatment was initiated
with a bolus of either epinephrine (4.0
mg) or phenylephrine (40.0 mg) followed
by an infusion of either epinephrine
(0.05 mg×kg-1×min-1) or
phenylephrine (0.5 mg×kg-1×min-1),
respectively. If systolic blood pressure
did not increase with the initial infusion,
repeat bolus doses could be given and
the infusion rate could be doubled until

Our data show that epinephrine restored
systolic blood pressure and increased
heart rate and cardiac output after spinal
anesthesia, but it did not restore MAP
and diastolic blood pressure.
Phenylephrine restored systolic, MAP,
and diastolic blood pressure in all
patients, but it decreased heart rate and
cardiac output. Using the Doppler
transmitral flow—velocity integral as an
approximation of stroke volume, we
observed that epinephrine significantly

Liguori GA,Sharrock NE. Asystole and Severe
Bradycardia during Epidural Anesthesia in Orthopedic
Patients.Anesthesiology 1997;89:250-257
This is a report of 7 cases of severe
bradycardia and 5 cases of asystole that
occurred during orthopedic surgery
under epidural anesthesia during the
past 9 yr at our institution. These include
one case of asystole and one case of
severe bradycardia that occurred in the
post anesthesia care unit (PACU).
Although this report does not provide
data on the incidence of bradycardia,
these individual cases provide the
greatest experience on patterns of onset

Asystole and Severe Bradycardia during
Epidural Anesthesia in Orthopedic
Patients

Bernards CM,Hymas NJ.
Progression of first degree heart block to high grade
second degree block during spinal anesthesia
ABSTRACT: A case is presented in
which a patient with pre-existing first
degree heart block developed high-
grade second degree heart block during
spinal anaesthesia. Progression of the
block was associated with blockade of
cardiac sympathetic neurons induced by
spinal anaesthesia. This suggests that
patients with pre-existing heart block
may be at increased risk for
development of higher grade block
during spinal anaesthesia.

Progression of first degree heart block to
high grade second degree block during
spinal anesthesia

spinal anesthesia
An 18-gauge intravenous catheter
was placed and 600 ml Ringer's
lactate and 4 mg morphine were
given iv. The blood pressure was
118/58, and heart rate was 84
beats per minute (sinus rhythm).
She was placed in the left lateral
decubitus position and 60 mg 5%
lidocaine in 10% dextrose with 200
mg epinephrine was injected into
the subarachnoid space at the L4

spinal anesthesia
She remained in the left lateral
decubitus position for two minutes and
was then turned supine. Seven minutes
later sensory block was evaluated by pin
prick and found to be at the level of T4
on the right and T3 on the left. Over the
next several minutes she developed
Type I second degree heart block
(Wenckebach) with a 4:3 conduction
ratio which progressed within 15 sec to
high-grade second degree block with a
2:1 conduction ratio (). Blood pressure

risk factors for side effects of spinal
anesthesia Anesthesiology 76:906-916,
1992
We prospectively studied 952 patients to
identify the incidence of hypotension
(systolic blood pressure < 90 mmHg),
bradycardia (heart rate < 50 beats/min),
nausea, vomiting, and dysrhythmia
during spinal anesthesia. Historical,
clinical, and physiologic data were
correlated with the incidence of these
side effects by univariate and
multivariate analysis. Hypotension
developed in 314 patients (33%),
bradycardia in 125 (13%), nausea in 175

Incidence and risk factors for side effects
of spinal anesthesia.

MS†; Crumrine, Robert, MD*
Sympatovagal effects of spinal anesthesia
assessed by heart rate variability analysis
Heart rate variations (HRV) result from
moment-to-moment changes in
sympathetic and parasympathetic
activity in response to many conditions.
These two neural inputs to the heart can
be identified by analyzing power spectra
of HRV for frequency components at the
vasomotor (low-frequency [LF]) and the
respiratory (high-frequency [HF])
rhythms. HRV analysis has been used
successfully in humans to noninvasively
evaluate the autonomic responses to

Assessment of autonomic function in a
clinical setting has been difficult to
accomplish, depending on the
techniques used . Normally, the
autonomic nervous system maintains a
sympathovagal balance that modulates
heart rate to accommodate bodily
demands subsequent to physiologic and
environmental changes. Oscillations in
heart rate that result from this
modulation can reveal markers for
sympathetic and parasympathetic

The cephalad progression of spinal
block to higher dermatome levels after
injection of the local anesthetic into the
lumbar space was accompanied by a
quantitative reduction of HRV, as
reflected by changes in the power of all
components between 0.03 and 0.5 Hz
within the HRV power spectra. In those
patients whose spinal blocks were
adequate for surgery, the reduction in
total HRV power became significant
when sensory blocks reached T3-4.

Kawamoto M, Tanaka N, Takasaki M. Power spectral
analysis of heart rate variability after spinal
anesthesia. Br J Anaesth 1993; 71:523-7.

Coronary perfusion pressure during cardiopulmonary
resuscitation after spinal anesthesia in dogs.Anesth
Analg 1996; 82:84-7
Cardiac arrest during spinal anesthesia is a rare
event, but when it does happen cardiopulmonary
resuscitation (CPR) is often ineffectual. This study
examines the effect of spinal anesthesia on coronary
perfusion pressure (CPP) during CPR and the
subsequent response of CPP to epinephrine
administration. Twenty mongrel dogs were
anesthetized, and randomly assigned to a spinal
injection with either 0.5 mg/kg bupivacaine or with an
equivalent volume of normal saline. 20 minutes later,
ventricular fibrillation was electrically induced and after
1 min CPR was started. CPP was measured every
minute. After 4 min of CPR, epinephrine 0.01 mg/kg

Coronary perfusion pressure during
cardiopulmonary resuscitation
after spinal anesthesia in dogs.

Increase in coronary perfusion pressure
with increase in epinephrine dose
0
0,5
1
1,5
2
2,5
3
3,5
4
CPP increase in
mmHG
0,01 0,1 0,2 0,4
bupi spinal
saline spinal

resuscitation
0
10
20
30
40
50
60
70
80
90
100
%
0,01 0,1 0,2 0,4
bupi spinal
saline spinal

Thgese dta demonstarte that spinal
anesthesia decrease CPP during
CPR to levels below the threshold
established for successful
resuscitation ant that epinephrine is
effective in increasing CPP during
CPR above the critical threshold

to cardiac arrest( from
Rosember et al
Mean noerpi change from baseline ng/mn
0
500
1000
1500
2000
2500
post 1 3
control
bupi

Clòaims in Finland
Patient Iniry Act(PIA) from May 1 1987
23500 claims up to 31/12/1993
86 claims associated with
spinaòl/peidural anesth;estimated at
550.000 spinal & 170.000 epid.
SPINAL 25(/550.000)0,45/10.000:
Cardiac arrest 2
paraplegia 5
permamnet cauda equina 1
peorneal nerve paresis 6
neurological deficits 7

Matta BF,Magee P.Wenckebach type heart block
following spinal anesthesia for caesarean section. CAN
J ANAESTH 1992 / 39: 10 / pp1067-8
ABSTRACT: A case is described of
complete heart block during spinal
anaesthesia for Caesarean section in a
fit 23 yr-old-woman. This developed
shortly after the institution of the
block(left side,L2,3 iuntespace,bupi 12,5
mg!!), with the height of the block below
T5 and in the absence of hypotension.
The patient was resuscitated
successfully with vagolytic and alpha-
agonist drugs. A Wenckebach block
persisted for a short period

Cardiac arrest (or severe
arrhytmia)cases...
author drug Site of
inj.
level other
matta Bupi
12,5
L2-3 T5 Done
on l
side
bernard
s
Lido 60
mg 5%
+ epi
200
micr
L4-5 T4-3 Left
side

Cardiac arrest associated
900 cases in claims 1988;14 cases
of neuraxial cardiaca rrest…..,all
pts were resuscitated,8 survived
but only 1 regained a sufficiemnt
neurologic function…..

Geffin B, Shapiro L. Sinus bradycardia
and asystole during spinal and epidural
anesthesia: J Clin Anesth 1998; 10:278–
85.<ldn>!
MEDLINEÒ RECORD:
AB - STUDY OBJECTIVE: To
characterize the clinical features that
predispose to sinus bradycardia and
cardiac arrest during spinal and epidural
anesthesia. DESIGN: Retrospective
clinical review. SETTING: University

Pollard
This consistent pattern suggests
that the risk factors for bradycardia
may help identify patients who are
more susceptible to vagal
predominance leading to circulatory
collapse and asystole during spinal
anesthesia.

Pollard
Could such reflex responses to
decreases in preload cause more than
bradycardia? Studies of the
hemodynamic effects of graded
hypovolemia have demonstrated
progressive vagal symptoms including
sweating, nausea, and syncopeMurray
RH, Thompson LJ, Bowers JA, Albright
CD. Hemodynamic effects of graded
hypovolemia and vasodepressor
syncope induced by lower body negative
pressure. Am Heart J 1968; 76:799–809.

Pollard
Taken together, these studies
demonstrate that decreases in preload
can precipitate not only classic vagal
symptoms, but also full cardiac arrest.
Although one might assume that
maintaining preload during spinal or
epidural anesthesia is a uniform practice
of anesthetists, the literature
demonstrates otherwise. Geffin and
Shapiro reported that prophylactic
preloading with a bolus of 300 to 750 mL
was not practiced during the 5-yr period

Pollard
Often two or more of these factors are
present in patients who receive spinal or
epidural anesthesia for labor analgesia
or for cesarean delivery. With the
similarities between spinal and epidural
anesthesia one might expect a
comparable rate of cardiac arrest during
epidural anesthesia. The decreased
incidence of cardiac arrest associated
with epidural anesthesia compared with
spinal anesthesia is a relatively new
finding that has not been explained .

Impaired neuroendocrine response mediates
refractoriness to cardiopulmonary resuscitation in
spinal anesthesia.Crit.care Med.26; 533-537: 1998
Objective: To determine the extent of neurogenic
control on adrenal secretion in a canine model of high
spinal anesthesia and cardiac arrest.
Design: Randomized, controlled, acute intensive
study.
Setting: University intensive care laboratory.
Subjects: Nineteen healthy, anesthetized, mongrel
dogs.
Interventions: Cardiac arrest was induced in 11
spinally anesthetized dogs and 8 sham-control
animals; cardiopulmonary resuscitation (CPR) was
started 60 secs later. Epinephrine was injected at 4
mins and every 2 mins thereafter. Arterial blood

Measurements and Main Results: At 1 and 3 mins
after cardiac arrest, the control group exhibited
significant increases of epinephrine and
norepinephrine concentrations (p < .05) that were
absent in the spinal anesthesia group. Plasma renin
increased in both groups whereas aldosterone and
cortisol remained unchanged.
Conclusions: Spinal anesthesia abolishes the
catecholamine release that follows cardiac arrest,
while a previously postulated direct adrenal effect of
hypoxia stimulating catecholamine release was not
confirmed in these experiments. Since epinephrine
treatment restores coronary perfusion pressure (CPP)

Introduction
The central role of the central nervous
system (CNS) in the generation of the
hormonal responses to maximal stress
has been examined in human and
animal models of cardiac arrest [1-7].
The main target organ of the endocrine
reaction to stress is the adrenal gland,
which is under the control of neurogenic
and humoral factors. The importance of
adrenal activation in cardiac arrest is
underlined by the results of experiments

mediates refractoriness to
cardiopulmonary resuscitation in spinal
anesthesia.Crit.care Med.26; 533-537: 1998
MATERIALS AND METHODS
Twenty, 18 to 35 kg, fasted, flatchested,
mongrel dogs of random sex were
anesthetized with 20 mg/kg of thiopental
and 2 [micro sign]g/kg iv of fentanyl,
followed by 50 mg/kg of chloralose
(0.8% in normal saline) in an
intravenous bolus and continued at 20
mg/kg/hr (0.4% in normal saline),
according to the protocol approved by
the Animal Care Committee at the
University of Michigan School of

Norepinephrine response to cardiac arrest
Bupivicaine, closed circles black;
control, open circlesred
Rosenberg: Crit Care Med, 26(3). 1998.533-
537

Epinephrine response to cardiac arrest (top). The log
mean change in serum epinephrine +/- SEM from
baseline is shown. Epinephrine levels increased in
both groups over time (p < .001). Mann-Whitney U
testing demonstrated a significant difference between
groups after 3 mins of cardiopulmonary resuscitation
(CPR) (p = .014).
Aldosterone response to cardiac arrest shown as
mean change in serum concentration +/- SEM from
baseline (middle). There was no significant difference
between groups or over time.
Renin response to cardiac arrest shown as mean
change in serum concentration +/- SEM from baseline

mediates refractoriness to
cardiopulmonary resuscitation in spinal
anesthesia.Crit.care Med.26; 533-537: 1998
RESULTS
Eleven of the twenty dogs were included
in the bupivacaine spinal group and
eight dogs were included in the sham-
spinal group. One dog was excluded
from the study because of the technical
difficulties which occurred during
placement of the spinal needle. Before
arrest, the central venous pressure was
similar in both groups [15]: 1 +/- 2 (SD)
vs. 0 +/- 2 mm Hg (p > .1). The mean
arterial pressure was, however,

Discussion from Rosenberg: Crit Care
Med, Volume 26(3).March 1998.533-537
The present work demonstrates that spinal anesthesia
produces significant suppression of the
norepinephrine and probably epinephrine responses
to maximal stress, as represented by cardiac arrest.
Since CPP is restored after epinephrine injection [15],
the data herein confirm that catecholamine deficiency
is an important physiologic mechanism for
refractoriness to CPR during spinal anesthesia. Thus,
the significant reduction in catecholamine release in
the bupivacaine group strongly suggests that low
catecholamine concentrations would be associated
with relaxation or poor constrictory response of aortic
root vascular tone thereby decreasing coronary

Med, Volume 26(3).March 1998.533-537
Comparison of the CPP data in this work regarding
dogs with spinal anesthesia with the results reported
by Foley et al. [1] regarding adrenalectomized dogs
undergoing CPR [1] shows decreases in CPP similar
in both profile and magnitude. Foley et al. [1] observed
a 30% increase in norepinephrine in sham-
adrenalectomized dogs as compared with 100% (ten-
fold) seen in control animals in the current work. This
difference is probably the result of the different
anesthetic agents that were used in the two sets of
experiments (barbiturate as compared with
chloralose). An additional difference with the work of
Foley et al. [1] is their finding of higher cortisol

Med, Volume 26(3).March 1998.533-537
It is still unclear whether the
norepinephrine plasma response to
stress originates from the adrenal
medulla or from peripheral sympathetic
nerve endings. Our experimental model
with both widespread sympathetic
blockade and suppression of afferent
adrenal neurogenic stimulation could not
differentiate between those sources.
However, if norepinephrine released into
the blood was derived from the
peripheral sympathetic system, as

Med, Volume 26(3).March 1998.533-537
While previous studies of cardiac arrest
have largely focused on the cardiovascular
involvement, the present investigation
provides a basis for further research into the
role of the CNS as an integral component,
rather than an affected end organ in
resuscitation. Norepinephrine deserves
reconsideration as an important factor in
resuscitation as it may be the native,
resuscitative catecholamine. Functional
studies of the neural centers supplying the
excitatory stimulus for activation of the
sympathetic system (hypothalamus and

patient insurance claims Acta
Anaesthesiologica Scandinavica.
41(4):445-452 1997
The Patient Injury Act has been in effect
in Finland since 1 May 1987. This
legislation is a no-fault compensation
scheme and implies that if a patient
during the course of medical treatment
suffers any injury as a result of that
treatment he or she may file a claim to
the Patient Insurance Association (PIA).
From 1 May 1987 to 31 December 1993,
23 500 claims for compensation were
made.

devices in prevention of anesthetic
mishaps: a closed claims analysis.
1999;71:535-540.
Caplan RA et al. Adverse
respiratory events in anesthesia: a
closed claims analysis.
Anesthesiology 1990;72:828
6. Kroll DA et al. Nerve injury
associated with anesthesia.
Anesthesiology 1990;73:202-7.
Cheney F et al, Nerve injury
associated with anesthesia.

32 y,110 kg for repair of ventral hernia
700 m l preload,16
gauge,Ecg,NIBP;SaO2 monit
fent 100 microgr premed(rekease of
vasopressin inhibited by low dose
morphine
left lat dec;at L2-3 15 mg of bupi
0.75%+d8,25%2 min later
supine,nause+ tingling hands;C5-C6
block!--15 sec…lost consciousenne no

Danno materno;CS vs vaginale
0
5
10
15
20
25
%
CS vag
morte materna
cefalea
morte neonatale
dolore dur.anest
danno neurale
danno cerebrale paz
distress emoz
dolore dorso
*

Biblio ASa closed claims and
others…..
Posner KL, Sampson, PD, Caplan RA, Ward RJ, Cheney FW: Measuring interrater reliability
among multiple raters: An example of methods for nominal data [published erratum appears in
Stat Med 1992; 11:1401]. Stat Med 9:1103-15, 1990<ldn>!
2: Caplan RA, Ward RJ, Posner K, Cheney FW: Unexpected cardiac arrest during spinal
anesthesia: A closed claims analysis of predisposing factors. ANESTHESIOLOGY 68:5-11,
1988<ldn>!
3: Frerichs RL, Campbell J, Bassell, MB: Psychogenic cardiac arrest during extensive
sympathetic blockade. ANESTHESIOLOGY 68:943-4, 1988
4: Chester, WL: Spinal anesthesia, complete heart block, and the pericardial chest thump: An
unusual complication and a unique resuscitation. ANESTHESIOLOGY 69:600-2, 1988
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2000

Eventi dannosi nei claims ostetrici
0
2
4
6
8
10
12
14
%
ob nonob
ventilaz inadeguata
iot difficile
aspiraz
intub esofag
broncospasmo
FiO2 inadeg
ostruz vie aeree
estubaz prematura
convuls
probl attrezz
errore farmacol
errore idrico..
perdite ematiche
errore trasf
*
*
*
Probl.resp
Probl cardiocirc

Outcome from literature
All patients resuscitated;all
neurologically intact
Drugs:
» Vagolytics
» Vasopressors
» Chronotropics
» Pacing thumps
» ECM

Mortalità in anestesia

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