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January
1998
Light versus heavy sedation after cardiac surgery: myocardial ischemia and
the stress response.
Hall RI, MacLaren C, Stafford Smith M, McIntyre AJ, Allen CTB, Murphy
JT, Sullivan J, Wood J, Ali I, Kinley E; Anesthesia and Analgesia 1997;85:971-8.
[ see abstract below ]
The advent of managed care in the 1990s brought with it vigorous efforts
to reduce costs by shortening postoperative intensive care unit and hospital
length of stay. The established routine of postoperative overnight mechanical
ventilation after uncomplicated cardiac surgery was reexamined, and gave
birth to the concept of "fast tracking" - i.e. ventilatory weaning and tracheal
extubation within six hours of operation.
Opposed to this notion were the observations regarding postoperative myocardial
ischemia generated particularly by Dennis Mangano and his colleagues in
the multicenter McSPI outcomes research group1. They found a
high incidence of electrocardiographic ischemia in the early period after
cardiac surgery, which appeared to correlate with subsequent adverse cardiac
outcomes. Mangano proposed that ischemia could be lessened by an intense
analgesic-sedative regimen using sufentanil infusion plus midazolam for
24 hours after surgery2.
In a study published in the November 1997 issue of Anesthesia and Analgesia,
Hall et al compared the effects "low" and "high" levels of postoperative
sedation on myocardial ischemia and the endocrine stress response in 50
patients undergoing uncomplicated coronary artery bypass graft (CABG) surgery3.
Sedation was provided by a continuous infusion of propofol with an endpoint
guided by the Ramsay Sedation Score4:
| Sedation Score |
Clinical Assessment |
| 1 |
restless, agitated |
| 2 |
awake, calm |
| 3 |
drowsy |
| 4 |
asleep; brisk response to glabellar tap or loud noise |
| 5 |
asleep; sluggish response to glabellar tap or loud |
| 6 |
asleep; no response to glabellar tap or loud noise
|
Patients were randomized to receive "light" or "heavy" sedation and the
propofol infusion was adjusted to achieve a Sedation Score of 2 or 4 respectively.
Analgesia was provided by a sufentanil infusion with superadded boluses
of morphine as necessary to keep the visual analog scale (VAS) pain score
less than 7 (0 = no pain, 10 = worst pain). Myocardial ischemia was assessed
by Holter ECG monitoring, myocardial infarction by CK-MB isoenzyme levels,
and endocrine stress response by serum cortisol and plasma and urine catecholamines.
There were no differences between the groups with respect to ECG evidence
of myocardial ischemia, postoperative myocardial infarction by CK-MB criteria
(three patients in each group) or endocrine stress response. The authors
concluded that light sedation does not increase the endocrine stress response
or the risk of myocardial infarction after uncomplicated CABG surgery.
My reason for reviewing this paper this month is that I am concerned lest
you, gentle reader, interpret this study as refuting the findings of Mangano
et al.
Firstly, it is very important to differentiate between sedation and analgesia,
which are often used synonymously. In this context, and in particular,
with regard to the administration of propofol (or for that matter, benzodiazepines),
sedation implies one or all of the properties of hypnosis (sleep induction),
anxiolysis or amnesia. It does not include analgesia. In this study the
authors took pains (no pun intended) to ensure that adequate levels of
analgesia were provided to both groups. It seems to be a reasonable assumption
that pain is generally a far more potent trigger of the endocrine stress
response (and thereby, myocardial ischemia) than awareness. Indeed, the
lack of difference between the two groups could simply be taken as supportive
evidence that sedation is not as important as analgesia in preventing
the postoperative stress response and myocardial ischemia.
Second, I think that the authors should be challenged to produce a power
analysis that suggests that they would be able to identify a significant
difference in outcomes such as myocardial infarction or ischemia with
as few as 25 patients in each group.
The assurance of adequate levels of sedation to alleviate anxiety, prevent
recall and, if necessary, induce sleep, is one of the primary goals of
critical care. Indeed, there are other advantages of combining sedative
and analgesic infusions - in particular, a reduction in the potential
for tachyphylaxis and excessive single drug administration (on the other
hand, side effects such as respiratory depression are exacerbated). Also,
the routine use of a Sedation Scale should be encouraged to standardize
the assessment and targets of levels of sedation. But it remains essential
not to confuse sedation with pain control. Clearly the intent of Hall
et al. was to inform, not to confuse - but we should make sure that we
take away the right message from this study!
Notes:
1Postoperative myocardial ischemia in patients undergoing coronary
artery bypass graft surgery. Smith RC, Leung JM, Mangano DT, The SPI Research
Group; Anesthesiology 1991;74:464-73.
2Postoperative myocardial ischemia: therapeutic trials using
intensive analgesia following surgery. Mangano DT, Siliciano D, Hollenberg
M et al. Anesthesiology 1992;76:342-53.
3Light versus heavy sedation after cardiac surgery: myocardial
ischemia and the stress response. Hall RI, MacLaren C, Stafford Smith
M, McIntyre AJ et al. Anesthesia and Analgesia 1997;85:971-8.
4Controlled sedation with alphaxalone-alphadolone. Ramsay MAE,
Savage TM, Simpson BRJ et al. Br Med J 1974;2:656-9.
Return to the Current Literature Review Front
Page , or read the abstract:
ABSTRACT
The influence
of light versus heavy sedation after coronary artery bypass graft (CABG)
surgery on the devlopment of postoperative myocardial ischemia has not been
described. After uncomplicated CABG surgery, 50 pateints were randomly assigned
to receive LOW (n=24;target Ramsey Sedation Score [RSS] = 2) or HIGH
(n=26; target RSS = 4) sedation with propofol. Analgesia was provided
to maintain a visual analog scale (VAS) pain score <7.
Myocardial ischemia was identified perioperatively using continuous 3-lead
Holter monitoring. By measuring creatine kinase (CK) MB levels preoperatively,
at entry to the intensive care unit (ICU), and every 12 h for 48 h; and
by obtaining aerial 12-lead electrocardiograms (ECG)(preoperatively; 2,
4, 12, 24, and 48 h after ICU admission, 8:00AM the morning after surgery;
and 5 min pre- and postextubation), myocardial infraction was identified.
Endocrine stress response was assesed by measuring serum cortisol levels
preoperatively, on admission to the ICU, and 24 h postoperatively. In a
subset of patients (LOW n=10, HIGH n=11), plasma and urinary
catecholamine levels were also measured.
There were no between-group differences in demographics, operative course,
hemodynamic variables, or cortisol levels while in the ICU. The VAS pain
score and target RSS were achieved and sustained, and they differed between
groups. There were three myocardial infractions in each group by CKMB criteria
alone. No ECG-identifiable myocardial infraction occurred. The ST segment
versus time curve (LOW 187 +/- 295 versus HIGH 1071 +/- 2137 mm/min) differed
between groups. Urinary and plasma catecholamine levels were similar between
groups over the observation period.
We conclude that the use of a reduced sedation regimen in combination with
adequate analgesia did not result in an increased endocrine stress response
or risk of myocardial ischemia.
Implications: This randomized study of patients after coronary artery bypass
surgery examined whether light (versus heavy) sedation with propofol in
the intensive care unit was associated with an increased degree of myocardial
ishemia. Using techniques to deflect myocardial ischemia, including Holter
monitoring, electrocardiogram,a nd myocardial enzyme measurements, no differences
were found. We conclude that light sedation does not increase the endcorine
stress response or the risk of myocardial infraction.
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