MSO4 for MI Pain
                            ================

>         I was recently surprised to hear from one of my collegues that the
> use of morphine sulfate in patients with acute MI had become passe; the
> premise being that pain directly correlates with active myocardial ischemia
> and, therefore, should not be masked by MSO4 but relieved by precise
> titration of the Tridil drip. While this theory sounds plausible, I wonder
> if there is any scientific evidence to support such practice.
>         My medline search did not reveal any evidence to support this
> theory, but maybe I missed something? Do any of you agree with the above
> premise? Are there any studies which support this? Anybody disagree? Is
> anyone still using MSO4, or is the rumor true that it is passe?


        Heather, you've become quite a prolific writer during your short
time on emed.

        In any case, I think that most clinicians would agree that
nitroglycerine is a first line adjunctive agent to manage ischemia, and
thus pain, in the setting of acute MI. Nevertheless, there may be a role
for pure analgesics such as morphine.  The rationale being that pain
results in sympathetic activation which, in itself, may worsen ischemia.
Some have experimented in the use of epidural morphine in the
postoperative period and report that it may lessen the extent of ischemia
(1,2). This may be true in the case of ongoing ischemia as well (3,4).
Recent reivews (5) as well as anectodal reports (6) continue to advocate
the use of morphine particularly with failure to achieve complete pain
relief with NTG alone.

        Your observation that, in some cases, morphine may  mask symptoms of
ongoing ischemia is a concern that has been raised before (7).


H. Louzon MD


(1)


de Leon-Casasola OA, Lema MJ, Karabella D, Harrison P
Postoperative myocardial ischemia: epidural versus intravenous
patient-controlled analgesia. A pilot project.
Reg Anesth 1995 Mar-Apr;20(2):105-12

BACKGROUND AND OBJECTIVES. Continuous postoperative epidural analgesia with
bupivacaine (BUP) and morphine (MS) may be associated with a decreased
incidence of postoperative myocardial ischemia (ISCH) and infarction (MI).
This study evaluated the incidence of ISCH and MI in patients with two or
more risk factors for coronary artery disease (CAD) who were admitted to the
ICU after upper abdominal surgery for cancer. METHODS. During a 1-year
period, 198 patients were studied for the incidence of ISCH and MI in a
prospective, nonrandomized fashion. The epidural group (EPI, n = 110)
received continuous epidural anesthesia by injection at the T7-9 interspaces
with 0.5% BUP/0.013% MS and light general anesthesia followed by 0.1%
BUP/0.01% MS epidural analgesia for 5-7 days. The general anesthesia group
(GEN, n = 88) received a balanced technique followed by intravenous
patient-controlled analgesia with 0.1% MS for 5-7 days. All patients had
preoperative and postoperative 12 lead ECGs every 6 hours on the first 3
postoperative days. Patients with ECG changes consistent with myocardial
ischemia had creatine kinase levels with isoenzymes drawn every 8 hours.
RESULTS. There were no differences in age, sex, number of cardiac risk
factors, number taking anti-anginal medication, preoperative heart rate (75
+/- 5 [EPI] vs. 73 +/- 4 [GEN]), and incidence of preoperative or
intraoperative ischemia between the two groups. All patients had adequate
analgesia. Postoperatively, patients in the EPI group had a lower incidence
of tachycardia (15 [14%] vs. 58 [65%], P < .00001), ischemia (5 [5%] vs. 15
[17%], P < .004), and infarction (0 vs. 3 [20% of patients with ischemia]).
All episodes of ischemia were silent and occurred more frequently during the
first 36 hours postoperatively (14 episodes or 72%). Overall 60% of the ISCH
episodes were associated with tachycardia (5/5 in the EPI group and 7/15 in
the GEN group). There were no deaths in either group. CONCLUSIONS. These
preliminary results suggest that epidural anesthesia and analgesia may
decrease the incidence of postoperative tachycardia, ischemia, and possibly
infarction in patients undergoing upper abdominal procedures.

(2)


Beattie WS, Buckley DN, Forrest JB
Epidural morphine reduces the risk of postoperative myocardial ischaemia in
patients with cardiac risk factors.
Can J Anaesth 1993 Jun;40(6):532-41

Perioperative myocardial ischaemia is a predictor of postoperative cardiac
morbidity (PCM). Epidural anaesthesia and adequate perioperative analgesia
have been shown to improve myocardial oxygen dynamics due to interruption of
pain and sympathetic pathways. The aim of the present study was to compare
the incidence of ischaemia after either general anaesthesia followed by
parenteral analgesia with morphine or combined epidural/general anaesthesia
followed by analgesia with epidural morphine. In a prospective
observer-blinded analysis of the occurrence of ischaemia, 55 patients
(epidural = 29/parenteral = 26) scheduled for elective surgery with defined
risks for ischaemic cardiac disease were entered and followed for 24 hr
after surgery with two-lead continuous Holter monitoring. Groups were
similar with respect to age, weight, modified Goldman (Detsky) risk
classification and the use of cardiac medications. Fewer patients receiving
the epidural anaesthesia/analgesia had ischaemic episodes (17.2 vs 50.0%, P
= 0.01), and tachyarrhythmias (20.7 vs 50.0%, P < 0.05). Epidural patients
had a four-fold reduction of the relative risk for either event (P < 0.001).
All ischaemic events were asymptomatic and unrecognized (silent). All major
morbid events (n = 5) (MI, congestive heart failure and death) occurred in
patients who had perioperative episodes of ischaemia. There were three
distinct peaks in onset of ischaemia, at 1-4 hr, 9-12 hr and 22-24 hr
postoperatively. One third of postoperative ischaemic events occurred within
the first four hours after operation and lasted from 1 to 31 min. Forty-two
percent of ischaemic episodes were associated with a heart rate > 100 bpm,
or an increase of 20% over the baseline heart rate. We conclude that
epidural anaesthesia/analgesia reduces but does not eliminate the risk of
myocardial ischaemia and tachyarrhythmia. We were unable to determine any
associated reduction in the risk of PCM.

(3)


Dzizinskii AA, Tumak VN, Zhatkin SI
[The effect of prolonged morphine epidural analgesia on the clinical course
and size of the necrotic area in patients with an acute myocardial
infarct]
Ter Arkh 1991;63(12):35-7

The effect of conventional and prolonged epidural analgesia (PEA) with
morphine on the clinical course and the size of the focus of necrosis was
studied and compared in 60 patients with acute myocardial infarction. In the
basic group (n = 30), analgesia was carried out for 7 days with the aid of
PEA. In the control group (n = 30), analgesia was performed by intravenous
injection of morphine. In both the groups, the clinical course ant the size
of the focus of myocardial necrosis were estimated (precordial cartography
and detection of creatine phosphokinase made in series). PEA was established
to bring about complete analgesia rapidly and safely, which in turn favours
noticeable limitation of the focus of necrosis and amelioration of the
clinical course of acute myocardial infarction. The effect produced by PEA
was considerably higher in all the parameters as compared to that attained
with conventional analgesia.


(4)


Dzizinskii AA, Tumak VN, Bidagaev VB
[The use of prolonged epidural analgesia with morphine for relief of the
pain syndrome in patients with acute myocardial infarct]
Anesteziol Reanimatol 1991 Sep-Oct;(5):43-5

Nociceptive effect of conventional and morphine-prolonged epidural analgesia
(MPEA) has been compared in 60 patients with acute myocardial infarction
(AMI). In 30 patients of the test group pain was relieved with MPEA used
during 7 days, while in 30 control patients analgesia was performed with the
intravenous administration of morphine or fentanyl, or neuroleptanalgesia
was used. MPEA was shown to produce a more prompt and reliable anesthetic
effect, thus improving the clinical course of AMI. As regards all the
parameters, the effect of MPEA was higher compared to conventional analgesia
techniques.

(5)


Reeder GS
Adjunctive therapy in the management of patients with acute myocardial
infarction.
Mayo Clin Proc 1995 May;70(5):464-8

Adjunctive therapy for acute myocardial infarction should include aspirin,
beta-adrenergic blocking agents, and, in most patients, consideration of the
use of angiotensin-converting enzyme inhibitors, especially if left
ventricular function is reduced. Heparin has an important adjunctive role in
enhancing early vessel patency in patients who receive tissue-type
plasminogen activator and in decreasing the frequency of reocclusion of an
infarct-related artery during any thrombolytic therapy. Heparin must also be
administered to all patients who undergo primary angioplasty. Intravenously
administered nitroglycerin and orally administered nitrates are probably
most effective in patients with symptomatic ischemia. Calcium channel
blockers and prophylactic antiarrhythmic agents are not indicated for most
patients with acute myocardial infarction. Currently, insufficient evidence
is available to recommend the widespread use of intravenously administered
magnesium sulfate in the setting of acute myocardial infarction. In patients
with ischemic pain, judicious intravenous administration of morphine can
provide relief. Use of warfarin sodium should be reserved for patients at
risk for left ventricular mural thrombus. Although the use of lipid-lowering
agents after myocardial infarction has been controversial, recent studies
have demonstrated the importance of such therapy for secondary prevention of
death and morbidity.


(6)


Yanagisawa H
Acute myocardial infarction improved by neuroleptic analgesic therapy.
South Med J 1990 Jul;83(7):839-42

Treated with orthodox therapy, a 58-year-old man with acute myocardial
infarction of the anteroseptal and lateral walls continued having lethal
arrhythmias, reinfarction, low blood pressure, and anuria. With modified
neuroleptic analgesic therapy, which consisted only of a continuous drip
injection of morphine and chlorpromazine, his condition improved
dramatically. Our patient's coronary spasms, which occurred after acute
myocardial infarction, might have been triggered by mental stress due to
anxiety and pain, and the use of neuroleptic analgesic agent therapy
prevented further coronary spasm and reinfarction.


(7)

Dershwitz M, Sherman EP
Acute myocardial infarction symptoms masked by epidural morphine?
J Clin Anesth 1991 Mar-Apr;3(2):146-8

This report describes the case of an 80-year-old woman with a long history
of chronic, stable angina pectoris who underwent resection of an abdominal
aortic aneurysm and placement of an aortobifemoral bypass graft under a
combination of epidural and general anesthesia. Epidural morphine was
administered postoperatively for pain management. The patient suffered a
massive myocardial infarction (MI) in the immediate postoperative period but
experienced no chest pain or discomfort similar to her usual anginal
symptoms. The use of epidural and spinal opioids in the treatment of anginal
pain is reviewed and discussed in terms of the possibility that such
epidural opioid therapy may have masked this patient's anginal symptoms.