<Case Report> Coronary Artery Spasm during Epidural Plus General Anesthesia 利用統計を見る

Case

Yamanashi Med. J. 2 (4), l59N163,

Report

Coronary Artery Spasm during Epidural Plus

General Anesthesia

Satoshi Kashimoto, Eiji Kitagawa and Tertio Kamazawa

DePartnzent of Anesthesiolog>), Yamanashi, A4edicctl College*

Abstract: XiVe present a case o￡ coronary artery spasm during epidural plus general thesia. A 7i-year-old man was scheduled for pancreatoduodenectomy. A continuous thoracic epiclurai block was performed at the Th IO-ll interspace and gei}eral anesthesia was maintained with enfiurane and nitrous oxide in oxygen. Thirty minutes after the start of the operatioil, hypotension occurred suddenly and the ECG showe(l elevation of the ST segment, widening of the QRS complex and occasional velttricular premature beats. These changes resolved abruptiy without treatment. The same episodes occurrecl both 1 hour and 30 min before the end of the operation, and were considered to be catised by coronary artery spasm. We used a continuous nitroglycerin infusion to prevent the coronary spasm. No fttrther episodes of the coronary vasospasm occurrecl. It is uncertain that the coroRary spasms in this patient were clue to the hyperventilation or epidural anesthesia. Key words: Anesthesia, Coronary spasm, Nitroglycerin

INrrRoDuc'rloN

During the operative period, myocardial

ischemia is often caused by an increase in

myocardial oxygeR consumptien in

pati-ents with coronary artery disease. In

con-trast to effort-induced ischemia, myocardial

ischemia can also result from coronary

artery spasm. The systemic hemodynamic

pattern associated with coronary artery

spasm differs from that associated witl}

ef-fort-induced ischemia. Coronary

vasos-pasm occurs suddenly without a

provoca-tive increase in blood pressure or heart

rate and ir}ay frequently provoke

li￡e-threatening dysrhythmias.

Kano et al.L') reviewed the I4 cases of

coroRary artery spasm LiRder epidural or

spinal anesthesia reported in the Japanese

}987

* Tamaho, Nakakoma,

Received June 5, 1987

Yamanashi, 409-38, Japan

literaure. However, a patient m whom

coronary spasm occurred more than twice

has seldom been reported. Mle present

st}ch a case of coronary artery spasm

dur-ing epidural pltis general anesthesia.

REpoRT oF A CASE

A 71-year-old man was schedulecl for

pancreatoduodenectomy. He had

experi-enced the first a￡tack of angina pectoris 5

years ago, btit hacl not experienced the

pain for the past l year. He had not

re-ceived medical treatment for this symptom.

The chest X-ray aRd the electrocardiogram

(ECG) at rest were norraal. An exercise

tolerance test revealed the depression of

the ST segmentin leads II, III and aVf in

ECG. Results oE enzyme studies were

normal except Eor SGOT, SGPT, CPK and

To-Bil (90mlU, I06mlU, 607mlU, 4.0

160 S. Kashimoto, E. Kitagawa and "I'.

_Kumazawa

The patient was premedicated with

hydroxyzine 25mg and atropine O.5mg

intramusculary 30 min before arriving in

the operating room. IRtravenous and

intra-arterial catheters were inserted and

ECG lead V5 was monitored. A continuous

￡horacic epidural block was performed at

the Th 10-II interspace. Anesthesia was

induced with intravenous thiamylal 250

mg while the patieRt breathed IOO per cent

oxygen. Following loss of consciousness,

succinylcholine 60mg was administered,

and the trachea was intubated. Anesthesia

was maintained with enfluraRe and nitrous

oxide in oxygen. Five millilitre of O.25%

bupivacaine was injected to produce an

epidurai block. Arterial pressure

de-creased from }80/80 te 102/66 mmHg over

a 10-min period.

Thirty minutes after the start of

opera-tion, the ECG suddenly showed elevation

of the ST segment, widening of the QRS

complex and eccasional ventricular

pre-mature contractions. The arterial pressure

decreased to 65/89mmHg" (Fig. 1). These

changes resolved abruptly without

treat-meRt 3 minutes later. As the bleod gas

analysis showed respiratory alkalosis (pH

ECG

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ECG and blood pressure changes during coronary artery spasm. ECG showed ele-vation of the ST segment and widening of the QRS complex. The arterial pressure decreased to 65139 mmHg,

Coronary spasm during anesthesia

7.53, PaC02 24.6, Pa02 186). Ventilation

was controlled to maintain PaCOg･ between

85 and 4e torr. However, the same episode

occurred l hour before the end of

opera-tion. This episode also was not preceded by

any rise in heart rate or arterial blood

pres-sure. When the third similar event

oc-curred, a continuous nitroglycerin infusion

was administered at a rate oE 1.0 ptg/kg/

min through ￡he line for nitroglycerin.

The arterial pressure retumed to normal

(BP 120/80mmHg, HR 76 beats/min).

After the operation, results of enzyme

stu-dies (SGOT, LDH, CPK) were almost

identical to those before the operation. As

for LDH isoenzymes, LDHi/LDH2 ratio

was }ess than 1, and there was no difference

between the ECG before and after the

operation. These findings did not indicate

myocaydial infarction. No further episodes

of ST segment elevation or dysrhythmias

occurred, and the patient was discharged

from the hospital.

DIscussloN

Three paroxysmal episodes of

myocar-dial ischemia observed during epidural

plus general aResthesia in this patient were

probably caused by coronary artery spasm,

as the ST segment elevation was not

pre-ceded by an increase in either heart rate

or arterial pressure. Effort-induced

myo-cardial ischemia in patients with fixed

coronary stenoses occurs when myocardial

oxygeR demand is increased by an increase

in heart rate, blood pressure, or

contrac-tility. In contrast, coronary vasospasm

decreases blood fiow and oxygen delivery

to the myecardium, and the onset of

spasm-induced ischemia is sudden and

without waming9). Systemic arterial

pres-sure and cardiac output fall, and left

ven-tricular end-diastelic pressure increases.

However, most episodes resolve withiR

2--5 min2--5). If vasospasm is marked and

16I

longed it can lead to an acute myocardial

infarctioR7).

We can enly speculate as to the origin of

the vasospasm during anesthesia. First,

hyperventilation can be the cause. The

vasoconstriction occurs if the hydrogen ion

concentration decreases by

hyperventila-tioni2). There are reports that

hyperven-tilation causes coronary vasoconstriction

in both normal subjectsii) and patients

with stable exertional angina pectoris6).

The first attack in this patient may have

been due to the hyperventilation. SecoRd,

epidural anesthesia may be the cause4).

Above the level of sympathetic blockade,

compensatory vasoconstrlctlon may occur,

presumab}y in an effort to offset the

reduc-tion iR peripheral resistance caused by the

block. This reflex sympathetic activity may

involve the cardiac sympathetic nerves

causing coronary vasoconstriction. In

con-trast to this view, thoracic epidural block

produces coronary vasodilation and

de-creased myocardial oxygen consumptioniO).

Sympathectomy by thoracic epidural

an-esthesia redistributes coronary blood flow

to the endocardium with an improvement

in the endocardial/epicardial ratio, both

infarcted and uninfarcted hearts3). Kano

et al.-") reviewed the cases of coronary

artery spasm under epidural or spinal

anesthesia reported in the Japanese

litera-ture, classified them into two groups

ac-cording to the existence of denervatiolt of

the cardiac sympathetic nerves, and

dis-cussed the possible factors of triggering

coronary artery spasm in each group.

Third, vagal refiex due to surgical

stirflula-tion may be the cause. However,

brady-cardia and hypotension were not seen

be-fore the attack in this patient.

We used a continuous nitroglyceyin

in-fusion to prevent the coronary vasospasm.

The efficacy o･f Ritrates in preventing

at-tacks of variant angina has been recognized

162 S. Kashimoto, E.

since Prinzinetal's first report9).

Hypoten-sioR accompanying myocardial ischemia

suggests cautiot}s administration of tt

vaso-dilator drL}g such as nitrogiycerin,

kow-ever, aggressive treatment is required in

cases of ischemia caused by coronary

spasm. Doses of nitroglyceriR should be

ad.justed to avoicl tachycardia or

hypoten-SiOII.

Although we did not administer calcium

chaRnel blocking drugs, they are also

coronary vasodilatoirs that decrease the

freqReRcy of variant angina attacks in

clinical situationsi･gi).

In summary, we encountered a patient

undergeing surgery and epidural pltis

geReral anesthesia who･ had three tlmes

episodes of myocardial ischemia probably

caused by coronary artery spasm. The

in-travenous nitroglycerin was useful in

pre-veBting coronary spasm diiriRg anesthesia.

REFERENCES

l) Antman E., MullerJ., Goldberg S., MacAIpin R., Rubenfu"e M., Tabatznik B., Liang C., Heupler I., Achuf'r S., Rcichek N., Geltman E., Kerin N. Z., Nefir R. K., and B}"aunwald E.: Nifedipine therapy for coronary-artery spasm. Experience

in l27 patients. New Engl. .I. Me(l., ge.9,

l278, l980.

2> Kano T., Ushijima K., and Sait'o Y.: Two c:･ises

of coronary artery spasm under epidural

thesia. Japanese Journftl o￡ anesthesiology, 35,

1896-I905, I986.

3) Klassen G. A., Bramwell R.. S., Bromage P. R., and Zborowska-Sluis l). T.: Effect of acute

J

Kitagawa

and T. Kumazawa

pathectomy by epidural anesthesia on the canine coronary circulation. Anesthesiology, 52, 8-l5, }980.

4) KraRtz E. M., Viljoem J. F., and Gilbert M. S.: Prinzmetal's variant angina cluring extradural

ai}aesthesia. Br. J. Anaesth., 52, 945-949, I980.

.V_{･)) Maseri A., Severi S., de Nes M., L'Abbate A.,}

C}}ierchia S., Marzil]i M., Ballestra A. M., Parodi

O., Biagini A., and Distante A.: "Variant al}gina": one aspect of a continuous spectrum of vasospastic myocardial ischemia. Am. J.

Car(liol., 42, 1019-I035, 1978.

6) Neill W. A., and Hattenhauer IN{{.: Impairment

of O,, supply due to ILyperventilatioi/). tion, 52, 854-858, 1975.

7) Oliva P. B., and Breckinridge J. C.: graphic evidence of coronary arterial spasm in acute myocardial iBfarction. Circulation, 56, 366-374, l977.

8) P}'evitali M., Saierno J. A., 'I{ravazzi L., Ray M.,

Medici A., Chimienti M., Specchia G., and Bobba P.: rlCreatment of angina at rest with nifedipine: a short-terin controlled stucly. Am. J. Cardiol., 45, 825-830, 1980.

9) Prinzmetal M., Kennamer R., Merliss R., Wada T., and Bor N.: Angina pectoris I. A variant form o￡ angina pectoris. Am, J. Med., 27, 888, l959.

IO) R.eiz S., Nath S., and Rais O.: Effects of thoracic

epi(hiral block and prenalterol on coronary vascular resistance and myocardial metabolism in patients with coronary artery disease. Acta

anaesth. scand., 24, 11-16, 1980.

II> Rowe G. G., Castillo C. A., and Crumpton C. W.:

Efrects of l}yperventilation on systemic and

nai+y hemodynamics. Ain. Heart J., 63, 67-77, l962.

I2) Yasue K., Nagao M., Ornote S., Takizawa A., Miwa I<., and Tanaka S.: Coroi}ary arterial spasm ancl Prinzmetal's variant form of angina induced by hyperventilation and tris-buffer

fusion. Circulation, 58, 56-62, l9'N/8.

Coronary sp盆s㎜during anes￡hesia 163 硬膜外と全身麻酔の併用下に起きた冠動脈スパスムの一例 樫本 温，北側恵史，熊沢光生   山梨医科大学麻酔科  症例は71歳の男性で脾頭十二指腸切除術が方笹行された。麻酔は硬膜外カテーテルを胸椎の10級！ に挿入し，エンフルレンの全身麻酔とした。手術開始30分後に，突然血圧が低下し，心電図はSTの 上昇，蠣の広いΩRS，心室性期外収縮を示した。これらは約1分後に自然に軽快した。同じような 発作が手術終了30分と1時間前におこった。冠動脈スパスムが原因と考えられたので，3度欝の発作 の時にニトログリセリンの静注を行った。以後発作は退院時までおこらなかった。この症例の冠動脈 スパスムの原因として，術中の過換気や硬膜外麻酔が考えられるが，確定はできない。 キーワード 冠動脈スパスム，麻酔，ニトログリセリン