UHM 2016, Vol. 43, No.

1 CARBON MONOXIDE AND ST-ELEVATION MYOCARDIAL INFARCTION: CASE REPORTs

Carbon monoxide and ST-elevation myocardial infarction: case reports

Douglas G. Sward, M.D. 1, Kinjal N. Sethuraman, M.D., MPH 1, Jennifer S. Wong, D.O. 2,
Robert E. Rosenthal, M.D. 1
1 Department

of Emergency Medicine and Program in Trauma, Section of Hyperbaric Medicine,

University of Maryland School of Medicine, Baltimore, Maryland, U.S.
2 Department of Emergency Medicine, Henry Ford Macomb Hospital, Detroit, Michigan, U.S.
CORRESPONDING AUTHOR: Douglas G. Sward, M.D. dgsward@hotmail.com
______________________________________________________________________________________________________________________________________________________

ABSTRACT

We describe two cases of myocardial infarction

with ST-segment elevation on electrocardiogram
associated with carbon monoxide (CO) poisoning, a
condition rarely reported in the literature. The first
was a 62-year-old woman who experienced chest
pain in the emergency department (ED) while being assessed for exposure to carbon monoxide in
her home. The second was an 80-year-old man who
fainted at home and was found to have ST elevation during the ED workup. After hospitalization, he
returned home and soon thereafter had difficulty
walking and speaking. The responding paramedics
detected a very high CO level in the home. Both

patients received hyperbaric oxygen therapy within

the first several hours of presentation. For this
combination of conditions, it is difficult to derive
evidence-based management recommendations,
given the paucity of cases reported to date. We
conclude that rapid consultation with interventional
cardiology and consideration of angioplasty or
stenting are appropriate, especially when electrocardiographic findings and echocardiography point
to a specific coronary distribution. Hyperbaric
oxygen therapy might have a role in the treatment,
based on its effects on myocardial ischemia and
injury in other models.

______________________________________________________________________________________________________________________________________________________

Introduction
Carbon monoxide (CO) poisoning is commonly associated with a wide variety of cardiac effects, but
it is rarely reported in association with ST-segment
myocardial infarction. The number of publications
providing details about such presentations is limited.
We recently treated two patients with concomitant CO
toxicity and ST-segment elevation myocardial infarction (STEMI). In the first case, CO toxicity was the
presenting complaint and STEMI was discovered
later. In the second case, STEMI was the presenting
complaint and CO toxicity was discovered after a
considerable delay. These cases frame the difficulties
in diagnosis and management of concomitant CO poisoning and STEMI.

Case 1
An ambulance crew was called to the home of a 62year-old woman who was confused and nauseated,
experiencing episodes of vomiting. She required
assistance to leave her home. Suspecting CO poisoning, the emergency medical services (EMS) personnel tested the environment and found the ambient CO
level to be 250 ppm. At the scene, the patients vital
signs were as follows: blood pressure 158/90 mmHg,
heart rate 107 beats/minute, respiratory rate 20 breaths/
minute, temperature 36.3C. The patient was given
high-flow oxygen through a non-rebreather mask.
She continued to complain of nausea and began to
experience substernal chest pain, which she described
as similar to the pain she had felt during a heart attack

_______________________________________________________________________________________________________________________

KEYWORDS: carbon monoxide, cardiac toxicity, hyperbaric oxygen, ST-elevation myocardial infarction

Copyright 2016 Undersea & Hyperbaric Medical Society, Inc.

63

UHM 2016, Vol. 43, No. 1 CARBON MONOXIDE AND ST-ELEVATION MYOCARDIAL INFARCTION: CASE REPORTs
11 years earlier. She reported that she had not undergone stent placement. Her only prescription medications were antihypertensives (hydrochlorothiazide and
an angiotensin receptor blocker), and she did not have
follow-up care with a cardiologist. The patient was not
a smoker.
In the emergency department, the patient was given
aspirin, her pain was controlled with fentanyl, and she
continued to receive oxygen via non-rebreather mask.
Her mental status gradually returned to normal, and
she returned to baseline shortly after arrival. Initial
laboratory data showed a carboxyhemoglobin level of
15.8% and a troponin-I concentration <0.02 ng/mL.
An electrocardiogram (ECG) showed ST elevations in
the inferior leads, with reciprocal depressions in
the anterior leads (Figure 1). Previous ECGs were not
available for comparison.
Cardiology and hyperbaric medicine were both consulted. The cardiologist recommended an intravenous
heparin infusion as well as administration of metoprolol, 25 mg PO. Emergent cardiac catheterization
was discussed but was deferred by cardiology. The
patient was then given hyperbaric oxygen therapy at
2.8 atmospheres absolute (atm abs) for 46 minutes.
About 20 minutes into her hyperbaric oxygen treatment, the cardiac monitor showed a six-beat run of
ventricular tachycardia. The patient was asymptomatic
and her vital signs remained stable. She was given a
150-mg bolus of intravenous amiodarone and completed her hyperbaric session without further incident.
Following the session, the patients chest pain had
resolved, and a repeat ECG showed that her ST segments had normalized.
Her troponin level peaked at 3.63 ng/mL the following day. She underwent an additional hyperbaric
treatment that morning at 2.0 atm abs for 120 minutes. A transthoracic echocardiogram showed her left
ventricular systolic function to be mildly decreased
at 45%, with segmental wall motion abnormalities
consistent with a right coronary artery distribution,
with inferior and posterior basal akinesis and midsegment hypokinesis. That afternoon, she underwent
cardiac catheterization, which revealed 70% stenosis
in the proximal right coronary artery (Figure 2). A
drug-eluting stent was placed in that artery, administration of clopidogrel and atorvastatin was initiated,

64

and the aspirin and metoprolol were continued.

The patient remained asymptomatic and stable for
the remainder of her hospitalization, and she was
discharged on the third day after admission.
Case 2
An 80-year-old man with a history of diabetes mellitus,
hypertension, and congestive heart failure was transported via ambulance to a hospital after experiencing
syncope and slurred speech at home. A computed
tomography scan of his brain was negative. On evaluation in the emergency department, an ECG showed
evolving ST elevation in V1 through V3 (Figure 3), and
the patients troponin level was 0.12 ng/mL. He underwent left heart catheterization, which showed clear
coronary arteries, cardiomyopathy, and an ejection
fraction of 35% to 45%. He was hospitalized for
four days and then discharged to a subacute
rehabilitation facility, from which he eventually
returned home.
Later on the day the patient arrived home, his
nephew called 911 after finding his uncle to be difficult
to arouse and to have an unsteady gait. The responding paramedics measured the ambient carbon monoxide
level at >350 ppm. In the field, the patient had a carboxyhemoglobin level of 34%, as measured by pulse
CO-oximetry, and a blood carboxyhemoglobin level of
27.7%. State EMS protocol directs that patients with
suspected CO toxicity be transferred to our facility.
At the emergency department, the patient was found
to be in congestive heart failure, with a pro-BNP level
>14,000 pg/mL. An ECG showed first-degree atrioventricular block, cardiomegaly, and sinus arrhythmia.
The patients troponin concentration was 0.03 ng/mL.
The patient was treated with hyperbaric oxygen
three times: once at 2.8 atm abs for 46 minutes then
at 2.0 atm abs for two 90-minute sessions. His maximum troponin concentration on this admission was
0.1 ng/mL. We treated this heart failure patient cautiously and monitored him for any decline in
ventricular function and the development of pulmonary edema, as these are risks associated with
hyperbaric oxygen. Cardiac catheterization was not
repeated at our hospital because the results of the
procedure done at the other hospital were available
to us.

Sward DG, Sethuraman KN, Wong JS, Rosenthal RE

UHM 2016, Vol. 43, No. 1 CARBoN MoNoXIDE AND ST-ElEVATIoN MYoCARDIAl INFARCTIoN: CASE REPoRTS

Figure 1: Case 1 ECG

Figure 2: Results of cardiac catheterization in Case 1,

revealing stenosis in the proximal right coronary artery

Echocardiography revealed an ejection fraction of

20%. After reviewing this patients presentation at the
first hospital, the treating physicians felt that CO toxicity was likely responsible for his initial cardiac event.

Sward DG, Sethuraman KN, Wong JS, Rosenthal RE

dIscussIon
Carbon monoxide produces a wide spectrum of cardiotoxicity. Over one-third of patients with CO toxicity
show evidence of cardiotoxicity on an ECG or with
cardiac biomarker measurement [1,2]. Cardiac toxicity
should be considered after CO exposure, particularly
in patients with hypotension or a decreased level of
consciousness. The clinical spectrum of cardiotoxicity includes chest discomfort, tachycardia, arrhythmia,
elevated troponin levels, and ventricular dysfunction
[3]. Numerous electrocardiographic alterations are
possible: ST-segment changes, prolongation of the
QTc interval, and prolongation of both Tp-e and Tp-e
dispersion. (On an electrocardiogram, Tp-e is the interval from the peak to the end of a T-wave; Tp-e dispersion is a measurement of the variation of the
Tp-e interval in different areas of the myocardium.)
When advanced imaging is indicated, echocardiography and myocardial perfusion single-photon
emission computed tomography are recommended.
Mechanisms of injury include global hypoxemia
caused by the formation of carboxyhemoglobin, interference with the mitochondrial cytochrome respiratory
chain, binding to myoglobin, and inflammation. The

65

UHM 2016, Vol. 43, No. 1 CARBoN MoNoXIDE AND ST-ElEVATIoN MYoCARDIAl INFARCTIoN: CASE REPoRTS

Figure 3: Case 2 ECG

development of a prothrombotic state has also been described, involving the coronary and pulmonary arteries
as well as the deep venous system [4]. The mechanism
for thrombosis is unclear but is postulated to be severe
generalized tissue hypoxia as well as increased platelet
stickiness [5]. CO poisoning is suspected to cause inflammation through the production of various species
of microparticles, activation of neutrophils, and modulation of intracellular calcium influx [6,7]. It is proposed
that CO toxicity can unmask occult coronary artery
disease. Carbon monoxide toxicity has been implicated
as the cause of in-stent thrombosis and increased atherosclerosis [8]. Punctate necrosis and subendocardial
hemorrhage have been documented on pathology reports
[9]. Endomyocardial biopsy has demonstrated mitochondrial swelling in the presence of abnormal glycogen
stores. These findings have been described in patients
with and without known coronary artery disease, including those with normal coronary angiograms [10,11].
The long-term mortality rate from cardiotoxicity

66

induced by carbon monoxide is suspected to be significant [4,12].

The spectrum of presentations is wide. Some patients
demonstrate only a rise and fall in cardiac biomarkers.
Angiography might demonstrate diffuse coronary
artery disease without acute obstruction [1]. Kalay and
associates [1] found significant correlation between
carboxyhemoglobin levels, brain naturetic peptide
levels, and ventricular ejection fractions [1]. In their
series, all patients with elevated cardiac biomarkers
were referred for cardiac catheterization. Interestingly,
all had negative coronary catheterizations, and most
cases of ventricular impairment resolved rapidly.
Some patients exposed to CO experience chest pain
and have electrocardiographic changes characteristic of
acute coronary syndrome. Dziewierz noted that if
a subsequent angiogram is negative, it is presumed
that coronary vasospasm or transient thrombosis was
the cause of the infarction [10]. The discovery of an
obstructing thrombus during cardiac catheterization

Sward DG, Sethuraman KN, Wong JS, Rosenthal RE

UHM 2016, Vol. 43, No. 1 CARBON MONOXIDE AND ST-ELEVATION MYOCARDIAL INFARCTION: CASE REPORTs
______________________________________________________________________________________________________________________________________________________

Table 1: Case reports describing concomitant CO poisoning and STEMI: clinical findings and treatment
Author/
Reference

COHb
level

coronary
obstruction

Grieb [17]
(case 1)

4% (late
LAD
specimen)

coronary
intervention

ventricular
dysfunction

HBO2 outcome

PCI

Yes

not reported

______________________________________________________________________________________________________________________________________________________

Grieb [17]
20%
unknown
none
*
Yes stable
(case 2)
______________________________________________________________________________________________________________________________________________________
Dziewierz
22%
distal LAD
LAD
apical
No
persistent ST changes,
[10]
angioplasty
hypokinesis
mild apical hypokinesis
______________________________________________________________________________________________________________________________________________________
Hsu [18]
19.3%
100% mid-LAD
LAD stent
not reported
No
Stable
______________________________________________________________________________________________________________________________________________________
Shih [5]
5.5%
no cardiac
None
global hypokinesis
No
Stable

catheterization
with ejection

performed
fraction 27%
______________________________________________________________________________________________________________________________________________________
Varol [8]
**
presumed but
Surface oxygen, *
No
angiogram 1 week later;

not verified
IV streptokinase
30% in-stent restenosis,

70% stenosis in second

obtuse marginal branch

of circumflex artery and

in LAD
______________________________________________________________________________________________________________________________________________________
Watanabe [19] *
no large vessel
cardiac
*
No
not reported

obstruction, marked
catheterization

delayed enhancement

of microcirculation
______________________________________________________________________________________________________________________________________________________
Kim [14]
2.6%
total obstruction of
cardiac
inferior wall
No
follow-up angiogram

posterior descending catheterization
hypokinesis with
negative for obstruction

branch of RCA
preserved ejection

fraction
______________________________________________________________________________________________________________________________________________________
Isik [20]
14%
100% obstruction
LAD stent
apical septal hypo- No
TIMI 3 flow

to proximal LAD
kinesis, ejection

fraction 42%
______________________________________________________________________________________________________________________________________________________
Unlu [13]
28.1%
LAD
tenecteplase,
mild
No
good

heparin
______________________________________________________________________________________________________________________________________________________
* not reported; **not measured; COHb, carboxyhemoglobin; HBO2, hyperbaric oxygen; LAD, left anterior descending artery; PCI, percutaneous
coronary intervention; RCA, right coronary artery; TIMI, Thrombolysis in Myocardial Infarction Study Group grading system

has been reported [13]. Other cases of transmural infarction have been attributed to inadequate oxygen
delivery resulting from CO poisoning in addition to
underlying coronary artery disease [9]. Diffuse myocardial stunning is possible after severe CO toxicity.
The echocardiograms of the patients described in this
article demonstrated global as well as regional wall
motion hypokinesis. Severe but reversible cardiomyopathies with associated transient conduction blocks
have been described [14]. Treatments have included
intra-aortic balloon propulsion and inotrope infusions.
Interestingly, severe myocardial dysfunction usually
resolves rapidly [8]. There have been cases of severe
CO toxicity with aspiration pneumonitis complicated

Sward DG, Sethuraman KN, Wong JS, Rosenthal RE

by severe biventricular hypokinesis requiring vasopressors; all of these patients recovered within one to
two weeks [15,16].
Grace and Platt called carbon monoxide toxicity
a great imitator [4]. They described a patient who
was diagnosed as having a viral syndrome but returned to the ED with chest pain and ST elevations
suspected to be indicative of acute coronary syndrome.
Eventually, the combination of CO toxicity and pulmonary embolism was diagnosed.
Tanindi described the management of a patient with
known coronary artery disease with two-vessel bypass grafts and stents, who presented with typical
acute coronary syndrome symptoms [3]. She had

67

UHM 2016, Vol. 43, No. 1 CARBON MONOXIDE AND ST-ELEVATION MYOCARDIAL INFARCTION: CASE REPORTS
undergone cardiac catheterization two days prior, and
it had indicated patent stents. Upon re-presentation,
a second cardiac catheterization was undertaken, and
an unexpectedly high carboxyhemoglobin concentration of 30% was discovered after the procedure.
Diagnostic and therapeutic approaches to the combination of CO exposure and STEMI have varied widely.
Information from published case reports, including
carboxyhemoglobin levels, degree of ventricular dysfunction, location of coronary obstruction, coronary
intervention, use of hyperbaric oxygen, and clinical
outcome, is presented in Table 1 [5,10,14,17-20]. Of
note, it is difficult to explain how several of the reported
cases had relatively low levels of carboxyhemoglobin.
The pathway to choosing which hyperbaric oxygen
therapy protocol to use is unclear, as there is considerable variation in protocols across institutions [21].
Our institutional protocol (2.8 atm abs for 46 minutes,
followed by two additional treatments of 2.0 atm abs
for 120 minutes at the discretion of the treating
physician) was used in both cases discussed in this
paper. The protocol is based on earlier work done
at our facility [22] and approximates the protocol
described by Weaver [23].
Predicting which patients have coronary lesions
amenable to intervention can be difficult. Several
patients described in the existing literature had few
to no coronary artery disease risk factors yet had
focal coronary lesions. Liberal consideration of
percutaneous coronary intervention (PCI) seems to be
a reasonable approach. Further research is warranted.

Conclusion
Our two cases demonstrate the difficulties with diagnosis as well as treatment of patients with concomitant
CO poisoning and STEMI. Our review of the published
cases on this topic highlighted the heterogeneity of
this complex disease process and the challenge in
determining whether cardiac injury is metabolic or
mechanical in origin. We contend that both hyperbaric
oxygen and percutaneous coronary intervention (PCI)
are reasonable approaches to consider in the management of patients with this combination. In resourcelimited environments, other options include administration of 100% surface oxygen and intravenous
thrombolysis. PCI should be considered strongly when
electrocardiographic ischemic patterns correlate with
wall motion defects on echocardiography. Typical
risk factor analysis is not valid when considering PCI.
Finally, further research is necessary to help guide
clinicians when faced with concomitant CO poisoning
and STEMI.
Acknowledgment
The manuscript was copy edited by Linda J. Kesselring, MS,
ELS, the technical editor/writer in the Department of
Emergency Medicine at the University of Maryland School
of Medicine.
Conflict of interest
The authors have declared that no conflict of interest exists
with this submission.


n

______________________________________________________________________________________________________________________________________________________

REFERENCES

1. Kalay N, Ozdogru I, Centinkaya Y, et al. Cardiovascular effects of carbon monoxide poisoning. Am J Cardiol
2007; 99: 322-324.
2. Satran D, Henry CR, Adkinson C, et al. Cardiovascular
manifestations of moderate to severe carbon monoxide
poisoning. J Am Coll Cardiol 2005; 45: 1513-1516.
3. Tanindi A, Yalcin R. Misdiagnosis of carbon monoxide
intoxication in a patient with known coronary artery disease:
a case report and review of cardiovascular effects of carbon
monoxide poisoning. West Indian Med J 2009; 58: 485-487.
4. Grace TW, Platt FW. Subacute carbon monoxide
poisoning: another great imitator. JAMA 1981; 246:
1698-1700.

68

5. Shih YC, Tsai CT, Chiang FT. Acute myocardial injury

mimicking an ST-elevation myocardial infarction secondary
to carbon monoxide poisoning. Acta Cardiol Sin 2006; 22:
229-233.
6. Xu J, Yang M, Kosterin P, et al. Carbon monoxide
inhalation increases microparticles causing vascular and
CNS dysfunction. Toxicol Appl Pharmacol 2013; 273:
410-417.
7. Weaver LK. Clinical practice: carbon monoxide
poisoning. N Engl J Med 2009; 360: 1217-1225.

Sward DG, Sethuraman KN, Wong JS, Rosenthal RE

UHM 2016, Vol. 43, No. 1 CARBON MONOXIDE AND ST-ELEVATION MYOCARDIAL INFARCTION: CASE REPORTs
8. Varol E, Ozaydin M, Aslan SM, Doan A, Altinbas A.
A rare cause of myocardial infarction: acute carbon
monoxide poisoning. Anadolu Kardiyol Derg 2007; 7:
322-323.
9. Diltoer MW, Colle IO, Hubloue I, et al. Reversible
cardiac failure in an adolescent after prolonged exposure to
carbon monoxide. Eur J Emerg Med 1995; 2: 231-235.
10. Dziewierz A, Ciszowski K, Gawlikowski T, et al.
Primary angioplasty in patient with ST-segment elevation
myocardial infarction in the setting of intentional carbon
monoxide poisoning. J Emerg Med 2013; 45:831-834.
11. Whyte G, Godfrey R, OHanlon R, et al. Acute
myocardial infarction in the presence of normal coronaries
and the absence of risk factors in a young, lifelong regular
exerciser. BMJ Case Rep 1009; 2009: bcr07.2008.0384.
12. Henry CR, Satran D, Lindgren B, et al. Myocardial
injury and long-term mortality following moderate to severe
carbon monoxide poisoning. JAMA 2006; 295: 298-402.
13. Unlu M, Ozturk C, Demirkol S, et al. Thrombolytic
therapy in a patient with inferolateral myocardial infarction
after carbon monoxide poisoning. Hum Exp Toxicol 2016;
35: 101-105.
14. Kim S, Lim JH, Kim Y, Oh S, Choi WG. A case of acute
carbon monoxide poisoning resulting in an ST elevation
myocardial infarction. Korean Circ J 2012; 42: 133-135.
15. Tritapepe L, Macchiarelli G, Rocco M, et al. Functional
and ultrastructural evidence of myocardial stunning after
acute carbon monoxide poisoning. Crit Care Med 1998; 26:
797-801.

Sward DG, Sethuraman KN, Wong JS, Rosenthal RE

16. McMeekin JD, Finegan BA. Reversible myocardial

dysfunction following carbon monoxide poisoning. Can J
Cardiol 1987; 3: 118-121.
17. Grieb G, Simons D, Piatkowski A, et al. Carbon
monoxide intoxication versus myocardial infarction:
an easy diagnosis? Burns 2001; 37: 29-31.
18. Hsu PC, Lin TH, Su HM, et al. Acute carbon monoxide
poisoning resulting in ST elevation myocardial infarction:
a rare case report. Kaohsiung J Med Sci 2010; 26: 271-275.
19. Watanabe K, Katayama T, Okuyama E, et al. A case of
myocardial infarction induced by coronary microvascular
spasm after acute carbon monoxide poisoning [in Japanese].
JJAAM 2012; 23: 787-792.
20. Isik T, Tanboga IH, Guvenc TS, Uyare H. ST-elevation
myocardial infarction after acute carbon monoxide poisoning.
Anadolu Kardiyol Derg 2012; 12: 276-284.
21. Byrne BT, Lu JJ, Valento M, Bryant SM. Variability
in hyperbaric oxygen treatment for acute carbon monoxide
poisoning. Undersea Hyperb Med 2012; 39(2): 627-638.
22. Britten JS, Myers RA. Effects of hyperbaric treatment
on carbon monoxide elimination in humans. Undersea
Biomed Res 1985; 12(4): 431-438.
23. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric
oxygen for acute carbon monoxide poisoning. N Engl J Med
2002; 347: 1057-1067.

69