Bedside Critical Care Guide

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Edited by
www.esciencecentral.org/ebooks Ramzy H Rimawi
001
Bedside Critical Care Guide

Chapter: Acute Myocardial Infarction in an ICU

Edited by: Ramzy H. Rimawi

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Acute Myocardial Infarction in an
ICU
Ramzy H Rimawi*, Matthew R Gay, Joshua R Howell, Endya
L Frye, Nyria L Muhirwa and Jered K Cope Meyers
East Carolina University – Brody School of Medicine, Department
of Internal Medicine, Section of Pulmonary, Critical Care and Sleep
Medicine, USA
*Corresponding author: Ramzy H. Rimawi, East Carolina University
– Brody School of Medicine, Department of Internal Medicine, Section
of Pulmonary, Critical Care and Sleep Medicine, USA, Fax: 252-744-
3472; E-mail: RIMAWIR@ECU.EDU

Epidemiology
Approximately 15 million Americans over 20 years of age have coronary heart disease (CHD), in which the prevalence for myocardial
infarction (MI) is 2.9% [1]. The prevalence of an MI is higher for men (4.2%, average age 65 years) than for women (1.7%, average age
72 years) and increases with age [1-3]. Moreover, age above 75 years is the strongest predictor of 90-day mortality in patients with ST-
segment elevation MI (STEMI) undergoing PCI [3]. The incidence of a MI is 525,000 first occurrences per year and 190,000 recurrent
attacks annually, of which approximately 15% die from the acute infarction. The American Heart Association estimates an MI to occur
in the US every 44 seconds [1]. CHD remains the number one cause of death in the United States; accounting for 1 of every 6 deaths in
the US. Although these mortality rates are concerning, there has been a decline in cardiovascular deaths within the past four decades
due to progress made in earlier diagnosis and management [2]. Percutaneous coronary intervention (PCI), antithrombotic therapy and
antihypertensive and lipid-lowering preventive measures have contributed to a significant reduction in hospital mortality related to MI.
In the ICU, the identification and management of MI remains a challenge. Epidemiologic data of MI in an ICU setting is often
underreported as MI can often be missed due to masked symptoms secondary to sedatives, analgesic medications or concomitant
critical conditions (sepsis, traumatic injuries, and cerebrovascular accidents), inability to communicate ischemic symptoms because of
endotracheal intubation or coma, and/or misinterpretation of non-coronary causes of elevated cardiac enzymes. In an ICU, patients
with acute coronary syndromes (STEMI, non-STEM (NSTEMI), stable angina, and unstable angina) exhibit exceedingly higher
morbidity, mortality, length of stay and healthcare costs [4,5]. Ischemic changes can occur in up to 21% of ICU patients with CAD (or
risk factors for CAD) and 37% of ICU patients with troponin elevation.

Definition
Acute MI occurs when there is an abnormal ischemic alteration of the myocardium due to an inability of the coronary perfusion to
meet the myocardial contractile demand [5]. In 2012, the Joint Task Force of the European Society of Cardiology, American College of
Cardiology Foundation, the American Heart Association, and the World Health Federation (ESC/ACCF/AHA/WHF) redefined MI as
a rise and/or fall of cardiac biomarkers with at least 1 value above the 99th percentile of the upper reference limit together with evidence
of myocardial ischemia with at least 1 of the following [4]:
• Symptoms of myocardial ischemia
• Development of pathologic Q waves on electrocardiogram (ECG)
• New ST-T changes or new left bundle branch block (LBBB)
• Acute loss of viable myocardium or a new regional wall motion abnormality
• Identification of an intracoronary thrombus by angiography or autopsy
• Sudden, unexpected cardiac death with symptoms suggestive of myocardial ischemia and presumed new ST-segment elevation,
LBBB, and/or evidence of fresh thrombus by coronary angiography and/or autopsy.

Diagnosis
The preliminary evaluation of a patient suspected of an acute MI begins with a thorough clinical history and physical examination.
The diagnosis of a myocardial infarction relies heavily on clinical signs, symptoms, electrocardiogram changes, cardiac enzymes, and
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radiologic tests [2]. While algorithms may not always be standardized, a possible algorithmic approach to the diagnosis of MI in an
ICU setting may be used (Figure 1).

003
 Figure 1 Legend: USA= unstable angina; STEMI: ST-segment elevation MI; NSTEMI: non-ST-segment elevation MI; ECG: electrocardiogram;
cTN: cardiac troponin; DX: diagnosis

Figure 1: Diagnostic Algorithm of Acute Coronary Syndromes.

A. Clinical exam: On presentation the patient is likely to present with chest pain or discomfort posterior to the sternum that is not
relieved with rest or exacerbated by movement of the thoracic cage (i.e. when breathing deeply or coughing) [6-8]. Other symptoms
include fatigue, shortness of breath, dizziness, diaphoresis, dyspnea, nausea, vomiting and syncope (Table 1) [2,6-8]. Unfortunately,
patients in an ICU setting may not be able to communicate these symptoms. Furthermore, providers often relate these symptoms to
other non-cardiac causes, including iatrogenic causes (mechanical ventilation, endotracheal tube), sepsis, shock, etc. That said, a clinical
history and physical examination may not always be the best diagnostic modality for acute MI in an ICU setting.
Chest Pain:
Posterior to the sternum
Descriptors: Crushing/Burning/Squeezing
+ Absence of relief on exertion or rest
Often lasting >20 minutes
Radiating to left arm, jaw, neck, shoulder, epigastrum
Fatigue
Dyspnea
Vertigo
Diaphoresis
Syncope
Palpitations
Nausea
Vomiting

Table 1: Classic Signs and Symptoms of Acute Myocardial Infarction

B.Daily ECG Recording: Previous studies using once daily 12-lead ECGs show dissociations between ischemia and troponin
elevation in the ICU, more especially in patients with septic shock [9-11]. The sensitivity and specificity of diagnosing acute MI (AMI)
in an ICU setting is very low and thus, using this method alone is not advised.
C. Continuous 12-lead ECG Recording: This should be initiated within 10 min of presentation in order help to detect episodes of
ST-segment deviations or other signs of ischemia. The precise sensitivity and specificity for detecting acute MI using continuous 12-lead
ECH monitoring is unknown.
D. Serum Biomarkers: Initial measurement should be done at presentation followed by second reading 6-9 hours after AMI.
Cardiac troponin, or cTN, is the preferred test. As prolonged myocardial ischemia preceded troponin elevation, myocardial ischemia
with elevated troponin is directly related to short-term and long-term mortality, Acute Physiology and Chronic Health Evaluation
(APACHE)-II score, mechanical ventilation, length of stay, and vasopressor support [12]. Myocardial ischemia can be detected in up
to 37% of patients with elevated troponins, likely related to prolonged ventricular wall stress as a result of the critical illness. Sepsis
without myocardial ischemia can elevate cTNs, likely related to increased myocardial oxygen supply and/or demand, coronary blood
flow, myocardial lactate consumption, biventricular dilatation, coronary plaque rupture, and myocardial injury [13,14].
E. Echocardiography: Early echosonography of the heart can help assess the prevalence of cardiac abnormalities, including wall
motion defects and vegetations [15]. In turn, this can fasten therapeutic decision.
F. Angiography: Myocardial infarction cab be confirmed via angiographic loss of patency of a major or side branch coronary artery
+/- persistently slowed, or no, flow due to embolization. Angiography can also allow for detection of stent thrombosis associated with
MI.

Medical Management
Treatment for a myocardial infarction (MI) in ICU patients should be initiated early and individualized and geared towards the
underlying cause, if identified. While the recommended treatment algorithms for critically ill patients with STEMI, NSTEMI and
unstable angina in the ICU are similar in non-critically ill patients, there may be exceptions depending on the clinical situation (i.e.
renal failure, active bleeding, and hemodynamic instability). The goals for management of an ICU patient with AMI include analgesia,
hemodynamic stability, electrolyte control, fluid balance, anticoagulation and/or anti-thrombotic therapy. Acute coronary syndrome
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therapies, including beta-blockades and antiplatelets should be given cautiously in critically ill patients with AMI, depending on
hemodynamic stability, renal function, and hepatic function. As thrombocytopenia is often found in patients with sepsis, antiplatelet
agents may not always be feasible.
A. Oxygen: often aimed at a goal of O2 saturation >90% [16-18].
B. Fibrinolysis: A potential therapeutic agent used in STEMI patients. Pretreatment with antiplatelet agents (i.e. clopidogrel) is often
recommended [7]. 004
 C. Nitrates: Assuming the blood pressure can tolerate, nitroglycerin can be used for analgesia. Intravenous nitroglycerin is used for
pain that is not controlled by sublingual administration. Medications should be reviewed for phosphodiesterase inhibitors taken within
the preceding 24 hours [16-18].
D. Morphine: Morphine can be also used from chest pain or anxiety if nitrates have not given a satisfactory affect [16-18].
E. Beta-blockade: As patients with AMI or unstable angina often have tachycardia and elevated blood pressures, beta-blocking agents
can reduce heart rate, blood pressure and the workload of the heart. In turn, this can reduce myocardial oxygen consumption. Beta-
blockers also reduce the risk of MI recurrence [19].
F. Statins: A lipid panel should be taken and, if possible, statin therapy started while tended for in the ICU. Follow-up lipid panels
should be postponed for 2 months following discharge, as MI alone can reduce LDL levels [16-18].
G. Antiplatelet: Aspirin in combination with glycoprotein IIb/IIIa inhibitors is recommended. In patients mechanically ventilated,
aspirin can be crushed and administered via gastric tube [20].
H. Anticoagulant: Unfractionated heparin with reperfusion therapy can reduce mortality [16-18] Anticoagulation therapy with
prasugrel and ticagrelor are currently preferred over clopidogrel [21].
I. Anti-arrhythmic Agents: Lidocaine is discouraged in acute MI. Rapid correction of electrolytes, particularly potassium and
magnesium, may help in acute MI with arrhythmia [16-18].
J. Hypothermia: There is promising evidence supporting induced hypothermia to reduce the extent of cardiomyocytes damage and
improve patient outcome while the cause of a ST-segment elevated myocardial infarction (STEMI) is determined [20, 22].

Percutaneous Coronary Intervention

Although early detection and rapid intervention of myocardial infarction can lead to fewer adverse cardiac effects and reduced
mortality, the identification of acute coronary syndrome in an ICU setting may be challenging. Not only are the patients critically ill from
concomitant conditions (i.e. sepsis, respiratory failure), but also 34% of patients in an ICU setting have elevated cardiac enzymes [23].
Regardless of whether a patient is critically ill in an ICU or clinically stable on a hospital ward when acute coronary syndrome is identified,
early invasive strategies continues to have more favorable outcomes compared to conservative methods in patients with ST-segment
elevation myocardial infarction (STEMI), non-ST-segment myocardial infarction (NSTEMI), and unstable angina [21-25]. Furthermore,
coronary angiography is favored to fibrinolytic therapy in other instances that may cause ST-segment elevations (i.e. pericarditis) [26].
An average of 500,000 percutaneous coronary interventions (PCI) are performed annually in the US averages [27]. However, critically
ill patients are often at high risk for adverse outcomes related to coronary angiography. High risk patients include those with ongoing
chest pain >20 minutes, ST depression ≥ 1mm in ≥ 2 leads, recent PCI in the past 6 months or prior coronary artery bypass grafting
(CABG), heart failure, sustained ventricular tachycardia, hemodynamic instability, elevated cardiac enzymes, LVEF <40%, and/or diabetes
mellitus [28]. Low risk patients are those with negative troponins, non-diagnostic EKGs, and lack ongoing chest pain. While STEMI
often necessitates immediate PCI, low-risk patients with unstable angina or NSTEMI may be treated medically with aspirin, heparin,
antiplatelet agents (i.e. clopidogrel), beta-blockers, statins and nitrates. Some of these agents may need to be avoided in patients with
contraindications, including hemodynamic compromise, bleeding disorders, and coagulopathy. If acute coronary symptoms continue in
these low risk patients, coronary angiography is then warranted within 12-14 hours. Depending on the angiographic findings, the patient
can then be treated with medical therapy, PCI (followed by glycoprotein IIb/IIIa inhibitors), or CABG.

References
1. Go AS, Mozaffarian D, Roger VL, Benjamin EJ, Berry JD, et al. (2013) Executive summary: heart disease and stroke statistics--2013 update: a report
from the American Heart Association. Circulation 127: 143-152.

2. Boateng S, Sanborn T (2013) Acute myocardial infarction. Dis Mon 59: 83-96.

3. Gharacholou SM, Lopes RD, Alexander KP, Mehta RH, Stebbins AL, et al. (2011) Age and outcomes in ST-segment elevation myocardial infarction
treated with primary percutaneous coronary intervention: findings from the APEX-AMI trial. Arch Intern Med 171: 559-567.

4. Ammann P, Maggiorini M, Bertel O, Haenseler E, Joller-Jemelka HI, et al. (2003) Troponin as a risk factor for mortality in critically ill patients without
acute coronary syndromes. J Am Coll Cardiol 41: 2004-2009.

5. Lim W, Qushmaq I, Cook DJ, Crowther MA, Heels-Ansdell D, et al. (2005) Elevated troponin and myocardial infarction in the intensive care unit: a
prospective study. Crit Care 9: R636-644.

6. Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, et al. (2012) Third universal definition of myocardial infarction. Circulation 126: 2020-
2035.

7. The Joint European Society of Cardiology/American College of Cardiology Committee (2000) Myocardial infarction redefined- A consensus document
of the Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. European Heart
Journal 21: 1502-1513.

8. Sabatine MS (2011) Pocket medicine. The Massachusetts General Hospital Handbook of Internal Medicine (4thedn).

9. Guest TM, Ramanathan AV, Tuteur PG, Schechtman KB, Ladenson JH, et al. (1995) Myocardial injury in critically ill patients. A frequently unrecognized
complication. JAMA 273: 1945-1949.

10. Spies C, Haude V, Fitzner R, Schröder K, Overbeck M, et al. (1998) Serum cardiac troponin T as a prognostic marker in early sepsis. Chest 113:
1055-1063.
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11. Turner A, Tsamitros M, Bellomo R (1999) Myocardial cell injury in septic shock. Crit Care Med 27: 1775-1780.

12. Landesberg G, Vesselov Y, Einav S, Goodman S, Sprung CL, et al. (2005) Myocardial ischemia, cardiac troponin, and long-term survival of high-
cardiac risk critically ill intensive care unit patients. Crit Care Med 33: 1281-1287.

13. Parker MM, Shelhamer JH, Bacharach SL, Green MV, Natanson C, et al. (1984) Profound but reversible myocardial depression in patients with septic
shock. Ann Intern Med 100: 483-490.

14. Turner A, Tsamitros M, Bellomo R (1999) Myocardial cell injury in septic shock. Crit Care Med 27: 1775-1780.
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15. Blanc P, Boussuges A, Souk-aloun J, Gaüzere BA, Sainty JM (1997) Echocardiography on HIV patients admitted to the ICU. Intensive Care Med
23: 1279-1281.

16. Braell JA, Aroesty JA, Simons M (2013) Overview of the acute management of unstable angina and non-ST elevation myocardial infarction. In:
UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA.

17. Hochman JS (2013) Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction. In: UpToDate, Basow, DS (Ed),
UpToDate, Waltham, MA.

18. Reeder GS, Kennedy HL, Rosenson RS (2013) Overview of the acute management of ST elevation myocardial infarction. In: UpToDate, Basow, DS
(Ed), UpToDate, Waltham, MA.

19. Yang EH (2008) ST-segment elevation myocardial infarction. In: Fuster V et al., eds., Hurst’s The Heart, (12thedn), 1375-14040. New York: McGraw-
Hill Medical.

20. Roe MT, Messenger JC, Weintraub WS, Cannon CP, Fonarow GC, et al. (2010) Treatments, trends, and outcomes of acute myocardial infarction
and percutaneous coronary intervention. J Am Coll Cardiol 56: 254-263.

21. Birkmeier S, Thiele H, Dörr R (2013) Management of acute myocardial infarction with ST-segment elevation : Update 2013. Herz .

22. Schwartz BG, Kloner RA, Thomas JL, Bui Q, Mayeda GS, et al. (2012) Therapeutic hypothermia for acute myocardial infarction and cardiac arrest.
Am J Cardiol 110: 461-466.

23. Webb I, Coutts J (2008) Myocardial infarction on the ICU: can we do better? Crit Care 12: 129.

24. Jneid H, Anderson JL, Wright RS, Adams CD, Bridges CR, et al. (2012) ACCF/AHA focused update of the guideline for the management of patients
with unstable angina/Non-ST-elevation myocardial infarction (updating the 2007 guideline and replacing the 2011 focused update): a report of the
American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. Aug 14: 126(7): 875-910.

25. Zijlstra F, Patel A, Jones M, Grines CL, Ellis S, et al. (2002) Clinical characteristics and outcome of patients with early (<2 h), intermediate (2-4 h)
and late (>4 h) presentation treated by primary coronary angioplasty or thrombolytic therapy for acute myocardial infarction. Eur Heart J 23: 550-557.

26. Acute Coronary Syndromes and Acute Myocardial Infarction. Chapter 31: 589-646 In: Critical Care Medicine: Principles of diagnosis and management
in the adult, Third Edition. Ed: Parillo JE, Dellinger RP. Mosby Inc.

27. Marso SP, Teirstein PS, Kereiakes DJ, Moses J, Lasala J, et al. (2012) Percutaneous coronary intervention use in the United States: defining
measures of appropriateness. JACC Cardiovasc Interv 5: 229-235.

28. Albert RK, Slutksy AS, Ranieri VM, Takala J, Torres A (2006) Acute Coronary Syndrome. Chapter 30, 301-318. In: Clinical Critical Care Medicine,
First Edition.

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