Case 1

49-year-old man with acute onset of chest pain - Mr.

Monson
Author: L. James Nixon, M.D., Associate Professor, Department of Internal
Medicine and Pediatrics, University of Minnesota Medical School

Summary of clinical scenario: Mr. Monson is a 49 year-old man who presents

to the Emergency Department with a first episode of exertional substernal chest
discomfort that resolved following five minutes of rest. He has a 33 pack-year
history of smoking and a family history of early onset coronary artery disease in
his father. He is pain free now, and his exam reveals stable vital signs and no
other abnormalities. Initial lab tests are significant for a normal EKG and chest
xray, and negative troponins. He then redevelops chest pain and is found to have
an acute ST elevation MI.

Key Findings from History:

Substernal Chest Discomfort
Nausea
Dyspnea
Smokes 1 ppd
+Family Hx of Coronary Artery Disease
Exertional Onset

Key Findings from PE:

Elevated BP (148/89)
Normal HR
Normal oxygen saturation

Final diagnosis: Acute Myocardial Infarction

Key Teaching Points

Knowledge:
ACS: The American Heart Association defines Acute Coronary Syndrome (ACS) as

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 an umbrella term to cover any group of clinical symptoms compatible with acute
myocardial ischemia. This term therefore includes unstable angina as well as both
ST segment elevation and non ST segment elevation myocardial infarction (STEMI
and NSTEMI).

Acute MI: The current definition of acute MI per the American College of
Cardiology is the typical rise and fall of troponin or creatinine kinase myocardial
band (CK-MB) plus ONE of the following:

Symptoms consistent with myocardial ischemia

Electrocardiogram changes indicating myocardial ischemia (ST-segment
elevation or depression)
New pathologic Q waves
Findings on percutaneous coronary intervention (PCI).

In addition, she points out that any patient who presents with a clinical history
consistent with acute MI and has a new left-bundle branch block should be triaged
as STEMI.
Differentiating between unstable angina and NSTEMI is based on whether the
troponins increase, so determining whether a patient has unstable angina or
NSTEMI may require serial measurements of troponins. Remember, No troponin
increase = No MI.

Atypical Symptoms of ACS: Atypical symptoms are particularly common in

diabetics, women, and the elderly. The most common reason for failure to
diagnose ACS is to ignore noncardiac or atypical symptoms such as dyspnea,
fatigue, nausea, abdominal discomfort, or syncope. If a patient has these
symptoms, with or without chest discomfort, it’s important to remember only
about 25% of patients who come to the ED with an MI have the “classic” severe
substernal chest pressure.

Critical Pathway/Practice Guideline: Research has shown that the items on

the checklist seen in this case clearly benefit patients with suspected ACS. This
checklist ensures we don't overlook a simple, but highly effective, intervention like
aspirin. Standard order sets provide a systematic approach to optimal care. These
checklists also allow an outside organization to make sure that our hospital is
doing what it should and improves standardization across hospitals.

Angina: Angina is related to an imbalance between myocardial oxygen supply and

demand that is related to atherosclerotic plaque. Classic angina is retrosternal
chest pain that comes on with exertion and is relieved with rest or nitroglycerin.
Unstable angina is when the chest pain occurs at rest, is new, is increasing in
frequency, or when its onset is triggered with a lower level of exertion. An acute
MI on the other hand results from rupture of an unstable plaque with subsequent
occlusive coronary artery thrombosis and myocardial necrosis. Stable angina is
thought to be caused by a stable atherosclerotic plaque, while unstable angina is
caused by an unstable plaque that has ruptured and caused a non-occlusive
thrombus.

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 EKG Findings: All patients presenting with chest pain should have an EKG done
immediately to look for ST segment abnormalities that indicate myocardial injury.
ST segment elevations are present in a STEMI; in a NSTEMI, ST segment
depressions may occur or the ST segments may be normal. It is important to
recognize the initial EKG may be non-diagnostic in half of patients. For this
reason, serial EKGs are recommended in patients suspected of angina, unstable
angina, or MI. An EKG's ability to diagnose Acute Myocardial Infarction (AMI) is
greater if performed during an episode of chest pain. In patients with ST elevation
on the EKG, do not delay further management while awaiting laboratory results.

A normal EKG in the presence of chest pain should not really change your opinion
about unstable angina, and really only suggests that he has not had an MI in the
past.

Echocardiography: Echocardiography is commonly used for risk stratification

since the left ventricular ejection fraction is a major predictor of long-term
prognosis after both ST elevation and non-ST elevation infarctions.
Echocardiography may also detect other complications of myocardial infarction
including aneurysm, thrombus, rupture, VSD, papillary muscle rupture, Mitral
regurgitation, Right Ventricular infarct and pericardial effusion.

Cardiac Monitoring/Arrhythmias: Continuous cardiac monitoring is indicated to

detect tachyarrhythmias and bradyarrhythmias that may occur in the setting of an
acute MI.
Sustained ventricular tachyarrhythmias in the peri-infarction period must be
treated immediately because of their negative effect on cardiac output and
possible exacerbation of myocardial ischemia. Additionally, they may lead to a
V-Fib arrest.

Supraventricular tachyarrhythmias may pose less immediate risk of cardiac arrest,

but they can increase myocardial oxygen demand exacerbating ischemia and
decreasing cardiac output.
Bradyarrhythmias early in the setting of an inferior wall MI (first 24 hours) may
respond to atropine treatment. Later or wide QRS-complex bradyarrhythmias as
well as bradyarrhythmias in the setting of an anterior wall MI usually require
placement of a temporary pacemaker.

Skills:
History-taking:

In all patients with suspected Acute Coronary Syndrome (ACS), you should
determine if there are associated symptoms like nausea, diaphoresis, and
shortness of breath. Be sure to ask about cardiac risk factors such as smoking,
hypertension, dyslipidemia (elevated LDL or total cholesterol or low HDL
cholesterol), diabetes, and previously documented coronary artery disease as well
as a family history of CAD.

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 Often the objective in characterizing chest pain is to distinguish ischemic from
non-ischemic pain. Symptoms of angina or MI may be difficult for patients to
describe, but some features are more characteristic of ischemia than others.

Substernal chest discomfort that began with exertion along with the associated
nausea and dyspnea are characteristic findings suggestive of a cardiac origin for
the chest pain. Smoking and a positive family history are risk factors for
developing coronary artery disease and thus increase his prior probability of
having angina. When interviewing this patient, much of your initial history has
been geared toward better characterizing the patient’s chest pain and then
determining what his risk factors are for coronary artery disease as well as other
diagnoses you may be considering. It is useful to have a mnemonic for recalling
the typical questions you want to know about symptoms in general. An example of
such a mnemonic is LAQ CODIERS.

Location (Where is the chest pain?)

Associated symptoms (nausea? diaphoresis? dyspnea? radiation? fever?
cough?)
Quality (pressure? dull? sharp? burning?)
Chronology (Since onset, is it getting better or worse? Has it changed in
position or character?)
Onset (What were you doing when it started? Any idea why it started when
it did?)
Duration (Does it come and go? How long does it last when present?)
Intensity (Compared to worst pain you’ve ever had, how bad is this pain on
a scale from 1-10?)
Exacerbating (Anything make it worse? What happens if you . . .?)
Relieving (Anything make it better? Have you tried anything? What do you
do when you get this symptom?
Situation (Where or when does it usually occur? What were you doing the
first time you noticed it?)

After you have better characterized the symptoms you should try to determine
risk factors for your primary and secondary diagnoses.

Physical exam:

The physical exam can be helpful in making a diagnosis of acute MI. First, check
the vital signs--tachycardia or hypertension can be found with acute MI because of
increased circulating levels of catecholamines. There are cardiac exam findings
that may be suggestive for MI. A new murmur may be caused by papillary muscle
rupture or dysfunction. An S3 or S4 may be heard as a result of damage
associated with heart failure or decreased diastolic relaxation.

The exam can also be useful to support or refute alternate explanations for the
patient’s symptoms. For instance:

Pericardial rub on initial presentation suggests pericarditis.

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 Lung crackles alone suggest heart failure, while the combination of fever,
crackles, and decreased breath sounds is suspicious for pneumonia.
Unilateral leg swelling hints at DVT/PE.
RUQ tenderness can be seen with acute cholecystitis.
Patients with GERD may have epigastric discomfort on palpation.
Chest wall tenderness is noted in patients with trauma, costochondritis, and
other muscular causes of chest pain. Be careful, however--patients with ACS
may also report chest wall tenderness.

Differential Diagnosis:

A useful way to organize your initial differential is to ask yourself,

1. “What do I think is most likely at this point based on what I know so far,
and why is that most likely?”
2. “What are the possible diagnoses based on what I know so far that I can’t
miss because the outcome would be really bad if I did?”
3. “What are the other diagnoses that remain on the list based on the story
so far?”

These are the diagnoses that you will come back to if your initial workup doesn’t
pan out as you expect.

Each of these categories is important considering each will decrease the likelihood
you miss something important or prematurely latch onto a diagnosis at the
exclusion of other potential explanations for a patient’s symptoms.

In this case, we initially have a rather broad list of explanations for this patient's
symptoms, but little history and no exam or labs. We do know, however, that he is
a male in his late 40's with substernal chest pain that began with exertion. This
history alone puts his pretest probability for coronary artery disease at over 90%.

When you initially encounter a patient with chest pain, you should have a rather
large list in mind its potential causes. Obtain your history, exam, and subsequent
lab tests with the goal of narrowing the differential while considering typical and
atypical presentations for these chest pain causes:

Cardiac causes:

Stable angina
Unstable angina
Acute MI
Atypical or variant angina (coronary vasospasm, Prinzmetal angina)
Cocaine-induced chest pain
Pericarditis
Aortic dissection: tearing chest pain radiating to back
Valvular heart disease, i.e., critical aortic stenosis

Gastrointestinal disorders:

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 Esophageal disease (GERD, esophagitis, esophageal dysmotility)
Biliary disease (cholecystitis, cholangitis): typically RUQ with radiation to
shoulder, may be referred to chest
Peptic ulcer disease
Pancreatitis

Pulmonary disorders:

Pneumonia
Spontaneous pneumothorax
Pleurisy
Pulmonary embolism
Pulmonary hypertension/cor pulmonale

Musculoskeletal causes:

Costochondritis
Rib fracture
Myofascial pain syndromes
Muscular strain
Herpes zoster

Psychogenic causes:

Panic disorders
Hyperventilation
Somatoform disorders

Laboratory interpretation:

Serum biomarkers of myocardial necrosis (i.e. Troponins, CK-MB) are elevated in

MI and indicate death of cardiac myocytes. If initial markers are normal, repeat
these measurements at 6 and 12 hours. Cardiac troponins are highly sensitive and
specific for an MI within the last 24 hours. They will be elevated in both STEMI
and NSTEMI.

Communication:

The patient in this case should improve his diet and stop smoking. Since he
expressed some interest in stopping smoking, you have him enrolled in your
hospital's smoking cessation program and give him the link to the American Heart
Association's smoking cessation resources:

http://www.americanheart.org/presenter.jhtml?identifier=3019598

There is no reason to not return to a normal sex life immediately.

Management:
Aspirin should be given to all patients suspected of an acute coronary syndrome

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 without contraindication. Aspirin reduces the risk of myocardial infarction (MI) in
unstable angina and reduces mortality in patients with an MI by reversibly
inhibiting thromboxane A2. Patients should receive 160-325 mg on arrival and
continue daily aspirin at 81 mg per day. Clopidogrel can be given to those with
aspirin allergy.

All patients with chest pain and possible MI should receive supplemental oxygen
as it may help diminish myocardial ischemia.

With active pain, nitrates are given by sublingual administration followed by

intravenous infusion (unless it causes hypotension, which can compromise
coronary perfusion pressure).

Early intravenous administration of beta blockers is used to reduce myocardial

oxygen demand by decreasing heart rate, blood pressure, and cardiac
contractility. They should be used carefully in those with severely decreased LV
function. Avoid pindolol and other beta blockers with intrinsic sympathomimetic
activity. Beta blockers reduce infarct size and the frequency of myocardial
ischemia. They also improve short- and long-term survival. Beta blockers are
effective because they decrease myocardial oxygen demand by reducing heart
rate, blood pressure, and myocardial contractility. The prolonged diastole may also
help to augment myocardial perfusion, which occurs mainly during diastole.

Begin with oral
-blockers within a few days of the event, if not begun acutely,
and continue them indefinitely. Goal heart rate is <70 and blood pressure
<130/80.

Anticoagulation therapy with either subcutaneous low molecular weight heparin or

intravenous unfractionated heparin should be added to antiplatelet therapy in
patients with likely or definite acute unstable angina.

Patients with a non-ST elevation acute coronary syndrome who meet intermediate
or high-risk criteria benefit from an early angiography and percutaneous coronary
intervention (PCI). A widely used predictive model is the TIMI risk score.

A fasting lipid profile should be obtained within 24 hours of hospitalization and

statin therapy should then be instituted prior to hospital discharge if indicated.
HMG CoA reductase inhibitors (statins) should be started while in the hospital in
patients with ACS with a target LDL of <100.

Short-term acute use of ACE inhibitors does not seem to add significant benefit in
unstable angina therapy, although later chronic therapy is indicated. That stated,
ACE inhibitors should be started within the first 24 hours of acute MI with
ST-segment elevation in 2 anterior precordial leads or in those with clinical heart
failure in the absence of hypotension (systolic BP < 100 mm Hg) if there are no
contraindications to an ACE inhibitor.

The coronary arteries can be directly visualized in the cath lab and stenotic
vessels can be dilated, thus relieveing ischemia. Urgency is critical as you want to

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 prevent further myocardial damage. Immediate diagnostic coronary angiography
should be considered in patients with chest pain and STEMI (like Mr. Monson) or
new Left Bundle Branch Block (LBBB) with the goal of angioplasty within 90
minutes (Joint Commission Guidelines).

It is essential to restore normal blood flow in the infarct-related artery ASAP in

order to save myocardium and improve survival in patients with an STEMI. The
chance for salvaging significant myocardium is greatest in the first few hours after
symptom onset, so a decision must be made immediately as to whether
reperfusion will be achieved with angioplasty (also known as primary
percutaneous coronary intervention (PCI)) vs. fibrinolytic therapy. Primary PCI is
preferred when performed in a timely manner by an expert operator; however,
when a patient presents to a hospital without PCI capability, the choices becomes
transfering the patient to a hospital with primary PCI capability or performing
fibrinolytic therapy at the place of presentation. Hospitals should have a protocol
outlining which is the best approach considering time from presentation to therapy
and expected outcomes.

Thrombolytic agents, such as Tissue Plasminogen Activator (tPA), activate

plasminogen with lysis of fibrin (and fibrinogen), resulting in in rapid lysis of clot
with reperfusion of the infarct-related territory and improving survival.
Thrombolytics are indicated in patients with acute STEMI or new LBBB MI when
primary PCI is not performed. The major complications associated with these
agents are bleeding and hemorrhagic stroke.

The absolute contraindications for thrombolytic therapy include:

Strong suspicion of dissection of the aorta

Pericardial effusion
Active gastrointestinal or other internal bleeding
Brain tumor, arteriovenous malformation, or aneurysm
Ischemic stroke in preceding 6 months (a verified transient ischemic attack
(TIA) is an exception)
Previous intracerebral hemorrhage or subarachnoid hemorrhage
Intracranial procedure or recent head trauma
Severe known bleeding disorder: coagulation abnormality,
thrombocytopenia, etc.

The decision about coronary artery bypass graft (CABG) versus angioplasty is
often complex. Percutaneous transluminal angioplasty (PTCA) with or without
stenting produces a similar survival rate to CABG but is associated with a higher
rate of recurrent symptoms and target vessel revascularization, although this may
be changing with the use of drug-eluting stents. CABG may be preferred in left
main lesions or in complex proximal LAD disease with other unfavorable lesions or
in patients with left ventricular dysfunction or diabetes mellitus.

GP IIa/IIIb antibodies and receptor antagonists are potent inhibitors of platelet

aggregation. In addition they may prevent platelet adhesion to the vessel wall.

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 These agents increase the risk of bleeding compared to placebo especially when
used in combination with fibrinolytics. Thromocytopenia can also result within 24
hours of initiating therapy. A meta-analysis of randomized trials looking at the
adjunctive use of abciximab for STEMI showed a significant reduction in thirty day
and long term mortality in patients treated with angioplasty but not in those
receiving fibrinolysis. Thirty-day reinfarction rate was significantly reduced in both
groups.

Sublingual nitroglycerin should be sent home with patients post-admission.

Clopidogrel is given in addition to aspirin in all patients undergoing coronary

artery stenting to reduce the risk of stent thrombosis. According to the 2007
ACC/AHA/SCAI focused update, clopidogrel therapy (in addition to aspirin) should
be continued for at least one month after bare metal stent implantation and if
possible up to one year. In patients with drug eluting stents who are not at
increased risk of bleeding, clopidogrel 75 mg daily is recommended for at least
one year (the efficacy of continuation beyond one year is not well established).

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