Chest Pain Case File

Chest Pain Case File

Eugene C. Toy MD, Donald Briscoe, MD, FA  AFP, Bruce Britton, MD, Joel J. Heidelbaugh, MD, FA  AFP, FACG

Case 20

A 56-year-old man is brought to the emergency department (ED) complaining of chest discomfort for about 90 minutes. He has had occasional symptoms for a month, but it is worse today. Today's symptoms began while he was walking his dog and decreased slightly with rest, but have not resolved. He describes the feeling as a pressure sensation in the left substernal area of his chest associated with shortness of breath and mild diaphoresis. He does not have any radiation of the discomfort today, but has experienced radiation to the left upper extremity in the past. The patient denies any health problems, but his wife reports that he has not seen a physician in years. His wife made him come in because his younger brother had a heart attack 6 months ago. He is a vice president of a bank and lives with his wife and three daughters. He has smoked 1½ pack of cigarettes per day for more than 30 years and denies drinking alcohol or any drug use.

On physical examination he is an anxious, obese gentleman who appears pale and has a moist brow. His temperature is 98.8°F (37. 1°C), his pulse is 105 beats/min, his respirations is 18 breaths/min, his blood pressure is 190/95 mm Hg, his height is 74 in, and his weight is 250 lb. Cardiac examination reveals regular rhythm without murmur, but he has an S4 gallop. Lungs are clear to auscultation. Neck is without carotid bruits or jugular venous distension. Abdomen is normal. He does have a right femoral bruit. Extremities reveal trace edema but no clubbing or cyanosis. He has 2+ pulses in radial and dorsal pedalis arteries. Rectal examination has no masses or tenderness with a normal prostate, and is guaiac negative.

⯈ What is your most likely diagnosis?

⯈ What is your next diagnostic step?

⯈ What is the next step in therapy?

ANSWER TO CASE 20:

Chest Pain

Summary: A 56-year-old obese man presents to the ED with chest discomfort. He has a pressure sensation in the left substernal area of his chest associated with shortness of breath and diaphoresis. His symptoms began with minimal exertion. The patient is without prior medical care. He has a family history of coronary artery disease (CAD) and a history of tobacco abuse. He is hypertensive and tachycardic. He has a cardiac gallop. Lower extremities have trace edema and a femoral bruit.

• Most likely diagnosis: Unstable angina pectoris; must rule out myocardial infarction (MI)

• Next diagnostic step:

Initial studies in the emergency room: complete blood count (CBC), electrolytes, blood urea nitrogen (BUN), creatinine, prothrombin time (PT), partial thromboplastin time (PTT), international normalized ratio (INR), glucose, 12-lead electrocardiography (ECG), and chest x-ray (CXR); markers of myocardial damage including creatine kinase (CK) and MB isoenzyme (CK-MB), troponin T and troponin I to be done STAT and every 6 to 10 hours for three cycles; oxygen saturation must be monitored, as well

Studies that can be performed later: fasting lipids, liver function tests, magnesium, homocysteine level, urine drug screen, urinalysis, and myoglobin

• Next step in therapy: MONA therapy: Morphine, Oxygen, Nitroglycerin, Aspirin

Morphine can achieve adequate analgesia which decreases levels of circulating catecholamines, thus reducing myocardial oxygen consumption. It must be initiated rapidly if nitroglycerin cannot alleviate the discomfort.

Oxygen 2 to 4 L/ min by nasal cannula; may be discontinued after 6 hours if oxygen saturation remains normal without other complications.

Nitroglycerin must be given sublingually initially every 5 minutes for a total of three doses (in the absence of hypotension or contraindications such as sildenafil [Viagra] use), then advanced to IV or transdermal routes.

Aspirin 325 mg should be chewed and swallowed (clopidogrel may be used if allergy to aspirin exists).

β-Adrenergic antagonist reduces myocardial damage and may limit infarct size.

Glycoprotein (GP) IIb/IIIa inhibitors reduce end point of death or recurrent ischemia when given in addition to standard therapy for patients with highrisk unstable angina or non-ST-elevation MI treated with percutaneous coronary intervention, or who are refractory to prior treatment.

ANALYSIS

Objectives

1. Understand a diagnostic approach to chest pain and how to reduce potential damage to myocardium by implementing rapid evaluation.
2. Know the acute evaluation of chest pain and how to best implement the primary and secondary treatment of chest pain.
3. Identify the risks and the need to educate patients to reduce their risks.
4. Be familiar with the differential diagnosis of chest pain and how to best rule in and out the more life-threatening problems.

Considerations

This 56-year-old man has unstable angina with a variety of risk factors for CAD. All patients who present to primary care physicians with chest pain are immediate challenges. Most resources emphasize the life-threatening etiologies; however, the non-life-threatening etiologies are far more common in presentation. Physicians must master a cost-effective approach to diagnosing the various etiologies of chest pain, determining which patients warrant further evaluation, putting a large emphasis on thorough history and physical examination. The cause of this patient's symptoms must be determined as soon as possible. If the etiology is determined to be cardiac, there are medications and interventions that can dramatically reduce both morbidity and mortality. A complete history and physical examination can give information that can guide if and when other more expensive and invasive tests are necessary. The patient's most immediate problem is his acute symptoms. His anxiety will decrease slightly when he perceives that he is getting adequate care and information.

Nearly 1½ million people in the United States experience an MI each year. This is fatal approximately one-third of the time. However, there has been a continuous decline in the mortality rate over the past three decades because of a better understanding of the etiology and pathophysiology of MI, and because of advances in therapeutic treatments.

The first priority is to obtain ECG and CXR, while giving medications to decrease the damage caused to his myocardium and simultaneously reducing his blood pressure. Nitroglycerin and β-adrenergic antagonists will begin achieving these goals. He will need constant monitoring and continuous telemetry. Oxygen needs to be continued as well. Before the ECG and CXR have been completed, aspirin, oxygen, nitroglycerin, morphine, and β-adrenergic antagonist should be given. The providers must assume cardiac etiology until it has been effectively ruled out to limit possible morbidity and mortality to the patient.

The laboratory tests previously listed need to be drawn, at which time IV access can be started in two places. The results of the tests will determine if the patient has other risk factors in addition to his known hypertension, family history of CAD, tobacco abuse, and obesity. If he routinely walks his dog, his lifestyle contains at least minimal physical activity.

The changes seen in an ECG that are indicative of angina include ST-segment elevation or depression and/ or T-wave inversion. MIs include these changes plus elevated CK-MB and/ or troponin levels. Pathologic Q waves may also indicate cardiac pathology, but typically represent myocardial tissue necrosis from a completed infarction. When Q waves are present, the benefits of thrombolytic therapy are uncertain. Not all MIs will have ECG changes. A normal ECG reduces the likelihood of MI but does not rule out cardiac pathology. Any person with symptoms of angina who has a left bundle branch block (LBBB) on ECG must have serum cardiac enzymes drawn, because there is a high degree of correlation between LBBB and organic heart disease, especially CAD. LBBB can mask signs of myocardial pathology, as it can mimic both acute and chronic ischemic changes. All of the listed ECG changes have a differential diagnosis that includes MI. The clinical picture is of utmost importance, again demonstrating the need for complete history and physical examination.

Approach To:

Chest Pain

DEFINITIONS

ANGINA PECTORIS: Severe pain around the heart caused by a relative deficiency of oxygen supply to the heart muscle.

MYOCARDIAL INFARCTION: Cardiac muscle death caused by partial or complete occlusion of one or more of the coronary arteries.

NEW YORK HEART ASSOCIATION FUNCTIONAL CLASSIFICATION OF ANGINA:

Class I-Angina only with unusually strenuous activity

Class II-Angina with slightly more prolonged or slightly more vigorous activity than usual

Class III-Angina with usual daily activity

Class IV-Angina at rest

UNSTABLE ANGINA: Angina of new onset, angina at rest or with minimal exertion, or a crescendo pattern of angina with episodes of increasing frequency, severity, or duration.

CLINICAL APPROACH

Etiologies

Atherosclerosis leading to plaque rupture and then cascading to coronary artery thrombosis is the cause of an acute MI approximately 90% of the time, but many different conditions can be the culprit for angina. Coronary artery spasm, including cocaine-induced injury, can cause angina. Aortic dissection extending into a coronary artery will cause extensive damage. An embolus to a coronary artery can be caused by endocarditis, prosthetic heart valves, or myxoma. Embolism can also cause cerebral vascular accidents, increasing the extent of the initial evaluation that is warranted.

Chest pain or discomfort is one of the most common complaints in both the outpatient and emergency setting. Assessing the cause of such symptoms in a rapid fashion is of utmost importance. If the patient is experiencing myocardial ischemia or infarction, time is myocardium. Initial evaluation should be done within 10 minutes of presentation and the goal of this evaluation should be to determine the need for further testing such as cardiac enzymes, stress test, or angiography. Ischemic heart disease remains the leading cause of morbidity and mortality in the United States. It is important to identify risk factors for coronary artery disease in patients, the presence of which would indicate an increased suspicion for an acute MI. Male gender, age older than 60 years, diaphoresis, radiation of pain to neck, arm, shoulder, or jaw, and a past history of angina or acute MI are all considered risk factors.

TREATMENT

Primary Treatment

All patients who rule in for MI should receive aspirin and an antithrombotic treatment, if there are no contraindications. Aspirin and heparin reduce the risk of subsequent MI and cardiac death in patients with unstable angina. Studies present different recommendations for using clopidogrel in addition to aspirin and heparin. Current American College of Cardiology I American Heart Association recommendations advise withholding clopidogrel for 5 to 7 days before planned bypass surgery. It is reasonable to give clopidogrel 300 mg orally to patients with suspected acute coronary syndrome (ACS) (without ECG or cardiac marker changes) who are either allergic to or have gastrointestinal intolerance of aspirin.

Heparin usually should be continued for 48 hours or until angiography is performed. Patients suffering from unstable angina with ECG changes should also be given platelet glycoprotein IIb/IIIa receptor inhibitors because the composite risk of death, MI, and recurrent ischemia is significantly reduced with these medications.

Nitroglycerin is best given IV initially because of the ability to achieve predictable blood levels rapidly. Once stabilized after 24 hours, the asymptomatic patient should be switched to a long-acting oral or transdermal nitrate. A β-adrenergic antagonist should also be given, unless contraindicated. The combination of nitroglycerin and β-adrenergic antagonist reduces the risk of subsequent MI. β-Adrenergic antagonists decreased mortality and reduced infarct size in many clinical trials.

Angiotensin-converting enzyme (ACE) inhibitors reduce short-term mortality when started within 24 hours of acute MI. Postinfarction ACE inhibitors prevent left ventricular remodeling and recurrent ischemic events. It is reasonable to recommend their indefinite use in the absence of any contraindications. All trials with oral ACE inhibitors have shown benefit from their early use, including those in which early entry criteria included clinical suspicion of acute infarctions. Magnesium sulfate should be given if levels are low, as hypomagnesemia can increase the incidence of torsade de pointes-type ventricular tachycardia.

Despite the widespread use of calcium channel blockers both during and after myocardial ischemia, no evidence exists supporting any benefit when taking these medications. Rapid release, short-acting dihydropyridines (eg, nifedipine) are contraindicated because they increased mortality in multiple trials.

Patients who are asymptomatic after 48 hours of drug therapy can perform a modified Bruce protocol stress test. Patients who have a markedly positive stress test should be referred for angiography. There is some debate concerning when angiography should be done. One approach shows that an early invasive approach with angiography within 24 to 48 hours is beneficial, whereas others recommend a more conservative approach, doing angiography only if recurrent ischemia is present or a stress test was positive. There is no clear consensus as to which approach is superior.

All patients admitted for angina or MI should receive a reduced saturated fat and cholesterol diet. These patients may benefit from nutrition counselors to help them develop healthy lifestyle changes.

Secondary Treatment

Primary prevention of CAD must be encouraged for all patients. Risk factors for CAD include diabetes mellitus, dyslipidemia, age, hypertension, tobacco abuse, family history of premature CAD, male gender, postmenopausal status, left ventricular hypertrophy, and homocystinemia (Table 20-1). Modification of these risk factors has a direct link to reduce morbidity and mortality. Patient education is particularly important.

Aspirin, nitrates, and β-adrenergic antagonist have proven benefits for both primary and secondary treatment. Prolonged treatment with aspirin reduces risks for

Abbreviations: CAD, coronary artery disease; HDL, high-density lipoprotein; LDL, low-density lipoprotein; Ml, myocardial

infarction; TC, total cholesterol; TG, triglyceride.

both CAD and cerebrovascular disease. β-Adrenergic antagonist reduces firstyear mortality. If no adverse effects are experienced, patients should continue β-adrenergic antagonist 2 to 3 years or longer. Long-acting nitrates can treat angina symptoms.

β-Hydroxy-β-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) have documented a consistent decrease in the incidence of major adverse cardiovascular events when given within a few days after onset of ACS. There are few data on patients treated within 24 hours of the onset of symptoms. It is safe and feasible to start statin therapy early (within 24 hours) in patients; once started, continue statin therapy uninterrupted. The American College of Cardiology/ American Heart Association recommendations are for all persons with known atherosclerotic cardiovascular disease (ASCVD) to be treated with high-intensity statin therapy.

Hypertension must be treated using agents that reduce cardiac complications, as previously discussed. If further reduction is necessary, many medications treat hypertension and angina. Blood pressure and coronary pathology have a linear relationship; as blood pressure is reduced, the risk, morbidity, and mortality of cardiac disease are also reduced. Agents used often depend on a patient's comorbid conditions.

Physical activity is an important component of lifestyle change. Recommendation of a minimum goal of 30 minutes of exercise on most days should be given to all patients. Weight management is also encouraged, but often requires numerous interventions. A minimum of a 5% reduction in weight will provide benefits to the patient. Body mass index needs to become part of the vital signs examined every visit.

CLINICAL PRESENTATION

The history should focus on onset and evolution of the chest pain. The cardinal features of all chief complaints should be followed, paying attention to patient's description of the pain/ discomfort, location, radiation of pain, quality of pain, severity of pain, duration, associating factors, and aggravating and/ or alleviating factors (Table 20-2). Many people do not describe angina as chest pain. It is more effective to ask the patient to describe the discomfort. Some describe it as pressure, squeezing, crushing, or smothering. Some may use a "Levine sign;' a fist held firmlyagainst the chest. The discomfort is usually central and substernal. It may radiate to the jaw, shoulder, arm, or hand, usually to the left side. Cardiogenic nausea and vomiting are associated with larger MIs.

The relationship of the symptoms to exertion is very important. Exertion, emotional

stress, or other situations that either increase myocardial oxygen demand or

decrease oxygen supply can increase symptoms. Angina usually responds promptly to

measures that reduce myocardial oxygen demand, such as rest. Pain typically resolves

in less than 5 minutes. If angina persists for longer than 20 to 30 minutes, a MI is

more likely. In this setting, hospitalization and further evaluation are warranted.

The targeted history in patients with angina needs to ascertain whether the patient has had prior episodes of myocardial ischemia (stable or unstable angina, MI, interventions such as bypass surgery or angioplasty). Evaluation of the patient's complaints should focus on chest discomfort, associated symptoms, gender and

Abbreviations: ↓, decreasing; ↑, increasing; CAD, coronary artery disease; CT, computed tomography; CXR, chest x-ray; ECG, electrocardiogram; JVD, jugular venous distension; MI, myocardial infarction; MRI, magnetic resonance imaging; NTG, nitroglycerin; N/V, nausea and vomiting; PPI, proton pump inhibitor; SOB, shortness of breath; TEE, transesophageal echocardiogram.

age-related differences in presentation, hypertension, diabetes mellitus, possibility of aortic dissection, risk of bleeding, and clinical cerebrovascular disease (amaurosis fugax, face/limb weakness or clumsiness, face/limb numbness or sensory loss, ataxia, or vertigo).

The physical examination needs to concentrate on evidence that supports or disproves a diagnosis of cardiovascular disease. General appearance and vital signs can reveal much about the patient and the patient's stability. Hypertension, evidence of elevated lipids, changes consistent with diabetes mellitus, and signs of peripheral vascular disease all increase the risk of CAD.

Funduscopic examination can show signs of chronic hypertension or diabetes mellitus. All blood vessels must be auscultated for bruits, a direct sign of atherosclerotic disease. Diminished peripheral pulses are also a sign of atherosclerotic disease. Signs of heart failure include pulmonary edema, rales, jugular venous distension, and hepatojugular reflux. New gallops or murmurs can signal myocardial ischemia. Shallow, painful breathing suggests chest pain with a pleural cause. Asymmetric expansion of the chest with unilateral hyperresonance to percussion and diminished breath sounds are indicative of a possible pneumothorax.

The cardiac examination requires careful evaluation. Unequal carotid pulses or upper extremity pulses can indicate aortic dissection, but most patients with dissection will not have pulse deficit. The murmur of aortic stenosis can be significant, as aortic stenosis can present with angina, which can then lead to syncope and heart failure.

The patient's chest wall should be palpated. If this examination reproduces the chest pain, costochondritis becomes more likely. Musculoskeletal causes of chest pain are the most common etiology in an outpatient setting. Abdominal examination is also important, as gastrointestinal etiology is the second most common culprit for chest pain in an outpatient setting. Careful examination of both upper quadrants and epigastric area must be done. The abdominal aorta warrants careful examination. Additionally, panic disorder and anxiety can cause chest pain, tightness and shortness of breath. Physicians should use a questionnaire to evaluate any possible psychogenic causes when this is suspected.

COMPREHENSION QUESTIONS

20.1 A 58-year-old man presents to his physician for follow-up of his hypertension and hyperlipidemia. He also reports chest pain and feeling short of breath after climbing two flights of stairs or walking three to four blocks. The symptoms resolve after several minutes of rest. Which of the following drugs is contraindicated as a first-line agent in the treatment of this patient's new condition?

A. Labetalol

B. Nitroglycerin

C. Enalapril

D. Nifedipine

E. Aspirin

20.2 Which one of the following patients presenting with chest pain is at the highest risk for an acute myocardial infarction?

A. A 40-year-old woman on proton pump inhibitor for reflux disease

B. A 75-year-old man with parasternal chest pain, lipid abnormalities, and no past history or cardiac disease

C. A 23-year-old man recently diagnosed with hypertrophic cardiomyopathy

D. A 67 -year-old man with a history of a prior angioplasty, with chest pain radiating to the neck and complaint of diaphoresis

20.3 Which of the following ECG changes makes the determination of acute MI the most difficult?

A. Qwave

B. ST-segment elevation

C. Left bundle branch block

D. First-degree atrioventricular block

E. T-wave inversion

20.4 A 64-year-old woman with a history of hypertension and angina pectoris presents with chest pain for the last 3 hours. She describes the pain as "sharp;' it is worse when she inhales deeply, and it is not relieved by sublingual nitroglycerin. Her ECG shows ST elevation in most leads. Which of the following is the most likely diagnosis in this patient?

A. Unstable angina pectoris

B. Myocardial infarction

C. Aortic dissection

D. Congestive heart failure

E. Pericarditis

ANSWERS

20.1 D. This patient has new onset of angina. Rapid release, short-acting dihydropyridines (nifedipine) are contraindicated because they increased mortality in multiple trials. β-Blocking agents are the agents of choice since they increase survival; nitroglycerin helps to abate chest pain, but has not been shown to impact survival.

20.2 D. Risk factors for increased likelihood of acute MI are male gender, age older than 60 years, chest pain radiating to neck, jaw, arm, or shoulder, and a prior history of angina or acute MI.

20.3 C. The changes of left bundle branch block make the determination of an acute MI by an ECG extremely difficult. In these patients, it is particularly important to obtain serum markers of myocardial damage.

20.4 E. This patient likely has pericarditis. The pain is described as sharp in nature rather than dull, aching, pressure. The pain is exacerbated by inspiration, and finally there is global ST-segment elevation noted on the ECG.

CLINICAL PEARLS

⯈ Angina pectoris is the most frequent symptom of intermittent ischemia.

⯈ Targeted history and physical examinations of patients with angina are vital to expedite proper diagnosis and treatment of patients. The patient's description of their discomfort is key; history must be given attention because it is the most important diagnostic factor.

⯈ Physical examination may be normal in many patients with angina.

⯈ Aspirin, nitrates, β-adrenergic antagonists, and statins are the backbone in treatment and prevention of myocardial pathology, having proven benefit for both primary and secondary treatment.

⯈ Time is myocardium. Initial diagnosis and treatment must be done as soon as possible.

⯈ Be mindful of polypharmacy, as many drugs have side effects that can exacerbate myocardial damage.

⯈ The most common etiology of chest pain in the primary care setting is musculoskeletal. However, it is imperative to rule out cardiac cause of chest pain before making a musculoskeletal-related diagnosis.

REFERENCES

American Heart Association. 2005 International consensus conference on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Dallas, Texas. January 23-30, 2005. 

Bosker G. Textbook of Adult and Pediatric Emergency Medicine. 2nd ed. Atlanta, GA: American Health Consultants; 2002. 

Braunwald E, Antman EM, Beasly JW, et al. ACC/ AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction: executive summary and recommendations. Circulation. 2000 Sep 5;102(10):1193-1209. 

Elliott A. ACC/ AHA guidelines for the management of patients with ST-elevation myocardial infarction-executive summary. A report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines. Circulation. 2004;110:588-636. 

Marshall S. On Call Principles and Protocols. 3rd ed. Philadelphia, PA: WB Saunders; 2000. 

McConaghy JR, Oza RS. Outpatient diagnosis of acute chest pain in adults. Am Fam Physician. 2013 Feb 1;87(3):177-182. 

Sabatine M. P ocket medicine. The Massachusetts General Hospital Handbook of Internal Medicine. Baltimore, MD: Lippincott Williams & Wilkins; 2000. 

Shubhada A, Kellie F, Subramanian P. The Washington Manual of Medical Therapeutics. 30th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2001. 

Wiviott S, Braunwald E. Myocardial infarction. Am Fam Physician. 2004;70:535-538.

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