chest pain case 1

>Chest pain Case 1

A 45-year-old man presents to the emergency department complaining of chest pain, which began twenty minutes before while he was filling
up his car with gasoline. He describes the pain as substernaI, intense, dulI, and squeezing. It does not change with respiration. He also
complains that he is nauseated. He has never experienced anything like this before. His temperature is 37.5 C (99.5 F), blood pressure is
124/76 mm Hg, pulse is 80/min, respiratory rate is 22/min, and oxygen saturation is 95% on room air. On physical examination, he is
diaphoretic. His lungs are clear, his heart rate is regular, and he has a normaI S1 and S2 without murmur, rub, or gallop. The examiner
estimates that his jugular venous pressure is elevated to the angle of the jaw. His abdomen is nontender, with normal bowel sounds. An
electrocardiogram is performed, which reveals sinus rhythm, normal axis, normal intervals, and ST elevation in leads lI, III, and aVF. A chest x-
ray film reveals no apparent cardiac or pulmonary abnormalities.

Question 1 of 7
Which of the following is the most likely diagnosis?
A. Acute myocardial infarction
B. Aortic dissection
C. Gastroesophageal reflux

D. Pericarditis
E. Pulmonary embolus


Question 2 of 7
What is the pathophysiologic process most likely to be responsible for this patient's presentation?
A. Atherosclerotic plaque rupture resulting in thrombus formation
B. Buildup of atherosclerotic stenosis to produce high-grade obstruction of the artery
C. Dissection of the vessel
D. Embolization of blood clot, air, or foreign material
E. Myocardial hypertrophy resulting in vessel narrowing


Question 3 of 7
Which of the following vessels is most likely to be diseased in this patient?
A. Coronary sinus
B. Left anterior descending coronary artery
C. Left circumflex coronary artery
D. Left main coronary artery
E. Right coronary artery


Question 4 of 7
This patient is given aspirin in the emergency department. Decreased production of which of the following mediators is responsible for the
beneficial effects of aspirin in this disorder?
A. cAMP
B. PIatelet glycoprotein lIB/IIIA
C. Prostacyclin
D. Thromboxane A2
E. Ubiquinone (coenzyme Q)


Question 5 of 7
EIevation of which of the following serum proteins is the most specific biochemical marker for this patient's condition?
A. AIanine aminotransferase
B. Creatine phosphokinase
C. Lactate dehydrogenase
D. Transferrin
E. Troponin


Question 6 of 7
Three days after hospital admission, the patient suddenly develops shortness of breath and becomes hypotensive. His heart rate is 100/min,
with a normaI PR and QRS intervaI. His blood pressure is 75/50 mm Hg. His respiratory rate is 38/min and his oxygen saturation on 2 Iiters
via nasal cannula drops to 60%. A chest x-ray reveals bilateral fluffy infiltrates in the lung fields. Which of the following complications of his
condition has most likely occurred?
A. Dilation of the left ventricle
B. Dressler syndrome
C. Rupture of the left ventricular free wall
D. Rupture of the posteromedial papillary muscle
E. Ventricular tachycardia


Question 7 of 7
The patient is taken emergently to the operating room. During surgery, a sample of affected myocardial tissue is sent to the pathology
Iaboratory for examination. Which of the following would be the likely pathologic finding(s)?
A. Acellular fibrosis
B. Monocyte infiltration, absent nuclei and striations
C. Myocyte disarray
D. Myocyte edema, hemorrhage, and dense neutrophil infiltration
E. Wavy myofibers with eosinophilic contraction bands

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Chest pain Case 1 answers

Q1
The correct answer is A. The differential diagnosis of chest pain is broad and includes all the answers on this list, all of which can present, as in this patient, with a relatively normal examination of the heart and lungs. Acute myocardial infarction is the only one of these findings that is associated with ST segment elevation in an anatomical distribution (in this case, the "inferior" leads). His elevated jugular venous pressure is also a clue to abnormal cardiac function; however, this might be present in severe constrictive pericarditis or pulmonary embolism as well.
Aortic dissection (choice B) often presents with chest pain or pain radiating to the back. It is not, however, typically associated with ST segment changes on the EKG, unless the dissection extends proximally into the ostia of the coronary arteries, obstructing flow, and resulting in secondary acute myocardial infarction, in which case a patient could present like this. However, this presentation would be an uncommon presentation of a relatively uncommon disease. The risk for aortic dissection is increased with long-standing essential hypertension, other peripheral vascular disease, hyperlipidemia, and advanced age, as well as connective tissue disorders such as Marfan syndrome or Ehlers-Danlos syndrome.
Patients with gastroesophageal reflux (choice C) may complain of intense substernal chest pain that is difficult to distinguish from the pain of myocardial infarction. However, the ST elevations on the EKG suggest transmural ischemia of the myocardium and do not occur with isolated gastroesophageal reflux. Do not let relatively normal vital signs and gastrointestinal symptoms such as nausea fool you!
Pericarditis (choice D), an inflammatory disease of the pericardium, presents with chest pain and is often associated with ST elevation on the EKG, as well as PR interval depression. However, the ST elevation usually involves multiple leads of the EKG, and is not in a strictly anatomic distribution. Pericarditis is often associated with a friction rub.
Pulmonary thromboembolism (choice E) can also present with chest pain. A patient who has had a large PE, however, typically will not have normal vital signs, and is likely to have tachycardia, tachypnea, and possibly hypoxemia. Hemodynamically significant pulmonary embolism can present with elevated JVP due to right heart strain. The patient might have ST depression in the inferior leads, but will not have ST elevation. The pain associated with pulmonary embolus is generally pleuritic in nature, that is, lateralizing, and changing with inspiration. Risk factors for pulmonary embolism include hypercoagulable states, immobilization, and vascular injury (Virchow's triad).


Q2
The correct answer is A. Acute coronary syndromes are thought to be the result of rupture of a pre-existing atherosclerotic plaque, often one that is not producing high-grade stenosis. When the endothelial surface covering the lipid core of an unstable plaque ruptures, a platelet plug forms and the clotting cascade is activated, rapidly propagating thrombus formation and suddenly occluding the vessel. This results in transmural ischemia, which becomes infarction, should the clot fail to recanalize quickly.
Atherosclerotic stenosis (choice B) is an important pathologic component of coronary artery disease. However, high-grade coronary stenoses most frequently cause stable angina, that is, chest pain and myocardial ischemia induced when an increase in myocardial oxygen demand exceeds the fixed supply that can be obtained through a severely stenotic vessel. As vessels progressively narrow over time, they produce ischemia, but not sudden infarction. Often distal to a narrowed vessel, collaterals will form from less diseased vessels, compensating for the reduced flow.
Coronary artery dissection (choice C) is a rare phenomenon that can produce transmural ischemia and infarction, but most commonly occurs in the setting of instrumentation of the vessel.
Embolization (choice D) is a relatively rare phenomenon in the coronary circulation under normal circumstances. Foreign material can only enter the left side of the heart via right-to-left intracardiac shunt, pulmonary vein interruption, or surgical opening of the left heart. Thrombus that forms in the left atrium (usually the result of low-flow states such as mitral stenosis or atrial fibrillation) can also embolize; patients with atrial fibrillation are anticoagulated to reduce the risk of cerebral embolization of left atrial clot.
Myocardial hypertrophy (choice E) can restrict subendocardial oxygen supply by creating high capillary pressure relative to arteriolar pressure. This does not occur in large coronary vessels, but can produce subendocardial ischemia in disease states that are associated with hypertrophic myocardium, such as aortic stenosis, long-standing essential hypertension, and idiopathic hypertrophic subaortic stenosis (IHSS).


Q3
The correct answer is E. Acute myocardial infarction is usually due to obstruction of one coronary vessel. The right coronary artery exits the right sinus of Valsalva of the aorta and gives off branches to the right ventricle, the SA nodal artery (in 70% of patients), the AV nodal artery, and, in the 85% of patients whose circulations are said to be "right-dominant," the posterior descending artery, which supplies the inferior wall of the RV and the LV as well as the posterior 1/3 of the interventricular septum. This patient has EKG signs of an inferior myocardial infarction, with ST elevation in the inferior leads, II, III, and aVF. He also has a physical sign of right ventricular dysfunction (elevated jugular venous pressure).
The coronary sinus (choice A) is the principal vein draining the left ventricle and runs alongside the circumflex artery in the posterior AV groove. It is not a common site for atherosclerotic disease or for obstruction.
The left anterior descending artery (choice B) supplies the anterior and anteroseptal portions of the left ventricle. Obstruction would produce ST elevation in the anterior (V2-V6) and occasionally the lateral (I, aVF) leads of the EKG, with possible "reciprocal" ST depression in the inferior leads.
The left circumflex artery (choice C) supplies the lateral wall of the left ventricle. 85% of patients have a "right-dominant" coronary anatomy. That is, the right coronary artery gives off the posterior descending artery (PDA). In the "left-dominant" remaining 15%, the PDA comes off the circumflex. Isolated inferior EKG lead changes are, therefore, most likely to be due to RCA obstruction; circumflex obstruction typically produces EKG lead changes in the lateral (I, aVL, V5, V6) leads.
The left main coronary artery (choice D) exits the aorta at the left sinus of Valsalva and divides into the left anterior descending and left circumflex arteries. Obstruction of the left main makes the entire left ventricle ischemic, often resulting in cardiogenic shock. This would produce ST segment elevation in leads I, aVL, and V2-V6.


Q4
The correct answer is D. Aspirin irreversibly inhibits the enzyme cyclooxygenase, which produces all the prostaglandin mediators from arachidonic acid. Cyclooxygenase in platelets produces thromboxane A2, which is a potent promoter of platelet aggregation and vasoconstriction. By blocking this, aspirin irreversibly inhibits platelet function, preventing aggregation at the site of plaque rupture. Platelets, having no nuclei, are unable to synthesize more cyclooxygenase, and therefore thromboxane production is inhibited for the life of the platelet, approximately 10 days.
Cyclic AMP (choice A) is an intracellular small molecule responsible for multiple signal transduction pathways. In cardiac myocytes, it activates protein kinases responsible for the phosphorylation of calcium channels, promoting entry of calcium into the cell. cAMP is broken down by phosphodiesterase, the inhibition of which is responsible for the beneficial effects of inotropic phosphodiesterase inhibitors such as milrinone.
Platelet surface glycoprotein IIb/IIIA (choice B) binds fibrinogen and von Willebrand factor, promoting aggregation and clot formation. It is inhibited by drugs like eptifibatide and tirofiban, which are used in acute coronary syndromes to further inhibit platelet aggregation and thrombus formation.
Prostacyclin (choice C) is produced by cyclooxygenase in endothelial cells, where it promotes vasodilation and inhibits platelet aggregation. Prostacyclin should therefore be a beneficial mediator. Aspirin inhibits prostacyclin formation, however, endothelial cells can produce more cyclooxygenase and are able to continue to synthesize adequate amounts of prostacyclin.
Ubiquinone (choice E), or coenzyme Q, is a naturally occurring coenzyme that plays a vital role in the mitochondrial electron transport chain. Studies have shown an association between decreased levels of coenzyme Q and heart disease, so inhibition of ubiquinone production would not likely be beneficial.


Q5
The correct answer is E. Troponins (in isoforms troponin C, troponin I, and troponin T) are required for actin-myosin cross linking in cardiac muscle. Small elevations in serum troponin levels are currently the most sensitive clinical serum markers for myocardial injury, elevating within 3-12 hours of infarction. Levels remain elevated for 5-14 days.
Alanine aminotransferase (choice A) occurs in both cardiac muscle and in the liver, and has been used in the past as a marker of cardiac injury. However, currently, its more common clinical use is as a marker of hepatocyte injury. Its time course of elevation in MI is intermediate between CPK and LDH (see below).
Creatine phosphokinase (choice B) has been the mainstay of diagnosis of myocardial injury for many years. CPK has several isoforms, of which the MB isoform is specific for cardiac muscle. The fraction of the total CPK that is the MB isoform has been used to differentiate myocardial injury from other injury processes elevating CPK. CPK is also elevated with skeletal muscle and with brain injury, but neither of these tissues contains significant amounts of MB isoform. In MI, CPK levels usually rise within 8 to 24 hours and return to normal after 48 to 72 hours.
Lactate dehydrogenase (choice C) is, like alanine aminotransferase, an enzyme that is released both with cardiac injury and with hepatocellular injury. It can also be elevated in hemolysis and with some neoplasms. In MI, it generally rises within 12 hours and peaks after 24-48 hours, remaining elevated for 10-14 days. These properties made LDH, prior to the introduction of troponin assays, the test used to detect MI occurring more than a day previously.
Transferrin (choice D) is a plasma protein responsible for the uptake of iron after absorption in the small intestine, and is responsible for iron-binding capacity in the blood. It is measured (usually as "total iron-binding capacity") in the differential diagnosis of the anemias.


Q6
The correct answer is D. This patient is suddenly in cardiogenic shock with severe pulmonary edema. This could be the result of arrhythmia, cardiac tamponade, or left ventricular valvular dysfunction. He had an inferior MI, which is most likely due to thrombosis of the right coronary artery. The posteromedial papillary muscle is supplied by the RCA alone in most patients and is prone to rupture in inferoposterior MI. Rupture leads to acute and severe mitral valve dysfunction, resulting in pulmonary edema and poor forward ejection.
Dilation of the left ventricle (choice A) typically occurs after extensive damage occurs, which would have appeared on this patient's acute EKG as ST elevation in the anterior leads. Dilation can result in mitral regurgitation, but typically of an insidious onset.
Dressler syndrome (choice B) is a late complication of MI that may occur weeks to months later, characterized by symptoms of pericarditis including pleuritic chest pain, fever, friction rub, and elevated white blood cell count. Patients can also develop early postinfarction pericarditis in the days to weeks following MI with friction rub and pericardial effusion. This is seldom associated with cardiac tamponade.
Rupture of the LV free wall (choice C) is a complication more likely to occur with more extensive damage to the LV than is produced in an inferior MI such as this patient had. However, LV free wall rupture would produce cardiac tamponade, which could produce this clinical picture.
Ventricular tachycardia (VT) (choice E) is a complication of MI (though risk is highest early in the course of infarction) and could also produce this clinical picture. However, it is excluded by the EKG, which reveals an atrial-ventricular conducted rhythm (VT displays no P waves) and a narrow-complex QRS (VT typically has a QRS much greater than 0.12 s).


Q7
The correct answer is B. Three days after infarction, coagulation necrosis is complete, with complete loss of cellular structure (hence the high risk of mechanical complications such as rupture) and infiltration of monocytes to phagocytize debris.
Acellular fibrosis (choice A) replaces necrosis after many weeks when debris is removed and fibroblasts have invaded the dead tissue and replaced it with collagen.
Myocyte disarray (choice C) is associated with hypertrophic subaortic stenosis (IHSS), rather than myocardial infarction.
Myocyte edema, with hemorrhage and neutrophil infiltration (choice D) occurs within 4-12 hours after infarction.
Wavy myofibers and contraction bands (choice E) are the first light microscopic pathologic changes to occur after MI, and appear within 1-3 hours after infarction.