Ischemia and infarction patterns US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Ischemia and infarction patterns. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Ischemia and infarction patterns US Medical PG Question 1: A 58-year-old man comes to the emergency department for complaints of crushing chest pain for 4 hours. He was shoveling snow outside when the pain started. It is rated 7/10 and radiates to his left arm. An electrocardiogram (ECG) demonstrates ST-segment elevation in leads V2-4. He subsequently undergoes percutaneous coronary intervention (PCI) and is discharged with aspirin, clopidogrel, carvedilol, atorvastatin, and lisinopril. Five days later, the patient is brought to the emergency department by his wife with complaints of dizziness. He reports lightheadedness and palpitations for the past 2 hours but otherwise feels fine. His temperature is 99.7°F (37.6°C), blood pressure is 95/55 mmHg, pulse is 105/min, and respirations are 17/min. A pulmonary artery catheter is performed and demonstrates an increase in oxygen concentration at the pulmonary artery. What finding would you expect in this patient?
- A. Widespread ST-segment elevations
- B. Harsh, loud, holosystolic murmur at the lower left sternal border (Correct Answer)
- C. Pulseless electrical activity
- D. Drop of systolic blood pressure by 20 mmHg during inspiration
- E. Normal findings
Ischemia and infarction patterns Explanation: ***Harsh, loud, holosystolic murmur at the lower left sternal border***
- This patient's presentation, including recent **anterior STEMI**, dizziness, lightheadedness, palpitations, hypotension, tachycardia, and **increased oxygen saturation in the pulmonary artery** (oxygen "step-up" indicating a left-to-right shunt), is highly suggestive of **ventricular septal rupture (VSR)**.
- VSR is a **mechanical complication** of MI that typically occurs **3-7 days post-infarction** when the necrotic myocardium is weakest.
- A **VSR** causes a **harsh, loud, holosystolic murmur** best heard at the **lower left sternal border** due to turbulent blood flow through the septal defect from the left ventricle to the right ventricle.
- The left-to-right shunt results in oxygenated blood from the left ventricle mixing with deoxygenated blood in the right ventricle, causing the characteristic oxygen saturation step-up detected by pulmonary artery catheterization.
*Widespread ST-segment elevations*
- Widespread ST-segment elevations are characteristic of **acute pericarditis**, which typically presents with **pleuritic chest pain** that improves when leaning forward and a **friction rub**, not the hemodynamic compromise described here.
- While **Dressler syndrome** (post-MI pericarditis) can occur weeks after MI, the acute hemodynamic instability, left-to-right shunt evidence, and 5-day timeframe point to VSR rather than pericarditis.
*Pulseless electrical activity*
- **Pulseless electrical activity (PEA)** indicates cardiac arrest with organized electrical activity but no mechanical cardiac output, resulting in an **unpalpable pulse**.
- The patient has a documented pulse of **105/min**, which directly contradicts PEA.
- A patient in PEA would be unconscious and unable to report symptoms for 2 hours.
*Drop of systolic blood pressure by 20 mmHg during inspiration*
- A drop in systolic blood pressure >10 mmHg during inspiration (**pulsus paradoxus**) is characteristic of **cardiac tamponade** or severe obstructive airway disease.
- While **free wall rupture** leading to tamponade is another mechanical complication post-MI, the **oxygen saturation step-up** in the pulmonary artery is pathognomonic for an **intracardiac shunt** (VSR), not tamponade.
- Tamponade would show equalization of diastolic pressures across all chambers, not increased PA oxygen saturation.
*Normal findings*
- The patient presents with clear evidence of hemodynamic compromise: **hypotension (95/55 mmHg)**, **tachycardia (105/min)**, dizziness, and lightheadedness.
- The **oxygen saturation step-up** in the pulmonary artery is an objective abnormal finding indicating an intracardiac left-to-right shunt.
- Therefore, normal findings are incompatible with this clinical presentation.
Ischemia and infarction patterns US Medical PG Question 2: A 53-year-old man with a past medical history significant for hyperlipidemia, hypertension, and hyperhomocysteinemia presents to the emergency department complaining of 10/10 crushing, left-sided chest pain radiating down his left arm and up his neck into the left side of his jaw. His ECG shows ST-segment elevation in leads V2-V4. He is taken to the cardiac catheterization laboratory for successful balloon angioplasty and stenting of a complete blockage in his left anterior descending coronary artery. Echocardiogram the following day shows decreased left ventricular function and regional wall motion abnormalities. A follow-up echocardiogram 14 days later shows a normal ejection fraction and no regional wall motion abnormalities. This post-infarct course illustrates which of the following concepts?
- A. Coronary collateral circulation
- B. Ventricular remodeling
- C. Myocardial hibernation
- D. Myocardial stunning (Correct Answer)
- E. Reperfusion injury
Ischemia and infarction patterns Explanation: ***Myocardial stunning***
- This refers to a temporary **post-ischemic contractile dysfunction** that persists even after blood flow has been restored following an acute ischemic event.
- The return to normal left ventricular function and absence of regional wall motion abnormalities after successful reperfusion indicates that the initial dysfunction was transient and not due to permanent myocardial damage.
- Classic timeframe: recovery occurs over **days to weeks** after reperfusion, as seen in this patient (14 days).
*Coronary collateral circulation*
- This involves the development of alternative pathways for blood supply to the myocardium when the primary coronary arteries are occluded.
- While it can mitigate the extent of myocardial injury, it generally doesn't explain the reversal of severe regional wall motion abnormalities and low ejection fraction to normal in such a short period after a complete blockage.
*Ventricular remodeling*
- This refers to changes in the **size, shape, and function of the ventricles** in response to myocardial injury or chronic pressure/volume overload, often leading to progressive heart failure.
- It typically involves *persistent* and *often detrimental* changes, which is contrary to the improvement seen in this patient's echocardiogram.
*Myocardial hibernation*
- This is a state of **persistently impaired myocardial function at rest** due to **chronic inadequate blood flow** that can improve with revascularization.
- Hibernation requires **pre-existing chronic ischemia** with baseline dysfunction prior to intervention, not an acute complete occlusion presenting as STEMI.
- This patient had an **acute presentation** with complete blockage and no history suggesting chronic stable ischemia, making stunning (not hibernation) the correct answer.
*Reperfusion injury*
- This is damage to the myocardial tissue that occurs **after blood flow is restored** to an ischemic area, often involving oxidative stress and inflammation.
- While it can worsen myocardial function, it is a complication of reperfusion that causes *additional damage*, not a phenomenon that explains the *recovery* of cardiac function after reperfusion.
Ischemia and infarction patterns US Medical PG Question 3: A 66-year-old female with hypertension and a recent history of acute ST-elevation myocardial infarction (STEMI) 6 days previous, treated with percutaneous transluminal angioplasty (PTA), presents with sudden onset chest pain, shortness of breath, diaphoresis, and syncope. Vitals are temperature 37°C (98.6°F), blood pressure 80/50 mm Hg, pulse 125/min, respirations 12/min, and oxygen saturation 92% on room air. On physical examination, the patient is pale and unresponsive. Cardiac exam reveals tachycardia and a pronounced holosystolic murmur loudest at the apex and radiates to the back. Lungs are clear to auscultation. Chest X-ray shows cardiomegaly with clear lung fields. ECG is significant for ST elevations in the precordial leads (V2-V4) and low-voltage QRS complexes. Emergency transthoracic echocardiography shows a left ventricular wall motion abnormality along with a significant pericardial effusion. The patient is intubated, and aggressive fluid resuscitation is initiated. What is the next best step in management?
- A. Immediate cardiac catheterization
- B. Immediate transfer to the operating room (Correct Answer)
- C. Emergency pericardiocentesis
- D. Intra-aortic balloon counterpulsation
- E. Administer dobutamine 5-10 mcg/kg/min IV
Ischemia and infarction patterns Explanation: ***Immediate transfer to the operating room***
- The patient's presentation with sudden onset chest pain, shortness of breath, profound cardiogenic shock, and a new **holosystolic murmur at the apex radiating to the back** in the context of a recent **STEMI**, strongly suggests **acute papillary muscle rupture** causing severe mitral regurgitation. This is a surgical emergency requiring immediate intervention.
- The holosystolic murmur at the apex is pathognomonic for acute mitral regurgitation, distinguishing this from ventricular free wall rupture (which would present with tamponade physiology without a murmur).
- The patient requires urgent surgical repair (mitral valve replacement or repair) to address this mechanical complication of **myocardial infarction (MI)**, which is causing severe hemodynamic compromise.
*Immediate cardiac catheterization*
- While cardiac catheterization is essential for diagnosing coronary artery disease and revascularization, in this emergent situation with profound shock and a mechanical complication (papillary muscle rupture), the primary issue is structural cardiac damage requiring surgical repair, not ongoing ischemia alone.
- Delaying surgical intervention for catheterization in this hemodynamically unstable patient would be detrimental and potentially fatal.
*Emergency pericardiocentesis*
- Although there is a **pericardial effusion** on echocardiography, the patient's presentation with a new holosystolic murmur and profound shock after STEMI indicates **papillary muscle rupture with acute mitral regurgitation**, not cardiac tamponade.
- The presence of a loud murmur excludes ventricular free wall rupture as the primary cause. The effusion is likely reactive or incidental.
- Pericardiocentesis would not address the underlying mitral valve pathology causing the hemodynamic collapse.
*Intra-aortic balloon counterpulsation*
- **Intra-aortic balloon pump (IABP)** can improve cardiac output and reduce afterload, which may provide temporary hemodynamic support in cardiogenic shock.
- However, in cases of **papillary muscle rupture** with severe acute mitral regurgitation, IABP provides only temporary support and does not fix the underlying structural problem.
- It could be considered as a bridge to surgery, but the definitive treatment is surgical repair, which should be expedited without delay.
*Administer dobutamine 5-10 mcg/kg/min IV*
- **Dobutamine** is an inotrope that increases cardiac contractility. While it might improve cardiac output in some forms of cardiogenic shock, in the setting of **acute severe mitral regurgitation from papillary muscle rupture**, it cannot resolve the structural valvular incompetence.
- Increasing contractility may paradoxically worsen the regurgitant fraction and further compromise forward cardiac output.
- Medical management alone cannot resolve this mechanical complication, necessitating urgent surgical intervention.
Ischemia and infarction patterns US Medical PG Question 4: A cardiologist is studying how a new virus that infects the heart affects the electrical conduction system of the cardiac myocytes. He decides to obtain electrocardiograms on patients with this disease in order to see how the wave patterns and durations change over time. While studying these records, he asks a medical student who is working with him to interpret the traces. Specifically, he asks her to identify the part that represents initial ventricular depolarization. Which of the following characteristics is most consistent with this feature of the electrocardiogram?
- A. Elevated in patients with full thickness ischemic injury of the heart
- B. Becomes peaked in states of hyperkalemia
- C. Becomes prominent in states of hypokalemia
- D. Normal duration defined as less than 120 milliseconds (Correct Answer)
- E. Normal duration defined as less than 200 milliseconds
Ischemia and infarction patterns Explanation: ***Normal duration defined as less than 120 milliseconds***
- The question asks for the representation of **initial ventricular depolarization**, which corresponds to the **QRS complex** on an ECG.
- The normal duration of the **QRS complex** is typically less than **0.12 seconds (120 milliseconds)**, reflecting efficient ventricular depolarization.
*Elevated in patients with full thickness ischemic injury of the heart*
- This description refers to the **ST segment elevation** seen in **ST-segment elevation myocardial infarction (STEMI)**, which represents myocardial injury, not initial ventricular depolarization.
- While related to cardiac electrical activity, **ST segment elevation** is a consequence of injury and refers to repolarization abnormalities, not the QRS complex itself.
*Becomes peaked in states of hyperkalemia*
- **Peaked T waves** are characteristic of **hyperkalemia**, indicating altered ventricular repolarization, not ventricular depolarization.
- The T wave represents ventricular repolarization, and its morphology changes significantly with potassium imbalances.
*Becomes prominent in states of hypokalemia*
- A **prominent U wave** is sometimes observed in **hypokalemia**, which follows the T wave and is thought to represent repolarization of Purkinje fibers.
- The U wave is distinct from the QRS complex and does not represent initial ventricular depolarization.
*Normal duration defined as less than 200 milliseconds*
- A duration of less than 200 milliseconds (0.20 seconds) typically refers to the normal duration of the **PR interval**, which represents atrial depolarization and conduction through the AV node.
- The **QRS complex** (initial ventricular depolarization) has a shorter normal duration, typically less than 120 milliseconds.
Ischemia and infarction patterns US Medical PG Question 5: A 55-year-old man comes to the emergency department because of left-sided chest pain and difficulty breathing for the past 30 minutes. His pulse is 88/min. He is pale and anxious. Serum studies show increased cardiac enzymes. An ECG shows ST-elevations in leads I, aVL, and V5-V6. A percutaneous coronary intervention is performed. In order to localize the site of the lesion, the catheter must pass through which of the following structures?
- A. Left coronary artery → left circumflex artery (Correct Answer)
- B. Right coronary artery → posterior descending artery
- C. Left coronary artery → left anterior descending artery
- D. Right coronary artery → right marginal artery
- E. Left coronary artery → posterior descending artery
Ischemia and infarction patterns Explanation: ***Left coronary artery → left circumflex artery***
- **ST-elevations** in leads I, aVL, and V5-V6 are indicative of a **lateral myocardial infarction**.
- The **left circumflex artery** primarily supplies the lateral wall of the left ventricle.
*Right coronary artery → posterior descending artery*
- The **posterior descending artery** (PDA) typically supplies the inferior wall and posterior interventricular septum.
- An occlusion here would cause **ST-elevations** in leads II, III, and aVF, which is not seen in this case.
*Left coronary artery → left anterior descending artery*
- The **left anterior descending** (LAD) artery supplies the anterior wall and apex of the left ventricle.
- Occlusion of the LAD would typically cause **ST-elevations** in leads V1-V4, indicating an anterior MI.
*Right coronary artery → right marginal artery*
- The **right marginal artery** is a branch of the right coronary artery and supplies part of the right ventricle.
- Occlusion here would primarily affect the **right ventricle**, and is not typically associated with the given ECG changes.
*Left coronary artery → posterior descending artery*
- While the **posterior descending artery** can sometimes originate from the left circumflex artery (**left dominant circulation**), it primarily supplies the inferior wall.
- The observed ECG changes in leads I, aVL, and V5-V6 are characteristic of a **lateral wall infarct**, which is supplied by the left circumflex artery.
Ischemia and infarction patterns US Medical PG Question 6: An 80-year-old man presents to the emergency department because of gnawing substernal chest pain that started an hour ago and radiates to his neck and left jaw. A 12-lead ECG is obtained and shows ST-segment elevation with newly developing Q waves. He is admitted for treatment. 4 days after hospitalization he suddenly develops altered mental status, and his blood pressure falls from 115/75 mm Hg to 80/40 mm Hg. Physical examination shows jugular venous distention, pulsus paradoxus, and distant heart sounds. What is the most likely cause of this patient's condition?
- A. Pericardial inflammation
- B. Compression of heart chambers by blood in the pericardial space (Correct Answer)
- C. Arrhythmia caused by ventricular fibrillation
- D. Rupture of papillary muscle
- E. Acute pulmonary edema from left heart failure
Ischemia and infarction patterns Explanation: ***Compression of heart chambers by blood in the pericardial space***
- The patient's initial presentation with ST-elevation myocardial infarction (STEMI) and subsequent development of **hypotension**, **jugular venous distention**, **pulsus paradoxus**, and **distant heart sounds** (Beck's triad) is highly indicative of **cardiac tamponade.**
- In the context of a recent MI, this constellation of symptoms strongly suggests a **cardiac free wall rupture**, leading to blood accumulation in the pericardial sac and compression of the heart.
- Free wall rupture typically occurs **3-7 days post-MI** and is a life-threatening mechanical complication.
*Pericardial inflammation*
- While pericardial inflammation (pericarditis) can occur post-MI, it typically manifests with **pleuritic chest pain** that is relieved by leaning forward and is often associated with a **pericardial friction rub.**
- It does not typically lead to acute, severe hypotension, pulsus paradoxus, or sudden circulatory collapse in this manner without significant effusion and tamponade physiology.
*Arrhythmia caused by ventricular fibrillation*
- **Ventricular fibrillation** would cause immediate cardiac arrest and loss of consciousness, not a gradual development of hypotension, JVD, and pulsus paradoxus.
- While arrhythmias are common post-MI, the specific physical findings point away from isolated VFib as the primary cause of hemodynamic collapse.
*Acute pulmonary edema from left heart failure*
- **Acute pulmonary edema** is a manifestation of **left heart failure**, characterized by severe dyspnea, orthopnea, and crackles on lung auscultation.
- While left heart failure can cause hypotension in cardiogenic shock, it would not typically present with the classic signs of cardiac tamponade such as pulsus paradoxus, distant heart sounds, and prominent JVD without pulmonary congestion findings.
*Rupture of papillary muscle*
- **Papillary muscle rupture** leads to severe **acute mitral regurgitation**, causing acute pulmonary edema, a new holosystolic murmur, and often cardiogenic shock.
- While it can lead to hypotension, it doesn't typically present with the classic signs of cardiac tamponade such as pulsus paradoxus and distant heart sounds; instead, a loud murmur would be prominent.
Ischemia and infarction patterns US Medical PG Question 7: A 71-year-old woman with a past medical history of type 2 diabetes, hypercholesterolemia, and hypertension was admitted to the hospital 8 hours ago with substernal chest pain for management of acute non-ST-elevated myocardial infarction (NSTEMI). The ECG findings noted by ST-depressions and T-wave inversions on anterolateral leads, which is also accompanied by elevated cardiac enzymes. Upon diagnosis, management with inhaled oxygen therapy, beta-blockers and aspirin, and low-molecular-weight heparin therapy were initiated, and she was placed on bed rest with continuous electrocardiographic monitoring. Since admission, she required 2 doses of sublingual nitroglycerin for recurrent angina, and the repeat troponin levels continued to rise. Given her risk factors, plans were made for early coronary angiography. The telemetry nurse calls the on-call physician because of her concern with the patient's mild confusion and increasing need for supplemental oxygen. At bedside evaluation, The vital signs include: heart rate 122/min, blood pressure 89/40 mm Hg, and the pulse oximetry is 91% on 6L of oxygen by nasal cannula. The telemetry and a repeat ECG show sinus tachycardia. She is breathing rapidly, appears confused, and complains of shortness of breath. On physical exam, the skin is cool and clammy and appears pale and dull. She has diffuse bilateral pulmonary crackles, and an S3 gallop is noted on chest auscultation with no new murmurs. She has jugular venous distention to the jaw-line, rapid and faint radial pulses, and 1+ dependent edema. She is immediately transferred to the intensive care unit for respiratory support and precautions for airway security. The bedside sonography shows abnormal hypodynamic anterior wall movement and an ejection fraction of 20%, but no evidence of mitral regurgitation or ventricular shunt. The chest X-ray demonstrates cephalization of pulmonary veins and pulmonary edema. What is the most appropriate next step in the stabilization of this patient?
- A. Obtain blood cultures and start preliminary broad-spectrum antibiotics
- B. Start intravenous fluids and epinephrine therapy
- C. Intubate the patient and perform an emergency cardiocentesis
- D. Initiate dopamine therapy and diuresis (Correct Answer)
- E. Insert two large-bore intravenous catheters and start rapid fluid resuscitation
Ischemia and infarction patterns Explanation: ***Initiate dopamine therapy and diuresis***
- This patient is presenting with **cardiogenic shock** secondary to extensive NSTEMI, characterized by **hypotension**, signs of **end-organ hypoperfusion** (confusion, cool clammy skin), **pulmonary edema** (crackles, dyspnea, elevated jugular venous pressure), and **severely reduced ejection fraction**. Dopamine is a vasopressor that can increase cardiac output and blood pressure.
- **Diuresis** with loop diuretics such as furosemide is crucial to reduce the fluid overload contributing to the pulmonary edema and jugular venous distention.
*Obtain blood cultures and start preliminary broad-spectrum antibiotics*
- While infection is a concern in critically ill patients, there are **no signs of infection** in this clinical presentation. The patient's symptoms are clearly attributable to acute cardiac decompensation.
- A delay in treating cardiogenic shock to investigate for infection would be detrimental and potentially fatal.
*Start intravenous fluids and epinephrine therapy*
- Intravenous fluids would **worsen the existing pulmonary edema and fluid overload** in a patient with an ejection fraction of 20% and clinical signs of volume overload (crackles, JVD, S3 gallop).
- Epinephrine is a potent vasopressor but is generally reserved for more severe shock refractory to other inotropes, or in cases of **cardiac arrest**, not typically first-line for cardiogenic shock with significant pulmonary congestion.
*Intubate the patient and perform an emergency cardiocentesis*
- While the patient is confused and has respiratory distress, **intubation** should be considered after hemodynamic stabilization, if respiratory failure persists or worsens.
- **Cardiocentesis** is indicated for **cardiac tamponade**, which is not supported by the absence of an effusion on bedside sonography and the finding of hypodynamic anterior wall movement, which points to pump failure.
*Insert two large-bore intravenous catheters and start rapid fluid resuscitation*
- This patient is in **cardiogenic shock with clear evidence of fluid overload**, including pulmonary edema and elevated jugular venous pressure.
- **Rapid fluid resuscitation would exacerbate heart failure** and worsen respiratory compromise due to increased preload.
Ischemia and infarction patterns US Medical PG Question 8: A 50-year-old man presents the emergency department for intense chest pain, profuse sweating, and shortness of breath. The onset of these symptoms was 3 hours ago. The chest pain began after a heated discussion with a colleague at the community college where he is employed. Upon arrival, he is found conscious and responsive; the vital signs include a blood pressure of 130/80 mm Hg, a heart rate at 90/min, a respiratory rate at 20/min, and a body temperature of 36.4°C (97.5°F). His medical history is significant for hypertension diagnosed 7 years ago, which is well-controlled with a calcium channel blocker. The initial electrocardiogram (ECG) shows ST-segment depression in multiple consecutive leads, an elevated cardiac troponin T level, and normal kidney function. Which of the following would you expect to find in this patient?
- A. Subendocardial necrosis (Correct Answer)
- B. Transmural necrosis
- C. Incomplete occlusion of a coronary artery
- D. Coronary artery spasm
- E. Ventricular pseudoaneurysm
Ischemia and infarction patterns Explanation: ***Subendocardial necrosis***
- This patient's presentation with **ST-segment depression** and **elevated troponin T** indicates a **Non-ST-segment Elevation Myocardial Infarction (NSTEMI)**, which typically results from subendocardial ischemia and necrosis.
- Subendocardial tissue is most vulnerable to ischemia due to its high oxygen demand and distal location from the coronary arteries, making it the first region to suffer damage when oxygen supply is compromised.
*Transmural necrosis*
- **Transmural necrosis** is characteristic of a **ST-segment Elevation Myocardial Infarction (STEMI)**, which presents with persistent **ST-segment elevation** on ECG.
- This patient's ECG shows **ST-segment depression**, ruling out transmural involvement at the time of presentation.
*Incomplete occlusion of a coronary artery*
- While an NSTEMI usually involves an **incomplete occlusion** or **critical stenosis** of a coronary artery, the question asks what would be *found* in the patient's heart tissue, not the mechanism.
- The direct tissue consequence of incomplete occlusion leading to NSTEMI is **subendocardial necrosis**, which is a more specific answer about the pathological finding.
*Coronary artery spasm*
- Although **coronary artery spasm (Prinzmetal angina)** can cause chest pain and ECG changes, it typically presents with **transient ST-segment elevation** (not depression) and often resolves spontaneously.
- The elevated troponin T indicates myocardial necrosis, which is not typically a feature of uncomplicated coronary artery spasm, and the duration of symptoms (3 hours) suggests a more sustained event than a transient spasm.
*Ventricular pseudoaneurysm*
- A **ventricular pseudoaneurysm** is a **late complication of myocardial infarction**, typically occurring weeks to months after the acute event, due to rupture of the ventricular free wall contained by pericardium.
- Given the 3-hour symptom onset, it is highly unlikely to be present in the acute phase of myocardial infarction.
Ischemia and infarction patterns US Medical PG Question 9: A 49-year-old man was brought to the emergency department by ambulance with complaints of sudden-onset chest pain that radiates into his neck and down his left arm. This substernal pain started 2 hours ago while he was having dinner. His past medical history is remarkable for hypercholesterolemia that is responsive to therapy with statins and coronary artery disease. His temperature is 37.0°C (98.6°F), blood pressure is 155/90 mm Hg, pulse is 112/min, and respiratory rate is 25/min. Troponin I levels are elevated. A 12-lead ECG was performed (see image). What is the most likely etiology of this patient’s presentation?
- A. Coronary vasospasm
- B. Right coronary artery occlusion (Correct Answer)
- C. Left circumflex artery occlusion
- D. Left anterior descending artery occlusion
- E. Left main coronary artery occlusion
Ischemia and infarction patterns Explanation: ***Right coronary artery occlusion***
- The ECG shows significant **ST elevation in inferior leads (II, III, aVF)** and **ST depression in anterior leads (V1-V4)**, which is characteristic of an **inferior wall myocardial infarction**.
- **Inferior wall MIs** are typically caused by occlusion of the **right coronary artery (RCA)**. The reciprocal changes (ST depression in anterior leads) support this, indicating involvement of the posterolateral wall often supplied by the RCA.
*Coronary vasospasm*
- While coronary vasospasm (e.g., in **Prinzmetal angina**) can cause ST elevation, it usually presents with more transient symptoms that resolve with vasodilators, and the ST segment elevations are typically regional but often more widespread or dynamic.
- The patient's history of **coronary artery disease (CAD)** and persistent symptoms with elevated troponin point towards a fixed obstruction rather than vasospasm.
*Left circumflex artery occlusion*
- **Left circumflex artery occlusion** typically causes changes in leads I, aVL, V5, and V6 (high lateral or lateral wall MI), and sometimes posterior leads.
- The predominant ST elevation in leads II, III, and aVF is not characteristic of a primary **left circumflex artery occlusion**.
*Left anterior descending artery occlusion*
- **Left anterior descending (LAD) artery occlusion** usually results in **anterior or anteroseptal MI**, characterized by ST elevation in leads V1-V4 and potentially I and aVL.
- The ECG shows ST depression in V1-V4, which are reciprocal changes rather than direct signs of an **LAD occlusion**.
*Left main coronary artery occlusion*
- **Left main coronary artery occlusion** is a catastrophic event, often presenting with widespread ST depression in multiple leads with ST elevation in aVR (and sometimes V1).
- While life-threatening, the ECG pattern here with prominent inferior ST elevation and reciprocal anterior depression is more indicative of an **RCA occlusion** than a left main occlusion.
Ischemia and infarction patterns US Medical PG Question 10: A 57-year-old man is brought to the emergency department for crushing substernal chest pain at rest for the past 2 hours. The pain began gradually while he was having an argument with his wife and is now severe. He does not take any medications. He has smoked 1 pack of cigarettes daily for 35 years. He is diaphoretic. His temperature is 37.1°C (98.8°F), pulse is 110/min, respirations are 21/min, and blood pressure is 115/65 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 97%. Cardiac examination shows an S4 gallop. The lungs are clear to auscultation. An ECG is shown. Which of the following is the most likely underlying cause of this patient's condition?
- A. Occlusion of the left circumflex artery
- B. Diffuse coronary vasospasm
- C. Tear in the intimal lining of the aorta
- D. Occlusion of the left anterior descending artery (Correct Answer)
- E. Thromboembolism to the right interlobar pulmonary artery
Ischemia and infarction patterns Explanation: ***Occlusion of the left anterior descending artery***
- The ECG shows significant **ST-segment elevation** in leads V1, V2, V3, and V4, which are contiguous leads indicative of an **anterior myocardial infarction**.
- The **left anterior descending (LAD) artery** supplies the anterior wall of the left ventricle and the anterior two-thirds of the interventricular septum, making its occlusion the most likely cause of an anterior STEMI.
*Occlusion of the left circumflex artery*
- Occlusion of the left circumflex artery typically causes an **inferior or lateral myocardial infarction**, evidenced by ST elevation in leads II, III, aVF (inferior) or I, aVL, V5, V6 (lateral).
- This ECG pattern does not correspond to a left circumflex artery occlusion.
*Diffuse coronary vasospasm*
- Diffuse coronary vasospasm (as seen in **Prinzmetal angina**) can cause transient ST-segment elevation, but it is typically not sustained for 2 hours and often resolves with nitrates.
- While it can present with chest pain at rest, the prolonged nature of the pain and clear localization on ECG points more towards a fixed **thromboembolic occlusion**.
*Tear in the intimal lining of the aorta*
- A tear in the intimal lining of the aorta (**aortic dissection**) causes severe, tearing chest pain that often radiates to the back.
- While severe and substernal, the pain in aortic dissection is not typically associated with these specific **ECG changes (anterior STEMI)**, which strongly indicate myocardial ischemia.
*Thromboembolism to the right interlobar pulmonary artery*
- A thromboembolism to the pulmonary artery (**pulmonary embolism**) would typically present with **pleuritic chest pain** and **dyspnea**, sometimes accompanied by hypoxemia and tachycardia.
- The ECG in pulmonary embolism might show signs of **right heart strain** (e.g., S1Q3T3 pattern, right axis deviation), but not the clear anterior ST-segment elevations seen here.
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