ECG interpretation in ACS US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for ECG interpretation in ACS. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
ECG interpretation in ACS 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
ECG interpretation in ACS 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.
ECG interpretation in ACS US Medical PG Question 2: 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
ECG interpretation in ACS 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.
ECG interpretation in ACS US Medical PG Question 3: 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
ECG interpretation in ACS 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.
ECG interpretation in ACS US Medical PG Question 4: Two days after undergoing an uncomplicated total thyroidectomy, a 63-year-old woman has acute, progressive chest pain. The pain is sharp and burning. She feels nauseated and short of breath. The patient has a history of hypertension, type 1 diabetes mellitus, medullary thyroid cancer, multiple endocrine neoplasia type 2A, anxiety, coronary artery disease, and gastroesophageal reflux disease. She smoked half a pack of cigarettes daily for 24 years but quit 18 years ago. Current medications include lisinopril, insulin glargine, insulin aspart, sertraline, aspirin, ranitidine, and levothyroxine. She appears anxious and diaphoretic. Her temperature is 37.4°C (99.3°F), pulse is 64/min, respirations are 17/min, and blood pressure is 148/77 mm Hg. The lungs are clear to auscultation. Examination shows a 3-cm linear incision over the anterior neck with 1 mm of surrounding erythema and mild serous discharge. The chest wall and abdomen are nontender. There is 5/5 strength in all extremities and decreased sensation to soft touch on the feet bilaterally. The remainder of the examination shows no abnormalities. Which of the following is the most appropriate next step in management?
- A. Obtain an ECG and troponin T levels (Correct Answer)
- B. Administer IV pantoprazole and schedule endoscopy
- C. Discontinue levothyroxine and obtain fT4 levels
- D. Administer IV levofloxacin and obtain chest radiograph
- E. Obtain urine and plasma metanephrine levels
ECG interpretation in ACS Explanation: **Obtain an ECG and troponin T levels**
- The patient presents with acute, progressive **chest pain that is sharp and burning**, along with nausea and shortness of breath, which are classic symptoms of an acute coronary syndrome, especially given her history of **coronary artery disease**, hypertension, diabetes, and prior smoking.
- An **ECG** and **troponin T levels** are crucial first steps to evaluate for myocardial ischemia or infarction in this high-risk patient.
*Administer IV pantoprazole and schedule endoscopy*
- While the patient has a history of gastroesophageal reflux disease (GERD) and her pain is described as "burning," the **acuteness, progression, and associated symptoms** (nausea, shortness of breath) in a patient with significant cardiac risk factors make a GI cause less likely as the primary concern.
- Empiric treatment for GERD without first ruling out a life-threatening cardiac event would be inappropriate and potentially dangerous.
*Discontinue levothyroxine and obtain fT4 levels*
- The patient is taking levothyroxine after a thyroidectomy for medullary thyroid cancer, but there is no immediate indication of thyroid hormone imbalance (e.g., hyperthyroidism causing chest pain) that would warrant discontinuing her medication or rushing fT4 levels as the first step in an acute chest pain presentation.
- Her pulse of 64/min is not suggestive of hyperthyroidism, which typically causes tachycardia.
*Administer IV levofloxacin and obtain chest radiograph*
- While shortness of breath can be a symptom of pneumonia, the **sharp, burning nature of the chest pain**, coupled with the absence of fever (temperature 37.4°C is mild), cough, or abnormal lung sounds (lungs clear to auscultation), makes an acute infection like pneumonia less probable as the primary diagnosis.
- Antibiotics and a chest radiograph would be considered after ruling out more immediate life-threatening conditions like acute coronary syndrome.
*Obtain urine and plasma metanephrine levels*
- The patient has a history of multiple endocrine neoplasia type 2A (MEN2A), which includes medullary thyroid cancer and can be associated with pheochromocytoma (adrenal tumor secreting catecholamines). However, her blood pressure (148/77 mm Hg) is not acutely elevated to crisis levels, and her symptoms are more consistent with cardiac ischemia than a pheochromocytoma crisis.
- While metanephrine levels would be important for long-term follow-up of MEN2A, they are not the immediate next step for acute chest pain in a patient with known coronary artery disease.
ECG interpretation in ACS US Medical PG Question 5: A 23-year-old man comes to the emergency department because of palpitations, dizziness, and substernal chest pain for three hours. The day prior, he was at a friend’s wedding, where he consumed seven glasses of wine. The patient appears diaphoretic. His pulse is 220/min and blood pressure is 120/84 mm Hg. Based on the patient's findings on electrocardiography, the physician diagnoses atrial fibrillation with rapid ventricular response and administers verapamil for rate control. Ten minutes later, the patient is unresponsive and loses consciousness. Despite resuscitative efforts, the patient dies. Histopathologic examination of the heart at autopsy shows an accessory atrioventricular conduction pathway. Electrocardiography prior to the onset of this patient's symptoms would most likely have shown which of the following findings?
- A. Epsilon wave following the QRS complex
- B. Prolongation of the QT interval
- C. Cyclic alteration of the QRS axis
- D. Slurred upstroke of the QRS complex (Correct Answer)
- E. Positive Sokolow-Lyon index
ECG interpretation in ACS Explanation: ***Slurred upstroke of the QRS complex***
- The patient's presentation with **atrial fibrillation with rapid ventricular response** and subsequent collapse after verapamil administration—a calcium channel blocker—is classic for a pre-excitation syndrome like **Wolff-Parkinson-White (WPW) syndrome**.
- In WPW, an accessory pathway (bundle of Kent) bypasses the AV node, leading to a **short PR interval** and a **delta wave** (slurred upstroke of the QRS complex) on ECG during normal sinus rhythm.
*Epsilon wave following the QRS complex*
- An **epsilon wave** is characteristic of **arrhythmogenic right ventricular cardiomyopathy (ARVC)**, representing delayed depolarization of the right ventricle.
- While ARVC can cause arrhythmias, it is distinctly different from the pre-excitation syndrome described, which involves an accessory pathway.
*Prolongation of the QT interval*
- **Prolonged QT interval** is associated with an increased risk of **torsades de pointes**, a polymorphic ventricular tachycardia.
- This finding is typical of **long QT syndrome** and does not directly relate to an accessory atrioventricular conduction pathway.
*Cyclic alteration of the QRS axis*
- **Cyclic alteration of the QRS axis** or electrical alternans is seen in conditions causing swings in cardiac position, most notably **pericardial effusion with tamponade**.
- This ECG finding is unrelated to accessory pathways or the mechanisms of pre-excitation syndromes.
*Positive Sokolow-Lyon index*
- A **positive Sokolow-Lyon index** signifies **left ventricular hypertrophy (LVH)**, characterized by large QRS voltages (e.g., SV1 + RV5/V6 ≥ 35 mm).
- While LVH can be associated with various cardiac conditions, it is not a direct ECG manifestation of an accessory atrioventricular conduction pathway.
ECG interpretation in ACS US Medical PG Question 6: A 40-year-old woman comes to the physician for a 6-month history of recurrent episodes of chest pain, racing pulse, dizziness, and difficulty breathing. The episodes last up to several minutes. She also reports urinary urgency and two episodes of loss of consciousness followed by spontaneous recovery. There is no personal or family history of serious illness. She does not smoke or drink alcohol. Vitals signs are within normal limits. Cardiopulmonary examination shows no abnormalities. Holter monitoring is performed. ECG recordings during episodes of tachycardia show a QRS duration of 100 ms, regular RR-interval, and absent P waves. Which of the following is the most likely underlying cause of this patient's condition?
- A. AV node with slow and fast pathway (Correct Answer)
- B. Pre-excitation of the ventricles
- C. Mutations in genes that code for myocyte ion channels
- D. Macroreentrant rhythm in the right atria through cavotricuspid isthmus
- E. Fibrosis of the sinoatrial node and surrounding myocardium
ECG interpretation in ACS Explanation: ***AV node with slow and fast pathway***
- This describes **AV nodal reentrant tachycardia (AVNRT)**, a common cause of **paroxysmal supraventricular tachycardia (PSVT)**. The ECG findings of **narrow QRS (100 ms)**, regular RR-interval, and **absent P waves** (often hidden within the QRS complex) are characteristic of AVNRT.
- The patient's symptoms of recurrent chest pain, racing pulse, dizziness, and spontaneous recovery from loss of consciousness fit the episodic nature of **AVNRT**. The presence of two pathways (slow and fast) within the AV node facilitates the reentrant circuit.
*Pre-excitation of the ventricles*
- **Pre-excitation syndromes** (e.g., Wolff-Parkinson-White syndrome) involve an accessory pathway that bypasses the AV node, leading to a **delta wave** and **short PR interval** on the baseline ECG.
- While they can cause SVT, the ECG during tachycardia would typically show a **wide QRS complex** if the accessory pathway is part of the reentrant circuit (antidromic), or a narrow QRS with a visible P wave if orthodromic and the accessory pathway is used for retrograde conduction, which doesn't fully align with the absent P waves and typically *normal* QRS during tachycardia as described.
*Mutations in genes that code for myocyte ion channels*
- This refers to **channelopathies** (e.g., long QT syndrome, Brugada syndrome), which predispose to **ventricular arrhythmias** like **polymorphic ventricular tachycardia** and **ventricular fibrillation**.
- These conditions typically cause **wide QRS tachycardias** and have distinct ECG patterns (e.g., prolonged QT interval, Brugada pattern) not described here. The narrow QRS and regular rhythm point away from primary ventricular channelopathies as the cause of this specific tachycardia.
*Macroreentrant rhythm in the right atria through cavotricuspid isthmus*
- This describes **atrial flutter**, which typically presents with characteristic **"sawtooth" F waves** on ECG, representing atrial activity.
- While atrial flutter can cause recurrent episodes of rapid heart rate, the ECG description of **absent P waves** and a **narrow QRS complex** without F waves makes atrial flutter less likely.
*Fibrosis of the sinoatrial node and surrounding myocardium*
- **Sinoatrial node dysfunction (sick sinus syndrome)** can lead to bradycardia, sinus pauses, or alternating bradycardia and tachycardia (tachy-brady syndrome).
- It does not primarily cause the described paroxysmal narrow-complex tachycardia with absent P waves. The patient's symptoms are more consistent with an abrupt-onset, regular supraventricular tachycardia.
ECG interpretation in ACS US Medical PG Question 7: A 30-year-old man is brought into the emergency room for complaints of acute onset chest pain and shortness of breath. He has a history of mental retardation and lives at home with his adoptive parents. His parents inform you that he has not seen a doctor since he was adopted as child and that he currently takes no medications. The patient's temperature is 99.1°F (37.3°C), pulse is 108/min, blood pressure is 125/70 mmHg, respirations are 25/min, and oxygen saturation is 92% on 2L nasal cannula. Physical exam is notable for a tall, thin individual with high-arched feet and mild pectus excavatum. There is mild asymmetry in the lower extremities with discomfort to dorsiflexion of the larger leg. Lung auscultation reveals no abnormalities. What is the most appropriate next step in management?
- A. Chest radiograph
- B. Serum blood test
- C. Genetic testing
- D. Angiogram
- E. Electrocardiogram (Correct Answer)
ECG interpretation in ACS Explanation: ***Correct: Electrocardiogram***
- **Acute chest pain** mandates an immediate **ECG** as the first diagnostic test to rule out **ST-elevation myocardial infarction (STEMI)**, which requires emergent intervention (PCI or thrombolysis).
- While this patient's presentation is highly suspicious for **pulmonary embolism (PE)** given the **unilateral leg swelling with pain on dorsiflexion** (suggestive of DVT), **tachycardia**, **tachypnea**, and **hypoxemia**, the ECG remains the most appropriate initial step per ACLS protocols for chest pain.
- ECG can also show findings suggestive of PE (sinus tachycardia, S1Q3T3 pattern, right heart strain) and help differentiate cardiac from pulmonary etiologies.
- The **Marfanoid features** (tall, thin, pectus excavatum, high-arched feet) raise concern for **aortic dissection**, which ECG can help evaluate alongside clinical assessment.
*Incorrect: Chest radiograph*
- Chest X-ray is critical in the workup and would typically be ordered simultaneously with or immediately after ECG in this patient with suspected PE.
- CXR helps exclude pneumothorax, pneumonia, and can show classic PE findings (Westermark sign, Hampton's hump), though it is often normal in PE.
- In the context of Marfan syndrome, CXR can reveal a widened mediastinum suggesting aortic dissection.
- However, ECG takes precedence as the immediate first step for any acute chest pain presentation.
*Incorrect: Serum blood test*
- Laboratory tests including **cardiac troponins** (for MI), **D-dimer** (for PE), and **CBC** are important but take time to result.
- D-dimer would be useful in this moderate-to-high probability PE case, but imaging (CT pulmonary angiography) would be more appropriate given the high clinical suspicion.
- Blood tests do not provide the immediate actionable information needed as the first diagnostic step in acute chest pain.
*Incorrect: Genetic testing*
- While the patient's phenotype suggests **Marfan syndrome** or another connective tissue disorder, genetic testing is an outpatient diagnostic tool for long-term management.
- It provides no immediate utility in the acute management of chest pain and respiratory distress.
- Genetic counseling and testing would be appropriate after stabilization and initial workup.
*Incorrect: Angiogram*
- **CT pulmonary angiography** would be the definitive test for PE diagnosis after initial ECG and CXR, but is not the immediate first step.
- **Cardiac catheterization** would be indicated if ECG showed STEMI or if there was high suspicion for ACS after initial workup.
- **CT aortography** might be needed if aortic dissection is suspected based on initial findings.
- Angiography is an invasive or advanced imaging procedure performed after non-invasive screening tests guide the diagnosis.
ECG interpretation in ACS US Medical PG Question 8: A 45-year-old man comes to the physician for a routine health maintenance examination. He feels well. He underwent appendectomy at the age of 25 years. He has a history of hypercholesterolemia that is well controlled with atorvastatin. He is an avid marathon runner and runs 8 miles per day four times a week. His father died of myocardial infarction at the age of 42 years. The patient does not smoke or drink alcohol. His vital signs are within normal limits. Cardiopulmonary examination shows no abnormalities. His abdomen is soft and nontender with a surgical scar in the right lower quadrant. Laboratory studies are within normal limits. An ECG is shown. Which of the following is the most likely diagnosis?
- A. Mobitz type II AV block
- B. First-degree AV block
- C. Mobitz type I AV block (Correct Answer)
- D. Third-degree AV block
- E. Atrial fibrillation
ECG interpretation in ACS Explanation: ***Mobitz type I AV block***
- The ECG shows progressive prolongation of the **PR interval** followed by a dropped QRS complex, which is characteristic of a **Mobitz type I (Wenckebach) AV block**.
- This rhythm disturbance is often benign, especially in athletes with high **vagal tone**, and does not usually require treatment.
*Mobitz type II AV block*
- **Mobitz type II AV block** is characterized by a constant PR interval before the dropped QRS complex.
- This type of block is generally more serious and indicative of a conduction disturbance below the AV node, often requiring a **pacemaker**.
*First-degree AV block*
- A **first-degree AV block** presents with a consistently prolonged PR interval (greater than 0.20 seconds) on every beat, without any dropped beats.
- In this patient's ECG, there is a dropped QRS complex after progressive PR prolongation.
*Third-degree AV block*
- **Third-degree (complete) AV block** is characterized by complete dissociation between the P waves and QRS complexes.
- There is no relationship between atrial and ventricular activity, and the ventricular rate is typically very slow and escape rhythms are observed.
*Atrial fibrillation*
- **Atrial fibrillation** is an irregularly irregular rhythm with no discernible P waves and varying R-R intervals.
- The ECG provided shows clear P waves and a regular, albeit interrupted, rhythm pattern.
ECG interpretation in ACS US Medical PG Question 9: A 56-year-old patient developed excruciating chest discomfort in the past 72 hours, relieved by GTN spray. Troponin I is normal, and the ECG shows features of left ventricular hypertrophy (LVH) with T wave flattening. The patient is already on statins, aspirin, and metoprolol 50 mg . What is the next best step in management?
- A. LMWH (Low Molecular Weight Heparin)
- B. Increase beta blocker dose
- C. IV NTG Drip
- D. Add Clopidogrel (Correct Answer)
- E. Arrange urgent coronary angiography
ECG interpretation in ACS Explanation: ***Add Clopidogrel***
- The patient presents with **unstable angina** (chest discomfort relieved by GTN, normal troponin, and ECG changes indicative of ischemia) and is already on aspirin, statins, and a beta-blocker.
- Adding **clopidogrel** (or another P2Y12 inhibitor) is crucial for **dual antiplatelet therapy (DAPT)**, which is a cornerstone in the management of unstable angina/NSTEMI to prevent further thrombotic events.
- This is the **immediate next step** to optimize medical therapy before considering invasive strategies.
*LMWH (Low Molecular Weight Heparin)*
- While **anticoagulation** is important in acute coronary syndromes and would be appropriate to add, the question asks for the **next best step** given the patient's existing management.
- LMWH would typically be added alongside DAPT, but establishing dual antiplatelet therapy takes priority.
*Increase beta blocker dose*
- The patient is already on metoprolol 50 mg, and while **titrating beta-blockers** is important for symptom control and reducing myocardial oxygen demand, the immediate priority in unstable angina is to address the underlying thrombotic process with DAPT.
- Beta-blocker optimization can be done after ensuring adequate antiplatelet therapy.
*IV NTG Drip*
- **Intravenous nitroglycerin (IV NTG)** is used to relieve ongoing chest pain and reduce preload/afterload, especially in severe or refractory symptoms.
- However, the patient's chest discomfort was already **relieved by GTN spray**, indicating that immediate pain control with IV NTG is not the most urgent next step compared to preventing further thrombotic events with DAPT.
*Arrange urgent coronary angiography*
- While **coronary angiography** is indicated in high-risk unstable angina, the immediate next step is to **optimize medical management** with dual antiplatelet therapy.
- Angiography timing depends on risk stratification; in a stable patient already on aspirin, beta-blockers, and statins, adding clopidogrel first ensures optimal antiplatelet coverage before any invasive procedure.
- Early invasive strategy (angiography within 24-72 hours) would be appropriate after medical stabilization.
ECG interpretation in ACS US Medical PG Question 10: 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
ECG interpretation in ACS 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.
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