ECG interpretation

ECG interpretation US Medical PG Question 1: An ECG from an 8-year-old male with neurosensory deafness and a family history of sudden cardiac arrest demonstrates QT-interval prolongation. Which of the following is this patient most at risk of developing?

• A. Hypertrophic cardiac myopathy
• B. Cardiac tamponade
• C. Essential hypertension
• D. Torsades de pointes (Correct Answer)
• E. First degree atrioventricular block

ECG interpretation Explanation: ***Torsades de pointes*** - The combination of **neurosensory deafness**, **QT-interval prolongation**, and a family history of **sudden cardiac arrest** is highly suggestive of **Jervell and Lange-Nielsen syndrome**, a form of **long QT syndrome**. - Patients with long QT syndrome are at significant risk for developing **polymorphic ventricular tachycardia** known as **Torsades de pointes**, which can degenerate into **ventricular fibrillation** and cause sudden cardiac death. *Hypertrophic cardiac myopathy* - This condition involves thickening of the **ventricular walls** and is associated with outflow tract obstruction, not primarily with QT prolongation. - While it can cause sudden cardiac arrest, it typically presents with symptoms like **dyspnea, chest pain**, or syncope during exertion, and its ECG findings usually include **left ventricular hypertrophy** and **deep Q waves**. *Cardiac tamponade* - **Cardiac tamponade** results from the accumulation of fluid in the **pericardial sac**, compressing the heart and impairing its filling. - This condition is not related to **QT prolongation** or **sensorineural deafness** and would present with signs of **hemodynamic instability**, such as **pulsus paradoxus** and muffled heart sounds. *Essential hypertension* - **Essential hypertension** is chronic high blood pressure with no identifiable secondary cause, commonly affecting adults. - It is not associated with **congenital neurosensory deafness** or significant **QT-interval prolongation** in childhood. *First degree atrioventricular block* - **First-degree AV block** is characterized by a prolonged **PR interval** on ECG, indicating delayed conduction through the AV node. - While it's an electrical abnormality, it is distinct from **QT prolongation** and is not typically associated with **neurosensory deafness** or the same risk of sudden cardiac arrest as long QT syndrome.

ECG interpretation US Medical PG Question 2: A researcher is studying how electrical activity propagates across the heart. In order to do this, he decides to measure the rate at which an action potential moves within various groups of cardiac muscle tissue. In particular, he isolates fibers from areas of the heart with the following characteristics: A) Dysfunction leads to fixed PR intervals prior to a dropped beat B) Dysfunction leads to increasing PR intervals prior to a dropped beat C) Dysfunction leads to tachycardia with a dramatically widened QRS complex D) Dysfunction leads to tachycardia with a sawtooth pattern on electrocardiogram Which of the following is the proper order of these tissues from fastest action potential propagation to slowest action potential propagation.

• A. B > D > C > A
• B. D > C > A > B
• C. B > C > D > A
• D. A > D > C > B (Correct Answer)
• E. A > C > D > B

ECG interpretation Explanation: ***A > D > C > B*** * **Purkinje fibers (A)** have the fastest conduction velocity in the heart to ensure rapid and synchronous ventricular depolarization. The description of "fixed PR intervals prior to a dropped beat" in **Mobitz type II second-degree AV block** indicates an issue with conduction distal to the AV node, often in the His-Purkinje system, while still maintaining typical conduction through the atria and AV node for conducted beats. * **Atrial muscle (D)** has a faster conduction velocity than the AV node but slower than Purkinje fibers. The "sawtooth pattern on electrocardiogram" unequivocally points to **atrial flutter**, which is characterized by rapid, regular depolarization of the atria. * **Ventricular muscle (C)** has a conduction velocity slower than Purkinje fibers but faster than the AV node. "Tachycardia with a dramatically widened QRS complex" is characteristic of **ventricular tachycardia (VT)**, which arises from abnormal electrical activity within the ventricles. * **AV node (B)** has the slowest conduction velocity in the heart, which allows for proper ventricular filling. "Increasing PR intervals prior to a dropped beat" describes **Mobitz type I second-degree AV block (Wenckebach phenomenon)**, which is due to progressive prolongation of conduction delay within the AV node itself. *B > D > C > A* * This order incorrectly places the **AV node (B)** as the fastest and **Purkinje fibers (A)** as the slowest, which is contrary to the known conduction velocities in the heart. * The AV node is critical for delaying the impulse, making it the slowest, while Purkinje fibers are designed for rapid spread, making them the fastest. *D > C > A > B* * This option incorrectly places **atrial muscle (D)** as faster than **Purkinje fibers (A)**. Purkinje fibers have the fastest conduction velocity in the heart, considerably faster than atrial muscle. *B > C > D > A* * This arrangement incorrectly lists the **AV node (B)** as the fastest and **Purkinje fibers (A)** as the slowest. The AV node is the slowest for its physiological role of delaying ventricular contraction, while Purkinje fibers are optimized for rapid conduction. *A > C > D > B* * While placing **Purkinje fibers (A)** as the fastest and the **AV node (B)** as the slowest is correct, this order incorrectly places **ventricular muscle (C)** as faster than **atrial muscle (D)**. Atrial muscle generally conducts faster than ventricular muscle in normal physiology.

ECG interpretation US Medical PG Question 3: A 72-year-old man comes to the physician because of a 2-month history of intermittent retrosternal chest pain and tightness on exertion. He has type 2 diabetes mellitus, osteoarthritis of the right hip, and hypertension. Current medications include insulin, ibuprofen, enalapril, and hydrochlorothiazide. Vital signs are within normal limits. His troponin level is within the reference range. An ECG at rest shows a right bundle branch block and infrequent premature ventricular contractions. The patient's symptoms are reproduced during adenosine stress testing. Repeat ECG during stress testing shows new ST depression of > 1 mm in leads V2, V3, and V4. Which of the following is the most important underlying mechanism of this patient's ECG changes?

• A. Diversion of blood flow from stenotic coronary arteries (Correct Answer)
• B. Transient atrioventricular nodal blockade
• C. Reduced left ventricular preload
• D. Ruptured cholesterol plaque within a coronary vessel
• E. Increased myocardial oxygen demand

ECG interpretation Explanation: ***Diversion of blood flow from stenotic coronary arteries*** - The **adenosine stress test** induces **submaximal coronary vasodilation** in healthy vessels, diverting blood flow away from stenosed areas that are already maximally dilated, a phenomenon known as **coronary steal**. - This **relative hypoperfusion** in areas supplied by stenotic arteries leads to myocardial ischemia, manifested as **new ST depression** on the ECG due to **subendocardial oxygen supply-demand mismatch**. *Transient atrioventricular nodal blockade* - While adenosine can cause transient AV nodal blockade, leading to AV blocks, this would manifest as specific changes in **PR interval** or **QRS drop-out**, not ST segment depression indicative of ischemia. - The patient's symptoms and ECG changes point towards myocardial ischemia, not an AV conduction disturbance. *Reduced left ventricular preload* - Reduced preload can occur in certain cardiac conditions but is not the primary mechanism behind ST depression during an adenosine stress test. - ECG changes due to reduced preload are usually nonspecific, such as **sinus tachycardia** or **low voltage**, and do not typically cause new ST depression in specific leads. *Ruptured cholesterol plaque within a coronary vessel* - A ruptured plaque with subsequent **thrombus formation** would lead to **acute coronary syndrome (ACS)**, characterized by persistent chest pain, **elevated troponins**, and potentially **ST elevation** or new **pathologic Q waves** if complete occlusion occurs. - The patient's troponin level is normal, and his symptoms are intermittent and reproducible on stress testing, which is more consistent with **stable angina**. *Increased myocardial oxygen demand* - While increased myocardial oxygen demand is a component of angina pectoris, adenosine primarily causes **coronary vasodilation**, which can worsen ischemia in stenotic areas by diverting blood flow, rather than directly increasing myocardial oxygen demand itself. - **Dobutamine stress testing** would be the test that primarily increases myocardial oxygen demand.

ECG interpretation US Medical PG Question 4: 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

ECG interpretation 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.

ECG interpretation US Medical PG Question 5: A 65-year-old woman comes to the physician because of a 3-month history of intermittent palpitations and shortness of breath. Cardiopulmonary examination shows no other abnormalities. An ECG shows an absence of P waves, an oscillating baseline, and irregular RR intervals at a rate of approximately 95 beats per minute. The difference between atrial and ventricular rates in this patient is most likely due to which of the following?

• A. Prolonged influx through voltage-gated Ca2+ channels in the bundle of His
• B. Transient activation of K+ current in Purkinje fibers
• C. Inhibition of the Na+/K+-ATPase pump in ventricular cells
• D. Limited speed of conduction through the left bundle branch
• E. Temporary inactivation of Na+ channels in the AV node (Correct Answer)

ECG interpretation Explanation: ***Temporary inactivation of Na+ channels in the AV node*** - The ECG findings are classic for **atrial fibrillation**, characterized by a rapid, irregular atrial rhythm (oscillating baseline with no P waves) and an irregularly irregular ventricular response. - The **AV node's refractory period** and the number of sodium channels available for conduction dictate the rate at which atrial impulses can pass to the ventricles, preventing a dangerously fast ventricular rate. *Prolonged influx through voltage-gated Ca2+ channels in the bundle of His* - The **bundle of His** primarily conducts impulses rather than primarily regulating the rate difference between atria and ventricles through calcium channel kinetics. - Prolonged calcium influx would generally **slow conduction** or decrease excitability, but it's not the primary mechanism explaining the ventricular rate control in atrial fibrillation. *Transient activation of K+ current in Purkinje fibers* - **Purkinje fibers** are involved in rapid ventricular depolarization, but their primary role is not to mediate the rate difference between atria and ventricles in atrial fibrillation. - Activation of K+ current typically leads to **repolarization**, affecting action potential duration, not the overall filtering of atrial impulses. *Inhibition of the Na+/K+-ATPase pump in ventricular cells* - Inhibition of the **Na+/K+-ATPase pump** would lead to intracellular sodium accumulation and depolarization, potentially causing arrhythmias, not regulating the ventricular rate in atrial fibrillation. - This is the mechanism of action for **digoxin**, which can slow AV nodal conduction but through a different primary pathway affecting the pump. *Limited speed of conduction through the left bundle branch* - While conduction system abnormalities can occur, a **limited speed of conduction** specifically in the left bundle branch would cause a wide QRS complex or bundle branch block, not the inherent rate-limiting seen in atrial fibrillation. - The AV node is the primary regulator of ventricular response rate in atrial fibrillation due to its inherent physiological properties.

ECG interpretation US Medical PG Question 6: In a patient with acute myocardial ischemia, which of the following cardiovascular structures is at greatest risk of damage?

• A. Pulmonary valve
• B. Cardiac conduction system (Correct Answer)
• C. Coronary artery
• D. Cardiac septum
• E. Temporal artery

ECG interpretation Explanation: ***Cardiac conduction system*** - The **cardiac conduction system** is highly dependent on a constant oxygen supply, and its disruption by ischemia can lead to serious **arrhythmias** and **heart blocks**. - Ischemia in critical areas like the **AV node** (supplied by the RCA) or the **bundle branches** can severely impair the heart's electrical activity. *Pulmonary valve* - The **pulmonary valve** is primarily a passive structure and is generally not directly damaged by acute myocardial ischemia. - Its function is more affected by changes in **pulmonary artery pressure** or **ventricular remodeling**, not immediate ischemic injury. *Coronary artery* - While **coronary artery disease (CAD)** is the *cause* of myocardial ischemia, the coronary artery itself is not the structure *damaged* in the sense of functional impairment due to lack of blood flow in acute ischemia. - The damage occurs downstream in the **myocardium** that the artery supplies. *Cardiac septum* - The **cardiac septum** can be damaged by myocardial ischemia, particularly the **interventricular septum**, leading to complications like **septal rupture**. - However, the conduction system is at *greatest* immediate risk of functional damage leading to life-threatening events due to its critical role in rhythm generation. *Temporal artery* - The **temporal artery** is a blood vessel located in the head, entirely separate from the heart. - It is not involved in myocardial ischemia and is not at risk of damage from a cardiac event.

ECG interpretation US Medical PG Question 7: Cardiac muscle serves many necessary functions, leading to a specific structure that serves these functions. The structure highlighted is an important histology component of cardiac muscle. What would be the outcome if this structure diffusely failed to function?

• A. Failure of potassium channels to appropriately open to repolarize the cell
• B. Failure of propagation of the action potential from the conduction system (Correct Answer)
• C. Ineffective excitation-contraction coupling due to insufficient calcium ions
• D. Inappropriate formation of cardiac valve leaflets
• E. Outflow tract obstruction

ECG interpretation Explanation: ***Failure of propagation of the action potential from the conduction system*** - The highlighted structure, the **intercalated disc**, contains **gap junctions** which are crucial for the rapid, synchronized spread of **action potentials** between cardiac muscle cells. - A diffuse failure of these structures would prevent the coordinated electrical activation of the myocardium, leading to a failure of impulse propagation and **compromised cardiac contraction**. *Failure of potassium channels to appropriately open to repolarize the cell* - This scenario describes a problem with **ion channel function** within individual cardiomyocytes, affecting their repolarization phase. - While critical for a single cell's electrical activity, it does not directly relate to the primary function of **intercalated discs** in *propagating* action potentials across multiple cells. *Ineffective excitation-contraction coupling due to insufficient calcium ions* - This outcome would result from issues with **calcium handling** mechanisms, such as problems with the **sarcoplasmic reticulum** or **calcium channels**, which are internal to the cardiomyocyte. - It is distinct from the role of **intercalated discs** in facilitating intercellular communication and electrical spread. *Inappropriate formation of cardiac valve leaflets* - The formation of cardiac valve leaflets is an intricate process during **embryological development** involving specific signaling pathways and cell migration. - This structural defect is not directly related to the function of **intercalated discs** in mature cardiac muscle, which are involved in electrical and mechanical coupling. *Outflow tract obstruction* - **Outflow tract obstruction** is a congenital or acquired structural defect affecting the major arteries leaving the heart (e.g., aortic or pulmonary stenosis). - This is a macroscopic structural anomaly that is not caused by a primary failure of **intercalated disc** function.

ECG interpretation US Medical PG Question 8: A 17-year-old boy comes to the physician for a follow-up examination. Two months ago, he suffered a spinal fracture after a fall from the roof. He feels well. His father has multiple endocrine neoplasia type 1. Vital signs are within normal limits. Examination shows no abnormalities. Laboratory studies show: Hemoglobin 13.7 g/dL Serum Creatinine 0.7 mg/dL Proteins Total 7.0 g/dL Albumin 4.1 g/dL Calcium 11.4 mg/dL Phosphorus 5.3 mg/dL Alkaline phosphatase 100 U/L Which of the following is the most likely cause of these findings?

• A. Immobilization (Correct Answer)
• B. Parathyroid adenoma
• C. Paraneoplastic syndrome
• D. Sarcoidosis
• E. Pseudohypercalcemia

ECG interpretation Explanation: ***Immobilization*** - Prolonged **immobilization**, especially after a spinal fracture, leads to **bone resorption**, releasing calcium and phosphorus into the bloodstream, causing **hypercalcemia** and **hyperphosphatemia**. - Though calcium and phosphorus are elevated, the **alkaline phosphatase** is normal, which is consistent with immobilization-induced bone resorption rather than primary bone disease. *Parathyroid adenoma* - A **parathyroid adenoma** causes primary **hyperparathyroidism**, characterized by **hypercalcemia** and **hypophosphatemia** (due to increased renal phosphate excretion), which contradicts the elevated phosphorus level seen here. - Although the father has MEN1, a personal history of parathyroid adenoma is not indicated by the lab results. *Paraneoplastic syndrome* - **Paraneoplastic syndrome** causing hypercalcemia is typically due to ectopic production of **parathyroid hormone-related peptide (PTHrP)**, leading to **hypercalcemia** with **low PTH** and generally **low phosphorus** levels. - This condition most commonly occurs with malignancies, such as squamous cell carcinoma, which is not indicated in this healthy-appearing young man with a recent fracture. *Sarcoidosis* - **Sarcoidosis** causes hypercalcemia due to increased synthesis of **1,25-dihydroxyvitamin D** by activated macrophages, leading to increased intestinal calcium absorption. - This typically results in **hypercalcemia** with **normal or low PTH** and **normal or low phosphorus** levels; it is not associated with elevated phosphorus. *Pseudohypercalcemia* - **Pseudohypercalcemia** is an artifactual elevation of total calcium, usually due to **severe dehydration** or **elevated protein** levels, particularly **albumin** or **immunoglobulins**. - In this case, the albumin and total protein levels are within the normal range, making pseudohypercalcemia unlikely.

ECG interpretation US Medical PG Question 9: A 52-year-old man is brought to the emergency department by ambulance after a motor vehicle accident. He was an unrestrained passenger who was ejected from the vehicle. On presentation, he is found to be actively bleeding from numerous wounds. His blood pressure is 76/42 mmHg and pulse is 152/min. Attempts at resuscitation fail, and he dies 25 minutes later. Autopsy shows blood in the peritoneal cavity, and histology of the kidney reveals swelling of the proximal convoluted tubule epithelial cells. Which of the following is most likely the mechanism underlying the renal cell findings?

• A. Decreased activity of caspase 7
• B. Increased activity of caspase 9
• C. Increased function of the Na+/K+-ATPase
• D. Increased activity of caspase 8
• E. Decreased function of the Na+/K+-ATPase (Correct Answer)

ECG interpretation Explanation: ***Decreased function of the Na+/K+-ATPase*** - The patient experienced **hypovolemic shock** due to severe blood loss, leading to a significant drop in blood pressure and organ perfusion. This results in **ischemia** of the renal cells. - **Ischemic injury** impairs ATP production, which is essential for the function of the **Na+/K+-ATPase pump**. Failure of this pump leads to intracellular accumulation of sodium and water, causing **cellular swelling**, particularly noticeable in the proximal convoluted tubules. *Decreased activity of caspase 7* - **Caspases**, including caspase 7, are involved in **apoptosis** (programmed cell death), which involves cell shrinkage and fragmentation, not the swelling observed here. - Decreased caspase activity would generally *reduce* apoptosis, which is not the primary mechanism of acute cell injury in shock. *Increased activity of caspase 9* - Increased activity of **caspase 9** is indicative of the **intrinsic apoptotic pathway**, typically initiated by mitochondrial damage. - While prolonged ischemia can eventually lead to apoptotic changes, the acute finding of **cellular swelling** points more directly to immediate membrane pump dysfunction due to ATP depletion. *Increased function of the Na+/K+-ATPase* - **Increased function** of the Na+/K+-ATPase would actively pump sodium out of the cell and potassium in, *preventing* intracellular swelling. - This option contradicts the observed finding of proximal convoluted tubule epithelial cell swelling, which is characteristic of acute cellular injury due to pump failure. *Increased activity of caspase 8* - **Caspase 8** is a key initiator caspase in the **extrinsic apoptotic pathway**, often triggered by death receptor signaling. - Similar to caspase 9, increased caspase 8 activity would lead to apoptosis, characterized by cell shrinkage, not the **cellular swelling** seen in acute ischemic injury.

ECG interpretation US Medical PG Question 10: An investigator develops a new drug that decreases the number of voltage-gated potassium channels in cardiac muscle cell membranes. Which of the following is the most likely effect of this drug on the myocardial action potential?

• A. Delayed repolarization (Correct Answer)
• B. Delayed depolarization
• C. Accelerated repolarization
• D. Decreased resting membrane potential
• E. Accelerated depolarization

ECG interpretation Explanation: ***Delayed repolarization*** - **Voltage-gated potassium channels** are primarily responsible for the efflux of potassium ions during the **repolarization phase** (phase 3) of the cardiac action potential. - A decrease in the number of these channels would reduce potassium efflux, thus slowing down the repolarization process and prolonging the **action potential duration**. *Delayed depolarization* - **Depolarization** (phase 0) of the cardiac action potential is primarily mediated by the rapid influx of **sodium ions** through voltage-gated sodium channels. - Changes in potassium channels do not directly affect the speed of depolarization. *Accelerated repolarization* - Accelerated repolarization would occur if there were an *increase* in the number or activity of **potassium channels**, leading to a faster efflux of potassium ions. - A *decrease* in these channels would have the opposite effect. *Decreased resting membrane potential* - The **resting membrane potential** is primarily maintained by the **leak potassium channels** and the **Na+/K+ ATPase pump**, not directly by voltage-gated potassium channels involved in repolarization. - A decrease in voltage-gated potassium channels would not significantly alter the resting membrane potential. *Accelerated depolarization* - Accelerated depolarization would result from an *increase* in the speed or magnitude of **sodium influx** during phase 0. - A reduction in potassium channels has no direct impact on the rate of sodium channel activation or current.

ECG interpretation Flashcard 1 of 10

Question: The end of rapid ventricular ejection corresponds with the onset of the _____ wave on ECG

Answer: T

ECG interpretation Flashcard 2 of 10

Question: The _____ on ECG represents the entire period of ventricular depolarization, contraction, and repolarization

Answer: QT interval

ECG interpretation Flashcard 3 of 10

Question: The onset of reduced ventricular ejection corresponds with the onset of the _____ wave on ECG

Answer: T

ECG interpretation Flashcard 4 of 10

Question: The _____ refractory period refers to the period in which a(n) conductive action potential cannot be generated

Answer: effective

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ECG interpretation Flashcard 5 of 10

Question: A(n) negative dromotropic effect increases the _____ interval on an ECG

Answer: PR

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ECG interpretation Flashcard 6 of 10

Question: Hypo-kalemia induced arrhythmias may present on ECG with _____ waves at the end of the T wave

Answer: U

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ECG interpretation Flashcard 7 of 10

Question: The output of the Purkinje cells is always _____

Answer: inhibitory

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ECG interpretation Flashcard 8 of 10

Question: The _____ on ECG represents the entire period of ventricular depolarization, contraction, and repolarization

Answer: QT interval

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ECG interpretation Flashcard 9 of 10

Question: Phase _____ of the myocardial action potential is characterized by rapid upstroke/depolarization

Answer: 0

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ECG interpretation Flashcard 10 of 10

Question: If the stereocilia are bent toward the kinocilium, the hair cell _____-polarizes

Answer: de

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