Cardiac axis determination US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Cardiac axis determination. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Cardiac axis determination US Medical PG Question 1: A 75-year-old man presents to the emergency department after an episode of syncope while walking outside with his wife. His wife states that he suddenly appeared pale and collapsed to the ground. She says he remained unconscious for 1 minute. He says he noticed a fluttering in his chest and excessive sweating before the episode. He has type 2 diabetes mellitus, essential hypertension, and chronic stable angina. He has not started any new medications in the past few months. Vital signs reveal: temperature 37.0°C (98.6°F), blood pressure 135/72 mm Hg, and pulse 72/min. Physical examination is unremarkable. ECG shows an old bifascicular block. Echocardiogram and 24-hour Holter monitoring are normal. Which of the following is the best next step in the evaluation of this patient's condition?
- A. Cardiac enzymes
- B. Continuous loop recorder (Correct Answer)
- C. Valsalva maneuver
- D. Electroencephalography (EEG)
- E. Tilt-table test
Cardiac axis determination Explanation: ***Continuous loop recorder***
- This patient's syncope is preceded by **palpitations (fluttering in chest)** and **sweating**, suggesting a cardiac etiology, specifically a **transient arrhythmia** not captured on a standard ECG or 24-hour Holter.
- A continuous loop recorder provides prolonged monitoring (months to years), increasing the likelihood of detecting intermittent arrhythmias responsible for syncopal episodes.
*Cardiac enzymes*
- While cardiac enzymes (e.g., troponin) are crucial for evaluating **acute myocardial ischemia** or infarction, the patient presents with syncope and no new chest pain, and his stable angina suggests chronic disease rather than an acute event leading to syncope in this specific instance.
- An **ECG showing an old bifascicular block** and an **unremarkable physical exam** make an acute cardiac event less likely as the primary cause of syncope when an arrhythmia is suspected.
*Valsalva maneuver*
- The Valsalva maneuver is a diagnostic tool often used to differentiate between certain types of **tachyarrhythmias** or to evaluate for **autonomic dysfunction**, but it is not an evaluative step for a patient presenting with unexplained syncope where an arrhythmia has not yet been documented.
- It would not help in identifying the cause of intermittent syncope in a patient whose standard workup has been unremarkable, as it's a test for immediate physiological response, not prolonged cardiac rhythm monitoring.
*Electroencephalography (EEG)*
- EEG is indicated when **seizure disorder** is suspected as the cause of loss of consciousness, often characterized by tonic-clonic movements, post-ictal confusion, or focal neurologic signs, which are absent in this patient's presentation.
- The patient's pre-syncopal symptoms of **palpitations and sweating** point away from a seizure and towards a cardiac cause.
*Tilt-table test*
- A tilt-table test is used to evaluate for **vasovagal syncope** or **postural orthostatic tachycardia syndrome (POTS)**, often considered when other cardiac causes are ruled out or when syncope is typically triggered by prolonged standing.
- Given the patient's pre-syncopal **palpitations**, a **cardiac arrhythmia** remains a higher suspicion than vasovagal syncope at this stage, especially after normal echocardiogram and Holter monitoring, necessitating further arrhythmia investigation.
Cardiac axis determination US Medical PG Question 2: A researcher measures action potential propagation velocity in various regions of the heart in a 42-year-old Caucasian female. Which of the following set of measurements corresponds to the velocities found in the atrial muscle, AV Node, Purkinje system, and ventricular muscle, respectively?
- A. 0.05 m/s, 1.1 m/s, 2.2 m/s, 3.3 m/s
- B. 2.2 m/s, 0.3 m/s, 0.05 m/s, 1.1 m/s
- C. 0.3 m/s, 2.2 m/s, 0.05 m/s, 1.1 m/s
- D. 0.5 m/s, 1.1 m/s, 2.2 m/s, 3 m/s
- E. 1.1 m/s, 0.05 m/s, 2.2 m/s, 0.3 m/s (Correct Answer)
Cardiac axis determination Explanation: ***1.1 m/s, 0.05 m/s, 2.2 m/s, 0.3 m/s***
- This option correctly lists the approximate conduction velocities for the **atrial muscle (1.1 m/s)**, **AV node (0.05 m/s)**, **Purkinje system (2.2 m/s)**, and **ventricular muscle (0.3 m/s)**, respectively.
- The **AV node has the slowest conduction velocity (~0.05 m/s)**, which is crucial for delaying ventricular contraction and allowing complete ventricular filling.
- The **Purkinje system has the fastest conduction velocity (~2-4 m/s)**, ensuring rapid and coordinated ventricular depolarization.
- **Atrial muscle (~1 m/s)** and **ventricular muscle (~0.3-0.5 m/s)** have intermediate velocities.
*0.05 m/s, 1.1 m/s, 2.2 m/s, 3.3 m/s*
- This sequence is incorrect because it places the **AV node's velocity (0.05 m/s)** first (as atrial muscle) and significantly overestimates ventricular muscle velocity (3.3 m/s).
- Atrial muscle conducts faster than 0.05 m/s, and ventricular muscle velocity should be approximately 0.3-0.5 m/s, not 3.3 m/s.
*2.2 m/s, 0.3 m/s, 0.05 m/s, 1.1 m/s*
- This option incorrectly assigns the **highest velocity (2.2 m/s)** to atrial muscle, which is characteristic of the Purkinje system, and misplaces the **slowest velocity (0.05 m/s)** in the Purkinje system instead of the AV node.
- The values do not align with known physiological conduction speeds across cardiac tissues.
*0.3 m/s, 2.2 m/s, 0.05 m/s, 1.1 m/s*
- This sequence incorrectly places the **slowest velocity (0.05 m/s)** in the Purkinje system, which is known for the most rapid conduction, and assigns an unrealistically high velocity (2.2 m/s) to the AV node.
- The arrangement directly contradicts the physiological function and relative speeds within the cardiac conduction system.
*0.5 m/s, 1.1 m/s, 2.2 m/s, 3 m/s*
- This option underestimates the **atrial muscle velocity** (0.5 m/s instead of ~1 m/s) and significantly overestimates the **ventricular muscle velocity** (3 m/s instead of ~0.3-0.5 m/s).
- The provided values do not accurately represent the typical ranges of conduction velocities for each specified cardiac region.
Cardiac axis determination US Medical PG Question 3: A 56-year-old man comes to the physician for a 5-month history of progressive bilateral ankle swelling and shortness of breath on exertion. He can no longer walk up the stairs to his bedroom without taking a break. He also constantly feels tired during the day. His wife reports that he snores at night and that he sometimes chokes in his sleep. The patient has smoked 1 pack of cigarettes daily for 25 years. He has a history of hypertension treated with enalapril. His pulse is 72/min, respirations are 16/min, and blood pressure is 145/95 mmHg. There is jugular venous distention. The lungs are clear to auscultation bilaterally. The extremities are warm and well perfused. There is 2+ lower extremity edema bilaterally. ECG shows right axis deviation. Which of the following is the most likely cause of this patient's condition?
- A. Alveolar destruction
- B. Ischemic heart disease
- C. Left ventricular hypertrophy
- D. Chronic hypoxia (Correct Answer)
- E. Chronic kidney damage
Cardiac axis determination Explanation: ***Chronic hypoxia***
- The patient's history of **heavy smoking**, snoring with choking episodes suggestive of **sleep apnea**, and symptoms of **right-sided heart failure** (bilateral ankle swelling, JVD, right axis deviation on ECG) point to chronic hypoxia as the underlying cause.
- **Chronic hypoxia** leads to **pulmonary vasoconstriction** and subsequent pulmonary hypertension, which eventually causes **right ventricular hypertrophy** and failure (cor pulmonale).
*Alveolar destruction*
- While **alveolar destruction** (emphysema) can lead to hypoxia in smokers, the normal auscultation of the lungs makes this less likely to be the primary cause of his symptoms, although it could contribute.
- The **ECG showing right axis deviation** more strongly suggests a primary pulmonary vascular issue or sustained right ventricular strain rather than solely alveolar destruction.
*Ischemic heart disease*
- Although the patient has risk factors for **ischemic heart disease** (smoking, hypertension), his symptoms and signs (bilateral ankle swelling, JVD, right axis deviation, clear lungs) are more consistent with isolated **right-sided heart failure** due to a pulmonary issue, not acute or chronic ischemia.
- **Left-sided heart failure** due to ischemic heart disease would typically present with pulmonary congestion (crackles, dyspnea) before isolated right-sided symptoms appear.
*Left ventricular hypertrophy*
- **Left ventricular hypertrophy** (LVH) is often seen in hypertension, but the patient's presentation of **right-sided heart failure** symptoms (JVD, edema, right axis deviation) with clear lungs does not directly point to LVH as the primary cause of his current condition.
- While his hypertension could lead to LVH, the symptoms described are more consistent with **pulmonary hypertension** and cor pulmonale.
*Chronic kidney damage*
- **Chronic kidney damage** would explain the bilateral ankle swelling, but it would typically be associated with other signs like elevated creatinine, uremia, or proteinuria, which are not mentioned.
- It would also not explain the **shortness of breath on exertion**, **snoring with choking**, or the **right axis deviation** on ECG, which directly points to a cardiac or pulmonary issue.
Cardiac axis determination US Medical PG Question 4: A 58-year-old man presents to the emergency department for evaluation of intermittent chest pain over the past 6 months. His history reveals that he has had moderate exertional dyspnea and 2 episodes of syncope while working at his factory job. These episodes of syncope were witnessed by others and lasted roughly 30 seconds. The patient states that he did not have any seizure activity. His vital signs include: blood pressure 121/89 mm Hg, heart rate 89/min, temperature 37.0°C (98.6°F), and respiratory rate 16/min. Physical examination reveals a crescendo-decrescendo systolic murmur in the right second intercostal area. An electrocardiogram is performed, which shows left ventricular hypertrophy. Which of the following is the best next step for this patient?
- A. Transthoracic echocardiography (Correct Answer)
- B. Chest radiograph
- C. Computed tomography (CT) chest scan without contrast
- D. Cardiac chamber catheterization
- E. Transesophageal echocardiography
Cardiac axis determination Explanation: ***Transthoracic echocardiography***
- The patient's symptoms (chest pain, exertional dyspnea, syncope) and physical exam findings (**crescendo-decrescendo systolic murmur at the right second intercostal space**, ECG showing **left ventricular hypertrophy**) are highly suggestive of **aortic stenosis**.
- **Transthoracic echocardiography** is the gold standard for diagnosing and assessing the severity of valvular heart diseases like aortic stenosis, quantifying valve area, pressure gradients, and ventricular function.
*Chest radiograph*
- A chest radiograph provides information about lung fields, cardiac size, and aortic calcification, but it cannot directly visualize or assess the function of heart valves.
- While it may show signs of heart failure (e.g., **pulmonary congestion**) or **cardiomegaly**, it is insufficient for a definitive diagnosis or severity assessment of valvular lesions.
*Computed tomography (CT) chest scan without contrast*
- A CT scan can detect calcification of the aortic valve, but it is not the primary imaging modality for assessing valvular function or the severity of stenotic lesions.
- CT is more useful for evaluating the **aorta for aneurysm** or dissection, or for **pulmonary pathology**, neither of which is the most likely diagnosis given the presenting symptoms.
*Cardiac chamber catheterization*
- Cardiac catheterization is an **invasive procedure** that is typically reserved for cases where non-invasive imaging is inconclusive or when planning for intervention (e.g., prior to valve replacement).
- It involves risks and is not the initial best step for diagnosis when a less invasive and highly informative test like echocardiography is available.
*Transesophageal echocardiography*
- **Transesophageal echocardiography (TEE)** provides more detailed images of the heart and valves compared to TTE because it avoids acoustic shadowing from the ribs and lungs.
- However, TEE is more invasive than TTE and is usually reserved for situations where TTE is inadequate or when a higher resolution view is needed, such as for infective endocarditis, prosthetic valve dysfunction, or before/during surgical procedures.
Cardiac axis determination US Medical PG Question 5: An abnormal wave is noted on a routine ECG. The wave in question represents which of the following electrical events in the cardiac cycle?
- A. Period between ventricular depolarization and repolarization
- B. Atrial repolarization
- C. Ventricular repolarization (Correct Answer)
- D. Ventricular depolarization
- E. Atrial depolarization
Cardiac axis determination Explanation: ***Ventricular repolarization***
- The **T wave** represents ventricular repolarization, which is the electrical recovery phase of the ventricles after contraction
- T wave abnormalities are among the most common ECG findings and include **T wave inversions** (myocardial ischemia, ventricular hypertrophy), **peaked T waves** (hyperkalemia), **flattened T waves** (hypokalemia, ischemia), and **biphasic T waves**
- The T wave corresponds to **phase 3** of the ventricular action potential when potassium channels open and the membrane repolarizes
*Period between ventricular depolarization and repolarization*
- This describes the **ST segment**, which represents the period when ventricles are completely depolarized before repolarization begins
- The **QT interval** encompasses both ventricular depolarization and repolarization (QRS + ST segment + T wave)
- These are intervals or segments, not waves
*Atrial repolarization*
- Atrial repolarization occurs during ventricular depolarization and is represented by the **Ta wave**
- This wave is typically **not visible** on standard ECG because it is **masked by the much larger QRS complex** and has very low amplitude
- It cannot be identified as a distinct wave on routine ECGs
*Ventricular depolarization*
- The **QRS complex** represents ventricular depolarization, the electrical activation that triggers ventricular contraction
- Normal QRS duration is **0.06-0.10 seconds** (3 small boxes or less)
- QRS abnormalities include bundle branch blocks, ventricular hypertrophy patterns, and pre-excitation
*Atrial depolarization*
- The **P wave** represents atrial depolarization, the electrical activation that triggers atrial contraction
- Normal P wave characteristics: **upright in leads I, II, aVF**; duration less than 0.12 seconds; amplitude less than 2.5 mm
- P wave abnormalities include left atrial enlargement (broad, notched P waves) and right atrial enlargement (tall, peaked P waves)
Cardiac axis determination US Medical PG Question 6: 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
Cardiac axis determination 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.
Cardiac axis determination US Medical PG Question 7: A 17-year-old girl suddenly grabs her chest and collapses to the ground while playing volleyball at school. The teacher rushes to evaluate the situation and finds that the girl has no pulse and is not breathing. He starts chest compressions. An automated external defibrillator (AED) is brought to the scene within 3 minutes and a shock is delivered. The girl regains consciousness and regular sinus rhythm. She is rushed to the emergency department. The vital signs include: blood pressure 122/77 mm Hg and pulse 65/min. The pulse is regular. An electrocardiogram (ECG) shows a shortened PR interval, a wide QRS complex, a delta wave, and an inverted T wave. Which of the following is the most likely pathology in the conduction system of this patient’s heart?
- A. Impulse generation by tissue in atrioventricular node
- B. Accessory pathway from atria to ventricles (Correct Answer)
- C. Automatic discharge of irregular impulses in the atria
- D. Wandering atrial pacemaker
- E. Blockage in conduction pathway
Cardiac axis determination Explanation: ***Accessory pathway from atria to ventricles***
- The ECG findings of a **shortened PR interval**, **delta wave**, and **wide QRS complex** are characteristic of **Wolff-Parkinson-White (WPW) syndrome**, which involves an **accessory pathway** (Bundle of Kent) bypassing the AV node.
- This accessory pathway allows for pre-excitation of the ventricles, predisposing patients to **tachyarrhythmias** like the one experienced by the patient (sudden cardiac arrest).
*Impulse generation by tissue in atrioventricular node*
- This describes a **junctional rhythm**, which would present with a **normal or long PR interval** and a **narrow QRS complex**, contrasting with the given ECG findings.
- A junctional rhythm typically results in a slower heart rate and is not generally associated with sudden cardiac arrest in healthy individuals.
*Automatic discharge of irregular impulses in the atria*
- This typically refers to **atrial fibrillation** or multifocal atrial tachycardia, which would show an **irregularly irregular rhythm** or multiple P-wave morphologies, not the specific PR and QRS abnormalities seen.
- While atrial fibrillation can occur with WPW, the primary pathology described by the ECG findings is the accessory pathway itself.
*Wandering atrial pacemaker*
- A **wandering atrial pacemaker** is characterized by varying P-wave morphology and PR intervals as the pacemaker shifts between different atrial sites, but it generally maintains a normal QRS duration.
- It is typically a benign arrhythmia and does not cause the pre-excitation or the risk of sudden cardiac death seen in this patient.
*Blockage in conduction pathway*
- A **blockage in the conduction pathway** (e.g., AV block) would result in a **prolonged PR interval** or dropped QRS complexes, which is the opposite of the shortened PR interval observed.
- While heart block can cause syncope, it wouldn't explain the pre-excitation pattern (delta wave, wide QRS) seen in the ECG.
Cardiac axis determination US Medical PG Question 8: A 55-year-old man presents to his physician with weakness and fatigue for 1 week. There is no significant past medical history. He mentions that he is very health conscious and has heard about the health benefits of juices. He is following a juice-only diet for the last 2 weeks. His physical examination is completely normal, except for depressed deep tendon reflexes. The only abnormality in a complete laboratory evaluation is a serum potassium level of 6.0 mEq/L (6.0 mmol/L). There are significantly peaked T-waves on ECG. Which of the following pathophysiologic mechanisms best explains the patient’s symptoms?
- A. Decreased resting membrane potential of skeletal muscle cells (Correct Answer)
- B. Prolonged release of Ca2+ ions after stimulation of Ryanodine receptors
- C. Hyperpolarization of skeletal muscle cells
- D. Dysfunction of Na+ channels
- E. Dysfunction of dystrophin-glycoprotein complex
Cardiac axis determination Explanation: ***Decreased resting membrane potential of skeletal muscle cells***
- The patient's **hyperkalemia** (serum potassium 6.0 mEq/L), evidenced by peaked T-waves, reduces the electrochemical gradient for potassium, making the **resting membrane potential less negative (more depolarized)**.
- While seemingly contradictory, a persistent partial depolarization due to high extracellular potassium can lead to inactivation of voltage-gated sodium channels, preventing the generation of new action potentials and causing **muscle weakness and depressed reflexes**.
*Prolonged release of Ca2+ ions after stimulation of Ryanodine receptors*
- This mechanism is associated with conditions like **malignant hyperthermia** or certain myopathies, characterized by muscle rigidity, cramps, or excessive heat production, which are not seen here.
- Hyperkalemia primarily affects **membrane excitability** rather than intracellular calcium release pathways directly.
*Hyperpolarization of skeletal muscle cells*
- **Hyperpolarization** would make the resting membrane potential more negative, making it harder to reach the threshold for an action potential, leading to weakness.
- This typically occurs in conditions causing **hypokalemia**, as a lower extracellular potassium concentration increases the electrochemical gradient and causes a net efflux of potassium ions.
*Dysfunction of Na+ channels*
- Dysfunction of **sodium channels** can cause various neuromuscular disorders, including periodic paralysis or myotonic conditions.
- While hyperkalemia indirectly affects sodium channel function by altering the resting membrane potential, the primary pathophysiologic insult here is the altered potassium gradient, not an intrinsic channel defect.
*Dysfunction of dystrophin-glycoprotein complex*
- This complex is crucial for maintaining muscle fiber integrity and is defective in **muscular dystrophies** (e.g., Duchenne muscular dystrophy).
- Such conditions cause progressive muscle degeneration and weakness, which develop over a much longer period than the acute symptoms described here and are not related to electrolyte imbalances.
Cardiac axis determination US Medical PG Question 9: 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
Cardiac axis determination 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.
Cardiac axis determination US Medical PG Question 10: 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
Cardiac axis determination 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.
More Cardiac axis determination US Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
