Cardiac conduction system development US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Cardiac conduction system development. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Cardiac conduction system development 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
Cardiac conduction system development 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.
Cardiac conduction system development US Medical PG Question 2: A 21-year-old man presents to a physician with repeated episodes of syncope and dizziness over the last month. On physical examination, his pulse is 64/min while all other vital signs are normal. His 24-hour ECG monitoring suggests a diagnosis of sinus node dysfunction. His detailed genetic evaluation shows that he carries a copy of a mutated gene “X” that codes for an ion channel, which is the most important ion channel underlying the automaticity of the sinoatrial node. This is the first ion channel to be activated immediately after hyperpolarization. Which of the following ion channels does the gene “X” code for?
- A. Fast delayed rectifier (IKr) voltage-dependent K+ channels
- B. Stretch-activated cationic channels
- C. L-type voltage-dependent calcium channels
- D. T-type voltage-dependent calcium channels
- E. HCN-channels (Correct Answer)
Cardiac conduction system development Explanation: ***HCN-channels***
- **HCN-channels (hyperpolarization-activated cyclic nucleotide-gated channels)** are responsible for the **funny current (If)**, which is the initial inward current that depolarizes the sinoatrial node after hyperpolarization.
- This current is crucial for **pacemaker activity** and the automaticity of the heart, aligning with the description of the gene and associated sinus node dysfunction.
*Fast delayed rectifier (IKr) voltage-dependent K+ channels*
- These channels are primarily involved in the **repolarization phase** of the cardiac action potential, particularly in the ventricles and atria, by carrying an outward potassium current.
- While important for heart rhythm, they are not the primary channels responsible for the **initial diastolic depolarization** in the sinoatrial node.
*Stretch-activated cationic channels*
- These channels respond to **mechanical stretch** and play a role in mechanosensation and mechanotransduction in various tissues, including the heart.
- They are not directly responsible for the intrinsic **automaticity** of the sinoatrial node immediately after hyperpolarization.
*L-type voltage-dependent calcium channels*
- These channels are activated at more positive potentials during the action potential and are responsible for the **upstroke and plateau phases** of the sinoatrial node action potential.
- They are crucial for transmitting the action potential but are not the **first ion channel** to be activated immediately after hyperpolarization.
*T-type voltage-dependent calcium channels*
- **T-type calcium channels** contribute to the late phase of diastolic depolarization but are activated at less negative potentials compared to HCN channels.
- They are involved in the **initial rapid depolarization**, but the funny current (HCN channels) is generally considered the *first* to be activated after hyperpolarization, especially at the most negative membrane potentials.
Cardiac conduction system development US Medical PG Question 3: A 38-year-old woman, gravida 2, para 1, at 24 weeks' gestation comes to the physician for a routine prenatal evaluation. She has no history of major medical illness and takes no medications. Fetal ultrasonography shows a cardiac defect resulting from abnormal development of the endocardial cushions. This defect is most likely to result in which of the following?
- A. Transposition of the great vessels
- B. Atrioventricular septal defect (Correct Answer)
- C. Dextrocardia
- D. Patent foramen ovale
- E. Sinus venosus defect
Cardiac conduction system development Explanation: ***Atrioventricular septal defect***
- **Endocardial cushion defects** are a hallmark of atrioventricular septal defects, leading to a common atrioventricular valve and an interatrial and/or interventricular communication.
- This defect commonly presents in individuals with **Down syndrome (Trisomy 21)**, though it can occur in isolation.
*Transposition of the great vessels*
- This defect results from abnormal **spiraling of the conotruncal septum**, not from endocardial cushion malformation.
- It leads to the **aorta arising from the right ventricle** and the **pulmonary artery from the left ventricle**, a circulation incompatible with life without a shunt.
*Dextrocardia*
- **Dextrocardia** is a condition where the heart is located on the right side of the chest, usually due to abnormal embryonic folding, and is not directly caused by endocardial cushion defects.
- It can occur as an isolated finding or as part of a more complex syndrome like **Kartagener syndrome**.
*Patent foramen ovale*
- A **patent foramen ovale** is a common remnant of fetal circulation, occurring when the foramen ovale fails to close after birth.
- It is a defect of the **atrial septum secondary to incomplete fusion between the septum primum and septum secundum**, not an endocardial cushion defect.
*Sinus venosus defect*
- A **sinus venosus defect** is a type of atrial septal defect occurring near the entrance of the superior or inferior vena cava.
- It is caused by **abnormal development of the sinus venosus** and is not directly related to endocardial cushion malformation.
Cardiac conduction system development US Medical PG Question 4: A 40-year-old man is brought to the emergency department 20 minutes after his wife found him unconscious on the bathroom floor. On arrival, he is conscious and alert. He remembers having palpitations and feeling lightheaded and short of breath before losing consciousness. He takes captopril for hypertension and glyburide for type 2 diabetes mellitus. His vitals are within normal limits. Physical examination shows no abnormalities. Random serum glucose concentration is 85 mg/dL. An ECG shows a short PR interval and a wide QRS complex with initial slurring. Transthoracic echocardiography reveals normal echocardiographic findings with normal left ventricular systolic function. Which of the following is the most likely underlying cause of this patient's findings?
- A. Ischemic myocardial necrosis
- B. Ectopic foci within the ventricles
- C. Accessory atrioventricular pathway (Correct Answer)
- D. A dysfunctional AV node
- E. Low serum glucose levels
Cardiac conduction system development Explanation: ***Accessory atrioventricular pathway***
- The ECG findings of a **short PR interval**, **wide QRS complex**, and **initial slurring (delta wave)** are characteristic of **Wolff-Parkinson-White (WPW) syndrome**, which is caused by an **accessory atrioventricular pathway**.
- Symptoms like **palpitations, lightheadedness, and syncope** in a patient with these ECG findings suggest an underlying **tachyarrhythmia originating from the accessory pathway**.
*Ischemic myocardial necrosis*
- While syncope can be a symptom of **myocardial ischemia**, the ECG findings (short PR, wide QRS with delta wave) are not typical for **ischemia or infarction**.
- The **normal echocardiogram** and absence of chest pain also make **ischemic myocardial necrosis** less likely.
*Ectopic foci within the ventricles*
- **Ventricular ectopic foci** can cause wide QRS complexes (e.g., in ventricular tachycardia), but they typically do not involve a **short PR interval or a delta wave**.
- The characteristic ECG pattern observed points away from primary **ventricular ectopy** as the underlying cause.
*A dysfunctional AV node*
- A **dysfunctional AV node** typically leads to **AV blocks** (prolonged PR interval, dropped beats) or sometimes reentrant tachycardias, but it does not cause a **short PR interval with a delta wave and wide QRS complex**.
- The described ECG pattern indicates a bypass of the **AV node's normal delay function**.
*Low serum glucose levels*
- Although the patient takes **glyburide** (which can cause hypoglycemia), his **random serum glucose** was 85 mg/dL, which is within the normal range and does not indicate **hypoglycemia**.
- While hypoglycemia can cause syncope, it does not explain the specific ECG abnormalities observed.
Cardiac conduction system development US Medical PG Question 5: 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
Cardiac conduction system development 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.
Cardiac conduction system development 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
Cardiac conduction system development 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.
Cardiac conduction system development US Medical PG Question 7: While explaining the effects of hypokalemia and hyperkalemia on the cardiac rhythm, a cardiologist explains that the electrophysiology of cardiac tissue is unique. He mentions that potassium ions play an important role in the electrophysiology of the heart, and the resting membrane potential of the cardiac myocytes is close to the equilibrium potential of K+ ions. This is because of the high resting potassium conductance of the ventricular myocytes, which is regulated by specific potassium channels. These are open at rest and are closed when there is depolarization. Which of the following potassium channels is the cardiologist talking about?
- A. Inward rectifier IKACh potassium channels
- B. Fast delayed rectifier IKr potassium channels
- C. Slow delayed rectifier IKs potassium channels
- D. Inward rectifier IK1 potassium channels (Correct Answer)
- E. Transient outward current Ito potassium channels
Cardiac conduction system development Explanation: ***Inward rectifier IK1 potassium channels***
- These channels are primarily responsible for maintaining the **resting membrane potential** of ventricular myocytes close to the **equilibrium potential of potassium (EK)**.
- They exhibit **inward rectification**, meaning they conduct potassium current more readily in the inward direction (at negative potentials) than outward. They are open at negative resting potentials and **close upon depolarization due to blockage by intracellular magnesium and polyamines**.
- They contribute to phase 4 of the action potential and prevent early repolarization during the plateau phase.
*Inward rectifier IKACh potassium channels*
- These channels are activated by **acetylcholine** via muscarinic receptors (M2), leading to hyperpolarization and reduced heart rate.
- They are primarily found in the **sinoatrial (SA) node and atrioventricular (AV) node**, not the main determinants of ventricular myocyte resting potential.
*Fast delayed rectifier IKr potassium channels*
- These channels contribute to the **repolarization phase (phase 3)** of the cardiac action potential, along with IKs.
- Their primary role is in **potassium efflux during repolarization**, not in establishing the resting membrane potential.
*Slow delayed rectifier IKs potassium channels*
- These channels also contribute to the **repolarization phase (phase 3)** of the cardiac action potential, acting more slowly than IKr.
- Their main function is to **terminate the action potential**, not to set the resting membrane potential.
*Transient outward current Ito potassium channels*
- These channels contribute to **early repolarization (phase 1)** in ventricular and atrial myocytes, and some Purkinje fibers.
- They cause a **brief outward potassium current** after the upstroke of the action potential, but do not maintain the resting membrane potential.
Cardiac conduction system development US Medical PG Question 8: A 42-year-old Caucasian woman is enrolled in a randomized controlled trial to study cardiac function in the setting of several different drugs. She is started on verapamil and instructed to exercise at 50% of her VO2 max while several cardiac parameters are being measured. During this experiment, which of the following represents the relative conduction speed through the heart from fastest to slowest?
- A. Purkinje fibers > ventricles > atria > AV node
- B. Purkinje fibers > atria > ventricles > AV node (Correct Answer)
- C. Atria > Purkinje fibers > ventricles > AV node
- D. AV node > ventricles > atria > Purkinje fibers
- E. Purkinje fibers > AV node > ventricles > atria
Cardiac conduction system development Explanation: ***Purkinje fibers > atria > ventricles > AV node***
- The **Purkinje fibers** have the fastest conduction velocity, ensuring rapid and synchronous ventricular depolarization.
- The **atria** conduct impulses faster than the ventricles, but slower than the Purkinje fibers, allowing for atrial contraction before ventricular systole.
*Purkinje fibers > ventricles > atria > AV node*
- This option correctly identifies the **Purkinje fibers** and **AV node** at the fastest and slowest ends, respectively, but incorrectly orders the atria and ventricles.
- While Purkinje fibers are fastest, cardiac muscle cells (atria then ventricles) conduct slower than Purkinje fibers.
*Atria > Purkinje fibers > ventricles > AV node*
- This option incorrectly places the **atria** as having the fastest conduction speed, which is not true as Purkinje fibers are significantly faster.
- It also misorders the Purkinje fibers relative to the atria in terms of speed.
*AV node > ventricles > atria > Purkinje fibers*
- This option is incorrect as it places the **AV node** as the fastest conductor and the **Purkinje fibers** as the slowest, which is the exact opposite of their actual conduction speeds.
- The AV node is known for its slow conduction to allow for ventricular filling.
*Purkinje fibers > AV node > ventricles > atria*
- This option incorrectly places the **AV node** as the second fastest conductor, and the ventricles as slower than the atria.
- The AV node is specifically designed to slow the impulse to allow for proper ventricular filling.
Cardiac conduction system development US Medical PG Question 9: A 60-year-old African American gentleman presents to the emergency department with sudden onset "vice-like" chest pain, diaphoresis, and pain radiating to his left shoulder. He has ST elevations on his EKG and elevated cardiac enzymes. Concerning his current pathophysiology, which of the following changes would you expect to see in this patient?
- A. No change in cardiac output; decreased venous return
- B. Increased cardiac output; increased systemic vascular resistance
- C. Decreased cardiac output; increased systemic vascular resistance (Correct Answer)
- D. Increased cardiac output; decreased systemic vascular resistance
- E. Decreased cardiac output; decreased venous return
Cardiac conduction system development Explanation: ***Decreased cardiac output; increased systemic vascular resistance***
- The patient's symptoms (chest pain, diaphoresis, ST elevations, elevated cardiac enzymes) are classic for an **acute myocardial infarction (MI)**, which directly impairs the heart's pumping function, leading to **decreased cardiac output**.
- In response to decreased cardiac output and reduced tissue perfusion, the body activates the **sympathetic nervous system** and **renin-angiotensin-aldosterone system**, causing **vasoconstriction** and thus **increased systemic vascular resistance** to maintain blood pressure.
*No change in cardiac output; decreased venous return*
- An acute MI significantly compromises the heart's ability to pump blood, meaning **cardiac output will almost certainly change** (decrease).
- While venous return might be affected, it's not the primary compensatory mechanism often leading to **decreased CO** in acute MI, which is largely due to impaired systolic function.
*Increased cardiac output; increased systemic vascular resistance*
- **Increased cardiac output** is highly unlikely in the context of an acute myocardial infarction because the heart muscle is damaged and unable to pump effectively.
- While **increased systemic vascular resistance** occurs as a compensatory mechanism, it's in response to a failed heart, not one that is effectively increasing its output.
*Increased cardiac output; decreased systemic vascular resistance*
- Both **increased cardiac output** and **decreased systemic vascular resistance** are typically signs of a hyperdynamic state (e.g., sepsis in its early stages) or vasodilation, which is contrary to the pathophysiology of an MI.
- An MI causes **cardiac dysfunction** and **compensatory vasoconstriction**, not increased output and vasodilation.
*Decreased cardiac output; decreased venous return*
- While **decreased cardiac output** is expected, **decreased venous return** is not the primary or most impactful immediate systemic response; the body often tries to maintain venous return initially to optimize filling pressures, although severe MI can eventually lead to overall circulatory collapse.
- The more prominent and immediate compensatory mechanism for a failing heart is often **increased systemic vascular resistance** to maintain perfusion pressure.
Cardiac conduction system development US Medical PG Question 10: A 35-year-old G2P1 delivers a boy in the 40th week of gestation. The pregnancy was uncomplicated. The newborn had Apgar scores of 7 and 9 at the 1st and 5th minutes, respectively. On physical examination, the newborn is noted to have a left-sided cleft lip. The hard palate and nose are normal. Which of the following statements describes the cause of the abnormality?
- A. Failure of fusion of the left maxillary prominence and the medial nasal process of the frontonasal prominence (Correct Answer)
- B. Failure of fusion of the left maxillary prominence and the lateral nasal process of the frontonasal prominence
- C. Failure of development of the left maxillary prominence
- D. Partial resorption of the first pharyngeal arch
- E. Failure of development of the first pharyngeal arch
Cardiac conduction system development Explanation: ***Failure of fusion of the left maxillary prominence and the medial nasal process of the frontonasal prominence***
- **Cleft lip** results from the **failure of fusion** between the **maxillary prominence** and the **medial nasal process** during the 6th to 7th week of embryonic development.
- The **medial nasal processes** form the philtrum of the upper lip, the primary palate, and the central part of the upper jaw, while the **maxillary prominences** form the lateral parts of the upper lip and the secondary palate.
*Failure of fusion of the left maxillary prominence and the lateral nasal process of the frontonasal prominence*
- The **lateral nasal processes** form the alae of the nose but do not directly contribute to the upper lip formation; therefore, their failure to fuse with the maxillary prominence would not cause a cleft lip.
- Fusion issues involving the lateral nasal process are associated with anomalies of the nasal structures, not the lip itself.
*Failure of development of the left maxillary prominence*
- Complete failure of development of the maxillary prominence would lead to a more severe facial defect, often involving hypoplasia or absence of the maxilla and not just an isolated cleft lip.
- Such a severe defect would likely impact other craniofacial structures more broadly than described.
*Partial resorption of the first pharyngeal arch*
- The **first pharyngeal arch** forms many structures of the face, including the maxilla and mandible, but cleft lip is a failure of fusion, not a resorption defect of a fully formed structure.
- Resorption issues are typically associated with conditions like Treacher Collins syndrome, affecting bones and soft tissues derived from the arch.
*Failure of development of the first pharyngeal arch*
- Complete or significant failure of development of the **first pharyngeal arch** would result in severe facial malformations, including micrognathia, severe ear abnormalities, and hypoplasia of the maxilla and mandible.
- A simple cleft lip, especially when the nose and hard palate are normal, does not typically point to a global failure of the first pharyngeal arch development.
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