Cardiology

Cardiology US Medical PG Question 1: A 66-year-old man comes to the emergency department because of a 1-day history of chest pain, palpitations, and dyspnea on exertion. He had a similar episode 3 days ago and was diagnosed with an inferior wall myocardial infarction. He was admitted and a percutaneous transluminal coronary angioplasty was successfully done that day. A fractional flow reserve test during the procedure showed complete resolution of the stenosis. Laboratory tests including serum glucose, lipids, and blood count were within normal limits. He was discharged the day after the procedure on a drug regimen of aspirin, simvastatin, and isosorbide dinitrate. At the time of discharge, he had no chest pain or dyspnea. Presently, his vitals are normal and ECG at rest shows new T-wave inversion. Which of the following is the most reliable test for rapidly establishing the diagnosis in this patient?

• A. Creatine kinase MB
• B. Lactate dehydrogenase
• C. Copeptin
• D. Aspartate aminotransferase
• E. Cardiac troponin T (Correct Answer)

Cardiology Explanation: ***Cardiac troponin T*** - **Cardiac troponin T** is a highly sensitive and specific biomarker for **myocardial injury**, making it the most reliable test for rapidly diagnosing acute coronary syndrome or re-infarction. - Its elevation indicates ongoing **myocardial necrosis**, even after a recent MI, and is crucial for guiding immediate management. *Creatine kinase MB* - While CK-MB is used for diagnosing myocardial infarction, its levels can also be elevated in cases of **skeletal muscle injury** or **after cardiac procedures**, reducing its specificity in this context. - CK-MB also has a **shorter window of elevation** compared to troponins, potentially missing later presentations of myocardial injury. *Lactate dehydrogenase* - **LDH** is a relatively **nonspecific marker** that can elevate due to various conditions affecting different organs (e.g., liver disease, hemolysis, renal injury). - Its elevation onset is **slower** and its diagnostic window is longer, making it less suitable for rapid diagnosis of acute myocardial injury. *Copeptin* - **Copeptin** is a marker of **endogenous stress** and is often used in conjunction with troponins to rule out NSTEMI, especially at early presentation. - However, it is not a direct marker of myocardial necrosis itself and is **not as specific** as troponin for diagnosing a re-infarction. *Aspartate aminotransferase* - **AST** is a **nonspecific enzyme** found in various tissues, including the liver, skeletal muscle, and heart. - Elevated AST levels are frequently seen in **liver damage** and are not a primary biomarker for diagnosing acute myocardial infarction or re-infarction.

Cardiology US Medical PG Question 2: A 55-year-old woman comes to the physician because of involuntary hand movements that improve with alcohol consumption. Physical examination shows bilateral hand tremors that worsen when the patient is asked to extend her arms out in front of her. The physician prescribes a medication that is associated with an increased risk of bronchospasms. This drug has which of the following immediate effects on the cardiovascular system? Stroke volume | Heart rate | Peripheral vascular resistance

• A. ↓ ↓ ↓
• B. ↓ ↓ ↑ (Correct Answer)
• C. ↓ ↑ ↑
• D. ↑ ↑ ↑
• E. ↑ ↑ ↓

Cardiology Explanation: ***↓ ↓ ↑*** - This patient likely has **essential tremor**, which is characterized by **bilateral hand tremors** that improve with alcohol and worsen with intention (postural tremor). The prescribed medication is a **beta-blocker** (e.g., propranolol), which is associated with an increased risk of bronchospasms due to blocking **beta-2 receptors** in the airways. - Beta-blockers **decrease heart rate** (negative chronotropic effect) and **stroke volume** (negative inotropic effect) by blocking beta-1 receptors in the heart, reducing cardiac output. - **Peripheral vascular resistance increases** acutely due to: (1) **unopposed alpha-1 adrenergic tone** in blood vessels (loss of beta-2 mediated vasodilation), and (2) baroreceptor-mediated reflex vasoconstriction in response to decreased cardiac output. This helps maintain blood pressure despite reduced cardiac output. *↓ ↓ ↓* - While beta-blockers decrease **heart rate** and **stroke volume**, peripheral vascular resistance does not decrease acutely. A decrease in all three parameters would cause severe hypotension. - The loss of beta-2 receptor-mediated vasodilation and baroreceptor reflexes lead to increased, not decreased, peripheral vascular resistance. *↓ ↑ ↑* - Beta-blockers **decrease heart rate** through beta-1 blockade, not increase it. This is their primary cardiac mechanism of action. - An increase in heart rate would be expected with sympathomimetic drugs or anticholinergics, not beta-blockers. *↑ ↑ ↑* - This combination indicates increased cardiovascular activity, which is the opposite effect of **beta-blockers**. - Beta-blockers reduce heart rate and stroke volume by blocking beta-1 receptors; they do not increase these parameters. - This pattern would suggest sympathetic activation or administration of an adrenergic agonist. *↑ ↑ ↓* - Beta-blockers **decrease** (not increase) both heart rate and stroke volume through beta-1 receptor blockade. - While decreased peripheral vascular resistance occurs with vasodilators, beta-blockers acutely **increase** PVR due to unopposed alpha-adrenergic tone.

Cardiology US Medical PG Question 3: A healthy 22-year-old male participates in a research study you are leading to compare the properties of skeletal and cardiac muscle. You conduct a 3-phased experiment with the participant. In the first phase, you get him to lift up a 2.3 kg (5 lb) weight off a table with his left hand. In the second phase, you get him to do 20 burpees, taking his heart rate to 150/min. In the third phase, you electrically stimulate his gastrocnemius with a frequency of 50 Hz. You are interested in the tension and electrical activity of specific muscles as follows: Biceps in phase 1, cardiac muscle in phase 2, and gastrocnemius in phase 3. What would you expect to be happening in the phases and the respective muscles of interest?

• A. Increase of tension in experiments 2 and 3, with the same underlying mechanism
• B. Increase of tension in all phases (Correct Answer)
• C. Recruitment of large motor units followed by small motor units in experiment 1
• D. Fused tetanic contraction at the end of all three experiments
• E. Recruitment of small motor units at the start of experiments 1 and 2

Cardiology Explanation: ***Increase of tension in all phases*** - In **phase 1**, lifting a 2.3 kg weight requires the **biceps** to contract, generating sufficient force (**tension**) to overcome gravity. - In **phase 2**, the **cardiac muscle** increases its contractile force (**tension**) to meet the metabolic demands of **exercise**, leading to a heart rate of 150/min. - In **phase 3**, electrical stimulation of the **gastrocnemius** at 50 Hz triggers muscle contraction, leading to an increase in **tension**. *Increase of tension in experiments 2 and 3, with the same underlying mechanism* - While tension increases in phases 2 and 3, the **underlying mechanisms differ**: cardiac muscle tension increases due to increased sympathetic stimulation and preload, while skeletal muscle tension increases due to unfused or fused tetanus from electrical stimulation. - Cardiac muscle contraction is regulated by **calcium-induced calcium release**, while skeletal muscle involves direct coupling of DHP receptor and ryanodine receptor. *Recruitment of large motor units followed by small motor units in experiment 1* - **Motor unit recruitment** follows the **size principle**, meaning smaller, more easily excitable motor units are activated first, followed by larger ones as more force is needed. - Therefore, in phase 1, **small motor units** would be recruited first, not large ones. *Fused tetanic contraction at the end of all three experiments* - **Fused tetanic contraction** occurs in **skeletal muscle** when stimulation frequency is high enough that individual twitches summate completely, leading to sustained contraction. - This phenomenon is **not possible in cardiac muscle** due to its long **refractory period**, which prevents sustained contraction and allows for adequate filling time. *Recruitment of small motor units at the start of experiments 1 and 2* - **Motor unit recruitment** applies to **skeletal muscle** (phase 1) and involves recruiting small motor units first for fine or gentle movements. - **Cardiac muscle** (phase 2) does not have motor units; instead, it relies on the **Frank-Starling mechanism** and hormonal/nervous regulation to adjust its contractile force as a syncytium.

Cardiology US Medical PG Question 4: An 83-year-old male presents with dyspnea, orthopnea, and a chest radiograph demonstrating pulmonary edema. A diagnosis of congestive heart failure is considered. The following clinical measurements are obtained: 100 bpm heart rate, 0.2 mL O2/mL systemic blood arterial oxygen content, 0.1 mL O2/mL pulmonary arterial oxygen content, and 400 mL O2/min oxygen consumption. Using the above information, which of the following values represents this patient's cardiac stroke volume?

• A. 30 mL/beat
• B. 70 mL/beat
• C. 40 mL/beat (Correct Answer)
• D. 60 mL/beat
• E. 50 mL/beat

Cardiology Explanation: ***40 mL/beat*** - First, calculate cardiac output (CO) using the **Fick principle**: CO = Oxygen Consumption / (Arterial O2 content - Venous O2 content). Here, CO = 400 mL O2/min / (0.2 mL O2/mL - 0.1 mL O2/mL) = 400 mL O2/min / 0.1 mL O2/mL = **4000 mL/min**. - Next, calculate stroke volume (SV) using the formula: SV = CO / Heart Rate. Given a heart rate of 100 bpm, SV = 4000 mL/min / 100 beats/min = **40 mL/beat**. *30 mL/beat* - This answer would result if there was an error in calculating either the **cardiac output** or if the **arteriovenous oxygen difference** was overestimated. - A stroke volume of 30 mL/beat with a heart rate of 100 bpm would yield a cardiac output of 3 L/min, which is sub-physiologic for an oxygen consumption of 400 mL/min given the provided oxygen content values. *70 mL/beat* - This stroke volume is higher than calculated and would imply either a significantly **lower heart rate** or a much **higher cardiac output** than derived from the Fick principle with the given values. - A stroke volume of 70 mL/beat at a heart rate of 100 bpm would mean a cardiac output of 7 L/min, which is inconsistent with the provided oxygen consumption and arteriovenous oxygen difference. *60 mL/beat* - This value is higher than the correct calculation, suggesting an error in the initial calculation of **cardiac output** or the **avO2 difference**. - To get 60 mL/beat, the cardiac output would need to be 6000 mL/min, which would mean an avO2 difference of 0.067 mL O2/mL, not 0.1 mL O2/mL. *50 mL/beat* - This stroke volume would result from an incorrect calculation of the **cardiac output**, potentially from a slight miscalculation of the **arteriovenous oxygen difference**. - A stroke volume of 50 mL/beat at 100 bpm would mean a cardiac output of 5 L/min, requiring an avO2 difference of 0.08 mL O2/mL, which is not consistent with the given values.

Cardiology US Medical PG Question 5: 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

Cardiology 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.

Cardiology US Medical PG Question 6: A 67-year-old man presents to the emergency department for squeezing and substernal chest pain. He states that he was at home eating dinner when his symptoms began. The patient has a past medical history of diabetes, hypertension, and dyslipidemia. He is currently taking atorvastatin, lisinopril, insulin, metformin, metoprolol, and aspirin. Six days ago he underwent percutaneous coronary intervention. His temperature is 99.5°F (37.5°C), blood pressure is 197/118 mmHg, pulse is 120/min, respirations are 17/min, and oxygen saturation is 98% on room air. Physical exam reveals an uncomfortable elderly man who is sweating. An ECG is ordered. Which of the following is the best next step in management for this patient?

• A. Stress testing
• B. Angiography (Correct Answer)
• C. Cardiac troponins
• D. Creatine kinase-MB
• E. Myoglobin

Cardiology Explanation: ***Correct: Angiography*** - This patient presenting with **acute chest pain 6 days post-PCI** is at high risk for **stent thrombosis or acute in-stent restenosis**, which represents a life-threatening emergency. - Given the **clinical instability** (severe hypertension 197/118, tachycardia 120/min, diaphoresis) and classic ACS symptoms in the immediate post-PCI period, **urgent coronary angiography** is the best next step in management. - While ECG and troponins are important diagnostic tools, this patient requires **immediate intervention** to evaluate the recent PCI site and potentially perform emergent revascularization. - In the setting of suspected **acute stent thrombosis**, time to reperfusion is critical, and angiography allows both diagnosis and treatment. *Incorrect: Cardiac troponins* - While troponins are essential biomarkers for myocardial injury and should be obtained, they are a **diagnostic test** rather than definitive management. - Waiting for troponin results would delay definitive management in a patient with clear clinical evidence of ACS. - In this high-risk post-PCI patient with active symptoms, management should not wait for biomarker confirmation. *Incorrect: Stress testing* - Stress testing is **absolutely contraindicated** in patients with active chest pain and suspected acute MI. - It could precipitate further myocardial ischemia, arrhythmias, or cardiac arrest. - Stress testing is reserved for risk stratification in stable patients or after ACS has been ruled out. *Incorrect: Creatine kinase-MB* - CK-MB is less sensitive and specific than troponins for myocardial injury, as it can be elevated in skeletal muscle conditions. - It has a shorter elevation window and has largely been replaced by troponins in modern practice. - Like troponins, it would not change the immediate management need in this clinically unstable patient. *Incorrect: Myoglobin* - Myoglobin lacks cardiac specificity (present in both cardiac and skeletal muscle) and has poor diagnostic accuracy for MI. - Its rapid rise and fall make it unreliable, and it generates many false positives. - It has no role in guiding management decisions in suspected ACS.

Cardiology US Medical PG Question 7: A 72-year-old woman is brought to the emergency department with dyspnea for 2 days. She is on regular hemodialysis at 3 sessions a week but missed her last session due to an unexpected trip. She has a history of congestive heart failure. After urgent hemodialysis, the patient’s dyspnea does not improve as expected. The cardiologist is consulted. After evaluation of the patient, he notes in the patient’s electronic record: “the patient does not have a chronic heart condition and a cardiac cause of dyspnea is unlikely.” The following morning, the nurse finds the cardiologist’s notes about the patient not having congestive heart failure odd. The patient had a clear history of congestive heart failure with an ejection fraction of 35%. After further investigation, the nurse realizes that the cardiologist evaluated the patient’s roommate. She is an elderly woman with a similar first name. She is also on chronic hemodialysis. To prevent similar future errors, the most appropriate strategy is to use which of the following?

• A. Two patient identifiers at every nurse-patient encounter
• B. A patient’s medical identification number at every encounter by any healthcare provider
• C. Two patient identifiers at every patient encounter by any healthcare provider (Correct Answer)
• D. Two patient identifiers at every physician-patient encounter
• E. A patient’s medical identification number at every physician-patient encounter

Cardiology Explanation: ***Two patient identifiers at every patient encounter by any healthcare provider*** - This strategy ensures that **all healthcare providers**, not just nurses or physicians, verify the patient's identity using at least **two distinct identifiers** before any interaction, greatly reducing the risk of mix-ups. - This comprehensive approach prevents errors like the one described, where a cardiologist evaluated the wrong patient due to similar names and circumstances, ensuring **patient safety** and appropriate care delivery. *Two patient identifiers at every nurse-patient encounter* - While important, limiting identification to nurse-patient encounters would **miss opportunities for error by other healthcare providers**, such as physicians, technicians, or pharmacists. - The scenario explicitly states the error was made by a **cardiologist**, indicating that relying solely on nurses for identification is insufficient. *A patient’s medical identification number at every encounter by any healthcare provider* - Although the **medical identification number** is a valid identifier, relying on a *single* identifier still carries a risk, especially if typed or read incorrectly. - **Two distinct identifiers** (e.g., name and date of birth, or name and medical record number) are the **gold standard** to minimize errors. *Two patient identifiers at every physician-patient encounter* - This option, while improving physician encounters, **fails to cover interactions with other crucial healthcare team members** (e.g., nurses, phlebotomists, imaging technicians) where patient misidentification can still occur. - A comprehensive patient safety strategy must extend beyond physician interactions to **all points of care**. *A patient’s medical identification number at every physician-patient encounter* - This option combines the weaknesses of using only a **single identifier** and limiting the scope to **only physician encounters**, leaving multiple vulnerabilities for patient misidentification throughout the healthcare process. - The **Joint Commission's National Patient Safety Goals** explicitly recommend using at least **two patient identifiers**.

Cardiology US Medical PG Question 8: A 70-year-old male presents for an annual exam. His past medical history is notable for shortness of breath when he sleeps, and upon exertion. Recently he has experienced dyspnea and lower extremity edema that seems to be worsening. Both of these symptoms have resolved since he was started on several medications and instructed to weigh himself daily. Which of the following is most likely a component of his medical management?

• A. Lidocaine
• B. Verapamil
• C. Carvedilol (Correct Answer)
• D. Aspirin
• E. Ibutilide

Cardiology Explanation: ***Carvedilol*** - The patient exhibits classic symptoms of **heart failure**, such as **dyspnea on exertion**, **orthopnea** (shortness of breath when he sleeps), and **lower extremity edema**. - **Beta-blockers** like carvedilol are essential for managing **chronic heart failure** by reducing myocardial oxygen demand and improving cardiac function. *Lidocaine* - **Lidocaine** is primarily an **antiarrhythmic drug** used for acute treatment of **ventricular arrhythmias**, not for chronic heart failure management. - It works by blocking sodium channels and has no direct benefit in addressing the underlying pathophysiology of heart failure. *Verapamil* - **Verapamil** is a **non-dihydropyridine calcium channel blocker** typically used for hypertension, angina, and supraventricular tachyarrhythmias. - It can have **negative inotropic effects**, which are generally contraindicated or used with extreme caution in patients with **systolic heart failure** due to its potential to worsen cardiac function. *Aspirin* - **Aspirin** is an **antiplatelet agent** used for primary or secondary prevention of **atherosclerotic cardiovascular disease** (e.g., in patients with coronary artery disease). - It does not directly manage the symptoms or pathophysiology of **heart failure** unless there is a coexisting ischemic etiology. *Ibutilide* - **Ibutilide** is an **antiarrhythmic drug** specifically used for the rapid conversion of **atrial flutter and atrial fibrillation** of recent onset to sinus rhythm. - It is not a medication used for the long-term management of **heart failure** symptoms described in the patient.

Cardiology US Medical PG Question 9: A 71-year-old man presents to the emergency department for shortness of breath. The patient was returning from a business trip to China, when he suddenly felt short of breath during the taxi ride home from the airport. The patient has a past medical history of poorly controlled diabetes mellitus and a 50 pack-year smoking history. The patient is non-compliant with his medications and is currently only taking ibuprofen. An initial ECG demonstrates sinus tachycardia. A chest radiograph is within normal limits. Laboratory values are notable for a creatinine of 2.4 mg/dL and a BUN of 32 mg/dL as compared to his baseline creatinine of 0.9 mg/dL. His temperature is 98.8°F (37.1°C), pulse is 122/min, blood pressure is 145/90 mmHg, respirations are 19/min, and oxygen saturation is 93% on room air. On physical exam, you note an older gentleman in distress. Cardiac exam is notable only for tachycardia. Pulmonary exam is notable for expiratory wheezes. Which of the following is the best confirmatory test for this patient?

• A. Ventilation perfusion scan
• B. Lower extremity ultrasound with Doppler
• C. CT angiogram (Correct Answer)
• D. Arterial blood gas
• E. D-dimer

Cardiology Explanation: ***CT angiogram*** - This patient presents with multiple risk factors for **pulmonary embolism (PE)**, including a recent long-haul flight and acute onset of dyspnea with tachycardia and hypoxemia. CT pulmonary angiography (CTPA) is the **gold standard confirmatory test** for PE, directly visualizing thrombi in the pulmonary arteries with high sensitivity (>90%) and specificity. - While this patient has **acute kidney injury** (creatinine elevated from 0.9 to 2.4 mg/dL), raising concerns about contrast-induced nephropathy, the **high clinical probability of PE** (recent long flight, acute dyspnea, tachycardia, hypoxemia) makes urgent diagnosis critical. In hemodynamically stable patients with intermediate-to-high PE probability and renal insufficiency, CTPA with appropriate precautions (IV hydration, minimizing contrast dose, avoiding nephrotoxic agents) is still preferred as it provides the most definitive diagnosis. - The patient's hemodynamic stability (BP 145/90) allows time for renal protective measures before contrast administration. *Ventilation perfusion scan* - A V/Q scan is an important **alternative** for diagnosing PE, particularly valuable in patients with severe renal insufficiency (CKD Stage 4-5) or contrast allergy where CTPA is truly contraindicated. - However, in this patient with **expiratory wheezes** suggesting possible underlying obstructive lung disease (50 pack-year smoking history), a V/Q scan has higher likelihood of **indeterminate results** (intermediate probability), which would not confirm or exclude PE and might necessitate additional testing anyway. - V/Q scans also have lower sensitivity than CTPA and require the patient to cooperate with breathing maneuvers, which may be difficult in an acutely dyspneic patient. *Lower extremity ultrasound with Doppler* - This test diagnoses **deep vein thrombosis (DVT)**, the most common source of PE. While a positive DVT in a patient with suspected PE would support treatment, a **negative study does not rule out PE** since the thrombus may have already completely embolized. - This is a supportive test, not a confirmatory test for PE itself. The patient's symptoms require direct assessment of the pulmonary vasculature. *Arterial blood gas* - An ABG typically shows **hypoxemia and respiratory alkalosis** in PE due to V/Q mismatch and hyperventilation, but these findings are **non-specific** and occur in many cardiopulmonary conditions (pneumonia, asthma, COPD exacerbation, heart failure). - ABG is a supportive tool that may guide oxygen therapy but does not confirm PE diagnosis. *D-dimer* - D-dimer has excellent **negative predictive value** and is useful to exclude PE in patients with **low clinical probability** (Wells score <2 or PERC rule negative). - In this patient with **high clinical probability** of PE (recent long flight, acute symptoms, risk factors), D-dimer would almost certainly be elevated and thus **not helpful for confirmation**. Elevated D-dimer occurs in many conditions including infection, inflammation, malignancy, recent surgery, and advanced age, making it non-specific in this context.

Cardiology US Medical PG Question 10: 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

Cardiology 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.

Cardiology Flashcard 1 of 10

Question: How do PCWP and preload change during distributive shock?_____

Answer: Decreased

Cardiology Flashcard 2 of 10

Question: One ECG change associated with cardiac tamponade is _____, which occurs due to "swinging" movement of the heart in a large effusion

Answer: electrical alternans

Cardiology Flashcard 3 of 10

Question: _____ and _____ are first line treatment for hypertension in patients with heart failure, MI, and/or diabetes

Answer: ACE inhibitors

Extra Information:   Sketchy Pharmacology: Cardiovascular (Antihypertensives) Watch Primary hypertension & hypertensive emergency [https://dashboard.sketchy.com/study/medical/courses/medical-pharmacology/units/medical-pharmacology-cardiovascular-renal/videos/medical-pharmacology-cardiovascular-and-renal-antihypertensives-primary-hypertension-and-hypertensive-emergency?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical]Watch associated Bootcamp video [https://app.bootcamp.com/med-school/cardiology/videos/hypertension?index=12] https://onlinemeded.org/spa/cardiology/hypertension/acquire?ref=anki 

Cardiology Flashcard 4 of 10

Question: Ca2+ channel blockers may be used to treat _____ if -blockers/nitrates have not worked or are contraindicated

Answer: stable angina

Cardiology Flashcard 5 of 10

Question: One ECG change associated with cardiac tamponade is a _____ QRS complex

Answer: low-voltage

Cardiology Flashcard 6 of 10

Question: What cardiac pathology results in global enlargement of the heart and dilation of all chambers?_____

Answer: Myocarditis

Cardiology Flashcard 7 of 10

Question: _____ is defined as compression of the heart by fluid

Answer: Cardiac tamponade

Cardiology Flashcard 8 of 10

Question: What is Ebstein's anomaly?

Answer: atrialized right ventricle

Cardiology Flashcard 9 of 10

Question: medial medullary syndrome

Answer: stroke in paramedian branches of ASA and/or vertebral arteries

Extra Information: lower limb hemiparesis, loss of proprioception, tongue deviation

Cardiology Flashcard 10 of 10

Question: migraine headache

Answer: irritation of CN 5, meninges, and/or blood vessels

Extra Information: release of substance P, CGRP, vasoactive peptidespulsating unilateral headache; 4-72 hr duration; +/- nausea, photophobia, phonophobia, auraabortive - triptans prophylactic - propranalol, topiramate