Cardiovascular

Cardiovascular US Medical PG Question 1: A 58-year-old man comes to the emergency department for complaints of crushing chest pain for 4 hours. He was shoveling snow outside when the pain started. It is rated 7/10 and radiates to his left arm. An electrocardiogram (ECG) demonstrates ST-segment elevation in leads V2-4. He subsequently undergoes percutaneous coronary intervention (PCI) and is discharged with aspirin, clopidogrel, carvedilol, atorvastatin, and lisinopril. Five days later, the patient is brought to the emergency department by his wife with complaints of dizziness. He reports lightheadedness and palpitations for the past 2 hours but otherwise feels fine. His temperature is 99.7°F (37.6°C), blood pressure is 95/55 mmHg, pulse is 105/min, and respirations are 17/min. A pulmonary artery catheter is performed and demonstrates an increase in oxygen concentration at the pulmonary artery. What finding would you expect in this patient?

• A. Widespread ST-segment elevations
• B. Harsh, loud, holosystolic murmur at the lower left sternal border (Correct Answer)
• C. Pulseless electrical activity
• D. Drop of systolic blood pressure by 20 mmHg during inspiration
• E. Normal findings

Cardiovascular Explanation: ***Harsh, loud, holosystolic murmur at the lower left sternal border*** - This patient's presentation, including recent **anterior STEMI**, dizziness, lightheadedness, palpitations, hypotension, tachycardia, and **increased oxygen saturation in the pulmonary artery** (oxygen "step-up" indicating a left-to-right shunt), is highly suggestive of **ventricular septal rupture (VSR)**. - VSR is a **mechanical complication** of MI that typically occurs **3-7 days post-infarction** when the necrotic myocardium is weakest. - A **VSR** causes a **harsh, loud, holosystolic murmur** best heard at the **lower left sternal border** due to turbulent blood flow through the septal defect from the left ventricle to the right ventricle. - The left-to-right shunt results in oxygenated blood from the left ventricle mixing with deoxygenated blood in the right ventricle, causing the characteristic oxygen saturation step-up detected by pulmonary artery catheterization. *Widespread ST-segment elevations* - Widespread ST-segment elevations are characteristic of **acute pericarditis**, which typically presents with **pleuritic chest pain** that improves when leaning forward and a **friction rub**, not the hemodynamic compromise described here. - While **Dressler syndrome** (post-MI pericarditis) can occur weeks after MI, the acute hemodynamic instability, left-to-right shunt evidence, and 5-day timeframe point to VSR rather than pericarditis. *Pulseless electrical activity* - **Pulseless electrical activity (PEA)** indicates cardiac arrest with organized electrical activity but no mechanical cardiac output, resulting in an **unpalpable pulse**. - The patient has a documented pulse of **105/min**, which directly contradicts PEA. - A patient in PEA would be unconscious and unable to report symptoms for 2 hours. *Drop of systolic blood pressure by 20 mmHg during inspiration* - A drop in systolic blood pressure >10 mmHg during inspiration (**pulsus paradoxus**) is characteristic of **cardiac tamponade** or severe obstructive airway disease. - While **free wall rupture** leading to tamponade is another mechanical complication post-MI, the **oxygen saturation step-up** in the pulmonary artery is pathognomonic for an **intracardiac shunt** (VSR), not tamponade. - Tamponade would show equalization of diastolic pressures across all chambers, not increased PA oxygen saturation. *Normal findings* - The patient presents with clear evidence of hemodynamic compromise: **hypotension (95/55 mmHg)**, **tachycardia (105/min)**, dizziness, and lightheadedness. - The **oxygen saturation step-up** in the pulmonary artery is an objective abnormal finding indicating an intracardiac left-to-right shunt. - Therefore, normal findings are incompatible with this clinical presentation.

Cardiovascular US Medical PG Question 2: A 67-year-old man comes to the emergency department because of retrosternal chest pressure and shortness of breath for 4 hours. The symptoms started while he was walking to work and have only minimally improved with rest. He has a history of type 2 diabetes mellitus. He has smoked one pack of cigarettes daily for 35 years. He appears uncomfortable. His pulse is 95/min. Serum studies show a normal troponin concentration. An ECG shows no abnormalities. Which of the following is the most likely underlying cause of this patient's symptoms?

• A. Atherosclerotic plaque thrombus with complete coronary artery occlusion
• B. Stable atherosclerotic plaque with 85% coronary artery occlusion
• C. Aortic valve thickening and calcification
• D. Disruption of an atherosclerotic plaque with a non-occlusive coronary artery thrombus (Correct Answer)
• E. Coronary artery occlusion due to transient increase in vascular tone

Cardiovascular Explanation: **Disruption of an atherosclerotic plaque with a non-occlusive coronary artery thrombus** - This scenario describes **unstable angina (UA)**, characterized by chest pain at rest or with minimal exertion, increased frequency/intensity of angina, or new-onset severe angina. - While troponin is normal and ECG shows no abnormalities, the persistent symptoms and minimal improvement with rest, along with risk factors like **diabetes** and **smoking**, strongly suggest an **unstable coronary lesion** that is not yet fully occlusive. *Atherosclerotic plaque thrombus with complete coronary artery occlusion* - **Complete coronary artery occlusion** typically leads to myocardial infarction (MI), which would manifest with **elevated troponin levels** and often **ECG changes** (e.g., ST elevation or depression). - The patient's normal troponin and ECG rule out an acute MI at this stage. *Stable atherosclerotic plaque with 85% coronary artery occlusion* - **Stable angina** symptoms usually improve promptly with rest and are predictable, occurring only during significant exertion. - The described symptoms, including minimal improvement with rest and 4 hours duration, are not typical of stable angina. *Aortic valve thickening and calcification* - While **aortic stenosis** can cause chest pain and shortness of breath, these symptoms are typically exertional and not usually described as "retrosternal pressure" that minimally improves with rest in this acute context without other signs of flow obstruction. - This condition is unlikely to be the sole cause of these acute, persistent symptoms without findings on initial workup. *Coronary artery occlusion due to transient increase in vascular tone* - **Coronary vasospasm** (Prinzmetal angina) can cause chest pain at rest and transient ECG changes, but it's typically **recurrent** and responds well to **vasodilators**. - This patient's symptoms, combined with risk factors for atherosclerosis and the prolonged nature of the pain, are less indicative of vasospasm as the primary underlying cause.

Cardiovascular US Medical PG Question 3: A medical research study is evaluating an investigational novel drug (medication 1) as compared with standard therapy (medication 2) in patients presenting to the emergency department with myocardial infarction (MI). The study enrolled a total of 3,000 subjects, 1,500 in each study arm. Follow-up was conducted at 45 days post-MI. The following are the results of the trial: Endpoints Medication 1 Medication 2 P-Value Primary: death from cardiac causes 134 210 0.03 Secondary: hyperkalemia 57 70 0.4 What is the relative risk of death from a cardiac cause, expressed as a percentage? (Round to the nearest whole number.)

• A. 64% (Correct Answer)
• B. 42%
• C. 72%
• D. 36%
• E. 57%

Cardiovascular Explanation: ***64%*** - The **relative risk (RR)** is calculated as the event rate in the exposed group divided by the event rate in the unexposed (control) group. - For cardiac death, the event rate for Medication 1 is 134/1500 = 0.0893, and for Medication 2 is 210/1500 = 0.14. Therefore, RR = 0.0893 / 0.14 = 0.6378. - Expressing as a percentage: 0.6378 × 100 = 63.78%, which rounds to **64%**. - This indicates that Medication 1 has 64% of the risk of cardiac death compared to Medication 2, representing a **36% relative risk reduction**. *42%* - This option is incorrect as it does not reflect the accurate calculation of **relative risk** using the provided event rates. - A calculation error or conceptual misunderstanding of the relative risk formula would lead to this value. *72%* - This percentage is higher than the calculated relative risk, suggesting an incorrect application of the formula or a misinterpretation of the event rates. - It does not represent the ratio of risk between the two medication groups for cardiac death. *36%* - This value represents the **relative risk reduction** (100% - 64% = 36%), not the relative risk itself. - This is a common error where students confuse relative risk with relative risk reduction. *57%* - While closer to the correct answer, this value is not the precise result when rounding to the nearest whole number. - Small calculation discrepancies or rounding at intermediate steps could lead to this slightly different percentage.

Cardiovascular US Medical PG Question 4: A 55-year-old man comes to the physician because of a 4-month history of episodic, pressure-like chest pain. The chest pain occurs when he is walking up stairs and improves with rest. He has hypertension and type 2 diabetes mellitus. His father died from a myocardial infarction at the age of 50 years. Current medications include hydrochlorothiazide and metformin. His pulse is 85/min, respirations are 12/min, and blood pressure is 140/90 mm Hg. Cardiac examination shows normal heart sounds without any murmurs, rubs, or gallops. An ECG shows high amplitude of the S wave in lead V3. An exercise stress test is performed but stopped after 4 minutes because the patient experiences chest pain. An ECG obtained during the stress test shows sinus tachycardia and ST-segment depressions in leads V1–V4. Which of the following is the most appropriate long-term pharmacotherapy to reduce the frequency of symptoms in this patient?

• A. Metoprolol (Correct Answer)
• B. Clopidogrel
• C. Aspirin
• D. Nitroglycerin
• E. Isosorbide mononitrate

Cardiovascular Explanation: ***Metoprolol*** - **Beta-blockers** like metoprolol are first-line agents for **symptom relief** in stable angina by reducing myocardial oxygen demand. - They decrease **heart rate**, **blood pressure**, and **myocardial contractility**, thereby reducing the frequency and severity of anginal episodes. *Clopidogrel* - **Clopidogrel** is an antiplatelet agent used primarily to prevent **thrombotic events** in patients with established cardiovascular disease or acute coronary syndromes. - It does not directly reduce the frequency of anginal symptoms, but rather prevents progression to **myocardial infarction** or **stroke**. *Aspirin* - **Aspirin** is an antiplatelet medication used for **secondary prevention** of cardiovascular events by inhibiting platelet aggregation. - While crucial for reducing cardiovascular risk, it does not directly alleviate the **frequency of anginal symptoms** themselves. *Nitroglycerin* - **Nitroglycerin** is a short-acting nitrate used to provide **immediate relief** of anginal pain during an acute episode. - It is not a long-term pharmacotherapy for reducing the *frequency* of symptoms. *Isosorbide mononitrate* - **Isosorbide mononitrate** is a long-acting nitrate used to *prevent* angina, but it is typically a **second-line agent** after beta-blockers due to potential for **tolerance** and side effects. - While it can reduce symptom frequency, beta-blockers are generally preferred as initial long-term therapy for symptom control.

Cardiovascular US Medical PG Question 5: 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. ↑ ↑ ↓

Cardiovascular 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.

Cardiovascular US Medical PG Question 6: A 44-year-old man presents for a checkup. The patient says he has to urinate quite frequently but denies any dysuria or pain on urination. Past medical history is significant for diabetes mellitus type 2 and hypertension, both managed medically, as well as a chronic mild cough for the past several years. Current medications are metformin, aspirin, rosuvastatin, captopril, and furosemide. His vital signs are an irregular pulse of 74/min, a respiratory rate of 14/min, a blood pressure of 130/80 mm Hg, and a temperature of 36.7°C (98.0°F). His BMI is 32 kg/m2. On physical examination, there are visible jugular pulsations present in the neck bilaterally. Laboratory findings are significant for the following: Glycated Hemoglobin (Hb A1c) 7.5% Fasting Blood Glucose 120 mg/dL Serum Electrolytes Sodium 138 mEq/L Potassium 3.9 mEq/L Chloride 101 mEq/L Serum Creatinine 1.3 mg/dL Blood Urea Nitrogen 18 mg/dL Which of the following is the next best step in the management of this patient?

• A. Replace captopril with valsartan.
• B. Stop furosemide.
• C. Stop metformin.
• D. Start rosiglitazone.
• E. Start exenatide. (Correct Answer)

Cardiovascular Explanation: ***Correct: Start exenatide.*** * The patient has **diabetes mellitus type 2** with an **HbA1c of 7.5%**, indicating suboptimal glycemic control despite being on metformin. Exenatide, a **GLP-1 receptor agonist**, helps improve glycemic control by increasing insulin secretion, decreasing glucagon secretion, and slowing gastric emptying. * Given his BMI of **32 kg/m²**, exenatide is particularly beneficial as it also promotes **weight loss**, addressing an important comorbidity. *Incorrect: Replace captopril with valsartan.* * The patient is currently on captopril, an **ACE inhibitor**, for hypertension. Replacing it with valsartan, an **ARB**, is generally considered if the patient develops an ACE inhibitor-induced cough or angioedema. * While the patient has a chronic cough, it's been present for several years, making a **long-standing smoker's cough or COPD more likely** than an ACE-inhibitor-induced cough, which usually resolves within a few weeks of stopping the drug. His blood pressure and renal function are stable on captopril. *Incorrect: Stop furosemide.* * The presence of **visible jugular pulsations** in the neck suggests **elevated central venous pressure**, which could indicate **fluid overload** or heart failure. Stopping a diuretic like furosemide in this context would likely worsen fluid retention. * Furosemide is currently helping to manage the patient's fluid status, and discontinuing it could lead to **decompensation**, especially given the potential cardiac involvement hinted at by the jugular pulsations and irregular pulse. *Incorrect: Stop metformin.* * The patient's **HbA1c of 7.5%** indicates that his diabetes is **not well-controlled** on metformin alone, but this does not warrant stopping metformin, which is a first-line agent. * Metformin should only be stopped in cases of severe renal impairment (eGFR <30 mL/min/1.73m²), which is not indicated by his **creatinine of 1.3 mg/dL**, or other contraindications such as metabolic acidosis. *Incorrect: Start rosiglitazone.* * Rosiglitazone is a **thiazolidinedione (TZD)** that can improve insulin sensitivity and lower blood glucose. However, it is associated with side effects such as **weight gain** and **fluid retention**, which would be undesirable in this patient given his obesity and potential signs of fluid overload (jugular pulsations). * Additionally, TZDs have been linked to an increased risk of **congestive heart failure**, a concern given his irregular pulse and jugular pulsations suggesting potential cardiac issues.

Cardiovascular US Medical PG Question 7: A 67-year-old man presents to the emergency department with a 1-hour history of nausea and upper abdominal and substernal chest pain radiating to his lower jaw. He vomited several times before arriving at the hospital. His last visit to the primary care physician was 6 months ago during which he complained of fatigue, ‘slowing down’ on his morning walks, and abdominal pain that exacerbated by eating spicy food. His current medications include atorvastatin, metformin, insulin, omeprazole, aspirin, enalapril, nitroglycerin, and metoprolol. Today, his blood pressure is 95/72 mm Hg in his right arm and 94/73 in his left arm, heart rate is 110/min, temperature is 37.6°C (99.6°F), and respiratory rate is 30/min. On physical examination, he is diaphoretic and his skin is cool and clammy. His cardiac enzymes were elevated. He is treated appropriately and is admitted to the hospital. On day 5 of his hospital stay, he suddenly develops breathlessness. His blood pressure drops to 80/42 mm Hg. On examination, bibasilar crackles are heard. Cardiac auscultatory reveals a high pitched holosystolic murmur over the apex. Which of the following most likely lead to the deterioration of this patient’s condition?

• A. Scarring of mitral valve as a complication of childhood illness
• B. Ballooning of mitral valve into the left atrium
• C. Age-related fibrosis and calcification of the aortic valve
• D. Papillary muscle rupture leading to reflux of blood into left atrium (Correct Answer)
• E. Aortic root dilation

Cardiovascular Explanation: **Papillary muscle rupture leading to reflux of blood into left atrium** - The patient's initial presentation with chest pain, nausea, and elevated cardiac enzymes is consistent with an acute **myocardial infarction (MI)**. The sudden breathlessness, drop in blood pressure, bibasilar crackles (indicating **pulmonary edema**), and a **new holosystolic murmur over the apex** suggest acute **mitral regurgitation**, a common mechanical complication of MI. - **Papillary muscle rupture**, particularly of the posterior medial papillary muscle due to its single blood supply from the posterior descending artery (often involved in inferior MIs), can lead to severe acute mitral regurgitation, causing rapid hemodynamic deterioration and **cardiogenic shock**. *Scarring of mitral valve as a complication of childhood illness* - **Rheumatic heart disease**, typically resulting from childhood illnesses like **streptococcal pharyngitis**, can cause mitral valve scarring (often **mitral stenosis** or chronic regurgitation). However, this would be a pre-existing condition and less likely to cause a sudden, acute decompensation solely on day 5 post-MI. - While it can lead to cardiac issues, the sudden onset of symptoms and their direct association with a recent MI point away from a chronic, pre-existing valvular condition as the primary cause of acute decompensation. *Ballooning of mitral valve into the left atrium* - This describes **mitral valve prolapse (MVP)**, which is usually a chronic, benign condition, though it can cause mitral regurgitation. - Acute, severe mitral regurgitation leading to cardiogenic shock post-MI is more characteristic of structural damage like papillary muscle rupture rather than the typical progression of MVP. *Age-related fibrosis and calcification of the aortic valve* - This describes **aortic stenosis**, a chronic condition characterized by obstruction of blood flow from the left ventricle. - Aortic stenosis typically presents with a **systolic ejection murmur** best heard at the right upper sternal border, radiating to the carotids, and symptoms like angina, syncope, and dyspnea, which are different from the patient's acute presentation of a **holosystolic murmur at the apex** and pulmonary edema. *Aortic root dilation* - **Aortic root dilation** can lead to **aortic regurgitation**, characterized by a **diastolic decrescendo murmur**. - While causes of aortic root dilation can include hypertension, Marfan syndrome, or syphilis, it does not explain a **holosystolic murmur at the apex** or acute mitral regurgitation secondary to an MI.

Cardiovascular US Medical PG Question 8: A 47-year-old man presents for a routine physical examination as part of an insurance medical assessment. He has no complaints and has no family history of cardiac disease or sudden cardiac death. His blood pressure is 120/80 mm Hg, temperature is 36.7°C (98.1°F), and pulse is 75/min and is regular. On physical examination, he appears slim and his cardiac apex beat is of normal character and non-displaced. On auscultation, he has a midsystolic click followed by a late-systolic high-pitched murmur over the cardiac apex. On standing, the click and murmur occur earlier in systole, and the murmur is of increased intensity. While squatting, the click and murmur occur later in systole, and the murmur is softer in intensity. Echocardiography of this patient will most likely show which of the following findings?

• A. Left atrial mass arising from the region of the septal fossa ovalis
• B. Doming of the mitral valve leaflets in diastole
• C. Prolapse of a mitral valve leaflet of ≥2 mm above the level of the annulus in systole (Correct Answer)
• D. Retrograde blood flow into the right atrium
• E. High pressure gradient across the aortic valve

Cardiovascular Explanation: ***Prolapse of a mitral valve leaflet of ≥2 mm above the level of the annulus in systole*** - The clinical presentation with a **midsystolic click** followed by a **late-systolic high-pitched murmur over the cardiac apex** is characteristic of **mitral valve prolapse (MVP)**. - The changes in the click and murmur timing and intensity with **standing (earlier, louder)** and **squatting (later, softer)** are classic findings, reflecting changes in left ventricular volume that affect the onset of valve prolapse. *Left atrial mass arising from the region of the septal fossa ovalis* - This description is highly suggestive of a **myxoma**, typically found in the left atrium, which can cause symptoms of **obstructive heart failure** or **embolism**. - A myxoma would not typically present with the characteristic **midsystolic click** and **late-systolic murmur** that changes with position. *Doming of the mitral valve leaflets in diastole* - **Doming of the mitral valve leaflets in diastole** is characteristic of **mitral stenosis**, where the valve fails to open properly. - Mitral stenosis would present with a **diastolic murmur**, not a midsystolic click and late-systolic murmur. *Retrograde blood flow into the right atrium* - **Retrograde blood flow into the right atrium** indicates **tricuspid regurgitation**, which would typically manifest as a **holosystolic murmur** best heard at the lower left sternal border, often with prominent jugular venous pulsations. - This finding is inconsistent with the patient's auscultatory findings at the cardiac apex. *High pressure gradient across the aortic valve* - A **high pressure gradient across the aortic valve** signifies **aortic stenosis**, which is characterized by a **systolic ejection murmur** best heard at the right upper sternal border with radiation to the carotids. - This condition would not produce a midsystolic click or a late-systolic murmur at the apex.

Cardiovascular US Medical PG Question 9: A 56-year-old Caucasian male presents to the clinic to establish care. He has never seen a physician and denies any known medical problems. Physical examination is notable for central obesity, but the patient has regular heart and lung sounds. He has a blood pressure of 157/95 mm Hg and heart rate of 92/min. He follows up 2 weeks later, and his blood pressure continues to be elevated. At this time, you diagnose him with essential hypertension and decide to initiate antihypertensive therapy. Per the Joint National Committee 8 guidelines for treatment of high blood pressure, of the following combinations of drugs, which can be considered for first-line treatment of high blood pressure in the Caucasian population?

• A. ACE inhibitor, ARB, CCB, or thiazide (Correct Answer)
• B. ACE inhibitor, angiotensin receptor blocker (ARB), beta-blocker (BB), or thiazide
• C. ACE inhibitor, ARB, CCB, or loop diuretic
• D. ACE inhibitor, ARB, alpha-blocker, or loop diuretic
• E. ACE inhibitor, ARB, alpha-blocker, or direct vasodilator

Cardiovascular Explanation: **ACE inhibitor, ARB, CCB, or thiazide** - The **JNC 8 guidelines** recommend **ACE inhibitors**, **ARBs**, **calcium channel blockers (CCBs)**, and **thiazide diuretics** as first-line agents for essential hypertension in the general non-Black population. - These drug classes have demonstrated efficacy in reducing cardiovascular events and are generally well-tolerated. *ACE inhibitor, angiotensin receptor blocker (ARB), beta-blocker (BB), or thiazide* - While **ACE inhibitors**, **ARBs**, and **thiazides** are first-line, **beta-blockers** are generally not considered first-line for uncomplicated hypertension unless there are specific compelling indications (e.g., post-MI, heart failure). - **Beta-blockers** are less effective than other first-line agents in preventing stroke in the elderly and may have more side effects in some populations. *ACE inhibitor, ARB, CCB or loop diuretic* - **ACE inhibitors**, **ARBs**, and **CCBs** are first-line options, but **loop diuretics** are typically reserved for patients with fluid overload or chronic kidney disease, not for initial management of essential hypertension. - **Loop diuretics** have a shorter duration of action and a greater electrolyte-wasting effect compared to thiazide diuretics, making them less suitable for long-term monotherapy. *ACE inhibitor, ARB, alpha-blocker, or loop diuretic* - **Alpha-blockers** and **loop diuretics** are not considered first-line agents for essential hypertension. **Alpha-blockers** are typically used for benign prostatic hyperplasia or as add-on therapy for resistant hypertension. - **Alpha-blockers** can cause significant orthostatic hypotension, particularly with the first dose, and have not shown the same cardiovascular protective benefits as true first-line agents. *ACE inhibitor, ARB, alpha-blocker, or direct vasodilator* - **Alpha-blockers** and **direct vasodilators** (e.g., hydralazine, minoxidil) are not first-line treatments for essential hypertension. - **Direct vasodilators** are potent but often cause reflex tachycardia and fluid retention, requiring co-administration with other agents, and are typically reserved for severe or resistant hypertension.

Cardiovascular US Medical PG Question 10: A 21-year-old man presents to his physician for a routine checkup. His doctor asks him if he has had any particular concerns since his last visit and if he has taken any new medications. He says that he has not been ill over the past year, except for one episode of the flu. He has been training excessively for his intercollege football tournament, which is supposed to be a huge event. His blood pressure is 110/70 mm Hg, pulse is 69/min, and respirations are 17/min. He has a heart sound coinciding with the rapid filling of the ventricles and no murmurs. He does not have any other significant physical findings. Which of the following best describes the heart sound heard in this patient?

• A. Fourth heart sound (S4)
• B. Opening snap
• C. Third heart sound (S3) (Correct Answer)
• D. Second heart sound (S2)
• E. Mid-systolic click

Cardiovascular Explanation: ***Third heart sound (S3)*** - An **S3 heart sound** is a low-pitched sound heard during **rapid ventricular filling** in early diastole, immediately after S2. - In young, healthy individuals, especially athletes, an S3 can be a normal physiological finding, representing rapid filling of a **compliant ventricle**. *Fourth heart sound (S4)* - An **S4 heart sound** occurs during **atrial contraction** against a stiff or non-compliant ventricle, just before S1. - It is typically associated with conditions like **ventricular hypertrophy** or **ischemia** and is less likely to be a normal finding in a young, healthy individual. *Opening snap* - An **opening snap** is a high-pitched, crisp sound heard after S2, caused by the sudden opening of a **stenotic mitral** or **tricuspid valve**. - It indicates valvular pathology, specifically **mitral stenosis**, and is not related to ventricular filling in a healthy heart. *Second heart sound (S2)* - The **S2 heart sound** represents the **closure of the aortic and pulmonary valves** at the end of ventricular systole. - While it marks the beginning of diastole, it does not coincide with the rapid filling of the ventricles itself. *Mid-systolic click* - A **mid-systolic click** is typically associated with **mitral valve prolapse**, caused by the sudden tensing of the chordae tendineae or valve leaflets. - It occurs during systole, not diastole, and is not related to ventricular filling.

Cardiovascular Flashcard 1 of 10

Question: What is the effect of thyroid hormone on the cardiovascular and respiratory systems? _____

Answer: Increased activity

Cardiovascular Flashcard 2 of 10

Question: What is the effect of cardiogenic shock on pulse pressure?_____

Answer: Decreased pulse pressure

Cardiovascular Flashcard 3 of 10

Question: What causes the midsystolic click in a murmur due to mitral valve prolapse?_____

Answer: Sudden tensing of chordae tendinae

Cardiovascular Flashcard 4 of 10

Question: When total myocardial ischemia lasts less than 30 minutes, restoration of blood flow leads to _____ dysfunction

Answer: reversible contractile

Cardiovascular Flashcard 5 of 10

Question: How does the cardiac output of the left heart compare to the right heart?_____

Answer: Equal (in steady state)

Cardiovascular Flashcard 6 of 10

Question: What is the clinical significance of watershed zones in cerebral circulation?

Answer: areas at the border of two artery distributions are prone to hypoxia and infarction during severe hypotension

Cardiovascular Flashcard 7 of 10

Question: Which basal ganglia pathway inhibits movement?

Answer: indirect mnemonic: indirect inhibits

Cardiovascular Flashcard 8 of 10

Question: What is the phrase used to describe action potential conduction in myelinated nerves?

Answer: saltatory conduction i.e. AP basically jumps from node to node

Cardiovascular Flashcard 9 of 10

Question: What is the function of myelin?

Answer: increases neuronal conduction velocity

Cardiovascular Flashcard 10 of 10

Question: Give the stages of mitosis.

Answer: prophase, metaphase, anaphase, telophase mnemonic: PMAT