CVS – 2024

The Fick principle is a method for measuring cardiac output (CO) based on oxygen consumption:

• Principle: The total uptake or release of a substance (e.g., O₂) by an organ is equal to the product of blood flow through the organ and the arteriovenous concentration difference of that substance.

• Applied to the whole body:

CO = O2 consumption / (Arterial O2 – Venous O2)

• O₂ consumption is measured (e.g., via a metabolic cart).

• Arterial O₂ content comes from arterial blood sampling.

• Venous O₂ content comes from mixed venous blood (e.g., from the pulmonary artery).

❌ Why the other options are incorrect

Cardiac output = Mean arterial pressure / Total peripheral resistance – This comes from Ohm’s law analogy (MAP = CO × TPR), not the Fick principle.

Cardiac output = Stroke volume × Systolic pressure – Stroke volume alone contributes to CO; systolic pressure is unrelated in Fick’s calculation.

Cardiac output = Pulse pressure × Heart rate – Pulse pressure reflects stroke volume indirectly; this is not the Fick principle.

Cardiac output = Heart rate × Stroke volume – This gives CO mathematically, but the Fick principle specifically uses oxygen consumption and arteriovenous O₂ difference.

Coronary blood flow is influenced by:

• Ventricular contraction – Compresses intramyocardial vessels, especially in the left ventricle.

• Ventricular relaxation – Relieves compression, allowing blood flow primarily during diastole.

Early ventricular systole:

• Left ventricular pressure rises sharply.

• Intramural vessels are compressed maximally.

• This causes minimal coronary perfusion, especially in the subendocardium.

Diastole (early, mid, late) and atrial systole allow coronary blood flow because ventricular contraction is absent or minimal.

❌ Why the other options are incorrect

Late ventricular systole – Flow begins to improve slightly as ventricular pressure approaches peak and relaxation starts.

Early diastole – Coronary perfusion increases significantly as the ventricle relaxes.

Atrial systole – Contributes to ventricular filling; coronary flow is not impeded.

Mid-diastole – Maximum coronary perfusion occurs here because the ventricle is fully relaxed.

Stroke volume (SV) is the volume of blood ejected from the ventricle per beat and is influenced primarily by:

• Preload – the end-diastolic volume or ventricular filling.

  • According to the Frank-Starling law, the more the ventricular fibers are stretched during filling, the stronger the subsequent contraction, increasing stroke volume.

❌ Why the other options are incorrect

Arterial blood pressure – Refers to afterload, which can influence stroke volume inversely but is not the strongest determinant.

Ventricular compliance – Modulates how easily the ventricle fills, indirectly affecting SV, but less directly than preload.

Atrial contraction – Contributes to late ventricular filling, especially at high heart rates, but preload (total EDV) is more critical.

Heart rate – Determines cardiac output (CO = HR × SV), but does not directly set stroke volume under normal conditions.

On a normal chest X-ray, the right cardiac border is formed almost entirely by the:

✔ Right atrium

However — right atrium is NOT listed among the answer choices.
So from the given options, the closest and most reasonable structure is:

👉 Right ventricle

Even though:

• The right ventricle is the most anterior chamber,

• It does NOT normally form the right mediastinal border,

• The question forces you to choose the closest possible answer.

Why the others are incorrect

❌ Left atrial appendage
Forms part of the left cardiac border.

❌ Pulmonary trunk
Also part of the left upper mediastinal border.

❌ Left ventricle
Forms the left lower cardiac border.

❌ Aortic arch
Visible on the left as the “aortic knob.”

Correct anatomical teaching (important to remember):

Right border = Right atrium

Left border = Aortic arch → Pulmonary trunk → Left atrial appendage → Left ventricle

When discussing dietary fats and heart-disease prevention, trans fats are the most dangerous and the first type of fat that should be eliminated.

Why trans fats are the worst

• Increase LDL (bad cholesterol)

• Decrease HDL (good cholesterol)

• Promote inflammation

• Strongly associated with atherosclerosis and heart attacks

• Found in deep-fried foods, baked goods, margarine, processed snacks

Even small amounts significantly raise cardiovascular risk, especially in someone with a family history of early heart disease.

Why the other options are incorrect

❌ Saturated fat
Unhealthy in excess, but less harmful than trans fats. Reducing is advisable, but not the most important.

❌ Monounsaturated fat
Heart-healthy (olive oil, nuts). Should not be avoided.

❌ Polyunsaturated fat
Also cardioprotective (sunflower oil, fish). Should not be avoided.

❌ Omega-6
Part of polyunsaturated fats. Safe in moderate amounts.

Among the listed drugs, Hydralazine is the one that acts as a direct arteriolar vasodilator.

✔ Hydralazine

• Directly relaxes arterial smooth muscle

• ↓ Peripheral resistance

• Used in hypertension and hypertensive emergencies

• Side effect: reflex tachycardia, lupus-like syndrome

Why the other options are incorrect

❌ Spironolactone
Aldosterone antagonist (potassium-sparing diuretic), not a vasodilator.

❌ Furosemide
Loop diuretic — increases Na⁺/water excretion, not a vasodilator.

❌ Metoprolol
β₁-blocker — reduces heart rate and cardiac output, not a vasodilator.

❌ Verapamil
Calcium channel blocker — decreases cardiac contractility and AV conduction, not used primarily as a vasodilator (DHP CCBs like nifedipine/amlodipine are vasodilators, but Verapamil is non-DHP).

Coronary blood flow is unique because:

• Most perfusion occurs during diastole, especially in the left ventricle.

• During systole, myocardial contraction compresses intramural vessels, reducing flow.

• Driving pressure for coronary flow in diastole is the pressure difference between the aortic diastolic pressure and left ventricular end-diastolic pressure.

• Therefore, aortic diastolic pressure is the primary determinant of coronary perfusion, particularly for the left coronary artery.

❌ Why the other options are incorrect

Left ventricular end-diastolic pressure – Acts as a back pressure, opposing flow, but is not the primary driving force.

Mean arterial pressure – Reflects average arterial pressure over the cardiac cycle, but coronary flow is diastole-dependent, so diastolic pressure is more directly relevant.

Stroke volume – Influences systolic pressure but is not the main determinant of coronary perfusion during diastole.

Heart rate – Affects the duration of diastole; higher rates reduce diastolic time, but the driving pressure remains aortic diastolic pressure.

Class I antiarrhythmic drugs (Class IA, IB, IC) all share one fundamental mechanism:

✔ They block fast voltage-gated Na⁺ channels in cardiac myocytes.

This action:

• Slows Phase 0 depolarization

• Decreases conduction velocity

• Helps suppress abnormal pacemaker activity

• Stabilizes the cardiac membrane

All subclasses differ in strength of Na⁺ block and effect on action potential duration, but Na⁺ channel blockade is the core mechanism.

Why the other options are incorrect

❌ Ca²⁺ channel blockade
Class IV drugs (Verapamil, Diltiazem).

❌ K⁺ channel blockade
Class III drugs (Amiodarone, Sotalol).

❌ Na⁺ channel opening
No antiarrhythmic drug works by opening sodium channels.

❌ K⁺ channel opening
Not a primary mechanism of antiarrhythmics.

Angiotensin Receptor Blockers (ARBs) block AT₁ receptors, preventing the action of angiotensin II → vasodilation, reduced aldosterone, lowered BP.

Losartan is the classic prototype ARB.

Common ARBs include:

• Losartan

• Valsartan

• Irbesartan

• Telmisartan

• Candesartan

Why the other options are incorrect

❌ Hydralazine
Direct arteriolar vasodilator.

❌ Metoprolol
Selective β₁-blocker.

❌ Labetalol (Lavetalol)
Combined α₁ + β-blocker.

❌ Prazosin
Selective α₁-blocker.

Only Losartan is an ARB.

Risk factors for cardiovascular diseases are divided into:

Modifiable Risk Factors (can be changed)

• High cholesterol

• Hypertension

• Smoking

• Obesity

• Physical inactivity

• Poor diet

• Diabetes

• Stress

Non-modifiable Risk Factors (cannot be changed)

• Age

• Gender

• Ethnicity

• Family history/genetics

In this question, only cholesterol level is something the industrialist can actively control or improve through:

• Workplace wellness programs

• Healthy food options

• Fitness activities

• Regular screening

Thus, it is the modifiable risk factor.

Why the other options are incorrect

❌ Family history – Non-modifiable
❌ Ethnicity – Non-modifiable
❌ Gender – Non-modifiable
❌ Age – Non-modifiable

A persistent, dry cough is the classic adverse effect of ACE inhibitors.
Captopril is an ACE inhibitor.

Why ACE inhibitors cause cough

• ACE inhibitors block degradation of bradykinin.

• ↑ Bradykinin levels lead to:

  • Persistent dry cough

  • Sometimes angioedema

This is the hallmark side effect of ACE inhibitors.

Why the other options are incorrect

❌ Nifedipine
Calcium channel blocker → causes flushing, edema, headache — not cough.

❌ Metoprolol
β₁-blocker → causes bradycardia, fatigue — not cough.

❌ Prazosin
α₁-blocker → causes orthostatic hypotension — not cough.

❌ Losartan
ARB → does NOT cause cough because it does not increase bradykinin.
(Used as an alternative when ACE inhibitors cause cough.)

Let’s line up the clues:

• 70-year-old man

• Heavy smoker

• History of myocardial infarction

• Hypertension (165/100 mmHg)

• Poor peripheral pulses in lower limbs → peripheral arterial disease

• 6-cm pulsating mass in the midline of the lower abdomen

This is the classic picture of an abdominal aortic aneurysm (AAA), most commonly due to atherosclerosis.

Why it’s an atherosclerotic aneurysm

• Location: Midline, lower abdomen → typically infrarenal abdominal aorta

• Risk factors:

  • Age

  • Male sex

  • Smoking

  • Atherosclerosis

  • Hypertension

• Pulsatile mass + peripheral vascular disease + IHD = textbook atherosclerotic aneurysm.

The aneurysm is caused by destruction and thinning of the aortic media due to atherosclerotic changes, leading to dilation and risk of rupture.

Why the other options are incorrect

❌ Thromboangiitis obliterans (Buerger disease)

• Occurs in younger male smokers

• Affects small and medium arteries of hands and feet, not the abdominal aorta

• Causes ischemia, claudication, gangrene—but not a 6-cm abdominal pulsating mass.

❌ Arteriovenous fistula

• Abnormal direct connection between artery and vein.

• Can cause high-output heart failure or local bruits, but not a large midline pulsatile abdominal mass.

❌ Polyarteritis nodosa (PAN)

• Necrotizing vasculitis of medium-sized arteries, affects multiple organs.

• Causes systemic symptoms (fever, malaise, abdominal pain, renal involvement), not a big, localized pulsatile aneurysm like this.

❌ Aortic dissection

• Sudden, severe tearing chest or back pain, usually involving the thoracic aorta.

• Not typically a chronic, palpable 6-cm abdominal pulsatile mass.

Systemic hypertensive heart disease refers to the changes in the heart caused by long-standing systemic (left-sided) hypertension.

The key sequence is:

↑ Systemic blood pressure → ↑ Afterload on LV → LV hypertrophy → LV stiffness → impaired filling → Left atrial enlargement

So the classic morphological findings include:

• Concentric left ventricular hypertrophy (LVH)

• Left atrial enlargement due to increased filling pressures

• Myocyte hypertrophy with increased transverse diameter

These occur because the left ventricle must pump against chronically elevated systemic resistance.

Why the other options are incorrect

❌ Decrease in transverse diameter of myocyte
Opposite of what happens.
Hypertrophy → increased transverse diameter (thickened myocytes).

❌ Right ventricular hypertrophy
Seen in pulmonary hypertension, not systemic hypertension.

❌ Right ventricle is dilated
Occurs in right-sided heart failure or pulmonary hypertension, not systemic hypertension.

❌ Thick pulmonary valve
Unrelated. Pulmonary valve changes occur with congenital defects, not hypertension.

Atherosclerosis is a chronic inflammatory disease of large and medium-sized arteries.
The classic lesion is the atherosclerotic plaque (fibrofatty plaque).

Key Morphological Features of Atherosclerosis

The plaque has three main components:

1. Fibrous cap (outer layer)

   • Made of smooth muscle cells, collagen, and extracellular matrix

   • This is the characteristic raised, firm part of the plaque

2. Necrotic lipid core

   • Cholesterol & cholesterol esters

   • Foam cells, macrophages

   • Cell debris, calcium

3. Shoulder region

   • T-cells, macrophages, smooth muscle cells

Thus, the most accurate morphological statement is:

✔ Fibrous cap is present

Why the other options are incorrect

❌ Hyaline deposition is present in the center
This describes hyaline arteriolosclerosis, not atherosclerosis.

❌ Eosinophils with cholesterol crystals
Wrong. The core contains foam cells, macrophages, cholesterol clefts, NOT eosinophils.

❌ Calcification is seen in early stage
Calcification occurs late (in advanced plaques).

❌ The lesions are not raised
Incorrect — atheromatous plaques are raised lesions that protrude into the lumen.

The timeline of morphological changes after myocardial infarction (MI) is well-defined.

At 12 hours, the heart muscle has already undergone irreversible injury, and the characteristic change you see on light microscopy is:

✔ Early coagulative necrosis

• Myocytes become hypereosinophilic

• Loss of nuclei (karyolysis) begins

• Neutrophils start to infiltrate the tissue

• Cell outlines remain preserved → classic for coagulative necrosis

This corresponds exactly to the 12–24 hour window after an MI.

Why the other options are incorrect

❌ Waviness of myocardial fibers
Occurs 1–3 hours after MI due to stretching by surrounding viable fibers.

❌ Dense collagenous scar
Occurs weeks later (around 7 weeks after MI).

❌ Endothelial injury
Not the characteristic microscopic change after 12 hours of MI.

❌ No changes
Incorrect — no changes are seen during the first 30 minutes. After 12 hours, definite necrosis is present.

This patient has a long history of poorly controlled hypertension, which has now suddenly accelerated to malignant hypertension (BP ≈ 250/125 mm Hg).

Malignant hypertension causes acute vascular injury, especially in the kidneys.

Classic Renal Lesion in Malignant Hypertension

Necrotizing arteriolitis (a.k.a. Fibrinoid necrosis of arterioles)

• Seen in malignant (accelerated) hypertension

• Characterized by:

  • Fibrinoid necrosis of vessel walls

  • Hyperplastic arteriolosclerosis (“onion-skin” appearance)

  • Acute renal failure or rising creatinine

This matches the patient’s rapidly worsening BP and rising serum creatinine.

Why the other options are incorrect

❌ Granulomatous arteritis
Seen in conditions like Giant Cell Arteritis, not hypertension.

❌ Fibromuscular dysplasia
Causes renovascular hypertension, usually in young women; produces a “string-of-beads” appearance—not malignant HTN changes.

❌ Renal arterial stenosis
Causes secondary hypertension, but the lesion seen is atherosclerosis or FMD, not necrotizing arteriolitis.

❌ Polyarteritis nodosa (PAN)
A systemic necrotizing vasculitis affecting medium arteries, but presents with multiple systemic symptoms, not just malignant hypertension.

A mid-systolic click on auscultation is the hallmark of mitral valve prolapse (MVP).

Over time, MVP can lead to:

• Progressive mitral regurgitation

• Symptoms like dyspnea, palpitations, and fatigue

• Valve leaflet billowing into the left atrium

The pathologic change responsible for MVP is:

Myxomatous degeneration

• Accumulation of mucoid (myxoid) material within the valve leaflet.

• Loss of collagen and elastin → floppy, redundant leaflet.

• Leads to elongation of chordae tendineae and eventual regurgitation.

This is the classic pathology in primary MVP, especially in otherwise healthy women.

Why the other options are incorrect

❌ Dystrophic calcification
Seen in calcific aortic stenosis, not MVP.

❌ Infective vegetations
Seen in infective endocarditis, cause fever, murmurs, emboli—not a mid-systolic click.

❌ Rheumatic vegetations
Seen on mitral regurgitation/stenosis after rheumatic fever—valve becomes thickened, fused, not floppy.

❌ Fibrinoid necrosis
Occurs in immune-mediated vasculitis, not in MVP.

The infant presents with:

• Cyanosis

• Heart murmur

• Overriding aorta

• Ventricular septal defect (VSD)

• Right ventricular hypertrophy (RVH)

• Pulmonary stenosis

These four classic defects together define:

Tetralogy of Fallot (TOF)

The tetralogy consists of:

1. Pulmonary stenosis

2. Right ventricular hypertrophy

3. Ventricular septal defect (VSD)

4. Overriding aorta

This leads to a right-to-left shunt, causing cyanosis shortly after birth.

Why the other options are incorrect

❌ Transposition of great arteries
Cyanotic, but shows aorta arising from RV and pulmonary trunk from LV, not VSD + overriding aorta.

❌ Patent ductus arteriosus
Causes continuous “machinery” murmur. Not associated with the four defects listed.

❌ Eisenmenger Syndrome
Occurs later in life due to long-standing L→R shunt reversing to R→L. Not present at birth with these anatomy findings.

❌ Coarctation of aorta
Presents with BP differences in arms vs legs, not VSD/overriding aorta.

To synthesize triglycerides (TAGs) and lecithin (phosphatidylcholine), the body needs a common intermediate called phosphatidic acid.

Why phosphatidic acid?

Phosphatidic acid is formed by adding two fatty acyl-CoA molecules to glycerol-3-phosphate:

1. Glycerol-3-phosphate → acylated → Lysophosphatidic acid

2. Lysophosphatidic acid → acylated again → Phosphatidic acid

From this step:

• Phosphatidic acid → Diacylglycerol (DAG) → TAGs (Triglycerides)

• Phosphatidic acid → CDP-diacylglycerol → Glycerophospholipids like:

  • Lecithin (phosphatidylcholine)

  • Phosphatidylserine

  • Phosphatidylethanolamine

So, phosphatidic acid is the branch point for both TAG and phospholipid synthesis.

Why the other options are incorrect

❌ Glycerol phosphate acyltransferase
An enzyme, not an intermediate.

❌ Monoacyl glycerol acyltransferase
Also an enzyme involved in TAG synthesis in the intestine.

❌ Lysophosphatidyl acyltransferase
Enzyme that forms phosphatidic acid — not the intermediate itself.

❌ Phosphatidyl transferase
General enzyme term — not the required intermediate.

The major reactive species (oxidative radicals) responsible for free-radical injury in the human body are:

1. Superoxide anion (O₂⁻)

• Produced mainly during mitochondrial oxidative phosphorylation.

• First radical formed when oxygen is reduced.

• Precursor of many other ROS.

2. Hydroxyl radical (•OH)

• Most destructive reactive oxygen species.

• Formed from:

  • Fenton reaction (Fe²⁺ + H₂O₂ → •OH)

  • Radiolysis of water

  • Haber–Weiss reaction

• Causes lipid peroxidation, DNA breaks, protein cross-linking.

3. Nitric oxide (NO)

• A reactive nitrogen species (RNS).

• Produced by nitric oxide synthase.

• Combines with superoxide to form peroxynitrite (ONOO⁻) → highly damaging.

Why others are wrong

❌ Glutathione
Not an oxidant — it is a major antioxidant that neutralizes free radicals.

❌ Ascorbic acid (Vitamin C)
Also a powerful antioxidant, not a radical.

❌ Organic peroxides
These may form in lipid peroxidation but are not the primary physiological radicals.

The dicrotic notch (also called the incisura) is a small downward deflection in the arterial pressure waveform, observed in aortic or ventricular pressure tracings:

• Occurs at the end of ventricular systole.

• Caused by closure of the aortic valve:

  • When the ventricle finishes ejecting blood, the aortic valve snaps shut.

  • This briefly increases aortic pressure due to elastic recoil and transient backflow, producing the notch.

• It marks the end of systole and beginning of diastole..

❌ Why the other options are incorrect

Blood ejection into the aorta – Causes the systolic upstroke, not the dicrotic notch.

Opening of the mitral valve – Marks ventricular filling, occurring later in diastole; not responsible for the notch.

Pulmonary valve closure – Produces a similar effect in the pulmonary artery, but the question refers to the aortic/atrial waveform.

Ventricular relaxation – Begins after the notch, but the notch itself is due to valve closure, not relaxation per se.

• Preload is the end-diastolic volume (EDV) or ventricular wall stretch at the end of filling.

• According to the Frank-Starling law of the heart:

  • An increase in preload stretches the myocardial fibers more.

  • This leads to stronger contraction (up to an optimal point).

• If afterload and contractility remain constant, the result is:

  • Greater stroke volume

  • Increased cardiac output (CO = HR × SV)

This is a fundamental principle by which the heart matches output to venous return.

❌ Why the other options are incorrect

Increased systemic vascular resistance – Afterload is constant, so SVR does not change.

Reduced end-diastolic volume – Preload is increased, so EDV rises, not decreases.

Lower systolic pressure – Systolic pressure usually rises with increased stroke volume, not decreases.

Decreased stroke volume – Stroke volume increases due to greater preload if contractility is unchanged.

The Bainbridge reflex is a cardiovascular reflex that helps maintain cardiac output in response to increased venous return:

• Trigger: Increased atrial pressure / stretch due to higher venous return.

• Afferent pathway: Stretch receptors in the atria and vena cavae send signals via the vagus nerve to the medulla.

• Efferent response: Increased sympathetic stimulation of the heart → increased heart rate (positive chronotropy).

• Purpose: Prevent atrial overfilling and maintain efficient circulation.

This reflex complements the baroreceptor reflex, which responds primarily to arterial pressure, whereas the Bainbridge reflex responds to venous pressure.

❌ Why the other options are incorrect

Decreases contractility in response to low venous return – Bainbridge reflex increases heart rate, not decreases contractility.

Decreases heart rate in response to high blood pressure – This describes the baroreceptor reflex, not the Bainbridge reflex.

Increases blood pressure in response to high heart rate – Not a feature of the Bainbridge reflex; it specifically regulates heart rate, not blood pressure.

Reduces cardiac output when venous return decreases – The Bainbridge reflex responds to increased venous return, not reduced.

Cardiac output (CO) is defined as:

CO = Heart Rate × Stroke Volume

During exercise:

1. Sympathetic stimulation increases:

   • Heart rate (chronotropy)

   • Contractility (inotropy) → increases stroke volume

2. This directly increases cardiac output, ensuring adequate oxygen delivery to muscles.

3. Other mechanisms (like vasodilation or increased venous return) support increased CO but are not the primary direct contributors.

Thus, increased heart rate and contractility are the main drivers of increased cardiac output during exercise.

❌ Why the other options are incorrect

Decrease in systemic vascular resistance – Helps reduce afterload and facilitate flow, but does not directly increase CO.

Increased parasympathetic activity – Would slow heart rate, reducing CO.

Increase in end-systolic volume – Means more blood remains in the ventricle after contraction, which reduces stroke volume, not CO.

Reduced ventricular filling – Lowers preload, decreasing stroke volume and CO.

• Atrial repolarization occurs after atrial depolarization.

• The atrial muscle cells repolarize slowly, but this electrical activity is masked by the much larger ventricular depolarization.

• Ventricular depolarization corresponds to the QRS complex, which has a much higher amplitude than atrial repolarization.

• Therefore, atrial repolarization occurs during the QRS complex and is not visible as a separate wave on a standard ECG.

❌ Why the other options are incorrect

QT interval – Represents ventricular depolarization and repolarization, not atrial repolarization.

ST segment – Corresponds to early ventricular repolarization; atrial repolarization has already occurred.

P wave – Represents atrial depolarization, not repolarization.

T wave – Represents ventricular repolarization, not atrial repolarization.

S3 heart sound characteristics:

• Occurs early in diastole, immediately after S2.

• Produced during rapid passive filling of the ventricle when the ventricular wall is compliant or overloaded.

• Physiologic S3: Seen in children and young adults due to highly compliant ventricles.

• Pathologic S3: Seen in elderly or adults and often indicates:

  • Heart failure (volume overload, dilated ventricles)

  • Mitral regurgitation

• Low-pitched “ventricular gallop,” best heard at the apex in the left lateral decubitus position with the bell of the stethoscope.

❌ Why the other options are incorrect

Ejection click – Heard early systole; associated with valve opening (e.g., aortic or pulmonary stenosis).

S1 – Occurs at ventricular contraction; closure of mitral and tricuspid valves.

S2 – Occurs at ventricular relaxation; closure of aortic and pulmonary valves.

S4 – Occurs just before S1 during atrial contraction; associated with stiff or hypertrophic ventricles (e.g., hypertension, LVH), not rapid filling.

Afterload is the resistance the ventricle must overcome to eject blood, usually determined by aortic or pulmonary arterial pressure.

• Ventricular pressure-volume (PV) loop changes with increased afterload:

  • Isovolumetric contraction pressure rises: The ventricle must generate a higher pressure during contraction before the semilunar valves can open.

  • Stroke volume may decrease slightly if contractility does not change.

  • End-systolic volume (ESV) may increase because less blood is ejected.

  • End-diastolic volume (EDV) may remain similar initially but can increase over time with chronic afterload elevation.

Key point: The immediate effect of increased afterload is seen as a higher peak pressure during isovolumetric contraction on the PV loop.

❌ Why the other options are incorrect

Increased compliance of the ventricle – Compliance is an intrinsic property of the myocardium and does not acutely change with afterload.

Decreased end-systolic pressure – Actually, end-systolic pressure rises with increased afterload.

Increased end-diastolic volume – May occur chronically if the heart dilates, but not the immediate effect.

Reduced preload – Preload depends on venous return, not afterload; it is unaffected acutely by afterload changes.

The ventricular action potential has distinct phases:

• Phase 0 (rapid depolarization):

  • Triggered when the membrane potential reaches threshold.

  • Fast voltage-gated sodium (Na⁺) channels open, allowing a rapid influx of sodium ions into the cell.

  • This causes a steep upstroke (high slope) of phase 0.

  • The steepness of the slope determines conduction velocity in the ventricular myocardium.

❌ Why the other options are incorrect

Potassium – Responsible for repolarization in phase 3, not the rapid depolarization.

Magnesium – Plays a cofactor role in enzymatic processes; does not determine phase 0 slope.

Chloride – Minor influence on resting potential; not involved in phase 0 depolarization.

Calcium – Contributes to the plateau (phase 2) and pacemaker depolarization, not the steep upstroke of phase 0.

When ventricular filling pressures drop suddenly (e.g., after hemorrhage or trauma):

• Cardiac output (CO) decreases because stroke volume falls.

• The body activates compensatory mechanisms to maintain arterial pressure and tissue perfusion.

• Baroreceptors in the carotid sinus and aortic arch detect the drop in mean arterial pressure almost immediately.

• They trigger a reflex increase in sympathetic tone and decrease parasympathetic tone, resulting in:

  • Tachycardia (increased heart rate)

  • Increased myocardial contractility

  • Peripheral vasoconstriction

Timing matters:

• Neural (baroreceptor) mechanisms respond within seconds.

• Renin-angiotensin-aldosterone system and vasoconstriction of coronary vessels are slower, taking minutes to hours.

❌ Why the other options are incorrect

Vasoconstriction of coronary vessels – Would reduce blood supply to the heart, not a compensatory mechanism; coronary vessels actually dilate to meet cardiac oxygen demand.

Increased parasympathetic tone – Would slow the heart, opposite of what is needed to maintain cardiac output.

Renin release from the kidney – Hormonal mechanism, slower response (minutes to hours).

Increased afterload – Not a direct immediate compensatory mechanism; afterload is more a result of systemic vascular resistance.

Cardiac muscle has distinctive features that differentiate it from skeletal and smooth muscle:

• Striated fibers – similar to skeletal muscle, but shorter and branched.

• Single centrally located nucleus – occasionally two.

• Intercalated discs – specialized cell junctions between adjacent cardiac myocytes.

Functions of intercalated discs:

• Mechanical connection via desmosomes – hold cells together during contraction.

• Electrical connection via gap junctions – allow rapid spread of action potentials for synchronized contraction.

❌ Why the other options are incorrect

Nuclei are peripherally arranged – Characteristic of skeletal muscle, not cardiac muscle.

Cells have multiple nuclei – Skeletal muscle is multinucleated; cardiac muscle usually has one central nucleus.

Fibers are non-striated – Smooth muscle is non-striated; cardiac muscle is striated.

Has diads – Found in cardiac muscle at the level of T-tubules and sarcoplasmic reticulum, but intercalated discs are more visually obvious under the microscope for identification.

The inner lining of the heart is called the endocardium:

• The endocardium is continuous with the tunica intima of blood vessels.

• Its epithelium is simple squamous, also called endothelium.

• Functions:

  • Provides a smooth surface for blood flow

  • Reduces friction

  • Forms a barrier between blood and myocardial tissue

  • Participates in hemostasis and vascular signaling

❌ Why the other options are incorrect

Pseudostratified ciliated columnar – Found in respiratory tract, not in the heart.

Stratified cuboidal – Rare; found in some gland ducts, not in endocardium.

Simple columnar – Found in digestive tract; not in blood vessels or heart chambers.

Simple cuboidal – Found in kidney tubules and some glands; not in endocardium.

Large arteries such as the aorta and pulmonary trunk are classified as elastic arteries. Their key features:

• Walls contain many layers of elastic laminae in the tunica media.

• Elastic fibers allow the arteries to expand during ventricular systole and recoil during diastole, which helps maintain continuous blood flow.

• These fibers are more abundant in large arteries than in medium or small muscular arteries.

• Muscular fibers (smooth muscle) are present but less dominant in the tunica media compared to elastic fibers in these vessels.

❌ Why the other options are incorrect

Connective tissue type 1 fibers – Found in tendons, ligaments, and dense connective tissue; not the main fibers for elastic recoil in large arteries.

Connective tissue type 2 fibers – Found in cartilage; irrelevant for arterial wall structure.

Reticular fibers – Provide support in soft tissues like lymphoid organs, not dominant in large arteries.

Muscular fibers – Smooth muscle is present in the tunica media, but elastic fibers dominate in large elastic arteries.

On a frontal chest X-ray, the cardiac silhouette is formed by different chambers of the heart:

• Right border – right atrium and superior vena cava

• Left border – mainly the left ventricle, with a small contribution from the left auricle

• Superior border – aortic arch, pulmonary trunk, left atrium

Left ventricle:

• Forms the apex and the left lateral border of the heart on X-ray

• Appears as the prominent left-sided cardiac shadow

• This is clinically important when evaluating cardiomegaly or left ventricular enlargement

❌ Why the other options are incorrect

Superior vena cava – Forms the right superior border, not the left border.

Right ventricle – Forms the inferior border and part of the right border.

Right auricle – Contributes to the right border, not the left.

Right atrium – Forms the right border of the heart, not the left border.

The coronary sinus is a large venous structure located in the posterior part of the coronary sulcus. Key points:

• Collects deoxygenated blood from most of the myocardium via tributaries like the great cardiac vein, middle cardiac vein, and small cardiac vein.

• Its main function is to return venous blood from the heart wall itself to the circulation.

• The coronary sinus opens directly into the right atrium, near the inferior aspect of the interatrial septum, just proximal to the tricuspid valve.

❌ Why the other options are incorrect

Inferior vena cava – Drains systemic venous blood from the lower body, not the heart wall.

Superior vena cava – Drains systemic venous blood from the upper body, not the heart wall.

Pulmonary trunk – Carries deoxygenated blood from the right ventricle to the lungs; coronary sinus does not drain here.

Left atrium – Receives oxygenated blood from the pulmonary veins, not venous blood from the myocardium.

Pericardium consists of:

1. Fibrous pericardium – tough outer layer

2. Serous pericardium – thin inner layer, divided into:

   • Parietal layer – lines the fibrous pericardium

   • Visceral layer (epicardium) – covers the heart surface

Pericardial cavity is the potential space between the visceral and parietal layers of the serous pericardium.

• Fluid accumulation (pericardial effusion) occurs in this space.

• This allows the heart to beat smoothly within the pericardial sac and prevents friction.

❌ Why the other options are incorrect

Endocardium and myocardium – This is the inner lining and muscle of the heart, not the pericardial space.

Myocardium and pericardium – Fluid does not accumulate inside the heart muscle.

Epicardium and pericardium – The epicardium is the visceral layer, so the correct term is visceral and parietal layers; this option is imprecise.

Myocardium and epicardium – Again, this is within the heart wall, not the pericardial cavity.

The Left anterior descending (LAD) artery is a branch of the left coronary artery. It:

• Runs in the anterior interventricular groove toward the apex.

• Supplies:

  • Anterior wall of the left ventricle

  • Anterior two-thirds of the interventricular septum

  • Sometimes the apex of the left ventricle

• Because it supplies such a large portion of the left ventricle, blockage can lead to significant myocardial infarction, hence the nickname “widow-maker.”

❌ Why the other options are incorrect

Inferior wall of left ventricle – Supplied primarily by the right coronary artery or posterior descending artery, not LAD.

Right ventricle – Mainly supplied by the right coronary artery.

Right atrium – Supplied by right coronary artery branches, not LAD.

Left atrium – Supplied mostly by circumflex branch of the left coronary artery, not LAD.

Pericardium has two main layers:

1. Fibrous pericardium – tough outer layer

2. Parietal serous pericardium – inner layer lining the fibrous pericardium

Visceral layer of serous pericardium is insensitive to pain.

• Pain from fibrous and parietal layers is somatic in nature.

• These layers are supplied by the phrenic nerve (C3–C5), which carries afferent fibers responsible for pain sensation.

• This explains why pericarditis pain often radiates to the shoulder or neck, following the C3–C5 dermatomes.

❌ Why the other options are incorrect

First intercostal – Supplies skin and muscles of the upper thoracic wall, not the pericardium.

Subcostal – T12 nerve; supplies abdominal wall muscles and skin, unrelated to pericardium.

Axillary – Branch of the brachial plexus, supplies shoulder region; does not innervate the pericardium.

Vagus – Provides parasympathetic fibers to the heart, but does not mediate pain sensation from the pericardium.

The circumflex branch of the left coronary artery:

• Arises from the left coronary artery.

• Runs in the atrioventricular (coronary) groove, which separates the atria from the ventricles.

• It travels posterolaterally around the heart, giving off branches to the left atrium and lateral/posterior walls of the left ventricle.

• This groove is also called the coronary sulcus, and it houses the right coronary artery on the right side and the circumflex on the left.

❌ Why the other options are incorrect

Posterior interventricular groove – Runs along the posterior surface between the right and left ventricles, primarily carrying the posterior descending artery.

Anterior interventricular groove – Runs along the anterior surface between the ventricles, mainly carrying the left anterior descending artery (LAD).

Posterior interatrial groove – Located on the posterior aspect of the atria; not associated with the circumflex artery.

Anterior interatrial groove – Located between the atria anteriorly; unrelated to the course of the circumflex artery.

During atrial septation in the fetal heart:

1. The septum primum is the first structure to grow downward from the roof of the primitive atrium toward the endocardial cushions, beginning the division of the atrium.

2. Initially, there is an opening near the cushions called the ostium primum.

3. Before the ostium primum closes, apoptosis creates perforations higher up in the septum primum, which coalesce to form the ostium secundum.

4. Later, the septum secundum grows adjacent to the septum primum but leaves the foramen ovale, allowing right-to-left shunting of blood in utero.

❌ Why the other options are incorrect

Interventricular septum / Ventricular septum – These separate the ventricles; the ostium secundum is not located here.

Septum secundum – Develops after the ostium secundum forms. It partially overlaps the ostium secundum to form the foramen ovale but does not contain the ostium secundum itself.

Atrial septum – This is a broad term; the ostium secundum forms specifically within the septum primum, not the atrial septum generally.

Verapamil is a non-dihydropyridine calcium channel blocker. Its mechanism of action:

• Blocks L-type (slow) Ca²⁺ channels in cardiac myocytes, nodal tissue, and vascular smooth muscle.

• In cardiac tissue, this slows phase 2 of the action potential, reducing contractility (negative inotropy) and conduction through the AV node (negative dromotropy).

• In vascular smooth muscle, it causes vasodilation, lowering systemic vascular resistance.

• Clinically, verapamil is used for angina, hypertension, and certain arrhythmias (like supraventricular tachycardia).

❌ Why the other options are incorrect

Activates Na ion channels – Verapamil does not increase sodium influx; this is unrelated to its mechanism.

Reduces blood pressure – While verapamil lowers blood pressure, this is an effect, not its primary mechanism.

Blocks K ion channels – Verapamil does not block potassium channels; potassium blockers are drugs like amiodarone or sotalol.

Increases heart rate – Verapamil may decrease heart rate by slowing AV nodal conduction; it does not increase it.

Atherosclerosis develops due to a combination of modifiable and nonmodifiable risk factors. Risk factors accelerate endothelial damage, lipid deposition, and plaque formation in arteries.

• Cigarette smoke, hyperlipidemia, hypertension, and diabetes are well-established risk factors.

• Young age, on the other hand, is not a risk factor. The risk of atherosclerosis increases with age; younger individuals generally have lower cumulative exposure to damaging factors.

❌ Why the other options are incorrect

Cigarette smoke – Contains toxins that damage endothelium, promote inflammation, and accelerate plaque formation.

Hyperlipidemia – High LDL cholesterol leads to lipid deposition in arterial walls, a key step in atherogenesis.

Hypertension – High pressure damages endothelial lining, promoting plaque formation.

Diabetes – Hyperglycemia causes endothelial dysfunction, oxidative stress, and inflammation, all accelerating atherosclerosis.

The cardiac conducting system ensures coordinated contraction of the heart. Different parts of the system conduct impulses at different velocities:

1. Sinoatrial (SA) node – the natural pacemaker; slow conduction to allow atrial contraction before ventricular activation.

2. Atrial internodal tracts – transmit impulses from SA node to AV node; faster than SA node but not the fastest.

3. Atrioventricular (AV) node – slowest conduction; creates a delay so ventricles fill properly before contraction.

4. Bundle of His – conducts impulses from AV node to the ventricles; faster than AV node.

5. Purkinje fibres – fastest conduction in the heart. They rapidly distribute impulses throughout the ventricular myocardium to ensure synchronized ventricular contraction.

• Purkinje fibres have high density of gap junctions and specialized architecture, which explains their very high conduction velocity (~4 m/s) compared to the AV node (~0.05 m/s).

❌ Why the other options are incorrect

Atrial internodal tracts – Faster than SA node but slower than Purkinje fibres; primarily transmit impulses to AV node.

Atrioventricular node – Slowest conduction; creates physiologic delay for ventricular filling.

Sinoatrial node – Pacemaker activity is fast in terms of automaticity, but conduction velocity is slow.

Bundle of His – Faster than AV node, but slower than Purkinje fibres in transmitting impulses to ventricles.

Atherosclerosis is influenced by a combination of modifiable and nonmodifiable risk factors:

• Nonmodifiable risk factors are those that cannot be altered by medical or lifestyle interventions.

• Age is one of the classic nonmodifiable risk factors. The risk of atherosclerosis increases naturally with aging due to cumulative endothelial damage, oxidative stress, and vascular changes over time.

Identifying nonmodifiable factors helps clinicians stratify risk, but interventions focus primarily on modifiable factors.

❌ Why the other options are incorrect

Cigarette smoking

• A modifiable behavioral risk factor; quitting reduces atherosclerosis risk.

Diabetes mellitus

• Modifiable to some extent through glycemic control, diet, and medications.

Hyperlipidemia

• Modifiable through diet, lifestyle, and lipid-lowering drugs.

Hypertension

• Modifiable with medications, exercise, and dietary changes.

After a myocardial infarction (MI), secondary prevention focuses on reducing the risk of future cardiac events. Two key interventions are:

• Diet modification (low saturated fat, more fruits and vegetables)

• Regular physical activity

These interventions primarily aim to improve lipid profile, especially to lower total cholesterol and LDL cholesterol, which are major contributors to atherosclerosis.

• A decrease in cholesterol levels (particularly LDL) indicates that lifestyle changes are effectively reducing the patient’s cardiovascular risk.

• While physical activity itself increases, the goal marker of success for diet/exercise is cholesterol reduction rather than the activity itself.

❌ Why the other options are incorrect

Physical activity

• Increasing activity is part of the intervention, not a marker of success. The question asks for a biological indicator showing improvement.

Vitamins

• Diet may change vitamin intake, but vitamins are not a primary marker for cardiovascular risk reduction post-MI.

Minerals

• Similar to vitamins, minerals can change with diet but are not direct indicators of atherosclerosis risk reduction.

Proteins

• Protein intake may be affected by diet, but it does not reflect cardiovascular improvement.

Captopril is an ACE inhibitor (Angiotensin-Converting Enzyme inhibitor). Its mechanism of action:

• Blocks ACE, which normally converts angiotensin I → angiotensin II.

• By inhibiting angiotensin II formation, it reduces vasoconstriction and aldosterone-mediated sodium and water retention, leading to lower blood pressure.

• It is used in hypertension, heart failure, and post-myocardial infarction management.

❌ Why the other options are incorrect

Hydralazine

• Direct vasodilator of arterioles.

• Does not affect the renin-angiotensin system or the formation of angiotensin.

Propranolol

• Non-selective beta-blocker.

• Reduces heart rate and cardiac output, and decreases renin release indirectly, but it does not directly inhibit angiotensin formation.

Metoprolol

• Selective beta-1 blocker.

• Similar to propranolol, it reduces renin secretion indirectly, but angiotensin formation is not directly blocked.

Digitoxin

• Cardiac glycoside used for heart failure/arrhythmias.

• Works by inhibiting Na⁺/K⁺ ATPase.

• No effect on the renin-angiotensin system.

In this case:

• The patient is 18 years old, presenting with palpitations.

• He has a history of recurrent joint pain for 4 years, which raises suspicion for rheumatic heart disease (RHD) or another chronic inflammatory condition affecting the heart.

• On examination, a mild systolic murmur at the apex is present, suggesting possible mitral valve involvement.

• Vital signs show mild tachycardia but normal blood pressure.

Trans-thoracic echocardiography (TTE) is the investigation of choice because:

• It is non-invasive and safe in young patients.

• Provides detailed anatomical assessment of cardiac valves and chambers.

• Can detect valvular regurgitation or stenosis, chamber dilation, and any structural abnormalities that may explain both the murmur and palpitations.

• Particularly useful in suspected RHD given his chronic joint history (likely secondary to rheumatic fever).

❌ Why the other options are incorrect

Dobutamine stress echocardiography
Used to assess ischemia or contractile reserve in patients who cannot exercise. Not indicated in a young patient with likely structural/murmur-related pathology.

Exercise tolerance test
Primarily evaluates exercise-induced ischemia or arrhythmias. This patient’s history and murmur point more toward structural disease, not coronary artery disease.

Coronary angiography
Indicated for suspected coronary artery disease or acute coronary syndrome. Extremely unlikely in an 18-year-old with normal blood pressure and no chest pain.

Nuclear imaging
Used for myocardial perfusion or viability assessment. Not indicated here because the problem is structural, not ischemic.

In the cardiac ventricular myocyte action potential, potassium permeability is highest during Phase 3, the rapid repolarization phase.

Here’s why:

• After the plateau (Phase 2), L-type Ca²⁺ channels close, but several types of K⁺ channels open, especially the delayed rectifier potassium channels.

• This causes a large efflux of K⁺, driving the membrane potential back toward the potassium equilibrium potential (around –90 mV).

• Because many potassium channels are simultaneously active here, Phase 3 has the highest total potassium conductance in the entire action potential cycle.

❌Why the other options are incorrect

Phase 4 (Resting membrane potential)
Potassium conductance is high here because of inward-rectifier K⁺ channels, but not as high as during Phase 3, where multiple K⁺ currents are active simultaneously.

Phase 2 (Plateau phase)
Calcium influx through L-type Ca²⁺ channels balances potassium efflux.
K⁺ permeability is present, but less dominant than in Phase 3.

Phase 1 (Initial repolarization)
Some K⁺ channels (transient outward current, Ito) contribute to a brief repolarization, but this is short-lived and does not represent the maximum K⁺ permeability.

Phase 0 (Rapid depolarization)
Dominated by Na⁺ influx through fast sodium channels.
Potassium permeability is low here.

✅ Lack of obesity

Explanation:
Hypertension (high blood pressure) is influenced by multiple lifestyle and dietary factors:

• High alcohol consumption: Excessive alcohol raises blood pressure by increasing sympathetic activity and vascular resistance. ✅ Implicated

• Low potassium intake: Potassium helps excrete sodium and relax vascular smooth muscle. Low intake can increase blood pressure. ✅ Implicated

• High sodium intake: Sodium retention increases blood volume and peripheral resistance. ✅ Implicated

• Lack of exercise: Physical inactivity reduces cardiovascular efficiency and promotes weight gain, contributing to hypertension. ✅ Implicated

• Lack of obesity: Obesity is a risk factor for hypertension. If obesity is absent, it does not contribute to hypertension; in fact, normal weight is protective. ✅ This is not an etiological factor

Explanation:
Triglyceride synthesis occurs stepwise:

1. Glycerol-3-phosphate → Lysophosphatidic acid (LPA) via Glycerol-3-phosphate acyltransferase (GPAT)

2. LPA → Phosphatidic acid (PA) via Lysophosphatidic acyltransferase (LPAAT)

3. PA → Diacylglycerol (DAG) via Phosphatidic acid phosphatase

4. DAG → Triacylglycerol (TAG) via Monoacylglycerol acyltransferase (MGAT / DGAT)

The final step, adding the third fatty acid to DAG to form TAG, is catalyzed by MGAT/DGAT, making it the terminal enzyme.

Why the other options are incorrect:

❌ Glycerol-3-phosphate acyltransferase (GPAT): Catalyzes the first step, not the final one.

❌ Glycerol phosphate acyltransferase: Another name for GPAT, still not terminal.

❌ Lysophosphatidyl acyltransferase (LPAAT): Converts LPA → PA; an intermediate step, not terminal.

❌ Phosphatidyl transferase: Involved in phospholipid metabolism, not the final step of TAG synthesis.

All the carbon atoms in cholesterol synthesized originate from acetyl-CoA ✅

Every single carbon in cholesterol ultimately comes from acetyl-CoA.
The pathway begins with acetyl-CoA, builds up to HMG-CoA, proceeds through mevalonate, and eventually forms squalene and the sterol nucleus.

Acetyl-CoA is the universal 2-carbon building block of cholesterol biosynthesis.

Incorrect Options

The rate-limiting step is the formation of HMG-CoA by the enzyme HMG-CoA synthase ❌
The rate-limiting step is actually the conversion of HMG-CoA → mevalonate by HMG-CoA reductase, not its formation.
This is the step inhibited by statins.

Squalene is the first cyclic intermediate in the pathway ❌
Squalene is linear, not cyclic.
The first cyclic intermediate is lanosterol, formed after squalene undergoes cyclization.

Synthesis occurs in the cytosol of the cell ❌
Only partially true, but not the best answer.
Cholesterol synthesis occurs in both the cytosol and the smooth endoplasmic reticulum.
Because they want the most correct statement, this one is rejected.

The initial substrate is mevalonate ❌
Mevalonate is an early product, not the starting point.
The pathway starts with acetyl-CoA.

All the carbon atoms in cholesterol synthesized originate from acetyl-CoA ✅

Every single carbon in cholesterol ultimately comes from acetyl-CoA.
The pathway begins with acetyl-CoA, builds up to HMG-CoA, proceeds through mevalonate, and eventually forms squalene and the sterol nucleus.

Acetyl-CoA is the universal 2-carbon building block of cholesterol biosynthesis.

Incorrect Options

The rate-limiting step is the formation of HMG-CoA by the enzyme HMG-CoA synthase ❌
The rate-limiting step is actually the conversion of HMG-CoA → mevalonate by HMG-CoA reductase, not its formation.
This is the step inhibited by statins.

Squalene is the first cyclic intermediate in the pathway ❌
Squalene is linear, not cyclic.
The first cyclic intermediate is lanosterol, formed after squalene undergoes cyclization.

Synthesis occurs in the cytosol of the cell ❌
Only partially true, but not the best answer.
Cholesterol synthesis occurs in both the cytosol and the smooth endoplasmic reticulum.
Because they want the most correct statement, this one is rejected.

The initial substrate is mevalonate ❌
Mevalonate is an early product, not the starting point.
The pathway starts with acetyl-CoA.

Syndrome of inappropriate antidiuretic secretion (SIADH) ✅

SIADH causes excess ADH, leading the kidneys to retain free water.
Water retention dilutes serum sodium, producing euvolemic hyponatremia.

Key hallmarks of SIADH:
• Low serum sodium
• Low serum osmolality
• Inappropriately concentrated urine
• Normal body fluid volume (not dehydrated, not overloaded)

This makes SIADH the classic and most commonly tested cause of hyponatremia.

Incorrect Options

Hyperaldosteronism ❌
Aldosterone retains sodium, not water. This causes hypernatremia or normal sodium—not hyponatremia.

Diabetes insipidus ❌
Loss of ADH (or renal insensitivity to it) leads to water loss, creating hypernatremia, not hyponatremia.

Addison’s disease ❌
Primary adrenal insufficiency can cause hyponatremia, but it is less common compared with SIADH and occurs due to loss of both aldosterone and cortisol. It is not the classic answer.

Dehydration ❌
Pure water loss raises sodium (hypernatremia). Sodium loss dehydration (rare) can cause hyponatremia, but this is not the most common association.

7–10 days ✅

After an acute myocardial infarction:

• Troponin I typically stays elevated for 7–10 days.
• Troponin T may persist slightly longer (up to 10–14 days), but standard exam answers align with 7–10 days as the recognized interval.

This prolonged elevation helps diagnose MI when patients present late.

Incorrect Options

14–21 days ❌
Too long. Troponins don’t remain elevated for three weeks.

25–28 days ❌
Much too prolonged. No cardiac troponin persists for nearly a month.

3–5 days ❌
This corresponds more to CK-MB, not troponins.

1–2 days ❌
Way too short. Troponins are not early-washout markers.

When glucose supply is less ✅

Low glucose means low insulin and high glucagon.
This hormonal shift activates lipolysis, sends fatty acids to the liver, and stimulates ketogenesis.

Situations where this occurs:
• Prolonged fasting
• Uncontrolled diabetes
• Low-carbohydrate diets
• Starvation states

The liver converts acetyl-CoA (from β-oxidation of fatty acids) into ketone bodies—acetoacetate, β-hydroxybutyrate, and acetone—which act as emergency fuel for the brain, heart, and skeletal muscle.

Incorrect Options

When glucose supply is constant ❌
Stable glucose → adequate insulin → no need for ketone production.

When glucose supply is high ❌
High glucose boosts insulin, suppresses lipolysis, and shuts down ketogenesis.

When protein supply is high ❌
High protein stimulates gluconeogenesis, not ketogenesis, because amino acids can be converted into glucose.

When protein supply is less ❌
Low protein doesn’t directly trigger ketogenesis; the key driver is lack of carbohydrates, not protein.

Hydroxyl ion (representing the hydroxyl radical) ✅

Even though the option says hydroxyl ion, exam questions often use this wording loosely to point toward the hydroxyl radical (•OH).
The hydroxyl radical is the most reactive and most damaging oxygen-derived free radical in the body.

It attacks lipids, proteins, DNA—anything within molecular reach.
Nothing outruns •OH once it forms.

Incorrect Options

Hydrogen peroxide ❌
Not a free radical. It’s a reactive oxygen species but relatively mild. It requires conversion (Fenton reaction) to produce hydroxyl radicals.

Chloride ion ❌
Not a free radical at all. Completely stable and essential for normal physiology.

Superoxide ❌
A true free radical, but far less reactive than the hydroxyl radical. Often serves as a precursor to more dangerous species.

Oxygen ❌
Molecular oxygen is stable in its ground state. It can form radicals but is not itself highly reactive.

Free fatty acids and monoglycerides ✅

Pancreatic lipase hydrolyzes triglycerides at the 1 and 3 positions, releasing:

• Two free fatty acids
• One monoglyceride (2-monoacylglycerol)

These products then join bile salt micelles, stroll toward the brush border, and get absorbed. No monosaccharides, no cholesterol—just classic lipid digestion products.

Incorrect Options

Free fatty acids and monosaccharides ❌
Monosaccharides (glucose, fructose, galactose) are carbohydrate products, made by amylase and brush-border enzymes—not lipase.

Monosaccharides and monoglycerides ❌
Again, monosaccharides belong to carb digestion, not fats.

Free fatty acids and triglycerides ❌
Lipase breaks down triglycerides; it does not produce or preserve them.

Free fatty acids and cholesterol ❌
Cholesterol comes from dietary intake or liver synthesis, but pancreatic lipase has nothing to do with releasing cholesterol from substrates.

Capillary blood flow ✅

Increasing the radius of arterioles (the main resistance vessels) dramatically reduces resistance.
According to Poiseuille’s law, resistance is inversely proportional to the fourth power of radius.
Even a small dilation leads to a large drop in resistance and a big increase in flow into the capillaries.

So, wider arterioles → less resistance → more capillary flow.

Incorrect Options

Diastolic blood pressure ❌
Arteriolar dilation reduces systemic vascular resistance, lowering diastolic pressure.

Systolic blood pressure ❌
Reduced resistance decreases afterload, which generally lowers systolic pressure rather than raising it.

Viscosity of the blood ❌
Viscosity depends on hematocrit and plasma proteins, not vessel radius.

Hematocrit ❌
Hematocrit is a property of blood composition, unaffected by vessel diameter.

Drain venous blood from the myocardium ✅

The coronary sinus collects deoxygenated venous blood from most of the myocardium through the cardiac veins and delivers it into the right atrium.
It functions as the major venous drainage channel of the heart itself.
No pressure balancing, no oxygen delivery, no blood storage—just steady drainage.

Incorrect Options

Equalize left and right ventricular pressures ❌
Pressure balance is maintained through valves and ventricular mechanics, not a venous structure.

Provide oxygenated blood to the left atrium ❌
That’s the job of the pulmonary veins.
The coronary sinus carries deoxygenated blood.

Store deoxygenated blood temporarily ❌
It acts as a conduit, not a reservoir.

Control coronary artery blood flow ❌
Arterial flow is regulated by metabolic demand and arterial tone.
The venous side has no regulatory authority over arterial perfusion.

S wave in V1 and R wave in V5/V6 > 35 mm ✅

This is the classic Sokolow–Lyon criterion for LVH.
The logic is simple: a thick left ventricle produces huge depolarization forces moving toward the left side of the chest. That creates:

• Very deep S wave in V1 (because the electrical vector moves away from V1)
• Tall R wave in V5 or V6 (because the vector moves toward these lateral leads)

When the sum exceeds 35 mm, the likelihood of LVH is high.

Often accompanied by T-wave inversions in the lateral leads (called “strain pattern”), but these are secondary, not the main diagnostic criterion.

Incorrect Options

Inverted T waves in inferior leads ❌
This reflects ischemia, inferior wall injury, or sometimes pericarditis—not LVH. LVH produces T-wave inversion in lateral leads, not inferior ones.

R wave in V1 and V2 > 25 mm ❌
Tall R waves in V1–V2 suggest right ventricular hypertrophy or posterior wall MI. LVH causes deep S waves in V1, not tall R waves.

Prominent Q wave in aVF ❌
A prominent Q in aVF points toward old inferior myocardial infarction, not ventricular hypertrophy.

Prolonged PR interval ❌
This represents first-degree AV block, a conduction delay between atria and ventricles. It has nothing to do with ventricular muscle mass.

6300 mL/min ✅

Cardiac Output formula:

CO = Heart Rate × Stroke Volume

Plug in the numbers:

CO = 90 beats/min × 70 mL/beat
CO = 6300 mL/min

That’s the amount of blood the heart ejects every minute.

Incorrect Options

7500 mL/min ❌
Would require a stroke volume of 83 mL at 90 bpm. Not what we’re given.

7000 mL/min ❌
Would require a stroke volume of about 78 mL. Again, doesn’t match the data.

5500 mL/min ❌
This would imply a stroke volume of around 61 mL. Too low for the given stroke volume.

6000 mL/min ❌
This matches 66–67 mL stroke volume at 90 bpm. Doesn’t fit the numbers.

Increased vascular resistance ✅

Diastolic blood pressure is determined mainly by systemic vascular resistance (SVR).
When arterioles constrict—common in chronic hypertension—the blood faces more resistance as it flows through the vascular tree. This resistance prevents pressure from falling during diastole, so the diastolic number climbs.

It’s the classic “narrow pipes keep pressure high” situation.

Incorrect Options

Increased cardiac output ❌
This raises systolic pressure more prominently. Diastolic pressure is only modestly affected because diastole reflects downstream resistance, not upstream pumping force.

Increased venous return ❌
More venous return stretches the ventricles and increases stroke volume (Frank–Starling), again pushing up systolic pressure more than diastolic. Venous return doesn’t directly control vascular tone.

Decreased blood volume ❌
Lower blood volume reduces pressure across the board. It would lower both systolic and diastolic pressures, often causing hypotension.

Increased heart rate ❌
A very fast heart rate shortens diastole and may slightly raise diastolic pressure, but it isn’t the fundamental cause in chronic hypertension. The main culprit is increased arteriolar resistance, not rate-driven mechanics.