MD3 Block 1 Cardiovascular System Quiz 1 Flashcards

A comprehensive set of 93 flashcards covering heart development, anatomy, physiology, and pathology based on lecture notes.

What are the five regions of the primitive heart tube listed from cranial to caudal?

Truncus arteriosus → Bulbus cordis → Primitive ventricle → Primitive atrium → Sinus venosus

What structures does the truncus arteriosus become, and what divides it?

It becomes the aorta and pulmonary trunk, divided by the spiral (aorticopulmonary) septum.

What is the most common congenital heart defect and its clinical sound?

Ventricular Septal Defect (VSD); it presents as a harsh holosystolic murmur at the left lower sternal border.

List the five cyanotic congenital heart defects using the '5 T's' mnemonic.

1) Tetralogy of Fallot, 2) Transposition of Great Vessels, 3) Truncus Arteriosus, 4) Tricuspid atresia, 5) Total anomalous pulmonary venous return

Name the four defects associated with Tetralogy of Fallot (PROVe).

1) Pulmonary stenosis, 2) Right Ventricular Hypertrophy (RVH), 3) Overriding aorta, 4) VSD

What is the classic presentation of Tetralogy of Fallot on X-ray and how do infants resolve 'tet spells'?

Boot-shaped heart on X-ray; squatting relieves symptoms by increasing SVR to decrease the R→L shunt.

Why is Transposition of the Great Vessels fatal without a mixing defect?

The aorta arises from the RV and the pulmonary artery from the LV, creating two parallel circuits with no mixing of oxygenated blood.

What medications are used to keep a Patent Ductus Arteriosus (PDA) open versus closing it?

Prostaglandins (alprostadil) keep it open; indomethacin (an NSAID) closes it.

Where is Coarctation of the Aorta usually located, and what is its pathognomonic X-ray finding?

Usually at the ligamentum arteriosum (juxtaductal); rib notching on CXR due to collateral intercostal arteries.

What is Eisenmenger Syndrome?

A long-standing L→R shunt causes pulmonary HTN leading to RV pressure rise and shunt reversal to R→L, causing irreversible late-onset cyanosis.

How do ASD and VSD murmurs differ clinically?

ASD causes a fixed split $S_2$ and soft systolic murmur; VSD causes a harsh holosystolic murmur at the left lower sternal border.

What do aortic arches 1 and 2 become?

They mostly regress; Arch 1 becomes part of the maxillary artery and Arch 2 becomes the stapedial and hyoid arteries.

What is the bilateral adult derivative of aortic arch 3?

Common carotid artery and proximal internal carotid artery.

Identify the adult structures derived from aortic arch 4.

Left side: aortic arch; Right side: proximal right subclavian artery.

What are the derivatives of aortic arch 6?

Bilateral: pulmonary arteries; Left side only: ductus arteriosus (ligamentum arteriosum).

What is the clinical significance of a right-sided aortic arch on CXR?

It is seen as trachea deviation and is associated with Tetralogy of Fallot and truncus arteriosus.

List the three layers of the heart wall from outer to inner.

Epicardium (visceral pericardium) → Myocardium → Endocardium

What are the components of the serous pericardium?

The parietal layer (lining the fibrous pericardium) and the visceral layer (epicardium on the heart surface).

Define Beck's Triad for cardiac tamponade.

Hypotension, Muffled heart sounds, and Jugular Venous Distension (JVD).

What is pulsus paradoxus and when is it seen?

A drop in SBP >$10\,mmHg$ on inspiration; it is pathognomonic for cardiac tamponade.

What does electrical alternans on an ECG indicate?

Cardiac tamponade, reflecting the alternating QRS height as the heart swings in fluid.

What are the classic ECG findings for acute pericarditis?

Diffuse saddle-shaped ST elevation in all leads and PR depression.

What is Kussmaul sign and with which condition is it associated?

JVP rises on inspiration; it is associated with constrictive pericarditis.

Identify the conduction system of the heart in the correct order.

SA node → AV node → Bundle of His → Left and Right Bundle Branches → Purkinje fibers

Where are the SA and AV nodes located anatomically?

SA node: junction of SVC and right atrium (crista terminalis); AV node: floor of right atrium near coronary sinus (triangle of Koch).

What are the intrinsic firing rates of the SA node, AV node, and Purkinje fibers?

SA node: $60-100\,bpm$; AV node: $40-60\,bpm$; Purkinje fibers: $20-40\,bpm$

Which coronary artery supplies the anterior LV wall and the anterior 2/3 of the interventricular septum?

Left Anterior Descending (LAD) artery.

A blockage in the Right Coronary Artery (RCA) most likely affects which wall and which ECG leads?

Inferior wall of the LV; leads II, III, and aVF.

Which coronary artery typically supplies the SA and AV nodes?

The Right Coronary Artery (RCA) supplies the SA node in $60\%$ of people and the AV node in $85\%$.

How is coronary dominance determined?

By which artery (RCA or LCx) gives rise to the posterior descending artery (PDA).

Where does the coronary sinus drain its venous blood?

Into the right atrium.

What are the effects of sympathetic versus parasympathetic stimulation on the heart?

Sympathetic increases HR, contractility, and conduction; Parasympathetic (Vagus) decreases HR and AV conduction velocity.

What mnemonic is used for superior mediastinum contents?

'BIG TEN' (Brachiocephalics, aortic arch, InnominaTe veins, Great vessels, Thymus, Esophagus, Nerves).

What is found in the posterior mediastinum?

Esophagus, descending aorta, thoracic duct, azygos/hemiazygos veins, and sympathetic trunk.

Describe the presentation and risk factors of aortic dissection.

Sudden severe tearing/ripping chest pain radiating to the back; risk factors include hypertension (#1), Marfan syndrome, and bicuspid aortic valve.

Contrast Stanford Type A and Type B aortic dissections.

Type A involves the ascending aorta and is a surgical emergency; Type B involves the descending aorta only and is managed with IV beta-blockers.

Which infection is associated with thoracic aortic aneurysms characterized by 'tree bark' calcification?

Syphilis (obliterative endarteritis of vasa vasorum).

Distinguish cardiac muscle from skeletal muscle histologically.

Cardiac: 1 central nucleus, branched, intercalated discs, involuntary; Skeletal: multiple peripheral nuclei, unbranched, voluntary.

What are the two components of intercalated discs?

1) Gap junctions (electrical coupling) and 2) Desmosomes/fascia adherens (mechanical coupling).

Describe the histological appearance and function of Purkinje fibers.

Large, pale-staining cells with abundant glycogen and few myofibrils; they function in rapid impulse conduction, not contraction.

What is the 'Windkessel effect' in elastic arteries?

The expansion during systole and recoil during diastole to maintain continuous blood flow.

Identify the characteristic features of muscular artery histology.

Thick tunica media with up to 40 layers of smooth muscle and a prominent internal elastic lamina.

What are the three tunics of blood vessels and which is thickest in veins?

Tunica intima, tunica media, and tunica adventitia; adventitia is thickest in veins.

Compare the three types of capillaries.

1) Continuous: tight junctions (least permeable); 2) Fenestrated: pores (kidney/intestine); 3) Sinusoidal: large gaps (most permeable).

What ion is responsible for Phase 0 (rapid depolarization) of the ventricular action potential?

Rapid influx of $Na^+$ via voltage-gated channels.

Explain Phase 2 (plateau) of the ventricular action potential.

$Ca^{2+}$ influx through L-type channels balanced by $K^+$ efflux; unique to cardiac muscle for excitation-contraction coupling.

Why is the long refractory period created by the plateau phase essential?

It prevents tetanic contractions, which would be fatal for heart function.

How does the SA node action potential differ from the ventricular action potential?

It has no fast $Na^+$ channels, depolarizes via slow $Ca^{2+}$ influx, and features a Phase 4 spontaneous 'funny' current ($I_f$).

Distinguish between Absolute Refractory Period (ARP) and Relative Refractory Period (RRP).

ARP: cell cannot be stimulated (Phases 0-early 3); RRP: cell can be stimulated by a suprathreshold stimulus (late Phase 3).

What is the Frank-Starling Law?

Increased preload (stretch) leads to a greater force of contraction and increased stroke volume due to optimal actin-myosin overlap.

What factors increase versus decrease preload?

Increase: fluid overload, exercise; Decrease: diuretics, venodilators like nitroglycerin.

Define afterload and contractility.

Afterload: resistance the ventricle pumps against (SVR); Contractility: intrinsic force of contraction independent of load.

Provide the formulas for Cardiac Output and Cardiac Index.

$CO = HR \times SV$; $Cardiac Index = CO / BSA$

Describe isovolumetric contraction in the cardiac cycle.

All valves are closed, and LV pressure rises with no change in volume.

When does the mitral valve close, and what heart sound does it produce?

It closes when LV pressure exceeds LA pressure, producing the $S_1$ heart sound.

When does the aortic valve close, and what heart sound does it produce?

It closes when aortic pressure exceeds LV pressure, producing the $S_2$ heart sound.

Define Stroke Volume (SV) and Ejection Fraction (EF).

$SV = EDV - ESV$; $EF = (SV / EDV) \times 100$ ($55-65\%$ is normal).

How does increased afterload affect the Pressure-Volume (PV) loop?

The loop shifts up and to the left, resulting in a smaller SV and larger ESV.

What is physiologic splitting of $S_2$?

A normal finding where $A_2$ occurs before $P_2$, and the split widens on inspiration due to increased RV filling.

What causes wide splitting versus paradoxical splitting of $S_2$?

Wide: delayed $P_2$ (RBBB/pulmonary stenosis); Paradoxical: delayed $A_2$ (LBBB/aortic stenosis), split narrows on inspiration.

What does an $S_3$ gallop ('Kentucky') indicate in an adult?

Volume overload, such as in heart failure or mitral regurgitation.

When is an $S_4$ gallop ('Tennessee') heard, and what does it suggest?

Late diastole; suggests a stiff ventricle as seen in LVH, hypertension, or aortic stenosis.

Describe the murmur associated with Aortic Stenosis.

Harsh crescendo-decrescendo systolic murmur at the right upper sternal border radiating to the carotids.

Identify the 'SAD' triad of symptoms in Aortic Stenosis.

Syncope, Angina, and Dyspnea on exertion.

What are the classic physical signs of Aortic Regurgitation?

Wide pulse pressure, bounding 'water hammer' pulse (Corrigan's), and head bobbing (de Musset sign).

Describe the Mitral Regurgitation murmur.

High-pitched, blowing, holosystolic murmur at the apex radiating to the left axilla.

What is the most common cause of Mitral Stenosis and its associated heart sound?

Almost always rheumatic fever; associated with an opening snap (OS) followed by a diastolic rumble.

How does the Mid-systolic click of Mitral Valve Prolapse (MVP) respond to Valsalva?

The click moves earlier in systole because decreased preload increases prolapse.

What is Carvallo sign?

The increase in intensity of tricuspid regurgitation murmurs with inspiration.

How does the Hypertrophic Obstructive Cardiomyopathy (HOCM) murmur respond differently to preload changes compared to AS?

HOCM murmur increases with decreased preload (Valsalva/standing), which is the opposite of Aortic Stenosis.

State the relationship between MAP, CO, and SVR.

$$MAP = CO \times SVR$$

Provide the formula for calculating Mean Arterial Pressure (MAP) using DBP and SBP.

$$MAP = DBP + 1/3(SBP - DBP)$$

According to Poiseuille's Law, what is the dominant determinant of resistance?

Radius ($r$); Resistance is proportional to $1/r^4$.

Name three substances that raise SVR and one that lowers it.

Raise: Norepinephrine, Angiotensin II, Vasopressin; Lower: Nitric Oxide.

Define the pressure thresholds for Systemic and Pulmonary Hypertension.

Systemic: Stage 2 is $\ge 140/90\,mmHg$; Pulmonary: Mean PA pressure >$25\,mmHg$ at rest.

What distinguishes hypertensive urgency from emergency?

Both involve BP >$180/120$, but hypertensive emergency involves acute end-organ damage.

Describe the short-term baroreceptor reflex response to a fall in BP.

Decreased firing of baroreceptors → increased sympathetic tone → increased HR, SVR, and contractility.

Explain the first step of the RAAS cascade.

Kidney juxtaglomerular cells release renin in response to low BP, which cleaves angiotensinogen into Angiotensin I.

What is the effect of Angiotensin II on the adrenal cortex and blood vessels?

It causes vasoconstriction ($\uparrow SVR$) and stimulates aldosterone release ($\uparrow Na^+$/water retention).

What are the '5 Ps' of Pheochromocytoma?

Pressure (HTN), Pain (headache), Perspiration (sweating), Palpitations, and Pallor.

List the stages of atherosclerosis pathogenesis in order.

Endothelial injury → LDL oxidation → Monocyte migration/Macrophage foam cell formation → Fatty streak → Fibrous plaque → Complicated plaque.

What are foam cells?

Macrophages that have engulfed oxidized LDL within the arterial intima.

Distinguish between Stable Angina and Unstable Angina.

Stable: predictable pain with exertion, fixed plaque, normal troponin; Unstable: pain at rest or worsening, plaque rupture, normal troponin.

What defines an NSTEMI versus a STEMI?

NSTEMI: subendocardial ischemia, elevated troponin, ST depression/T-wave changes; STEMI: transmural infarct, elevated troponin, ST elevation.

Provide the timeline for Troponin I/T elevation.

Rises in $3-6h$, peaks at $24h$, and remains elevated for $7-10$ days.

Why is CK-MB clinincally useful despite being less specific than troponin?

It normalizes in $48-72h$, making it useful for detecting reinfarction.

What is the most vulnerable period for myocardial rupture post-MI?

3 to 14 days, during the macrophage/granulation tissue phase.

Define Dressler syndrome.

Post-MI autoimmune pericarditis occurring 2 to 10 weeks after infarction.

What does the P wave represent on an ECG?

Atrial depolarization.

State the normal ranges for the PR interval and QRS duration.

PR interval: $0.12-0.20\,sec$; QRS duration: <$0.12\,sec$.-

How do you calculate heart rate from a regular ECG rhythm?

$300$ divided by the number of large squares between R waves.

Which ECG leads represent the lateral LV wall?

Leads V5, V6, I, and aVL.

What constitutes a pathologic Q wave and what dose it signify?

A Q wave >$1$ small square wide or >$25\%$ of the R wave height; it signifies an old/completed MI.

What ECG findings characterize pericarditis?

Diffuse saddle-shaped ST elevation and PR depression.