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Anatomy and Physiology: Cardiovascular System (University)

40 cards · 13 topics · by Quizcard team · 0 hearts · Updated 2026-11-03

Heart LayersHeart ChambersHeart ValvesBlood Flow Through the Heart & LungsCoronary CirculationConduction System & ECGCardiac Cycle & Heart SoundsCardiac Output & Stroke VolumePreload, Afterload & ContractilityBlood Pressure RegulationVessel StructureCapillary ExchangeMajor Arteries & Veins
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Heart Layers

What are the three layers of the heart wall, and what are the two layers of the pericardium?

Answer: Wall (outside→inside): epicardium, myocardium, endocardium. Pericardium: fibrous pericardium (outer sac) + serous pericardium, which has a parietal layer and a visceral layer (= epicardium), separated by pericardial fluid.

Explanation

Epicardium = visceral serous layer; myocardium = cardiac muscle doing the pumping; endocardium = endothelial lining continuous with vessel lining. Pericardial fluid reduces friction as the heart beats.

Heart Chambers

Name the four chambers of the heart.

Answer: Right atrium, right ventricle, left atrium, left ventricle.

Explanation

Atria receive blood and act as priming pumps; ventricles are the main pumping chambers.

Which heart chamber has the thickest wall, and why?

Answer: The left ventricle, because it must generate high pressure to pump blood through the entire systemic circulation.

Explanation

The right ventricle is thinner-walled since it only needs to pump blood through the low-resistance pulmonary circuit.

What structures separate the atria from each other and the ventricles from each other?

Answer: Interatrial septum (contains the fossa ovalis, a remnant of the fetal foramen ovale) separates the atria; interventricular septum separates the ventricles.

Heart Valves

Name the two atrioventricular (AV) valves and their locations.

Answer: Tricuspid valve (right AV, between right atrium and right ventricle) and mitral/bicuspid valve (left AV, between left atrium and left ventricle).

Name the two semilunar valves and their locations.

Answer: Pulmonary valve (right ventricle → pulmonary trunk) and aortic valve (left ventricle → aorta).

What prevents the AV valve leaflets from prolapsing (ballooning) into the atria during ventricular systole?

Answer: Chordae tendineae, which anchor the valve leaflets to papillary muscles in the ventricular walls.

Explanation

Papillary muscles contract with the ventricles, pulling taut on the chordae to keep valve cusps closed.

When are the AV valves open versus the semilunar valves, and can both sets be open at once?

Answer: AV valves open during ventricular diastole (filling); semilunar valves open during ventricular systole (ejection). They are never both open at the same time normally.

Explanation

This alternating pattern ensures unidirectional blood flow through the heart.

Blood Flow Through the Heart & Lungs

Trace the path of deoxygenated blood from the body into the lungs.

Answer: Superior/inferior vena cava → right atrium → tricuspid valve → right ventricle → pulmonary valve → pulmonary trunk → pulmonary arteries → lungs.

Trace the path of oxygenated blood from the lungs into systemic circulation, and explain why pulmonary vessels seem to break the 'arteries carry oxygenated blood' rule.

Answer: Pulmonary veins → left atrium → mitral valve → left ventricle → aortic valve → aorta → systemic circulation. Pulmonary arteries carry deoxygenated blood and pulmonary veins carry oxygenated blood.

Explanation

Vessel naming (artery/vein) is based on direction relative to the heart (away from/toward), not oxygen content — the pulmonary circuit is the exception to the usual pattern.

Coronary Circulation

What are the two main coronary arteries, when do they fill, and where does cardiac venous blood drain?

Answer: Left coronary artery (branches into LAD and circumflex) and right coronary artery; both fill mainly during diastole. Venous blood drains via cardiac veins into the coronary sinus, which empties into the right atrium.

Explanation

During systole, aortic valve cusps cover the coronary ostia and myocardial contraction compresses the vessels, impeding coronary flow — so the heart perfuses itself mainly when relaxed.

What does the left anterior descending (LAD) artery supply?

Answer: The anterior wall of the left ventricle and the anterior two-thirds of the interventricular septum.

Explanation

Occlusion of the LAD ('the widow-maker') causes a large anterior MI.

What does the right coronary artery (RCA) typically supply?

Answer: Right atrium, right ventricle, and in most people the SA node, AV node, and the inferior wall of the left ventricle.

Explanation

This is why inferior MIs (RCA occlusion) commonly cause bradyarrhythmias/heart block.

Conduction System & ECG

List the normal conduction pathway of an electrical impulse through the heart.

Answer: SA node → atria (internodal pathways) → AV node → bundle of His → right and left bundle branches → Purkinje fibers.

Why is the SA node the heart's natural 'pacemaker'?

Answer: It has the fastest intrinsic rate of spontaneous depolarization (~60–100 bpm), so it sets the heart rate before other tissues can.

Explanation

If the SA node fails, the AV node (≈40–60 bpm) or Purkinje fibers (≈20–40 bpm) can take over at a slower rate.

Why does the AV node delay the electrical impulse?

Answer: To allow atrial contraction to finish and the ventricles to fill completely before ventricular contraction begins.

Explanation

This delay corresponds to the PR interval on the ECG.

Identify the waves of a normal ECG and what each represents.

Answer: P wave = atrial depolarization; QRS complex = ventricular depolarization (atrial repolarization is hidden within it); T wave = ventricular repolarization.

Explanation

The PR interval (start of P to start of QRS, normally 0.12–0.20 s) reflects AV nodal conduction delay; the QT interval reflects total ventricular depolarization + repolarization time.

Cardiac Cycle & Heart Sounds

What are the main phases of the cardiac cycle?

Answer: Atrial systole → isovolumetric ventricular contraction → ventricular ejection → isovolumetric relaxation → ventricular filling (rapid filling, then slow filling/diastasis).

Explanation

Isovolumetric phases occur with all valves closed, so ventricular volume doesn't change even though pressure does.

What causes heart sound S1 ('lub')?

Answer: Closure of the AV valves (mitral and tricuspid) at the start of ventricular systole.

What causes heart sound S2 ('dub')?

Answer: Closure of the semilunar valves (aortic and pulmonic) at the start of ventricular diastole.

What are S3 and S4 heart sounds and what do they indicate?

Answer: S3: sound of rapid ventricular filling; can be normal in children/young athletes but suggests heart failure/volume overload in older adults. S4: sound of atrial contraction against a stiff, non-compliant ventricle; often indicates ventricular hypertrophy.

Cardiac Output & Stroke Volume

What is the formula for cardiac output?

Answer: CO = HR × SV

Explanation

CO = cardiac output (L/min); HR = heart rate (beats/min); SV = stroke volume (mL/beat). Example: HR 70 bpm × SV 70 mL/beat = 4900 mL/min ≈ 4.9 L/min.

What is the formula for stroke volume?

Answer: SV = EDV − ESV

Explanation

EDV = end-diastolic volume (volume just before contraction); ESV = end-systolic volume (volume remaining after contraction). Example: EDV 120 mL − ESV 50 mL = SV 70 mL.

What is the formula for ejection fraction and its normal range?

Answer: EF = (SV / EDV) × 100%; normal ≈ 55–70%.

Explanation

Example: SV 70 mL / EDV 120 mL = 58%. EF is a key clinical measure of systolic (pump) function.

Preload, Afterload & Contractility

Define preload.

Answer: The degree of stretch on ventricular muscle fibers at the end of diastole, determined mainly by venous return (reflected as end-diastolic volume).

Explanation

Increased venous return (e.g., from increased blood volume or venoconstriction) increases preload.

Define afterload and state how increased afterload affects stroke volume.

Answer: Afterload is the resistance/pressure the ventricle must overcome to eject blood (determined largely by systemic vascular resistance and arterial pressure). Increased afterload decreases stroke volume, all else equal.

Explanation

E.g., hypertension (high SVR) increases LV afterload, making ejection harder and reducing SV unless contractility compensates.

Define contractility (inotropy) and give examples of what changes it.

Answer: Contractility is the intrinsic strength of ventricular contraction at a given preload and afterload. Positive inotropes (sympathetic stimulation, catecholamines, increased intracellular Ca2+) increase it; negative inotropes (beta-blockers, hypoxia, acidosis) decrease it.

State the Frank-Starling law of the heart.

Answer: Within physiological limits, increased venous return/preload (greater stretch of myocardial fibers) leads to a greater force of contraction and increased stroke volume.

Explanation

A failing heart shows a flatter, downward-shifted Frank-Starling curve — it produces less stroke volume for the same preload due to reduced contractility.

Blood Pressure Regulation

What is the formula for mean arterial pressure (MAP)?

Answer: MAP = DBP + 1/3(SBP − DBP), approximately equal to CO × SVR.

Explanation

DBP = diastolic BP, SBP = systolic BP, CO = cardiac output, SVR = systemic vascular resistance. Example: BP 120/80 mmHg → MAP = 80 + 1/3(120−80) = 93 mmHg.

How does the baroreceptor reflex regulate blood pressure?

Answer: Baroreceptors in the carotid sinus and aortic arch sense arterial stretch. A rise in BP increases their firing, which increases parasympathetic (vagal) and decreases sympathetic output, lowering heart rate, contractility, and causing vasodilation to reduce BP; a drop in BP does the opposite.

Explanation

This is a fast, short-term negative feedback mechanism for beat-to-beat BP control.

Outline the Renin-Angiotensin-Aldosterone System (RAAS) pathway.

Answer: Low BP/renal perfusion → kidneys release renin → renin converts angiotensinogen to angiotensin I → ACE (lungs) converts angiotensin I to angiotensin II → angiotensin II causes vasoconstriction and stimulates aldosterone release from the adrenal cortex → aldosterone increases Na+ and water reabsorption in the kidneys → increased blood volume and BP.

Explanation

Angiotensin II also directly raises BP via potent arteriolar vasoconstriction and stimulates thirst and ADH release.

What is the role of ADH (vasopressin) in blood pressure regulation?

Answer: Released from the posterior pituitary in response to low blood volume/pressure or high plasma osmolality; it promotes water reabsorption in the renal collecting ducts and, at high levels, causes vasoconstriction — raising blood volume and BP.

Vessel Structure

What are the three layers (tunics) of a blood vessel wall?

Answer: Tunica intima (innermost; endothelium), tunica media (smooth muscle and elastic fibers), tunica externa/adventitia (outer connective tissue).

How do arteries and veins differ structurally, and why do veins have valves?

Answer: Arteries have a thicker, more muscular/elastic tunica media to withstand high pulsatile pressure. Veins have thinner walls, larger lumens, and contain one-way valves to prevent backflow and assist venous return against gravity/low pressure (aided by the skeletal muscle pump).

What makes capillary walls structurally suited for exchange?

Answer: Capillaries consist of a single layer of endothelial cells with no tunica media or externa, allowing efficient diffusion of gases, nutrients, and wastes.

Capillary Exchange

What are the main mechanisms of capillary exchange?

Answer: Diffusion (main route for gases and small solutes, down concentration gradients), filtration (fluid pushed out by hydrostatic pressure), reabsorption (fluid pulled in by oncotic/osmotic pressure), and vesicular transport (transcytosis of larger molecules).

What determines net fluid movement across a capillary (Starling forces)?

Answer: Net filtration = (capillary hydrostatic pressure − interstitial hydrostatic pressure) − (capillary oncotic pressure − interstitial oncotic pressure).

Explanation

At the arterial end, hydrostatic pressure dominates, favoring filtration out of the capillary; at the venous end, oncotic pressure dominates, favoring reabsorption back in. Imbalance (e.g., low plasma protein) causes edema.

Major Arteries & Veins

What are the major branches off the aorta, in order from the heart?

Answer: Ascending aorta (gives rise to the coronary arteries) → aortic arch (brachiocephalic trunk, left common carotid artery, left subclavian artery) → descending aorta (thoracic then abdominal branches, ending by splitting into the common iliac arteries).

What do the superior and inferior venae cavae drain, and where do they empty?

Answer: Superior vena cava drains the head, neck, upper limbs, and thorax; inferior vena cava drains the lower limbs and abdomen. Both empty into the right atrium.

What is the hepatic portal system?

Answer: Venous blood from the GI tract and spleen drains via the hepatic portal vein into the liver before returning to systemic circulation through the hepatic veins into the IVC.

Explanation

This 'portal' detour lets the liver process absorbed nutrients and toxins before they reach the rest of the body.

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