❤️ A&P II · Cardiovascular System

Memory tricks for the heart, blood vessels, and circulation

Heart anatomy, the conduction system, cardiac cycle, blood pressure, Frank-Starling law, blood vessel types, and circulation pathways — these memory tricks unite the anatomy of the cardiovascular system with the physiology of how it pumps and regulates blood flow.

❤️ Cardiovascular System

Memory Tricks

Proven Mnemonics & Acronyms — fast to learn, hard to forget.

Heart Anatomy
Blood flows: RA → RV → Lungs → LA → LV → Body
Right side = pulmonary circuit · Left side = systemic circuit
Blood flow through the heart — the two circuits in one pump
The heart has four chambers in two functional pumps. Right side (pulmonary circuit): deoxygenated blood enters right atrium (RA) from superior and inferior vena cava → tricuspid valve → right ventricle (RV) → pulmonary semilunar valve → pulmonary arteries → lungs (gas exchange). Left side (systemic circuit): oxygenated blood returns from lungs via pulmonary veins → left atrium (LA) → mitral/bicuspid valve → left ventricle (LV) → aortic semilunar valve → aorta → body. Left ventricle has thicker wall (pumps against higher systemic resistance). Both sides contract simultaneously. Pericardium: double-walled sac surrounding heart — fibrous outer layer + serous inner (parietal and visceral/epicardium).
Tricuspid
Right AV valve — 3 cusps. Between RA and RV. "Try" to remember right = tri.
Bicuspid/Mitral
Left AV valve — 2 cusps. Between LA and LV. Most commonly diseased valve.
Semilunar valves
Pulmonary (RV → pulmonary artery) and Aortic (LV → aorta). Half-moon shaped.
Left ventricle
Thicker wall — pumps against systemic resistance (~120 mmHg vs ~25 mmHg in RV).
Conduction System
SA → AV → Bundle of His → Bundle branches → Purkinje fibers
Sinoatrial node → AV node → His → left/right bundles → Purkinje
The cardiac conduction system — the heart's own electrical wiring
SA node (sinoatrial node): right atrium near SVC — the pacemaker. Fires at 60-100 bpm. Sets heart rate. Signal spreads across both atria → atria contract. AV node (atrioventricular node): at junction of atria and ventricles — intentional delay (0.1 sec) allows atria to finish emptying into ventricles before ventricles contract. Only electrical pathway between atria and ventricles. Bundle of His (AV bundle): through interventricular septum. Bundle branches: left and right — travel down each side of septum. Purkinje fibers: spread through ventricular walls from apex upward — rapid conduction causes ventricles to contract from bottom up, ejecting blood upward into great vessels. ECG: P wave (atrial depolarization) → QRS complex (ventricular depolarization) → T wave (ventricular repolarization).
SA node
Pacemaker — 60-100 bpm. Right atrium. Vagus nerve slows it (parasympathetic).
AV node delay
0.1 sec pause — lets atria empty before ventricles fire. Only electrical bridge between chambers.
P wave
Atrial depolarization. SA node fires → spreads across atria → atria contract.
QRS complex
Ventricular depolarization (and atrial repolarization hidden within). Ventricles contract.
Cardiac Cycle
Diastole = filling · Systole = pumping · Lub = valves closing · Dub = semilunar closing
Ventricular filling → isovolumetric contraction → ejection → isovolumetric relaxation
The cardiac cycle — four phases and the heart sounds explained
Diastole (relaxation and filling): AV valves open → blood flows passively from atria into ventricles. Atrial systole (atrial kick) completes filling — adds last 20-30%. Isovolumetric contraction: ventricles contract, pressure rises → AV valves close (Lub = S1) → both sets of valves closed briefly. Ventricular ejection: pressure exceeds arterial pressure → semilunar valves open → blood ejected. Stroke volume (~70 mL). Isovolumetric relaxation: ventricles relax → semilunar valves close (Dub = S2) → pressure drops until below atrial pressure → AV valves open again. Heart sounds: S1 (Lub) = AV valve closure. S2 (Dub) = semilunar valve closure. S3 = ventricular gallop (heart failure). S4 = atrial kick into stiff ventricle.
S1 (Lub)
AV valve closure — mitral + tricuspid. Start of systole. Heard at apex.
S2 (Dub)
Semilunar valve closure — aortic + pulmonary. End of systole. Split on inspiration (normal).
Stroke volume
~70 mL per beat at rest. EDV (~120) − ESV (~50) = SV (~70 mL).
Cardiac output
CO = HR × SV. Normal ~5 L/min. Can increase to 20-25 L/min during exercise.
Frank-Starling Law
More stretch = more force — the heart pumps what it receives
Increased venous return → increased EDV → increased stretch → stronger contraction → increased SV
Frank-Starling law — why the heart automatically matches output to input
The Frank-Starling law states that the more the ventricle is stretched during filling (↑ preload = ↑ EDV), the more forcefully it contracts — up to a physiological limit. Mechanism: more stretch → more optimal actin-myosin overlap (length-tension relationship) → more cross-bridges formed → stronger contraction → higher stroke volume. This ensures the heart pumps exactly what it receives — left output = right output, preventing blood from pooling in either circuit. Preload: the degree of stretch before contraction — determined by venous return and EDV. Afterload: the resistance the ventricle must overcome to eject blood (systemic vascular resistance). ↑ afterload → ↓ SV. Contractility: intrinsic strength of contraction — increased by sympathetic stimulation, Ca2+, positive inotropes (digoxin).
Preload
EDV — stretch before contraction. ↑ venous return → ↑ preload → ↑ SV.
Afterload
Resistance against ejection — systemic BP. ↑ afterload → harder to eject → ↓ SV.
Contractility
Intrinsic force. ↑ by sympathetic (NE), Ca2+, digoxin. ↓ by acidosis, hypoxia.
Clinical
Heart failure = heart on descending limb of Starling curve — more stretch = less force.
Blood Pressure
BP = CO × SVR — Cardiac Output × Systemic Vascular Resistance
Normal 120/80 · Systolic = contraction · Diastolic = relaxation
Blood pressure regulation — what raises and lowers it
Blood pressure = Cardiac Output × Systemic Vascular Resistance. CO = HR × SV. SVR = determined by arteriole diameter (vasoconstriction raises BP, vasodilation lowers). Normal: 120/80 mmHg. Systolic (120): pressure during ventricular contraction. Diastolic (80): pressure during ventricular relaxation. Pulse pressure = systolic − diastolic = 40 mmHg. Mean arterial pressure (MAP) = diastolic + 1/3 pulse pressure ≈ 93 mmHg. Hypertension (>130/80): ↑ CO, ↑ SVR, or both. Long-term: baroreceptor reflex (carotid sinus and aortic arch detect stretch → adjust HR and SVR). RAAS (renin-angiotensin-aldosterone system): low BP → renin → angiotensin II → vasoconstriction + aldosterone → Na+ retention → ↑ blood volume → ↑ BP.
BP = CO × SVR
Raise HR or SV → ↑ CO → ↑ BP. Vasoconstrict arterioles → ↑ SVR → ↑ BP.
Baroreceptors
Carotid sinus and aortic arch. ↑ BP → stretch → vagus → ↓ HR. Fast reflex.
RAAS
Kidney → renin → angiotensin I → ACE → angiotensin II → vasoconstriction + aldosterone.
MAP
Mean arterial pressure = DBP + 1/3(PP). Must be >60 mmHg to perfuse vital organs.
Blood Vessel Types
AACCVV — Arteries · Arterioles · Capillaries · Capillaries · Venules · Veins
High pressure delivery → resistance vessels → exchange → collection → return
Five blood vessel types — structure matches function at every level
Arteries: thick walls, elastic (large) or muscular (medium) — carry blood AWAY from heart under high pressure. Aorta is most elastic — stretches during systole, recoils during diastole (Windkessel effect). Arterioles: small arteries with abundant smooth muscle — primary resistance vessels, regulate blood flow to capillary beds. Vasodilation/constriction controlled by sympathetic tone, local metabolites, hormones. Capillaries: single layer of endothelium + basement membrane — site of ALL exchange (O2, CO2, nutrients, waste). Continuous, fenestrated, sinusoidal types. Venules: collect blood from capillaries. Veins: thin walls, large lumen, valves — carry blood TOWARD heart under low pressure. Veins hold ~64% of blood volume — capacitance vessels. Skeletal muscle pump and respiratory pump aid venous return.
Arterioles
Resistance vessels — control distribution of blood. Greatest pressure drop here.
Capillaries
Exchange vessels — only 1 cell thick. O2/CO2, glucose/waste, fluid exchange.
Veins
Capacitance vessels — hold 64% of blood. Valves prevent backflow. Thin walls.
Venous return
Skeletal muscle pump, respiratory pump, venous valves, sympathetic venoconstriction.
Capillary Exchange
Starling Forces — Hydrostatic pushes out · Oncotic pulls in
Net filtration = capillary HP − interstitial HP − plasma oncotic + interstitial oncotic
How fluid moves between capillaries and tissues — Starling forces
Fluid movement across capillary walls is determined by four Starling forces. Capillary hydrostatic pressure (CHP): blood pressure inside capillary pushes fluid OUT into interstitium — higher at arterial end (~35 mmHg), lower at venous end (~15 mmHg). Plasma oncotic pressure (COP): proteins (albumin) in blood pull fluid IN — ~25 mmHg throughout. Net result: arterial end — filtration (fluid leaves capillary). Venous end — reabsorption (fluid returns). Excess filtered fluid drained by lymphatics. Edema: occurs when filtration > reabsorption + lymphatic drainage. Causes: ↑ CHP (heart failure), ↓ COP (low albumin — liver disease, malnutrition), blocked lymphatics, increased capillary permeability (inflammation).
Hydrostatic pressure
Blood pressure pushes OUT. Higher at arterial end → filtration dominates.
Oncotic pressure
Protein (albumin) osmotic pull pulls IN. ~25 mmHg. Constant throughout capillary.
Edema
↑ HP (CHF), ↓ COP (cirrhosis, malnutrition), blocked lymph (filariasis), inflammation.
Lymphatics
Return ~3 L/day excess filtrate to blood. Right lymphatic duct + thoracic duct.
Coronary Circulation
LCA → LAD + Circumflex · RCA → SA node + RV · Fill during diastole
Left coronary artery · Right coronary artery — heart's own blood supply
Coronary arteries — which artery supplies which part of the heart
The heart receives its own blood supply from two coronary arteries that branch off the aorta just above the aortic valve. Left coronary artery (LCA): divides into Left Anterior Descending (LAD) — supplies anterior LV, interventricular septum, "widow maker" — most critical and Circumflex — supplies lateral and posterior LV. Right coronary artery (RCA): supplies RA, RV, SA node, AV node (in 85% of people — "right dominant"). Coronary arteries fill during diastole (heart relaxed) — that is when myocardium is not compressed. During systole, myocardial contraction squeezes vessels closed. MI (myocardial infarction): blocked coronary artery → ischemia → cell death. LAD occlusion most deadly.
LAD
Left anterior descending — anterior LV and septum. "Widow maker" — most critical.
Circumflex
Lateral and posterior LV. Runs in left atrioventricular groove.
RCA
RA, RV, SA node, AV node. Right dominant in 85%. Inferior MI from RCA occlusion.
Diastolic filling
Coronaries fill during diastole — tachycardia shortens diastole → reduces coronary perfusion.
Special Circulations
Portal = gut → liver · Pulmonary = right → lungs → left · Fetal = placenta bypasses lungs
Three specialized circulatory pathways with unique anatomy and physiology
Three special circulations — portal, pulmonary, and fetal
Hepatic portal circulation: blood from GI tract (stomach, intestines, spleen, pancreas) drains into portal vein → liver (first pass metabolism — detoxifies absorbed substances, processes nutrients). Then drains into hepatic veins → IVC. Portal hypertension: liver disease → increased resistance → varices (dilated collateral veins in esophagus and rectum). Pulmonary circulation: only arterial blood that is deoxygenated (right side) — pulmonary arteries carry deoxgenated blood to lungs. Unique: hypoxic vasoconstriction (low O2 → constrict → redirect blood to better-ventilated areas). Fetal circulation: fetus bypasses lungs — foramen ovale (RA→LA) and ductus arteriosus (pulmonary artery→aorta). Close at birth when lungs inflate.
Portal vein
GI → liver → hepatic veins → IVC. First-pass metabolism. Liver gets nutrient-rich blood first.
Portal hypertension
Cirrhosis → ↑ resistance → esophageal varices, ascites, splenomegaly.
Foramen ovale
Fetal RA→LA shunt. Closes at birth (pressure reversal). Patent = PFO in adults.
Ductus arteriosus
Pulmonary artery → aorta in fetus. Closes with O2 exposure. Patent = PDA (closes with indomethacin).
🎓 Common Exam Questions
Q: Describe the cardiac cycle including all pressure and volume changes.
A: Ventricular filling (late diastole): AV valves open, semilunar valves closed, ventricles fill passively then via atrial kick. EDV ~130 mL. Isovolumetric contraction: all valves closed, ventricular pressure rises rapidly. Ventricular ejection: semilunar valves open when ventricular pressure exceeds aortic (80 mmHg left, 25 mmHg right). SV = EDV - ESV = ~70 mL. Isovolumetric relaxation: all valves closed, pressure falls rapidly. Diastole: AV valves reopen when ventricular pressure < atrial pressure. S1 = AV valves closing (onset systole). S2 = semilunar valves closing (onset diastole). S3 (ventricular gallop) = early diastole, volume overload/HF. S4 (atrial gallop) = late diastole, stiff ventricle.
Q: What is the Frank-Starling Law and what is preload vs afterload?
A: Frank-Starling Law: the greater the end-diastolic volume (stretch), the greater the force of contraction and stroke volume — up to a point. The heart pumps what it receives. Preload: ventricular filling pressure = EDV. Increased by: increased venous return, fluid overload, bradycardia. Decreased by: hemorrhage, diuretics, venodilators (nitroglycerin). Afterload: resistance against which ventricle pumps = systemic vascular resistance (left) / pulmonary vascular resistance (right). Increased by: hypertension, aortic stenosis, vasoconstriction. Contractility (inotropy): independent of preload/afterload. Increased by: catecholamines, digoxin, Ca2+. Decreased by: beta-blockers, heart failure, acidosis.
Q: Explain the cardiac conduction system and what happens when each part fails.
A: SA node (pacemaker, 60-100 bpm) → AV node (delay 0.1 sec, allows ventricular filling, 40-60 bpm) → Bundle of His → Left and Right bundle branches → Purkinje fibers (20-40 bpm). If SA fails: AV node takes over at 40-60 bpm. If AV node fails: ventricular escape rhythm at 20-40 bpm. AV blocks: 1st degree (prolonged PR >200ms), 2nd degree Mobitz I (progressive PR lengthening then dropped beat), Mobitz II (fixed PR with intermittent dropped beats — dangerous), 3rd degree (complete AV dissociation — emergent pacemaker).
Q: What determines blood pressure and how is it regulated short vs long term?
A: BP = CO × SVR. CO = HR × SV. Short-term (seconds-minutes): baroreceptors in carotid sinus and aortic arch detect stretch → signal to medulla → autonomic adjustment (HR, contractility, vascular tone). Long-term (hours-days): kidneys via RAAS — aldosterone increases Na+/water retention → increased blood volume → increased BP. ADH increases water retention. Atrial natriuretic peptide (ANP) released by stretched atria → promotes Na+ and water excretion → lowers BP. Antihypertensives target these mechanisms: diuretics (volume), beta-blockers (HR/CO), ACE inhibitors (RAAS), calcium channel blockers (SVR).
Q: What is coronary artery anatomy and which vessel supplies what?
A: Left main coronary artery → Left anterior descending (LAD) + Left circumflex (LCx). LAD supplies: anterior LV wall, anterior 2/3 of interventricular septum, apex, anterior papillary muscle. LCx supplies: lateral and posterior LV wall, SA node in 40%. Right coronary artery (RCA) supplies: right ventricle, SA node in 60%, AV node in 85%, posterior LV wall in right-dominant system (85% of people). LAD occlusion = anterior MI (most common, most deadly — 'widow maker'). RCA occlusion = inferior MI (bradycardia, heart block common). LCx occlusion = lateral MI.