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