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Cardiovascular Physiology

Usually weeks 9-12 of a medical physiology course — the course's largest unit

Cardiovascular physiology is the longest unit in the course because it stacks every earlier one: membrane potentials become the cardiac action potential, muscle mechanics become Frank-Starling and afterload, and endocrine loops become the renin-angiotensin-aldosterone system. Build it in the order the blood experiences it — the electrical event, the mechanical cycle it triggers, the stroke volume that cycle produces, the vessels that stroke volume has to push through, and the reflexes that keep arterial pressure steady. The exam leans hardest on graphs (the ventricular and nodal action potentials, the Wiggers diagram, pressure-volume loops, and the cardiac function and venous return curves) and on prediction questions — what happens to stroke volume, pressure, and heart rate after a hemorrhage, a change in posture, a drug, or a leaky valve. If you can draw each graph from memory and push each variable in both directions, the unit becomes very scoreable.

On the PANCE this unit feeds:Cardiovascular · 11%Pulmonary · 9%Renal · 5%

This guide is the frame. The exams are written from your lectures— drop this unit's slides on the dashboard to get flashcards and board-style questions from your own course, and quiz them all semester (a course whose exams re-test earlier units rewards nothing more than early, repeated self-testing). The physiology playbook has the weekly loop.

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Lectures you file for this course live under Physiology → My Lectures in your library — pick it from the Module box as you upload, or from any card's Move menu afterwards.

AI-authored study notes, not faculty-reviewed and not medical advice. Verify every mechanism against your course materials and faculty; programs differ in emphasis.

High-Yield Pearl

Anchor every cardiovascular question to MAP = CO × TPR and CO = HR × SV, name which of preload, afterload, contractility, or rate the scenario touched first, and then let the baroreceptor reflex push the other variables the opposite way.

What the exam asks
Mechanisms, curves, and what happens when each one fails.
  • The circuit, its pressures, and where the blood sits. The two sides of the heart pump in SERIES, so their outputs must match over time, while the systemic organs sit in PARALLEL, each on its own arteriole. Resting pressures (mmHg) worth knowing cold: right atrium 0–5; right ventricle 25/0–5; pulmonary artery 25/10 (mean ~15); pulmonary capillary wedge ~8 (an estimate of left atrial pressure); left ventricle 120/0–10; aorta 120/80 (mean ~93). Most of the blood volume — roughly two-thirds — sits in the systemic VEINS, the compliant capacitance vessels; arteries hold about 15% and capillaries only about 5%. Flow velocity is inversely proportional to total cross-sectional area (v = Q/A), so blood moves fastest in the aorta and slowest in the capillaries, whose combined area is hundreds of times larger — slow enough for exchange.
  • The ventricular action potential, phase by phase. Phase 4: stable resting potential near −90 mV, held there by the inward-rectifier K+ current (IK1). Phase 0: fast voltage-gated Na+ channels open and Na+ rushes in — a steep upstroke to about +20 mV; class I antiarrhythmics block these channels and slow conduction. Phase 1: brief partial repolarization (the notch) as Na+ channels inactivate and a transient outward K+ current (Ito) flows. Phase 2: the PLATEAU — L-type Ca2+ channels let Ca2+ in, balanced by delayed-rectifier K+ efflux; this Ca2+ triggers contraction. Phase 3: L-type channels close while delayed-rectifier K+ currents (IKr, IKs) and then IK1 repolarize the cell; class III drugs block IKr and prolong this phase (a longer QT). The Na+/K+-ATPase and the Na+/Ca2+ exchanger restore the gradients. Because Na+ channels stay inactivated until the membrane repolarizes, the effective refractory period lasts nearly as long as the contraction — the heart cannot be tetanized.
  • The SA node's pacemaker potential and autonomic control of rate. Nodal cells have no stable resting potential. Phase 4 is a slow diastolic depolarization from a maximum diastolic potential near −60 mV: the FUNNY current (If) — a mostly Na+ inward current through HCN channels that OPEN on hyperpolarization — plus declining K+ conductance and, late, T-type Ca2+ entry. At threshold (about −40 mV), phase 0 is carried by L-type Ca2+ channels — slow, which is why nodal conduction is slow and why calcium channel blockers slow the AV node. Phase 3 is K+ efflux; there is no phase 1 or 2. Sympathetic stimulation (norepinephrine on β1 receptors → more cAMP) increases If and the Ca2+ currents: a STEEPER phase 4 slope reaches threshold sooner — positive chronotropy. Vagal acetylcholine (M2 receptors, Gi) lowers cAMP, reduces If, and opens ACh-activated K+ channels, which hyperpolarize the cell and flatten the slope — negative chronotropy. Ivabradine blocks If and slows the rate without changing contractility.
  • Conduction, velocity, and the EKG. Normal order: SA node → atrial muscle (with an interatrial bundle to the left atrium) → AV node → bundle of His → right and left bundle branches → Purkinje fibers → ventricular muscle, endocardium to epicardium and apex to base. Conduction velocity is fastest in Purkinje fibers (~2–4 m/s), then atrial muscle, then ventricular muscle, and slowest in the AV node (~0.05 m/s); the ~0.1 s AV nodal delay lets the atria finish emptying before the ventricles contract and limits how many atrial impulses reach the ventricles in atrial fibrillation. Intrinsic rates set the hierarchy: SA node 60–100/min, AV junction 40–60, Purkinje/ventricle 20–40 — the fastest pacemaker suppresses the rest (overdrive suppression). On the EKG, the P wave is atrial depolarization; the PR interval (0.12–0.20 s) is mostly AV nodal conduction time; the QRS complex (<0.12 s) is ventricular depolarization and hides atrial repolarization; the ST segment is the plateau, when the whole ventricle is depolarized and isoelectric; the T wave is ventricular repolarization; and the QT interval approximates the duration of the ventricular action potential.
  • Cardiac excitation-contraction coupling and relaxation. During the plateau, Ca2+ entering through L-type channels in the T-tubules opens nearby RyR2 channels on the sarcoplasmic reticulum — calcium-induced calcium release — and the resulting Ca2+ transient binds troponin C. How much Ca2+ is released sets the force: that is contractility. Relaxation requires removing Ca2+: SERCA2a pumps most of it back into the SR, and the Na+/Ca2+ exchanger ejects the amount that entered. Phospholamban tonically brakes SERCA; when β1 stimulation activates protein kinase A, it phosphorylates phospholamban (releasing the brake → faster reuptake and faster relaxation, LUSITROPY), L-type channels (more trigger Ca2+ and bigger SR stores → stronger contraction, INOTROPY), and troponin I (faster Ca2+ release from troponin). Digoxin inhibits the Na+/K+-ATPase; the rise in intracellular Na+ slows Ca2+ extrusion by the exchanger, loading the SR and raising contractility.
  • The cardiac cycle, heart sounds, and murmurs. Late diastole: atrial contraction tops off the ventricle (the a wave) — a modest share of filling at rest, more at high heart rates and in stiff ventricles. When ventricular pressure exceeds atrial pressure the mitral and tricuspid valves close (S1) and ISOVOLUMETRIC CONTRACTION begins — all valves closed, pressure rising steeply, volume constant. When LV pressure exceeds aortic pressure (~80 mmHg) the aortic valve opens and EJECTION begins, rapid then reduced; the aortic valve closes when LV pressure falls below aortic pressure, producing S2 and the dicrotic notch (incisura) on the aortic trace. ISOVOLUMETRIC RELAXATION follows until LV pressure falls below left atrial pressure, the mitral valve opens, and rapid filling begins, then slow filling (diastasis). S2 splits physiologically on inspiration because more venous return delays pulmonic closure. S3 is heard in early rapid filling — normal in children, athletes, and pregnancy, but a sign of volume overload and a dilated ventricle in heart failure. S4 is atrial contraction against a stiff ventricle (hypertrophy, ischemia) and can never occur in atrial fibrillation. Murmurs follow the valves: a systolic crescendo-decrescendo murmur is aortic stenosis; a holosystolic murmur is mitral (or tricuspid) regurgitation or a VSD; an early diastolic decrescendo murmur is aortic regurgitation; a diastolic rumble after an opening snap is mitral stenosis.
  • Stroke volume: preload, afterload, contractility — and cardiac output. Stroke volume = EDV − ESV (~70 mL), ejection fraction = SV/EDV (normal about 55–70%), and cardiac output = HR × SV (~5 L/min). PRELOAD is the stretch of the myocardium before contraction — best indexed by end-diastolic volume, estimated by end-diastolic pressure; more filling means more sarcomere overlap and greater Ca2+ sensitivity, so a stronger beat (Frank-Starling), which is how the two ventricles keep their outputs matched. AFTERLOAD is the wall stress the ventricle must overcome to eject; by the law of Laplace, wall stress ∝ pressure × radius / wall thickness, so afterload rises with aortic pressure, with aortic stenosis, and with a DILATED ventricle, and falls when the wall thickens. CONTRACTILITY (inotropy) is force at a given preload and afterload, raised by sympathetic stimulation, digoxin, and higher heart rate (the staircase effect), and lowered by ischemia, acidosis, β-blockers, and calcium channel blockers. Cardiac output can be measured by the Fick principle: CO = O2 consumption ÷ (arterial − mixed venous O2 content) — for example 250 mL O2/min ÷ (200 − 150 mL O2/L) = 5 L/min.
  • Pressure-volume loops. A left ventricular PV loop plots pressure against volume and runs COUNTERCLOCKWISE: filling along the bottom (volume rises, pressure barely moves, tracing the end-diastolic pressure-volume relationship) → mitral closure at the bottom right (EDV) → isovolumetric contraction straight up → aortic opening → ejection across the top to the left → aortic closure at the top left (ESV) → isovolumetric relaxation straight down → mitral opening at the bottom left. The loop's WIDTH is stroke volume, its area is stroke work, and its top-left corner lies on the end-systolic pressure-volume relationship (ESPVR), whose slope indexes contractility. Increased PRELOAD moves the bottom-right corner rightward — a wider loop, bigger SV, ESV nearly unchanged. Increased AFTERLOAD makes the loop taller and narrower: the aortic valve opens at a higher pressure and ejection stops at a larger ESV along the same ESPVR. Increased CONTRACTILITY steepens the ESPVR, moving the top-left corner leftward — a wider loop with a smaller ESV and a higher EF. A stiff (diastolic dysfunction) ventricle has a steeper filling curve: higher pressure at any volume.
  • Cardiac function and venous return curves. Two curves share one x-axis, right atrial pressure. The cardiac function (Starling) curve shows cardiac output RISING as RAP (preload) rises, then plateauing. The venous return curve shows venous return FALLING as RAP rises, because RAP is the back-pressure against flow into the heart; it reaches zero at the MEAN SYSTEMIC FILLING PRESSURE (~7 mmHg) — the pressure throughout the circulation if the heart stopped — and flattens at negative RAP as the great veins collapse. The heart operates where the curves intersect (output = return). Blood volume and venous tone set mean systemic filling pressure: transfusion or venoconstriction shifts the venous return curve RIGHT in parallel; hemorrhage or venodilation shifts it LEFT. Positive inotropes shift the cardiac function curve UP (higher output at a lower RAP); heart failure shifts it DOWN (lower output at a higher RAP). Changing TPR rotates the venous return curve about the same x-intercept — higher TPR flattens it — and moves the cardiac function curve in the same direction, so output changes while RAP stays about the same.
  • Hemodynamics: pressure, flow, resistance, and compliance. Flow Q = ΔP / R (the hemodynamic Ohm's law), so MAP ≈ CO × TPR (right atrial pressure being near zero). Resistance follows Poiseuille: R = 8ηL / (πr⁴) — halving a vessel's radius raises its resistance 16-fold, which is why the arterioles, with their muscular walls and sympathetic innervation, are the main site of resistance and the largest pressure drop. Resistances in SERIES add; resistances in PARALLEL add as reciprocals, so the total is lower than any single branch, and adding or dilating a parallel bed lowers TPR. Flow is normally laminar; turbulence (bruits, murmurs) is predicted by the Reynolds number, Re = ρvd/η, which rises with velocity and diameter and falls with viscosity — so stenosis (a high-velocity jet) and anemia (low viscosity, high velocity) both cause turbulent flow. Viscosity rises mainly with hematocrit (polycythemia). Compliance C = ΔV/ΔP is highest in veins (roughly 20 times arterial), and it falls in arteries with age. Pulse pressure = systolic − diastolic and rises with stroke volume and with stiffer arteries (isolated systolic hypertension in older adults). Mean arterial pressure ≈ diastolic + ⅓ pulse pressure at rest — not the simple average, because diastole lasts longer than systole.
  • The microcirculation and Starling forces. Fluid movement across a capillary: Jv = Kf [(Pc − Pi) − σ(πc − πi)]. Capillary hydrostatic pressure (Pc, falling from about 35 to 15 mmHg along the capillary) and interstitial oncotic pressure (πi, low) push fluid OUT; plasma oncotic pressure (πc, ~25 mmHg, mostly albumin) and interstitial hydrostatic pressure (Pi, near zero) pull it IN. Kf is the capillary's water permeability; σ, the reflection coefficient, is how well the wall holds back protein. In the classic picture, filtration dominates the arterial end and reabsorption the venous end; in most tissues net filtration slightly exceeds reabsorption, and the LYMPHATICS return the excess (a few liters a day) along with escaped protein. Arteriolar dilation raises Pc and favors filtration; arteriolar constriction lowers Pc and favors absorption. EDEMA follows from any imbalance: raised Pc (heart failure, venous obstruction, dihydropyridine vasodilators), lowered πc (nephrotic syndrome, cirrhosis, malnutrition), raised Kf or leaky walls (burns, sepsis, inflammation), or blocked lymphatics (lymph node dissection, filariasis).
  • Local control and the special circulations. Tissues set their own flow: MYOGENIC autoregulation (stretching arteriolar smooth muscle makes it contract) and METABOLIC control (adenosine, CO2, H+, K+, lactate, low O2, and NO dilate arterioles in proportion to metabolic rate) hold flow nearly constant across a range of pressures and match it to demand — active hyperemia with work, reactive hyperemia after an occlusion is released. CORONARY: extraction of O2 is already ~70–80% at rest, so extra demand must be met by more flow (adenosine, NO); left ventricular flow occurs mostly in diastole because systolic compression squeezes the vessels, which makes the subendocardium most vulnerable and tachycardia (shortened diastole) dangerous. CEREBRAL: autoregulated across roughly MAP 60–150 mmHg and exquisitely sensitive to PaCO2 — hypercapnia dilates, hyperventilation constricts (lowering intracranial pressure briefly). SKELETAL MUSCLE: sympathetic α1 tone dominates at rest; in exercise local metabolites override it. SKIN: sympathetic control for thermoregulation, including arteriovenous anastomoses. PULMONARY: a low-pressure, low-resistance bed where hypoxia CONSTRICTS arterioles (hypoxic pulmonary vasoconstriction, diverting blood to ventilated alveoli) — the opposite of the systemic response. KIDNEY: autoregulated by the myogenic response and tubuloglomerular feedback.
  • Reflex and hormonal control of arterial pressure. Short term, the BARORECEPTOR reflex: stretch receptors in the carotid sinus (afferents in CN IX) and aortic arch (CN X) fire in proportion to pressure and its rate of change, projecting to the nucleus tractus solitarius in the medulla. A fall in pressure reduces their firing → less vagal and more sympathetic outflow → higher heart rate and contractility, arteriolar constriction (higher TPR), and venoconstriction (higher mean systemic filling pressure). The reflex buffers moment-to-moment changes but resets within days to a sustained pressure. PERIPHERAL CHEMORECEPTORS (carotid and aortic bodies) respond to low PaO2, high PaCO2, and acidosis and add sympathetic drive in severe hypotension; brain ischemia triggers the strongest sympathetic response of all (the CNS ischemic response). Long term, the kidney sets pressure by controlling volume: low renal perfusion, low macula densa NaCl, and β1 stimulation release RENIN; angiotensin II constricts arterioles, stimulates aldosterone (Na+ retention), ADH, and thirst, and enhances proximal Na+ reabsorption. ADH (V1) constricts vessels and (V2) retains water once volume loss is substantial. Atrial stretch releases ANP, which acts through cGMP to dilate vessels, increase GFR and Na+ excretion, and inhibit renin and aldosterone.
  • Integrated responses: exercise, hemorrhage, standing, and Valsalva. EXERCISE: central command and muscle receptors raise sympathetic and lower vagal outflow (higher HR and contractility, venoconstriction), while the muscle and respiratory pumps raise venous return; local metabolites dilate working-muscle arterioles, so TPR FALLS even as renal and splanchnic beds constrict. Cardiac output can rise four- to fivefold; systolic pressure and pulse pressure rise, diastolic changes little, MAP rises modestly. HEMORRHAGE: lost volume lowers mean systemic filling pressure → venous return, RAP, SV, and MAP fall (pulse pressure narrows) → the baroreflex raises HR, contractility, TPR, and venous tone; lower capillary pressure draws interstitial fluid into the plasma (which dilutes the hematocrit over hours), and RAAS, ADH, and thirst restore volume over hours to days. STANDING: roughly half a liter of blood pools in the legs → venous return and SV fall → the baroreflex raises HR and TPR within seconds, helped by the skeletal muscle pump. VALSALVA (forced expiration against a closed glottis): phase I, raised intrathoracic pressure briefly raises aortic pressure; phase II, venous return falls, so BP falls and HR rises reflexly; phase III, release causes a brief further dip; phase IV, restored venous return ejects into constricted vessels — a BP overshoot with reflex bradycardia. Reduced preload during the strain softens most murmurs but LOUDENS the murmur of hypertrophic cardiomyopathy.
Worth drilling · 50 concepts
Each with the one fact that identifies it. Your course's slides are the authority; use this to check your list against.
  1. 1Systemic veins — hold about two-thirds of the blood volume; the capacitance vessels
  2. 2Arterioles — the major site of systemic vascular resistance and the largest pressure drop
  3. 3Capillaries — greatest total cross-sectional area and slowest flow velocity
  4. 4Pulmonary capillary wedge pressure — catheter estimate of left atrial pressure (~8 mmHg)
  5. 5Poiseuille equation — resistance varies inversely with the fourth power of the radius
  6. 6Parallel resistances — total is lower than any single branch; the arrangement of the organs
  7. 7Reynolds number — predicts turbulence; rises with velocity, falls with viscosity
  8. 8Pulse pressure — systolic minus diastolic; rises with stroke volume and stiff arteries
  9. 9Mean arterial pressure — diastolic plus one-third of pulse pressure at rest
  10. 10Inward rectifier K+ current — IK1; holds the ventricular resting potential near −90 mV
  11. 11Fast Na+ current — phase 0 upstroke of ventricular muscle; blocked by class I drugs
  12. 12Transient outward K+ current — Ito; the phase 1 notch
  13. 13Plateau phase — phase 2; L-type Ca2+ entry balanced by K+ efflux
  14. 14Delayed rectifier K+ current — phase 3 repolarization; blocked by class III drugs
  15. 15Funny current — If; HCN channels opened by hyperpolarization drive nodal phase 4
  16. 16Nodal upstroke — phase 0 of SA and AV nodes, carried by L-type Ca2+ channels
  17. 17SA node — dominant pacemaker; fastest intrinsic rate (60–100/min)
  18. 18AV node — slowest conduction; its delay lets the ventricles finish filling
  19. 19Purkinje fibers — fastest conduction in the heart (~2–4 m/s)
  20. 20Overdrive suppression — the fastest pacemaker silences the slower latent ones
  21. 21Effective refractory period — no propagated response possible; outlasts most of contraction
  22. 22PR interval — mostly AV nodal conduction time; normally 0.12–0.20 s
  23. 23QRS complex — ventricular depolarization; hides atrial repolarization
  24. 24ST segment — ventricles fully depolarized during the plateau; normally isoelectric
  25. 25QTc — rate-corrected duration of ventricular depolarization plus repolarization
  26. 26Calcium-induced calcium release — L-type Ca2+ entry opens RyR2 on the SR
  27. 27Phospholamban — SERCA brake released by PKA phosphorylation
  28. 28Lusitropy — the rate of myocardial relaxation; raised by β1 stimulation
  29. 29Isovolumetric contraction — all valves closed; ventricular pressure rises at constant volume
  30. 30Isovolumetric relaxation — all valves closed; pressure falls from aortic closure to mitral opening
  31. 31Dicrotic notch — incisura on the aortic trace marking aortic valve closure
  32. 32Atrial a wave — atrial contraction on the atrial or venous trace; absent in atrial fibrillation
  33. 33First heart sound — mitral and tricuspid closure at the start of systole
  34. 34Second heart sound — aortic and pulmonic closure; splits on inspiration
  35. 35Third heart sound — early rapid filling of a dilated, volume-overloaded ventricle
  36. 36Fourth heart sound — atrial kick into a stiff, hypertrophied ventricle
  37. 37Frank-Starling mechanism — greater end-diastolic volume yields a stronger contraction
  38. 38Law of Laplace — wall stress rises with pressure and radius, falls with wall thickness
  39. 39Ejection fraction — stroke volume divided by end-diastolic volume; normal about 55–70%
  40. 40Fick principle — cardiac output equals O2 consumption over the arteriovenous O2 difference
  41. 41End-systolic pressure-volume relationship — its slope indexes contractility
  42. 42Mean systemic filling pressure — x-intercept of the venous return curve (~7 mmHg)
  43. 43Plasma oncotic pressure — albumin's pull that opposes capillary filtration
  44. 44Lymphatics — return filtered fluid and protein; blockage causes lymphedema
  45. 45Myogenic response — arteriolar smooth muscle contracts when stretched
  46. 46Metabolic hyperemia — blood flow rises in proportion to tissue metabolic rate
  47. 47Hypoxic pulmonary vasoconstriction — lung arterioles constrict to low alveolar O2
  48. 48Baroreceptor reflex — carotid sinus and aortic arch stretch receptors buffer arterial pressure
  49. 49Carotid body — peripheral chemoreceptor firing to low PaO2, high PaCO2, and acidosis
  50. 50Atrial natriuretic peptide — atrial-stretch hormone that dilates vessels and excretes Na+
Practice it
Active recall over the drill list — flip and claim, match the pairs, produce the answers cold, fill in the diagram, or read the curves like the exam does.

Every concept on the drill list, one card at a time — the name up front, the fact that identifies it on the flip. Claim each card honestly and the deck learns what to lead with next time. Progress lives in this browser only.

What everyone misses
The distinctions that lose points on this material, year after year.
  • The narrowest vessel is not the most resistant bed. Each capillary is narrower than an arteriole, but capillaries are arranged in enormous parallel networks, so their COMBINED resistance is modest and their combined area is the largest in the circuit. The arterioles — few enough, muscular, and sympathetically controlled — are where the largest pressure drop occurs and where TPR is adjusted. The same parallel logic explains why velocity is SLOWEST in the capillaries even though each is so narrow.
  • Nodal phase 0 is calcium, not sodium. The reflex answer 'Na+ channels open' is right for atrial, ventricular, and Purkinje cells, but in the SA and AV nodes the upstroke is carried by L-type Ca2+ channels. That is why calcium channel blockers (and not class I Na+ blockers) slow AV nodal conduction, and why nodal cells conduct so slowly. The funny current is a phase 4 current, not the upstroke.
  • Preload is volume (stretch), not pressure. End-diastolic pressure is used as a stand-in for preload, but the Frank-Starling mechanism responds to fiber LENGTH. A stiff, hypertrophied ventricle can have a high end-diastolic pressure with a small end-diastolic volume — high filling pressure, LOW preload. Read the volume axis on a PV loop before calling preload increased.
  • A dilated heart has MORE afterload. Students equate afterload with aortic pressure alone. By the law of Laplace, wall stress also rises with chamber radius, so a dilated failing ventricle faces higher afterload at the same blood pressure, and a thickened wall lowers it. That is why afterload reduction helps heart failure and why concentric hypertrophy is an adaptation to pressure overload.
  • Which corner moves: EDV for preload, ESV for afterload and contractility. On a PV loop, a preload change moves the bottom-right corner (EDV) with ESV nearly unchanged. Afterload and contractility both act on the top-left corner (ESV): more afterload slides it up and RIGHT along the same ESPVR line (smaller SV), more contractility steepens that line and moves it LEFT (larger SV). If the ESPVR slope changed, it was contractility.
  • Mean arterial pressure is not the average of systolic and diastolic. At resting heart rates the heart spends about two-thirds of each cycle in diastole, so MAP ≈ diastolic + ⅓ pulse pressure (120/80 → about 93, not 100). As heart rate rises and diastole shortens, MAP moves toward the arithmetic average.
  • Hypoxia dilates systemic vessels but constricts pulmonary ones. In the systemic circulation low O2 is a metabolic vasodilator; in the lung it constricts arterioles so blood is diverted away from poorly ventilated alveoli. Generalized alveolar hypoxia (high altitude, COPD) therefore raises pulmonary vascular resistance and can cause pulmonary hypertension and right heart strain.
  • Right atrial pressure plays a different role on each curve. On the cardiac function curve a higher RAP means more preload and more output; on the venous return curve a higher RAP means less pressure gradient and less return. Students who treat RAP as good on both curves misread the shifts: a failing heart settles at a HIGHER RAP with a LOWER output, and a positive inotrope raises output while LOWERING RAP.
Clinical correlations
Where this unit shows up again — in clinic, on rotations, and on the boards.
  • Hemorrhagic shock. A trauma patient is tachycardic with cool, pale skin and a narrowing pulse pressure before the systolic pressure falls — the baroreflex is compensating with tachycardia, vasoconstriction, and venoconstriction. Hypotension usually appears only after large losses (roughly 30% of blood volume), which is why a normal blood pressure does not exclude significant bleeding. The early hematocrit can be normal because whole blood was lost; it falls as interstitial fluid shifts in and IV fluids are given.
  • Orthostatic hypotension. A sustained drop of at least 20 mmHg systolic or 10 mmHg diastolic within three minutes of standing, with lightheadedness. Causes map onto the reflex: volume depletion (too little to pool), α1 blockers and other vasodilators (effector blocked), and autonomic neuropathy from diabetes or Parkinson disease (reflex arc broken — a hallmark is that the heart rate FAILS to rise). A large heart-rate rise without hypotension suggests postural orthostatic tachycardia syndrome.
  • Heart failure with reduced ejection fraction. Depressed contractility shifts the cardiac function curve down and the PV loop's ESPVR flatter: EF falls, EDV and filling pressures rise. Low output activates the sympathetic system and RAAS, which retain Na+ and water and raise afterload — helpful at first, harmful long term. High left atrial pressure raises pulmonary capillary pressure (pulmonary edema, dyspnea, orthopnea); an S3 reflects the volume-overloaded ventricle. ACE inhibitors or ARBs, β-blockers, aldosterone antagonists, and diuretics each target a piece of this physiology.
  • Aortic stenosis. An older adult with exertional angina, syncope, or dyspnea and a harsh systolic crescendo-decrescendo murmur at the right upper sternal border radiating to the carotids. LV systolic pressure far exceeds aortic pressure to force blood through the narrowed valve, so afterload is high, the ventricle hypertrophies concentrically (an S4), and the carotid pulse is weak and delayed (pulsus parvus et tardus). Coronary supply-demand mismatch and a fixed output that cannot rise with exercise explain the symptoms.
  • Aortic regurgitation. A widened pulse pressure with bounding pulses and an early diastolic decrescendo murmur. Blood leaking back into the ventricle in diastole drops diastolic pressure and enlarges EDV, so stroke volume (and systolic pressure) rise — the loop is wide, with no true isovolumetric relaxation because the aortic valve never fully seals. The ventricle dilates eccentrically under chronic volume overload.
  • Hyperkalemia and the EKG. Rising K+ depolarizes the resting membrane (less K+ gradient), which inactivates fast Na+ channels and slows conduction: peaked T waves first, then a prolonged PR, a flattened P wave, a widening QRS, and eventually a sine-wave pattern and ventricular fibrillation or asystole. IV calcium stabilizes the membrane immediately; insulin with glucose and β2 agonists shift K+ into cells.
  • AV nodal block. First-degree block is a PR interval over 0.20 s with every P wave conducted. Second-degree Mobitz I shows progressive PR lengthening until a beat drops (usually AV nodal, often benign, worsened by β-blockers, calcium channel blockers, digoxin, and high vagal tone). Mobitz II drops beats without warning and is infranodal. In third-degree block the atria and ventricles beat independently and a slow junctional or ventricular escape rhythm sets the rate — the hierarchy of latent pacemakers made visible; pacing is the treatment.
  • Edema at the bedside. Pitting leg edema with jugular venous distension is raised capillary hydrostatic pressure from right heart failure; generalized edema with heavy proteinuria and low albumin is lost oncotic pressure (nephrotic syndrome); ascites and edema with liver disease combine low albumin and portal hypertension; ankle edema after starting amlodipine is arteriolar dilation raising capillary pressure; non-pitting arm swelling after axillary node dissection is lymphedema. Each is one term of the Starling equation.
  • Hypertrophic cardiomyopathy and dynamic murmurs. A young athlete with exertional syncope and a systolic murmur that gets LOUDER with Valsalva or standing and softer with squatting or handgrip. Asymmetric septal hypertrophy obstructs the LV outflow tract, and the obstruction worsens when the ventricle is smaller (less preload) or ejects harder. Maneuvers that reduce preload soften nearly every other murmur, so the opposite response points to this diagnosis (and mitral valve prolapse, whose click comes earlier). β-blockers help by slowing the rate and lengthening filling.

Frequently asked

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