7.3 Cardiovascular Physiology

Why cardiovascular physiology is a scored Physiology topic

Cardiovascular physiology is 12% of the Physiology domain. Official bullets: cardiac pump; electrophysiology of the heart; hemodynamics; regulation of circulation; circulation in organs; lymphatics; hematology and immunity. Chamber names and coronary ostia are General Anatomy. This section is pressures, intervals, resistances, and control loops. Gas transport details continue in /study-guides/nbce-part1/physiology-respiratory-gi/respiratory-physiology.

Cardiac pump and cycle

Cardiac output (CO) = heart rate × stroke volume. Resting adult teaching values: heart rate about 70/min, stroke volume about 70 mL, CO about 5 L/min (range often 4–6). Ejection fraction = SV / EDV; with EDV ~120 mL and SV ~70 mL, EF is ~60% (normal band about 55–70%). Pulse pressure = systolic − diastolic arterial pressure; it rises when stroke volume rises or arterial compliance falls.

Mean arterial pressure (MAP) is the time-weighted arterial pressure. Teaching approximation: MAP ≈ diastolic + 1/3 pulse pressure. For 120/80 mmHg, MAP ≈ 80 + 13 ≈ 93 mmHg. Because systole is shorter than diastole, MAP is closer to diastolic than to the arithmetic mean of systolic and diastolic.

Wiggers phases (left ventricle)

Right-sided events are similar but at lower pressure (pulmonary artery ~25/8 mmHg versus aorta ~120/80). Right ejection starts slightly earlier and lasts slightly longer, which splits S2 with inspiration (increased venous return delays pulmonary valve closure).

Preload is wall stretch before contraction, indexed by EDV or end-diastolic pressure (and, upstream, venous return). Afterload is the load during ejection, indexed by aortic pressure or, more precisely, Laplace wall stress. Contractility is the inotropic state at a given preload and afterload (the Starling-curve height). Venous return is driven by the gradient from mean systemic filling pressure (about 7 mmHg teaching value) to right-atrial pressure; the Guyton intersection of the venous-return curve with the cardiac-function curve sets steady-state CO.

Laplace for a sphere: wall tension (or stress) T ≈ P × r / (2h). A dilated ventricle (large r, often thinner h) must generate more wall stress for the same pressure—higher myocardial oxygen demand. The same relation explains why a small-radius capillary can tolerate its transmural pressure and why an enlarging aneurysm is mechanically unstable.

Electrophysiology of the heart and the ECG

Hierarchy of pacemakers. Sinoatrial (SA) node intrinsic rate about 60–100/min (vagal tone holds the resting adult nearer 70). Atrioventricular (AV) node about 40–60/min. His–Purkinje about 20–40/min. The fastest pacemaker overdrive-suppresses the others by driving Na+/K+ ATPase (more negative diastolic potential in latent pacemakers).

SA-node action potential. Maximal diastolic potential is only about −60 to −70 mV (few IK1 channels, so not −90 mV). Phase 4 is a spontaneous drift: funny current If (HCN channels, mixed Na+/K+, activated by hyperpolarization and by cAMP), then T-type Ca2+, then the L-type Ca2+ upstroke. There is no fast INa upstroke in true nodal cells. Acetylcholine (M2) lowers cAMP, reduces If and Ca2+ currents, raises IK,ACh → slower rate. Norepinephrine (β1) raises cAMP → faster rate and faster AV conduction.

AV node is the delay site (small cells, Ca2+-dependent upstroke, few gap junctions). Delay of about 0.09–0.12 s lets atria finish emptying. It is also a filter against atrial tachyarrhythmias. His–Purkinje conduction is fast (large diameter, lots of INa and connexin) so the ventricular endocardium depolarizes nearly together → a narrow QRS.

Mean QRS axis teaching range is about −30° to +90° (some sources +100°). Left-axis and right-axis deviation are vector facts; chamber-hypertrophy criteria are low yield unless a stem hands you them. Atrial repolarization is buried in the QRS.

Excitation–contraction in the ventricle is CICR, already covered. The ECG does not show contraction; the mechanical lag after QRS is electromechanical delay (excitation–contraction coupling time).

Hemodynamics: Ohm, Poiseuille, and resistance networks

Ohm's law for flow: Q = ΔP / R. For the whole systemic circuit, CO = (MAP − RAP) / TPR, so MAP − RAP = CO × TPR. Right-atrial pressure is normally near 0–5 mmHg, so MAP ≈ CO × TPR. If CO is 5 L/min and MAP is 93 mmHg (RAP ≈ 0), TPR ≈ 18.6 mmHg·min·L^−1. Raising TPR at constant CO raises MAP; raising CO at constant TPR raises MAP. Baroreflexes usually move both.

Poiseuille's law for laminar flow in a rigid cylinder:

R = 8 η L / (π r^4) and Q = (π r^4 ΔP) / (8 η L)

Resistance is linear in viscosity (η) and length (L) and inverse to radius to the fourth power. Halving radius multiplies resistance by 16 and, at a fixed ΔP, cuts flow to 1/16. Doubling radius multiplies flow by 16. That is why arterioles—not capillaries, not the aorta—are the resistance vessels: they have adjustable r and sit where r^4 has leverage. Viscosity rises with hematocrit (polycythemia, dehydration) and with hypothermia; anemia lowers viscosity. In tubes the size of arterioles, the Fåhraeus–Lindqvist effect lowers apparent viscosity (cells stream centrally).

Series resistances add (Rtotal = R1 + R2). Parallel beds add as reciprocals (1/Rtotal = 1/R1 + 1/R2), so opening a new parallel bed (exercise muscle) lowers TPR even if other arterioles constrict. Reynolds number predicts turbulence (high velocity, large diameter, low viscosity)—the physiology of bruits and Korotkoff sounds, not a fluid-mechanics course.

Arterial compliance (ΔV/ΔP) stores stroke volume in systole and recoils in diastole (Windkessel). Aging stiffens arteries: systolic pressure and pulse pressure rise, diastolic pressure may fall. Capillaries have huge total cross-sectional area, so velocity is lowest there—time for diffusion. Veins hold ~60–70% of blood volume (capacitance); venoconstriction is a preload maneuver.

Regulation of circulation

Arterial baroreceptors. Carotid sinus (CN IX) and aortic arch (CN X) are stretch receptors. Increased MAP or pulse pressure increases firing. Primary synapse is nucleus tractus solitarius (NTS). NTS excites the nucleus ambiguus / dorsal vagal complex (raise parasympathetic outflow to SA and AV nodes) and excites the caudal ventrolateral medulla, which inhibits the rostral ventrolateral medulla (RVLM) (cut sympathetic preganglionic drive). Net: bradycardia, lower contractility, vasodilation. A fall in MAP does the opposite (diagram). The reflex is a beat-to-beat buffer; it resets in sustained hypertension and does not set the long-term MAP by itself.

Peripheral chemoreceptors (carotid and aortic bodies) fire when PaO2 falls (also high PaCO2 / H+). They raise ventilation and, if ventilation is not allowed, raise sympathetic vasoconstriction. Central chemoreceptors on the ventral medulla sense brain-ECF H+ tightly coupled to PaCO2—primarily a respiratory story, with cardiovascular spillover.

Renin–angiotensin–aldosterone. Juxtaglomerular cells release renin when renal perfusion pressure falls, when NaCl delivery to the macula densa falls, and when sympathetic β1 input rises. Renin cleaves angiotensinogen to angiotensin I; angiotensin-converting enzyme (pulmonary endothelium) makes angiotensin II. AT1 receptors: arteriolar constriction, aldosterone secretion, ADH and thirst, renal Na+ reabsorption, sympathetic facilitation. Aldosterone retains Na+ (and therefore volume). ADH (vasopressin) at V2 retains water; at high levels V1 constricts vessels. ANP/BNP from stretched atria/ventricles oppose the cascade (natriuresis, vasodilation).

Local metabolic control dominates in heart, brain, and exercising muscle: adenosine, K+, H+, CO2, lactate, and low PO2 dilate arterioles. Myogenic (Bayliss) constriction when transmural pressure stretches vascular smooth muscle contributes to autoregulation. Endothelium: nitric oxide (cGMP) and prostacyclin dilate; endothelin constricts. Reactive hyperemia is repayment of a flow debt after occlusion; active hyperemia is matching flow to metabolism.

Circulation in organs

Lymphatics and Starling forces

Capillary exchange is convection plus diffusion. Starling relationship: net filtration pressure ≈ (Pc − Pi) − σ(πc − πi). Teaching numbers: arterial-end Pc ~30–35 mmHg, venous-end Pc ~15 mmHg, plasma oncotic πc ~25–28 mmHg. Filtration at the arterial end, absorption at the venous end, with a net filtration that lymphatics return—about 2–4 L/day of fluid, plus protein that leaked. Thoracic duct (left) drains most of the body to the left venous angle; right lymphatic duct drains the right upper quadrant.

Edema when Pc rises (heart failure, venous obstruction), πc falls (hypoalbuminemia), permeability rises (σ falls; inflammation), or lymph is blocked. Skeletal-muscle and arterial pulsation pump lymph through valved vessels; smooth muscle in larger lymphatics has intrinsic pacemakers.

Hematology and immunity as blood-cell function

This bullet on the Part I physiology plan is blood-cell function, not the full microbiology immunology chapter. Keep the overlap tight.

Whole blood is about 5 L in a 70 kg adult: roughly 3 L plasma and 2 L red-cell volume at hematocrit ~40–45%. Red cells (~5 × 10^6/μL; hemoglobin ~15 g/dL) carry oxygen on hemoglobin (four heme sites) and carry much of the blood's buffering and CO2 as bicarbonate after carbonic anhydrase. They lack mitochondria and live ~120 days. Anemia lowers O2 content and viscosity; polycythemia raises both and can throttle flow via η in Poiseuille's law.

Platelets (150–400 × 10^3/μL) form the primary hemostatic plug: adhesion (von Willebrand factor–GPIb), activation (ADP, thromboxane A2), aggregation (GPIIb/IIIa–fibrinogen). They are innate first responders at a break in endothelium, not adaptive lymphocytes.

Innate immunity: barriers, phagocytes, complement (opsonization C3b, membrane-attack C5–9, anaphylatoxins C3a/C5a), pattern-recognition receptors, NK cells. Adaptive immunity: clonal B and T cells, MHC I (all nucleated cells → CD8) versus MHC II (professional APCs → CD4), antibodies (IgM first, IgG later, IgA mucosa, IgE mast cells, IgD B-cell receptor). Complement and phagocytes link the two. Full hypersensitivity types and vaccine classes belong to pathology and microbiology; here you need to know which circulating cell does which job and how that cell load changes viscosity, O2 content, and hemostasis—the cardiovascular consequences of blood as a tissue.

Plasma proteins (albumin oncotic pressure, clotting factors, immunoglobulins) sit in the same fluid that Starling forces and lymph are moving. A stem that drops albumin is asking for edema from low πc, not for a GI lecture.