Cardiovascular Physiology: Structure, Function, and Regulation

Cardiac Physiology

Heart Structure and Conduction System

The heart functions as a dual pump, ensuring blood flows efficiently through the body. Its muscle cells are interconnected by gap junctions, allowing coordinated contraction. The conduction system consists of specialized, non-contractile cardiac muscle cells that initiate and distribute electrical impulses, producing action potentials (APs) spontaneously at different rates.

• Sinoatrial (SA) node: Located in the right atrium, acts as the primary pacemaker, generating APs at 100/min (modified to 75/min by the parasympathetic nervous system).

• Atrioventricular (AV) node: Also in the right atrium, generates APs at 50/min and delays conduction to allow ventricular filling.

• Bundle of His (AV bundle): The only route for electrical activity from atria to ventricles.

• Bundle Branches: Right and left branches, APs at 30/min.

• Purkinje fibers: Terminal fibers stimulating ventricular myocardium contraction.

Additional info: If the conduction system is damaged, the next fastest part becomes the pacemaker. Artificial pacemakers are used if SA or AV nodes are damaged.

Action Potentials in Cardiac Cells

Cardiac muscle cells are either autorhythmic (self-excitable) or contractile. The SA and AV nodes have no resting membrane potential, and their APs cycle continuously.

• Pacemaker Potential: Slow inward Na+ leak causes depolarization toward threshold (-40mV).

• AP Depolarization: Ca2+ influx causes rapid depolarization.

• AP Repolarization: K+ outflow restores membrane potential.

• Ventricular Myocardial APs: Contractile cells, resting MP = -90mV, phases include rapid Na+ influx, plateau (Ca2+ influx), and repolarization (K+ outflow).

Excitation-Contraction Coupling: AP triggers Ca2+ release from sarcoplasmic reticulum, binding to troponin, exposing myosin binding sites, and initiating contraction. The duration of AP (~250 ms) and twitch (~300 ms) prevents summation and tetanus.

Cardiac Cycle

Electrical Activity (ECG)

The ECG records the sum of electrical activity from all myocardial cells, not individual APs. It is measured using electrode pairs (leads) and displayed as waves:

• P wave: Atrial depolarization, followed by contraction.

• QRS wave: Ventricular depolarization, followed by contraction; masks atrial repolarization.

• T wave: Ventricular repolarization, followed by relaxation.

ECG intervals indicate phases of contraction and relaxation. Abnormalities include tachycardia (>100 bpm), bradycardia (<60 bpm), and heart block (impaired AV node conduction).

Mechanical Activity

Each heartbeat consists of systole (contraction, emptying) and diastole (relaxation, filling) for both atria and ventricles. Electrical activity initiates these events.

• Average resting HR = 75 beats/min; cardiac cycle duration = 0.8 sec.

• Atria: Systole for 0.1 sec, diastole for 0.7 sec.

• Ventricles: Systole for 0.3 sec, diastole for 0.5 sec (begin systole after atria).

Blood Flow Through the Heart

Blood flow is driven by pressure changes, valve function, and myocardial contraction. During ventricular systole, AV valves shut (first heart sound, LUB), and semilunar valves open. During diastole, semilunar valves shut (second heart sound, DUB), and AV valves open when ventricular pressure drops below atrial pressure.

Heart Sounds: Turbulent flow occurs when valves shut; laminar flow is silent. Korotkoff sounds are heard during blood pressure measurement.

Cardiac Output (CO)

Definition and Calculation

Cardiac output is the volume of blood ejected by each ventricle per minute. It is calculated as:

• Stroke Volume (SV): Volume ejected per beat, SV = EDV – ESV.

• End Diastolic Volume (EDV): Volume at end of diastole (~120 ml).

• End Systolic Volume (ESV): Volume at end of systole (~50 ml).

• SV = 120 ml – 50 ml = 70 ml.

• CO = HR × SV.

At rest, CO ≈ 5.25 L/min per ventricle; total blood volume passes through each ventricle every minute.

Control of Cardiac Output

• Heart Rate: Intrinsic control by SA node; extrinsic control by neural (SNS, PSNS), hormonal (epinephrine, NE, thyroid hormone), and other factors (ions, fever, age, fitness).

• Stroke Volume: Intrinsic control (Frank-Starling's Law: force of ejection proportional to fiber length), extrinsic control (SNS, hormones, drugs, pH, ion concentrations).

Additional info: SNS increases both HR and force of contraction; PSNS decreases HR only.

Blood Circulation

Blood Flow and Resistance

Blood flow (F) is determined by the pressure gradient (ΔP) and resistance (R):

• Resistance depends on vessel length, blood viscosity, and radius (controlled by smooth muscle).

• Vasodilation increases radius, decreases resistance, and increases flow.

• Vasoconstriction decreases radius, increases resistance, and decreases flow.

Blood flow to organs is regulated by intrinsic (myogenic, metabolic) and extrinsic (neural, hormonal) mechanisms.

Blood Pressure

Definition and Regulation

Blood pressure is the hydrostatic pressure exerted by blood on vessel walls. Systolic pressure is produced by ventricular contraction; diastolic pressure by elastic arteries during relaxation. Pulse pressure = systolic - diastolic. Mean arterial pressure (MAP) is the average pressure during the cardiac cycle:

• MAP = diastolic pressure + 1/3 pulse pressure.

• MAP is regulated by cardiac output, total peripheral resistance (TPR), and blood volume.

Key equations:

• $\Delta P = F \times R$

• $\text{MAP} = \text{Cardiac Output} \times \text{Total Peripheral Resistance}$

Extrinsic Regulation of MAP

MAP is regulated by neural (baroreceptor and chemoreceptor reflexes) and hormonal mechanisms. Baroreceptors in the carotid sinus and aortic arch monitor MAP and trigger responses to maintain homeostasis.

Hormonal control includes epinephrine, renin-angiotensin system, and atrial natriuretic peptide (ANP).

Additional info: Angiotensin II increases vasoconstriction, aldosterone, ADH, and thirst, raising blood volume and MAP. ANP decreases MAP by promoting urine production and vasodilation.

Capillary Exchange

Mechanisms of Exchange

Solutes and fluids move between blood and interstitial fluid (ISF) via diffusion, vesicular transport, and mediated transport. Fluid movement is governed by osmosis and bulk flow, driven by four pressures:

• Blood hydrostatic pressure (BHP): Pushes fluid out of capillaries.

• Blood osmotic pressure (BOP): Pulls fluid into capillaries.

• ISF hydrostatic pressure (IFHP): Pushes fluid into capillaries.

• ISF osmotic pressure (IFOP): Pulls fluid out of capillaries.

Net filtration pressure (NFP) determines whether filtration or absorption occurs:

• At arteriolar end: NFP = 10 mmHg (filtration).

• At venous end: NFP = -9 mmHg (absorption).

90% of filtered fluid is reabsorbed; 10% enters lymph. Edema results from imbalances in these pressures.

Hemostasis

Stages of Hemostasis

Hemostasis is the process of stopping bleeding, involving:

• Vascular spasm: Vasoconstriction reduces blood flow.

• Platelet plug formation: Platelets adhere to damaged vessels, releasing factors to promote clotting.

• Clot formation: Three stages—production of prothrombin activator, conversion of prothrombin to thrombin, and conversion of fibrinogen to fibrin.

Clot retraction and repair follow, with fibroblasts and endothelial cells restoring vessel integrity. Fibrinolysis dissolves the clot via plasmin.

Additional info: Hemophilia is a disorder of clotting, most commonly due to deficiency of factor VIII.