Mizzou Physiology Block 3 Exam Study Guide

Blood

Connective tissue that transports gases, nutrients, wastes, hormones and cells throughout the body.

Main components of blood

Plasma (liquid extracellular matrix) and formed elements (red blood cells, white blood cells, platelets).

Plasma composition

~90% water; contains solutes: ions (Na⁺, K⁺, Cl⁻, HCO₃⁻), nutrients (glucose, amino acids, lipids), metabolic wastes, gases (dissolved CO₂), hormones, and plasma proteins (albumin, globulins, fibrinogen).

Albumin

Most abundant plasma protein; generates osmotic (oncotic) pressure that draws water into capillaries from interstitial fluid.

Major function of red blood cells

O₂ transport (and some CO₂ transport/buffering).

Hemoglobin (Hb)

Key protein in RBCs that binds O₂ reversibly; each Hb can carry 4 O₂ molecules.

Role of the heart

Pump that generates pressure to move blood through pulmonary and systemic circulations, maintaining perfusion and pressures.

Heart anatomy

4 chambers: right atrium (RA), right ventricle (RV), left atrium (LA), left ventricle (LV). Two separate series circuits: pulmonary (RV → lungs → LA) and systemic (LV → body → RA).

Heart valves

Ensure unidirectional flow: AV valves (tricuspid right, mitral/bicuspid left) between atria and ventricles; semilunar valves (pulmonary and aortic) at ventricular outflow tracts.

Systole

Ventricular contraction and ejection; LV pressure rises above aortic pressure → aortic valve opens → ejection (ventricular volume decreases).

Diastole

Ventricular relaxation and filling; ventricular pressure falls below atrial pressure → AV valves open → passive filling; atrial contraction (late diastole) adds final volume.

Pressure/volume relationship

Volume highest at end-diastole (EDV), lowest at end-systole (ESV). Aortic pressure peaks during ventricular ejection and falls during diastole.

Cardiac output

Heart rate * stroke volume.

Heart rate (HR) control

Autonomic nervous system: ↑ sympathetic (NE) ↑ HR via pacemaker cell slope and threshold; ↑ parasympathetic (ACh) ↓ HR by hyperpolarization and slowed depolarization. Hormones (epinephrine) also increase HR.

Stroke volume (SV) control

Determined by preload (EDV), contractility (inotropy; sympathetic stimulation, circulating catecholamines, Ca²⁺ availability), and afterload (arterial pressure/TPR).

Venous return (VR)

Volume flow of blood back to the heart per minute (must equal CO at steady state).

End-diastolic volume (EDV)

Volume in ventricles at end of filling; VR determines EDV — more VR → higher EDV. Preload sets initial sarcomere length and thus influences SV via Frank-Starling mechanism.

Pathway of red blood cell

Systemic circuit (return to heart): Tissue capillaries → venules → veins → vena cavae → right atrium → tricuspid valve → right ventricle → pulmonary valve → pulmonary artery → lungs (pulmonary capillaries).

Pulmonary to systemic circulation

Pulmonary capillaries → pulmonary veins → left atrium → mitral valve → left ventricle → aortic valve → aorta → arteries → arterioles → tissue capillaries.

Valves ensuring one-way flow

Valves that control blood entry into the ventricles and those that control blood exit from ventricles into the main arteries.

AV valves

Tricuspid (right) and mitral/bicuspid (left) valves that control entry into the ventricles.

Semilunar valves

Valves that control exit from the ventricles; include pulmonary (RV → pulmonary artery) and aortic (LV → aorta) valves.

Isovolumetric contraction

Phase at the start of systole where ventricles contract with all valves closed, causing pressure to rise without volume change.

Ejection

Phase where semilunar valves open when ventricular pressure exceeds arterial pressure, allowing blood ejection and decreasing ventricular volume.

Isovolumetric relaxation

Early diastole phase where ventricles relax, semilunar valves close, and AV valves remain closed until ventricular pressure falls below atrial pressure.

Frank-Starling Law

Principle stating that stroke volume increases in response to increased end-diastolic volume (EDV) due to increased sarcomere length.

End diastolic volume (EDV)

Ventricular volume immediately before contraction, reflecting stretch of myocardial fibers; referred to as preload.

Afterload

The pressure the ventricle must overcome to eject blood, influenced by arterial pressure and total peripheral resistance.

Cardiac output (CO)

Volume of blood pumped by one ventricle per minute, calculated as CO = stroke volume (SV) × heart rate (HR).

Heart rate (HR)

Number of heartbeats per minute, primarily controlled by the SA node and modulated by autonomic inputs.

Sympathetic stimulation

Increases heart rate (positive chronotropy), contractility (positive inotropy), and conduction velocity (dromotropy) via NE/E and β₁ receptors.

Parasympathetic stimulation

Decreases heart rate (negative chronotropy) and slightly decreases conduction velocity in the AV node, with minimal direct effect on ventricular contractility.

Venous return

The flow of blood back to the heart, which affects end-diastolic volume and subsequently stroke volume and cardiac output.

Stroke volume (SV)

The amount of blood ejected by the ventricle with each heartbeat, influenced by preload, afterload, and contractility.

Autonomic nervous system

Regulates heart rate and contractility through sympathetic and parasympathetic pathways.

Circulating hormones

Substances like catecholamines that influence heart function, including heart rate and contractility.

Baroreflex

A reflex mechanism that helps regulate blood pressure by adjusting heart rate and vascular resistance.

Atrial kick

The final contraction of the atria during diastole that contributes to ventricular filling.

Pressure-volume loop

A graphical representation of the relationship between pressure and volume in the heart throughout the cardiac cycle.

SV

Stroke volume, which is influenced by preload, contractility, and afterload.

Preload (EDV)

End-diastolic volume; an increase in preload leads to an increase in stroke volume according to the Frank-Starling mechanism.

Contractility

The ability of the heart muscle to contract; increased by sympathetic stimulation and positive inotropes like EPI and digitalis, leading to increased stroke volume.

Increased contractility

A positive inotropic state that raises stroke volume at the same end-diastolic volume, often due to sympathetic stimulation or circulating catecholamines.

Decreased afterload

A reduction in resistance that increases stroke volume without changing end-diastolic volume.

Factors influencing venous return

Blood volume, venous tone, skeletal muscle pump, respiratory pump, gravity/posture, and venous valves.

Increase venous return

Can be achieved by increasing venous tone, blood volume, activating the skeletal muscle pump, or increasing respiratory drive.

Cardiac muscle features

Intercalated discs containing gap junctions for electrical coupling and desmosomes for mechanical linkage, allowing coordinated contraction.

Contractile cells

Striated myocardial cells responsible for force generation, with abundant sarcomeres and large sarcoplasmic reticulum and T-tubules.

Autorhythmic cells

Specialized pacemaker cells that generate spontaneous depolarization, with fewer contractile fibers and lack of stable resting potential.

Cardiac electrical conduction system

Includes the SA node, internodal pathways, AV node, Bundle of His, bundle branches, and Purkinje fibers.

Excitation travel pathway

SA node → atrial myocardium → AV node → Bundle of His → bundle branches → Purkinje fibers → ventricular myocardium.

Contractile vs autorhythmic cells

Contractile cells have a stable resting potential and rapid upstroke, while autorhythmic cells have an unstable resting potential and spontaneous firing.

Tetany in cardiac muscle

Cardiac myocytes do not undergo tetany due to a prolonged absolute refractory period caused by the plateau phase.

Voltage-gated channels in cardiac muscle

L-type Ca²⁺ channels are prominent in cardiac cells, producing a plateau phase, unlike skeletal muscle which has fast Ca²⁺ release.

Pacemaker potential

The gradual depolarization in pacemaker cells caused by the slow influx of sodium ions.

Threshold in pacemaker cells

When the pacemaker potential reaches threshold, an action potential is triggered.

Sympathetic vs parasympathetic stimulation

Sympathetic stimulation increases heart rate by accelerating pacemaker potential, while parasympathetic stimulation decreases heart rate.

Voltage-gated Ca²⁺ channels

Channels that open at threshold, producing the action potential upstroke.

Sympathetic stimulation (β₁)

Increases funny current and Ca²⁺ channel activity, leading to steeper diastolic depolarization and shorter time to threshold, resulting in increased heart rate (HR).

Parasympathetic stimulation (ACh via M₂)

Increases K⁺ conductance and decreases funny current, resulting in a more negative max diastolic potential and slower depolarization, leading to decreased heart rate (HR).

P wave

Represents atrial depolarization, occurring just before atrial contraction.

PR interval

Conduction time from atria to ventricles, indicating AV node delay.

QRS complex

Represents ventricular depolarization, which masks atrial repolarization.

ST segment

Indicates that the ventricles are depolarized, representing the plateau phase.

T wave

Represents ventricular repolarization.

QT interval

Duration of ventricular depolarization plus repolarization, indicating electrical systole.

QRS complex and isovolumetric contraction

The QRS complex precedes and coincides with the onset of isovolumetric contraction; mechanical contraction starts just after ventricular depolarization.

T wave and isovolumetric relaxation

The T wave occurs during ventricular repolarization and is followed by isovolumetric relaxation; mechanical relaxation begins as repolarization completes.

Large arteries (elastic)

Conduct blood away from the heart and act as pressure reservoirs, storing energy during systole and releasing it during diastole.

Arterioles

Resistance vessels that are major controllers of flow distribution and total peripheral resistance (TPR) via vasoconstriction and vasodilation.

Capillaries

Thin exchange vessels that enable diffusion and fluid exchange between blood and interstitial fluid (ISF).

Venules/veins

Low-pressure volume reservoirs that return blood to the heart; veins have high compliance and valves to prevent backflow.

Skeletal muscle blood flow

Can consume the highest fraction of cardiac output during exercise, but kidneys receive approximately 20-25% of cardiac output at rest for filtering blood and regulating volume/composition.

Common layers of blood vessels

Include tunica intima (endothelium), tunica media (smooth muscle, elastic fibers), and tunica externa (connective tissue).

Large arteries structure

Have a thick elastic tunica media that allows stretch and recoil, functioning as a pressure reservoir.

Arterioles structure

Possess prominent smooth muscle for regulation of diameter, affecting resistance.

Capillaries structure

Feature a single endothelial cell layer plus a basement membrane, maximizing exchange.

Veins structure

Have thinner walls, larger lumen, more compliance, and less muscle/elasticity, functioning as volume reservoirs that can hold large blood volumes at low pressure.

Aorta's pressure reservoir function

Stores energy by stretching during systole and maintains aortic pressure and forward flow into peripheral vessels during diastole, smoothing pulsatile output into steady flow.

Characteristics of capillaries

Thin walls (single endothelial layer), narrow diameter, large total surface area, slow blood velocity in capillaries, and permeability (tight junctions or fenestrations depending on capillary type) enable efficient diffusion and exchange.

Filtration

Net movement of fluid out of capillary into ISF (driven by capillary hydrostatic pressure > oncotic pressure).

Absorption

Net movement into capillary from ISF (oncotic pressure > hydrostatic pressure).

Starling forces

Capillary hydrostatic pressure (Pc) pushes fluid out; interstitial hydrostatic pressure (Pif) pushes in; plasma oncotic pressure (πc, mainly from albumin) pulls fluid in; interstitial oncotic pressure (πif) pulls fluid out. Net filtration = (Pc + πif) − (Pif + πc).

Pressure at arteriole end

Pc high → filtration tends to dominate.

Pressure at venous end

Pc lower, πc unchanged → absorption can dominate. Overall, slight net filtration across bed is returned by lymphatics.

Venous system as volume reservoir

Veins have high compliance, store large blood volume at low pressure (volume reservoir).

Mechanisms aiding venous return

Venous valves (prevent backflow), skeletal muscle pump (compresses veins during activity), respiratory pump (negative intrathoracic pressure during inspiration pulls blood toward heart), venoconstriction (sympathetic) reduces compliance and increases venous return.

Functions of the lymphatic system

Lymphatics return excess interstitial fluid and proteins to the circulation, transport absorbed fats from intestines (chyle), and provide immune surveillance (lymph nodes).

Edema

Excessive accumulation of interstitial fluid due to: ↑ capillary hydrostatic pressure (e.g., heart failure), ↓ plasma oncotic pressure (e.g., hypoalbuminemia), ↑ capillary permeability (inflammation), lymphatic obstruction (lymphedema).

Pressure changes in circulation

Highest pressure in aorta/arteries, declines across arterioles and capillaries, lowest in vena cava. Pressure drop across the systemic circuit equals energy delivered by the heart and is dissipated by resistance.

Effect of vessel diameter on flow

Flow ∝ radius⁴ (Poiseuille's law relationship for laminar flow): small changes in radius produce large changes in flow. Doubling radius → 16× flow (if other factors constant). Vasoconstriction strongly decreases flow; vasodilation strongly increases flow.

Major factor opposing blood flow

Resistance (R) is major opposing factor; depends on viscosity, vessel length, and radius (most powerful).

Total peripheral resistance (TPR)

Combined resistance of systemic arterioles. Vasoconstriction ↑ TPR → ↓ flow for given pressure; vasodilation ↓ TPR → ↑ flow.

Differences between pulmonary and systemic circulations

Pulmonary circulation: lower pressures and lower resistance, but high flow equal to systemic flow (same CO).

Pulmonary arteries

More compliant; right ventricle ejects against low afterload.

Systemic circulation

Higher pressures and much higher resistance (TPR) to perfuse whole body.

Sympathetic signals

Increase HR and contractility → ↑ CO; vasoconstriction of most systemic arterioles → ↑ TPR and ↑ arterial pressure.

Parasympathetic signals

Mainly decreases HR (↓ CO); overall tends to lower blood pressure via HR reduction.

Sympathetic tone

Baseline sympathetic nerve activity causing partial vasoconstriction at rest; neurotransmitter: norepinephrine (NE).

α-adrenergic receptors

Cause vasoconstriction in many vascular beds (skin, splanchnic).