exam 3 human phys fall 2026

Capillary

Smallest blood vessel; site of exchange (O2 and nutrients leave blood, CO2 and wastes enter). Connects arterioles to venules.

Artery

Vessel that carries blood AWAY from the heart (thick, muscular, elastic walls).

Vein

Vessel that carries blood TOWARD the heart (thinner walls, less smooth muscle, larger lumen; has valves).

Septum

Wall in the heart dividing the left and right sides.

Pulmonary arteries

Carry deoxygenated blood from the right ventricle to the lungs.

Pulmonary veins

Carry oxygenated blood from the lungs to the left atrium.

Superior and inferior vena cava

Largest veins; return deoxygenated blood from the upper body (superior) and lower body (inferior) to the right atrium.

Aorta

Largest artery; carries oxygenated blood from the left ventricle to the systemic circuit.

Resistance (blood flow)

Opposition to blood flow; mainly determined by blood vessel radius (also length and blood viscosity).

Vasoconstriction

Narrowing of blood vessels from smooth muscle contraction; decreases flow, increases resistance and blood pressure.

Vasodilation

Widening of blood vessels from smooth muscle relaxation; increases flow, decreases resistance and blood pressure.

Pericardium

Fluid-filled sac that encases and protects the heart.

Myocardium

Thick middle layer of the heart wall made of cardiac muscle.

Layers of the heart wall (outside to inside)

Pericardium/epicardium → myocardium → endocardium.

Autorhythmic cells

Pacemaker cells that spontaneously generate action potentials and set the heart rate (no neuron needed).

Electrocardiogram (ECG/EKG)

Recording of the heart's electrical activity from the body surface.

Systole

Contraction phase of the cardiac cycle (ventricles eject blood).

Diastole

Relaxation/filling phase of the cardiac cycle.

End-diastolic volume (EDV)

Volume of blood in a ventricle at the end of diastole (~120 mL at rest, just before contraction).

End-systolic volume (ESV)

Volume of blood left in a ventricle after systole (~50 mL).

Stroke volume (SV)

Volume of blood pumped by a ventricle per beat. SV = EDV − ESV.

Cardiac output (CO)

Volume of blood pumped by a ventricle per minute. CO = SV × heart rate.

Venous return

Rate at which blood returns to the right atrium; determines EDV.

Ejection fraction (EF)

Percent of EDV ejected per beat. EF = (SV / EDV) × 100.

Order of blood vessels in the systemic circuit

Heart → aorta → arteries → arterioles → capillaries → venules → veins → vena cava → heart.

Pathway of blood through the heart (full)

Vena cava → right atrium → tricuspid valve → right ventricle → pulmonary valve → pulmonary artery → lungs → pulmonary veins → left atrium → mitral (bicuspid) valve → left ventricle → aortic valve → aorta → body.

Which side of the heart serves which circuit?

Right side → pulmonary circuit (to lungs). Left side → systemic circuit (to body).

Blood flow and pressure gradient

Blood always flows down its pressure gradient (high to low). Flow is proportional to the pressure difference (ΔP) between two points. Flow = ΔP / R.

Radius and resistance relationship

Resistance is proportional to 1/r^4. Small changes in radius cause huge changes in resistance and flow.

If a vessel's radius is cut in half, what happens to resistance?

Resistance increases 16-fold (2^4 = 16). If radius doubles, resistance drops to 1/16.

Real-life importance of vessel diameter changes

Redirects blood flow (e.g., to muscles during exercise), regulates blood pressure, and helps with temperature control (skin vasodilation releases heat).

Function of heart valves

One-way doors that keep blood flowing forward and prevent backflow.

Why is an "incompetent" (leaky) valve bad?

Blood leaks backward, so the heart must pump the same blood repeatedly. Less forward output and extra workload on the heart.

Two sets of heart valves

AV valves (tricuspid, mitral/bicuspid) between atria and ventricles; semilunar valves (pulmonary, aortic) between ventricles and arteries.

Why are cardiac muscle cells connected by gap junctions?

They let ions and electrical signals pass directly between cells, so the heart contracts as a coordinated unit.

Intercalated discs

Specialized junctions connecting cardiac muscle cells (contain gap junctions and desmosomes).

How can heart cells generate action potentials on their own?

Autorhythmic pacemaker cells (SA node) have an unstable resting potential that drifts to threshold spontaneously.

Path of electrical conduction in the heart

SA node → atria → AV node (delay) → AV bundle (bundle of His) → bundle branches → Purkinje fibers → ventricles.

Natural pacemaker of the heart

SA (sinoatrial) node.

Function of the AV node delay

Slows the signal so the atria finish contracting and filling the ventricles before the ventricles contract.

P wave

Atrial depolarization (followed by atrial contraction).

PR segment

Flat segment between P and QRS; AV node conduction delay.

QRS complex

Ventricular depolarization (followed by ventricular contraction). Atrial repolarization is hidden within it.

ST segment

Ventricles are fully depolarized and contracting (plateau phase); ejecting blood.

T wave

Ventricular repolarization (ventricles relax).

First heart sound (S1, "lub")

AV valves closing at the start of ventricular systole.

Second heart sound (S2, "dub")

Semilunar valves closing at the end of ventricular systole.

Cardiac cycle: ventricular filling phase

AV valves open, semilunar valves closed; blood flows from veins into atria and ventricles; atrial contraction tops off ventricular filling.

Cardiac cycle: isovolumetric contraction

Ventricles contract with ALL valves closed; pressure rises but volume does not change.

Cardiac cycle: ejection

Ventricular pressure exceeds aortic pressure, semilunar valve opens, blood ejected into the aorta.

Cardiac cycle: isovolumetric relaxation

Ventricles relax with all valves closed; pressure falls until AV valves open.

Dicrotic notch

Small bump in aortic pressure curve when the aortic valve closes.

How does increased venous return affect cardiac output?

More venous return → greater EDV → ventricle stretches more → stronger contraction (Frank-Starling) → greater SV → greater CO.

How does sympathetic stimulation affect the heart?

Increases heart rate and contractility (stroke volume), so cardiac output increases.

How does parasympathetic (vagal) stimulation affect the heart?

Decreases heart rate, so cardiac output decreases.

Factors that increase cardiac output

Higher heart rate, higher stroke volume, higher venous return/blood volume, sympathetic activity (e.g., exercise).

Factors that affect venous return

Skeletal muscle pump, respiratory pump, venoconstriction (sympathetic), valves in veins, blood volume.

Arteriole

Small branch of an artery; main site of regulation of blood flow and peripheral resistance (has a smooth muscle layer).

Venule

Small vessel that collects blood from capillaries and drains into veins.

Endothelium

Smooth single-cell lining of all blood vessels.

Three types of capillaries

Continuous (least leaky), fenestrated (pores), sinusoid (largest gaps, discontinuous).

Continuous capillary

Tight junctions with small gaps; allows small molecules through. Found in muscle, skin, brain (very tight in brain).

Fenestrated capillary

Capillary with pores (fenestrations) for rapid movement of fluid and larger solutes. Found in kidney, small intestine, and endocrine glands.

Why are fenestrated capillaries found in the kidney and intestine?

Those organs need to filter or absorb large volumes of fluid and solutes quickly.

Sinusoid capillary

Very leaky capillary with large gaps; allows cells and proteins through. Found in liver, spleen, bone marrow.

Angiogenesis

Growth of new blood vessels from existing vessels.

Atherosclerosis

Buildup of fatty plaque and hardening in artery walls that narrows and stiffens arteries.

Coronary heart disease

Narrowing or blockage of coronary arteries (often from atherosclerosis), reducing blood and O2 supply to heart muscle (chest pain, heart attack).

Systolic pressure

Peak arterial pressure during ventricular contraction (~120 mm Hg).

Diastolic pressure

Lowest arterial pressure during ventricular relaxation (~80 mm Hg).

Pulse pressure

Systolic pressure − diastolic pressure.

Mean arterial pressure (MAP)

Average driving pressure in the arteries. MAP = diastolic + 1/3 (systolic − diastolic).

Calculate MAP: BP = 120/80

MAP = 80 + 1/3(120 − 80) = 80 + 13.3 ≈ 93 mm Hg.

Peripheral resistance

Resistance to flow in the systemic circuit, mostly set by arteriole diameter.

Baroreceptors

Stretch-sensitive receptors in the carotid sinuses and aortic arch that monitor arterial blood pressure (MAP).

Baroreceptor reflex: blood pressure too HIGH

Baroreceptors stretch more, signals to medulla → decreased sympathetic and increased parasympathetic → lower heart rate, lower contractility, vasodilation → BP falls.

Baroreceptor reflex: blood pressure too LOW

Less stretch, fewer signals to medulla → increased sympathetic and decreased parasympathetic → higher heart rate, stronger contraction, vasoconstriction → BP rises.

Where is the cardiovascular control center?

Medulla oblongata.

How do the kidneys adjust blood pressure over minutes to hours?

By changing how much water is retained or excreted, which changes blood volume → venous return → SV → cardiac output → BP.

Effect of increased HR, SV, blood volume, venous return, or vasoconstriction on blood pressure

Each one INCREASES blood pressure (and decreases do the opposite).

Sympathetic control of arterioles

Norepinephrine acts on alpha-1 receptors → vasoconstriction (e.g., digestive tract, skin, kidneys). Less NE → vasodilation.

Where does the sympathetic system dilate vs constrict vessels (fight or flight)?

Constrict: digestive organs, kidneys, skin. Dilate: skeletal muscle (and heart, brain maintained) to supply more blood where it is needed.

Sympathetic tone

Baseline level of sympathetic activity on arterioles; lets vessels dilate (tone decreases) or constrict (tone increases).

Structure of arteries vs veins

Arteries: thick, muscular, elastic walls to handle high pressure. Veins: thinner walls, less smooth muscle, larger diameter, hold most blood volume, valves.

Structure of capillaries

Single layer of endothelial cells on a basement membrane (no smooth muscle); thin for exchange.

Where is blood flow fastest and slowest?

Fastest in the aorta/arteries (small total cross-sectional area). Slowest in capillaries (largest total cross-sectional area).

Why is slow flow in capillaries a good thing?

Gives time for exchange of gases, nutrients, and wastes between blood and tissue.

Major functions of the lymphatic system

(1) Returns excess interstitial fluid and proteins to the blood, (2) absorbs fat from the small intestine, (3) filters pathogens (immune function).

Ventilation

Movement of air into and out of the lungs.

Inspiration

Air flowing into the lungs; caused by contraction of the diaphragm and external intercostal muscles expanding the thoracic cavity.

Expiration

Air flowing out of the lungs; at rest it is passive (muscles relax and lungs recoil).

Alveoli

Tiny air sacs at the end of the airways where gas exchange with pulmonary capillaries occurs.

Diaphragm

Dome-shaped skeletal muscle under the lungs; contracts and flattens (moves down) during inspiration.

Pleura

Membrane around the lungs; fluid between layers keeps the lungs stuck to the chest wall so they expand with it.

Surfactant

Substance secreted in alveoli that reduces surface tension and prevents alveoli from collapsing.

Partial pressure

Pressure exerted by one gas within a mixture of gases (proportional to its concentration).

Tidal volume (TV)

Volume of air moved in or out of the lungs in one normal breath (~500 mL).

Inspiratory reserve volume (IRV)

Extra air that can be forcibly inhaled after a normal inspiration.

Expiratory reserve volume (ERV)

Extra air that can be forcibly exhaled after a normal expiration.

Residual volume (RV)

Air remaining in the lungs after a maximal exhalation; cannot be exhaled (keeps alveoli from collapsing).