human physiology exam three

Velocity vs flow

Flow = volume/time, velocity = distance/time

Velocity vs area

Velocity = Flow ÷ Area (↑area → ↓velocity)

Fastest velocity

Aorta (smallest total cross-sectional area)

Slowest velocity

Capillaries (largest area allows exchange)

Driving force of flow

Pressure gradient (ΔP)

Flow equation

Flow = ΔP / Resistance

What is the most important factor affecting blood flow resistance?

Radius (∝ 1/r⁴)

Other factors affecting resistance

vessel length and blood viscosity

Sarcomere

Contractile unit from Z line to Z line

A band

Region of the sarcomere containing thick filaments (myosin) that does not change length during contraction

I band

Thin filament region that shortens during contraction

H zone

region of thick filaments only (no overlap) — shortens during contraction

What shortens (during contraction)

Sarcomere, I band, H zone

What part of the sarcomere does NOT change length during contraction?

A band

Blocking protein in muscle

Tropomyosin

Exposing mechanism

Ca²⁺ binds to troponin, causing tropomyosin to move and expose myosin-binding sites on actin

Thick filament protein

Myosin

Thin filament proteins

Actin, troponin, tropomyosin

skeletal vs cardiac muscle

Skeletal is voluntary, multinucleated, and independent, while cardiac is involuntary, branched, has gap junctions, and contracts together

What are the three factors affecting stroke volume

Preload (ventricular filling), afterload (resistance to ejection), and contractility (strength of contraction)

Cardiac connection

Gap junctions let ions pass between cardiac cells → rapid signal spread → coordinated contraction (functional syncytium).

Cardiac fatigue resistance

high mitochondrial content and continuous oxygen-rich blood supply

Excitation-contraction coupling

Electrical depolarization triggers Ca²⁺ influx and release from the sarcoplasmic reticulum, leading to muscle contraction

First step (pacemaker potential)

Slow Na⁺ influx through funny channels initiates pacemaker depolarization

AP propagation

The action potential spreads along the sarcolemma and down T-tubules to trigger muscle contraction

What triggers Ca²⁺ release from the SR?

Ca²⁺ influx → opens ryanodine receptors → SR releases more Ca²⁺

Ca²⁺ role in muscle contraction

Binds troponin → exposes myosin binding sites

Blood flow through heart

body —> vena cava —> right atrium —> tricuspid → right ventricle —> pulmonary valve —> pulmonary artery —> lungs —> pulmonary veins —> left atrium —> bicuspid —> left ventricle —> aortic valve —> aorta —> body

Valve function

Ensure one-way flow and prevent backflow

What determines when heart valves open and close?

Heart valves open and close based on pressure differences between chambers

Funny channels

Slow Na⁺ influx in SA node

Pacemaker mechanism

Spontaneous depolarization in SA node cells due to funny Na⁺ channels that slowly bring the membrane to threshold, followed by Ca²⁺ influx causing an action potential

Pacemaker vs contractile AP

Pacemaker cells have unstable resting potential and automatic depolarization, while contractile cells have stable resting potential with fast Na⁺ depolarization and a Ca²⁺ plateau

Pacemaker depolarization

Ca²⁺ influx via L-type Ca²⁺ channels (slow upstroke)

What ion causes depolarization in cardiac contractile cells?

Na⁺ influx

Plateau phase

Ca²⁺ influx balances K⁺ efflux → membrane potential stays stable (in cardiac contractile cells)

P wave

Atrial depolarization

QRS complex

ventricular depolarization (atrial repolarization is hidden)

T wave

Ventricular repolarization when the ventricles relax

PR interval

Time from start of P wave to start of QRS, representing AV node delay

Normal PR

0.12–0.20 s

Normal QRS

0.06–0.12 s

No P waves

Atrial fibrillation

Long PR interval

Heart block

Wide QRS

Delayed ventricular conduction

S1

First heart sound caused by closure of the AV valves, marking the start of systole (LUB)

S2 heart sound

Closure of semilunar (aortic and pulmonary) valves marking the start of ventricular diastole (DUB)

Electrical pathway

SA node → AV node → bundle of His → Purkinje fibers

AV node delay

Allows ventricular filling

Pressure-volume loop

Graph of ventricular pressure vs volume showing filling, contraction, ejection, and relaxation

EDV

Max ventricular filling

ESV

Volume after contraction

Stroke volume

Stroke volume is the amount of blood ejected by one ventricle with each heartbeat (SV = EDV − ESV)

Isovolumetric contraction

Phase of the cardiac cycle where ventricular pressure increases while volume remains the same because all valves are closed

Ejection phase

Volume decreases as blood leaves

Isovolumetric relaxation

Pressure decreases volume same

Wiggers events

QRS marks start of ventricular contraction, S1 is AV valve closure, T wave marks ventricular relaxation, and S2 is semilunar valve closure

Stroke volume factors

Preload, contractility, afterload

Preload

degree of ventricular stretch at end-diastole (depends on venous return)

Contractility

Strength of heart contraction independent of preload and dependent on Ca²⁺

Afterload

The pressure or resistance that the ventricles must overcome in order to eject blood into the arteries, mainly determined by arterial blood pressure (especially aortic pressure)

Cardiac output

CO = SV × HR

Systolic pressure

Pressure during contraction

Diastolic pressure

Pressure during relaxation

Pulse pressure

The difference between systolic and diastolic blood pressure (systolic − diastolic)

MAP

MAP = DBP + 1/3 (SBP − DBP)

BP factors

CO, resistance, blood volume, vessel elasticity

Venous return

The flow of blood returning to the heart through the veins, which determines how much the ventricles fill (preload)

Effect of an increase in venous return

increase preload → increase stroke volume

Systemic control

brain + hormones control blood vessels to regulate blood pressure

Local control

Blood flow is regulated by tissue metabolic needs (e.g., O₂ ↓, CO₂ ↑) causing vasodilation or vasoconstriction

Upper respiratory tract

nose, nasal cavity, paranasal sinuses, and pharynx

Lower respiratory tract

Trachea, bronchi, bronchioles, and lungs (including alveoli)

Gas exchange location

Alveoli

Gas exchange mechanism

Diffusion

Driving force

Partial pressure gradients

O₂ movement

Alveoli → blood

CO₂ movement

Blood → alveoli

Type I alveolar cells

Thin cells specialized for gas exchange by diffusion across the alveolar membrane

Type II alveolar cells

produce surfactant

Surfactant

Reduces surface tension

Respiratory pump

Breathing changes thoracic pressure to enhance venous return to the heart

Alveolar pressure rest

0 cm H₂O

Pleural pressure rest

Negative

Inspiration

Alveolar pressure decreases - air flows in

Expiration

Alveolar pressure increases - air flows out