physio exam 3

Flow definition

Volume per unit time

Velocity definition

Distance per unit time

Velocity equation

Velocity = Flow ÷ Area

Where velocity fastest

Aorta (small total cross-sectional area)

Where velocity slowest

Capillaries (largest total area)

Why capillary velocity is slow

Allows time for exchange

Driving force of blood flow

Pressure gradient (ΔP)

Flow equation

Flow = ΔP / Resistance

What increases flow

↑Pressure or ↓Resistance

Main resistance factor

Radius (∝ 1/r⁴)

Other resistance factors

Length and viscosity

Thick filament

Myosin

Thin filaments

Actin, troponin, tropomyosin

Sarcomere

Contractile unit from Z disk to Z disk

A band

Length of thick filament

I band

Thin filament only

H zone

Thick filament only

What shortens

Sarcomere, I band, H zone

What stays constant

A band

Sliding filament theory

Actin and myosin slide past each other

What blocks binding

Tropomyosin

What exposes binding

Ca²⁺ binds troponin

Power stroke

Myosin pulls actin when Pi released

Rigor state

Myosin stuck without ATP

Excitation-contraction coupling

ACh → AP → Ca²⁺ release → contraction

DHP receptor

Voltage sensor in T-tubule

RyR receptor

Releases Ca²⁺ from SR

Relaxation

Ca²⁺ pumped back into SR

Skeletal muscle control

Somatic motor neurons

Cardiac muscle control

Autonomic + hormones

Cardiac vs skeletal

Both striated and use actin/myosin

Cardiac unique features

Gap junctions, autorhythmic cells

Why cardiac cannot tetanize

Long refractory period

Left heart blood flow

LA → mitral → LV → aorta

Right heart blood flow

RA → tricuspid → RV → pulmonary artery → lungs

Valve function

Ensure one-way flow

AV valves

Prevent backflow into atria

Semilunar valves

Prevent backflow into ventricles

Electrical pathway

SA → AV → bundle of His → bundle branches → Purkinje

Pacemaker

SA node

Funny channels

Allow Na⁺ and K⁺ influx

Function of funny channels

Create pacemaker potential

Pacemaker AP

Unstable resting potential

Pacemaker depolarization

Ca²⁺ influx

Pacemaker repolarization

K⁺ efflux

Contractile depolarization

Na⁺ influx

Plateau phase

Ca²⁺ influx

Repolarization

K⁺ efflux

P wave

Atrial depolarization

QRS complex

Ventricular depolarization

T wave

Ventricular repolarization

Arrhythmia

Abnormal rhythm

Tachycardia

Fast heart rate

Bradycardia

Slow heart rate

S1 sound

AV valves closing

S2 sound

Semilunar valves closing

EDV

Volume before contraction

ESV

Volume after contraction

Stroke volume

SV = EDV − ESV

Cardiac output

CO = HR × SV

Normal CO

~5 L/min

Systolic pressure

Pressure during contraction

Diastolic pressure

Pressure during relaxation

Pulse pressure

Systolic − diastolic

MAP

Diastolic + 1/3(pulse pressure)

Blood pressure determinants

Cardiac output + resistance

What increases BP

↑Volume or ↑Resistance

Venous return

Blood returning to heart

What increases venous return

Muscle pump, respiratory pump, sympathetic tone

Local control of flow

NO, CO₂, metabolites cause vasodilation

Systemic control

Baroreceptors and nervous system

Upper respiratory tract

Nose, pharynx, larynx

Lower respiratory tract

Trachea, bronchi, bronchioles, alveoli

Gas exchange location

Alveoli

Gas exchange mechanism

Diffusion

Driving force for gas exchange

Partial pressure gradients

Type I alveolar cells

Gas exchange

Type II alveolar cells

Produce surfactant

Surfactant function

Reduces surface tension and prevents collapse

Inspiration

Diaphragm contracts, volume ↑, pressure ↓

Expiration

Passive recoil, air flows out

Pleural pressure

Always negative

Respiratory pump

Helps venous return

Boyle’s law

↑Volume → ↓Pressure

Dalton’s law

Total pressure = sum of partial pressures

Pressure-volume loop phases

Filling → isovolumetric contraction → ejection → isovolumetric relaxation

Isovolumetric contraction

All valves closed, pressure ↑, volume constant

Isovolumetric relaxation

All valves closed, pressure ↓, volume constant

Ejection phase

Semilunar valves open, blood leaves ventricle

Filling phase

AV valves open, ventricles fill

When AV valves open

During filling phase

When semilunar valves open

During ejection

Wiggers diagram

Shows pressure, volume, ECG, and heart sounds over time

When S1 occurs in Wiggers diagram

AV valves close (start of systole)

When S2 occurs in Wiggers diagram

Semilunar valves close (end of systole)

Aortic pressure

Rises during ejection, falls after

Ventricular pressure

Rises in systole, falls in diastole

Atrial pressure

Small changes with filling and contraction

Ventricular volume

Increases during filling, decreases during ejection

PR interval

Time from atrial depolarization to ventricular depolarization (AV delay)