Equations and OO stuff

Air flow

Palveolar - patmospheric / resistance

Minute ventilation

TV X RR

TLC

IRV+ERV+TV+RV

MAP

CO x TPR

DBP + 1/3(SBP-DBP)

1/3 PP+DBP

Flow

Pressure gradient/resistance of blood vessels

CO

HR x SV

Ejection fraction

SV/EDV x 100

SV

EDV-ESV

SV (including EDV and stuff)

extrafusal fiber

Alpha motor neuron (Ach nicotinic receptor)

Intrafusal

gamma neuron

spindles

stretch and length

more tension

more xbridges, more AP’s, more ca

(if maximally generating tension: motor unit recruitment)

Role of ATP for muscle contraction

1.Release myosin head from actin

2.Provides ADP and Pi which powers the power stroke

3.Movement of calcium back to the SR (calcium ATP pump)

load > tension

Isometric

Still forming xbridges, just attaching and reattaching to the same spot

tension> load

can lift object

Latent period

AP has arrived, takes time for SR to release ca

Summation

Send more ca before relaxed

Muscle relaxer

Ach inhibitor

slow, fast fibers telling you what

how fast they twitch

High intensity vs low intensity

High intensity: more carbs

Low intensity: more fats

Use fibers in what order

type I

type IIa

type IIx

golgi tendon organs detect too much stretch

they contract in the antagonist muscle

Smooth muscle innervated by

ANS

plasma protein NTK

Albumin

more EDV

more stretch

Frank starling effect

To increase contractility

1.Frank starling effect

2.SNS using Epi

Frank starling effect

Process of increased contractility

TPR

how dilated/constricted a vessel is

Increase FSE

Increased contractility, increased SV, increased CO, increased MAP

Laying down

Greatest venous return because of gravity

Afterload

Pressure causing the valve to have a harder time opening

Major resistance vessels

Arterioles

Resistance increases what happens to afterload

Increases, SV decreases

TPR increases

Afterload increases, SV decreases, CO decreases

HR max

220-age

208-.7xage

Heart failure

Inability to eject enough blood

Poor venous valves

decreased preload, decreased EDV, decreased SV, decreased CO

If heart not ejecting enough blood which valves should you be thinking

AV

Starling forces

Fluid exchange

Dilate vessels

Less pressure

Constrict arterioles

More pressure

What dilates vessels extrinsically

1.SNS

2.Angiotensin II

3.Vasopressin/ADH

What dilates vessels intrinsically

nitric oxide

Bohr effect

Increased metabolites, increased unloading of O2 at the tissue level

Increased metabolism

Shift to the right - unload more o2

CO2 transport

Tissue into blood, enters erythrocyte, meets up with water, Co2 and water, transferred into carbonic acid by enzyme carbonic anhydrase, dissociates into bicarbonate and H ion, H ion moves onto hemoglobin (what binds to heme sites in hglob? Oxygen) bicarbonate circulates in lungs, goes back into RBC, meets up with H, those two convert back to carbonic acid, carbonic acid back to co2 and water is carbonic anhydrase.

To buffer pH

Central chemoreceptors

• Increased CO₂ → increased H⁺ → decreased pH → increased ventilation.

Remember: Central chemoreceptors primarily respond to changes in CO₂ (through H⁺)

Peripheral chemoreceptors

• Detect:

  • Decreased arterial PO₂ (low oxygen)

  • Increased arterial PCO₂

  • Increased arterial H⁺ (decreased pH)

These stimulate increased ventilation.

Remember: Peripheral chemoreceptors detect O₂, CO₂, and H⁺ in arterial blood.

Increase in H, CO2

Increased minute ventilation

Decreased in O2

Increased minute ventilation

Compliance vs elasticity

Compliance: stretch

Elasticity: stretch and return to original shape

type i alveoli

gas exchange

autorhythmic cells where

SA/AV node

Cardiac/skeletal need to phosphorylate?

no. only smooth muscle

fibrin

polymer that forms clot

what detaches xbridge

ATP

what breaks atp to adp and pi

ATPase

VC

IRV+TV+ERV

Diaphragm contracts

Volume increases, pressure decreases

Inspiration

Two things that keep lungs from collapsing

Surfactant

RV