Cardiac Output

CO

SV dependent on force of contraction and can vary force.

Amount of blood pumped out is proportional to blood returning.

More blood returning stretches heart muscles more (Preload). Increases contraction force and increases SV (Afterload).

Frank-Starling Mechanism

Increasing stretch increases force

Optimal length in skeletal muscles for maximal force. Resting heart is not at optimal length. Contraction force can also affect SNS and PNS activity.

PNS and SNS on the Heart

Innervates the heart.

Influence pumping action by affecting HR & SV.

Maintains BP, O2 & CO2, and pH levels

PNS

Vagus nerve carries PNS fibers to heart. Innervates the SA node. Pacemaker.

PNS neurons produce ACh which binds to ionotropic receptors on cardiac cells and cause K+ efflux and cell hyperpolarization. Decreases Na+ permeability & Ca2+ which means it takes longer to depolarize and leads to decreased HR.

AChR2 in the Heart: M2

M2 muscarinic receptors in heart act to slow HR to normal sinus after stimulation of sympathetic system. Slows depolarization speed.

SNS on the Heart

Sympathetic nerves from thoracic region project to the heart as cardiac nerves

Innervates SA and AV nodes, Coronary vessels and atrial and ventricular myocardiums.

Stimulation increases HR and contractino force

Regulation

Sympathetic - Catecholamines

• Main NT in SNS are norepi and epi

• Catecholamines derived from tyrosine. Hormones or NTs.

• Epi derived/made from norepi

• Catecholamines bind to alpha and beta adrenergic receptors

• Adrenergic neurons secrete adrenergic NTs

  • Norepi-secreting neurons are noradrenergic

Norepinephrine

NT from SNS. Postganglionic sympathetic neurons

Increases rate & degree of cardiac muscle depolarization

increases AP frequency & force and velocity of contraction

Agonist for cell surface beta-andrenergic receptors

G-protein mediated synthesis. Accumulation of cAMP in cardiac cells

Opens Ca2+ slow channels and increases ability to depolarize

Also helps open Na+ channels

Epinephrine

Hormone from the adrenal medulla.

Basically same effect as norepinephrine

Conversion of norepi & epi:

Increases CO and blood glucose

Increases activity, excitement, stress → sympathetic stimulation of cardio-regulating center in medulla

Causes heart sympathetic stimulation and adrenal gland secretes epi and norepi into blood

Transported in blood to cardiac muscles and binds to beta-adrenergic receptors

Epi & Norepi Effects

Preps for fight or flight and increases BP HR and up-regulates blood & oxygen supply to muscles

Causes shorter and stronger beats

1. Affects Ca2+ channels into cell

2. Affects Ca2+ channels out sarcoplasmic reticulum

3. Affects Ca2+ troponin interactions

4. Affects Ca2+ reuptake into sarcoplasmic reticulum

Faster Ca2+-troponin interactions mean faster heart contractions which leads to more completely emptying of the heart and increasing SV