Cardiac Physiology

Heart rate (HR)

number of cardiac cycles completed in one minute, expressed as b/min (avg at rest:  60-80 b/min)

Stroke Volume (SV)

volume of blood ejected by EACH ventricle per beat (avg at rest:  70 ml/beat)  - each ventricle should eject an equal amount 

Cardiac output (CO/Q)

volume of blood ejected by EACH ventricle per minute (avg at rest:  5000 ml/min or 5 L/min) (HR x SV)

Ejection Fraction (EF):

percentage of blood ejected by (each) ventricle per beat, indicative of pump function  (EF = SV/EDV X 100) (avg at rest:  55-65+%)

Cardiac Index (CI):

cardiac function as indicated by cardiac output divided by body surface area – determined from charts – estimates used as indicator of pump function in critical care units (clinical unit) (avg at rest:  2.8–4.2)

Diastole

relaxation of myocardium

Systole

contraction of myocardium

Cardiac mechanical cycle:

normal cycle = .7-.8 seconds

Cycle stages:

Early systole, late systole, early diastole, mid-diastole, late diastole

Early systole

depolarization from AV to ventricles → contraction begins → AV valves close “Lub” → semilunar valves remain closed briefly → isometric contraction

Late systole

ventricular pressure is greater than aortic / pulomary pressure → SL valves open → ejection occurs → leaves small amount of blood in ventricals = ESV (end systole volume -amount of blood remaining in ventricles after contraction ~ 50-60 ml)

Early diastole

wave of repolarization to relaxation so then ventircular pressure is less than atrial pressure → SL valves close “Dub” → isovolumetric relaxation while all the valves are closed → continues until atrial pressure is greater than ventricular pressure causing AV valves to open (70-80% of total volume)

Mid-diastole

Phase of slow ventricular filling atria & ventricles are relaxed, the AV valves remain open while the SL are closed.

Late diastole

Atrial systole occurs here, delivering the final 20% of blood = EDV (amount of blood in each ventricle at the end of ventricular diastole / rest) = 120-130 ml

Normal CO

5.25 L/min, maximal CO 4-5 times resting CO in nonathletic people, whereas athletes may reach 35 L/min.

Factors effecting stroke volume

1) preload, contractility, afterload

Preload

amount othat ventricles are stretched by contained blood (dependent on venous return)

→ contributes to contractility

Frank-Starling law of the heart

more stretch in cardiac muscle cells = greater contraction force due to optimal actin/myosin overlap

Contractility

• cardiac cell contractile availability due to interaction at cross bridges of myofilaments

• dependent on increased calcium availability and increased sympathetic nervous system input

• changes in force of contraction occuring is INDEPENDENT of myocardial muscle fiber length (ie. preload)

Drugs that affected contractility (iontropics)

adrenergics (+), B-blockers (-), Ca2+ channel blockers (-)

Afterload

back pressure exerted by blood in the large arteries leaving the heart (just the pressure that has to be overcome)

What effects afterload?

if arterial pressure increases → afterload increases

If afterload increases → stroke volume decreases

if aortic / pulonary pressure increase → afterload increases

if ventricle radius increases → afterload increases

if ventricle thickness increases → afterload decreases

Which cycle directs which?

The electrical cycle is directing the mechanical cycle

SA (sinoatrial) node (pacemakrer)

generates impulses about 75 times/min (sinus rythm), depolarizes faster than any other part of the myocardium

AV node

• smaller diameter fibers, fewer gap junctions (dont want it to contract at AV node bc we dont want blood coming out from the bottom of the heart we need it bottom up)

• delays impulses approximately .1 second (to allow for increased time for the ventircles to fill)

• depolarizes 50 time/min

AV buncle (bundle of his)

only electrical connection between the atria and the ventricles

R and L buncle branches

two pathways in the interventricular spetum that carry the impulses toward the apex of the heart.

Purjunke fibers

completes the pathway into the apex and ventricular walls

depolarize at 30 times per minute in absence of AV node input

Cardiac muscle

self excitable and contracts as a unit

• has a long (250 ms) absolute refractory period

Autorhythmic cells

all myocites are autorthymic measning they initiate action potentials

they contain unstable resting potentials (pacemaker potentials)

use Ca2+ influx for rising phase of action potential

Cardiac Muscle Contraction steps

1) calcium influx triggers openning of calcium channels in the SR, liberating burts of calcium

2) ca2+ binds to toponin and sliding of the filaments begin

3) duration of AP and contractile phase is much greater in cardiac muscle than skeltal

4) repolarization results from inactivation of ca2+ channels and opening of voltage gated K+ channels

Homeostatic imbalances can lead to..

1) Arrhythmias (irregular heart rhythms)

2) Uncoordinated atrial and ventricular contractions

3) Fibrillation (rapid, irregular contractions useless for pumping blood)

Ectopic focus

abnormal pacemaker takes over

Defective SA node can result in?

ectopic focus or AV node takes over (junctional rythm of 40-60bpm)

Defective AV node results in?

• partial or total heart block

• few or no impulses from SA node reach the ventricles

Where are cardiac centers located in the brain?

Medulla oblongata

P wave

depolarization of SA node

QRS complex

ventricular depolarization

T wave

ventricular repolarization

Absolute / effective refractory period (ERP)

Portion of AP during which cardiac cells are completely insensitve to further electrical stimulation (and thus mechanical systole)

• protective mechnism to prevent uncontrolled ventricular contraction