cardiac cells are interconnected allowing the action potential spreads when one cell becomes excited.

Intercalated disc of the cell membranes are fused

with one another = gap junctions

Opening of 2 channels:

1. Opening of fast sodium channels 

2. slow opening of slow calcium channels or calcium-sodium channels (stay opening for several tenths of a second)

large quantities of Ca and Na ions into the interior of the cardiac muscle fiber allow for prolonged periods of depolarization

Ca ions that enter during the plateau phase activate the muscle contractile phase

0.05sec 

the muscle is more difficult than normal to excite, but can be excited by a strong excitatory signal

action potential->membrane of transverse (T) tubules->longitudinal sarcoplasmic tubules->release of Ca -> into muscle sarcoplasm -> into myofibrils -> catalyze the chemical reactions ->sliding of actin-myosin filaments

Large amts of Ca ions from the T tubules and SR

Strength of contraction cardiac muscle = concentration of Ca ions in ECF

atrium 0.2 seconds

ventricle 0.3 seconds

spread of depolarization through the atria and followed by atrial contraction

slight rise in atrial pressure curve immediately after P wave

0.16 seconds after onset of P wave

result of depolarization of the ventricles

begins slightly before the onset of ventricular systole

repolarization of the ventricles

Occurs before the end of ventricular contraction

 - lg amts of blood accumulate in R & L atria bc of closed AV valves

 - when systole is over, the ventricular pressures fall 

 - increased pressure in the atria cause AV valves to open

1st 1/3 diastole = rapid filling

2nd 1/3 diastole = small amt of blood of flows

3rd 1/3 diastole = atria contracts

1. period of isovolumic (isometric) contraction

2. Period of ejection

3. period of isovolumic (isometric) relaxation

4. End-diastole volume, end-systolic volume, & Stroke volume output

-after ventricle contraction begins, pressure increases, causing AV valve to close

-Tension increases in the muscle but little or no shortening of the muscle fibers is occuring 

-LV pressure rises about 80mmHg & RV pressure rises about 8mmHg

-semilunar valves open

-65-70% empties during the first 1/3 of period = rapid ejection

-30% during last 2/3 = slow ejection

-end of systole

- R & L intraventricular pressures decrease rapidly

- AV valves close

-normal filling of the ventricles increases the volume of each ventricle to about 110 - 120 ml = end-diastolic volume

 - ventricles empty during systole, the volume decreases to about 70ml = stroke volume output

-the remaining volume in each ventricle, about 40-50 ml = end systolic volume

the fraction of the EDV that is ejected

usually about 60%

AV valve

aka tricuspid valve

aka mitral valve

-papillary muscles contract when the ventricular walls contract

-they pull the vanes of the vavles inward toward the ventricles to prevent their buildging too far back toward the atria during ventricular contraction

-aortic and pulmonary artery semilunar valves

-high pressures in the arteries at the end of the systole cause the semilunar valves to snap closed

-velocity of blood ejection through the semilunar valves is far greater than through larger AV valves

-constructed with pliable fibrous tissue

-occurs on the aortic pressure curve when the aortic valve closes and backflow of blood is stopped

-closing of the AV valves during ventricular contraction

-lower in pitch, longer

-closing of semilunar valves

-at the end of systole, rapid snap

the total amount of energy converted to work in 1 minute

MW=SWxHR

1. a major proportion is used to move the blood from the low pressure veins to the high pressure arteries (volume-pressure work or external work)

2. a minor proportion of the energy is used to accelerate the blood to its velocity of ejection into arteries through semilunar valves (kinetic energy of blood flow)

Phase 1 - period of filling

Phase 2 - period isovolumic contraction

Phase 3 - Period of ejection

Phase 4 - Period of isovolumic relaxation

the degree of tension on the muscle when it begins to contract

- considered the end-diastolic pressure when the ventricle becomes filled

to specify the load against which the muscle exerts its contractile force

- afterload of the ventricle is the pressure in the artery leading from the ventricle

-chemical energy is used to provide the work of contraction

-derived from oxidative metabolism of fatty acids using oxygen

-during contraction, expended chemical energy is converted to heat and a small amt of work output

the ratio of work output to total chemical energy expenditure

-maximum efficiency of the normal heart is btw 20 - 25%

-the intrinsic ability of the heart to adapt to increasing volumes of inflowing blood

-the greater the heart muscle is stretched during filing, the greater the force of the contraction & the greater the quanitity of blood pumped into the aorta

-the cardiac output can be increased more than 100% by sympathetic stimulation

-can increase the HR from 70 bpm to 180 - 200

-increases the force of the heart contraction to as much as double which increases the volume of blood pumped and ejection pressure

-can increase maximum cardiac output as much as two - three fold 

-cardiac output can be decreased to as low as zero

-can stop the heart for a few seconds

-can decrease the strength of the heart muscle contractions by 20 - 30%

-the great decrease in HR combined with slight decrease in heart contraction strength can decrease ventricular pumping by 50%+

-causes heart to bc dilated and flaccid -> slows the HR

-lg amts can block the conduction through the AV bundle >8mEq/L = cause weakness of the heart & abnormal rhythm = death

-opposite of K effects

-increased activity ->spastic contractions

-spastic contractions ->lower Ca ions -> cardiac flaccidity