HeartPrepared by Dr F.NikbakhtAssistant professor of Medical school

Cardiac muscle

Cardiac Muscle

Sinus node and the Purkinje system of the heart, showing also the A-V node, atrial internodal pathways, and ventricular bundle branches

Organization of the A-V node. The numbers represent the interval of time from the origin of the impulse in the sinus node. The values have been extrapolated

to human beings .

Transmission of the cardiac impulse through the heart, showing the time of appearance (in fractions of a second after initial appearance at the sinoatrial

node) in different parts of the heart .

Rhythmical action potentials (in millivolts) from a Purkinje fiber and from a ventricular muscle fiber, recorded by means of microelectrodes

Rhythmical discharge of a sinus nodal fiber. Also, the sinus nodal action potential is compared with that of a ventricular muscle fiber .

Force of ventricular heart muscle contraction, showing also duration of the

refractory period and relative refractory period, plus the effect of premature

contraction. Note that premature contractions do not cause wave summation, as

occurs in skeletal muscle.

Denervated HeartHeart Rate ~100/min (Intrinsic Heart Rate)

Parasympathetic Nervous System)PNS: Vagus Nerve(

Could Decrease HR to Zero (Cardiac Arrest)

Sympathetic Nervous System)SNS: Cardiac Nerves(

Could Increase HR by 300%

Normal HR (~72/min) Is dominated by PNS

Parasympathetic NS,Inhibits cardiac APs

Sympathetic NS stimulates cardiac APs

Vagal Nerve Terminals

Neurotransmitter = Acetylcholine

Muscarinic Receptors

K Channels

Hyperpolarization

Longer time to reach threshold (Slower Heart Rate)

Sympathetic Nerve Terminals

Neurotransmitter = Norepinephrine

Beta-adrenergic Receptors

Leak Na Channels

Faster Rate of Spontaneous Depolarization

Faster to reach threshold (Faste Heart Rate)

Conducting System of Heart

Cardiac CycleHeart is two pumps that work together,

right and left halfRepetitive contraction (systole) and

relaxation (diastole) of heart chambersBlood moves through circulatory system

from areas of higher to lower pressure.Contraction of heart produces the pressure

The cardiac cycleThe cardiac cycle

Cardiac cycle

Ejection Fraction = Stroke Volume/End-Diastolic Volume

Ejection Fraction is a measure of cardiac contractility

The pressure-volume loop

Heart SoundsFirst heart sound or “lubb”

Atrioventricular valves and surrounding fluid vibrations as valves close at beginning of ventricular systole

Second heart sound or “dupp”Results from closure of aortic and pulmonary semilunar valves at beginning of ventricular diastole, lasts longer

Third heart sound (occasional)Caused by turbulent blood flow into ventricles and detected near end of first one-third of diastole

Sound Origin

1st sound Closure of mitral and tricuspid valves

2nd sound Closure of aortic and pulmonary valves

3rd sound Rapid ventricular filling in early diastole

4th sound Ventricular filling due to atrial contraction

Regulation of stroke volume & heart rate

Measurement of cardiac outputRegulation of heart rate

neuralRegulation of stroke volume

PreloadAfterloadNeural

Control of cardiac output

Sympathetic nervous system–sympathetic nerves release norepinephrine–plus circulating epinephrine from adrenal

medulla–both act on ß-receptors on sinoatrial node–increases slope of the pacemaker potential –increases heart rate = tachycardia

+25

0

-25

-50

-75

mV

Parasympathetic nervous system–vagus releases ACh –acts on muscarinic receptors on sinoatrial

node–hyperpolarises cells and decreases slope of

pacemaker potential–decreases heart rate = bradycardia

+25

0

-25

-50

-75

mV

Regulation of stroke volume - preload

Starlings Law states - the energy of contraction is proportional to the initial length of the cardiac

muscle fibre

Length

Ten

sion

=)preload(

Regulation of stroke volume - preload

In vivo, preload is affected by the End Diastolic Volume

End Diastolic Volume

Str

oke

Volu

me

Increased venous return, increases EDV, and therefore increases stroke volume = self-

regulation

Resting EDV

Regulation of stroke volume - afterload

Afterload is the load against which the muscle tries to contract

In vivo, afterload is set by the arterial pressure against which the blood is expelled (this in turn

depends on the Total Peripheral Resistance)If TPR increases, stroke volume will go down

Regulation of stroke volume - neural

End Diastolic Volume

Str

oke

Volu

me +sympathetic stimulation

Control of cardiac outputHR increases

via decrease vagal tone & increased sympathetic tone

Contractility increases via increased sympathetic tone alters inotropic state & shortens systole

Venous return increases via venoconstriction & skeletal/respiratory pumps maintains preload

Total peripheral resistance falls due to arteriolar dilation in muscle, skin & heart reduces afterload

CO increase 4-6 times

HR x SV = CO