Refractory period of cardiac Refractory period of cardiac musclemuscle

cardiac muscle has refractory period, cardiac muscle has refractory period, preventing restimulationpreventing restimulation

during this interval, a normal cardiac during this interval, a normal cardiac impulse cannot re-excite an already excited impulse cannot re-excite an already excited area of the heartarea of the heart

ventricles: 0.25-0.30 secventricles: 0.25-0.30 sec another, relative refractory period of 0.05 another, relative refractory period of 0.05

sec, muscle is more difficult to excite, but sec, muscle is more difficult to excite, but can be stimulatedcan be stimulated

atria: ~0.15 secatria: ~0.15 sec relative refractory: 0.03 secrelative refractory: 0.03 sec rhythmical rate of atria can be faster than rhythmical rate of atria can be faster than

that of ventriclesthat of ventricles

Cardiac CycleCardiac Cycle

beginning of heart beat to beginning of the beginning of heart beat to beginning of the nextnext

R to R or P to P wave is often how one is R to R or P to P wave is often how one is measuredmeasured

Systole and DiastoleSystole and Diastole

relaxation phase: heart fills with blood, relaxation phase: heart fills with blood, diastolediastole

work phase: heart pumps blood, systolework phase: heart pumps blood, systole cardiac cycle curvecardiac cycle curve

DiastoleDiastole

first third: rapid fillingfirst third: rapid filling middle third: small amount of fillingmiddle third: small amount of filling last third: atria contract, ~25% of blood last third: atria contract, ~25% of blood

flows into ventriclesflows into ventricles

SystoleSystole

Isovolumic or isovolumetric contraction Isovolumic or isovolumetric contraction occurs at onset of ventricular contractionoccurs at onset of ventricular contraction

ventricles need to develop sufficient ventricles need to develop sufficient pressure to open semilunar valves against pressure to open semilunar valves against the aorta and pulmonary arterythe aorta and pulmonary artery

ventricles contract isometrically, volume ventricles contract isometrically, volume does not changedoes not change

Ejection nextEjection next

pressure in L vent. >80 mm Hg and R vent. > pressure in L vent. >80 mm Hg and R vent. > 8 mm Hg, valves open8 mm Hg, valves open

first third: rapid ejection, 70% of blood is first third: rapid ejection, 70% of blood is ejectedejected

next two-thirds: final 30% is ejected, slow next two-thirds: final 30% is ejected, slow ejectionejection

isovolumic relaxationisovolumic relaxation sudden onset, rapid drop in pressure, no sudden onset, rapid drop in pressure, no

change in volumechange in volume intraventricular pressure drops to diastolic intraventricular pressure drops to diastolic

levellevel

End Diastolic Volume (EDV)End Diastolic Volume (EDV)

volume in ventricles after the period of volume in ventricles after the period of fillingfilling

usually ~110-120 ml of blood/ventricleusually ~110-120 ml of blood/ventricle

Stroke Volume (SV)Stroke Volume (SV)

volume ejected during systolevolume ejected during systole ~70 ml~70 ml

End Systolic Volume (ESV)End Systolic Volume (ESV)

volume in ventricles after systole, ~40-50 volume in ventricles after systole, ~40-50 mlml

Ejection Fraction (EF)Ejection Fraction (EF)

fraction of EDV that is ejectedfraction of EDV that is ejected usually ~ 60%usually ~ 60% when contraction force is strong, ESV can when contraction force is strong, ESV can

fall to 10-20 mlfall to 10-20 ml EDV can be as high as 150-180 ml of EDV can be as high as 150-180 ml of

bloodblood increase EDV and decrease ESV, SV can increase EDV and decrease ESV, SV can

double resting SVdouble resting SV

Volume Pressure curves for Volume Pressure curves for Systole and DiastoleSystole and Diastole

Phase I: filling phase ESV to EDV Phase I: filling phase ESV to EDV increase vol. ~70 ml pressure rises ~5 increase vol. ~70 ml pressure rises ~5 mm Hg (diastolic)mm Hg (diastolic)

Phase II: isovolumic contraction, Phase II: isovolumic contraction, increase pressure (~80 mm Hg), not increase pressure (~80 mm Hg), not volumevolume

Phase III: ejection periodPhase III: ejection period Phase IV: isovolumic relaxation ventricle Phase IV: isovolumic relaxation ventricle

pressure decreases to diastolic levelspressure decreases to diastolic levels

Preload: degree of tension on the Preload: degree of tension on the heart muscle when it begins heart muscle when it begins

contractioncontraction

Volume of blood in the ventricle at the Volume of blood in the ventricle at the end of diastole (EDV)end of diastole (EDV)

Afterload: load against which the Afterload: load against which the muscle exerts its contractile forcemuscle exerts its contractile force

Pressure in artery leading from the Pressure in artery leading from the ventriclesventricles

Regulation of the heart’s pumpingRegulation of the heart’s pumping

@ rest, Q is usually 4-6 l/min@ rest, Q is usually 4-6 l/min Q is reliant upon rate of blood flow into Q is reliant upon rate of blood flow into

heart (venous return)heart (venous return) Frank-Starling Mechanism: increase in Frank-Starling Mechanism: increase in

venous return (EDV) increases the amount venous return (EDV) increases the amount of blood pumped into the aortaof blood pumped into the aorta

F-S: Heart pumps what heart getsF-S: Heart pumps what heart gets

Due to increased return: increased stretch of the Due to increased return: increased stretch of the heart heart increase force of the contraction increase force of the contraction (optimal length for force)(optimal length for force)

Increase in force is also seen in skeletal muscleIncrease in force is also seen in skeletal muscle Stretch R atrial wall can increase heart rate by Stretch R atrial wall can increase heart rate by

10-20% increasing Q (less than from F-S 10-20% increasing Q (less than from F-S mechanism)mechanism)

High pressure in the arteries does not increase High pressure in the arteries does not increase QQ

Ventricular Function CurvesVentricular Function Curves

As arterial pressure increases, work output As arterial pressure increases, work output of stroke volume increases until it reaches of stroke volume increases until it reaches the limit of the heartthe limit of the heart

As arterial pressure increases (EDV) EF As arterial pressure increases (EDV) EF also increasesalso increases

Extrinsic Regulation of the Heart Extrinsic Regulation of the Heart RateRate

Neural influences can be superimposed on Neural influences can be superimposed on inherent rhythmicity of heartinherent rhythmicity of heart

Originate in CVC in medulla Originate in CVC in medulla Transmitted via autonomic NS via Transmitted via autonomic NS via

sympathetic and parasympatheticsympathetic and parasympathetic Ventricles: sympatheticVentricles: sympathetic Atria: both Atria: both

Sympathetic InnervationSympathetic Innervation

Can increase Q by 100%Can increase Q by 100% Causes release of epi and norepi, Causes release of epi and norepi,

speeding rate of SA depolarizationspeeding rate of SA depolarization Result: tachycardiaResult: tachycardia Also increases the force of contractionAlso increases the force of contraction Inhibition of sympathetic NS can decrease Inhibition of sympathetic NS can decrease

HR and pumpingHR and pumping

Mechanism the continuously Mechanism the continuously discharges, maintains HR ~30% higher discharges, maintains HR ~30% higher than if there were no stimulation than if there were no stimulation

If depress sympathetic stimulation, HR If depress sympathetic stimulation, HR and force of contraction decrease, and force of contraction decrease, decreasing Q ~30%decreasing Q ~30%

Adrenal glands are also active and can Adrenal glands are also active and can release epi with general sympathetic release epi with general sympathetic activationactivation

Parasympathetic innervationParasympathetic innervation

Can slow HR to almost zeroCan slow HR to almost zero Ach released, decreasing the rate of sinus Ach released, decreasing the rate of sinus

discharge: bradycardiadischarge: bradycardia Cell bodies are in cardioinhibitory center of Cell bodies are in cardioinhibitory center of

medullamedulla With strong stimulus, heart can stop With strong stimulus, heart can stop

beating for few seconds, start again, at a beating for few seconds, start again, at a rate of 20-30 bpmrate of 20-30 bpm

Strong parasympathetic stimulation will Strong parasympathetic stimulation will decrease the force of contraction by 20-decrease the force of contraction by 20-30%30%

Decrease is not great in its extent, most Decrease is not great in its extent, most fibers are in atria, few in ventriclesfibers are in atria, few in ventricles

Large decrease in HR combined with Large decrease in HR combined with small decrease in contractility: decrease small decrease in contractility: decrease ventricular pumping 50%ventricular pumping 50%

Training EffectTraining Effect

Exercise favors vagal dominanceExercise favors vagal dominance Increase in parasympathetic activity, may Increase in parasympathetic activity, may

also have a decrease in sympathetic also have a decrease in sympathetic activityactivity

Training may also reduce intrinsic firing Training may also reduce intrinsic firing rate of SA noderate of SA node

Peripheral inputPeripheral input

Peripheral receptors in blood vessels, Peripheral receptors in blood vessels, joints, musclesjoints, muscles

Input to ventrolateral medullaInput to ventrolateral medulla Modify vagal or sympathetic outflowModify vagal or sympathetic outflow Baroreceptors in aortic arch and carotid Baroreceptors in aortic arch and carotid

sinus (alterations in BP)sinus (alterations in BP)

Increase BP: reflex slowing of HR and Increase BP: reflex slowing of HR and dilation of peripheral vasculaturedilation of peripheral vasculature

Decrease BP to normal levelsDecrease BP to normal levels This feedback is overridden during This feedback is overridden during

exerciseexercise But, still may act to prevent abnormally But, still may act to prevent abnormally

high BP during ex.high BP during ex.