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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.