Refractory period of cardiac muscle cardiac muscle has refractory period, preventing restimulation cardiac muscle has refractory period, preventing restimulation during this interval, a normal cardiac impulse cannot re-excite an already excited area of the heart during this interval, a normal cardiac impulse cannot re-excite an already excited area of the heart ventricles: sec ventricles: sec another, relative refractory period of 0.05 sec, muscle is more difficult to excite, but can be stimulated another, relative refractory period of 0.05 sec, muscle is more difficult to excite, but can be stimulated

atria: ~0.15 sec atria: ~0.15 sec relative refractory: 0.03 sec relative refractory: 0.03 sec rhythmical rate of atria can be faster than that of ventricles rhythmical rate of atria can be faster than that of ventricles

Cardiac Cycle beginning of heart beat to beginning of the next beginning of heart beat to beginning of the next R to R or P to P wave is often how one is measured R to R or P to P wave is often how one is measured

Systole and Diastole relaxation phase: heart fills with blood, diastole relaxation phase: heart fills with blood, diastole work phase: heart pumps blood, systole work phase: heart pumps blood, systole cardiac cycle curve cardiac cycle curve

Diastole first third: rapid filling first third: rapid filling middle third: small amount of filling middle third: small amount of filling last third: atria contract, ~25% of blood flows into ventricles last third: atria contract, ~25% of blood flows into ventricles

Systole Isovolumic or isovolumetric contraction occurs at onset of ventricular contraction Isovolumic or isovolumetric contraction occurs at onset of ventricular contraction ventricles need to develop sufficient pressure to open semilunar valves against the aorta and pulmonary artery ventricles need to develop sufficient pressure to open semilunar valves against the aorta and pulmonary artery ventricles contract isometrically, volume does not change ventricles contract isometrically, volume does not change

Ejection next pressure in L vent. >80 mm Hg and R vent. > 8 mm Hg, valves open pressure in L vent. >80 mm Hg and R vent. > 8 mm Hg, valves open first third: rapid ejection, 70% of blood is ejected first third: rapid ejection, 70% of blood is ejected next two-thirds: final 30% is ejected, slow ejection next two-thirds: final 30% is ejected, slow ejection isovolumic relaxation isovolumic relaxation sudden onset, rapid drop in pressure, no change in volume sudden onset, rapid drop in pressure, no change in volume intraventricular pressure drops to diastolic level intraventricular pressure drops to diastolic level

End Diastolic Volume (EDV) volume in ventricles after the period of filling volume in ventricles after the period of filling usually ~ ml of blood/ventricle usually ~ ml of blood/ventricle

Stroke Volume (SV) volume ejected during systole volume ejected during systole ~70 ml ~70 ml

End Systolic Volume (ESV) volume in ventricles after systole, ~40-50 ml volume in ventricles after systole, ~40-50 ml

Ejection Fraction (EF) fraction of EDV that is ejected fraction of EDV that is ejected usually ~ 60% usually ~ 60% when contraction force is strong, ESV can fall to ml when contraction force is strong, ESV can fall to ml EDV can be as high as ml of blood EDV can be as high as ml of blood increase EDV and decrease ESV, SV can double resting SV increase EDV and decrease ESV, SV can double resting SV

Volume Pressure curves for Systole and Diastole Phase I: filling phase ESV to EDV increase vol. ~70 ml pressure rises ~5 mm Hg (diastolic) Phase I: filling phase ESV to EDV increase vol. ~70 ml pressure rises ~5 mm Hg (diastolic) Phase II: isovolumic contraction, increase pressure (~80 mm Hg), not volume Phase II: isovolumic contraction, increase pressure (~80 mm Hg), not volume

Phase III: ejection period Phase III: ejection period Phase IV: isovolumic relaxation ventricle pressure decreases to diastolic levels Phase IV: isovolumic relaxation ventricle pressure decreases to diastolic levels

Preload: degree of tension on the heart muscle when it begins contraction Volume of blood in the ventricle at the end of diastole (EDV) Volume of blood in the ventricle at the end of diastole (EDV)

Afterload: load against which the muscle exerts its contractile force Pressure in artery leading from the ventricles Pressure in artery leading from the ventricles

Regulation of the heart’s rest, Q is usually 4-6 rest, Q is usually 4-6 l/min Q is reliant upon rate of blood flow into heart (venous return) Q is reliant upon rate of blood flow into heart (venous return) Frank-Starling Mechanism: increase in venous return (EDV) increases the amount of blood pumped into the aorta Frank-Starling Mechanism: increase in venous return (EDV) increases the amount of blood pumped into the aorta

F-S: Heart pumps what heart gets Due to increased return: increased stretch of the heart  increase force of the contraction (optimal length for force) Due to increased return: increased stretch of the heart  increase force of the contraction (optimal length for force) Increase in force is also seen in skeletal muscle Increase in force is also seen in skeletal muscle Stretch R atrial wall can increase heart rate by 10-20% increasing Q (less than from F-S mechanism) Stretch R atrial wall can increase heart rate by 10-20% increasing Q (less than from F-S mechanism) High pressure in the arteries does not increase Q High pressure in the arteries does not increase Q

Ventricular Function Curves As arterial pressure increases, work output of stroke volume increases until it reaches the limit of the heart As arterial pressure increases (EDV) EF also increases

Extrinsic Regulation of the Heart Rate  Neural influences can be superimposed on inherent rhythmicity of heart  Originate in CVC in medulla  Transmitted via autonomic NS via sympathetic and parasympathetic  Ventricles: sympathetic  Atria: both

Sympathetic Innervation  Can increase Q by 100%  Causes release of epi and norepi, speeding rate of SA depolarization  Result: tachycardia  Also increases the force of contraction  Inhibition of sympathetic NS can decrease HR and pumping

 Mechanism the continuously discharges, maintains HR ~30% higher than if there were no stimulation  If depress sympathetic stimulation, HR and force of contraction decrease, decreasing Q ~30%  Adrenal glands are also active and can release epi with general sympathetic activation

Parasympathetic innervation  Can slow HR to almost zero  Ach released, decreasing the rate of sinus discharge: bradycardia  Cell bodies are in cardioinhibitory center of medulla  With strong stimulus, heart can stop beating for few seconds, start again, at a rate of bpm

 Strong parasympathetic stimulation will decrease the force of contraction by %  Decrease is not great in its extent, most fibers are in atria, few in ventricles  Large decrease in HR combined with small decrease in contractility: decrease ventricular pumping 50%

Training Effect  Exercise favors vagal dominance  Increase in parasympathetic activity, may also have a decrease in sympathetic activity  Training may also reduce intrinsic firing rate of SA node

Peripheral input  Peripheral receptors in blood vessels, joints, muscles  Input to ventrolateral medulla  Modify vagal or sympathetic outflow  Baroreceptors in aortic arch and carotid sinus (alterations in BP)

 Increase BP: reflex slowing of HR and dilation of peripheral vasculature  Decrease BP to normal levels  This feedback is overridden during exercise  But, still may act to prevent abnormally high BP during ex.