Lecture 7 - Cardiac Cycle, Factors Affecting Cardiac Output, Stroke Volume & Heart Rate - PDF

The Cardiac Cycle Cardiac Output: Stroke Volume and Heart Rate Sherwood: Chapter 9-10 Objectives The Cardiac Cycle Cardiac Output, Stroke Volume and Heart Rate 2 The Cardiac Cycle  Late diastole—both sets of...

The Cardiac Cycle Cardiac Output: Stroke Volume and Heart Rate Sherwood: Chapter 9-10 Objectives The Cardiac Cycle Cardiac Output, Stroke Volume and Heart Rate 2 The Cardiac Cycle  Late diastole—both sets of chambers are relaxed and ventricles fill passively. START Isovolumic ventricular relaxation—as ventricles relax; pressure in ventricles Atrial systole—atrial contraction falls, blood flows back into forces a small amount of cusps of semilunar valves additional blood into ventricles. and snaps them closed. Definitions for systole and diastole Atrial systole S1 and diastole S2 Ventricular systole and diastole Ventricular ejection— Isovolumic ventricular as ventricular pressure contraction—first phase of rises and exceeds ventricular contraction pushes pressure in the arteries, AV valves closed but does the semilunar valves not create enough pressure to open and blood is open semilunar valves. ejected. Pressure-Volume Curve (Loop) This is another way to represent one cardiac cycle. It represents the changes in volume and pressure that happen over one cardiac cycle. Pressure = y-axis Volume = x-axis Pressure-Volume Curve A. Ventricle is relaxed and filling with blood A’  B. Atrial contraction adds final amount of blood to ventricle B. The volume of blood in the ventricle at the end of filling is called end-diastolic Ventricular contraction volume begins Both the AV valves and semilunar valves are closed! Blood has nowhere to go. Pressure rises rapidly without change in volume Pressure-Volume Curve BC. Change in pressure without volume called isovolumic contraction C. Pressure in ventricle exceeds aorta, and aortic valve opens CD. Pressure rises as ventricle continues to contract, but volume decreases as blood leaves through aorta. -Volume of blood leaving ventricle is stroke volume (SV) D. Volume remaining in ventricle is end-systolic volume (ESV) DA. Ventricles relax, semilunar valves close -Ventricle once again sealed chamber -This region of the loop is called isovolumic relaxation Normal Heart Sounds Noises generated by the beating heart Can be heard with a stethoscope First heart sound (LUB) Also called S1 Closure of mitral valve and tricuspid valve at start of ventricular systole Second heart sound (DUB) Also called S2 Closure of aortic valve and pulmonary valve at start of ventricular diastole  Time (msec) Putting everything 0 100 QRS 200 300 400 500 600 700 800 QRS together… complex complex Electro- cardiogram P T P (ECG) 120 The next several slides will 90 B Aorta Dicrotic notch detail what happens during Pressure A the cardiac cycle (mm Hg) 60 Left ventricular -Will look at things one step at pressure a time 30 Left atrial pressure D 0 C Heart sounds S1 S2 135 E Left ventricular volume (mL) 65 F Atrial Ventricular Ventricular Atrial systole systole diastole systole Atrial systole Isovolumic Ventricular Early Late Atrial systole ventricular systole ventricular ventricular contraction diastole diastole ECG Trace P wave = atrial depolarization *atrial contraction occurs following P-wave* QRS complex = ventricular depolarization *ventricular contraction occurs following QRS complex* T wave = ventricular repolarization *absolute refractory period = NO more Time (msec) contractions* 0 100 200 300 400 500 600 700 800 QRS QRS complex complex Electro- cardiogram P T P (ECG) Atrial Ventricular Ventricular Atrial systole systole diastole systole Atrial systole Isovolumic Ventricular Early Late Atrial systole ventricular systole ventricular ventricular contraction diastole diastole Left Ventricular Volume Atrial systole -Atria contract and pump blood into the ventricles, therefore volume in ventricles increases Ventricular systole -Begins with isovolumetric contraction, where volume does not change -Aortic valve opens (E), and blood ejected Time (msec) through aorta (stroke volume = amount 135 of 0 100 200 300 400 500 600 700 800 E blood ejected from ventricle) Left ventricular volume (mL) Ventricular diastole 65 F Atrial Ventricular Ventricular Atrial -Begins with isovolumetric relaxation, systole systole diastole systole where volume does not change -Aortic valve closes, tricuspid valve opens (F), and ventricle passively fills Atrial systole Isovolumic Ventricular Early Late Atrial systole ventricular systole ventricular ventricular contraction diastole diastole Left Atrial Pressure Time (msec) 0 100 200 300 400 500 600 700 800 120 Atrial systole -Atria contact and pressure 90 increases Pressure (mm Hg) -2nd “small” bump is back pressure 60 from tricuspid valve closing 30 Left atrial pressure Ventricular systole -Atrial pressure low but slowly 0 135 increases Left E -Remember that atria are in diastolevolume ventricular (mL) right now, so they are passively 65 F filling, thus explaining why pressure Atrial systole Ventricular systole Ventricular diastole Atrial systole would slowly increase Ventricular diastole -Tricuspid valve open, so pressure in Atrial systole Isovolumic Ventricular Early Late Atrial systole atria drops as ventricles are now ventricular systole ventricular ventricular contraction diastole diastole passively filling with blood coming from atria. Note that this is still Left Ventricular Pressure Atrial systole 0 100 200 Time (msec) 300 400 500 600 700 800 -Pressure in ventricle increases 120 slightly because of blood coming from atria during atria contraction. 90 Pressure briefly drops when Pressure tricuspid valve closes (mm Hg) 60 Left ventricular pressure Ventricular systole 30 -Ventricle contracts. Isovolumetric contraction occurs when all valves 0 are closed but pressure is building. Heart sounds S1 S2 Pressure reaches peak just after Atrial systole Ventricular systole Ventricular diastole Atrial systole aortic valve opens (coincides with faint grey line) and blood is ejected into circulation Atrial systole Isovolumic Ventricular Early Late Atrial systole Ventricular diastole ventricular contraction systole ventricular diastole ventricular diastole -Tricuspid valve open, and ventricle passively fills until atrial systole Left Ventricular Pressure and Volume Atrial systole Time (msec) -Pressure increase in ventricle 0 100 200 300 400 500 600 700 800 caused by increased volume of 120 blood entering ventricle due to atrial contraction. 90 Pressure (mm Hg) Left Ventricular systole 60 ventricular pressure -AV valve closes, and isovolumetric contraction occurs 30 -Pressure builds until it exceeds aortic pressure 135 0 E -Aortic valve opens (E), and blood ventricular Left ejected from heart volume (mL) 65 F Atrial Ventricular Ventricular Atrial Ventricular diastole systole systole diastole systole -Isovolumetric relaxation occurs when all 4 valves are shut and pressure drops -Passive filling begins when tricuspid Atrial systole Isovolumic ventricular Ventricular systole Early ventricular Late ventricular Atrial systole contraction diastole diastole valve opens (F) -Pressure and volume in ventricle Aorta Pressure Atrial systole -Pressure in the aorta much higher than within heart Dicrotic Notch: Time (msec) -Pressure is slowly dropping because 0 100 200 300 400 500 600 700 800 Closure of the blood is exiting arterial circulation 120 aortic valve creates and entering venous pool (venules a disturbance B and veins) 90 Aorta Dicrotic notch aortic pressure Pressure (mm Hg) A curve Ventricular systole 60 Left ventricular First heart sound pressure -”A” corresponds to aortic valve (LUB) opening 30 Also called S1 -Pressure “flips” and now ventricular Closure of mitral pressure greater than aortic 0 valve and tricuspid Heart pressure sounds S1 S2 valve at start of -Continues until “B” which Atrial systole Ventricular systole Ventricular diastole Atrial systole ventricular corresponds to aortic valve closing; systole pressure “flips” again and now aortic pressure greater than Second heart sound ventricular pressure Atrial systole Isovolumic Ventricular Early Late Atrial (DUB) systole ventricular systole ventricular ventricular contraction diastole diastole Also called S2 Ventricular diastole Closure of aortic valve and Left Atrial Pressure Atrial systole -Pressure higher in atria than 0 100 200 Time (msec) 300 400 500 600 700 800 ventricle; ensures blood flowing 120 “forward” into ventricle B 90 Aorta Dicrotic notch Ventricular systole Pressure A (mm Hg) -”C” corresponds to tricuspid valve 60 Left ventricular pressure opening -Pressure “flips” and now ventricular 30 Left atrial D pressure pressure greater than atrial pressure 0 C Heart Ventricular diastole sounds S1 S2 Atrial Ventricular Ventricular Atrial -Continues until “D” which systole systole diastole systole corresponds to tricuspid valve opening; pressure “flips” again and now atrial pressure greater than ventricular pressure Atrial systole Isovolumic ventricular Ventricular systole Early ventricular Late ventricular Atrial systole -Ventricular pressure only greater contraction diastole diastole than atrial pressure from isovolumetric contraction until Atrial Systole 0 100 Time (msec) Electro- ECG cardiogram (ECG) P -P wave occurs prior to atrial contraction 120 Pressure 90 Aorta -Aortic pressure drops as blood Pressure (mm Hg) continues to enter venous pool 60 -Atrial and ventricular pressure Left increase when atria contract 30 Left atrial pressure ventricular pressure -Tricuspid valve open but aortic C valve closed 0 Heart sounds 135 Volume Left ventricular -Left ventricle volume increases volume (mL) because blood is ejected out of the 65 Atrial atrium and into the ventricle systole Atrial systole Isovolumetric 0 100 QRS Time (msec) Contraction complex Electro- cardiogram P (ECG) ECG 120 -QRS means ventricle is depolarized and is beginning to contract from 90 Aorta apex to base Pressure (mm Hg) Left 60 ventricular pressure Pressure -Ventricular pressure rises causing 30 Left atrial pressure tricuspid valve to close (pressure in ventricle greater than atria), and Heart 0 C backflow causes small pressure spike sounds S1 135 in atria Left -Ventricular pressure continues to riseventricular volume (mL) and exceeds that of the aorta 65 Atrial systole Volume -Left ventricular volume DOES NOT CHANGE -S1 = “Lub” sound – tricuspid valve Isovolumic ventricular closes contraction Ventricular 0 100 QRS 200 Time (msec) 300 Systole complex Electro- cardiogram P T (ECG) ECG 120 -Ventricle depolarized, and starts to B repolarize by the end of phase 90 Aorta *absolute refractory period* Pressure (mm Hg) A Left 60 ventricular pressure Pressure -Ventricular pressure peaks. A and B 30 Left atrial pressure are opening and closing of aortic valve Heart 0 C -Ventricular pressure HIGHER than sounds S1 135 aortic pressure during this phase Left E -Atrial pressure slowly rises becausevolume ventricular (mL) this is atrial diastole, and passive 65 filling is occurring Atrial systole Ventricular systole -*Only time during cardiac cycle that aortic/systemic pressure is increasing since blood is leaving the heart, and entering systemic circulation Ventricular systole Isovolumetric 0 100 QRS 200 Time (msec) 300 400 Relaxation complex Electro- cardiogram P T (ECG) ECG 120 -Nothing happens here B 90 Aorta Dicrotic notch Pressure Pressure (mm Hg) A Left -Pressure drops in left ventricle 60 ventricular -B is closing of aortic valve and is pressure Dicrotic Notch: Closure of the also the “Dub” sound (S2) 30 Left atrial pressure aortic valve creates a disturban Volume 0 C aortic pressure curve Heart -Left ventricular volume DOES NOT sounds S1 S2 135 CHANGE Left E ventricular volume (mL) 65 Atrial Ventricular systole systole Early ventricular diastole Ventricular 0 100 QRS 200 Time (msec) 300 400 500 600 700 800 Diastole complex Electro- cardiogram P T (ECG) ECG 120 -End of phase signified by next P- B wave 90 Aorta Dicrotic notch Pressure A (mm Hg) Left Pressure 60 ventricular pressure -Aortic pressure slowly drops as blood enters venous pool 30 Left atrial pressure D -D is opening of tricuspid valve and atrial pressure drops because blood 0 Heart C enters ventricle (see below) sounds S1 S2 135 E Left Volume ventricular volume (mL) -Left ventricular volume increases 65 F during this phase; passive filling Atrial systole Ventricular systole Ventricular diastole Late ventricular diastole  Time (msec) 0 100 200 300 400 500 600 700 800 QRS QRS complex complex Electro- cardiogram P T P (ECG) 120 B 90 Aorta Dicrotic notch Pressure A (mm Hg) Left 60 ventricular pressure 30 Left atrial pressure D 0 C Heart sounds S1 S2 135 E Left ventricular volume (mL) 65 F Atrial Ventricular Ventricular Atrial systole systole diastole systole Atrial systole Isovolumic Ventricular Early Late Atrial systole ventricular systole ventricular ventricular contraction diastole diastole Study Guide Phase ECG Heart Ventricular Ventricular Sound Volume pressure Filling/Diastole Isovolumetric Contraction Ejection Isovolumetric Relaxation Cardiac Output, Stroke Volume and Heart Rate Filling Time - + + - + Afterload Stroke Volume and Cardiac Output Stroke volume Stroke volume: amount of blood pumped by one ventricular contraction Measured in mL/beat Can be calculated by: EDV – ESV = SV Cardiac output Cardiac output: volume of blood pumped by one ventricle per minute CO = HR x SV Average SV: 70mL Average CO: ~5 L/minute Several factors affect these values If the heart contracts harder, more blood volume will leave the ventricle. If the heart contracts faster, more blood may leave the ventricle per minute. Stroke Volume and Cardiac Output Definitions: SV = end diastolic volume (EDV) minus end systolic volume (ESV) EDV = amount of blood collected in a ventricle during diastole ESV = amount of blood remaining in a ventricle after contraction Preload – amount ventricles are stretched by the contained blood Afterload – back pressure exerted by blood in the large arteries leaving the heart Cardiac Output and Stroke Volume Calculate the cardiac output (L/min) from the following information. Heart rate: 80 beats/min End diastolic volume: 130 ml End systolic volume: 60 ml Heart Rate Normal resting heart rate: 60-100bpm Initiated by autorhythmic cells Remember the If channels and the T-type Calcium Channels What regulates heart rate? Both branches of autonomic nervous system regulate HR 1. PNS Activation - Decreases HR 2. SNS Activation - Increases HR They regulate it by changing membrane potential How?? 1) Parasympathetic Control of Heart Rate Parasympathetic Nervous System Released Acetylcholine Binds to muscarinic receptor On the SA nodal cells Increases the K+ efflux Hyperpolarizes the cell And decreases rate of depolarization Begins at a lower membrane potential. HR Decreases Therefore it takes longer to reach threshold  HR 2) Sympathetic Control of Heart Rate Sympathetic Nervous System Released norepinephrine Binds to β1 receptor On the SA nodal cells Increases the Na+ and Ca2+ influx Increases rate of depolarization It takes less time to reach the threshold potential  HR Increases HR What Factors Influence Stroke Volume? Directly related to force generated by heart during contraction Force of ventricular contraction determined by: 1) Length of the muscle fibers Ability of muscle fibers to contraction directly related to length of fiber 2) Contractility Intrinsic ability of a cardiac muscle fiber to contract Function of Ca2+ interaction with contractile filaments 3) Venous return Amount of blood that returns to heart from veins 4) Skeletal muscle Contraction of skeletal muscle 1 and 2) Frank-Starling Law of the Heart Length-Tension Relationship More blood flows into ventricle  muscle fibers stretch more  more forceful contraction Even in the absence of any nervous input! Frank-Starling Law: SV is proportional to end-diastolic volume Force: Indicated by stroke volume Stretch: indicated by end- diastolic volume SV is proportional to the EDV This relationship holds true in the absence of neural input! What would happen to contractility if 1 and 2) Norepinephrine: Effect on Contractility Remember:  force of contraction = SV Norepinephrine increases force of contraction! Any substance that affects contractility is called an inotropic agent Inotropic agents cause inotropic effects 1 and 2) Norepinephrine: Effect on Contractility Norepinephrine binds to B1 receptors Same receptors that increase HR (see slide 28) G-protein reaction activates cAMP cAMP activates secondary messengers Secondary messengers: 1. Increase calcium entry into cell 2. Increase calcium release from SR Increased calcium spark + calcium signal 3. Enhance actin-myosin interaction Greater crossbridge formation, etc 4. Increase calcium binding to RyR Increased calcium release from SR 3 – 5) Other Factors that Affect Stroke Volume 3) Venous Return Amount of blood that returns to heart from veins More blood returns to heart = more blood pumped out 4) Skeletal muscle: Contraction of skeletal muscle around veins pushes blood back to heart Increases stroke volume by increasing venous return 5) Respiratory Pump: When you breath in, pressure is decreased in lungs Takes pressure off veins of lungs and increases amount of blood that flows through them and back to heart  SNS Filling Time - + + - + Afterload Quiz 1) What is the difference between atrial and ventricular systole? 2) What is isovolumetric contraction and isovolumetric relaxation? 3) What is cardiac output if HR is 60 and SV is 100mL? 4) What regulates HR at rest, and what system takes over during exercise? 5) What does norepinephrine release do to a) HR, b) SV and c) CO? What does acetylcholine do to the above parameters? 6) What 5 factors influence SV? 7) How does blood flow into the ventricle increase