Cardiac Cycle Notes

NOTES NOTES CARDIAC CYCLE MEASURING CARDIAC OUTPUT FICK PRINCIPLE osms.it/Fick-principle ▪ Model used to measure cardiac output (CO) ▫ Output of left, right ventricles equal during normal cardiac function ▪ Steady state: rate of O2 consumption = amount of O2 leaving lungs via pulmonary vein - amount of O2 returning via pulmonary arteries x CO ▪ Pulmonary blood flow of right heart = CO of left heart: used to calculate CO Cardiac Output = O2 consumption [O2] pulmonary vein - [O2] pulmonary artery ▪ 250mL/minute = total O2 consumption (70kg, biologically-male individual); pulmonary venous O2 content = 0.20/mL; pulmonary arterial O2 content = 0.15/mL Cardiac Output = 250mL/min = 5000mL/min 0.20mL - 0.15mL ▪ Also measures blood flow to individual organs ▫ Renal blood flow = renal O2 consumption / renal arterial O2 - renal venous O2 CARDIAC & VASCULAR FUNCTION CURVES osms.it/cardiac-and-vascular-function-curves ▪ Curves depicting functional connections between vascular system, right atrial pressure, and CO CARDIAC FUNCTION CURVE (CO CURVE) ▪ Plot of relationship between left ventricle (LV) CO, right atrial (RA) pressure ▪ Based on Frank–Starling relationship describing CO dependence on preload ▫ Preload (determined by RA pressure), independent variable; CO, dependent variable ▫ ↑ venous return → ↑ RA pressure → ↑ LV end-diastolic volume (EDV)/preload, myocardial fiber stretch → ↑ CO ▫ LV CO (L/min) = LV venous return/ preload (RA pressure in mmHg) ▫ Relationship remains intact with steady state of venous return ▫ RA pressure 4mmHg → curve levels off at maximum 9L/min OSMOSIS.ORG 111

VASCULAR FUNCTION CURVE ▪ Plot of relationship between venous return, RA pressure ▪ Independent of Frank–Starling relationship ▫ Venous return independent variable; RA pressure dependent variable ▫ Venous return, RA pressure: inverse relationship ▪ ↑ RA pressure → ↓ pressure gradient between systemic arteries, RA → ↓ venous return to RA; CO Mean systemic pressure (MSP) ▪ Pressure equal throughout vasculature ▪ Influenced by blood volume, distribution Total peripheral resistance (TPR) ▪ Primarily determined by pressure in arterioles; determines slope of curve ▪ ↓ TPR (↓ arteriolar resistance) → ↑ flow from arterial to venous circulation → ↑ venous return → clockwise rotation of curve ▪ ↑ TPR (↑ arteriolar resistance) → ↓ flow from arterial to venous circulation → ↓ venous return → counterclockwise rotation of curve ALTERING CARDIAC & VASCULAR FUNCTION CURVES osms.it/altering-cardiac-vascular-function-curves ▪ Curves combined → changes in CO visualized, cardiovascular parameters altered ▪ Curves can be displaced by changes in blood volume, inotropy, TPR INOTROPIC AGENTS ▪ Alters cardiac curve ▪ Positive inotropic agents (e.g. digoxin) at any level of RA pressure ▫ ↑ contractility, stroke volume (SV), CO → (1) cardiac curve shifts upward, (2) vascular function curve not affected, (3) x-intercept (steady state) shifts upward, to left ▪ Negative inotropic agents (e.g. betablockers) ▫ Opposite effect BLOOD VOLUME ▪ Alters vascular curve ▪ ↑ circulating volume (e.g. blood transfusion) ▫ ↑ MSP → (1) curves intersect at ↑ CO, RA pressure, (2) parallel shift of x-intercept (steady state), vascular curve 112 OSMOSIS.ORG to right, (3) no change in TPR ▪ ↓ circulating volume (e.g. hemorrhage) ▫ Opposite effect ▪ Changes in venous compliance are similar to blood volume changes ▫ ↓ venous compliance → changes similar to ↑ circulating volume ▫ ↑ venous compliance → changes similar to ↓ circulating volume TOTAL PERIPHERAL RESISTANCE ▪ Alters both curves due to changes in afterload (cardiac curve), venous return (vascular curve) ▪ ↑ TPR → ↑ arterial pressure → ↑ afterload → ↓ CO → (1) downward shift of cardiac curve, (2) counterclockwise rotation of vascular curve, (3) ↓ venous return, (4) RA pressure unchanged, ↓/↑ (depending on cardiac, venous curve alteration), (5) curves intersect at altered steady state ▪ ↓ TPR (arteriolar dilation) ▫ Opposite effect

Chapter 16 Cardiovascular Physiology: Cardiac Cycle PRESSURE-VOLUME LOOPS osms.it/pressure-volume_loops ▪ Graphs represent pressure, volume changes in LV during one heartbeat (one cardiac cycle/“stroke work”) ▪ Pressure in left ventricle on y axis, volume of left ventricle on x axis FOUR PHASES Ventricular filling during diastole ▪ At end of this phase: ▫ Mitral valve closed ▫ Left ventricle filled (EDV); relaxed, distended ▫ EDV = 140mL Isovolumic contraction ▪ Systole begins (ventricular contraction) ▪ No changes to ventricular volume (mitral, aortic valve closed) ▪ Pressure builds Ventricular ejection ▪ Pressure in left ventricle > aortic pressure → aortic valve opens → blood ejected Isovolumic relaxation ▪ Ventricle starts relaxing → aortic pressure > LV pressure → aortic valve closes ▪ End of systole ▪ ESV = 70mL STROKE VOLUME (SV) ▪ STROKE VOLUME (SV) ▪ Amount of blood pumped by ventricles in one contraction ▪ SV = EDV - ESV STROKE WORK (SW) ▪ Work of ventricles to eject a volume of blood (i.e. to eject SV) ▪ Represented by area inside of loop Figure 16.1 Measurements that can be obtained from the pressure-volume loop graph. Pulse pressure is measured in mmHg and reflects the throbbing pulsation felt in an artery during systole. Pulse pressure = systolic blood pressure - diastolic blood pressure. Stroke volume is measured in mL and is blood volume ejected by left ventricle during every heartbeat. Stroke volume = end-diastolic volume - end systolic volume. OSMOSIS.ORG 113

Figure 16.2 The four phases of the pressure-volume loop and the condition of the heart during each phase. 114 OSMOSIS.ORG

Chapter 16 Cardiovascular Physiology: Cardiac Cycle CHANGES IN PRESSURE-VOLUME LOOPS osms.it/changes_in_pressure-volume_loops ▪ Cardiac parameters change → volumepressure loops change ▪ ↑ preload (↑ EDV) → ↑ strength of contraction → ↑ stroke volume → larger loop ▪ ↑ afterload → ↑ ventricular pressure during isovolumetric contraction → ↑ less blood leaves ventricle → ↑ end-systolic volume (ESV) → ↓ SV → loop narrower, taller (smaller SV, higher pressure; stroke work remains relatively stable) ▪ ↑ contractility → blood under ↑ pressure → longer ejection phase → left ventricular pressure = aortic pressure → ↑ SV, stroke work, ↓ ejection fraction (EF), EDV → loop widens Figure 16.3 Changes in stroke work as a result of increased preload (B), afterload (C), and contractility (D) represented on pressure-volume loop graphs. OSMOSIS.ORG 115

CARDIAC WORK osms.it/cardiac-work ▪ Work heart performs as blood moves from venous to arterial circulation during cardiac cycle PHASES OF CARDIAC WORK Atrial systole ▪ Begins when atria, ventricles in diastole ▪ Atrioventricular (AV) valves open → passive ventricular filling ▪ Atrial depolarization → atria contract (atrial kick during systole) → completes ventricular filling (EDV) ▪ Venous pulse: “a” wave (↑ atrial pressure) ▪ ECG ▫ P wave, PR interval Isovolumetric ventricular contraction ▪ Ventricular contraction begins (ventricular systole) → ventricular pressure > atrial pressure → AV valves close (S1); semilunar valves closed ▪ ECG ▫ QRS complex Rapid ventricular ejection ▪ Ventricular systole continues → left ventricular pressure > aortic pressure → aortic valve forced open → blood ejected (SV) (blood also ejected into pulmonary vasculature via pulmonic valve) ▪ ↑ aortic pressure ▪ Atrial filling begins ▪ ECG ▫ ST segment ▪ ▪ ▪ ▪ ventricular pressure < aortic pressure → aortic valve closes (S2); causes dicrotic notch on aortic pressure curve All valves closed Ventricular volume ▫ Constant Complete ventricular repolarization ECG ▫ T wave ends Rapid ventricular filling ▪ Ventricular diastole continues → ventricular pressure < atrial pressure → AV valves open ▪ Passive ventricular filling (ventricles relaxed, compliant) ▪ S3 (normal in children) produced by rapid filling Reduced ventricular filling (diastasis) ▪ Ventricular diastole continues; ventricles relaxed ▪ Mitral valve open ▪ Changes in heart rate (HR) alter length of diastasis TYPES OF CARDIAC WORK Internal work ▪ Pressure work: within the ventricle to prepare for ejection ▪ Quantified by multiplying isovolumic contraction time by ventricular wall stress ▪ Accounts for 90% of cardiac work Reduced ventricular ejection ▪ ↓ ventricular ejection velocity ▪ ↑ atrial pressure ▪ Ventricular repolarization begins ▪ ECG ▫ T wave External work ▪ Volume work: ejecting blood against arterial resistance; product of pressure developed during ejection, SV ▪ Represented by area contained in pressurevolume loop ▪ Accounts for 10% of cardiac work Isovolumetric ventricular relaxation ▪ Ventricles relaxed (ventricular diastole); Myocardial oxygen consumption ▪ Pressure work > volume work 116 OSMOSIS.ORG

Chapter 16 Cardiovascular Physiology: Cardiac Cycle ▪ Aortic stenosis → ↑↑ pressure work → ↑↑ oxygen consumption, ↓ CO ▪ Strenuous exercise → ↑ volume work → ↑ oxygen consumption, ↑ CO LV and right ventricle (RV) ▪ Volume work: CO LV = RV CO ▪ Pressure work: LV (aortic pressure 100mmHg) > RV (pulmonary pressure 15mmHg) ▫ ↑ systemic pressure (e.g. hypertension) → ↑ LV pressure work → ventricular wall hypertrophy ▫ Law of Laplace for sphere (e.g. heart): thickness of heart wall increases → greater pressure produced CARDIAC PRELOAD osms.it/cardiac-preload ▪ EDV: volume load created by blood entering ventricles at end of diastole before contraction ▪ Establishes sarcomere length, ventricular stretch as ventricles fill (length-tension relationship) FACTORS AFFECTING PRELOAD Venous pressure ▪ Includes blood volume, rate of venous return to RA ▪ ↑ blood volume, venous return → ↑ preload Ventricular compliance ▪ Flexibility: ability to yield when pressure applied ▪ Compliant, “stretchy” ventricles → ↑ preload ▪ Noncompliant, stiff ventricles → ↓ preload Atrial contraction ▪ Early ventricular diastole → ventricles relaxed, passively fill with blood from atria via open AV valves → late ventricular diastole atrial systole (atrial kick) → additional blood into ventricles ▪ Accounts for 20% of ventricular preload Resistance from valves ▪ Stenotic mitral, tricuspid valves create inflow resistance → ↓ filling → ↓ preload ▪ Stenotic pulmonic, aortic valves create outflow resistance → ↓ emptying → ↑ preload HR ▪ Normal heart rate allows adequate time for ventricles to fill ▪ Tachyarrhythmias → ↓ filling time → ↓ preload OSMOSIS.ORG 117

CARDIAC AFTERLOAD osms.it/cardiac-afterload ▪ Amount of resistance ventricles must overcome during systole ▪ Establishes degree, speed of sarcomere shortening, ventricular wall stress (forcevelocity relationship) ▪ ↑ afterload → ↓ velocity of sarcomere shortening ▪ ↓ afterload → ↑ velocity of sarcomere shortening FACTORS AFFECTING AFTERLOAD LV ▪ Systemic vascular resistance (SVR) ▪ Aortic pressure RV ▪ Pulmonary pressure Resistance from valves ▪ Stenotic pulmonic, aortic valves create outflow resistance → ↑ afterload LAW OF LAPLACE osms.it/law-of-Laplace ▪ Describes pressure-volume relationships of spheres ▪ Blood vessels ▫ > radius of artery = > pressure on arterial wall ▪ Heart ▫ Wall tension produced by myocardial fibers when ejecting blood depends on thickness of sphere (heart wall) ▪ Laplace’s formula: tension on myocardial fibers in heart wall = pressure within ventricle x volume in ventricle (radius) / wall thickness 118 OSMOSIS.ORG ▪ T= Pxr h ▫ T = wall tension ▫ P = pressure ▫ r = radius of ventricle ▫ h = ventricular wall thickness ▪ Dilation of heart muscle increases tension that must be developed within heart wall to eject same amount of blood per beat ▪ Myocytes of dilated left ventricle have greater load (tension) ▫ Must produce greater tension to overcome aortic pressure, eject blood → ↓ CO

Chapter 16 Cardiovascular Physiology: Cardiac Cycle FRANK–STARLING RELATIONSHIP osms.it/Frank-Starling_relationship ▪ Loading ventricle with blood during diastole, stretching cardiac muscle → force of contraction during systole ▪ Length-tension relationship ▫ Amount of tension (force of muscle contraction during systole) → depends on resting length of sarcomere → depends on amount of blood that fills ventricles during diastole (EDV) ▫ Length of sarcomere determines amount of overlap between actin, myosin filaments, amount of myosin heads that bind to actin at cross-bridge formation ▫ Low EDV → ↓ sarcomere stretching → ↓ myosin heads bind to actin → weak contraction during systole → ↓ SV ▫ Too much sarcomere stretching prevents optimal overlap between actin, myosin → ↓ force of contraction → ↓ SV ▪ Allows intrinsic control of heart = venous return with SV ▪ Extrinsic control through sympathetic stimulation, hormones (e.g. epinephrine), medications (e.g. digoxin) → ↑ contractility (positive inotropy), SV ▪ Negative inotropic agents (e.g betablockers) → ↓ contractility → ↓ SV Figure 16.4 Graphical representation of the Frank–Starling relationship and sarcomere length at low, mid-range, and high EDVs. A mid-range EDV (B), where the volume of blood returning to the ventricles is increasing but is not too large (C), allows for best myosin-actin binding → ↑ strength of contractions → ↑ stroke volume. Figure 16.5 Graphical representation of positive and negative inotropic effects on the Frank–Starling relationship. OSMOSIS.ORG 119

STROKE VOLUME, EJECTION FRACTION, & CARDIAC OUTPUT osms.it/stroke-volume-ejection-fraction-cardiac-output SV ▪ Volume of blood (mL) ejected from ventricle with each contraction ▪ Calculated as difference between volume of blood before ejection/EDV, after ejection (ESV) ▪ EDV (120mL) - ESV (50mL) = 70mL ▪ SV affected by preload, afterload, inotropy EF ▪ Fraction of EDV ejected with each contraction ▪ SV (70)/EDV (120) = 58 (EF) ▪ Average = 50–65% CO ▪ Volume of blood ejected by ventricles per minute ▪ SV (120) x HR (70) = 4900mL/min 120 OSMOSIS.ORG