Changes in pressure-volume loops_ Video & Anatomy _ Osmosis

ARDIAC CYCL MEASURING CARDIAC OUTPUT - FICK PRINCIPLE NOTES osms.it/Fick-principle = Model used to measure cardiac output (CO) = Qutput of left, right ventricles equal during normal cardiac function = Steady state: rate of O, consumption = amount of O, leaving lungs via pulmonary vein - amount of O, returning via pulmonary arteries x CO = Pulmonary blood flow of right heart = CO of left heart: used to calculate CO Cardiac Output = O, consumption [O,] pulmonary vein - [O,] pulmonary artery = 250mL/minute = total O, consumption (7/0kg, biologically-male individual); pulmonary venous O, content = 0.20/mL; pulmonary arterial O, 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 O, consumption / renal arterial O, - renal venous O, 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 = 1 venous return — 1 RA pressure — 1 LV end-diastolic volume (EDV)/preload, myocardial fiber stretch — 1 CO = |V 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

112 OSMOSIS.ORG 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 = 1 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) — 1 flow from arterial to venous circulation — 1 venous return — clockwise rotation of curve = 1 TPR (1 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 s 1 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. beta- blockers) = Opposite effect BLOOD VOLUME = Alters vascular curve = 1 circulating volume (e.g. blood transfusion) s+ MSP — (1) curves intersect at 1 CO, RA pressure, (2) parallel shift of x-intercept (steady state), vascular curve to right, (3) no change in TPR = | circulating volume (e.g. hemorrhage) = Opposite effect = Changes in venous compliance are similar to blood volume changes s | venous compliance — changes similar to 1 circulating volume s 1 venous compliance — changes similar to | circulating volume TOTAL PERIPHERAL RESISTANCE = Alters both curves due to changes in afterload (cardiac curve), venous return (vascular curve) = 1 TPR — 1 arterial pressure — 1 afterload — | CO — (1) downward shift of cardiac curve, (2) counterclockwise rotation of vascular curve, (3) | venous return, (4) RA pressure unchanged, |/1 (depending on cardiac, venous curve alteration), (5) curves intersect at altered steady state = | TPR (arteriolar dilation) = Opposite effect

© ETECTION ISOVOLUME TRIC CONTRACTION \ J SYSTOLE T @ Mitral valve opens @ Mitral valve closes @ Aortic valve opens HEARTREAT 0 Aortic valve closes ( STROKE) Q 2 3 > LV Volume DIASTOLE / N (® 1SOVOLUME TRIC RELAXATION (® RELAXATION AorTiC MITRAL AorTIC MITRAL VALVE VALVE VALVE VAWE 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 — volume- (ESV) — | SV — loop narrower, taller pressure loops change (smaller SV, higher pressure; stroke work = 1 preload (1 EDV) — 1 strength of remains relatively stable) contraction — 71 stroke volume — larger = 1 contractility — blood under 1 pressure loop — longer gjection phase — left ventricular = 1 afterload — 1 ventricular pressure during pressure = agrtic pressure — T SV, stroke isovolumetric contraction — 1 less blood work, | ejection fraction (EF), EDV — loop leaves ventricle — 1 end-systolic volume widens A. NORMAL PRESSURE-VOLUME LOOP B. INCREASED PRELOAD A AN ESP - -T ESP - - i | | GTROKE | STROKE ‘: WORK 5 WORK I , | e : " : LARGER i | 3 : 3 | a |\ a \ 3 Li— N 1 . 3 L—— I o LV Volume | STK(le& g LV Volume STR'OK& ! END- systone VOLUME ENTiDAsTOLIC VOLUME VOLUME C. INCREASED AFTERLOAD D. INCREASED CONTRACTILITY | r\ | T/ ESP J-==-- N i § | [STROKE CTROKE : Remauns l LAR,G‘ o ! relative % : S&uble9 3 | [ / \/ % ;‘Ur‘—---[ ------- 1 . % s e i R LV Volume STR&K& LV Volume STR'OK& VOLUME VOLUME 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

= Aortic stenosis — 11 pressure work — 11 oxygen consumption, | CO = Strenuous exercise — 1 volume work — 1 oxygen consumption, 1 CO LV and right ventricle (RV) = Volume work: CO LV =RV CO Chapter 16 Cardiovascular Physiology: Cardiac Cycle = Pressure work: LV (aortic pressure 100mmHg) > RV (pulmonary pressure 15mmHgQ) s 1 systemic pressure (e.g. hypertension) — 1 LV pressure work — ventricular wall hypertrophy = | aw 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 * |ncludes blood volume, rate of venous return to RA = 1 blood volume, venous return — 1 preload Ventricular compliance = Flexibility: ability to yield when pressure applied = Compliant, “stretchy” ventricles — 1 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 — 1 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 FACTORS AFFECTING AFTERLOAD overcome during systole : LV = Establishes degree, speed of sarcomere _ . shortening, ventricular wall stress (force- * Systemic vascular resistance (SVR) velocity relationship) = Aortic pressure = 1 afterload — | velocity of sarcomere RV shortening : = Pulmonary pressure = | afterload — 1 velocity of sarcomere yP shortening Resistance from valves = Stenotic pulmonic, aortic valves create outflow resistance — 1 afterload LAW OF LAPLACE osms.it/law-of-Laplace = Describes pressure-volume relationships of = T=Pxr spheres h = Blood vessels o T = wall tension ° P = pressure o r = radius of ventricle o 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 = > 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 - Myocytes of dilated left ventricle have fibers in heart wall = pressure within ) , , . greater load (tension) ve_ntrlcle X volume in ventricle (radius) / wall - Must produce greater tension to thickness overcome aortic pressure, gject blood — } CO 118 OSMOSIS.ORG

STROKE VOLUME, EJECTION FRACTION, & CARDIAC OVTPUT osms.it/stroke-volume-e jection-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