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Ventricular Pressure-Volume Loops Steve Wood, PhD

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Presentation on theme: "Ventricular Pressure-Volume Loops Steve Wood, PhD"— Presentation transcript:

1 Ventricular Pressure-Volume Loops Steve Wood, PhD scwood@salud.unm.edu

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5 Cardiac Output Cardiac Output Heart Rate Heart Rate Stroke Volume Stroke Volume Preload Afterload Inotropy SNS PNS + + - - + + + + - - + + + + + + 5 II. The Ventricle as a Pump: Cardiac Output = HR x SV

6 Single Starling Curve Normal values are LVEDP 8 mmHg and SV of 70 ml/beat. Cytosolic Ca ++ constant. Inotropy (contractility) is constant. The increased force of contraction at greater preload is due to: (1) favorable overlap of thin and thick filaments; and (2) increased affinity of Ca ++ for Troponin C. Single Starling Curve Normal values are LVEDP 8 mmHg and SV of 70 ml/beat. Cytosolic Ca ++ constant. Inotropy (contractility) is constant. The increased force of contraction at greater preload is due to: (1) favorable overlap of thin and thick filaments; and (2) increased affinity of Ca ++ for Troponin C. 6 III. The Ventricle as a Pump: Frank-Starling Curves Preload

7 Inotropy afterload Frank-Starling Curves inotropy afterload 7 Changes in afterload and contractility (inotropy ) shift the Frank-Starling curve up or down (at any given preload) PV loops explain this – slide 18 Changes in afterload and contractility (inotropy ) shift the Frank-Starling curve up or down (at any given preload) PV loops explain this – slide 18 Preload

8 8 A drug which caused vasoconstriction of systemic veins (alpha agonist) would shift point 1 to point ___. A B C D

9 Stroke Volume (or cardiac output) Left Ventricular end-diastolic pressure (or end-diastolic volume) Normal Heart failure Increased contractility a b c Starling Curves in Heart Failure Hypotension Pulmonary congestion 9

10 10 This isovolumic curve is also called P o (pressure at zero ejection), or the end-systolic pressure volume relationship (ESPVR). This "resting" curve represents pressures during diastolic filling of the ventricle, and reflects passive properties of the ventricular wall that resist stretch; i.e., the compliance of the ventricle and factors that impair Ca++ reuptake into SR (e.g., hypoxia) (Lusitropy) IV. Pressure-Volume Relationships in the Ventricles

11 1 2 3 4 11 V. PRESSURE-VOLUME LOOPS LV Volume, ml LV Pressure, mm Hg a LV Volume, ml 020050120 LV Pressure, mm Hg 0 100 ESV EDV b c d ESPVR EDPVR 1 2 3 4 SV Preload Afterload

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14 14 Work = force x distance = force x cm P = force/unit area = force/cm 2 Volume = cm 3 P x V = force/cm 2 x cm 3 = force x cm Work = force x distance = force x cm P = force/unit area = force/cm 2 Volume = cm 3 P x V = force/cm 2 x cm 3 = force x cm Work of the Heart Cardiac Work = Stroke work x HR Work of the Heart Cardiac Work = Stroke work x HR

15 15 Oxygen Demand of the Heart HR x SBP VO 2

16 Inotropy Stroke Work Curve inotropy Stroke Work (P x V) Stroke Work (P x V) 16 When stroke work is plotted against preload ONLY changes in inotropy will shift curve.

17 17 At constant afterload and inotropy SV increases and ESV remains constant EF increases Dashed lines are systolic and diastolic pressures At constant afterload and inotropy SV increases and ESV remains constant EF increases Dashed lines are systolic and diastolic pressures Effect of Increased Preload A. Effect of Preload on Stroke Volume VI. Effects of Preload, Afterload, Inotropy and Lusitropy on Ventricular Pressure-Volume Loops

18 18 At constant afterload and inotropy SV decreases and ESV remains constant EF decreases slightly At constant afterload and inotropy SV decreases and ESV remains constant EF decreases slightly Effect of Decreased Preload Effects of changing preload = Starlings Law

19 19 At constant preload and inotropy SV decreases and ESV increases EF decreases No change in contractility (aortic closure occurs on the same line) This is an acute effect of sudden increase in afterload; in subsequent beat increased EDV will increase SV At constant preload and inotropy SV decreases and ESV increases EF decreases No change in contractility (aortic closure occurs on the same line) This is an acute effect of sudden increase in afterload; in subsequent beat increased EDV will increase SV Effect of Increased Afterload B. Effect of Afterload on Stroke Volume

20 20 Effect of Decreased Afterload At constant preload and inotropy SV increases and ESV decreases EF increases No change in contractility (aortic closure occurs on the same line) At constant preload and inotropy SV increases and ESV decreases EF increases No change in contractility (aortic closure occurs on the same line)

21 21 C. Effect of Contractility on Stroke Volume At constant preload and afterload SV increases and ESV decreases EF increases At constant preload and afterload SV increases and ESV decreases EF increases Effect of Increased Contractility (+ Inotropy)

22 22 At constant preload and afterload SV decreases and ESV increases EF decreases Over time, EDV increases causing increased LV and LA pressure – next slide At constant preload and afterload SV decreases and ESV increases EF decreases Over time, EDV increases causing increased LV and LA pressure – next slide Effect of Decreased Contractility (- Inotropy)

23 23 D. Systolic and Diastolic Heart Failure Systolic Failure EDV increases with loss of inotropy because increased ESV is added to normal venous return. Increased EDV causes increased LV and LA pressure. EF decreased Systolic Failure EDV increases with loss of inotropy because increased ESV is added to normal venous return. Increased EDV causes increased LV and LA pressure. EF decreased

24 24 Diastolic Failure Reduction in ventricular compliance Mechanisms: Hypertrophy; Reduced Lusitropy LV Increased LA and pulmonary venous pressure pulmonary congestion RV Increased RA pressure and systemic venous pressure peripheral edema EF may not change Diastolic Failure Reduction in ventricular compliance Mechanisms: Hypertrophy; Reduced Lusitropy LV Increased LA and pulmonary venous pressure pulmonary congestion RV Increased RA pressure and systemic venous pressure peripheral edema EF may not change Compliance = V/ P

25 25 Combined Systolic & Diastolic Failure Decreased SV and EF Increased end diastolic pressure Compensatory volume expansion further increases end diastolic pressure Combined Systolic & Diastolic Failure Decreased SV and EF Increased end diastolic pressure Compensatory volume expansion further increases end diastolic pressure

26 VII. Practice Questions 26 http://www.unmphysiology.org/boardreview/cardioquestions.html

27 Summary 27

28 28 Huh?


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