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Cardiac Physiology and Hemodynamics

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Cardiac Physiology and Hemodynamics 2017-09-22 objectives cardiac function & • review the principles of electromechanical coupling hemodynamics • master the concept of preload, afterload, and contractility Lars Grosse-Wortmann • understand the difference between pressure and resistance • comprehend the indication of CMR in shunt lesions … or: what do contact lenses and cardiac catheterization have in common ? • speak a common language • electro-mechanical coupling • determinants of cardiac output • the cardiac cycle • hemodynamics 1 2017-09-22 1. Ca++ enters sarcoplasm 2. binds to troponin-C 3. actin binds to myosin 4. ATP binds to myosin 5. ATP → ADP + P 6. release of P 7. power stroke 8. release of ADP 9. ATP binds to myosin 10. muscle relaxes • electro-mechanical coupling • determinants of cardiac output • the cardiac cycle • hemodynamics Otto Frank Ernest Starling 2 2017-09-22 Frank Starling law cardiac output • CO = amount of blood pumped by each ventricle in one minute • CO = heart rate (HR) X stroke volume (SV) • CI = CO, indexed to BSA = CO / BSA • example: – BSA 2.0 m2 – HR 60 bpm, SV 90 ml • CO = 5.4 l/min • CI = 2.7 l/min/m2 regulation of CO factors affecting SV • HR, SV • PRELOAD – extend of myocardial stretch by contained blood • SV = amount of blood pumped by one – ~ CVP ventricle during one contraction = EDV (enddiastolic volume) – • AFTERLOAD – load against the ventricle must pump ESV (endsystolic volume) – ~ BP • EF = portion of EDV that is pumped during • CONTRACTILITY one contraction – force of myocardial “squeeze” = SV / EDV – ~ EF 3 2017-09-22 preload or afterload ? afterload preload • mitral regurgitation • pulmonary stenosis • VSD • ASD • coarctation of aorta • H(o)CM • PDA which heart would you want ? nl. DCM HCM d X Law of Laplace • What we know is not much. What we do not know is immense. • The weight of evidence for an extraordinary claim must be proportioned to its strangeness. 4 2017-09-22 contractility • contractility from: – increased sympathetic stimuli – Ca++, positive inotropes and other drugs • contractility from: – acidosis – intrinsic myocardial diseases – ischemia – hypoxia – sympathetic inhibition ejection fraction • EF = (EDV-ESV/EDV) x 100 • Estimates global ventricular performance • Echo: – M mode – Simpson’s – 3D echo • dependent on preload / afterload / heart rate • no information on regional wall motion, synchronicity, AV valve function 5 2017-09-22 ejection fraction M-mode ejection fraction Simpson‘s myocardial mechanics Courtesy of P. Claus / M. Friedberg Courtesy of B. Eidem / M. Friedberg 6 2017-09-22 cardiac cycle • electro-mechanical coupling 1 Late diastole: both sets of START chambers are relaxed and ventricles fill passively. Isovolumic ventricular 5 relaxation: as ventricles 2 Atrial systole: atrial contraction relax, pressure in ventricles forces a small amount of • determinants of cardiac output falls, blood flows back into additional blood into ventricles. cups of semilunar valves and snaps them closed. • the cardiac cycle • hemodynamics Isovolumic ventricular Ventricular ejection: 3 4 contraction: first phase of as ventricular pressure ventricular contraction pushes rises and exceeds AV valves closed but does not pressure in the arteries, create enough pressure to open the semilunar valves semilunar valves. open and blood is ejected. the cardiac cycle Time (msec) 0 100 200 300 400 500 600 700 800 Electro- QRS QRS Cardiac cycle complex cardiogram complex (ECG) P T P 120 90 Dicrotic Aorta Pressure notch (mm Hg) Left 60 ventricular Pulmonary artery pressure Left atrial Mitral valve 30 pressure Tricuspid valve ejection S2 Heart S1 sounds 135 Left ventricular volume (mL) 65 Atrial Ventricular Ventricular Atrial systole systole diastole systole Wigger‘s diagram Atrial systole Isovolumic Ventricular Early Late Atrial ventricular systole ventricular ventricular systole contraction diastole diastole 7 2017-09-22 the cardiac cycle the cardiac cycle Aorta Aorta Pulmonary artery Pulmonary artery Mitral valve Mitral valve Tricuspid valve Tricuspid valve filling isovolumetric relaxation the cardiac cycle the cardiac cycle Aorta diastesis Aorta Pulmonary artery Pulmonary artery Mitral valve Mitral valve Tricuspid valve filling Tricuspid valve isovolumetric contraction 8 2017-09-22 tachycardia shortens diastole • electro-mechanical coupling • determinants of cardiac output Chung et al., Am J Physiol Heart Circ Physiol 287:2003-08, 2004 • the cardiac cycle 60 bpm 1000 ms • hemodynamics 150 bpm 400 ms how do we know ... ? cardiac catheterization 2006 BC Imhotep observations on the pulse 400 BC Hippocrates signs and symptoms of heart disease blood, phlegm, black bile, yellow bile 300 BC Aristotle beating heart in a chick embryo 250 BC Erasistratus anatomy of the heart with 4 valves 129-199 Galen heart is a muscle, but liver moves the blood, blood passes through pores in the septum 1540 Servetus pathway of blood, oxygenation in the lungs 1904 - 1979 1628 Harvey heart is a pump, circulatory system http://www.ptca.org/archive/bios/forssmann.html 9 2017-09-22 X-rays “Röntgen-rays“ pulmonary arterial pressure • 15 – 25mmHg / 8-12mmHg – in • left to right shunt • PAH • pulmonary vein stenosis, MS, elevated LVEDP 1845 - 1923 vascular resistance 6 L 9 L Qp / Qs • R = ΔP / Q Ohm‘s law (R=V/I) 3 L 1.5:1 – mmHg / [ml/(min x m2)] – in Wood units x m2 • Rs = (AO-P – RA-P) / Qs (15-30 WU*m2) • Rp = (PA-P – LA-P) / Qp (<3 WU*m2) 6 L 3 L 3 L – increases with acidosis, pCO2 ++ – decreases with O2, NO, (prostacyclin, Ca -block., sildenafil, bosentan) 10 2017-09-22 ways to measure Qp and Qs • dilution (dye, heat) – Fick 1829 - 1901 14 year ♀ the Fick principle MAPCA anatomy ? surgical options ? PHtn ? I = I2-I1 = V*CI2 – V*CI1 V = I / (CI2–CI1) V/t = I / [t*(CI2–CI1)] CO = VO2 / (O2venous – O2arterial) 11 2017-09-22 PAPVC Qs = SVC + DAO flows 2 = 2.40 l/min/m2 • RPA = 4.0 l/min/m Qp = pulmonary vein flow • LPA = 5.0 l/min/m2 = 6.20 l/min/m2 • Qp = 9.0 l/min/m2 Qp/Qs = 2.58 • Qs = ascending aorta = 3.0 l/min/m2 r-MAPCA r-MAPCAs: inaccurate l-MAPCAs = 3.61 l/min/m2 • Qp / Qs = 3.0 RPVs = 2.16 l/min/m2 • total left-to-right shunt = 6.0 l/min/m2 r-mAP = 61mmHg, wedge 15mmHg 2 r-PVRi = 21 WU * m2 • vertical vein = 1.5 l/min/m l-mAP = 17mmHg • calculated LRS via ASD l-PVRi = 0.6 WU * m2 2 l-MAPCA • total LRS – vertical vein = 4.5 l/min/m CHD – made simple summary how does the blood • relaxation consumes energy go ‘round ? • pulmonary blood flow • myocardial performance depends on • systemic blood flow preload, afterload, and contractility • intracardiac shunts • extracardiac shunts • blood follows the path of least resistance • path of least resistance • pressure + resistance + shunt • RV preload / afterload • LV preload / afterload • ventricular function 12.
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