Cardiac Physiology an Overview Dr L J Solomon Department of Paediatrics and Child Health School of Medicine Faculty of Health Sciences University of the Free State and PICU Universitas Academic Hospital Bloemfontein
Overview Haemodynamic Principles Cardiac Cycle events and (LV) Pressure and volume changes Whole Heart flow Length tension relationships (Starling Mechanisms) Subcellular E-C coupling mechanisms Determinants of myocardial performance Adrenergic effects Starling effects Force-frequency relation Vascular function Pleural Pressure and Cardiac function Software simulator to illustrate priciples
The heart is just a pump! Dr. Christiaan Barnard of South Africa, left, with Dr. Michael E. DeBakey and Dr. Adrian Kantrowitz of Brooklyn in 1967 July 13, 2008
Cardiac Physiology Theoretical Model: Pumps Left side Right side Pipes Pulmonary Systemic Central Peripheral Resistance (variable) Tissue arteriolar and capillary networks Preload Contractility HR Afterload Peripheral Resistance CO = HR X SV
Haemodynamic principles Flow (Q), Velocity (v), Cross sectional area (A) v = Q/A v Aorta Cap bed Large veins
Haemodynamic principles
Haemodynamic principles Resistances in series = R1 +R2 + R3 etc. Resistances in parallel = 1/R1 + 1/R2 + 1/R3 etc. P Aorta Arterioles Cap bed Large veins
Model limitations Non-Newtonian Fluids Blood: viscosity decreases with increased shear rate http://en.wikipedia.org/wiki/hemorheology#cite_ref-2 Non-linear Pressure Flow relationships Curved, branched, tapered, distensible arteries Non-laminar, pulsatile flow Cardiopulmonary interactions Complexities of flow through heart Twist Asymmetric redirection of flow
Cardiac Physiology Cardiac Cycle Systole http://library.med.utah.edu/kw/pharm/hyper_heart1.html Diastole Artificial Organs 35(5):454 458
Cardiac Physiology Asymmetric redirection of flow through the heart Philip J. Kilner, Guang-Zhong Yang, A. John Wilkes, Raad H. Mohiaddin, David N. Firmin & Magdi H. Yacoub Nature 404, 759-761(13 April 2000) doi:10.1038/35008075 http://www.nature.com/nature/journal/v404/n6779/fig_tab/404759a0_f3.htmlnature a, In the linear arrangement in systole, contraction of the ventricle (thick boundary) pulls on the atrium (white arrowheads), contributing to atrial expansion. Inflow gives rise to recirculation bilaterally (thin arrows), a relatively unstable pattern of flow that redirects blood inappropriately for subsequent ventricular filling. Any recoil of the ventricle (black arrowheads) away from blood accelerated to the outflow (thick arrows) would push back against the atrium, counteracting atrial expansion. b, In diastole, recirculation in the expanding ventricle redirects fluid away from the outflow tract.
Cardiac Physiology Asymmetric redirection of flow through the heart Philip J. Kilner, Guang-Zhong Yang, A. John Wilkes, Raad H. Mohiaddin, David N. Firmin & Magdi H. Yacoub Nature 404, 759-761(13 April 2000) doi:10.1038/35008075 http://www.nature.com/nature/journal/v404/n6779/fig_tab/404759a0_f3.htmlnature c, In a sinuously looped arrangement in systole, ventricular contraction also expands the adjacent atrium (white arrowheads). Atrial filling is now asymmetric and more stable, streamlines being accommodated by wall curvatures in a way that redirects momentum towards the atrio-ventricular valve. Recoil of the ventricle away from ejected blood (black arrowheads) now adds to the pull on the atrio-ventricular junction, enhancing rather than suppressing atrial expansion. d, In diastole, redirected intra-atrial momentum can contribute to ventricular filling, which occurs with asymmetric recirculation, redirecting flow preferentially towards the outflow tract. Looped curvature thus allows the sinuous redirection of momentum and dynamically enhanced reciprocation between atrial and ventricular function.
Cardiac Physiology http://www.nature.com/nature/journal/v404/n6779/fig_tab/404759a0_f1.html#figure-title a, In the right atrium in ventricular systole, viewed in a sagittal plane from the subject's right side, blood entering from superior and inferior caval veins contributes to the forward rotation of blood in the expanding chamber. Coloured streamlines computed from magnetic resonance velocity acquisitions show local speed, as indicated by the colour scale. b, In early ventricular diastole, further inflow of blood is again redirected forwards and down the front of the right atrium, and away from the viewer (out of plane) through the open tricuspid valve. Asymmetric redirection of flow through the heart Philip J. Kilner, Guang-Zhong Yang, A. John Wilkes, Raad H. Mohiaddin, David N. Firmin & Magdi H. Yacoub Nature 404, 759-761(13 April 2000) doi:10.1038/35008075
Cardiac Physiology http://www.nature.com/nature/journal/v404/n6779/fig_tab/404759a0_f1.html#figure-title c, In the left atrium in ventricular systole, blood enters from the upper and lower pulmonary veins on each side, indicated by arrows in this coronal plane viewed from the front (lower veins lie out of plane posteriorly). Streamlines are redirected asymmetrically round towards the mitral valve, which is closed, but pulled by contraction of the left ventricle. d, In early ventricular diastole, there is further inflow from veins while blood passes through the open mitral valve to the left ventricle. Vertical and oblique dotted lines indicate planes orthogonal to this panel Asymmetric redirection of flow through the heart Philip J. Kilner, Guang-Zhong Yang, A. John Wilkes, Raad H. Mohiaddin, David N. Firmin & Magdi H. Yacoub Nature 404, 759-761(13 April 2000) doi:10.1038/35008075
Cardiac Physiology http://www.nature.com/nature/journal/v404/n6779/fig_tab/404759a0_f1.html#figure-title e, In the left ventricle in systole, streamlines pass from the left ventricle through the aortic valve, viewed here in an oblique long-axis plane from above left, the front of the subject being located to the left of the image. f, In early diastole, streamlines pass from the left atrium through the open mitral valve to the left ventricle, with asymmetric recirculation (curved arrow) round the anterior leaflet of the mitral valve. Asymmetric redirection of flow through the heart Philip J. Kilner, Guang-Zhong Yang, A. John Wilkes, Raad H. Mohiaddin, David N. Firmin & Magdi H. Yacoub Nature 404, 759-761(13 April 2000) doi:10.1038/35008075
Frank-Starling Law / mechanism of the http://en.wikipedia.org/wiki/otto_frank_(physiologist) Heart http://en.wikipedia.org/wiki/ernest_starling Otto Frank 1865-1944 Ernest Starling 1866 to 1927 Stroke Volume increases with increasing End Diastolic Volume which stretches the ventricular wall, causing cardiac muscle to contract more forcefully (the so-called Frank-Starling mechanism). Stroke volume may also increase due to greater contractility of the cardiac muscle during exercise, independent of end-diastolic volume. Stroke volume is influenced more by the Frank-Starling mechanism at lower work rates while contractility has a greater influence at higher work rates.
Length Tension Sarcomere (Starling mechanism) R. John Solaro Advan in Physiol Edu 277:S155-S163, 1999
Subcellular mechanism Ca ++ Flux Influx during systole Efflux during diastole influx efflux Donna H. Korzick Adv Physiol Educ 35: 22 27, 2011
Contractile mechanism:
Sarcomere Length Tension and Ca++
Pump Performance Determinants Neuro-humeral tone Adrenergic receptor regulation Frank Starling Effects Force Frequency Relation Vascular Function
Adrenergic receptor regulation
Frank Starling effects Cardiac output CO = HR X SV SV ~ Contractility, Preload, Afterload Decreased Afterload or Increased contractility CO or SV Normal Increased Afterload or Decreased contractility (Preload)
Force frequency relation force-frequency relationship represents an intrinsic regulatory factor essential for immediate adjustment of cardiac contractile function to rapidly changing requirements of blood supply. This frequency-dependent gain in contractility is intrinsic to mammalian cardiac muscle and allows for greater contractile force [Eur J Pharmacol 2004, 500:73-861]. The heart generally beats stronger when it is stimulated to contract faster, AND it displays frequency-dependent acceleration of relaxation (FDAR) [Eur J Pharmacol 2004, 500:73-861, J Mol Cell Cardiol 2007, 43:523-5312]. From a physiological perspective, FDAR participates in the maintenance of efficient ventricular filling and coronary blood flow at higher heart rates, despite a decreased diastolic time interval. Critical Care 2009, 13:R14
Force recordings from isolated muscle strips from RA and LV from explanted human hearts. Münch G et al. Am J Physiol Heart Circ Physiol 2000;278:H1924-H1932 2000 by American Physiological Society
Vascular Function Curve CO effect on CVP CO CVP Peripheral Resistance CVP CO
Vascular Function Curve CO effect on CVP CO CVP Peripheral Resistance CVP CO
Vascular Function Curve CO effect on CVP CO CVP Peripheral Resistance CVP CO
Cardiac Physiology Interactions between Vascular function curve and Starling curve http://en.wikipedia.org/wiki/frank%e2%80%93starling_law_of_the_heart
Cardiac Physiology Functional Anatomy Circulation Compartments: Intra-thoracic Abdominal Peripheral Pressure gradients Flow From Shekerdemian and Bohn: Arch. Dis. Child 1999;80;475-480
Cardiac Physiology Right Ventricular Preload, Pleural Pressure, Cardiac output Pleural Pressure +2 CO 0-2 -4-6 -4-2 0 +2 +4 Right Atrial Pressure
Cardiac Physiology Right Ventricular Afterload and Lung Volume Total PVR Alveolar Vessels Parenchymal Vessels RV FRC TLC Lung Volume
Cardiac Physiology Left Ventricular Afterload Transmural Pressure = Pressure inside pressure outside Therefore P LVTM = P Ao P PL Afterload increases with: High P Ao Low P PL
Cardiac Physiology Artificial Organs 35(5):454 458,