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Edit Comment Close Premium member Presentation Transcript PowerPoint Presentation: Moderator: Dr Mohan Speaker: Dr Nabeel Heart-lung interactionsPowerPoint Presentation: 5/4/2012 2 LA RA Pab ANS Diaphragm Extra-alveolar vessels Ppl P alv Alveolar vessels Non-abdominal compartment Abdominal compartment Pulmonary circulation Systemic circulation RV LV Thorax P syst Pra Venous return Cardiac output Patm P pcPowerPoint Presentation: 5/4/2012 3 Venous return LV afterload LV preload LV Contractility RV preload RV output Pulmonary Circulation Baseline Inotropic state Intravascular volume Lung compliance Ventricular interdependence LV stroke volume Parallel connection Series connection MODEL OF CIRCULATIONDeterminants of cardiac output: 5/4/2012 4 Determinants of cardiac output Heart rate Stroke volume Preload Contractility Afterload × Cardiac output = Myocardial fibre length at start of systole Myocardial fibre tension during systole Ventricular wall stress during ejectionPowerPoint Presentation: 5/4/2012 5 A=Preload dependence Frank Starling principle Failing heart Introduction: Introduction Intimately coupled Heart and lungs share same space in thorax and both are surrounded by pleural pressure Heart and great vessels exist in ‘ cardiac fossa’ surrounded by tissues Interactions subtle during normal health but profound during critical illness Respiratory disease exaggerates normal stresses of breathing and circulatory disease compromises response to these stresses. 5/4/2012 6Cardio-respiratory Interactions: Cardio-respiratory Interactions Transient effects: Periodic changes induced by inspiratory/expiratory cycle (phasic effects) or unsustained effects of various respiratory maneuvres (eg. recruitment maneuvres ) Steady state effects: Impact of sustained alterations of respiratory conditions Steady state effects depend on both mechanical and neuro-humoral factors PEEP/ CPAP, Weaning 5/4/2012 7PowerPoint Presentation: 5/4/2012 8 RV LV Thorax 1 3 2 4 Basic framework of Heart-lung interactions 1 = venous return 2= ventricular interdependence 3 = RV afterload / PVR 4 = LV afterloadPowerPoint Presentation: Determinants of heart-lung interactions ITP Pleural pressure Pericardial pressure Lung volume Transpulmonary Pressure 5/4/2012 9PowerPoint Presentation: 5/4/2012 10 ↑ LUNG VOLUME Hemodynamic effects of changes in lung volume Spontaneous Ventilation Positive Pressure Ventilation Autonomic tone PVR VALI/VILI due to high lung volumes can lead to ‘ventilator-associated heart injury’ Mechanical interactions Humoral factorsPowerPoint Presentation: Changes In Lung Volume Autonomic tone Respiratory sinus arrhythmia (normal autonomic responsiveness) Lung inflation at Vt >15 ml/kg ↓ heart rate by sympathetic withdrawal Reflex vasodilation with lung hyperinflation Humoral factors Sustained hyperinflation induce fluid retention by↑ plasma norepinephrine and renin and ↓ A trial natriuretic peptide (ANP) Mechanical interactions ( compression of heart in cardiac fossa by juxtacardiac ITP at high lung volumes) ↑ PVR (by hyperinflation) 5/4/2012 11PowerPoint Presentation: 5/4/2012 12 THORAX Venous return LV ejection Hemodynamic effects of changes in ITP Spontaneous Ventilation ↓ pressure gradient for venous return and LV ejection ↑ ITP ↓ ITP ↑ pressure gradient for venous return and LV ejection Positive Pressure VentilationVenous Return and RV filling (RV preload): Venous Return and RV filling (RV preload) Reservoir of circulation: SMALL VEINS (highly distensible) Capacitance (total volume at given pressure): Unstressed volume : Volume in venous reservoir when transmural /distending pressure nearly zero. Stressed volume : Additional volume in excess of unstressed volume generating + ve transmural pressure ( Psyst /MSFP) . 5/4/2012 13 Venous return = (MSFP−RAP) / Rv (MSFP−RAP) =5mm Hg approx.PowerPoint Presentation: 5/4/2012 14 Unstressed (Vo) “Stressed” (Vs) Psyst Venous return (Passive) Pra HEART Arterial resistance (Active ) Psyst = MSFP Pra = Right Atrial Pressure Rv= Resistance to venous return Reservoir: VEINS 70% blood volume. Venous return = (MSFP−RAP) / Rv Magder’s representation of venous capacitance Upstream DownstreamPowerPoint Presentation: 5/4/2012 15 RA LV Veins Arteries High Compliance Low Resistance Low Pressure Much Volume Low Compliance High Resistance High Pressure Little VolumePowerPoint Presentation: Psyst = upstream pressure for venous blood flow (nearly 7mm Hg) Average weighted pressure of venous reservoirs of systemic circulation Psyst depends on elastic properties and volume of blood in systemic veins Psyst/MSFP is closer to central venous than to arterial pressure 5/4/2012 16 Psyst Factors influencing MSFP/ Psyst Total volume of reservoir Compliance/diameter of reservoir S tressed VolumePowerPoint Presentation: 5/4/2012 17 Pra (mm Hg) 0 Guytonian Venous return curve ↑Rv Venous return (Pcrit) Slope=1/ Rv ↑MSFP Psyst = MSFP Pra = Right Atrial pressure VR=venous return CO=cardiac output Venous return = (MSFP−RAP) / Rv Flow limitation Flow-limitation of venous return (Venous return cannot increase indefinitely by ↓Pra ): Flow-limitation of venous return (Venous return cannot increase indefinitely by ↓ Pra ) 5/4/2012 18PowerPoint Presentation: 5/4/2012 19 (Vo) (Vs) Psyst Pcrt Flow limitation Pcrt=Critical closing pressure of veins=Patm Pra < Pcrt ThoraxPowerPoint Presentation: 5/4/2012 20 PEEP Transmission of ↑ITP into RA ↑RAP Constant p ressure gradient for venous return “Reflex matching of ↑RAP by equivalent ↑MSFP “ Cardiovascular Adaptation to PEEPPowerPoint Presentation: 5/4/2012 21↓Venous return by PEEP: ↓Venous return by PEEP Diaphragmatic descent ↑Intra-abdominal pressure( ↑ IAP) Distortion of venous geometry Compression of portal circulation by liver 5/4/2012 22 ↑Pcrt of veins ↑ITP Compression of veins at thoracic inlet ↑Rv ↑ resistance to venous return (Rv)↓Venous return by PEEP: 5/4/2012 23 Unstressed (Vo) “Stressed” (Vs) Psyst Pra ↑Pcrt ↑Rv ↓Venous return by PEEP ThoraxPowerPoint Presentation: Action of PEEP is modulated by volume status : Hypovolemia : prevents compensatory rise in MSFP systemic veins more compressible to PEEP 5/4/2012 24 Hypovolemia aggravates negative effects of PEEP on cardiac output.Guytonian Cardiac function curve (frank starling curve): Guytonian Cardiac function curve (frank starling curve) 5/4/2012 25 Pra Pcrt Cardiac output Venous return = cardiac output (Steady-state conditions) For any given set of cardiac function and venous return curves, only one combination of RAP and cardiac output (= venous return) exists at which steady-state conditions apply.PEEP and cardiac output (normal heart): 5/4/2012 26 RAP(mm Hg) Venous return 0 3 2 1 4 5 6 0 PEEP ZEEP PEEP+ hypovolemia PEEP+ volume expansion ↑MSFP ↑ITP PEEP and cardiac output (normal heart)PEEP and cardiac output (failing heart): PEEP and cardiac output (failing heart) 5/4/2012 27 RAP(mm Hg) Venous return 0 3 2 1 4 5 6 0 PEEP ZEEP ↑MSFP ↑ITPRV Output: RV Output RV output depends on: RV filling volume (preload) RV contractility RV afterload (maximal RV systolic wall stress) Pulmonary circulation is high flow, low-impedance circuit. Pulmonary vascular resistance (PVR) , R = 8 µ L/ ∏ r 4 (Poiseulle’s equation for flow) µ = viscosity, r= radius of pulmonary vessel, L= length of pulmonary vessel 5/4/2012 28 lung volume and PVR (bimodal relation) : lung volume and PVR (bimodal relation) 5/4/2012 29 PVR Lung volume) Alveolar vessels Extra-alveolar vessels RV TLC FRC Combined PVRPowerPoint Presentation: 5/4/2012 30 West zones of pulmonary circulation Pa >Pv >PA PA >Pa >Pv Pa >PA >Pv Pa=Pulmonary arterial pressure PA=Alveolar pressure Pv =Pulmonary venous pressurePulmonary vasculature: Pulmonary vasculature Alveolar vessels capillaries in alveolar walls surrounded by alveolar pressure (Palv) Extra-alveolar vessels vessels in corner of alveolar junctions larger vessels which feed or drain capillaries Pulmonar arteries and veins Behave as if surrounded by pleural pressure(Ppl) 5/4/2012 31PowerPoint Presentation: 5/4/2012 32 Extra-alveolar vessels Alveolar vessels Extra-alveolar vessels Extra-alveolar vessel compression by ↓↓ lung volume Extra-alveolar vessel (collapsed) Alveolar vessel (0pen)PowerPoint Presentation: 5/4/2012 33 Alveolar vessel compression by ↑↑ lung volume Extra-alveolar vessels Alveolar vessels Extra-alveolar vessels Corner vessels Corner vessels Radial traction on extra-alveolar vessels during inspiration Dilation of extra-alveolar vessels by ↑ lung volume Corner vesselPowerPoint Presentation: 5/4/2012 34 Hemodynamic effects of increased PVR RVSP > 35 mmHgPowerPoint Presentation: 5/4/2012 35 Pulmonary embolism/ Asthma exacerbation/ Hyperinflation/ HPV/ Pericardial tamponade RV/LV >0.6PowerPoint Presentation: Parallel Interdependence Diastolic filling of one ventrice influences geometry and stiffness of other ventricle RV & LV mechanically coupled: common septum & circumferential fibres (Diastolic septal interaction) expansion of both ventricles constrained by a common pericardium (Pericardial constraint) Cardiac fossa LV preload during spontaneous inspiration predominantly affected by parallel effects. Series Interdependence Propagation of changes in RV output to LV output LV preload during PEEP predominantly affected by series effects. Parallel interactions have limited effects, unless acute cor pulmonale is present. 5/4/2012 36 Ventricular interdependence LV preload and ventricular interdependence (parallel interdependence) : 5/4/2012 37 LV preload and ventricular interdependence (parallel interdependence) LV RV RV dilation LV ↑RV afterload (zone I/II) Impaired LV filling Induction /Aggravation of ‘acute cor pulmonale ’ Elongated, crescentic shaped RV Round -shaped RV RV/LV<0.6 (normal) (ratio between end-diastolic areas) RV/LV>0.6PowerPoint Presentation: 5/4/2012 38 LV end diastolic volume LV pressure RV end diastolic volume 0 50 35 20 Parallel connection 10 20 30 40LV preload and series interdependence: 5/4/2012 39 LV preload and series interdependenceVentricular afterload : Ventricular afterload Ventricular afterload : Ventricular afterload is the force opposing ventricular ejection. RV afterload : level of transmural pressure within pulmonary artery trunk (PVR) LV afterload : level of transmural pressure within aortic root 5/4/2012 40PowerPoint Presentation: LV ejection and afterload 5/4/2012 41 Law of Laplace links transmural pressure (P) to surface tension (T) and radius (r) of vessel. P T = Pr/h T rPowerPoint Presentation: 5/4/2012 42LAPLACE LAW: LAPLACE LAW Myocardial Systolic wall Tension, T= (P TM × r) P TM = ( P LV − P pl ) r= radius; LV wall geometry 5/4/2012 43 P pl P AO Thorax P TM P LV T + + + + + +PowerPoint Presentation: 5/4/2012 44 ↑ITP ↓ITPRole of changes in ITP to define cardiovascular performance : Role of changes in ITP to define cardiovascular performance 5/4/2012 45 Effect of changes in ITP in CHF and normo -/ hypervolemia Effect of changes in ITP in hypovolemiaPowerPoint Presentation: 5/4/2012 46 LV pressure LV volume LVESP Diastolic pressure volume relationship a b c d Ventricular ejection Ventricular filling Isometric relaxation Isometric contraction Diastolic dysfunction Systolic dysfunction Pressure - Volume loop of left ventricle (LVESP=LV end systolic pressure)PowerPoint Presentation: 5/4/2012 47 LV pressure LV volume ↑ITP ↓ ITP ↓LV ejection pressure ↓LV preload Effect of changes in ITP in CHF and normo -/ hypervolemia Failing hearts are more sensitive to afterload changes than normal heartsHemodynamic effects of ventilation: Hemodynamic effects of ventilation Hemodynamic effects of spontaneous ventilation (connection in parallel / ventricular interdependence) Hemodynamic effects of mechanical ventilation (connection in series) 5/4/2012 48PowerPoint Presentation: Pleural pressure↑ Transpulmonary pressure↑ RV preload↓ RV afterload↑ LV preload↑ (squeezed alveolar vessels) LV afterload↓ RV ejection↓ LV ejection↑ LV preload↓ LV ejection ↓ INSPIRATION EXPIRATION SBP, PP increases Aortic blood velocity increases (CHF and hypervolemia ) SBP, PP decreases Aortic blood velocity decreases ( Hypovolemia ) pulmonary circulation transit time Hemodynamic effects of positive pressure inspiration (connection in series) 5/4/2012 49 ↑ITP LV preload↓ SBP, PP decreases Aortic blood velocity decreases (Acute cor pulmonale Reversed pulsus paradoxusPowerPoint Presentation: Pleural pressure ↓ RV preload↑ LV preload↓ LV afterload ↑ LV ejection↓ INSPIRATION EXPIRATION SBP, PP decreases Aortic blood velocity decreases Hemodynamic effects of spontaneous inspiration (connection in parallel) 5/4/2012 50 LV RV RV ejection ↑ LV preload↑ LV ejection↑ SBP, PP increases Aortic blood velocity increases ↓ITP pulsus paradoxusApplications in critically ill: Applications in critically ill Assessment of fluid responsiveness ALI/ARDS Congestive heart failure (CHF) COPD, OSA Weaning failure (cardiac origin) 5/4/2012 51PowerPoint Presentation: 5/4/2012 52 Assessment of fluid responsivenessPEEP in ARDS/ALI: 5/4/2012 53 PEEP in ARDS/ALI ALI/ARDS: High recruitment potential and low chest wall elastance Lower risk of negative effects of PEEP on hemodynamics Poor recruitability and ↑ chest wall elastance ( ↑ IAP>12): : Higher risk of negative effects of PEEP on hemodynamics ARDS & compliant chest walls ↑transmission to intrapleural space ↓RV preload ARDS & stiff chest walls ↓ transmission to intrapleural spaceHemodynamic effects of ventilation depend on cardiopulmonary status: Hemodynamic effects of ventilation depend on cardiopulmonary status Less tolerant of PPV Hypovolemic patients (nomal cardiac function) RV dysfunction More tolerant of PPV LV dysfunction (with hypervolemia) COPD (no RV dysfunction), OSA Benefit of abolishing negative swings in ITP 5/4/2012 54PowerPoint Presentation: 5/4/2012 55 PEEP in acute cardiogenic pulmonary edemaWeaning failure from cardiac region: Weaning failure from cardiac region Weaning from mechanical ventilation can be considered as ‘hemodynamic stress test’. Transition from positive pressure ventilation to spontaneous breathing is an exercise Weaning should be done ‘gradually’ in patients with limited cardiovascular reserve. Improving cardiovascular reserve/ inotropic support may be helpful in weaning such patients 5/4/2012 56PowerPoint Presentation: 5/4/2012 57 Weaning as ‘Hemodynamic stress test’PowerPoint Presentation: THANK YOU You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.