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Cardiopulmonary Interaction in Critically Ill Patients

Cardiopulmonary Interaction in Critically Ill Patients. 吳健樑 馬偕醫院 胸腔內科. Major Determinants of Cardiovascular Responses to Ventilation. Thoracic cage. R ventricle L ventricle. 1. Lung Volume 2. Intrapleural pressure. Venous Return. LV Afterload.

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Cardiopulmonary Interaction in Critically Ill Patients

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  1. Cardiopulmonary Interaction in Critically Ill Patients 吳健樑 馬偕醫院 胸腔內科

  2. Major Determinants of Cardiovascular Responses to Ventilation Thoracic cage R ventricle L ventricle 1. Lung Volume 2. Intrapleural pressure Venous Return LV Afterload

  3. Influence of Pleural Pressure on Hemodynamic Monitoring 15 15 -5 5 15 -5 LA LA LA Low Myocardial Compliance High Pleural Pressure Normal PIP = PEEP x {CL/ (CL + CCW)}

  4. Physiological Changes Induced by Ventilation • Lung volume increases • Pleural pressure (intrathoracic pressure, ITP) change in VR • Transpulmonary pressure increase in RV afterload

  5. Heart – Lung Interaction • Hemodynamic effects of lung volume change (肺容積) • Hemodynamic effects of change in intrathoracic pressure (胸腔內壓力)

  6. Hemodynamic Effects of Lung Volume Change • Autonomic tone • Pulmonary vascular resistance • Mechanical heart-lung interaction

  7. Autonomic Tone • Lung inflation decrease HR • Lung inflation leads to reflex arterial vasodilatation (Inflation–vasodilatation response)

  8. 機械通氣中的右心室後負荷 • RV afterload is estimated as RV systolic wall stress • LaPlace equation: • Maximum wall stress =1/2 x (Ptm x r)/wall thickness • Transmural Ppa defines systolic RV pressure • Mechanical ventilation  transmural Ppa • Pulmonary vascular resistance 

  9. Pulmonary Vascular Resistance Change in Ventilation • 肺血管阻力下降的因素 • Increasing alveolar O2 tension • blunting hypoxic pul vasoconstriction • Re-expanding collapsed alveolar units • Reversing acute respiratory acidosis • Decreasing central sympathetic tone • 肺血管阻力上升的因素 • Overdistending lung units

  10. 肺內血管之種類 • Alveolar vessels • 肺泡壁內的small pulmonary arterioles, venules and capillaries • Extra-alveolar vessels • large pulmonary arteries, venues in the “corner” between alveoli

  11. Extra-alveolar vessels Alveolar vessels Resting (FRC) Low lung volume High lung volume Size and shape of alveolar and extra-alveolar vessels at different lung volumes

  12. Total Alveolar Extra-alveolar The effects of lung volume on pulmonary vascular resistance Pulmonary vascular resistance RV TLC FRC

  13. Diagram of Anatomical and Mechanical Relationship between Heart and Lung Pericardium R lung L lung RV LV S Pperi PIP RV S LV Prv

  14. S LV Mechanical Heart - Lung Interaction L lung • Mechanical heart-lung • interaction is most influential in diastole during total lung capacity • 2. This effect is caused by juxtacardiac pleural pressure greater than lateral pleural pressure R lung 吐氣 S LV 右心室 吸氣

  15. Intrathoracic Pressure對血行動力之影響 • Systemic venous return • Left ventricular preload • Biventricular interdependence • Left ventricular afterload

  16. Systemic Venous Return • 血液從週邊流至右心 – 靜脈系統是一low pressure and low resistance 循環 • 靜脈回流決定於1) pressure gradient between Pra and Mean CirculatoryPressure; 2) resistance to venous flow

  17. Systemic Venous Return • Factors determining VR • Intrathoracic pressure • Right atrial pressure (Pra) • Resistance to venous flow (Rv) • Mean circulatory pressure (MCP) • Venous return (VR) = (MCP-Pra) / Rv

  18. venous return CF- CFN  CF+ Point of flow limitation   Curves of Venous Return and Cardiac Function Cardiac output determined by the intersection of venous return and cardiac function 2.0 1.5 Venous return/cardiac output 1.0 0.5 5 10 -15 -10 -5 0 MCP Right Atrial Pressure

  19. Systemic Venous Return • ITP increases • Pra  • Pressure gradient between MCP and Pra • VR • RV stroke volume • ITP decreases • The reverse occurs

  20. Limit of “cardiac function” Limit of “return function” Concept of Limits Q Raising MCP will not increase Q Lowering Pra will not increase VR Pra

  21. When the Return Curve intersects the plateau of Cardiac Function Curve does not change Q Q Increasing MCP does not change Q (or SV) Pra E4

  22. CF nl  CF theoretical  CF reality Effects of Sustained Decrease in Intrathoracic Pressure on Venous Return and Cardiac Output VR Venous return/cardiac output Right Atrial Pressure

  23. ZEEP PEEP10 PEEP20 VRp      MCP peep Effects of PEEP on Venous Return and Cardiac Output VR0 Venous return/cardiac output Right Atrial Pressure MCP zeep

  24. Effects of PEEP on Venous Return • Decreasingvenous return, but less than expected • Increasing mean circulatory pressure due to increased abd pressure and sympathoadrenal response to PEEP • Compressing the IVC through inflation of lower lobe of Rt lung

  25. Hemodynamic Effects of Changes in Intrathoracic Pressure • Systemic venous return • Left ventricular preload • Biventricular interdependence • Left ventricular afterload

  26. Left Ventricular Preload • A change in VR to RV  a change in LV preload and LV cardiac output • Sustained increase in ITP (PPV)  RV filling  LV preload and CO after 2-3 heart beats, usually occurs in expiratory phase

  27. Hemodynamic Effects of Changes in Intrathoracic Pressure • Systemic venous return • Left ventricular preload • Biventricular interdependence • Left ventricular afterload

  28. Ventricular Interdependence R lung L lung RV LV S RV PIP RV end-diastolic volume S LV

  29. VentricularInterdependence • 右心室和左心室共用一interventricular septum • 右心室舒張末期容積增加 心室中隔偏向左心室 左心室舒張末期容積減少  左心室stroke volume 和CO減少 BP 下降  Pulsus paradoxus

  30. Hemodynamic Effects of Normal Inspiration 自發性呼吸 expiration inspiration

  31. Hemodynamic Effects of Obstructed Inspiration 氣道阻塞時呼吸 expiration inspiration

  32. Left Ventricular Afterload • ITP 上升 • LV transmural pressure • LV afterload • LV injection and LV stroke volume • The augmenting effect is usually limited • ITP 下降 • The converse occurs

  33. Clinical Implication of Increasing ITP • Large decrease in ITP in pulmonary diseases (obstructive and restrictive) LV preload ↓ and LV afterload  • Preventing exaggerated negative ITPswings improvescardiac function, such as severe UAO(上呼吸道阻塞) • An important factor in cardiac dysfunction and respiratory failure

  34. Clinical Implication of Increasing ITP(continued) • Weaning from positive pressure ventilation is a form of cardiac stress • Transition from PPV to spontaneous ventilation會造成左心室負荷增加 • PEEP augments LV ejection and decreases LV load by impeding venous return

  35. RVpreload RVejection Pleural pressure LVpreload & ejection RVafterload Trans - pul pressure LVafterload LVejection LVpreload SBP, PP Maximal at the end of inspiration SBP, PP Minimal at the end of expiratory period Sequential changes in hemodynamics during MV cycle

  36. Insp Insp Insp Respiratory Changes in Systolic Pressure in Mechanical Ventilated Patient Baseline (“apnea”) mmHg 150- dUP SPV dDown 75- PAP CVP 0-

  37. Respiratory Changes in Systolic Pressure in Mechanical Ventilated Patient Michard F. yearbook of ICM ,2000.

  38. Respiratory Changes in Systolic Pressure • up reflect the increased LV stroke volume related to increased LV preload and decreased LV afterload • up increase in LV dysfunction • down reflect the expiratory decreased LV preload and stroke volume • down is main component of SPV in hypovolemia

  39. 5 seconds Respiratory Changes in Pulse Pressure in Mechanical Ventilated Patient PPmax PPmin PP (%) = (PPmax – PPmin) / (PPmax + PPmin)/2 Michard et al. Am J Respir Cit Care Med 20000;162:134-8

  40. Respiratory Changes in Pulse Pressure • Pulse pressure is maximal (PPmax) at the end of inspiratory period • Pulse pressure is minimal (PPmin): usually 3 heart beats later during the expiratory period • PP (%) = (PPmax – PPmin) (PPmax + PPmin)/2

  41. Relationship between respiratory change in pulse pressure before volume expansion and changes in cardiac index Michard F. AMJCCM 2000

  42. Relationship between respiratory change in pulse pressure on ZEEP and changes in cardiac index Michard F. AMJCCM 1999

  43. SV Decreased contractility LVEDV Fluid Responsiveness in Critically ill • Volume expansion is commonly used in critically ill pts to improve hemodynamics • Based on Frank-Starling relationship, the expected hemodynamic response to volume expansion is: ↑RVEDV, LVEDV, SV and CO In reality: - only40-72% of pts have positive fluid response Nl CV function

  44. Indicators of fluid responsiveness in critically ill • Bedside indicators of ventricular preload • RAP (CVP) • PAOP • RVEDV • LVEDA • 2. Dynamic changes in preload induced by changes in ITP • - Δ RAP • - Δ PP • - Δ down

  45. Mean RAP before volume expansion in responders and nonresponders • Conclusions: • Before volume expansion, Rap was not significantly different between individuals • Marked overlap of RAP values did not allow identification of a threshold value to predict fluid response * * RAP (mmHg) * P < 0.05

  46. Mean PAOP before volume expansion in responders and nonresponders • Conclusions: • Before volume expansion, PAOP was variable between studies • None of these studies presented a PAOP cutoff value to predict hemodynamic response to volume expansion * * * * P < 0.05

  47. PPV and NPV of Dynamic Parameters

  48. Clinical Significance of Respiratory Changes in Pulse Pressure • PP discriminate between responder and nonresponder to volume expansion: threshold value 13% • The baseline PP closely correlated with increase in CI in response to volume expansion • PP on ZEEP closely correlated with PEEP induced decrease in CI. The higher PP on ZEEP, the greater the decease in CI with PEEP

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