Cardiorespiratory Interactions

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Cardiorespiratory Interactions

  1. 1. Cardiorespiratory Interactions: The Heart - Lung Connection Jon N. Meliones, MD, MS, FCCM Professor of Pediatrics Duke University Medical Director PCICU
  2. 2. Optimizing CRI • Cardiorespiratory Economics O2: supply vs. demand  CRI: The Heart  CRI: The Lung  Conventional Ventilation  Non-Conventional Ventilation  Clinical Applications
  3. 3. Cardiorespiratory Economics • O2 Demand: O2 consumption = C. O. x (CaO2 - CvO2) O2 Consumption = amount of oxygen used for aerobic metabolism •Failure to meet the demands results in anaerobic metabolism
  4. 4. Cardiorespiratory Economics Optimizing CRI O2 delivery   O2 content:  Hgb,  O2 sat,  PaO2  cardiac output cardiac interventions: another talk pulm interventions: this talk   O2 consumption:  patient WOB
  5. 5. Cardiorespiratory Interactions A Definition Effects of intrathoracic pressure, lung volume, and gas exchange on: Cardiovascular events such as venous return, ventricular performance, and arterial outflow.
  6. 6. Normal Function LA RA LV RV
  7. 7. Decreased Function QuickTime™ and a Cinepak decompressor are needed to see this picture.
  8. 8. Right Ventricular Filing Effects on RV Vena Cava Positive Pressure RA Thorax Ventilation RV PA
  9. 9. Systemic Venous Return (RV Preload) PSV RAP = mean systemic venous pressure PPV increases right atrial pressure Right spontaneous Atrial breathing Pressure 0 0 Max Systemic Venous Return
  10. 10. Effects of PPV on Right Ventricle   es in intrathoracic pressure  C.O.   ing RV preload   ing RV afterload by  ing PVR  Best strategy for the failing RV is to limit intrathoracic pressure
  11. 11. Effects of PPV on LV Filling Thoracic Pump Augmentation Lung Lung Positive LA Pressure Ventilation LV AO
  12. 12. Effects of PPV on LV Afterload 100 100 AO AO LVTM=130 LVTM=70 70 Thorax 130 LV LV +30 -30 Spontaneous PPV
  13. 13. Effects of PPV on Left Ventricle es in intrathoracic pressure  C.O.:   ing LV preload when low   ing LV afterload  preload when excessive (RV) effects  Best strategy for the failing LV is to utilize intrathoracic pressure to optimize preload & afterload
  14. 14. Optimizing CRI  Cardiorespiratory Economics  CRI: The Heart  CRI: The Lung  The pulmonary vasculature  Conventional Ventilation  Non-conventional Ventilation  Clinical Applications
  15. 15. Effect of Lung Volume on PVR Overexpansion Atelectasis PVR Total PVR Small Vessels Large Vessels FRC Lung Volume
  16. 16. LA RA QuickTime™ and a Microsoft Video 1 decompressor are needed to see this picture. LV RV
  17. 17. RA RV TR Jet TR Jet = 103: PRV= 103 + PRA
  18. 18. Effects of of pH on PVR Effects pH on PVR *p p <0.05vs Hypoxia * < 0.05 vs * 40 * 35 PVR 30 (mmHg) 25 (l x Min) 20 15 10 5 0 Hypoxia Respiratory Metabolic Hypoxia CTL Alkalosis Alkalosis Lyrene RK, 1985
  19. 19. Effects of PaCO2 on PVR pH = 7.4 PCaO2 r=0.7, P<0.05 40 2 PCaO2 r=0.11, P=ns 30 2 20 Change in 10 PVR -10 -20 -30 -20 -10 10 20 30 Change in PaCO2 Malik, 1973, J Appl Phys
  20. 20. Pulmonary Vasculature • Optimize lung volume: • Avoid overexpansion / atelectasis  Avoid hypoxic vasoconstriction  Avoid hypercapnia; promote alkalosis  Neonates at ed risk for pulm HTN  Inhaled gases modify PVR
  21. 21. Overdistention Exhalation 40 Over 30 Volume Expansion (mL) 20 10 Inspiration 0 0 15 30 45 Airway Pressure (cmH20)
  22. 22. Overdistention and C.O. 1000 950 PEEP 5 PEEP 10 900 Cardiac 850 Output 800 750 (mL/min) 700 650 600 550 500 10 15 20 Tidal Volume (mL/kg) Cheifetz: CCM 1998
  23. 23. Overdistention and PVR 5000 4500 PEEP 5 PEEP 10 PVR 4000 5 (d-sec/cm 3500 ) 5 3000 2500 2000 1500 1000 10 15 20 Tidal Volume (mL/kg)
  24. 24. Overdistention  Pulmonary effects Barotrauma; pneumothroax  Cardiac effect Increased RV afterload Increased PVR Decreased cardiac output
  25. 25. Intrinsic PEEP Beginning Premature initiation of of Inspiration Inspiration End of Inspiration Retained Gas Results in PEEP Termination Beginning Premature of of Termination of Exhalation Exhalation Exhalation
  26. 26. Intrinsic PEEP • Expiratory gas flow continues at the end of the time allotted for exhalation. • PEEPi may lead to excessive MAP. – Pulmonary effects: • Barotrauma – Cardiac effects: • Impedance of venous return • Decreased cardiac output
  27. 27. Optimizing CRI  Cardiorespiratory Economics  CRI: The Heart  CRI: The Lung  Conventional Ventilation  Non-conventional Ventilation  Clinical Applications
  28. 28. Non-conventional Ventilation  HFOV  HFJV  Negative pressure ventilation  Inhaled nitric oxide
  29. 29. PIP at HFOV Machine PIP at MAP Alveolus at Alveolus Delta P at Machine Delta P at MAP Alveolus at PEEP Machine at Alveolus PEEP at Machine
  30. 30. HFOV  HFOV decreases cardiac output??  Traverse et al Pediatr Res. 1988.  Traverse et al. Chest. 1989.  Laubscher et al. Arch Dis Child. 1996. Theme: Cardiac output decreases with “significantly” ed MAP But, studies did not control for preload.
  31. 31. Preload Augmentation PSV HFOV Right Atrial Pressure CMV 0 0 Systemic Venous ReturnMax
  32. 32. HFOV and CRI: Summary Cardiac output is maintained during HFOV  In a given pt, C.O may be ed if:  MAP is “significantly” ed.  Consider volume loading  Consider inotropes  Bottom line: Oxygen delivery  If C.O. can be maintained & oxygenation is ed  Oxygen delivery will 
  33. 33. High-frequency Jet Ventilation  Intermittent pulse delivery of gas  Frequency: 180 - 900  Passive exhalation  Special ETT adaptor required  Weight/size limitation (Bunnell Jet)
  34. 34. HFJV 20 Volume Limited Airway Pressure HFJV 15 MAP 10 MAP 5 0.3 0.6 0.1 0.2 0.4 0.5 0
  35. 35. RA LA QuickTime™ and a RV Cinepak decompressor are needed to see this picture. LV
  36. 36. Effects of HFJV on CRI * p < 0.01 vs HFJV * * 10 Pre HFJV 9.4 9.4 8 Post 6 * * 4 4.6 * * 3.8 3.7 2.9 2 2.3 2.4 1.6 0 Paw PVR C.I.
  37. 37. Inhaled NO  PAO2,  cGMP Oxygen A 2,  Ca++,  PVR NO Epithelial Cells Interstitium Muscle Endothelial Cells cGMP NO Injured CA++ EDRF Relaxation NO Capillary Hgb Met Hgb
  38. 38. NNitric Oxide In CHD OI Miller, SF Tang, A Keech, NB Pigott, E Beller and DS Celermajer: Lancet 2000 • 126 Pts, randomized • Less Pulm HTN crisis, Less Vent Days. • No difference in mortality • Patients with passive flow, worse response, better in “small vessels” • Use lowest dose, wean daily. • Use sildenafil
  39. 39. RV Dysfunction Pulmonary HTN Ventilation Manipulations • Conventional Ventilatory Strategies – MAP but maintain FRC – Alkalinize with normocapnia • Nonconventional Modes – HFJV – Negative pressure ventilation • Inhaled Medical Gases –FiO2 ( CaO2) –Nitric oxide
  40. 40. LV Dysfunction • Conventional Ventilatory Strategies –Thoracic pump augmentation of LV preload (“low” ventilatory rate with “high” TV) – LV afterload MAP but maintain FRC •Nonconventional Modes –HFJV or HFOV if MAP > 15 - 20 cm H2O (optimize O2 delivery &  barotrauma) • Inhaled Medical Gases –FiO2 ( CaO2)
  41. 41. Respiratory Dysfunction Ventilation Manipulations • Conventional Ventilatory Strategies –Maintain ideal lung volume –Titrate PEEP / optimize MAP –Alkalosis • Nonconventional Modes –HFOV if PAW > 15 - 20 cm H2O –(optimize O2 delivery &  barotrauma) • Inhaled Medical Gases –FiO2 ( CaO2) –Nitric oxide
  42. 42. Optimizing CRI • Clinical Applications  Single Ventricle Physiology made easy….sure
  43. 43. AORTA
  44. 44. Single Ventricle Pulm Veins Vena Cava LA RA 65 99 LV 80 RV 80 PA AO PDA
  45. 45. Causes of Systemic Desaturations • Sao2 is dependent on – 1. SmvO2 – 2. SpvO2 – 3. Volume of Pulmonary venous vs systemic venous return • Decreased oxygen delivery to the tissues – Lowering of SmvO2 i.e QS • Alveolar arterial gradient – Lowering SpvO2 • Alterations in QP/QS
  46. 46. Norwood With BT Shunt Procedure: 3 1. Create unobstructed SBF outlfow to aorta = create PBF neoaorta 2. Unobstructed mixing in atrium = atrial septectomy 21 3. Stable PBF = BT shunt vs RV-PA shunt (Sano) Benefits: – Not ductal dependent – RV is systemic pump – Coronary perfusion stable Problems: – Gore-Tex doesn’t grow – Shunts clot – Still cyanotic (80%)
  47. 47. Norwood With Sano Procedure: 1. Create unobstructed SBF outlfow to aorta = create 3 PBF neoaorta 2. Unobstructed mixing in atrium = atrial septectomy 3. Stable PBF = RV-PA 21 shunt (Sano) Benefits: – Not ductal dependent – RV is systemic pump and SANO may provided better function – Coronary perfusion stable Problems: – Shunts clot – Still cyanotic (and lower SaO2 vs BT shunt) – RV is still volume
  48. 48. Single Ventricle Management Key Points Pulmonary Blood BT shunt Sano flow Flow occurs during Systole & Systole diastole SaO2 Higher lower Less diastolic run off No Yes and possible better ventricular function
  49. 49. Qp / Qs Ratio = Ratio of Oxygen Extraction of the Systemic vs Pulmonary Bed Qp SaO2 – SmvO2 SpvO2 – SpaO2 Qs a= arterial mv= mixed venous pv= pulmonary vein pa= pulmonary artery
  50. 50. Qp:Qs Ratio Since Aortic and Pulmonary Blood Flow both come from the Aorta: Aortic Sat. = Pulmonary Sat. SaO2 – SmvO2 SpvO2 – SaO2 In a SV patient: a= arterial mv= mixed venous pv= pulmonary vein
  51. 51. Qp:Qs Ratio If one assumes Pulmonary Venous Sat. = 95% then: Qp:Qs = SaO2 – SmvO2 95 – SaO2 In a SV patient: Assume: SpaO2 = SaO2 SPVO2 = 95 Measure: SaO2 and SmvO2
  52. 52. Qp:Qs Ratio = 1/1 Balanced Pulmonary Blood Flow 15 1 80 – 65 = = 1 15 95 – 80 In a SV patient: Assume: SpaO2 = SaO2 = 80 SPVO2 = 95 Measure: SaO2 = 80 SmvO2 = 65
  53. 53. Qp:Qs Ratio = 2/1 Excessive Pulmonary Blood Flow 30 2 80 – 50 = = 1 15 95 – 80 In a SV patient: Excessive shunt flow: Increase PVR: CO2, Keep FI02 low Decrease SVR: Milrinone, Nipride
  54. 54. Qp:Qs Ratio = 1 / 2 Inadequate Pulmonary Blood Flow 10 1 75 – 65 = = 2 20 95 – 75 In a SV patient: Decreased shunt flow: Decrease PVR: Lower CO2, O2 Increase SVR: Epin.
  55. 55. Qp:Qs Ratio = 1/1 Balanced Pulmonary Blood Flow 35 1 60 – 25 = = 1 35 95 – 60 In a SV patient: Balanced shunt flow: Low CO Increase CO: Epin., Milrinone
  56. 56. Effects of Inspired Gas on Pre-op Single Ventricle 6 Difference in DO2 5 4 3 2 1 0 Hypoxia Hypercapnea Pre Post
  57. 57. What are the Key Issues for the management of a post Norwood patient? • SaO2 target is between 70-80% so keep Hgb >15 • SmvO2 target = >55 but usually common atrial line so use cerebral O2 (are they any good? Yes for trends) • Lactates are followed on all pts. If < 2.5 good. If increases > 1/hr bad sign. Keep they alive. • Chest is usually open… risk for tamponade! • The answer is always!!! Increase QT! • Steroids although no data
  58. 58. Post Op Management • Balance Qp/QS (careful! Just increase the PaCO2) – Low FI02 with B-T shunt – FIO2 = 0.4 with sano – Consider adding CO2 – NEVER use hypoxia – NEVER bag with FIO2 = 1.0
  59. 59. Optimizing CRI • Cardiorespiratory Economics O2: supply vs. demand  CRI: The Heart  CRI: The Lung  Conventional Ventilation  Non-Conventional Ventilation  Clinical Applications

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