1. Cardiorespiratory
Interactions:
The Heart - Lung
Connection
Jon N. Meliones, MD, MS, FCCM
Professor of Pediatrics Duke University
Medical Director PCICU

2. Optimizing CRI
• Cardiorespiratory Economics
O2: supply vs. demand
 CRI: The Heart
 CRI: The Lung
 Conventional Ventilation
 Non-Conventional Ventilation
 Clinical Applications

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. 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. 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. Normal Function
LA
RA
LV
RV

7. Decreased Function
QuickTime™ and a
Cinepak decompressor
are needed to see this picture.

8. Right Ventricular Filing
Effects on RV
Vena Cava
Positive
Pressure
RA
Thorax Ventilation
RV
PA

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. 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. Effects of PPV on LV Filling
Thoracic Pump Augmentation
Lung Lung
Positive
LA
Pressure
Ventilation
LV
AO

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. 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. Optimizing CRI
 Cardiorespiratory Economics
 CRI: The Heart
 CRI: The Lung
 The pulmonary vasculature
 Conventional Ventilation
 Non-conventional Ventilation
 Clinical Applications

15. Effect of Lung Volume on PVR
Overexpansion
Atelectasis
PVR
Total PVR
Small Vessels
Large Vessels
FRC
Lung Volume

16. LA
RA
QuickTime™ and a
Microsoft Video 1 decompressor
are needed to see this picture.
LV
RV

17. RA
RV
TR Jet
TR Jet = 103: PRV= 103 + PRA

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. 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. 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. Overdistention
Exhalation
40
Over
30
Volume Expansion
(mL) 20
10 Inspiration
0
0 15 30 45
Airway Pressure (cmH20)

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. 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. Overdistention
 Pulmonary effects
Barotrauma; pneumothroax
 Cardiac effect
Increased RV afterload
Increased PVR
Decreased cardiac output

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. 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. Optimizing CRI
 Cardiorespiratory Economics
 CRI: The Heart
 CRI: The Lung
 Conventional Ventilation
 Non-conventional Ventilation
 Clinical Applications

28. Non-conventional Ventilation
 HFOV
 HFJV
 Negative pressure ventilation
 Inhaled nitric oxide

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. 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. Preload Augmentation
PSV
HFOV
Right Atrial
Pressure CMV
0
0
Systemic Venous ReturnMax

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. High-frequency Jet Ventilation
 Intermittent pulse delivery of gas
 Frequency: 180 - 900
 Passive exhalation
 Special ETT adaptor required
 Weight/size limitation (Bunnell Jet)

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. RA LA
QuickTime™ and a
RV Cinepak decompressor
are needed to see this picture.
LV

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. 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. 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. 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. 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. 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. Optimizing CRI
• Clinical Applications
 Single Ventricle
Physiology made
easy….sure

43. AORTA

44. Single Ventricle
Pulm Veins
Vena Cava
LA
RA 65 99
LV
80
RV
80
PA AO
PDA

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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. Effects of Inspired Gas on
Pre-op Single Ventricle
6
Difference in DO2
5
4
3
2
1
0
Hypoxia Hypercapnea
Pre Post

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. 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. Optimizing CRI
• Cardiorespiratory Economics
O2: supply vs. demand
 CRI: The Heart
 CRI: The Lung
 Conventional Ventilation
 Non-Conventional Ventilation
 Clinical Applications