Cardiorespiratory Interactions:
Transcript of Cardiorespiratory Interactions:
CardiorespiratoryInteractions:
The Heart - Lung Connection
Jon N. Meliones, MD, MS, FCCM
Professor of Pediatrics Duke University Medical Director PCICU
Optimizing CRI
• Cardiorespiratory Economics
O2: supply vs. demand
CRI: The Heart
CRI: The Lung
Conventional Ventilation
Non-Conventional Ventilation
Clinical Applications
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
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
Cardiorespiratory Interactions
Effects of intrathoracic pressure,
lung volume, and gas exchange
on:Cardiovascular events such as venous
return, ventricular performance, and
arterial outflow.
A Definition
Normal Function
LA
LV
RA
RV
Decreased Function
QuickTime™ and aCinepak decompressor
are needed to see this picture.
Effects on RVEffects on RV
ThoraxThoraxRA
RV
PA
Positive
Pressure
Ventilation
Positive
Pressure
Ventilation
Right Ventricular Filing
Vena Cava
Systemic Venous Return
(RV Preload)PSV RAP = mean systemic venous pressure
00
Right
Atrial
Pressure
PPV increasesright atrial pressure
spontaneous breathing
MaxSystemic Venous Return
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
Thoracic Pump Augmentation
Lung Lung
LA
LV
AO
Effects of PPV on LV Filling
Positive
Pressure
Ventilation
Positive
Pressure
Ventilation
Effects of PPV on LV Afterload
130
-30
SpontaneousSpontaneous
100100
70
+30
100100
PPVPPV
LVTM=130LVTM=130 LVTM=70LVTM=70
AOAO AOAO
LVLV LVLV
ThoraxThorax
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
Optimizing CRI
Cardiorespiratory Economics
CRI: The Heart
CRI: The Lung
The pulmonary vasculature
Conventional Ventilation
Non-conventional Ventilation
Clinical Applications
Lung VolumeLung Volume
PVRPVRTotal PVRTotal PVR
Large VesselsLarge Vessels
Small VesselsSmall Vessels
AtelectasisAtelectasis
OverexpansionOverexpansion
Effect of Lung Volume on PVR
FRCFRC
QuickTime™ and aMicrosoft Video 1 decompressorare needed to see this picture.
LA
LV
RV
RA
RV
RA
TR JetTR Jet = 103: PRV= 103 + PRA
Effects of pH on PVREffects of pH on PVR
PVR(mmHg)
(l x Min)
CTL Hypoxia RespiratoryAlkalosis
MetabolicAlkalosis
Hypoxia00
55
1010
1515
2020
2525
3030
3535
4040
Lyrene RK, 1985Lyrene RK, 1985
** **
*p < 0.05 vs* p < 0.05 vs Hypoxia
40
30
20
10
-10
-20
40
30
20
10
-10
-20
-30 -20 -10 10 20 30-30 -20 -10 10 20 30
Change in PaCO2
Change in
PVR
Change in
PVR
r=0.7, P<0.05r=0.11, P=ns
r=0.7, P<0.05r=0.11, P=ns
PCaO2
PCaO2
PCaO2
PCaO2
Malik, 1973, J Appl PhysMalik, 1973, J Appl Phys
pH = 7.4pH = 7.4Effects of PaCO2 on PVR
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
15 30 4515 30 45
Volume(mL)
3030
2020
1010
0000
4040
Over
Expansion
Exhalation
Inspiration
Airway Pressure (cmH20)
OverdistentionOverdistention
500
550
600
650
700
750
800
850
900
950
1000
10 15 20
PEEP 5 PEEP 10
Overdistention and C.O.Overdistention and C.O.
Cardiac
Output
(mL/min)
Cardiac
Output
(mL/min)
Tidal Volume (mL/kg)Tidal Volume (mL/kg)Cheifetz: CCM 1998
Overdistention and PVROverdistention and PVR
1000
1500
2000
2500
3000
3500
4000
4500
5000
10 15 20
PEEP 5 PEEP 10
Tidal Volume (mL/kg)Tidal Volume (mL/kg)
PVR
(d-sec/cm5)
PVR
(d-sec/cm5)
Overdistention
Pulmonary effects
Barotrauma; pneumothroax
Cardiac effect
Increased RV afterload
Increased PVR
Decreased cardiac output
Intrinsic PEEP
Terminationof
Exhalation
Beginningof
ExhalationPremature
Termination of Exhalation
Retained Gas Results in PEEPi
Beginningof
Inspiration
Endof
Inspiration
Premature initiationof Inspiration
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
Optimizing CRI
Cardiorespiratory Economics
CRI: The Heart
CRI: The Lung
Conventional Ventilation
Non-conventional Ventilation
Clinical Applications
Non-conventional Ventilation
HFOV
HFJV
Negative pressure ventilation
Inhaled nitric oxide
HFOV PIPat
Machine
PEEPat
Machine
PEEPat
Alveolus
PIPat
AlveolusMAPat
Alveolus
Delta Pat
Alveolus
Delta Pat
Machine
MAPat
Machine
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.
Preload Augmentation
PSV
00
Right Atrial
Pressure
HFOV
CMV
MaxSystemic Venous Return
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
High-frequency Jet Ventilation
Intermittent pulse delivery of gas
Frequency: 180 - 900
Passive exhalation
Special ETT adaptor required
Weight/size limitation (Bunnell Jet)
VolumeLimitedVolumeLimited
HFJVHFJV
5
10
15
20
0 0.1 0.30.2 0.4 0.5 0.6
Airw
ay P
ressure
MAPMAP
MAPMAP
HFJVHFJV
QuickTime™ and aCinepak decompressor
are needed to see this picture.
RA
LV
RV
LA
PawPaw PVRPVR C.I.C.I.00
22
44
66
88
1010 PreHFJVPost
PreHFJVPost
* p < 0.01 vs HFJV* p < 0.01 vs HFJV
**
**
**
** **
**
9.4 9.4
4.63.8
1.6
3.7
2.32.9
2.4
Effects of HFJV on CRIEffects of HFJV on CRI
PAO
2, cGMP
Ca++, PVR
PAO
2, cGMP
Ca++, PVR
Hgb
Endothelial Cells
Injured
Capillary
MuscleInterstitium
Epithelial Cells
Oxygen
NO
NO cGMP
CA++
RelaxationNO
Met Hgb
EDRF
Inhaled NOInhaled NO
NNitric Oxide In CHD
• 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
OI Miller, SF Tang, A Keech, NB Pigott, E Beller and DS
Celermajer: Lancet 2000
RV Dysfunction Pulmonary HTNVentilation Manipulations
• Conventional Ventilatory Strategies– MAP but maintain FRC
– Alkalinize with normocapnia
• Nonconventional Modes– HFJV
– Negative pressure ventilation
• Inhaled Medical Gases–FiO2 ( CaO2)
–Nitric oxide
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)
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
Optimizing CRI
• Clinical Applications
Single Ventricle
Physiology made
easy….sure
AORTA
Single Ventricle
Vena Cava
RA
RV
PA
Pulm Veins
LA
LV
AO
65
80
80
99
PDA
Causes of Systemic Desaturations
• Sao2 is dependent on– 1. SmvO2
– 2. SpvO2
– 3. Volume of Pulmonary venous vssystemic venous return
• Decreased oxygen delivery to the tissues– Lowering of SmvO2 i.e QS
• Alveolar arterial gradient– Lowering SpvO2
• Alterations in QP/QS
Procedure:
1. Create unobstructed outlfow to aorta = create neoaorta
2. Unobstructed mixing in atrium = atrial septectomy
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%)
– RV is volume overloaded
Norwood With BT Shunt
12
3
PBF
SBF
Procedure:1. Create unobstructed
outlfow to aorta = create neoaorta
2. Unobstructed mixing in atrium = atrial septectomy
3. Stable PBF = RV-PA 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
overloaded
12
3 PBF
SBF
Norwood With Sano
Single Ventricle Management Key Points
Pulmonary Blood
flow
BT shunt Sano
Flow occurs during Systole &
diastole
Systole
SaO2 Higher lower
Less diastolic run off
and possible better
ventricular function
No Yes
Qp / Qs Ratio =
Ratio of Oxygen Extraction of the
Systemic vs Pulmonary Bed
SaO2 – SmvO2
SpvO2 – SpaO2
a= arterialmv= mixed venouspv= pulmonary veinpa= pulmonary artery
Qp
Qs
Qp:Qs Ratio
Since Aortic and Pulmonary Blood
Flow both come from the Aorta:
Aortic Sat. = Pulmonary Sat.
SaO2 – SmvO2
SpvO2 – SaO2In a SV patient:
a= arterialmv= mixed venouspv= pulmonary vein
Qp:Qs Ratio
If one assumes Pulmonary
Venous Sat. = 95% then:
Qp:Qs =
SaO2 – SmvO2
95 – SaO2In a SV patient:Assume:SpaO2 = SaO2
SPVO2 = 95
Measure:SaO2 and SmvO2
Qp:Qs Ratio = 1/1
Balanced Pulmonary Blood
Flow
80 – 65
95 – 80
15
15
1
1==
In a SV patient:Assume:SpaO2 = SaO2 = 80SPVO2 = 95
Measure:SaO2 = 80SmvO2 = 65
Qp:Qs Ratio = 2/1
Excessive Pulmonary Blood
Flow
80 – 50
95 – 80
30
15
2
1==
In a SV patient:Excessive shunt flow:Increase PVR: CO2, Keep FI02 lowDecrease SVR: Milrinone, Nipride
Qp:Qs Ratio = 1 / 2
Inadequate Pulmonary Blood
Flow
75 – 65
95 – 75
10
20
1
2==
In a SV patient:Decreased shunt flow:Decrease PVR: Lower CO2, O2Increase SVR: Epin.
Qp:Qs Ratio = 1/1
Balanced Pulmonary Blood
Flow
60 – 25
95 – 60
35
35
1
1==
In a SV patient:Balanced shunt flow: Low COIncrease CO: Epin., Milrinone
Effects of Inspired Gas on
Pre-op Single Ventricle
0
1
2
3
4
5
6
Hypoxia Hypercapnea
Pre Post
Diffe
ren
ce
in D
O2
• 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
What are the Key Issues for the management of
a post Norwood patient?
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
Optimizing CRI• Cardiorespiratory Economics
O2: supply vs. demand
CRI: The Heart
CRI: The Lung
Conventional Ventilation
Non-Conventional Ventilation
Clinical Applications