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