Heartlung Interaction

Cardiopulmonary Interaction in Critically Ill Patients

吳健樑馬偕醫院胸腔內科

1. Lung Volume

2. Intrapleural pressure

R ventricle

L ventricle

Venous Return LV Afterload

Major Determinants of Cardiovascular Responses to Ventilation

Thoracic cage

Influence of Pleural Pressure on Hemodynamic Monitoring

5 15 15-5 -5 15

LALA LA

HighPleural

Pressure

Normal LowMyocardialCompliance

PIP = PEEP x {CL/ (CL + CCW)}

Physiological Changes Induced by Ventilation

• Lung volume increases

• Pleural pressure (intrathoracic pressure, ITP) change in VR

• Transpulmonary pressure increase in RV afterload

Heart – Lung Interaction

• Hemodynamic effects of lung volume change ( 肺容積 )

• Hemodynamic effects of change in intrathoracic pressure ( 胸腔內壓力 )

Hemodynamic Effects of Lung Volume Change

• Autonomic tone

• Pulmonary vascular resistance

• Mechanical heart-lung interaction

Autonomic Tone

• Lung inflation decrease HR

• Lung inflation leads to reflex arterial vasodilatation (Inflation–vasodilatation response)

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

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

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

Low lung volume High lung volume

Size and shape of alveolar and extra-alveolar vessels at different lung volumes

Resting (FRC)

Alveolar vesselsExtra-alveolar vessels

Total

Alveolar

Extra-alveolar

RV FRC TLC

Pu

lmo

nar

y va

scu

lar

resi

stan

ce

The effects of lung volume on pulmonary vascular resistance

R lung L lung

LVRV

LVRV

Pericardium

Pperi

PIP

Prv

S

S

Diagram of Anatomical and Mechanical Relationship between Heart and Lung

S LV

R lung L lung

右心室

LV吐氣

吸氣

Mechanical Heart - Lung Interaction

S

1. 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

Intrathoracic Pressure 對血行動力之影響

• Systemic venous return

• Left ventricular preload

• Biventricular interdependence

• Left ventricular afterload

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 Circulatory Pressure; 2) resistance to venous flow


• Factors determining VR

– Intrathoracic pressure

– Right atrial pressure (Pra)

– Resistance to venous flow (Rv)

– Mean circulatory pressure (MCP)

• Venous return (VR) = (MCP-Pra) / Rv

CFN

Right Atrial Pressure

Ve

no

us

ret

urn

/car

dia

c o

utp

ut

-15 -5 0 5 10-10

MCP

venous return

Point of flow limitation

CF-

CF+

0.5

1.0

1.5

2.0

Curves of Venous Return and Cardiac FunctionCardiac output determined by the intersection of venous return and cardiac function


• ITP increases– Pra – Pressure gradient between MCP and Pra– VR– RV stroke volume

• ITP decreases– The reverse occurs

Concept of Limits

Q

Pra

Limit of “return function”

Limit of “cardiac function”

Lowering Pra will not increase VR

Raising MCP will not

increase Q

When the Return Curve intersects the plateau of

Cardiac Function Curve does not change Q

Q

Pra

Increasing MCP does not change Q

(or SV)

E4

Effects of Sustained Decrease in Intrathoracic Pressure on Venous Return and Cardiac Output


Ve

no

us

ret

urn

/car

dia

c o

utp

ut

VR CF nl

CF theoretical

CF reality


Ve

no

us

ret

urn

/car

dia

c o

utp

ut

MCP zeep

ZEEPVR0

PEEP20

PEEP10

MCP peep

VRp

Effects of PEEP on Venous Return and Cardiac Output

Effects of PEEP on Venous Return

• Decreasing venous 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

Hemodynamic Effects of Changes in Intrathoracic Pressure





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

Hemodynamic Effects of Changes in Intrathoracic Pressure





R lung L lung

LVRV

LVRVPIP

RV end-diastolic volume

S

S

Ventricular Interdependence

Ventricular Interdependence

• 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

Hemodynamic Effects of Normal Inspiration

expiration inspiration

自發性呼吸

Hemodynamic Effects of Obstructed Inspiration

expiration inspiration

氣道阻塞時呼吸

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

Clinical Implication of Increasing ITP

• Large decrease in ITP in pulmonary diseases (obstructive and restrictive)

LV preload ↓ and LV afterload

• Preventing exaggerated negative ITP

swings improves cardiac function, such as severe UAO( 上呼吸道阻塞 )

• An important factor in cardiac dysfunction and respiratory failure

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 　

RV ejection

LV ejection

SBP, PPMaximal at the end of inspiration

LV preload & ejection

SBP, PPMinimal at the end of expiratory period

Sequential changes in hemodynamics during MV cycle

RV afterload

LV preload

Trans - pulpressure

Pleural pressure

RV preload

LV afterload

Respiratory Changes in Systolic Pressure in Mechanical Ventilated Patient

0-

150-

75-

mmHg

dUP

dDown SPV

Baseline(“apnea”)

Insp Insp Insp

PAPCVP

Respiratory Changes in Systolic Pressure in Mechanical Ventilated Patient

Michard F. yearbook of ICM ,2000.

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

Respiratory Changes in Pulse Pressure in Mechanical Ventilated Patient

Michard et al. Am J Respir Cit Care Med 20000;162:134-8

PPmax

PPmin

5 seconds

PP (%) = (PPmax – PPmin) / (PPmax + PPmin)/2

Respiratory Changes in Pulse Pressure 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

Relationship between respiratory change in pulse pressure before volume expansion and

changes in cardiac index

Michard F. AMJCCM 2000

Relationship between respiratory change in pulse pressure on ZEEP and changes in

cardiac index

Michard F. AMJCCM 1999

Fluid Responsiveness in Critically ill

1.Volume expansion is commonly used in critically ill pts to improve hemodynamics

2.Based on Frank-Starling relationship, the expected hemodynamic response to volume expansion is: ↑RVEDV, LVEDV, SV and CO

LVEDV

S V

Nl CV function

Decreasedcontractility

In reality: - only 40-72% of pts have positive fluid response

Indicators of fluid responsiveness in critically ill

1.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

Mean RAP before volume expansion in responders and nonresponders

RA

P (

mm

Hg

)

0

2

4

6

8

10

12

Responsers Nonresponsers

* *

* P < 0.05

Conclusions:1. Before volume

expansion, Rap was not significantly different between individuals

2. Marked overlap of RAP values did not allow identification of a threshold value to predict fluid response

Mean PAOP before volume expansion in responders and nonresponders

* P < 0.05

Conclusions:1. Before volume

expansion, PAOP was variable between studies

2. None of these studies presented a PAOP cutoff value to predict hemodynamic response to volume expansion

Responders NonrespondersCalvin 8 ± 1 7 ± 2

Schneider 10 ± 1 10 ± 1

Reuse 10 ± 4 10 ± 3

Diebel 14 ± 7 7 ± 2

Diebel 16 ± 6 15 ± 5

Wagner 10 ± 3 14 ± 4

Tavernier 10 ± 4 12 ± 3

Tousignant 12 ± 3 16 ± 3

Michard 10 ± 3 11 ± 2

*

*

*

PPV and NPV of Dynamic Parameters

Study Pt No. ParameterCut-off value PPV NPV

Magder 1992

33 ΔRAP 1 mmHg 84 93

Tavernier 1998

35 Δdown 5 mmHg 95 93

Magder 1999

29 ΔRAP 1 mmHg 77 81

Michard 2000

40 ΔPP 13% 94 96

Feissel 2001

19 ΔVpeak 12% 91 100

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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Heartlung Interaction