heartlung interaction
TRANSCRIPT
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
Systemic Venous Return
• 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
Systemic Venous Return
• 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
Right Atrial Pressure
Ve
no
us
ret
urn
/car
dia
c o
utp
ut
VR CF nl
CF theoretical
CF reality
Right Atrial Pressure
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
• Systemic venous return
• Left ventricular preload
• Biventricular interdependence
• Left ventricular afterload
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
• Systemic venous return
• Left ventricular preload
• Biventricular interdependence
• Left ventricular afterload
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