Cardiopulmonary Interaction in Critically Ill Patients

Major Determinants of Cardiovascular Responses to Ventilation

Thoracic cage

R ventricle L ventricle
1. Lung Volume 2. Intrapleural pressure

Venous Return

LV Afterload

Influence of Pleural Pressure on Hemodynamic Monitoring

5 15
LA

-5

15
LA

-5

15
LA

High Pleural Pressure

Normal

Low Myocardial Compliance

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 ()
Hemodynamic effects of change in

intrathoracic pressure (

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

(Inflationvasodilatation response)


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

Increasing alveolar O2 tension
blunting hypoxic pul vasoconstriction

Re-expanding collapsed alveolar units Reversing acute respiratory acidosis Decreasing central sympathetic tone

Overdistending lung units


Alveolar vessels
small pulmonary arterioles, venules and capillaries

Extra-alveolar vessels
large pulmonary arteries, venues in the corner between alveoli

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

Resting (FRC)

Low lung volume

High lung volume

The effects of lung volume on pulmonary vascular resistance

Pulmonary vascular resistance

Total Alveolar

Extra-alveolar RV FRC

TLC

Diagram of Anatomical and Mechanical Relationship between Heart and Lung

Pericardium

RV

R lung
S

L lung

LV

Pperi PIP
RV
S

Prv

LV

Mechanical Heart - Lung Interaction

R lung L lung
S

LV

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

LV

Intrathoracic Pressure

Systemic venous return

Left ventricular preload

Biventricular interdependence

Left ventricular afterload

Systemic Venous Return

low pressure and low resistance 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

Curves of Venous Return and Cardiac Function

Cardiac output determined by the intersection of venous return and cardiac function

Venous return/cardiac output

venous return
2.0 1.5 1.0 0.5

CF-

CFN

Point of flow limitation

CF+

-15

-10

-5

10

MCP

Right Atrial Pressure

Systemic Venous Return

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

ITP decreases
The reverse occurs

Concept of Limits
Limit of return function

Limit of cardiac function

Raising

Lowering
Pra will not increase VR

MCP will not increase Q

Pra

When the Return Curve intersects the plateau of Cardiac Function Curve does not change Q

Q
Increasing MCP does not change Q (or SV)

E4

Pra

Effects of Sustained Decrease in Intrathoracic Pressure on Venous Return and Cardiac Output
Venous return/cardiac output

VR

CF nl

CF
theoretical

CF
reality

Right Atrial Pressure

Effects of PEEP on Venous Return and Cardiac Output

Venous return/cardiac output

VR0

ZEEP

PEEP10 PEEP20

VRp

Right Atrial Pressure

MCP zeep

MCP peep

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

Ventricular Interdependence
RV
R lung
S

L lung

LV

PIP RV end-diastolic volume

RV

LV

Ventricular Interdependence
interventricular septum
stroke volume CO BP Pulsus paradoxus

Hemodynamic Effects of Normal Inspiration

expiration

inspiration

Hemodynamic Effects of Obstructed Inspiration

expiration

inspiration

Left Ventricular Afterload

ITP
LV transmural pressure LV afterload LV injection and LV stroke volume The augmenting effect is usually limited

ITP
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() 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 PEEP augments LV ejection and decreases LV load by impeding venous return

Sequential changes in hemodynamics during MV cycle

RV preload

Pleural pressure Trans - pul pressure

RV ejection

LV preload & ejection

RV afterload

LV afterload
LV ejection

LV preload

SBP, PP Maximal at the end of inspiration

SBP, PP Minimal at the end of expiratory period

Respiratory Changes in Systolic Pressure in Mechanical Ventilated Patient

Baseline mmHg 150(apnea)

dUP dDown SPV

75-

PAP CVP 0-

Insp

Insp

Insp

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

PPmax PPmin

5 seconds

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

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

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

Nl CV function

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

SV

Decreased contractility

LVEDV

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

- RAP - PP - down

Mean RAP before volume expansion in responders and nonresponders

Responsers Nonresponsers

12 10
RAP (mmHg)

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 W M ich ag predict fluid ne ar r d response

8 6 4 2 0
Ca l vin Sc hn ei Re u de r se

* P < 0.05

Mean PAOP before volume expansion in responders and nonresponders

Responders
Calvin Schneider Reuse Diebel Diebel Wagner Tavernier Tousignant Michard 81 10 1 10 4 14 7 16 6 10 3 10 4 12 3 10 3

Nonresponders
72 10 1 10 3 72 15 5 14 4 12 3 16 3 11 2

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

*
*

* P < 0.05

PPV and NPV of Dynamic Parameters

Study
Magder
1992

Cut-off Pt No. Parameter value PPV NPV

33 35 29 40 19 RAP down RAP PP Vpeak 1 mmHg 5 mmHg 1 mmHg 13% 12% 84 95 77 94 91 93 93 81 96 100

Tavernier
1998

Magder
1999

Michard
2000

Feissel
2001

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