Monitorización hemodinámica - aymon.es · •Mediciones de las presiones de llenado ventricular ... Precarga Presión tele-diastólica (PAD o POAP) CURVA DE FUNCIÓN CARDÍACA CURVA

1

Monitorización hemodinámica

José A. Lorente

Hospital Universitario de Getafe

CIBER de Enfermedades Respiratorias

Universidad Europea de Madrid

Respimad 2011

2

•Monitorización de la precarga

•Mediciones de las presiones de llenado ventricular

•Función cardíaca

•Relación presión/volumen en el corazón

•Presión de llenado sistémica

Monitorización hemodinámica

-5 20

0

5

Gasto

cardíaco

Precarga

Presión tele-diastólica (PAD o POAP)

CURVA DE FUNCIÓN CARDÍACA

CURVA DE FUNCIÓN CARDÍACA / RETORNO VENOSO

Función cardíaca y precarga

-5 20

0

5

Gasto

cardíaco



Precarga



-5 20

0

5

Volumen

ventricular

(Precarga)

Presión tele-diastólica

(PAD o POAP)PAD

Relación normal entre el

volumen y la presión

¿Qué es la precarga?

-5 20

0

5

Volumen

ventricular

Presión tele-diastólica

(PAD o POAP)

Compliance elevada

Compliance normal

Compliance disminuída

PAD

Compliance = volumen / presión

•Estimación de la precarga (volumen) mediante la presión:

•Tres “precargas” diferentes para la misma presión!!!

•necesitamos conocer la compliance

•(la relación de P con V)


-5 20

0

5

Gasto

cardíaco


Volumen (telediastólico)

“Estiramiento”



•La precarga es una “distensión”

•No es una “presión de llenado”

•No es un volumen

•Se estima por el volumen


¿Por qué conocer la precarga?


-5 20

0

5

Gasto

cardíaco




Diferente respuesta (GC)

al aumentar PAD ó POAP

dependiendo de la

“precarga basal”


-5 20

0

5

Gasto

cardíaco




Diferente respuesta (GC)

dependiente de la función

ventricular (relación

precarga/GC)


•PRESIONES DE LLENADO VENTRICULAR

•VD: PRESIÓN VENOSA CENTRAL → catéter venoso central

•VI: POAP → catéter de arteria pulmonar (Swan Ganz)

Presión venosa central

5 cm

5 cm debajo del

ángulo esternal:

No cambia con la

posición del paciente

Plano torácico medio

al nivel de la 5ª

costilla

(sobreestima 3 mm Hg)



Presión capilar pulmonar

PEEP=0

PEEP=15

PEEP=20


PEEP=0

PEEP=15

PEEP=20


•Determinante del llenado no es PVC sino Presión transmural

•Efecto de la Ppl sobre la PVC

•i.e. Espiración forzada

•¿Por qué se mide al final de la espiración?




¿Dónde se ha de medir?



•La PVC como indicador de la precarga

•Gold standard: reto de fluidos

•Rápido

•Aumentar PVC≥2 mm Hg

•La pendiente de la zona “dependiente”:

•5 L/min en el rango de PVC 0-10 mm Hg

•Luego: GC ≥ 300 ml por PVC cada 1 mm Hg

(y todavía se infraestima el aumento de GC)


-5 20

0

12

Gasto

cardíaco



-5 20

0

12

Retorno

venoso

PAD

CURVA DE RETORNO VENOSO

Presión sistémica

media

PAD

RV=(PAD-Psm)/RRV

-5 20

0

12

Gasto

cardíaco

CURVA DE FUNCIÓN CARDÍACA / RETORNO

VENOSO

Presión tele-diastólica (PVC o POAP)

PAD

-5 20

0

12

Gasto

cardíaco

Presión tele-diastólica (PVC o POAP)


Contractilidad

Compliance ventricular

Postcarga

0 120

0

200

Presión

VI

RELACIÓN PRESIÓN / VOLUMEN VENTRICULAR

VOLUMEN VI

8040

Llenado ventricular durante

la diástole

(relación P/V diastólica)

0 120

0

200

Presión

VI


VOLUMEN VI

8040

Aumento de

presión

ventricular

al comienzo

de la sístole,

sin cambio

en el

volumen

0 120

0

200

Presión

VI


VOLUMEN VI

8040

Eyección de la

sangre cuando

la PVI excede

Pao, hasta

alcanzar el

volumen tele-

sistólico

(determinado

por la

contractilidad)

0 120

0

200

Presión

VI


VOLUMEN VI

8040

Relajación

isovolumétrica

0 120

0

200

Presión

VI


VOLUMEN VI

8040

Emax

0 120

0

200

Presión

VI


VOLUMEN VI

8040

Efecto del

aumento de

la postcarga

0 120

0

200

Presión

VI


VOLUMEN VI

8040

Efecto del

aumento de la

precarga

(sin cambios en

relación P/V

diastólicos!)

0 120

0

200

Presión

VI


VOLUMEN VI

8040

Efecto del

aumento de

la “rigidez”

Presión

tele-

diastóli

ca

0 120

0

200

Presión

VI


VOLUMEN VI

8040

Efecto de la

disminución

de la

contractilidad

0 120

0

200

Presión

VI


VOLUMEN VI

8040

Cambios

en la

sepsis

36

•Clearly, measures of central venous pressure (Pcv) as estimates of right

atrial pressure (Pra) bear little relation to cardiac preload.

•Most physicians adhere to the philosophy that the energy necessary to

cause cardiac output is due to the mechanical force of ventricular contraction.

•Most analysis of the determinants of cardiac output centralizes in the

influence of

•preload

•contractility

•afterload

•heart rate

Mean systemic filling pressure and venous return

37

•The venous system contains as much as 75% of the total blood volume, with

approximately three-fourths of it in the small veins and venules.

•It is the pressure difference between these venous capacitance vessels and

the right atrium that defines the pressure gradient for venous return.

•This venous driving pressure reflects only stressed volume and not the total

venous blood volume.

•Changes in venous vasomotor tone and blood flow distribution can markedly

alter this upstream venous pressure without any change in total blood

volume.


38

Parameters for venous return:

•mean systemic filling pressure

•right atrial pressure

•resistance to venous return

•systemic compliance

•stressed and unstressed volume


39

Mean systemic filling pressure

•A measure of effective volume status (the effective circulating blood

volume).

•Independent of cardiac function.

•Volume status and fluid responsiveness (i.e. a significant increase in cardiac

output on fluid loading) are not synonymous.

•Even hypovolemic patients can be nonresponders to fluid loading.

•Fluid responsiveness depends on the intersection of the venous return curve

and the cardiac function curve.

•Fluid expansion will lead to a greater improvement in cardiac output in a

patient with a normal cardiac function than in a patient with impaired cardiac

function.


40

Venous resistance

•The slope of the venous return curve is proportional to the reciprocal of the

resistance to venous return.

•Venous resistance can be altered in many ways:

•constriction of the conducting veins; however, unlike the arterial

side, which has thick muscular vessel walls, venoconstriction

causes only a minimal increase in Rv.

•by increased blood viscosity.

•the major mechanism by which Rv is altered is by redistribution of

blood between different vascular beds.


41

Venous resistance

•Venoconstriction of an organ decreases its unstressed blood volume,

•Its local upstream pressure transiently rises.

•Expells blood into the systemic circulation because some of the unstressed

volume is shifted to stressed volume.

•Most of the venoconstriction with change in unstressed volume occurs in the

splanchnic circulation, which has a more prominent innervation.

•As splanchnic blood flow must subsequently pass across a second

parenchymal bed, the liver, splanchnic Rv is much higher than for other

organs, and any change in splanchnic Rv has minimal effect on total Rv

•Accordingly, venoconstriction of the splanchnic circulation has a minimal

incremental effect on Rv but a significant ability to increase Pmsf.


42

Compliance, stressed and unstressed volume

•The intravascular volume can be divided into unstressed volume and

stressed volume.

•The intravascular volume that fills these vessels up to the point where

intravascular pressure starts to rise is called unstressed volume, whereas the

volume that stretches the blood vessels and causes intravascular pressure to

rise is called the stressed volume.

•Administration of vasopressors and inotropes can be used to enlarge or

reduce stressed volume.

•Vasopressors increase stressed volume by recruiting volume from the

unstressed compartment.

•The increase in venous resistance and total peripheral resistance on itself

would diminish cardiac output. The increase in cardiac output by the increase

in Pmsf dominates the negative impact on cardiac output by the increase in

arterial and venous resistance.


43

Compliance, stressed and unstressed volume

•Knowledge of the volume status is of great importance before administrating

these drugs into a critically ill patient whose endogenous adrenergic

stimulation is already maximal.

•Norepinephrine may reduce splanchnic blood pooling, increase Pmsf, Rs and

Rsys of the splanchnic circulation, but the resulting decrease in flow of the

splanchnic circulation may increase ischemia in the gut and liver.


44

Localization of Pmsf

• Pmsf reflects a physiological concept: the circulation behaves as if the

upstream pressure for venous return is Pmsf because if Pra is rapidly varied,

blood flow co-varies in a fashion consistent with that specific Pmsf.

•The localization of Pmsf reflects a lumped parameter of all the vascular

beds.

•Its position in the pooled vascular beds will shift depending on changes in

arterial and venous resistances.

•The ratio of the resistance of venous return and systemic vascular

resistance describes the location within the circulation where Pmsf exists.

•A higher ratio implies a more upstream Pmsf location.

•Pmsf usually resides in the small venous lacunae downstream from the

capillary beds.


45Jansen, Curr Op Crit Care 2010;16:231

Bedside assessment of mean systemic filling pressure





¡Gracias!

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CAMBIOS CÍCLICOS EN LA

PRESIÓN DE PULSO

Mo

nit

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de

la

pre

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rga

Variación de la presión de pulso

PPmax – PPminPPV =

PPmean

PPmax

PPmean

PPmin

Pulse pressure variation (PPV) represents the variation of the pulse

pressure

over the ventilatory cycle.

PPV is

•measured over last 30s window

•only applicable in controlled mechanically ventilated patients with regular beat

rhythm

Mo

nit

ori

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de

la

pre

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rga

Análisis del contorno del pulso: gasto cardíaco y volumen de eyección

Mechanical

ventilation

↑↑↑Airway pressure

↑Ppl

↑Transpulmonary pressure

Capillary bed compression

(~100 ml)

↑LV filling

↑Systolic pressure

↑PP

↓RVEDV

↑RV afterload

↓RV ejection

↓Systolic pressure

↓PP

↓Venous return

↓LV filling↓LV ejection

Mo

nit

ori

zac

ión

de

la

pre

ca

rga


Mo

nit

ori

zac

ión

de

la

pre

ca

rga


Mo

nit

ori

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ión

de

la

pre

ca

rga


Mo

nit

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de

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Jardin ICM 2004;30:1047

Mo

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de

la

pre

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Jardin ICM 2004;30:1047

Mo

nit

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de

la

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Fluid overload versus hypovolemia

Jardin ICM 2004;30:1047

Mo

nit

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de

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pre

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rga


RV dysfunction

Monnet et al, AJRCCM 2000;162:134

Patients on MV

with sepsis and

acute circulatory

failure

Mo

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de

la

pre

ca

rga


VPP inducida

por la VM

http://ajrccm.atsjournals.org/content/vol162/issue1/images/large/RCCM9903035.f3.jpeg


Mo

nit

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de

la

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VPP inducida

por la VM


VPP inducida

por la VM


Mo

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ión

de

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pre

ca

rga



↑EDV as a result of fluid therapy depends on the partitioning of fluid into the different vascular

compartments (with different compliances) organized in series

↑SV depends on ventricular function

↓ventricular contractility → ↓slope of EDV/SV relationship

A patient can be a non responder because of:

•↑ Venous compliance

•↓ Ventricular compliance

•Ventricular dysfunction

Variación de la presión de pulso: “pitfalls”

Falses negatives:

Small VT (i.e., ≤8 ml/kg)

MV associated with spontaneous inspirations that ↓effects on venous return

False positives:

↑RV afterload

(DPP indicates LV preload-dependence but not RV-preload dependence)

Measurement error when than manually


Monnet et al. CCM 2009

Predicting volume responsiveness by using the end-expiratory occlusion in

mechanically ventilated patients

Análisis del contorno del pulso: índice de función cardíaca

t [s]

P [mm Hg]

dPmx* = dP/dtmax of arterial pressure curve

dPmx* represents left ventricular pressure velocity increase and thus is

a parameter of myocardial contractility


SVmax

SVmin

SVmean

SVmax – SVminSVV =

SVmean

Stroke Volume Variation (SVV) represents the variation of stroke volume

(SV) over the

ventilatory cycle.

SVV is


•only applicable in controlled mechanically ventilated patients with regular heart

rhythm


PPmax – PPminPPV =

PPmean

PPmax

PPmean

PPmin

Pulse pressure variation (PPV) represents the variation of the pulse

pressure

over the ventilatory cycle.

PPV is


•only applicable in controlled mechanically ventilated patients with regular beat

rhythm


ANÁLISIS DEL CONTORNO

DEL PULSO

Pulse Contour Analysis

CV Bolus

injection

PULSIOCAT

H

CALIBRATION

Transpulmonary Thermodilution injection

t

T

P

t

pulse contour analysis

Bolus Injection

Lungs

PiCCO Catheter e.g. in femoral artery

Transpulmonary thermodilution

measurement only requires

central venous injection of a

cold

(< 8°C) or room-tempered

(< 24°C) saline bolus…

Thermodilution parameters

Lt HeartRt Heart

RA PBV

EVLW

* LA LV

EVLW

*

RV

* not available in the USA (p 63)

Tb injection

t

Transpulmonary thermodilution: Cardiac

Output

Tb = Blood temperature

Ti = Injectate temperature

Vi = Injectate volume

∫ ∆ Tb. dt = Area under the thermodilution curve

K = Correction constant, made up of specific weight and

specific heat of blood and injectate

CO Calculation:

Area under the

Thermodilution Curve

After central venous injection of the indicator, the thermistor at the tip of

the arterial catheter measures the downstream temperature changes.

Cardiac output is calculated by analysis of the thermodilution curve

using a modified Stewart-Hamilton algorithm:

For correct calculation of CO, only a fraction of the total injected indicator

needs to pass the detection site. Simplified, only the change of temperature

over time is relevant.

Advanced Thermodilution Curve

Analysis

Transpulmonary thermodilution: Volumetric

parameters

Mtt: Mean Transit time

time when half of the indicator has

passed the point of detection in the

artery

DSt: Down Slope time

exponential downslope time of the

thermodilution curve

For the calculations of volumes…

ln Tb

injection

recirculation

MTt

t

e-1

DSt

Tb

All volumetric parameters are obtained by advanced analysis of the

thermodilution curve:


parameters

RAEDV

Thermodilution curve

measured with arterial

catheter

CV Bolus Injection

LAEDV LVEDVRVEDV

Right

Heart

Left

Heart

Lungs

After injection, the indicator passes the following intrathoracic

compartments:

The intrathoracic compartments can be considered as a series of “mixing

chambers” for the distribution of the injected indicator (intrathoracic thermal

volume).

ITTV

PTV

The largest mixing chamber in this series are the lungs, here the

indicator (cold) has its largest distribution volume (largest thermal volume).


parameters

Transpulmonary thermodilution: Newman Model

ITTV = RAEDV + RVEDV + Lungs + LAEDV + LVEDV = MTt x

Flow (CO)

PTV = Thermal Volume of the Lungs = DSt x Flow

(CO)Newman et al, Circulation 1951

RAEDV

detectioninjection

LAEDV LVEDVRVEDV

Rt Heart Lt Heart

Lungs

PTV

flow

ITTV

Multiplication of MTt (Mean Transit time) with CO results in the

complete Intrathoracic Thermal Volume (ITTV) which is the whole

needle to needle volume.

Multiplication of DSt (Downslope time) with CO yields the largest mixing

volume which is the lungs.

80

Intrathoracic Blood Volume

Intrathoracic Blood Volume

(ITBV)

is Global End-Diastolic Volume

(GEDV) + the blood volume in the

pulmonary vessels (PBV).ITBV = PBV + GEDV RVEDV LAEDVLVEDVPBVRAEDV

ITBV can be directly measured with thermal dye dilution technique (COLD System)

and has shown to be consistently 25% greater than GEDV measured by single

thermodilution technique (PiCCO).

Therefore it is possible to compute ITBV based on measurement of GEDV: ITBV =

1,25 x GEDV

ITB

VT

D (m

l)

r = 0.96

ITBV = 1.25 * GEDV – 28.4 [ml]GEDV vs. ITBV in 57 intensive care

patients

Sakka et al, Intensive Care Med 26: 180-

187, 2000

Transpulmonary thermodilution : ITBV as preload



Transpulmonary thermodilution: ITBV as preload

Transpulmonary thermodilution: ITBV as preload

Limitations

•Overestimates preload

•Aortic aneuyrysm

•Radial artery

•Intracardiac shunts

•Underestimates preload

•PTE

•Reduction of PBV (i.e. pneumonectomy)PBV will be 10% of ITBV and not 20%

Extravascular Lung Water*

EVLW*

EVLW*

RAEDV RVEDV LAEDV LVEDVPTV

EVLW

ITBV

ITTV

RAEDVRVEDV LAEDV LVEDVPBV

Extravascular Lung Water (EVLW*) represents the amount of water

content of the lungs and is calculated by subtraction of ITBV from ITTV.

=

Transpulmonary thermodilution: EVLW

87

Global Ejection Fraction (GEF)

(transpulmonary thermodilution)

GEF =GEDV

4 x SV

RVEF =RVEDV

SVLVEF =

LVEDV

SV

RV ejection fraction (RVEF)

(pulmonary artery thermodilution)

LV ejection fraction

(LVEF)

(echocardiography)

1 2& 3

Global Ejection Fraction

Right Heart Left HeartLungs

PBV

EVLW*

EVLW*RAEDV RVEDV LVEDV

Stroke Volume SV

LAEDV

Ejection Fraction: Stroke Volume related to End-Diastolic Volume

* not available in the USA (p 63)

Transpulmonary thermodilution

Transpulmonary thermodilution: GEF & PVPI

PBV

elevated

elevated

EVLW*

PBV

elevated

normal

PBV

normal

normal

Pulmonary Vascular Permeability Index

Pulmonary Vascular Permeability Index (PVPI) is the ratio of

Extravascular Lung Water (EVLW) to pulmonary blood volume (PBV). It

allows to identify the type of pulmonary oedema.

Pulmonarv Blood

Volume

Hydrostatic

pulmonary edema

Permeability

pulmonary edema

PVPI

=normal

PVPI* =EVLW*

elevated

PVPI

=

EVLW*

normal

PBV

EVLW*

PBV

EVLW*

PBV

EVLW*

Normal Lungs

Extra Vascular

Lung Water

Transpulmonary thermodilution: PVPI

Documents

Monitorización hemodinámica - aymon.es · •Mediciones de las presiones de llenado ventricular ... Precarga Presión tele-diastólica (PAD o POAP) CURVA DE FUNCIÓN CARDÍACA CURVA