Monitoring

Steve Blackburn

Intensiviste

Anesthésiologiste

2010

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Cas clinique

• Patient 50 ans, post op PAC

– ATCD IRC; Db; Coronaro J2

• TA labile

• Tachycardie

• Diurèse limite

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4

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Plan

• Monitoring TVC

• Monitoring Swan Ganz

– Cas clinique

– détermination causes d’erreurs d’interprétation

– American Thoracic Society

• Section Critical Care

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Introduction

• Facteur clé outcome ICU

– Optimisation fonction cardiovasculaire

• volume circulant adéquat

• pré-charge

• fonction inotropique cardiaque

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Monitoring

• TVC

• Swan Ganz

• Echo cardiaque

• doppler oesophagien

• Discussion utilisation et limitations

– monitoring fréquent ICU

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Définition

• Qu’est-ce que la pression veineuse

centrale

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• Pression intravasculaire dans les gros

vaisseaux veineux thoracique

• Par convention

– prise au niveau jonction OD et VCS

– estimation pression OD

• Pression vs Volume

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Ondes PVC

• les ondes sont décrites en terme de ses

composantes

– 3 ondes ascendantes

– 2 ondes descendantes

• a contraction auriculaire

• x relaxation auriculaire

• c fermeture valve tricuspide a/n début systole

ventriculaire et le bulging des feuillets dans OD

• v retour veineux dans OD en présence valve

tricuspide fermée

• y à la fin systole ventriculaire (vidange OD vers VD)7

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Modification des ondes selon

pathologies• FA

• Dissociation AV / rythme jonctionnelle

• Régurgitation tricuspidienne

• Sténose tricuspidienne

• Pathologies avec réduction compliance VD

• Constriction péricarde

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FA

• perte onde a

• onde c plus proéminente

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•Dissociation AV / rythme jonctionnelle

• Contraction auriculaire survenant durant la

systole ventriculaire

• Onde a canon 2nd contraction auriculaire

contre valve tricuspide fermée

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Onde A canon

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•Régurgitation tricuspidienne

• sang éjecté à rebourd durant systole

ventriculaire du VD vers OD

• Production onde C-V large fusionnée

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Régurgitation Tricuspidienne

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• Sténose tricuspidienne

• flow du sang OD vers VD se fait contre

résistance fixe

• onde a augmentée

• descente y atténuée

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• Pathologies avec réduction compliance VD

• maladie péricardique

• maladie myocardique

– HVD 2nd HTP

– cardiopathie hypertrophique

– onde a augmentée

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• Constriction péricarde

• descente y steep short

• tamponnade : monophasique avec single x

descente.

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Péricardite constrictive

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Déterminants de TVC

• TVC est influencée par :

– volume sang dans le compartiment veineux

central

– compliance de ce compartiment

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étude de Starling

• relation entre TVC et CO

• relation entre retour veineux et TVC

• Si tous les facteurs sont constants, une tvc

donnée est associée avec un seul CO

possible. 16

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facteurs affectant ces 2 courbes

• Volume sang total

• Distribution du volume de sang dans les

différents compartiments

– (déterminés par le tonus vasculaire)

• Etat inotropique du VD

– (affecte la forme de la courbe fonction

ventriculaire)

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• lorsque ces facteurs sont affectés, il y a

débalancement entre CO et retour veineux

ad nouvel équilibre.

• De plus, la VCS est une structure

intrathoracique, ainsi les variations de

pressions intrathoracique affecterons la

TVC

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Implications importantes en

clinique lors de la mesure de la

TVC• Variation clinique de la respiration

• PEEP intrinsèque ou thérapeutique

• De plus, maladie valve tricuspide,

myocarde et péricardique et anomalie du

rythme

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TVC et prédicteur précharge

cardiaque• Optimisation CO suite administration

liquide

– précharge et stroke volume

• Problématique de REA liquidienne

excessive

• objectif ultime: atteindre une précharge

minimale afin d’obtenir le maximum stroke

volume 22

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définition de la précharge

• longueur des fibres musculaires cardiaque

à la fin de la diastole

• En terme d’indice de précharge

– 2 assumptions

• TVC est équivalent pression remplissage du coeur

• longueurs des myofibriles est proportionnel au

remplissage cardiaque

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courbe P-V

• modification de la courbe 2nd facteurs

modifiant la compliance ventriculaire

– oedeme myocardique

– ischémie myocardique

– état inotropique

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Si TVC = indice précharge

• début onde c

– fermeture valve tricuspide (début systole

ventriculaire donc RVEDP)

• exeption : sténose tricuspidienne (présence

gradient de pression entre les 2 chambres)

• pression moyenne durant onde a

– Si absence onde c

• FA

– Donc absence onde a

» prendre pression au point Z

» point sur onde TVC correspondant fin QRS20

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Monitoring commercial

• Génération d’une moyenne de TVC durant

tout le cycle cardiaque et prend une

moyenne sur plusieurs cycle.

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• Corrélation TVC mesurée et pression

distension OD en fin diastole

– souvent absente

• ex:

– appareil display

– pression transmurale : P intravasculaire (- P

extravasculaire

» chgt P intrathoracique lors de la respiration

» degré de transmission pression intrathoracique

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Solution

• Mesure manuelle

• Fin expiration

• Absence de PEEP

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Evidence clinique

• Absence corrélation

– TVC-CI

– stroke volume index

– intrathoracique blood volume index

– LVEDV index

– RVEDV

• LV preload est relié EDLAP

• Perte prédictibilité TVC + wedge si

pathologie présente. 27

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Evidence clinique

• Chirurgie hanche

• transplant rénale

– études monitoring Volume circulant bas

• Chirurgie cardiaque

– TVC ≥ 15

• Ventilation mécanique

– TVC ≤ 10 : réduction CI28

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TVC vs Swan

• Morbidité swan vs TVC

• $

• Absence avantage low risk surgical patient– Pearson, KS., Analg & Anesth 69:336-341

• Réduction outcome 2nd complications et

temps d’intubation – Stewart RD., Ann.Thorac.Surg. 66:1306-1311

• Goal directed therapy

– outcome identique• Rivers NEJM 345; 1368-1377

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TVC vs Swan

• The incidence of major morbidity in critically ill patients managed with

pulmonary artery catheters: a meta-analysis, Crit. Care Med.,

Mar;28(3):615-9

– 12 RCT

– 1610 patients

• Réduction morbidité en faveur du Swan Ganz

• A randomized, controlled trial of the use of pulmonary-artery catheters in

high-risk surgical patients. NEJM 2003 Jan 2;348(1): 5-14

– ASA III / IV

– 1994 patients

• Absence de bénéfice en faveur du Swan

• Morbidité idem

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Swan Ganz

• Développement initale

– mesure des pressions V. Pulmonaires

• Alternatives moins invasives

– ETO

– Sonde doppler oesophagienne

• Avantage du Swan vs Echo : Suivi étroit

– PAP

– CO

– SvO231

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Installation du Swan

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Sources D’erreurs

• système monitoring

– cathéter

– connecteur tubulaire

– transducer

• conversion énergie mécanique en signal électrique

– processeur

– résonnance naturelle du système

• élasticité et capacitance

– hyperésonnance

– damping32

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Hyperrésonnance

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ARDS

Ventilation spontanée

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A 45 yr-old man is hospitalized in ICU for sudden hypotension associated with fever (38 C), six days after an

infero-lateral myocardial infarction associated with transient cardiogenic shock requiring the infusion of 5

g/kg/min of dobutamine.

A faint systolic murmur is heard on cardiac auscultation, and the chest radiograph and ECG are not changed on

day 6.

A pulmonary artery catheter is inserted.

The cardiac index is 2.5 L/min/m2, SvO2 is 45% and the pulmonary artery pressure (PAP) and wedge pressure

(WP) tracings (upper panel), associated with right atrial (RAP) and right ventricular pressure tracing (lower

panel) are presented below. These data suggest which of the following diagnoses:

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A.

Severe tricuspid regurgitation

B.

Acute left ventricular failure

C.

Cardiac tamponade

D.

Mitral insufficiency

E.

Ventricular septal rupture

F.

Septic shock

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• Correct answer is A.

• The patient presents with a low cardiac output syndrome (CI = 2.5, SvO2 = 45%), RV dysfunction (RAP = 22), and no clinical, radiologic or hemodynamic (WP = 10) signs of left ventricular dysfunction. The findings do not support the diagnosis of "acute left ventricular failure" or "mitral regurgitation".

• The very low SvO2 eliminates the diagnosis of "ventricular septal rupture". In addition the right atrial and RV compliance (constrictive pericarditis or RV ischemia). Taking into account the history of the patient, this tracing is probably secondary to recent RV infarction.

• Moreover, the systolic upstroke (arrow) observed on the RAP tracing is due to severe tricuspid regurgitation, confirmed by echocardiography.

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• A supine patient has a Ppw of 12 mm Hg. He is on 5 cm H20 PEEP. One hour later the nurse informs you

that the Ppw is now 22 mm Hg. Which of the following could explain the change in Ppw (measured at end-

expiration)? TRUE or FALSE for each answer.

a.

Increased respiratory muscle activity

b.

Myocardial ischemia

c.

PEEP increased to 15 cm H20

d.

Transducer inadvertently positioned 5 inches below previous location

e.

Incomplete (partial) wedging

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Answer: A, B, D, E - True;

C- False.

Increased expiratory muscle activity can cause substantial elevation in juxtacardiac pressure and the end-expiratory Ppw (see Question 5).

Ischemia often leads to an acute decrease in LV compliance, resulting in a higher Ppw for the same LV end-diastolic volume.

A transducer that is 5 inches (12.5 cm) below the previous level will result in about a 10 mmHg increase of the Ppw (12.5 cm H20 ~ 10 mmHg).

Incomplete wedging may also lead to overestimation of the Ppw (see Question 8).

A PEEP of 15 cm H20 (~ 12 mmHg) would not cause Ppw to increase by 10 mm Hg. Normally, only about 1/2 of PEEP is transmitted to the juxtacardiac space, and the fraction is even less when lung compliance is reduced as in ARDS.

An increase in Ppw equivalent to the increase in PEEP would require non-Zone 3 conditions. However, in this example the Ppw can not be tracking alveolar pressure (PEEP), because the measured Ppw of 22 mmHg is much higher than the level of PEEP. REFS. # 3, 12

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• Match the hemodynamic set given below with the most likely cause of hypotension. Use each number only

once.

.

Pra

Ppa

Ppw

CO(L/min)

A. 18 30/19 18 3.5

B. 6 40/28 27 3.4

C. 17 30/15 14 3.2

D. 14 45/28 14 3.9

E. 10 32/16 14 8.0

1. Acute anterior MI

2. Gram negative sepsis

3. Cardiac tamponade

4. Acute inferior MI with RV involvement

5. Acute pulmonary embolism37

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Answer: A-3, B-1, C-4, D-5, E-2.In E the CO is elevated and sepsis is the only condition listed that is

associated with a high CO. In the other instances, the cause of low CO must be deduced from pressure data.

With anterior MI only the LV is involved so that Pra may be normal despite a very high Ppw (B).

With massive PE the pulmonary vascular resistance is significantly increased, as reflected in a widened Ppa-Ppw gradient and Pra may be quite elevated (D).

Equalization of the Pra and Ppw (A) is a cardinal feature of tamponade, but could also be seen with inferior MI with RV involvement.

However, RV infarct often results in Pra > Ppw (C); the latter would not be seen in tamponade. REFS. # 1, 4

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A 55 year old woman presents with acute respiratory failure. Initial exam shows bilateral crackles and a

systolic murmur. A chest radiograph is consistent with pulmonary edema, but heart size is normal and

there are no pleural effusions. A PA catheter is inserted. The following data are obtained: CO 5.0 L/min

(CI 2.7 L/min/M2), Pra 18 mmHg, Ppa 65/33 mmHg, Ppw (mean) 34 mmHg, SvO2 68 % (SaO2 92%). A

pressure tracing recorded from the distal lumen is shown, with arrow indicating balloon inflation.

• Which of the following scenarios could reasonably explain the above data ? (True or False for each

statement).

a.

Acute inferior MI with papillary muscle ischemia

b.

Post-infarct VSD in a hypotensive patient with mottled extremities

c.

Major pulmonary embolism with incomplete catheter wedging upon balloon inflation

d.

Acute renal failure with normal LV function and no mitral insufficiency

e.

Pulmonary hypertension due to small vessel veno-occlusive disease

Answer

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• Answer: A,B,D are True. C and D are False. The tracing shows an elevated Ppw with a prominent V

wave. Inferior MI with papillary muscle ischemia (A) may present with pulmonary edema and a

prominent V wave due to mitral regurgitation; a normal CO and SvO2 may be seen if global systolic

function is well preserved. However, a prominent V wave can occur in the absence of mitral

insufficiency if blood returning from the lungs during ventricular systole encounters a left atrium

that is noncompliant or is overdistended due to hypervolemia; disorders that increase pulmonary

blood flow will increase the volume of drainage of from the pulmonary veins and therefore

accentuate the V wave. A post-infarct VSD (B) increases pulmonary blood flow and this, together

with high left atrial pressure due to impaired LV systolic function and/or decreased LV compliance,

explains why a prominent V wave is sometimes seen with a post-infarct VSD. Also, the

thermodilution cardiac output (right sided output) is significantly higher than systemic cardiac

output and the left-to-right shunt causes a step-up in O2 saturation from right atrium to right

ventricle. This accounts for the apparent paradox of a shocked patient with mottled extremities

despite measurements of CO and SvO2 that are normal (or elevated), and SVR that is normal or

low. (SVR is a calculated value, so erroneous or misleading CO measurements will produce an

erroneous or misleading SVR). Hypervolemia due to acute renal failure (D) can be associated with

a large V wave in the absence of mitral regurgitation, and the size of the V wave will decrease after

diuresis or dialysis. In this setting, there may also a prominent A wave. (Indeed, the tracing shown

in Question 6 is from a patient with acute renal failure whose echocardiogram revealed no mitral

insufficiency; following aggressive diuresis the Ppw was 12 mmHg and the V wave was negligible).

Pulmonary hypertension from pulmonary embolism (C) is associated with a widened Ppad-Ppw

gradient and a normal Ppw. In the pressure tracing shown, the timing of the A and V waves is

typical of a left atrial waveform, so there is no reason to suspect incomplete wedging. A widened

Ppad-Ppw gradient and a normal Ppw is also expected in small vessel veno-occlusive disease (E),

because the inflated catheter records pressure in medium-large pulmonary veins, downstream

from the site of increased resistance. Rarely, vascular obstruction of large pulmonary veins due to

mediastinal fibrosis can lead to pulmonary hypertension with an elevated Ppw (and the Ppw is

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A 42 year old man presents with acute, severe pancreatitis. Because of hypotension, he receives 1 L normal

saline, with a transient increase in blood pressure. An arterial blood gas shows a PaO2 70 mmHg, PaCO2 24

mm Hg, pH 7.20 and HCO3 12 mEq/L on room air. On exam he appears to be in respiratory distress and has a

tender abdomen. He has cool extremities with livedo reticularis, poor capillary refill, and absent dorsalis pedis

pulses. Urine output is < 20 ml/hr. A chest radiograph shows minimal bibasilar infitrates. ECG = tachycardia

without ST-T abnormalities. The patient is intubated and mechanically ventilated in the assist-control mode with

Vt=700 ml and PEEP=5 cmH20. Tachypnia and increased respiratory efforts persist despite mechanical

ventilation and midazolam infusion. A PA catheter is inserted and the following data is obtained, with Ppa, Ppw,

and Pra (in mmHg) measured at end-expiration. The Ppw tracing is shown below.

BP 82/60, HR 130/min, CO 3.6 L/min, SV 30 ml, SvO2 40 %, Ppa 45/30, Ppw 22-26, Pra 16-20

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• Question 1. Based on the available data, what is the most likely cause of shock and which empiric

therapeutic approach would be most appropriate? (One best answer)

Diagnosis

Therapy

a

Myocardial depression

Dobutamine

b.

Sepsis

Norepinephrine

c.

Hypovolemia

IV saline

d.

Myocardial depression

Dopamine & IV bicarbonate.

e.

Massive PE

TPA42

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Answer 1 is C. The clinical picture of severe pancreatitis with hypotension, cool extremeties, oliguria, and acidosis in a patient who received only a modest amount of fluid (1 L) is highy suggestive of profound hypovolemia. The recorded Ppw is 22-26 mmHg. However, the tracing shows very large respiratory excursions, greatly increasing the probability that the high end-expiratory Ppw is due to increased juxtacardiac pressure from abdominal expiratory activity. As such, the measured end-expiratory Ppw may greatly overestimate transmural filling pressure and LV preload. Abdominal muscle contraction at end-expiration is a common cause of errors in use of the Ppw and can usually be easily detected by palpation of the upper abdomen.

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A 56 year old man, who has a 60 pack-year history of cigarette smoking, is admitted with two hours of

substernal pressure and dyspnea. A duodenal ulcer was diagnosed 3 weeks previously and has been treated

with cimetidine. On examination he is in marked respiratory distress, using accessory muscles of respiration,

and cyanotic. Following intubation, mechanical ventilation, and sedation, the blood pressure is 110/85, heart

rate 117, and temperature 36.8. On assist-control with a rate of 20, Vt 500, PEEP of 10cmH2O, and FiO2 0.6,

the PO2 is 68mmHg, PCO2 44, and pH 7.27. The hemoglobin concentration is 14.2g/dL. The ECG shows an

acute inferior myocardial infarction. The chest radiograph reveals diffuse, four-quadrant airspace filling with

Kerley B lines and a normal sized heart. A pulmonary artery catheter is inserted. You are called because the tip

of the catheter cannot be wedged successfully. A tracing from the distal tip of the catheter during inflation of the

balloon and attempted wedging is shown:

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• What can you conclude from this tracing?

A.

The catheter is "over-wedged".

B.

The catheter is appropriately wedged.

C.

Catheter whip makes it impossible to determine the location of the tip of the catheter.

D.

The catheter is not wedged.

E.

It is likely that the balloon of the catheter is ruptured, perhaps during passage through the introducer sheath.

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Answer/Discussion. B is the correct answer. There are four criteria for a wedged catheter: a) conversion of the tracing from a pulmonary artery waveform to an atrial waveform ("damping"); b) a fall in the mean intravascular pressure; c) arterialized blood can be withdrawn from the tip of the catheter; and d) fluoroscopic evidence of fixation (wedging) of the tip of the catheter in a pulmonary artery. The final two of these are relatively cumbersome and used only occasionally. The first is widely used, but suffers from its failure in patients with substantial mitral regurgitation, as in the tracing shown, when a typical atrial waveform can never be seen, and in conditions where the waveform dampens, but a wedge is not attained (as in partial obstruction of the catheter, for example against the wall of the pulmonary artery). The most reliable and sensitive criterion for a wedged catheter is a fall in the mean pressure, which must occur when the tip of the catheter senses pulmonary artery pressure (unwedged) versus when it senses left atrial pressure (wedged). Before attempting to wedge a catheter, the operator should ascertain both the waveform and the mean pressure, then inflate the balloon. The waveform and mean pressure should be compared after attempted wedging. If the waveform fails to dampen, but the mean pressure falls, the catheter is wedged. This patient had an acute myocardial infarction complicated by acute, severe mitral regurgitation and pulmonary edema. Note the giant V wave in the wedge tracing (and in the pulmonary artery tracing). When a giant V wave is present, a pressure should be reported for the height of the V wave (54mmHg in this example) as well as for the pressure immediately preceeding the onset of the V wave, which best estimates left ventricular end-diastolic pressure (here, 26 mmHg).

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Zoning Artéfact

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Zoning Artéfact

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algorithme

REA liquidienne et inotropes• REA (volémie ad TVC cible 10-15)

• Si TVC 15+

– Pathologies sous jacentes identifiables

• physiologique vs potentiellement mortelle

– Réponse clinique

– Investigation supplémentaire

• RX pulmonaire

• sédation

• Swan ganz

– PAP

– CO

• Echo cardiaque

– TVC élevée et CO bas

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