Prezentare caz

• CA, barbat, 68 ani

• APP -Infarcte cerebrale multiple sechelare

-Tulburare neurocognitiva de origine vasculara
-Atrofie cerebrala
-HTA.Dislipidemie.AOMI grad III
-BPOC, tabagism cronic (38 PA)

15.04- se prezinta la camera de garda pentru durere retrosternala iradiata in epigastru, dispnee, transpiratii,
sincopa, alterarea starii generale, somnolent, dezorientat temporospatial, febra (38.6)
Clinic: Constient, greu cooperant, dezorientat temporospatial, GCS 13, febril, stabil hemodinamic si respirator
Paraclinic: -Leucocitoza cu neutrofilie
-EAB: ph-7.46, pCo2-24, pO2-63, Hco3-17, lactat 1.48
troponina:16.2, CK-423, CK-MB16

Dg: Infarct miocardic acut NSTEMI, Killip II

Suspiciune endocardita valva aortica infirmata ecografic
Regurgitare mitrala grad II/IV degenerative
24.04 – ADMISIE STI
ADMISIE STI:
-constient, greu cooperant, dezorientat temporo-spatial, GCS 13
-MV prezent bilateral, incarcat traheobronsic, raluri ronflante si sibilante bilateral
-Zgomote cardiace ritmice, echidistante, echipotente, fara sufluri
-Abdomen suplu, nedureros spontan si la palpare, fara semen de iritatie peritoneala
-echilibrat respirator si hemodinamic
-Diureza prezenta, tranzit prezent

Paraclinic:
• Leucocitoza (18,13) cu neutrofilie (14.17), Hb-13.8 g/dl, Trombocite- 269.000
• Sindrom de citoliza hepatica: Alt 82 U/l, AST 123 U/l
• Cr-1.45, uree 80 mg/dl
• Fibrinogen 595 mg/dl, procalcitonina 2 ng/ml

EAB: ph7.5, pO2-58, pCO2-31, bicarbonate-24, lactat 1

Rx: microopacitati de intensitate sechelara supraclavicular pe partea dreapta, infiltrate interstitiale cu

aspect reticular in ambele campuri pulmonare

TAZOCIN-4.5G/8H, VANCOMICINA 1G/12H

SOFA=4, APACHE=12
• CT- fara semne de AVC
• Ecografie cardiacă-infirma endocardita
• Urocultura/sumar de urina-negativ
• Exudat nazal- screening negative pentru
colonizare nazala cu S.aureus
• Exudat faringian-Streptococ beta-hemolitic
absent
-Staphylococcus aureus absent
-Levuri prezente: Candida albicans
Rx-Opacități sechelare apicale drepte si benzi fibrotice bazale.Desen interstițial si
reticulomicrovascular accentuat (25.04)
Rx 07.05- Fără modificări
10.05-Ziua 16 TI
-Leucocitoza cu neutrofilie
-Hb-8.7g/dl
-Trombocite-150.000
Consult cardio - Suspiciune endocardita valva mitrala cu hemoculturi negative in
momentul consultului
-Se initiaza trat atb-Ceftriaxona 2g/12h, Linezolid 600 mg/12h, Gentamicina 160mg/zi

12.05- puseu febril (39,3): Hemoculturi pozitive Acinetobacter baumanii sensibil la

Colistin
--instabil hemodinamic, oligoanurie, trombocitopenie
 Evoluție pacient
45

38.3
40 38 37.5 39 38.2 38.6 38.5 38.8
36.8
35

30

25

20

15

10

Leucocite Fibrinogen Procalcitonina Temp

Colistin
Cefort Cefort+Linezoli
Vancomicina 1g/12h + Tazocin 4.5g/8h d+ 1milU/8h+Tigacyl
1g/12h Gentamicina 500mg/8h
• 14.05- IOT-VM-BiPAP-FiO2-50%, PEEP-9, Pins-
17

• 15.05-Leucocitoza-28.000 cu neutrofilie-
26.000, Hb-8.7g/dl, Tr-124.000,
Procalcitonina>100, Uree 180 mg/dl, Cr-3.93
mg/dl
CT 15.05- Modificări pulmonare ce asociaza condensări bazale
si pleurezie postero-bazală minimă.
• 16.05-Leucocite-4230,Hb-9g/dl, Tr-32.000,
Uree 244 mg/dl, Cr-4.73 mg/dl

Exitus 16.05, ora 08:30

ARDS
 “Acute Respiratory Distress Syndrome  (ARDS) is
an acute diffuse, inflammatory lung injury, leading to
increased pulmonary vascular permeability, increased
lung weight, and loss of aerated lung tissue with
hypoxemia and bilateral radiographic opacities,
associated with increased venous admixture, increased
physiological dead space and decreased lung
compliance.”
 Definitia Berlin
• debut <1 saptamana
• opacitati bilaterale (Rx pulmonar/ CT)
neexplicate de efuziuni, noduli, zone de
atelectazie
• indice de hipoxemie < 300 mmHg
• insuficienta respiratorie neexplicata de
insuficienta cardiaca sau hipervolemie
 Clasificare
• Usor: indice de hipoxemie 200-300
- mortalitate 27%
• Moderat: indice de hipoxemie 100-200
- mortalitate 32%
• Sever: indice de hipoxemie <100
- mortalitate 45%
 Factori de risc
Directi Indirecti
Pneumonie Sepsis non-pulmonar

Aspiratia continutului gastric Pancreatita

Contuzia pulmonara Transfuzia masiva

Embolia Politrauma

Inecul Bypass cardio-pulmonar

Injurii inhalatorii
• ARDS primar/ pulmonar : condensari, aspect
asimetric, opacifieri si aspect de ‘geam mat’

• ARDS secundar/ extrapulmonar: colaps

alveolar, opacifieri cu aspect simetric,
atelectazii
 Simptome
• dispnee
• tahipnee
• hipoxemie
• tahicardie
• simptomele bolii de baza
 Fiziopatologie
• injurie
• exudativa – distrugerea mb alv-cap cu aparitia
infiltratului inflamator si exudat proteic ce
formeaza membrane hialine
• proliferativa – proliferarea pneumocitelor tip II si a
cel
• fibrotica – infiltrare cu fibroblaste care inlocuiesc
alveolele si ductele cu zone de fibroza
• rezolutie – restaurare inceata si incompleta
 Etapa exudativa
• dureaza 3-7 zile
• injurie alveolara difuza cu
* acumulare de apa extravascular si celule
inflamatorii
* necroza celulelor alveolare
* hemoragie intraalveolara
=> scade vent alv, sunt intrapulmonar, scade
complianta, creste efortul resp
 Etapa proliferativa
• dureaza 2-3 saptamani
• creste nr de pneumocite II
• eliminarea resturilor intraalveolare
• scaderea edemului
 Etapa fibrotica
• apare dupa 2-3 sapt
• fibroza interstitio-alveolara
• bule de emfizem
• dependenta de ventilatie mecanica
 Baby lung model

The “baby lung” is actually the “small” lung open at end-

expiration; it may become larger during inspiration due to newly
recruited tissue, according to the recruitment-pressure curve and
the opening pressure distribution. The “baby lung” is not healthy
but it is aerated. Its specific elastance, however, is usually near-
normal. The smaller the “baby lung,” the greater the potential
for VILI.
Interconexiune:
* edem pulmonar cu distrugerea barierie
alveolo-capilare
* infiltrate inflamatorii
* deficit al surfactantului
Membrana alveolo-capilara
• Injurie bidirectionala : proteine si fluid in
alveole/ surfactant si citokine alveolare in
plasmadamage with bidirectional flow
disfunctie de surfactant
• proliferare anormala de pneumocite tip II
-> perturbarea balantei dintre procesele
reparatorii si fibroza
Infiltrate inflamatorii
• Migrarea neutrofilelor in alveole cu eliberarea
speciilor reactive de O2, citokine, proteaze ->
distructie tisulara
• Celule endoteliale, plachete, macrofage
alveolare -> inflamatie alveolara
Disfunctia de sufactant
• scaderea compliantei pulmonare
• scaderea productiei si legarea de proteinele
plasmatice
 Efecte
• hypoxaemia (V/Q mismatch, impaired hypoxic pulmonary
vasoconstriction)
• increase in dependent densities (surfactant dysfunction, alveolar
instabilities)
• decreased compliance (surfactant dysfunction, decreased lung
volume, fibrosis)
• collapse/consolidation (increased compression of dependent lung)
• increased minute ventilation (increased in alveolar dead space)
• increased work of breathing (increased elastance, increased minute
volume requirement)
• pulmonary hypertension (vasoconstriction, microvascular thrombi,
fibrosis, PEEP)
 Ventilator Induced Lung Injury
• volutrauma: injurie fizica prin supradistensie
• barotrauma: ruptura cailor aeriene
determinata de ppv
• atelectrauma: forte de frecare la interfata
plaman deschis/inchis=> colaps
• biotrauma: injurie mediata de citokine
 Tratament
• tratamentul cauzei
• terapie suportiva: fluide, nutritie, ventilatie
mecanica, pozitionare, terapie farmacologica,
terapii de salvare
 Ventilator management of patients with ARDS

Ventilator Mode
Volume assist/control until weaning
Tidal Volume (VT)
• Initial Vt: 4-6 mL/kg predicted body weight.
• Measure inspiratory plateau pressure (Pplat, 0.5 sec inspiratory pause) every 4 hours AND after each change in
PEEP or Vt.
• If Pplat > 30 cm H2O, decrease Vt to 5 or to 4 mL/kg.
• If Pplat < 25 cm H2O and Vt < 6 mL/kg PBW, increase Vt by 1 ml/kg PBW .

Respiratory Rate (RR)

With initial change in Vt, adjust RR to maintain minute ventilation.
• Make subsequent adjustments to RR to maintain pH 7.30-7.45, but do not exceed RR = 35/min, and do not increase
set rate if Paco2 < 25 mm Hg.
I : E Ratio
Acceptable range = 1 : 1 to 1 : 3 (no inverse ratio).
FIO2 , Positive End-Expiratory Pressure (PEEP), and Arterial Oxygenation
Maintain Pao2 = 55-80 mm Hg or Spo2 = 88%-95% using the following PEEP/Fio2 combinations:
FIO2 0.3-0.4 0.4 0.5 0.6 0.7 0.8 0.9 1
PEEP 5-8 8-14 8-16 10-20 10-20 14-22 16-22 18-25
Acidosis Management
• If pH < 7.30, increase RR until pH ≥ 7.30 or RR = 35/min.
• If pH remains < 7.30 with RR = 35, consider bicarbonate infusion.
• If pH < 7.15, Vt may be increased (Pplat may exceed 30 cm H2O).
Alkalosis Management
If pH > 7.45 and patient not triggering ventilator, decrease set RR but not below 6/min
Fluid Management
• Once patients are out of shock, adopt a conservative fluid management strategy.
• Use diuretics or fluids to target a central venous pressure (CVP) of < 4 or a pulmonary artery occlusion pressure (PAOP)
of < 8.
Liberation from Mechanical Ventilation
• Daily interruption of sedation.
• Daily screen for spontaneous breathing trial (SBT).
• SBT when all of the following criteria are present:
(a) Fio2 < 0.40 and PEEP < 8 cm H2O.
(b) Not receiving neuromuscular blocking agents.
(c) Patient awake and following commands.
(d) Systolic arterial pressure > 90 mm Hg without vasopressor support.
(e) Tracheal secretions are minimal, and the patient has a good cough and gag reflex.
Spontaneous Breathing Trial
• Place patient on 5 mm Hg pressure support with 5 mm Hg PEEP or T-piece.
• Monitor HR, RR, oxygen saturation for 30-90 minutes.
• Extubate if there are no signs of distress (tachycardia, tachypnea, agitation, hypoxia, diaphoresis).
 Recruitment maneuvers
• A RM is a dynamic, transient increase in transpulmonary
pressure (difference between airway pressure and pleural
pressure) which is directly proportional to the reopening of
lung units
Increasing PEEP from 5 to 15 cm H2O has been demonstrated to
yield increased lung volume (anatomical recruitment) in half of
patients, while in other patients, higher PEEP results in
improvement of lung volume and perfusion (functional
recruitment). In other words, opening of alveolar units does not
necessarily entail restoration of lung perfusion in that specific
region. In cases of functional recruitment, an increment in
PaO2/FiO2 can be expected
 Terapia farmacologica
• surfactant replacement therapy: theoretically good,
improves oxygenation but no improvement in mortality,
problems with distribution to alveoli
• glucocorticoids: improvement in ventilator free days and
shock, no improvement in mortality and increase in
weakness
• ketoconazole: antifungal that inhibits thromboxane
synthase and 5-lipooxygenase -> early data but not
confirmed.
• others: cytokine antagonism, NSAIDS, scavengers of O2
radicals, lisofylline -> no success, APC in sepsis
 Prone position
As in the case of PEEP, the use and indications of prone positioning in
patients with ARDS has changed over time. While decades ago this
procedure was only used to improve arterial oxygenation in life-
threatening acute respiratory failure , it is nowadays clear that prone
positioning, allowing for a more homogeneous distribution of stress and
strain, helps to protect lung against the VILI . The most important
consequences of prone positioning, which can explain its final effect are:
a better ventilation/perfusion matching with a consequent improvement
in CO2 clearance, a more homogenous distribution of ventilation with a
reduction of VILI and a recruitment of dorsal regions through the
redistribution of lung densities . Therefore, prone positioning should be
reserved to all patients with severe ARDS, especially in the acute phase,
because of the higher probability to recruit lung parenchyma.
• scade compresia cardiaca si abdominala
asupra lobilor inferiori
• uniformizeaza raportul V/Q si elastanta
pulmonara
• faciliteaza drenajul
• potenteaza efectele benefice ale manevrelor
de recrutare
Contraindicatii absolute:
- arsuri/ fracturi deschise
- instabilitate spinala
- fracturi pelvice
- Instabilitate hemodinamica marcata
- hic
Complicatii:
- edem facial
- leziuni de decubit
- obstructie cai aeriene
- dislocare IOT/ CVC/sonde
- hipotensiune
- varsaturi
 Terapii de salvare
• iNO - optimisation of V/Q mismatch, 1-60ppm,
40-70% will respond, monitor for metHb
• prostacicline inhalatorii - optimisation of V/Q
mismatch, 1-50ng/kg/min, as effective as iNO
• HFOV – optimisation of oxygenation in severe
hypoxemia
• ECMO
• ECCO2 R
 ECMO in ARDS
INDICATIONS
• acute, severe REVERSIBLE respiratory or
cardiac failure with a high risk of death that is
refractory to conventional management
• poor gas exchange
• compliance < 0.5mL/cmH2O/kg
• P:F ratio < 100
• shunt fraction > 30%
GENERAL CONTRAINDICATIONS
Absolute
• progressive non-recoverable cardiac disease (not transplant candidate)
• progressive and non-recoverable respiratory disease (irrespective of
transplant status)
• chronic severe pulmonary hypertension
• advanced malignancy
• >120kg
• unwitnessed cardiac arrest
Relative
• age > 75
• multi-trauma with multiple bleeding sites
• CPR > 60 minutes
• multiple organ failure
• CNS injury
 ECCO2 R
Until recently, the primary use of ECCO2R has been as a bridge to
recovery in cases of severe hypercapnic acidosis (HCA) that are
refractory to mechanical ventilation. In the vast majority of cases, this
has been in the context of ARDS, although it has also been used in a
variety of other situations. The threshold at which a HCA requires
treatment is debatable and will vary depending on the clinical
situation but most would agree that there comes a point at which
intervention is required. More recently, ECCO2R has been used to
allow protective ventilation in patients with acute respiratory distress
syndrome (ARDS) in whom HCA has not yet become refractory and
this is likely to be where its role lies in the future. It is now well
established that mechanical ventilation can initiate and exacerbate
lung injury.
In clinical practice, ECCO2R often exceeds
expectations with regards to oxygenation, which
can be explained by two other factors:
1. As the ECCO2R system lowers the PaCO2, the
alveolar concentration of O2 will increase in
accordance with the alveolar gas equation.
2. By removing CO2, ECCO2R allows ventilation
strategies that are focused on oxygenation
rather than CO2 elimination.