INSUFICIENȚA RESPIRATORIE

ACUTĂ

Prof.dr.Şerban Bubenek MD
INSUFICIENŢA RESPIRATORIE ACUTĂ

Definiție

• incapacitatea plamanilor de a face fata nevoilor metabolice

ale organismului adică asigură doar un aport insuficient de O2
tisular sau o eliminare insuficienta de CO2

• se traduce printr-o presiune partiala scazuta a O2 in sangele

arterial (PaO2<60mmHg) si/sau o presiune partiala crescuta a
CO2 in sangele arterial (PaCO2>50mmHg)
 Fiziopatologie
Sistemul respirator este alcatuit din:
• caile respiratorii superioare

• Plaman (organul la nivelul caruia se realizeaza schimburile

gazoase, format din arborele bronsic si alveolele)

• peretele toracic care actioneaza ca o pompa

• sistemul nervos central cu eferentele si aferentele sale care

realizeaza controlul si adaptarea respiratiei la nevoile organismului

• sitemul vascular care asigura caile de transport ale gazelor

 hipoventilatia
2 mari TIPURI de IRA secundară
disfuncției de
5
Insuficienta pompă a
Insuficienta
mecanisme aparatului
respiratorie respiratorie
fiz-pat respirator.
hipoxemică hipercapnică
(Tip I) (Tip II)

PaO2 Scăzut Normal sau

scăzut
PaCO2 Normal sau Crescut
scăzut (↑ )
Δ(A-a)O2 Crescut Normal
 Alte 2 tipuri………
Tipul III = insuficienta respiratorie postoperatorie
• este de fapt o insuficienta respiratorie mixta.
• o componenta hipercapnica este generata de utilizarea medicamentelor depresoare ale
SNC (opioidele,hipnotice) și effect residual al miorelaxantelor de tip curare, care genereaza
hipoventilatie
• o componenta hipoxemica secundara atelectaziei postoperatorii.
Atelectaziile post chirurgie sunt multifactoriale, influentate de: tipul de interventie
chirurgicala, localizarea plagii operatorii, pozitia pe masa de operatie, durata interventiei
chirurgicale, etc…
• alte cauze de insuficienta respiratorie postoperatorie sunt: edemul pulmonar
(supraincarcare lichidiana), embolia pulmonara precum si infectia pulmonara
postoperatorie.

Tipul IV = insuficienta respiratorie din starile de șoc

• se refera la pacienții IOT+VM in cursul procesului de resuscitare a unui soc.
• Scopul ventilatiei este de a ameliora schiburile gazoase și de a diminua travaliul muschilor
 DO2 = CO x CaO2
CaO2 = (Hb x 1.36 x SaO2) + ( PaO2 x 0.0031)
if: Hb=15 g%

CaO2 = 20,1 + 0,3

DEFINITIONS
 Atmosphere and OXYGEN
Dalton's Law Of Partial Pressures
• Azot (N2) - 78,0 %;
• Oxigen (02) - 20,93 %;
• Dioxid de carbon (C02) - 0,03 %; AIR
• Argon (Ar) - 0,937 %;
• He, H+, etc.
• in a mixture of gases the pressure exerted by each gas is equal to
the pressure which would be exerted if that gas alone were present
PressureTotal = Pressure1 + Pressure2 …Pressuren
TBP (P.atm.) = PN2 + PO2 + PCO2 + PAr+ ………. = 760 mm.Hg

• The partial pressure of a gas in a mixture is obtained by multiplying

the total pressure by the fractional concentration of the gas. 8
O2 ? : PO2atm, PiO2 , PAO2 , PaO2
Ventilation and Perfusion at the Level of the Whole Lung

Dead Space ventilation

2250 mL/min
 Alveolar Gas Equation !!!!!
PiO2= FiO2 x ( TBP – H2O vapor pressure )

PAO2 = FiO2 x ( TBP – H2O vapor pressure ) – (PACO2/R)

PiO2

PAO2 = PiO2 – (PaCO2/R)

PaCO2 approximates PACO2 due to the rapid diffusion of CO2

R = Respiratory Quotient (VCO2/V02) = 0.8 100

40

in a normal individual breathing room air:

 Gas Composition in the Normal Alveolar Space
Trachea: partial pressure of CO2 is approximately 0
PiO2 = FiO2 x (barometric pressure-H2O vapor pressure)
= (760 – 47) x 0.21 =150 mmHg
PAO2 = 100 mm.Hg In the alveolar space,
oxygen diffuses into the
blood and CO2 diffuses
into the alveolus from the
blood.

D (diffusion coefficient) = Solubility / √ Mol. weight

 HYPOXEMIA
Learning objectives

• To be familiar with the 5 basic mechanisms of hypoxemia.

• To know the differential diagnosis of hypoxemia.

To understand the mechanisms of HYPOXEMIA,
one should be aware about 2 fundamental EQUATIONS !

• Alveolar Gas Equation

PAO2 = FiO2x (TBP- PH2O) – (PaCO2/R) (R=0,8)
for FiO2 = 0.21: PAO2 = 150 – (PaCO2/R)

• Aa-O2 gradient = PAO2 – PaO2 ( n= 14 – 20 mm.Hg.)

Alveolar arterial
- estimated from Alveolar Gas Eq. - measured by blood gases

- is a measure of how difficult is for O2 to cross the alveoli-capillary membrane

- larger the gradient = more severe is the disease !
 Aa-O2 gradient = PAO2 – PaO2
• n= 14- 20 mm.Hg. for FiO2 = 0,21

4 mm.Hg.

40 mm.Hg.
 Mechanisms of HYPOXEMIA
PaO2 = PAO2 – AaO2 gradient

PaO2 = FiO2x (TBP- PH2O) – (PaCO2/R) – AaO2 gradient

low PiO2 high High A-a gradient
- impaired diffusion
- shunt
- V/Q mismatch
The potential reasons of Hypoxemia:
1. Low PiO2
2. High PaCO2
3. High A-a O2 gradient
 1. Low PiO2 due to High altitude & Hypoxemia
• TBP sea level = 760 mm.Hg. ( O2 = 21 % )
• TBP decrease as altitude increase! (but O2=21% constant)
• sea level: saturated vapor pressure = 47 mm.Hg.

Pinsp.O2 = FiO2 x (TBP- PH2O)

• at sea level: Pinsp.O2 = 0.21 x (760 – 47) = 150 mm.Hg.

• 1500m: TBP = 719 mm.Hg

• 2000m: TBP = 600mm.Hg.: PinspO2 = 116 mm.Hg !!! PAO2= 116-50=66 mmHg

• 6000m : TBP= 380 mm.Hg.

• Pinsp.O2 = (380-47) x 0.21= 70 mm.Hg !
• PAO2 = PiO2 – (PACO2/R) = 70 – 50 = 20 mm.Hg. !!!

• HYPERVENTILATION DO NOT SOLVE THE PROBLEM !!!

1. Low PiO2 due to low FiO2 = Hypoxemia due to MISTAKES

The ANAESTHESIOLOGIST’s place

• An accidental decrease in FiO2

- the anesthetist does not supply enough oxygen
- improper installation of oxygen supply lines
- a leak in the breathing circuit
 1. Low PiO2 & Hypoxemia

• Hypoxemia appears due to ↓ TBP or by error↓

FiO2

• responds to 100 % O2 by ↑ Pinsp.O2 = correction of

Hypoxemia

• normal A-a O2 gradient ( PAO2 – PaO2)

• body : Hyperventilation and ↓paCO2

2. HYPOVENTILATION & Hypoxemia
Consequences of Inadequate Ventilation
• Apnea:
– PACO2 rises
– PAO2 falls until there is
no gradient for diffusion
into the blood

• Hypoventilation:
– Inadequate ventilation
for perfusion
– PACO2 rises
– PAO2 falls, but diffusion
continues
 2. Hypoventilation & Hypoxemia
• Causes: Tidal Volume or resp.rate or both ↓↓↓
• consequences in the alveoli: ↑PACO2 and: ↓ PAO2

• PAO2= FiO2 x (TBP- PH2O) – (PACO2 / 0.8)

• if PACO2 ↑ = final PAO2 ↓, in consequence PaO2 ↓ = Hypoxemia !

• AaO2 gradient is NORMAL, but if FiO2=21%: HYPOXEMIA is present !

• ROOM AIR: ph= 7,25, PaCO2 =60 BE = HCO3=

• PAO2= 150 – 60/0,8 = 150- 75 = 75 mm.Hg. ! AaO2= 15 (normal)
• PaO2= 75 -15 = 60 ( SpO2= 89 - 90 %) !
• O2 4 l/min : FiO2 = 0,3 : PAO2= (0,3 x713) – 75 = 210 - 75= 135
• PaO2 = 135 -15 = 120 mm.Hg ( SaO2= 100 %) but still Hypercapnia !
2. Hypoventilation & Hypoxemia

For a FiO2 0.4

an O2 flow ≥ 4 l/ min is safe
for avoiding hypoxemia
in pts with hypoventilation!
How Can We Tell if Alveolar
Ventilation is Adequate?
 PaCO2 and Alveolar Ventilation
• PaCO2 is:
– directly related to CO2 production (tissue metabolism)
– inversely related to alveolar ventilation (VA )

VCO 2
PaCO »
2 VA
• Increased PaCO2 (hypercarbia)
is always a reflection of inadequate alveolar ventilation (VA) !
 2. Hypoventilation & Hypoxemia
• Hypoventilation:

FiO2 21% + Hypoventilation = Hypoxemia !!!

- A-aO2 normal

- responds to supplemental O2 very well !

- treatment of severe hypoventilation is not O2

supplement, but assisted / mechanical VENTILATION !
 Causes of Hypoventilation

• 1. Depression of CNS by drugs (opioids, hypnotics, etc)

• 2. Inflammation, trauma or hemorrhage in the brainstem
• 3. Abnormal spinal cord pathway
• 4. Disease of the motoneurons of the brain stem/spinal
cord
• 5. Disease of the nerves supplying the respiratory
muscles (PRNevrites)
• 6. Disease of the neuromuscular junction (M.Gravis)
• 7. Disease of the respiratory muscles (myopathies)
• 8. Abnormality of the chest wall
• 9. Upper airway obstruction (CPOD)
 3. DIFFUSION & Hypoxemia
Fick’s Law of Diffusion
Dx AxΔP
Vx = Vx = rate of diffusion
ΔX D = diffusion coefficient ( ͠solubility)
A = surface area
Δ P = partial pressure gradient
Δ X = thickness of membrane

“impaired diffusion” is reserved for pathologic states characterized by

↑ thickness of the alveolar-capillary membrane.
( e.g.: pulmonary FIBROSIS)
 3. DIFFUSION & Hypoxemia
• sea level FiO2 21 %: - P insp O2 = 150 mm.Hg.
- PAO2= 100 mm.Hg
- PaO2 = 86-90 mm.Hg.

• normal AaO2 gradient = 14 – 20 mm.Hg

• the “calculated normal AaO2 gradient” = (Age/4) + 4

Diffusion Hypoxemia
- responds to 100% O2 but still ↑ AaO2 gradient !
- Fibrosis + exercising , or + causes of ↑ CO ( sepsis, septic shock )
- in states of impaired diffusion, hypoxemia is exacerbated by high
altitude and high CO !
 4. SHUNTING & Hypoxemia
• SHUNT = pulmonary blood has NO contact with ventilated alveoli !

SvO2= 70%
a. 70 % → SO2=96 %
84 %
b. 70 % → SO2= 70%
c. pulm. veins:
50 % flow with SaO2 98 %
50% flow with SaO2 70 %
- AaO2 gradient is ↑ mean =84 %

- if we give O2 100% :
pulm. veins: 100% O2 do NOT really improve Hypoxemia !
50 % flow with maximal SaO2 100%
50% flow with SaO2 70 % 85 %
 Causes of Shunt
n= 2 % of CO
up to 5 % of CO
• Physiologic shunt (Venous Admixture):
pulm.: bronchial & pleural veins
A. Normal true (anatomic) shunt:
extra-pulm.: Thebesian Veins
B. regional differences V / Q areas

• Pathologic shunts:
– Intracardiac
– Intrapulmonary
• Vascular malformations
• Unventilated or collapsed alveoli !
 4. SHUNTING & Hypoxemia
• SHUNT:
- Do NOT respond to 100% O2
- AaO2 gradient is ↑

Pathophysioloy : R → L Shunt

Causes of R → L Shunt :
1. intracardiac (Fallot , old VSD, ASD )
2. intrapulmonary
- ARDS ( fluid & proteins into the alveoli)
 5. V/Q mismatch & Hypoxemia

V/Q Matching
• 300 million alveoli

• Different alveoli may have widely differing amounts of ventilation and

of perfusion

• Ventilation-Perfusion matching is the process by which areas of the

lung which are best ventilated also receive the highest blood flow!

• Key for normal gas exchange is to have matching of ventilation and

perfusion for each alveolar unit !
– Alveoli with increased perfusion also have increased ventilation
– Alveoli with decreased perfusion also have decreased ventilation
– V/Q ratio = 1.0
 Two Lungs, Not One
• Suppose the left lung is ventilated but not
perfused (dead space). V/Q = V/0 = ȹ

• Suppose the right lung is perfused but not

ventilated (shunt). V/Q = 0/Q = 0

• Total V/Q = 1, but there is NO gas exchange !!!!!

• V/Q must be matched “at the level of alveolar unit” !

Why is the V / Q ratio important ?

V / Q ratio is a major factor in the regulation of ALVEOLAR

(and therefore ARTERIAL) levels of:

PaO2 & PaCO2

 V / Q ratio
upright position

V/Q
V / Q ratio

w
flo
od
o
bl

l ation
ve nti

APEX BASE
distance down lung P
 Pa O2 ~ 130 mm Hg

Pa CO2 ~ 28 mm Hg

V >>> Q high V / Q

V~Q V/Q~1
Pa O2 ~ 100 mm Hg

Pa CO2 ~ 40 mm Hg

Q >> V low V / Q
Pa O2 ~ 89 mm Hg

Pa CO2 ~ 42 mm Hg
 e.g. V/Q mismatch : 2 different areas of the LUNG

100 % O2 V/Q ↑

SO2
SvO2 70 % smaller area blood
98 %

SaO2 ?
bigger area blood
95 %
SO2
80 %

V/Q ↓

- resultant SaO2 is NOT the mean ( 98+80)/2 = 89 %!, but maybe 85 % !

- 100 % O2: improves Oxygenation !
 V/Q mismatch
• Responds to 100 % O2

• ↑ Aa-O2 gradient

• Causes
- ARDS
- Pneumonia V/Q mismatch
- Pulmonary embolism is
- COPD the most
- Fibrosis common cause
- Asthma of Hypoxemia
 Pulmonary EMBOLISM

• diverting blood has 2 adverse effects ( according Fick’s Law):

- decrease of A = the total surface area of capillary membrane ( ↓diffusion rate)
- increase the flow to a capillary bed of finite cross sectional area = ↑velocity =
decrease cross time = ↓diffusion rate

• Consequence: even if alveolar capillary membrane in remaining lungs is normal,

blood crossing this area can be incompletly oxygenated !!!

PaO2 is low because = V/Q m + impaired diffusion

 Etiologies of HYPOXEMIA with high Aa-O2 gradient
Impaired Diffusion
- Pulmonary Fibrosis
shunt
- Interstitial Lung Disease
V/Q Mismatch Shunt
- ARDS - R→ L intracardiac
- Pulmonary Edema - Atelectasis
- COPD - Mucus plugging
- Pulm. Embolism - Pulmonary AVM
- Pleural Efussion - Difuse Alveolar
- Pneumothorax HEMORRHAGE
- Pulm.HYPERTENSION - Hepatopulmonary
- Pulm. CONTUSION Syndrome
 ,

C.O..
C.O..
C.O..

C.O.

C.O..
 Hypoxemia and the response to 100% FiO2
• SaO2 in shunts do NOT fully correct with 100 % O2, unless the shunt
is small ( Qs /Qt ≤ 30 %)
- when the Qs/Qt > 0.4, even providing inspiratory fraction of oxygen up to 100 % is
not sufficient to ensure an adequate oxygenation and some degrees of hypoxia should
be expected.
- if Qs/Qt > 0.4, oxygenation provided by the native lung cannot sustain vital oxygen
delivery!

• SaO2 in: impaired diffusion and V/Q mismatch usually fully corrects
with 100% FiO2, unless the underlying pathology is very severe
and/or advanced.

• SaO2 in hypoventilation always fully corrects with 100 % O2 !

• but: appropriate treatment for Hypoventilation is VENTILATION !
 Detecting V/Q Mismatching and Shunt

• Radiotracer assessments of regional

ventilation and perfusion.

• Multiple inert gas elimination.

– Takes advantage of the fact that rate of
elimination of a gas at any given V/Q ratio varies
with its solubility.

• A-aO2 Gradient
 Approach to Hypoxemia
Check Aa-O2 gradient( adjusted for age and FiO2)
normal elevated

Hypoventilation SaO2 completely corrects with 100% O2 ?

or
Low PiO2n
NO
YES

L-R Shunt
V/Q mismatch
and/or
impaired diffusion

1. Review history and Exam

2. Check CXR
3. if SHUNT is present, consider TTE with bubble study

Almost all causes of Hypoxemia associated with an elevated Aa-gradient

have more than one mechanism at work and there is no single algorithm to indentify the
diagnosis !
 Cauze de insuficienta respiratorie acuta
Tipul 1 Hipoxemica Tipul 2 Hipercapnica

ARDS Obstructia de CRS

Cauze pulmonare infectioase Cauze neurologice de hipoventilatie (miastenia gravis)

Cauze cardiace (edemul pulmonar acut) Epansamente pleurale

Embolia pulmonara Pneumotorax

Atelectazia Criza astmatica

Acutizare BPCO Acutizare BPCO

Depresia centrilor respiratori (intoxicatii)

Diselectrolitemii (hipopotasemie, hipomagnezemie)

Acute Respiratory Distress Syndrome
 ARDS
The Berlin Definition
• No change in the underlying conceptual understanding of ARDS

– “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 (shunt) + V/Q mismatch

- increased physiological dead space
- decreased lung compliance.

• .
 New: BERLIN DEFINITION (2012)

- based on 4,000 pts. data, according to BERLIN definition:

only HYPOXEMIA contributed to the predictive validity of
the definition!
et al. JAMA 2012; 307:2530
ARDS Diagnosis
• Clinical pattern & blood gas analysis

• Imaging
Chest radiograph
Computed tomography
Lung ultrasound
Positron emission tomography
 Differentials
• Left ventricular failure/volume overload
• Mitral stenosis
• Pulmonary veno-occlusive disease
• Lymphangitic spread of malignancy
• Interstitial and/or airway disease
– Hypersensitivity pneumonia
– Acute eosinophilic pneumonia
– Acute interstitial pneumonitis
 ARDS
Pathological Stages

• Initial "exudative" stage-diffuse alveolar damage

within the first week

• “Proliferative" stage-resolution of pulmonary edema,

proliferation of type II alveolar cells, squamous
metaplasia, interstitial infiltration by myofibroblasts,
and early deposition of collagen

• Some patients progress to a third "fibrotic" stage,

characterized by obliteration of normal lung
architecture, diffuse fibrosis, and cyst formation
 Pathophysiology
1. Direct or indirect injury to
the alveolus causes alveolar
macrophages to release pro-
inflammatory cytokines

Ware et al. NEJM 2000; 342:1334

 Pathophysiology
2. Cytokines attract /
activate neutrophils into
the alveolus and
interstitum, where they
damage the alveolar-capillary
membrane (ACM).

Ware et al. NEJM 2000; 342:1334

Pathophysiology
3. ACM integrity is lost,
interstitial and alveolus fills
with proteinaceous fluid,
surfactant can no longer suppor
alveolus

Ware et al. NEJM 2000; 342:1334

 Pathophysiology
• Consequences of lung injury include:

– IMPAIRED GAS EXCHANGE

– Decreased Compliance

– Increased pulmonary arterial pressure (HTP)

 Impaired Gas Exchange

• V/Q mismatch
– related to filling of alveoli
– shunting causes hypoxemia

• Increased dead space

– Related to capillary dead space and V/Q mismatch
– Impairs carbon dioxide elimination
– Results in high minute ventilation
 Decreased Compliance

• Hallmark of ARDS

• Consequence of the stiffness of poorly or

nonaerated lung

• Fluid filled lung becomes stiff/boggy

• Requires increased pressure to deliver Vt !!!!!

 Increased Pulmonary Arterial Pressure
• Occurs in up to 25% of ARDS patients

• results from hypoxic vasoconstriction

• Positive airway pressure causing vascular

compression

• Can result in right ventricular failure

• Not a practice we routinely measure !

Evidence based management of ARDS
• Treat the underlying cause

• Low tidal volume ventilation

• use PEEP

• Monitor Airway pressures

• Conservative fluid management

• Reduce potential complications

 Brower RG, Matthay MA, Morris A, Schoenfeld D, Thompson BT, Wheeler A

Hypothesis:
In patients with ALI, ventilation with smaller tidal volumes (6 mL/kg) will
result in better clinical outcomes than traditional tidal volumes (12 mL/kg)
ventilation.

ARDS Network N Engl J

 Low Tidal Volume Ventilation

Protective measure to avoid over distention

of normal alveoli:

• uses low (normal) tidal volumes

• minimizes airway pressures

• uses Positive end-expiratory pressure (PEEP)

 PEEP
• Higher levels of PEEP/ FiO2 does not improve
outcomes
– may negatively impact outcomes:
• causing increased airway pressure
• increase dead space
• decreased venous return
• barotrauma
 PEEP

• Every ARDS patient needs it !

• Goal is to maximize alveolar recruitment and

prevent cycles of recruitment/derecruitment
 PEEP

• As FiO2 increases, PEEP should also increase !

ARDSnet. NEJM 2004; 351,

 Airway Pressures in ARDS
• Plateau pressure is most predictive of lung injury !

• Goal Plateau Pressure < 30 cmH2O, the lower the better

• Decreases alveolar over-distention and reduces risk of lung
strain !

• Adjust tidal volume to ensure Plateau Pressure at goal !

• It may be permissible to have plateau pressure > 30 cm.H2O

in some cases:
• Obesity
• Pregnancy
• Ascites
Terragni et al. Am J Resp Crit Care Med. 2007; 175(2):160
 Mechanical Ventilation
• MV is not a cure but a supportive measure

• to ensure gas exchange while minimizing risk of VILI and reducing respiratory
muscle activity

• target in Oxygenation is 88-95% SpO2 (PaO2=55-80 mmHg)

– No benefit from a liberal oxygenation with SpO2 > 95% (Panwar, AJRCCM
2016)

• Permissive Hypercapnia with PaCO2 up to 70mmHg with Ph>7.20

 Refractory Hypoxemia

• Mechanical Trouble (tubing, ventilator, ptx, plugging)

• Neuromuscular blockade

• Recruitment maneuvers – positioning, “good lung down” optimizes V/Q

mismatch

• Increase PEEP

• Inhaled PROSTAGLANDINE !
When inhaled, the vasodilator reaches the normal lung, is concentrated in
normal lung segments and recruits blood flow to functional alveoli where it is
oxygenated. This decreases shunting and hypoxemia !
• NO !?
• Prone position
• ECMO
 Supportive Therapies
• Sedation / analgesia / NMBA for 24- 48 hrs.

• Treat underlying infection

• DVT prophylaxis / stress ulcer prevention

• HOB 30°

• Hand washing

• Use full barriers with chlorhexidine

• Feeding protocol

• Avoid contrast nephropathy

• Pressure ulcer prevention, turning Q2h

• Avoid steroid use

v
 CARDS (Covid-19-ARDS) has 2 phenotypes:
“type L”: “type H”:
• low lung elastance (high compliance) - high elastance (low Compliance )
• Alower
fundamental role isbyplayed
lung weight estimated CT scan by disproportionate
- higher endothelial
lung weight damage that:
• low response to PEEP - high PEEP responders
• Minute ventilation is high +
•
- Infiltrates
disrupts pulmonary vasoregulation
are often limited in extent and, initially - extensive CT consolidations
at CT usually showind a ground-glass pattern on CT
- signifies
(that promotes ventilation-perfusion
interstitial rather than alveolar edema) mismatch (the primary cause of initial hypoxemia)
• many patients do not appear overtly dyspneic.

- fosters thrombogenesis
• Another feature consistently reported in CARDS is a highly activated coagulation cascade, with widespread
micro- and macro-thromboses in the lung and in other organs, very elevated serum D-dimer levels are a
consistent finding associated with adverse outcomes.
The COVID-19 infection induces: vasoplegia, VA/Q mismatch, and hypoxemia
 COVID- 19 ARDS

• COVID-19 causes unique lung injury

• COVID-19 is a systemic disease that primarily injures the vascular endothelium

• it affects both gas and vascular poles of the alveoli

• it may be helpful to categorize patients as having either type L or H phenotype.

• Different ventilatory approaches are needed, depending on the underlying

physiology
THANK YOU !