oxy lesson 4

1. upper airway

2. lower airway

CLASSIFICATION OF AIRWAY 2

• Oral cavity

• Nasal cavity

• Pharynx

• Larynx

Upper airway 4

Trachea

Bronchi

Bronchioles

Alveoli

Lower airway 4

• portion of larynx below the vocal folds

• Trachea

• Bronchi 

• Bronchioles

Lower airway

Includes: 4

Lower airway

• Conducts air to lungs = facilities gas exchange

Lower airway

• Uses mucus & cilia to trap and expel particles

gas exchange

Lower airway

faci:

• mucus and cilia

Lower airway

USES ( 2) to expel particles

Acute Respiratory Distress Syndrome (ARDS)

• Lower airway disorder

Acute Respiratory Distress Syndrome (ARDS)

• “Wet lung” “shock lung syndrome” 

Acute Respiratory Distress Syndrome (ARDS)

• Severe form of acute respiratory failure characterized by:

  • Diffuse inflammation 

  • Increased permeability of alveolar-capillary membrane

Acute Respiratory Distress Syndrome (ARDS)

• Leads to:

  • Noncardiogenic pulmonary edema 

  • Reduced lung compliance

  • Severe hypoxemia (often does not respond to conventional oxy therapy)

• “Wet lung” “shock lung syndrome” 

ARDS AKA 2

syndrome

group of symptoms that occur together

• Diffuse inflammation 

• Increased permeability of alveolar-capillary membrane

ARDS

• Severe form of acute respiratory failure characterized by: 2

• Noncardiogenic pulmonary edema 

• Reduced lung compliance

• Severe hypoxemia (often does not respond to conventional oxy therapy)

ARDS LEADS TO 3

• Severe hypoxemia

• (often does not respond to conventional oxy therapy)

ARDS

• Rapid onset (12-48 hours) or typical onset (72 hours - 7 days) 

ARDS

• After severe respiratory failure caused by diffuse (widespread) inflammation & injury to the ALVEOLAR- CAPILLARY MEMBRANE 

ARDS

• Injury increases permeability of pulmonary capillaries, allows: (to enter the alveolar spaces)

  • Fluid

  • Proteins

  • Inflammatory cells 

• 12 - 48 hours

• 72 - 7 days

ARDS

rapid onset _____

typical onset _______

• severe respi failure

• diffuse (widespread) inflammation

• alveolar capillary membrane

ARDS

rapid and typical onset After _________caused by ______ (________) _____ & injury to the _____

Fluid

Proteins

Inflammatory cells

ARDS

• Injury increases permeability of pulmonary capillaries, allows: (to enter the alveolar spaces) 3

• Pulmonary edema (noncardiogenic)

• Impaired gas exchange

• Decreased lung compliance (STIFF)

• hypoxemia

ARDS

characterized by 4

Pulmonary edema (noncardiogenic)

Develops even when heart functions Normally

Impaired gas exchange

Due to accumulation of fluid in the alveoli

Decreased lung compliance (STIFF)

Due to

• Edema

• Inflammation 

• Collapse of alveoli support

• Edema

• Inflammation 

• Collapse of alveoli support

Decreased lung compliance (STIFF)

Due to 3

hypoxemia

• Refractory 

hypoxemia

• impaired O2 diffusion

• Refractory 

does not adequately improve with standard O2 therapy alone

standard O2 therapy

Refractory

does not adequately improve with_________ alone

1. Initiation phase

2. Amplification phase

3. Injury phase

pathogenesis ARDS

Initiation phase

Triggering / injuring event

Initiation phase

Precipitating event & inflammatory response

Amplification phase

Immune cells (neutrophils/ WBC) are recruited & activated —> pulmonary parenchyma

• Neutrophils/ WBC

• pulmonary parenchyma

Amplification phase

Immune cells (________) are recruited & activated —> _________

Injury phase

Immune cells release damaging substances = injure lung tissue

1. Injury to the alveolar-capillary membrane

2. Development of noncardiogenic pulmonary edema

3. ventilation-perfusion (V/Q) mismatch & shunting

4. reduced lung compliance

Pathophysio ARDS 4

• Cytokines

• Proteases

• Reactive oxy species

• Endothelial (within lungs)

• Epithelial cells (within lungs)

• Permeable

• plasma and protein

• interstitial space and alveoli

ARDS pathophysio Injury to the alveolar-capillary membrane

• neutrophils (WBC) release inflammatory: 3

• Damages 2

• more ____ = ( 2 ) leak into ( 2 )

• Alveolar-capillary mem

• fluid

• lungs

• hydrostatic pressure

• Inefficient gas exchange

• Low oxy

ARDS

Development of noncardiogenic pulmonary edema

• Disrupted ______ = _____accumulates within _____

  • Even if ______ in pulmonary circulation may be NORMAL

• Result: ( 2 )

• fluid

• surfactant

• blood flow

• physiologic shunting

• oxygenated

• limited improvement

• functional alveoli

• gas exchange

ARDS

ventilation-perfusion (V/Q) mismatch & shunting

• Type II pneumocytes 

  • Many alveoli is filled with _______ or collapses due to loss of ___

• Severe hypoxemia

  • ____ still passes through = ____________

  • Blood passes without adequately _____

• Increase FiO2 = _________

  • Due to lack of _________ available for ______

• Severe hypoxemia

• Type II pneumocytes

• Increase FiO2 = limited improvement

ARDS

ventilation-perfusion (V/Q) mismatch & shunting 3

• Alveolar edema + inflammation + collapse

• stiff

• expand

• compliance

• breathing

• functional alveoli

reduced lung compliance

• _______ + ___ + _____ = _____lungs & difficult to (reduced _____)

  • Increase work for _____ = lack of ______ available for gas exchange

• PHASE 1: Acute injury

• PHASE 2: Latent 

• PHASE 3: Acute Respiratory Failure

• PHASE 4: Severe Abnormalities

ARDS

Clinical Phases 

PHASE 1: Acute injury

• Manifestations 

  • Edema

  • Thick alveolar capillary membrane 

• Chest x-ray = Normal

PHASE 1: Acute injury

• Early changes:

  • Dyspnea

  • Tachypnea

• edema

• Thick alveolar capillary membrane

• normal

PHASE 1: Acute injury

manifestation 2

chest x ray

• Dyspnea

• Tachypnea

PHASE 1: Acute injury

• Early changes: 2

Endothelial

(within lungs)

Epithelial cells

(within lungs)

Oxygen therapy and support

PHASE 1: Acute injury

intervention

PHASE 2: Latent

• 6-38 hours after injury

PHASE 2: Latent

• Manifestations 

  • Increase edema 

  • Right —> left pulmonary shunting

  • V/Q mismatch

  • Hyperventilation

PHASE 2: Latent

• Early stage change

  • Patchy infiltrated form (from pulmonary edema) 

6 - 38 h

PHASE 2: Latent

____ hours after injury

• Increase edema 

• Right —> left pulmonary shunting

• V/Q mismatch

• Hyperventilation ( leads to hypocapnia

PHASE 2: Latent

Manifestations 4

• Patchy infiltrated form (

ARDS

PHASE 2: Latent 

Early stage change

pulmonary edema)

• Patchy infiltrated form (from

• Mechanical ventilation

• Prevent complications

ards

PHASE 2 intervention 2

PHASE 3: Acute Respiratory Failure

• Inflammatory damage of type II alveolar cells

  • Result: inhibition of surfactant production 

PHASE 3: Acute Respiratory Failure

• Inhibition = causes decreased compliance = increased work of breathing such as: 

  • Tachypnea 

  • Dyspnea 

  • High pitched and diffused crackles 

• type II alveolar cells

• surfactant production

PHASE 3: Acute Respiratory Failure

• inflammatory damage of ______

• Result: inhibition of ________

• inhibition

• compliance

• work of breathing

PHASE 3: Acute Respiratory Failure

• _______= causes decreased ______ = increased_______

• Tachypnea 

• Dyspnea 

• High pitched and diffused crackles

PHASE 3: Acute Respiratory Failure

• Inhibition = causes decreased compliance = increased work of breathing such as: 3

PHASE 4: Severe Abnormalities

• Chronic phase

  • Later effect that develop overtime

PHASE 4: Severe Abnormalities

• Includes:

  • fibrin deposition resulting in fibrosis

  • permanent alveolar damage

  • severe hypoxemia

    • unresponsive to therapy, metabolic & respiratory acidosis 

PHASE 4: Severe Abnormalities

• Occurs after: (may lead to pulmonary fibrosis) 

  • 10 days

• May be irreversible 

PHASE 4: Severe Abnormalities

• fibrin deposition resulting in fibrosis

• permanent alveolar damage

• severe hypoxemia (metabolic & respiratory acidosis )

PHASE 4: Severe Abnormalities

Includes 3

• 10 days

• pulmonary fibrosis

PHASE 4: Severe Abnormalities

occurs after ___ and may lead to ___

1.  severe shortness of breath

2. rapid breathing 

3. increased work of breathing 

4. use of accessory respiratory muscles 

5. cyanosis in severe cases

ARDS CM 5

: 1 week of a known clinical insult or development of new respiratory symptoms

onset of ards

Lung parenchyma

• end-stage fibrosis (thickening or scarring)

fibrosis

Lung parenchyma

is the end stage

Lung parenchyma

remodeling of lung architecture

“honeycomb lung”

Lung parenchyma AKA

“honeycomb lung”

• heavily scarred & destroyed lung tissue (contains clusters of small, thick-walled cystic airspaces) 

• Lung tissue

• small thick walled cystic airspaces

• “honeycomb lung”

  • heavily scarred & destroyed _____ (contains clusters of ______)

• NO, there are patches of Normal lung

• 20 - 30 percent

does ARDS affect all parts of the lung?

lung size reduction to

Berlin definition

• Diagnosis for ARDS

1. Timing

2. Chest imaging findings

3. Origin of Edema

4. Oxygenation Severity

ARDS - BERLIN DEF

CLINICAL CRITERIAS 4

• SX must develop 1 week of a known clinical insult / new respiratory sx

BERLIN

Timing

• Chest radiography (CXR) or computed tomography (CT/ lung scan) 

• bilateral infiltrates 

• opacities

• pulmonary edema

berlin definition

Chest imaging findings

• ( 2 )

  • Show

  • Show ______ that are consistent with ____

1. pleural effusion

• excess fluid

• LUNGS AND CHEST WALL

2. Lung collapse

3. Pulmonary nodules

BERLIN DEF

Chest imaging findings

• AB cannot be fully explained by 

  • _________

    • AB buildup of ___ in the spaces between ____and ___

  • _______

  • _________

• pulmonary edema

1. cardiac failure

2. fluid overload

Origin of Edema

_________observed must not be caused by: ( 2 )

cardiac function

i f cause of pulmonary edema is uncertain test for

Echocardiography (ECG

• To evaluate left ventricular function & filling pressures

Echocardiography (ECG

• identify signs of congestive heart failure 

• left ventricular function & filling pressures

• congestive heart failure

  
  

Echocardiography (ECG]

evaluates (2)

identifies sign of ___

Brain natriuretic peptide (BNP)

• biomarker measured to help support or argue against heart failure

• heart failure

Brain natriuretic peptide (BNP)

• biomarker measured to help support or argue against _______

central venous pressure (CVP)

trends to assess venous congestion & right ventricular function

• venous congestion & right ventricular function

central venous pressure (CVP)

assess 2

1. no cardiomegaly or pleural effusions on imaging 

2. no jugular venous distension

3. NO

• S3 (ventricular – systolic heart failure or volume overload)

• S4 (atrial – diastolic heart failure, left ventricular hypertrophy, or hypertension) gallop

FINDINGS (against cardiogenic pulmonary edema) 3

1. abg

2. Chest Imaging

3. chest radiography (CXR)

4. computed tomography (CT / lung scan) 

5. berlin definition

Diagnostic Evaluation5 ARDS

ABG

ARDS

dx for

• severe hypoxemia 

  • low PaO2 BUT high levels of supplemental O2

chest imaging

identifies the bilateral infiltrates reflect fluid accumulation & inflammatory changes within the lungs:

• chest radiography (CXR)

• computed tomography (CT / lung scan) 

chest imaging 2 types