Respiratory Failure Respiratory Failure - PowerPoint Presentation

Slide1

Respiratory Failure

Slide2

Respiratory Failure

Defined as the impairment of the lung’s ability to maintain adequate oxygen and carbon dioxide homeostasis.

Slide3

Respiratory Failure - Definition

PaO

2

< 60 mm Hg

and/or

PaCO

2

> 50 mm Hg

Slide4

Respiratory Failure

Can be acute, sub acute, or chronic.

If chronic then compensation has developed to maintain pH.

Respiratory failure defined by pH < 7.25 in these patients.

Slide5

Types of Respiratory Failure

Type 1 = Hypoxemic Respiratory Failure.

Type 2 = Hypercapnic/Hypoxemic respiratory failure.

Slide6

Type 1 Respiratory Failure

Primarily a failure to maintain adequate oxygenation.

PaO

2

< 60 mm Hg.

Ventilation is not impaired.

PaCO

2

<= 40 mm Hg.

Slide7

Type 1 Respiratory Failure Examples

Pneumonia – any etiology.

Acute (Adult) Respiratory Distress Syndrome (ARDS).

Reduced FiO

2

(High Altitude).

Slide8

Examples – Patient A

A 24 y/o man with acute pneumonia.

ABG on room air

PaO

2

= 55 mm. Hg

PaCO

2

= 28 mm. Hg

pH = 7.49

Slide9

Type 2 Respiratory Failure

Failure of the lungs to maintain ventilation.

PaCO

2

> 50 mm. Hg

Resulting hypercarbia may lead to hypoxemia alone.

Usually V/Q mismatch and/or shunt is also present.

Etiology more varied.

Slide10

Example – Patient B

A 23 y/o woman presents in coma:

ABG on room air:

Pa02 = 62 mm Hg

PaCO2 = 86 mm Hg

pH = 7.04

Slide11

Type 2 Respiratory Failure - Examples

Pneumonia – any etiology

Drug overdose

COPD

Upper airway obstruction

Slide12

Type 2 Respiratory FailureEtiologic Locations

CNS

Peripheral nervous system

Chest wall disorders

Lung parenchyma

Extrapulmonic organs – heart etc.

Slide13

Mechanisms of Hypoxemia

Hypoventilation

è

Check PaCO

2

V/Q mismatch

è

Resolves with 100% O

2

Shunt

è

Doesn't resolve with 100% O

2

Insufficient FiO

2

è

Check FiO

2

at mouth

Diffusion Block

è

Exceedingly rare

Slide14

Symptoms of Respiratory Failure

Often nonspecific (and unrecognized)

Dyspnea

Headache

Chest pain

“Feeling of Impending Doom”

Slide15

Signs of Respiratory Failure

Mental status changes.

Respiratory Distress.

Accessory muscle use.

Inability to speak.

Rate, depth and noise of breathing.

Slide16

Treatment of Respiratory Failure

Immediate stabilization.

Determination of the inciting event.

Treatment of the precipitating event.

Treatment of co-existing lung disease.

Slide17

Treatment of Respiratory Failure - Stabilization

Call for help.

Supplemental oxygen.

Tracheal intubation.

Mechanical ventilation.

Slide18

Central Nervous System Causes of Respiratory Failure

Drugs

Hypothyroidism

Brainstem injury or tumor

Primary alveolar hypoventilation

Central sleep apnea

Slide19

Extrapulmonary Respiratory Failure

Hypoxemic with normal A-a gradient

Hypercarbic acute or chronic

CNS

PNS

Respiratory muscles

Chest Wall

Pleura

Upper Airways

Slide20

Pulmonary Causes of Respiratory Failure

Lower airway

Asthma, COPD

Parenchymal

Pulm. Edema, infections, interstitial lung dz

Pulmonary vasculature

PE, Primary pulmonary hypertension

Slide21

Upper Airway Obstruction

Acute epiglottitisAcute laryngeal edemaAnaphylaxisTraumaForeign body aspirationRetropharyngeal hemorrhage

Bilateral vocal cord paralysis

Tracheal stenosis

Tracheomalasia

Tumors

Slide22

Chest Wall and Pleural Disorders

Kyphoscoliosis

Obesity hypoventilation

Flail chest

Fibrothroax

Thoracoplasty

Ankylosing spondylitis

Slide23

Respiratory Muscle Dysfunction

Muscular dystrophies

Myotonic dystrophies

Polymyositis

Periodic paralysis

Electrolyte disorders

Slide24

Peripheral Nervous System Causes of Respiratory Failure

Spinal cordTetanusStrychnineALSGuillain Barre Synd.ShellfishBilateral phrenic nerve palsy

Diptheria

Pseudocholinesterase deficiency

Myasthenia Gravis

Eaton-Lambert

Botulism

Organophosphate poisoning

Slide25

ARDS

Acute Respiratory Distress

Syndrome

Slide26

History

Adult hyaline membrane diseaseDa nang lungPump lungShock lungTraumatic lungTransplant lungWet lungWhite lungPost transfusion lung

Adult respiratory distress syndrome:ARDS

(Ashbaugh 1967)

Acute respiratory distress syndrome:ARDS

(AECC 1994)

Slide27

Definition(American-European Consensus Conferense: AECC 1994)

ARDSAcutePaO2/FiO2<200 mmHgBilateral interstitial or alveolar infiltratesPcwp <18 mmHg

ALI

Acute

<300 mmHg

Same

same

Slide28

Etiology

Direct lung injuryAspiration of gastric contentsPulmonary contusionToxic gas inhalationNear drowningDiffuse pulmonary infectionFat embolism

Indirect lung injurySevere sepsisMajor traumaHypertransfusionAcute pancreatitisDrug overdoseReperfusion injuryPost cardiac bypass/lung transplants

Slide29

Incidence

United States:

150,000 cases per year (75/100,000

population)

Recent studies:

Lower annual incidence of 3 to 5/100,000 population

Slide30

Prognosis

its cause, the patient's age, and co- morbid factors

Low:

chronic disease, multiple organ dysfunction syndrome (MODS), and sepsis

Slide31

Pathogenesis

systemic inflammatory response

complement system

coagulation cascade

cyclooxygenase

leukotriene pathways

cytokines

chemokines

nitric oxide (NO)

Slide32

Pathology

diffuse alveolar damage (DAD)

Acute alveolar injury

Exudative phase

Pulmonary vascular lesions

Proliferative phase

(honeycomb lung)

Slide33

Pathology Typical histologic findings with ARDS which includes alveolar inflammation, thickened septal from protein leak (pink), congestion and decreased alveolar volume

Slide34

Infectious causesBacteria - Gm neg & pos , mycobacteriae, mycoplasma, rickettsia, chlamydiaViruses- CMV, RSV, hanta virus, adeno virus, influenza virusFungi- H.capsulatum, C.immitisparasites- pneumocytis carinii, toxoplasma gondii

Differential Diagnosis

Slide35

Differential Diagnosis

Non infectious causes

Drugs & toxins

(paraquat, aspirin, heroin, narcotics, toxic gas, tricyclic anti depressants, acute radiation pneumonitis)

Idiopathic

(esinophilic pneumonia, Acute interstitial pneumonitis, sarcoidosis, rapidly involving idiopathic pulmonary fibrosis)

Immunologic

(acute lupus pneumonitis, Good Pastures syndrome, hypersensitivity pneumonitis)

Metabolic

(alveolar proteinosis)

Miscellaneous

(fat embolism, neuro/high altitude pulmonary oedema)

Neoplastic

(leukemic infiltration, lymphoma)

Slide36

Differential Diagnosis

Slide37

Physiology

Hypoxemia

Increased dead space

Low lung compliance

Low chest wall compliance

Measurement of respiratory compliance

Slide38

Treatment of ARDS

General measures

Specific therapy

Mechanical ventilation

Ancillary ventilatory strategies

Slide39

General measures

Diagnosis& Treatment of underlying condition

Hemodynamic management

Hemodynamic monitoring

Early treatment of sources of inflammation and sepsis

Treatment of infections

Nutrition

Avoidance of iatrogenic complications

Support of other organ system function

Slide40

Support of other organ system function

Hemodynamics

Renal function

Skeletal muscle

GI tract

Slide41

Specific therapy

Bronchodilator Anti inflammatory therapy corticosteroidsShort termLong term NSIDSProstaglandinsPGE1PGI2Immunotherapy Antiendotoxin Anticytokine antibodiesCytokine-receptor antagonistsCyclo oxygenase inhibitors

Antioxidant

Ketoconazole

Ketanserin

Almitrine

Pentoxiphyline

Slide42

Mechanical ventilation

VALI

Traditional approach

V

T

=10-15 ml/kg, PEEP=10-20 CmH2O

Limiting the FIO

2

Normal ABG

This traditional philosophy has been challenged

Barotrauma

Diffuse nonhomogeneous lung injury

The ideal method of MV for these patients is still controversial

Slide43

Mechanical ventilation

TPP≤30 CmH

2

O

Adequate lung expansion

Appropriate level of both EEAP and EIAP

Using semi-static compliance

Slide44

Mechanical ventilation

Recruitment maneuvers

High and short term CPAP(40CmH

2

O, 30 min)

Pressure limited ventilation

The initial IFR is high and variable

The maximal AP is reached early in inspiration

Slide45

Recruitment maneuvers Portable chest computed tomography of a patient withsevere acute respiratory distress syndrome (ARDS). On the left, thepatient is ventilated on 20 cm H2O positive end-expiratory pressure(PEEP). On the right, the patient is on 25 cm H2O PEEP after a recruit-ment maneuver consisting of PEEP 40 cm H2O, pressure control 20 cmH20, respiratory rate 10/min, inspiratory to expiratory (I:E) ratio 1:1for 2 minutes. (Courtesy of Dr. Benjamin Medoff, MassachusettsGeneral Hospital.)

Slide46

Ancillary ventilatory strategies

ECMO

IVOX

Exogenous surfactant

HFV

Inhaled NO

Prone ventilation

Partial liquid ventilation

Slide47

ECMO

Slide48

Suggested algorithm for mechanical

ventilation in patients with ARDS and other

forms of severe respiratory failure

Secure the airway and deliver positive-pressure ventilation with

5-10 cm H

2

O PEEP

• Obtain hemodynamic stability and patient comfort

• Pursue diagnosis and therapy of the cause

Set FlO

2

to keep SpO

2

> 90% or PaO

2

> 60 mm Hg

With the ventilator in pressure-limited assist control mode, set

pressure control and PEEP:

A.

Empiric

way (fast):

• Set pressure control <20-25 cm H

2

O (vt = 500-600 ml)

and respiratory rate aiming for a PacO

2

and pH close to

normal or mild respiratory acidemia.

• Increase PEEP by 2.5 cm H

2

O steps every 20-30 min, as

long as SpO

2

and vt increase or stay the same. Consider

decreasing pressure control and increasing rate if the sum

of PEEP and pressure control settings is >35 cm H

2

O.

B.

Physiologic

way (slow):

• Perform a static P-V curve of the respiratory system, and

set PEEP and pressure control just above and below the

lower and upper inflection points, respectively.

• Reassess pressure control and PEEP settings daily.

Slide49

•

If high ventilatory requirements persist (e.g., FiO

2

> 0.6, PEEP >

10 cm H

2

O), consider:

A. Increasing sedation, considering neuromuscular blockade.

B. Recruitment maneuver.

C. Permissive hypercapnia.

D. Increasing inspiratory time.

E. Prone ventilation.

F. Inhaled NO.

G. If beyond 7 days of ARDS and no evidence of infection,

consider corticosteroids.

•

If ventilatory requirements decrease and the patient is generally

stable, consider:

A. Decreasing FlO

2

by 0.05-0.1 steps every 2-4 h, keeping

SpO

2

> 90%.

B. Discontinuing neuromuscular blockade, decrease sedation.

C. Decreasing I: E ratio toward =1:3 (inspiratory time 1.0-1.5 s).

D. Decreasing respiratory rate to allow spontaneous

ventilation.

E. Setting ventilator mode to PSV.

Slide50