Acute Respiratory Failure

32

Transcript of Acute Respiratory Failure

Page 1: Acute Respiratory Failure
Page 2: Acute Respiratory Failure

علما زدني و قل رب ١١٤سورة طه آية . صدق اهللا العظيم

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Respiratory Disorders Associated With Acute

Respiratory Failure

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By

Prof. Adel Mohamad SaeedProfessor of Chest Diseases

Ain Shams University

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Definition:The term Acute Respiratory Failure (A.R.F ) is used clinically to indicate a disease or disorder of the respiratory system , recent in onset, which has resulted in a level or pattern of external gas exchange that is inadequate for the metabolic needs of the body .

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This deficiency is reflected in arterial hypoxemia, hypercapnia and respiratory acidosis. If the initiating mechanism is not arrested, corrected & reversed the abnormalities in the blood gases are apt to progress to intolerable levels. There is no precise level of arterial Po2 or Pco2 that defines [ARF]. However, an arterial Pao2< 50-60 mmHgcan be life threatening because further impairment of gas exchange can cause a drop in Pao2 to levels that would compromise Oxygen Delivery [Do2] to vital organs.

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Acute rise of PaCo2 to >50 mmHg i.e. Acute Hypercapnia with Respiratory Acidosis result in mental confusion, depressed sensorium that end in coma and death.

The effects of acute hypoxemia and acute hypercapnia may overlap, resulting in severe C. N. S depression .

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The respiratory apparatus consists of two components :

1- Pump system: includes the entire ventilatory apparatus [Respiratory Center, Thoracic Cage, Air ways].

2- Gas Exchange system : pulmonary parenchyma [alveoli with alveolar air & alveolo-capillary membrane.

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Respiratory Failure can therefore be divided into :

Pump Failure or hypercapnic respiratory failure with Co2 retention.

Lung Failure or gas exchange failure with arterial hypoxemia i.e. hypoxemic respiratory failure.

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Lung Failure (Hypoxemic Respiratory Failure):

Adult respiratory distress syndrome ARDS.

Cardiogenic pulmonary edema.

End stage pulmonary fibrosis, resulting from different fibrotic lung diseases.

Massive Pulmonary Embolism.

Severe Pneumonia.

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Pump Failure ( Hypercapnic Respiratory Failure ):

Neuromuscular disease, atrophic or pseudo hypertrophic myopathies.

Guillain Barre syndrome.

Myasthenia gravis.

Amyotrophic lateral sclerosis.

Cervical quadriplegia.

Botulism.

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Respiratory Poliomyelitis.

Bilateral diaphragmatic paralysis.

Hereditary myopathies.

Multiple sclerosis.

Collagen vascular disease e.g. vanishing lung syndrome in SLE.

Central nervous disorders “C.V.S”.

Drug over dose.

Head trauma.

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Hypothyroidism e.g. myxedema coma.

Brain stem infarction& brain neoplasm.

Disorders of the chest bellows.

Kyphoscoliosis & Chest wall deformities.

Chest trauma and Flail Chest.

Tension pneumothorax.

Massive pleural effusion.

Airway obstruction.

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Acute severe asthma.

COPD "Chronic Obstructive Pulmonary Disease"

Anaphylaxis

Cystic fibrosis

Upper airway obstruction e.g. Epiglottitis & F.B inhalation.

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Hypercapnia due to hypercapnic respiratory failure can arise in one of two ways:

1) Alveolar hypoventilation secondary to a subnormal low minute ventilation .

2) Ventilation-Perfusion (V /Q ) mismatch .

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Pathophysiologic mechanisms in Acute Respiratory Failure:

Mechanism Type of failure FeatureGlobal alveolar hypoventilation

Pump Hypercapnia

Ventilation –perfusion mismatch

Pump and /or lung Hpercapnia and /or hypoxemia

Shunt Lung Hpoxemia

Diffusion abnormality

Lung Hpoxemia

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BASIC PRINCIPLES OF OXYGEN TRANSPORT■ Gas exchange in the lungs concerns ventilation,

perfusion and diffusion.■ Arterial hypoxemia may occur because of:

– A decrease in PIO2.– Alveolar hypoventilation.– Ventilation/perfusion disturbance.– Impaired diffusion at the alveolar capillary

barrier.

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150.7 150

100 99

40 40

020406080

100120140160180

Atm. air(Dry)

TrachealGas

AlveolarGas

Arterialblood

Tissue Venousblood

150.7 150

100 99

40 40

020406080

100120140160180

Atm. air(Dry)

TrachealGas

AlveolarGas

Arterialblood

Tissue Venousblood

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Oxygen Delivery and Utilization

DO2 = CO x CaO2 x 10– DO2 = O2 delivery, ml/min.– CO = Cardiac output L/min.– CaO2 = O2 content of arterial blood ml/dl.

CaO2 = ([Hb] x 1.34 x Sa O2%) + (PaO2 x 0.003)– Hb = Hemoglobin conc. gm/dl.– 1.34 = O2 carrying capacity of Hb at 37°C ml/gm.– Sat. O2% = Percentage saturation of Hb with O2.– 0.003 = Solubility coefficient for O2.

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Delivery system Description L/min flow rate

delivers FIO2 Complications

Nasal cannula

Flow rate of 1-6 L/min

Delivers approx 4%/L

Prongs insert 1 cm into each nare

Comfortable and inexpensive

Patient can eat and talk

1 L/min = 24%

2 L/min = 28%

3 L/min = 32%

4 L/min = 36%

5 L/min = 40%

6 L/min = 44%

Delivered FIO2 depends on tidal

volume and ventilatory rate Nasal passages must be patent

Easily dislodged May irritate

nasal passages and eyes at

higher flow rates

Delivery system Description L/min flow rate

delivers FIO2 Complications

Nasal cannula

Flow rate of 1-6 L/min

Delivers approx 4%/L

Prongs insert 1 cm into each nare

Comfortable and inexpensive

Patient can eat and talk

1 L/min = 24%

2 L/min = 28%

3 L/min = 32%

4 L/min = 36%

5 L/min = 40%

6 L/min = 44%

Delivered FIO2 depends on tidal

volume and ventilatory rate Nasal passages must be patent

Easily dislodged May irritate

nasal passages and eyes at

higher flow rates

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Venturi

mask**

Flow rates are variable

Clear plastic mask with different

adapters that determine FIO2

Provides exact oxygen concentrations

Inspired concentrations do not vary

with ventilatory rate and tidal volume

Delivery device of choice for COPD

patients depending on hypoxic drive

2 L/min = 24%

3 L/min = 28%

4 L/min = 31%

6 L/min = 35%

8 L/min = 40%

10 L/min = 45%

12 L/min = 50%

14 L/min = 55%

Same as

for simple

mask

Venturi

mask**

Flow rates are variable

Clear plastic mask with different

adapters that determine FIO2

Provides exact oxygen concentrations

Inspired concentrations do not vary

with ventilatory rate and tidal volume

Delivery device of choice for COPD

patients depending on hypoxic drive

2 L/min = 24%

3 L/min = 28%

4 L/min = 31%

6 L/min = 35%

8 L/min = 40%

10 L/min = 45%

12 L/min = 50%

14 L/min = 55%

Same as

for simple

mask

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Simple mask*

Flow rate of 5-

8 L/min

Clear plastic,

must fit tightly

on patient's

face

5-8 L/min = 50-60%

Need minimum of 5 L/min to adequately flush carbon

dioxide and avoid rebreathingUse cautiously on comatose

patients Must fit securely to patient's face to avoid entrainment of

room air and dilution of inspired FIO2

Increased risk of aspiration Less comfortable than nasal

cannula Easily removed

Simple mask*

Flow rate of 5-

8 L/min

Clear plastic,

must fit tightly

on patient's

face

5-8 L/min = 50-60%

Need minimum of 5 L/min to adequately flush carbon

dioxide and avoid rebreathingUse cautiously on comatose

patients Must fit securely to patient's face to avoid entrainment of

room air and dilution of inspired FIO2

Increased risk of aspiration Less comfortable than nasal

cannula Easily removed

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Partial rebreathing

mask*

Flow rate of 6-10 L/min

Clear palstic mask that incorporates reservoir bag into system to deliver

oxygen concentrations >

60%

6-10 L/min = 55-70%

Flow should be sufficient to keep

reservoir bag inflated on inspiration

Other complications

same as for simple mask

Nonrebreathing mask*

Flow rate of 10-12 L/min

Clear plastic mask with reservoir bag

and 2 one-way valves (1 on mask

and 1 between reservoir bag and

mask

10-12 L/min = 80-100%

Flow should be sufficient to keep

reservoir bag inflated on inspiration

Other complications

same as for simple mask

Partial rebreathing

mask*

Flow rate of 6-10 L/min

Clear palstic mask that incorporates reservoir bag into system to deliver

oxygen concentrations >

60%

6-10 L/min = 55-70%

Flow should be sufficient to keep

reservoir bag inflated on inspiration

Other complications

same as for simple mask

Nonrebreathing mask*

Flow rate of 10-12 L/min

Clear plastic mask with reservoir bag

and 2 one-way valves (1 on mask

and 1 between reservoir bag and

mask

10-12 L/min = 80-100%

Flow should be sufficient to keep

reservoir bag inflated on inspiration

Other complications

same as for simple mask

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Advantages and disadvantages of oxygen sources

Oxygen source

Advantages Disadvantages

Cylinders

Reliable Easy maintenance High purity oxygen No additional noises Much experience

User-unfriendly Heavy with small capacity Limited freedom of movement Requires frequent delivery Relatively high cost

Concentrator

User-friendly Safe No delivery problem Universally usable Relatively low cost

Requires electricity Produces vibrations and noise Unreliable at > 3 l/min Critical storage conditions Requires regular maintenance

Liquid oxygen

User-friendly Easy to transport High purity oxygen Reliable Easy maintenance

Not universally usable Spontaneous evaporation Requires regular delivery Dependent on storage container Various types incompatible

Oxygen source

Advantages Disadvantages

Cylinders

Reliable Easy maintenance High purity oxygen No additional noises Much experience

User-unfriendly Heavy with small capacity Limited freedom of movement Requires frequent delivery Relatively high cost

Concentrator

User-friendly Safe No delivery problem Universally usable Relatively low cost

Requires electricity Produces vibrations and noise Unreliable at > 3 l/min Critical storage conditions Requires regular maintenance

Liquid oxygen

User-friendly Easy to transport High purity oxygen Reliable Easy maintenance

Not universally usable Spontaneous evaporation Requires regular delivery Dependent on storage container Various types incompatible

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Oxygen Therapy in Acute exacerbation of COPD:Rationale: low flow O2 by nasal cannula or venturamask is given during acute vent. failure to achieve PaO2 of 60 Hg and SaO2 of 92%.Intubation is indicated on the basis of objective undersirable effects of respiratory acidosis (PH< 7.20) ,consciousness level deterioration or development of arrhythmias. O2 induced hypercapnia is related to an increase in (VD/VT) or (V/Q) mismatch.NPPV significantly decreased the rate of intubation.

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Domiciliary ODomiciliary O22 & Long Term & Long Term Oxygen TherapyOxygen Therapy

Indications of LTOT:Chronic airflow obstruction specially if PaCO2 > 45 mmHg. Advanced interstitial pulmonary disease.Advanced pulmonary malignancy. Advanced cystic fibrosis.Severe congestive heart failure.Cong. cyanotic heart disease.

(Breslin et al., 1991).

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Patients who need oxygenCardio pulmonary Resuscitation [CPR] in

Respiratory or Cardio pulmonary arrest.

Fluid in the alveoli .

• Pulmonary edema .

• Pneumonia .

• Near drowning .

• Chest trauma .

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• Collapsed alveoli (alveolar atelectasis ) as in cases of :

a) Airway obstruction : Any unconscious patient.

Choking & FB inhalation.

b) Failure to take deep breaths : Severe pain as in rib fracture & severe pleurisy ) .

Paralysis of the respiratory muscles .

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Depression of the respiratory center (head injury ,drug overdose )

c) Collapse of an entire lung (pneumothorax or massive pleural effusion )

Other gases in the alveoli :a) Smoke inhalation .

b) Toxic inhalations .

c) Carbon monoxide poisoning .

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Any patient complaining of shortness of breath .

Any patient in shock .

any patient with signs of respiratory insufficiency .

Any patient breathing fewer than 10 times / minute i.e. bradypnea.

Any patient in cardiac arrest.

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Any patient complaining of chest pain .

Any patient suspected to be suffering a stroke .

( Caroline , 1995 )

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Adverse Effects of OAdverse Effects of O22 TherapyTherapy

These may be related to the device used e.g. nasal irritation, epistaxis, conjunctivitis inspissated secretions or barotrauma and volutrauma associated with mech. ventilation.O2 induced hypercopnia in COPD is due to V/Q mismatch.Hyperoxia produces pulmonary toxicity through production of O2 free radicals (O2-, OH-, O1, H2O2) at a rate that overwhelmes the antioxidant defences.O2 free radicals damage cell membranes, enzymes and nucleic acids leading eventually to cell death.