RESPIRATORY FAILURE

Definition
Pulmonary gas exchange fails to maintain normal arterial O2 & CO2 levels.
Classified into types I and II.

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Pathophysiology

Type I Respiratory Failure Type II Respiratory Failure

When disease impairs ventilation of part of a lung

(asthma or pneumonia), perfusion of that region Arterial hypoxia with hypercapnia.
results in hypoxic, CO2-laden blood entering the In conditions that cause generalised,
severe ventilation-perfusion mismatch --
pulmonary veins.
> insufcient normal lung to correct
Increased ventilation of neighboring regions of
PaCO2
normal lung can CO2 excretion, correcting
A disease that total ventilation (not
arterial CO2 to normal, but cannot augment O2
just diseases of the lung but also
uptake because the haemoglobin owing through
disorders affecting any part of the
these regions is already fully saturated.
neuromuscular mechanism of
Admixture of blood from the underventilated and
ventilation).
normal regions --> hypoxia + normocapnia

ventilatory drive: rapid respiratory

rate and accessory muscle recruitment.
/ inadequate respiratory effort.

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Management of Acute Respiratory Failure
Type I Respiratory Failure
Treat underlying cause.
O2 (3560%) by facemask to
correct hypoxia.
Assisted ventilation if PaO2
<8kPa despite 60% O2.
Humidified O2 in patients
who need high
concentrations of O2 for >
few hours.
Type II Respiratory Failure
Treat underlying cause.
Controlled O2 therapy: start at 24% O2. (respiratory centre
may be insensitive to CO2 & respiration is driven by hypoxia.)
Recheck ABG after 20min.
If PaCO2 is steady / lower, O2 concentration to 28%.
If PaCO2 >1.5kPa & the patient is still hypoxic: assisted
ventilation (NIPPV).
Rarely a respiratory stimulant (doxapram 1.54mg/min IVI).
Consider intubation and ventilation, if appropriate.
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Chronic & "Acute on Chronic" Type II Respiratory Failure
Most common cause of chronic type II respiratory failure: severe COPD.
Although PaCO2 may be persistently , there is no persisting acidaemia because the kidneys
retain bicarbonate, correcting arterial pH to normal.
This compensated pattern, which may also occur in chronic neuromuscular disease or
kyphoscoliosis, is maintained until there is a further acute illness, such as an exacerbation of
COPD which precipitates an episode of acute on chronic respiratory failure, with acidaemia and
initial respiratory distress followed by drowsiness and eventually coma.
These patients have lost their chemosensitivity to PaCO2, and so they may paradoxically
depend on hypoxia for respiratory drive, and are at risk of respiratory depression if given high
concentrations of oxygen.
Patients may not be distressed, despite being critically ill with severe hypoxaemia, hypercapnia
and acidaemia.
While the physical signs of CO2 retention (confusion, flapping tremor, bounding pulses) can be
helpful if present, they may not be, so arterial blood gases are mandatory in the assessment of
initial severity and response to treatment.

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HOME VENTILATION FOR CHRONIC RESPIRATORY FAILURE
Non-invasive ventilation (NIV) is of great value in the long-term treatment of respiratory failure
due to spinal deformity, neuromuscular disease and central alveolar hypoventilation.
Some patients with advanced lung disease (cystic fibrosis) also benefit from NIV.
In these conditions, the onset of type II respiratory failure can be very gradual.
Morning headache (due to PaCO2) & fatigue are common symptoms but, in many cases, the
diagnosis is only revealed by sleep studies or morning blood gas analysis.
In the initial stages, ventilation is insufficient for metabolic needs only during sleep, when there is
a physiological decline in ventilatory drive.
Over time, CO2 retention becomes chronic + renal compensation of acidosis.
Home-based NIV overnight is sufficient to restore the daytime PCO2 to normal, and to relieve
fatigue and headache.
In advanced disease (muscular dystrophies or cystic fibrosis), daytime NIV may also be required.

LUNG TRANSPLANTATION

Single lung
Advanced emphysema, lung fibrosis
transplantation
Cystic fibrosis, bronchiectasis
Bilateral Lungs (Transplanted lung is vulnerable to cross-infection in the context of post-
transplantation transplant immunosuppression, thus single lung transplantation is
contraindicated.)

Combined heart-
Advanced congenital heart disease: Eisenmengers syndrome.
lung
Primary pulmonary hypertension unresponsive to medical therapy.
transplantation

Acute rejection Corticosteroid

Chronic rejection Ciclosporin, mycophenolate, tacrolimus (inhibit cel-mediated immunity)

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 PULMONARY EOSINOPHILIA
Definition
Association of radiographic (usually pneumonic) abnormalities & peripheral blood eosinophilia.
Eosinophils are the predominant cell recovered in sputum or BAL.
Eosinophil products are likely to be the prime mediators of tissue damage.

Etiology

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Acute Eosinophilic Pneumonia
An acute illness (<5 days) characterized by diffuse pulmonary infiltrates &
Definition
hypoxic respiratory failure.

Pathology Diffuse alveolar damage.

Etiology Idiopathic / drug reaction.
Dx BAL: >25% eosinophils.
Rx Corticosteroid

Chronic Eosinophilic Pneumonia

Presents in an insidious manner with malaise, fever, weight loss,
Definition
breathlessness and unproductive cough.

Incidence Common in middle-aged females.

Chest X-ray appearance has been likened to the photographic negative of

pulmonary edema + bilateral, peripheral & predominantly upper lobe
parenchymal shadowing.
Dx Peripheral blood eosinophil count .
ESR and total serum IgE .
BAL: proportion of eosinophils in the lavage fluid.

Prednisolone (2040 mg daily).

Rx Prednisolone can be withdrawn after a few weeks without relapse, but long-
term, low-dose therapy is occasionally necessary

Tropical Pulmonary Eosinophilia

Mosquito-borne filarial infection caused by the tissue-dwelling human
Definition
nematode Wuchereria bancrofti / Brugia malayi.
Clinical Features Fever, weight loss, dyspnoea, asthma-like symptoms.

Peripheral blood eosinophilia

Dx total IgE.
anti-filarial antibody titres.

Rx Diethycarbamazine.

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