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ACUTE RESPIRATORY FAILURE

ACUTE RESPIRATORY FAILURE

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Published by Cayunk Norliana

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Published by: Cayunk Norliana on Mar 28, 2011
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02/04/2013

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ACUTE RESPIRATORY FAILUREDefinition-Pathophysiology-Clinical picture-Signs and Symptoms  -Diagnosis-Treatment-Croup-Asthma-COPD-ARDS  DefinitionAcute respiratory failure (ARF) exists when the patient's breathingapparatus fails in its ability to maintain arterial blood gases within thenormal range. By definition, ARF is present when the blood gasesdemonstrate:
y
 
An arterial oxygen tension (PaO2) of < 8 kPa (60 mmHg) withnormal or low PaCO2 (Type I or hypoxaemic respiratoryfailure)or 
y
 
An arterial carbon dioxide tension (PaCO2) of > 6.7 kPausually accompanied by a fall in pH (<7.3,H+ > 45 n mols l-1)in addition to hypoxaemia (Type II or ventilatory respiratoryfailure)Hypoxaemia on its own does not always mean respiratory failure, for example, if the subject is at altitude or has a right to left shunt due tocongenital heart disease.We are concerned only with ARF, one of the most dramatic and lifethreatening emergencies that the casualty officer and the house officemay have to deal with in the hospital setting.PathophysiologyAny part of the respiratory system may be involved in the causationof a respiratory emergency, i.e.
y
 
The respiratory centre in the CNS
y
 
The respiratory apparatus (e.g. chest wall and lungs)
y
 
The respiratory muscles including the diaphragm, the mainrespiratory pump
y
 
The gas exchanging units in the lung i.e. the respiratorybronchioles and the alveoliIt is pertinent to remember that in assessing patient¶s with ARF, mostattention is paid to what is happening at the alveolar level i.e. theblood gasesExamples of conditions causing ARF are shown in Table 1
 
 Clinical PictureThe clinical picture varies with the cause but any of those mentionedin Table 1 leads to a deterioration in the patient's respiratory gasexchange. The subsequent changes which occur in blood gases,particularly carbon dioxide, cause stimulation of the medullarychemo-receptor and compensatory mechanisms to be activated. Thepatient becomes aware of the necessity to breathe, and as theprecipitating cause progresses, exhibits overt signs of distress, i.e.dyspnoea. Eventually blood gases can no longer be kept in the normalrange and ARF supervenes.ARF resulting from CNS depression as a result of drugs or injurydoes not produce overt signs of respiratory distress. Accuratediagnosis is dependent on a high index of suspicion and is confirmedby arterial blood gas analysis.TABLE 1 Causes of respiratory failureSite ExamplesRespiratory centre(CNS)Depressant drugs, opiates; traumatic andischaemic lesionsLoss of respiratory sensitivity to CO2Spinal cord andperipheral nervesSpinal injury, Guillain Barre,poliomyelitisNeuromuscular junction Myasthenia, neuromuscular blockingdrugsMuscle Myopathies, respiratory muscle fatigue inCOPDPleura and thoraciccageFlail chest, pneumothorax, haemothoraxDeformities, trauma (e.g. rib fractures),loss of optimal shape due to chronic lunghyperinflationAirways Extrathoracic: foreign bodies, croupIntrathoracic: asthma, bronchiolitis,bronchitisGaseous exchange Emphysema, pulmonary oedema, ARDS,pneumoniaLung vasculature Pulmonary embolus, ARDSARDS refers to adult respiratory distress syndrome (see later)
 
 Clinical signs and symptomsGenerally, the patient becoming anxious and completely preoccupiedwith the necessity to concentrate every effort on ventilation heraldsthe onset of ARF. The eyes are closed, the accessory muscles of ventilation are fully used; often a characteristic position is adopted,such as sitting forward with drooling secretions, as in the child withacute epiglottitis. Hypoxia and hypercarbia produce characteristiceffects on the CNS and cardiovascular system (CVS), for example:1
Hypoxia
:CNS - Uncooperative, confused, drunken-like stateCVS - Bradycardia, variable blood pressure, cyanosis2 Hypercarbia:CNS - Tremor and overt flapCVS - Raised pulse rate, peripheral vasodilation with pink peripheries, blood pressure changes are variableDiagnosisDiagnosis depends on history, clinical examination and specialinvestigations such as chest X-ray, peak expiratory flow rate andarterial blood gas analysis. It is important to establish the causativesite (Table 1).For example, the history gives a clue to pre-existing disease such aschronic bronchitis and asthma, or may distinguish between acuteepiglottitis (sudden onset) and laryngo-tracheobronchitis (slower onset over 24 hours), when the clinical signs are equivocal. Onclinical examination, expiratory wheeze suggests intrathoracic airwayobstruction whilst inspiratory wheeze suggests that it is extrathoracic.Chest X-ray will reveal parenchymal causes such as pneumonia,airway obstruction due to foreign bodies (ipsilateral hyperinflation of lung), pleural and thoracic cage causes, such as effusion,pneumothorax and fractured ribs. Raised bicarbonate levels in theblood gases suggest chronic pre-existing disease, and a combinationof hypoxia, hypocarbia and an initial metabolic alkalosis followed byacidosis is a common accompaniment of ARDS.

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