Clinical features and management of respiratory failure
Acute hypoxaemia or hypercapnia is less well toleratedthan chronic gradual alteration in blood gases. Virtually allpatients with respiratory failure, with the exception ofsome with CNS dysfunction (e.g. drug overdose), arebreathless. Acute hypoxaemia causes restlessness, confusionand sweating, with a tachycardia, poor peripheralperfusion and central cyanosis.Patients with acute severe hypercapnic ventilatoryfailure are breathless and cyanosed, and in addition may have confusion, flapping tremor of the hands, warm peripheries,bounding pulse and occasionally papilloedema. Themental state is probably the best clinical index to follow, asincreasing confusion and restlessness often parallel a risingPaco2. When patients (for instance those with advancedchronic bronchitis) progress to severe chronic respiratoryfailure, with a compensated respiratory acidosis,symptoms may also include sleep disturbance with earlymorning headache and personality change. Such patientsdevelop polycythaemia, pulmonary hypertension and corpulmonale.Chronic hypercapnic respiratory failure can occur despite normal lung function. Sleep apnoea syndromes, may be severe enough to produce pulmonaryhypertension and cor pulmonale. Patients withneuromuscular disorders (e.g. myasthenia gravis or theGuillain-Barre syndrome) may also have life-threateningventilatory failure despite normal lungs.
Management of Acufe respiratory failure
The general principles for the management of acute respiratoryfailure are those of any other respiratory emergency.The airway should be kept clear of sputum and protected.Oxygen should be given in sufficient concentration toensure a Pao2 of 8kPa (60mmHg). This can be deliveredvia a Venturi mask, which will give a fixed inspired oxygenconcentration of 24, 28 or 35%, or a Hudson or MC maskwhich will deliver variable, but higher, inspired oxygenconcentrations. In practice it is difficult to administer morethan 40% O2 by conventional face masks. Higher concentrationscan be given using a tight-fitting face mask; thisalso permits the application of continuous positive airwaypressure (CPAP), which further increases Pao2. If an adequatePao2 can only be achieved by a high FiO2 or CPAP,the patient is oxygen dependent and requires carefulobservation. In all patients with hypoxia the non-invasivemonitoring of SaO2 is useful; however, in patients withventilatory failure it is also crucial to monitor arterial pHand Pco2. If identifiable, the underlying cause should betreated: for example, antibiotics for acute bacterial pneumonias,or bronchodilators and corticosteroids for acuteasthma. If the patient's condition is worsening, withdeepening cyanosis, disturbance of consciousness, a risingPaco2, and progressive acidosis, then a decision whether tointubate and employ assisted mechanical ventilation mustbe made. This decision is based on a number of considerations,including the previous exercise capacity, thepossibility of treating the underlying cause, the overallclinical state of the patient and serial arterial blood gasmeasurements.
Chronic respiratory failure
Patients with chronic respiratory disease who developadditional acute problems require a rather differentpattern of management. Patients with long-standinghypoxaemia and hypercapnia are dependent on hypoxaemiato maintain ventilatory drive. High concentrationsof inspired oxygen reduce respiratory drive and ventilation,resulting in a rise in Paco2 and a worsening respiratoryacidosis. Oxygen must therefore be given in acontrolled fashion, starting with an inspired concentrationof 24% and with repeated monitoring of arterial bloodgases. It should be emphasized that it is not necessary toraise the Pao2 into the physiological range: a Pao2 of morethan 6 kPa (45 mmHg) is usually sufficient to maintain thepatient in a reasonable clinical state.
Although it is correct to exercise caution when administering oxygen to hypercapnic patients, it should be remembered that severehypoxaemia - Pao2 less than 5kPa (38mmHg) - is lifethreateningand must be relieved, and hypoxaemic patientswithout CO2 retention (a common situation in fibrotic lungdisease, for example) can receive high inspired oxygenconcentrations without developing hypercapnia.If, with the proper use of oxygen supplements, the Paco2continues to rise, and particularly if the respiratory acidosisworsens, a respiratory stimulant such as doxapram may,in the short term, occasionally be helpful. This may allowthe use of a higher inspired oxygen concentration withoutprecipitating a rise in Paco2. However, some patients willcontinue to deteriorate, and the point may come when adecision will have to be made about whether to offerassisted mechanical ventilation. In this group of patients,above all, their background in terms of respiratory function,exercise tolerance, and when they were last reasonablywell, must be taken into consideration. Discussions should involve the patient's family and, very often, thepatient.For selected patients with ventilatory failure, including those with chronic bronchitis, the technique of noninvasive intermittent nasal positive pressure ventilation may obviate the need for intubation and reduce mortality.
Questions and Answers
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respiratory failure
The state in which the lungs cannot perform the function of gas exchange adequately during rest and exercise is called respiratory failure. In this condition, the resting PaO2 falls below 60mm Hg (60 torr or 8 KPa) and/or the PaCO2 rises above 49mm Hg (49 torr or 7 KPa), when breathing room air at sea level. How relevant is this clinical situation?
This is the mainstay in the management of respiratory failure. Oxygen is administered with nasal catheter or by more effective methods such as masks or tents. If given by nasal catheter, the rate is 2-3 liters per minute and the catheter tip should be located 15cm from the nostril. What makes this corrective method very effective?
There is no precise clinical definition of respiratory failure; the diagnosis rests on the interpretation of arterial blood gas measurements. A patient can be said to be in respiratory failure if the arterial oxygen tension (-Pao2) falls below 8.0 kPa/60 mmHg (normal range 11.3-13.3kPa or85-100mmHg) or if the arterial carbon dioxide tension(Paco2) rises above 6.6kPa/50mmHg (normal range4.6-6.0kPa or 35-45 mmHg), when the subject is at sealevel, awake and breathing air.
The clinical features of respiratory failures are hypoxia and hypercapnia. The manifestations of hypoxia and hypercapnia vary from each other.
When the pulmonary parenchyma is grossly and irreversibly damaged, hypoxemia and hypercapnia may persist despite treatment. In such cases partial relief can be obtained by giving long term continuous or intermittent oxygen therapy.
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