2 Postgrad Med J: first published as 10.1136/pgmj.34.387.2 on 1 January 1958. Downloaded from RESPIRATORY FAILURE AND CARBON DIOXIDE NARCOSIS By E. KEITH WESTLAKE, M.A., M.D., M.R.C.P. Senior Medical Registrar, Middlesex Hospital All physicians are familiar with the clinical and and the prevailing barometric pressure (B). For biochemical manifestations of cardiac and renal example, when the respiratory quotient is 0.79 and failure, but the syndrome of respiratory failure has the barometric pressure 760 mm., this equation gained recognition more slowly. The primary simplifies to: P02 = 150 - 1.21 x alveolar pCO2. function of the lungs is to maintain a constant Thus at the normal alveolar pCO2 of 40 mm., the exchange ofoxygen and carbon dioxide between the corresponding pO2 will be o02 mm., but if the blood and air. This is achieved by intermittent alveolar pCO2 rises to 80 mm., the alveolar pO0 flushing of the alveoli with inspired air and the must fall to 53 mm. (I50- I.21 x 80). Capillary continuous diffusion of oxygen and carbon dioxide blood leaving the alveoli cannot have an oxygen across the alveolar membrane. In normal indi- tension higher than this figure and the oxygenProtected by copyright. viduals, these processes maintain the mean carbon saturation of arterial blood will therefore be dioxide tension (pCO2) in the alveoli at 40 ± 5 reduced to about 80 per cent. with the appearance mm. Hg. and the oxygen tension (pO2) at Ioo I 5 of central cyanosis. mm. Hg. Respiratory failure may be said to be When the alveolar pCO, is suddenly raised from present when there is inability or failure of the 40 to 80 mm., the volume of carbon dioxide dis- repiratory centre and neuro-muscular mechanism solved in the arterial plasma increases from 2.8 to prevent the alveolar pCO2 rising above, and the vols. per 00oo ml. to 5.6 vols. with consequent fall alveolar pO0 falling below their normal values. in blood pH from 7.4 to 7.I. Renal compensation The level of alveolar pCO, is determined by two for this respiratory acidaemia, with partial restora- variables: (a) the rate of carbon dioxide produc- tion of the arterial pH toward normal, is brought tion by the body i.e. the metabolic rate and (b) about over a period of days by increased tubular the adequacy of alveolar ventilation. If the reabsorption of bicarbonate and the excretion of a metabolic rate remains constant, the alveolar highly acid urine (pH 4.6-4.8) containing in- pCO2 will vary inversely with alveolar ventilation. creased amounts of ammonium and chloride ions. http://pmj.bmj.com/ If the latter is halved, the pCO2 will rise to double Thus the biochemical effect of respiratory failure its original level and vice-versa. Similarly, if the is the combination of hypercapnia, hypoxaemia rate of carbon dioxide production is doubled, and acidaemia. alveolar ventilation must increase to the same extent if the alveolar pCO2 is to remain unchanged. Causes of Respiratory Failure Respiratory failure is therefore characterized by failure result from relative underventilation of the alveoli in Respiratory may organic lung disease of the central nervous system (for example, on September 23, 2021 by guest. relation to body metabolism. encephalitis lethargica (Barach and Woodwell, When breathing air, alveolar hypoventilation I92I), bulbo-spinal poliomyelitis (Plum and inevitably causes hypoxaemia (arterial oxygen un- Wolff, I951), motor neurone disease (Feltman saturation) as well as hypercapnia (raised arterial et al., 1952), brain stem haemorrhage) or of the pCOg) since as the level of alveolar pCO, rises, the respiratory muscles (for example, dystrophia alveolar P02 falls. The relationship between the myotonica (Benaim and Worster-Drought, I954), alveolar gas tensions can be appreciated from the myasthenia gravis, dermatomyositis). In general equation derived by Fenn, Rahn and Otis (I946)* medicine, respiratory failure is most commonly and depends on the respiratory quotient (R.Q.) encountered in patients with long standing chest * disease whose is Mean alveolar pO2 = (B - 47) x 0.21 - alveolar ventilatory capacity grossly 0.79 diminished e.g. in chronic bronchitis and emphy- pC02(o.2I + ). sema (Baldwin et al., 1949) and severe kypho- R.Q. scoliosis (Fishman et al., I956). Patients who are WESTLAKE: Failure and Carbon Dioxide Narcosis January 1958 Respiratory 3 Postgrad Med J: first published as 10.1136/pgmj.34.387.2 on 1 January 1958. Downloaded from association with gross obesity (Burwell et al., I956). 90. The Diagnosis of Respiratory Failure OQ ..... Clinical recognition of alveolar hypoventilation may be difficult and the only certain method of diagnosis is the demonstration of a raised level of 65 pCO2. This is most conveniently achieved by 60 analysis of arterial blood since the pCO2 of alveolar air and arterial blood are virtually identical. With practice, samples of arterial blood can be readily obtained by puncture of the brachial artery under 455 local analgesia. Direct determination of both pCO2 and pO2 in arterial blood can be made by the bubble equilibration technique devised by Riley. Jo This method has been extensively used in 0O 25 30 35 40 45 50 5S 60 65 0 75 80 85 90 05 00 respiratory research but is technically too difficult ARTERIAL CO, TENSION for routine use in a biochemical laboratory. arterial can be . Chronic Bronchiti with Cor Pulmonok with However, pCO2 estimated No . accurately or without Emphysma. congestve cardiac by an indirect method. Blood pH, pCO2 and fallure. total content are the FIG. i.-Respiratory failure precipitated by an acute plasma CO2 related by well- chest infection in patients with chronic lung disease. known Henderson-Hasselbalch equation. If any Arterial oxygen saturation and carbon dioxide two of these variables are known, then the third on tension admission with, and recovery from, an can be calculated. Thus, rearranging the equation: Protected by copyright. acute respiratory infection. Single points represent Total patients who died. plasma CO2 content mM/L pCO2 = - 0.03 x (antilog blood pH - 6.09) + i able to maintain a normal alveolar pCO2 when well, Total plasma CO2 content is measured by the frequently develop acute respiratory failure with manometric method of Van Slyke and Neill (1924) severe hypoxaemia and hypercapnia when sub- and blood pH with a glass electrode and pH meter. jected to the stress of a respiratory infection Practical details for measuring blood pH at body (Westlake, 1954). This is illustrated in Fig. i. temperature are to be found in the papers ofWilson In this diagram the arterial oxygen saturation and (1951), Severinghaus, Stupfel and Bradley (1956) pCO2 during the course of an acute respiratory and Wynn and Ludbrook (I957). infection have been plotted as oblique arrows. The six normal subjects i.e. those without previous The Clinical Manifestations of Respiratory black Failure respiratory symptoms (represented by http://pmj.bmj.com/ triangles) were all suffering from extensive lobar The disturbances of blood gas tensions and in pneumonia and in five the pCO2 on admission to blood pH caused by respiratory failure have pro- hospital was lower than that on recovery. This found physiological effects on the brain, cerebral may be taken as the normal response to an acute vessels, heart and lungs and are responsible for the chest infection. In the 39 patients with a previous appearance of certain characteristic signs and history of chest disease (chronic bronchitis, symptoms which may make a bed-side diagnosis emphysema and cor pulmonale), the arterial pCO2 of respiratory failure possible. on admission was higher than on recovery in 37. Mental disturbance in respiratory failure varies on September 23, 2021 by guest. In many instances the initial levels of pCO2 were with its severity. In mild cases the patient may be 30 to 40 mm. higher than those on recovery. euphoric or mildly confused. More severe de- Other factors that may precipitate respiratory grees of hypoxaemia and hypercapnia cause pro- failure in patients with chronic chest disease are gressive deterioration in mental function with severe asthma (Schiller et al., 1951; Sieker and visual and auditory hallucinations, delusions, Hickam, 1956), chest surgery (Bjork and stupor and finally coma. Although disturbed Engstr6m, 1955) and the ill-advised administra- mental function is principally due to cerebral tion of morphine and other drugs which depress anoxia (Simpson, 1957), the effects of hyper- the sensitivity of the respiratory centre (Roussak, capnia and acidaemia on the brain should not be I951; Samuelsson, I952; Wilson, Hoseth and neglected. The effect of breathing Ioo per cent. Dempsey, 1954). In rare instances, chronic oxygen shows that hypoxaemia is only one of the respiratory failure occurs in the absence of either factors concerned since the patient in respiratory pulmonary or neurological disease, usually in failure, although considerably improved, often POSTGRADUATE MEDICAL 4 JOURNAL January 1958 Postgrad Med J: first published as 10.1136/pgmj.34.387.2 on 1 January 1958. Downloaded from remains confused and disorientated despite full (Stone et al., 1953; Fulton, 1953; Flint, 1954). saturation of the arterial blood with oxygen. If The cardiac output is usually normal or even mental disturbance were solely due to hypoxaemia, moderately raised (Ferrer et al., 1950; Mounsey an immediate return to mental clarity would be et al., I952) and this, together with the vasodilator expected. Impaired memory is usual during a effect of hypoxaemia and hypercapnia on the small period of respiratory failure, even in the absence vessels of the limbs, is responsible for the warm of obvious mental disturbance. After recovery extremities and bounding pulse present during from an acute respiratory infection, carefulenquiry episodes of congestive failure-in contrast to con- will often reveal that the patient has complete gestive failure in mitral stenosis, hypertension or amnesia (lasting days or even a week or two) for ischaemic heart disease where the cardiac output the early phase of his illness, although at the time, is low and the extremities cold.