Ventilatory failure

Chapter 27 Ventilatory failure




KEY POINTS



image Ventilatory failure occurs when alveolar ventilation becomes too low to maintain normal arterial blood gas partial pressures.

image There are many causes, involving the respiratory centre, the respiratory muscles or their nerve supply and abnormalities of the chest wall, lung or airways.

image Modest increases in the inspired oxygen concentration will correct hypoxia due to ventilatory failure, but may worsen hypercapnia.



Definitions


Respiratory failure is defined as a failure of maintenance of normal arterial blood gas partial pressures. Hypoxia as a result of cardiac and other extra-pulmonary forms of shunting are excluded from this definition. Respiratory failure may be subdivided according to whether the arterial Pco2 is normal or low (type 1) or elevated (type 2). Mean of the normal arterial Pco2 is 5.1 kPa (38.3 mmHg) with 95% limits (2 s.d.) of±1.0 kPa (7.5 mmHg). The normal arterial Po2 is more difficult to define because it decreases with age (page 194), and is strongly influenced by the concentration of oxygen in the inspired gas. Mechanisms that contribute to respiratory failure include ventilatory failure (reduced alveolar ventilation) and venous admixture as a result of either pure intrapulmonary shunt or ventilation perfusion mismatch (Chapter 8).


Ventilatory failure is defined as a pathological reduction of the alveolar ventilation below the level required for the maintenance of normal alveolar gas partial pressures. Because arterial Po2 (unlike arterial Pco2) is so strongly influenced by shunting, the adequacy of ventilation is conveniently defined by the arterial Pco2, although it is also reflected in end-expiratory Pco2 and Po2. This chapter is concerned mainly with pure ventilatory failure; other causes of respiratory failure are described in the next four chapters.



Pattern of Changes in Arterial Blood Gas Tensions


Figure 27.1 shows, on a Po2/Pco2 diagram, the typical patterns of deterioration of arterial blood gases in respiratory failure. The shaded area indicates the normal range of values with increasing age corresponding to a leftward shift. Pure ventilatory failure in a young person with otherwise normal lungs would result in changes along the broken line. Chronic obstructive pulmonary disease (COPD), the most common cause of predominantly ventilatory failure, occurs in older people, and the observed pattern of change is shown within the upper arrow in Figure 27.1. The limit of survival, while breathing air, is reached at a Po2 of about 2.7 kPa (20 mmHg) and Pco2 of 11 kPa (83 mmHg). The limiting factor is not Pco2 but Po2. This prevents the rise of Pco2 to higher levels except when the patient’s inspired oxygen concentration is increased. It may also be raised above 11 kPa by the inhalation of carbon dioxide. In either event, a Pco2 in excess of 11 kPa may be considered an iatrogenic disorder. Figure 27.1 also shows the pattern of blood gas changes caused by shunting or pulmonary venous admixture (Chapter 8).


image

Fig. 27.1 Pattern of deterioration of arterial blood gases in chronic obstructive pulmonary disease and pulmonary shunting. The shaded area indicates the normal range of arterial blood gas partial pressures from 20 to 80 years of age. The oblique broken line shows the theoretical changes in alveolar Po2 and Pco2 resulting from pure ventilatory failure. In chronic obstructive pulmonary disease, the arterial Po2 is always less than the value that would be expected in pure ventilatory failure at the same Pco2 value. Discussion of shunting is to be found in Chapter 8 and further discussion of chronic obstructive pulmonary disease in Chapter 28.


In general, the arterial Po2 indicates the severity of respiratory failure (assuming that the patient is breathing air), while the Pco2 indicates the differential diagnosis between ventilatory failure and shunting as shown in Figure 27.1. In respiratory disease it is, of course, common for ventilatory failure and shunting to coexist in the same patient, and the relative contribution of each mechanism will determine whether type 1 or 2 respiratory failure develops.



Time Course of Changes in Blood Gas Tensions in Acute Ventilatory Failure


Although the upper arrow in Figure 27.1 shows the effect of established ventilatory failure on arterial blood gas tensions, short-term deviations from this pattern occur in acute ventilatory failure. This is because the time courses of changes of Po2 and Pco2 in response to acute changes in ventilation are quite different.


Body stores of oxygen are small, amounting to about 1550 ml while breathing air. Therefore, following a step change in the level of alveolar ventilation, the alveolar and arterial Po2 rapidly reach the new value and the half-time for the change is only 30 seconds (see page 205 and Figure 11.19). In contrast, the body stores of carbon dioxide are very large: of the order of 120 litres. Therefore, following a step change in the level of alveolar ventilation, the alveolar and arterial Pco2 only slowly attain the value determined by the new alveolar ventilation. Furthermore, the time course is slower following a reduction of ventilation than an increase (Figure 10.11) and the half-time of rise of Pco2 following a step reduction of ventilation is of the order of 16 minutes.


The practical point is that, during the early phase of acute hypoventilation, there may be a low Po2 while the Pco2 is increasing but is still within the normal range. Thus the pulse oximeter may, under certain circumstances such as when breathing air, give an earlier warning of hypoventilation than the capnograph. This breaks the rule that the Pco2 is the essential index of alveolar ventilation, and it may be erroneously believed that the diagnosis is shunting rather than hypoventilation.



Causes of Ventilatory Failure1,2


The causes of ventilatory failure may be conveniently considered under the headings of the anatomical sites where they arise. These sites are indicated in Figure 27.2. Lesions or malfunctions at sites A to E result in a reduction of input to the respiratory muscles. Dyspnoea may not be apparent and the diagnosis of ventilatory failure may be overlooked on superficial inspection of the patient. Lesions or malfunctions at sites G to J result in evident dyspnoea and no one is likely to miss the diagnosis of hypoventilation. The various sites will now be considered individually.


A. The respiratory neurones of the medulla are depressed by hypoxia and also by very high levels of Pco2, probably of the order of 40 kPa (300 mmHg) in the healthy unanaesthetised subject, but at a lower Pco2 in the presence of some drugs (see below). Reduction of Pco2 below the apnoeic threshold results in apnoea in the unconscious subject but usually not in the conscious subject. Loss of respiratory sensitivity to carbon dioxide occurs in various types of long-term ventilatory failure, particularly COPD, and this is discussed further on page 412.
image

Fig. 27.2 Summary of sites at which lesions, drug action or malfunction may result in ventilatory failure. (A) Respiratory centre. (B) Upper motor neuron. (C) Anterior horn cell. (D) Lower motor neuron. (E) Neuromuscular junction. (F) Respiratory muscles. (G) Altered elasticity of lungs or chest wall (H) Loss of structural integrity of chest wall and pleural cavity. (I) Increased resistance of small airways. (J) Upper airway obstruction.


A wide variety of drugs may cause central apnoea or respiratory depression (page 77) and these include opioids, barbiturates and most anaesthetic agents, whether intravenous or inhalational. The respiratory neurones may also be affected by a variety of neurological conditions such as raised intracranial pressure, stroke, trauma or neoplasm.


B. The upper motoneurones serving the respiratory muscles are most likely to be interrupted by trauma. Only complete lesions above the third or fourth cervical vertebrae will affect the phrenic nerve and result in total apnoea. However, fracture dislocations of the lower cervical vertebrae are relatively common and result in loss of action of the intercostal and expiratory muscles while sparing the diaphragm. Upper motoneurones may be involved in various disease processes, including tumours, demyelination and, occasionally, in syringomyelia.

C. The anterior horn cell may be affected by various disease processes, of which the most important is poliomyelitis. Fortunately, this condition is now rare in the developed world but it can produce any degree of respiratory involvement up to total paralysis of all respiratory muscles.

D. Lower motoneurones supplying the respiratory muscles are prone to normal traumatic risks and, in former times, the phrenic nerves were surgically interrupted for the treatment of pulmonary tuberculosis. The later stages of motoneurone disease may cause ventilatory failure at this level. Idiopathic polyneuritis (Guillain–Barré syndrome) remains a relatively common neurological cause of ventilatory failure. The syndrome results from an immune-mediated aetiology and is characterised by a rapidly ascending motor nerve paralysis, which in one-third of patients progresses to quadriplegia and total respiratory muscle paralysis.3

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Jun 12, 2016 | Posted by in RESPIRATORY | Comments Off on Ventilatory failure

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