~une1974~·I.-

S.A. MEDICAL JOUR"l"'L 1257

'dextrocardia' should be regarded with suspicion andtreated as a diaphragmatic hernia until proved otherwise.A systematic approach to the investigation is vital (TableI), and should always be associated with an adequatepostero-anterior and lateral chest X-ray film. The inter­pretation of chest radiographs in the newborn may bedifficult. Poor quality X-ray films are extremely misleading.

Since there are many factors in the interpretation thatmay require expert knowledge, the attending doctor shouldnot hesitate to seek expert advice after excluding grossradiological abnormalities_

Constant monitoring of the child's progress is vital andrespiratory difficulty can be anticipated by regular bloodgas and pH estimations_

Pathophysiology and Treatment of AcuteRespiratory Failure in the Postoperative Patient

R. J. JEDEIKIN

SUMMARY

The pathophysiology and treatment of acute respiratoryfailure in the postoperative patient is discussed. Specialemphasis is placed on the concept of closing volumes,which forms the basis for the understanding of thepathophysiology, and is used as an index for patientassessment.

In the treatment of acute respiratory failure post­operatively, the discussion has been confined to prophy­laxis, use of intravenous analgesia, intermittent positivepressure ventilation and the dramatic use of positive end­respiratory pressure.

S. Afr. Med. J., 48, 1257 (1974).

The recent advances in anaesthesia and intensive carehave resulted in a better understanding of the patho­physiology of acute respiratory failure (ARF) andconsequent improvement in its management. The aim of

Department of Anaesthetics, University of Cape TownR. J. JEDEIKIN, B.SC., M.B. CH.B., F.F.A. (S_A.) (Present

address: University of Vermont, Department of Anes­thesiology, Mary Fletcber Hospital, Burlington, Vermont,USA)

Date received: 11 February 1974.

this review is to briefly discuss these two aspects of ARF,because it is a serious postoperative complication thatcan usually be avoided.

Ventilation per se is extremely difficult to monitorproperly, while cyanosis is a notoriously unreliablephysical sign. For these reasons there is no recognisedclinical definition of respiratory failure. The diagnosis ofARF is made solely on blood gas estimation: 'acuterespiratory failure is a state where the arterial oxygentension (PaO,) is 60 mmHg or less, and/or the arterialcarbon dioxide tension (PaCO,) is 49 mmHg or higher'.]

In essence, this is a measure of the ability of thelungs to carry out their primary function in life-gaseousexchange.

PATHOPHYSIOLOGY

During normal tidal-volume breathing, the volume of airleft in the lungs at the end of expiration is ± 3 000 ml,and is known as the functional residual capacity (FRC).Following maximal expiration there is usually a residualvolume (RV) of ± 1200 ml in the alveoli that cannotbe exhaled. However, during forceful exhalation, as thevolume of the lungs is reduced, small airways (less than2-mm diameter) tend to collapse! Furthermore, it is thesmall airways in the dependent lung regions (where there isless negative pressure) that tend towards early closure. Thevolume of air left in the lungs when airway closure occurs

1258 S.-A. MEDIESE TYDSKRIF 15 Junie 1974

-100 0

Po°280(mm Hg)

60

7 TLC

6

5

LUNG 4VOLUME

(LI r)3

2

YEARS 20 30 40 50 60NORMAL ADULT

(AI

70 ADULTWITH

ARF(8)

Fig. 1. Increasing closing volume shown in relation to age.

is known as the closing volume, and will vary accordingto position and age"" The older the person the earliersmall airway closure during expiration will occur, andtherefore the larger will be the closing volume (Fig. 1).

In the young person, airway closure only tends tooccur during forced expiration at volumes approximatelyequal to RV, while in the elderly, probably because ofloss of elasticity, airway closure may occur during tidalvolume expiration. The above holds true for the uprightposition. In the recumbent position, the diaphragm willencroach on the expiratory volume resulting in earlierairway closure.

Normally, those small airways that have closed will openon inspiration, sighing or yawning, and at the end ofinspiration, regardless of age, all regions of the lung areopen. If, however, they should fail to open due to anabnormality, air which is trapped behind the collapsedpassages is absorbed, resulting in alveoli collapse andatelectasis. Pulmonary capillaries continue to perfuse tbisnon-ventilated area of lung tissue, resulting in ventilation­perfusion imbalance, wbich manifests clinically as a dropin the partial pressure of oxygen (PaG,).

This is exactly what can happen postoperatively andexplains why the obese, elderly patient so often developspostoperative basal atelectasis. The lung ba~es are parti­cularly prone because there is less negative pressure andthe alveoli are already small. As the patient is recumbentpostoperatively, the diaphragm is raised .and the lungvolume decreased. In the immediate postoperative periodfollowing a general anaesthetic, the patient is usuallyunable to take a deep breath, sigh or cough in order

to reopen collapsed or closed alveoli.If the patient is broncbitic, or even has just a plain

cold, the airways may already be partially closed withmucus as well as being congested. This results in collapseand consolidation, and the patient is on the way torespiratory failure.

When a patient is already in acute respiratory failurehis lung volumes are usually decreased and there is adrop in the FRC. The cycle perpetuates itself, and withfurther diminution of FRC there is an increased tendencyfor early airway closure in expiration. The extent towhich this occurs will be influenced by 3 factors: (a)the nature of the acute process, e.g. mucous plugging,pulmonary emboli, Mendelsohn's syndrome, etc; (b)integrity of the surfactant system, e.g. the f :esence ofpulmonary oedema will, for instance, increase \he surfacetension by destruction and surfactant; and (c) low com­pliance and/or increased airway resistance as can occurin chronic obstructive airway disease, kyphoscoliosis, etc.

PATIENTS AT RISK

There are basically 2 groups of factors (explained interms of airway closure) wbich, unless attended to, willprecipitate ARF. Awareness of these factors and anti­cipation of the suspect patient can lead to better pre­operative workup, followed by a drop in the incidenceof postoperative ARF, more thoughtful anaesthesia, andearly recognition of respiratory problems postoperatively,resulting in early, vigorous therapy.

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ps

15 June 1974 S.A. MEDICAL JOURNAL 1259

Group A (Nou-Pulmonary Factors)

The obese patient' or the patient with abdominaldistension is a poor risk. Anaesthesia per se: the supineand head-down position," as well as inadequate turningof patients, potentiate airway closure, as do too vigorousairway suction and expiratory efforts. Paralysis, debility,narcotic drugs and pain result in poor inspiratory effortand failure to open closed airways:

Group B (Pulmonary Factors)

There are basically 3 pathological factors that areassociated with most pulmonary conditions: increasedsurface tension; interstitial oedema' (e.g. a patient incongestive cardiac failure); and inflammation (includingthe common cold), resulting in swelling of the bronchialmucosa and the intrabronchial tree.

PATIENT ASSESSMENT

A full clinical history and examination is mandatory,and only from a sound clinical basis can the decision bemade as to what further sophisticated tests should b.e done.It is, however, rare for a patient about to undergo surgerytoday, not to have a pre-operative chest X-ray film taken,and if he is over 40 years of age, an ECG. The respiratoryand cardiovasculature status of the patient is of extremeimportance. Where a patient with chronic obstructiveairway disease is coughing copious amounts of sputum,it is often of more consequence than his lung functionstudies. It is the patient with undiagnosed myocardialischaemia who is likely to be tipped into pulmonar:yoedema by the injudicious administration of intravenousfluid. Furthermore, the type of operative procedure inconjunction with the patient's clinical state may influencethe clinician in having the patient artificially ventilatedduring the immediate postoperative period.

The basic lung function tests are the vital capacity(VC) and the forced expiratory volume in the first second(FEV,), which are indicative of the ventilatory reserveand mechanics. Occasionally FEV, and YC are used indeciding whether a patient may have the respiratoryreserve necessary in order to recover from a pneumo­nectomy or lobectomy.

It is occasionally necessary to do full pulmonaryvolume studies including single-breath and steady-statemeasurements. Assessment of ventilation is done byassessing the PaCO, while the PaO, and inspired oxygenconcentration (FiO,) are for assessing oxygenation of thepatient. It is important that the PaO, be related to theFiO, in order to estimate the efficiency of oxygenation.

TREATMENT

Prophylaxis is the cornerstone of all medical treatments.The importance of early recognition of risk factors andsubsequently the timely treatment of these patients pre­operatively, will result in a marked clinical and laboratory

improvement with Iow morbidity and Iow mortality post­operatively.

Adequate treatment of underlying disease is wellappreciated, as is the ever-increasing and important roleof the chest physiotherapist, before as well as afteroperation.

Perhaps the most difticuIt problem facing the clinicianin the postoperative period is the adequate treatmentof pain. Too little analgesia can result in hypoventilation,ineffectual coughing with poor clearance of secretions,and subsequent atelectasis and infection. Over-sedationor too much analgesia, especially in the at-risk patientwith emphysema, by depressing the respiratory centre,will result in the same sequence of events as those thatfollow on too little analgesia.

Regional anaesthesia and local anaesthetic blocks arecommonly used in some centres and are an excellent wayof treating pain. However, not all parts of the body areaccessible to this form of treatment, and opiates stillpresent an important method of pain relief. Moreover.it is thought that judicious small amounts of opiates canbe used in the treatment of pain if given by intravenousinjection.

The aim of intravenous analgesia is to titrate smalldoses of either morphine or pethidine against the patient'spain threshold. In other words, following an initial 2 - 3mg of morphine intravenously (depending on the sizeand the age of the patient), intravenous increments ofJ mg morphine may be repeated at half-hourly intervalsuntil there is adequate pain relief without the unwantedsequel of respiratory depression. Such patients, however,will require careful monitoring of the respiratory rate,depth of respiration, blood pressure and pulse rate, andideally this should be practised in an intensive careenvironment. Similarly, intravenous morphine is oftenof great advantage in alleviating the pain of vigorouschest physiotherapy when given 15 minutes beforehand.

ARTIFICIAL VENTILATION

In the past, intermittent positive pressure ventilation(IPPY) was associated with serious complications anda high mortality. With the exception of cases of polio­myelitis, IPPY was the last resort when all conservativemeasures had failed.

Today IPPV is not only more frequently used in thetreatment of acute respiratory failure, but has aplace in the prevention of ARF. When ARF is a!1ticipatedpostoperatively, IPPY may be continued from the operat­ing theatre to the ward. As a rule, in most centres,patients who have had an open-heart operation areventilated for a minimum of 12 hours afterwards. Thepractice of artificial ventilation during the postoperativeperiod has now extended to the genera! surgical wards.and postoperative IPPY is mainly indicated for thosepatients with poor lung function studies pre-operatively,certain neurosurgical operations, certain upper abdominaloperations, especially where it is thought the patientwill have much pain (abdominal thoracic incisions, etc.),and fixed cardiac outout states.

1260 S.-A. MEDIESE TYDSKRIF 15 Junie 1974

It is usually unnecessary to venWate these patientsfor over 48 hours, 12 - 24 hours being the mean extubationtime.'"

Equally vexing is the problem of when to initiateartificial ventilation in the patient already in respiratoryfailure. Respiratory failure is not usually a precipitousevent, but more commonly the result of inadequate careand monitoring. There' is no doubt that the morbidityand mortality of ARF increases with the severity, despiteintervention with IPPY. The longer the delay in startingtreatment, the more likely that IPPY at a late stage mayin fact add to the damage, owing to the need for higherinspiratory oxygen concentration (FiO,) and the use ofhigh tidal volumes and high airway pressure. As aguideline it is suggested that ventilatory support beinitiated in adults when the respiratory rate increases toover 35/rnin, the pO, drops to under 70 rnmHg whileon oxygen, and the PaCO, is over 55 rnmHg.ll These are,however, not absolute figures and it is very importantto note the trend, e.g. regular monitoring of bloodgases may show a progressive drop in po, associatedwith an ever-increasing FiO,. The clinician's clinical judge­ment should be linked with the laboratory information.

It has recently been shown that the pattern of ventilationmay profoundly affect the oxygenation and ventilationof the patient. During prolonged IPPY with a constantvolume ventilator, it was noted that there was a pro­gressive drop in Pao, which was reversed by intermittenthyperventilation and/or sighs." This has, however, beenrefuted by some observers."

What does appear to be accepted is that ventilation withlow tidal volumes tends to drop the PaO" while largertidal volumes (10 - 15 mI/kg) are able to maintain abetter PaO,. No lung damage is noted at these hightidal volumes. Excessive low PaCO, is treated by meansof an external deadspace.14

The most important advance in the management ofacute respiratory failure during the last 5 years has beenthe advent of PEEP (positive end expiratory pressure)."'"PEEP enables the patient to keep a positive and expiratorypressure in his lungs. It has been shown that if apatient eXhales against a resistance this tends to keepsmall dependent airways open, and will therefore increasehis FRC. 17 Thus, during inspiration more alveoli are keptopen and the arterial pO, is improved. It is also thoughtthat PEEP, by virtue of the increased pressure in thelungs, will push fluid out of the alveoli into the interstitialspace and perhaps even into the pulmonary vasculature."PEEP is usually introduced when, despite ever-increasinginspired oxygen content, the PaO, continues to decrease.Absolute figures that may be used as a guide are a pO,

of under 70 when the patient is on 50% oxygen andintermittent POSitive pressure ventilation." InitiaJly, PEEPwas only used when a situation with the above figureshad been reached, but there is an increasing tendency touse PEEP earlier in anticipation of further deterioration.

PEEP or constant positive pressure breathing (CPPB)can be used either with artificial ventilation with aventilator, or by spontaneous breathing," with PEEPranging anywhere from 2 - 10 cm of ao. Levels of 15cm and more have been recorded. PEEP may be simplyapplied to a ventilator by attaching the expiratory limbof the ventilator to a calibrated tube immersed in water.

In some patients PEEP may not improve the Pao"and may even worsen it, and it may also result in twomajor complications: increased tendency to tension pneu­mothorax, and hypotension, usually in patients alreadydehydrated or hypovolaemic. According to Deane et al.'"the incidence of tension pneumothorax has been markedlydecreased by the use of non-depolarising agents onpatients on CPPB, while deleterious drops in bloodpressure can be avoided by adequate hydration of thepatient.

I should like to thank Professor A. B. Bull, Head of theDepartment of Anaesthetics, Uriiversity of Cape Town andGroote Schuur Hospital, for his encouragement, critical reviewand help with this manuscript.

REFERENCES

1. Bates, D. V., Macklem, P. T. and Christie, R. V. (1971): Respira­tory Function in Disease. An IncToduction to the Integrated Studyof the Lung, 2nd ed., p. 442. Philadelphia: W. B. Saunders.

2. Burger, E. J. J. and Macklem, P. T. (1968): J. Appl. Physiol., 25,139.

3. Holland, J., Milic-Emili, J. and Macklem, P. T. (1968): J. Clin.Invest., 47, 81.

4. Leblanc, P., Rut!, F. and Milic-Emili, J. (1970): J. Appl. Physiol.,28, 448.

5. Holley, H. S., Milic-Emili, J. and Becklate, M. ·t. (1967): J. Clin.Invesr.. 46, 4'15.

6. Don, H. F., Wahba, W. M. and Cuadrado, L. (970): Anesthesio­logy, 32, 521.

7. Don, H. F., Craig, D. B. and Wahba, W. M. (1971): Ibid., 35,582.

8. Bendixen, H. H., Egbert, L. O. and Hedley-Whyte, J. (1965):Respiratory Care. St. Louis: C. V. Mosby.

9. Hugbes, J. M. B. and Rosenzweig, D. Y. (1970): J. AppI. PhysioI.,29, 332.

10. PODloppidan, H., Laver, M. B. and Geffin, B. (1970): Advanc.Surg., 4, 163.

11. PonlOppidan, H., Geffin, B. and Lowenstein, E. (1972):: N. EngI.J. Med., 287, 799.

12. Bendixen, H. H., Hedley-Whyte, J. and Laver, M. B. (1963): Ibid.,269, 991.

13. Bergman, N. A. (1970): Anesthesiology, 32, 297.14. Suwa, K., Geflin, B. and Pontoppidan, H. (1968): Ibid., 29, 1206.15. Kumar, A., Falke, K. J. and Geffin, B. (1970): New EngI. J. Med.,

283, 1430.16. Ashbaugh, D. G., Petty, T. L. and Bigelow, D. B. (1969): J.

Thorac. Cardiovasc. Surg., 57, 31.17. McIntyre, R. W., Laws, A. K. and Ramachandran, P. R. (1969):

Canad. Anaesth. Soc. J., 16,477.18. Staub, N. C. (1970): Hum. Path., I, 419.19. Gregory, G. A., Kitterman, J. A. and Phibbs, R. H. (1971): New

EngI. J. Med., 284, 1333. .20. Deane, R. t Morgan. J. G. and Shinosaki. T. Personal communication.