Recognizing and treating respiratory problems in the surgical patient

Recognizing and treating respiratory problems in the surgical patient John

H Eisele, MD

Postoperative respiratory problems may be secondary to the operation or to the anesthesia, but most often are related to both. The frequency of postoperative respiratory complications remains surprisingly high despite the advent of antibiotics and the use of better techniques for anesthesia and respiratory care. The incidence of pulmonary problems following abdominal and nonabdominal surgery over a 40-year span is shown in Table 1. The wide variation is probably due to an unclear definition of complications. A list of the types of complications (Fig 1) represents a retrospective study of 48,000 patients.' Atelectasis, together with pneumonias which some believe are always preceded by atelectasis, constitute 50% to 70% of John H Eisele, MD, i s an associate professor i n the department of anesthesiology a t t h e University of California School of Medicine, Sacramento M e d i c a l Center. H e i s a graduate of Cornell University, Ithaca, NY, and of A l b a n y M e d i c a l College, NY.

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all postoperative respiratory complications. Consequently, most of this discussion concerns the prevention of atelectasis. Atelctasis is generally agreed to be the most common postsurgical problem, but there is no general agreement on its definition. Hamilton2 proposed that we forget the classic concept of airway obstruction, distal gas absorption, and mass localized lesions, and think instead of atelectasis as small diffuse lesions, nonobstructive in origin, due primarily to lack of adequate inflations. The work of Clements? indicates that there is a change in the surface tension of an alveolus when it is not moved or stretched. Surfactant is the film-like substance lining the alveoli and helping to maintain their spherical shape. Hours of constant volume ventilation, even though adequate for gas exchange, tend to reduce surfactant and thus increases the surface f o ~ c e sthat collapse 01' decrease the size of the alveoli. The net result

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is higher pressures needed for inflation. These changes under anesthesia may lead to a decreased lung volume, a decreased lung compliance, and a fall in arterial oxygenation-findings which furnish a reasonable clinical definition of atelectasis.

Adequacy of ventilation during anesthesia. Thus, inadequate ventilation is the most common cause of a fall in compliance and oxygen concentration under anesthesia and in the recovery room. Often we think our patients are being sufficiently ventilated with 8 to 10 L/min, but in actuality their alveolar ventilation is insufficient. Alveolar ventilation is total ventilation minus dead space ventilation. Dead space includes all lung areas where gas enters but does not contact blood. If ventilation to some areas increases out of proportion to its blood flow, or if perfusion decreases more than ventilation in other areas, the outcome is more dead space ventilation, which means less air goes to the well-perfused areas. Does this happen under anesthesia? Bendixen4 demonstrated that

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reduced arterial oxygenation may occur even during controlled ventilation unless occasional hyperinflations are given. This has not been confirmed by all investigators but is generally accepted by anesthesiologists. Recently, the idea of airway closure has been offered to explain some of the fall in arterial oxygen concentration during anesthesia. It has been shown that under anesthesia the amount of air in the lungs a t the end of an expiration may fall to a point below which airways closure O C C U ~ S . ~This point, the closing volume, is relatively constant so that a fall in the end-expiratory volume during anesthesia may cause closing of airways 1 mm or less in diameter. The reasons for a reduction in lung volume during anesthesia are not entirely clear but may be related to loss of muscle tone, the supine position, and upward pressure of abdominal contents. These changes are more likely to develop during upper abdominal surgery when retractors push viscera against the diaphragm. The elderly are more susceptible to

Table 1 Incidence of postoperative pulmonary complications following general anesthesia

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Author

Date

King Rovenstine Pooler

1933 1936 1939 1946 1953 1954 1957 1964 1968

Dripps Palmer Thoren Fomon Hamilton Wightman

May 1973

Number of subjects

7,000 7,874 6,000 1,240 180 343 800 27 700

Incidence

% Abdominal % Non-abdominal

14 6 12.5 5.5 26 27 6.6 25 10.3

1 ....

0.7 ..~. -.._ .... ..~. . . . .

0.6

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Type of complication Asthma Pneumothorax, hemothorax, or pleural effusion Hypoventilation secondary to anesthesia or surgery Pulmonary edema other than cardiac Aspiration Increased secretions or hemorrhage

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Fig I. A list shows the types of pulmonary complications following general anesthesia and a variety of surgical procedures. These are plotted as a relative incidence of the total complications among 48,000 cases reported by Modell and Moya.1

Atelectasis Acute lower respiratory tract infection Pulmonary embolism Miscellaneous

I 1

4

25 50 75 I00 Percent of Total Pulmonary Complications

airway closure, and the obese have a reduced end-expiratory volume. Both of these situations promote air trapping, which in turn adds to wasted ventilation.

How to treat inadequate ventihtion. What is adequate ventilation during anesthesia? The physiologists have defined hyperventilation as ventilation out of proportion to metabolic needs. In normal man this means a pC0, below 40 mm Hg. When we control ventilation we often reduce the pC0, to 30 mm Hg or lower. Are we doing any harm by producing severe hyperventilation with the pC0, below 20 mm Hg? So long as the airway pressure is not over 40 cm H,O, there is no evidence to show that alveoli are injured or that pulmonary blood flow is compromised. However, lowering the pCO,, regardless of the pressure or flows required, will reduce cerebral blood flow as much as 50% a t a pC0, of 20. This

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may be critical in patients with cerebral vascular disease or marked anemia. Hyperventilation also reduces sympathetic tone to the heart and blood vessels, and decreases cardiac output, especially if there is hypovolemia. The lowered cardiac output is more dependent on ventilator pressures than on the NO,. Also, increased ventilation raises the amount of anesthetic delivered. In conducting deliberate hyperventilation we must be aware of these possible disadvantages. T h o s e who advocate it seem to think that hyperventilation is better than underventilation. The proponents state that less anesthesia is required because the total neural input from the muscles of respiration is reduced. This, however, has not been proven in terms of the requirements for inhalation agents. Throughout this argument there is an implication that hypoventilation,

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or a pC0, over 40 mm Hg, is a bad state of affairs. This has not been proven true. Small elevations (5 to 10 mm Hg) in pC0, usually result from spontaneous breathing during anesthesia. This rise in pC02 can produce an increase in systemic perfusion by catecholamine stimulation. However, under halothane anesthesia the blood pressure and heart rate responses to increased CO, are unpredictable. In patients with heart disease I do not recommend hypoventilation because of a greater potential for arrhythmias, an increase in cardiac work, and because these patients have a diminished inotropic response to C0,.6 Inadequate oxygenation is always a danger during spontaneous breathing, particularly if the patient is in an unusual position. The patients able to tolerate mildly elevated pC0, are healthy and free of cardiovascular disease. Patients with pulmonary or cardiac disease should not be allowed to retain CO,. In general, these patients and critically ill patients should be hyperventilated and monitored closely. When a patient’s status is in doubt, it is wiser to overventilate than to underventilate.

Adequacy of oxygenation during anesthesia. Inadequate oxygenation is another probIem related to ventilation and to postoperative respiratory problems. Numerous studies have shown decreased arterial oxygen in the postoperative Many factors including age can be associated with postoperative hypoxemia. More important than the type of anesthetic or the anesthetic technique are the status of the patient, the type of surgery, and length of surgery. We often think the patient

May 1973

is safe when he may have a seriously low pO,, not low enough to produce cyanosis or dark blood, but low enough to impair oxygen reserves in some areas. In a large county hospital over a two-year period, arterial sampling of patients inspiring 30% 0, revealed a mean PO, of 79 mm Hg. Those inspiring 40% 0, had 85 mm Hg, and those receiving 50% 0, had 110 mm Hg. In most cases, arterial blood was drawn because of the anesthesiologist’s concern. However, it points out that many times we keep patients at unsafe inspired 0, levels. What is optimal? I suggest 100% saturated hemoglobin for all patients under general anesthesia. This can only be ensured when the p0, is above 100 mm Hg. How do we diagnose hypoxia under anesthesia? Looking for cyanosis of the skin under indirect lighting may be deceiving but we must always look for changes in color. The mucous membranes and conjunctivae are better indicators than the extremities or nail beds, which may be blue from cold. The color of the blood in the surgical field may indicate impaired oxygenation provided it has not come from areas of stasis. The anesthesiologist who waits for changes in vital signs may be completely fooled, because the classic tachycardia and hypertension secondary to the hypoxia induced norepinephrine secretion may not occur. In patients with diseased hearts and in small children, bradycardia should be considered evidence of hypoxemia until proven otherwise. The final diagnosis depends upon an arterial blood gas measurement. Treating hypoxemia under anesthesia is simple since it is imperative

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to increase the inspired 0, when we suspect low oxygenation. When should we anticipate hypoxemia? If the patient has lung disease and major surgery is planned, we should know his preoperative PO, on room air. In some conditions like sarcoidosis the ventilation-perfusion problems may be out of proportion to the patient's symptoms. A case to illustrate this concerned a 35-year-old man with asymptomatic pulmonary sarcoidosis who was anesthetized for repair of a retinal detachment. His preoperative PO, was 70 mm Hg. Shortly after induction cyanosis was noted. The 0, concentration was changed from 40% to 60% 0,. Ten minutes later the PO, was 70 mm Hg -the same as the awake value.

How to prevent atelectasis dwing anesthesia. The concept of airways closure during anesthesia is useful not only because it offers an attractive explanation of how atelectasis and hypoxemia can develop under anesthesia, but also because it suggests prevention of atelectasis by increasing the end-expiratory volume or preventing its fall. A small amount of end-expiratory pressure achieves results when the pop-off valve is closed just enough to keep the expiratory pressure at 5 to 10 cm H,O a t the end of expiration. Frumin," Cheney,'O and others have measured small increases in PaO, after adding expiratory resistances in normal patients and animals under anesthesia. One should expect a larger rise in PO, with this maneuver in patients with lung disease or in prolonged abdominal operations. These measures are not novel, since we often use manual pressure on the anesthesia rebreathing bag during expiration of the patient with ob-

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structive lung disease or asthma. I suggest that we consider using endexpiratory pressure in cases where the risk of hypoxemia is high, like during major abdominal surgery and particularly when high concentrations of N,O are used; in trauma cases where shock lung may be a threat; and when patients are in the lateral or prone positions where large pulmonary ventilation-perfusion abnormalities can be expected. When employing end-expiratory pressure, the blood pressure should be monitored carefully for evidence of decreased cardiac output consequent to reduced venous return. The breath sounds should be checked frequently because of the increased chance of pnuemothorax. Whenever possible the arterial PO, should be measured to determine the effectiveness of this simple maneuver. It has been suggested that end-expiratory pressure be used during the latter part or a t the end of the operation to re-expand collapsed alveoli. We do not know if this is effective or any better than a few super inflations just before extubation.

Recoveryj room problems. As a general rule, it is best to give supplemental 0, to all elderly patients, all extremely ill patients, and all patients following major surgery. I think most recovery room patients should receive 0, until they are able to sit up or meet the criteria for discharge. Following prolonged anesthesia and/or rapid emergence, we often note shivering and increased muscle tone. This means increased 0, consumption in a situation where respiration probably is unable to meet the additional metabolic demands. This calls for more 0,.

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The major question in the recovery room is the adequacy of ventilation. Airway obstruction is usually obvious and calls for immediate correction. However, the effect of residual anesthetic, narcotic or muscle relaxant drugs may be very subtle. The first thing to remember is that anesthetic gas must be eliminated by the lungs, and if it was the only agent given then we must promote effective breathing. This can often be achieved by raising the patient's head slightly. This is especially important if the patient is obese. Adding one to two feet of dead space tubing to the airway to allow CO, rebreathing has been recommended by Hamilton,2 (Fig 2) both to stimulate respiration and establish a pattern of deeper breaths. This is also good anti-atelectasis treatment, since it may open up closed airways. Neither of these procedures are recommended if residual narcotic and anesthetic are present. Elevating the head of a patient given narcotics is likely to cause postural hypotension. At the same time raising the pC0, with added dead space may not stimulate breathing due to the narcotic induced respiratory depression. A potent narcotic antagonist, Narcan, is effective against all narcotics and does not have narcotic properties itself. It has been a great help in sorting out and correcting respiratory depression in the recovery room. Administering 1/8 to 1/4 cc of Narcan every two to three minutes will determine the presence of narcotic depression. It is very easy to give more than enough and find the patient screaming in pain. The difficulty is that Narcan is only effective for about two hours. The effects of morphine and Demerol outlast the Nar-

M a y 1973

Fig 2. A standard anesthesia face mask connected t o a length of corrugated anesthesia hose into which the patient breathes and rebreathes some of his expired air depending on the lenqth of the hose.

can, a situation which can be very dangerous if the patient has been returned to the ward. Patients given large doses of narcotic for anesthetic management should be kept in the recovery room for a longer period. More Narcan may be needed after two hours and again after four hours. We still have the problem of reversal of muscle relaxants to consider. If the narcotics are antagonized and the patient is awake but unable to cough or sit up, we should suspect some residual curarization. Neither inspection of the ventilatory effort nor the ability to raise the head off the pillow are sufficient indicators. Walts" suggested eliciting a five second sustained tetanic contracture with the nerve stimulator. If nerve stimulators are not available the ability of the patient t o raise his head and hold it up should represent a sustained tetanus, and is a useful index that the curare is not a factor. The

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problem is that the patient may not be awake enough to carry out this request. Therefore, it makes sense to attempt to reverse the narcotic first. In most cases involving curare or gallamine some prolonged muscle relaxant effect will require reversal. We think of 40 minutes as the effective duration of curare, but some factors alter the time period. Among the factors are depth of anesthesia; the blood pH which when low can intensify the neuromusculas block; the temperature which may produce the rewarming curarization phenomenon; the electrolytes sodium, potassium, and calcium, which when low can prolong the neuromuscular blockade; and finally, the presence of antibiotics which themselves have a neuro-

muscular blocking effect. Many of these antibiotics are sensitive to calcium reversal of the block, though some are not (Table 2).12 Once the anesthetic, the narcotic and the relaxant are reversed, pain can promote ineffective breathing. The pattern may be too shallow to clear the normal anatomic dead space. In addition, tight binding dressings about the chest and abdomen may constrict breathing efforts. Peridural or intercostal blocks are effective in the recovery room. Relief of the pain of breathing is usually associated with improved blood gases. Also, the patient can get up sooner, reducing the chance for atelectasis. These postoperative nerve

Table 2 Anfibiofic Group I Aminasidine Dihydrostreptomycin Gentamicin Kanamycin Neomycin Paromomycin Viomycin

Side effects Neuromuscular blockade reversible with calcium salts, also with neostigmine if block is incomplete. Some ganglionic blocking activity. Smooth muscle depression and obtotoxicity.

Group II Polymixin A Polymixin B Colistin

Neuromuscular paralysis not reversed b y calcium or neostigmine.

Group I l l Lincomycin

Neuromuscular blockage not consistently reversed with calcium or neostigmine.

Commonly used antibiotics are grouped according to general chemical structure. The side effects concerning surgical patients are listed on the right.. Note that the neuromusclar blocking properties may not b e reversed with any agent, occasionally prolonging paralysis postoperatively.

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blocks have been used extensively at some hospitals. Preventing postoperative respiratory problems really starts by assessing and identifying them preoperatively. Ask patients to stop smoking the day before surgery because acute exposure to smoke can depress the lungs' defense rnechani~ms.'~The filtering action of the cilia and the clean-up work of alveolar macrophages are hindered by smoke, while the important muco-ciliary lining and the humidification machinery are damaged by habitual smoking. Patients with obvious lung disease who have not been checked previously should undergo blood gas and forced expiratory volume (FEV) analyses. Make sure the chest x-ray has been evaluated and be certain that purulent sputum is not present. If we do all of the reasonable tests preoperatively then we know if oxygenation will be a concern; we will not administer 70% N 2 0even though the N,O-narcotic-relaxant technique is so popular; and we will not be satisfied to see the bag or bellows move a magic 8 or 10 L/min. If we are forewarned then we can draw an arterial sample or more simply, an arterialized venous sample for a PO, and pC0, determination. This preventive action may avoid an anesthetic catastrophe and may reduce the occurrence of postoperative respiratory complications.

0

REFERENCES I. J H Modell and F Moya, "Postoperative pulincidence and managemonary complications ment," Anesthesia and Analgesia, 45 (July-August

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I966), 432-439. 2. W K Hamilton, "Postoperative complications,"

respiratory Respiratory Therapy Clinical Anes-

thesia (Philadelphia:

F A Davis Co. 1965), chapter

10. 3. J A Clements, "Surface tension o f lung extracts," Proceedings of the Socidy for Experimental Biology and Medicine, 95 ( M a y I957), 170- 172. 4. H H Bendixen, e t al, "Impaired oxygenation i n surgical patients during general anesthesia with controlled ventilation: A concept of atelectasis," New England Journal of Medicine, 269 (November

I963), 99 1-996. 5. H F Don, e t al, "Airway closure, gas trapping, and the functional residual capacity during anesthesia," Anesthesiology, 36 (June 1972), 533-

539. 6. J P Blackburn, e t al, "PaC02 and the preejection period: The paCOJinotropy response curve," Anesthesiology, 37 (September 1972),

268-2 76. 7. J F Nunn, "Influence of age and other factors on hypoxaem'a i n the postoperative period," Lancet,

2 (September 1965), 466-568. 8. G R Sellery, " A review of the causes of postoperative hypoxia," Canadian Anaesthefisfs' Society Journal, 15 (March 1968), 142-151. 9. M J Frumin, e t al, "Alveolar-arterial 0 2 differences during artificial respiration i n man," Journal of

A p p l i e d Physiology,

I959), 694-700. 10. F W Cheney,

14 (September

e t al, "The effect of expiratory

resistance on t h e blood gas tensions of anesthetized patients," Anssthesiology, 28 (July-August

1967)

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670-676.

I I. G E Strobel, "An in-vitro model of anesthetic hypertonic hyperpyrexia, halothane-caffeine-induced muscle contractures: Prevention of contracture by Procainamide," Anesthesiology, 35 (November 19711, 465-473. 12. C Pittinger and R Adamson, "Antibiotic blockade of neurornuscular function," Annual Review of Pharmacology, 12 ( 1972), 169-184. 13. G M Green and D Carolin, "The depressant effect of cigarette smoke on the in vitro antibacterial activity of alveolar macrophages," New h g l a n d Journal of Medicine, 276 (February 1967), 42 I-42 7.

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May 1973

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