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Postgrad Med J: first published as 10.1136/pgmj.40.465.404 on 1 July 1964. Downloaded from

POSTGRAD. MED. J. (1964), 40, 404

PULMONARY CEDEMA RONALD FINN, M.D., M.R.C.P. Senior Medical Registrar, Royal Southern Hospital, Liverpool, Research Fellow, Department of , University of Liverpool.

OEDEMA of the was defined by TABLE I. Lznnec (1829) as . .. "the infiltration of THE CAUSES OF PULMONARY OEDEMA serum into the substance of this organ, in such A. Disease: degree as to diminish its 1. . evidently perme- 2. Aortic and disease. ability to the air, in ." hennec also 3. Myocardial disease. observed that pulmonary cedema was most 4. . commonly caused by disease of the heart, B. Central Nervous System: and could manifest itself as "suffocative 1. Trauma. orthopnoea". James Hope (1832) noted that 2. Haemorrhage and Thrombosis. obstruction of the left heart would lead to 3. Encephalitis. pulmonary congestion associated with severe C. : 1. -(especially influenzal). dyspnoea, and wrote that . . . " has 2. and . been too much regarded as independent of the 3. of irritant gases. heart. Long treatises have even been written 4. Chest trauma. (Traumatic wet ). by copyright. upon it without ever mentioning disease of D. Allergy: this organ as one of its causes. It is, therefore, 1. Angioneurotic cedema. necessary to dwell a little on this subject, not 2. Serum sickness. only for showing the magnitude of this error, E. Miscellaneous Causes: but of the reader with 1. Distension of cesophagus, stomach, gall making acquainted all bladder. the habitudes and aspects of a complaint, 2. Excessive transfusion. which is perhaps the most distressing in the 3. Overhydration in acute renal failure. whole catalogue of human maladies". 4. Manipulation of stellate ganglion. 5. Overdosage with morphia, , me-http://pmj.bmj.com/ thyl salicylate. Causes of Pulmonary Oedema 6. High altitude pulmonary cedema. Pulmonary cedema may be due to multiple and the resulting pulmonary congestion causes, and extensive aetiological classifications renders the lungs turgid and less distensible, have been given by Cameron (1948), Luisada and the resultant difficulty in expanding and and Cardi (1956) and Visscher, Haddy and retracting the stiffened lung is responsible for Stephens (1956). The more common causes the primary symptom of dyspnoea. If the pul- on September 30, 2021 by guest. Protected are listed in Table 1. monary rises still further and exceeds the osmotic pressure, then true Aetiological Considerations pulmonary cedema occurs. Congestion of the bronchial mucosa and secondary broncho- In the ultimate analysis pulmonary cedema spasm may lead to and must be due to one or more of the following thus further contribute to the sensation of factors; a rise in pulmonary capillary pressure, dyspnoea. a fall in intravascular osmotic pressure, an The classical relationship between cardiac increase in capillary permeability, or a fall in dyspnoea and posture (orthopnoea) is probably tissue pressure. due to increased right ventricular output con- Left Ventricular Failure: sequent on increased right atrial filing in the Failure of the left is the most horizontal position (McMichael, 1937); and it common cause of pulmonary cedema, and may has been estimated that the lungs contain an be acute or chronic. Left ventricular failure extra 500 ml. of in the recumbent pos- leads to damming back of blood in the lungs, ture (McMichael, 1939). The decrease in vital Postgrad Med J: first published as 10.1136/pgmj.40.465.404 on 1 July 1964. Downloaded from July', 1964 FINN: Pulmonary Oedema 405

>Left Ventricular Failure

a Tachycardia I~~~~~Raisedcu/n Cap. Pressulre Increased Anoxia and Metabolic RJY Out Acidosis

Anx ity Suction Effect Pulmonary Oedema.

Ventilation Defect Dyspnoea (foaming})-

FIG. 1.-The vicious circle operating in left ventricular failure whereby increasing pulmonary cedema progressively impairs myocardial function, thereby leading to further degrees of pulmonary cedema. This chain reaction is potentially self perpetuating and unless broken at some point may prove fatal. capacity due to upward displacement of the Sampson and Friedman 1962) have demon- diaphragm is a further factor leading to strated very large increases in flow from increased pulmonary congestion in the hori- the lung, and it has therefore been suggested by copyright. zontal position. that reduced lung motion at night decreases pulmonary lymph flow and hence predisposes Paroxysmal nocturnal dyspnoea (cardiac to pulmonary cedema. asthma, acute left ventricular failure) usually Once the attack has started a vicious circle occurs in patients with chronically congested develops (Fig. 1), whereby increasing degrees lungs, and is due to the sudden trapping of an of pulmonary cedema further reduce myocard- extra few hundred millilitres of blood in the ial function. There are several mechanisms by already congested . These means of which pulmonary cedema further attacks usually occur at night and various ex- embarrasses the left ventricle. Thus the severe http://pmj.bmj.com/ planations have been offered to account for dyspnoea leads to intense , and the this phenomenon. The failing heart is more resultant tachycardia and diminished coronary able to meet demands during the night when filling time place severe demands on the failing the requirements are reduced, and thus ventricle. The intense inspiratory efforts tend to balance is temporarily restored. This allows suck more blood into the pulmonary circulation the resorption of postural cedema which has thus collected in the dependent parts of the body tending to further cedema formation.

Pullmonary cedema may produce a severe vent- on September 30, 2021 by guest. Protected during the day, leading to a nocturnal increase ilation defect due to obstruction of the airways in blood volume, and the chronically raised by frothy fluid, and the resulting anoxia and pulmonary venous pressure tends to redistri- metabolic acidosis further impairs myocardial bute this cedema fluid in the lungs. The as- function leading to further degrees of failure sumption of the horizontal position during and progressively severe pulmonary cedema. sleep also tends to increase pulmonary conges- This chain mechanism is potentially self tion by increasing right ventricular filling perpetuating and unless broken at some point pressure and decreasing . Com- the sequence of increasing pulmonary cedema pensatory mechanisms are delayed because of and sleep, and thus the patient does not wake and diminishing myocardial function may sit up until pulmonary congestion is well prove fatal. advanced. During sleep less fluid is lost by Mitral Valve Obstruction: evaporation from the lung, thus potentiating the Obstruction at the mitral valve is usually due cedematous state. Recent experimental studies to a tight mitral stenosis, but on rare occasions in rabbits in whom cardiac failure has been ball valve thrombi and atrial myxomata may induced by artificial A-V shunts (Uhley, Leeds, be present. Severe obstruction at the mitral Postgrad Med J: first published as 10.1136/pgmj.40.465.404 on 1 July 1964. Downloaded from 406 POSTGRADUATE MEDICAL JOURNAL .July, 1964 valve leads to pulmonary congestion with a strictor potential (Sarnoff, 1952). The resultant raised pulmonary capillary pressure and sub- overloading of the pulmonary circulation pre- sequent pulmonary aedema, which can be acute disposes to pulmonary oedema. The peripheral or chronic. shut down in the systemic circulation impairs Acute pulmonary cedema in mitral stenosis, left ventricular output and thus strains the unlike that in left ventricular failure, usually left ventricle, and there is evidence that neuro- occurs during exercise. The resulting tachy- genic pulmonary oedema usually occurs in as- cardia decreases the diastolic filling period, sociation with hypertension and coronary thus leading to a hold-up of blood in the left disease which act as predisposing factors . Tachycardia associated with acute (Paine, Smith & Howard, 1952). The extreme and the onset of an abnormal rhythm bradycardia which sometimes occurs in severe such as auricular fibrillation may similarly intracranial damage may also predispose to precipitate an attack of acute pulmonary pulmonary oedema (Campbell, Haddy and cedema. It is also well known that a chest infec- Visscher, 1949). tion may act as a precipitating factor by Acute pulmonary oedema can occur in increasing capillary permeability, and the heroin poisoning, particulary in "main-line" increased blood volume associated with preg- addicts. (Silber and Clerkin, 1959). The patho- nancy may also precipitate an episode of genesis is not clear, but due to respir- pulmonary cedema. atory depression may lead to increased capillary permeability (Drinker, 1945). Morphia is also Other Causes: known to increase intracranial pressure (Keats Irritant gases such as phosgene produce lung and Mithofer, 1955) and may stimulate the cedema by a direct action on the pulmonary vasomotor centres (Schmidt and Livingstone, , and increased capillary permeability 1933) and thus the oedema might be partly cedema associated is responsible for pulmonary neurogenic in origin. Pulmonary cedema by copyright. in with serum sickness and acute angioneurotic salt water drowning is due to an imbalance cedema. Acute renal failure produces cedema of hydrostatic and osmotic in the by excessive fluid intake in the face of anuria pulmonary capillary bed set up by the inhal- or severe oliguria, with resultant circulatory ation of salt water into the alveoli; hypoxic overload. Excessive transfusion may have damage to the capillaries and neurogenic similar effects in elderly subjects with poor factors probably also contribute (Lancet 1962). renal and cardiac reserves. Pulmonary oedema may accompany lung infec- Pulmonary cedema may occur in association tions, particularly influenzal pneumonia and with intracranial disease of many kinds, and is probably due to the local release of vaso-http://pmj.bmj.com/ it is of historical interest that asthma was dilator substances as part of the inflammatory linked with the central nervous system long reaction. The mechanism of high altitude pul- before the relationship to was monary cedema is uncertain (Hultgren, Spickard suspected. Thomas Willis (1679) divided and Lopez, 1962). asthma into two groups, one associated with bronchial obstruction, and the other he called Clinical Picture convulsive asthma, in which the lungs were . (Acute left ventricular fail- normal and the cause of the disorder lay in ure). on September 30, 2021 by guest. Protected the nerves controlling respiration. Thus Willis The clinical picture of acute pulmonary stated that he had . . . "clearly unfolded by is similar whatever the underlying cause. anatomical observations that the cause of a In routine clinical practice however acute pul- convulsive asthma sometimes consists in the monary cedema is usually due to left ven- hinder part of the head near the origin of the tricular failure. nerves." Morgagni (1769) in the famous De The clinical picture was well described in Sedibus et Causis Morborum (The Seats and 1832 by James Hope (Fig. 2) who in discussing Causes of Disease) describes the relationship asthma noted that cardiac asthma comprised between head and subsequent pulmonary .. . "by far the greatest number of the most cedema. It is now suggested that any acute severe and fatal cases of the disease." Hence cerebral disturbance may lead to massive stimu- the term cardiac asthma derives historically lation of the sympathetic system with a result- from the fact that hitherto severe paroxysmal ant shift of blood from areas of high constrictor dyspnoea arising from the heart had not been potential in the systemic circulation to the differentiated from other forms of asthma. pulmonary circulation which is of low con- Hope's description of cardiac asthma is so Postgrad Med J: first published as 10.1136/pgmj.40.465.404 on 1 July 1964. Downloaded from July, 1964 FINN: Pulmonary Oedema 407 his chest and muttering a fervent invocation for death to put a period to his sufferings." Hope also notes that the respiration might be ."wheezing and performed with violent efforts of all the muscles of respira- tion both ordinary and auxiliary. The inspi- rations are high and accomplished with apparently little descent of the diaphragm, and the expirations are short and imperfect. The surface is chilly, the extremities are cold, and the face is pale and sometimes, livid." He goes on to say that often . . . "There is violent and in suffocative paroxysms, accompanied, at first, with scanty expecto- ration of viscid , but ending in a copious and free discharge of thin, trans- parent, frothy fluid, occasionally intermixed with blood. This evacuation by disgorging the pulmonary capillaries, affords great relief to the cough and dyspnoea." Apart from noting that the patient will often go to the window in an attempt to get fresh air, and that he is usually soaked in , there is little to add to Hope's clinical descrip- tion. There is a tachycardia and there may by copyright. be a pulsus alternans. The may be either raised or lowered. Occasionally FIG 2.-James Hope (1801-1841). (Courtesy of the an arrhythmia is present, and a Wellcome Historical Medical Museum). Born is usually audible. Pulmonary signs depend on in Stockport, Cheshire, and became a Physi- cian to St. George's Hospital. Attributed his the site of the cedema; thus if it is pericapillary success to the advice given him by his father: little abnormal will be heard, but if it is intra- 1. Never keep a patient ill longer than you can alveolar then crepitations and fine rales will help. 2. Never take a fee to which you do not be audible throughout the lung fields. Oedema feel yourself entitled. 3. Always pray for your

patients. of the bronchial walls together with excessive http://pmj.bmj.com/ bronchi,al secretions may lead to secondary detailed and well written that it could hardly bronchospasm. In some patients bronchospasm be bettered today .. . "The fit is, on the whole, may appear to dominate the clinical picture, more apt to supervene during the evening or and this is said to occur mainly in those with early part of the night. From a slumber fraught pre-existing or asthma. with the horrors of a hideous dream he starts Investigations are rarely carried out in acute up with a wild exclamation ... sitting with the pulmonary cedema. The chest X-ray will show trunk bent forwards and the elbows or fore- fleecy mottling spreading from the hila (Figs. on September 30, 2021 by guest. Protected arms resting on the drawn-up knees. The latter 3 and 4). The electrocardiogram may show an position he assumes when attacked by a arrhythmia or evidence of myocardial damage, paroxysm of dyspnoea, sometimes however ex- and catheter studies have demonstrated a tending the arms against the bed on either side, markedly raised pressure. to afford a firmer fulcrum for the muscles of respiration. With eyes widely expanded and Subacute Pulmonary Oedema starting, eyebrows raised, nostrils dilated, and The dividing line between pulmonary con- the head thrown back at every respiration, gestion (pulmonary venous hypertension) and ghastly and haggard he casts around a hurried, subacute pulmonary oedema is not clear, and distracted look of horror, of anguish, and of it is likely that dyspnoea in chronic heart failure supplication; now imploring, in plaintive moans, is partly due to pulmonary cedema. quick, broken accents and stifled voice, the Several factors tend to prevent the develop- assistance already lavished in vain, now up- ment of cedema in the chronically congested braiding the impotency of medicine; and now, lung. Recent studies on artificially induced in an agony of despair, dropping his head on failure in animals (using A-V shunts) have Postgrad Med J: first published as 10.1136/pgmj.40.465.404 on 1 July 1964. Downloaded from 408 POSTGRADUATE MEDICAL JOURNAL July, 1964

(a) by copyright. http://pmj.bmj.com/ on September 30, 2021 by guest. Protected

(b) FIG. 3.-(a) Pulmonary cedema associated with acute nephritis. (b) Resolution of cedema 10 days later. demonstrated greatly increased ly,mph drainage from the lung (Uhley and others, 1962). It FIG. 4.-(a) Acute pulmonary cedema caused by left has therefore been suggested that chronic ex- ventricular failure and cessive ultrafiltration leads to an increased run- in a patient with chronic bronchitis. off capacity of the lymphatics, with resultant (b) Resolution of cedema 48 hours later. Note presence of fibrosis and emphysema together protection from overt oedema. That this with an old tuberculous lesion at the right mechanism is operative in man is well demon- apex. Postgrad Med J: first published as 10.1136/pgmj.40.465.404 on 1 July 1964. Downloaded from

July, 1964 FINN: Pulmonary Oedema 409 and bronchospasm dominate the picture. The heart is often enlarged, pulsus alternans may be noted, and a triple rhythm is often heard. The pulmonary circulation time is increased, and there is a reduction in all fractions of the lung volume except the residual air. Catheter studies will show a raised end-diastolic pressure in the left ventricle, and a raised left atrial pressure with a steep Y descent. A large "a" wave may be seen on the apex cardiogram (Coulshed and Epstein, 1963). Much recent work has shown that subacute pulmonary oedema and pulmonary venous hypertension may first be demonstrated radio- logically. The radiological signs have been well documented and include enlarged hilar shadows with fuzzy outlines, enlargement of the upper lobe pulmonary , small bilateral pleural effusions and some perihilar shadowing (Simon, 1961). Subacute pulmonary oedema is common in mitral stenosis, and engorged basal pulmonary lymphatics (Kerley's lines) are well seen, but also occur to a lesser extent in other forms of pulmonary oedema. Haemo-

may be seen in long standing cases by copyright. and occasionally intrapulmonary ossific nodules FIG. 5.-Long standing pulmonary venous hyper- may develop (Galloway, Epstein and Coulshed, tension with basal septal lines and a fibrosed 1961). interlobar fissure in a patient with mitral stenosis (By courtesy of Dr. C. M. Ogilvie). Treatment of Acute Pulmonary Oedema strated by the engorged basal pulmonary lym- 1. Posture: Placing the patient in a sitting phatics or septal lines, so commonly seen in position will reduce intrapulmonary blood mitral stenosis (Fig. 5). Further protective volume by increasing the vital capacity and by http://pmj.bmj.com/ mechanisms such as thickening of the capillary lowering right ventricular filling pressure. The walls and , probably conscious patient will naturally assume the most contribute to the long survival in mitral stenosis. comfortable position, but the importance of The clinical picture requires no elaboration. posture should not be forgotten in the confused There is dyspnoea which is at first exertional, or semi-conscious patient. This simple pro- but which gradually progresses until present cedure will often abort nocturnal episodes of at rest. The dyspnoea due to pulmonary con- cardiac asthma without recourse to other gestion is related to posture (orthopncea). The methods. on September 30, 2021 by guest. Protected sudden development of "bronchitis" or a noc- 2. Morphia: is undoubtedly the most valuable turnal cough in the elderly should always drug in the treatment of acute pullmonary raise the suspicion of impending left ventricular cedema, and a i to i grain (15-20 mg.) should failure. Bronchitic symptoms such as a chronic be given intramuscularly or a i grain (10 mg.) cough associated with a little and intravenously. Its life saving action rests on wheezing, may occur in subacute pulmonary its ability to break the vicious circle (Fig. 1) oedema, and are particularly common in which operates in acute pulmonary cedema. patients with mitral stenosis. The intense dyspnoea produces great distress Physical examination may reveal evidence and anxiety, leading to a rapid tachycardia of the underlying cause, such as aortic or mitral which further increases the work of the already vailve disease, and there may be a history of failing left ventricle, thus leading to further anginal pain, and appropriate electrocardio- decompensation and pulmonary cedema, and graphic evidence of underlying coronary artery hence to even greater dyspnoea. As the pul- disease. Basal crepitations or small basal monary oedema increases exchange is effusions may be detected; occasionally rales impaired and severe hypoxia may develop which Postgrad Med J: first published as 10.1136/pgmj.40.465.404 on 1 July 1964. Downloaded from 410 POSTGRADUATE MEDICAL JOURNAL July, 1964 further reduces myocardial efficiency, and may able left ventricular failure. It acts by rapidly lead to loss of vascular tone and the develop- reducing intrapulmonary blood volume. About ment of profound circulatory collapse. The one pint of blood should be taken from an arm principle site of action of morphia is on the , but in exceptional circumstances intra- higher cortical centres, lowering the level of arterial puncture of the femoral artery can be consciousness and thus relieving the intense employed. Medical venesection using tourni- anxiety which perpetuates this vicious circle. quets applied to the limbs will have the same The direct depressant action of morphia on the effect. respiratory centre is probably of secondary im- 6. Oxygen: Severe pulmonary cedema may portance. produce arterial hypoxia due primarily to air- 3. Aminophylline: This drug is commonly way obstruction caused by fluid. The resulting used in this country, and is given intravenously anoxia further reduces myocardial efficiency in a dose of 0.25-0.5 gram. Its principle action and the administration of oxygen is of value. is the relief of airway obstruction due to expira- 7. Atropine: This drug has been recommended tory bronchospasm. It also 'lowers venous to reduce bronchial secretions, but it is of doubt- pressure, acts as a respiratory stimulant, and ful value in pulmonary oedema. It has been may be a myocardial stimulant. The value used in neurogenic pulmonary cedema associat- of aminophylline in acute pulmonary cedema ed with extreme bradycardia of vagal origin. has however been questioned (Luisada and 8. The Management of Abnormal Rhythms: Cardi, 1956), and it should never be used in In cases which do not preference to In certain cases respond to treatment morphia. it can fairly rapidly it is always worthwhile doing an be difficult to distinguish between cardiac and electrocardiogram, as an abnormal rhythm bronchial asthma, especially in subjects with such as ventricular tachycardia or uncontrolled a history of chronic bronchitis or asthma; and auricular fibrillation may be detected. by copyright. The in these circumstances morphia could be abnormal dangerous and a trial of aminophylline is justi- rhythm may have precipitated the fied. attack of pulmonary cedema, or it may have started during the attack. Reversion to sinus 4. Digitalis: It is welil known that digitalis rhythm by suitable methods, such as intra- strengthens the myocardial muscle in the heart- venous procaine amide (under ECG control) lung preparation, and recent studies using strain in ventricular tachycardia, will often terminate gauges applied to the exposed human heart the attack of pulmonary cedema. The sudden during extra-corporeal by-pass procedures have onset of a rapid auricular fibrillation often fully confirmed this finding (Braunwald, Blood- precipitates acute pulmonary cedema in patientshttp://pmj.bmj.com/ well, Goldberg and Morrow, 1961). Intravenous with mitral stenosis, and the use of digitalis in use of the short acting glycosides such as this situation is justified. Complete heart block strophanthin (1 mg. of ouabain) is usually may precipitate pulmonary cedema following recommended, but it is doubtful whether they a myocardiall infarct, and the use of steroids have any advantage over intravenously admin- may restore sinus rhythm, possibly by reducing istered digoxin (1 mg.). Care should be taken cedema and hence hypoxia in the region of the if digoxin has been given previously, and A-V node (Printzmetal and Kemmamer, 1954). smaller doses used. Digoxin is absolutely con- In these circumstances the sodium-retaining on September 30, 2021 by guest. Protected traindicated in acute pulmonary cedema due action of steroids should be counteracted by to mitral stenosis, as it will increase right ven- the concomitant use of a diuretic. tricular output and further increase the pulmon- 9. Intermittent Positive Pressure ary cedema. It has furthermore been suggested : that (I.P.P.B./I-02). This technique utilising oxygen digoxin may always have a greater effect and inspiratory up to 45 cm. of water, on a healthy ventricle, and it may therefore has been used by Miller and Sproule (1959) in increase right ventricular outputl to a greater over 350 cases, and they describe their results extent than that of the failing left ventricle, thus as usually remarkable and often dramatic. In exaggerating the degree of pulmonary cedema. the apparatus described, 100% oxygen was Thus some authorities would not recommend used and the intravenous digoxin in the treatment of acute inspiratory pressure could be pulmonary cedema due to left ventricular readily adjusted. This technique should be failure. used only when simple measures have failed. It is now well recognised that the anoxic 5. Venesection: If other methods fail vene- disturbance in acute pulmonary cedema can section may be life saving in otherwise intract- be profound, and arterial oxygen saturations Postgrad Med J: first published as 10.1136/pgmj.40.465.404 on 1 July 1964. Downloaded from July, 1964 FINN: Pulmonary Oedema 411 as low as 30% have been recorded. The anoxia tion of , inhalation should be discon- is not due to a defect, but is a dis- tinued for 15 'minutes per hour. tribution defect, and is largely due to the 11. The Artificial Kidney: Dialysis offers a frothy fluid which obstructs the airways. rational method of rapidly removing excess Physiological studies have shown that I.P.P.B./ fluid from the body, and thus reducing pulmon- I-02 rapidly corrects the arterial oxygen satura- ary congestion. Pulmonary cedema due to cir- tion, and this in turn will improve cardiac culatory overload is most commonly seen in function and increase vascular tone. patients with anuria when the fluid intake has It has previously been pointed out that the not been satisfactorily regulated, but can also dyspncea in acute pulmonary cedema is prim- occur in elderly subjects who have been over- arily due to the increased transfused. Ultrafiltration with the artificial resulting from the increased kidney can be achieved by raising the pressure due to frothy cedema fluid, and the diminished in the venous circuit, and lowering the dialysing compliance. The latter factor is due to a com- fluid pressure by limiting its flow. The success- bination of interstitial congestion, increased pul- ful use of this technique in pulmonary cedema monary vascular pressure, and increased pul- associated with acute renal failure has recently monary blood volume. been described (Logan, Williams, Edwards and I.P.P.B./I-02 may be of value in several Watson, 1964). It should of course be empha- ways. I.P.P.B./I-02 significantly decreases the sized that rigid restriction of fluid intake (to work of respiration and so relieves the sensation about 400 ml. daily) will usually prevent, or of dyspnoea. The improved ventilation relieves control, pulmonary oedema associated with hypoxia and also increases lymphatic flow, thus anuria or severe oliguria. Exchange trans- helping to reduce the cedema. The positive fusion can also be carried out during dialysis pressure during inspiration increases the intra- by the replacement of whole blood with packed alveolar pressure, and so decreases the trans- by copyright. capillary pressure gradient, and hence the cells. This procedure effectively reduces plasma tendency towards cedema formation. The re- volume and there is no risk of inducing hyper- lief of dyspnoea will tend to reduce the increas- kalaemia during dialysis. ed depth of respiration during extreme volun- 12. Diuretics: There is no time for diuretics tary effort, and will therefore lower the cardiac to act in acute pulmonary cedema, but they in-flow load and hence reduce right ventricular are of great value in the management of sub- output. acute pulmonary cedema. With the plethora Acute pulmonary cedema can never exist in of diuretics now available, resistant cedema is a "steady state", and must therefore always be not commonly seen in medical wards. The http://pmj.bmj.com/ progressive, increasing pulmonary cedema commonest cause of failure to respond to diur- throwing an extra load on the heart and leading etic therapy is hypokalaemia, and severe hypo- to further ventricular decompensation. I.P.P.B./ kalaemia may be present with a normal serum 1-02 breaks this vicious circle of progressive potassium level. The diagnosis of potassium decompensation at many points, and may there- depletion is best made by a high index of clinical fore be life-saving. suspicion of the circumstances, such as pro- longed diuretic therapy, in which potassium loss 10. Antifoaming Agents: Oedema fluid in the may have arisen. The clinical picture of on September 30, 2021 by guest. Protected alveoli and smaller bronchi is not of great anorexia, apathy, mental confusion, unusual significance until the of the muscle weakness and abdominal distension, to- fluid reaches a critical point and foaming occurs. gether with oliguria and a moderately raised This leads to an enormous increase in volume blood urea should suggest hypokalaemia; and and rapidly gives rise to a ventilation defect and the electrocardiographic picture of S.T. de- hypoxia, which reduces myocardial efficiency pression, T wave inversion, and "U" waves and produces further transudation and foaming. in the left praecordial leads should support This vicious circle can be broken by the use the diagnosis. Hypokalaemia is best corrected of antifoaming agents (Luisada and Cardi, with oral potassium. Diuretic resistance also 1956). Ethyl alcohol is an efficient antifoaming occurs with low chloride levels, and ammonium agent, and oxygen bubbling through a 95% chloride 8 grammes daily in divided doses for alcohol is administered via a nasal a few days is worth trying. Sodium restriction catheter, and can also be given by I.P.P.B./I-02. is a valuable adjunct to diuretic therapy, and The flow rate is gradually increased to 10 litres severe restriction using a rice diet for a few a minute. In order to avoid excessive absorp- days will often improve resistant cedema as- Postgrad Med J: first published as 10.1136/pgmj.40.465.404 on 1 July 1964. Downloaded from 412 POSTGRADUATE MEDICAL JOURNAL July, 1964 sociated with pulmonary congestion and other- emboli, and introspection leading to mental wise intractable dyspnoea. In terminal cases depression. which have proved resistant to all diuretics It should be remembered that rest includes great relief from dyspnoea may be afforded by mental rest, and reassurance and nocturnal simple mechanical measures such as the use of sedation are therefore of great importance. a cardiac bed, pleural aspiration and acupunc- Fear of the night is very common in patients ture. with orthopnoea, and the provision of a good 13. The Underlying Cause: It is rarely pos- night's sleep can lead to considerable clinical sible to treat the underlying cause during an at- improvement. If the simpler barbiturates do tack of pulmonary cedema, and one has to not prove satisfactory, then more powerful seda- rely on general measures to reduce intrapul- tives of the morphia group are justified. monary blood volume. Attention to the general health is important The reversion of abnormal rhythms is an as the correction of associated conditions will exception to this rule, and occasionally in re- often greatly improve myocardial function. sistant pulmonary cedema due to hypertension Thus anaemia, obesity and minor grades of it is justifiable to lower the blood pressure; thyrotoxicosis should be looked for, and cor- subcutaneous ansolysen in small doses is a rected if necessary. Infections increase capil- powerful hypotensive agent, but must be used lary permeability in patients with mitral steno- with caution. Intractable pulmonary cedema sis. It is therefore mandatory to treat infections occasionally occurs in mitral stenosis, especially promptly and vigorously, and there is a case during pregnancy, and emergency mitral valvot- for prophylactic vaccination in omy has been used in these circumstances, but patients with mitral stenosis. Women with carries a high mortality. is known valvular disease should be advised as to their to increase capillary permeability and may pre- ability to undertake a pregnancy. If pregnancy cipitate acute pulmonary cedema, and in this is thought to incur a significant risk, then opera-by copyright. situation therapy is indicated. In tive intervention or some form of birth control acute allergy where the pulmonary cedema is should be considered. due to increased capillary permeability, corti- Treatment of the underlying cause is oc- sone and antihistamines are valuable. casionally possible in heart disease, and would include the use of hypotensive agents, and the correction of valve lesions by valvotomy and Preventive Measures valve The most common cause of acute pulmonary replacement.

oedema is left ventricular failure, and it is now http://pmj.bmj.com/ generally accepted that this is usually due to the Summary sudden trapping of an extra few hundred milli- litres of blood in a previously congested pul- 1. The various causes of pulmonary cedema monary circulation. In other words acute pul- are reviewed. monary cedema is usually a of 2. It is stressed that acute pulmonary oedema subacute pulmonary cedema and rarely arises cannot exist in a "steady state", but is in a previously normal lung. The vital import- usually progressive by means of a vicious ance of this point is not always appreciated, circle mechanism. on September 30, 2021 by guest. Protected but it does suggest that the early recognition 3. Morphia is the most valuable drug in the and treatment of subacute pulmonary cedema treatment of acute pulmonary cedema, but should prevent many cases of cardiac asthma. numerous other measures are currently Diuretic therapy supplemented by salt restric- available. tion is of great value in controlling subacute pulmonary cedema, and maintenance therapy 4. Acute pulmonary cedema in routine clin- with digoxin will improve myocardial function. ical practice is usually due to left ventricu- Patients with mild heart failure should avoid lar failure. It is emphasized that acute excessive exercise, and the amount of rest re- attacks of pulmonary cedema (cardiac quired should be estimated for each individual asthma) usually occur in a previously con- patient. With modern diuretic therapy the gested lung, and hence the recognition and tendency has been to allow more activity, and treatment of subacute pulmonary cedema it should be remembered that the present trend may prevent their occurrence. in is to avoid prolonged immobility I wish to thank Dr. E. Noble Chamberlain and because of the twin dangers of pulmonary Dr. C. A. St. Hill for their valuable comments. Postgrad Med J: first published as 10.1136/pgmj.40.465.404 on 1 July 1964. Downloaded from July, 1964 FINN: Pulmonary Oedema 413 REFERENCES BRAUNWALD, E., BLOODWELL, R. D., GOLDBERG, L. I. and MORROW, A. G. (1961): Studies on Digitalis: IV. Observations in man on effects of digitalis preparations on contractility of the non-failing heart and on total . J. clin. Invest. 40, 52. CAMERON, G. R. (1948): Pulmonary Oedema. Brit. med. J., i, 965. CAMPBELL, G. S., HADDY, F. J. and VISSCHER, M. B. (1949): Effect of acute bradycardia on pulmon- ary vascular pressures in anaesthetised dogs. Proc. Soc. exp. Biol. (N.Y.). 71, 52. COULSHED, N. and EPSTEIN, E. J. (1963): The apex cardiogram. Its normal features explained by those found in heart disease. Brit. Heart J. 25, 697. DRINKER, C. K. (1945): and . Cambridge, Mass.: Harvard University Press. GALLOWAY, R. W., EPSTEIN, E. J. and COULSHED, N. (1961): Pulmonary ossific nodules in mitral valve disease. Brit. Heart J. 23, 297. HOPE, J. (1832): A treatise on the diseases of the heart and great vessels. p. 346. London: William Kidd. HULTGREN, H., SPICKARD, W. and LOPEZ, C. (1962): Further studies of high altitude pulmonary cedema. Brit. Heart. J. 24, 95. KEATS, A. S. and MITHOFER, J. C. (1955): The mechanism of increased intracranial pressure induced by . New Engl. J. Med. 252, 1110. LAENNEC, R. T. H. (1829): A treatise on diseases of the chest and on mediate . p. 178. Translated by Forbes, J. London: J. T. Underwood. LEADING ARTICLE (1962): Lancet, i, 468. LOGAN, W. F. W. E., WILLIAMS, A. J., EDWARDS, E. C. and WATSON, D. C. (1964): Pulmonary cedema complicating acute renal failure. Postgrad med. J. 40, 24. LUISADA, A. A. and CARDI, L. (1956): Acute pulmonary edema. Circulation. 13, 113. MCMICHAEL, J. (1937): Postural charges in cardiac output and respiration in man. Quart. J. exp. Physiol. 27, 55. MCMICHAEL, J. (1939): Hyperpncea in heart failure. Clin. Sci. 4, 19. MILLER, W. F. and SPROULE, B. J. (1959): Studies on the role of intermittent inspiratory positive pressure oxy- by copyright. gen breathing (I.P.P.B./1-02) in the treatment of pulmonary cedema. Dis. Chest. 35, 469. MORGAGNI, J. P. (1769): De Sedibus et Causis Morborum. Book 4. Letter 52, Article 9. Translated by Alexander, B. (London). PAINE, R., SMiTH, J. R. and HOWARD, F. A. (1952): Pulmonary edema in patients dying with disease of the central nervous system. J. Amer. med. Ass. 149, 643. PRINTZMETAL, M. and KENNAMER, R. (1954): Emergency Treatment of Cardiac Arrhythmias. J. Amer. med. Ass. 154, 1049. SARNOFF, S. J. (1952): Neurohamodynamics of acute pulmonary cedema. J. Physiol. 117, 38p.

SCHMIDT, C. F. and LIVINGSTON, A. E. (1933): The action of morphine on the mammalian circulation. J. http://pmj.bmj.com/ Pharmacol. exp. Ther. 47, 411. SIBLER, R. and CLERKIN, E. P. (1959): Pulmonary edema in acute heroin poisoning. Amer. J. Med. 27, 187. SIMON, M. (1961): The pulmonary vessels in incipient left ventricular decompensation. Circulation. 24, 185. UHLEY, H. M., LEEDS, S. E., SAMPSON, J. J. and FRIEDMAN, M. (1962): Effect of pulmonary lymphatics in chro- nic pulmonary edema. Circulat Res. 11, 966. VISSCHER, M. B., HADDY, F. J. and STEPHENS, G. (1956): The physiology and pharmacology of pulmonary cede- ma. Pharmacol. Rev. 8, 389. WILLIS, T. (1679): Pharmaceutice Rationalis, 2nd Part, p. 82. London: Dring, Harper and Leigh. on September 30, 2021 by guest. Protected