OR~IGINAL CONTRIBUTION
Arterial Blood Gases in Acute Pulmonary Edema Norman J. Diamond, MD Jerome Schofferman, MD John W. Elliott* Torrance, California
rterial b l o o d gas and pH m e a s u r e m e n t s in 82 patients with acute pulL0nary e d e m a of c a r d i o g e n i c origin entering the e m e r g e n c y departLent varied w i d e l y and w e r e unpredictable using clinical examination. he m e a n arterial o x y g e n t e n s i o n (PaO2) m e a s u r e d in 71 p a t i e n t s ireathing r o o m air w a s 59 mm Hg. Fourteen of the 82 patients were ~cidemic; 35, a l k a l e m i c a n d 33 h a d a pH in the n o r m a l range. The icidemic g r o u p h a d m a r k e d l y l o w e r PaO2, all u n d e r 60 mm Hg. Oxygen ld f u r o s e m i d e w e r e u s e d in all cases and effectively c o r r e c t e d the gpoxia and r e d u c e d p u l m o n a r y congestion. Other drugs u s e d included ~inophylline (14 patients), m o r p h i n e sulfate (9 patients) and digoxin (3 ~tients). Five o f the nine patients w h o r e c e i v e d m o r p h i n e w e r e hyper!arbic initially but the CO2 retention did not w o r s e n . No patient died luring the initial 48 hours. This study reiterates the i m p o r t a n c e of diecting t h e r a p y at ventilatory and cardiac abnormalities and points out ~e value of arterial b l o o d gas monitoring to a s s e s s the initial status, 0nitor the patient's course, and to select drug therapy.
~iamond NJ, Schofferman J, Elliott JW: Arterial blood gases in acute pulmonaryedema. JACEP 5:497-500, July 1976. edema, pulmonary; blood gases and. ~NTRODUCTION Arterial blood gases m a y be one of e best p a r a m e t e r s to e v a l u a t e the verity of acute p u l m o n a r y e d e m a p a t i e n t s s e e n in t h e e m e r g e n c y ~epartment. Much h a s been w r i t t e n ~egarding the implications of abnor-
l!~
•~ientific r e s eatAssembly nthet eannual d in
ACEP/EDNA Las Vegas,
~evada, October, 1975. ~r0m the Receiving-Emergency Depart~eat Harbor General Hospital, Torrance, California, and UCLA School of Medi~iae,* Los Angeles, California. dress for reprints: Norman J. Diamond, , Receiving-Emergency Department, arbor General Hospital, 1000 West Car~0aStreet, Torrance, California 90509.
~P
July 1976
malities. Anthonisen and Smith 1 suggest t h a t r e s p i r a t o r y acidosis signals a t e r m i n a l stage in p u l m o n a r y edema. However, more r e c e n t l y Miller's 2 w o r k h a s shown low m o r t a l i t y r a t e when hyp'ercarbia is recognized and t r e a t e d a p p r o p r i a t e l y . A v e r y 3 est i m a t e d t h a t a t least 25% of his patients with pulmonary edema had a combined r e s p i r a t o r y a n d metabolic acidosis. A b e r m a n 4 observed a wide s p e c t r u m of a c i d - b a s e d i s t u r b a n c e s w i t h frequent metabolic acidosis. In addition, s e v e r a l e d i t o r i a l s have rec e n t l y called a t t e n t i o n to t h e wide r a n g e of a c i d - b a s e d i s t u r b a n c e s in acute p u l m o n a r y edema.~, ~ We have reviewed t h e records of 82 e m e r g e n c y d e p a r t m e n t p a t i e n t s with
acute p u l m o n a r y e d e m a in order to e v a l u a t e a r t e r i a l blood gas r e s u l t s b e f o r e t r e a t m e n t a n d to c o r r e l a t e them with morbidity, mortality, choice of t h e r a p y a n d p a t i e n t outcome.
METHOD H o s p i t a l r e c o r d s of 138 p a t i e n t s with the p r i m a r y diagnosis of acute cardiogenic p u l m o n a r y edema, seen from July, 1974, to May, 1975, in our e m e r g e n c y d e p a r t m e n t , w e r e reviewed. The diagnosis of acute pulm o n a r y e d e m a r e q u i r e d the presence of b i b a s i l a r rales u n e x p l a i n e d by infection or a n y other cause and a chest x - r a y film i n t e r p r e t e d as d e m o n s t r a t ing p u l m o n a r y v a s c u l a r congestion. P a t i e n t s w i t h o u t b i b a s i l a r r a l e s or w i t h o u t x - r a y film evidence of congested p u l m o n a r y v a s c u l a t u r e were excluded. Those with significant p r e - e x i s t i n g l u n g p a t h o l o g y (chronic obstructive p u l m o n a r y disease) were also e x c l u d e d . E i g h t y - t w o p a t i e n t s fulfilled our criteria. T h e i r presenting symptoms, physical findings, electrocardiograms, chest x.-ray films, initial arterial blood gas results, emergency department treatment and final outcome provide the basis for this report.
RESULTS Clinical Findings. Presenting s y m p t o m s a n d p h y s i c a l findings in t h e 82 p a t i e n t s were reviewed (Table
Volume 5 Number 7 Page 497
Table 2 ARTERIAL BLOOD GAS RESULTS N=82
Table 1 INITIAL S Y M P T O M S AND PHYSICAL FINDINGS N=82 Presenting Symptoms
PaO2 (71 Patients) measured while breathing room air Average PaO2 = 59 mm Hg No. %
Sudden onset of breathlessness Orthopnea Chest pain
75 (91) 45 (55) 33 (40)
Paroxysmal nocturnal dyspnea
25 (30)
Physical Findings
Hypertension
40 (49)
Hypotension Tachycardia
0 35 (43)
Peripheral edema
32 (39)
Atrial fibrillation
15 (18)
1). S h o r t n e s s o f b r e a t h , 75 c a s e s (91%), a n d h y p e r t e n s i o n , 40 cases (49%), w e r e o b s e r v e d m o s t frequently. A t r i a l f i b r i l l a t i o n was prese n t in 15 (18%) p a t i e n t s . A c u t e m y o c a r d i a l infarction w a s suspected first by h i s t o r y a n d i n i t i a l electroc a r d i o g r a m in 20 p a t i e n t s a n d was c o n f i r m e d by t y p i c a l e l e c t r o c a r d i o graphic or enzyme evolution in 15. A r t e r i a l o x y g e n t e n s i o n (Pa(h). Arterial blood gas results were a v a i l a b l e for all 82 p a t i e n t s (Table 2). In 71, e v a l u a t e d while b r e a t h i n g room a i r a n d s t u d i e d before t r e a t ment, the a v e r a g e PaO~ was 59 m m Hg. Of these, 36 (44%) h a d a PaO2 less t h a n 60 m m Hg a n d 16 (20%) h a d a P a ( h less t h a n 50 m m Hg. Arterial carbon dioxide tension (PaCO~). H y p e r c a p n i a was p r e s e n t in 11 patients; h y p o c a p n i a in 41; 30 pat i e n t s h a d n o r m a l PaCO2. All b u t one of t h e h y p e r c a p n i c p a t i e n t s h a d acidemia. A r t e r i a l b l o o d p H (Table 2). The acid-base s t a t u s of t h e 82 p a t i e n t s was assessed by the c r i t e r i a proposed by the Ad Hoc C o m m i t t e e of the New Y o r k A c a d e m y of S c i e n c e Conference. 7 A n o r m a l pH was observed in 33 (40%) p a t i e n t s a l t h o u g h five of these had a m i x e d acid-base abnormality. A c i d e m i a ( p H < 7.36) was p r e s e n t in 14 (17%) patients. A m o n g these, five h a d p u r e r e s p i r a t o r y acidosis,
Page 498 Volume 5 Number 7
No.
%
36
(44)
16
(20
Normal pH (7.36-7.44) Mixed acid/base abnormality
33 5
(40)
Acidemia (pH < 7.36) Pure respiratory acidosis
14 5
(17)
PaO2 60 mm Hg PaO2 50 mm Hg pH Distribution
Respiratory & metabolic acidosis
5
Respiratory acidosis & metabolic alkalosis
1
Metabolic acidosis & respiratory alkalosis
3
Alkalemia (pH >7.44) Pure respiratory alkalosis Respiratory alkalosis & metabolic acidosis Respiratory alkalosis & metabolic alkalosis
35 23
(43)
9
3
/
Table 3 T R E A T M E N T MODALITIES No. of patients
Oxygen
82
Furosemide Aminophylline
82 14
Morphine Rotating tourniquets
9 9
Digoxin
3
Phlebotomy
3
five h a d c o m b i n e d r e s p i r a t o r y a n d metabolic acidosis, one h a d respiratory acidosis w i t h metabolic alkalosis and t h r e e had p r i m a r y metabolic acidosis w i t h c o m p e n s a t o r y respiratory alkalosis. A l k a l e m i a (pH >7.44) was found in 35 (43%) cases. Of these, 23 (28%) had pure respiratory alkalosis, 9 ' (1L%) h a d r e s p i r a t o r y a l k a l o s i s with metabolic acidosis and 3 (4%) h a d respiratory alkalosis combined with metabolic alkalosis. I n i t i a l t r e a t m e n t (Table 3). All 82 patients received oxygen and furosemide. Aminophylline was given to 14 (17%), m o r p h i n e sulfate
to 9 (11%) and d i g i t a l i s glycosides t~ 3 (4%). A d d i t i o n a l m e a s u r e s include the use of r o t a t i n g tourniquets in~ (11%) and p h l e b o t o m y in 3 (4%). T h e p a t i e n t s who r e c e i v e d m0r: phine sulfate (Table 4) Were am0n~ t h e m o s t a g i t a t e d a n d decompen. sated in our group. No d e a t h s occurred e i t h e r in the e m e r g e n c y d e p a r t m e n t or during ths i n i t i a l 48 hours of h o s p i t a l care. DISCUSSION A r t e r i a l blood gas measurements have become e s s e n t i a l in the care of the c r i t i c a l l y ill. Since medical stu.{ dents, nurses a n d respiratory' t h e r a p i s t s have a s s u m e d the resp0n' sibility for o b t a i n i n g a r t e r i a l blood, it is i m p o r t a n t to a s c e r t a i n the useful" n e s s of a r t e r i a l b l o o d g a s meas" u r e m e n t s in acute p u l m o n a r y edema. T h i s r e t r o s p e c t i v e s t u d y of 82 pa, t i e n t s was u n d e r t a k e n to determine t h e f r e q u e n c y of v a r i o u s acid-base a n d v e n t i l a t o r y d i s t u r b a n c e s re. v e a l e d b y t h e b l o o d g a s meaS' u r e m e n t s in the e m e r g e n c y depart" m e n t a n d t h e i m p l i c a t i o n of the arte' r i a l blood gas r e s u l t s with regard ~' s u b s e q u e n t t h e r a p y a n d outcome. ' T h e a v e r a g e a r t e r i a l oxygen teN' sion in t h i s group was 59 m m I4g,
July 1976
Table 4 ARTERIAL BLOOD GASES OF PULMONARY EDEMA PATIENTS GIVEN MORPHINE SULFATE 1
Age Sex
Blood Pressure
Pulse Rate
Respiratory Rate
Pa0=*
PaC0=*
pH*
62
M
260/140
140
28
38
50
7.12
48
35
7.31t
50
56
24
7.52
65
M M
250/140
74
F
76 59 34
6.96 7.15t 7.39
69
30
158/100
140 (30 minutes) 100
40
43 52 54
M
120/90
100
20
54
30
7.42
52
M
140/80
150
40
70
M
120
56 64 65 31 62
46 69 34 63 43
7.26 7.19t 7.53t 7.20 7.34t
72
M
130/90 62 20 (respiratory arrest-intubate)
44 104
56 40
7.00 7.27
56
M
160/80
57 71
61 39
7.21 7.43t
(after 24 hrs.)
120
40
*Breathing room air tSubsequent blood gases somewhat higher t h a n the 49 m m Hg reported by A b e r m a n i n 1971 in 50 similar p a t i e n t s . 4 This m a y be explained, in part, by exclusion of the sickest p a t i e n t s i n our group, who were g i v e n s u p p l e m e n t a l o x y g e n prior to m e a s u r e m e n t of blood gases. Respiratory alkalosis was present in half of our cases. The hyperventilation m i g h t be e x p l a i n e d by t h e hypoxic r e s p i r a t o r y d r i v e coupled with the effect of t h e s t i m u l a t e d pulmonary nerve fibers stretched by an e n g o r g e d p u l m o n a r y c a p i l l a r y bed." S i m i l a r to A b e r m a n ' s report, 4 metabolic acidosis was commonly associated w i t h t h e r e s p i r a t o r y alkalosis. H u c k a b e e s a t t r i b u t e s t h e metabolic acidosis to i n c r e a s i n g lactate production by poorly perfused tissues i n p a t i e n t s with hypoxia and reduced cardiac output. Eichenholz 9 adds that metabolic acidosis may result as a f a i l u r e of i n t e r m e d i a r y '~etabolism i n the presence of primary hypercapnia. Acidemia - - pure respiratory, pure ~etabolic or combined - - was present in 14 p a t i e n t s . P a t i e n t s w i t h Prior history of s i g n i f i c a n t obstructive lung disease were omitted from this report. Therefore, this hypoventilation m a y be r e l a t e d to a i r w a y °bStruction s e c o n d a r y to b r o n c h o -
J • PJuly 1976
spasm, peribronchial edema or foam. West TM has shown t h a t CO2 elimination is reduced a n d a r t e r i a l hypoxemia develops i n states of ventilation/ perfusion imbalance. Respiratory alkalosis was the most c o m m o n a b n o r m a l i t y a n d was associated more often with less hypoxic patients. However, a sizeable n u m b e r of a c i d e m i c p a t i e n t s was observed and who they were was not predictable, clinically, either i n our series or in others. 2-4 Clearly, the classical use of oxygen a n d m o r p h i n e to t r e a t p u l m o n a r y edema has been replaced by oxygen a n d f u r o s e m i d e . All 82 Of our pat i e n t s r e c e i v e d o x y g e n a n d furosemide. T h e r e were no d e a t h s a n d only rare deterioration. Plentiful oxygen delivery m a y f r e q u e n t l y be all t h a t is necessary to p a r t i a l l y relieve bronchospasm', tachypnea, metabolic acidosis and anxiety. Rotating t o u r n i q u e t s and phlebotomy w e r e n o t u s e d o f t e n e n o u g h to evaluate adequately. Neither our house staff nor other investigators 2-4 commonly used morphine. This may be due to the realization t h a t hypercapnia is seen more frequently t h a n previously appreciated. Nevertheless, our data on those p a t i e n t s given m o r p h i n e is r e a s s u r i n g (Table 4).
N i n e p a t i e n t s , ages 50 to 74, with m o d e r a t e to s e v e r e h y p o x i a a n d m a r k e d l y a b n o r m a l clinical findings were given m o r p h i n e sulfate i n the emergency department. All had EKG evidence of coronary a r t e r y disease and six h a d acute myocardial infarction. Five p a t i e n t s had hypercapnia (PaCO2 >50) and were acidemic. In three of these cases, with a very low i n i t i a l pH a n d high P a C ( h , the abn o r m a l blood gases were rapidly reversed by t h e t r e a t m e n t described a n d t h e y w e r e c e r t a i n l y n o t adversely affected by morphine sulfate. One p a t i e n t with elevated P a C ( h initially became more hypercapnic but reverted to n e a r n o r m a l values over 24 hours. A n o t h e r p a t i e n t suffered a respiratory arrest shortly after 4 mg of m o r p h i n e were a d m i n i s t e r e d intravenously. Immediate intubation was performed and the p a t i e n t was successfully resuscitated. Thus, morphine sulfate seems to be a safe drug when given to p a t i e n t s with severe p u l m o n a r y edema, provided arterial blood gases are monitored ser i a l l y a n d the p a t i e n t carefully observed. The r o u t i n e m o n i t o r i n g of blood gases i n p u l m o n a r y e d e m a i n the emergency department may have additional value. Rapid i m p r o v e m e n t in blood gases m a y postpone or prev e n t t h e u s e of m o r e h a z a r d o u s a g e n t s , s u c h as g l y c o s i d e s or aminophylline. These drugs and a c i d e m i a are very common precursors of cardiac arrest.11,12 The absence of s u d d e n death in our group of patients is e n c o u r a g i n g and m a y be r e l a t e d to less f r e q u e n t u s e of a m i n o p h y l l i n e a n d glycosides a n d rapid use of oxygen and furosemide.
REFERENCES 1. Anthonisen UR, Smith HJ: Respiratory acidosis as a consequence of pulmonary edema. A n n I n t e r n M e d 62:993-999, 1965. 2. Miller A, Chisid L, S a m a r t i n TG: Acute reversible respiratory acidosis in cardiogenic pulmonary edema. J A M A 216:1315-1319, 1971. 3. Avery WG, Samet P, Sackner MA: The acidosis of pulmonary edema. A m J M e d 48:320-324, 1970. 4. Aberman A, Fulop M: The metabolic and respiratory acidosis of acute pulmonary edema. A n n I n t e r n M e d 76:173-184, 1972. 5. Editorial: Acid-base imbalance in pulmonary edema. J A M A 216:1337, 1971.
V o l u m e 5 Number 7 Page 499
6. Editorial: Blood gas tensions in acute p u l m o n a r y edema. Lancet 1:1106-1107, 1972. 7. Ad-Hoc Committee of t h e New York Academy of S c i e n c e s Conference (November 23-24, 1964): S t a t e m e n t on acid-base terminology. A n n Intern Med 63:885-890, 1965.
Page 500 Volume 5 Number 7
8. Huckabee WE: Lactic acidosis. A m J Cardiol 12:663-666, 1963. 9. Eichenholz A: P r i m a r y hypocapnia: A cause of m e t a b o l i c acidosis. J A p p l i e d Physiol 17:283-288, 1962.
11. C a m a r a t a SJ, Weil MH, Hanashir, PK, et al: Cardiac arrest in the critiealll ill. I. A study of predisposing causes il 132 p a t i e n t s . C i r c u l a t i o n 44:688-69ii 1971. '~
10. West JB: Causes of carbon dioxide retention in lung disease. N Engl J Med 284:1232, 1971.
12. Kastor JA: Digitalis intoxicatio~ i~ patients with atrial fibrillation. Circala. tion 47:888-896, 1973.
July 1976 ~ )
Arterial Blood Gases in Acute Pulmonary Edema Norman J. Diamond, MD Jerome Schofferman, MD John W. Elliott* Torrance, California
rterial b l o o d gas and pH m e a s u r e m e n t s in 82 patients with acute pulL0nary e d e m a of c a r d i o g e n i c origin entering the e m e r g e n c y departLent varied w i d e l y and w e r e unpredictable using clinical examination. he m e a n arterial o x y g e n t e n s i o n (PaO2) m e a s u r e d in 71 p a t i e n t s ireathing r o o m air w a s 59 mm Hg. Fourteen of the 82 patients were ~cidemic; 35, a l k a l e m i c a n d 33 h a d a pH in the n o r m a l range. The icidemic g r o u p h a d m a r k e d l y l o w e r PaO2, all u n d e r 60 mm Hg. Oxygen ld f u r o s e m i d e w e r e u s e d in all cases and effectively c o r r e c t e d the gpoxia and r e d u c e d p u l m o n a r y congestion. Other drugs u s e d included ~inophylline (14 patients), m o r p h i n e sulfate (9 patients) and digoxin (3 ~tients). Five o f the nine patients w h o r e c e i v e d m o r p h i n e w e r e hyper!arbic initially but the CO2 retention did not w o r s e n . No patient died luring the initial 48 hours. This study reiterates the i m p o r t a n c e of diecting t h e r a p y at ventilatory and cardiac abnormalities and points out ~e value of arterial b l o o d gas monitoring to a s s e s s the initial status, 0nitor the patient's course, and to select drug therapy.
~iamond NJ, Schofferman J, Elliott JW: Arterial blood gases in acute pulmonaryedema. JACEP 5:497-500, July 1976. edema, pulmonary; blood gases and. ~NTRODUCTION Arterial blood gases m a y be one of e best p a r a m e t e r s to e v a l u a t e the verity of acute p u l m o n a r y e d e m a p a t i e n t s s e e n in t h e e m e r g e n c y ~epartment. Much h a s been w r i t t e n ~egarding the implications of abnor-
l!~
•~ientific r e s eatAssembly nthet eannual d in
ACEP/EDNA Las Vegas,
~evada, October, 1975. ~r0m the Receiving-Emergency Depart~eat Harbor General Hospital, Torrance, California, and UCLA School of Medi~iae,* Los Angeles, California. dress for reprints: Norman J. Diamond, , Receiving-Emergency Department, arbor General Hospital, 1000 West Car~0aStreet, Torrance, California 90509.
~P
July 1976
malities. Anthonisen and Smith 1 suggest t h a t r e s p i r a t o r y acidosis signals a t e r m i n a l stage in p u l m o n a r y edema. However, more r e c e n t l y Miller's 2 w o r k h a s shown low m o r t a l i t y r a t e when hyp'ercarbia is recognized and t r e a t e d a p p r o p r i a t e l y . A v e r y 3 est i m a t e d t h a t a t least 25% of his patients with pulmonary edema had a combined r e s p i r a t o r y a n d metabolic acidosis. A b e r m a n 4 observed a wide s p e c t r u m of a c i d - b a s e d i s t u r b a n c e s w i t h frequent metabolic acidosis. In addition, s e v e r a l e d i t o r i a l s have rec e n t l y called a t t e n t i o n to t h e wide r a n g e of a c i d - b a s e d i s t u r b a n c e s in acute p u l m o n a r y edema.~, ~ We have reviewed t h e records of 82 e m e r g e n c y d e p a r t m e n t p a t i e n t s with
acute p u l m o n a r y e d e m a in order to e v a l u a t e a r t e r i a l blood gas r e s u l t s b e f o r e t r e a t m e n t a n d to c o r r e l a t e them with morbidity, mortality, choice of t h e r a p y a n d p a t i e n t outcome.
METHOD H o s p i t a l r e c o r d s of 138 p a t i e n t s with the p r i m a r y diagnosis of acute cardiogenic p u l m o n a r y edema, seen from July, 1974, to May, 1975, in our e m e r g e n c y d e p a r t m e n t , w e r e reviewed. The diagnosis of acute pulm o n a r y e d e m a r e q u i r e d the presence of b i b a s i l a r rales u n e x p l a i n e d by infection or a n y other cause and a chest x - r a y film i n t e r p r e t e d as d e m o n s t r a t ing p u l m o n a r y v a s c u l a r congestion. P a t i e n t s w i t h o u t b i b a s i l a r r a l e s or w i t h o u t x - r a y film evidence of congested p u l m o n a r y v a s c u l a t u r e were excluded. Those with significant p r e - e x i s t i n g l u n g p a t h o l o g y (chronic obstructive p u l m o n a r y disease) were also e x c l u d e d . E i g h t y - t w o p a t i e n t s fulfilled our criteria. T h e i r presenting symptoms, physical findings, electrocardiograms, chest x.-ray films, initial arterial blood gas results, emergency department treatment and final outcome provide the basis for this report.
RESULTS Clinical Findings. Presenting s y m p t o m s a n d p h y s i c a l findings in t h e 82 p a t i e n t s were reviewed (Table
Volume 5 Number 7 Page 497
Table 2 ARTERIAL BLOOD GAS RESULTS N=82
Table 1 INITIAL S Y M P T O M S AND PHYSICAL FINDINGS N=82 Presenting Symptoms
PaO2 (71 Patients) measured while breathing room air Average PaO2 = 59 mm Hg No. %
Sudden onset of breathlessness Orthopnea Chest pain
75 (91) 45 (55) 33 (40)
Paroxysmal nocturnal dyspnea
25 (30)
Physical Findings
Hypertension
40 (49)
Hypotension Tachycardia
0 35 (43)
Peripheral edema
32 (39)
Atrial fibrillation
15 (18)
1). S h o r t n e s s o f b r e a t h , 75 c a s e s (91%), a n d h y p e r t e n s i o n , 40 cases (49%), w e r e o b s e r v e d m o s t frequently. A t r i a l f i b r i l l a t i o n was prese n t in 15 (18%) p a t i e n t s . A c u t e m y o c a r d i a l infarction w a s suspected first by h i s t o r y a n d i n i t i a l electroc a r d i o g r a m in 20 p a t i e n t s a n d was c o n f i r m e d by t y p i c a l e l e c t r o c a r d i o graphic or enzyme evolution in 15. A r t e r i a l o x y g e n t e n s i o n (Pa(h). Arterial blood gas results were a v a i l a b l e for all 82 p a t i e n t s (Table 2). In 71, e v a l u a t e d while b r e a t h i n g room a i r a n d s t u d i e d before t r e a t ment, the a v e r a g e PaO~ was 59 m m Hg. Of these, 36 (44%) h a d a PaO2 less t h a n 60 m m Hg a n d 16 (20%) h a d a P a ( h less t h a n 50 m m Hg. Arterial carbon dioxide tension (PaCO~). H y p e r c a p n i a was p r e s e n t in 11 patients; h y p o c a p n i a in 41; 30 pat i e n t s h a d n o r m a l PaCO2. All b u t one of t h e h y p e r c a p n i c p a t i e n t s h a d acidemia. A r t e r i a l b l o o d p H (Table 2). The acid-base s t a t u s of t h e 82 p a t i e n t s was assessed by the c r i t e r i a proposed by the Ad Hoc C o m m i t t e e of the New Y o r k A c a d e m y of S c i e n c e Conference. 7 A n o r m a l pH was observed in 33 (40%) p a t i e n t s a l t h o u g h five of these had a m i x e d acid-base abnormality. A c i d e m i a ( p H < 7.36) was p r e s e n t in 14 (17%) patients. A m o n g these, five h a d p u r e r e s p i r a t o r y acidosis,
Page 498 Volume 5 Number 7
No.
%
36
(44)
16
(20
Normal pH (7.36-7.44) Mixed acid/base abnormality
33 5
(40)
Acidemia (pH < 7.36) Pure respiratory acidosis
14 5
(17)
PaO2 60 mm Hg PaO2 50 mm Hg pH Distribution
Respiratory & metabolic acidosis
5
Respiratory acidosis & metabolic alkalosis
1
Metabolic acidosis & respiratory alkalosis
3
Alkalemia (pH >7.44) Pure respiratory alkalosis Respiratory alkalosis & metabolic acidosis Respiratory alkalosis & metabolic alkalosis
35 23
(43)
9
3
/
Table 3 T R E A T M E N T MODALITIES No. of patients
Oxygen
82
Furosemide Aminophylline
82 14
Morphine Rotating tourniquets
9 9
Digoxin
3
Phlebotomy
3
five h a d c o m b i n e d r e s p i r a t o r y a n d metabolic acidosis, one h a d respiratory acidosis w i t h metabolic alkalosis and t h r e e had p r i m a r y metabolic acidosis w i t h c o m p e n s a t o r y respiratory alkalosis. A l k a l e m i a (pH >7.44) was found in 35 (43%) cases. Of these, 23 (28%) had pure respiratory alkalosis, 9 ' (1L%) h a d r e s p i r a t o r y a l k a l o s i s with metabolic acidosis and 3 (4%) h a d respiratory alkalosis combined with metabolic alkalosis. I n i t i a l t r e a t m e n t (Table 3). All 82 patients received oxygen and furosemide. Aminophylline was given to 14 (17%), m o r p h i n e sulfate
to 9 (11%) and d i g i t a l i s glycosides t~ 3 (4%). A d d i t i o n a l m e a s u r e s include the use of r o t a t i n g tourniquets in~ (11%) and p h l e b o t o m y in 3 (4%). T h e p a t i e n t s who r e c e i v e d m0r: phine sulfate (Table 4) Were am0n~ t h e m o s t a g i t a t e d a n d decompen. sated in our group. No d e a t h s occurred e i t h e r in the e m e r g e n c y d e p a r t m e n t or during ths i n i t i a l 48 hours of h o s p i t a l care. DISCUSSION A r t e r i a l blood gas measurements have become e s s e n t i a l in the care of the c r i t i c a l l y ill. Since medical stu.{ dents, nurses a n d respiratory' t h e r a p i s t s have a s s u m e d the resp0n' sibility for o b t a i n i n g a r t e r i a l blood, it is i m p o r t a n t to a s c e r t a i n the useful" n e s s of a r t e r i a l b l o o d g a s meas" u r e m e n t s in acute p u l m o n a r y edema. T h i s r e t r o s p e c t i v e s t u d y of 82 pa, t i e n t s was u n d e r t a k e n to determine t h e f r e q u e n c y of v a r i o u s acid-base a n d v e n t i l a t o r y d i s t u r b a n c e s re. v e a l e d b y t h e b l o o d g a s meaS' u r e m e n t s in the e m e r g e n c y depart" m e n t a n d t h e i m p l i c a t i o n of the arte' r i a l blood gas r e s u l t s with regard ~' s u b s e q u e n t t h e r a p y a n d outcome. ' T h e a v e r a g e a r t e r i a l oxygen teN' sion in t h i s group was 59 m m I4g,
July 1976
Table 4 ARTERIAL BLOOD GASES OF PULMONARY EDEMA PATIENTS GIVEN MORPHINE SULFATE 1
Age Sex
Blood Pressure
Pulse Rate
Respiratory Rate
Pa0=*
PaC0=*
pH*
62
M
260/140
140
28
38
50
7.12
48
35
7.31t
50
56
24
7.52
65
M M
250/140
74
F
76 59 34
6.96 7.15t 7.39
69
30
158/100
140 (30 minutes) 100
40
43 52 54
M
120/90
100
20
54
30
7.42
52
M
140/80
150
40
70
M
120
56 64 65 31 62
46 69 34 63 43
7.26 7.19t 7.53t 7.20 7.34t
72
M
130/90 62 20 (respiratory arrest-intubate)
44 104
56 40
7.00 7.27
56
M
160/80
57 71
61 39
7.21 7.43t
(after 24 hrs.)
120
40
*Breathing room air tSubsequent blood gases somewhat higher t h a n the 49 m m Hg reported by A b e r m a n i n 1971 in 50 similar p a t i e n t s . 4 This m a y be explained, in part, by exclusion of the sickest p a t i e n t s i n our group, who were g i v e n s u p p l e m e n t a l o x y g e n prior to m e a s u r e m e n t of blood gases. Respiratory alkalosis was present in half of our cases. The hyperventilation m i g h t be e x p l a i n e d by t h e hypoxic r e s p i r a t o r y d r i v e coupled with the effect of t h e s t i m u l a t e d pulmonary nerve fibers stretched by an e n g o r g e d p u l m o n a r y c a p i l l a r y bed." S i m i l a r to A b e r m a n ' s report, 4 metabolic acidosis was commonly associated w i t h t h e r e s p i r a t o r y alkalosis. H u c k a b e e s a t t r i b u t e s t h e metabolic acidosis to i n c r e a s i n g lactate production by poorly perfused tissues i n p a t i e n t s with hypoxia and reduced cardiac output. Eichenholz 9 adds that metabolic acidosis may result as a f a i l u r e of i n t e r m e d i a r y '~etabolism i n the presence of primary hypercapnia. Acidemia - - pure respiratory, pure ~etabolic or combined - - was present in 14 p a t i e n t s . P a t i e n t s w i t h Prior history of s i g n i f i c a n t obstructive lung disease were omitted from this report. Therefore, this hypoventilation m a y be r e l a t e d to a i r w a y °bStruction s e c o n d a r y to b r o n c h o -
J • PJuly 1976
spasm, peribronchial edema or foam. West TM has shown t h a t CO2 elimination is reduced a n d a r t e r i a l hypoxemia develops i n states of ventilation/ perfusion imbalance. Respiratory alkalosis was the most c o m m o n a b n o r m a l i t y a n d was associated more often with less hypoxic patients. However, a sizeable n u m b e r of a c i d e m i c p a t i e n t s was observed and who they were was not predictable, clinically, either i n our series or in others. 2-4 Clearly, the classical use of oxygen a n d m o r p h i n e to t r e a t p u l m o n a r y edema has been replaced by oxygen a n d f u r o s e m i d e . All 82 Of our pat i e n t s r e c e i v e d o x y g e n a n d furosemide. T h e r e were no d e a t h s a n d only rare deterioration. Plentiful oxygen delivery m a y f r e q u e n t l y be all t h a t is necessary to p a r t i a l l y relieve bronchospasm', tachypnea, metabolic acidosis and anxiety. Rotating t o u r n i q u e t s and phlebotomy w e r e n o t u s e d o f t e n e n o u g h to evaluate adequately. Neither our house staff nor other investigators 2-4 commonly used morphine. This may be due to the realization t h a t hypercapnia is seen more frequently t h a n previously appreciated. Nevertheless, our data on those p a t i e n t s given m o r p h i n e is r e a s s u r i n g (Table 4).
N i n e p a t i e n t s , ages 50 to 74, with m o d e r a t e to s e v e r e h y p o x i a a n d m a r k e d l y a b n o r m a l clinical findings were given m o r p h i n e sulfate i n the emergency department. All had EKG evidence of coronary a r t e r y disease and six h a d acute myocardial infarction. Five p a t i e n t s had hypercapnia (PaCO2 >50) and were acidemic. In three of these cases, with a very low i n i t i a l pH a n d high P a C ( h , the abn o r m a l blood gases were rapidly reversed by t h e t r e a t m e n t described a n d t h e y w e r e c e r t a i n l y n o t adversely affected by morphine sulfate. One p a t i e n t with elevated P a C ( h initially became more hypercapnic but reverted to n e a r n o r m a l values over 24 hours. A n o t h e r p a t i e n t suffered a respiratory arrest shortly after 4 mg of m o r p h i n e were a d m i n i s t e r e d intravenously. Immediate intubation was performed and the p a t i e n t was successfully resuscitated. Thus, morphine sulfate seems to be a safe drug when given to p a t i e n t s with severe p u l m o n a r y edema, provided arterial blood gases are monitored ser i a l l y a n d the p a t i e n t carefully observed. The r o u t i n e m o n i t o r i n g of blood gases i n p u l m o n a r y e d e m a i n the emergency department may have additional value. Rapid i m p r o v e m e n t in blood gases m a y postpone or prev e n t t h e u s e of m o r e h a z a r d o u s a g e n t s , s u c h as g l y c o s i d e s or aminophylline. These drugs and a c i d e m i a are very common precursors of cardiac arrest.11,12 The absence of s u d d e n death in our group of patients is e n c o u r a g i n g and m a y be r e l a t e d to less f r e q u e n t u s e of a m i n o p h y l l i n e a n d glycosides a n d rapid use of oxygen and furosemide.
REFERENCES 1. Anthonisen UR, Smith HJ: Respiratory acidosis as a consequence of pulmonary edema. A n n I n t e r n M e d 62:993-999, 1965. 2. Miller A, Chisid L, S a m a r t i n TG: Acute reversible respiratory acidosis in cardiogenic pulmonary edema. J A M A 216:1315-1319, 1971. 3. Avery WG, Samet P, Sackner MA: The acidosis of pulmonary edema. A m J M e d 48:320-324, 1970. 4. Aberman A, Fulop M: The metabolic and respiratory acidosis of acute pulmonary edema. A n n I n t e r n M e d 76:173-184, 1972. 5. Editorial: Acid-base imbalance in pulmonary edema. J A M A 216:1337, 1971.
V o l u m e 5 Number 7 Page 499
6. Editorial: Blood gas tensions in acute p u l m o n a r y edema. Lancet 1:1106-1107, 1972. 7. Ad-Hoc Committee of t h e New York Academy of S c i e n c e s Conference (November 23-24, 1964): S t a t e m e n t on acid-base terminology. A n n Intern Med 63:885-890, 1965.
Page 500 Volume 5 Number 7
8. Huckabee WE: Lactic acidosis. A m J Cardiol 12:663-666, 1963. 9. Eichenholz A: P r i m a r y hypocapnia: A cause of m e t a b o l i c acidosis. J A p p l i e d Physiol 17:283-288, 1962.
11. C a m a r a t a SJ, Weil MH, Hanashir, PK, et al: Cardiac arrest in the critiealll ill. I. A study of predisposing causes il 132 p a t i e n t s . C i r c u l a t i o n 44:688-69ii 1971. '~
10. West JB: Causes of carbon dioxide retention in lung disease. N Engl J Med 284:1232, 1971.
12. Kastor JA: Digitalis intoxicatio~ i~ patients with atrial fibrillation. Circala. tion 47:888-896, 1973.
July 1976 ~ )
