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Blood Gases:
Not as Complicated as They Seem
Version 2.01 December 4, 2007 updates at: www.conovers.org
Keith Conover, M.D., FACEP
Attending Staff, Mercy Hospital of Pittsburgh, Department of Emergency Medicine
Clinical Assistant Professor, Department of Emergency Medicine, University of Pittsburgh
Adjunct Clinical Assistant Professor, Department of Internal Medicine / Emergency Medicine, Lake Erie College of Osteopathic Medicine
What to do when someone hands you a blood gas:
First, DON'T PANIC. Analyzing a blood gas, even in the face of a complicated acid-base disorder, is well within the scope of even a beginning student. There is so much written about blood gases and acid-base disorders, however, and from so many perspectives, that it might look like a hopeless task. Never fear. With a few simple guidelines that you can keep on a card or in a pocket notebook, you can face the numbers without fear. The trick is to start the right way. There's lots of information on a blood gas. For simplicity's sake ignore it all except the pO2, pCO2, and pH; add to this the bicarbonate ("bicarb," CO2) from an SMA panel (Chem-8, Basic Metabolic Panel) or set of electrolytes, and you're all set to evaluate oxygenation and diagnose acid-base status.
Arterial or Venous? VBGs rule!
The first question, before we even start delving deep into equations, and for that matter even before you order a gas, is whether to order an arterial or a venous gas. Yes, we talk about ABGs all the time. Yes, in community hospitals (and some teaching hospitals for that matter), the RTs will say you want a what? A venous gas? [aside to the other RT do we do those?]
Yes, ABG is a much more traditional term and what we always used to do. But, hey, do you want someone to stick a needle in your artery if they can stick a needle in your vein and get the same exact information?
Back in the old days, we got ABGs mostly to find out how well oxygenated people were. Why? Because back before the days of pulse oximiters (you know, the evil humour days?), it was the only way. But now with pulse oximeters everywhere (I even have one in my car first-aid kit), thats much less of an argument. Indeed, we know that pulse oximetry, at least if youve got a good wave form, is quite accurate. Indeed, knowing the confusion about ABG results in sick-sick patients (is this arterial or venous? maybe its a mixed-venous gas get another one, OK?), pulse oximetry is likely, in real, practical terms, better than an ABG. Well, this is true at least in the initial stages of evaluation, and as an emergency physician, thats my main interestbut its also true when a patient on the floor suddenly decompensates.
Yes, if you have an indwelling arterial line in the ICU, and youre sure its working OK, then following ABGs makes sense. But thats a tiny fraction of the patients who need their oxygenation checked.
And, it turns out that a venous blood gas can give you all the information you need to diagnose someones acid-base status. OK, OK, there are a few exceptions, like someone in cardiac arrest or who is peri-arrest (that means either you just got them back or theyre about to arrest). But for the majority of patients who are sick-sick but not circling the drain right on the edge, a VBG is just fine. Its faster and easier to draw, easier on the patient, and less likely to cause arterial bleeding or arterial clots. (Ever heard of the Allen test youre supposed to do before drawing an ABG at the wrist? Thats to make sure the patient has two arteries to the handso if you wreck one, the hand doesnt turn black and fall off. Think about it.)
As you would expect, venous blood has much less oxygen than arterial blood. Normal arterial pO2 (pAO2) is about 80-100 mm; the corresponding oxygen saturation is anything greater than 95% saturation.
Yes, there are few times when the pulse oximetry and the pO2 dont match, primarily in carbon monoxide poisoning, so for carbon monoxide poisoning, a single ABG may make sense, at least for patients who are obviously sick. However, if the patient isnt sick and you just want to rule out CO poisoning, you can just get a venous CO levelthey are just as good as arterial levels. ADDIN EN.CITE Touger19955532553217Touger, M.Gallagher, E. J.Tyrell, J.Department of Medicine, Bronx Municipal Hospital, Albert Einstein College of Medicine.Relationship between venous and arterial carboxyhemoglobin levels in patients with suspected carbon monoxide poisoningAnn Emerg MedAnn Emerg Med481-3254AdultArteriesBlood Specimen Collection/methodsCarbon Monoxide Poisoning/*bloodCarboxyhemoglobin/*metabolismComparative StudyEmergency Service, HospitalFemaleHumansMaleMiddle AgedPredictive Value of TestsProspective StudiesVeins1995Apr7710152http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=7710152 1
The vast majority of the time, as long as you can get a good pulse ox reading, you dont need an arterial blood gas. The table below is also available on a card at the end of this article, so you can keep it in your pocket:
SaO2 PaO2@pH7.3 PaO2@pH7.4 PaO2@pH7.5
--------------------------------------------------
99 171 158 143
98 122 111 101
97 101 92 84
96 89 82 74
95 82 74 68
94 76 69 63
93 72 66 60
92 68 62 57
91 66 60 55
90 63 58 53
88 59 54 49
86 56 51 47
84 53 49 44
82 51 47 42
80 49 45 41
78 47 43 39
76 45 41 38
74 44 40 35
72 42 39 34
OK, so what are normal values for a venous blood gas?
The venous pO2 is easy. Venous pO2 is normally 40 mm Hg. This is the same as the normal arterial pCO2, making it easy to remember.
The venous pCO2 is also pretty easy. The venous pCO2 is 5.7 mm Hg higher than arterial. For practical purposes, call it 6 mm Hg. Normal arterial pCO2 is 40 (same as the venous pO2 remember?), so normal venous pCO2 is 46. Simple, really.
Normal pH for an arterial blood gas is 7.35-7.45, and normal for a venous gas is just a little more acidotic, as youd expect: 7.32-7.42. So the venous pH is usually just 0.03 lower than the arterial. So take your venous pH and add 0.03 to it to get the equivalent in arterial-pH terms. But, really, 0.03 is a very small number, and probably not all that clinically significant, so if you just remember that the venous and arterial pH are about the same, thats good enough for government work.
Venous Blood Gas:
pH - 0.03 lower than arterial pH unless low-flow state (basically the same)
pO2 - 40-50
pCO2 - 5.7 higher than arterial pCO2 (46 rather than 40)
So, if youre worried your patient has acidosis or carbon dioxide retention, just check a venous gas. If its OK, then sos the patients CO2 level and acid-base status. ADDIN EN.CITE Gennis19855524552417Gennis, P. R.Skovron, M. L.Aronson, S. T.Gallagher, E. J.The usefulness of peripheral venous blood in estimating acid-base status in acutely ill patientsAnn Emerg MedAnn Emerg Med845-9149Acid-Base Imbalance/*diagnosis/drug therapyAdolescentAdultAgedBicarbonates/*blood/therapeutic useBlood PressureCarbon Dioxide/bloodEmergenciesFemaleHeart Arrest/*blood/therapyHumansHydrogen-Ion ConcentrationMaleMiddle AgedResuscitationVeins1985Sep3927796http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3927796 Weil19865525552517Weil, M. H.Rackow, E. C.Trevino, R.Grundler, W.Falk, J. L.Griffel, M. I.Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitationN Engl J MedN Engl J Med153-63153*Acid-Base EquilibriumAgedArteriesBicarbonates/bloodCarbon Dioxide/bloodFemaleHumansHydrogen-Ion ConcentrationMaleMiddle AgedPartial PressureResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.*ResuscitationVeins1986Jul 173088448http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=3088448 Durkin19935526552617Durkin, R.Gergits, M. A.Reed, J. F., 3rdFitzgibbons, J.Lehigh Valley Hospital, Allentown, Pennsylvania 18105-1556.The relationship between the arteriovenous carbon dioxide gradient and cardiac indexJ Crit CareJ Crit Care217-2184AgedAged, 80 and overArteriesBlood Gas Analysis*Body Surface AreaCarbon Dioxide/*blood*Cardiac OutputCatheterization, PeripheralCatheterization, Swan-GanzComparative Study*Critical IllnessEvaluation StudiesFemaleHumansLinear ModelsMaleMiddle AgedOxygen/*blood/*pharmacokineticsThermodilutionTissue DistributionVeins1993Dec8305959http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8305959 Durkin19935526552617Durkin, R.Gergits, M. A.Reed, J. F., 3rdFitzgibbons, J.Lehigh Valley Hospital, Allentown, Pennsylvania 18105-1556.The relationship between the arteriovenous carbon dioxide gradient and cardiac indexJ Crit CareJ Crit Care217-2184AgedAged, 80 and overArteriesBlood Gas Analysis*Body Surface AreaCarbon Dioxide/*blood*Cardiac OutputCatheterization, PeripheralCatheterization, Swan-GanzComparative Study*Critical IllnessEvaluation StudiesFemaleHumansLinear ModelsMaleMiddle AgedOxygen/*blood/*pharmacokineticsThermodilutionTissue DistributionVeins1993Dec8305959http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=8305959 Adrogue19895527552717Adrogue, H. J.Rashad, M. N.Gorin, A. B.Yacoub, J.Madias, N. E.Department of Medicine, Baylor College of Medicine, Houston.Assessing acid-base status in circulatory failure. Differences between arterial and central venous bloodN Engl J MedN Engl J Med1312-632020*Acid-Base EquilibriumAdultAgedAged, 80 and overArteriesBicarbonates/blood/therapeutic useCardiovascular Diseases/physiopathologyHeart Arrest/*bloodHumansHydrogen-Ion ConcentrationMiddle AgedPartial PressureResearch Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.Respiration, ArtificialShock/bloodVeins1989May 182535633http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2535633 2-5
Quick and Dirty
Looking t o f i g u r e o u t s o m e o n e s a c i d - b a s e s t a t u s i n a h u r r y ? I g n o r e a l l t h e v e r b i a g e i n t h i s h a n d o u t e x c e p t w h a t s i n t h e t w o c h u n k s o f b o x e d t e x t b e l o w . ( S o m e t h i n g e l s e t h a t s o n t h e c a r d a t t h e e n d s o y o u c a n k e e p h a n d y . )
T%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%W%
Q% C h e c k t h e p H o n t h e b l o o d g a s t o t e l l w h e t h e r t h e p a t i e n t h a s a n Q%
Q% A c i d e m i a ( p H ) o r A l k a l e m i a ( p H ) o r E u p H e m i a ( n o r m a l p H ) . Q%
`%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%c%
Q% C h e c k t h e b i c a r b o n t h e S M A - 6 a n d t h e p C O 2 o n t h e g a s . p H w i t h Q%
Q% [ H C O 3 - ] , o r p H w i t h [ H C O 3 - ] , i n d i c a t e s a p r i m a r y m e t a b o l i c a c i d o s i s Q%
Q% o r a l k a l o s i s ; p H w i t h p C O 2 , o r p H w i t h p C O 2 , i n d i c a t e s a p r i m a r y Q%
Q% r e s p i r a t o r y a c i d o s i s o r a l k a l o s i s . Q%
`%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%c%
Q% C h e c k f o r t h e e x p e c t e d d e g r e e o f c o m p e n s a t i o n . ( E m p i r i c E q u a t i o n s B e l o w ) Q%
`%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%c%
Q% F o r m e t a b o l i c a c i d o s i s , c h e c k t o s e e i f i t i s a n a n i o n g a p a c i d o s i s , a Q%
Q% n o n - a n i o n g a p a c i d o s i s , o r a m i x e d d i s o r d e r . I f a l l o f t h e a c i d o s i s Q%
Q% i s d u e t o a n i o n - g a p a c i d s , t h e n t h e i n c r e a s e i n t h e a n i o n g a p s h o u l d Q%
Q% b e t h e s a m e a s t h e d e c r e a s e i n t h e [ H C O 3 - ] . E . g . , i f t h e A . G . i s 2 0 Q%
Q% ( n o r m a l 1 2 ) , a n d t h e [ H C O 3 - ] i s 1 9 ( n o r m a l 2 7 ) , t h e n a l l o f t h e Q%
Q% a c i d o s i s ( a l l o f t h e [ H C O 3 - ] ) i s d u e t o t h e A . G . f r o m e x c e s s o r g a n i c Q%
Q% a c i d s t h a t f o r m t h e a n i o n g a p . A G = [ N a + ] - ( [ C l - ] + [ H C O 3 - ] ) Q%
Z%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%]%
T h e r e a r e a b o u t a z i l l i o n e m p i r i c e q u a t i o n s t h a t r e l a t e C O 2 , p H , a n d b i carbonate. There are also complicated-looking graphs ("nomograms") that do essentially the same thing for you.
Just pick a couple of the simple equations to memorize or write down. Ignore all the rest unless someone forces you to look at them. My best picks are in the box below.
T%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%W%
Q% F o r m e t a b o l i c a c i d o s i s , W i n t e r s ' e q u a t i o n : Q%
Q% p C O 2 = 1 . 5 ( [ H C O 3 - ] ) + 8 2 = l a s t 2 d i g i t s o f p H Q%
Q% f o r g o o d c o m p e n s a t i o n e x c e p t : Q%
Q% l a c t i c a c i d o s i s m a y h a v e o v e r c o m p e n s a t i o n d u e t o C N S e f f e c t s . Q%
`%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%c%
Q% F o r m e t a b o l i c a l k a l o s i s o r a c i d o s i s , w i t h r e s p i r a t o r y c o m p e n s a t i o n : Q%
Q% p C O 2 = l a s t 2 d i g i t s o f t h e p H = [ H C O 3 - ] + 1 5 Q%
Q% ( f o r [ H C O 3 - ] f r o m 8 t o 3 5 ) Q%
`%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%c%
Q% F o r r e s p i r a t o r y a c i d o s i s , e v e r y i n c r e a s e i n p C O 2 h a s a n e x p e c t e d Q%
Q% d e c r e a s e i n p H : Q%
Q% p C O 2 1 0 = p H . 0 8 ( a c u t e ) Q%
Q% p C O 2 1 0 = p H . 0 3 ( l a t e r , w i t h m e t a b o l i c c o m p e n s a t i o n ) Q%
`%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%c%
Q% F o r r e s p i r a t o r y a l k a l o s i s , e a c h d e c r e a s e i n p C O 2 h a s a n e x p e c t e d Q%
Q% i n c r e a s e i n b i c a r b o n a t e : Q%
Q% p C O 2 1 0 = [ H C O 3 - ] 2 ( a c u t e ) Q%
Q% p C O 2 1 0 = [ H C O 3 - ] 5 ( c h r o n i c / c o m p e n s a t e d ) Q%
Z%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%P%]%*
A n d t h a t s a l l y o u need to know about blood gas analysis.
Wellll, not really... you might want to know a bit more about what causes and maintains each of the four main abnormalities, and what to do about the problems you detect.
The remainder of this handout is a reference to the four primary acid-base disturbances, and the essential clinical features of each, also with postscripts on the A-a gradients and on blood gases and hypothermia. We start with the simple, and move to the more complex. The information in small print is somewhat esoteric, just some of my own notes from past lectures Ive attended myself.
Respiratory Acidosis
First, remember the treatment for respiratory acidosis. It is not calculations, it is not drugs, it is airway and breathing. (Remember your ABCs?)
Second, respiratory acidosis tends to cause Cl- loss and volume depletion by unknown mechanisms. (Source: Burton David Rose, Clinical Physiology of Electrolyte and Acid-Base Disorders, which is a just outstanding book.)
Respiratory Alkalosis
Causes:
Salicy l a t e o v e r d o s e , e s p e c i a l l y i n c h i l d r e n ( m i x e d w i t h a n i o n - g a p m e t a b o l i c a c i d o s i s , w h i c h p r e d o m i n a t e s i n l a t e r s t a g e s ) .
C i r r h o s i s ( p r o g e s t e r o n e i n b l o o d ? ) a n d l i v e r f a i l u r e ( a m i n e s i n b l o o d ? )
E a r l y s t a g e s o f s e p s i s .
P s y c h o g e n i c h y p e r v e n t i l a t i o n .
P r e g n a n c y ( p r o g e s t e r o n e ) .
P o n t i n e l e s i o n s .
A c u t e h y p o x i a ( e . g . , P E ) .
R e s p i r a t o r y a l k a l o s i s w i l l H C O 3 - s l i g h t l y d u e t o c o n v e r s i o n t o C O 2 .
W i l l h a v e s h i f t f r o m p y r u v a t e t o l a c t a t e i n b l o o d , c a u s i n g m i l d a n i o n g a p c o m p e n s a t o r y a c i d o s i s .
U s u a l l y c o m p e n s a t e s t o t a l l y o v e r 2 - 3 d a y s .
M a y c a u s e a s y m p t o m a t i c P O 4 .
M e t a b o l i c A c i d o s i s
F i r s t q u e s t i o n : i s i t a d e q u a t e l y c o m p e n s a t e d ?
U s e o n e o f t h e t w o f o r m u l a s i n t h e b o x a b o v e .
S e c o n d q u e s t i o n : i s i t a n A n i o n G a p o r a N o n - a n i o n - g a p ( h y p e r c h l o r e m i c ) m e t a b o l i c a c i d o s i s ?
[ N a + ] - ( [ C l - ] + [ H C O 3 - ] ) > > 1 2 i s a n i o n g a p a c i d o s i s
[ N a + ] - ( [ C l - ] + [ H C O 3 - ] ) = 1 2 i s h y p e r c h l o r e m i c ( n o n - a n i o n g a p ) a c i d o s i s
i n a n i o n g a p s h o u l d b e s a m e a s i n H C O 3 - , o r h a s B O T H a n i o n - g a p a n d n o n - a n i o n - g a p m e t a b o l i c a c i d o s e s .
H i g h A n i o n G a p M e t a b o l ic Acidoses
Mnemonic-- KUSMAL:
K- ketoacidosis
U- uremia
S- salicylates
M- methanol (and ethylene glycol, paraldehyde)
A- alcohol (EtOH)
L- lactic acidosis
Normal Anion Gap (Hyperchloremic) Metabolic Acidoses
divided into high K+ vs. low K+
a. high K+
1. hyperal and increased amino acid catabolism
2. post-hypocapnic (it takes a while for the HCO3- to rise)
3. dilutional
4. hypoaldo (either from low renin or adrenal dysfunction)
5. NH4Cl, CaCl2, lysine, or arginine (effectively adds HCl)
b. low K+
1. GI: diarrhea, fistulas (K+ loss and high aldo)
2. GU: surgical ureteral conduits
3. RTA: Renal Tubular Acidosis. Complex subject best left to outside reading or a nephrology rotation.
Metabolic Alkalosis
Metabolic alkalosis is a complex disorder, and understanding of metabolic alkaloses has generally been an arcane art, whose practitioners are suspected of pacts with the devil. However, it need not be quite so complex. This presentation provides three different views of metabolic alkalosis: Pathophysiology, Classification, and Treatment.
Pathophysiology of Metabolic Alkalosis
PRIMARY EVENT
The primary event is either loss of H+ or gain of HCO3-. Examples: upper GI losses from vomiting or NG suction, H+ loss from the kidney. Or, H+ may move into the cells because of a low serum K+. Alkalosis may also result from addition of HCO3- or (purportedly) "contraction" of fluid volume around a fixed amount of HCO3-.
MAINTENANCE
Alkalosis will quickly be corrected by compensatory m e c h a n i s m s u n l e s s s o m e f a c t o r i s a c t i n g t o m a i n t a i n t h e a l k a l o s i s . S e v e r a l f a c t o r s m a y m a i n t a i n a n a l k a l o s i s , a l l b y d e c r e a s i n g H C O 3 - e x c r e t i o n ( i t a l i c s b e l o w ) :
A h i g h a l d o s t e r o n e s t a t e , e i t h e r p r i m a r y o r s e c o n d a r y
K + o r C l -
T h e r e n a l T m f o r H C O 3 - m a y b e r e s e t b y a l l o f t h e a b o v e , a n d b y v o l u m e .
N o n - r e s o r b a b l e a n i o n s ( e . g . , p e n i c i l l i n , c a r b e n i c i l l i n ) t a k e H C O 3 - w i t h t h e m .
p C O 2 s e c o n d a r y t o a l k a l o s i s c a u s e s a T E R T I A R Y r e n a l H C O 3 - r e t e n t i o n ( u p t o 4 0 % o f t h e H C O 3 - i n m e t a b o l i c a l k a l o s i s m a y b e s e c o n d a r y t o t h i s ) .
R e n a l f a i l u r e w i t h d e c r e a s e d H C O 3 - f i l t r a t i o n ( r a r e )
A m e t a b o l i c a l k a l o s i s ( b u t n o t a l k a l e m i a ) m a y b y a c o m p e n s a t o r y l o s s o f H + d u e t o p r i m a r y r e s p i r a t o r y o r m e t a b o l i c a c i d o s i s . ( C a u s e d b y H + i n r e n a l t u b u l e c e l l s . )
C L A S S I F I C A T I O N O F METABOLIC ALKALOSIS:
This section is in smaller print because it's more complicated than the rest and probably not worth reading until you actually have a patient with metabolic alkalosis in front of you. Three different views of metabolic alkalosis are presented. Each classifies all the alkaloses in a different way. No one classification is clearly superior.
Classification #1: Chloride-responsive vs. Non-chloride responsive Metabolic Alkalosis
Chloride Responsive Metabolic Alkalosis Urinary Cl- < 20 mEq/l means chloride-responsive, which will respond to NaCl. Most alkaloses are in this category and are associated with normal or low blood volumes:
Gastric fluid loss
Diuretics
Posthypercapnic
Diarrheal losses of Cl- (congenital or villous adenoma)
Chloride Unresponsive Metabolic Alkalosis Urinary Cl- > 20 mEq/l means not chloride-responsive. These alkaloses are rare, and are associated with normal to increased plasma volume. The problem is volume expansion secondary to hyperaldo., severe K + , o r s e v e r e C l - , + l e a d i n g t o H C O 3 - l o s s ; g i v e p l e n t y o f K + , t r e a t w i t h l a r g e d o s e s o f A l d a c t o n e ( s p i r o n o l a c t o n e ) t o i n h i b i t t h e a l d o e f f e c t . C a u s e s :
C o n n ' s d i s e a s e ( p r i m a r y h y p e r a l d o )
C u s h i n g ' s s y n d r o m e ( c o r t i s o l h a s s o m e m i n e r a l o c o r t i c o i d e f f e c t )
C o n g e n i t a l a d r e n a l h y p e r p l a s i a
B a r t t e r ' s s y n d r o m e ( c o n g e n i t a l h y p e r t r o p h y o f j u x t a g l o m e r u l a r a p p a r a t u s w i t h r e n i n a n d i n a b i l i t y t o r e a b s o r b C l - )
t r u e l i c o r i c e i n g e s t i o n ( g l y c y r r h i z i c a c i d i n l i c o r i c e i s s i m i l a r t o a l d o )
? p r o f o u n d K + d e p l e t i o n w i t h G F R
Unclassified Metabolic Alkalosis
alkali administration
milk-alkali syndrome
glucose ingestion after starvation (unknown mechanism)
blood transfusion (citrate)
large doses of penicillin or carbenicillin (cause increased excretion of K+ and H+ due to large filtered load of - ions)
Classification #2: Metabolic Alkalosis by Root Causes
Upper GI H+ losses (vomiting or NG suction)
Renal H+ losses (e.g. diuretics, hyperaldo)
Diuretics ("contraction"); actually, diuretics probably cause metabolic alkalosis by mech a n i s m s d e s c r i b e d u n d e r " p a t h o p y s i o l o g y " r a t h e r t h a n b y c o n t r a c t i o n a r o u n d t h e H C O 3 -
P r i m a r y m i n e r a l o c o r t i c o i d e x c e s s
K + ( s e v e r e ) w i t h G F R
C o l o n i c H + l o s s e s ( d i a r r h e a o r v i l l o u s a d e n o m a o r l a x a t i v e a b u s e w i t h s e c o n d a r y r e n a l d y s f u n c t i o n ? )
A l k a l i i n g e s t i o n ( I V o r P O b i c a r b o r C a C O 3 ) ( r a r e )
P o s t h y p e r c a p n i c : a f t e r C O 2 n o r m a l i z e d , t a k e s a w h i l e f o r t h e c o m p e n s a t o r y H C O 3 - t o n o r m a l i z e .
H y p o p a r a t h y r o i d i s m : P T H c a u s e s H C O 3 - e x c r e t i o n , l a c k > r e t e n t i o n .
C l a s s i f i c a t i o n # 3 o f M e t a b o l i c A l k a l o s e s : A n i o n G a p v s . n o n - A n i o n G a p
H i g h A n i o n G a p M e t a b o l i c A l k a l o s e s
+ c h a r g e s o n p l a s m a p r o t e i n s f r o m p H
i n c r e a s e d l a c t a t e p r o d u c t i o n
d e c r e a s e d l a c t a t e m e t a b o l i s m ( e . g . i n l i v e r f a i l u r e w i t h h y p e r a l i m e n t a t i o n )
N o r m a l A n i o n G a p M e t a b o l i c A l k a l o s e s
C a + +
M g + +
p a r a p r o t e ins
lithium
Treatment of Metabolic Alkalosis
PH < 7.6, ASYMPTOMATIC (CHLORIDE-RESPONSIVE ASSUMED)
volume depleted: give IV-NS and K+ (base amount of K+ on urine Cl-); see below.
edematous but intravascularly depleted (CHF, nephrosis, cirrhosis): give albumin to i n t r a v a s c u l a r v o l u m e i f a p p r o p r i a t e , r e p l e t e K + a g g r e s s i v e l y , a n d c o n s i d e r D i a m o x ( s e e b e l o w )
v o l u m e e x p a n d e d ( r a r e ) : g i v e K C l p o o r I V
P H > 7 . 6 , S Y M P T O M A T I C ( C H L O R I D E - R E S P O N S I V E A S S U M E D )
m o n i t o r e d b e d
N H 4 C l o r H C l I V
2 0 - 4 0 m E q / h r o f 0 . 1 N o r 0 . 1 5 N H C l t h r o u g h c e n t r a l l i n e ( N H 4 C l c a n b e g i v e n P O , b u t m u s t b e a v o i d e d i n c i r r h o s i s o r r e n a l f a i l u r e b e c a u s e o f N H 3 b u i l d u p )
1 0 0 m E q H + s h o u l d H C O 3 - b y 7 m E q / L
f o l l o w h o u r l y p H , p C O 2 , H C O 3 -
s t o p w h e n p H < 7 . 6 a n d p a t i e n t a s y m p t o m a t i c
A c e t a z o l a m i d e ( D i a m o x )
w a t c h f o r K + ; m u s t s u p p l e m e n t w i t h m a s s i v e a m o u n t s K C l
2 5 0 m g I V Q 8 H
s t o p w h e n p H < 7 . 6 a n d p a t i e n t a s y m p t o m a t i c
N O N - C H L O R I D E - R E S P O N S I V E :
U r i n a r y C l - > 2 0 m E q / l m e a n s n o t c h l o r i d e - r e s p o n s i v e ( r a r e ) , s o p r o b l e m i s p r o b a b l y p r i m a r y h y p e r a l d o , o r s e v e r e l a c k o f K+ leading to HCO3- loss; give plenty of K+, and give large doses of Aldactone (spironolactone) to block aldo receptors.
Further Reading
If you are still puzzled by acid-base balance, and not too nauseated by the dense information above, you should pick up a good book on the topic. There's a book by Stryer that is very well-though-of, but my personal favorite is Clinical Physiology of Acid Base and Electrolyte Disorders by Burton David Rose. If you can't find it in the bookstore, get it from www.amazon.com .
I h o p e y o u f i n d t h i s l i t t l e h a n d o u t u s e f u l . I t ' s j u s t c o b b l e d t o g e t h e r f r o m m y o w n n o t e s , a n d i s p r e t t y r o u g h , b u t r e m e m b e r , i t ' s a t l e a s t w o r t h w h a t y o u ' r e p a y i n g f o r i t ( n o t h i n g ) .
A p p e n d i x I : O x y g e n a t i o n : t h e A - a g r a d i e n t
E v a l u a t i n g t h e p O 2 o n r oom air is easy: the lab usually prints out normal values for you, and even puts a little asterisk next to low values. But what if the patient's pO2 is low normal, but the pCO2 is below normal. Could this mean the patient is having to work hard to keep the pO2 up, causing a low pCO2? Could this mean the patient has a big pulmonary embolism or a bad pneumonia, despite a "normal" pO2? You betcha.
Is there any scientific way to factor the pCO2 into your figuring? Sure enough.
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$' `d \$ ]`gd"` - a b r ، ` b z 0 2 ؐ ڐ b d n p r ޒ & ( , - o t v z Ե hy CJ OJ QJ h? CJ OJ QJ hy 6] h? H*h? 5OJ QJ \ h"` h? H* h? 6] !hMV h? 5CJ OJ QJ \] h? H* h? 5\ h? hy ? r t x | ~ җ $$If a$ $a$gd"` gd"` gd"` 2 = ? v x $ y { ( ) , . 3 V X & ' ~ + , Y hK 5OJ QJ \ hK 6 hK 5\ Uho] hK H*hK j h? 0J U h? H*h? N This calculation has the intimidating name of the Aa Gradient. And, deriving it from first principles can be difficult. But using the formula is incredibly simple. Just keep it written down somewhere so you can find it when you need it.
A-a Gradient (Alveolar-arterial Oxygen Gradient)
Use: To quantify ABG results to estimate the average gradient across the alveolar membrane. An increased A-a gradient is seen in pulmonary embolism, pneumonias, ARDS, etc.
Normal A-a gradient:
AgeUpper Limit of Normal2017302140245027603170348038
From: Morris A, Kamer R, Crapo R, et al. Clinical pulmonary function: a manual of uniform laboratory procedures, 2E. Salt Lake City: InterMountain Thoracic Society, 1984:45. Quoted in Emergency Medicine Reports, 12/14/92.
Normal values increase with age, and smoking or occupational pneumoconiosis will also increase the A-a gradient.
Equation: A-a gradient = (713 (FIO2) - 1.2 (pCO2)) - (pO2)
For room air: A-a gradient is: 150 - 1.2(pCO2) - pO2
Derivation:
(pAlveolarO2) = (Fractional Inspired O2) * (Atmospheric Pressure - partial pressure of water in saturated air) - (pAlveolar CO2/R) -- (where R is the respiratory coefficient, the amount of CO2 produced per molecule of O2 used) or:
pAO2 = (FIO2(760-47)) - (pACO2/R) or,
since rapid diffusion of CO2 across the alveolar membrane means that pACO2 and paCO2 are the same:
pAO2 = 713(FIO2) - 1.2(paCO2)
therefore: A-a O2 = (713(FIO2) - 1.2(pCO2)) - pO2
Appendix II: Hypothermia and blood gases
You may hear about "correcting blood gases for hypothermia." The blood gas blood is warmed to room temperature when the syringe is injected into the ABG machine. Therefore, the lab wants to know if the patient is hypothermic, so they can "correct" the numbers. Lab people want to "correct" the numbers so that they give you exactly correct numbers, reflecting exactly what the pH and pCO2 are in the patient's blood. Despite these good intentions of the lab people, LIE TO THEM. If they ask if the patient is hypothermic, say no. If someone is taking the gas to the lab, and might tell the lab the patient is hypothermic, use duct tape over the person's mouth before sending him or her to the lab.
Why? One very important reason.
You've invested considerable time and energy in learning about room temperature blood gases. But, do you have any idea what a normal pH or pCO2 is at 30(C? At 25(C? I don't, and hypothermia is one of my specialties. But it turns out that if you warm the blood gas to a normal temperature, and don't correct for hypothermia, then the numbers you get compare almost perfectly with a room-temperature gas. For example, the patient is hypothermic to 25(C. You get an uncorrected pH of 7.4. This means the patient is not acidotic (acidemic), and not alkalotic (alkalemic). If you got a "corrected" gas, you'd have to go look up in a table what the normal pH is for a core temperature of 25 (C. The normal pH at 25(C is not 7.4. Same thing for pCO2. The normal pCO2 at 25(C is not 40.
Got it?
There is one exception, though. Correcting for temperature is appropriate when you're considering pO2 on an arterial gas. Here's the trick I use: send the gas up without any mention of hypothermia, then use the pCO2 and pH to figure out the patient's acid-base status. Then call the lab and say "oh, by the way, the patient's core temperature is 25(C, so you could you tell me the corrected pO2?" And when they try to give you the corrected pH and pCO, just put your fingers in your ears.
Well, now you know why you keep the lab people in the dark about your patient's temperature: to keep them from confusing you, and to let you use your room-temp acid-base knowledge to properly manage your patient.
ADDIN EN.REFLIST 1. Touger M, Gallagher EJ, Tyrell J. Relationship between venous and arterial carboxyhemoglobin levels in patients with suspected carbon monoxide poisoning. Ann Emerg Med 1995;25(4):481-3.
2. Gennis PR, Skovron ML, Aronson ST, Gallagher EJ. The usefulness of peripheral venous blood in estimating acid-base status in acutely ill patients. Ann Emerg Med 1985;14(9):845-9.
3. Weil MH, Rackow EC, Trevino R, Grundler W, Falk JL, Griffel MI. Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation. N Engl J Med 1986;315(3):153-6.
4. Durkin R, Gergits MA, Reed JF, 3rd, Fitzgibbons J. The relationship between the arteriovenous carbon dioxide gradient and cardiac index. J Crit Care 1993;8(4):217-21.
5. Adrogue HJ, Rashad MN, Gorin AB, Yacoub J, Madias NE. Assessing acid-base status in circulatory failure. Differences between arterial and central venous blood. N Engl J Med 1989;320(20):1312-6.
Yes, yes, I know the footnote on page 3 talks about SMA-6 and evil humours as being good examples of traditional terms I like to use. So Im inconsistent.
SMA-6 is the old name for chem-6 or basic metabolic panel. It means BUN, Cr, electrolytes; SMA-7 adds a glucose. SMA is Sequential Multi-Analyzer which was the first commercial multiple-test lab chemistry machine. Yes, its an old fashioned term, but hey, whats the matter with that? A sense of tradition is important, thats why I still use words like monilial intertrigo and evil humours.
None but respiratory alkalosis can have compensation all the way back to a normal pH. A normal pH with any other disorder indicates a second, superimposed, acid-base disorder. Also, note that SMA-6 autoanalyzer may not accurately determine very high HCO3-, so the [HCO3-] must be done manually by the lab.
SECONDARY HYPERALDO may be due to: v o l u m e , o r e f f e c t i v e v o l u m e ( e . g . i n c i r r h o s i s , C H F , n e p h r o t i c s y n d r o m e ) ; o r C l - ( p e r h a p s t h e e f f e c t o r o f d e c r e a s e d v o l u m e ) ; b o t h c a u s e s e c o n d a r y a l d o ( w h i c h c a u s e s s o d i u m a v i d i t y i n t h e d i s t a l t u b u l e ) .
P R I M A R Y H Y P E R A L D O m a y b e d u e t o : t u m o r , l i c o r i c e ( g l y c y r r h i z i c a c i d i n l i c o r i c e i s s i m i l a r t o a l d o ) , o r B a r t t e r ' s s y n d r o m e : c o n g e n i t a l h y p e r t r o p h y o f j u x t a g l o m e r u l a r a p p a r a t u s w i t h r e n i n a n d i n a b i l i t y t o r e a b s o r b C l - .
H i g h a l d o ( a l o n g w i t h N a + d e l i v e r y t o t h e d i s t a l a l d o - s e n s i t i v e a r e a s o f t h e t u b u l e f r o m d i u r e t i c s o r H C O 3 - o v e r w h a t t h e p r o x i m a l t u b u l e c a n a b s o r b ) c a u s e s N a + r e a b s o r b t i o n a n d o b l i g a t e K + o r H + e x c r e t i o n . A t t e m p t s t o r e t a i n N a + / H C O 3 - b y t h e d i s t a l t u b u l e l e a d t o s e c r e t i o n o f H + t o p e r m i t r e c o v e r y o f t h e H C O 3 - ; o t h e r w i s e , a l a r g e a m o u n t o f N a + w o u l d b e l o s t a l o n g w i t h t h e H C O 3 - , r e s u l t i n g i n v o l u m e d e p l e t i o n .
M e c h a n i s m : i n c r e a s e d H + i n r e n a l t u b u l e c e l l s ( b e c a u s e o f K + e f f l u x i n K + ) c a u s e s H + e x c r e t i o n .
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One note: if trying to diagnose pulmonary embolism in a patient with chest pain, syncope, or unexplained tachycardia, dont use the A-a gradient, or a pO2, or even a pulse oximeter reading to help you decide if its a PE. It just doesnt help. Yes, by all means check the patients oxygenation to see how sick the patient is and whether the patient needs oxygen. But the majority of people with a PE will not have low oxygenation. Indeed, its even said (correctly) that, if you have two young healthy women with pleuritic chest pain, and one has a normal pulse ox and the other has a low pulse ox, the one with the normal pulse ox is more likely to have a PE. True. The one with the low pulse is is more likely to have a pneumonia.
Conover's ABG Handout
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