Acid Base Introduction

Acid Base Interpretation
Part III
Clinical correlation
Jakub Matera
5 steps to analyse acid base
• Step 1
Look at the pH. Acidaemia or alkalaemia?
• Step 2
Who is responsible for this change in pH ( primary culprit )?
• Step 3
Calculate compensatory changes.
Adequate compensation?
Acute or chronic process?
• Step 4
Calculate AG and ∆ gaps.
Is there any additional pathological process?
Mixed metabolic or respiratory disturbance?
• Step 5
Clinical correlation? Find the diagnosis.
Analyse the following blood gas and electrolyte values:
pH 7.47, PCO2 20, HCO3 15, Na 145, Cl 100
The pH is elevated (alkalaemia), with a low PCO2 and a low HCO3.
Because the pH is high, the low PCO2 represents a primary disorder (RO), so
a respiratory alkalosis is present.
Expected HCO3 based on metabolic compensation should be: in acute (The 2 for 10 Rule) = 20; in
chronic (The 5 for 10 Rule) = 14.
At first inspection, the low HCO3 level appears to be metabolic compensation for a chronic
respiratory alkalosis.
Follow the fourth step rule, however, and calculate the AG: 145 – (100+15) = 30
Because the wide anion gap exists a metabolic acidosis (WAGMA) is also present.
Now calculate the ∆ AG: 30 - 12 = 18, and add it to the measured HCO3 : 15. The sum, 33 mmol/L,
is higher than a normal HCO3 concentration, indicating a metabolic alkalosis is also present.
The near-normal pH reflects the competing effects of these three primary disorders.
This patient had findings of bacterial pneumonia (hence the respiratory alkalosis), history of
vomiting (the metabolic alkalosis) and evidence of alcoholic ketoacidosis (causing metabolic
acidosis). These three independent disorders can occur concurrently in other clinical settings.
Four primary acid-base disorders cannot coexist, as a patient cannot hypoventilate and
hyperventilate at the same time.
• What if a patient presents with a
pH of 7.10, a PCO2 50, HCO3 15, Na 145, Cl 100 ?
• The person is acidaemic with an elevated PCO2, and low HCO3
• Because the pH is low, the increased PCO2 (respiratory acidosis)
and decreased HCO3 (metabolic acidosis) are both primary
disorders (ROME).
• The anion gap is increased : AG = 145 – (100+15) = 30;
therefore, the metabolic acidosis is of the wide anion gap
variety (WAGMA).
• Because the sum of the ∆ AG (18) and the measured HCO3 (15)
is 33 mmol/L. So, greater than the normal HCO3 concentration,
a metabolic alkalosis is also present: three primary disorders.
• This patient presented in an obtunded conscious state
(respiratory acidosis),with a history of vomiting (metabolic
alkalosis) and laboratory findings consistent with diabetic
ketoacidosis (metabolic acidosis).
• Interestingly, identical blood gas values
pH of 7.10, a PCO2 50, HCO3 15, Na 145, Cl 100
could occur in a patient with chronic respiratory acidosis and
metabolic compensation in whom an acute anion gap metabolic
acidosis developed.
Example: Patient with COPD and T2DM who developed
metformin induced lactic acidosis
• Although the pH, PCO2, and HCO3 values would be the same in
both these patients, clinical correlation would readily
differentiate between the two.
• As is the case for other diagnostic tests, acid-base abnormalities
cannot and should not be interpreted without knowledge of the
clinical context.
Metabolic acidosis
• Wide anion gap (WAGMA)
increased H+ consumes HCO3-
• Non anion gap (NAGMA)
loss of HCO3- (kidney or gut) will raise Clhence non anion gap
Metabolic acidosis
[Na+] + [K+] = [Cl-] + [HCO3-] + [AG- ]
Normal AG
Excess AG
Mnemonics for Wide AG Metabolic Acidosis
A- Analgesics (massive NSAID,
C- Cyanide, Carbon monoxide
A- Arsenic, Alcoholic ketoacidosis
T- Toluene
Methanol, Metformin
Diabetic ketoacidosis
Paraldehyde, Phenformin
Iron, Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates, Starvation
R- Renal failure
Methanol, metformin
Alcoholic ketoacidosis
Paraldehyde, Phenformin
Lactic acidosis
Ethylene glycol
Salicylates, Starvation
a useful misspelling of Adolph Kussmaul's name
Salicylate poisoning
Aldehyde (paraldehyde)
Ethylene glycol
Dr Adolph Kussmaul( 1822 -1902)
German physician and a leading clinician of his time
•First to describe dyslexia. (He called it 'word blindness'.)
•First to describe polyarteritis nodosa.
•First to describe progressive bulbar paralysis.
•First to diagnose mesenteric embolism.
•First to perform pleural tapping and gastric lavage.
•First to attempt oesophagoscopy and gastroscopy.
He described two medical signs and one disease which
have eponymous names that remain in use:
•Kussmaul breathing - very deep and laboured breathing
seen in severe metabolic acidosis
•Kussmaul's sign - paradoxical rise in the JVP on
inspiration in constrictive pericarditis, RV strain (TS) and
•Kussmaul disease (also called Kussmaul-Maier disease) Polyarteritis nodosa.
GOLD MARK: an anion gap mnemonic for the 21st century.
Mehta AN, Emmett JB, Emmett M. Lancet 2008;372(9642):892.
Over the past couple decades, the dynamic
of conditions that can cause an anion gap
metabolic acidosis has changed and a list has
Metabolic acidosis due to excessive
paraldehyde use has become exceedingly
Iron and isoniazid are just two of many drugs
and toxins that cause hypotension and lactic
Three “new” organic anion-gap-generating
acids and acid precursors have been
recognised in recent years. They are:
D-lactic acid, which can occur in some
patients with short bowel syndromes;
5-oxoproline (or pyroglutamic acid)
associated with chronic paracetamol use,
often by malnourished women;
high-dose propylene glycol infusions;
Propylene glycol, the solvent used for several
parenteral medications including lorazepam,
diazepam, phenobarbital, and others is
metabolised to lactate.
Therefore we propose a new anion gap
mnemonic for the 21st century: GOLD MARK.
This acronym represents :
Glycols (ethylene and propylene),
M- Methanol,
A- Aspirin,
R- Renal failure, and
K- Ketoacidosis.
Mnemonic aids are only helpful if they are
easily remembered and we believe GOLD
MARK fits that requirement.
increased H+ consumes HCO3
↓ acid excretion
renal failure (acute or chronic)
↑ acid load
 Ketoacids
DKA, Alcoholic, starvation
 Lactic acid
L-lactate and D-lactate
 Exogenous acids
ethylene glycol – oxalic acid, methanol – formic acid,
oxoproline acid
Lactic acidosis
overproduction, underutilisation, decreased excretion
• Type A – caused by tissue ischaemia
• Type B – caused by impaired mitochondrial O2
utilisation and impaired excretion
Type A
– all state of shock (cardiogenic, hypovolaemic, septic);
– excessive exercise, seizures, respiratory failure;
– mesenteric ischaemia, limb ischaemia, compartment
– haemoglobin abnormality: severe anaemia, COHb (CO
poisoning), MetHb (nitropruside).
Lactic acidosis
Type B - impaired mitochondrial O2 utilisation and
impaired excretion
• B1 – systemic disease
Leukaemia, Lymphoma, Thiamine deficiency, Infections,
Pancreatitis, Short bowel syndrome (D-Lactate),
Failures: hepatic, renal, diabetic;
• B2 – toxins and drugs: alcohols –glycols, iron, isoniazid,
biguanides (metformin), salicylates, AZT (zidovudine),
and cyanide poisoning;
• B3 – inborn metabolic errors (eg G6PD).
Non anion gap metabolic acidosis
loss of HCO3- (kidney or gut) will raise Cl- , hence non anion gap.
 K+ normal or ↑
• Mineralocorticoid deficiency (Addison’s )
• Addition of Cl (Saline)
 K+ ↓
• Lower GI losses (diarrhoea)
• Renal losses (CA inhibitors, RTA)
• Urinary diversion (vesico-colic, uretero-enterostomy)
Mnemonic for NAGMA
Small bowel fistula
Extra chloride (K+ normal or ↑)
Carbonic anhydrase inhibitor
Addison’s disease (K+ ↑)
Renal tubular acidosis (RTA)
Pancreatic fistula
NAGMA – kidney or gut ?
• NAGMA – loss of HCO3- (kidney or gut) will raise Cl• Urine Anion Gap (UAG) – helps differentiate
between GIT and renal causes of hyperchloraemic
metabolic acidosis (NAGMA with ↓K+)
• UAG = Nau + Ku – Clu
• UAG – normal close to 0
• neGUTive = GI loss of HCO3 (eg diarhoea, fistulas)
• Positive = impaired renal acidification (eg RTA, CAI)
Metabolic alkalosis
Volume loss
Saline responsive
Urinary chlorine < 10 mmol/L
• Upper GI losses
vomiting, gastric alkalinisation, gastric
• Lower GI losses
chronic diarrhoea (Cl-)
• Renal diuretic losses
remote diuretic use
• Skin loss (Cl-)
• Cystic fibrosis
• Milk-alkali syndrome
chronic ingestion of large doses of
CaCO3 . Hypercalcemia increases
renal bicarbonate reabsorption
Volume normal or overloaded
Saline unresponsive
Urine chlorine > 20 mmol/L
• Conn’s Syndrome
primary hyperaldosteronism
• Cushing’s Syndrome
• Bartter’s Syndrome
inherited thick ascending limb of
the loop of Henle and excretion
excessive amounts of Na, K, Cl.
• Renal artery stenosis
stimulates the renin-angiotensinaldosterone system
• Severe hypo K+ and hypo Mg2+
• Current diuretics use
Respiratory disturbance
 Acute
 Central / supratentorial
Severe pneumonia
Severe head injury
Sedative use
General anaesthetics
 Chronic
• Intracranial tumours
• Neuromascular disease
Mild to moderate HI
Anxiety (fear, stress)
Voluntary hyperventilation
 Systemic
• Liver failure
• Pregnancy
 Respiratory
Pulmonary fibrosis
Mild pneumonia
Alveolar-arterial Gradient
It is simply the difference between Alveolar concentration of
O2 (PAO2), and arterial concentration of O2 (PaO2).
• A-a gradient = PAO2 – PaO2
• The PaO2 is obtained from the ABG
• The PAO2 is obtained from the Alveolar Gas equation:
• Alveolar Gas equation: PAO2 = PIO2 – PaCO2/R
• The PIO2 is PO2 inspired in trachea
• The PaCO2 is a value from your ABG
• R – respiratory quotient ( 0.8 or 1.0 if patient is on 100% FiO2)
• PIO2 = (PB – 47) x FiO2
• PB is barometric pressure of the inspired air (760 mm Hg at sea level)
• 47 mm Hg is a water vapour pressure (47 mm Hg)
• PAO2 = (760-47) x FiO2 – PaCO2/R
Alveolar Gas equation
PAO2 = (760-47) x FiO2 – PaCO2/R
FiO2 = 0.21
PAO2 = (760-47) x 0.21 – 40/0.8
PAO2 = 149 – 50
PAO2 = 99
FiO2 = 0.5
PAO2 = (760-47) x 0.5 – 40/0.8
PAO2 = 356 – 50
PAO2 = 306
FiO2 = 0.3
PAO2 = (760-47) x 0.3 – 40/0.8
PAO2 = 214 – 50
PAO2 = 164
FiO2 = 0.7
PAO2 = (760-47) x 0.7 – 40/0.8
PAO2 = 499 – 50
PAO2 = 449
FiO2 = 0.4
PAO2 = (760-47) x 0.4 – 40/0.8
PAO2 = 285 – 50
PAO2 = 235
FiO2 = 1.0
PAO2 = (760-47) x 1.0 – 40/1.0
PAO2 = 713 – 40
PAO2 = 673
A-a gradient
Normally some A-a gradient
exists b/o anatomical
barriers between alveolar
air and the blood that
would become arterial
• thin layer of epithelial cells
of the alveolar wall,
• very thin layer of interstitial
potential space,
• equally thin layer of arterial
endothelial lining.
Normal A-a gradient
• 5-25 mmHg or
• < age/4 + 4
• < (age+10)/ 4
Abnormal A-a gradient
 Elevated > 25 mmHg – oxygenation failure
• anything that come between those thin layers - interstitial
fluid and alveolar oedema (APO, Pneumonia, ARDS);
• V/Q mismatches (Pneumonia, PE, atelectasis);
• R-to-L shunts (PFO, ASD, PE, Pulmonary AVM).
 Low < 5 mmHg – ventilation failure
• CNS disorders, neuromuscular disease, oversedation;
• Low FiO2 (high altitude).
Is the A-a gradient helpful ?
• On a busy night at the ED, a nurse slips you
the ABG result of a patient that you had seen
60 minutes ago.
• You'd almost forgotten the details of the
history already; except that the patient was
symptomatically breathless, but you could not
identify any focal signs.
• You had seen another 3 patients since then,
and another 3 are waiting for you.
• ABG that is shown to you: pH 7.34, pO2 94, pCO2 40
and HCO3 25
• You probably think that it is not too bad, right ? Not
too abnormal results, huh ?
• And if you are anything like me, you may be
grumbling to yourself that your very own ABG may
not be anywhere near that good. Ahaa !
• The problem is that, you have forgotten that due to
the symptomatic breathlessness, the patient has
been on a nasal prongs oxygen at 3 L/min, which
probably gives an FiO2 of around 0.3 [30% oxygen].
• So the oxygen concentration should be much higher.
pH 7.35, PO2 94, PCO2 40, HCO3 25
• Let's try calculating the A-a gradient and see what it tells us.
• Alveolar Oxygen Concentration is calculated as follows: at sea level BP =
760 mm Hg, at 37 C water pressure = 47 mm Hg
PAO2 = (760-47) x FiO2 – PaCO2/R
= [(760-47) x 0.30] - [40/0.8]
= 164 mm Hg.
Measured PaO2 = 94 mm Hg
Which gives an A-a gradient of a whopping 70 mm Hg !!!!
• So there are huge problems with the lungs; and the ABG is no where near
as normal as initially thought !
• What could be the problem ?
• Did you really narrow your DD ?
• Calculating the A-a gradient is more academic then making a
difference in diagnosis
• It doesn't tell you what the problem is it just tells you that there is a
• Most of the time you would not need an A-a gradient to tell you
that there is a problem and most of the time clinical history and
assessment will tell you what the problem is.
• In general we would not do an ABG unless the patient is in severe
respiratory distress and you are unable to check saturation using a
non invasive sats probe.
• In an intubated patient ABG maybe more useful for obvious
reasons. In ED, non intubated patients, it maybe quite unnecessary.
The time and risk involved outweighs its clinical usefulness..
• The procedure to procure an ABG is not without risk. It is only a
matter of time before some patient ends up with an ischemic hand.
What we should remember?
• Step wise approach to acid base analysis
• Look at the pH: acidaemia or alkalaemia ?
If pH within a normal limit but abnormal PCO2 or HCO3 look at pH again –
whichever side of 7.40 the pH is on, the process that caused it to shift to that side
is the primary abnormality
Principle: The body does not fully compensate for primary acid-base disorders
• Indentify primary process: remember ROME
alkalosis ↑ pH, ↓ PaCO2
acidosis ↓ pH, ↑ PaCO2
alkalosis ↑ pH, ↑ HCO3
acidosis ↓ pH, ↓ HCO3
Compensation rules and limits
Expected PCO2
• Metabolic acidosis The One & a Half plus 8 Rule
Winter’s formula
• Metabolic alkalosis The Point Nine plus Nine Rule
Expected HCO3
• Respiratory acidosis acute
• Respiratory alkalosis acute
The 1 for 10 Rule
The 4 for 10 Rule
The 2 for 10 Rule
The 5 for 10 Rule
Compensation Limits
 Metabolic acidosis
 Metabolic alkalosis
PaCO2 ≥ 10mmHg
PaCO2 ≤ 60mmHg
 Respiratory acidosis
 Respiratory alkalosis
HCO3 ≤ 40mmol/L
HCO3 ≥ 10mmol/L
(≥ 18 in acute)
• Calculate the anion gap: Na – (Cl + HCO3)
If AG is ≥ 20, there is a primary metabolic acidosis
regardless of pH or HCO3
Principle: The body does not generate a large
anion gap to compensate for a primary disorder
• Calculate the excess anion gap: ∆ AG = AG – 12
• Add ∆ AG to the measured HCO3
 if the sum is greater than a normal HCO3 (>30) there is
an underlying metabolic alkalosis;
if the sum is less than a normal HCO3 (<22) there is an
underlying non anion gap metabolic acidosis
Principle: 1 mmol of unmeasured acid titrates 1
mmol of bicarbonate (+ ∆ AG= - ∆ HC03 )
Clinical correlation
Know the causes of WAGMA and lactic acidosis
Know the causes of NAGMA – USED CARP
Metabolic acidosis (kidney and gut)
Metabolic alkalosis (saline responsive or not?)
Respiratory disorders
A-a gradient – limitations and usefulness
questions ?
• Describe
state the characteristics or appearance of the
subject, including relevant negatives.
• Interpret
state a conclusion or conclusions which
includes a differential diagnosis, but excludes
• An 84 year old man is brought to your ED following a high
speed car accident.
• He has sings of multiple rib fractures.
• Two hours after arriving in the ED he becomes more
breathless and distressed.
• His observations are:
GCS 14, HR 75, BP 100/60, RR 24.
• He is on 50% O2, ABGs are performed:
pH 7.14, pCO2 60, pO2 114, HCO3 17,
Lactate 1.4, Na 139, K 4.8, Cl 116, Glucose 11.3.
• Describe and interpret his results.
• An 8 year old girl is brought to your ED with a 3 week
history of general malaise. On the morning of
presentation, she was found by her mother to be very
lethargic and difficult to rouse.
• Her observations are:
GCS 9, HR 110, BP 85/50, RR 18, temp 36oC
• VBG results:
pH 7.31, PCO2 31, HCO3 17, Na 128, K 5.9, Cl 100, Gluc 1.5
• Describe and interpret the results of her investigations

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