Acid-base disorder

ACID–BASE disorder
Look at the values obtained from “Arterial Blood Gas (ABG)” to diagnose acid-base disorder and the cause of
it. 1st We’ve to look at serum pH, whether it’s acidic or basic or Normal? Then next step is to find out which
one (PaCO2 or HCO3 - ) value correlates with the pH status.
Few imp points to be understood

1. pH ∝ HCO3 - , so if serum HCO -  then pH , if P CO (H+) increases then pH 

3 a 2
PaCO2 (H+)

2. Normal pH = 7.35 – 7.45

3. Normal value of HCO3 - is 24 mEq/L +/- 3 and HCO3 - content is always controlled metabolically. If
it’s high then the metabolic component is increasing the alkalotic content of blood - and vice versa.
MRS. HCO3 3 2-3-4, so N value is 24 +/- 3.
4. Normal value of PaCO2 (H+) is 40 mmHg – and always controlled by respiratory component. If it’s
high then it’s increasing the acid content, if it’s  then it’s decreasing the acid content of arterial
blood.
5. Compensation is Never Complete (for e.g. respiratory compensation of metabolic acidosis can
never bring-back the pH to normal) – the only Exception to this rule is “High-altitude alkalosis”.
6. If pH is N and HCO3 - or PaCO2(H+) is deranged, then it should be a mixed disorder of primary acid/
primary base, because we all know that “Compensation is never complete”.
Note- Respiratory compensation of either acid or base disorder is immediate, so most of the Non-respiratory
causes of acid-base disorders will have respiratory compensation. Whereas metabolic compensation, usually
by the kidneys, takes 2-3 days to kick in, via increasing re-absorption of HCO3 - or increasing excretion of
HCO3 - in urine. So primary respiratory acid/base disorder may not have metabolic compensation especially if
the respiratory P/P is acute in process.
So let’s play with some ABG values- try to explain it 1st and then only look at the ans.

No. pH PaCO2(H+) HCO3 -

7.31 45 25 pH ∝ HCO3 -
7.33 45 30  PaCO2 (H+)
7.33 34 14
7.20 50 14  Normal pH = 7.35 – 7.45
7.40 50 34
7.40 32 17  Normal value of HCO3 - is 24 mEq/L +/- 3
7.47 32 23
 Normal value of PaCO2 is 40 mmHg
7.46 32 30
7.46 45 18
Answers –

1. pH is acidic, now look “which one of the values correspond with the pH status?” The  in PaCO2(H+) is
causing acidic pH. So the Dx is primary Respiratory acidosis (always due to Alveolar hypoventilation).
HCO3 - value is within the N range, so metabolic compensation by kidney hasn’t kicked in. Dx is Acute
Hypoventilation - Commonly seen in ER with (1) Benzodiazepines + alcohol or (2) Phenobarbitals or
(3) Opiate (heroin) - overdose.

2. pH is acidic; PaCO2 (H+) is, so it’s primary respiratory acidosis. HCO3 - is , so metabolic compensa-
tion (mostly by kidney) has kicked in now. Dx is Chronic Hypoventilation - Commonly seen in Chronic
Bronchitis.

3. pH is acidic, now the value of PaCO2(H+) is , so it doesn’t correspond with pH status. Now look at HCO3
-
value which is, so it corresponds to the pH value, so it’s primary Metabolic acidosis with instantly
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starting – compensatory respiratory alkalosis. NSIDx is Calculate serum Anion Gap.
 Acid-base disorder

4. pH is acidic and too low, and there’s Respiratory acidosis (PaCO2(H+) is ) and metabolic acidosis
(HCO3 - is ), so Dx is mixed acid/acid disorder - seen in cardiopulmonary arrest (cardiac arrest causes
Lactic acidosis and Pulmonary arrest causes Alveolar hypoventilation).
5. pH is N, PaCO2 (H+) is ( so respiratory acidosis) and HCO3 - is ( so metabolic alkalosis)- this is a
mixed acid/base disorder. But wait “Can there be full compensation?” No, it can’t be because remember
that COMPENSATION IS NEVER COMPLETE.
6. pH is N , PaCO2(H+) is  (respiratory alkalosis) and HCO3 - is ( metabolic acidosis)- This can be due
to
 Mixed acid-base disorder, as in cases of overdose of Aspirin in Adults.

 The only one situation where compensation is complete, in which primary respiratory alkalosis is
fully compensated by metabolic acidosis i.e. Acclimatization in High–altitude.
7. pH is high, so Alkalosis, PaCO2  and HCO3 - is within N range. Dx is respiratory alkalosis - No metabolic
compensation yet – cause is Acute Hyperventilation due to (1) acute Hypoxemia or (2) Panic attack.
8. pH is Alkalotic, PaCO2  and HCO3 -  . Dx is Primary Respiratory alkalosis with metabolic acidosis as
compensation - due to Chronic Hyperventilation of any cause for e.g. in Anemia.
9. pH is Alkalotic and PaCO2  (respiratory acidosis) – which must be compensatory. HCO3 - is , so it is
Metabolic alkalosis with Respiratory compensation. Dx can be
 Renal loss (Conn’s or Cushing)

 GI loss (vomiting/diarrhea) or

 Diuretics- except Acetazolamide and K+ sparing diuretics

A simplified Algorithm for Acid-base disorders

1st step is to look at pH-

pH  pH 

if PaCO2 is > 40 mmHg if HCO3 - is < 24 if PaCO2 is < 40 mmHg if HCO3 - is > 24
it's Respirtory Acidosis It's Metabolic Acidosis It's Respiratory Alkalosis It's Metabolic Alkalosis

NSIDx is
calculation of serum ANION GAP

if < 12 then NSIDX if > 12 then

Urine anion gap it must be KUSSMEIL1

if - ve if +ve

Non-renal cause of Renal cause of acidosis

Acidosis

1. See Metabolic Acidosis chapter

Respiratory acidosis
Alveolar Hypoventilation is the cause. Primary respiratory acidosis is most of the time managed with
120 noninvasive Bi-PAP or Invasive Intubation and ventilation.
 Acid-base disorder

RESPIRATORY ALKALOSIS
Hyperventilation due to conditions like (1) Hypoxia or (2) Respiratory stimulators or (3) panic attack - can
cause acute Resp alkalosis, which can cause acute Hypocalcemia resulting in Neuro-muscular excitation with
S/S of paresthesia, hyper-active Deep Tendon Reflexes, peri-oral numbness, carpo-pedal spasm and tetany to
seizures.

1. Hypoxia- leads to compensatory increase in ventilatory drive which flushes out the CO2.

2. Increase in Progesterone (which is a respiratory stimulant) for e.g. in

 pregnancy

 Cirrhosis –due to decreased metabolism of progesterone.

3. Panic/Anxiety Attack. CCS- patient with sudden onset of chest pain, sweating and palpitation.
Rule out Pulm-Embolism and MI by doing EKG and CXR. If ABG is done, it will show respiratory
alkalosis without metabolic compensation. NSIM  ask the patient to breathe in a closed bag, if still
not responding then Diazepam can be given to the patient. (But personally in my experience, rather
than breathing into an air bag I’ve found that it’s more effective to show and empower the patient
on how to control respiration. If asked to breathe into the bag the patient can get more anxious and
hypoxemic with more increase in Respiratory Rate.)

METABOLIC ACIDOSIS (MAC)

 With compensatory Respiratory alkalosis (deep and fast breathing which is called Kussmaul breathing)

 NSIDx after ABG’s shows MAC is measurement of anion gap.

 What’s anion gap? It‘s the “sum of all the +ve charged ions” minus “sum of all –ve charged ions”, in serum
electrolyte panel

i.e. (Na+ + k+) – (Cl- + HCO3- ) = which should normally be < 12.

 If Anion Gap is < 12, then it’s Normal anion gap Metabolic acidosis(MAC)

 If Anion Gap is ≥ 12, then there’s presence of unmeasured Cations in blood causing MAC.
Careful review of H/O patient would point to the cause.

High Anion Gap MAC

 MRS--KUSSMEIL is the cause of Kussmaul breathing with high anion gap MAC.

 K- ketoacidosis –which can develop in Diabetic Ketoacidosis, Alcoholism and Malnutrition.

 U- Uremia – H/O CRF or ARF.

 SS- Salicyclates – H/O oral ingestion of Salicyclates and S/S associated with it.

 M- Methanol – usually with H/O alcoholism or a Homeless person presenting with - confusion +
visual disturbances

 E- Ethylene gycol (anti-freeze)- usually with H/O alcoholism or a Homeless person presenting with
- Confusion + Renal failure.

 I- Inorganic acids like PO4--and SO4--accumulation, for e.g. in Chronic Renal failure (CRF). Note in
later stages of CRF, MAC can develop due to impaired NH4+ excretion.
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 Acid-base disorder
 L- Lactic acidosis- The causes are hypoxemia ischemia excessive anaerobic glycolysis- this
can occur in conditions like (1) Septic shock, (2) transient Post-seizure acidosis, and (3) bowel
ischemia- CCS an old patient with unrecognized lactic acidosis with H/O abdominal pain after
meals.
Normal anion gap MAC
 If Dx is not clear about what is causing this acid imbalance, then NSIDx is urinary anion gap, which is
very helpful in delineating the cause.

 The idea of Urinary Anion Gap (UAG) is same as serum anion gap with, “Sum of all +ve anions” minus
“sum of all –ve Cations” in urine.

 (Na+ + k+) – (Cl- ) = Urinary Anion Gap (UAG)

Note; Urinary Cl- concentration directly correlates with Urinary NH4+secretion so UAG can be used to measure
urine NH4+ concentration

 If UAG is negative then Cl- is high, so NH4+ must be high in urine, suggesting an appropriate increase
in excretion of acid (H+) in the form of NH4+ to compensate for Non-renal cause of MAC. Fluid
loss in Diarrhea or Duodenal fistula results in HCO3 - loss causing metabolic Acidosis - and kidneys
compensate by  NH4+ secretion, so urinary Cl- content will be high and UAG would be –ve.

 If there’s defective NH4+ production and secretion, then the NH4+ will be low in urine and MAC will
develop. So as the Urinary Cl- is low, UAG will be +ve  as in renal cause of N anion gap MAC
for e.g. in Renal-Tubular-Acidosis 1, 2 and 4 or Acetazolamide.
Remember that Gastric acid secretion is acidic and loss of it causes Metabolic alkalosis, but beyond
stomach, in the intestines fluid loss results in HCO3- loss which will result in MAC.

Types of Renal Tubular Acidosis (RTA)

RTA 1 (distal RTA) RTA 2 (proximal RTA) RTA 4
P/P Distal H+ ion pump is In the Proximal  The Juxta-glomerular
not working – so K+ is Convoluted Tubule, apparatus is knocked off –
excreted to reabsorb Na+ HCO3- reabsorption low Renin- low Aldosterone
in distal tubules, so K+ pump isn’t working acidosis. Diabetes- MCC
is   Low Aldosterone/high renin
in Addison’s disease
Imp association Renal stones Osteomalacia S/S of Hyperkalemia for e.g.
weakness
Serum potassium  N or  
Tx Oral HCO3- and K+ Thiazide diuretics and Replace Aldosterone with
1
replacement replace K+. Fludrocortisone
1. Thiazide induced Mild vol. depletion enhances absorption of HCO3 -
from Proximal Convoluted
Tubule.

 Causes of RTA are very vast, and knowing its etiology is less imp than how to make Dx and How to
Treat.

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 Acid-base disorder

METABOLIC ALKALOSIS
This is the MC acid-base disorder in hospitalized patients, due to common things like (1) diuretics and (2) Gastric
fluid loss from procedures like NG tube aspiration. Compensation is immediate respiratory hypoventilation
with Hypocapnia.

Approach for Dx of Metabolic Alkalosis

Metabolic alkalosis

assess the volume status and serum K+

Hypertensive and Normotensive/Hypotensive

Hypokalemia usually due to
usually due to primary ECF loss and compounded by secondary
HyperAldesteronemia or Hyperaldosteronemia
Hypercortisolemia
 Conn's Syndrome
Cushing' syndrome
 Renal artery stenosis NSIDx is Urinary Cl-

low Urinary Cl- high Urinary Cl-

1. Gastric Fluid loss 1. Current diuretic ingestion
2. Prior diuretic ingestion 2. Bartter and Gittleman's syndrome
collectively called Contraction
alkalosis

Causes of Metabolic alkalosis

1. Loss of gastric fluid—for e.g. (1) Too much vomiting or (2) NG tube aspiration. Loss of K+, Cl-, H+
and water (which are the major contents of Gastric juice). NSIM is IV Normal saline.
2. Diuretics- most of the diuretics results in Metabolic alkalosis with secondary volume depletion- ex-
ception is Acetazolamide which causes MAC.
3. Bartter’s syndrome- which is due to genetic deficiency in Na+-K+-2Cl- co-transporter in Thick
Ascending loop of Henle- MRS- think that Bartter’s patients are on Chronic Furosemide Tx as
Furosemide blocks the same co-transporter. Barter lasix
4. Gittleman’s syndrome which is due to genetic deficiency in Na+Cl- co-transporter if Distal convo-
luted tubule-MRS- think that these patients are on Chronic Thiazide Tx as Thiazide blocks the
same co-transporter. Gittleman-thiazide
5. Hepatic encephalopathy- Hyperammonemia-this is a basic ion.
6. Citrate- which is basic (–ve charged ion) for e.g. in cases of too much blood transfusion.
7. Conn’s syndrome - high levels of Aldosterone which re-absorbs Na+ in exchange for K+ or H+
which are increasingly excreted in urine. Note a mimicker of Conn’s syndrome is Liddle syndrome-
this genetic disease results in over activity of Aldosterone receptors.
8. Too much Glucocorticoids- which acts like its’ close relative Aldosterone, for e.g. in Cushing syn-
drome.
9. Renal artery stenosis with resultant secondary Hyperaldosteronism and resulting HTN
10. MgOH2 and CaCO3 antacid over ingestion -- which is called the Milk-Alkali syndrome, but it is
very rare nowadays, due to better medication for acute Peptic Ulcer Disease. 123