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Acid-base disorder

ACIDBASE disorder
Look at the values obtained from Arterial Blood Gas (ABG) to diagnose acid-base disorder and the cause of it. 1st Weve to look at serum pH, whether its 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. 2. 3. pH HCO3 - , so if serum HCO - then pH , if P CO (H+) increases then pH 3 a 2 PaCO2 (H+) Normal pH = 7.35 7.45 Normal value of HCO3 - is 24 mEq/L +/- 3 and HCO3 - content is always controlled metabolically. If its 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. Normal value of PaCO2 (H+) is 40 mmHg and always controlled by respiratory component. If its high then its increasing the acid content, if its then its decreasing the acid content of arterial blood. 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. 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.

4.

5. 6.

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 lets play with some ABG values- try to explain it 1st and then only look at the ans. No.

1) 2) 3) 4) 5) 6) 7) 8) 9)

pH 7.31 7.33 7.33 7.20 7.40 7.40 7.47 7.46 7.46

PaCO2(H+) 45 45 34 50 50 32 32 32 45

HCO3 25 30 14 14 34 17 23 18 30 30 18

pH HCO3 PaCO2 (H+) Normal pH = 7.35 7.45 Normal value of HCO3 - is 24 mEq/L +/- 3 Normal value of PaCO2 is 40 mmHg

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 hasnt kicked in. Dx is Acute Hypoventilation - Commonly seen in ER with (1) Benzodiazepines + alcohol or (2) Phenobarbitals or (3) Opiate (heroin) - overdose. pH is acidic; PaCO2 (H+) is, so its primary respiratory acidosis. HCO3 - is , so metabolic compensation (mostly by kidney) has kicked in now. Dx is Chronic Hypoventilation - Commonly seen in Chronic Bronchitis. pH is acidic, now the value of PaCO2(H+) is , so it doesnt correspond with pH status. Now look at HCO3 value which is, so it corresponds to the pH value, so its primary Metabolic acidosis with instantly starting compensatory respiratory alkalosis. NSIDx is Calculate serum Anion Gap.

2.

3.

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Acid-base disorder
4.

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pH is acidic and too low, and theres 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). 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 cant be because remember that COMPENSATION IS NEVER COMPLETE. 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

5.

6.

fully compensated by metabolic acidosis i.e. Acclimatization in Highaltitude.

7. 8. 9.

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. 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. 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 (Conns 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 it's Respirtory Acidosis

if HCO3 - is < 24 It's Metabolic Acidosis

if PaCO2 is < 40 mmHg It's Respiratory Alkalosis

if HCO3 - is > 24 It's Metabolic Alkalosis

NSIDx is calculation of serum ANION GAP

if < 12 then NSIDX Urine anion gap if - ve Non-renal cause of Acidosis

if > 12 then it must be KUSSMEIL1 if +ve Renal cause of acidosis

1.

See Metabolic Acidosis chapter

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

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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. 2. Hypoxia- leads to compensatory increase in ventilatory drive which flushes out the CO2. 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 Ive found that its 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 ABGs shows MAC is measurement of anion gap. Whats anion gap? Its 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 its Normal anion gap Metabolic acidosis(MAC) If Anion Gap is 12, then theres 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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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. 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.

If theres defective NH4+ production and secretion, then the NH4+ will be low in urine and MAC will

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)

P/P RTA 1 (distal RTA) Distal H+ ion pump is not working so K+ is excreted to reabsorb Na+ in distal tubules, so K+ is Renal stones Oral HCO3- and K+ replacement RTA 2 (proximal RTA) In the Proximal Convoluted Tubule, HCO3- reabsorption pump isnt working RTA 4 The Juxta-glomerular apparatus is knocked off low Renin- low Aldosterone acidosis. Diabetes- MCC Low Aldosterone/high renin in Addisons disease Osteomalacia S/S of Hyperkalemia for e.g. weakness N or 1 Thiazide diuretics and Replace Aldosterone with Fludrocortisone replace K+.
-

Imp association Serum potassium Tx 1.

Thiazide induced Mild vol. depletion enhances absorption of HCO3 Tubule.

from Proximal Convoluted

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 Hypokalemia usually due to primary HyperAldesteronemia or Hypercortisolemia Conn's Syndrome Cushing' syndrome Renal artery stenosis

Normotensive/Hypotensive usually due to ECF loss and compounded by secondary Hyperaldosteronemia

NSIDx is Urinary Cl-

low Urinary Cl1. Gastric Fluid loss 2. Prior diuretic ingestion collectively called Contraction alkalosis

high Urinary Cl1. Current diuretic ingestion 2. Bartter and Gittleman's syndrome

Causes of Metabolic alkalosis

1. 2. 3. Loss of gastric fluidfor 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. Diuretics- most of the diuretics results in Metabolic alkalosis with secondary volume depletion- exception is Acetazolamide which causes MAC. Bartters syndrome- which is due to genetic deficiency in Na+-K+-2Cl- co-transporter in Thick Ascending loop of Henle- MRS- think that Bartters patients are on Chronic Furosemide Tx as Furosemide blocks the same co-transporter. Barter lasix Gittlemans syndrome which is due to genetic deficiency in Na+Cl- co-transporter if Distal convoluted tubule-MRS- think that these patients are on Chronic Thiazide Tx as Thiazide blocks the same co-transporter. Gittleman-thiazide Hepatic encephalopathy- Hyperammonemia-this is a basic ion. Citrate- which is basic (ve charged ion) for e.g. in cases of too much blood transfusion. Conns 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 Conns syndrome is Liddle syndromethis genetic disease results in over activity of Aldosterone receptors. Too much Glucocorticoids- which acts like its close relative Aldosterone, for e.g. in Cushing syndrome. Renal artery stenosis with resultant secondary Hyperaldosteronism and resulting HTN
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4.

5. 6. 7.

8. 9.

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.