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.
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Look at the pH.Acidaemia or alkalaemia?
Who is responsible for this change in pH ( primary culprit )?
Calculate compensatory changes.
Acute or chronic process?
Calculate AG and ∆ gaps.
Is there any additional pathological process?
Mixed metabolic or respiratory disturbance?
Clinical correlation? Find the diagnosis.
pH 7.47, PCO2 20, HCO3 15, Na 145, Cl 100
pH of 7.10, a PCO2 50, HCO3 15, Na 145, Cl 100 ?
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
increased H+ consumes HCO3-
loss of HCO3- (kidney or gut) will raise Cl-
hence non anion gap
[Na+] + [K+] = [Cl-] + [HCO3-] + [AG- ]
A CAT MUDPILES
A-Analgesics (massive NSAID, acetaminophen)
C-Cyanide, Carbon monoxide
A-Arsenic, Alcoholic ketoacidosis
M- Methanol, metformin
A- Alcoholic ketoacidosis
a useful misspelling of Adolph Kussmaul's name
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 COPD.
Kussmaul disease (also called Kussmaul-Maier disease) - Polyarteritis nodosa.
G- Glycols (ethylene and propylene),
R- Renal failure, and
renal failure (acute or chronic)
DKA, Alcoholic, starvation
L-lactate and D-lactate
ethylene glycol – oxalic acid, methanol – formic acid, oxoproline acid
Type B - impaired mitochondrial O2 utilisation and impaired excretion
LUKE TIPS FAILURES:
Leukaemia, Lymphoma, Thiamine deficiency, Infections, Pancreatitis, Short bowel syndrome (D-Lactate), Failures: hepatic, renal, diabetic;
loss of HCO3- (kidney or gut) will raise Cl- , hence non anion gap.
S- Small bowel fistula
E- Extra chloride (K+ normal or ↑)
C- Carbonic anhydrase inhibitor
A- Addison’s disease (K+↑)
R- Renal tubular acidosis (RTA)
P- Pancreatic fistula
Urinary chlorine < 10 mmol/L
Volume normal or overloaded
Urine chlorine > 20 mmol/L
inherited thick ascending limb of the loop of Henle and excretion excessive amounts of Na, K, Cl.
Renal artery stenosis
stimulates the renin-angiotensin-aldosterone system
Severe hypo K+ and hypo Mg2+
Current diuretics use
vomiting, gastric alkalinisation, gastric aspiration
chronic diarrhoea (Cl-)
remote diuretic use
chronic ingestion of large doses of CaCO3 . Hypercalcemia increases renal bicarbonate reabsorption
Central / supratentorial
Mild to moderate HI
Anxiety (fear, stress)
It is simply the difference between Alveolar concentration of O2 (PAO2), and arterial concentration of O2 (PaO2).
PAO2 = (760-47) x 0.21 – 40/0.8
PAO2 = 149 – 50
PAO2 = 99
PAO2 = (760-47) x 0.3 – 40/0.8
PAO2 = 214 – 50
PAO2 = 164
PAO2 = (760-47) x 0.4 – 40/0.8
PAO2 = 285 – 50
PAO2 = 235
PAO2 = (760-47) x 0.5 – 40/0.8
PAO2 = 356 – 50
PAO2 = 306
PAO2 = (760-47) x 0.7 – 40/0.8
PAO2 = 499 – 50
PAO2 = 449
PAO2 = (760-47) x 1.0 – 40/1.0
PAO2 = 713 – 40
PAO2 = 673
Normally some A-a gradient exists b/o anatomical barriers between alveolar air and the blood that would become arterial blood:
Normal A-a gradient
= [(760-47) x 0.30] - [40/0.8] = 164 mm Hg.
Measured PaO2 = 94 mm HgWhich gives an A-a gradient of a whopping 70 mm Hg !!!!
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
alkalosis ↑ pH, ↓ PaCO2
acidosis ↓ pH, ↑ PaCO2
alkalosis ↑ pH, ↑ HCO3
acidosis ↓ pH, ↓ HCO3
chronic The 4 for 10 Rule
chronic The 5 for 10 Rule
(≥ 18 in acute)
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
Principle: 1 mmol of unmeasured acid titrates 1 mmol of bicarbonate (+ ∆ AG= - ∆ HC03 )
state the characteristics or appearance of the subject, including relevant negatives.
state a conclusion or conclusions which includes a differential diagnosis, but excludes management.
GCS 14, HR 75, BP 100/60, RR 24.
pH 7.14, pCO2 60, pO2 114, HCO3 17,
Lactate 1.4, Na 139, K 4.8, Cl 116, Glucose 11.3.
GCS 9, HR 110, BP 85/50, RR 18, temp 36oC
pH 7.31, PCO2 31, HCO3 17, Na 128, K 5.9, Cl 100, Gluc 1.5