2. Acid-base Balance Flashcards
POCT (point of care testing / bedside testing)(8)
1) Faster result
2) Small sample size
3) Reduced preanalytic errors
4) Eliminate / minimize preparation steps
5) Improved patient satisfaction
6) Faster decision making and follow-up with patient
7) Better management of therapy
8) Convenience
PH of extracellular vs intracellular space
Ec: 7,38 - 7,42
Ic: 6,8
Sources of H+
- Intake, metabolism (50 mmol/d) = metabolic
- CO2 (12500 mmol/d) = respiratory
Elimination of H+
- Kidney
- Lung (CO2)
- GI
- Liver
Buffer with highest buffer capacity in body
Bicarbonate
Methods for evaluation of metabolic changes
1) Henderson-Hasselbalch (HCO3-)
2) Siggaard-Andesson (BE-)
3) Stewart (strong ion difference), anion gap
PH arterial vs venous BG
Arterial: 7,35 - 7,45
Venous: 7,35 - 7,43
PCO2 arterial vs venous BG
Arterial: 35 - 46 mmHg
Venous: 37 - 50 mmHg
Bicarbonate arterial vs venous BG
Both: 21 - 26 mmol/l
BE arterial vs venous BG
Both: +/- 2,5 mmol/l
Anion gap arterial vs venous BG
Both: 10 - 14 mmol/l
Practical classification of acid-base disorders
- Iatrogenic
- Fixed
- Symptom of ongoing acute illness
- Only metabolic acidosis has real clinical importance
Increased AG metabolic acidosis
MUDPILES M: Methanol U: Uremia D: (Diabetic) ketoacidosis (or alcoholic, starvation, metabolic error) P: Paracetamol, phenformin, paraldehyde I: Iron, Isoniazide L: Lactic acidosis E: Ethanol S: Salicylates
Non-anion gap acidosis causes
- Renal tubular acidosis
- GI acidosis
- Iatrogenic acidosis
Symptoms metabolic acidosis (10)
1) Increased symp activity
2) Decreased inotropy, arterial dilation (critical pH 7,2)
3) Decreased oxygen binding to Hgb
4) Hyperkalemia
5) Insulin resistance
6) Free radical formation
7) Bone demineralization
8) Emesis
9) Decreased sensorium
10) Hyperventilation
