Acid-base, electrolytes and fluid balance Flashcards
Acidosis vs Acidaemia
acidiosis is an abnormal condition which tends to decrease arterial pH, and similarly alkalosis is an abnormal condition which tends to increase arterial pH
Compensation
Normal body process which attempt to return the arterial pH to normal - uses respiratory and renal buffering mechanisms
Why is the number of H+ important?
Cellular machinery is very sensitive to changes in H+
Intracellular H+ is related to extracellular H+ and Na and K+ ions
Acid-base balance
At normal pH [H+] is 40nmol/L, as pH is -log10[H+] = 7.4
Between pH 6-7 there is a 10x change in H+
Normal pH is 7.35-7.45
Behavior of weak acids
HA H+ & A-
The law of mass action –> [H+][A-]/[HA] = K
Henderson Hasselbach equation: pH=pKa + log10[A-]/[HA]
Buffering theory
Enables the body to handle H+ without a change in pH
This is most effective when th pKa of the buffer is close to the working pH
Buffering molecules
Haemoglobin Proteins Phosphate (PO4--) Bicarbonate (HCO3-) (Renal) Carbon Dioxide (about 60%) (Respiratory)
Carbonic acid and bicarbonate system
CO2 + H20 HCO3- + H+ (speeded by carbonic anhydrase) –> very rapid changes
Rise in PCO2 increases [H+] and lowers pH
Decrease in PCO2 reduces [H+] and increases pH
Renal compensation mechanisms
H+ is secreted and HCO3 is reabsorbed by renal tubules
(dependent on filtered load of HCO3 and GFR)
H+ secretion is dependent on arterial PCO2
In a respiratory acidosis more H+ is secreted and in a alkalosis secretion is decreased and HCO3 reabsorption is depressed
Clinical Signs of Acidosis
CVS –> neg. inotropic effect, catecholamine release, tachy, arrhythmias, peripheral vasodilation, renal and GI vasoconstriction
GI –> Decreased Gut motility
RS –> pulmonary vasoconstriction, increased ventilatory drive until PCO2>13Kpa, Bronchodilation,
Electrolytes –> High Ca++ and K+
CNS –> reduced GCS, Changes in CBF/ICP,
Clinical Signs of Alkalosis
CVS –> Increased coronary & systemic vascular resistance, Left shift in Hb/O2 dissociation curve, decreased DO2
Electrolytes –> Low Ca++ and K+
CNS –> epilepsy
Causes of Respiratory alkalosis
Cental –> CNS lesions, aspirin, anxiety, pregnancy, septicaemia, liver failure
Pulmonary –> pneumonia, asthma, CCF, PE, hyperventilation
Causes of Respiratory acidosis (Hypoventilation)
CNS trauma –> trauma/infection/tumor/etc
Drugs –> sedatives or narcotics
Neuromuscular compromise
Airway obstruction –> FB, asthma, COPD
Causes of Metabolic alkalosis
Loss of H+ –> gastric (vomiting or drainage), urine (Cushings or diuretics), Potassium deficiency (drives H+ into cells)
Excessive intake of HCO3 –> As bicarbonate, lactate or citrate
Causes of Metabolic acidosis
Increased H+ –> renal failure, ketoacidosis, lactate acidosis, ingesting aspirin/glycol/ethanol
Decreased H+ secretion –> renal failure, renal tubular acidosis, mineralocorticoid deficiency
Loss of bicarbonate –> diarrohea or pancreatic fistula, proximal RTA
Blood gas interpretation
- pH –> acidosis or alkalosis
- CO2 –> if it agrees with the pH it is resp, if not metabolic
- BE –> HCO3 -25 is BE, -ve is acidotic, +ve is alkalotic
Electrolyte normal values
Na+ 134-141mmol/L
K+ 3.5-4.5 mmol/L
Cl- 100-105mmol/L
HCO3— 24-28mmol/L
Electrolyte daily intake
Na+ –> 80mmol/day (0.5L of 0.9% saline)
K+ –> 80mmol/day
Water –> ~ 3L per day
Fluid compartments of the body
The whole body is: 18% protein, 7% mineral, 15% fat, 60% water
Intracellular water is 40% of body weight
Extracellular water is 20% of body weight
Causes of Hyponatraemia
Artifact or contamination of the sample
Severe hyperlipidaemia or hyperproteinaemia
Reduced Na intake is rare but increased Na loss is common
Hyponatraemia with normal ECF volume
Water excess –> psychogenic polydipsia, disorders of the thirst centre, beer drinkers potomania or normal intake with poor renal function
SIADH –> CNS disease, tumor, chest disease, carbamazapine
Or increased sensitivity to ADH (or oxytocin) or abnormal ADH release (hypothyroid, Addisons, vagal neuropathy)
Hyponatraemia with decreased ECF volume
GI –> Vomiting, diarrhoea, haemorrhage
Kidney –> osmotic diuresis, diuretics, recovery of acute tubular necrosis, renal artery stenosis
Management of Hyponatraemia
Na, limit fluid, enhance water excretion, demeclocycline or hypertonic saline
Demeclocycline
An antibiotic which is actually used to induce nephrogenic diabetes insipidus by reducing the sensitivity of collecting duct cells to ADH and so it is used to treat hyponatraemia
Hypernatraemia
ADH deficiency (diabetes insipidus) or insensitivity (Li, ATN or tetracyclines) Iatrogenic from hypertonic solution Osmotic duresis (TPN or hyperosmolar coma) Deficient water intake
Management of Hypernatraemia
Na>145mmol/L
thirst, confusion, coma, cerebral thrombosis,
Treat with slow correction with 0.9% saline and beware cerebral oedema
Causes of Hypokalaemia
reduced intakes (anorexia) or artefact Usually due to a shift into cells --> alkalosis, insulin, catecholamines, paralysis (rare) Increased loss--> Renal (alkalosis, diuretics, tubular damage, hyperaldosteronism, hypomagnesaemia) or GI (vomiting, diarrhoea or laxatives)
Management of Hypokalaemia
Symptoms –> weakness and lethargy, arrhythmias,
Treatment –> careful supplementation and treat underlying cause
Causes of Hyperkalaemia
Artefacts (common) – haemolysis, contaminated sample
Increased intake from supplements (rare)
Shift out of cells –> acidosis, cell lysis (burns or crush injuries)
Decreased Loss –> acidosis, renal failure, K+ sparing diuretics, addisons, ACEis, cyclosporin
Management of Hyperkalaemia
Symptoms –> Ca gluconate –> protect the myocardium, arrhythmias or cardiac arrest, ECG changes
Treatment –> Oral cation exchange resin (polystyrene sulphonate) to increase gut excretion, glucose and insulin
Insulin management of hyperkalaemia
- Sodium bicarbonate 50ml of 8.4% IV
- -> Ca gluconate (protect the myocardium) - Glucose (200ml of 10%) plus 10 units of insulin
ECG changes in severe hyperkalaemia
Broad QRS
Peaked T
ST depression
Absent P
Perioperative fluid management
Aim to maintain circulating volume
Normal electrolyte balance, with normal Hb and glucose
Replace ongoing fluid losses with fluid or blood
Replacing fluid deficit due to starvation
Hourly maintenance x hours starved
Hourly maintenance of fluid
0-10kg = 4ml/kg/hr
10-20kg = (40ml + 2ml/kg)hr
>20kg = (60ml + 1ml/kg)hr
Eg 85kg man requires 125ml/hr maintenance
Where does fluid go?
Water or detrose will distribute across all body fluid, only 5-10% stays in blood
30-35% of saline stays in blood while all of blood stays in the blood
Causes of anion gap metabolic acidosis (CAT MUDPILES)
Cyanide, CO, congestive heart failure Aminoglycosides Theophylline Methanol Uraemia Diabetic (EtOH/starvation) ketoacidosis Paraldehyde, paracetamol, phenformin Iron, isoniazid, inborn errors Lactic acidosis Ethanol/ethylene glycol Salicylate
