Acid-base, electrolytes and fluid balance Flashcards

1
Q

Acidosis vs Acidaemia

A

acidiosis is an abnormal condition which tends to decrease arterial pH, and similarly alkalosis is an abnormal condition which tends to increase arterial pH

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2
Q

Compensation

A

Normal body process which attempt to return the arterial pH to normal - uses respiratory and renal buffering mechanisms

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3
Q

Why is the number of H+ important?

A

Cellular machinery is very sensitive to changes in H+

Intracellular H+ is related to extracellular H+ and Na and K+ ions

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4
Q

Acid-base balance

A

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

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5
Q

Behavior of weak acids

A

HA H+ & A-
The law of mass action –> [H+][A-]/[HA] = K
Henderson Hasselbach equation: pH=pKa + log10[A-]/[HA]

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6
Q

Buffering theory

A

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

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7
Q

Buffering molecules

A
Haemoglobin
Proteins
Phosphate  (PO4--)
Bicarbonate (HCO3-) (Renal)
Carbon Dioxide (about 60%) (Respiratory)
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8
Q

Carbonic acid and bicarbonate system

A

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

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9
Q

Renal compensation mechanisms

A

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

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10
Q

Clinical Signs of Acidosis

A

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,

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11
Q

Clinical Signs of Alkalosis

A

CVS –> Increased coronary & systemic vascular resistance, Left shift in Hb/O2 dissociation curve, decreased DO2
Electrolytes –> Low Ca++ and K+
CNS –> epilepsy

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12
Q

Causes of Respiratory alkalosis

A

Cental –> CNS lesions, aspirin, anxiety, pregnancy, septicaemia, liver failure
Pulmonary –> pneumonia, asthma, CCF, PE, hyperventilation

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13
Q

Causes of Respiratory acidosis (Hypoventilation)

A

CNS trauma –> trauma/infection/tumor/etc
Drugs –> sedatives or narcotics
Neuromuscular compromise
Airway obstruction –> FB, asthma, COPD

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14
Q

Causes of Metabolic alkalosis

A

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

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15
Q

Causes of Metabolic acidosis

A

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

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16
Q

Blood gas interpretation

A
  1. pH –> acidosis or alkalosis
  2. CO2 –> if it agrees with the pH it is resp, if not metabolic
  3. BE –> HCO3 -25 is BE, -ve is acidotic, +ve is alkalotic
17
Q

Electrolyte normal values

A

Na+ 134-141mmol/L
K+ 3.5-4.5 mmol/L
Cl- 100-105mmol/L
HCO3— 24-28mmol/L

18
Q

Electrolyte daily intake

A

Na+ –> 80mmol/day (0.5L of 0.9% saline)
K+ –> 80mmol/day
Water –> ~ 3L per day

19
Q

Fluid compartments of the body

A

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

20
Q

Causes of Hyponatraemia

A

Artifact or contamination of the sample
Severe hyperlipidaemia or hyperproteinaemia
Reduced Na intake is rare but increased Na loss is common

21
Q

Hyponatraemia with normal ECF volume

A

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)

22
Q

Hyponatraemia with decreased ECF volume

A

GI –> Vomiting, diarrhoea, haemorrhage

Kidney –> osmotic diuresis, diuretics, recovery of acute tubular necrosis, renal artery stenosis

23
Q

Management of Hyponatraemia

A

Na, limit fluid, enhance water excretion, demeclocycline or hypertonic saline

24
Q

Demeclocycline

A

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

25
Hypernatraemia
``` ADH deficiency (diabetes insipidus) or insensitivity (Li, ATN or tetracyclines) Iatrogenic from hypertonic solution Osmotic duresis (TPN or hyperosmolar coma) Deficient water intake ```
26
Management of Hypernatraemia
Na>145mmol/L thirst, confusion, coma, cerebral thrombosis, Treat with slow correction with 0.9% saline and beware cerebral oedema
27
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) ```
28
Management of Hypokalaemia
Symptoms --> weakness and lethargy, arrhythmias, | Treatment --> careful supplementation and treat underlying cause
29
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
30
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
31
Insulin management of hyperkalaemia
1. Sodium bicarbonate 50ml of 8.4% IV - -> Ca gluconate (protect the myocardium) 2. Glucose (200ml of 10%) plus 10 units of insulin
32
ECG changes in severe hyperkalaemia
Broad QRS Peaked T ST depression Absent P
33
Perioperative fluid management
Aim to maintain circulating volume Normal electrolyte balance, with normal Hb and glucose Replace ongoing fluid losses with fluid or blood
34
Replacing fluid deficit due to starvation
Hourly maintenance x hours starved
35
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
36
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
37
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 ```