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
Q

Hypernatraemia

A
ADH deficiency (diabetes insipidus) or insensitivity (Li, ATN or tetracyclines)
Iatrogenic from hypertonic solution
Osmotic duresis (TPN or hyperosmolar coma)
Deficient water intake
26
Q

Management of Hypernatraemia

A

Na>145mmol/L
thirst, confusion, coma, cerebral thrombosis,
Treat with slow correction with 0.9% saline and beware cerebral oedema

27
Q

Causes of Hypokalaemia

A
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
Q

Management of Hypokalaemia

A

Symptoms –> weakness and lethargy, arrhythmias,

Treatment –> careful supplementation and treat underlying cause

29
Q

Causes of Hyperkalaemia

A

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
Q

Management of Hyperkalaemia

A

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
Q

Insulin management of hyperkalaemia

A
  1. Sodium bicarbonate 50ml of 8.4% IV
    - -> Ca gluconate (protect the myocardium)
  2. Glucose (200ml of 10%) plus 10 units of insulin
32
Q

ECG changes in severe hyperkalaemia

A

Broad QRS
Peaked T
ST depression
Absent P

33
Q

Perioperative fluid management

A

Aim to maintain circulating volume
Normal electrolyte balance, with normal Hb and glucose
Replace ongoing fluid losses with fluid or blood

34
Q

Replacing fluid deficit due to starvation

A

Hourly maintenance x hours starved

35
Q

Hourly maintenance of fluid

A

0-10kg = 4ml/kg/hr
10-20kg = (40ml + 2ml/kg)hr
>20kg = (60ml + 1ml/kg)hr
Eg 85kg man requires 125ml/hr maintenance

36
Q

Where does fluid go?

A

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
Q

Causes of anion gap metabolic acidosis (CAT MUDPILES)

A
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