Intensive care
Pulse oximetry
- Non invasive estimation of arterial Hb O2 saturation
- Depends on 2 main principles;
- Different light absorption between Hb and oxyHb
- Identification of pulsatile blood component of the signal
- Different light absorption between Hb and oxyHb
- Provides no information about ventilation including CO2 status
- Inaccuracies;
- Bright overhead lighting may give pulsatile waveforms and saturation values when there is no pulse
- Dyes and pigments including nail vanish may give low values
- Abnormal haemoglobins such as methaemoglobinaemia cause reading which tend towards 85%
- Carboxyhaemoglobin caused by CO poisoning causes saturation values of 100%
- Oxygen values less than 70% become inaccurate
- Cardiac arrhythmias may interfere with the oximeter picking up the pulsatile signal and calculating the pulse rate
- Vasoconstriction and hypothermia which cause reduced tissue perfusion can cause failure to register a signal
- Cardiac valve defects may cause venous pulsations and so venous saturation is recorded by the oximeter
- Bright overhead lighting may give pulsatile waveforms and saturation values when there is no pulse
Acid-Base Balance
See acid-base notes (chemical pathology)
Acidosis
Lactate acidosis
- A form of high anion gap metabolic acidosis
- Lactic acid is produced by anaerobic glycolysis
- It may be oxidized to CO2 and water in the Krebs cycle or reconverted to glucose by gluconeogenesis in the liver. Both these processes require oxygen
- Most forms are due to high levels of L-lactate although is some malabsorption states, with bacterial overgrowth a D-lactate acidosis occurs
- The Cohen and Woods classification of lactate acidosis;
- Type A; hypoxia/poor circulation - this is the most common
- Cardiovascular shock
- Hypoxia
- Severe anaemia
- CO poisoning
- Asphyxia
- Respiratory and cardiac failure
- Sepsis
- Type B1 – miscellaneous diseases
- Cirrhosis
- Fulminant hepatic failure
- Widespread malignant disease – prob because carcinoma tissue produce lactate acid
- Type B2 – drugs and toxins
- Biguinides
- Salicylate
- Ethanol
- Methanol
- Ethylene glycol
- Iron overdose
- HIV retroviral therapy
- Type B3; metabolic disorders and inborn errors
- Glucose-6-phosphate deficiency
- Pyruvate dehydrogenase deficiency
- Mitochondrial defects
- Beri beri (thiamine deficiency)
- Type A; hypoxia/poor circulation - this is the most common
Renal tubular acidosis
- There are 2 main types;
- Type I
- Due to a distal tubular defect
- The distal luminal cells are abnormally permeable to H+ - impairing the ability to build up an [H+] gradient between the lumen and the tubular cells
- The urinary pH therefore cant fall much below that of the plasma
- Type II;
- Impairment of bicarbonate reabsorption in the proximal tubule
- Loss of bicarbonate may cause a systemic acidosis
- In Fanconi’s syndrome, Type II RTA is also associated with amino aciduria, phosphaturia and glycosuria
- Type I
Glycol-induced acidosis
- Causes increased H+ formation
- Causes a metabolic acidosis, renal and hepatic dysfunction and also a hypocalcaemia (due to oxalate conversion and calcium chelation as calcium oxalate)
Fluid balance
- Input – assume 750ml from food and measure how much has been drunk
- ‘Insensible losses’ are considered to be 1l
- However there is endogenous water production of 500ml per day
- Therefore overall insensible losses are taken to be 500ml
- The required daily input is calculated from the previous days output plus an extra 500ml
- Pyrexia patients may sweat lose an additional 1L in sweat and if hyperventilating respiratory water loss may be considerable
- The volume of fluid given should be based upon calculated cumulative balance and on the clinical evidence of the state of hydration. Composition should be adjusted to maintain normal plasma electrolyte concentrations
- Evidence of haemodilution;
- Increasing plasma volume with protein free fluids leads to a fall in proteins and haemoglobin
- However findings may be affected by pre-existing abnormalities in protein and red cell concentrations
- Evidence of haemoconcentration
- Depletion of water and small molecules results in a rise in the concentration of proteins and blood cells with a rise in Hb and haematocrit
Sodium status
- Sodium and its associated anions (chloride and bicarbonate) account for a least 90% of extracellular osmolality
- Plasma sodium status is important because of its osmotic effect on fluid distribution
- The volume of ECF is directly dependant upon total body sodium content since water intake and loss are regulated to hold the concentration of sodium in the ECF constant and because sodium is virtually confined to the ECF
- Plasma sodium concentrations should be monitored whilst fluid is being corrected to ensure the distribution of fluid between the intracellular and extracellular compartments is optimal
- Water and sodium depletion    Â
- The plasma sodium concentrations can give an indication of the relative amounts of water and sodium that have been lost;
- Plasma sodium will be normal if isotonic fluid has been lost
- Plasma sodium will be increased if hypotonic fluid has been lost
- With severe sodium depletion, increased ADH causes water retention to maintain plasma volume at the expense of osmolality – hyponatraemia develops and the sodium level will be low
- Loss of pure water results in an increased sodium concentration and thus osmolality
- The plasma sodium concentrations can give an indication of the relative amounts of water and sodium that have been lost;
- Excess water and sodium
- Can be due to a failure of normal excretion or from excessive intake
- Water excess
- Increased load is shared by the ICF and ECF fluid compartments
- Results in hyponatraemia
- Sodium excess
- Clinical features are related primarily to the expansion on the ECF volume
- When due to excessive intake hypernatraemia is normal
- In patients whose sodium overload is due to reduced excretion, it is most commonly due to secondary aldosteronism – seen in patients who despite having clinical evidence of increased ECF volume, they appear to have a decreased effective plasma volume due to e.g. venous pooling or a disturbance in the normal distribution of ECF between the vascular and extravascular compartments therefore in these patients the sodium excess can manifest as hyponatraemia implying the co-existence of a defect in free water excretion
In isolation plasma concentration provides no information about the sodium content of the ECF as it may be raised, normal or low in causes of sodium excess or depletion depending on the amount of water in the ECF
- Plasma sodium should be measured in the following circumstances;
- Patients with dehydration or excessive fluid loss as a guide to appropriate replacement
- Patients who are on parenteral fluid replacement who are unable to indicate or respond to thirst e.g comatose, elderly, infants
- Patients with unexplained confusion, abnormal behaviour or signs of CNS irribility
Fluid Balance Points to Bear in Mind
·       Blood transfusions are equivalent to giving saline.
·       Giving dextrose is equivalent to giving water.
Creatine
- Plasma creatine concentration is the most reliable simple biochemical test of glomerular function
- Reference range is 60-120μmol/L – day to day variation in an individual varies much less
- Plasma creatine levels vary inversely with the GFR
- Although it takes drop in GFR of 50% before plasma levels of GFR rise – after this point the creatine concentration doubles for every 50% drop in GRF
- Therefore a normal creatine value doesn’t exclude renal impairment but a raised creatine does indicate impaired renal function
- Drawbacks
- Samples should be taken after an overnight fast as ingestion of meat can increase values up to 30% 7 hours after the meal]
- Strenuous exercise can cause a transient slight increase in plasma creatine concentrations
- Values are related to muscle bulk however although muscle bulk tends to decrease with age so does GFR and so creatine concentrations remain fairly constant
- Assay is prone to analytical interferenceby substances such as bilirubin, ketone bodies and drugs
- Changes in creatine concentration can occur independently of renal function due to changes in muscle mass;
- Decreased in starvation and wasting diseases, immediately after surgery and patients treated with corticosteroids
- In pregnancy the GFR increases but this is balanced by the increase in creatine synthesis
Oligouria
- Defined as a urine output of less than 400ml/day or 15ml/hour
- Usually indicates low GFR and acute renal failure
- Biochemical values in oligouria due to pre-renal and intrinsic causes
|
|
Pre renal failure |
Intrinsic failure |
|
Urine sodium concentration |
<20mmol/L |
40mmol/L |
|
Urine:plasma urea concentration |
>20:1 |
<10:1 |
|
Urine:plasma osmolality |
1.5:1 |
<1.1:1 |
Tests for Rhabdomyolysis
·       Most specific:
o      CK – mainly CK-MM
o      Aldolase A (glycolytic enzyme in skeletal muscle, but not advantage over CK and rarely used; Type B is only found in liver, kidney, and intestine but not muscle).
o      Isoenzyme LDH5 (in liver & skeletal muscle).
o      Myoglobin (precipitates out in renal tubules → acute renal failure)
Phosphate level
- Phosphate, like potassium, enters cells from the ECF if the rate of glucose metabolism is increased
- This may be associated with glucose infusion during the treatment of a diabetic coma with insulin
- Consequences of severe hypophophataemia;
- Rhabdomyolysis
- Muscle weakness and myopathy
- Impaired diaphragmatic contractility
- Seizures
- Parasthesia
- Osteomalacia
- Thrombocytopenia, impaired clotting and reduced leukocyte function
- Particularly a problem if phosphate levels are already low, due to;
- Poor intake
- Malabsorption states
- Chronic alcoholism
- Renal tubular loss