Investigation of salt and water and acid/base balance Flashcards
What is water balance determined by?
- Intake
- Output - obligatory losses (sweat, exhaling), controlled losses (renal function, ADH, gut absorption)
- Redistribution (between compartments)
How does water redistribute?
- Osmotically active substances in the blood may result in water distribution to maintain osmotic balance
- Water will transfer into a compartment with much higher solute levels
- Excess solute in ECFV -> cell shrinkage
- Excess solute IC -> cell swelling
What are the physiological responses to water loss?
- Stimulation of ADH release - renal water retention
- Stimulaiton of hypothalamic thirst centre - increase intake
- Redistribution of water from ICF - increased ECF water
What is sodium balance determine by?
- Intake - dietary
- Output - obligatory losses (skin), controlled excretion (kidneys, aldosterone, GFR, gut absorption/pathological loss)
What hormones are involved in salt and water balance?
Sodium
- Aldosterone from adrenal cortex - regulates Na and K homeostasis
- Natriuretic hormones (ANP and BNP) - promote Na excretion and decrease BP (look for n-terminus of both when looking at heart failure)
Water
- ADH - synthesised in hypothalamus and store in posterior pituitary. Release causes increase in water absorption in CDs
- Aquaporins - AQP1 in PCT, AQP2 and 3 in CD under control of ADH
Briefly describe the RAAS system
- Juxtoglomerular cells recognise hypotension and macula densa recognises sodium depletion
- These signal juxtoglomerular cells to release renin
- renin released, converts angiotensionigen to angiotensin I
- This is converted to angII by ACE
- AngII acts on adrenal cortex to release aldosterone
What is freezing point depression osmometry?
- Looks at the colligative properties of a solution
- If you increase the number of particles in a soln, the osmotic pressure will increase
- Increasing more solute will increase the boiling point
- Decreasing the solute will decrease the boiling point
- Can decrease the freezing point with more solute
Case 1 - drowsy and confused, dry tongue, low BP and high pulse.
Blood results - high sodium, urea and creatinine
Renal impairment
- dry tongue = dehydration
- BP low and pulse fast = dehydration
- Na high = dehydration
- Urea and creatinine high = poor renal perusion -> increased reabsorption
Case 2 - confusion, drinking lots of water
- lab results - v low sodium
- Very low sodium - cause confusion, can become violent and have other psychiatric problems
- Psychogenic polydipsia - drink lots and lots of water
What clinical questions do you have to ask when looking at a sodium related case?
- Are they euvolaemic, or hypo-/hyper-?
- What is the underlying cause of the hyponatraemia?
- What other lab tests might help interpret the data?
- What is the kidney doing with sodium etc
How do you assess a pt with possible fluid/electrolyte disturbance?
- History - fluid intake/output, vomiting/ diarrhoea, past history, medication
- Examination - lying and standing BP, pulse, oedema, tongue, JVP/ CVP
- Fluid chart
What brain probs can sodium probs cause?
- Hyponatraemia - over-rapid correction may lead to central pontine myelinolysis
- Hypernatraemia - over-rapid correction may lead to cerebral oedema - too much water in brain causes it to start pushing down through the foramen magnum
Sodium balance summary
- BP/ volume sensed - baroreceptors and renal perfusion pressure
- Aldosterone produced from renal cortext
- Causes action at DCT - sodium reabsorption and loss of H+/K+
Why do we have to balance acid-base?
- Large amounts of hydrogen ions are a by-product of ATP production
- Maintenance of EC H+/ pH is essential to maintain protein/ enzyme function
- Depends on the relative balance between acid production and excretion (CO2 production and excretion - respiration; and H+ production and excretion - renal)
What i significant about the pH being a log scale?
- Changes in H+ ions doesnt seem that much
- A drop in 40mM from 80 to 40mM is only a drop in 0.3 pH from 7.4 to 7.1
What is the henderson-hasselbalch equation?
CO2 + H20 H2CO3 H+ + HCO3
What happens in metabolic acidosis?
The H+ generation exceeds the excretion - H+ goes up
- Try to get equilibrium to bring back normality
- increase bicarbonate levels and remove CO2
- Kussmaul respiration is deep sighing breahing to get rid of CO2 to compensate for metabolic acidosis
What happens in respiratory acidosis?
- Rate of CO2 excretion < generation
- Ability to excrete CO2 is impaired, but still producing a lot
- H+ conc goes up because of the CO2 retention
- Have to try and improve the renal excretion od H+ and regeneration of bicarb
- Metabolic compensation takes longer than respiratory
What are the 3 main buffer systems we have in the body?
- Bicarbonate in the serum, phosphate in the urine
- Skeleton - good at taking up H+
- IC accumulation/ loss of H+ ions in exchange for K+ - proteins and phosphate act as buffers
What are the differences in compensation speeds between resp and metabolic?
- Respiratory can occur very rapidly - kussmaul breathing in response to diabetic ketoacidosis
- Metabolic takes around 36-72 hrs
. need enzyme induction for increased genetic transcription and translation
. no compensation seen in acute resp acidosis such as asthma
. requires more chronic scenario to include compensation mechanism
What is the mechanism of renal bicarb regeneration?
- We reclaim most bicarb in PCT, and only generate bicarb in the DCT
- Sodium goes into the cell in exchange for K which gets excreted
- Carbonic acid dissociates to form bicarb and H+ which are excreted
- When we excrete H+ ions, we dont excrete sodium ions to regulate the electrochemical gradient
How do we interpret ABG?
- pO2 - have to also check FiO2
- pH - is it normal?
- pCO2 - primary resp, or compensatory response?
- HCO3 - metabolic component (dont measure on ABG< we calculate using H-H)
What are some causes of resp acidosis?
- Airway obstruction - bronchospasm, COPD, aspiration, strangulation
- Resp centre depression - anaesthetics, sedatives, cerebral trauma, tumours
- Neuromuscular disease - Motor neurone disease, Gullain-Barre syndrome
- Pulmonary disease - pulmonary fibrosis, respiratory distress syndrome, pneumonia
- Extrapulmonary thoracic disease - flail chest
Case 3 - RTA, flail chest, unable to oxygenate, cant blow off CO2
- Low O2, low pH (acidotic), high pCO2, normal bicarb
= Uncompensated acute respiratory acidosis + impaired oxygenation
What are the main causes of respiratory alkalosis?
- Hypoxia - high altitude, severe anaemia, pulmonary disease (oedema or embolism)
- mechanical overventilation
- Increased respiratory drive - resp stimulants (salicylates), cerebral disturbance (trauma, infection, tumours), hepatic failure, G-ve septicaemia, primary hyperventilation syndrome, voluntary hyperventilation
Case 4 - increasingly anxious, tingling in fingers and toes
- Tingling from change in ionised ca levels
- more is bound to protein because you are trying to release H+ from protein
- high pH (alkalotic)
- Low pCO2
- normal bicarb
- uncompensated, acute respiratory alkalosis
(should compensate by decreasing bicarb)
What are the main causes of metabolic acidosis?
- Increased H+ formation - ketoacidosis, lactic acidosis, posioning, inherited organic acidosis
- Acid ingestion
- Decreased H+ excretion - renal tubular acidosis, renal failure, carbonic dehyrdratase inhibitors
- Loss of bicarbonate - diarrhoea, pancreatic, intestinal or biliary fistulae
Case 5 - type 1 diabetes, not taken isnulin for 24 hrs
- normal pO2
- acidotic low pH
- Normal pCO2
- Low bicarb
- uncompensated acute metabolic acidosis
What are main causes of metabolic alkalosis?
- Increased addition of base
- Decreased elimination of base
- Increased loss of acid - GI loss - hypovolaemia from persistent vomiting (loss of HCl, loss of K and loss of fluid)
- renal loss (diuretics, K depletion, mineralocorticoid excess)
Case 6 - vomiting last 48 hrs
- normal PO2 and CO2
- alkalotic high pH
- High bicarbonate
- uncompensated metabolic alkalosis
Acid base clinical scenarios summary
Resp acidosis
- CO2 retention
- Compensation is metabolic alkalosis
Resp alkalosis
- Increased CO2 loss
- Compensation is metabolic acidosis
Metabolic acidosis
- Acid ingestion
- Increased acid production
- Reduced acid excretion
- Compensation is resp alkalosis
Metabolic alkalosis
- very difficult primary disturbance to produce and maintain - very specific factors required
- Compensation is resp acidosis
Why is it that when you are acidotic, you tend to also have hyperkalaemia?
- Exchange of cations to keep neutral charge
Hyper vs hypokalaemia
Hyper
- increased intake
- Decreased loss - reduced GFR, reduced tubular loss (K+ sparing diuretics, ACEIs, mineralocorticoid deficiency)
Hypo
- increased loss - gut, kidney (diuretics, Mg deficiency, mineralocorticoid excess, renal tubular abnoralities)
- Decreased intake - alcohol, anorexia
Why would you get K+ redistribution?
Can get redistribution between ICF and ECF
- Alkalosis, insulin and beta agonists into the cell
- Acidosis, decreased insulin and tissue damage - out of the cell
