Investigation of Salt & Water and Acid/Base Balance Flashcards by Sharjeel Ahmad

Distribution of body fluids - describe

Extracellular Fluid Compartment = 20%
Interstitial = 15%
Intravascular = 5%
Transcellular = 1%
H2O in connective tissue = <1%

Intracellular Fluid Compartment = 40%

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Water balance are determined by what? (w/sodium)

Intake
 - Dietary intake (Thirst)
Output 
 - Obligatory losses
         Skin
         Lungs
- Controlled losses – these depend on:
         Renal function
         Vasopressin/ADH (anti-diuretic 
         hormone)
         Gut (main role of the colon)
         Redistribution

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Sodium balance are determined by what? (w/water)

Intake

Dietary (unless vegan and doesn’t add salt)
Western diet 100-200 mmol/day

Output
- Obligatory losses
Skin

- Controlled losses – these depend on:
      Kidneys     
      Aldosterone
      GFR
      Gut - most sodium is reabsorbed; loss 
       is pathological

Determined by intravascular volume

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Hormones involved in water and salt balance for sodium

Aldosterone produced in the adrenal cortex: regulates sodium and potassium homeostasis

Natriuretic hormones (ANP cardiac atria, BNP cardiac ventricles) promote sodium excretion and decrease blood pressure

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Hormones involved in water and salt balance for sodium for just water

ADH/vasopressin: synthesised in hypothalamus and stored in posterior pituitary. Release causes increase in water absorption in collecting ducts

Aquaporins (AQP1 proximal tubule and not under control of ADP) AQP2 and 3 present in collecting duct and under control of ADH

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Effect of osmotically active substances in blood

Osmotically active substances in the blood may result in water redistribution to maintain osmotic balance but cause changes in other measured solutes

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Define osmometer and its action

An osmometer is a device for measuring the osmotic strength of a solution, colloid, or compound.

Freezing point depression
Uses colligative properties of a solution
More solute – lower the freezing point

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List methods for analysing sodium

Indirect Ion selective electrodes (main lab analysers)

Direct Ion selective electrodes (Blood gas analyser)

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How to assess a patient with possible fluid/electrolyte disturbance using history

History

Fluid intake / output
Vomiting/diarrhoea
Past history
Medication

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How to assess a patient with possible fluid/electrolyte disturbance using examination

Examination - Assess volume status

Lying and standing BP
Pulse
Oedema
Skin turgor/Tongue
JVP / CVP

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How to assess a patient with possible fluid/electrolyte disturbance using examination apart from history + examination

Fluid chart

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Action at DCT

Sodium reabsorption

Loss of H+/K+

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By-prod of ATP prod

Large amounts of protons/hydrogen ions are an inevitable by-product of energy/ATP production

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Maintenance of extracellular [H+]/pH depends on what ?

depends on the relative balance between acid production and excretion
carbon dioxide production and excretion (respiration)
hydrogen ion production and excretion (renal)

maintain protein/enzyme function

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Effect of decreased buffering

Decr. Buffering – consumption of HCO3

= Removal of CO2

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Define metabolic acidosis

Metabolic acidosis
(rate of H+ generation > excretion)

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Effect of increased renal excretion

🡩 renal excretion of H+ & regeneration of HCO3

🡩retention of CO2
(H20 + CO2 ⮀ H2CO3)

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pH equation in terms of HCO3 and CO2

pH = HCO3/CO2

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Describe attempt to return acid / base status to normal by buffering

Bicarbonate buffer in serum, phosphate in urine (for excretion)
Skeleton
Intracellular accumulation/loss of H+ ions in exchange for K+ , proteins and phosphate act as buffers

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Describe attempt to return acid / base status to normal by compensation

Diametric opposite of original abnormality
Never overcompensates
Delayed and limited

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Describe attempt to return acid / base status to normal by treatment

By reversal of precipitating situation

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Describe the speed of respiratory compensation with an example

Respiratory compensation for a primary metabolic disturbance can occur very rapidly
Kussmaul breathing (respiratory alkalosis) in response to DKA

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Describe the speed of metabolic compensation + its requirements

Metabolic compensation for primary respiratory abnormalities take 36-72 hours to occur

requires enzyme induction from increased genetic transcription and translation etc

Requires more chronic scenario to include compensation mechanism

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When is compensation absent

No compensation seen in acute respiratory acidosis such as asthma

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Mechanism of renal bicarbonate regeneration

H+ moves out from tubular cell into renal lumen, Na+ moves in - H+ from H20 + CO2 ⮀ H2CO3 K+ movement stopped HCO3- from H20 + CO2 ⮀ H2CO3 - Regenerated and reclaimed bicarbonate

Pitfalls of ABG

``` Expel air Mix sample Analyse ASAP Plastic syringes OK at room temp for ̴ 30mins Ice not required Ensure no clot in syringe tip ```

Errors in blood gas analysis are dependent more on what

Errors in blood gas analysis are dependent more on the clinician than on the analyser

Causes of respiratory acidosis

``` Airway obstruction Neuromuscular disease Pulmonary disease Extrapulmonary thoracic disease Respiratory centre depression ```

Respiratory acidosis - describe compensation

Increased renal acid excretion (metabolic alkalosis, 36-72 hrs delay)

Respiratory acidosis - describe correction

Requires return of normal gas exchange

Respiratory acidosis - features (acute and chronic)

Features acute: 🡻pH (🡹[H+]), 🡹pCO2, 🡺[HCO3-],– ie. no compensation chronic: 🡻pH (🡹[H+]), 🡹pCO2, 🡹[HCO3-],– ie. compensation

Causes of respiratory alkalosis

Hypoxia Pulmonary disease Mechanical overventilation Increased respiratory drive

List what would cause increased respiratory drive

``` Respiratory stimulants eg salicylates Cerebral disturbance eg trauma, infection and tumours Hepatic failure G-ve septicaemia Primary hyperventilation syndrome Voluntary hyperventilation ```

List what would cause respiratory centre depression

Anaesthetics Sedatives Cerebral trauma Tumours

List what would cause airway obstruction

Bronchospasm (Acute) COPD (Chronic) Aspiration Strangulation

List what would cause pulmonary disease

Pulmonary fibrosis Respiratory Distress Syndrome Pneumonia Pulmonary oedema Pulmonary embolism

List what would cause an extrapulmonary thoracic disease

Flail chest

List what would cause neuromuscular disease

Guillain-Barre Syndrome | Motor Neurone Disease

List what would cause hypoxia

High altitude Severe anaemia Pulmonary disease

Respiratory alkalosis - describe compensation

Increased renal bicarbonate excretion (metabolic acidosis, 36-72 hrs delay)

Respiratory alkalosis - describe features (acute and chronic)

acute: high pH, low [H+], n[HCO3-], low pCO2 – no compensation chronic: high pH, low [H+], low [HCO3-], low pCO2

Causes of metabolic acidosis

``` Increased addition of acid Increased H+ formation Acid ingestion Decreased H+ excretion Loss of bicarbonate ```

List what would cause increased H+ formation

Ketoacidosis Lactic acidosis Poisoning – methanol, ethanol, ethylene glycol, salicylate Inherited organic acidosis

List what would cause acid ingestion

Acid poisoning | XS parenteral administration of amino acids eg arginine

List what would cause decreased H+ excretion

Renal tubular acidosis Renal failure Carbonic dehydratase inhibitors

List what would cause loss of bicarbonate

Diarrhoea | Pancreatic, intestinal or biliary fistula/drainage

Metabolic acidosis | - describe compensation

hyperventilation, hence low pCO2

Metabolic acidosis | - describe correction

of cause | increased renal acid excretion

Metabolic acidosis | - features

low pH, high [H+], low [HCO3-], low pCO2

Causes of metabolic alkalosis

Increased addition of base Increased loss of acid Negative effects on renal system Decreased elimination of base

List what would cause increased addition of base

Inappropriate Rx of acidotic states | Chronic alkali ingestion

List what would cause increased loss of acid

GI loss - Gastric aspiration - Vomiting with pyloric stenosis

List what would cause negative effects on the renal system that would lead to metabolic alkalosis

Diuretic Rx (not-K+sparing) Potassium depletion Mineralocorticoid excess- Cushing’s, Conn’s Drugs with mineralocorticoid activity – carbenoxolone

Metabolic alkalosis | - describe compensation

Hypoventilation with CO2 retention (respiratory acidosis)

Metabolic alkalosis | - describe correction

increased renal bicarbonate excretion | reduce renal proton loss

Metabolic alkalosis | - features

high pH, low [H+], high [HCO3-], N/highpCO2

Hypovolaemia from persistent vomiting | leads to

Loss of HCl Loss of potassium Loss of fluid

Diuretics lead to

Chronic K+ depletion

Describe response to fluid loss

Response to fluid loss is aldosterone activation - Reabsorb NaCl/H2O at distal convoluted tubule in kidney in exchange for K+ /H+

Hyperkalaemia causes

If increased intake: Usually parenteral if decreased loss: ``` Reduced GFR Reduced tubular loss (potassium sparing diuretics anti-inflammatories, ACEIs, mineralocorticoid deficiency) ```

Hypokalaemia causes

If increased loss: ``` Gut (diarrhoea, laxatives) Kidney (diuretics, magnesium deficiency, mineralocorticoid XS renal tubular abnormalities) ``` if decreased intake: Often alcohol Anorexia

Investigation of Salt & Water and Acid/Base Balance Flashcards

(61 cards)