Investigations of Salt & Water and Acid/Base Balance Flashcards
(105 cards)
1
Q
How much water does our body contain?
A
Total body fluids = 60% of body weight
ECF: 20% ICF: 40% - Interstitial: 15% - Intravascular: 5% - Transcellular: 1% - Connective tissue: <1%
2
Q
How is Water and Na+ balance determined?
A
By input and output of both
3
Q
What are the main intake methods of Na+ and water?
A
Water Intake: Dietary intake (Thirst)
Na+ intake: Dietary (Western diet 100-200 mmol/day)
4
Q
What are the obligatory water losses causing water output?
A
Obligatory losses
- Skin (sweat)
- Lungs (breath)
5
Q
What are the controlled water losses
A
Controlled losses depend on:
- Renal function
- Vasopressin/ADH (antidiuretic hormone)
- Gut (main role of the colon)
6
Q
What are the obligatory Na+ losses
A
Obligatory loss
- Skin (sweat)
7
Q
Describe the controlled Na+ losses
A
Controlled losses / excretion
- Kidneys
- Mineralocorticosteroid Aldosterone
- GFR
- Gut - most sodium is reabsorbed; loss is pathological
8
Q
How does redistribution occur in order to maintain Na+ and water balance?
A
determined by intravascular volume
9
Q
How does aldosterone effect Na+ balance?
A
Aldosterone produced in the adrenal cortex: regulates sodium and potassium homeostasis
10
Q
What is the role of natriuretic hormones in Na+ balance?
A
Natriuretic hormones (ANP cardiac atria, BNP cardiac ventricles) promote sodium excretion and decrease blood pressure
11
Q
How does ADH maintain water balance?
A
ADH/vasopressin: synthesised in hypothalamus and stored in posterior pituitary. Release causes increase in water absorption in collecting ducts
12
Q
What is the role of aquaporins in water balance?
A
Aquaporins (AQP1 proximal tubule and not under control of ADP) AQP2 and 3 present in collecting duct and under control of ADH
13
Q
What hormones help maintain Na+/water balance?
A
Na+
- Aldosterone
- ANP/BNP
Water
- ADH/vasopressin
- AQP1/2/3
14
Q
What is the effect of osmotic pressure on water movement?
A
Water moves from a high Ψ to low Ψ
15
Q
How does osmotic potential control water movement in blood?
A
Osmotically active substances in blood may result in water redistribution to maintain osmotic balance but cause changes in other measured solutes
16
Q
What processes occur in response to water loss
A
Water loss = inc. ECF osmolality
- ADH release stimulated
= renal water retention - Hypothalamic thirst centre
= inc. water intake - water redistribution from ICF
= inc. ECF water
Restoration of ECF osmolality
17
Q
Which members of population are more susceptible to dehydration?
A
Dehydration common in elderly and v. young babies who can’t access water themselves
18
Q
Describe what happens to Na+ in renal tubules
A
GFR ~95-98% of Na+ filtered by glomeruli undergoes obligatory reabsorption driven by renal perfusion
19
Q
Where in the renal tubules is Na+ mainyl reabsorbed?
A
Most Na+ reabsorbed in proximal tubule
Distal tubule reabsorption due to aldosterone
20
Q
Where does ADH produce its reabsorption effects?
A
ADH stimulates water reabsorption from the collecting duct
21
Q
Outline the aldosterone mechanism in hypertension / Na+ depletion
A
- Juxtaglomerular cells produce renin
- Renin = conversion of angiotensinogen → angiotensin I
- Angiotensin I circulates body and (in lungs) ACE (angiotensin-converting enzyme) converts into angiotensin
- Angiotensin stimulates adrenal cortex to produce aldosterone
Helps maintain our circulating volume
22
Q
How can we measure the osmometry of Na+?
A
Freezing point depression
Uses colligative properties of a solution
> More solute (Salt) – lower the freezing point
23
Q
How can we measure electrolytes such as Na+?
A
- Indirect Ion selective electrodes (main lab analysers)
- Direct Ion selective electrodes (Blood gas analyser) - measure concentrations rather than ion activity
24
Q
What is hypernatraemia?
A
Increased water loss and sodium gain
25
What is hyponatraemia?
Increased sodium loss and water gain
26
How do we assess a possible fluid / electrolyte disturbance?
1. history
2. Examination
3. Fluid chart
27
What should a patient history determine?
Fluid intake / output
Vomiting/diarrhoea
Past history
Medication
28
What examination can be done on a patient with NA+/water imbalance?
Assess volume status
- Lying and standing BP
- Pulse
- Oedema
- Skin turgor/Tongue
- JVP / CVP
29
What risks should we consider before treating hyper/hyponatraemia?
Hyponatraemia
- Over-rapid correction may lead to central pontine myelinolysis (shrinkage)
Hypernatraemia
- Over rapid correction may lead to cerebral oedema (expansion)
30
How can we overcome the potential life damaging risks of treating Na+ imbalance?
Important to correct sodium at the same speed - no more than 10mmol/L per 24 hours sodium change
31
What are important lab investigations for Na+/water imbalance?
- Paired serum + urine osmolality and electrolytes
- Urea/creatinine ratio = inc. Urea = dehydration
- Serum osmolality
= Indicates presence of other osmotically active
substances
Urinary sodium – ignore reference interval
<20 mmol/L = conservation
>20 mmol/L = loss
Urinary osmolality - ignore reference interval
Relate to serum osmolality
Urine /serum osmolality
>1 = water conservation
< 1 = water loss
32
What is hypovolaemia?
Hypovolaemic - Low BP due to low circulating volume of blood, Na+ &/or water
33
What is menat byeuvolaemic?
Euvolemic - normal Na+ and bodily fluid stores and normal BP
34
What is hypervolaemia?
Hypervolemic - excess fluids (blood, water etc.)
35
What mechanisms are in place to determine Na+ balance?
- Baroreceptors = Blood pressure/volume sensed
- Renal perfusion pressure = Aldosterone produced
- Adrenal cortex = Action at DCT
- Sodium reabsorption = Loss of H+/K+
(reference range 133-145 mmol/L)
(Life threatening range <115 >160 mmol/L)
36
What causes build up of H+ in the body?
Large amounts of protons/hydrogen ions are an inevitable by-product of energy/ATP production
37
Why do we need to regulate H+ levels in the body?
Maintenance of extracellular [H+]/pH is essential to maintain protein/enzyme function
38
What is H+ balance dependent upon?
Balance depends on relative balance between acid production and excretion
- carbon dioxide production + excretion (respiration)
- hydrogen ion production + excretion (renal)
39
What are the threats to normal pH?
Carbonic acid = from burning carbohydrates (CO₂)
Non-Carbonic acids = from metabolising amino acids
40
How is H+ balance restored?
Majority of CO₂ removed via lungs
| H+ excreted mainly through kidneys
41
Outline the pH calcualtion
pH = -log10[H+] or pH = log101/[H+]
pH from 7.4-7.1
[H+] 40-80
ie [H+] doubled for pH fall of 0.3
42
What is metabolic alkalosis?
Rate of H+ generation > excretion
| [H+] increases, pH falls - acidosis
43
How is normal pH restored from metabolic alkalosis?
To restore normal neutral:
- Buffer consumption of HCO₃⁻
- CO₂ removal (kussmaul respiration)
44
What is respiratory acidosis?
Rate of CO₂ excretion < generation
CO₂ increase ⇒ [H+] increase
pH falls = acidosis
45
How is respiratory acidosis resolved?
There is increased CO₂ retention which can only be converted into HCO₃⁻ via normal renal function
46
Why does compensation occur?
Attempt to return acid / base status to normal
47
What are the body's methods of compensating?
1. Buffering
2. Compensation
3. Treatment
48
Outline how the body buffers changes in acid base balance
- 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
49
Outline the compnestaion techniques in the body
- Diametric opposite of original abnormality
- Never overcompensates
- Delayed and limited
50
What treatment is there for loss of acid base balance?
Reversal of precipitating situation
51
How quickly does respiratory compensation occur?
Respiratory compensation for a primary metabolic disturbance can occur very rapidly
Kussmaul breathing (respiratory alkalosis) in response to DKA
52
How fast is metabolic compensation?
Metabolic compensation for primary respiratory abnormalities take 36-72 hours to occur
53
Why is metabolic compensation slower?
requires enzyme induction from increased genetic transcription and translation etc
54
Why does metabolic compensation not always occur?
No compensation seen in acute respiratory acidosis such as asthma
Requires more chronic scenario to include compensation mechanism
55
Where is bicarbonate produced in the kidneys?
Bicarbonate produced in 2 places:
- renal lumen
- renal tubular cells
56
How does renal lumen restore acid base balance?
Renal lumen exchanges Na+/K+
| K+ excreted in urine
57
How do tubular cells regenerate bicarbonate?
Tubular cell undergoes buffer mechanism
H₂O + CO₂ H₂CO₃
Water & carbon dioxide form carbonic acid which breaks down into hydrogen ions and bicarbonate
H₂CO₃ ⇆ HCO₃⁻ + H+
58
How is bicarbonate regenerated in kidneys?
In the proximal renal lumen bicarbonate is reclaimed, and in the distal tubular cells, bicarbonate is regenerated and H+ ions are removed
59
Why is H+ and K+ unable to be excreted at the same time?
H+ and K+ removal can’t occur simultaneously due to electrochemical imbalance - only occurs one at a time
60
What are the pitfalls of using ABG
```
Expel air
Mix sample
Analyse ASAP
Plastic syringes OK at room temp for ̴ 30mins
Ice not required
Ensure no clot in syringe tip
```
61
How do errors in ABG analysis arise?
Errors in blood gas analysis are dependent more on the clinician than on the analyser
62
How do we interpret ABG results?
pO2 remember to check FiO2
pH – Normal or does it show an acidosis or alkalosis
pCO2 – primary respiratory or compensatory response
HCO3 – metabolic component (calculated using Henderson-Hasselbach)
63
What causes respiratory acidosis?
Retention of Carbon dioxide may be due to:
- Airway obstruction
- Respiratory centre depression
- Extrapulmonary thoracic disease: flail chest
- Pulmonary disease
- Neuromuscular disease
64
What airway obstructions lead to respiratory acidosis?
Airway obstructions include:
- Bronchospasm (Acute)
- COPD (Chronic)
- Aspiration
- Strangulation
65
What causes respiratory centre depression leading to respiratory acidosis?
- Anaesthetics
- Sedatives
- Cerebral trauma
- Tumours
66
What neuro-muscular diseases lead to respiratory acidosis?
Guillain-Barre Syndrome
| Motor Neurone Disease
67
What aspects of pulmonary disease can lead to acidosis?
- Pulmonary fibrosis
- Respiratory Distress Syndrome
- Pneumonia
68
Describe respiratory acidosis compensation
Compensation - Increased renal acid excretion (metabolic alkalosis, 36-72 hrs delay)
Correction - Requires return of normal gas exchange
69
Describe features of acute and chronic resp. acidosis
Acute:
🡻pH (🡹[H+]),
🡹pCO2,
🡺[HCO3-],– ie. no compensation
Chronic:
🡻pH (🡹[H+]),
🡹pCO2,
🡹[HCO3-],– ie. compensation
70
Outline the condition of the following patient:
21 y/o male
RTA (road traffic accident) flail chest
Low pO2 - pt can’t oxygenate properly
Low pH = acidic and raised CO2
Normal HCO3 - not compensating
Uncompensated acute respiratory acidosis +impaired oxygenation
71
What is a flail chest?
Flail chest - broken ribs front & back
72
How does the body compensate for respiratory alkalosis?
Compensation - Increased renal bicarbonate excretion (metabolic acidosis, 36-72 hrs delay)
Correction - Of cause
73
Outline acute and chronic resp. alkalosis
Acute:
high pH
low [H+], n[HCO3-]
low pCO2 – no compensation
Chronic:
high pH, low [H+]
low [HCO3-]
low pCO2
74
What causes respiratory alkalosis?
Low pCO2 – excess removal of carbon dioxide
75
What conditions lead to resp alkalosis?
- Hypoxia
- Pulmonary disease
- Mechanical overventilation
- Increased respiratory drive
76
What may cause an increased respiratory drive?
```
Respiratory stimulants > eg. salicylates
Cerebral disturbance > eg. trauma, infection and tumours
Hepatic failure
G-ve septicaemia
Primary hyperventilation syndrome
Voluntary hyperventilation
```
77
What causes hypoxia?
- High altitude
- Severe anaemia
- Pulmonary disease
78
What causes pulmonary disease?
Pulmonary oedema
| Pulmonary embolism
79
A Student volunteered to have arterial blood sample taken, but became increasingly anxious and had tingling in fingers and toes
Patient began hyperventilating ⇒ excessive CO2 removal
High pH = alkalotic
Normal HCO3 - not compensating
What condition has the following patient developed?
Uncompensated acute respiratory alkalosis
Tingling sensation due to low [H]+ ions (alkalotic) - albumin proteins buffer a lot of H+ ions
Albumin also has bound Ca2+
⇒ H+ ions come off albumin, and more Ca2+ is bound, so to compensate Ca2+ is dropped from albumin causing tingling
80
What are the causes of metabolic acidosis?
Increased addition of acid
- Increased H+ formation
- Acid ingestion
Decreased H+ excretion
- decreased H+ excretion
- loss of bicarbonate
81
How do we get increased H+ forming?
- Ketoacidosis
- Lactic acidosis
- Poisoning – methanol, ethanol, ethylene glycol, salicylate
- Inherited organic acidosis
82
How can acid ingetsion occur?
Acid poisoning
| XS parenteral administration of amino acids eg arginine
83
What causes decreased H+ excretion?
- Renal tubular acidosis
- Renal failure
- Carbonic dehydratase inhibitors
84
What conditions lead to a loss of bicarbonate?
Diarrhoea
| Pancreatic, intestinal or biliary fistulae/drainage
85
How is metabolic acidosis comepnsated for
Compensation - hyperventilation, hence low pCO2
| Correction - of cause, increased renal acid excretion
86
Outline the features of metabolic acidosis
low pH
high [H+]
low [HCO3-], low pCO2
87
Diagnose the following:
17 year old male – Type 1 diabetes – not taken insulin for 24 hours
Low pH = acidotic
Low HCO3
Uncompensated acute metabolic acidosis
88
What are the common causes of metabolic alkalosis?
- Increased addition of base
- Increased loss of acid
- Decreased elimination of base
89
How does base addition increase to a pathological level?
Inappropriate Rx of acidotic states
Chronic alkali ingestion
90
Describe the causes of acid loss through GI
Gastric aspiration
| Vomiting with pyloric stenosis
91
How is acid lost through the kidneys?
- Diuretic Rx (not-K+sparing)
- Potassium depletion
- Mineralocorticoid excess- Cushing’s, Conn’s
- Drugs with mineralocorticoid activity – carbenoxolon
92
Describe the compensation mechanism for metabolic alkalosis
Compensation - hypoventilation with CO2 retention (respiratory acidosis)
Correction - increased renal bicarbonate excretion, reduce renal proton loss
93
Outline the features of metabolic alkalosis
High pH
Low [H+]
High [HCO3-], N/highpCO2
94
What condition does a 56 year old female – vomiting last 48 hours with High pH = alkalotic and High HCO3 - not compensating have?
Uncompensated acute metabolic alkalosis
95
How can metabolic alkalosis arise due to hypovolemia?
Hypovolaemia from persistent vomiting
- Loss of HCl
- Loss of potassium
- Loss of fluid
96
How do diuretics lead to metabolic alkalosis?
Chronic K+ depletion
97
How does the body respond to fluid loss?
Response to fluid loss is aldosterone activation
Reabsorb NaCl/H2O at distal convoluted tubule in kidney in exchange for K+ /H+
98
Summarise resp acidosis
CO2 retention
| Compensation is metabolic alkalosis
99
Summarise respiratory alkalosis
increased CO2 loss
| Compensation is metabolic acidosis
100
Summarise metabolic alkalosis
Very difficult primary disturbance to produce and maintain in proton producers!
(Very specific factors required) - need to switch off RAAS via antiemetics and fluids to replace ciruclating volume
Compensation – respiratory acidosis
101
Summarise metabolic acidosis
Acid ingestion
Increases acid production
Reduced acid excretion
Compensation respiratory alkalosis
102
How does hyperkalaemia arise?
Acidosis usually associated with hyperkalemia as more significant to remove H+ than K+ ⇒ K+ build up
103
What is hypokalaemia?
excess k+ loss associated with alkalosis
104
Describe regular K+ redistribution in the body
K+ redistributes between ICF and ECF very rapidly
105
When does artifactual hyperkalaemia occur?
Artifactual hyperkalemia usually when patients take K+ into wrong tube or contaminated with K+ EDTA
