Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MSC: Disease of major orgns > Assessment and Disorders of Acid Base Balance > Flashcards

Assessment and Disorders of Acid Base Balance Flashcards

1
Q

What do blood gas analysers measure?

A
  • Electrolytes: Sodium, Potassium, Chloride, Ionised calcium
  • Metabolites: Glucose, Lactate
  • Co-oximetry: Total Hb, O2 saturation, Oxy-Hb, CO-Hb, Met-Hb
  • Calculated parameters: Base excess, Standard bicarbonate, Anion Gap, Total CO2
  • Gases: PCO2, PO2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are methods of measures within the blood gas analysers?

A
  • Potentiometric: pH, pCO2, Na+, K+, Cl-, Ca++
  • Amperometric: pO2, glucose, lactate
  • Spectrophotometry: co-oximetry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is an Anion Gap?

A
  • Difference between sum of measured cations and anions:

Anion gap = ([Na+] + [K+]) – ([Cl-] – [HCO3-])

  • Most individuals have excess measured cations i.e. an anion gap due to unmeasured anions. (An osmolar gap indicates the presence of uncharged species e.g. ethanol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What could unmeasured anions and cations be?

A

Unmeasured cations: Calcium, Magnesium, (Lithium), (Cationic Igs)

Unmeasured anions (in metabolic acidosis; ¯HCO3-): Proteins, b-Hydroxybutyrate, Acetoacetate, Lactate, Sulphates, Phosphates, Formate, Glycolate, Oxalate, Hippurate, Salicylate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When does an absent anion gap occur?

A

Occurs with increased unmeasured cations, hypoalbuminaemia, Bromide toxicity (spurious ­Cl-), Nitrates.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does a low or negative anion gap occur?

A

Observed when hyperchloremia is caused by high levels of cations (lithium toxicity), monoclonal IgG gammopathy, or hypercalcaemia / hypermagnesaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does the Anion Gap chanage with Albumin?

A
  • Adjust anion gap for albumin concentration, since albumin is a weak acid that may account for up to 75% of the anion gap. Without correction clinically significant increases in anions (>5mmol/L) may be missed in >50% cases.
  • For every 10 g/L albumin decrease, increase calculated anion gap by 2.3 - 2.5 mmol/L.
  • Albumin-corrected anion gap is still an approximation. Does not account for ions like magnesium, calcium, and phosphate.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are Characteristic Biochemistry results for metabolic acidosis?

A
  • pH - Low
  • [H+] - Increased
  • [HCO3-] - Increased
  • PCO2 - Normal or low
  • PO2 - Increased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are further biochemical investigations for Metabolic Acidosis?

A
  • U&Es
  • Anion gap
  • Osmolal gap
  • Plasma glucose
  • Lactate
  • Ketones
  • Drugs/poisons (e.g. paracetamol / salicylate / ethanol / methanol / ethylene glycol)
  • Other e.g. urine pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are causes of metabolic acidosis?

A

Increased acid formation

  • Ketoacidosis: Diabetic, Alcoholic, Starvation
  • Lactic acidosis: Type A (tissue hypoxia), Type B (drugs, liver disease, IEMs), D-lactic acidosis
  • Poisoning: Salicylate, Toxic alcohols (Methanol, Ethanol, Ethylene glycol), Inherited organic acidosis

Decreased acid excretion

  • Uraemic acidosis
  • RTA: Type 1, Type 4

Gain of acid

  • Ingestion of strong acid: Hydrochloric acid, Sulphuric acid
  • Infusion of ammonium chloride
  • I.V. feeding with excess cationic amino acids: Arginine, Lysine

Loss of base

  • GI loss: Diarrhoea, Pancreatic fistula
  • Renal loss: RTA type 2, Acetazolamide, Ureteroenterostomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the acronym for causes of Increase Anion Gap metabolic acidosis?

A
  • M: Methanol toxicity
  • U: Uraemia of renal failure (AKI and severe CKD)
  • D: Diabetic ketoacidosis (alcoholic and starvation ketoacidosis)
  • P: Paraldehyde toxicity
  • I: Isoniazid, Iron or Ischaemia
  • L: Lactic acidosis ***
  • E: Ethylene glycol toxicity (other toxic alcohols)
  • S: Salicylate toxicity (also paracetamol)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are causes of Norma Anion Gap metabolic Acidosis?

A

GI fluid loss

  • Diarrhoea (severe): Hypokalaemia, hypomagnesaemia
  • Pancreatitis
  • Intestinal fistulae

Renal tubular acidosis (RTA)

  • Type 1 (distal): Urine pH > 5.5, Hypokalaemia
  • Type 2 (proximal): Urine pH < 5.5, normo- or hypokalaemia
  • Type 4: Urine pH < 5.5, Hyperkalaemia

Other

  • Carbonic anhydrase inhibitors (e.g. Acetazolamide)
  • Saline infusion
  • Ingestion of HCl / ammonium chloride
  • Recovery from ketoacidosis
  • Adrenal insufficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the Pneumonic for causes of Normal Anion Gap Metabolic Acidosis?

A
  • Hyperalimentation
  • Acetazolamide
  • RTA
  • Diarrhoea
  • Uteroenterostomy
  • Pancreatic fistula
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Type 1 Renal Tubular acidosis and its mechanism and cause?

A

Type 1 (Distal). More common than Type 2

Mechanism

  • ↓ Distal tubular secretion of H+;Inability to acidify urine.

Biochemical Features

  • Urine pH > 5.5
  • Hypokalaemia
  • Hypercalciuria
  • Nephrocalcinosis
  • Renal calculi
  • Osteomalacia / Rickets

Investigations

  • Urine acidification test: failure to acidify urine pH <5.5 in response to an acid load (e.g.ammonium chloride or furosemide) supports the diagnosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Type 2 Renal Tubular Acidosis?

A

Type 2 (Proximal). Genetic diseases (e.g. cystinosis) and nephrotoxins (e.g. myeloma light chains) may cause proximal tubular damage

Mechanism

  • ↓ Proximal reabsorption of filtered bicarbonate. Distal tubular function is good enough so urine acidification is normal.

Biochemical Features

  • Urine pH < 5.5
  • Hypokalaemia
  • Urinary glucose, phosphate & urate excretion may be increased with aminoaciduria and hypercitraturia in Fanconi syndrome
  • Osteomalacia and calciuria without stone formation.

Investigations

  • Abnormally high fractional excretion of bicarbonate load when plasma bicarbonate is ~ 20 mmol/L.
  • Treatment with sodium bicarbonate and potassium supplements. Vitamin D and phosphate supplements if needed.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Type 4 Renal Tubular Acidosis?

A

Type 4 (Hypoaldosteronism). May occur in adrenal failure, hyporeninaemic hypoaldosteronism or drugs inhibiting RAA axis.

Mechanism

  • Hypoaldosteronism causing sodium wasting and decreased H+ and K+ excretion by H+ ATPase in distal tubule. Urine acidification still occurs in distal tubules.

Biochemical Features

  • Urine pH < 5.5
  • Hyperkalaemia
  • Sodium wasting

Investigations

  • Measure renin / aldosterone
  • Hyperkalaemia treated with diuretics.
  • Mineralocorticoid replacement as required.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are systemic effects fo metabolic acidosis?

A

Cardiovascular

  • Negative inotropic effect
  • Arteriolar vasodilation
  • Constriction of peripheral veins
  • Impaired myocardial contractility (severe acidosis)

Oxygen Delivery

  • Immediate right shift (Bohr) in oxyHb dissociation curve
  • Slower left shift in oxyHb dissociation curve (¯synthesis ­breakdown 2,3-DPG)

Nervous system

  • Decreased consciousness

Potassium

  • K+ movement from ICF to ECF causing hyperkalaemia
  • Decreased renal excretion
  • Frequently K-depleted; hypokalaemia common with correction (unless replaced)

Bone

  • Decalcification with negative calcium balance
  • Renal osteodystrophy (CKD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are responses to Metabolic acidosis?

A

Buffering

  • Acute increased­H+ resisted by bicarbonate buffering causing decreased HCO3-
  • Tissue proteins and bone important in chronic acidosis (decalcification)

Respiratory Compensation

  • Develops rapidly but takes several hours to become maximal (12-24h)
  • Peripheral chemoreceptors and respiratory centre stimulated resulting in hyperventilation
  • Self-limiting as hyperventilation generates additional CO2. Lower limit for PCO2 is 1.4-1.6 kPa

Renal Compensation

  • Urine H+ excretion maximised (pH 4.2)
  • Urea production inhibited and glutaminase induced (producing NH4+for excretion and regenerating bicarbonate) (chronic acidosis)
  • Increased renal gluconeogenesis (to utilise 2OG derived from glutamine)
  • Increased rate of regeneration of bicarbonate
  • Increased Na+/H+ exchange
19
Q

How is Metabolic Acidosis managed?

A

Identify and treat cause

Alkali administration:

  • I.V sodium bicarbonate: Usually only given if [H+] > 100 nmol/L (pH 7.0)
  • Oral bicarbonate: CKD, RTA types 1 & 2
  • Rapid correction impairs O2 delivery to tissues (until 2,3-BPG normalises). Rebound alkalosis, hypernatreamia, volume overload possible

Dialysis (some cases of uraemia / overdose)

20
Q

What are Characteristic Biochemistry results for respiratory acidosis?

A
  • pH - Low
  • [H+] - High
  • [HCO3-] - Increased/Normal
  • PaCO2 - High
21
Q

What are further investigations for Respiratory Acidosis?

A
  • Chest radiograph
  • Lung function tests
22
Q

What are causes of Respiratory Acidosis?

A
  • Defective control of Respiration
  • Defective Respiratory Function
23
Q

What are causes of Defective Control of Respiration?

A

CNS depression (respiratory centre)

  • Anaesthetics
  • Narcotics
  • Severe hypoxia
  • Opiates
  • Sedatives

CNS disease

  • Trauma
  • Stroke
  • Infarction / ischaemia
  • Haemorrhage
  • Tumour
  • Infection

Neurological disease

  • Spinal cord lesions
  • Poliomyelitis
  • Guillan-Barre syndrome
  • Motor neurone disease
  • Neurotoxins (e.g. organophosphates, snake venom)
24
Q

What are causes of Defective Control of Respiratory Function?

A

Mechanical

  • Myasthenic syndrome (myasthenia gravis)
  • Myopathies (e.g. muscular dystrophy)
  • Thoracic trauma / tumours / deformities
  • Pneumothorax
  • Pleural effusion
  • Diaphragm paralysis
  • Inadequate mechanical ventilation

Pulmonary disease

  • COPD
  • Restrictive defects
    • Fibrosis
    • Pulmonary oedema
    • Infiltrative tumours
  • Obstructive defects
    • Chronic bronchitis
    • Emphysema
    • Severe asthma
    • Laryngospasm
    • Bronchospasm
    • Tumour / aspiration

Impaired perfusion

  • Massive pulmonary embolism
25
Q

What systemic effects of respiratory Acidosis?

A

Hypoxaemia:

  • Breathlessness, cyanosis, drowsiness

Neurological (Hypercapnia):

  • Headache, papilloedema, extensor plantar responses, myoclonus (chronic)
  • Anxiety, confusion, impaired consciousness

Effects of acidosis (as for metabolic) e.g. Bohr shift, hyperkalaemia, etc.

26
Q

What is the response of the Body towards Respiratory Acidosis?

A

Buffering

  • Limited buffering by haemoglobin (rapid)
  • Other intracellular buffers important in chronic acidosis

Respiratory Compensation

  • Increase ­PCO2 stimulates respiratory centre (hyperventilation) but underlying disease prevents adequate response

Renal Compensation (2-5 days)*

  • Maximal bicarbonate reabsorption
  • Almost all phosphate excreted as H2PO4-
  • Marked increase in urinary ammonium
  • Increased Na+/H+ exchange
27
Q

How is Respiratory Acidosis managed?

A
  • Treat underlying cause if possible
  • Maintain adequate arterial PO2, avoid loss of hypoxic stimulus to respiration
  • Avoid rapid correction of PCO2 (risk of alkalosis due to persistence of compensation)
  • Bronchodilators (e.g. salbutamol in COPD)
28
Q

What are Characteristic Biochemistry results for metabolic Alkalosis?

A
  • pH - High
  • [H+] - Low
  • [HCO3-] - High
  • PaCO2 - Normal or High
  • K+ - Low
29
Q

What are further investigations of Metabolic Alkalosis?

A
  • U&Es (Na+, K+, Cl-, urea, creatinine)
  • Calcium and albumin
  • Magnesium
  • Urine pH*
  • Urine chloride (spot urine)
  • Blood pressure
30
Q

What are causes of Metabolic Alkalosis?

A

Saline responsive (urine Cl- < 20 mmol/L)

  • Gastrointestinal: Vomiting / Pyloric stenosis (common), Gastric drainage, Congenital Cl-losing diarrhoea
  • Exogenous alkali administration: Sodium bicarbonate (IV), Lactate, Citrate (transfusion), Acetate (especially if ¯GFR), Milk alkali syndrome (rare)
  • Other exogenous: Diuretics (Common), Diuretic administration post ­PCO2, Poorly reabsorpable anion therapy (e.g. penicillin, carbenicillin)

Saline unresponsive (urine Cl- > 20 mmol/L)

  • Association with hypertension (mineralocorticoid excess): Primary hyperaldosteronism (Conn’s), Secondary hyperaldosteronism, Cushing’s Syndrome, 11-β-hydroxylase and 17-α-hydroxylase deficiencies (CAH), Carbenoxalone and Liquorice (glycrrhizic acid)
  • Other: Barter’s syndrome, Gitelman’s syndrome, Refeeding syndrome, Severe potassium depletion, Magnesium deficiency, Extreme hypercalcemia
31
Q

How does Gastric Losses lead to Metbolic Alkalosis?

A
  • Gastric Loss of [Cl-], [Na+], [K+], [H+]
  • Loss of [Cl-] leads to retention of [HCO3-] so increased [HCO3-]
  • Loss of [Na+], [K+], [H+] leads to rention of [Na+], [K+] at the expenses of [H+]. This leads to low [H+]
  • This can lead to metabolic alkalosis
32
Q

What are systemic effects of metabolic alkalosis?

A

Generally opposite to those of acidosis. Less pronounced CV effects and no apparent bone effects

  • Impaired O2 delivery to tissues
  • Potassium depletion, which sustains alkalosis and may manifest as muscle weakness.
  • Neuromuscular hyperexcitability (acute): parasthesia, muscle cramps, tetany, convulsions. This is due binding of H+ to albumin increases Ca2+binding, lowering ionised calcium)
33
Q

What are responses to metabolic alkalosis?

A

Buffering

  • Release of buffered H+, with increased ­HCO3-

Respiratory Compensation (24 – 36h)*

  • Decreased stimulation of chemoreceptors but self-limiting as ­PCO2 stimulates ventilation (maximal pCO2 ~ 8 kPa)
  • Hypoxic stimulus also overrides decreased H+ stimulus at respiratory centre.

Renal Compensation

  • Inappropriate reabsorption of HCO3- due to decreased GFR/increased tubular function.
  • If decreased ECF volume associated with [Cl-] deficiency, obligatory increased [­HCO3-] reabsorption which exacerbates alkalosis.
  • Potassium deficiency contributes to persistence of alkalosis. Increased mineralocorticoid activity promotes distal tubular Na+ (with increased K+ and H+ excretion)
34
Q

How is metabolic alkalosis managed?

A
  • Treat underlying cause
  • Treat factors that sustain alkalosis: Volume expansion (saline responsive), Potassium replacement, Magnesium replacement
  • Dangerous to give saline in saline-unresponsive causes (e.g. sodium excess)
  • Spironolactone or amiloride (hyperaldosteronism)
35
Q

What are Characteristic Biochemistry results for Respiratory Alkalosis?

A
  • pH - High
  • [H+] - Low
  • [HCO3-] - Normal/Low
  • PaCO2 - Low
  • K+ - Low
  • Phos - Low
36
Q

What are further investigations for Respiratory Alkalosis?

A
  • LFTs
  • Salicylate
  • FBC (? Sepsis (WCC), ?anaemia). Possibly cultures.
  • Chest radiograph
  • Lung function tests
37
Q

What are causes of respiratory alakalosis?

A

Non-pulmonary stimulation of respiratory centre

  • Cortical influences (common): Pain, Fever, Anxiety
  • Drugs / toxins: Salicylate, Catecholamines, Progesterone, Theophylline, Thyroxine
  • Endogenous compounds: Hepatic failure (toxins), Pregnancy (progesterone), Sepsis (cytokines), Thyroid crisis
  • CNS lesions: Encephalitis, Meningitis, SAH, Tumours, Trauma / Head injury, Stroke
  • Hypoxia: High altitude, Severe anaemia, Right-to-left shunts

Hyperventilation

  • Voluntary
  • Mechanical

Pulmonary disorders

  • Pneumonia
  • Pulmonary oedema (all types)
  • Lung fibrosis
  • Pneumothorax
  • Pulmonary embolism
  • Asthma
  • Interstitial lung disease
  • Chronic bronchitis
38
Q

What are systemic effects of Respiratory Alkalosis?

A
  • Manifestations of underlying disease predominate
  • Acute hypocapnia decreases cerebral blood flow causing light-headedness, confusion, etc.
  • Perioral and peripheral parasthesia (¯ionised calcium)
  • Cardiovascular: increased heart rate, tightening of chest, angina
  • Mild hypokalaemia
  • Hypophosphataemia
39
Q

How is Respiratory Alkalosis Compensated?

A

Buffering

  • Release of H+ from non-bicarbonate buffers
  • New steady state achieved quickly. Persists for up to 6 hours (when renal compensation becomes evident)

Respiratory Compensation

  • Inhibitory effect of ¯PCO2 on respiration overwhelmed by primary cause which stimulates hyperventilation

Renal Compensation (2-5 days)*

  • Decreased renal generation of bicarbonate (CO2is substrate). Decreased urinary acidification.
40
Q

How is Respiratory Alkalosis managed?

A
  • Treat underlying cause
  • Rapid symptomatic relief by re-breathing from paper bag
  • Sedation or prevention of hyperventilation by mechanical hyperventilation (in severe cases)
41
Q

What are causes of Hypoxaemia?

A
  • Hypoventilation e.g. Head injury, drugs (morphine or barbiturates), respiratory muscle weakness, chest trauma, COPD, obesity, etc.
  • Diffusion impairment e.g. Lung Fibrosis
  • Ventilation-perfusion mis-matching
  • Right-to-left shunt
  • Low inspired pO2 e.g. high altitude
42
Q

What is Pulse Oximetry?

A
  • Non-invasive, transcutaneous estimation of arterial oxygen saturation (SaO2). Differential light absorption by haemoglobin and oxyhaemoglobin sensed through a pulsatile signal
  • SaO2 may be normal if tissue hypoxia caused by Low cardiac output states, Anaemia, Failure of tissue oxygen use, Severe hypoxia in a single organ.
43
Q

What can cause inaccuracies of Pulse Oximetry?

A
  • Bright light (pulsatile waveforms and saturation).
  • Dyes and pigments e.g. nail varnish (artificially low).
  • Abnormal haemoglobins e.g. methaemoglobinaemia.
  • Carboxyhaemoglobin in CO poisoning (saturation since oxyhaemoglobin and carboxyhaemoglobin cannot be distinguished).
  • Cardiac arrhythmias (interfere with detection of pulsatile signal).
  • Vasoconstriction / hypothermia (desaturation, failure to register signal due to reduced perfusion).
  • Movement e.g. shivering.
  • Saturations < 75%
44
Q

What is the Haber-Weiss equation?

A

[H+] = K ([pCO2]/[HCO3])

K – embraces dissociation constants and solubility coefficient of carbon dioxide

K – 180 when H+ in nmol/L, HCO3 in mmol/L and pCO2 kPa

MSC: Disease of major orgns (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions