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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
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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
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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
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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

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5
Q

When does an absent anion gap occur?

A

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

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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.

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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.
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8
Q

What are Characteristic Biochemistry results for metabolic acidosis?

A
  • pH - Low
  • [H+] - Increased
  • [HCO3-] - Increased
  • PCO2 - Normal or low
  • PO2 - Increased
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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
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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
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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)
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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
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13
Q

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

A
  • Hyperalimentation
  • Acetazolamide
  • RTA
  • Diarrhoea
  • Uteroenterostomy
  • Pancreatic fistula
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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.
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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.
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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.
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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)
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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)

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