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Metabolic Emergencies (C 12) Flashcards

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1
Q

Describe the relationship between acid-base status and potassium.

A

Acidaemia results in an extracellular shift of potassium that can result in significant hyperkalaemia. Increase in serum K+ of 0.4-0.6 mmol/L for each decrease in pH of 0.1

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2
Q

What are the mechanisms by which acid-base disturbances can be compensated?

A

Buffering, respiratory manipulation of CO2, renal handling of bicarbonate

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3
Q

What is timing of the different forms of compensation?

A

Immediate: buffering with plasma proteins, haemoglobin and the carbonic-acid-bicarbonate systems. Slower, within minutes: respiratory compensation by alterations in alveolar ventilation. Hours-days: renal compensation

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4
Q

Define acidaemia.

A

Presence of an increased concentration of H+ ions in the blood

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5
Q

What are the physiological effects of acidaemia?

A

(1) Decrease in affinity of Hb for oxygen, (2) Increased serum K+

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6
Q

Define metabolic acidosis.

A

Increase in the [H+] of the blood as a result of increased acid production or bicarbonate wasting from the GIT or renal tract.

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7
Q

What is non-anion gap metabolic acidosis also known as?

A

Hyperchloraemic metabolic acidosis

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8
Q

What is the equation to calculate the anion gap?

A

Anion gap = [Na+] - [Cl-] + [HCO3-]

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9
Q

What does an anion-gap metabolic acidosis imply and indicate?

A

That there is an increase in the ‘unmeasured’ anions - generally the upper limit of a normal anion gap is 14 (range 5-12!).The anions that are responsible for a raised anion gap depend on the cause of the acidosis. Examples: lactic acid in shock/hypoxia, PO4/SO4 in renal failure, ketoacids in ketoacidosis, oxalic acid in ethylene glycol poising

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10
Q

What are the acids that increase the anion-gap in ethylene glycol and methanol poisoning?

A

Ethylene glycol: oxalic acid, Methanol: formic acid

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11
Q

What are the causes of high lactate?

A

Type A: Imbalance between oxygen demand and supply. Including CO poisoning, excessive O2 demand (seizures, hyperpyrexia, shivering, exercise), shock, severe anaemia, severe hypoxia. Type B: Metabolic derangements. Including: beta-2 agonists, cancer, cyanide, ethanol, liver failure, inborn errors of metabolism, ketoacidosis, meformin, sepsis, vitamin deficiency (thiamine, biotin)

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12
Q

What is the hallmark of non-anion gap acidosis?

A

Elevation of serum chloride (secondary to urinary retention by the renal tubules which HCO3- is lost)

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13
Q

What is non-anion-gap metabolic acidosis the result of?

A

Loss of HCO3- from the body rather than increased acid production

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14
Q

How can the causes of non-anion gap metabolic acidosis be classified?

A

The site of HCO3- losses.GIT losses: fluid losses rich in bicarbonate, cholestyramine ingestion (binds HCO3- in the gut). Renal losses: renal tubular acidosis, carbonic anhydrase inhibitor therapy, adrenocortical insufficiency. Large volume chloride-rich crystalloid administration

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15
Q

What is the acid-base disturbance with someone who receives excessive normal saline resuscitation?

A

Due to direct chloride excess there is renal bicarbonate loss driving a non-anion gap metabolic acidosis

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16
Q

What is renal tubular acidosis?

A

Group of conditions where there is an impaired ability to secrete H+ in the distal convoluted tubule or a problem with the absorption of HCO3- in the PCT.

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17
Q

What blood test abnormalities do patients with renal tubular acidosis have?

A

Chronic metabolic acidosis with hypokalaemia, nephrocalcinosis, rickets or osteomalacia

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18
Q

What drugs can cause renal tubular acidosis?

A

Ibuprofen, toluene, carbonic anhydrase inhibitors

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19
Q

Describe how you would treat a patient with metabolic acidosis.

A

Correction of the underlying causes. Consider HCO3 use in selected circumstances.

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20
Q

In what circumstances may you consider bicarbonate use in metabolic acidosis?

A

If there is acidosis and (a) severe hyperkalaemia, (b) severe sodium channel blocker poisoning, (c) salicylate poisoning or (d) methanol poisoning

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21
Q

In who should HCO3 use be avoided?

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A

Patients with DKA and lactic acidosis associated with sepsis or severe cardiorespi disease - it does not improve outcomes

22
Q

What are the potential hazards of HCO3 therapy?

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A

High solute load, hyperosmolarity, hypokalaemia, decreased ionised serum calcium and worsening intracellular/CSF fluid acidosis. The latter may precipitate hepatic encephalopathy.

23
Q

Define alkalaemia.

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A

Decrease in [H+] in the blood

24
Q

What are the possible effects of extreme alkalaemia? What are these the consequence of?

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A

Altered mental status, tetany and seizures. These are due to a reduction in ionised calcium concentration - especially common with respiratory alkalosis due to anxiety

25
What can alkalaemia in patients with chronic airways disease cause?
Exacerbate tissue hypoxia due to a leftward shift of the oxygen-dissociation curve
26
What are the causes of metabolic alkalosis?
Most commonly: loss of acid from the GIT. Others: renal acid losses or exogenous bicarbonate. Classification: (a) Chloride/saline-responsive or (b) Not chloride/saline-responsive. (a) GIT volume loss (vomiting), diuretics, licorice, hypokalaemia. (b) Hyperaldosteronism, apparent mineralocorticoid excess, Liddle's, Cushing's, conn's, bartter's, gitelman's and excessive bicarb ingestion 
27
What are possible sources of exogenous bicarbonate?
Antacids, dialysis and milk-alkali syndrome
28
Describe chloride-responsive metabolic alkalosis.
Arises from conditions that result in both chloride and volume loss. Reduced extracellular volume --> increased mineralocorticoid activity --> sodium reabsorption + hydrogen secretion. This then causes increased bicarbonate formation and the kidney cannot excrete it all. Causes: GIT volume loss (vomiting), diuretics, licorice, hypokalaemia
29
What is the urine chloride in patients with metabolic alkalosis typically?
If fluid responsive: low (<10 mmol/L) because it is not excreted to maintain electroneutrality. If not fluid responsive: higher (>10)
30
Describe chloride-unresponsive metabolic alkalosis.
Due to disease states that either result in inappropriate excessive mineralocorticoid secretion (ie no volume loss/chloride wasting). Other causes would be due to ionic transport channel defects in the kidneys (congenital). Causes: hyperaldosteronism, apparent mineralocorticoid excess, Liddle's, Cushing's, conn's, bartter's, gitelman's and excessive bicarb ingestion 
31
What are several physiological causes for respiratory alkalosis?
(a) Exercise, (b) Altitude-related hypoxia, (c) Stimulation of respiratory centre by progesterone in pregnancy 
32
Discuss the causes for respiratory alkalosis.
(1) CNS mediated hyperventilation: increased ICP, CVA, psychogenic, (2) Hypoxia-mediated hyperventilation: altitude, anaemia, V/Q mismatch, xanthines, (3) Pulmonary: CCF, mechanical hyperventilation, pneumonia, PE, (4) Sepsis, (5) Toxin-induced: salicylate or nicotine
33
What are toxins that can cause metabolic alkalosis?
Salicylates, nicotine 
34
Discuss the Cameron's approach to Acid-Base Disturbances.
(1) What is the pH? (2) Primary process - respi, metabolic, both? (3) Calculate the anion gap, (4) Check for degree of compensation, (5) Presence of delta gap 
35
What does the delta gap mean?
In an anion-gap metabolic acidosis, this step determines whether there is a non-anion-gap (hyperchloraemic) component as a contributing explanation of the bicarbonate fall. There should be a 1:1 relationship between the rise in the anion gap over normal and the decrease in the bicarbonate. If the bicarbonate is higher than predicted then a metabolic alkalosis is also present. If the bicarbonate is lower than predicted then a non-anion gap acidosis is also present
36
Discss the causes of acute respiratory acidosis.
Airway obstruction, aspiration, bronchospasm, drug-induced CNS depression, hypoventilation (CNS/muscular origin), hypoventilation (PNS origin - GBS, OP, poisoining), pulmonary diseases
37
Discuss the causes of chronic respiratory acidosis.
Lung diseases (COPD, pulmonary fibrosis), NMD - muscular atrophy, obesity, severe kyophoscoliosis
38
Discuss compensation in metabolic acidaemia.
For every 1 decrease in HCO3-, PaCO2 should decrease by 1.3
39
Discuss compensation in metabolic alkalaemia.
For every 1 increase in HCO3-, PaCO2 should increase by 0.6 
40
Discuss compensation in chronic respiratory acidaemia.
For every 10 increase in PaCO2, HCO3 should increase by 4 
41
Discuss compensation in acute respiratory acidaemia.
For every 10 increase in PaCO2, HCO3 should increase by 1
42
Discuss compensation in acute respiratory alkalaemia.
For every 10 DEcrease in PaCO2, HCO3 should decrease by 2
43
Discuss compensation in chronic respiratory alkalaemia.
For every 10 DEcrease in PaCO2, HCO3 should decrease by 5
44
Causes of anion-gap acidosis.
CO/cyanide, Alcohol incl ketoacidosis, Toluene, Metformin/methanol, Uraemia, DKA, Paracetamol/propylene glycol/paraldehyde/phenformin, Iron/isoniazid, Lactic acidosis, Ethylene glycol, Salicylcates/starvation ketoacidosis
45
Causes of low anion gap.
<6. Increased unmeasured cations: hypercalcaemia, hypermagnesaemia, lithium, multiple myloma/gammopathies, decrease unmeasured anions, dilution, hypoalbuminaemia. Artefactual hyperchloraemia: bromism, iodism, hypertriglycidaemia, propylene glycol
46
Causes of non-anion gap metabolic acidosis.
Ureterostomy, Small bowel fistula, Excess chloride, Diarrhoea, Carbonic anhydrase inhibitors, Adrenal insufficiency, Renal tubular acidosis, Pancreatic fistula 
47
What are drugs that can cause non-anion gap metabolic acidosis?
Acetazolamide (other CA-inhibitors such as topiramate), Acidifying agents (ammonium chloride), Cholestyramine
48
If pH is < 7.40 and PaCO2 > 44, then it is:
Respiratory acidosis
49
If pH is < 7.40 and HCO3 is < 25, then it is:
Metabolic acidosis
50
If pH is > 7.44 and PaCO2 is < 40, then it is:
Respiratory alkalosis
51
If pH is > 7.44 and HCO3 is > 25, then it is:
Metabolic alkalosis 

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