Brainscape's Knowledge GenomeTM

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


See full index

ABGs > Metabolic Emergencies (C 12) > Flashcards

Metabolic Emergencies (C 12) Flashcards

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

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

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

A

Buffering, respiratory manipulation of CO2, renal handling of bicarbonate

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

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

Define acidaemia.

A

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

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

What are the physiological effects of acidaemia?

A

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

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

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

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

A

Hyperchloraemic metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the equation to calculate the anion gap?

A

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Chronic metabolic acidosis with hypokalaemia, nephrocalcinosis, rickets or osteomalacia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What drugs can cause renal tubular acidosis?

A

Ibuprofen, toluene, carbonic anhydrase inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe how you would treat a patient with metabolic acidosis.

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In who should HCO3 use be avoided?

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?

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.

A

Decrease in [H+] in the blood

24
Q

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

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
Q

What can alkalaemia in patients with chronic airways disease cause?

A

Exacerbate tissue hypoxia due to a leftward shift of the oxygen-dissociation curve

26
Q

What are the causes of metabolic alkalosis?

A

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
Q

What are possible sources of exogenous bicarbonate?

A

Antacids, dialysis and milk-alkali syndrome

28
Q

Describe chloride-responsive metabolic alkalosis.

A

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
Q

What is the urine chloride in patients with metabolic alkalosis typically?

A

If fluid responsive: low (<10 mmol/L) because it is not excreted to maintain electroneutrality. If not fluid responsive: higher (>10)

30
Q

Describe chloride-unresponsive metabolic alkalosis.

A

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
Q

What are several physiological causes for respiratory alkalosis?

A

(a) Exercise, (b) Altitude-related hypoxia, (c) Stimulation of respiratory centre by progesterone in pregnancy

32
Q

Discuss the causes for respiratory alkalosis.

A

(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
Q

What are toxins that can cause metabolic alkalosis?

A

Salicylates, nicotine

34
Q

Discuss the Cameron’s approach to Acid-Base Disturbances.

A

(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
Q

What does the delta gap mean?

A

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
Q

Discss the causes of acute respiratory acidosis.

A

Airway obstruction, aspiration, bronchospasm, drug-induced CNS depression, hypoventilation (CNS/muscular origin), hypoventilation (PNS origin - GBS, OP, poisoining), pulmonary diseases

37
Q

Discuss the causes of chronic respiratory acidosis.

A

Lung diseases (COPD, pulmonary fibrosis), NMD - muscular atrophy, obesity, severe kyophoscoliosis

38
Q

Discuss compensation in metabolic acidaemia.

A

For every 1 decrease in HCO3-, PaCO2 should decrease by 1.3

39
Q

Discuss compensation in metabolic alkalaemia.

A

For every 1 increase in HCO3-, PaCO2 should increase by 0.6

40
Q

Discuss compensation in chronic respiratory acidaemia.

A

For every 10 increase in PaCO2, HCO3 should increase by 4

41
Q

Discuss compensation in acute respiratory acidaemia.

A

For every 10 increase in PaCO2, HCO3 should increase by 1

42
Q

Discuss compensation in acute respiratory alkalaemia.

A

For every 10 DEcrease in PaCO2, HCO3 should decrease by 2

43
Q

Discuss compensation in chronic respiratory alkalaemia.

A

For every 10 DEcrease in PaCO2, HCO3 should decrease by 5

44
Q

Causes of anion-gap acidosis.

A

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
Q

Causes of low anion gap.

A

<6.Increased unmeasured cations: hypercalcaemia, hypermagnesaemia, lithium, multiple myloma/gammopathies, decrease unmeasured anions, dilution, hypoalbuminaemia. Artefactual hyperchloraemia: bromism, iodism, hypertriglycidaemia, propylene glycol

46
Q

Causes of non-anion gap metabolic acidosis.

A

Ureterostomy, Small bowel fistula, Excess chloride, Diarrhoea, Carbonic anhydrase inhibitors, Adrenal insufficiency, Renal tubular acidosis, Pancreatic fistula

47
Q

What are drugs that can cause non-anion gap metabolic acidosis?

A

Acetazolamide (other CA-inhibitors such as topiramate), Acidifying agents (ammonium chloride), Cholestyramine

48
Q

If pH is < 7.40 and PaCO2 > 44, then it is:

A

Respiratory acidosis

49
Q

If pH is < 7.40 and HCO3 is < 25, then it is:

A

Metabolic acidosis

50
Q

If pH is > 7.44 and PaCO2 is < 40, then it is:

A

Respiratory alkalosis

51
Q

If pH is > 7.44 and HCO3 is > 25, then it is:

A

Metabolic alkalosis

ABGs (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions