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SEM3: CLIP30230 GI/GU Therapeutics > L19 Acid/Base Disorders > Flashcards

L19 Acid/Base Disorders Flashcards

1
Q

Systems that maintain acid homeostasis?

A

Buffer systems
Lungs
Kidneys

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2
Q

Normal pH in the body?

A

Normal pH 7.35-7.45

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3
Q

First/Second Line Defences against pH shifts?

A
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4
Q

Physiological Buffer Systems?

A

To regain acid-base balance, the lungs may respond to a metabolic disorder, and the kidneys may respond to a respiratory disorder

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5
Q

Time course of buffering, respiratory compensation & renal excretion of an acid load?

A
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6
Q

ABG:

pH 7.24 (7.35-7.45)

pCO2 8kPa (4.5-6)

pO2 6.9kPa (>11)

HCO3- 27mmol/L (22-28)

A

Acute Respiratory Acidosis

Morphine has dropped respiratory drive (Retaining CO2) => Elevated PCO2 => Volatile acid that drops pH.

Acute
↑[HCO3-] = 0.75 mEq/L for every 1kPa ΔPCO2

HCO3 (Bicarbonate): Normal, trying to compensate

Reflects intracellular buffering (hemoglobin, intracellular proteins)

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7
Q

U&E:
Na+ 134mmol/L (135-145)

Urea 12 mmol/L (5-10)

K+ 2.9 mmol/L (3.5-5.2)

Creatinine 70μmol/L (50-100)

Cl- 107 mmol/L (95-105)

ABG:
pH 7.30 (7.35-7.45)

pCO2 4.4kPa (4.5-6)

pO2 12.4kPa (>11)

HCO3- 16 mmol/L (22-28)*

A

Metabolic Acidosis with Normal Anion Gap

Metabolic Acidosis: Lung compensation, increasing respiratory rate => decreased CO2

Anion Gap= Na+ - (Cl- + HC03) = 134 - (107+16)= 11 (Normal 6-12)

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8
Q

U&E:

Na+ 140 mmol/L (135-145)

Urea 35 mmol/L (5-10)

K+ 6.2 mmol/L (3.5-5.2)

Creatinine 417 μmol/L (50-100)

Cl- 90 mmol/L (95-105)

ABG:
pH 7.18 (7.35-7.45)

pCO2 3.0 kPa (4.5-6)

pO2 11.2 kPa (>11)

HCO3- 18 mmol/L (22-28)

A

High Anion Gap Metabolic Acidosis

Anion Gap (AG) = Na+ - (Cl- + HCO3-)

AG= 140- (90+18) = 22 HIGH (Normal 6-12)

Potential Causes:
Lactic Acidosis, Casued by Septic Shock

Acute kidney injury (HIGH Creatinine)

T1D => if poorly managed => diabetic ketoacidosis (look for glucose and ketone levels

MUDPILERS

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9
Q

ABG

pH 7.31 (7.35 -7.45)

pCO2 8.0 kPa (4.5 – 6 kPa)

pO2 8.8 kPa (11-14 kPa)

HCO3- 34 mmol/L (22-28)

A

Chronic Respiratory Acidosis

Longstanding COPD, has had ample time for Renal compensation

Chronic Acidosis
↑[HCO3-] = 2.56 mEq/L for every 1kPa ΔPCO2

Reflects generation of new HCO3- due to the increased excretion of ammonium (Kidneys have had time to compensate)

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10
Q

Acute vs. Chronic respiratory acidosis

A

Acute
↑[HCO3-] = 0.75 mEq/L for every 1kPa ΔPCO2

Reflects intracellular buffering (hemoglobin, intracellular proteins)

Chronic
↑[HCO3-] = 2.56 mEq/L for every 1kPa ΔPCO2

Reflects generation of new HCO3- due to the increased excretion of ammonium (Kidneys have had time to compensate)

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11
Q

Role of the Kidneys in Acid-Base Balance

A

Reabsorb almost all of the filtered HCO3

Generate new HCO3 (By excreting acid!)

Excretion of titratable acid

Excretion of ammonium (NH4+)

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12
Q

For every ______ that is excreted by the kidneys a new _______ is generated

A

Ammoniagenesis
Production of HCO3− and NH4+ from the renal metabolism of glutamine

For every NH4+ that’s excreted by the kidney, a new HCO3- is generated.

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13
Q

How is the Anion Gap Measured?

What is a normal AG?

A

Routine lab tests don’t measure ALL ions

Na+ + “unmeasured cations” = Cl- + HCO3- + “unmeasured anions”

Anion Gap (AG) = Na+ - (Cl- + HCO3-)

AG= “unmeasured anions”-“unmeasured cations”

We get a + value because there are more “unmeasured anions” than “unmeasured cations”

Normal AG: 10±2

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14
Q

Significance of The Anion Gap

A

Primarily used in the evaluation of Metabolic Acidosis: Can divide metabolic acidosis by those yielding a high anion gap and those with a low anion gap

Determines presence of unmeasured anions: Under normal conditions, it’s mainly due to albumin & phosphate

Sum of major cations less the sum of major anions:
Anion Gap (AG) = Na+ - (Cl- + HCO3-)

Normal AG: 10±2

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15
Q

Metabolic Acid-Base Disorders with HIGH Anion Gap

A

MUDPILERS

Methanol
Uraemia
DKA/Alcoholic KA
Paraldehyde
Isoniazid
Lactic Acidosis
Ethylene Glycol/EtOH
Rhabdomyolysis/Renal failure
Salicylates

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16
Q

Metabolic Acid-Base Disorders with LOW Anion Gap

A

HARDUPS

Hyperalimentation
Acetazolamide
Renal tubular acidosis
Diarrhoea
UreteroEnteric fistula/shunt
Post Hypocapnia
Spironolactone

17
Q

Causes of Metabolic Alkalosis?

A

Vomiting
Villous Adenoma
Hypercalcaemia
Hypokalaemia
Contraction Alkalosis
Diuretics (loop, thiazides)
Mineralocorticoid Excess

18
Q

Disorders leading to Respiratory Acidosis?

A

↓ Respiratory Drive
CNS: stroke or tumour
Drugs: sedatives, narcotics

↓ Chest Wall Movement
Neuromuscular disease
Muscle relaxants
Chest wall trauma, tension pneumothorax

Obstructive Pulmonary Disease
COPD, Asthma

19
Q

Disorders leading to Respiratory Alkylosis?

A

↑ Respiratory Drive
Stroke, pregnancy, thyrotoxicosis
Aspirin OD
Anxiety, pain, fever

Hypoxaemia Induced
PE, Asthma, pneumonia, Congenital heart disease

Latrogenic
Mechanical Ventilation

20
Q

Approach to Acid-Base Disorders?

A
  1. What is the pH? Acidaemic or Alkalaemic?
  2. What is respiratory involvement? pCO2
  3. What is metabolic involvement? [HCO3-]
  4. Determine if compensation is present
  5. For metabolic acidosis, what’s the AG?
21
Q

Disorders leading to Respiratory Acidosis?

A

↓ Respiratory Drive
CNS: stroke or tumor
Drugs: sedatives, narcotics

↓ Chest Wall Movement
Neuromuscular disease
Muscle relaxants
Chest wall trauma, tension pneumothorax

Obstructive Pulmonary Disease
COPD, Asthma

22
Q

Casues of Lactic Aciodis?

A

Lactate/lactic acid is a normal end-product of anaerobic metabolism

Elevated levels in shock, hypotension, ischaemia, hypoxia

Metformin induced lactic acidosis
Rare complication

Renal impairment, sepsis, older age, and dehydration all increase likelihood of development

Metformin contraindicated in renal impairment (eGFR < 30mls/min)

23
Q

ABG

pH 7.56 (7.35 -7.45)

pCO2 6.9 kPa (4.5 – 6 kPa)

pO2 12.5 kPa (11-14 kPa)

HCO3- 43 mmol/L (22-28)

A

Metabolic Alkalosis

CO2 Elevated, compensation

HCO3- 43 mmol/L (22-28) ALKYLOSIS

24
Q

pH <7.35
Low pCO2
Low HCO3

A

Metabolic Acidosis

25
Q

pH <7.35
High pCO2
High HCO3

A

Respiratory Acidosis

26
Q

pH >7.35
High pCO2
High HCO3

A

Metabolic Alkalosis

27
Q

pH >7.35
Low pCO2
Low HCO3

A

Respiratory Alkalosis

28
Q

Physiological Compensatory Mechanisms to acidosis?

A

To regain acid-base balance, the lungs may respond to a metabolic disorder, and the kidneys may respond to a respiratory disorder.

Metabolic Acidosis (Lung Response):
increase respiratory rate to blow off more CO2
Pt. feels short of breath
ABG partial pressure of CO2 is low.

Resipratory Acidosis (Kidney Response):
Get rid of Amonia
Retain more bicarbonate

29
Q

Presentation of Aspirin Overdose?

A

Early: tinnitus, vertigo, n+v+d (vomiting may be severe)

Later: altered mental state, coma, hyperthermia

Initially Respiratory ALKYLOSIS
HYPERPNOEA (early) due to stimulation of the medullary respiratory centre => excess CO2 blown off=>Fall in pCO2 =>Respiratory Alkalosis

Then a High AG Metabolic Acidosis develops due to the accumulation of organic acids (lactic acid, ketoacids)

30
Q

Treatment of Aspirin Overdose?

A

Sodium Bicarbonate (IV bolus then IV infusion)
*“Alkalinisation” reduces the diffusion of salicylate into CNS & reduces its reabsorption in the renal tubules
*Raise the systemic & urine pH
*Reduces the fraction of the uncharged form, which moves easily across cell membranes

Activated charcoal (given w/i 2 hours of ingestion) binds it effectively (patient must be alert)

Salicylate removal can be enhanced by hemodialysis

31
Q

Respiratory Acidosis Treatments?

A

Treat underlying causes:
COPD, asthma
Reduced resp drive (CNS, narcotics)

Naloxone for opiate overdose
Flumazenil for benzodiazepine overdose

32
Q

Opioid antagonist

First line for the treatment of opiate overdose

0.4-2mg IV repeat every 2-3 mins

A

NALOXONE

33
Q

A competitive antagonist of benzodiazepines, reverses their effects

Normally used if resp. rate is severely depressed

Acts quickly when given IV (0.2mg initially) Short action: only ~2 hours

Risk of withdrawal seizures

A

FLUMAZENIL

34
Q

Respiratory Alkalosis Treatments?

A

Some important causes… anxiety, aspirin toxicity, CNS causes, asthma, excessive mechanical ventilation

Hyperventilation syndrome: treat underlying psychological stress, reassurance, paper bag

If pCO2 is corrected rapidly in chronic resp. alkalosis, metabolic acidosis may occur

35
Q

Metabolic Acidosis Treatments?

A

Remember the important causes…. DKA, lactate (ischaemia, sepsis), RTA, diarrhea, aspirin OD

TREAT THE UNDERLYING CAUSE

Sodium Bicarbonate use is controversial

  • Raising the pH may cause myocardial depression or intracellular acidification
  • Generally reserved for acute severe metabolic acidosis
36
Q

Metabolic Alkylosis Treatments?

A

Reduce GI losses E.g. antiemetic for vomiting

Stop loop/thiazide diuretic if causing contraction alkalosis

Volume contraction + reduced chloride: both can be treated with 0.9% NaCl

SEM3: CLIP30230 GI/GU Therapeutics (19 decks)

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