L19 Acid/Base Disorders Flashcards by Jackson Barrett

Systems that maintain acid homeostasis?

Buffer systems
Lungs
Kidneys

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Normal pH in the body?

Normal pH 7.35-7.45

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First/Second Line Defences against pH shifts?

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Physiological Buffer Systems?

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

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ABG:

pH 7.24 (7.35-7.45)

pCO2 8kPa (4.5-6)

pO2 6.9kPa (>11)

HCO3- 27mmol/L (22-28)

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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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)*

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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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)

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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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)

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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Acute vs. Chronic respiratory acidosis

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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Role of the Kidneys in Acid-Base Balance

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

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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How is the Anion Gap Measured?

What is a normal AG?

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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Significance of The Anion Gap

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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Metabolic Acid-Base Disorders with HIGH Anion Gap

MUDPILERS

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

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Metabolic Acid-Base Disorders with LOW Anion Gap

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HARDUPS

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

Causes of Metabolic Alkalosis?

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

Disorders leading to Respiratory Acidosis?

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↓ 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

Disorders leading to Respiratory Alkylosis?

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

Hypoxaemia Induced
PE, Asthma, pneumonia, Congenital heart disease

Latrogenic
Mechanical Ventilation

Approach to Acid-Base Disorders?

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What is the pH? Acidaemic or Alkalaemic?
What is respiratory involvement? pCO2
What is metabolic involvement? [HCO3-]
Determine if compensation is present
For metabolic acidosis, what’s the AG?

Disorders leading to Respiratory Acidosis?

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↓ 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

Casues of Lactic Aciodis?

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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)

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)

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Metabolic Alkalosis

CO2 Elevated, compensation

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

pH <7.35
Low pCO2
Low HCO3

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Metabolic Acidosis

pH <7.35 High pCO2 High HCO3

**Respiratory Acidosis**

pH >7.35 High pCO2 High HCO3

**Metabolic Alkalosis**

pH >7.35 Low pCO2 Low HCO3

**Respiratory Alkalosis**

Physiological Compensatory Mechanisms to acidosis?

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

Presentation of Aspirin Overdose?

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)

Treatment of Aspirin Overdose?

**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**

Respiratory Acidosis Treatments?

Treat underlying causes: **COPD, asthma** Reduced resp drive (**CNS, narcotics**) **Naloxone** for opiate overdose **Flumazenil** for benzodiazepine overdose

Opioid antagonist First line for the treatment of opiate overdose 0.4-2mg IV repeat every 2-3 mins

**NALOXONE**

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

**FLUMAZENIL**

Respiratory Alkalosis Treatments?

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*

Metabolic Acidosis Treatments?

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

Metabolic Alkylosis Treatments?

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

L19 Acid/Base Disorders Flashcards

(36 cards)