L19 Acid/Base Disorders Flashcards
Systems that maintain acid homeostasis?
Buffer systems
Lungs
Kidneys
Normal pH in the body?
Normal pH 7.35-7.45
First/Second Line Defences against pH shifts?
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
Time course of buffering, respiratory compensation & renal excretion of an acid load?
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)
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)
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
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)
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)
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+)
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.
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
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
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
Metabolic Acid-Base Disorders with LOW Anion Gap
HARDUPS
Hyperalimentation
Acetazolamide
Renal tubular acidosis
Diarrhoea
UreteroEnteric fistula/shunt
Post Hypocapnia
Spironolactone
Causes of Metabolic Alkalosis?
Vomiting
Villous Adenoma
Hypercalcaemia
Hypokalaemia
Contraction Alkalosis
Diuretics (loop, thiazides)
Mineralocorticoid Excess
Disorders leading to Respiratory Acidosis?
↓ 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?
↑ 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?
- 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?
↓ 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?
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)
Metabolic Alkalosis
CO2 Elevated, compensation
HCO3- 43 mmol/L (22-28) ALKYLOSIS
pH <7.35
Low pCO2
Low HCO3
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
