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Acid-Base Disorders
Acidemia vs Acidosis
• Acidemia
• Describes concentration of hydrogen ions [H+] in plasma; this it includes all
conditions where H+ in plasma is higher than the values observed in normal
subjects (40 +/- 2nmol/L), or a pH less than 7.38
• Acidosis
• Any process by which there is increased H+ and a decrease in the concentration
and/or content of bicarbonate (HCO3-) in the extracellular fluid compartment
• 2 causes
• High CO2 tension in arterial blood (PaCO2) – Respiratory Acidosis
• High H+ in plasma from a low bicarb – Metabolic Acidosis
Alkalemia vs Alkalosis
• Alkalemia
• It includes all conditions where H+ in plasma is lower than the values observed
in normal subjects (40 +/- 2nmol/L), or a pH greater than 7.42
• Alkalosis
• Any process by which there is decrease H+ and an increase in the
concentration and/or content of bicarbonate (HCO3-) in the extracellular fluid
compartment
Acid-Base Disorder
• Step 1: Measure pH
• Step 2: Check the Compensatory or secondary response of PCO2 or HCO3- to
see if the disorder is simple or mixed
• Step 3: Calculate serum Anion Gap
• Step 4: Determine cause of acid-base disorder
• Step 5: Treat
Identifying the Disorder
• Check pH, pCO2, and HCO3- (CO2 in Basic Metabolic Panel)
• Normal pH 7.40
• Normal pCO2 40
• Normal HCO3- 24
• First determine if acidemia or alkalemia is present
• Then determine primary generating change (check pCO2)
• Finally determine degree of compensation, or secondary/tertiary disturbances
Consequences of Severe Acid-Base Disturbances
Organ System
Cardiovascular
Respiratory
Acidemia (pH < 7.38)
contractility , arteriolar vasodilation
MAP and CO; response to catecholamines
risk of arrhythmias
Hyperventilation, resp muscle strength
Alkalemia (pH > 7.42)
Arteriolar vasoconstriction
coronary blood flow
risk of arrhythmias
Hypoventilation
Metabolic
K, insulin resistance
K, ICa, Mg, PO4
Neurologic
MS
MS, seizures, tetany
ABG vs VBG
• Concordant for pH (~0.04 difference)
• HCO3 changes by ~2 mEq but not PaCO2 (8+/-17 mmHg)
• VBG can be used to screen for hypercarbia w PaCO2 cutoff >/= 45
mmHg (100% sensitive)
• Does not accurately assess degree of hypercarbia
Metabolic Acidosis
• pH <7.40
• pCO2 > 40 (compensatory mechanism)
• Remember: Hyper/Hypoventilation alters pCO2 to counteract 1ry metabolic process
• HCO3 < 24
• Check for AG always!!
• AG = Na – (Cl + HCO3-)
• Increased AG = there are increased unmeasured anions
• Organic acids, phosphates, sulfates
• Decreased AG = decreased Albumin or increased unmeasured cations
• Ca, Mg, K, Li, bromine, immunoglobulins
• If increased AG,
• Check delta-delta (delta AG / delta bicarb)
• Delta = change in
Increased Anion Gap Met Acidosis
• 3 major causes
• Ketoacidosis
• When glucose is not available to cells because of lack of insulin, cell dysfunction, or glucose depletion
• Fatty acids are oxidized to yield energy
• Acetone and 2 ketoacids (acetoacetic and B-hydroxybutyric)
• H+ produced are consumed by HCO3- (buffered), producing carbonic acid
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3 –
• Ketoanions accumulate in serum, increasing AG
• Lactic acidosis
• Glucose anaerobic glycolysis to pyruvate ! lactate
• Type A lactic acidosis: primary inadequate delivery of oxygen to tissues
• Shock most common cause
• Type B lactic acidosis: tissue oxygenation is normal but they cannot use oxygen normally or need
excessive amounts
• Hepatic failure, malignancy, drugs, seizures
• Toxicities
Increased Anion Gap Met Acidosis
• 3 major causes
• Ketoacidosis
• Lactic acidosis
• Toxicities
• Ethylene glycol, methanol, salicylate intox, pyroglutamic acidosis from acetaminophen
• Check Osmolal gap
• Calc Sosm = 2xNa + glu/18 + BUN/2.8
• If difference is greater than 10 suggests ingestion; >25 mOsm/kg of serum, the presence of a
toxic alcohol is probable
Ingestions
AG
OG
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Ingestion
Other manifestations
Acetaminophen
Hepatitis
Salicylates
Fever, tachycardia, tinnitus; met acid + resp alk
Ethanol
Alcoholic fetor, changes mental status, hepatitis, keto + lactic acid
+/- met alkalosis (vomiting)
Methanol
Changes mental status, blurred vision, pupillary dilation,
papilledema
Ethylene Glycol
Changes mental status, cardiopulmonary failure, hypocalcemia, Ca
oxalate crystals ! renal failure; urine flouresces under UV light
Prolylene gluycol
AKI
Isopropyl alcohol
Changes mental status, fruity breath (acetone)
Normal Anion Gap Met Acidosis
• 3 causes
• GI HCO3- loss
• Diarrhea and external drainage of pancreatic, biliary, or small bowel juices
• Chloride-rich fluid remains behind generating a hyperchloremic met acidosis (normal AG)
• Renal
• HCO3- loss or H+ retention
• Renal Tubular Acidosis
• Inorganic acid intake
Normal Anion Gap Met Acidosis
• Work-up
• History
• Urine Anion Gap
• UAG = (Urine Na + Urine K) – Urine Cl
• UAG = unmeasured anions – unmeasured cations
• As NH4+ is primary unmeasured cation, UAG is indirect assay for renal NH4+ excretion
• Negative UAG !
increased renal NH4+ excretion (appropriate response to acidemia
• DDx: GI causes, proximal RTA, ingestions or dilutional
• Positive UAG!
failure of kidneys to secrete NH4+
• DDx: distal or hypoaldo RTA, early renal failure
Renal Tubular Acidosis
• Proximal (old type II RTA)
• Defect in proximal tubular HCO3- reabsorption
• Most common cause in children is cystinosis (causing Fanconi Syndrome)
• Most common cause in adults are paraproteinemias and autoimmune
disorders
• Distal (old type I RTA)
• Defect in collecting duct with defect in net distal H+ secretion
• 2 varieties
• Hypokalemic distal RTA
• Hyperkalemic distal RTA
Renal Tubular Acidosis
• Distal
• Hypokalemic
• Collecting duct potassium secretion is intact
• Enhanced by small amount of bicarbonaturia
• Seen with Sjögren’s syndrome, ampho B tox, cirrhosis of liver, medullary sponge kidney,
etc
• Hyperkalemic
• Hypoaldosteronism (old type IV RTA)
• Can be caused by DM, mild chronic renal failure
• Tubular defect
• Can be caused by chronic obstruction of kidney, SLE, and sickle cell disease
Recall Aldosterone…
https://cjasn.asnjournals.org/content/10/2/305
Hypoaldosteronism
• Increase K ! Decrease in NH3 synthesis/delivery !
carrying capacity
• 3 variants:
• Decrease Renin
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diabetic nephropathy
NSAIDs
CIN
HIV
• Normal Renin
• Decrease aldo synthesis (1ry adrenal disorders, ACEi, ARBs, Heparin)
• Decrease response to aldosterone
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K-sparing diuretics
TMP-SMX
Pentamidine
CIN (calcineurin inhibitors)
Tubulointerstitial disease (sickle cell, SLE, amyloid, diabetes)
decrease urine acid
Treatment (severe met acidosis pH <7.2)
• DKA: insulin and IVFs
• Replete K, Mg, PO4 as needed
• Lactic acidosis
• Treat underlying condition
• Renal failure
• Hemodialysis
• Methanol and ethylene glycol
• Early fomepizole, Vit B6, folate, HD (especially if late presentation)
• Alkali therapy: NaHCO3
Metabolic Alkalosis
• 3 causes
• Loss of volume
• Cl depletion from extrarenal losses of hydrogen ion or chloride
• Gastric acid loss, vomiting, renal chloride loss, diuretics, posthypercapnia, cystic fibrosis
• Gain of volume due to mineralocorticoids
• Chloride replete Urine Cl spot > 20 mmol/L
• Kidney is not avid for salt because of volume expansion and therefore excretes the daily Na+ and Clload without difficulty
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Hyperaldosteronism
Gitelman’s syndrome
Bartter’s syndrome
Cushing’s syndrome
Licorice excess
• Miscellaneous factors
• Profound K depletion
Approach to Metabolic Alkalosis
• Urine Cl
• < 20 Saline-Responsive
• GI losses, Prior diuretics, posthypercapnia
• > 20 Saline-Resistant
• Hypertensive
• 1ry Hyperaldo
• 2ry Hyperaldo
• Non-aldosterone
• Hypo- or normotensive
• Current diuretics
• Severe Hypokalemia
• Exogenous alkali
• Barter’s
• Gitelman’s
Respiratory Acidosis
• Increase in pCO2
• Etiologies:
• CNS depression
• Sedatives, CNS trauma, O2 in chronic hypercapnia (decreases hypoxemic drive), central
sleep apnea
• Neuromuscular disorders
• MG, Guillain-Barré, poliomyelitis, ALS, muscular dystrophy, severe hypophosphatemia,
high spinal cord injury, drugs (paralytics)
• Upper airway abnormalities
• Obstruction, laryngospasm, OSA, esophageal intubation
• Lower airway abnormalities
• Asthma, COPD
Respiratory Alkalosis
• Decrease in PCO2
• Hypoxia ! hyperventilation
• Pneumoniae, pulm edema, PE, restrictive lung disease
• Primary hyperventilation
• CNS stimulation, pain, anxiety, fever, trauma, stroke, voluntary
• Drugs: salicylates, progesterone, methylxanthines, nicotine, pregnancy, hepatic
failure, sepsis
• Pseudorespiratory alkalosis
• Decreased perfusion with preserved ventilation
• CPR, severe HoTN !
increase tissue CO2
decreased delivery of CO2 to lungs for excretion; low PaCO2 but
Compensations
• Metabolic Acidosis
• Winter’s Formula
• PaCO2 = (1.5 x HCO3) + 8 ±2
• PaCO2 last two digits of pH
• Metabolic alkalosis
• PaCO2 = 0.7 x ΔHCO3
Compensations
• Respiratory Acidosis
• Acute
• HCO3 = 0.1 x ΔPaCO2
• Chronic
• HCO3 = 0.35 x ΔPaCO2
• Respiratory Alkalosis
• Acute
• HCO3 = 0.2 x ΔPaCO2
• Chronic
• HCO3 = 0.4 x ΔPaCO2
Examples
You are evaluating a 55 y/o man who just arrived to ED with shortness
of breath. He has a history of emphysema
• pH 7.32
• PCO2 80 mmHg
• HCO3- 40 mmol/L
Examples
You are evaluating a 55 y/o man who just arrived to ED with shortness
of breath. Patient also complains of episodes of diarrhea He has a
history of emphysema. Calculated AG 11
• pH 7.10
• PCO2 80 mmHg
• HCO3- 26 mmol/L
Examples
You are evaluating a 55 y/o man who just arrived to ED with shortness
of breath. AG 35.
• pH 7.44
• PCO2 12 mmHg
• HCO3- 8 mmol/L
Examples
You are evaluating a 55 y/o man who just arrived to ED with shortness
of breath. BP on arrival 70/30. AG 33.
• pH 7.14
• PCO2 22 mmHg
• HCO3- 8 mmol/L
Examples
You are evaluating a 55 y/o man who just arrived to ED with shortness
of breath.
• pH 7.55
• PCO2 35 mmHg
• HCO3- 30 mmol/L
Examples
You are evaluating a 55 y/o man who just arrived to ED with shortness
of breath.
• pH 7.55
• PCO2 21 mmHg
• HCO3- 20 mmol/L