Acid/Base Flashcards
Acidosis
Metabolic: decrease HCO3 or =45 mmHg
Alkalosis
Metabolic: increase HCO3 > or = 28 mEq/L
Respiratory: decrease pCO2
Lungs
- regulate ACUTE changes (occurs w/in seconds)
- regulates PCO2 through respiration rate and depth changes
Renal
- regulates CHRONIC changes (takes hours- days to compensate)
- regulates HCO3 and H through excretion/reabsorption/buffer
Primary METABOLIC disorder–> Respiratory compensation
meta acidosis –> compensate w/respiratory alkalosis
meta alkalosis–> compensate w/respiratory acidosis
Primary RESPIRATORY disorder–> Metabolic compensation
resp acidosis–> compensate w/metabolic alkalosis
resp alkalosis–> compensate w/metabolic acidosis
Acidosis Clinical Manifestation
- hyperventilation
- CNS depression
- Hypotension
- Hyperkalemia
- Arrhythmias
- decrease contractility
Alkalosis Clinical Manifestation
- nerve excitation
- Arrhythmias
- respiratory depression
- hypoventilation
- hypokalemia
Step 1.
evaluate the pH
- pH acidemia
- pH > 7.40–> alkalemia
Step 2.
Is the primary disorder respiratory or metabolic?
–> it is problem with the HCO3 or the PCO2?
Step 3.
Calculate the anion gap.
AG= Na- Cl- HCO3
Step 4.
Check for compensation
- winter’s formula for METABOLIC acidosis
- -> pCO2= 1.5 (HCO3)+8 (+-2)
- expected increase in pCO2 w/METABOLIC alkalosis
- -> pCO2= 0.75 (pt’s HCP3- norm HCO3) (-+2)
Step 5.
If AGMA, check corrected HCO3
- -> corrected HCO3= pt’s HCO3 + (pt’s AG- norm AG)
- **norm AG= 12
Corrected HCO3
- relationship between the serum HCO3 & AG
- Indicates if degree of compensation is appropriate or if another metabolic acid/base disorder is present
- for rise in AG by 1–> corresponding decrease of HCO by 1 mEq/L
- if calculated HCO3 is not in the reference range (22-28 mEq/L)–> coexisting metabolic disturbance
- —> if > norm, metabolic alkalosis
- —> if
Causes of NAGMA
H: Hyperalimentation (high Cl soln) TPN & NS
A: Acetazolamide (inhibit Na reabsorption)
R: Renal tubular acidosis (proximal, distal, & hyperaldosteronism type 4)
D: Diarrhea
U: Uretero-pelvic shunt (fistula)- excessive loss of HCO3 from surgery or cancer
P: Post-hypocapnia (decreased CO2)
S: Spironolactone
Causes of AGMA
M: Methanol/Metformin U: Uremia (high BUN)--> CKD or AKI D: Diabetic acidosis (DKA), ketoacidosis P: Poisoning/ propylene glycol/ paraldehyde I: Intoxication/ infection/ isoniazid (INH) L: Lactic acidosis (shock) E: Ethylene glycol (antifreeze) S: Salicylates/Sepsis
Winter’s Formula
expected pCO2= 1.5 (HCO3) +8 (+-2)
- pCO2 predicted: coexisting respiratory acidosis
Osmolar Gap
- if you can’t easily identify a cause for an AGMA, calculated the osmolar gap.
- osmolar gap= measured Osm- calculated Osm
- calculated Osm= 2(Na) + BUN/2.8 + glucose/18 + EtOH/4.6
- -> norm gap Osm gap > 10
Typical Treatment for Metabolic acidosis
- if pH is 7.20-7.35: focus on cause
- if pH
Treatment Options for Metabolic acidosis- Sodium Bicarbonate
***Goal: target pH 7.2
tab: 3.9 mEq/ 325 mg, chronic replacement in renal failure or renal tubular acidosis
IV: 50 mEq or mmol ampule; isotonic soln in D5W or SW 150 mEq NaHCO3/ 1 L, reserve for acute situations no evidence-based benefit
Treatment Options for Metabolic acidosis- Sodium citrate/ citric acid
Alkali: 1 mEq/ mL soln
- chronic replacement in renal failure or renal tubular acidosis
Treatment Options for Metabolic acidosis- Tromethamine (THAM)
Alkali: sodium-free buffer
- reserve for acute situations
- no benefit over sodium bicarbonate
Treatment Options for Metabolic acidosis- Hemodialysis
A: E: I: O: U: - reserved for acute situations
Metabolic Alkalosis Causes
C: contraction L: Licorice E: Endocrine (Conn's, Cushing's, Bartter's syn) V: vomiting E: excess alkali (Sodium bicarb) R: refeeding alkalosis (malnurished pt's) P: post-hypercapnia D: diuretics
Compensation for metabolic alkalosis
exp increase in pCO2= 0.75 (pt’s HCO3- norm HCO3 {12})
- if pCO2 predicted: respiratory acidosis
Treatment for metabolic alkalosis: volume-dependent or saline-responsive
- vomiting
- nasogastric suction
- diuretics
Urine Chloride:
Treatment for metabolic alkalosis: volume-independent or saline-resistant
- mineralcorticoid excess
–> Cushing’s syn
–> Conn’s syn - hypokalemia
Urine Chloride: > 20 mEq/L
Treat:
- treat underlying disorder
- potassium replacement
Respiratory Acidosis causes
C: CNS depression (stroke, opiate OD, seizures, sedation, head trauma)
A: Airway obstruction (COPD)
N: Neuromuscular disorders (ALS, Guillain Barre, Myasthenia gravis)
S: Severe pneumonia, pulmonary embolism, pulmonary edema
Compensation for Respiratory Acidosis
- for each 10 mmHg increase in pCO2, pH will decrease by:
- -> 0.08 units in ACUTE respiratory acidosis
- -> 0.03 units in CHRONIC respiratory acidosis
Treatment for Respiratory Acidosis
- Focus on cause
- Oxygen therapy
- ***NEVER use added base for respiratory acidosis
Respiratory Alkalosis cause
C: CNS stimulation (pain, anxiety, fever, tumors, stroke, head trauma)
H: hypoxia
A: anxiety
M: mechanical ventilation
P: progesterone (pregnancy & cirrhosis)
S: salicylates/sepsis
Compensation for Respiratory Alkalosis
- for each 10 mmHg decrease in pCO2, pH will increase by
- -> 0.08 units in ACUTE respiratory alkalosis
- -> 0.03 units in CHRONIC respiratory alkalosis
Treatment for Respiratory Alkalosis
- focus on cause
- hypoventilation
- breathe into a bag for anxiety
- sedation
General Treatment Principles
- ALWAYS correct underlying etiology
- ->DKA: stop ketoacid production, correct volume depletion, and normalize blood glucose
- ->Uremia: renal replacement therapy (dialysis)
- -> excessive vomiting: antiemetics
- -> COPD exacerbation: oxygen, bronchodilators, corticosteroids, possibly antibiotics
- -> narcotic OD: opiod antagonist
- Alkali or acid replacement
- -> reserved for critically-ill pt’s
- -> only provides a “temporary fix”
