Kirila Acid Base Flashcards
normal electrolytes: Na, K, Cl, CO2
Na = 135-145 (140) K = 3.5-5 (4) Cl = 98-106 (103) CO2 = 21-28 (24)
Anion Gap: calculation and normal values, and what it means
ANION GAP:
Na- (CL + HCO3) = AG
Normal: 12 +/- 2
Anion gap – reflects concentration of anions that aren’t routinely measured. (Sulfates, phosphates, acetoacetic acid, beta hydroxybutric acid)
Normal ABGs (pH, PaCO2, PaO2, HCO3, O2)
pH 7.35 – 7.45 (7.4) PaCO2 35 – 45 (40) PaO2 80 – 100 (90) HCO3 22 – 26 (24) O2 Sat 92-100%
what do you request to completely evaluate acid base states: shock, low perfusion state, lactic acid level?
Basic metabolic panel
Normal O2 calculations
104 - (.27 x age) or 100 - (1/3 x age)
o2 naturally declines with age
causes of hypoxia
Hypoventilation
V/Q (Ventilation/Perfusion)
mismatch as seen in
Pulmonary Embolus (PE)
Shunting e.g. cardiac anomalies
Low inspired fraction of O2 (FiO2)
High altitude
Diffusion abnormalities e.g.
Alveolar Hemorrhage, Connective Tissue disorder
values defining Acidosis, alkalosis, hypoxia, hypercapnia, hypocapnia
Acidosis pH < 7.35
Alkalosis pH > 7.45
Hypoxia pO2 < 60 Hypercapnia pCO2 > 45 Hypocapnia pCO2 < 35
3 step approach to determining alkalosis or acidosis
1) is pH high or low?
2) is it respiratory or metabolic?
3) if its respiratory in nature, is it a pure respiratory process or is there a metabolic component?
pH and pCO2 are both elevated
metabolic process
pH and pCO2 are in opposite directions
respiratory process
in a PURE respiratory process…..
for each 10 mmHg change in PaCO2, the pH should move in the opposite direction by .08 (+/- .02) ((so .06-.1 ))
PURE Respiratory:
If PaCO2 is 30, the pH should be
If PaCO2 is 30 ( a decrease of 10 mmHg from 40) the pH should be 7.48 (7.4 + .08)
PURE Respiratory:
If PaCO2 is 60, the pH should be….
If PaCO2 is 60 (an increase of 20 mmHg) the pH should be 7.24 (7.4 – 2 x .08 or .16) a decrease of .16 or .08 for each 10 mmHg rise in pCO2
If the rule for a pure respiratory process is (meaning the pH and PaCO2 go in opposite directions but not in their respective proportions) is not consistent with the measured findings
“a second metabolic process is present”
referred to as a mixed process
metabolic acidosis with high anion gap: diagnosis
Acute heart failure Atrial Fibrillation with Rapid Ventricular Response Hyponatremia Azotemia Metabolic acidosis Mitral regurgitation
Metabolic acidosis: defined and causes
Metabolic acidosis – decrease in extracellular pH caused by a decrease in HCO3
- Loss of HCO3 – GIT (Gastrointestinal Tract), renal
- Increase Hydrogen load – DKA or lactic
- Decrease hydrogen excretion by kidney – uremic acidosis or RTA
types of metabolic acidosis
- elevated anion gap
2. normal anion gap with hyperchloremia
lactic acidosis: type A
shock, severe anemia, heart failure, CO poisoning
lactic acidosis type B1
associated with systemic disorders, DM, liver failure, spesis, seizures
lactic acidsosis type b2
associated with drugs/toxins, ethanol, methanol, ethylene glycol, ASAw
tests when metabolic acidosis is suspected
Echocardiogram
Lactic acid level
Cardiac Enzymes (Troponin I, CK MB)
Treatment of the acidotic patient
Oxygen 2-4 liters/min N/C
IV – loop diuretic
Fluid restriction 1-1.5 L/day
Na HCO3 – cautiously (why?)
ACEI – cautiously (why?)
Normal anion gap
12 +/- 2 (10-14)
Normal anion gap met acid – what it means
HCO3 falls and CL rises (hyperchloremic met acid)
HARDUPS
H - Hyperalimentation
A - Acid infusion, acetazolamide
R – RTA – renal loss of HCO3/or decreased H sec
D – Diarrhea – losing HCO3, K
U – Ureteral sigmoid or ileal diversion – losing HCO3 / increased CL and H resorption
P – Pancreatic fistula – losing HCO3, K
S – Spironolactone
RTA types 1-3
1) Distal – decreased secretion of H+, so not getting rid of acid, ie “failure to acidify urine” – aka Type I Possible causes: SLE (Lupus), Sjögren’s, toluene
2) Proximal – decreased absorption of HCO3 , so not absorbing buffer – aka Type II
Possible causes: multiple myeloma, heavy metal poisoning, Wilson’s Disease, amyloidosis
3) Hyperkalemic RTA – Hyporenin and hypoaldosterone – decreased NH4 excretion and decreased HCO3 production – aka Type IV
Possible causes: analgesic nephropathy, sickle cell disease and SLE
analgesic nephropathy, sickle cell disease and SLE
type IV normal anion gap metabolic acidosis
multiple myeloma, heavy metal poisoning, Wilson’s Disease, amyloidosis
type II normal anion gap metabolic acidosis
SLE (Lupus), Sjögren’s, toluene
type 1 normal anion gap metabolic acidosis
tx for mixed high anion gap metabolic acidosis and respiratory acidosis
Dialysis – hemodialysis
Na HCO3
Synthyroid
Aerosol treatments with nebulizers
tx for normal anion gap metabolic acidosis
IV fluids for volume restoration (careful not to give too much NaCL or N/S)
Could give fluids of ½ strength N/S with Na HCO3 and K
Rx underlying cause
Rx of CV compromise; pH <7.2, HCO3 <10
HCO3 deficit = desired HCO3 – measured HCO3 x (.5 x wt kg)
RX NaHCO3
1 amp 8.5%, 50 mEq/50cc
Tablets – 650 mg
metabolic alkalosis
pH increase, HCO3 doubly increases, paCO2 increases
Compensatory paCO2 .7 increase for every 1 increase in HCO3
paCO2 = (.9 x HCO3) +9 (+/- 2)
Causes “CLEVER PD”
CL loss or HCO3 excess
Volume contraction
CL loss – vomiting, N/G suction, villous adenoma, diuretics
HCO3 excess – enhanced HCO3 resorption (hyperaldo, licorice excess)
METABOLIC ALKALOSIS CAUSES “CLEVER PD”
C – Contraction of volume L – Licorice E – Endocrine (Conns, Cushing's, Bartters) V – Vomiting E – Excess Alkali R – Refeeding alkalosis
P – Post Hypercapnia
D – Diuretics
METABOLIC ALKALOSIS
TWO TYPES
chlorine reponsive and chlorine unresponsive
cl responsive
one type of metabolic alkalosis
CL (Chloride) Responsive -Urine CL < 10-20 mEq/l -Improves with NaCl and Volume -a decrease in Serum CL and Volume Contraction Vomiting, NG suction, diuretics
cl unresponsive
one type of metabolic alkalosis
CL (Chloride) Unresponsive
Urine CL > 10-20 mEq/l
Unresponsive to saline
Endocrine causes: Bartters, severe K depletion, hyperaldo, Cushing’s
paCO2 =
paCO2 = (.9 x HCO3) +9 (+/- 2)
Compensatory paCO2
Compensatory paCO2: .7 increase for every 1 increase in HCO3
ꜜ pH. ꜜ PaCO2, ꜜꜜ HCO3
metabolic acidosis
metabolic acidosis compensation
ꜜ paCO2 = 1.2 for ea 1 ꜜ HCO3
paCO2 = 1.5 x HCO3 + 8
paCO2 = last 2 digits of pH
paCO2 = HCO3 + 15
↑ pH, ↑ PaCO2, ↑↑ HCO3
metabolic alkalosis
metabolic alkalosis compensation
↑ paCO2 = .7 for each 1↑ HCO3
↑ paCO2 by 6 for each 10 ↑ in HCO3
↓ pH, ↑ ↑ PaCO2, ↑ HCO3
respiratory acidosis
respiratory acidosis compensation
↑ HCO3 = 1 for ea 10 ↑ paCO2
pH ↓ by .08 for ea 10 ↑ paCO2
conn’s syndrome
Primary Hyperaldosteronism
Mineralocorticoid excess
Saline resistant (UCL >20)
Increased HCO3 excretion in urine
drugs, CVA, Neuromuscular Airway obstruction, pneumonia, Pulmonary edema, pneumothorax, pleural disease, COPD, restrictive disease (disorders of the chest wall, resp. muscles)
cause hypoventilation–> resp acidosis
hyperventilation causes and mnemonic
Septic – pyelonephritis, renal abscess Hyperthyroid Anxiety – biochemistry test Pain/fever Respiratory hyperventilation may also be due to infection (sepsis)
C – CNS disease H – Hypoxia A – Anxiety M – Mechanical Ventilation P – Progesterone S – Salicylates/Sepsis/Stress
