Describe normal arterial blood gases (ABG’s)
PH: 7.35-7.45 (7.4) PaCO2: 35-45 (40) PaO2: 80-100 (90) HCO3: 22-26 (24) O2 Sat: 92-100%
What should you get to completely evaluate acid base states?
Basic metabolic panel
What is important about hypoxemia?
Subnormal oxygenation in blood
Normal O2 = 104-.27 x age = 100-1/3 x age = decreases with age
What are cause of hypoxia?
Hypoventilation
Ventilation/Perfusion mismatch as seen in pulmonary embolus
Shunting, eg cardiac abnormalities
Low inspired fraction of O2 (FiO2)
High altitude
Diffusion abnormalities, eg alveolar hemorrhage, connective tissue disorder
Describe ABG terms
Acidosis pH7.45
Hypoxia pO245
Hypocapnia pCO2
When does kidney start to retain HCO3?
In 12-16 hrs
Max conc in 1 week
What is the 3 step approach to ABG analysis?
How do you determine respiratory vs metabolic acidosis/alkalosis?
If pH and pCO2 are both increased or decreased in same direction, then the process is metabolic
If one is increased, while the other is decreased (opposite), the process is respiratory
-as pCO2 increases, then pH decreases
Describe the change in a pure respiratory process of acidoss/alkalosis
For each 10 mmHg change in PaCo2, the pH should move in opposite direction by 0.08 (+/- 0.02)
If PaCO2 is 30, what should the pH be?
If PaCo2 is 60, what should the pH be?
A decrease of 10 mmHg from 40 will lead to pH of 7.48 (7.4+0.08)
An increase of 20 mmHg from 40 will lead to pH of 7.24 (7.4-(2x0.08)), a decrease of 0.16, or 0.08 for each 10 mmHg rise in pCO2
Describe the mixed process of acidosis/alkalosis
Step 3 of ABG analysis compares the “should be” (expected/calculated) pH to actual measured pH
If actual pH is not what it should be, is it higher or lower?
If higher, there must be a concomitant metabolic alkalosis
If lower, there must be a concomitant metabolic acidosis
70 y/o M presents to ED with increasing dyspnea (RR 25 breaths/min)
PE: JVD at 45 degrees, estimated CVP 11mm H2O
Lungs: b/l crackles in bases and scattered wheezes
Heart: grade 3/6 systolic murmur at apex with radiation into left axilla, S3 gallop heard, no S4
B/l peripheral edema of legs. Cool extremities
BP 100/68, P 115/min, afebrile, O2 sat 78%
Venous lab: Na 128 K 5.8 Cl 92 HCO3 12 BUN 42 Cr 2.1 BNP 500
4. Oxygen 2-4 L/min N/C IV - loop diuretic Fluid restriction 1-1.5 L/day Na HCO3 - cautiously ACEI - cautiosly
What are normal electrolytes values?
Na 135-145 (140)
K 3.5-5 (4)
Cl 98-106 (103)
CO2 21-28 (24)
What is the anion gap?
Na-(Cl + HCO3)
12+/-2
Reflects concentration of anions that are not routinely measured (sulfates, phosphates, acetoacetic acid, beta hydroxybutyric acid)
Describe metabolic acidosis
Decrease in extracellular pH caused by a decrease in HCO3
2 types:
Elevated anion gap
Normal anion gap with hyperchloremia
What are causes of high anion gap?
High anion gap, metabolic acidosis: MUDPILES
Methanol: formic A
Uremia (renal failure)
Diabetic ketosis
Paraladehyde
INH, iron
Lactic acid
-shock, sepsis, low perfusion, marathon runners
Ethylene glycol, glycolic
Salicylates
CCAT
-CO, cyanide, alcohol, toluene
Describe lactic acidosis
Type A (tissue hypoxia) -shock, severe anemia, heart failure, CO poisoning
Type B1 (associated with systemic disorders) -DM, liver failure, sepsis, seizures
Type B2 (associated with drugs/toxins) -ethanol, methanol, ethylene glycol, ASA
Type B3 (associated with inborn errors of metabolism) -G6PD deficiency
68 y/o F presents to ED in lethargic state. Past 3-4 weeks, anorexia, confusion, edema, and weight gain.
PMH positive for poorly controlled HTN and diabetes mellitus, DJD, and hypothyroidis
Meds: HCTZ 50 mg daily, Lantus insulin 20 units hs, NSAID for arthritis, and synthyroid 0.05 mg orally daily
Arousable but lethargic
BP 158/88, P 90/min, R 10 breaths/min, temp 98F, O2 sat 88%
Neck veins mildly distended at 45
Heart: 2/6 systolic murmur 2nd ICS, RSB with slight radiation into R carotid
Lungs: basilar crackles, R>L
Abdomen: tenderness RUQ, edge of liver is 3 fingers below costal margin. Percussion span of liver is 8 cm (normal)
Extremities: marked pitting edema of feet, calves, and thighs
2. Myxedema Ischemic cerebral vascular disease Valvular heart disease Heart failure Hypertension
37 y/o F presents to ED with 6 day history of diarrhea. Approximately 7 stools/day and up 3-4 times through night with watery, non-bloody stools. Able to drink fluids, soups, jello. Hasn’t traveled out of country, camped outdoors, or ingested spring/river water. Aunt has Crohn’s disease. No antibiotics over past 4 months.
BP 80/50, P 110/min, R 18/min, Temp 100F, O2 Sat 94
General: pale, poor skin turgor, dry mucous membranes
Neck veins flat
Heart: no murmur, S3 or S4.Tachycardia 110 p/min
Lungs: clear
Abdomen: hyperactive bowel sounds, mildly tender diffusely, no organomegaly
Extremities: coo to touch. Tattoo R ankle
Neurologic: normal
What are causes of normal anion gap metabolic acidosis (HCO3 falls and Cl rises. hyperchloremic met acid)?
HARDUPS
Hyperalimentation
Acid infusion, acetazolamide
Renal tubular acidosis
-Renal loss of HCO3 or decreased H sec
Diarrhea
-losing HCO3, decreases K
Ureteral sigmoid or ileal diversion
-losing HCO3/increasing Cl and H resorption
Pancreatic fistula
-losing HCO3, decreased K
Describe distal renal tubular acidosis
Type I
Decreased secretion of H, so not getting rid of acid, ie failure to acidify urine
Possible causes: SLE, Sjogren’s, toluene
Describe proximal renal tubular acidosis
Type II
Decreased absorption of HCO3, so not absorbing buffer
Possible causes: multiple myeloma, heavy metal poisoning, Wilson’s disease, amyloidosis
Describe hyperkalemic renal tubular acidosis
Type IV
Hyporenin and hypoaldosterone
Decreased NH4 excretion and decreased HCO3 production
Possible causes: analgesic nephropathy, sickle cell disease, and SLE
Describe treatment of metabolic acidosis
Rx underlying cause
Rx of CV compromise; pH