Introduction to Acid-Base Disturbances and CIS-Wolff Flashcards
compensation for A-B disturbance FASTEST to SLOWEST
- ECF buffering (with the enviornment)
- Cellular buffering (K+ out /H+ in exchange)
- Respiratory compensation
- Renal base (HCO-3) excretion
- Renal Acid (H+) excretion
high NH4+ in urine means what
a lot of H+ has been excreted
causes of Respiratory Acidosis ACUTE
CANS
- CNS depressed
- Airway obstructed
- Neuromuscular disorder
- severe pneumonia, pulmonary embolism, pulmonary edema
causes of Respiratory acidosis CHRONIC
- COPD
- impaired ventilation diseases (inhibition of medullary respiratory centers –X–> peripheral chemorecpetors, Guillain Barrè syndrome)
Respiratory Alkalosis
CHAMPS
- CNS causing hyperventilation
- Hypoxia (high altitude)
- Anxiety
- Pregesterone (stimulates medulla resp center)
- Salicylates (NSAIDS, Aspirin = acids causing increased breathing) Sepsis (esp gram-), severe anemia
what to calculate if you find metabolic acidosis
Compensation Anion Gap (12 or under is normal)
what to calculate if you find metabolic alkalosis
Compensation (only not on test I think)
Cl- responsive or resistant or not (20 or under is normal)
Metabolic Acidosis causes WITH ANION GAP
HAGMA (GOLDMARK)
- Glycols (ethylene) **
- Oxoproline (Tylenol) **
- Lactic Acid ** (ISCHEMIA)
- D -Lactate (from carbs by bacteria in SI) = short bowel syndrome **
- Methanol
- Asprin, NSAIDS **
- Renal Failure **
- Ketoacidosis **
- Uremia
Metabolic Acidosis WITH NO anion gap
NAGMA (HARDUPS)
- Hyperalimentation (high Cl- )
- Acetazolamide
- RENAL TUBULAR ACIDOSIS **
- Diarrhea, V **
- Ureterosigmoid fistula (colon wastes HCO-3)
- Pancreatic fistula (eastes HCO-3)
- Spironolactone
Renal Tubular Acidosis is what
ACEDIMIA
+
normal Anion gap (nagma), serum Cr, and NO diarrhea
Type 1 Renal tubular acidosis
what , and exs
X secrete H+ from a-intercalated cells
= hypokalemia + normal AG
Sjögrens syndrome, Sickle cells anemia, liver cirrhosis)
Type 2 Renal tubular acidosis
what , and exs
X HCO3- reabsorption in PT
= hypokalemia
Fanconi’s syndrome (children), multiple myeloma, drugs
Type 4 Renal tubular acidosis
what , and exs
X aldosterone or kidney response to Aldosterone
= HYPERKALEMIA* (X K+ secreted and peed out= X H+ secreted out) + Normal AG
Diabetic nephropahty, chronic interstitial nephritis, drugs (NSAIDS, heparin)!!
What causes Metabolic Alkalosis
CLEVER PD
- Contraction of ECF (loss of NaCl)
- Licorice
- Endocrine problem (Cushing, Conns, Bartter)
- Vomit (loose HCl, form tummy)
- Post- hypercapnia
- diuretics –> K+ loss and H+ loss = volume contraction
HTN
high H+
Hypotention
HIGH HCO-3
cause and TX of Cl- responsive metabolic alkalosis
V, diuretics,
Tx: normal saline with Cl-
cause and TX of Cl- restrictive metabolic alkalosis
HIGH aldosterone (RTA) = increased H+ and K+ excretion and NaCl, NaHCO3 reabsoption, diuretics Tx: cause of this Cl- in urine loss (hyperaldosteronism, K+ loosing diuretics)
Patient with Respiratory Acidosis ACUTE will present with
headache, confusion, anxiety, tremor, coma maybe, convulsions, drowsy
Patient with Respiratory Acidosis CHRONIC will present with
COPD
memory loss, sleep loss, sleepy during day, personality changes, tremor, gait changes, loss of reflex, papilledema, twitching
Patient with Respiratory Alkalosis ACUTE will present with
light-headed, confusion, paresthesia (numbness and tingling), cramps, syncope, tachypnea*, hypocalcemia (decreases threshold for AP)
Patient with Respiratory Alkalosis CHRONIC will present with
asymptomatic usually
Patient with Metabolic Acidosis MILD will present with
asymptomatic usually
Patient with Metabolic Acidosis pH< 7.10 will present with
N, V, malaise
= respiratory compensation seen : DEEP breaths (X DYSPNEA)
