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Renal II Final > Acid/Base Disorders > Flashcards

Acid/Base Disorders Flashcards

1
Q

Describe normal arterial blood gases (ABG’s)

A 
PH: 7.35-7.45 (7.4)
PaCO2: 35-45 (40)
PaO2: 80-100 (90)
HCO3: 22-26 (24)
O2 Sat: 92-100%
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2
Q

What should you get to completely evaluate acid base states?

A

Basic metabolic panel

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3
Q

What is important about hypoxemia?

A

Subnormal oxygenation in blood

Normal O2 = 104-.27 x age = 100-1/3 x age = decreases with age

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4
Q

What are cause of hypoxia?

A

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

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5
Q

Describe ABG terms

A

Acidosis pH7.45

Hypoxia pO245
Hypocapnia pCO2

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6
Q

When does kidney start to retain HCO3?

A

In 12-16 hrs

Max conc in 1 week

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7
Q

What is the 3 step approach to ABG analysis?

A
  1. Does patient have acidosis or alkalosis? pH high or low?
  2. Is acidosis/alkalosis a respiratory or metabolic process?
  3. If it is a respiratory acidosis/alkalosis, is it a pure respiratory process, or is there a metabolic component?
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8
Q

How do you determine respiratory vs metabolic acidosis/alkalosis?

A

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

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9
Q

Describe the change in a pure respiratory process of acidoss/alkalosis

A

For each 10 mmHg change in PaCo2, the pH should move in opposite direction by 0.08 (+/- 0.02)

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10
Q

If PaCO2 is 30, what should the pH be?

If PaCo2 is 60, what should the pH be?

A

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

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11
Q

Describe the mixed process of acidosis/alkalosis

A

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

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12
Q

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
  1. What is his anion gap?
  2. What is his diagnosis?
  3. What other tests would you use?
  4. How would you treat this pt?
A
  1. Na - (Cl + HCO3)
    128 - (92+12)
    24
  2. Metabolic acidosis with high anion gap
    Acute HF
    Atrial fibrillation with rapid ventricular response
    Hyponatremia
    Azotemia
    Mitral regurgitation
  3. Echocardiogram, lactic acid level, cardiac enzymes (troponin I, CK MB)
4. Oxygen 2-4 L/min N/C
IV - loop diuretic
Fluid restriction 1-1.5 L/day
Na HCO3 - cautiously 
ACEI - cautiosly
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13
Q

What are normal electrolytes values?

A

Na 135-145 (140)
K 3.5-5 (4)
Cl 98-106 (103)
CO2 21-28 (24)

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14
Q

What is the anion gap?

A

Na-(Cl + HCO3)
12+/-2
Reflects concentration of anions that are not routinely measured (sulfates, phosphates, acetoacetic acid, beta hydroxybutyric acid)

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15
Q

Describe metabolic acidosis

A

Decrease in extracellular pH caused by a decrease in HCO3

  1. Loss of HCO3: GI tract, renal
  2. Increase hydrogen load: DKA or lactic
  3. Decrease hydrogen excretion by kidney: uremic acidosis or RTA

2 types:
Elevated anion gap
Normal anion gap with hyperchloremia

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16
Q

What are causes of high anion gap?

A

High anion gap, metabolic acidosis: MUDPILES
Methanol: formic A

Uremia (renal failure)

  • increased BUN, Cr
  • increased sulfates, phosphates as unmeasured anions

Diabetic ketosis

  • increased glucose. Starvation, alcohol abuse
  • acetoacetic acid, B-hydroxybutyric acid

Paraladehyde

INH, iron

Lactic acid
-shock, sepsis, low perfusion, marathon runners

Ethylene glycol, glycolic

Salicylates

CCAT
-CO, cyanide, alcohol, toluene

17
Q

Describe lactic acidosis

A 
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
18
Q

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

  1. What is your diagnosis?
  2. Differential diagnosis?
  3. What tests do you order?
  4. PH 7.1, pCO2 45, pO2 68, HCO3 8. Analysis?
  5. Na 150, K 7, Cl 115, HCO3 10. Anion gap?
  6. Interpretation?
  7. How would you treat the pt?
A
  1. Metabolic encephalopathy: R/O hypothyroid (myxedema)
    Likely ischemic cerebral vascular disease due to poorly controlled hypertension
    Electrolyte/acid-base disorder
    Fluid overload
2. Myxedema
Ischemic cerebral vascular disease
Valvular heart disease
Heart failure
Hypertension
  1. CBC: Hgb 9 g, Hct 27%
    CMP
    TSH: 10
    HbA1C
  2. Metabolic and respiratory acidosis
  3. 150 - (115+10) = 25
  4. High anion gap metabolic acidosis because of renal failure (retention of hydrogen ions) in uremic acidosis
    And respiratory acidosis: lungs haven’t compensated as you’d expect for metabolic acidosis by decreasing pCO2
  5. Dialysis: hemodialysis
    Na HCO3
    Synthyroid
    Aerosol treatments with nebulizers
19
Q

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

  1. Diagnosis/differential diagnosis?
  2. CBC Hb16, Hct 50%, WBC 14,000
    CMP: Na 148, K 2.6, Cl 114, HCO3 20
    Stools: culture for enteric pathogens, ova parasites, WBC’s/hemoccult of stool
    ABG: pH 7.1, pCO2 34, pO2 92, HCO3 20
    Anion gap?
  3. ABG analysis?
  4. Treatment?
A
  1. Diarrhea: secretory, infectious, consider inflammatory bowel disease
    Hypovolemia: volume contracted, possible electrolyte/acid base disturbance
    Hypotension
  2. 148 - (114+20) = 14 (normal)
  3. Metabolic acidosis (normal anion gap, low HCO3, elevated Cl)
  4. IV fluids for volume restoration (careful not to give too much NaCl or N/S)
    Could give fluids of 1/2 strength N/S with Na HCO3 and K
20
Q

What are causes of normal anion gap metabolic acidosis (HCO3 falls and Cl rises. hyperchloremic met acid)?

A

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

21
Q

Describe distal renal tubular acidosis

A

Type I
Decreased secretion of H, so not getting rid of acid, ie failure to acidify urine
Possible causes: SLE, Sjogren’s, toluene

22
Q

Describe proximal renal tubular acidosis

A

Type II
Decreased absorption of HCO3, so not absorbing buffer
Possible causes: multiple myeloma, heavy metal poisoning, Wilson’s disease, amyloidosis

23
Q

Describe hyperkalemic renal tubular acidosis

A

Type IV
Hyporenin and hypoaldosterone
Decreased NH4 excretion and decreased HCO3 production
Possible causes: analgesic nephropathy, sickle cell disease, and SLE

24
Q

Describe treatment of metabolic acidosis

A

Rx underlying cause

Rx of CV compromise; pH

25
Q

46 y/o M presents to your office with weakness and one week history of vomiting. Not able to even drink water, tea, or soup without vomiting. Hasn’t eaten any solid food for past 6 days. Denied diarrhea or hematemesis. Admits to chills, malaise, and felt hot. PMH unremarkable. No meds or allergies.
BP 90/52, P 118/min, R 20/min, 101F, O2 Sat 90%
General appearance: dry mucous membranes, poor skin turgor with mild tenting
Neck veins flat
Lungs: clear
Heart: no murmur, S3 or S4. Normal S1 and S2 splits on inspiration
Abdomen: vitiligo areas on abdomen, no distention or organomegaly
Extremities: no edema, normal temperature to touch, no rashes
Neurologic: normal

  1. Diagnosis/differential diagnosis?
  2. CBC, Hb 16.5, Hct 49%, WBC 11,500
    CMP Na 130, Cl 88, K 3.0, HCO3 31
    Urine Cl 10 mEq/L
    Stool hemoccult negative
    Blood cultures pending
    ABG: pH 7.5, pCO2 45, pO2 90, HCO3 31
    Analysis?
  3. How would you treat this pt?
A
  1. Vomiting complicated by volume contraction
    Hypotension, tachycardia secondary volume loss
    Fever: R/O intestinal infection
  2. Metabolic alkalosis (due to vomiting with contraction alkalosis: volume loss)
  3. IV fluids (0.9% N/S with KCL) to replenish volume loss and dehydration
26
Q

Describe metabolic alkalosis

A

Increase pH, big increase HCO3, increase paCO2
Compensate paCO2 increase 0.7 for every 1 increase in HCO3
PaCO2=0.9xHCO3 +9 (+/-2)
Causes: CLEVER PD
Cl loss of HCO3 excess
Volume contraction
Cl loss: vomiting , N/G suction, villous adenoma, diuretics
HCO3 excess: enhanced HCO3 resorption (hyperaldo, licorice excess)

27
Q

What are causes of metabolic alkalosis?

A

CLEVER PD

Contraction of volume
Licorice
Endocrine (Conns, Cushing's, Bartters)
Vomiting
Excess Alkali
Refeeding alkalosis

Post hypercapnia
Diuretics

28
Q

Describe metabolic alkalosis: Cl responsive

A

Urine Cl

29
Q

Describe metabolic alkalosis: Cl unresponsive

A

Urine Cl> 10-20 mEq/L
Unresponsive to saline
Endocrine causes: Bartters, severe K depletion, hyperaldo, Cushing’s

30
Q

Describe treatment for metabolic alkalosis

A

Rx underlying cause
NaCl, KCl, Magnesium
Spironolactone for mineralocorticoid excess

31
Q

52 y/o F presents to office with CC of feeling weak all over. Has had this complaint on other visits. Being treated for HTN, but her BP has been more resistant to control despite medications. Meds: beta-blocker, ACEI, and vasodilator. She does not smoke or take hormones or use NSAIDs. She drinks 1-2 glasses of wine every 2-3 weeks
BP 168/104, P 84/min, R 14/min, 98.6, O2 sat 94%
Diffuse muscle weakness in hands, arms, and legs
Remainder normal

  1. Differential diagnosis?
  2. CMP: Na 140, K 2.7, Cl 102, HCO3 30.
    Mg, Ca normal. BUN 20, Cr 1.
    CBC and TSH normal
    Analysis?
  3. Urine Cl high>20
    Aldosterone level high
    Plasma renin level low
    Diagnosis?
  4. Treatment?
A
  1. Diffuse muscle weakness
    -Hypothyroidism
    -Electrolyte disorder. Low levels of Na, K, Mg, Ca
    HTN becoming resistant to treatment
  2. Metabolic alkalosis
  3. Combination of HTN, hypokalemia
    Metabolic alkalosis
    Hyperaldosteronism (Conn’s syndrome)
  4. CT of adrenals
    Adenoma (solitary) 85% laparoscopic excision
    bilateral hyperplasia (15%): spironolactone to inhibit hyperplasia and aldosterone production (mineralocorticoid excess)
    Correct hypokalemia
32
Q

Describe Conn’s syndrome

A

Primary hyperaldosteronism
Mineralocorticoid excess
Saline resistant (UCL>20)
Increased HCO3 excretion in urine

33
Q

74 y/o M presents to ED with dyspnea, cough, and fever. Onset was 6 days ago. Cough is productive of yellowish-greenish sputum. Dyspnea is at rest and on any exertional activity. Temp has been up to 101F with shaking chills
PMH: COPD, oxygen dependent, DJD, and IBS. Smokes 1/2 ppd of cigarettes
Meds: Spiriva inhaler 2 puffs daily, symbicort MDI 2 puff BID, aerosol nebulizer with albuterol with N/S 3-4x/day and prednisone 20 mg po daily for past 6 months
General: respiratory distress, using accessory muscles of respiration. 26-28 breaths/min and shallow, lips are pursed
BP 110/70, P 120 irregular/min, R 28/min, temp 101F, O2 sat 70% (on ambient/room air)
Neck veins distended
Lungs: decreased breath sounds bilaterally with suspected crackles left lung lower lobe
Heart: irregular rhythm, rapid rate (120/min), no murmur
Abdomen: thin, no organomegaly, decreased bowel sounds, non-distended, scar RLQ
Extremities: nicotine stain on fingers. Feet cold with bluish colored toes, no pulses in either foot palpable
Neuro: brisk reflexes arms and legs
No cranial nerve deficit. Alert and oriented

  1. Diagnosis?
  2. CXR, ECG
    CBC: WBC 17,500, Hb 12, Hct 36
    CMP: Na 130, K 3.8, Cl 102 HCO3 29, BUN 54, creatinine 1.4
    Sputum: epithelial cells, no WBC’s
    Blood cultures pending
    ABG: pH 7.14, pCO2 70, pO2 50, HCO3 29
    ABG analysis?
  3. Treatment?
A
  1. Probable pneumonia, CAP (community acquired pneumonia): immunosuppressed due to chronic steroid use
    Exacerbation of COPD secondary to infection
    Tobacco addiction
    Peripheral Vascular Disease secondary to Arterial Sclerosis Obliterans (PVD 2nd ASO)
  2. Respiratory acidosis (acute) with hypoxia
  3. Admit to ICU, cardiac monitor, and continuous oximetry
    Aerosol treatments every 4h around clock (beta agonists, inhaled steroids)
    Nasal and oral tracheal suction prn
    If airway compromised or gases worsen, BiPAP or CPAP, may need intubation and mechanical ventilation
    IV steroids: methylprednisolone 125 mg IV
    Sputum for gram stain and C&S
    Blood cultures
    Begin IV antibiotic with coverage against community acquired pathogens
34
Q

Describe respiratory acidosis and hypoxia

A

Decrease pH, big increase paCO2, increase HCO3
Anything that causes hypoventilation CNS depression:
-Drugs, CVA, neuromuscular airway obstruction, pneumonia, pulmonary edema, pneumothorax, pleural disease, COPD, restrictive disease (disorders of chest wall, respiratory muscles)

35
Q

21 y/o F college student presents to ED with a history of right flank pain, fever, chills, and dyspnea. She has a biochemistry test in the morning. No significant PMH.
BP 100/68, P 110/min, R 28/min, temp 100F, O2 sat 89%
Neck: thyroid enlarged, nontender, no JVD
Lungs: clear
Heart: no murmur, S3 or S4. Soft 1/6 systolic murmur over apex
Abdomen: soft, no guarding or rigidity. Decreased bowel sounds. Tenderness to light percussion/palpation over right costovertebral angel (right flank)
Extremities: warm but no rash
Neurologic: brisk DTRs (+2/4) b/l, slight tremor of hands

  1. Diagnosis?
  2. Differential diagnosis?
  3. CBC: Hb 15, Hct 45, WBC 21,000: infection
    CMP normal
    Blood cultures pending
    TSH decreased, free T4 increased
    UA: TNTC WBC’s in urine, cloudy, and nitrate positive
    C&S pending
    Renal ultrasound: L kidney normal. R kidney mildly enlarged
    ABG: pH 7.56, pCO2 20, pO2 89, HCO3 20
    Analysis?
  4. Why is she breathing so fast?
  5. Treatment?
A
  1. Probably UTI (pyelonephritis)
  2. Sepsis, renal abscess, hyperventilation, R/O hyperthyroidism
  3. Respiratory alkalosis (acute)
  4. ? Septic: pyelonephritis, renal abscess
    ? Hyperthyroid
    ? Anxiety: biochem test
    Pain/fever
  5. IV’s to hydrate N/S
    IV antibiotics
    CT of abdomen and pelvis
    Note: respiratory hyperventilation may also be due to infection (sepsis)
    Other factors include hyperthyroidism and anxiety
36
Q

What causes respiratory alkalosis?

A

Increase pH, big decrease paCO2, decrease HCO3
Anything that causes hyperventilation
CHAMPS

CNS disease
Hypoxia
Anxiety
Mechanical ventilation
Progesterone
Salicylates/sepsis/stress

Renal II Final (8 decks)

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