Acid/Base Disorders Flashcards by Nicole Cabalo

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%

How well did you know this?

Not at all

Perfectly

What should you get to completely evaluate acid base states?

Basic metabolic panel

How well did you know this?

Not at all

Perfectly

What is important about hypoxemia?

Subnormal oxygenation in blood

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Describe ABG terms

Acidosis pH7.45

Hypoxia pO245
Hypocapnia pCO2

How well did you know this?

Not at all

Perfectly

When does kidney start to retain HCO3?

In 12-16 hrs

Max conc in 1 week

How well did you know this?

Not at all

Perfectly

What is the 3 step approach to ABG analysis?

Does patient have acidosis or alkalosis? pH high or low?
Is acidosis/alkalosis a respiratory or metabolic process?
If it is a respiratory acidosis/alkalosis, is it a pure respiratory process, or is there a metabolic component?

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

What is his anion gap?
What is his diagnosis?
What other tests would you use?
How would you treat this pt?

Na - (Cl + HCO3)
128 - (92+12)
24
Metabolic acidosis with high anion gap
Acute HF
Atrial fibrillation with rapid ventricular response
Hyponatremia
Azotemia
Mitral regurgitation
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

How well did you know this?

Not at all

Perfectly

What are normal electrolytes values?

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

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

Describe metabolic acidosis

Decrease in extracellular pH caused by a decrease in HCO3

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

2 types:
Elevated anion gap
Normal anion gap with hyperchloremia

How well did you know this?

Not at all

Perfectly

What are causes of high anion gap?

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

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

What is your diagnosis?
Differential diagnosis?
What tests do you order?
PH 7.1, pCO2 45, pO2 68, HCO3 8. Analysis?
Na 150, K 7, Cl 115, HCO3 10. Anion gap?
Interpretation?
How would you treat the pt?

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

CBC: Hgb 9 g, Hct 27%
CMP
TSH: 10
HbA1C
Metabolic and respiratory acidosis
150 - (115+10) = 25
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
Dialysis: hemodialysis
Na HCO3
Synthyroid
Aerosol treatments with nebulizers

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

Diagnosis/differential diagnosis?
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?
ABG analysis?
Treatment?

Diarrhea: secretory, infectious, consider inflammatory bowel disease
Hypovolemia: volume contracted, possible electrolyte/acid base disturbance
Hypotension
148 - (114+20) = 14 (normal)
Metabolic acidosis (normal anion gap, low HCO3, elevated Cl)
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

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

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?

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

Describe metabolic alkalosis

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)

What are causes of metabolic alkalosis?

CLEVER PD ``` Contraction of volume Licorice Endocrine (Conns, Cushing's, Bartters) Vomiting Excess Alkali Refeeding alkalosis ``` Post hypercapnia Diuretics

Describe metabolic alkalosis: Cl responsive

Urine Cl

Describe metabolic alkalosis: Cl unresponsive

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

Describe treatment for metabolic alkalosis

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

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?

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

Describe Conn's syndrome

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

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?

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

Describe respiratory acidosis and hypoxia

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)

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?

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

What causes respiratory alkalosis?

Increase pH, big decrease paCO2, decrease HCO3 Anything that causes hyperventilation CHAMPS ``` CNS disease Hypoxia Anxiety Mechanical ventilation Progesterone Salicylates/sepsis/stress ```