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Flashcards in Acid/Base Deck (34):
1

Acidosis

Metabolic: decrease HCO3 or =45 mmHg

2

Alkalosis

Metabolic: increase HCO3 > or = 28 mEq/L
Respiratory: decrease pCO2

3

Lungs

- regulate ACUTE changes (occurs w/in seconds)
- regulates PCO2 through respiration rate and depth changes

4

Renal

- regulates CHRONIC changes (takes hours- days to compensate)
- regulates HCO3 and H through excretion/reabsorption/buffer

5

Primary METABOLIC disorder--> Respiratory compensation

meta acidosis --> compensate w/respiratory alkalosis
meta alkalosis--> compensate w/respiratory acidosis

6

Primary RESPIRATORY disorder--> Metabolic compensation

resp acidosis--> compensate w/metabolic alkalosis
resp alkalosis--> compensate w/metabolic acidosis

7

Acidosis Clinical Manifestation

- hyperventilation
- CNS depression
- Hypotension
- Hyperkalemia
- Arrhythmias
- decrease contractility

8

Alkalosis Clinical Manifestation

- nerve excitation
- Arrhythmias
- respiratory depression
- hypoventilation
- hypokalemia

9

Step 1.

evaluate the pH
- pH acidemia
- pH > 7.40--> alkalemia

10

Step 2.

Is the primary disorder respiratory or metabolic?
--> it is problem with the HCO3 or the PCO2?

11

Step 3.

Calculate the anion gap.
AG= Na- Cl- HCO3

12

Step 4.

Check for compensation
- winter's formula for METABOLIC acidosis
--> pCO2= 1.5 (HCO3)+8 (+-2)
- expected increase in pCO2 w/METABOLIC alkalosis
--> pCO2= 0.75 (pt's HCP3- norm HCO3) (-+2)

13

Step 5.

If AGMA, check corrected HCO3
--> corrected HCO3= pt's HCO3 + (pt's AG- norm AG)
***norm AG= 12

14

Corrected HCO3

- relationship between the serum HCO3 & AG
- Indicates if degree of compensation is appropriate or if another metabolic acid/base disorder is present
- for rise in AG by 1--> corresponding decrease of HCO by 1 mEq/L
- if calculated HCO3 is not in the reference range (22-28 mEq/L)--> coexisting metabolic disturbance
----> if > norm, metabolic alkalosis
----> if

15

Causes of NAGMA

H: Hyperalimentation (high Cl soln) TPN & NS
A: Acetazolamide (inhibit Na reabsorption)
R: Renal tubular acidosis (proximal, distal, & hyperaldosteronism type 4)
D: Diarrhea
U: Uretero-pelvic shunt (fistula)- excessive loss of HCO3 from surgery or cancer
P: Post-hypocapnia (decreased CO2)
S: Spironolactone

16

Causes of AGMA

M: Methanol/Metformin
U: Uremia (high BUN)--> CKD or AKI
D: Diabetic acidosis (DKA), ketoacidosis
P: Poisoning/ propylene glycol/ paraldehyde
I: Intoxication/ infection/ isoniazid (INH)
L: Lactic acidosis (shock)
E: Ethylene glycol (antifreeze)
S: Salicylates/Sepsis

17

Winter's Formula

expected pCO2= 1.5 (HCO3) +8 (+-2)
- pCO2 predicted: coexisting respiratory acidosis

18

Osmolar Gap

- if you can't easily identify a cause for an AGMA, calculated the osmolar gap.
- osmolar gap= measured Osm- calculated Osm
- calculated Osm= 2(Na) + BUN/2.8 + glucose/18 + EtOH/4.6
--> norm gap Osm gap > 10

19

Typical Treatment for Metabolic acidosis

- if pH is 7.20-7.35: focus on cause
- if pH

20

Treatment Options for Metabolic acidosis- Sodium Bicarbonate

***Goal: target pH 7.2
tab: 3.9 mEq/ 325 mg, chronic replacement in renal failure or renal tubular acidosis
IV: 50 mEq or mmol ampule; isotonic soln in D5W or SW 150 mEq NaHCO3/ 1 L, reserve for acute situations no evidence-based benefit

21

Treatment Options for Metabolic acidosis- Sodium citrate/ citric acid

Alkali: 1 mEq/ mL soln
- chronic replacement in renal failure or renal tubular acidosis

22

Treatment Options for Metabolic acidosis- Tromethamine (THAM)

Alkali: sodium-free buffer
- reserve for acute situations
- no benefit over sodium bicarbonate

23

Treatment Options for Metabolic acidosis- Hemodialysis

A:
E:
I:
O:
U:
- reserved for acute situations

24

Metabolic Alkalosis Causes

C: contraction
L: Licorice
E: Endocrine (Conn's, Cushing's, Bartter's syn)
V: vomiting
E: excess alkali (Sodium bicarb)
R: refeeding alkalosis (malnurished pt's)
P: post-hypercapnia
D: diuretics

25

Compensation for metabolic alkalosis

exp increase in pCO2= 0.75 (pt's HCO3- norm HCO3 {12})
- if pCO2 predicted: respiratory acidosis

26

Treatment for metabolic alkalosis: volume-dependent or saline-responsive

1. vomiting
2. nasogastric suction
3. diuretics
Urine Chloride:

27

Treatment for metabolic alkalosis: volume-independent or saline-resistant

1. mineralcorticoid excess
--> Cushing's syn
--> Conn's syn
2. hypokalemia
Urine Chloride: > 20 mEq/L
Treat:
- treat underlying disorder
- potassium replacement

28

Respiratory Acidosis causes

C: CNS depression (stroke, opiate OD, seizures, sedation, head trauma)
A: Airway obstruction (COPD)
N: Neuromuscular disorders (ALS, Guillain Barre, Myasthenia gravis)
S: Severe pneumonia, pulmonary embolism, pulmonary edema

29

Compensation for Respiratory Acidosis

- for each 10 mmHg increase in pCO2, pH will decrease by:
--> 0.08 units in ACUTE respiratory acidosis
--> 0.03 units in CHRONIC respiratory acidosis

30

Treatment for Respiratory Acidosis

- Focus on cause
- Oxygen therapy
****NEVER use added base for respiratory acidosis

31

Respiratory Alkalosis cause

C: CNS stimulation (pain, anxiety, fever, tumors, stroke, head trauma)
H: hypoxia
A: anxiety
M: mechanical ventilation
P: progesterone (pregnancy & cirrhosis)
S: salicylates/sepsis

32

Compensation for Respiratory Alkalosis

- for each 10 mmHg decrease in pCO2, pH will increase by
--> 0.08 units in ACUTE respiratory alkalosis
--> 0.03 units in CHRONIC respiratory alkalosis

33

Treatment for Respiratory Alkalosis

- focus on cause
- hypoventilation
- breathe into a bag for anxiety
- sedation

34

General Treatment Principles

- ALWAYS correct underlying etiology
-->DKA: stop ketoacid production, correct volume depletion, and normalize blood glucose
-->Uremia: renal replacement therapy (dialysis)
--> excessive vomiting: antiemetics
--> COPD exacerbation: oxygen, bronchodilators, corticosteroids, possibly antibiotics
--> narcotic OD: opiod antagonist
- Alkali or acid replacement
--> reserved for critically-ill pt's
--> only provides a "temporary fix"