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PHYSIOLOGY > ACID BASE BALANCE > Flashcards

ACID BASE BALANCE Flashcards

1
Q

DIARRHEA

A
  • washed out a lot of HCO3 (decrease in HCO3)
  • thus generating H+ ion fix acid metabolic acidosis
  • is due to INCREASE in H+ ion fixed acids
  • second by DECREASE in HCO3
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2
Q

RESPIRATORY ACIDOSIS (acute)

A
  • respiratory depression (anesthetics, morphine)
  • pulmonary edema, cardiac arrest
  • airway obstruction
  • muscle relaxant
  • sleep apnea
  • chronic obstructive lung disease
  • restrictive lung disease
  • neuromuscular defects (MS, muscular dystrophy)
  • obesity hypoventilation syndrome
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3
Q

RESPIRATORY ALKALOSIS (acute)

A
  • anxiety
  • fever
  • hypoxemia
  • pneumothorax ( in some cases) atelectasis pulmonary shunt increase ventilation leading to LOW arterial CO2
  • ventilation- perfusion inequality
  • hypotension
  • high altitude
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4
Q

RESPIRATORY ACIDOSIS

A
  • Hypoventilation
  • INCREASE PaCO2
  • will make the curve shift to the R
  • INCREASE H+ is the cause of acidosis
  • slight INCREASE HCO3 it is not part of the compensation, rather part of the disturbance (22-26)
  • an increase of 10 mm Hg of CO2 will increase HCO3 by 1 mmol
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5
Q

RESPIRATORY ALKALOSIS

A
  • HYPERVENTILATION
  • that causes a DECREASE in PaCO2 (main cause)
  • shift to the L
  • decrease in H+ ion caused the alkalosis
  • slight DECREASE in HCO3
  • a decrease of PaCO2 by 10 mm Hg, the HCO3 decreases by 2 mmol
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6
Q

METABOLIC ACIDOSIS

A
  • LACTIC ACIDOSIS (increase acid production)
  • KETOACIDOSIS (increase acid production faster than the kidney produced)
  • RTA type II (loss of HCO3)
  • DIARRHEA (loss of HCO3)
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7
Q

METABOLIC ACIDOSIS

A
  • decrease ability of the nephron to excrete fixed acid and thus, failure to add new HCO3 to body stores
  • acute and chronic renal disease or failure
  • inability to synthesize ammonia
  • RTA type I
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8
Q

METABOLIC ALKALOSIS

A
  • VOMITING
  • GASTRIC SUCTIONING
  • PRIMARY HYPERALDOSTERONISM, results from too much lost in H+ ions in the urine
  • LOSS OF BICARBONATE-FREE FLUID (contraction alkalosis)
  • maintenance:
  • volume depletion
  • increase aldosterone
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9
Q

METABOLIC

A
  • main causes are HCO3 or H+
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10
Q

METABOLIC ACIDOSIS

A
  • excess of H+ ions
  • shift to the L
  • BIG DECREASE in HCO3
  • assuming CO2 is 40
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11
Q

METABOLIC ALKALOSIS

A
  • caused by DECREASE IN H+ ions
  • vomiting stomach contents
  • BIG INCREASE IN HCO3
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12
Q

RESPIRATORY ACIDOSIS

A
  • increase CO2
  • decrease pH
  • normal to increase HCO3
    to compensate increase above normal HCO3
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13
Q

RESPIRATORY ALKALOSIS

A
  • decrease CO2
  • increase pH
  • normal to decrease HCO3 to compensate decrease HCO3 to below normal
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14
Q

METABOLIC ACIDOSIS

A
  • no change CO2 40 mm Hg
  • decrease pH
  • big decrease HCO3 to compensate increase it
  • hyperventilating
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15
Q

METABOLIC ALKALOSIS

A
  • no change in CO2 40 mm Hg
  • increase pH
  • big increase in HCO3 to compensate decrease it
  • hypo-ventilating
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16
Q

normal values:

pH first

A
  • 7.4
  • low- acidosis
  • high- alkalosis
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17
Q 
normal values:
PCO2 second (RESPIRATORY COMPONENT)
A
  • 40 mmHg
  • high- acidosis
  • low- alkalosis
18
Q

normal values: (METABOLIC COMPONENT)

HCO3 last

A
  • 24 mmol/L
  • low- acidosis
  • high- alkalosis
19
Q

CONCEPT:

A

pH low plus PCO2 high = respiratory acidosis but if you add HCO3 low= metabolic acidosis or mixed acidotic problem VIA

20
Q 
case:
arterial components:
pH = 7.3 low acidosis
PCO2 = 30 mm Hg low rule out respiratory component, metabolic (40)
PO2 = 95 mm Hg distractors
serum:
HCO3 = 14 mEq/L low acidosis
A
  • METABOLIC due to low PCO2 and big decrease in HCO3 ACIDOSIS due to low pH
21
Q

case:

arterial component:
pH = 7.6 high alkalosis
PCO2 = 20 mm Hg low rule in respiratory
PO2 = 95 mm Hg
serum:
HCO3 = 18 mEq/L low acidosis
A

RESPIRATORY due to low PCO2 ALKALOSIS due to high pH

22
Q

concept;

A

HCO3 low

23
Q

concept:

A

HCO3 high > PCO2 low meaning it is more of a METABOLIC PROBLEM

24
Q

case:

arterial components:
pH = 7.2 low acidosis
PCO2 = 80 mm Hg high rule in respiratory component
PO2 = 70 mm Hg
serum:
HCO3 = 30 mEq/L high saying no metabolic acidosis

A

RESPIRATORY ACIDOSIS

25
Q

case:

arterial component:
pH = 7.6 high alkalosis
PCO2 = 52 mm Hg high rule out respiratory component hypoventilation compensation to the problem
PO2 = 70 mm Hg
serum:
HCO3 = 44 mEq/L high rule in metabolic
A

METABOLIC ALKALOSIS

26
Q

arterial PCO2 = 55 mm Hg
serum HCO3 = 20 mEq/L
no pH

A

mixed respiratory and metabolic alkalosis

due to PCO2 is inverse to HCO3

27
Q

CO2

A
  • respiratory compensation
28
Q

HCO3 (distal tubule collecting duct)

A
  • renal compensation

if the kidney is working otherwise it would be respiratory

29
Q

H+ ions

A
  • increase acidosis
  • to become normal shift to the L going to CO2 respiratory variable thus decrease it by hyperventilating and increase in plasma HCO3
  • WINTERS FORMULA
30
Q

H+ ions

A
  • decrease in alkalosis

- to become normal shift to the R by hypo-ventilating and increase CO2 and decreasing HCO3 by dumping it in urine

31
Q

“Winters’ Formula”,[1] named for Dr. R.W. Winters,[

A

is a formula used to evaluate respiratory compensation when analyzing acid-base disorders and a metabolic acidosis is present. It can be given as

P_{CO_2} = (1.5 \times HCO_3^-) + 8 \pm 2,

where HCO3− is given in units of mEq/L and pCO2 will be in units of mmHg.

Winters’ formula gives an expected value for the patient’s PCO2; the patient’s actual (measured) PCO2is then compared to this.

If the two values correspond, respiratory compensation is considered to be adequate.

If the measured PCO2 is higher than the calculated value, there is also a primary respiratory acidosis.

If the measured PCO2 is lower than the calculated value, there is also a primary respiratory alkalosis.

Alkalosis
Note that Winter’s formula pertains to settings of metabolic acidosis.

To calculate the expected pCO2 in the setting of metabolic alkalosis, the following equations are used:

pCO2 = 0.7 [HCO3] + 20 mmHg +/- 5
pCO2 = 0.7 [HCO3] + 21 mmHg
32
Q

acute metabolic/respiratory
acute hypoventilation/hyperventilation
acute lactic acidosis

A
  • no compensation
33
Q

ACIDOSIS

A
  • INCREASE HCO3 forming acid urine
34
Q

ALKALOSIS

A
  • DUMP/DECREASE HCO3 in the urine causing an alkaline urine
35
Q

The urine anion gap

A

is calculated using measured ions found in the urine. It is used to aid in the differential diagnosis of metabolic acidosis.

The term “anion gap” without qualification usually implies serum anion gap. The “urine anion gap” is a different measure, principally used to determine whether the kidneys are capable of appropriately acidifying urine.

Determining the cause of a metabolic acidosis that lacks a serum anion gap often depends on determining whether the kidney is appropriately excreting acid.

36
Q

Urine anion Gap (NH4)

A

Urine anion gap is calculated by subtracting the urine concentration of chloride (anions) from the concentrations of sodium plus potassium (cations):

= Na+ + K+ − Cl−

A positive urine anion gap suggests a low urinary NH4+ (e.g. renal tubular acidosis).
A negative urine anion gap suggests a high urinary NH4+ (e.g. diarrhea).

37
Q

positive ions in plasma anion gap

A
  • measure only SODIUM (140)
38
Q

negative ions in plasma anion gap

A
  • measure CHLORIDE (108) and HCO3 (24) = 132 meaning less than the SODIUM CONCENTRATION
  • difference between SODIUM and the total negative ion is the ANION GAP (140- 132) = 8 mmol
39
Q

DIARRHEA

A
  • washed out HCO3

- and Na

40
Q

LACTIC ACIDOSIS

A
  • H+ neutralized by using HCO3

- HCO3 IS CONVERTED TO LACTATE

41
Q

just got off the airplane

A
  • acute respiratory alkalosis no compensation

PHYSIOLOGY (40 decks)

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