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CPR 2 > Acid Base Disorders 1 > Flashcards

Acid Base Disorders 1 Flashcards

1
Q

What is renal compensation in respiratory/metabolic acidosis?

A
  • Chronic acidosis (if kidney normal)
  • IncreasedH+ secretion by tubule
  • Filtered bicarbonate is reabsorbed
  • Urinary acid phosphate (titratable acidity) is increased
  • Ammonium in urine is increased
  • Urine pH b3comes acidic
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2
Q

Describe renal compensation in Respiratory/metabolic alkalosis

A
  • Alkalosis (if kidney normal and fluid volume normal)
  • Decreased H+ secretion by tubule
  • Filtered bicarbonate NOT reabsorbed
  • Urinary bucarbonate loss increases
  • Acid phosphate and ammonium in urine decreases
  • Bicarbonate also secreted by tubular cells
  • Urine pH becomes alkaline

Increased bucarbonate loss in uribe

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3
Q

Summarize assessment of acid-base status

A

Clinical assessment is done by arterial blood fas (ABG) analysis
Arterial blood gas analysis: arterial pH, HCO3^-, PaCO2

Normal levels
PH: 7.35-7.45
PaCO2(PCO2): 33-45 mmHg
HCO3^-: 22-28mmol/L

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4
Q

How can we classify acid-base disorders?

A

Acidosis: pH is less than 7.35
Alkalosis: pH is greater than 7.45

Respiratory acid base disorders: dysfunction of respiratory system and characterized by primary changes in PaaCO2

metabolic acid base disorders: metabolic or renal disorders and characterized by primary changes in [HCO3^-]

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5
Q

What is the compensation of metabolic acidosis ?

A

Respiratory compensation

Leading to PCO2 below 40 mmHg

Renal compensation only if kidney is normal

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6
Q

What is the compensation mechanisms of respiratory acidosis ?

A

Renal compensation

Leads to b8carbonate compensation above 24 Mm

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7
Q

What is the compensatory mechanism of metabolic alkalosis ?

A

Respiratory compensation

Leads to PCO2 over 40 mmHg

Renal compensation only if kidney is normal and if fluid volume is adequate

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8
Q

What is the compensatory mechanism of respiratory alkalosis?

A

Renal compensation

Bicarbonate concentration below 24 Mm

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9
Q

What is the effect of compensatory mechanism on ratio of HCO3/PCO2?

A

If primary disorder is characterized by an increase in PaCO2 compensatory mechanisms will increase HCO3, to bring ratio towards normal and pH comes closer towards normal

-If primary disirder is characterized by a decrease in HCO3, compensatory mechanisms will decrease PaCO2, to bring ratio towards normal and pH comes closer to normal

COMPENSATION always in the SAME DIRECTION

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10
Q

Give an example of respiratory acidosis

A

A 45 year old man comes to the physician because of a 1-day history of fever and cough. He is a chronic smoker for the past 20 years. He was diagnosed with chronic obstructive pulmonary 2 years ago.

Arterial blood gas shows
Ph: 7.25 (acidosis)
PCO2: 60 mmHg (primary Distrpurbance) respiratory
Bicarbonate conc.: 25 mmol/L(acute)

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11
Q

Describe respiratory acidosis

A

Characterized by decreased rate of respiration/decreased lung function/ decreased air entry into the lungs

  • As a result, CO2 is NOT washed out (CO2 accumulation), resulting in elevation of PaCO2 (primary abnormality)
  • Remember, CO2 is an ACID, and it’s accumulation causes respiratory acidosis

Acute stage:

  • pH decreased (lower than 7.36)
  • PaCO2 elevated (primary disturbance)
  • HCO3 ^- is almost normal
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12
Q

give an e ample of chronic respiratory acidosis

A

A 45 year old man 5 days of onset of lung infection (if not treated or treatment not effective)

Arterial blood gas analysis (chronic respiratory acidosis)
Ph: 7.32(compare to day 1, closer to normal) acidosis
PCO2: 60 mmHg (primary change) respiratory
Bicarbonate conc.: 32 mmol/L (compensated by kidneys)

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13
Q

Describe chronic respiratory acidosis with compensation

A
  • During compensation, renal system comes to rescue
  • Kidneys excrete more H+, and generate more HCO3^- , and serum bicarbonate conc levels increase.
  • Increased excretion of phosphate (titratable acid) and ammonium in urine

Chronic respiratory urine

  • pH: lower than normal (<7.36)- closer to normal pH, when compared to acute stage
  • PaCO2: elevated (primary defect is still not corrected- respiratory system is still not functioning optimally)
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14
Q

Explain the impact of the Henderson hassalbach equation in respiratory acidosis

A

pH= pka+ logincreased [HCO3^-]/0.03 x increased PCO2

Primary abnormality increases PCO2 due to respiratory disease—> fall in pH

Compensation by renal system, increases serum [HCO3^-], and ratio of [base]/[acid] returns almost to normal, and pH comes toward normal (still below normal)

Compensation always in same direction to bring ratio towards normal

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15
Q

What are the causes of respiratory acidosis ?

A

Airway obstruction by foreign body

Central causes: opioids, anesthetics

Disease/injury to phrenic nerve: guillian barre syndrome; multiple sclerosis

Lung diseases: COPD, RDS, fibrosis of lung, collapse of lung

  • Drugs which inhibit respiratory center (opioids, anesthetics)
  • Diseases/injury of phrenic (supplies diaphragm)
  • Lung diseases: chronic obstructive pulmonary disease(COPD), fibrosis, respiratory distress syndrome infants or in chronic smokers (Acute respiratory distress syndrome, ARDS)
  • Foreign body in Respiratiry tract
  • Demyelinating disorders: Gillian barre syndrome, multiple sclerosis
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16
Q

Give an example of acute respiratory alkalosis

A

A 25 year old student has been out camping in the himalaya (high altitude) . She is hyperventilating.

Hypoxia stimulates the respiratory center

Secondary day of her stay, her arterial blood gas results:

  • ph: 7.57 alkalosis
  • PaCO2: 20 mmHg Respiratiry
  • bicarbonate conc. 22 mmol/L acute
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17
Q

What is acute respiratory alkalosis ?

A

Respiratory alkalosis characterized by increase in rate of respiration (hyperventilation) —> increased washout of CO2. —> decreased PaCO2 (primary disturbance)

Acute respiratory alkalosis

  • ph is decreased (greater than 7.44)
  • PaCO2 is decreased (below 35mmHg)
  • bicarbonate conc. Is almost normal
18
Q

What is the arterial blood gas of chronic respiratory alkalosis ?

A

Arterial blood gas:
Ph: 7.46 (compare to 2 days, it is closer to normal) alkalosis
PaCO2: 20 mmHg (primary disturbance)
Bicarb9nate conc. 17 mmol/L(renal compensation and increased bicarbonate conc. In ursine)(chronic)

19
Q

What is the bodily response to chronic respiratory alkalosis?

A

Renal system tries to bring pH back towards normal

Kidneys do NOT secrete H+ into urine

Increased urinary HCO3^- excretion (beta intercalated cells) and pH of ursine Becomes alkaline, and serum HCO3^- falls

Chronic respiratory alkalosis

  • pH: higher than normal- closer to normal pH, when compared to acute stage
  • PaCO2: decreased (primary defect still not corrected- respiratory system is still hyperventilating)
  • bicarbonate concentration: decreased (renal compensation)
20
Q

What is the impact of Henderson-hassalbach equation in respiratory alkalosis?

A

pH= pKa+ log decreased [HCO3^-]/ 0.03 x PaCO2

Primary abnormality decreased PaCO2 due to hyperventilation, which results in rise in pH (alkalosis)

-Compensation by renal system, decreases serum [HCO3^-], ratio of [base]/[acid] ratio returns closer to normal, and pH comes toward normal (still above normal)

Compensation always in same direction to bring ratio towards normal

21
Q

What are the causes of respiratory alkalosis?

A

Causes of hyperventilation

  • Anxiety, fever, somatic symptoms disorder
  • high altitude: hypoxia stimulates respiratory center and increases rate of respiration. When a person stays for a long time at elevated altitude, renal compensatory mechanisms are active and bicarbonate concentration levels fall
    • Refer to hemoglobin lecture: identify changes in oxygen dissociation curve when a person is adapted to high altitude
  • Mechanical ventilation: (over ventilation)
  • Drugs that stimulate respiratory center (acute salicylate poisoning)
22
Q

What is the arterial blood gas metabolic acidosis?

A 
pH: 7.2
PaCO2: 30 mmHg
Bicarbonate conc. : 12 mmol/L (bucarbonate loss for buffering ketone bodies- primary abnormality)
Na+: 140 mEq/L
CL-: 100 mEq/L
K+: 5.2 mEq/L

Plasma glucose: 500 mg/dL
Dipstick test with urine for ketone bodies and glucose is positive

She is hyperventilating (kussmaul breathing)

23
Q

What are the characteristics of metabolic acidosis?

A

Characterized by acidosis Decreased bicarbonate conc. and low pH

Bicarbonate Conc. Is low due to

  • increased nonvolatile acids [HCO3^-] is lost by buffering
  • or due to increased losses of HCO3^-

Acidosis stimulates respiratory center—> hyperventilation and a fall in PaCO2 (remember, respiratory center responds within minutes)
-When plasma pH falls, respiratory center stimulated—> increased rate and depth of respiration —> increased CO2 washout leads to decreased PaCO2(compensatory hyperventilation)

24
Q

What is the role of kidney in metabolic acidosis?

A
  • If kidney is functioning, can also compensate to increase H+ excretion, increases formation of new HCO3^-
  • Renal system takes hours to days to respond
  • Increased H+ secretion in renal tubules
  • Increased excretion of acid phosphate (titratable acid) and ammonium in urine
  • However, until cause of acidosis is treated, pH doesn’t come back to normal
25
Q

What is the Henderson-hassalbach equation impact in metabolic acidosis?

A
  • Primary abnormality is decreased HCO3^-, which results in a fall in pH
  • Compensation by respiratory system, results in hyperventilation, and decreases PaCO2, and ratio of base/acid conc. returns almost to normal, and pH comes toward normal (it is below normal)

The kidneys can compensate too, if they are normal- they try to increase the serum HCO3^-

26
Q

Describe H+ and K+ interrelations in acidosis/alkalosis

A

K+ (major intracellular cation)

K+ and H+ are intricately related

Diabetes mellitus-insulin deficiency and hyperglycemia (hyper osmolarity)-K+ shift from ICF to ECF (hyperkalemia)

Changes in pH affect serum (DCF) K+ levels

  • metabolic acidosis- hyperkalemia
  • metabolic alkalosis- hypokalemia

Also, changes in serum K+ affects pH

  • Hyperkalemia- acidosis
  • Hypokalemia- alkalosis
27
Q

What is the role of serum K+ and diabetic ketoacidosis?

A

Serum K+ is increased(K+: 5.3 mEq/L)

  • plasma glucose: 500 mg/dL (ECF hyper osmolarity causes K+ to shift from ICF to ECF with osmotic fluid shift)
  • Insulin deficiency in type 1 diaabetes mellitus prevents K+ entry into ICF (K+ levels in ECF increase)- remember, insulin activated Na-K ATPase
28
Q

What is the anion gap?

A

Anion gap= cations- sum of anions

Anion= [Na+] -([Cl- ]-[HCO3-])

Normal anion gap is 8- 14 mEq/L

Due to presence of unmeasured anions

Unmeasured anions: phosphate, sulfate, lactate, ketone bodies and protein

In some forms of metabolic acidosis, there is increase in unmeasured anions, resulting in increased anion gap

29
Q

How can we calculate the anion gap?

A 
pH: 7.2
PaCO2: 30 mmHg
[HCO3-]:12 mmol/L
Na+: 140 mEq/L
Cl-: 100 mEq/L
K+: 5.3 mEq/L

140-112=28 mEq/L(normal 8-16 mEq/L)

High anion gap metabolic acidosis

In ketoacidosis, ketone bodies are the unmeasured anions

30
Q

What ABG of metabolic acidosis with a normal anion gap?

A 
ABG:
pH: 7.24
PCO2: 30 mmHg
Bicarbonate conc.: 12 mmol/L(bicarbonate loss in intestinal secretions- primary abnormality)
Na+: 140 mEq/L 
CL-: 116 mEq/L

Calculate anion gap:140-128= 12 mEq/L(8-14 mEq/L)
Normal anion gap (hyperchloremic) metabolic acidosis

31
Q

What are the causes of metabolic acidosis?

A

Increased production of non-volatile acids (high anion gap metabolic acidosis)- increased unmeasured anions

Increased loss of HCO3^-(base)- normal anion gap metabolic acidosis- hypercholermic acidosis

32
Q

What is the effect of metabolic acidosis dye to increased production 9f nonvolatile acidosis?

A

High anion gap metabolic acidosis-increased unmeasured anions

Leads to:
- diabetic ketoacidosis (increased ketone body production)

  • lactic acidosis (increased lactate)
  • chronic renal failure(decreased excretion of sulfate, phosphate)
  • Methanol and ethylene glycol poisoning
33
Q

What is the effect of metabolic acidosis due to increased HCO3^-

A

Normal anion gap metabolic. Acidosis- hyperchloremic acidosis

  • Diahrrea (increased loss of HCO3^- rich intestinal secretions)
  • Renal tubular acidosis(failure to secrete H+ and reabsorb HCO3^-)
  • Acetazolamide treatment (inhibits renal carbonic anhydrase)
34
Q

Whaat is the metabolic alkalosis ABG?

A

pH: 7.56
PaCO2: 50 mmHg
Bicarbonate conc.: 30 mmol/L (primary abnormality) metabolic

35
Q

What is the effect of vomiting/ nasogastric suction ?

A

Loss of acid

Parietal cells contain carbonic anhydrase

For every H+ pumped into the gastric lumen, one HCO3^- gained by blood

36
Q

What are the characteristics of metabolic alkalosis?

A

Increased bicarbonate conc. ( relative excess of HCO3^-)

Increased pH (alkalosi) inhibits respiratory center, there is a decrease in rate of respiration (hypoventilation)—> decreased washout of CO2 (CO2 retention )—> increased PaCO2

Metabolic alkalosis

  • pH- higher than normal
  • bicarbonate conc. Is increased (primary abnormality)
  • PaCO2 is increased (compensatory mechanism)
37
Q

Give renal compensation if metabolic alkalosis.

A
  • Renal system compensates, if it is functioning normally, by excreting more HCO3^-(alkaline urine)
  • Beta-intercalated cells secrete bicarbonate into urine
38
Q

What is the impact on the Henderson hassalbach equation in metabolic alkalosis?

A
  • Primaary abnormality is increased HCO3^-, which results in a rise in pH
  • Compensation by respiratory system, increases PaCO2, and the ratio of base:acid ratio returns almost to normal, and pH comes toward normal (it is still above normal)

Kidneys can compensate if they are normal and if fluid volume is adequate

39
Q

What is the renal response in metabolic alkalosis that results in volume contraction ?

A

When there is volume depletion, renal compensation firvalkalosis may not be seen

RAAS is active

Kidneys try to conserve sodium and secrete protons in urine (Na-H+ exchanger active )- resulting in aacidic urine- paradoxical aciduria

40
Q

What is the cause of metabolic alkalosis?

A
  • Vomitting, pyloric stenosis (gastric outlet obstruction)
    • Loss of acidic contents of stomach, results in relative HCO3^- excess
  • Nasogastric suction: a tube removes acidic contents of stomach
  • Excessive consumption of antacids
  • Primary hyperaldosteronism causes hypokalemia and metabolic alkalosis
  • Hypokalemia
  • diuretics (cause bulk of Na in tubules) —> K+ secretion —> hypokalemia—> alkalosis

CPR 2 (32 decks)

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