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S2B5 Physiology > Acid Base > Flashcards

Acid Base Flashcards

1
Q

What must happen to maintain acid-base balance?

What are the 2 ways this occurs?

A

excrete an amount of acid equal to the production of non-volatile acids

Volatile acid - CO2 is “blown off” by the lungs

Kidneys are responsible for the excretion of non-volatile acids (50-150 mEq/day & requires proton acceptors in the tubule)

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2
Q

What are the sources of H+ in the kidney?

This requires what enzyme?

A
  1. dissociation of H2CO3
    • requires enzyme carbonic anhydrase
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3
Q

What measurement is an index of H+ secretion?

A

HCO3- reabsorption

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4
Q

What are buffers?

What is the equilbrium constant?

How is equilbrium shifted?

A

buffers are a mixture of relatively weak acids & its conjugate base

Ka is the equilibrium constant, pKa = -log Ka

Adding or removing H+ causes this equilbrium to shift either left or right

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5
Q

What is the Henderson-Hasselbalch Equation?

A
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6
Q

pH is dependent on what two factors?

A
  1. The [A-]/[HA] ration (regardless of the concentrations)
  2. the pKa of the buffer system
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7
Q

What are the pH levels & subsequent [H+] under normal, acidosis, and alkalosis situations?

A
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8
Q

Acid-base regulation refers to what phenomena?

A

regulation of the [H+] in the body fluids

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9
Q

What 4 systems are involved in the regulation of pH?

A
  1. Chemical buffers
  2. Respiratory system (controling ventilation)
  3. Kidney (controling excretion fixed acid & generating bicarbonate)
  4. Bone (long-term)
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10
Q

How quickly do chemical buffers respond to an acid or base challenge?

What is the isohydric principle?

A

instantaneously - both intracellular & extracellular - due to a change in the acid/base ration

Isohydric principle: all of the chemical buffer systems participate simulatneously in defending against disturbances in acid-base status

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11
Q

How quickly does the respiratory system compensate for challenges to acid/base status?

How does it do this?

A

minutes to hours

Regulates PaCO2 by altering alveolar ventilation

Acidosis stimulates ventilation

Alkalosis reduces ventilation

  • Alveolar ventilation equation
    • VCO2 = rate of CO2 production
    • VA = rate of alveolar ventilation
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12
Q

How quickly does it take the kidney to compensate for challenges to acid/base status?

What are these responses?

A

hours to days

  • Acidosis:
    • excrete more H+ (as NH4+ and TA) and produce and reabsorb more HCO3-
  • Alkalosis
    • secrete less H+ and excrete more HCO3-
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13
Q

Where do the buffers in the blood come from?

A
  • Most of the buffer is through bicarbonate (plasma & erythrocyte) –53%
  • hemoglobin & oxyhemoglobin are also important – 35%
  • organis phosphate – 3%
  • inorganic phosphate – 2%
  • plasma proteins – 7%
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14
Q

What is the most powerful extracellular buffer?

pKa?

Why is it effective at blood pH?

Describe the components of this system & include relevant equations.

A

CO2 - bicarbonate buffer system

pKa = 6.1

  • Effective at pH 7.4 b/c
    • CO2 and HCO3- can be controlled independently
      • ventilation takes care of CO2
      • kidney takes care of bicarbonate
    • HCO3- can be replaced nearly as fast as it is used up in buffering pH changes
  • CO2 - volatile acid
    • Produce ~15,000 mEq/day from cellular metabolism
    • Lungs (respiratory system) regulates arteiral PaCO2 by controlling alveolar ventilation
  • HCO3- - base
    • kidney contorl body fluid [HCO3-] by excreting excess HCO3- in the urine (in alkalosis), or by makign “new” HCO3- (in acidosis)
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15
Q

Describe the equation for the mass action relationship

A

because we can independntly regulate CO2 on one side of the system and independnetly regulate HCO3- on the other side of the system

this makes the CO2 / bicarb system important in regulating pH

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16
Q

What are the normal values of the following variables with relation to the mass action equation

PaCO2

Dissolved CO2

Plasma [HCO3-]

pHa

A
  • PaCO2 = 40 mmHg
  • Dissolved CO2 = 0.03 * PaCO2 = 1.2
  • Plasma [HCO3-] = 24 mM
  • pHa = 7.4 or [H+] = 40 nM (40 x 10-9 M)
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17
Q

Do absolute concentrations of HCO3- and CO2 matter?

A

no, for pH 7.4 all that matter is that the ratio is 20/1

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18
Q

What is the role of “non-respiratory buffers” ?

A

the H+ are also in equilibrium with “non-respiratory” buffers

so, when we look at changes in CO2 that drive the reaction left or right, these changes in H+ will result in relative changes to the A- / HA form of the “non-respiratory buffers”, which influences our acid/base status

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19
Q

What ratio of HCO3- to dissolved CO2 denotes acidosis?

What ratio of HCO3- to dissolved CO2 denotes alkalosis?

A
  • acidosis
    • <20/1
  • alkalosis
    • `>20/1
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20
Q

Describe what happens variable under acidosis & then under alkalosis?These measurements indicated respiratory or metabolic conditions?

HCO3- / CO2 ratio

PaCO2

plasma HCO3-

A
  • Primary Acid-Base Disturbances
    • Acidosis
      • HCO3- / CO2 decreases
        • Respiratory: increase PaCO2 (decrease VA) - increasing the denominator by decreasing ventilation
        • Metabolic: decrease plasma HCO3-
    • Alkalosis
      • HCO3- / CO2 increases
        • Respiratory: decrease PaCO2 (increase VA) - decrease the amount of acid by increasing ventilation
        • Metabolic: increase plasma HCO3-
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21
Q

What is the difference between correction & compensation?

A
  • Correction
    • the elimination of the cause of the acid-base disturbance
    • all values return to normal
  • Compensation
    • minimized the pH disturbance by adjusting the ratio of conjugate base to acid
      • returning the HCO3- / CO2 ratio toward 20/1
        • so, if CO2 goes up, need to increase HCO3- as well
      • compensation is NOT corrective and a small pH disturbance will remain
22
Q

What type of compensation occurs for respiratory disorder?

What type of compensation occurs for metabolic disorder?

A
  • Respiratory disorder
    • compensation is renal (hours to days)
  • Metabolic disorder
    • compensation is respiratory (minutes to hours) & renal (hours to days)
23
Q

What does “primary disturbance” refer to?

In what direction do compensatory changes occur

A
  • Primary disturbance is the initial change
    • All chemical buffers are involved in any pH change, and the buffering is instantaneous
  • Compensatory changes occur in the “same direction” as the primary disturbance, and bring the base/acid ratio back toward 20/1
    • respiratory compensation takes minutes to hours ( & typically accompanies the development of the disorder)
    • renal compensation takes hours to days
24
Q

What type of disturbance occurs when the change pH and plasma [HCO3-] occur in the same direction?

A

metabolic disturbance

pH is directly proportional to [HCO3-]

25
Q

What type of disturbance occurs when the change of pH and plasma [HCO3-] occur in opposite directions?

A

respiratory disturbance

pH is inversely proportional to dissolved CO2

26
Q

Fill out the provided diagram

A
27
Q

How can you determine the degree of compensation?

A

from the change in the “other” variable

if you have had time to compensate & bring the ratio back to 20/1, you will minimize the magnitude of the change in pH

28
Q

How can you determine if there is a base excess vs. deficit?

A

Total base in the system is determine by HCO3- + A-

  • Base excess
    • increase in total base contents (HCO3- + A-)
  • Base deficity
    • decrease in total base contents (HCO3- + A-)
    • base deficit is somethign referred to as “negative base excess”
29
Q

What impact does hypoventilation have on acid/base status?

A
  • Hypoventilation –> Respiratory Acidosis
    • leading to CO2 retention
    • increased PaCO2 (hypercapnia)
30
Q

What conditions indicate acute respiratory acidosis?

How would you calculate [HCO3-​]?

A
  • Change in opposite directions
    • increased PaCO2 ( >40mmHg)
    • decreased pH (increased [H+])
  • Small increase in HCO3- – but no base excess
    • new HCO3- can be approximated by:
31
Q

What conditions indicate chronic respiratory acidosis?

How would you calculate [HCO3-]?

A
  • Renal compensation (hours to days)
    • The kidneys secrete more H+ (due to increased PaCO2)
      • reabsorb all the filtered HCO3-
      • increase formation of TA and NH4+
      • increase new HCO3- production (increase HCO3-)
      • excrete an acidic urine
    • plasma HCO3- increases– a base excess develops
    • Expected HCO3- at madimal compensation:
32
Q

What conditions can lead to acute ihibition of the medullary respiratory center?

Chronic?

A
  • Acute
    • drugs, opiates, anesthetics, seditives
    • oxygen in chronic hypercapnia
    • cardiac arrest
    • central sleep apnea
  • Chronic
    • extreme obesity (Pickwickian syndrome)
    • central nervous system lesion (rare)
33
Q

What disorders of the respiratory muscles and chest wall can lead to acute respiratory acidosis?

Chronic respiratory acidosis?

A
  • acute
    • muscle wakness - myasthenia gravis, periodic paralysis, aminoglycosides, Guillain-Barre syndrome, severe hypokalemia or hypophosphatemia
  • chronic
    • muscle weakness - poliomyelitis, amyotrophic lateal sclerosis, multiple sclerosis, myxedema
    • kyphoscoliosis
    • extreme obesity
34
Q

What type of airway obstruction can lead to acute respiratory acidosis?

A
  • acute
    • aspiration of foreign body or vomitus
    • obstructive sleep apnea
    • langospasm
35
Q

What disorders affecting gas exchange across the pulmonary capillary can cause acute respiratory acidosis?

Chronic respiratory acidosis?

A
  • acute
    • exacerbation of underlying lung disease (including increased CO2 production with high carbohydrate diet)
    • adult respiratory distress syndrome
    • acute cardiogenic pulmonary edema
    • sever asthma or pneumonia
    • pneumothorax or hemothorax
  • chronic
    • chronic obstructive pulmonary disease: bronchitis, emphysema
36
Q

What impact does hyperventilation have on acid/base status?

A
  • Hypoventilation –> Respiratory Alkalosis
    • leading to excess CO2 elimination
    • decreased PaCO2 (hypocapnia)
37
Q

What conditions indicated acute respiratory alkalosis?

How would you calculate [HCO3-​]?

A
  • Opposite directions
    • decrease PaCO2 ( <40 mmHg)
    • incrase pH (decrease [H+])
  • Small decrease in HCO3 but no base deficit,
  • the new HCO3 concentration can be approximated by:
38
Q

What conditions indicated chronic respiratory alkalosis?

How would you calculate [HCO3-​]?

A
  • Renal compensation (hours to days)
    • The kidneys secrete less H+ (due to decreased PaCO2)
      • fail to reabsorb all the filtered HCO3- and some HCO3- and some HCO3- stays in teh tubule and is excreted
      • relatively alkaline urine
    • Plasma HCO3- decreases and a base deficit develops
    • Expected HCO3- at maximal compensation
39
Q

What conditions can cause hypoxemia, leading to respiratory alkalosis?

A
  • Alkalosis
    • pulmonary disease: pneumonia, interstitial fibrosis, emboli, edema
    • congestive heart failure
    • hypotension or severe anemia
    • high-altitude residence
40
Q

What conditions directly stimulate the medullary respiratory center leading to respiratory alkalosis?

A
  • Stimuation of Medullary Respiratory Center
    • psychogenic or voluntary hyperventilation
    • hepatic failure
    • gram-negative septicemia
    • salicylate intoxicatoin
    • postcorrection of metabolic acidosis
    • pregnancy and the luteal phase of the menstrual cycle (due to progesterone)
    • neurologic disorder: cerebrovascular accidents, pontine tumors
41
Q

What is the primary disturbance in metabolic acidosis?

A

derease in plasma HCO3

  1. increased H+ (diabetic ketoacidosis)
  2. loss of HCO3- (diarrhea)
  • Combination of decrease in pH and a decrease in [HCO3-] in teh same direction
    • a base deficit develops & can be used to assess the severity of the disturbance
42
Q

Describe respiratory compensation in metabolic acidosis.

How would you calculate the expected PaCO2?

A
  • Respiratory compensation (…minutes to hours)
    • low pH stimulates peripheral chemoreceptors which increase ventilatio, leading to a decrease in PaCO2
    • no real “acute” phase b/c respiratory system begins increasing ventilation with the onset of the acidosis, and PaCO2 begins to fall
    • Tendency for the central chemoreceptors to limit the extent of the hyperventilation (low PaCO2 reduces drive to breathe)
    • Expected PaCO2 with respiratory compensation:
43
Q

Describe renal compensation of metabolic acidosis.

What is the maximally acidic urine?

A
  • Renal compensation (hours to days)
    • since the primary disturbance is a fall in plasma HCO3-, the filtered load of HCO3 will be reduced
    • Total H+ secretion is reduced (decreaed FLHCO3 and decreased PCO2)
    • Instead, the kidney forms more TA and NH4+ and therefore excretes more H+
    • Produces more new HCO3 to reduce the base deficit
    • maximally acidic urine (~pH 4.5)
44
Q

Why is there an anion gap in metabolic acidosis & how do you calculate it?

What is the normal value?

A

Anion gap develops due to the accumulationof fixed acids

Anion gap represents “unmeasured anoins” taht balance Na+ in place of the lost HCO3-

normal value is 9-13

45
Q

What are the most common causes of metabolic acidosis with an anion gap?

A

MULEPAK

  • M: methanol
  • U: uremia
  • L: lactate
  • E: ethylele glycol
  • P: paraldehyde
  • A: aspirin
  • K: ketones
46
Q

What is the primary disturbance of metabolic alkalosis?

A

increase in plasma HCO3-

  1. loss of H+ (excessive vomiting)
  2. gain of HCO3- (overuse of diuretics)
  • the combination of increase in pH and increase in HCO3- confirms metabolic alkalosis – change in the same direction
  • A base excess ([HCO3-] and [A-]) develops and can be used to assess the severity of the disturbance
47
Q

Describe respiratory compensation of metabolic alkalosis

How would you calculate the expected PaCO2?

A

not very good & doesn’t last very long

  • Respiratory compensation (minutes to hours)
    • High pH inhibits peripheral chemoreceptors which decreases ventilation, leading ot an increase in PaCO2
    • tendency for the chemoreceptors to limit the extend of the hypercapnia (central) and hypoxemia (peripheral) due to hypoventilation
    • Expected PaCO2 with respiratory compensation:
48
Q

Describe renal compensation of metabolic alkalosis

A
  • Renal compensation (hours to days)
    • since the primary disturbance is an increase in plasma HCO3-, the filtered load of HCO3- is increased
    • the increased PaCO2 increases renal H+ secretion and increases HCO3- reabsorption, compromising the degree of compensation
    • excess HCO3- is excreted resultin in a realtively alkaline urine
49
Q

Renal compensation of metabolic alkalosis is impaired under what two conditions?

Describe why this is the case.

A
  • Volume depletion
    • increase aldosterone release increases distal nephron Na+ reabsorption and increases H+ (and K+) secretion
      • increase in new HCO3-
  • K+ - depletion
    • decreases in Na+- K+ exchange in the distal nephron and increases H+ secretion ( to offset the reduced K+ secretion)
      • increase new HCO3-
  • BOTH conditions increase new HCO3- production and reabsorption perpetuating the alkalosis
50
Q

Why might someone fail to achieve the expected degree of compensation?

A

It is possible to have 2 acid-base disorders at the same time

this may reflect a mixed disorder

51
Q

What conditions might suggest that a person has mixed acidosis and alkalosis conditions?

A

pH in the normal range

PaCO2 and HCO3- out of normal ranges

one is probably a chronic condition

S2B5 Physiology (10 decks)

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