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A Physiology > 3.8. The role of ventilation in the regulation of the pH, in the development and compensation of the acid-base imbalances in the body. > Flashcards

3.8. The role of ventilation in the regulation of the pH, in the development and compensation of the acid-base imbalances in the body. Flashcards

1
Q

I. Alveolar CO2-tension
1. Which organ does pCO2 depend mostly on?

A

respiration (alveolar ventilation equation)

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2
Q

I. Alveolar CO2-tension
2. Which equations we can you to find pCO2?

A

pCO2 depends mostly on respiration (alveolar ventilation equation), and since we can find pCO2 in the Henderson- Hasselbalch equation as well:
- We can alter the pH of the blood with our respiration (easily and quickly)

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3
Q

I. Alveolar CO2-tension
3. How does rate of ventilation determine the pCO2?

A
  • Increase in alveolar ventilation -> lower pCO2
  • Decrease in alveolar ventilation -> higher pCO2
  • The relationship between the ventilatory rate and the pCO2 is expressed as following:
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4
Q

I. Alveolar CO2-tension
4. What are the consequences of changing pCO2 in blood?

A
  • Increase in pCO2 -> lower pH
  • Decrease in pCO2 -> higher pH
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5
Q

I. Alveolar CO2-tension
5. Why isn’t the key thing for our respiration necessarily O2?

A

Key thing for our respiration is not necessarily O2, but to maintain pCO2-levels for the pH

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6
Q

II. Effect of alveolar ventilation on pCO2 and pO2
1. Characteristics of Hyperventilation

A

Hyperventilation: when ventilation is more than metabolically necessary
- pCO2 < 40mmHg
- pCO2 decreases => pH↑

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7
Q

II. Effect of alveolar ventilation on pCO2 and pO2
2. Characteristics of Hypoventialtion

A

Hypoventilation: when ventilation is less than metabolically necessary
- pCO2 > 40mmHg
- pCO2 increases => pH↓

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8
Q

II. Effect of alveolar ventilation on pCO2 and pO2
3. Can respiration regulate pH? Give examples

A

Respiration can regulate the pH: can either be the solution to the problem or the cause of the problem
- Ex: in high altitudes, where O2-levels are low, we ventilate a lot (hyperventilation = pH↑)
- pH increase important for saturation of Hb (pushes the Hb-saturation curve to the left)

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9
Q

III. Chemoreceptors and acid-base balance
1. What are the 2 types of chemoreceptors participate in acid-base balance?

A
  1. Central chemoreceptors (CCR)
  2. Peripheral chemoreceptors (PCR)
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10
Q

III. Chemoreceptors and acid-base balance
2A. How can Central chemoreceptors (CCR) regulate pH?

A
  • represents 75% of the ventilation drive at rest
  • located in CNS (ventrolateral medulla)
  • CCRs senses ([H+]) pH in ECF and CSF, indirectly by measuring the pCO2
    +) There is a BBB here: only CO2 can pass – H+ and HCO3- cannot
    +) CO2 will become H+ and HCO3-, and there will be an increase in HCO3- and H+ in CSF
    o H+ is in nmol-range, while HCO3- are in mmol-range
    => pCO2↑ = pH↓: HCO3- - level cannot change it (short term)
    => Adaptation, due to many mechanism the HCO3- level will increase and decrease the pH to normal values (long term)
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11
Q

III. Chemoreceptors and acid-base balance - Central chemoreceptors (CCR)
2B. Why isn’t the HCO3- changing?

A

o Because there is no other buffer in the CSF, only the CO2/HCO3- -
buffer
o But if a change happens in HCO3-:
- It cannot buffer so much because H+ is increasing (due to CO2)
- HCO3- should counter the pH-changing effect of CO2, but it is
difficult since no others are present

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12
Q

III. Chemoreceptors and acid-base balance
3. How can Peripheral chemoreceptors (PCR) participate in acid-base balance?

A
  • Located in the aortic arch (aortic bodies) and carotid bifurcation (carotid bodies)
  • Senses pH and arterial pO2 directly (+ CO2-levels)
  • Less sensitive to pCO2
    => If the CCRs have adapted to some unusual pCO2-levels, the PCRs can detect that the pH is not normal (very important mechanism)
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13
Q

IV. ACID-BASE DISORDERS
1. Integration of pH control systems
a) How does pH control system work?

A

There is a constant acid challenge in the body. Therefore, we have different lines of defenses
- 1st line of defense: chemical buffering
- 2nd line of defense: respiratory buffering
- 3rd line of defense: renal buffering

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14
Q

IV. ACID-BASE DISORDERS
1. Integration of pH control systems
B) How does 1st line of defense: chemical buffering work?

A
  • Chemically buffer the protons that are being produced
  • 70mmol of nonvolatile acids are to be buffered
  • Works rapidly (second-scale)
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15
Q

IV. ACID-BASE DISORDERS
1. Integration of pH control systems
B) How does 2nd line of defense: respiratory buffering work?

A
  • Buffer mainly the CO2 (volatile acid)
  • Exhale 15,000mmol of CO2
  • Works relatively fast (minute-scale)
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16
Q

IV. ACID-BASE DISORDERS
1. Integration of pH control systems
C) How does 3rd line of defense: renal buffering work?

A
  • Acts slowly (hour-scale)
  • Production of ‘’new’’ HCO3-
  • H+ excreted (combined with urinary buffers)
  • NH4+ traps H+
    => Last to processes protect the bladder, without the buffer the environment in the urinary bladder would be very acidic (like in the stomach!)
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17
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
A. What are Acidosis & Alkalosis?

A
  1. Acidosis = acidemia (pH < 7,35) and/or altered pCO2 +/- act [HCO3-]
  2. Alkalosis = alkalemia (pH > 7,45) and/or altered pCO2 +/- act [HCO3-]
    => Acidosis and alkalosis are not about pH of the blood, these are situations that are acid-base disorders
18
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
B. What happen if a patient with acid-base disorder goes to the doctor?

A
  • Measure pH (decide if acidosis or alkalosis)
  • Then look at pCO2 and HCO3- - levels (respiratory / metabolic)
    => But if both pCO2 – and HCO3- - levels have changed, then we the doctor needs to think about which of these changes would lead to acidosis/alkalosis on its own
19
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
C2. What are Causes of RESPIRATORY ACIDOSIS?

A
  • pulmonary diseases, ex: obstructive lung diseases – pulmonary emphysema (lung damaged, ventilation not working, reduced gas exchange)
  • high pCO2 in the inhaled air (gas exchange does not function)
  • drugs (overdose of opioids => inhibits medullar respiratory centers = lower ventilation) DEADLY!
20
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
D2. What are Causes of Respiratory alkalosis?

A
  • voluntary hyperventilation
  • high altitude (low pO2 and higher pCO2 => hyperventilate)
  • Iatrogenic (induced by doctors) drug side effects (e.g., aspirin => stimulate respiratory centers => hyperventilation)
21
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
C3. What are Compensation of RESPIRATORY ACIDOSIS?

A

Compensation: pH gets closer to 7,4 (renal compensation = slow)
- renal NAE increases -> kidney produces new HCO3-
- increased BB and BE
- increased standard [HCO3-] > 24mM
- increased further in actual [HCO3-]&raquo_space; 24mM
=> as long as the original problem is there, pCO2 remains high (pulmonary emphysema)

22
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
D1. What are characteristics parameters of Respiratory alkalosis?

A
  • pH > 7,45
  • paCO2 < 40mmHg (pH↑)
  • no change in buffer base (BB) and buffer excess (BE)
  • unchanged standard [HCO3-]
  • decreased actual [HCO3-] < 24mM
23
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
D3. What is the Compensation of Respiratory alkalosis?

A

Compensation: => pH gets closer to 7,4
- renal NAE decreases -> H+ - excretion
- decreased BB and BE
- decreased standard [HCO3-] < 24mM (↓HCO3- -
reabsorption)
- further decrease in actual [HCO3-]

24
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
E1. What are the characteristics parameters of Nonrespiratory (metabolic) acidosis?

A
  • pH < 7,35
  • unchanged paCO2
  • decreased BB (<44mEq/L) and decreased BE (<2,5mEq/L)
  • decreased standard [HCO3-] < 24mM
  • decrease in actual [HCO3-] <24mM (pH↓)
25
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
E2. What are the Causes of Nonrespiratory (metabolic) acidosis?

A
  • diabetes (accumulation of keto acids)
  • renal failure (inability of kidneys to get rid of 70mmole of fixed acid)
  • diarrhea (lose HCO3- via feces)
  • physical exercise (increased production of lactate – eat up HCO3-)
26
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
E3. What is the compensation of Nonrespiratory (metabolic) acidosis?

A

Compensation: pH gets closer to 7,4
- hyperventilation -> paCO2 < 40mmHg (Kussmaul – respiratory pattern of a diabetic patient => deep respiration + high frequency = ↓paCO2)
- renal NAE increases (if it can – diabetes)
- partial restoration of BB and BE (if possible)
- partial restoration of standard [HCO3-], but still <24mM
- complex changes, but still decreased actual [HCO3-]
>24mM

27
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
F1. What are characteristic parameters of Nonrespiratory (metabolic) alkalosis?

A
  • pH > 7,45
  • unchanged paCO2
  • increased BB (>49mEq/L) and BE (>2,5mEq/L)
  • increased standard [HCO3-] > 24mM (pH↑)
  • increased actual [HCO3-] > 24mM
28
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
F2. What are the causes of Nonrespiratory (metabolic) alkalosis?

A
  • lost gastric acid (by vomiting due to drug overdose -> ↑ [HCO3-] in the blood)
  • Hyperaldosteronism (increased [aldosterone] -> ↑H+-secretion = alkalosis)
  • Uncontrolled intake of alkalis (used for ulcers – damaging the stomach = overused)
29
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
F3. What is the compensation for Nonrespiratory (metabolic) alkalosis?

A

Compensation: pH gets closer to 7,4
- Hypoventilation -> paCO2 > 40mmHg
- renal NAE decreases
- partial restoration of BB and BE (if possible)
- partial restoration of standard [HCO3-], but still > 24mM
- complex changes but still increased actual [HCO3-] > 24mM

30
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
G1. What are the characteristic parameters of Mixed type acidosis?

A
  • pH &laquo_space;7,35
  • paCO2 > 40mmHg
  • decreased BB (<44mEq/L) and BE (<2,5mEq/L)
  • decreased actual [HCO3-] <24mM
  • complex changes in actual [HCO3-]
31
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
G2. What are the Causes of Mixed type acidosis?

A

Causes: more than 1 disease!
- E.g., diabetes + chronic obstructive pulmonary disease (COPD) or kidney failure + drug overdose

32
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
G3. What is the compensation for Mixed type acidosis?

A

Compensation: -> pH gets closer to 7,4 (options limited + takes time)
*** Situation where doctor needs to buy time by adding acids/bases to patient pushing pH to normal, till they find a treatment for the root cause of the underlying problem
- Increased ventilation to decrease paCO2 (if possible)
- renal NAE increases (if it can)
- partial restoration of BB and BE (if possible)
- partial restoration of [HCO3-]
- complex changes in actual [HCO3-]

33
Q

IV. ACID-BASE DISORDERS
2. Acid-base disorders
H. Fill in the table

34
Q

IV. ACID-BASE DISORDERS
3. Anion gap
A. What is anion gap?

A

Anion gap is the difference between measured cations (Na+) and measured anions in plasma. Usually use this technique to diagnose metabolic acidosis.

35
Q

IV. ACID-BASE DISORDERS
3. Anion gap
B. How do we use anion gap?

A
  1. Useful value because metabolic acidosis has many causes
    - Accumulation of ‘’new’’ acids => dissociate to proton and anion (lactate)
    - Net loss of HCO3-
  2. With this technique, we can find the unmeasured anions in the blood = protein, phosphate, citrate, sulfate
  3. Usually: AG ≈ 8-16 mEq/L
  4. If AG is high or sum of cations is higher than sum of anions, there must be unmeasured anions (ex: proteins) in the plasma
    => Metabolic acidosis is then due to something that has been produced in the body, which is an acid
36
Q

IV. ACID-BASE DISORDERS
4. Ca2+ and K+ - levels in acid-base disorders
A1. Why are Calcium levels affected a lot by pH?

A

Ca2+-levels are affected a lot by pH, because:
- Calcium likes to bind to albumin
- If albumin and plasma proteins have more negative charges -> Ca2+ will bind more frequently
=> Shift from freely available Ca2+ to protein bound Ca2+ (freely available Ca2+↓)

37
Q

IV. ACID-BASE DISORDERS
4. Ca2+ and K+ - levels in acid-base disorders
A2. How and when can this Shift from freely available Ca2+ to protein bound Ca2+ (freely available Ca2+↓ happen?

A
  • Plasma proteins are buffers -> buffering means if there is a change in pH, they may bind or release a proton
  • If pH↑ -> the buffers (plasma proteins) start to release their H+ = more negative charges in their structure
    => Ca2+-ions will bind = [Ca2+] of freely available↓
38
Q

IV. ACID-BASE DISORDERS
4. Ca2+ and K+ - levels in acid-base disorders
A3. Why is it a problem if there are abnormal Ca2+ levels?

A
  • [Ca2+]-ions↓ = threshold for voltage-gated Na+-channels also↓
    => Action potentials occur more easily -> causes random body contractions
    => Deadly if contractions are related to respiratory muscles
39
Q

IV. ACID-BASE DISORDERS
4. Ca2+ and K+ - levels in acid-base disorders
B1. Why are K+ levels important?

A
  1. Important molecule in setting the membrane potential.
  2. Depends on pH
40
Q

IV. ACID-BASE DISORDERS
4. Ca2+ and K+ - levels in acid-base disorders
B2. How can K+ can cause cardiac arrythmia?

A

Important molecule in setting the membrane potential. If K+-levels change:
- Whole GHK- and Nernst-equation changes
- If we alter the [K+], then membrane and equilibrium potential changes
- Functions which rely on the membrane a lot, can have problems (heart, SA node rely on proper membrane potential-related changes)

41
Q

IV. ACID-BASE DISORDERS
4. Ca2+ and K+ - levels in acid-base disorders
B3. How can K+ cause problem in pH regulation?

A

Potassium levels also depend on the pH-value:
- (+) 0,1 pH -> (-) 0,5mM [K+]
- Acidosis -> hyperkalemia ([K+]↑)
- Alkalosis -> hypokalemia ([K+]↓)

During acidosis, the return of K+ into the tubular lumen (via ROMK1) is inhibited
=> K+-reabsorption↑ -> hyperkalemia [K+]↑

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