Lecture 26 - Acid Base and Control of Ventilation Flashcards
Henderson-Hasselbach equation?
pH = 6.1 + log (HCO3-)/0.03 PCO2
Result of rise in CO2?
Respiratory acidosis
Result of fall in CO2?
Respiratory alkalosis
Result of rise in HCO3-?
Metabolic alkalosis
Result of fall in HCO3-?
Metabolic acidosis
How does the transport of CO2 in blood affect blood?
Powerful effect on the acid-base balance of the blood
Normal pH?
7.4
“-emia”?
Blood
What does alkalemia mean?
High blood pH > 7.4
What does acidemia mean?
Low blood pH < 7.4
What does alkalosis mean?
Disease leading to alkalemia
What does acidosis mean?
Disease leading to acidemia
What 2 systems manage the acid-base balance of the blood? Compare them.
- Lung with CO2 management: QUICK
2. Renal metabolic system with HCO3- management: SLOW
6 primary disorders of acid base balance?
- Acute respiratory acidosis
- Chronic respiratory acidosis
- Acute respiratory alkalosis
- Chronic respiratory alkalosis
- Metabolic acidosis
- Metabolic alkalosis
Change in pH due to acute change in PaCO2 of 10 mmHg in clinically relevant pH range?
Change pH by 0.08 in opposite direction
Change in pH due to acute change in PaCO2 of 20 mmHg in clinically relevant pH range?
Change pH by 0.16 in opposite direction
How do the kidneys function to manage the acid-base balance of the blood when hyper or hypoventilation alter the CO2 content in blood? What is this called? What to note?
Over hours/days they retain/release HCO3- leading to a compensatory acidosis or alkalosis correcting the pH partially = chronic compensated respiratory alkalosis/acidosis
Never fully compensated because the abnormality is causing the compensation so when pH reaches the normal range the compensatory mechanism stops instead of continuing until 7.4 => pH will still be acidemic or alkalemic
2 types of respiratory acidosis or alkalosis?
- Acute uncompensated
2. Chronic compensated
Change in pH due to chronic change in PaCO2 of 10 mmHg in clinically relevant pH range?
Change pH by 0.03-0.05 in opposite direction
Does the pH ever reach 7.4 in chronic compensated respiratory alkalosis/acidosis?
NEVER
Describe metabolic acidosis.
Drastic reduction in HCO3- => acidosis => lungs quickly react and hyperventilate to partially correct it => pH remains low (acidemia) + HCO3- is low (metabolic acidosis) + PCO2 is low (respiratory compensation)
Can one distinguish an acute metabolic derangement from a chronic one based on blood gas alone? Why?
NOPE cause lungs are so quick to compensate
Describe metabolic alkalosis.
Drastic increase in HCO3- => alkalosis => lungs quickly react and hypoventilate to partially correct it => pH remains high (alkalemia) + HCO3- is high (metabolic alkalosis) + PCO2 is high (respiratory compensation)
How can acid base status of blood be measured?
Using an arterial blood gas test to measure:
- PaO2
- PaCO2
- pH
- HCO3- (computer calculate using HH equation)
How to determine which primary disorders of acid base balance it is? What 2 numbers are needed?
- Primary disorder: alkalemia or acidemia determines acidosis or alkalosis
OR if pH is normal but CO2 is not: that means there are 2 primary disorders working in opposite directions - Respiratory derangement? If it does not match the primary disorder than the primary disorder must be metabolic
- If primary disorder is respiratory, is it acute or chronic? OR if pH change is higher than 0.8, both respiratory and metabolic disorders happening in same direction?
- If chronic, what is the compensatory metabolic disorder (always opposite the primary disorder)?
ONLY pH and PaCO2 needed
If the pH change is HIGHER than 0.8 per 10 mmHg, what can we assume?
BOTH metabolic and respiratory disorders happening together in the same direction
What are the axes of a Davenport diagram?
- X-axis: pH
- Y-axis: plasma HCO3-
- Z-lines: PCO2 (number to left of line)
How to read a point on a Davenport diagram to determine primary disorder?
- Track to x-axis to read pH
- Follow the z-line for PCO2
Follow the technique!
Normal plasma HCO3-?
24 mEq/L blood
What does it mean if the pH is deranged, but the CO2 is normal?
Metabolic disorder + respiratory issue so lungs cannot compensate
Davenport diagram: jump from one line to line to the right?
Respiratory alkalosis
Davenport diagram: jump from one line to line to the left?
Respiratory acidosis
Which nerves are responsible for controlling respiratory output? What brain center controls these?
Phrenic nerves controlled by pons and medulla, which can be overriden by the cortex
From what do the pons and medulla receive input to control respiratory output?
- Chemoreceptors
- Lungs
- Cortex
2 types of chemoreceptors regulating respiratory output? Describe each.
- Central chemoreceptors in medulla responding to changes in blood pH and PaCO2
- Peripheral chemoreceptors in aortic and carotid bodies responding to hypoxia (low PaO2 causing low CaO2), pH, and PaCO2
What are peripheral chemoreceptors most sensitive to? List the 3 factors in order. Which one determines minute ventilation? Why?
- Hypoxia
- pH
- PaCO2***
Because the hypoxia has a lower threshold to kick in (PaO2 of 50 mmHg) and the body maintains constant pH
Trick to be able to hold your breath for longer? Why is this dangerous?
- Hyperventilate to lower CO2
- Hold your breath
=> PaCO2 threshold of chemoreceptors will take longer to be reached
Dangerous because person may not have enough time to surface to avoid drowning secondary to hypoxia
Main 2 causes of COPD?
- US: smoking
2. Most of the world: cooking over biomass fuels
2 types of COPD? Describe each.
- Emphysema: damaged alveoli
2. Chronic bronchitis: more narrow airways
In patients with COPD, which factor determines the minute ventilation? Big treatment mistake if they come into hospital being sick?
Because breathing is difficult, the patient’s body will adjust over time to decrease respiratory rate => decreased respiratory rate will augment CO2 retention => respiratory acidosis => over time the kidneys adjust to release HCO3- in attempt to maintain pH => chronic compensated respiratory acidosis => dangerous cycle where the chemoreceptors become increasingly desensitized to a continuous increase in PaCO2 as the patient breathes less over time => silenced CO2 alarm => after a certain period, the patient’s oxygen levels will become so low that hypoxic drive becomes the main input controlling respiration
Big treatment mistake if they come in to hospital hypoxic because they are sick and you give them 100% O2 they will stop breathing because no more respiratory drive = hypercapnic coma
Which response is slower: central or peripheral chemoreceptor response to increase PaCO2?
Central chemoreceptor response is SLOWER
How does the ventilatory response vary during sleep?
It decreases
How does the ventilatory response vary if the work of breathing is increased?
It decreases
What is the major stimulus to ventilation at high altitude?
Hypoxia
PaO2 in mild CO poisoning?
Normal
