Respiratory acidosis or alkalosis occurs when a change in respiratory function causes a disturbance in pH
what is blood pH proportional to?
what is it called when pH is low? High?
what happens when one system is dysfunctional?
explain how the different systems can change the pH
As blood pH is proportional to the ratio of HCO3- to CO2, excessive changes may result from respiratory (CO2) or metabolic (HCO3-) dysfunction (↓pH = acidosis, ↑pH = alkalosis).
If one system is dysfunctional, other system will try to compensate and bring pH back to normal e.g respiratory acidosis by hyperventilation -> the metabolic system will try to compensate by inducing metabolic alkalosis
↑Ventilation = ↓PaCO2= ↑ pH ↓Ventilation = ↑PaCO2= ↓ pH ↓ HCO3 excretion = ↑[HCO3-] =↑ pH ↑ HCO3 excretion = ↓[HCO3-] =↓pH (unless PaCO2 or HCO3 changes proportionally, in the opposite direction)
what causes the increased pH?
Low pH accompanied by high PaCO2 is termed respiratory acidosis, as hypoventilation is responsible for the increase in CO2 levels and decreased pH
↓ventilation ↓ ↑PACO2 ↓ ↑PaCO2 (hypercapnia) ↓ ↑[H+] = ↓pH (acidosis)
Respiratory acidosis - what happens in the case of chronic hypo-ventilation?
what happens if no chronic hypo-ventilation?
In the event of chronic hypo-ventilation, HCO3- excretion must decrease to maintain normal pH.
↓HCO3 excretion by kidney as the renal system will detect there is a decrease in pH therefore try to retain bi-carbonate in the body -> as it is alkaline so up pH
Also, there will be an increased chemoreceptor feedback to increase repsiratory rate hence increase ventilation
If any pathology affects this, it’ll cause chronic respiraotry acidosis/hypoventilation
what causes this and the high pH?
High pH accompanied by low PaCO2 is termed respiratory alkalosis, as hyperventilation is responsible for the decrease in CO2 levels and increased pH
↑ventilation ↓ ↓PACO2 ↓ ↓PaCO2 (hypocapnia) ↓ ↓[H+] = ↑pH (alkalosis)
Respiratory alkalosis - what happens in the case of chronic hyper-ventilation?
if not chronic hyper-ventilation?
In the event of chronic hyperventilation, HCO3- excretion must increase to maintain normal pH.
↑HCO3 excretion by kidney as a means to lower pH
Also, there will be an decreased chemoreceptor feedback to decrease repsiratory rate hence decrease ventilation
Causes of hyperventilation: anxiety
what does anxiety cause?
what reflex follows up on this?
why isnt this sufficient enough to bring the breathing rate down?
Anxiety trigger → panic attack ↓ Increased ventilation (tachypnoea) without increased metabolic demand ↓ Hyperventilation → Decreased PaCO2 ↓ Respiratory alkalosis
the reflex in a healthy person will still be there hence decreased chemoreceptor feedback and decreased respiratory rate
BUT because of the strength of the kind of emotional stimulus + anxiety panic attack, it isn’t suffiecient to bring breathing rate down so breathing rate remains high
Intervention for anxiety attack
why does this intervention work?
classic intervention is to get the person to breathe into a paper bag -> inspiring expired air will recycle the co2 + keep in body rather than expel into the environment
Hence you will breathe in more co2 and keep more co2 in body
therefore correct co2 previously lost + correct alkalosis
Causes of respiratory alkalosis: altitude
what happens at higher altitude? how does body accomodate to this and effect of this?
At sea level, PAtm ≈ 100kPa 100kPa x 21% O2 ≈ 21kPa, CO2 ≈ 0kPa ↓ At 8000ft, PAtm ≈ 75kPa 75kPa x 21% O2 ≈ 15kPa, CO2 ≈ 0kPa ↓ ↑ alveolar ventilation to try and maintain normal PAO2 & PaO2 (via hypoxic drive) ↓ Increased ventilation = ↓PaCO2 ↓ Respiratory alkalosis
Higher altitude - what happens if breathing at normal rate?
why? and effect of this?
If breathing normally, individual will become hypoaemic due to decreased pressure gradient in the alveoli
This will be detected by peripheral chemoreceptors (hypoxia + less o2) hence there will be increased alveolar ventilation by hypoxic drive to maintain normal level of o2
How to avoid respiratory alkalosis with increased altitude?
To avoid respiratory alkalosis, try to ascend at a relatively low rate
Compensatory mechanisms in body e.g. renal system can excrete more HCO3 to compensate for the increase in pH
what causes the low pH? (3 things that can do this)
what is the compensatory reflex and how does it recognise it?
Low pH accompanied by low [HCO3-] is termed metabolic acidosis, as excessive metabolic acid production and/or increased excretion of HCO3- is responsible for the decreased pH
𝑝𝐻∝(↓[𝐻𝐶𝑂3− )/〖𝑃𝑎 𝐶O2 )
↓absorption or ↑excretion of HCO3- OR Addition of H+ (reacts with available HCO3-)
Unless PaCO2 changes in proportion with [HCO3-] (in the opposite direction), acidosis (↓pH) will occur.
Respiratory compensation (↑ventilation) occurs almost instantly, and attempts to return pH back to normal range (impacts the levels of co2 in CSF and central/peripheral chemo recptors separately inducing a reflex compensation)
Metabolid acidosis - correction pathway
Excessive acid production and/or insufficient [HCO3-] ↓ ↑[H+] = ↓pH (acidosis) ↓ ↑Chemoreceptor feedback ↓ ↑Respiratory rate ↓ Respiratory compensation (↑ventilation) ↓ ↓PaCO2
Causes of metabolic acidosis: Lactic acidosis (sepsis)
Infection ↓ Pathological immune response ↓ Septic shock ↓ ↓oxygen delivery to tissues (hypoxia) ↓ ↑Lactic acid production & ↓pH
Respiratory compensation to ↑O2 delivery and ↑lactic acid conversion
Causes of metabolic acidosis: other
3 other causes?
which of the 3 parameters do they relate?
↑ fatty acid release from liver due to insulin deficiency =↑ (acidic) ketone body production
Diarrhoea (e.g. decreased HCO3- absorption in colon)
Renal failure (e.g. decreased HCO3- reabsorption in proximal tubule)
what causes this? 3 things
High pH accompanied by high [HCO3-] is termed metabolic alkalosis, as reduced metabolic acid production or reduced excretion of HCO3- is responsible for the increased pH
𝑝𝐻 ∝ (↑𝐻𝐶𝑂3− )/(𝑃𝑎 𝐶𝑂2)
Removal of H+ (less reacts with available HCO3-)
↑absorption or ↓excretion of HCO3-
Unless PaCO2 changes in proportion with [HCO3-] (in the opposite direction), alkalosis (↑pH) will occur. Respiratory compensation (↓ventilation) attempts to return pH back to normal range.
Metabolic alkalosis - correction pathway
Excessive acid removal and/or Excessive [HCO3-] ↓ ↓[H+] = ↑pH (alkalosis) ↓ ↓Chemoreceptor feedback ↓ ↓Respiratory rate ↓ Respiratory compensation (↓ventilation) ↓ ↑PaCO2
Causes of metabolic alkalosis
3 causes? which parameter effected?
Diuretics (changes to H+ and HCO3- reabsorption)
Antacids (↑HCO3- consumption)
Vomiting (loss of H+ in stomach acid)
Examples of the effects of acid-base disorders: acidosis-induced hyperkalaemia
name the two exchangers for cells? net effects?
why is there an issue with acidosis?
what is the overall effect? what pathologies can this lead to?
one mechanism is via initial exchange of H+ and Na+ (hydrogen efflux, sodium influx), followed by Na+ and K+ exchange (sodium efflux, potassium influx) – the net effect is that potassium ions enter the cell in exchange for hydrogen ions leaving.
However the initial step involving diffusion of H+ out of the cell in exchange for Na+, relies on the presence of a H+ concentration gradient – the concentration of H+ inside the cell must be greater than the concentration outside the cell. In the event acidosis, this process breaks down as pH falls, representing an increase in blood and extracellular [H+].
The overall effect is that uptake of K+ by cells is reduced in response to acidosis, leading to potassium accumulation within the extracellular fluid in blood. Because K+ have critical roles in membrane potential and muscle function, cells such as skeletal muscle and cardiac pacemaker cells are adversely effect, as can be observed by the symptoms of cardiac arrhythmia and muscle weakness observed in patients with hyperkalaemia
Acidosis = ↑[H+]extracellular ↓ ↓H+ conc. gradient ↓ ↓H+ excretion = ↓H+ - Na+ exchange = ↓Na+ - K+ exchange ↓ ↓Na+ - K+ exchange = ↓K+ absorption ↓ K+ accumulation in serum = hyperkalaemia ↓ Cardiac arrhythmias + Muscle weakness
Examples of the effects of acid-base disorders: alkalosis-induced cerebral vasoconstriction
what acts as a vasodilator? which vessels are particualry sensitive?
issue with hyperventilation? effects?
CO2 (via H+) acts as a vasodilator in blood vessels (cerebral arteries particularly sensitive)
Hyperventilation = ↓CO2 and ↓H+ (alkalosis)
Alkalosis causes vasoconstriction of cerebral arteries
↓ cerebral blood flow = headache, lightheadedness, confusion, seizures
Minute ventilation of the lungs rapidly increases rapidly after exercise begins.
Q: How would you expect this response to be mediated/controlled?
why may PaCO2 decrease a bit with exercise?
In healthy individuals, PaCO2 does not increase during exercise (in fact it may decrease slightly). This is because ventilation increases before the extra CO2 produced by muscles can increase PaCO2.
The mechanism of this response is not fully understood; proposed hypotheses involve direct feedback between muscle activity/motor cortex and respiratory centres, changes in body temperature, or micro-oscillations in PaO2/PaCO2.
acidosis summary - causes
Arterial ph = <7.35
increased lactic acid (sepsis)
Increased ketone bodies (diabetes)
Decreased kidney acid secretion (renal failure)
decreased HCO3- reabsorption (renal acidosis)
Diarrhoea (loss of HCO3- from gut)
acidosis summary - effects
Tachypnoea - abnormal rapid breathing muscular weakness headache confusion, coma cardiac arrythmia hyperkalaemia
acidosis summary - compensatory mechanisms
Hyperventilation (decreased PaCO2, respiratory compensation)
Decreased HCO3- excretion (renal compensation)
alkalosis summary - causes
arterial pH = >7.45
Vomiting (loss of H+ in HCL)
Increased Kidney acid excretion (diuretics)
Increased Alkalotic agent consumption (antacids, NaHCO3)
alkalosis summary - effects
Bradypnoea Muscular weakness, cramps, tetany Heachache, Nausea Lightheadness, confusion, coma Cardiac arrhythmia Hypokalaemia
alkalosis summary - compensatory mechanisms
Hypoventilation (increased PaCO2, respiratory compensation)
Increased HCO3- excretion (renal compensation)