Acidosis = 7.2
Alkalosis = 7.6
Normal = 7.35-7.45
Art Blood = 7.5
Venous Blood = 7.4
1. Changes in excitability of nerves and mucles cells
2. Marked influuence on enzyme activity
- proteins can become denatures
- pH is too low
- neurons become less excitable
- CNS depression
- pH too high
- neurones becomes hyperexcitable
- tingling, sustaines muscle contractions
- intermediates of citirc acid cycle
- AA
- Lactic acid
- breakdown of fates making ketoacids
- biggest source is CO2
1. Chemical buffers
- quickest response
2. Ventilation
- rapid but slower than buffer response
3. Renal regulation of H and HCO3
- slowest response
- large amts of HCO3 prod from CO2
- HCO3 buffers H
- Hb can bind to H in RBC
- HCO3 is available to buffer H from other sources
- deviations in H are not swiftly corrected the lungs come into action
- 2nd line of defense
- RPS only compensate for changes in CO2 and pH that arent regulated by this system
- can only partially correct abnormalities in pH 50-75%
1) Peripheral and central chemoreceptors change ventilation in response to diff mechs
- peripheral response to changes in H
- central response to changes in CO2
2) Rise in ventilation reduces H driving from the peripheral chemoreceptors is dimished
- H increase triggers peripheral chemoreceptors to increase ventilation to release more CO2
- CO2 removal from increased ventilation the central chemoreceptors inhibit the respiratory centre
- Kidneys deal with compensation of pH that RPS cannot correct completely
1) H secretion/excretion
2) HCO3 reabsorption/excretion
- located in collecting duct
- deals with acidosis
- excretes H
- reabsorbs HCO3 and K
1. HCO3- buffers H+ that comes from the blood to make CO2
2. The CO2 diffuses into the type A cell
3. Carbonic anhydrase (CA) reforms HCO3- and H+
4. H+ is exchanged for K+ via the H+/K+ pump
5. H+ is excreted
6. K+ is reabsorbed
- located in collecting duct
- deals with alkalosis
- reabsorb H
- excrete HCO3
1. Carbonic anhydrase (CA) reforms HCO3- and H+
2. H+ is exchanged for K+ via the H+/K+ pump
3. K+ is excreted
4. H+ is reabsorbed
- Can arise from either respiratory dysfunction or metabolic disturbances
4 Deviations:
1) respiratory acidosis
2) respiratory alkalosis
3) metabolic acidosis
4) metabolic alkalosis
- result of abnormal CO2 retention from hypoventilation
Possible Causes:
- lung disease
- depression of RP centre by drugs or disease
- nerve or muscle disorders that reduce respiratory muscles activity
- holding breath
Compensations:
- chemical buffers immediately take up add H
- kidneys
- due to excessive loss of CO2 from body causing hyperventilation
Possible Causes:
- fever
- anxiety
- aspirin poisoning
- physiologic mechs at high altitude
Compensations:
- chemical buffer systems liberate H
- Con't for few days then kidneys help converse H and excretes more HCO3
- all types of acidosis other than those cause by excess CO2 in body fluids
Causes:
- severe diarrhea
- diabetes mellitus
- strenuous exercise
Compensation:
- buffers take up extra H
- lungs blow off add CO2 gen
- kidneys excrete more H and conserve more HCO3
- reduction in plasma pH caused by relative deficiency of noncarbonic acids
Causes:
- vomiting
- ingestion of alkaline drugs
Compensations:
- chem buffer systems liberate H
- vent reduced
- persists for serveral days then kidneys ceonserve h and excrete excess HCO3
