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Acid and Base Balance

Acid-Base Balance

Acidosis = 7.2
Alkalosis = 7.6


Normal = 7.35-7.45

Art Blood = 7.5

Venous Blood = 7.4

Effects of Change in Hydrogen

1. Changes in excitability of nerves and mucles cells
2. Marked influuence on enzyme activity

- proteins can become denatures

Acidosis

- pH is too low
- neurons become less excitable

- CNS depression

Alkalosis

- pH too high
- neurones becomes hyperexcitable

- tingling, sustaines muscle contractions

Sources of Hydrgron in the Body

- intermediates of citirc acid cycle
- AA

- Lactic acid

- breakdown of fates making ketoacids

- biggest source is CO2

ph Homeostasis

1. Chemical buffers
- quickest response


2. Ventilation

- rapid but slower than buffer response


3. Renal regulation of H and HCO3

- slowest response

Chemical Buffers

- 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

Ventilatory Regulation of pH

- 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

Ventilation and ACID-BASE Balance

- 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

Peripheral and Ventilation Chemoreceptors

- H increase triggers peripheral chemoreceptors to increase ventilation to release more CO2
- CO2 removal from increased ventilation the central chemoreceptors inhibit the respiratory centre

Renal Regulation of pH

- Kidneys deal with compensation of pH that RPS cannot correct completely

1) H secretion/excretion

2) HCO3 reabsorption/excretion

Type A intercalated cells

- located in collecting duct
- deals with acidosis

- excretes H

- reabsorbs HCO3 and K

Type A intercalated cells STEPS

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

Type B Intercalated Cells

- located in collecting duct
- deals with alkalosis

- reabsorb H

- excrete HCO3

Type B Intercalated Cells STEPS

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

Acid-Base Imbalances

- Can arise from either respiratory dysfunction or metabolic disturbances

4 Deviations:

1) respiratory acidosis

2) respiratory alkalosis

3) metabolic acidosis

4) metabolic alkalosis

Respiratory Acidosis and an Increase in [CO2]

- 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

Respiratory Alkalosis and a Decrease in [CO2]

- 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

Metabolic Acidosis and a Fall in [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

Metabolic Alkalosis and an Elevation in [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

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