acid base chem lab

1. Lab 11: Acid - Base Balance of the Arterial
Plasma

2. Lab 11 - Carbonic Acid Buffering System
Important to maintain blood pH at intermediate set point (pH = 7.4)
- For metabolic processes and systems to work well
- Lot of the proteins are pH-dependent
: Homeostatic mechanism in which the lungs and/or
kidneys will maintain arterial blood pH approximately at 7.4.

3. Lab 11 - Causes of Blood pH Imbalance
(in arterial plasma)
Blood pH is mainly determined by the in the plasma.

4. Lab 11 - Acidosis and Alkalosis Disorders
Respiratory acidosis: a disorder where the respiratory system fails to eliminate
CO2 as fast as it is produced thus H+ concentration in the arterial plasma is
increased above normal (pH < 7.35).
Respiratory alkalosis: a disorder where the respiratory system eliminates CO2
faster than it is produced thus H+ concentration in the arterial plasma is
decreased below normal (pH > 7.45).
Metabolic acidosis: a disorder where there is an increase of arterial H+
concentration due to some cause other than a primary change in PCO2 (pH <
7.35).
Metabolic alkalosis: a disorder where there is a decrease of arterial H+
concentration due to some cause other than a primary change in PCO2 (pH >
7.45).

5. Lab 11 - Respiratory Acid-Base Disorders –
Cause and Compensatory Mechanism
Cause: Respiratory system (PCO2)
•
• Increase CO2 production to alveolar
ventilation (Net gain of plasma CO2)
•
• Decrease CO2 production to alveolar
ventilation (Net loss of plasma CO2)
Compensatory: Kidneys slowly adjust HCO3
-
• via secretion of H+
(No net gain of plasma HCO3
-)
• (Net gain of plasma HCO3
-)
• Binding to filtered nonbicarbonate
buffer via secretion of excess H+
• Glutamate breakdown and secretion of
NH4
+
• (Net loss of plasma HCO3
-)
• Insufficient secretion of H+
Respiratory Acidosis
Respiratory Alkalosis

6. Lab 11 - Metabolic Acid-Base Disorders – Cause
and Compensatory Mechanism
• Respiratory rate
• Tidal volume
Influence net gain or loss of plasma CO2
Cause: Any situation other than the
respiratory system
• Excessive production of lactic acid
• Excessive diarrhea
• Persistent vomiting
Compensatory:
Secondary: Kidneys
slowly adjust HCO3
-
Primary: Lungs quickly
adjust PCO2
• “Reabsorption” of
filtered HCO3
-
• New HCO3
-
•
Metabolic acidosis
Metabolic alkalosis
• • Excretion of
HCO3
-

7. Lab 11 – Goals (aka Learning Outcomes)
• Explain the homeostatic regulation of arterial pH using the
carbonic acid buffering system.
• Examine respiratory and metabolic acidosis and alkalosis
under various conditions.
o Predict and justify the cause of the acid-base disorder.
o Predict and justify the compensatory system and
mechanisms to correct pH imbalances.

8. Lab 11 – Experimental Setup for Part 1
Animal model: None, but there is an
inanimate model
Experimental Setup: PhysioEx simulation
Renal Responses to Respiratory Acidosis and Alkalosis

9. Lab 11 – Experimental Setup for Part 2
Metabolic Acidosis and Alkalosis
Animal model: Unknown
Experimental Setup: Case study
Initial pH
change
Values before compensation Compensated state (steady state)
pH
Arterial
PCO2
(mmHg)
Alveolar
ventilation
(ml/min)
Arterial
HCO3
-
(mMol/L)
pH
(log
molar)
Arterial
CO2
(mmHg)
Alveolar
ventilation
(breaths/min)
Arterial
HCO3
-
(mMol/L)
How these variables change 5
minutes after compensation
relative to before compensation