1. Resting Membrane Potential
Represents the period of time when excitable cells, such as nerve fibers, are not transmitting signals
All body cells are electrically polarized with the inside more negatively charged than the outside
Difference in charge is a result of the differences in ionic composition of the ICF(mostly K+) and ECF (mostly Na+)
Concentration difference is maintained by the active transport of Na+ and K+ (sodium-potassium pump)
Plasma membrane is more permeable to K+ then Na+, K+ diffuses easily from the ICF to the ECF
Net result is an excess of ions inside the cell

2. Sodium-Potassium Pump

3. Blood K+ Levels Control Resting Potential

4. Acid–Base Balance

5. Understanding pH
pH = a calculation based on the percentage of hydrogen (H+) ions in a solution and the amount of acids and bases
Body normally maintains pH within a narrow range ( )
Acid (by-product of metabolic processes) is defined as a compound that can dissociate and release a hydrogen ion
Base is defined as a compound that can accept or combine with a hydrogen (H+) ion
Calculated using the Henderson-Hasselbalch equation
pH is inversely related to H+ concentration
a low pH = high concentration of H+
a high pH = low concentration of H+

6. Understanding CO2
Metabolic by-product which diffuses from cell  tissue spaces  circulation
Transported in the circulation:
Dissolved in plasma (10%) exhaled through lungs
As bicarbonate (70%)
Attached to Hgb (20%)
Combines with water to form H2CO3

7. Regulation of pH Chemical buffer systems in body fluid
Bicarbonate buffer system
Transcellular hydrogen-potassium exchange system
Body proteins
Lungs
Changes in PCO2 and pH in the blood are sensed by brainstem and peripheral chemoreceptors which alter the respiratory rate
Kidneys
Hydrogen/bicarbonate exchange (secretes excess H+ and reabsorbs HCO3)
Ammonia buffer system (generation of new HCO3)
Phosphate buffer system (intratubular)

8. Buffer Systems

9. Laboratory Tests Arterial blood gases
Assess the respiratory component of acid-base balance
Serum electrolytes
Base excess or deficit
Measure of the bicarbonate (HCO3-) excess or deficit
Anion gap
Difference between serum concentration of Na+ and the sum of Cl- and HCO3-
Normal range is 8 to 12 mEq/L
 in lactic acidosis and diabetic ketoacidosis

10. Metabolic Acidosis and Alkalosis
CO2 + H2O  H2CO3  H+ + HCO3−
Metabolic Acidosis
Metabolic Alkalosis
 H+ =  pH (<7.35)
 serum HCO3-
RR  PCO2 and H2CO3-
 H+ =  pH (>7.45)
 serum HCO3-
RR  PCO2

11. Causes of Metabolic Acidosis
Increased production of metabolic acids
Accumulation of lactic acid (inadequate O2 delivery, intense exercise)
Ketoacidosis (uncontrolled DM, fasting or dieting)
Decreased renal function
Kidneys lose ability to eliminate metabolic acids and nitrogenous waste
Increased bicarbonate losses
loss of intestinal fluids (diarrhea, intestinal suction, fistulas)
Hyperchloremic acidosis
Abnormal absorption of Cl- by the kidneys
Treatment with chloride containing medications

12. Manifestations of Metabolic Acidosis
Laboratory Tests
pH 
HCO3 (primary) 
PCO2 (compensatory) 
Signs of Compensation
Respiratory rate
Hyperkalemia
Acidic urine
 Ammonia in urine
GI effects
Anorexia
Nausea and vomiting
Abdominal pain
Neurological effects
Weakness, lethargy
Confusion, stupor, coma
Cardiovascular effects
Peripheral vasodilation
 Cardiac output
Cardiac arrhythmias
Skin
Warm, flushed

13. Causes of Metabolic Alkalosis
Excess bicarbonate base
Excess ingestion of bicarbonate-containing antacids (Alka-Seltzer)
IV infusion of base solution (blood transfusions, TPN, LR)
Loss of fixed acids
Loss of acid from stomach (vomiting, gastric suction)
Loss of chloride from the urine
Loss of potassium (diuretics)

14. Manifestations of Metabolic Alkalosis
Laboratory Tests
pH 
HCO3 (primary) 
PCO2 (compensatory) 
Signs of Compensation
 Respiratory rate
Hypoxia
Respiratory acidosis
Neurological effects
Hyperactive reflexes
Tetany
Confusion
Seizures
Cardiovascular effects
Hypotension
Cardiac arrhythmias

15. Treatment of Metabolic Acidosis
Correct the underlying cause
Restoring fluid and electrolytes
Correct chloride and/or potassium deficiencies
NaHCO3 for normal anion gap acidosis
Insulin and fluid replacement for patients in diabetic ketoacidosis

16. Respiratory Acidosis and Alkalosis
CO2 + H2O  H2CO3  H+ + HCO3−
Respiratory Acidosis
Respiratory Alkalosis
 H+ =  pH (<7.35)
 PCO2
 H2CO3-
 HCO3−
 H+ =  pH (>7.45)
 PCO2
 H2CO3-
 HCO3−

17. Causes of Respiratory Acidosis
Represents a decrease in pH caused by an elevation in PCO2
Usually due to conditions that impair alveolar ventilation such as:
Acute disorders of ventilation (narcotic overdose, lung disease, chest injury, weakness or respiratory muscles or airway obstruction
Chronic disorders of ventilation (COPD)-sustained increase in PaCO2 resulting in renal adaptation with marked increase in serum HCO3 and a lesser decrease in pH.
Increased CO2 production (exercise, fever, sepsis, burns, CHO-rich diet)

18. Manifestations of Respiratory Acidosis
Laboratory Tests
pH 
HCO3 (primary) 
PaCO2 > 50
Signs of Compensation
Acidic urine
GI effects
Anorexia
Nausea and vomiting
Abdominal pain
Neurological effects
Headache, behavioral changes
Depression, paranoia
Confusion, stupor, coma
Tremors, paralysis
Skin
Warm, flushed

19. Treatment of Respiratory Acidosis
Correct the underlying cause
Directed toward improving ventilation
Correct chloride and/or potassium deficiencies

20. Causes of Respiratory Alkalosis
Systemic acid-base disorder characterized by a primary decrease in PaCO2 which produces an elevation in pH and subsequent decrease in HCO3
Causes:
Hyperventilation
Central stimulation of the medullary respiratory center (anxiety pain, pregnancy, sepsis, encephalitis, salicylate toxicity)
Peripheral pathways of the medullary respiratory center
Mechanical ventilation (if rate and volume are such that expired CO2 exceeds production

21. Manifestations of Respiratory Alkalosis
Laboratory Tests
pH 
HCO3 (primary) 
PCO2 (compensatory) 
Signs of Compensation
 Respiratory rate
Hypoxia
Respiratory acidosis
Neurological effects
Hyperactive reflexes
Tetany
Confusion
Seizures
Cardiovascular effects
Hypotension
Cardiac arrhythmias

22. Treatment of Respiratory Alkalosis
Correct the underlying cause
Supplemental O2 for hypoxia
Adjust ventilator settings
Reassurance, rebreathing and psychological support for hyperventilation syndrome