5.1 Acid Base Balance and Disorders Flashcards
pH
- Level of acidity or alkalinity of fluids
- If pH moves from 6 to 5 concentration of H+ has increased by 10 times
- If H+ is high the fluid is acidic
- If H+ is low the fluid is alkaline
Regulation of pH
- Acid is the end product of protein, fat, and carbohydrate metabolism
VOLATILE - Carbonic Acid (H2CO3) (Eliminated as CO2)
NONVOLATILE - Sulfuric, Phosphoric, other Organic Acids
Eliminated as Ammonium (NH4+) and regulation of Bicarbonate (HCO3-)
pH
Normal range 7.35 - 7.45
- Regulated mainly by lungs and kidneys
Buffers
- They are weak acids and conjugate bases that bind to excessive H+ or OH- without causing change in pH
- Lungs blow off CO2 to regulate Carbonic Acid
- Kidneys excrete HCO3- by producing alkaline/acidic urine.
- These are compensatory mechanisms
Buffering Action of Hemoglobin
- CO2 is a waste product of cellular metabolism
- O2 is exchanged for CO2
- When CO2 enters the blood it is quickly dissolved and ionized
Hemoglobin in Acidosis
- Potassium and H+ have inverse relationship in acidosis. Potassium leaves cells and H+ goes into cells. Because of this acidosis may cause hyperkalemia
- The same is true vice-versa
Buffering Action of Kidneys
Kidneys excrete ammonia and phosphate to maintain the bodies pH levels.
Protein Buffer System
- Largest buffer system in the body
- Proteins can function as both acid or bases
BONE BUFFER SYSTEM - Excess H+ can be exchanged for sodium and potassium on the bone surfaces.
- Dissolution of bone minerals cause the release of sodium bicarbonate and calcium bicarbonate into ECF
- These can be used to buffer acids
Acid-Base Imbalance
Acidosis - Increased H+
(pH < 7.35)
Alkalosis - Decreased H+
(pH > 7.45)
Acidosis/Alkalosis
Respiratory Acidosis - Elevation of CO2 (Less Respirations)
Respiratory Alkalosis - Decreased CO2 (Hyperventilation)
Metabolic Acidosis - Decrease in HCO3 or increase in non-carbonic acids
Metabolic Acidosis - Elevation in HCO3 usually due to excessive loss of metabolic acids
The Anion Gap
(Na+ + K+) - (Cl- + HCO3-) = Anion Gap
Normal Range 10 - 12 mEq/L
Abnormal > 14
Other Anions (lactate, pyruvate, other metabolic acids)
Respiratory Buffer
- An increase in respiration rate or blowing off CO2 quickly compensates for acidosis
- It is not a good system to compensate for metabolic alkalosis
Renal Buffer System
- Conversion/Excretion of HCO3-
- Takes a long time
- Useful for chronic hypercapnia
- Not very useful in acute respiratory acidosis
Normal ABG Ranges
pH (7.35 - 7.45) - Lower is acidosis, higher is alkalosis
PCO2 (Respiratory) 35-45 mmHg
Higher is acidosis, lower is alkalosis
HCO3 (Metabolic) 22-26 mEq/L
Lower in acidosis, higher in alkalosis
BE (Base Excess) +/- 2 mEq/L
Lower in acidosis, higher in alkalosis
How to Interpret ABG
Step 1 - Is it normal, acidosis or alkalosis
Step 2 - Is it Respiratory or Metabolic Acidosis
(ROME) - Respiratory Opposite, Metabolic Equal
Compensation
- Patient has normal pH but abnormal CO2 or HCO3
Primary Respiratory Acidosis
- Increase in Carbonic Acid (H2CO3)
- Retention of CO2
Etiology/Common Causes (Respiratory Acidosis)
Etiology - Hypoventilation (Increased CO2)
Common Causes
- Over sedation and depression of respiratory system
- Brain stem trauma with damage to respiratory center
- COPD (CO2 Retention)
- Sleep Apnea (retention of co2 due to obstructed airway)
Compensation/Correction (Respiratory Acidosis)
Compensation - Stimulates kidneys to excrete H+ as ammonia or H2PO4 and retain Bicarbonate
Correction - Increase alveolar ventilation
Clinical Manifestation (Respiratory Acidosis)
Clinical Manifestations - Notable decrease in rate/depth or respirations - Sensorium CO2 crosses BBB (lipophilic) HCO3 Does not Cross (hydrophilic) - Headache, Restlessness, Apprehension (anxiety) - Confusion, Lethargy, Tremors - Seizures and Coma
Diagnosis/Treatment Respiratory Acidosis
pH - Less than 7.5
- Increased pCO2 (Hypercapnia) and decreased O2 (Hypoxia)
- Increased HCO3- (Bicarbonate) which results in renal compensation
- Lactic Acidosis, in presence of anaerobic metabolism
Treatment
- Restore alveolar ventilation.
- Oxygen, intubation, mechanical Ventilation
- Narcotic reversal agent (if due to narcotic overdose)
Primary Respiratory Alkalosis
- Decrease in carbonic acid due to hyperventilation and excess loss of carbon dioxide.
Common Causes (Respiratory Alkalosis)
- Hypoxemia (low oxygen) pulmonary/circulatory disease
- Hyperdynamic states (sepsis, fever, thyrotoxicosis too much thyroid hormone)
- Improper ventilator settings
- Brain stem lesions
- Salicylate (OTC) poisoning (in combination with metabolic acidosis
Etiology/Compensation (Respiratory Alkalosis)
Etiology - Hyperventilation (decreased co2)
Compensation
- Begin exchanging H+ for K+ in RBC
- Kidneys compensate by retaining H+ and excreting HCO3-
Clinical Manifestation (Respiratory Alkalosis)
- Increased rate/depth of respirations (blowing out co2)
- Alkalization of plasma leading to decrease in ionized calcium
- This causes tingling in extremities, circumoral numbness, neuromuscular weakness, changes in sensorium, dizziness, confusion, seizures.
Diagnosis/Treatment (Respiratory Alkalosis)
Diagnosis
- pH > 7.45
- Decreased pCO2 < 35 mmHg (Hypocapnia)
- Normal or slightly elevated HCO3
Treatment
- Administer oxygen for hypoxic
- Adjust mechanical ventilation
- Assist with rebreathing CO2 (paper bag)
Primary Metabolic Acidosis
- Increase in non-carbonic acids or loss of bicarbonate
Common Causes (Metabolic Acidosis)
- Lactic Acidosis from reliance on Anaerobic Metabolism
- Renal Failure (retention of metabolic acids)
- Diabetic Ketoacidosis (reliance of protein and fat for energy resulting in production of acids)
- Diarrhea (loss of alkaline duodenal secretions)
Etiology (Metabolic Acidosis)
- Decrease in Base (HCO3-) due to loss
- Increase in Metabolic Acid (H+) due to retention or increased production
Compensation (Metabolic Acidosis)
- Respiratory system blows off CO2
- Renal system increases excretion of ammonium and phosphate. This lowers H+ available to form carbonic acid.
Clinical Manifestation (Metabolic Acidosis)
- Headache, Lethargy
- Anorexia, Nausea, Vomiting
- Progression to Coma
- Hyperventilation
- Kussmaul (rapid, deep, heaving) respirations to compensate severe metabolic acidosis
- Lethal Dysrhythmias
Diagnosis/Treatment (Metabolic Acidosis)
- pH < 7.35
- Normal/Decreased pCO2 (Insufficient to offset acidosis)
- Decreased HCO3
- Serum Lactate/Ketones for lactic acidosis or diabetic ketoacidosis.
Treatment
- Treat underlying cause
- Judicious use of sodium bicarbonate (if used at all)
Primary Metabolic Alkalosis
- Decrease of non-carbonic acids or gain in bicarbonate via reabsorption or lack of consumption.
Common Causes Diabetic Alkalosis
- Loss of gastric acids from prolonged vomiting or GI suction
- Renal Retention of Bicarbonate
- Excess consumption of antacids such as magnesium hydroxide
- Excessive bicarbonate intake
- Diuretic Therapy
Etiology of Diabetic Alkalosis
- Increase in base (HCO3) due to retention or decreased consumption
- Decrease in metabolic acids (H+) due to loss of production resulting in net gain of base bicarbonate
Compensation (Diabetic Alkalosis)
Respiratory - Hypoventilation resulting in increase of PaCO2 and H2CO3
Renal - Kidneys retain H+ and excrete bicarbonate
(Not effective if patient is dehydrated or has electrolyte imbalance)
Clinical Manifestation
- Signs and symptoms of underlying cause (GI)
- Paresthesia (pins and needles) and muscle weakness with decreased ionized calcium (alkaline environment)
- Hypoventilation (retention of co2)
- Confusion/seizures in severe cases
Diagnosis/Treatment Metabolic Alkalosis
- pH > 7.45
- Normal or increased PCO2 (Insufficient to offset alkalosis)
- Increased HCO3
Hypochloremia (gastric suctioning)
Treatment
Treat underlying cause
Complex Acid Base Balances
- Primary imbalance is offset my a secondary imbalance that returns pH to normal ranges. (2 wrongs make a right)
- Mixed imbalances of both respiratory and metabolic acidosis/alkalosis.
(Diabetic Ketoacidosis and Lactic Acidosis)
