- 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

- 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-)

- 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

Acidosis - Increased H+ (pH 7.45)

- An increase in respiration rate or blowing off CO2 quickly compensates for acidosis - It is not a good system to compensate for metabolic alkalosis

- Conversion/Excretion of HCO3- - Takes a long time - Useful for chronic hypercapnia - Not very useful in acute respiratory acidosis

- Patient has normal pH but abnormal CO2 or HCO3

5.1 Acid Base Balance and Disorders Flashcards by David Li

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

How well did you know this?

Not at all

Perfectly

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-)

How well did you know this?

Not at all

Perfectly

Normal range 7.35 - 7.45

- Regulated mainly by lungs and kidneys

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Buffering Action of Kidneys

Kidneys excrete ammonia and phosphate to maintain the bodies pH levels.

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Acid-Base Imbalance

Acidosis - Increased H+
(pH < 7.35)
Alkalosis - Decreased H+
(pH > 7.45)

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

The Anion Gap

(Na+ + K+) - (Cl- + HCO3-) = Anion Gap
Normal Range 10 - 12 mEq/L
Abnormal > 14

Other Anions (lactate, pyruvate, other metabolic acids)

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Renal Buffer System

Conversion/Excretion of HCO3-
Takes a long time
Useful for chronic hypercapnia
Not very useful in acute respiratory acidosis

How well did you know this?

Not at all

Perfectly

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 well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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)