Acid-Base Disorders Flashcards
Definitions: acidemia, alkalemia, acidosis, alkalosis
- Acidemia: increase in [H+] > 44 mEq/L or a pH < 7.36
- Alkalemia: decrease in [H+] < 36 mEq/L or a pH > 7.44
- Acidosis: a physiological disorder which causes acidemia if not counterbalanced
- Alkalosis: a physiological disorder which causes alkalemia if not counterbalanced
Describe how the pH of the extracellular fluid is controlled in health and in disease.
• Normal pH maintained between 7.36 and 7.44
• Homeostasis maintained by:
o Body buffers (ex. Proteins, phosphate, etc.)
• Important extracellular buffer = HCO3-/H2CO3 (bicarbonate/carbonic acid)
o Pulmonary regulation of PaCO2
o Renal reabsorption/excretion of HCO3- and acid
Illustrate how the Henderson-Hasselbach equation can be used to explain the importance of H+ and HCO3- in the determination of blood pH.
- Acid-base status of arterial blood:
- pH = 6.1 + log [HCO3-/H2CO3]
o 6.1 = pKa of buffer pair
o HCO3- = concentration of bicarbonate in plasma (normally 24 +/- 2 mEq/L)
o H2CO3 = concentration of carbonic acid in plasma
• Calculated as PaCO2 x 0.03
Define primary and secondary acid-base disorders
- Primary acid-base disorders involve changes in PaCO2 (or HCO3-) that raise or lower pH
- Secondary/compensatory changes are the metabolic (change in HCO3-) or respiratory (change PaCO2) responses
Define the four primary acid-base disorders
Respiratory acidosis: PaCO2 > 46 mmHg and pH < 7.35
Respiratory alkalosis: PaCO2 < 35 mmHg and pH > 7.45
Metabolic acidosis: decreased HCO3-; compensated with hyperventilation and decreased PaCO2
Metabolic alkalosis: increased HCO3-
Causes of CO2 retention
o High CO2 production o Low minute ventilation • High mechanical load • Weak or inefficient muscles • Insufficient drive o Ventilation-perfusion inequality o Abnormal breathing pattern (low VT, high f)
Diseases and consequences associated with respiratory acidosis
Central depression
• Drugs: opiates, sedatives, anesthetics
• Oxygen therapy in chronic obstructive lung disease
• Obesity-hypoventilation syndrome
• CNS disorders
Neuromuscular disorders
• Neurologic: multiple sclerodis, poliomyelitis, phrenic nerve injuries, high cord lesions, Guillain-Barre, botulism, tetanus
• End-plate: myasthenia gravis, succinylcholine chloride, curare, aminoglycosides, organophosphates
• Muscle: muscular dystrophy
Airway obstruction (most common cause of respiratory acidosis)
• COPD
• Acute aspiration, laryngospasm
Chest wall restriction
• Pleural: massive effusions or emphysema, pneumothorax
• Chest wall: kyphoscoliosis, scleroderma, ankylosing spondylitis, extreme obesity
Severe pulmonary restrictive disorders
• End-stage pulmonary fibrosis
• Parenchymal infiltration: pneumonia, edema
• Consequences:
o CO2 diffuses into cells and CSF → cerebral vasodilation and possible cerebral edema
o Increased circulating catecholamines → sweating, hypertension, flushing
Diseases and consequences associated with respiratory alkalosis
Primary central disorders • Hyperventilation syndrome, anxiety • Cerebrovascular disease • Meningitis, encephalitis Hypoxia Pulmonary disease • Interstitial fibrosis • Pneumonia • Pulmonary embolism • Pulmonary edema (some patients) Septicemia, hypotension Hepatic failure Drugs: • Salicylates • Nicotine • Xanthines • Progestational hormones High altitude Mechanical ventilation
• Consequences:
o Cerebral vasoconstriction → reduced cerebral blood flow
o Reduced Ca2+ bonding and reduced ionized calcium may lead to paresthesias and tetany
Diseases and consequences associated with metabolic acidosis
High anion gap metabolic acidosis:
• Methanol
• Uremia (Renal failure)
• Diabetic Ketoacidosis (also alcoholic or starvation ketoacidosis)
• Paraldehyde
• Infection (lactic acid)
• Ethylene glycol
• Salicylates
• (MUD PIES)
Metabolic acidosis with normal anion gap:
• Loss of bicarbonate: diarrhea, pancreatic or biliary drainage, ureterosigmoidostomy
• Carbonic anhydrase inhibitors
• Renal tubular acidosis
• Addition of acid: hyperalimentation, NH4Cl, HCl
• Villous adenoma
Diseases and consequences associated with metabolic alkalosis
Initiating factors:
• Loss of H+ from extracellular fluid: vomiting or nasogastric suctioning
• External loss of chloride: diuretics
• Addition of HCO3-: massive blood transfusion (blood contains citrate = metabolized to HCO3-)
Maintenance of metabolic alkalosis (via mechanisms that impair kidney’s abilities to excrete excess HCO3-):
• Extracellular fluid volume contraction
• Decreased glomerular filtration rate
• Increased tubular reabsorption of HCO3-
• Mineralcorticoid excess = stimulates H+ and K+ secretion
• Hypokalemia
Consequences: Neuromuscular • Neural hyperexcitability • Lethargy and confusion Respiratory • Hypoventilation • Left shift of oxyhemoglobin dissociation curve • Increased 2,3-DPG (shifts curve to the right) Cardiac • Myocardial irritability (arrhythmias) • Enhanced digitalis toxicity Metabolic • Decreased ionized calcium • Increased lactate production • Slight increase in anion gap
Explain how the body compensates for acidosis or alkalosis and the magnitude of compensatory change expected for a defined change in PaCO2 or in HCO3
• For acute respiratory processes:
o Measured change in PaCO2 of 10 should cause an expected change in pH by 0.1
• For chronic processes:
o When pH is close to normal (7.38-7.42) → compensation is adequate
Stepwise approach to ABG analysis
- Are results possible? (Especially for extreme pH values: < 6.9 or > 7.6)
a. Use the H-H equation - What is the primary disorder?
a. Acid or base?
b. Respiratory or metabolic? - How much compensation is present?
a. For metabolic acidosis → what is the anion gap?
i. Calculate Delta-delta in anion-gap disorder
b. For metabolic alkalosis → what is the urine chloride? - For metabolic processes, what subset is most likely?
- Is there a secondary process?
a. Historical clues!
b. Other clues:
i. Compensation equations don’t add up
ii. Directions of change for PaCO2 and HCO3- are opposite
iii. Change in HCO3- differs from change in anion gap - For really sick patients (especially ICU patients with altered mentation) are there hidden problems?
a. Usually in setting of overdose
i. Calculate osmole gap
b. Can also occur in patients on multiple medications with effects on kidney electrolyte homeostasis +/- diabetes
c. Examples: salicylates, alcohol (other than ethanol), renal transplant patients +/- diabetes (at risk for renal tubular acidosis)
Explain how the pattern of changes in acid-base values differs between acute and chronic respiratory disorders.
- Metabolic processes don’t happen quickly (kidneys need time to adjust)
- Result: if pH is close to normal (7.38-7.42) = compensation is adequate
- Metabolic acidosis: PaCO2 (expected) = 1.5 x HCO3 (measured) + 8
- Metabolic alkalosis: PaCO2 (expected) = 0.7 x HCO3 (measured) + 20
Explain how to recognize combined (or mixed) acid-base disorders.
• Direction and magnitude of pH change is determined by relative magnitude of severity of simultaneously present disorders
• Result: pH may be misleading if opposing disorders are present
• Other clues:
o Compensation equations don’t add up
o Directions of change for PaCO2 and HCO3- are opposite
o Change in HCO3- differs from change in anion gap
Base Excess
• Pure metabolic estimate
• Methods:
o In lab, adjust the PaCO2 in a blood sample to 40 by equilibrating with overlayed/admixed CO2
o Adjust pH back to 7.4 by adding HCL or NaOH as needed
• Convention:
o Positive base excess: metabolic alkalosis
o Base deficit/negative base excess: metabolic acidosis
• Used as a measure of resuscitation efficacy in patient presenting with acute trauma
• Often doesn’t reflect complete picture in medial ICU patients
