5 Acidosis, Alkalosis, & Acid-Base Disorders Flashcards
Chemical Equilibria
Association ↔ Dissociation H2CO3 ↔ H+ + HCO3¯ HProtein ↔ H+ + Protein¯ HA ↔ H+ + A¯ H2O ↔ H+ + OH¯ HHb ↔ H+ + Hb PO4 3¯ ↔ HPO4 2¯ ↔ H2PO4 1¯ ↔ H3PO4
STRONG Electrolytes
Produce strong ions Completely dissociates → one way 100% dissociation; no backwards movement NaOH, NaCl, HCl, KCl, Lactic Acid, Keto Acids, Sulfate Na+ K+ Ca2+ Mg2+ NaCl → Na+ + Cl¯ HCl → Cl¯ + H+ Lactic Acid → H+ + Lactate¯ Strong acids "PUSH" the equilibria of weak acids (to protonate or associate)
WEAK Electrolytes
Partially dissociate
Able to move forwards & backwards to maintain homeostasis/equilibrium
HCO3¯, H2O, HA, HProtein, H2CO3, CaProtein
Plasma proteins/Hgb and PO43 ¯
HProtein ↔ H+ + Protein¯
HA ↔ H+ + A¯
Anion Gap
= Unmeasured anions – Unmeasured cations = Weak anions (A¯) + Strong acids (SA¯) = Na+ – (Cl¯ + HCO3¯) Predicted AG = Albumin x 3 Normal range = 8-16mEq/L r/t Metabolic Acidosis Helps determine the source
Strong Ion Difference
= (Strong cations) – (Strong anions) = Unmeasured weak anions
= (Na+ + K+ + Ca2+ + Mg2+) – (Cl¯ + Lactate)
Normal range = 40-45mEq/L
Conjugate Acid/Base
AH + B ↔ BH+ + A¯
Acid + Base ↔ Conjugate acid + Conjugate base
NH3 + HCl ↔ NH4+ + Cl¯
Base (NH3) accepts H+ to form conjugate acid (NH4+)
Acid (HCl) donates H+ to form conjugate base (Cl¯)
CO2 Hydration Reaction
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3¯
Acidosis Physiological Effects
○ Myocardial and smooth muscle depression
○ Activates SNS activity in heart OR remains unchanged
More drastic increase in SNS activity r/t respiratory over metabolic acidosis
○ Decreased cardiac contractility ↓CO ↓BP
○ Increased coronary perfusion in heart by affecting diastolic filing time
○ Decreased peripheral vascular resistance via arterial vasodilation ↓BP
○ Increased cerebral blood flow d/t cerebral vasodilation ↑CBF
CNS metabolic effect (vascular smooth muscle cells in acidic environment)
Relax and dilate
Carbon dioxide = anesthetic
CO2 narcosis
○ Coronary and systemic vasculature DILATE
○ Pulmonary vessels CONSTRICT during hypoxemia, hypercapnia, and acidemia
Opposite effect compared to systemic vasculature
High CO2 w/ elevated H+ ion concentration will cause increase in extracellular Ca2+ which causes pulmonary vasoconstriction
○ Vasculature less responsive to endogenous catecholamines - net effect less
Normal pH = body hormones allow permissive effect of endogenous catecholamines (Epi and NE) work to increase HR via β1 receptor stimulation
○ Tissue hypoxia causes right shift = more O2 dropped off at the tissues
Example: Increased O2 available at tissues during exercise
○ Progressive hyperkalemia
Increased H+ ion causes K+ ions to move out intracellular space and into extracellular
Plasma K+ increases approximately 0.6mEq/L for each 0.1 decrease in pH
Alkalosis Physiological Effects
○ Increased binding sites on plasma proteins for Ca2+
Decreased serum Ca2+
Respiratory and circulatory depression
Neuromuscular irritability
○ Increased systemic vascular resistance ↑SVR
○ Decreased cerebral blood flow d/t cerebral vasoconstriction ↓CBF
○ Coronary and systemic vasculature CONSTRICT
○ Pulmonary vessels DILATE
Decreased pulmonary vascular resistance ↓PVR
Increased bronchial smooth muscle tone (bronchoconstriction)
○ Oxyhemoglobin dissociation curve left shift
More difficult Hgb to release O2 at tissues
○ Hypokalemia
Movement K+ ions into cells in exchange H+
○ Hypoxic pulmonary vasoconstriction
Base Excess
Index that quantifies the metabolic acidosis
Negative BE or “base deficit” or “acid excess”
BE = Weak acid + bicarbonate
BE = HCO3¯ − 24
Normal − 2 to + 2
< −2 suggests primary metabolic acidosis (base deficit or acid excess)
> +2 primary metabolic alkalosis (excess base)
BE also abnormal during metabolic compensation for primary respiratory disorders
Strong Acids
Irreversible dissociation (one way →) Readily & irreversibly give up H+ ions Lactic acid Hydrochloric acid (HCl) Nitric acid (HNO3) Sulfuric acid (H2SO4) Hydrobromic acid (HBr) Hydroiodic acid (HI) Perchloric acid (HClO4) Chloric acid (HClO3)
pH/pCO2/pO2/HCO3¯
7.35-7.45
35-45
80-100
22-26
High Anion Gap Causes
Increased strong nonvolatile acids (lactic or keto acids) concentration → no compensatory Cl¯ increase → increased anion gap
Methanol intoxication Uremia Diabetic ketoacidosis Paraldehyde Isoniazid or Iron overdose (metabolism inborn error) Lactic acidosis Ethylene glycol Intoxication Salicylate intoxication
Normal Anion Gap Causes
Hyperchloremic acidosis - primary HCO3¯ loss compensated w/ increased Cl¯ → unchanged anion gap
Fistula (biliary, pancreatic) Ureterogastric conduit Saline administration Endocrine (Addison's, hyper-PTH) Diarrhea Carbonic anhydrase inhibitor Ammonium Renal tubular acidosis Spironolactone
Weak Acid
Carbonic acid Phosphoric acid Acetic acid HProtein Ammonium ion (NH3 conjugate acid)
Volatile Acid
H2CO3
Strong Cations
POSITIVE
Na+ K+ Ca2+ Mg2+
Strong Anions
NEGATIVE
Cl¯ Lactate¯
Relationship b/w pH & H+
Logarithmic pH <7.4 ↑H+ >7.4 ↓H+ Equal change in pH = 7.2 → 7.1 H+ 16nEq/L larger increase 7.5 → 7.6 H+ 7mEq/L smaller decrease
pH Importance
H+ involved in nearly all biochemical reactions
Component of homeostasis - affects ionization status (ion concentration equilibrium) & responsible for movement of certain molecules in & out of cells (osmolarity)
Enzyme systems operate at optimal pH and variations can impact enzyme activity (Na+/K+ ATP-ase pump)
Changes in ventilation, perfusion, & electrolyte composition rapidly alters H+ & acid-base balance → dynamic process w/ multiple equilibrium reactions occurring at the same time (w/in microseconds)
pH & pCO2 demonstrate fairly predictable changes in many pathological conditions
Alters ionization degree of proteins & drugs administered
Importance out of proportion to its relatively miniscule concentration in the body
Henderson-Hasselbalch
pH = 6.1 + log(HCO3¯/(PaCO2 x 0.03))
Volatile Acids
Carbonic acid
Aerobic metabolism
Nonvolatile Acids
Lactic acid
Hydrogen phosphate
Anaerobic metabolism
How are body acids generated?
Aerobic metabolism produces volatile acids
Anaerobic metabolism produces nonvolatile acids
-OSIS
Any (one) pathological process that alters arterial pH
Acidosis or Alkalosis
-EMIA
NET EFFECT of all primary processes and compensatory physiological responses on arterial blood pH
Acidemia pH < 7.35
Alkalemia pH > 7.45
Kidney Function Impact on Acid-Base Balance
Controls HCO3¯ reabsorption from tubular fluid
Forms new bicarbonate
Eliminates H+ in the form of titratable & ammonium acids
Respiratory Acidosis
pH < 7.35 CO2 > 45
Drives CO2 hydration reaction to the right (↑ CO2)
Problem: Alveolar hypoventilation
Acute - compensatory response limited; chemical buffer instant response
Chronic - full renal compensation (12-24hrs and peak 3-5 days)
Compensatory mechanism: ↑ HCO3¯
Respiratory Alkalosis
pH > 7.45 CO2 <35
Inappropriate increase in alveolar ventilation relative to CO2 production
Acute - regulated by buffers in blood; variable compensatory response d/t unable to decrease RR below certain point
Chronic - decrease bicarb absorption via renal system and increase H+ excretion
Compensatory mechanism: ↓ HCO3¯
Metabolic Acidosis
pH < 7.35 HCO3¯ < 22
Primary mechanisms lead to decrease HCO3¯
1. Consumption HCO3¯ by strong nonvolatile acid (lactic, pyruvic, keto acid)
2. Renal/GI HCO3¯ loss
3. Rapid ECF compartment dilution w/ HCO3¯ free solutions (saline administration)
Anion gap r/t metabolic acidosis
Base excess < -2
Compensation: ↓CO2
Chemoreceptors sense increased H+ concentration & respond w/ increased ventilation to blow off CO2
Metabolic Alkalosis
pH > 7.45 HCO3¯ > 26 Compensation: ↑CO2 Base excess > +2 Physiological compensatory response will not increase PaCO2 > 55 Indicates primary acid-base disturbance
Strength & Efficiency of the Buffer Systems
- Buffers - immediate - weakest
- Respiratory - couple to 24hrs - moderate
- Renal - 3-5days - strongest
Strength & Efficiency of the Buffer Systems
- Buffers - immediate - weakest
- Respiratory - couple to 24hrs - moderate
- Renal - peak 3-5days - strongest
Acidemia Anesthetic Considerations
Potentiates CNS depressant effects of most sedative and anesthetic agents - adjust dosage
Increased sedation and depression of airway reflexes (may predispose to aspiration) - protect the airway
Direct circulatory depressant effects of anesthetics can be exaggerated
Anesthetic agents that rapidly decrease sympathetic tone can indirectly produce unopposed circulatory depression
Avoid succ d/t potential for hyperkalemia
Alkalemia Anesthetic Considerations
Prolongs the duration of opioid-induced respiratory depression
General ischemia can occur w/ marked reduction in CBF during respiratory alkalosis (particularly when hypotension present) systemic vascular vasoconstriction
Alkalemia & hypokalemia can precipitate arterial & ventricular dysrhythmias
Excitable cardiac cells d/t decreased VG Na+ channels stabilization
