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)
