5 Acidosis, Alkalosis, & Acid-Base Disorders Flashcards Preview

AS - N927 Chem/Physics > 5 Acidosis, Alkalosis, & Acid-Base Disorders > Flashcards

Flashcards in 5 Acidosis, Alkalosis, & Acid-Base Disorders Deck (35)
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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)





High Anion Gap Causes

Increased strong nonvolatile acids (lactic or keto acids) concentration → no compensatory Cl¯ increase → increased anion gap

Methanol intoxication
Diabetic ketoacidosis
Isoniazid or Iron overdose
(metabolism inborn error)
Lactic acidosis
Ethylene glycol
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)
Carbonic anhydrase inhibitor
Renal tubular acidosis


Weak Acid

Carbonic acid
Phosphoric acid
Acetic acid
Ammonium ion (NH3 conjugate acid)


Volatile Acid



Strong Cations

Na+ K+ Ca2+ Mg2+


Strong Anions

Cl¯ Lactate¯


Relationship b/w pH & H+

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



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



Any (one) pathological process that alters arterial pH
Acidosis or Alkalosis



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