5 Acidosis, Alkalosis, & Acid-Base Disorders Flashcards

1
Q

Chemical Equilibria

A
Association ↔ Dissociation
H2CO3 ↔ H+ + HCO3¯
HProtein ↔ H+ + Protein¯
HA ↔ H+ + A¯
H2O ↔ H+ + OH¯
HHb ↔  H+ + Hb 
PO4 3¯ ↔ HPO4 2¯ ↔ H2PO4 1¯ ↔ H3PO4
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2
Q

STRONG Electrolytes

A
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)
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3
Q

WEAK Electrolytes

A

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¯

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4
Q

Anion Gap

A
= 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
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5
Q

Strong Ion Difference

A

= (Strong cations) – (Strong anions) = Unmeasured weak anions
= (Na+ + K+ + Ca2+ + Mg2+) – (Cl¯ + Lactate)
Normal range = 40-45mEq/L

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6
Q

Conjugate Acid/Base

A

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¯)

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7
Q

CO2 Hydration Reaction

A

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3¯

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8
Q

Acidosis Physiological Effects

A

○ 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

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9
Q

Alkalosis Physiological Effects

A

○ 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

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10
Q

Base Excess

A

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

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11
Q

Strong Acids

A
Irreversible dissociation (one way →)
Readily &amp; 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)
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12
Q

pH/pCO2/pO2/HCO3¯

A

7.35-7.45
35-45
80-100
22-26

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13
Q

High Anion Gap Causes

A

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
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14
Q

Normal Anion Gap Causes

A

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
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15
Q

Weak Acid

A
Carbonic acid
Phosphoric acid
Acetic acid
HProtein
Ammonium ion (NH3 conjugate acid)
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16
Q

Volatile Acid

A

H2CO3

17
Q

Strong Cations

A

POSITIVE

Na+ K+ Ca2+ Mg2+

18
Q

Strong Anions

A

NEGATIVE

Cl¯ Lactate¯

19
Q

Relationship b/w pH & H+

A
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
20
Q

pH Importance

A

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

21
Q

Henderson-Hasselbalch

A

pH = 6.1 + log(HCO3¯/(PaCO2 x 0.03))

22
Q

Volatile Acids

A

Carbonic acid

Aerobic metabolism

23
Q

Nonvolatile Acids

A

Lactic acid
Hydrogen phosphate
Anaerobic metabolism

24
Q

How are body acids generated?

A

Aerobic metabolism produces volatile acids

Anaerobic metabolism produces nonvolatile acids

25
Q

-OSIS

A

Any (one) pathological process that alters arterial pH

Acidosis or Alkalosis

26
Q

-EMIA

A

NET EFFECT of all primary processes and compensatory physiological responses on arterial blood pH
Acidemia pH < 7.35
Alkalemia pH > 7.45

27
Q

Kidney Function Impact on Acid-Base Balance

A

Controls HCO3¯ reabsorption from tubular fluid
Forms new bicarbonate
Eliminates H+ in the form of titratable & ammonium acids

28
Q

Respiratory Acidosis

A

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¯

29
Q

Respiratory Alkalosis

A

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¯

30
Q

Metabolic Acidosis

A

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

31
Q

Metabolic Alkalosis

A
pH > 7.45 HCO3¯ > 26
Compensation:  ↑CO2
Base excess > +2
Physiological compensatory response will not increase PaCO2 > 55
Indicates primary acid-base disturbance
32
Q

Strength & Efficiency of the Buffer Systems

A
  1. Buffers - immediate - weakest
  2. Respiratory - couple to 24hrs - moderate
  3. Renal - 3-5days - strongest
33
Q

Strength & Efficiency of the Buffer Systems

A
  1. Buffers - immediate - weakest
  2. Respiratory - couple to 24hrs - moderate
  3. Renal - peak 3-5days - strongest
34
Q

Acidemia Anesthetic Considerations

A

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

35
Q

Alkalemia Anesthetic Considerations

A

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