129) Respiratory Alkalosis (p. 130) Etiology -Concentration of non-carbonic acids ↑’s or Hco3 is lost from ECF or can’t be regenerated by the kidneys -Hco3 concentration is ↑’d, usually caused by excessive loss of metabolic acids. -caused by alveolar hypoventilation -occurs when hyperventilation & ↓’d concentration of co2 (hypocapnia) Epidemiology -RF, Dka, prolonged Diarrhea w/ Hco3 loss -prolonged vomiting, gastric suction, excessive bicarb intake, hyperaldosteronism, w/ ↓’d K, duretics -depression of resp. center (brainstem trauma, over sedation) -paralysis of resp. muscles -disorders of chest wall (kyphoscoliosis, pickwickian syndrome, flail chest) -disorders of lung parenchyma (pneumonitis, pulm. Edema, emphysema, asthma, bronchitis) -may be acute or chronic - acute: acute resp. acidosis -Chronic: assoc’d w/ COPD & chest wall deformities or neuromuscular disorders -Hypermetabolic states (fever, anemia, thyrotoxicosis) -early salicylate intoxication - anxiety or panic disorders -improper use of mech. Ventilation -hyperventilation manifestations -Changes to neuro, resp. GI & CV systems. -HA, lethargy (early) -coma, severe acidosis (late) -Kussmaul respirations, anorexia, N/V/D , abd. Discomfort. -Severe acidosis can compromise ventricular contraction & produce life- threatening dysrhythmias. -symptoms vary -weakness, muscle cramps, hyperactive reflexes -paresthesias, tetany seizures -RR slow/ shallow -severe: confusion, convulsions -Atrial tach & other dysthymias -symptoms are r/t level of acuity of onset & severity of Paco2 retention - acute: -Ha, restlessness, blurred vision, apprehension, Rapid RR -Chronic: lethargy, muscle twitching, tremors, convulsions, coma, RR depressed over time -dizziness, confusion, paresthesias, carpopedal spasm convulsions, coma -tachypnea Pathophysiology -The buffer systems compensate for the excess acid & attempt to maintain pH wnl. -H+ ions will move to intracellular space, & K+ will -Resp. compensation occurs when resp center is inhibited by↑’d pH. -> ↓’d rate/depth -> co2 retention -> hco3 to hcco3 concentration normalizes -alveolar hypoventilation causes co2 retention, ↑ing H+-> produces acidosis (hypercapnia). - hyperventilation & ↓’d concentration of co2 (hypocapnia)-> hypoventilation precipitated by hypoxia
move to extracellular to maintain ionic balance. -Bicarb buffers-> lowers H+ & ↑’s the pH-> stimulates hyperventilation-> lowers the Paco2 & the amt. of H2Co3 in bld. -Kidneys excrete excess Acid as Nh4 & titratable acid. -When acidosis is severe, cant compensate bc buffers become depleted- so pH continues to ↓ causing the ration to fall <20:1 -K+ redistributed to the extracellular space & reabsorbed @ apical membrane of renal collecting tube. -renal compensation not effective- causes paradoxical response bc of ↓’d vlm. & electrolyte loss -> kidneys ↑ Hco3 & Na reabosorption -> H+ excreted & reabsorption of hco3prevents correction -oxyhgb curve shifted to left - acute: attempts at compensation is not effective bc renal buffer mechanism takes time -protein buffers provide some compensation -hco3 not a good buffer for co2 -Chronic: renal compensation is effective-> acidosis
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- Fall '15
- Spring 2018