Clinical Disturbannces Charles L. Webber, Jr., Ph.D.

Learning Objectives: You should be able to:

• Show how specific cardiopulmonary disturbances that can precipitate as problems of acidosis or alkalosis.
• Explain in detail how pathophysiological upsets in potassium ion concentration can lead to serious acid-base abnormalities.
• Explain in detail how pathophysiological upsets in potassium ion concentration can lead to serious acid-base abnormalities.
• Cite several examples of how the physician might induce acid-base imbalances in patients being treated for other maladies.
• Discuss the acid-base ramifications of multiple organ system failures as in concurrent lung and renal diseases.

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Cardiopulmonary Disturbances

1. Metabolic Acidosis
   • congestive heart failure
     •  cardiac output  blood pressure  GFR  H+ secretion  [H+]
     •  blood pressure  blood flow  anaerobic metabolism  lactic acid production
   • hypovolemic shock
     •  circulating blood volume  blood pressure  GFR
        H+ secretion  [H+]
     •  blood pressure  blood flow  anaerobic metabolism
        lactic acid production

    

2. Metabolic Alkalosis
   • contraction alkalosis
     • diuretic therapy excretion of isotonic NaCl  ECF volume
        [HCO3-]
   • massive blood transfusions
     • blood bank blood anticoagulated with acid-citrate dextran (a colloid)
     • citrate (organic anion) + O2 CO2 + H2O + HCO3-
     • must give at least 8 units of blood (4000 mL) before significant
        plasma pH is induced
   • posthypercapnic alkalosis
     • initiation of ventilator therapy for COPD fast  PaCO2 and slow  [HCO3-]
     • delay in restoration of high [HCO3-] values down toward normal  plasma pH

    

3. Respiratory Acidosis
   • chronic obstructive pulmonary disease (COPD)
     •  VþA  PaCO2
     • seen in emphysema, asthma, severe kyphoscoliosis, extreme obesity, and post-surgical patients

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Renal Disturbances

1. Metabolic Acidosis
   • renal failure
     •  GFR  filtration of titratable acids (HPO4- -)  H+ secretion  [H+]
     •  GFR  filtration of glutamine  NH3 load to tubular cells  NH4+ formation
     •  NH4+ formation  H+ secretion  [H+]
   • proximal renal tubular acidosis (type II RTA)
     • impaired Na+/H+ exchanger in luminal membrane
        H+ secretion  [H+]
     •  Na+/K+/ATPase in basolateral membrane
        Na+/H+ exchanger energy  H+ secretion
     •  carbonic anhydrase activity in brush border
        HCO3- reabsorption  H+ secretion
   • distal renal tubular acidosis (type I RTA)
     •  permeability of distal nephron to H+  H+ back-leaks
        H+secretion  [H+]
     • inability to acidify urine below pH of 5.3
       (normal pH minimum is 4.5 to 5.0)

    

2. Metabolic Alkalosis
   • hyperreninism (Fig. 30)
     •  renin from juxtaglomerular apparatus hyperplasia and tumors
     •  renin  angiotensin II & III  aldosterone
        K+ secretion  [K+]extracell &  [K+]intracell
     •  [K+]intracell  [H+]intracell (intracellular acidosis)
        [HCO3-]out (extracellular alkalosis)
     •  [H+]intracell  H+ secretion &  HCO3- reabsorption
        [H+] &  [HCO3-]
     • this is hypokalemic metabolic alkalosis with paradoxically acidic urine
     • K+/H+ exchanger plays an important role in this mechanism

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Gastrointestinal Disturbances

1. Metabolic Acidosis
   • aspirin ingestion
     • þ acetylsalicylic acid salicylic acid  [H+]
     • þ chronic use of aspirin for controlling inflamation can induce acid/base problems
   • hyperalimentation
     • þ hyperalimentation fluids can contain an excess of cationic amino acids (e.g. arginine & lysine)
     • þ R-NH3+ + O2 urea + CO2 + H2O + H+
   • diarrhea
     • þ loss of intestinal fluids below stomach (lower GI tract) loss of HCO3-  [HCO3-]
     • þ excessive fluid loss can also result from laxative abuse
   • fistulas
     • þ removal of alkaline secretions from body by tube drainage loss of HCO3-  [HCO3-]
     • þ pancreatic and biliary secretions are alkaline
   • ureterosigmoidostomy
     • þ surgical rerouting of ureters from bladder to sigmoid colon  Cl- delivery to colon
     • þ  Cl- load to colon  Cl- reabsorption &  HCO3- secretion loss of HCO3-  [HCO3-]
     • þ Cl-/HCO3- exchanger in ilium and colon plays an important role in this mechanism

    

2. Metabolic Alkalosis
   • protracted vomiting
     • þ loss of gastric fluids (upper GI tract) loss of H+  [H+]
     • þ repeated vomiting loss of gastric HCl  [H+]
     • þ nasogastric suction loss of gastric HCl  [H+]
   • congenital chloridorrhea
     • þ intestinal Cl-/HCO3- exchanger defect  Cl- reabsorption &
        HCO3- secretion  [HCO3-]
   • dietary hypokalemia
     • þ  K+ ingestion  [K+]extracell  [K+]intracell
     • þ  [K+]intracell  [H+]intracell (intracellular acidosis)
        [HCO3-]extracell (extracellular alkalosis)
     • þ  [H+]intracell  H+ distal secretion &  HCO3- proximal reabsorption  [H+] &  [HCO3-]
   • liver cirrhosis with ascites
     • chronic alcoholism hepatic disease  portal pressure
       ( plasma hydrostatic forces) ascites
     • chronic alcoholism hepatic disease hypoalbuminemia
       ( plasma oncotic forces) ascites
     • ascites  abdominal pressure  femoral venous pressure
       permeability edema  CBV  renin
       hypokalemic metabolic alkalosis
     • 3-4 L of ascites fluid can be removed by paracentesis

    

3. Respiratory Alkalosis
   • aspirin ingestion
     • þ acetylsalicylic acid salicylic acid chemoreceptor stimulation  VþA  PaCO2  [H+]
     • þ again, chronic use of aspirin for controlling imflamation can induce acid/base problems

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Endocrine Disturbances

1. Metabolic Acidosis
   • hypoaldosteronism
     • þ  aldosterone  K+ secretion  [K+]extracell &  [K+]intracell
     • þ  [K+]intracell  [H+]intracell (intracellular alkalosis)
        [HCO3-]extracell (extracellular acidosis)
     • þ  [H+]intracell  H+ secretion &  HCO3- reabsorption  [H+] &  [HCO3-]
   • diabetes mellitus
     • þ lack of insulin altered metabolism of free fatty acids in liver
     • þ free fatty acid (health) triglycerides
     • þ free fatty acid (diabetes) ketoacids (e.g. þ hydroxybutyric acid, acetoacetic acid)
     • þ ketoacidosis is associated with an abnormally high anion gap
       (A- = Na+ - Cl- - HCO3- > 15 mM)

    

2. Metabolic Alkalosis
   • mineralocorticoid excess (primary hyperaldosteronism)
     • þ  aldosterone  K+ secretion  [K+]extracell &  [K+]intracell
     • þ  [K+]intracell  [H+]intracell (intracellular acidosis)
        [HCO3-]extracell (extracellular alkalosis)
     • þ  [H+]intracell  H+ secretion &  HCO3- reabsorption
        [H+] &  [HCO3-]
     • þ autonomous hypersecretion of aldosterone from adenoma or hyperplasia of adrenal cortex
   • glucocorticoid excess
     • þ  ACTH from anterior pituitary  cortisol from adrenal cortex (Cushing's Syndrome)
     • þ  ACTH  permissive action of AT-II & AT-III on adrenal cortex  aldosterone release
     • þ  aldosterone  K+ secretion  [K+]extracell &  [K+]intracell
     • þ  [K+]intracell  [H+]intracell (intracellular acidosis)  [HCO3-]extracell (extracellular alkalosis)
     • þ  [H+]intracell  H+ secretion &  HCO3- reabsorption  [H+] &  [HCO3-]
   • hypoparathyroidism
     • þ  parathyroid hormone (PTH)  HCO3- reabsorption  [HCO3-]
     • þ  PTH  Ca++ reabsorption +  HPO4- - reabsorption

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