Kategorier: Alle

av R G 15 år siden

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Acid-Base Disorders

Acid-base disorders involve imbalances in the body's pH levels, leading to either acidemia or alkalemia. Alkalemia occurs when the pH exceeds 7.45 and can result from respiratory factors such as hyperventilation or metabolic factors like a gain of bicarbonate or loss of hydrogen ions.

Acid-Base Disorders

Acid-Base Disorders

pH > 7.45

Alkalemia

Respiratory

Hyperventilation

Secondary response:



  • Bicarb generation
  • Cellular buffering & Renal
  • Hepatic failure
    Distress

    Pregnancy

    Pain

    Anxiety

    Hypoxemia

    CNS lesions
    Metabolic

    Gain of bicarb or loss of H+

    Secondary response:


  • Decreased ventilation
  • Cl- resistant

    Stimulates Aldo

    Severe hypokalemia

    RAAS, Adrenal tumors

    Cl- sensitive (volume depleters)

    Vomiting

    Loop, Thiazide Diuretics

    Decreased ECV

    Increased RAAS

    Increased Aldo

    Decreased H+, K+

    pH < 7.35

    Acidemia

    PCO2
    > 45

    Compensatory response to respiratory acidosis

    Causes

    Miscellaneous

    Obesity

    Hypoventilation

    Pulmonary

    Parenchyma

    Airway

    Neuromuscular

    Central

    Anesthetics

    Infection

    Stroke

    Compensatory Rate

    4 Bicarb per 10 pCO2

    Chronic Respiratory Acidosis (Single Disorder)

    1 Bicarb per 10 pCO2

    Compensation not as good: needs to regenerate bicarb

    Acute Respiratory Acidosis (Single Disorder)

    < 35

    Compensatory response to metabolic acidosis

    (Hyperventilation)

    HCO3

    > 28

    Mixed

    < 24

    Metabolic Acidosis (Single)

    Anion Gap

    > (10-12)

    High AG

    Delta Ratio

    >3

    High AG + concurrent met. alk or pre-existing comp. resp acid

    1-2

    Pure High AG Acidosis

    <1

    High AG & Normal AG acidosis

    <0.4

    Hyperchloremic normal anion gap acidosis

    Osmolar Gap

    > (10-15)

    Think ingestion

    Propylene glycol

    Ethylene glycol

    Produces glycolic, oxalic acids

    EtOH

    Methanol

    Methanol/formaldehyde intoxicatoin

    Produces formic acid

    Rx: Dialysis

    10-15

    MUDPILES

    Salicylates

    Also causes respiratory alkalosis (BRS phys)

    Lactic acid

    Hypoxia

    Rx: Pressors

    INH

    TB Rx

    Young women, Suicide

    Paraldehyde

    DKA

    Acetoacetic acid

    B-OH-butyric acid

    Rx: Insulin

    Uremia

    Typically doesn't get that high because we dialyze before they get that sick.

    GFR < 15-20

    Rx: Dialyze

    Malnutrition

    10-12

    Hyperchloremic

    Urine anion gap

    > -20

    Renal

    RTA of renal insufficiency

    GFR usu. >15 ml/min

    Hyperkalemic

    Type 4 RTA

    Hyporeninemic, hypoaldosteronemic distal RTA

    Most common seen

    Diabetic patients

    You can generate a Type 4 RTA w/ drugs that limit Aldo fx on kidney





  • ACE
  • ARB
  • Aldo antagonists


  • Kidney for some reason doesn't respond to aldosterone

    OR aldosterone effects on kidneys are being blocked (drugs)

    Hypokalemic

    NH4CL Admin.

    No change in Urine pH

    Classical distal RTA

    Type 1 (only because it was discovered first)

    Proton back leak distally



  • Amphotericin B (makes holes)

  • K+ leaks out (hypokalemic) to compensate

    Urine pH < 5

    Proximal RTA

    Rare (Paraproteinemias --> Excessive amt of a single monoclonal gammaglobulin in the blood)

  • Waldenstrom's macroglobulinemia
  • Amyloidosis
  • Multiple myeloma

  • Abnormal protein damages the proximal tubule

    Iatrogenic


  • CA inhibitors (Acetazolamide)
  • Gentamicin

  • Part of generalized disorder of proximal tubular function known as --> Fanconi syndrome


  • Self-limiting

  • Problem w/ Bicarb reabsorption --> Serum bicarb load delivered to kidney reduces, so kidney can handle new steady state due to distal effects

  • Aldosterone action leads to hypokalemia




    HCO3 not reabsorbed --> Na+ travels with it --> juxtaglomerular apparatus senses sodium load passing through --> secretes renin --> Angiotensinogen to Angiotensin I (by renin)--> AgI to AgII (by ACE) --> Vasoconstriction + Aldosterone stimulation --> sodium intake distally, potassium excreted --> hypokalemia

  • < -20

    Extrarenal

    Ext. loss of secretions in GI

    Biliary

    Pancreatic

    Diarrhea