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pH<7.35 with decreased HCO3 and a decreased PCO2 |
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pH<7.35 with increased PCO2 with increased HCO3 |
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pH>7.45 with decreased PCO2 and decreased HCO3 |
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pH>7.45 with increased HCO3 and increased PCO2 |
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carbonic acid/bicarbonate |
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determined by ratio of PCO2 to HCO3 |
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Respiratory Regulation of pH |
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Definition
rate/depth of ventilation can be varied to modify CO2 excretion; increasing respirations increases CO2 excretion which increases pH; when used as a compensatory mechanism, ONSET is QUICK but capacity to reverse pH is LIMITED |
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H & NH4 are ions excreted in urine; HCO3 is reabsorbed; when used as a compensatory mechanism, ONSET is SLOW but capacity to reverse pH is GREAT |
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Causes of Metabolic Acidosis (low pH with low HCO3 and low PCO2) |
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Definition
caused by anion gap acidosis (MUDPILES), lactic acidosis (shock, severe anemia, heart failure, metformin [rare], NRTIs [HIV meds], ethanol), hyperchloremic acidosis (diarrhea, renal tubular acidosis) |
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Elevated serum anion gap (SAG) acidosis |
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Definition
type of metabolic acidosis; SAG = Na - (Cl + HCO3); SAG > 11 suggest excess unmeasured anions |
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Definition
form of metabolic acidosis associated with diabetes (decreased insulin causes increased fatty acid levels which are converted to ketoacids by excess glucagon) and alcoholism or starvation (decreased carb intake causes decreased levels of insulin & increased levels of glucagon) |
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form of metabolic acidosis caused by accumulation of lactic acid during anaerobic metabolism of glucose occurs; may occur in pts with large sections of small intestine removed |
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form of metabolic acidosis that occurs when Cl is present in diarrhea |
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Clinical Presentation of Metabolic Acidosis |
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Definition
pt presents generally as asymptomatic; chronic: bone demineralization; Severe symtpoms: tachycardia, decrease in cardiac output, nausea/vomiting, hyperventilation (compensatory), hyperglycemia & hyperkalemia |
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Treatment of Chronic Asymptomatic Metabolic Acidosis |
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Definition
treat condition over weeks; use NaHCO3 products, NaCitrate (Bicitra), KCitrate (Urocit K, Polycitra-K), KHCO3/citrate (K-Lyte), Na/K/Citrate (Polycitra) |
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Definition
used in treatment of chronic asymptomatic and severe metabolic acidosis; MoA: neutralizes H & raises pH; ADRs: bloating, hypernatremia, fluid overload; ADRs for severe tx: impaired O2 release from Hb, Na/fluid overload, paridoxical tissue acidosis, decreased myocardial contractility, many incompatibilities; Efficacy: slow but generally effective; Efficacy in severe tx: may be deleterious in lactic acidosis, limit use to pH<7.1, not for routine use in advanced cardiac life support |
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used to treat chronic asymptomatic metabolic acidosis; MoA: oxidized to HCO3 |
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potassium citrate (Urocit-K, Polycitra-K) |
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Definition
used to treat chronic asymptomatic metabolic acidosis & also hypokalemia; MoA: oxidized to HCO3; ADRs: hyperkalemia, GI ulceration, bradycardia, bloating; Efficacy: alternative for pts have fluid overload/hypokalemia |
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potassium HCO3/citrate (K-Lyte) |
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Definition
used to treat chronic asymptomatic metabolic acidosis; MoA: oxidized to HCO3; ADRs: hyperkalemia, GI ulceration, bradycardia, bloating; Efficacy: also alternative for pts w/ fluid overload/hypokalemia |
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Definition
used to treat chronic asymptomatic metabolic acidosis; MoA: oxidized to HCO3; ADRs: hyperkalemia, GI ulceration, bradycardia, bloating, fluid overload, hypernatremia; Efficacy: good if pt is hyponatremia/hypokalemic |
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Treatment of Severe Metabolic Acidosis |
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Definition
some pts require emergent HD; those with hyperchloremic acidosis may require several days of IV therapy; can't rely on hepatic conversion of acetate, citrate, or lactate to HCO3; treat with NaHCO3 and/or tromethamine (THAM) |
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Definition
used to treat severe metabolic acidosis; MoA: alkaline organic amine that neutralizes H & acts as osmotic diuretic; ADRs: respiratory depression, inflammation, hyperkalemia, impaired coagulation; Efficacy: no evidence to show its more efficacious than NaHCO3, use with extreme caution in pts with severe liver or kidney failure |
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Monitoring Parameters for Metabolic Acidosis |
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Definition
mild-moderate: periodic K & HCO3 levels; severe: ABGs 30 min after administration of NaHCO3 |
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Epidemiology & Etiology of Metabolic Alkalosis (high pH with high HCO3 and high PCO2) |
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Definition
very common in hospitalized patients; caused by: NaCl responsive (vomiting, gastric drainage, diuretic therapy), NaCl unresponsiveness (hyperaldosteronism, Cushing's syndrome), unclassified reasons (refeeding syndrome) |
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Pathophysiology of Metabolic Alkalosis |
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Definition
GI balance: H secreted in stomach, HCO3 secreted by pancreas --> NG suctioning & vomiting cause alkalosis; Diuresis: loop & thiazide diuretics cause Cl loss in association with Na & K --> minimizes HCO3 loss & results in alkalosis; Mineralcorticoid: excess mineralcorticoid activity stimulates H secretion & ammoniagenesis; PCNs: act as non-reabsorbable anions which enhances K & H secretion in renal tubules |
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Clinical Presentation of Metabolic Alkalosis |
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Definition
mild-moderate: asymptomatic; Severe: arrhythmias, mental confusion, tetany, muscle cramping, hypoventilation (compensatory) |
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Treatments of Metabolic Alkalosis |
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Definition
for NaCl responsive disorders: volume replacement with NS; if HF, acetazolamide (Diamox); if above measures are not effective: give hemodialysis (HD), hydrochloric acid, ammonium chloride, arginine monohydrochloride; NaCl resistant disorders: treat mineralcorticoid etiology --> switch to corticosteroid with less mineralcorticoid activity |
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Definition
used to treat metabolic acidosis if heart failure is occurring; MoA: carbonic anhydrase inhibitor that reduces H secretion at renal tubule & increases excretion of Na, K, HCO3, & water; ADRs: low Na, K, hepato- & nephrotoxic, NVD; Efficacy: helps lower pH but may not normalize pH |
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used to treat metabolic alkalosis if acetazolamide & NS are not working(not common); MoA: H dissociates from Cl to lower pH; ADRs: hemolysis, acidosis; Efficacy: should be discontinued at pH 7.5 |
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used to treat metabolic alkalosis if acetazolamide & NS are not working; MoA: liver converts ammonium chloride to HCl & urea; ADRs: ammonia toxicity (bradycardia, arrhythmias, coma), avoid in pts with severe hepatic or renal diseases; Efficacy: improvement in metabolic status seen within 24 hrs |
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arginine monohydrochloride |
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Definition
used to treat metabolic alkalosis in patients not responding to acetazolamide & NS; MoA: converted to HCl in liver; ADRs: accumulation of urea; Efficacy: not FDA approved, but better than ammonium chloride in pts with hepatic dysfunction |
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Monitoring Parameters for Metabolic Alkalosis |
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Definition
mild-moderate: ABGs, chem-7 after fluid resuscitation, periodically there after; severe: ABGs, chem-7 q4-8 hrs |
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Epidemiology & Etiology of Respiratory Acidosis |
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Definition
more common in ICU/hospital settings; Caused by: neuromuscular abnormalities (meds [anesthetics, opioids, sedatives], seizures), pulmonary abnormalities (COPD/asthma, severe pneumonia, severe pulmonary edema, massive PE), feeding (aggressive parenteral feeding), cardiac (cardiac arrest) |
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Pathophysiology of Respiratory Acidosis |
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Definition
increased PCO2 causes decreased pH, CO2 causes vasodilation of cerebral arteris resulting in CNS symptoms; pts with chronic condition utilize low O2 levels as a stimulus for breathing as PCO2 levels can be chronically elevated; in acute setting, hypoxia is prinicipal threat to life; Acute compensation: elevated PCO2 causes increase in carbonic acid --> dissociates to HCO3 which helps increase pH; in Delayed compensation: HCO3 reabsorption, ammoniagenesis, distal H secretion |
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Clinical Presentation of Respiratory Acidosis |
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Definition
Neurologic: altered mental status, seizures, coma; Cardiovascular: increased CO & hypotension (depending on severity); electrolytes: mild increase in K |
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Treatment of Acute Respiratory Acidosis |
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Definition
establish patent airway (may require mechanical ventilation); discontinue/reverse benzodiazepines (w/ flumazenil) & opioids (w/ naloxone), bronchodilators (albuterol) |
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Treatment of Decompensated Respiratory Acidosis |
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Definition
only administer O2 if PO2 < 50 mmHg (administration may result in depressed respiratory function); treat underlying conditions; utilize bronchodilators if possible |
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Monitoring Parameters of Respiratory Acidosis |
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Definition
acute/severe: ABGs q2-4 hrs, then q12-24 hrs as acidosis improves |
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Epidemiology & Etiology of Respiratory Alkalosis (low pH with low PCO2 and low HCO3) |
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Definition
most frequently occurring acid-base disorder, occurs in pregnancy & high altitudes, common in hospitalized pts; caused by: central stimulation of respiration (anxiety, catecholamines, nicotine), hypoxemia/tissue hypoxia (high altitude), peripheral stimulation of respiration |
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Pathophysiology of Respiratory Alkalosis |
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Definition
decrease in PCO2 results in elevated pH, decreased PCO2 causes reduced cerebral blood flow, Compensation: acute --> intracellular proteins, phosphates, Hgb release H to lower HCO3; delayed compensation: HCO3 reabsorption in kidney is inhibited, decreased H & NH4 secretion |
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Clinical Presentation of Respiratory Alkalosis |
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Definition
mostly asymptomatic, CNS/Neuromuscular: confusion, syncope, seizures, muscle cramps/tetany; CV: arrhythmias; GI: N/V; Respiratory: HYPERventilation |
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Treatment of Moderate Respiratory Alkalosis |
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Definition
treat underlying causes: relieve pain, treat infection, breathe into paper bag is useful for anxiety/hyperventilation syndrome, O2 therapy if severe hypoxemia; Severe: mechanical ventilation with sedation +/- paralysis |
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Monitoring Parameters for Respiratory Alkalosis |
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Definition
if severe: take pH, ABGs, and set ventilator frequently |
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