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WorksheetsAcevedo exam nephrology 3
Total questions: 65
Worksheet time: 37mins
►Normal pH: 7.40 (7.35-7.45)
true
false
►pH<7.35 (acidic)
Acidemia:
Alkalemia:
HCO3-: bicarbonate
CO2 blood test is really a measure of your blood HCO3- level because most of the CO2 in the body is in the form of HCO3-
unit (mEq/L or mmol/L) on ABG panel (“metabolic base”)
CO2 blood test is really a measure of your blood H3CO2- level because most of the CO2 in the body is in the form of HCO3-
PO2 which are true?
PCO2: partial pressure (mmHg) of carbon dioxide (“respiratory acid”) dissolved in blood;
Low levels can be caused by hypoventilation
high levels can be caused by hypoventilation
May be measured from the arteries PaO2 (ABG)
the amount of oxygen attached to hemoglobin in arterial blood (e.g., oxygen saturation)
SaO2 (%):
Hypoxia:
Hypoxemia
insufficient oxygen supply to body tissues/organs
Hypoxemia:
Hypoxia:
insufficient oxygen in the blood Reduction of PO2 to below 80mmHg
Hypoxia:
Hypoxemia:
substance that can donate protons (hydrogen ion [H+])
►Base:
►Acid:
substance that can accept protons
►Base:
►Acid:
Renal regulation
Slower onset (~24-48 hours): controls HCO3-
increase HCO3- and increase pH
decrease HCO3- decrease pH
pH <7.4 increase
PCO2 increase a >40 mmhg
respiratori acidosis
metabolic acidosis
pH<7.4
decrease in bicarbonate <24 mEq/L
metabolic acidosis
respiratory acidosis
pH >7.4 decrease of PCO2 <40 mmhg
respiratory alkalosis
metabolic alkalosis
pH>7.4 increase HCO3 >24 mEq/L
respiratory alkalosis
metabolic alkalosis
Respiratory regulation
►Chemoreceptors (arterial/medulla)
increase RR/tidal volume increase CO2 excretion
decrease PCO2 increasepH
Slow & shallow: retains CO2
Fast & deep: blows off CO2
Respiratory regulation
►Chemoreceptors (arterial/medulla)
decrease RR/tidal volume decrease CO2 excretion
increase PCO2 decrease pH
Slow & shallow: retains CO2
Fast & deep: blows off CO2
Renal regulation: Mechanisms of homeostasis
Slower onset (~24-48 hours): controls HCO3- decrease HCO3- increase pH and decrease HCO3- increase pH .
Generation of HCO3-
Filtration or reabsorption of HCO3-
Excretion of H+
Slower onset (~24-48 hours): controls HCO3- increase HCO3- increase pH and decrease HCO3- decrease pH .
Arterial Blood Gas (ABG) Analysis step:
none
►Step 1. Analyze the pH ►Step 2. Analyze the CO2
►Step 3. Analyze the HCO3- ►Step 4. Determine the primary disturbance
►Step 5. Evaluate for compensation ►Step 6. Evaluate the PO2 and SO2
*Compensation will always be from the opposite regulatory system and will always go in the same direction as the primary disturbance*
true
false
Respiratory acidosis
Metabolic acodosis
Respiratory alkalosis
Metabolic alkalosis
Respiratory acidosis
Metabolic acidosis
Respiratory alkalosis
Metabolic alkalosis
Respiratory acidosis
Metabolic acidosis
Respiratory alkalosis
Metabolic alkalosis
Respiratory acidosis
Metabolic acidosis
Respiratory alkalosis
Metabolic alkalosis
High anion gap metabolic acidosis
Non-anion gap:hyper choleemos metabolic acidosis (CURSED +AP
High anion gap metabolic acidosis
Non-anion gap:hyper choleemos metabolic acidosis (CURSED +AP
Loss H+
Exogenous alkali
Volumen loss
Others
Loss H+
Exogenous alki
Volumen loss
Other
Loss H+
Exogenous alki
Volumen loss
Other
Loss H+
Exogenous alki
Volumen loss
Other
Metabolic acidosis
Acute respiratory acidosis
Chronic respiratory acidosis
Metabolic acidosis
Acute respiratory acidosis
Chronic respiratory acidosis
Metabolic acidosis
Acute Respiratory acidosis
Chronic respiratory acidosis
Metabolic alkalosis
Acute respiratory alkalosis
Chronic respiratory alkalosis
Metabolic alkalosis
Acute respiratory alkalosis
Chronic respiratory alkalosis
Metabolic alkalosis
Acute respiratory alkalosis
Chronic respiratory alkalosis
Metabolic acidosis
Acute respiratory acidosis
Chronic respiratory acidosis
Metabolic acidosis
Acute respiratory acidosis
Chronic respiratory acidosis
Metabolic acidosis
Acute respiratory acidosis
Chronic respiratory acidosis
Metabolic alkalosis
Acute respiratory alkalosis
Chronic respiratory alkalosis
Metabolic alkalosis
Acute respiratory alkalosis
Chronic respiratory alkalosis
Metabolic alkalosis
Chronic respiratory alkalosis
Acute respiratory alkalosis
Loss of HCO, replaced by Cl
and/or gain of H+
gain of H+
gain of H+H
Loss of HCO, replaced by Cl
and/or gain of H+
metabolic acidosis? which are true
Rapid administration of non-alkali-containing IV fluids
Loss of HCO3- through body fluids Diarrhea, biliary drainage, pancreatic fistula
Consumption of HCO3- in order to neutralize acids (e.g., buffering)Endogenous acids Exogenous acid Organic acids accumulating because of a metabolic disturbance (e.g., lactic acid, ketoacids)
none
►Serum anion gap (SAG) Otherwise known as anion gap (AG) Used in the differential diagnosis for metabolic acidosis To maintain electroneutrality: cations = anions [Na+] + [UCs] = [Cl-] + [HCO3-] +[UAs]
none
UAs = unmeasured anions: proteins, sulfates (SO42-) phosphates (PO43-), organic anions
UCs = unmeasured cations: Mg2+, Ca2+, K+
UCs = unmeasured cations: proteins, sulfates (SO42-) phosphates (PO43-), organic anions
UAs = unmeasured anions:Mg2+, Ca2+, K+
SAG = [Na+] – [Cl-] – [HCO3-] Combining the equation
SAG = [Na+] – [Cl-] – [HCO3-]
with the equation
[Na+] + [UCs] = [Cl-] + [HCO3-] +[UAs]
Normal SAG = 9 mEq/L (mmol/L) (range 3-11)
SAG = [UAs] – [UCs]
SAG = [UAs] + [UCs]
SAG =[UCs] – [UAs]
Two major types of metabolic acidosis
Non anion gap/hyperchloremic metabolic acidosis
anion gap/hyperchloremic metabolic acidosis
High anion gap metabolic acidosis
low anion gap metabolic acidosis
Results in a normal SAG because HCO3- losses from ECF are effectively replaced by Cl-
SAG = [Na+] – [ Cl-] – [ HCO3-]
High anion gap acidosis
Non-anion gap(non AG)/hyperchloremic metabolic acidosis
SAG = [Na+] – [Cl-] – [ HCO3-]
When SAG >20 to 25 mEq/L (mmol/L) a significant organic acidosis is likely
High anion gap acidosis (high AG)
Non-anion gap(non AG)/hyperchloremic metabolic acidosis
Metabolic Acidosis: Clinical Presentation
Hyperkalemia
Severe acidemia: pH<7.15-7.20, plasma HCO3-<8 mEq/L (mmol/L) Hallmarks: dyspnea, hyperventilation with deep, rapid respirations (to increase CO2 excretion)
Mild to moderate acidemia: pH 7.2-7.4 Usually asymptomatic
Compensation: hyperventilation leading to decrease PaCO2
Low serum CO2
metabolic acidosis treatment ►Asymptomatic/mild to moderate: pH 7.2-7.4
Oral alkali replacements (i.e., sodium bicarbonate) Over 3-5 days
HD (cardiac instability/electrolyte disturbances) IV alkali therapy
metabolic acidosis treatment ►Severe acidemia: pH<7.15-7.20, plasma HCO3-<8mEq/L (mmol/L)
Oral alkali replacements (i.e., sodium bicarbonate) Over 3-5 days
HD (cardiac instability/electrolyte disturbances) IV alkali therapy
Metabolic Alkalosis: Clinical Presentation
►Hypokalemia
►Mild to moderate alkalemia (pH 7.4-7.6) May have symptoms related to underlying cause of disorder (e.g., muscle weakness with hypokalemia, postural dizziness or orthostatic hypotension with volume depletion, etc.
►Decreased iCa (increase albumin binding due to decrease competition from H+ ions)
►Severe alkalemia: pH>7.60 Cardiac arrhythmias Particularly in patients with heart disease, hyperventilation, hypoxemia Neuromuscular irritability w/signs of tetany or hyperactive reflexes due to secondary decreased iCa
►Compensation: hypoventilation resulting in increase PaCO2
Metabolic Alkalosis:Treatment
Acetazolamide PO 250-350mg QD or BID
Persistent alkalosis or if initial pH >7.60 use agents RARE!) Hydrochloric acid (preferred for those with renal failure, liver failure, or decompensated CHF) Ammonium chloride Arginine monohydrochloride Hemodialysis using a low-bicarbonate dialysate
Sodium chloride resistant or unclassified Correct underlying or potentially contributing causes concomitant electrolyte imbalances
Exogenous corticosteroid therapy: decrease dose or switch to one with less mineralocorticoid activity
Liddle syndrome: amiloride or triamterene
Endogenous mineralocorticoid excess (e.g., Bartter’s or Gitelman): spironolactone, amiloride, or triamterene (if no response, consider surgery)
Severe potassium depletion (<3 mEq/L): PO or IV K+ supplementation
Excess alkali intake, refeeding syndrome, high dose PCN: adjust therapy
Ammonium chloride (Rare! treatment) Liver converts ammonium chloride (NH4Cl) to urea and free hydrochloric acid
True
FAlse
Arginine monohydrochloride (Rare!)
Off-label dosing (not FDA-approved) 10 g/h IV
Similar to ammonium chloride: arginine is metabolized by the liver to produce H+ ions, with a conversion of 100 g to 475 mEq (mmol) of H+
Administer cautiously to patients with impaired kidney or hepatic function
Impaired kidney function: increase urea synthesis and associated BUN may be associated with severe hyperkalemia caused by arginine-induced shifts of potassium from ICF -> ECF
Impaired hepatic function: Can be used in patients with relative hepatic insufficiency (unlike ammonium chloride) because arginine combines with ammonia in the body to synthesize urea
Decreased iCa (increase albumin binding due to decrease competition from H+ ions)
metabolic acidosis
metabolic alkalosis
Mild to moderate acidosis: pH 7.2-7.4, PaCO2>50-55 mmHg, up to 80mmHg
Mild to moderate acidosis:
Severe acidosis:
pH<7.15-7.20, PaCO2>80 mmHg
Severe acidosis:
Mild to moderate acidosis:
Respiratory Acidosis:
►Hypoxia is often present (PaO2 <70 mmHg)
►Moderate (PaCO2 of 50-55 mmHg) to severe (PaCO2 >80 mmHg) hypercapnia
►Hyperkalemia
Respiratory alkalosis
hypokalemia
Mild to moderate alkalemia: pH 7.4-7.6
sually relatively asymptomatic Hyperventilation or symptoms related to decreased PaCO2 or decreased cerebral blood flow: light-headedness, confusion, seizures, nausea/vomiting, etc.
Severe alkalemia: pH>7.60 Cardiac arrhythmias Neuromuscular irritability
hyperkalemia
High anion gap acidosis (high AG)
When SAG >20 to 25 mEq/L a significant organic acidosis is likely
When SAG <20 to 25 mEq/L a significant organic acidosis is likely
AG >17-20 mEq/L (mmol/L): possible organic acidosis
A 23 YOM is admitted to the hospital due to extreme fatigue and vomiting. He is also experiencing significant muscle weakness…
ABG: 7.48/48/80/36
metabolic alkalosis
metabolic acidosis
Address hypokalemia (along with magnesium first if low) + normal saline
Address hyperkalemia (along with magnesium first if low) + normal saline
A 28 YOF presents to the ED with chief complaint of severe diarrhea over the last week…
metabolic acidosis
metabolic alkalosis
respiratory acidosis
respiratory alkalosis
