Acid Base Disorders 1 Flashcards
What is renal compensation in respiratory/metabolic acidosis?
- Chronic acidosis (if kidney normal)
- IncreasedH+ secretion by tubule
- Filtered bicarbonate is reabsorbed
- Urinary acid phosphate (titratable acidity) is increased
- Ammonium in urine is increased
- Urine pH b3comes acidic
Describe renal compensation in Respiratory/metabolic alkalosis
- Alkalosis (if kidney normal and fluid volume normal)
- Decreased H+ secretion by tubule
- Filtered bicarbonate NOT reabsorbed
- Urinary bucarbonate loss increases
- Acid phosphate and ammonium in urine decreases
- Bicarbonate also secreted by tubular cells
- Urine pH becomes alkaline
Increased bucarbonate loss in uribe
Summarize assessment of acid-base status
Clinical assessment is done by arterial blood fas (ABG) analysis
Arterial blood gas analysis: arterial pH, HCO3^-, PaCO2
Normal levels
PH: 7.35-7.45
PaCO2(PCO2): 33-45 mmHg
HCO3^-: 22-28mmol/L
How can we classify acid-base disorders?
Acidosis: pH is less than 7.35
Alkalosis: pH is greater than 7.45
Respiratory acid base disorders: dysfunction of respiratory system and characterized by primary changes in PaaCO2
metabolic acid base disorders: metabolic or renal disorders and characterized by primary changes in [HCO3^-]
What is the compensation of metabolic acidosis ?
Respiratory compensation
Leading to PCO2 below 40 mmHg
Renal compensation only if kidney is normal
What is the compensation mechanisms of respiratory acidosis ?
Renal compensation
Leads to b8carbonate compensation above 24 Mm
What is the compensatory mechanism of metabolic alkalosis ?
Respiratory compensation
Leads to PCO2 over 40 mmHg
Renal compensation only if kidney is normal and if fluid volume is adequate
What is the compensatory mechanism of respiratory alkalosis?
Renal compensation
Bicarbonate concentration below 24 Mm
What is the effect of compensatory mechanism on ratio of HCO3/PCO2?
If primary disorder is characterized by an increase in PaCO2 compensatory mechanisms will increase HCO3, to bring ratio towards normal and pH comes closer towards normal
-If primary disirder is characterized by a decrease in HCO3, compensatory mechanisms will decrease PaCO2, to bring ratio towards normal and pH comes closer to normal
COMPENSATION always in the SAME DIRECTION
Give an example of respiratory acidosis
A 45 year old man comes to the physician because of a 1-day history of fever and cough. He is a chronic smoker for the past 20 years. He was diagnosed with chronic obstructive pulmonary 2 years ago.
Arterial blood gas shows
Ph: 7.25 (acidosis)
PCO2: 60 mmHg (primary Distrpurbance) respiratory
Bicarbonate conc.: 25 mmol/L(acute)
Describe respiratory acidosis
Characterized by decreased rate of respiration/decreased lung function/ decreased air entry into the lungs
- As a result, CO2 is NOT washed out (CO2 accumulation), resulting in elevation of PaCO2 (primary abnormality)
- Remember, CO2 is an ACID, and it’s accumulation causes respiratory acidosis
Acute stage:
- pH decreased (lower than 7.36)
- PaCO2 elevated (primary disturbance)
- HCO3 ^- is almost normal
give an e ample of chronic respiratory acidosis
A 45 year old man 5 days of onset of lung infection (if not treated or treatment not effective)
Arterial blood gas analysis (chronic respiratory acidosis)
Ph: 7.32(compare to day 1, closer to normal) acidosis
PCO2: 60 mmHg (primary change) respiratory
Bicarbonate conc.: 32 mmol/L (compensated by kidneys)
Describe chronic respiratory acidosis with compensation
- During compensation, renal system comes to rescue
- Kidneys excrete more H+, and generate more HCO3^- , and serum bicarbonate conc levels increase.
- Increased excretion of phosphate (titratable acid) and ammonium in urine
Chronic respiratory urine
- pH: lower than normal (<7.36)- closer to normal pH, when compared to acute stage
- PaCO2: elevated (primary defect is still not corrected- respiratory system is still not functioning optimally)
Explain the impact of the Henderson hassalbach equation in respiratory acidosis
pH= pka+ logincreased [HCO3^-]/0.03 x increased PCO2
Primary abnormality increases PCO2 due to respiratory disease—> fall in pH
Compensation by renal system, increases serum [HCO3^-], and ratio of [base]/[acid] returns almost to normal, and pH comes toward normal (still below normal)
Compensation always in same direction to bring ratio towards normal
What are the causes of respiratory acidosis ?
Airway obstruction by foreign body
Central causes: opioids, anesthetics
Disease/injury to phrenic nerve: guillian barre syndrome; multiple sclerosis
Lung diseases: COPD, RDS, fibrosis of lung, collapse of lung
- Drugs which inhibit respiratory center (opioids, anesthetics)
- Diseases/injury of phrenic (supplies diaphragm)
- Lung diseases: chronic obstructive pulmonary disease(COPD), fibrosis, respiratory distress syndrome infants or in chronic smokers (Acute respiratory distress syndrome, ARDS)
- Foreign body in Respiratiry tract
- Demyelinating disorders: Gillian barre syndrome, multiple sclerosis
Give an example of acute respiratory alkalosis
A 25 year old student has been out camping in the himalaya (high altitude) . She is hyperventilating.
Hypoxia stimulates the respiratory center
Secondary day of her stay, her arterial blood gas results:
- ph: 7.57 alkalosis
- PaCO2: 20 mmHg Respiratiry
- bicarbonate conc. 22 mmol/L acute
What is acute respiratory alkalosis ?
Respiratory alkalosis characterized by increase in rate of respiration (hyperventilation) —> increased washout of CO2. —> decreased PaCO2 (primary disturbance)
Acute respiratory alkalosis
- ph is decreased (greater than 7.44)
- PaCO2 is decreased (below 35mmHg)
- bicarbonate conc. Is almost normal
What is the arterial blood gas of chronic respiratory alkalosis ?
Arterial blood gas:
Ph: 7.46 (compare to 2 days, it is closer to normal) alkalosis
PaCO2: 20 mmHg (primary disturbance)
Bicarb9nate conc. 17 mmol/L(renal compensation and increased bicarbonate conc. In ursine)(chronic)
What is the bodily response to chronic respiratory alkalosis?
Renal system tries to bring pH back towards normal
Kidneys do NOT secrete H+ into urine
Increased urinary HCO3^- excretion (beta intercalated cells) and pH of ursine Becomes alkaline, and serum HCO3^- falls
Chronic respiratory alkalosis
- pH: higher than normal- closer to normal pH, when compared to acute stage
- PaCO2: decreased (primary defect still not corrected- respiratory system is still hyperventilating)
- bicarbonate concentration: decreased (renal compensation)
What is the impact of Henderson-hassalbach equation in respiratory alkalosis?
pH= pKa+ log decreased [HCO3^-]/ 0.03 x PaCO2
Primary abnormality decreased PaCO2 due to hyperventilation, which results in rise in pH (alkalosis)
-Compensation by renal system, decreases serum [HCO3^-], ratio of [base]/[acid] ratio returns closer to normal, and pH comes toward normal (still above normal)
Compensation always in same direction to bring ratio towards normal
What are the causes of respiratory alkalosis?
Causes of hyperventilation
- Anxiety, fever, somatic symptoms disorder
- high altitude: hypoxia stimulates respiratory center and increases rate of respiration. When a person stays for a long time at elevated altitude, renal compensatory mechanisms are active and bicarbonate concentration levels fall
- Refer to hemoglobin lecture: identify changes in oxygen dissociation curve when a person is adapted to high altitude
- Mechanical ventilation: (over ventilation)
- Drugs that stimulate respiratory center (acute salicylate poisoning)
What is the arterial blood gas metabolic acidosis?
pH: 7.2 PaCO2: 30 mmHg Bicarbonate conc. : 12 mmol/L (bucarbonate loss for buffering ketone bodies- primary abnormality) Na+: 140 mEq/L CL-: 100 mEq/L K+: 5.2 mEq/L
Plasma glucose: 500 mg/dL
Dipstick test with urine for ketone bodies and glucose is positive
She is hyperventilating (kussmaul breathing)
What are the characteristics of metabolic acidosis?
Characterized by acidosis Decreased bicarbonate conc. and low pH
Bicarbonate Conc. Is low due to
- increased nonvolatile acids [HCO3^-] is lost by buffering
- or due to increased losses of HCO3^-
Acidosis stimulates respiratory center—> hyperventilation and a fall in PaCO2 (remember, respiratory center responds within minutes)
-When plasma pH falls, respiratory center stimulated—> increased rate and depth of respiration —> increased CO2 washout leads to decreased PaCO2(compensatory hyperventilation)
What is the role of kidney in metabolic acidosis?
- If kidney is functioning, can also compensate to increase H+ excretion, increases formation of new HCO3^-
- Renal system takes hours to days to respond
- Increased H+ secretion in renal tubules
- Increased excretion of acid phosphate (titratable acid) and ammonium in urine
- However, until cause of acidosis is treated, pH doesn’t come back to normal
What is the Henderson-hassalbach equation impact in metabolic acidosis?
- Primary abnormality is decreased HCO3^-, which results in a fall in pH
- Compensation by respiratory system, results in hyperventilation, and decreases PaCO2, and ratio of base/acid conc. returns almost to normal, and pH comes toward normal (it is below normal)
The kidneys can compensate too, if they are normal- they try to increase the serum HCO3^-
Describe H+ and K+ interrelations in acidosis/alkalosis
K+ (major intracellular cation)
K+ and H+ are intricately related
Diabetes mellitus-insulin deficiency and hyperglycemia (hyper osmolarity)-K+ shift from ICF to ECF (hyperkalemia)
Changes in pH affect serum (DCF) K+ levels
- metabolic acidosis- hyperkalemia
- metabolic alkalosis- hypokalemia
Also, changes in serum K+ affects pH
- Hyperkalemia- acidosis
- Hypokalemia- alkalosis
What is the role of serum K+ and diabetic ketoacidosis?
Serum K+ is increased(K+: 5.3 mEq/L)
- plasma glucose: 500 mg/dL (ECF hyper osmolarity causes K+ to shift from ICF to ECF with osmotic fluid shift)
- Insulin deficiency in type 1 diaabetes mellitus prevents K+ entry into ICF (K+ levels in ECF increase)- remember, insulin activated Na-K ATPase
What is the anion gap?
Anion gap= cations- sum of anions
Anion= [Na+] -([Cl- ]-[HCO3-])
Normal anion gap is 8- 14 mEq/L
Due to presence of unmeasured anions
Unmeasured anions: phosphate, sulfate, lactate, ketone bodies and protein
In some forms of metabolic acidosis, there is increase in unmeasured anions, resulting in increased anion gap
How can we calculate the anion gap?
pH: 7.2 PaCO2: 30 mmHg [HCO3-]:12 mmol/L Na+: 140 mEq/L Cl-: 100 mEq/L K+: 5.3 mEq/L
140-112=28 mEq/L(normal 8-16 mEq/L)
High anion gap metabolic acidosis
In ketoacidosis, ketone bodies are the unmeasured anions
What ABG of metabolic acidosis with a normal anion gap?
ABG: pH: 7.24 PCO2: 30 mmHg Bicarbonate conc.: 12 mmol/L(bicarbonate loss in intestinal secretions- primary abnormality) Na+: 140 mEq/L CL-: 116 mEq/L
Calculate anion gap:140-128= 12 mEq/L(8-14 mEq/L)
Normal anion gap (hyperchloremic) metabolic acidosis
What are the causes of metabolic acidosis?
Increased production of non-volatile acids (high anion gap metabolic acidosis)- increased unmeasured anions
Increased loss of HCO3^-(base)- normal anion gap metabolic acidosis- hypercholermic acidosis
What is the effect of metabolic acidosis dye to increased production 9f nonvolatile acidosis?
High anion gap metabolic acidosis-increased unmeasured anions
Leads to:
- diabetic ketoacidosis (increased ketone body production)
- lactic acidosis (increased lactate)
- chronic renal failure(decreased excretion of sulfate, phosphate)
- Methanol and ethylene glycol poisoning
What is the effect of metabolic acidosis due to increased HCO3^-
Normal anion gap metabolic. Acidosis- hyperchloremic acidosis
- Diahrrea (increased loss of HCO3^- rich intestinal secretions)
- Renal tubular acidosis(failure to secrete H+ and reabsorb HCO3^-)
- Acetazolamide treatment (inhibits renal carbonic anhydrase)
Whaat is the metabolic alkalosis ABG?
pH: 7.56
PaCO2: 50 mmHg
Bicarbonate conc.: 30 mmol/L (primary abnormality) metabolic
What is the effect of vomiting/ nasogastric suction ?
Loss of acid
Parietal cells contain carbonic anhydrase
For every H+ pumped into the gastric lumen, one HCO3^- gained by blood
What are the characteristics of metabolic alkalosis?
Increased bicarbonate conc. ( relative excess of HCO3^-)
Increased pH (alkalosi) inhibits respiratory center, there is a decrease in rate of respiration (hypoventilation)—> decreased washout of CO2 (CO2 retention )—> increased PaCO2
Metabolic alkalosis
- pH- higher than normal
- bicarbonate conc. Is increased (primary abnormality)
- PaCO2 is increased (compensatory mechanism)
Give renal compensation if metabolic alkalosis.
- Renal system compensates, if it is functioning normally, by excreting more HCO3^-(alkaline urine)
- Beta-intercalated cells secrete bicarbonate into urine
What is the impact on the Henderson hassalbach equation in metabolic alkalosis?
- Primaary abnormality is increased HCO3^-, which results in a rise in pH
- Compensation by respiratory system, increases PaCO2, and the ratio of base:acid ratio returns almost to normal, and pH comes toward normal (it is still above normal)
Kidneys can compensate if they are normal and if fluid volume is adequate
What is the renal response in metabolic alkalosis that results in volume contraction ?
When there is volume depletion, renal compensation firvalkalosis may not be seen
RAAS is active
Kidneys try to conserve sodium and secrete protons in urine (Na-H+ exchanger active )- resulting in aacidic urine- paradoxical aciduria
What is the cause of metabolic alkalosis?
- Vomitting, pyloric stenosis (gastric outlet obstruction)
- Loss of acidic contents of stomach, results in relative HCO3^- excess
- Nasogastric suction: a tube removes acidic contents of stomach
- Excessive consumption of antacids
- Primary hyperaldosteronism causes hypokalemia and metabolic alkalosis
- Hypokalemia
- diuretics (cause bulk of Na in tubules) —> K+ secretion —> hypokalemia—> alkalosis
