Nephrology > Acid-Base and the Renal System > Flashcards

Acid-Base and the Renal System Flashcards

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1
Q

pH is determined by what?

Henderson-Hasselbach equation?

A

the ratio of CO2 to HCO3

pH = 6.10 + log ([HCO3] ÷ [0.03 X PCO2])

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2
Q
  1. Each day the body generates acids that must be what? 2
  2. How much CO2 produced daily?
  3. Cellular metabolism generates organic acids which are metabolized to what?
A
  1. buffered or excreted
  2. 15,000 mmol of CO2 produced daily
  3. metabolized to
    - glucose,
    - CO2 or
    - water
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3
Q

Acid base balance is maintained by what? 3

A
  1. Respiratory: CO2 is exhaled via the respiratory system
  2. Metabolism: Metabolic utilization of organic acids
  3. Renal: excretion of nonvolatile acids
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4
Q

Renal excretion of acid is accomplished how?

A
  1. H+ ions combined with urinary buffers
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5
Q

H+ ions combined with urinary buffers are excreted by the urine. Which buffers are we talking about?
4

Give an example of a major adaptive response that happens due to this process?

A
  1. Phosphate (HPO4 = H → H2PO4)
  2. Urate
  3. Creatinine
  4. Ammonia (NH3 + H → NH4)

Major adaptive response is an increase in ammonium excretion in the urine

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6
Q

What are the three kinds of buffers we talked about?

A
  1. Respiratory
  2. Renal
  3. Carbonic acid-bicarbonate buffer
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7
Q

Describe the physiology of the Respiratory Buffer system?

How soon may compensation occur?

A

pH will trigger an increase or decrease in the rate and depth of ventilation until the appropriate amount of CO2 has been re-established

Compensation may occur within minutes

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8
Q

Respiratory compensation

Within an intact respiratory system there is a prediactable amount of buffer for CO2. Describe this for:

  1. Metabolic acidosis?
  2. Metabolic alkalosis?
A

Metabolic acidosis
1. PCO2 will decrease by 1.3 mmHg for every 1 mEq/L drop in the serum HCO3

Metabolic alkalosis
2. PCO2 will increase 0.7mmHg for every 1 mEq/L increase in HCO3

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9
Q

Bicarbonate HCO3-:

  1. Is what kind of ion?
  2. What is it a buffer for?
  3. What maintains the balance of HCO3- and H+?
  4. There is a small immediate change due to what?
  5. Kidneys affect changes in the pH which take how long?
A
  1. Base
  2. Buffer for hydrogen ions
  3. Renal system maintains the
  4. whole body buffering system
  5. 3-5 days
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10
Q

Bicarbonate buffer: How much will HCO3- change in the following settings:

  1. Acute respiratory acidosis
  2. Chronic respiratory acidosis
  3. Acute respiratory alkalosis
  4. Chronic respiratory alkalosis
A
  1. HCO3 will increase 1 mEq/L per 10mmHg increase in PCO2
  2. HCO3 will increase 3.5 mEq/L per 10mmHg increase in PCO2
  3. HCO3 will decease by 2 mEq/L per 10mmHg decrease in PCO2
  4. HCO3 will decrease by 5 mEq/L per 10mmHg decrease in PCO2
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11
Q

Carbonic acid-bicarbonate buffer system
1. Whats the chemical equation again?

  1. If there is an increase in the H+ concentration in the blood it can be converted into what?
  2. If H+ concentrations in the blood drop below the desired level then carbonic acid will do what?
  3. When CO2 levels increase it is converted into?
A
  1. CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-
  2. carbonic acid
  3. dissociate
  4. carbonic acid
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12
Q

The end goal of blood gas analysis is what?

What are the 4 etiologies?

A

Determine if the acid base disturbance is metabolic or respiratory in etiology

  1. Respiratory acidosis
  2. Respiratory alkalosis
  3. Metabolic acidosis
  4. Metabolic alkalosis
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13
Q

Respiratory acidosis

  1. What is the main problem?
  2. What is this caused by?
  3. How do we correct this?
A
  1. too much CO2.
  2. something wrong with ventilation (rib fractures, something wrong with the pulmonary cap membrane)
  3. Ventilator, meds etc
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14
Q

Respiratory acidosis occurs at what levels:
pH?
PaCO2?

A

pH less than 7.35 with a PaCO2 > than 45 mm Hg

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15
Q

Causes of Respiratory Acidosis

4

A
  1. Central nervous system depression
  2. Impaired respiratory muscle function
  3. Pulmonary disorders
  4. Hypoventilation
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16
Q

Describe what could cause the following resulting in respiratory acidosis?

  1. Central nervous system depression 2
  2. Impaired respiratory muscle function 3
A
    • medications (narcotics, sedatives, or anesthesia)
    • head injury
    • spinal cord injury,
    • neuromuscular diseases
    • neuromuscular blocking drugs
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17
Q

Describe what could cause the following resulting in respiratory acidosis?

  1. Pulmonary disorders 7
  2. Hypoventilation 5
A
    • Atelectasis
    • Pneumonia
    • Pneumothorax
    • Pulmonary edema
    • Bronchial obstruction
    • Massive pulmonary embolus
    • Respiratory failure
    • Pain
    • Chest wall injury/deformity
    • Abdominal distension
    • Obesity
    • Trauma
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18
Q

Respiratory Alkalosis
1. What is the main problem?

  1. How do you correct that?
A
  1. Hyperventilation

2. Correct the underlying cause
fever, sepsis, anxiety, pain

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19
Q

Respiratory Alkalosis
pH at?
PaCO2 at?

A

pH >7.45 with a PaCO2 less than 35 mm Hg

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20
Q

Causes of respiratory alkalosis?

4

A
  1. Psychological responses (anxiety, fear)
  2. Increased metabolic demands
  3. Medications, such as respiratory stimulants
  4. Central nervous system lesions
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21
Q

What would cause increased metabolic demands that lead to respiratory alkalosis?
4

A
  1. Fever,
  2. sepsis,
  3. pregnancy
  4. thyrotoxicosis
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22
Q

What is the problem in Metabolic acidosis?

A

Not enough HCO3- to buffer the acidic state of the body (not enough bicarb to buffer or too much acid)

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23
Q

Metabolic acidosis:
How can bicarb be lost? 1

Or too much acid can build up? How? 3

A
  1. GI or renal losses
  2. Excretion problem- Renal disease
  3. Intake - Overdose
  4. Metabolism issues – anaerobic, ketone bodies
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24
Q

Metabolic Acidosis
HCO3- level at?
pH at?

The presence of metabolic acidosis should spur a search for what?

A

bicarbonate level of less than 22 mEq/L with a pH less than 7.35

hypoxic tissue somewhere in the body.

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25
Metabolic Acidosis can be caused by? | 6
1. Renal failure 2. Diabetic ketoacidosis 3. Diarrhea 4 Anaerobic metabolism --from tissue hypoxia 5. Starvation 6. Salicylate intoxication
26
1. The anion gap can be used for what? 2. Whats the equation? 3. Whats the nromal range?
1. Can be used to narrow down the etiology of the metabolic acidosis 2. AG = Na – (HCO3 + Cl) 3. Traditionally normal range 12 +/- 4 mEq/L (if measured automatically the reference range may be different) Just the difference between the cations and anions
27
Non acid base disorders that may cause errors in AG interpretation?
1. Low albumin 2. Hypernatremia 3. Hyponatremia 4. Certain antibiotics
28
For every __mEq/L decrease in serum albumin the AG will decrease by __mEq/L
1 2
29
Major unmeasured cations? 4 Major unmeasured anions? 4 Why dont we measure these? So if the Anion Gap is altered how does this inform us there is abnormalities in these?
1. Ca++ 2. Mg++ 3. Gamma-glubulins 4. K+ 1. Albumin 2. Phosphate 3. Sulfate 4. Lactate (sepsis, hypoxemia, exercise) Because they dont change Because these readily change and if one is elevated then it will dump the opposite anion or cation to compensate. (ex. dump Cl- if K+ is low)
30
Why the AG should always be calculated | 2
1. It is possible to have an abnormal AG even if the sodium, chloride and bicarbonate levels are normal 2. A large AG (>20) suggests a primary metabolic acid-base disturbance regardless of the pH or serum bicarbonate levels (respiratory system would never get that out of range)
31
Increased AG metabolic acidosis 1. First step should be? 2. In an increased AG acidosis there should be a mole for mole ________in HCO3 as the AG _______? 3. A corrected HCO3 higher or lower than normal (24) indicates the concomitant presence of what? 2
1. Calculate the corrected HCO3 2. decrease increases 3. metabolic alkalosis or normal AG gap metabolic acidosis
32
Increased anion gap metabolic acidosis : Causes? | MUDPILES.
``` M – methanol intoxication U - uremia D – diabetic or alcoholic ketoacidosis P – paraldehyde I – Isoniazide or iron overdose L – lactic acid E – ethylene glycol intoxication S – salicylate overdose ```
33
Non-anion gap metabolic acidosis: Causes? | USED CAR
U - Ureteral- sigmoid diversions -accumulate urine in intestine, reabsorb Cl- -H20 in intestine, secrete bicarb in intestine S – small bowel fistula, saline administration E – Endocrinopathies -Addison’s, Hyperparathyroidsim D – Diarrhea C – carbonic anhydrase inhibitors A - (hyper)alimentation (TPA) R - Renal tubular acidosis
34
Metabolic alkalosis: What is the problem? How can this occur? 2
Too much HCO3- 1. Can occur with excessive H+ loss - -GI or renal 2. Or a gain in HCO3-
35
Metabolic Alkalosis: | bicarbonate level___ mEq/L with a pH ____
> 26 | > 7.45
36
How can you get too much bicarb? 3 How can you lose too much acid?5
Excess base occurs from ingestion of: 1, antacids 2. excess use of bicarbonate 3. use of lactate in dialysis Loss of acids can occur secondary to: 1. protracted vomiting (loss of Cl- and you dont get that chloride coming in) 2. gastric suction (same as above) 3. Hypochloremia* 4. Excess administration of diuretics 5. High levels of aldosterone Lack of H+ then doesnt get down to the small bowel to connect with bicarb
37
Symptoms of Alkalosis | 3
1. Increased neuromuscular irritability Severe alkalosis 2. Pt may become belligerent 3. CNS depression
38
Signs of increased neuromuscular irritability that is caused by alkalosis? 3 What happens in CNS depression? 2
1. Paresthesias of the fingers and toes 2. Tetany 3. Seizures 1. Confusion—lethargy 2. Death at a pH around 7.8
39
Gastric hydrogen loss in metabolic alkalosis: 1. Each mEq of H+ lost generates __mEq of HCO3- 2. Normally H+ is secreted into the stomach. Explain why it might not be and how this is occurs in alkalosis? 3
1. 1 2. - When acidic chyme enters small intestine HCO3- is secreted into the lumen - Person vomiting—H+ being lost so HCO3- not secreted - Cl- also secreted with H+ so lost with vomiting
40
Renal H+ loss with metabolic alkalosis caused by what? | 3
1. Loop or thiazide diuretics 2. Excess aldosterone: 3. Posthypercapnic alkalosis
41
1. Renal H+ loss with metabolic alkalosis caused loop or thiazide diuretics: How does this occur? 3
1. -Increased flow to DCT and CT—increased reabsorption of Na+ 2. -As Na+ reabsorbed increased secretion H+ and increase HCO3- reabsorption 3. -May also get volume contraction
42
Renal H+ loss with metabolic alkalosis caused by excess aldosterone: 1. Causes? 2 2. Secreting what? 3. Retaning what?
1. Steriods, tumor 2. K 3. Na
43
Renal H+ loss with metabolic alkalosis caused by Posthypercapnic alkalosis: HOw does this occur? 2
1. Rapid lowering of chronically elevated PCO2 (usually by mechanical ventilation) results in metabolic alkalosis 2. The fall in PCO2 acutely raises the cerebral intracellular pH
44
What is contraction alkalosis? | 2
1. Loss of large volumes of fluid | 2. Contraction of extracellular volume around relatively constant quantity of bicarbonate
45
Causes of contraction alkalosis? | 4
1. IV loop diuretics with rapid fluid removal 2. Thiazides 3. Vomiting (prolonged)‏ 4. Sweat losses in pts w/ cystic fibrosis
46
1. Metabolic alkalosis can be further characterized by what? 2. In two basic categories of diseases the kidneys retain HCO3 - How can they be differentiated? 3. What should we order to determine this? 2 4. What are the two kinds of metabolic alkalosis that we are talking about?
1. Urinary chloride 2. They can be differentiated in terms of response to treatment with sodium chloride 3. By the level of urinary Cl- as determined by ordering a 1. spot, or 2. random urinalysis for chloride (UCl). 4. - Chloride Sensitive (Responsive) Metabolic Alkalosis - Chloride-Insensitive (Resistant) Metabolic Alkalosis
47
1. Urine chloride that is under 10 mEq/L is considered what? | 2. Over 10?
1. Chloride responsive metabolic alkalosis | 2. Chloride resistant metabolic alkalosis
48
1. What can Chloride responsive metabolic alkalosis be caused by? 2 2. What can Chloride resistant metabolic alkalosis be caused by?
1. - Renal loss of chloride - GI loss of H+, Cl- 2. Excess mineralcorticoid use
49
What causes renal loss of chloride in Chloride responsive metabolic alkalosis? 3 What causes GI loss of H+ and Cl- in Chloride responsive metabolic alkalosis? 3 What causes excess mineralcorticoids? 3
1. Diurectics 2. Cystic fibrosis (other diseases) 3. Posthypercapnia 1. NG sunctioning 2. Vomiting 3. Chloride-wasting diarrhea 1. Adrenal (cushings, hyperaldosteronism) 2. Exogenous steriod administration 3. Bartter's syndrome
50
Chloride Sensitive (Responsive) Metabolic Alkalosis: 1. What is the inital problem? 2. This chloride depletion results in what? 3. In this category of metabolic alkalosis, the urinary Cl- is at what level? 4. The disorders respond to treatment with what?
1. a sustained loss of chloride out of proportion to the loss of sodium (either by renal or GI ) 2. in renal sodium conservation leading to a corresponding reabsorption of HCO3 - by the kidney 3. less than 10 mEq/L, 4. intravenous NaCl
51
Chloride-Insensitive (Resistant) Metabolic Alkalosis: 1. Describe the pathophysiology. 2. The urinary Cl- is at what level? 3. these disorders do not respond to what?
1. Direct stimulation of the kidneys to retain bicarbonate irrespective of electrolyte intake and losses 2. >10 mEq/L, and 3. NaCl administration
52
Treatment of Metabolic Alkalosis: Correct the underlying disorder. 1. Chloride responsive? 3 2. Chloride resistant?
Chloride-responsive 1. Replace volume with NaCl if depleted 2. Correct hypokalemia if present 3. Administration of NH4Cl and HCl should be reserved for extreme cases Chloride-resistant 1. Treat underlying problem, such as stopping exogenous glucocorticoids
53
Alkali Administration can cause | 3
1. Milk-alkali syndrome- 2. Post-correction metabolic alkalosis 3. Administration of large quantities of citrate (i.e. w/ infusion of 8 or more units of blood, or giving fresh frozen plasma in plasmapheresis)
54
What is milk alkali syndrome?
too much Ca+ intake with absorbable alkali. This occurs through too much Ca++ supplements or dairy through treatment of osteoporosis. Triggered by the alkali administration.
55
Post-correction metabolic alkalosis by administration of what?
by administration of NaHCO3 to treat lactic acidosis or ketoacidosis
56
Administration of large quantities of citrate (i.e. w/ infusion of 8 or more units of blood, or giving fresh frozen plasma in plasmapheresis). 1. Each mmol of citrate creates how much bicarb? 2. What can occur because of this and why?
1. each mmol of citrate generates 3 mEq of bicarbonate (for a total of 23 meq of bicarbonate in each unit of blood) 2. metabolic alkalosis can occur if the renal ischemia or underlying renal disease prevents the excess bicarbonate from being excreted in the urine
57
1. Whats the equation for the anion gap? 2. What do lab values for the anion gap reflect? 3. What is the normal anion gap?
1, (Na+) – (HCO3- + Cl-) 2. Reflects the concentration of nonbicarbonate buffers: albumin, phosphate, sulfate, organic acids 3. Range 12 +/- 4 but can be depending on the instrument used to measure serum electrolytes (esp. chloride)
58
1. High serum anion gap most often due to? | 2. What must you rule out? 2
1. Most often due to an increase in unmeasured anions, and this is almost always caused by one of the organic metabolic acidoses 2. - lactic acidosis - ketoacidosis
59
When do we figure out the Delta Gap/Delta HCO3-?
Use only if the anion gap is elevated for metabolic acidosis
60
What is the Delta Gap/Delta HCO3-? | Whats the equation? Delta Gap (Delta Bicarb)
Ratio of the increase in anion gap compared to the decrease in the HCO3 concentration 1. AG measured - 12 = delta AG (∆AG) 2. 24 – measured HCO3 = delta bicarb(∆BC)
61
Delta Gap: 1. If ∆AG is > ∆BC then you have what also? 2. If ∆AG is less than ∆BC then NON-AG? 3. If they are equal (=/- 2) ?
1. metabolic alkalosis present (excess bicarb along with lactate or metabolic acidosis) 2. metabolic acidosis:+ An additional NON-AG metabolic acidosis (ex: lactic acidosis superimposed on severe diarrhea) 3. then NO ADDITIONAL DISTURBANCE
62
Respiratory compensation for metabolic acidosis: 1. PCO2 should decrease by mmHg for every __meq/L decrease in the serum HCO3 2. Why would it be helpful to determine what the respiratory compensation should be? 3. What are our PCO2 limits?
1. 1.3 and 1 2. If the respiratory compensation isnt what it should be then they have a respiratory problem 3. Limits: PCO2 can only fall to 8-12 mmHg
63
When is WInter's formula used? What is it used ot predict? What is the equation? 3 things to remember
1. Use in metabolic acidosis only 2. Used in metabolic acidosis to predict the PaCO2 you should have if there is appropriate respiratory compensation for the metabolic acidosis 3. - Predicted PaCO2 =1.5 * (HCO3-) + 8 (+/- 2) - Rough estimate is HCO3 + 15 - Or PCO2 should be similar to the decimal digits of the pH. (pH 7.25, the PCO2 should be about 25)
64
Winter's formula: 1. Higher than predicted = ? 2. Lower than predicted = ?
1. concomitant respiratory acidosis | 2. concomitant respiratory alkalosis
65
Respiratory compensation in Metabolic alkalosis: 1. For every 1 meq/L elevation in the HCO3 the PCO2 should increase by about ___ mmHg 2. Upper limit for increasing the CO2 is about ___mmHg
1. 0.7 | 2. 55
66
1. What is Summer's formula used in? 2. What is it used to calculate? 3. If the calculated CO2 is higher than actual = ? 4. If the calculated CO2 lower than actual = ? 5. Whats the formula?
1. Use in metabolic alkalosis only 2. Used to calculate respiratory compensation (CO2) for metabolic alkalosis 3. concomitant respiratory alkalosis 4. concomitant respiratory acidosis 5. PCO2 = 0.7 ( HCO3+21) +/-2
67
1. When is MUDPILES used? 2. When is USED CAR used? 3. Name 4 causes of metabolic acidosis? 4. Name 5 causes of metabolic alkalosis? 5. What is the underlying problem with respiratory acidosis? 6. What is the underlying problem with respiratory alkalosis? 7. How long does it take for the renal system to compensate by increasing the HCO3? - Chronic? 8. When might it be helpful to measure a urine chloride?
1. Increased an gap 2. Non-anion gap met acido 3. - DKA, - lactate acidosis, - alcoholic acidosis. - Asa overdose 4. - vomiting, - gastric suction, - diuretics, - antacid overdose, - dehydration 5. ventilation 6. hyperventilation 7. 6-12 hours. - Chronc in 3-5 days 8. Metabolic alkalosis
68
``` History: pt with respiratory distress ABG: pH 7.32, PCO2 70, HCO3 35 1. What is your initial interpretation? Can we apply any of the new info here 2. When do you use delta gap? 3. When do you use Winter’s formula? 4. When do you use Summer’s formula? ```
1. Respiratory acidosis with partial renal metabolic compensation (probably already had an intially increase in bicarb because of chronic respiratory acidosis- Acute on Chronic) 2. no 3. no 4. no
69
Pt presents with diarrhea ABG: pH 7.24, PCO2 24, HCO3 10 1. What is the initial interpretation? 2. How do we figure out the appropriate degree of respiratory compensation? - What should the PCO2 be? 3. What if the CO2 was higher or lower than expected? 2
1. Metabolic Acidosis with partial respiratory compensation 2. Predicted PaCO2 =1.5 * (HCO3-) + 8 (+/- 2)= 23 (+/-2) - CO2 is low to compensate - 24 is what it should be when bicarb is at 10. 3. - If Co2 was higher than predicted then they would also have a respiratory acidosis - If the CO2 was lower than predicted they would have an underlying respiratory alkalosis
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