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864 > Acid-Base Balance - metabolic > Flashcards

Acid-Base Balance - metabolic Flashcards

1
Q

Acid-Base Regulation

normal: physiological pH: ___ - ___
- < = acidemia
- > = alkalemia

HCO3- = ___ = ___
CO2 = ___ = ___
- compensation for a particular disorder involves the opposite part (lungs compensate metabolix disorder, kidneys compensate respiratory disorders)

A

7.35-7.45
- kidneys, metabolic
- lungs, respiratory

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2
Q

pH of blood determined by ratio of ___ to ___ , not the relative amounts of each

A
  • HCO3-
  • pCO2
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3
Q

normal blood gas values ( ___ blood)
PaCO2: 35 - 45 mmHg
- remember: ___

HCO3: 22-26 mEq/L
- remember ___

A

arterial
40
24

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4
Q

adverse consequences - acidemia

CV
- ___ CO
- impairment in ___
- ___ pulmonary vascular resistance and arrhythmias

Metabolic
- ___ resistance
- inhibition of anaerobic ___
- ___ kalemia

CNS
- ** ___ or altered mental stauts**

Others:
- decreased ___ muscle strength
- ___ (correct acidosis and blow out CO2)
- dyspnea

A

CV
- decreased
- contractility
- increased

metabolic
- insulin
- glycolysis
- hyperkalemia

CNS
- coma

others
- respiratory
- hyperventilation

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5
Q

adverse consequences - alkalemia

CV
- ___ coronary blood flow due to arterial ___
- ___ anginal threshold
- arrythmias

Metabolic
- ___ K+ , Ca, and Mg
- ___ of anaerobic glycolysis

CNS
- ___ cerebral blood flow
- seizures

others
- decreased ___ (lungs trying to retain as much CO2 as they can)

A

CV
- decreased, constriction
- decreased

Metabolic
- decreased
- stimulation

CNS
- decreased

Others
- respirations

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6
Q

acid generation

1) diet: ~ __ mEqkg/day of acid consumed per day - comes from oxidation of proteins and fats
2) aerobic metabolism of ___ produces 15-20 K mmol of CO2 each day
3) Nonvolatile acids also formed

A

1
glucose

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7
Q

Acid Regulation - 1) buffering

  • first line of defense
  • buffer: ability of weak acid and its base to resist change in pH with addition of a strong acid or base

prinicple buffer: ___
- ___ onset with intermediate capacity
- HCO3- buffer present in largest [ ]
- how well you can utilize this buffer depends on how well you kidneys and lungs work

when acid is added
- large amount of ___ can be exhaled very rapidly
- body needs new ___ added to system in amount same to H+ loas ingested each day

A
  • bicarbonate
  • rapid
  • CO2
  • HCO3-
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8
Q

Acid Regulation - 1) buffering

phosphates
- intermediate onset and capacity ( ___ )
- ___ inorganic phosphated, limited activity
- ___ organic phosphates (more useful)
- Ca Phos in ___ relatively inaccessible (unless long period of acidosis_

A
  • slower
  • extracellular
  • intracellular
  • bone
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9
Q

Acid Regulation - 1) buffering

proteins
- ___ / ___ : rapid onset, limited capacity

A

albumin/hemoglobin

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10
Q

Acid Regulation - 2) renal system regulation

kidney serves 2 main purposes:
- reabsord filtered ___
- excrete ___ released from nonvolatile acids

A
  • HCO3-
  • H+
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11
Q

Acid Regulation - 2) renal system regulation

HCO3- reabsorption
- 4000-4500 mEq of HCO3- is filtered through kidney daily
- 85-90% reabsorbed by ___ tubule
- virtually no HCO3- in ___

Net effect: filtered HCO3- is reabsorbed without any net loss of H+

A
  • proximal
  • urine
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12
Q

Acid Regulation - 2) renal system regulation

HCO3- reabsorption
anything limiting H+ sectretion into the proximal tubule lumen results in urinary ___ losses

example drug class ___
- decreases entry of ___ and ___
- metabolic ___ occurs with increased HCO3- excretion

A
  • HCO3-
  • carbonic anhydrase inhibitors
  • CO2, H2O
  • acidosis
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13
Q

Acid Regulation - 2) renal system regulation

HCO3- generation = ___ excretion
- delayed onset but large capacity (slower)
- reclamation of all filtered HCO3- is not sufficient to maintain normal blood pH
- kidney works hard to excrete huge daily acid load and replete the HCO3- used in the process
- H+ excretion takes place in the ___ tubule

ammonium excretion: ___ mEq/day
titratable acidity: ___ mEq/day

A
  • H+
  • distal
  • 300
  • 30
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14
Q

Acid Regulation - 2) renal system regulation

distal tubular H+ secretion
- 50% of net acid axcretion
- CO2 combines with water in the presence of carbonic anhydrase to form H2CO3 -> breaks down to H+ and HCO3-
- the H+ is transported back into the tubular ___ by ATPase
- HCO3- freely crosses the distal tubular membrane and enters the peritubular ___ for absorption

A
  • lumen
  • capillary
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15
Q

Acid Regulation - 3) ventilatory regulation

  • rapid onset and ___ capacity

chemoreceptors detect an increase in PaCO2 and ___ rate/depth of ventilation
- CO2 diffuses easily from tissues to capillary blood to the alveoli

A
  • LARGE
  • increase
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16
Q

Acid Regulation - 4) Hepatic regulation

  • oxidation of proteins generates ___ and ___
  • NH4+ can be eliminated via urea synthesis or renal ammoniagenesis
  • is liver diminished hepatic urea synthesis, metabolic ___ may occur or an acidotic state will be corrected
  • an increase or decrease in the urea cycle will affect the HCO3- pool
  • if we dont make urea, we will have more ___ sitting around
A
  • HCO3-, NH4+
  • alkalosis
  • HCO3-
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17
Q

Compensation Chatacteristics for Acid-Base Disorders

  1. respiratory compensation very ___
  2. renal compensation takes 3-5 ___ for maximum effect
  3. compensation moves the pH towards normal, but rarely corrects the pH to normal
A
  • rapid
  • days
18
Q

Compensation Chatacteristics for Acid-Base Disorders

metabolic acidosis
- ___ HCO3
- ___ PaCO2

metabolic alkalosis
- ___ HCO3
- ___ PaCO2

respiratory acidosis
- ___ HCO3
- ___ PaCO2

respiratory alkalosis
- ___ HCO3
- ___ PaCO2

A

metabolic acidosis
- decreased HCO3
- decreased PaCO2

metabolic alkalosis
- increased HCO3
- increased PaCO2

respiratory acidosis
- increased HCO3
- increased PaCO2

respiratory alkalosis
- decreased HCO3
- decreased PaCO2

19
Q

Guidelines for Initial Interpretation of Acid-Base Disorders

metabolic acidosis
- PaCO2 should decrease by ___ times the fall in plamsa HCO3-

when numbers fall outside the above range
- ___ acid base balance
- inadequate extent and/or time for compensation

A

1.25x
mixed

20
Q

metabolic acidosis

  • pH < ___
  • low serum HCO3 ( < __ mEq/L)
  • compenatory decrease in PaCO2 from ____

classified as either ___or ___
- SAG = _____
- normal: __ - __

A
  • 7.35
  • 24
  • hyperventilation
  • non-anion gap, anion gap
  • SAG = Na - (Cl + HCO3)
21
Q

Metabolic acidosis - patho of non-anion gap (hyperchloremic acidosis)

  • overall, there is a loss of plasma ___ replaced by ___

Causes
GI HCO3- loss: ___ , pancreatic fistulas/biliary drainage

renal HCO3- loss: type II renal tubular acidosis (proximal):
- ___ , topiramate, HIV
- reabsorption threshold for HCO3 decreased in proximal tubule
- loss of HCO3 -> loss of ___ -> loss of ___ -> activate ___ -> secondary ___
- leads to hypo ___

A
  • HCO3
  • Cl
  • diarrhea
  • CAIs
  • Na, fluid, RAAS, hyperaldosteronism
  • hypokalemia
22
Q

Metabolic acidosis - patho of non-anion gap (hyperchloremic acidosis)

Causes (cont):
reduced renal H+ excretion (distal tubule RTAs)

Type I RTA ( ___ RTA)
- H+ cannot be pumped into tubule lumen
- urine cant be maximally acidified
- increase in ___ excretion

Type IV RTA (hypoaldosteronism or ___ RTA)
- less aldosterone and hyperkalemia = H+ ___ = acidosis

chronic renal failure
- ___ H+ secretion
- less ___ production

A
  • hypokalemia
  • K+
  • hyperkalemia
  • retention
  • decreased
  • ammonia
23
Q

Metabolic acidosis - patho of non-anion gap (hyperchloremic acidosis)

Causes (cont)
___ and ___ administration
- TPN administration
- HCl or ammonium Cl adminitrations

A

acid, chloride

24
Q

Metabolic acidosis - patho of anion gap

MULEPAK

A

Methanol intoxication
Uremia
Lactic acidosis
Ethylene glycol
Paraldehyde ingestion
Aspirin (salicylates)
Ketoacidosis

25
Q

Metabolic acidosis - patho of anion gap

MUDPILES

A

Methanol intoxication
Uremia
Diabetic ketoacidosis
Poisoning/propylene glycol ingestion
Intoxication/infection
Lactive acidosis
Ethylene glycol
Salicylate/sepsis

26
Q

Metabolic acidosis - patho of anion gap

Overall ___ losses are replaced with another anion besides Cl

Delta Gap = ____
- when delta added to patient’s measured HCO3, result should be in normal HCO3 range
- if elevated, indicates metabolic ___ in addition to acidosis, (mixed)

A
  • HCO3
  • pt’s anion gap - 10
  • alkalosis
27
Q

Causes of Anion Gap Metabolic Aciosis

___ acidosis (most common cause)
- lactate is a normal product of anaerobic metabolism (pyruvate -> lactate)
- lactate formation essential for RBCs and exercising muscle
- increased levels always result from decreased clearance versus overproduction
- HCO3- buffers lactate
- persistent failure to oxizide will exhause buffer

A

lactic

28
Q

causes of lactic acidosis

1) ___
2) drugs/toxins: alcohol, ___ , propylene glycol
3) ___ - self limiting
4) ___ : packed poorly perfused bone marrow cavities
5) hepatic/renal failure
6) ___ : formation of ketones/lactate
7) malnutrition: deficiencies of vitamins and thiamine
8) rhabdomyolysis

A
  • shock
  • metformin
  • seizures
  • leukemia
  • diabetes mellitus
29
Q

Causes of Anion Gap Metabolic Aciosis (cont)

Ketoacidosis
- increase in acetoacetic acid

Drug intoxications: ___ toxicity
- respiratory ___ - stimulation of respiratory drive
- metabolic ___
- also methanol/ethylene glycol ingestion

A
  • salicylate
  • alkalosis
  • acidosis
30
Q

Symptoms of lactic acidosis

  • Kussmauls ___ (compensation)
  • peripheral ___ causing flushing and tachycardia; as acidosis worsens, ventricular arrhythmias or reduced contractilty may occur
  • ___ kalemia
  • lethargy/coma
  • nausea/vomiting
  • ___ demineralization in chronic acidotic states
A
  • respirations
  • vasodilation
  • hyperkalemia
  • bone
31
Q

Anion Gap metabolic acidosis treatment

treat underlying cause

acute ___ therapy (for severe and acute bicarb losses)
- consider use if pH < ___

Dose (mEq) = ___
- use ___ for desired HCO3
- give ___ - ___ the calculated dose
- during cardiac arrests ~1 mEq/kg may be given
- supplement ___ if needed

A
  • HCO3
  • 7.1
  • Dose (mEq) = (0.5 x IBW) x (desired HCO3 - actual HCO3)
  • 12
  • 1/3 - 1/2
  • K
32
Q

Hazards of HCO3 therapy

  • overalkanization can reduce cerebral flow and can impair oxygen ___ from Hgb to tissues (shift to left)
  • ___ /hyperosmolality
  • CSF ___ accurs from the CO2 that is generated, which readily diffuses into the CSF

electrolyte shifts
- K sucked back into cells = ___
- decreased ionized Ca = decreased myocardial contractility

A
  • release
  • hypernatremia
  • acidosis
  • hypokalemia
33
Q

chronic bicarb therapy for chronic metabolic acidosis
- average dose: __ - __ mEq/kg/day (may go up to 10+ mEq/kg/day)

A

1-3

34
Q

Metabolic alkalosis

  • increased pH (> ___ )
  • increased HCO3 ( > __ mEq/L), and a compensatory ____ resulting in increased PaCO2
A
  • 7.45
  • 30
  • hypoventilation
35
Q

Metabolic alkalosis patho

3 mechanisms
1. loss fo acid from ___ or ___
2. administration of HCO3 or bicarb precursor
3. contraction alkalosis

often, ___ and ___ depletion contribute

A
  • GI, urine
  • volume, Cl
36
Q

Metabolic alkalosis - saline responsive

saline responsive
- urinary chloride < ___ - ___ mEq/L

hypochloremic state
- normally, Cl- is anion absorbed with Na
- without Cl, Na is reabsorbed with ___

causes
- ___ therapy
- ___ and NG suction
- exogenous HCO3 administration or ___ transfusion

A
  • 10-20
  • HCO3
  • diuretic
  • vomiting
  • blood
37
Q

Metabolic alkalosis - saline resistant

saline resistant
urinary chloride > ___ mEq/L
- key difference: no ___ depletion

causes
- increased ___ activity
- hypokalemia
- renal tubular ___ wasting

Increased aldosterone = H+ ___ and ___

A
  • 20
  • Cl
  • mineralcorticoid
  • chloride
  • secretion, hypokalemia
38
Q

Metabolic alkalosis symptoms

  • muscle ___ ; weakness; parathesias
  • postural dizziness
  • cellular hypoxia, mental ___ , coma, seizures
  • diect ___ suppression; CV collapse; arrhythmias
A
  • cramps
  • confusion
  • myocardial
39
Q

Metabolic alkalosis - treatment

  • correct underlying cause
  • rapid correction not necessary but treatment still needed

saline responsive
- fluid/electrolyte replacement with ___ or ___
- use caution with HF, hepati/renal failure patients

Ex. NS with 20-40 mEq/L KCl over 4-5 hours then NS with 20-40 mEq/L KCl at 125-200 mL/hr
- may also used LRs for certain patients
- but lactate will be come HCO3 so be careful

___ ___ inhibitors
- cause acidosis (good for correcting)
- helpful in patients who cannot tolerate excess fluids/Na
- ___ wasting; supplement
- not helpful in volume depletion, renal dysfunction, or severe alkalosis

alternatives for persistent metabolic alkalosis
- ___ acid in D5W or NS
- monitoring: ABG and K+ at least q4h during infusion
- ammonium chloride
- monitoring: ABG every 4 hrs; mental status; electrolytes

adjunct therapy: ___ or ___ in patients with vomiting or NG suctions

A
  • NaCl or KCl
  • carbonic anhydrase
  • K
  • HCl
  • H2RA, PPIs
40
Q

Metabolic alkalosis treatment - saline resistant alkalosis

saline resistant
- correct ___ with K sparking diuretic or KCl supplementation
- decrease dose of ___ or change steroids to one with less activity
- administer ___ - antagonizes mineralcorticoid receptor (inhibits aldosterone stimulation of H+ ___ )
- correct ___ - give fluids

A
  • hyokalemia
  • mineralcorticoid
  • spironolactone, secretion
  • hyperaldosteronism

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