Acid-Base Balance - metabolic Flashcards
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)
7.35-7.45
- kidneys, metabolic
- lungs, respiratory
pH of blood determined by ratio of ___ to ___ , not the relative amounts of each
- HCO3-
- pCO2
normal blood gas values ( ___ blood)
PaCO2: 35 - 45 mmHg
- remember: ___
HCO3: 22-26 mEq/L
- remember ___
arterial
40
24
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
CV
- decreased
- contractility
- increased
metabolic
- insulin
- glycolysis
- hyperkalemia
CNS
- coma
others
- respiratory
- hyperventilation
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)
CV
- decreased, constriction
- decreased
Metabolic
- decreased
- stimulation
CNS
- decreased
Others
- respirations
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
1
glucose
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
- bicarbonate
- rapid
- CO2
- HCO3-
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_
- slower
- extracellular
- intracellular
- bone
Acid Regulation - 1) buffering
proteins
- ___ / ___ : rapid onset, limited capacity
albumin/hemoglobin
Acid Regulation - 2) renal system regulation
kidney serves 2 main purposes:
- reabsord filtered ___
- excrete ___ released from nonvolatile acids
- HCO3-
- H+
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+
- proximal
- urine
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
- HCO3-
- carbonic anhydrase inhibitors
- CO2, H2O
- acidosis
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
- H+
- distal
- 300
- 30
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
- lumen
- capillary
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
- LARGE
- increase
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
- HCO3-, NH4+
- alkalosis
- HCO3-
Compensation Chatacteristics for Acid-Base Disorders
- respiratory compensation very ___
- renal compensation takes 3-5 ___ for maximum effect
- compensation moves the pH towards normal, but rarely corrects the pH to normal
- rapid
- days
Compensation Chatacteristics for Acid-Base Disorders
metabolic acidosis
- ___ HCO3
- ___ PaCO2
metabolic alkalosis
- ___ HCO3
- ___ PaCO2
respiratory acidosis
- ___ HCO3
- ___ PaCO2
respiratory alkalosis
- ___ HCO3
- ___ PaCO2
metabolic acidosis
- decreased HCO3
- decreased PaCO2
metabolic alkalosis
- increased HCO3
- increased PaCO2
respiratory acidosis
- increased HCO3
- increased PaCO2
respiratory alkalosis
- decreased HCO3
- decreased PaCO2
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
1.25x
mixed
metabolic acidosis
- pH < ___
- low serum HCO3 ( < __ mEq/L)
- compenatory decrease in PaCO2 from ____
classified as either ___or ___
- SAG = _____
- normal: __ - __
- 7.35
- 24
- hyperventilation
- non-anion gap, anion gap
- SAG = Na - (Cl + HCO3)
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 ___
- HCO3
- Cl
- diarrhea
- CAIs
- Na, fluid, RAAS, hyperaldosteronism
- hypokalemia
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
- hypokalemia
- K+
- hyperkalemia
- retention
- decreased
- ammonia
Metabolic acidosis - patho of non-anion gap (hyperchloremic acidosis)
Causes (cont)
___ and ___ administration
- TPN administration
- HCl or ammonium Cl adminitrations
acid, chloride
Metabolic acidosis - patho of anion gap
MULEPAK
Methanol intoxication
Uremia
Lactic acidosis
Ethylene glycol
Paraldehyde ingestion
Aspirin (salicylates)
Ketoacidosis
Metabolic acidosis - patho of anion gap
MUDPILES
Methanol intoxication
Uremia
Diabetic ketoacidosis
Poisoning/propylene glycol ingestion
Intoxication/infection
Lactive acidosis
Ethylene glycol
Salicylate/sepsis
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)
- HCO3
- pt’s anion gap - 10
- alkalosis
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
lactic
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
- shock
- metformin
- seizures
- leukemia
- diabetes mellitus
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
- salicylate
- alkalosis
- acidosis
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
- respirations
- vasodilation
- hyperkalemia
- bone
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
- HCO3
- 7.1
- Dose (mEq) = (0.5 x IBW) x (desired HCO3 - actual HCO3)
- 12
- 1/3 - 1/2
- K
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
- release
- hypernatremia
- acidosis
- hypokalemia
chronic bicarb therapy for chronic metabolic acidosis
- average dose: __ - __ mEq/kg/day (may go up to 10+ mEq/kg/day)
1-3
Metabolic alkalosis
- increased pH (> ___ )
- increased HCO3 ( > __ mEq/L), and a compensatory ____ resulting in increased PaCO2
- 7.45
- 30
- hypoventilation
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
- GI, urine
- volume, Cl
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
- 10-20
- HCO3
- diuretic
- vomiting
- blood
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 ___
- 20
- Cl
- mineralcorticoid
- chloride
- secretion, hypokalemia
Metabolic alkalosis symptoms
- muscle ___ ; weakness; parathesias
- postural dizziness
- cellular hypoxia, mental ___ , coma, seizures
- diect ___ suppression; CV collapse; arrhythmias
- cramps
- confusion
- myocardial
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
- NaCl or KCl
- carbonic anhydrase
- K
- HCl
- H2RA, PPIs
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
- hyokalemia
- mineralcorticoid
- spironolactone, secretion
- hyperaldosteronism
