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Principles II > acids and bases and ABG interpretation > Flashcards

acids and bases and ABG interpretation Flashcards

1
Q

how can mechanical ventilation alter the acid/base balance?

A

its effect on PCO2

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2
Q

how can blood loss effect acid/base balance?

A

potential to impact the pH buffering ability because of lost hemoglobin

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3
Q

what is homeostasis of acid base balance based on?

A

a balance between….

  • intake and production of H+
  • removal and elimination of H+
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4
Q

why is H+ concentration essential?

A
  • it is essential for proper functioning of enzymatic reactions
  • cell functions are altered when H+ changes
  • requires more precision regulation compared to other ions since it is lower than other ions in the body
    ex: Na+ over 3.5 million times greater than H+
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5
Q

what is an acid?

A

a molecule that releases H+ ion
-proton donators

HA - H+ + A-

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6
Q

what are some examples of acids?

A
  • H2CO3 (Carbonic acid): dissociates to form H+ and HCO3- (bicarbonate ions)
  • HCL (hydrochloric acid): dissociates to form H+ and Cl- (chloride ions)
  • Phosphoric and sulfuric acids
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7
Q

what is considered the most important acid/base reaction in the body?

A

H2CO3 - H+ + HCO3-

-the dissociation of carbonic acid into H+ and bicarbonate ions or vice versa

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8
Q

what is a base?

A

molecule or ion that accepts H+ ion

  • proton acceptor
  • HCO3-, ammonia, and proteins are the body’s bases

B + H+ - BH+

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9
Q

what are some examples of bases?

A
  • HCO3- (bicarbonate ion): accepts/combines with H+ to form H2CO3 (carbonic acid)
  • HPO4-: accepts/combines with H+ to form H2PO4-
  • net negatively charged proteins (amino acids) also accept H+ (ex: Hgb)
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10
Q

what are the most important acid and base in the body?

A

carbonic acid and bicarbonate

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11
Q

what is the most important protein base?

A

hemoglobin

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12
Q

describe strong acids and bases

A

acid: releases H+ rapidly and in large amounts
base: rapidly reacts with and quickly removes H+

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13
Q

describe weak acids and bases

A

acid: slow to dissociate and release H+
base: binds to H+ much slower and weaker bond

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14
Q

which type of acids and bases does acid base regulation involve?

A

weak acids and bases

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15
Q

what is the pH of solution related to ?

A

the ratio of the undissociated to the dissociated acid

  • acidosis: ratio of HCO3- to CO2 decreases
  • alkalosis: ratio of HCO3- to CO2 increases
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16
Q

how are pH and H+ concentration related?

A

inversely related

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17
Q

what determines the pH of the blood?

A

ratio of HCO3- to H2CO3 (or PCO2)

  • PCO2 determines the amount of H2CO3 formed
  • at a normal pH of 7.4 ratio of bicarb to carbonic acid is 20:1
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18
Q

what is seen with respiratory acidosis primarily?

A

increased PaCO2

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19
Q

what is seen with compensated respiratory acidosis?

A

increased PaCO2 and increased HCO3-

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20
Q

what is seen with respiratory alkalosis primarily?

A

decreased PaCO2

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21
Q

what is seen with compensated respiratory alkalosis?

A

decreased PaCO2 and decreased HCO3-

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22
Q

what is seen with metabolic acidosis primarily?

A

decreased HCO3-

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23
Q

what is seen with compensated metabolic acidosis?

A

decreased HCO3- and decreased PaCO2

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24
Q

what is seen with metabolic alkalosis primarily?

A

increased HCO3-

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25
Q

what is seen with compensated metabolic alkalosis?

A

increased HCO3- and increased PaCO2

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26
Q

what is normal arterial and venous blood pH?

A

arterial blood: 7.4

venous blood: 7.35

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27
Q

what is considered acidosis?

A

arterial pH less than 7.35

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28
Q

what is considered alkalosis:

A

arterial pH > 7.45

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29
Q

what pH range is compatible with life?

A

approx. 6.8-7.8

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30
Q

how does CO2 effect amount of H2CO3?

A

CO2 released from tissues combine with H2O via carbonic anhydrase to form H2CO3

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31
Q

what is the first H+ regulation mechanism to respond to acid/base imbalance?

A

buffering systems

32
Q

describe buffering systems

A
  • reversibly combine with acids or bases to prevent excess changes in H+
  • reacts within seconds
  • does not eliminate H+; keeps it bound up until balance can be re established
33
Q

how do buffering systems work?

A

-buffers bind with free H+ to form a weak acid (H buffer)

Buffer + H+ HBuffer

  • when H+ concentration increases the reaction is forced right and H+ binds to buffer
  • when H+ concentration decreases the reaction is forced left and H+ releases from buffer (mass action)
34
Q

describe the bicarbonate buffer system

A
  • most powerful and most important extracellular buffer system in the body
  • effective for metabolic acidosis (NOT respiratory)
  • HCO3- changes very little in response to increased pCO2
35
Q

describe the phosphate buffer system (HPO4-)

A
  • strong acids such as HCl are buffered
    ex: HCl + Na2HPO4 => NaH2PO4 + NaCl
  • strong bases such as OH are buffered
    ex: NaOH + NaH2PO4 => Na2HPO4 + H2O
36
Q

describe the protein buffer system

A
  • protein are anions (negative charge) that easily accept H+ proton
  • most abundant intracellular buffers in the body
  • hemoglobin is an effective buffer
    ex: H+ + Hgb HHgb
37
Q

what is the second H+ regulation mechanism for acid/base balance?

A

Lungs

*reacts within minutes

38
Q

how do the lungs help balance acid/base?

A
  • regulates removal of CO2 which effectively eliminates H2CO3
  • regulate pCO2
  • chemoreceptors in the brainstem respond to CO2 “indirectly” but “directly” to H+ after CO2 crosses the BBB and chemical reaction occurs that liberates H+
39
Q

how do central chemoreceptors assist the lungs in acid/base regulation?

A

respond to changes in the H+ concentration of CSF

  • increased H+ (decreased pH) = increased ventilation
  • decreased H+ (increased pH) = decreased ventilation
  • although the BBB is impermeable to H+, CO2 easily diffuses across and liberates H+ ions from another ion that stimulates the receptors
40
Q

how does CO2 lead to acidosis?

A
  • aerobic cellular respiration process produces CO2 and H2O
    ex: C6H12O6 + 6O2 => 6CO2 + 6H2O + 36 or 38 ATP
  • CO2 reacts with H2O through carbonic anhydrase to form H2CO3
    ex: CO2 + H2O H2CO3
  • H2CO3 then easily donates H+ through carbonic anhydrase, leaving HCO3-
    ex: H2CO3 H+ + HCO3-
  • carbonic anhydrase inhibitors (diuretics) cause metabolic acidosis
41
Q

where is carbonic anhydrase found?

A
  • lungs
  • RBCs
  • kidney
42
Q

what is the 3rd H+ regulation mechanism?

A

kidneys: eliminate acids and bases from the body
* last compensatory mechanism to respond
* reacts in hours and days (slowest)

43
Q

describe the renal acid/base regulatory system

A
  • kidneys regulate HCO3-
  • most effective regulatory system for controlling H+ (since its actually eliminating rather than shifting)
  • regulate extracellular fluid H+ using three mechanisms:
    1) secretion of H+
    2) reabsorption of filtered HCO3-
    3) production of new HCO3-
44
Q

describe renal secretion of H+ to balance acid/base

A
  • usually a 1:1 ratio; for every H+ secreted an HCO3- enters the blood; approx. 4320 meq HCO3- filtered and 4320 meq of H+ secreted daily
  • if a greater amount of one is lost then the blood becomes more acid or alkaline
  • both excretion of H+ and the reabsorption of HCO3- are controlled by the H+ secretion process
  • filtered HCO3- must react with H+ to form H2CO3 before it can be reabsorbed
  • when H+ concentration is low, the kidneys cant reabsorb all of the filtered HCO3- which results in increased secretion of HCO3- (lost in urine), balancing the decrease in H+
45
Q

describe renal production of new HCO3-

A

1) secreted H+ combines with phosphate and ammonia buffers to yield new HCO3-
* ammonia is the more important, most used system
2) glutamine, formed by amino acid metabolism, is changed to ammonium (NH4-) by renal tubular cells
* 1 glutamine form 2 NH4- and 2 HCO3-
* *NH4- excreted in urine and the HCO3- is reabsorbed into the blood as new HCO3-

46
Q

describe renal correction of acidosis

A
  • increased H+ stimulates glutamine metabolism, resulting in increased production of NH4-
  • NH4- causes increased secretion of H+ and addition of new HCO3-
  • excess H+ is eliminated through urine
  • newly produced HCO3- enters the blood
  • *most effective, but slowest, way to correct acidosis
47
Q

describe renal correction of alkalosis

A
  • ratio of HCO3- to CO2 (H+) increases (more HCO3-)
  • HCO3- cant be reabsorbed (needs to be bound with H+)d/t the decrease secreted H+
  • this process results in an overall decrease in plasma HCO3- and correction of alkalosis
48
Q

what factors may increase H+ secretion and HCO3- reabsorption?

A
  • increased PCO2
  • increased H+ w/ decreased HCO3-
  • decreased extracellular fluid volume
  • increased angiotensin II
  • increased aldosterone
  • hypokalemia
49
Q

what factors may decrease H+ secretion and HCO3- reabsorption

A
  • decreased PCO2
  • decreased H+ w/ increased HCO3-
  • increased extracellular fluid
  • decreased angiotensin II
  • decreased aldosterone
  • hyperkalemia
50
Q

what is the anion gap?

A

gap b/w anions and cations from a practical medical evaluation standpoint in which only certain cations and anions are measured (so looks like a gap)

  • no “true” plasma anion gap
  • concentration of anions and cations must be equal to maintain neutrality electrically
51
Q

what is the normal plasma anion gap range?

A

7-14 mEq/L
= [Na+] - [HCO3-] - [Cl-]
= 144 - 24 - 108
=12 mEq/L

52
Q

what cations and anions are measured?

A

HCO3-
Na+
Cl-

53
Q

what is the diagnostic purpose of anion gap?

A
  • differentiating causes of metabolic acidosis
  • movement of HCO3- or other anions up or down causes a compensatory up or down movement of Cl-
  • hyperchloremic metabolic acidosis (normal anion gap metabolic acidosis): if decreased in HCO3- and Na+ is unchanged, then Cl- must increase to maintain electric neutrality
54
Q

what are causes of metabolic acidosis associated with an increased anion gap (normal Cl-)?

A
  • DM (ketoacidosis)
  • lactic acidosis
  • chronic renal failure
  • aspirin (salicylate acid) poisoning
  • methanol poisoning
  • ethylene glycol poisoning
  • starvation
  • rhabdomyolysis
55
Q

what are causes of metabolic acidosis associated with a normal anion gap (hyperchloremia)?

A
  • increased GI loss (diarrhea, ingestion of CaCl2, MgCl2, fistulas)
  • renal tubular acidosis
  • carbonic anhydrase inhibitor
  • Addison’s disease (hyperaldosteronism)
  • increased intake of chloride containing acids (ammonium chloride, lysine hydrochloride, arginine hydrochloride)
  • TPN (Cl- salts of amino acids)
  • dilutional (large amount of bicarb free fluids, i.e. NS)
56
Q

what are physiological effects of alkalosis?

A
  • increased affinity of hemoglobin for O2: harder for hgb to release form O2 to tissues; Oxyhgb curve shifts left
  • plasma proteins have increased affinity for ionized Ca++ causing increased binding: hypocalcemia, CV/circulatory depression and collapse; NM irritability (tetany; laryngospasm?)
  • H+ moves out of the cell while K+ moves into the cell, resulting in HYPOkalemia
57
Q

what are side effects seen d/t alkalosis?

A
  • CNS: decreased CBF, seizures, lethargy, delirium, tetany
  • CV: arteriolar vasoconstriction, decreased coronary blood flow, decreased threshold for angina, predisposition to refractory dysrhythmias
  • Resp: hypoventilation, hypercarbia, arterial hypoxemia
  • metabolism: hypokalemia, hypocalcemia, hypomagnesemia, hypophosphatemia, stimulation of anaerobic glycolysis
58
Q

describe respiratory alkalosis

A
  • decrease in pCO2, which decreases H+
  • d/t increased alveolar ventilation: CO2 eliminated more rapidly than produced
  • tx: correct the cause of increased ventilation; during GA, reduce Vt and RR or if spontaneously breathing, give fentanyl or something to calm down
59
Q

what are common causes of respiratory alkalosis?

A
  • central: pain, anxiety, ischemia, stroke, tumor, infection, fever, drug-induced (salicylates, progesterone [pregnancy], analeptics [doxapram])
  • peripheral: hypoxemia, high altitude, pulmonary disease (CHF, noncardiogenic pulmonary edema, asthma, PE), severe anemia
  • sepsis
  • metabolic encephalopathies
  • ventilator-induced
60
Q

describe metabolic alkalosis

A
  • excess HCO3- or loss of H+
  • less common than metabolic acidosis
  • causes: HCl loss; Na+ reabsorption and HCO3- secretion
  • sx: hypokalemia (alkalosis causes K+ to shift intracellular)
  • tx: PPIs (keep acid out of GI tract); K+ sparing diuretics (increases excretion of HCO3-
61
Q

what are common causes of metabolic alkalosis?

A
  • GI: vomiting, NG suction, choride diarrhea
  • renal: diuretics, posthypercpanic, low Cl- intake
  • sweat: cystic fibrosis
  • increased mineralocorticoid activity: hyperaldosteronism, cushing’s syndrome, licorice ingestion, bartter’s syndrome
  • severe hypokalemia
  • massive blood transfusion
  • acetate-containing colloid solutions
  • alkaline administration w/ renal insufficiency (antacids)
  • hyperkalemia
  • sodium PCNs
  • glucose feeding after starvation
62
Q

what are physiological effects of acidosis?

A
  • decreased affinity of hgb for O2: easier for hgb to release O2 to the tissue
  • sympathoadrenal activation
  • CNS depression/lethargy: CO2 narcosis (CO2, not H+, penetrates BBB)
  • cardiac and vascular smooth muscle less responsive to catecholamines
  • H+ moves into cell while K+ move out of cell, resulting in Hyperkalemia
  • K+ increases 0.6 mEq for every 0.1 decrease in pH
63
Q

what are side effects seen with acidosis?

A
  • CNS: obtundation, coma
  • CV: impaired myocardial contractility, decreased CO, decreased arterial BP, sensitization to reentrant dysrhythmias, decreased threshold for V fib, decreased responsiveness to catecholamines
  • Resp: hyperventilation, dyspnea, fatigue of resp. muscles
  • metabolism: hyperkalemia, insulin resistance, inhibition of anaerobic glycolysis
64
Q

describe respiratory acidosis

A
  • increase in PCO2, which increases H+
  • d/t decreased alveolar ventilation (worse when renal function poor)
  • tx: normalize alveolar ventilation
  • correct chronic CO2 SLOWLY to allow renal elimination of HCO3- (correcting too fast can lower CO2 faster than kidneys can excrete excess compensatory HCO3- and cause metabolic alkalotic state)
  • correct chronic CO2 retainers back to their baseline (correcting to normal value results in respiratory alkalosis)
65
Q

what are common causes of respiratory acidosis?

A
  • hypoventilation
  • CNS depression: drug-induced, sleep disorders, OHS, cerebral ischemia, cerebral trauma
  • NM disorders: myopathies, neuropathies
  • chest wall abnormalities: flail chest, kyphoscoliosis
  • pleural abnormalities: pneumothorax, pleural effusion
  • airway obstruction: upper (foreign body, tumor, laryngospasm, sleep disorders), lower (severe asthma, COPD, tumor)
  • parenchymal lung disease: pulmonary edema, PE, pneumonia, aspiration, interstitial lung disease
  • ventilator malfunction
  • increased CO2 production
  • large caloric loads
  • malignant hyperthermia
  • intensive shivering
  • prolonged seizure activity
  • thyroid storm
  • extensive thermal injury (burns)
66
Q

describe metabolic acidosis

A
  • acidosis not caused by excess CO2
  • d/t renal failure, excess production of acids, ingestion of acids, loss of HCO3- (diarrhea, intestinal vomiting), DM
  • tx: correct the cause; if chronic conditions (resp. or renal failure) then neutralize acid (Bacitra, oxidizes to NaHCO3-)
67
Q

what are common causes of metabolic acidosis?

A
  • increased anion gap
  • increased production of nonvolatile acids: renal failure, ketoacidosis (DM and starvation), lactic acidosis, alcoholic, inborn errors of metabolism
  • ingestion of toxin: salicylate, methanol, ethylene glycol, paraldehyde, toluene, sulfur
  • rhabdomyolosis
  • normal anion gap (hyperchloremic)
  • increased GI losses of HCO3-: diarrhea, anion exchange resins (cholestyramine), ingestion of CaCl2 & MgCl2, fistulas (pancreatic, biliary, or small bowel), ureterosigmoidostomy or obstructed ileal loop
  • increased renal losses of HCO3-: renal tubular acidosis, carbonic anhydrase inhibitors, hypoaldosteronism
  • dilutional: large amount of bicarb free fluids, i.e. NS
  • TPN: Cl- salts of amino acids
  • increased intake of chloride-containing acids: ammonia chloride, lysine hydrochloride, arginine hydrochloride
68
Q

how does acidosis effect K+ and Ca++?

A
  • increased K+: H+ shifts into cell and K+ out of cell; increased excitation and depolarization; high T waves
  • high serum K+ moves resting membrane potential higher which depolarizes
  • increased Ca++: albumin less bound to Ca++ and releases easier causing an increase; depressed sensation of nerves, NM junctions, and reflexes; hypotonia
  • raises the threshold potential moving it further from resting potential
69
Q

how does alkalosis affect K+ and Ca++?

A
  • decreased K+: H+ shifts out of cell and K+ moves in; muscular weakness, cramps, PVCs, U wave, flat T wave
  • low K+ moves resting potential lower which hyperpolarizes
  • decreased Ca++: albumin get more negatively charged in alkalosis; more ionized Ca++ to bind to albumin causing a drop; oversensitization of nerves and NM junction causing spasm
  • lowers threshold potential closer to resting potential
70
Q

what are normal ABG values?

A
  • pH: 7.35-7.45
  • pCO2: 35-45 mmHg
  • pO2: 80-100 mmHg
  • HCO3-: 22-26 mEq/L
  • BE: 0 + or - 2 mEq/L
  • SaO2: > 97%
71
Q

what are the steps to ABG interpretation?

A

1) arterial pH: acidosis, alkalosis, normal
2) arterial pCO2: does it explain the pH?
3) arterial HCO3-: does it explain the pH?
4) any compensation: did non-contributing factor react and correct the pH?

72
Q

how does temperature affect ABG measurement?

A
  • affects pO2, pCO2, and pH, NOT HCO3-
  • pO2 and pCO2 (gas tensions) decrease with hypothermia bc it lowers the partial pressure of gas in solution (total CO2 content unchanged, but partial pressure decreased)
  • gas solubility indirectly proportional to temperature (gas solubility increases as temperature decreases)
  • pH increases with hypothermia (pCO2 decreases but HCO3- unchanged)
73
Q

describe ABG temperature correction

A
  • uncorrected: regardless of temp, ABGs are typically warmed to 37 degrees for measurement (alpha stat management) when the patient is hypothermic
  • corrected: table or program estimates what gas tension and pH would be at patient’s actual temperature (pH stat management) when the pt. is hypothermic
  • goal: practitioner to maintain pCO2 40 mmHg, pH 7.4 when patient is hypothermic
74
Q

why is temperature correction important?

A
  • pt. having CABG on CPB pump temp 25 degrees C
  • uncorrected (alpha stat): pCO2 40, pH 7.40 at 37 C
  • corrected (pH stat): pCO2 23, pH 7.60
  • cerebral vasoconstriction reduces CBF; decreased K+, coronary vasospasm, increased SVR may occur
  • perfusionist adds CO to oxygenator on CPB pump
  • evidence shows that alpha stat preserves CBF autoregulation
  • no appreciable differences in outcomes except in children b/w the two strategies
75
Q

describe ABG use in determining A-a gradient

A

PAO2 - PaO2

  • ABGs provide a PaO2: can determine V/Q mismatch, shunt, blood-gas barrier such as pulmonary edema, CHF, ARDS, atelectasis
  • normal youth adult on room air = 5-10 mmHg
  • increases 1 mmHg for every decade lived
76
Q

what is base excess?

A
  • amount of excess or insufficient level of bicarb
  • positive number = metabolic alkalosis
  • negative number = metabolic acidosis
77
Q

describe mixed acid/base disorders

A
  • mixed acid base disorders characterized by abnormal compensatory response
  • two or more causes of acid/base imbalance
    ex: pH low = acidosis, both pCO2 increased and HCO3- decreased (metabolic and respiratory component = mixed acidosis)
  • diarrhea induced HCO3- loss in pt. with COPD

Principles II (18 decks)

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