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1

how can mechanical ventilation alter the acid/base balance?

its effect on PCO2

2

how can blood loss effect acid/base balance?

potential to impact the pH buffering ability because of lost hemoglobin

3

what is homeostasis of acid base balance based on?

a balance between....
-intake and production of H+
-removal and elimination of H+

4

why is H+ concentration essential?

-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+

5

what is an acid?

a molecule that releases H+ ion
-proton donators

HA - H+ + A-

6

what are some examples of acids?

-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

7

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

H2CO3 - H+ + HCO3-
-the dissociation of carbonic acid into H+ and bicarbonate ions or vice versa

8

what is a base?

molecule or ion that accepts H+ ion
-proton acceptor
-HCO3-, ammonia, and proteins are the body's bases

B + H+ - BH+

9

what are some examples of bases?

-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)

10

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

carbonic acid and bicarbonate

11

what is the most important protein base?

hemoglobin

12

describe strong acids and bases

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

13

describe weak acids and bases

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

14

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

weak acids and bases

15

what is the pH of solution related to ?

the ratio of the undissociated to the dissociated acid
-acidosis: ratio of HCO3- to CO2 decreases
-alkalosis: ratio of HCO3- to CO2 increases

16

how are pH and H+ concentration related?

inversely related

17

what determines the pH of the blood?

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

18

what is seen with respiratory acidosis primarily?

increased PaCO2

19

what is seen with compensated respiratory acidosis?

increased PaCO2 and increased HCO3-

20

what is seen with respiratory alkalosis primarily?

decreased PaCO2

21

what is seen with compensated respiratory alkalosis?

decreased PaCO2 and decreased HCO3-

22

what is seen with metabolic acidosis primarily?

decreased HCO3-

23

what is seen with compensated metabolic acidosis?

decreased HCO3- and decreased PaCO2

24

what is seen with metabolic alkalosis primarily?

increased HCO3-

25

what is seen with compensated metabolic alkalosis?

increased HCO3- and increased PaCO2

26

what is normal arterial and venous blood pH?

arterial blood: 7.4
venous blood: 7.35

27

what is considered acidosis?

arterial pH less than 7.35

28

what is considered alkalosis:

arterial pH > 7.45

29

what pH range is compatible with life?

approx. 6.8-7.8

30

how does CO2 effect amount of H2CO3?

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

31

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

buffering systems

32

describe buffering systems

-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

how do buffering systems work?

-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

describe the bicarbonate buffer system

*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

describe the phosphate buffer system (HPO4-)

-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

describe the protein buffer system

-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

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

Lungs
*reacts within minutes

38

how do the lungs help balance acid/base?

-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

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

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

how does CO2 lead to acidosis?

-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

where is carbonic anhydrase found?

-lungs
-RBCs
-kidney

42

what is the 3rd H+ regulation mechanism?

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

43

describe the renal acid/base regulatory system

-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

describe renal secretion of H+ to balance acid/base

-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

describe renal production of new HCO3-

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

describe renal correction of acidosis

-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

describe renal correction of alkalosis

-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

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

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

49

what factors may decrease H+ secretion and HCO3- reabsorption

-decreased PCO2
-decreased H+ w/ increased HCO3-
-increased extracellular fluid
-decreased angiotensin II
-decreased aldosterone
-hyperkalemia

50

what is the anion gap?

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

what is the normal plasma anion gap range?

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

52

what cations and anions are measured?

HCO3-
Na+
Cl-

53

what is the diagnostic purpose of anion gap?

-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

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

-DM (ketoacidosis)
-lactic acidosis
-chronic renal failure
-aspirin (salicylate acid) poisoning
-methanol poisoning
-ethylene glycol poisoning
-starvation
-rhabdomyolysis

55

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

-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

what are physiological effects of alkalosis?

-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

what are side effects seen d/t alkalosis?

-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

describe respiratory alkalosis

-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

what are common causes of respiratory alkalosis?

-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

describe metabolic alkalosis

-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

what are common causes of metabolic alkalosis?

-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

what are physiological effects of acidosis?

-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

what are side effects seen with acidosis?

-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

describe respiratory acidosis

-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

what are common causes of respiratory acidosis?

*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

describe metabolic acidosis

-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

what are common causes of metabolic acidosis?

*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

how does acidosis effect K+ and Ca++?

-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

how does alkalosis affect K+ and Ca++?

-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

what are normal ABG values?

-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

what are the steps to ABG interpretation?

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

how does temperature affect ABG measurement?

-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

describe ABG temperature correction

-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

why is temperature correction important?

-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

describe ABG use in determining A-a gradient

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

what is base excess?

-amount of excess or insufficient level of bicarb
-positive number = metabolic alkalosis
-negative number = metabolic acidosis

77

describe mixed acid/base disorders

-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