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Clin Path > Water, Lytes, Acid/Base Ch5 D&P > Flashcards

Water, Lytes, Acid/Base Ch5 D&P Flashcards

1
Q

Total body water is approximately what percentage of body weight?

A

60%

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2
Q

How is total body water divided up in the body?

A 
Intracellular fluid
Extracellular fluid (Blood, intercellular fluid, transcellular fluid like third space peritoneaum etc, and GI tract like in ruminants).
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3
Q

What are the factors that influence effective circulating blood volume?

A

BLood volume AS WELL AS arterial blood pressure, arterial resistance and delivery of blood to volume receptors.

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4
Q

What are the 4 laboratory abnormalities associated with dehydration?

A

Increased hemtocrit
Increasted protein
INcreased BUN /; Crea
High urine SG

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5
Q

Increased total body water is best measured how and where does this accumulate?

A

Increased body weight.

It accumulates in the extracellular fluid or third spaces. (edema, ascites etc)

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6
Q

How can you have hypovolemia and increased total body water at the same time?

A

yes when water accumulates in third spaces or the GI tract like in ruminants where fluid is trapped in the rumen.

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7
Q

What is osmolality definition?

A

The number of solute particles/unit weight of a solution. (osmolarity is the number of solute particles per unit volume of a solution - usually in ECF they are about the same). THESE MAINTAIN FLUID INSIDE CELLS, DONT CONFUSE WITH COLLOID OSMOTIC PRESSURE WHICH MAINTAINS FLUID INSIDE A VESSEL (IE GLUCOSE AND PROTEIN)

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8
Q

What is the average ECF osmolality and what are the main contributors to osmolality?

A

Usually around 300milliosmoles per kilogram.
Electrolytes and small molecules like glucose and urea .
Larger stuff like proteins doesn’t contribute much to osmolality but does contribute to colloid osmotic pressure to keep fluid in vessels.

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9
Q

What is tonicity and ineffective osmoles versus effective?

A

The effective osmolality of a solution, ie the concentration of solutes that can cause shifts in water across a semipermeable membrane. Remember only solultes that DO NOT cross the membrane are effective osmoles and contribute to tonicity.
Urea freely passes between the ECF and ICF so it is an ineffective osmole and doesn’t contribute to tonicity.

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10
Q

What is the osmolar gap?

A

The numerical difference between measured osmolality and estimated osmolality. It usually ranges from -5 to 15 mOsm/L depending on the formula used to estimate and method used to measure.

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11
Q

What does an increase in osmolal gap mean?

A

The presence of unmeasured non polar, low molecular weight (ie small, not like protein which is large) substances such as ethylene glycol, propylene glycole, etc).

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12
Q

What can cause hyperosmolality?

A

Hypernatremia (all animals hypernatremic are also hyperosmolal).
Accumulation of other endogenous solutes like BUN or glucose.

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13
Q

What is hypertonicity and what may cause it?

A

Increase in effective osmoles like Na, Glc, ethylene glycol etc taht causes water to shift from ICF to ECF causing cell shrinkage.

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14
Q

What results from a rapid return to isotonicity from hypertonicity in the ECF?

A

Cellular edema as fluid flows back into cells > dire consequences. (ie as in cerebral cellular edema causing brain damage and death.)

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15
Q

Does hyperosmolality always mean you have hypertonicity in the ECF?

A

NO, not if the osmole is ineffective, ie BUT concentration does not increase tonicity or cause ICF or ECF water shifts b/c it is freely moveable across membranes (but it can produce changes in pH! - ie acidosis)

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16
Q

What can cause hypoosmolality?

A

Its always always associated with hyponatremia, BUT not all cases of hyponatremia are associated with hypoosmolality (ie like when you have hyperglycemia) which is also an effective osmole, and this is why you use D5W when you want to give an animal straight water IV without sodium in it so its isoosmolality with respect to serum/ECF.

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17
Q

What are the consequences of hypoosmolality?

A

Hypotonicity, fluid shifts ECF > ICF and cell swelling.
Intravascular hemolysis as fluid rushes into RBCs
Neurologic disorders

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18
Q

What happens if you have deydration and hypoosmolality?

A

Loss of ECF volume is even faster due to movement into cells / ICF so you can get circulatory collapse, shock etc.

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19
Q

With blood gas analysis, what values are measured and whats calculated from the measured values?

A

Measured: PO2, PCO2, pH (hydrogen ion conc).
Calculated: Blood bicard / HCO3 and standard bicarb and base excess values are calculated from the measured values.

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20
Q

When can you use venous versus arterial samples for blood gas measurement?

A

Arterial ONLY FOR PO2

Arterial or venous for pH, HCO3 and PCO2.

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21
Q

What does PO2 reflect?

A

Not the total O2 in the blood because most of it is bound to hemoglobin so it doesn’t contribute to PO2 but it does influence the percent saturation of Hgb with oxygen.

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22
Q

When does high and low PO2 occur?

A

High can only occur if the animal is on oxygen and low occurs in respirator disorders or with derangement of the respiratory control mechs.

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23
Q

What does PCO2 tell you?

A

Its proportional to dissolved CO2 in the plasma. Dissolved CO2 is in equilibrium with carbonic acid.
Its a measure of alveolar ventilation, if ventilation decreases, it increases and visa versa.

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24
Q

How is the blood bicarbonate level / ion determined HCO3-? How is the bicarb concentration maintained in health?

A

Calcuated from pH and PCO2 using Henderson Hasselbalch.

Its maintained in health by conservation and production of NaHCO3 by the renal tubules.

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25
Q

What is base excess, what does it relfect?

A

Reflects metabolic acid-base disorders; BE greater than 0 indicates metabolic alkalosis and BE below 0 indicates metabolic acidosis.

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26
Q

What is the other way to measure HCO3-?

A

TCO2 is the other way. HCO3- is the major contributor to TC02 do changes in TC02 are interpreted as changes in bicarb.

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27
Q

What is SaO2?

A

Oxygen saturation of hemoglobin, whats measured on the pulse ox. Its proportional to arterial P02, an indirect measure of arterial oxygenation.

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28
Q

*What is the ratio that determines acid base regulation?

What does changes in each of 2 the values mean?

A

HCO3- / H2CO3 (bicarb to carbonic acid, which is the only acid secreted as a gas by the lungs). THINK OF ACID BASE IN TERMS OF THIS RATIO, IF ONE GOES UP THE BODY TRIES TO RAISE THE OTHER ETC.

  • Changes in bicarb (aka metabolic acidosis or alkalosis) produced respiratory compensation in minutes.
  • Changes in carbonic acid (aka respiratory acidosis or alkalosis) produce metabolic compensation but it takes longer, often days.(NOTE CARBONIC ACID IS ASSESSED INDIRECTLY AS PCO2)
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29
Q

How do acid base compensatory changes occur? Is it possible to overcompensate?

A

Compensation produces unidirectional change in the components of the buffer to restore the bicarb/carbonic acid ratio. (ie if bicarb is low the body will lower PCO2, which indirectly represents carbonic acid, to keep the ratio the same to maintain pH.)
NO the body WILL NOT overcompensate.

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30
Q

What happens if HCO3- and PCO2 (representing carbonic acid) change in opposite direction (ie one goes up and the other goes down?)

A

That means there is a mixed respiratory and metabolic disorder. (pg 150)

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31
Q

How is bicarb measured in blood?

A

Either as HCO3- from blood gas or via TCO2. TCO2 = bicab. (don’t confuse with PC02 which is the measure of respiratory disorders representing carbonic acid)

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32
Q

How do you calculate the anion gap and what is it?

A

([Na + K] - [Cl + HCO3])
Used to help determine cause of acid base abnormalities. The total serum cations are equal to those commonly measured like sodium and potassium plus the unmeasured ones (UC).
Total anions are equal to those commonly measured like Cl and bicarb plus the unmeasured ones (UA).

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33
Q

So what is the relationship between cations and anions in serum and what is the actual calculation for anion gap once you rearrange the equation?

A

By the law of electrical neutrality they are equal. TA = TC (ie Na + K + UC = Cl + bicarb + UA) NOW if you rearrange the equation you get:
Na + K -Cl - HCO3 = UA - UC and so therefore
AG = UA - UC (just remember A comes before C)
pg152

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34
Q

What substitutes for bicarb in anion gap calculation?

A

TCO2 but you have to use a slightly different reference interval than if you are using HCO3 cause they are a little different.

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35
Q

In health, what are the major anions and cations?

A

Unmeasured anions = Albumin; phosphates, sulfates, small organic acids.
Unmeasured cations = ionized Ca++, Mg++, some gamma globulins.

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36
Q

When there are changes in anion gap, what is causing most of the changes?

A

UA.

The UC remain quite constant in health and dz.

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37
Q

Name some diseases that may cause an increased anion gap? (4)

A 
Lactic acidosis (lactate), 
diabetic ketoacidosis (acetoacetate, beta-hydroxybutyrate), 
renal insufficiency (salts of uremic acids) and 
certain toxicities like ethylene glycol.
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38
Q

What causes a decreased anion gap? (3)

A

This is uncommon.

Causes include hemodilution, hypoalbuminemia and increases in certain cations like hypercalcemia. (ie the THREE H’s)

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39
Q

How does albumin contribute to anion gap?

A

Remember its an anion so:
Hyperalbuminemia causes high AG.
Hypoalbuminemia causes low AG.
Note albumin mediated changes in AG are primarily mediated by albumin concentration rather than pH mediated shifts in H+.
*You can get offsets such has hypoalbuminemia and lactic acidosis where the AG would essentially be normal.

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40
Q

What does blood pH do post prandial?

A

Monogastrics > slight transient increase in blood pH.
Urine becomes alkaline (secretion of gastric acid leads to increases in plasma sodium bicarb which is excreted in the kidneys and raises pH of urine).
Ruminants > also have a net alkalinizing effect (but diets can be acidified).

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41
Q

What do you want to do to the blood pH just prior to parturition?

A

It goes down which increases the blood ionized Calcium and reduces milk fever in cattle.

42
Q

What is the influence of exercise on acid base balance?

A

Two opposing change occur:

  • Lactic acid production by hypoxic muscles
  • Hyperventilation decreases PC02, increasing blood pH by hypocapnia.
43
Q

What pattern of change occurs in horses involved in endurance exercise?

A

Hypokalemia, hypochloridmia and slight hyponatremia and equine sweat has high concentrations of Cl, K and equal concentrations of Na compared to plasma.

44
Q

What is the job of serum sodium and where is most of it located in the body?

A

Maintains ECF osmolality and essential for renal water retention (minimal Na in the ICF).
Essentially all Na in the body is in ECF and so ECF Na is an estimate of total body Na.

45
Q

What are causes of hyponatremia with decreased ECF water (ie dehydration)?

A 
Loss of Na rich fluids.
Diarrhea
Addisons
osmotic diuresis in diabetes mellitus
renal dz in cattle
46
Q

Causes of hyponatremia with normal fluid, normal hydration?

A

Dietary salt def
Loss of Na rich fluid or txment with low Na fluids
Rapidly occuring hyperglycemia that pulls fluid in
Ruptured urinary bladder
Hypersalivation in horses

47
Q

In what conditions may you see hypernatremia and the animal is NOT dehydrated?

A

Primary hyperaldosteronism
Salt poisoning
If water has shifted into GI tract as in grain overload acidosis, propylene glycol toxicosis
Urea toxicosis (cattle)
Third space water shift like bile peritonitis

48
Q

What does it mean to have hyponatremia in a dehydrated animal?

A

loss of Na and water but Na losses wehre greater than water losses so you get a total body decrease in Na.

49
Q

What does it mean to have hyponatremia in an animal with edema or ascites?

A

Water accumulation greater than Na increases. Total Na may be normal or increased but fluid has increased even more..

50
Q

Hypernatremia in a dehydrated animal means what?

A

Loss of water without loss of Na. ECF is decreased but Na is normal.

51
Q

What does hypernatremia mean in an animal with normal ECF volume?

A

Increased total body Na usually doe to excess intake of salt without access to water.

52
Q

What is Sodium : potassium ratio used for and what is the number that indicates dz?

A

Hypoaldoesteronism. Addisons associated with a calculated Na/K less than 24. Probabliity of Addisons increases as it decreasesa dn ratio of less than 19 is highly associated with but nor specifc for hypoaldosteronism. Remember there is other stuff that will decrease the Na:K ration.

53
Q

What are4 other conditions that will decrease the Na:K ratio?

A

Renal dz
Diarrhea due to Trichuris vulpis
Repeated drainage of chylothorax
Large volume of peritonitis and pleuritis

54
Q

How may shifts or alterations in serum potassium occur?

A

Shifts of K+ between ICF and ECF (normal body K+)
Increases or decreases in total body K+
Mixed disorders of both internal and external K

55
Q

Which animal species has high intra RBC potassium?

A

Horses, pigs and primates.

Low in most cats and dogs except certain dog breeds like Akitas, Shiba Inus and some other Japanese breeds.

56
Q

What are some reasons for erroneously high K+

A

Leakage from platelets during clotting like in marked thrombocytosis (or if serum not seperated from clot right away.
Leakage from high K+ RBCs like during hemolysis even if there isn’t enough hemolysis to make the serum pink.

57
Q

What are the causes of hyperkalemia due to external changes in K+ balance?

A
  • Decreased urinary excretion (anuric or oliguric renal disease) > **like post blockage in a cat or foal with ruptured urinary bladder; dogs and ruminants usually DO NOT have hyperkalemia with postrenal obstruction or ruptured bladder.
  • Hypoaldosteronism (Addison’s disease) > hyperkalemia and hyponatremia.
  • Increased body cavity fluid > hyperkalemia & hyponatremia that looks like addisons and may occur with repeated drainage of chylothorax causing retentio of K+; also peritoneal efffusions in cats.
  • Parenteral admin of K+
58
Q

Which conditions may cause hyperkalemia due to secondary changes in internal K+ balance?

A

Acidemia with shifts of K+ out of cell and H+ in to ICF.
In acidosis it usually occurs d/t selective loss of Sodium Bicarb (NaHCO3-) and retention of Cl- like in secretory diarrhea and then you get ICF > ECF shifts in K+ and in these cases the plasma Cl- is usually also elevated.
Cell membrane damage
Tissue necrosis
Insulin defeciency, which facilitates K+ entry into ICF normally, (diabetes causes renal loss of K+).
Inherited HYPP in horses.
Intracellular K+ depletion due to other problems above can cause large shifts in K+ after correction of above problems and quickly lower K+.
Note: rapid alkinalization of an acidotic patient via therapy can produce life threatening hypokalemia as K+ races into ICF.

59
Q

What are the top 7 causes of Hyperkalemia to remember (3 external and 4 internal)?

A

Renal failure
Addisons
Post obstruction or bladder rupture (cats and foals)
Acidosis, secretory loss of bicarb
Insulin deficiency like in diabetes
Muscle exertion or damage / necrosis.
Inherited hyperkalemic periodic paralysis in horses

60
Q

What are the top 7 causes of hypokalemia (4 external, 3 internal)?

A

Anorexia / low K+ diet
Loss of GI fluids (diarrhea / vomiting, including into rumen).
Renal loss (osmotic diuresis, tubular acidosis, metabolic alkalosis, hyperaldosteronism[tumor-opposite of addisons], renal dz etc.)
Profuse sweating in horses
Alkalemia
*Insulin therapy (especially if the patient is already K+ depleted; *bicarb therapy if acidotic will do the same thing)
Refeeding syndrome after starvation

61
Q

Hypokalemia is almost always due to what general process and what may this perpetuate and what may result?

A

Almost always associated with depletion of ICF K+.
Can result in myopathy, cardiac abnormalities, loss of renal concentrating abilities and can perpetuate metabolic alkalosis as acid shifts out of the cell and K+ enters the cell to compensate for the alkalosis. (paradoxic aciduria b/c the kidney has to exchnage H+ for Na+ instead of K+ as it resorbs sodium in the distal convuluted tubule, which is stimulated by aldosterone due to hypovolemia and hypochloremia, seen with vomiting or sequestration of HCl rich gastric contents.)

62
Q

Cl- is an important component of what in the body?

A

Many secretions like gastric fluid, sweat and saliva in horses.

63
Q

Total body Cl- often changes in parallel to what?

A

Na+; increases or decreases may reflect changes in ECF not total body Cl-.

64
Q

What conditions does Cl- change in that is not related to Na?

A

Loss of HCl- or KCl- secretions

65
Q

What may result in relative increase in serum or plasma Cl- ?

A

Loss of NaHCO3- rich fluids in intestinal secretions or urine (but actual Cl- may be normal or decreased depending on hydration status).

66
Q

Selective decreases in Cl- are almost always associated with what?

A

Loss of HCl- rich fluids and metabolic alkalosis

67
Q

Selective increase in Cl- may be present with what condition?

A

Metabolic acidosis due to selective loss of NaHCO3 (ie secretory acidosis)

68
Q

Loss of what other substance from the blood may produce hyperchloridemia?

A

Hypoalbuminemia becuase albumin is an anion. The AG may also be decreased (but maybe not if the increase in Cl is matched to the decrease in Albumin; Cl- accounts for the majority of the anions).

69
Q

What are the consequences of Cl- deficiency?

A

Usually associated with metabolic alkalosis (you lose Cl then bicarb has to go up to maintain electrical neutrality as Cl and HCO3- acct for the majority of anions).
Causes polydipsia and decreased renal concentrating ability.

70
Q

Which change tells you that you have a metabolic acidosis? How is respiratory compensation achieved?

A

Decreased plasma HCO3- or serum TCO2.

Hyperventilation to exhale CO2 and restore HCO3-/H2CO3 ration.

71
Q

What are the two basic ways you can get a metabolic acidosis?

A
  1. Loss of bicarb in a secretory acidosis.
  2. Gain of acids (organic acid excess) in a TITRATIONAL acidosis as the bicarb titrates the excess acid.
    * Can also have mixed secretory & titrational acidosis (like with diarrhea and dehydration in which case the acidosis may be marked)
72
Q

What are the mechanisms and causes of bicarb loss from the body?

A

Fluids rich in NaHCO3- or KHCO3- are lost such as in:

  • Saliva in animals that can’t swallow (ruminants not horses)
  • intestinal or pancreatic secretions (trapped or lost)
  • bicarb rich urine in renal tubular acidosis
73
Q

What is the normal electrolyte pattern in HCO3- loss acidosis?

A

Low plasma bicarb to serum TCO2

Serum Cl- is increased and AG is normal.

74
Q

What is the patterns of AG, bicarb and Cl in a secretory acidosis?

A

Low bicarb, high Cl and normal AG (where ag represents anion gap and titrated excess organic acids).

75
Q

What is the patterns of AG, bicarb and Cl in a titrational acidosis?

A

Low bicarb, normal Cl and excess AG (where ag represents anion gap and titrated excess organic acids)

76
Q

What is the patterns of AG, bicarb and Cl in a simple metabolic alkalosis?

A

AG is normal and there is excessive bicarb due to low Cl (remember the body never over produces base-just like albumin- and you will almost never gain a base, so alkalosis is due to loss of the other main anion, which is Cl- ).

77
Q

What is the patterns of AG, bicarb and Cl in a mixed alkalosis and acidosis?

A

High AG due to addition of an acid and so some base is lost to titrate it (ie titrational acidosis), but Cl- has also gone down in an alkalosis so there is some increase in bicarb on the other end so its mixed.
- This may occur due to vomiting and loss of Cl- (and acid) to produce an alkalosis, as well as dehydration and increased lactic acid that would normally produce an acidosis).

78
Q

What exactly happens in a titrational acidosis?

A

The bicarb buffers the organic acid and is converted to a salt of the acid, ie: Sodium bicarb + acid > Carbonic acid/H2CO3(carbon dioxide and water) + NaAcid.
The presence of SaltAcid is recognized as an increased anion gap/AG.

79
Q

What are some of the clinically important organic acids?

A

L-Lactic acid from mammalian anaerobic glycolysis
D-Lactic acid from bacterial catabolism (usually ruminants and horses)
Acetoacetic acid and Betahydroxybuteric acid (ketones) in DKA
Uremic acids in renal failure
Some organic poisons and their metabolites (ie ethylene glycol, propylene glycol).

80
Q

What is the electrolyte pattern in titrational acidosis?

A

Low bicarb / TCO2
Cl- is WNL
High Anion Gap

81
Q

How does a mixed titrational and secretory acidosis occur?

A

Dehydration from diarrhea (secretory acidosis, loss of bicarb) leads to accumulation of lactic acid (titrational acidosis) from hypovolemic shock > may combine to produce a marked acidemia.

82
Q

What are the electrolyte patterns in a mixed titrational and secretory acidosis?

A

Markedly low plasma HC03- / TCO2
Cl- may be WNL or have mild changes
Mild to Mod increase in AG

83
Q

What is the indicator of metabolic alkalosis?

A

Increased serum HC03- or serum TCO2;

respiratory compensation often poor cause hypoventilation to retain CO2 is restricted by need for O2.

84
Q

What is almost always the cause of metabolic alkalosis? What occurs with the electrolyte and AG changes, and compare monogastrics to ruminants to horses in how this occurs.

A

Loss of gastric or abomasal HCl.
[Loss of HCl, gain of bicarb b/c Cl is lost as well as H+ so you ahve alkalosis, hypochloridemia and the AG is WNL.
-Vomiting in monogastrics
-Abomasal or high gut obstruction in ruminants and reflux from abomasum into rumen (internal or ruminal vomiting).
-Horses > Proximal jejunitis-ileitis produces mild metabolic alkalosis d/t pooling of HCl in stomach

85
Q

**How does paradoxical aciduria occur in metabolic acidosis due to HCl loss?

A

The kidney should be secreting excess NaHCO3- and retaining H+ ions in this case but the kidney often cannot correct the alkalosis. > paradoxical aciduria.

  • Its due to hypovolemia, hypochloridemia and total body K+ depletion.
  • Kidney retains water via Na+ retention d/t hypovolemia and needs an anion to retain with it and Cl- is depleted so it uses HCO3- (which perpetuates the alkalosis).
  • Na+ resporbtion requires exchange with another cation, either K+ or H+, and K+ is also depleted (much has gone intracellular d/t alkalosis) so H+ is exchanged with Na+ and excreted into urine producing paradoxical aciduria.
86
Q

Other less common conditions that can cause alkalosis?

A

Liver failure in horses > excess bases (NH3 and amines) in circulation, hyperammonemia basically results in metabolic acidosis.
Hypochloridemia from any cause and hypokalemia associated with hypovolemia may also lead to metabolic alkalosis.

87
Q

What is the electrolyte pattern in hypochloremic metabolic alkalosis?

A

Increased HCO3- or TCO2.
Decreased Cl-
+/- Hyponatremia

88
Q

What are the mechanisms and causes of mixed metabolic acidosis and alkalosis?

A
  • Loss of HCl rich fluids leads to metabolic alkalosis and increased bicarb BUT this is offset by hypovolemia and increased lactic acidosis (and AG) that will titrate the Bicarb excess bringing it within ref interval, BUT Cl- wil\l be VERY low and the AG will be very high.
  • Other examples include when titration acidosis produces vomiting like in DKA and renal failure where the acids themselves cause vomiting with the same results as above.
89
Q

What are the lab findings with Mixed metabolic acidosis and alkalosis? How do you detect it?

A
  • HCO3- or TCO2 near or WNL *NOTE measurement of TCO2/bicarb will NEVER detect a mixed metabolic alkalosis / acidosis, gotta look at AG.
  • Decreased Cl-
  • Very high AG
90
Q

What does PO2 measurement tell you?

A

Its a measure of intrapulmonary gas exchange.

91
Q

What is the cause of and what conditions result in hypoxemia and compensatory hyperventilation?

A

Decreased gas exchange and concomitant continuation of CO2 exchange, ie low PO2 and normal or low PCO2 d/t hyperventilation (Resp alkalosis).
Examples:
-Perfusion/diffusion abnormalities, (ie pneumonia, pulmonary edema, pulmonary thormbosis.)
-Decreased intrapulmonary gas exchange (thickened alveolar septa, pulmomary fibrosis, pulmonary edema)

92
Q

What are the categories of dzs (4) and some important ones associated with hypoventilation with hypoxemia and hypercapnia leading to respiratory acidosis (not blowing of enough CO2).

A

Aka Hypoxemia without hyperventilatory compensation:
- Abnormalities of neurologic control (sedation, anesthesia, head trauma).
-Muscular or mechanical failure in breathing (neurotoxins-botulism, myasthenia, pleural effusion, pneuomothorax.)
-Upper airway obstruction (calf diptheria, tracheal collapse, laryngeal edema or constriction)
-Pulmonary abnormalities (severe edema or pneumonia, chronic obstructive lung dz).
(note less severe forms of pneumonia and edema may cause hypoxemia without resulting in respiratory acidosis).

93
Q

What is arterial PCO2 a measure of?

A

Alveolar ventilation. This is what controls respiration in health minute to minute.
-In chronic hypoxemia the aortic and carotid bodies can respond to total O2 content being low and become the major controllers of respiration (ie they override the CO2 based control.)

94
Q

What are the conditions where respiratory acidosis occurs (3) and what are the values associated with this?

A
  • Hypercapnia/PCO2 above the ref interval, which indicates hypoventilation.
  • D/t deranged central control, failure of mechanical apparatus of breathing and severe pulmonary abnormalities.
95
Q

Dzs associated with respiratory acidosis are also associated with what other abnormality of oxygen? Why?

A
  • Hypoxemia cause O2 exchange is LESS efficient than CO2 exchange.
96
Q

How does Respiratory compensation for metabolic alkalosis occur and how effective is it? Why?

A

It occurs via HYPOventilation to cause Hypercapnia to compensate for the alkalosis BUT its blunted by the need for oxygen and development of hypoxemia so its not that effective.

97
Q

How does respiratory alkalosis occur and what does it cause?

A

Hypocapnia which indicates hyperventilation and is associated with altered respiratory control.

98
Q

Altered respiratory control may occur under what two conditions (very general)?

A

Physiologic like heat control, panting.
Pathologic like with hepatic encephalopathy where substances chemically effect the respiratory center.
(I think also with respiratory compensation for metabolic acidosis would also be included here.)

99
Q

What kind of lab changes can you expect in mixed respiratory and metabolic acid base disorders? There are two general patterns that clue you in to this.
(NOTE: DO NOT confuse this scenario with mixed secretional and titrational acidosis or mixed metabolic acidosis and alkalosis).

A
  • Lack of expected compensation (like normal PCO2 and abnormal HCO3-, aka lack of compensation or abnormal PCO2 and normal HCO3-); BLUF if the compensatory response is absent think about this.
  • PCO2 changes and HCO3-/TCO2 changes that produce both alkalosis and acidosis (ie low PCO2 and high bicarb, or high PCO2 and low bicarb).
100
Q

Compare respiratory compensation to metabolic compensation for acid base disorders.

A
  • Respiratory compensation occurs within minutes after a pH abnormality and can last long term.
  • Metabolic compensation may lag several days after onset of respiratory disorder.
  • Mixed disorders may lead to severe blood pH abnormalities.
101
Q

What are some things that can produce hyperventilation and hypocapnia and respiratory alkalosis?

A

Altered Resp control > convulsions, fear, fever, heat exposure, hepatic encephalopathy.
Hypoxemia > Hypotension, pulmonary shunts, fibrosis, pneumonia, pulmonary edema.

Clin Path (14 decks)

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