Acid Base II Flashcards

1
Q

Describe the isohydric principle.

Do we measure acid/base on arterial or venous side? Why?

A

Isohydric Principle-in plasma space. body contains many buffer systems- each of which competes for the same H ions. how many types of protons are there in plasma space? ONE. “iso” … how many protein buffers? multiple

  • so when loading plasma w protons, they’re buffered by 3 diff systems (or more)
  • only one buffer system needs to be closely examined to understand the H in the plasma space- possible bc all buffer systems are linked together through a common H (isohydric principle)

acid/base measure arterial side, not venous
in exercise pour CO2 and H into venous blood but lungs take care of that. so look at arterial blood for assessment

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2
Q

Describe protons in the plasma and interstitial space and intracellular.

Is pH slighly higher or lower in intracellular space?

A

(plasma perfuses all body tissues) by regulation of plasma proton conc we then regulate the interstitial H ion conc. then regulate intracellular.

bottom line is regulation of intracellular (gradient from intercell to interstitial to plasma) 7.4 is usually less in intracellular spaces (lower pH in cells, higher proton conc. and takes time for protons to diffuse out of cells into interstitium)

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3
Q

How is intracellular pH affected when one hyperventilates or holds their breath?

A

transfer of protons from cell to interstitium to plasma (motion from intracellular to interstitium is slow-means when hyperventilate and blow off CO2 and pH high or hold breath and pH falls…doesnt affect intracellular pH that much bc of the slow transfer…means can’t hyperventilate yourself to death in terms of status… protected!
slow transfer is important

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4
Q

Describe the bicarbonate buffer system. Open/closed? How is the hydrogen ion conc. calculated?

What is the pK? Why is the bicarb system so useful?

A

open system in communication with the external environment

[H+] =Kal x (0.03 x PaCO2)/[HCO3-]

main focus is bicarb system -OPEN system.. so we can excrete CO2 by breathing…goes out to environment, pK is 6.1 which is more than 1 unit away from pH of 7.4 still a VERY useful system bc we breathe out CO2 and secrete protons and reabsorb bicarb

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5
Q

Describe the phosphate and protein buffer systems.

Open/closed?

Equation?

A

closed systems within the body -

closed system (buffering protons while in transit from tissue space and back to lungs and so forth) picking up protons and buffer them, take care of at lung and also kidney space to bring back to normal value
protein system is closed system bc when buffers protons we don't bleed and lose that proton to environment

phosphate is sorta closed bc its in plasma space at low concentration. secrete/excrete phosphate salts so partially open to environment

[H+]=Ka2 x [H2PO4-]/[HPO42-]

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6
Q

Which buffer system is the most important to look at to understand the H in the plasma space?

Which is of second/third importance?

A

bicarb is most important…
[H+]=24 x (PaCO2)/[HCO3-]

  • hemoglobin buffer is of secondary importance
  • phosphate buffer is of tertiary importance
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7
Q

Draw a diagram of the isohydric principle.

A

Figure 8

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8
Q

Describe how a malfunctioning respiratory system can lead to acid-base disturbances.

A

insufficient CO2 removal- respiratory acidosis –acidemia

excessive CO2 removal-
respiratory alkalosis -alkalemia

alveolar ventilation is inadequate for metabolic demands - means alveolar ventilation is either too low (COPD) or too high (panic attack, over ventilated)
alveolar ventilation is geared to perfectly match metabolic processes in body so maintain constant PaCO2 at 40mmHg…so insufficient removal of CO2 is respiratory acidosis (my patient has “acidemia” or is “acidotic” NOT “acidic” …) if body fluids at 7.0 that is severe acidosis.. excessive removal of CO2 alveolar ventilation too high

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9
Q

Describe malfunctioning metabolic systems. (2 types)

A

renal (improper processing of H+ or HCO3-)

extra-renal (excessive metabolic CO2 and H+ production)

renal component and extra-renal component (everything else except lungs)

renal -improper processing of protons, (not secreted right) bicarb (not being reabsorbed)

extra-renal processes- prod. of ketoacids, can have aldosterone tumors leaking to alkalosis..
if acid based problem, get hint by differential diagnosis, look at anion gap to see if problem lies in kidney or else place.

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10
Q

What are the compensations for dysfunctional lungs or kidneys or extra-renal? Which are fast/slow compensations?

Describe HOW.

A

kidneys can compensate for dysfunctional lungs (renal system responds after a couple of days- slow) if lungs retain CO2, kidney takes that CO2 convert its to bicarb, secrete the proton, increase base-load and work as a buffer.

the lungs can compensate for dysfunctional kidneys (respiratory system responds within minutes- fast) if kidneys retaining protons, that proton conc. will stimulate kidney receptors and alveolar ventilation will go up and ventilates off as a volatile acid, CO2. responds in minutes

lungs and kidneys can both compensate for acid-base disturbances of extra-renal origin

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11
Q

How can the origin of acid- base disturbances and presence of compensations be determined?

A

measurement of bicarb buffer system components and pH (simple)
- looking at bicarb buffer system variables (bicarb, PaCO2, pH) …can calculate one by using other 2

interpretation of plasma electrolytes concentrations (Na, HCO3-, Cl-) (more complicated)

(anion gap is imp. K conc. are important) esp bc of proton/K exchange

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12
Q

Describe the anion gap. What does it account for. What does it differentiate between?

A

anion gap… accounts for unmeasured anions that must be present to neutralize the charge of the measured Na+ (plasma electroneutrality maintained)

anion gap differentiates between acid/base disorders due to renal/GI systems (normal A- gap) vs other metabolic disorders (high A- gap)

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13
Q

How do you rearrange the pH Henderson/H eq. to solve for a missing value. Solve for HCO3-, pH, PaCO2 and A-.

A

pH = 6.1 + log10 [HCO3-]/(0.03 x PaCO2))

HCO3- (mM) = 0.03 x PaCO2 x 10^(pH-6.1)

PaCO2 (mmHg) = [HCO3-]/(0.03 x 10^(pH-6.1))

[A-] (mEq/L) = [Na+] - [HCO3-] - [Cl-]

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14
Q

What are the normal limits for pH, PaCO2, [HCO3-], [H+], [A-]?

A
pH- 7.35 to 7.45
PaCO2 - 35mmHg to 45mmHg
[HCO3-] 22mM to 28mM 
[H+] 35 nM to 45nM
A- 10meq/L to 15meq/L
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15
Q

When does an uncompensated acid-base disturbance exist?

What values cause acidemia or alkalemia?

A

exists if pH is out of its normal range

acidemia - pH less than 7.35 or H+ greater than 45nM
alkalemia - pH greater than 7.45 or H+ less than 35nM

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16
Q

If an uncompensated acid-base disturbance exists, how can the primary cause be determined?

metabolic acidosis
respiratory acidosis
metabolic alkalosis
respiratory alkalosis

A

can be determined from the one bicarbonate system variable that is not normal

metabolic acidosis- HCO3 less than 22 mM

respiratory acidosis -PaCO2 greater than 45mmHg, retaining CO2, suppressed alveolar ventilation

metabolic alkalosis HCO3- greater than 28nM

respiratory alkalosis -PaCO2 is less than 35mmHg

17
Q

When would a double acid-base disturbance exist?

When would a mixed acid-base disturbance exist?

A

double acid-base disturbance- if plasma pH is abnormal and both bicarbonate system variables are abnormal on the same side of pH

severe acidosis- HCO3 is less than 22mM and PaCO2 is greater than 45mmHg

18
Q

When does a mixed acid-base disturbance exist?

Give examples using HCO3 and PaCO2.

A

if plasma pH is within its normal range (compensatory situation) but both bicarb system variables are not normal

HCO3- less than 22mN and PaCO2 is less than 35mmHg

HCO3- greater than 28mM and PaCO2 greater than 45mmHg

large anion gaps also are mixed disorders (A- is greater than 15mEq/L

19
Q

Evaluate/work through Figure 10.

A

Figure 10.

compensation does not CURE. kidney can compensate for acid/base disturbances introduced by sick lung. just compensates, does not correct it..

20
Q

If a compensatory situation exists, how can primary disturbance be determined?

A

by examining which side of normal the pH value resides

Figure 11

21
Q

Given the following case, what is the diagnosis?

data:
pH= 7.35 units
PaCO2= 30mmHg
[HCO3-] =16mmol/L

primary disturbance?
compensation?
full/partial compensation?

A

diagnosis:

pH-normal, acid
PaCO2- low, pul. alkalosis
HCO3– low, metabolic acidosis

primary metabolic acidosis (since pH resides on acid side of normal
secondary respiratory alkalosis (compensation)
full compensation

22
Q

Given the following case, what is the diagnosis?

data:
pH= 7.45 units
PaCO2= 30mmHg
[HCO3-] =20mmol/L

primary disturbance?
compensation?
full/partial compensation?

A

pH-normal, alk
PaCo2, low pul alk
HCO3- low metabolic acid

primary respiratory alkalosis
secondary metabolic acidosis

full compensation

23
Q

Clinical observations:
are acidotic or alkalotic problems more common?

are respiratory or metabolic disorders more complicated?

A

acidotic more common and more easily regulated

respiratory less complicated than metabolic

24
Q

Describe primary respiratory acidosis.

What is the initiating event? (Possible causes)
What are the resultant effects on CO2, PaCO2, H+, and pH

What are compensations?

A

What would suppress alveolar ventilation? bronchitis, emphysema, COPD (fibrosis NO bc its low compliance disease), barbiturate poisoning (CNS depression), weak respiratory muscles (neuromuscular disease

retain CO2, PaCO2 goes up, proton conc. in blood goes up, pH down

compensation - actually have increase at kidney level of more bicarb being reabsorbed, if PaCO2 higher in blood.. (CO2 rep. in blood in bicarb, carbamino-compounds and dissolved CO2 which filters)
if excess CO2 load in renal filtrate, then excess renal reab. of bicarb… secrete the proton. PCO2 response. kidney can take the CO2, keep the bicarb and secrete the proton (good thing) secondary metabolic alkalosis..nothing wrong, its compensating

25
Q

Describe primary respiratory alkalosis.

What is the initiating event? (Possible causes)
What are the resultant effects on CO2, PaCO2, H+, and pH

What are compensations?

A

anything that causes ventilation to increase, causes resp. alkalosis, PaCO2 falling below 35mmHg partial pressure, blowing it off.

  • salicylate intoxication (low-dose aspirin therapy)
  • CNS disorders and hyperexcitability
  • psychogenic paroxysmal hyperventilation “panic attack”
  • hyperventilation, on ventilator in hospital, in hospital and adjust parameters.. (volume and freq. parameters) if chest isn’t moving and you give more volume…no! measure CO2 in blood don’t look at chest wall. don’t want to over-ventilate.

reverse CO2 effect on kidney, filtering less CO2, less change to secrete protons and reabs. bicarb, get secondary metabolic acidosis..
(HCO3- retention via reverse PaCO2 effect on renal proximal tubules)

26
Q

Describe primary metabolic acidosis.

What is the initiating event? (Possible causes)
What are the resultant effects on CO2, PaCO2, H+, and pH

What are compensations?

A

initiating events: renal and extrarenal
-diabetes mellitus, ketoacidosis (larger than normal anion gap)
-severe shock or heart failure and lactic acidosis (larger than normal anion gap)
-diarrhea and loss of bicarbonate ions (normal anion gap)
renal tubular acidosis and retention of H ions (normal anion gap)
salicylate intoxication (normal anion gap)

retain protons, bicarb goes down, pH down bc H ion goes up
compensation for primary metabolic acidosis? what does acidosis do to pul. system? stimulates it. so alveolar ventilation goes up.. central kidney receptors at floor of 4th ventricle where brain bathed by CSF.
secondary if high enough can get peripheral kidney receptors.. stimulate peripherals in extreme ex.

heaving of chest wall- metabolic acidosis.. acid driven, if severe metabolic acidosis, severe drive in ventilation..while doing that you’re eliminating CO2, not exercising, you’re prod. this acid bc of some other problem.

27
Q

What is Kussmaul respiration? What is it an example of?

A

characteristic deep labored breathing with chest heaving

ex of primary metabolic acidosis

28
Q

Describe primary metabolic alkalosis.

What is the initiating event? (Possible causes)
What are the resultant effects on CO2, PaCO2, H+, and pH

What are compensations?

A

initiating events: renal and extrarenal

causes: chronic K ion depletion, if body is losing K, can be due to aldosterone secreting tumor in adrenal cortex, too much aldosterone, too much Na reabsorption, extracellular volume expansion and K secretion goes up, followed by protons which are also secreted
- protracted vomiting and loss of gastric acids (pyloric obstruction, gastric ulcers)
- dehydration and depletion of extracellular fluid volume (contraction alkalosis)

(hypokalemic metabolic alkalosis!!!)

resultant effects: decreased H+ or increased HCO3- and pH increases

compensations: secondary respiratory acidosis (with renal participation if possible)
- increased CO2 retention via decrease in acid drive on ventilation
- hypoventilation also decrease PaO2 which may limit compensation (hypoxic drive on breathing)

29
Q

Will urine pH be low or high if there is chronic depletion of K ions?

A

will be LOW (acidic) w depletion of K ions

(hypokalemic metabolic alkalosis!!!)

hyperkalemic metabolic ACIDosis…! shifts in K conc. also give you shifts in proton. if losing K lose protons. then sample urine, pH really low, so many protons in urine bc secreting too many, leaving deficit and thats why he’s in alkalosis! (thats why insufficient to look at what’s in urine alone)

30
Q

What effect will a suppression of alveolar ventilation have on CO2?

What will it due to oxygen partial pressure if you hypoventilate?

What happens to O2 saturation when hypoventilate? Why?

A

suppression of alveolar ventilation will retain CO2.

O2 partial pressure goes down when hypoventilate

what happens to O saturation when hypoventilate? goes down but not far bc hemoglobin curve flat in loading zone 80-100 mmHg. (imp. of oxyhemoglobic curve being sigmoidal not straight)

if PO2 falls to 70mmHg cant go further than that..there’s limit.

31
Q

Why do you offer bag on face therapy to people who are hyperventilating?

A

bag over face so when breath out CO2 breath it back in… brings PCO2 back UP.

32
Q

Given the following case provide diagnosis and compensation:

pH= 7.55
PaCO2 =27mmHg
HCO3- = 23mmol/L
PaO2=104mmHg
SaO2=98%
A
pH= 7.55 (high, alk) 
PaCO2 =27mmHg (low, pul alk, primary) 
HCO3- = 23mmol/L (normal)
PaO2=104mmHg (high)
SaO2=98% (normal) 

diagnosis: primary respiratory alkalosis
no compensation at all (“get back out!!”

33
Q

Given the following case provide diagnosis and compensation:

pH= 7.30
PaCO2 =34mmHg
HCO3- = 24mmol/L

A

pH= 7.30 (low, acid)
PaCO2 =34mmHg (low pul alk)
HCO3- = 24mmol/L (normal)

diagnosis: data incompatability… one of these is wrong, test out with table

34
Q

Of the following, which are examples of resp acidosis/alkalosis or metabolic acidosis/alkalosis:

low dose aspirin therapy
high dose aspirin therapy
COPD
heart failure
diabetes mellitus 
chronic K ion depletion
dehydration and depletion of ECF volume
diarrhea
severe shock
artificial ventilation
psychogenic paraoxysmal hyperventilation
vomiting
CNS disorders
barbituate poisoning
lactic acidosis, 
renal tubular acidosis
weak respiratory mus
ketoacidosis
A

COPD, weak respiratory muscles and barbituate poisoning - primary resp. acidosis

low-dose aspirin therapy (salicylate intoxication), CNS disorders and hyperexcitability, psychogenic paroxysmal hyperventilation, artificial ventilation -primary resp. alkalosis

diabetes mellitus, ketoacidosis, sever shock or heart failure, lactic acidosis, diarrhea, renal tubular acidosis, salicylate intoxication (high does aspiriin therapy)
-metabolic acidosis

chronic K ion depletion, protracted vomiting, loss of gastric acids, dehydration and depletion of ECF volume - metabolic alkalosis

35
Q

Of the following examples which would have a normal anion gap and which would have a large anion gap?

diabetes mellitus
severe shock
diarrhea
high dose aspirin therapy (salicylate intox)
renal tubular acidosis
heart failure
lactic acidosis
ketoacidossi
A

diabetes mellitus, ketoacidosis, severe shock, heart failure, lactic acdidosis- all larger than normal anion gap

normal gap:
diarrhea, loss of bicarb ions
renal tubular acidosis and retention of H ions
salicylate intoxication (high dose aspirin therapy