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N361: Pathophysiology II > Module 3 - Alterations in Acid-Base Balance > Flashcards

Module 3 - Alterations in Acid-Base Balance Flashcards

1
Q

How many acid base disturbances are important to us?

A

4

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2
Q

How does ABG help us with acid base imbalances?

A

Gives us numbers from arterial blood that can indicate any acid base disturbances and imbalances

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3
Q

What needs to be done before each ABG?

A

An Allens Test

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4
Q

Hydrogen Ions (H+)

A

Ions vital to life with low concentration in the body compared to Na, K, etc, but equally as important

Has 2 forms

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5
Q

How are H+ ions expressed

A

They are expressed as pH (logarithmic form)

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6
Q

What are the 2 forms of Hydrogen Ions in the Body

A
  1. Volatile Hydrogen of Carbonic Acids
  2. Nonvolatile form of Hydrogen and Organic Acids (Fixed)
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7
Q

Carbonic Acid

A

Most important acid in the body

H2CO3

It breaks down into and is made up of CO2 and H2O (think of breathing!)

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8
Q

What two areas of the body control acid base balance?

A

Lungs
Kidneys

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9
Q

What area of the body controls volatile forms of hydrogen ions?

A

Lungs

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10
Q

What area of the body controls nonvolatile forms of hydrogen ions?

A

Kidneys

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11
Q

What is the normal pH range for the body?

A

7.35 to 7.45 (slightly alkalotic)

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12
Q

Acids

A

produced as the end products of metabolism (ex: Lactic acids cause achy muscles from anaerobic glycolysis)

Contain H+ Ions

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13
Q

Acids are Hydrogen Ion ___

A

Donors

they give up H+ to neutralize or decrease the strength of an acid or to form a weaker base (makes acid weaker giving away H+)

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14
Q

Strength of an acid is determined by …

A

the number of hydrogen ions it contains

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15
Q

The number of hydrogen ions in body fluid determines…

A

acidity, alkalinity, or neutrality of the body fluid

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16
Q

More H+ = More ____ = ___ pH

A

More H+ = More acidic = lower pH

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17
Q

Discuss Lung excretion of acids

A

Lungs excrete 13000-30000 mEq of volaile hydrogen per day in the form of carbonic acid (H2CO3) as CO2

The respiratory rate increases to get rid of the acids make things more alkalotic/neutral

The fast workhorse of acid base balance

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18
Q

Discuss Kidney excretion of acids

A

Kidneys excrete 50mEq of nonvolatile acids per day

The kidney releases a lot less than the lungs but the difference they make could be what determines the difference between life and death

The slow fine tuners of acid base balance

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19
Q

Bases

A

contain no Hydrogen ions (H+)

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20
Q

Most important Base in the body?

A

Bicarb (HCO3-)

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21
Q

Bases are hydrogen ion (H+) ____

A

acceptors

they accept H+ from acids to neutralize or decrease the strength of a base or to form a weaker acid

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22
Q

What is pH

A

it reflects the hydrogen ion concentration (H+) in a fluid

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23
Q

The greater the concentration of H+ ions, the ___ the pH and the more ___ the blood

A

lower the pH; the more acidic the blood

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24
Q

The lower the concentration of H+ ions, the ___ the pH and the more ___ the blood

A

higher the pH; the more alkalotic the blood

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25
Q

Acids are formed from …

A

Metabolic activity (or other substances)

ex: Glucose –> Carbonic Acid (H2CO3)

ex: incomplete oxidation of fats –> Ketoacids

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26
Q

What is the normal ratio of alkali (bicarbonate) to acid (H2CO3) ?

A

20:1

1 part acid to 20 part alkali

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27
Q

What balance situations lead to acidosis?

A

Increased acid with normal alkali

Normal acid with decreased Alkali

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28
Q

What balance situations lead to alkalosis?

A

Normal acid with increased alkali

Decreased acid with normal alkali

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29
Q

What is the acidosis (non death) range of pH

A

<7.35 but > 6.80

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30
Q

What is the alkalosis (non death) range of pH

A

> 7.45 but <7.80

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31
Q

What is the acidosis (death) range of pH

A

< 6.80

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32
Q

What is the alkalosis (Death) range of pH

A

> 7.80

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33
Q

What is an example of acidosis?

A

DKA

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34
Q

What is an example of alkalosis

A

Hyperventilation (blowing off a lot of CO2 and Water (which makes up carbonic acid) which raises pH and you become more numb, tingling, etc)

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35
Q

Buffer

A

a weak acid/base that can combine with strong acids/bases to minimize changes in pH of the blood

they sense what is wrong in the body and try to keep pH in a healthy range

End Goal - keep pH 7.35 to 7.45

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36
Q

Major Intracellular Buffer System

A

Potassium - Hydrogen Ion Exchange

H+ increase (acidic)–> H+ moves into cells and K+ moves out

H+ decreases (alkalotic) –> H+ moves out of cells and K+ moves in

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37
Q

Major Extracellular Buffer Systems

A

Protein Buffers
Bicarbonate Buffers
Phosphate Buffers
Bone Buffers

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38
Q

What makes up 80% and 20% of Protein Buffers Respectively?

A

80% - Hgb

20% - Albumin and plasma globulin

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39
Q

Bicarbonate Buffer

A

ECF Buffer

Exchange of Carbonic Acid in the Lungs w/ breathing (Fast) and Bicarbonate from the Kidneys (Slow)

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40
Q

Bone Buffer

A

ECF Buffer

More common in chronic conditions

Exchanges of pH between bones and blood

Causes kidney stones and demineralization of bones)

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41
Q

Where else can buffer systems take place?

A

Cells
Blood
interstitial Tissue
Bones
Etc

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42
Q

What are the 3 most important things to know for Buffers as a Regulatory System of H+ Concentration in the Blood?

A
  1. Fast Acting
  2. Reacts Immediately - protection against H+ changes in ECF
  3. Functions to keep pH in narrow limits of stability where there is too much acid or base released
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43
Q

What other things do Buffer Systems do?

A

Absorb or release H+ as needed

Serve as a transport mechanism that carries excess hydrogen ions (H+) to the lungs

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44
Q

What is important to know about what happens after a primary buffer system reacts?

A

Once they are consumed, the body is less able to withstand further stress until the buffers are replaced (autonomic process)

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45
Q

What is the major intracellular buffer and how does it shift pH?

A

Potassium

The K level changes to compensate for H+ level changes

There is tons of K+ in cells

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46
Q

How does the Potassium Buffer work with Acidosis?

A

The body protects itself from the acid state by moving H+ INTO cells –> K+ then moves out to make room for the H+ in the cells and serum potassium levels rise

This is when Serum H+ is high and pH is low

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47
Q

How does the Potassium Buffer work with Alkalosis?

A

Cells release hydrogen ions (H+) into the blood in an attempt to increase acidity of the blood and combat alkalinity –> K+ then moves into the cells and serum K+ levels decrease

This is when Serum H+ is low and pH is high

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48
Q

The body prioritized what balance?

A

pH balance before electrolyte balance (so temporary imbalances can occur)

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49
Q

What can happen regarding potassium and alkalosis? Acidosis?

A

Hypokalemia/ Hyperkalemia can occur making people not feel well for a little while

Ex: cardiac arrhythmias, GI issues with innervation

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50
Q

What is the Major Buffer System of ECF and how does it balance pH?

A

HG Systems (80%)

Acid Base balance is maintained with chloride exchanges for bicarbonate between the RBCs/HGB

Chloride shifts in and out of cells in response to level of O2 in the blood

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51
Q

A cation must be exchanged for a ___ and an anion must be exchanged for a ___

A

cation; anion

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52
Q

How does the HGB buffer fix low serum bicarbonate (Acidosis)?

A

Less base = acidic –> pH is lower –> RBC will let HCO3 out and Cl- in –> Serum chloride decreases

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53
Q

How does the HGB buffer fix high serum bicarbonate (Alkalosis)?

A

More base= alkalotic –> pH is higher –> RBC lets HCO3- in and Cl- out –> Serum Chloride increases

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54
Q

The benefit of the HGB system is what?

A

You do not feel symptoms of hypo or hyperchloremia unless it is extreme

Hyper - Fluid Volume Excess
Hypo - Dehydration, Fluid Loss, Vomiting, Diarrhea

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55
Q

Plasma Protein Systems

A

ECF Buffer

Functions in conjunction with the liver (via albumin, globulin, etc) to vary the amount of hydrogen ions (H+) in the chemical structure of protein

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56
Q

What special acid base function does plasma proteins have?

A

they have the ability to attract or release H+ ions

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57
Q

What would the action be of the Plasma Protein Buffer System if there is Metabolic Alkalosis?

A

H+ ions release from plasma proteins and enter serum to increase acidity –> H+ will then bind to unbound calcium and decrease total ionized calcium –> nL pH with Hypocalcemia occurs

ex: Hyperventilation –> Alkalosis –> Correction –> Serum Ionized Levels Drop –> Hypocalcemia w/ dizziness, tingling, etc because of lowered threshold

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58
Q

What would the action be of the Plasma Protein Buffer System if there is Metabolic Acidosis?

A

Too many serum H+ –> H+ goes into a plasma protein and calcium unbinds and enters the blood –> Increase in ionized Ca and decrease in bound Ca –> Hypercalcemia and nL pH

ex: DKA –> Acidosis –> Correction –> Serum ionized levels rise –> hypercalcemia w/ longer distance to firing and slowing of muscle and nerve innervation

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59
Q

Phosphate buffer system

A

ECF Buffer

present in cells and body fluids

especially active in the kidneys

acts like bicarb and clears spare H+ ions by exchanging phosphorous with calcium at the level of the kidneys

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60
Q

The only acid that the lungs can get rid of, unlike the kidneys which can get rid of many, is what?

A

Carbonic Acid

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61
Q

What does the Carbonic Acid/Bicarbonate System do?

A

it is a buffer system for ECF

it maintains a pH of 7.4 with a 20 bicarb to 1 carbonic acid ratio (20:1)

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62
Q

The 20:1 ratio determines what?

A

Hydrogen ion (H+) concentration of body fluid

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63
Q

Carbonic acid concentration is controlled by what?

A

The excretion of CO2 by the LUNGS

The rate and depth of respiration changes then in response to the changes in CO2

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64
Q

Bicarbonate concentration is controlled by what?

A

the KIDNEYS which selectively retain or secrete bicarb in response to body needs

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65
Q

How does DKA cause Kussmaul breathing?

A

DKA occurs with productions of ketoacids which lower pH and deplete bicarb while creating carbonic acid. The buildup leads to an increase in rate and depth of respiration by the lungs to try and raise the pH

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66
Q

In what directions/areas can Carbonic Acid go

A

To the lungs: H2CO3 H2O and CO2

To the Kidney H2CO3 H+ and HCO3-

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67
Q

What is needed for carbonic acid to turn into bicarb and hydrogen or carbon dioxide and water?

A

Carbonic Anhydrase - an enzyme that breaks down carbonic acid into these components

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68
Q

If blood buffer systems are the first defense for acid base balance, what are the second and third/final?

A

second - lungs

third/final - Kidneys

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69
Q

What occurs during Acidosis regarding the lungs and pH?

A

pH decreased so RR and Depth increase to try and blow off acids

Carbonic acid can be carried to the lungs and reduced to CO2 and Water to be exhaled, thus H+ ions are inactivated and excreted

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70
Q

What occurs during Alkalosis regarding the lungs and pH?

A

pH increased so RR and Depth decrease to try and blow off acids

CO2 is retained and carbonic acid builds up (CO2 + H2O) to neutralize and decrease the strength of excess bicarbonate

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71
Q

How do the lungs mechanically compensate for acidosis and alkalosis?

A

Acidosis: increase RR and Depth

Alkalosis: decrease RR and depth

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72
Q

How fast are the lungs in fixing excess or deficit?

A

The action of the lungs is reversible and only takes 10-30 seconds to correct

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73
Q

Why is Bicarbonate considered volatile?

A

it is in a gaseous form - in lungs 30,000 mEq of volatile acids are removed with only 50 mEq removed via kidneys so we do need constant buffering

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74
Q

What occurs with acid base balance, buffering, and diarrhea?

A

Diarrhea gets rid of bases, letting the body get acidotic. So respiration rate and depth increase to blow off carbonic acids and raise pH. This only takes 10-30 seconds to correct.

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75
Q

The lungs can only deal with ___ ___, everything else is handled by the ___

A

deal with CARBONIC ACID

handled by the KIDNEYS

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76
Q

Why can the lungs only deal with carbonic acid?

A

the lungs can only inactivate H+ carried by carbonic acid, excess H+ on other carriers and from other problems need to be excreted by the kidneys

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77
Q

How does the lungs exactly retain or get rid of H+ ions

A

Lungs can either hold H+ with CO2 and making Carbonic acid until deficit is corrected

Or it can inactivate H+ and turn them into water molecules to be exhaled as CO2 to correct excess

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78
Q

How long does acid base compensation by the kidneys take?

A

Few hours to several days, but this is more selective and thorough than other regulators as its the ultimate correction

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79
Q

What is the action of correcting acidosis for the kidneys?

A

pH has gone down, so excess H+ are secreted into the tubules and combine with buffers for excretion in the urine

the urine is outside normal pH and more acidic but we only care about blood pH at the moment so this is ok

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80
Q

What is the action of correcting alkalosis for the kidneys?

A

pH has gone up, so bicarbonate ions move into the tubules, combine with sodium, and are excreted in the urine

this urine is outside normal pH and more alkalotic but we only care about blood pH at the moment so this is ok

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81
Q

What are the 3 methods for the kidneys to selectively regulate bicarbonate and rid of acids?

A
  1. Conservation of bicarbonate that is filtered by releasing H+ and holding onto Bicarb ions
  2. Extra H+ is turned into phosphoric acid (using phosphorous) and is excreted in urine
  3. Amino Acid alteration in renal tubules diffuses ammonia into the kidneys which then combines with excess H+ (into ammonium) and is excreted in the urine
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82
Q

Respiratory: ___ + ___ Carbonic Acid __ + __ :Renal

A

Respiratory: CO2 + H2O Carbonic Acid (via Carbonic Anhydrase) H+ + HCO3- :Renal

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83
Q

In health there is a ratio of what?

A

20 bicarb (base) for 1 part Carbonic acid (acid) (or CO2)

20b:1a –> pH of 7.4 (within 7.35 to 7.45)

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84
Q

What happens if the ratio of bases:acids increases?

A

ex: 30:1 –> blood pH increases –> alkalosis

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85
Q

What happens if the ratio of bases:acids decreases?

A

ex: 13:1 –> blood pH decreases –> Acidosis

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86
Q

Slower and shallower breathing leads to …

A

retention of CO2 –> production of acid

can correct alkalosis

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87
Q

Faster and deeper breathing leads to …

A

elimination of CO2 –> elimination of acid

can correct acidosis

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88
Q

Response difference between the lungs and kidneys?

A

Lungs: Rapid response occurring within minutes with a maximum of 12-24 hours (with effect declining thereafter)

Kidney: Slow response occurring within 1 to 2 days

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89
Q

Decreased pH (acidosis) leads to what occurring in the kidneys?

A

decreased pH –> secrete more H+ (and less K+) and phosphate –> reabsorb more bicarbonate (and less Cl-)

this can raise the pH

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90
Q

Increased pH (alkalosis) leads to what occurring in the kidneys?

A

increased pH –> secrete less H+ (and more K+) –> Reabsorbs less bicarb (and more Cl-)

this can lower the pH

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91
Q

BMP

A

Basic Metabolic Panel

Drawing venous blood (rather than arterial for ABG) to check electrolyte and acid base balance

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92
Q

A BMP CO2 levels comes from what type of blood and represents what?

A

venous blood

Venous CO2 is actually a measure of Bicarbonate

so, high CO2 values means alkalosis, and low CO2 levels means acidosis

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93
Q

Metabolic Acidosis

A

Total concentration of buffer base (Bicarbonate) is lower than normal with a relative increase in H+ concentration

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94
Q

Metabolic means what?

A

it is dealing within the body

so in the case of metabolic acidosis, there is a kidney problem and the lungs must compensate

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95
Q

When does Metabolic Acidosis occur?

A

as a result of losing too many bases (ex: diarrhea) and holding too many acids without sufficient bases (ex: DKA)

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96
Q

Potential causes for Metabolic Acidosis

A

Diabetes and DKA

Renal Insufficiency or Failure

Insufficient Metabolism of Carbohydrates

Excessive ingestion of Acetylsalicylic Acid (Aspirin)

Severe Diarrhea

Malnutrition

High Fat Diet

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97
Q

The most common and main reason for Metabolic Acidosis is?

A

DKA and Diabetes

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98
Q

Why are kidneys the problem for Metabolic Acidosis?

A

kidneys will hold back bicarbonate, but eventually this system is exhausted. The lungs will then blow off carbonic acid to try and compensate

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99
Q

How does DKA and Diabetes lead to Metabolic Acidosis

A

insufficient insulin causes increased fat metabolism because the glucose cannot get into cells

this leads to accumulation, in excess, of ketones and other acids that exhaust the bicarbonate system

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100
Q

How does Renal Failure/Insufficiency cause Metabolic Acidosis

A

Increased waste products of protein metabolism are retained because the kidney cannot metabolize them and rid of the acids

excessive acid build up thus overpowers bicarbonates ability to maintain balance

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101
Q

How does Insufficient metabolism of carbohydrates cause Metabolic Acidosis

A

insufficient supplies of O2 are available for proper burning of CHO, glc, and H2O –> this leads to lactic acid buildup, and insufficient metabolism of carbs causes Lactic Acidosis

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102
Q

What must the lungs do when there is Lactic Acidosis causing Metabolic Acidosis?

A

It cannot blow off lactic acid, so it must blow off Carbonic acid

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103
Q

How does excessive ingestion of acetylsalicylic acid (aspirin) cause Metabolic Acidosis?

A

excessive ingestion of acetylsalicylic acid causes an increase in H+ concentration because it metabolizes into H+

This is a mixed imbalance though

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104
Q

How is Acetylsalicylic Acid causing a mixed imbalance of Metabolic Acidosis?

A

Aspiring poisoning in the early stages is associated with respiratory alkalosis -d/t aspirin impact on resp centers - so they will breath fast, but once aspirin is metabolized the acids will build up and metabolic acidosis occurs

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105
Q

How does severe diarrhea cause Metabolic Acidosis

A

intestinal and pancreatic secretions are normally alkaline so excessive loss of base in this case causes MA

faster and deeper respirations occur as a result

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106
Q

How does malnutrition lead to Metabolic Acidosis

A

improper metabolism of nutrients causes fat catabolism leading to excess build up of ketones and acids (like DKA a little)

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107
Q

How does a High fat Diet lead to metabolic acidosis

A

high intake of fat causes a much too rapid accumulation of waste products of fat metabolism leading to a build up of ketones and acids

think Atkins diet

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108
Q

Anion Gap

A

Lab that describes the difference between the serum concentration of the major measured cation, Sodium (Na+), and the sum of measured major anions, Chloride and Bicarbonate.

The difference between the major measured cation and the major measured anions represents the concentration of unmeasured anions (like phosphates, sulfates, ketone bodies, lactic acid, and proteins)

AG = [Na+] - ([HCO3-]+[Cl-])

This will tell us whether they have too much acid or loss of bases

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109
Q

Anion Gap is only looked at in the case of …

A

metabolic acidosis

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110
Q

Normal Anion Gap range?

A

12 +/- 2 mEq/L

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111
Q

What does elevated anion gap mean?

A

elevation is occurring from accumulation of acids (these are the unmeasured anions of acids)

ex: lactate in lactic acidosis, acetoacetate in ketoacidosis, sulfates and phosphates in RF - unmeasured anions of acids

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112
Q

What does a Normal Anion Gap represent?

A

a loss of base (bicarb)

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113
Q

What does a lowered anion gap mean?

A

It is a rare occurrence

It occurs from a decrease in proteins like in cancer and cirrhosis

it either comes from a decrease in unmeasured anions or an increase in unmeasured cations

ex: low albumin, hyperkalemia, hypercalcemia, hypermanesemia

114
Q

What are the etiologies for a High anion gap?

A
  1. Excess production of metabolic acids (lactic acidosis, DKA, starvation, alcoholic intoxication, aspirin poisoning)
  2. Impaired elimination of metabolic acids (ex: RF)
115
Q

What are the etiologies for a Normal anion gap?

A
  1. Loss of intestinal secretions (diarrhea, intestinal suction, biliary or pancreatic fistula)
  2. increased renal losses (renal tubular acidosis, tx with carbonic anhydrase inhibitors, HYPOaldosteronism)
  3. Increased chloride levels (excess reabsorption of chloride by the kidney, sodium chloride infusion, ileal conduit)
116
Q

Ileal Conduit

A

placed for bladder cancer

ureter attached to Small intestine instead of emptying urine via the bladder

urine then mixes with feces causing chloride absorption allowing for a normal anion gap and thus loss of bases

117
Q

Assessment of Metabolic Acidosis shows what?

A

Headache
Nausea
Vomiting (low pH stims vomit centers)
Diarrhea
Fruit smelling breath from improper fat metabolism
Twitching
Mental Dullness (!!)
Drowsiness
Stupor
Coma
Convulsions

Hyperpnea with Kussmaul Breathing - due to an attempt to blow off extra CO2 and compensate for the acidosis

118
Q

Neural Manifestations of Metabolic Acidosis

A

Weakness
Lethargy
General Malaise
Confusion
Stupor
Coma

119
Q

Cardiovascular Manifestations of Metabolic Acidosis

A

Peripheral Vasodilation (Decreased HR and BP)

Decreased HR

Cardiac Dysrhythmias

120
Q

GI Function Manifestations of Metabolic Acidosis?

A

Anorexia

Nausea and Vomiting

Abdominal Pain

121
Q

Non Cardiac, GI, or Neural Manifestations of Metabolic Acidosis?

A

Skeletal - bone disease if MA is chronic

Skin - flushed warm and dry (from peripheral vasodilation)

122
Q

What is the Stupor, Coma, and Confusion related to in metabolic acidosis manifestations?

A

An increase in ionized calcium from the plasma protein buffer system (H+ moves to proteins but those proteins release Ca2+)

123
Q

The most important Metabolic Acidosis manifestations are?

A

Neural
Cardiovascular
GI Function

124
Q

How does the Body compensate for Metabolic Acidosis?

A

Respiratory: Kussmaul breathing - increased RR and depth

Hyperkalemia

Acidic Urine

Increased Ammonium in Urine

*kidneys are trying, but they are also the issue, so lungs are the compensatory part

125
Q

General Interventions for Metabolic Acidosis

A

Determine the Cause of the Acidosis!!!

Maintain a patent airway

Assess LOC for CNS depression - a chance of seizure exists if the body is acidotic

Monitor Lyte values

maintain I and O and assist with fluid and lyte replacement as prescribed

Initiate safety precautions for convulsions and coma

Prepare to administer IV solutions like isotonic saline, 5d1/2NS (hypertonic to pull fluid from cells to return circulating volume), sodium lactate or bicarbonate to increase the buffer base

Monitor K level very closely (as K moves with GIK for example)

126
Q

Why do Potassium levels need to be monitored very closely in Metabolic Acidosis?

A

When acidosis is being treated, K will move back into the cell and blood levels will drop rapidly

127
Q

Metabolic Acidosis Interventions if it is caused by DKA

A

Insulin (GIK) is given to hasten movement of serum glucose into cells –> decreases concurrent ketosis (making ketone acids)

When glc is being properly metabolized, body will stop making fats into glucose

Monitor for circulatory collapse d/t polyuria which may come from the hyperglycemic state, as polyuria or diuresis may lead to ECF volume deficit

128
Q

Metabolic Acidosis Interventions if it caused by Renal Failure

A

Dialysis may be used to remove protein and waste products thereby lessening the acidosis state - potential primary need / main treatment

Diets low in protein and high in calories will lessen the amount of protein waste products d/t protein catabolism; this in turn will lessen acidosis - but this is slower and not the main fix in the end

129
Q

Treatments for Metabolic Acidosis

A

Monitor patients at risk (DM, sepsis, shock)

Monitor VS (esp RR and depth)

Monitor ABGs and K+ levels

Administer Sodium Bicarb (NaHCO3)

Cardiac Monitoring for low serum K+ levels

CORRECT UNDERLYING CAUSE OF ACIDOSIS

Administer IV fluids with lactate (unless contraindicated)

130
Q

Treatment for DKA Metabolic Acidosis?

A

Insulin + Normal Saline

131
Q

Treatment for Lactic Acidosis Metabolic Acidosis

A

IV fluids and oxygen

132
Q

Treatment for Renal Failure, Drug Overdose, or Drug Poisoining Metabolic Acidosis

A

Dialysis

133
Q

Treatment for CHRONIC Metabolic Acidosis

A

Increase in Carbohydrates and Decrease in Fat diet

134
Q

Why is DKA Metabolic Acidosis treatment so serious?

A

Metabolic acidosis compensation is making K+ move into cells which then is lost in urine, while DKA GIK treatment moves it in so we are at double risk for low potassium levels that could lead to arrhythmias (higher resting membrane to reach)

135
Q

Define Metabolic Acidosis

A

Fixed Acid Excess - too much acid

136
Q

Causes of Metabolic Acidosis

A
  1. Acid Accumulation - excessive Metabolic acids
  2. Loss of bicarbonate base (HCO3-)

This is a problem via the KIDNEYS

137
Q

What compensates for Metabolic Acidosis

A

Respiratory excretion of H2CO3 (CO2 + H2O)

the LUNGS ARE COMPENSATORY

138
Q

What are normal PaCO2 levels?

A

35-45 (thinks of 7.35-7.45)

PaCO2 is the respiratory marker and partial pressure of CO2

139
Q

What are normal HCO3- levels?

A

22-26

HCO3- is the renal/metabolic marker

140
Q

What are the pH, PaCO2, and HCO3- levels like in uncompensated Metabolic Acidosis?

A

pH - &laquo_space;7.35 (ex: 7.3)

PaCO2 - normal range (35-45)

HCO3- -<22 (low)

141
Q

What are the pH, PaCO2, and HCO3- levels like in partially compensated Metabolic Acidosis?

A

pH - <7.35 (slightly low)

PaCO2 - <35 (slightly lower now)

HCO3- - No change (still <22)

142
Q

What are the pH, PaCO2, and HCO3- levels like in compensated Metabolic Acidosis?

A

pH - low normal (ex: 7.35 exactly)

PaCO2 - &laquo_space;35 (much lower)

HCO3- - No change (still <22)

143
Q

Why are the pH, PaCO2, and HCO3- levels like an elevator?

A

the levels never increase or decrease compared to one another, they either decrease together, increase together, or they may increase or decrease with some having no change (all going in same direction)

144
Q

Why does PaCO2 decrease and HCO3- stay relatively the same in Metabolic Acidosis compensation?

A

PaCO2 decreases because the compensatory system for MA (lungs) will blow it off fast to correct/raise pH

Bicarbonate stays largely the same (low) because the kidneys are the problem here, not the compensatory mechanism

145
Q

Why does the body allow such a drop in PaCO2 for metabolic acidosis compensation?

A

Because it cares more about correcting pH than the Co2 amount

146
Q

How may the ratio of bases:acids be in normal, uncompensated, and compensated Metabolic Acidosis?

A

Normal: 20:1 with ex: 24 mEq/L of Bicarb and 40 mmHg of PaCO2 and a pH of 7.4

Uncompensated: 13:1 with ex: 16 mEq/L of Bicarb and 40 mmHg of PaCO2 with a pH of 7.2

Compensated: 20:1 with an ex: 18 mEq/L of bicarb (largely the same but slightly corrected since kidneys are still working) and 30 mmHg of PaCO2 with a pH of 7.38

147
Q

Metabolic Alkalosis

A

Issue with the kidneys, compensated by the lungs

Deficit of carbonic acid (H2CO3) and a decrease in hydrogen ion concentration

pH > 7.45

2nd most common acid base disorder in hospital patients

opposite effect of metabolic acidosis

148
Q

What can result in metabolic alkalosis?

A

Results from the accumulation of base or from a loss of acid without a comparable loss of base in body fluids

149
Q

What are 2 potential causes for the increase in available basic solution in the blood and decrease in available acids in the blood in Metabolic Alkalosis?

A
  1. Ingestion of excess sodium bicarbonate (ex: excessive ingestion of sodium bicarb like in Alka-Seltzer or baking soda causes an increase in the amount of base in the blood
  2. Excessive Vomiting (leads to an excessive loss of acids)
150
Q

What are some examples of events/disease that cause Metabolic Alkalosis?

A
  1. GI Suctioning - leads to an excessive loss of acids from the suctioning
  2. Diuretics - loss of H+ ions and K+ ions causes a compensatory increase in the bicarbonate in the blood
  3. Hyperaldosteronism - increased renal tubule reabsorption of sodium occurs with the resultant loss of H+
  4. Massive Transfusion of Whole Blood - citrate, and anticoagulant in the whole blood, metabolizes into bicarb
151
Q

What is the most common reason for causing Metabolic Alkalosis

A

Gastrointestinal Suctioning

152
Q

How does Hyperaldosteronism cause Metabolic Alkalosis?

A

The increased reabsorption of sodium causes Na to stay and H+ to leave in the urine

Also called Conns Syndrome

153
Q

General Etiologies for Metabolic Alkalosis

A

Excess gain of bicarb.

Increased bicarb retention

Excessive H+ loss

Volume contraction

Abrupt correction of respiratory acidosis by mechanical ventilation

154
Q

What are some ways a person with metabolic alkalosis ended up with excess gain of bicarbonate

A
  1. Administration/Ingestion of HCO3 (e.g. alka seltzer)
  2. Adminsitration of TPN containing ACETATE, solutions with LACTATE, or CITRATE in whole blood - all will metabolize into Bicarb
  3. NaHCO3 administration during CPR
155
Q

Why is bicarbonate retention increased in Metabolic Alkalosis?

A

d/t a loss of chloride

156
Q

How can H+ be lost in excess leading to Metabolic Alkalosis?

A
  1. NG Suctioning (most common reason)
  2. Vomiting
  3. Bulimia
  4. Potassium Deficit d/t diuretic therapy or hyperaldosteronism
157
Q

What does volume contraction mean as an etiology for metabolic alkalosis

A

loss of body fluids through something like diuretic therapy

158
Q

Things that can be seen on assessment for Metabolic Alkalosis

A

DECREASED RR AND DEPTH OF BREATHING (conserve volatile acid CO2)

Nausea and Vomiting

Diarrhea

Numbness and Tingling in the extremities

Restlessness and twitching in the extremities

Hypokalemia

Hypocalcemia

Sinus Tachycardia

Dysrhythmias

159
Q

What is causing the twitching/neuro excitability and hypocalcemia in Metabolic Alkalosis?

A

Low H+ leads to calcium attaching to plasma proteins to release H+ which lowers the unbound amount of calcium. There is then hypocalcemia occurring which lowers the threshold for firing allowing for neuro excitability

160
Q

Important Areas of Manifestations in Metabolic Alkalosis?

A

Neural
Cardiovascular
GI Function
Compensatory

161
Q

Neural Manifestations of Metabolic Alkalosis?

A

Confusion

Hyperactive DTR

Tetany

Paresthesias in the Fingers and Toes

Circumoral Paresthesias (tingling around the mouth)

Carpopedal Spasm

*All of this d/t hypocalcemia lowering threshold

162
Q

Cardiovascular Manifestations of Metabolic Alkalosis?

A

Hypotension

Dysrhythmias

163
Q

What are the compensatory manifestations of Metabolic Alkalosis?

A

Respiratory rate decreases and depth decreases

Urine pH increases because the kidneys are trying to get rid of some bicarb - but these areas are the problem still and cannot do too much

164
Q

Interventions for Metabolic Alkalosis?

A

Maintain a patent airway (may have spasms)

Monitor vitals, I&O, Lyte values, muscle weakness

Institute safety precautions for tetany and convulsions

Prepare K and Cl– as prescribed, to administer meds as prescribed to promote kidney excretion of excess bicarb, and to administer acidifying solutions as ammonium chloride and arginine chloride as prescribed

165
Q

Treatments for Metabolic Alkalosis?

A

Monitor pts at risk (ex: those with GI fluid loss)

Assess I&O

Monitor VS (esp., RR and Depth)

Monitor ABGs

Correct the underlying cause of imbalance

IV fluids (NS) and lyte supplements to replace fluid volume and K+ and Cl- losses

Supply sufficient Cl- to enable renal reabsorption of NaCl and renal excretion of excess Bicarb

Cardiac monitor for hypokalemia

teach about excess sodium bicarb ingestion and supplemental KCl for thiazide and loop diuretic therapy

166
Q

What is the hallmark/most important treatment for Metabolic Alkalosis behind treating the underlying cause?

A

Teaching them about other methods of treating dyspepsia (not alka seltzer or baking soda)

167
Q

Definition of Metabolic Alkalosis

A

Fixed acid deficit

168
Q

Causes for Metabolic Alkalosis

A

Base Accumulation

Loss of Acids

169
Q

Compensation Mechanism for Metabolic Alkalosis

A

Respiratory retention of H2CO3 (CO2+H2O)

170
Q

What would pH, PaCO2, and HCO3- levels look like in Uncompensated Metabolic Alkalosis?

A

pH&raquo_space; 7.45 (ex: 7.5)

PaCO2 = normal range (35-45)

HCO3- > 26 (high like 32)

171
Q

What would pH, PaCO2, and HCO3- levels look like in Partially compensated Metabolic Alkalosis?

A

pH > 7.45 (slightly lower now - maybe 7.48)

PaCO2 > 45 (retention of CO2 is occurring to lower pH)

HCO3- = No change (still greater than 26 since this is not really the compensatory thing)

172
Q

What would pH, PaCO2, and HCO3- levels look like in Compensated Metabolic Alkalosis?

A

pH = High normal (ex: pH = 7.45 - compensated)

PaCO2 &raquo_space; 45 (much greater because it was retained to lower pH)

HCO3- = no change (still greater than 26, maybe a little lower like 28-30, but this is not the compensatory mechanism)

173
Q

Respiratory Acidosis

A

Total concentration of buffer base is lower than normal with a relative increasing H+ concentration - a greater number of H+ ions are circulating in the blood than can be absorbed by the buffer system (too much acid not enough base)

In this case respiratory is where the problem is at with metabolic/kidney being the compensator

174
Q

Root Mechanical Cause for Respiratory Acidosis

A

Defects in the function of the lungs or by changes in normal respiratory patterns due to secondary problems (like lack of perfusion)

Any condition that causes an obstruction of the airway or depresses respiratory status can cause respiratory acidosis

175
Q

What is pH and PaCO2 like in (uncompensated) respiratory acidosis?

A

pH < 7.35 and PaCO2 >45

176
Q

Potential Causes for Respiratory Acidosis

A

Hypoventilation

Infection

Medications

Pneumonia

Atelectasis

Brain Trauma

emphysema

asthma

bronchitis

pulmonary edema

bronchiectasis

177
Q

How does Hypoventilation cause Resp Acidosis

A

CO2 is retained and H+ increase causing an acidic state

Carbonic acid is retained d/t slow and shallow breaths making pH lower

178
Q

How does Infection cause Resp Acidosis

A

inflammation and bacterial agents can decrease aeration in the lungs from obstruction leading to acid buildup

179
Q

How do Medications and what Medications cause Resp Acidosis

A

Sedatives, narcotics, anesthetics

They depress the respiratory center leading to hypoventilation –> increase in H+ then leads to CO2 narcosis

180
Q

Narcosis

A

stupor or unconsciousness due to medication impact

181
Q

How does Pneumonia cause Resp Acidosis

A

infection, irritants, and immobility lead to pneumonia which causes obstruction of airway passages leading to inadequate oxygenation from fluid accumulation

COVID pneumonia leads to consolidation that decreases lung volume potentially even

182
Q

How does Atelectasis (lung collapse) cause Resp Acidosis

A

Excessive mucus collection with the collapse of alveolar sacs d/t mucus plugs, infectious drainage, or anesthetic medication causes decreases respiration or no exchange occurring

183
Q

How does Brain trauma cause Resp Acidosis

A

excessive pressure on the respiratory center or medulla oblongata depresses respiration ability/rate

184
Q

How does Emphysema cause Resp Acidosis

A

Loss of elasticity of alveoli sacs restricts air flow in and out, mostly out, leading to an increased CO2 level

185
Q

How does Asthma cause Resp Acidosis

A

spasms from allergens, irritants, or emotions can lead to smooth muscles of the bronchioles constricting causing decreased oxygenation and loss of CO2

186
Q

How does Bronchitis cause Resp Acidosis

A

Inflammation causes airway obstruction

187
Q

How does Pulmonary Edema cause Resp Acidosis

A

Extracellular accumulation of fluid in acute CHF causes disturbances in alveolar diffusion and perfusion (plus it is more difficult to expand the lungs)

188
Q

How does bronchiectasis cause Resp Acidosis

A

Bronchi become dilates from inflammation; destructive changes and weakness of the bronchi then occur which leads to decreased and hindered perfusion and less effective bronchiole walls

this is a part of COPD

189
Q

Acute Etiologies of Respiratory Acidosis

A

Lung Disease - Acute pulmonary edema, aspiration, atelectasis, pneumothorax, severe pneumonia

Depression of respiratory center - sedative or narcotic overdose, head injury

190
Q

Chronic Etiologies of Respiratory Acidosis

A

Chronic lung diseases - chronic bronchitis, asthma, cystic fibrosis, emphysema, COPD

Chest wall and respiratory muscle issues - obesity, post op pain, high abdominal or thoracic incisions, abdominal distension from ascites or bowel obstruction (all of these prevent lung expansion)

191
Q

Why are acute problems particularly/especially dangerous for Respiratory Acidosis in comparison to chronic issues?

A

Acute happens quickly, but the compensatory mechanisms of the kidneys are very slow - therefore we may need to give outside help in the hospital because of the low speed

With chronic, the kidneys have time to compensate, so while lyte balance may be abnormal, it can still be compensated for efficiently

192
Q

Things assessed and found for Respiratory Acidosis?

A

RR and depth drop

headaches and mental status changes (ex: confusion, drowsiness, restlessness, visual disturbances)

Diaphoresis

cyanosis as hypoxia becomes mroe acute

hyperkalemia

rapid and irregular pulse leading to dysrhythmias and ventricular fibrillation

The nervous system is depressed, much like Metabolic Acidosis in many ways

193
Q

___ leads to restlessness in people

A

hypoxemia

194
Q

Important group Manifestations of Respiratory Acidosis

A

Neural
Cardiac
Skin
Respiratory

195
Q

Neural Manifestations of Respiratory Acidosis

A

Dilation of cerebral vessels and depression of neural function (to get oxygen to the brain)

Feeling of fullness in the head

headache

weakness

behavior changes like confusion, depression, paranoia, hallucinations

tremors

paralysis

depressed DTR

*neural depression from hypercalcemia

196
Q

Skin Manifestations of Resp Acidosis

A

warm and flushed from dilation of vessels to get more O2 and get rid of more CO2

197
Q

Cardiac Manifestation of Resp Acidosis

A

Tachycardia

198
Q

Respiratory Manifestations of Resp Acidosis

A

Dyspnea
Cyanosis

199
Q

How does the kidney compensate for Resp Acidosis

A

Makes the urine more acidic by getting rid of acids (H+)

200
Q

Interventions for Respiratory Acidosis

A

Maintain patent airway

improve ventilation and aeration based on the clinical manifestations

Monitor for signs of respiratory distress

administer O2 as prescribed

place in semi fowlers unless contraindicated since they may have orthopnea

encourage and assist client to turn cough and deep breath

prepare to administer chest physiotherapy and postural drainage as prescribed

encourage hydration to thin secretions unless excess fluid intake is contraindicated

201
Q

What needs to be reduced, monitored, avoided, and administered with Respiratory Acidosis

A

Reduce - restlessness by improving ventilation rather than by administering sedatives or narcotics

Monitor - lyte values

Avoid - tranquilizers, narcotics, hypnotics because they depress respiration

Administer - antibiotics for infection as prescribed

202
Q

Treatment for Respiratory Acidosis

A

TCDB (turn cough deep breathing) every 2 hours

IS - incentive spirometer use

chest PT

suctioning

semi fowlers or orthopneic position

encourage fluids (unless contraindicated)

supplemental O2 to treat hypoxemia

Monitor VS, ABGs, Serum K+

use bronchodilators

give antibiotics for pneumonia

administer sedatives with caution

be prepared for intubation and mechanical ventilation

203
Q

Why do we need to be careful giving supplemental O2 to treat hypoxemia in respiratory acidosis for COPD patients?

A

it may cause a loss of hypoxemic stimulus to breath

204
Q

Definition of Respiratory Acidosis

A

Carbonic Acid (H2CO3) excess

205
Q

Cause of Respiratory Acidosis

A

Altered alveolar ventilation leading to retention of CO2

206
Q

Compensation for Respitaory Acidosis

A

Occurs in the kidneys

Renal retention of HCO3- occurs slowly

acidic urine is excreted

207
Q

If Metabolic Acid-Base issues are like an elevator, what are Respiratory Acid-Base issues like?

A

A see saw/ teeter totter

because values move in opposite directions rather than together

208
Q

What is the respiratory and metabolic markers for Respiratory acid base disturbances and what is the marker we are most concerned with?

A

Resp - PaCO2

Metabolic - HCO3-

We are most concerned with the PaCO2 since it is what is causing this issue (and the lungs)

209
Q

pH, PaCO2, and HCO3- values in uncompensated Respiratory Acidosis

A

pH &laquo_space;7.35 (very low)

PaCO2 > 45 (very high)

HCO3- normal range (22-26)

210
Q

pH, PaCO2 and HCO3- values in partially compensated Respiratory Acidosis

A

pH < 7.35 (still low but slight increase/H+ decreases to make it more basic)

PaCO2 - no change (slightly lower but not much)

HCO3- >26 (increased)

211
Q

pH, PaCO2, and HCO3- values in compensated Respiratory Acidosis?

A

pH = low normal (7.35 ish)

PaCO2 - not much change (slight decrease)

HCO3-&raquo_space; 26 (much higher)

212
Q

Respiratory Alkalosis

A

deficit of carbonic acid (H2CO3) and a decrease in H+ concentration

results from the accumulation of base or from loss of acid without a comparable loss of base in body fluids

213
Q

What are the pH and CO2 levels like in Respiratory Alkalosis

A

pH&raquo_space; 7.45

CO2 <35

214
Q

Causes for Respiratory Alkalosis Occurring

A

Conditions that cause over stimulation of the respiratory system:

Hyperventilation
Hysteria
Overventilation by Mechanical Ventilators

Conditions that increase metabolism such as

Fever
Pain or Brain Trauma
Salicylates
Hypoxia

215
Q

What happens calcium levels in Respiratory Alkalosis?

A

they drop (hypocalcemia) since calcium binds to plasma proteins to release H+

This leads to neuromuscular excitability and cardiac issues

216
Q

How does Hyperventilation cause Respiratory Alkalosis

A

rapid respiration causes blowing off of CO2 –> leads to a decrease in carbonic acids

217
Q

How does Hysteria cause Resp Alkalosis

A

often neurogenic in nature and related to psychoneurosis, but this conditions causes hyperventilation and excessive exhaling of CO2

218
Q

How does Over-Ventilation by mechanical ventilators cause Resp Alkalosis

A

administration of O2 and the depletion of CO2 can end up occurring and the patient may be hyperventilated by the mechanical ventilator

219
Q

What do we commonly do in regard to acid-base balance if a patient has cranial swelling?

A

We want to vasoconstrict to prevent too increased ICP so we might keep them slightly alkalotic on a ventilator to cause vasodilation

220
Q

What stimulates change in blood vessel tone?

A

pH O2 and CO2 levels

221
Q

What levels will cause vasoconstriction?

A

high pH, high O2, low CO2

222
Q

What levels will cause vasodilation?

A

low pH, low O2, high CO2

223
Q

How does Pain or Brain Trauma cause Resp Alkalosis

A

overstimulation of the resp center in the brain stem with a resultant carbonic acid deficit due to the changes

224
Q

How do Salicylates cause Resp Alkalosis?

A

They stimulate the respiratory center causing hyperventilation initially

225
Q

What is unique about acid base changes and Salicylates/Aspiring?

A

It will cause initial Resp Alkalosis by stimulating the respiratory center in the brain to lead to hyper ventilation

Later on though it will cause Metabolic Acidosis as more acids are absorbed and then the lungs need to try and compensate

226
Q

How does hypoxia cause resp Alkalosis?

A

causes resp stimulation with resultant carbonic acid deficit

227
Q

Main Etiologies of Resp Alkalosis

A

Excessive Ventilation
Excessive Mechanical Ventilation
Pregnancy
Hyperventilation during Labor and Delivery

228
Q

Examples of Excessive Ventilation leading to Resp Alkalosis?

A

Extreme Anxiety (most common)

Hypoxemia

Stimulation of Resp Center d/t high fever, early salicylate poisoning, encephalitis, CNS lesions affecting resp center, increased blood ammonia

229
Q

Why may excessive mechanical ventilation be deliberate?

A

to cause vasoconstriction to prevent cerebral edema

230
Q

Why does pregnancy and labor and delivery sometimes cause respiratory alkalosis

A

Pregnant women are more sensitive to CO2 and are stimulated to breath more

L&D causes hyperventilation potentially when pushing

231
Q

What is seen on Assessment of Resp Alkalosis

A

Initially hyperventilation and resp stimulation will cause abnormal rapid respiation (Tachypnea), in an attempt to compensate, resp rate and depth will then go down!

headache

Mental status changes

vertigo

lightheadedness

paresthesias as tingling of the fingers and toes

Hypokalemia

Hypocalcemia (lowers threshold)

tetany

convulsions

232
Q

Manifestations of Resp Alkalosis?

A

Cerebral Vasoconstriction from pH and O2 increases and CO2 decreases

Neuromuscular Irritability

Cardiovascular Dysrhythmias

Hyperventilation (high RR and depth)

Dry mouth

GI function problems like pain

233
Q

Cerebral Vasoconstriction manifestations for Respiratory Alkalosis?

A

lightheadedness, syncope

inability to concentrate

blurred vision, vertigo

loss of consciousness

234
Q

Neuromuscular Irritability manifestations for Respiratory Alkalosis

A

paresthesias

tinnitus

carpopedal spasms (Trousseaus sign)

Spasms (chvostek))

tetany and twitching

hyperactive DTR

seizure, convulsion, coma

235
Q

Interventions for Respiratory Alkalosis

A

Emotional support and reassurance

Maintain patent airway

encourage appropriate breathing patterns

assist with breathing techniques and apply breathing aids as prescribed

voluntary holding of breath

rebreathe exhaled CO2

rebreathing mask as prescribed

CO2 breaths as perscribed

provide cautious care with ventilator clients so that the client is not forced to take breaths too deeply or rapidly

monitor lyte values

administer meds as ordered

prepare to administer calcium gluconate for tetany as prescribed

236
Q

Calcium Gluconate for tetany treats the underlying issue of ___

A

hypocalcemia

237
Q

Treatments for Respiratory Alkalosis

A

Monitor VV especially RR and Depth

Encourage slow breathing and less deep breathing

Breathe into paper bag

use rebreather mask

administer sedatives (FOR ANXIETY NOT RESP DEPRESSION)

correct underlying cause (pain, anxiety)

monitor ABGs

adjust mechanical ventilator settings

monitor serum K+ levels

provide emotional support

238
Q

Definition of Respiratory Alkalosis

A

Carbonic Acid (H2CO3) deficit

239
Q

Cause of Respiratory Alkalosis

A

Hyperventilation leading to excessive elimination of CO2

240
Q

Compensation for Respiratory Alkalosis

A

Renal Excretion of HCO3-

241
Q

What does pH, PaCO2, and HCO3- looks like in uncompensated Resp Alkalosis

A

pH&raquo_space; 7.45 (high, up)

PaCO2 <35 (low, down)

HCO3- Normal

242
Q

What does pH, PaCO2, and HCO3- looks like in partially compensated Resp Alkalosis

A

pH >7.45 (still up)

PaCO2 No change (it is the problem)

HCO3- <22 (lower now, down)

243
Q

What does pH, PaCO2, and HCO3- looks like in compensated Resp Alkalosis

A

pH High Normal (7.45) (this is now corrected)

PaCO2 - no change - may be slightly higher but not by much since its not the compensator

HCO3- «22 (very low, down to correct pH)

244
Q

What to do before obtaining an Arterial Blood Gas Specimen?

A

Obtain VS

Determine if there is an Arterial Line

Performed Allen’s Test

Assess factors that may impact accuracy

Assist with specimen draw by having a heparinized syringe

Provide emotional support

Apply pressure

Label specimen and transport on ice to Lab

Record clients Temp, and type of supplemental O2 that client is receiving on lab form

245
Q

What does an Allen Test do?

A

it determines the presence of collateral circulation

246
Q

What must be done to take an ABG Specimen after a suctioning or client activities?

A

Wait 20 minutes

247
Q

How long must you put pressure on an ABG site after getting a specimen?

A

apply pressure for 5 to 10 minutes (since anticoagulants)

248
Q

How to do an Allen’s Test

A
  1. Ask client to make a tight fist
  2. Occlude ulnar and radial arteries
  3. tell them to open their hands with occlusion still occurring
  4. let go of one artery and check for color return
  5. Do it again for the other side
249
Q

Normal H+ concentration

A

7.35-7.45

250
Q

pH range that leads to acidosis

A

<7.35

251
Q

pH range that leads to Alkalosis

A

> 7.45

252
Q

pH ranges that are deadly?

A

<6.8 or >7.8

253
Q

Normal PaCO2 level (partial pressure of CO2 in arterial blood)

A

35-45 mmHg

254
Q

A PaCO2 <35 indicates what

A

hypocapnia/hypocarbia and Respiratory Alkalosis

255
Q

A PaCO2 >45 indicates what

A

Hypercapnia/Hypercarbia and Respiratory Acidosis

256
Q

What is the normal PaO2 (partial pressure of O2 in arterial blood)

A

80-100 mmHg

257
Q

What does PaO2s of <80, <60, and <40 indicate?

A

<80 - mild hypoxemia

<60 - moderate hypoxemia

<40 - severe hypoxemia

258
Q

What is the normal HCO3- Concentration

A

22-26 mEq/L

259
Q

% Hgb molecules saturated with O2 in a normal healthy person is..

A

> 95%

260
Q

HCO3- concentration <22 indicates?

A

Metabolic Acidosis

261
Q

HCO3- concentration >26 indicates?

A

Metabolic Alkalosis

262
Q

What are the 3 important indicators on an ABG to look at

A

pH, PCO2, and HCO3- concentration

263
Q

Why is PaO2 not a good thing to know, but a non-used indicator for acid base imbalance on an ABG?

A

You can have normal PaCO2 and be hypoxemic or have normal O2 with Hypercarbia

The levels depend on what is wrong with the person. Such as a COPD patient can get O2 in (normal) but cannot get CO2 out (Hypercarbia)

So the level changes do not necessarily mean much for acid base

264
Q

Major Forms of Acid Base Imbalances

A

Primary Imbalance

Compensated Imbalances

Combined or Mixed Imbalances

265
Q

Primary imbalance

A

Primary cause of the problem

originates from an acute condition

either respiratory or metabolic in origin

266
Q

Compensated Imbalances

A

Respiratory imbalances compensated by the renal system

Metabolic imbalances compensated by the respiratory system

267
Q

Combined or Mixed Imbalances

A

involve both respiratory and metabolic imbalances at the same time (both acidosis, both alkalosis, or one acidosis and one alkalosis)

ex: Salicylate Poisoning causes initial Respiratory Alkalosis followed by Metabolic Acidosis

268
Q

Steps for Analyzing ABG Results

A
  1. Look at blood gas report
  2. look at pH, is it up or down? if up then its alkalosis, if down then its acidosis
  3. Look at PCO2, is it up or down? If it is an opposite response/direction to pH then it is d/t a respiratory imbalances. if not reflecting opposite response as pH then move to next step
  4. Look at HCO3-, does it reflect a corresponding/same direction response with the pH? If so, then condition is metabolic imbalance
  5. Keep in mind compensation has occurred if pH in 7.35 to 7.45 range (low and high ends), and if the pH is not in normal limits it is important to look at the resp or metab function indicators to determine if partially compensated (pH starting to go in normal direction) or uncompensated
269
Q

In Respiratory Acidosis, pH is ___ and PCO2 is ___

A

pH down, PCO2 up

270
Q

In Respiratory Alkalosis, pH is __ and PCO2 is ___

A

pH is up and PCO2 is down

271
Q

In Metabolic Acidosis, pH is ___ and HCO3 is ___

A

pH is down and HCO3 is down

272
Q

In Metabolic Alkalosis, pH is ___ and HCO3 is ___

A

pH is up and HCO3 is up

273
Q

When compensation has occurred for Respiratory Acidosis and Alkalosis, what occurs to the ABG levels

A

compensation -pH is in normal limits

partial compensation if HCO3 is abnormal

Uncompensated if HCO3 is normal

274
Q

When compensation has occurred for Metabolic Acidosis and Alkalosis, what occurs to the ABG levels

A

Compensation - pH in normal limits

Partial - PCO2 is abnormal

Uncompensated - PCO2 is normal

275
Q

In acidosis, pH is ___

A

down

276
Q

In alkalosis, pH is __

A

UP

277
Q

The respiratory function indicator is the ___

A

PCO2

278
Q

The metabolic function indicator is the ___

A

HCO3

279
Q

What sort of thing could cause a Mixed Imbalance of Metabolic and Respiratory Acidosis

A

Cardiopulmonary Arrest

  • the hypoxemia –> lactic acidosis and CO2 retention
280
Q

What sort of thing could cause a Mixed Imbalance of Metabolic and Respiratory Alkalosis

A

Vomiting during pregnancy

  • out of breath/hyperventilate + losing acids
281
Q

What sort of thing could cause a Mixed Imbalance of metabolic acidosis and respiratory alkalosis?

A

Salicylate/ASA poisoning

  • first Aspirin stimulates resp centers to cause respiratory alkalosis
  • second the metabolism of the aspirin causes acids leading to metabolic acidosis (which increases breathing yet again)

N361: Pathophysiology II (20 decks)

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