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Principles of Anesthesia 1 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What does hydrogen ion concentration give us?

A

pH

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2
Q

What do we know if the H+ ion concentration exceeds hydroxyl ions?

A

Solution is acidic

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3
Q

What do we know if the H+ ion concentration is less than the hydroxyl ions?

A

Solution is aklalotic

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4
Q

Which substances dissociate or dissolve into their component parts in water?

A

Those with polar bonds

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5
Q

What determines whether a substance is a strong acid or strong base?

A

The degree of dissociation in water

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6
Q

What is the Law of Mass Action?

A

Rate of chemical reaction is proportional to product of masses of the reacting substances

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7
Q

Which three rules must be followed for acid and base balance?

A
  1. Electrical neutrality
  2. Dissociation equilibrium which follow the law of mass action
  3. Mass conservation
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8
Q

What are pH alterations due to that lead to metabolic acidosis or alkalosis?

A

Abnormal bicarbonate reabsorption and hydrogen ion elimination by the kidneys

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9
Q

What are pH alterations due to that lead to respiratory acidosis or alkalosis?

A

Altered respiratory drive and CO2 levels

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10
Q

Do respiratory and metabolic disorders occur independently?

A

Rarely, you can have mixed or complex acid-base disorders

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11
Q

What is the degree of water dissociation and hydrogen ion concentration affected by in the modern approach to acid-base balance?

A

Strong ions, weak acids and carbon dioxide

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12
Q

Which approach to acid-base disorders is explained by the effect of PCO2, SID, Atot?

A

Stewart Approach

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13
Q

How do you calculate the SID?

A

(Na+ + K+ + Ca2+ + Mg2+) - (Cl- + lactate-)

strong cations - strong anions

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14
Q

Changes in SID will cause changes in what two concentrations?

A

Hydrogen ion and hydroxyl ion concentrations

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15
Q

Which ions dissociate completely leading to a direct affect on acid-base balance?

A

Na+ and Cl-

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16
Q

What does increased SID indicate?

A

alkalosis and presence of unmeasured cations

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17
Q

What does decreased SID indicate?

A

acidosis and presence of unmeasured anions

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18
Q

Describe SID in ECF

A

It is positive and 40-44 mEq/L

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19
Q

What is the degree of dissociation determined by for weak acids?

A

Temperature and pH

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20
Q

Give an example of two weak acids

A

albumin and phosphate

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21
Q

What does an increase in weak acid concentration indicate?

A

acidosis

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22
Q

What does a decrease in weak acid concentration indicate?

A

alkalosis

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23
Q

Describe SID and total weak acids in relation to the presence of acid base disorders

A

They are independent variables and are inversely related in the presence of acid base disorders

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24
Q

What does the Boston approach use for ABG analysis?

A

acid-base maps and the relationship between CO2 and bicarb

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25
Q

5 questions we ask when analyzing ABGs?

A
  1. What is the suspected or actual cause?
  2. Does my physical assessment support these findings?
  3. How do I treat the disorder?
  4. Do I treat the disorder?
  5. Did I cause it preoperatively?
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26
Q

What is the first thing we should ask when looking at any acid-base disorder?

A

Is the patient hypoxic

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27
Q

What lab value change do we see in respiratory alkalosis?

A

decreased PCO2 and increased pH

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28
Q

What do we see in the Stewart approach with respiratory alkalosis?

A

decreased PaCO2

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29
Q

Primary cause of respiratory alkalosis?

A

Increased minute ventilation/mechanical hyperventilation

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30
Q

Symptoms of respiratory alkalosis? (5)

A
  1. Vasoconstriction
  2. Lightheadedness
  3. Visual disturbances
  4. Dizziness
  5. Possible hypocalcemia
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31
Q

Other causes of respiratory alkalosis? (6)

A
  1. Abnormal respiratory drive from stimulants or toxins such as anxiety or pain
  2. CNS abnormalities
  3. Pulmonary insult/injury such as PE
  4. Liver failure
  5. Sepsis
  6. Pregnancy
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32
Q

What do we expect to see in the HCO3- with acute compensation of respiratory alkalosis?

A

HCO3- will decrease 2 mEq/L for every 10 mmHg decrease in PCO2 down to a 20 mmHg decrease

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33
Q

What do we expect to see in the HCO3- with chronic compensation of respiratory alkalosis?

A

HCO3 will decrease 5 mEq/L for every 10mmHg decrease in PCO2 down to a 20 mmHg decrease

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34
Q

Treatment for respiratory alkalosis?

A

decrease minute ventilation/ventilator change, treat cause

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35
Q

What lab value change do we see in respiratory acidosis?

A

Increased PaCO2 and decreased pH

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36
Q

Primary cause of respiratory acidosis?

A

Failure of the lungs to eliminate CO2/hypoventilation

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37
Q

Symptoms of respiratory acidosis? (3)

A
  1. Vasodilation
  2. Narcosis
  3. Cyanosis
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38
Q

Other causes of respiratory acidosis? (5)

A
  1. Drug associated respiratory depression
  2. Neurologic injury
  3. Lung injury/disease
  4. Neuromuscular and musculoskeletal disease
  5. Inadequate NMBD reversal
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39
Q

What change in HCO3 would we expect to see in acute compensation of respiratory acidosis?

A

HCO3 will increase 1 mEq/L for every 10 mmHg increase in PCO2 > 40mmHg

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40
Q

What change in HCO3 would we expect to see in chronic compensation of respiratory acidosis?

A

HCO3 will increase by 4 mEq/L for every 10 mmHg increase in PCO2 > 40 mmHg

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41
Q

Treatment for respiratory acidosis?

A

increase minute ventilation/ventilator changes, treat cause

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42
Q

Which acid-base disorder do you anticipate in a patient who has poor mechanical ventilation, narcosis and/or incomplete reversal of neuromuscular blockade?

A

respiratory acidosis

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43
Q

What lab value changes would we expect to see in metabolic alkalosis?

A

increase in bicarb and increased pH

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44
Q

What would the Stewart approach show in metabolic alkalosis?

A

Increased SID, increased concentration of cations vs anions

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45
Q

What does metabolic alkalosis result from?

A

net loss of hydrogen ions and or addition of bicarb

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46
Q

What is the most common cause of metabolic alkalosis?

A

GI acid loss from vomiting or NG suctions causing chloride loss

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47
Q

Symptoms of metabolic alkalosis? (4)

A
  1. Widespread vasoconstriction
  2. lightheadedness
  3. Tetany
  4. Paresthesia
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48
Q

Other causes of metabolic alkalosis? (4)

A
  1. Diuretics
  2. Third spacing
  3. Bleeding
  4. Hypokalemia
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49
Q

Expected PCO2 compensation in metabolic alkalosis?

A

0.7 x HCO3 + 20

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50
Q

Treatment for metabolic alkalosis?

A

Hypoventilation, fluid replacement, treat cause

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51
Q

What lab value changes would we expect to see in metabolic acidosis?

A

Decreased bicarb and decreased pH

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52
Q

Symptoms of metabolic acidosis? (5)

A
  1. Vasodilation
  2. Hypotension
  3. Diminished muscular performance esp heart
  4. Arrhythmias
  5. Can lead to shock
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53
Q

How does the oxyhemoglobin dissociation curve shift in metabolic acidosis and what does it cause?

A

To the right causing increase oxygen delivery to tissues

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54
Q

Causes of metabolic acidosis? (9)

A
  1. Renal injury/failure
  2. DKA
  3. Sepsis
  4. Drugs/toxins
  5. Lactic acidosis
  6. GI losses with a normal AG
  7. Diarrhea
  8. Carbonic anhydrase inhibitor use
  9. Renal tubular acidosis
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55
Q

What is the expected PCO2 in acute compensation of metabolic acidosis?

A

Winter’s Formula is (1.5 X HCO3) + 8 +/- 2

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56
Q

What does the anion gap represent?

A

The total serum concentration of unmeasured anions and is the difference between measured cations minute measured anions, this is used to investigate metabolic acidosis

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57
Q

Conventional AG calculation?

A

(Na+ + K+) - (HCO3- + Cl-) = 14-18 mEq/L

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58
Q

Modern AG calculation?

A

(Na+ + K+) - (HCO3- + Cl- + lactate) = 14-18 mEq/L

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59
Q

What does an abnormal or increased AG indicate?

A

Metabolic acidosis is caused by unmeasured anions

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60
Q

What does a normal AG indicate?

A

Metabolic acidosis is caused by lactate build up or hyperchloremia such as excess normal saline use preoperatively

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61
Q

What issue do critically ill patients usually have in the presence of metabolic acidosis and a normal AG?

A

Hypoalbuminemia

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62
Q

Which have a far greater impact on the anion gap and why?

A

UMA because they are found in higher concentrations

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63
Q

What is the delta anion gap or delta ratio equation?

A

(Measured AG - Normal AG) / (Normal HCO3 - Measured HCO3)

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64
Q

What does the delta ratio dictate?

A

If the AG is normal, HCO3 decreases and the ratio will be less than 0.4 or low, supporting hyperchloremic metabolic acidosis; if the ratio is between 1 and 2 the acidosis is likely from UMAS and anticipate an abnormal AG

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65
Q

When might the Boston approach to ABG analysis be deficient?

A

Metabolic disorders

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66
Q

Which two approaches to ABG analysis are often combined to incorporate the sum of the difference in charge of the common ECF ions?

A

AG and Boston

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67
Q

What is a normal base excess?

A

-2 to +2

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68
Q

What does full compensation of acid-base imbalance yield?

A

normal pH

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69
Q

Expected HCO3 in acute respiratory acidosis?

A

24 + [(PaCO2 - 40)/10]

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70
Q

Expected HCO3 in chronic respiratory acidosis?

A

24 + 4[(PaCO2 - 40)/10]

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71
Q

Expected HCO3 in acute respiratory alkalosis?

A

24 - 2[(40 - PaCO2)/10]

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72
Q

Expected HCO3 in chronic respiratory alkalosis?

A

24 - 5[(40 - PaCO2)/10] range +/- 2

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73
Q

What is lactic acidosis a product of?

A

Production of lactate > the liver’s ability to clear it and is a product of glucose metabolism

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74
Q

What levels of lactate are significant? Severe?

A

> 2mEq/L is significant, > 5 mEq/L with metabolic acidosis is severe

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75
Q

What is Type A lactic acidosis?

A

Seen in hypovolemic or hemorrhagic shock with inadequate oxygen delivery

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76
Q

What is Type B lactic acidosis?

A

Occurs despite normal oxygen delivery

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77
Q

Causes of metabolic acidosis from wide AG (unmeasured anions) (4)

A
  1. Hypoperfusion
  2. Lactic acidosis
  3. DKA
  4. Renal failure
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78
Q

Causes of metabolic acidosis from measured anions (4)

A
  1. Hyperchloremia
  2. Normal saline and saline containing fluids
  3. Renal tubular acidosis
  4. Bladder reconstructions
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79
Q

Causes of metabolic acidosis from free water excess such as hyponatremia and dilation acidosis? (6)

A
  1. Hypotonic fluid administration
  2. Sodium loss
  3. Diarrhea
  4. Hyperosmolar fluids such as mannitol and alcohol
  5. Hyperproteinemia
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80
Q

Causes of metabolic alkalosis?

A
  1. Hyperventilation of patient with hx of CO2 retention such as COPD
  2. Sodium gain from things such as sodium bicarb and massive transfusions
  3. Chloride loss such as in NGT suctioning
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81
Q

Does sodium bicarb improve long term outcomes?

A

It has not been shown to

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82
Q

What would be an example of a metabolic disorder that we may intentionally cause?

A

Acidosis caused by permissive hypercapnia to prevent ventilator related lung injury because treatment may cause reverse effects

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83
Q

What is the A-aDO2 equation?

A

FIO2 (760-47) - PaCO2/0.8

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84
Q

What does A-aDO2 approximate?

A

Partial pressure of oxygen in the alveoli

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85
Q

What does A-aDO2 allow for the calculation of?

A

Alveolar-arterial gradient of oxygen and the amount of respiratory/cardiac shunt

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86
Q

What is a normal A-aDO2?

A

5-10mmHg, although age or chronic lung disease may cause an increase

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87
Q

What is the required cardiovascular monitoring and frequency?

A

BP and HR monitoring every 5 minutes

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88
Q

When is thermoregulation monitoring required?

A

When clinically significant changes in body temp are anticipated or suspected or for SCIP protocol

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89
Q

What must be done if we omit a standard of care?

A

Reason for omission must be charted

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90
Q

What does the beer-lambert equation describe?

A

The law of absorption

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91
Q

What is the law of absorption in relation to pulse oximetry?

A

If a known intensity of light illuminates a chamber of known dimensions then the concentration of a dissolved substance can be determined

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92
Q

What must light absorption be measured at?

A

Wavelengths equal to the number of solutes

More solutes such as oxygen = more absorption

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93
Q

4 variations of hemoglobin?

A
  1. Oxyhemoglobin (HbO2)
  2. Deoxyhemoglobin
  3. Methemoglobin (metHb)
  4. Carboxyhemoglobin (COHb)
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94
Q

What is the gold standard number of wavelength for pulse-oximetry?

A

4 wavelengths

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95
Q

What does more wavelengths give us in pulse-oximetry?

A

Greater assurance of looking at HbO2 and Deoxyhemoglobin

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96
Q

What are the 5 layers that light is transmitted through for pulse-oximetry?

A
  1. Skin
  2. Soft tissue
  3. Venous blood
  4. Arterial blood
  5. Capillary blood
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97
Q

What type of movement increases length of the light path and increases absorbency?

A

Pulsatile expansion of the artery

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98
Q

How was the problem of ambient light solved for pulse-oximetry?

A

alternating red/infared light

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99
Q

How do we solve low perfusion issues with pulse-oximetry readings?

A

signal amplified, but the artifact is also amplified

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100
Q

Describe venous blood pulsations

A

longer signal averaging time, slower to report changes

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101
Q

What is an intervention we utilize that can also absorb light from a pulse-ox?

A

Intravenous dyes

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102
Q

What is the definition of SaO2?

A

Ratio of oxyhemoglobin to all hemoglobin

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103
Q

What are fingers relatively sensitive to?

A

vasoconstriction

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104
Q

Where is the detection of desaturation and resaturation slower on a pulse-ox?

A

Peripherally

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105
Q

Which finger do we avoid placing the pulse-ox?

A

index finger

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106
Q

What is a more reliable place for a pulse-ox with epidural blocks?

A

Toes due to vasodilation

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107
Q

What are three other areas for pulse-ox placement that are less affected by vasoconstriction and reflect desaturation quicker?

A

tongue, cheek, forehead

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108
Q

How accurate is a pulse-ox?

A

+/- 2% when measured against ABGs if sat is >70%

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109
Q

Do anesthetic vapors affect pulse-ox?

A

no

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110
Q

What type of pressures do pulse-oximeters have difficulty detecting?

A

high partial pressures

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111
Q

At what wavelength range does carboxyhemoglobin absorb as much light as oxyhemoglobin?

A

660 nm

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112
Q

What is the effect of carboxyhemoglobin on SpO2?

A

Falsely elevates SpO2; for every 1% increase COHb will increase SpO2 by 1%

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113
Q

What is the COHb of many smokers?

A

> 6%

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114
Q

Who invented the sphygmomanometer?

A

Samuel von Basch

115
Q

What are korotkoff sounds produced by?

A

turbulent flow beyond the partially occluding cuff

116
Q

Phase 1 korotkoff sound?

A

The most turbulent/audible (SBP)

117
Q

Phase 2-3 korotkoff sound?

A

Sound character changes, turbulent flow decreases

118
Q

Phase 4-5 korotkoff sound?

A

muffled/absent sounds (DBP)

119
Q

4 limitations to auscultation of blood pressure?

A
  1. Decreased peripheral flow
  2. Changes in vessel compliance
  3. Shivering
  4. Incorrect cuff size
120
Q

What is the maximum cuff pressure for adults? neonates?

A

300 mmHg for adults; 150 mmHg for neonates

121
Q

Cuff bladder standards for BP monitoring?

A

40% of arm circumference

80% of length of upper arm

122
Q

4 Descriptors of automatic non-invasive techniques for BP?

A
  1. Maximal amplitude is MAP
  2. SBP and DBP calculated from algorithm
  3. SBP usually 25-50% of MAP amplitude
  4. DBP is least accurate
123
Q

When is automatic non-invasive techniques for BP measurement rough equal to arterial pressure?

A

when MAP is 75 mmHg or lower

124
Q

Standards of non-invasive BP monitoring?

A

+/- 5 mmHg, can be larger depending on the circumstances

125
Q

Non-invasive BP measuring of MAP during hypertension?

A

underestimation

126
Q

Non-invasive BP measuring of MAP during hypotension

A

overestimation

127
Q

What is the more reliable way to determine blood pressures from non-invasive monitoring?

128
Q

Clinical limitations of non-invasive BP monitoring?

A

extremes of heart rate and pressure

129
Q

4 trauma factors related to frequent cycling of non-invasive blood pressure?

A
  1. Coagulopathies
  2. Peripheral neuropathies
  3. Arterial/venous insufficiency
  4. Compartment syndrome
130
Q

What is the most common monitoring site for arterial blood pressure?

A

Radial, it is easy to access and complications are uncommon

131
Q

4 steps to the Allens’ test?

A
  1. Examiner compresses radial and ulnar artereis
  2. Patient makes a tight fist which exsanguinates the palm
  3. Patient opens hand
  4. Examiner releases ulnar artery and color to the palm should return in less than 10 seconds
132
Q

What is the diagnostic accuracy of the Allens’ Test?

133
Q

What is unique about the transfixion technique of arterial line placement?

A

Front and back walls are punctured intentionally and the catheter is withdrawn until pulsatile blood flow appears

134
Q

Is the transfixion technique of arterial line placement associated with more frequent complications?

135
Q

5 other common sites of arterial blood pressure monitoring?

A
  1. Brachial: not the best collateral flow
  2. Posterial tibial
  3. Axillary
  4. Dorsalis pedis: smaller and more difficult
  5. Femoral: higher complication rate
136
Q

Describe the automatic flush function of A-lines

A
  1. 1-3 mL/hr to prevent thrombus formation
  2. lack of dextrose
  3. lack of heparin
137
Q

Where do we typically level an A-line?

A

Midchest/midaxillary line to look at the aortic root

138
Q

How is the waveform maximized with A-lines?

A

limit stopcocks, limit tubing length, and non-distensible tubing

139
Q

What is distal pulse amplification due to?

A

Due to impedance changes along vascular tree

140
Q

What are the changes in A-line as pressure wave moves to periphery?

A
  1. Arterial upstroke steeper
  2. Systolic peak higher
  3. Dicrotic notch later because longer for wave to transmit
  4. End-diastolic pressure lower
141
Q

What is the summation of sine waves?

A

fundamental wave + harmonic wave = typical pressure wave (fourier analysis)

142
Q

What does the square wave test occur from?

A

From compressing fast flush, rapid rise in pressure and waiting for it to respond

143
Q

What should we see post square wave form test?

A

1-2 rebound oscillations at bottom of square

144
Q

What does the damping capability of A-line systems do?

A
  1. Decreases system resonance

2. Prevents exaggerated waveforms

145
Q

What do we see with an underdamped A-line?

A

Systolic pressure elevated, more exaggerated movement and steeper systolic upstroke

146
Q

What issues could we have with an underdamped A-line?

A

tubing too long, wrong tubing

147
Q

What issues could we have with an overdamped A-line?

A

air bubble, tubing too long, pressure bag empty

148
Q

What do we see with overdamped A-lines?

A
  1. Systolic pressure decreased
  2. Decreased pulse pressure
  3. Loss of detail
149
Q

7 pathology that can cause A-line waveform changes?

A
  1. Age: loss of distensibility
  2. Atherosclerosis
  3. Embolism
  4. Arterial dissection
  5. Shock
  6. Hypothermia
  7. Vasopressor infusions
150
Q

When compared with central aortic pressure, peripheral arterial waveforms have a _____ pulse pressure?

A

Wider pulse pressure because higher SBP and lower DBP in periphery

151
Q

What initially occurs as a result of increased lung volume from the ventilator delivering a breath? (5)

A
  1. Compression of lung tissue
  2. Increased LV preload
  3. Increases intrathoracic pressure
  4. Decreases afterload
  5. Increased LV stroke volume
152
Q

What occurs as intrathoracic pressure continues to increase as the ventilator delivers a breath?

A
  1. Reduction in venous return and right heart preload
  2. Increased PVR causes increased R heart afterload
  3. R heart stroke volume drops
  4. Left heart preload falls
  5. Arterial BP declines
153
Q

What is systolic pressure variation (SPV)?

A

Increase or decrease in systolic pressure in relation to end-expiratory presssure

154
Q

What is normal SPV in ventilated patients?

155
Q

With SPV what is the normal increase?

156
Q

With SPV what is the normal decrease?

157
Q

What does increased SPV indicate?

A

early hypovolemia

158
Q

What is the pulse pressure variation (PPV)?

A

Utilizes maximum and minimum pulse pressures over entire respiratory cycle

159
Q

What is a normal PPV?

160
Q

How do you calculate PPV?

A

[(PPmax-PPmin)/(PPmax+PPmin)]/2

161
Q

What does an increase in PPV indicate?

A

Patient could benefit from fluids

162
Q

What is stroke volume variation (SVV)?

A

Computer analysis of arterial pulse pressure waveform to correlate resistance and compliance based on age and gender to calculate SV

163
Q

What is the equation for SVV?

A

SV max - SV min / SV mean

164
Q

What is a normal SVV?

165
Q

What is required to calculate SVV?

A

ventilated patient with stable RR and Vt 8cc/kg

166
Q

When is SVV not accurate?

A

Severe tachycardia and dysrhythmias

167
Q

2 descriptors of non-diverting sampling?

A
  1. Gas is not removed from the circuit

2. Also called main-stream

168
Q

2 descriptors of diverting sampling?

A
  1. Gas IS removed from the circuit for analysis elsewhere

2. Also called side-stream

169
Q

4 challenges of mainstream sampling?

A
  1. Water vapor
  2. Secretions
  3. Blood
  4. More interfaces for disconnections
170
Q

4 challenges of sidestream sampling?

A
  1. Kinking of sampling tube
  2. Water vapor
  3. Failure of sampling pump
  4. Leaks in the line
171
Q

What is Dalton’s Law?

A

The total pressure exerted by a mixture of gases is equal to the sum of the partial pressure of each gas

172
Q

What is mass spectrometry?

A

Concentration determined according to mass

173
Q

How many gases can mass spectrometry calculate?

A

Up to eight different gases

174
Q

What can mass spectrometry calculate?

A

Partial pressure from measured proportion (%)

175
Q

What is the total partial pressure from ventilated patients?

176
Q

What is normal ETCO2?

A

35.65 mmHg

177
Q

What does infared analysis calculate?

A

The number of molecules based on absorption of IR radiation (partial pressures)

178
Q

What does more molecules mean with infrared analysis?

A

more IR radiation is absorbed and the more motion from IR (or partial pressure)

179
Q

How must gas monitoring be calibrated?

A

For high and low concentrations

180
Q

What does gas monitoring sampling inside the inspiratory limb give us? (2)

A
  1. Ensures oxygen delivery

2. Analyzes hypoxic mixtures

181
Q

What does gas monitoring sampling on the expiratory side give us? (2)

A
  1. Ensures complete pre-oxygenation “denitrogenation”

2. ET O2 above 90% is adequate

182
Q

Is there oxygen monitoring at auxiliary sites?

183
Q

3 reasons for the low alarm with gas monitors

A
  1. Pipeline crossover
  2. Incorrectly filled tanks
  3. Failure of a proportioning system
184
Q

2 reasons for high alarms with gas monitors

A
  1. Premature infants

2. Chemotherapeutics drugs such as bleomycin

185
Q

What does airway pressure monitoring assess?

A

Patients mechanical and or spontaneous ventilation

186
Q

What does airway pressure monitoring determine?

A

Presence of PEEP

187
Q

3 descriptors of mechanical airway pressure gauges?

A
  1. No recording data so no trends
  2. No alarm system
  3. Must be continually scanned
188
Q

2 descriptors of electronic pressure gauges?

A
  1. Built within ventilator or anesthesia machines

2. Alarm system is integrated

189
Q

When are low peak inspiratory pressure alarms on?

A

When the ventilator is on

190
Q

When does a low peak inspiratory pressure alarm go off?

A

When pressure does not exceed a preset minimum

191
Q

Causes of low peak inspiratory pressure alarms? (5)

A
  1. Disconnects
  2. Apnea
  3. Vent failure
  4. Leaks in system
  5. OGT in lung on suction
192
Q

What do you want to do if you see a low peak inspiratory pressure alarm?

A

Start at one end of circuit and trace it to another, the most common causes is for something to get disconnected

193
Q

When is a high pressure alarm non-functional?

A

Pressure controlled ventilation

194
Q

What is a high pressure alarm usually fixed at?

A

50-80 cmH20

195
Q

3 causes of high pressure alarms?

A
  1. Obstructions
  2. Reduced compliance
  3. Coughing/straining
196
Q

Describe sustained elevated pressure alarms

A

Pressure that remains elevated during respiratory cycle

197
Q

3 causes of sustained elevated pressure alarms?

A
  1. Improperly adjusted APL valve
  2. Activation of oxygen flush system
  3. Malfunctioning PEEP
198
Q

What type of pattern does the reaction of a single muscle fiber to a stimulus follow?

A

all-or-none pattern

199
Q

What does the repose of the whole muscle depend on?

A

How many muscle fibers are activated

200
Q

4 most common patterns of nerve stimulation?

A
  1. Single
  2. TO4
  3. Tetanic Stimulation
  4. Post-tetanic stimulation
201
Q

How many Hz is usually used for single twitch nerve stimulation?

A

0.1-1.0 Hz

202
Q

What type of muscle relaxants do we see fade with?

A

Non-depolarizers such as Rocuronium

203
Q

What is the TOF ratio?

A

4th twitch/1st twitch

204
Q

What would be the issue with having no twitches?

A

Will be unable to reverse and giving something such as neostigmine could actually cause the block to be deeper

205
Q

What do we expect to see with surgical blocks?

A

A couple of twitches

206
Q

Describe the diaphragm and resistance to both types of NMBD? (3)

A
  1. Needs up to 2x as much drug for identical block
  2. Recovers faster than periphery
  3. Onset of blocks is faster than adductor pollicis
207
Q

What do we consider if we see the diaphragm moving before the thorax after NMBD reversal?

A

This does not indicate adequate ventilation!

208
Q

What are the most sensitive muscles to paralysis?

A

Orbicularis occuli, masseter, upper airway

209
Q

What most closely reflects laryngeal adductor muscle?

A

Corrugator supercilli of facial nerve

210
Q

What does the EEG show us?

A

Summation of excitatory and inhibitory PSP’s

211
Q

How are electrodes placed for EEGs?

A

So that surface anatomy relates to cortical regions

212
Q

Where are the odd numbers found with EEGs?

A

all are on the left side of the cranium

213
Q

What does the “z” indicate with EEG electrodes?

A

midline along the central sulcus

214
Q

EEG beta signal Hz for Awake?

215
Q

EEG alpha signals Hz for Eyes closed?

216
Q

EEG theta and delta signals showing depressed EEG?

A

Theta: 4-7 Hz
Delta: <4 Hz

217
Q

What is a processed EEG a combination of?

A

16 channel EEG to 2-4 channels

218
Q

What does an ideal EEG show?

A

Bilateral hemispheres

219
Q

What does the BIS monitor do?

A

Processes EEG signal to monitor LOC

220
Q

What is the lag time of BIS monitors?

A

20-30 seconds

221
Q

What was BIS monitor use proposed for?

A

To prevent intraoperative awareness

222
Q

3 facts of the B-Unaware trial

A
  1. Multicenter
  2. Compared age-adjusted end-tidal MAC
  3. to BIS 40-60, no significant difference
223
Q

What is temperature mainly regulated by?

A

Hypothalamus

224
Q

What is temperature control mediated by? (4)

A

Dopamin, norepinephrine, acetylcholine, prostaglandins

225
Q

What nerve fibers generally detect cold?

A

a-delta fibers

226
Q

What nerve fibers generally detect warmth?

227
Q

What does temperature vary by?

A
  1. Sex
  2. Exercise
  3. Food intake
  4. Thyroid function
  5. Drugs such as alcohol, nicotine, anesthetics
228
Q

Describe heat transfer significance in surgery as radiation

A

Major type of loss in surgical patients

229
Q

Describe heat transfer significance in surgery as conduction

A

negligible, patients are on thick foam pads

230
Q

Describe heat transfer significance in surgery as convection

A

negligible, rate of air speed in OR small

231
Q

Describe heat transfer significance in surgery as evaporation

A

less than 10% in the absence of sweating

232
Q

Initial temperature in GA?

A

rapid decrease

233
Q

What is the initial rapid decrease of temperature in GA due to? (3)

A
  1. Volatiles causing direct vasodilation
  2. Increases heat loss
  3. Preferentially distributes more heat to periphery than core
234
Q

Continual temperature drop due to GA occurs when and because of what

A
  1. Heat loss exceeds production

2. Occurs hour 2-4

235
Q

Describe the plateau phase of hypothermia with GA?

A
  1. thermal steady state
  2. Heat loss equals heat production leading to being unable to warm-up
  3. Occurs 3-4 hours after anesthesia
  4. Vasoconstriction prevents loss of heat from core but peripheral heat continues to be lost
236
Q

5 factors associated with hypothermia in regional anesthesia such as epidural and spinals?

A
  1. Decreases the threshold that triggers vasoconstriction
  2. Induces vasodilation in the periphery below area of the block
  3. Redistributes heat to periphery similar to GA
  4. Decreases shivering threshold
  5. Sedatives also inhibit thermoregulatory control
237
Q

What is normal core temp?

A

37 degrees celsius or 98.6 F

238
Q

5 complications associated with hypothermia

A
  1. 3x the incidence of morbid cardiac outcome
  2. 3x the incidence of wound infection
  3. Impairs platelets, PT, and PTT function
  4. Increase need for transfusion by 20%
  5. Increases duration of NMB
239
Q

4 benefits of hypothermia

A
  1. Improved outcome during recovery from cardiac arrest
  2. Protective against cerebral ischemia
  3. More difficult to trigger MH
  4. Reduces metabolism 6% per degree C
240
Q

4 common sites for core temperature monitoring

A
  1. Nasopharynx
  2. Esophagus
  3. Pulmonary artery
  4. Tympanic membrane
241
Q

5 factors associated with nasopharynx monitoring of temperature?

A
  1. Close to hypothalamus
  2. Not affected by inspired gas if intubated
  3. Easy to find
  4. Sensor must contact posterior wall
  5. Epistaxis
242
Q

Where do we place esophageal monitoring for temperature?

A

lower 1/4 to 1/3 of esophagus between the heart and descending aorta

243
Q

What temperature monitoring site could we have maximal heart sounds?

A

esophageal

244
Q

5 not so good sites of core temperature monitoring?

A
  1. Oral
  2. Axillary
  3. Rectal
  4. Bladder
  5. Skin
245
Q

What is considered room temp?

A

70 degrees F = 21 degrees C

65 degrees F = 18 degrees C

246
Q

What does a single blanket reduce heat loss by? 3 blankets?

A 
1 = 30% reduction in heat loss 
3 = 50% reduction in heat loss
247
Q

What do we do with our ETCO2 to approximate PaCO2?

A

Add about 4 mmHg

248
Q

What would be the issue with with approximating PaCO2 from ETCO2 in COPD patients?

A

COPD patients would have a higher PaCO2 than approximated due to increased alveolar dead space

249
Q

5 physiological effects from hypercarbia?

A
  1. Respiratory acidosis
  2. Increase cerebral blood flow due to cerebral vasodilation
  3. Increases ICP in susceptible patients
  4. Increased pulmonary vascular resistance
  5. Potassium shifts from intracellular to intravascular
250
Q

4 physiological effects from hypocarbia?

A
  1. Respiratory alkalosis
  2. Decreased CBF
  3. Potassium shifts to the intracellular space
  4. Blunts normal urge to breathe
251
Q

6 other things that ETCO2 informs us of other than ventilation

A
  1. Pulmonary blood flow
  2. Aerobic metabolism
  3. ETT/LMA placement
  4. Integrity of breathing circuit
  5. Adequacy of cardiac output
  6. VD to Vt
252
Q

What is Bohr’s equation?

A

VD/Vt = (PaCO2 - PeCO2)/(PaCO2)

253
Q

What is capnometry?

A

The measurement and quantification if inhaled/exhaled CO2

254
Q

What is capnography?

A

The method of measurement but also the graphic display or time of inhaled/exhaled CO2

255
Q

What is the best method to confirm endotracheal intubation?

A

Detection of carbon dioxide breath-by-breath

256
Q

Describe what you would see on a monitor to confirm ETT placement?

A

3 successive CO2 waveforms of the same height

257
Q

3 descriptors of chemical indicators of ETT placement

A
  1. Semi-quantitative
  2. Color change of pH sensitive paper
  3. A type of capnometer, doesn’t give waveform but does give quantitative information
258
Q

Relate CO2 concentration to IR reaching the detector

A

The greater the CO2 in the sample, the less IR that reaches the detector

259
Q

What is the issue with sidestream analyzers of CO2?

A

They have a delay time and rise time

260
Q

4 CO2 monitor requirements?

A
  1. CO2 reading within +/- 12% of actual value
  2. Manufacturers must disclose interference caused by ethanol, acetone,, halogenated volatiles
  3. Must have a high CO2 alarm for inhaled and exhaled CO2
  4. Must have an alarm for low exhaled CO2
261
Q

Two reasons for low exhaled CO2 alarm

A
  1. D/c

2. No pulse

262
Q

CO2 production/Delivery to Lungs causes of Increased PetCO2 (7)

A
  1. Increased metabolic rate
  2. Fever/Sepsis
  3. Seizures
  4. MH
  5. Thyrotoxicosis
  6. Increased cardiac output
  7. Bicarb admin
263
Q

Equipment malfunction causes of increased PetCO2 (3)

A
  1. Rebreathing
  2. Exhausted CO2 absorber
  3. Faulty inspiratory/expiratory valves
264
Q

Alveolar ventilation causes of increased PetCO2 (5)

A
  1. Hypoventilation
  2. Respiratory center depression
  3. Neuromuscular disease
  4. High spinal anesthesia
  5. COPD
265
Q

Equipment causes of decreased PetCO2 (4)

A
  1. Ventilator disconnect
  2. Esophageal intubation
  3. Complete airway obstruction
  4. Leak around ETT
266
Q

CO2 Production/Delivery to lungs causes of decreased PetCO2 (5)

A
  1. Hypothermia
  2. Cardiac arrest
  3. Pulmonary embolism
  4. Hemorrhage
  5. Hypotension
267
Q

Alveolar ventilation cause of decreased PetCO2?

A

Hyperventilation

268
Q

What is the simple and most widely used technique for monitoring exhaled CO2?

A

Time capnogram

269
Q

What does the time capnogram display?

A

inspiratory and expiratory phases over time

270
Q

Phase 1 of capnogram? (3)

A
  1. Baseline
  2. Exhalation of dead space from central conducting airways
  3. Essentially no CO2
271
Q

Phase 2 of capnogram? (3)

A
  1. Expiration
  2. Sampling of gases at transition of airway and alveoli
  3. Normally steep
272
Q

Phase 3 of capnogram? (3)

A
  1. Plateau phase
  2. Normally representative of CO2 in alveolus
  3. Can be representative of ventilation heterogeneity
273
Q

Phase 0 or 4 of capnogram? (2)

A
  1. Inspiration of Fresh gas flow (FGF)

2. Remaining CO2 washed out

274
Q

Where is ETCO2 measured?

A

End-point of phase 3 at the beta angle

275
Q

Characteristics of capnogram of inadequate seal around ETT or faulty inspiratory valve (3)

A
  1. Reduced plateau phase 3
  2. No beta angle
  3. Sloped phase 4 inspiratory phase
276
Q

Characteristics of capnogram of hyperventilation (2)

A
  1. Reduced inspiratory phase and expiratory phase over time

2. Seen during induction

277
Q

Characteristics of capnogram of hypoventilation (3)

A
  1. Increased expiratory upstroke
  2. ETCO2 increases, alveoli will eventually collapse causing an increased risk of hypoxemia
  3. Seen as the case goes on
278
Q

Characteristics of capnogram of increased airway resistance (4)

A
  1. P3 slope increased
  2. P2 upstroke decreased
  3. Beta angle and inspiratory phase normal at beginning but reduced over time
  4. Shark fin appearance of wave
279
Q

3 causes of increased airway resistance and which is the most common?

A
  1. Bronchospasm
  2. Increased Secretions
  3. COPD (most common)
280
Q

What type of patients is it normal to see cardiac oscillations on capnogram?

A

Skinny people

281
Q

Characteristics of capnogram of patients re-breathing or soda lime exhaustion (2)

A
  1. Doesn’t return to baseline CO2

2. Should not be rebreathing CO2

282
Q

Characteristic of capnogram for NMBD’s wearing off?

A

Curare cleft, the patient doesn’t finish inspiring like normal

283
Q

How do you differentiate esophageal intubation/cardiac arrest capnogram waveform from patient disconnect?

A

Esophageal intubation/cardiac arrest will have a slow decline, disconnect will show a flatline and immediate drop

Principles of Anesthesia 1 (3 decks)

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