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Semester 2 TxWes > AP II Unit 4 > Flashcards

AP II Unit 4 Flashcards

1
Q

Describe the basics of the FEF 25-75 test

A

It’s the same information as the FEV1/FVC test, you just ignore the first 25% and last 25% and focus on the middle 50%. The idea is that if there is going to be variability in the test it is most likely to show up during this portion of the FVC measurement

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2
Q

What specifically is the FEF 25-75 supposed to be sensitive to?

A

Small/medium airway obstruction

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3
Q

Per lecture, what is the most sensitive PFT to changes and why?

A

Closing capacity test; because it measures airway collapse without forceful expiration

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4
Q

What is the “ballpark” desirable range for the FEF 25-75 in an asthmatic?

A

500 - 1000 cc/second

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5
Q

What change would occur to lung volumes if the lung had less inward recoil?

A

The chest wall still has the same opposing recoil and is now greater than the lungs inward recoil, lung volume would expand (volume would increase)

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6
Q

What happens to lung volumes as you lose/gain elastance?

A

Less elastance = less recoil opposing the chest wall = higher lung volumes (think obstructive lung disease)
More elastance = more recoil opposing the chest wall = lower lung volumes (think restrictive lung disease)

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7
Q

How does supine vs standing affect chest recoil?

A

Upright = more outwards chest recoil
Supine = less outwards chest recoil (this contributes to lower FRC when supine)

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8
Q

What happens to lung volumes after you give a paralytic?

A

The diaphragm loses all tone and relaxes, this allows the diaphragm to creep upwards and reduce lung volume

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9
Q

What controls our rate/depth of breathing?

A

The medulla

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10
Q

What is the main element of blood/CSF that central chemoreceptors are concerned with?

A

Protons

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11
Q

What is the main component of the blood that peripheral chemoreceptors are concerned with?

A

Oxygen

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12
Q

What is the normal arterial/CSF pH and concentration CO2?

A

Arterial = 7.4 pH and PCO2 of 40
CSF = 7.31 pH and PCO2 of 50

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13
Q

Exactly where would you expect to find central chemoreceptors?

A

The antro-lateral medulla

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14
Q

What fraction of blood gas management is performed by the central and peripheral chemoreceptors?

A

Central = 85%
Peripheral = 15%

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15
Q

What houses peripheral chemoreceptors? Where would you find them?

A

Bodies, 2 pairs are at the bifurcation of the internal/external carotids and 3-5 are in the region of the aorta

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16
Q

What transmits information from the carotid and aortic chemoreceptors?

A

Carotid = Glossopharyngeal nerve (CN IX)
Aortic = Vagus nerve (CN X)

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17
Q

At what PO2 do peripheral chemoreceptors begin to rapidly fire?

A

less than 60 mmHg of PO2

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18
Q

What are the 2 primary ways the body can respond to changes in blood gas CO2?

A

By modifying ventilation or respiratory rate

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19
Q

If the body wants to increase respiration, what is the most effective change to make?

A

Increase tidal volume before increasing RR (increasing Vt doesn’t increase dead space ventilation, whereas an increase in RR will increase dead space ventilation)

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20
Q

Per lecture, what is a non-pharmacologic method to reduce BP?

A

Hyperventilate = blow off CO2 = less metabolic byproducts in circulation, BP should decrease

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21
Q

What is the relationship of CO2 to iCal?

A

As you blow off CO2, less protons occupy albumin, as they leave albumin this leaves room for the Ca++ to occupy sites on albumin and plasma iCal should decrease which slows down HR or reduce CO

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22
Q

Why do infants not handle changes to blood gases?

A

Their respiratory systems haven’t fully developed and the brainstem isn’t able to fully respond to blood gas changes

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23
Q

What are the pulmonary pleural layers?

A

Visceral = attached to the lung tissue
Parietal = attached to the chest wall

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24
Q

How does each layer of the intercostals affect breathing?

A

External = help with inspiration
Internal = help with expiration

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25
Q

What muscles help keep the rib cage from moving downwards when breathing?

A

Scalene muscles and the sternocleidomastoid muscles

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26
Q

What muscles other than the diaphragm assist with breathing (discount muscles that stabilize the rib cage for this question)?

A

Internal/external intercostals, serratus anterior and the abdominal muscles

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27
Q

What muscle are you optimizing when you put your hands on your knees when trying to breath?

A

Pectoralis minor

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28
Q

What are the abdominal muscles involved with expiration?

A

rectus abdominus, the internal/external obliques and transverse abdominus

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29
Q

What are the 2 names of the ear canal?

A

pharyngotympanic tube or the eustachian canal

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30
Q

2 primary functions of the nose?

A

Humidification and filtration

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31
Q

Why do DIC patients frequently experience nosebleeds?

A

Because the nose gets its blood from vessels with protected circulation (meaning they get blood no matter what is going on in the body), the internal/external carotids

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32
Q

What is the primary source of blood for the nose?

A

External carotid artery

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33
Q

What vessels bridges the internal carotid to the smaller nasal blood vessels?

A

Ophthalmic artery

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34
Q

What are the 2 names of the structures that create air turbulence in the nose?

A

Concha or turbinates

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35
Q

Which of the concha is most fragile?

A

The middle and superior concha as they are made up of the ethmoid bone

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36
Q

Describe the basic nerve innervation of the upper airway

A

Trigeminal nerve (V) = Mouth and nose
Glossopharyngeal (IX) = covers the area above larynx
Vagus (X) = back of the throat, trachea and larynx

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37
Q

What tonsils are at the back of the throat? Back of the nose? under the tongue?

A

Throat = palatine tonsils
Nose = pharyngeal tonsils
Tongue = lingual tonsils

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38
Q

What are the 3 salivary glands listed in lecture?

A

Side of the cheek = Parotid (most important)
Under the tongue = sublingual
Further back and under the mandible = submandibular

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39
Q

Per lecture, what is the 100% most correct/scientifically accurate way to describe a brain freeze?

A

ICE CREAM FOG

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40
Q

What nerve is responsible for creating a brain freeze?

A

Trigeminal (V)

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41
Q

What are the 3 divisions of the trigeminal (V) nerve?

A

V1 = comes off the top and turns into the ophthalmic branch
V2 = maxillary division
V3 = mandibular division

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42
Q

What innervates somatic sensation of the tongue?

A

Front 2/3 = V3 branch of the trigeminal (V) nerve
Back 1/3 = Glossopharyngeal nerve (IX)

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43
Q

What innervates taste to the tongue?

A

Glossopharyngeal (IX) and facial nerve VII

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44
Q

What nerve is the primary source of innervation to the epiglottis?

A

Vagus (X) nerve

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45
Q

Filtration of the nose relies on what?

A

Momentum

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46
Q

What kind of particles are unlikely to be trapped in mucus?

A

Small particles, like smoke

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47
Q

Per lecture, what does smoke inhibit?

A

A1-alpha antitrypsin

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48
Q

Why would coughing dramatically increase 2 weeks after smoking cessation?

A

The cilia have now grown back and are now assisting to expel things from the lungs

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49
Q

Other than smoking, per lecture, what else could disrupt the cilia?

A

Insertion of an ET tube

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50
Q

What blade is seated in the vallecula to help with DL?

A

Miller blade

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51
Q

What blade gets behind the lingual tonsil to help with DL?

A

MAC blade

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52
Q

What cartilage forms a complete circle?

A

Cricoid cartilage

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53
Q

Per lecture, what is a potential downside of using cricoid pressure?

A

Increased gastric pressure blowing out the LES

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54
Q

What 3 ligaments connect the hyoid bone to the thyroid cartilage?

A

Median thyrohyoid ligament, thyrohyoid membrane and thyrohyoid ligament

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55
Q

What enters the foramen in the thyrohyoid membrane?

A

The internal superior laryngeal artery/vein and nerve

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56
Q

What do the internal/external superior laryngeal nerves innervate?

A

External = motor function of the cricothyroid muscles
Internal = sensory function of the larynx

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57
Q

What is the only muscle involved with phonation that is not innervated by the internal branch of the superior laryngeal nerve?

A

Cricothyroid muscles

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58
Q

Describe the R/L area of recurrence for the laryngeal nerves

A

L = aorta, R = brachiocephalic artery/trunk

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59
Q

What points connect the thyroid cartilage and the hyoid bone via the thyrohyoid membrane?

A

The superior horns connect to the hyoid bone

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60
Q

What connects the inferior horns of the thyroid cartilage to the cricoid cartilage?

A

The cricothyroid joint

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61
Q

What are the pivot points on the cricoid cartilage called?

A

Facet joints

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62
Q

Name the upper facet

A

articular facet for arytenoid cartilage

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63
Q

Name the lower facet

A

articular facet for the thyroid cartilage

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64
Q

What connects the cricoid cartilage to the trachea?

A

Crico-tracheal ligament

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65
Q

Per lecture, what is the advantage of not having continuous tracheal rings?

A

It allows for flexibility, resist crush injury, and useful during coughing or when the esophagus needs to expand in the presence of food

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66
Q

What are the airflow velocities of a cough/sneeze?

A

Cough = 50 mph
Sneeze = 100 mph

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67
Q

What is the length of the trachea? How much is intra/extra thoracic?

A

11 - 13 cm total, 2-4 is extra-thoracic

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68
Q

How many tracheal rings are there? What connects them to each other?

A

20, and annular ligaments

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69
Q

What is the total angle between the mainstem bronchi? Angle of R/L?

A

70 total, R = 25 degrees, L = 45 degrees

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70
Q

Per lecture, what can change the angle of the mainstem bronchi?

A

Deep inspiration (narrows the angle less than 70 degrees)

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71
Q

What happens during swallowing if the cricothyroid muscles contract?

A

Helps pivot the thyroid cartilage down which pulls down the epiglottis

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72
Q

What muscles tighten the vocal cords?

A

Cricothyroid and vocalis muscles

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73
Q

What muscles have no effect on the opening of the rima glottidis?

A

Cricothyroid and vocalis muscles

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74
Q

What muscles adduct the vocal cords?

A

Thyroarytenoid, transverse arytenoid and lateral cricoarytenoid muscles

75
Q

What muscles close the rima glottidis?

A

Thyroarytenoid, transverse arytenoid and lateral cricoarytenoid muscles

76
Q

What muscles abduct the children…I mean abduct the vocal cords?

A

Posterior cricoarytenoid muscles

77
Q

What muscles open the rima glottidis?

A

Posterior cricoarytenoid muscles

78
Q

What is the narrowest part of the airway in an adult? Non-adult?

A

Adult = Vocal cords/trans-glottic space
Non = Cricoid cartilage

79
Q

Why would our PO2 and PAO2 be substantially lower at altitude?

A

There is less atmosphere on top of us at elevation, meaning there is less driving pressure to force air into our lungs

80
Q

How does the body adapt to living at altitude in terms of optimizing oxygenation?

A

The body expands the RBC count by releasing erythropoietin from the kidneys (increases RBC count/HCT)

81
Q

What would occur if you spontaneously went from atmospheric to 0 mmHg of atmospheric pressure?

A

TOTAL RECALL!!! Gas in the body would revert from dissolved to gas phase and your blood would boil

82
Q

What regions make up the pharynx?

A

Nasopharynx (top part) oropharynx (back of the mouth) and laryngopharynx

83
Q

If possible, what muscles would you want contracting when attempting to intubate a patient?

A

Posterior cricoarytenoid muscles

84
Q

What is the max altitude a plane can pressurize to? What is the more likely range it will pressurize to?

A

Max = 15,000 feet
Range = 7,000 - 12,000 feet

85
Q

Per lecture, what are the 2 adaptations of Sherpas’?

A

The have “higher” cardiac function and larger lungs

86
Q

How much water above you is equivalent to adding 1 atm of pressure?

A

Every 33 feet

87
Q

At significant depth of water, what would you expect to happen to the partial pressures of gas in your lungs?

A

They should greatly increase; assume 3 atm of pressure:
3 x 760 = 2280
N2: .79 x 2280 = 1801
O2: .21 x 2280 = 478
this does not take into account water vapor for gas going into the lungs, this is just to show how increasing atm increases partial pressure

88
Q

How does the body get rid of N2?

A

Respiratory exchange

89
Q

Describe decompression sickness (or its much more scientific name, the bends)?

A

You go from an environment of high pressure to low pressure quickly. This creates a pressure gradient that allows dissolved gas to go back into the gaseous form. This is dangerous with N2, as the body can’t metabolize or store it and it can create air emboli

90
Q

What gas could you replace nitrogen with in a gas tank to avoid sudden decompression issues?

A

Helium; it’s an inert gas that is less likely to cause bubbles like N2 does

91
Q

What is advantageous about nitrogen being present in the lungs?

A

Because it doesn’t like to go into solution, it stays in the lungs and helps prop the airways open

92
Q

What is more likely to occur if you denitrogenate a lung?

A

With no insoluble gas in the lungs, they are at higher risk of airway collapse causing absorption atelectasis

93
Q

What position would you expect to find the vocal cords in during phonation?

A

Close together, almost fully closed

94
Q

What is the basic idea behind a hyperbaric chamber?

A

It can mimic the higher pressure experienced a significant depth to allow time for the body to breath off the excess N2

95
Q

Why does total arterial oxygen linearly increase after Hgb is 100% bound?

A

At this point, the only way oxygen can get into the blood is by dissolving, which it does so at a rate of 0.003 ml per 1 mmHg making it a linear increase

96
Q

At what partial pressure is oxygen liable to become toxic?

A

~1500 mmHg

97
Q

Why is excess oxygen potentially toxic?

A

Oxygen likes to rust/oxidize things and in great excess it can overwhelm the body’s compensatory mechanisms and start oxidizing tissues in the body

98
Q

What are the 4 dangerous oxygen molecules?

A

O2- (super oxide)
OONO- (peroxynitrite)
H2O2 (hydrogen peroxide)
NO (nitric oxide)

99
Q

If you have a massive excess of oxygen in the body, what oxygen molecule is most likely causing the most oxidative stress?

A

Super oxide (O2-)

100
Q

What does super oxide bind to that can create a very toxic compound that destroys DNA (causing replication and cancer problems)?

A

Nitric oxide, once bound, it creates OONO- (peroxynitrite)

101
Q

What can occur if you have an excess of NO donors?

A

They can negatively affect Hgb and its ability to carry oxygen (think met-Hgb)

102
Q

What enzymes can interact with H2O2?

A

Peroxidase and catalase

103
Q

What does acetylcysteine do?

A

It scavenges free radicals (common to use in tylenol OD patients)

104
Q

What enzyme is responsible for prevent super-oxides from accumulating in the body?

A

super oxide dismutase

105
Q

What 4 substances were mentioned in lecture as having a role in managing the 4 dangerous oxygen molecules?

A

super oxide dismutase, peroxidase, catalase and acetylcysteine’s

106
Q

Per lecture, why is the iron lung a “better” long term treatment option for impaired ventilation?

A

It more closely mimics the body’s natural modality of breathing because it uses negative pressure breathing

107
Q

How did polio spread?

A

Via public pools, the virus does very well in water

108
Q

What were the 2 initial polio vaccines? Which worked better?

A

1 = dead virus
2 = a modified but alive polio virus (this is the one that worked better)

109
Q

What is A-a shorthand for?

A

the alveolar - arterial difference of a gas (usually oxygen)

110
Q

What is the formula to estimate age-related decline of A-a?

A

Age + 10 / 4

111
Q

Why does A-a increase as you age?

A

You develop more alveolar dead space and slowly shunt more and more

112
Q

What is the alveolar gas equation?

A

PAO2 = (Pb - pH2O) x FiO2 / R

113
Q

In the alveolar gas equation, what is R?

A

The respiratory quotient, also known as RQ

114
Q

How would you calculate R or RQ in the alveolar gas equation?

A

it’s the ratio of oxygen consumption and CO2 production

R = CO2 per min production / O2 consumption per minute

115
Q

How does R or RQ change when burning solely carbs, fat or protein for energy?

A

Carbs = higher, 1.0
Fats = lower, 0.7
Proteins = same, 0.8

116
Q

Why does burning fats create a lower R or RQ?

A

Fats have the long fatty acid tails that when consumed released carbon which latches onto oxygen to form CO2, but release far more hydrogen which also bonds to O2 to form H2O which reduces that amount of CO2 that is created relative to when you burn carbs

117
Q

What is RER?

A

The respiratory exchange ratio (essentially the same thing as R or RA), it’s just the actual measurement of CO2 coming out and O2 going in

118
Q

If healthy, what is a normal end-tidal CO2 to PaCO2 gradient?

A

~3 mmHg

119
Q

Why does the end-tidal CO2 to PaCO2 gradient increase with age?

A

As you develop more dead space, you have less CO2 in parts of the lungs getting ventilation without blood flow (dead space) which dilutes CO2. When you exhale, end-tidal CO2 is then reduced which increases the gradient

120
Q

Other than aging, what can increase the end-tidal CO2 to PaCO2 gradient?

A

V/Q mismatch or abnormal diffusion barrier

121
Q

What 2 factors greatly reduce FRC when administering anesthesia?

A

The patient being supine (1L decrease to FRC) and giving anesthetics/paralytics (another 1L decrease)

122
Q

Why do you hyperoxygenate a patient before intubating (show your work you tired ass anesthesia student, Schmidt demands this of you!)

A

Assuming 1L FRC, 0.13 x 1 = 130 ml of oxygen, with 250 cc/min of oxygen consumption, you have about 30 seconds worth of O2 in the lungs. If you get that up to say, 60% oxygen, then you have 600 ml of oxygen in the lungs, which gives you just over 2 minutes worth of oxygen

123
Q

Why do we want a fairly static PACO2 to PaCO2 gradient?

A

This prevents variability in arterial CO2. If arterial CO2 fluctuates it can cause changes in BP and cerebral perfusion (too little CO2 = drop in BP/CO/CBF, if it increases, BP/CO/CBF would increase)

124
Q

What is the concentration of hydrogen ions in the blood?

A

0.00004 mEq/L

125
Q

In HCl, what is the conjugate base?

A

Cl-

126
Q

What are the alkaline metals mentioned in lecture?

A

Na, K and Li

127
Q

If you have elevated CO2 in the blood, based on the carbonic anhydrase reaction, what other products would you expect to be elevated?

A

Bicarb and protons

128
Q

Why are ketone acids difficult to get rid of?

A

Because they are non-volatile acids we can’t breath them off, the only way we can get rid of them is by the kidneys

129
Q

Per lecture, ingestion of what compound can cause acidosis?

A

ASA (Acetylsalicylic acid)

130
Q

Bicarb’s chemistry does not explain its ability to buffer, so why is it such a good buffer?

A

Think of LaPlace’s experiment; it predicted that alveoli that are already full would fill with air first, but the inverse is true in the body. Similar to bicarb, biologic control mechanisms allow bicarb to exert it’s effect

131
Q

What is the urinary pH limit?

A

4.5

132
Q

How much urine would you have to make to get rid of an adequate amount of protons if they didn’t have urinary buffers?

A

2,000 L/day

133
Q

What is the primary urinary buffer? Secondary?

A

Primary = phosphates
Secondary = ammonia

134
Q

List these systems by speed of responding to pH changes: blood buffers, kidneys and lungs

A

Slowest = kidneys, intermediate = lungs, fastest = blood buffers

135
Q

How would you differentiate metabolic vs respiratory pH problems on an ABG?

A

In metabolic, the bicarb levels should be variable, in respiratory it should be variability in CO2 levels (be careful as bicarb can increase/decrease in response to CO2 levels, pay close attention to what the bicarb level is relative to CO2)

136
Q

Can the lungs fully compensate for a metabolic acidosis?

A

No, it can only partially compensate

137
Q

In general, is the body more capable or responding to acidosis or alkalosis problems?

A

Acidosis

138
Q

Per lecture, what is an example of acute respiratory alkalosis? Chronic respiratory alkalosis?

A

Acute = hyperventilating such as when anxious
Chronic = Normalizing to a high altitude environment

139
Q

What is the name of this graph?

A

Nomogram

140
Q

As you increase ventilation, your BP drops. What are the 2 mechanisms leading to the reduction in BP?

A

The primary mechanism is the reflex of the central chemoreceptors responding to lower CO levels, the other is a lower plasma iCal level

141
Q

What ribs have intercostal muscles?

A

Ribs 1 - 10

142
Q

What bone is the inferior concha a part of?

A

The maxilla or maxillary bone (upper jaw)

143
Q

What bone is the middle and superior concha mainly a part of?

A

The ethmoid bone

144
Q

What bone of the coronal sinuses anchors the falx cerebri?

A

The crista galli

145
Q

What is the basic difference in placement of a MAC vs a miller blade?

A

MAC = you get behind the lingual tonsil
Miller = placed in the vallecula

146
Q

What connects the superior horn to the hyoid bone?

A

Thyrohyoid ligament

147
Q

What are some substances mentioned in lecture that can act as buffers?

A

Bicarb, proteins, phosphates, ammonia, sulfur

148
Q

What is the pH of venous vs arterial blood?

A

A = 7.4
V = 7.35

149
Q

What are the 3 pathology examples given in lecture that can be sources of acid?

A

DM, poor renal function (can’t build new bicarb) or pathology of the lungs (not enough surface area to get rid of CO2)

150
Q

What are the main examples of respiratory alkalosis, per lecture?

A

Anxiety related, high altitude, ventilatory changes or progesterone related

151
Q

What is methanol metabolized into?

A

Formic acid

152
Q

What is the relationship of Hgb concentration to bicarb?

A

Linear, as Hgb concentration increases bicarb levels can also increase d/t Hgb’s ability to buffer (Hgb can buffer the proton, when you lose protons you favor the creation of more bicarb)

153
Q

Describe how the proximal tubule allows us to retain bicarb

A

Protons come into the filtrate and combine with bicarb to form H2O and CO2, CO2 is then reabsorbed and via CA reaction turned into bicarb and a proton. The proton is then secreted back into the filtrate via the Na/H exchanger and we reabsorb a Na in exchange for secreting the proton

154
Q

What increases the cycling rate of secretion/Na reabsorption in the proximal tubule?

A

The AT-1 receptor which can be sped up by angiotensin II binding to it

155
Q

How do diuretics affect sodium reabsorption?

A

With diuretics, more Na reaches the distal tubule and the exchangers in the distal tubule will secrete a lot of protons in exchange for reabsorbing Na

156
Q

What type of pH problem can diuretics cause?

A

Metabolic alkalosis

157
Q

Where are the 2 primary sites of acid/base management in the kidneys?

A

The proximal tubule and the intercalated cells

158
Q

What is the formula to solve for anion gap? Normal range?

A

Na - Bicarb - Cl = anion gap, normal is 12

159
Q

How can certain kinds of metabolic acidosis cause the anion gap to increase? Examples?

A

As bicarb levels decrease but Cl isn’t rising as there is other sources of negatively charged compounds making up the difference, creating a metabolic acidosis with an increased or open anion gap

Ex: DKA, DM, ETOH, starvation, lactic acidosis, methanol, salicylates, ethylene glycol, ammonium chloride can all cause this

160
Q

Per lecture, what type of metabolic acidosis has a normal anion gap?

A

Metabolic acidosis related to diarrhea (pancreatic fluid loss was also mentioned, but Schmidt said to focus on diarrhea as the primary example)

161
Q

What muscles warp around the airway and higher up in the throat?

A

The pharyngeal constrictors

162
Q

What muscles connect to the hyoid bone and the floor of the jaw? Name them

A

The suprahyoid muscles

Anterior/posterior diagastric muscle, stylohyoid, mylohyoid and geniohyoid muscle

163
Q

What are the infrahyoid muscles?

A

Omohyoid, sternohyoid, sternothryoid and thyrohyoid

164
Q

Where would you find irritant receptors? What nerve innervates them?

A

Throughout the lungs and airways and the Vagus (X)
In the nose is the Trigeminal (V)

165
Q

What are the J-receptors? Describe their location as well

A

The are stretch receptors in the lungs that look at how much blood volume is in the lungs. They are located in juxtaposition to the capillaries (meaning the receptor itself in in the alveoli, but in very close proximity to the capillary). Too much blood in the lungs sets off these receptors causing us to feel dyspneic.

166
Q

What do the pulmonary stretch receptors do?

A

They sense the volume of air in the lungs. As you breath to maximal volumes, further attempts to inspire make you feel “uncomfortable” as a way to discourage you from breathing further

167
Q

Describe Cheyne-stokes breathing

A

You have a cyclic ratio of very deep breathing followed by periods of apnea

168
Q

What are the causes mentioned in lecture of Cheyne-stokes breathing?

A

A delay in getting oxygenated blood to the brainstem (such as extreme physical labor) or brain damage

169
Q

What are some of the respiratory drive disorders listed in class?

A

Elevated ICP (MOA on breathing unclear), OD on opiates (pentobarbital specifically mentioned)

170
Q

What are the 2 types of OSA?

A

CNS dysfunction related or airway obstruction related

171
Q

What surgical procedure may alleviate airway obstruction related OSA?

A

Uvuloplasty

172
Q

What is the trigger to break a breath holding manuever?

A

Elevated PCO2

173
Q

What causes hiccups?

A

Phrenic nerve firing

174
Q

What nerve is irritated when you “get the wind knocked out of you”?

A

Phrenic nerve -> this leads to the diaphragm relaxing and makes you feel apneic/dyspneic

175
Q

What is the difference tachypnea and hyperventilation?

A

Tachy = rapid breathing that is NOT in excess of metabolic needs
Hyperventilation = rapid breathing that is in excess of metabolic needs

176
Q

Describe Kussmaul respirations

A

Very deep/rapid breathing to try and increase pH. Common in DKA

177
Q

What is the difference in Biot vs ataxic breathing?

A

Biot = irregular rate with minimal variability in volume
Ataxic = irregular rate and irregular volume

178
Q

What is the basic function of a ventilator “sigh”?

A

It acts as an occasional large breath to help re-recruit portions of the lung

179
Q

What are some examples of conditions that can increase/decrease the capnograph waveform?

A

Increase = fever, bicarb infusion (you create more CO2 from the CA reaction which is then expired), release a tourniquet, increase CO, hypoventilation and MH

Decrease = hypothermia, decreased CO, PE, hyperventilation, extubation, airway obstruction, circuit disconnect, dead space development, esophageal intubation

180
Q

What is the primary determinant of lung ventilation and blood flow?

A

Gravity

181
Q

When supine, what portions of the lung would get the most ventilation?

A

Posterior portion of the lung, which would also mean the pleural pressure would be more negative there as well

182
Q

At low lung volumes, the lung doesn’t ventilate in an ideal way. What is the fix for this?

A

Increase tidal volume or use extra PEEP

183
Q

What nerve controls the inner muscles of the larynx?

A

Inferior laryngeal nerve

Semester 2 TxWes (16 decks)

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