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pharm 4 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is the goal of Arterial O2 sats?

A

> 94% (healthy patient)

COPD 88-92%

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2
Q

What is the goal for Arterial O2 tension (PaO2/partial pressure in vasculature)?

A

80mmHg

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3
Q

What is the PaO2/FiO2 ratio in the vented patient?

A

Goal of 400-500

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4
Q

What is the calculation for Alveolar-arterial gradient?

A

2.5+0.21 (RA) x AGE

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4
Q

What is the Alveolar-aterial gradient?

A

O2 in the alveoli (PAO2)

VERSUS

O2 dissolved in the plasma (PaO2)

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5
Q

The Alveolar-arterial gradient increases with

A

An increase in FiO2

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6
Q

What does the oxyhemoglobin Dissociation Curve tell us?

A

The correlation between saturated HGB with partial pressure

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7
Q

What causes a LEFT shift on the oxyhemoglobin dissociation curve?

A

LOW temp/DPG

LESS O2 delivery to TISSUES

ELEVATED pH & Affinity (O2)

FETAL

“Meth” “LEFT”

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8
Q

What causes a RIGHT shift on the oxyhemoglobin dissociation curve?

A

REDUCED O2 affinity

INCREASED O2 delivery, DPG, H+ & Temp

More acidic

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9
Q

When HGB has a high affinity for O2

A

It will hold on to it

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10
Q

Hypoxemia is low O2 in the

A

Blood

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11
Q

Hypoxia is low O2 in the

A

Tissues

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12
Q

Hypoventilation will cause what issues?

A

Increase in PaCO2 & PACO2

Decrease in PAO2 & diffusion

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13
Q

How can hypoxemia be corrected?

A

Small increases in FiO2

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14
Q

Ventilation is….
Oxygenation is….

A

Co2 out

O2 in

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15
Q

Examples of Low flow

A

NC

Simple face mask

Face tent

NRB

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16
Q

Examples of High Flow

A

HFNC

Venturi Mask

Neb

Non-invasive/invasive vent (mechanical)

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17
Q

What is the FiO2 & LPM of venturi & trach collar?

A

FiO2= 0.24-0.6

LPM= 2-15

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18
Q

What is the FiO2 & LPM of NC?

A

FiO2= 0.24-0.4

LPM= 1-6

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19
Q

What is the FiO2 & LPM of simple mask?

A

FiO2= 0.35-0.55

LPM= 5-10

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20
Q

What is the FiO2 & LPM of NRB?

A

FiO2= 0.80-0.95

LPM= 10-15

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21
Q

FiO2 will increase by what percent per liter of O2?

A

4%

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22
Q

NRB is ideal for

A

Severely hypoxic, but ventilating well

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23
Q

Venturi is good for

A

COPD

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24
Q

Pre-oxygenation is known as

A

Denitrogenation

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25
Q

When we pre-oxygenate, our reserved is increased by

A

1.5-4L

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26
Q

What is the 2nd biggest reservoir of O2 besides the plasma?

A

FRC, which is the lung volume held after exhalation

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27
Q

What is the targeted end tidal O2?

A

90%, but most likely 88-92%

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28
Q

Where should FiO2 be to prevent hyperoxia?

A

40-50%

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29
Q

Hyperoxia can cause

A

Pulmonary/CNS/Ocular toxicity

Pro-inflammatory & cytotoxic effects

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30
Q

Will an increase in FiO2 help a patient hemmoraging?

A

NO

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31
Q

In HOTN, 100% O2 will cause

A

A reduce in SV & CO through an increase in SVR

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32
Q

100% O2 in cardiac ischemia can increase

A

Coronary vasoconstriction

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33
Q

100% O2 in cerebral ischemia can cause

A

A decrease in CBF

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34
Q

What system controls the airway?

A

PSNS by affecting the size, gland activity & microvasculature

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35
Q

What receptors are on the airway smooth muscle?

A

Adrenergic & an abundance of Beta 2 receptors (postgang/cholinergic)

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36
Q

SNS has this effect on airway smooth muscle

A

Indirect control

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37
Q

The NANC has this influence on smooth muscle tone

A

Direct

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38
Q

The NANC has a role in

A

The inflammatory process

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39
Q

What cells cause bronchoconstriction?

A

Histamine

Prostaglandin D2 & F2

Leukotrienes C4, E4 & D4

Platelet activating factor

Bradykinin

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40
Q

What preganglionic and postganglionic receptors are involved in PSNS influence?

A

Vagus pregang

Cholinergic postgang

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41
Q

How does contraction occur in the airway smooth muscle when the PSNS system is activated?

A

Vagus pregang–> Cholinergic post gang–>

ACh–>M3–>Gq (stimulatory)

Phospholipase C–> Increased IP3

SR releases Ca+–>MLCK activated

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42
Q

Which C fibers cause bronchoconstriction?

A

Sub P

NKa

Calcitonin gene related peptide

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43
Q

Catecholamine release can

A

Bind Beta-2 receptors indirectly through the SNS

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44
Q

Beta 2 during SNS activation will

A

Inhibit the release of ACh by causing hyperpolarization and stimulating adenyl cyclase, which increases cAMP & causes smooth muscle relaxation

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45
Q

cAMP in the smooth muscle will cause

A

Relaxation

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46
Q

Beta 2 stimulated which G protein?

A

Gs, which increases cAMP, which also created hyperpolarization, leading to HYPOKALEMIA

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47
Q

In the NANC system, what is inhibitory & what is excitatory?

A

Inhibitory- Nitric Oxide & Vasoactive Intestinal Peptide

Excitatory- Sub P & NKa

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48
Q

M2 involves which G protein?

A

Gi, which inhibits adenyl cyclase, leading to NO increase in cAMP, causing constriction

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49
Q

Asthma will cause these changes

A

Hyper-irritability

Airway remodeling

Mucous

Hypertrophy

Angiogenesis

Decrease in diameter & airflow

Increase in resistance

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50
Q

What are the long term effects of Asthma?

A

Epithelial damage

Submucosal edema

Mucous secretion/plugging

Increase in vascular permeability

Vasoconstriction

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51
Q

Definition of COPD

A

Chronic Obstructive Pulmonary disease where expiratory airflow limitations are NOT fully reversible

52
Q

COPD can be classified as

A

Emphysema

Chronic Bronchitis

53
Q

Characteristics of Emphysema

A

Parenchymal destruction

Loss of elastic recoil & structural integrity

54
Q

Characteristics of Chronic Bronchitis

A

Small airway narrowing & inflammation

Mucous

55
Q

COPD will cause

A

Bronchial inflammation

Fibrosis & narrowing

Goblet cell metaplasia

Mucous hypersecretion

Alveolar destruction (emphysema)

Decrease in elastic recoil & airflow

increased resistance

56
Q

Patients with COPD often

A

Air-trap

Hyperinflate

57
Q

What can be causing a bronchospams?

A

Anaphylaxis to ABX or NMB

Mechanical?

Histamine release (atracurium, meperidine or morphine)

Hyperactive airway

58
Q

What will you see with a bronchospasm?

A

Increase in peak airway pressures (Early)

Decrease in tidal volume (early)

Capnography changes (early)

Changes in SaO2 & PaCO2

59
Q

What will you feel or hear with a bronchospasm?

A

Difficult to bag

Wheezing

60
Q

What is a poor indicator of airway obstruction?

A

Wheezing

61
Q

Increased levels of cAMP cause

A

Inhibition of MLCK

62
Q

What are examples of Inhaled short acting Beta 2 agonists?

A

Albuterol

Levalbuterol

63
Q

What are examples of inhaled long acting Beta 2 agonist?

A

Salmeterol

Formoterol

64
Q

What are examples of IV Beta agonists? Think IV SET

A

Salbutamol

Epinephrine

Terbutaline

65
Q

Beta agonists will cause dilation & relaxation. They will also cause

A

Decrease in diastolic pressure 9SVR)

Hepatic glycogenolysis

Pancreatic release of glucagon

Stimulates Na/K ATPase (hypokalemia)

66
Q

What are the systemic side effects of Beta agonists?

A

Tremor

Tachycardia

HYPERglycemia

HYPOkalemia

HYPOmagnesium

Decrease in PaO2 (by vasodilating poorly vented areas=shunting)

67
Q

Careful giving Beta. 2 agonists to

A

Cards

DM

Hyperthyroid

Diuretic

Digoxin

68
Q

Albuterol has some

A

Beta 1 activity

69
Q

What is airway onset of albuterol?

A

5-10min

70
Q

What is the PO inhaler onset of albuterol?

A

15-30min

71
Q

What is the duration of albuterol?

A

4-6 hours

72
Q

What is the acute dose of albuterol?

A

4-8 puffs Q20min

90mcg/puff

73
Q

Epi has both

A

Beta 1 & Beta 2 effects

74
Q

What is the dose of Racemic EPI

A

0.5mL of 2.25% in 4mL NS

Improvement in 20-30min

Monitor of systemic effects

75
Q

Vasoconstriction in tracheal mucosa

A

Relieves edema

76
Q

Muscarinic Antagonists (anticholinergics) block

A

ACh from binding M3, which binds to Gq, cascading with Phospholipase C, increasing the formation of IP3, causing constriction

77
Q

Which Muscarinic Antagonists (anticholinergic) is inhaled & long acting?

A

Tiotropium

78
Q

Which Muscarinic Antagonists (anticholinergic) is inhaled & short acting?

A

Ipratropium (tx COPD)

79
Q

Which Muscarinic Antagonists (anticholinergic) are given IV?

A

Atropine (crosses BBB)

Glycopyrrolate

80
Q

Anticholinergic side effects?

A

Tachycardia

Dry mouth

Blurred vision

Mydriasis

Urinary retention

Tremors

81
Q

What is the example of Methylxanthines?

A

Theophylline

82
Q

What are the 2 MOA of Theophylline, a Methylxanthine?

A

Phosphodiesterase Inhibitor (increased cAMP)

Blocks Adenosine 2B receptor

83
Q

What are the side effects Theophylline, a Methylxanthine?

A

GI upset

HA

Restlessness

Seizures

Arrhythmias

Death

Toxic >20mcg/mL

84
Q

Corticosteroids effects

A

DNA transcription & proteins

85
Q

Glucocorticoids increase

A

Beta 2 receptors

86
Q

Glucocorticoids decrease

A

Inflammatory cells

Mucus Secretion

Cytokine

Leak

87
Q

Steroid & beta agonist combination therapy is reserved for

A

COPD

88
Q

What are the combo drug examples of corticosteroids & beta 2 agonists?

A

Fluticasone/Salmeterol

Budesonide/Formoterol

89
Q

What are examples of Corticosteroids used to treat respiratory problems?

A

Fluticasone

Mometasone

Methylprednisolone…

90
Q

What are the side effects of corticosteroids?

A

Infection

HYPERglycemia

HTN

Adrenal Suppression

Psychosis

Ulcer

Osteoporosis

Increased IOP

91
Q

What are examples of Leukotriene Modifiers?

A

Montelukast

Zileuton

92
Q

What is the MOA of Leukotriene Modifiers?

A

Blocks Leukotriene receptors

Blocks conversion of arachidonic acid to leukotrienes

93
Q

What are the examples of Mast cell stabilizers?

A

Cromolyn Sodium

Nedocromil

94
Q

What is the MOA of Mast cell stabilizers?

A

Blocks mast cell degranulation

Blocks release of histamine, bronchoconstriction, mucosal edema & mucous secretion

95
Q

Which medications DO NOT decrease bronchomotor tone?

A

Desflurane

Nitrous Oxide

96
Q

Which channels are sensitive to anesthesia?

A

T-type Ca+ channels

97
Q

Beta 2 are bound to…

Alpha 2 are bound to…

A

Beta-Gs

Alpha- Gi

98
Q

What is bound to Gq?

A

Alpha 1

ET-A

M3

99
Q

What happens when Alpha1, ET-A & M3 are bound to Gq proteins?

A

IPs increases, increasing the release of intracellular Ca+= constriction

100
Q

Activated Ca+ in the endothelial cell will eventually lead to

A

Vasodilation

101
Q

What is the pathway of cGMP?

A

Ca+–>NOS–>L-arg–>NO

Activation of guanylyl cyclase–> GTP to cGMP= relaxation

102
Q

cGMP activates

A

MLCP, which breaks down myosin light chains

103
Q

What is the mean pulmonary artery pressure?

A

> 20-25mmHg

104
Q

Increased Pulm vascular resistance

A

> 2 Woods units

105
Q

Normal mean PAP

A

12 (or less than 20)

106
Q

Normal PVR

A

Anything <2

107
Q

What is the pathology of PH?

A

Decreased NOS & prostacyclin

Increase in thromboxane & endothelin-1

108
Q

When dealing with PH, it is important to avoid

A

PVR

Hypothermia

Ketamine

Nitrous Oxide

Acidosis

Lrg decreases in SVR

109
Q

What should be used in the management of PH?

A

Vasopressors intra-op for HOTN

Etomidate

Opioids

Low volatile agents

110
Q

In PH, there is a decrease in

A

The blood flow to the right side

111
Q

What is the main treatment for acute PH?

A

Inhaled Nitric Oxide

112
Q

Inhaled Nitric Oxide activates

A

Guanyl cyclase to increase cGMP

113
Q

Inhaled Nitric Oxide reduces

A

Shunt fraction

114
Q

IV Nitric oxide causes

A

Vasodilation everywhere, which can lead to perfusion of poorly vented lungs, which will increase the shunt and decrease PaO2, PVR & SVR (hypoxemia)

115
Q

Nitric Oxide will cause

A

Vasodilation

Bronchodilation

Anti thrombotic/inflammatory/proliferation

116
Q

What are examples of Phosphodiesterase Inhibitors?

A

Milrinone (PDE3/cardiac)

Sildenafil (PDE5/lungs)

Tadalafil (PDE5/lungs)

117
Q

What is the MOA of Phosphodiesterase Inhibitors?

A

Increases & prevents the breakdown of cGMP & cAMP

Targets Nitric Oxide pathway

Ca+ levels are decreased

Inhibits Phosphodiesterase enzymes

118
Q

PDE5 side effects

A

HA

Nasal congestion

Dyspepsia

Flushing

Priapism

119
Q

PDE-4 side effects

A

HA

Nausea

Diarrhea

120
Q

PDE3 side effects

A

V Arrythmias

HA

HOTN

121
Q

What are examples of Endothelin Receptor Antagonists?

A

Bosentan

Ambrisentan

122
Q

What is the MOA of Endothelin Receptor Antagonists?

A

Blocks ET-A &/or ET-B

Decreases smooth muscle cell proliferation

123
Q

Endothelin Receptor Antagonists side effects

A

Related to vasodilatory properties

Flushing

HA

HOTN

124
Q

What is the MOA of Prostacyclin derivatives/ Prostaglandins?

A

Increases PGI2 to target IP receptors

Relaxes vascular smooth muscle

Inhibits muscle cell growth 7 PLT aggregation

125
Q
A
126
Q
A
127
Q

Prostacyclin derivatives/ Prostaglandins improves

A

Oxygenation

128
Q

Prostacyclin derivatives/ Prostaglandins drug examples

A

Prostacyclin

Epoprostenol (inhaled)

Iloprost (inhaled)

Trepostinil (inhaled)

Remodulin (IV)

pharm 4 (4 decks)

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