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PAS 506 > Exam 4 (Pulmonary and Cardiac) > Flashcards

Exam 4 (Pulmonary and Cardiac) Flashcards

1
Q

Pnea

A

Breathing

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2
Q

Eupnea

A

Normal breathing

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3
Q

Hypopnea

A

Decreased breathing

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4
Q

Hyperpnea

A

Increased breathing

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5
Q

Apnea

A

No breathing

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6
Q

Dyspnea

A

Difficulty breathing

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7
Q

Orthopnea

A

Dyspnea lying down

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8
Q

AP diameter

A

Distance of chest front to back

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9
Q

What drives the body to breathe

A

Get CO2 out. NOT get O2 in because CO2 directly affects pH and we have a very narrow range of pH we can live at

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10
Q

Carbonic acid

A

H2CO3, formed when CO2 meets water in the lungs

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11
Q

Causes of hypoxia

A

ischemia - decreased blood flow
hypoxemia - decreased PaO2
Hemoglobin issues like anemia

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12
Q

Diffusion

A

Hemoglobin exchanging CO2 for O2 in the alveoli.
No ATP or carriers

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13
Q

Alveolar capillary membrane

A

Very thin with large SA.
Fluid line alveoli
Alveolar epithelium
Epithelial basement membrane
Fluid in interstitial space
Capillary endothelium
Endothelial basement membrane

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14
Q

What is directly proportional to rate of diffusion

A

Pressure
SA
Temp
Solubility

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15
Q

What is inversely proportional to rate of diffusion

A

Molecular size
Thickness of membrae

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16
Q

Can O2 or CO2 diffuse more easily

A

CO2
It is smaller and 24x more soluble.
Overall 20x better

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17
Q

Elastin

A

Important in lung recoil

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18
Q

Expiration

A

Passive
Longer
Decreases lung volume
Increases pressure to +1
Diaphragm ascends
Internal intercostals and abdominals used in forced expiration

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19
Q

Inspiration

A

Active
Shorter
Lung expands
Decreases pressure to -1
Sternoclediomastoid, serratus anterior, and scalene muscles used in forced inspiratoin

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20
Q

Flow in lungs

A

Volume of air per unit of time
(P1-P2)/Resistance

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21
Q

What part of lungs has greatest resistance

A

Bronchi

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22
Q

Does inspiration or expiration have most resistance

A

Expiration because airways are getting smaller

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23
Q

Intrapulmonary/intra-alveolar pressure

A

Can be positive or negative
Pressure inside the lungs.

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24
Q

Intrapleural/intra thoracic pressure

A

Always negative
Pressure between the two pleural layers
Pulls esophagus open increasing its volume and decreasing pressure until it becomes negative.
EQUAL to esophagus pressure
Normally -2 at end of expiration and -7 at end of inspiration.
Gets more negative as chest wall expands away from lung

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25
Q

Transpulmonary/Transmural pressure

A

Difference between intrapulmonary/intra-alveolar and Intrapleural/intra thoracic.
Always positive

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26
Q

Boyles law

A

Volume is inversely proportional to pressure

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27
Q

When is the lowest pressure in the lung

A

Mid-inspiration

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28
Q

When is the highest pressure in the lung

A

mid-expiration

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29
Q

What would happen if you were stabbed in a lung without negative pleural pressure

A

Lung collapses
Lung would recoil until relaxed and chest wall would expand until relaxed

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30
Q

Dead space of lung

A

Volume that does not undergo gas exchange

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31
Q

Anatomical space (conducting zone) of lung

A

1/3 of tidal volume that it takes to fill up conducting parts of lung

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32
Q

Physiological dead space

A

Anatomical deadspace + alveolar dead spaces (not normal.
Equals anatomical dead space in healthy

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33
Q

Conducting zone

A

No gas exchange
Nose
Nasal cavity
Pharynx
Trachea
Primary, secondary, and tertiary bronchi

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34
Q

Tidal volume

A

Amount of air breathed in and out on normal breath.
about 500 mL

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35
Q

Compliance

A

Change in V/change in P
Expansibility
Opposite to surface tension
Opposite to elasticity and recoil
Surfactant helps overcome surface tension

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36
Q

What causes recoil of lung

A

Surface tension
Elasticity (elastin and collagen)

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37
Q

Surfactant

A

Keeps aveoli and lung partially open so you don’t have to inflate lung from nothing.
Helps break surface tension of water in lungs to prevent lungs from collapsing and let air sink for gas exchange

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38
Q

Type 1 pneumanocytes

A

do gas exchange

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39
Q

Type 2 pneumanocytes

A

Function as stem cells and produce surfactant

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40
Q

What stimulates surfactant production

A

Cortisol
Thyroxin
Prolactin

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41
Q

Inspiratory reserve volume (IRV)

A

Amount of air that can be inspired above tidal volume.
About 3000 mL

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42
Q

Inspiratory capacity (IC)

A

Tidal volume + inspiratory reserve volume.
3500 mL

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43
Q

Expiratory Reserve Volume (ERV)

A

Amount of air that can be expired below the tidal volume.
1100mL

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44
Q

Residual Volume (RV)

A

Air that remains in lungs after maximal forced expiration.
Important to perform gas exchange because heart is sending more blood than you are breathing.
1200mL
Can’t be measured with spirometry

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45
Q

Functional residual capacity (FRC)

A

expiratory reserve volume + residual volume
2300mL

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46
Q

Vital Capacity (VC)

A

inspiratory reserve, tidal, and expiratory reserve volume.
(Everything but the residual volume)

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47
Q

Total lung capacity TLC)

A

Everything
5800 mL

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48
Q

COPD and asthma (obstructive lung disease)

A

Can get air in but it can’t get out.
Increased residual volume (RV)
RV/TLC ratio >30%

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49
Q

Average healthy RV/TLC ratio

A

21%

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50
Q

FEV1

A

Forced expiratory volume.
Amount of air you can forcibly exhale in one second

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51
Q

FVC

A

Forced vital capacity.
Amount of air you can forcibly exhale after maximal inhalation

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52
Q

FEV1/FVC ratio

A

Should be 80% (4L/5L)

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53
Q

Ventilation

A

Process of air getting into alveoli
AKA (V)
AKA PAO2

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54
Q

Perfusion

A

Blood flow to the lungs for gas exchange.
AKA (Q)
AKA PaO2

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55
Q

Aa gradient

A

Difference betwen PAO2 and PaO2
(oxygen in in alveoli vs in the arteries)
Or difference in PACO2 and PaCO2

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56
Q

PAO2

A

O2 in alveoli
105mmHg

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57
Q

PaO2

A

O2 In arteries
100 mmHg

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58
Q

PACO2

A

CO2 in alveoli
40 mmHg

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59
Q

PaCO2

A

40 mmHg

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60
Q

Alveolar ventilation perfusion ratio

A

Normally 0.8.
3 at apex of lung
0.6 at base of lung

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61
Q

Ventilation Defect

A

Air is unable to get to alveoli
So ventilation is lowered.
V/Q is decreased

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62
Q

Pulmonary shunt

A

Blood flowing past poorly ventilated alveoli doesn’t pick up oxygen and mixes with oxygenated blood.
Produces hypoxemia.
V/Q is decreased

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63
Q

Perfusion defect

A

Occurs when there is a prob with pulmonary artery or blood supply to lung.
V/Q is increased

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64
Q

Response to hypoxia in most organs

A

Blood vessels dialate to get more blood (and O2) to area

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65
Q

Lung response to hypoxia

A

Vessels constrict so other normal alveoli will get blood and effected area will not

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66
Q

Hypocapnea

A

Too little CO2.
Causes alkalosis

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67
Q

Is partial pressure of O2 in alveoli greater or less than that in blood

A

Greater.
Must be for O2 to diffuse across to capillaries to Hgb

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68
Q

Hemoglobin

A

4 subunits each with heme and iron molecule made of two alpha and two beta chains.
Each of the four iron atoms can reversibly bind to O2

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69
Q

O2 saturation

A

% of hemoglobin bound to O2.
Normal is 97%

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70
Q

What does the O2 binding curve/hemoglobin dissociation curve show

A

The more O2 thats on a heme, the easier it is to bind the next

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71
Q

Voluntary control of breathing

A

In cerebral cortex
Sends messages along the corticospinal tracts.

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72
Q

Automatic control breathing

A

In pre-Botzinger complex of medulla
Messages sent via cervical cord and activate diaphragm via phrenic nerve

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73
Q

What change is CSF most sensitive to

A

Change in hydrogen ion concentration

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74
Q

Normal PaCO2

A

34-45 mmHg

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75
Q

Central chemoreceptor

A

Monitor H+ concentrations in CSF

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76
Q

Peripheral chemoreceptors

A

Monitor pCO2 or pO2

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77
Q

Normal PaO2

A

80-100 mmHg

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78
Q

What does a left shift in the oxygen dissociation curve mean

A

Hemoglobin has increased affinity for O2
More difficult for O2 to unbind and perfuse the tissues.
Found in alveolus when CO2 is decreasing and pH is increasing (basic conditions)

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79
Q

What does right shift of oxygen dissociation curve mean

A

Hemoglobin has decreased affinity for oxygen.
Easier for oxygen to dissociate from hemoglobin to perfuse with tissues.
Found in peripheral tissue when CO2 increasing and pH is decreasing (acidic conditions)

80
Q

2,3-diphosphoglycerate (2,3-DPG)

A

Inversely related to pH
Facilitates O2 transport within RBC
Increases at high pH, hypoxia, and low Hgb
Decreases at low pH

81
Q

Normal arterial pH

A

7.35-7.45

82
Q

Lung jobs as buffer

A

Maintain CO2 levels by either holding in or blowing off CO2

83
Q

Kidney jobs as buffer

A

Regulates bicarbonate.
HCO3- + H+ <–> H2CO3

84
Q

Metabolic acidosis

A

Decrease in serum HCO3- which means low pH

85
Q

Metabolic alkalosis

A

Disorder that has high HCO3- which means there aren’t many H+ which means high pH

86
Q

Respiratory acidosis

A

Disorder that has high arterial PaCO2 causing decreased pH

87
Q

Respiratory alkalosis

A

Disorder that has low arterial PaCO2 causing increased pH

88
Q

Normal HCO3- levels

A

22-26 mEq/L

89
Q

Largest artery in the body

A

Aorta

90
Q

Largest vein in the body

A

Inferior vena cava

91
Q

Tunica Intima of artery

A

Inside
Exchange of gases and nutrients

92
Q

Tunica Media of artery

A

Middle
Smooth muscle fibers of vascoconstriction/vasodilation

93
Q

Tunica Externa of artery

A

Outside
Anchors and protects vessel, contains nerve fibers and lymphatics

94
Q

Tunica Intima of veins

A

Inside
Endothelial tissue
Frictionless pathway for blood movement

95
Q

Tunica Media of vein

A

Middle
Elastic and muscular tissue that vasoconstricts/dialates

96
Q

Tunica Adventitia of Vein

A

Outer layer which provide support of vessel.

97
Q

Are blood clots more commonly found in veins or arteries

A

Veins bc blood can pool.
Bc blood moved by muscle movement and has valves

98
Q

What ion does most work in the heart

A

Calcium

99
Q

Anneurism

A

Bulging of vessel wall from increased blood pressure/blockage

100
Q

RAAS system

A

Renin
Angiotensin
Aldosterone
Causes vasoconstriction and Na/H2O retention
Angiotensin converted to Angiotensin I by Renin.
Angiotensin I converted to Angiotensin II by ACE
Angiotensin II causes Aldosterone and ADH to be released

101
Q

What increase vasoconstriction/Na reabsorption/H2O retension/increase bloodflow

A

RAAS
ADH
Epi+NE
Endothelin’s

102
Q

What causes Vasodilation/decrease Na/H2O Retension/decrease BP

A

Nitric oxide
CO2
Histamine
Acetylcholine
Prostaglandin
ANP

103
Q

Cardiac output

A

Total volume ejected by ventricles per minute
Avg is 5L/min
Stroke volume x HR

104
Q

Preload

A

end-diastolic volume created by venous return.
Volume in ventricles at end of diastole

105
Q

Afterload

A

Fixed load cardiac muscle needs to overcome to shorten during contraction.
Pressure left ventricle must oppose to get blood out.
Affected by diameter of vessels

106
Q

Contractility

A

Inotropy.
ability of heart to contract.
Directly related to ejection fraction

107
Q

Ejection Fraction

A

stroke volume/end-diastolic volume
usually 50-70%

108
Q

Positive inotropes

A

Increase contractility
Sympathetic

109
Q

Negative inotropes

A

decrease contractility.
Parasympathetic

110
Q

Pacemaker cells

A

Generate spontaneous action potentials and create conduction system in heart.
SA, AV, bundle of His, right and left bundle branches, Purkinje fibers

111
Q

Contractile Cells

A

99% of myocardium.
Cardiac myocytes responsible for contraction of heart.
Rely on pacemaker cells to become depolarized

112
Q

Cardiac index

A

Cardiac output relative to body surface area.
CI=CO/BSA

113
Q

Invasive ways to measure cardiac output

A

Right heart catheterization
Indwelling swan ganz catheter
Indwelling pulmonary artery catheter

114
Q

Noninvases ways to measure cardiac output

A

echocardiogram

115
Q

Right Coronary Artery

A

On inferior wall
Provide blood to right ventricle, right atrium, SA, AV, and inferior heart.

116
Q

What to do and look for with inferior right MI

A

Give lots of fluid and watch for slow HR bc pt is at higher risk for clots.

117
Q

Left Anterior Decending Artery (LAD)

A

On anterior wall
Supplies about 60% of heart
Branches into left main coronary artery.
Perfuses septum (bundle of his and bundle branches), left ventricle, and apex

118
Q

Left Circumflex artery (LCX)

A

Travels in left actrioventricular groove between left ventricle and left atrium.
Perfuses lateral and posterolateral walls of left ventricle

119
Q

Three major types of cardiac muscle

A

Atrial muscle
Ventricular muscle
Specialized excitatory or conductive muscle fibers.

120
Q

Synctium

A

Cardiac tissue in atria and ventricles form a unit

121
Q

Three types of channels used in heart action potential

A

Fast sodium channels
Slow sodium-calcium channels
Potassium channels

122
Q

Phase 0 of myocyte action potential

A

Sodium influx depolarizes cell

123
Q

Phase 1 of myocyte action potential

A

potassium efflux makes it slightly less depolarized

124
Q

Phase 2 of myocyte action potential

A

Calcium influx causing plateau

125
Q

Phase 3 of myocyte action potential

A

Potassium eflux repolarizing the cell

126
Q

Phase 4 of myocyte action potential

A

Resting potential

127
Q

What determines heart rate

A

balance between inhibition of SA node by vagus nerve and stimulation of SA node by sympathetic nervous system

128
Q

Heart conduction order

A

SA –> AV –> bundle of His –> Bundle branches –> Purkinje fibers

129
Q

SA Node

A

Sinoatrial node
upper right atrium
Primary pace maker
60-100 bm

130
Q

Bachman’s bundle

A

Conducts impulses from SA node to left atrium.

131
Q

AV Node

A

Atrioventrcular node
In lower right atrium near interatrial septum.
Slows the conduction of electrical impulses from the SA node.
Tells SA node to chill out
40-60 BPM

132
Q

Right and left bundle branches

A

20-40 BPM

133
Q

Purkinje fibers

A

Conduct impulse to myocardial cells of ventricle causing ventricular depolarization.
20-40 BPM

134
Q

Ventricle fire rate

A

30-40 BPM

135
Q

Acetylcholine effect on HR

A

lowers

136
Q

Baroreceptors

A

Nerve endings in aortic arch and carotid sinus that tell brain blood pressure and flow.
Adjust HR to fix pressure

137
Q

Vagus nerve stimulation effect on cardiovascular system

A

Vasodilation and decrease in BP and HR

138
Q

Vagal maneuvers

A

Slow HR
Cough
Bear down
Squat
Hold breath
gag
cold water on face
low up balloon
blow into syringe

139
Q

Electrocardiogram

A

12 leads
12 diffeent views of heart

140
Q

P wave

A

Atrial depolarization

141
Q

QRS complex

A

Ventricle depolarization

142
Q

T wave

A

Ventricle repolarization

143
Q

Bronchodialaters

A

Short/long acting beta-2 agonist (-terol)
Short/long acting muscarinic antagonist (-ium)

144
Q

Antiinflammatory

A

Inhaled corticosteroids (-sone)
LTD4-receptor blockers (-lukast)

145
Q

Inhibitors of angiotensin

A

ACEi (-pril)
Ang II receptor blockers (-sartan)
Direct renin inhibitor (aliskiren)

146
Q

Vasodilators

A

Dihydropyridine Calcium channel blockers with (-ipine)
Non-dihydropyridine (diltiazem and verapamin)
Beta-blockers (lol)

147
Q

Allergic asthma physiology

A

Inflammation.
Bronchoconstriction
Mucus secretion

148
Q

What does a beta 2 agonist cause

A

bronchodilation
Rapid relief
NO antiinflammatory effect
Also causes tachycardia and restlessness

149
Q

What is used for maintenance of asthma

A

Inhaled corticosteroid.
Reduces inflammation

150
Q

Beta-2 agonist mechanism of action

A

Bind to beta 2 receptor.
Activates G protein
Activates adenylyl cyclase.
Increase cAMP.
Inhibit Ca release.
Airway smooth muscle relaxation and dilation

151
Q

Short acting Beta-2 agonist

A

-uterol.
acts quick.
short duration
NO anti-inflammatory effects

152
Q

Long acting beta-2 agonist

A

-terol
Last up to 12 hrs.
Used with ICS for asthma or LAMA for COPD.
Given to pts with more freq asthma attacks

153
Q

ACh effect on airway

A

Bind to M3 causing bronchoconstriction and increased mucus secretion.
Can also cause smooth muscle thickening and fibrosis

154
Q

Muscarinic antagonist

A

-ium
Causes bronchodilation
Less effective than beta-2 agonist

155
Q

Muscarinic antagonist method of mechanism of action

A

Completely blocks muscarinic receptors in lungs.
Block vagally mediated contraction of airway

156
Q

Muscarinic antagonist adverse effects

A

Little systemic absorption.
Dy mouth
Urinary retention

157
Q

Inhaled corticosteroids

A

-asone, -ide
Long-term control of persistant asthma.
Can be used by itself to treat asthma.
Decreases inflammatory cascade
Decreases mucus secretion
Decreases capillary permeability
Inhibits leukotriene release.
Reduce freq of exacerbations
Long term use decreases airway hyperresponsiveness
DO NOT relax airway smooth musle

158
Q

Inhaled corticosteroids method of action

A

Block phospholipase A. –> Block arachidonic acid release. –> prevent leukotriene release

159
Q

Inhaled corticosteroid adverse effects

A

Oropharyngeal candidiasis (yeast infection)
So pt should rinse mouth after use.

160
Q

PO cortico steroid

A

For mild-moderate exacerbations
Prednisolone
Prednisone
Methylprednisolone

161
Q

Parental corticosteroid

A

Used for severe exacerbations.
Methylprednisolone sodium succinate

162
Q

LTD4 receptor blockers

A

-luk-
add on therapy for pts with asthma not well controlled on ICS.
Prevent allergic rhinitis and exercise-induced asthma.
No role in COPD

163
Q

LTD4 receptor blockers method of action

A

Blocks Cys-LT1(an LTD4 receptor) receptor on mast cell –> decreased bronchial reactivity, decreased mucosal edema, decreased mucus secretion

164
Q

LTD4 receptor blockers adverse affects

A

May stress liver and cause hepatic dysfunction
Mountelukast - neuropsychiatric effects on box

165
Q

COPD

A

Chronic, progressive loss of pulmonary function.
Decreased SA for gas exchange.
Excessive mucus blocks airway.
Not fully reversible.

166
Q

Pathophysiology of COPD

A

Caused by irritant, mostly cigs.
Changes epithelial cells and activates macrophages.
Fibrosis.
Narrowing of airways.
Inflammatory mediators destroy alveolar walls increasing mucus secretion.

167
Q

COPD treatment

A

SABA, SAMA, and systemic steroid for acute
LABA, LAMA, and ICS for persistent.
ICS monotherapy NOT recomended

168
Q

Most prevalent modifiable risk factor for CVD

A

BP

169
Q

Baroreceptor reflexes for BP regulation

A

Maintain cardiac output and SVR
Moment to moment control via autonomic nerves.

170
Q

Humoral mechanisms to regulate BP

A

Maintain cardiac output or long-term control of BP

171
Q

Endothelin 1

A

constricts blood vessels

172
Q

Nitric oxide

A

Dilates blood vessels

173
Q

How do kidneys control BP

A

Controling sodium and water through RAAS system

174
Q

ACE

A

Angiotensin converting enzyme.
Converts Ang I to Ang II.
Breaks down bradykinin

175
Q

Angiotensin II

A

Bindst to angiotensin-1 receptor on blood vessel causing vasoconstriction.
Signal adrenal gland to release aldosterone
Signals pituitary to release ADH

176
Q

Aldosterone

A

Signals kidney to increase Na and water reabsorption causing increased blood volume and therefore pressure.

177
Q

ACE inhibitor and mechanism

A

-pril
Bind to ACE inhibiting conversion of ang I to ang II.
Decrease aldosterone secretion
Decreased Na and water retention, decreased sympathetic output.
Prevents breakdown of bradykinin causing increase in vasodilation
Decrease BP

178
Q

Uses for ACEi

A

Control HTN.
Heart Failure
post heart attack
Prevention of kidney disease

179
Q

ACEi adverse affects

A

Dry cough and angiodema from build up of bradykinin.
Hyperkalemia.
Orthostatic hypotension.
TETRATOGENIC ON BOX. can’t give to pregnant

180
Q

Angiotensin II receptor blockers (ARBs) and mechanism

A

-sartan
Binds to angiotensin-1 receptor.
Decreases activation of AT1 receptor by ang II.
Causes vasodilation, decreased Na and water rentention, decreased sympathetic output.
No effect on bradykinin system.
More selective than ACEi

181
Q

Uses of ARBs

A

HTN
Heart failure
TETRATOGENIC ON BOX. can’t use in pregnancy

182
Q

Direct renin inhibitor

A

Aliskerin
Binds directly to renin.
Inhibits enzymatic effects of renin.
Reduces conversion of ang to ang I.
Causes vasodilation, decreased sodium and water retention. decreased sympathetic output.

183
Q

Uses for direct renin inhibitor

A

Not used much
HTN only

184
Q

Direct renin inhibitor adverse affects

A

Dry cough
Angiodema
hyperkalemia
renal impairment
diarrhea
TETRATOGENIC ON BOX. Can’t give to pregnant

185
Q

Dhydropyridine

A

Subclass of calcium channel blocker.
-pine
Work in peripheral vasculature to lower BP.
Results in vasodilation in peripheral arterioles

186
Q

Non-dihydropyridine

A

Verapamil, Diltiazem
Work in SA and AV node to fix arrhythmias.
Results in decreased cardiac conduction and contractility.
Decreases O2 demand

187
Q

Calcium channel blockers mechanism

A

Bind and inhibit L-type (long acting) ca channels in heart an vascular smooth muscle
Decrease Ca intry into cells.

188
Q

Ca channel blocker uses

A

HTN
Arrhythmias/dysrhythmias
Pulmonary hypertension
Migraine headaches
NOT heart failure

189
Q

B1 receptor

A

in heart.
Epi and NE bind to increase contractility and HR thus increasing cardiac output.
On kidney, induces renin release

190
Q

B2 receptor

A

In lungs.
Epi and NE bind causing relaxation of smooth muscles and dilation of bronchioles

191
Q

B3 receptor

A

In adipose tissue

192
Q

Beta Blockers

A

-lol
Antagonize Beta receptors.
Decrease HR and contractility thus decreased CO.
Decreased BP.
Decreased Renin secretion.
Some also block alpha 1 receptors causing vasodilation decreasing BP even more

193
Q

Beta-blocker uses

A

HTN
Arrhythmias
Heart Failure

194
Q

Beta blocker adverse effects

A

Bradycardia
Hypotension
May mask symptoms of hypoglycemia.
Insomnia

195
Q
A

PAS 506 (9 decks)

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