Exam 4 (Pulmonary and Cardiac) Flashcards
1
Q
Pnea
A
Breathing
2
Q
Eupnea
A
Normal breathing
3
Q
Hypopnea
A
Decreased breathing
4
Q
Hyperpnea
A
Increased breathing
5
Q
Apnea
A
No breathing
6
Q
Dyspnea
A
Difficulty breathing
7
Q
Orthopnea
A
Dyspnea lying down
8
Q
AP diameter
A
Distance of chest front to back
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
10
Q
Carbonic acid
A
H2CO3, formed when CO2 meets water in the lungs
11
Q
Causes of hypoxia
A
ischemia - decreased blood flow
hypoxemia - decreased PaO2
Hemoglobin issues like anemia
12
Q
Diffusion
A
Hemoglobin exchanging CO2 for O2 in the alveoli.
No ATP or carriers
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
14
Q
What is directly proportional to rate of diffusion
A
Pressure
SA
Temp
Solubility
15
Q
What is inversely proportional to rate of diffusion
A
Molecular size
Thickness of membrae
16
Q
Can O2 or CO2 diffuse more easily
A
CO2
It is smaller and 24x more soluble.
Overall 20x better
17
Q
Elastin
A
Important in lung recoil
18
Q
Expiration
A
Passive
Longer
Decreases lung volume
Increases pressure to +1
Diaphragm ascends
Internal intercostals and abdominals used in forced expiration
19
Q
Inspiration
A
Active
Shorter
Lung expands
Decreases pressure to -1
Sternoclediomastoid, serratus anterior, and scalene muscles used in forced inspiratoin
20
Q
Flow in lungs
A
Volume of air per unit of time
(P1-P2)/Resistance
21
Q
What part of lungs has greatest resistance
A
Bronchi
22
Q
Does inspiration or expiration have most resistance
A
Expiration because airways are getting smaller
23
Q
Intrapulmonary/intra-alveolar pressure
A
Can be positive or negative
Pressure inside the lungs.
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
25
Transpulmonary/Transmural pressure
Difference between intrapulmonary/intra-alveolar and Intrapleural/intra thoracic.
Always positive
26
Boyles law
Volume is inversely proportional to pressure
27
When is the lowest pressure in the lung
Mid-inspiration
28
When is the highest pressure in the lung
mid-expiration
29
What would happen if you were stabbed in a lung without negative pleural pressure
Lung collapses
Lung would recoil until relaxed and chest wall would expand until relaxed
30
Dead space of lung
Volume that does not undergo gas exchange
31
Anatomical space (conducting zone) of lung
1/3 of tidal volume that it takes to fill up conducting parts of lung
32
Physiological dead space
Anatomical deadspace + alveolar dead spaces (not normal.
Equals anatomical dead space in healthy
33
Conducting zone
No gas exchange
Nose
Nasal cavity
Pharynx
Trachea
Primary, secondary, and tertiary bronchi
34
Tidal volume
Amount of air breathed in and out on normal breath.
about 500 mL
35
Compliance
Change in V/change in P
Expansibility
Opposite to surface tension
Opposite to elasticity and recoil
Surfactant helps overcome surface tension
36
What causes recoil of lung
Surface tension
Elasticity (elastin and collagen)
37
Surfactant
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
38
Type 1 pneumanocytes
do gas exchange
39
Type 2 pneumanocytes
Function as stem cells and produce surfactant
40
What stimulates surfactant production
Cortisol
Thyroxin
Prolactin
41
Inspiratory reserve volume (IRV)
Amount of air that can be inspired above tidal volume.
About 3000 mL
42
Inspiratory capacity (IC)
Tidal volume + inspiratory reserve volume.
3500 mL
43
Expiratory Reserve Volume (ERV)
Amount of air that can be expired below the tidal volume.
1100mL
44
Residual Volume (RV)
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
45
Functional residual capacity (FRC)
expiratory reserve volume + residual volume
2300mL
46
Vital Capacity (VC)
inspiratory reserve, tidal, and expiratory reserve volume.
(Everything but the residual volume)
47
Total lung capacity TLC)
Everything
5800 mL
48
COPD and asthma (obstructive lung disease)
Can get air in but it can't get out.
Increased residual volume (RV)
RV/TLC ratio >30%
49
Average healthy RV/TLC ratio
21%
50
FEV1
Forced expiratory volume.
Amount of air you can forcibly exhale in one second
51
FVC
Forced vital capacity.
Amount of air you can forcibly exhale after maximal inhalation
52
FEV1/FVC ratio
Should be 80% (4L/5L)
53
Ventilation
Process of air getting into alveoli
AKA (V)
AKA PAO2
54
Perfusion
Blood flow to the lungs for gas exchange.
AKA (Q)
AKA PaO2
55
Aa gradient
Difference betwen PAO2 and PaO2
(oxygen in in alveoli vs in the arteries)
Or difference in PACO2 and PaCO2
56
PAO2
O2 in alveoli
105mmHg
57
PaO2
O2 In arteries
100 mmHg
58
PACO2
CO2 in alveoli
40 mmHg
59
PaCO2
40 mmHg
60
Alveolar ventilation perfusion ratio
Normally 0.8.
3 at apex of lung
0.6 at base of lung
61
Ventilation Defect
Air is unable to get to alveoli
So ventilation is lowered.
V/Q is decreased
62
Pulmonary shunt
Blood flowing past poorly ventilated alveoli doesn't pick up oxygen and mixes with oxygenated blood.
Produces hypoxemia.
V/Q is decreased
63
Perfusion defect
Occurs when there is a prob with pulmonary artery or blood supply to lung.
V/Q is increased
64
Response to hypoxia in most organs
Blood vessels dialate to get more blood (and O2) to area
65
Lung response to hypoxia
Vessels constrict so other normal alveoli will get blood and effected area will not
66
Hypocapnea
Too little CO2.
Causes alkalosis
67
Is partial pressure of O2 in alveoli greater or less than that in blood
Greater.
Must be for O2 to diffuse across to capillaries to Hgb
68
Hemoglobin
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
69
O2 saturation
% of hemoglobin bound to O2.
Normal is 97%
70
What does the O2 binding curve/hemoglobin dissociation curve show
The more O2 thats on a heme, the easier it is to bind the next
71
Voluntary control of breathing
In cerebral cortex
Sends messages along the corticospinal tracts.
72
Automatic control breathing
In pre-Botzinger complex of medulla
Messages sent via cervical cord and activate diaphragm via phrenic nerve
73
What change is CSF most sensitive to
Change in hydrogen ion concentration
74
Normal PaCO2
34-45 mmHg
75
Central chemoreceptor
Monitor H+ concentrations in CSF
76
Peripheral chemoreceptors
Monitor pCO2 or pO2
77
Normal PaO2
80-100 mmHg
78
What does a left shift in the oxygen dissociation curve mean
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)
79
What does right shift of oxygen dissociation curve mean
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
2,3-diphosphoglycerate (2,3-DPG)
Inversely related to pH
Facilitates O2 transport within RBC
Increases at high pH, hypoxia, and low Hgb
Decreases at low pH
81
Normal arterial pH
7.35-7.45
82
Lung jobs as buffer
Maintain CO2 levels by either holding in or blowing off CO2
83
Kidney jobs as buffer
Regulates bicarbonate.
HCO3- + H+ <--> H2CO3
84
Metabolic acidosis
Decrease in serum HCO3- which means low pH
85
Metabolic alkalosis
Disorder that has high HCO3- which means there aren't many H+ which means high pH
86
Respiratory acidosis
Disorder that has high arterial PaCO2 causing decreased pH
87
Respiratory alkalosis
Disorder that has low arterial PaCO2 causing increased pH
88
Normal HCO3- levels
22-26 mEq/L
89
Largest artery in the body
Aorta
90
Largest vein in the body
Inferior vena cava
91
Tunica Intima of artery
Inside
Exchange of gases and nutrients
92
Tunica Media of artery
Middle
Smooth muscle fibers of vascoconstriction/vasodilation
93
Tunica Externa of artery
Outside
Anchors and protects vessel, contains nerve fibers and lymphatics
94
Tunica Intima of veins
Inside
Endothelial tissue
Frictionless pathway for blood movement
95
Tunica Media of vein
Middle
Elastic and muscular tissue that vasoconstricts/dialates
96
Tunica Adventitia of Vein
Outer layer which provide support of vessel.
97
Are blood clots more commonly found in veins or arteries
Veins bc blood can pool.
Bc blood moved by muscle movement and has valves
98
What ion does most work in the heart
Calcium
99
Anneurism
Bulging of vessel wall from increased blood pressure/blockage
100
RAAS system
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
What increase vasoconstriction/Na reabsorption/H2O retension/increase bloodflow
RAAS
ADH
Epi+NE
Endothelin's
102
What causes Vasodilation/decrease Na/H2O Retension/decrease BP
Nitric oxide
CO2
Histamine
Acetylcholine
Prostaglandin
ANP
103
Cardiac output
Total volume ejected by ventricles per minute
Avg is 5L/min
Stroke volume x HR
104
Preload
end-diastolic volume created by venous return.
Volume in ventricles at end of diastole
105
Afterload
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
Contractility
Inotropy.
ability of heart to contract.
Directly related to ejection fraction
107
Ejection Fraction
stroke volume/end-diastolic volume
usually 50-70%
108
Positive inotropes
Increase contractility
Sympathetic
109
Negative inotropes
decrease contractility.
Parasympathetic
110
Pacemaker cells
Generate spontaneous action potentials and create conduction system in heart.
SA, AV, bundle of His, right and left bundle branches, Purkinje fibers
111
Contractile Cells
99% of myocardium.
Cardiac myocytes responsible for contraction of heart.
Rely on pacemaker cells to become depolarized
112
Cardiac index
Cardiac output relative to body surface area.
CI=CO/BSA
113
Invasive ways to measure cardiac output
Right heart catheterization
Indwelling swan ganz catheter
Indwelling pulmonary artery catheter
114
Noninvases ways to measure cardiac output
echocardiogram
115
Right Coronary Artery
On inferior wall
Provide blood to right ventricle, right atrium, SA, AV, and inferior heart.
116
What to do and look for with inferior right MI
Give lots of fluid and watch for slow HR bc pt is at higher risk for clots.
117
Left Anterior Decending Artery (LAD)
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
Left Circumflex artery (LCX)
Travels in left actrioventricular groove between left ventricle and left atrium.
Perfuses lateral and posterolateral walls of left ventricle
119
Three major types of cardiac muscle
Atrial muscle
Ventricular muscle
Specialized excitatory or conductive muscle fibers.
120
Synctium
Cardiac tissue in atria and ventricles form a unit
121
Three types of channels used in heart action potential
Fast sodium channels
Slow sodium-calcium channels
Potassium channels
122
Phase 0 of myocyte action potential
Sodium influx depolarizes cell
123
Phase 1 of myocyte action potential
potassium efflux makes it slightly less depolarized
124
Phase 2 of myocyte action potential
Calcium influx causing plateau
125
Phase 3 of myocyte action potential
Potassium eflux repolarizing the cell
126
Phase 4 of myocyte action potential
Resting potential
127
What determines heart rate
balance between inhibition of SA node by vagus nerve and stimulation of SA node by sympathetic nervous system
128
Heart conduction order
SA --> AV --> bundle of His --> Bundle branches --> Purkinje fibers
129
SA Node
Sinoatrial node
upper right atrium
Primary pace maker
60-100 bm
130
Bachman's bundle
Conducts impulses from SA node to left atrium.
131
AV Node
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
Right and left bundle branches
20-40 BPM
133
Purkinje fibers
Conduct impulse to myocardial cells of ventricle causing ventricular depolarization.
20-40 BPM
134
Ventricle fire rate
30-40 BPM
135
Acetylcholine effect on HR
lowers
136
Baroreceptors
Nerve endings in aortic arch and carotid sinus that tell brain blood pressure and flow.
Adjust HR to fix pressure
137
Vagus nerve stimulation effect on cardiovascular system
Vasodilation and decrease in BP and HR
138
Vagal maneuvers
Slow HR
Cough
Bear down
Squat
Hold breath
gag
cold water on face
low up balloon
blow into syringe
139
Electrocardiogram
12 leads
12 diffeent views of heart
140
P wave
Atrial depolarization
141
QRS complex
Ventricle depolarization
142
T wave
Ventricle repolarization
143
Bronchodialaters
Short/long acting beta-2 agonist (-terol)
Short/long acting muscarinic antagonist (-ium)
144
Antiinflammatory
Inhaled corticosteroids (-sone)
LTD4-receptor blockers (-lukast)
145
Inhibitors of angiotensin
ACEi (-pril)
Ang II receptor blockers (-sartan)
Direct renin inhibitor (aliskiren)
146
Vasodilators
Dihydropyridine Calcium channel blockers with (-ipine)
Non-dihydropyridine (diltiazem and verapamin)
Beta-blockers (lol)
147
Allergic asthma physiology
Inflammation.
Bronchoconstriction
Mucus secretion
148
What does a beta 2 agonist cause
bronchodilation
Rapid relief
NO antiinflammatory effect
Also causes tachycardia and restlessness
149
What is used for maintenance of asthma
Inhaled corticosteroid.
Reduces inflammation
150
Beta-2 agonist mechanism of action
Bind to beta 2 receptor.
Activates G protein
Activates adenylyl cyclase.
Increase cAMP.
Inhibit Ca release.
Airway smooth muscle relaxation and dilation
151
Short acting Beta-2 agonist
-uterol.
acts quick.
short duration
NO anti-inflammatory effects
152
Long acting beta-2 agonist
-terol
Last up to 12 hrs.
Used with ICS for asthma or LAMA for COPD.
Given to pts with more freq asthma attacks
153
ACh effect on airway
Bind to M3 causing bronchoconstriction and increased mucus secretion.
Can also cause smooth muscle thickening and fibrosis
154
Muscarinic antagonist
-ium
Causes bronchodilation
Less effective than beta-2 agonist
155
Muscarinic antagonist method of mechanism of action
Completely blocks muscarinic receptors in lungs.
Block vagally mediated contraction of airway
156
Muscarinic antagonist adverse effects
Little systemic absorption.
Dy mouth
Urinary retention
157
Inhaled corticosteroids
-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
Inhaled corticosteroids method of action
Block phospholipase A. --> Block arachidonic acid release. --> prevent leukotriene release
159
Inhaled corticosteroid adverse effects
Oropharyngeal candidiasis (yeast infection)
So pt should rinse mouth after use.
160
PO cortico steroid
For mild-moderate exacerbations
Prednisolone
Prednisone
Methylprednisolone
161
Parental corticosteroid
Used for severe exacerbations.
Methylprednisolone sodium succinate
162
LTD4 receptor blockers
-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
LTD4 receptor blockers method of action
Blocks Cys-LT1(an LTD4 receptor) receptor on mast cell --> decreased bronchial reactivity, decreased mucosal edema, decreased mucus secretion
164
LTD4 receptor blockers adverse affects
May stress liver and cause hepatic dysfunction
Mountelukast - neuropsychiatric effects on box
165
COPD
Chronic, progressive loss of pulmonary function.
Decreased SA for gas exchange.
Excessive mucus blocks airway.
Not fully reversible.
166
Pathophysiology of COPD
Caused by irritant, mostly cigs.
Changes epithelial cells and activates macrophages.
Fibrosis.
Narrowing of airways.
Inflammatory mediators destroy alveolar walls increasing mucus secretion.
167
COPD treatment
SABA, SAMA, and systemic steroid for acute
LABA, LAMA, and ICS for persistent.
ICS monotherapy NOT recomended
168
Most prevalent modifiable risk factor for CVD
BP
169
Baroreceptor reflexes for BP regulation
Maintain cardiac output and SVR
Moment to moment control via autonomic nerves.
170
Humoral mechanisms to regulate BP
Maintain cardiac output or long-term control of BP
171
Endothelin 1
constricts blood vessels
172
Nitric oxide
Dilates blood vessels
173
How do kidneys control BP
Controling sodium and water through RAAS system
174
ACE
Angiotensin converting enzyme.
Converts Ang I to Ang II.
Breaks down bradykinin
175
Angiotensin II
Bindst to angiotensin-1 receptor on blood vessel causing vasoconstriction.
Signal adrenal gland to release aldosterone
Signals pituitary to release ADH
176
Aldosterone
Signals kidney to increase Na and water reabsorption causing increased blood volume and therefore pressure.
177
ACE inhibitor and mechanism
-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
Uses for ACEi
Control HTN.
Heart Failure
post heart attack
Prevention of kidney disease
179
ACEi adverse affects
Dry cough and angiodema from build up of bradykinin.
Hyperkalemia.
Orthostatic hypotension.
TETRATOGENIC ON BOX. can't give to pregnant
180
Angiotensin II receptor blockers (ARBs) and mechanism
-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
Uses of ARBs
HTN
Heart failure
TETRATOGENIC ON BOX. can't use in pregnancy
182
Direct renin inhibitor
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
Uses for direct renin inhibitor
Not used much
HTN only
184
Direct renin inhibitor adverse affects
Dry cough
Angiodema
hyperkalemia
renal impairment
diarrhea
TETRATOGENIC ON BOX. Can't give to pregnant
185
Dhydropyridine
Subclass of calcium channel blocker.
-pine
Work in peripheral vasculature to lower BP.
Results in vasodilation in peripheral arterioles
186
Non-dihydropyridine
Verapamil, Diltiazem
Work in SA and AV node to fix arrhythmias.
Results in decreased cardiac conduction and contractility.
Decreases O2 demand
187
Calcium channel blockers mechanism
Bind and inhibit L-type (long acting) ca channels in heart an vascular smooth muscle
Decrease Ca intry into cells.
188
Ca channel blocker uses
HTN
Arrhythmias/dysrhythmias
Pulmonary hypertension
Migraine headaches
NOT heart failure
189
B1 receptor
in heart.
Epi and NE bind to increase contractility and HR thus increasing cardiac output.
On kidney, induces renin release
190
B2 receptor
In lungs.
Epi and NE bind causing relaxation of smooth muscles and dilation of bronchioles
191
B3 receptor
In adipose tissue
192
Beta Blockers
-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
Beta-blocker uses
HTN
Arrhythmias
Heart Failure
194
Beta blocker adverse effects
Bradycardia
Hypotension
May mask symptoms of hypoglycemia.
Insomnia
195
