Phys Exam 2 Flashcards
(299 cards)
1
Q
what does the cardiovascular system do
A
moves materials entering the body, cell to cell, and moves stuff out of the body
2
Q
what are examples of a closed loop system
A
systemic/caval system: vena cavas, coronary system, portal systems
3
Q
what is a pulmonary embolism
A
clot that eventually gets stuck in lung -> no blood to heart = no blood to brain
4
Q
what is a stroke from
A
clot on arterial side that got into a small enough vessel that gets STUCK
5
Q
what is a portal system
A
systemic circulation in which blood draining from capillary bed of one structure flows through a larger vessel to supply capillary bed of another structure before returning to heart
6
Q
what are examples of portal systems
A
hepatic (liver), renal (kidneys), hypothalamic-hypophyseal
7
Q
average pressure in arteries and veins
A
arteries: 100 mmHg (aorta has highest pressure
veins: 0 mmHg (vein cava has lowest)
8
Q
what is static pressure influenced by
A
- fluid volume (increase in fluid, increase in pressure)
- wall compliance (increase in compliance, increase in pressure)
think of tubes connected with common tube on the bottom that is plugged. the water is exerting pressure on the walls of the container -> hydrostatic pressure
9
Q
hydraulic pressure in influenced by
A
driving force/pressure: pumping force
pressure gradient: must be present for flow
resistance to flow: diameter and total length of vessel AND viscosity of fluid
thing of 4 tubes lined up, connected with one common tube on bottom plugged. once you remove the plug, pressure falls with distance as energy is lost because of friction (this is how our cardiovascular system works)
10
Q
do arteries or veins have more smooth muscle
A
arteries have much more -> regulates blood flow to tissues
11
Q
Fluid pressure basics:
what is the driving force in the heart
A
pressure created by the heart muscle contraction -> driving pressure
12
Q
Fluid pressure basics:
flow is proportional to ______
flow is inversely proportional to _______
A
flow is proportional to CHANGE IN PRESSURE GRADIENT
flow is inversely proportional to RESISTANCE
13
Q
what happens when we have a higher system pressure gradient in terms of flow and resistance
A
Flow: increases (proportional to pressure gradient)
resistance: decreases (inversely proportional to flow)
increase in flow and decrease in resistance
14
Q
Fluid pressure basics:
resistance to flow is a function of (3)
A
vessel length
blood viscosity
vessel diameter
15
Q
Fluid pressure basics:
what is the most significant influence in our bodies when it comes to resistance and flow
A
VESSEL DIAMETER! it is the only thing that can change in our body
16
Q
what happens to our bp with vasoconstriction
A
increase bp
17
Q
what happens to our bp with vasodilation
A
decrease bp
18
Q
what controls vessel diameter
A
changes in volume (dehydration) and wall compliance
this can also affect bp
19
Q
what happens to our bp is we are very dehydrated
A
can faint bc our bp decreases
20
Q
what happens to our bp with an increase of plaque in arteries
A
increases bp
21
Q
what organ regulates blood volume
A
kidney (renal)
22
Q
what really affects blood flow the most
A
RESISTANCE!!
23
Q
small change in vessel diameter does what to flow
A
HUGE EFFECT. Going from 1mm to 3mm increases flow from 1 to 81
to the 4th power
24
Q
what is the volume of blood called
A
flow rate
25
what is the distance an amount of blood travels called
flow velocity
26
what is the heart mostly composed of
myocardium
27
what are the two types of myocardium and what has only 1%
myocardial CONTRACTILE: majority of heart
myocardial AUTO-RHYTHMIC: 1% of heart
28
what are the cells called that are the pacemakers of the heart
myocardial autorhythmic cells
29
what heart cells have sarcomeres
myocardial contractile cells
30
what are unique features about myocardial autorhythmic cells
no sarcomeres
smaller and no driving pressure force
conducting cells -> set rate of beat
31
what sets the pace of the heart
SA node. 70/80 bpm
32
what is the backup pacemaker cell
AV node. 40-60 bpm
33
what the the backup pacemaker if a "heart block" occurs?
bundle of His and Purkinje fibers 20-40 bpm
34
what is the purpose of 2 way valves
ensures one-way flow
35
what are the AV valves
tri and bicuspid
36
what are the semilunar valves
aortic and pulmonary valves
37
what do papillary muscles and cordae tendinae do
prevents blood from shooting back into atrium
38
do cardiac cells do E-C coupling?
YES!
39
are autorythemic cardiac cells spontaneous or non?
spontaneous
40
what ion plays a HUGE role in cardiac AP
Ca2+!!!!!
41
are myocardial contractile forces variable or all or nothing?
VARIES!
42
What determines the force of a myocardial contractile cell generated
the force is generated by cardiac cell is proportional to the number of crossbridges that are active AND sarcomere length at the beginning of contraction
43
what determines the # of crossbridges that are active
the amount of Ca2+ available to bind to troponin
44
what does more stretch and more blood mean in terms of force generated? small or large?
the more stretch and more fluid = GREATER FORCE
45
how are myocardial contractile cells SIMILAR to neurons (2)
1. DEpolarization due to Na+ ENTER
2. REpolarization due to K+ EXIT
46
how are myocardial contractile cells DIFFERENT from neurons (1)
LOOONG AP due to Ca2+ entry in cell -> prevents tetanus
47
what is tetanus and what could it do to the heart
a continuous tonic spasm of muscle
could result in fainting or be fatal
48
5 phases of AP of myocardial contractile cells
1. resting membrane potenital
2. depolarization -> Na+ entry
3. initial repolarization -> Na+ channels CLOSE
4. Repolarization Plateau: Ca+ OPEN and FAST K+ CLOSE
5. Rapid Repolarization: Ca+ CLOSE and SLOW K+ OPEN
49
do cardiac cells have long or short refractory periods?
LONG! lasts almost as long as the muscle twitch
50
how does lidocaine work
blocks fast-voltage gated Na+ channels in the neuronal cell membrane that is responsible for signal propagation.
51
how do we not feel pain with lidocaine
the membrane of the postsyn. neuron will NOT depolarize because there was no AP.
It doesn't prevent the pain signals going to the brain but rather it doesnt allow pain signals to even be produced
52
what is the point of epinephrine in lidocaine
vasoconstrictor -> prolongs numbing effect
53
what could happen if a patient was hyper-reactive to lido?
because the heart has voltage gated Na+ channels, they could potentially go into cardiac arrest or faint
54
what cells makes up the conducting system of the heart (SA, AV, Pukinjie, His)
myocardial autorhythmic cells! 1% !!
55
what cells control the heartbeat rhythm and pace
myocardial autorhythmic cells
56
what causes autorhythmic cells to have an unstable membrane potential
leaky channels
57
what is the resting membrane potential called for autorhythmic cells?
pacemaker potential -> has an unstable membrane potential
58
what is the autorhythmic cell's resting potential called?
pacemaker potential phase
59
what happens during the pacemaker potential phase
Na+ flows in through If channels -> as membrane potential slowly rises, If channels CLOSE and one set of SLOW Ca2+ channels open
60
what happens during the depolarization phase of autorhythmic cells
threshold is reached -> AP due to voltage gated FAST Ca2+ channels. TONS OF Ca2+ during this following in!!
61
what happens during the rapid repolarization phase in autorhythmic cells
at peak AP, Ca2+ CLOSE and K+ channels OPEN -> repolarization -> K+ channels close at the end of this phase
62
what would happen if If channels were blocked
heart would stop
63
how do depolarizations of autorhythmic cell spread to adjacent contracile cells?
Gap junctions!! intercalated discs!
64
rising phase of AP in autorhythmic cells is due to
Ca2+ entry
65
rising phase of AP in contractile cells is due to what
Na+ entry
66
what is the repolarization phase like in contractile cells?
EXTENDED plateau due to Ca2+ entry
RAPID phase caused by K+ efflux
67
what is the repolarization phase like in autorhythmic cells
RAPID -> caused by K+ efflux (flowing out)
68
do heart cells have a hyperpolarization?
not normally
69
what heart cells have a refractory period?
contractile cells do. its long due Na+ channel gated not resetting until end of AP
70
pathway of electrical conduction in heart
1. SA node depolarizes
2. electrical activity goes to AV node
3. depolarization spreads slowly across atria (conduction slows through AV node)
4. depolarization moves rapidly through ventricular conducting system to apex of heart
5. depolarization wave spreads upward from the apex
71
what is the internodal pathway
pathway from SA -> AV
routes the direction of electrical signals through atria so the heart contracts in a coordinated fashion to pump efficiency from atria -> ventricles (atria contract first -> SA node sets pace)
72
AV node during conduction:
signal from SA reaches AV. AV delays, allowing ventricles to fill before they contract
73
Bundle of His action in conduction:
signal continues down bundle of His, through L and R bundle branches into Purkinjie fibers.
ventricles contract bottom up
74
what is the purpose of the AV valves (bi/tricuspids) during contraction
AV valves stays closed to prevent backflow during contraction
75
what does an ECG show
heart's electrical activity and sum of many AP
76
what do the waves show on an ECG in general
show depolarization/repolarization of atria and ventricles
77
what does the P wave represent
the atria depolarize then contract
78
what does the P-R segment represent
atria contraction continues. electrical signal travels through AV node and bundle of His -> slows signal down/AV node delay
79
what does the QRS wave show
ventricular contraction begins @ end of Q wave and continues through T wave. atrial repolarization occurs during R wave
80
what does the T wave show
ventricles repolarization
81
what does the T-P segment show
heart is silent- everything is relaxed
82
EKG segment shows
baseline between waves
83
EKG interval shows
combo of wave and segment
84
mechanical events are slightly ______ behind electrical events
depolarization vs. muscle contraction
LAGGED
85
diastole means
relaxed
86
systole means
contraction
87
MECHANIAL EVENTS
what is happening in the heart at the beginning of cycle
R atria filling with blood from vena cavas
L atria filling with blood from pulmonary veins
AV valves open -> ventricles filling
88
MECHANIAL EVENTS
what happens during #2 -> atrial systole/atria contract
completes last 20% of ventricular filling
some blood is forced back into vena cava
89
MECHANIAL EVENTS
isovolumic ventricular contraction -> first phase of ventricular contraction
what happens
AV valves forced closed -> LUB
semilunar valves still closed until pressure inside ventricular becomes greater than pressure in aorta
atrial diastole is going on during this time -> all 4 valves closed (isometric contraction of heart, atria relaxed and blood begins to flow back into atria)
90
MECHANIAL EVENTS
ventricular ejection events
completion of ventricle systole: ventricle contraction pressure becomes high enough to push semilunar valves OPEN and blood ejected to arteries.
blood is pumped into the pulmonary/peripheral systems
atria -> relaxed, continuing to fill with blood
91
MECHANIAL EVENTS
isovolumic ventricle relaxation events
ventricular diastole: ventricular relaxation and pressure drops -> still higher than atrial pressure
arterial blood pressure flows backward pushing semilunar valves shut -> second heart sound DUB
cardiac muscle cells of ventricles are relaxing. AV valves wont open until pressure within ventricles decreases lower than pressure in atria
92
at what point could you hear blood regurgitating through the semilunar valve back into the left ventricle?
isovolumic ventricular relaxation
93
what is stroke volume
amt of blood pumped per contraction/heartbeat "one pump"
94
what is end diastolic volume
max volume of blood in ventricle during mechanical heart cycle (max amt before contraction) EDV
95
what is end systolic volume ESV
the least volume of blood in a ventricle during a mechanical heart cycle (min. amt after contraction)
96
is there blood left in the ventricular after contraction?
yes, safety mech. allows for compensatory change w/ change in vessel capacity
97
what is stroke volume
volume of blood before contraction minus volume of blood after contraction
98
is stroke volume constant
no. exercise and other factors can change it
99
what is cardiac output
volume of blood pumped by 1 ventricle in a given period of TIME (1 min)
indictor of total blood flow in body but DOESNT reflect where the distribution occurs in the various body tissues
100
what are the 4 determinates of cardiac output
1. heart rate
2. preload
3. contractility
4. afterload
stroke volume = 2,3,4
101
what happens to blood if one side of the heart begins to fail?
blood pools in the circulation behind failing side
LV fails -> blood pools in lungs (LA goes to lungs) -> problems in limbs -> swelling of ankles/feet
everything gets backed up!
102
SA node control is dominated by which branch on NS
PNS -> slows/narrows ion channels -> slow HR
103
tonic control of HR is dominated by what NS
PNS
104
why cant heart transplant patients do exercise?
increase HR due to loss of PNS control and decrease in HR response during exercise -> chronotropic incompetence
105
increase in Na and Ca2+ does what to HR and what NS
SNS -> increases HR
106
increase in Ca2+ and decrease in K+ does what to HR and what NS
PNS -> decrease heart rate
107
what is epinephrine
synthetic form of adrenaline
increases HR
relaxes smooth muscle in airways (dilation)
constricts blood vessels -> decreases swelling
SNS
108
what is cholinergic
PNS
form of AcH -> PNS drug
PNS is known as the cholinergic system
slows HR -> vasodilation
109
what is a chronotropic drug
increases of decreases HR
110
what is chronotropic incompetence
the inability of the heart to increase its rate in proportion with increased activity or demand
111
what controls HR during exercise
catecholamines
slow HR at start of exercise then reduced peak HR and a delay return towards resting values after cessation of exercise
112
what is preload (SV)
stretch of myocardial cells in ventricular walls (determined by volume of blood in the ventricle at the beginning of contraction)
113
what influences the contractility of the heart
the stretch of muscle cells, chemical/electrical factors (hormones drugs etc)
114
what is the Frank-Starling Law
increase in SV -> increase in EDV
115
how is EDV determined via a process
venous return
116
what 3 things affect venous return
1. skeletal muscle pump
2. respiratory pump
3. sympathetic innervation of veins
117
what would venous dilation due to SV
reduce it -> reduction in venous return
118
what is iontropic
a chemical that changes the force/speed of contractility
119
what does a POS. inotropic drug do and examples of them
increase/strengthen contractility -> pump MORE blood
increase SV with fewer heart beats (forceful and shorter contractions)
epi. norepi and adrenaline
used for congestive heart failure
120
what does a NEG. inotropic drug do and examples
weaken/decrease contractility -> pump LESS blood
decreases SV with fewer heartbeats
beta-blockers -> vasodilation
used for hypertension, chronic heart failure
121
what is afterload
combined load of EDV and arterial resistance during ventricular contraction
122
what factors affect afterload
arterial constriction -> vasoconstriction increases BP
BP is an indirect measure of afterload
123
what is ejection fraction
percentage of EDV ejected with 1 contraction
amt of blood pumped out of ventricles in 1 heartbeat relative to total amt of blood in ventricle
124
what factors determine cardiac output -3
heart rate and SV and afterload
125
does pulmonary BP have higher or lower BP than systemic
LOWER! would damage lungs if high
has much lower resistance too
126
where is the site of exchange in the vascular system
capillaries
127
what vessel has a lot of elasticity and collagen
large arteries
128
capillary microcirculation:
what has HIGH hydrostatic pressure and LOW oncotic pressure
capillary side. fluid OUT
129
capillary microcirculation:
what has LOW hydrostatic pressure and HIGH oncotic pressure
venule side.
fluid IN
130
capillary microcirculation:
what factors determine direction of water exchange
hydrostatic and oncotic pressure
131
capillary microcirculation:
what determines the rate of exchage
permeability of the capillary itself
132
how is systemic blood pressure created -3
1. ventricular contraction
2. elastic recoil in arteries sustains driving force - windkessel effect
3. blood flow obeys the rules of fluid flow
133
what is the most important factor influencing blood flow
RADIUS!!!
134
what is MAP
avg pressure in large arteries over a cardiac cycle
135
flow of blood in veins is influenced by -3
1. one-way valves
2. skeletal muscle/diaphragm
3. gravity
136
what is MAP proportional to
CO x peripheral resistance in arterioles
137
what 4 things influence MAP
1. blood volume
2. CO
3. blood flow into/out of arteries
4. distribution of blood b/w arteries and veins
138
what NS controls the heart
PNS and SNS
139
what NS controls vessels?
SNS! NOT PNS
140
what vessel has the greatest influence on resistance
arterioles (accounts for 60% of total resistance)
141
what influences arteriolar resistance -3
local tissues metabolic needs via signaling (exercise)
ANS sympathetic reflexes (paracrine)
hormones
142
active hyperemia
increases metabolic activity and increases blood flow (blushing/redness) can be from exercise
143
reactive hypereria
vessel occlusion, increase flow
144
adenosine (paracrine)
released by cardiomyocytes low on O2
145
histamine (paracrine)
vasodilator
146
serotonin (paracrine)
vasoconstrictor
147
how do different receptors respond to the SAME NT
different receptors will cause different responses!
148
what organs gets the most amount of blood due to their filtering jobs
kidney and liver!
149
what is the most observable sign of any type of hyperemmia?
blushing/redness
150
does reactive hyperemia do in terms of homeostasis
goes AGAINST it
151
what is systemic control
hormones influence kidney excretion of ions and H2O
hormones such as atrial natriuretic peptide and angiotension III
152
what is systemic control in terms of NS
ANS sympathetic reflexes --> CNS mediated, MAP maintenance and body temp. homeostasis
such as norepine and epine
153
norepine and epine are what
types of catecholamines. act as NT and hormones
154
where does norepine come from (NS)
ANS -> sympatheic division.
PNS DOES NOT AFFECT VESSELS
155
does PSNS affect vessels?
NO! SNS does (autonomic)
156
what does norepinephrine do
CONSTRICTION. tonic control of arteriolar diameter
increase in norep = vasoconstriction
decrease in norep = vasodiliation
157
Norepine from from the ANS neurons do what
help maintain arteriole wall SM tone
158
Blood flow through individual blood vessels is determined by what
vessel's resistance to flow
159
what happens to the blood pressure proximal and distal to the constriction
proximally the pressure INCREASES
distally the pressure DECREASES
160
increase to resistance does what to flow
DECREASES
inversely proportional
161
what are baroreceptors sensitive to
pressure!
162
what does carotid reflexes detect
PRESSURE. sends feedback to medullary cardiovascular control center if there is an increase in P
163
what do carotid chemoreceptores respond to
blood O2 levels
164
what does the hypothalamus regulate
temp and SNS reponses
165
what does the cerebral cortex regulate
emotional responses (blushing)
166
what is vasovagal syncope
seeing blood and fainting. CV system overreaction to certain emotional triggers
167
what is syncope and what causes it
fainting
no blood to brain
dehydration, SNS dysfunction, heart failure (hypotension)
168
normal BP
systolic < 120mmHg
diastolic < 80mmHg
169
why does tachycardia decrease the perfusion of the coronary circulation? EXAM Q!!!
bc the amt of tine the ventricles spend in diastole is decreased over the span on a minute
170
air follows the principle of
bulk flow
171
what moves air?
we use muscles like the diaphragm to create a pressure gradient
NO muscular pump like the CV system!
172
what is external respiration
movement of gases b/w the environment and body's cell
173
what is cellular respiration
intracellular rxn of O2 w/ organic molecules
174
main steps of external respiration (4)
1. atmosphere to lung
2. lung to blood exchange
3. transport of gases in the blood
4. blood to tissue exchange --> cellular respiration
175
what are the 2 functional divisions of the pulmonary system
conducting zone and respiratory zone
176
what is the conducting zone
provides rigid conduits for air to reach the sites of gaseous exchange
nose, pharynx, larynx, trachea, bronchi, bronchioles
warms, humidifies and filters air
gaseous exchange doesn't take place in this zone
177
does gas exchange take place in conducting or respiratory zone?
respiratory zone
178
what is the respiratory zone
site of gaseous exchange!
respiratory bronchioles, alveolar ducts and alveoli
179
what are the sites of the conducting zone
nose, pharynx, larynx, trachea, bronchi, bronchioles
180
what are the sites of the respiratory zone
respiratory bronchioles, alveolar ducts and alveoli
181
what is involved in quite inspiration
diaphragm
182
what is involved in quite expiration
NO muslces
183
what muscles are used during inspiration during exercise
accessory ms, diaphragm, external intercostal, scalene, SCM
184
what muscles are used during expiration during exercise
abdominal ms, internal intercostal
185
what happens to thoracic volume and air pressure during inspiration
thoracic volume INCREASES
air pressure DECREASES
186
is expiration a passive or active phenomenon
passive!
muscles of expiration are only needed during forced breathing and NOT quite
187
how can you strengthen your abs and obliques
blowing balloons
188
what are the branching structures of airways that supply air
in the lungs -> trachea, brochi, and bronchioles
189
what are the functional units of the respiratory system where the exchange of respiratory gases occur
alveoli
190
is air exchange 100% ?
no! not everything makes it to the alveoli!
191
where does the exchange of respiratory gases occur
alveoli
192
where does the blood-air barrier exist in gas exchange
in the lungs -> alveoli
193
where does pulmonary gas exchange occur
across the fused basement membrane of the type I pneumocytes and endothelim
194
what is the point of the fused BM in the type I pneumo and endothelium
prevents air bubbles from forming in the blood and from blood entering the alveoli
195
what epi is the trachea lined with
PSCC with goblet cells
196
what is mucus secreted by in the airway
goblet cells and seromucus cells
197
how does saline play a role in the airway
epi cells secrete saline -> lowers mucous viscosity and allow cilia to push mucus towards the pharynx (from the trachea)
198
where does cilia move mucous towards from the trachea
pharynx!
199
what is Dalton's Law
total P of a mixture of gases in the sum of the P of the individual gases
200
what is a partial P
P of an indivudal gas in a mixture
201
what does the presence of water vapor do gas
it dilutes the contribution of other gases
humidity makes it hard to breathe since the O2 has been diluted with H2O
202
what is Boyle's Law
increase V, decrease P
203
during fetal development, what grows faster than the lungs
the thoracic cage and parietal pleura -> neg. pleural cavity P
204
what maintains the sub-atmosphere intrapleural P
2 opposing forces -> elastic recoil of the lung creating an inward P and the chest wall pulling outward
205
what does the pleural fluid serve as
a lubricant so lungs can move freely in chest wall
206
what allows for chest expansion
parietal (outside) and visceral (inside) pleura
(these two together create the pleural cavity)
207
during inspriation, what ms contract
diaphragm, external intercostal, scalene
208
what happens during inspriation
increase in thoracic volume and decrease in air pressure and air moves into lungs
diaphragm contracts and flattens
209
what happens during expiration
inspriatory muscles RELAX --> decrease in thoracic volume and increase in air pressure --> outward movement of air = expiration
210
are expiratory muscles involved during quite expiration
NO!
211
T/F: inspiration is the expansion of the lungs
FALSE! it is drawing of air into lungs
212
T/F: expiration is NOT the contraction of the lungs
True! it is releasing air from lungs
213
what are the 4 pressure changes during quiet breathing
1. inspiration
2. expiration
3. alveolar pressure
4. intrapleural pressure
214
is expiration or inspriation take longer
expiration
215
what is residual volume (lungs)
amt of air leftover after exhaling. never really changes. always have leftovers
216
what is tidal volume
amt of air that moves in/out lungs w/ each cycle
217
what is inspiratory reserve volume
forced inspiration. more than normal
218
what is expiratory reserve volume
forced expiratory. more than normal
219
what is total lung capacity
amt of air lungs can hold (abt 6 liters)
220
what is pneumothorax
a collapsed lung that cannot function normally
221
what happens when you get stabbed in the lung
when air/fluid enters space b/w parietal and visceral linings -> lung collapses due to subatmo. and atmo pressure equalizing
222
T/F: a normal lung is both complaint and elastic
TRUE
223
what is compliance and equation
ability to stretch
change in V / change in P
224
what is elastance and equation
ability to recoil
= 1/complaince
225
what does restrictive lung disease mean
lungs cant fully EXPAND/INHALE (Decrease in V)
226
examples of restrictive lung diseases
fibrotic lung diseases, scoliosis, obesity, inadequate surfactant production
227
what does obstructive lung disease mean
lungs cant EXHALE normally (increase in residual V)
228
examples of obstructive lung diseases
COPD, emphysema, and asthma
229
what do we use to test for lung diseases
spirometry. do forced expiratory volume in 1 second
230
an infant that lacks surfactant has what type of lung disease
restrictive.
decreases inspiratory reserve V
231
obstructive lung disease treatment
pursed-lip breathing
232
surfactant increases/reduces surface tension
REDUCES
233
what happens if there is no surfactant
the alveoli will collaspe
234
smaller alveoli produce more/less surfactant than larger ones
MORE -> P is inversely proportional to radius
235
what is in surfactant
surface active agents
proteins and phospholipids -> disrupt cohesive forces b/w H2O molecules
236
what cells secrete surfactant
type II pneumocytes cells
237
what is the one factor that changes in our system
RADIUS! inversely proportional to resistance
238
what is alveolar dead space
volume of air inhaled that does not take part in gas exchange
inspired air at the end of each inspiration in the anatomic dead space is exhaled unchanged bc it remains in the conducting airways
239
slower breathing means what it terms of O2 exchange
MORE O2 exchange and O2 moving through system
240
eupnea is
normal quiet breathing
241
hyperpnea is
increased respiratory rate and/or V in response to increased metabolism
242
hyperventilation is
increased respiratory rate and/or V without increased metabolism
243
hypoventilation is
decreased alveolar ventilation
244
tachypnea is
rapid breathing -> usually increased respiratory rate with decreased depth
245
dyspnea is
difficulty breathing
246
apnea
cessation of breathing
247
what is hyperventilation
fast breathing unaccompanied by increased metabolic demands of your body
increase O2 and decrease in CO2 partial pressure
248
what is hypoventilation
super slow breathing
decrease in P O2, increase in P CO2
249
blood flowing past an under ventilated alveoli does/does not get oxygenated
does NOT!
leads to constriction of arterioles so that the blood is diverted to a better ventilated alveoli
250
changes in bronchiole diameter is mediated by what
levels of CO@ in the exhaled air passing through them
251
is pO2 lower in arterial blood or alveoli's
arterial blood pO2 is lower than alveolis
O2 moves down conc. gradient
252
tissue pCO2 is lower/higher than that of blood
lower! CO2 moves down conc. gradient
253
in the venous blood, pCO2 is higher/lower than alveoli's
HIGHER
CO2 moves down conc. gradient -> exhaled out
254
breathing super slow does what in terms of rate of exchagne
you get a higher rate of exchange
255
is the pH in arterial or venous higher
higher in arterial
arterial 7.4
venous 7.37 (little more acidic)
256
what is hypoxic hypoxia
low arterial pO2 (high altitude)
257
what is anemic hypoxia
decreases amt of O2 bound to hemoglobin (blood loss)
258
what is ischemic hypoxia
reduced blood flow (heart failure)
259
what is histotoxic hypoxia
failure to use O2 bc of poison (cyanide)
260
what does the total oxygen content of arterial blood depend on
amt of O2 dissolved in plasma and bound to Hb
261
how does O2 enter the plasma
diffuses across alveolar epi cells and capillary endothelial cells
262
what affects diffusion
gas solubility
263
is CO2 or O2 more soluble in liquid
CO2 is 20x more soluble in liquid than O2
harder for O2 to go into bloodstream since it's MUCH easier for CO2
264
Hb + O2 =
HbO2 -> oxyhemoglobin
265
what are 2 characteristics of Hb-O2 binding
its reversible and co-operative! (one binds, they all do)
266
total blood O2 content =
dissolved O2 + O2 bound to Hb
267
more than 98% of O2 in blood is bound to
Hb in RBC
less than 2% is dissolved in plasma
268
what does O2 diffuse through to attach to a RBC
alveolar, BM, capillary endothelium, cell membrane of RBC
269
can cells survive without hemoglobin?
NO!
4x more O2 available than is needed by cells at rest.
270
what is the primary factor that determines the % of available Hb binding sites that are occupied by O2
plasma P O2
271
what is percent saturation of hemoglobin
plasma p O2 is the primary factor that determines the % of available hemoglobin binding sites are occupied by O2
272
what are. the3 determinates of arterial pO2
1. gas composition of inspired air
2. alveolar ventilation rate
3. efficiency of gas exchange b/w alveoli and blood
273
how does altitude sickness occur
decrease in barometric P and decrease in pO2 = O2 is more dispersed in air. NO pressure gradient for it to travel down
274
a right shift on the graph for O2-Hb binding means
decrease Hb affinity for O2 -> O2 actively unloads
275
a left shift on the graph for O2-Hb binding means
increase Hb affinity for O2 -> reluctant to release O2
276
CO2 reacts with H2O to form
carbonic acid
277
what is the Bohr Effect
increase in CO2 in plasma -> lower blood pH
hemo releases O2 (occurs with exercise)
278
what does a decrease in CO2 do to blood pH
increases blood pH (more basic)
hemo picks up or retains O2 (wont release O2)
279
increasing temp does what to the affinity of Hb for O2
DECREASES affinity of Hb for O2
280
a decrease in 2,3-BPG does what to the affinity of Hb for O2
INCREASES affinity of Hb for O2
chronic hypoxia and anemia both increase 2,3-BPG production
281
low P in fetus does what to O2 affinity
increases O2 affinity
low pO2 environment
282
3 ways CO2 is transported
7% dissolved in plasma
23% bound to Hb
70% converted to bicarb ion (most CO2 is transported as bicarb -> buffer)
283
Does the diaphragm fire sponetaneously?
NO! requires neural control
284
what controls the diaphragm
control is based on monitoring of O2, CO2, H+ levels in arterial blood and extracellular fluid
285
ventilation is based on what
chemoreceptor and mechanoreceptor linked reflexes (neg. feedback loops) modulated by brainstem neurons
286
respiratory neurons in the medulla nucleus tractus solitarius control what
inspiratory (dorsal respiratory group) and expiratory (ventral respiratory group) ms
287
what do neurons in the pons do
integrate sensory info and interact w/ medullary neurons to influence ventilation
288
what is found in the dorsal respiratory group and where is it
nucleus tractus solitarius
IN MEDULLA
289
in the pons, the pontine respiratory group do what
they recieve sensory info from DRG -> influences the initiation and termination of respiration
290
what do the pons do
coordinate a smooth respiratory rhythm and influence ventilation
291
what primarily regulates ventilation
CO2
levels of respiratory gases are sensed by central and peripheral chemoreceptors which are associated with arterial circulation
292
where are peripheral chemoreceptors
located outside CNS in carotid/aortic bodies -> ALWAYS exposed to arterial blood
293
where do peripheral chemoreceptors sense changes in
CO2, O2, and pH
carotid/aortic O2 sensors release NT when pO2 in lowered
294
CO2 crosses BBB to react with water to form
H2CO3 -> H+ and HCO3-
295
H+ and HCO3- have a potent direct stimulatory effect on what kind of chemoreceptor?
CNS!
296
do pH changes in plasma influence the CNS chemoreceptors directly?
NO!
CO2 enters the CSF easily, H+ ions cross very slowly
297
is pCO2 remains high for several days, what do the CNS chemorec. do
adapt to it by increasing the concentration of HCO3- that buffer the H+
298
what are irritant receptors?
receptors in the airway that are stimulated by irritants that enter airway (coughing and bronchoCONSTRICTION)
299
what are stretch receptors? how do they get activated?
receptors in the lung that signal brainstem to terminate inspiration (Hering-Breuer inflation reflux).
activated by increase in tidal volume
