Respiratory Flashcards
(299 cards)
1
Q
pleural fluid
A
negative pressure making the lung stick to chest wall
2
Q
pleurisy
A
inflammation of pleural cavity, sharp pain worse on inspiration
3
Q
visceral pleura
A
insensitive to pain, relay stretch sensation only
4
Q
cause of pleurisy
A
viral infections, pulmonary embolism, myocardial infarction, pneumothorax, pericarditis, pneumonia
5
Q
airway geometry
A
divides 23 times, exchange only in last 4 generations (alveolar ducts and alveoli)
6
Q
compliance definition
A
delta volume over delta pressure
7
Q
hydrostatic pressure
A
relative to barometric pressure, cm of water above atmospheric
8
Q
pleural pressure
A
subatmospheric, mouth is open and lungs are held inflated by difference in pressure
9
Q
elastic recoil forces
A
inward for lungs, outward for chest, equal and opposite at FRC
10
Q
functional residual capacity
A
amount of gas present in lungs when mouth is open and respiratory muscles are relaxed
11
Q
source of lung elastic recoil
A
lung tissue elastic from collagen and elastin, surface tension forces (surface tension main contributor to lung recoil)
12
Q
surface tension
A
from cohesive forces between liquid molecules
13
Q
surface tension on alveolus
A
surface tension forces tend to collapse it, towards the center
14
Q
shunt
A
vascular pathway in which there is no gas exchange
15
Q
pulmonary surfactant
A
90% phospholipids and 10% proteins, secreted by alveoli type II cells, mostly dipamitoyl phosphatidyl choline
16
Q
surface tension and pulmonary surfactant
A
more concentrated the surfactant is, more the surface tension is lowered
17
Q
ARDS
A
reduced production of surfactant or increased destruction of surfactant
18
Q
IRDS
A
high level of collapse, administer surfactant using bronchoscope, grunting noises, acts like a shunt
19
Q
inhalation
A
active process, diaphragm, external intercostal muscles (lift the ribs when they contract)
20
Q
accessory muscles
A
shoulder girdle, used in exercise, coughing, sneezing, COPD and emphysema
21
Q
tripod position
A
assumed by people in respiratory distress, optimizes mechanics of respiration by utilizing accessory muscles of neck and upper chest
22
Q
exhalation
A
passive process, diaphragm relaxes, volume decreases, alveolar pressure becomes positive
23
Q
forced exhalation
A
contract internal intercostals, contract abdominal muscles (push guts into the diaphragm)
24
Q
Boyle’s Law
A
pressure inverse to volume
25
transmural pressure
palv-ppl
26
begin inhalation transmural pressure
transmural greater than recoil so lung begins to expand, alveoli increase in size and decrease in pressure
27
end inhalation transmural pressure
forces are balanced, flow is zero
28
chest flail
chest wall caves in, moves in the opposite manner, cannot generate sufficiently low intrapleural pressure during inhalation, mechanical ventilation with positive pressure
29
pneumothorax-tension vs non-tension
shift of mediastinum away from pneumothorax
tension-more air in pleural cavity with each breath
non-tension-not as dangerous
30
atelactasis
no air entering pleural caivty, mediastinal shift to side of collapse
31
spontaneous pneumothorax
without blunt force
32
primary spontaneous pneumothorax
without any existing lung pathology
33
secondary spontaneous pneumothorax
arising due to lung disease
34
traumatic pneumothorax
blunt force trauma
35
iatrogenic pneumothroax
trauma due to medical procedure
36
treatment of pneumothorax
needle aspiration or insertion of one-way chest tube
37
specific compliance
normalizes compliance value to the total lung capacity
38
measurement of compliance
spirometry
39
total compliance
from lung and chest wall, 1/total=1/chest+1/lung
40
lung compliance measurement
esophageal balloon
41
alveolar simplification
tissue destruction due to increased breakdown of structural proteins, happens in emphysema
42
Emphysema morphological
alveolar simplification increases compliance, increases FRC, gas transfer diminished
43
centrilobar emphysema
central portion of secondary pulmonary lobules, superior parts of lung, exposure to chemicals and smoking
44
panacinar emphysema
uniformly destroys alveolus, mainly lower half of lungs. alpha 1 antitrypsin and Ritalin induced emphysema
45
decrease in compliance
fibrosis-more difficult to inflate, loss of surfactant
46
increase in compliance
emphysema, loss of elastic fibers, age, easier to inflate
47
airways resistance
should be in greatest in small airways but decreased by parallel arrangement, greatest airway resistance is in the largest airways
48
silent zone
low airway flow velocity and low airway resistance, applies to small airways
49
expansile forces
positive alveolar and negative pleural keep airway open
50
dynamic compression
pressure outside is greater than the pressure inside, collapsing more likely in forced exhalation because pleural pressure becomes positive
51
Bernoulli's effect on airway
faster airflow=lower pressure, lower pressure promotes collapse
52
cartilaginous rings
prevent collapse caused by high flow rates
53
airway in emphysema
loss of radial traction
loss of tissue
high velocity, low pressure
54
asthma
edema of wall
mucus narrowing airway
high velocity, low pressure
55
tethering
resist collapse better, loss in emphysema patients
56
tidal volume
volume of air inspired or expired with each breath
57
dead space
aire which a person breathes but is not used for gas exchange (fills respiratory passages like the nose, pharynx, and trachea)
58
residual volume
amount of air in lungs which cannot be exhaled or pushed out of lungs
59
total lung capacity
volume of air in the lungs after a maximal inspiratory effort
60
forced vital capacity
amount of air that can be exhaled as quickly during a forced exhalation
61
forced expiratory volume in 1 second
amount exhaled in first second, should be 80% of FVC
62
functional residual capacity
volume of air in lung when lung and chest wall have equal recoil force
63
lung capacity
sum of two or more volumes
64
direct measure of spirometry
TV, FVC, FEV1, FEF
65
not measured on spirometry
RV, FRC, TLC
66
measure of FRC
helium dilution test, COPD use box body plethysmography
67
FRC supine
lesser, body contents pushing into chest
68
FRC and RV with age
increase (softer)
69
obesity and pregnancy on FRC
decrease FRC
70
kyphoscoliosis
abnormal curvature of spine, decrease FRC
71
emphysema
increase FRC, barrel chest syndrome
72
obstructive diseases
```
emphysema
asthma
bronchitis
cystic fibrosis
COPD
```
73
restrictive disease
```
pulmonary fibrosis
sarcoidosis
silicosis
asbestosis
Wegener's granulomatosis
```
74
FEV1 and FEF 25-75
lower in patient with obstructive pulmonary disease
75
FEV/FVC
increased in restrictive
| decreased in obstructive
76
slope PEF curve
decreased in obstructive
| increased in restrictive
77
flow loop obstructive
shift to left (larger volumes)
78
flow loop restrictive
shift to right (smaller volumes)
79
flow loop high airway resistance
no change in volumes
80
variable intrathoracic lesion
tumor of lower trachea, inside the thoracic cage, problem with expiration
81
variable extrathoracic lesion
vocal cord paralysis, fat deposits, outside thoracic cage, airway compressed on inspiration
82
fixed obstructions
foreign bodies or scarring, affect both inspiration and expiration
83
methacholine challenge test
concentrations of methacholine increase, decline in 20%, if less than 8 hyperactive airways
84
problems with methacholine challenge
COPD or allergic rhinitis test positive, asthma with anti-inflammatory will test negative, asthma triggered by specific agents may test positive
85
DLCO
depends on area available for exchange and thickness of the alveolar capillary membrane
measure of conductance
86
Henry's law
amount of gas dissolved in fluids depends on their solubility coefficients and partial pressures
87
flow of gases
always move down partial pressure gradients
88
compartments of O2
dissolved (insolube)-contributes to partial pressure
| bound to hemoglobin-does not contribute to partial pressure
89
Hb
bind 4 O2 molecules, acts as buffer (tissue PO2 only changes a bit from large drop in PO2)
90
alveolar movement of O2
moves from alveolus into capillary and then binds to Hb
91
tissue movement of O2
dissolved oxygen into tissue, lowers PO2 and causes Hb to release O2
92
O2 content
total amount of O2 in blood, dissolved plus bound to Hb
93
arterial to venous
drops 5%
94
anemia
PaO2 normal, PvO2 low, extraction is difficult
95
CO poisoning
reduces O2 transport, PaCO=0, reduces O2 transport, unloading of O2 can only happen when PO2 is very low
96
carboxyhemoglobin
cherry red in color, CO poisoning cherry red skin
97
therapy for CO poisoning
95% O2 or pure O2
| 95% stimulates respiratory centers in brain
98
O2 capacity
maximal amount of oxygen Hb is capable of carrying
decreased-anemia, CO poisoning
increased-polycythemia
99
pulse oximeter
measures saturation of Hb (650 red and 900 blue), does not tell how much Hb and what it is saturated with (not helpful with CO poisoning or anemia)
100
arterial blood gas
tells pulmonary function, venous does not
101
P50
partial pressure of oxygen when Hb is 50% saturated
102
shift to right
H increase
temperature increase
PCO2 high
increase 2,3 DPG
103
erythropoesis
increased blood volume and increased viscosity of blood create increase in workload (polycythemia)
104
transport of CO2
dissolved
as bicarbonate
bound to hemoglobin (carbamino)
105
diffusion of CO2
diffuses faster, requires less of a pressure gradient
106
CO2 in lungs
Cl moves out and CO2 moves in
107
CO2 in tissue
Cl moves in and CO2 moves out
108
carbamino transport
only 5%, fast reaction
109
Haldane effect
PO2 is low and affinity of Hb for CO2 increases, aids in loading of RBCs with CO2
110
CO2 and partial pressure
linear, no saturation kinetics
111
defense mechanism of lung
macrophages released
112
air conditioning
nasal mucosa and nasal turbinates heat and humidify air
113
olfaction
detect odors
114
filtration
particles removed by nose, cilia lining moves others up (mucociliatory escalator)
115
immotile cilia syndrome
scarring and inflammation
116
blood filter
can trap clots, bubbles, fat cells
117
blood reservoir
blood is expelled from pulmonary circulation to systemic
118
metabolism of circulating substances
E1, E2, F2 alpha removed from lungs, A1, A2, I2 are unaffected
119
bronchial circulation
2% of CO, drains into pulmonary veins, shunt
120
pulmonary circulation
represents total cardiac output
121
characteristics of pulmonary circulation
small, low resistance, soft and distensible, low resistance and low pressures
122
zone 1
not perfused (A>a>v)
123
zone 2
intermittently at systolic pressure (a>A>v)
124
zone 3
always perfused (a>v>A)
125
resistance in lung
resistance decreases as you go to the bottom of the lung, perfusion greatest at bottom of lung
126
hemorrhage and general anesthesia
high amounts of zone 1
127
exercise
increase in zone 2 and zone 3
128
PEEP
zone 1, can lead to right heart failure
129
alveolar hypoxia
smooth muscle contracts in low PO2 to try to V/W mismatch
130
recruitment
passive, blood into unperfused capillaries
131
distension
stretching of existing pulmonary capillaries
132
alveolar vessels
high volume, high resistance
| low volume, low resistance
133
extra-alveolar vessels
high volume, low resistance
low volume, high resistance
radial traction helps keep it open
134
mechanical ventilation
PVR elevated, high resistance, leads to right heart failure
135
pulmonary angiography
into pulmonary artery, monitored by X rays, Xenon is insolube
136
V/Q scan
albumin microaggregates with Tc or I, gamma rays, few capillaries=dark
137
pulmonary edema
results in impaired gas exchange
138
hydrostatic edema
caused by increased capillary pressure
no change in Kf and sigma
usually occurs in left heart failure (ex. mitral stenosis), shows Kerly B lines
139
permeability edema
increase in permeability of vessel wall, wall is more porous, principal in ARDS, Kf can change because of bacterial toxins
140
ARDS
persistent lung inflammation and increased capillary permeability, diffuse alveolar damage and pulmonary edema
141
high altitude pulmonary edema
atmospheric PO2 is low, leads to low alveolar PO2, vasoconstriction due to hypoxia, leaking across membranes
142
rate of diffusion
highly impacted by changes of partial pressure
143
factors governing gas exchange
gradient in partial pressure
thickness and properties of membrane
surface area of alveolus
144
perfusion limitation
gas diffuses through the membrane and equilibriates quickly, O2, CO2, N2O
145
diffusion limited
PaCO=0, ability of membrane to transfer CO by diffusion is low
146
DLCO
measure how well a patient's lungs exchange gases, measurement of conductance
147
decrease DLCO
obstructive (decrease area)
restrictive (increase thickness)
pulmonary edema-increase tension
embolus, edema, tumors, sarcoidosis, lupus, anemia, pregnancy, alveolar proteinosis, smokers, lung resection, pulmonary hypertension
148
no change in DLCO
bronchitis
myasthemia gravis
chest wall deformities
asthma
149
increase in DLCO
supine, exercise, polycythemia, asthma, hemorrhage, left to right shunt, obesity
150
ventilation distribution
higher at the bottom of the lung
151
compliance distribution
higher at the bottom of the lung
152
oxygen consumption and CO2 production
250 for O2 and 200 for CO2
153
alveolar ventilation
takes into consideration dead space
154
anatomical dead space
large airways
155
physiological dead space
alveoli that are ventilated but not perfused
156
Bohr's assumption
CO2 in atmosphere is negligible, CO2 expired comes from alveoli (alveoli that are ventilated and perfused)
157
hyperventilation
decreases PACO2
158
hypoventialtion
increases PACO2
159
alveolar ventilation proportions
proportional to metabolic rate, inverse to CO2
160
central chemoreceptors
located in brainstem, sensitive to CO2 in brain interstitium, can adapt
161
peripheral chemoreceptors
cannot adapt, neck region, most sensitive to PO2 (also H and PCO2), located in carotid and aortic bodies
162
Blood brain barrier
permeable to CO2, poorly permeable to H or HCO3
163
buffering capacity of CSF
low, lacks hemoglobin, low HCO3, low protein levels
164
amplification of respiration
adding hypoxia, hypercapnia, and acidosis all work together to amplify respiration
165
supplemental O2 in lung disease
ventilation dependent on hypoxia, giving O2 to patient can depress ventilation
166
phrenic nerve
C3-C5, controls muscles of inspiration, FRC most near normal if damaged phrenic nerve
167
dorsal respiratory groups
inspiratory neurons, responsible for basic rhythm of breathing
168
ventral respiratory groups
inspiratory and expiratory, controls upper airways
169
apneustic
pons, stimulates VRG and DRG, if cut will hold inspiration
170
pneumotaxic center
pons, prevents apneuistic, enhances and fine tines rhythmicity of breathing
171
congenital central hypoventilation syndrome
central pattern generator is inoperative, insensitive to chemoreceptors, no automatic control but voluntary breathing is intact, danger at night when they sleep (permanent tracheostomy)
172
increase in respiratory drive
cocaine, amphetamines, caffeine
173
decrease in respiratory drive
cerebral edema, intracerebral abnormality, acute poliomyelitis, ingestion of alcohol, opiates, benzo, barbituates, anesthetics
174
body temperature on ventilation
deep hypothermia depresses ventilation
fever increases ventilation
painful stimuli increase ventilation and panic
175
cheyne-stokes breathing
gradual increase in volume and frequency of breathing, PCO2 changes in advance of PCO2 in respiratory neurons, corresponds to brain PCO2
176
Biots respiration
hyperapnea, meningitis patients, deep long pauses
177
Kussuads
deep movements, drive high and more frequent, diabetic ketoacidosis
178
obstructive sleep apnea
inspiratory process is intact
179
central sleep apnea
signal from thoracic fades
180
high pressure environments
treatment of gaseous gangrene (wound healing)
SCUBA
caissons for bridges
181
increase in pressure
1 atmosphere every 10 meters
182
compression on descent
mask squueze
ear drum rupture
middle ear squeeze
183
expansion on ascent
pneumothorax, dissection of mediastinum, gas emboli, exhale continuously when going to surface to avoid
184
oxygen toxicity
too much can cause alveolar and endothelial membrane damage, due to peroxide and oxygen radical interactions (normal air at 6 ATA can cause seizures in 5-10 minutes)
185
nitrogen toxicity
acts the same way as alcohol, the bends if rise too rapid-bubbles
186
hypoxia of high altitude
peripheral chemoreceptors sense hypoxia, increase ventilation
187
acute adjustments
acute increase in ventilation due to peripheral chemoreceptors
188
acclimation to altitude
hyperventilation, increased hematocrit, increased capillary growth, plasma volume decrease (reduced water intake)
189
acute mountain sickness
greater than 8000 feet, experience headaches, insomnia, weakness, associated with fluid retention, treated with diuretic
190
high altitude cerebral edema
ataxia, swelling causes brain ischemia and herniation
191
high altitude pulmonary edema
most serious, highest mortality, most commonly seen in athletic young males
192
ideal V/Q ratio
0.8
193
shunt
ventilation but not perfused
194
A-a gradient
bigger the gradient, poorer the exchange, normal between 5 a and 15
195
V/Q top of the lung
over ventilated and contribute to dead space (high at the top)
196
V/Q bottom of the lung
shunt like exchange (low at the bottom)
197
lung transplant outcomes
successful in fibrosis, in emphysema single lung transplant didnt help because air went to the bad lung (higher recoil in new lung vs high compliance in old lung)
198
V/Q to partial pressures
inverse to PaCO2
| direct to PaO2
199
treatment for right heart failure
nitric oxide reverses hypoxic pulmonary vasoconstriction, selectively dilates ventilated blood vessels
200
nitroprusside
increases blood flow to all lung segments, including those that are not well ventilated
201
right to left shunt
leaves left atrium without being oxygenated
202
absolute intrapulmonary shunts
true shunts
203
low V/Q mismatch
hypoxemia
increased A-a gradient
hypercapnia
204
compensation mechanism for V/Q mismatch
alveolar hypoxia leading to smooth muscle contraction
| stimulation of ventilation
205
result of compensation of V/Q mismatch
normalizes carbon dioxide
| does not normalize oxygen
206
limit of ventilation
```
emphysema
bronchitis
asthma
restrictive disease
pneumonia is a classic shunt
```
207
A-a gradient contributions
gravity causing V/Q mismatch
shunts
increases with age due to wear and tear
smaller in supine position
208
diagnosing a shunt
100% oxygen, if PaO2 increases drastically it is a low V/Q mismatch
209
causes of hypoxemia
```
air with low PO2
hypoventilation
shunts
low V/Q mismatch
diffusion problem
```
210
high V/Q ratios
pulmonary emboli, top of the lung
211
pulmonary embolus
high V/Q, local inflammation which then destroys surfactant and alters capillary permeability that causes combination of low and high V/Q mismatches
212
pulmonary embolism ventilation
increase in ventilation, work harder to breathe leading to low V/Q
213
contents of perinephric spaces
kidneys, adrenal glands, proximal ureters, perirenal fat
214
contents of anterior pararenal space
pancreas (except tail), second and third part of duodenum, aorta, inferior vena cava, ascending and descending colon
215
intravenous pyelogram
replaced by CT
216
pyelonephritis
striated nephrogram-alternating stripes or wedges of opacified and nonopacified parenchyma caused by nonhomogeneous edema
217
renal cysts
ubiquitous, easily recognized but complicated cysts are more difficult to assess in terms of a benign or malignant lesion
218
chest imaging modalities
plain radiography
computed tomography
magnetic resonance imaging
219
technique
AP-at bedside
PA-preferred
lateral
220
level of inspiration
10th rib posteriorly
221
penetration
lower thoracic vertebrae should be visible, bronchial and vascular structures behind the heart should be seen
222
rotation
spinous processes should be at the medial end of the clavicles
223
angulation
if beam is angled toward head, lordotic view results
| clavicles above the level of the ribs
224
hilum
Right anterior
| left superior
225
pleura
should not be visible
226
fissures of lung
minor is seen on PA
| major is seen on lateral
227
right hemidiaphragm
higher due to presence of liver
228
left bumps of mediastinum
aortic arch
pulmonary trunk
left ventricle
229
retrosternal
RV
230
right side
right atrium
231
airspace opacity
alveoli are filled with dense material
232
silhouette sign
airspace opacity resulting in loss of lung-mediastinum or lung-diaphragm interface
233
interstitial opacities
thin linear or reticular opacities
234
patterns of pneumonia
lobar-pneumococcal
lobular-staphyloccocal
interstitial-viral, mycoplasma
235
atelectasis
collapse of lung, post operative due to mucus plugging, mediastinum shifts toward opposite side due to contralateral hyperinflated lung
236
transudative
low protein
237
exudative
high protein
238
diagnosing pulmonary embolism
CTA
239
lung masses
solitary-primary lung carcinoma
| multiple bilateral masses-metastatic disease
240
renal capsule
fibrous capsule that can be stripped off the surface of the kidney
241
renal cortex
outer zone of kidney
242
renal medulla
inner zone of kidney consisting of pyramids and columns
243
renal sinus
space within the kidney that is occupied by the renal pelvis, calices, vessels, nerves, fat
244
renal papilla
apex of renal pyramid where urine is excreted into the minor calyx
245
minor calyx
receives urine at the papilla, several minor calyces combine to form major calyx
246
major calyx
formed by union of minor calyces, combine to form the renal pelvis
247
renal pelvis
funnel shaped superior end of the ureter that lies within the renal sinus
248
ureter
muscular duct that carriers urine from the kidney to the urinary bladder
249
risks for hypertension
coronary artery disease, congestive heart failure, stroke
| highest correlation is with stroke
250
normal
251
pre hypertension
120-139/80-89
252
stage 1
140-159/90-99
| treat with mono drugs
253
stage 2
>160/>100
| treat with combo drugs
254
benefits of lowering blood pressure
prevents strokes better than MI
255
compelling indications
```
heart failure
diabetes with proteinuria
Coronary artery disease (prior MI)
chronic renal insufficiency
CVA
```
256
Guyton model
altered renal set point necessary to maintain hypertension
257
renovascular hypertension
arteriograms remain gold standard
| stenosis causes one to sense low BP and secrete renin
258
hyperaldosteronism
nonstimulatable renin and nonsuppressable aldosterone
hypokalemia in face of ACE inhibitor is red flag
stimulate renin with diuretic and suppress aldo with volume expansion
259
pheochromocytoma
autonomous production of vasoconstrictors (epinephrine and norepinephrine)
260
hypertension in CRF
significant renin stimulation, inhibitor of sodium pump
261
essential hypertension
genetics
| environmental-stress, alcohol, dietary salt, smoking, sedentary
262
causes of hypertension
primary (essential) more common than secondary
263
malignant hypertension
medical emergency, acute vascular injury in context of HTN, found on retinal examination
264
secondary hypertension
early, without family history, severe or difficult to control
265
types of renovascualr hypertension
fibromuscular dysplasia-young, female, familial
266
atheromatous
older, correlates with PVD
267
grading of fundoscopic exam
I-narrowing
II-AV nicking
III-hemorrhages or exudate
IV-papilledema
268
risk factors for atherosclerosis
```
smoking
dyslipidemia
>60
male or postmenopausal female
family history
```
269
uncompicated hypertension
diuretics
270
diabetes
ACE inhibitors or ARB
271
myocardial infarction
beta blocker
272
systolic heart failure
ACE inhibitors or ARB
273
pulmonary responses to exercise
increased ventilation and improved V/Q matching
274
cardiovascular responses to exercise
increase in cardiac output and redistribution of blood flow
| important in determining maximum O2 consumption
275
VO2 max
highest rate of O2 consumption that can be achieved during maximal exercise
276
plateau in VO2
primary criterion that indicates VO2 max has been reached
277
determinants of VO2 max
genetics is major determinant, training, peaks at 18 and then declines, females lower (gap decreases with training)
278
O2 uptake
increases linearly until plateau
279
minute ventilation
increases linearly until disproportionate increase at ventilatory threshold
280
arterial CO2
constant until ventilatory threshold is reached, metabolic acidosis triggers increase in ventialtion that causes PaCO2 to drop
281
arterial pH
constant until ventilatory threshold where acidosis occurs
282
PaO2
relatively constant during exercise
283
initial increase in ventilation
mediated by central command mechanism, delayed responses are mediated by mechanical and chemical signals arising from skeletal muscles and cardiovascualr reflexes
284
autonomic nervous system activation
mechanoreceptors and chemoreceptors, feed forward mechanism in anticipation of exercise (decreases vagal output and increases sympathetic output), net result is increase in force and rate of contraction
285
mechanical mechanisms
muscle pump activity, respiratory activity to enhance blood flow and venous return
286
metabolic mechanisms
vasodilator metabolites for contracting muscles
287
cardiac output from exercise
increases due to increase in heart rate and stroke volume
288
heart rate
increases in direct proportion to exercise intensity
289
stroke volume
moderate increases but plateaus, maintained by pumping muscles, larger inspirations, venoconstriction and arterial vasodilation, sympatheric stimulation, lusitropy, atrial kick, declines when those mechanisms cannot keep up
290
systemic vascular resistance
decreases as intensity increases due to vasodilation
291
systolic blood pressure
increases progressively, pulse pressure also increases
292
mean arterial pressure
increases less than would be expected because CO increases and SVR decreases
293
blood pressure and HR
usually inverse but arterial baroreceptor reflex is operating at higher set point so it does not fire to slow HR
294
blood flow to skeletal muscles
net effect of widespread sympathetic stimulation is shunting of blood flow from inactive tissues to actively contracting muscles
295
blood flow to skin
increased due to vasodialtion sensed by hypothalamus, if it is too intense then sympathetic will divert it away
296
blood flow to kidney and splanchnic circulation
decreases due to sympathetic activity
297
changes in cardiac vascular function curves
increases equilibrium point where both increase (due to decrease in SVR and increase in CO)
298
training
increases O2 delivery and O2 extraction, increases maximal stroke volume does not change heart rate), extraction improved by increased capillary proliferation and increased density to decrease diffusion barrier, increased mitochondria, increased plasma compartment (sports anemia)
299
factors to training
genetic component
