1
Q
3 determinants of O2 supply
A
- arterial O2 saturation- % hgb, 97% O2 bound to Hgb
- O2 transport in blood- Hgb level and affinity
- Cardiac output- SV x HR
2
Q
what is a key determinant of O2 saturation?
A
Alveolar gas exchange- cross A-C membrane
3
Q
oxygenation is influenced by what 3 things
A
- Ventilation- ability
- V/Q matching- concentration of O2
- Diffusion- effectiveness
4
Q
PaCO2 is determined primarily by?
A
Ventilation
5
Q
minute ventilation?
A
RR x Vt
6
Q
hyperventilation does what to CO2
A
decreases. more is blown off
7
Q
how do you measure PaO2
A
arterial blood sample
8
Q
what is V/Q matching
A
relationship between air reaching alveoli (vent) and blood reaching alveoli (perfusion- Q)
9
Q
what 4 things determine diffusion
A
- driving pressure - difference in concentration gradient
- diffusion coefficient - how fast it can dissolve/diffuse
- anatomical surface area -pulm edema, fibrosis
- thickness of A-C mem - inflam process
10
Q
what influences driving pressure?
A
Difference of concentration of gases.
the greater the difference the greater the driving pressure
11
Q
what is diffusion coefficient
A
how readily a gas will diffuse across
CO2 is 20 x faster than O2
12
Q
what influences anatomical surface area?
A
lobectomy, plural effusion
13
Q
arterial O2 sat 2 main components
A
- vent
2. gas exchange
14
Q
arterial O2 sat is influenced by? 3
A
- movement of air in and out
- concentration of inspired O2
- gas exchange at the A-C membrane
15
Q
which process of ventilation is active? passive?
A
active - inhalation
passive - exhale
16
Q
pressures when you inhale
A
increases the intrapulmonary pressure
decreases pulmonary pressure
- relative to atmospheric pressure
17
Q
WOB functional residual capacity FRC
A
- volume of air left in lungs after passive expiration
- needed for gas exchange
18
Q
WOB vital capacity
A
- vol of air breathed out after the deepest inhale
19
Q
WOB tidal volume
A
- amount of air moved into and out of the lungs during normal breathing aprox 500cc
shallow resps = decreased Vt
20
Q
WOB is influenced by? 3
A
- resp muscle function
- lung compliance
- airway resistance
21
Q
WOB is
A
overcoming elastic and resistance properties of lungs
22
Q
lung compliance. 3
A
- measure of distension ability. stretch and force required
- chest wall elasticity
- airway resistance
- alveolar compliance
fibrosis
23
Q
if a PT has poor lung compliance…
A
they will have rapid and shallow breaths
24
Q
airway resistance
A
resistance of resp tract to airflow during inspire and expire. Diameter
wheezing, asthma
25
arterial O2 content.
amount to O2 being carried by blood. includes O2 bound to Hgb and O2 dissolved in plasma
26
determinants of O2 transport in blood
1. Hgb level
| 2. Affinity (dissociation curve)
27
stroke vol =
amount of blood ejected from heart
mls/beat
28
stroke vol is influenced by 3
1. preload
2. contractility
3. afterload
29
contractility
ability of heart myofibrils to change their strength of contraction
SNS response
30
preload
volume of blood in the ventricles at the end of diastole
crackles, CVP, JVD norm 2-6), tachycardia
- increased force of diastole = increased preload
31
preload is influenced by
circulating vol and venous return
32
afterload
force or resistance against which the vents have to pump in order to eject blood
DBP, PP, cap refill, skin temp, periph pulses, pt hx
33
primary determinant of afterload
1. diameter of arterioles
| 2. arotic impedance (valve stenosis, vasoconstrict)
34
contractility primary determinant
preexisting medical condition
35
aortic impedance
the sum of external forces that resist left vent ejection
36
oxygen demand is influenced by 3
1. temp (normal 36.4-37.6)
2. physical activity
3. stress physiological or perceived
37
type 1 alveolar cell
more surface area. cover 90-95 %
gas exchange
38
type 2 alveolar cells
smaller only 5%
secrete pulm surfactant to decrease surface tension
found at blood/air barrier
39
minute ventilaion
relationship with blood and CO levels
| RR x Vt = min vol
40
central chemoreceptors
CNS
located in ventrolateral medulary surface of cranial nerves
- sensitive to pH of environment of CSF of altered O2 and CO2** levels
- a rise in CO2 causes = tension of arteries
41
periph chemoreceptors
PNS
in carotid and aortic bodies
- sensitive to chemical concentrations in blood.
- low O2 (hypoxia)**, high CO2, hypoglycemia
when O2 in arterial blood falls, send message to brain to increase ventilation
*****only when O2 falls below 60mmHg****
42
how much O2 is inhaled through the air?
21%
| some gets dissolved into humidity
43
how much atmospheric pressure is inspired O2
159mmHg (21% of atmospheric pressure of 766mmHg)
44
humidification of upper airways drops pressure to
150mmHg
45
pressure pulm/arterial O2 level
40mmHg
46
alveolar partial pressure = ?
100mmHg
47
arterial PaO2 is dependant on 2 factors?
1. inspired O2 pressure (FiO2)
| 2. FRC
48
2 main factors that influence ventilation and CO2 level
1. RR
| 2. Vt
49
aterial CO2 is dependent on 2?
1. CO2 production
| 2. CO2 removal
50
when FRC is decreased?
there is less air in the lungs at the end of expire
51
deadspace
vol gas that passes through the lung that is not perfused and does not take part in gas exchange
- decreases Vt
52
anatomical shunt
blood that passes through venous to arterial circulation that does not take part in gas exchange
- septal or vent defects
53
physiological shunt
alveoli perfused but not ventilated
pneumonia
54
lung compliance dependent on 3 factors
1. chest wall elasticity
2. airway resistance
3. alveolar compliance
55
during inspiration 3:
1. intrathoracic and intrapulmonary pressure decreases
2. diaphragm contracts
3. intercostal muscles contract and thoracic cavity increases in size
56
resp gas is not exchanged in
terminal bronchioles
57
what decreases airway resistance
SNS
58
the most sensitive region of resp tract for trigger cough
carina- the biforcation of trachea that separates L and R broncioles
59
pulm surfactant 4:
1. prevent alveolar collapse
2. reduce alveolar surface tension
3. increases lung compliance
4. secreted by type 2 cells
60
peripheral chemoreceptors are located in
aortic arch
61
V/Q mismatch primarily affects?
O2 levels in arterial blood
62
external vs. internal compliance
ex- stab wound, corset, deformity. prob with diaphragm, broken ribs
in- fibrosis
63
airway resistance is influenced by?
diameter of airway.
wheezing, bronchospasms, increased secretions
64
respiratory muscle function
MS, Guillain Barre, poor nutrition, broken robs, abd ascites, ALS
PT would need mechanical vent to replace muscle function for thoracic abnormalities
65
for CCN what are the significant pulmonary volumes?
VC, Vt, FRC
increased WOB = decreased Vt = increased RR
Assess PTs RR and tidal vol
66
Vital Capacity
indicates if a PT can cough and clear their throat. Do determine if the PT can be extubated.
can they protect their airway?
67
FRC
functional residual capacity
amount of air left in lungs at the end of exhale.
many small airways remain open post-exhale. If airway collapse it is more WOB to open on the next inhale
increased FRC = decreased WOB
decreased FRC = decreased arterial oxygenation = decreased O2 supply to tissues
68
ABG gold standard for ventilation
PaCO2
Alveoli should have a lower concentration of CO2 than in the blood for the CO2 to be expelled toward lower concentration.
Shunt/shunt-like - reduces clearance of CO2 from alveoli disrupting concentration gradient and CO2 cant diffuse out of blood will build up as PaCO2
69
tidal volume
amount of air inhaled with each breath. inverse relationship with RR
```
hypervent = decreased TV
shallow = decresed TV
```
70
what are chemoreceptors
plays feedback that incresaes ventilation. central and peripheral both sensitive to CO2 levels in blood
sense change and send message to brainstem to increase ventiation by increasing RR and/or depths of breath
71
PaCO2 is the primary influence on?
ventilation
72
< 60mmHg O2 in arterial blood =
moderate degree of hypoxemia
73
what is the key determinant to O2 saturation and supply?
1. alveolar gas exchange
74
diffusion is influenced by?
1. thickness of membrane
| 2. difference in concentration of gasses
75
external respiration
takes place in lungs and across alveolar mem
76
internal respiration
gas exchange across the membrane that separate tissues and cells of body organs from blood
77
what is alveolar gas exchange
physical movement of gas by diffusion across A-C membrane (ACM)
78
what are the two components of gas exchange?
1. diffusion
| 2. V/Q matching
79
4 main factors that influence diffusion in lungs
1. thickness of A-C mem
2. driving pressure -concentration gradient. supplemental O2 NP
3. anatomical surface area
4. diffusion coefficient - what is more diffusable, CO2
80
CO2 levels determined primarily by
ventilation
81
when ventilation inadequate what happens to driving pressure
decreased CO2 exhaled = Pa CO2 increases = decreases driving pressure
82
the movement of O2 across the membrane is influenced by? 2
1. ventilation
| 2. diffusion
83
diffusion impared
O2 less diffusable that CO2. decresaed surface area would impact decrease O2sat
84
when V/Q properly matched...
optimal gas exchange
85
what happens to air if person lying on their side
the lung below will receive more air = more blood
ex. if PT has right lung pneumonia - position PT on left side
86
shunt/shunt-like
alveoli partial or non-ventilated but fully perfused
part: secretions, bronchoconstrict
shunt: pneumonia, atelectasis
87
dead space/dead space-like
alveoli fully ventilated but not perfused
dead-like : person with low CO
dead : PE
88
ventilation influenced by factors that affect getting air into and out of the lungs : 3
1. compliance
2. resistance
3. resp muscle strength
vent assessed by PaCO2 values
89
why does hypoxemia occur in V/Q mismatch?
causes local or regional hypoxia, triggering vasoconstricion
O2 cannot pass the barrier (A-C mem) and then less in bloodstream for tissues
90
what affects Hgb dissociation curve
1. pH
2. PaCO2
3. temp
91
right shift curve
decreased pH (acidic), increased CO2 and increased Temp
decreased affinity- increases cellular oxygenation but could cause depletion eventually
Right Release
92
left shift curve
increased pH (alkolitic), decreased CO2, decreased Temp
increased affinity - Hgb remains saturated but PaO2 driving pressure affected impacting cellular oxygenation
Left
93
normal PaO2 =
normal SaO2 =
normal PaCO2 =
PaO2 = 80-100mmHg
<80- >60 = mild hypoxemia
<60- >40 =mod hypoxemia
<40 = severe hypoxemia
SaO2 = 93-100%
PaCO2 = 35-45
94
Hgb O2 trasport:
inspired O2 meets prefusion--> PaO2 in plasma binds to Hgb becomes SaO2 (oxyhemaglobin)--> released back into plasma again as PaO2 to diffuse into cells to meet demand
95
% SaO2 in blood to Hgb
97% to Hgb and 3% left in plasma
96
what percent of O2 carried in blood is used at cellular level?
25%
| 75% venous returns to heart and lungs remains saturated
97
diffusion is reliant on
driving pressure
concentration gradient
98
if there is low Hgb then what happens to O2
there will be less avail for O2 to bind with Hgb so less to be transported to tissues
99
if there is a left shift then...
the increased affinity means that for any given SaO2, the PaO2 will be lower than normal.
need SaO2 higher to ensure adequate PaO2
less avail for tissues
drive more O2, warm her up, give PRBC transfuse
100
CO =
HR x SV (amount of blood in one beat mls)
the amount of blood pumped out of the heart in 1 min
75mls of blood per beat, HR 70/min x 75mls = 5250 mls or 5.2L/min
101
S1 is associated with
closure of mitral and tricuspid valves
high pitched and heard at apex
102
S2
aortic and pulmonary valves closing
103
pulse pressure is? normal number
difference between systolic and diastolic 120-80 = 40
104
these decrease contractility 3
1. decreased O2
2. Inotropic drugs
3. electrolyte imbalance
105
veins can be referred to as
capacitance vessels (active constriction)
106
veins contain what % of circulating blood vol?
75%
107
stimulation of SNS =
1. increased HR
| 2. increased contractility
108
primary pacemaker of heart
SA node
109
optimal stretch of cardiac myofibrils that support optimal contractility =
starlings law
110
tone of vessels?
diameter and elasticity
111
primary indicators of preload
1. CVP
2. S3- hear second dubb = PT need lasix
3. POCUS - point of care ultrasound
4. JVD? (right side heart)
112
secondary indicators of preload
1. crackles - decide if HF issue or infectious issue (left side heart)
2. edema
3. skin turgur
4. mucus membranes
5. in/outs / daily weights
113
common afterload assess parametres:
1. PP (norm 40)
2. DBP <80 = dilated, >80 = constricted
3. cap refill
4. color limbs
5. temp limbs
6. periph pulses
114
vasoconstriction is what type of response?
SNS and RAAS
115
what happens to CO and SV if vasodialted?
SV increased. vents can eject more
| CO - increased even though BP low
116
vasoconstricted
can have normal BP but low CO because heart is working harder to eject through narrow arteries
117
diastolic BP is the best indicator of?
Tone. indicates the degree of vasodilate/constrict
118
PP is altered by
force of contraction of vent, arterial tone and vessel diameter
119
what is a good indicator of organ perfusion?
Mean BP or MAP
often used to titrate drugs and fluid therapy
2distolic + systolic / 3 = organ perfusion
120
what will the body do if contractility of heart impaired?
SV will fall so HR will increase to maintain CO
compensatory response by SNS
121
SV has 3 determinants
1. contractility
2. preload
3. afterload
122
increased preload examples 5
1. excess circulating vol
2. decrease intrathoracic pressure
3. increase vent filling time
4. constrict veins (decreases venous capacitance)
5. increase venous return
123
decreased preload ex. 6
1. decreased circulate vol
2. increased intrathoracic pressure (harder for blood to return to heart)
3. decreased vent filling time
4. dilated veins
5. decreased venous return
6. tachycardia
124
if preload is decreased what happens to contractility
decreased
125
frank starling law =
if you increase the vol into heart, CO will increase to a point when the actin/myosin molecules cannot stretch any farther then contractility can be impaired and over stretched
- increased preload = increased contractility
- increased pressure = increased stretch myofibrils
- overstretched myofibrils = decreased contractility
126
what happens to contractility and preload if a PT has HF?
If contractility imapired then vents dont empty effectively during systole = more vol left in vents at end systole (increased ESV) = heart fills with more blood during diastole = greater than normal amount to blood in vents at end of diastole (increased EDV) = increase in preload.
less stretch = greater pressure
vents less distensible = less compliant
127
what happens to afterload if you decrease contraction?
decreases SV and blood flow leaving heart
128
how do you assess vessel diameter? and what does that affect?
measure the pulse pressure
<40 = narrow/ vasoconstriced = increased afterload and resistance
129
what does the inflammatory response and hyperthermia do to afterload?
decreases
130
what are catecholimines? and what do they do to afterload?
epi/norepi (from adrenal glands)
increase
131
name things that determine contractility
1. preload
2. SNS
3. amount of Ca+ in myocardial cell
132
name things that decrease contractility
1. low O2 supply to the heart
2. negative inotropis drugs (BB's, CCB's)
3. electrolyte imbalance
4. preexist medical cond
133
name things that increase contractility
1. electrolyte imbalance
2. circulating catecholemines (epi/norepi)
3. inotropic drugs (digoxin, dopamine, dobutamine)
134
how is ejection fraction measured?
what is normal %?
what is measured?
if EF < 30% = ?
Echo
>50%
% blood going into right left atrium and % leaving left vent
if < 30 = decreased contractility
135
the ANS key role 3:
1. regulate cardiovascular system
2. alters HR
3. changes SV by exerting influence on contractility and arterial tone.
these manipulate CO and vessel diameter and are important in mntning organ perfusion.
136
the ANS has 2 divisions:
SNS and PNS
which neurotransmitters are for SNS? PNS?
SNS: epi and norepi (adrenergic or adrenalin)
PNS: acetlylcholine (cholinergic)
137
PNS receptors location and 2 main effects
maybe not important
atria, AV junction and vents of heart
leaves brain to vegas nerve
1. slow down rate of impulse at SA node
2. slow transmissions of impulses through the AV node
= decreased HR
138
SNS receptors location and innervates:
maybe not important
receptors in:
1. systemic vasculature
2. skin
3. lungs
4. GI system
5. kidneys
innervates: SA node, AV node, ventricular myocardium
139
SNS receptors 2 main types
what is it designed for?
Alpha and Beta
short term action. in chronic PTs SNS in overdrive = increased cell metabolism and O2 demand
140
Beta 1 receptors located? what do they do?
one heart
located: SA node, AV node and myocardial cells
they:
1. increase HR,
2. speed on conduction,
3. automaticity (firing of cell) and
4. force of contraction
141
Beta 2 receptors located? results in ?
two lungs/two legs
located: smooth muscles of bronchioles and arterioles supplying skeletal muscle
they:
1. vasodilate arterioles**
2. bronchodilation**
3. increase intestinal motility
4. increase breakdown of glycogen and lipids
142
Alpha receptors located and results?
located: skin**, peripheral circulation, gut** and kidneys**
they:
1. vasoconstrict** arterioles in skin and peripheral circulation
2. vasoconstrict** in gut and kidneys
= increase BP
143
what do BB do?
block beta receptors so neurotransmitters cannot connect inhibiting the effects of SNS
= decrease HR, conduction, firing and contraction
144
what does inotropic drugs so?
dopamine and dobutamine...
mimic action of SNS stimulating beta receptors
= increased HR, conduction, firing and contraction
145
norepiepherine does what
vasoconstricts
drug of choice for excess dilation like sepsis
146
key source of input to regulate the ANS? sensed by what?
BP
sensed by barroreceptors
147
where are barroreceptors located? what do they do?
aortic body and carotid sinuses .
sense changes of stretch of vessel wall
148
factors influencing metabolic and O2 demands 3.
1. temp
2. physical activity
3. stress
149
3 main compensatory mechanisms
1. neurological: SNS
2. hormonal :RAAS
3. chemical: action from chemoreceptor response
150
if CO decreases, explain compensatory mechanisms...
if decreases to alveoli perfusion is deminished (creating dead space or dead space-like)...
- decrease in pressure changes will be sensed by the baoreceptors
- triggers ANS to compensate: SNS will increase HR, increase contractility and vasoconstrict
- arterial O2 falls and will be sensed by chemoreceptos to stimulate resp centers in brainstem to increase RR and depth (when PaO2 < 60mmHg)
- the increase in ventilation will increase O2 avail at A-C membrane, support diffusion, and help O2 saturation = increase O2 supply from source
151
if CO drops that blood flow though kidneys is reduced (and urine output drops)?
- kidneys will respond by releasing hormones in RAAS which will increase circulating preload, and BP by increasing afterload (vasoconstrict)
152
what 4 outcomes does the RAAS provide?
1. increased preload
2. increased afterload
3. increased CO
4. increased BP
153
what does angiotensin 2 do? 3
1. potent vasoconstrictor = increased afterload and BP
2. stimulate release aldosterone from adrenal cortex = reabsorbs Na+ and H2O = increased vol and preload
3. triggers production of vassopressin (ADH) = reabsorb H2O = increased vol and preload
154
what happens to the chemoreceptors if SaO2 is decreased?
what else is activated?
chemorecptors trigger resp center to increase RR and Vt.
SNS also activated
both attempt to restore O2 supply
155
what will the SNS do if there is decreased Hgb
Hgb = deceased transport = SNS to increase HR
156
how do cells get from aerobic to anaerobic?
hypoxia cells shift from aerobic to anaearobic = lactic acid.
locally this causes - pre-capillary sphincters to relax = increased blood flow and O2 supply
globally - chemoreceptors sense decrease in pH and trigger center responses = increase RR and Vt, increase vent and SaO2
NOTE: this also increases cardiac work, resp work, and muscle work = increase O2 demand
mod 2 CC
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