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Physiology Flashcards

1
Q

Dead space

A

Area of the lung that is not perfused but is ventilated, meaning there is no gas exchange

Like peor long standing disease

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2
Q

A-a gradient change in a shunt

A

In a shunt A-a gradient is elevated because when you jack up o2 the alveolar o2 goes up but arterial stays the same so the gradient increases

Need to increase areas of ventilation like recruitment maneuver

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3
Q

Oxygen content eqution

A

Cao2 = [hb x saturation x 1.34] +.003 x Pao2

1.34 is how many ml of 2 a hgb can carry

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4
Q

Consumption of o2

A

Vo2 = hb x (Sat a- sat mv) x 1.34 x co

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5
Q

Delivery of o2

A

C art o2 x cardiac output

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6
Q

Svo2 mixed venous o2 decrease

A 
Mv sat (svo2) depends on hgb co and art sat as well as vo2 or also known as consumption of o2
If consumption goes up or other go down that will dec mvo2
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7
Q

Arterial content of o2 factors

A

The major factor is hgb x sat x 1.34

The minor factor is .003 x pao2

This means that arterial content is mostly dependent on the hgb and minorly on the pao2
The pao2 is roughly estimated by 5x o2 inhaled
Normal is 21% so pao2 is normall 100
Arterial saturation is pulse ox

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8
Q

Normal cardiac outputting

A

5 l/min

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9
Q

Svr

A

1200 dynes/sec/cm5

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10
Q

Normal oxygen consumption vo2

A

250 ml/ min
Or 3.5 cc/kg
Normal 70 kilo person is 240

Stated as vo2

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11
Q

Normal mixed venous sat

A

75 % o2

46 for co2

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12
Q

Dysoxia

A

Point where oxygen consumtpion vo2 decreases due to do2 decreaseing

Do2 is delivery of o2

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13
Q

Dysoxia and svo2

A

When vo2 starts outpacing do2, svo2 drops

Delivery of oxygen is equal to cardiac output times arterial o2
Arterial o2 is equal to hemoglobin x arterial o2 sat(pulse ox) x 1.34 +.003 x the pao2

So when mixed venous sat starts dropping we can increase co with inotropes / fluids, or increases artrial o2 by increasing hgb / increasing peep/ or increasing fio2

If that doesnt work then you can decreasin vo2 oxygen consumption

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14
Q

Shunt

A

An area of the lung that is perfused but not ventilated

V/q ratio is 0

Can be from vsd, mucous plug, right mainsten

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15
Q

Oxygen produces how much atp per molecule of glucose

A

38

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16
Q

Atp synthase and h+

A

Allows the h+ to enter the mitochondria after being pumped out by the electron transport chain and makes atp

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17
Q

Post op fever

A

Day 1-2 wind (pna aspiration pe poss atlectasis)
Day 3-5 water (uti 2/2 foley during sx)
Day 4-6 walking ( weins) dvr or pe
Wound 5-7 surgical sight infection
Wonder drug 7+ drug feber or infection 2/2 iv line

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18
Q

Nitroglycerin affect

A

Mainly on preload does not affect svo2

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19
Q

Nitroprusside

A

Causes cyanide toxicity ehich dec use of o2 falsely elevates o2 but at cellular level patient is hypoxic

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20
Q

Ci

A

Co/ body surface area

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21
Q

Sepsis and mixed venous sat

A

Increases because mitchondrial use of o2 is impaired

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22
Q

Bohr affect

A

Essentially means increase co2 binding to hgb causes increwsed release of o2 ( right shift)

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23
Q

Haldane affect statea

A

Deoxy blood can bind co2 as a buffer

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24
Q

Fick equation

A

Relates consumption to delivery

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25
Respiratory quotient
Production of co2 for every o2 consumed Carbs make 1 to 1 o2 consumed Protein is .8 Fat is .7 In patients nearing respiratory failure you can dec carbs and more lipids to dec co2 produxtion
26
Carbonic anyhydrase
Found in rbc and endothelium Makes co2 + water into bicarb Majority of co2 is bicarb. Only a little is actually bond to hgb
27
Normal paco2 svco2
40 46
28
Pao2/fio2 ration in ards
29
Pcwp in ards
Generally less than 18 to rule out cardiogenic causes
30
Ards cc/kg
Initially starts at 8cc per kg then decrease to 6cc/kg | When patient has more then 30 pleatue lressure decrease the tidal volume
31
Tidal volume increass in ards with resp acidosis
Cant increase tv can only change rr or peep
32
In patients with ards and low po2 inc peep or fio2
Increasing peep is better because long term inc of o2 over 60 causes more oxygen radicles
33
Aprv assist pressure release ventilation
Aprv applies two levels of coao. One high, one very low. The high is long low pressure is short. The low pressure is used to ventilate and remove co2 The patient can spontaneously breath at both levels of cpap In ards mean pressure shud stay below 30
34
Rsbi
Rr / tv Less than 100 is consistent with. Succesful extubation
35
Pressure control / pressure limited
A pressure is given irrespective of volume given
36
Gastric feed stoppage before sx
Should be stopped 6 hrs before surgery | Duodenal is safe
37
Tpn
Insulin is added for hyperglycemia | High levels of carbs lead to resp failure because of high rq
38
Regarding stress which conditions is h2 blockers helpful
Mechanical bent > 48 hrs or coagulaopathy Anytging that dec prefusion to stomach cells to make buffer Liver dx or >30% burns severe head injury or hypotension but two must be present
39
A calculous cholecysistis can lead to
Perforation within 48 hrs Three buggest risk factors include trauma tpn and surgery
40
Copd o2 sat to avoid co2 narcosis
35 % o2
41
Rules for o2 mask nc etc
``` 2l nasal canula is 25% 6l nc 40% Simple facemask 40 Venturi mask - can be adjusted Non rebreather >90 ```
42
Bohr affect
Means increasing co2 increases oxygen leaving hgb
43
Haldane means
The hgb without o2 can bind co2
44
Increasing both vo2 and do2
By inc cardiac out You increase the o2 deleivered and consumed You can tell this cuz the mixed venous goes up which means more o2 is making it back to venous blood
45
Main determinents of arterial o2
Mainly hgb x sat x 1.34 | Dissolved o2 is just .003 x arterial pao2
46
Elimination of co2
Vco2 =hb x svco2 x co2
47
Resp quotient
Rq= vo2/vco2
48
Volatile anesthic affect on resp
Dec co2 responsiveness and hypoxic drive
49
Troponin
In the muscle is an inhibatory protein which binds to actin in the resting state
50
Tropomyosin
An inhibatoryprotein which binds to myosin in a resting state
51
Calcium in mh
Calcium inhibits the inhibiton of troponin. In resting muscle tropnin is tightly bound to actin. Calcium inhibits this binding. As this union is weakened tropomyosin is able to act on actin which causes muscle contraction
52
Mh and nmdp
Ndmb cannot block a mh contracture because calcium js already released
53
Earliest sign kf mh
Hypercarbia and tachycadia
54
Dantrolene
It inhibits transmembrane calcium flux and excitation coupling In other words decreesses ca release Must be made i. Sterile water
55
Mh testing
Halothane caffiene contraction test Conducted to samples of muscles Indicated for children w distant relatives
56
Approximate shunt fraction
5% | From pulmonary veins, thesbian, veins and pleural veins going directly to left atrium
57
Above which shunt fraction does increasing fio2 not affect pao2
Above 30% shunt there is minimal affect
58
How will decreasing erv increase shunt
Decreasing frc which means decreasing erv and rv will decrease the total lung capacity for o2 which increases the shunt.
59
Fvc /fev1
Should be within 20% of normal to be normal Only in restrictive disease do u see a 20% drop woth mild disease. With obstructive disease if it is mild frc/fev1 and each individually is preserved
60
Fef 25-75%
It is an early indicator of medium and small airway disease. It has alot of variability and therefore is not used but it is sensitive meaning if u have it then it probably means u have the diseas
61
Factors that increase periopetive complications
Copd smoking obesity exercise intolerance asthma and age >65 Surgical factors include abdominal thoracix or length of sx
62
Frc is lowest
12 hours post op 2/2 splinting stlectasis and pos op pain control
63
Copd and ecg
Right heart stuff with poor r wave progression | Rbb enlarged p wave and mat
64
Abdominal surgery does what to pft
Decreases frc 25% by decreasing the experiatory reserve vplume shifting the graph down because of atlectasis affecting the top of the graph
65
Peak pressure
Dynamic compliance The pressure required to keep lungs inflated includes static Dynamic compliance =volume/peak-peep
66
Pleatue pressure
Measured w inspiratory hold for pleatue pressure Static compliance
67
Pip
Peak - pleatu | This is the resitance flow. Pressure needed tk overcome resistance to flow within airways
68
Muscle of respiration
Inhalation- external intercostal scm large back maucles | exhalation- internal intercostals and abdominal
69
Density of gas affecting flow
The higher the density the faster the flow the more turbulent Reynolds number > 2000 is turbulent
70
Where are chemoreceptos in brain
4th ventricle
71
Resp quotiejt
Vco2 / vo2
72
Co2 increase with apnea
During apnea co2 rises 6mmhg in the first minute and 3mmhg for every minute there after
73
Hypoxic ventilatory drive
Mainly regulated by carotid bodies at bifurcation of the common carotid artery
74
Bezold jerish
Brady cardia and hypotenson following pooling of blood when u wud expect tachy
75
Anticholnergic affects (atropine / glyco)
Anti sialogogue, sedative, increased hr, decreased ion secretion, prevent motion induced nausea, mydriasis dilation, relaxation of les

Anatomy (9 decks)

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