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Anatomy > Physiology > Flashcards

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
Q

Respiratory quotient

A

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

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26
Q

Carbonic anyhydrase

A

Found in rbc and endothelium
Makes co2 + water into bicarb

Majority of co2 is bicarb. Only a little is actually bond to hgb

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27
Q

Normal paco2 svco2

A

40 46

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28
Q

Pao2/fio2 ration in ards

A
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29
Q

Pcwp in ards

A

Generally less than 18 to rule out cardiogenic causes

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30
Q

Ards cc/kg

A

Initially starts at 8cc per kg then decrease to 6cc/kg

When patient has more then 30 pleatue lressure decrease the tidal volume

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31
Q

Tidal volume increass in ards with resp acidosis

A

Cant increase tv can only change rr or peep

32
Q

In patients with ards and low po2 inc peep or fio2

A

Increasing peep is better because long term inc of o2 over 60 causes more oxygen radicles

33
Q

Aprv assist pressure release ventilation

A

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
Q

Rsbi

A

Rr / tv

Less than 100 is consistent with. Succesful extubation

35
Q

Pressure control / pressure limited

A

A pressure is given irrespective of volume given

36
Q

Gastric feed stoppage before sx

A

Should be stopped 6 hrs before surgery

Duodenal is safe

37
Q

Tpn

A

Insulin is added for hyperglycemia

High levels of carbs lead to resp failure because of high rq

38
Q

Regarding stress which conditions is h2 blockers helpful

A

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
Q

A calculous cholecysistis can lead to

A

Perforation within 48 hrs

Three buggest risk factors include trauma tpn and surgery

40
Q

Copd o2 sat to avoid co2 narcosis

A

35 % o2

41
Q

Rules for o2 mask nc etc

A 
2l nasal canula is 25% 
6l nc 40%
Simple facemask 40
Venturi mask - can be adjusted
Non rebreather >90
42
Q

Bohr affect

A

Means increasing co2 increases oxygen leaving hgb

43
Q

Haldane means

A

The hgb without o2 can bind co2

44
Q

Increasing both vo2 and do2

A

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
Q

Main determinents of arterial o2

A

Mainly hgb x sat x 1.34

Dissolved o2 is just .003 x arterial pao2

46
Q

Elimination of co2

A

Vco2 =hb x svco2 x co2

47
Q

Resp quotient

A

Rq= vo2/vco2

48
Q

Volatile anesthic affect on resp

A

Dec co2 responsiveness and hypoxic drive

49
Q

Troponin

A

In the muscle is an inhibatory protein which binds to actin in the resting state

50
Q

Tropomyosin

A

An inhibatoryprotein which binds to myosin in a resting state

51
Q

Calcium in mh

A

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
Q

Mh and nmdp

A

Ndmb cannot block a mh contracture because calcium js already released

53
Q

Earliest sign kf mh

A

Hypercarbia and tachycadia

54
Q

Dantrolene

A

It inhibits transmembrane calcium flux and excitation coupling

In other words decreesses ca release

Must be made i. Sterile water

55
Q

Mh testing

A

Halothane caffiene contraction test
Conducted to samples of muscles

Indicated for children w distant relatives

56
Q

Approximate shunt fraction

A

5%

From pulmonary veins, thesbian, veins and pleural veins going directly to left atrium

57
Q

Above which shunt fraction does increasing fio2 not affect pao2

A

Above 30% shunt there is minimal affect

58
Q

How will decreasing erv increase shunt

A

Decreasing frc which means decreasing erv and rv will decrease the total lung capacity for o2 which increases the shunt.

59
Q

Fvc /fev1

A

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
Q

Fef 25-75%

A

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
Q

Factors that increase periopetive complications

A

Copd smoking obesity exercise intolerance asthma and age >65

Surgical factors include abdominal thoracix or length of sx

62
Q

Frc is lowest

A

12 hours post op 2/2 splinting stlectasis and pos op pain control

63
Q

Copd and ecg

A

Right heart stuff with poor r wave progression

Rbb enlarged p wave and mat

64
Q

Abdominal surgery does what to pft

A

Decreases frc 25% by decreasing the experiatory reserve vplume shifting the graph down because of atlectasis affecting the top of the graph

65
Q

Peak pressure

A

Dynamic compliance
The pressure required to keep lungs inflated includes static

Dynamic compliance =volume/peak-peep

66
Q

Pleatue pressure

A

Measured w inspiratory hold for pleatue pressure

Static compliance

67
Q

Pip

A

Peak - pleatu

This is the resitance flow. Pressure needed tk overcome resistance to flow within airways

68
Q

Muscle of respiration

A

Inhalation- external intercostal scm large back maucles

exhalation- internal intercostals and abdominal

69
Q

Density of gas affecting flow

A

The higher the density the faster the flow the more turbulent

Reynolds number > 2000 is turbulent

70
Q

Where are chemoreceptos in brain

A

4th ventricle

71
Q

Resp quotiejt

A

Vco2 / vo2

72
Q

Co2 increase with apnea

A

During apnea co2 rises 6mmhg in the first minute and 3mmhg for every minute there after

73
Q

Hypoxic ventilatory drive

A

Mainly regulated by carotid bodies at bifurcation of the common carotid artery

74
Q

Bezold jerish

A

Brady cardia and hypotenson following pooling of blood when u wud expect tachy

75
Q

Anticholnergic affects (atropine / glyco)

A

Anti sialogogue, sedative, increased hr, decreased ion secretion, prevent motion induced nausea, mydriasis dilation, relaxation of les

Anatomy (9 decks)

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