Physiology Flashcards
Dead space
Area of the lung that is not perfused but is ventilated, meaning there is no gas exchange
Like peor long standing disease
A-a gradient change in a shunt
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
Oxygen content eqution
Cao2 = [hb x saturation x 1.34] +.003 x Pao2
1.34 is how many ml of 2 a hgb can carry
Consumption of o2
Vo2 = hb x (Sat a- sat mv) x 1.34 x co
Delivery of o2
C art o2 x cardiac output
Svo2 mixed venous o2 decrease
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
Arterial content of o2 factors
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
Normal cardiac outputting
5 l/min
Svr
1200 dynes/sec/cm5
Normal oxygen consumption vo2
250 ml/ min
Or 3.5 cc/kg
Normal 70 kilo person is 240
Stated as vo2
Normal mixed venous sat
75 % o2
46 for co2
Dysoxia
Point where oxygen consumtpion vo2 decreases due to do2 decreaseing
Do2 is delivery of o2
Dysoxia and svo2
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
Shunt
An area of the lung that is perfused but not ventilated
V/q ratio is 0
Can be from vsd, mucous plug, right mainsten
Oxygen produces how much atp per molecule of glucose
38
Atp synthase and h+
Allows the h+ to enter the mitochondria after being pumped out by the electron transport chain and makes atp
Post op fever
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
Nitroglycerin affect
Mainly on preload does not affect svo2
Nitroprusside
Causes cyanide toxicity ehich dec use of o2 falsely elevates o2 but at cellular level patient is hypoxic
Ci
Co/ body surface area
Sepsis and mixed venous sat
Increases because mitchondrial use of o2 is impaired
Bohr affect
Essentially means increase co2 binding to hgb causes increwsed release of o2 ( right shift)
Haldane affect statea
Deoxy blood can bind co2 as a buffer
Fick equation
Relates consumption to delivery
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
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
Normal paco2 svco2
40 46
Pao2/fio2 ration in ards
Pcwp in ards
Generally less than 18 to rule out cardiogenic causes
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
Tidal volume increass in ards with resp acidosis
Cant increase tv can only change rr or peep
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
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
Rsbi
Rr / tv
Less than 100 is consistent with. Succesful extubation
Pressure control / pressure limited
A pressure is given irrespective of volume given
Gastric feed stoppage before sx
Should be stopped 6 hrs before surgery
Duodenal is safe
Tpn
Insulin is added for hyperglycemia
High levels of carbs lead to resp failure because of high rq
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
A calculous cholecysistis can lead to
Perforation within 48 hrs
Three buggest risk factors include trauma tpn and surgery
Copd o2 sat to avoid co2 narcosis
35 % o2
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
Bohr affect
Means increasing co2 increases oxygen leaving hgb
Haldane means
The hgb without o2 can bind co2
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
Main determinents of arterial o2
Mainly hgb x sat x 1.34
Dissolved o2 is just .003 x arterial pao2
Elimination of co2
Vco2 =hb x svco2 x co2
Resp quotient
Rq= vo2/vco2
Volatile anesthic affect on resp
Dec co2 responsiveness and hypoxic drive
Troponin
In the muscle is an inhibatory protein which binds to actin in the resting state
Tropomyosin
An inhibatoryprotein which binds to myosin in a resting state
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
Mh and nmdp
Ndmb cannot block a mh contracture because calcium js already released
Earliest sign kf mh
Hypercarbia and tachycadia
Dantrolene
It inhibits transmembrane calcium flux and excitation coupling
In other words decreesses ca release
Must be made i. Sterile water
Mh testing
Halothane caffiene contraction test
Conducted to samples of muscles
Indicated for children w distant relatives
Approximate shunt fraction
5%
From pulmonary veins, thesbian, veins and pleural veins going directly to left atrium
Above which shunt fraction does increasing fio2 not affect pao2
Above 30% shunt there is minimal affect
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.
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
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
Factors that increase periopetive complications
Copd smoking obesity exercise intolerance asthma and age >65
Surgical factors include abdominal thoracix or length of sx
Frc is lowest
12 hours post op 2/2 splinting stlectasis and pos op pain control
Copd and ecg
Right heart stuff with poor r wave progression
Rbb enlarged p wave and mat
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
Peak pressure
Dynamic compliance
The pressure required to keep lungs inflated includes static
Dynamic compliance =volume/peak-peep
Pleatue pressure
Measured w inspiratory hold for pleatue pressure
Static compliance
Pip
Peak - pleatu
This is the resitance flow. Pressure needed tk overcome resistance to flow within airways
Muscle of respiration
Inhalation- external intercostal scm large back maucles
exhalation- internal intercostals and abdominal
Density of gas affecting flow
The higher the density the faster the flow the more turbulent
Reynolds number > 2000 is turbulent
Where are chemoreceptos in brain
4th ventricle
Resp quotiejt
Vco2 / vo2
Co2 increase with apnea
During apnea co2 rises 6mmhg in the first minute and 3mmhg for every minute there after
Hypoxic ventilatory drive
Mainly regulated by carotid bodies at bifurcation of the common carotid artery
Bezold jerish
Brady cardia and hypotenson following pooling of blood when u wud expect tachy
Anticholnergic affects (atropine / glyco)
Anti sialogogue, sedative, increased hr, decreased ion secretion, prevent motion induced nausea, mydriasis dilation, relaxation of les
