Question Answer
For gas to flow through an airway what must exist a pressure gradient
the airway begins that the mouth
pleural pressure is usually what compared to the alveoli negative
Paw press at the airway opening -mouth
Palv press of the alveoli (although not the same, it can be interchangeable with Pplat)
Pbs press of the body surface, or atmospheric pressure
Ppl intrapleural press
Pta Transairway pressure, Paw-palv, causes air to move into lungs (also same as PIP-Pplat, press needed to overcome resistance on inhalation)
Ptt Transthoracic pressure, Pbs-Palv, press needed to allow NPV to work, press needed to expand lungs and chest wall at the same time
Ptp Transpulmonary pressure, Palv-Ppl, press needed to keep alveoli open
Ptr Transrespiratory pressure, Paw-Pbs, press needed to allow for positive press ventilation (same as CS+RAW)
Pta+Palv PIP
what type of ventilation is most similar to spontaneous breathing NPV
how does NPV work vacuum press against the chest wall puts sub-atmospheric press at the body surface that is transmitted to the pleural space and then to the alveoli
In NPV, Paw pressure is what (high or low) compared to pressure in the alveoli Paw is high (0) and alveoli is negative-allowing gas to flow into lungs
Hazards of NPV <Venous return, abdominal pooling, <blood press, “tank shock” <venous return caused by abdominal pooling
What is passive recoil all exhalation is passive, regardless of type of breath and vent mode
what type of ventilation reverses the normal pressure gradients PPV
What type of hypoxemia is most responsive to O2 therapy V/Q mismatch
What are the 4 factors that determine the ability to oxygenate surface area(can improve), diffusion coefficient(cannot), press gradient (can-fio2)), a/c membrane thickness(cannot)
What is the most important factor in ability to oxygenate surface area
O2 content is directly related to? Hb saturation and PaO2
CaO2 and CvO2 CaO2 eqs (Hbx1.34)SaO2+(PaO2x.003), norm 20 Vol%, CvO2 eqs (Hbx1.34(Svo2+(PvO2x.003), norm 15 Vol%
What can affect O2 content? decreased Hb, decreased O2 saturation, anemia, PaO2 is down (hypoxemia), surface area
Oxygen delivery is a function of CaO2 and CO, DO2 eqs (CaO2xCO)x10
Normal DO2 1000mL/O2/min, 900-1200 mL/O2/min
Normal CaO2 is 20vol%
Transpulmonary Pressure Ptp, maintains alveolar inflation, keeps alveoli open and stable, Ptp eqs (Palv-Ppl)
Transthoracic pressure Ptt, across the chest, press needed to expand the lungs and chest wall at the same time, (allows NPV to work), press required to overcome elastance, Ptt eqs (Pbs-Palv)
Transairway pressure Pta, press required for air to flow into lungs, press to overcome Raw, Pta eqs (Paw-Palv)
Transrespiratory Pressure Ptr, press required to inflate lungs during PPV, therefor Ptr is press required to overcome elastance and resistance, Ptr eqs (Paw-Pbs)
How is volume determined V eqs FxT(I), lung volumes change as a result of flow caused by a change in pressure (or flow x inspired time)
Alveolar pressure during NPV (spontaneous breathing) 0 at rest, neg on insp, O at PIP, positive on expiration and back to O for rest (0-0+0)
Alveolar pressure for PPV O at rest, positive on inspiration, positive at PIP, positive on expiration and back to 0 at rest(0+++0)
Alveolar air equation (Hb-47)FIO2-(PaCO2x1.25), norm is 80-100 mmHg, can be 675 mmHg on 100% FIO2
Oxygen consumption VO2, norm is 250 mL/O2/L/min, VO2 eq (CaO2-CvO2)10xCO
How can PEEP improve oxygenation increased FRC causes increased surface area, also improves distribution by recruiting alveoli (atelectasis, consolidation) >RV and CL
How does PEEP contribute to MAWP increases it 1:1, peep up 1-map up 1
What is the purpose of using PEEP helps to open (recruit) and stabilize collapsed or fluid filled alveoli to increase surface area and diffusion, improves V/Q mismatch, and PaO2. >FRC, >RV, >CS, >PaO2
What are the hazards of PEEP barotrauma, auto-PEEP, >VD, overdistention, <CL, and >MAWP
What kinds of barotrauma’s are caused by high PEEP pneumothorax, PIE (pulm interstitial emphysema), sub q emphysema, pneumopericardium and pneumoparitineum (air in stomach cavity)
PEEP of +5 will cause what increased CS, increased PaO2 with no effect on CO
PEEP of +10 will cause what increased CS, increased PaO2 and increased CO
PEEP of +15 will cause what over distention, decreased CS, decreased PaO2. Causes blood flow to be redistributed to poorly ventilated alv and increases shunting
How does PEEP or PPV cause increased VD? <CL (>press and <vol) causes a decrease in perfusion, increasing deadspace.
VT for ARDS, COPD, Normal and Neuro ACNN, 4-8, 8-10, 10-12, 12-15, ARDS is 6-8, but but can go down to 4 for permissive hypercapnia
RR for ARDS, COPD, Normal and Neuro ACNN, 12-15, 10-12, 10-12, 8-10
What is the starting VT and RR for most pts RR-10 and VT at 10, ABG at 20 mins
What can cause PaO2 decrease with PPV overdistention, supine position causes >V/Q mismatch, atelectasis with >secretions
What is the best position for oxygenation of ARDS pt? prone to improve V/Q
A-a gradient aka A-aDO2 norm (on vent) is 5-10 mmHg on 21%, 30-60 on 100%, potential to oxygenate vs actual, every 50 above norm is approx 2% shunt above norm of 2-3%
What is resp acidosis CO2 >45 and PH <7.35, occurs when VE is inadequate (hypoventilation)
what can cause resp acidosis on ventilated pt VT set to low or RR set to low, VT lost to small ET tube, increased VD/VT ratio, PEEP to high, pulm emboli
Signs vented pt has resp acidosis restless and anxious causing asynchrony, dyspneic,
How can RT better manage vent pt for resp acidosis appropriate VT and mandatory RR settings, VE
finding the desired VE, RR, VT or CO2 (VExCO2)/CO2(D) eqs VE(D) or (RRxCO2)/CO2(D) eqs RR(D) where D is desired
Physiological changes from resp acidosis cerebral vasodilation causing increased ICP, <PH can alter tissue function, Hyperkelemia can cause disrythmias, rt shift in disassociation curve-releases O2 more readily
How can excessive PEEP cause >PaCO2? blood flow is diverted from ventilated alveoli to hypoventilated, resulting in >V/Q ratio
Respiratory Alkalosis defined hyperventilation causes PaCO2 <35 with Ph >7.45, can be caused by dyspnea, anxiety, pain or asynchrony
How can mach cause resp alk VT to high, RR to high, trigger to sensitive (auto-triggering)
Prolonged resp alk can cause what hypokalemia, cardiac arrhythmia’s (av block, PVC, tachycardia, atrial flutter), left shift causes tissue hypoxia from hypokalemia
NaHCO3 required (.25 x BW(kg)) x base deficit/2 equals NaHCO3 required
What is a time constant resistance x compliance and it is always equal for inhalation and exhalation
How long does it take a to expire 95% of VT (RAW x CS)3, because 3 is equal to 95%
PIP peak airway pressure, max pressure of inspiration and the sum of raw and cl or the sum of Pta and Palv
What factors determine PIP press of airway and press nec to inflate alv, so PIP eqs (Paw+Palv) CL+Raw
Pplat plateau pressure, press to overcome elastance (Palv)
How does RT obtain plat press at end of inspiration, during an inspiratory breath hold for .5 to 1.5 seconds, press necessary to inflate alveoli, norm on vent is <30-35cmH2O
What problems can occur with plat press is above 35 cmH2O trauma from sheer force, air leakage from alveoli, release of inflammatory mediators, multisystem organ failure
RAW (RIA) (PIP-Pplat)/(flow in mins/60), norm on vent is 5-12 cmH2O/L/sec, > with edema, bronchospasm, secretions
CS (CVAE) VT(L)/(Pplat-PEEP), norm on vent is .035-.055 L/cmH20, represents lung elasticity and chest wall recoil, < with stiff lungs like ARDS
COPD RAW and CL >RAW and >CL
Mean airway pressure average press above baseline during the entire vent cycle I and E
Calculating Mean airway press (PIP(IT/TCT).5
Calculating mean airway press with PEEP .5(PIP-PEEP)x(IT/TCT)+PEEP
What factors can increase mean airway pressure auto-PEEP, complications of PPV, Etime to short, PEEP to high, manditory breath modes, I time to long, <CL, >RAW, >PIP
Extrinsic PEEP preset PEEP by RT on mach, end exp press above zero
Effect of PEEP on MAWP 1:1, every 1 cmH20 of PEEP applied increases MAWP 1cmH2O
What effect does increased MAWP have on FRC? as MAWP increases, FRC increases, resulting in increased surface area increasing diffusion and increasing PaO2
VC-CMV time or pt triggered, volume limited-volume(time) cycled, continuous mandatory ventilation, press is variable so watch for cardiac probs, best way to control CO2, to long and muscle atrophy
VC-SIMV flow or press triggered, volume limited-volume(time) cycled, synchronized intermittent mandatory ventilation,
Physiologic effects of VC-SIMV <MAP, partial support, min RRset + spontaneous, decreased cardiac problems
ASV adaptive support ventilation, dual support, only available on Hamilton Galileo, RT inputs wt, press, PEEP, FIO2, Itime, cycle time, machine monitors CL and Raw to determine RRset, time or pt trigger based on lung mechanics
PC-CMV aka PCV press Control ventilation, time or pt trigger, press limited-time cycled. Press constant during insp RT sets IT, press and RR, VT based on CL and RAW, mach, pt effort and set press
APRV aka Bilevel airway press relief ventilation, modified CPAP, similar to PC-IRV but for spont breathing pt. Intermittently relieves press from insp to allow for PaCO2 removal
What is the benefit of APRV (bilevel) benefit of CPAP (alveolar recruiting) with improved ventilation, but few vents offer it
PSV press support ventilation, pt triggered, press limited-flow cycled with supplemental press at the beginning of inspiration. Helps overcome resistance of ET and trach tubes, secretions, spasms, and imposed mach resistance, helps insure good spont VT
What are the benefits of PSV <RR, >VT, <muscle activity, <O2 consumption, and pt comfort
VAPS volume assured press support, dual control that guarantees volume, 2 flow sources, first flow rectangle w/constant volume, second descending at press limit
Benefit of VAPS allows VT according to pt demand, improves synchrony, flow one < press-time to <WOB, flow two < airway press by early high flow in insp and lower flow on end expiration
CPAP cont positive press ventilation, small alveolar press to spont breathing pts on I and E to increase alv press, causes alveolar recruiting, benefit is lower FIO2 to maintain PaO2
Bilevel aka APRV CPAP with separate press for insp and exp, great for COPD and ARDS
What is benefit of Bilevel for COPD less alv collapse at end expiration
What is benefit of Bilevel for ARDS <PIP and end exp pressures, with lower FIO2 while maintaining PaO2 and Co2 removal
ATC automatic tube compensation, mach calculates and adjusts for tube resistance automatically based on input of tube size and type by RT
Advantages of ATC better and more accurate than RT calculating, may help w/auto-PEEP, more comfortable for pt than adjusting PSV for tube
PAV proportional assisted ventilation, press, flow and volume are delivered proportional to pt effort, improves synchrony while maintaining good WOB, good for pts w/changing lungs, experimental
CT Tube compliance, CT eq V/P (during insp), since the circuit tubing expands under the press of inspiration, some volume never makes it to the lungs, but exhalation is passive so it is registered by exhalation valve
Why or when might CT be important not enough to be significant in adult with normal lungs, but with child or infant, or very small VT even small loss of volume could be critical
Compressed or compressible volume volume of gas in the circuit or the volume lost in the circuit due to CT, varies based on type of circuit and mach. Most mach’s are capable of measuring and adjusting for CT, if not RT can calc during set up and adjust
Unless contraindicated, how often should a ventilated pt be turned Q2hrs
Best position for pt on a ventilator semi-recumbent head at 30-45 degrees
What is best position for pt on a mach with unilateral lung disease affected lung in non dependent position (bad lung up), > blood flow to good alveoli causing >PaO2, also puts bad lung in postural drainage position (drains secretions)
Best position for pt on mach with ARDS? if able to tolerate, prone is best, recruits dependent zones, improves oxygenation and allows for <FIO2.
Cardiovascular effects of PVV <CO, <venous return, <BP, compression of coronary blood vessels, all can lead to < coronary perfusion and MI, >afterload <contractility and <HR
CO cardiac output, stroke volume x HR
CI cardiac index, CO (L/min)/body surface in sq meters
MAP, mean arterial pressure norm 93mmHg (if Bp is 120/80), <MAP can be caused by shock, >PEEP, >MAWP
ICP intercranial pressure, norm is 5 mmHg, can be increased from brain injury, brain hemorrhage, stroke, masses
How can RT manipulate MAP (mean arterial press) RR, VT, IT, insp pause, ET, PIP, baseline press, insp flow, waveform
what should RT use as determining factor in <MAP (arterial) ABG, to <MAP, if PaO2 is up then reduce PEEP
CPP cerebral perfusion press, quantifies perfusion of the brain, norm is 88-93 mmHg, has the ability to auto regulate (to some degree), CPP eqs (MAP-ICP)
What is PPV effect on kidneys longterm PPV causes pts to retain salt and water, increased plasma renin activity, plasma aldosterone and vasopressin (ADH) and <atrial natriuretic hormone, all leading to reduced urine output
what effect does PPV have on liver and spleen can cause hepatic dysfunction even in normal liver, > bilirubin caused by <blood flow
what is PPV effect on GI tract high incidence of GI bleed and stress ulcers in long term PPV caused by gastric mucosal ischemia. Impaired blood flow to mucosa, < motility causes >bacteria and >infections, gastric distention from cuff leaks, malnutrition
Complications from NG tubes during mech vent include epitaxis, sinusitis, ischemia and necrosis in nares, >raw from small tube size, hard to suction
Complications from ET tubes during mech vent include pressure sores, bronchoventilation, larengealventilation, inadequate cuff inflation, aspiration, cuff press to high, <humidity
Acute complications of mechanical ventilation hemorrhage, canulation of pretrach space, subcutaneous emphysema and pneumothorax
Long term complications of mechanical ventilation artery erosion, hemorrhage, trach erosion
Barotrauma extra alveolar air escapes, where it escapes to is a complication of pressure. Pneumothorax, pheumomediastanum, pneumoparacardium, subcutaneous emphysema, pneumoperitoneum
Oxygen toxicity causes lung tissue damage, increased permeability of A-C membrane, caused by O2 >50% FOR LONGER THAN 24-48 HOURS
What is the physiologic effect of O2 toxicity high O2 exposure causes free radicals production, normally quickly detoxed by antioxidants, but >FIO2 causes >free radicals and free radicals cause >permeability leading to fluid in the alveoli and <CL and more FIO2 to keep PaO2(viscous circle)
VAP ventilator associated pneumonia number 2 nosocomial infection, most often caused by aspiration,vented pt is esp vulnerable (airway is bi-passed), most are gram negative, more are multi-drug resistant staph A
RSBI rapid shallow breathing index, calculates WOB, >105 indicates pt can successfully be weaned, RSBI eqs F/VT
What is best way for RT to prevent vent associated pneumonia semi-recumbent positioning head at 30-45 degrees and gentle suctioning to prevent aspirations, vent change every 48hrs, drain and discard tube condensation, suction top of cuff, gloves and hand washing
What are the usual causes of a vent circuit malfunction cuff rupture, mainstem, laryngeal or esophageal intubation, press caused soft tissue erosion, circuit disconnect, circuit leak (connector, Neb MDI humidifier)
What are the usual causes of vent mach malfunction elec failure, microprocessor failure, exhalation valve failure, internal valve leak, gas supply failure
What are the signs and symptoms of a malfunction dyspnea, tachycardia, tachypnea, hypotension, diaphoresis, access muscles, retractions, paradoxal breathing, asynchrony
What the cardiac hazard of PEEP increases intrathoracic pressure causing increased plural press around the heart, to much can < venous return and < CO
Optimal PEEP PaO2 >60 w/out depressing CO. This allows for adequate PaO2 for tissue delivery, but keeps FIO2 below toxicity <50%
VT on mach for ARDS 6-8, can go down to 4 for ARDS if using permissive hypercapnia as treatment
VT on mach for COPD 8-12
VT on mach for normal lungs 10-12
VT on mach for neuro 12-15
RRset is dependant on what pt status, post op-10-12 (norm), >for ICP and met acidosis, <for COPD and acute asthma
Why do we < RRset for COPD and acute asthma? to allow for >Etime, avoids airtrapping
How does RT increase VE on mach >VT, RRset, or both, VE eq VTxRR
Why is A-a Gradient usually up with PPV gas distribution is redistibuted to nondependented zones with less perfusion, increasing deadspace
Increased VD causes what to the PaCO2 increase, if VE stays the same same
If the Time constant decreases will the alveoli fill faster or slower? faster
Restrictive diseases like ARDS need what kind of I:E times longer I, shorter E
Obstructive diseases like COPD need what kid of I:E times short I and longer E
How does RT measure auto-PEEP end expiration pause, during pause Palv and Paw equalize and total PEEP registers on mach. Intrinsic PEEP eqs Total PEEP-Extrinsic PEEP
What is the best triggering for decreasing WOB flow
When mach is in SIMV, most RT’s add what to spnt breaths to overcome the imposed WOB due to the system curcuits and trach tubes PSV
Max PIP 40cmH2O (not an absolute)
Factors that increase RAW on vented pt airway edema, spasm and secretions
Best way for RT to prevent increased RAW adequate humidy, bronchial hygene, bronchodilators and antiinflamitories
factors that decrease CL alv and interstitial edema, fibrosis and chest wall restrictions
Best ways for RT to manage < CL advocate for pt to med staff for drugs that < vascular load, vasodilators, diaretics and > contractility
Vented pt reaches 35 cmH20 Pplat on VC, what should RT do <VT or change to PC
Hazard of >MAWP reduced venous return and CO in cardiac comprimised pts
Benefits of PEEP >FRC (alv recruiting), <shunting, >CL, <WOB, >PaO2
Hazards of inappropriate PEEP barotrauma, <venous return and CO, >WOB, >Pulm Vascular resistance, >ICP, <renal blood flow, >MAWP
dynamic hyperinflation auto-peep or intrinsic peep
contraindications of PEEP unilateral lung disease and >ICP
why is PPV+PEEP or PPV+CPAP indicated for a pt with refractory hypoxemia? decreased physiological shunts-recruits
what is the benefit of a decelerating flow pattern improves gas distribution to lung units with long time constants by <PIP, <WOB, <VD/VT and <A-a gradient
If inflationary hold has the effect of alv recruitment why dont we use it only used to obtain Pplat, pt’s dont like it, so causes asyncrony, >MAWP, airtrapping in pts with obstructions
where is VT and Peak insp flow the highest at the tip of the ET tube
where is VT and peak insp flow the lowest in the circuit
transpulmonary and transrespiratory have in common both are A-, transpulmonary is palv-ppl and transrespiratory is paw-pbs
transthoracic and transairway have in common both are -A, transthoracic is pbs-palv, and transairway is paw-palv
finding VT VT(D) eqs VTxCO2/CO2(D), where D is desired, used to find target CO2
ALI Acute Lung Injury, is the beginning stage of ARDS, P/F ratio <300
the difference between ALI and ARDS 48 hrs, ALI is P/f ratio <300, ARDS is P/F ratio <200