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Mech vent chapt 40
WillWallace Mech Vent chapt 40
| 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 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 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 effect 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 |
| difference between ALI and ARDS | 48 hrs, ALI is P/f ratio <300, ARDS is P/F ratio <200 |
Created by:
williamwallace
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