| Question | Answer |
| S&S of decreased vent drive are | bradypnea is hallmark and ultimately apnea, decreased RR causes a decreased LOC |
| *VD/VT norm | 25 to 40% |
| PEEP | Positive End Exp Press, norm 5-15, application and maintenance of press at the airway throughout the exp phase of pos press ventilation. |
| *Imposed WOB | press created by endotracheal tube, vent circuit or autopeep that causes increase pressure and therefore increases WOB |
| Shunt | (type 1) aka Refractory Hypoxemia, complete block of ventilation to alveoli, most common cause atelectasis, pulm ed and pneumonia. Does not respond to FIO2, refractory to O2 |
| What is the most common cause of Type II vent failure | increased WOB |
| Extrinsic PEEP | Set by RT on Vent machine |
| *VT norm | 5-8mL/Kg IBW |
| *Indication for vent w/refractory hypoxemia | A-aDO2 >350 on 100% or P/F value <200 |
| 3 types of respiratory muscle weakness are | central failure, transmission failure, contractile failure |
| *What is the cardinal sign of increased WOB | tachypnea (causes decreased VT which causes decreased CO2) |
| Why do severe burns cause increased WOB | severe burns over large area of body causes hypermetibolic state which causes increased CO2 production which in turn causes increased VE |
| Type I Failure | Hypoxemic respiratory failure, PaO2 <60 on R/A, caused by VQ mismatch, shunt, diffusion impairment, perfusion/diffusion impairment, altitude |
| *Resp muscle fatigue/failure | (type II) neuromuscular, resp pump fails, caused by ALS, GB, MG, muscular dystrophy. |
| *Decreased P/F ratio | increased shunt |
| Most extreme shunt | ARDS |
| Altitudes effect on FIO2 | (type 1) increased altitude decreases BP, this causes decreased press in alveoli and not enough press to oxygenate, decreases PaO2 |
| *Indications for vent w/inadequate lung expansion | VT <5mL/kg, VC <10mL/kg, RR >35/min |
| *Indications for vent w/inadequate muscle strength | MIP ≥-20, VC<10mL/kg, MVV <2L/minxVE |
| Indications for vent support are | severe refractory hypoxemia, inadequate alv vent, inadequate lung expansion, inadequate muscle strength and increased WOB |
| *MIP norm | -80 to -100 cmH2O |
| *VC norm | 65-75mL/Kg IBW |
| *Type II failure | hypercarbia, PaCO2 >50 on R/A, caused by decreased vent drive, resp muscle fatigue or increased WOB |
| *Most easily reversible respiratory muscle weakness is | contractile, (overworked) |
| Transmission failure/fatigue | exertion induced, reversible impairment in the transmission of neural impulses |
| *P/F value norm | 350-450 |
| What are the 3 causes of acidosis | resp center not responding to incr in CO2, Resp center responding but signal not getting through, or brain & nerves working but bellows are not (contractile failure). |
| What is the relationship between RAW and WOB | conditions that cause increased RAW make pts work harder to exhale |
| *A-aDO2 norm | 10-20 on room air, 25-65 on 100% O2, every 50 is approx 2% shunt above norm of 2-5% |
| *Chronic vent failure | (type II) develops over days, weeks or months, COPD (hypercapnia), Obesity (hypoventilation) and kyphoscoliosis are most common causes. Kidneys compensate w/incr HCO3 (50-50club) |
| Increased WOB | (type II) pt has normal drive to breath, normal nerves and muscles, but workload to great. Most common causes are COPD and Asthma, also in pneumo, rib fract, pleur effusion, severe burns & Obs Sleep Apnea |
| AutoPEEP | dynamic hyperinflation, causes over distention, decr CO, incr intra-thoracic press, and decr venous return |
| What is the most common cause of V/Q mismatch | COPD |
| *How does RT measure PH for acute or chronic vent failure | (Type I&Type II) in chronic PH will drop .03 for every 10mmHg rise in PaCO2, acute PH will drop .08 for every 10mmHg rise in PaCO2 |
| *Indications for vent w/inadequate alv vent | PaCO2 >55torr and or PH <7.20 (or 7.25) |
| S&S of V/Q mismatch | increased HR, increased RR, use of accessory muscles |
| *Vent support with CHI | hyperventilate to decrease CO2 to 25 -30mmHg causing alkalosis to reduce ICP |
| Respiratory failure | inability to maintain normal delivery of O2 to tissue or normal removal of CO2 from tissues. PaO2 <60 and or a PaCO2 >50 on room air |
| Intrinsic PEEP | aka autoPEEP, inadvertent buildup of poss press in the alveoli due to incomplete exhale, results in progressive hyperinflation rise in end-expiratory press |
| *Indications for vent w/increased WOB | VE>10L/min, VD/VT >60% |
| *VE norm | 5-6L/min |
| *VD/VT Ratio | used as indicator for vent support in increased WOB, norm is 25 to 40%, >60% indicates need of support |
| *Three most common causes of Type I hypoxemic resp failure | V/Q mismatch (COPD), Shunt (atelectasis, pulm ed, pneumonia), secondary to hypoventilation |
| Acute ventilator failure | PaCO2 >50 with uncompensated bicarb. Thoracic pump or bellows failure |
| Central failure/fatigue | exertion-induced, reversible decrease in central respiratory drive |
| Increased WOB equals shallow breathing, signs are | decr VT, decr VC, incr VE, decr CO2 |
| *How does RT recognize Type I from Type II from ABG on R/A | add PaO2 and PaCO2, if between 110-130 then Type II, less than 110-then Type I |
| Perfusion/diffusion impairment | (type 1) rare cause of hypoxic resp failure caused by anatomical shunt secondary to liver disease, causes impaired gas exchange, FIO2 can help |
| V/Q mismatch | (type 1) perfusion in excess of ventilation, COPD is most common cause, blood flow is good but airtrapping, swelling, mucus etc. causes decrease in ventilation, Responds to FIO2 |
| a/A Gradient | norm is 74% |
| What is significance of increased PaCo2 | Body is hardwired to blow off CO2, so incr CO2 equals inc RR, so inc CO2 suggests hypoventilation and acidosis |
| *Acute on Chronic ventilator failure | aka combined Type I Type II failure, chronic respiratory failure with an acute complication. Emphysema pt with bacterial or viral infection |
| *MIP | max inspiration press (bedside test), norm 80-120, manometer measures neg press, not pt dependent, can be done w/mask, most reliable bedside assessment |
| *What effect does an increased RR (VE) have on VT | decreases VT and blows off CO2 |
| *Contractile failure/fatigue | reversible impairment in the contractile response to a NEURAL IMPULSE IN AN OVERLOADED MUSCLE (COPD) |
| Diffusion impairment | (type 1) usually not a problem when pt at rest, but exertion causes hypoxemia. Most often caused by interstitial lung disease, pulm fibrosis, asbestosis, sarcoidosis |
| Managing COPD’er on vent | COPD causes incr RAW and decreases exp flow, can easily cause autoPEEP aka hyperinflation and over distension, manage w/ decreased VT & rates and exp time |
| *Bedside assessment of resp muscles are | MIP (most reliable), VC, MVV (not often) |
| MVV | max voluntary ventilation, bedside test with hand held spirometer, not often used because pt dependent. |
| Complications of acute respiratory failure | secondary to ARDS (sepsis, multiorgan failure) secondary to TX(emboli, barotraumas, infection) non pulm (arrhythmias, hypotension, GI ailment, renal) Hosp acquired (bacterial, malnutrition, psychosis) |
| *Decreased vent drive | (type II) chemoreceptor’s responding to increased CO2 stimulate drive to breath, decreased by CNS depression (OD, brain lesion, hypothyroidism, obesity, cent sleep apnea, hypothermia) hallmark is brandypnea |
| What is the most common cause of increased WOB | COPD and asthma |
| Most common complaint seen in diffusion impairment | exertional dyspnea |
| *MVV norm | 120-180L/min |
