Respiratory failureinability 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
Type I FailureHypoxemic respiratory failure, PaO2 <60 on R/A, caused by VQ mismatch, shunt, diffusion impairment, perfusion/diffusion impairment, altitude
*Three most common causes of Type I hypoxemic resp failureV/Q mismatch (COPD), Shunt (atelectasis, pulm ed, pneumonia), secondary to hypoventilation
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
S&S of V/Q mismatchincreased HR, increased RR, use of accessory muscles
What is the most common cause of V/Q mismatchCOPD
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
*Decreased P/F ratioincreased shunt
Most extreme shuntARDS
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
Most common complaint seen in diffusion impairmentexertional dyspnea
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
Altitudes effect on FIO2(type 1) increased altitude decreases BP, this causes decreased press in alveoli and not enough press to oxygenate, decreases PaO2
*Type II failurehypercarbia, PaCO2 >50 on R/A, caused by decreased vent drive, resp muscle fatigue or increased WOB
*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
S&S of decreased vent drive arebradypnea is hallmark and ultimately apnea, decreased RR causes a decreased LOC
*Resp muscle fatigue/failure(type II) neuromuscular, resp pump fails, caused by ALS, GB, MG, muscular dystrophy.
*What effect does an increased RR (VE) have on VTdecreases VT and blows off CO2
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
What is the most common cause of Type II vent failureincreased WOB
What is the most common cause of increased WOBCOPD and asthma
What is the relationship between RAW and WOBconditions that cause increased RAW make pts work harder to exhale
PEEPPositive End Exp Press, norm 5-15, application and maintenance of press at the airway throughout the exp phase of pos press ventilation.
Intrinsic PEEPaka autoPEEP, inadvertent buildup of poss press in the alveoli due to incomplete exhale, results in progressive hyperinflation rise in end-expiratory press
Extrinsic PEEPSet by RT on Vent machine
Why do severe burns cause increased WOBsevere burns over large area of body causes hypermetibolic state which causes increased CO2 production which in turn causes increased VE
*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)
*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
*How does RT recognize Type I from Type II from ABG on R/Aadd PaO2 and PaCO2, if between 110-130 then Type II, less than 110-then Type I
What is significance of increased PaCo2Body is hardwired to blow off CO2, so incr CO2 equals inc RR, so inc CO2 suggests hypoventilation and acidosis
What are the 3 causes of acidosisresp 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).
Acute ventilator failurePaCO2 >50 with uncompensated bicarb. Thoracic pump or bellows failure
*Acute on Chronic ventilator failureaka combined Type I Type II failure, chronic respiratory failure with an acute complication. Emphysema pt with bacterial or viral infection
Complications of acute respiratory failuresecondary to ARDS (sepsis, multiorgan failure) secondary to TX(emboli, barotraumas, infection) non pulm (arrhythmias, hypotension, GI ailment, renal) Hosp acquired (bacterial, malnutrition, psychosis)
Indications for vent support aresevere refractory hypoxemia, inadequate alv vent, inadequate lung expansion, inadequate muscle strength and increased WOB
a/A Gradientnorm is 74%
*A-aDO2 norm10-20 on room air, 25-65 on 100% O2, every 50 is approx 2% shunt above norm of 2-5%
*P/F value norm350-450
*Indication for vent w/refractory hypoxemiaA-aDO2 >350 on 100% or P/F value <200
*VT norm5-8mL/Kg IBW
*VC norm65-75mL/Kg IBW
*Indications for vent w/inadequate lung expansionVT <5mL/kg, VC <10mL/kg, RR >35/min
*Indications for vent w/inadequate alv ventPaCO2 >55torr and or PH <7.20 (or 7.25)
*MIP norm-80 to -100 cmH2O
*Indications for vent w/inadequate muscle strengthMIP ≥-20, VC<10mL/kg, MVV <2L/minxVE
*MVV norm120-180L/min
*VE norm5-6L/min
*VD/VT norm25 to 40%
*Indications for vent w/increased WOBVE>10L/min, VD/VT >60%
*Bedside assessment of resp muscles areMIP (most reliable), VC, MVV (not often)
*MIPmax inspiration press (bedside test), norm 80-120, manometer measures neg press, not pt dependent, can be done w/mask, most reliable bedside assessment
MVVmax voluntary ventilation, bedside test with hand held spirometer, not often used because pt dependent.
*Imposed WOBpress created by endotracheal tube, vent circuit or autopeep that causes increase pressure and therefore increases WOB
*What is the cardinal sign of increased WOBtachypnea (causes decreased VT which causes decreased CO2)
*VD/VT Ratioused as indicator for vent support in increased WOB, norm is 25 to 40%, >60% indicates need of support
Increased WOB equals shallow breathing, signs aredecr VT, decr VC, incr VE, decr CO2
3 types of respiratory muscle weakness arecentral failure, transmission failure, contractile failure
Central failure/fatigueexertion-induced, reversible decrease in central respiratory drive
Transmission failure/fatigueexertion induced, reversible impairment in the transmission of neural impulses
*Contractile failure/fatiguereversible impairment in the contractile response to a NEURAL IMPULSE IN AN OVERLOADED MUSCLE (COPD)
*Most easily reversible respiratory muscle weakness iscontractile, (overworked)
*Vent support with CHIhyperventilate to decrease CO2 to 25 -30mmHg causing alkalosis to reduce ICP
Managing COPD’er on ventCOPD causes incr RAW and decreases exp flow, can easily cause autoPEEP aka hyperinflation and over distension, manage w/ decreased VT & rates and exp time
AutoPEEPdynamic hyperinflation, causes over distention, decr CO, incr intra-thoracic press, and decr venous return