Question Answer
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
Type I Failure Hypoxemic 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 failure V/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 mismatch increased HR, increased RR, use of accessory muscles
What is the most common cause of V/Q mismatch COPD
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 ratio increased shunt
Most extreme shunt ARDS
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 impairment exertional 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 failure hypercarbia, 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 are bradypnea 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 VT decreases 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 failure increased WOB
What is the most common cause of increased WOB COPD and asthma
What is the relationship between RAW and WOB conditions that cause increased RAW make pts work harder to exhale
PEEP Positive End Exp Press, norm 5-15, application and maintenance of press at the airway throughout the exp phase of pos press ventilation.
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
Extrinsic PEEP Set by RT on Vent machine
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
*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/A add PaO2 and PaCO2, if between 110-130 then Type II, less than 110-then Type I
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
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).
Acute ventilator failure PaCO2 >50 with uncompensated bicarb. Thoracic pump or bellows failure
*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
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)
Indications for vent support are severe refractory hypoxemia, inadequate alv vent, inadequate lung expansion, inadequate muscle strength and increased WOB
a/A Gradient norm is 74%
*A-aDO2 norm 10-20 on room air, 25-65 on 100% O2, every 50 is approx 2% shunt above norm of 2-5%
*P/F value norm 350-450
*Indication for vent w/refractory hypoxemia A-aDO2 >350 on 100% or P/F value <200
*VT norm 5-8mL/Kg IBW
*VC norm 65-75mL/Kg IBW
*Indications for vent w/inadequate lung expansion VT <5mL/kg, VC <10mL/kg, RR >35/min
*Indications for vent w/inadequate alv vent PaCO2 >55torr and or PH <7.20 (or 7.25)
*MIP norm -80 to -100 cmH2O
*Indications for vent w/inadequate muscle strength MIP ≥-20, VC<10mL/kg, MVV <2L/minxVE
*MVV norm 120-180L/min
*VE norm 5-6L/min
*VD/VT norm 25 to 40%
*Indications for vent w/increased WOB VE>10L/min, VD/VT >60%
*Bedside assessment of resp muscles are MIP (most reliable), VC, MVV (not often)
*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
MVV max voluntary ventilation, bedside test with hand held spirometer, not often used because pt dependent.
*Imposed WOB press created by endotracheal tube, vent circuit or autopeep that causes increase pressure and therefore increases WOB
*What is the cardinal sign of increased WOB tachypnea (causes decreased VT which causes decreased CO2)
*VD/VT Ratio used as indicator for vent support in increased WOB, norm is 25 to 40%, >60% indicates need of support
Increased WOB equals shallow breathing, signs are decr VT, decr VC, incr VE, decr CO2
3 types of respiratory muscle weakness are central failure, transmission failure, contractile failure
Central failure/fatigue exertion-induced, reversible decrease in central respiratory drive
Transmission failure/fatigue exertion induced, reversible impairment in the transmission of neural impulses
*Contractile failure/fatigue reversible impairment in the contractile response to a NEURAL IMPULSE IN AN OVERLOADED MUSCLE (COPD)
*Most easily reversible respiratory muscle weakness is contractile, (overworked)
*Vent support with CHI hyperventilate to decrease CO2 to 25 -30mmHg causing alkalosis to reduce ICP
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
AutoPEEP dynamic hyperinflation, causes over distention, decr CO, incr intra-thoracic press, and decr venous return