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110 Cards in this Set

  • Front
  • Back
what primary or secondary disorders of what areas can lead to ARF? (4)
2.lung parenchyma
3.chest wall
4.neural processes
important facotr in development of ARF?
fatigue of muscles of breathing
how is ARF distinguished from CRF?
ARF - abrupt increase of PaCO2 and decreases of pH

CRF - pH 7.35-7.45 despite increased PaCO2
what happens to the following in ARF?

a.PaO2 = <70mmHg on 50% O2
b.PaCO2 = >50-55mmHg (can also be decreased or not changed)
c.pH = <7.3
d.RR = >35breaths/min (tachypnea)
what happens to the following in ARF?

e.vital capacity
f.inspiratory force
h.lung compliance
h.pulmonary vascular resist
e.vital capacity = <15mL/kg
f.inspir force = <25cmH2O
g.FRC = decreased
h.lung compliance = decreased
i.PAPW = <15mmHg despite pulm edema
h.pulmonary vascular resist = increased w/ pulm HTN
in ARF, PaO2 is low despite what 2 things?
1.supplemental O2
2.absence of rt to lft intracardiac shunt
in ARF, name 3 causes of low PaO2
1.v/q mismatching
2.rt to lft pulmonary shunting
3.alveolar hypoventilation
what influences whether CO2 changes in ARF?
relation of alveolar ventilation to metabolic produciton of CO2
when PaCO2 in increased, how do you know if hypoxemia is due to hypoventilation or a combination of hypoventilation and v/q mismatching?
by calculating the A-a gradient (PAO2-PaO2)
how do you calculate PAO2?
PAO2 = (%FiO2x713)-PaCO2/0.8
where do the 713 come from in PAo2 equation?
barometric pressure at sea level 760 - water vapor pressure 47 = 713
some causes of hypoventilation?
1.resp muscle wkness
2.decreased vent drive
cause of v/q mismatch?
when A-a gradient is normal, arterial hypoxemia is due to ? what is normal A-a gradient?
pure hypoventilation

no more than 15mnmHg
when A-a gradient is increased, arterial hypoxemia is due to?
v/q mismatching and/or right-to-left intrapulmonary shunting

> 15mmHg
what is the compensatory mechanism that creates a normal pH with elevated PaCO2 in chronic resp failure?
renal tubular reabsorption of bicarbonate
acute respiratory distress syndrome (ARDS)
arterial hypoxemia associated w/ acute lung injury
what lung injury characterizeds ARDS?
1.diffuse alveolar damage (influx of protein rich edema fluid into alveoli due to increased permeability of alveolar capillary membranes)

2.noncardiogenic pulmonary edema
what prevents adeq gas exchange in ARDS?
fluid filled alveoli
what is normal gas exhange in the lungs?
exchange of gases across alveolar walls allowing uptake of fresh O2 and relaease of CO2
name some direct causes of ARDS (5)
1.aspiration (gastric contents, fresh/salt water, hydrocarbon fluids)
2.lung contusion
3.pneumonia (viral, bacterial, TB, fungal, pnuemonocyctis carinii)
4.fat, air, amniotic fluid emboli
5.inhalational injury (smoke, high concent of O2, corrosive chemicals)
name some indirect causes of ARDS (8)
2.nonthoracic trauma
3.drugs (heroin, methadone, propoxyphene, barbs, colchicine, asa, hztz)
4.shock (hematologic DO, massive blood transfusion, DIC, cardiopulmonary bypass)
5.metabolism (acute pancreatitis, uremia)
6.increased ICP
7.ascent to high altitudes
S&S of ARDS (5)
1.arterial hypoxemia resistant to treatment w/ supplemental O2
2.CXR that look like cardiogenic pulmonary edema
3.fibrosing alveolitis
4.pulmonary HTN progressing to rt side heart failure
characters of fibrosing alveolitis
1.persistant arterial hypoxemia
2.increased alv deadspace
3.further dec in pulm compliance
when do survivors of ARDS regain normal lung fxn?
6-12 months
3 principle treatment goals for ARF?
1.correct arterial hypoxemia
2.remove excess CO2
3.provide patent upper airway
ways to correct arterial hypoxemai in ARF?
1.maintain pao2 60-80

2.spontaneously breathing patients: supplmental O2 via n/c, venturi mask, nonrebreathing mask, or T-piece (attached to free end of tracheal tube)

3.continuous positive airway pressure w/BIPAP or CPAP to open previously closed alveoli

4.ETT w/ mechanical vent if previous interventions do not work
what is the disadvantage of n/c, venturi mask, nonrebreathing mask, or T-piece?
seldom provide inspired oxygen concentrations higher than 50% in severe ARF
what is the disadvantage of high concentrations of O2?
toxic to lungs b/c
1.excessive production of free O2 radicals
2.replacing all nitrogen w/ O2 removes the "nitrogen splint" which leads to collapse of alveoli and absorption atelectasis
non-resp way to facilitate the removal of excessive carbon dioxide
increasing CO by
1.optimizing IV fluid
2.positive inotropes
when is it necessary to provide tracheal intubation w/ mechanical ventilation in ARF patients?
if PaO2 cannot be maintained at 60mmHg with 50% oxygen
2 modes of ventilation
1.volume-cycled ventilation
2.pressure-cycled ventilation
what are the subclasses of volume-cycled ventilation?
a.assist-control ventilation (AC)

b.synchronized intermittent mandatory ventilation (SIMV)

c.postitive end-expiratory pressure (PEEP)
3 characteristics of assist-control ventilation (AC)
1.patient initiates breath
2.breath delivered at preset Vt
3.set rate of Vt breaths
synchronized intermittent mandatory ventilation (SIMV)
1.patient initiates breath
2.patient initiates Vt
3.certain minute ventilation delivered from ventilator
postitive end-expiratory pressure (PEEP)
allows positive pressure throughout resp cycle
when is postitive end-expiratory pressure (PEEP) beneficial?
when exhalation is incomplete during airway obstruction
what population are pressure cycled ventilation typically used?
what 3 classes of drugs may be used to help manage patients receiving mechanical ventiliation?
what sedatives may be used during mech ventilation? what are their benefit?

prevent self extubation, barotrauma, and excessive deterioration in gas exchange
why are propofol and remifentanil good choices for mech vent support?
disappears fast so can cut off to do neuro assessments and can be weaned off quick
when are paralytics good for mech ventilated patients? what should be considered in regard to clearance of NMBAs?
if sedation is inadeq or hemodynamic instability is present

dependenc of certain NMBAs on renal clearence (pancuronium, vercuronium, rocuronium) should be considered
risk associated with paralytic use?
prolonged durg-induced paralysis in diffuse polyneuropahtys that may accompnay critical illnesses
what analgesics may be used during mech vent management?
complications of ET intubation and mechanical ventilation (5)
2.alveolar overdistension
5.critical illness myopathy
name of infection associated w/ ETT & mech vent.
ventilator-associated pneumonia
prevention of alveolar overdistension
1.smaller Vt 5-8ml/kg
2.airway pressure no more than 30
ABG effect of alveolar overdistension
2 effects of barotrauma
tension pneumothorax
arterial gas embolism
most common cause of arterial hypoxemia secondary to mech vent?
treatment of atelectasis
bronchoscopy to remove mucus plugs
what is critical illness myopathy?
neuromuscular weakness that persists long after resp failure is resolved
what can critical illness myopathy reflect?
axonal disorder occuring w/ sepsis and multiple system organ failure
what can accentuate critical illness myopathy?
to dc mechan vent where should the following measurable factors be:

a.gas exchange
b.vital capacity
d.max insp pressure
h.condiser coexist abnorm
a.gas exchange: maintain PaO2 and eliminate CO2
b.vital capacity >15ml/kg
c.PaO2 >60mmHg on <50% O2
d.max insp pressure >-20cmH2O
e.pH = normal
f.RR <20 breaths/min
g.Vd/Vt ration < 0.6
h.consider coexist abnorm: anemia, hypokalemia, hypovolemia
to dc mechan vent subjective factors should be present?
3.tolerate sponteneous vent w/o tachypnea, tachycardia, or distress laryngeal reflexes (cough, clear secretions, glottic fxn not impaired)
methods used to withdraw mechanical vent and benefit of each.
1.SIMV (allows spontan breathing & diminished mandatory breaths per min until pt is breathing completely spont)
2.T-piece (intermittent trials & total removal from mech vent while breathing spont)
3.decreasing levels of pressure-support vent
with method used to withdraw mech vent is least effective?
decreasing levels of pressure-support vent
signs that COPD is acutely deteriorating to ARF (4)
1.increased dyspnea
2.altered consciousness
3.retention of secretions
4.further deterioration of gas exchange
how can vicious cycle of COPD progressing to ARF be prevented? give examples.
by treating triggering events
--increased production of CO2 by fever
treatment goals for COPD exacerbations (7)
1.analyze ABGs
2.maintain pao2 at least 50-60
3.accept PaCO2 changes as long as pH >7.2
4.bronchopulmonary lavage
5.encourage coughing
6.meds: antibiotics, bronchodilators, corticosteroids
7.mechan vent
when would you use noninvasive vent methods to treat COPD exacerabations? what would you use?
alert despite hypercarbia

BIPAP via tight fitting face mask
what is benefit of noninvasive vent methods?
decreased risk of nosocomial infection
what pressures do BIPAPs deliver?
ins pressure 15-20 cmH2O
exp pressure 3-5 cmH2O
when would you use tracheal intubation to treat COPD exacerabations?
1.hemodynamically unstable
3.secretions can't be cleared
what is the disadvantage of tracheal intubation?
risk of nosocomial infections
which indirect lung injury is associated with highest risk of progression to ARDS?
death associated with ARF in pts with acute lung injury and ARDS is most often attributed to ____ or ____ rather than primary resp causes
sepsis or multi-organ failure
treatment of ARF associated with acute lung injury and ARDS (7) for underlying cuase
2.prevent: further infection, GI bleeding, thromboembolism
3.adeq nutrition
4.ventilation via trachal intubations w/ mech vent & inverse-ratio ventilation
5.fluid & hemodynamic mgmt
6.drugs: diuretics, corticosteroids
7.removal of secretions
in ARF associated with acute lung injury and ARDS:

ways of preventing further infection
proper respiratory
oral care
keep et cuff inflated
in ARF associated with acute lung injury and ARDS:

which method of nutritional support is preferred? why?
enteral feeding
no risk of catheter sepsis
in ARF associated with acute lung injury and ARDS:

how can you minimize barotrauma?
PaO2 60-80 using Vt 8-10ml/kg
disadvantage of excessive levels of PEEP
1.overdistended alveoli
2.compressed capillaries
3.decreased VR
4.decreases CO
5.decreased PaO2 (b/c blood is shunted away from full alveoli)
advantages and disadvantages of inverse-ratio vent
1.insp time exceeds exhalation time
2.may improve arterial oxygenation w/out PEEP

2.hypotension d/t auto PEEP
what are the signs of adeq organ perfusion adn CO?
1.metabolic acid/base balance
2.adeq renal fxn (UOP 0.5-1 ml/kg/hr)
what pulm artery occlusion pressure reflects inadeq IV fluid volume?
< 15
how can you improve secretion removal?
1.adeq systemic and humidification of inspired gases
2.fiberoptic bronchoscopy
compensatory responses to arterial hypoxemia
1.increased alveolar ventilation (from carotid body stimulation)
2.regional pulmonary artery vasocon (to divert blood flow from hypoxic alveoli)
3.increases SNS activity (to enhance tissue O2 delivery by increased CO)
significant desaturation occurs once PaO2 decreases to below what?
< 60
at what PaO2 do compensatory mechanisms fail? what will occur?
PaO2 of 30

cell damage and death
what should be monitored during ARF treatment?
1.pulmonary gas exchange
a.O2 exchanges and PaO2
b.CO2 elimination
c.mixed PvO2
d.arterial pH
e.intrapulmonary shunting

2.cardiac fxn
b.cardiac filling pressures
c.intrapulmonary shunt

3.PA catheter
what does Vd/Vt ratio reflect?
efficacy of CO2 transfer across membrane
what is Vd/Vt?
dead space volume/tidal volume ratio which depicts lung areas that receive adeq ventilation but inadeq or no pulm blood flow
normal Vd/Vt
< 0.3
what dz processes can Vd/Vt be incrased to 0.6 or more?
decreasead CO
what dose mixed PvO2 represent?
oxygen transport system: O2 delivered vs amt of O2 taken up by tissues
what is intrapulmonary shunting?and what happens to PaO2?
perfusion of alveoli not being ventilated

Lung Transplantation
Four approaches.
1.Single lung transplant
2.Bilateral lung transplant
3.Heart-lung transplant
4.Transplantation of lobes
Name some indications for lung transplant. (4)
Any end stage resp failure condition such as:

1.Cystic fibrosis
3.Pulmonary fibrosis
4.Primary pulmonary hypertension
why is aseptic technique important in lung transplant pts?
monitoring devices & equipment during lung transplantation
PA catheter
postop mech vent
name some pathophysiology issues of patients undergoing lung transplant.
1.Pts. will demonstrate restrictive patterns (mild to moderate pulm HTN & some rt sided heart failure)
2.Strict asepsis
3.Arterial hypoxemia with one-lung ventilation
4.Pulm. HTN when PA clamped
bad drugs & good drugs for pts undergoing lung tranplant?
bad: histamine releasing

good: bronchodilators
how to correct Arterial hypoxemia with one-lung ventilation
trial of PEEP to dependent lung
treatment of pulm HTN during PA clamping in lung transplant surgery
1.prostacylcin infusion extreme cases cardiopulmonary bypass is necessary
POSITIVE physiologic effects after Lung Transplantation
1.Peak improvement in 3-6 months
2.Arterial oxygenation returns to normal
3.Pulmonary vascular resistance normalizes
4.↑ CO
5.Improved exercise tolerance
6.inhaled b2 agonists produce bronchodilation
NEGATIVE physiologic effects after Lung Transplantation
Lung denervation (loss of cough reflex, blunted vent response to CO2, and mucociliary clearance impaired)
Complications of lung transplantation (7)
1.Pulmonary edema
2.Dehiscence of bronchial anastomosis
3.Anastomotic stenosis
5.Acute rejection
6.Chronic rejection - Bronchiolitis obliterans
what are the anesthesia considerations when working with a patient who has had a lung transpant?
1.Function of transplanted lung
2.Possibility of rejection or infection
3.Effects of immunosuppressive therapy
4.Disease of the native lung
5.Planned surgical procedure and its effects on the lungs
Preop. Evaluation of a pt with a Transplantated Lung (4)
1.History of increasing dyspnea or need for supplemental oxygen
2.SE of immunosuppressive drugs 3.Chronic rejection
4.Preop. medications
when does acute lung transplant reject typically occur?
100 days after transplantation
what is Bronchiolitis obliterans in relation to
Chronic lung rejection?
--fibroproliferative process that targets small airways and leads to submucousal fibrosis and luminal obliteration

--uncommon during first 6 months

--incidence exceeds 60% in pts who survive for 5 years
name 2 side effects of immunosuppressive drugs
pulm HTN, renal dysfxn
what can chronic lung transplant rejection hard to differentiate from?
resp infection
signs of chronic lung transplant rejection
Forced exp vol, vital capacity and TLC will be dec., arteial hypox., inc. A-a gradient, chronic cough may be sign of brochiolitis obliterans
what are some preop meds that may be given to lung transplantees that are have surgery? considerations of each?
1.opioids (will have inc. sensitivity)
2. supp. corticosteroids (for long stressful operations)
3.prophylactic abx
4.fluid (preload cautiously)
best Choice of Anesthetic Technique for Lung Transplantees having surgery?
Regional is best
--Decreased cough reflex
--Potential for bronchoconstriction
--Increased risk of aspiration & pulmonary infections
anesthesia managemnt, monitoring, and goals of lung transplantees having surgery (3)
1.Fluid with caution
3.Prompt recovery and early extubation
if you intubate a pt with a lung transplant, what is important to remember?
ETT cuff just beyond the vocal cords to prevent tracheal or bronchial anastomosis trauma
what 2 things do a TEEs show you?
1.cardiac function
2.volume status