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97 Cards in this Set

  • Front
  • Back
Barotrauma
trauma associated with pressure.

-results in the formation of subcutaneous emphysema, pneumothorax, pneumonmediastinum, pneumoperitonem, and pneumopericardium.

-caused by high PIP w/low EEP, bullous lung disease such as may occure with emphysema or a history of TB, high level PEEP with high Vt, aspiration of gastric acid, necrotizing pneumonias, ALI/ARDS
Volutrauma
damage from high distending volumes rather than high pressures
Biotrauma
release of chemical mediators.

-overdistention lung injury causes excess stretching of alveolar cells, the formation of edema, and the release of inflammatory mediators. Lung begins to resemble that of a lung with ALI/ARDS. The release of the mediators may actually result in multiple organ failure.
Shear stress
occurs when an alveolus that is normally expanded is adjacent to one that is collapsed (atelectasis) adn unstable.

-in the interstitial space between the two, force is exerted as these units move or slide against eachother. Stress pulls normal tissue apart, resulting in physical damage to the alveolar cells, particularly the epithelial and endothelial.
Overdistention
pressure volume curve w/duck billed appearance
Auto PEEP
whenever flow does not return to baseline in either a flow time curve or a flow volume loop
Inadequate flow
pressure time graphic is concave or downward scoop and the flow curve is constant.
Leaks
key indicator: the expiratory volume curve-if the expiratory volume does not return to zero a leak is present.
Ringing
when flow and pressure delivery is very high at the beginning of a breath results in the oscillation of air in the pt ventilator circuit and at the upper airway at the beginning of inspiration
Importance of PEEP
helps restore FRC by recruiting previously collapsed alveoli.

-Adequate PEEP levels prevent repeated collapse and reopening of alveoli and help maintain lung recruitment.

-In ALI, PEEP seems to offer some protection from tissue damage from high pressures.
VAP
refers to a pneumonia acquired 48 hours after intubation. Incidence of VAP ranges from 6% to 52% per 100pts. 6 to 21x higher for intubated pts.

-Mortaility rates range from approx 5% to 40%. Increases hospital sty 6.1 days and MV length 9.6 days.
Factors predisposing pts to VAPS:
nasopharynx and tracheal surface injury, ineffective cough mechanism, passage of bacteria into trachea, poor nutrition.
Diagnosis of VAP:
Fever (38.2), elevated WBC (leukocytosis), purulent secretions, new infiltrates on xray, bronchoscopy with protected brush catheter.
Causes of VAP:
colonization of the oropharynx and the stomach with potentially pathogenic organisms, chronic micoraspiration of subglottic secretions
Endogenous
microorganisms from nose, mouth, oropharynx, and trachea
Exogenous
microorganisms are the biofilm of the tracheal tube, circuits, nebulizers, humidifies, and health care workers.
Prevention of VAP
hand washing, oropharynx cleaning and decontaminations, noninvasive ventilation, semi recumbent pt positioning and eternal feeding, kinetic beds, selecting, changing and suctioning the ET tube and care of the trach tube, CASS
Oxygen toxicity
can induce pulmonary changes in humans in as little as 6 hours, exposures for more than 72 hours cause development of pattern similar to ARDS
Absorption atelectasis
concentratoin more than 70% lead to rapid absorption atelectasis increases intrapulmonary shunt
Depression of ventilation
pts with chronic CO2 retention (COPD), high oxygen levels can increase PaCO2
Ventilator related problems
if the pts severe respiratory distress is relieved by manual ventilation with 100% oxygen, then the problem is associated with the ventilator or with ventilator management. Leaks, inadequate oxygentation, inadequate ventilatory support, trigger sensitivity, inadequat flow settings, auto-PEEP, increased ventilatory drive, need for sedation, pt ventilator dyssyncrony.
Pt related problems:
airway problems, pneumothorax, bronchospasm, secretions, pulmonary edema, dynamic hyperinflation, abnormalities, in respiratory drive, change in body position, drug induced distress, abdominal distention, pulmonary embolism
Airway complications
kinking of the ET tube in the back of the throat, impingement of the tube on the carina, adn displacement of the tupe upward, above the vocal cords, or into the right mainstem bronchus, rupture of leakage of the ET cuff, pt biting the ET tube, airway secreitons, and mucus plugging of airways, cuff herniation over the end fo the ET tube, development of a tracheoesophageal fistula, rupture of the innominate artery.
Treatment of pt related problems
-disconnect pt from ventilator
-manual ventilation (80-100%O2)
-maintaining normal ventilating pressures (PEEP valve if need)
-evaluate compliance adn resistance through bag ventilation
-rapid physical evaluation and assess monitored indexes and alarms, check the patency of the airway by passing a suctio catheter
Activation of low pressure, low volume, and low VE alarms may indicate:
a leak, low pressure alarms are most often activated by leaks
High pressure alarms
airway problems, change in lung characteristics or pt related conditions or problems related to the ventilator or pt circuit.

-commonly activated when pt coughs or bites ET tube or secretions build up in the airway
Low PEEP/CPAP alarms activated when:
pressure falls below the desired baseline during PEEP or CPAP. May occur when the ventilator cannot compensate for a leak in the circuit or active inspiration.
Apnea alarms indicate:
pt apnea or pt disconnection, systme leaks, inadequate machine sensitivity or inappropriate set apnea parameters
Negative pressure ventilation
1950's peaked
-increase lung volumes by intermittenly applying negative pressure to the entire body below the neck or just the upper resion of the chest (increased transpulmonary pressure, passive exhalation)

-Iron lung, chest cuirass
Nebulizers and external flow
pts on PSV must initiate a breath by creating a slightly negative pressure or drop in flow in the circuit, which is detected by the ventilator. When a continuous flow nebulizer is placed between the pt and the sensing mechanism, the pt finds it more difficult to generate the effort to trigger the ventilator. This problme may arise with microprocessor controlled ventilators whenever a nebulizer powered by an external gas source is used.
NPPV
very effective in the treatment of acute respiratory failure caused by COPD exacerbation
In acute care NPPV used to treat:
COPD exacerbation, asthma, hypoxemic respiratory failure (including the following disease processes: pneumonia, ARDS, trauma, cardiogenic pulmonary edema), community acquired pneumonia, cardiogenic pulmonary edema (mask CPAP proven very effective)
In chronic care NPPV used for:
supportive therapy rather than a lifesaving treatment

-chronic hypoventilation, nocturnal desaturation, respiratory muscle fatigue, and poor sleep quality, restricitve thoracic disorders (include: chest wall deformaties and neuromuscular weakness, hypoventilation adn respiratory failure), chronic stable COPD, cystic fibrosis
Goals and indications for NPPV:
avoidance of intubation, improve gas exchange by resting the respiratory muscles and increasing alveolar ventilation, help offset intrinsic PEEP.
Selection process for NPPV must consider:
pt diagnosis and clinical characteristics.
-1st establishe the need for ventilaitory support assistance according to clinical and blood gas criteria.
-2nd exclude pts at increased risk of failure of complications such as respiratory arrest, hemodynamic instability, excessive secretions, and inability to protect airway, agitation, confusion, facial burns or deformities.
-Finally, the potential reversibility of the disease process.
Pt should be considered for NPPV if they have:
-severe daytime CO2 retention (PaCO2 >52)
-nocturnal hypoventilation despite the administration of nocturnal oxygen therapy
Indicatios of NPPV:
Exac. COPD
acute asthma
hypoxemic RF
CAP
card. pulm. edema
immunocompromised
postoperative
postextubation
DNR
acute care setting
Signs/Symptoms for NPPV:
mod to severe dyspnea
RR >24bpm
accessory muscle use
paradoxical breathing
Selection criteria for NPPV:
PaCO2 >45
pH < 7.35
PaO2/FiO2 < 200
Consider several factors for discontinuation of vent:
ventilatory support during weaning, oxygenation and PEEP, maintenance of artificial airway even after ventilatory support discontinued, pts may require more than one of the first three therapies. Ventilator and airway should be discontinued ASAP to avoid risks associated with MV, weaning decisions depend greatly on pts recovery form the problems that imposed the need for MV.
Rapid shallow breathing index
most reliable test for determining a pts weaning status.

-Cal by: RR/VT
this measurement is taken 1min after disconnecting the spont breathing pt from the vent and O2. Successful weaning is more likely if the RSBI is below 105 (normal range 60 to 105)
CROP index
evaluates complinace, RR, oxygenation, and inspiratory pressure. may provide good assessement of potential respiratory msucle overload and fatigue.

Cal: (CdxPImax x [PaO2/PAO2])/RR

>13 indicate the likelihood of successful ventilator withdrawal.
Airway occlusion pressure
PO.1
inspiratory drive to breath
-to obtain the PO.1 the airway is occluded during the first 100 msec of inspiration and the pressure at the upper airway is measured. This value is believed to reflect both the drive to breathe and ventilatory muscle strenght. Normal range is 0 to -2 cmH2O.
Values below -6 cmH2O may indicate a high drive to breathe and suggest that weaning is not likely to succeed.
Techniques of weaning:
SIMV
PSV
T-piece weaning
T-piece through vent
Synchronized intermittent mandatory ventilation (SIMV)
reduction in mandatory rate progressively and pressure support added to reduce increased WOB
PSV
pt controls rate, timing and depth
T-piece weaning
removes the pt from vent according to predetermined schedule (heated humidification, high flow of gas, large bore tubing pre/post ETT adaptor)
T-piece through ventilator
CPAP
Modes helpful in ventilator discontinuation:
-automatic tube compensation
-volume targeted PSV
-automode and variable pressure support/variable pressure control
-mandatory minute ventilation
-adaptive support ventilation
-knowledge based weaning system
Automatic tube compensation:
desinged to specifically reduce the work associated with ET resistance
Volume targeted PSV
pressure support with a volume target
Automode and variable pressure support/vairable pressure control:
ventilator can switch form a time triggered mandatory breath to a pt-triggered support breath (VC-CMV to VS or PC-CMV to PSV, or PRVC to VS)
Mandatory minute ventilation
ventilator automatically increased the level of support if the pts spontaneous ventilation decreases, thus maintaing a consistent minimum VE
Adaptive support ventilation
increases or decreases ventilatory support based on monitored pt parameters (pressure limited breaths that target a volume and rate)
Knowlege based weaning system:
ventilator measures parameters such as Paw, Vt, RR, and PetCO2, and adjusts the PS level or the mode to accommodate the pt (PS to PC-CMV)
Weaning failure
if the pt fails the SBT, the cause of the failure must be determined and corrected when possible: cardiac factors, acid-base factors, metabolic factors, pharamocological agents, psychological factors, nutritional status and exercise.
Hypophosphatemia
phosphate deficiency

-may contribute to musle weakness and failure to wean
Hypomagnesaemia
low magnesium

-associated with muscle weakness
Hypothyroidism
may impaire respiratory muscle function; blunt the central response to hypercarbia and hypoxemia
Malnutrition
reduced central response to hypoxemia and hypercapnia and an impaired immune response.
Underfeeding
muscle wasting (including the diaphragm, heart, and other organ tissues) particularly in pts under the stress of an acute, severe illness.
Overfeeding
increase O2 consumption (VO2), increased VCO2 and increased VE
Problems and mortality associatedd with long term ventilation
moratlity rate with LTMV are high: 57% for 2 year mortality, 66 to 97% for 5 year moratlity
Long term mechanical ventilation
required by two general categoires of pts:
-those recovering from an acute illness
-those chronic progressive disorders
Goals of LTMV
enhancing the individuals living potential, improving physical and physiological level of function, reducing morbitiy, reducing hospitalizations, extending life, providing cost effective care.
Three considerations of patient selection:
-disease process and clinical stability: pts recovering from acute illnesses and acute respiratory failure who do not respond to repeated attempts at liberation from the ventilator.
-pts with chronic disorders who only require mechanical ventilation for part of the day
-pts requiring continuous ventilatory support to survive
Psychological evaluation of pt and family:
psychological stability and coping skills are critical to the success of long term ventilation. Family must be aware of prognosis, advantages, and disadvantages, availability of other support systems (respite care and psychological consultants)
Finances:
overal cost of caring for ventilator dependent pts at home may strain family budget even for those who are insured.
Discharge planning considerations
a thorough examination and preparation for discharge requires:
-geographical and home assessment, family education, and home care service (nursing services, emergency care)
Important factors in choosing a vent:
reliability, safety, versatility, user friendly, easy pt cycling, all pts must be supplied with manual resuscitation device.

-PPV is the most commonly used device. ventilator should be easy to operate, light weight, and portable, have AC current, internal DC battery, and external DC battery.
First generation portable volume venilators
can serve as both transport and long term ventilator, piston driven.

-Modes: VC-CMV and VC-IMV (external H valve assembly), FiO2 greater than 21% require bled in O2 (some can provide 100%), PEEP provided with external threshold resistor.
Second generation portable ventilators
PPV that are primarily micorprocessor-controlled and piston driven, more features than 1st generation vents, electrically powered (LTV), volume or pressure targeted mandatory breaths, have greater flexibility.
Equipment:
vent circuits, humidifies, heater, HME, temp probe, power supply, tracheostomy attachments, replacement ventilator circuit filters, communication aids, pts interfaces, suction machine, suction container, suction catheters, connecting tubes, gloves, oxygen tubing.
HFOV controls and features
helps recruit the lung and avoid lung injury. It is a method of high freq vent in which gas is oscillated at high frequencies (3 to 15Herts).

High freq oscillations are produced by a reciprocating piston that is magnetically driven. Pressure is positive in the airway during the inspiratory phase (forward stroke) and negative during the expiratory phase (return stroke) The amplitude (set by power) determines the forward and backword excursion.
Indications for HFOV:
ARDS pts not responding to conventional mechanical ventilation, air leaks, early intervention to recruit lungs, clinical staff comfort in using the equipment.
Controls of HFOV:
mPaw (analogous to Paw on conventional ventilator),

set 3 to 5 cm H2O above the observed Paw
Amplitude HFOV:
adjusted by the power control and influence ventilation (PaCO2). Amplitude affects piston displacement (determine Vt) ; power should be initially started at 6 to 7 for adults, appropriate power setting is determined by chest wiggle factor (CWF) visible from clavical to mid thigh. Amplitude should be adjusted for high PaCO2 not the frequency.
Frequency HFOV:
controls the time allowed for the piston to move forward and back.

Initial setting is 5 to 6 Hz (300 to 360 cycles/min)
Inspiratory time percent HFOV:
represents the portion of the respiratory cycle that the piston spends in a forward mostion.

Set initially at 33% (I:E of 1:2)
Bias flow HFOV:
first parameter set, affects mPaw and range is 25 to 40L/min
FiO2 HFOV:
initially set at 100% and decreased in increments of 10% as tolerated.
Heliox therapy
20/80
used in tx of disorders that cause airway obstruciton: postextubation, stridor, asthma, tracheobronchitis, viral larnygitis, bronhiolitis, tumors, (laryngeal or mediastinal), foreign body aspiration, vocal cord paralysis, dyskinesia, COPD
Helium
low density, inert gas that lowers the resistance to turbulent flow in obstructed airways and reduces respiratory muscle load and dyspnea. Effective only when turbulent flow is present and is expected to be more beneficial in diseases affecting the larger airways and partially obstructed airways.

Heliox is proven effectvie in reducing risk of respiratory muscle fatigue in pts with acute exacerabtion of asthma
Devices for delivering heliox:
mask heliox (in conjunction iwth aerosolized bronchodilators), use of two flowmeters and t-piece attach to a mask, non rebreather with nasal cannula.
APRV
a mode of venilatory support desinged to provide two levels of CPAP and allow SPONT breathing at both levels when spont effort is present. It provides a moderately high level of pressure:
(P-high) 15 to 30 cmH2O that is considered the baseline pressure. occasionally interrupted with a brief time at lower pressure:
(P-low) 0 to 15 cmH2O. the brief interval at P-low is called release time and allows for removal of CO2.
Time triggered and time cycled when spont efforts detected.
-Not spont = pressure curve looks like pressure controlled inverse ration ventilation.
APRV advantages:
lower PIP, better O2, less circulatory interference, improved gas exchange without compromising hemodynamics, reduced physiological dead space, provides better ventilation-perfusion matching, reduced risk of acute lung injury (ALI), may recruit consolidated lung areas, prevent opening and closing of alveoli, less sedation, improved pt comfort, preserves spont ventilation.
Compared to PCV APRV:
reduces P-peak and Paw, increases cardiac index, decreases CVP, increases urine output, increases O2 delivery, reduces need for sedation and paralysis
APRV disadvantages:
pressure targeted mode so volume delivery is dependent on lung compliance, airway resistance, and pt spont effort, possible incomplete elimination of CO2, not all ventilators with APRV allow pt triggering in the phase of P-high to P-low and from P-low to P-high, limited staff experience.
ILV
independent lung ventilation
-technique that allows gas flow to each lung to be controlled separately, is accomplished by using a specialized double lumen ET tube (DLET)

-considered when Vt and PEEP requirement of one lung would compromise the other lung.
Indications ILV:
thoracoabdominal aortic aneurism repair, thoracic organ transplant, lung volume reduction surgery, pneumonetomy, pulmonary hemorrhage, isolation of infected secretions, video-assisted thoracospopic procedures.
Atelectrauma
injury to the lungs that occur because of repeated opening and closing of lung units at lower lung volumes
Webb and Tierney study
high peak inspiratory pressures without PEEP resulted in death (rats)
Hypoventilation:
occurs with inadequate alveolar ventilation, result in increase PaCO2 levels, acidotic pH causing right shift in the oxyhemoglobin dissociation curve and reduces the ability o fthe hemoglobin to bind and carry oxygen. Increase PaCO2 can lead to coma, elevated hydrogen ion content-hyperkalemia, cardiac dysrhythmias, increased ICP
Hyperventilation:
inappropriate vent settings or pt induced (pain, airway inflammation, anxiety syndromes), lower than normal PaCO2 level, alkalosis causing a left shift in the oxyhemoglobin dissociation curve enhances the ability of hemoglobin to pick up oxygen in the lungs but makes it less available at the tissue level = Haldane effect
Severe Hypocapnia and lead to:
tetany, reduced cerebral perfusion, increased ICP and cerebral edema, and reduces drive to breathe
Pneumothorax
recognized as increase WOB, nasal flaring, use of accessory muscles, uneven chest wall movement, and absence of breath sounds on the affected side.
Bronchospasm
may be manifested by dyspnea, wheezing, increased WOB such as use of accessory muscles, lack of coordination of chest or abdominal wall movement, retractions of the suprasternal, supraclavicular and intercostal spaces, increased Raw, increased PIP and transairway pressure.