Mechanical Ventilation/Pulmonary Alternations Flashcards
Nasal Cannula
1 L/min = 24%
2 L/min = 28%
3 L/min = 32%
4 L/min = 36%
5 L/min = 40%
6 L/min = 44%
ET Tube PEDI/EASY-CAP
purple -> gold = CO2 > 2%
gold = good
sitting midline
CO2 coming from both sides of lungs
Simple Mask
**uses: short term O2 therapy **
contraindicated of CO2 retention
Low flow 6-10 L/min, 35%-60%
min 5L needed to flush out CO2
Non-Rebreather
More O2 sat. (not breathing atmospheric air or CO2)
If unable to wean w/i 6 hours -> intubate
Air Entrainment Mask
Optiflow
High flow w/ spread N/C prongs
5-60 L/min of O2
21%-80% Oxygen
Only resp. can touch
Ambu
Oxygenates + Ventilates
Artifical Airways
Phargyngeal airways: stops tongue from obstructing the appear airways
Oropharyngeal airway
Nasophargnygeal airway: used for pt w/ lots of secretions
* thread suction catheter through
* contraindicated w/ facial fracture pt
* Aka nasal trumpet
Nursing Management
Protect airway, prevent dislodge, secure tape/ ties
sterile suctioning
Cuff management, humidification, communication
oral hygiene Q 2-4
Endotracheal Tube
Always attached to ventilator
short term airway management - 2wks
Cough + gag reflexes compromised
Rotate site/side of tube Q shift ( L,R, middle)
Most adults get cuffed ETT
* Children w/o cuff
* burn/smoke inhalation pts no cuff (air leaking sound when balloon needed)
* Deflated cuff before removal !
Complications
nasal/ oral inflammation/ ulcers
vocal cord injuries - cuff presser on cords
tube obstruction + displacement
Tracheostomy
Preferred for long term intubation
avoids oral, nasal, pharyngeal, + largyngeal complications
Does not have to be attached to vent
inner cannula changed Q shift
Ventilators
Tidal Volume : volume of air needed to vent per breath (mL) 350-550 mL
Rate: resp rate
FiO2: fraction of inspired O2 ( degree of O2 saturation of Tv)
PEEP: positive end resp pressure
* allows alveoli to stay open during exhalation
* prompts better oxygenation
* delay alveoli collapse
* cautions w/: non-compliant lungs - COPD (hypovolemia/ decrease CO)
* Side Effects: decrease decrease CO/BP (Vt compresses heart)
Pt breaths < vent. setting = problem w/ machine (takes pt off, bag pt, call resp)
Assist Control
**Most invasive **
Pre-set: RR/Vt/ FiO2/ Peep
if pt breaths over vent, they get pre-set Vt
Setting: AC: 16/400/40%/+5
Reading: RR20, HR85, SPO2 96%
( 4x pt induced breaths, vent setting good)
Sychronized Intermittent Mandatory Vent. (SIMV)
Weaning mode
has present Vt + RR
Pt may take breaths @ own rate + volume
Vent breaths synchronized to pts resp. effort
Setting: 8/400/40%/+5
Reading: RR 16, HR 95, SPO2 94%
(8x pt induced breaths -> Vt, FiO2, Peep, controlled by pt)
Pressure Support
weanding mode
preset pressure to assist inspiration (reduces workload)
pt takes own RR/ Vt
Good for ARDS
Will convert to SIMV if pt= Apneic
Artifical Airway Nursing
Q 2-4 oral hygiene ( prevent VAP)
HOB increase 30 ( prevent vap)
Gastric residuals WNL -> Avoid vomiting / aspiration
PRN suctioning (prevent VAP)
Chest PT
Change inner cannula Qshift
Rotate ET tube site Q shift
Ambu bag @ bedside, working suctions @ beside
Verify ETT placement, check freq and after turning
Reasses sedation
DVT prophylaxis - move pt to chair
High Pressure Alarm
relieve underlying cause
ex. biting ET tube, kinked tubing, bulit up secretions
Low Pressure Alarm
Emergency !
Discounted line ? -> reconnect to pt
ET Tube out ? _ bag pt, call resp
Monitor For Complications
Monitor BP + HR for vent. tolerance
Barotrauma to alveoli ( increase pressure)
Volutrauma (increase volume) to non compliant lungs
VAP, GI distrubance, Pt- vent dyssynchrony
Acute Respiratory Failure
Resp system fails in oxygenation or CO2 elimination => altered gas exchange
Type 1: hypoxemic, oxygen failure
Type 2: hypercapnic, ventilatory failure (drug OD) (ABG : PaCO2 increase)
Clinical Presentation: mental status change, tachypnea, decrease RR after failure/ pulses
Diagnosis: ABG’s, CxR, SPO2
Managment: Maintain airway, call RRT!, Optimize O2 delivery, minimize O2 demand, Treat cause, Drugs: bronchodilators, steroids, ssedatives, analgesics, temp. NM blockers
Acute Respiratory Distress Syndrome
Pulmonary manifestation of MODS, sepsis
Non-cardiac pulmonary edema- fluids in alveolar space
Causes: Direct: apiration, near drowning, pneumonia
Indirect: sepsis, CABG, DIC, Shock states
Acute Phase: Insidous < 72 hrs.
Fluids shifts into alveolar space (pressure builds up), impeded gas exchange/ decrease compliance
Fibroproliferative Phase: Late phase
Scar tissue builds up + captures fluid -> lung stiffening (harder to remove fluid (refractory)), pulmonary HTN
Clinical presentation:
Early: tachypnea, restlessness, normal PaO2, normal CXR, lungs may be clear
Late: accessory muscle use, crackles, increase agitation, CXR infiltrates “white out”, lactic acidosis, increase HR/ decrease BP, hyperventilation
Resolution Phase: takes several weeks
Alveoli restoration, fluid out, cells multiply, macrohages removes debris
Management: mechanical ventilation, bronchodilators, sedative, analgesis, NM Blocker, lasix, prone position, suctioning, nutrition, increase PEEP
Pneumonia
Acute inflammation caused by infection
* community acquired, hospital associated, ventilator assoicated aspiration
Risk Factors: ETOH abuse, COPD, comorbidites, impaired swallowing (strokes), tube feeds, smokers, DM, immunocompromised, age, ventilators
Diagnostics: CXR, bronchoscopy, CBC, blood cultures, chem panel, ABG’s
Manifestations: cough, fever, dyspnea, tachypnea, chest pain, abnormal breathe sounds, confusion, loss of appetite
* Atypical/ one sided crackles!
Management: abx, O2, bronchodilators, cough/ deep breathing, positioning, chest PT, R+R
Pulmonary Embolism
Pulmonary arterial bed clot -> interferes w/ oxygenation
Risk Factors: DVTs, A-fib, surgery, cancers, trauma, preg
Manifestation: abrupt!
* increase HR, RR, dyspnea, SOB, decrease SpO2, crackles, hemoptysis
Diagnostics: CXR, D-dimer, ABG’s, V-Q mismatch, DVT studies
Treatment: anticoags-heparin! O2, greenfield filter, surgery
Prevention: prophylatic anticoags, compression stockings, SCDs
