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Problems of Diffusion
Pulmonary Edema
Acute Adult Respiratory Syndrome (ARDS)
Pneumoconioses
Asbestosis
Silicosis
Black Lung
Sarcoidosis
Pulmonary Edema
Abnormal accumulation of fluid in the lung tissue that can move into the alveoli
Fluid in the alveoli → impaired gas exchange and difficulty breathing
Often a medical emergency
Flash pulmonary edema = develops very rapidly
Pulmonary Edema - Cardiogenic
Caused by a cardiac problem
Common with:
Left-sided heart failure (LVF)
MI
Pulmonary fluid overload
Pulmonary Edema - Non-cardiogenic
Not primarily caused by heart failure
Causes include:
Direct lung injury → smoke inhalation, aspiration, trauma
Hematogenous injury → sepsis, pancreatitis, multiple transfusions, cardiac bypass
Pulmonary Edema - Clinical Manifestations
Respiratory distress
Frothy pink sputum**
Tachypnea
Tachycardia
Anxious/agitated/ confused/ stuporus
Cough
Air hunger; Central cyanosis
Early sign will be confusion/agitation- late sign will be cyanosis.
Pt is literally drowning in their own fluids.
Pulmonary Edema - Assessment
Crackles to auscultation
inspiratory
bases, ascending
Ascending crackles as fluid progresses upward
Pulmonary Edema - Diagnosis
CXR
ABGs
BNP
Echo
Pulse ox
Pulmonary Edema - Medical Treatment
Goal: Treat the underlying cause and improve oxygenation/respiratory status.
Oxygen
Often NRB (nonrebreather mask)
Intubation/mechanical ventilation if severe
Diuretics
Lasix (furosemide) → loop diuretic
Removes excess fluid
Vasodilators
Nitroglycerin (nitro) or nitroprusside IV
Helps reduce cardiac workload/vascular pressure
Only use if BP is stable
Closely monitor BP, HR, and SpO₂
Positive inotropes
Increase the force of cardiac contraction
Helps the heart pump blood more effectively
Example: digoxin
Morphine
No longer routinely recommended for acute pulmonary edema
Balloon pump
May be needed if the patient does not respond to medications
Pulmonary Edema - Nursing Management
Position client for comfort
High-Fowler’s
Legs dependent/dangling over the side of the bed
Helps decrease venous return and ease the workload on the heart
1:1 monitoring
Often cared for in ICU/CC setting
Bed rest / encourage rest
Reduce oxygen demand
Strict I&O
Monitor fluid balance closely
Continuous cardiac monitoring
Monitor respiratory status
RR, SpO₂, lung sounds, work of breathing
Diuretic therapy
Bedside commode (BSC) may be needed because of increased urination
Provide emotional support
Address anxiety after immediate physical needs are managed
Acute Respiratory Distress Syndrome (ARDS)
Acute = sudden onset and life-threatening
Begins after exposure to a trigger/risk factor
Trigger → inflammatory response
Inflammation causes lung damage and alveolar collapse
Acute Respiratory Distress Syndrome (ARDS) - Syndrome characterized by:
Pulmonary edema
Progressive hypoxemia
Refractory to O₂ → oxygen does not adequately correct the low oxygen level
Reduced lung compliance
Lungs become stiff/hard to expand
High mortality rate
ARDS - Chest X Ray

Risk Factors/Causes of ARDS
Direct Injury
Smoke inhalation
Chest trauma
Aspiration
TB
Obstructed airways
Burns
Cardiac bypass
Radiation
Indirect Injury
Sepsis
Multiple transfusions
Pneumonia
Shock
Burns
Head trauma
Pancreatitis
Overdose ingestions
All causes damage alveolar-capillary membrane
ARDS - Clinical Manifestations
Rapid onset of severe dyspnea, usually within 72 hours of the triggering event
May initially look like pulmonary edema
Crackles
Intercostal retractions
Severe respiratory distress
Arterial hypoxemia that does NOT improve adequately with O₂
Lung injury → fibrosing alveolitis
Thickening of alveolar walls
Lungs become stiff
↓ lung compliance
Causes persistent, severe hypoxemia
High mortality
Death commonly occurs from MODS (multiple organ dysfunction syndrome)
ARDS - Diagnostics
Pulse oximetry
Monitors oxygen saturation
ABGs
Shows hypoxemia and other oxygenation/ventilation problems
CXR
May show patchy → diffuse opacities
Severe “white-out” appearance = ominous sign
BNP
Helps differentiate cardiogenic pulmonary edema from ARDS
Higher BNP suggests a cardiac cause such as heart failure
Echocardiogram (ECHO)
Evaluates heart function and helps assess for a cardiac cause
PFTs
May be used to evaluate lung function
Assess respiratory effort
Use of accessory muscles indicates increased work of breathing
Medical Management of ARDS
Treat the underlying cause + improve oxygenation + support organ function + prevent further lung damage.
Treat underlying condition/cause
Identify and treat what triggered the ARDS
Supplemental O₂
May require ETT + mechanical ventilation
PEEP (Positive End-Expiratory Pressure)
Keeps alveoli open at the end of expiration
Prevents alveolar collapse
Improves gas exchange/oxygenation
Does not cure ARDS; it supports oxygenation
PEEP is a critical component of ARDS treatment
Circulatory support
Maintain adequate blood pressure and perfusion
Vasopressors may be needed for hypotension
Fluid management
Give enough fluid to maintain circulation
Avoid fluid overload because excess fluid can worsen pulmonary edema
Nutritional support
Important because ARDS is a severe, high-metabolic-stress condition
Monitor
ABGs
SaO₂/SpO₂
PFTs as ordered
Medical Management of ARDS - Meds
Treatment is mainly supportive and may include medications based on the patient's condition:
Antibiotics → if infection is the cause/suspected
Steroids
Diuretics → help manage excess fluid
Bronchodilators → if indicated
Anxiolytics/sedation → e.g., Ativan, Versed, Diprivan
Paralytics may be used in severe cases to facilitate mechanical ventilation
Nursing Management - ARDS
Close monitoring and supportive nursing care are critical.
Close respiratory + cardiac monitoring
SpO₂, ABGs, respiratory status, HR, BP
Monitor PA pressures if available
Mechanical ventilation
Manage PEEP
Positioning
Prone positioning or HOB elevated as ordered
Prone positioning can improve oxygenation and help recruit alveoli
Helps drain secretions and reduce ventilator-associated lung injury
Frequent turning/repositioning
CPT (chest physiotherapy)
Suctioning
Suction only when needed to remove secretions
Nebulizer treatments as ordered
ARDS - Prone Positioning
May:
Improve oxygenation
Keep improvement in oxygenation sustained
Reduce lung injury/barotrauma
Reduce ventilator time
Reduce ICU stay
Help drain pulmonary secretions
Reduce compression of the lungs by the heart
ARDS - Nursing Care
Skin care
High risk for pressure injuries because of immobility/ventilation
Oral care
Eye care
Sedated/paralyzed patients may not blink → eye drops and/or tape eyes closed as ordered
Foley catheter
Monitor urine output
Nutrition
Enteral or parenteral nutrition as needed
35–45 kcal/kg/day
Fluid management
Crystalloids as ordered while avoiding fluid overload
Anxiety/Agitation
Provide reassurance and communication
Medications may include:
Versed
Ativan
Fentanyl
Neuromuscular blocking agents
May be used with severe mechanical ventilation needs
Closely monitor
Remember: paralysis does not mean loss of hearing/sensation
Hemodynamic Support
Vasopressors
Used for hypotension
Cause vasoconstriction → increase BP
ARDS
Care is aggressive and supportive
Survival and prevention of complications depend heavily on nursing care
Can cause permanent injury and scarring of the alveolar-capillary membrane
Amount of scarring varies:
Minimal → severe/crippling
Severe permanent lung damage may result in being oxygen-dependent long-term or for life
Sarcoidosis
Interstitial lung disease
Cause is unknown
Usually develops slowly/insidiously
Most common in adults around 20–40 years
More common African-American
Lungs are most commonly affected, but any organ can be involved
May involve an abnormal hypersensitivity/inflammatory response to triggers such as bacteria, fungi, viruses, or chemicals
Causes granulomas and eventually fibrosis in the lungs
Fibrosis → lungs can become stiff/hard
↓ lung function
Sarcoidosis - Clinical Manifestations
Often has few obvious respiratory symptoms
General symptoms may include:
Fatigue
Fever
Joint pain
Anorexia/loss of appetite
May go into remission without treatment
Sarcoidosis - Diagnosis
CT scan
Lung biopsy
Sarcoidosis - Management
Usually symptomatic/supportive
Corticosteroids
Methotrexate may be used
Outpatient follow-up/monitoring
Pneumoconioses
Lung diseases caused by repeated exposure to harmful/noxious substances
Dust
Mineral particles
Metal particles
Fumes/chemicals
Inhaled substance → immune/inflammatory response
Insidious (slow) onset
May develop over many years
Causes lung scarring/pulmonary fibrosis
Fibrosis → restrictive lung disease
Lungs become stiff
Difficulty fully expanding the lungs
Cigarette smoking can worsen the disease
Can lead to chronic disease and disability
Management/Goal
Prevention is the main goal
Reduce or eliminate occupational exposure
Control exposure to harmful substances
Pneumoconioses - Silicosis
inhalation exposure to silica dust
glass manufacture, stone cutting, pottery
enlarging nodular lesions throughout lung
20 yrs before onset
Pneumoconioses - Asbestosis
inhalation to asbestos dust
mining, roofing, demolition
asbestos fibers become surrounded by fibrous tissue
associated with lung cancer
Pneumoconioses - Black lung
inhalation of coal dust
coal mining
fibrotic lesions form due to over-exposure
development of emphysema
Pneumoconioses- H&P
History- inquire about exposure/time frame
Physical Exam:
May be symptomatic for many years as this onset is insidious
Dyspnea, chronic cough
Loss of appetite
Hypoxemia
Cor pulmonale
Respiratory failure
Diagnostics: H&P; CT; CXR
Pneumoconioses- Nursing Management
Maintain oxygenation
Monitor respiratory status and O₂ saturation
Supportive care
Lifestyle changes
Teach patient to stop further exposure
Avoid/reduce exposure to dust, minerals, metals, fumes, etc.
Stop smoking
Smoking can worsen the condition
Monitor for:
Cor pulmonale
Respiratory failure
Employee advocate
Help protect the patient from continued workplace exposure
Problems of Transport
Pulmonary embolism
Cor pulmonale
Pulmonary Hypertension
Problems of Transport - Examples of Nursing Diagnoses
Decreased Cardiac Output
Decreased Tissue Perfusion
Pulmonary Embolism - PE
Obstruction of the pulmonary vasculature by:
Blood clot
Air
Fat
Septic material
Amniotic fluid
Foreign bodies (e.g., IV catheter fragments)
Effects of PE
↓ Systemic oxygenation
Pulmonary tissue hypoxia
Severe can lead to death
May recur
Outcomes depend on the patient’s co-morbidities
PE - Origin
Usually originates in the venous system, most commonly from a DVT
Can also originate from the right side of the heart
PE – Pathophysiology
One of the most common acute pulmonary diseases among hospitalized clients
Most frequent etiology: DVT (deep vein thrombosis) ⭐
A clot can break loose → travel through the right side of the heart → pulmonary artery
Can cause sudden obstruction of pulmonary blood flow
Severe PE can cause rapid cardiovascular/respiratory collapse
Saddle embolism: embolus becomes lodged at the bifurcation of the pulmonary artery
PE - Risk Factors
Prolonged immobilization
Surgery
Obesity
Advancing age
Hypercoagulability → blood is more likely to form clots
Dehydration
Malignancy (cancer)
History of thromboembolism
Sickle cell disease (SCD)
PE - Clinical Manifestations: Respiratory
Sudden onset
Dyspnea
Tachypnea
Chest pain
Cough
Hemoptysis
Crackles
Pleural friction rub
PE - Clinical Manifestations: Cardiovascular
Tachycardia
Distended neck veins
Syncope
Cyanosis
Hypotension
PE - Diagnosis
H&P → health history + physical assessment
CXR
Mainly used to rule out other causes of symptoms
CT / Spiral CT
Chest CTA (CT pulmonary angiography) ⭐
Visualizes the pulmonary blood vessels
Common/important test for PE
V/Q scan
Used when CTA cannot be performed or is unavailable
Compares ventilation (airflow) with perfusion (blood flow)
EKG
May show sinus tachycardia
May show T-wave inversion
Pulse oximetry / ABGs
May show hypoxemia
ABGs can sometimes be normal
D-dimer
Elevated D-dimer can indicate increased clot formation/breakdown
Not specific for PE
Coagulation studies
PE - Medical Treatment
Goal: Improve respiratory and vascular status
Supplemental O₂
IV fluids
IV vasopressors if needed
Anticoagulation therapy
Heparin
Warfarin
Low-molecular-weight heparin (LMWH)
Monitor for bleeding
Bleeding gums
Heavier menstrual period
Unusual bleeding
Bleeding anywhere
Thrombolytic therapy
tPA
Breaks up the clot
Surgical intervention
Embolectomy → removes clot
IVC filter (Greenfield/umbrella)
Helps prevent clots from traveling to the lungs
May be used for recurrent/chronic PE or when anticoagulation cannot be used
PE - Nursing Management
Monitor oxygenation
Pulse oximetry
Respiratory status
Monitor anticoagulation
IV Heparin
Monitor PTT/aPTT
Goal: 1.5–2.5 × normal per lecture
Warfarin
Takes about 4–5 days to become effective
Monitor PT/INR
Goal: INR 2.0–3.0
Heparin is continued while warfarin becomes therapeutic, then heparin is decreased/stopped as ordered
Thrombolytic therapy - ase
Used for severe, unstable PE
Contraindications:
Recent CVA/stroke (lecture: within 2 months)
Active bleeding
Recent surgery (lecture: within 10 days)
Recent trauma
Severe hypertension
Monitor closely for bleeding
Surgical intervention
Clot removal (embolectomy)
Transvenous/IVC filter insertion
Monitor for bleeding and infection
Monitor WBC/CBC as ordered
PE – Prevention
Overall goal: Prevention
Identify patients at risk for DVT/PE
Early ambulation/walking
SCDs (sequential compression devices)
Compression stockings as ordered
Hydration
Prevent prolonged immobility
Anticoagulant prophylaxis when ordered:
Low-dose heparin
Lovenox (enoxaparin) SQ
Other prophylaxis as prescribed
Pulmonary Hypertension (PHT)
“The other high blood pressure”
Elevated pressure in the pulmonary arteries
Pulmonary artery pressure is normally much lower than systemic blood pressure
Normal mean pulmonary artery pressure is about 14 mmHg
Reflects the pressure the heart needs to pump blood from the heart to the lungs
Narrowing of pulmonary arteries → harder for blood to flow
Heart must work harder to pump blood to the lungs
Increased workload → right ventricular hypertrophy/weakening → right-sided heart failure
Can be fatal
Usually not curable, but treatment can improve symptoms and quality of life
May not be recognized until late in the disease
Suspect with DOE (dyspnea on exertion) without another obvious cause
Pulmonary Hypertension - Risk Factors / Causes
Idiopathic → cause unknown
Sickle cell disease
Altered immune response/HIV
COPD
Obesity
Sarcoidosis
Smoking
Valvular heart disease
Congenital heart defects
Pulmonary Hypertension - S/S
Dyspnea
Begins as dyspnea on exertion (DOE)
Progresses to dyspnea at rest
Weakness
Fatigue/tiredness
Dizziness
Syncope (fainting) may occur
Anorexia/loss of appetite
Signs of right-sided heart failure:
Pedal/peripheral edema
Ascites
JVD
Liver enlargement/congestion
Weight gain
Swelling of extremities
Murmur may be present
Symptoms are generally insidious (develop slowly)
Pulmonary Hypertension - Diagnosis
H&P
Pulmonary artery pressure (PAP)
Echocardiogram
EKG
CXR
PFTs
V/Q scan
CTA may also be used
Pulmonary Hypertension - Medical Management
Manage underlying disease
Long term medication
Heart-lung transplant
Cure?
Pulmonary Hypertension - Nursing Management
Identify at risk
Teaching re: lifestyle changes, medications, travel, support groups
Nursing Assessment
O₂/oxygenation
Edema
JVD
Daily weight/weight gain
Swelling of extremities
Monitor for right-sided heart failure
Cor Pulmonale - Pathophysiology
Right-sided heart failure caused by pulmonary hypertension (PH)
Usually related to chronic lung disease, especially COPD
Chronic lung disease can cause:
Hypoxemia → low O₂
Hypercapnia → high CO₂
↑ pulmonary vascular resistance/ pulmonary hypertension
Increased pressure in pulmonary circulation makes the right ventricle work harder
Right ventricle enlarges (hypertrophies) → eventually weakens and fails
Leads to right-sided heart failure
Also called pulmonary heart disease
Cor Pulmonale - Medical Management
Improve ventilation
Improve heart failure
Bed rest, sodium restriction, digitalis (get rid of fluids)
Improve underlying disease
Pulmonary hygiene and CPT
Cor Pulmonale - Nursing Management
Observe for acute respiratory failure
Teaching re: activity, diet, medications
Acute Respiratory Failure
Failure of any component of breathing
ventilation
diffusion
transport of gases
Rapid – minutes to hours
Acute Respiratory Failure - ABG 50/50 rule
pH < 7.35
Pa O2 < 50
PCO2 > 50
Causes of Respiratory Failure - Ventilatory Failure
Extra-pulmonary
Neuromuscular disorders
Spinal cord injuries (SCI)
CNS dysfunction
Chemical depression (O.D.)
Others
Intra-pulmonary
Airway disease
Pulmonary edema
Pneumonia
COPD
Causes of Respiratory Failure - Oxygenation Failure
Low atmospheric oxygen concentration
Abnormal hemoglobin
Pulmonary embolism
HF
Hypovolemic shock
Hypoventilation
Mechanical obstruction
S&S of Respiratory Failure
Restlessness/confusion/headache- early signs
Pallor advancing to cyanosis (Central cyanosis is a late sign)
Diaphoresis (sweating)
Anxiety
Tachycardia/Tachypnea
Shallow respirations with accessory muscle usage
Diminished Lung Sounds- no lung sounds (late)
Lethargy/Fatigue (later)
Treatment- Mechanical Ventilation Indications:
Airway protection
Compromised or at risk
Acute respiratory failure
Diagnosed emergently on clinical presentation or based on diagnostics
Treatment- Mechanical Ventilation Goals:
Identify and correct the underlying cause
Improve oxygenation and gas exchange
Eliminate/remove excess CO₂
Reduce work of breathing (WOB)
Minimize risk of lung injury
Improve patient comfort
ETT insertion + mechanical ventilator may be required
Ventilator air is warmed and humidified
Intubation Steps
“Before we vent them, we have to tube them.”
Preparation
Gather equipment and medications
Position patient
Pre-oxygenation
Give O₂ before intubation
Pretreatment
Medications may be given before induction
Paralysis with induction
RSI (Rapid Sequence Intubation)
Protection and positioning
Protect airway and position appropriately
Placement with proof
Insert ETT
Confirm correct placement
Post-intubation management
Connect to mechanical ventilator
Monitor patient closely
Nursing Role
Nurse usually does not intubate
Nurse assists with intubation according to hospital policy
Respiratory therapist commonly performs/assists with intubation depending on facility protocol
Intubation Preparation
Gather all equipment needed- crash cart
Light source
Skilled personnel
Difficult airway cart
Glide scope
Ensure sx properly working!!
SOAP ME (ACLS)
S – Suction
Turned on and working
O – Oxygen
Include backup oxygen supply
A – Airway equipment
Laryngoscope/handles
Endotracheal tubes
Stylets
Supraglottic airways
P – Pharmaceuticals
Induction agent
Muscle relaxant
Adjuvant medications
Emergency medications
M – Monitors
Audible SpO₂ tone
BP at least every 5 minutes
E – Emergency equipment
Defibrillator
Emergency/invasive airway equipment
Preoxygenation
Give 100% oxygen for 3–5 minutes
Can use:
NRB (nonrebreather mask)
Ambu bag/BVM
Allow patient to breathe spontaneously when possible
Position:
Prefer head-elevated/sitting position if tolerated
If spinal injury is suspected and the patient must remain immobilized → reverse Trendelenburg
Helps prevent hypoxemia during intubation/apnea
Helps reduce risk related to aspiration
May be performed by RN or RT
With an Ambu bag: 4–8 breaths may be sufficient per lecture
A healthy patient may only have about 1 minute of safe apnea on room air
Pre-medication
Purpose: Medications are given before intubation to decrease unwanted effects of intubation
Often used as part of RSI (Rapid Sequence Induction and Intubation)
LOAD
L – Lidocaine
1.5 mg/kg IV
May help blunt increase in ICP
May decrease bronchospasm
O – Opiates
Fentanyl 2–5 mcg/kg IV
Helps blunt the response to intubation
A – Anticholinergics
Atropine for children
Glycopyrrolate may be used
Helps reduce secretions/bradycardia
D – Defasciculating dose
Small dose of a nondepolarizing neuromuscular blocker
May be given if succinylcholine is planned
Placement with Proof
Each attempt should not exceed 30 seconds, maximum of 3 attempts
If more than one attempt is needed, ventilate the patient 30-60 seconds between
After intubation, inflate the cuff
Confirm tube placement with exhaled carbon dioxide detector and CXR
Have to hear lung sounds on both side when tube is in
Tape near lips – remember number
Post-intubation Mgmt
Secure endotracheal tube in place
Set ventilator settings
Continue to medicate
Recheck V/Sand pulse ox
Malfunctions- what to do?
Document
Sizes
Depth markings on shaft/lip line
Cuff/ balloon
How placement was confirmed
Work with collaboration with RT!
Vent Settings - Rate & Tidal Volume
RR-How many breaths will the vent deliver per min?
The pre-set number of positive pressure breaths per minute.
The pt can breathe more depending on the mode
Tidal Volume :The amount of air the ventilator has been set to deliver during a single breath. Reflects the amount of air inspired and expired
This is the minimum amount the pt will breath
V T estimated at 6-12 ml/kg of IBW (may initially be higher).
FiO2 Setting
FiO₂ = Fraction of inspired oxygen
Represents the amount/percentage of oxygen delivered by the ventilator
Range:
0.21 = 21%
1.0 = 100%
Room air = 20.8% ≈ 21% O₂
FiO₂ setting is based on:
Patient’s condition
Recent ABG results
How the patient is responding to treatment
Example:
FiO₂ 0.40 = 40% O₂
FiO₂ 1.0 = 100% O₂
May start with a higher FiO₂ for severe hypoxemia and then decrease it as oxygenation improves.
Goal: Use the lowest FiO₂ necessary to maintain adequate arterial oxygenation.
Normal PaO₂ = about 80–100 mmHg
Always look at recent ABGs—do not use an old admission ABG if the patient’s condition has changed.
Positive End Expiratory Pressure -PEEP
Increases pressure in the lungs at the end of expiration
Helps keep alveoli open
Prevents atelectasis
Improves:
Oxygenation
Alveolar ventilation
Lung compliance
Used along with other ventilator modes
Complications of PEEP
Barotrauma → lung injury from excessive pressure
↓ Venous return
↓ Cardiac output (CO)
↑ Intracranial pressure (ICP)
Pulmonary edema
Very high PEEP can damage alveoli and cause air leaks/lung injury
Continuous Positive Airway Pressure (CPAP)
Positive pressure during inhalation and exhalation
Requires spontaneous breathing
PEEP ≈ CPAP in terms of continuous positive pressure
Delivery
Invasive
Endotracheal tube
Tracheostomy
Noninvasive
Tight-fitting face mask
Good seal required
Ventilator
CPAP is set using the PEEP setting
Example:
FiO₂ = 40%
PEEP/CPAP = 10 cm H₂O
Candidates
COPD
Pulmonary edema
Chronic respiratory failure
Chronic heart failure
Sleep apnea
Some patients who do not want intubation
Can be used for weaning from mechanical ventilation
Noninvasive PPV
CPAP
BiPAP
Important
Patient must be able to breathe spontaneously
Avoid/use cautiously with head, neck, or facial trauma that prevents a proper mask seal
Synchronized Intermittent Mandatory Ventilation - SIMV
Often used as a weaning mode
Patient breathes spontaneously between machine-delivered breaths
Machine provides a set number of mandatory breaths
Useful when ABGs and respiratory rate are improving/normal
Goal is to gradually allow the patient to do more of the breathing
Assist Control - AC
Used when patient is still breathing but breaths are not effective
Patient may have shallow or inadequate breaths
Ventilator delivers a full supported breath when the patient initiates a breath
Provides more support than SIMV
Controlled Mechanical Ventilation - CMV
Used for patients who are not breathing adequately or at all
Example: comatose or overdose patient
Ventilator provides the patient's breaths
Used for the sickest patients who cannot adequately breathe on their own
BiPAP – Bilevel Positive Airway Pressure
Provides 2 levels of positive airway pressure
IPAP = inspiratory positive airway pressure
EPAP = expiratory positive airway pressure
IPAP is higher than EPAP
More pressure is needed during inspiration
Lower pressure during exhalation makes it easier to breathe out
Example:
FiO₂ = 40%
IPAP = 10 cm H₂O
EPAP = 6 cm H₂O
Noninvasive ventilation
Delivery:
Nasal/oral mask
Nasal pillows
Mouthpiece
Compliments/supports the patient’s own breathing
Requires the patient to be spontaneously breathing
Indications
Sleep apnea
COPD
Other patients who need noninvasive respiratory support
Tolerance
Tolerance varies
Often used at night
Hazards of Mechanical Ventilation
ETT (Endotracheal Tube) complications
Dislodgement/malposition
Tube may enter right mainstem bronchus
Tube may be positioned too high in the mid-trachea
Kinking → obstructs airflow
Cuff failure
Air leak
Inadequate seal
Obstruction
Secretions
Cuff/balloon problems
Pressure necrosis
Excessive cuff pressure can damage tracheal tissue
Aspiration
Can lead to aspiration pneumonia
Children
pediatric ETTs may not have a cuff
Aspiration prevention
Anti-ulcer/stress-ulcer medications may be used to help maintain gastric pH and reduce complications if aspiration occurs
Maintain appropriate cuff pressure
Cuff pressure
Keep adequate but not excessive
Lecture: <20 mm Hg to reduce risk of tracheal necrosis
Hazards of Mechanical Ventilation
Excessive pressure
Barotrauma → lung damage from high pressure
Pneumothorax → alveoli can rupture and air enters pleural space
Alveoli can rupture
Decreased cardiac output (CO)
Positive pressure compresses the heart and great vessels
↓ Venous return
↓ CO
↓ Tissue perfusion
Signs of decreased CO
↓ Urine output (UOP)
Monitor pulmonary artery catheter readings if present
Pulmonary infection
VAP – Ventilator-Associated Pneumonia
HOB 30°
Mouth care q4h
Turn q2h
Hand hygiene
Key concern
Mechanical ventilation can cause a ventilator-acquired pneumothorax
Nursing Care r/t Mechanical Ventilation
Daily CXR
Daily ABG
Daily weight
Turn/ROM
I&O
Lab values
Hydration, nutrition, O2 carrying capacity, muscle strength
Na+, K+, Mg++, serum osmolality, H&H, BUN, creatinine
Suctioning PRN
For all ventilator alarms: Assess patient first!
cause unknown- bag patient and call RT!
High-pressure alarm
Possible kinked tubing
Secretions/obstruction can also increase pressure
Low-pressure alarm
Possible disconnection from the ventilator
Possible leak
Nutrition
Monitor nutrition closely
Carbohydrate metabolism produces CO₂
Too much carbohydrate can increase CO₂ production
Adequate protein is needed for respiratory muscle strength
Troubleshooting
Identify the problem quickly
Is it a patient problem or a ventilator problem?
Manage the patient, not the alarm! ⭐
If in doubt → bag the patient
DOPE
D – Displaced
ETT may be displaced/dislodged
O – Obstructed
Secretions
Kinked tube
Patient biting tube
P – Pneumothorax
E – Equipment failure
“Bucking the Vent”
Patient is out of sync with the ventilator
Example: patient tries to exhale while the ventilator is delivering inspiration
May need:
Suctioning
Sedation adjustment
Ventilator adjustment
Low-Pressure Alarm = LEAK
Tube disconnection
Cuff leak
Tube dislodgement/extubation
Leak in tubing/system
Gas-flow/equipment problem
High-Pressure Alarm = BLOCKAGE/RESISTANCE
Secretions
Kinked tube
Pulmonary edema
Patient coughing
Patient biting the tube
May need suctioning
May need sedation if inadequately sedated
If the Cause Cannot Be Identified Quickly
Assess the patient first
If becoming deoxygenated:
Disconnect from ventilator
Use manual resuscitation bag (Ambu/BVM) with 100% O₂
Call RT/help
Continue manual ventilation until the problem is corrected
Manual Ventilation
100% O₂: use 10+ L/min
Bag-mask ventilation: 1 breath every 5–6 seconds
10–12 breaths/min
Advanced airway: 1 breath every 6–8 seconds
8–10 breaths/min
Suctioning
PRN (as needed) — do NOT suction routinely
Indications:
Visible secretions in tubing
Coarse crackles
↓ O₂ saturation
↑ Work of breathing (WOB)
Asymmetrical chest movement
Before Suctioning
Pre-oxygenate the patient ⭐
Monitor:
Vital signs
Cardiac rhythm
Watch for:
PVCs
Bradycardia
During Suctioning
Insert the catheter without suction
Apply intermittent suction while withdrawing
Suction only while coming OUT
Limit passes according to facility policy/protocol
Lecture: may go in up to 3 times
After Suctioning
Post-oxygenate
Reassess:
O₂ saturation
Respiratory status
Breath sounds
VS/rhythm
Evaluate whether secretions were effectively removed
Saline
Do NOT routinely instill saline
May be considered for thick, tenacious secretions per policy
Weaning from the Vent
Look for trends of improving clinical picture
Physically & Psychologically ready
Collaborative Effort- HC Team
Extubation
Observe for fatigue and hypoxia
Increased WOB
Increased RR, HR
Diaphoresis/anxiety
Falling SpO2, rising BP or falling BP
Look for signs of exhaustion!
Weaning- simply means withdrawing client from vent. Pt must be stable enough to come off.
3 stages: 1) vent, 2) ETT 3) oxygen
Want to wean them as quickly as we can or as they can tolerate for pt safety
Tracheostomy
Surgical opening in trachea
Long term ventilation
By-pass obstruction
Can only stay down for 2 weeks
If pt doesn’t get better from ventrilor , put in tracheostomy
Complications:
bleeding
pneumothorax
aspiration
air embolism
laryngeal nerve damage
tracheal wall damage
airway obstruction