Transcript NURS 2140 Pulmonary Disorders WI 2012

Nursing Management of Patients
with Respiratory Disorders
NURS 2140
Winter Quarter 2012
Teresa M. Champion, RN MSN
ASSESSMENT OF PATIENTS
WITH RESPIRATORY
DISORDERS
Anatomy Physiology of Pulmonary
System
Ventilation – movement of air in and out
of lungs
 Respiration – consists of diffusion of
oxygen across alveolar-capillary
membrane into pulmonary circulation and
release of carbon dioxide molecules
across the alveolar- capillary membrane
through the airways out into the
environment

Exchange of Gases during
Respiration

Respiration Perfusion – the exchange of O2
and CO2 across the alveolar membrane
◦ Alveoli – place in lungs where exchange occurs
and must be adequately expanded by air to have
adequate contact with hemoglobin
 If alveoli are expanded adequately but unable to
exchange due to edema or secretions – a
ventilation(V)/perfusion(Q) mismatch occurs
 If alveoli are not expanded adequately despite blood flow
– Ventilation (V) and Perfusion (Q) mismatch will also
occur
Mechanisms of Respiration

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
Ventilation – dependent on neuromuscular
and musculoskeletal integrity
CNS – medulla and Pons respond to changes
to carbon dioxide and oxygen levels in the
blood by increasing or decreasing rate and
depth of respiration
Musculoskeletal – assist and influence
respiration - intercostal muscles, diaphragm,
abdominal muscles, thoracic muscles
(scalene, sternomastoid and trapezius)
Inspiration and Expiration

Influenced by intrapleural pressures
◦ When the pressure of air in the lungs reaches
capacity during inspiration, expiration begins
 Inspiration is active
 Expiration is passive
Movement of air in one breath is the tidal
volume
 Movement of air over one minute is minute
ventilation
 Normal tidal volume at rest is ~500ml, but
can increase if more is demanded by the
body (i.e. exercise and stress)

Collection of Patient Data

History
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Biographic and demographic data
Chief complaint - dyspnea
Past medical history, allergies
Family history
Risk factors
Social history, Cultures
Medications
Nutrition
Travel and Areas of Residence
PHYSICAL EXAMINATION

Inspection
◦ General Appearance
◦ Mentation
◦ Rate, Depth and Rhythm of Respirations
 Tachypenea, Bradypnea, Orthopnea, Apnea, Hyperpnea
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Thoracic Size and Shape
Thoracic Expansion and Symmetry
Use of Accessory Muscles
Color and Appearance of Skin and Extremities
 Pallor
 Cyanosis
◦ Neck Inspection – Tracheal Deviation
ABNORMAL BREATHING
PATTERNS

Cheyenne Stokes
• Breaths are deep than become shallow followed
by periods of apnea
• Causes: severe brain pathology - brain stem
herniation, Increased ICP, compression on Brain
Stem
Kussmal’s
• Breaths are deep, rapid and labored
• Rates are >20 bpm
• Causes: metabolic acidosis, renal failure,
diabetic ketoacidosis

PHYSICAL EXAMINATION

Palpatation of Skin and Extremities
◦ Edema – Caused by Pulmonary HTN
 8mm – 4+, 6mm – 3+, 4mm – 2+, 2 mm – 1+
◦ Skin Temperature & Moisture
 warm moist skin r/t increased effort of breathing, possible fever
from pulmonary infection
 Dry skin-moisture lost from increased respirations
◦ Clinical Reference Points – landmarks
 Trachea, nipple line, sternum, intercostals, axillary line, midaxillary
line, midclavicular line
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Chest Excursion – should be equal and up to 5-10 cm
Tactile Fremitus – palpations of vibration in thorax
Tenderness
Crepitus – also called “subcutaneous emphysema – air
trapped under the subcutaneous tissue
PHYSICAL EXAMINATION

Auscultation of the lungs – 4 types of
breath sounds
◦ Tracheal Breath Sounds –
 loud and high pitched – over the largest airway and are the
loudest – length of time heard is equal during expiration and
inspiration
◦ Bronchial Breath Sounds –
 loud and high pitch, harsh and less turbulent and lower in
frequency than tracheal – Expiration is heard longer than
inspiration
◦ Bronchovesicular –
 Midway in pitch between Bronchial and Vesicular and are
heard during inspiration and expiration
◦ Vesicular
 Soft and low pitched – heard longer during expiration, heard
over most of thorax
ADVENTITIOUS BREATH SOUNDS

Crackles (Rales)
◦ Indicate fluid, inflammation in airways – snapping sound
when airways open – can be heard when airways close too
but softer sounding than on inspiration
◦ Intermittent or discontinuous.
◦ Fine or Course

Wheezes
◦ High-pitched musical sounds caused by inflammation in
narrowing airways or bronchospasms
◦ Rhonchi – indicate mucus secretions in the airways
◦ Caused by air passing through mucus strands
◦ Can be heard on inspiration and expiration
◦ Continuous/ discontinuous (intermittent),
◦ Mild/moderate/severe
ADVENTITIOUS BREATH SOUNDS

Stridor
◦ Heard only during inspiration as air attempts
to flow though an obstruction, high pitched
crowing sound – needs immediate
intervention

Pleural Friction Rub
◦ Indicate inflamed pleural surfaces – easily
heard on inspiration – hold breath to
determine it is not pericardial
USING THE STEHASCOPE

Diaphragm - best for
higher pitched sounds, like
breath sounds and normal
heart sounds.

Bell - is best for
detecting lower pitch
sounds, like some heart
murmurs, and some
bowel sounds. It is used
for the detection of
bruits, and for heart
sounds (for a cardiac
exam, listen with the
diaphragm, and repeat
with the bell).
PHYSICAL EXAMINATION

Percussion
◦ Dull - Abnormal Finding
 Heard over solid tissue, occurs when air is absent, can be
heard over consolidation areas with pneumonia, pleural
effusion, hemothorax, solid tumors
 Dull thumping sound without vibration
◦ Resonant – Normal Finding
 heard over lung fields during inspiration while lungs are full of
air
 low pitched clear sounds – Normal Finding
◦ Hyperresonant – Abnormal Finding
 Very loud, lower pitched longer sound than resonance
 Drum like sound with vibration
 indicates hyperinflamation – emphysema, pneumothorax
PAIN
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Pain in association with breathing may be related
to Pulmonary Embolism, Pneumothorax, Pleural
Disease, Pericarditis, Musculoskeletal Disease or
Pneumonia
Sudden onset shortness of breath may be related
to Pulmonary Embolism or pneumothorax
Pain during respiration may decrease tidal
volumes
Pain management enables participation in
rehabilitative activities and promotes deep
breathing to prevent pneumonia and atelectasis
Use cough suppressants with caution
GERONTOLOGICAL
CONSIDERATIONS

Aging decreases respiratory function
◦ Osteoporosis – stooped posture, decreased rib
expansion
◦ Anterior to posterior diameter increases
◦ Alveolar surface decreases
◦ Decreased elasticity
◦ Increased atelectisis
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Lower arterial oxygen values – decreased
exchange of O2/CO2
Increase risk of pneumonia – Decreased tidal
volumes, ineffective cough
Risk of aspiration may increase with aging
Aging may affect patient comfort needs during
the examination
HEALTH PROMOTION
Smoking cessation
 Decrease exposure to second-hand smoke
 Hand Hygiene
 Flu and Pneumonia Vaccines
 Instruction and use of Personal Protective
Equipment (PPE) especially in the
workplace for workers exposed to
allergens, mold, bird, bat and rat feces and
other toxins like asbestos

STANDARD OF CARE

For patients with cardiac and respiratory
illness, standard is:
◦ Continuous or intermittent observation of the
patient’s oxygen saturation (most cost effective)
◦ End-tidal carbon dioxide levels (being used more,
but is more costly but most accurate).
◦ Monitoring Peak Flow results is utilized to trend
treatment effectiveness in patients with asthma
RESPIRATORY MONITORING

Pulse Oximetry
◦ Measures saturation of hemoglobin
◦ May NOT be accurate with patients with low Hgb,
hypovolemia and shock states
◦ Nail polish, ambient light may interfere with
reading
◦ Wave forms should match pulse rate and should
not be dampened
RESPIRATORY MONITORING

Peak Flow Meters
◦ Evaluate air movement to determine severity of
asthma exacerbation
◦ Measure Peak Expiratory Flow Rate
◦ Measurements are based on age and body size
◦ Red Zone (Dangerous) – less than 50% of the
normal value
◦ Yellow Zone (caution) – Between 50% to 80%
below normal value
◦ Green Zone (Good) – meets 80% to 100% of
normal value
RESPIRATORY MONITORING

Arterial Blood Gases
◦ Determine Respiratory Acidosis and Alkalosis
◦ PaO2 levels below 80mmHg and/or SaO2 <95%
indicate hypoxemia
◦ Cost $800 to $1500.00 per draw
◦ Invasive procedure
RESPIRATORY MONITORING

Capnography
◦ Measures exhaled carbon dioxide or End Tidal CO2
(ETCO2)
◦ Small disposable capnographers are used to check ET
Tube placement after intubation and/or continuous
monitoring of tube placement
◦ Capnography monitoring has been added to the 2010
– 2015 ACLS Guidelines for Compression
Effectiveness.
◦ Normal ETCO2 values are 35mmHg to 45mmHg.
◦ ETCO2 values between 10-20mmHg indicate high
quality compressions
◦ ETCO2 less than 10mmHg – quality of chest
compressions need improvement
MONITOR SHOWING ETCO2
WAVEFORM
RESPIRATORY PATHWAY
DISORDERS
SLEEP APNEA
 AIRWAY OBSTRUCTION
 TRACHEOSTOMY

ANATOMY OF RESPIRATORY TRACT
SLEEP APNEA
Defined – a person stops breathing for
more than 10 seconds, more that 20-30
times in an hour
 3 types –

◦ Central
 Brain fails to send signal to the breathing muscles to
initiate respirations (less common)
◦ Obstructive
 Physical obstruction from tissues in upper airway
◦ Combination of both or Mixed Sleep Apnea
RISK FOR SLEEP APNEA
Overweight/Obesity
 High Blood Pressure
 Decreased Airway Size – congestion,
inflammation (allergies), anatomical
abnormalities
 Family History

MEDICAL MANAGEMENT FOR
SLEEP APNEA
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Weight loss
Avoid alcohol, tobacco and sleeping pills
(sedatives)
Use side-lying positions when sleeping
Dental devises that move tongue or mandible
forward
Continuous Positive Airway Pressure (CPAP)
Machines
Surgical Interventions – UVPPP – resection of
the uvula and soft palate, Tracheotomy
Focus is on airway patency
AIRWAY OBSTRUCTION
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Potentially life threatening – requires immediate
intervention
Types: foreign object, allergy, lesions, stenosis,
swelling
Causes:
◦ Viral and Bacterial Infections, fire or inhalation burns,
allergic reactions (foods/medications/bee stings)
◦ Infections after dental extractions
◦ Laryngeal trauma-MVA, Strangulation or surgical
procedures
◦ Large tumors
◦ Aspiration of foreign objects
Clinical Manifestations of Airway
Obstruction
STRIDOR
 Inability to speak (partial or complete)
 Labored breathing and use of accessory
muscles
 Air Hunger (mild)
 Cyanosis (severe)

Medical Management of Airway
Obstruction
Diagnosis and treat the cause
 Provide Oxygenation Support!!
 Sit in upright position
 Keep patient’s airway patent (if partial or
mild obstructions get worse – need
immediate intervention)
 Secure and protect airway – Endotracheal
Intubation, Cricothyroidotomy or
tracheotomy – bag/mask ventilation will not
work with obstruction!

Tracheotomy
Insertion of artificial airway in the trachea
 Recommended for oral/nasal
endotracheal intubations lasting longer
than 1 – 2 weeks. (book says 7 – 10 days)
 Usually is temporary to protect airway
until underlying cause can be fixed or
corrected

Tracheotomy
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Incision is below the prominent thyroid cartilage
(Adam’s Apple) and below the cricoid cartilage –
between 2 – 3 OR 3 – 4 tracheal cartilages
A tube is placed and secured (Sutured) to keep the
tracheal stoma open
The tube is also secured with ties
The tube remains in place until the tracheal stoma is
well established and won’t close back up
A post tracheotomy kit is kept at bedside or on the
nursing unit if accidental decannulation occurs
An Obturator is kept at bedside to prevent stoma
closure if decannulation occurs until new
tracheotomy tube can be put in immediately
TYPES OF TRACHEAL TUBES
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Made of silicone, plastic, stainless steel or
silver
With or without an inner cannula
With or with out a cuff
◦ Mechanical ventilation requires cuffed tubes to seal
the airway to maintain pressures for ventilation
◦ Cuffed tracheal tubes decrease aspiration risk
◦ Inner cannulas prevent tube obstructions from
thick crusted secretions

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Average adult size are 7 to 8
Shiley or Bivona are most common
Assessment of New Tracheal
Artificial Airway
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Auscultation of the lungs
Monitoring Oxygenation saturations
Assessment of increased amount of blood in
the sputum and around site
Subcutaneous emphysema (crepitis) around
the neck
Respiratory distress
Patency of tracheal tube
Postoperative pulmonary edema (POPE)
Interventions following
Tracheostomy
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Encourage cough and deep breathing
Suction as necessary, but keep to a minimum
Provide supplemental oxygen
Pre-oxygenate with 100% Oxygen when
suctioning
Hyperventilate (bag – suction) when
necessary
Suction limited to 5-10 seconds with each
pass
Insert catheter till patient starts to cough or
meet slight resistance – do not use force
Tracheostomy Cares
Tracheotomy cares should be done every 8
to 12 hours with cleaning the inner cannula
or changing the disposable cannula
 Most medical institutions no longer use
Hydrogen peroxide to clean around
tracheostomy site (book says use halfstrength)
 Aseptic technique is used when cleaning
the inner cannula (sterile gloves)

Laryngectomy
Trachea is sutured to the stoma
 Oral airway is permanently bypassed
 Patients lose the ability to speak because
the vocal cords are bypassed permanently
 Patient only breath out of their stoma
 The esophagus still follows the normal
pathway and patients can still eat normally

LOWER AIRWAY DISORDERS
Restrictive lung diseases (interstitial
lung diseases)
◦ Result in reduced lung volumes
◦ Alteration in lung parenchyma (alveolar tissue
w/ terminal bronchioles, respiratory
bronchioles, alveolar ducts)
◦ Disease of pleura, chest wall or
neuromuscular apparatus
◦ Characterized by reduced total lung capacity,
vital capacity, or resting lung volume
Obstructive lung diseases
◦ Common characteristic – chronic and
recurring blockage of airways
◦ Limit airflow through the airways and out of
the lungs
LOWER AIRWAY DISORDERS
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Infections and Inflammatory Disorders of the
Lungs
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Acute or Chronic Bronchitis
Influenza – complication - pneumonia
Pneumonia – 6th leading cause of death
Tuberculosis – Mycrobacterium tuberculosis
Lung Abcesses/Empyema
Pneumonia
Inflammatory process that results in
edema of the parenchymal lung tissue
(aveoli and bronchioles) caused by
inhalation of bacteria, viruses, fungi,
protozoa or parasites or enter lungs via
the blood stream
 Aspiration of water, food, vomitus, toxic
gases, chemicals and smoke
 Radiation therapy
 Effects terminal gas exchange

Classifications of pneumonia
Type of agent causing infection
 Distribution of the infection (lobar consolidation of a lobe, or bronchial –
patchy consolidation)
 Setting (community or healthcare
(hospital) aquired

Community Acquired Pneumonia
(CAP)

CAP: begins outside hospital or is
diagnosed w/in 48 hours after admission
◦ Patient did not reside in a long-term facility
prior to admission
◦ Incidence of CAP is highest in winter months
◦ Smoking an important risk factor
Healthcare (Hospital) Acquired
Pneumonia (HAP)

HAP: occurs > 48 hours after hospital
admission
◦ HAP has a mortality rate of 20% to 50%
◦ 90% of HAP infections are bacterial
◦ Compromised immune systems, chronic lung
disease, intubation and mechanical ventilation
increase risk
Severe Acute Respiratory Syndrome
Severe acute respiratory syndrome (SARS) is a
serious form of pneumonia. It is caused by a virus
that was first identified in 2003. Infection with the
SARS virus causes acute respiratory distress
(severe breathing difficulty) and sometimes death.
 SARS is a dramatic example of how quickly world
travel can spread a disease. It is also an example of
how quickly a connected health system can respond
to a new health threat
 World Health Organization (WHO) physician Dr.
Carlo Urbani identified SARS as a new disease in
2003.

Clinical Manifestations of
Pneumonia
Fever, chills
 Increased respiratory rates
 Rusty bloody sputum
 Crackles
 X-ray abnormalities
 Chest discomfort
 Cough
 Fatigue, muscle aches, headache, nausea

Nursing Management of Pneumonia

Administer antibiotics (prime treatment)
 Antibiotic Type depend on organism
Primary nursing intervention: Maintain
airway and O2 saturation above 93%
 Promote nutrition and hydration
 Provide small, frequent, high-carb, highprotein meals

Discharge Priorities/Prevention

Teach patient about
◦ Continue deep breathing and coughing
exercises 4x/day, 6-8 weeks
◦ Signs and symptoms to report to health care
provider
◦ Continue and complete antibiotic therapy as
directed
◦ Rest, fluids and nutrition important
Pulmonary Tuberculosis

Mycobacterium tuberculosis (bacteria)
◦ Transmitted via aerosolization (i.e., an airborne
route)
◦ Affects people with repeated close contact with
an infected but undiagnosed person
◦ TB an opportunistic infections common with
HIV/AIDS
◦ The newest form of TB is multidrug-resistant
tuberculosis (MDRTB)
◦ Resistant TB is difficult and costly to treat and can
be fatal
Clinical Manifestations
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Dyspnea
Weight loss
Cough
Sputum production, streaked with blood
Sleep disturbances
Lethargy, exhaustive fatigue, activity
intolerance, nausea, irregular menses
Low-grade fever may have occurred for
weeks or months
Fever also may be accompanied by night
sweats
Laboratory and Diagnostic
Procedures
Tuberculin skin test
 Chest x-ray
 Acid-fast bacillus smear
 Sputum culture
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Nursing Management
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Administer drug therapy as ordered by
health care provider
Report the diagnosis to the local health
department
Keep patient in negative pressure room with
respiratory airborne isolation
Maintain isolation until three consecutive
sputum cultures have tested negative
Focus on preventing the spread of the
infection
Discuss pain management, handling fatigue,
importance of good nutrition
Health Promotion and Prevention of
TB
The main focus of TB management is
preventing spread of the infection
 Patient typically must take drugs for 9
months
 Test and treat all persons in close contact
with the infected individual

Lung Abcess
Most often abscess is secondary to
anaerobic and aerobic organisms that
colonize the upper respiratory tract.
 Formation of multiple abscesses and
cavities occurs commonly in patients with
TB or fungal infections of the lung.
 Pulmonary Empyema - is a collection of pus
in the space between the lung and the inner
surface of the chest wall (pleural space).

Clinical Manifestations of Lung
Abcess
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Spiking temperature with rigors and night sweats
Cough with foul sputum
Pleural chest pain
Tachycardia
Dullness on percussion over the abcessed area.
Oxygen saturation may decrease with larger
abcesses
Laboratory and Diagnostic
Procedures for Lung Abcess
CT scan
 Pleural fluid and blood cultures may be
obtained (thoracentesis)
 Bronchoscopy
 Transtracheal aspiration via suction
sputum collection for cultures

Nursing Management of Lung Abcess
Penicillin G or clindamycin is the
pharmacologic therapy of choice
 Administer antipyretic, antibiotic, and pain
medications
 Assess for recent history of influenza,
pneumonia, febrile illness, cough, and sputum
production
 Space physical care to allow for periods of
rest between activities

Chronic Obstructive Pulmonary
Disease (COPD)
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
Characterized by chronic, recurrent
obstruction in pulmonary airways
Encompasses chronic bronchitis and
emphysema
◦ Obstruction is generally permanent and progressive

Unifying symptoms
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Dyspnea
Wheezing
Use of accessory muscles
Ventilation/perfusion (V/Q) mismatching
Decreased forced expiratory volume
Chronic Obstructive Pulomary
Disease (COPD)
Emphysema: abnormal, permanent
enlargement of the aveoli (air sacs)
accompanied by destruction of their walls
 Chronic bronchitis: characterized by
hypersecretion of mucus and chronic
productive cough that continues at least 3
months of the year for at least two
consecutive years

Etiology of COPD
The primary cause of COPD is exposure
to tobacco smoke. Clinically significant
COPD develops in 15% of cigarette
smokers.
 Age of initiation, total pack-years, and
current smoking status predict COPD
mortality

Pathophysiology of COPD

Obstructed airways close on expiration and
traps air in the distal portions of the lung,
causing:
◦ Hypoventilation (increased PaCO2)
◦ Ventilation/perfusion mismatching
◦ Hypoxemia
Edema and accumulation of inflammatory cells
lead to bronchial wall inflammation and
thickening
 Airway enlargement, loss of elastic recoil in the
alveoli trap air, limit outflow
 Enzymes called proteases break down elastin,
cause alveolar destruction

Nursing Management
Assess for dyspnea, muscle fatigue,↑ work of
breathing, worsening symptoms
 Monitor ABG results
 Manage the anxiety
 A major role of the nurse is patient and
family education

◦ Breathing retraining
◦ Use of postural drainage techniques
◦ Energy conservation

Single most important factor in preventing
COPD – smoking cessation
Cystic Fibrosis (CF)
A person is born with CF, and it affects boys
more than girls
 Affects Caucasians 5 times more often than
African American people
 Typical features: mucous plugging, chronic
inflammation, infection
 Peripheral bullae or blebs may develop due to
obstruction, airway wall weakening
 Affects mucous glands of the lungs, liver,
pancreas, and intestines
 Causes progressive disability due to multiplesystem failure

Clinical Manifestations of CF

Acute exacerbation characterized by:
◦
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Increasing breathlessness
Change in sputum volume, color, and viscosity
Tiredness
Loss of appetite
Weight loss
Include barrel chest and digital clubbing
GI: malabsorptive symptoms e.g. frequent loose and
oily stools, cramping, rectal prolapse
 Signs and symptoms of diabetes including abnormal
glucose tolerance, polydipsia, polyuria, and polyphagia
 Subtle manifestations: chronic sinusitis, nasal polyps


Nursing Management of CF
Assist patient to maintain adequate airway
clearance, reduce risk factors, perform
ADLs
 Involve patient/family in planning and
implementing the therapeutic regimen
 Encourage use of corticosteroids,
bronchodilators, and antibiotics
 Postural drainage techniques – percussion
and vibration

Diagnostic Tests for CF
Possibly abnormal ABGs and PFTs
 Abnormal sweat chloride test >60 mEq/L
 Chest x-ray – densities w/o consolidation
 Fecal fat analysis – fat concentration is
elevated
 Pacreatic Enzymes decreased
 Serum Glucose Increased
 Sperm count low
 Genetic Analysis – positive for CF
 Liver enzymes - elevated

Pulmonary Embolism (PE)
Thrombus breaks loose and blocks a
pulmonary artery
 Produces widespread pulmonary
vasoconstriction and impairs ventilation
and perfusion (V/Q) resulting in lifethreatening hypoxemia, pulmonary
ischemia and pulmonary infarction

Epidemiology of PE
Occurs mostly in older individuals, males
more than females
 Highest incidence in hospitalized patients
 In patients younger than 55 yrs of age
occurs more in females
 Patients who have survived PE have
higher incidence of recurring PE and the
development of pulmonary hypertension
and cor pulmonale

Etiology of PE
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
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Complication of a Deep Vein Thrombosis
(DVT) common after surgery, trauma,
childbirth, stroke, heart failure, Myocardial
Infarction (MI), Atrial Fibrillation, Cancer and
prolonged immobilization
Arise from thrombi in proximal deep veins
Can also arise from pelvis from childbirth or
pelvic fractures
Risk Factors of PE
Most common – prior history of DVT or PE
 Venous stasis with hypercoagulation states
or a clotting tendency of the blood
 Long trips in airplanes, trains and cars
 Oral contraception
 Pelvic, Hip or femur fractures
 Central venous catheters
 Genetic conditions causing increased clotting
disorders

Pathophysiology of PE
Pulmonary occlusion occurs when a bloodborne
substance occludes a branch of the pulmonary
artery and obstructs blood flow
 Embolism – thrombus, air (accidental air injection),
fat from bone marrow after a fracture, amniotic
fluid that enters the mother’s blood stream after
rupture of membranes at birth, piece of an IV
catheter that sheared off
 Atelectasis (lung collaspe) may occur from loss of
surfactant, pulmonary infiltrates can occur
 Systemic hypotension, decreased cardiac output,
pulmonary hypertension and right ventricular
failure and death.

Four types of PE Occurances
Massive occlusion of pulmonary
circulation
 Infarction of a portion of the lung
 Embolus without infarction
 Multiple pulmonary emboli that may be
chronic or recurrent

Clinical Manefestations
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Triad of symptoms – hemoptysis, dyspnea
(sudden onset), and chest pain
Many signs and symptoms are atypical –
pleural chest pain, chest wall tenderness,
friction rub
Small repeating emboli – decreases
pulmonary bed
Massive PE – tachypnea, S3 and S4 gallop,
tachycardia, sudden crushing chest pain and
are usually fatal
Diagnostic Testing for PE










AGB’s – abnormal in some cases
Pulse Oximetry – sometimes abnormal
WBC – may be elevated
ECG – tachycardia, peaked T-waves in lead II, right axis
deviation, right bundle branch block
D-dimer – positive >500 mg/L
V/Q scan – somes shows abnormal perfusion patern
Pulmonary Angiogram – positive
Lower extremity dopplers (U/S) – positive for DVT
Echocardiography – right sided heart failure
Spiral CT - positive
Nursing Management of PE
Evaluation of risk factors on admission and during
hospital stay
 Encourage maximal mobility, range of motion and
ambulation when appropriate or leg compression
devices if on bed rest
 Administer anticoagulant medication - heparin
continuous IV drip until coumadin started and PT/INR
is theraputic

◦ Monitor liver function when patients receive anticoagulants
Monitor Lab for anticoagulant effectiveness (Heparin PTT q 6 hrs till in range then q day)
 Assess for symptoms of bleeding and heparin-induced
thrombocytopenia (HIT)
 IVC Filter – vena cava filter

Discharge Teaching

Discharge priorities include educating the
patient and family about risk factors and
following treatment regimes
(anticoagulant therapy)
◦ Coumadin – routine INR
◦ Diet – low in vitamin K
Saddle
Pulmonary
Embolism
Cor Pulmonale

Alteration in the structure and function of
the right ventricle caused by a primary
disorder of the respiratory system
◦
◦
◦
◦

Chronic lung disease
Pulmonary embolism
Interstitial lung disease
Primary pulmonary hypertension
Right sided heart failure caused by the left
side of the heart or congenital heart disease
is NOT considered cor pulmonale
Pathophysiological causes of Cor
Pulmonale

Pathophysiological respiratory mechanisms
lead to Primary Pulmonary Hypertension
(PPH) then to cor pulmonale these include:
◦ Pulmonary vasoconstriction due to alveolar
hypoxia
◦ Anatomic compromise of the pulmonary vascular
bed
◦ Increased blood viscosity secondary to blood
disorders
◦ Idiopathic primary pulmonary hypertension
Two types of Cor Pulmonale
Acute: usually results from massive PE or
injury d/t mechanical ventilation for ARDS
 Chronic cor pulmonale usually caused by
COPD

Diagnostic Testing for Cor
Pulmonale
Echocardiography gives information about
the size of the heart
 Chest x-rays and CAT scan
 PFT evaluate ventilation/perfusion
mismatch
 ABG tests identify gas exchange, presence
of acidosis and alkalosis

Clinical Manifestations of Cor
Pulmonale


Asymptomatic initially
Later, as right ventricular (RV) pressures increase,
physical signs commonly include:
◦ Left parasternal systolic lift (visible pulsations to left
midsternal)
◦ Loud pulmonic component of the second heart sound (S2)
◦ Murmurs of functional tricuspid and pulmonic insufficiency
◦ Then even later, an RV gallop rhythm (third [S3] and fourth
[S4] heart sounds)
◦ Distended jugular veins, hepatomegaly
◦ Lower extremity edema, fatigue, dyspnea, chest pain on
exertion, cough
◦ In advanced stages, hepatic congestion leads to anorexia,
RUQ abdominal discomfort
Physical Assessment Findings and
Nursing Management









Increased chest diameter
Labored respirations with retractions of the chest
wall and use of accessory muscles
Hyperresonance to percussion
Diminished breath sounds
Cyanosis
Manage dyspnea by administration of oxygen
Administer medications to treat right ventricular
hypertrophy and pulmonary hypertension
Provide patient education re: managing equipment
and medications
Refer to home health and pulmonary rehabilitation
Nursing Management of Cor
Pulmonale







Manage dyspnea by administration of oxygen
Administer medications to treat right ventricular
hypertrophy and pulmonary hypertension
(vasodilators, calcium channel blockers)
Provide patient education re: managing equipment and
medications
Refer to home health and pulmonary rehabilitation
Regularly assess oxygen needs and medications
Single most preventive measure – encourage smoking
cessation
Avoid exposure to secondhand smoke and respiratory
pollutants
Complex Respiratory Disorders
The Alveolar-Capillary (A-C)
Membrane
Ventilation/Perfusion
Ventilation (V) – movement of air
 Perfusion (Q) – the movement of blood
carrying oxygen
 Near equal relationship of ventilation is
4L/min and perfusion 5L/min
 Acute Respiratory Failure commonly
caused by mismatch of ventilation and
perfusion

Ventilation is 4L/Min and Perfusion is 5L/min
Normal ventilation to perfusion is 4/5 or 0.8
V/Q is equal to 0.8
– no miss match
(b) V/Q is >0.8 – there
is ventilation but
no perfusion
(c) V/Q is <0.8 – there
is perfusion but
little or no
ventilation
(d) V/Q no perfusion
and no ventilation
(a)
Acute Respiratory Failure
Respiratory system unable to provide O2
and remove CO2
 Lungs can not meet the physiological
needs of the body due to failure of heart,
lungs or both.
 Hallmark of Acute Respiratory Failure is
respiratory difficulty with abnormal ABG’s

Three main categories of Acute
Respiratory Failure

Hypoxemia (deprived of oxygen)
◦ Caused by failure of oxygenation

Hypercapnea (high CO2 in blood)
◦ Caused by failure of respiratory system to
ventilate

Failure of respiratory centers in the brain
ABG Findings for ARF

Hypoxemia:
◦ PaO2 below normal (<60 mmHg)
◦ SaO2 <90% on room air

Hypercapnea:
◦ PaCO2 above normal (>50 mmHg)
◦ pH <7.3
Pathophysiology of Acute
Respiratory Failure

Alteration in oxygenation is most common
form of Acute Respiratory Failure
◦ Perfusion (Q)exceeds ventilation (V)
◦ A low V/Q ratio causes decreased oxygenation
of venous blood & a mixing of less oxygenated
blood with arterial blood
◦ Reduced arterial oxygen value (hypoxemia)

Hypoventilation
Pulmonary Edema

Types
◦
◦
◦
◦
◦
◦
Acute Pulmonary Edema
Cardiogenic Pulmonary Edema (CPE)
Noncardiogenic Pulmonary Edema (NCPE)
Neruogenic Pulonary Edema
Negative Pressure Pulmonary Edema
Pulmonary Edema in Specific Populations
Acute Pulmonary Edema
Abnormal accumulation of fluid in the
lungs
 Occurs rapidly – over minutes or hours
 Etiologies – all relate to failure of heart
and/or lungs

Cardiogenic Pulmonary Edema
(CPE)

Initial insult is caused by heart failure
◦ ↑ Pulmonary venous pressure leads to
◦ ↑ Hydrostatic pressure in pulmonary
capillaries
 Result: pulmonary edema
Cardiac dysfunction is most common
factor
 Fluid overload, and chronic hypoxemia
may also be present

Noncardiogenic Pulmonary Edema
(NCPE)
Insult to the A-C membrane
 Changes the permeability of the A-C
membrane
 Major causes: sepsis, inflammation, inhaled
toxins, drugs

Clinical Manifestations of
Cardiogenic PE/Non-Cardiogenic PE
Respiratory clues are identical
 Agitation, confusion common to both
CPE and NCPE
 Distinguishing factors are subtle
 Most evident in cardiac assessment, skin
appearance

Differentiating CPE/Non-CPE

Mostly evident in cardiac assessment, skin
appearance
◦ Example 1: tachycardia with hypotension and
cool diaphoretic skin suggests CPE
◦ Example 2: tachycardia with hypertension,
bounding pulses and dry skin suggests NCPE
Differentiating CPE/Non-CPE

Other Distinguishing Factors
◦ Jugular Vein Distension more common in
CPE
◦ If coronary artery catheter is used,
Pulmonary Artery Occlusion Pressures
(PAOP) or Pulmonary Capillary Wedge
Pressure (PCWP) above 18mmHg confirms
CPE
Neurogenic Pulmonary Edema

Direct insult to central nervous system
◦ Examples: seizures, cerebral hemorrhage, head
injury

Dyspnea (shortness of breath) is primary
presenting symptom
◦ Other symptoms may be present
◦ Crackles, pink frothy sputum
Negative Pressure
Pulmonary Edema
Caused by ventilation with airway
obstruction
 High pressures required
 When obstruction is relieved

◦ Hydrostatic pressure pushes fluid into lungs
Pulmonary Edema and Specific
Populations
Mountain climbers – HAPE (high altitude
pulmonary edema) – causes vasoconstriction
and hypoxemia and confusion –
vasoconstriction causes increased pulonary
pressures and forses fluid in the aveoli and
interstical spaces
 Heroin users
 Scuba divers/hyperbaric chamber users
 Excessive intravenous fluid administration

Acute Respiratory Distress
Syndrome (ARDS)
Most severe type of respiratory failure
 Caused by injury to A-C membrane
 Mortality rate = 40%
 Acute lung injury (ALI) less severe than
ARDS

Acute Respiratory Distress
Syndrome (ARDS)
ARDS leads to a buildup of fluid in the air sacs. This
fluid prevents enough oxygen from passing into the
bloodstream.
 The fluid buildup also makes the lungs heavy and
stiff, and decreases the lungs' ability to expand.
 The level of oxygen in the blood can stay
dangerously low, even if the person receives oxygen
from a breathing machine (mechanical ventilator)
through a breathing tube (endotracheal tube).
 ARDS often occurs along with the failure of other
organ systems, such as the liver or kidneys. Cigarette
smoking and heavy alcohol use may be risk factors.

Treatment for ARDS
Typically people with ARDS need to be in an intensive care
unit (ICU).
 The goal of treatment is to provide breathing support and
treat the cause of ARDS. This may involve medications to
treat infections, reduce inflammation, and remove fluid
from the lungs.
 A breathing machine is used to deliver high doses of
oxygen and continued pressure called PEEP (positive endexpiratory pressure) to the damaged lungs. Patients often
need to be deeply sedated with medications when using
this equipment. Some research suggests that giving
medications to temporarily paralyze a person with ARDS
will increase the chance of recovery.
 Treatment continues until you are well enough to breathe
on your own.

Causes of ARDS
ARDS can be caused by any major injury to
the lung. Some common causes include:
 Breathing vomit into the lungs (aspiration)
 Inhaling chemicals
 Lung transplant
 Pneumonia
 Septic shock (infection throughout the
body)
 Trauma

How the Ventilator Works
Monitors respiratory rate, pressure,
volume
 Delivers specified volume, pressure, or
both
 Controls concentration of oxygen
 Mixes compressed air with oxygen to
reach desired FiO2

Nursing Issues
Complexity of equipment is increasing
 Variety of equipment is increasing
 No standard terminology among
manufacturers

Terminology
Spontaneous breaths
 Mandatory breaths
 Assisted breaths
 Types of ventilation
 Modes

Types of Breath

Spontaneous breaths
◦ Patient initiates breath
◦ Patient controls switch from inspiration to
expiration

Assisted breaths
◦ Patient initiates breath
◦ Ventilator controls switch to expiration
◦ Ventilator controls volume and pressure
Terminology

Mandatory breaths – controlled entirely
by ventilator
◦ Inspiration
◦ Expiration
◦ Volume/pressure of gas delivery
Types of Ventilation
Volume – clinician controls tidal volume;
pressure can vary – can set rate, set
volume
 Pressure – clinician controls pressure;
tidal volume can vary - set rate, set
pressure, need to monitor minute
volumes – pressure is determined by lung
compliance – used for ARDS
 No clinical consensus on preferred type

Common Ventilator Modes
Mode: describes the pattern of breath
delivery
 Common modes

◦ Assist control mode (ACM) (A/C)
◦ Synchronized mandatory intermittent
ventilation (SIMV)
◦ Pressure support (PS or PSV) – assists
spontaneous breathing
◦ Pressure controlled ventilation (PCV)
Assist Control Mode
ACM delivers a preset volume or a preset
pressure for each breath
 Patient can trigger a breath or the breath
can be time triggered (CMV, A/C)
 Commonly used in care of in the
postoperative patient

Assist Control Mode

Nursing Implications of ACM
◦ As patient awakens, she or he may begin
initiating breaths
◦ Machine may not have time to deliver set
volume
◦ Patient can become hypoxic by attempt to
breathe faster, stacking breaths
◦ Pressure builds; lungs may be injured
Assist Control Mode

Nursing Implications of ACM
◦ Nurse must monitor to assure that patient
and machine are working together
◦ At high respiratory rates – air trapping may
occur and cause high pressures and the high
pressure to alarm on the ventilator
Synchronized Intermittent
Mandatory Ventilation
Very common mode in US
 SIMV sets the mandatory respiratory rate
(VE )
 Ventilator will deliver a set volume or
pressure
 Patient can also initiate a breath

◦ Ventilator waits for the patient, to breathe
◦ Synchronizes delivery of breath in concert
with the patient
Synchronized Intermittent
Mandatory Ventilation

Nursing Implications of SIMV
◦ Desirable for patient to “overbreathe” the
machine; i.e. breathe faster than the VE
◦ In SIMV, patient may initiate breaths, some are
assisted and some are not
◦ Team should evaluate VE, level of sedation or
analgesia
Pressure Support
PS is a form of assisted ventilation
 Requires stable respiratory effort from
patient
 IF ventilator senses negative pressure on
inspiration

◦ THEN ventilator supports the patientinitiated breath
Pressure Support

Does not control the rate or tidal volume
◦ Therefore, usually used with SIMV, CPAP
mode
◦ PS not triggered unless patient breathes
above the VE (mandatory rate)
Pressure Support

Nursing Implications of PS with SIMV
◦ If patient does not “overbreathe” the machine,
no benefit from PS
◦ The nurse should assess the patient and talk
to the team to determine a course of action
Pressure Control Ventilation
Clinician sets rate and pressure
 Tidal volume is allowed to vary
 Usually reserved for patients with
noncompliant lungs, difficult to ventilate
and oxygenate
 Gas delivery distinguishes PCV from PS

◦ Breath triggers rapid delivery of gas to reach
set pressure, then the flow is decelerated
Pressure Control Ventilation

Nursing Implications of PCV
◦ The nurse should trend the VE and the
expiratory volume over time
◦ Volume decrease may indicate lungs are
becoming less compliant
◦ Adjust Pressure to Achieve the Same Volume
Positive End-Expiratory Pressure
PEEP is a ventilator setting, not a mode
 Provides resistance at end of exhalation
 Prevents alveoli from collapsing
 CPAP – continuous positive airway
pressure – related to PEEP

Three Types of PEEP
Physiological PEEP – 5 cm of H2O
 Treatment PEEP – >5 cm of H2O
 Auto-PEEP - gas trapped in alveoli at end

expiration, due to inadequate time for
expiration, bronchoconstriction or mucus
plugging. It increased the work of breathing.

For most ventilated patients, PEEP of at
least 5 cm of H2O required to prevent
alveolar collapse
Nursing Implications of PEEP
PEEP of greater than 5 cm of H2O can
cause decreased cardiac output – and
CAUSE HYPOTENSION
 Pneumothorax at higher levels of PEEP
 The nurse should be aware of the level of
PEEP, especially if patient is hypotensive

Auto-PEEP
•
Potential problems
◦ Ventilator set rate is too high
◦ Overaggressive use of an Ambu bag
•
Result: pressure builds in the lungs
◦ Disconnect the ventilator or Ambu briefly
◦ Allows the excess pressure to dissipate
CPAP
Commonly used prior to extubation
 Patient is breathing spontaneously
 Ventilator support at end of expiration
only

Nursing Assessment in ARF
Priorities are airway and oxygenation
status
 Frequent, ongoing assessment is vital

Assessment Data
Ask if the patient feels s/he is getting
enough air
 Evaluate for anxiety
 Respiratory rate, work of breathing, SO2,
vital signs
 Assess skin and nail beds for cyanosis and
pallor

Nursing Diagnosis
Impaired gas exchange
 Ineffective tissue perfusion:
cardiopulmonary and peripheral
 Deficient knowledge related to the
disease process
 Self-care deficit
 Ineffective airway clearance
 Ineffective breathing pattern

Nursing Interventions in ARF
Encourage deep breathing and coughing
 Encourage incentive spirometer use, if
ordered
 Frequent turning and repositioning

Indications for
Endotracheal Intubation
Inability to maintain oxygenation/
ventilation
 Airway protection
 Elective surgery

Nurse’s Role
Know the proper equipment and its use
 Anticipate the health provider’s needs
 Position the patient
 Preoxygenate the patient
 Provide suction as necessary
 Monitor the patient
 Provide information and reassurance

How Intubation Works
Figure 36.6 Endotracheal tube.
Documentation
Size of ET tube
 Location of ET tube in airway
 Medications administered
 Patient’s tolerance of procedure

Suctioning
Performed based on assessment only
 Never routinely ordered
 DO: Hyperoxegenate before/after
suctioning
 DON’T: Routinely instill normal saline
before suctioning
 10 seconds for each pass, up to three
times only

Complications
Hypoxemia
 Bronchospasm
 Cardiac arrhythmias
 Tissue injury
 Increased risk of infection

Closed Suctioning System

Patient with high PEEP, high FiO2
◦ Closed system keeps pressure up
Patient cannot tolerate use of open
system
 Patient with airborne infectious disease

◦ Avoids exposing others to aerosolized
infectious secretions