Professional Documents
Culture Documents
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.
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
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)
Characterized by chronic, recurrent
obstruction in pulmonary airways
Encompasses chronic bronchitis and
emphysema
◦ Obstruction is generally permanent and progressive
Unifying symptoms
◦ 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 multiple-
system failure
Clinical Manifestations of CF
Acute exacerbation characterized by:
◦ 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 life-
threatening 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
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
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