Course
Objectives Upon
completion of this course, the student will be able to:
Be able to define
Pulmonary Edema
List 2 causes of
Pulmonary Edema
List 2 early and 2 late
signs and symptoms of Pulmonary Edema
Describe 2 nursing
interventions for caring for the patient with a Pulmonary Embolism
Identify 2 appropriate
nursing diagnosis’ for patient’s with a Pulmonary
Embolism
Explain primary and
secondary causes of Pulmonary Hypertension
Discuss 2 medical
treatment options for Pulmonary Hypertension
State 2 nursing
interventions for the care and management of the patient with Pulmonary
Hypertension
Definition
Pulmonary edema refers to extravasation of fluid from the pulmonary
vasculature into the interstitium and alveoli of the lung.
Causes
Increased capillary
hydrostatic pressure
Increased capillary
permeability
Decreased plasma
oncotic pressure
Lymphatic obstruction
Pathophysiology The
process of excess fluid accumulation in the lungs (Pulmonary Edema) can
be divided into three phases and occurs as follows:
Stage 1 –
Fluid transfer is increased into the lung interstitium because
lymphatic flow increases.
Stage 2 – The
capacity of the lymphatics to drain excess fluid is overwhelmed and
fluid begins to accumulate in the interstitial space that surrounds the
bronchioles and lung vasculature.
Stage 3 – As
fluid continues to build up, increased pressure causes it to track into
the interstitial space around the alveoli and disruption to the
alveolar membrane occurs. Once this occurs, gas exchange becomes
impaired
Contributing
Factors
Infectious pulmonary
edema (viral or bacterial)
Inhaled toxins
Circulating toxins
Vasoactive substances
(histamine, kinins)
Disseminated
intravascular coagulation
Immunologic reactions
Radiation pneumonia
Uremia
Near-drowning
Aspiration pneumonia
Smoke inhalation
Adult respiratory
distress syndrome
Diagnosis
Clinical findings on
assessment
ABG (PO2 low)
Chest X-ray (may reveal
fluid in/around lung space or enlarged heart)
Ultrasound (may reveal
weak heart muscle or leaking/narrow heart valves)
Symptoms
(may develop slowly or acutely) Early
signs:
Shortness of breath on
exertion
Sudden respiratory
distress after sleep
Difficulty breathing
unless sitting upright
Cough
Late
signs:
Labored and rapid
breathing (causing respiratory alkalosis)
Frothy or bloody sputum
Tachycardia
Cardiac Arrhythmias
Cold, clammy, sweaty,
bluish skin
Decreased blood pressure
Thready pulse
Anxiety
Pulse oximetry is
commonly less than 85% and arterial Po2 of 30 to 50 mm Hg
Note: Non-specific
symptoms may include weakness, light-headedness, abdominal pain,
malaise, wheezing and nausea. Medical
Treatment
Medical treatment for
Pulmonary Edema is considered an emergency
If possible, find and
treat the underlying cause of Pulmonary Edema
O2 via nasal cannula or
mask
Intubation and
mechanical ventilation may be necessary
If intubated, pulmonary
toilet, respiratory medication treatments
Furosemide (Lasix)
– increases urine output and works quickly to remove excess
fluid from the body
Morphine Sulfate
– decreases anxiety and work load of breathing.
Dobutamine –
dilates the peripheral vessels to decrease work load of left ventricle
Aspirin –
helps decrease blood viscosity for easy oxygen delivery.
If required, titrate
inotropic and Vasoactive medications to maintain contractility, preload
and afterload parameters
Nursing
Care and Management Assessment:
Identify type of
artificial airway or supplemental oxygen
If intubated, assess
and document ET Tube size, position and stability
Check respirations for:
Rate
Depth
Rhythm
Symmetry
Accessory muscle use
If present note color,
consistency and odor of sputum (pink frothy is usually noted in
Pulmonary Edema)
Auscultate
lungs for equality and/or adventitious breath sounds
Rales – also
known as crackles are heard when fluid or exudates is present in the
terminal bronchioles. Most notable on inspiration and are described as
fine or coarse
Rhonchi – is
produced by passage of air through fluid filled narrow air passages.
Heard on both inspiration and expiration and are described as musical,
squeaky, rattling, high pitched or low pitched
Pleural Friction Rub
– is produced by pleural inflammation and is heard on both
inspiration and expiration. Described as rough or grating sound that
varies depending on patient position
Interventions:
Monitor for symptoms of
heart failure/decreased cardiac output
Monitor vital signs
Observe for confusion,
restlessness, agitation (may be sign of decrease cardiac output)
Monitor for chest pain,
discomfort (note severity, radiation and duration)
If chest pain present
(have patient lie down, give O2, medicate for pain and notify physician)
Cardiac monitor for
dysrhythmias
If patient has a
Pulmonary Artery Catheter, monitor for increased PAWP, SVR and a
decreased cardiac output
O2 per physicians order
If patient intubated,
pulmonary toilet, suction, med-neb treatments
Monitor intake and
output (kidney perfusion may be compromised if cardiac output low)
Note results of EKG,
chest X-ray and other diagnostic tests
Monitor labs work such
as ABG, CBC, electrolytes (blood work should be routine)
Assist patient to
understand need for lifestyle changes
Side effects of
medications
Early reporting of SOB
or other respiratory difficulty
Provide specific
self-care and disease process information to patient prior to discharge
Possible
Nursing Diagnosis (NANDA)
Alteration in Comfort:
Pain
Altered Breathing
Pattern
Ineffective Airway
Impaired Gas Exchange
Altered Tissue
Perfusion: (peripheral, cardiac)
Anxiety
Ineffective Coping
Knowledge Deficit
Impaired Nutrition
Potential for Skin
Breakdown
Pulmonary
Embolism
Definition A
Pulmonary Embolism is a sudden lodgment of a blood clot in a
pulmonary artery that causes an obstruction of blood supply to lung
tissue.
Causes A
pulmonary embolism is most often caused by blood clots from veins in
the legs (Deep Vein Thrombosis DVT) or in the pelvis or hip area. They
can also be caused by air bubbles, fat droplets, amniotic fluid or
tumor cells that clump and obstruct pulmonary vessels. Pathophysiology Once
a thrombus separates from its site of origin, it travels through the
circulation to the inferior vena cava. From the inferior vena cave, it
then passes through the right ventricle which pumps the thrombus into
the pulmonary arteries where it finally lodges. Once a Pulmonary
embolism has lodged in an artery, a disruption of both pulmonary
hemodynamics and gas exchange occurs. Diagnosis
Physical Exam
(Pulmonary Hemodynamics if Pulmonary Artery Catheter in place)
Chest X-ray
Pulmonary
ventilation/perfusion scan
Pulmonary Angiogram
Doppler Ultrasound (to
rule out DVT)
Venogram (to rule out
DVT)
Elevated Troponin Level
(which indicates right ventricular micro-infarction)
Elevated pro-B-type
peptide Level (which indicates right ventricular overload)
Symptoms
(may be vague or resemble other disease processes)
Cough (sudden onset)
Bloody sputum
Shortness of breath
(sudden onset)
Splinting of ribs with
breathing
Chest pain (under the
breast bone described as sharp, stabbing, burning)
Tachycardia
Tachyapnea
Wheezing
Cool clammy skin (may
be sweaty)
Bluish skin
discoloration
Nasal flaring
Pelvis/Leg pain (DVT)
Swelling of leg (DVT)
Hypotension
Weak pulse
Anxiety/Nervousness
Lightheadedness/Dizziness
Medical
Treatment Anticoagulation
- When acute Pulmonary Embolism is suspected, anticoagulation should be
started immediately (Heparin 80 unit/kg bolus followed by 18
units/kg/hr). Target of activated partial thromboplastin should be
between 60-8- seconds (Patient should eventually be weaned of IV
Heparin and oral Warfarin (Coumadin) should be started).
Inferior Vena Caval
Filters – Filters
can be inserted percutaneously to prevent further Pulmonary Embolism,
but they do not stop an already activated thrombolic process. They are
indicated for recurrent Pulmonary Embolism and for cases when
anticoagulation is contraindicated. Because these filters are
retrievable, they can be used on a temporary basis.
Thrombolysis
– Recombinant Tissue Plasminogen (rt-PA) is a treatment
option for lysing Pulmonary Embolism. If ordered it should be given as
a 100mg IV infusion over 2 hours. (This treatment is somewhat
controversial due to the fact that most patients with Pulmonary
Embolism also have increased systemic arterial pressure and/or moderate
to severe right ventricular dysfunction). Other medications include
Streptokinase and Urokinase.
Embolectomy
– When thrombolysis is contraindicated, a catheter (angio
procedure that delivers high velocity jet saline that blasts the clot)
can be attempted or surgical embolectomy can be considered.
Note:
More than 600,000 people in the United States have a pulmonary embolism
each year, and more than 60,000 die Nursing
Care and Management Assessment:
Identify patients at
risk for the development of Pulmonary Emboli and put preventative
measures in place (ambulation, range of motion, sequential/ted hose).
Assess for
Homan’s sign (may indicate impending thrombosis of leg veins)
Complete respiratory
assessment to include complaints of pleural pain, pain on inspiration,
presence of crackles
Assess for hemoptysis
Interventions:
Avoid leaving IV
catheters in place for long periods of time
If SOB, HOB should be
in semi-fowler’s position to assist with air distribution
O2 as prescribed
(monitor for signs of hypoxia)
Pulse Oximetry
Administer Opioids for
sever pain
Administer
anticoagulation as prescribed and monitor for untoward bleeding (gums,
bruising)
Encourage verbalization
of fear and anxiety
Respiratory
toilet to include:
Nebulizer treatments
Incentive spirometry
Postural drainage
(vibration and percussion)
Possible
Nursing Diagnosis (NANDA)
Alteration in Comfort:
Pain
Altered Breathing
Pattern
Ineffective Airway
Impaired Gas Exchange
Altered
Tissue Perfusion: (peripheral, cardiac)
Anxiety
Ineffective Coping
Knowledge Deficit
Impaired Nutrition
Potential for Skin
Breakdown
Pulmonary
Hypertension
Definition Pulmonary
Hypertension is a continuous high blood pressure in the pulmonary
artery caused by increased hydrostatic pressure in the pulmonary
system. With Pulmonary Hypertension, pulmonary artery pressures reach
mean of 25mmHg or higher (normal mean being 14mmHg).
Causes The
causes of Pulmonary Hypertension are not well known, but primary
Pulmonary Hypertension is considered to be an inherited disease process
and secondary Pulmonary Hypertension is thought to be caused by an
associated disease process such as:
Chronic lung or heart
disease
Liver Cirrhosis
Stimulant abuse
HIV infection
Pulmonary Embolism
Connective tissue
diseases (Schleroderma, Lupus)
Pathophysiology Similar
to the cause, the pathophysiology of Pulmonary Hypertension is also
poorly understood. What is clear is that there is an insult to the
endothelium of the lung that results in vascular scaring endothelial
dysfunction and smooth muscle proliferation. There are three
predominant mechanisms that occur with Pulmonary Hypertension and they
are:
Hypoxic vasoconstriction
A decreased size of the
pulmonary vascular bed
Volume or pressure
overload
Diagnosis Invasive:
Hemodynamic right heart
catheterization (can determine type and severity of Pulmonary
Hypertension)
Pulmonary angiography
(gives view of pulmonary blood vessels)
Non-Invasive:
ECG and chest x-ray
(shows right ventricular hypertrophy and hypertrophy of the pulmonary
artery)
Echocardiogram (views
effectiveness of hearts pumping ability)
Pulmonary function test
(measures lung capacity)
Perfusion lung scan
(measures flow of blood)
CT (measures blood flow
and can see blockage)
MRI (views and measures
blood flow)
Symptoms Difficulty
breathing and shortness of breath are the hallmark symptoms of
Pulmonary Hypertension, but other common symptoms include:
Fatigue
Dizziness
Syncope
Dependant edema
Cyanosis (clubbing of
fingers)
Tachycardia
Heart palpitation
Medical
Treatment The
primary goals of treatment for Pulmonary Hypertension are to treat the
underlying cause, reduce symptoms to improve quality of life, slow the
growth of smooth muscle cells and increase oxygen supply.
Oxygen therapy for
patients who:
Have PaO2 of less than
55 mm Hg at rest from any cause
Desaturate during
exercise
Perform better on
oxygen therapy
Medication
options include:
Anticoagulation
– to reduce blood clot formation
Calcium Channel
Blockers – to relax smooth muscle and increase oxygen
delivery from the heart
Prostacyclin
– also produced in cells of the body, it dilates the blood
vessels
Treprostinil
– another prostacyclin that also relaxes and dilates blood
vessels
Bosentan
– a relatively new treatment that widens the lung arteries
and reduces blood pressure
Nitric oxide inhalation
– causes the pulmonary arteries to widen or open, is also
being used by some doctors
Sildenafil
(Viagra) – causes the pulmonary arteries to open and is being
tested for treatment of Pulmonary Hypertension
Diuretics –
thought ease symptoms and improve the heart's performance
Note:
Lung Transplant is a consideration for severe Pulmonary Hypertension Nursing
Care and Management
Assessment:
Identify those at risk
(pts. with COPD, CHF and mitral disease)
Obtain history
regarding onset of symptoms
Assess degree of
dyspnea (usually starts with exertion only and progresses to dyspnea at
rest)
Assess skin
color/temperature, peripheral pulses and for presence of peripheral
edema.
Assess respiratory
rate, rhythm, and effort.
Assess intake and
output and weight every day.
Assess neurological
status (orientation, level of consciousness)
Assess ABG which will
show a decreased PaO2 (hypoxemia)
Interventions:
Manage the underlying
cardiac or pulmonary condition
Continuous O2 (hypoxia
is most common cause of pulmonary vasoconstriction)
Administer cardiac
medications as ordered (digitalis can improve cardiac function)
Diuretics
Rest/Activity balance
Initial fluid
restriction
Monitor hemodynamics
via pulmonary artery catheter if present
Patient/Family
Education:
Stress and relaxation
exercises may assist with the ability to maintain regular activities
Exercise is important
(may be to exhausting in late stages)
Encourage activities
that are not strenuous
May require portable
oxygen
Ongoing medication and
medical appointments will be required
Maintain healthy diet
Refrain from smoking
High altitudes,
pregnancy and air travel can worsen symptoms
Possible Nursing Diagnosis
(NANDA)
Activity Intolerance
Alteration in Cardiac
Output
Fatigue
Fluid Volume Excess
Knowledge Deficit
Impaired Gas Exchange
Anxiety
Ineffective Coping
(grieving)
References
Marini, J., J. MD.
Wheeler, A., P. (2009). Critical care medicine: the essentials. (4th
ed.). Lippincott, Williams & Wilkins. Philadelphia
Hargrove-Huttel, R., A. (2008). Lippincott’s review series:
medical-surgical nursing. (2nd ed.). Lippincott, Williams &
Wilkens. Philadelphia
Grossman, Shamai, MD., MS. (2004). Congestive Heart Failure and
Pulmonary Edema. Retrieved on February 4, 2005 at: www.emedicine.com
Field, C. M.D. (2006). Pulmonary embolism. Retrieved on December 15,
2006 at:
http://www.emedicine.com/EMERG/topic490.htm
Lerner, S., E., & Associates. (2003). Pulmonary and Critical
Care Medicine. Retrieved on February 3, 2005 at:
www.lectlaw.com/med/med08.htm
Mayo Clinic. (2006). Pulmonary edema. Retrieved on December 15, 2006 at:
http://www.mayoclinic.com/health/pulmonary-edema/DS00412
Medline Plus. (2004). Pulmonary Embolis. Retrieved on February 2, 2005
at:
www.nlm.nih.gov
Merck Manual of Diagnosis and Therapy. (2004). Pulmonary Disorders.
Retrieved on February 2, 2005 at:
www.merck.com
National Heart, Lung and Blood Institute Diseases and Conditions Index.
(2004). What is Pulmonary Artery Hypertension? Retrieved on February 5,
2005 at:
www.nhlbi.nih.gov
Oudiz, R., J., MD. (2005). Pulmonary Hypertension, Primary. Retrieved
on February 5, 2005 at:
www.emedicine.com
Sharma, Sat., MD. (2005). Pulmonary Hypertension, Secondary. Retrieved
on February 5, 2005 at:
www.emedicine.com
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