PULMONARY DISORDERS - 3 Nursing CEs

Author: Kristi Hudson RN MSN CCRN

Written: February 6, 2005

Updated: September 11, 2009

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)
• Place patient in semi-fowlers or upright position
• Activity/Rest balance (gradually increase activity)
• If eating, diet should be sodium restricted, low cholesterol (limit caffeine)
• Serve smaller more frequent meals
• Monitor bowel and bladder function (stool softeners prn)
• Minimize environmental stimuli (decrease anxiety for patient and family)
• Daily weight
• Refer appropriately (heart failure programs, cardiac rehab, support groups)

Patient/Family Education:

• Signs and symptoms of heart failure
• Importance of smoking cessation/avoidance of alcohol
• Stress reduction
• Diet restrictions (sodium, fluid intake guidelines)
• 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

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