Asthma

A chronic inflammatory Disease of the airways that causes airway:

• Hyper responsiveness

• Mucosal edema

• Mucus production

• This inflammation leads to recurrent episodes

Signs and Symptoms

• Cough

• Chest tightness

• Wheezing

• Dyspnea

Note: Asthma differs from the other obstructive lung disease in that it is largely
reversible, either spontaneously or with treatment patients with asthma may experience
symptom free periods alternating with acute exacerbations, which last from minutes to
hours or days.

• Most common chronic disease in childhood

• Occur at any age

Note: a disruptive disease affecting school and work attendance occupational choices,
physical activity and general quality of life.

Allergy

• The strongest predisposing factor for asthma chronic exposure to airway irritants
or allergens also increase the risk for develop asthma
 • EG. Grass, Tree, and weed pollens, mold dust, roaches or animal dander.

• Note: most people who have asthma are sensitive to a variety of triggers a
patients asthma condition will change depending upon the environment, activities
management practices and other factors.

The 3 most common symptoms of asthma are cough, dyspnea, and wheezing in some
instances cough will be the only symptoms

• Asthma attacks often occur at night or early morning

• There is cough with or without mucus production

• There maybe generalized wheezing

• Generalized chest tightness and dyspnea occur

• Asthma is categorize according to symptoms and objective measures of airflow

obstruction

Assessment and Diagnostic Findings

• Complete family, environmental, and occupational history is essential

• Determine that periodic symptoms of airflow obstruction are present

• Positive family history and environmental factors including seasonal changes

particularly cold air and air pollution are associated with asthma

• Determines meds. E.g. (Aspirin, antibiotics, piperazine, limetidine)

• Comorbid conditions such as GERD, Drug induce asthma, and allergic

bronchopulmonary aspergillosis

• Others include Eczema, rashes, and temporary edema

• During acute episodes, sputum and blood test may disclose eosinophillia
elevated levels of eosinophils

• PaCO2 may rise

Prevention
 • Patients with recurrent asthma should undergo test to identify the substance that
precipitate the symptoms

• The patient is instructed to avoid the causative agents whenever possible

• Knowledge to the diseases

Complications

• Status asthmaticus

• Respiratory Failure

• Pneumonia

• Atelectasis

Medications

• Corticosteroids

• Cromolyn NA (intal) and Nedocromic (Tilade)

• Methylxantines (theophylline)

• Leukotriene modifiers

Management of asthma Exacerbation

• Best manage by early treatment and education of the patient

• Beta adrenergic meds. Are first used for prompt relief airflow obstruction

• Corticosteroids decrease airway inflammation who failed to respond in inhaled

beta adrenergic meds.

• Oxygen supplementation maybe required to relieved hypoxemia

• Written action plan (guide patient in self mgt.)

Peak flow monitoring

 • Peak flow meters measure the highest airflow during a force expiration

• Recommended for all patients with moderate or severe asthma

• Helps asthma severity and added symptoms monitoring the current degree of
asthma control

• Monitoring peak flow for 2-3 weeks after receiving optimal asthma therapy

Nursing Management

• Patient treatment successfully as an out patient if asthma symptoms are

relatively mild

• ICU or hospitalization for acute and severe asthma

• Dyspnea is present ( calm approach is important)

• Obtain history of allergy reactions to meds.

• Fluid administered if the patient is dehydrated

• Patient with incubation because of acute respiratory failure nurse must assist
intubations procedure, continues close monitoring of the patient

Status Asthmaticus

• Sever and persistent asthma that does not respond to conventional therapy

• Longer than 24 hrs

• Infection, anxiety, nebulizer abuse, dehydration may contribute to these episodes

• Acute episodes may be precipitated by hypersensitivity to aspirin

Signs and Symptoms

• Labored breathing

• Prolong exhalation

• Engorge neck veins

• Wheezing (frequently disappear a sign of impending respiratory failure)

Assessment

• Pulmonary functions studies are the most accurate means of assessing acute
airway obstruction

Medical Management

• Short acting beta adrenergic agonist

• Corticosteroids

• Intravenous fluid for hydration

• O2 therapy to treatment dyspnea, centro cyanosis, and hypoxemia

Note: Death from asthma is associated with several risk factors

• Past history of sudden and severe exacerbations

• Prior endotracheal intubation for asthma

• Prior admission to ICU for an asthma exacerbation

• Two or more hospitalization for asthma within past year

• Excessive used of beta adrenergic inhalers

• Recent withdrawal form systemic corticosteroids

• COPD

• Psychiatric disease

• Low socio economic

• Urban residence

Nursing Management

• Monitor patient for the first 12 to 24 hrs. until status is under control

• Assess pt. skin turgor

• Room should be quite and free of respiratory irritants.

PULMONARY EDEMA

-is defined as abnormal accumulation of fluid in the lung tissue or alveolar space.
It is a severe, life threatening condition.

PATHOPHYSIOLOGY

Pulmonary edema most commonly occurs as a result of increase micro vascular

pressure from abnormal cardiac function. The backup of blood into the pulmonary
vasculature resulting from inadequate left ventricular function causes an increased
micro vascular pressure, and fluid begins to leak into the interstitial space and alveoli.

Other causes of pulmonary edema are:

a. hypervolemia or a sudden increase in the intravascular pressure in the lung

-when one lung has been removed, all the cardiac output then goes to the
remaining lung. If the patient’s fluid status is not monitored closely, pulmonary edema
can quickly develop in the post operative period as the patient’s pulmonary vasculature
attempts to adapt. This type of pulmonary edema is sometimes termed “flash”
pulmonary edema.

Example: patient who has undergone pneumonectomy

b. re-expansion pulmonary edema

-this may due to rapid reinflation of the lung after removal of air from
pneumothorax or evacuation of fluid from large pleural effusion.

CLINICAL MANIFESTATIONS

The patient has:

-increasing respiratory,

-dyspnea

-air hunger

-central cyanosis
**The patient is usually very anxious and often agitated. The patient coughs up or the
nurse sections out these foamy, frothy and often blood-tinged secretions. The patient
has acute respiratory distress and may become confuse or stuporous.

ASSESMENT AND DIAGNOSTIC FINDINGS

Auscultation reveals crackles in the lung bases (especially in the posterior bases)
that rapidly progressed toward the apaces of the lungs. These crackles are due to the
movement of air through the alveolar fluid. The chest x-ray reveals increase interstitial
markings. The patient may be tachycardic, the pulse oximetry values begin to fall, and
arterial blood gas analysis demonstrates increasing hypoxemia.

MEDICAL MANAGEMENT

Management focuses on correcting the underlying disorder. If the pulmonary

edema is cardiac in origin, then improvement in left ventricular function is the goal.
Vasodilators, inotropic medications, afterload or preload agents, or contractility
medications may be given. Additional cardiac measures (e.g. intra-aortic balloon pump)
may be indicated if the patient does not respond. If the problem is fluid overload,
diuretics are given and the patient is placed on fluid restrictions. Oxygen is administered
to correct the hypoxemia; in some circumstances, intubation and mechanical ventilation
are necessary. The patient is extremely anxious, and more pain is administered to
reduce anxiety and control pain.

NURSING MANAGEMENT

Nursing management of the patient with pulmonary edema includes:

1. Assisting with administration of oxygen and intubation and mechanical ventilation if

respiratory failure occurs.

2. The nurse also administers medication (i.e., more pain, vasodilators, inotropic
medications, and preload and afterload agents.) as prescribed and monitors the
patient’s response.
ACUTE RESPIRATORY DISTRESS SYNDROME

-is a clinical syndrome characterized by a sudden and progressive pulmonary

edema, increasing bilateral infiltrates on chest x-ray, hypoxemia refractory to oxygen
supplementation, and reduced lung compliance. These signs occur in the absence of
left side failure. Patients with ARDS usually require mechanical ventilation with a higher
than normal airway pressure.

PATHOPHYSIOLOGY

ARDS occurs as a result of inflammatory trigger that initiates the release of

cellular and chemical mediators, causing injury to the alveolar capillary membrane.
These result in leakage of fluid into the alveolar interstitial spaces and alterations in the
capillary bed. Severe ventilation-perfusion mismatching occurs in ARDS. Alveoli
collapse because of the inflammatory infiltrate, blood, fluid, and surfactant dysfunction.
Small airways are narrowed because of interstitial fluid and bronchial obstruction. The
lung compliance becomes markedly decreased (stiff lungs), and the result is a
characteristic decrease in functional residual capacity and severe hypoxemia. The blood
determines to the lung or gas exchange is pumped through the nonventilated,
nonfunctioning areas of the lung, causing a shunt to develop. This means that blood is
interfacing with nonfunctioning alveoli and gas exchange is markedly impaired, resulting
in severe, refractory hypoxemia.

ETHOLOGIC FACTORS RELATED TO ARDS:

• Aspiration (gastric secretions, drowning, hydrocarbons)

• Drug ingestion and over dose

• Hematological disorders (disseminated intravascular coagulopathy [DIC],

massive transfusions, cardiopulmonary bypass)

• Prolonged inhalation of high concentrations of oxygen, smoke or corrosive

substances.

• Localized infection (bacterial, fungal, viral pneumonia)

• Metabolic disorders (pancreatitis, uremia)

• Shock
 • Trauma (pulmonary contusion, multiple fractures, head injury)

• Major surgery

• Fat or air embolism

• Systemic sepsis

CLINICAL MANIFESTATIONS

Clinically, the acute phase of ARDS is marked by a rapid offset of severe

dyspnea that usually occurs 12-48 hours after the initiating event. A characteristic
feature is arterial hypoxemia that does not respond to supplemental oxygen. On chest
x-ray, the findings are similar to those seen with cardiogenic pulmonary edema and
present as bilateral infiltrates that quickly worsen. The acute lung injury then progresses
to fibrosing alveolitis with persistent, sever hypoxemia. The patient also has increased
alveolar dead space (ventilation to alveoli, but poor perfusion) and decrease pulmonary
compliance (“stiff lungs”, which are difficult to ventilate). Clinically, a patient is thought to
be in the recovery phase if the hypoxemia gradually resolves, the chest x-ray improves,
and the lungs become more compliant.

ASSESSMENT AND DIAGNOSTIC FINDINGS

Intercostals retractions and crackles, as the fluid begins to leak into the alveolar
interstitial space, are evident on physical examination. A diagnosis of ARDS maybe
made based on the following criteria:

• a history of systemic or pulmonary risk factors

• acute onset of respiratory distress

• bilateral pulmonary infiltrates

• clinical absence of left sided heart failure

• ratio of partial pressure of oxygen of arterial blood to fraction of inspired oxygen

(PaO2/FiO2) less than 200 mmHg (severe factory hypoxemia)
MEDICAL MANAGEMENT

The primary focus in the management of ARDS includes identification and

treatment of the underlying condition. Aggressive, supportive care must be provided to
compensate for the severe respiratory dysfunction. This supportive therapy almost
always includes intubation and mechanical ventilation. In addition, circulatory support,
adequate fluid volume, and nutritional support are important. Supplemental oxygen is
used as the patient begins the initial spiral of hypoxemia. As the hypoxemia progresses,
intubation and mechanical ventilation are instituted. The concentration of oxygen and
ventilator settings and modes are determined by patient’s status. This is monitored by
arterial blood gas analysis, pulse oximetry, and bedside pulmonary function testing.

• Positive end-expiratory pressure (PEEP) is a critical part of the treatment of

ARDS. PEEP usually improves oxygenation, that it does not influence the natural
history of the syndrome. Use of PEEP helps to increase functional residual
capacity and reverse alveolar collapse by keeping the alveoli open, resulting in
improved arterial oxygenation and a reduction in the severity of the ventilation-
profusion and balance.

• Systemic hypotension may occur in ARDS as a result of hypovolemia secondary

to leakage of fluid into the interstitial spaces and depressed cardiac output from
high levels of PEEP therapy. Hypovolemia must be carefully treated without
causing further overload. Intravenous crystalloid solutions are administered with
careful monitoring of pulmonary status. Inotropic or vasopressor agents may be
required. Pulmonary artery pressure catheters are used to monitor patient’s fluid
status and the severe and progressive pulmonary hypertension sometimes
observed in ARDS.

NURSING MANAGEMENT

• Positioning is important. The nurse should turn the patient frequently to improve
ventilation and profusion in the lungs and enhance secretion drainage.

• The nurse must closely monitor the patient for deterioration in oxygenation with
changes in position.
 • Oxygenation in the ARDS patient is sometimes improved in the prone position
and may be used in special circumstances; studies to asses the benefits and
problems of such positioning are on going.

• The patient is extremely anxious and agitated because of the increasing

hypoxemia and dyspnea. The nurse should explain all procedures and provide
care in calm, reassuring manner. It is important to reduce the patient’s anxiety
because anxiety prevents rest and increase oxygen expenditure. Rest is
essential to reduce oxygen consumption, thereby reducing oxygen needs.

Pulmonary Embolism (PE)

 Refers to the obstruction of the pulmonary artery or one of its branches by

thrombus (Thrombi) that originates in the venous system or in the right side of
the heart.
 TYPES OF EMBOLI
a. Blood clot – Most common
b. Air
c. Fat
d. Amniotic Fluid
e. Septic – from bacterial invasion of the thrombus
1. Risk factor for pulmonary emboli
a. Venous stasis – slowing of blood flow in veins
- Prolonged immobilization
- Prolonged periods of sitting/ traveling
- Varicose veins
- Spinal cord injury
b. Hypercoagulability – due to release of tissue thromboplastin after surgery.
- Injury
- Tumor – pancreatic, GU, GI, breast , lung
- Increased platelet count – polycythemia, splenectomy.
c. Venous Endothelial Disease
- Thrombophlebitis
- Vascular disease
- Foreign bodies – IV/ central venous catheter
d. Certain Disease State – combination of stasis coagulation alteration and
venous injury
- Heart Disease
- Trauma – fracture of the hip, pelvic, vertebrae, lower extremities
- Post operative state/ postpartum period
- DM
- COPD
e. Other Predisposing Conditions
- Advanced age
 - Obesity
- Pregnancy
- Oral contraceptive use
- History of previous thrombophlebitis, pulmonary embolism
- Constrictive clothing
2. most thrombi originate in the deep veins of the legs, other sites include the pelvic
veins and the right atrium of the heart
3. venous thrombosis can result from slowing of blood flow (stasis), secondary to
damage to the blood vessel wall ( Endothelial lining) or changes in the blood
coagulation mechanism
4. Atrial Fibrillation causes pulmonary embolism. An enlarged right atrium in
fibrillation causes blood to stagnate and form clot in this area. This clots are
prone to travel into the pulmonary circulation
PATHOPHYSIOLOGY

5. When a thrombus completely or partially obstructs a pulmonary artery or its

branches, the alveolar dead space is increased. Area though continue to
ventilate, receives little or no blood flow. Thus gas exchange is impaired or
absent in this area.
6. The hemodynamic increased pulmonary vascular resistance from the regional
vasoconstriction and reduced size of the pulmonary vascular bed. This result in
an increase in pulmonary arterial pressure and an increased in right ventricular
requirements of the right ventricle exceed its capacity, right ventricular failure
occurs leading to a decrease in cardiac output followed by decreased in systemic
blood pressure and development of shock.

CLINICAL MANIFESTATION

- dyspnea
- tachypnea
- chest pain
- Anxiety
- Fever
- Tachycardia
- Apprehension
- Cough
- Diaphoresis
- Hemoptysis
- Syncope
- Rapid weak pulse
- Shock
- Sudden onset of pain or warmth/ swelling of the proximal or distal
extremity skin discoloration superficial vein distention
- Pain is relieve when elevated
ASSESSMENT AND DIAGNOSTICS

- death is common in PE if not detected early

♦
1. Chest x ray usually normal but may show infiltrate, atelectasis,
elevation of the diaphragm on the affected side.
2. ECG shows sinus tachycardia, PR interval depression and
nonspecific T wave changes
3. Peripheral Vascular Studies – Doppler, ultrasonography,
venosenography
4. Arterial Blood Gas – show hypoxemia and hypocapnia
5. Ventilation Perfusion Scan test choice in patients with suspected PE
6. Pulmonary Angiography – gold standard for the diagnosis of PE
PREVENTION

- To prevent PE is to prevent Deep Venous Thrombosis

- Active exercise to avoid venous stasis
- Early ambulation
- Use of elastic compression stockings
- Low dose of heparin before the surgery to reduce the risk of post
operative deep venous thrombus
- Low dose of heparin is thought to enhance the activity of antithrombin
III a major plasma inhibitor of clotting factor X. this regimen is not
recommended for patients with active thrombotic process, major
orthopedic surgery, open prostatectomy
- Low molecular weight heparin is alternative
- Intermittent pneumatic leg compression device is useful in preventing
thromboembolism

MEDICAL MANAGEMENT

a. Emergency Management
- Massive PE is a life threatening emergency.
- Objective is to stabilize the cardiopulmonary system. Because a
sudden rise in pulmonary resistance increases the work of the right
ventricle which causes acute right sided heart failure with cardiogenic
shock.
- Patients die in the 1st 1 hour to 2 hours after the embolic event.
The following are some of the emergency management

a. Nasal Oxygen- to relieve hypoxemia, respiratory distress and central

cyanosis
b. Intravenous infusion lines- to establish routes for medication or fluids
that will be needed
c. Perfusion Scan, hemodynamic measurements and arterial blood gas
d. Slow infusion of dobutamine for hypotension
 e. ECG- monitor for dysrrhythmias and right ventricular failure
f. Digitalis glycosides- diuretics and antiarrhythmic agents
g. Blood- for serum electrolyte, CBC, HCT
h. Indwelling catheter- to monitor urinary output if the pt. has suffered
massive embolism
i. Small dose of morphine and sedatives- to relieve the patient’s anxiety,
to alleviate chest discomfort, to improve the endotracheal tube, to ease
adaptation to the mechanical ventilator.
b. General Management-
- Oxygen therapy to correct hypoxemia, relieve the pulmonary vascular
vasoconstriction and reduce the pulmonary hypertension.
- Using Elastic compression
- Elevate the leg to increase venous flow
b. Pharmacologic Therapy
- Anticoagulation Therapy (heparin and warfarin sodium) are primary
method in managing acute deep vein thrombosis and PE
- Heparin to prevent the recurrence of Emboli but no effect on emboli
that are already present.
- Goal is to keep the partial thromboplastin time 1.5-2.5 times normal
- Warfarin administration is start within 24 hrs after the start of heparin
because the onset of action of 4 to 5 days
- Prothrombin time is maintained at 1.5 to 2.5 times the normal
- Anticoagulation therapy is contraindicated in pt. who are at risk for
bleeding

- Thrombolytic therapy (urokinase, streptokinase, alteplase,

anistreplase, reteplase)

- Patients who are severely compromised hypotension and hypoxemia

despite oxygenation therapy

- This therapy resolves the thrombi or emboli more quickly and restore
more than hemodynamic functioning of the pulmonary circulation
reducing pulmonary hypertension and improve perfusion,
oxygenation and cardiac output, bleeding

- Before thrombolytic therapy obtained prothrombin time and partial

thromboplastin time, HCT, Platelet counts

- Heparin is stopped prior to the administration of thrombolytic agents.

 - All but essential invasive procedures are avoided because of
potential bleeding

- Contraindicated to thrombolytic therapy CVA within 2 mo. Active ICP,

Active bleeding, surgery within the past 10 days of the thrombotic
events, recent labor and delivery, trauma or severe hypertension

c. Surgical Management
- Embolectomy indicated if the p. has massive PE
- Transvenous catheter embolectomy is a technique in which a
vacuum cupped catheter is introduced transvenously into the affected
pulmonary artery.
- Pulmonary embolectomy requires a thoracotomy with
cardiopulmonary bypass.

NURSING MANAGEMENT

1. Minimizing the risk of pulmonary Embolism

2. Preventing thrombus Formation- encourages early ambulation, active and
passive exercise, don’t wear constrictive clothes.
3. Assessing Potential for Pulmonary Embolism- monitor for positive homan’s
sign
4. Monitoring Thrombolytric Therapy
5. Managing Pain- Semi fowlers position, turn and reposition the pt. to improve
ventilation perfusion ratio. Administer analgesics for severe pain
6. Managing oxygen therapy- deep breathing and incentive spirometry are
indicated for all patients to minimize or prevent atelectasis and improve
ventilation
7. Relieving Anxiety-
8. Monitor for complication – cardiogenic shock and Right ventricular failure.
9. Providing Post operative nursing care- After the surgery measure the pt.
pulmonary arterial pressure and urinary output.