RESPI REVIEW1

7/31/2019 RESPI REVIEW1

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MAJOR DISORDERS OF THERESPIRATORY SYSTEM

Sheryll Joy Lopez-Calayan, RN, MSN


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PULMONARY EMBOLISM AND

INFARCTION Etiology and pathophysiology

Emboli develop from thrombi in peripheralcirculation; associated with venous stasis resultingfrom immobility, coagulopathy, vasculardisease, surgery, aging, oral contraceptives,obesity, and constrictive clothing

When an embolus lodges in the pulmonary arterycausing hemorrhage and necrosis of lung tissue itis called a pulmonary infarction


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Clinical findings

Subjective: severe dyspnea that occurs suddenly;

anxiety;

restlessness;

sharp pleuritic pain

Objective:

increased temperature, pulse, and respirations;

violent coughing with hemoptysis;

diaphoresis


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Therapeutic interventions

Anticoagulant therapy

Thrombolytic therapy

Angiography; if the condition is severe, anembolectomy may be indicated

Vena caval interruption; a filter may be

implanted in the inferior vena cavapreventing the passage of large thrombi


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Nursing Care of Clients with

Pulmonary Embolism and

Infarction PLANNING/IMPLEMENTATION

Place in the high-Fowlers position andadminister oxygen

Monitor for hypoxemia and right heart failure

Administer thrombolytics/anticoagulants asordered; monitor for bleeding

Maintain calm environment to decrease fear Educate client regarding anticoagulants and

prevention of thrombophlebitis


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PULMONARY EDEMA

Etiology and pathophysiology

An acute emergency situation conditioncharacterized by a rapid accumulation of fluid inalveolar spaces resulting from increased pressurewithin the pulmonary system

Possible causes include valvular disease, left-ventricular failure, circulatory overload,aspiration of gastric contents, drowning


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PULMONARY EDEMA

Clinical findings Subjective: history of premonitory symptoms such as shortness

of breath, paroxysmal nocturnal dyspnea,

wheezing, and orthopnea; acute anxiety, apprehension, restlessness Objective: rapid, thready pulse and rapid respirations; pink, frothy sputum; wheezing; crackles; pallor or cyanosis; low PO2; elevated pulmonary capillary wedge pressure and central venous

pressure


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Pulmonary Edema

PLANNING/IMPLEMENTATION Support client in the orthopneic, high-Fowlers or

semi-Fowlers position with legs dependent

Observe and record vital signs and monitor cardiacactivity and intake and output

Provide a reassuring environment to allay anxiety;administer morphine sulphate to relieve anxiety

Suction as needed to maintain a patent airway Administer and monitor effects of medications to

reduce preload and afterload

Educate client regarding pharmacology andprevention of heart failure


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PNEUMONIA

Etiology and pathophysiology Inflammatory disease usually caused by infectious agent (bacterial,

viral, protozoal, or fungal) but may also be caused by inhalation ofchemicals and aspiration of gastric contents

Pneumonia is commonly spread by respiratory droplets

Pnemococcal pneumonia usually caused by Streptococcus pneumoniae;incidence highest in winter; other bacterial causes include Klebsiella

pneumoniae, Haemophilus influenzae, Pseudomonas, and Staphylococcusaureus

Aspiration pneumonia occurs when gastric contents and the normalflora of the upper respiratory tract are aspirated into the lung

Pneumocystis cariniipneumonia, a rare protozoal infection, is seen in

clients with impaired immune function {e.g., AIDS) Viral pneumonia include influenza virus type A and cytomegalovirus May cause a collection ofpus (empyema) or fluid (pleural effusion) within

the pleural space


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PNEUMONIA

Clinical findings Subjective: lassitude; dyspnea; chest pain that

increases on inspiration

Objective Elevated temperature; increased WBC

Chest x-ray examination shows pulmonary infiltration

Cough with sputum production

Pneumococcal: purulent, rusty sputum

Staphylococcal: yellow, blood-streakedsputum

Klebsiella: red, gelatinous sputum

Mycoplasmal: non-productive that advances to mucoidsputum


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PNEUMONIA


If bacterial pneumonia, culture and sensitivitytests will be done on blood and sputum todetermine appropriate antibiotic therapy

Oxygen therapy usually via nasal cannula


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PLANNING/IMPLEMENTATION Encourage coughing and deep breathing after chest

physiotherapy, splinting the chest as necessary

Collect sputum specimen for culture and sensitivity tests insterile container; notify the physician if organism is resistant tothe antibiotic being given

Increase fluid intake to 3 liters daily

Maintain semi-Fowlers position

Monitor for signs of respiratory distress, such as laboredrespirations, cool clammy skin, cyanosis and change inmental status

Plan rest periods

Instruct client to cover nose and mouth when coughing

Administer antibiotics as ordered Teach preventive measures including: role ofnutrition and

fluids; avoiding respiratory irritants (e.g., smoking);vaccination against Streptococcus pneumoniae andinfluenza; balance of activity and rest


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CHRONIC OBSTRUCTIVE PULMONARY

DISEASE (COPD) Etiology and pathophysiology

Group of diseases that result in chronic airflowlimitation (CAL); also called chronic obstructive

lung disease (COLD); causes include airpollution, smoking, chronic respiratoryinfections, exposure to molds and fungi, andallergic reactions


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DISEASE (COPD) Types Asthma: reversible bronchospasms and increased secretions

that last from 1 to several hours; obstruction of the bronchiolescharacterized by attacks that occur suddenly and last from 30 to60 minutes; an asthmatic attack that is difficult to controlis

referred to as status asthmaticus Chronic bronchitis: inflammation of the bronchial walls with

hypertrophy of mucous goblet cells; characterized by a chroniccough

Emphysema: characterized by distended, inelastic, or destroyedalveoli with bronchiolar obstruction and collapse; these alterations

greatly impair the diffusion of gases through the alveolarcapillary membrane

Bronchiectasis: chronic dilation of the bronchi and bronchiolesas a result of infection or obstruction


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UNDERSTANDING ASTHMA


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1. Histamine attaches to receptor sites in thelarger bronchi, where it causes swelling in

smooth muscles


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2. Slow reacting ,a substance of anaphylaxis

attaches to receptor sites in the smaller

bronchi and causes swelling of smooth musclethere.


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3. Histamine stimulates the mucuos membranes

to secrete excessive mucus , further narrowingthe bronchial lumen, as show below.


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4. On inhalation, the narrowed bronchial lumen

can still expand slightly, allowing air to

reach the alveoli. On exhalation , increased

intrathoracic pressure closes the bronchial

lumen completely.


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5. Mucus fills the lung bases, inhibiting

alveolar ventilation .


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PATHOPHYSIOLOGY

Exposure to allergies and irritants

Stress

Cold Air

Exercise

Immunoglobulin E Stimula

tion

STEROIDS


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Mast cells degranulation

MAST CELL

STAB.

Hista

mine

SRS-

A

Pros

Ta

Glan

din

Brady

kinin

Leuko

triene

Anti

hist


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Mucus

Secretion Inflammation Bronchospasm

Broncho

dilators

SOB

WheezingNon Productive

Cough


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WHAT TO LOOK FOR!!!!

Dyspneic

Marked respiratory effort

Marked respiratory effort Wheezing upon auscultation


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DISEASE (COPD)

Clients with COPD become accustomed toan elevated residual carbon dioxide leveland do not respond to high CO2concentrations as the normal respiratorystimulant; they respond instead to a drop inoxygen concentration in the blood

May precipitate pulmonary hypertension,cor pulmonale, and right ventricular heartfailure


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DISEASE (COPD)

Clinical findings Subjective: fatigue and weakness; dyspnea;

headache; impaired sensorium

Objective Orthopnea, expiratory wheezing, sterious breathing

sounds, cough

Barrel chest, cyanosis, clubbing of fingers, use ofaccessory muscles; pursed lip breathing

Increased PCO2 and decreased PO2 of arterial bloodgases; polycythemia

Distended neck veins, peripheral edema (with right heartfailure)


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DISEASE (COPD)

Therapeutic interventions Steroids to prevent and reduce inflammation

Antibiotics to prevent/treat infection

Bronchodilators to reduce muscular spasm Mucolytics and expectorants to liquefy secretions

and to facilitate their removal

Oxygen at 1 to 2 L even if hypoxia is severe

Respiratory therapy program to include nebulizertherapy, postural drainage, and exercise

High-protein soft diet in small, frequent feedings ismost easily tolerated


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Nursing Care of Clients

with Chronic ObstructivePulmonary Disease PLANNING/IMPLEMENTATION

Advise the elimination ofsmoking and other externalirritants, such as dust, as much as possible

Supervise the clients respiratory exercises, such as pursed

lip or diaphragmatic breathing Teach proper use of inhalers and other special equipment

(e.g., spacer)

Carefully observe for symptoms ofhypoxia and carbondioxide intoxication (CO2 narcosis) if oxygen is beingadministered

Teach client to adjust activities to avoid overexertion

Teach clients to avoid people with respiratory infections

Teach the client to avoid the use of sedatives orhypnotics, which could compromise respirations


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Nursing Care of Clients

with Chronic ObstructivePulmonary Disease Teach client to maintain the highest resistance possible by

getting adequate rest, eating nutritious food, dressingproperly for weather conditions, maintaining fluid intake,receiving vaccinations against S. pneumoniae and influenza

Teach client to be alert to early symptoms of infection,hypoxia, hypercapnea, or adverse response tomedications

Encourage client to continue with close medicalsupervision; monitor compliance

Encourage client to express feelings about disease andtherapy

Accept feelings about life-long restrictions in activity

Encourage client and family to take an active role inplanning therapy


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PNEUMOTHORAX/CHEST INJURY

Etiology and pathophysiology

Collapse of a lung resulting from disruption of thenegative pressure that normally exists within the

intrapleural space caused by the presence of airin the pleural cavity; may be associated withfractured ribs

Reduces the surface area for gaseous exchangeand leads to hypoxia and retention of carbondioxide (hypercarbia)


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Types Spontaneous: thought to occur when a weakened area of the

lung (bleb) ruptures; air then moves from the lung to the

intrapleural space causing collapse; highest incidence is inmen 20 to 40 years of age

Open: laceration (e.g., a stab wound) through the chest wallinto the intrapleural space

Hemothorax: collection of blood within the pleural cavity

Hydrothorax: accumulation of fluid in the pleural cavity Tension: buildup of pressure as air accumulates within the

pleural space; the pressure increase is likely to induce amediastinal shift

Mediastinal shift may occur toward the uninvolved side as a

result of increased pressure within the pleural space; thisinvolves the trachea, esophagus, heart, and great vessels

Flail chest: instability of chest wall related to fractures of theribs or detached sternum; caused by crushing chest injuries


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How open pneumothorax occurs ?

Complete

Collapse

Knife wound


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Partial collapse

Rupture bleb

SPONTANEOUS

PNEUMOTHORAX


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UNDERSTANDING TENSION

PNEUMOTHORAX On Expiration, the mediastinal shift distortsthe vena cava and reduces venous return


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On inspiration, the mediastinum

shifts toward the unaffected lung,

impairing ventilation


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Clinical findings Subjective: chest pain, usually described as sharp and

increasing on exertion; dyspnea; drowsiness Objective

Tachycardia; hypotension; rapid, shallow respirations(nonsymmetric)

Flail chest: loose chest segment moves inward duringinspiration and outward during expiration (paradoxicalrespiration)

Breath sounds on the affected side will be diminished orabsent

Chest x-ray examination will reveal extent of thepneumothorax


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Bed rest initially

Analgesics and antibiotics

Negative pressure is returned to the intrapleuralspace by the insertion ofchest tubes attached tounderwater drainage

Restoration of blood volume loss as a result oftrauma

Volume controlled ventilation


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Pneumothorax

PLANNING/IMPLEMENTATION

Maintain constant supervision until stable

Maintain patency of chest tubes

Place in high-Fowlers position

Offer fluids frequently

Monitor vital signs, particularly respirations

EVALUATION/OUTCOMES Maintains adequate gas exchange

Verifies reduction or absence of chest pain


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Nursing care: without suction

1. prepare the unit for use and connect the chest catheter to the drainage tubing

2. examine the entire system to ensure airtightness and absence of obstructionfrom kinks or dependent loops of tubing

3. note oscillation of the fluid level within the water-seal tube. It will rise oninspiration and fall on expiration due to changes in the intrapleural pressure. Ifoscillation stops and system is intact, notify the physician

4. milk the chest tubes and drainage tubing every 1-2 hours as ordered todislodge mucus and blood clots. Hold the proximal part of tubing with one handand squeeze the distal portion in a downward direction

5. check the color, amount and characteristics of the drainage. If drainage ceasesand system is not blocked, assess for signs of respiratory distress from fluid / airaccumulation.

6. always keep drainage system lower than the level of the clients chest 7. keep Vaseline gauze at bedside at all times in case chest tube falls out.

8. encourage coughing and deep breathing to facilitate removal of air anddrainage from pleural cavity

9. provide ROM exercises


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Nursing care: with suction

1. attach suction tubing to suction apparatus and chest catheter to drainagetubing

2. open suction slowly until a stream of bubbles is seen in the suction chamber.There should be continuous bubbling in this chamber and intermittentbubbling in the water seal. Check for an air leak in the system if bubbling inwater seal is constant; notify physician if no air leak

3. check drainage, keep drainage system below level of clients chest, keepVaseline gauze at bedside, encourage coughing and deep breathing, provideRom exercises as noted above.

I. never clamp chest tubes unless a specific order is written by the physician.Clamping the chest tubes of a client with air in the pleural space will causeincreased pressure build up and possible tension pneumothorax.

J. removal of the chest tube: instruct the client to perform Valsalva maneuver;apply a Vaseline pressure dressing to the site.

K if the water seal bottle should break immediately obtain some type of fluid-filled container to create an emergency water seal until a new unit can beobtained


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ADULT RESPIRATORY DISTRESS

SYNDROME (ARDS)

Etiology and pathophysiology Respiratory failure as a complication of trauma,

aspiration, prolonged mechanical ventilation,severe infection, open-heart surgery, fat emboli,

shock Involves:

Pulmonary capillary damage with loss of fluid andinterstitial edema

Impaired alveolar gas exchange and tissue hypoxia

resulting from pulmonary edema Alteration in surfactant production; collapse of alveoli

Atelectasis resulting in labored and inefficientrespiration


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CAUSES OF ARDS

Fat emboli

Sepsis

Shock

Pulmonary contusions

Multiple transfusions


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Control Complications

Improve General

health


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PLATELETS AGGREGATE

AND RELEASE ( H),

(S) & ( B)


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(H ) Inflame and damage the

alveolocapillary

mem,increasing capillaryper.Fluid shifts to interstitial

space


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Capillary perm.

Increases, Protein leak

out,Inc. Interstitial

osmotic pressure,PULMONARY EDEMA


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Decreased bld. Flow

ALVEOLI COLLAPSE

IMPAIRING GAS

EXCHANGE


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SUFFICIENT OXYGEN

CANT CROSS THE

ALVELOCAPI.MEMBRANE, BUT CO2

CAN


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PULMONARY EDEMA

WORSENS,

INFLAMMATION LEADS

TO FIBROSIS


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What to look for !!!!

Rapid ,shallow breathing and dypnea

Hypoxemia

Crackles and rhonchi


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WHAT TESTS TELL YOU !!!

Arterial Blood Gas- respiratory alkalosis

Pulmonary Artery Catheterization- capillarywedge pressure

Chest X ray- bilateral infiltration

Whiteouts of both lung fields


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SYNDROME (ARDS)

Clinical findings Subjective: restlessness;

anxiety;

dyspnea Objective: tachycardia;

grunting respirations;

intercostals retractions;

cyanosis; PCO2 initially decreased and later increased, and

decreased PO2 arterial blood gases;

chest x-ray examination reveals pulmonary edema


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SYNDROME (ARDS)


Relieve the underlying cause

Mechanical ventilation with positive endexpiratory pressure (PEEP): this setting on amechanical ventilator maintains positivepressure within the lungs at the end of

expiration, which increases the residualcapacity, reducing hypoxia

Corticosteroids may be used


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SYNDROME (ARDS) PLANNING/IMPLEMENTATION

Allow frequent rest periods between therapeutic interventions

Provide tranquil, supportive environment; sedation is contraindicated

because of its depressant effect on respirations Observe behavioural changes and vital signs because confusion and

hypertension may indicate cerebral hypoxia

Auscultate breath sounds to observe for signs ofpneumothorax when theclient is on PEEP (lung tissue that is frail may not withstand increased

intrathoracic pressure, and pneumothorax occurs) Monitor arterial blood gases, as ordered; use a heparinized syringe

Maintain a patent airway

Care for the client on mechanical ventilation

Measure central venous and pulmonary artery pressures


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CARBON MONOXIDE POISONING

Etiology and pathophysiology:

carbon monoxide combines with haemoglobinmore readily than does oxygen, resulting in tissue

anoxia; caused by inadequately ventedcombustion devices

Clinical findings

Subjective: headache; faintness; vertigo; tinnitus Objective: color normal, cyanotic, or flushed but

usually cherry pink; paralysis; loss ofconsciousness; ECG changes


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PLEURISY

Inflammation of the visceral and parietal membranes

These membranes rub together during respiration andcause pain

May be caused by pulmonary infarction or pneumonia

It usually occurs on one side of the chest, usually in lowerlateral portions in the chest wall

Assessment

Knife like pain that is aggravated on deep breathing andcoughing

Dyspnea Pleural friction rub on auscultation

Apprehension

Pleurisy


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Implementation

Identify and treat the cause

Monitor lung sounds

Analgesics as prescribed Hot and cold applications

Coughing and deep breathing

Lie on affected side to splint chest


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Mechanical ventilation with 100% oxygen untilcarboxyhemoglobin is reduced to less than 5%

and respirations are normal Hyperbaric pressure chamber to increase oxygen

concentration and accelerate formation of carbondioxide which can be exhaled


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ASSESSMENT

History to determine extent of exposure

Color of skin

Level of consciousness

ANALYSIS/NURSING DIAGNOSIS

Impaired gas exchange related to chemical

imbalance Alteration in thought processes related to hypoxia


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CARBON MONOXIDE POISONING PLANNING/IMPLEMENTATION

Remove the individual from the immediate areaof poisoning

Evaluate for cardiopulmonary resuscitation if

necessary and maintain until additional helparrives

Administer oxygen as prescribed

Maintain respirations with assistance if needed

Monitor vital signs, with special concern forrespirations


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EVALUATION/OUTCOMES

Maintains adequate oxygen levels

Remains conscious and alert

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