Download nursing management

Respiratory
Maladaptations
M. DuBois Fennal, PhD,
RN, CNS
1/15/15
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CHRONIC
OBSTRUCTIVE
PULMONARY DISEASE
(COPD)
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Major obstructive
disorders
Emphysema, Chronic bronchitis,
 Definition: A term applied in the clinical
setting to refer to pulmonary disorders
that hinder expiratory flow (preferred
term, chronic airflow limitation).
Asthma, Cystic fibrosis (Kidd &
Wagner,2001).
Chronic Bronchitis, emphysema, asthma
(Hudak, Gallo & Martin,1998)
Chronic bronchitis, emphysema (Lemone &
Burke,2000)
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ETIOLOGY
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Smoking
Air pollution
Smog
Irritating fumes
Occupational exposures
Infection
Heredity
Aging
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INCIDENCE
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Approximately fourteen million
Americans have COPD. It is the fourth
leading cause of death in the United
States. Mortality 90,000 deaths in 1996.
Mortality is still higher in men than in
women in 2002, however, prevalence is
increasing in women and decreasing in
men.
Lost work hours 250 million in 1998.
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PATHOPHYSIOLOGY
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COPD is a slowly developing
disease, manifest by obstruction of
the airways. Excessive secretions,
increase size of airways, loss of
alveolar wall elasticity and the loss
of the ability of the lungs to recoil
may all be found in the pathology
of COPD, but may be in lesser
combinations.
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CHRONIC BRONCHITIS
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Chronic infection or irritation of the
bronchi can lead to bronchitis.
Bronchitis is defined as; excessive
secretion of bronchial mucus
characterized by a productive
cough lasting three or months in
two consecutive years (Tierney
1998).
“BLUE BLOATER”
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SIGNS AND SYMPTOMS
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Shortness of breath
Anorexia and weight loss
Fever
Chronic productive cough
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CLINICAL
PRESENTATION
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Bronchospasms
Hypoxia
Hypoventilation
Diminished breath sounds
Cyanosis
Tachycardia
Tachypnea
Mucus plugs
*May have symptomatology of right
sided heart failure.
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MEDICAL
MANAGEMENT
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Maintain a patent airway
Oxygen, low dose
Bronchodilators
Prevent infection or additional
infection.
Improve circulation and perfusion
Maintain fluid and electrolyte
balance
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NURSING
MANAGEMENT
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Airway maintenance
Prevention of infection
Maintenance of circulation and perfusion.
Safety
Skin integrity
Nutrition
Comfort
Psychosocial support.
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EMPHYSEMA
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Irreversible destruction of the
alveoli and the alveolar walls.
Theories under investigation
include; neutrophils and
macrophages which can release
elastase.
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SIGNS AND SYMPTOMS
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Shortness of breath
Anorexia and weight loss
Fever
Chronically productive cough
especially in the morning
Barrel chest
“PINK PUFFER”
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CLINICAL
MANIFESTATIONS
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Bronchospasms
Hypoxia
Hypoventilation
Diminished breath sounds
Cyanosis
Tachycardia
Tachypnea
Excessive mucus
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Classification
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Panilobular – destruction of
bronchioles, alveolar ducts, and
alveoli.
Centritobular – change in center of
secondary lobule, chronic hypoxia,
hypercapnia and polycythemia,
cyanosis, peripheral edema,
respiratory failure.
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MEDICAL
MANAGEMENT
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Blood gas determination
Chest x-ray
Pulmonary studies
Allergy test
Ventilation perfusion studies
CT scan
Echocardiogram
Oxygenation
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NURSING
MANAGEMENT
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Maintenance of airway
Maintenance of circulation and
perfusion
Prevention or treatment of
infections.
Maintenance of fluid and
electrolyte balance.
Maintenance of cardiac status
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CARE OF THE PATIENT
WITH COPD
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Improve the quality of life or assist to a
peaceful death.
Oxygen in low doses
Intubations and mechanical ventilation
as necessary
Bronchodilators such as
proventil,alupent, brethine, adrenalin,
isurprel, theophylline, aminophylline and
expectorants such as robitussin.
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NURSING DIAGNOSIS
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Impaired gas exchange
Ineffective airway clearance
Self-care deficit
Activity intolerance
Ineffective coping
Knowledge deficit
Altered nutrition
Decisional conflict.
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PULMONARY
EMBOLISM
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Definition: Sudden obstruction of
one or more of the pulmonary
arteries by a thrombus that
originates somewhere in the
venous system.
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ETIOLOGY
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90% of all pulmonary emboli
originate from deep venous
thrombosis of the legs.
10% result from stasis, pelvic veins
and damaged blood vessels.
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INCIDENCE
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Over 5 million individuals per year in the
United States will experience a
pulmonary embolism.
250, 000 hospitalizations
50,000 death, 90% within the first 1-2
hours.
Incidence is increased in clients with
venous stasis, hypercoagulability,
vascular disease, heart disease, post-op,
the elderly, and on oral contraceptives.
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PATHOPHYSIOLOGY
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When a clot block circulation in a branch
of the pulmonary artery, alveoli are
ventilated but not perfused, thereby
producing areas of mismatched
ventilation and perfusion. Decrease
pulmonary blood flow and deficient
surfactant, leading to atelectasis. May
also cause right ventricular failure,
pulmonary hypertension, and increase
vascular resistance.
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SIGNS AND SYMPTOMS
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Dyspnea
Substernal chest pain
Rapid weak pulse
Shock
Syncope
Cough with pleuritic pain
Sudden death
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CLINICAL
PRESENTATION
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Dyspnea at rest
Tachycardia
Tachypnea
Anxious
Systemic hypotension
Rales
Hemoptysis
Gallop rhythm
Pleural friction rub
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MEDICAL
MANAGEMENT
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Electrocardiogram, chest x-ray, ABG’s,
Ventilation/perfusion lung scan,
pulmonary angiography.
Thrombolytic therapy,
Anticoagulation therapy
Correction of hypoxemia
Oxygen
Surgery
Intubations & mechanical ventilation
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NURSING
MANAGEMENT
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Oxygenation
Reduction of clotting mechanisms
Assessment for complications
Sedation
Prevention of additional emboli
Emotional and psychological
support.
Safety
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NURSING DIAGNOSIS
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Impaired gas exchange
Decrease cardiac output
Risk for injury
Anxiety
Ineffective coping, patient and
family.
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PULMONARY
HYPERTENSION
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Definition: A condition in which the
pulmonary arterial pressure is
elevated to an abnormal level. May
be a primary disorder, but is
usually secondary to another
condition
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ETIOLOGY
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Primary, unknown. Secondary, a
reduction in the vascular bed. May result
from vasoconstriction or wide spread
vessel destruction. Initiating factors
include: hypoxemia, COPD, sleep
apnea, hypoventilation due to obesity.
Left ventricular failure, mitral stenosis,
and core pulmonale, a condition or right
ventricular hypertrophy and failure.
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INCIDENCE
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Seventy-five percent of the cases
are caused by core pulmonale.
A significant number of cases are
caused by multiple pulmonary
emboli, lung disease and left sided
heart failure.
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PATHOPHYSIOLOGY
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When the pressure in a low-pressure,
low-resistance chamber increases,
resistance is increased.
As resistance increases, the chamber
enlarges (right ventricle), because of the
increase work load. When the pressure
in the pulmonary system becomes too
great, the right ventricle fails causing
stasis of venous blood in the systemic
system.
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CLINICAL
MANIFESTATIONS
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Peripheral edema
Cyanosis
Changes in mental status
Dyspnea
Increased jugular venous
distention
Fatigue, ascities, nocturia, weight
gain, anorexia and nausea
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MEDICAL
MANAGEMENT
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Flow directed catheter, ABG’s, chest xray, hemoglobin and hematocrit.
Check history for smoking, COPD, high
altitude experiences.
Decrease the fluid overload, decrease
pulmonary vascular resistance, decrease
work load of the heart. Oxygen,
bronchodilators, diuretics,
echocardiogram
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NURSING
MANGAGEMENT
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Continuous assessment to prevent
complications.
Auscultation of heart sounds
Measurement of pulmonary artery
pressures
Evaluation of laboratory data
Evaluation of medications
Conservation of energy
Interpretation of ABG’s, and
dysrhythmias
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NURSING DIAGNOSIS
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Impaired gas exchange
Fluid volume excess
Anxiety
Ineffective coping (patient and
family)
At risk for injury
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RESPIRATORY FAILURE
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Definition: A Pao2 less than 55
mm Hg, and a PCo2 greater than
50 mm Hg.
An imbalance between in supply
and demand of O2
The inability of the pulmonary
system to maintain adequate gas
exchange.
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ETIOLOGY
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Inadequate ventilation
impaired gas exchange
Ventilation/perfusion mismatch
Disease processes
Injuries
Cardiac and neuromuscular
disorders
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INCIDENCE
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Occurs most frequently as a
complication of other disease
processes, COPD, Pneumonia,
pulmonary edema, chest injuries
and drug overdose is at the top of
the list. Occurs more often in
males and more often in older
adults.
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PATHOLOGY
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May be acute or chronic
Failure of oxygenation is a problem
of hypoxemia, such as in ARDS,
pulmonary embolus, acute
asthmatic attacks, and pneumonia.
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Failure of ventilation (acute
respiratory acidosis) is caused by
alveolar hypoventilation, such as
with COPD, neuromuscular
disorders respiratory muscle
fatigue etc. Ventilation failure
allows for the build up of high
levels of carbon dioxide
(hypercapnia)
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H
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SIGNS AND SYMPTOMS
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D
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Hypoxemia
Dyspnea
Tachypnea
Cyanosis
Anxiety
Dysrhythmias
Hypertension
Metabolic acidosis
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CLINICAL
MANIFESTATIONS
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Dyspnea
Tachypnea
Tachycardia
Cool to cold skin
Increase blood pressure
Varying states of consciousness
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MEDICAL
MANAGEMENT
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Will depend on the cause and the
type of failure. Correct the
hypoxemia or hypercapnia and
treat the underlying cause.
Oxygen, intubation, mechanical
ventilation, bronchodilators, muscle
relaxants i.e. morphine.
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NURSING
MANAGEMENT
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Airway management
Safety
Skin integrity
Nutrition
Monitor laboratory results and
arterial blood gas results, intervene
for abnormals.
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NURSING DIAGNOSIS
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Ineffective airway clearance
Impaired gas exchange
Self-care deficit
Activity intolerance
Risk for injury
Anxiety
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RESPIRATORY
DISTRESS SYNDROME
(ARDS)
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Definition: characterized by
noncardiogenic pulmonary edema,
collapsed and fluid filled alveoli
and subsequently severe
hypoxemia.
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ETIOLOGY
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Occurs in a usually healthy
individual after some sort of insult
to the body, i.e. sepsis, aspiration,
trauma, hemorrhagic shock.
The process will usually manifest
itself within seventy two hour of a
pulmonary insult.
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INCIDENCE
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Highest in individuals who present
with shock, sepsis, hypo or
hyperthermia, drug overdose, DIC,
multiple blood transfusions,
cardiopulmonary bypass,
eclampsia, burns, pancreatitis,
pneumonia, inhalation injury and
stress.
200, 000 cases per year, mortality
rate of 40% – 90%
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PATHOPHYSIOLOGY
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ARDS may present as mild to
severe. In mild no other organs
are involved, in severe, multiple
organs are involved.
Associated with a systemic
inflammatory response syndrome
(SIRS) (Vollman and Aulbach,
1998).
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Capillary endothelial cell becomes
injured and allows protein and
water to leak out into the interstitial
and alveolar spaces, producing
interstitial edema.
Protein destroys surfactant
Capillary narrow and finally
collapse.
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Hemorrhage occurs into interstitum
Pulmonary edema occurs
Blood flow in lungs cease
Hyaline membrane develops
making the lungs less compliant.
Increase PCO2, decrease O2
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SIGNS AND SYMPTOMS
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Tachypnea
Cyanosis
Grunting respirations
Intercostal retractions
Extreme agitation
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Clinical manifestations
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Marked dyspnea
Restlessness and agitation
Cyanosis
Bilateral alveolar infiltrates
Elevated PaCO2 and decreased
PaO2, severe respiratory acidosis,
rales, decreased breath sounds,
pulmonary friction rub.
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MEDICAL
MANAGEMENT
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Admit to critical care
Intubations and mechanical
ventilation
Arterial blood gas and chest x-ray
IV access (2)
Positive end expiratory pressure
(PEEP) or
Continuous positive airway
pressure (CPAP)
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NURSING
MANAGEMENT
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Airway management
Control and or support ventilation
and gas exchange
Restrict fluids
Constant assessment
Monitor diagnostic studies, cardiac
monitor and physical assessment
Psychological support
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COMPLICATIONS
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Oxygen toxicity
Sepsis
Fluid imbalance
Injury from tracheotomy and
suctioning
Complications of PEEP, decrease
cardiac output subcutaneous
emphysema, pneumothorax,
pneumomediastium
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Nursing Diagnosis
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Impaired gas exchange
Ineffective airway clearance
Potential for aspiration
Decrease cardiac output
Altered nutrition
Potential for infection
Sensory-Perceptual alterations
Anxiety
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