Respiratory Flashcards
S/S of sarcoidosis
systemic inflammatory disease that can affect any organ, Common symptoms, which tend to be vague, include fatigue (unrelieved by sleep; occurs in 66% of cases), lack of energy, weight loss, joint aches and pains (which occur in about 70% of cases),[6] arthritis (14–38% of persons), dry eyes, swelling of the knees, blurry vision, shortness of breath, a dry, hacking cough, or skin lesions.[1][12][13][14] Less commonly, people may cough up blood.[1] The cutaneous symptoms vary, and range from rashes and noduli (small bumps) to erythema nodosum, granuloma annulare, or lupus pernio. Sarcoidosis and cancer may mimic one another, making the distinction difficult.[15]
ARDS
Respiratory failure results from an acute inflammation resulting in diffuse alveolar damage, non-cardiac pulmonary edema, poor lung compliance and significant hypoxemia
Causes of ARDS
indirect (transfusion reactions, sepsis, pancreatitis,) or direct (trauma, aspiration, pneumonia) insult to the lungs that results in diffuse alveolar damage
S/S of ARDS
tachypnea
progressive hypoxemia.
Appropriate laboratory and radiologic studies should be directed to the underlying disease. For example, if pneumonia is suspected, blood and sputum cultures may be appropriate. If the patient had significant trauma, radiologic studies should be directed to evaluate the extent of the injury. It is imperative to evaluate the arterial oxygen and carbon dioxide tension with arterial blood gas monitoring in all these patients.
Dx ARDS
- Respiratory symptoms must occur or become worse within one week of the initial insult
- Bilateral pulmonary opacities consistent with pulmonary edema on radiographic imaging (not be due to pleural effusions, lobar or lung collapse, or pulmonary nodules)
- The respiratory failure must not be due to cardiac failure or volume overload. This must be verified by an objective measure such as (echocardiogram, pulmonary occlusion pressure, etc.) to exclude hydrostatic pulmonary edema if there is no risk factors explain the ARDS.
- Impaired oxygen exchange must be present as defined by the ratio of arterial oxygen tension to fraction of inspired oxygen (PaO2/FiO2).
How are COPD and asthma intially managed?
rapid bronchodilators, anti-inflammatory steroids, and oxygenation via invasive and non-invasive ventilation
COPD
characterized by persistent non-reversible airflow obstruction due to destruction of the distal airways from local inflammation as a result of exposure to noxious particles and gases (mostly from tobacco abuse). This permanent change in lung structure coupled with chronic inflammation leads to a progressive decline in lung function, abnormal gas exchange, pulmonary hypertension, air trapping (inability to deflate the lung), increased sputum production, skeletal muscle wasting and cachexia
Pulmonary embolism
the sudden blockage of an artery in the lung, usually by a blood clot . In most cases, the clots are small and are not deadly, but they can damage the lung. But if the clot is large and stops blood flow to the lung, it can be deadly and require immediate treatment.
S/S of PE
· Sudden shortness of breath.
· Sharp chest pain that is worse when you cough or take a deep breath.
· A cough that brings up pink, foamy mucus.
Labs for PE
- D-dimer. A D-dimer blood test measures a substance that is released when a blood clot breaks up. D-dimer levels are usually high in people with pulmonary embolism.
- CT (computed tomography) scan or CT angiogram. These tests might be done to look for a pulmonary embolism or for a blood clot that may cause a pulmonary embolism.
- Ventilation-perfusion scanning. This test scans for abnormal blood flow through the lungs after a radioactive tracer has been injected and you breathe a radioactive gas.
- Magnetic resonance imaging (MRI). This test may be used to view clots in the deep veins and lungs.
- Doppler ultrasound. A Doppler ultrasound test uses reflected sound waves to determine whether a blood clot is present in the large veins of the legs.
- Echocardiogram (echo). This test detects abnormalities in the size or function of the heart’s right ventricle, which may be a sign of pulmonary embolism. - Pulmonary angiogram. This invasive test is done only in rare cases to diagnose pulmonary embolism.
Treatment of PE
Treatment usually includes anticoagulant use to prevent further clots and many patients have to be on a anticoagulant regime for a few months. Aggressive treatments may include a thrombolytic to dissolve the clot quickly or a embolectomy which is where the clot is removed surgically. A filter may be placed inside the inferior vena cava (IVCF) to prevent further clots reaching the lungs, this is usually only if anticoagulants are not an option or are not working.
Atelectasis
Atelectasis is when the alveoli within the lung become deflated. It is one of the most common respiratory complications after surgery. Atelectasis is also a possible complication of other respiratory problems, including cystic fibrosis, inhaled foreign objects, lung tumors, fluid in the lung, severe asthma and chest injuries. They can be diagnosed via chest x-ray.
S/S of atelectasis
· Difficulty breathing (dyspnea)
· Rapid, shallow breathing
· Coughing
· Low-grade fever
What is pneumonia?
a. Acute inflammation of lung parenchyma (alveoli and respiratory bronchioles)
b. Interstitial – inflammation of the interstitial tissues that is characterized by progressive scarring(fibrosis) of the lungs
Risk factors for pnemonia
People over age 65
· Conditions that produce mucus or bronchial obstruction and interfere with normal lung draining (I.e. cancer, cigarette smoking, COPD)
· Immunosuppressed patients and those with low neutrophil count
· Prolonged immobility and shallow breathing patterns
S/S of viral pneumonia
Fever: low grade
Cough: non-productive
White blood cell count: normal to low elevation
Chest x-ray: minimal changes
Clinical course: less severe than pneumonia of bacterial cause
S/S of bacterial pneumonia
Fever: high Cough: productive White blood cell count: high elevation Chest xray: obvious infiltrates Clinical course: more severe than viral cause
S/S of lung cancer
A cough that doesn't go away and gets worse over time Chest pain that doesn't go away Coughing up blood Feeling short of breath Wheezing Losing your voice (hoarseness) Getting sick with pneumonia and bronchitis a lot Swollen neck and face Not hungry, losing weight without trying Feeling tired
Describe lung cancer staging
Staging (Canadian Cancer Society, 2013)
-is a way to describe the cancer based on where the cancer is in the body
-the stage is determined by:
Location of the primary tumour
Size of the tumour
Amount of spread to surrounding tissues
If the cancer has spread to the lymph nodes
If the cancer has spread to other parts of the body
Why Stage?
To help choose the most effective treatment
To evaluate treatment of a particular stage of cancer
Estimate a person’s chance of recovery or prognosis
Stages of cancer
stage 0 – carcinoma in situ
stages I and II – the cancer is limited to the organ or location where it began or it may have spread to a nearby structure (localized spread)
stage III – the cancer has spread further into a surrounding structure or to the regional lymph nodes (regional spread)
stage IV – the cancer has spread to a distant site in the body (metastatic spread)
Cystic Fibrosis
fatal autosomal recessive multisystem disorder characterized by exocrine gland dysfunction. CF results from a mutation in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which is
located on chromosome 7 and regulates the flow of chloride, sodium, and bicarbonate ions across the epithelium. The mutation results in abnormal secretions and thick mucus that obstruct glands and ducts, damaging tissues and seriously affecting the pulmonary, gastrointestinal, endocrine/metabolic, and reproductive systems.
S/S of CF
Signs and symptoms of CF include meconium ileus in newborns; increased anterior/posterior chest diameter; digital clubbing; dry or productive cough; wheezing; constipation; abdominal distention; foul-smelling, fatty stools; decreased weight gain/growth; recurrent pneumonia and bronchitis; and bloodstained sputum.
Cor pulmonale
right ventricle of the heart enlarges (with or without right-sided heart failure) as a result of diseases that affect the structure or function of the lung or its vasculature
type of pulmonary arterial hypertension due to a known cause
any disease affecting the lungs and accompanied by hypoxemia may result in cor pulmonale
frequent cause is COPD, certain disorders of the nervous system, respiratory muscles, chest wall and pulmonary arterial tree also may be responsible
Pathophysiology of Cor pulmonale
oxygen deprivation of lungs, causes hypoxemia and hypercapnia, resulting in ventilatory insufficiency - results in pulmonary arterial vasoconstriction and possibly reduction of the pulmonary vascular bed - net effect: increased resistance in the pulmonary circulatory system, resulting in increased pulmonary bp
mean pulmonary arterial pressure of 45 mm Hg or more may occur in cor pulmonale
right ventricular hypertrophy may result, followed by right ventricular failure
s/s of cor pulmonale
symptoms usually related to underlying lung disease
Right ventricular failure:
increasing edema of the feet and legs, distended neck veins, enlarged palpable liver, pleural effusion, ascites, heart murmur.
increased levels of carbon dioxide: headache, confusion, somnolence
pts often complain of increasing SOB, wheezing, cough and fatigue
Medical management of cor pulmonale
objectives of treatment are to improve the patient’s ventilation and to treat both the underlying lung disease and the manifestations of heart disease
supplemental oxygen is administered to improve gas exchange and to reduce pulmonary arterial pressure and pulmonary vascular resistance
improved survival rates and greater reduction in pulmonary vascular resistance have been reported with continuous 24 hour oxygen therapy for pts with severe hypoxemia
chest physical therapy and bronchial hygiene manoeuvres to remove accumulated secretions, administration of bronchodilators
respiratory failure - endotracheal intubation and mechanical ventilation may be necessary
reduction of peripheral edema: bed rest, sodium restriction, diuretic therapy
digitalis may be prescribed to relieve pulmonary htn if the pt also has left ventricular failure, a supraventricular dysrhythmia or right ventricular failure that does not respond to therapy
ECG monitoring- high prevalence of dysrhythmias in pts with cor pulmonale
pulmonary inf’n must be treated promptly to avoid further impaired gas exchange and exacerbations of hypoxemia and pulmonary heart disease
prognosis depends on whether the pulmonary hypertension is reversible
Define Acute Respiratory Failure
exchange of oxygen for carbon dioxide in the lungs cannot keep up with the rate of oxygen consumption and carbon dioxide production by the cells of the body
1) fall in arterial oxygen tension (PaO2) to less than 50 mm Hg (hypoxemia- decrease in arterial oxygen tension in the blood)
2) rise in arterial carbon dioxide tension (PaCO2) to greater than 50 mm Hg (hypercapnia)
3) with an arterial pH of less than 7.35
common causes of ARF
can be classified into 4 categories: decreased respiratory drive, dysfunction of the chest wall, dysfunction of the lung parenchyma, other causes
s/s of ARF
early signs: those ass’d with impaired oxygenation and may include restlessness, fatigue, headache, dyspnea, air hunger, tachycardia, increased bp
progressively: confusion, lethargy, tachycardia, tachypnea, central cyanosis, diaphoresis and respiratory arrest
physical findings: accessory muscle use, decreased breath sounds, findings related to cause of ARF
