Test 3 Flashcards
Air moving in and out of the lungs
Ventillation
Ventilation depends on three things:
- Distensibility: the ease of which the lungs can inflate or distend
- Resistance: Amount of force that the lungs have to work against
- Elasticity: How well the lungs can recoil
Blood needs to flow to the lungs and provide oxygen. The air needs to be able to flow from the lungs into the blood stream. CO2 needs to be able to leave the blood stream and go to the lungs.
Perfusion
For every __L of air we inhale we need ___L of blood/min.
4L or air, 5L of blood/min
Clinical Manifestations of Respiratory Dysfunction
Sneezing Dysphagia Dysphonia Dyspnea Abnormal Respiratory Rates -Tachypnea -Bradynea Abnormal Respiratory Patterns -Kussmaul -Cheyne Stokes
Caused by Irritation in upper respiratory tract
Sneezing
difficulty swallowing
• Dysphagia
coarse voice
• Dysphonia
protective from irritants. Normal in healthy individuals. Must determine if ______ is productive or not. Persons with decreased _______ reflex have increase chances of infection
cough
coughing up blood
Hemoptysis
shortness of breath. (Can still have normal respiratory rate & be in severe respiratory distress)
• Dyspnea
positional. Person needs to sit up to breath – unable to lie flat & breathe properly
o Orthopnea
Wake up at night with extreme SOB, gasping for air
o Paroxysmal nocturnal dyspnea (PND)
slower than normal breathing
o Bradypnea
faster than normal breathing
o Tachypnea
Increase in depth of breathing. Increase in tidal volume. (can be normal after exercise, persons at rest should not have this pattern of breathing)
o Kussmaul
Progressive increase in the rate and depth of breathing followed by a period of apnea. Alternating periods of deep and rapid breathing.
o Cheyne Stokes
often seen in children. Not often seen in adults as the cartilage of the adult nose is harder than that of a child.
o Nasal flaring
Suprasternal, supraclavicular, substernal, subcostal, intercostal indrawing – seen in children, _____ _____ ______ ___at the subcostal area below the rib cage
chest wall caves in
snoring – indicates an obstruction usually in upper respiratory tract
o Sonorous breathing
Upper respiratory blockage, high pitched musical sound
o Stridor
Popping sound
o Crackles
Continuous musical quality
o Wheezes
Visceral pleura and parietal pleura rub against each other. Inflammation of pleura may cause this.
o Friction rub
usually from coughing. Cough so hard they strain muscles in the chest.
• Pain in chest
Respiratory pain is reproducible (act of coughing will elicit pain). Cardiac pain is described as a pressure and constant.
o Pleuritic
________poisoning is the exception person looks red
CO2
Sign of hypoxemia. Occurs in cystic fibrosis, COPD
• Clubbing of digits
early signs of hypoxemia. You will see this before changes in vitals occur
• Anxiety/Restlessness/Confusion
o Elevated carbon dioxide levels in the blood
o May also be referred to as hypercarbia
• Hypercapnia
o Decreased O2 concentration in the blood o Causes: Hypoventilation Diffusion abnormalities Ventilation-perfusion mismatch
• Hypoxemia
o Inadequate oxygen supply to the cells
• Hypoxia
End result of pulmonary disease
Respiratory Failure
Respiratory disease interferes with ______ _________or transport and can lead to ________ _______ as defined by either
o Arterial Blood O2 (PAO2) ___ mmhg/pH
Oxygen Intake, and can lead to respiratory failure
oArterial Blood O2 (PAO2) 45 mmhg/pH
Respiratory Failure May also result from
cardiac dysfunction, drugs, prolonged tachycardia in other disorders such as metabolic acidosis
Treatment of respiratory failure is based on the:
etiology of respiratory failure. Must treat whatever is causing the respiratory failure.
Tests to Evaluate Respiratory Function (6)
- Chest Xray (CXR): easiest & least expensive. Won’t tell you everything.
- Computed tomography (CT scan)
- Blood gas analysis (ABG’s)
- Pulmonary function tests (PFT)/spirometry
- Sputum analysis (C&S, cytology – looking for cancer cells, Acid Fast Bacilli – TB test)
- VQ scan (Ventilation/Perfusion Scan) – done in nuclear medicine. Measuring how well the lungs are being perfused with blood and oxygen
Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:
Resistance to air flow. Air has trouble getting in and out of the lungs. Diseases that block the flow of air in and out of the lungs are obstructive disorders
• Obstructive disorders
Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:
Air does not have trouble getting in and out of the lungs. The lungs have poor distensibility. Cannot fully expand
• Restrictive disorders
Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:
Caused by a pathogen (pneumonia, croup)
• Infectious disorders
Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:
Nothing wrong with lungs. There is a problem with blood flow to the lungs. (blood clot, pulmonary embolism)
• Disorders of Vascular Origin
Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:
Cancers
• Malignancies
OBSTRUCTIVE DISORDERS
10
Croup Epiglottitis Bronchiolitis Bronchitis Asthma COPD: Umbrella term for Chronic Bronchitis & Emphysema Chronic Bronchitis Emphysema Bronchiectasis
• Caused by parainfluenza virus, influenza A or respiratory syncytial virus (RSV)
o Attacks upper respiratory structures
• Most commonly occurs in 6 months to 5 years age group.
Croup
Croup is characterized by ____________ extending from _____ _______to bronchial lumina
inflammation, vocal cords
Clinical Manifestation of Croup (6)
o catarrhal symptoms: sick looking eyes – red, runny eyes o rhinorrhea: runny nose o low-grade fever o barking cough o stridor o nasal flaring
Croup is not usually fatal; however, more serious in?
<6 months old.
• Causative organisms (not viral)
o Haemophilus influenzae type B – immunization helps prevent epiglottitis
o Streptococcus pneumoniae
Epiglottitis
Most common in ____ to _____ year age group, but may also affect adults
2 to 6
Epiglottitis Clinical manifestations: sudden onset
o sore throat, dysphagia, drooling, fever
o “sniffing position”, muffled voice, anxious
o stridor, respiratory distress
Epiglottitis Evaluation: based on symptoms:
o X-ray of soft tissues of neck.
o Characteristic “thumbprint”
o Do not attempt to examine pt’s throat. Depressing the tongue can cause laryngospasm – may not be able to be intubated after.
Epiglottitis can be _______________________
• Fatal: death may occur in a few hours
Epiglottitis treatment:
IV antibiotics quickly; may require rapid intubation.
widespread infection of the bronchioles
Bronchiolitis
_______ ______ _____causes bronchiolitis (majority of cases)
respiratory syncytial virus (RSV)
True or False
Bronchiolitis not contagious?
False
It is highly contagious
Bronchiolitis is more prevalent is what age group and what time of year?
2 – 24 month age group, o November to February
Clinical manifestations of Bronchiolitis (7)
o Nasal congestion, mild conjunctivitis
o Inspiratory crackles, expiratory wheezes
o Use of accessory muscles, (such as intercostal indrawing), nasal flaring, increased work of breathing
o Tachypnea (with resp rate 50 – 60 per min. Can go up to 80)
o Tachycardia, poor feeding
o Pallor, cyanosis, hypoxemia
o Episodes of apnea
Pathogenesis of Bronchiolitis (4)
o Respiratory virus attacks lower bronchioles
o Bronchiole walls become very swollen & obstructed.
o Edema of submucosa, increase in mucus secretion
o Necrosis of bronchial epithelium
Virus causes epithelial layers to slough off
Clogs up bronchioles so air cannot get past them into the alveoli
Management of Bronchiolitis
o Humidity, fluids, rest
o Infection control precautions
- Inflammation of the trachea and bronchi
* Acute or chronic
Bronchitis
Etiology of Bronchitis
influenza virus A or B, parainfluenza virus, respiratory syncytial virus (RSV); smoke or inhalation of chemical irritants
Pathogenesis of Bronchitis (5)
o Bronchi become invaded by viruses o Edema of mucous membranes o Increased mucous production o Loss of ciliary function o Causing bronchiole irritation
Manifestations of Bronchitis
o Expiratory wheezing, dyspnea, malaise
o Cough (productive or nonproductive) from increased mucus production
o Chest pain r/t persistent coughing
• Treatment – Acute Bronchitis
o Increase fluids, smoking cessation, expectorants(thins out secretions)/antitussives(suppresses cough), antibiotics not routinely prescribed
Chronic Bronchitis
permanent increase in thickness of the bronchi, and increase in the number of goblet cells. Which means increased mucus productions, increased cough, decreased cilia
• Clinical Manifestations of Asthma (6)
o Dyspnea, with increased respiratory effort
o Wheezing (inspiratory and expiratory), SOB
o Prolonged expiration
o Cough – nonproductive during acute attack; productive with thick mucus as attack resolves
o Use of accessory muscles, respiratory distress with severe attacks
o May lead to respiratory failure
treatment of asthma
o Acute attacks: inhaled bronchodilators, oral corticosteroids, oxygen prn
o Chronic management: avoidance of allergens and triggers, patient education, anti-inflammatories (ie. inhaled corticosteroids), antileukotrienes. Airway inflammation & fluid may be still be present in some individuals, even though they are asymptomatic
- Permanent damage
- Cannot be cured
- Person must live with symptoms
COPD: Umbrella term for Chronic Bronchitis & Emphysema
- Hypersecretion of mucus and chronic productive cough for 3 months a year for 2 consecutive years
- Increase in the size and number of mucous glands and goblet cells
- Airway obstruction caused by chronic infection and injury
Chronic Bronchitis
• Clinical Manifestations of Chronic Bronchitis (4)
o increased mucus productions, increased cough
o At risk for recurrent pulmonary infections
o Peripheral & central edema
o Right sided heart failure (blue bloaters)
Edemic, bloated, cyanotic
• Loss of elastic recoil occurs from destruction of alveolar walls resulting in permanent enlargement of gas-exchange airways (Like a balloon that has been inflated too many times)
Emphysema
In emphysema the _____big, boggy and stretched (ENLARGED)
o Alveoli
_____ _ -______protects us from these enzymes that want to destroy our lungs tissue. Emphysema has a deficiency in this which is a primary cause.
Alpha1-antitripsin
Secondary cause to emphysema
injury to lungs from inhaled toxins
o Cigarette smoke – toxins within cigarettes destroys alpha1-antitripsin
• Clinical manifestations of emphysema (4)
o Barrel chest (anterior-posterior diameter of chest is larger than it should be because the lungs are always in a state of hyperinflation)
o Pursed lip breathing – they have to make the extra effort to exhale. It isn’t natural for them, they have to force air out of lungs.
o Sit in tripod position – most comfortable way they can breath
o Weight loss – thin, emaciated appearance
People with emphysema are at High risk for pneumonia as they cannot _____________ ___________
effectively expectorate
- Dilation of the bronchi
* Pocket forms on side of bronchi and they have different shapes
Bronchiectasis
Bronchiectasis can develop _________ ____________ _____________
abscess, infection, burst
Bronchiectasis Occurs as a result of __________ of muscle and elastic fibers of bronchial wall
weakening
RESTRICTIVE DISORDERS (2)
Pneumonia
Atelectasis
Pneumonia
• Etiology (3)
o Begins with Inhalation of pathogens. Pathogens then establish themselves inside the lungs
o Aspiration – vomiting and inhaling gastric contents. Burns the bronchi and respiratory passages
o Endogenous – infection that occurs somewhere else in the body. Travels to the lungs and establishes infection there
Pneumonia
• Pathogenesis
o Set off inflammatory reaction
o Alveoli fill with exudate (drainage)
o Consolidation
Pneumonia
• Clinical manifestations may vary with cause, age and severity of illness (3)
o Fever, chills
o Cough (may or may not be productive)
o Dyspnea, crackles over affected lobe
collapse of lung tissue
Atelectasis
Atelectasis two types:
o Obstruction
o Compression by external mass
Atelectasis • Pathogenesis (3)
o Airless alveoli shrivel due to elasticity – because they are not receiving air
o Interferes with blood flow through lungs (decreased gas exchange & oxygenation)
o Client will become hypoxemic very quickly
Atelectasis • Risk factors (2)
o Immobility – secretions pool in lungs and clog small bronchioles. And alveoli that are passed the area of obstruction do not receive air and shrivel. Inhibits blood vessels. If oxygen isn’t restored the tissue becomes necrotic and dies.
o Surgery
Atelectasis • Clinical manifestations (9)
o Dyspnea o Cough o Fever o Leukocytosis o Tachypnea o Focal decreased breath sounds o Increased crackles at lung bases o Hypoxemia o Decreased depth of respiratory excursions
Chest Wall Structural Abnormalities – prevent lungs from expanding
Hunched back. Elderly with osteoporosis. Inhibits chest expansion
• Kyphosis
Chest Wall Structural Abnormalities – prevent lungs from expanding
(chest excavation) Sternum is displaced backwards
• Pectus excavatum
Chest Wall Structural Abnormalities – prevent lungs from expanding
Sternum is protruding forward. Bird chest.
• Pectus carinatum
Chest Wall Structural Abnormalities – prevent lungs from expanding
spine is ‘S’ shaped. Interferes with movement of ribs and inhibits movement of chest wall.
• Scoliosis
Painful interferes with lung expansions. Leading to pneumonia or atelectasis
• Rib fractures
o Usually 2 fractures per rib in consecutive ribs or fracture of sternum plus consecutive ribs.
o Results in paradoxical breathing
o Treatment: pain control and management of underlying pulmonary and/or cardiac injury (Chest tubes, mechanical ventilation)
o Can cause pneumothorax
• Flail chest (multiple rib fractures)
• An accumulation of air in the pleural space
o Causes atelectasis (greater amount of air = more severe atelectasis)
• May result from underlying disease (such as COPD) or from chest trauma (rib fractures)
Pneumothorax
• Types of pneumothorax
o Spontaneous Primary Secondary o Open o Tension
Pneumothorax: Spontaneous
• Primary
o Spontaneous rupture of blebs (air blister) on visceral pleura. May occur during rest, exercise, or sleep.
o Usually occurs in men between 20 – 40 yrs
Pneumothorax: Spontaneous
• Secondary
o Resulting from trauma or spontaneous rupture of bleb on visceral pleura secondary to pre-existing pulmonary disease
• Opening in chest wall secondary to trauma such as stab wounds, bullet wounds. (CHEST INJURY)
• Air is drawn through the wound into the pleural space during inspiration and forced back out during expiration. Wound in the chest wall appears to be “sucking air” and is visibly bubbling; therefore referred to as “sucking wound”
o Leads to atelectasis
• Pressure in pleural space equals atmospheric pressure
Pneumothorax: Open
As person inhales, air is entering through chest wall. The issue is a flap will develop. Air cannot escape bc of flap. Every time they inhale more and more air get into the pleural space. Increases pressure inside thoracic cavity.
Pneumothorax: Tension (WORST PNEUMOTHORAX)
• Air enters the pleural space during inspiration; on expiration, opening is sealed and air becomes trapped, increasing the pressure within the thoracic cavity
Pneumothorax: Tension (WORST PNEUMOTHORAX)
manifestations of tension pneumothorax
o Initially: Chest pain, dyspnea, tachycardia, decreased breath sounds on affected side,
o As pneumothorax progresses: absent breath sounds on affected side, hypoxemia, laboured breathing, jugular venous distension, hypotension, contralateral tracheal shift.
- Accumulation of excessive fluid in the pleural space
* Fluid is heavy and sits at bottom of pleural space
Pleural Effusion – same principle as pneumothorax but instead of air it is fluid in the pleural space
blood in pleural space usually associated with trauma
o Hemothorax
watery drainage in pleural space, low protein count (seen in pneumonia)
o Transudate
watery but has high protein count (seen in tumors – lung cancer)
Exudate
pus in pleural space (seen in lung abscesses)
Empyema
lymphatic fluid leaking into pleural space
Chylous pleural effusion
• Clinical manifestations are associated with the extent of atelectasis (amount of drainage) Symptoms worsen as drainage increases (3)
o Dyspnea, tachypnea, tachycardia, decreased breath sounds on affected side
o Fever associated with infection (empyema)
o Hypoxemia, laboured breathing, hypotension, contralateral tracheal shift
• Form of respiratory failure
• Causes
o Direct – pneumonia, smoke inhalation, chemical inhalation, inhalation of toxic fumes, near drowning
o Indirect – caused by other diseases such as pancreatitis, drug overdose
Acute Respiratory Distress Syndrome (ARDS)
Fibroblast cells deposit protein along walls of alveoli occur with the increased inflammation. This increases the thickness of the alveoli and decreases gas exchange.
Prominent fibrosis (thickening)
o Fibroproliferative phase
• Pathogenesis of ARDS
o Acute phase
Inflammatory mediators damage structure of alveoli
At the same time we have an increase in coagulation factors
Lots of inflammation at site
Alveolar membrane becomes damage as a result of inflammation & edema
Increase in coagulation factors causes increase in blood clotting inside the lungs
Can recover from this phase If damage isn’t too severe
• Clinical manifestations of ARDS
o Dyspnea, tachypnea, tachycardia, increased respiratory effort.
o Hypoxemia unresponsive to increasing fractions of inspired oxygen (Fi02), poor lung compliance
o Can result in respiratory failure and if not reversed – death
o Restlessness, exhaustion, decreased mental status
Inherited disease. Genetic abnormality. Respiratory, pancreatic, and GI tract ducts become clogged with a very thick mucus. Normally, we have a little bit of mucus in secretions. In cystic fibrosis, the mucus is so thick it plugs the ducts.
Cystic Fibrosis (cystic = duct)
• CF gene located on chromosome __
7
• CFTR (cystic fibrosis transmembrane regulator)
Abnormal expression of protein
• Characterized by ______ _________ __ ____ _______and concentrated sweat, often causing obstruction of GI and respiratory tracts
excessive secretion of thick mucus
CF Respiratory effects (blocks ducts in respiratory tract)
o Cough, wheeze, recurrent pneumonia o Barrel chest, clubbing bc of hypoxemia o Bronchospasm o Mucus in lung o Causes hypoxemia
CF Gastrointestinal effects (mucus prevents liver and pancreas from secreting enzymes)
o Failure to thrive, malabsorption
o Diabetes, pancreatitis, hepatic failure
No tx for CF only Manage symptoms by supplementing digestive enzymes
Cotezyme
• As the client with cystic fribrosis ages they can develop:
o Pancreatitis
o Liver failure
o Diabetes
o Respiratory problems bc lungs begin to fail, become hypoxemic
Can go into respiratory failure
Usually need lung transplant eventually
Etiology – Lung disease caused by chronic exposure to industrial products
Pneumoconiosis
fine particle silica(dust) inhalation
• Silicosis
in buildings in 50s as fire retardant
• Asbestosis
coal miner’s lung, accumulation of soot, fine particle dust
• Anthracosis
pesticides, fine hay particles
• farmer’s lung
• Macrophages (WBCs) secrete____________which destroy alveolar walls
lysozymes
• Causative organism: Bordetella pertussis
Pertussis – whooping cough
• Droplet infection of Pertussis – whooping cough
highly contagious
Pertussis – whooping cough Pathogenesis
o Attached to cilia in respiratory tract produces a toxin which initiates an inflammatory response
Incubation Period 5 – 21 days
Prodrome: 1 – 2 wks; Rhinorrhea (runny nose), fever, malaise (resembles bad cold)
Paroxysm : 1 – 6 wks; Paroxysmal coughing spasm (associated with vomiting)
Convalescence: wks – months
Can be dangerous in infants and babies bc of coughing spams – cause vomiting. This causes increased risk for aspiration.
Pertussis – whooping cough Clinical Manifestations
- Bruising around eyes
* Broken blood vessels in eye from coughing
Pertussis – whooping cough • Complication:
o Risk of aspiration in infants ( 1 – 3 infants deaths per year in Canada)
o Petechiae, bruising, fractured ribs, pneumonia
Tuberculosis • Mode of transmission
caused by inhalation of bacterium
o aerosolized droplet
Tuberculosis • Populations at risk (large populations living in small areas)
o Elderly o HIV o Homeless o Refugee camps o Travelers
TB Clinical Manifestations:
• Primary infection may be asymptomatic
• Active disease:
o Fever, fatigue, malaise, weight loss, night sweats, cough (may be productive, may cough up blood), sputum production, hemoptysis
• A severe form of pneumonia caused by:
SARS associated coronavirus (SARS-CoV).
SARS quickly leads to ___________ ____________
respiratory failure
SARS Pathogenesis
o Incubation period 2 to 7 days
o Onset: fever, chills, myalgia, headache
o Nonproductive cough; progresses to pneumonia
o May develop hypoxemia
o Period of communicability:
when pt symptomatic.
CDC recommends isolation for 10 days post symptoms
• Mode of transmission for SARS
airborne (CDC) – highly contagious
• WHO guidelines: SARS may be suspected in a patient with
o Fever of 38°C and
o History of
travel to high risk areas OR
Contact with someone with a diagnosis of SARS
Influenza – respiratory illness. Can have gastro symptoms comes from the
• Orthomyomyxoviridae – family that influenza comes from…. Awe (comes from birds)
• Influenza A
• Influenza B
• Influenza C
Which is the most serious
Influenza A – most serious
Influenza – respiratory illness Complications
o Croup, viral pneumonia, secondary bacterial infections
o Cardiac complications
o Reye’s syndrome (encephalopathy – brain damage, secondary to infection)
o Guillain-Barre syndrome
Blood clots have developed in lungs or develop elsewhere in the body. An embolus (piece of blood clot) breaks off and travels to lungs
Pulmonary Embolism – blood clot to lungs
often caused by DVT Prolonged immobility
o Venous stasis (sluggish blood flow)
often caused by DVT
Polycythemia vera (increase coagulability)
Medications (birth control)
o Hypercoagulability (promote blood clotting)
often caused by DVT
Hyperglycemia can inflame blood vessel
When we start an IV (venipuncture)
Smoking
o Inflammation of blood vessel
Pulmonary Embolism – blood clot to lungs Pathogenesis
o Initially a blood clot (thrombus) forms within the deep veins. The clot becomes embolus, by becoming dislodged from its original site and travels through the systemic circulation and into the pulmonary circulation. The clot eventually travels into a branch of the pulmonary circulation. It can either occlude a small vessel causing temporary symptoms until the fibrinolytic system destroys it. It may manifest as multiple small emboli, or it may be large enough to block the flow of blood distal to the obstruction, creating death of pulmonary tissue (an infarction).
o Can have multiple small emboli or one large one
Pulmonary Embolism – blood clot to lungs
• Clinical Manifestations varies with severity
o Initially – anxiety, restlessness
o Dyspnea, tachypnea, chest pain, tachycardia
o As it worsens – May experience hemoptysis
o Hypoxia/cyanosis
o Massive occlusion from poor blood flow to tissue – profound shock
Lung Cancer
• Small cell
o Rapid growing o Unresponsive to treatment o Grows in central bronchi region o Grows from the outside of lung inside o Doubles in size in 33 days o Usually isn’t found until it has spread considerable o Has poorest outcome
Lung Cancer
• Non-small cell
o Squamous cell
grows centrally
easily found
grows slowly
o Adenocarcinoma Slow growing cancer Grows peripherally Grows more quickly than squamous cell o Large cell carcinoma Grows in cluster Grows peripherally Slow growing Fairly easy to find & indentify o If found early there may be success in treating them
Lung Cancer what is the first sign
Persistent nagging cough
Lung Cancer effects
o Obstruction of airflow
o Inflammation
o Pleural effusion, hemothorax, pneumothorax
o Paraneoplastic syndrome (SIADH) – tumors manufactures and secretes ADH
Swelling
Hyponatremia
