respiratory

Question 1

influenza patho

Answer 1

Upper respiratory virus that is easily spread from person to person due to inappropriate hand washing
Can lead to more severe respiratory conditions such as pneumonia or even death

Question 2

influenza clinical manifestations

Answer 2

Cough, fever and myalgia accompanied by a headache and sore throat
Mild conditions are similar to a common cold
Dyspnea, diffuse crackles

Question 3

influenza nursing assessment

Answer 3

I-PAP
Airway compliance, perfusion, gas exchange
NEURO: fever, headache, LOC, alert, orientated, lethargic, dizziness, light headedness, (related to impaired gas exchange); CV: color, hemodynamic status- is the patient pale, pink, grey, cyanotic, tachycardia, pulses x 6, capillary refill; RESP: do you hear inspiratory or expiratory crackles in the lungs where (course, fine), is gas exchange impaired, is the patient tachypneic; cough; expectorant MSK: arthralgia
Gonna start with resp then go to hemodynamic and neuro assessment

Question 4

conditions of the lower respiratory system

Answer 4

Disorders of the chest wall and pleura 
Pleural Effusions and Pneumothorax
Restrictive lung diseases
Aspiration, Atelectasis, Pulmonary Edema, ARDS, ALI, COVID-19
Obstructive Airway disorders
Asthma (pediatric), COPD, Emphysema
Respiratory tract infections
Pneumonia, TB, and Acute Bronchitis
Pulmonary Vascular disorders
Pulmonary Embolus, Pulmonary HTN, Cor Pulmonale

Question 5

pleural effusion clinical manifestations

Answer 5

Trapped lung can occur when the visceral pleura becomes encased with a fibrous peel or rind pulmonary restriction
Progressive dyspnea and decreased movement of the chest wall on the affected side
Manifestations of an empyema include fever, night sweats, cough and weight loss
lungs can’t fully expand

Question 6

pleural effusion nursing assessment

Answer 6

Dullness to percussion and absent or decreased breath sounds over affected area

Question 7

pleural effusion nursing assessment

Answer 7

Dullness to percussion and absent or decreased breath sounds over affected area

Question 8

Pleural effusion summary of assessment

Answer 8

Condition: Collection of excess fluid in the intrapleural space, with compression of overlying lung tissue. Effusion may contain watery capillary fluid (transudative), protein (exudative), purulent matter (empyemic), blood (hemothorax), or milky lymphatic fluid (chylothorax). Gravity settles fluid in dependent areas of thorax. Presence of fluid subdues all lung sounds.
Inspection: Increased respirations, dyspnea; patient may have dry cough, tachycardia, cyanosis, abdominal distension.
Palpation: Tactile fremitus decreased or absent. Tracheal shift away from affected side. Chest expansion decreased on affected side.
Percussion: Dull to flat. No diaphragmatic excursion on affected side.
Auscultation: Breath sounds decreased or absent. Voice sounds decreased or absent. When remainder of lung is compressed near the effusion, bronchial breath sounds may be heard over the compression along with bronchophony, egophony, whispered pectoriloquy.
Adventitious sounds: None.

Question 9

pneumothorax patho

Answer 9

Presence of air in the pleural space that results in a complete or partial collapse of a lung
Should be suspected after blunt trauma to the chest wall
May also be associated with a hemothorax
Classified as either closed, open or tension pneumothorax

Question 10

closed pneumothorax

Answer 10

No associated external wound
Spontaneous pneumothorax witch is the accumulation of air in the pleural space without an apparent event
Caused by rupture of small blebs on the visceral pleural space underweight, male, cigarette smokers between 20-40 yrs old

Question 11

open pneumothorax

Answer 11

Air enters the pleural space through an opening in the chest wall
Penetrating chest wound is referred to as a sucking chest wound
can lead to a tension pneumothorax

Question 12

tension pneumothorax

Answer 12

Pneumothorax with a rapid accumulation of air in the pleural space causing severely high intrapleural pressures
Occurs from either open or closed pneumothorax
In an open chest wound, the flap acts as a one-way valve where air can enter on inspiration but not escape
May occur in chest tubes are clamped or become blocked with a patient who has a pneumo
This is a medical emergency
late manifestation is a tracheal shift (to unaffected side)

Question 13

hemothorax

Answer 13

Accumulation of blood in the intrapleural space
Causes include chest trauma, lung malignancy, complications of anticoagulant therapy, pulmonary embolus and tearing of pleural adhesions

Question 14

chylothorax

Answer 14

Presence of lymphatic fluid in the pleural space because of a leak in the thoracic duct
Causes include trauma, surgical procedures and malignancy

Question 15

pneumothorax clinical manifestations

Answer 15

In a small pneumothorax, patients may exhibit mild tachycardia and dyspnea
In a larger pneumothorax, patients may exhibit respiratory distress, shallow, rapid respirations, dyspnea, air hunger, decreased oxygen saturation, chest pain, cough with or without hemoptysis
Chest pain because the cardiac myocytes don’t get enough oxygen (type 2 MI)

Question 16

pneumothorax nursing assessment

Answer 16

Upon auscultation, there are no breath sounds over the affected area and hyper-resonance may be present
If a tension pneumothorax develops, the patient may have severe respiratory distress, tachycardia and hypotension
Mediastinal displacement occurs with tracheal shift (always deviates to the unaffected side)
Changes in blood pressure, pulse

Question 17

pneumothorax assessment summary

Answer 17

Condition: Free air in pleural space causes partial or complete lung collapse. Air in pleural space neutralizes the usual negative pressure present; thus lung collapses. Usually unilateral. Pneumothorax can be (a) spontaneous (air enters pleural space through rupture in lung wall), (b) traumatic (air enters through opening or injury in chest wall), or (c) tension (trapped air in pleural space increases, compressing lung and shifting mediastinum to the unaffected side).
Inspection: Unequal chest expansion. If pneumothorax is large, patient may have tachypnea, cyanosis, apprehension, bulging in interspaces.
Palpation: Tactile fremitus decreased or absent. Tracheal shift to opposite side (unaffected side). Chest expansion decreased on affected side. Tachycardia, decreased blood pressure.
Percussion: Hyperresonant. Decreased diaphragmatic excursion.
Auscultation: Breath sounds decreased or absent. Voice sounds decreased or absent.
Adventitious sounds: None.

Question 18

restrictive lung disease: aspiration

Answer 18

Passage of fluid and solid particles into the lung
May be related to impair levels of consciousness (LOC), seizure disorders, cerebrovascular accident, and neuromuscular disorders that cause dysphagia
May cause severe pneumonitis
Lung becomes still and noncompliant leading to edema and collapse

Question 19

restrictive lung disease: atelectasis

Answer 19

Collapse of lung tissue
Three types which are: compression atelectasis, absorption atelectasis and surfactant impairment
Tends to develop after surgery
Clinical manifestations include: dyspnea, cough, fever and leukocytosis

Question 20

atelectasis summary of assessment

Answer 20

Condition: Collapsed shrunken section of alveoli, or an entire lung, as a result of (a) airway obstruction (e.g., the bronchus is completely blocked by thick exudate, aspirated foreign body, or tumour), the alveolar air beyond it is gradually absorbed by the pulmonary capillaries, and the alveolar walls cave in; (b) compression on the lung; and (c) lack of surfactant (hyaline membrane disease).
Inspection: Cough. Lag on expansion on affected side. Increased respiratory rate and pulse. Possible cyanosis.
Palpation: Chest expansion decreased on affected side. Tactile fremitus decreased or absent over area. With large collapse, tracheal shift toward affected side.
Percussion: Dull over area (remainder of thorax sometimes has hyperresonant note).
Auscultation: Vesicular decreased or absent over area. Voice sounds variable, usually decreased or absent over affected area.
Adventitious sounds: None if bronchus is obstructed. Occasional fine crackles if bronchus is patent.

Question 21

restrictive lung disease: pulmonary edema

Answer 21

excess water in the lung, actually within the alveoli
common clinical manifestation for a lot of other diseases
most common problem is as a result of a left sided heart problem

Question 22

pulmonary edema patho

Answer 22

Most common cause is left-sided heart disease
May be related to capillary injury that increases capillary permeability
May also be caused by obstruction in the lymphatic vessels
When hydrostatic pressure exceeds oncotic pressure (holds fluid in the capillary) fluid moves out into the insterstitial space , when the flo of fluid out of the capillaries exceeds the lumphatic systenms ability to remove it, pulmonary edema develops.
Capillary injury and inflammation cause water and plasma proteins to leak out of the capillary and move intot he instestitial space. The insterstitial oncotic pressure begins to exceed capillary oncotic pressure, water moves out of the capillary and into the lung

Question 23

pulmonary edema clinical manifestations

Answer 23

Dyspnea and increased work of breathing
Fine inspiratory crackles and dullness to percussion of the lung bases
V/Q mismatch (low) leads to hypoxemia
In severe cases, pink, frothy sputum

Question 24

pulmonary edema nursing assessment

Answer 24

I-PAP

Auscultation, Percussion

Question 25

restrictive lung disease: acute respiratory distress syndrome (ARDS)

Answer 25

Characterized by acute lung inflammation an diffuse alveolocapillary injury
Acute Lung Injury (ALI) is a less severe form of lung inflammation
Most Common Causes:
Sepsis and multiple trauma, pneumonia, burns, aspiration, cardiopulmonary bypass, surgery, pancreatitis, blood transfusions, drug overdose, inhalation of smoke or noxious gases, fat emboli, high concentrations of supplemental oxygen, radiation therapy, and disseminated intravascular coagulation (DIC)

Question 26

ARDS patho

Answer 26

There is massive pulmonary inflammation that injures the alveoli-capillary membrane and produces severe pulmonary edema
V/Q mismatching (shunting)
Hypoxemia
Endothelial damage initiates the complement cascade
Toxic mediators such as tumor necrosis factor and interleukin 1
Inflammatory mediators are released
Alveoli and respiratory bronchioles fill with fluid or collapse
Lungs become less compliant increasing the work of breathing, ventilation of alveoli decrease and hypercapnia develops leading to acute
ARDS creates a stiff lung
neutrophils and macrophages want to come along as a natural immunity response

Question 27

ARDS clinical manifestation

Answer 27

Dyspnea, rapid, shallow breathing
Inspiratory crackles
Respiratory alkalosis
Decreased lung compliance
Hypoxemia unresponsive to oxygen therapy
Diffuse alveolar infiltrates without evidence of cardiac disease
early stages = blow off co2
end stages = higher levels of co2

Question 28

ARDS nursing assessment

Answer 28

I-PAP
Related to symptoms
go from early stage down to late stage
Dyspnea and hypoxemia
↓
Hyperventilation and respiratory alkalosis
↓
Decreased tissue perfusion, organ dysfunction, and metabolic acidosis
↓
Increased work of breathing, decreased tidal volume, and hypoventilation
↓
Respiratory acidosis and worsening hypoxemia
↓
Hypotension, decreased cardiac output, death
monitor and intervene

Question 29

ARDS summary of assessment

Answer 29

Condition: An acute pulmonary insult (trauma, gastric acid aspiration, shock, sepsis) damages alveolar capillary membrane, leading to increased permeability of pulmonary capillaries and alveolar epithelium, and to pulmonary edema. Gross examination (autopsy) would show dark red, firm, airless tissue, with some alveoli collapsed, and hyaline membranes lining the distended alveoli.
Subjective: Acute onset of dyspnea, apprehension.
Inspection: Restlessness; disorientation; rapid, shallow breathing; productive cough; thin, frothy sputum; retractions of intercostal spaces and sternum. Decreased PaO2, blood gases show respiratory alkalosis, radiographs show diffuse pulmonary infiltrates, a late sign is cyanosis.
Palpation: Hypotension.
Auscultation: Tachycardia.
Adventitious sounds: Crackles, rhonchi.

Question 30

severe pulmonary illness/acute lung illness

Answer 30

September 6, Health Canada issued an advisory
Stemmed from the CDC and FDA reports of severe pulmonary illness and deaths related to the use of vaping
No specific device or substance has been linked to the illness but it is believed to be as a result of chemical exposure

Question 31

acute lung illness patho

Answer 31

Although there is limited research, based on accounts there are pathophysiological changes that may contribute to patient compromise:
Bronchiolitis obliterans (popcorn lung) = inflammatory obstruction of the airways
Acute eosinophilic pneumonia = inflammatory stimulus that recruits macrophages and neutrophils to lung tissue 
Diffuse alveolar damage = hemorrhage in alveolar 
Idiopathic interstitial pneumonia = inflammation and scarring in the alveoli
Lipoid pneumonia = presence of lipids within alveolar space
most often patients come in with lipoid pneumonia

Question 32

acute lung illness clinical manifestations

Answer 32

May include flu-like symptoms such as cough, fever, malaise, fatigue and weight loss.
Gradual onset of shortness of breath and dry cough
Tachycardia
Tachypnea
Potential to develop acute respiratory distress quickly requiring supportive measures
Vomiting and diarrhea
Long-term effects and lung damage still unknown
Scarring, chronic inflammation, cost to treat, addictions

Question 33

covid 19 patho

Answer 33

SARS-CoV-2 enters the host cell by biding to the ACE2 receptor in the lung membrane fusion of the virus and the host cell is activated after the binding, viral RNA is released into the cytoplasm, establishing infection
ACE-2 is expressed on the type II alveolar epithelial cells (surfactant), and weekly expressed on the surface of the epithelial cells, proximal tubule cells of the kidney and bladder urothelial cells, as well as the enterocytes of the small intestine, especially in the ileum
RAS plays a significant role in COVID-19 infections

Question 34

covid 19 adults nursing assessment

Answer 34

NEURO: fever, headache, LOC, alert, orientated, lethargic, dizziness, light headedness, (related to impaired gas exchange); CV: color, hemodynamic status- is the patient pale, pink, grey, cyanotic, tachycardia, pulses x 6, capillary refill, peripheral edema, chest pain, tachycardia; RESP: do you hear inspiratory or expiratory crackles in the lungs where (course, fine), is gas exchange impaired, is the patient tachypneic, non-productive cough, expectorant, cyanosis, oxygen required, pleuritic chest pain; RENAL: urine output > or < 30 cc/hr, colour, consistency, frequency, 24 hour fluid balance; GI: taste, smell, nausea, vomiting, diarrhea, anorexia MSK: is the gait steady

LAB Values: CBC: WBC (neutrophils, bands), platelets, hemoglobin; Electrolytes: sodium, potassium, and BNP levels, creatinine, BUN, GFR, magnesium; Clotting Factors: INR, PTT, D-Dimer; MISC: CRP, lactate, ABG

Question 35

covid 19 pediatrics clinical manifestations

Answer 35

Multisystem Inflammatory Disease
Increase in children with symptoms of Kawasaki disease (CV lecture)
Inflammation in multiple body systems such as: heart, lungs and kidneys, brain, skin, eyes, and GI organs

Clinical Manifestations: 
Fever
Abdominal pain
Vomiting
Diarrhea
Neck pain
Rash
Bloodshot eyes
Feeling extra tired

Question 36

obstructive airway disorders: chronic obstructive pulmonary disorder (COPD) patho

Answer 36

Group of chronic diseases that cause obstruction in airflow.
Pathophysiology:
 in the exhaled air flow caused by a narrowing or obstruction of the airways
e.g., emphysema, chronic bronchitis, bronchiectasis (Abnormal widening of the bronchi or their branches, causing a risk of infection)
Emphysema & chronic bronchitis are often clinically grouped together and referred to as COPD.
Many patients have overlapping features of damage at both the acinar level (emphysema) and bronchial level (bronchitis)

Question 37

COPD risk factors and other info

Answer 37

Risk factors include environmental – smoking, occupational exposure (dusts, cadmium, gold dust, coal dust, grain dust), outdoor air pollution, repeated childhood respiratory tract infections
COPD is the result of long-term heavy cigarette smoking; about 10% of pts are non-smokers
Elastic recoil – low
Airway resistance – normal or slightly increased
Bronchial wall becomes inflamed and fibrosed, with breakdown of alveolar tissue and loss of elasticity, hyper mucus secretion, airway obstruction, air trapping.

Question 38

COPD emphysema patho

Answer 38

Loss of lung elasticity
Pathophysiology:
Enlargement on alveoli due to air trapping; hyperinflation of lungs and increased Total Lung Capacity
“over-inflation” enlargement of airspaces unaccompanied by destruction

Question 39

COPD emphysema clinical manifestations

Answer 39

Dyspnea
Hyper inflated chest (Barrel chest)
Use of accessory muscles
Pursed lip breathing
Weight loss and anorexia
Prolonged expiratory phase, wheezes, decreased breath sounds
Tripod position
cacepnic (use more calories)

Question 40

COPD emphysema nursing assessment

Answer 40

I-PAP
Inspection for the way the patient is breathing, position, chest wall
Auscultation over all lung fields
Vital signs, oxygenation, perfusion

Question 41

COPD emphysema breathing

Answer 41

Emphysema patient use of prominent accessory muscles to breathe
Features include:
purse-lip breathing with intense dyspnea
patient is often thin and elderly
little sputum produced
edema and overt heart failure are rare complications

Question 42

COPD emphysema summary of assessment

Answer 42

Condition: Caused by destruction of pulmonary connective tissue (elastin, collagen); characterized by permanent enlargement of air sacs distal to terminal bronchioles and rupture of interalveolar walls. Airway resistance is increased, especially on expiration, which causes hyperinflation of the lung and an increase in lung volume. Cigarette smoking accounts for 80%-90% of cases of emphysema.
Inspection: Increased anteroposterior diameter. Barrel chest. Use of accessory muscles to aid respiration. Tripod position. Shortness of breath, especially on exertion. Respiratory distress. Tachypnea.
Palpation: Decreased tactile fremitus and chest expansion.
Percussion: Hyper-resonant. Decreased diaphragmatic excursion.
Auscultation: Decreased breath sounds. Expiration may be prolonged. Muffling of heart sounds as a result of overdistension of lungs.
Adventitious sounds: Usually none; occasionally, wheeze.

Question 43

COPD chronic bronchitis patho

Answer 43

Airway obstruction caused by inflammation of airways
Characterized by hypersecretion of mucus and chronic productive cough for at least 3 months
Pathophysiology:
Inspired irritants result in airway inflammation with infiltration of neutrophils, macrophages and lymphocytes
Continued bronchial inflammation leads to bronchial edema and increases the size and number of mucous glands leading to the production of thick tenacious mucus
Often combined with emphysema

Question 44

COPD bronchitis summary of assessment

Answer 44

Condition: Proliferation of mucous glands in the passageways, resulting in excessive mucus secretion. Inflammation of bronchi with partial obstruction of bronchi by secretions or constrictions. Sections of lung distal to obstruction may be deflated. Bronchitis may be acute or chronic with recurrent productive cough. Chronic bronchitis is usually caused by cigarette smoking.
Inspection: Hacking, rasping cough productive of thick mucoid sputum. Chronic: dyspnea, fatigue, cyanosis, possible clubbing of fingers.
Palpation: Tactile fremitus normal.
Percussion: Resonant.
Auscultation: Normal vesicular. Voice sounds normal. Chronic: prolonged expiration.
Adventitious sounds: Crackles over deflated areas. Wheeze may be present.

Question 45

respiratory tract infection pneumonia

Answer 45

Infection of the lower respiratory tract caused by bacteria, viruses, fungi, protozoa, or parasites
Defined in two ways:
Location in the lungs
Lobar Pneumonia (occurs in one lobe of the lung).
Bronchopneumonia (tends to be patchy).
Origin of Infection
Community-acquired (pneumonia contracted outside the hospital)
Hospital-acquired pneumonia – nosocomial; particularly gram-negative bacteria and staphylococci

Question 46

pneumonia patho

Answer 46

Acquire organisms three primary routes: aspiration, inhalation and hematogenous
Macrophages in the alveolar recognize the pathogens and activates the innate and adaptive immune responses
Release of tumor necrosis factor-alpha and interleukin-1 from macrophages contributes to inflammation
Inflammatory mediators and immune complex damage bronchial mucous membranes and alveoli-capillary membranes causing alveoli to fill with infectious debris and exudate causing lung damage and consolidation
Accumulation in the acinus leads to dyspnea and to V/Q mismatching and hypoxemia
could lead to ARDS

Question 47

pneumonia clinical manifestations

Answer 47

Sudden onset of fever, chills, productive cough of purulent sputum and pleuritic chest pain
Confusion or stupor (related to hypoxia) may be predominant
pneumonia differs from chronic bronchitis because of the fever (response to the infection)

Question 48

pneumonia nursing assessment

Answer 48

I-PAP
Inspection: increased work of breathing, cough, changes in perfusion and oxygenation
Percussion/Palpate: dullness and increased fremitus over areas of pulmonary consolidation
Auscultate: may have decreased breath sounds or bronchial breath sounds or crackles
Lab Values: Complete Blood Count (CBC), C-Reactive Protein (CRP), Electrolytes, Arterial Blood Gas (ABG)

Question 49

pneumonia complications

Answer 49

Pleurisy (inflammation of the pleura) can lead to pleural effusion
Pleural Effusion (can lead to pneumothorax)
Atelectasis
Empyema
Pericarditis
Endocarditis

Question 50

pneumonia summary of assessment

Answer 50

Condition: Infection in lung parenchyma leaves alveolar membrane edematous and porous, and so red blood cells (RBCs) and white blood cells (WBCs) pass from blood to alveoli. Alveoli progressively fill up (become consolidated) with bacteria, solid cellular debris, fluid, and blood cells, all of which replace alveolar air. This results in decreased surface area of the respiratory membrane, which causes hypoxemia.
Inspection: Increased respiratory rate. Guarding and lag on expansion on affected side. Children: sternal retraction, nasal flaring.
Palpation: Chest expansion decreased on affected side. Tactile fremitus increased if bronchus patent, decreased if bronchus obstructed.
Percussion: Dull over lobe.
Auscultation: Breath sounds louder with patent bronchus, as if coming directly from larynx. Voice sounds have increased clarity, bronchophony, egophony, whispered pectoriloquy present. Children: diminished breath sounds may occur early in pneumonia.
Adventitious sounds: Crackles, fine to medium.

Question 51

respiratory tract infection: tuberculosis (TB) patho

Answer 51

Infection caused by mycobacterium tuberculosis, an acid-fast bacillus that affects the lungs
Pathophysiology:
Highly contagious transmitted through airborne droplets
Immunocompetent patients, microorganism is contained by the inflammatory and immune response systems that results in latent TB infection (LTBI)
After latent period in the upper lobe, bacilli are inspired into the lungs where they multiply and cause nonspecific pneumonitis activates alveolar macrophages and neutrophils
May lay dormant but can also be reactivated

Question 52

TB clinical manifestations

Answer 52

LTBI is asymptomatic
Symptoms of active disease develop gradually and usually unnoticed: fatigue, weight loss, lethargy, anorexia and low grade fever
Cough that produces purulent sputum, night sweats and general anxiety, dyspnea, chest pain and hemoptysis

Question 53

TB nursing assessment

Answer 53

I-PAP

Lab Values: CBC, acid-fast bascilli (AFB)

Question 54

TB summary of assessment

Answer 54

Condition: Inhalation of tubercle bacilli into the alveolar wall starts course of disease: (a) Initial complex is acute inflammatory response; macrophages engulf bacilli but do not kill them. Tubercle forms around bacilli. (b) Scar tissue forms, and lesion calcifies and is visible on radiograph. (c) Previously healed lesion is reactivated. Dormant bacilli now multiply, producing necrosis, cavitation, and caseous lung tissue (cheeselike appearance). (d) Extensive destruction occurs as lesion erodes into bronchus, forming air-filled cavity. Apex usually has the most damage.
Subjective data: Initially no symptoms, manifests as positive result of skin test or on radiograph. Progressive tuberculosis involves weight loss, anorexia, easy fatigability, low-grade afternoon fevers, night sweats. Patient may have pleural effusion, recurrent lower respiratory infections.
Inspection: Cough initially nonproductive, later productive of purulent, yellow-green sputum, may be blood-tinged. Dyspnea, orthopnea, fatigue, weakness.
Palpation: Skin moist at night from night sweats.
Percussion: Resonant initially. Dull over any effusion.
Auscultation: Normal or decreased vesicular breath sounds.
Adventitious sounds: Crackles over upper lobes common, persist after full expiration and cough.

Question 55

pulmonary vascular condition: pulmonary embolus patho

Answer 55

Occlusion of the pulmonary vascular bed by an embolus
Pathophysiology:
May occur as: embolus with infarction, embolus without infarction, massive occlusion, or multiple pulmonary emboli
Significant obstruction of the pulmonary vasculature leads to increased pulmonary artery pressures (pulmonary hypertension)
Effect of the embolus depends on the extent of pulmonary blood flow obstruction
Release of neurohumoral substances such as serotonin, histamine, catecholamines, angiotension II, and inflammatory mediators such as endothelin, leukotrienes, thromboxanes, and toxic free oxygen free radicals
Increased vasoconstriction
Leads to increased PA pressures (pulmonary HTN), can lead to RV dilation and increased pulmonary afterload
Absent blood flow causes V-Q mismatch (dead space) and decrease surfactant production resulting in atelectasis contributing to hypoxemia
virchow’s triad puts patients more at risk

Question 56

pulmonary embolus clinical manifestations

Answer 56

Sudden onset of pleuritic chest pain (hurts with inspiration), dyspnea, tachypnea, tachycardia and unexplained anxiety
Occasional syncope or hemoptysis
Pleural friction rub, pleural effusion, fever and leukocytosis
hemoptysis

Question 57

pulmonary embolus nursing assessment

Answer 57

I-PAP
Vital signs with careful monitoring of HR and sp02 levels (moderate hypoxemia), fever, hypotension
Inspect: Perfusion, color, level of consciousness,
Auscultate: crackles
Increased oxygen requirements
Lab Values: CBC, d-dimer (classic test for PE), troponin, BNP level, ABG

Question 58

pulmonary embolus summary of assessment

Answer 58

Condition: Undissolved materials (e.g., thrombus, or air bubbles, fat globules) originating in legs or pelvis, detach and travel through venous system returning blood to right heart and lodge to occlude pulmonary vessels. More than 95% arise from deep vein thrombi in lower legs as a result of stasis of blood, vessel injury, or hypercoagulability. Pulmonary occlusion of the vascular bed results in ischemia of downstream lung tissue, increased pulmonary artery pressure, decreased cardiac output, and hypoxia. In rare cases, a saddle embolus in bifurcation of pulmonary arteries leads to sudden death from hypoxia. More often, small to medium pulmonary branches occlude, leading to dyspnea. These may resolve by fibrolytic activity.
Subjective data: Chest pain, worse on deep inspiration, dyspnea.
Inspection: Apprehensiveness, restlessness, anxiety, mental status changes, cyanosis, tachypnea, cough, hemoptysis, PaO2 < 80 on pulse oximetry. Arterial blood gases show respiratory alkalosis.
Palpation: Diaphoresis, hypotension.
Auscultation: Tachycardia, accentuated pulmonic component of S2 heart sound.
Adventitious sounds: Crackles, wheezes.

Question 59

respiratory dysfunction in pediatric patients

Answer 59

Upper Respiratory Tract Diseases

Lower Respiratory Tract Disease

Question 60

approach to acute respirology

Answer 60

upper respiratory tract = croup, epiglottitis
lower respiratory tract = bronchiolitis/respiratory syncytial virus (RSV), pneumonia, asthma
upper/lower respiratory tract = foreign body

Question 61

upper respiratory tract diseases

Answer 61

Diseases above the thoracic inlet.
Characterized by inspiratory stridor, hoarseness, and suprasternal retractions.
Differential diagnosis of stridor:
Croup
Epiglottitis
Foreign body aspiration

Question 62

croup

Answer 62

definition = paroxysmal attacks (spasm of the larynx)
epidemiology = 6months-4years, peak incidence: fall and early winter
etiology = influenza A and B, RSV, allergic component
clinical presentation = hoarse voice, barking cough, inspiratory stridor, most common onset at night, shortness of breath, anxiety
investigation = clinical diagnosis, chest xray (“steeple sign” from subglottic narrowing)
prognosis = excellent (but likely to recur)

Question 63

epiglottitis

Answer 63

definition = extremely acute, severe, and rapid progressive swelling (due to infection of epiglottis and surrounding tissue)
epidemiology = rare, 2-8years
etiology = bacterial (H. influenza type b)
clinical presentation = abrupt onset-rapid progression, medical emergency (severe airway obstruction), excessive drooling, stridor, anxiety, shortness of breath, difficulties swallowing (dysphagia), usually sitting in tripod position, cherry red/swollen epiglottis
investigation = clinical diagnosis, avoid examining the throat to prevent further respiratory exacerbation
prognosis = very good if detected and treated early, preventable via haemophilus influenzae type b vaccine

Question 64

tripod position

Answer 64

Trunk leaning forward, neck extended, and chin thrust forward

Question 65

lower respiratory tract diseases

Answer 65

Obstruction of airways below thoracic inlet, produces more expiratory sounds.
Classic symptom: wheezing
Common differential diagnosis of wheezing:
-Bronchiolitis: first episode of wheezing.
-Pneumonia: fever, cough, fatigue.
-Asthma: recurrent wheezing episodes, identifiable triggers.

Question 66

bronchiolitis/respiratory syncytial virus (RSV)

Answer 66

definition = acute viral infection of lower respiratory tract (small bronchioles) with resultant trapping of air
epidemiology = infants (2-12 months), peak incidence at 6 months, winter or early spring, occurs in children prone to airway reactivity, increase incidence of asthma in later life
etiology = respiratory syncytial virus (80% of cases)
clinical presentation = coughing, fever, feeding difficulties, irritability, wheezing, respiratory distress, tachypnea, tachycardia, retractions, poor air entry, acute/severe respiratory distress for the first 48-72 hours followed by rapid recovery
investigation = chest xray, nasopharyngeal swab, complete blood count
prognosis = excellent (less than 1% mortality rate)

Question 67

pneumonia

Answer 67

definition = inflammation of pulmonary tissue associated with consolidation of alveolar spaces
epidemiology = common in childhood but occurs more frequently in infancy and early childhood, incidence is greatest in the first year of life
etiology = viral agents are responsible for most pneumonias: RSV and influenza virus, bacterial causes: S. pneumonia, GBS, and S. aureus
clinical presentation = tachypnea, increased work of breathing (intercostal, suprasternal, subcostal, nasal flaring, use of accessory muscles), cyanosis, respiratory fatigue, auscultation: crackles, wheeze, decreased air entry over affected side
investigation = clinical diagnosis, chest xray
prognosis = good with rapid recovery when symptoms are recognized and treated early

Question 68

asthma

Answer 68

definition = lower airway disorder characterized by heightened airway reactivity with bronchospasm and obstruction
epidemiology = 75% of children with asthma have a positive family history for asthma, onset is usually before 5 years old and the disorder remains with the child throughout life, common in adults (7-10%) especially in children (10-15%)
etiology = unknown
clinical presentation = anxiety, cough, shortness of breath, crackles, tachycardia, cyanosis, use of accessory muscles, expiratory wheeze, tachypnea
classifications = mild asthma = occasional attacks of wheezing or coughing, symptoms respond quickly to inhaled bronchodilators, moderate asthma = more frequent episodes with symptoms persisting and chronic cough, decreased exercise tolerance, severe asthma = daily and nocturnal symptoms, frequent ER visits and hospitalization
investigation = clinical diagnosis, pulmonary functional studies
prognosis = progressive worsening over time is unusual

Question 69

asthma (reactive airway disease) summary of assessment

Answer 69

Condition: An allergic hypersensitivity to certain inhaled allergens (pollen), irritants (tobacco, ozone), microorganisms, stress, or exercise that produces a complex response characterized by bronchospasm, and inflammation, edema in walls of bronchioles, and secretion of highly viscous mucus into airways. These factors greatly increase airway resistance, especially during expiration, and produce the symptoms of wheezing, dyspnea, and sensation of tightness in the chest.
Inspection: During severe attack: increased respiratory rate, shortness of breath with audible wheeze, use of accessory neck muscles, cyanosis, apprehension, retraction of intercostals spaces. Expiration laboured, prolonged. When asthma is chronic, barrel chest may develop.
Palpation: Tactile fremitus decreased; tachycardia.
Percussion: Resonant. May be hyperresonant if asthma is chronic.
Auscultation: Diminished air movement. Breath sounds decreased, with prolonged expiration. Voice sounds decreased.
Adventitious sounds: Bilateral wheezing on expiration; sometimes inspiratory and expiratory wheezing.

Question 70

foreign body aspiration (upper or lower tract)

Answer 70

definition = child usually presents after a sudden episode of coughing or choking while eating with subsequent wheezing, coughing or stridor
epidemiology = usually occurs in children less than 5
clinical presentation = symptoms depend on the whether event was witnessed, size of object, elapsed time since event, location of object, degree and duration of airway blockage, signs and symptoms include: sudden onset of respiratory distress, abnormal respiratory sounds, coughing, gagging, agitation, cyanosis
investigation = clinical diagnosis, xray if opaque object swallowed, bronchoscopy if object in the larnx and trachea, direct laryngoscopy-visualize the object and remove with forceps
prognosis = potentially life-threatening, good if diagnosed soon after the event, there is usually little damage to the airway or the lungs

Question 71

summary of pediatric respiratory

Answer 71

Respiratory infections account for the majority of acute illness in children.
There are numerous differences in a pediatric airway versus an adult, some of these include large tongue, trachea is narrow, and epiglottis is large and floppy.
Upper respiratory tract infections include croup and epiglottitis.
Lower respiratory tract infections include bronchiolitis/RSV, pneumonia, and asthma.
Upper/lower respiratory tract infections include foreign body aspiration.