infections and disorders of the pulmonary system

What is …

• ____Inflammation_____ of parenchymal structures in the lower respiratory tract (bronchioles & alveoli) 

• Infectious or non-infectious causes 

• Pathophysiology:

  • Defense mechanisms and anatomic structures assist in keeping the lower respiratory tract a sterile environment 

  • Organisms that make it past these barriers are eaten by macrophages in the alveoli 

  • Inflammatory process ensues (swelling(getting narrower), pain, warmth, increased capillary permeability —> fluid leaks into alveoli) 

  • Endotoxins are released by some microorganisms – damaging the mucus membranes of the bronchi & alveoli – resulting in inflammation and edema 

  • Exudate can then build up in the distal airways affecting Ventilation and Gas Exchange 

pneumonias

(lower respiratory tract infection)

Patho of pneumonia

• Defense mechanisms and anatomic structures assist in keeping the lower respiratory tract a sterile environment 

• Organisms that make it past these barriers are eaten by macrophages in the alveoli 

• Inflammatory process ensues (swelling(getting narrower), pain, warmth, increased capillary permeability —> fluid leaks into alveoli) 

• Endotoxins are released by some microorganisms – damaging the mucus membranes of the bronchi & alveoli – resulting in inflammation and edema 

• Exudate can then build up in the distal airways affecting Ventilation and Gas Exchange 

 

Classifications of pneumonia: Community vs Hospital-Acquired 

Community-Acquired Pneumonia

Hospital-Acquired Pneumonia

Infection that begins outside the hospital or is diagnosed within 48 hours after admission to the hospital in a person who has not resided in a long-term care facility for 14 days or more before admission.  Bacterial or viral  Most common organism: S. Pneumoniae  Other organisms:  H. influenzae, S. aureus, gram-negative bacilli  Mycoplasma pneumoniae, Legionella, Chlamydia species, viruses (atypical agents)

Lower respiratory tract infection not present or incubating on admission to the hospital; usually > 48 hours or more after admission  Mostly bacterial  P. aeruginosa, S. aureus, Enterobacter species, Klebsiella species, E. coli, Serratia  30-50% mortality  Multiple causative agents  Risk factors for HAP

What is being described

• Infection that begins outside the hospital or is diagnosed within 48 hours after admission to the hospital in a person who has not resided in a long-term care facility for 14 days or more before admission. 

• Bacterial or viral 

• Most common organism: S. Pneumoniae 

• Other organisms: 

• H. influenzae, S. aureus, gram-negative bacilli 

• Mycoplasma pneumoniae, Legionella, Chlamydia species, viruses (atypical agents) 

community-ccquired pneumonia

What is being desribed

• Lower respiratory tract infection not present or incubating on admission to the hospital; usually > 48 hours or more after admission 

• Mostly bacterial 

• P. aeruginosa, S. aureus, Enterobacter species, Klebsiella species, E. coli, Serratia 

• 30-50% mortality 

• Multiple causative agents 

• Risk factors for HAP 

Hospital-Acquired Pneumonia 

What is being descibed?

• S. Pneumonia is the most common cause of bacterial pneumonia 

• Organisms in the upper airways may travel to the lower airways by aspiration 

• Defense mechanisms prevent infection under normal conditions 

**Pneumonia vaccine ***

Acute Bacterial Pneumonia (Typical pneumonia) 

What are the manefestations of Acute Bacterial Pneumonia (Typical pneumonia) 

• Chills 

• Fever (Elderly???) 

• Elderly present with confusion

  

• Fine crackles 

  • Lung sound, sounds like popping noise  

• Malaise 

  • Feeling bad 

• Pleuritic chest pain 

  • In Pleural space, pain around the lungs  

• Productive cough(coughing stuff up)  with blood tinged / rusty colored / purulent sputum 

 

What is being described?

• Often referred to as “walking pneumonia”  

  • Not as severe, patient can walk around 

• Most common organism: Mycoplamsa pneumoniae 

• Usually mild 

Primary Atypical Pneumonia 

What are the manfestations of Primary Atypical Pneumonia 

• Dry hacking nonproductive cough  

• Fever 

• Headache 

• Muscle aches 

  • Because your coughing so much 

What is being desribed:

• Mycobacterium tuberculosis 

• One of the leading causes of death for people with HIV. (opportunistic infection) 

• People with increased risk for TB: people from foreign countries, living in congested populations(bunch of people living in close quarters), people with HIV, the elderly, and other immunocompromised individuals 

• Waxy outer capsule is difficult to destroy. May be referred to as acid-fast bacilli (retains red dye on waxy capsule) 

• May affect other organs besides the lungs 

• Transmitted via very tiny droplet nuclei (1 – 5 microns [1 inch = 42,540 microns]) that remain in the air for several hours 

• Latent vs Active TB 

  • Latent may develop to active TB if the immune system fails 

• TB skin test  

• BCG vaccine  

TUBERCULOSIS (TB) 

(lower respiratory tract infection)

How is TUBERCULOSIS (TB)  transmitted?

via very tiny droplet nuclei (1 – 5 microns [1 inch = 42,540 microns]) that remain in the air for several hours 

How may latent TB devlop to active TB

if the immune system fails 

What is the Pathogenesis of latent TB

• Droplet nuclei eludes defense mechanisms in upper respiratory tract and lodges in bronchiole or alveoli. 

• Inflammatory process begins. However, macrophages are unable to kill the bacilli by phagocytosis because of the waxy outer capsule protecting the bacteria. Because it cannot be killed, a cell mediated response is initiated that “contains” the organism. 

• A “tubercle” is formed. 

  • Tissue within the tubercle dies, and a cheese-like center forms

• Scar tissue develops around the tubercle. Lesions calcify and are able to be visualized on a chest x-ray. 

• Adequate immune system: Bacilli remain contained and the patient will not develop active TB. 

• If immune system fails: Bacilli will not be contained. Active TB may develop – extensive lung damage can occur. 

  • Bacteria break out and go to other parts of the lung, and starts to destroy the lungs 

What are the manefestations of Latent TB

none

What is the skin test restult of latent TB

positive

What is the ability of latent TB to spread to others, how does it grow, spread, and advance

• TB lives but doesn’t grow in the body 

• Doesn’t make a person feel sick or have symptomps  

• Cant spread from person to person 

• Can advance to TB disease

How does a chest x-ray look for latent TB

May or may not see anything

What are the manefestations of active TB

• Anorexia 

• Blood tinged sputum 

• Cough – dry or productive

 

• Fatigue 

• Fever 

• Night sweats 

• Weight loss 

What is the skin test restult of active TB

positive

What is the ability of active TB to spread to others

• TB is active and grows in the body 

• Makes a person feel sick and have symptoms  

• Can spread from person to person 

• Can cause death if not treated  

How does a chest x ray look for active TB

Cavitary lesions, opacities, infiltrates, or consolidations. 

What is being desribed

• Risk factors: Smoking, occupational/environmental hazards, genetics  

• Most are carcinomas that originate in lung tissue  

• Primary cancers from other tissues can metastasize to the lung 

4 types:

• Small-Cell Carcinoma (“Oat Cell”)

• Squamous Cell Carcinoma  25% - 40% 

• Adenocarcinoma 20% - 40%  

• Large-Cell Carcinoma  10%-15%

lung cancer

What kind of lung cancer is being desribed

charcteristics:

• Cells grow in clusters 

• Strong association with smoking 

• Highly malignant - Poor prognosis 

• Metastases usually evident at time of diagnosis 

• Brain metastases are common 

• Commonly associated with paraneoplastic syndromes (occur when cancer cells secrete hormones or other chemicals, this one secretes antidiuretic hormone)

Small-Cell Carcinoma (“Oat Cell”) 

What kind of lung cancer is being desribed

charcteristics:

• Found most commonly in men 

• Associated with smoking 

• Usually originates in central bronchi 

• Hypercalcemia 

Squamous Cell Carcinoma 

25% - 40% 

What kind of lung cancer is being desribed

charcteristics:

• Most common type in North America 

• Weaker association with smoking 

• Most common type for women and non-smokers 

• Originate in bronchiolar or alveolar tissue 

• Associated with areas of scarring in lungs 

Adenocarcinoma 

20% - 40%  

What kind of lung cancer is being desribed

charcteristics:

• Poor prognosis 

• Spreads very early 

• Invade subsegmental bronchi and larger airways 

Large-Cell Carcinoma  

10% - 15% 

Manifestations of lung cancer depend on location, metastasis, and stage. In general: 

• Anorexia 

  • Lack of appetite  

• Chronic cough 

  • Usually a dry cough 

• Hemoptysis  

  • Productive cough with blood in it  

• Pain  

• Shortness of breath 

• dyspnea 

• Wheezing 

  • Lung sound, sounds like a whistle  

• Metastasis is most common to brain, bone, and liver 

DISORDERS OF VENTILATION / PERFUSION RATIO AND GAS EXCHANGE 

 

DISORDERS OF THE PLEURA :

• pleural effusion

• hemothorax

• pneumothorax

• tension pneumothorax

• atelectasis

What is being described?

• Abnormal collection of fluid in the pleural cavity. Fluid may be: exudates, purulent drainage (empyema), chyle(lymphatic fluid), blood, or serous transudate (hydrothorax). May be unilateral or bilateral. 

• Causes: 

  • Heart failure  

  • Renal failure 

  • Liver failure 

  • Malignancy 

  • Infections 

PLEURAL EFFUSION 

causes of pleural effusion

• Heart failure  

• Renal failure 

• Liver failure 

• Malignancy 

• Infections

What is the patho of PLEURAL EFFUSION 

• Increased capillary permeability  

• Decreased colloidal osmotic pressure  

• Albumin contributes to colloidal osmotic pressure, so low albumin  

• Increased negative intrapleural pressure  

• Impaired lymph drainage 

 

Manefestations of pleural effusion

• Dyspnea  

• Decreased lung expansion 

• Diminished breath/lung sounds  

• Hypoxemia  

• Pleuritic pain (Large effusion- constant pain) 

  • Pain in pleural space, we have nerve endings here  

• Fever, increased WBC, and other signs of inflammation (with empyema) 

What is being described:

• specific type of pleural effusion: Blood in the pleural cavity 

• Causes: 

  • Chest injury 

  • Complication of surgery 

  • Malignancies 

  • Vessel rupture 

• Variations in severity based on size: 

  • Minimal: < 250 mL  

  • Moderate: 500 mL – 1000 mL (~ 1/3 of pleural space) 

  • Large: > 1000 mL (1/2 or more of one side of the chest)  

hemothorax

causes of hemothorax

• Chest injury 

• Complication of surgery 

• Malignancies 

• Vessel rupture 

What are manefestaitons of a hemothorax

Dyspnea, Hypoxemia, & Hypovolemia —> SHOCK

What is being described:

• Condition in which air enters the pleural space, causing a partial or complete collapse of the affected lung. Pneumothorax is usually expressed in percentages (5%-95%). 

• Types: 

  • Spontaneous Pneumothorax (no injury): Rupture of air-filled bleb or blister on the surface of the lung.  

    • Primary pneumothorax

    • Secondary pneumothorax:

  • Traumatic Pneumothorax (injury)

PNEUMOTHORAX  

What is spontaneous pneumothorax (no injury)

• Rupture of air-filled bleb or blister on the surface of the lung.  

  • Primary pneumothorax: Healthy individuals. Seen most often in tall boys and young men (10-30 years old). Smoking and family history may play a role. 

  • Secondary pneumothorax: Underlying lung disease. Common cause- emphysema (Other conditions- asthma, TB, cystic fibrosis, lung cancer). 

Spontaneous Pneumothorax (no injury):

What is primary pneumothorax

• Healthy individuals.

• Seen most often in tall boys and young mean (10-30 years old).

• Smoking and family history may play a role. 

Spontaneous Pneumothorax (no injury):

What is secondary pneumothorax

• Underlying lung disease.

• Common cause-

  • emphysema (Other conditions- asthma, TB, cystic fibrosis, lung cancer).

What is Traumatic Pneumothorax (injury):

• Penetrating or non-penetrating chest injury 

  • Gun shots, stabbing, medical procedures, rib fractures  

  • Hemothorax commonly occurs with traumatic pneumothorax 

Manefestations of PNEUMOTHORAX   (depend on severity)

• Asymmetrical chest expansion  

  • Only one side expanding  

• Chest pain  

• Decreased or absent breath sounds over site 

• Dyspnea 

• Hypoxemia 

• Tachycardia 

• Tachypnea 

 

What is being described:

• Air enters pleural space but cannot escape  

• Pressure increases with each breath. 

• As pressure increases, the affected lung collapses. The heart and great vessels are compressed. Mediastinal structures shift to the opposite side of the chest. The trachea is pushed from the normal, midline position. The unaffected lung becomes compressed. 

• Patient is breathing in and air is leaking out into pleural space  

• Ventilation is severely impaired: Life-threatening, medical emergency!!! 

• More common with traumatic pneumothorax 

TENSION PNEUMOTHORAX 

Manefestations of TENSION PNEUMOTHORAX 

• Hypotension  

  • Because CO is being decreased  

• Distended neck veins  

  • Jugular veins drain into superior vena cava, so when blood backs up it goes into these neck veins  

• Subcutaneous emphysema 

  • Air that’s gotten into subcutaneous tissue  

• Tracheal deviation toward unaffected side 

  • As pressure increases it pushes trachea away to unaffected side 

• May lead to shock 

 

What is being described

• Incomplete expansion of a lung/portion of a lung 

• Results in partial or complete lung collapse 

• Decreased surface area for gas exchange 

• Causes: 

  • Airway obstruction 

  • Lung compression 

  • Absence or loss of pulmonary surfactant (newborns) 

  • Increased risk after surgery secondary to pain, pain medications, and immobility 

ATELECTASIS 

causes of atelectisis

• Airway obstruction 

• Lung compression 

• Absence or loss of pulmonary surfactant (newborns) 

• Increased risk after surgery secondary to pain, pain medications, and immobility 

Manfestations of ATELECTASIS 

• Cyanosis 

• Decreased/absent breath sounds over the affected area

• Dyspnea 

• Fever, s/s infection 

• Hypoxemia 

• Tachycardia 

• Tachypnea 

Obstructive airway disorders:

• asthma

• Chronic obstructive pulmonary disease (COPD)

• Cystic fibrosis

• chronic intersistial lung diseases

What is being described:

• Chronic disorder of the airways that causes episodes of airway obstruction, bronchial hyperresponsiveness, airway inflammation, and airway remodeling (in some cases). 

• Affects individuals of every age; many cases develop in childhood 

 

• Risk factors for development: 

  • Genetic predisposition* for the development of an IgE response to common allergens 

  • Allergies 

  • Antenatal exposure to tobacco smoke and pollution 

asthma

• Risk factors for development asthma

• 
  

  • Genetic predisposition* for the development of an IgE response to common allergens 

  • Allergies 

  • Antenatal exposure to tobacco smoke and pollution 

What is the patho of asthma

• Exposure to stimulus (allergen) triggers the onset of an “asthma attack” 

• Inflammatory response ensues, extreme response  

• Inflammatory mediators are released- stimulating the PNS, resulting in bronchoconstriction 

• Mucosal edema and mucous production 

• Airway narrows 

  • =Wheezing  

• Air becomes trapped distal to the edematous airway- resulting in distended alveoli 

• Blood flow to distended alveoli is reduced (decreased gas exchange) 

Manefestations of asthma

• Anxiety 

• Chest tightness 

• Cough  

  • Cough may be chronic  

• SOB 

• Tachycardia 

• Tachypnea 

• Accessory muscle use 

  • Ex: intercostal muscles, neck muscles: Someone whose struggling to breathe we can see these muscles retract  

• Wheezing 

 

What is being described:

• Progressive worsening of lung tissue  

• Group of chronic airway diseases characterized by chronic and recurrent obstruction of airflow in the pulmonary airways 

• Leading cause of morbidity and mortality worldwide 

• Most common cause: smoking

• Less common cause: Hereditary deficiency in a1 antitrypsin 

  • Enzyme that protects lungs during inflammation, 

    • Without it inflammation continues until lungs are damaged  

• Periodic exacerbations of dyspnea and increased sputum production; lung tissue progressively worsens after each exacerbation 

• Two types: Emphysema & Chronic Bronchitis (may have both) 

 

CHRONIC OBSTRUCTIVE PULMONARY DISEASE 

Most common cause of COPD

smoking

least common cause of COPD

• Hereditary deficiency in a1 antitrypsin 

  • Enzyme that protects lungs during inflammation, 

    • Without it inflammation continues until lungs are damaged  

TWO types of COPD:

Emphysema	Chronic Bronchitis
Known as the “pink puffers” because:  1) no cyanosis 2) accessory muscle use   Associated with smoking or inherited alpha1- antitrypsin    Pathophysiology:  Recurrent inflammation results in the release of enzymes causing irreversible enlargement of the distal air spaces   Loss of lung elasticity: lungs stretched and don’t get back smaller   Abnormal enlargement of distal airspaces distal (results in hyperinflation of lungs)  Destruction of alveolar walls and capillary beds  Elastic recoil is lost  Air trapping results à Volume of air passively expired is reduced  Hyperventilation and decreased cardiac output  Lung is oxygenated, but limited blood flow prevents oxygenation of body tissues  Proportionate decrease in ventilation & perfusion	“Blue bloaters”          Pathophysiology:  Chronic inflammatory process with excessive bronchial mucous secretion  Airflow is obstructed
Manifestations of Emphysema:  Barrel chest – there is an increased anterior-posterior diameter of the chest (related to hyperinflation), rounded chest  Diminished lung sounds due to air trapping  Dyspnea – begins as exertional(ex:walking), but worsen as the disease progresses  Relatively normal ABG’s (until late stages)  Muscle wasting   Sitting upright/leaning forward  Prolonged expiration (when they breathe out they breathe out longer than someone w/o this because air is trapped)  Pursed lip breathing   Accessory muscle use	Manifestations of Chronic Bronchitis:  Increased sputum production , more prone to infection  Coarse lung sounds – fluid/secretions.     Cyanosis (blue)  Respiratory acidosis (Compensated?)  Hypercapnia and Hypoxemia  Frequent respiratory infections  Polycythemia  May develop pulmonary HTN and/or right-sided HF  Accessory muscle use

Pick the description that best fits EMPHYSEMA (COPD)

Known as the “pink puffers” because:  1) no cyanosis 2) accessory muscle use   Associated with smoking or inherited alpha1- antitrypsin    Pathophysiology:  Recurrent inflammation results in the release of enzymes causing irreversible enlargement of the distal air spaces   Loss of lung elasticity: lungs stretched and don’t get back smaller   Abnormal enlargement of distal airspaces distal (results in hyperinflation of lungs)  Destruction of alveolar walls and capillary beds  Elastic recoil is lost  Air trapping results à Volume of air passively expired is reduced  Hyperventilation and decreased cardiac output  Lung is oxygenated, but limited blood flow prevents oxygenation of body tissues  Proportionate decrease in ventilation & perfusion

Manifestations of Emphysema:  Barrel chest – there is an increased anterior-posterior diameter of the chest (related to hyperinflation), rounded chest  Diminished lung sounds due to air trapping  Dyspnea – begins as exertional(ex:walking), but worsen as the disease progresses  Relatively normal ABG’s (until late stages)  Muscle wasting   Sitting upright/leaning forward  Prolonged expiration (when they breathe out they breathe out longer than someone w/o this because air is trapped)  Pursed lip breathing   Accessory muscle use

What kind of COPD is best know as the pink puffers because:

1: no cyanosis 2) accessory muscle use  

emphysema

What is the patho of emphysema

• Recurrent inflammation results in the release of enzymes causing irreversible enlargement of the distal air spaces  

• Loss of lung elasticity: lungs stretched and don’t get back smaller  

• Abnormal enlargement of distal airspaces distal (results in hyperinflation of lungs) 

• Destruction of alveolar walls and capillary beds 

• Elastic recoil is lost 

• Air trapping results → Volume of air passively expired is reduced 

• Hyperventilation and decreased cardiac output 

• Lung is oxygenated, but limited blood flow prevents oxygenation of body tissues 

• Proportionate decrease in ventilation & perfusion 

What are the Manifestations of Emphysema: 

• Barrel chest – there is an increased anterior-posterior diameter of the chest (related to hyperinflation), rounded chest

 

• Diminished lung sounds due to air trapping 

• Dyspnea – begins as exertional(ex:walking), but worsen as the disease progresses 

• Relatively normal ABG’s (until late stages)

 

• Muscle wasting  

• Sitting upright/leaning forward 

• Prolonged expiration (when they breathe out they breathe out longer than someone w/o this because air is trapped) 

• Pursed lip breathing  

• Accessory muscle use 

What kind of COPD is known as “blue bloaters”

chronic bronchitis

What desciption best fits chronic bronchitis (type of COPD)

“Blue bloaters”          Pathophysiology:  Chronic inflammatory process with excessive bronchial mucous secretion  Airflow is obstructed

Manifestations of Chronic Bronchitis:  Increased sputum production , more prone to infection  Coarse lung sounds – fluid/secretions.     Cyanosis (blue)  Respiratory acidosis (Compensated?)  Hypercapnia and Hypoxemia  Frequent respiratory infections  Polycythemia  May develop pulmonary HTN and/or right-sided HF  Accessory muscle use

What is the patho of chronic bronchitis

• Chronic inflammatory process with excessive bronchial mucous secretion 

• Airflow is obstructed 

What are the Manifestations of Chronic Bronchitis: 

• Increased sputum production , more prone to infection 

• Coarse lung sounds – fluid/secretions.    

• Cyanosis (blue) 

• Respiratory acidosis (Compensated?) 

• Hypercapnia and Hypoxemia 

• Frequent respiratory infections 

• Polycythemia 

• May develop pulmonary HTN and/or right-sided HF 

• Accessory muscle use 

What is being described:

• Genetic disorder: Autosomal Recessive 

• Affects respiratory, gastrointestinal, and reproductive systems 

• More common in Caucasians  

• Excessive, thick mucous that obstructs the lungs and pancreas 

Pathophysiology: 

• Genetic mutation increases absorption of sodium and water(makes sectretion thick) from the airways into the blood, causing the mucociliary blanket of the respiratory epithelium to become more viscid 

• Result is the accumulation of thick respiratory secretions that predispose the individual to recurrent pulmonary infections 

cystic fibrosis

Patho of cystic fibrosis

• Genetic mutation increases absorption of sodium and water(makes sectretion thick) from the airways into the blood, causing the mucociliary blanket of the respiratory epithelium to become more viscid 

• Result is the accumulation of thick respiratory secretions that predispose the individual to recurrent pulmonary infections 

Manefestations of cystic fibrosis

• Thick secretions → mucous plugs 

• Frequent lung infections 

• Structural changes in bronchial wall 

• Malnutrition 

• High levels of NaCl in sweat  

• Abnormal pancreatic function 

• SALTY:

  • SKINNY

  • AUTOSOMAL RECESSIVE

  • LUNG INFECTIONS

  • THICK MUCOUS

  • YOUNG AGE

What is being described

• Group of diseases resulting from inflammatory conditions that cause the lung tissue to become stiff and difficult to expand (decreased compliance) 

• Affects collagen and elastic connective tissues in the interstitium of alveolar walls 

 

• Multiple causes: 

  • Injury —> Inflammation —> Scarring(makes diffusion difficult) 

  
  

  • Occupational 

    • “Coal miner’s lung” 

    • Asbestosis 

    • Gases/fumes 

  
  

  • Drugs / Medications 

    • Cancer drugs and others 

  
  

  • Immunologic 

    • Sarcoidosis (inflammation, increased collagen & connective tissue) 

    • Collagen vascular disease (example: Lupus) 

CHRONIC INTERSTITIAL LUNG DISEASES 

causes of CHRONIC INTERSTITIAL LUNG DISEASES 

• Injury —> Inflammation —> Scarring(makes diffusion difficult) 

• Occupational 

  • “Coal miner’s lung” 

  • Asbestosis 

  • Gases/fumes 

• Drugs / Medications 

  • Cancer drugs and others 

• Immunologic 

  • Sarcoidosis (inflammation, increased collagen & connective tissue) 

  • Collagen vascular disease (example: Lupus) 

Manefestations of CHRONIC INTERSTITIAL LUNG DISEASES 

• Increased work of breathing 

• Exercise intolerance 

• Small, frequent breaths 

• Hypoxemia 

What disorders of pulmonary circulation is this

• Occlusion of pulmonary vessel with an embolus(traveling clot) 

• Embolism may be a blood clot, air, fat, amniotic fluid, fat from bone marrow 

• Common cause: Deep vein thrombosis**  

• Risk factors: 

  • Virchow’s Triad  

    • Stasis of blood flow 

    • Endothelial injury 

    • hypercoagulability 

  • Immobility 

  • Post-surgical 

  • Pregnancy 

  • Oral contraceptives/hormone replacement 

• May result in loss of alveolar surfactant (alveolar collapse) 

• May result in pulmonary hypertension → right-sided heart failure 

• Ventilation-Perfusion mismatching 

pulmonary embolism

What is a common cause of Pulmonary embolism

deep vein thrombosis

Massive pulmonary embolism :

Occlusion of major artery —> Infarction of large portion of lung tissue 

Smaller pulmonary embolsim:

embolism lodged in a more distal site → May not cause infarction of lung tissue 

risk facotrs of pulmonary embolism

• Virchow’s Triad  

  • Stasis of blood flow 

  • Endothelial injury 

  • hypercoagulability 

• Immobility 

• Post-surgical 

• Pregnancy 

• Oral contraceptives/hormone replacement 

Manefestations of a pulmonary embolism

• Chest pain* 

• Dyspnea* 

• Tachypnea* 

• Anxiety 

• Cough (may be blood tinged) 

• Hypoxemia 

• Tachycardia 

What is being described:

• Result of another problem 

• Gas exchange failure / Ventilation failure 

• Failure to oxygenate the blood and/or eliminate CO2  

• Acute Lung Injury  

• Acute Respiratory Distress Syndrome 

 

respiratory failure

Manefestations of respiratory failure

• Change in level of consciousness 

• Cyanosis 

• Hypoxemia 

• Hypercapnia 

• Tachycardia 

• Tachypnea