Disorder of ventilation and gas exchange CH 23 Flashcards Preview

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Flashcards in Disorder of ventilation and gas exchange CH 23 Deck (25):
1

Discuss the causes, diagnosis and treatments of dyspnea

-difficulty breathing
-causes is unknown, but four types of mechanisms to explain the sensation:
-Stimulation of lung receptors
-increased sensitivity to changes in ventilation perceived through the CNS mechanism
-reduced ventilatory capacity or breathing reserve
-stimulation of neural receptors in the muscle fibers of the intercostal and diaphragm and of receptors in the skeletal joins

DIAGNOSIS
-visual analog scale

TREATMENT
-depends on the cause
-o2 therapy
-pulmonary edema requires improvement in heart function
-decrease anxiety, breathing retraining and energy conservation

2

Define hypoxia

-deficiency in the amount of oxygen reaching the tissue

3

Define hypoxemia and causes and manifestation

-reducing of oxygen in the arterial blood

CAUSE
-inadequate oxygen in air
-disease of the respiratory system
-dysfunction of the neurological system
-alterations in circulatory function resulting in inadequate pulmonary capillary circulation
-PO2 <60 mmhg

MANIFESTATION
-increase HR
-peripheral vasoconstriction
-diaphoresis
-increase in BP
-impairment of mental performance
-metabolic acidosis

CHRONIC HYPOXEMIA
-increased ventilation
-vasoconstriction
-increase production of RBC
-cyanosis

4

Define hypercapnia and causes and manifestation

-increase in carbon dioxide in the blood
-caused by hypoventilation or mismatching of ventilation and perfusion

MANIFESTATION
-respiratory acidosis
-vasodilation
-nervous system dysfunction

5

State the characteristics of pleural pain and differentiate it from other types of chest pain

-since the visceral pleura does not contain pain receptors, the pain results from somatic pain fibers that innervate the parietal pleura

-musculoskeletal pain (sharp)
-bronchi pain (substernal and dull)
-Myocardial pain (aching, burning, stabbing)

6

Characterize the pathogenesis, manifestations and treatment options of pleural effusion

-an abnormal collection of fluid in the pleural cavity
PATHO
-rate of fluid formation exceeds the rate of its removal

Types of Fluid
Transudative - (hydrothorax) due to heart failure
Exudative - high specific gravity with inflammatory cells
purulent, chyle, sanguineous

Empyema - refers to an infection that results in exudate containign glucose, protein, leukocytes and debris (d/t infectious)

Chylothorax - refers to effusion of the lymph. Lymph fluid. D/T trauma, inflammation and malignancy

Hemothorax - presence of blood in the pleural cavity. Injury, surgery, aortic aneurism rupture

MANIFESTATION
-Vary with cause
Dyspnea, tachypnea
Decreased breath sounds
Percussion = dull/flat sounds
Hypoxemia (d/t less area for gas exchange)
If inflammation exists…
Pleuritic pain, fever, increased WBC

TREATMENT
-directed at the cause of the disorder
Thoracentesis
Injection of a sclerosing agent into the pleural cavity
Open surgical drainage
Treat cause


7

Cause and manifestation of spontaneous pneumothroax

-is the ruptured of the air-filled blister on lung surface
-atmospheric air inhaled enters pleural cavity; lung collapse

TWO TYPES
PRIMARY (healthy people)
-risk factor: tall people, smokers, talc inhalation
SECONDARY (underlying lung disease)
-emphysema (most common), asthma, TB, CF, sarcoidosis, CA

MANIFESTATION
-Ipsilateral chest pain
Tachypnea
Dyspnea
Asymmetry of chest
Hyper-resonant percussion
Decreased/absent breath sounds over area of pneumo

8

causes and manifestations of traumatic/open pneumothorax

-causes by a penetrating or non-penetrating fracture of ribs into the pleura
Causing a increase pressure and moving the affected side to the unaffected side

MANIFESTATION
-sucking chest wound

9

causes and manifestation of tension pneumothorax

-occurs when intrapleural cavity pressure exceeds atmospheric pressure
-results in a rapid increase in pressure within the chest that causes compression atelectasis of the unaffected lung
-the shift in the mediastinum to the opposite side causing compression of the vena cava in which decreases venous returns therefore decreases cardiac output

-common with trauma pneumothorax
-hypoxemia and hypotension
-shock


10

Discuss possible treatments for the various types of pneumothorax

ABGs, CXR, CT
Treatment varies with cause
May resolve if small spontaneous
Oxygen
Analgesic
Chest tube
Tension: Large-bore needle to affected side
Open: cover with airtight covering, then chest tube

11

Describe the causes and manifestations of atelectasis

-incomplete expansion of the alveoli
-caused by airway obstruction, pneumothorax or pleural effusion

MANIFESTATION
-tachypnea, tachycardia, dyspnea, cyanosis, hypoxemia, diminish chest expansion, absent in breath sound, intercostal retraction

TREATMENT
-deep breathing, coughing, position change

12

Describe the interaction between heredity, alterations in the immune response, and environmental agents in the pathogenesis of bronchial asthma

CAUSE
-Chronic inflammatory airway disorder characterized by airflow obstruction and hyperresponsiveness

Release cytokines in response to allergens or bacteria/virus
TH1
Respond to microbes
Cause B cells to differentiate into IgM & IgG
TH2
Respond to allergens
Stimulate B cells to differentiate into IgE (immunoglobin E = antibody)

Allergen elicit response of the early phase and late phase response
Allergen triggers mast cells to release cytokines in which causes bronchospasm in early phase, or infiltration of inflammatory cells in which causes airway inflammation in late phase








Risk factors include:
Genetics
Environmental
Presence of inflammatory cells
Damage to bronchial epithelium

13

Compare and contrast extrinsic (atopic) asthma and intrinsic (nonatopic) asthma

-extrinsic is an hypersensitivity reaction induced by exposure to allergies such as dust, pollin, mites, cockroach, animal dander
-often have other allergic disorder
-consist of early and late phase response

-intrinsic is triggered by respiratory tract infection, exercise, cold air, drugs, chemicals, hormones, polutants, emotions, and gerd

14

Characterize the early-phase and late-phase responses in the pathogenesis of bronchial asthma and relate them to the manifestations of this disorder

EARLY PHASE
-10 to 20 mins
-TH2 stimulates B cells to differentiate into IGE
-mast cells release chemical mediator such as interleukin, histamine, prostaglandins
-mucous production
-bronchospasm
-BRONCHODILATOR NEEDED

LATE PHASE
-4 to 8 hours after exposure
-inflammation
-increase airway responsiveness
-inflammatory mediators continues to be released, causing epithelial damage, edema, reduced clearance of secretion
-all these prolongs attack

15

Describe chronic bronchitis pathology and manifestation

-inflammation airway obstruction of the major and small airways. Chronic inflammation from smoking and recurrent infections
PATHOGENESIS
-hypersecretion of mucous and hypertrophy of submucosal glands in the trachea and bronchi

MANIFESTATION
-cyanosis, fluid retention due to right heart failure
-Hypercapnia/hypoxemia/polycythemia
-sob, rhonchi
-sputum

Blue bloaters (usually bronchitis)*
Cannot increase respiration enough to maintain oxygen levels
Cyanosis and polycythemia
Cor pulmonale (RVF)

16

Describe emphysema and its pathology and manifestation


Inflammatory response releases proteases that digest elastin
Destruction/thinning of alveolar walls, capillary beds
Loss of lung elasticity
Enlargement of distal airspaces

RISK FACTOR
Smoking history
Hereditary deficiency in type of antitrypsin

MANIFESTATION
Barrel chest (d/t air trapping)
Weight loss
Lack of cyanosis
Use of accessory muscles
Pursed-lip breathing (prevent the airway from collapsing during expiration)
Decreased breath sounds
Increase respiration to maintain oxygen levels
dyspnea


17

Describe appropriate diagnostic and treatment measure for COPD

-physical exam
-history
-pulmonary function test
-chest xray
-labs

Treatment (dependent on stage)
Smoking cessation
Breathing exercises
Avoidance of infections
Bronchodilators, corticosteroids
Oxygen therapy

18

Describe bronchiectasis and its manifestation

Permanent dilation of the bronchi and bronchioles d/t destruction of muscle and elastic tissue

Secondary to persisting infection or obstruction

MANIFESTATION
Coughing/copious amounts of foul-smelling, purulent sputum/hemoptysis
Weight loss and anemia are common

19

Discuss the genetic abnormality responsible for cystic fibrosis and state its effect on lung and pancreatic function

-caused by the genetic mutation of chromosome 7
-this chromosome encodes the Cystic fibrosis trans-membrane regulator (CFTR) mutation – inherited that has an accumulation of fluid in the lungs

LUNG
-dehydration of mucous layer, defective mucociliary function, accumulation of viscous secretion which can obstruct airways and lead to recurrent infections, salty sweat
-coughing, SOB

PANCREAS
-abnormal pancreatic secretion
-unable to digest fats and proteins
-ABD pain, steatorrhea (pale poo), diarrhea/constipation

20

Discuss typical diagnostic and treatment measure for cystic fibrosis

CF Diagnosis
Sweat test
CFTR genetic test
Blood levels trypsinogen (pancreatic enzyme)

CF Treatment
Antibiotics, PT, routine re-assessments
Diet control
Enzymes to dissolve thick mucous
Lung transplant

21

Describe the basic pathophysiology and manifestations with sarcoidosis

-multisystem disorder in which granulomas(collection of inflammatory cells) are found in many tissues and organ but mainly lungs

PATHOLOGY
-Fibrosis causes restrictive, stiff, non-compliant lung

MANIFESTATION
-Dyspnea
cough, chest pain, Tachypnea, shallow breaths
Decreased exercise tolerance
Skin, eyes, lungs

22

State the most common causes of pulmonary embolism and manifestations

Causes
- blood-borne substance (thrombus), air (from IV), or fat (mobilized from bone marrow after fracture or trauma), or amniotic fluid

MANIFESTATION

Respiratory
Dyspnea
Tachypnea
Pleuritic pain (severe on inspiration)
Cough/blood-tinged sputum
Hypoxemia

CVS
Tachycardia
angina

CNS
loss of consciousness
anxiety
fever

23

Discuss diagnostic and treatment measure for pulmonary embolism

Diagnostic
Arterial Blood Gases
D-dimer – fibrin degenerative product, small protein fragment, present in the blood after a blood clot is degraded by fibrinalysis
CT
Pulmonary angiography
ECG
Venous studies
R/O other causes

TREATMENT
Fibrinolytic therapy (emergency)
Streptokinase
Urokinase
Tissue plasminogen activator (TPA)

Anticoagulation
Heparin
Oral (long-term)

24

Compare primary and secondary pulmonary hypertension

PRIMARY
-inherited abnormal elevation pressure in the pulmonary system
-blood vessel wall thickens/constricts
-fibrosis and destruction

SECONDARY
-Elevation of pulmonary venous pressure
Mitral valve/LV disorders

Increased pulmonary blood flow
Left to right shunts

Pulmonary vascular obstruction
Emboli

Hypoxemia
Vasoconstriction of pulmonary arteries

25

Discuss the pathophysiology of cor pulmonale

-right sided heart failure from lung disease or pulmonary Decreased lung ventilation
-Pulmonary vasoconstriction
-Increased workload on right heart
-Decreased oxygenation
-Kidney releases erythropoietin = more RBCs made
-Polycythemia makes blood more viscous
-Increased workload on heart