Disorder of ventilation and gas exchange CH 23 Flashcards
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
Define hypoxia
-deficiency in the amount of oxygen reaching the tissue
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
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
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)
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
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
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
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
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
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
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
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
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
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)
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
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
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
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
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
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
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
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)
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
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
