Disorders of Respiratory Function Pt. 2 Flashcards
Mr. K’s Girlfriend Stabbed Him with a Knitting Needle …Now he is having breathing problems, and his breath sounds are diminished on the side with the wound
His trachea seems to be slanting toward the other side of his chest, and his heart sounds are displaced away from the wound
He has an increased respiration rate and blood pressure, is pale and sweating with bluish nail beds, and has no bowel sounds
What is going on?
Tension Pneumothorax
Asthma
Chronic inflammatory disorder of the bronchial mucosa.
Causes bronchial hyperresponsiveness, constriction of the airways and variable airflow obstruction that is reversible.
Big inflammatory response/Episodic attacks of bronchospasm, bronchial inflammation, mucosal edema, and increased mucous production
Early Asthmatic Response
Immunoglobulin E (IgE) causes the mast cells to degranulate, releasing a large number of inflammatory mediators.
Vasodilation
Increased capillary permeability
Mucosal edema
Bronchial smooth muscle contraction (bronchospasm)
Tenacious mucous secretion
FLU SHOT IS BEST FOR PATIENTS WITH ASTHMA BECAUSE OF HIGH RISK OF PNEUMONIA
True
Late asthmatic response
Begins 4 to 8 hours after the early response.
Chemotactic recruitment of lymphocytes, eosinophils, and neutrophils occurs.
Prolonged smooth muscle contraction
Airway scarring
Increased bronchial hyperresponsiveness
Impaired mucociliary function with accumulation of mucous and cellular debris, forming plugs in the airways
Remodels airways
S/S of Late Asthmatic Response
Air trapping
Hyperinflation distal to obstructions
Increased work of breathing
Hypoxemia
Clinical Manifestations of Asthma
Asymptomatic between attacks
Chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, tachypnea
Pulsis Paradoxus
Drop in systolic BP in inspiratory phase
Status asthmaticus
Bronchospasm not reversed by usual measures (treatment)
Life threatening
Ominous signs of impending death in an Asthma patient
Silent Chest, and a PaCO2 greater than 70 mm Hg
Asthma Treatment
Immediate administration of oxygen and inhaled beta-agonist bronchodilators
Oral corticosteroids administration early in the course of management
Careful monitoring of gas exchange and airway obstruction in response to therapy
Antibiotics are not indicated for acute asthma unless a bacterial infection is documented
Status asthmaticus
Prolonged asthma attack that does not respond to typical drug therapy
May last several minutes to hours
Medical emergency
A child has asthma. Which pathophysiologic process occurs in this disease?
Chronic inflammatory disorder, causing mucosal edema and reversible airflow obstruction
COPD
COPD describes a group of conditions characterized by obstruction to airflow in the lungs
Emphysema and Chronic Bronchitis
Emphysema
Loss of lung elasticity, permanent enlargement of the air spaces, destruction of the alveolar walls & capillary beds, with hyperinflation of the lungs (The respiratory tissues)
Inflammation and fibrosis of bronchial wall
Hypertrophied mucus glands excess mucus
Obstructed airflow
Loss of alveolar tissue and elastin lung fibers
Effective respiration is impaired, Air spaces enlarge
Chronic Bronchitis
inflammation of major and small airways and excessive mucous production in the large airways (The conducting airways)
What’s one factor that differentiates COPD from Asthma?
Asthma is reversible, COPD is not
Risk Factors for COPD
Exposure to particles Tobacco smoke Occupational dusts Oxidative stress Gender: Male (Bronchitis) Female (Emphysema) Age Nutrition
A genetic defect in alpha1-antitrypsin synthesis leads to alveolar damage
True. Neutrophils in alveoli secrete trypsin
can damage alveoli particularly elastic walls
Alpha1-antitrypsin inactivates the trypsin before it can damage the alveoli
Bleb (complication of Emphysema)
Intrapleural airspace separated from alveoli by a thin pleural covering
Caused by structural changes in lung tissue
Can rupture and lead to pneumothorax.
Bulla: (Large complication of Emphysema)
Subpleural airspace that results from the destruction of pulmonary tissue
Caused by structural changes in lung tissue
Can rupture and lead to pneumothorax.
Chronic Bronchitis
Chronic irritation of airways
Increased number of mucus cells
Mucus hypersecretion
Productive cough
The mucus glands of the tracheobronchial tree become thickened and encroach on the diameter of the airway lumen.
Increased mucus production in the peripheral airways.
Prolonging the inhalation of toxic inhalants
Blue Boater
Cannot increase respiration enough to maintain oxygen levels.
Hypoxemia, hypercapnia (excessive CO2) → Cyanosis, polycythemia (bone marrow increases RBC/hemoglobin)
Pulmonary HTN→ Rt. Heart failure → peripheral edema (“bloater”)
Pink Puffers
(emphysema)
Increase respiration to maintain oxygen levels
Dyspnea; increased ventilatory effort
Use accessory muscles; pursed-lip breathing (“puffers”)
Clinical Manifestations of Emphysema
Accessory muscle use Pursed-lip breathing Prolonged exhalation Barrel chest Weight loss
Clinical Manifestations of Chronic Bronchitis
Dyspnea ↓exercise tolerance Expiratory wheezes & crackles Hypoxemia, hypercapnia Cyanosis Polycythemia Peripheral edema
Dx of COPD
Spirometry, Bronchodilator reversibility testing
History and Physical
Treatment of COPD
Reduce airflow limitations Prevent secondary medical complications Reduce Respiratory symptoms Improve quality of life Pharmacology Avoiding risk factors Pulmonary rehabilitation Oxygen supplementation
You Are Caring for a COPD Client … He has chronically high PCO2
He is being given low-flow oxygen and complains all the time that he “needs more air,” so you turn up his oxygen. As a result, he is unconscious and not breathing. What happened?
Hypoxic drive was eliminated (the need to take in oxygen based on the CO2 levels). Balance must exist between PCO2 and PO2
Pulmonary Embolism
Obstruction of the pulmonary artery or one of its branches by a thrombus/clot
Originates somewhere in the venous system or in right side of heart
Due to a Blood clot: thrombis
Risk Factors for Pulmonary Embolism
Virchow’s Triad!! Venous Stasis (Prolonged immobilization
Varicose veins), Hypercoagulability (Inherited coagulation disorders, Smoking, Malignancies, Hormone Therapy), and Venous Endothelial Disease (foreign bodies/trauma)
Pulmonary Embolism Pathophysiology
Damaged endothelial wall
Thrombus completely or partially obstructs pulmonary artery or its branches
Alveolar dead space increased
Continues to be ventilated but receives little to no blood flow
Impaired gas exchange
Ventilation-perfusion imbalance
Pulmonary Embolism
Increased pulmonary resistance→ increased right heart workload→ right ventricular failure→ decreased cardiac output→ SHOCK!!
Clinical Manifestations of Pulmonary Embolism
Dyspnea is most frequent symptom Chest pain (Pleuritic in origin) Sudden onset May mimic MI (heart attack), angina, bronchopneumonia or heart failure Apprehension Cough Diaphoresis Hemoptysis Syncope: passing out
Size of thrombus contributes to symptoms
Pulmonary Hypertension (primary)
Blood vessel walls thicken and constrict
Pulmonary Hypertension (secondary)
Elevation of pulmonary venous pressure MS, LV heart failure. Increased pulmonary blood flow L→R shunts septal defects Pulmonary vascular obstruction (PE) Hypoxemia (Stimulus for pulmonary vasoconstriction)
Cor Pulmonale
Right-sided heart failure secondary to respiratory disease 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
Pulmonary Edema
Excess water in the lung from disturbances of capillary hydrostatic pressure, capillary oncotic pressure, or capillary permeability
Most common cause of pulmonary edema: Left-sided heart disease
Clinical manifestations of Pulmonary Edema
Dyspnea, orthopnea, hypoxemia, and increased work of breathing, cough with pink/frothy sputum
Pulmonary Edema Treatment
Increased hydrostatic pressure caused by heart failure
Improve cardiac output and volume status with diuretics, vasodilators, and drugs that improve the contraction of the heart muscle.
Increased capillary permeability resulting from injury
Remove offending agent and supportive therapy to maintain adequate oxygenation, ventilation, and circulation.
Oxygen/Mechanical Respiration
Ventilation/perfusion mismatching occurs in
COPD and Atelectasis
Impaired diffusion hypoxemia but not hypercapnia
occurs in
ARDS
Pulmonary edema
What causes respiratory failure?
Hypoventilation: hypercapnia, hypoxia
Hypoxemia
PO2 <60 mm Hg
Cyanosis
Activation of compensatory mechanisms (Sympathetic system activation)
Hypercapnia
PCO2 >50 mm Hg
Respiratory acidosis
Decreased muscle contraction, increased respiration
