Disorders of Respiratory Function Pt. 2 Flashcards by Eddie Peterson

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

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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

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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

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FLU SHOT IS BEST FOR PATIENTS WITH ASTHMA BECAUSE OF HIGH RISK OF PNEUMONIA

True

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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

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S/S of Late Asthmatic Response

Air trapping
Hyperinflation distal to obstructions
Increased work of breathing
Hypoxemia

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Clinical Manifestations of Asthma

Asymptomatic between attacks

Chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, tachypnea

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Pulsis Paradoxus

Drop in systolic BP in inspiratory phase

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Status asthmaticus

Bronchospasm not reversed by usual measures (treatment)

Life threatening

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Ominous signs of impending death in an Asthma patient

Silent Chest, and a PaCO2 greater than 70 mm Hg

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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

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Status asthmaticus

Prolonged asthma attack that does not respond to typical drug therapy
May last several minutes to hours
Medical emergency

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A child has asthma. Which pathophysiologic process occurs in this disease?

Chronic inflammatory disorder, causing mucosal edema and reversible airflow obstruction

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COPD

COPD describes a group of conditions characterized by obstruction to airflow in the lungs

Emphysema and Chronic Bronchitis

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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

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Chronic Bronchitis

inflammation of major and small airways and excessive mucous production in the large airways (The conducting airways)

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What’s one factor that differentiates COPD from Asthma?

Asthma is reversible, COPD is not

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Risk Factors for COPD

Exposure to particles
Tobacco smoke
Occupational dusts
Oxidative stress
Gender: Male (Bronchitis) Female (Emphysema)
Age
Nutrition

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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