Case study 4

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Alterations in Pulmonary Function

Objectives

Describe signs and symptoms with pulmonary disease

Define hypoxia and hypercapnia

Identify types of pulmonary disease and injuries

Identify types of restrictive, obstructive, and infective lung diseases

Relate the etiology and pathophysiology to the clinical manifestations of pulmonary disease

List treatments for pulmonary diseases

Lecture Outline

Clinical Manifestations of Pulmonary Alterations

Signs & Symptoms

Conditions caused by Pulmonary Disease/Injury

Pleural Abnormality

Pulmonary Disorders:

Restrictive Lung Disease

Obstructive Lung Disease

Respiratory Tract Infections

Lecture Outline (with examples)

Clinical Manifestations of Pulmonary Alterations

Signs & Symptoms

dyspnea, cough, abn. sputum, hemoptysis, abn. breathing patterns, hypo/hyper ventilation, cyanosis, clubbing, pain

Conditions caused by Pulmonary Disease/Injury

hypercapnia, hypoxemia, ventilation-perfusion

Pleural Abnormalities

Pneumothorax

Signs and Symptoms:

Dyspnea

Definition: shortness of breath

Etiology

Damage to lung tissue, disturbance in ventilation, stimulation of receptors, increased work of breathing

Signs / Symptoms

Shortness of breath, “breathlessness”, nostril flaring, use of accessory muscles

Types

Dyspnea on exertion (DOE)

Orthopnea – shortness of breath when laying down

Paroxysmal nocturnal dyspnea (PND) – waking up at night gasping for air

Signs and Symptoms:

Abnormal Breathing Patterns

Definition: change in rate, depth, regularity, effort of breathing

Etiology: Physiologic or pathologic

Types

Kussmaul - slightly increased ventilatory rate (rapid), very large tidal volume (deep), and no expiratory pause: exercise, Metabolic acidosis

Labored – increased work of breathing

Restricted - disorders that stiffen the lungs or chest wall and decrease compliance

Cheyne-Stokes - alternating periods of deep and shallow breathing; apnea lasting 15 to 60 seconds, followed by ventilations that increase in volume until a peak is reached, after which ventilation decreases again to apnea: neurologic conditions

Signs and Symptoms:

Hypoventilation

Definition: Inadequate alveolar ventilation in relation to metabolic demands

Etiology: alteration in drive to breathe (neurologic) or ability to respond to that drive (pulmonary)

airway obstruction, chest wall restriction, or altered neurologic control of breathing

Retain CO2 = acidosis

Hyperventilation

Definition: Alveolar ventilation exceeding metabolic demands

Etiology: anxiety, acute head injury

Blow off CO2 = alkalosis

Signs and Symptoms:

Cough

Acute or chronic

Abnormal sputum

Change in the amount, color, consistency

Hemoptysis

Coughing up blood or bloody secretions

Pain

May originate in the pleurae, airways, or chest wall

Cyanosis

Bluish discoloration due to desaturation or reduced hemoglobin

Clubbing

Chronic hypoxemia

Conditions Caused by Pulmonary Disease or Injury

Hypercapnia

↑ CO2 in the arterial blood (PaCO2)

Etiology: Hypoventilation of alveoli

Respiratory acidosis

Decreased drive to breathe

Inadequate ability to respond to ventilatory stimulation

Increased dead space

Air trapping

Hypocapnia

CO2 in the arterial blood (PaCO2)

Etiology: Hyperventilation of alveoli

Respiratory alkalosis

Questions to think about:

What are examples of Hyper- or Hypocapnia?

What is the result of Hyper- or Hypocapnia?

Questions to think about:

What are the causes of each?

What is the result of Hypercapnia Hypocapnia?

↑ CO2 in the arterial blood (PaCO2)

Causes: Occurs from decreased drive to breathe or an inadequate ability to respond to ventilatory stimulation

Hypercapnia, or increased CO2 concentration in the arterial blood (increased Paco2), is caused by hypoventilation of the alveoli. Remember that CO2 is easily diffused from the blood into the alveolar space; thus minute volume (respiratory rate × tidal volume) determines not only alveolar ventilation, but also Paco2.

Hypoventilation is often overlooked because breathing pattern and ventilatory rate may appear normal; it is important to obtain blood gas analysis to determine the severity of hypercapnia and resultant respiratory acidosis.

There are many causes of hypercapnia. Most are a result of a decreased drive to breathe or an inadequate ability to respond to ventilatory stimulation. Causes include: (1) depression of the respiratory center by drugs; (2) diseases of the medulla, including infections of the central nervous system or trauma; (3) abnormalities of the spinal conducting pathways, as in spinal cord disruption or poliomyelitis; (4) diseases of the neuromuscular junction or of the respiratory muscles themselves, as in myasthenia gravis or muscular dystrophy; (5) thoracic cage abnormalities, as in chest injury or congenital deformity; (6) large airway obstruction, as in tumors or sleep apnea; and (7) increased work of breathing or physiologic dead space, as in emphysema.

Hypercapnia and the associated respiratory acidosis can result in several important clinical manifestations. Of greatest concern are electrolyte abnormalities that occur in response to the low pH that may cause dysrhythmias. Individuals also may have somnolence and even be in a coma because of changes in intracranial pressure associated with high levels of arterial carbon dioxide, which causes cerebral vasodilation. Alveolar hypoventilation with increased alveolar carbon dioxide limits the amount of alveolar oxygen available for diffusion into the blood, leading to secondary hypoxemia.

Conditions Caused by Pulmonary Disease or Injury

Hypoxemia

Reduced oxygenation of arterial blood (Reduced PaO2)

Caused by respiratory alterations

Can lead to tissue hypoxia

Hypoxia

Reduced oxygenation of cells in tissues

Caused by respiratory alterations and/or alterations of other systems – i.e low cardiac output, cyanide poisoning

Questions to think about:

What are examples of Hyper- or Hypocapnia?

What is the result of Hyper- or Hypocapnia?

Hypoxemia, or reduced oxygenation of arterial blood (reduced Pao2), is caused by respiratory alterations, whereas hypoxia, or reduced oxygenation of cells in tissues, may be caused by alterations of other systems as well. Although hypoxemia can lead to tissue hypoxia, tissue hypoxia can result from other abnormalities, such as low cardiac output or cyanide poisoning.

Hypoxemia results from problems with one or more of the major mechanisms of oxygenation:1.Oxygen delivery to the alveolia.Oxygen content of the inspired air (Fio2)

2.Ventilation of the alveoli

3.Diffusion of oxygen from the alveoli into the blood:

A) Balance between alveolar ventilation and perfusion ( mismatch); B) Diffusion of oxygen across the alveolocapillary membrane

4.Perfusion of pulmonary capillaries

The amount of oxygen in the alveoli is called the Pao2 and is dependent on two factors. The first factor is the presence of adequate oxygen content of the inspired air. The amount of oxygen in inspired air is expressed as the percentage or fraction of air that is composed of oxygen, called the Fio2. The Fio2 of air at sea level is approximately 21% or 0.21. Anything that decreases the Fio2(such as high altitude) decreases the Pao2. The second factor is the amount of alveolar minute ventilation (tidal volume × respiratory rate). Hypoventilation results in an increase in Paco2 and a decrease in Pao2 such that there is less oxygen available in the alveoli for diffusion into the blood. This type of hypoxemia can be completely corrected if alveolar ventilation is improved by increases in the rate and depth of breathing. Hypoventilation causes hypoxemia in unconscious persons; in people with neurologic, muscular, or bone diseases that restrict chest expansion; and in individuals who have COPD.

Diffusion of oxygen from the alveoli into the blood is also dependent on two factors. The first is the balance between the amount of air getting into alveoli () and the amount of blood perfusing the capillaries around the alveoli (). An abnormal ventilation-perfusion ratio () is the most common cause of hypoxemia (Figure 35-2).

What is shunting? Normally, alveolocapillary lung units receive almost equal amounts of ventilation and perfusion. The normal is 0.8 to 0.9 because perfusion is somewhat greater than ventilation in the lung bases and because some blood is normally shunted to the bronchial circulation. Mismatch refers to an abnormal distribution of ventilation and perfusion. Hypoxemia can be caused by inadequate ventilation of well-perfused areas of the lung (low ). Mismatching of this type, called shunting, occurs in atelectasis, in asthma as a result of bronchoconstriction, and in pulmonary edema and pneumonia when alveoli are filled with fluid. When blood passes through portions of the pulmonary capillary bed that receive no ventilation, right-to-left shunt occurs, resulting in decreased systemic Pao2 and hypoxemia. Hypoxemia also can be caused by poor perfusion of well-ventilated portions of the lung (high ), resulting in wasted ventilation. The most common cause of high is a pulmonary embolus that impairs blood flow to a segment of the lung. An area where alveoli are ventilated but not perfused is termed alveolar dead space.

The second factor affecting diffusion of oxygen from the alveoli into the blood is the alveolocapillary barrier. Diffusion of oxygen through the alveolocapillary membrane is impaired if the alveolocapillary membrane is thickened or the surface area available for diffusion is decreased. Abnormal thickness, as occurs with edema (tissue swelling) and fibrosis (formation of fibrous lesions), increases the time required for diffusion across the alveolocapillary membrane. If diffusion is slowed enough, the oxygen in the alveolar gas (Pao2) and capillary blood does not have time to equilibrate during the fraction of a second that blood remains in the capillary. Destruction of alveoli, such as that which occurs in emphysema, decreases the surface area available for diffusion. Hypercapnia is rarely produced by impaired diffusion, because carbon dioxide diffuses so easily from capillary to alveolus that the individual with impaired diffusion would die from hypoxemia before hypercapnia could occur.

Hypoxemia most often is associated with a compensatory hyperventilation and resultant respiratory alkalosis (i.e., decreased Paco2 and increased pH). However, in individuals with associated ventilatory difficulties, hypoxemia may be complicated by hypercapnia and respiratory acidosis. Hypoxemia results in widespread tissue dysfunction and, when severe, can lead to organ infarction. In addition, hypoxic pulmonary vasoconstriction can contribute to increased pressures in the pulmonary artery (pulmonary artery hypertension) and lead to right-sided heart failure and cor pulmonale (see p. 1276). Clinical manifestations of acute hypoxemia may include cyanosis, confusion, tachycardia, edema, and decreased renal output.

Conditions Caused by Pulmonary Disease or Injury

Ventilation – Perfusion (VQ)

What lung diseases cause a VQ mismatch?

Asthma

Pulmonary edema

Emphysema

Pulmonary

Bronchiectasis

Cystic fibrosis

Interstitial lung diseases

Pulmonary hypertension

Conditions Caused by Pulmonary Disease or Injury

Ventilation-perfusion (VQ)

Normal VQ: oxygen fills the alveolus and oxygenates blood

Low VQ: impaired ventilation impedes oxygen causing hypoxemia (blood not oxygenated adequately)

Shunt (very low) VQ: blocked ventilation causes collapsed alveoli (so no oxygen is getting to blood) causing severe hypoxemia

High VQ: the obstruction is in the venous system (from the pulmonary artery) where there is oxygen, but it can’t be absorbed causing hypoxemia (think pulmonary emboli)

A low ventilation and perfusion ratio will result in shunting.

Pleural Abnormality

Pneumothorax

Definition: Air or gas in the pleural space

Types:

Open pneumothorax (damaged chest wall)

Tension pneumothorax (air trapped in pleural space, pressure goes from negative to +)

Spontaneous pneumothorax (just happens)

Secondary pneumothorax (happens because of something- central line insertion, chest surgery)

Bleb

Pleural Abnormality

Pneumothorax

Clinical Manifestations:

Acute pleural pain

Tachypnea, dyspnea

Absent or decreased breath sounds

Hyperresonance to percussion on affected side

Diagnostics:

CXR, US, MRI

Treatment:

Chest tube and fixing underlying problem

Lecture Outline (with examples)

2. Pulmonary Disorders:

Restrictive Lung Disease

aspiration, atelectasis, bronchiectasis, pulmonary edema, pulmonary fibrosis, inhalation disorders, ARDS

Obstructive Lung Disease

asthma, COPD-chronic bronchitis/emphysema

Respiratory Tract Infections

pneumonia

Pulmonary Disorders: Restrictive Lung Disease

Characterized by decreased lung tissue compliance and increased effort to expand lungs on inspiration

Clinical Manifestations

Dyspnea

Increased respiratory rate

Tachypnea

Assessment Findings

SPIROMETRY FINDINGS: Decreased Tidal Volume; Decreased FEV1, Decreased Forced Vital Capacity (FVC)

Hypoxemia

V/Q mismatch = decreased diffusion capacity of O2 from alveoli to blood

Crackles

People suffering from restrictive lung disease have a hard time fully expanding their lungs when they inhale. That is, it’s more difficult to fill lungs with air. This is a result of the lungs being restricted from fully expanding. This can occur when tissue in the chest wall becomes stiffened, or due to weakened muscles or damaged nerves. Any of these factors can restrict the expansion of the lungs. Some of the conditions classified as restrictive lung disease include:

Interstitial lung disease ; Sarcoidosis; Neuromuscular disease, such as amyotrophic lateral sclerosis (ALS); Pulmonary fibrosis; Asbestosis; and Silicosis

In restrictive lung disease, the total volume of the lungs is reduced; this is seen in pulmonary fibrosis, when scarring in the lung tissue causes ‘stiffening’ of the lungs, typically resulting in progressive and marked breathlessness on exertion. The breathing tests show a reduction in both the FEV1 and FVC (‘small’ lungs) but the FEV1/FVC ratio is normal (above 70%) as there is no narrowing in the airways. Restrictive lung volumes are also seen where the chest wall is unable to expand normally – e.g. obesity, kyphoscoliosis or conditions that result in weak respiratory muscles, such as myasthenia gravis or muscular dystrophy.

Restrictive Lung Diseases

Aspiration

Atelectasis

Bronchiectasis

Bronchiolitis

Pulmonary fibrosis

Inhalational disorders

Pneumoconiosis

Allergic alveolitis

Pulmonary edema

Acute respiratory distress syndrome (ARDS)

Some of the most common restrictive lung diseases in adults are aspiration, atelectasis, bronchiectasis, bronchiolitis, pulmonary fibrosis, inhalational disorders, pneumoconiosis, allergic alveolitis, pulmonary edema, and acute respiratory distress syndrome. Restrictive lung volumes are also seen where the chest wall is unable to expand normally – e.g. obesity, kyphoscoliosis or conditions that result in weak respiratory muscles, such as myasthenia gravis or muscular dystrophy.

Restrictive Lung Disease:

Aspiration

Etiology

Passage of fluid and solid particles into the lungs Compression atelectasis

Clinical manifestations

Dyspnea, cough, fever, and leukocytosis

Infection – aspiration pneumonia

Treatment Prevention

Eat slowly and chew food

Eat sitting upright at least at 45 degrees

Restrictive Lung Disease:

Atelectasis

Collapse of lung tissue

Compression atelectasis

External compression on the lung

Absorption atelectasis

Gradual absorption of air from obstructed or hypoventilated alveoli

Surfactant impairment

Decreased production or inactivation of surfactant

Clinical manifestations

Dyspnea, cough, fever, and leukocytosis

Treatment Prevention

Deep breathing

FIGURE 35-5 Pores of Kohn.

A, Absorption atelectasis caused by lack of collateral ventilation through pores of Kohn. Whereas in

B, Restoration of collateral ventilation during deep breathing.

Absorption atelectasis & normal

Atelectasis is the collapse of lung tissue. There are three types of atelectasis: compression, absorption, and surfactant impairment:

1.Compression atelectasis is caused by the external pressure exerted on lung tissue, such as occurs with tumors, or by fluid or air in the pleural space. Atelectasis at the base of the lungs can be caused by abdominal distention pressing on a portion of the lung, causing the alveoli to collapse.

2.Absorption atelectasis results from gradual absorption of air from obstructed or hypoventilated alveoli or from inhalation of concentrated oxygen or anesthetic agents.

3.Surfactant impairment results from decreased production or inactivation of surfactant, which is necessary to reduce surface tension in the alveoli and thus prevent lung collapse during expiration. Surfactant impairment can occur because of premature birth, acute respiratory distress syndrome, anesthesia, or mechanical ventilation.

When does atelectasis occur?

Atelectasis tends to occur after surgery and with use of general anesthesia.

In addition, individuals are often in pain, breathe shallowly, are reluctant to change position, and produce viscous secretions that tend to pool in dependent portions of the lung after surgical procedures, especially those involving the thorax or upper abdomen.

Clinical manifestations of atelectasis are similar to those of pulmonary infection: dyspnea, cough, fever, and leukocytosis. Prevention and treatment of postoperative atelectasis usually include deep breathing exercises (often with the aid of an incentive spirometer), frequent position changes, and early ambulation. Deep breathing is beneficial because it (1) promotes the ciliary clearance of secretions, (2) stabilizes the alveoli by redistributing surfactant, and (3) permits collateral ventilation of the alveoli through pores of Kohn in the alveolar septa. The pores of Kohn, which open only during deep breathing, allow air to pass from well-ventilated alveoli to obstructed alveoli, minimizing their tendency to collapse and facilitating expectoration of the bronchial obstruction (Figure 35-5).

Restrictive Lung Disease:

Bronchiolitis

Diffuse inflammation of small airways or bronchioles

Most common in children

Occurs in adults with chronic bronchitis or those with a viral infection or who have inhaled toxic gases

Clinical manifestations

Rapid ventilatory rate; significant use of accessory muscles; low-grade fever; dry, nonproductive cough; and hyperinflated chest, hypoxemia

Treatment

Antibiotics, steroids, and chest physical therapy, humidified air, deep breathing, coughing, postural drainage)

With diffuse inflammation comes PAIN…..

Bronchiolitis is usually diffuse. The resulting decrease in the ventilation-perfusion ratio results in hypoxemia. A decrease in minute ventilation with resulting carbon dioxide retention also may occur as lung restriction worsens.

Restrictive Lung Disease:

Bronchiolitis Obliterans

Late-stage fibrotic disease of the airways

Can occur with all causes of bronchiolitis

Complication: Bronchiolitis obliterans Organizing Pneumonia (BOOP)

Restrictive Lung Disease:

Pulmonary Edema

Excess water in the lung from disturbances of capillary hydrostatic pressure, capillary oncotic pressure, or capillary permeability

Etiology: Left-sided heart failure (most common)

Postobstructive pulmonary edema (POPE): Negative pressure pulmonary edema

Rare life-threatening complication that can occur after relief of upper airway obstruction

Pulmonary edema is excess water in the lung. The normal lung is kept dry by lymphatic drainage and a balance among capillary hydrostatic pressure, capillary oncotic pressure, and capillary permeability. In addition, surfactant lining the alveoli repels water, keeping fluid from entering the alveoli. Predisposing factors for pulmonary edema include heart disease, ARDS, and inhalation of toxic gases.

The most common cause of pulmonary edema is left-sided heart disease. When the left ventricle fails, filling pressures on the left side of the heart increase and an increase in pulmonary capillary hydrostatic pressure. When the hydrostatic pressure exceeds oncotic pressure, fluid moves into the interstitium. Fluid moves to the lymphatic vessels and is then removed from the lung. When the flow of fluid out of the capillaries exceeds the lymphatic system’s ability to remove it, pulmonary edema develops.

If the capillary oncotic pressure is decreased for any reason (e.g., anemia or decreased levels of plasma proteins), pulmonary edema also develops but at a lower hydrostatic pressure.

Another cause of pulmonary edema is capillary injury that increases capillary permeability. Capillary injury causes edema in cases of adult respiratory distress syndrome (ARDS) or inhalation of toxic gases, such as ammonia. Capillary injury causes water and plasma proteins to leak out of the capillary and move into the interstitium.

Pulmonary edema also can result from obstruction of the lymphatic system. Drainage can be blocked by compression of lymphatic vessels caused by edema, tumors, and fibrotic tissue or by increased systemic venous pressure that elevates the hydrostatic pressure of the large pulmonary veins into which the pulmonary lymphatic system drains. This can happen in left-sided heart failure.

Pulmonary Edema Pathophysiology

If the capillary oncotic pressure is decreased for any reason (e.g., anemia or decreased levels of plasma proteins), pulmonary edema also develops but at a lower hydrostatic pressure.

Pulmonary Edema: Clinical Manifestations

Clinical manifestations

Dyspnea

Orthopnea

Hypoxemia

Increased work of breathing

Rales

Dullness

S3 Gallop

Hypoventilation / Hypercapnia

Clinical manifestations

Dyspnea

Orthopnea

Hypoxemia

Increased work of breathing

Examination Findings

Rales

Dullness

S3 Gallop

Hypoventilation / Hypercapnia

Pulmonary Edema Treatment

Treatment

↑ hydrostatic pressure caused by heart failure

Improve cardiac output & volume status with diuretics, vasodilators, and drugs that improve the contraction of the heart muscle

↑ capillary permeability resulting from injury

Remove offending agent and supportive therapy to maintain adequate oxygenation, ventilation, and circulation.

POPE

Provide PEEP ventilation

Any type of pulmonary edema

Provide supplemental oxygen and/or mechanical ventilation

Diuretics

Restrictive Lung Disease:

Pulmonary Fibrosis

Excessive amount of fibrous or connective tissue in the lung

SPIROMETRY: Decreased Functional Residual Capacity (FRC)

Inhalation Disorders

Exposure to toxic gasses

Pneumoconiosis

Silica

Asbestos

Coal

Allergic Alveolitis

Extrinsic allergic alveolitis (hypersensitivity pneumonitis)

Restrictive Lung Disease:

Acute respiratory distress syndrome (ARDS)

Fulminant form of respiratory failure characterized by acute lung inflammation and diffuse alveolocapillary injury

Injury to the pulmonary capillary endothelium

Inflammation and platelet activation

Surfactant inactivation

Atelectasis

Acute Respiratory Distress Syndrome (ARDS)

Clinical Manifestations

Hyperventilation - Rapid shallow breathing pattern

Crackles auscultated in lungs on inspiration

Respiratory alkalosis

Dyspnea and Hypoxemia

Metabolic acidosis

Hypoventilation

Respiratory acidosis

Further hypoxemia

Hypotension, decreased cardiac output, death

Evaluation and treatment

Physical examination, blood gases, and radiologic examination

Supportive therapy with oxygenation and ventilation and prevention of infection

Treat underlying cause

Acute Respiratory Distress Syndrome (ARDS)

Postoperative Respiratory Complications

Atelectasis

Pneumonia

Pulmonary edema

Pulmonary emboli

Prevention Frequent turning, deep breathing, early ambulation, air humidification, and incentive spirometry

Treatment

Prevention, oxygenate, antibiotics (pneumonia) anticoagulation (pulmonary emboli)

Obstructive Lung Diseases

What are the characteristics of Obstructive lung disease?

All obstructive lung diseases

Narrowing of pulmonary airways

Air trapping

Common Obstructive Lung Diseases:

Asthma

Chronic Obstructive Pulmonary Disease (COPD)

Emphysema

Chronic Bronchitis

the characteristics of Obstructive lung diseases include narrowing of pulmonary airways which hinders a person’s ability to completely expel air from the lungs. The practical result is that by the end of every breath, quite a bit of air remains in the lungs. Some common conditions related to obstructive lung disease include:

Asthma; Chronic Obstructive Pulmonary Disease (COPD); Emphesema and Chronic Bronchitis; Bronchiectasis; Cystic Fibrosis

Part of the process of assessing patients who present with breathlessness, cough or other respiratory symptoms involves undertaking breathing tests to determine how well the lungs are functioning.

At its most basic, this involves measuring the amount of air that can be forcefully exhaled from a full breath through a device called a spirometer.

These measurements are compared to values that would be expected for someone of similar height, age and gender to achieve (called predicted values) and, together with clinical history and examination, help to judge whether symptoms are the result of an obstructive or restrictive process.

The volume exhaled in the first second (Forced Expiratory Volume – FEV1) is expressed as a percentage of the total volume exhaled (Forced Vital Capacity – FVC) or FEV1/FVC ratio and is normally above 70%.

Obstructive lung disease

In obstructive lung disease, the airways are narrowed, making it difficult to exhale quickly giving a reduced FEV1/FVC ratio. This may be temporary, such as in acute asthma, when the airways can rapidly constrict in response to a trigger (e.g. pollen, house dust mite or pet dander in someone with sensitivity to those inhalants) and with treatment with inhaled bronchodilators and inhaled corticosteroids may go back to normal.

In chronic obstructive disease such as emphysema, long standing damage to the airways causes permanent and irreversible narrowing which does not respond very well to inhaled therapy, resulting in long term symptoms of breathlessness, which progress over time.

The lungs become enlarged, or hyperinflated, increasing the work of breathing.

Obstructive Lung Disease

Inspiration

Increased difficulty with activity or exertion

Expiration

Airway obstruction is worse with expiration

More force/more time is required to expire a given volume of air

Longer / Emptying the lungs is slowed

Rate of breathing increases

Lungs work harder

Fresh air circulated into the lungs, and spent air circulated out, decreases

Unifying signs and symptoms

Wheezing and dyspnea

Clinical manifestations

Increased work of breathing, ventilation-perfusion mismatching, decreased forced expiratory volume in one second (FEV1).

Obstructive pulmonary disease is characterized by airway obstruction that is worse with expiration. More force (i.e., use of accessory muscles of expiration) or more time is required to expire a given volume of air and emptying of the lungs is slowed.

The unifying symptom of obstructive pulmonary disease is dyspnea; the unifying sign is wheezing. Individuals have an increased work of breathing, ventilation-perfusion mismatching, and a decreased forced expiratory volume in one second (FEV1).

Obstructive Lung Disease:

Asthma

Chronic inflammatory disorder of the bronchial mucosa

Causes bronchial hyperresponsiveness, constriction of the airways and variable airflow obstruction that is reversible

Increased mucus secretion, bronchoconstriction, and airway edema is caused by airway obstruction which contributes to increased airflow resistance and hypoventilation

Can lead to obstruction and status asthmaticus

Asthma is chronic inflammatory disorder of the bronchial mucosa

Causes bronchial hyperresponsiveness, constriction of the airways and variable airflow obstruction that is reversible.

Many cells and cellular elements contribute to the persistent inflammation of the bronchial mucosa and hyperresponsiveness of the airways, including macrophages (dendritic cells), T helper 2 (Th2) lymphocytes, B lymphocytes, mast cells, neutrophils, eosinophils, and basophils.

Asthma Pathophysiology

Think about ALL of the cell communication and cell signalling going on here!

Asthma: Early Response

Antigen exposure  bronchial mucosa  activates dendritic cells  present the antigen to CD4+ T cells.

Interleukin 4 (IL-4) stimulates B-cell activation and the production of antigen-specific IgE ------ WHY is this important?

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

There is both an immediate (early asthmatic response) and a late (delayed) response.

Airway epithelial exposure to antigen initiates both an innate and an adaptive immune response in sensitized individuals.

In the early asthmatic response…. antigen exposure to the bronchial mucosa activates a cascade of events….. dendritic cells (antigen-presenting cells) to present the antigen to CD4+ T cells, which differentiate into Th2 cells. These Th2 cells release numerous cytokines including IL-4, IL-5, IL-8, IL-13, IL-17, and IL-22. IL-4 stimulates B-cell activation, proliferation, and production of antigen-specific IgE.

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

Asthma: Early Response

IL-5 stimulates the activation of eosinophils, which contributes to increased bronchial hyperresponsiveness, fibroblast proliferation, epithelial injury, and airway scarring

IL-8 activates neutrophils that cause a more exaggerated inflammatory response

IL-13 impairs mucociliary clearance, enhances fibroblast secretion, and contributes to bronchoconstriction

IL-17 increases neutrophilic inflammation

IL-22 stimulates airway epithelial cells, causing further innate and adaptive immune responses

IL-5 stimulates the activation, migration, and proliferation of eosinophils, which cause direct tissue injury and release of toxic neuropeptides that contribute to increased bronchial hyperresponsiveness, fibroblast proliferation, epithelial injury, and airway scarring.

IL-8 activates neutrophils that contribute to a more exaggerated inflammatory response. IL-13 impairs mucociliary clearance, enhances fibroblast secretion, and contributes to bronchoconstriction and airway remodeling. IL-17 increases neutrophilic inflammation and IL-22 stimulates airway epithelial cells, which play an important role in stimulating further innate and adaptive immune responses.

Ultimately there is activation of surface mediators…. A portion of preformed IgE binds to receptors on the surface of mast cells. Once bound to antigen, the IgE causes the mast cells to degranulate, releasing a large number of inflammatory mediators. Together these mediators do a number of things. They cause vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction (bronchospasm), and tenacious mucus secretion from mucosal goblet cells with narrowing of the airways and obstruction to airflow.

Asthma: Late Response

Occurs 4-8 hours after early response

Chemotactic recruitment of lymphocytes, eosinophils, and neutrophils

Prolonged smooth muscle contraction

Airway scarring

Increased bronchial hyperresponsiveness

Impaired mucociliary function with accumulation of mucous and cellular debris, forming plugs in the airways

Leads to airway remodeling if left untreated

The late asthmatic response begins 4 to 8 hours after the early response. Chemotactic recruitment of lymphocytes, eosinophils, and neutrophils during the acute response causes a latent release of inflammatory mediators, again inciting bronchospasm, edema, and mucus secretion with obstruction to airflow. Synthesis of leukotrienes contributes to prolonged smooth muscle contraction. Eosinophil mediators cause direct tissue injury with fibroblast proliferation and airway scarring.

Release of toxic neuropeptides contribute to increased bronchial hyperresponsiveness. Damage to ciliated epithelial cells contributes to impaired mucociliary function with accumulation of mucus and cellular debris forming plugs in the airways (increased synthesis of nitric oxide contributes to oxidative injury and chronic inflammation).74 A decrease in the number or function of T regulatory (Treg) cells are associated with asthma.69 Untreated inflammation can lead to long-term airway damage that is irreversible, known as airway remodeling (subepithelial fibrosis, smooth muscle and mucous gland hypertrophy).75

Asthma: Late Response

Air Trapping

Hyperinflation

Increased work of breathing

Hypoxemia

CO2 retention

Respiratory Alkalosis       Respiratory Acidosis = EMERGENCY

Airway obstruction increases resistance to airflow and decreases flow rates, especially expiratory flow.

Impaired expiration causes air trapping, hyperinflation distal to obstructions and increased work of breathing. Changes in resistance to airflow are not uniform throughout the lungs and the distribution of inspired air is uneven, with more air flowing to the less resistant portions. Continued air trapping increases intrapleural and alveolar gas pressures and causes decreased perfusion of the alveoli. Increased alveolar gas pressure, decreased ventilation, and decreased perfusion lead to variable and uneven ventilation-perfusion relationships within different lung segments.

Hyperventilation is triggered by lung receptors responding to increased lung volume and obstruction. The result is early hypoxemia without CO2 retention. Hypoxemia further increases hyperventilation through stimulation of the respiratory center, causing Paco2 to decrease and pH to increase (respiratory alkalosis).

With progressive obstruction of expiratory airflow, air trapping becomes more severe and the lungs and thorax become hyperexpanded, putting the respiratory muscles at a mechanical disadvantage. This leads to a fall in tidal volume with increasing CO2retention and respiratory acidosis. Respiratory acidosis signals respiratory failure, especially when left ventricular filling and, thus, cardiac output become compromised because of severe hyperinflation.

Asthma: Clinical Manifestations

What physical assessment signs is the RN looking for with Asthma?

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

Pulsus paradoxus

Status asthmaticus

Bronchospasm not reversed by usual measures

Life threatening

Ominous signs of impending death

Silent chest (no audible air movement) and a Paco2 greater than 70 mm Hg

Persons with asthma are asymptomatic between attacks and pulmonary function tests are normal. No clinical symptoms are present during partial remission, but pulmonary function tests are abnormal.

At the beginning of an attack, the individual experiences chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, and tachypnea. Severe attacks involve the use of accessory muscles of respiration, and wheezing is heard during both inspiration and expiration. Asymptomatic between attacks

A pulsus paradoxus (decrease in systolic blood pressure during inspiration of more than 10 mmHg) may be noted. Peak flow measurements should be obtained. Because the severity of blood gas alterations is difficult to evaluate by clinical signs alone, arterial blood gas tensions should be measured if oxygen saturation falls below 90%. Usual findings are hypoxemia with an associated respiratory acidosis, NOT alkalosis as your book indicates! . In the late asthma response, symptoms can be even more severe than the initial attack.

If bronchospasm is not reversed by usual measures, the individual is considered to have severe bronchospasm or status asthmaticus. If status asthmaticus continues, hypoxemia worsens, expiratory flows decrease further, and effective ventilation decreases. Acidosis develops as arterial Paco2 begins to rise. Asthma becomes life threatening at this point if treatment does not reverse this process quickly. A silent chest (no audible air movement) and a Paco2 greater than 70 mmHg are ominous signs of impending death.

Chronic Obstructive Pulmonary Disease: COPD

Chronic Obstructive Pulmonary Disease

Defined:

Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.

Airflow limitation that is not fully reversible

Usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases

Chronic obstructive pulmonary disease (COPD) is defined as a “preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible.

As you can see COPD is a leading cause of death both in the US and worldwide. Overall mortality from COPD has increased in the United States over the past 30 years; however, mortality in women has increased more than twice that much.

Chronic Obstructive Pulmonary Disease

COPD is currently the fourth leading cause of death in the world.1

COPD is projected to be the 3rd leading cause of death by 2020.2

More than 3 million people died of COPD in 2012 accounting for 6% of all deaths globally.

Globally, the COPD burden is projected to increase in coming decades because of continued exposure to COPD risk factors and aging of the population.

1. Lozano R, Naghavi M, Foreman K, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet 2012; 380(9859): 2095-128.

2. Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med 2006; 3(11): e442.

The most common respiratory symptoms include dyspnea, cough and/or sputum production. These symptoms may be under-reported by patients.

The main risk factor for COPD is tobacco smoking but other environmental exposures such as biomass fuel exposure and air pollution may contribute.

Besides exposures, host factors predispose individuals to develop COPD. These include genetic abnormalities, abnormal lung development and accelerated aging.

COPD may be punctuated by periods of acute worsening of respiratory symptoms, called exacerbations.

In most patients, COPD is associated with significant concomitant chronic diseases, which increase its morbidity and mortality.

Direct costs of COPD are $32 billion in US

Indirect costs $20.4 billion in US

COPD Pathophysiology

Expiration becomes difficult because loss of elastic recoil reduces the volume of air that can be expired passively and air is trapped in the lungs. Air trapping causes hyperexpansion of the chest, which puts the muscles of respiration at a mechanical disadvantage. This results in increased work of breathing, so that many individuals will develop hypoventilation and hypercapnia late in the course of the disease

COPD: Overview

Emphysema and Chronic bronchitis

COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease

Clinical Manifestations

Patient c/o increased mucus, dyspnea, cough, sometimes wheezing

Diagnostics:

Spirometry is required to make the diagnosis; the presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation.

Evaluate ABG/BMP  Respiratory acidosis  Metabolic alkalosis

Treatment:

Dependent on stage of disease

Education

Diagnosis

COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease.

Clinical Manifestations: Patient c/o increased mucus, dyspnea, sometimes wheezing,

Diagnostics: Spirometry is required to make the diagnosis; the presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation.

Evaluate ABG/BMP  patient has retention of CO2 which is respiratory acidosis, but if the kidneys are doing their job they will retain bicarb to compensate by having a metabolic alkalosis and because the renals are retaining bicarb it must secrete another negatively charged ion. The ion that is secreted is chloride. Now when chloride is excreted by the rule of neutrality it needs to pull a positively charged ion so it excretes potassium in the form of potassium chloride causing hyponatremia, hypochloremia, and elevated bicarb. Again this is the kidneys way of creating a metabolic alkalosis trying to compensate for the respiratory acidosis.

Treatment: Use the guidelines

The goals of COPD assessment are to determine the level of airflow limitation, the impact of disease on the patient’s health status, and the risk of future events (such as exacerbations, hospital admissions, or death), in order to guide therapy.

COPD: Chronic Bronchitis

Chronic bronchitis

Hypersecretion of mucus and chronic productive cough that lasts for at least 3 months of the year and for at least 2 consecutive years

Inspired irritants increase mucus production and the size and number of mucous glands

The mucus is thicker than normal

Bronchodilators, expectorants, and chest physical therapy used to treat

COPD: Emphysema

Emphysema

Abnormal permanent enlargement of the gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis

Loss of elastic recoil

Centriacinar emphysema (damage to bronchioloes)

Panacinar emphysema (damage to alveoli)

Obstructive Pulmonary Disease: Emphysema

COPD: Alpha 1 Antitrypsin Deficiency

Alpha 1 Antitrypsin Deficiency

What is it?

Genetic deficiency

Proteinase and elastase deficiency

Starts as an adolescent

Screening: All patients with a diagnosis of COPD should be screened

There is a form of emphysema that is genetic and is proteinase and elastase deficiency. It usually develops later in the teenager years and is pure emphysema. It can be misdiagnosed as asthma because it is started in adolescence.

The World Health Organization recommends that all patients with a diagnosis of COPD should be screened once especially in areas with high AATD prevalence.

AATD patients are typically < 45 years with panlobular basal emphysema

Delay in diagnosis in older AATD patients presents as more typical distribution of emphysema (centrilobular apical).

A low concentration (< 20% normal) is highly suggestive of homozygous deficiency.

COPD Assessment Scales

COPD Assessment Test (CAT TM )

Chronic Respiratory Questionnaire (CCQ® )

St George’s Respiratory Questionnaire (SGRQ)

Chronic Respiratory Questionnaire (CRQ)

Modified Medical Research Council (mMRC) questionnaire

COPD: Management and Treatment

Treatment depends on severity

Bronchodilators

Inhaled or oral steroids

Antibiotics for exacerbation

Vaccinations for influenza and pneumonia

Oxygen therapy

Breathing training – Pursed lip

Lung transplant

Education and self-management

Physical activity

Pulmonary rehabilitation programs

Exercise training

End of life and palliative care

Nutritional support

Avoiding Infections

Although it is important to take preventive measures to avoid lung infections, you do not need to isolate yourself from other people. There is no guaranteed way to prevent infections, however, if you are proactive with your vaccines (link to adult vaccines) and take the time to wash your hands, and are aware of your surroundings, then you will increase your chances of living an infection-free life. Learn about avoiding infections.

Medications

Your health care provider may prescribe medications to control the symptoms of COPD, like bronchodilators for COPD, combination bronchodilators and anti-inflammatories, and antibiotics. Learn about COPD medicines, tips for managing all your medications and techniques to inhale medications.

Oxygen Therapy

Some people with COPD may benefit from oxygen therapy. Oxygen therapy is used to ensure there is enough oxygen in the blood to provide for the body's needs. Learn about oxygen therapy.

Pulmonary Rehabilitation

Because of the many aspects involved in the care and management of life with COPD, you may choose to participate in a pulmonary rehabilitation program, which involves tailored treatment for your needs. Learn about pulmonary rehabilitation.

Lung Volume Reduction Surgery (LVRS)

Lung volume reduction surgery is considered for adults with certain patterns of severe emphysema. Specific tests are done to determine if lung volume reduction surgery is recommended. These tests include breathing tests, a chest CT scan, arterial blood gas (ABG), lung perfusion study and exercise test. Learn more about LVRS.

Oxygen

COPD: Chest X-Ray

X-Rays of COPD will reveal long lungs with a flattened diaphragm

ASTHMA VS. COPD

SIMILARITIES

DIFFERENCES

Asthma is a leading chronic childhood disease affecting about 10 percent of the U.S. population, chronic obstructive pulmonary disease (COPD) is a leading chronic adult disease, is currently the third leading cause of death and second leading cause of disability. Some people have both asthma and COPD. Studies show a direct correlation between severity of asthma as a child and the incidence of COPD. Meaning that children who suffer from severe, persistent asthma are nearly 32 times more likely to develop COPD in adulthood, where children with mild asthma were not at an increased risk. Many people with long-standing asthma develop airway remodeling that causes a chronic irreversible airflow obstruction, or COPD. Many people who develop COPD will need to continue to treat the inflammation caused by their asthma as well as add treatments to manage the symptoms of COPD and retain as much lung function as possible. Here are some examples about similarities and difference between the two diseases:

References

Eckert, D., Jordan, A., Merchia, P., & Malhotra, A. (2007). Central sleep apnea: Pathophysiology and treatment. Chest, 131, 595-607.

Levitzky, M. (2008). Using the pathology of obstructive sleep apnea to teach cardiopulmonary integration. Adv Physiol Educ 32, 196-202.

Malhotra, A. & Owens, R. (2010). What is central sleep apnea. Respir Care, 55, 1168-1178.

Mbata, G. & Chukwuka, J. (2012). Obstructive sleep apnea hypopnea syndrome. Ann Med Health Sci Res, 2, 74-77.

Miller, J. & Berger, A. (2016). Screening and assessment for obstructive sleep apnea in primary care. Sleep Medicine Reviews, 29, 41-51.

Susheel, P., Schneider, H., Scwartz, A., & Smith, P. (2007). Adult obstructive sleep apnea. Chest, 132. doi:10.1378/chest.07-0040.

http://emedicine.medscape.com/article/295807-overview

Respiratory Tract Infections:

Pneumonia

Responsible for more disease and death than any other infection

Inflammation of the parenchymal structures of the lung, such as the alveoli and bronchioles

Infection of the lower respiratory tract

https://en.wikipedia.org/wiki/Pneumonia

Pneumonia

Classification:

Typical

Bacteria

Lobar pneumonia – consolidation in part or all of one lobe

Bronchopneumonia – patchy consolidation in > 1 lobe

Atypical

Viral

Mycoplasma

Typical pneumonias are a result from infection by bacteria that multiply extracellularly in the alveoli and cause inflammation and exudation of fluid into the air-filled alveolar spaces.

Atypical pneumonias are caused by viral and mycoplasma infections that invade the alveolar septum and the interstitium of the lung. They produce less striking symptoms and physical findings than bacterial pneumonia. There is a lack of alveolar infiltration and purulent sputum, leukocytosis, and lobar consolidation on the radiograph

Pneumonia

Classification:

Community-acquired pneumonia (CAP)

Bacterial caused by Streptococcus pneumonia, H. influenza, S. aureus or Atypical

Viral

Health care–associated pneumonia (HCAP)

Staphylococcus aureus (MRSA)

Haemophilis influenza

Hospital-acquired pneumonia (HAP) ** nosocomial

Haemophilis influenza

Ventilator-associated pneumonia (VAP)

Pseudomonas aeruginosa / E.Coli / Klebsiella pneumonia / Acinetobacter / Staphylococcus aureus

Infection of the lower respiratory track

Community-acquired pneumonia (CAP)

Streptococcus pneumonia

Atypical

Health care–associated pneumonia (HCAP)

Staphylococcus aureus (MRSA)

Haemophilis influenza

Hospital-acquired pneumonia (HAP) ** nosocomial

Haemophilis influenza

Ventilator-associated pneumonia (VAP)

Pseudomonas aeruginosa / E.Coli / Klebsiella pneumonia / Acinetobacter / Staphylococcus aureus

Pneumonia: Clinical Manifestations

Clinical Manifestations

Preceded by an upper respiratory infection

Cough, dyspnea, fever, chills, malaise, and pleuritic chest pain

Subcostal and intercostal retractions from dyspnea

Pulmonary consolidation on CXR

Fever, cough productive

Hyporesonnance (dullness over consolidation), rales, diminished, pleural friction rub, egophany (E changes to Aaaa sound), increased tactile fremitus “99” (Vibration increases)

Pneumonia: Treatment

Treatment

ALL pneumonias

Establish adequate ventilation & oxygenation

Mechanical ventilation may be needed

Adequate hydration

Pulmonary hygiene (deep breathing, coughing, chest PT, IS, flutter)

Bacterial pneumonia

Antibiotics

Viral pneumonia

Supportive therapy

Antiviral medications