Transcript Document
PATHOPHYSIOLOGY OF RESPIRATORY SYSTEM DISEASES
Mehtap KAÇAR KOÇAK M.D. PhD Yeditepe University Medicine School, Pathophysiology
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General Introduction
Respiratory diseases is often classified as acute or chronic, obstructive or restrictive, and infectious or noninfectious.
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Reduction of Pulmonary Function
1.
2.
Inadequate blood flow to the lungs –
hypoperfusion
Inadequate air flow to the alveoli -
hypoventilation
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Signs and Symptoms of Pulmonary Disease
Dyspnea, Abnormal breathing patterns, Hypoventilation and hyperventilation, Cough, Hemoptysis, Cyanosis, Pain, Clubbing, Abnormal sputum. 4
Dyspnea
Dyspnea breath” – subjective sensation of uncomfortable breathing, feeling “short of Ranges from mild discomfort after exertion to extreme difficulty breathing at rest.
Usually caused by diffuse and extensive rather than focal pulmonary disease.
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Dyspnea
Due to: Airway obstruction • Greater force needed to provide adequate ventilation • Wheezing sound due to air being forced through airways narrowed due to constriction or fluid accumulation Decreased compliance of lung tissue 6
Signs of dyspnea:
Flaring nostrils Use of accessory muscles in breathing Retraction (pulling back) of intercostal spaces 7
Types of dyspnea
Orthopnea;
is caused by the horizontal position, which redistributes body water, causes the abdominal contents to exert pressure on the diaphragm, and decreases the efficiency of the respiratory muscles.
Some individuals with left ventricular failure wake up at night gasping for air and must sit up or stand to relieve the dispnea, this type of positional dyspnea is termed
Paroxysmal nocturnal dyspnea (PND)
PND results from fluid in the lungs caused by the redistribution of of body water while the individual is recumbent.
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Abnormal breathing patterns
Normal breathing (eupnea) is rhythmic and effortless. Ventilatory rate is 8 to 16 breaths per minute, and tidal volume ranges from 400 to 800 ml.
The rate, depht, regulatory and effort of breathing undergo characteristic alterations in response to physiologic and pathophysiologic conditions…..
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Kussmaul respiration (hyperpnea);
→ no expiration pause.
is characterized by →a slightly increased ventilatory rate, → very large tidal volume, Strenous exercise or metabolic acidosis induces Kussmaul respiration.
Labored or obstructed breathing
on the site of obstruction.
consists of slow ventilatory rate, large tidal volume, increased effort, and prolonged inspiration or expiration, depending Audible wheezing (whistling sounds) and stridor (high-pitched sounds made during inspiration) is often present. 10
Restricted breathing
is characterized by small tidal volumes and rapid ventilatory rate (tachypnea).
Restricted breathing is commonly caused by disorders such as pulmonary fibrosis that stiffen the lungs or chest wall and decrease compliance.
Panting
occurs with exercise. Shock and severe cerebral hypoxia contribute to
gasping respirations
that consist of irregular, quick inspirations with an expiratory pause. 11
Sighing respirations
consists of irregular breathing characterized by frequent, deep sighing inspirations. Sighing respirations are caused by anxiety.
Cheyne-Stokes respirations
are characterized by alternating periods of deep and shallow breathing. Apnea lasting 15 to 60 seconds is followed by ventilations that increase in volume until a peak is reached, after which ventilation (tidal volume) decreases again to apnea. This respirations results from any condition that slows the blood flow to the brain stem, which in turn slows impulses sending information to the respiratory centers of the brain stem. 12
Hypoventilation and hyperventilation
Hypoventilation
is inadequate alveolar ventilation in relation to metabolic demands. It is caused by alterations in pulmonary mechanics or in the neurologic control of breathing.
With hypoventilation, CO2 removal does not keep up with CO2 production and PaCO2 increases, causing hypercapnia (PaCO2>44 mmHg). This results in respiratory acidosis, which can affect the function of many tissues throughout the body. (somnolence or disorientation) 13
Hyperventilation is alveolar ventilation that exceeds metabolic demands. The lungs remove CO2 at a faster rate than it is produced by cellular metabolism, resulting in decreased PaCO2 or hypocapnia (PaCO2<36 mmHg).
Hyperventilation results in a respiratory alkalosis that also can interfere with tissue function.
Hyperventilation commonly occurs with severe anxiety, acute head injury, and conditions that cause insufficient oxygenation of the blood.
Hypoventilation and hyperventilation can be determined only by arterial blood gas analysis.
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Blood Gas Analysis
Factors Connected with blood gas measurements
Abnormalities of respiratory control
Gas exchange
Respiratory mechanics
Circulation
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Blood Gas Analysis
Blood gas values
pH : 7.35
—7.45
PaO 2 : 80 —100mmHg(10.6~13.3kpa) SaO 2 : 91 —97.7% PaCO 2 : 35 —45mmHg(4.67~6.0kpa)
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Cough
Attempt to clear the lower respiratory passages by abrupt and forceful expulsion of air Most common when fluid accumulates in lower airways Most coughs are initiated in the larynx and in the tracheabronchial tree by both mechanical and chemical irritant receptor stimulation.
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Other cough receptors are located: The external auditory canal, Diaphragm, Pericardium, Pleura, Stomach, The most distal bronchioli and the alveoli (a few).
Stimulation of cough receptors is transmitted centrally through the vagus nerve. (this way is inhibited by opiates and serotoninergic agents) 18
Acute cough:
It is cough that resolves within 2 to 3 weeks of the onset of illness or resolves with treatment of the underlying condition.
It is commonly the result of; Upper respiratory infections, Allergic rhinitis, Acute bronchitis, Pneumonia, Congestive heart failure, Pulmonary embolus, Aspiration.
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Chronic cough:
It is defined as cough that has persisted for more than 3 weeks.
In nonsmokers, chronic cough is almost always caused by postnasal drainage syndrome, Asthma, Gastroesophageal reflux disease.
In smokers, chronic bronchitis is the most common cause of chronic cough.
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Hemoptysis:
Hemoptysis is the coughing up of blood or bloody secretion.
Hemoptysis is sometimes confused with hematemesis, which is the vomiting of blood.
Blood that is coughed up is usually bright red, has an alkaline pH, and is mixed frothy sputum, whereas blood that is vomited is dark, has an acidic pH, and is mixed with food particles.
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Hemoptysis results from damage to the lung parenchyma with rupture of pulmonary vessels or from inflammation, injury, or cancer of the bronchial tree. 22
The most common causes of hemoptysis are:
Tuberculosis, Bronchiectasis, Lung cancer, Bronchitis, Pneumonia.
23
Cyanosis
Cyanosis is bluish discoloration of the skin and mucous membranes caused by increasing amounts of desaturated or reduced hemoglobin (which is bluish) in the blood.
Cyanosis generally develops when 5 g of hemoglobin is desaturated, regardless of hemoglobin concentration. 24
Cyanosis can be caused by decreased arterial oxygenation (low PaO2), pulmonary or cardiac right-to-left shunts, decreased cardiac output, cold environments, or anxiety.
Lack of cyanosis does not necessarily indicate that oxygenation is normal. For example, severe anemia and CO poisoning can cause inadequate oxygenation of tissues without causing cyanosis.
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Most cases arise as a result of peripheral vasoconstriction – result is reduced blood flow, which allows hemoglobin to give up more of its oxygen to tissues-
peripheral cyanosis.
Best seen in nail beds Due to cold environment, anxiety, etc.
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Central cyanosis
can be due to : Abnormalities of the respiratory membrane Mismatch between air flow and blood flow Expressed as a ratio of change in ventilation (V) to perfusion (Q) : V/Q ratio • Pulmonary thromboembolus - reduced blood flow • Airway obstruction – reduced ventilation
In persons with dark skin can be seen in the whites of the eyes and mucous membranes.
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Pain
Pain caused by pulmonary disorders originates in the pleurae, airways or chest wall.
Pleural pain is the most common pain caused by pulmonary disease and is usually sharp or stabbing in character. (infection and inflammation) Pleural pain is also common with pulmonary infarction caused by pulmonary embolism.
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Pulmonary pain is central chest pain that is pronounced after coughing and occurs in individulas with infection and inflammation of the trachea or bronchi. (it is differentiated from cardiac pain).
Pain in the chest wall is muscle pain or rib pain. (excessive coughing, costochondritis) 29
Clubbing
Clubbing is the selective bulbous enlargement of the end (distal segment) of a digit (finger or toe), whose severity can be graded from 1 to 5 based on the extend of nail bed hypertrophy and the amount of changes in the nails themselves.
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Clubbing is commonly associated with diseases that interfere with oxygenation, such as bronchiectasis, cystic fibrosis, pulmonary fibrosis, lung abscess and congenital heart disease.
Lung cancer is sometimes associated with clubbing even in the absence of significant hypoxemia. This syndrome is called
hypertrophic osteoarthropathy
(HOA) and its pathogenesis is unknown.
32
Abnormal sputum
The color, consistency, odor and amount of sputum vary different pulmonary disorders. 33
Conditions Caused by Pulmonary Disease or Injury
Hypercapnia, Hypoxemia, Acute respiratory failure, Pulmonary edema, Aspiration, Atelectasis, Bronchiectasis, Bronchiolitis, Pleural abnormalities (pneumothorax, pleural effusion, empyema) Abscess formation and cavitation, Pulmonary fibrosis
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Hypercapnia
Hypercapnia or increased CO2 in the arterial blood is caused by hypoventilation of the alveoli.
Causes include; * depression of the respiratory center by drug, * infection of CNS or trauma, * spinal cord disruption or poliomyelitis, * diseases of the neuromuscular junction (MG, MD) * chest injury, * large airway obstruction.
Hypercapnia and the associated respiratory acidosis can result in several important clinical manifestations. (dysrythmia, coma, somnolence) 35
Hypoxemia
Hypoxemia or reduced oxygenation of arterial blood is caused by respiratory alterations.
The five causes of hypoxemia are; * decreased oxygen content in inspired gas (high altitude), * hypoventilation (drug overdose, neurologic damage), * diffusion abnormalities (emphysema, fibrosis, edema), * abnormal ventilation-perfusion ratios (asthma, chronic bronchitis, ARDS), * pulmonary right-to-left shunt (congenital heart defects).
Hypoxemia is often associated with a compensatory hyperventilation and resultant respiratory alkalosis.
Hypoxemia result in widwspread tissue dysfunction and when severe can lead to organ infarction.
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Acute respiratory failure
Respiratory failure is defined as inadequate gas exchange, that is hypoxemia, where PaO2 is ≤50 mmHg PaCO2 is ≥50mmHg, (hypercapnia) pH ≤7.25.
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Pulmonary edema
Pulmonary edema is excess water in the lung.
The normal lung contains very little water or fluid.
It is kept dry by lymphatic drainage and a balance among capillary hydrostatic pressure, capillary oncotic pressure and capillary permeability. The most common cause of pulmonary edema is heart disease. 39
Pulmonary Circulation
:
•
Consists of:
•
Pulmonary artery & its branches
•
Thin-walled, easily distensible Pulmonary
• • • • •
capillaries Pulmonary venous system Left Atrium Low pressure Low resistance to blood flow Accepts all blood from right heart
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PA pressure: Sys: 20 – 30 mm Hg Dias: 8 – 12 mmHg.
12 – 15 mm Hg mean Normal L.A.Pr: 8 mm Hg with an Upper limit of 15 mm Hg Blood vol: About 1 litre.
More than 100 ml in capillaries.
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Pulmonary Circulation
Pul cap pr.: about 10 mm Hg
Oncotic pressure: 25 mm Hg
Inward gradient: 15 mm Hg
Pul congestion and oedema result when the pul cap pr is >25 mm Hg (“backward failure”)
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Pulmonary Arterial Pressure rises during:
Negative pressure breathing
Supine position
Systemic venous congestion from any cause
Overtransfusion
Left ventricular failure
43
Pulmonary Arterial Pressure falls during:
Positive pressure breathing
Upright position
Valsalva manuevre
After haemorrhage
Systemic vasodilatation from any cause.
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PULMONARY EDEMA
Classified into: Cardiogenic: Otherwise called as Hydrostatic or Transudative.
Non-Cardiogenic: Other-wise called as Permeability or Exudative.
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Cardiogenic Pulmonary Edema
Increased pulmonary vascular pressure
Transudation of fluid across endothelium into pulmonary interstitium and then into the alveolar space.
Noncardiogenic Pulmonary Edema
Low pressure pulmonary edema Injured microvascular endothelium allows protein-rich fluid to enter the extravascular spaces.
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Cardiogenic Pulmonary Edema Causes:
Left ventricular failure Volume overload Mechanical obstruction of left outflow tract e.g. Mitral stenosis Other valvular diseases like Mitral stenosis, PDA, Aortic valvular diseases & also in congestive failure and hypertension.
Noncardiogenic Pulmonary Edema Causes:
Toxins: eg. Smoke, ozone, phosgene, Nitrogen dioxide, Emboli: Air, thrombotic, amniotic fluid Trauma and burns Aspiration of gastric contents Acute radiation Pneumonitis D.I.C.
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PULMONARY EDEMA MIXED PATHOGENESIS
Incompletely understood:
High altitude pulmonary edema
Neurogenic: midbrain lesions, Middle/Posterior cranial fossa surgeries
Reperfusion pulmonary edema
Narcotic overdose
Tocolytic therapy
Uraemia
Negative pressure pulmonary edema.
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PUL EDEMA – SIGNS & SYMPTOMS
Symptoms: Acute Dyspnea Cough, Pink frothy sputum Signs: Tachycardia Blood Pressure: variable Lung crepitations 50
PUL EDEMA – SIGNS & SYMPTOMS
Other signs of congestion: Increased JVP Peripheral edema Cardiac enlargement -- apex beat displaced S3 Gallop – apical 3 rd heart sound 51
Atelectasis
Atelectasis is the collaps of lung tissues. The two types of atelectasis: 1-
Compression atelectasis
is caused by the external pressure exerted by a tumor in the lung, or by fluid or air in the pleural space.
2-
Absorption atelectasis
results from gradual absorption of air from obstructed or hypoventilated alveoli or from inhalation of concentrated oxygen or anesthetic agent. .
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Clinical manifestations of atelectasis are dyspnea, cough, fever and leukocytosis.
Atelectasis tends to occur after surgery.
Prevention and treatment of postoperative atelectasis usually include deep breathing. (open pore of Kohn)
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Bronchiectasis
Bronchiectasis is persistent abnormal dilatation of the bronchi.
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Pathophysiology
It results from two causes: Infectious insult Impairment of drainage, airway obstruction, and/or a defect in host defense. 57
Infection: Bacterial, mycobacterial, central airway bronchiectasis Airway obstruction: intraluminal tumor, foreign body, lymph nodes, COPD Immunodeficiency: ciliary dyskinesia, HIV, hypogammaglobulinemia, cystic fibrosis (obstruction and immunodef.) 58
Bronchial dilatation may be;
Clindrical bronchiectasis
, (with symmetrically dilated airways as is commonly seen after pneumonia and is reversible)
Saccular bronchiectasis
(in which the bronchi become large and balloon-like),
Varicose bronchiectasis
constrictions and dilations deform the bronchi).
(in which 59
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Clinical manifestations of bronchiectasis:
Cough (90 %) Daily sputum production (76%) Dyspnea (72%) Hemoptysis (56%) Recurrent pleurisy 61
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Bronchiectasis
If wide spread Dyspnea Clubbing of the fingers h pulmonary blood pressure Cor pulmonale 64
Pneumothorax
Pneumothorax is the presence of air or gas in the pleural space caused by a rupture in the visceral pleura or parietal pleura and chest wall. 65
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PULMONARY DISORDERS
Acute Respiratory Distress Syndrome (ARDS) Obstructive Pulmonary Diseases : *Chronic obstructive pulmonary diseases (Chronic bronchitis and Emphysema) *Asthma Respiratory Tract Infections (Tuberculosis) Pulmonary Vascular Disease (Pulmonary Embolism and Pulmonary Hypertension) 67
Acute Respiratory Distress Syndrome :
Acute Respiratory Distress Syndrome (or Adult Respiratory Distress Syndrome) • Rapid and severe onset of respiratory failure characterized by acute lung inflammation and diffuse injury to the respiratory membrane with noncardiogenic edema.
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ARDS
Identified in last 25 years Affects 200 -250 thousand people each year in U.S. Mortality in persons < 60 is 40% ( ↓ 67%) Those over 65 and immuno compromised still have mortality over 60 % Most survivors have almost normal lung function 1 year after acute illness.
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Pathophysiology of ARDS
All disorders causing ARDS acutely injure the respiratory membrane and produce severe pulmonary edema, shunting, and hypoxemia.
Shunting: blow flow is normal, but gas exchanged is decreased. V/Q ratio changes: the same effect as if blood were shunting or bypassing the lungs.
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Damage can occur directly:
Aspiration of acidic gastric contents
Inhalation of toxic gases
Or indirectly:
Chemical mediators from systemic disorders
71
Result is massive inflammatory response by lungs
Initial injury damages the pulmonary capillary epithelium, causing platelet aggregation and intravascular thrombus formation.
Platelets release substances that attract and activate neutrophils. Damage also activates the complement cascade which also activates neutrophils and the inflammatory response.
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Role of neutrophils is central to the development of ARDS.
Neutrophils release inflammatory mediators: Proteolytic enzymes Toxic oxygen products Prostaglandins and leukotrienes Platelet activating factors These damage the respiratory membrane and increase capillary permeability, allowing fluids, proteins, and blood cells to leak into alveoli → pulmonary edema and hemorrhage 73
Reduces pulmonary ventilation and compliance Neutrophils and macrophages release mediators that cause pulmonary vasoconstriction → pulmonary hypertension Type II alveolar cells also damaged, see decreased surfactant production Alveoli fill with fluid or collapse.
Lungs become less compliant, and ventilation decreases.
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After 24 – 48 hours hyaline membranes form After about 7 days, fibrosis progressively obliterates the alveoli, respiratory bronchioles and interstitium Result is acute respiratory failure 75
In addition, chemical mediators often cause widespread inflammation, endothelial damage and increased capillary permeability throughout the body This leads to systemic inflammatory response syndrome, which leads to multiple organ dysfunction syndrome (MODS) Death may not be caused by ARDS alone, but by MODS 76
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Clinical manifestations:
Symptoms develop progressively:
Hyperventilation →
respiratory alkalosis→ dyspnea and hypoxemia→ metabolic acidosis→ respiratory acidosis → further hypoxemia → hypotension → decreased cardiac output →
death
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Evaluation and Treatment
Diagnosis based on physical examination, blood gases and imaging Treatment is based on early detection, supportive therapy and prevention of complications, esp. infection Often requires mechanical ventilation Many studies underway for treatment: Prophylactic immunotherapy Antibodies against endotoxins Inhibition of inflammatory mediators Inhalation of nitric oxide to reduce pulmonary hypertension Surfactant replacement 80
Obstructive and Inflammatory Lung Disease
Chronic Bronchitis Emphysema Asthma
Christine Hooper, Ed.D., RN Spring 2006
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A- Normal lung, B- Emphysema, C- Chronic bronchitis, D- Asthma
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Chronic Obstructive Pulmonary Disease: COPD
Disease of airflow obstruction that is not totally reversible
Chronic Bronchitis
Emphysema
83
Risk Factors for COPD
Nutrition Infections Socio-economic status Aging Populations
84
COPD: Etiology
Cigarette smoking #1 Recurrent respiratory infection Alpha 1-antitrypsin deficiency Aging 85
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Mucous plug
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Chronic Bronchitis
Recurrent or chronic productive cough for a minimum of 3 months for 2 consecutive years.
Risk factors Cigarette smoke Air pollution 89
Chronic Bronchitis Pathophysiology
Chronic inflammation Hypertrophy & hyperplasia of bronchial glands that secrete mucus Increase number of goblet cells Cilia are destroyed 90
Chronic Bronchitis Pathophysiology
Narrowing of airway Starting w/ bronchi smaller airways airflow resistance work of breathing Hypoventilation & CO2 retention hypoxemia & hypercapnea 91
Chronic Bronchitis Pathophysiology
Bronchospasm often occurs End result Hypoxemia Hypercapnea Polycythemia (increase RBCs) Cyanosis Cor pulmonale (enlargement of right side of heart) 92
Chronic Bronchitis: Clinical Manifestations
In early stages Clients may not recognize early symptoms Symptoms progress slowly May not be diagnosed until severe episode with a cold or flu Productive cough • • Especially in the morning Typically referred to as “cigarette cough” Bronchospasm Frequent respiratory infections 93
Chronic Bronchitis: Clinical Manifestations
Advanced stages Dyspnea on exertion Dyspnea at rest Hypoxemia & hypercapnea Polycythemia Cyanosis Bluish-red skin color Pulmonary hypertension Cor pulmonale 94
Chronic Bronchitis: Diagnostic Tests
PFTs FVC: FEV1: Forced vital capacity Forcible exhale in 1 second FEV1/FVC = <70% ABGs PaCO2 PaO2 CBC Hct 95
Emphysema
Abnormal distension of air spaces Actual cause is unknown 96
Emphysema: Pathophysiology
Structural changes Hyperinflamation of alveoli Destruction of alveolar & alveolar-capillary walls Small airways narrow Lung elasticity decreases 97
Emphysema: Pathophysiology
Mechanisms of structural change
Obstruction of small bronchioles Proteolytic enzymes destroy alveolar tissue Elastin & collagen are destroyed Support structure is destroyed “paper bag” lungs 98
Emphysema: Pathophysiology
The end result: Alveoli lose elastic recoil, then distend, & eventually blow out.
Small airways collapse or narrow Air trapping Hyperinflation Decreased surface area for ventilation 99
Healthy Lung
elastic clean many alveoli with large surface areas healthy capillaries clear airways 100
Emphysema Lung
loss of elasticity filled with toxins from tobacco smoke fewer alveoli with smaller surface areas destroyed capillaries blocked airways 101
Types:
acinus according to distribution within the
Panacinar: Uniform involvement
of the acinus Associated with
α1-antitrypsin deficiency Centriacinar: Enlargement of central parts of the acinus
(respiratory bronchioles and alveolar duct),
sparing
the peripheral alveoli
(distal alveoli
) More common and more severe in apical segments of
upper lobes In heavy smokers Chronic bronchitis
and often associated with 102
A- Centriacinar emphysema, B- Panacinar emphysema
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Emphysema: Clinical Manifestations
Early stages Dyspnea Non productive cough Diaphragm flattens A-P diameter increases • “Barrel chest” Hypoxemia may occur • • Increased respiratory rate Respiratory alkalosis Prolonged expiratory phase 104
Emphysema: Clinical Manifestations
Later stages Hypercapnea Purse-lip breathing Use of accessory muscles to breathe Underweight • No appetite & increase breathing workload Lung sounds diminished 105
Emphysema: Examination
Pulmonary function • residual volume, lung capacity, DECREASED FEV 1 , vital capacity maybe normal Arterial blood gases Normal in moderate disease May develop respiratory alkalosis Later: hypercapnia and respiratory acidosis Chest x-ray Flattened diaphragm hyperinflation 106
Goals of Treatment: Emphysema & Chronic Bronchitis
Improved ventilation Remove secretions Prevent complications Slow progression of signs & symptoms Promote patient comfort and participation in treatment 107
Asthma
Asthma is defined as A chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cellls.
In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particulary at night or in the early morning. 108
Asthma
Reversible inflammation & obstruction Intermittent attacks Sudden onset Varies from person to person Severity can vary from shortness of breath to death Triggers Allergens Exercise Respiratory infections Drugs and food additives Nose and sinus problems Emotional stress 109
Asthma: Pathophysiology
Swelling of mucus membranes (edema)
Spasm of smooth muscle in bronchioles
Increased airway resistance
Increased mucus gland secretion
110
Asthma: Pathophysiology
Early phase response: 30 – 60 minutes
Allergen or irritant activates mast cells Inflammatory mediators are released • histamine, bradykinin, leukotrienes, prostaglandins, platelet activating-factor, chemotactic factors, cytokines Intense inflammation occurs • • • Increased vasodilation and permeability Epithelial damage Bronchospasm • • Bronchial smooth muscle constricts Increased mucus secretion Edema 111
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Asthma: Pathophysiology
Late phase response: 5 – 6 hours
Characterized by inflammation Eosinophils and neutrophils infiltrate Mediators are released mast cells release histamine and additional mediators Self-perpetuating cycle Lymphocytes and monocytes invade as well Future attacks may be worse because of increased airway reactivity that results from late phase response • Individual becomes hyperresponsive to specific allergens and non-specific irritants such as cold air and dust • Specific triggers can be difficult to identify and less stimulation is required to produce a reaction 113
Asthma: Early Clinical Manifestations
Expiratory & inspiratory wheezing Dry or moist non-productive cough Chest tightness Dyspnea Anxious &Agitated Prolonged expiratory phase Increased respiratory & heart rate Decreased PEFR 114
Asthma: Early Clinical Manifestations
Wheezing Chest tightness Dyspnea Cough Prolonged expiratory phase [1:3 or 1:4] 115
Asthma: Severe Clinical Manifestations
Hypoxia Confusion Increased heart rate & blood pressure Respiratory rate up to 40/minute & pursed lip breathing Use of accessory muscles Diaphoresis & pallor Cyanotic nail beds Flaring nostrils 116
Classifications of Asthma
Mild intermittent Mild persistent Moderate persistent Severe persistent 117
Asthma: Diagnostic Tests
Pulmonary Function Tests FEV1 decreased • Increase of 12% - 15% after bronchodilator indicative of asthma PEFR decreased Symptomatic patient eosinophils > 5% of total WBC Increased serum IgE Chest x-ray shows hyperinflation ABGs Early: respiratory alkalosis, PaO2 normal or near-normal severe: respiratory acidosis, increased PaCO2, 118
Asthma: Collaborative Care
Mild intermittent Avoid triggers Premedicate before exercising May not need daily medication Mild persistent asthma Avoid triggers Premedicate before exercising Low-dose inhaled corticosteroids 119
Asthma: Collaborative Care
Moderate persistent asthma Low-medium dose inhaled corticosteroids Long-acting beta2-agonists Can increase doses or use theophylline or leukotriene-modifier [singulair, accolate, zyflo] Severe persistent asthma High-dose inhaled corticosteroids Long-acting inhaled beta2-agonists Corticosteroids if needed 120
Asthma: Collaborative Care
Acute episode FEV1, PEFR, pulse oximetry compared to baseline O2 therapy Beta2-adrenergic agonist • • via MDI w/spacer or nebulizer Q20 minutes – 4 hours prn Corticosteroids if initial response insufficient • • Severity of attack determines po or IV If poor response, consider IV aminophylline 121
Asthma: Client Teaching
Correct use of medications Signs & symptoms of an attack Dyspnea, anxiety, tight chest, wheezing, cough Relaxation techniques When to call for help, seek treatment Environmental control Cough & postural drainage techniques 122
COPD Complications
Cor pulmonale
Pulmonary hypertension
Acidosis
Polycythemia
123
COPD Complications
Right side of the heart must increase to push blood into the lungs
•
Right-sided heart failure develops
•
Subsequent intravascular volume expansion
•
Systemic venous congestion
124
Pathophysiology of Cor Pulmonale
125
Cor pulmonale signs&symptoms
Heart sound changes to the second heart sound, right-sided ventricular diastolic S 3 gallop, and early ejection click along left sternal border Distended neck veins Hepatomegaly with upper quadrant tenderness Ascites Epigastric distress Peripheral edema Weight gain Acute exacerbations of chronic bronchitis Acute respiratory failure 126
Tuberculosis
Pathophysiology Mycobacterium tuberculosis Tubercle bacillus 127
Tuberculosis
Etiology Assoc. w/ Poverty Malnutrition Overcrowding Substandard housing Inadequate health care Elderly HIV Prison 128
Tuberculosis
5-10% become active Only contagious when active Primarily affect lungs but… Kidneys Liver Brain Bone 129
Tuberculosis
Pathophysiology Mode of transmission Air-borne alveoli Multiplies in alveoli 130
Tuberculosis
Immune response phase Macrophages attack TB TB has waxy cell wall that protects it from macrophages Immune system surrounds the infected macrophages Forms a Lesion Called a Tubercle 131
Clinical manifestations of Tuberculosis
(active phase) NOC sweats Low grade fever Weight loss Chronic productive cough Rust colored sputum Thick Hemoptysis 132
Natural history of tuberculosis in a
newly infected
not necessarily disease)
(adult) contact
(infection is NO INFECTION CONTACT
Defenses
NO DISEASE (90%) INFECTION
Cell-mediated immunity
EARLY DISEASE (5%) DISEASE LATE DISEASE (5%)
133
TB
PATHOPHYSIOLOGY
systemic infection primary infection/disease progressive primary disease miliary disease meningitis chronic TB (re-activation) 134
Inhalation of Infected Droplet Nuclei non-specific bronchopneumonia 1) skin test sensitization 2) resistance to exogenous reinfection 3) lympho-hematogenous spread complete resolution (rare) progression healing with granuloma formation massive necrosis (rare) breakdown with development of (re-activation)TB DISEASE stable
135
TB:
PRIMARY
Infection
95% of cases begin with pulmonary focus usually a SINGLE focus hypersensitivity develops 2 to 6 weeks until then, focus may grow larger hypersensitivity brings caseation 136
PRIMARY
Infection: Lympho-hematogenous spread
8-14 weeks after onset of TB usually occult Mantoux positive during this phase body wide seeding occurs during this phase bone, kidney, meninges etc.
3% of children with nl CXR’s develop calcifications in lung apices (SIMON FOCI) 137
138
PRIMARY
TB: endo-bronchial consequences
lymph nodes draining primary infection site become involved lymph node capsule becomes adherent to bronchial wall infection can progress to ulceration into the bronchial wall bronchial compression occurs with more than one node at same level with healing, bronchial constriction/stenosis can occur 139
INFECTION
TO ENDO-BRONCHIAL
DISEASE
TO
STENOSIS
140
HEALED PRIMARY INFECTION
SIMON FOCI CALCIFIED nodes and peripheral lesion
(Ghon complex)
other VISCERAL sites
141
USUAL PROGRESSION OF
PRIMARY
INFECTION infection lympho-hematogenous spread healed PRIMARY infection
142
PROGRESSIVE PRIMARY
TB
(
DISEASE)
occasional (3.7%) local progression, despite hypersensitivity (more common in younger pt) can be cavitary can have endo-bronchial spread similar in appearance to adult type, “reactivation” disease 2/3 of cases progress to death in the untreated 143
PROGRESSIVE PRIMARY DISEASE lymph node involvement cavitation pleural effusion
144
Progressive Primary Disease
145
ENDOBRONCHIAL SPREAD WITH SUBSEQUENT BRONCHOPNEUMONIA
146
MILIARY
Disease Generalized Hematogenous Tuberculosis
generalized dissemination through bloodstream caseous focus ruptures into blood vessel growth of tubercle within the blood vessel may be acute, occult or chronic uniformly fatal if not treated rare usually occurs in the first 4 months after primary infection 147
CHRONIC PULMONARY
TB (re-activation/adult type)
occurs only after primary infection 0.5-10 % incidence (7% by Lincoln) usually not less than 1 year of age most cases occur when primary infection aquired after 7 years of age minute areas of bronchopneumonia tissue hypersensitivity (Type IV hypersensitivity reaction - cavity formation few symptoms early on in disease 148
Pulmonary embolism
149
Epidemiology & Pathophysiology-1
Thrombi commonly form in deep veins in the calf propagate into the proximal veins, including & above the popliteal veins from which they are more likely to embolize 150
Epidemiology & Pathophysiology-2
About 79% of patients with PE have evidence of DVT in their legs PE occurs in up to 50% of patients with proximal DVT Dual pulmonary circulation ( pulmonary & bronchial arteries ), pulmonary infarction : not usually present 151
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Epidemiology & Pathophysiology-3
APE, anatomical obstruction is the most important cause of compromised physiology release of vasoactive & bronchoactive agents (serotonin from platelets )--- deleterious ventilation – perfusion matching 153
Epidemiology & Pathophysiology-4
As RV afterload increases, tension in RV wall rises dilatation, dysfunction, & ischemia of RV Death results from RV failure.
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Virchow's classic triad of risk
Hypercoagulability Stasis Venous injury 156
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NURSING 621 Adult Respiratory Pathophysiology W. Rose
Pulmonary hypertension
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Predisposing factors
Defective fibrinolytic systems
Presence of lupus-like anticoagulant
Deficiency of protein C, protein S, and antithrombin III
Malignancy
Atrial septal defects
Indwelling venous catheters
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Pulmonary Hypertension
Etiology/Contributing factors • • • • • Primary: Rare Female > Male Age 20-40 years hereditary tendency usually die within 5 years of diagnosis • Secondary: • • Existing cardiac or pulmonary disease Mitral valve disease COPD 160
Pulmonary Hypertension
Pathophysiology • Pulmonary arteries narrow Vasoconstriction • Increased Pulmonary BP (>30 mmHg) • How do you measure pulmonary BP?
Only can be measured during right side heart catheterization 161
Pulmonary Hypertension
Pathophysiology If increase in BP Right ventricle has to work harder Right ventricle hypertrophy • enlargement and dilation Right ventricle fails Precursor to Cor Pulmonale 162
Pulmonary Hypertension in COPD
Chronic hypoxia Pulmonary vasoconstriction Pulmonary hypertension Cor pulmonale Edema Muscularization Intimal hyperplasia Fibrosis Obliteration Death
Source : GOLD 2007 163
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Selected etiologic conditions giving rise to pulmonary hypertension
“
honeymoon period”
The existence of a
“honeymoon period”
during which time pulmonary hypertension is present but the subject exhibits few symptoms, if any. It is during this time that compensatory hypertrophy of the right ventricle occurs in an effort to maintain cardiac output in the presence of increased pulmonary vascular resistance (PVR).
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The pathophysiological events in the progression of pulmonary hypertension during this period have not been well defined.
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Pulmonary Hypertension
Clinical manifestations of • • • • Pulmonary hypertension without right sided heart failure (Not clinically evident until late in progression) Dyspnea and fatigue that worsens over time Cyanosis and Tachypnea Crackles and decrease breath sounds 168
Pulmonary Hypertension
Clinical manifestations of… Right sided heart failure • • • • • • Peripheral edema Ascites Distended neck veins Liver engorgement Crackles Heart murmur 169
Pulmonary Hypertension
Diagnostic exams/procedures ABG’s: • PaO2 • • Decreased Hypoxemia • • • PaCO2 Decreased Hypercapnia 170
Pulmonary Hypertension
Diagnostic exams ECG • Shows right ventricular hypertrophy Cardiac catheterization • Right sided heart catheterization only way to measure pulmonary pressure X-ray Pulmonary function test 171
Pulmonary Hypertension
Treatment Oxygen therapy • Vasodilators (in some people) Anticoagulants – Warfarin (Coumadin) Diuretic to decrease blood volume Heart/lung transplant • Really there is no cure – death within 2-3 years of diagnosis unless transplant 172
Pulmonary Hypertension
A 66-year-old client takes a potassium depleting diuretic. Foods that will help to keep the client’s potassium level within normal limits include • • • • • • Bananas Oranges Cantaloupe fish Spinach whole-grain cereals 173
Restrictive lung disease: idiopathic pulmonary fibrosis
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Background
The lung volumes are reduced either because of: 1.
Alteration in lung parenchyma.
2.
Diseases of the pleura, chest wall or neuromuscular apparatus.
Physiologically restrictive lung diseases are defined by reduced total lung capacity, vital capacity and functional residual capacity, but with preserved air flow.
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Restrictive lung diseases may be divided into the following groups: Intrinsic lung diseases (diseases of the lung parenchyma) Extrinsic disorders (extra-parenchymal diseases) 176
Intrinsic Lung Diseases
These diseases cause either: Inflammation and/or scarring of lung tissue (interstitial lung disease) or Fill the air spaces with exudate and debris (pneumonitis).
These diseases are classified further according to the etiological factor.
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Extrinsic Lung Diseases
The chest wall, pleura and respiratory muscles are the components of respiratory pump.
Disorders of these structures will cause lung restriction and impair ventilatory function.
These are grouped as: Non-muscular diseases of the chest wall.
Neuromuscular disorders.
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Pathophysiology
Intrinsic lung diseases: Diffuse parenchymal disorders cause reduction in all lung volumes.
This is produced by excessive elastic recoil of the lungs.
Expiratory flows are reduced in proportion to lung volumes.
Arterial hypoxemia is caused by ventilation/perfusion mismatch.
Impaired diffusion of oxygen will cause exercise induced desaturation.
Hyperventilation at rest secondary to reflex stimulation.
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Extrinsic Disorders
Diseases of the pleura, thoracic cage, decrease compliance of respiratory system.
There is reduction in lung volumes.
Secondarily, atelectasis occurs leading to V/Q mismatch hypoxemia.
The thoracic cage and neuromuscular structures are a part of respiratory system.
Any disease of these structures will cause restrictive disease and ventilatory dysfunction.
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Diffuse Interstitial Pulmonary Fibrosis
Synonyms: idiopathic pulmonary fibrosis, interstitial pneumonia, cryptogenic fibrosing alveolitis.
Pathology:
Thickening of interstitium.
Initially, infiltration with lymphocytes and plasma cells.
Later fibroblasts lay down thick collagen bundles.
These changes occur irregularly within the lung.
Eventually alveolar architecture is destroyed – honeycomb lung 181
Etiology
Unknown, may be immunological reaction.
Clinical Features Uncommon disease, affects adults in late middle age.
Progressive exertional dyspnea, later at rest.
Non-productive cough.
Physical examination shows finger clubbing, fine inspiratory crackles throughout both lungs.
Patient may develop respiratory failure terminally.
The disease progresses insidiously, median survival 4-6 years.
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