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CHRONIC OBSTRUCTIVE PULMONARY DISEASE

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE RESPIRTORY DEPARTMENT RENJI HOSPITAL DEFINITION OF COPD Chronic obstructive pulmonary disease (COPD) is a preventable and ... – PowerPoint PPT presentation

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Title: CHRONIC OBSTRUCTIVE PULMONARY DISEASE


1
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
  • RESPIRTORY DEPARTMENT
  • RENJI HOSPITAL

2
DEFINITION OF COPD
  • Chronic obstructive pulmonary disease (COPD) is a
    preventable and treatable disease state
    characterized by air flow limitation that is not
    fully reversible.
  • Air flow limitation is usually progressive and is
    associated with an abnormal inflammatory response
    of lungs to noxious particles or gases,primarily
    caused by cigarette smoking.

3
Component of COPD
  • The definition Include chronic bronchitis
    ,emphysema with airflow limitation.
  • The definition exclude other causes of chronic
    airflow obstruction such as Pulmonary cystic
    fibrosis , diffuse panbronchiolitis and
    bronchiectasis etc.

4
COPD
  • Component part

5
Process of copd
  • Chronic Bronchitis ??????
  • Obstructive emphysema ??????
  • COPD airflow limitation
  • Pulmonary artery hypertension ?????
  • Col pulmonal heart disease ???

6
Chronic Bronchitis
7
Chronic Bronchitis
  • Chronic bronchitis is defined clinically as the
    presence of a cough productive of sputum not
    attributable to other causes on most days for at
    least 3 months over 2 consecutive years.
  • Clinical and epidemiological term

8
Chronic Bronchitis
  • Chronic nonspecific inflammation
  • Symptoms of cough and sputum production with or
    without gasping
  • Recurrent attacks
  • Chronic proceeding

9
Classification of Chronic Bronchitis
10
Stages of Chronic Bronchitis
11
Diagnosis of chronic bronchitis
  • Cough Sputum expectoration Gasping
  • Three months /per year or longer
  • Continuously longer than two years
  • Exclude other lung and heart disease
  • If shorter than three months /per year then
    definite objective evidences are demanded (such
    as X-Ray and lung function et al.)to diagnose.

12
Obstructive Emphysema
13
Definition of Emphysema
  • Pulmonary emphysema
  • (a pathological term)
  • is characterized by abnormal,permanent
    enlargement of air spaces distal to the terminal
    bronchioles ,accompanied by destruction of their
    walls and hyperdistension leading to reduction
    in lung elastics recoil and airway obstruction.

14
Classification of Emphysema
15
Risk factor for COPD
Genes Exposure to particles Tobacco smoke
Occupational dusts, organic and inorganic
Indoor air pollution from heating and cooking
with biomass in poorly vented dwellings
Outdoor air pollution Lung Growth and
Development Oxidative stress Gender/ Age/
Respiratory infections /Socioeconomic
status Nutrition Comorbidities
16
Pathogenesis of COPD
17
Pathogenesis
The inflammation in the respiratory tract of COPD
patients appears to be an amplification of the
normal inflammatory response of the respiratory
tract to chronic irritants such as cigarette
smoke. Inflammatory Cells Involve neutrophils,
macrophages, and lymphocytes. These cells
release inflammatory mediators and interact with
structural cells in the airways and lung
parenchyma. Inflammatory Mediators The
inflammatory mediators attract inflammatory
cells from the circulation (chemotactic factors),
amplify the inflammatory process (proinflammatory
cytokines), and induce structural changes (growth
factors).
18
Oxidative Stress Oxidative stress may be an
important amplifying mechanism in COPD. Oxidants
are generated by cigarette smoke and other
inhaled particulates, and released from activated
inflammatory cells such as macrophages and
neutrophils.
Protease-Antiprotease Imbalance Protease-mediated
destruction of elastin, a major connective tissue
component in lung parenchyma, is an important
feature of emphysema and is likely to be
irreversible.
19
Difference in inflammation between
COPD and asthma
Although both COPD and asthma are associated with
chronic inflammation of the respiratory tract,
there are marked differences in the inflammatory
cells and mediators involved in the two diseases,
which in turn account for differences in
physiological effects, symptoms, and response to
therapy .
20
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21
Pathology
Pathological changes characteristic of COPD are
found in the proximal airways, peripheral
airways, lung parenchyma, and pulmonary
vasculature. These changes include chronic
inflammation, and structural changes .
22
  • Proximal airways (trachea, bronchi gt 2 mm
    internal diameter)
  • Goblet cells, enlarged submucosal glands (both
  • leading to mucus hypersecretion), squamous
    metaplasia of epithelium
  • Peripheral airways (bronchioles lt 2mm i.d.)
  • Airway wall thickening, peribronchial fibrosis,
    luminal
  • inflammatory exudate, airway narrowing
    (obstructive bronchiolitis)
  • Increased inflammatory response and exudate
    correlated with disease severity.

23
  • Lung parenchyma (respiratory bronchioles and
    alveoli)
  • Alveolar wall destruction, apoptosis of
    epithelial
  • and endothelial cells.
  • Centrilobular emphysema dilatation and
    destruction of respiratory bronchioles most
    commonly seen in smokers
  • Panacinar emphysema destruction of alveolar
    sacs as well as respiratory bronchioles most
    commonly seen in alpha-1 antitrypsin deficiency

24
Normal distal lung acinus
25
Centriacinar(centrilobular) emphysema
26
Panacinar emphysema
27
  • Pulmonary vasculature
  • Thickening of intima, endothelial cell
  • dysfunction, smooth muscle
  • pulmonary hypertension.

28
PATHOPHYSIOLOGY
  • Airflow Limitation and Air Trapping
  • The inflammation, fibrosis, and luminal exudates
    in small airways is correlated with the
    reduction in FEV1and FEV1/FVC ratio.
  • The peripheral airway obstruction traps air
    during expiration,resulting in hyperinflation.
  • Emphysema is more associated with gas exchange
    abnormalities than with reduced FEV1.

29
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30
  • Gas Exchange Abnormalities
  • VA/Q imbalance
  • Reduced pulmonary vascular bed
  • Mucus Hypersecretion
  • Pulmonary Hypertension
  • Hypoxic vasoconstriction of small pulmonary
    arteries eventually result in structural changes
    that include intimal hyperplasia and later smooth
    muscle hypertrophy/hyperplasia.
  • The loss of the pulmonary capillary bed in
    emphysema may also contribute to increased
    pressure in the pulmonary circulation.
  • Progressive pulmonary hypertension may lead to
    right ventricular hypertrophy and eventually to
    right-side cardiac failure (cor pulmonale).

31
  • Systemic features
  • They have a major impact on survival and
    comorbid diseases.
  • Cachexia
  • a loss of skeletal muscle mass and weakness
  • increased likeliness of having osteoporosis,
    depression and chronic anemia.
  • Increased concentrations of inflammatory
    mediators,
  • including TNF-, IL-6, and oxygen-derived free
    radicals,
  • There is an increase in the risk of
    cardiovascular diseases.

32
Clinical Manifestation
  • History
  • History of exposure to risk factors,
  • Tobacco smoke.
  • Occupational dusts and chemicals
  • Smoke from home cooking and heating fuels.
  • Age of onset After middle age
  • Seasonwinter

33
Clinical Manifestation
  • Symptoms
  • Gradually progressive dyspnea is the most common
    presenting character.
  • Dyspnea that is
  • Progressive (worsens over time)
  • Usually worse with exercise
  • Persistent (present every day)
  • Described by the patient as an increased effort
    to breathe,heaviness, air hunger, or
    gasping.

34
  • Chronic Cough
  • May be intermittent and may be unproductive.
  • Chronic sputum production
  • Recurrent respiratory infection
  • Recurrent attacks leading to cor pulmonal
  • heart disease
  • Unexpected weigh loss
  • Decreased food appetite

35
  • Physical Signs
  • Earlier periodMinimal/Nonspecific signs
  • Advanced Stage
  • Inspection
  • Barrel-shaped chest ,
  • accessory respiratory muscle participate ,
  • prolonged expiration during quiet breathing.
  • Palpation
  • Weakened fremitus vocalis

36
Clinical Manifestation
Percussion Hyperresonant depressed
diaphragm, dimination of the area of absolute
cardiac dullness. Auscultation Prolonged
expiration reduced breath sounds The presence
of wheezing during quiet breathing Crackle can
be heard if infection exist. The heart sounds are
best heard over the xiphoid area.
37
Auxillary Examination
Chronic bronchitis
  • Chest Radiograph(X-Ray)
  • Non apparent abnormality
  • Or thickened and increased of the lung markings
    are noted.

38
Auxiliary Examination
  • Chest X-Ray --emphysema
  • Chest findings are also varible.
  • Marked over inflation is noted with flattend and
    low diaphragm
  • Intercostal space becomes widen
  • A horizontal pattern of ribs
  • A long thin heart shadow
  • Decreased markings of lung peripheral vessels

39
Chest X-Ray
40
Auxiliary Examination
  • Pulmonary function Test
  • Determination of a forced vital capacity and
    FEV1is necessary for the diagnosis and assessment
    of the severity of the disease and helpful in
    following its progress.
  • FEV1 /FVC is the best index of airflow
    obstruction?

41
Auxiliary Examination
  • Pulmonary function Test
  • diagnostic criteria
  • A post-bronchodilator
  • (FEV1)/forced vital capacity(FVC) 70
  • confirm the presence of airflow limitation
    that is not fully reversible.
  • FEV1 pred is used for evaluation of the
    severity of pulmonary function status.
  • The FEV1 and the FEV1/FVC ratio fall
    progressively as the severity of COPD increases.

42
Pulmonary function Test
  • Elevations of total lung capacity (TLC)
  • Functional reserve capacity(FRC)
  • Residual volume(RV)
  • RV/TLCgt40 for emphysema
  • Vital capacity (VC)
  • Peak expiratory flow(PEF)

43
spirometric classification of COPD
  • FEV1/FVC FEV1pred
  • mild lt70 80
  • moderate lt70 5080
  • severe disease lt70 3050
  • Very severe lt 70 30orlt50
  • following with
    respiratory failure
  • right heart
    failure



44
Auxiliary Examination
  • CT(Computed tomography) greater sensitivity and
    specificity for emphysema than CXR , especially
    for the diagnosis of bronchiectasis and
    evaluation of bullous disease

45
Computed Tomography
46
Labortory Examination
  • Blood examination
  • In excerbation or acute infection in airway,
    leucocytosis may be detected.
  • Sputum examination
  • ????? streptococcus pneumonia
  • ?????? Haemophilus influenzae
  • ????? Moraxella catarrhalis
  • ??????? klebsiella pneumonia

47
Auxiliary Examination
  • Blood gas analysis
  • Arterial blood gas analysis may reveal
    hypoxemia,particularly advanced disease.
  • In patients with severe hypoxemia ,CO2
    retention,it shows low arterial PO2 and high
    arterial PCO2.

48
Diagnosis of COPD
  • Clinical manifestation
  • Auxiliary examinations
  • Significant importance of Pulmonary function test
  • Spirometry should be obtained in all patients
    with
  • Exposure to cigarettes
  • Environmental or occupational pollutants
  • presence of cough ,sputum production or dyspnea

49
Stage
  • Exacerbation
  • Gradually progressive
  • Cough and sputum
  • Dyspnea and gasping
  • Increased
  • purulence sputum
  • followed by recurrent
  • respiratory infection.
  • Stable
  • Stable systoms of
  • Cough and sputum
  • ,gasping and dyspnea are alleviated.

50
Differential Diagnosis of COPD
  • Suggestive features
  • 1. Mid-life onset
  • 2. Slowly progressing symptoms
  • 3. Long history of smoking
  • 4.Dyspnea during exercise
  • 5.largely irreversible airflow limitation
  • 1.Early onset
  • 2. Symptoms vary from day to day
  • 3. Symptoms at the night/early morning
  • 4. A family history
  • 5. Airflow limitation that is largely reversible
  • 6.largely reversible airflow limitation
  • 7.Allergy,rhinitis,eczema
  • Diagnosis
  • COPD
  • Asthma
  • ---??

51
Differential Diagnosis of COPD
  • Diagnosis
  • Pulmonary carcinoma
  • - --??
  • Tuberculosis
  • ---???
  • Suggestive features
  • Commonly occurs in patients over 40 years old
  • with cigarette smoking.
  • Obvious radiological abnormality
  • Onset at all ages
  • Tuberculosis toxic syndrome
  • Lung infiltrate on chest radiography
  • Microbiological confirmation
  • Sputum examination of positive TB
    bacterium can confirms the diagnosis

52
Differential Diagnosis of COPD
  • Diagnosis
  • Bronchiectasis
  • ??
  • Non-obstructiveemphysema
  • Suggestive features
  • 1. Large volume of purulent sputum
  • 2. Commonly associated with bacterial infection
  • 3. Coarse crack/clubbing on auscultation
  • 4. Bronchial dilation and bronchial wall
    thickening on X-ray /CT
  • pulmonary function tests

53
  • Complication
  • chronic respiratory failure
  • Pneumothorax
  • Chronic pulmonary heart disease

54
TREATMENT
  • Aim
  • Based on the principles of
  • prevention of further progress of disease
  • preservation and enhancement of pulmonary
    functional capacity
  • avoidance of exacerbations in order to improve
    the quality of life.

55
TREATMENT
  • Stop smoking
  • Avoid environment pollution
  • Antibiotic therapy
  • Bronchodilators
  • Glucocorticoids
  • Expectorant
  • Respiratory stimulant
  • Oxygen therapy
  • Rehabilitation care
  • Lung volume reduction surgery

56
stable COPD(I)
avoid risk factors
  • Education and smoking cessation
  • Smoking cessation has the greatest capacity to
    influence the natural history of COPD.
  • Control the occupational and environmental
    pollution

57
stable COPD(II)
  • Drug therapy
  • Prevent and control symptoms ,
  • increase exercise capacity,
  • reduce the frequency and severity
  • of exacerbations ,
  • improve health status.

58
Drug Therapy
  • 1.Bronchodilators??????
  • Bronchodilators are central to the symptomatic
    management of COPD.
  • improve emptying of the lungs,reduce dynamic
    hyperinflation and improve
  • exercise performance .

59
Drug Therapy
  • Bronchodilators
  • Three major classes of bronchodilators
  • ß2 - agonists
  • Short acting salbutamol terbutaline
  • Long acting Salmeterol formoterol
  • Anticholinergic agents
  • Ipratropium,tiotropium
  • Theophylline (a weak bronchodilator, which may
    have some anti-inflammatory properties)

60
Drug Therapy
  • 2.Glucocorticoids
  • Regular treatment with inhaled glucocorticoids
    is appropriate for symptomatic patients with
    anFEV1lt50pred and repeated exacerbations.
  • Chronic treatment with systemic glucocorticoids
    should be avoided because of an unfavorable
    benefit-to-risk ratio.

61
  • 3. COMBINATION THERAPY
  • Combination therapy of long acting ß2-agonists
    and inhaled corticosteroids show a significant
    additional effect on pulmonary function and a
    reduction in symptoms.
  • Mainly in patients with an FEV1lt50pred

62
Drug Therapy
  • 4.Others
  • Antioxidant agents---????
  • Immunoregulators---?????
  • Vaccine---??
  • Traditional Chinese medicine---????
  • Alpha-1 antitrypsin augmentation
  • Mucolytic(mucokinetic,mucoregulator)
  • agents
  • Antitussives

63
Oxygen Therapy
  • Oxygen -- gt15 h /d
  • Long-term oxygen therapy (LTOT) improves
    survival,exercise,sleep and cognitive performance
    in patients with respiratory failure.
  • The therapeutic goal is to maintain SaO2
    90 and PaO2 60mmHg at sea level and rest .

64
Long-term Oxygen therapy LTOT
  • Indication
  • For patients with a
  • PaO2 55 mmHg or SaO288 ,
  • with or without hypercapnia
  • For patients with a
  • PaO2 of 5570(60)mmHg or SaO289 as well as
    pulmonary hypertension / heart failure /
    polycythemia (hematocrit gt55)

65
  • Pulmonary rehabilitation
  • Nutrition
  • Surgery
  • Bullectomy
  • Lung volume reduction surgery(???)
  • Lung transplantation (???)

66
Manage exacerbation
  • Identify the cause of exacerbation
  • Virus or Bacteria or Other uncertain reasons
  • Assessment of severity
  • The proceeding history and disease must be
    considered and comparison is very important.

67
Oxygen therapy
Controlled oxygen therapy. Supplemental oxygen
should be titrated to improve the patients
hypoxemia. Adequate levels of oxygenation (PaO2 gt
8.0 kPa, 60 mm Hg, or SaO2 gt 90) are easy to
achieve in uncomplicated exacerbations, but
CO2 retention can occur insidiously with little
change in symptoms. Once oxygen is started,
arterial rrr blood gases should be checked 30-60
minutes later to ensure satisfactory oxygenation
without CO2 retention or acidosis.
68
Bronchodilators Increase dose and times
properly Atomization and inhalation
Glucocorticoids Oral or intravenous
glucocorticosteroids are recommended. Thirty to
40 mg of oral prednisolone daily for 7-10 days is
effective and safe.
69
  • Antibiotics
  • Respiratory infection is the usual predisposing
    factor.
  • It is advocated to select antibiotics
    according to culture of sputum and
    drug-sensitivity test.
  • Mechanical Ventilation
  • Noninvasive mechanical ventilation
  • Invasive mechanical ventilation
  • Others

70
Chronic Pulmonary Heart Disease
  • Respiratory Department
  • Renji Hospital

71
DEFINITIONS
  • Enlargement of the right ventricle (RV)
  • due to pulmonary artery hypertension
  • which arises from structural or functional
  • abnormalities of the lungs, chest wall
    ,vascular.

RV FAILURE
72
  • Cor pulmonale may be
  • acute or chronic.
  • The most common cause of acute cor pulmonale
  • --- thromembolism
  • The most common cause of chronic cor pulmonale
  • ---copd

73
Bronchial
pulmonary diseases The main diseases chronic
bronchitis,
copd,(8090) Others asthma,
bronchiectasis,
pulmonary fibrosis,sarcoidosis Severe thoracic
deformity cause
compression of the lung
Aetiology
74

Aetiology
  • Pulmonary vascular diseases
  • primary pulmonary hypertention
  • pulmonary embolism
  • Neuromuscular disorder


75
PATHOLOGY
  • Primary lung
  • Chronic bronchitis pulmonary emphysema
  • Pulmonary vessel
  • 1. Stenosis of pulmonary artery thicken of
    the vessel wall
  • 2. Loss and fracture of the alveolar capillary
  • 3. Distortion of the pulmonary vascular bed

76
PATHOLOGY
  • Heart
  • Increase of the heart weight
  • Thicken of the heart muscle
  • The enlarged right ventricle

77
????????,?????
Cor pulmonale
78
  • PATHOPHYSIOLOGY
  • Pulmonary arterial hypertension?????
  • 1. Structural

Smooth muscular thickening
of the smaller arteries Anatomic
reduction of the vascular bed Pulmonary
vascular remodeling--?????
79
  • PATHOPHYSIOLOGY
  • Pulmonary arterial hypertension
  • 2. Functional

Pulmonary vasoconstriction secondary to
alveolar hypoxia, acidosis, and hypercapnia.
1.humoral factor???? 2.tissue
factor---???? 3.nerve factor---????
80
PATHOPHYSIOLOGY
  • Pulmonary arterial hypertension

3. The increase of pulmonary blood flow ,
blood volume and blood viscosity?
(caused by polycythemia secondary to

hypoxia.)
81
PATHOPHYSIOLOGY
  • Failure of right ventricle
  • Pulmonary hypertension
  • Myocardial anoxia
  • Repeatedly pulmonary infection
  • effect of bacterial toxin to the heart
  • Acid base disorder
  • arrhythmia

82
  • Clinical Manifestation
  • Historial information varies with
  • the underlying
    etiology.
  • For COPD patient
  • Productive cough and dyspnea, wheezing
  • Breathlessness limits the patient's ability .
  • Dyspnea and cardiopalmus after movement
  • A history of emergency hospital admissions
    because of

  • respiratory infection.
  • Dyspnea on exertion is the most common
  • presenting manifestation of pulmonary
  • hypertension.

83
Clinical Manifestation
Physical examination
  • Compensation period
  • For copd
  • Pulmonary arterial hypertension signs
  • (S3) and a systolic murmur of tricuspid
    regurgitant
  • P2gtA2
  • a right ventricular parasternale impulse

84
Clinical Manifestation
  • Decompensation period
  • Physical examination
  • Respiratory failure
  • Respiratory infection is the usual predisposing
    factor .
  • Clinical manifestation hypercapnia and hypoxia
  • Such as dyspnea,cyanosis,increase in heart
    rate,peripheral
  • venous dilation.
  • Sweaty and nero-psychiatric symptoms (
    headaches,
  • letharfy,exciation,delirium,tremor,t
    ic,papilloedema,etc).
  • .

85
Clinical Manifestation
  • Physical examination
  • Right ventricular failure
  • Tachynea,
  • elevated jugular venous pressure,
  • right ventricular parasternum impulse
  • hepatomegaly,
  • peripheral edema
  • positive hepatojugular reflux
  • total cardia failure with arrhythmia

86
X-Ray Diagnostic Criteria
  • (I) Distension of the low right pulmonary artery
    trunk
  • Diameter transversa gt15mm
  • Or diameter transversa (right hyop-
  • pulmonary artery /trachea) gt1.07
  • Or widen gt2mm(compare to the
  • primary right pulmonary artery trunk)
  • (II) Midrange projecture of pulmonary artery
    trunk
  • or the altitude 3mm

87
X-Ray Diagnostic Criteria
  • (III) Significant projecture of the conus
  • portion 7mm
  • (IV) Enlargement of the main pulmonary
  • artery,rapid tapering of pulmonary
    arterial branches toward lung periphery
  • Right ventricle enlarged
  • Various pulmonary parenchymal,pleural,and/
    or thoracic abnormalities dependent on underlying
    etiology of cor pulmonale.
  • One item can be diagnosed.

88
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89
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90
Electrocardiogram Diagnostic Criteria
  • Main Conditions
  • Mean QRS axis gt?90?
  • Vl R/S1
  • Marked clockwise rotation of the electric axis(V5
    R/S 1)
  • P-pulmonary pattern (an increase in P-wave
    amplitude )
  • RV1?SV5gt1.05mV
  • aVR R/S or R/Q1 (except for myocardial
    infarction)
  • V1-3 QS?Qr?qr pattern

91
Electrocardiogram Diagnostic Criteria
  • Secondary Conditions
  • Low-voltage ORS in Limb lead
  • Right bundle-branch block (Incomplete or rarely
    complete)
  • One item in main condition can be diagnosed
  • Two or more than two items in secondary condition
    is to suspect.

92
Echocardiogram Diagnostic Criteria
  • Main Conditons(I)
  • Internal diameter of right ventricular outflow
    tract 30mm
  • Right ventricular internal dimension 20mm
  • The thickeness of right ventricular anterior wall
    5.0mm
  • Left/right ventricular internal dimension lt2

93
Echocardiogram Diagnostic Criteria
  • Main Conditons(II)
  • Internal dimension of right pulmonary artery
    18mm or pulmonary artery trunk 20mm
  • Right ventricular outflow tract/internal
    dimension of left atrium gt1.4
  • Pulmonary artery hypertension signs(low a-wave
    lt2mm) or midsystolic closure

94
Echocardiogram Diagnostic Criteria
  • Reference conditions
  • Interventricular septal thickness 12mm
  • Pulsation altitude lt5mm or paradoxical motion
  • Right atrium enlarged 25mm
  • Curve DE EF of anterior tricuspid leaflet
    accelerate
  • E-peak sharp AC period prolong .
  • Low curve amplitude of anterior leaflet of mitral
    valve ,CElt18mmCD section slowly upgrade and
    prolong as horizontal positionEF rate of decay
    lt90mm/s

95
Echocardiogram Diagnostic Criteria
  • Notice
  • The diagnostic criteria is only fit for the
    Detection Position of praecordium
  • Patient who has lung or chest disease,could be
    diagnosed if he or she has two items above
  • (including one main condition at least)

96
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97
Auxiliary Examination echocardiogram Arterial
blood gases Analysis of blood
98
Diagnosis
  • Chronic respiratory disease or thoracic cage
    disease
  • Pulmonary arterial hypertension
  • Right ventricular hypertrophy or dilatation
  • Right heart insufficienacy
  • Other reason heart diseases must be ruled out

99
Differential Diagnosis
  • Coronary artery disease ---???
  • Angina cordis, Myocardial infarction history
  • Left ventricular hypertrophy (EKG)
  • Rheumatic heart disease---??????
  • History echocardiogram
  • Myocardial disease ---??????
  • Without chronic respiratory disease
  • Echocardiogram
  • The total heart enlarged

100
  • Complication
  • Pulmonary encephalopathy
  • Acid-base disorder and electrolyte disturbances
  • Shock
  • DIC
  • Arrhythmia
  • Gastrointestinal hemorrhage

101
Treatment
  • Acute exacerbation period
  • Antibiotics
  • Respiratory insufficiency therapy
  • Airway Management
  • (Oxygen,Bronchidilator
    ,secretion clean)
  • Respiratory stimulant
  • Mechanical ventilation
  • Acid-base imbalance and electrolyte disturbance

102
Treatment(I)
  • Acute exacerbation period
  • Therapeutic principle of heart failure
  • Antibiotics most important
  • Oxygen
  • low concentration and careful administration
    are essential to avoid depressing respiratory
    drive and causing hypercapnea.
  • Bronchodilator
  • can reduce the effort of breathing and
    decrease dyspnea.
  • beta-adrenergic stimulants, theophylline
    compounds

103
Treatment(II)
  • Diuretic agent
  • low dose ,short course
  • Cardiant
  • Low dose,fast effect, quick metabolism
  • Hypoxemia,acidosis and catecholamine
    excess
  • can increase the adverse effects of
    digitalis.
  • indications
  • left heart failure
  • Infection has been controlled and diuretic
    agent has been used,heart failure still exist
  • Right heart failure without severe infection
  • Cardiac arrhythmia

104
Vasodilating agentControl the arhythmia
Corticosteroids The value is depend on the
likely responsiveness of the underlying
ventilatory functional abnormality.Others
prevent complication
105
Treatment(III)
  • Compensation
  • Breath training
  • Elevate the power of resistance
  • Chinese medicine and immunoenhancer
  • Improve nutritional status
  • Home oxygen therapy
  • Long term oxygen therapy is indicated for
    patients with persistent arterial hypoxemia at
    rest or after exercise (arterial oxygen tension
    consistently below 55mmHg while breathing room
    air.

106
Treatment
  • Preventive measure
  • Prevent respiratory infection
  • Physical exercise
  • Environmental health
  • Stop smoking
  • Lung function monitoring

107
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