sesak napas arimbi ( pbl )
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Sesak Napas Arimbi ( PBL )TRANSCRIPT
DYSPNEA¶
dr. Arimbi, Sp.PFK UWK Surabaya
Introduction
Discomfort feeling inbreathing Subjective and difficult to measure Etiology: lung, hearth, endocrine,
kidney, neurology, hematology, rheumatology and phsycology
Prevalence of dyspnea: no accurate data
Definition of Dyspnea
The America Thoracic Society ( ATS ): The term of discomfort perception
subjective in breathing that consist of sensation with different intensity as a results of interaction of various phsycology, social and enviromental factors.
Mechanism of Dyspnea
Interaction between signal and receptor in otonomic nerve system, motoric cortex, airway receptor, lung and thoracic cage.
Dyspnea
Emotion
Cognitive
Behavior
Complex of
breathing
Lung & Thorax cage
Primary motoric cortex
Primary Sensory cortex
Exercise
Chemoreceptor
stimulant
Mechanism of Dyspnea
Pathophysiology of dyspnea
Heightened ventilatory demand Respiratory muscle
abnormalities Abnormal ventilatory
impedance Abnormal breathing patterns Blood-gas abnormalities
Causa of Dyspnea
1. Respiratory dyspnea – a. Inspiratory dyspnea
b. Expiratory dyspnea c. Mixed dyspnea
2. Cardiac dypnea –a. Left Hearth Failure a.1. Ortopnea
a.2.PND b. Right Hearth failure
3. Toxic dyspnea - metabolic / Poisson4. Hematologi dissorder dyspnea5. NeuroPsichogenic dissorder dyspnea
Respiratory Dyspnea (1)
Caused by abnormal ventilation and gas exchange, reduction in ventilatory capacity, hypercapnia and hypoxemia resulting from respiratory disease.
Three clininal types: Inspiratory dyspnea
Expiratory dyspnea
Mixed dyspnea
Inspiratory Dyspnea (1a)
Tends to occur primarily when there is
obstruction ( such as inflammation,
edema, tumor and foreign body) in
larynx, trachea and major bronchi.
Characterized by the depression sigh, in
which visible indrawing over the sternal
notch, the supraclavioular spaces, the
intercostal spaces and the epigastrium
in the inspiration can be seen.
Often accompanied by a coarse, low
pitched inspiratory wheezing and dry
cough.
Expiratory Dyspnea (1b)
Expiratory dyspnea is due to the decrease of lung elasticity and spasm / narrowing of the bronchioles and smaller bronchi as in emphysema, bronkhitis, bronchial asthma.
Expiration is prolonged and laboured with wheezing.
Mixed Dyspnea (1c)
Occurs with the extensive lung disease, such as severe pneumonia, pulmonary fibrosis, massive atelectasis, pleural effusion and pneumothorax.
Results in the decrease of ventilators and gas exchange capacity.
Breathing is difficult during both inspiration and expiration.
Cardiac Dyspnea (2)
Cardiac dyspnea is usually
attributable to pulmonary
vascular congestion
resulting from the left
and/or right heart failure.
Cardiac dyspnea (2a)
In Left-sided heart failure, compliance is reduced, and therefore, ventilation is decreased to the edematous lung regions and vital capacity reduced. Alveoli are stiff and more work is needed to overcome elastic recoil, the high alveolar pressure will stimulate stretch receptor and initiate the inflation reflex resulting in early turning off of inspiration and an increase in respiratory rate.
Cardiac dyspnea (2b)
The dyspnea caused by right-sided heart failure is less severe than that one caused by left-sided.
Mechanism: (1) The pressure of right atrial
and superior vena cava is the natural stimulus of respiratory center. (2) The decrease of oxygen content and the accumulation
of the acid metabolites, such as lactic, stimulate
respiratory center. (3) The restriction of the respiratory
movement caused by enlargement of liver resulting
from congestion, ascites and pleural effusion.
Cardiac dyspnea
Symptoms of congestive heart failure
can cause
orthopnea and paroxysmal nocturnal
dyspnea
when elevated-filling pressure is present.
Orthopnea (2a.1)
Orthopnea is difficulty in
breathing in the supine position,
this may be relived by sitting up,
which reduces the degree of
pulmonary congestion by
pooling blood in the lower
extremities and lowering left
ventricular filling pressures,
improving the diaphragmatic
movement, increasing vital
capacity.
Paroxysmal Nocturnal Dyspnea (2a.2)
Symptoms: The patient awakes short of breath at night, but often obtain relief by sitting up for a period of time. In the most advanced cases, the patients become acutely dyspneic, cyanotic and very frequently produce foamy sputum tinged with blood.
Signs: Moist rales at the both lung bases, tachycardia, wheezing and bronchospasm, the markedly accentuated second heart sound in the pulmonic area.
Paroxysmal nocturnal dyspnea (2a.2)
Mechanism: Supine posture for sleep results in resorbtion of extracellular fluid into the intravascular space, causing arise in filling pressure.
The paroxysmal dyspnea is termed as cardiac asthma. It can be seen in the hypertensive heart disease and coronary heart disease.
Toxic dyspnea (3)
In the metabolic acidosis (uremia and diabetic ketosis), the acid metabolites stimulate the respiratory center, causing deep and regular respiration with snoring.
The overdose of morphine and pentobarbital can depress respiratory center causing deep respiration or Cheyne-Stokess respiration
1. Paroxysmal dyspnea with wheezing.
2. Dyspnea with chest pain.
3. Dyspnea with fever.
4. Dyspnea with cough and purulent sputum.
5. Dyspnea with coma.
Various Accompanied Symptom of dyspnea
It is present in bronchial asthma and cardiac asthma. Paroxysmal severe dyspnea is often seen in acute larynx edema, foreign body in bronchi, massive pulmonary embolism, and spontaneous pneumothorax.
Paroxysmal dyspnea with wheezing (1)
It is frequently observed in lobar pneumonia, pulmonary infarction, spontaneous pneumothorax, acute exudative pleurisy / dry pleurisy, acute myocardial infarction, and bronchial carcinoma.
Dyspnea with chest pain (2)
It is commonly noted in pneumonia, lung abscess,
pulmonary tuberculosis, pleurisy, acute pericarditis,
and nervous system diseases.
Dyspnea with fever (3)
It is often present in chronic bronchitis, emphysema
with infection, purulent pneumonia, and lung abscess.
Dyspnea with large amount of foamy sputum is often
seen in acute left ventricular heart failure / Pulmonary edema and Organophosphorus
poisoning.
Dyspnea withcough and purulent sputum (4)
It suggests Cerebral hemorrhage, Meningitis,
Pneumonia with shock, Uremic lung / CKD, Diabetic Ketoacidosis / KAD , and acute
poisoning.
Dyspnea with coma (5)
Cause of dyspnea ( location )
Lower airway:-Pulmonary edema-Asthma / COPD-Pleural Efusion -Pneumothorax-Pneumonia
Cardiac:-Decomp cordis-Acute MI -Cardiomyopathy-Pericarditis-Arrythmia
Upper airway:-Foreign body obstruction-Pharyngeal edema-Epiglotidis- Croup
Dyspnea in upper airway (1)
• Foreign body obstruction ( Partial or complete, cause of pediatric airway obstruction )
• Pharyngeal edema• Epiglottitis• Croup
Foreign Body obstruction
Partial / total Obstruction Most common cause pediatric airway
obstruction Suspect in any child with:
- Suddent onset of dyspnea- Decreased loss of conciuosness
Suspect in any adult who develops dyspnea or losses concioucness while eating
Pharyngeal edema Swealling of soft tissue of throat Allergic reaction, upper airway burns Hoarseness, stridor and drooling
Epiglotidis Bacterial infection Cause edema of epiglotis Children age 4 – 7 years Increasingly common in adult Rapid onset, high fever, stridor,
sorethroat and drooling
Croup
Laryngotracheobronkhitis Viral infection Cause edema of larynx / trachea Children ages 6 moth – 4 years Slow onset, hoarseness, brassy
cough, nightime stridor, dyspnea. When in doubt, manage as
Epiglottitis
Dyspnea in Lower airway (2)
1. Abnormality of breathing mechanism, lung became more stiff, weakness of ventilation muscles
2. Restritive lung disease3. Obstructive lung disease4. Disturbance of lung diffusion5. Disturbance of lung perfusion
Restrictive Lung Disease
• Lung Atelectasis
FibroticLung
TumourBullaeLung
Abcess• Mediastinal
Mediastinal Tumour
CardiomegalyPericardial
Effusion
Restrictive Lung Disease
• Pleura Pleural EffusionPleural TumourPneumothorax
• Diafragma Hernia of Diafragma
Paralize of Diafragma
• Bone Rib fracturePectus excavatumScoliosis, Kyphosis
Obstructive lung disease
• Asthma• COPD Chronic
Bronkhitis
Emphysema• Bronchiectasis• Carcinoma
Bronchogenic• Foreign Body
Diffusion • Alveolar
wall• Interstitial
Space• Arterial wall• Plasma• Red blood
cell wall
Perfusion • Pulmonary
Emboly• Congestive
Hearth Failure
Disturbance of lung
Asthma ( 1 )
Reversible obstruction pulmonary disease Younger person disease ( 80% have first
episode before 30 years ) Lower airway hypersensitive to allergen,
emotional stress, irritant and infection Bronkhospasm Bronkhial edema Increase mucus product and plugging Resistant to airflow, Work of breathing
increase
Asthma ( 2 )
Airway narrowing interferes with exhalation Air trappinng in chest interferes with gas
exchange Wheezing, coughing and respiratory
distress All that wheezes is not Astma Other possibilities:
- Pulmonary edema- Pulmonary embolism- Anaphilaxtic ( severe allergent reaction )- foreign body aspiration- Pneumonia
COPD Prone to periodes of “
decompensation “ Trigger by respiratory infection,
chest trauma Sign / symptom:
- Respiratory distress - Tachypnea
- Cough productive of green or yellow sputum
There are: - Chronic Bronkhitis ( Blue bloater ) - emphysema ( Pink Puffer )
Chronic Bronchitis
Chronic lower airway inflamation- Increased bronchial mucus product- Productive cough
• Urban male smoker > 30 years old• Mucus, swelling interfere with
ventilation• Increased CO2, decreased O2
• Cyanotic occurs early in disease• Lung disease overwork right
ventricle• Right hearth failure occurs• RHF product periferal edema
Emphysema Loss of elasticity of small airway
Destruction of alveolar wall Urban, male, smoker > 40-50 yars
olds Lungs lose of elastic recoil Retan CO2, maintain near normal
O2 Cyanotic occure late in disease Barrel chest ( increase AP
diameter ) Thin, wasted Prolonge exhalation throught
pursed lips
Alveolar Function Problem (1)
( Pulmonary edema )
Fluid in / around alveoli , small airway Cause: LVH, toxic inhalant, aspiration,
drowning, trauma Sign / symptom:
- Labored breathing’- Coughing- Rales, ronchi- Wheezes, pink frothy sputum- Sit up, hight concent O2- Assist ventilation
Alveolar Function Problem (2)
( Pulmonary edema )
Clot from venous circulation Passed trought right hearts Lodges in pulmonary circulation Shut of blood flow past part of alveoli Sign / symptom: dyspnea, chespain,
tachypnea, tachycardi,haemoptisis
Sudden dyspnea + no readily identifiable cause
= Pulmonary Embolism
ATS Dyspnea Scale
Grade 1 : No dyspnea except severe exercise activity
Grade 2: Dyspnea when climb the step in hurry or climb a small hiil
Grade 3: Walk slower compound to common people
Grade 4: Must stop for brething after 100 yard walk
Grade 5: Dyspnea while put or off the clothes
Evaluation Dyspnea
Critical aspect for patients evaluation and management, by :
1. History, physical examinations, laboratorium & Röntgen
2. Exercise performance 3. Questionnaires relating to exercise tolerance4. Questionnaires relating Quality of Life (QOL)
and dyspnea 5. Rating the symptom of dyspnea
Assessment (1)
History:1. Persistence or variability of the symptom
( intermittent, persistent, or progressive)2. Aggravating or precipitating factors
( activity, timing, position, exposures, eating )
3. Actions or medications effective in decreasing the symptom
Assessment (2)
Physical examinations: Pattern of breathing ( kussmaul,
cheyne-stokes, use of pursed lips or accessory muscle )
Body habitus ( cachexia, obesity, barrel chest )
Posture ( leaning forward on elbow )
Skeletal deformity Emotional state Clubbing finger Edema of the lower extremities
Assessment (3)
Other examinations: Laboratory ( anemia, polycythemia, BGA, ESR ) Chest X-ray, CT scan thorax Spirometry, bronchial challenge/provocation
test Skin prick test, Eos count, Ig E ( allergic
condition ) Electrocardiography, echocardiography Otolaryngologic assessment Sleep studies Psychologic assessment
Assessment (4)
Exercise performance: 6 minutes walk Cycle ergometryQuestionnaires relating to exercise
tolerance: American Thoracic Society Scale Baseline Dyspnea IndexQuality of Life and Dyspnea: Chronic Respiratory Disease
QuestionnairesRating symptom of dyspnea: Borg scale Visual analogue scale
Treatment
* Symptomatic treatment of dyspnea / medical
* Reduce sense of effort and improve respiratory muscle function ( Rehabilitation )
- Energy conservation ( pacing ) - Breathing strategies ( pursed-
lips breathing ) - Position ( leaning forward ) - Correct obesity or malnutrition - Inspiratory muscle exercise - Respiratory muscle rest - Medications ( theophylline )
Conclusion
Dyspnea is subjective symptom Various abnormality may cause
dyspnea Severity of dyspnea can be measure
COUGH¶
dr. Arimbi,Sp.P
FK UWK Surabaya
Introduction
Cough is not a common occurrence in healthy people.
Cough present and persistent Clinical problems. It can be an important defense mechanism.It can be an important factor in the spread of
infection.It is one of the most common symptoms for which patients seek medical attention.
Function of Cough
* To prevent foreign material from entering the
lower respiratory tract.* To clear foreign material and excessive
secretions from the lower respiratory tract.
Mechanism of cough* Phase inspiration:
Deep inspiration before cough* Phase Compressive :
Glottis anb bronkhus close* Phase Expulsive :
Then the glottis opens, allowing expiratory airflow a forced expiration. Expiratory muscles contract increase pleural, abdominal, and alveolar pressures to a level of > 100 mm Hg.
Cough can be initiated
* Involuntarily. Involuntary coughing to be entirely a vagal phenomenon
Innervated by the vagus nerve and its branches. These include: the lower part of the oropharynx, the larynx, and the lower respiratory tract, as well as tympanic membrane and the external auditory meatus.
Irritation at all these sites can cause coughing. * Voluntarily
Cough is not mediated by vagally reflex. Cough is the only one defensive reflex mechanism that we can mimic voluntarily and accurately. We can also inhibit it voluntarily.
Cough divided
* Acute Cough ( lasting less than 3 weeks )
Acute cough can be transient and of minor consequence
Such as ( severe attack of Asthma, Acute lung edema, Pneumonia, Pulmonary
embolism, and Aspiration, the viral or bacterial upper respiratory tract
infections, Allergic rhinitis, and Environmental irritant rhinitis )
* Sub acute cough ( 3 – 8 weeks )
* Chronic cough ( lasting 8 weeks or more )
Such as : Postnasal drip syndrome (PNDS) secondary to rhinosinus conditions,
Asthma, Gastro-esophageal reflux disease (GERD), Chronic bronchitis or
Bronchiectasis, Chronic infections like Pulmonary TB, Carcinoma, and cough
induced Angiotensin-Converting Enzyme Inhibitor.
Evaluation of cough• History ( cough, smoking cessation, or
discontinuation of the ACEI )• Physical examination• Laboratory, such as:
- Chest / sinus roentgenogram
- Allergic evaluation (PNDS)
- Spirometry before and after bronchodil / methacholine challenge (Asthma)
- Modified barium esophagography / 24-hour esophageal PH ( GERD )
- Acid-fast bacilli sputum smear ( Pulmonary TB )
- Flexible bronchoscopy ( carcinoma bronchogenic / endobronchial TB )
- Chest computed tomographic scan ( ca- bronchogenic, pulmonary tumour )
- Noninvasive cardiac studies
- Blood CD4 lymphocyte count (immunocompromised patients)
Treatment of cough (1)
1. Antitusif Controls, prevents or eliminate cough
2. Protusif makes cough more effective Antitusif :
- Directed at the cause or the presumed operant pathophysiologic mechanism of a particular disorder.- Decreased sensitivity sensoric receptor- Decreased frekwency cough
- There are 2 anti tusive: * Antitusif perifer ( H1-antihistamin ) * Antitusif sentral ( Codein )
Treatment of cough (2)
a. Antihistamin : - First generation of Antihistamin is
more effective - Non sedation
- Anticolinergic activity- Central penetration more effecttives
b. Codein - Best and powerfull antitusive ( until
now )
Treatment of cough (3)
Protusif / mucolitic - Increase mucus ekspektoration
- Decrease mucus viscocity - Effectivity cough depent on: mucocilliary
clearance, closed of glottis, FEV1 > 1l/mnt, and mucus viscocity - There are: Carbocystein, Bromhexine, Gliceril Guaicolat