DYSPNEA

dr. Arimbi, Sp.P FK 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

Mechanism of Dyspnea
Interaction between signal and

receptor in otonomic nerve system, motoric cortex, airway receptor, lung and thoracic cage.

Mechanism of Dyspnea
Emotion Cognitive Behavior

Dyspnea
Chemoreceptor stimulant

Primary motoric cortex

Complex of breathing

Primary Sensory cortex

Exercise

Lung & Thorax cage

Pathophysiology of dyspnea
Heightened ventilatory

demand Respiratory muscle abnormalities Abnormal ventilatory impedance Abnormal breathing patterns

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 / Poisson 4. Hematologi 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

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

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
Cardiac

(2)

dyspnea is usually

attributable to pulmonary vascular congestion resulting from the left and/or right heart failure.

Cardiac dyspnea
In Left-sided heart failure,

(2a)

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

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,

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,

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

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

Various Accompanied Symptom of dyspnea

1. Paroxysmal dyspnea with wheezing.
2. Dyspnea with chest pain. 3. Dyspnea with fever. 4. Dyspnea with cough and purulent sputum.

Paroxysmal dyspnea with wheezing (1) 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.

Dyspnea with chest pain (2)

It is frequently observed in lobar pneumonia, pulmonary infarction, spontaneous pneumothorax, acute exudative pleurisy / dry pleurisy, acute myocardial infarction, and bronchial carcinoma.

Dyspnea with fever (3)

It is commonly noted in pneumonia, lung abscess, pulmonary tuberculosis, pleurisy, acute pericarditis, and nervous system diseases.

Dyspnea with cough and purulent sputum (4)

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 /

Dyspnea with coma (5)

It suggests Cerebral hemorrhage, Meningitis, Pneumonia with shock, Uremic lung / CKD, Diabetic Ketoacidosis / KAD , and acute poisoning.

Cause of dyspnea ( location )

Upper airway:Lower airway: -Foreign body-Pulmonary obstruction edema -Pharyngeal -Asthma / edema COPD -Epiglotidis -Pleural - Croup Efusion -Pneumothora x -Pneumonia Cardiac: -Decomp cordis -Acute MI -Cardiomyop athy -Pericarditis -Arrythmia

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 disease 3. Obstructive lung disease 4. Disturbance of lung diffusion 5. Disturbance of lung perfusion

Restrictive Lung Disease

Atelectasis Fibrotic Lung Tumour Bullae Lung Abcess Mediastinal Mediastinal Tumour Cardiomegaly
Lung

Restrictive Lung Disease

Pleura

Pleural

Effusion
Pleural Tumour Pneumothorax Diafragma Hernia of Diafragma Paralize of Diafragma Bone Rib fracture

Obstructive lung disease

Asthma COPD

Chronic

Bronkhitis Emphysema Bronchiectasis Carcinoma Bronchogenic Foreign Body

Disturbance of lung

Diffusion Alveolar wall Interstitial Space Arterial wall Plasma Red blood cell

Perfusion Pulmonary Emboly Congestive Hearth Failure

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

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

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 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

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

( Pulmonary edema )

(1)

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

( Pulmonary edema )

(2)

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

Evaluation Dyspnea
Critical aspect for patients evaluation and management, by : 1. History, physical examinations, laboratorium & Rntgen 2. Exercise performance 3. Questionnaires relating to exercise tolerance 4. Questionnaires relating Quality of Life (QOL) and 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

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

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

Assessment

(4)

Exercise performance: 6 minutes walk Cycle ergometry Questionnaires relating to exercise tolerance: American Thoracic Society Scale Baseline Dyspnea Index Quality of Life and Dyspnea: Chronic Respiratory Disease Questionnaires Rating symptom of dyspnea: Borg 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

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

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

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.

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,

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 )

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 )

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