sesak napas arimbi ( pbl )

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