Hendarsyah Suryadinata, dr., SpPD

Hendarsyah Suryadinata, dr., SpPD
Tempat/Tanggal Lahir : Bandung, 24 November 1977 Pekerjaan : Departemen Ilmu Penyakit Dalam Divisi Respirologi dan Respirasi Kritis Jabatan : Staff Departemen Ilmu Penyakit Dalam RSHS Bandung

Hendarsyah Suryadinata
Management of Dyspnea Hendarsyah Suryadinata Divisi Repirologi dan Kritis Respirasi Departemen/SMF Ilmu Penyakit Dalam FK Unpad/RSUP Dr Hasan Sadikin Bandung

Dyspnea on Effort (DOE)
Exertion-induced SOB Orthopnea Recumbent-induced SOB Paroxysmal nocturnal dyspnea (PND) Sudden SOB after recumbent Sever breathness at night relieved when patient sits up

Dyspnea Rapid Assessment ABC’s Mental status Presence of cyanosis

D Dyspnea Initial Interventions IV assess
Pulse oximetry; supplemental O2 Cardiac monitor

What Are the Indications for Airway Management?
Secure & maintain patency Protection Oxygenation Ventilation Treatment – Suction, medications

Dyspnea : History Prolonged questioning can be counterproductive
Yes/No questions if significantly dyspneic Unlike pain, severity of dyspnea = severity of disease What does patient mean by SOB? How long has SOB been present? Is it sudden or gradual Does anything make it better or worse?

Has there been similar episodes? Are there associated symptoms?
Dyspnea : History Has there been similar episodes? Are there associated symptoms? What is the past medical Hx? Smoking Hx? Medications?

Cause : Acute Bronchial asthma Pneumonitis Pneumonia Pneumothorax Thromboembolic disease Cardiac Pulmonary Edema Non Cardiac Pulmonary Edema Psychogenic

Cause : Chronic Pulmonary Cause COPD Bronchial Asthma Emphysema Chronic Bronchitis Restrictive Lung Disease Sarcoidosis Rheumatoid lung fibrosing alveolitis Pneumoconosis

Dyspnea : Etiologies

Dyspnea Etiologies: Pulmonary Causes

Dyspnea Common Pulmonary Causes
Obstructive lung disease Asthma/COPD Pneumonia Pulmonary embolism Pneumothorax

Dyspnea Etiologies: Nonpulmonary Causes

Dyspnea Common Cardiac Causes
Acute coronary syndromes CHF Dysrhythmias Valvular heart disease

Dyspnea Common Miscellaneous Causes
Metabolic acidemias Severe Anemia Pregnancy Hyperventilation Syndrome

Pulmonary Diseases & Disorders
Pulmonary Disease & Conditions may result from: Infectious causes Non-Infectious causes Adversely affect one or more of the following Ventilation Diffusion Perfusion

The Respiratory Emergency may stem from dysfunction or disease of (examples only): Control System Hyperventilation Central Respiratory Depression CVA Thoracic Bellows Chest/Diaphragm Trauma Pickwickian Syndrome Guillian-Barre Syndrome Myasthenia Gravis COPD

The Respiratory Emergency may affect the upper or lower airways Upper Airway Obstruction Tongue Foreign Body Aspiration Angioneurotic Edema Maxillofacial, Larnygotracheal Trauma Croup Epiglottitis

Lower Airway Obstruction Emphysema Chronic Bronchitis Asthma Cystic Fibrosis

The Respiratory Emergency may stem from Gas Exchange Surface Abnormalities Cardiogenic Pulmonary Edema Non-cardiogenic Pulmonary Edema Pneumonia Toxic Gas Inhalation Pulmonary Embolism Drowning

Dyspnea Physical Examination: Vital Signs
BP  if dyspnea significant  = life-threatening problem Pulse Usually  Bradycardia - severe hypoxemia Respiratory rate Sensitive indicator of respiratory distress DANGER = > bpm or < bpm

Dyspnea Physical Examination: Observation
Ability to speak Patient position Cyanosis Central vs. peripheral (Acrocyanosis) Mental status Altered MS - Hypoxemia/Hypercapnia

Dyspnea Physical Examination
Pulmonary Use of accessory muscles Intercostal retractions Abdominal-thoracic discoordination Presence of stridor Cardiac Check neck for presence of JVD Signs of severe respiratory distress

Dyspnea Physical Examination: Pulmonary
Inspection Use of accessory muscles Splinting Intercostal retractions Percussion Hyper-resonance vs. dullness Unilateral vs. bilateral

Dyspnea Physical Examination: Pulmonary
Auscultation Air Entry Stridor = Upper Airway Obstruction Breath sounds Normal Abnormal Wheezing, Rales, Rhonchi, etc. Unilateral vs Bilateral

Dyspnea Physical Examination: Cardiac
Neck JVP ? Auscultation Abnormal S2 splitting Present of S3 and/or S4 Rubs Murmurs

What does clubbing suggest? Chronic Hypoxemia

Pneumonia Fever with Chill Pleuratic Chest Pain Purulent Sputum History of Upper Respiratory Symptoms Signs of Consolidation CXR CBC Blood Culture BGA

Pneumonia Inflammation of the bronchioles and alveoli
Products of inflammation (secretions, pus) add to respiration difficulty Gas exchange is impaired Work of breathing increases May lead to Atelectasis Sepsis V/Q Mismatch Hypoxemia

Pneumonia: Etiology Viral Bacterial Fungi Protozoa (pneumocystis)
Aspiration

Management of Pneumonia
Treatment mostly based upon symptoms Oxygen Rarely is intubation required IV Access & Rehydration B2 agonists may be useful Antibiotics Antipyretics

Pneumonia: Management
MD follow-up for labs, cultures & Rx Transport considerations Elderly have significant co-morbidity Young have difficulty with oral medications ED vs PMD office/clinic Transport in position of comfort

Acute Bronchial Asthma
Age Start in Young Age Family History H/O Allergic Rhinitis Physical Examination Barrel Shape CXR BGA

Asthma: Signs and Symptoms
Onset of attacks associated with “triggers” Dyspnea Non-productive cough Tachypnea Expiratory wheezing Accessory muscle use Retractions

Asthma : Signs and Symptoms
Absence of wheezing IMPENDING RESPIRATORY ARREST!

Lethargy, confusion, suprasternal retractions RESPIRATORY FAILURE

Early Blood Gas Changes Decreased PaO2 Decreased PaCO2 WHY?

Later Blood Gases Decreased PaO2 Normal PaCO2 IMPENDING RESPIRATORY FAILURE

Still Later Blood Gases Decreased PaO2 Increased PaCO2 RESPIRATORY FAILURE

Asthma : Management Airway Breathing
Sitting position or position of comfort Humidified O2 by NRB mask Dry O2 dries mucus, worsens plugs Encourage coughing Consider intubation, assisted ventilation Impending respiratory failure Avoid if at all possible

Obtain medication history Consider
Asthma : Management Circulation IV TKO Assess for dehydration Titrate fluid administration to severity of dehydration Trial bolus of 250 cc Monitor ECG, Pulse Oximetry Obtain medication history Consider Overdose Dysrhythmias

Nebulized Beta-2 agents Nebulized anticholinergics
Asthma : Management Nebulized Beta-2 agents Salbutamol Nebulized anticholinergics Ipratropium Atropine IV Corticosteroid Methylprednisolone Combination

Magnesium Sulfate (IV) Methylxanthines
Asthma : Management Rarely used Questionable efficacy, Potential Complications Magnesium Sulfate (IV) Methylxanthines Aminophylline (IV)

COPD : Management Causes of Decompensation
Respiratory infection (increased mucus production) Chest trauma (pain discourages coughing or deep breathing) Sedation (depression of respirations and coughing) Spontaneous Pneumothorax Dehydration (causes mucus to dry out)

TRUE HYPOXIC DRIVE IS VERY RARE
COPD: Management Airway and Breathing Sitting position or position of comfort Calm & Reassure Encourage cough Avoid exertion Oxygen Don’t withhold Maintain O2 saturation above 90 % TRUE HYPOXIC DRIVE IS VERY RARE

COPD: Management Ventilation Circulation
Avoid intubation unless absolutely necessary Near respiratory failure Exhaustion Circulation IV TKO Titrate fluid to degree of dehydration 250 cc trial bolus Excessive fluid may precipitate CHF Monitor ECG

COPD : Management Drug Therapy Obtain thorough medication history
Nebulized Beta 2 agonists Albuterol Terbutaline Metaproterenol Isoetharine

COPD : Management Drug Therapy Ipratropium (anticholinergic) by SVN
(Beta-2 agonist) by MDI, SQ or IV Corticosteroids (Anti-inflammatory agent) by IV

Pneumothorax Suden Chest Pain Dyspnea, Cough H/O Asthma COPD Examination  Trachea, Shifted to Opposite side, Absent Breath Sound CXR

Acute Pulmonary edema Previous H/O Heart Disease Hyperthyroidism
Rheumatic Heart Disease  MS Sign of LVF Tachycardia Pulses alternant Basal Criptation/Fine Crackles ECG Change CXR ( cardiomegaly) Echo

Pulmonary Edema High Pressure (Cardiogenic)
AMI Chronic HTN Myocarditis High Permeability (Non-Cardiogenic) Poor perfusion, Shock, Hypoxemia High Altitude, Drowning Inhalation of pulmonary irritants

Cardiogenic Pulmonary Edema: Etiology
Left ventricular failure Valvular heart disease Stenosis Insufficiency Hypertensive crisis (high afterload) Volume overload Increased Pressure in Pulmonary Vascular Bed

Non-Cardiogenic Pulmonary Edema: Etiology
Toxic Inhalation Near Drowning Liver Disease Nutritional Deficiencies Lymphomas High Altitude Pulmonary Edema Acute Respiratory Distress Syndrome Increased Permeability of Alveolar-Capillary Walls

Pulmonary Edema: Signs &Symptoms
Dyspnea on Exertion Paroxysmal Nocturnal Dyspnea Orthopnea Noisy, Labored Breathing Restlessness, Anxiety Productive Cough (Frothy Sputum) Rales, Wheezing Tachypnea Tachycardia

Management of Non-Cardiogenic Pulmonary Edema
Position Oxygen PPV / Intubation CPAP PEEP IV Access; Minimal fluid administration Treat the underlying cause Diuretics usually not helpful; May be harmful Transport

Acute Respiratory Distress Syndrome
AKA: Non-Cardiogenic Pulmonary Edema A complication of : Severe Trauma / Shock Severe infection / Sepsis Bypass Surgery Multiple Blood Transfusions Drug Overdose Aspiration Decreased Compliance Hypoxemia

Pulmonary Embolism History of Prolonged Imobilization Pelvic Surgery Contraceptive Pills Cyanosis ECG CXR BGA Echo V/Q Study

Pulmonary Embolism A disorder of perfusion
Combination of factors increase probability of occurrence Hypercoagulability Platelet aggregation Deep vein stasis Embolus usually originates in lower extremities or pelvis

Pulmonary Embolism Risk factors Venostasis or DVT
Recent surgery or trauma Long bone fractures (lower) Oral contraceptives Pregnancy Smoking Cancer

Management Based on Severity of Sx/Sx Airway & Breathing
Pulmonary Embolism: Management Management Based on Severity of Sx/Sx Airway & Breathing High Concentration O2 Consider Assisting Ventilations Early Intubation Circulation IV, 2 Large Bore Sites Fluid Bolus then TKO; Titrate to BP ~ 90 mm Hg Monitor ECG Rapid transport

Rapid transport to appropriate facility
Pulmonary Embolism: Management Thrombolytics Aspirin & Heparin Rapid transport to appropriate facility Embolectomy or thrombolytics at hospital (rarely effective in severe cases due to time delay) Poor prognosis when cardiac arrest follows

IV Heparin vs Low Molecular Weight Heparin (LMWH)
Pulmonary Embolism: Management IV Heparin vs Low Molecular Weight Heparin (LMWH) IV Un-fractionated (UF) Heparin: Hypotension, massive PE, RF units/kg bolus over 10 minutes Infusion 20 units/kg/h Maintain Prothrombin time (PTT) seconds Oral or LMWH follow up to Heparin LMWH Dosing: For hemodyanamically stable pts Enoxaparin > 2mo/age: 1mg/kg SQ BID < 2mo/age: 1.5 mg/kg SQ daily Reviparin > 5kg: 100 U/kg SQ BID

Pleurisy Inflammation of pleura caused by a friction rub
Layers of pleura rubbing together Commonly associated with other respiratory disease

Presentation of Pleurisy
Sharp, sudden and intermittent chest pain with related dyspnea Possibly referred to shoulder May  or  with respiration Pleural “friction rub” may be audible” May have effusion or be dry

Pleurisy Management Based upon severity of presentation
Mostly supportive

Laryngotracheobronchitis (Croup)
Common syndrome of infectious upper airway obstruction Viral Infection Parainfluenza Virus Subglottic Edema Larynx, Trachea, mainstem bronchi Usually 3 months to 4 years of age

Croup: Management Usually requires little out of home treatment Calm & Prevent agitation Moist cool air - mist Humidified O2 by mask or blowby Do Not Examine Upper Airways

If in respiratory distress:
Croup: Management If in respiratory distress: Racemic epinephrine via nebulizer Decreases subglottic edema (temporarily) Necessitates transport for observation for rebound IV TKO - ONLY if severe respiratory distress Transport

Epiglottitis Bacterial infection (Hemophilus influenza ) Edema of epiglottis (supraglottic) partial upper airway obstruction Typically affects 3-7 year olds

Epiglottitis: Management
Immediate life threat (8-12% die from airway obstruction) Do NOT attempt to visualize airway Allow child to assume position of comfort AVOID agitation of the child AVOID anxiety of the healthcare providers O2 by high concentration mask

Epiglottitis: Management
If respiratory failure is eminent: IV TKO ONLY if eminent or respiratory arrest Be prepared to take control of airway Intubation equipment with smaller sized tubes Needle cricothyrotomy & jet ventilation equipment Rapid but calm transport Appropriate facility

Upper Respiratory Infection
Common illness Rarely life-threatening Often exacerbates underlying pulmonary conditions May become more significant in some patients Immunosuppressed Elderly Chronic pulmonary disease

Usually requires no intervention
Management of URI Usually requires no intervention Oxygen if underlying condition has been exacerbated Rarely, pharmacologic interventions are required Bronchodilators Corticosteroid

Hyperventilation Syndrome

A diagnosis of EXCLUSION!!! An increased ventilatory rate that DOES NOT have a pathologic origin Results from anxiety Remains a real problem for the patient

Hyperventilation Syndrome: Pathophysiology
Tachypnea or Hyperpnea secondary to anxiety Decreased PaCO2 Respiratory alkalosis Vasoconstriction Hypocalcemia Decreased O2 Release to Tissues

Hyperventilation Syndrome : Signs & Symptoms
Light-headedness, giddiness, anxiety Numbness, paresthesias of: Hands Feet Circumoral area Cold hands, feet Carpopedal spasms Dyspnea Chest pain

Hyperventilation Syndrome : Signs & Symptoms
Rapid breathing Cool & possibly pale skin Carpopedal spasm Dysrhythmias Sinus Tachycardia SVT Sinus arrhythmia Loss of consciousness and seizures (late & rare)

Hyperventilation Syndrome : Management
Educate patient & family Consider possible psychopathology especially in “repeat customers” Transport occasionally required If loss of consciousness, carpopedal spasm, muscle twitching, or seizures occur: Monitor EKG IV TKO Transport

Serious diseases can mimic hyperventilation Hyperventilation itself can be serious

Central Respiratory Depression

Respiratory Depression : Causes
Head trauma CVA Depressant drug toxicity Narcotics Barbiturates Benzodiazepines ETOH

Respiratory Depression : Recognition
Decreased respiratory rate (< 12/min) Decreased tidal volume Decreased LOC Use Your Stethoscope Look, Listen, Feel THEY PROBABLY AREN’T If you can’t tell whether a patient is breathing adequately...

Respiratory Depression : Management
Airway Open, clear, maintain Consider endotracheal intubation The need to VENTILATE is not the same as the need to INTUBATE

Respiratory Depression: Management
Breathing Oxygenate, ventilate Restore normal rate, tidal volume Oxygen alone is INSUFFICIENT if Ventilation is INADEQUATE

Respiratory Depression: Management
Circulation Obtain vascular access Monitor EKG (Silent MI may present as CVA) Manage Cause Check Blood Sugar Consider Narcan 2mg IV push if S/S suggest narcotic overdose Intubate if can not find or treat cause

Guillian-Barre´ Syndrome
Autoimmune disease Leads to inflammation and degeneration of sensory and motor nerve roots (de-myelination) Progressive ascending paralysis Progressive tingling and weakness Moves from extremities then proximally May lead to respiratory paralysis (25%)

Guillian-Barre´ Syndrome Management
Treatment based on severity of symptoms Control airway Support ventilation Oxygen Transport in cases of respiratory depression, distress or arrest

Causes loss of ACh receptors at neuromuscular junction
Myasthenia Gravis Autoimmune disease Causes loss of ACh receptors at neuromuscular junction Attacks the ACh transport mechanism at the NMJ Episodes of extreme skeletal muscle weakness Can cause loss of control of airway, respiratory paralysis

Myasthenia Gravis Presentation
Gradual onset of muscle weakness Face and throat Extreme muscle weakness Respiratory weakness -> paralysis Inability to process mucus

Myasthenia Gravis Management
Treat symptomatically Watch for aspiration May require assisted ventilations Assess for Pulmonary infection Transport based upon severity of presentation Plasmapharesis

Thank You !

Hendarsyah Suryadinata, dr., SpPD

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