Learning on approach to breathlessness.pptx

about all causes of breathlessness

1. Approach to breathlessness (dyspnea) Prepared by : Fatin Ilyana

2. Introduction Dyspnea is a subjective feeling of difficulty in breathing Not all cases of dyspnoea are caused by cardiorespiratory pathology. Metabolic causes also may manifest primarily with acute dyspnoea. Elderly patients / Patients with DM may manifest dyspnoea as the presenting complain with/without chest pain.

3. anatomy of respiratory system Right lungs has 3 lobes, left has 2 lobes Covered by a connective tissue called pleura. Acts as a cushion and also a line of defense for the lungs. Muscles involved in respirations : Diaphragm, intercoastal muscles, sternocleidomastoid and abdominal muscles. Blood supply of the lungs is dual : Deoxygenated blood and oxygenated blood coming form the pulmonary artery and pulmonary vein respectively. Nerve supply to the lung : Coming from both parasympathetic and sympathetic fibres arising from vagus nerve and sympathethic chain. No innervation to the visceral pleura

4. Pathophysiology Hypoxia - Insufficient delivery of oxygen at tissue level Hypoxemia - Abnormally low arterial oxygen tension [PaO2 < 60mmHg Mechanisms - Hypoxemia Hypoventilation - Hypoxemia from hypoventilation always associated with raised Pco2. Two possible factors [low inspired oxygen level, decrease in minute ventilation] Right to Left shunt - Blood that enters the systemic circulation without traversing ventilated lung/Intracardiac shunt. Variety of pathologies such as consolidation, atelectasis and vascular malformations. Ventilation-Perfusion mismatch - Regional alteration of either ventilation or perfusion can affect the gas exchange which results in hypoxemia. Pathologies such as pulmonary embolism, pneumonia, reactive airway disease. Diffusion impairment - Mainly depends on the alveolar-capillary barrier.

5. 55 year old male, dropped at ED entrance by son. Patient’s son went to park the car and was not available for about 30 min. Patient was tachypnoiec , RR 52/min . Primary triage triaged the patient to Red zone/Resus. How to approach this patient?

6. Clinical examination Vital signs - Bp, Hr, Oxygen saturation, Temperature, Pain score Airway - Any signs of upper / lower airway obstruction (Stridor, wheezing, angioedema - swelling of lips, periorbital, tongue/hoarseness of voice ) Breathing - Respiratory rate [ Tachypnea ] / Recruitment of accessory muscles, Speaking in sentences, phrases, words / Central or peripheral cyanosis / Tripod position or pursed lips / Lung Auscultation Circulation - Pulse ~ Rate, volume, rhythm / CRT / Peripheries Disability - GCS status, Altered mental status, Confusion, Restless

7. Cardiovascular - Raised JVP, S3 Heart sound, Systolic/Diastolic murmur, Pitting pedal oedema Respiratory – Rhonchi / Bibasal crepitations / Focal crepitation / Reduce Breath sound/ Tracheal shift Renal - AV Fistula / Pallor / Bilateral Pitting oedema over lower limb / Uraemic frost Clinical examination

8. FOCUSED HISTORY TAKING Age/Demographic details Smoking history Baseline ADL Compliance To medications Details of dyspneoa should be elicited. Recent History of trauma/Fall Recent Travel history --> MERS Pet exposure Possible psychiatric illness [Diagnosis of exclusion]*

9. INVESTIGATIONS Investigations will be primarily guided by the history and physical examinations. Bedside Investigation:

10. INVESTIGATIONS

11. INVESTIGATIONS Imaging : Chest X-ray Point of care ultrasound

12. Bronchial Asthma Asthma is a chronic inflammatory disorder characterized by variable airway obstruction with recurrent or chronic wheeze / cough It is characterized by bronchial hyper-responsiveness and variable airflow obstruction, that is often reversible either spontaneously or with treatment.

13. pathogenesis

14. ASTHMA MANAGEMENT

15. Chronic obstructive pulmonary disease Is defined as a preventable and treatable disease characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases.

16. Risk factors Genes Exposure to particles - Tobacco smoke - Occupational dust, organic and inorganic - Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings - Outdoor air pollution Lung growth and development Oxidative stress Gender Age Respiratory infections Socioeconomic status Key features to make diagnosis of COPD: Chronic cough Chronic sputum production Dyspnea : progressive and worsening with time Hx of exposure to risk factors

17. investigations Full blood count Chest X ray ABG ECG Spirometry post bronchodilator Exercise test

18. Initial pharmacotherapy GROUP E LABA + LAMA Consider LABA + LAMA + ICS if blood eos > 300 GROUP A Bronchodilator GROUP B LABA + LAMA

19. Heart failure DEFINITION : Clinical syndrome which develops when the heart cannot maintain adequate output, or can do so only at the expense of elevated ventricular filing pressure. In mild to moderate cases, CO is normal at rest and is impaired when metabolic demand increases during exercise or some form of stress. Most commonly, HF is due to myocardial dysfunction- either systolic, diastolic, or both. However, pathology of the valves, pericardium, and endocardium, and abnormalities of heart rhythm and conduction can also cause HF. Etiology of HF MUST BE IDENTIFIED in order to reverse/control the condition

20. HF can be classified according to: Phenotypes. These descriptions may reflect the: - Temporal characteristics (e.g., acuteness, chronicity) - Affected circulatory systems (e.g., left vs right) - Clinical context and trajectory (e.g., decompensated, improved, advanced, end-stage) . Stages of HF : A - “At Risk” B - “Pre HF” C - “Symptomatic HF with previous or current symptoms” D - “Advanced HF” The severity of symptomatic HF and the exercise capacity of the patient can be assessed using the New York Heart Association (NYHA) functional Class (Table 9, page 50).

21. Pathophysiology Starling’s Law. It’s not HF until the afterload is reduced. When there’s reduced afterload, the sympathethic system is activated causing peripheral vasoconstriction(raise preload) , increased inotrope and chronotrope activity to compensate.(increase afterload) Prolonged stimulation causes the negative effects : Myocyte apoptosis, hypertrophy, focal myocyte necrosis

22. Etiology The common underlying causes of HF in adults are: Coronary artery disease (CAD) Hypertension Dilated cardiomyopathy-idiopathic, familial Valvular heart disease Diabetic cardiomyopathy Comorbidities are common and include hypertension, diabetes, and dyslipidemia.

23. DIAGNOSIS 1. Identify etiology 2. Is ventilation and perfusion adequate? History : SOB, ACS ssx , previously known diseases, edematous , raised JVP, NYHA Bloods : proBNP (In patient with no apparent ssx ), identify risk factors ECG : LVH patterns ECHO : Dilated/hypertrophy, EF CXR : Features of HF

24. Acute Heart Failure Managements Phase Based Management : Phase 1 - Urgent treatment and stabilization in ED Phase 2 - In ward Management Phase 3 - Discharge and Post discharge “vulnerable” period Phase 1 Rapid recognition and identifying the signs and symptoms HF is crucial + Identify the possible provoking cause as well Assess the Haemodynamic status of the patient --> Mainly identify any evidence of shock or Hypoperfusion/Congestion

25. Acute Heart Failure Managements Treat the precipitating factors for the Acute HF -- “CHAMPION” C - Coronary artery disease H - Hypertensive emergency A - Arrhythmias M - Mechanical causes [Valvular heart disease] P - Pulmonary embolism/Pneumonia I - infections O - Other medications N - non-compliance to therapy/Non-compliance to fluid overload

26. Warm and Wet - Adequate perfusion but congested (lungs and/or periphery). Cold and Dry - Hypoperfusion* and dehydrated/not congested**. Cold and Wet - Hypoperfusion* and congested** (lungs and/or periphery). Warm and Dry - Adequate perfusion and dehydrated/not congested.** These patients have either mild HF or are in the compensated stage of HF. Hypoperfusion: cold peripheries, capillary refill time more than 2 seconds, diaphoresis, oliguria, dizziness, confusion, narrow pulse pressure, hypotension. Congestion: peripheral edema, orthopnoea , paroxysmal nocturnal dyspnea, lung crepitations, jugular venous dilatation, positive hepatojugular reflux, congested hepatomegaly, gut congestion, ascites. Most patients admitted with Acute HF are in the ‘wet-warm’ category. The goal of therapy is to make them ‘dry-warm’- optimal perfusion and fluid status.

27. HYPERVENTILATION SYNDROME Hyperventilation attack/syndrome - Diagnosis of exclusion [Can achieved with proper history and physical examination without extensive investigations] Precipitated by a stressor - stressful event Symptoms – Numbness, cramping of hands and feet, perioral tingling, non specific dizziness, sensation of suffocation, near-syncope, chest tightness Management : - Provide reassurance - Advise on the breathing techniques

28. SUMMARY Step-wise approach is essential Focussed History and Clinical assessment is crucial Not to miss metabolic causes/Drug toxicity - Salicylates Hyperventilation syndrome is a diagnosis of exclusion Pathologies with Normal breath sound and Equal air entry: DKA/Pulmonary embolism

29. REFERENCES Pulmonary Physiology for Pre-clinical Students Guide to the Essentials in Emergency Medicine 2nd Edition Tintinallis Emergency Medicine

30. THANK YOU