Apprenticeship: Dyspnoea & Respiratory Conditions | PDF

Dyspnoea and Respiratory Conditions AAP Apprenticeship Learner Outcomes For the learning outcomes that are associated with this presentation please refer to the AAP Apprenticeship Learner Outcome: Dyspnoea and Respiratory Conditions Respiratory Assessment Respiratory Asse...

Dyspnoea and Respiratory Conditions AAP Apprenticeship Learner Outcomes For the learning outcomes that are associated with this presentation please refer to the AAP Apprenticeship Learner Outcome: Dyspnoea and Respiratory Conditions Respiratory Assessment Respiratory Assessment What are the elements of a medical patient assessment? What breathing assessments should be undertaken as part of the Primary Survey ? Respiratory Assessment From your general impression of the patient what features would suggest abnormal respiratory function? How should respiratory rate be obtained? What ‘normal’ breathing characteristics be expected an adult? Recap: Primary Survey – B Expose the chest and assess respiratory rate and depth as well as effectiveness of respiration. Look for: Cyanosis or pallor peripherally and centrally Adequacy of chest movement Symmetry of chest movement Inspect the chest anteriorly and posteriorly Recap: Primary Survey – B Cyanosis, anaemia or pallor is more difficult to detect in people with darker skin tones. Look for central cyanosis around the lips and inside the mouth. Peripheral cyanosis is usually seen in the hands or feet and may occur with or without central cyanosis. In anaemia the conjunctiva may appear to be pale pink or white, regardless of the patient’s skin tone. In patients with darker skin tones there may be reduced darkness in the palmar creases, although this sign alone cannot be used. Recap: Primary Survey – B Feel for: Any instability of the chest wall and note any areas of tenderness. Note depth and equality of chest movement. Feel the chest anteriorly and posteriorly where achievable. Recap: Primary Survey – B Auscultate altered breathing patterns with a stethoscope What are the landmarks for auscultation? Recap: Primary Survey – B Record oxygen saturations Normal range is 94-98%, or 88-92% for patients with COPD (unless patient’s documentation says it is normal for them) SpO2 40 (Children 1 – 5) Heart rate: – >110 (adults) – >125 (children >5) – >140 (children 1 – 5) Inability to complete a sentence in one breath. Severities of Asthma cont… Moderate exacerbation Able to speak in sentences. Increasing symptoms: dyspnoea, wheeze. Peak expiratory flow (PEF) >50-75% best or predicted. No features of acute severe asthma. Heart rate ≤140/min children 1–5, ≤125/min in children >5. Respiratory rate ≤40/min in children 1–5, ≤30/min in children >5 Mild: Below best level of functioning due to wheeze. PEF >75% best or predicted. No features of moderate or acute asthma. Asthma Assessment and Management For the Assessment and Management of asthma please refer to the AAP Scope of Practice and the following JRCALC Plus App guideline: Medical / Asthma in Adults and Children Within YAS, Paramedics can administer Prednisolone for mild/moderate Asthma, and Prednisolone/Hydrocortisone for severe/life threatening Asthma. They can also administer Adrenaline 1:1000 for life threatening Asthma. Consider Critical Care support for Severe / Life threatening presentations Key Points Asthma is a common life-threatening condition. Its severity is often not recognised. Accurate documentation is essential. A silent chest is pre-terminal. Paramedics have additional drug therapies that can benefit management of asthma exacerbations.  Chronic Obstructive Pulmonary Disease (COPD) Chronic Obstructive Pulmonary Disease (COPD) What is COPD? Introduction COPD is a chronic progressive disorder characterised by airflow obstruction. The two main COPD conditions are Emphysema and Chronic Bronchitis. It is estimated that approximately 3 million people in the UK have COPD – affecting 2-4% of the population; however, only 1.5% are diagnosed. Patients with COPD usually present with an exacerbation of their underlying condition. Some patients with severe COPD have an individualised care plan to assist in their care. Pathophysiology Emphysema Destruction of alveolar wall by enzymes leading to permanently enlarged air spaces beyond terminal bronchioles. Loss of surface area for gas exchange. Lack of support for other surrounding structures, such as small bronchi, which can lead to collapse and further obstruction of airflow during expiration. Causes of Emphysema Cigarette smoking is implicated in most cases, however a genetic pre-disposition can contribute to early onset of the disease in non-smokers. Normal lungs Exposure to other air pollutants also contributes to developing the disease. The other main cause is hereditary protein deficiency. Smoker’s lungs Chronic Bronchitis Inflammation and narrowing of bronchioles. Increased mucus secretions. Inhibition of cilia. Accumulation of secretions. Bronchoconstriction. Chronic productive cough. Chronic Bronchitis Causes of Chronic Bronchitis Patients usually have a history of cigarette smoking or living/working in an urban industrialised area. A prolonged exposure to inhaled irritants leads to inflammation and recurrent infections, starting the cycle. Exacerbation of COPD Patients usually call for an ambulance during an infective exacerbation (sudden worsening) of their COPD. There is no single feature that defines an exacerbation. Some exacerbations are mild and self-limiting, whilst others are more severe, potentially life-threatening, and require intervention. Alert Cards and Care Plans Why should the information on alert cards and care plans be considered in the treatment and management of patients with COPD? Features of an acute exacerbation Increased dyspnoea Increased sputum production/ purulence (containing pus) Increased cough Increased wheeze Chest tightness Reduced exercise tolerance Fluid retention Increased fatigue Acute confusion Worsening of a previously stable condition Severe features of an acute exacerbation Marked dyspnoea Tachypnoea Pursed-lips breathing Use of accessory muscles Acute confusion New-onset cyanosis New-onset peripheral oedema Marked reduction in activities of daily living Conditions with similar features to COPD Some conditions may present with similar conditions to an exacerbation of COPD (see below). Consider these when diagnosing an exacerbation of COPD: Asthma Pneumonia Pneumothorax LVF PE Lung cancer Upper airway obstruction Pleural effusion Recurrent aspiration  COPD Assessment and Management For the Assessment and Management of COPD please refer to the AAP Scope of Practice and the following JRCALC Plus App guideline: Medical / Chronic Obstructive Pulmonary Disease Salbutamol and Ipratropium Bromide must always be administered separately. These drugs must not be mixed together in the nebulising chamber under any circumstance  Hypercapnic respiratory failure (HCRF) HCRF (also known as Type 2 respiratory failure) occurs when the oxygen level of arterial blood (PaO2) is low, and the carbon dioxide level (PaCO2) is high. The majority of patients who present with an acute exacerbation of COPD will not be at risk of HCRF and, when assessing these patients, SpO2 Scale 1 should be used to calculate a NEWS score. Scale 2 must only be used when there is documented evidence that states the patient is at risk of HCRF. All patients should be managed according to JRCALC guidelines irrespective of which SpO2 scale is used. PARI mini air driven portable nebuliser Refer to YAS Standard Operating Procedure: PARI mini® Air-Driven Portable Nebuliser for Preparation and Usage Guidance PARI mini air driven portable nebuliser The Trust is no longer able to procure these devices due to manufacturer discontinuation. Consequently, not every frontline vehicle will be equipped with one. If patients with COPD require nebulised Salbutamol or Ipratropium, and an air driven nebuliser is not available, they should be treated as per JRCALC guidelines using an oxygen driven nebuliser with a maximum nebulisation time of 6 minutes. Consider Sepsis Exacerbations of COPD predominantly arise from an infective origin. Therefore it is important to consider sepsis as a differential diagnosis. For the Assessment and Management of sepsis please refer to the AAP Scope of Practice and the following JRCALC Plus App guideline: Medical / Adult Sepsis Screening Tool Pulmonary Embolism (PE) Pulmonary Embolism What is a pulmonary embolism (PE)? Pulmonary Embolism A pulmonary embolism is a blood-borne substance, such as a clot, which reduces or obstructs blood flow through the pulmonary vessels. Affecting approximately 21 per 10,000 per annum. PE can be life threatening, leading to death in 7-11% of cases. However, treatment is effective if given early.  Causes of PE Over 70% of PEs originate from deep leg veins (deep vein thrombosis - DVT) and most deaths occur within the first hour after symptoms develop. Early DVT The blockage causes an infarction, which usually involves a part of the lung and the pleural membrane in that area. PEs that block moderate sized arteries usually cause respiratory impairment. Late DVT Predisposing Factors The risk factors for developing a venous thromboembolism are well known and can help to identify patients who may have a PE. Medical / Pulmonary Embolism / Introduction Presentation PEs usually present as one of four types: 1. Multiple small pulmonary emboli – Characterised by progressive breathlessness more commonly identified at outpatient appointments than through emergency presentation due to the long- standing nature of the problem. 2. Segmental emboli with pulmonary infarction – May present with pleuritic pain and/or haemoptysis but with little or no cardiovascular compromise. Presentation continued… 3. Major pulmonary emboli obstruction of the larger branches of the pulmonary tree – May present with sudden onset of shortness of breath with transient rise in pulse and/or fall in blood pressure. Often a precursor to a massive PE. 4. Massive pulmonary emboli – Often presenting with loss of consciousness, tachypnoea and intense jugular vein distension, and may prove immediately or rapidly (within 1 hour) fatal or unresponsive to cardiopulmonary resuscitation. Signs and Symptoms PE can present with a wide range of signs and symptoms The presence of predisposing factors should increase the index of suspicion of PE PE Assessment and Management For the Assessment and Management of pulmonary embolism please refer to the AAP Scope of Practice and the following JRCALC Plus App guideline: Medical / Pulmonary Embolism (The Wells Criteria can be used to assess the probability of a PE; however, a low score cannot rule out a PE and further investigation is required.) Take a defibrillator at the earliest opportunity to a patient with dyspnoea and keep with the patient until handover (JRCALC) Assessment and Management Clinically stable patients may be suitable for assessment at a Same Day Emergency Care (SDEC) facility according to local pathways, providing the 4 hours timeline can be met. Medical / Pulmonary Embolism Pneumonia Introduction Pneumonia is an infection of the terminal bronchioles and alveoli. It is more common in the elderly and during the winter months. Results from a bacterial or viral infection. Pneumonia can develop secondary to aspiration or other airway infections (i.e. influenza). However, in the majority of cases, people catch pneumonia from inhaled pathogens. Pneumonia can be community or hospital acquired. Pathophysiology Inflammation and oedema cause the alveoli to fill with fluid and blood cells (red and white). This is known as consolidation. Consolidation disrupts external respiration. Signs and Symptoms Dyspnoea Fever with or without rigors Cough (often productive of green, blood-stained or rusty coloured sputum) Pleuritic chest pain Muscle or joint pain Assessment Findings Upon assessment may also find the following signs: High temperature (pyrexia) Increased respiratory rate (tachypnoea) Increased heart rate (tachycardia) Crackles or bronchial breath sounds (rhonchi) on auscultation Reduced SpO2 Pneumonia Assessment and Management For the Assessment and Management of Pneumonia please refer to the AAP Scope of Practice and the following JRCALC Plus App guideline: Medical / Dyspnoea Consider the potential for Sepsis. Take a defibrillator at the earliest opportunity to a patient with dyspnoea and keep with the patient until handover (JRCALC) Pneumothorax Pneumothorax The presence of air in the plural cavity separating the plural membranes. What are the two pleural layers called and what is found between them? Pathophysiology Spontaneous - No obvious causal factor. Traumatic - External cause. Atelectasis - Partial or complete collapse of lung. Open - Communication between atmospheric and pleural space. Tension – Increasing intra-pleural pressure causing worsening of lung collapse. Signs and Symptoms Signs and symptoms can include: Dyspnoea (usually sudden onset). Chest pain (non-specific, often pleuritic). Reduced breath sounds. Signs and Symptoms Additionally, in Tension Pneumothorax, the following may be noted: Chest wall may be moving poorly or not at all on the affected side, while appearing over expanded. Hyper-resonant to percussion. Distended neck veins. Later, tracheal deviation and cyanosis. Tachycardia and hypotension. Difficulty in manual ventilation. Cardiac arrest. Pneumothorax Assessment and Management For the Assessment and Management of pneumothorax please refer to the AAP Scope of Practice and the following JRCALC Plus App guideline: Medical / Dyspnoea  Pneumothorax Assessment and Management For the Assessment and Management of pneumothorax with a history of trauma please refer to the AAP Scope of Practice and the following JRCALC Plus App guideline: Trauma / Thoracic Trauma Request a Paramedic for patients presenting with signs and symptoms of a tension pneumothorax, as they can attempt needle thoracocentesis to temporarily reduce the pressure Hyperventilation Syndrome (HVS) Introduction Common pre-hospital presentation. Defined as ‘a rate of ventilation exceeding metabolic needs and higher than that required to maintain normal plasma carbon dioxide levels’. Hyperventilation can occur in a range of life-threatening conditions including: PE, Diabetic Ketoacidosis, Asthma and Hypovolaemia. Always assume that hyperventilation is secondary to hypoxia, or another underlying respiratory or metabolic disorder, until proven otherwise. Hyperventilation Syndrome is a diagnosis of exclusion Pathophysiology The cause of HVS is unknown, but it is hypothesised that stress may result in an exaggerated respiratory response. Stressors include psychological distress and caffeine. Other causes include elevated levels of CO2. Over breathing results in decreased level of CO2 in the blood, causing respiratory alkalosis and resulting in a number of signs and symptoms. Clinicians are required to undertake a comprehensive history, physical assessment and rule out all other possible diagnoses and red flags. Be aware of the possibility of unconscious bias where the patient has a history of anxiety. Signs and Symptoms For signs and symptoms of HVS by body system, please refer to: Medical / Hyperventilation Syndrome 4. Pathophysiology. Table 3.69 HVS Assessment and Management For the Assessment and Management of HVS please refer to the AAP Scope of Practice and the following JRCALC Plus App guideline: Medical / Hyperventilation Syndrome Review For the learning outcomes and reference standards that are associated with this presentation please refer back to the AAP Apprenticeship Learner Outcome: Dyspnoea and Respiratory Conditions Any questions?