Respiratory Emergencies PDF

🫁 Respiratory Emergencies Lecturer Lecture Notes Type ABCDE Approach in the Peri-Arrest Patient Airway You should speak to the patient and assess whether the airway...

🫁 Respiratory Emergencies Lecturer Lecture Notes Type ABCDE Approach in the Peri-Arrest Patient Airway You should speak to the patient and assess whether the airway is in tact Perform basic airway manoeuvres - Jaw thrust or a Head tilt child lift OPA or NPA → give oxygen too Check for foreign bodies and remove them Dentures, Food Suction especially if there are secretions Consider NIV Anaesthetist if it involves invasive airway management Breathing Check the respiratory rate Check SPO2 Quick respiratory examination Take an ABG A CXR might be useful Respiratory Emergencies 1  Circulation Pulse, Rhythm and Blood pressure JVP Check the capillary refill time Perform abdominal palpation Insert large bore cannulas if the patient is hemodynamically unstable Take bloods; CBC, U&E, INR, Group and save ECG and attach to cardiac monitor Give a fluid bolus of normal saline unless they have heart failure and pulmonary oedema (acute heart failure) Auscultate the heart Disability - mostly neurology Blood glucose Temperature AVPU assessment (Shorter Glasgow Coma scale) Alert Verbalising Induce pain Unresponsive Pupils → if they’re reactive or unreactive Neck stiffness - in meningitis Tone and Power Plantars Exposure Scars Trauma Respiratory Emergencies 2  Pressure sores Skin integrity in general Catheterisation Malena, bleeding, hemoptysis Dyspnoea It must be differentiated from pain, fatigue, weakness and deconditioning It must be qualified and quantified Check specific impairments and use a standardised scale like the MRC dyspnoea scale It can be respiratory, cardiovascular, metabolic or other Causes of Dyspnoea Location Causes Anaphylaxis, foreign body, tumour, vocal Upper Airways cord dysfunction Lower airways Anaphylaxis, foreign body, tumour, bronchospasm, exacerbation of obstructive Respiratory Emergencies 3  Location Causes lung disease, toxic inhalation and infection Chest wall/pleura Effusion and tumour Parenchyma Infectious, inflammatory, neoplastic and CHF Vasculature PE, chronic pulmonary hypertension CHF, Arrhythmia, effusion, tamponade, Cardiovascular valvular dysfunction (aortic stenosis and mitral regurgitation), shock Metabolic Anaemia, acidosis and intoxications Pregnancy, Pain and anxiety, Others hyperventilation and neuromuscular disorders Respiratory Failure - Type 1 PaO2 less than 8 KPa with a low or normal pCO2 Most common cause Hyperventilation, blowing away all their CO2 therefore they would have a low CO2 Vascular Pulmonary embolism Pulmonary oedema Intra cardiac shunt AV malformation Pulmonary arterial hypertension Pulmonary Asthma Pneumonia Pneumothorax Respiratory Emergencies 4  Pulmonary haemorrhage Exacerbation of COPD, bronchiectasis and ILD Upper Airway Acute epiglottitis Tumour Foreign Body Respiratory Failure - Type 2 A pO2 which is less than 8kPa with a raised CO2 of more than 6 kPa Hypoventilation leaving to increased PaCO2 and carbon dioxide retention Seen in NM disorders Reduction in minute ventilation Neuromuscular disorders CNS depression like during a drug overdose, brainstem disease and hypothyroidism Chest wall abnormalities Morbid obesity Increased dead space ventilation Obstructive airway disease, asthma, COPD and CF Upper airway obstruction, epiglottitis, tracheal tumours Alveolar abnormalities Secondary to type 1 respiratory failure: severe pulmonary oedema, pneumonia, pulmonary haemorrhage. Respiratory Emergencies Respiratory Emergencies 5  Common causes → Infection, bronchospasm (COPD and Asthma), Pneumothorax Less common → massive hemoptysis, pulmonary embolus, anaphylaxis, foreign bodies, opiate overdose, ARDS, pulmonary-renal syndromes, pleural effusion and infection and inhalation injuries Common Causes Acute Severe Asthma Predictors of a life threatening attack Prior ICU stay More than 2 hospitalisations or more than 3 emergency visits in the past year History of brittle asthma → appears well and then within a few hours they become severely sick Poor perception of symptoms by patients Frequent use of salbutamol Has cardiovascular and respiratory co-morbidities → COPD, smoking, overweight, heart issues Psychiatric illness, social isolation, alcohol and drug use Examination Increased RR (more than 25) Increased HR (more than 120) PEFR → less than 1/3 predicted Type 2 respiratory failure on ABG An SPO2 less than 92% Respiratory Emergencies 6  Life threatening → looks cyanosed, short of breath, trouble breathing Severe asthma treatment Oxygen to increase the Oxygen saturation (more than 90%) Nebulised bronchodilators: High dose beta agonist (salbutamol), anticholinergic (ipratropium) every 20 mins continuously Intravenous or oral corticosteroid (hydrocortisone 200mg IV) Reassess after therapy to determine appropriate next steps; admission to ward, ITU ect Severe Acute Asthma - other treatment options NIV → decreases work of breathing, alleviates muscle fatigue and allows spontaneous ventilation. This may help avoid intubation IV magnesium sulphate → 1.2-2g IV over 20 mins Heliox → this is a mix of helium and oxygen which allows for greater oxygen delivery during inspiration, reduces airway resistance and work of breathing until the primary therapies have time to act Respiratory Emergencies 7  IV Ketamine → produces bronchodilation of airway smooth muscle, improves gas exchange, compliance and overall lung function Therophylline (not really used) - this is toxic and can cause arrhythmias Severe COPD Exacerbation Physical signs Accessory muscle use Paradoxical chest movements Central cyanosis Peripheral Oedema Haemodynamic instability Altered mental state Decreased air entry with wheezing and sometimes a silent chest similar to what is seen in asthma. Tests at the bedside Pulse oximetry Arterial blood gas CXR ECG CBC Electrolytes and Glucose Sputum culture and Sensitivity - bacteria is often found In the case of an emergency, DO NOT perform as a spirometry - it is used to monitor and assess patients in the outpatient settings Hospital referral criteria Marked increase in symptoms, particularly dyspnoea Respiratory Emergencies 8  Severe COPD Frequent exacerbations Cyanosis Peripheral oedema Co-morbidities Arrhythmias Older Age Insufficient home support Treatment of an Exacerbation of COPD If it is mild, where the peak flow is still quite preserved (50% or more) you can treat the patient at home → Increase the Beta Agonist, add an anticholinergic and consider a short course of steroids If lung function is less than 70%, opt for inpatient treatment → use nebulised treatment, systemic corticosteroids (for about 1-2 weeks). Antibiotics are given if there is purulent sputum and fever Respiratory Emergencies 9  Chest X-rays and ABGs can be done to exclude other causes like pneumonia, tumours If they’re acidosis, one might opt for non invasive ventilation (hypercapnia and retaining CO2 - type 2) If type 1 resp failure, nebulised oxygen with a venturi mask Pharmacological treatment Bronchodilators Antibitoics Corticosteroids Respiratory management NIV → non invasive ventilation MV → mechanical ventilation Oxygen Non-invasive ventilation Respiratory Emergencies 10  When there is type II reps failure and the CO2 goes up, attach them to an NIV Oxygen is pushed in forcefully down the lungs. It improves oxygenation and eliminated CO2 from the lungs. Reduces the severity of breathlessness almost immediately Patient has to be conscious for this to happen It decreases the length of the hospital stay Mortality and intubation rates are reduced Reduces mortality and intubation rates - less patients are referred to intensive care Mechanical Ventilation Indications If one is unable to tolerate the NIV If NIV fails Altered level of consciousness and agitation Life threatening hypoxaemia Apnoea and respiratory arrest - barely breathing Aspiration risk or actually aspirated Inability to remove secretions Haemodynamically inability Arrhythmias Intensive care unit admission If there is severe dyspnoea refractory to emergency treatment If there is an altered mental state If there is haemodynamic instability Need for mechanical ventilation If they have a PaO2 of less than 40, with pH less than 7.25 despite the patient being on NIV Respiratory Emergencies 11  Pulmonary Embolism Most often, pulmonary embolism has a non-scpecific clinical presentation. It is most common in hospitalised patients. There is haemodynamic compromise Classified into submassive or massive Risk Factors of PE Can be divided into major and minor risk factors Major Minor Immobilisation CVS disease Surgery COPD Obstetrics Oestrogens Maliignancy Obesity Lower limb fractures Long distance travel Previous DVT Chronic diseases like CNS, CKD Thrombophilia Diagnosis of PE High clinical probability - WELL’s score D-Dimer assay → high in many states therefore it is not specific. A low D- dimer means that the likely hood that there is thrombosis is practically zero CTPA VQ scan - used in pregnancy and CKD Lower limb doppler ultrasound Treatment of PE Submassive PE LMWH given subcutaneously and IVC filters to prevent further embolisation Respiratory Emergencies 12  With LMWH be careful in → renal failure, recent surgery, pelvic fractures and pregnancy Massive PE (when the systolic blood pressure is less than 90 mmHg → Thrombolysis Alteplase followed by unfractionated heparin One has to be cautious with fluids as these may compromise the RV Massive Haemoptysis Relatively rare and Classified as loss of 500ml or more of blood over 24 hours at a bleeding rate of more than 100mls per hour Causes of Haemoptysis Common Causes Less common causes Bronchial carcinoma Pulmonary embolism Pneumonia AV malformations TB Mitral stenosis Bronchiectasis Pulmonary oedema CF (who get bronchiectasis) Vasculitis, Goodpasture’s Aspergilloma Clotting disorders Anticoagulants Management of Massive Haemoptysis In this case, supportive care is critical ABCDE approach mentioned before is empirical ICU admission Correct coagulopathy and haemodynamics to try stop the bleeding Cross match and keep units in reserve Respiratory Emergencies 13  Once the patient is stable, take a focused history and physical examination Order a CXR/CT with angiography protocol Intubation might be required if respiratory failure is present or if very large amounts of blood is expectorated This is contraindicated if the patient has terminal disease like cancer Bronchoscopy might be done to localise the bleed however timing of this is controversial. There is no specific agent that can be administered to stop bleeding. Adrenaline and saline might be given to help. The first line definitive procedure is bronchial artery embolisation. This is a radiological intervention (through the femoral approach) Stopps the blood supply to a particular area Upper Airway Obstruction This could be due to foreign bodies such as food or toys, the patients own tongue or swelling of the wairway If there’s an underlying problem, it is always important to ventilate When assessing a patient with suspected upper airway obstruction, check for Airway movement Ability to speak Dyspnoea Hypoxia Sounds - like snoring and stridor Low oxygen levels on pulse oximetry Toxic Inhalation This could be due to - Respiratory Emergencies 14  Inhalation of super heated air Hazardous chemicals Combustion products Steam Toxic inhalation causes → bronchiolitis, obliterative bronchiolitis, organising pneumonia, ARDS. 1. Bronchospasm 2. Bronchial oedema 3. Ciliary dysfunction 4. Reduced surfactant 5. Haemorrhage 6. Systemic inflammation Some associated symptoms include burns to the face, nose and mouth and stridor Management of toxic inhalation includes Rescuer safety - your safety is important, useless going in if you’re going to risk your life Remove from further exposure Rapid transport Secure airway – may need intubation Correct hypoxia - give him oxygen Check for COHb - give high flow oxygen to try reverse this IV access and fluids Correct wheezing with beta 2 agonist Sometimes Steroids/antibiotics in the setting of infection and inflammation of the lower airway Respiratory Emergencies 15  Carbon Dioxide Monitoring Inhalation of the carbon monoxide gas allows its binding with haemoglobin resulting in cellular hypoxia Assessment of the patient includes checking for the following Headache Irritability Errors in judgment Confusion Vomiting Flu like symptoms Pink/Red colour Severe presentations of carbon monoxide poisoning Pulmonary oedema Myocardial ischaemia Arrhythmias Seizures Coma What are some late presentations of carbon monoxide poisoning Focal neurology Cognitive defect Personality change Treatment for carbon monoxide poisoning includes Securing of the airway Removal from the source High flow oxygen Hyperbaric chambers Respiratory Emergencies 16  Pneumothorax Air rushing into the pleural cavity causing lung collapse and pleuritic pain History Acute onset of pleuritic chest pain usually at rest with or without dyspnoea Symptoms can be out of proportion to the extend of lung collapse especially in secondary pneummothorax where the reserve is limited Trauma might cause a pneumothorax - broken rubs, hitting the chest Examination Hypoxaemia Major alterations in vitals usually seen in tension pneumothorax Hyperexpanded hemithorax with increased resonance, decreased vesicuar sounds and fremitus (decreased air entry) Contralateral teacheal deviation might be noted Mannan sign → this is a clicking, crunching sound with heart beats influenced by position and respiration Patients will be hypoxic Classification Spontaneous Primary PTx: in a patient without apparent underlying pulmonary disease Thought to be caused by the rupture of an air-containing space within or in vicinity to the visceral pleura, usually at the apex Although patients have no apparent underlying lung disease, up to 80% have blebs or bullae on CT examination Male sex, smoking, tall stature, and genetics are risk factors Recurrence rate of 39% in ipsilateral lung and 15% in contralateral lung Respiratory Emergencies 17  Spontaneous Secondary PTx: in a patient with underlying pulmonary disease Almost any lung condition can be associated with the development of a PTx COPD is by far the most common etiology nowadays Although the exact mechanism varies, the principles underlying the development of primary PTx are likely also playing a role (exacerbated by airway/parenchymal inflammation and architecture disruption) Recurrence rates are usually higher and depend on the underlying etiology Traumatic Pneumothorax Iatrogenic falls under this Radiological Diagnosis A standard erect PA CXR is sufficient → expiratory views are not recommended for routine use A sharply demarcated white pleural line without lung markings lateral to it is diagnostic Mimickers: skin fold, tubings, ribs Use of expiratory views /lateral decubitus views if unclear A pleural effusion is present in up to1 5-25% of cases (usually an eosinophilic pleuritis in reaction to the presence of air; rarely hemorrhagic) Supine patients Deep sulcus sign / upper quadrant lucency / ↑sharpness of cardiac border or hemidiaphragm CT scan recommended only if: Diagnosis suspected despite normal CXR To better define underlying disorder Respiratory Emergencies 18  Management There has been a shift towards more conservative initial treatment and reliance on patient status rather than the pneumothorax size Treatment is more aggressive if the cause of the pneumothorax is secondary Tension Pneumothorax Clinical Diagnosis Evidence of sudden deterioration in a patient known to have a PTx or highly suspected of having one should prompt initiation of therapy Severe hypocaemia, tachycardia, contralateral tracheal shift, increased JVP and shock Mediastinal shift to the contralateral side It is caused by a one way valve phenomenon producing a positive pleural pressure during most of the resp cycle The main consequence is reduction of venous return and cardiac output Treatment Oxygen administration Immediate needle aspiration in the second interocostal space at mid- clavicular line Insertion of a chest drain If you do not do this, you would be risking cardiac arrest Anaphylaxis This is a type 1 hypersensitivity reaction. It is IgE mediated Respiratory Emergencies 19  Characterised by vasodilation, bronchial mucosal oedema, bronchoconstriction Treatment includes IV fluids Oxygen Hydrocortisone Adrenaline Chlorphenamine Nebulised bronchodilators IV adrenaline only if there is circulatory compromise Intubation and tracheostomy but there are rare Infection This can be pleural or parenchymal Pleural - Empyema This is frank pus in the pleural space It needs drainage via an intercostal drain Administration of broad spectrum antibiotics Parenchymal/Pneumonia Ascess, sepsis, respiratory failure, ARDS Respiratory Emergencies 20  The list at the bottom, describes a complicated pneumonia where people might need intensive treatment ARDS Pulmonary insult resulting in non-cardiogenic pulmonary oedema and hypoxaemia refractory to oxygen therapy. Cytokines secrete fluid which cannot be removed by diuretics. This results in death. Criteria Acute onset Bilateral infiltrates on CXR PCWC