Common Respiratory Disorders.pdf

Common Respiratory Disorders Foundations of Critical Care 2024 D.Freer Learning Outcomes Identify the aetiology, pathophysiology, clinical and diagnostic features and management of the following acute respiratory disorders: COPD Pulmonary Embolism Pneu...

Common Respiratory Disorders Foundations of Critical Care 2024 D.Freer Learning Outcomes Identify the aetiology, pathophysiology, clinical and diagnostic features and management of the following acute respiratory disorders: COPD Pulmonary Embolism Pneumonia Asthma APO will be discussed with Heart Failure Causes of respiratory distress What commonly causes respiratory distress in your patients? Ventilatory problems Obstructive / restrictive Acute / Chronic OR impaired pulmonary ventilation or perfusion Infectious processes Impaired CNS drive Heart failure Metabolic problems Normal during increased activity Take a good history Important in every area, not just the ED Length of time? Onset (gradual vs abrupt)? Position of comfort? Orthopnea? Coughing? Productive? Character? Haemoptysis? Pain? Onset, quality, radiation, severity, duration ? PMHx? Occupational Hx? Current medications & allergies? Focussed assessment Don’t forget the ABCs Signs & manifestations of shortness of breath Cough – recent vs chronic Sputum – colour & amount Fever Chest pain – localised, worse on Haemoptysis – distinguish from haematemesis, epistaxis, maxillofacial Children – head bobbing, nasal flaring, Dyspnoea Causes Cardiovascular… Respiratory… Metabolic… Mechanical… Extra-pulmonary… Acute dyspnoea with no previous heart or lung disease Chronic Lung Disease Obstructive – cannot get the air out Asthma Bronchiectasis Chronic Bronchitis Emphysema Chronic obstructive pulmonary disease (COPD) Chronic obstructive airways disease (COAD) Chronic airway limitation (CAL) Restrictive – cannot get the air in -osis (interstitial pulmonary fibrosis, asbestosis, cystic fibrosis)  COPD 5% of the population May present as life threatening respiratory failure Common co-morbidity Often have a combination of chronic bronchitis and emphysema +/- asthma Chronic Bronchitis Clinical diagnosis: “Chronic cough with sputum production for at least 3 months per year for 2 consecutive years” Emphysema Pathological diagnosis: “Destruction of lung units distal to terminal bronchioles leading to abnormal permanent airspace enlargement” Chronic Bronchitis Long-standing inflammation of the lower airways Mucus +++ Infections Wheeze Coughing and mucus for at least 3 months a year for 2 years in a row Chronic Bronchitis Increased mucus secreting cells Productive cough Vital capacity decreased Tidal volume is normal or decreased Alveoli walls not severely affected and diffusion is relatively normal Alveolar ventilation reduced Emphysema Destroys the alveoli Lungs lose elasticity Alveoli become enlarged Emphysema Destruction of the alveolar walls Decreased alveolar surface membrance Pulmonary capillaries decrease in number Increased dead-space ventilation (V>Q) Weakens walls of small bronchioles, causes: Loss of recoil Air trapping Increased residual volume Hypoxia, inflammation, loss of capillaries, and hypercarbia Leads to pulmonary hypertension & cor pulmonale (R heart failure) Alveolar destruction in emphysema Attraction of Smoking inflammatory cells Release of elastase Decreases Inherited Action inhibited by a1-antitrypsin a1-antitrypsin a1-antitrypsin activity deficiency Destruction of elastic fibres No Damage in lung Emphysema Emphysema Smoker history Barrel-chested, AP ratio 1:1 Unable to fully exhale ABG normally shows low PaO2, high PaCO2 and high HCO3 (chronic) COPD Treatment Relieve hypoxia – hypoxia kills faster than hypercarbia Titrate oxygen to SpO2 88-92% Positioning – seated / semi-seated Bronchodilators – salbutamol & Ipratropium – MDI / neb NIV – BiPAP for ventilatory support & alveolar recruitment Corticosteroids Antibiotics ? When? Oxygen & CO2 retention Excessive oxygen administration can lead to hypercapnic respiratory failure in some COPD patients COPD patients with more severe hypoxemia are at higher risk of CO2 retention from uncontrolled O2 administration The same phenomenon has also been described in Severe asthma Community-acquired pneumonia Obesity hypoventilation syndrome Neuromuscular conditions Any patient with chronic respiratory failure may be at risk Oxygen and CO2 retention The traditional theory is that oxygen administration to CO2 retainers causes loss of hypoxic drive, resulting in hypoventilation and type 2 respiratory failure. This is a myth. Patients suffering from COPD exacerbations, regardless of whether they have CO2 retention, generally have HIGH respiratory drive (unless there is impending hypercapnic coma) The real explanation involves: Increased V/Q mismatch (most important) The Haldane effect How oxygen causes CO2 retention V/Q mismatch In COPD, over time patients optimise their gas exchange by hypoxic vasoconstriction (i.e. they reduce blood supply to areas where gas exchange does not occur well). Administering a high level of oxygen will increase oxygen tension, reducing hypoxic pulmonary vasoconstriction. Results in increased perfusion to areas where ventilation is poor Increased dead space ventilation & higher PaCO2 due to overall lack of ventilation at the alveolar level How oxygen causes CO2 retention The Haldane effect: Describes the difference in the quantity of carbon dioxide carried in oxygenated and deoxygenated blood. CO2 has a higher affinity for deoxygenated Hb than oxygenated Hb Giving a patient high levels of oxygen will decrease the affinity of CO2 for Hb. Carbon dioxide will be displaced by oxygen, resulting in a higher PaCO2. For patients who cannot increase their minute ventilation and blow off this CO2 (i.e. those with COPD), the Haldane effect accounts for about 25% of their total PaCO2 increase. What do we do? In patients with COPD, hypoxic pulmonary vasoconstriction is the most efficient way to optimise the V/Q ratio to improve gas exchange. This physiological mechanism is counteracted by oxygen therapy and accounts for the largest increase of oxygen-induced hypercapnia. A titrated oxygen therapy to achieve saturations of 88%-92% is recommended in patients with an acute exacerbation of COPD. “permissive hypoxemia” to avoid hypercarbia In extremist, always give oxygen Hypoxia kills faster than hypercarbia Pneumonia – ‘Old mans best friend’ Definition: Acute inflammation of the lung parenchyma 10% mortality rate in Australia 2nd most common hospital-acquired infection Highest mortality rate for HAI Common cause of death in elderly Pneumonia Classification Classified into groupings. Community Acquired pneumonia Hospital Acquired (nosocomial) pneumonia Pneumonia in the immuno-compromised patient Aspiration pneumonia Community – acquired pneumonia Large majority of presentations to ED Typical (common bacteria) / atypical (uncommon bacteria) Mostly managed in the community Hospital acquired pneumonia (nosocomial) Pneumonia acquired during a hospital stay (in hospital after 72 hours) The leading cause of death among hospital acquired infections Broad range of causative organisms some being antibiotic resistant Pneumonia Risk Factors Advanced Age >65years Smoking history Stroke / swallowing difficulty URTI Tracheal intubation Prolonged immobility Immunosuppressive therapy Non-functional immune system Malnutrition Dehydration Co-Morbidities I.e; CAL, Diabetes, CHD Pneumonia Pathophysiology Inflammatory response Lung defence mechanisms overwhelmed (COUGH/ CILIARY ACTION) Infective agent penetrate the lower respiratory tract Inflammation and colonization Inflamed alveoli fill with exudate Increased capillary permeability Diffusion of O2 and CO2 altered A-a gradient increased or decreased? Pneumonia Pathophysiology Bacterial pneumonia can lead to significant V/Q mismatch with significant increase in pulmonary shunting. Leads to hypoxia ARF / pleural effusions can develop Causes of Pneumonia Bacteria Viruses Mycoplasma’s Fungal agents Protozoan Aspiration of food, fluids, vomitus Inhalation of toxic or caustic chemicals, dust, smoke, or gases Pneumonia - Typical (Bacterial) Gram positive Strep. Pneumoniae (most common) Staph. Aureus Gram negative (highest mortality) e.g. haemophilus influenza bacillus, klebsiella frequent cause of nosocomial pneumonia Esp. in the critically ill due to altered defences, intubation, poor oral hygiene, suctioning… Pneumonia - Atypical Influenza virus strains Can rapidly progress to picture of ARDS. Mycoplasma (younger adults, teenagers) PCP ( severely immuno-suppressed patients) Pneumocystis carinii pneumonia – CXR (diffuse bilateral interstitial shadowing), Pneumonia Clinical Signs Fever / rigors / sweats Dyspnoea, headache, fatigue Tachycardia Low saturations, cyanosis (severe , late) Dull percussion over area of consolidation Crackles, bronchial breathing Altered mental state Sputum Pneumococcal – bloody or rust coloured Pseudomonas – green Haemophilus – green Klebsiella – currant jelly Pneumonia Management Antibiotic therapies commence as soon as possible broad spectrum until the specific organism is isolated Respiratory support a needed Oxygen to correct hypoxia Enable expectoration – Chest Physiotherapy Bronchodilator therapies – open airways/loosen consolidation Fluids and Electrolyte management Nutritional support Prevention – Tracheal suction IPPV pt Handwashing  Pulmonary Embolism Blockage of the pulmonary artery by: Air Blood clot Other foreign material Thrombus can be loosened by: Trauma Clot dissolution Sudden muscle spasm Intravascular pressure changes or alterations in peripheral blood flow Most common is dislodgement of emboli from deep veins in the thigh and pelvis Pulmonary embolism Risk Factors: Immobility Venous injury Hypercoagulability Pregnancy / post-partum Oral contraceptive tablet Multi-trauma (long bone #s) IVDU Symptomatic PE occurs in approximately 50% of untreated DVT. Pulmonary embolism Consider a PE in any patient who has cardio-respiratory problems that cannot be otherwise explained; look for risk factors Wells’ criteria for PE: - Clinical signs - Probability of PE - HR>100 - Immobilisation (3 days) or surgery in past 4 weeks - Previous PE - Hemoptysis - Malignancy with treatment in last 6 months or palliative Pathophysiology of PE Venous stasis Vessel Injury Hypercaogulability Thrombus Formation Dislodgement of Portion of Thrombus Occlusion of pulmonary circulation Increase in dead-space ventilation Hypoxic vasoconstriction Decreased surfactant Release of neuro-hormonal inflammatory substances Pulmonary oedema Atelectasis Pathophysiology of PE Tachypnoea Dyspnoea – most common Chest Pain Increased Dead Space V/Q imbalances Decreased PaO2 Pulmonary infarction Decreased cardiac output Systemic hypotension Shock Pulmonary Embolism Treatment Closely observe – continuous Sp02 and cardiac monitoring. Oxygen Fluid loading Anticoagulation Thrombolytics (massive PE) ETT & IPPV Inotropes Surgery Asthma Inflammatory disease Episodic periods of reversible bronchospasm, mucous plugging and air trapping Epidemiology 1 in 10 Australians have asthma – approx. 2.8 million people More common in females after adolescence Approximately 500 deaths per year ‘Thunderstorm Asthma’ 2016 unusual ‘cluster of allergic asthma flare-ups’ with springtime thunderstorms High grass pollen count for first 30 min of storm Thousands of emergency calls 9 deaths, state of emergency in Victoria Asthma Pathophysiology Chronic inflammatory disorder of the lower airways Mast cells, eosinophils, & T lymphocytes mobilised Bronchospasm to cause inflammation Many and varied triggers Inflammation leads to increase in airway responsiveness: Bronchial hyper-responsiveness Airway remodelling occurs secondary to the inflammation: Thickening and Fibrosis of brochioles Bronchial Edema Increased Mucus Production Asthma Pathophysiology Mediated by immune system Mast cells activated by allergens Bronchoconstrictive substances (e.g. histamine) released Eosinophils release protein that damages the epithelium T cells stimulate IgE Acute broncho constriction (contraction of smooth 2 muscle) 1 Swelling of airway wall Secondary to inflammation 3 Chronic mucous plug formation (mucous hyper secretion & inflammatory exudate) Direct & indirect airway Hyper responsiveness Asthma triggers Extrinsic Type 1 – allergic (e.g. pollen) Type II – prolonged exposure (e.g. mites) Commonly accompanied by other allergies (eczema & allergic rhinitis) Intrinsic attacks (no known cause in 30% - ? Exercise) E.g. infection, emotional stress, anxiety, coughing or laughing Most episodes occur following respiratory infection Asthma patient history Recent viral infection? Exposure to known allergen? Activity prior to presentation? High risk History Childhood onset Steroid dependence Previous ICU admissions Signs of severe asthma Classic triad of cough, wheeze, and dyspnea Difficulty speaking – Single words Rib retractions Pulse > 130, Resps > 30 SaO2 < 90% on air Altered mental status – Lethargy/confusion? Signs of life-threatening asthma Inability to speak Silent chest Sweating & vomiting Panic SaO2 < 90% with O2 Golden Rule All that wheezes is not asthma Pulmonary Edema Allergic reactions Pneumonia Foreign body aspiration Asthma Treatment Bronchodilators 12x salbutamol & 8 Atrovent via MDI with spacer Can give 5mg salbutamol & 500mcg ipratropium neb Repeat / continuous bronchodilators May need K+ replacement Oxygen – titrate to 93-95% If no response, add IV Magnesium Sulfate Systemic corticosteroids – 100mg Hydrocortisone Ventilate………. NIV or invasive…….Difficult Zeep & permissive hypercapnea Increased I:E ratio, longer expiratory time Continue to treat underlying cause Questions? We are sitting in the shade today because someone planted a tree a long time ago