Summary Notes PDF

1.0 Overview 1.1 Respiratory anatomy The conducting airways - Air is inhaled through the nasopharynx and down into the trachea and then into the bronchi - Right main bronchus almost forms a straight line with trachea (25 degrees) - most common for foreign bodies and aspiration - deep intubation - L-...

1.0 Overview 1.1 Respiratory anatomy The conducting airways - Air is inhaled through the nasopharynx and down into the trachea and then into the bronchi - Right main bronchus almost forms a straight line with trachea (25 degrees) - most common for foreign bodies and aspiration - deep intubation - L-mainstem bronchus is more angulated and less prone to these issues - Bronchioles come off bronchi, end up in alveolar ducts and then into alveoli where gaseous exchange occurs Right lung Left lung Larger 3 lobes Smaller 2 lobes (plus lingula) Terminology Dyspnoea A subjective perception of shortness of breath Respiratory distress A term combining the patient's subjective sensation of dyspnea with signs indicating difficulty breathing. Hypoxia Insufficient delivery of oxygen to the tissues The brain is the most sensitive organ to hypoxia therefore is an early clinical sign. Hypoxemia Deficiency of oxygen in arterial blood Causes 1. Hypoventilation 2. Right to left shunt (intrapulmonary shunt) 3. Ventilation-perfusion (V/Q) mismatch 4. Diffusion impairment 5. Low inspired oxygen Anoxia No oxygen Hypercapnia PaCO2 >45mmHg Normal 35-45mmHg Commonly caused by alveolar hypoventilation: slow, shallow breathing, small tidal volumes, under ventilation Rarely results from increased CO2 production alone Effects - Seizures, coma, death - Reduced myocardial and diaphragmatic contraction - Arrhythmias, hypotension, cardio/respiraotry arrest, death - Right shift on Oxy-Hb curve - Decreased O2 affinity to Hb at the alveolus PaO2 The partial pressure of O2 in the blood This is dissolved oxygen in the blood, not bound to Hb SaO2 Measures the percentage of Hb saturated with O2 Accessory muscle use Important to see what muscles are being recruited in the laboured breathing patient Laboured inhalation Laboured exhalation (e.g. COPD, asthma) Muscles - Scalenes - Sternocleidomastoid - Trapezius - Intercostals - Restrictive conditions Laboured - Raise the ribs and sternum to increase the anterior posterior diameter - Increase the AP diameter of the thorax - Their contraction prevents collapse under high negative pressures Muscles - Intercostals - Obliques (internal/external) - contract trying to force air out of chest - Obstructive lung disease Laboured - The abdominal muscles are the most noticeable muscles of expiration - Increase intra-abdominal pressure, thereby moving the diaphragm upward - This helps with expiration against lower airway obstruction in obstructive lung disease Pulmonary compliance: refers to the amount of pressure that must be generated to expand the lungs with a given volume. E.g. some balloons are harder to inflate than others Good compliance Poor compliance Means you need little pressure to generate a big volume change Means you need a large pressure to create that same or less volume change - stiff lungs Lung volumes and capacities (sums of volumes) - Tidal volume: the amount of air you inhale in a normal breath a rest - Inspiratory reserve: amount you can possibly inhale over and above your tidal volume - Expiratory reserve volume: amount you can possibly exhale below normal tidal volume - Residual volume: prevents lungs from collapsing entirely - Expiratory reserve + residual volume = functional residual capacity (FRC) - Tidal volume + inspiratory reserve volume (IRV) = inspiratory capacity (IC) 1.2 Respiratory physiology Ventilation (V) - Volume of air that moves into and out of the mouth Minute ventilation = RR x TV FiO2 = fraction of inspired oxygen: an estimation of the oxygen content a person inhales and is thus involved in gas exchange at the alveolar level Perfusion (Q) - Flow of blood through the tissues or to an area E.g. CO = 6l/min = the lungs are perfused with 6L of blood per minute Under ideal conditions, ventilation should match perfusion (V = Q) Intrapulmonary shunt (occurs in bronchospasm) - V/Q ratio decreases (<1) - E.g. 5L air enters the lungs and CO=6l/min then 5/6 = 0.83 - Result is decreased arterial oxygen concentration Dead space: volume of gas that does not take part in gaseous exchange (ventilated but not perfused) There are three types of dead space 1. Alveolar dead space - Alveoli that are ventilated but not perfused Changes from minute to minute Evident in shock states, emphysema, pulmonary embolism little to no perfusion but still good ventilation 2. Anatomical dead space - Parts of respiratory tract that are ventilated but not perfused (trachea, bronchi, bronchioles) Fixed anatomy that does not change About 33% of every breath is anatomical dead space 3. Apparatus dead space - From equipment such as filter and EtCO2 Don't add unnecessary apparatus as this increases dead space and traps CO2 1.3 Acid base disorders, O2 delivery and O2 dissociation Main buffer system: lungs and kidneys must work together to keep or restore balance (normal pH 7.4) CO2 + H2O > H2CO3 > H+ + HCO3Lungs: acid is excreted as carbon dioxide Kidneys: bicarbonate is altered to counteract altered CO2 Respiratory acidosis Respiratory alkalosis Definition High PaCO2/EtCO2 Retained CO2 = increase resp rate to blow off CO2 (hyperventilation) Leads to formation of carbonic acid when CO2 combines with water, more H+ ions, lower pH Lower CO2 = decreased resp rate to retain CO2 (hypoventilation) Low PaCO2/EtCO2 Less carbonic acid, thus less H+ in blood, pH increase Causes Lung disease causing impaired gas exchange and CO2 retention Opioid overdose Head injury Any condition resulting in hypoventilation (cardiac arrest) ROSC target CO2 is lower end of normal (35-40) to reduce acidosis from no respiration Salicylate overdose High fever Hysteria/voluntary over breathing Passive over ventilation by hand delivered ventilations via BVM or incorrectly adjusting the mechanical ventilator Any condition resulting in hyperventilation Oxygen delivery to tissues - Partial pressure of gas: the total pressure of a mix of gases is equal to the sum of their own individual pressures - Dalton’s law states that the total pressure exerted by a mixture of non-reacting gases is equal to the sum of the partial pressures of each individual gas in the mixture. - Henry’s law states that the amount of a gas dissolved in a liquid is directly proportional to the partial pressure of that gas above the liquid. It describes the relationship between the concentration of a gas in a solution and its partial pressure. - Ficks law states that the rate of gas diffusion across a permeable membrane is determined by - The partial pressure gradient of the gas - The thickness of the membrane (APO, fibrosis) - important - The surface area of the membrane (COPD, fibrosis) - important - Chemical features of the gas and the membrane - The Bohr effect refers to the phenomenon in which the affinity of haemoglobin for oxygen is reduced under conditions of low pH (acidic environment) and high levels of carbon dioxide (CO2). Oxygen dissociation The O2-Hb dissociation curve is an S shaped curve that illustrates the % of Hb saturated with O2 at different partial pressure levels of arterial oxygen. Left shift Right shift Hb holds tighter onto O2 and does not easily release to the tissues Hb holds less tightly to the O2 and releases it easily to the tissues General RSA RIPAP assessment for all patients with respiratory compromise Normal Mild/moderate Severe Life-threatening Conscious state Alert Alert May be altered Altered or unconscious General appearance Calm, quiet Calm, mildly anxious Distressed Distressed, anxious, fighting to breathe, exhausted, catatonic Speech Clear and steady sentences Full sentences, pausing to catch breath Short phrases only Words only, or unable to speak Skin Normal, pink Normal, may be pale, sweaty Pale, sweaty, may be cyanosed (cyanosis SpO2 <90) Pale, sweaty, cyanosed Work of breathing (inspect use of accessory muscles) Normal chest Slight increase in movement (nil normal chest accessory muscles) movement Marked chets movement + use of accessory muscles Marked chest movement with accessory muscle use, intercostal retraction +/tracheal tugging (suprasternal retractions) or exhaustion SaO2 88-92% for COPD patients is normal ask what patients normal sats is 94-98% >94% 90-94% <90% Rate/rhythm 12-16 Regular event cycles 20-25 Asthma may have slightly longer expiratory phase >25 Asthma prolonged expiratory phase >25 or <8 Asthma prolonged expiratory and inspiratory phase Inspect Symmetrical rise and fall of chest bilaterally, nil scars, patches N/A N/A Asymmetrical rise and fall of chest, unilateral/bilateral hyperinflation (tension pneumo) Palpation N/A N/A N/A N/A Auscultation Usually quiet, no wheeze Normal vesicular sounds Asthma: mild expiratory wheeze +/- inspiratory wheeze LVF: may be some fine crackles at bases, progresses to mid zone Athma: expiratory wheeze +/inspiratory wheeze LVF: fine crackles full field with possible wheeze Upper airway obstruction: inspiratory stridor Silent chest, faint adventitious sounds Percussion Resonance: normal Dull: fluid filled compartment, solid organ Hyperresonant: air field compartment Resonant bilaterally N/A N/A Hyperresonance with tension pneumothorax Percussion sounds Hyperresonant Hollow sound Air filled cavity = pneumothorax which can progress to tension pneumothorax Normoresonant Between dull and hollow Air filled alveoli Hyporesonant Dull sound Fluid filled cavity For hyper resonant and hyperresonant sound, the potential space between the visceral pleura and parietal pleura becomes an actual space as the layers separate due to being filled with air or fluid. Pneumothorax COPD can cause bullae which is a rupture/tear in visceral pleura which leads to pneumothorax Pneumothorax Tension pneumothorax Hemodynamically stable Hemodynamically unstable History Chief complaint Allergies Medications Past medical Hx Last email Events proceeding What's been going on today? When did the symptoms start? Did it come on suddenly or has it gotten worse? Duration? Gotten better or worse? Always there or does it come and go? SOB only on exertion or at rest as well? Pain = OPQRST Cough Dry or productive cough? Acute <3 weeks Subacute 3-8 weeks Chronic >8 weeks Presence of blood or precipitants? Can develop after starting new medications such as ACE inhibitors Occupational Hx Work exposures e.g. smoke, asbestos, silica, coal mine dust Social Hx Alcohol, drug use, smoking history Travel Hx High risk areas? India, Pakistan, Africa Recent long haul flights = PE Sputum Frothy, sometimes with a pink tinge’ think purulent: congestive heart failure, pulmonary oedema Yellow or green: infectious Brown: tobacco smokers, old blood Clear or white: Viral bronchitis, COPD, asthma Blood streaked: tumour, tuberculosis, pulmonary oedema, trauma from coughing Volume/viscosity Auscultation Term Acoustic characteristics Description Course crackle Discontinuous sound: loud, low in pitch Pulling apart strips of velcro Predominantly heard during inspiration Loudest in the bases Fine crackles Discontinuous sound: sift, higher pitch, shorter duration Unilateral crackles = infection (pneumonia) can be secondary to COPD Wheeze Continuous sound: high pitched, dominant High/low pitched, continuous musical sound Stridor Loud, musical sound of definite and constant pitch Identical to wheezing except for following characteristics 1. Confined to inspiration 2. Always louder over neck where wheezing is loudest (wheezing is louder over the chest) Pleural rub Discontinuous sound: low or high pitch. Short duration Predominantly during expiration Confined mostly to expiration Loud grating or rubbing sounds Sometimes had crackling character, resembles parenchymal crackles Arterial Blood Gas Analysis Only pO2 will be different between arterial and venous, the other parameters will be the same. pH Normal 7.35 to 7.45 Changes depending on level of CO2/bicarbonate PaO2 Normal >75mmHg Hypoxia kill first before hypercarbia PaCO2 Normal 35 to 45mmHg Oxygen can absorb without ventilation while CO2 requires ventilation to blow off Bicarb Normal 22 to 26 mmol Bicarb increases slowly over hours to weeks to compensate for acidosis therefore usually only evident in chronic conditions Acute conditions: no change to bicarb due to time to change COPD is chronic and shows high bicarb due to metabolic system working hard to compensate for acidosis Respiratory/ventilatory failure Occurs when the lungs and ventilatory muscles cannot move enough aim in and out of the alveoli to adequately oxygenate arterial blood and eliminate carbon dioxide. Type 1 (hypoxemic) Type 2 (hypercapnic) PaO2 <60mmHg with normal or subnormal PaCO2 E.g. APO/CAPO, pneumonia PaCO2 >50mmHg E.g. respiratory pump failure Diagnosis template Respiratory acidosis/alkalosis (depending on pH) with or without metabolic compensation (depending on bicarb) the patient is in type I/II respiratory failure Ventilation strategy Adult Paediatric One breath every 5-6 seconds 10-12bpm One breath every 3-5 seconds 12-20bpm Start in guideline and titrate to effect based on 1. Alveolar plateau - alveolar is empty - end of expiration 2. Good rise and FALL (no breath stacking) AND 1. SpO2 2. EtCO2 - “Supplement the patient's breath and stick 2 breaths in between giving a resp rate of 18/min” - “I want to increase the patient's minute volume (resp rate x tidal volume)” - Tidal volume aim: 6-8 ml/kg - One breath over 1 second Gas trapping/breath stacking: air accumulates due hyperventilation where inspiratory volume exceeding expiratory volume (due to expiratory outflow issue) - Shark fin on capnography: air is struggling to get out - prolonged expiratory phase - no alveolar plateau Permissive hypoxia/hypercapnia: settling for lower respiratory rate to prevent breath stacking Hyperventilation complications 1) Barotrauma 2) Gastric inflation - causes regurgitation to aspiration to pneumonia 3) Increase in intrathoracic pressure causes a decrease in BP O2 delivery systems Mask Litres per minute Nasal cannula 1 to 6 Simple face mask 5 to 10 Nebuliser 6-8 (8 gold standard) Non-rebreather 10 to 15 BVM 10 to 15 (usually always 15) CPAP 5 cm H2O 8 10 cm H2O 12 15 cm H2O 15 2.0 Asthma 2.1 Burden of asthma and asthma phenotypes Asthma: is a heterogeneous disease, usually characterised by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, SOB, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation (obstructive lung disease, expiratory outflow obstruction that can progress to inspiratory) 2.2 Phenotypes and asthma journey Phenotypes Obesity Some obese patients with asthma have prominent respiratory symptoms and little eosinophilic airway inflammation Allergic Commences in childhood, past and/or family history of allergic disease. They respond well to inhaled corticosteroids ICS. Examples: pollen, grass, cats MHx: hay fever, eczema and asthma When pollen particles are inhaled, the antibodies bind to the antigen, causing mast cell activation. IgE mediated Non-alle rgic Idiosyncratic, often respond less well to ICS - Infection - Exercise - Cold air - Drugs (aspirin or other NSAID) - interfere with prostaglandin production - decreases all prostaglandins (PGE2 is a bronchodilator) - PGD2 can cause bronchoconstriction Allergies: nil - still gets asthma MHx: healthy until recently. Started getting chest tightness when exercising and exposed to cigarette smoke When exercising, the SNS response causes mast cell activation Idiosyncratic Late onset Some adults present with asthma for the first time in adult life, nonallergic, often require higher doses of ICS Fixed airflow Long-standing asthma develop fixed airflow limitation - airway wall remodelling 2.3 Pathophysiology Asthma cascade Acute phase Late phase Allergen to mast cell Mast cell release histamine Histamine binds and activated H1 and H2 receptors Activation of H1 receptors causes bronchoconstriction and inflammation from increased vascular permeability Activation of H2 increases mucus production Prostaglandins and leukotrienes cause more bronchoconstriction making it more difficult to reverse Increase in cytokines Eosinophils release mediators which further bronchoconstrict (principal cell involved in this phase of asthma) Lymphocytes further activate mast cells and eosinophils Respiratory Tract Infections (RTIs) bypass the acute phase and go straight to the late phase. The result is more severe bronchospasm. Ask about genetic history of asthma (parents) - child is likely to have asthma - Question allergies, house dust mites, domestic animals, mould/fungi - Are you a known asthmatic? - How often do you have symptoms? - How often do you use your reliever? - Do you get symptoms during the night or when you wake up? - Do you take your preventer as prescribed? - Age of onset? - How bad are your exacerbations? - Previous hospital presentations in the last 12 months? - Doy ou know of anything that triggers asthma? - Any other medical conditions? Long term effects - Airway remodelling: hypertrophy and hyperplasia of ASM cells, goblet cell hyperplasia - With remodelling, even the smallest exacerbations can cause severe airway obstruction. Airway is already somewhat constricted. 2.4 Treatment Short Acting Beta Agonist (SABA) Blue puffer - reliever Beta 2 agonist - smooth muscle relaxant Corticosteroids Red puffer - preventer Moderate exacerbations and up will most likely require corticosteroids Short Acting Muscarinic Agents (SAMA) Ipratropium bromide Cuts off parasympathetic innovation that may be activated mast cells Beta 2 agonist Adrenaline 2.5 Management 1. Classify current exacerbation (mild to life threatening) from RSA 2. Classify chronic status: intermittent (blue puffer) vs persistent (blue and red puffer) 3. Current control: ask patient about their symptoms over the last few weeks Good control Partial control Poor control Daytime symptoms or need reliever < 2 days per week No limitations of activities No symptoms during night on Daytime symptoms or need for reliever >2 days per week Any limitation of activities Any symptoms during night or on Daytime symptoms or need for reliever >2 days per week Any limitation of activities Any symptoms during night or on waking waking waking 4. Treatment Metered Dose Inhaler (MDI) Indications: For the delivery of MDI medications Contraindications: FBAO with spacer, for connector nil Complications: poor procedural compliance reducing drug delivery Time release of medication with inspiration Mild/moderate Severe Life-threatening Oxygen Salbutamol Ipratropium bromide Hydrocortisone Oxygen Salbutamol Ipratropium bromide Hydrocortisone Adrenaline Magnesium sulphate CPAP Oxygen Salbutamol Ipratropium bromide Hydrocortisone Adrenaline Magnesium sulphate If RR <10 commence IPPV with nebuliser CPAP Pharmacology COPD or any patient with wheezes treated with nebulised salbutamol and ipratropium bromide Drug Indications Contraindications Adult dose Paediatric dose Salbutamol Bronchospasm Allergy ADR Patients <1 year of age 12 (1.2mg) MDI SDO NEB 5mg repeated PRN >6 years 12 (1.2mg) MDI 1-5 years 6 (600 micro g) MDI Ipratropium bromide Moderate bronchospasm (unresponsive to initial QAS salbutamol neb) Severe bronchospasm Allergy ADR Patients <1 year of age NEB 500 microg repeated 20 minute intervals Total max 1.5mg (3 doses) >6 years NEB 500 microg repeated 20 minute intervals Total max 1.5mg (3 doses) 1-5 years 250 microg repeated at 20 minute intervals Total max 750 microg (3 doses) Hydrocortis one Asthma Allergy ADR Acute exacerbation of COPD (with evidence of respiratory distress) IM 100mg SDO IV slow push over 1 minute 4 mg/kg SDO not to exceed 100 mg IV slow push over 1 minute Adrenaline Severe life threatening bronchospasm or silent chest (patients must be able to speak in single words and/or have haemodynamic compromise and/or an ALOC IM 500 microg repeated 5 minute intervals no max IM >6 300 microg 1-6 years 150 microg 6 months - <1 year 100 microg <6 months 50 microg Repeated at 5 minute intervals no max dose 3.0 COPD Nil 3.1 Overview and pathophysiology COPD: is a common, preventable, chronic, irreversible and treatable disease that is characterised by persistent respiratory symptoms and airflow limitation that is due to airways dn/ir alveolar abnormalities (an inflammatory response of the lung) usually caused by significant exposure to noxious particles or gases Key pathology - Airflow limitation that is - Usually progressive and - Associated with an abnormal inflammatory response of the lungs due to noxious particles or gas Exacerbation of COPD An event in the natural course of disease, characterised by change in the patient's baseline dyspnoea, cough and/or sputum that is beyond normal day to day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD. These are commonly precipitated by viruses or bacteria. Exacerbations are associated with significant morbidity and mortality. 3.2 Pathophysiology Expiratory airflow obstruction - leads to hypercapnia 1. Tobacco smoke and air pollutants (oxidants) enter the lungs 2. Inflammation of the airway epithelium 3. Infiltration of inflammatory cells and release of cytokines (neutrophils and macrophages) 4. Muscle weakness, weight loss, inhibition of normal endogenous antiproteases Causes 1. Continuous bronchial irritation and inflammation 2. Chronic bronchitis: bronchial edema, hypersecretion of mucus, bacterial colonisation of airways 1. Breakdown of elastin in connective tissue of lungs 2. Emphysema: Destruction of alveolar septa and loss of elastic recoil of bronchial walls Causes - Airway obstruction - Air trapping - Loss of surface area for gas exchange - Frequent exacerbations (infection, bronchospasm) - Dyspnoea - Cough - Hypoxaemia and hypercapnia - Cor pulmonale Inherited alpha1 antitrypsin deficiency is a rare genetic condition causing breakdown of elastin = emphysema Pulmonary blebs Are small subpleural thin walled air containing spaces, not larger than 1-2 cm in diameter. Theri walls are less than 1mm thick. Can coalesce to form larger cystic spaces called bullae, if they rupture, they allow air to escape into pleural space resulting in a spontaneous pneumothorax. Hypoxic drive Normal COPD CO2 is principle stimulant for respiration Due to chronically high levels of CO2, sensitivity to CO2 levels is decreased, with a higher threshold required. O2 takes over as principal stimulant for respiration, as patients develop a hypoxic drive. One of the most clinically interesting and least understood theories in respiratory medicine is the hypoxic-drive theory. This holds that people who chronically retain carbon dioxide lose their hypercarbic drive to breathe. Thus, according to the theory, since the brain no longer responds to hypercarbia, the only remaining autonomic drive is hypoxemia. It then follows that, should patients in this condition be given enough supplemental oxygen to drive their PaO2 levels much higher than 60 mm Hg, they will also lose their hypoxemic drive to breathe. Hypoxic pulmonary vasoconstriction Main primary issue with O2 administration Compensatory mechanism to improve VQ matching a) Normal lung with good V/Q matching b) Ventilation impaired in COPD in certain parts of the lung, compensation HPV in those areas to improve V/Q matching c) If O2 is administered, the compensatory HPV is lost. Blood flow increases, delivering more CO2 to that alveolus. CO2 is transferred into the alveolus, but cannot escape the narrowed bronchi. CO2 builds up in alveolus, and travels back into the blood. Haldane effect Oxygenation of blood in the lungs displaces carbon dioxide from haemoglobin, increasing the removal of carbon dioxide. Consequently, oxygenated blood has a reduced affinity for carbon dioxide. Thus, the Haldane effect describes the ability of haemoglobin to carry increased amounts of carbon dioxide (CO2) in the deoxygenated state as opposed to the oxygenated state. A high concentration of CO2 facilitates dissociation of oxyhemoglobin. 3.3 Clinical features Finger clubbing Increased infections due to cilia malfunction Gasping Home oxygen Barrel chest (increased AP diameter) Hoover's test: lung hyperinflation leading to a flattened diaphragm which causes the lower rib cage to move paradoxically during inhalation, in an inward direction rather than outward. Positive (abnormal) Negative (normal) Normal for COPD patients Inhale: fingers wrapped around chest get closer together Inhale: fingers wrapped around chest get further apart Pursed lips breathing - Reduces RR - Increases TV - Increases SaO2 - Intrinsic PEEP - increases pressure to expand alveoli and allow for more gas exchange Cor Pulmonale 1. RHF is caused by respiratory disease 2. Patents often develop enlarged hearts 3. Long term HPV causes remodelling of pulmonary vasculature and persistent narrowing of those vessels which causes pulmonary hypertension. 4. The right side of the heart has a harder time pumping blood to the lungs when this happens. If this high pressure continues, it puts strain on the right side of the heart, leading to RVH, then RA dilation, followed by RVF or Cor Pulmonale 5. Signs of RVH: peripheral oedema and elevated JVP 6. ECG: RVH and RBBB Cor Pulmonale ECG Tall P waves: right atrial dilation RVH with RV strain pattern RBBB 3.4 Chronic medications Reduced frequency and severity of exacerbations Elude to severity of disease progression/chronic status The triple therapy 1. S/LABA 2. S/LAMA 3. ICS is less effective for COPD because inflammatory cells are different to asthma Inflammatory cells Asthma COPD Eosinophils Mast cells Neutrophils Macrophages 3.5 Prehospital treatment O2 administration in AECOPD O2 administration should be administered carefully as it affects the following compensatory mechanisms which may lead to oxygen induced respiratory depression - HPV (abolishes) - Hypoxic drive (abolishes) - Haldane effect Low dose controlled supplemental O2 therapy TTE SaO2 of 88 to 92%. Neb for 6 minutes at 6 litres and reassess History taking - Are you a known CO2 retainer? - Has a doctor told you what your normal oxygen level is? Step 1: classify current exacerbation (mild/moderate/severe/life threatening) Step 2: classify chronic status Mild Moderate Severe SABA SABA LAMA/LABA ICS SABA LAMA/LABA ICS O2 therapy Step 3: classify risk for exacerbation Low risk High risk 0 or 1 exacerbation not leading to hospital admission >2 exacerbations in previous year, or > 1 exacerbation leading to hospital admission 4.0 Acute Pulmonary Oedema and ARDS 4.1 General pathophysiology - APO Cardiogenic Non-cardiogenic Increase in hydrostatic pressure due to cardiac issue Increase in permeability of pulmonary capillaries Valvular dysfunction Coronary artery disease LV dysfunction Injury to capillary endothelium Causes Increased capillary permeability and disruption of surfactant produced by alveoli Causes Increased left atrial pressure Causes Causes Increased pulmonary capillary hydrostatic pressure Movement of fluid and plasma proteins from capillary to interstitial space (alveolar septum) and alveoli 4.2 Specific pathophysiology Condition Pathophysiology Neurogenic/drugs CNS insult (seizure, head injury) Drugs (naloxone, opioids) Catecholamines released Increased cardiac output Pulmonary vasoconstriction Increased hydrostatic pressure in pulmonary capillaries Fluid plasma pushed out into alveolus Chemical burns/smoke inhalation Chemical burns (chlorine) Toxic inhalation (smoke, cyanide poisoning) Direct injury to lung tissue from - The chemical burn - Variety of toxic substances Increased capillary permeability (direct injury to endothelium) Fluid leaks out from capillaries into alveoli Bronchospasm may occur in presence of APO Drowning 3 mechanisms Direct injury from water Causes direct injury to lung tissue Leads to increased capillary permeability Fluid leaks out into alveolus Laryngospasm Laryngospasm causes large negative intrathoracic pressure against obstructed airway Pulls fluid into alveolus Hypoxia Lack of O2 and HPV Negative pressure Negative pressure: 1. Vocal cords snap shut - laryngospasm (protective mechanism) 2. Diaphragm expands and no air can get in due to now closed system 3. Negative pressure (pressure decrease) generated from increase in volume 4. Negative pressure sucks fluids in from capillaries. In closed system pressure is inversely proportional to volume - fluid moves down the pressure gradient Hypoxia and HPV also present High altitude pulmonary edema Thinks that oxygenation is poor due to decrease partial pressure of oxygen (hypoxia) Body tries to fix V/Q mismatch by HPV All vessels constricts, increasing hydrostatic pressure minimally - doesn't compare to large hydrostatic pressure increase like in CAPO - occasional HSP mechanism with other mechanisms Fluid moves from capillaries into alveoli down the concentration gradient ARDS Acute respiratory distress syndrome 1. Injury to lung form direct/indirect causes disruption and infiltrate 2. Exudative phase (early) - alveolar capillary membrane 3. Proliferative phase - multiplication of abnormal alveolar cells and inflammatory cells 4. Fibrotic phase - infiltration with fibroblasts replace alveoli and alveolar ducts with fibrosis 5. Resolution - slow and incomplete repair of alveoli Direct Indirect Pneumonia Chest trauma Smoke inhalation Systemic sepsis Burns Pancreatitis Drug overdose Effects of ARDS Pulmonary oedma + inflammatory infiltrates + surfactant disruption = hypoxia 4.3 Management Aim is to reverse hypoxia and prevent HPV - Treat underlying cause - Position semi-fowlers (30 degrees head/torso up) O2 therapy - aim for SpO2 96+ Ventilations with PEEP - ensure adequate ventilation before adding PEEP CPAP therapy early (form of PEEP) Consider GTN (withhold for as long as possible) - exhaust patient on CPAP before GTN administration For GTN, must understand pathophysiology and identity a hydrostatic pressure issue e.g. pink frothy sputum Cautious fluid therapy - keep them dry - Unless hypovolemic/septic shock - Maintain BP >90 and radial pulses CPAP Indications APO Contraindications - BP <90 GCS <=8 Age <16 Inadequate ventilatory drive Pneumothorax Facial trauma Epistaxis Mechanism - Recruits and re-expands collapsed alveoli (higher pressures) - Increases surface area to improve gaseous exchange - Splints/keeps open alveoli - Decreased WOB - May assist with pushing fluid back into capillaries PEEP Indications Contraindications Pulmonary edema (cardiogenic and noncardiogenic) Asthma and COPD (SpO2 <90) Profound hypoxemia associated with - Flail segments - Pulmonary contusions - Aspiration Newborn resuscitation Absolute - BP <90 Relative - Pneumothorax - Unilateral lung disease - Broncho-plueral fistula - Hypovolemia - Extrinsic PEEP should always be set to a low pressure to ensure it is lower than intrinsic PEEP 5-20 cm of water Do not increase PEEP over 5 cm of water for patients with obstructive lung disease PEEP may be increased to 10 cm of water for APO if SpO2 does not rise above 90% 5.0 Putting It All Together Asthma-COPD Overlap Syndrome (ACOS) - A growing body of evidence suggests that many patients meet diagnostic criteria for both asthma and COPD - The distinction between asthma and COPD is obscured in this patient population, which is now categorised at ACOS - 2% prince - ACOS is characterised by the presence of persistent airflow limitation nd identified by features it shares with both asthma and COPD including airway obstruction, exacerbation and respiratory symptoms - Patients with ACOS are often smoker that have asthma, which my progress to fixed airway diseases - Patients with ACOS experience more frequent exacerbations, hospitalisations and rapid decline in lung function versus patients with either asthma or COPD. Asthma vs COPD characteristics Characeterics Asthma COPD Age of onset <20 >40 Pattern and persistence of symptoms Regular changes Worse at night or early morning Obvious triggers: exercise, emotions, pollutants, allergens Every day, exertional dyspnea History of chronic cough and sputum with no obvious triggers Expiratory airflow limitation Variable Lung function normal between symptoms Persistent Abnormal lung function between symptoms/exacerbations History Previous diagnosis of asthma Family history of asthma and allergies Previous diagnosis of COPD, CB or emphysema Heavy past exposure to smoke, pollutants Long term clinical trajectory Seasonal/yearly variation in symptoms Medications often provide relief, lasting weeks Progressively worsens over years Limited and short-term relief to medications Clinical features Chest size normal between exacerbations Severe hyperinflation (barrel chest) Conflicting pathologies - General rule in medicine when there are conflicting diagnosis/treatments is to treat the dominant pathology - Ask yourself: is this patient more on the COPD or asthma side of the spectrum? - Administer oxygen therapy according to predominant pathology - Rest of management prehospitally is very similar: SABAs, SAMA and adrenaline if severe/life threatening Secondary spontaneous pneumothorax due to asthma/COPD Secondary spontaneous pneumothorax Primary spontaneous pneumothorax A PTX that occurs as a complication of underlying lung disease Occurs without precipitating event in the absence of clinical lung disease Tension pneumothorax pathophysiology: - Lung pushes on mediastinum - Aortocaval compression - Causes hypotension, ALOC, radial pulses, absent or diminished breath sounds on affected side Clinical deterioration can involve marking the location for the needle decompression RIPAP first and identifying PTX will prevent unnecessary adrenaline administration Hydrocortisone prevents flare ups in the short term management CPAP is indicated for APO only, not dual lung pathologies such as in the presence of asthma. If unsure to administer adrenaline, see if nebulised drugs work first then reassess. Causes of SSP - COPD is most common with 50-70% of SSP caused by COPD - Rupture of apical blebs is the usual cause - Severity of COPD correlates with the likelihood of developing SSP - Asthma is a much less common cause, often due to over-zealous ventilation (barotrauma) Important differential diagnosis for a wheezing patient - Enlarged thyroid (goitre) stridor sound - Cardiac asthma (cardiogenic APO) - Airway obstruction - Bronchitis - Anaphylaxis Difficulty with BVM ventilations B Beard M Mask seal Tegader/glad wrap O Obese O Obesity/obstruction Ramp/semi fowlers N No teeth A Ages Mask of inside of patients lower lip E Elderly N No teeth Teeth out to intubate, teeth in to ventilate Rolled gauze on inside of mouth S Sleep apnoea/snoring S Stiffness (resistance to ventilation) OPA/NPA Difficulty with extraglottic/LMA placement R Registered mouth opening O Obstruction/obesity D Distorted anatomy S Stiffness (resistance to ventilation) 6.0 LRTIs and URTIs Inflammatory response: inflammation is a protective response from the bodies immune system Inflammation is a critical innate defence in the war between microbial invaders and their hosts microorganisms 1. They trigger inflammation when they're introduced into the body and begin to grow and produce compounds that damage host cells 2. Resident immune cells called macrophages may wander into the infected area and engulf the invading organisms 3. The macrophages digest the material and in this way help clean up the infection 4. In response to the infection macrophages releasing a number of chemicals including those called cytokines 5. Cytokines are small proteins that regulate the immune response some diffuse into the vasculature and stimulate endothelial cells to express specific receptors called selectins 6. Selectins binds to carbohydrates on the surface of neutrophils snagging the cells as they flow by in the bloodstream and slowing them down such that they roll along the endothelium inflammatory signals trigger these rolling neutrophils to express adhesion 7. Molecules called integrins on their surface the integrins lock onto adhesion molecules called AI cam 1 and V cam 1 on endothelial cells 8. The tight adhesion stops the rolling and the neutrophils begin to scratch out along the endothelial surface 9. Damaged tissue cells in the area of inflammation release bradykinin a nine amino acid polypeptide that helps loosen the tight junctions between endothelial 10. Cells neutrophils can now initiate extravasation in which they squeeze through the loosened endothelial wall and into the tissues where they can help macrophages attack the invading microbes 11. Bradykinin molecules also bind to other cells of the immune system called mast cells that are in the area causing them to release histamine 12. The histamine further loosens the endothelial cell junctions allowing more fluid in cells to move out of the capillaries 13. Kinin when it attaches to capillary cells induces the cells to synthesise prostaglandins 14. Prostaglandins stimulate nerve endings causing pain which draws awareness to the infected area The five cardinal signs of inflammation: - Redness - Warmth - Pain - Swelling - Altered function of the affected site Due to - Capillary dilation - Increased capillary activity - White blood cell infiltration - Capillary leakage - Sensation of pain Infections - Bacteria and virus cause most human infections - Disease: when the cells of the body are damaged Difference between bacteria and a virus Bacteria Both Viruses Living organism, unicellular Larger Fission: a form of asexual reproduction Localised Usually treated with antibiotics In latin means little stick Can cause disease Spreads by roots of coughing, sneezing, coming into contact with contaminated animals, people Does not have nuclei Possibility to be vaccinated Capable of killing humans and raging human health Not living, no cells Smaller Reproduction: invades host cell, taking control an copies the DNA/RNA destroying the host cell Systemic Antibiotics will not affect the disease In latin means poison Portals of entry Respiratory tract Directly via the nose and mouth (eyes) Gastrointestinal Directly via contaminated food/water Indirectly mouthing contaminated surfaces or fluids Genitourinary tract Poor hygiene STI’s Skin Animal bites Trauma, lacerations, punctures Upper Respiratory Tract Infections (URTI) Upper airway: C6 up - Microbes constantly enter here - Cilia and goblet cells clean the area Types of infections Nasal Rhinitis: runny nose Sinusitis: change in voice. No echo Pharynx Pharyngitis: sore throat Tonsils: lymph tissue and front line immune system Tonsillitis: painful to swallow Strep throat: pus Larynx Laryngitis: hoarse voice Epiglottis: supraglottic Apiglottitis: global vaccination make this rare - unable to swallow Croup: subglottic Laryngotracheobronchitis Trachea Tracheitis Influenza: often portal of entry in the URT Type A Most common Mutates easily Acquire immune system may not recognise the mutation Hard to vaccinate against Spread - Via droplets: gibe your infected patient a mask - Can live outside host for several hours - wash hands and wipe areas Influenza vs cold Influenza Cold None None Fever Headache Runny nose Sneezing None None Bacteria Virus Gradual onset Localised symptoms Pus (exudate) (from snot) Swollen/tender glands Rapid onset Systemic symptoms Watery discharge (from snot) Less likely Paramedics and the flu - Stay at home of you have it - Give patients P2 mask (duck bill) - Wash your hands - Low transport threshold if: <6 months, pregnant, >65, chronic disease, immunocompromised - Provide symptomatic relief: panadol, remove heavy clothing, rigours Lower respiratory tract infections Acute Bronchitis - Swelling of the bronchus Often secondary to URTI Acute and persistent cough - With other signs and symptoms Chronic bronchitis (COPD) - Cough and daily mucus production For at least 3 months For two or more consecutive years Pneumonia - alveolar - Community acquired - many types Hospital acquired Aspiration Populations at risk - Severity of infection - Associate symptoms - Comorbidities - Age - Immunocompromised Sepsis Sepsis: Life threatening organ dysfunction due to dysregulated host response to infection Septic shock: A subset of sepsis with profound circulatory, cellular and metabolic abnormalities. Mortlites = 20-30%. This is a syndrome: a group of signs and symptoms that occur together Diagnosis: based on a combination of various signs and clinical features Sepsis risk High risk Moderate risk RR >25 SpO2 <92% Systolic BP <90mmHg HR >130 GCS <15 Skin changes Reduced urine output Diarrhoea RR 21-24 Temp <35.5 or > 38.4 Systolic BP 90-99mmHg HR 90-129 Reduced urine output Treatment - Panadol - Oxygen - Fluid - aim for MAP >65mmHg - Adrenaline will increase MAP by shunting blood away from peripheries (vasoconstriction) 7.0 Paediatrics With a Noisy Airway Paediatric assessment Paediatric Assessment Triangle (PAT) Appearance WOB Circulation to skin Tone Interactiveness Gaze Cry Conscionability Breath sounds Positioning Retractions Nasal flaring Pallor Mottling Cyanosis O2 therapy - Children desaturate faster due to higher metabolic demands and lower functional residual capacity, so keep on higher end of 94-98% to buy time especially if/when condition suddenly deteriorates - Flow via nasal cannula to children should not exceed 2 lpm, as these higher flows are uncomfortable for the child and can cause drying and potential bleeding of the nasal mucosa. For infants who have a requirement of >2L/min, oxygen should be delivered via hudson face mask starting at 4L/min Types of coughs Whooping cough Caused by bacteria - hear the whoop at the end gasping for air Croup Caused by virus Swelling of vocal cords Dry cough Caused by asthma Influenza Pneumonia Productive/wet cough Pneumonia Cold Virus vs bacteria Virus Bacteria Systemic form start - e.g. general malaise and weakness Inside the cell Localised source then systemic Can be treated with antibiotics Outside the cell and multiply Epiglottitis vs croup Epiglottitis Croup Drooling (swollen and too painful to swallow) Neck extended Increased pulse Age usually 3-7 years Fast onset (within hours) Supraglottic (higher up) Systemically unwell No cough Temp >38.5 - high grade fever Vaccination helpful No obvious drooling (area affected is lower) No extended neck Hoarseness of voice with or without respiratory distress Stridor auscultated over trachea only - narrowing not in lungs but in larynx and trachea Age usually <3yo Slow onset (1-3 days) Glottic and subglottic (lower down) Coryza (catarrhal inflammation of the mucous membrane in the nose, caused especially by a cold or by hay fever), RTI Seal-like barking Temp <38.5 - low grade fever Vaccination less useful Rapidly developing inflammation of the epiglottis and adjacent tissues, due to bacterial infection, may cause life-threatening airway obstruction. Refers to an infection of the upper airway which obstructs breathing and causes characteristic barking cough. The cough and other symptoms of croup are the result of swelling around the vocal cords (larynx), trachea (windpipe) and bronchial tubes (bronchi) A common viral inflammatory illness causing narrowing of the supraglottic airway. Bacterial - influenza type B Viral: - Parainfluenza virus - Flu A Flu B Rhinovirus RSV Wheeze or stridor Phase of respiratory cycle Wheeze Stridor Consistent throughout lung fields Localised over trachea Start with inspiration - the more severe it gets progresses to inspiration and expiration Asthma Croup Mostly expiratory wheeze (sometimes inspiratory when severe/life threatening) Inspiratory wheeze localised over the trachea Upper airway wheeze inspiration and expiration biphasic stridor - sign of severe croup impending upper airway obstruction Respiratory Syncytial Virus (RSV) Causes infection of the lungs and breathing passages, is a major cause of respiratory illness in young children Asthma Bronchiolitis Wheezes >2 yo Family Hx Allergen or respiratory pathogen Fever if caused by RTI Good response to B2 agonists Wheezes <2 yo URI, coryza RSV Fever Little to none response to B2 agonists Brief periods of apnoea Pertussis - 100 day cough - whooping cough - Infants <1yo make up 50-70% of cases - Common 3-12 days after exposure - Lasts up to 6 weeks - Whoop sound occurs with the forceful inspiration after a coughing fit Treatment Westley croup score Mild <=2 Moderate 3-7 Severe >=8 Dexamethasone (PO) Neb adrenaline (5mg SDO) Dexamethasone (PO) Neb adrenaline (5mg SDO) Dexamethasone (PO) All patients with suspected croup should be transported to hospital for assessment Condition Treatment Pharmacology Croup Westley croup score Dexamethasone Neb adrenaline 5mg (f moderate to severe) Paracetamol Localised effects of adrenaline wanted (alpha): vasoconstriction properties to minimise leaky capillaries - quick fix Dexamethasone: slower working agent reduces inflammation (like hydrocort - not in acute phase) Epiglottitis Paracetamol IV fluids Sit on hands - no drugs that can help O2 sats right up with O2 Bronchioliti s Transport Asthma Neb salbutamol Neb ipratropium bromide Hydrocortisone Whooping cough (pertussis/1 00 day cough) O2 therapy 8.0 Pulmonary Embolism Pulmonary embolism - About 90% of pulmonary emboli come from the legs, with most involving the proximal veins - Prevention of PE therefore requires both prevention of venous thromboembolism and effective treatment of DVT when it occurs - Other types of PE include fat, air and amniotic fluid embolism PE vs DVT DVT PE Thrombus that forms in a deep vein of the leg or pelvis either partially or totally blocking the flow of blood. A DVT of part of it breaks off from the vein The break away clot travels through the bloodstream to the hart and migrates towards the lung The clot blocks a vessel in the lung, interrupting blood supply Pathophysiology Virchow’s triad 1. Stasis: abnormalities in blood flow such as immobilisation including lengthy bed rest or travel, obesity, pregnancy, paralysis, atrial fibrillation, tremors 2. Vessel wall injury: injuries to vascular endothelium such as surgery, hypertension, atherosclerosis, chronic inflammation and infection 3. Hypercoagulability: causes include: estrogens, birth control pills, pregnancy, cancer, inherited protein deficiencies, post operative, any medication that reduces blood viscosity. Risk factors for PE - Recent surgery/immobility - Pregnancy - Oral contraceptive pill - Extended travel >12 hours - Acute or chronic illness - Malignancy - interfere with coagulation - make blood more viscous - Smoking - interfere with coagulation - make blood more viscous Pathophysiology overview 1. Sudden obstruction of blood flow to the lungs, pulmonary hypertension and severe strain on the heart 2. Lung tissue becomes infarcted and the patient perceives this as sharp pleuritic chest pain. Because part of the lung is now dead or dying, the patient becomes hypoxic and the RR increases to compensate for the non-functioning lung tissue. The patient may then begin to have massive haemoptysis (coughing up blood from lungs). 3. The CV system undergoes sudden changes as well due to the acute obstruction. The HR increases as it initially tries to compensate for the impaired blood flow, but, if the size of the clot is overwhelming, it can't keep forward flow and obstructive shock occurs. Pathophysiological response to PE - Infarction followed by inflammation in the lung and pleura - Increased dead space causes an increase in V/Q mismatch, causing abnormal gas exchange. This does not cause hypoxia. - Shunting attempts to compensate for this increases dead space by sending all CO to the remaining lung tissue. This can work well, but if the clot is too large, then capillaries become engorged, and the diffusion distance for O2 and CO2 is too far. Hypoxia and eventually hypercapnia (late sign) follow. Clinical features Symptoms Frequency in PE Signs Frequency in PE Dyspnoea (rest or exertional) 60% Tachypnoea 60% Pleuritic chest pain 60% Tachycardia 40% Calf or thigh pain 44% Atelectasis 30% Calf or thigh swelling 41% Crackles on auscultation (rales) 18% Fever 15% JVD 10% Cough 10% Wells score Estimates the clinical probability of the patient having a PE PE and ECG - all a result of higher pressures on the right side - mainly ventricle - Sinus tachycardia - most common finding - Nonspecific ST segment and T wave changes - Abnormalities in <10%: S1Q3T3 (deep S wave lead I, Q wave and T wave inversion in lead III) - New incomplete RBBB conduction abnormality from RV dilation - RV strain: indicates myocardial ischemia in the RH as it is being stretched due to increased volume and pressure load from PE. V1-V3, II, III, aVF. - Right axis deviation - Right atrial enlargement (peaked T wave in lead II) PE and EtCO2 - Increased dead space means that lung ventilation is normal, but not all parts have been perfused. This causes reduced EtCO2 as some air goes in and out of the lungs without coming into contact with blood. - Further with the compensatory pulmonary shunting that follows, the perfusion distance within the capillaries prevents optimal gas exchange. Less CO2 can be exhaled in the parts of the lung that are still being perfused. - A reduction in CO also affects EtCO2 - The EtCO2 is not reflective of the PaCO2 in this case - a term referred to as an increased A-a gradient. Types of haemoptysis (blood coughed up) Pink frothy sputum CAPO Frank blood Artery been severely damaged Red tinged streaky sputum Small trauma from coughing - PE infected tissue in lung Diffusion vs perfusion issues CAPO PE Diffusion issue because O2 and CO2 struggle to get across PE is perfusion issue due to occluded pulmonary artery May be diffusion issue when blood vessels become enlarged due to HPV PE fluid resuscitation RV is struggling: more volume = right sided failure - biventricular failure - cardiogenic shock and die PE and pain Infarcted lung tissue causes adjacent inflammation of visceral pleura and rubbing against parietal pleura PE cardiac arrest - PEA in PE arrest - heart is trying to beat but its mechanically obstructed - PE less susceptible to lysis as opposed to AMI (due to clot coming from leg and is hardened) - ROSC patients will be in respiratory and metabolic acidosis - Stacked shocks: witnessed arrest from cardiac cause - is PE a cardiac cause? 9.0 Interstitial and Occupational Lung Disease Interstitial lung disease - Encompasses a group of disorder which all have varying degrees of fibrosis and inflammation in the lung interstitium - Interstitium is the region between the alveolar epithelium and capillaries - Cells present there include fibroblasts, myofibroblasts, macrophages - Other components: elastin, collagen Pneumoconiosis - Interstitial lung disease caused by inhalation of certain dusts and the immune response to these dusts - Usually occupational Main types Aetiology Coal workers pneumoconiosis Inhalation of coal dust Silicosis Inhalation of crystalline silica Asbestosis Inhalation of asbestos Interstitial lung disease pathogenesis 1. Most commonly due to dust, silica and asbestos 2. Particles that are 1 to 5 micrometres are most dangerous since they get lodged in the bifurcation of distal airways 3. Bigger unlikely to reach distal airways 4. Small act like gases and move in and out of alveoli freely 5. Macrophages dealing with the particles leads to cytokine release - inflammation - fibrosis and collagen deposition 6. Due to inhalation of mineral dust into the lungs - interstitial fibrosis 7. Smoking makes this all worse Lungs are essentially trapped in a cage of their own fibrosis which leads to 1. Small tidal volumes as lungs cannot expand well 2. Increased RR to maintain MV 3. Diffusion impairment (O2 battles to cross thickened fibrotic alveolar membrane) 4. In severe form can lead to hypoxia and cor pulmonale or respiratory failure Obstructive lung disease (OLD) Restrictive lung disease (RLD) Examples COPD, asthma, bronchiectasis ILD, neuromuscular disease, morbid obesity End result Air remains inside lung after a full exhalation leading to breath stacking Difficulty inhaling due to stiffness inside lung tissue or chest wall Problem Reduction in air flow (exhalation affected worse than inhalation) Reduction in lung volume Mechanism of hypoxaemia Ventilation issue Diffusion with ILD Ventilation issue with other conditions Ventilation strategy Slower rates (4 to 6), larger tidal volumes (produce visible chest rise) Faster rates (>10), smaller tidal volumes (produce visible chest rise) Asbestosis - High risk occupations: asbestos waste handler, construction worker, shipyard worker - Fibrosing condition of the lungs caused by inhalation of substantial asbestos dust - Lag period for 20 years before symptoms develop - It is usually slowly progressive with patients presenting with exertional breathlessness and a dry cough - Late inspiratory crackles and finger clubbing may be present - Most common presentation is incidental finding on chest X-ray of pleural plaques: thickened areas in the pleura visible on X-ray, but do not cause symptoms - Come patients develop diffuse pleural thickening which is extensive and progressive pleural fibrosis occurs, which involves both the visceral and parietal pleura - In contrast to pleural plaques, diffuse pleural thickening may markedly reduce lung volumes, resulting in exertional dyspnoea Coal workers pneumoconiosis (CWP) - Results from the inhalation of particles of coal mine dust, which are engulfed by macrophages which then accumulate to form the coal macule - Pneumoconiosis appears on the chest X-ray as small rounded opacities, typically appearing in upper and middle zones - Simple coal worker’s pneumoconiosis is not associated with abnormal clinical signs or significant impairment of lung function - If breathlessness and lung function impairment are present likely due to associated lung or heart disease - Progressive massive fibrosis (PMF) refers to the coalescence of macules to form irregular masses of fibrous tissue and is associated with increasing impairment of lung function and symptoms Silicosis - Workplace activities such as cutting, grinding and polishing produce fine dusts that contain respirable crystalline silica 1. 2. 3. 4. Once silicosis occurs the damage is irreversible and in contrast to coal workers pneumoconiosis, the condition may continue to progress after the individual is removed from the exposure Although subjects may be asymptomatic, as the condition progresses increasing levels of breathlessness can be anticipated Macrophages ingest the silica particles and triggers a massive inflammatory response This causes fibroblasts to multiply and produce collagen, causing fibrosis of the interstitium Silica particles also trigger formation of oxygen free radicals which further damage the lung Macrophages are outlived by the silica deposits in the lung, and so are engulfed by new macrophages, and the cycle of destruction continues, as the deposits cannot be removed. Silicosis types Classic silicosis Symptoms 10-20 years after exposure Accelerated silicosis Symptoms 5-10 years after exposure Silicoproteinosis Very high levels of exposure may induce symptoms within 1 year of exposure and death within 5 years Work related occupational lung disease - Both conditions will be managed according to COPD and asthma protocols - Additionally, the removal of the trigger may involve alternative occupation and may involve workers compensation Work related asthma Work related COPD Asthma originally caused by work vs existing asthma exacerbated by work Occupational asthma further divided into sensitiser induced (immune-mediated sensitization to an occupational agent) and irritant induced (non-immunological) Difficult to show causation in patient's history with a strong smoking history Easier to demonstrate causation in patients who are non-smokers E.g. machine operators and bus drivers (fumes), cotton workers (dust), cleaners (vapours) Cystic fibrosis - Abnormal CFTR channel does not move chloride ions, causing sticky mucous to build up on the outside of the cell - Normal CFTR channel moves chloride ions to the outside of the cell where sodium follows and water fallows keeping mucous thin - Inability to clear mucus from airways - Environment where bacteria etc thrive - Chronic colonisation of bacteria Clinical features - Clubbing of digits - Pallor of conjunctiva due to anaemia of chronic disease and iron deficiency - Mild hyper-resonance to percussion (OLD) - Coarse crepitations which may change/clear on coughing, may hear audible crackles at the mouth (bronchiectasis causing thick secretions) - Wheeze (OLD) Bronchiectasis - When bronchi and bronchioles become scarred and elated, allowing infected mucus to build up in pockets - Cilia also damaged which results in poor removal of mucous Management - Oxygen treatment includes controlled low dose oxygen therapy aiming for 88-92% - Nebulised therapy for bronchospasm. May consider nebulised hypertonic saline which has shown to act as a mucolytic - Escalate oxygen therapy and NIV as required to reverse persistent hypoxia unresponsive to convention O2 therapy - IV therapy: fluid therapy may be indicated for dehydrated patients - If patient becomes unresponsive start at the beginning - Response - A: patency - B: Patients intrinsic resp rate, tidal volume - are they moving any air? If no take control of breathing - C: pulse rate, BP, ECG (Fix A/B and C will follow) Management considerations - Use of supplemental breathing: working against pt forces air down the path of least resistance into oesophagus causing aspiration - Adrenaline opens up the airway in life threatening pts - If suspected pneumoconiosis: look for signs of heart failure - Ventilation strategy - Obstructive lung disease Restrictive lung disease Slow rates with big tidal volumes - as fast as they will allow to rescue acidosis 6-8 ml/kg Weak lungs Smaller tidal volumes at faster rate Smaller tidal volumes but still sufficient enough to produce visible chest rise Push 20 bpm in APO Caution with PEEP valve in OLD as increased extrinsic PEEP may override intrinsic PEEP Must monitor for aorto-caval compression via BP 10.0 Pleural Disease Haemoptysis Massive haemoptysis Pseudo haemoptysis Bleeding that is potentially acuity life-threatening 100 to >600 ml in 24 hour period Coughing of blood from a source other than the lower respiratory tract Sources - Nasopharynx - Oral cavity - Haematemisis aspirated into the lungs Lung blood supply Lung has dual blood supply - Low pressure (pulmonary) - Systemic pressure supply (bronchial artery) Bronchial artery responsible for 90% of cases Mechanisms - Neoplasms - Pulmonary venous hypertension - Infection History Physical examination - Volume in the past 24-48 hours? Is the blood mixed with white or purulent phlegm? Frequency of haemoptysis New or recurrent symptoms? Dyspnoea? Other symptoms of infection (e.g. fever, chills, night sweats) Sputum: amount and colour off blood: concomitant purulent secretions Respiratory distress? Tachypnoea/tachycardia? Accessory muscle use, cyanosis, bruising on skin suggestive of coagulopathy Focal wheeze or diffuse crackles Pleural effusion - 10-2