2024 COPD Module 2 Answers PDF

Module 2: Exacerbation of COPD ============================== Key concepts ------------- - Describe the components for optimal gas exchange and alveolar ventilation. - Describe how airflow obstruction effects gas exchange. - Describe compensatory mechanisms that aim maintain homeostas...

Module 2: Exacerbation of COPD ============================== Key concepts ------------- - Describe the components for optimal gas exchange and alveolar ventilation. - Describe how airflow obstruction effects gas exchange. - Describe compensatory mechanisms that aim maintain homeostasis. - Describe the clinical manifestations of COPD. - Recognise treatment priorities for the management of patients experiencing acute exacerbation of COPD. +-----------------------+-----------------------+-----------------------+ |  | A picture containing |  | | | text, font, | | | | screenshot | | | | Description | | | | automatically | | | | generated | | +=======================+=======================+=======================+ | Section: The | Section X: Management | Section: Primary | | mechanics of | Exacerbations. Pg | Survey & Physical | | breathing | 139-142 | assessment in | | | | Kenneally, J & | | Penola, D & McDonald, | | Flenady, T. | | V. 2024. The | | Respiratory | | structure & function | | Emergencies (Ch 21). | | of the pulmonary | | 2024 in K, Curtis et | | system (Ch 24) in J, | | al. Emergency and | | Craft et al. | | Trauma Care. Elsevier | | understanding | | | | | | | | | | Section: COPD | | | | | | | | Penola, D. Maltby, S | | | | & McDonald, V. 2024. | | | | Alterations of | | | | pulmonary system | | | | across the life span | | | | | | | | (Ch 25) in J, Craft | | | | et al. understanding | | | | pathophysiology | | | | (4^rd^ Edn). Pgs. | | | | 712-763. Elsevier. | | | | | | | +-----------------------+-----------------------+-----------------------+ +-----------------------------------------------------------------------+ | What is COPD? | | | | Chronic obstructive pulmonary disease includes chronic bronchitis and | | emphysema[.] As the name suggests it is an obstructive | | pulmonary disease (as opposed to a restrictive pulmonary disease) | | which means there is an obstruction to airflow in the lungs. [COPD | | includes two diseases: chronic bronchitis and emphysema.] | | | | [Chronic bronchitis] is defined as hypersecretion of | | mucus and chronic productive cough for at least 3 months of the year | | (usually the winter months) for at least 2 consecutive years. | | | | [Emphysema] is abnormal permanent enlargement of gas | | exchange airways accompanied by destruction of alveolar walls. | | Obstruction results from changes in lung tissues, rather than mucus | | production and inflammation as in chronic bronchitis. The major | | mechanism of airflow limitation is loss of elastic recoil. | | | | **Pathogenesis of emphysema & chronic bronchitis. What is happening | | to the alveoli and the bronchioles?** | | | | Alveoli: Emphysema is a disease of the alveoli. The fibres that make | | up the walls of the alveoli become damaged. The damage makes them | | less elastic and unable to recoil on expiration, making it hard to | | exhale carbon dioxide out of the lungs, causing increased volume of | | air in the alveoli. Degradation of the capillary/alveolar membrane | | also occurs. | | | | =LOSS OF ELASTIC RECOIL AND DEGRADATION OF THE ALVEOLI-CAPILLARY | | MEMBRANE | | | | Bronchioles: in chronic bronchitis the small airways become inflamed | | and fill with mucus. Initially this process affects only the larger | | bronchi, but eventually all airways are involved. As the airways | | become increasingly narrowed, airway obstruction results (see Figs | | 25.11 and 25.12). The airways collapse early in expiration, trapping | | gas in the distal portions of the lung. Production of thick, | | tenacious mucus that cannot be cleared because of impaired ciliary | | function increasing susceptibility to pulmonary infection and injury. | | Frequent infectious exacerbations are complicated by bronchospasm | | with dyspnoea and a productive cough. | | | | = SWOLLEN AND MUCUS FILLED AIRWAY, IMPAIRED COUGH | | | | **Effect of disease on respiratory function?** | | | | **[Impaired gas exchange:]** large floppy alveoli make | | expiration difficult because loss of elastic recoil reduces the | | volume of air that can be expired passively and results in decrease | | alveolar ventilation. Less volume of air during inspiration and | | expiration means less gas exchange. Degradation of the | | capillary/alveolar membrane results in a loss of the respiratory | | membrane where gases cross between air and the blood, resulting in a | | significant ventilation--perfusion mismatching and | | [hypoxemia]. | | | | **[Decreased minute volume:]** hypoventilation occurs in | | later stages of the disease due to difficulty in expiration and | | reduced exhaled tidal volume. | | | | **[Increased work of breathing:]** loss of elastic recoil | | impeded expirations and air is trapped in the lungs. Air trapping | | causes an increase in expansion of the chest, which puts the muscles | | of ventilation, such as the diaphragm not as effective. This means | | that more effort is required to expire the air from the lungs from | | other muscles (accessory muscles of the neck, intercostal and | | abdomen) results in increased workload of breathing, so that late in | | the course of disease, many individuals will develop [hypoventilation | | and hypercapnia]. Eventually ventilation--perfusion | | mismatching, and hypoxaemia occurs. Extensive air trapping puts the | | respiratory muscles at a mechanical disadvantage, resulting in | | hypoventilation and hypercapnia. | | | | Figure 25.10 (Chapter 25: Craft et al, 2024) | | | |  | | | | Activity Case study: JOHN HAMPTON presents with Exacerbation of COPD | | -------------------------------------------------------------------- | | | | A new admission has arrived. You receive the following handover: | | | | +--------------------------------+--------------------------------+ | | | S | John Hampton, a 74-year-old | | | | | male presented to the | | | | | Emergency Department with | | | | | shortness of breath that has | | | | | been getting worse over the | | | | | last few days. He has an | | | | | increasing amount of mucus | | | | | which is different in colour | | | | | and is feeling generally | | | | | unwell. He visited his GP | | | | | during the week who started | | | | | him on a course of antibiotics | | | | | and oral corticosteroids. He | | | | | self-medicated with a Ventolin | | | | | inhaler prior to admission but | | | | | this had not resolved his | | | | | symptoms. He became | | | | | increasingly breathless and | | | | | distressed and was brought to | | | | | the Emergency Department by | | | | | ambulance. | | | +================================+================================+ | | | B | Diagnosed with Emphysema 5 | | | | | years ago. Smokes pack/day for | | | | | 40 years. ETOH occasional | | | +--------------------------------+--------------------------------+ | | | A | A-G Assessment | | | | | | | | | | Airway: Clear | | | | | | | | | | **Breathing:** | | | | | | | | | | - Severe shortness of breath | | | | | and coughing | | | | | | | | | | - Using accessory muscles of | | | | | respiration | | | | | | | | | | - Unable to speak. | | | | | | | | | | - On auscultation of the | | | | | chest there is diminished | | | | | air entry | | | | | | | | | | | | | | | | | | | | - Respiratory rate 36 | | | | | breaths/min | | | | | | | | | | - SpO~2~ 84% on room air | | | | | | | | | | **Circulation:** | | | | | | | | | | - Heart rate: 140 beats/min | | | | | ↑ | | | | | | | | | | - BP 150/88mmHg ↑ | | | | | | | | | | - Temperature: 38.2 | | | | | | | | | | **Disability:** | | | | | | | | | | - GCS 15, PEARTL. Equal | | | | | strength X 4 | | | | | | | | | | **Exposure:** | | | | | | | | | | - No bruising, wounds | | | | | | | | | | - IV cannula left cubital | | | | | fossa. | | | | | | | | | | - Height: 195cm | | | | | | | | | | - Weight: 88kg | | | | | | | | | | **Fluids:** | | | | | | | | | | No IV fluids in progress | | | | | | | | | | **Glucose:** | | | | | | | | | | - BGL: 5mmol/L | | | +--------------------------------+--------------------------------+ | | | R | Continuous nebulized Ventolin | | | | | | | | | | Hydrocortisone 100mg IVI stat | | | | | then 6 hourly | | | | | | | | | | CXR | | | | | | | | | | Sputum culture | | | | | | | | | | Keep Oxygen saturations | | | | | \~88-92% | | | | | | | | | | ABG on RA: | | | | | | | | | | pH:7.32 | | | | | | | | | | PaO2: 54 | | | | | | | | | | PaCO2: 58 | | | | | | | | | | HCO3: 26 | | | | | | | | | | SaO2: 84% | | | | | | | | | | BE- 4 | | | +--------------------------------+--------------------------------+ | | | | **Question 1:** Assessment of John Hampton: Based on the handover | | determine your treatment priorities. Read section: Primary Survey & | | Physical assessment from Ch 13 pg 225-264, Curtis et al, 2024 | | | | +---------------------+---------------------+---------------------+ | | | Assessment | Finding | Treatment | | | +=====================+=====================+=====================+ | | | Airway | Patent. No sign of | Keep NBM | | | | | obstruction | | | | +---------------------+---------------------+---------------------+ | | | Breathing | Hypoxia | Apply Oxygen VM @ | | | | | | 28%. Continuous | | | | | | saturation | | | | | | monitoring | | | | | | | | | | | | Adjuncts: Arterial | | | | | | blood gas & CXR | | | +---------------------+---------------------+---------------------+ | | | | Chest auscultation: | Sit in high fowlers | | | | | decreased air entry | | | | | | & expiratory wheeze | | | | +---------------------+---------------------+---------------------+ | | | | Tachypnoea, equal | | | | | | chest rise & fall | | | | +---------------------+---------------------+---------------------+ | | | | Forced & prolonged | | | | | | expiration | | | | +---------------------+---------------------+---------------------+ | | | | Increased work of | | | | | | breathing | | | | +---------------------+---------------------+---------------------+ | | | Circulation | Tachycardia | Observe place on | | | | | | continuous cardiac | | | | | | monitor. | | | | | | | | | | | | Document on | | | | | | observation | | | | | | | | | | | | Inform Doctor (if | | | | | | on wards call rapid | | | | | | response) | | | +---------------------+---------------------+---------------------+ | | | | Hypertension | | | | +---------------------+---------------------+---------------------+ | | | | Peripherally cool | | | | +---------------------+---------------------+---------------------+ | | | Disability | GCS 15 | Observe, drowsiness | | | | | | is a sign of | | | | | | deterioration | | | +---------------------+---------------------+---------------------+ | | | Exposure | Skin intact, no | Nil. Maintain | | | | | bruises or wounds, | dignity | | | | | cannula | | | | +---------------------+---------------------+---------------------+ | | | Glucose | Normal | Nil | | | +---------------------+---------------------+---------------------+ | | | Other | High risk for | Triage to resus, | | | | | deterioration | continuous | | | | | | monitoring of | | | | | | pulse, and oxygen. | | | | | | BP 15 minutely. | | | | | | Doctor should be in | | | | | | attendance | | | +---------------------+---------------------+---------------------+ | | | | **Question 2**: Describe the pathogenesis of the clinical | | manifestations: | | | | Hypoxia V/Q mismatch- alveoli hypoventilation | | ----------------------------- ------------------------------------- | | --------------------------------------------------------------------- | | --------------------------------------------------------------------- | | --------------------------------------------------------------- | | Cough Increased sputum and purulence | | Wheeze Narrowing of the airway due to inflam | | mation, oedema and sputum | | Hypercarbia (high CO2) V/Q mismatch- alveoli hypoventilation | | Tachypnoea Chemoreceptors detect hypoxia and fee | | dback to respiratory center to increase respiratory rate | | Increased work of breathing Increased tension caused by narrow ai | | rways and floppy alveoli required increased effort to expire air from | | lungs. Accessory muscles are required, and diaphragm effectiveness i | | s reduced due to squashing from over inflated lungs | | Dyspnoea Hypoxia cause air hunger combined wit | | h increase work of breathing to overcome tension of narrow airways lo | | ng-term evaluation involves measurement of dyspnea on a valid scale s | | uch as Modified Medical Research Council Dyspnea Scale (MMRC) | | Expiratory flow limitation Narrow airways cause obstruction to a | | irflow | | Hyperinflation Gas trapping from loss of elastic rec | | oil and narrow bronchioles from inflammation and sputum increase the | | volume of air left in the alveoli at the end of expiration. | | | | The clinical manifestations of COPD exacerbations can be highly | | variable and reflect broad heterogeneity in the underlying | | pathophysiology of COPD as well as diversity in the nature and effect | | of the inciting agent. Expiratory flow limitation (EFL), because of | | airway inflammation, is the pathophysiological hallmark of COPD. | | Exacerbations fundamentally reflect acute worsening of EFL, and there | | is evidence for both increased airway inflammatory activity and | | worsening airway obstruction as plausible explanations. | | | | Hypoxemia is a common problem in acute exacerbations. Worsening of | | ventilation--perfusion matching is the most important determinant of | | hypoxemia in this setting. Higher oxygen use from the increased work | | of breathing as well as by inadequate cardiac reserve to increase | | cardiac output can worsen hypoxia. Finally, especially in severe | | COPD, both the increase in airway resistance and the decrease in | | inspiratory to expiratory time ratio led to hyperinflation. | | Hyperinflated lungs impede the efficiency of the respiratory muscles, | | thereby contributing to the breathlessness experienced during these | | acute events. Measurements of arterial blood gases are therefore very | | important in the assessment of patients with acute exacerbations. | | Generally, an arterial Pa~O2~ of less than 60mmHg or an acute or | | acute-on-chronic respiratory acidosis indicates acute respiratory | | failure requiring hospitalization. Particular attention should be | | paid to changes in mental status, which might also indicate the | | presence of respiratory failure. | | | |  | | | | Respiratory pathophysiol-Ventilation-Perfusion | | | | **Question 3:** A plain chest-x-ray is taken. Compare and contrast | | John's x-ray below and a normal chest x-ray on the right. Look at | | John's diaphragm and consider how this may impact of John's | | breathing. | | | | Normal chest radiograph (male) \| Radiology | | Case \... | | | | Xray findings for COPD: | | | | Findings of chronic bronchitis on chest radiography** **are | | non-specific and include increased [bronchovesicular | | markings](https://radiopaedia.org/articles/missing?article%5Btitle%5D | | =bronchovascular-markings&lang=us) and [cardiomegaly](https://radiopa | | edia.org/articles/cardiomegaly?lang=us). | |  Emphysema manifests as [lung | | hyperinflation](https://radiopaedia.org/articles/lung-hyperinflation- | | 1?lang=us) with | | flattened hemidiaphragms, a small heart, and possible bullous | | changes.  On the lateral radiograph, a \"barrel chest\" with widened | | anterior-posterior diameter may be visualized. The \"[saber-sheath | | trachea](https://radiopaedia.org/articles/saber-sheath-trachea-2?lang | | =us)\" sign | | refers to marked coronal narrowing of the intrathoracic trachea | | (frontal view) with concomitant sagittal widening (lateral view). | | | | **Question 4: How is an exacerbation of COPD diagnosis made?** | | | | The simple pragmatic definition of a COPD exacerbation recently | | provided by the Canadian Thoracic Society: | | | | "*a sustained worsening of dyspnea, cough or sputum production | | leading to an increase in the use of maintenance medications and/or | | supplementation with additional medications."* | | | | Spirometry during an acute exacerbation: | | | | The routine use of pulmonary function tests to aid in the diagnosis | | and characterisation of severity of stable COPD has been suggested by | | recent clinical practice guidelines. However, the usefulness of | | spirometry or pulmonary function tests for the diagnosis of acute | | exacerbations or for the prediction of clinical outcomes remains | | unknown. The changes in spirometry variables observed during | | exacerbations of COPD are variable, and the time course of recovery | | of such physiological parameters following an exacerbation does not | | always follow that of symptom recovery. Lastly, given the | | heterogeneity of the structural abnormalities and pathophysiology | | which characterise COPD, the overall degree of impairment during | | exacerbations may not be adequately reflected in simple spirometry | | parameters. | | | | **Question 5:** Describe lung hyperinflation. What is causing this | | and how is this effecting John's breathing? | | | | Hyperinflation, defined as an increased volume of air remaining in | | the lung at the end of spontaneous expirations, is present when | | resting FRC or EELV is increased above normal. A significant | | proportion of patients with COPD have some degree of lung | | hyperinflation, which often remains undetected in the absence of | | detailed physiological analysis. | | | | Lung hyperinflation alters the geometry of the thorax and shortens | | the diaphragm, thereby placing the diaphragm in a suboptimal | | contractile position to generate pressure. This mechanical | | disadvantage reduces the force-generating capacity of the inspiratory | | muscles and is likely to become further exaggerated in patients who | | dynamically hyperinflate. the ability of the respiratory muscles to | | generate pressure decreases at high lung volumes in humans. | | | | Hyperinflation and the associated increase in work and oxygen cost of | | breathing may compromise blood flow to the periphery, leading to | | compromised oxygen delivery and therefore causing increased leg | | fatigue.  | | | | **Question 6: COPD is now recognised as a systematic disorder that | | has extrapulmonary manifestations. What are some might be some of the | | effects on the other organs:** **Ch 25 Craft, Fig 25.8 pg 712-763** | | | |  | | | | Extrapulmonary manifestations of COPD are also caused by an | | inflammatory process. Importantly, there is a general association | | between the severity of the airflow obstruction and the severity of | | extrapulmonary end-organ damage in patients with COPD. Recently it | | has been observed that COPD exacerbations are associated with | | increased levels of soluble markers of systemic inflammation in | | serum. Furthermore, the degree of systemic inflammation correlated | | with the degree of lower airway inflammation and was greater in the | | presence of a sputum bacterial pathogen, suggesting that the systemic | | inflammatory response at exacerbation is proportional to that | | occurring in the lower airway and is greater in the presence of a | | bacterial pathogen. | | | | **Heart: RV enlargement and eventually failure (**Cor pulmonale); | | vasoconstriction and pulmonary hypertension caused by | | hypoxia/hypercapnia and/or increased alveolar pressure can cause | | increase afterload to the right ventricle and when sustained will | | cause right ventricular failure. | | | | Skeletal muscle dysfunction: muscle wasting and osteoporosis cause | | specific anatomic and functional changes and contributes | | significantly to limited exercise capacity and reduced quality of | | life | | ([](https://www.atsjournals.org/doi/full/10.1513/pats | |.200512-125SF)). | | Lower peripheral muscle force occurs during acute COPD exacerbations | | ([](https://www.atsjournals.org/doi/full/10.1513/pats | |.200512-125SF)), | | and the reduced peripheral muscle force present at hospital admission | | partially recovers at discharge | | | | **Question 7:** John's has a arterial blood sample taken. Below is | | the result, **what are your nursing priorities based on the above | | result?** | | | | **The most important and first step should be to look at the | | patient's oxygenation.** | | | | **It is evident that the ABG shows hypoxia and initiating controlled | | oxygen therapy is needed to achieve a target saturations of 88-92%.** | | | | ABG on RA: | | | | pH:7.32 | | | | PaO~2~: 54 | | | | PaCO~2~: 58 | | | | HCO~3~: 26 | | | | SaO2: 84% | | | | BE- 4 | | | | **Question 8:** Refer to the Evidence-based guidelines under the | | additional resources tab (page 138 X2.1). What is treatment | | evidence-based recommendation for JOHN? | | | | Assess severity: Assessment of severity of the exacerbation includes | | a medical history, examination, spirometry and, in severe cases (FEV1 | | \< 40% predicted), blood gas measurements, chest x- rays and | | electrocardiography. | | | | Optimise treatment: | | | | An exacerbation of COPD may involve an increase in airflow | | limitation, excess sputum production, airway inflammation, infection, | | hypoxia, hypercarbia and acidosis. Treatment is directed at each of | | these problems. | | | | Bronchodilators: Inhaled beta-agonist (e.g., salbutamol, | | 400--800mcg; terbutaline, 500-- 100mcg) and antimuscarinic agent | | (ipratropium, 80mcg) can be given by pressurised metered dose inhaler | | and spacer, or by jet nebulisation (salbutamol, 2.5--5 mg; | | terbutaline, 5 mg; ipratropium, 500mcg). The dose interval is | | titrated to the response and can range from hourly to six-hourly. | | There is a lack of evidence in favour of one mode of delivery over | | another for bronchodilators during exacerbations of COPD. | | | | Corticosteroids: Oral corticosteroids hasten resolution and reduce | | the likelihood of relapse. Up to two weeks' therapy with prednisolone | | (40--50 mg daily) is adequate. Longer courses add no further benefit | | and have a higher risk of adverse effects. | | | | Antibiotics: Antibiotics are given for purulent sputum to cover | | typical and atypical organisms. | | | | Controlled oxygen therapy: This is indicated in patients with | | hypoxia, with the aim of improving oxygen saturation to 88 to 92%. | | Use nasal prongs at 0.5--2.0 L/minute or a Venturi mask at 24% or | | 28%. Minimise excessive oxygen administration, which can worsen | | hypercapnia. | | | | Ventilatory assistance: This is indicated for increasing | | hypercapnia and acidosis. Noninvasive ventilation by means of a mask | | is the preferred method. Although the adherence to pharmacological, | | rehabilitation and vaccination management as recommended in GOLD have | | each been shown to reduce health care costs, uptake of GOLD | | recommendations has had little evaluation. A study in a Victorian | | hospital setting demonstrated significant overuse of antibiotics and | | oxygen therapy, as well as a greater evidence practice gap in general | | medical units than respiratory medical units (Tang 2014) | | | | **Question 9**: Spirometry is used to diagnose and evaluate response | | to treatment. How are lung function tests effected in COPD? | | | | ###### The diagnosis of COPD rests on the demonstration of airflow li | | mitation which is not fully reversible ([Global Initiative for Chroni | | c Obstructive Lung Disease 2017](https://copdx.org.au/copd-x-plan/ref | | erences/references-a-g/#135a)). Spirometry is not useful during exac | | erbation due to individual variation. | | | | Because COPD is defined by demonstration of airflow limitation which | | is not fully reversible, spirometry is essential for its diagnosis | | and this may be performed in the community or prior to discharge from | | hospital. Most spirometers provide predicted ("normal") values | | obtained from healthy population studies, and derived from formulas | | based on height, age, sex and ethnicity. | | | | Airflow limitation is not fully reversible when, after | | adminis­tration of bronchodilator medication, the ratio of FEV~1~ to | | forced vital capacity (FVC) is \