Respiratory Flashcards
What is pneumonia?
Inflammation of the alveoli of the lungs, usually this is as a result of a bacterial infection
What organisms commonly causes typical CAPs and what are the specific features seen in each?
- Streptococcus Pneumoniae – high fever, rapid onset, pleuritic chest pain and herpes labialis (cold sores on the lip)
- Haemophilus Influenza – common in COPD
- Staph Aureus – commonly following influenza infection
What organisms commonly causes atypical CAPs and what are the specific features seen in each?
- Mycoplasma pneumoniae – dry cough, atypical chest signs, autoimmune haemolytic anaemia and/or thrombocytopenia, erythema multiforme and nodosum, often in younger patients – diagnosis from mycoplasma serology
- Legionella – hyponatraemia and lymphopenia, classically secondary to infected air conditioning units – diagnosis from urinary antigen
- Klebsiella Pneumoniae – typically following aspiration in alcoholics or diabetics, has a typical red-currant jelly sputum and most commonly affects the upper lobes.
- Pneumocystis Jiroveci – HIV patients, dry cough, exercise induced desaturations and absence of chest signs – manage with co-trimoxazole
- Chlamydia psittaci – causes psittacosis, suspect with a combination of fever and history of bird contact
What organisms often cause hospital acquired pneumonia?
- Staph Aureus
- Enterobacteriaciae
- Pseudomonas species
- Haemophilus Influenzae
- Acinetobacter baumanii
- Fungal such as candida
What are the clinical features of pneumonia?
Productive cough Dyspnoea Pleuritic chest pain or ache Fever Tachycardia Haemoptysis Dull to percussion Bronchial breathing Reduced breath sounds Crackly chest
What investigations should be done in someone suspected of having a pneumonia?
Routine bloods – especially FBC, U&Es and CRP
CXR
ABG
Sputum sample
Pneumococcal and legionella urinary antigen test
How should suspected pneumonia be assessed for management in the primary care setting?
CRB65 – Primary Care Confusions (AMTs < 8/10) Respiratory rate > 30 Blood pressure <90/60 Age of 65
0 = low risk
1 – 2 = intermediate risk
3-4 = high risk
Home based care for CRB65 of 0
Use clinical judgement for those with a score of 1
Hospital assessment if 2 or more
Point of care CRP test
< 20 – do not routinely offer antibiotics
20 – 100 – consider delayed antibiotics
> 100 – offer antibiotics therapy
How is suspected pneumonia assessed for management in the secondary care setting?
CURB65 – secondary Care Confusions (AMTs < 8/10) Urea > 7 Respiratory rate > 30 Blood pressure <90/60 Age of 65
0 = treat in community
1 = safely managed in community if O2 sats > 92% and not bilateral or multi-lobar
2 or more = manage in hospital
3 or more = intensive care assessment
What general management should be offered to patients with suspected pneumonia?
Oxygen as needed
Monitor urine output
Sepsis 6 if appropriate
What antibiotics should be offered to patients with pneumonia?
If low severity CAP, then give 5-day course of amoxicillin or a macrolide, or tetracycline if pencilling allergic
If moderate severity CAP give 7-10-day course of dual antibiotic therapy – amoxicillin and a macrolide
If high severity CAP give 7-10-day course of dual antibiotic therapy – co-amoxiclav/tazocin and a macrolide
If HAP – give co-amoxiclav or cefuroxime within 5 days of admission. If more than 5 days after admission give Tazocin or ceftazidime or ciprofloxacin
What is COPD?
Definition – COPD is airflow obstruction which is usually progressive, not fully reversible and does not change markedly over several months. The disease is predominantly caused by smoking.
COPD is umbrella term encompassing both emphysema and chronic bronchitis and patients may have features of both.
What causes COPD?
Smoking
Alpha 1 antitrypsin deficiency
Occupational exposure such as coal dust, cadmium, cotton, cement, and grain
Pollution
What are the clinical features of COPD?
Exertional breathlessness – purse lip breathing Chronic cough Excess sputum production Frequent respiratory infections Wheeze Right sided heart failure Smoker or ex-smoker
What signs can be elicited in patients with COPD?
Bullae forming because of emphysema and destruction of alveoli
Hyperinflation
Cyanosis
Co2 retention (flap)
Cor pulmonale causing (right heart failure secondary to respiratory disease) – peripheral oedema, raised JVP, systolic parasternal heave and a loud P2
What investigations should be done in patients with COPD?
Spirometry FEV1/FVC ratio < 70%. Stage 1, Mild – FEV1 > 80% Stage 2, Moderate – FEV1 = 50-79% Stage 3, Severe – FEV1 = 30-49% Stage 4, Very Severe – FEV1 < 30%
Chest X-ray – hyperinflation, bullae, flat hemidiaphragm and exclude lung cancer
ABG
FBC
Genetic test for alpha 1 antitrypsin deficiency
CT scan if considering for surgery
What is the dyspnoea score?
- Not troubled by breathlessness except on strenuous exercise
- Short of breath when hurrying or walking up a slight hill
- Walks slower than contemporaries on level ground because of breathlessness or must stop for breath when waling at own pace.
- Stops for breath after walking about 100m or after a few minutes on level ground
- Too breathless to leave the house, or breathless when dressing or undressing.
What is the general management of someone with COPD?
Smoking cessation and offering nicotine replacement therapy, varenicline or bupropion
Annual flue vaccine and one-off pneumococcal vaccine
Pulmonary rehabilitation
What pharmacological management is offered to someone with COPD?
Short acting bronchodilators i.e. SABA (salbutamol) and/or SAMA (ipratropium)
Next you must determine whether patient has any asthmatic features or features suggesting they are likely to be steroid responsive:
• Any previous asthma diagnosis or atopy
• High blood eosinophil account
• Substantial variation in FEV1 over time (at least 400ml)
• Substantial diurnal variation in PEFR (at least 20%)
If they are like asthmatic or steroid responsive then switch to SABA + LABA (formoterol) + Inhaled corticosteroid, with the option of adding in a LAMA (tiotropium bromide) if still struggling (discontinue the SAMA if still on it). Use combined inhalers where possible.
If they do not have asthmatic features or are unlikely to be steroid responsive then switch to a LABA + LAMA and a SABA (discontinue the SAMA if still on it).
Oral theophylline can be added if patient is still breathless or if patient cannot use inhalers. Dose must be reduced if a macrolide or fluoroquinolone are co-prescribed.
What antibiotics can be offered prophylactically to COPD patients and what criteria must be met first?
Antibiotic prophylaxis may be recommended in select patients, azithromycin is usually used but patients must not be smoking, and must have had a CT scan to exclude bronchiectasis and a sputum culture to exclude atypical infections and tuberculosis
What drugs can we offer to help reduce the volume of sputum?
Mucolytics can be considered in chronic productive cough and continued if it improves symptoms, the most common drug used is carbocysteine.
How should cor pulmonale be managed in COPD?
In cor pulmonale treat with diuretics and consider long term oxygen. Do not use ACEi, Ca+ blockers or alpha blockers.
What are the last choice options for managing COPD
Long term oxygen therapy and lung volume reduction are last resorts
Which COPD patients shoud be assessed for long term oxygen assessment?
Must be used for at least 15 hours a day and patients CAN NOT be smoking, cigarettes or e-cigarettes. Assess patient who have any of the following. Before commencing must make a risk assessment include risk of fire and risk of falls from equipment.
• Very severe airflow obstruction (FEV1 < 30%), consider if only severe (FEV1 30-49%)
• Cyanosis
• Polycythaemia
• Peripheral oedema or raised JVP
• Oxygen saturations = 92%
How is someone assessed for long term oxygen therapy?
Assess by measured ABG on 2 occasions at least 3 weeks apart
Offer to those with pO2 < 7.3kPa
Offer to those with pO2 between 7.3-8kPa and one of the following
• Secondary polycythaemia
• Peripheral oedema
• Pulmonary hypertension
How does an exacerbation of COPD present?
Presentation – increased SOB, cough, wheeze, sputum, hypoxia, and confusion.
What often causes exacerbation of COPD?
Causes – can be non-infective but if infective then most commonly due to Haemophilus influenzae, others include strep pneumoniae and Moraxella catarrhalis. Viruses can also cause exacerbation and the most common cause is Rhinovirus.
How is exacerbation of COPD managed?
Treat with famous 5
• High flow oxygen by venturi mask 24% - use oxygen flow as instructed by mask
• Antibiotics (if infective cause) – amoxicillin/clarithromycin/doxycycline
• Nebulised Salbutamol
• Nebulised Ipratropium
• Corticosteroid – oral prednisolone 30mg for 5 days or IV hydrocortisone
• Oral theophylline with senior input
• NIV or BiPAP (Not CPAP which is better for HF and OSA)
Describe the systematic approach to interpreting an ABG
- Check pH – is it alkalotic or acidotic
- Check oxygen partial pressure and saturation to determine if arterial or venous
- Check PaCO2 – does this match the pH
- Check the HCO – does this match the pH
- Check the lactate levels
- Check Anion gap
- Check everything else including electrolytes
What causes a metabolic acidosis?
Occurs due to a reduction in plasma bicarbonate levels by one of two mechanisms
- Gain of strong acid e.g. ketones in DKA or lactate in sepsis
- Loss of base e.g. from bowel in diarrhoea
How do we determine what has causes a metabolic acidosis?
This can be determined by calculating the anion gap. (Na + K) – (Cl + HCO), the normal range for the anion gap is 10-18mmol/L.
What does a normal anion gap in a metabolic acidosis suggest?
If the Anion gap is normal this suggests a hyperchloraemic metabolic acidosis i.e. bicarb has been lost and replaced with chloride ions.
Causes include:
• GI loss in diarrhoea, fistula, ureterosigmoidostomy
• Renal tubular acidosis
• Drugs such as acetazolamide
• Ammonium chloride injection
• Addison’s disease
What does a raised anion gap in a metabolic acidosis mean?
If the anion gap has been raised, then this suggests that bicarbonate has been used up by new acids and not replaced.
Causes include
• Lactate from shock or hypoxia or sepsis
• Ketones in DKA or alcohol
• Urate in renal failure
• Acid poisoning such as salicylates or methanol
Why does a metabolic alkalosis occur?
Occurs either due to an increase in plasma bicarbonate levels or a loss of hydrogen ions. This usually occurs in the kidney or the GI tract. Primarily this revolves around activation of the renin-angiotensin II-aldosterone system. Aldosterone causes reabsorption of Na in exchange for H+ in the kidneys. Fluid loss such as vomiting, and diuretics causes loss of Na and Cl which activates aldosterone causing a loss of H+. In hypokalaemia K+ inside cells is switched for H+.
What are the common causes of a metabolic alklaosis?
Causes: • Vomiting/aspiration • Diuretics • Hypokalaemia • Primary hyperaldosteronism • Cushing’s syndrome • Congenital adrenal hyperplasia • Bartter’s syndrome
What is a respiratory acidosis?
Rise in CO2 that results in alveolar hypoventilation, renal compensation by increasing HCO can lead to a compensation respiratory acidosis.
What commonly causes a respiratory acidosis?
Causes
• COPD
• Decompensation respiratory conditions e.g. pulmonary oedema or asthma
• Sedative drugs such as opiates or benzodiazepines
What is a respiratory alkalosis?
Hyperventilation resulting in excess loss of CO2 resulting in an increase in pH.
What causes a respiratory alkalosis?
Causes
• Psychogenic – anxiety
• Hypoxia causing subsequent hyperventilation e.g. PE or high altitude
• Early salicylate poisoning (simulates the respiratory centre early but later on the acidic effect of salicylate causes a metabolic acidosis)
• CNS stimulation e.g. stroke, subarachnoid haemorrhage, and encephalitis
• Pregnancy
What is type 1 respiratory failure?
Gas exchange in the lungs in inadequate resulting in hypoxia, it is defined as a PaO2 < 8kPa with a normal or low PaCO2.
What causes type 1 respiratory failure?
This occurs primarily due to ventilation perfusion mismatching, hypoventilation, abnormal diffusion or right to left cardiac shunts. Examples of V/Q mismatching: • Pneumonia • Pulmonary oedema • Pulmonary embolism • Asthma • Emphysema • Pulmonary fibrosis • ARDS
What is type 2 respiratory failure?
Gas exchange in the lungs in inadequate resulting in hypoxia, it is defined as a PaO2 < 8kPa with a high PaCO2 >6kPa.
What causes type 2 respiratory failure?
Causes
This occurs due to alveolar hypoventilation with or without V/Q mismatching
• Pulmonary disease – asthma, COPD, pneumonia, pulmonary fibrosis and obstructive sleep apnoea
• Reduced respiratory drive – sedative drugs, CNS tumour or trauma
• Neuromuscular disease – cervical cord lesion, diaphragmatic paralysis, polio, myasthenia gravis and Guillain barre syndrome
• Thoracic wall disease – flail chest and kyphoscoliosis
How does respiratory failure present?
Hypoxia – dyspnoea, restlessness, agitation, confusion, central cyanosis, polycythaemia, pulmonary hypertension and cor pulmonale.
Hypercapnia – headache, peripheral vasodilation, tachycardia, bounding pulse, tremor/flap, papilloedema, confusion, drowsiness, and coma.
How should a suspected respiratory failure be investigated?
Routine bloods ABD CXR Sputum and blood culture if febrile Spirometry
How should type 1 respiratory failure be managed?
Type 1 – treat cause, give oxygen by facemask – 24-60%, and assisted ventilation if PaO2 < 8kPa despite 60% oxygen.
How should type 2 respiratory failure be managed?
Type 2 – be aware as the respiratory drive could be relying on oxygen. Treat underlying cause, controlled oxygen therapy starting at 24%. Repeat ABG in 20 minutes if CO2 is steady or lower then increase oxygen concentration. If CO2 has risen by >1.5kPa consider ventilatory support i.e. NIPPV or intubation and ventilation
What is acute respiratory distress syndrome? (ARDS)
Definition – acute lung injury characterised by severe hypoxaemia without a cardiac cause. The disease is self-perpetuating as more alveoli are damaged the swelling causes more trauma to more alveoli.
What causes ARDS?
Inflammatory damage to the alveoli causing pulmonary oedema, respiratory compromise, and consequently acute respiratory failure.
Describe the direct and indirect causes of ARDS?
Direct Pneumonia Smoke inhalation Aspiration Fat embolus
Indirect Sepsis Acute Pancreatitis Polytrauma Transfusion reaction Head injury – sympathetic stimulation leading to pulmonary hypertension
Describe the clinical features of someone with ARDS?
Can start hours to days after the event Dyspnoea Cyanosis and hypoxia Inspiratory crackles on auscultation Multiorgan failure Rising ventilatory pressures
In early stages – exudative phase with injury due to oedema
Later stage – fibroproliferative changes leading to scarring and poor lung function
How should someone with ARDS be investigated?
Routine bloods including amylase, clotting, CRP and blood cultures
Blood cultures
Arterial blood gas
CXR which usually shows bilateral pulmonary infiltrates
Pulmonary artery catheter to measures pulmonary capillary wedge pressure
What are the diagnostic criteria for ARDS?
Diagnostic criteria
• Acute onset
• CXR showing bilateral infiltrates
• PCWP < 19 or lack of clinical congestive cardiac failure
• Refractory hypoxaemia with PsO2:FiO2 <200
How should ARDS be managed?
Treat underlying cause e.g. antibiotics if signs of sepsis
Negative fluid balance with diuretics
Circulatory support – inotropes such as dobutamine, vasodilators and blood transfusions
Prone ventilation and use of PEEP
Mechanical ventilation using low tidal volumes to avoid pneumothorax
What is a pneumothroax?
Definition – Air in the pleural space
What are the risk factors for pneumothorax?
Tall, young, thin and male Marijuana smoking COPD Interstitial lung disease Cystic fibrosis Sub pleural blebs HIV leading to PCP Marfan’s or rheumatoid arthritis NIPPV
What can causes a pneumothroax?
Traumatic
Iatrogenic - chest drain, biopsy, subclavian line, ventilation in ITU etc.
Spontaneous – usually due to small blebs that burst on the lung surface.
What is the difference between a primary and secondary pneumothorax?
Pneumothorax in normal lung = primary pneumothorax
Pneumothorax in diseased lung = secondary pneumothorax
What are the clinical features of a pneumothorax?
Pleuritic chest pain especially on inspiration
Breathlessness and low saturation
How should someone with a suspected pneumothorax be investigated?
Investigated by X-ray on inspiration and if greater than 2cm from edge of rib cage then it equals a large pneumothorax as lung is 50% collapsed.
CT scan allows us to differentiate between pneumothorax and complex hollows lung disease, also of emphysema obscuring chest X-ray and finally if there is suspicion of aberrant drain position.
How are pneumothoraxes managed?
ABCDE and management of symptoms i.e. pain, SOB and blood sats.
Definitive management by aspiration or chest drain acutely or surgery – pleurectomy, fixing the bleb or pleuradhesis
Primary
Small – discharge home unless breathless in which case aspirate
Large – aspirate if this fails then chest drain
Secondary
If >50yrs, and large and/or patient is short of breath then a chest drain should be used
If 1-2cm attempt aspiration, if this fails (pneumothorax still greater than 1cm) then chest drain. Patient should be admitted for at least 24 hours.
If <1cm then give oxygen and admit for 24 hours
Are there any restriction after having a pneumothorax?
After a pneumothorax scuba diving should be permanently avoided unless the patient has undergone bilateral pleurectomy and has normal lung function and chest CT scan postoperatively.
Where are chest drains inserted?
Insertion of chest drain – triangle of safety in the mid axillary line, 5th intercostal space. This is bordered by the anterior edge of latissimus Dorsi, the lateral border of pectoralis major, a line superior to the horizontal level of the nipple and the apex below the axilla.
There is another triangle situation behind the scapula. Bounded by the trapezius above, latissimus dorse below and laterally by the vertebral border of the scapula.
What are the relative contraindications of a chest drain?
Relative Contraindications • INR > 1.3 • Platelet count < 75 • Pulmonary bullae • Pleural adhesions
What is a tension pneumothorax?
This is where a flap has been created in the lungs and the pleural space fills up with more air with each breath. This places pressure on the mediastinum and will cause a tracheal deviation.
