Breathlessness- core conditions Flashcards
Asthma
A chronic inflammatory condition of the airways which is characterised by recurrent symptoms and airflow obstruction which is usually variable and reversible
Pathophysiology of asthma
Inhaled allergens stimulate the development of T helper cells which produce a variety of cytokines which stimulate the production of IgE, eosinophils and mast cells. IgE then binds to mast cells and is cross linked by antigens lead to cell degeneration and the release of mediators such as histamine, prostaglandin and leukotrienes. This causes bronchoconstriction and the early athematic response. The late asthmatic response is associated with increased airway inflammation and is driven mainly by Eosinophils.
When to consider asthma
• Symptoms of SOB, cough, wheeze and chest tightness
• Recurrent/variable nature of symptoms
• Diurnal variation in symptoms- morning increase in symptoms and overnight
• Personal and family history of atopy
• Identifiable triggers i.e. exercise, infection, pollen, dust, animal dander, NSAID’s etc
Asthma- common investigations
• Peak expiratory flow (PEF)- measures maximum speed of expiration, usually monitored over 2-4 weeks. Variability of 20% or more is significant
• Spirometry: main investigation for identifying obstruction, measures how much air is breathed out and how quickly. An FEV1/FVC ratio of less than 70% means there is an obstruction
• Reversibility: for patients with obstructive spirometry, patient is given dose of bronchodilator and spirometry is re-performed. Increase in FEV1 of both 12% and 200mL in volume is positive
• Fractional exhaled Nitric oxide (FeNo): a positive FeNo (>40ppb) suggests eosinophilic inflammation
• These investigations have a high rate of false negatives
Stepwise management for asthma
Different therapies are added in till the asthma is controlled. You move up and down the treatment ladder as needed in order to maintain the lowest controlling therapy.
• Step 1 (suspected asthma)- Short acting Beta-2 agonist (Salbutamol): use when required. Consider a low dose inhaled corticosteroid (ICS) i.e. beclomethasone
• Step 2- add inhaled long acting beta agonist (LABA) i.e. Salmeterol to low dose ICS
• Step 3- consider increasing ICS to medium dose or adding Leukotriene receptor antagonist (LTRA) i.e. Montelukast. If there is no improvement with the LABA this can be stopped.
• Step 4- refer patients for specialist care
Aims of treatment
• No daytime symptoms
• No night time awakening due to asthma
• No need for rescue medication
• No exacerbation
• No limitations on activity including exercise
• Normal lung function (FEV1 and or PEF >80% predicted or best)
• Minimal side effects
Moderate acute asthma exacerbation
• Increasing symptoms
• PEF >50-75% best or predicted
• No features of acute severe asthma
Severe acute asthma exacerbations
Any one of:
• PEF 33-50% best or predicted
• Respiratory rate >25/min
• Heart rate >110/min
• Inability to complete sentences in a breath
• Altered consciousness
• Exhaustion
• Arrhythmias
• Hypotension
• Cyanosis
• Silent chest
• Poor respiratory effort
Near fatal acute asthma exacerbation
Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressure
Investigations for acute asthma
• Peak expiratory flow (PEF)- this is expressed as a % of the patients previous best value, in the absence of this % of predicted is a rough guide
• Pulse oximetry/arterial blood gas- the aim of oxygen therapy is to maintain SpO2 94-98%. Patients with an SpO2 of <92% or features of life threatening asthma require ABG
Investigations for acute asthma: Chest x-ray
Chest x-ray is not routinely recommended in patients except for:
• Suspected pneumomediastinum or pneumothorax
• Suspected consolidation
• Life threatening asthma
• Failure to respond to treatment satisfactorily
• Requirement for ventilation
Management of acute asthma
• A to E structure
• Controlled oxygen therapy (94-98%)
• Salbutamol nebulisers, can be given back to back if there is a poor response to the initial dose
• Hydrocortisone (IV) or Prednisolone (PO)
• Ipratropium nebulisers- in severe or life threatening cases or where there is an inadequate response to initial treatment
• Magnesium sulphate (IV) or Theophylline (as aminophylline infusion IV) can be considered under specialist guidelines
• Incubation and ventilation may also be required
COPD
Airway obstruction which is chronic and progressive, includes chronic bronchitis and emphysema
Chronic bronchitis- a productive cough that lasts at least three months of two consecutive years
Emphysema- the abnormal, permanent enlargement of the air spaces due to the breakdown of alveoli.
Consider COPD when they present with:
• Are over 35 with a risk factor i.e. smoking
• Exertional breathlessness
• Chronic cough
• Regular sputum production
• Wheeze
• Frequent winter ‘bronchitis’
Clinical signs and risk factors for COPD
Clinical signs include: Barrel chest, Cyanosis, Flapping tremor, Pursed lip breathing, Use of accessory muscles, wheeze
Risk factors: smoking, pollution and exposure to dust, Alpha 1 antitrypsin deficiency
Investigations into COPD
chest x-ray
• Useful to exclude other causes like malignancy
• In COPD you will see Hyperextended lungs, Flattened Hemidiaphragm, Bullae
Spirometry
• FEV1/FVC ratio <70% (below)
• Scalloping of flow/volume curve
Management of COPD- non medical
• Smoking cessation
• Pneumococcal vaccination and annual influenza vaccine
• Pulmonary rehab- combines physical therapy with disease education and nutritional, psychological and behavioural intervention. Programme is done in groups and lasts 6-8 weeks
COPD- medication: short acting and combination therapy
• Short acting bronchodilator i.e. salbutamol. They will initially be offered either a SABA or a Short Acting Muscarinic antagonist
• Combination therapy: Long acting beta agonist (LABA) and Long Acting Muscarinic Antagonist (LAMA) or
a Long Acting Beta Agonist and Inhaled Corticosteroid (ICS). The second option is normally for patients with asthmatic features
Medications: triple therapy and extra
• Triple therapy- for patients who still have day to day symptoms which affect the quality of their life or they have one severe or two moderate exacerbations within a year. LABA + LAMA + ICS
• May need long term oxygen therapy, home nebulisers, prophylactic antibiotics and mucolytics. Some patients may need lung volume reduction surgery
You go from short acting to combination therapy to triple therapy if symptoms are not controlled
Acute exacerbations of asthma
Sustained worsening of the patients symptoms from their usual stable state which is beyond normal day to day variations and is acute in onset
Management of acute exacerbations of COPD
• A to E assessment
• Controlled oxygen therapy- should be monitored with ABG’s to ensure they are not hypercapnic
• Steroids (PO)
• Salbutamol nebulisers (bronchodilator)
• Ipratropium nebulisers (bronchodilator)
• Consider antibiotics- if symptoms are severe or there are changes to the sputum
• Non invasive ventilation- if there is hypercapnia and acidaemia
• Intubation and ventilation can be considered in patients with severe exacerbations who don’t respond to treatment
Investigations for acute exacerbations of COPD
• Blood tests- including FBC, urea and electrolytes, C reactive protein
• Cultures- blood cultures, sputum cultures. Will show if there is a source of infection
• Arterial blood gas- is there evidence of hypercapnia, acidosis. Is oxygen appropriate
• Chest x-ray: to exclude pneumonia/ other pathology
Shock
Failure of the circulatory system which results in inadequate tissue perfusion. This leads to anaerobic respiration, cellular hibernation and death, Organ dysfunction, Organ damage, death.
Types of shock
• Hypovolaemic shock: too little blood
• Cardiogenic shock: the heart fails
• Obstructive shock: blockage of blood vessels
• Distributive shock (Vasogenic/vasodilatory): the vessels distend
Blood flow equations
MAP= CO x SVR (systemic vascular resistance)
CO= HR x SV
Features of Hypovolaemic stroke
Reduced preload causes reduced stroke volume and so reduced cardiac output
• Low JVP/CVP
• Decreased circulating volume and venous return
Mechanism of cardiogenic stroke
• Reduced contractility: Decreased contractility causes reduced stroke volume.
• Reduced compliance: Reduced preload causes reduced stroke volume
• Vascular incompetence causes reduced forward flow
• Inflow obstruction: reduced preload causes reduced stroke volume
• Outflow obstruction: increased afterload causes reduced stroke volume
Arrhythmias
• Bradycardia- reduced heart rate causes reduced cardiac output
• Tachycardia- reduced preload causes reduced cardiac output
Vasogenic (distributive) shock mechanism of action
• Capacitance vessels: reduced preload causes reduced stroke volume
• Resistance vessels: systemic vascular resistance decreases, which will tend to increase CO and decrease MAP but redistribution of blood flow may cause cellular hypoperfusion
Features of shock
• Decreased blood pressure, increased heart rate
• Pallor with cool peripheries
• Slow capillary refill
• Increased respiratory rate, decreased urine output
• Altered conscious levels
• High lactate
Features of cardiogenic shock
• Decreased cardiac emptying causes venous congestion
• Increased JVP/CVP and/or pulmonary oedema
Features of obstructive shock
• Decreased cardiac filling/emptying
• Venous congestion
Features of vasogenic (distributive) shock
• Decreased vascular tone and venous return
• Leads to low JVP/CVP
• Warm peripheries
Hypovolaemic shock
• Conditions- haemorrhage (internal/external) due to trauma, GI bleed, ectopic pregnancy and ruptured AAA. Can also be due to fluid loss from diarrhoea, vomiting, burns, polyuria (DKA/DI) and third spacing
• Features of history: External bleeding, visible injury, haematemesis/melaena, abdo pain, chest/back/flank pain, sexual activity (ruptured ectopic pregnancy), input/output, recent surgery
Cardiogenic shock
• Conditions: Myocardial infarction, Myocarditis/Pericarditis, Atrial fibrillation/SVT/VT, Complete heart block, Valvulopathies (aortic stenosis/mitral regurgitation), Drug overdose (beta blockers/ Ca antagonist)
• Features of history: chest pain, shortness of breath, palpitations, murmur, irregular pulse, extreme tachy/bradycardia, drug history, cardiac risk factors
Obstructive shock
• Clinical conditions: Cardiac tamponade (trauma/metastases), Tension pneumothorax, Pulmonary embolism, Coarctation of the Aorta (during the first month of life when PDA closes), air embolus, Aortocaval compression
• Features: Injuries, PMH, Chest pain, Shortness of breath, risk factors for DVT (surgery, immobilisation, OCP), muffled heart sounds, central line, pregnancy
Vasogenic/distributive shock causes
• Clinical conditions: adrenal insufficiency, spinal cord injury, anaphylaxis, SIRS/ Sepsis, Drug overdose (Ca antagonist, Propofol)
• Features: injuries, medications, hyperpigmentation, allergen exposure, fever, cough, dysuria, abdo pain
Anaphylactic shock
Histamine release causes oedema due to increased capillary permeability. Fluid loss from the circulation causes Hypovolaemia, a combination of distributive and Hypovolaemic shock’
Septic shock
• Microvascular thrombosis causes tissue ischaemia and adrenal insufficiency
• There is vasodilation, increased permeability and decreased perfusion
• Systemic effects: fever, diminished myocardial contractility, metabolic abnormalities
Effect of shock
• Hypoperfusion
• Increased anaerobic respiration
• Cellular hibernation and death
• Organ dysfunction, organ damage, death
Initial management of stroke
• ABCD approach to all acutely ill patients
• Oxygen delivery is maximised with high flow oxygen given via a mask with a reservoir bag
• Blood flow is optimised usually by giving IV fluids in the first instance (even in cardiogenic shock)
• Treatment depends on the cause
Shock: fluid resuscitation
Aim to optimise circulating volume
• Fluid challenge: 250-500ml 0.9% NaCl or Hartmanns
• Given over no more than 15 minutes
• Assess for response and side effects
• Repeat if appropriate
• If you have given 2 litres and the patient isn’t better then its not working, get help
Definitive treatment for shock can also include
• Electrical cardioversion
• Pacemaker
• Inotrope infusion: Epinephrine, Norepinephrine, Dobutamine
• Thrombolysis
• Balloon angioplasty
• Surgery
• Needle thoracostomy
• Chest drain insertion
Treatment for anaphylaxis
• Epinephrine, 500mcm IM
• Hydrocortisone
• Chlorphenamine
The sepsis 6
• Give O2 to keep sats above 94%
• Take blood cultures
• Give IV antibiotics
• Give a fluid challenge
• Measure lactate
• Measure urine output
Sinus tachycardia
Sinus rhythm is accelerated by stressful factors, often systemic and non-cardiac (infections, dehydration, emotional stress, physical activity etc) with a heart rate >100.
Reentrant SVT’s: AVNRT (atrioventricular nodal reentry tachycardia)
• The most common cause of palpitations in patients with structurally normal hearts
• Typically paroxysmal, can occur spontaneously or upon triggers of exertion, caffeine, alcohol, beta-agonists (salbutamol)
• Sudden onset of regular, rapid palpitation. The patient may experience a brief fall in blood pressure (pre-syncope)
• Shortness of breath, anxiety and occasionally polyuria duet to elevated atrial pressure
• Tachycardia (140-280bpm), regular in nature, ceases spontaneously or continues indefinitely
AVNRT- ECG and causes
• ECG: regular tachycardia, usually narrow QRS complex unless pre-existing bundle branch block or rate related aberrant conduction. ST-segment depression may be seen with or without underlying coronary artery disease. P waves if visible exhibit retrograde conduction with P-wave inversion in leads II, III, aVF.
• Due to an extra pathway- called a reentrant circuit, located in or near the AV node that causes the heart to beat prematurely
Re-entrant SVT’s: ARVT (atrioventricular reentrant tachycadia)
• Similar clinical features with AVNRT
•Cause: there needs to be accessory pathway present. In optimal conditions (perfectly synchronised atrial/ventricular premature beat), a re-entry circuit forms. This re-entry circuit involves the atria, AVN, ventricles and back to the atria through the accessory pathway.
ARVT- ECG
Rate usually 200 – 300 bpm. P waves may be buried in QRS complex or retrograde. QRS Complex usually <120 ms unless pre-existing bundle branch block or rate-related aberrant conduction. T wave inversion, ST segment depression is common
Wolf Parkinson white syndrome
• Pre-excitation - early activation of the ventricles due to impulses bypassing the AV node via an accessory pathway
• Tachyarrhythmias can be facilitated by:
• Formation of a re-entry circuit involving the accessory pathway, AVRT
• Direct conduction from the atria to the ventricles via the accessory pathway, bypassing the AV node, seen with atrial fibrillation or atrial flutter in conjunction with WPW
Atrial flutter
Palpitations +/- SOB/CP/pre-syncope. If AV conduction is 1:1, then ventricular rate can be 300 bpm and haemodynamic instability occurs (red flag symptoms), with a high risk of ventricular fibrillation (cardiac arrest).
Atrial flutter- cause
Re-entry circuit within the right atrium. The length of the re-entry circuit corresponds to the size of the right atrium, resulting in a fairly predictable atrial rate of around 300 bpm. Ventricular rate is determined by the AV conduction ratio (“degree of AV block”). The commonest AV ratio is 2:1, resulting in a ventricular rate of ~150 bpm.
Atrial flutter- ECG
Narrow complex tachycardia, regular atrial activity at ~300 bpm, flutter waves (“saw-tooth” pattern) best seen in leads II, III, aVF — may be more easily spotted by turning the ECG upside down (flutter waves in V1 may resemble P waves). Loss of the isoelectric baseline
Atrial flutter 4:1 block (depolarisation front goes around the atria 4 times, while being conducted to the ventricles only once)
Atrial fibrillation
The most common sustained arrhythmia. The incidence and prevalence of AF is increasing. Lifetime risk over the age of 40 years is ~25%. Patients with AF have an increased risk of embolic events (stroke).
Management strategies: Rate control: beta-blockers, CCB, digoxin. Rhythm control: electrical/chemical cardioversion
The higher stroke risk should be addressed with anticoagulants
Causes of atrial fibrilation
Ischaemic heart disease, hypertension, valvular heart disease (esp. mitral valve disease), cardiomyopathies and /or acute infections, electrolyte disturbance (hypokalaemia, hypomagnesaemia)
Atrial fibrilation- ECG
Irregularly irregular rhythm. No P waves. Absence of an isoelectric baseline. Variable ventricular rate. Narrow QRS complexes, unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction. Atrial fibrillation waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude >0.5mm). They may mimic P waves leading to misdiagnosis.
