Shortness of Breath Flashcards
What simple things can be done during initial assessment of a breathless patient?
- Give salbutomol neubuliser
- Sit the patient upright to help with ventilating
Important associated symptoms to ask about in SoB history…
- Cough - if productive, what colour is sputum?
- Fever
- Palpitations
- Syncope
- Ankle swelling
- Orthopnoea
- Wheezing
- Chest pain - cardiac or pleuritic
What medications can precipitate breathlessness?
In asthma:
- B blockers
- NSAIDs
- Aspirin
Differentials for shortness of breath…
CARDIAC:
- Acute heart failure
- ACS
- Arrhythmia e.g. AF
- Pericarditis
- Cardiac tamponade
RESPIRATORY:
- Asthma
- COPD exacerbation
- Pneumothorax
- PE
- Pleural effusion
- Airway obstruction e.g. anaphylaxis
- ARDS
OTHER:
- Pain
- Medications
- Trauma
- Metabolic e.g. DKA
- Drug overdose
- Anxiety
Presentation of asthma…
- Classical sx: SoB, cough, tight chest
- Signs: widespread wheeze, prolonged expiratory phase, Harrison sulcus ( groove at inferior border of rib cage of children)
- Sx are worse at night, and in the morning
- Triggered by cold weather, exertion, alergens
What is the atopic triad?
Atopy = genetic predisposition to IgE-mediated allergen hypersensitivity
- Asthma
- Hayfever
- Eczema
What symptoms can be seen in aspirin induced asthma?
Samter’s triad:
- Asthma
- Aspirin sensitivity
- Nasal polyps
Diagnosis of asthma…
If high probability of asthma based on clinical features:
Trial of inhaled steroid treatment for 6/52 - patient asked to keep PEFR diary to check response:
- Initial diurnal variation >20%
- Improvement on treatment
If intermediate probability of asthma based on clinical features:
- Spirometry is normally required - FEV1/FVC= <0.7
AND
- Bronchodilator reversibility test - 400mg salbutomol= >12% increase in FEV1 200ml increase in vol
Eosinophilic testing includes:
- FeNO test: >40 parts per billion = diagnostic
- IgE testing
- Blood eosinophils
What are the typical spirometry findings with asthma?
FEV1= low
FVC = normal/ low (due to premature narrowing of the airways causing reduced expiration)
FEV1/ FVC = <0.7
RV = high (due to less air being expelled)
What normally occurs in annual asthma review?
3 important questions:
- Difficulty sleeping because of asthma sx?
- Usual asthma sx present throughout the day?
- Has asthma interfered with daily activities?
Check inhaler technique and PEFR diary
Take new PEFR reading in clinic
Lifestyle advice on smoking cessation, avoiding triggers and poor control
Asthma management regime…
*SABA e.g. salbutomol should be used throughout PRN - consider moving up ladder if using >3x per week at any point
Step 1: Regular preventer therapy = low dose ICS (beclametasone) , initially BD, then OD
Step 2: Inital add on therapy = LABA (formeterol) - ideally in combination inhaler with ICS
Step 3: Consider increasing dose of ICS to medium dose OR add LTRA
Step 4: If poor improvement - referral to specialist services is required
What is considered complete asthma control?
- No daytime symptoms
- No night-time awakening
- No need for rescue medication
- No asthma attacks
- No limitations on activity
- Normal lung function
What is the process of stepping down asthma treatment?
- Move down ladder when patient feels that asthma is well controlled and there is objective evidence
- Ask ‘3 questions’ to assess improvement
- Reduce ICS by 25-50% every 3 months to lowest possible dose
- Remove add-on therapies every 3 months
What is brittle asthma?
‘Brittle’ no longer used - referred to as severe asthma:
- Wide variation in PEFR
- Sudden , severe attacks on a background of good control
Risk factors for asthma attacks…
- Using > 3 classes of asthma medication
- Chronic LABA use
- Brittle/ severe asthma
Why can chronic LABA use predispose to asthma attacks?
Long term LABA exposure leads to reduced sensitivity to bronchodilator effects of SABA therefore may lead to worsening breathlessness.
Trigger for asthma attacks…
- Environmental allergens
- Infections
- Exercise
- Medications
- Emotional factors - stress, anxiety
What is the pathophysiology of acute severe asthma?
- End airway collapse occurs which leads to air trapping as more air is inspired than can be expired
- This causes increased positive end expiratory pressure (PEEP)
- Higher pressures therefore have to be overcome for inspiration, which eventually tires the patient
- Vicious cycle of increasing breathlessness occurs
Signs of acute severe asthma…
- PEFR = 33-50% of best/ predicted value
- SpO2 > 92%
- RR> 25/min
- HR > 110/min
- Inability to complete full sentences
Signs of life-threatening asthma…
- PEFR = <33% of best/ predicted value
- SpO2 <92%
- PaO2 <8kPa
- Silent chest
- Cyanosis
- Reduced GCS
Management of acute severe asthma
A-E assessment:
A:- Ensure airway is patent and then give 15L O2 via non-rebreathe
B: - Continuous oxygen sat , pulse rate and resp rate monitoring
- CXR ordered
C:- IV access and routine bloods for potential trigger
- ABG if SpO2 is reduced
- ECG
Medical management = O SHIT ME (not correct order!):
- Oxygen = High flow, aiming for 94-98% sats
- Salbutomol 5-10mg neb via 6L O2 , back-to-back every 15-30 mins
- Ipratropium bromide 0.5mg alongside Salbutomol nebs up to 3 back-to-back and then 4 hourly
- IV Hydrocortisone 100mg / Prednisolone 40-50mg 6 hourly then continued for 5 days
- IV Magnesium Sulphate 2g over 20 minutes if life-threatening
- Escalate to ITU for possible intubation and ventilation - they may then give Theophyline infusion
When is a patient allowed to be discharged after an acute severe asthma attack?
When PEFR > 75% of predicted/ best value
Ensure they have 5 day course of oral steroids
What is the typical presentation of pneumonia?
Lower respiratory tract infection symptoms:
- Breathlessness
- Productive cough - purulent sputum
- Pleuritic chest pain
- Systemic illness: fever, malaise, rigors
Examination findings:
- Reduced expansion
- Reduced breath sounds
- Dull percussion
- Coarse crepitations
What are the different types of pneumonia?
- Community accquired pneumonia:
- Typical = classic symptoms, most likely strep. pneumoniae
- Atypical = insidious onset, extrapulmonary sx e.g. abdominal pain, diarrhoea, arthralgia - caused by legionella, mycoplasma - Hospital accquired pneumonia:
- Defined as pneumonia contracted >48 hrs after hospital admission
- Most likely organisms = pseudomonas a. and staph a.
What warrants hospital admission for pneumonia in the community?
CRB 65 score (no urea measurement in community) = 1-2
OR
SpO2 <94%
…Should warrant secondary care
What investigations are required for pneumonia?
Bedside:
- ECG: cardiac cause of breathlessness
- Urine dip: for other source of infection
Bloods and Labs:
- FBC: raised WCC in infection
- ESR/CRP: raised in infection
- U&Es and LFTs: baseline for abx treatment, and for CURB 65
- ABG if SpO2 <94%
- Blood cultures
- Urine sample
- Sputum culture
Imaging:
- CXR: diagnostic if consolidation and air bronchograms seen
What is the CURB 65 score?
- Confusion of new onset
- Urea > 7mmol/L
- RR> 30/ min
- Blood pressure <90 systolic / < 60 diastolic
- Age> 65
Score: 0-1 = outpatient care, 2 = secondary care, >3= ICU
What is the generic antibiotic treatment for CAP?
Mild CAP:
- Amoxicillin 500mg TDS for 5-7 days
- Clarithromycin/ Doxycycline if allergic to Penicillin
Moderate CAP:
- Dual therapy of Amoxicillin with Clarithromycin: 7-10 day course
Where is legionella pneumoniae normally encountered?
People who have recently travelled on holiday - exposed to contaminated cooling systems/ humidifiers and showers in hotels/ apartments
What are some possible complications of pneumonia?
- Pneumothorax
- Parapneumonic effusion
- Empyema
- Abscess
What is the general management of pneumonia?
A-E assessment is required
- High flow oxygen to titrate sats between 94-98%
- IV fluids if pt is dehydrated - maintenance
- Analgesia - NSAIDs/ paracetamol for pain
Antibiotic therapy dependent on local trust guidelines
What is the generic antibiotic treatment for HAP?
Mild HAP:
- Co-amoxiclav 625mg TDS
Severe HAP:
- Tazocin 4.5g IV TDS
Causes of acute heart failure…
- ACS - lack of myocardial perfusion may lead to HF
- Acute mechanical disrupton : valve regurgitation / rupture of ventricular septum
- Arrhythmia
- Acute cardiac outflow obstruction: massive PE, tension pneumothorax, tamponade
What are the two main types of pulmonary oedema?
- Cardiogenic pulmonary oedema
- Non-cardiogenic pulmonary oedema:
- ARDS
- Neurogenic pulmonary oedema (significant CNS injury)
- Iatrogenic fluid overload (excessive fluids/ blood transfusion)
- Hypoalbuminaemia (fluid moving into intravascular space)
- Smoke inhalation
- Near-drowning incidents
Presentation of acute heart failure…
Symptoms:
- SoB
- Sweating, nausea
- Productive cough - pink frothy sputum
- PND/ orthopnoea
Signs:
- Raised JVP
- Crackles on auscultation
- Gallop rhythm
Investigations for acute heart failure…
Bedside:
- ECG : may see sinus tachycardia , arrhythmia/ ischaemia which is causing HF
Bloods:
- U&Es
- Troponins - to look for ischaemic cause
- INR
- BNP - >100mg/L
Imaging:
- CXR - ABCDE signs of heart failure
- Echocardiography - pericardial effusion or tamponade
Management of acute heart failure…
A-E assessment is with treatment:
- Sit patient up right
- Give high flow O2 via non-rebreathe
- 20-40mg Furosemide IV by slow injection
- Diamorphine 2.5-5mg IV with Metoclopramide 10mg IV
- GTN if SBP>90 mmHg
Once controlled, patient should be fluid restricted to 1.5L per day
What chest x-ray findings are seen in heart failure?
ABCDE:
- Alveolar oedema
- Kerley B lines
- Cardiomegaly
- Dilated upper lobe vessels
- Effusion
What are the two types of cardiogenic shock?
- Pump failure (problems specifically with cardiac function): MI, arrhythmia, myocarditis, acute valve failure, aortic dissection
- Obstruction: PE, tamponade, tension pneumothorax
What is the definition of respiratory failure?
Failure of the respiratory system to maintain adequate gas exchange :
- Lung failure = inability to maintain gas exchange leading to hypoxia
- Ventilatory failure = cannot ventilate properly therefore CO2 buildup will lead to hypercapnia
What are the normal ranges for oxygen and carbon dioxide?
Oxygen = 11.3-13.3 kPa
Carbon dioxide = 4.5-6.0 kPa
What is the definition of type 1 respiratory failure?
Type 1 = Low O2 ( PaO2< 8kPa) AND normal/ low CO2 (PaCO2 = 6kPa)
What is the definition of type 2 respiratory failure?
Type 2 = Low O2 (PaO2 <8 kPa) AND high CO2 (PaCO2 > 6kPa)
Why is the oxygen saturation target for T2RF patients at risk of CO2 retention, lower than normal?
Patients that tend to be affected = COPD, neuromuscular disorders, obesity and thoracic wall disease.
Oxygen saturation is lower because higher oxygen concentration will…
1. Lower the hypoxic drive to breathe which means that ventilation will be reduced and so less CO2 is blown off, leading to CO2 retention
- Have vasodilatory effects on dead space, leading to disruption of the perfusion of the respiratory system
What are the different causes of hypoxia?
- Hypoventilation - seen in neuromuscular disorders, low GCS, extreme fatigue
- Diffusion limitation - pulmonary oedema, ARDS (where there is an increased diffusion barrier)
- Shunt - AV malformation, VSD (leading to deoxygenated blood entering arterial system without passing through pulmonary circulation)
- V/Q mismatch - seen in COPD
- Reduced oxygen in the inspired air (FiO2) i.e. at high altitudes
What is V/Q mismatch?
V/Q mismatch occurs when the ventilation of the lungs does not match the perfusion of blood in the system.
When there is mismatch, some areas of the lungs are likely to have reduced oxygenation as there is ‘dead space’ (non/ poorly - ventilated areas of the lungs) or there is reduced perfusion to well ventilated areas.
What is the effect of hypercapnia on the brain?
Increased CO2 concentration in the blood will stimulate greater cerebral blood flow through its vasodilatory effect on cerebral vasculature.
This will likely lead to:
- Headache, raised CSF pressure, papilloedema
- Restlessness, tremor, slurred speech, asterixis, clouding of consciousness
What are some indications for the use of non-invasive ventilation?
- COPD with respiratory acidosis (pH 7.25-7.35)
- Type 2 RF secondary to chest wall deformity, neuromuscular disease/ obstructive sleep apnoea
- Cardiogenic pulmonary oedema unresponsive to CPAP
- Weaning from tracheal intubation
What is the difference between BiPAP and CPAP, and when are they used?
BiPAP = delivers airway pressure that cycles between high inspiratory pressure and low expiratory pressure - this increases tidal volume and clears CO2 - good in T2RF
CPAP = delivers constant airway pressure throughout the ventilatory cycle - provides high flow and PEEP which recruits collapsed alveoli for improved oxygenation. Mainly used in T1RF and cardiogenic pulmonary oedema
General management of respiratory failure…
- Address the hypoxaemia FIRST: aim for sats of 94-98% (in most people)
- Address hypercapnia - NIV (CPAP/ BiPAP)
- Treat the underlying cause of resp failure e.g. abx for infection
What is the definition of COPD, and what is it’s pathophysiology?
Fixed irreversible airflow obstruction - made up of 2 conditions:
- Chronic bronchitis = chronic cough that has lasted at least 3 months of a year (increased inflammation and mucus production)
- Emphysema = permanent dilatation of terminal air spaces (destruction of parenchymal tissue)
What is the typical presentation of COPD?
*Almost exclusively seen in smokers
Symptoms = productive cough, dyspnoea, wheeze
Signs = tachypnoea, use of accessory muscles, hyperinflation, reduced expansion, reduced breath sounds, widespread wheeze
Describe the levels of the MRC Dyspnoea scale…
1 = Dyspnoea on strenuous exercise 2 = Dyspnoea walking fast/ incline 3 = Dyspnoea on walking on flat ground 4 = Dyspnoea causes pt to stop for breath every few mins 5 = Too dyspnoeaic to leave the house
What are the different stage s of COPD according to spirometry findings?
FEV1/FVC <0.7 due to reduced FEV1 from obstructive airway causing expiration to be affected.
Stage 1 = FEV1 > 80% of predicted
Stage 2 = FEV1 50-79% of predicted
Stage 3 = FEV1 30-49% of predicted
Stage 4 = FEV1 <30% of predicted
How is COPD diagnosed?
COPD should be considered in:
- Age > 35 y/o
- Smokers/ ex smoker
- Sx = exertional dyspnoea, chronic cough/ sputum production
Investigations to carry out in suspected COPD…
- Spirometry - post bronchodilator will show irreversible airflow obstruction (FEV1/FVC = <0.7)
- CXR - shows flattened hemi-diphragm, hyperinflated chest, bullae
- FBC - exclude secondary polycythaemia
- BMI calculation
Conservative management of COPD…
- Smoking cessation! - single most effective intervention
- Pulmonary rehabilitation
- Immunisation - pneumococcal and influenza
- Education - early signs of exacerbation
Management regime of COPD…
Step 1 = SABA/ SAMA
Step 2 dependent on if pt has asthmatic features/ steroid responsiveness e.g.
- any previous diagnosis of asthma
- high blood eosinophil count
- variation in the FEV1 over time
- significant diurnal variation
IF patient has no features suggesting steroid responsiveness - add LABA + LAMA
IF patient has features of steroid responsiveness - add LABA + ICS
- if patient still remains breathless offer triple therapy:
LAMA+ LABA+ ICS
Final step = oral theophylline if short acting and long acting bronchodilators have not worked
What are some common features of AE of COPD?
- Increase in dyspnoea
- Increased frequency of cough
- Chest tightness
- Increase in sputum
- Patients may be hypoxic - leading to acute confusion
Management of AE of COPD…
O SHIT (not in that order!)
- Controlled Oxygen to meet target oxygen sats of 88-92%
- Salbutomol 5mg and Ipratropium bromide 500mcg via nebuliser
- IV Hydrocortisone 200mg + Prednisolone 30mg - continue for 7-14 days
- Antibiotics only if evidence of infection e.g. purulent sputum
** No response to nebulisers or steroids should prompt IV aminophylline and NIPPV
What are the indications for LTOT in COPD?
- Patients with resting PaO2 = 8.0 kPa AND evidence of peripheral oedema, polycythaemia or pulmonary HTN
- Patients with resting hypercapnia
Why is polycythaemia seen in COPD?
Chronic hypoxaemia stimulates increased production of EPO by the kidneys
What is the pathophysiology of interstitial lung disease?
- Thickening and fibrosing of the alveolar walls
- Reduced elasticity of the lung tissue which makes breathing more difficult
Causes of interstitial lung disease…
- Idiopathic = commonest cause
- Pneumoconiosis = caused by inhalation of dust - 3 primary types= coal workers’. silicosis, asbestosis
- Replacement fibrosis - after lung damage
- Extrinsic allergic alveolitis e.g. farmer’s lung, bird-keeper’s lung
- Granulomatous disease e.g. sarcoidosis
- Iatrogenic - medications e.g. amiodarone
- Connective tissue diseases e.g. SLE
Presentation of interstitial lung disease…
Symptoms:
- dyspnoea
- chronic non-productive cough
- wheeze
- chest pain
Signs:
- central cyanosis
- fine end-respiratory crackles
- finger clubbing
- signs of pulmonary HTN / RHF
Investigations in interstitial lung disease…
Bloods:
- FBC, ESR, CRP - signs of inflammation
- Autoantibody screen
- Serum IgG for different allergen epitopes (EAA)
- ABG (decreases sats)
Imaging:
- CXR: nodular opacities and widespread interstitial markings
- HRCT: ground glass appearance - diagnostic
Other:
- Spirometry : FEV1/FVC > 0.7 - restrictive pattern seen, reduced TLC and RV
- Lung biopsy using VATS/ thoracotomy
Management of interstitial lung disease…
Conservative management:
- Smoking cessation
- Immunisations
- Avoidance of triggers e.g. in bird keepers’ lung
- Long term/ ambulatory oxygen therapy - may be beneficial for some
Medical management:
- Corticosteroids for most types of ILD
Surgical management:
- Lung transplantation may be last resort
What are the different types of lung cancer?
Non-small cell : - Squamous cell carcinoma - Adenocarcinoma - Large cell carcinoma Small cell - most aggressive form, which frequently metastasises (liver, bone, brain, adrenals)
Presentation of lung cancer…
- Persistent cough
- Haemoptysis
- Chest pain - chest wall and pleural involvement
- Unexplained dyspnoea
- Weight loss/ anorexia
- Shoulder pain - referred pain from diaphragmatic involvement
- Pleural effusion
- Wheeze/ stridor
Indications for 2-week-wait referral for lung cancer…
- Chest x-ray findings suggesting lung cancer
- Aged over 40 and unexplained haemoptysis
Urgent chest x-ray should be considered for patients…
Aged over 40 with 2 or more unexplained symptoms:
- Cough
- Fatigue
- SoB
- Chest pain
- Weight loss
- Appetite loss
Investigations for lung cancer…
- Chest x-ray: location of lesion, and surrounding tissue damage
- HRCT: gold-standard investigation - shows tumour site and size
- Biopsy : FNA for palpable disease, bronchoscopy with central tumours, CT guided percutaneous transthoracic biopsy - peripheral tumuors
- PET scanning - metastases
Management of lung cancer…
Non-small cell lung cancer:
- Surgery: curative intent
- Radiotherapy: radical radiotherapy has curative intent- used when tumour is inoperable
- Chemotherapy: adjunct in stage 1/2 and palliative in stage 3/4
Small cell lung cancer:
- Surgery: if no evidence of metastases
- Chemotherapy: beneficial in limited disease
- Radiotherapy: in combination with chemo if positive response to chemo
Paraneoplastic syndromes of lung cancer…
Small cell:
- ADH -causing hyponatraemia
- ACTH - Cushing’s
- Lambert - Eaton Syndrome
Squamous cell:
- PTH-rp leading to hypercalcaemia
- Hyperthyroidism (high TSH)
Adenocarcinoma:
- Gynaecomastia
Features of non-small cell lung cancers…
Squamous cell:
- Commonest type
- Found centrally
- Strongly associated with clubbing
Adenocarcinoma:
- Typically peripheral
- Most common type in non-smokers
Large-cell :
- Typically peripheral
- Anaplastic - poorly differentiated tumours, poor prognosis
Signs of haemodynamic compromise…
- Hypotension (MAP <65mmHg)
- Systolic BP <90
- Tachycardia / bradycardia
- Increased cap refill time
- Oliguria
Basic management algorithim for tachyarrhythmia (with pulse) …
- A-E approach of the patient:
- A: patent
- B: Monitor SpO2 and give O2
- C: Monitor HR, BP, 12 lead ECG, get IV access for bloods - Is patient haemodynamically stable (shock, syncope, ischaemia, heart failure)?
- NO - unstable:
Then follow protocol for unstable tachycardia
YES - stable:
4. Is QRS complex narrrow (0.12s) ?
Then follow protocol depending on if it is a broad complex or narrow complex tachycardia…
Management algorithim for unstable tachyarrhythmia …
- A-E approach of the patient:
- A: patent
- B: Monitor SpO2 and give O2
- C: Monitor HR, BP, 12 lead ECG, get IV access for bloods - Adverse features indicating unstable arrhythmia present?:
- Shock
- Syncope
- Myocardial ischaemia (changes seen on ECG)
- Heart failure - Seek expert help and begin synchronised DC shock - 3 attempts
- Amiadarone 300mg IV over 10-20 mins
- Repeat shock
- Amiadarone 900mg IV over 24 hours
Management algorithim for broad complex tachycardia…
- Identify if irregular or regular broad complex tachycardia…
Irregular:
2. Seek expert help
Regular: Likely to be VT
2. Amiodarone 300 mg over 20-60mins
- Then Amiodarone 900mg over 24 hrs
Irregular:
- AF with BBB - treat as narrow complex tachycardia
- Polymorphic VT (torsades de pointes) -IV magnesium
Management algorithim for narrow complex tachycardia…
- Identify if irregular or regular narrow complex tachycardia…
Regular (probably SVT):
2. First line = vagal manouveres: carotid sinus massage, blowing into pressurised syringe (valsalva)
- Second line = Adenosine 6mg rapid IV bolus - if no effect give 12mg, then further 12mg
* Patient should have cardiac monitor with defibrillator pads ready in case cardiac arrest occurs from adenosine
4.Sinus rhythm achieved?
Yes = probable re-entry SVT , record 12 lead ECG
No= Consider atrial flutter - B blocker for rate control
Irregular:
2.Probably AF - rate control with B blocker/ diltiazem
- Assess VTE risk and anticoagulate
What are the shockable rhythms, and how are they incoporated into the algorithim?
VF and PULSELESS VT :
1. Confirm pt is in cardiac arrest after checking for signs of life
- Call resuscitation team
- Perform uninterrupted CPR whilst getting defibrillator/ monitoring pads and applying them
- Stop chest compressions while machine analyses rhythm and identifies if it is shockable
- Resume CPR, warning all rescuers to stand back as machine gets ready to shock - only person giving compressions should be in contact
- Once machine is charged tell rescuer giving compressions to stand clear then give shock
What are the causes of cardiac arrest?
4 Hs and 4 Ts:
- Hypoxia
- Hypovolaemia
- Hyperkalaemia, hypokalaemia - other metabolic disorders
- Hypothermia
- Thrombosis
- Toxins
- Tension pneumothorax
- Tamponade
Different types of AF…
Paroxysmal AF = self terminating AF - usually lasts <7 days
Persistent AF = not self-terminating and lasting >7 days, usually needs cardioversion to stop
Permanent AF = continuous AF which cannot be cardioverted
Presentation of AF…
Symptoms:
- Palpitations
- Dyspnoea
- Chest pain
- Fatigue
Signs:
- Irregularly irregular pulse
Investigations for AF…
Bedside:
ECG is diagnostic - may need 24 hr ambulatory ECG in paroxysmal AF
ECG findings:
- Irregularly irregular ventricular rhythm
- Absence of p waves
- Wandering baseline
- Tachycardia
Bloods:
- TFTs - hyperthyroid state can cause arrhythmias
- FBC
- U&Es - electrolyte abnormalities
- LFTs and coagulation profile - pre-warfarin
Imaging:
- CXR find structural causes
- Echo - for underlying structural heart disease
Long term management of AF…
Rate control (used mainly in >65y/o, IHD):
- First line = B blocker e.g. atenolol
OR Calcium channel blockers e.g. verapamil, diltiazem
- Digoxin in sedentary people
- Second line = Combination therapy of with 2 of:
- B blocker
- Diltiazem
- Digoxin
Rhythm control (used when continuing sx after rate control):
Pharmacological cardioversion:
- Flecainide
- Amiodarone
- Electrical cardioversion if AF persisting > 48hrs - should continue amiodarone for up to 12 months after
- Catheter ablation if pharmacological cardioversion has not worked
- Pace and ablate strategy for permanent AF (cardioversion has not worked) with symptoms of LV failure
Anticoagulation - CHADS-VASC2 score used to decide if necessary
Score =1 - consider anticoagulation
Score =/>2 - offer anticoagulation
What occurs in pace and ablate therapy?
DDD pacemaker insertion followed by AVN ablation (iatrogenic complete heart block)
Management of acute AF…
- Haemodynamically unstable - emergency electrical cardioversion required
- Haemodynamically stable :
- <48 hrs onset= rate/ rhythm control
- > 48hrs onset = rate control
What is atrial flutter?
Form of supraventricular tachycardia characterised by succession of atrial depolarisation waves for every ventricular depolarisation
What are the symptoms seen in atrial flutter?
- Main = palpitations
- Dyspnoea
- Fatigue
- Chest pain
REGULAR pulse - unlike AF
ECG findings in atrial flutter?
- Saw-tooth appearance of ECG
- QRS complexes follow after a certain number of p waves - depending on degree of AV block i.e. 2:1 means 2 p waves for every QRS
Management of atrial flutter…
- Catheter ablation is normally first line
- Electrical cardioversion may be attempted - but need anticoagulation
What are the different types of supraventricular tachycardia?
- Atrial tachycardia = atrial ectopics leading to abnormal p waves on ECG (negative in I,II, AvL, AvF)
- Atrioventricular nodal re-entry tachycardia (AVNRT) = atrial ectopic causing cycling of electrical signals within AV node - constant re-stimulation of AV node
- Atroventricular re-entry tachycardia = accessory pathways which bypass AV node
Presentation of SVT…
- Palpitations
- Syncope
- Dizziness/ light headed
- Tachycardia may be the only finding seen
Acute management of SVT…
- Identify precipitating factors e.g. caffeine, exercise, drugs
- Vagal manouveres
- Adenosine 6mg –>12mg–>12mg
Long term prevention of SVT…
- B blockers for rate control
- Radiofrequency ablation
ECG findings for SVT…
- Narrow complex tachycardia (140-280bpm)
- P waves appear very soon after QRS complex so R-P interval is very short
- May be P wave inversion in II,III, AvF due to retrograde conduction
Give an example of an AVRT?
Wolff-Parkinson White is most common form - needs urgent treatment due to risk of degenerating into VF.
ECG findings in Wolff-Parkinson White..
- Short PR interval
- Broad QRS complex
- Delta wave (slurred upstroke of QRS)
- Left axis deviation commonly
Management of Wolff-Parkinson White?
Definitive treatment = radiofrequency ablation of accessory pathway
What are the two types of ventricular tachycardia?
- Monomorphic VT- seen mainly post-MI
- Polymorphic VT -e.g. Torsades de Pointes (varying amplitudes causing crescendo-decrescendo)
ECG is diagnostic of VT…
- Fast rate >120bpm
- Regular rhythm
- No p waves
- Broad QRS complex
Management of VT…
Pulseless VT= unsynchronised DC cardioversion
Unstable VT with pulse:
- Antiarrhythmics e.g. amiodarone
- Synchronised defibrillation if drug therapy fails
*ICDs for patients with sustained VT, previous cardiac arrest due to VT and VT post-MI
What is a major risk factor for VF?
Ischaemic heart disease - leads to fast-conducting infarction scars.
ECG findings of VF…
- Very fast rate
- Irregular rhythm
- No p waves
- Broad QRS with abnormal morphology
Management of VF…
Defibrillation with ICD insertion
CABG if IHD is identified
Different types of broad complex tachycardia…
- Ventricular tachycardia
- Ventricular fibrillation
- Wolff Parkinson White
- Bundle branch block
Pathophysiology of bundle branch block…
- Bundle becomes injured which impairs electrical conduction
- As it can no longer be conducted along the preferred pathway, it instead moves through muscle fibres
- This leads to prolongation of conduction
ECG changes seen in RBBB…
- Broad complex (>120ms)
- RSR pattern in V1-3 meaning M shaped QRS complex - secondary R wave due to delayed repolarisation
- Wide, slurred ‘S’ wave in I, AvL, V5-6 (W shaped QRS complex)
ECG changes seen in LBBB…
- Broad complex (>120 ms)
- Dominant S wave in V1 - W shaped QRS complex
- Notched R wave in V6 - M shaped QRS complex
What are some common causes of heart block?
- Ischaemic event leading to fibrous tissue forming over AV node
- Lyme disease
- Myocarditis
- Endocarditis
- SLE
How does heart block present?
- Syncope
- Fatigue
- Dizziness
- Sometimes asymptomatic
What are the three types of heart block commonly seen, and their ECG changes?
First degree: PR interval > 0.2s - asymptomatic mainly
Second degree:
- Mobitz type 1 = progressive prolongation of PR interval until QRS complex is eventually dropped
- Mobitz type 2 = fixed pattern to conduction block - QRS complex is dropped after a certain number of p waves e.g. 3:1 ratio = 3 p waves for every 1 QRS
Third degree: No association between P waves and QRS complexes
Management algorithim of bradyarrhythmias…
- A-E approach of the patient:
- A: patent
- B: Monitor SpO2 and give O2
- C: Monitor HR, BP, 12 lead ECG, get IV access for bloods - Is patient haemodynamically stable (shock, syncope, ischaemia, heart failure)?
NO - unstable:
3. Atropine 500mcg IV - repeat to maximum of 3mg if no response OR
Adrenaline 2-10mcg/min IV
4. Seek expert help
YES - stable:
If there is risk of asystole commence treatment as above.
If there is no risk - continue to observe.
