Block 2: conduction defects, valves, pericarditis, cardiac tamponade Flashcards
(51 cards)
1
Q
AF with complete heart block
A
If the ‘baseline’ shows no clear P waves, or there is atrial fibrillation together with slow regular ventricular rhythm this also indicates complete heart block and is a medical emergency
2
Q
Bundle branch block
A
- Blockage in depolarisation of ventricles after bundle of His
- Complete: QRS >120
- Incomplete: same QRS changes but duration is <120
3
Q
Differentiating LBBB and RBBB
A
- Its WiLLiaM and MaRRoW
- in LBBB there is a ‘W’ in V1 and a ‘M’ in V6
- in RBBB there is a ‘M’ in V1 and a ‘W’ in V6
4
Q
Causes of LBBB
A
- Always pathological
- myocardial infarction
- diagnosing a myocardial infarction for patients withexistingLBBB is difficult
- the Sgarbossa criteria can help with this
- hypertension, aortic stenosis and left sided heart failure
- Can obscure diagnosis of left ventricular hypertrophy
- aortic stenosis
- cardiomyopathy
- rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
- Can be incomplete but unlike RBBB is likely to progress to complete
- Can require pacing
5
Q
Causes of RBBB
A
- normal variant - more common with increasing age. Especially if incomplete and QRS is <120ms
- right ventricular hypertrophy (can obscure diagnosis)
- chronically increased right ventricular pressure - e.g. cor pulmonale
- pulmonary embolism, COPD
- myocardial infarction
- atrial septal defect (ostium secundum)
- cardiomyopathy or myocarditis
6
Q
Management of Supraventricular tachycardia
A
- vagal manoeuvres: Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe. carotid sinus massage
- intravenous adenosine: rapid IV bolusof6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg. Contraindicated in asthmatics - verapamil is a preferable option
- electrical cardioversion
- Prevention of episodes: beta-blockers, radio-frequency ablation
7
Q
Supraventricular tacycardia
A
- Arise from the atria or AV node
- Fast regular rhythm, with or without P waves
- Episodes are characterised by the sudden onset of a narrow complex tachycardia
- Typically an atrioventricular nodal re-entry tachycardia (AVNRT): no visible P waves, they are hidden in the QRS complex, the atria and ventricles depolarise simultaneously
- Other causes include atrioventricular re-entry tachycardias (AVRT): P waves are on top of T waves, there is additional electrical connection between the atria and ventricle (accessory pathway)
8
Q
Atrial fibrillation
A
- Common and benign
- Very fast disorded atrial activity
- No P waves (no synchronised depolarisation) and fibrillatory waves (f-waves) due to disordered atrial activity
- Treated by DC-cardioversion or rate/rhythm controlled drugs
- Calculate stroke score with CHA2DS2-VASc score to consider anticoagulants
9
Q
Medications for A-fib
A
- Rate control: beta blockers, calcium channel blockers, digoxin
- Rhythm control: beta blockers, dronedarone,amiodarona
- ACEi, SGLT2
- Catheter ablation: if dont respond to treatment
- medical re-synchronisation: amiodarone
10
Q
Ventricular tachycardia
A
- A broad complex tachycardia origination from ventricular ectopic beats, can cause V-fib
- Usually due to cardiac ischaemia or myocardial scar
- Life threatening if untreated, if patient is haemodynamically compromised they will need urgent DC cardioversion, if not in shock give amiodarone
11
Q
The two main types of VT
A
- monomorphic VT: most commonly caused by myocardial infarction
- polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval.
12
Q
Ventricular fibrilation
A
- Completely disordered electrical activity in the ventricles
- Irregular with rate usually >300bpm
- Life threatening without electrical defibrillation
13
Q
Aortic regurgitation
A
- The leaking of the aortic valve causing blood to go in the opposite direction during ventricular diastole
- Causes: rheumatic fever, bicuspid aortic valve, infectine endocarditis, Marfans, syphilis
- Investigation: echocardiography
- Medical management of any heart failure and surgery in symptomatic patients with severe disease or asymptomatic patients with severe disease and LV systolic dysfunction
14
Q
Features of aortic regurgitation
A
- early diastolic murmur: intensity of the murmur is increased by thehandgrip manoeuvre
- collapsing pulse
- wide pulse pressure
- Quincke’s sign (nailbed pulsation)
- De Musset’s sign (head bobbing)
- mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
15
Q
Clinical features of aortic stenosis
A
- dyspnoea
- chest pain
- syncope / presyncope (e.g. exertional dizziness)
murmur - an ejection systolic murmur (ESM) is classically seen in aortic stenosis
- classically radiates to the carotids
- this is decreased following the Valsalva manoeuvre
16
Q
Examination features of severe aortic stenosis
A
- narrow pulse pressure
- slow rising pulse
- delayed ESM
- soft/absent S2
- S4
- thrill
- duration of murmur
- left ventricular hypertrophy or failure
17
Q
Causes of aortic stenosis
A
- degenerative calcification (most common cause in older patients > 65 years)- i.e. coronary artery disease
- bicuspid aortic valve (most common cause in younger patients < 65 years)
- William’s syndrome (supravalvular aortic stenosis)
- post-rheumatic disease
- subvalvular: HOCM
18
Q
Management of aortic stenosis
A
- if asymptomatic then observe the patient is a general rule
- ifsymptomatic then valve replacement
- if asymptomatic butvalvular gradient > 40 mmHgand with features such as left ventricular systolic dysfunction then consider surgery
- Balloon valvuloplasty can be used in children
19
Q
Mitral regurgitation
A
- When blood leaks through the mitral valve during systole
- Risk factors: female, low body mass, age
- Causes: post MI, mitral valve prolapse, infective endocarditis, rheumatic fever
- Tend to be asymptomatic but may get fatigue, SOB and oedema
- Signs: pansystolic murmur described as “blowing”. It is heard best at the apex and radiating into the axilla. S1 may be quiet as a result of incomplete closure of the valve. Severe MR may cause a widely split S2
20
Q
Mitral regurgitation: investigations and treatment
A
- ECG: broad P waves
- Chest x-ray: cardiomegaly
- Diagnose through an echocardiogram
- In acute cases: nitrates, diuretics, positive inotropes and an intra-aortic balloon pump
- Surgery: prefer repair but can have valve replacement
21
Q
Mitral stenosis
A
- Causes: rheumatic fever
- Obstruction of blood flow from left atrium to ventricle causes increased pressure in the right side of the heart
- Symptoms: dyspnoea, haemoptysis
- Mid late diastolic murmur (best heard in expiration)
- Loud S1
- Opening snap, low volume pulse, malar flush, atrial fibrilation
22
Q
Mitral stenosis: investigations and treatment
A
- Chest x-ray: left atrial enlargement
- Echocardiogram
- Patients with associated AF require anticoagulation (warfarin)
- In symptomatic patients use a percutaneous mitral ballon valotomy or mitral valve surgery
23
Q
Tricuspid regurgitation
A
- Signs: Pan-systolic murmur, prominent/giant V waves in JVP, pulsatile hepatomegaly, left parasternal heave
- Causes: right ventricular infarction, pulmonary hypertension i.e. COPM, rheumatic heart disease, infective endocarditis
24
Q
Rheumatic valve disease
A
Causes diffuse fibrous with leaflet thickening and commissural fusion. Valve resembles fish mouth. Occurs in mitral stenosis
25
Endocarditis causes
- Infective: bacterial (staphylococci, Streptococci), fungal infection
- Non-infective: due to hypercoagulable states like pregnancy, cancers or infection
26
Features of endocarditis
- Features associated with valve pathology, such as a new murmur or abnormal echo appearance
- Features of infection (fever, elevated biochemical and haematological markers)
- Features of systemic embolisation, such as stroke, renal or splenic infarction
Immunologic phemomena, and vasculitic phemomena
- Diagnosed using Duke’s criteria (for infective endocarditis)
27
Acute pericarditis
Inflammation of the pericardial sac lasting for less than 4-6 weeks
28
Diagnosing acute pericarditis
At least 2 of the 4 following criteria
- Pericarditic chest pain
- Pericardial rub
- New widespread ST elevation or PR depression on ECG
- Pericardial effusion (new or worsening)
29
Acute pericarditis supportive findings
- Elevation of markers of inflammation (i.e C-reactive protein, erythrocyte sedimentation rate, and white blood cell count)
- Evidence of pericardial inflammation and oedema by an imaging technique (CT, CMR)
30
Incessant/chronic pericarditis
Incessant pericarditis: Pericarditis with symptoms lasting for >4-6 weeks but <3 months without remission.
Chronic pericarditis: lasting for >3 months
31
Recurrent pericarditis
Recurrence of pericarditis after a documented first episode of acute pericarditis and a symptom-free interval of 4–6 weeks or longer (Usually within 18–24 months but a precise upper limit of time has not been established).
32
Causes of acute pericarditis
- viral infections (Coxsackie)
- tuberculosis
- uraemia
- post-myocardial infarction
- early (1-3 days): fibrinous pericarditis
- late (weeks to months): autoimmune pericarditis (Dressler's syndrome)
- radiotherapy
- connective tissue disease: systemic lupus erythematosus, rheumatoid arthritis
- hypothyroidism
- malignancy: lung cancer, breast cancer
- trauma
33
Features of acute pericarditis
- chest pain: may be pleuritic. Is often relieved by sitting forwards
- other symptoms include a non-productive cough, dyspnoea and flu-like symptoms
- pericardial rub
34
Investigations for acute pericarditis: ECG
- the changes in pericarditis are often global/widespread, as opposed to the 'territories' seen in ischaemic events
- 'saddle-shaped' ST elevation
- PR depression: most specific ECG marker for pericarditis. Seen in II, aVF and PR elevation in aVR
35
Investigations for acute pericarditis
- ECG
- all patients with suspected acute pericarditis should have transthoracic echocardiography
- CXR, Echocardiogram, CMR
- bloods
- inflammatory markers (CRP, ESR)
- troponin: around 30% of patients may have an elevated troponin - this indicates possible myopericarditis
36
Management of acute pericarditis
- Most patients are managed as outpatients and given anti-inflammatories and 1 week follow up= patients with high-risk features such as fever > 38°C or elevated troponin should be inpatients
- treat underlying cause= most patients however will have pericarditis secondary to viral infection, so no treatment indicated
- strenuous physical activity should be avoided until symptom resolution and normalisation of inflammatory markers- at least 3 months. In athletes wait till ECG and echocardiogram have normalised
- a combination of Asprin/NSAIDs and colchicine is now used first-line= until symptom resolution and normalisation of inflammatory markers (usually 1-2 weeks) followed by tapering of dose recommended over
- If Asprin/NSAID’s are contraindicated consider low dose corticosteroids
37
Predictors of poor prognosis in acute pericarditis
- Major: Fever >38 degrees, Subacute onset, Large pericardial effusion, Cardiac tamponade, Lack of response to aspirin or NSAID’s after 1 week of therapy
- Minor: Myopericarditis, Immunosuppression, Trauma, Anticoagulation
- Hospital admission: presentation that suggests underlying cause or one major or minor risk factor
38
Constrictive pericarditis
- Causes: particularly TB
- Features: SOB, right heart failure (elevated JVP, ascites, oedema, hepatomegaly), JVP shows prominent x and y descent, pericardial knock (loud S3), positive Kussmauls sign
- CXR: pericardial calcification
39
Recurrent pericarditis treatment
- First line: Asprin or NSAID + colchine + exercise restriction
- Second line: Low dose corticosteroids
- Third line: IV immunoglobulin
- Fourth line: Pericardectomy
40
Prognosis for acute pericarditis
- Mostly good long term prognosis
- Cardiac tamponade: more common with underlying cause like malignancy, TB or purulent pericarditis
41
Risk of developing constrictive pericarditis
- Low (<1%) for idiopathic and presumed viral pericarditis.
- Intermediate (2–5%) for autoimmune, immune mediated and neoplastic aetiologies.
- High (20–30%) for bacterial aetiologies, especially with TB and purulent pericarditis.
- Colchine reduces recurrence rate
42
Myopericarditis
- Predominant pericarditis with minor myocardial involvement
- Patient with definite criteria for acute pericarditis with elevated biomarkers of myocardial injury (troponin I or T, CK-MB fraction) without newly developed focal or diffuse impairment of LV function in echocardiography or CMR
- Reduce dosage of NSAID compared to pure pericarditis, don't need colchine
- Investigations: coronary angiography to rule out ACS, CMR
43
Cardiac tamponade
Characterised by the accumulation of pericardial fluid under pressure. Normally due to 300-600ml of fluid.
Cardiac tamponade is a life-threatening, slow or rapid compression of the heart due to the pericardial accumulation of fluid, pus, blood, clots or gas as a result of inflammation, trauma, rupture of the heart or aortic dissection.
44
Cardiac tamponade: Classification/causes
- Onset to (acute, subacute) or (chronic if more than three months).
- The size mild (<10 mm), moderate (10–20 mm) or large (>20 mm)
- Distribution (circumferential or loculated)
Causes: Pericarditis, Tuberculosis, Iatrogenic (post cardiac surgery), Trauma, Neoplasm/malignancy
45
Cardiac tamponade: Causes
- Elevated intra cardiac pressures.
- Progressive limitation of ventricular diastolic filling.
- Reduction in cardiac out put.
- Cardiac ouput is initially maintained due to increased adrenergic tone causing tachycardia and peripheral vasoconstriction
46
Cardiac tamponade: Beck's triad
Classical features (Beck’s triad): hypotension, raised JVP, muffled heart sounds.
47
Cardiac tamponade: other features
- dyspnoea, orthopnoea
- tachycardia
- Agitation, palpitation, drowsiness, decreased urine output, weight loss
- an absent Y descent on the JVP (jugular venous pressure) - this is due to the limited right ventricular filling
- pulsus paradoxus - an abnormally large drop in BP (>10 systolic) during inspiration
- Kussmaul's sign
- ECG: electrical alternans
- Management: urgent pericardiocentesis
- Raised central venous pressure (JVP) characterized by prominent x descent and attenuated or absent y decent.
- Pericardial friction rub
48
Cardiac tamponade: investigations
- CXR: cardiomegaly
- Echocardiogram: gold standard.
- Fluid analysis
- Treatment: normally pericardiocentesis or cardiac surgery
49
Cardiac tamponade signs on echocardiogram
- Chamber collapse: right atrial collapse begins in late diastole, precedes clinical signs. Right ventricular collapse occurs later on
- Increased ventricular interdependence: an increase in filling of one ventricle causes a decrease in the other. Mitral and tricuspid diastolic inflow velocities can quantify this. A drop of >40% of tricuspid inflow velocity is diagnostic, in mitral valves its a drop of >25%
- Inferior Vena Cava Plethora (IVC): a dilated >2.1cm with <50% respiratory change in the inferior vena cava. Reflects the intrapericardial pressure being transmitted to the right heart chambers
50
Cardiac tamponade management: drainage
- Pericardiocentesis: Advantages are that it allows rapid drainage, less invasive, minimal preparation. Complications are that it can lacerate the heart. Can cause incomplete drainage or recurrence. Is not recommended for small effusions (<1cm), loculation, adhesion or fibrinous stranding
- Surgical drainage: Advantages are its more complete, less likely to cause recurrence, gives access for tissue biopsy. Can drain loculated effusion. Causes more pain and longer recovery
- Percutaneous balloon pericardiotomy: for large effusions (particularly malignant), limited complications, recurrence is rare
51
Cardiac tamponade management: medical
- Fluids, Inotropic support if the patient is hypotensive
- Avoidance of diuretics or vasodilators
- If score >6 have urgent pericardiocentesis
