Cardiology Flashcards
AVN re-entry tachycardia (Causes/Path/CF/ECG/Mx/Sub-types)
Causes: Commonest cause of palpitations in patients with strucurally normal hearts. Typically spontaneously or with provocation (exertion, caffeine, alcohol, beta-agonists (salbutamol) or sympathomimetics (amphetamines). W>M (75%).
Path: Functional re-entry circuit with the AVN.
• Normal- impulse travels down fast and slow pathways simultaneously, fast impulse enters distal end of slow pathway and they cancel each other out.
• Abnormal- One of the pathways is in it’s refractory period, so the impulse goes down the other pathway, this then cyles round, back up the other pathway then cycling round.
CF: Sudden onset rapid/regular palpitations, syncope, chest pain (think underlying coronary artery disease), dyspnoea, anxiety. Regular tachycardia 140-280
ECG: Regular tachycardia 140-280, narrow complex unless there is co-existing BBB/rate related aberrant conduction. P waves, if visible, inverted in II, III, aVF. May see ST depression and QRS alterans (large complex alternating sized complex).
Mx: Vagal rhythm, adenosine. May use CCBs/amiodarone, DC cardioversion rarely needed. If recurrent episodes not amenable to medical treatement could consider catheter ablation.
Subtypes:
• Slow-Fast- (80-90%), anterograde slow pathway, retrograde fast pathway- likely no visible P wave.
• Fast-Slow- (10%), anterograde fast pathway, retrograde slow pathway- P wave after QRS (long ventriculo-atrial interval)
• Slow-Slow- (1-5%), anterograde & retrograde slow pathway- P wave prior to QRS (similar to sinus tachycardia)
Atrioventricular re-entry tachycardia (Path/ECG/Mx)
E.g. Wolff-Parkinson-White
Path: An accessory pathway allows electrical activity from the ventricles to pass to resting atrial myocytes.
• Orthodromic conduction- Via the AVN, anterograde, resulting in a regular narrow QRS comlpexes
• Antidromic- Via accessory pathway, going back through the AVN, producing a regular broad complex rhythm.
ECG:
• Orthodromic- 200-300 bpm, retrograde P waves, long RP interval, QRS <120 (unless pre-existing BBB or rate-related aberrant conduction, rate-related ischaemia is common. QRS alterans (QRS complexes large and alternating in size).
• Antidromic- 200-300 bpm, regular broad complexes
Mx:
• Orthodromic- If unstable DC cardiovert, if stable need to slow conduction via AVN, start with vagal manoeuvres then adenosine and/or verapamil. (note if verapamil used observe for at least 4 hours as may develop AF.)
• Antidromic- If any doubt if is VT treat accordingly, if stable try procainamide, Ibutilide/amiodarone second line., DC cardioversion if drug therapy fails.
Focal atrial tachycardia (Path/CF/ECG/Mx/Associations)
Path: Rapid regular rhythm arising from a discrete area within the atira.
CF: Palpitations, fatigue, chest pain, syncope.
ECG: Regular atrial tachycardia with P wave morphology different from sinus tachycardia.
Mx: Adenosine, withdrawing causative agent/treatin underlying cause. Can require ablation.
Associations: Coronary artery disease, CCF, surgery, digoxin tocicity, catecolamines, cocaine and alcohol excess
Sinus Tachycardia (Causes/Mx)
Causes:
1. Infection, pain, anxiety, dehydration, exercise, bleeding, systemic vasodilation( eg sepsis), anaemia, fever, PE, hyperthyroidism, pregnancy, hypercapnia, autonomic neuropathy (inappropriate sinus tachycardia)
2. Drugs- eg caffeine, nicotine, salbutamol
Mx:
1. If emergency treat as per ALS algorithm
2. Otherwise treat the underlying
Narrow complex tachycardias- ALS
A-E
Give O2 to maintain SpO2
IV access
Blood gas/bloods- correct clear abnormalities
If signs of shock (Hypotension, chest pain, syncope or heart failure):
1. Synchronised DC shock (up to 3 attempts)
2. Amiodarone 300mg IV over 10-20 minutes
3. Repeat shock
4. Amiodarone 900mg over 24 hours
Regular:
1. Vagal manoeuvres (blow through syringe, ice on face, carotid massage)
2. Adenosine 6mg IV bolus, if no effect then a further 12mg then a further 12mg.
3. NSR achieved- probably re-entry paroxysmal SVT, consider prophylaxis
4. NSR not achieved- possible atrial flutter
Irregular:
1. Probable AF
2. Rate control- B-blocker or diltiazem, if in HF consider digoxin or amiodarone.
3. Assess thromboembolic risk and consider anticoagulation
PE (RF/CF/Ix/Mx/Unprovoked PE)
RF: Recent surgery, thrombophilia, leg fracture, immobility, malignancy, pregnancy/post-partum, COCP/HRT and previous VTE.
CF:
1. Symptoms- acute SOB, pleuritic chest pain, haemoptysis, dizziness, syncope.
2. Pyrexia, cyanosis, tachypnoea, tachycardia, hypotension, raised JVP, pleural rub and pleural effusion.
Ix:
1. Bloods- Routine, D-dimer
2. ABG- T1RF
3. CXR- often normal, may show dilated pulmonary artery, linear atlectasis, small pleural effusion, wedge shaped opacities or cavitation(rare).
4. ECG- may be normal, often sinus tachy, also RBBB, right ventricular strain (TWI V1-V4), S1Q3T3 (deep S in I, pathological Q in III and TWI in III)
Mx:
1. Unstable- thrombolyse if massive/RHS, alteplase 10mg in 1 min then 90mg over 2 hours
2. Stable- DOAC (apixaban/rivaroxaban), can use warfarin (with LMWH bridging)
Unprovoked: If no known provoking factor consider Ix for malignancy/antiphospholipid/thrombophillia. Ix that can be done include: Bloods, CXR, breast exam, PSA and CT abdo/pelvis.
Cardiac myxoma (path/CF/Ix/Mx)
Path: Rare benign cardiac tumor, F:M 2:1, usually sporadic, but may be familial (carney complex, cardiac/cutaneous myxomas)
CF:
1. Can mimic IE- fever, weight loss, clubbing, raised EDR and systemic emboli
2. Can mimic MS- left atrial obstruction and AF.
3. Tumour plop, symptoms may vary with posture.
Ix: ECHO
Mx: Excision
Restrictive cardiomyopathy (causes/CF/Ix/Mx)
Causes: Idiopathic, amyloidosis, haemachromatosis, sarcoidosis, scleroderma, Loffler’s eosinophilic endocarditis, endomyocardial fibrosis.
CF: Features of RVF, raised JVP with prominent X/Y descents, hepatomegaly, oedema, ascities.
Ix: ECHO/MRI/cardiac catheterisation
Mx: Treat the underlying cause.
Hypertrophic cardiomyopathy (Path/inheritance/CF/Ix/Mx/Prognosis)
Path: LV outflow obstruction fromasymmetrical septal hypertrophy. Leading cause of sudden cardiac death in the young. 0.2% prevalence with AD inheritance but 50% sporadic, 70% have mutations encoding B-myosin/a-tropomyosin and troponin T.
CF:
1. Sudden cardiac death- ask about family
2. Angina, SOB, palpitations, syncope, CCF, jerky pulse, A wave in JVP, double apex beat, systolic thrill left sternal edge, harsh ejection systolic murmur.
Ix:
1. ECG- LVH, progressive Twave inversion, deep Qwaves (inferior+lateral), AF, WPW syndrome, ventricular ectopics and VT.
2. ECHO- asymmetrical septal hypertrophy, small LV cavity with hypercontractile posterior wall, midsystolic closure of aortic valve, systolic anterior movement of mitral valve.
3. Cardiac catheterisation- can be helpful to assess severity, but can cause VT.
4. Exercise test +/- holter- useful to risk stratify
Mx:
1. B-blockers or verapamil for symptoms (aim to reduce compatability), amiodarone for arrythmias.
2. Anticoagulate for paroxysmal AF or systemic emboli
3. Septal myomectomy- surgical/chemical(alcohol), to reduce LV outlow tract gradient is reserved for severe symptoms
4. Consider implantible defibrillator
Prognosis: if <14 then 5.9%/year, if >14 then 2.5%/year. Poor prognostic factors- age <14, syncope at presentation and FH of sudden cardiac death.
Dilated cardiomyopathy (Associations/CF/Ix/Mx/Prognosis)
Associations: Unknown cause, but associated with alcohol, high BP, chemotheraputics, haemochromatosis, viral infection, autoimmune, peri/postpartum, thyrotoxicosis, congenital (X-linked).
CF:
1. Fatigue, SOB
2. Pulmonary oedema, RVF, emboli, MR/TR, pleural effusion, oedema, jaundice, hepatomegaly, ascities, AF and VT.
3. Tachycardia, hypotension, raised JVP, diffuse apex S3.
Ix:
1. Bloods- High BNP, low Na (indicates poor prognosis.
2. CXR- Cardiomegaly, pulmonary oedema.
3. ECG- Tachycardia, non-specific T wave changes, poor R wave progression.
4. ECHO- globally dilated hypokinetic heart and low ejection fraction. MR/TR. LV mural thrombus.
Mx:
1. Bed rest
2. Diuretics, B-blockers, ACEi and anticoagulants
3. biventricular pacing/ICDs/LVAD/transplantation
Prognosis: Variable, mortalitiy ~40% in 2 years
Acute myocarditis (Causes/CF/Ix/Mx/Prognosis)
Causes:
1. Idiopathic- 50%
2. Viral- Enteroviruses, adenoviruses, HHv6, EBV, CMV, influenza, hepatitis, mumps, rubela, Coxsckie, polio, HIV, HSV
3. Bacterial- Staph, Strep, Clostridia, diptheria, TB, meningococcus, mycoplasma, brucellosis, psittacosis
4. Spirochaetes- Leptospirosis, syphylsis, Lyme disease
5. Protozoa- Chagas, Leishmania, toxoplasmosis
6. Drugs- Cyclophosphamide, trastuzumab, penicillin, chloramphenicol, sulfonamides, methyldopa, spironolactone, phenytoin, carbamezapine.
7. Toxins- Cocaine, lithium, alcohol, lead, arsenic
8. Immunological- SLE, sarcoid, Kawaski, scleroderma, heart transplant rejection
CF: Chest pain, HF symptoms, palpitaions and tachycardia, soft S1 and S4 gallop.
Ix:
1. ECG- ST changes and T wave inversion, atrial arrythmias, transient AV block and QT prolongation
2. Bloods- CRP/ESR and troponin raised, send viral serology
3. ECHO- diastolic dysfunction, regional wall abnormalities
4. Cadiac MRI if stable
5. Endomyocardial biopsy is gold standard
Mx: Treat underlying cause, treat HF/arrythmias, avoid exercise as it can precipitate arrythmias, NSAIDs controversial.
Prognosis: 50% recover within 4 weeks, 12-25% will develop dilated cardiomyopathy and severe heart failure (can also develop years later).
Tetralogy of fallot (Path/Features/CF/Ix/Mx/Prognosis)
Path: Most common cyanotic congenital heart disorder (3-6:10,000), 10% adult CHD. Thought to be due to abnormalities in the seperation of the truncus arteriosus into aorta and pulmonary arteries.
Features:
1. VSD
2. Pulmonary stenosis
3. RVH
4. Aorta overides the VSD accepting right heart blood.
CF:
1. Infants- may be acyanotic at work with pulmonary stenosis murmur, gradually become cyanotic after ductus arteriosus closeure with increasing right to left flow. Toddlers may squat as it increases peripheral vascular resistance, reducing R>L flow.
2. Adults- Often asymptomatic, if unoperated often have cyanosis.
3. Repaired patients- late symptoms include exertional dyspnoea, palpitations, clubbing, RV failure, syncope and sudden death.
Ix:
1. ECG- RVH with RBBB
2. CXR- normal or classical boot shaped heart
3. ECHO/cardiac CT/MRI- will show anatomy and provide information for surgery.
Mx: Surgery, usually done before 1 year old with closure of VSD and pulmonary stenosis.
Prognosis:
- Without surgery- 95% death by 20.
- After surgery- 85% survive to 35, with common issues being PR causing RV dilatation and failure, RV outflow tract obstructions, AR, LV dysfunction and arrythmias.
Coarctation of the aorta (Path/Associations/CF/Ix/Mx/Complications)
Path: Congential narrowing of the descending aorta, ususally just distal to the origin of the left subclavian artery.
Associations: Bicuspid aortic valve, Turner’s syndrome.
CF: Radiofemoral delay, weak femoral pulse, HTN, scapula bruit, systolic murmur (best heard over left scapula), cold feet.
Ix: CT/MRI aortogram. CXR may show rib notching as blood diverts down intercostal arteries to reach lower body causing them to dilate.
Mx: Surgery or balloon dilatation +/- stenting
Complications: HF from high afterload, IE, intracerebral haemorrhage.
Ventricular septal defects (Causes/CF/Ix/Mx/Complications)
Causes: Congential (1:2000), acquired- post MI
CF:
1. severe HF in infancy or asymptomatic.
2. Harsh pansystolic murmur at left sternal edge with a systolic thrill +/- parasternal heave (smaller holes give louder murmurs)
Ix:
1. ECG- Normal, can show LAD/LVH/RVH.
2. CXR- Normal heart size with mild pulmonary plethora (small VSD) or cardiomegaly with large pulmonary arteries and marked pulmoary pethora.
3. Cardiac catheterisation- raised O2 sats in right ventricle.
Mx: Initially medical management as many close spontaneously, indications for surgical closure are failed medical therapy, symptomatic, shunt >3:1, SBE/IE
Complications: AR, IE/SBE, pulmonary HTN, Eisenmenger’s complex, HF from volume overload.
Atrial septal defect (ASD) (Types/CF/Ix/Mx/Complications)
Types:
1. Ostium secundum- 80%, often asymptomatic until adulthood when develop L>R shunt, typically 40-60 year olds.
2. Ostium primum- associated with AV valve anomalties (e.g. Down;s), present in childhood.
CF:
1. Chest pain, palpitaions, SOB, haemoptysis. Increased frequency of migraines.
2. Arrythmias (AF), pulmonary systolic flow murmur, wide fixed split S2, pulmonary HTN may predispose PR/TR
Ix:
1. ECG- RBBB with LAD(primum) or with RAD(secundum).
2. CXR- small aortic knuckle, pulmonary plethora, atrial enlargement
Mx: May close spontaneously. Primum should be closed in childhood, Secundum should be closed if symptomatic or RV failure. Transcatheter closure more common than surgical.
Complications:
- Reversal of L>R shunt- (Eisenmenger’s complex), initial L>R shunt causes pulmonary HTN which increases RH pressures until they exceed left, at which point it reverses. Causes cyanosis as deoxygenated blood enters body.
- Paradoxical emboli- go through shunt into arterial circulation. ( e.g strokes)