Cardiology Flashcards
Chest pain
Differential diagnosis
• CVS: ACS, aortic dissection, pericarditis
• Pulmonary: PE, pneumothorax, pneumonia, pleuritis
• GI: GERD, PUD, Boerhaave’s perforation, gallstone, pancreatitis
• Superficial: costochondritis, rib trauma, herpes zoster
• Psychological: panic disorder
Important questions
• Characteristics: dull (ACS), pleuritic (i.e. pain when breathing maximally; PE, PTX, pericarditis), tearing (aortic
dissection)
• Radiation: jaw/ left arm (ACS), back (aortic dissection)
• Changes with position: better when sitting up (GERD, pericarditis)
• Respiratory: SOB, cough +/- sputum, fever (pneumonia)
• GI:
o Severe vomiting (MWS/ Boerhaave’s perforation)
o N/V, haematemesis, melena (PUD)
o Acid reflux, dysphagia (GERD)
Investigations
• Bloods: CBC, CRP/ESR, cardiac enzymes Q3h x 3, D-dimer, amylase
• ECG: sinus tachycardia, ST-T changes
• CXR: pneumothorax, widened mediastinum (aortic dissection), consolidation, lung mass
Palpitations
Differential diagnosis
• Cardiac: PE, arrhythmia, valvular heart disease, HCM
• Endocrine: thyrotoxicosis, hypoglycaemia, phaeochromocytoma
• Systemic: anaemia, fever
• Drugs: thyroxine, adrenergics, discontinuation of benzodiazepines
• Physiological: peri-menopause, pregnancy, caffeine, stress
• Psychiatric
Important questions
• Character: tap on the table
• Onset & cessation (arrhythmia usually abrupt)
• Previous episodes
• Associated symptoms
o CVS: chest pain, SOB, dizziness, LOC
o Thyrotoxicosis: heat intolerance, weight loss despite good appetite
o Phaeochromocytoma: episodic headache, flushing, tremor
o Hypoglycaemia: hunger, tremor, dizziness
o Anaemia: bleeding source (e.g. menorrhagia, PR bleed), malaise, postural hypotension
ECG
• 12-lead ECG
• Ambulatory continuous ECG monitoring:
o Holter monitor: 24h
o Event recorder: 4-6 weeks, triggered by patient
o Implantable loop recorder: implanted under chest skin, triggered by patient or program function
Cardiac enzymes
- Troponin
Most specific (TnI > TnT)
Persist longest
DDx: any ischaemic damage (e.g.
tachyarrhythmia, HF), myocarditis,
pericarditis, Takotsubo cardiomyopathy, CKD
(renally excreted) - Myoglobin
Rise earlier than troponin
DDx: myocarditis, muscular dystrophy, CKD
Echocardiography
• Transthoracic ECHO (TTE)
• Transesophageal ECHO (TEE): useful in
o Aortic dissection
o Atrial abnormalities
o Prosthetic valve: avoid acoustic shadowing
o When viewing posterior structures (Mitral valve)
• Echocardiogram views:
- Parasternal long axis(PSLA)
- Parasternal short axis (PSSA)
- Apical views (Apical 4-chamber)
- Subcostal view
- IVC view
Ischaemic heart disease
Anatomy of coronary arteries
LAD:
• Anterior and lateral wall of LV (inc. apex)
• Anterior 2/3 of septum
• RV
LCX:
• LA + small part of lateral LV
• AV node (if left-dominant)
RCA:
• Posterior wall of LV
• Posterior 1/3 of septum
• RV
• AV node (if right-dominant)
Pathology
• Imbalance of myocardial O2 demand and supply due to
o Coronary atherosclerosis (MC)
o Non-atherosclerotic causes:
- Vasculitis (e.g. Takayasu, PAN, Kawasaki, eGPA)
- Embolism: septic emboli
- Vasospasm (e.g. cocaine abuse, Prinzmetal’s variant)
- Dissection: retrograde extension of AD
Definitions
• Stable angina: chest pain upon exertion
• Acute coronary syndrome
o Unstable angina: defined as any one of
- Resting angina >20min
- New-onset angina that markedly limits normal activity
- Increasing angina that is more frequent, lasts longer or occurs with less exertion than previous angina
o MI: raised cardiac enzymes
- NSTEMI: without ST elevation, but may have ST depression or T wave inversion
- STEMI: with ST elevation or new LBBB
Pathology of atherosclerosis
• Fatty streaks: slightly raised yellow deposits
• Atheromatous plaque: fibrous cap + necrotic
centre
• Unstable plaque: thinner fibrous cap +
growing core, causing
o Plaque rupture: thrombus formation à
occlusion
o Aneurysm: pressure atrophy of tunica
media
o Atheroembolism
Causes of painless MI
• DM
• Complete infarct (>6h)
Stable angina
Clinical features
• Transient myocardial ischemia due to fixed atheromatous stenosis
• Central squeezing substernal/retrosternal chest pain/discomfort/tightness
o Radiation to C7-T4 dermatomes (lower jaw, shoulder and arm)
o Last <30minutes
o Triggers: eating, exertion, emotion, environment (hot / cold)
o Relieved by rest / TNG
Investigations
• Bloods: CBC, metabolic screening (FBG, HbA1c, lipid profile), LRFT, TFT (thyrotoxicosis)
• ECG: non specific +/- reversible ST-segment changes +/- evidence of previous MI
• Risk stratification by Framingham risk score
—> Further risk stratification if intermediate pre-test probability (see above)
o Stress test (exercise ECG) – monitor ECG, BP and general condition
- Ischemic: planar / down-sloping ST depression
o Stress echocardiogram (exercise / dobutamine / adenosine)
- Look for LV dysfunction, regional wall motion abnormalities
o CT/MR coronary angiogram
o Myocardial perfusion scan e.g. thallium
o Cardiac MRI
• If high risk: coronary angiography +/- revascularization (PCI/CABG)
o Gold standard: provide anatomical information about extent/mature of coronary artery disease
o Mortality: 1 vessel < 2 vessel < 3 vessel < left main stem disease
Management
Objective: symptomatic relief and prevent further cardiac events
• Treat exacerbating factors e.g. anaemia, thyrotoxicosis
• Manage risk factors:
o Lifestyle modification: dietary advice, exercise, body weight control, smoking cessation
o DM / HT / HL treatments (e.g. ACEI/ARB, statin)
• Anti-anginal therapy
o Nitrates: systemic vasodilation —> reduce preload (LV EDV) and afterload —> reduce cardiac demand
- For acute symptomatic relief: short-acting SL nitroglycerin 0.4-0.6mg prn
- Angina prophylaxis: long-acting nitrates (risk of nitrate tolerance: only use if BB/CCB ineffective)
- S/E: headache, dizziness, flushing, hypotension
- C/I: HOCM, PDE5 inhibitor (e.g. Viagra within 24h, tadalafil within 48h)
o Cardio-selective beta-blockers: negative inotropic & chronotropic effects
- Choices: atenolol, metoprolol, bisoprolol
- First-line monotherapy for stable angina
- S/E: hypotension, bronchospasm, exacerbate PVD, hypoglycemia
- Need to taper over 2 weeks: sudden discontinuation may intensify ischemia / thyroid storm
- C/I: CHF (may precipitate APO), heart block, asthma/COPD
o Calcium channel blockers
- Non-dihydropyridines (diltiazem, verapamil): vascular + cardiac effects
—> Used as alternative to BB (NOT given together)
—> S/E: constipation
- Dihydropyridines (amlodipine, SR nifedipine): vascular-selective
—> Used in combination with b-blockers, solo administration may cause reflex tachycardia
—> S/E: headache, dizziness, oedema not relieved by diuretics
o Others: ranolazine
• Prevent further cardiac events
o Antiplatelets: aspirin / clopidogrel
Acute coronary syndrome (Diagnostic criteria, type, bio marker, ECG of stemi and nstemi
Diagnostic criteria for myocardial infarction
• Detection of rise and/or fall of cardiac biomarker (preferably cardiac
troponin), with at least 1 value above 99th percentile of ULN
• AND at least one of:
o Clinical: ischemic chest pain
o ECG: new significant ST segment / T wave changes / new LBBB / pathological Q waves
o Imaging: new loss of viable myocardium / regional wall motion abnormality e.g. lateral wall hypokinesia
Types of AMI
• Type 1: atherosclerotic plaque disruption (MC)
• Type 2: mismatch between O2 supply and demand (e.g. vasospasm) – check CBC for anemia, PR for GIB
• Type 3: unexpected cardiac death before blood samples are drawn
• Type 4: PCI-associated (4a: PCI; 4b: stent thrombosis)
• Type 5: CABG-associated
Biomarkers
• Cardiac troponins: gold standard for myocardial ischaemia
o Diagnostic cut-off of hsTnT: positive if baseline > 14 and >100% rise 3-6h later
o Rise and fall patterns of hsTnT/hsTnI
- AMI: peak at 24-48h, return to baseline over 5-14 days
- Myocarditis: peak at 1 day, elevated for 7 days
o Other causes of elevated troponins: myocarditis, heart failure, CKD
• CK-MB: cardiac-specific (c.f. CK-MM for skeletal muscles, CK-BB for brain / GI tract smooth muscles)
• Other markers: urine myoglobin (first marker to rise), AST, LDH
ECG interpretation
STEMI
• STEMI: sequence of changes
o Hyperacute T wave (5-30mins)
o ST elevation (hours): ≥2mm in V2/V3 and ≥1mm in all other leads, require ≥2 anatomically contiguous leads
o Pathological Q wave (12-24h): >1mm wide / >2mm deep, often V1-3
o T wave inversion (late)
• Localizing the infarct (important!)
LAD
- anterior V1-V6
- anteroseptal V1-V3
- anterolateral V4-V6
LCX
- lateral I, aVL, V6
Distal RCA
- inferior II, III, aVF
Proximal RCA
- right ventricular V3R, V4R
Posterior descending artery of RCA/LCX
- posterior V1-V3
Left main/proximal LAD
- diffuse aVR
• Inferior STEMI: associated with right ventricular* (40%) & posterior (40%) as well as AV nodal block (AV nodal branch from RCA)
o Must perform right-sided ECG +/- Echo to rule out right ventricular involvement (C/I for nitrates)
• Posterior STEMI: rarely isolated, usually occur with inferior / lateral MI
o V1-V3: ST depression, tall broad R waves, upright T waves
o Flip the ECG upside down & Order posterior leads
• MI in the presence of LBBB: Sgarbossa’s criteria (≥3 points: 90% specificity)
• De Winter T waves (depressed ST take-off with hyperacute T wave in precordial leads): proximal LAD occlusion, Tx as anterior STEMI
• DDx of ST elevation:
o STEMI: convex ST elevation, associated with Q waves
o Acute pericarditis: diffuse concave ST elevation & PR depression
o LVH with strain pattern: concave ST elevation in V1-3,
associated with LVH features
o LBBB
• Bradycardia in STEMI: Bezold-Jarisch reflex (vagal response)
RV infarction
S/S:
- hypotension
- increase JVP
- kussmaul sign
ECG
- ST elevation in V1, III>II, depression in V2
NSTEMI
• ST depression and/or prominent T wave inversion (>1mm) in 2 contiguous leads (do NOT correlate with location of infarct)
o Usually widespread: subendocardial ischemia
o If localized: more likely reciprocal change – look for ST elevation in other leads
o Check ST elevation (>1mm) in aVR which suggests left main / severe triple vessel disease —> directly go for CABG
Wellen’s syndrome: critical proximal LAD stenosis
• Recent Hx of angina, but ECG taken pain-free (pain = NSTEMI)
o Type A (25%): biphasic T waves in V2-3
o Type B: (75%) deeply & symmetrically inverted T waves in V2-3
• Troponin should be normal (r/o NSTEMI)
• High risk: mean time of extensive anterior MI = 8 days
(first sign: pseudo-normalization of T wave during
pain)
Mx of ACS
Initial management
• Admit CCU for high risk cases*
• Complete bed rest + NPO for first 12h
• Close monitoring: BP/P, IO Q1h, cardiac monitoring with defibrillator standby
• Target Hx and PE to rule out other life-threatening emergencies: aortic dissection, pulmonary embolism, tension pneumothorax, perforated peptic ulcer / esophagus
• Initial investigations:
o 12-lead ECG: stat (repeat Q15min if high suspicion) + Q4-6h on D0, at least daily x 3 days,
o Serial hsTnT: stat + Q3h x 3, more if high suspicion, at least x 3 days
o CK-MB, LDH
o CBC, clotting profile (for heparin / thrombolytics), LFT, RFT (for possible PCI), TFT (r/o thyrotoxic MI)
o Random BG, lipid profile
o CXR, D-dimer
• Morphine: IV 2-5mg prn (S/E: hypotension, bradycardia, resp depression) with Maxolon cover
• Oxygen: supplementary O2 when SaO2 < 90%
• Stool softener
• Nitroglycerin: venous dilation (↓preload), arterial dilation (↓afterload), coronary arterial dilation (↑perfusion)
o SL GTN 1 tab Q5min (max 3 doses if ongoing ischemic discomfort)
o IV GTN (e..g IV isosorbide dinitrate 2-10mg/h): indicated in first 48h if persistent ischemia, heart failure or hypertension
o Monitor BP/P (withhold if SBP < 100, S/E: cardiogenic shock, headache, dizziness)
o C/I: PDE5 inhibitors taken in past 24h
• Dual Antiplatelet
o Aspirin (chewed non-enteric coated): 300mg stat
o P2Y12 inhibitor:
- PCI: clopidogrel 600mg loading —> 75mg maintenance (more preferred: ticagrelor 180mg – PLATO trial)
- Thrombolytic: clopidogrel 300mg loading —> 75mg maintenance if age ≤75 (cannot use others)
• Beta-blocker (cardio-selective): proven survival benefit, ↓HR/BP/contractility and improve coronary perfusion
o Usual regimen: metoprolol (25mg BD oral) / atenolol, titrate to HR <70
o If reduced EF: consider bisoprolol / carvedilol / metoprolol succinate
o Alternative: rate-limiting CCB (diltiazem / verapamil)
Contraindications of beta-blockers:
• Poor ventricular function
• Acute pulmonary oedema
• Heart block (2nd / 3rd degree)
• Asthma / COPD
• Low molecular weight heparin (Enoxaparin 1mg/kg sc Q12h) / UFH
o Choice: UFH if primary PCI (faster onset), LMWH if thrombolysis,
UFH/LMWH if not for reperfusion
o S/E: heparin-induced thrombocytopenia, osteoporosis, hyperkalemia
Further management of STEMI
• Coronary angiography +/- revascularisation by PCI [refer to separate section for details]
o Indications in STEMI
- Primary PCI (aim door-to-balloon time ≤90 minutes):
Ø Present <12 hours after onset of chest pain
Ø Clinical and/or ECG evidence of ongoing ischemia between 12-24 hours of onset
Ø Cardiogenic shock / Severe acute HF (irrespective of onset time)
- Rescue PCI: within 3 hours after failed thrombolysis
- Post-thrombolytic PCI: within 24 hours after successful thrombolysis to reduce re-infarction rate
o Pre-med: GP IIb/IIIa inhibitor (IV abciximab / eptifibatide) if heavy clot load
• Thrombolysis
o Indications: STEMI with symptom onset within 12h + PCI not available within 2h from diagnosis
- NOT used in NSTEMI / UA
o Contraindications: refer to [Neuro]
o Pre-treatment: full-lead ECG, clotting (INR, APTT), cardiac enzymes
o Choice of agent:
- Fibrin-specific: Tenecteplase (TNK-tPA) / Alteplase (tPA) / Reteplase (rPA) —> need LMWH cover
- Fibrin non-specific: streptokinase (cheaper) —> cannot give with IV heparin (∵long halflife: combined use = bleeding risk)
o After treatment: repeat ECG when new rhythm detected / pain subsided / 90 mins after thrombolytics
- Successful reperfusion (routine PCI in 2-24h) vs failure (rescue PCI stat)
o S/E: allergy / anaphylaxis (2%), haemorrhagic stroke (1%)
o Signs of reperfusion:
- Clinical: chest pain subsides
- Biochemical: early CPK peak (monitor Q8h x 3)
- ECG: accelerated nodal/idioventricular rhythm (AIVR), resolution of ST elevation of ≥50% in the worst ECG lead 90min post-fibrinolytic
Hypotension during thrombolysis:
Withhold infusion + check for cause
• Treatment-related: fluid replacement, resume infusion at ½ rate
• Cardiogenic: rescue PCI +/- mechanical circulatory support (e.g. IABP)
• Anaphylaxis: IM epinephrine + IV hydrocortisone
Management of NSTEMI/ UA
• Immediate revascularization if haemodynamically unstable / mechanical complications
• Risk assessment to determine need of revascularization
1. High Risk Complications of MI:
• Refractory angina
• Cardiogenic shock
• Acute pulmonary edema
• Ventricular arrhythmia
Other high risk feature
• ST segment changes ≥0.1mV
• New bundle branch block
• Elevated troponin >0.1mg/mL
• High risk score (TIMI ≥ 3, GRACE > 140)
Immediate invasive treatment:
Coronary angiogram —> revascularisation
(PCI/ CABG)
• GPIIb/ IIIa inhibitor is not routinely added unless evidence of ongoing ischaemia in the presence of DAPT (persistent chest pain, ECG evidence of ischemia)
- Low Risk
- For plaque stabilization [as above]; no need PCI (still recommend PCI if resources available)
- Medical therapy: beta-blocker, statin, DAPT
(total 12 months) + LMWH
Further Stratification by treadmill ECG +
echocardiogram
• High risk: PCI
• Low risk: Continue medical therapy
TIMI score
7 parameters: score ≥3 = indicated for revascularization
• Demographics: age ≥ 65 years
• Clinical:
o ≥3 CAD risk factors
o ≥2 angina events in 24 hours
o Aspirin use within 7 days
• Ix results:
o Known CAD with ≥50% coronary stenosis
o ST segment deviation ≥ 0.5mm
o Elevated cardiac enzymes (TnT / CK-MB)
Grace score
Score > 140: indicated for revascularization
• History: age
• Presentation: HR, SBP, CHF (Killip class), cardiac arrest
• Ix: ↑ creatinine, ↑ markers, ST elevation
Medications upon discharge of ACS
• Antiplatelets: aspirin 80mg daily for life, P2Y12i (e.g. clopidogrel 75mg, ticagrelor 90mg BD) for 12 months
• Beta blocker: e.g. metoprolol 100mg BD
• ACEI/ ARB: start within first 24h, especially if anterior MI / heart failure / EF < 40% / HT / DM / CKD
o Aldosterone antagonist (e.g. Aldactone) if EF<40% + DM/CHF and already on b-blocker and ACEI/ARB
• High dose statin: (e.g. atorvastatin 80mg/day) all patients regardless of LDL
• +/- LMWH if given thrombolysis, give up to 8 days or until revascularization
• +/- Sublingual GTN PRN for symptomatic relief
Complications of MI
• Arrhythmia: usually due to scar tissue after MI, Mx accordingly
o Tachyarrhythmia: e.g. ventricular ectopic (MC), SVT, AFib/AFlut, VT/VF (15%)
o Bradyarrhythmia: e.g. sinus bradycardia, heart block (all types)
• Ventricular dysfunction: ischemic APO
o RV dysfunction: Mx by volume expansion, Swan-Ganz catheter (fig.) to monitor pulmonary capillary wedge pressure (PCWP)
o LV dysfunction: Mx by ACEI/diuretics, inotropes (dopamine/milrinone), intra-aortic balloon pump (IABP), assistive device (LVAD)
• Myocardial rupture: Observe if stable, emergency cardiac catheterization and repair if unstable
o LV free wall rupture —> haemopericardium and cardiac tamponade
o Papillary muscle / chordae tendinae rupture —> ischemic MR (a/w inferior MI)
o Ventricular septum rupture (VSR) —> left-to-right shunt
• Thromboembolism: due to mural thrombus
• Pericarditis: inflammatory (1-7d) or autoimmune (Dressler’s syndrome: 2-8 weeks)
o Peri-infarction pericarditis: give aspirin, avoid NSAIDs / steroids
o Dressler’s syndrome: pericarditis, pleural effusion, low-grade fever, pleuritic chest pain, anaemia, ESR
- Mx: high-dose aspirin + colchicine, or NSAID + colchicine
Post ACS cardiac rehabilitation
• Exercise training: begin 1-2 weeks post-PCI
• Driving 2-3 weeks post-ACS, air travel 2 months post-ACS
• Return to work: 2 months post-MI (not allowed if pilots / air traffic controllers / divers)
• Echocardiogram: 6 weeks post-ACS, to detect LV aneurysm
o S/S of heart failure, ECG shows persistent ST elevation ≥ 2 weeks after MI
o Mx: ACEI, anticoagulation, aneurysmectomy, CABG
• ± Exercise stress test: 6 weeks post-ACS to assess adequacy of PCI —> coronary angiogram if +ve
• ICD indicated if NYHA III/IV HF or LVEF < 30% (high risk of sudden cardiac death due to VT/VF)
Percutaneous coronary intervention
• Indications
o Medically refractory angina
o NSTEMI/ UA with high TIMI risk score + single/ double-vessel disease or not a surgical candidate
o STEMI (primary/ delayed / rescue PCI)
• Procedure:
o Pre-med: DAPT
o Vascular access: femoral artery vs radial artery (preferred due to lower bleeding risk: radial artery is paired with ulnar artery, and can be compressed easily against radius)
o Coronary angiography: inject contrast at mouth of coronary artery
o Percutaneous transluminal coronary angioplasty (PTCA): balloon + stent placement
- Drug-eluting stent: drugs reduce neointimal proliferation —> reduce in-stent restenosis
Ø Drugs: paclitaxel (antiproliferative), sirolimus
- Bare metal stent: 30% risk of re-stenosis, used if high bleeding risk / cannot take DAPT (e.g. anticipated surgery within 12 months)
• Complications: overall mortality <0.5%, may require emergency CABG if unstable
o Puncture: pseudoaneurysm, aortic dissection, coronary artery dissection, myocardial infarction
o Balloon: in-stent restenosis (15%) - due to elastic recoil and neointimal hyperplasia
o Stenting: stent thrombosis (1-2%), stent infection (rare)
• Adjunctive therapy
o Pre-PCI: DAPT (aspirin + ticagrelor) ± heparin ± GPIIb/IIIa inhibitors (only in STEMI)
o Post-PCI (with stent):
- DAPT (aspirin + ticagrelor)
Ø 12 months if DES (drugs delay endothelialization —> require longer duration of DAPT) ± extra 18m if no S/E (∵late stent thrombosis)
Ø 4-6 weeks if BMS
- Lifelong aspirin 80mg/day
Coronary artery bypass surgery
• Indications for NSTEMI/ STEMI:
o Anatomical considerations: can apply SYNTAX score (≥23 favour CABG)
- Triple vessel disease (≥ 70% stenosis)
- Proximal LAD disease (≥ 70% stenosis)
- Left main disease (≥50% stenosis) or left main-equivalent disease (proximal LAD + proximal LCx)
o Post-MI mechanical complications:
- Ventricular septal rupture (VSR)
- LV free wall rupture/ aneurysm
- Acute severe ischemic MR
o Not suitable for PCI (e.g. small coronary arteries, anatomy)
• Procedure
o Type: on-pump (MC), off-pump, minimally invasive
o Incision: median sternotomy
o Grafts used: artery graft > vein graft
- Artery graft: left internal thoracic artery (LITA) > radial artery (prone to severe vasospasm due to
- Vein graft: GSV (longer length available, but only 60% patency over 10 years [improved with statin])
o Systemic heparinisation and connect to cardiopulmonary bypass with warm blood cardioplegia
o Grafting usually distal first (to coronary artery), then proximal (to aorta)
o Post-op ICU stay
• Specific complications
o Mortality 1-2%
o AF 30%
o Peri-op stroke 2.5% (microembolisation of gaseous & particulate matter)
o Peri-op MI
o Post-op low cardiac output syndrome (LCOS): due to ventricular dysfunction
o Graft occlusion: may require PCI to graft / re-CABG
• Pre-op assessment
o Vascular exam: varicose veins, carotid bruit, peripheral pulses
o Allen’s test: compress both radial & ulnar arteries —> clench + unclench hand x 10 —> release ulnar artery to note blood return (normal < 6s) - competent ulnar collaterals
o Investigations: CT thorax (aortic calcifications), coronary angiogram (surgical planning), echocardiogram (concomitant valvular heart diseases to be treated)
• Adjunctive therapy
o Before operation: withhold P2Y12 inhibitor
o After operation: DAPT for 12mo, then aspirin indefinitely
Myocardial infarction with no obstructive coronary atherosclerosis
• Evidence of MI with normal / near-normal coronary angiogram (<50% stenosis)
• Workup: echocardiogram, cardiac MRI, coronary angiogram
• Some causes:
o Vasospastic angina (Prinzmetal’s variant): recurrent typical angina occurring at rest at night (↑vagal tone)
- Mx: CCB (avoid beta-blocker)
o Stress (Takotsubo) cardiomyopathy (“broken heart syndrome”)
- Pathology: catecholamine-induced microvascular spasm
- S/S: acute substernal chest pain (~ACS), dyspnea, syncope triggered by emotional/physical stress
- Echo findings: transient LV wall motion abnormality (apical ballooning)
- Mx: self-limiting +/- anticoagulation if LV mural thrombus
Aortic dissection
Definition
• Tear in aortic intima, allowing blood to dissect into media
• Acute aortic syndrome (AAS): an umbrella term, all manage as aortic dissection
o Aortic dissection
o Intramural haematoma (IMH): haematoma within medial layer of aortic wall without the presence of intimal injury, due to rupture of vasa vasorum
o Penetrating atherosclerotic ulcer (PAU): ulceration of atheromatous plaques, allowing haematoma formation within the media
Classifications
• Stanford: 80% type A (involve Ascending aorta), 20% type B (below left subclavian)
• Debakey: type I, II, IIIA and IIIB (fig.)
Risk factors
• Uncontrolled HT, e.g. cocaine use, phaeochromcytoma
• Connective tissue disease (e.g. Marfan’s)
• Vasculitis, e.g. Takayasu arteritis
• Pregnancy
Clinical features
• Chest pain: sudden onset, tearing, radiate to back
• Asymmetric BP & pulse between arms (e.g. radial-radial delay for Type A, radial-
femoral delay for Type B)
• Complications:
o Ischaemia: MI, ischaemic stroke, mesenteric ischaemia, AKI, limb ischaemia, etc
o Rupture: aortic rupture, cardiac tamponade, acute aortic regurgitation (-> APO)
Investigations
• Bloods: TnT (rule out MI), lactate (elevated in ischaemic gut/ shock)
• ECG
• CXR: widened mediastinum, pleural effusion
• Echo (transesophageal: more sensitive): pericardial effusion, aortic
• Urgent CT aortogram: true lumen can be traced from normal aorta and is compressed by false lumen
o True lumen is more hyperdense (new blood), old lumen is more hypodense (old blood)
Management
• Supportive: NPO, complete bed rest, O2, cardiac monitor, analgesia
• Book CCU / ICU bed for intensive monitoring of BP/P, ECG, I/O
• Antihypertensive: stabilize dissection, prevent rupture & minimize Cx
o Target goal: SBP 100-120 (MAP 60-75), HR 60-70
o IV labetalol 10mg (BB): lower BP + reduce cardiac contractility
o IV sodium nitroprusside: caution if renal failure or HR not controlled (might lead to reflex tachycardia), C/I if pregnancy
o Diltiazem/ verapamil (non-DHP CCB): if BB contraindicated
o Hydralazine is C/I in aortic dissection
• CTS consultation:
o Indications: Type A (proximal) / complicated Type B (distal)
- Complication: e.g. shock, renal artery involvement, hemoperitoneum, limb / visceral ischaemia, aneurysm expansion / progression of dissection
o Surgical options: open repair / TEVAR (thoracic endovascular aortic repair) / endovascular stent graft
Diffuse ST depression in ECG
Can be NSTEMI
Or type 2 AMI —> O2 demand and supply mismatch, e.g. hypovolumea / anemia
—> after fluid resuscitation or blood transfusion —> may back to normal
don’t give DAPT and anticoagulation for anemia patient
Acute heart failure
Pathophysiology
• Volume overload (increased preload): valvular disease (e.g. MR, AR), renal impairment
• Pressure overload (increased afterload): hypertension, PE
• Myocardial lo. ss (impaired contractility): MI (MC)
• Impaired ventricular filling (reduced preload): pericardial disease
Clinical features and management
Classify by presence of congestion (wet vs dry) and adequacy of peripheral perfusion (warm vs cold)
• Sudden onset with rapid progression
• Vitals: ↑↑RR, ↑↑HR, ↑BP (if not shock)
Investigations
• CXR
• ECG
• Echocardiogram: LVEF, underlying cause
• Bloods: cardiac enzymes (TnT, CK, LDH), BNP, ABG
Acute management of APO (SAQ!!)
• General measures
o Complete bed rest, prop up
o High flow O2 by face mask – only if SaO2 ≤ 90%
o Low salt diet + fluid restriction (NPO if very ill)
• Identify and treat underlying cause e.g. arrhythmia, IHD, uncontrolled HT, chest infection
• Monitor BP/P, I/O, SaO2, CVP, RR Q30-60min
• If BP stable, consider
o IV Lasix (frusemide) 40-120mg: require high dose if chronically on diuretics
- S/E: hypotension, electrolyte disturbances (hypoK, hypoMg), AKI
o IV nitrate e.g. GTN 1 mcg/kg/min (withhold if SBP <100)
- C/I: hypotension, HOCM, PDE5 inhibitors within 24h
o +/- Morphine 2-5mg slow IV
• If BP unstable / unsatisfactory response to above: consider inotropes
o Dopamine (3-5 ug/kg/min as inotrope; >5 ug/kg/min as vasopressor)
o Dobutamine 2.5-15 ug/kg/min
o Milrinone (PDE inhibitor)
• Ventilate if needed (e.g. desaturation, cardiogenic shock): CPAP —> BiPAP —> intubation
Management of Refractory Heart Failure • Intra-aortic balloon pump (IABP): systolic unloading (deflate during systole to ¯afterload)+ diastolic augmentation (inflate during diastole to coronary perfusion); C/I in severe AR, aortic dissection • Transaxial pump (Impella): percutaneous pump • Extracorporeal membrane oxygenation (ECMO): promote circulation + oxygenation • LV assist device (LVAD): promote circulation, but not oxygenatio • Manage underlying cause: PCI for ischemic APO, intervention for significant valvular lesion • Heart transplant
Congestive heart failure
Definitions:
failure of heart to pump blood at rate sufficient to meet metabolic demands, or ability to do so only at
abnormally high cardiac filling pressure
Pathophysiology
• Cardiac output is determined by preload (EDV), afterload, contractility
o Frank-Starling law: increase EDV (preload) —> increase SV
Classification
• Low output vs high output
• Left-sided vs right-sided
• Systolic (inability to expel sufficient blood) vs diastolic (failure to relax and fill normally) ~ HFrEF vs HFpEF
• Reduced (HFrEF, EF ≤ 40%) vs mildly reduced (HFmrEF, EF 40-49%) vs preserved (HFpEF, EF ≥ 50%)
o Estimation of EF: Simpson’s bi-plane EF, 3D, eyeballing
- Decreased preload
- Diastolic dysfunction: fall in CO
- Reduced inflow: MS, TS
Myocardial: RCM, HCM, LVH with fibrosis
Pericardial: constrictive pericarditis, cardiac tamponade - Volume overload
- Raised preload past optimal point
- High-output state: anemia, thyrotoxicosis, fluid overload
Valvular: AR, MR - Pressure overload
- Increased afterload
- Left-sided: hypertension, AS
Right-sided: cor pulmonale, PS, PE - Reduced contractility
- Poorly coordinated
contractions
- Segmental: post-MI
Global: myocarditis, cardiomyopathy - Arrhythmia
- Inability to maintain proper coordination
- Tachycardia: AF
Bradycardia: complete heart block
Clinical features
1. Left heart failure
- Low CO (forward)
• Fatigue, decreased ET
• Cool extremities, dizziness
• Slow CR, peripheral cyanosis
• MR, S3 (volume overload)
• Cheyne-Stokes respiration (unstable
central respiratory control —> cyclic breathing with apnea followed by
progressive deeper breathing then
gradual decreases)
- Venous congestion (backward)
Pulmonary congestion
• SOB, orthopnoea, PND
• Cough with pinkish sputum
• Crackles
• Pleural effusion
- Causes
Myocardial diseases e.g. IHD
Volume overload: AR, MR
Pressure overload: systolic HT, AS
- Right heart failure
- Low CO
- Left failure symptoms if decreased RV output leads to LV underfilling
Functional TR, S3 (right-sided)
- Venous congestion
Systemic congestion
• Peripheral oedema (pitting)
• Elevated JVP, Kussmaul’s sign (paradoxical rise in JVP in aspiration due to poor RV compliance)
• Hepatomegaly, pulsatile liver
- Causes
Chronic lung condition: COPD
LV failure causing RV failure
Pressure overload: pulmonary HT
Diagnosis
• Clinical diagnosis based on S/S
o Framingham criteria
• Severity: New York Heart Association (NYHA) class
o Class I: no symptoms with ordinary activity
o Class II: symptoms with ordinary activity
o Class III: symptoms with minimal activity
o Class IV: symptoms at rest
• Killip class: predict mortality in post-MI HF
o Class I: no clinical signs of HF
o Class II: lung creps, S3 gallop, elevated JVP
o Class III: frank APO
o Class IV: cardiogenic shock (SBP < 90), peripheral
vasoconstriction (oliguria, cyanosis, sweating)
Investigations (SAQ!!)
Evaluation for the presence of heart failure
• Bloods: serial TnT, CBC, RFT (hypoNa), LFT (hepatic congestion)
• BNP (brain natriuretic peptide) / NT-proBNP (N-terminal BNP):
release from ventricles during overload, can help distinguish CHF
from other causes of SOB
o BNP: <100 rule out HF, >400 suggest CHF (DDx PE, pulmonary HT, renal failure)
o NT-proBNP: more specific for LV dysfunction
• CXR: ABCDE (Alveolar oedema/ perihilar haziness/ bat wing
opacities, Kerley B, Cardiomegaly, Dilated upper lobe vessels,
pleural Effusion)
• Bedside echocardiogram: reduced EF
Evaluation for potential causes of heart failure
• ECG: evidence of CAD, LVH, heart block
• TTE:
o LV & RV size and ejection fraction
o Valvular diseases: any prosthetic leak
o Regional wall motion abnormalities (MI / DCM)
o Pericardial thickening (constrictive pericarditis / effusion)
• Cardiac MRI: distinguish ischemic vs non-ischemic
• Coronary angiography
Treatment of HFrEF
• Lifestyle modification: weight reduction, stop smoking, avoid alcohol, fluid and salt restriction
• Manage risk factors: HT, HL, DM, arrhythmia, anemia, OSA
• Cardiac rehabilitation: structured exercise programme for NYHA class I-III HF
• Guideline-directed medical therapy (GDMT): 4 pillars of HFrEF
- ACEI (lisinopril 5mg-40mg daily, captopril, enalapril)
- All patients with HFrEF (decrease preload for less fluid retention, decrease afterload for decrease vasoconstriction)
- S/E: dry cough, angioedema, hyperK, renal impairment
-C/I: bilateral RAS, pregnancy - ARB (valsartan, losartan, candesartan)
- All patients with HFrEF (decrease preload for less fluid retention, decrease afterload for decrease vasoconstriction)
- Alternative if cannot tolerate ACEI - Beta blocker (metoprolol, bisoprolol, carvedilol)
- All patients with HFrEF, start low and go slow, start 2 weeks after ACEI since transiently worsen HR and contractility
- S/E: hypoglycaemia
- C/I: APO, 2nd/3rd heart block, asthma, copd - ARNI (angiotensin-receptor neprilysin inhibitors) (Entresto)
- alternative to ACEI/ARB. Stop ACEI 36hr before starting ARNI
- S/E: hypotension, hyperK, angioedema (since oincrease bradykinin)
- dose adjustment if eGFR <30 - Mineralocorticoid receptor antagonist (MRA) (spironolactone, eplerenone)
- NYHA class II-IV with LVEF </= 35%, post MI with LVEF </= 40%
- S/E: hyperK, tender gynaecomastia, decreased libido
- C/I: eGFR<30, hyperK>5
- dose adjustment if eGFR<50 - Sodium-glucose co-transporter 2 inhibitor (dapaglifozin, empaglifozin)
- weight loss, cardioprotective, renal protective
- S/E; UTI, euglycaemic DKA - Hydralazine + nitrates (direct vasodilator)
- patients who cannot tolerate ACEI/ARB - Ivabradine
- indication: Maximal dose / C/I to beta-blockers - Loop / thiazide diuretics (furosemide (start at 20-40mg), bumetanide, torsemide
- indicated if volume overload —> monitor RFT and body weight
- S/E: dizziness, GI discomfort, nocturia, HypoK - Digoxin
- indicated in patients with AF / persistna treatment despite treatment
- MOA: positive inotropic agent that increase contractility
- narrow therapeutic index: TDM 8h post-dose
- S/E: dizziness, n/v/d, arrhythmia
- renal excretion that affected by K/Ca
• Procedural interventions:
o Cardiac resynchronization therapy (CRT): “biventricular pacing” (DDD pacing to both RV and LV) – best for patients with LVEF<35% and wide QRS (especially LBBB)
o Implantable cardioverter-defibrillator (ICD): prevention of arrhythmias if LVEF <35% or Hx of VT/VF
o LV assisted device: artificial pump, now more common than heart transplant
o Heart transplant
HFpEF
• Pathophysiology: decrease compliance due to increase ventricle & artery stiffness
• Risk factors: female, aging, HT
• Clinical features: similar to HFrEF, but
o More venous congestion (backflow) - dyspnoea, pulmonary oedema
o More co-morbidities
• Management: no proven treatment shown to reduce mortality, below drugs only reduce risk of hospitalization
o Non-pharmacological: exercise, diet
o Pharmacological
• Management of co-morbidities: HT, DM, obesity, etc
• Volume overload: diuretics (caution for hypotension due to stiff LV)
• NYHA II/III + elevated BNP: SGLT2i —> add MRA 2 weeks later
o Not effective: ACEI/ARB, BB, CCB, nitrate, digoxin, PDE5i
Tachyarrhythmia
- Narrow complex
—> Regular
- Sinus tachycardia
- Atrial flutter
- Paroxymal SVT: AVRT/AVNRT/AT
—> irregular
- Atrial fibrillation
- Multi-focal atrial tachycardia
- Atrial flutter with variable AV block - Wide complex
—> Regular
- Ventricular tachycardia
- SVT with aberrancy (i.e. pre-existing/functional BBB)
- Antidromic AVRT
—> Irregular
- AF with pre-excitation (underlying WPW) / pre-existing or functional BBB – fast, broad and irregular (FBI)
- Polymorphic VT: normal / prolonged QT (TdP)
Sinus tachycardia
Features
• Rate > 150bpm, respond to carotid sinus massage
• ECG: normal P wave, narrow QRS complex
Causes
• Physiological: dehydration, exercise, pain, anxiety
• Anemia
• Endocrine: thyrotoxicosis, pheochromocytoma
• Vascular: pulmonary embolism
• Infection
• Drug-induced: beta-agonists, thyroxine, caffeine / alcohol
Atrial flutter
• Pathology: Macro re-entry circuit within RA, usually around tricuspid valve annulus
• Clinical S/S: palpitations, chest discomfort, heart failure
• Complications: thromboembolism, degeneration into AFib
ECG features
• Saw-tooth pattern (~300bpm) at inferior leads (II, III, aVF)
• RR intervals are multiples of PP intervals
o Atrial depolarisation rate ~300 bpm
o AV nodal blockade: 2:1 (150bpm) / 3:1 (100bpm)
• Two patterns:
o 80% counterclockwise (typical): negative flutter waves in II, III, aVF
o 20% clockwise: upright in all leads
• Carotid sinus massage: increase AV block and reveal flutter waves
Associated conditions
• Cardiac: cardiomyopathy, valvular heart disease, ischemic heart disease, pericarditis
• Non-cardiac: PE, alcoholism, thyrotoxicosis
Management
Similar to atrial fibrillation
• Haemodynamically unstable:
o DC cardioversion (50-100J biphasic) – different dosage as AFib
• Haemodynamically stable: refer to AFib
Atrial fibrillation
MC sustained cardiac arrhythmia
Pathology:
• Uncoordinated atrial contraction with multiple re-entrant circuits —> Ineffective atrial contraction
• Variable AV conduction rate —> Irregularly irregular rhythm
• Atrial fibrillation begets atrial fibrillation: structural and electrical modelling at each episode —> higher risk of AFib
Clinical S/S:
• Irregular palpitation, SOB due to low CO, syncope
• Irregularly irregular pulse with variable volume, absent a wave of JVP, mitral valve lesions
Classification
• Paroxysmal (self-terminating < 48h) vs persistent (>7d) vs long-standing persistent (>1y) vs permanent
• Non-valvular vs valvular (definition: moderate-to-severe MS or prosthetic heart valves)
Aetiology
• Old age (a/w sick sinus syndrome)
• Cardiac: HT, MI, mitral valve diseases (∵LA dilation), cardiomyopathy, post-cardiac surgery
• Metabolic: high catecholamine states (stress, infection, pheochromocytoma), thyrotoxicosis, hypoK, hypoMg
• Respiratory: hypoxemia (e.g. COPD, pneumonia), pulmonary embolism, OSA
• Drugs: alcohol (holiday heart syndrome: stress + dehydration + effect of alcohol), caffeine, smoking, ivabradine (IF
inhibitor)
Investigations
• Bloods: CBC, LRFT, bone, TFT, Mg
• ECG
o Absent P waves, irregular baseline
o Irregularly irregular RR intervals: usually fast (rapid ventricular response), if slow suspect heart block
• Echocardiogram for structural heart disease & LA thrombus
• +/- 24h Holter for slow AF / long pause
Management: Rate control + Rhythm control + Anticoagulation
Acute management
• Haemodynamically unstable:
o DC cardioversion (120-200J biphasic)
• Haemodynamically stable:
o Treat underlying cause if possible, e.g. hyperthyroidism, PE, sepsis / pneumonia, hypoK/Mg
o Rate control: must check whether there are features of APO —> avoid BB / CCB
- EF ≥ 40%
—> Beta blockers (e.g. IV metoprolol 2-5mg bolus over 2 min)
—> CCB: e.g. IV diltiazem 0.25mg/kg bolus over 2 min or IV verapamil - EF < 40%
- Beta blockers (e.g. IV metoprolol 2-5mg bolus over 2 min)
- IV digoxin 0.25mg
- IV amiodarone also can achieve rate control
o Cardioversion (terminate arrhythmia)
Types:
- Pharmacological:
1. Amiodarone (Class 3) 150mg over 10 min —> 1 mg/min x 6h —> 0.5mg/min x 18h
—> C/I: thyrotoxicosis (absolute C/I: precipitate thyroid storm), active liver disease
2. Flecainide / Propafenone (Class 1c): require BB/CCB 30 mins (?prevent atrial flutter)
3. Procainamide (Class 1a)
Timing
Haemodynamically unstable or refractory to amiodarone: DC cardioversion
- AF < 48h: no need anticoagulation before cardioversion
- AF > 48h: risk of unstable intra-atrial thrombus —> delayed cardioversion
—> Before cardioversion: TEE to rule out LA thrombus / anticoagulation for 3 weeks (usually
with UFH/LMWH)
—> After cardioversion: anticoagulation for at least 4 weeks (warfarin / NOAC) +/- long term depends on CHA2DS2-VASc score
Chronic Mx of AF
Comparing rate control vs rhythm control
• Similar mortality & thromboembolic events
• Rate control: symptomatic relief & prevent tachycardia-induced cardiomyopathy
o More simplified regimens, cheaper and fewer side effects
• Conclusion (AFFIRM trial, RACE trial):
o Rate control if asymptomatic/ mildly symptomatic, older
o Rhythm control if symptomatic (e.g. HF), younger, shorter disease duration (may prevent ventricular remodelling)
- Rate control
Target HR < 80 if symptomatic, < 110 if asymptomatic
• Pharmacological:
o Beta-blockers (Class II) (e.g. esmolol, metoprolol, propranolol) - most
effective and common
o Non-dihydropyridine calcium channel blockers (Class IV): (e.g. verapamil,
diltiazem) – C/I in CHF
o Digoxin: preferred if HFrEF, but C/I in renal impairment
o Amiodarone: last resort
• Surgical: when drugs fail
o Block and pace: AV node blockade drugs + pacemaker (usually VVI(R) / DDD(R))
o Ablate and pace: AV node RFA + pacemaker (usually VVI(R) / DDD(R))
** Note: All AV nodal blockers (BB/CCB) are C/I in pre-
excitations e.g. WPW: rapid accessory pathway
conduction —> rapid pre-excited AF —> VFib**
—> use procainamide - Rhythm control
• Pharmacological
o Na channel blockers (Class I): e.g. procainamide (1a), flecainide / propafenone (1c)
- Preferred in patients with no / minimal underlying heart disease
- Concomitant AV nodal blocking agents (BB/CCB) required: risk of atrial flutter
o K channel blockers (Class III): amiodarone, dofetilide/sotalol
- Preferred in patients with IHD / post-MI / heart failure
- S/E: QT prolongation —> TdP
• Catheter ablation (RFA/ cryoablation): electrically isolate areas around pulmonary veins
o Efficacy 75%, much lower if persistent AF
o Symptomatic relief only, not lower risk of stroke —> anticoagulation may still be required
• Surgery: MAZE ablation
- Anticoagulation
• Indications (must know!!)
o All valvular AF (high stroke risk)
o Non-valvular AF with CHA2DS2-VASc score ≥ 2 for male, ≥ 3 for female
- UTD: Also if 1 for male / 2 for female who is 65-74 years old (age as strongest risk factor)
• Drugs: warfarin (target INR: 2.0-3.0 in general, 2.5-3.5 if mitral/dual valve rep.) or NOAC
• Non-pharmacological prevention of stroke: considered for patients who cannot tolerate long-
term anticoagulation (e.g. previous life-threatening bleeding, high HAS-BLED score)
o Percutaneous left atrial appendage occlusion (LAAO): e.g. Watchman device
- Require coverage with short-course DAPT + longer course of aspirin
o Epicardial snare to ligate LAA
CHA2DS2-VASc score
Components
- Congestive heart failure (1)
- Hypertension (1)
- Age >/=75 (2)
- DM (1)
- Stroke /TIA (2)
- Vascular disease e.g. prior MI, PVD, aortic plaque (1)
- Age 65-74 (1)
- Sex: female (1)
Indicated for anticoagulation if non-valvular AF + score. >=2 for male and >=3 for female
HA financed NOAC if score>5
HAS-BLED score
- hypertension
- Abnormal LRT (max 2)
- Stroke
- Bleeding history
- Labile INR
- Elderly age > 65
- Drug use that promotes bleeding (e.g. anti platelet / NSAIDS) / excessive alcohol (max 2)
Score >3 indicated potentially high risk for bleeding: aim lower end of INR and careful monitoring
Multifocal atrial tachycardia
• ≥ 3 morphologically distinct non-sinus P waves (known as “wandering atrial pacemaker” if not tachycardic)
• Associated with COPD
• Exacerbated by digoxin, theophylline, hypoK/Mg
• Poor response to DC cardioversion
• Treatment: manage underlying cause, CCB if too fast, no need anticoagulation
Paroxymal supraventrilcular tachycardia
Pathophysiology
• Re-entry circuits
• Types
o AVNRT: most common form, often in teenagers / young adults
- AV node has fast pathway (↑conduction speed & ↑refractory period)
and slow pathway
- Typical “down slow, up fast”
o AVRT: extranodal accessory pathway
- Most common: Wolff-Parkinson-White syndrome (Bundle of Kent)
- Others: Lown-Ganong-Levine syndrome (LGLS)
Clinical features
• Rapid forceful regular heartbeat with sudden onset and termination
• Provoked by exertion, caffeine, alcohol, b-agonists
• Terminated by vagal maneuvers
• +/- Haemodynamic compromise: chest discomfort, syncope, SOB
• +/- Polyuria (↑ANP due to atrial activation)
ECG features
• Narrow complex tachycardia (HR 150-220)
• P waves
o AVRT: inverted P waves with a RP interval > 70ms
o AVNRT: no visible P waves, or inverted P waves with a RP interval < 70ms
o (AT: inverted P waves with a long RP interval)
• ST-T abnormalities
Management of regular narrow complex tachycardia
Acute management
• Unstable: synchronized DC cardioversion (50-100J biphasic, then 50-100J increment)
• Vagal maneuvers: ineffective in aborting AT & A flutter, but slowing HR can reveal underlying rhythm
o Carotid sinus massage (CSM) (C/I: carotid bruits, Hx of carotid stenosis)
- MOA: baroreceptor stimulation —> increased PSNS supply
- Technique: auscultate to r/o carotid bruits —> pressure applied to the carotid bifurcation for 10s (superior border of thyroid cartilage)
o Valsalva maneuver: deep inspiration —> forcefully exhale against a closed glottis / against syringe
o Ice pack to face/eye (C/I: IHD)
• Medical therapy: if vagal maneuvers failed (common)
o Adenosine: IV ATP 10mg bolus —> maximum 2 more trials of ATP 20mg Q1-2min
- MOA: AV nodal blocker (hyperpolarization of KATP channels in AV node), very quick onset (<10 sec)
- C/I: asthma, WPW syndrome (emergency trolley standby: WPW syndrome difficult to differentiate —>
transform into VF)
- S/E (warn the patient!): transient flushing, chest discomfort
• Check BP to ensure normal/elevated before the following
o CCB: IV verapamil 2.5-5mg bolus à 5-10mg after 15-30mins
o Consider other agents: b-blocker / digoxin / diltiazem / amiodarone
o Known WPW syndrome: procainamide
• If BP low: go for DCCV
Chronic management
• Infrequent attacks
o Education: self-termination by vagal maneuvers
o Pill in pocket approach: flecainide
• Frequent attacks / High-risk cases (e.g. antidromic AVRT / pre-excited AF)
o Catheter ablation: RFA / cryoballoon (1st line)
- Complications: AV node damage —> complete heart block requiring pacemaker, cardiac tamponade
o Medical therapy (2nd line): Class 1c (flecainide), CCB, BB
Wolff
Parkinson White syndrome
Definition: presence of accessory AV pathway (bundle of Kent)
• “WPW pattern”: pre-excitation on resting ECG but asymptomatic
• “WPW syndrome”: also with documented tachyarrhythmia / symptoms
• WPW is the most common form of AV re-entrant tachycardia (AVRT)
Possible ECG features of accessory AV pathway
• In Sinus rhythm
o Concealed pathway (only allows retrograde transmission): normal ECG in sinus rhythm + predisponse to AVRT
o Manifest pathway (fig.): WPW syndrome
- Short PR < 0.12: AP conducts quicker than AV node
- Delta wave: no AV node to delay conduction
- Wide QRS: pre-excitation of ventricles
- Type A (left-sided AP) = dominant R wave in V1; Type B (right-sided AP) = dominant S wave in V1
• In AVRT
Orthodromic AVRT (95%)
- narrow complex tachycardia
- delta waves absent
- treat as narrow complex tachycardia
Antidromic AVRT (down accessory, up AV node)
- wide complex tachycardia
- delta waves absent
- manage as VT
• In AF/ atrial flutter
o AF with pre-excitation: irregular wide complex tachycardia (all atrial depolarisation is conducted to ventricle via accessory pathway)
o A flutter: HR > 200, regular, wide QRS
o Possible degeneration into VT/ VF
Management
• Haemodynamically unstable: synchronised
DC cardioversion
• Haemodynamically stable:
o Acute: IV procainamide
o Chronic: catheter ablation, flecainide /
propefanone
• Must AVOID:
o Digoxin: shorten refractory period
o AV nodal blockers (e.g. amiodarone,
BB, CCB): increase conduction
through bypass tract —> ↑ventricular
response —> VF possible
Premature ventricular complex
• Very common in normal population, associated with HT, LVH, acute MI
• Pathophysiology: ectopic firing of focus within the ventricle
• Clinical S/S: skipped beat with palpitation (strong beat) after post-PVC pause
ECG features
• < 3 consecutive wide QRS complexes of abnormal shape, not
preceded by P wave
o If ≥ 3: defined as non-sustained VT
• Common descriptions:
o Monomorphic (all PVC look the same) vs polymorphic
o “Ventricular bigeminy”: every other complex is a PVC
o “Ventricular trigeminy”: every third complex is a PVC
Management
• Consider 24h Holter to quantify PVC burden and identify non-sustained VT
• Management: symptomatic (BB / CCB)
Ventricular tachycardia
• A series of ≥ 3 consecutive wide complex tachycardia
• Life threatening: decreased CO, decreased myocardial perfusion, possible degeneration into VF
• Classification:
o Morphology:
• Monomorphic e.g. RVOT (right ventricular outflow tract tachycardia)
• Polymorphic: e.g. Torsades de pointes (TdP)
o Duration:
• Non-sustained: self-terminating within 30s
• Sustained: >30s / symptomatic
Causes
• Valvular lesions
• Heart muscle problem:
cardiomyopathy, myocarditis
• Coronary artery disease
• Illicit drug use e.g. cocaine
• Long QT syndrome
• HypoK / hypoMg
ECG features
• Wide QRS complex
• AV dissociation
o Capture beat: normal QRS
o Fusion complex: sinus and
ventricular beat coincide
• Extreme axis deviation
• Absence of RBBB / LBBB
• Positive / negative concordance
• Brugada’s sign: RS interval > 100ms
• Josephson’s sign: notch near nadir of S wave
• RSR’ complex with tall “left rabbit ear” in V1 (specific for VT)
Ddx of regular wide complex tachycardia
- VT
- SVT with aberrany
—> BBB
—> WPW
VT
- age < 35
- structural heart disease
- ischemic heart disease / MI
- FHx of sudden cardiac death
SVT
- previous ECG: BBB/WPW
- Hx of Paroxymal tachycardia
• ECG – Brugada criteria: when in doubt, treat as VT
Acute management of stable wide complex tachycardia
If haemodynamically unstable:
• Wide regular (monomorphic VT): DC synchronized cardioversion 100J -> 200J -> 300J -> 360J
• Wide irregular (polymorphic VT / VF): Defibrillation
If haemodynamically stable:
• Monomorphic VT
o Non-sustained (<30 sec): usually self-limiting à treat underlying cause (e.g. hypoK, hypoMg)
o Sustained (≥30 sec): IV amiodarone 150mg over 10 min -> repeat PRN / infuse
• Alternatives: lignocaine, sotalol/procainamide (if EF normal), cardioversion (if EF <40%)
• Polymorphic VT
o Defibrillation due to imminent risk of degeneration into VF
o Evaluate QTc interval after revertion to sinus rhythm:
• QTc > 460 msec: Torsades de pointes
• Withdraw precipitating agent
• IV magnesium 5-10mmol over 15 minutes
• Isoprenaline infusion (increase HR to shorten QT, but may cause palpitations)
• Transcutaneous pacing
• QTc < 460 msec: treat as ischaemia (e.g. beta blockers, emergency PCI)
o Treat underlying cause of prolonged QT
Bazett’s formula: QTc = QT / √RR
(RR measured in seconds)
Subsequent management:
• Consider implantable cardioverter-defibrillator (ICD) especially if underlying heart failure
• Look for underlying cause: CBC, LRFT, TnT, Mg, CaPO4, urine toxicology
• Full cardiac workup: ECG, echocardiogram / cardiac MRI, stress imaging, etc.
Torsades de Pointes
• Specific form of polymorphic VT in the presence of long QT
o QRS complexes “twist” around isoelectric line
• “R on T” phenomenon: Ventricular premature complex (VPC) begin at / after apex of T wave à trigger VT/VF
Ventricular fibrillation
• Rapid and irregular electrical activity à
Unsynchronized contraction à Immediate loss of CO
• Immediately life threatening
• Mx: immediate defibrillation (200J biphasic)
ECG features
• Chaotic irregular appearance without discrete p waves,
QRS complexes or T waves
Acute Mx of bradycardia
• Identify and treat underlying cause; ABC; cardiac monitor; IV access; 12-lead ECG, K/Ca/Mg, TFT, digoxin lvl
• Stop offending drugs: e.g. beta-blockers, CCB, digoxin, amiodarone
• If haemodynamically stable: monitor and observe
o Consider transcutaneous pacing for bridging for 2nd degree Type II / 3rd degree heart block
• If haemodynamically unstable:
o Pharmacological Rx:
- IV atropine 0.5mg bolus à Repeat every 3-5 min (max 3mg)
- IV isoprenaline / dopamine / adrenaline infusion
- Not useful if 2nd degree Type II / 3rd degree heart block (esp with new wide QRS i.e. blockade distal to AV node) —> proceed to pacing
o Transcutaneous pacing: verify patient tolerance (CONSENT!) and mechanical capture (palpable
femoral pulse); give analgesia and sedation prn
• Consider cardiac consultation and permanent pacing after stabilization
Sick sinus syndrome
Definition: Dysfunction of SA node leading to variety of arrhythmias
Causes:
• Intrinsic: idiopathic degenerative fibrosis (MC), ischemia (RCA/LCX), cardiomyopathy
• Extrinsic: drugs, autonomic dysfunction, hypoT4
Clinical S/S: dizziness, presyncope, SOBOE, chest discomfort, Stokes-Adams attack (transient syncope due to ↓CO)
Possible arrhythmias
• Inappropriate sinus bradycardia: chronotropic incompetence (cannot increase rate during exercise)
• Sinus pause / arrest: pause is NOT multiple of PP interval
• SA exit block : pause is multiple of PP interval
• Others: tachycardia-bradycardia syndrome, pAF/pAT, atrial ectopic beats
Diagnosis
• 24h Holter ECG
Treatment
• Correct underlying cause
• If symptomatic with pause > 3sec: permanent pacemaker (AAI, DDD if AV nodal disease)
Escape / Extopic rhythms
• Distal latent pacemakers become active – can be transient (escape) or continuous (ectopic rhythm)
Atrioventricular block
Causes
• Idiopathic (~50%): progressive degeneration of conduction system
• Ischemic heart disease (40%): especially RCA infarct à AV node ischemia à high grade heart blocks
• Drugs (AV nodal blockers): beta blockers, non-dihydropyridine CCB, digoxin, adenosine, amiodarone
• Metabolic: hyperK, hypoT4
• Cardiac procedures: e.g. open heart surgery, TAVI
• Cardiomyopathies / Myocarditis
• Congenital heart disease: neonatal lupus with anti-Ro/La +ve —> complete heart block
Types
- 1st degree AV block
-> PR > 200ms (5 small squares) P:QRS = 1:1
- 2nd degree (Mobitz type 1)
P:QRS = n : n-1
- 2nd degree AV block (Mobitz type 2)
- 3rd degree AV block
Mobitz 1
- worsen in vagal maneuver, improved in IV atropine, improve with exercise
Mobitz type 2:
- improve with vagal manoeuvres, worsen with IV atropine and exercise
Management
• Acute management: stop offending medications (e.g. BB, CCB, digoxin), support ventricular bradycardia
(e.g. atropine, isoprenaline, temporary pacing)
• Definitive management: Re-evaluate cardiac rhythm after all reversible factors are corrected
o 1st degree / 2nd degree Type I: rarely symptomatic, no need treatment
o 2nd degree Type II / 3rd degree: permanent pacemaker (DDD)
- Complete heart block in AMI:
o Inferior MI: often revert to sinus after revascularization, Mx by atropine & temporary pacing
o Anterior MI: often irreversible heart block (LAD à extensive infarct), Mx by permanent pacing
RBBB
rSR’ in V1/V2
QRs in V6
Causes:
- normal variant
- ASD
- RV strain, e.g. PE, RVH, cor pulmonale
LBBB
- rS in V1
- R in V6
Causes:
- Lenegre disease: primary degenerating
- Heart disease: AMI, DCM, AS
- HyperK
- digoxin toxicity
LAFB
- Left axis deviation
- qR in I, aVL
- rS in II, III, aVF
Benign
LAFB
- Left axis deviation
- qR in I, aVL
- rS in II, III, aVF
Benign
LPFB
Right axis deviation
Absence of RVH
qR in II, III, aVF; rS in I, aVL
Bifascicular block
• RBBB + LAFB = RBBB features + left axis deviation
• RBBB + LPFB = BBB features + right axis deviation (after ruling out other DDx: RVH, PE, lateral STEMI)
Trifascicular block
• Incomplete trifascicular block
o Bi-fascicular block + 1st degree / 2nd degree AV block
o RBBB + alternating LAFB/LPFB
• Complete trifascicular block
o Bi-fascicular block + 3rd degree AV block
Brugada syndrome
Definition: AD mutation in cardiac Na channel gene (SCN5A), characterised by sudden cardiac death associated with
characteristic ECG abnormalities
Diagnostic criteria
• Clinical: syncope, documented VF/ VT, nocturnal agonal respiration, FHx of SCD < 45y +
• ECG abnormalities:
o Type 1: Brugada sign (coved ST elevation > 2mm in ≥1 of V1-V2 followed by T wave inversion)
o Type 2: Saddleback shaped ST elevation with terminal portion of ST segment elevated ≥ 1mm
o Type 3: similar to type 2, but terminal portion of ST segment is elevated < 1mm
o For types 2/3 ECG pattern, make the diagnosis by converting patient to type 1 ECG pattern
- Flecainide provocative test ± high V1/V2 placement (2nd ICS)
Management
• Symptomatic: ICD (1st line esp for Hx of cardiac arrest / VT), quinidine / amiodarone (if ICD refused or C/I)
• Asymptomatic (i.e. ECG Brugada sign only): watchful waiting
o Avoid inducing drugs, e.g. beta blockers
o Avoid excessive alcohol and heavy meals(pro-arrhythmic)
• Family screening
Long QT syndrome
Definition of long QT (UTD): ≥460ms (before puberty), ≥470ms (adult M), ≥480ms (adult F)
Clinical S/S: usually asymptomatic, may have palpitations / syncope / sudden cardiac arrest (TdP)
Aetiology
• Congenital long QT: cardiac ion channel mutation (e.g. Romano-Ward syndrome: AD mutation of KCNQ1 gene
—> K+ channel), other associations include syndactyly & Andersen syndrome
• Acquired:
o Drugs (5A): antiarrhythmic (class Ia/III), antipsychotic, antidepressant, antihistamine, antimicrobial
(macrolides, fluoroquinolones, azole antifungals)
o Metabolic: hypo-Ca/K/Mg, hypothyroidism
o Structural heart disease: HT, LVH
Investigations
• Schwartz score for diagnosis: ECG findings, clinical Hx (e.g. syncope), family Hx
• Holter + exercise stress test (QT not reduced by exercise)
• Genetic testing
Management
• Torsades de pointes: defibrillation, IV MgSO4, isoprenaline (β-agonist), transvenous ventricular pacing
• Remove/ treat underlying causes, e.g. avoid drugs that prolong QT interval, avoid stress (e.g. strenuous exercise),
correct electrolyte disturbances
• Beta blockers (e.g. propranolol): given to ALL patients, ↓syncope and ↓sudden cardiac death
• Implantable cardioverter-defibrillator (ICD) if initially present with cardiac arrest without reversible cause
Pacemaker
• Indications: supraventricular disease
o SA node dysfunction (MC): sick sinus syndrome, AF with
symptomatic bradycardia
o AV block: Mobitz II, complete heart block
o Bundle branch block: trifascicular block
• Temporary pacemakers:
o Transcutaneous (discomfort: forceful pectoral muscle contraction)
o Transvenous (via internal jugular, subclavian or femoral vein)
• Permanent pacemakers:
o Coding:
- 1st letter: chamber paced (A, V, D)
- 2nd letter: chamber sensed (A, V, D, O)
- 3rd letter: pacemaker response (Trigger, Inhibited, Dual)
- 4th letter: any rate modulation (R)
o Single chamber pacemaker: RV/ RA
- AAI: sinus node disease with intact AV node, e.g. sick sinus syndrome
-> ECG: pacing spike followed by normal P and QRS complex
- VVI: AF with symptomatic bradycardia
—> ECG: pacing spike followed by QRS complex with LBBB (RV
depolarized first)
o Dual chamber pacemaker: RA + RV
- DDD: for AV block with normal SA node, e.g. Mobitz Type II heart block, complete heart block
o Biventricular pacing: cardiac resynchronisation therapy pacemaker (CRT-P) – RV + LV
- Consider if LVEF <35% with wide QRS
• After care: full lead ECG, CXR
• Complications
o Due to implantation: pneumothorax, cardiac tamponade, lead malposition, pocket haematoma, infection
o Due to pacemaker: failed pacing, pulse generator failure
Indication for temporary pacing
- Mobitz type 2 HB
- 3rd degree HB
- Bifascicular block + 1st HB
- RBBB + alternating LAFB/LPFB
- Alternating LBBB + RBBB
Electrical cardio version and defibrillation
• Synchronised DC cardioversion: unstable haemodynamics or refractory medical treatment in
o SVT: PSVT, A flutter, AF
o Monomorphic VT (with pulse)
• Defibrillation (i.e. asynchronous DC cardioversion)
o Pulseless VT (mono/ polymorphic)
o VF
• Initial energy for cardioversion/ defibrillation (escalate if ineffective)
PSVT 100J
A flutter 100J
AF 150-200J
Stable wide complex
tachycardia 100J
Unstable wide complex
tachycardia 100J
Polymorphic VT 150-360J
Implantable cardioverter defibrillators (ICD)
• Detect ventricular arrhythmia, terminate them and prevent SCD
• Indications:
o Secondary prevention: prior VT/ VF (except VT/ VF within first 48h of MI)
o Primary prevention: congenital (e.g. long QT syndrome, Brugada syndrome, HOCM), severe HF (CRT-D)
Catheter ablation
• Intentionally damage a portion of re-entrant pathway by applying radiofrequency or freezing (cryoablation)
• Pathway determined by electrophysiologic study
General indications for valvular replacement
• Symptomatic (HF) despite optimal medical therapy
• Asymptomatic, but severe disease defined by
o Severe stenosis/ regurgitation by ECHO criteria
o LV dilatation: LV end-systolic diameter
o LV systolic dysfunction: Impaired LVEF < 50%
o Complications, e.g. new-onset AF, pulmonary HT
• Infective endocarditis despite optimal medical therapy
Aortic stenosis
Aetiology:
- bicuspid aortic valve (MC in young)
- Senile calcification (MC in old)
- Rheumatic heart disease
- IE
- Hyperuricemia
- William’s syndrome
S/S:
- Angina
- Syncope
- HF
Mx:
- avoid strenuous exercise
- HF: ACEI + diuretics
- Valvular replacement: open, transcatheter aortic valve implantation (TAVI)
Indication of surg
- symptomatic
- if asymptomatic
—>
valve area < 0.6cm2
VT
LV systolic gradient > 40mmHg
Concomitant heart surgery
Aortic regurgitation
Aetiology:
- valvular: degeneration,
- RHD,
- congenital (bicuspid)
- aortic root dilation
- hypertension
- infection (syphilitic aortitis)
- inflammatory (AS)
- CT disease (Marfan)
Acute AR: aortic dissection, IE
S/S:
- SOB
- fatigue
- chest pain more at night
Ix:
ECG, CXR, ECHO, CT thorax, coronary angiogram
Mx:
- diuretics
- vasodilators for HT: ACEI/ARB/CCB
- valvular replacement
Indications of surg:
- symptomatic
- if asymptomatic
—> LVEF < 50%
—> LV dilation
—> aortic root dilation
—> acute severe AR
Mitral regurgitation
Aetiology:
Chronic MR
- MVP
- RHD, IE
- LV dilation (functional)
- Connective tissue disease
- Cardiomyopathies
Acute MR:
- Post-MI ruptured chordae tendinae / papillary muscle
- IE
S/S:
- AF
- HF
Ix:
Double right heart border and splaying of carina
Mx:
- AF
- HF
Surgical options:
- MV repair: open, percutaneous MV clipping (MitraClip)
- Mechanical MV replacement
- Percutaneous MV replacement
Indications for surg:
- symptomatic
- LVEF 30-60%
- LV dilation: end systolic diameter>45mm
- new onset AF
- new onset pulmonary hypertension
Mitral stenosis
Aetiology:
- RHD
- IE
- Degenerative: mitral annular calcification
- Inflammatory
- Congenital
S/S:
- AF
- HOV (Ortner’s syndrome)
- Haemoptysis
- Concomitant MR
Mx:
- AF
- Valvular repair: Percutaneous transvenous mitral commissurotomy, open commissurotomy
- mitral valve replacement
C/I for PTMC:
- moderate severe MR
- LAA thrombus
- Calcified valve
Indicated for valvular replacement:
- pul HT
- Pul congestion
- haemoptysis
- recurrent embolism events despite anticoagulation
Pulmonary hypertension S/S
elevated JVP with systolic “v” waves (functional TR), parasternal heave (RV pressure overload), parasternal thrills (functional TR), loud P2,
pansystolic murmur of TR, Graham-Steell murmur of PR
Mitral valve prolapse
Primary:
myxomatous dengeneration of mitral valve (common in females)
Secondary:
- connective tissue disease
- SLE
- PCKD
S/S:
- Palpitation
- LLSB mid-systolic click followed by late systolic crescendo- decrescendo murmur
- angina, fatigue, dyspnea, anxiety
- complications:
—> embolism stroke
—> endocarditis
—> arrhythmia
—> progress to MR
Mx:
- Asymptomatic: reassure and FU
- Symptomatic: treat arrhythmia, treat chest pain with beta blockers
Rheumatic heart disease
Definition: immune-mediated multisystem disease secondary to group A Strep infection
• Pathophysiology: molecular mimicry – cross-react against cardiac proteins (anti-M)
Clinical features
• Acute rheumatic fever: Occur 2-6 weeks after pharyngeal (strep throat) or skin infection (scarlet fever)
• Chronic RHD: inflammation and scarring of cardiac valves after 1 or more episodes of rheumatic fever
o Valve involved: MV > AV > TV (~ SBE)
• Jones criteria:
o 2 major OR 1 major + 2 minor
o + Evidence of recent GAS infection: ↑ASOT / positive RAT / positive throat culture / recent scarlet fever
Major criteria:
Joints
Heart
Nodules
Erythema
Sydenham chorea.
Minor criteria:
Previous rheumatic fever
ECG with PR prolongation
Athralgias
CRP and ESR elevated
Elevated temperature
*Pancarditis: may have transient murmurs e.g. AR, MR, mid-diastolic murmur at apex (Carey-Coombs murmur)
Management
• Acute rheumatic fever:
o Eradication of Group A Strep (Tx & 2o prophylaxis): IM benzathine penicillin G x 10 days —> Q4 weeks until
21 year old / for 5 years (whichever is longer)
o Arthritis: NSAIDs
o Carditis: ECHO, treat HF
o Sydenham chorea & rash: no specific treatment
• Chronic rheumatic heart disease (CHRD): periodic clinical assessment + echocardiogram
Infective endocarditis
• Definition: infection of cardiac endothelium, most commonly the valves
• Valve involvement: MV»_space; AV > TV (common in IVDA) > PV
Subacute infective endocarditis
- tend to affect abnormal valve e.g. prosthetic valve, aortic/ mitral valvular disease, congenital heart disease
- Strep viridans, enterococci coagulate negative Staph
Acute infective endocarditis
- IVDA, tend to affect normal valves
- G+ S aureas
• Culture negative endocarditis: Coxiella burnetti (Q fever), Brucella, fungal infections
• Other causes of endocarditis: SLE (Libman-Sachs endocarditis), malignancy
Clinical features
• Constitutional symptoms: fever, loss of weight, chills
• Cardiac involvement: chest pain, heart failure symptoms (SOBOE, PND), new-onset TR
Investigations
• CBC, ESR/CRP, RFT, urinalysis for potential GN
• Blood culture: at least 3 sets at different sites to demonstrate persistent bacteremia (typical for IE)
• ECG / CXR
• Echocardiogram (TTE/TEE): detect vegetations, valvular lesions, abscesses
Modified Duke’s criteria
• Definite diagnosis if 1 pathologic criteria OR 2 major OR 1 major + 3 minor OR all minor
• Pathologic criteria (require cardiac surgery / autopsy): microorganisms demonstrated in vegetation, histologic exam
• Major: +ve blood culture x2, +ve echocardiogram (vegetation / abscess / new regurgitation / dehiscence of prosthetic valves, +ve serology for Coxiella
• Minor (“FIVE PM”):
o Fever
o Immune complex, e.g. GN, Osler’s node (tender raised), Roth spots, RF +ve
o Vascular, e.g. Janeway lesions (non-tender flat), mycotic aneurysm, intracranial haemorrhage, emboli, lung infact
o Predisposing heart conditions, e.g. IVDA
o Microbiological, e.g. +ve blood culture x 1
Management
• High dose IV antibiotics for 6 weeks: give empirically before C/ST to cover at least Staph, Strep & Enterococcus
E.g. vancomycin, ampicillin, gentamicin
• Surgical debridement and valvular replacement
o Indications: haemodynamically unstable, infected prosthesis, persistent infection despite ABx
• Follow-up blood culture Q3days
Tx steps:
1. R/o penicillin allergy
2. Acute MSSA in IVDA: IV cloxacillin + gentamicin for 5 days
3. Chronic MSSA: IV ampicillin + gentamicin for 6 weeks
4. MRSA: IV vancomycin + gentamicin
5. If prosthetic valve: +rifampicin
Antibiotic prophylaxis
Routine antibiotic prophylaxis is NOT recommended
Only indicated for high risk group during selected procedures
High risk
• Prosthetic valve replacement / repair
• Previous IE
• Congenital heart disease: unrepaired cyanotic CHD, repaired with residual defects, completely repaired within the first 6 months
• Dental procedures: amoxicillin 2g PO / ampicillin IV; single dose 30-60min before
procedure; clindamycin 600mg PO/IV if allergic to penicillin
• Other procedures: only in the context of infection
o Respiratory: anti-Staph
o GI / GU: anti-Enterococcal
o Skin / MSK: anti-Staph and anti-Strep
Acute pericarditis
Aetiology:
- Idiopathic/ viral (80%): Coxsackie, adenovirus, HIV
- Bacterial: TB, strep, staph
- CVS: post-STEMI (inflammatory,
autoimmune i.e. Dressler’s Sx)
- Metabolic: uraemic pericarditis
- Paraneoplastic
- Autoimmune: SLE, RA, vasculitis
- Iatrogenic: PCI / pacemaker insertion
S/S:
- Chest pain: pleuritic, positional
(↓sitting up and leaning forward), radiate to back (trapezius muscle)
- Low grade fever
- P/E: pericardial friction rub (classically triphasic: atrial systole, ventricular systole, rapid filling phase of early ventricle diastole)
Ix:
- CBC D/C, ESR/CRP
- Cardiac Tn, CK-MB
- *ECG: diffuse ST elevation
concaving upwards + PR
depression, Spodick’s sign if early (downsloping TP segment)
- Underlying cause: sputum for AFB & TB culture / IGRA, RF/ ANA, CXR mammography (malignancy)
Mx:
- treat underlying cause
- rest
- NSAID +/- colchicine for anti-inflammatory and analgesic action (alternative: low dose steroid)
- If recent MI: aspirin (avoid NSAID/steroid)
- Pericardiocentesis if fluid output more than 50ml/hr
Pericardial effusion
Aetiology:
- Acute pericarditis
- serous effusion: CHF, cirrhosis, nephrotic syndrome, hypoT4
- haemorrhagic: AD, trauma, LV rupture
S/S:
- compression symptoms: dysphagia, SOB, HOV, hiccups
P/E:
- muffled heart sound, Edward sign (dullness over left angle of scapula: compressive atelectasis)
Ix:
CXR
- globular shaped heart
- clear lung fields
- Oreo-cookie sign on lateral film
ECG:
- tachycardia
- low QRS voltage
- electrical alternans
ECHO:
- chamber collapse (RA most prone, distended IVC)
Mx:
- treat underlying cause
- pericardiocentesis
—> diagnostic: order gram stain, C/ST, AFB+TB culture, PCR, cytology +/- biopsy for histology
—> therapeutic
Cardiac tamponade
Aetiology:
- infection
- neoplastic
- uraemia
- trauma
Definition: pericardial effusion + haemodynamic compromise
S/S:
- Beck’s triad: hypotension, elevated JVP, muffled heart sound
- Pulsus paradoxus (decrease in 10mmHg SBP in inspiration)
- Kussmaul’s sign
- LL edema
Ix:
CXR
- globular shaped heart
- clear lung fields
- Oreo-cookie sign on lateral film
ECG:
- tachycardia
- low QRS voltage
- electrical alternans
ECHO:
- chamber collapse (RA most prone, distended IVC)
Mx:
- IV fluid (D5/NS/plasma)
- AVOID vasodilators and diuretics and PAP
- ECHO-guided percardiocentesis
—> apical / subcostal approach
—> complications: cardiac perforation, damage to pericardial coronary artery
- alternative: open drainage
- prevention: pericardial window
Constrictive pericarditis
Aetiology:
- progressive thickening, fibrosis and calcification of pericardium after any cause of acute pericarditis
- classically TB pericarditis
S/S:
- reduced CO: hypotension, reflex tachycardia, fatigue
- Kussmaul’s sign
- right HF: elevated JVP, hepatomegaly, peripheral oedema
- P/E: pericardial knock
Ix:
- CXR: pericardial calcification
- ECG: non-specific, low-voltage
- ECHO: thickened bright pericardium
- Cardiac catheterisation
Mx:
- anti-inflammatory agents
- surgical pericardiectomy
Myocarditis
Definition: non-ischaemic myocardial inflammation
Aetiology
• Idiopathic
• Infection:
o Viral (MC): e.g. Coxsackie virus, Influenza, COVID-19, adenovirus, enterovirus, CMV, HCV, HIV
o Bacterial: e.g. Rickettsial infections (Q fever, RMSF), TB, mycoplasma
o Fungal / Parasitic
• Autoimmune: rheumatic fever, SLE, RA
• Toxin: cocaine
• Hypersensitivity: drugs (e.g. antibiotics), insect/ snake bites
• Others: giant cell myocarditis, eosinophilic myocarditis
Clinical features
• Fever
• Chest pain
• Acute heart failure: SOB, tachycardia (out of proportion to fever), elevated JVP
• Chronic heart failure: dilated cardiomyopathy as a chronic insult (see below)
Investigations
• ECG: non-specific ST-T changes + conduction defects
• Bloods: CBC, CRP/ESR, cardiac enzymes, viral titres
• ECHO, cardiac MRI (to assess pathological and functional abnormalities)
• Coronary angiogram (to rule out IHD as the cause)
• Endomyocardial biopsy (if diagnosis uncertain): histology by Dallas criteria, IHC
Management
• Restrict activity
• Supportive care: HF, arrhythmia
• Treat underlying cause
Complication
• Dilated cardiomyopathy (DCM)
Cardiomyopathy
• Intrinsic or primary myocardial disease that is not secondary to congenital, hypertensive, coronary, valvular or pericardial disease
• Functional classification: dilated (MC), hypertrophic, restrictive
• Investigations: ECG, CXR, ECHO, exercise test / Holter monitoring (look for arrhythmias), coronary angiography (to rule out IHD), endomyocardial biopsy
Dilated cardiomyopathy
Definition:
- ventricular enlargement and decreased contractility with impaired systolic function
Aetiology:
- Familial
- Vascular: MI
- causes of myocarditis
- Toxins: alcohol, anthracyclines (e.g. doxorubicin)
S/S:
- may present as MR/TR (LV dilatation), left HF, tight HF
LVEF: <30%
Ix:
- CBC, LRFT, TFT, antibodies
- CXR: heart failure
- ECG: A/V enlargement, arrhythmia (AF, VT)
- Echo: LV size and EF, TR/MR
- Cardiac MRI / Endomyo Bx
Mx:
- treat underlying causes
- manage CHF and arrhythmia
- consider ICD/CRT if LVEF<35%
- heart transplant
Restrictive cardiomyopathy
Definition:
- decreased myocardial compliance in a non-dilated, non-hypertrophied ventricle
Aetiology:
- infiltrative: amyloidosis, glycogen storage disease
- fibrosis: scleroderma, radiation
S/S:
- may present as right HF, arrhythmia
- Kussmaul’s sign+ve
LVEF>50%
Ix:
- Echo: speckled myocardium exclude constrictive pericarditis (pericardial calcification on CXR, thickened pericardium on echo)
Mx:
- treat underlying causes
- manage arrhythmia and CHF
Arrhythmogenic RV cardiomyopathy (ARVC)
Definition:
- abnormal RV due to myocardial replacement by fibrofatty tissue
Aetiology:
- genetics: AD
S/S:
- right HF
- arrhythmia
Ix:
- ECG: Epsilon wave
Mx:
- avoid competitive sports
- medical: beta blockers
- ICD
- genetic counselling
Hypertrophic cardiomyopathy
Definition:
- Left ventricular hypertrophy without causative hemodynamic factors (e.g. HT, aortic valve disease, storage diseases)
- normal systolic function but abnormal diastolic relaxation
• Often affecting interventricular septum —> LV outflow tract obstruction
• Classification: non-obstructive (75%) vs obstructive (HOCM) (25%)
o Obstructive = evidence of LVOT gradient
Aetiology:
- Genetics (100%): AD
S/S:
- maybe asymptomatic or present as SOBOE, exertional chest pain, syncope (due to LV outflow tract obstruction), HF, sudden cardiac death
LVEF: 35-50%
Ix:
- ECG: dagger-like Q waves in inferior / lateral leads, LVH +/- strain, anterior leads T wave inversion, AF, WPW
- CXR: normal (early stage), cardiomegaly (late stage)
- ECHO: LVH, ASH, SAM of mitral valve, LVOT
- Holter monitoring +/- exercise test: arrhythmia
- genetic testing
Mx:
- avoid exacerbating factors e.g. dehydration, competitive sports
- family screening. Genetic counselling, CPR education
- If symptomatic / evidence of LVOT:
—> beta-blockers (propranolol / verapamil)
—> +/- diuretics for congestive symptoms
—> +/- Tx arrhythmias: amiodarone, anticoagulation
—> avoid vasodilators (e.g. nitrates, ACEI/ARB) and digoxin even in angina: decrease preload and increase LVOTO
- ICD
- surgical: surgical septal myomectomy, alcohol septal ablation (alcohol-induced infarction)
Hypertrophic obstructive cardiomyopathy (HOCM)
• Mechanism of LVOT obstruction in HOCM
o Asymmetrical septal hypertrophy (ASH) —> distort LV systolic movement
o Venturi effect due to increased ejection velocity —> systolic anterior motion (SAM) of mitral valve —> mitral-septal contact —> secondary MR
• Associations: WPW, Friedreich’s ataxia, Fabry’s disease
Physical findings of HOCM
• Jerky pulse +/- double carotid arterial impulse
• Prominent ‘a’ wave in JVP: reduced
compliance of RV due to septal hypertrophy
• Double apical impulse with heaving
character: pre-systolic impulse due to forceful
atrial contraction against non-compliant LV
• Late ejection systolic murmur (ESM) over
LLSB radiating up sternal edge but not to
carotid: LV outflow tract obstruction
• Pansystolic murmur at apex radiating to
axilla: systolic anterior motion (SAM) of mitral
valve —> MR
• Murmurs enhanced by Valsalva maneuver /
standing from squatting (∵↓preload)
• Reversed splitting of S2
• S4: due to atrial systole
Complications of HOCM
• Arrhythmia: AF (most common), ventricular arrhythmias
• Diastolic heart failure: pressure overload due to LVOT obstruction
• Sudden cardiac death
• Angina / MI: increased muscle load and myocardial O2 demand
• Infective endocarditis
• Systemic embolization
Risk factors for sudden cardiac death in HOCM
• Hx of syncope
• FHx of Sickle cell disease
• Abnormal BP response to exercise
• Non-sustained VT
• Severe LVH with thickness >30mm
Mx:
Mavacamten —> myosin inhibitor
Digoxin overdose
Digoxin > 2.6ng/ml = toxic
S/S:
- hyper K
Ix:
- RFT
- ECG
- TnT, CK
Common arrhythmia:
- bradycardia
- downward sloping scooped ST segment suggest digoxin therapy
- T wave inversion
- U wave —> chronic toxicity —> hypoK
- Heart block
Mx:
- resus
- stop all drugs
- serum digoxin level
- RFT for electrolyte disturbance
- cardiac markers
- activated charcoal if acute overdose
- anti-digoxin immunoglobulin = Digibind / ovine
- atropine
- synchronised DC cardioversion
- Tx underlying causes = hypoK = KCl in saline infusion
-admit to monitor in inpatient
- refer cardiologist, nephrologist and toxicologist
Risk factors for digoxin toxicity
- electrolyte —> hyperK/hypoK, hyperCa, hypoMg, hyperNa
- ABG —> acidosis, alkalosis
- Cardiovascular—> MI
- Endocirne -> hyper/hypoThyroid
- Renal insufficiency
- Hypoxemia
- DDI —> amiodarone, verapamil. Earthy my in and ditiazem for CYP450 inhibitors
