Cardiology Flashcards
(73 cards)
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
