Approach to Patient with Acute Chest Pain

 Hx of ISCHEMIC pain:
o Duration --> Minutes to Hours (typically >20-30min; NOT seconds or days)
o Quality --> Sore, dull, squeezing, crushing (NOT sharp or point-like; cannot point at it)
o Location --> 90% substernal (uncommon to left; very rare to right)
o Radiation --> Neck, arm
o Precipitating Factors --> Exertional
o Alleviating Factors --> Rest, nitroglycerine
 GORD can worsen with nitroglycerine
o Associated Symptoms
 SOB
 Vagal symptoms
 Inferior wall sits on diaphragm and is in contact with vagus
 Inferior wall MI cause vagal stimulation
o N+V
o Bradycardia (also due to 3rd degree AV block in inferior MI)
o Sweating
o Light headedness
o NON-associated symptoms
 Positional --> Change with position (? pericarditis)
 Pleuritic --> Changes with respiration (? PPPPP)
 PE, Pneumonia, Pericarditis, Pneumothorax, Pleuritis
 Tender --> Pain reproduced on palpation (? costochondritis)

 Examination of ISCHEMIC pain: Not very useful as signs often non-specific or absent
o Vitals: ↑RR, ↑HR (if ↓, ?inferior wall), BP ↑or↓ (>20mmHg difference between arms
present in 70% of aortic dissections)
o Heart sounds: Mostly normal, but sometimes...
 Widely split S2 (caused by anything delaying right sided conduction)
 Pulmonary HTN
 Pulmonary stenosis
 RVH
 RBBB
 Paradoxical S2 (caused by anything delaying left sided conduction)
 HTN
 Aortic stenosis
 LVH
 LBBB
 S3 Gallop
 S4 Gallop
 Aortic regurgitation
 Mitral regurgitation (papillary muscle dysfunction from posterior wall infarction)
 Mx of ISCHEMIC pain:
o First: ECG
 ST elevation --> Infarction (STEMI)
 Non-ST elevation (i.e. normal or ST depression [± t-wave inversion])

 DDx of Chest Pain:

o Non-Cardiac Chest Pain:
 GI:
 GERD
 Peptic Ulcers
 Gallbladder disease (right-sided; not easily confused with cardiac!)
 Costochondritis --> Chest wall tenderness
o Cardiac:
 MI --> Severe pain >20min duration
 Aortic stenosis --> systolic ejection murmur, SAD triad + CHF
 Myocarditis --> Vague and mild pain, mild SOB; variable presentation
 Pericarditis --> sharp, pleuritic, worse on leaning back, better on sitting forward
 Dissecting aortic aneurysm --> sharp, tearing, located in back, loss of pulses/arm-
arm BP deviation >20mmHg, aortic regurgitation, widened mediastinum
 Mitral prolapse --> Transient, mid-systolic click, young female w/ no risk
o Pulmonary:
 Pulmonary embolus --> SOB, pleuritic paincough?, hemoptysis?
 Pneumothorax --> Sudden onset pain + SOB, absent/reduced lung sounds (only if
tension pneumo), tracheal deviation, tall skinny people...
Basic Concepts

 Heart sounds – normal and abnormal:

o 1st heart sound  Mitral + tricuspid valves closing at beginning of systole
o 2nd heart sound  Aortic + pulmonary valves closing at end of systole
 Split S2:
 Physiological
o On inspiration there is more right heart but less left heart return
o More volume in R heart, less in L heart = P2 closes after A2
 Pathological
o Fixed split:
 ASD or VSD equalises blood at all times
 A2 + P2 are always in synch
o Widely split
 Right sided problems
o Paradoxical/reverse split:
 Left sided problems which slow conduction
 A2 slows down, P2 remains same = P2 closes before A2
 AS, HOCM, LBBB, LVH

 Loud or Soft S2:

 Loud  HTN
 Soft  Severe aortic stenosis

o 3rd heart sound “Kentucky”  Early diastolic extra sound

 What is it  Atria splashing blood into ventricle
 Causes  EARLY SIGN of LV dysfunction
 Innocent in <30 + athletic
 Rapid filling or poor LV function (CCF/DCM)
 Constrictive pericarditis (“Pericardial knock”)
 Mx  ↑Diuretic, ↑ACE-I, ↑B-blocker
 Can lead to acute pulmonary oedema if not rigorously treated

o 4th heart sound “Tennessee”  Early systolic extra sound (imagine split S1)
 What is it  Atrial systole splashing blood into stiff LV
 Causes  LVH, AS, HOCM, HTN
 Mx  Nil (benign), but treat underlying heart failure (and causative condition)

o Murmurs:
 AS  ejection systolic radiating to clavicle + carotids
 MS  mid-diastolic
 AR  early diastolic
 MR  pan-systolic radiating to axilla
 PS  ejection systolic radiating to back

o Other heart sounds:

 Mitral prolapse  Mid-systolic click
 Atrial myxoma  Atrial plop in late diastole
Cardiology Investigations

 Blood Pressure
o BP = CO x SVR
 CO = SV x HR
o Normal systolic = 100-160
o Mean arterial pressure (MAP) = ([2xdiastolic] + systolic)/3
 E.g. 120/80 = MAP of 93.3
 ~60 MAP needed for adequate organ perfusion (e.g. 80/50 = minimum)
 If hypertensive body used to high pressure and organ perfusion needs ~75 MAP (e.g.
145/80)
 Anaesthetists use MAP more than systolic BP as is better estimator of perfusion

 ECG

 Enzymes:
o Myoglobin  Most sensitive EARLY marker (<6hr) for MI (non-specific though)

o CKMB:
 Rises: 4-6 hours
 Peaks: 12-24 hours
 Normalizes: 3-4 days
 Hence best biomarker for early re-infarction as 4 days later CK-MB should
be normal, but troponin will still be elevated as it takes 2 wks to normalize
o E.g. Chest pain again 5 days later, troponin useless but CK-MB
helpful

o Troponin T/I (components of the cardiac myofibril [actin component])

 Physiology:
 Troponin is bound to tropomyosin
 Tropomyosin regulates actin + regulates the binding to myosin in myocytes
 Uses: ACS, routinely following PCI or CABG patients
 Difference: Nil, each of equal value
 Levels: Detectable at 3-6hr, peaks at 12-24hr, disappears by 14d
 Measure at presentation
 Measure again at 12hr post-chest pain (6hr if using hsTrop)

 Preferred to CK-MB in first instance

 Normal CK-MB but ↑troponin = minor myocardial damage

 Remains elevated for weeks (therefore good late marker of MI)

 TROPONIN IS PROGNOSTIC – higher = worse outcomes = higher mortality

 Artificially raised in:

 Renal disease
 CCF
 PE
 Pericarditis
 Myocarditis

*In these cases, take troponin and TREND IT (you MUST see rise and fall as
this indicates acute condition such as MI; stable trop = artificially raised)
o hsTrop
 Allows detection of smaller changes in troponin
 Useful as no need for admission + 12hr trop, can measure admission + 6hr trops
 Allows quicker decision to be made on diagnosis and quicker intervention

o hsCRP
 Detects smaller levels of CRP (i.e. the ones normally reported at <1, this will find)
 Clinically significant as some patients may benefit from STATIN therapy if hsCRP
raised (JUPITER trial), but trial done later found no association between hsCRP and
statin therapy benefit (Lancet study – Heart Protection Study Collab Grp)

o BNP  Raised in CCF, ACS and associated with mortality

 Scans
o CXR

o Echo
 TTE
 Easier to do
 Better tolerated
 Better visualisation of ventricles (esp ventricular apex)

 TOE
 Better visualisation of:
o Posterior structures (e.g. atria, pulmonary veins)
o Left atrial appendage (since transducer positioned against LA)
o Prosthetic valve assessment

 Notes
 Do not perform echo when patient has pH <7.3 – LV does NOT contract
well in acidotic conditions and this will misrepresent their LV function

o Cardiac CT (coronary artery calcium scoring [CACS])

 Types:
 Electron beam CT (EBCT) – more commonly used
 Multidetector CT (MDCT)

 Indications:
 Screening asymptomatic w/ one or more cardiac risk factors
 Screening with Framingham risk over 10yr @ 10-20%
 Strong FH of pre-mature CAD

 How:
 Scan for atherosclerotic plaque calcium
 Amount of calcium mathematically converted to “calcium score”
 Known correlation between calcium + risk of future ischaemic events
 Add in contrast  visualise lumen of coronary arteries

 Benefits: High negative predictive value for IHD (esp if contrast also used)

 Disadvantages: No functional capacity information, radiation

o Myocardial Perfusion Scan (MPI)
 How:
 Technitium-99m (99mTc) binds to ligand methoxyisobutyl isonitrile (MIBI)
 Radiotraced compound localises to viable myocardium
 Single Photon Emission CT (SPECT) used to assess radiotracer distribution
 Two sets of images  Rest + stress (w/ exercise OR
adenosine/dipyridamole)

 Interpretation:
 Non-viability on STRESS images, but same area viable on REST images =
likely succeed w/ PCI at recovering function and reducing symptoms

 Indications: Medium risk in angina, but ?why this over e.g. echo

 Notes: Shows very similar information to echocardiography for the most part, but
has some further specific information (as does Echo)

o Cardiac MRI (CMR)

 Indications: GOLD standard for providing structural images of heart
 Congenital heart disease
 LV + RV mass
 Assessing cardiomyopathy (differentiating between different types)

 How:
 MR images provide structure AND functional assessment
 Add in Gadolinium  Some information on myocardial perfusion
o Not in CKD 4/5 – risk of nephrogenic sclerosing fibrosis w/ eGFR
<30

 Benefits:
 Defines anatomy
 Can visualise wall motion
 With contrast, can visualise infarcted areas

 Drawbacks:
 Lack of resources and training precludes the use of CMR
 Does not tell too much about CAD (CT + MPI + angiography better)
 Angiography/Percutaneous Coronary Intervention
o Use: For stent insertion (balloon angioplasty is NOT performed alone anymore)

o Following stent insertion:

 Smooth muscle cells + fibroblasts adhere to stent
 Encase stent in due time
 Until stent is encased, there is a risk of stent thrombosis of stent
 When stent is encased, there is a risk of restenosis within stent

o Complications of Stents:
 Stent thrombosis
 1-2% (biggest risk = ↓compliance with anti-platelet Rx, esp clopidogrel),
poor prognosis
 First month biggest risk, but any time in first 12mo (esp if stops
clopidogrel)
 Presents like acute MI (rapid onset; will not be relieved by GTN)
 Higher risk in drug-eluting stent (due to slow endothelialisation)
 Rx: GP 2b/3a inhibitor + immediate PCI
o GP 2b/3a reduces morbidity and mortality if used pre-PCI in stent
thrombosis (PasTest)

 Restenosis
 15%, good prognosis
 First 6mo (due to excessive tissue proliferation around stent), but can
occur at any point in lifetime; Also has high risk thrombosis in first month
(just like DES – but after 1mo BMS is lower risk and DES still high risk to
12mo)
 Presents like recurrence of angina (slow onset; exertional; may be relieved
by GTN)
 Higher risk in bare metal stent
 Rx: Angina medications + angiogram (+/- angioplasty)

o Types of stents:
 Bare metal stent (BMS)
 Drug-eluting stent (DES)
 Coated with paclitaxel OR sirolimus (AKA rapamycin; inhibit local tissue
growth)
 Reduces re-stenosis rates
 Increases stent thrombosis rates as slower rate of stent endothelisation
hence why clopidogrel so important

o Which stent?: Cardiology opinion – must consider risks of anticoagulation, adherence to

therapy, etc.
o General complications:
 Cholesterol embolization
 Mechanism:
o Introduction of catheter breaks off atherosclerotic plaques in
femoral/iliac arteries or abdominal aorta
o Cholesterol embolises to feet
o Purpuric rash ensues in feet/levido reticularis OR renal artery
embolization
o Eosinophilia on bloods

 Notes: More common in arteriopaths

 Site-related complications (occur in 1%)

 Haematoma
 Pseudo-aneurysm (femoral)
 Retroperitoneal haemorrhage
o Fx: Lower abdo pain, flank pain, shock
o Ix: Contrast CT
o Rx: Conservative (fluids)
o Notes: Can be life threatening
Coronary anatomy

 Left main stem

o Left Anterior Descending (LAD)
 Septal branches
 Diagonal branches
o Left Circumflex
 Left marginal
 Right main stem
o Right marginal
o Posterior descending (determines dominance)

 Variations:
o 4% of people have third main stem – posterior coronary artery
o Artery dominance:
 The artery which supplies the posterior descending artery is dominant
 70% right dominant (supplied by right coronary artery)
 20% co-dominant (both RCA + circumflex)
 10% left dominant (supplied by circumflex)

 Territories of supply + dysfunction:

o Left main stem:
 LAD:
 Course: Behind pulm artery, down interventricular sulcus to apex
 Supply: Interventric septum, apex, 50% of LV (more than any other artery)
 ECG:
o Anterior + Septal (V1-V4)
o Sometimes lateral (LAD or circ; 1, aVL, V4-V6)
 LCX:
 Supply: 30% of LV, anterolateral papillary muscles, SA node (40%)
 ECG: Lateral changes (1, aVL, V5-V6)
o Right main stem:
 Right Marginal:
 Supply: Right ventricle
 ECG: Inferior or Posterior infarct
 Posterior Descending:
 Course: Posterior interventricular sulcus to apex where meets LAD
 Supply: Posterior intervent septum (33% of septum) + 20% of LV (posterior)
 ECG: Inferior or Posterior infarct

 NB: RCA supplies SA node (60%; also LCX) and AV node (90%; minimally supplied
also by LCX)
Cardiac Action Potential
Common Drugs Used in Cardiology

 ACE-I
o Monitoring  U+E (prior to Rx, within 2wk of initiation, after increasing dose [as ACE-I gets
titrated up], at least annually)
o S/E  Cough, AKI, hyperkalaemia, angioedema (can even be MANY YEARS after initiation!)
 Stop if K+ >6
 If K+ still >6 post-stopping, advise low K+ diet

 B-Blockers
o Selective  Bisoprolol, atenolol, Metoprolol (shorter acting, good for rate control in lung
disease where may want to ensure patient does not have SOB related to B-blockade
bronchoconstriction)

o Non-selective  Propranalol, carvedilol + labetalol (b-blocker and a-blocker), timolol

 Carvedilol used for CCF when 1st line beta-blockers not tolerated

o S/E  Bronchospasm, fatigue

o Overdose  Rx: First = Atropine; Second = Glucagon (activates adenyl cyclase promoting
formation of cyclic AMP [from cyclic ATP], which causes direct stimulation to heart), also by
increasing BMs (but less imp)

 CCBs
o Non-rate controlling (dihydropyridines)
 Ideal for >55 w/ systolic HTN
 Especially good in angina and PVD
 Poor in CCF due to fluid retention (except amlodipine is okay in CCF)
o Rate controlling (non-dihydropyridines)
 Types:
 Verapamil
 Diltiazem
 How they work:
 SA + AV node rely mainly on slow calcium channels for depolarisation
 Ca channel blockade = even slower depolarisation = reduced HR
 I.e. reduce frequency of impulse (whereas e.g. flecainide slows Na channels
used for conduction, so flecainide slows velocity of impulse)

o S/E  Headache, flushing, ankle oedema

 Diuretics
o Furosemide  For fluid off-loading
 Can cause ototoxicity if given in high doses (e.g. >2 GRAMS/day)

o Thiazides (e.g. HCTZ)  Previously used for HTN, but now thiaz-like preferred (indapamide +
chlorthalidone; still later options)
 S/E  Gout, impaired glu tol, hypokalaemia, hyponatraemia, hypercalcaemia
 Hypokalaemia caused by:
o 1) Increased sodium in tubules makes the Na/K exchangers more
active (resorb Na, excrete K)
o 2) Increased flow in distal tubule + collecting duct = K+ washes
away
 Spironolactone
o Use: CCF, cirrhosis (large doses), hyperaldosteronaemia (i.e. Conn’s), HTN (4 th line)
o Mechanism: Aldosterone antagonist acting at the DCT (and partly CDs)
o S/E: HyperK, gynaecomastia
o Notes: RALES trial  NYHA 3+4 and already on ACE-I would benefit from low dose spiro

 Digoxin**
o How does it work:
 Blocks Na/K ATPase (by preventing hydrolysis of the ATP)
 The increased intracellular sodium consequently causes ↑intracellular calcium (by
way of the Na/Ca exchange)  Positively inotropic
 AV blockage  Negatively chronotropic

o Indications: AF (1st if CCF present), CCF (late, but 1st line if also has AF), SVT (children)

o How to load (rapid digitalisation): Load within 24hr

 500mcg PO, then
 500mcg PO 8hr later, then
 250mcg PO 8hr later, then
 Maintenance dose (often 62.5mcg or 125mcg to start, depending on age/U+E/size)

o S/E: N+V, Gynaecomastia (with long-term use)

o Toxicity: Progressive between the levels of 1.5-3 (normal = 0.5-2)

 Symptoms  N+V+D, blurry green/yellow vision (xanthopsia), cardiac dysrhythmia
 Risk for toxicity  High dose, high age, hypokalaemia/magnasaemia, AKI/CKD (dig
retention)
 Rx
 Stop digoxin
 ECG + Cardiac monitor
o Bradycardia (AV block)
 Can cause ANY arrhythmia inc CHB + VF except CANNOT
cause 2nd deg HB Mobitz II
o Prolonged PR
o Down sloping ST depression [reverse tick]
o Flat T-waves
o Short QT
 Reduce absorption (ONLY if caused by taking too many pills, e.g. not in AKI)
o <4hr = lavage
o >4hr = cholestyramine
 Treat any arrhythmias
o Brady – atropine, temp pacing
o Tachy – amiodarone
 Digibind  Indication: Haemodynamic instability, resistant VT/VF
o Only once levels are back and found to be high
o Levels are taken 6hr post-dose (normal = 1-2.6)
 Dialysis

 Check electrolytes at earliest possible opportunity and correct K/Mg

 Doxazosin
o Mechanism: Alpha-1 adrenoreceptor antagonist
o Use: When concomitant BPH, or resistant HTN
o Notes: Other alpha blockers
 Alpha-1a antagonist = tamsulosin (urogenital specific)
 Non-selective = phenoxybenzamine (used in pheo)

 Amiodarone
o Indications: Atrial, nodal or ventricular tachycardias

o Mechanism: Block K+ channels (long half-life – 20-100d)

 Increase refractory period by inhibiting repolarisation
 Action potential is therefore longer
 HR slowed

o SEs: Hepatitis, pulm fibrosis, skin discolouration in sun (“slate grey appearance”), thyroid,
peripheral neuropathy, bradycardia, thrombophlebitis, corneal deposits, LQTS (anything that
blocks K+ channels will do this)

 Amiodarone-induced hypothyroidism (AIH):

 Mechanism: High iodine causing Wolff-Chaikoff effect
o Autoregulatory phenomenon where thyroxine production is shut
off due to high circulating levels of iodine
 Rx: CONTINUE amiodarone if needed + Rx with thyroxine

 Amiodarone-induced thyrotoxicosis (AIT):

 Mechanism: Jod-Basedow Phenomenon (too much iodine = high T3/T4
production)
 Rx: STOP amiodarone, and…

o Monitoring:
 Monitor TFT, LFT, U+E, CXR prior to Rx
 Check U+E prior as ?hypokalaemia (if present, increased risk arrhythmia)
 Monitor TFT + LFT 6-monthly

o Notes:
 Do NOT give with TCAs (risk of long QT, VT, VF, TdP); half the dose of digoxin (as
both affect K+)
 Long half-life (up to 3mo) hence need for carbimazole in AIT type 1, also drugs can
interact even up to 3mo after stopping amiodarone!
 Give in central vein (otherwise risk of thrombophlebitis)

 Sotalol (class III anti-arrhyth – NB: B-blockers are class II; this is class III along with K+ recept blockers)
o Increase refractory period hence slowing heart rate (like amiodarone as same mechanism)
o Used in AF when standard beta-blockers not effective
o The only anti-arrhythmic (perhaps also amiodarone) which may cause LQTS + TdP
 Flecainide
o Blocks sodium channels so slows conduction velocity
o Indications  AF (rhythm control), SVT w/ accessory pathway (e.g. WPW)
 Do NOT use flecainide in WPW if there is any doubt of ?WPW ?VT (also do NOT use
any AV node blocking drugs esp verapamil)
o S/Es  Neg inotropy, neg chronotropy (bradycardia), proarrhythmic, oral paraesthesia,
visual disturbances
o CI  Post MI, structural heart defects

 Aspirin  Blocks thromboxane production (prevents platelet aggregation)

 Clopidogrel  Blocks platelet ADP receptors (P2Y12 ADP receptor) – inactivates platelets
o Use: MI, Stroke, TIA (RCP favours this over A+D), PVD (1 st line now)
o Other similar drugs: Prasugrel, ticagrelor, ticlopidine
o Interactions: PPI (omeprazole, but lansoprazole is OKAY)

 Abciximab, Tirofiban  Blocks glycoprotein IIb/IIIa

o This is the common pathway for both thromboxane and ADP
o Therefore, this is the most potent/effective antiplatelet agent
o Indication: NSTEMI with 6mo GRACE >3% w/ PCI planned soon but patient cannot have it
immediately e.g. needs transfer (i.e. any delay)

 Adenosine
o Use: SVTs (if asthma, use IV verapamil)
o Dose: 6mg, 12mg, 12mg
o Mechanism: Transient AV node block via A1 receptor agonism (leads to hyperpolarisation by
creating outward potassium flux); but has short half life (8-10s)
o S/E: Chest pain (+feeling impending doom), bronchospasm, worsens WPW + access pathways
o Interactions: Dipyridamole enhances effect (inhibits the uptake of adenosine into platelets,
hence increasing extracellular concentration; caused prolonged arrest of rhythm!),
aminophylline reduces effect (will have minimal effect at AV node)

 Nicorandil
o Mechanism: Nitrate + potassium channel activator

 Ivabradine
o Effect: Reduce HR
o Use: Angina (once BB/CCB failed)
o Mechanism: If (funny current) inhibition
 Funny current seen in SA + AV nodes
 They help regulate the cardiac pacemaker activity
o S/E: Visual symptoms (e.g. luminuous phenomenon), bradycardia
 Cholesterol lowering drugs
Physiology
o Cholesterol
 Production: Made from steroids + fat in complex process starting w/ HMG-CoA Redu
 Aim (total cholesterol): <5mmol/L (only have targets in SECONDARY prevention)
 Average in UK: 5.9mmol/L (80% >50 = higher than 5)
 Target when on therapy: TChol <4mmol/L, LDL <2mmol/L
o Triglycerides
 Production: Ester + 3 fatty acids (both attained from e.g. oil + all sources of fat)
 Transport: From intestine to liver + muscle + adipose tissue via chylomicrons
 >6 = Risk of pancreatitis, retinal vein thrombosis
 >10 = Use fibrates ONLY if isolated (i.e. no hypercholesterolaemia, otherwise statin)
o Lipoproteins (transferring cholesterol and triglycerides in blood)
 HDL  Collect cholesterol from body tissues + return to liver (“good cholesterol”)
 LDL  Carry cholesterol from liver to cells of body (“bad cholesterol”)
 IDL  Between LDL and VLDL, not detectable in blood
 VLDL  Carry newly synthesised cholest + triglycerides from liver to adipose tissues
 Chylomicrons  Carry triglycerides from intestines to liver + muscle + adipose tissue

o Hyperlipoproteinaemias (e.g. Familial Hypercholesterolaemia – use Simon Broome Criteria)

 Type 1  Increased chylomicrons (eruptive skin xanthomas, pancreatitis)

 Type 2  Increased LDL + VLDL (xanthelasma, tendon xanthomas, corneal arcus)

 Type 2A = LDL only  Familial hypercholesterolaemia (auto dom)
o FH of early MI’s
 Type 2B = LDL + VLDL  Familial combined hyperlipidaemia

 Type 3 (Remnant)  Increased IDL (tubo-eruptive xanthomas, palmar xanthomas)

 Type 4  Increased VLDL AKA familial hypertriglyceridaemia (pancreatitis)

 Type 5  Increased VLDL and chylomicrons

NB: Pts will be heterozygotes; homozygote is rare and usually die of MIs in teens
 Statins
o Mechanism  Reduce hepatic cholesterol synthesis by blocking HMG-CoA reductase =
increased uptake of LDL from blood to the liver = less delivery of cholesterol to body cells =
less atheroma

 HMG CoA  Formed from acetyl CoA + acetoacetyl CoA; converted to mevalonate
by HMG-CoA reductase (target for statins)

o Indication (NICE Guidelines)

 History of cardiovascular disease (e.g. CAD, angina, stroke, TIA, PVD)
 >75 + any cardiovascular risk factors (esp smoking + HTN)
 Age 40-74 with 10yr CVD risk = 10% (using QRISK2 – advocated by NICE)
 Lipid disorders (e.g. familial hypercholesterolaemia) – start with MAX dose statin
 Diabetes + one additional risk factor (e.g. HTN, obesity, high-risk lipid profile, FH)
 High risk lipid profile  TChol >4, LDL >2, or Triglyc >4.5 (Clin Know Sum)

 TChol:HDL >6

o Initiation
 First  Simvastatin 40mg OD (20mg if increased risk myopathy) OR start with
Atorvastatin immediately (NICE 2014 Lipid Modification Guidelines)
 TChol >4 or LDL >2 despite Simva 40  Simva 80mg
o MHRA risk myopathy with Simva 80mg
 Failure of Simva 80mg  Atorva +/- ezetimibe
 Intolerant  Pravastatin 40mg OD
*Take at night as they have slightly greater effect then as most cholesterol synthesis
occurs at night

o Side-effects  Muscle, liver

 Myopathies  Measure CK (norm = 60-175)
 Normal CK + Muscle pain  Myalgia (continue statin)
 <10x upper limit of normal  Myositis (continue statin if tolerated)
 >10x upper limit of normal  Rhabdomyolysis (STOP statin)
NB: More common with lipophilic statins (simva + atorva) than hydrophilic
statins (rosuva, prava)

 Hepatitis  Discont if LFTs 3x ↑norm range, otherwise continue + rpt LFT in 1mo

o Monitoring  LFTs (at baseline, 3mo, 12mo)

o Targets

o Contraindications  STOP when starting a course of macrolides (erythro/clarithro) –

increased risk of myopathy + rhabdomyolysis
Ezetemibe  Indications = Statins CI’d, Statin therapy failure w/ MAXIMAL dose (TChol/LDL
still too high); Mechanism = reduce cholesterol absorption in small intestine; Efficacy =
Reduce LDL by ¬20%, triglyc by 5%, and increase HDL by 5% 

Fibrates (e.g. Fenofibrate)  Isolated severe hypertriglyceridaemia (TGs >10) WIHTOUT

hypercholesterolaemia (otherwise statin is still first choice), e.g. Type 4
hyperlipoproteinaemia – familial hypertriglyc; Mechanism = PPAR-alpha agonist (increases
lipoprotein lipase) – NB: glitazones are PPAR-gamma agonist

Nicotinic Acid  Best for raising HDL (use when statin working but HDL still too low); limited
by its side effects (flushing, impaired glucose tolerance, myositis) so often not used

Orlistat  Block pancreatic + gastric lipase (causes lack of fat digestion) – may cause steat
(can get OTC)
Indications  BMI >28 + risk factors CVD, BMI >30 alone, Wt loss on Rx 5% at 3mo,
use for <1yr
JVP

 Definition: Indirect measure of central venous pressure (CVP) using the internal jugular vein (IJV)

 Waveforms:
o A  Pre-systolic; Produced by right atrial contraction
o C  Early systole; Closure of tricuspid valve (not normally visible)
o X Descent  Atrial relaxation (occurs whilst ventricles contraction)
 Atria opens so negative pressure sucks blood in causing descent of JVP
o V  Late systole; Increased blood in right atrium from venous return
o Y Descent  Opening of tricuspid valve
 Blood exits atrium into ventricle allowing JVP blood to descend and fill atrium

 Diseases:
o A Wave
 Absent A waves  AF
 Large A waves  Tricuspid stenosis (RA contraction against a partially closed valve)
 Cannon A waves  CHB + VT (RA contraction against a fully closed valve, occur randomly)

o Prominent/Giant V Waves  TR

o Slow Y Descent  Tricuspid stenosis (blood exits RA slower, so blood from

JVP can only enter RA slower), RA myxoma

o Absent Y-descent  Cardiac tamponade

o Steep/Rapid Y Descent  Constrictive pericarditis, TR

 Notes:
o The double waveform seen is a result of the A + V waves
 A occurs before pulse
 V occurs toward end of pulse

o Distinguishing the C wave, X descent and Y descent is nearly impossible

Pulmonary Capillary Wedge Pressure (PCWP)

 Definition: Indirect estimate of LA pressure to determine if heart is being adequately filled with blood

 Method:
o Swan-Ganz catheter (two ports, one balloon)
o Insert into peripheral vein
o Advance catheter to RA  RV  Pulm art  Branch of pulm art
o Pressure tranducers record pressures in:
 Branch of pulm art (distal port)  ~25/10mmHg
 RA (proximal port)  ~0-3mmHg
o Balloon is then inflated to STOP pulmonary flow, and after few seconds atrial backflow
(which has the same pressure as the LA) reaches the distal port (ahead of the balloon) and
that pressure can be recorded to identify LA pressure  ~8-10mmHg
 This LA pressure = PCWP
 It will have arterial saturations
 It should be close to the same pressure as the LV diastolic pressure

 Uses:
o Severity of (all give ↑LA pressure and therefore ↑PCWP)
 LVH
 AS, AR, MS. MR
*Normal = 8-10mmHg
*Can guide the use of therapy e.g. nitrates, frusemide; more fluids

o Fluid status in shock

 Normal PCWP 8-10mmHg
 In shock, likely to be lower than 8-10mmHg
 In shock, aim for 12-14mmHg
 Give fluids until target PCWP of 12-14mmHg reached
 NB: When >20mmHg (mostly due to CCF), pulmonary oedema likely

o Oxygenation of various cardiac areas

 SVC should always have lower sats than IVC (due to high brain use of oxygen)
 PCWP should have arterial saturations

Cardiac Index (CI)

 Background: Cardiac output is not the same for all individuals, it is based on body size

 Formula: CI = (SV x HR) / BSA (Body surface area)

o Normal = 2.6-4.2 L/min/m2
o If <1.8, cardiogenic shock likely
Ischemic Heart Disease/Coronary Artery Disease***

 Cause: Atherosclerosis (most common)

 Pathogenesis of MI:
o Atherosclerosis breaks off to expose inside of plaque
o Platelets adhere to exposed plaque and block artery
o Platelets stabilised by fibrin (made from fibrinogen)
 Fibrin lysed by plasmin (made from plaminogen which is activated by Tissue
plasminogen activator [TPA]) unless F13 (clot stabilising factor) acts on clot
 Fibrin = Creator (Brahma); Plasmin = Destroyer (Shiva); F13 = Preserver (Vishnu)
o Drugs used:
 Aspirin + Clopidogrel  Prevents further aggregation of platelets (pre-fibrin)
 TPA  Breaks the fibrin meshwork to bust clot (pre-factor 13)
 Angioplasty  Compresses clot (post-factor 13)

 Risk Factors for IHD/CAD:

o Modifiable:
 Cholesterol  Most important
 Smoking  Quickest effect (↑HDL primarily, ↓vascular effects)
 HTN  Most common risk factor
 Diabetes
 If present, BP and cholesterol must be lower than normal recommended
 (Diet and Exercise)  ↑HDL primarily
 Obesity independently associated with mortality (i.e. even if not causing
HTN, diabetes, cholesterol, etc)
 For every kilotgram lost, 1mmHg lost
o Non-Modifiable:
 FH (esp if premature – men <50, women <60)
 Age (>65)
 Sex (male)
 Ethnicity (S Asian)
  Stable Angina** (chronic coronary syndrome/chronic ischemic heart disease)
o Definition: Coronary pain reproduced by predictable factors, usually exercise
o Risk: Cardiac risk, AS, HOCM

o Features: Exertional chest pain relieved by rest/GTN in ~5min

 If new, worse, rest, not relieved by GTN  UNSTABLE/Treat as ACS

o Diagnose:
 First:
 ECG (normal, unless in episode... ?q-waves, ?LBBB, ?LVH, ?ST depression)
 Bloods (cardiac risk, anaemia, TFTs, troponins)

*If ECG is normal (without ischaemic/infarction changes) and Troponin normal,

patient can almost always be sent home and Ix/Rx’d as OP*

 Second: Calculate Framingham risk

 If minimal risk (<10%), no investigation needed

 If low risk (10-30%), do CT calcium scoring (see above)

 If intermed risk (30-60%; or successfully tPA’d MI), do functional imaging

o Nuclear stress (exercise) imaging (sestamibi  imaged agent)
 ↓uptake in ischemic or infarcted tissues
 At rest ischemic tissue picks up sestamibi (not infarcted)
 Ischemic tissue can be reperfused (bypass or stent), not
infarcted tissue

o Stress (exercise) echo

 ↓wall motion

o Cardiac MRI

o NB: If unable to exercise, dobutamine stimulation (then apply NSI/SE)

o ?How do you pick between these

 If high risk (60-90%)  Angiography (also get angiography if medical failure)

 If very high risk (>90%)  Assume CAD present + consider intervention

*NB: Note exercise ECG is NEVER used anymore for investigating new chest pain (NICE guidelines)
o Treat: ALL PATIENTS GET “CARDIAC REHAB”
o Medical: Prior to angiography (in many cases)
 Acute chest pain: GTN x3 doses spaced 5min apart – after 3x/15min seek help
 Chronic disease management:
 Risk factor modification: Aspirin, Statins, ACE-I (if diabetic)
 NB: ACE-I provide benefit in ANY coronary artery disease, irrespective of LVH,
beyond just BP control (HOPE study)
 NB: Aspirin is the single most important intervention for stable angina

FOR ANGINA
 First line: B-blocker/atenolol 50mg OD (most important) + GTN (PRN)
o If B-blocker CI’d: Rate limiting CCB (e.g. dilt/verap monoRx)
 Second – refractory to low-dose BB: Increase BB/atenolol 100mg OD
 Third – refractory to high-dose BB: Add CCB (e.g. nifedipine MR)
 Fourth – if still refractory: Add one of the following (sometimes 2)
o Long-acting nitrate (e.g. ISMN + ISDN)
 Tolerance builds easily, may need to take more regularly if
this occurs (i.e. instead of 12 hours apart, take two doses 8hr
apart) – not seen in ISMN MR, just the non-MR version
o Ivabradine (Funny current inhibitor in sinoatrial node)
o Nicorandil (coronary artery dilation via NO + K+ ATP agonism)
o Ranolazine (reduced myocardial ischemia)
 o Definitive: Angiography (if medical failure [refractory to CCB stage], stress test pos [e.g. 30-60%
risk w/ MPS/Echo] OR high risk CAD [60-90% Framingham risk])
Aim  Reduce angina (NOT to reduce mortality or future MI)

 1-2 vessels w/ 70%+ stenosis (no diabetes if 2): Angioplasty (stent)

 Complication: Re-stenosis/Thrombosis (put on clopidogrel to lower risk)

 ≥3 vessel OR 2 vessel+diabetes OR Left main (>50% stenonsis) OR Need other cardiac

surgery also e.g. valve surgery: CABG
 LAD occlusion  Left Internal Mammary Artery (LIMA)
o LAD is hugely important artery (supplies anterior wall, ventricular
septum, apex)
o LIMA has 90% patency by 10yr, vein grafts have 50%
 LIMA avoids intimal hyperplasia and atheroma formation
more so than veins (e.g. saphenous)
o In-situ LIMA (still attached to subclavian) has better patency than free
graft (whole vessel removed and attached)
 Cut distal portion of LIMA
 Connect to LAD post-blockage
o ?Why ever use a vein

 Complications:
o Neurology (due to CardioPulm bypass)
o Cardiac tamponade
 Features: As per tamponade
 Ix: TOE
 Pericardial effusions may be loculated to posterior
aspect of heart, therefore TTE cannot reliably
exclude diagnosis as only TOE can see posteriorly
 Rx: As per tamponade
o Haemolysis (sheer stress due to bypass system)
 Features: As per anaemia
 Ix: Raised unconj bilirubin, NORMAL other LFTs,
schistocytes
 NB: Right heart failure gives you only direct
hyperbili and raised ALP

o Notes:
 Exercise stress test w/ ECG:
 Should not be done on b-blockers as cannot reach target heart rate
 Should not be done on digoxin as normally causes ↓-sloping ST segment
 A down or horizontal sloping ST segment is WORSE than an up-sloping ST
segment
 ST elevation or depression should be measured 80ms AFTER the J-point, as
tachycardia induced J-point depression and this is NORMAL
o E.g. young man with strong FHx, exercise test, ECG shows 1-2mm
J-point depression at 120bpm – NORMAL test.
 Considerations for stenting:
 Distal vessels must be adequate
 LV EF% must be intact (or else no improvement will be seen)

ECG EXERCISE TESTING HAS POOR SENSITIVITY AND SPECIFICITY AND NUMEROUS LIMITATIONS... CENTRES
NOW ARE PREFERRING TO DO CT Ca  SPECT/Echo/MRI  Angiography
Acute Coronary Syndrome (ACS)***

 Classification: SPECTRUM (one can progress to next)

o Unstable angina  New, Worse, Rest

o NSTEMI: Clot not fully occluding artery

o STEMI: Full occlusion of artery

 Symptoms of ALL: Substernal chest pain (enough to consider ACS) for >15min anytime in last 9hr
o See first section (above) for further symptoms + signs

 Signs:
o S3 or S4
o Pan-systolic murmur (new)
 MR  Posterior MI causing chordae rupture
 VSD  LAD MI causing septal infarct
o N+V+Sweating+Bradycardia  Inferior MI causing vagal stimulation/CHB

 Risk factors for poor prognosis, and necessity for angiography/angioplasty:

o UA w/:
 Hemodynamic instability (CP, SOB, HypoTN, confusion)
 Prolonged (>10min) chest pain, Syncope
 Persistent ECG changes, VTach
 ↑Trop, ↓Ejection fraction
 Diabetes, CKD (trops accumulate), Prior PCI or CABG

o NSTEMI with GRACE 6mo mortality of >3%

o All STEMIs
 Diagnose: ABCDE + ECG + O2 (if <95%) + Fluid... then begin Rx (as below)
o First: ECG (NB: Arrival-to-ECG time = 10min)
 UA + NSTEMI:
 ST depression >1mm
 T wave inversion >2mm in 2 adjacent leads
 Normal ECG
 STEMI  ≥1mm in 2 adjacent limb leads (2mm in chest leads)

 Notes
 Pure lateral infarcts often only affect the limb/augmented leads (I, aVL,
sometimes also II); likely anterolateral if any of V4-6 affected

o Second: Troponin T/I (UA from others)  If ST-elevation, troponin does not guide initial Mx
 Detectable at 3-6hr (take on admission and at 12hr post-onset)
 Peak 12-24hr (6-12hr with hsTrop)
 Remain raised up to 10-14d
 Since can be artificially raised, if this is thought then you should TREND the troponin
and expect to see a rise and drop (indicated acute rise of trop e.g. MI)
 Released most often in response to ISCHAEMIA, but INFARCTION will raise it highest
 Troponin CAN be elevated in 30% of UNSTABLE ANGINA (poorer prognosis, this is
basically NSTEMI though)
 Troponin levels are PROGNOSTIC – higher = worse prognosis = higher chance death

 If second attack 5d later, CK-MB useful as it normalises post-MI in 3-4d (hence if

raised indicates infarction but troponin less useful as will be up anyway)

o Other  Full bloods inc random glucose, random lipids, CXR, Echo, Angiography ± stenting

Unstable Angina NSTEMI STEMI

ECG - - +
Troponins - + +

TO DIAGNOSE STEMI, NEED 2/3 (Cardiac Chest Pain, ECG findings, Troponin rise) [WHO Guidelines]
 BEFORE STARTING TREATMENT IN UA/NSTEMI, ASSESS RISK: GRACE score (NICE recom)
o Factors assessed  Age, HR, SBP, Degree of CCF (if any), Creat, Arrest on admission?, ST
changes?, Trop raised?

o Interpretation
 Depends on whether STE or NSTE
 Predicts in-hospital mortality AND post-discharge mortality
 NSTEMI 6mo mortality of 3% = high risk = needs angiography in <96hr

o NB: WHO Criteria for MI (NSTEMI or STEMI) is 2 of the following 3:

 Ischaemic like chest pain (both will have)
 Evolutionary ECG changes (ST elevation = STEMI; depression = NSTEMI)
 Rise and fall in cardiac markers (only needed no signs of MI on ECG but cardiac chest
pain present)
 Hence  STEMI never needs troponins (unless ?silent MI therefore no
cardiac chest pain)
 Treat: Telemetry needed (not just a cardiac monitor) – death in 72hr is ventric arrhythmias
o Unstable Angina + NSTEMI:
 Immediate – all patients:
 Oxygen (ALL patients in first 2hr, and only after if Sats <90-94%)

 Nitrates (50mg in 50mL IV @ 1-12mg/hr  Reduces SOB/Pulm edema/Low sats)

o BP must be >90 systolic
o Titrate dosage up according to BP (start 1mg/hr, titrate up as tolerated)
o Use with caution in posterior infarction
o Has NO effect on long-term mortality

 Morphine (Diamorphine 2.5-5mg IV) + Metoclopramide 10mg IV over 2min

 Aspirin 300mg
o Start whilst history being taken! Do NOT wait for ECG
o Followed by 75mg Aspirin maintenance dose (continue lifelong)
o Do NOT use if aspirin allergy, use clopidogrel alone; beware of dissection

 Clopidogrel 300mg not for angio [UA, some NSTEMI], 600mg for angio [STEMI,
some NSTEMI] (cont 12mo in ALL patients with DES; 1mo BMS; stop before major
surgery but contact cardiologist first [risk stent thrombosis])
o Followed by 75mg Clopidogrel maintenance dose (continue for 12mo)
o NB: PPIs, particularly omeprazole, interact with clopidogrel
 Stop and replace with PO Ranitidine 300mg BD (e.g. if GORD)
 Use lansoprazole if treating gastric ulcer
o Relevant trials  CLARITY (proved 300mg effective), COMMIT (proved
75mg also effective, but less so than 300mg)
o May be soon replaced by Ticagrelor

 Heparin
o If no thrombolysis planned <24hr  LMWH (Fondaparinux 2.5mg OD
x8d)
 Not if eGFR <20 or creat >265
 If Trop neg at 12hr + pain free + no ECG changes  STOP
 NB: Enoxaparin also improves morbidity + mortality
o If thrombolysis likely in 24hr:
 UFH (can reverse with PS)
 Abciximab or Eptafibitide (GP 2b/3a inhibs)

 B-blocker – metoprolol 25-50mg TDS (max dose 100mg TDS)

o NOT if shocked/haemodynamically unstable/bradycardic, but ALWAYS
otherwise including in acute stage!
o Use atenolol 50-100mg OD if compliance an issue
o If concomitant LVH, use Bisoprolol 2.5mg OD (titrate up to 10mg OD)

 Sliding Scale (if diabetic T1 or T2 or random BM >11 in non-diabetic)  Keep BMs

<11 (DIGAMI study; DIGAMI2 did not support findings but still common practice)
o Measure ALL MIs (even NSTEMI but NOT UA) BMs
o If known diabetic  Sliding scale as per DKA protocol
o If not known diabetic but BG >11  Sliding scale as per DKA protocol

 Statin (can be started in acute stage)

 Possible further Rx if B-Blockers not tolerated: 1) Long-acting CCBs (Diltiazem MR

90mg BD [not usually in conjunction with b-blocker but can be done] or Amlodipine
5-10mg OD), 2) Oral nitrates (after IV nitrate finished; ISMN slow release 30-60mg
OM), 3) K+ channel activator (nicorandil 10mg BD, titrate to max 30mg BD if
necessary)
o Consider ITU if consistently hypotensive for inotropic support (?MI
induced CCF)
o If hypotensive, can consider intra-aortic balloon pump to increase
perfusion pressure
NB: Differences between cardiac monitoring and telemetry
Telemetry can be radio-signalled to central nurse station to view + be alerted to dangerous rhythms
Telemetry can be recorded

 If low risk – chronic management can start soon:

 Aspirin

 Clopidogrel (12mo)  All patients (used to be if GRACE >1.5%)

o 12mo irrespective of stents/STEMI/NSTEMI
o Clopidogrel monotherapy used if aspirin not tolerated
o Warfarin monotherapy used if both asp/clopid not tolerated

 B-Blocker (MUST be carvedilol OR bisoprolol for long-term)

o Write in TTO how to titrate up bisoprolol for GP (from 2.5 to 10mg as
tolerated)
o In COPD + asthma, still use low dose bisoprolol and titrate up slowly
(observational study [Quinit et al BMJ 2013] showed significant benefit
despite potential bronchoconstriction; perhaps weight up with how many
exacerbations + how severe [e.g. was ITU needed?])

 ACE-I (Ramipril 2.5mg titrated up to 10mg OD as tolerated)

 Simvastatin 40mg OD (all patients irrespective of LDL/Cholesterol!)

o Aim total cholesterol <4, LDL <2
o If ineffective, up to 80mg, then consider adding ezetimibe
o If intolerant, either lower dose or use atorvastatin or pravastatin
o This can/should ideally be started in ACUTE stage also

 Omega-3-acid ethyl esters (Omacor)  All post-MI patients who do NOT eat 2-4
portions of oily fish/wk
o Reduce risk of ventricular arrhythmias, especially after anterior MI

 Lifestyle modification, cardiac rehab, nitrates

 (Eplenerone – if CCF post-MI; start within 3-14d post-MI ideally after ACE-I started,
?convert to spiro after 14d post-MI)
 (No driving for 4 weeks post-MI)

 If intermediate/high risk (GRACE Score >3% 6mo mortality) OR ongoing chest pain: If in DGH
call primary centre as per STEMI protocol

 First: GP 2b/3a inhibitors (eptifibatide, tirofiban, abciximab)

o Give to ALL NSTEMI due to undergo angiography in next 96hr w/ GRACE
6mo mort >3% (unless bleeding risk e.g. recent surgery)
o ↓risk of vascular re-occlusion when angioplasty done
o Do NOT need to give if you are in PCI centre and patient will
IMMEDIATLEY be going up for angiogram/angioplasty (if there is ANY
delay e.g. even 1hr then give GP 2b/3a)

 <96hr: Angioplasty (NB: if GRACE 6mo <3% then angio can be done after 96hr!)
o NB: Even NSTEMI needs inpatient angiogram (+/- angioplasty) prior to
discharge EVEN if low risk and often within 5d
 STEMI:
o Acute:
 Immediate: Should take aspirin, ADP-receptor blocker (e.g. clopidogrel, prasugrel, ticragelor),
injectable anticoagulant (ideally bivaludin, NOT LMWH), and if being transferred GP 2b/3a
inhibitor (e.g. tirofiban, Abciximab) – ESC guidelines

 Definitive: TPA (not as good) or Angioplasty (better)  But SAME efficacy if <2hr, PCI better
if >2hr despite extra time needed for transport from DGH to PCI centre

 PCI can occur <90min: PCI

o Transfer to local PCI service if not avail @ local hosp
o Call tertiary centre, prep CCU + for PCI/thrombolysis (+fax ECG)
o Call ambulance service for transfer of patient
o Call cardio reg (on call reg if one available, otherwise any)
o Always stent, never just balloon angioplasty  Reduced re-infarction
o Ideally still needs glycoprotein IIb/IIIa inhibitor to prevent vascular
occlusion after PCI (eptifibatide, tirofiban, abciximab)

 PCI cannot occur <90min: tPA = Tenecteplase/Alteplase/Reteplase

o Must be done <12hr onset of CP and ideally <30min from entering door
o If PCI cannot be given in <90min, tPA administered if <12hr
 Reperfusion with tPA in <12hr reduces irreversible ventricular
damage
o Tenecteplase/Alteplate > Streptokinase as they…:
 Fibrin specific (better)
 Does not cause reactions with repeated use
 But streptokinase = lower risk of haemorrhagic stroke
o Tenecteplase = one bolus; Alteplase = one bolus + two IV infusions (AKA
accelerated regimen – standard regimen is INFERIOR to streptokinase
hence not used)
o Also give UFH or LMWH for 2d (but not with Streptokinase)
o Streptokinase CAN be given if CP onset was >4hr and never had
streptokinase before (otherwise CI’d) as:
 1) SK has equal reperfusion efficacy to tPA if CP >4hr ago
 2) Cheaper (80-90 quid/patient vs alteplase 600 quid/pt)
 3) Less risk of haemorrhage

o If TPA’d, must do ECG 90 min later to confirm lowering of ST elevation...

 >50% ST segment resolution, No chest pains,

Haemodynamically stable: Inpatient angiography ± PCI (during
same admission) – Resus UK ALS eLearning

 <50% ST segment resolution, Ongoing or recurrent chest pain,

shock: Rescue PCI (if still within 12hr from onset of chest pain)
 REACT trial
 “Rescue” = failed tPA now needing PCI

o Absolute CI’s: Prior IC hemorrhage, bleeding, suspected dissect,

pregnancy
o Relative contras: Recent surg, recent bleed, severe HTN

*TPA <12hr from onset + <30min from door, PCI <90min from door

 TPA not given: Treat as per UA/NSTEMI (i.e. add LMWH)

 Failed PCI/TPA: Emergency CABG

o Chronic: As per low risk in UA/NSTEMI

 Prognosis: 10% risk of death in next 12mo following an MI, and there is a 5% chance of death for any given
person in each year thereafter (use GRACE score for mortality in 6mo post-discharge)
Ways to get angioplasty
Stable angina with very high Framingham risk
Stable angina with positive exercise test who get angiogram with 1-2 vessel disease (3+ vessel = CABG)
UA/NSTEMI with low risk who then get follow up with exercise test (positive), angiography (2 vessel)
UA/NSTEMI with med-high risk (3% 6mo mortality on GRACE score)
STEMI
 Complications of ACS: DIM PTT

o Dysrhythmia  NB: RCA supplies both SA and AV node! Occur within first 48hr
 Slowing:
 SA node dysfunction  Bradycardia; SSS (RCA 75%, LCX 25%)

 AV node dysfunction  Heart block (inferior MI, RCA)

o 1st degree [PR >200]  No treatment
o 2nd degree  Mobitz 1 – No Rx, Mobitz 2 – Pace
o 3rd degree [disjointed P + QRS, regular P-P + R-R]
 Symptomatic  Isoprenaline then PACE (if hypotensive – give
adrenaline rather than isoprenaline)
 Asymptomatic  Pace, but IN THE CONTEXT OF MI – PCI is
MOST IMPORTANT (but if symptomatic then Rx as per non-MI
3rd degree HB)

o NB: Post-MI, you do NOT perform temporary pacing on asymptomatic +

stable 3rd deg HB due to INFERIOR MI (but MUST pace if ANTERIOR MI)

 Quickening
 Supraventricular tachy’s (Rx: Adenosine – IV Verapamil if asthma)

 Ventricular  V-Tach/V-Fib  See below

o Non-sustained V-tach <48hr post-MI
 Pathology: Due to automaticity
 Rx:
 First: Beta-blockers
 Second: Amiodarone (may suppress arrhythmia, but
does NOT improve long-term survival; useful if get VT
episodes even whilst on B-blocker)
 Other:
o Replace magnesium if low
o NO indication for ICD

o VF is the most common cause of death post-MI

o Rx of Sustained/Cardiac Arrest  Acute = ALS, Chronic = B-blocker, ICD

o Ischemic (use CK-MB to investigate as first line)

 Angina
 Re-infarction (3-5%)
 Infarct extension into new territory
 Stent thrombosis (most likely cause arrhythmia post-48hr [<48hr = peri-infarct arrhythmia])
 2% experience stent thrombosis in first month
 15% experience re-stenosis in first 6mo; 50% experience re-stenosis in the long-run
 o Mechanical/Pump Dysfunction
 CCF (↓wall motion) ± Cardiogenic shock
 Cardiogenic shock <24hr after tPA if <75 (i.e. early complication)
o Ix: PCWP (esp in inferior MI + cardiogen shock)
o Rx: “Rescue angioplasty” if previously tPA’d + IABPump (SHOCK trial) +
inotropes + ITU
 Re-tPA = More bleeding, no mortality benefit (REACT trial)
 NB: Eplenerone effective for post-MI CCF

o NB: Do NOT treat asymptomatic heart failure (i.e. low EF, no symptoms)
except with ACE-I (only one which shows mortality benefit)
 E.g. patient has MI, then echo shows low EF but asymptomatic –
do NOT give frusemide

 Cardiac rupture
 Septal rupture (↑O₂ sats from RA to RV [as RV+LV communicating], pulm oedema)
 Valve rupture (MR in posterior – leads to pulm oedema)

o Pericarditis
 Pericarditis; <48hr post-MI (often after transmural MI – 10% of these patients)
 Dressler Syndrome; 2-12wk after MI  NSAIDs, aspirin, ± steroids
 Can lead to cardiac tamponade

o Psychosocial
 Depression
 ED (1. Psychosocial, 2. B-blocker therapy)

o Thromboembolic (mural thrombus – clot forms in weak heart wall outpocket)  LMWH

Low BP post-MI

 +JVP, +pulm oedema  Acute CCF/LV dysfunction, Acute VSD, Acute MR, tamponade
 +JVP, -pulm oedema  3rd deg AV block (cannon A-waves), Tamponade, PE, RV infarct
 -JVP, -pulm oedema  Bleeding, dehydration
Posterior MI

 Pathology: RCA branches (70%), or sometimes LCX (if left dominant [20%] or co-dominant [10%])
 ECG changes: Look at leads V1-V3... V2 is the most important
o Dominant and slightly wide R waves (also seen in RVH, WPW)
o ST segment depression
o Upright T wave in V2  If inverted ?RVH

 Notes: There is no such thing as a pure posterior MI – you MUST have either an inferior MI with
posterior extension, or lateral MI with posterior extension (depending on which forms the dominant
circulation – the right heart with RCA or left heart with LCX – posterior MI is a distal occlusion of these
vessels)
o The ST elevation seen in a posterior MI e.g. in the inferior leads is truly an inferior STEMI, not
just reciprocal changes
o Reciprocal changes themselves represent ischaemia (even in e.g. anterior MI getting
reciprocal inferior changes) and signify worse MI – reciprocal changes are NOT just an ECG
phenomenon (they signify ischaemia in a different territory)

Features of Different MI’s

 Anterior (LAD)
o LVOT Obstruction
o LV mural thrombus
o LV aneurysm (which may cause persistent anterior ST elevation)
o Ventricular septal rupture
o Pericarditis (Dressler = 2-12wk post-MI)
o Heart block (less common than inferior, but if HB associated with ant MI = much worse as
more extensive area of myocardium damaged; hence MUST pace [inc temporary pacing]
even if asymptomatic + stable)

 Inferior (RCA)
o RV infarction (1/3 of inferior MI = RV infarction = RVHF = ↓pre-load = shock)
o MR (RCA supplies chordae tendinae + papillary muscles)
o Heart block (all degrees; RCA supplies AV node via AV nodal branch)
 More common than anterior MI CHB, can also occur if LCX supplies AV node (some
patients)
 Do NOT need to temporary pace if asymptomatic + stable
o Bradycardia (vagus stimulation, sick sinus syndrome [RCA supplies SA node also], CHB)
o N+V (vagus stimulation)

 Posterior (RCA or LCX)

o MR (less common than inferior)
o RVHF
Non-Atherosclerosis ACS

 Prinzmetal Angina  Coronary vasospasm, occurs at rest (usually smoker from sleeping)
o Risk: Age, smoking

o Features: Rest chest pain usually occurring during sleep, often in smoker

o Diagnose:
 First: ECG (ST↑!)
 Best: Angiogram (clean coronaries)
 Can use ERGONOVINE or intracoronary ACh to stimulate spasm (should not
happen in normal patients)
o If no vasospasm  ?cardiac syndrome X
 If stress test was done, would be normal too

o Treat: CCB + Nitrates

 Takotsubo Cardiomyopathy AKA Stress Cardiomyopathy AKA Apical Ballooning Syndrome AKA
Broken Heart Syndrome
o Definition: Transient systolic dysfunction of the apical and/or mid-segments of the LV that
mimics MI, but in the absence of CAD
 NB: Takotsubo = Octopus trap (has a similar shape to the apical ballooning)

o Epidemiology: Women account for at least 90% of cases (possibly 100%), mostly post-
menopausal

o Triggers:
 Significant illness
 Physical stress
 Emotional stress (e.g. death of relative, shocking news, domestic abuse, arguments,
financial losses, etc)

o Features: Chest pain following stressful trigger

 Unlikely to have significant cardiac risk

o Ix:
 ECG – ST elevation which often does NOT mimic single vascular territory, but many
 Echo
 Regional wall motion abnormalities (RWMA) extending beyond a single
vascular territory, which is likely to be transient
 May see apical ± mid-segment ballooning, but not always as may have
disappeared
 Angiogram – Clean coronary arteries (smooth, no occlusions, little-to-no CAD)

o Rx: As per CCF

o Prognosis: Post-event, LVEF recovers in 4 weeks 

  Cardiac Syndrome X (AKA Microvascular angina)
o Definition: Exercise-induced anginal symptoms with normal coronary arteries and an
INABILITY to induce coronary vasospasm (differentiates from Prinzmetal)

o Epidemiology: Mostly women, age 40-50

o Theories:
 Ischaemic: Abnormal coronary microvasculature
 Non-ischaemic: Altered cardiac pain perception + hypersensitivity

o Risk factors: As per CAD – the cholesterol builds up in the MICROVASCULATURE

o Features: Exercise induced angina pain (but may not be sub-sternal)

o Ix: As per CAD/ACS

 ECG  ST depression (down-sloping – important sign)
 Angiogram  Clean coronary arteries, inability to induce coronary vasospasm (e.g.
using ACh or ergonovine; as there is NO hyperspasm of arteries, just blocked
microvasculature)

o Rx: As per angina

 First: Lifestyle measures + statins (only if cholesterol high)
 Second: Beta-blockers
 Third: GTN spray (long-acting nitrates not as useful)
*NB: Microvasculature compromise too small for PCI or CABG

o DDx: CAD, Prinzmetal angina, Cardiomyopathy

o Notes: Do not confuse with Metabolic Syndrome X

 Others  Vasculitis (e.g. Kawasaki), cocaine use, hyperthyroidism, anaemia, hypoxia

IF A PATIENT ROCKS UP LATE TO THE GP WITH CHEST PAIN + ECG CONFIRMS RECENT MI (STEMI, T-
wave inversion...)

0-12hr from onset = Aspirin + URGENT AMBULANCE ADMISSION

12-72hr from onset = Aspirin + Same day referral (high risk arrhythmia)
>72hr = Attain troponin and decide on action on individual basis
Aortic Dissection***

 Pathology: Tear in intima  hematoma within aortic wall which extend in either direction
o Commonly 2cm from aortic valve, or distal to L subclavian in descending aorta
o Most prevalent in 50-70

 Classification: Standard = A + B; DeBakey = I, II, III

o Type A  Affects ascending aorta (70%)
 Debakey I  Ascending aorta affected + propagates to at least aortic arch
and sometimes beyond
 Debakey II  Confined to ascending aorta

 Worrying  Affects aortic root – can track blood into the pericardial space leading to cardiac
tamponade and death

o Type B (AKA Debakey III)  Does NOT affect ascending aorta at all (distal to L subclavian; 30%)

 Risk factors: Cardiac risk (esp poorly controlled HTN, biscuspid aortic valve), connective tissue disorders
o Many begin with an aneurismal aorta

 Features: Sudden, severe ripping/tearing/sharp chest pain radiating to back in a 60yr old, AR murmur
o NB: Pain is maximal at time of onset, MI gradually gets worse (and is dull)
o NB: Pain migrates as dissection progresses
o May get (proximal to distal): Aortic regurgitation, Cardiac tamponade, Angina (coronaries involvement),
Stroke-like symptoms, Distal limb ischemia (back pain, mesenteric ischemia, AKI, claudication...)
o May get Horner’s syndrome (mass effect of dissection causing sympathetic nerve blockage)

 Ix:
o ECG (MI or ST-depression changes)  May lead wrongfully to thrombolytic therapy!!
o CXR (widened mediastinum in 80%)
o TOE (very good and may be done in anaesthetic room/ITU [rather than in radiology])
o Best: CT/MRI  Confirms diagnosis and vessels involved
 Must be done in radiology where support is poor – patient MUST be stable!
 CT scanner = “Tube of Death” – ONLY for stable patients
 NB: Lumen of dissection can extend from aortic arch to iliacs!

 Rx: After ABCDE, type A = call surgeons; type b = IV labetalol

o First – resuscitate: ABCDE  O2, IV access + X-match + fluid, analgesia/morphine

o Second – lower BP: IV B-blocker (labetalol)

 ↓heart contract = reduce dP/dt (rate of change of art wall pressure) = slows prog of dissec
 NB: Get BP between 100-120 systolic
 If not done w/ b-blocker or they are CI’d then give further therapy
 Nitroprusside, GTN, CCB (reduce both arterial pressure and dP/dt)

o Third – definitive: Surgery – endovascular repair, graft  stenting, inc stenting of branch vessels
 Grafting performed via median sternotomy + cardiopulmonary bypass
 Defective aorta removed and replaced with graft
 Aortic valve spared if possible
 NB: Type A vs Type B  Type A always requires surgery, type B often medical (BP control)
 Surgery in type B has risk of paraplegia, so medical Rx first
 Surgery for type B if  aortic RUPTURE, limb ischaemia, unrelenting pain

 25% mortality when treated, 85% mortality when not treated

 Contraind’s: Evolving stroke OR established renal failure
Congestive Cardiac Failure (CCF)/Heart Failure***

 Types: (NB: normal EF = 55-75%)

o Systolic = Dilated = HF w/ Reduced Ejection Fraction (HF-REF) (<40%; displace apex)  ACE-I + digoxin
more useful
o Diastolic = HF w/ Preserved Ejection Fraction (HF-PEF) (normal apex)

o High output  Increased demands + normal pump (supranormal EF in some cases)

o Low output  Normal demands + dysfunctional pump (low EF)

 Cause: Of systolic + diastolic dysfunction both

o Low output failure
 Myocardial disease
 Ischemia (inc ACS)
 HTN
 Cardiomyopathy (hypertrophic, restrictive)
 Valvular disease (10%)
 Drugs, Toxins (e.g. alcohol, cocaine), Endocrine (e.g. thyroid), Infiltrative
 Arrhythmias

o High output failure  Anaemia, pregnancy, hyperthyroidism, hypoxia

 Symptoms:
o Left sided  SOB, cough (pink frothy), PND + Orthop
o Right sided  Ankle swelling, nocturia

 Signs:
o Left sided:
 Cardiomegaly
 End inspiratory crackles
 Dull lung bases
 Pulsus alternans (varying strong/weak beats; a sign of LV systolic dysfunction and poor
prognosis, usually associated with 3rd heart sound) – do not confuse with electrical alternans
of cardiac tamponade

o Right sided:
 ↑JVP
 Dependent oedema
 Hepatomegaly ± ascites
 Ix:
o Acutely:
 First: ECG  Rule out arrhythmias
 If in arrhythmia, correction of this = fastest correction of cardiac output
 Second: CXR
 Alveolar oedema (extending from hila)
 B lines (Kerley)  Horizontal lines @ bases = fluid btwn lobules (not lobes)
 Cardiomegaly
 Diversion of blood to upper lobe vessels (prominent upper lobe vessels)
Effusions (pleural)  Meniscus sign
*Lateral/decubitus X-ray = more sensitive than CXR for effusion
 Third: Echo (as inpatient)
 Third: PCWP (will guide whether fluid can be given and how to give diuretics)
 o Chronically: All patients get ECG first, and baseline bloods + CXR can be done

 If previous MI: Echo in 2wk  LV syst + diast func, LV thickness, valve disease

 If no previous MI: BNP OR NT-proBNP (lasts longer in blood)

 High BNP (>400): Echo in 2wk

 Raised BNP (100-400): Echo in 6wk

 Normal (BNP <100): Heart failure unlikely, consider other diagnoses (NICE
recommends BNP as a test to rule out CCF i.e. good NPV)

*BNP/NT-ProBNP aids diagnosis AND risk stratification, but mainly used in primary
care (funded there, but not in hosp – costs £15 in hosp)
*Released in response to LV strain
*Very good marker of prognosis
*Very good NEGATIVE PREDICTIVE VALUE (but poor PPV)
*Raised levels also seen in AKI/CKD, MI; reduced with ACE-I/ARB
*Effects  Vasodilate, diuretic + natriuretic, suppress RAAS + sympathetic tone

***Must ALWAYS ask... what precipitated this episode of decompensated heart failure?***
Common things are  Worsening ischemia/MI, additional valvular dysfunction, infection, arrhythmia

Staging  New York Heart Classification

1. No symptoms on physical activity
2. Moderate exercise brings on symptoms
3. Mild exercise brings on symptoms
4. Any exercise brings on symptoms
 Rx:

 Acute: IPOD MAN

o First:
 IV access
 Position upright
 Oxygen  High flow O2, CPAP
 Diuretics (IV frusemide infusion)
 Morphine (diamorphine) – give this BEFORE furosemide; important!
 Anti-emetic
 Nitrates (IV infusion; very, very important – best venodilator which is hugely important)
NB: Beta-blockers are contraindicated in acute pulmonary oedema, but patients in LVF
without pulmonary oedema MUST have b-blockers prescribed if BP allows (large benefit), and
if already on BB when admitted do not stop

o If refractory: This is verging on cardiogenic shock

 Inotrope (dobutamine or dopamine)  ↑contractility, ↓SVR/afterload
 This is why noradrenaline NOT used, it would INCREASE SVR
 Dobutamine is a strong positive inotrope than dopamine
 Dopamine dilates the renal arteries preferentially, so can help with diuresis
 Dopamine can be used in conjunction with other positive inotropes
 Inotropic support should be used in cardiogenic shock whilst awaiting an intra-
aortic balloon pump ± PCI if shock is associated with MI

 Intra-aortic balloon pump + sodium nitroprusside (vasodilator) - e.g. in aort sten

 Inserted via femoral artery into descending aorta
 Inflates during diastole – alters cardiac, cerebral blood flow via ↑back pressure
 Deflates during systole – increases BP via vacuum effect
 Works on principle of “counterpulsation”
 CI in aortic regurgitation, aortic dissection, severe aorto-iliac occlusive dissease

o F/U: 2wk from discharge with MDT OP appointment

  Chronic:
o All patients: Education, MDT (e.g. heart failure specialist nurse), lifestyle mod (avoid salt, reduce
weight, reduce alcohol), control cardiac risk (aspirin, statins)

o Systolic (<40% ejection fraction):

 Symptoms:
 First: ACE-I and B-Blocker (both ALWAYS) and Diuretic (when symptomatic ONLY)
o ACE-I (Ramipril 1.25mg BD titrated to 5mg BD [or as far as tolerated], or,
Lisinopril 2.5mg OD titrated to 35mg OD [or as far as tolerated]) 
↓afterload, ↓remodelling
 Monitor U+E initially after Day 3+7, then weekly after each dose
increase
 Only stop titrating up when – High K, High Creat, Low BP
 Lower DIURETIC first before ACE-I for hypoTN
 Use ARB if intolerant to ACE (Candesartan 4mg OD titrated up
by doubling dose every 2wk [and no less] to max 32mg OD as
tolerated)
SAVE, SOLVD, CONSENSUS trials

o B-Blocker  ↓work, ↑vent filling

 Bisoprolol 1.25mg OD  10mg OD as tolerated as per HR + BP
(CBIS-II Trial)
 Carvedilol (COPERNICUS Trial)
 Metoprolol controlled release (MERIT-HF Trial)

 Complications:
 Asymptomatic hypotension = Do NOT change drug
 Symptomatic bradycardia = Half dose
 2nd or 3rd deg HB = STOP
*NB: Beta-blocker therapy usually comes AFTER ACE-I initiation (usually
when ACE-I are beginning to be titrated up in dose  CBIS-III trial)

o Diuretic (furosemide 20-80mg OD, or, Bumetanide 1-2mg OD) 

Symptomatic treatment ONLY, so ONLY give if evidence of fluid retention

 Refractory, Type III + IV:

o Spironolactone 12.5-50mg OD (↓dose to inhibit RAAS, not diurese)
 Lowers mortality in Stage III/IV NYHC
 Given for ALL patients in Stage III or IV, or patients
transitioning from Stage II  Stage III

 Risk: Hyperkalemia, esp w/ ACE/B-blocker (but dose is LOW so if

NORMAL renal function UNLIKELY to develop hyperkalaemia –
likely avoid in poor renal function)

 Risk: Breast tender/enlarge (swap to eplenerone 25mg OD

increasing to 50mg OD by 4wk of Rx)
 Use Eplenerone if 3-14 days post-MI – better than
spiro in this situation
(EPHESUS trial)

o Ang II Receptor Blocker despite being on ACE-I

 CHARM study – 15% lower mortality when combined with B-
Blocker and ACE-I in refractory CCF

o Hydralazine + Nitrate (symptomatic control for Type III and IV, but of
PROGNOSTIC benefit in black people!)

NB: All calcium channel blockers (except amlodipine) and NSAIDs + COX-2 inhibitors are contraindicated in CCF
NB: Ideal to increase all medications to maximum dose, but this may be limited by S/Es (most importantly hypotension and
bradycardia) and hence cannot achieve maximum doses
  If still refractory, Type III + IV:
 Digoxin 125mcg (62.5mcg for elderly) (however, strongly indicated if also in AF but
still NOT before B-blockers [as B-blocker have MORTALITY benefit]! )
o ↑K+ = ↓Dig activity; ↓K+ = Dig toxicity
o Dig very effective at slowing HR, but NOT during exercise (however B-
blockers ARE good even during exercise)
o Works via reduced AV conduction, increased LV contraction (inhibition of
Na/K ATPase), vagal stimulation

o Toxicity: N+V, CNS, Blurred vision w/ yellow halo

o Rx:
 First: Stop drug, K+ replacement
 If CNS/ECG change: Digibind (Antibods)

 Ivabradine (inhibits funny current and slows down heart through different
mechanism than B-Blockers)

o Indications: Resting HR >75, Max dose ACE-I/ARB + B-Block, Spiro

o 2.5-5mg BD, then adjust dose to achieve HR ≤60 (yes – bradycardic!)

o Definitive/Surgical:
 Biventricular pacing/Cardiac resynchronisaton therapy ± ICD
 Indication: All must be met
o Maximal medical Rx in NYHC Stage 3/4
o EF <35%
o Prolonged QRS (>120; particularly with LBBB) or observed dyssynchrony

 Rationale: Improves exercise tolerance + survival

 Notes:
o Bivent pacing/CRT-P for dyssynchrony (one lead in RV, one lead in
coronary sinus to pace LV)
o ICD for poor EF
o Can combine CRT + ICD (CRT-D) if suitable for both, but if only suitable for
one then ONLY do that one (rather than prophylactically putting in CRT-D)

 PCI, CABG

 Valvular correction

 Symptomatic + maximum therapy?  Heart transplant

 Contraindications:
o Cancer (unless in remittance for >5yr)
o CrCl <50mL/min

 Diastolic (normal ejection fraction):

o Symptoms:
 First: Diuretics and B-Blocker (NO ACE-I if ↑ejection fraction)
 Can use rate-limiting CCBs if beta-blocker not tolerated
 Do not use RL-CCBs in low ejection fraction!

o Definitive: Identify cause + surgical correction (if possible)

Pathophysiology of Flash Pulmonary Oedema

 Due to rapid LA congestion

 Example 1
o Mitral stenosis  LA dilation  AF  Increased HR (in fast AF)  Reduced CO + Decreased
LV filling time in diastole  LA congestion  Pulmonary congestion
 Example 2
o Acute MI  Overall heart failure  Poor CO  Congestion
 Example 3
o MR  Backflow of blood rapidly
 Example 4
o RAS  Significant hypertension (= high afterload)  Overall heart failure  Poor CO 
Congestion
Valvular Heart Disease

 Mitral Stenosis** – mid-to-late diastolic rumbling murmur best heard with bell in left lateral position
o Cause:
 Rheumatic fever (most common; usually in immigrants – see below)
 SPECTRUM: Strep pyo pharyngitis  Scarlet Fever  Rheumatic fever
 Degenerative calcification

o Pres: SOB, haemoptysis, CHF, malar flush

 Thromboemboli (stagnant LA blood)
 Hoarseness (LA compressing recurrent laryngeal)
 Dysphagia (LA compressing esophagus)
 A-Fib  Independently associated, but not unique
 Heart sounds  Loud S1 + Opening snap (in early diastole) + TAPPING

o Ix:
 First: ECG
 LA enlargement; + RV + RA enlargement due to pulmonary HTN
 A-Fib
 Second: CXR
 LA enlargement  Straightening of right heart border + lifting up of left
main stem bronchus
 Third: Echo
 Diastolic mitral flow murmur, thickened mitral valve leaflets, LA dilatation
 If asymptomatic but significant murmur, follow-up every 2-3yr
 Fourth: Cardiac MRI (rarely needed)
 Best: Angiography (rarely done)

o Rx:
 Conservative: Salt restriction  ↓Pre-load

 Medical:
 Diuretics OR long acting nitrates  ↓Pre-load, relieve SOB
 B-blocker OR rate-limiting CCBs  Improve exercise tolerance
 Anticoagulation (based on CHADSVASC) if A-Fib

 Surgical:
 First: Percutaneous Mitral Commissurotomy (PMC AKA valvuloplasty)
o Insert catheter into vein  RA  Puncture septum  Enter LA 
Balloon valvuloplasty of MS
o Contraindicated in LAA clot (risk of breaking off embolism)
 If not candidate for PMC: Valve Replacement

o Notes:
 Swan-Ganz right heart catheter can suggest mitral stenosis
 Normally PCWP = LV diastolic pressure; if PCWP is
higher (i.e. >5mmHg different) then indicates
mitral stenosis
 Results also show pulmonary HTN (RV-to-pulm art
pressure rises, and pulm art pressure more than
20% of SBP), and aortic stenosis (LV-to-aortic
pressure has gradient >25 [it is 75 = very severe])
 Mitral Regurgitation**  Pan-systolic murmur + radiation to axilla; soft S1, wide split S2, S3 present
o Types:
 Primary  Intrinsic lesions affecting the valve
 Degenerative (most common)
 Ischemia (i.e. posterior MI causing chordae rupture)
 Infective endocarditis (mitral = most common valve affected in non-IVDU)
 Secondary  Secondary to left ventricular defects
 LV enlargement

o Pres:
 Acute MR (e.g. posterior MI)  SOB, cough
 Rapid pulmonary oedema – life threatening, needs emergency valve repair

 Chronic MR (e.g. degeneration)  Asymptomatic with progression to gradual SOB

o Ix:
 First: ECG
 LVH + LA enlargement
 Second: CXR
 Cardiomegaly
 Third: Echo
 Systolic mitral flow murmur, LA and/or LV dilation
 Fourth: Cardiac MRI
 Best: Angiography (rarely done)

 Other: On examination, isometric exercise tests (e.g. handgrip exercises) make the
MR murmur WORSE but make the AS, MVP and HOCM murmurs BETTER! Standing
makes the MR murmur better.

o Indications for Rx: Symptoms, LVH or CCF, Pulm HTN, New AF

 If no indications met: 6 monthly echocardiogram

o Rx:
 Medical: Can use nitrates, diuretics, sodium nitroprusside
 First: ACE-I if CCF present (↓pulmonary congestion, ↓pre-load = ↑CO)
o Beta-blockers, spironolactone also appropriate

 Surgical: Valve repair or replacement

 Indications:
o Acute MR (esp if leading to pulm oedema)
o Symptomatic despite medical therapy
o <60% EF  MR should have ↑EF; ↓EF = decompensation

 What type of valve?

o Metallic  If young, as can last whole life
 Rx: Warfain AND aspirin life-long, INR 2.5-3.5
o Bioprosthetic  If old (>70), as only lasts 10-15yr
 Rx: Warfarin 3mo INR 2-3, then aspirin lifelong

*Both have same risk of endocarditis

*Metallic has lower failure rate (+last longer)

 Complications  Cardiac tamponade

o PE unlikely as patients fully heparinised whilst on bypass
 Mitral Valve Prolapse  Mid-systolic click
o Definition: Abnormal bulging (>2mm) of one or both of the mitral valve leaflets into the
atrium during ventricular systole

o Epidemiology: Very common (3% of population, more in females) – risk for developing MR
 Risk factors for developing MR  >50, HTN, obese, thick mitral leaflet, AF, big LA...

o Cause: Dilated mitral annulus; often leaflets are thickened; associated diseases are:
 Marfan’s (NB: dilation of aortic sinuses/AR is the most common defect in Marfan’s)
 Ehlers-Danlos
 Osteogenesis imperfecta
 PCKD

o Pres of Prolapse: Pain, Palpitations, Panic attacks, Pectus excavatum, Presyncope

 Murmur loudens with Valsalva, quietens with squatting (vice versa for ALL left sided
except mitral prolapse or HOCM, hence why these DON’T get diuretics)
 Valsalva = ↓blood to LEFT heart makes murmur LOUDER (and with HOCM)

o Ix: ECG, CXR, Echo (systolic displacement of mitral leaflets), Cardiac MRI, Angiogram (rarely)

o Rx:
 Low risk of developing MR: Symptomatic treatment (e.g. b-blocker for panic)
 High risk of developing MR: Surgery  Valve repair ± annuloplasty
 Valve repair involved leaflet resection
 Annuloplasty makes annulus SMALLER, leaflets re-join
 This procedure is NOT percutaneous

o Complication:
 Endocarditis (3-8x relative risk)
 Stroke (rare)
 Arrhythmia + Sudden death
 Aortic Stenosis**  Ejection systolic murmur + radiation to carotids/clavicle; S2 single or paradox; S4
o Cause:
 Young <65:
 Bicuspid valve (present in 1% of population)
 William’s syndrome (supravalvular aortic stenosis)
 HOCM (subvalvular aortic stenosis)
 Rheum fever (mitral more common)

 Old >65: Calcification

o Pres - SAD: Syncope, Angina (most common), Dyspnea, CHF (worst prognosis)
 Asymptomatic  <5% incidence of death per year
 Angina  5 year median survival
 Syncope  3 year median survival
 CCF  2 year median survival
*Once symptoms appear, the prognosis is POOR; When asymptomatic, good prog

o Examination findings:
 Slow-rising (small + late) pulse... AKA pulsus parvus et tardus
 Narrow pulse pressure (syst + diast BP close together)
 Diminished S2 = severe AS... A2 is normal/loud in aortic sclerosis
 BOTH stenosis and sclerosis radiate to carotids!
 Aortic sclerosis is MORE COMMON in population than stenosis!
 Presence of S4 (marker of severity)

o Ix:
 First: ECG  LV Hypertrophy

 Second: CXR  Cardiomegaly + calcifications

 Third: Echo (sometimes with low-dose dobutamine stress)  Gradient assessment,

thick aortic valve leaflets, LVH/CCF, “contractile reserve” if with dobutamine

 >50mmHg gradient = severe (e.g. LV = 200mmHg, Aorta = 150mmHg)

 Jet velocity >4m/s = severe

 Valve area <1cm2 = symptomatic (indication for Sx), <0.5cm2 = severe

 Moderate gradient in CCF patient can actually be severe AS, therefore in

CCF it is better to use V-Max2 as marker of severity
o In AS + CCF, also use dobutamine stress test to determine if there
is any “contractile reserve” – if so, then valve replacement may
help but if not then valve replacement unlikely to be beneficial
(and just Rx as CCF)
o Gradient is sometimes imprecise with Echo  Angio best

 Fourth: Cardiac MRI

 Best: Angiography (R/O co-existing CAD, better assess gradient)

Exercise testing is CONTRAINDICATED in AS

o Rx: OBSERVE PATIENTS WHO ARE ASYMPTOMATIC OR VALVE GRADIENT <50mmHg
 All patients: Modify cardiac risk factors (AS is big risk for IHD)

 Surgery – first line: Surgical aortic valve replacement

 Indications**:
o Symptomatic (esp syncope) inc CCF (can partially resolve w/ TAVI!)
o Valve gradient >40-50mmHg
o Jet velocity >4m/s
o Valve area <1cm2
o AS + CCF ≥NYHA 2 + Surgical mortality ≥50%
If these indications are not present, WATCH AND WAIT

 Types  Bovine/porcine bioprosthetic (>65); metallic (<65)

o Bioprosthetic – warfarin x3mo then lifelong aspirin
o Metallic – warf + asp long-term (INR – aort = 2-3; mitral = 2.5-3.5)

 Unfit for surgery: Transcatheter Aortic Valve Implantation (TAVI)

o Efficacy
 Equal to surgical AVR
 10% 30d mortality

o Method
 Peripheral access e.g. via femoral artery
 Bring new valve into centre of existing stenotic aortic
valve
 Blow up balloon with new valve around it so native valve
gets compressed against endothelial walls
 New valve now expanded (and native valve compressed)
and new valve functional

 Unfit for surgical AVR and TAVI:

 Diuretics, Digoxin... ACE-I are CONTRAINDICATED (relative) with AS
 Balloon valvuloplasty (↓invasive than TAVI, but most re-stenose by 12mo)
o Use valvuloplasty if unfit for surgery, but does not work in calcified
valves (i.e. most older people, but good for young people!)

Severity: Loss of S2, slow rising pulse, narrow pulse pressure, ↓BP, radiating murmur
 Aortic Regurgitation**  Early diastolic murmur (at LLSB)
o Cause:
 Cardiac enlargement  HTN, IHD
 Congenital  bicuspid aortic valve (commonest congenital)
 Infective  Tertiary syphilis, infective endocarditis
 Rheumatological  AnkSpon, ReA, SLE
 Aortic dissection

o Pres: SOB, CHF

 Wide pulse pressure
 Watson’s water hammer pulse (rapidly collapsing; AKA “Corrigan pulse” – rarely felt)
 Quinky sign (fingers), Head bobbing, Austin flint murmur (apical rumbling murmur)

o Ix:
 First: ECG  LV Hypertrophy
 Second: CXR  LV or Aortic dilatation
 Third: Echo  Dilated LV and/or aorta, LV volume overload
 Fourth: Cardiac MRI
 Best: Angiogram

o Rx:
 Conservative: Salt restriction
 Medical:
 ACE-I (if hypertensive, LVH present, or cannot tolerate surgery)
 B-blocker (only if Marfan’s as it slows aortic root dilation)
 Surgical: Valve replacement
 Indications:
o Acute AR (esp w/ poor LV function - Sx should be done urgently)
o Symptomatic despite medical therapy
o Asymptomatic with LV dysfunction (EF <55%)
 AR should have ↑EF; ↓EF = decompensation
 MS AS MR AR MVP
Cause Rheumatic Young: Bicuspid Ischemia Ischemia Congential
Fever valve (dilation) (connect tissue)
HTN
Old:
Calcification
Key Findings Mid-Diastolic Ejection systolic Pan-systolic + Early diastolic Pain,
+ radiation to radiation to Palpitations,
Emboli/stroke carotids axilla S3 in Panic attacks,
decompensation SyncoP
Hoarseness S4 gallop; S2 S3 w/ soft S1
single or and widely split Wide pulse Mid-systolic
Dysphagia paradoxical S2 pressure click

A-Fib Slow-rising Worsens with

pulse Valsalva,
Loud S1 + improves with
Opening snap Narrow pulse squatting
(following S2) pressure
Ix LAH, ?RVH, LVH/Cardiomegaly Displacement
ECG, CXR, Echo ?RAH of leaflets

No
cardiomegaly
Rx Salt restriction Valve Salt restriction Salt restriction B-blocker
+ Replacement + +
Diuretics TAVI First: ACE-I First: ACE-I NO DIURETICS!
(if symptoms)
Surgical: If refractory: If refractory:
Balloon If unsuitable for ARB then other ARB then other
Valvuloplasty or surgery – vasodilator vasodilator
Valve balloon therapy therapy
Replacement valvuloplasty
(re-stenosis in Surgical: Valve Surgical: Valve
6-12mo ) repair or replacement
replacement
Bioprosthetic Valve (Bovine or Porcine) = For older people = WARFARIN x3mo, then ASPIRIN ONLY
Mechanical = For younger people = WARFARIN + ASPIRIN LONG-TERM
Tricuspid Valve Disease

 Epidemiology:
o Less common than aortic and mitral
o TR > TS
o TR usually associated with pulmonary HTN secondary to MS or MR

 Tricuspid stenosis: Rumbling mid-diastolic murmur at LLSB

o Cause: Always secondary to MS/MR, usually also caused by rheumatic fever
 Rarely  Carcinoid syndrome

o Features: General signs of right and left sided heart failure (esp right)
 LARGE A wave (JVP upstroke due to contraction against relatively closed tricuspid)
 NB: NOT Cannon A waves (this is seen in complete heart block)

o Ix: ECG, CXR, Echo, Cardiac MRI, Angiography

o Rx:
 Medical: Treat symptoms (e.g. of endocarditis, heart failure, arrhythmias)
 Surgical: Valve replacement (cannot repair as leaflet tissues not compliable)

 Tricuspid regurgitation: Pan-systolic murmur at LLSB

o Cause: RVH/Cor pulmonale causing annular dilatation (most com)
 Stab wound (tricusp most anterior valve)
 CARCINOID syndrome (any right sided lesion, most common tricuspid)
 Endocarditis
 Ebstein abnormality
 PE

o Features: Often asymptomatic unless with pulmonary HTN  Signs of right/left heart failure
 Giant V wave (more blood in venous system following systole, but cannot fill atrium
as already filled with regurgitant blood hence prominent V wave)
 cV = cardiovascular wave
 V = ventricular wave
*Same thing
 Rapid y-descent (blood rushing into ventricle from previously high pressure V wave
causes rapid Y-descent)
 Pulsatile liver in systole

o Ix: ECG, CXR, Echo, Cardiac MRI, Angiography

o Rx:
 Medical: Treat symptoms (e.g. of endocarditis, heart failure, arrhythmias)
 Surgical: Valve Annuloplasty (preferred) or Valve replacement (if severe, rare)
Pulmonary Valve Disease

 Epidemiology:
o Rare
o Congenital defects most common cause of PS or PR

 Pulmonary Stenosis: Ejection systolic murmur at ULSB radiating to back

o Cause: Congenital heart defects (10% of all CHDs)

o Features: In neonates
 SOB, syncope, heart failure (right and left)
 Cyanosis dependent on degree of PS
 Parasternal heave
 Sometimes prominent/cannon A waves (due to severe backlogging)

o Ix: ECG, CXR, Echo, Cardiac MRI, Angiography

o Rx:
 Medical:
 ABCDE resus + knees to chest (increase pulm circ in ToF)
 Prostaglandin E1 (keep PDA open)
 Surgical: Balloon valvotomy

 Pulmonary Regurgitation: Early diastolic murmur with loud P2, without a collapsing pulse (?AR)
o Cause: Rare congenital anomaly, OR after valvotomy of PS (e.g. in ToF)
 Others  Dilated annulus due to RVH, Pulmonary HTN, Marfan’s

o Features: Right sided heart failure

o Ix: ECG, CXR, Echo, Cardiac MRI, Angiography

o Rx: Usually conservative, rarely pulmonary valve replacement

NB: Severe stenosis of ANY valve is considered high risk for pregnancy (not as bad if tricuspid)
Myocardial + Pericardial Diseases

 Cardiomyopathy (Myocardial Diseases)

o General Points
 Definition: Conditions where heart muscle is structurally or functionally abnormal in
the ABSENCE of CAD, HTN, valve disease and congenital heart disease severe
enough (if present at all) to cause the degree of dysfunction observed

 Epidemiology: Can all occur at young ages – must have high suspicion (except for
restrictive)

 Ix options for all:

 ECG
 Urine dip
 Blood  Full workup including cardiac enzymes, TFTs, NTproBNP, ESR
 CXR
 Stress test
 Echo – important
 Cardiac MRI – important for cardiomyopathy
 Angiography
 Endomyocardial biopsy (only once underlying defects ruled out)

The goal of investigation is first aimed at determining if there is underlying

defects (e..g CAD, valve disease) which could be the cause – if not, then
further workup into cardiomyopathy is conducted (e.g. begin looking for
iron levels for haemochromatosis  endocardial biopsy)
o Dilated Cardiomyopathy = ↓EF (can relax, but not contract)
*This condition is IDENTICAL to systolic dysfunction CCF (i.e. HF-REF), except often in a
younger patient with a susceptible myocardium (i.e. not old, so not just “wear and tear”)
 Epidemiology: Most common form of CM

 Cause:
 Idiopathic (most common)
 Genetic (25%, auto-dom; family will have it)
 Alcohol
 Ischaemia
 Valvular
 Infective  Post-viral [e.g. adenovirus, myocarditis leading to DCM], HIV
 Tachycardia-induced DCM (e.g. AF, A-Flut, hyperthyroid, any chronic tachy)
 Sarcoid, Hemochromatosis
 Connective tissue disorders
 Chemotherapy

 Features: As per CCF, but likely YOUNG patient

 Sometimes with thromboembolism e.g. stroke
 Arrhythmia

 Rx: SAME as CCF

 First: ACE-I + B-Blocker  All pts
o Spironolactone  When above medication not controlling
o Diuretics + Nitrates  All symptomatic patients w/ fluid overload
o Digoxin
 If poorly controlled with above medications
 If in AF with fast ventricular response
 Also consider warfarin

 Definitive:
o Biventricular pacing (wide QRS [esp LBBB] w/ NYHC 3/4)
o Implantable defibrillator
o Valvular repair/replacement
o Heart transplant (esp if young)
o Hypertrophic Obstructive Cardiomyopathy/HOCM*** = ↑EF (can contract, but not relax)
 Epidemiology:
 Second most common CM (1/500 = 0.2% of population)
 Often presents 20-30y/o
 Most com cause sudden cardiac death in young people + athletes (inc female)

 Cause: Familial/genetic (auto dom [60%] frame-shift mutation, sporadic), HTN

 HOCM  unexplained hypertrophy of interventricular septum (asymmetrical)
 High penetrance, but variable expression (will be passed down, but ?severity)
 Most commonly due to mutation in gene encoding for beta-myosin heavy chain
protein (but also the myosin binding protein C)

 Pres: Syncope, Angina, Dyspnea, YOUNG, athlete, FH sudden cardiac death (SCD)
 Ejection systolic OR mid-systolic murmur which does NOT radiate to carotids
o DECREASES on squatting + leg elevation
o INCREASES on Val Salva
I.e. INCREASED murmur when pre-load DECREASED
 Classically JERKY pulse (vs AS = slow rising pulse)
 Large A waves
 Double apex beat
 Mid-to-late systolic precordial impulse

 Ix: As above, but on:

 ECG
o Non-spec ST abnorm (most com)
o LVH (2nd most com)
o Deep Q-waves inferior or anteroseptal (unknown why)
o Progressive T-wave inversion (i.e. LV strain in V4-6 usually)
o Episodes of non-sustained VT (on Holter monitor)

 Echo  MR SAM ASH

o Mitral regurgitation (MR)
o Systolic anterior motion (SAM) of anterior mitral valve leaflet (contacting
the interventricular septum)
o Asymmetrical hypertrophy (ASH)/LVH – ventricular septum thickening
(>3cm thickening = poor prognosis)

 Biopsy  Disorganised muscle + myofibrillar disarray

 Rx: ABCD – Amiodarone, Beta-blockers OR verapamil, Cardioverter defib, Dual chamber pace
 Conservative: Avoid strenuous activity

 First: B-Blocker
o Can also use verapamil if B-blockers CI’d
o Amiodarone can be used for arrhythmias

 Any VT (run or sustained) OR Syncope: Implantable cardiodefibrillator (ICD)

 Severe CCF: Consider bivent pacing

 Refractory to Medical: Surgical Myomectomy (5% of patients)

 DDx: LQTS (this does NOT have FH; this will have STRUCTUALLY NORMAL heart)
 Complications: Sudden death due to spontaneous ARRHYTHMIA
 Occurs secondary to ischemia of hypertrophied segment
 1% risk of SCD per year
 Risk of sudden death (1 = possibly significant; two or more = very significant)
o Unexplained syncope
o FH sudden death (<45y/o + history syncope)
o Episodes of VT (non-sustained OR sustained)
o LVOT obstruction (gradient >30mmHg)
o Septal thickening >30mm
o Exercise-induced hypotension (highly important risk factor)

 Associations: Friedreich’s ataxia, WPW

 Drugs to avoid: ACE-I  Outflow obstruct increases if ↓afterload; Nitrates; Inotropes

 Poor prognostic signs: As per above “Risk of sudden death”

o Restrictive Cardiomyopathy** (AKA Obliterative CM; uncommon; diastolic + systolic dysfunction)
 Definition: Filling + diastole impaired, but normal wall thickness + systolic function

 Epidemiology: Rare (<0.1% population)

 Causes: Amyloid (most com), Haemochromotosis, Sarcoid, Cancer (inc myeloma), Fibrosis
(e.g. endomyocardial fibrosis = most common cause of RCM; scleroderm)

 Pres:
 Pure diastolic heart failure (i.e. normal systolic function - normal EF)
o Kussmaul Sign  Inspiration = ↑JVP (should normally ↓JVP)
 Positive = Restrictive Cardiomyopathy, Constrictive Pericarditis,
or Cardiac Tamponade
 Often right sided heart failure symptoms (>> left)

 Ix: As above
 ECG (↓voltage – key sign)
o Also seen in – ↑fat, ↑muscle, ↑air (emphysema)
 CXR/CT (norm/mildly enlarged heart size, N pericardium [calcified = e.g.
constrictive pericarditis])
 Echo (rigid myocard, small thick vents, thick interatrial septum [amyloid deposits],
“granular sparkling”/”global speckled”/echogenic appearance [amyloid], mild
pericardial effusion [e.g. 5mm] but not enough to be tamponade)

 Rx:
 Medical: Manage heart failure
 Definitive:
o Pacing or implantable defibs
o Heart transplant

 Notes: Do NOT use digoxin in amyloid heart disease – amyloid can cause 2nd or 3rd deg HB,
and digoxin will exacerbate this (i.e. digoxin is CONTRAINDICATED)

o Arrhythmogenic Right Ventricular CM (ARVCM)

 Pathology: RV myocardium is replaced with fibrofatty tissue
 Epidemiology:
 25-40y/o, FH of condition OR sudden death (auto dom, 25% penetrance)
 2nd most common cause sudden cardiac death after HOCM
 Features: Syncope, palpitations, ↓exercise tolerance, dizzy spells during exercise
 VT often precipitated by catecholaminergic drive (e.g. exercise, anxiety, fright)
 Ix: No genetic tests
 ECG  Arrhythmias, often LBBB pattern (anyone with VT + LBBB = consider
ARVCM), V1-3 TWI, notch at end of QRS comp (epsilon wave; 50%)
 Echo  Dilated right heart (most common), hypokinetic right ventricle
 Cardiac MRI (MUST be done if suspected)  Fibro-fatty replacement of myocard
 Other  RV angiogram, RV myocardial biopsy
 Rx:
 First: Sotalol (treat VT episodes)
 Failed sotalol: ICD
o Not for ICD in first instance, thin wall of RV can lead to RV rupture with
ICD placement – ICDs much better for underlying LV issues
o But, this may be considered first line for some patients

 Notes: Naxos disease  Auto recessive ARVC, + palmoplantar keratosis + woolly hair
o Other considerations:
 Catecholaminergic polymorphic VT
 Definition: Inherited disorder of VT episodes
 Epidemiology: 1/10,000; 15% of SCD
 Features: Exercise-induced VT (presents w/ collapse), sometimes emotional
 Ix:
o ECG  Normal
o Echo  Normal (hence not cardiomyopathy)
o MRI  Normal (hence not cardiomyopathy)

o Stress echo  Irregularly shaped VT occurs

 Rx: Beta blockers, verapamil, flecainide, ICD

o Refractory: Sympathectomy

 Congenital LQTS (e.g. Romano-Ward [no deafness], JLN [deafness])

 Pericardial Disease
o General Points
 Anatomy: Outside to inside
 Outer fibrous layer (parietal pericardium)
 50mL plasma filtrate
 Inner serous layer (visceral pericardium)
 Function: Limit dilation, maintain compliance, preserve Starling curve, barrier to
malignancy (part of reason why not many cardiac tumours)

o Acute Pericarditis***
 Cause:
 Viral (most common)  Coxsackie virus
 Rheum  SLE, RA, Sarcoid
 Renal  Uraemia
 Cardiac  Post-MI (Dressler’s syndrome if 2-12wk)
 Drugs  Hydralazine
 Bacterial or Fungal
 Post-radiotherapy

 Pres:
 Pain  Classic cardiac pain and...
o Pleuritic
o Positional (better on sitting forward, worse on lying back)
 Pericardial friction rub (70%; pathognomonic)
o Best heard with patient sitting up and leaning forward
 Previous URTI (1wk ago)
 Pyrexia

 Ix: ECG + Auscultation = diagnostic

 Blood  FBC, ESR, CRP, U+E (urea), cardiac enzymes
o Troponins may be elevated, but not MI (unless Dressler)
o Troponin significantly elevated ONLY in 1/3 of cases
 ECG (diffuse saddle shaped ST-seg↑ w/ upright T-waves; PR depression
[most specific ECG finding of pericarditis])
 CXR  Flask shaped cardiac silhouette
 Echo
 CT/MRI  Pericardial thickening >5mm
 Pericardiocentesis (echo guided)  Place needle subcostal, aim toward
shoulder

 Rx: If develops pericardial effusion, transfer to CCU

 Acute attack:
o First: NSAIDs
o Second: Colchicine ± NSAIDs (esp if lasts >14d)
o Refractory to NSAIDs + Colchicine: Steroids (prednisolone)

 Long term:
o If first attack: Nil
o Following recurrence to prevent attacks: Colchicine

 Complications: Pericardial effusion ± tamponade, recurrence of pericarditis (10-15%

of cases in next one year!)
o Chronic Pericarditis
 Epidemiology: Rarely following acute pericarditis
 Types:
 Chronic effusive
 Chronic constrictive
 Features: Pain, palpitations, syncope, SOB... may progress to tamponade (Beck’s
triad, pulsus paradoxus, Kussmaul’s sign)
 Ix: Echo, Cardiac MRI, ?pericardial biopsy
 Rx:
 Effusive
o Not compromised  Nil
o Compromised/tamponade  As per tamponade
 Constrictive
o Medical  Salt restriction + diuretics
o Surgical  Pericardiectomy (85% cure rate, but 10% mortality
from procedure)

o Constrictive Pericarditis
 Cause: Idiopathic, post-heart surgery, thoracic radiation, post-viral

 Pathophys: Fibrosis of pericardium which constricts all four chambers of heart

 Pres:
 R+L sided failure symptoms (e.g. lung symptoms/SOB, fluid retention)
 Fatigue
 Kussmaul sign (↑ in JVP during inspiration [normally should reduce])
o RARELY seen in tamponade
 Pericardial knock (confused w/ S3)
 Rapid Y descent of JVP (as most ventricular filling occurs in early diastole)
o NB: In tamponade, the Y-descent is absent or blunted

 Ix:
 ECG (↓volt)  Same as restrictive cardiomyopathy
 CXR/CT/MRI (calcified pericard)  KEY DIFFERENCE to restrictive CM
 Cardiac catheterisation for pressures  Equal pressures in ALL chambers
in diastole, matching of RV + LV pressures in respiration

 Rx: Remove pericardium

 Notes: NO pulsus paradoxus (as seen in tamponade)

 o Cardiac Tamponade**  Pericardial effusions which restrict the heart
 Background:
 Slow fluid accumulation: Pericardial expansion + accommodation
o E.g. as per pericarditis (but may also be rapid in some cases)
 Rapid fluid accumulation: Tamponade

 Cause: Anything causing any pericardial disease/effusion can cause tamponade

 Young:
o Trauma (e.g. RTA inc airbag release into chest, other chest trauma)
o Pericarditis (acute or chronic)
 Old:
o Malignancy (breast/lung)  Most common cause bloody effusion
o Renal failure (uraemia)
o Acute MI
o Post-MI (Dressler’s)

 Pres:
 Beck’s Triad  ↑JVP, ↓BP/shock, Distant heart sounds
 Pulsus paradoxus  ↓10mmHg BP on inhalation
 Absent or Blunted Y descent due to limited RV filling (differentiates from
constrict pericard)

 Ix: Full bloods (inc U+E for urea, ANA, HIV testing, TB testing)
 First: ECG (electrical alternans  QRS alternates from ↑-↓ volts = severe!)
 Second: “Water bottle” heart – enlarged (acutely)
 Third: Echo (pericardial effusion, diastolic collapse of RA + RV)

 Rx: ABCDE (leg elevation, O2, IV fluids, inotropes)

 Immediately: Subxiphoid pericardiocentesis/pericardial drain (Echo
guided) + Treat cause
 Eventually: Pericardial Window
 If recurrent: Pericardiodesis

Acute pericard can lead to Chronic/Constrict Pericard OR Tamponade

Chronic/Constrictive pericarditis leads to chronic heart failure, tamponade leads to acute heart failure

TAMponade = TAMpaX (only X present, Y is absent)

Myocarditis

 Definition: Acute or chronic inflammation of the myocardium which may present like MI and may
progress to dilated cardiomyopathy

 Epidemiology: Incidence unknown, but may be implicated in 10% of SCD

 Causes:
o Infection
 Viral (most common)  Coxsackievirus, others (adenovirus, parvovirus, HIV, EBV…)
 Bacterial (much less common)  Diphtheria (most common bacterial)
 Protozoa  Chagas (trypanosomiasis [cruzi = American, Gambia [west Africa])

o Immune mediated (e.g. SLE, sarcoid, scleroderma…)

o Drugs
 Hypersensitivities  Various medications
 Toxins  Alcohol, chemotherapy (esp anthracyclines – e.g. doxorubicin), cocaine,
trastuzumab

o Other
 Metal poisoining
 Electrical shock
 Radiotherapy/radiation

 Features: May be asymptomatic or may present with fulminant CCF + SCD

o Fatigue (>50%)
o Chest pain (35%)
o Fever (20%)
o SOB
o Palpitations + tachycardia
o S4 gallop
o Signs of CCF

 Ix:
o ECG  ST elevation OR depression, TWI (diffuse), atrial arrhythmias, transient AV block
o Bloods  FBC (leucocytosis 25%), CK/Trop (often elevated), CRP/ESR (elevated in 60%)
o CXR  Signs of CCF
o Echo
o Cardiac MRI (can differentiate transient [myocarditis] from permanent [MI] tissue damage) –
VERY good test
o Endomyocardial biopsy (gold standard)

 Rx: Conservative (NB: Steroids have NO evidence for their use)

o Low threshold for ITU if CCF present (inotropic support)

 Prognosis: Some recover, some develop intractable/severe CCF

Amyloidosis**

 Definition: Extracellular and intracellular deposition of insoluble amyloid fibrils, which arise from
various proteins, causing parenchymal dysfunction

 Pathogenesis: 23 unrelated proteins are known to form amyloid fibrils

 Classification: Commonly affect cardio + renal, but can affect either one alone
o A Amyloidosis (AA)  Acute phase reactant amyloid, therefore seen in patients with chronic
inflammation
 Causes: e.g. RA, chronic microbial infections like TB, sometimes neoplasia like RCC
 Features: Renal most common, 10% cardaic

o Light Chain Amyloidosis (AL)  Monoclonal plasma cell disorder similar to multiple myeloma
OR from multiple myeloma itself
 Causes: Mult myel (BJ deposition), MGUS, Waldenstrom’s
 Features: Cardiac in 50% + neuro most common
 Fatal in 80% of cases

o Heavy Chain Amyloidosis (AH)  Rare

o Transthyretin-related Amyloidosis (TTR)  Precursor transport protein synthesised in liver

o Beta2-Microglobulin Amyloidosis  Associated with dialysis

o Cryopyrin-associated Periods Syndrome-associated Amyloidosis (CAPS)

o Hereditary Renal Amyloidoses  GROUP of conditions seen in families (specific mutations,

autosomal dominant)

o CNS Amyloidosis
 Beta-protein amyloid  Alzheimer’s
 Prion protein amyloid  CJD

 Cause: Unknown, but risk factors = chronic inflammation (e.g. RA), hereditary
  Features: Depends on organs affected, multiple systems often involved

o Cardiac (most common cause of death – arrhythmias + intractable heart failure)

 Affects all parts of heart
 Pericardial amyloid = pericardial effusion
 CAD amyloid = angina
 Myocardial amyloid = restrictive cardiomyopathy
 Electrical pathway amyloid = low voltage, heart block

 Syncope (marks the terminal stage of cardiac amyloidosis)

o Renal  Nephrotic syndrome

 Massive proteinuria (NB: can be <3.5g/day in some cases, but still presents like
nephrotic syndrome; still consider w/ any proteinuria esp w/ chronic inflame states)
 Normal or only slightly enlarged kidneys
 HTN is rare

o Hepatic  Hepatomegaly
 Rarely jaundice + cirrhosis
 LFTs normal, possibly raised ALP

o Neuro  Glove and stocking polyneuropathy

 Carpal tunnel
 Peripheral neuropathy (20%)

o GI  Poor motility and absorption of any part (oesophagus to colon)

o Haem  Spontaneous periorbital purpura (raccoon eyes)

o Thyroid  Firm, symmetrical, nontender goitre (resembles Hashimoto’s)

*Note the absence of hyperpigmentation, bronze diabetes (haemochromotosis) when considering the cause of
cardiomyopathy (and for amyloid cardiomyopathy, chronic inflammatory states are NOT needed)
 Ix:
o ECG  Low voltage DESPITE LVH (LVH should have large voltage – big clue to diagnosis)

o Urinalysis
 Proteinuria
 Light chains (on electrophoresis – essentially this is low levels of Bence Jones
protein which are immunoglobulin light chains)

o Blood
 FBC (anaemia)
 U+E (raised creatinine)
 LFT (raised ALP, low albumin)
 Inflammatory markers (raised ESR, normal CRP)
 Clotting (abnormal in 50% - INR or Factor X deficiency [PT/APTT])
 Blood film  Howell-Jolly bodies (splenic dysfunction)

o Renal USS  LARGE kidneys despite CKD (if renal failure is present)
 Only other large kidneys in advanced renal disease = Hydronephrosis, Diabetic
nephropathy, Acromegaly, Renal vein thrombosis

o Echo
 Ventricular thickening with reduced ventricle size
 Thickened intra-atrial septum
 Thickened valvular leaflets
 Speckled/granular myocardial appearance

o Cardiac MRI (very good test)

o Serum Amyloid P Scintigraphy (demonstrates distribution and amount of amyloid deposition

in the body without need for multiple biopsies!)

o Biopsy  Definitive histological diagnosis (diagnosis made in 80%)  RECTAL BIOPSY

 Biopsy affected organ (heart, kidney) OR rectum OR subcutaneous aspiration of
abdominal fat (best, preferred now)
 Red-green birefringence under polarised light with Congo red stain  DIAGNOSTIC

 Renal biopsy  Mesangial amyloid light chain protein deposition (lambda + kappa
chains) – light green staining in mesangium
 NB: Multiple myeloma = lambda + kappa light chains EXCRETED, not
deposited (but chains may block up tubules causing obstructive disease)

o Immunofixation electrophoresis  Determine what type of amyloidosis

 Rx: Only supportive treatment available

o CCF  Diuretics
 CCBs and Digoxin contraindicated as may be toxic at therapeutic levels
o Renal failure
 Fluid overload  Diuretics
 Anaemia  Epo
 Kidney transplant (will eventually recur in new kidney often >10yr though)
o Hepatic  Liver transplant
o Underlying inflammatory conditions  Treat on individual basis (e.g. RA)
o If AL  Chemo
o Stem cell transplant (must be <70, minimal heart failure, creatinine <177, <3 organs involved)
 No consistent evidence for stem cell transplant
Cardiac Tumours

 Types:
o Cardiac myxoma (usually in left atrium, hence Atrial Myxoma)  50% of cardiac tumours
 What is it:
 Polyp-like mass on pedicle usually coated in layer of thrombus
 Often in the left atrium, and often on the interatrial septum

 Features: Asymptomatic, usually incidental finding; can present like endocarditis

Triad of:
 Fever, tachycardia, SOB
 Embolic phenomenon (necrotic peripheries, mini-strokes…)
 Atrial plop (tumour plop) – impaction against endocard in atrial systole
 Clubbing

 Ix: ECG, CXR, Echo (pedunculated heterogenous mass typically attached to fossa
ovalis region of interatrial septum), Endocardial biopsy

 Rx: First line of treatment is immediate surgical removal

 Medical: B-blockers
 Surgical:
o Benign: Resection (1st line due to ↑↑ risk embolic phenomenon)
o Malignant: Heart transplant

o Secondary tumours (usually affect the pericardium; lung, breast, lymphoma)

o Rhabdomyoma (tuberous sclerosis)
o Papillary fibroelastoma
o Rare others

Dextrocardia

 Definition: Heart is situation on right side

 Types:
o Isolated dextrocardia  Heart is just pushed over more toward right (embryonic defect)
o Dextrocardia situs inversus  Heart (and JUST the heart) is mirror image on right side (this is
NOT situs inversus viscera)
 Cause: Kartagener’s (most common, see below)
 Situs inversus TOTALIS/Viscera + Bronchiectasis
 Ix: ECG, CXR, Echo (all can identify dextrocardia)
 Rx: Nil, but if defibbing must put pads on opposite sides!

Situs Inversus (Viscera)

 Definition: Major visceral organs are on opposite side in mirror image to normal
 Types:
o Situs inversus with dextrocardia (i.e. “totalis”)
o Situs inversus with levocardia (i.e. “incompletes”) – heart on normal side, other organs not
 *Associated with Kartagener’s syndrome  Dextrocardia + bronchiectasis + sinusitis
Rate and Rhythm Disturbances

 Disorder of SA Node

o Sinus Brady  HR <60, QRS <0.120 (normal)

 Cause:
 Normal variant
 Drugs (beta-blocker, verapamil, diltiazem, digoxin)
 Heart block (age, IHD)
 Ischemia (MIs  Sick sinus syndrome [poor SA node])
 Hypothyroidism, Hypothermia, Hypoxia

 Rx:
 Asymptomatic: Do not treat

 Symptomatic (light-headed, confusion) OR <40bpm OR hypotensive:

o First: (get cardiologist immediately, and transcut pacing equip)
 First line: Atropine 500mcg IV x6 doses max (3mg)
 ?600-1200mcg in first instance, then more as
necessary? (KH Blue Book) –check guidelines

 If hypotensive: Adrenaline 2-10mcg/min IV

o Second: Pace (First: Transcutaneous; Second: Transvenous ideally under

X-Ray guidance)

o Sinus Tachy (P wave present)  Cause: Everything and anything! Rx: Treat underlying cause
 AV Block/Heart Block**
o Causes for all:
 1st degree  Normal aging (common), athletes (common)
 All  Ischemia/Post-MI, drugs, structural abnormalities (e.g. valve disease)

o 1st Degree
 Definition: PR >0.2s, no dropped beats
 Rx: NO treatment – avoid AV node inhibiting drugs (e.g. b-blocker, CCBs, digoxin)

o 2nd Degree
 Types:
 Mobitz 1 (Wenckebach) – AV nodal hence normal QRS complexes
o Definition: PR elongating then drop
o Rx: NO treatment (unless post-MI and causing symptoms)
 Mobitz 2 – Infranodal (His/Purkinje) hence usually wide QRS complexes
o Definition: PR stable then drop
o Rx: PACE (progresses to 3rd degree)

o 3rd Degree – AV nodal OR infranodal (His/Purkinje)

 Definition: P-QRS disassociation, P-P + R-R constant, bradycardia
 Types:
 AV nodal:
o HR 45-60
o Narrow QRS (junctional escape rhythm – originates from AV node)
 P-waves will be inverted as atrial contraction occurs in
the backward direction if AV node is the primary
pacemaker
o Does not need urgent pacing if asymptomatic
 Infranodal:
o HR <45
o Wide QRS (ventricular escape rhythm – originates from ventricle)
o Haemodynamic compromise

 Pres (infranodal more severe):

 Bradycardia + Hypotension  Stokes-Adams Attack (sudden syncope)
 Cannon A(trial) waves (↑JVP from RA contracting against closed AV valve)
o These occur at IRREGULAR intervals
 Basal systolic murmur (patients develop constant background murmur)

 Treat:
 Symptomatic, Adverse signs (HR <40, BP <90, CCF), Risk of asystole (broad
QRS, ventricular pause >3s whilst awake/>5s whilst sleeping) 
Isoprenaline (then urgent pace) – beta agonist
o If hypotensive  Adrenaline
 Asymptomatic + none of other things above  Elective pacing
o NB: 3rd deg AV block associated with inferior MI often transient,
but may still requires pacing if HR remains slow after some time
o NB: 3rd deg AV block associated with anterior MI needs urgent
pacing irrespective of symptomatic/asymptomatic
o NB: Stable 3rd degree AV nodal block (HR 45-60) does not need
urgent pacing if asymptomatic, can DISCHARGE for ELECTIVE PPM
insertion (still need PPM as can progress unpredictably)
o Specific indications for pacing 2nd degree (Mobitz II) and 3rd degree AV block
 Symptomatic bradycardia
 Documented periods of asystole >3s when awake (this would make the HR at that
point 20BPM) or 5s when sleeping
 Any escape rate <40bpm in AWAKE patients (doesn’t count if asleep)
 Tachycardia Resus Council UK Algorithm
o First: Assess using ABCDE (in full)

o Are there adverse features?  Shock, Syncope, Myocardial ischemia, Heart failure

 Yes/Unstable  Synchronised DC shock x2 then Amiodorone

 No/Stable  What is the QRS?

 Broad (>0.12)
o Irregular
 AF with BBB
 Pre-excited AF
 Polymorphic VT (Torsades)

o Regular  VT, SVT with BBB/aberrancy, ?WPW

 Narrow
o Irregular  AF, AF with accessory pathway (irregular SVT-like)
o Regular  SVT or A-Flut
 1) Vagal manoeuvres
 2) Adenosine 6mg rapid IV
 3) Adenosine 12mg rapid IV
 4) Adenosine 12mg rapid IV (again)

 Restored rhythm?
 Yes  SVT
 No  A-Flut
 Supraventricular Tachycardia/SVT***  Definition: HR>100, QRS <0.120
o Paroxysmal Supraventricular Tachy  A type of AVNRT - (technically includes AF + A-Flut, but these
are generally considered on their own)
 Definition: Sudden onset ectopic tachy followed by abrupt cessation
 Cause: Re-entry @ AV node (hence why adenosine works – for AVNRT + AVRT)
 Pres: HR 130-200, narrow QRS, asymptomatic or syncope
 Key factors: No flutter wave, no fibrillatory wave, tachy (p-waves absent though)

 Ix: ECG (diagnostic)

 Others  Bloods (FBC, U+E [K+], Mg, TFTs), CXR, Echo
 Rx:
 Stable:
o First: Vagal manoeuvres (transiently ↑ AV block and may unmask
underlying rhythm, or may terminate rhythm in 25%! )
 Carotid massage (auscultate FIRST)
 Blow into syringe
 Valsalva
 Dip head in cold water OR eat/drink ice chinks
 Ocular massage (hard)

o Second: Adenosine 6mg/2sec, if no response in 1min then give 12mg

IV/2sec, and 12mg IV/2sec AGAIN (only for SVT)  Cures 90%
 ADENOSINE ONLY DRUG NEEDS TO BE PUSHED IN IV STAT, and
FLUSHED through
 Must push stat as it breaks down when touches blood

 Contra = asthma  If asthma: IV verapamil

 Verapamil is contraindicated in ANY wide QRS SVT
(e.g. SVT with abberancy, wide-complex WPW)
because the wide QRS indicates an accessory pathway
and verapamil will block the AV node thereby causing
shunting toward the accessory pathway thereby
worsening the arrhythmia, and flecainide may worsen
VT (if the wide-complex tachy was VT)

o Third: B-Blocker or CCB (verapamil or diltiazem)

 This is done in case the rhythm is actually atrial flutter (hence,
rate control is the management of choice)
 By the time this step is reached, expert advice should be sought

o Fourth: Digoxin

 Unstable (CP [ischaemia], SOB [CCF], ↓BP, Confusion [Syncope]): DC Cardioversion

 Long term: Beta-blocker e.g. sotalol (prevent), Ablation (cure)

o Multifocal Atrial Tachy

 Def: Electrical impulse generated in various places within the atria
 Cause: COPD (or other resp disease)
 Pres: HR 100-200, ECG (Irregular; P-wave shape + PR interval vary beat-to-beat)
 Irregular as may have variable block so QRS may conduct at random intervals but
AFTER p-waves
 Looks like 3rd degree HB, but is irregular (and P-waves perhaps going quite fast)
 Key factor: Changing morphology x3 in row, somewhat irregular
 Rx: Treat COPD, CCBs  DO NOT give B-Blockers (contra’d in pulm disease)
 Atrial Flutter (A type of SVT which falls into the category “atrial re-entrant SVT”)
o Def: Re-entrant rhythm which is regular w/ saw-toothed baseline + 2:1-5:1 AV block
 The re-entrant rhythm is within the right atrium

o Epidemiology: Much less common than AFib

o Types:
 Type 1 (typical)
 Baseline atrial rate ~300
 Subsequent 2:1 – 5:1 AV block (most commonly 2:1)
o The length of the circuit corresponds with size of RA, hence creating
predictable atrial rate at 300bpm (can be 200-400 though)
o 2:1 block is most common, giving ventricular rate of 150
 1:1 block is rare, often only seen in WPW when AV nodal
blocking drugs given – this leads to severe haemodynamic
instability and VT/VF
 Variable block – AV block may alternate between
2:1/3:1/4:1/5:1 giving an appearance like atrial fibrillation/AF,
but flutter waves present
 Anticlockwise re-entry in 90%
o Retrograde atrial conduction leading to:
 Inverted flutter waves in inferior leads (II, III, aVF)
 Positive flutter in V1 (may resemble upright P-waves)
(NB: the opposite is true in 10% of cases)

 Type 2 (atypical)  Baseline atrial rate >350 + less amenable to ablation

o Pathology:
 Atrial impulse occurs
 Some of atrial impulse travels down AV node to create QRS
 Some of atrial impulse travels back around the atria to then quickly meet again at
AV node
o AV node blocks
o Cycling of electricity continues
 AV node blocks at 2:1, 3:1, 4:1 (e.g. 4 re-entrant cycles AKA 4 p-
waves = 1 QRS)

o Features: Palpitations, syncope, angina, dyspnea, heart failure

o Ix:
 ECG (P’s present + saw-tooth, regular, 2/3/4:1 AV block [often 2:1 = 150bpm], narrow QRS)
 Can get VARIABLE BLOCK – swapping between e.g. 2:1, 3:1 and 4:1 blocks
 TOE (R/O LAA clot prior to DC cardioversion if flutter present for >48hr)

o Rx:
 Stable:
 First: B-Blocker or CCB (verapamil or diltiazem) or Digoxin
 Second: DC Cardioversion (MUST do TOE first if >48hr – rule out LAA clot)
o More effective than in AF so often less Joules can be used 
o Followed by 6wk warfarin
 Recurrent A-Flut: Catheter radiofrequency ablate (of tricuspid valve isthmus)

 Unstable or Failed Chemical: DC Cardioversion immediately

 Followed by 6wk warfarin
 Sometimes chemical [amiodarone, flecanide if no struc heart defects]

o Note:
 AV blocking meds + chemical cardioversion often unsuccessful 
 DC Cardioversion is followed by 6 weeks of warfarinisation
 Atrial Fibrillation/A-Fib/A Fib/AF*** (An atrial SVT)
o Def: Uncoordinated atrial activity leading to an irregularly irregular beat with disassociation
between the cardiax apex and radial pulse
 Source of ectopic electrical activity often pulmonary veins (whereas A-Flut =
tricuspid isthmus)

o Terminology/types:
 If LA size <5cm, more likely to be:
 Acute  <48hr onset
 Paroxysmal  Spontaneous termination within 7d, usually <48hr
o Recurrent  2+ episodes
o May degenerate into sustained forms
 If LA size >5cm, more likely to be:
 Persistent  Lasting >7d, or if does not self terminate (i.e. required rhythm
control)
o E.g. if DC cardioversion needed on D5 and successfully reverts, this
is still PERSISTENT
o May degenerate into permanent AF
 Permanent  >1yr and not terminated by cardioversion (if failed
cardioversion at 3mo, this is still PERSISTENT until it reaches 1yr)

 Other classification
 Recurrent  2 or more episodes of AF (usually paroxysmal, possibly
persistent [esp if needed cardioversion])
o This will require anticoagulation (whereas single episode will not)

o Epidemiology: Extremely common – most common sustained arrhythmia

o Cause: Atrial enlargement – CHAMP (just like thyroid mnemonic)

 Cardiac (HTN, Valvular disease, IHD/CAD, CCF), Thyrotoxicosis
 Holiday heart syndrome (excessive alcohol intake – binge drinking)
 Acute infections
 Metabol (↓Mg, ↓K)
 Pulmonary causes (COPD, PE, pulm HTN)

o Features: Spectrum – symptoms get worse as ventricular response gets faster/higher

 Asymptomatic (20%)
 Palpitations
 Heart failure
 Syncope

o Ix: ECG ± Holter monitor/Event recorder (if paroxysmal suspected)  No p-wave, irreg irreg
 CXR
 Echo (?LAA thrombus prior to cardioversion, ?LV function, ?LA size ?suitability for
cardioversion, ?valvular disease)
 CT/MRI if stroke...
  Rx: Paroxysmal = Always RHYTHM control, if persistent/permanent use below criteria
o Acute – Rate and Rhythm control:

 >65, Asymp, IHD/CAD  Rate Control (HR<80):

 First: B-Blocker or CCB (verap/diltiaz)  “Pill in Pocket”
o Bisoprolol  2.5-5mg PO (max 10mg PO)
o Diltiazem SR  60-90mg PO (max 180mg)

o Can give repeated doses of each to achieve max dose if not controlled as
long as BP syst >100
o CCB in asthma or if there is another B-Blocker CI

 Second: Digoxin (1st line in CCF ONLY; NOT for paroxysmal AF – exacerbates!)
o Loading: 500mcg PO, then 500mcg PO 6-8hr later, then 250mcg PO 6-8hr
later
Maintenance: 62.5mcg to 250mcg oD

*Rate control important as fast AF  Reduced diastolic LV filling time 

LA congestion  Pulmonary congestion  Flash pulmonary oedema

*If one medication doesn’t work alone, ADD the other (e.g.
bisoprolol/verapamil AND digoxin together)

 Third: Amiodarone
 Consider: Consider swapping b-blocker to sotalol?

Rate or rhythm control?

If >65, consider rhythm control for those who are SYMPTOMATIC as cardioversion aims to eliminate symptoms
If >65 and asymptomatic, rate control and anticoagulation is completely acceptable
 <65, Symptoms/unstable, severe CCF  Rhythm Control:

o Electrical: Nurse led service

 <48hr (stable or unstable): Heparin + Emerg DC Cardioversion (in A+E!)

 E.g. if palpitations for 36hr, cardiovert; 48hr is from FIRST onset of symptoms
 Perform under conscious sedation (e.g. in A+E) or GA
 Place pads in antero-posterior position (anterior pad slightly to right of chest,
posterior pad slightly to left of back)
 Must perform synchronised shock (press Sync button) otherwise risk of
precipitating VF if shock in refractory period
 Start 120-150J biphasic (200J monophasic), work up if fails
o NB: A-Flut = start 70-120J biphasic (100J monophasic)
 Hold shock button down until shock is delivered (may be delay to ensure synch)
 Post-cardioversion, NO further anticoagulation necessary (or ?4wk after – risk of
“atrial stunning” after DC cardiversion and risk of forming LAA thrombus)

 If fails: IV amiodarone 300mg in 10-20min, then 900mg in 24hr (as per ALS)

 >48hr + unstable: Rx dose heparin + Emerg DC Cardioversion

 If fails: IV amiodarone 300mg in 10-20min, then 900mg in 24hr (as per ALS)

 >48hr + stable:
 Option 1: Get TOE – if no clot, then heparin + DC cardioversion
o Continue warfarin for AT LEAST 4wk

 Option 2:
o Warfarin 3wk minimum
 Give Warfarin + bridge with Rx dose LMWH
 Continue until 3 consecutive weeks of INR therapeutic (2-3)

o DC cardioversion (100J then 200J then 360J then 360J with pads in AP

o Wafarin continues for MIN 4wk + weekly INR

 “Atrial stunning” occurs for few days after, and high risk of
developing LAA thrombus

o Amiodarone after also to help maintain sinus rhythm (for up to few

months!)

*Initial DC cardioversion has 80% success rate, but 40% relapse by 1 month and
80% by 1 year
*Sustained sinus rhythm most likely if AF <6mo (if >12mo = unlikely sustained sinus
– will revert back to AF eventually); young; small LA size
*Consider chemical agents PRIOR to DC cardioversion if cardioversion likely to fail

o Chemical:

 No structural problems/CCF/IHD: IV Flecainide 1-2mg/kg over 10min (max dose 150mg)

 Structural problems present (inc CAD): Amiodarone

 Can also use sotalol (young) as amiodarone has risk of epididymo-orchitis (infertility
– not good in young! But young more likely to have structurally normal hearts)
 Chemical sometimes used for 4wk before DC if high risk of DC failing (e.g. previous
failure/AF recurrence)
 o Surgical:
 Radiofrequency ablation
 For symptomatic paroxysmal AF unresponsive to medical Rx (both RATE and
RHYTHM control) – also for elderly! Not just young…
 Femoral vein catheter – IVC – RA – Puncture atrial septum – ablate LA + pulmonary
veins
o Risk of pulm vein stenosis, oesoph fistula, tamponade

 Alternative: Ablate AV node and insert pacemaker (sense atrial depol, pace ventricle)
 Makes people pacemaker dependent though

 Alternative: Close the LAA with a WATCHMAN device

 Deliver device by puncturing atrial septum and implant this net-like device to
occlude the LAA and therefore prevent clot formation in the area with the highest
implication of thrombus formation and subsequent embolic showering

Electrical of chemical first?  Can give chemical first, and if non-responder then DC cardioversion
For AF <48hr in young, chemical first (e.g. flecainide; no anti-coagulation needed) then if fails DC cardioversion
(with anticoag)
  Chronic - thromboprophylax: Warfarin or Dabigatran (better!) – SADCHAVS

 Oral anticoagulants
o Dabigatran (direct thrombin/F2 inhibitor – 110 or 150mg BD)
o Rivaroxaban (Factor Xa inhibitor – 15 or 20mg OD)
 Used more often for prophylactic and Rx DVT Rx
o Apixaban (Factor Xa inhibitor – 2.5mg or 5mg BD)

o All have more predictable anticoagulation effect + less regular monitoring

of INR + easier for patients to take
 Can only be prescribed by consultants

 Other notes regarding anticoagulation

o If single AF episode, then sinus  Can stop warfarin
o If second AF episode, then sinus (i.e. “recurrent”)  Warfarin life long

 Other considerations for definitive Rx:

 AV node ablation  Older patients with chronic/permanent AF (need perm pace)
 Atrial defibrillator (NOT an ICD – this is for ventricular arrhythmias)

 Notes:
o If paroxysmal AF with risk factor (e.g. alcohol, infection) spontaneously resolves  discharge with no Rx
o If paroxysmal AF with no risk factors spontaneously resolves  ?Rx – only if recurrent

NB: New guidelines state that if NO risk factors with AF (i.e. score = 0), then NO Rx preferred to aspirin
NB: New guidelines state that if ONE risk factor with AF (i.e. score = 1) then Warfarin/Dabigatran preferred to
aspirin! (“preferred to” means can still use aspirin, but most evidence says it is not as good)
 Wolff-Parkinson-White (WPW)**  An SVT which fits the category AVRT
o Def: Re-entrant rhythm where signal passes through AV node + Bundle of Kent:
 Orthodromic  Down AV node, back up BoK (10x more common)
 Antidromic  From atria to ventricle through the BoK, thereby bypassing the AV
node (hence short PR), but then back up AV node

o Epidemiology:
 Can occur from any age >20 (also affects older
people!)
 Most common ventricular pre-excitation syndrome

o Risk factors:
 MVP
 Cardiomyopathy (e.g. HOCM)
 Ebstein’s anomaly (see picture)

o Features: Episodic palpitations, dizziness, syncope

o ECG: Short PR (<.120), Slurred upstroke of QRS (delta

wave), Wide QRS, HR 150-250
 Pathophysiology of ECG in Pre-Excitation:
 SA node releases impulse
 Impulse travels down atria (P-wave formed)
o Some impulse travels down BoK without delay
o Some impulse travels down AV node with normal AV delay
 Impulse which travels down BoK causes delta wave – initial ventricular wall
depolarisation (through the muscle)
o This causes shortened PR interval since there was no delay (as
there would be at the AV node) for this electricity travelling down
BoK
 Impulse leaves AV node and travels down Bundle of His
o Now QRS becomes narrow, but since it started with the delta
wave it will overall be just a bit wide (slightly >120ms)

o Hence – short PR and delta wave can occur in BOTH orthodromic

and antidromic WPW (but when SYNDROME occurs i.e. the re-
entrant rhythm takes place, orthodromic more common)

 BoK impulse STOPS at ventricles

 There is NO re-entrant rhythm

 When AV pathway or BoK pathway gets taken over (due to refractory

times) then re-entry will begin and WPW SYNDROME will occur
o Often presenting with SYNCOPE/COLLAPSE
 Types:
o ECG Changes
 Type A (left-sided accessory pathway; with RAD)
 Delta wave + QRS complex upright in precordial leads (V1-V6)
 Dominant R wave in V1 (may be misinterpreted as RBBB or RVH) – positive
delta

 Type B (right-sided accessory pathway; with LAD) – more common

 Delta wave + QRS complex mainly negative in V1 + V2 (negative delta), but
positive in other precordial leads (resembling LBBB)

o Symptoms
 “Pre-Excitation”  WPW ECG but NO symptoms and NO tachycardia
 Occurs when impulse AV node reaches ventricles before impulse travelling
through the BoK (despite the AV delay at AV node)
 The impulse travelling through the BoK still creates the delta wave + wide
QRS as some early depolarisation occurs, but the impulse through AV node
predominates the cardiac depolarisation – hence, asymptomatic
 Since normal pathway dominates and refractory period sets in, merely get:
o SINUS RHYTHM
o Short PR interval
o Delta wave
o Slightly wide QRS

 WPW Syndrome  WPW ECG + tachycardia + symptomatic (e.g. syncope, collapse)

 Orthodromic: Narrow QRS (10x more common)
 Antidromic: Wide QRS
o One of few supraventricular causes of wide QRS – often mistaken
for VT – do NOT use flecainide or procainamide if in doubt of
diagnosis (but use if certain)
 Drugs to avoid in WPW Syndrome = ABCD (adenosine, B-
blockers, CCBs, Digoxin)
o Will still have P-wave, short PR and delta-wave (as with pre-
excitation)
o ↓PR + narrow QRS (+no delta) + SVT = Lown-Ganong-Levine
Syndrome (occurs without an accessory bundle, so ablation not an
option)
 Rx of WPW Syndrome:
o Acute episode – NARROW COMPLEX: SAME AS ANY SVT
 Stable – Medical Rx: (High efficacy )
 First: Vagal manoeuvres (Valsalva, carotid massage, splash cold water on
face)
 Second: IV Adenosine (NOT in asthma OR broad complex, but if given in
broad complex will not kill [so sometimes useful for testing ?SVT if thought
to be VT] unlike flecainide + verapamil which will precipitate VF)
 Third: IV Verapamil (NOT if broad complex/antidromic)
o Use flecainide first if patient has WPW with AF
o Digoxin contraindicated – accelerated tachycardias

 Unstable, or Refractory to Medical: Defib/Cardioversion

 Patients can enter VT/VF with bad WPW
 NB: Pts who DO NOT have AF are unlikely to enter VT – antidromic WPW
has wide QRS tachycardoa which looks like VT but is not (Rx with adenosine
still, not as per VT)

o Acute episode – BROAD COMPLEX or AF/AFlut also present with WPW:

 Stable: Flecainide – must be 100% certain this is SVT with broad complex!!!
 If VT cannot be ruled out: Amiodarone (before Flecainide)
 NB: May be hard to exclude VT – VT will kill, antidromic WPW less likely!
 Flecainide + verapamil will precipitate VF if actually VT and not WPW!

 Unstable: Cardioversion

o Chronic
 Medical: Flecainide (esp good for WPW with AF), amiodarone + verapamil, sotalol
(avoid if co-existing AF as prolongs refractory time at AV node, hence increases
transmission through accessory pathway, increased ventricular rate + risk of VT)
 Slow conduction rate
 Slow down refractory time of bypass tract
 Chronic medical Rx at reducing WPW episodes is unpredictable

 Definitive: RF catheter ablation of BoK (ALL symptomatic patients need this, and
some asymptomatic even [esp young]! 95% success rate)
 Young, No AF: Minimal risk, done early
 Concomitant AF: Inpatient RFA as HIGH risk of death due to VF

 Rx of WPW Pre-Excitation (asymptomatic):

o High risk profession (e.g. pilot, truck driver) OR FH SCD: Radifrequency ablation
o Low risk profession: Electrophysiological studies to stratify risk, then subsequent Rx
 Medicaly therapy first
 Ablative therapy if refractory

 Complications: Development of VF if WPW is

concomitant with AF
What does “unstable” mean with tachycardia rhythms?

 Signs of shock (BP <90, impaired consciousness)

 Syncope
 Myocardial ischaemia/chest pain
 Acute CCF

*These are all indications to DC Cardiovert a tachycardia rhythm in the FIRST instance (inc AF) WITHOUT
exceptions!

*Patients should be given IV UFH prior to emergency DC cardioversion to reduce risk of thromboembolism

*All SVTs can be differentiated by their P-wave presence + morphology (except WPW which has other classical
findings)
 Ventricular Arrhythmias***
o Ventricular Tachycardia/V-Tach/VT/Monomorphic VT
 Definition:
 Broad complex tachycardia originating from ventricular ectopic focus with potential
to RAPIDLY decompensate into VF + asystole (i.e. even if patient haemodynamically
stable, this is an extremely time-sensitive emergency)
 Must be at least 3 ventricular extrasystoles in a row @ >120bpm
o If 100-120BPM, termed “accelerated idioventricular rhythm”

 Cause:
 Ischemia (esp post-MI) – if patient in VT, MI = top differential
 Cardiomyopathy
 Metabolic/electrolyte deranged (K+, Mg, Ca)

 Features: Haemodynamically compromised, but not always (signs of heart failure)

 ECG: Wide, bizarre QRS complexes @ >120BPM (at least 3 beats)

 May see:
o Capture beats (ectopic focus stimulates SA node to make a normal beat,
and if ventricles are not refractory this will conduct through AV node and
cause narrow QRS beat)
o Fusion beats (where capture beat/normally conducted beat meets
ventricular conduction to create a superimposed beat)
o *see below for more on this*

 Left axis deviation (LV overpowers RV in ventricular rhythms)

 “Chest lead concordance”

o V1-6 all mainly positive = posterior wall ectopic focus for VT
o V1-6 all mainly negative = anterior wall ectopic focus for VT

 Sustained  >30s
 “Run”  <30s

 Types:
 Monomorphic  Constant QRS morphology (all look the same), 90% are >0.12s
width, regular aside from where fusion or capture beats seen
 Fascicular  Similar to monomorphic, but slightly narrower QRS (0.11-0.14s)
 RVOT origin VT  RAD + LBBB + VT pattern
 Polymorphic AKA Torsades  Risk factor is long QTc, and risk for this is:
o Congenital  Jervell-Lange-Neilsen OR Romano-Ward Syndromes
o Electrolytes  HypoCa, HypoMg, HypoK
o Drugs  Amiodarone, TCAs, dopaminergic drugs, methadone
o Other  IHD, SAH, Hypothermia
 Catecholeminergic VT  VT on exercise of emotional stress (e.g. fright, shock)
 Rx:
o Pulseless: Adult ALS  http://www.resus.org.uk/pages/alsalgo.pdf
 CPR + Emergency Cardioversion (exactly same as VF)
 Start at 150-200J biphasic, then subsequent shocks work-up to max 360J
 Give 3 shocks (1 immediately, then 2min apart), and if still in VT:
o Adrenaline 1mL of 1:1000 IV, AND
o Amiodarone 300mg IV, THEN

o 2 more min CPR, re-assess, shock if necessary, re-assess, AND

o Adrenaline 1mL of 1:1000 IV every alternate shock (i.e. every 3-5min)

o Pulse: http://www.resus.org.uk/pages/tachalgo.pdf
 Unstable: Cardioversion x3 SYNCHRONISED shocks (then IV amiod as above)
 NB: SYNCHRONISED shocks (shock aligned with peak of QRS) are used for ANY
unstable tachyarrhythmia WITH a pulse
 Stable:
 IV Amiodorone 300mg in 250mL D5W over 20-60min
THEN
 900mg further in 500mL D5W over next 24hr
IF STILL REFRACTORY after 24hr
 IV Lidocaine – bolus then infusion over 6.5hr (with caution in severe LVF)

 Co-administration of magnesium 8mmol (4mL of 50%) if hypomagnasaemic,

especially if refractory to amiod
NB: Flecainide and verapamil in stable VT may PRECIPITATE VF (hence if unsure
WPW/SVT or VT, Rx as VT as it is worse + giving WPW Rx would precipitate death in
VT!

o Chronic Management: Consider the following

 Implantable cardioverter defibrillator (ICD)
 Indications are:
o Sustained VT causing syncope
o Sustained VT with EF <35%
o Conditions complicated by non-sustained VT (i.e. VT run)
 MI
 HOCM
 LQTS
 Brugada syndrome
o Any EF <30% (with or without VT)

 Function:
o Anti-bradycardia pacing (like a normal pacemaker)
o Cardioversion shocks (to end VT – low energy – feels like a jolt)
o Defib shocks (to end VF – high energy – feels like kick to chest)

 Electrophysiological studies (EPS)

 DDx: SVT with aberrant conduction/aberrancy

VT SVT w/ Aberrant Conduction

AV disassociation (therefore will have
intermittent Cannon A waves)
Capture + fusion beats
(rarely seen, but presence =
pathognomonic)
Very broad complex (>160ms)
**Most important
Northwest axis
Does NOT respond to vagal maneouv
Chest leads have pos/neg concordance
i.e. all QRS either up or down
Cardiac history (e.g. CAD, MI, LV dysfunc
etc). If present, >95% chance = VT
AV still associated (A + V at same HR,
and no cannon A waves)
NO capture or fusion beats
(rarely seen in VT though so not helpful)
Borderline broad complex (just >120ms)
Normal axis
Responds to vagal manoeuvers
(blocks AV node)
Still has R-wave progression
No cardiac history, young

NB: Presence of BBB can be rate related, so not seeing BBB on previous patient ECG
does not rule out SVT w/ aberrant conduction
o Torsades de Pointes (TdP) AKA Polymorphic VT  V-Tach which gets larger and smaller
 Risk: LQTS, Drugs (anything dopaminergic or anti-arrhythmic)
 Congenital  Jervell-Lange-Neilsen (deaf) OR Romano-Ward Syndromes (not deaf)
 Electrolytes  HypoCa, HypoMg, HypoK
 Drugs  Amiodarone, TCAs, SSRIs, dopaminergic drugs, methadone, macrolides
 Other  IHD, SAH

 Bradycardia (often occurs in sinus bradycardic patients with long QTc)

 Rx:
 Pulseless: Treat at VF (ALS algorithm)
 Pulse:
o First: IV Mg EVEN IF Mg LEVEL IS NORMAL (serum Mg poorly reflects
intracell level)
o Then: Correct K+, Amiodarone
o If prolonged QT and bradycardia (if in terminating TdP): Temporary
pacing
 Pace 80-90bpm – this reduced QT, reduces chance to revert
back into TDP
 Do this ASAP if in and out of TDP + meets criteria (before
medical Rx)
 Complications: VF
 Note: Drug-induced TdP characteristically has small then large then small cycle (i.e. ceases
inbetween cycles, even if just for ONE sinus beat)
o

o Ventricular Fibrillation/V-Fib/VF (always going to be pulseless basically i.e. follow ALS pathway)
 Definition: Random ventricle contraction = poor CO  cardiac arrest/sudden death
 Risk: Post-MI, LQTS, Brugada
 Features: Heart failure symptoms

 Ix: ECG, blood (myoglobin, CK-MB, troponin, electrolytes inc K+ Mg Ca), etc

 Rx: Adult life support  CPR + Emergency Cardioversion

 Start at 150-200J biphasic, then subsequent shocks work-up to max 360J
 Give 3 shocks, and if still in VT:
o Adrenaline 1mg IV, AND
o Amiodarone 300mg IV, THEN

o 2 more min CPR, re-assess, shock if necessary, re-assess, AND

o Adrenaline 1mg IV every alternate shock (i.e. every 3-5min)
o Agonal Rhythm
 Definition: Slow, irregular, broad QRS complexes in dying patient, commonly seen in later
stages of an unsuccessful resuscitation attempt
 Complexes will eventually flatline into asystole


Advanced Life Support (ALS)

 Background
o What’s the point of an algorithm?
 Allow for rapid decisions in time sensitive emergency
 All cardiac arrest team members work from same
guideline, hence management is standardised and team members can predict next actions

o Chain of survival
 Early recognition + call for help
 Agonal breathing  Slow, sighing respirations
o Occurs early AFTER initiation of cardiac arrest (i.e. patient may be
arresting whilst agonal breathing present)

 Early CPR
 Technique for compressions  Good quality compressions related to outcome
o Centre of chest (middle of the lower half of the sternum)
o 5-6cm depth
o Allow full chest recoil before next compression
o 2/s (i.e. 100-120/min)
o 30 compressions – 2 breaths
 Once airway secured, continuous chest compressions and
asynchronous ventilation
o Swap compression provider every 2min to avoid fatigue

 Technique for respirations

o Start with high flow oxygen
 Face mask may be quickest
 Move to bag-valve-mask when available

 Get Guidel airway in ASAP w/ BVM

 Use LMA or iGel ASAP w/ BVM (can do continuous
compressions now)
 Intubation has no advantage over LMA or iGel, and is
more technically challenging (and unrecognised
oesophageal intubation is fatal)
o Avoid excessive ventilation/hyperventilation
o Consider capnography (can prove tube placement, quality of CPR, return
to spontaneous circulation)
 Rapid rise in end tidal CO2 = sign of return to life/circulation

 Other things
o Get IV access
 Can’t attain: IO access
 NB: Do NOT use central line unless patient ALREADY has a
patent one in situ
 Early defibrillation (in VF + VT)
 Attach ASAP (but do NOT interrupt chest compressions to attach)
 Once attached, pause chest compressions to assess rhythm
o Shockable  Shock + get medications ready
 VF – coarse or fine?
 Coarse – responds well to shock
 Fine – responds poorly to shock, progresses into
asystole (and often confused with asystole as chest
wall movement may give fine VF picture also – in this
case treat as asystole [as would be poor response to
shock anyway]) – high quality chest compressions in
fine VF may precipitate larger amplitude VF (good
thing) and hence increased response to shocking
o Non-shockable  Continue compressions + get medications ready
 Charge defibrillator WHILST compressions still occurring (i.e. you ONLY stop to
analyse rhythm – if for shock, continue compressions until charged then hands-off
again for shock delivery) – once charged, do NOT pause to re-check rhythm
 Deliver shock at appropriate energy (different for every machine)
o Use 150-200J biphasic starting, work up to 360J biphasic (or start 360J
monophasic)
o If unsure – use HIGHEST available energy; DO NOT delay shock deciding
what energy to use
 Post-shock IMMEDIATELY re-start CPR for 2 min
 ONLY check pulse when an organised rhythm compatible with life is present
 After third shock, give adrenaline (1mg IV) AND amiodarone (300mg IV) whilst
compressions occurring
o MUST flush with 20mL fluid
o Drugs are LESS important than good quality chest compressions and early
shocks (perhaps more importance in PEA/Asystole)
 Continuing resuscitation:
o VT/VF  attempt as long as patient remains in VT/VF – do NOT stop
attempting resuscitation
o PEA/Asystole  continue for 20min at least, always looking for reversible
causes (after 20min without identification of reversible cause, unlikely to
survive and reasonable to stop)

 Must reduce pre- and post-shock “hands-off” time as the longer spent not doing
CPR = reduced shock efficacy
 Post-resuscitation care
 Goals
o Normal cerebral function
o Stable cardiac rhythm
o Adequate organ perfusion
o Quality of life

 Post-cardiac arrest syndrome

o Brain injury  Coma, seizures, myoclonus
o Myocardial dysfunction
o Systemic ischaemia-reperfusion injury (sepsis-like response)
o Persistence of underlying pathology

 Tasks
o Get all obs
 Constantly monitor (including urine output)
 Consider arterial line for continuous BP monitoring (should
ALWAYS be present if patient transferred to ITU)

o A+B
 Controlled oxygen and ventilation (maintain 94-98% sats – NOT
higher)
 Ventilation ONLY if patient has low GCS post-arrest
 AVOID hyperventilation
 Monitor capnography aiming for normocarbia
 Check respiratory function via examination (broken ribs may
cause pneumothorax, or pneumothorax may be initial cause;
etc)
 Insert NG tube for decompression
 Following BVM ventilation or mouth-to-mouth some
air may go into stomach
 Decompression also improves lung compliance
 Portable CXR
 IV sedation (most will need this to maintain
intubation/mechanical ventilation – will also help with shivering
if therapeutic hypothermia to be conducted)

o C
 ECG monitor + 12-lead ECG (?MI)
 Assess cap refill
 Check for signs of CCF
 Get bloods (if not already taken during arrest)
 ABG – gives quick information on many reversible
causes (hypoxia, hyper/hypokalaemia, acid/base
status ?toxins)
 Venous bloods  FBC, U+E, CRP, Glucose, Troponin
 Echo
 Quantifies degree of post-arrest myocardial
dysfunction (i.e. weak heart despite optimal filling due
to reperfusion injury)
 Echo may help determine need for inotropes OR IABP
 A blood pressure should be attained to achieve urine
output of 1mL/kg/hr and normalising lactate
o D
 Therapeutic hypothermia (especially AVOID hyperthermia)
 Situations to use
o VF arrest  ROSC but unconscious still (most useful here – cool to 32-34
deg)
o Non-shockables after ROSC (may benefit)
 Contraindications
o Severe sepsis
o Coagulopathy
 How to use
o Induce  30mL/kg 4deg C IV fluid and/or external cooling
o Maintain (for 24hr)
 External cooling (ice packs, wet towels, cooling blankets or
pads, water-circulating gel-coated pads)
 Internal cooling (intravascular heat exchanger, cardiopulmonary
bypass)
o Rewarm slowly by 1 degree every 4hr
 Complications
o Shivering (which raises body temp)  Rx = sedate + neuromusc blocking
drugs
o Bradycardia + cardiovascular instability
o Infection
o Hyperglycaemia
o Impaired coagulation
o Reduced drug clearance
 Assess neurology (NB: successful CPR leaves patient without neurological compromise)
 GCS
 Pupils
 Limb tone and movement
 Posture

 NB: Neuro signs do NOT predict outcome within 24hr of ROSC

 NB: At 3 days the following have poor outcome associated:
o Absent pupillary light AND corneal reflexes (together)
o Absent or extensor motor response to pain
 Treat seizures (occur in 25% of patients who remain with low GCS)
 Attain glucose (aim for 4-10)

o E
 Look for and treat all possible underlying causes

o Further history
 Health before cardiac arrest
 Time delay before resuscitation
 Duration of resuscitation
 Cause of cardiac arrest

o Further tasks
 Discuss with relevant team/on call consultant; discuss with ITU
 Secure cannulae, tubes, etc
 Suction as necessary
 Regular monitoring by nursing staff
 Document
 Call family
 Re-assess yourself before leaving

o If patient dies – organ donation?

 Brain death, heart beating (DBD)
 Cardiac death (DCD)
o Reversible causes
 Hypoxia
 Attain airway
 Give high flow oxygen
 Do not hyperventilate (reduces coronary perfusion pressure = worse outcomes)
 Hyperkalaemia/Hypokalaemia
 Check latest lab results on system
 Check ABG
 Treat as per usual
o Hyper  Calcium gluconate, ins+dex
o HypoK/Mg  IV K+
 Hypovolaemia/hypotension
 Seek cause of hypovolaemia (e.g. inc surgical drains)
 IV fluids
 Hypothermia
 Check with low-reading thermomenter
 Treat with active re-warming (e.g. bair hugger, warm IV fluid, consider
cardiopulmonary bypass only if immediately available OR active re-warming
strategies fail)

 Tamponade
 Think of risk factors  Chest trauma, cardiac surgery
 Get urgent echo
 Rx with needle pericardiocentesis OR resuscitative thoracotomy
 Toxins
 Rare unless OD
 Check drug chart
 Tension pneumothorax
 Check tube position if intubated
 Resp examination (reduced breath sounds, hyper-resonant, tracheal deviation)
 Needle decompress to start (or thoracostomy [create incision] if chest wall is too
big for a cannula), then drain
 Thrombosis (PE, coronary thrombosis/ACS)
 If high risk PE, give thrombolysis
 If thrombolysis given, you MUST continue CPR for 60-90min before discontinuing
CPR (unless patient comes back before)
o Case reports demonstrating patients can come back from cardiac arrest
due to PE after this long without significant neurological damage
 Notes
o Predicting cardiac arrest
 50-80% deteriorate prior to cardiac arrest – hypoxia and hypotension are COMMON, and all
obs may start to worsen (high RR, tachycardia)
 Agonal breathing (patient may already be arresting)

o If someone can do USS at the arrest, reversible causes can be more readily identified
 What can be identified
 Tamponade
 PE
 Ischaemia (via RWMA)
 Hypovolaemia (IVC compression)
 Pneumothorax

 Where to put probe  Sub-xiphoid

 When to probe
 Place probe just before rhythm assessment
 Start scanning during rhythm assessment (only have 10s hence need well-trained
operator; can take Focused Echo Extended Life-support [FEEL] course)

o The crash team

 Team leader should be identified
 Should meet once a day with tasks allocated
 Directions should be clear
 E.g. “Dev – give 1mg adrenaline in 1 minute” (specific person, specific time, specific
instruction)
o Advanced decisions + DNAR
 Advanced decisions
 Should act on written or verbal advanced decisions (if patient competent)
o Written > verbal, but if repeatedly refuses treatment verbally this should
have same weighting
o However, if patient chooses to refuse life-sustaining treatment (e.g.
ventilation, BiPAP) their decision should be in writing
 If advanced decision is unknown, give CPR – can stop CPR if information on refusal
of treatment becomes available
 E.g.
o Friend says “don’t want CPR”, next week has arrest
 GIVE CPR (comment ?out of context)
o Find out friend had cancer + takes anti-depressants
 CONTINUE CPR (don’t know if palliative, if depressed may have
been lacking capacity)
o Next of kin says “stop CPR”
 CONTINUE CPR at least initially until you can involve the
consultant

 DNAR
 Most common reason for DNAR = futility – patient will have unacceptable QoL
following CPR
 Do NOT need to discuss DNAR with patients who are highly unlikely to have a
cardiac arrest OR patients who are at end of life (final stage of irreversible illness)
and CPR would be futile
 Aim to involve relatives, but if patient has capacity must respect if they refuse to
tell relatives
 If patient doesn’t have capacity use next of kin, and if not available then use IMCA
(Independent Mental Capacity Advocate) if not emergency and doctor’s belief of
best interest in emergency (it is accepted that there is a subjective element, but
discussion with other healthcare providers is essential to confirm decisions)
o Relatives CANNOT force CPR if doctor believes it will be futile
 DNAR (better/new term = DNACPR) is ONLY for withholding CPR, not other
treatments (otherwise this is palliative)

o Public places
 In UK there is NO legal obligation to offer medical assistance in public place
 If you stop to help, the legal situation changes and you assume duty of care
 There have been NO successful litigations against “good Samaritan” acts by doctors
in the UK
 This is NOT the case in Europe where it is MANDATORY to help

o Task management during an arrest

 Brief team (before patient contact ideally – crash team meets up and leader assigns role)
 If did not meet up, leader should be identified in 30s or less
 Give clear information
 Specific detail
 Specific structure
 Specific urgency
 Be honest
 Defibrillation BEFORE IV line + ABGs etc (i.e. do not delay – remove incomplete
cannulae/ABGs and SHOCK)
 Facilitating changing of compression giver
 Debrief team
 Fill out audit forms + any relevant incident reports
o ABCDE

o Special circumstances
 Types
 Anaphylaxis
 Asthma
 Electrolyte disorders (e.g. hyperkalaemia)
o If cardiac arrest – Rx hyperkalaemia DURING arrest (inc calcium
gluconate), consider haemodialysis DURING arrest if refractory to medical
Rx; give sodium bicarbonate (for hyperkalaemia and TCA OD)
 Hypovolaemia
 Poisoning
o E.g tricyclic – give sodium bicarbonate
 Pregnancy

o Statistics of cardiac arrest (in-hospital)

  Others
o Ventricular ectopics  Very common, can often be benign; No Rx unless symptomatic

o PEA + Asystole
 Background
 These are NOT shockable
 WORSE outcomes than VT + VF
 MORE common in hospital (VT+VF in community)
 UNLIKELY to recover from PEA/asystole unless reversible cause is found and treated
 PEA – rarely a perfectly straight line trace (if this occurs check lead placement)

 Management
 CPR 30:2
 IV Adrenaline 1mg immediately (continue every 3-5min) – this is the drug of choice
 Continue CPR without pausing during ventilation
 Consider reversible causes of PEA/Asystole (see below – H4 T4)
o E.g. if hypovolaemia present – Rx with fluids during arrest

o Peri-Arrest Rhythms – Bradycardia

 Broad complex CHB (narrow = much less risk; does not need urgent pacing unless
symptomatic or associated with ANTERIOR MI)
 Recent asystole
 Mobitz type II AV block
 Ventricular pause >3s whilst awake, of >5s whilst sleeping

o Reversible causes in cardiac arrest  4H + 4T

 Hypothermia
 Hypovolaemia
 Hypoxia
 Hypo/Hyper K+ (or other metabolic... Mg, Ca)

 Thrombosis (coronary or pulmonary)

 Tamponade (cardiac)
 Toxins
 Tension pneumothorax

**Biphasic defibrilliation used – needs much less energy for

successful defib than monophasic shocks (e.g. 150J vs 350J) – biphasic shocks therefore reduce the chance of
skin burns and myocardial damage
**Biphasic defib has a 90% first shock success rate in VF (vs 60% for monophasic)
Anti-Arrhythmic Drugs (Vaughan-Williams Classification)

 Class 1 – Na+ channel blockers (avoid in CAD/struc heart defect/CCF – ↑risk death; esp flecainide)
o 1A (fast channel blockers which affect QRS complex, lengthen cardiac action potential):
 Examples: Procainamide, quinidine
 Mechanism: Increases AP
 Uses: Ventricular arrhythmias, WPW
 Notes:
 Procainamide causes drug-induced lupus
 Quinidine (and quinine) causes cinchonism (headache, tinnitus, low plates)

o 1B (do NOT affect QRS complex, shorten cardiac action potential):

 Examples: Lidocaine, pheytoin
 Mechanism: Decreases AP
 Uses: V-Tach, AF

o 1C (do not affect cardiac action potential):

 Examples: Flecainide
 Mechanism: No effect on AP duration; slows down velocity of conduction
 Uses: AF, recurrent tachyarrhythmia with abnormal conduction (WPW)
 Contraindications: Structurally abnormal heart (CAST trial – 1989 – more death)

 Class 2 – Beta-blockers:
o Examples: Propranalol, metoprolol, atenolol, bisoprolol (NB: sotalol is Class 3)
o Mechanism:
 Beta-blockade (selective + non-selective [propranalol])
 Sinoatrial node blockade (mostly)
o Uses: Post-MI, prevent recurrence of tachyarrhythmias

 Class 3 – K+ Channel:
o Examples: Amiodarone, sotalol (also beta blocker), dofetilide
o Mechanism:
 K+ channel blockers; amiodarone has class 1,2,3,4 activity
 Widen cardiac action potential
o Uses: WPW (if with structural heart defects)
o S/E: Can prolong QT as they widen AP (as per all K+ channel blockers)

 Class 4 – Rate-limiting CCBs:

o Examples: Verapamil, Diltiazem
o Mechanism:
 Calcium channel blockade
 AV node blockade (mostly)
o Uses: Prevent recurrence of SVT, reduce ventricular rate in AF

 Class 5 – Unknown Mechanism:

o Examples: Adenosine, Digoxin, Mg Sulphate
o Mechanism: Unknown  Adenosine = AV blockade, Digoxin = K+ interaction
o Uses:
 Adenosine  SVTs
 Digoxin  CCF w/ AF
 Mg Sulphate  Torsades
Junctional Tachycardias

 Types:
o AV Nodal Re-Entrant Tachy (AVNRT)  Electrical signal MUST pass through AV node (e.g.
Paroxysmal SVT)
o AV Re-Entrant Tachy (AVRT)  Alternative pathways are made between the atria and
ventricles (e.g. WPW)
 Orthodromic  Atrial impulse passes through AV node, toward ventricles, back up
the atria, then toward AV node again (narrow QRS complex)
 Antidromic  Atrial impulse passes down accessory pathway, down ventricles
(wide QRS), up toward AV node, then around again to accessory pathway

 Notes:
o It can be EXTREMELY difficult to tell the difference between AVNRT (e.g. Paroxysmal SVT)
and Orthodromic AVRT (e.g. orthodromic WPW [most common form])

Sick Sinus Syndrome

 Definition: Collection of conditions with sinus node dysfunction with inappropriate atrial rate

 Cause: Idiopathic fibrosis (most common), fatty infiltration of SA node/AV node/His bundles/fascicles,
post-MI (RCA in 70%, LCX in 30%)

 Features: Episodes of:

o SA node blocks  bradycardia, sinus arrest (pt goes pulseless for short time period)
 Syncope
 Dizziness
 Faints
o AV node blocks  Heart block (2nd degree)
o SVTs  AF/A-flut, other SVTs
 Palpitations
 Embolic phenomenon (strokes from AF)

 Ix: ECG, Holter/24hr tape (often needed)

 Rx: Pace (Rx of choice)

Syncope

 Definition: Transient LoC caused by global cerebral hypoperfusion characterised by rapid onset, short
duration, and spontaneous recovery (i.e. excluding seizures, coma, shock)

 Causes:
o Neural mediated (AKA reflex syncope):
 Vasovagal (i.e. common faint)
 Situational (e.g. cough, sneeze, defecation, micturation)
 Carotid sinus hypersensitivity
o Cardiac (often during exercise)
 Arrhythmia
 Subclavian-steal
 Any cardiac disease (e.g. LVOT obstruction/HOCM/AS)
o Orthostatic hypotension (AKA postural hypotension)
o Autonomic problems:
 Diseases  Multiple system atrophy, PD, Diabetes
 Medication  Anti-HT
o Psychogenic  Factitious, anxiety, panic attack

 Ix: Score using the European Guidelines in Syncope score  BP + ECG + Bloods always
o Neural mediated/Reflex: Carotid sinus massage, tilt test, implantable loop recorder
 Do NOT carotid massage anyone with prior TIA or stroke (listen for bruits first)

o Cardiac:
 ECG ambulatory monitoring (e.g. Holter monitor, event recorder [e.g. Holter where
can press button to record when symptoms felt], external OR implantable loop
recorder, home telemetry)
 Implantable Loop Recorder – e.g. Reveal device
o Indications: REGULAR Syncope OR light headedness/dizziness OR
palpitations thought to be cardiac but not diagnosed on 24-hour
ECG or 30-day external monitor (i.e. so longer recording is needed
– ILRs can last 2-3yr)
 Especially indicated where ECG findings show risk factors
for arrhythmias (e.g. bifascicular block, long QT)

o Method: Size of pack of gum, implanted under skin over chest,

records arrhythmias in circular/loop memory, can store ~3
episodes, new episodes replace oldest, recordings made by
sudden rises/drops in HR OR patient activated
 Echo
 Angiography

 Rx:
o Neural mediated  Reassure these are benign
o Cardiac  Treat underlying defect
o Orthostatic
 Conservative: Stop offending drugs, raise bed head, hydration, support stockings
 Medical: Low dose fludrocortisone
Brugada Syndrome

 Definition: Genetic disease with abnormal ECG and increased risk

sudden death

 Cause: 20% due to SNC5A gene defect (codes for sodium channel;
most common abnormality)

 Epidemiology:
o More common in Asians
o 10x more common in MEN
 But genetic defects same in M/F
 Men have much higher penetrance (unknown why)

 Features:
o Syncope (most common presentation, due to runs of VT)
o Sudden cardiac death (often in sleep!)
o FH sudden cardiac death
o AF (20%)
o Nightmares + thrashing at night

o Classic ECG findings (ST elevation leads V1-3) – this is key to differentiate from ?HOCM
o Often unmasked by sodium channel blockers (e.g. flecainide)

 Ix:
o First: ECG (3 types, mainly ST elevation in V1-3, ?but may have completely normal ECG)
 Type 1: Raised J point with ST elevation, T-wave inversion V1 + V2
 Type 2: Saddle-backed ST segments with elevation
 Type 3: ST elevation only
o Second: Bloods (K+, Ca2+, Trop, SNC5A gene)
o Third: Echo (?Arrhythmogenic RVCM [must rule this out, can have similar ECG], ?HOCM)
o Fourth: Flecainide challenge/provocation (for ANY syncope w/o obvious cause, test for
channelopathies)
 This will unmask the classic ECG findings of Brugada syndrome or other channelop’s
o Fifth: Electrophysiology (test for inducible arrhythmias)

 Rx:
o Asymptomatic + No FH: Close monitoring
o Symptomatic OR FH sudden death: Implantable cardiac defibrillator (ICD)

o All patients with confirmed Brugada: Avoid competitive sports

 There is NO evidence for this, this is based on expert consensus that exercise
precipitates VT and VF so it is sensible to not exercise heavily

 Complications: Development of VT (inc polymorphic)  VF  Sudden death

 DDx: Other “inherited channelopathies”  E.g. inherited/congenital LQTS; HOCM

Pacing**

 Methods:
o Percussive/Percussion AKA Transthoracic mechanical
 Closed fist on left lower edge of sternum
 Strike this area (overlies the RV + IVC) at 10cm swing lengths
 Only use for interim in bradycardic cardiac arrest where electrical pacemaker is
being brought to patient
 Best if bradycardia with some output as saves patient trauma of CPR
 Should see a QRS complex – if not then move fist around precordium until
QRS generated
 If no QRS generated within a few seconds, start CPR

o Transcutaneous
 Give sedation + analgesia
 Apply defib pads to either under right clavicle and axilla (less preferred) or antero-
posterior over heart (more preferred, better success)
 Select pacing current (measured in mA) and increase until electrical capture is seen
(wide QRS, tall broad T-wave)
 Once capture seen, assess pulse to ensure electrical capture is associated with
mechanical capture
 Only use in emergencies (i.e. haemodynamically unstable) awaiting transvenous

o Transvenous
 This is a temporary measure
 Done for haemodynamically unstable patients
 Insert wire through vein into RA or RV – wire connected to pacer – pace
 Remove once:
 Permanent subclavicular pacemaker inserted
 There is no longer a need for pacing

o Epicardial
 During open heart surgery if patient enters AV block
 Place electrodes directly on epicardium
 Temporary measure until transvenous pacing achieved

o Subclavicular
 Permanent pacing measure
 Electrode wires pass through veins and connect to pacer which is inserted under the
skin below the clavicle
 Types:
 Single-Chamber
o One pacing lead
o One chamber of heart (atria or ventricle)
 Dual-Chamber (NB: different to bivent pacing)
o Two pacing leads
o One in atria, one in ventricles – mimics natural contraction
 Rate-Responsive
o Detects physical activity and automatically adjusts HR to fulfil
bodily metabolic needs

o Intracardial  New, wireless pacing inserted directly into myocardium (not available yet)
 o Biventricular (AKA Cardiac Resynchronization Therapy)  For severe heart failure with lack
of RV and LV synchronization (e.g. bundle branch blocks) leading to worsening of CCF
 Indications:

 Clinical  Refractory heart failure (NYHC III or IV) – i.e. medications maxed
AND
 ECG
o QRS >120ms (e.g. LBBB) especially if coupled with 1st deg AV block
OR
o Noticeable ventricular dysychrony on ECG
AND
 Other (more minor criteria)  EF <35%
BUT
 Cannot have arrhythmia (e.g. AF) – must be in sinus rhythm
 Why: Improves outcomes (↓mortality, morbidity – CARE-HF + COMPANION studies)
 How: Two leads, one through right side paces septum, left side lead paces LV,
coordinates with RV, sometimes has lead which senses RA also
 Other: Can be combined with ICD to protect against arrhythmia (known as CRT-D)

 Indications:
o Emergency/Acute  Start transcutaneous if dire emergency, then change to transvenous
 Asystole
 3s when awake
 5s when sleeping
 Symptomatic bradycardia
 Bilateral bundle branch block (i.e. bifascicular block) + trifascicular block
 Heart block – Mobitz 2 or 3rd degree HB w/:
o Symptoms (inc syncopal episode)
o Haemodynamic compromise
o BBB
o Following MI

o Elective:
 Refractory heart failure with LBBB (Bivent AKA CRT)
  Nomenclature: Four letters
o 1st: Chambers paced  Which chambers can receive an impulse to contract
 A = atrium can receive an impulse/contraction
 V = ventricle can receive an impulse/contraction
 D = both A+V

o 2nd: Chambers sensed  Which chambers are monitored for abnormal electrical activity
 A
 V
 D

o 3rd: Response to sensing  When the pacer detects electricity, what will it do?
 T = trigger an impulse
 I = inhibit an impulse
 D = have the capability for both T + I

o 4th: Rate modulation  If undergoing physical activity, can pacer respond by ↑HR?
 O = No
 R = Rate modulation – pacer CAN increase HR based on physical activity (detects
vibrations and increases HR (problems in Parkinson’s and shivering!)

*Cannon A waves can occur as a result of VVIR pacing  Ventricles may be paced, but since atria not sensed
the ventricles and atria may beat with disassociation, so if a A + V beat occur at same time then tricuspid will
be closed (due to overpowering pressure in RV to close tricuspid) causing a cannon A wave in JVP

*All pacemakers are now DDDR except for AF with (long pauses OR 3rd degree HB) which are VVIR
Other Pacing Notes

 Pacing the RV  Access via subclavian vein – SVC – RA – RV

 Pacing the LV  Access via subclavian vein – SVC – RA – Coronary sinus – Pass wire to LV region
o Coronary sinus is a collection of veins which gather blood after the coronary arteries and
return deoxygenated blood directly into the RA

 Pacing of LV causes RBBB; pacing of RV causes LBBB

o 20% of population may have PFO
o Pacing lead can theoretically pass through PFO to cause LV pacing when RV is intended

 What pacing based on ECG?

o Temporary pacing
 Often in context of CHB (e.g. post-MI or otherwise)
 Pacing spikes before each QRS rather than before each p-wave

o VVI
 Atria is not sensed nor paced, but ventricle is sensed and paced
 Will create pacing spikes before each QRS, and likely no P-waves present (unless
CHB)

o DDD
 Both right atria and right ventricle sensed and paced
 For when SA node not creating P-waves
 Will see pacing spikes before P-wave, and assuming normal AV node conduction will
have normal QRS without pacing spike OR may have packing spike also before QRS
(double pacing spike = definitive way of knowing dual chamber pacing)
 The ECG would be similar with an AAI pacemaker
Implantable cardiodefibrillator**  Restoration to sinus rhythm during arrhythmias (not constantly going)

 Indications:
o Episode of sustained VT causing syncope or EF <35%
o Previous MI due to VT/VF
o MI complicated by non-sustained VT (or sustained, but this is indication with or without MI)
o Familial conditions (e.g. LQTS, Brugada)
o HOCM with syncope

 Notes: Also known as “anti-tachycardia pacing” (though is not a pacemaker in the conventional sense)
Anderson-Fabry Disease

 Definition: Lack of a-galactosidase causing accumulation of glycosphingolipids in lysozomes

 Cause: Mutation at Gal gene at Xq22
 Features: LVH, Renal failure, Long-standing rash in bathing trunks distribution, strokes at young age

Marfan’s Syndrome**

 Definition: Inherited (auto dom) connective tissue disorder characterised by skeletal, dermatological, cardiac +
aortic, ocular and dural malformations

 Cause: Mis-sense mutation in chromo 15q21 gene encoding for fibrillin-1 (elastin-matrix glycoprotein)
o Inherited
o Sporadic (associated with increasing paternal age)

 Epidemiology: 2-3/100,000, affects all sexes + regions + ethnicity equally; prognosis 70yr old

 Features: Tall, thin, long arms + legs (arm span to height ratio >1.05), arachnodactyly
o Skin  Striae
o Heart + vessels  Aortic sinus dilation (90%) + AR (80%), MVP (75%), MR, AAA
o Eyes  Lens dislocation (superotemporal ectopia lentis; 75%), closed angle glaucoma
o Joints  Hypermobile
o Skeleton
 Pectus excavatum + pes planus
 Kyphoscoliosis
 Arachnodacytly
 Walker’s wrist sign (sounds rubbish!)
 Steinberg’s thumb sign (sounds rubbish!)
o Lung  Repeated pneumothorax
o Face  High arched palate, retrognathia

 Criteria: Ghent criteria  Green = Major criteria; Orange = Minor (non-spec)

 Ix:
o ECG  Aortic root dilation (?1st deg HB)
o Pelvic XR  Protrusio acetabula (50%!)
o Echo  Aortic root dilation (best for monitoring condition)
o MRI
 Spinal column  Dural ectasia
 Aorta  Measure dilation

 DDx:
o Ehlers-Danlos
o Fragile X
o Acromegaly
o Homocystinuria
 Fx: Learning difficulty, clots, no FH (recessive, Marfan’s =
Dom), epilepsy in 30%, inferior lens dislocation
 Ix=cyanide-nitroprusside test, homocysteine levels
 Rx=Vit B6/pryidoxine
o MEN 2b (Marfanoid phenotype + Follicular thyroid + Pheo)
 Rx: MDT – geneticist, ophthal, cardio, ortho
o Non-drug:
 Counselling
 Avoid vigorous activity + contact sports

o Drug:
 B-blockers (reduce MAP  Reduced aortic root dilation/rupture)
 ACE-I have emerging evidence

o Surgical: Aortic root graft (for root dilation)

 Prognosis: Much better now with BB + ACE-I therapy, and echo monitoring; death by aortic dissection + other
CVS disease
ECG Abnormalities

 Left axis deviation  LVH, Left anterior fascicular block, inferior MI

 Right axis deviation  RVH, left posterior fascicular block, PE
 LBBB
o Criteria:
 Rhythm must be supraventricular
 QRS >0.12
 QS or rS in V1, RsR’ + T-wave inversion relative to QRS in V6
 NB: if T-wave same direction, ?ischemia or MI

o Causes:
 Aortic stenosis, HTN
 DCM
 Acute MI, IHD
 Extensive CAD

o Rx:
 New LBBB in context of chest pain warrants PCI!

 RBBB
o Criteria:
 Rhythm must be supraventricular
 QRS >0.12 (or >0.10 for “incomplete block”)
 Terminal R wave in V1 (e.g. R, rR’, rsR’, qR)
 T-wave inversion relative to QRS in V1
 NB: if T-wave same direction, ?ischemia or MI
 Slurred S wave in lead I + V6

o Causes:
 RVH
 Pulmonary HTN (e.g. PE)

 Left anterior fascicular block

o Criteria:
 Left axis deviation (this will encompass the qR and rS essentially, so any LAD w/o
explanation = LAFB)
 qR in lateral leads (I + aVL)
 rS in inferior leads (II, III, aVF)

 Left posterior fascicular block (RAD w/o explanation)

 Bifascicular block  RBBB + (LAFB or LPFB)

 Trifascicular block  1st degree AV block + RBBB + (LAFB or LPFB)

o Risk: Can have episodes or can progress to CHB
o Rx: Cardiac telemetry and PPM insertion

*NB: Whenever a fascicle is blocked, conduction occurs to that area via the myocardium (e.g. in RBBB,
conduction and subsequent contraction of the RV occurs via trans-septal conduction of the LV
impulse through the myocardium to the RV) hence why conduction is significantly slowed
 Epsilon potential  Seen in ARV Cardiomyopathy, RV
dysplasia
o Seen in V1 + V2 (RV leads)
o Due to fat displacing myocytes

 U-wave  Hypokalaemia

 Reverse tick  Digoxin toxicity

 J-wave  Hypothermia

 Bigeminy
o Normal QRS followed by ventricular ectopic
o Benign in structurally normal hearts and people without CAD
o Pathological (increased risk arrhythmia and sudden death) in
those with CAD or structurally abnormal hearts

o Causes: CAD, LV dysfunction, Digoxin toxicity, normal variant

 Trigeminy
o Two normal QRS followed by ventricular ectopic
o Same significance as bigeminy (see above)
 Electrical alternans  Cardiac tamponade
o NB: Not to be confused with pulsus
anternans seen in heart failure
(alternating strong and weak beats
felt at the pulse)

 Capture beat
o In a ventricular arrhythmia (often VT), the ectopic focus causes a retrograde depolarisation
of the ventricles
o This can then stimulate the SA node to fire, causing synchronised atrial contraction and a p-
wave
o If the ventricles are not refractory at this point, then this beat will travel through the AV
node to cause a normal, narrow-complex QRS complex
o VT may continue afterwards

 Fusion beat
o Electricity from an ectopic focus and the normal cardiac pacemaker (i.e. sinoatrial node)
reach a particular area at the same time causing a bigger contraction (i.e. an ectopic beat
meets a capture beat in VT, or an ectopic beat meets a normal beat in someone who has
random ectopic beats)
o The resulting ECG change is a mix of both – the ectopic will be predominantly negative but
the capture/SA-originating beat will be positive, so the resultants will be a small wave
(usually slightly negative with a not-wide-but-not-narrow QRS complex)
 If in ventricles  Ventricular fusion beat
 If in atria  Atrial fusion beat

*Notice fusion beat still looks like a mini-VT complex as the VT wave will me the majority of the fusion
*Notice the capture beats look exactly like a normal QRS complex, and much different to that of the
VT complex


 Wave lengths:
o P-wave  0.12-0.2s

o PR interval (<0.2s)
 Prolonged  Idiopathic, athletes, IHD, Dig tox, hypoK+ and hyperK+ [rare], aortic
root pathology (e.g. abscess in endocarditis), Lyme, sarcoid
 Short  WPW, LGL
 Depressed  Pericarditis

o QRS  Normally 0.06-0.10s (acceptable is <0.12s = 3 small boxes)

 LQTS
o Causes:
 Genetics  14 genetic mutations which lead to LQTS (affecting K/Ca/Na channels)
 Romano Ward Syndrome (LQT1 – LQT6) – commonest
o Autosomal dominant

 Anderson Syndrome (LQT7)

 Timothy Syndrome (LQT8)

 LQT9-12

 Jervell and Lang-Neilsen Syndrome (JLN1-2)

o Autosomal recessive
o Deafness

 Drugs  Antihistamines (e.g. diphenhydramine), Anti-emetics (e.g. ondansetron),

Decongestants, Macrolides, Antipsychotics (esp typicals e.g. haloperidol), Sotalol
(causes TdP)

 Electrolyte disturbances (hypokalaemia, hypomagnesaemia)

o Ix  24hr tape, ?Reveal device

o Rx:
 Collapse with QTc <500: Beta-blockers (but NOT sotalol as this prolongs QT)
 Collapse with QTc >500 (i.e. high risk): ICD

 LVH  S in V1 + R in (V5 or V6 – whichever is bigger) >35mm

 RVH  R in V1 and S in V6 >15mm

 Normal variant ECGs in athletes

o Sinus bradycardia
o 1st degree HB + 2nd degree HB (Mobitz I/Wenckebach)

 Pulsus bisferiens  Double peak in the pulse per cardiac cycle; mixed AR + AS

 Pulsus paradoxus  Decrease >10 in BP during inspiration; Tamponade (NOT constrictive pericard)

 Pulsus alternans  Varying strong/weak pulse; LV failure

 Kussmaul sign  Rise in JVP on inspiration; constrictive pericarditis (NOT tamponade), restrictive CM
Endocarditis**
 Risk: DPIGS
o Structural heart  Prosthetic valve, Rheum valves (one of the biggest risk factors),
Congenital heart defect (repaired or not), HOCM
o IVDU
o GI  Colonic malignancy, chronic cholecystitis
o Pneumonia
o Dental surgery, poor oral hygiene
o (Previous endocarditis – biggest risk factor!)

 Pathogenesis: All vegetations consist of bacteria (non-sterile) AND platelets (sterile)

o Valves affected in decreasing frequency: Mitral  Aortic  M + A  Tricusp  Pulm (v rare)
o NB: IVDU get TRICUSPID (hits there first)

 Organisms:
o Staph
 Aureus (2nd most com; G+ coccus in grape-like clusters)  Risk: IVDU, Prosthet valve
 Most com when skin infection, abscess, or vascular access site (e.g. IVDU)
 Poor prognosis (30% mortality)

 Epidermidis (uncommon [1-3%] but most com 1st year post-valve surg [esp 2mo] +
may have delayed pres [e.g. 6mo post-surg but infection derived from events peri-
surgery) – e.g. without surgery, even Haemophilus is more prevalent than S epid

o Strep:
 Viridans (most com – 50%)  Risk: Oral surgery, poor dental hygiene
 Most com overall
 Better prognosis (5% mortality) than S aureus + neg-culture endocard
 E.g. S milleri (but this is a LARGE group of organisms)

 Strep bovis (3rd most com)  Risk: Colonic malignancy

 Intermediate-poor prognosis (15% mortality)

 Other streps (e.g. mitis – part of viridans group, after dental surgery)

o Others  Pseudomonas, HACEK organisms (culture negative), Fungi (Candida seen in IVDU
mostly), Non-infective  Libman-Sacks endocarditis AKA non-bacterial thrombotic
endocarditis AKA marantic endocarditis (e.g. SLE, cancer)
 Features: Fever (?few weeks), Murmur ONLY!  “Feel slightly off and under the weather”

o Systemic signs:
 Sore throat initially
 Weight loss + night sweats + loss of appetite

 TIAs (focal neurology)

 Lung infarcts (SOB at rest or on exertion)
 Spleen infarcts (enlarged spleen)
 Haematuria (renal infarcts)

o Possible signs (peripheral stigmata):

 Janeway Lesions  Macular, painless red/hemorrhagic lesions on hands and feet
 Osler Nodes  Painful and raised red lesion on hands and feet
 Splinter Hemorrhage  Vertical hemorrhage under nail
 Clubbing
 Roth spots  Retinal hemorrhage

 Diagnostic criteria – Modified Duke’s Criteria: Pathological Criteria OR 2 major OR 1 major + 3 minor
OR 5 minor

o PATHOLOGICAL criteria  Positive histology or microbiology at autopsy or cardiac surgery

o MAJOR criteria:
 Positive blood cultures
 Blood cultures x2 with TYPICAL organism (S viridans and HACEK)
OR
 Persistent bacteraemia from x2 cultures taken >12hr apart
OR
 X3 cultures (not 12hr apart each) where pathogen is less specific
OR
 Positive serology for Coxiella burnetii, Bartonella spp, or Chlamydia psittaci
OR
 Positive molecular assays for specific gene target

 Positive echo (new valvular regurgitation, oscillating structures, abscess formation,

dehiscence of prosthetic valves)

o MINOR criteria:
 Risk factor (e.g. predisposing heart condition or IVDU)
 Positive blood culture which does not meet major criteria
 Cultures x1
OR
 Atypical organism
 Fever >38
 Vascular phenomenon  Major emboli, splenomegaly, clubbing, splinter
haemorrhage, Janeway lesions, petechiae, purpura
 Immunological phenomenon  Osler’s nodes, Roth spots, glomerulonephritis
 Ix:
o First:
 Urine dip + MCS (haematuria ± proteinuria)

 Blood culture x3 taken >6hr apart each (i.e. need 18hr to collect)  >90% sensitive
(but cannot culture after ABx started)
 DO NOT do echocardiogram first
 Start empiric therapy AFTER culture taken, and if negative but positive
echocardiogram (vegetation seen) use FEVER, 1 RISK AND EMBOLIC
PHENOMENON to make diagnosis
 Cultures may not be useful if a patient has received empiric antibiotics prior
to culturing
 Cultures taken 6hr apart demonstrate CONSTANT bacteraemia – an
important feature of endocarditis
 Cultures DO NOT need to be taken from 3 separate sites (there is NO
evidence for this – PassMedicine)

 If antibiotics started already, patient not improving after some days, high
risk endocarditis: STOP antibiotics for 1 week, re-culture x3 taken 6hr apart
each (British Society for Antimicrobial Chemotherapy and European Society
for Cardiology)

 Other:
 ECG (1st degree HB = aortic root abscess  Must be Rx with valve replace)
 CXR

o Second: Trans-thoracic echo (TTE)  not as good as culture or TOE, but easy

o Best: Trans-oesophageal echo (TOE)  95% sensitive, not dependent on ABx use
  Treat:
o Empiric (waiting for culture): **Gentamicin mainly used to PREVENT penicillin resistance**!

 Native valve, non severe: Amoxicillin + Gent

 Native valve, severe: Vancomycin + Gentamicin

o After culture:
 MSSA: Penicillins (Flucloxacillin)

 MRSA: Vancomycin or Daptomycin (if VRSA also) + Rifampicin

 S viridians: Penicillins (e.g. BenPen)

 S bovis: Penicillins AND COLONOSCOPY (assoc with diverticuli/polyps/colon Ca!)

o Surgery?
 CONGESTIVE FAILURE FROM VALVE RUPTURE
 Uncontrolled infection
 Recurrent embolic phenomenon
 Large vegetations
 Aortic root abscess/vegetation causing 1st deg HB (i.e. presence of 1degHB = surg)
 Prosthetic valve endocarditis
 First: Treat any pulmonary oedema/major complications
 Second: Operate (metallic valve if young, bioprosthetic if old [as only has
10-15yr lifespan, therefore if young will need further high risk operation])
 Third: After operation, 4-6wk antibiotics

4-6wk Abx usually necessary

 Complications:
o Complete heart block
o TIA
o AKI
o CCF
o Painful swellings of fingers
o Bowel infarction
o Haematuria

 Prophylaxis: NO ANTIBIOTICS! METICULOUS ORAL HYGEINE, needle exchange programmes, etc

HACEK  Haemophilus, Actinobacillus, Cardiobacterium hominis, Eikenella corrodens, Kingella

These take longer to culture (up to 2 weeks)
Rheumatic Fever

 Cause: Group A Strep (Strep pyogenes)

 Presentation:
o Acute pharyngitis in recent past
o Febrile
o Symmetrical polyarthritis ± subcutaneous extensor surface nodules (e.g. elbows)
o MR (acute, then progresses to MS)

 Criteria: Modified Jones Criteria

o Major:
 Murmur (usually mitral, MR in acute stage, MS in chronic stage)
 Subcut nodules
 Arthritis
 Erythema marginatum (red geographical rash)  Rash moves day-to-day; may
leave white ring scar
 Chorea
o Minor - FLARE
 Fever
 Long PR (NB: consider endocarditis)
 Arthralgia
 Raised ESR/CRP

 Ix:
o ECG  1st degree HB (long PR)
o Throat swab
o Blood
 Raised WBC, CRP, ESR
 Anti-streptolysin O (ASO) titre  Peaks at 4-5wk post-pharyngitis
 Cultures
o CXR
o Echo

 Rx: Admit
o All cases: IM BenPen 1.2g
o If arthritis OR carditis present: Aspirin OR Naproxen
o If CCF: As per CCF

 Complications:
o Pregnancy may precipitate recurrence
o Higher risk endocarditis
o CCF
Other

 Cardiac disease in HIV/AIDS

o Conditions
 Pericardial effusions
 Endocarditis
 Myocarditis
 Pulm HTN
o Why
 HIV infection
 Cardiotoxicity of HAART

 Driving/DVLA in Cardiology
o HTN – can drive unless medication side effects
o Angioplasty (elective) – 1 wk
o Pacemaker insertion – 1wk
o CABG – 4wk
o ACS – 4wk (1wk only if successfully treated with angioplasty)
o Angina – Indefinite ONLY if episodes occur whilst driving
o ICD
 For sustained VT/VF – 6mo
 Prophylactically – 1mo
o Successful catheter ablation for arrhythmia – 2 days
o Aortic aneurysm >6cm – Still drive, need annual R/V
o Aortic aneurysm >6.5cm – Cannot drive
Paediatric Cardiology**
Common presentations in paediatric cardiology are:
Cyanosis  Must disting btwn resp and cardiac (NB: cardiac usually LACK of subcost/intercost
recession)
Heart failure
Heart murmur

Heart Failure (generally)

 Cause:
o L-to-R cardiac shunt (e.g. large VSD)
o Left sided obstruction (e.g. stenotic disease, coarctation, hypoplastic left heart)
o HOCM
 Features:
o Infant  Respiratory, hepatomegaly, failure to thrive
 General  Poor feeding, failure to thrive (fluid overload may put weight falsely
high)
 Left sided  ↑RR, cough/creps
 Right sided  Hepatomegaly
o Child  More similar to adult
 Ix: ECG, CXR, Echo (three tests for ALL congenital heart disease)
 Rx: O2, Diuretics, ACE-I

*LVH – occurs from CoA, PDA, VSD but NOT ToF (RVH) or ASD (RA enlargement)
*ECG – characteristic findings with AVSD, Tricuspid Atresia but NOT mild PS, PDA, VSD
Murmurs

Location Sound Diagnosis Features

Left clavicle/LUSE Continuous/Machinery PDA Acyanotic, fixed S2
LUSE Continuous/Machinery Total Anomalous Cyanotic 
Pulmonary Venous
Drainage
LLSE Pansystolic VSD Acyanotic unless
Eisenmenger’s occurs
LLSE + Apex (+ Heave) Pansystolic HOCM Acyanotic, brisk pulse
LUSE Ejection systolic Tetralogy of Fallot Cyanotic, RV heave
LUSE Ejection systolic ASD Secundum Primum: +Pansystolic
ASD Primum Secundum: +Mid-
diastolic

Both: Fixed wide split S2

Between shoulder blades - Coarctation of the Aorta Weak/absent femorals
BP (arm) >> BP (leg)
*LUSE – left upper sternal edge
NB: Benign murmur are SSSSS: soft, systolic, symptomless, S1/S2 normal, Special tests (ECG/CXR/Echo)
normal, NO THRILL, NO RADIATION
Congenital Heart Disease

Acyanotic Cyanotic
PDA Tetralogy of Fallot
ASD Transposition of Great Arteries
VSD (without Eisenmenger’s) Tricuspid Atresia
HOCM Total Anomalous Pulmonary Venous Drainage
Aortic Stenosis Hypoplastic Left Heart Syndrome
Coarctation of Aorta
Circulatory Adaptations at Birth

 Before birth
o Oxy blood from placenta  Placental vein  Bypass liver via ductus venosus  RA
 RA  Foramen ovale  LA  LV  Ascending aorta
 RA  RV  Pulmonary artery  Ductus arteriosus  Descending aorta
 RA  RV  Pulmonary artery  Pulmonary system (small amount)
 After birth
o O2 inhalation  closure of ductus arteriosus (ligamentum arteriosum now)
o O2 inhalation  pulmonary artery vasodilation  ↑pulmonary blood flow  ↑pulmonary
vein return to LA  closure of foramen ovale (fossa ovalis now)

NB: Only functional closure occurs now, TRUE closure of ductus arteriosus occurs by 3wk

PROSTAGLANDIN E1 (Alprostadil, Misoprostol) MAINTAINS PDA

INDOMETHACIN CLOSES PDA

NB: COMPLICATIONS OF ALL CONGENITAL HEART DISEASE IS: Poor growth, heart failure, endocarditis
Acyanotic Congenital Heart Disease: Patent Ductus Arteriosus

 Normally, DA becomes Ligamentum Arteriosum

 Definition: Failure of DA to close in 24hr post-birth (normally closes by 24hr, fully shuts at 3wk)
 Presentation:
o Small patency: Asymptomatic
o Large patency:
 Machinery murmur (continuous – sounds like a train with regular gushes)
 Heard at upper left sternal border
 Continuous murmur heard because aortic pressure > pulmonary pressure
in both systole + diastole hence blood travels BACKWARD across PDA
 As RVH ensues due to pulm HTN, RV > LV pressure, diastolic component of
murmur lost, then murmur completely lost when pressures equal (severe
disease and may now progress to cyanosis/low sats)
 Bounding pulses distal to the PDA with collapsing element
 SOB, poor leg perfusion (as deoxygenated blood is being sent there)
 Ix: ECG, CXR, Echo
 Rx:
o Asymptomatic: Observe
o Symptomatic:
 Conservative: Fluid restriction + O2 + Diuretics
 Medical: NSAID  Indomethacin, ibuprofen
 USE FOR <1yr (best for pre-term)
 Surgical – Best for term: Ligation  Cardiac cath + insertion of SPRING OCCLUDING
COIL
 USE FOR >1yr (as indomethacin will not be effective)
Acyanotic Congenital Heart Disease: Atrial Septal Defect (ASD) (Surgery in all cases)

 Types: L-to-R shunt

o Ostium Secundum  More common (70%), less serious, located at MID-ATRIA

 Pathology: ASD in foramen ovale area

 Features: Asymp until 3-5th decade (?early heart failure, paradoxical stroke from DVT), wide
fixed split S2, eject systolic + mid-diastolic (for secundum only), triphalageal thumbs (Holt-
Oram syndrome)

 Ix: In adulthood, RBBB with RAD

 Rx: Surgery in ALL cases, even if asymptomatic

o Ostium Primum  Less common (30%), more serious, located at BOTTOM of atria (hence can also
interfere with AV node)

 Pathology: Endocardial cushion defect affects AV valves; DOWN SYNDROME

 NB: All babies w/ Down Syndrome MUST be Echo’d (irrespective of symptoms)
o 50% have CHD, many with AVSD (ostium primum)

 Features: Asymptomatic (small)  Heart failure (large); wide fixed split S2, eject systole
 Presents at 10-20yr

 Ix:
 ECG – In adulthood
o RBBB with RAD = Secundum (more benign)
o RBBB with LAD = Primum (more worrying; DDx Trifascicular block)
 CXR
 Echo

 Rx: Surgery in ALL cases

 Complications in adulthood if not treated: 50% dead by age 50

o Eisenmenger’s in adulthood (pulmonary vascular and right heart pressures reach systemic pressure and
L-to-R ASD shunt turns to R-to-L [as systemic circulation now path of least resistance] and
deoxygenated blood enters systemic circulation – CYANOSIS)
 Poor prognosis
 Presents with SOB, cyanosis, clubbing in adulthood
 May cause polycythaemia
 Must NOT get pregnant – risk of maternal mortality
o Paradoxical emboli for stroke
Acyanotic Congenital Heart Disease: VSD (most common CHD, majority close spontaneously)

 Features: L-to-R shunt

o Asymptomatic (L-to-R shunt)  Heart failure  Cyanosis (Eisenmenger’s – R-to-L shunt)
o Panysystolic murmur at LLSE which does NOT change with inspiration/expiration
 Ix: ECG, CXR, Echo
 Rx: Majority close spontaneously
o Medical: Treat heart failure (O2, diuretics, digoxin, ACE-I)
o Surgery if severe heart failure, pulmonary HTN, cyanosis

 Complications in adulthood if not treated:

o Eisenmenger’s in adulthood (right heart pressures reach systemic pressure and L-to-R ASD shunt turns
to R-to-L and deoxygenated blood enters systemic circulation – CYANOSIS)
 Poor prognosis
 Presents with SOB, cyanosis, clubbing in adulthood
 May cause polycythaemia
 Must NOT get pregnant – risk of maternal mortality
o Paradoxical emboli for stroke
o Biventricular hypertrophy
Acyanotic Congenital Heart Disease: Coarctation of the Aorta (Balloon dilatation or graft)

 Definition: Constriction of the aorta distal to the left subclavian (98% of cases)
 Types:
o Infantile pre-ductal  PDA supplies blood to ↑volume + O2; when closes – leg cyanosis
 NB: even though PDA blood “deoxygenated”, some O2 is still carried 
o Child onset juxta-ductal  Less severe as heart grown properly
 Risk: Turner syndrome (45X)  90% of child onset coarctation
 Features: Asymptomatic  Heart failure in adulthood
o “Hypertension in the upper body, hypoperfusion in the lower body”  BP Arm > BP Leg
 BP R-Arm > BP L-Arm (if pre-left subclavian)
o Commonly has aortic regurgitation due to common association with bicuspid aortic valve
o Continuous murmur over thoracic spine if VERY stenotic coarctation (<2mm)
o May go unnoticed, collateral supply develops to leg and becomes asymptomatic!

o Radiofemoral delay (esp if coarctation distal to L subclavian [i.e. most of time]), but can get radio-radial
delay if pre-left subclavian
 Ix: ECG, CXR, Echo  CXR may show rib notching (often seen in ADULTHOOD)+ “3 sign”
 Rx:
o Neonates:
 First: Maintain PDA w/ Prostaglandin E1
 Second: Surgery
o Child:
 First: Treat HTN
 Second: Surgery in ALL cases, no exceptions! (NB: Surg may NOT
cure HTN)
 Balloon dilation
 Resect affected area + graft
 Complications:
o High risk for endocarditis
Acyanotic Congenital Heart Disease: Aortic Stenosis

 Types:
o Supra-aortic (least common – e.g. William syndrome)
o Aortic
o Sub-aortic (IHSS/HOCM)
 Features: Most have bicuspid aortic valve; EJECTION SYSTOLIC
o Infant  Heart failure, collapse
o Child  Syncope, chest pain on exertion
 Ix: ECG, CXR, Echo
 Rx: Balloon dilatation if symptomatic or severe, sometimes valve replacement

Acyanotic Congenital Heart Disease: HOCM (young teenagers)  See Cardiology

Cyanotic Congenital Heart Disease: Tetralogy of Fallot

 Most common cyanotic heart disease

 4 Cardinal Features:
o Pulmonary stenosis
o RV hypertrophy
o Large VSD
o Overriding aorta

 Features: E.g. Cyanotic spell in 3mo old after feeding, was sweaty, worsened w/ crying
o Cyanosis usually NOT present @ birth, usually at ~3mo or so
 Pulmonary stenosis is the most important factor
 Age of presentation is dependent upon degree of pulmonary stenosis (often worsens with
age)
 CAN present @ birth if PS severe; RVH will make PS worse hence some present later
o Paroxysmal hypercyanotic spells, especially during exertion (feeding, crying)
o Sweating
o SOBOE (resp signs WITHOUT chest recession), Heart failure, Fail-to-thrive, murmur

 Ix: Hyperoxic test (↑O₂, sats do not improve but should with resp disease) ECG, CXR (for resp disease; may show
“boot shaped heart”), Echo (not always readily available)
o NB: With hyperoxic test must cease test ASAP if sats do not rise or else PDA will close

 Rx: Consider Abx for ALL blue babies (pneumonia, Mec Asp Synd, etc)
o First: Place child w/ knees to chest (↑SVR therefore ↑pulmonary circulation )
o Second – Medical
 In neonates: Maintain PDA w/ IV Prostaglandin E1 (if at birth – will not work later)
 NB: PDA is aortic  pulmonary = more oxygenation
 In >1mo: Propranalol + refer for surgery
o Third – Surgery:
 Immediately: Blalock-Taussig shunt to delivery more blood to pulmonary circulation
 At 6mo+: Corrective surgery
Cyanotic Congenital Heart Disease: Transposition of the Great Arteries (ToGA)
*Second most common cyanotic heart disease, but most common cause of cyanosis at birth

 Features:
o Cyanosis in first few hours – days (@closure of PDA/FO)
o Hypoxia (PaO2 VERY low)
o Murmur, CXR “egg-on-string” appearance
 Wide cardiac silhouette, thin pedicle
 Ix: Hyperoxic test, ECG, CXR, Echo
 Rx:
o First - Supportive:
 Keep warm
 Correct acidosis + hypoglycemia
o Second - Medical: Maintain PDA + PFO w/ IV
Prostaglandin E1 (ALPROSTADIL)
 NB: PDA is pulmonary  aortic! (different) = more oxygenation
o Third – Surgery:
 Immediately:
 Balloon atrial septotomy (i.e. make big ASD)
 Subclavian Artery  Pulmonary artery SHUNT (Blalock-Taussig Shunt)
o This puts MORE blood into lungs which then passes through FO
 >2wk old: Corrective switch
Cyanotic Congenital Heart Disease: Hypoplastic Left Heart Syndrome (HLHS)

 Definition: Underdevelopment of left heart forcing right heart to supply both pulmonary + systemic
circs

 Mechanism:
o RV  Pulmonary vessels  LA (nearly fully blocked mitral valve)
o LA  PFO/ASD  RA  RV  Pulmonary vessels  PDA  Systemic perfusion

 Features:
o Cyanosis in first few days
o Heart failure + collapse in first couple weeks of life
o Weak peripheral pulses

 Ix: Hyperoxic Test, ECG, CXR, Echo

 Rx:
o First: Maintain PDA + FO w/ Prostaglandin E1
 NB: PDA goes FORWARDS as no aortic pressure
o Second: Surgery
 Reconstruction: 2-3 steps which correct the heart
 Definitive: Transplantation
Cyanotic Congenital Heart Disease: Tricuspid Atresia

 Definition: No connection between RA and RV

 Mechanism:
o RA  PFO  LA  LV
 LV  Aorta
 LV  VSD  Pulmonary system

 Features: Cyanosis in first few days to early months of life

 Ix: Hyperoxic test, ECG, CXR, Echo

 Rx:
o First: Maintain PDA w/ Prostaglandin E1
o Second: Surgery

Cyanotic Congenital Heart Disease: Total Anomalous Pulmonary Venous Drainage (TAPVD)

 Definition: Pulmonary veins drain into RA, so only blood through PFO enters left heart
 Features: Cyanosis in the first few days of life
 Ix: Hyperoxic test, ECG, CXR, Echo
 Rx:
o First: Maintain PDA w/ Prostaglandin E1
o Second: Surgery (insert PVs into LA)