Acute coronary syndrome D: spectrum of acute myocardial Hypertension Diagnosing hypertension

ischaemia or infarction • If clinic BP ≥140/90, measure

again after 5 min, measure on
Stage 1 HTN Stage 2 HTN Stage 3 HTN
STEMI: ECG+ve [ST- NSTEMI: ECG inconclusive Unstable angina: normal R: • Unmodifiable: ↑age, males, FHx Clinic BP ≥140/90 Clinic BP ≥160/100 Clinic BP ≥180/120
both arms, and check cuff
elevation], trops+ve [normal or other ∆], trops+ve ECG, normal trops • Modifiable: smoking, DM, HTN, placement
ABPM ≥135/85 ABPM ≥150/95 = HTN crisis
hypercholesterolaemia, obesity • Use ambulatory BP monitoring
Treat (ABPM) to Dx (clinic BP - white
STEMI criteria – ≥20 min s/smx, ECG features in ≥2 contiguous leads coat syndrome)
• 2.5 mm ST elevation in V2-3 in men ≤40yo, or ≥ 2.0 mm in men >40yo P: • Atherosclerosis in coronary vessels Treat if <80yo AND • target organ damage • Alternatively, home BP
• 1.5 mm ST elevation in V2-3 in women 2/2 endothelial dysfunction (smoking, • established CVD, AKI/CKD, T2DM monitoring – 2 readings in the
• 1 mm ST elevation in other leads • new LBBB (always pathological) HTN, hyperglycaemia) • 10y cardiovascular risk ≥10% morning, 2 at night, for 4-7d
• Plaque formation causes physical
S/Smx: angina at rest (>20 min) not relieved by GTN. Gripping/heavy pain, a/w blockage → ↓blood flow to without T2DM
nausea, sweating, dyspnea, palpitations, etc myocardium → ischaemia & angina Ix: Fundoscopy, urine dipstick,
• Plaque rupture may cause complete +T2DM <55yo, ≥55yo Black ECG, bloods (FBC, U&Es,
occlusion → myocardial infarction not black HbA1c, lipids, etc)
Ix: ECG, ABG, bloods (trops, FBC, lipids, HbA1c, U&E, LFT, TFT), CXR, echo,
blood glucose Hypertensive retinopathy
1. ACEI / ARB CCB
ECG cardiac territories • Grade I: barely detectable arterial
narrowing
All: Aspirin 300 mg, O2 if sats <94%, paracetamol 1g PO/IV [morphine if severe I aVR V1 V4 2. + CCB or thiazide-like + ACEI or ARB [if black] • II: obvious narrowing + focal
Mx pain only], GTN 1 spray (caution hypotension), ± ondansetron 4 mg IV irregularities
Lateral Anterior/ • III: flame haemorrhages, dot and blot
3. all classes (ACEI/ARB + CCB + thiazide)
= LCir septal = LAD haemorrhages, hard and soft
PCI possible within 2h no Fibrinolysis
+ spironolactone if K ≤4.5 mmol/L exudates, cotton wool spots
• Prasugrel • Alteplase etc II aVL V2 V5 4. • IV: papilloedema
STEMI: or + alpha/beta-blocker if K >4.5mmol/L
- clopidogrel if pt is on PO anticoag + antithrombin
(1) <12h of smx Inferior Lateral Lateral
- ticagrelor if pt is high risk bleeding • Thereafter,
AND = RCA
• Obtain radial access (preferred to ticagrelor
(2) is PCI possible D: persistently raised BP Antihypertensives: side effects
femoral) • If no ECG
within 2h? III aVF V3 V6
• UFH + bailout GPIIb/IIIa inhibitor resolution after
• PCI: Drug eluting stent 60-90 min, PCI Lateral R: obesity, metabolic syndrome, ACE-inhibitors: dry cough (15%; usually in 1st year

If pt presents >12h but has ongoing smx of STEMI or has cardiogenic shock, V1-6, aVL = Proximal LAD
↓exercise, ↑alcohol, DM, black ancestry, of starting), angiooedema, hyperkalaemia, first
dose hypotension
>60yo, FHx (HTN, CKD), sleep apnoea
consider sending for PCI anyway • If dry cough develops, switch to ARB
Posterior STEMI: • Avoid in pregnancy & breastfeeding
Low risk (≤3% 6mo mortality): fondaparinux & ticagrelor • Reciprocal V1-3 changes Aetiology: • CI/caution in renovascular disease (eg bilateral
NSTEMI Int/high risk (>3%): - ST depression • Essential HTN - no specific cause renal artery stenosis) and aortic stenosis,
(1) GRACE • If unstable: PCI immediately (see STEMI PCI) - tall, broad R waves • Secondary HTN hereditary idiopathic angioedema
≤3% or >3%? • If stable, PCI within 72h + give fondaparinux, prasugrel or - upright T waves - Primary hyperaldosteronism • May cause ↑creatinine (up to 30% acceptable)
ticagrelor, and UFH • Confirmed by ST elevation and Q waves in - Renal disease, eg glomerulonephritis,
posterior leads (V7-9) renal artery stenosis CCBs: Verapamil - constipation, hypotension,
GRACE score predicts all-cause mortality 6mo after discharge for ACS - Endocrine disorders, eg Cushing's, bradycardia, flushing; caution in HF
Unstable angina & 2' prevention (lifelong): (6As) aspirin 75 mg od, another Inferior MIs are a/w AV block phaeochromocytoma, acromegaly • Diltiazem - hypotension, ↓HR, ankle swelling,
- Drugs, eg steroids, COCP caution in HF
❗️
antiplatelet for 12mo (eg clopidogrel), atorvastatin 80 mg od, ACEI (eg ramipril), - Others: pregnancy, coarctation of the
atenolol (or bisoprolol), aldosterone antagonist for HF (eg eplenerone) DDx: DO NOT give verapamil & diltiazem with βB -
• Global T wave inversion: think non-cardiac aorta may result in heart block
Other notes Complications "DREAD": death, rupture of cause • Amlodipine, nifedipine, etc - flushing, HA, ankle
• MI a/w cocaine use: add IV myocardium, edema, arrhythmia and • Pericarditis: global ST elevation Other notes on Mx: swelling, reflex tachycardia. No issues with HF.
benzodiazepine, ?avoid βB aneurysms, Dressler's syndrome • PE: sinus tachy (most common), S1Q3T3 • DM: ACEI/ARB best
• Diet: Mediterranean style diet. • CKD: ACEI/ARB first line. Furosemide Thiazide-like diuretics: hypoK, hypoNa, hyperCa,
No rec for omega-3 or fish Post-MI ACS risk stratification using Killip classes useful in GFR<45 - monitor for gout, impaired glucose tolerance, impotence
• Exercise: 20-30 min daily I: no clinical signs of HF 6% Mean arterial pressure = dehydration • Rarely, pancreatitis, ↓platelets, agranulocytosis,
• Sex: ok to resume in 4w. II: lung crackles + S3 17% average arterial pressure • Isolated systolic hypertension - treat photosensitivity rash
• PDE-5 inhibs (sildenafil) can III: frank pulmonary edema 38% throughout systole & diastole same way as normal HTN
be used 6mo after MI. IV: cardiogenic shock 81% 30d mortality MAP = DBP + 1/3(SBP - DBP) Continued on 01.09
Avoid in pts prescribed
nitrates and nicorandil P: ~10% morbidity. ↑ risk for future events

01.01 Cardiology – Acute coronary syndrome, Hypertension

(c) qqm / jmsn
01.02 Cardiology – Ischaemic heart disease, Atrial fibrillation, ALS algorithm
Ischaemic heart disease Atrial fibrillation Advanced life support

D: inadequate blood supply to the D: supraventricular tachyarrhythmia Mx (continued) Unresponsive and not Cardiac arrest refers to
myocardium. Angina = chest pain due to causing uncoordinated and ineffective • Consider rhythm control if reversible breathing normally VT, VF, pulseless
reduced blood flow to the myocardium contractions of the atria cause, HF 2/2 AF, new-onset (<48h), electrical activity and
÷ new onset, paroxysmal, persistent AF atrial flutter manageable with ablation asystole
R: age, smoking, CAD, HTN, ↑chol, DM, • Electrical cv synchronised to R wave
IVDU, male, sedentary lifestyle. R: age, ↑↑alcohol, smoking, HTN, ↑chol, to prevent inducing VFib CPR 30:2
HF, T2DM, obesity, other heart disease, • Pharmacological cv: flecanide or Attach defib/monitor ROSC = return
hyperthyroidism, etc amiodarone (latter if structural heart of spontaneous
P: • Atherosclerosis in coronary vessels
disease present) circulation
2/2 endothelial dysfunction (smoking,
HTN, hyperglycaemia) A: [SMITH] sepsis, mitral valve • Anticoagulation for all pts: use Ax rhythm
• Plaque formation causes physical pathology, IHD, thyrotoxicosis, HTN / P:
blockage → ↓blood flow to
CHADSVASc score to calculate risk
anatomical, histological ∆ in atria due to
myocardium → ischaemia & angina
of stroke & ORBIT score for risk of
underlying heart disease, resulting in bleeding
conductive ∆. - if ≥1 (M) or ≥2 (F): DOAC indefinitely Shockable ROSC Non-shockable
S/smx: - warfarin only if mechanical heart [VF / pulseless VT] [PEA/asystole]
• Stable angina (all 3 features) S/Smx: palpitations, irregularly valves or severe mitral stenosis
- chest pressure / constriction <20min irregular pulse, SOB, CP, fatigue, - DOAC/warfarin for stroke/TIA + AF
- provoked by exertion dizziness, syncope adrenaline 1 mg asap
1 shock
- relieved by rest or GTN
CHA2DS2VASc score
• Atypical angina in women, DM, older Ix: ECG, bloods (FBC, clotting profile, Immediately resume
U&E, TFT, U&Es - including Mg) • Age 65-74yo =1 ≥75yo =2
people - 2 of 3 + GI discomfort, CPR for 2 min
• Sex Male =0 Female =1 Immediately resume
dyspnea, nausea
• Heart failure =1 CPR for 2 min
Mx: • Hypertension =1 Give adrenaline 1mg IV every
Ix: ECG, bloods (Hb, lipids, HbA1c) Haemodynamically unstable • Stroke/TIA/VTE =2 other cycle (every 3-5min)
• If stable angina cannot be excluded by (SBP<90, HR>150, syncope, CP etc) if arrest witnessed, 3 stacked shocks
• Vascular disease (prior MI, PAD) =1
clinical Ax alone, consider → electrical cardioversion (cv) after 3rd shock: adrenaline 1mg
-☝🏻 CT coronary angiography
• Diabetes =1
repeat adrenaline 1 mg every 3-5min ABCDE
-✌🏻 non-invasive functional imaging Stable + onset <48h Aim for O2 sats 94-98%,
☝🏻 ✌🏻
ORBIT score
- 3rd invasive coronary angiography • Rate control: βB or CCB digoxin after 3 shocks, amiodarone 300 mg + normal PaCO2
• Age ≥75yo =1
• Heparinise, and early rhythm control after 5 shocks, amiodarone 150 mg Ix: 12-lead ECG, CXR, ABG
✌🏻
• Bleeding Hx (GI bleed, ICH,
with electrical cv or pharmacological cv lidocaine Identify and treat causes
Mx: • Sublingual GTN for relief of smx haemorrhagic stroke) =2
(or before activities known to cause • GFR <60 mL/min =1
Onset >48 / uncertain onset
☝🏻 ✌🏻
angina) • Tx with antiplatelets =1
- 1 dose + rest → if no relief, take 2nd • Rate control: βB or CCB digoxin • Give O2, maintain airway Identify and treat reversible causes:
dose → if no relief, call 999 • If rhythm control considered, must Complications: stroke/TIA (5x ↑risk
• Use waveform capnography • Hypoxia • Hypovolemia
• Aspirin 75 mg OD, unless pt is anticoag for ≥3w before cv, then • Continuous compressions if • Hypo/hyperK • Hypo/hyperthermia
compared to non-AF pts), bradycardia,
already on antiplatelet (eg clopidogrel) elective electrical cv advanced airway • Thrombosis (MI or PE)
hypotension, heart failure, death, etc
• Statin, eg atorvastatin • OR, transoesophageal echo (TOE) to • IV or IO access • Tension pneumothorax
☝🏻
• Amiodarone - risk of thyroid issues
• β-blocker and/or CCB r/o left atrial appendage thrombus – • if PE suspected, admin thromboly- • Tamponade (cardiac) • Toxins
- don't give βB to asthmatics💡 can heparinise and cardiovert asap
• Catheter ablation if wishes to avoid
tic drugs, extend CPR to 60-90 min
- if CCB used as monotherapy, give
verapamil or diltiazem antiarrhythmics Ax of rhythm via defib or ECG monitor
- if CCB combined with βB, use - Femoral access → radiofrequency to • VF and VT: ventricular tachyarrhythmia causing unsynchronised and
amlodipine, nifedipine, etc burn off myocardial origin of aberrant ineffective contractions of the ventricles
•✌🏻 Long-acting nitrate (eg isosorbide electrical activity
- Requires anticoagulation 4w before
• Pulseless electrical activity (PEA): ECG detects some rhythm (eg
sinus tachy), but no there is no detectable pulse (eg on the carotids)
mononitrate), nicorandil, ivabradine or
ranolazine and during procedure ↳ electrical activity of heart present, but no mechanical activity
• In pts with DM, consider ACE inhibitor - Even after catheter ablation, risk of • Asystole: cessation of electrical and mechanical activity of the heart
• Lifestyle changes stroke remains – consider anticoag - Usually occurs as decompensation of VT, VF or PEA - terminal rhythm
- Smoking cessation, limit alcohol - Risk of cardiac tamponade, stroke, - Poor prognosis unless 2/2 choking or pacemaker failure
- Cardioprotective diet pulmonary vein stenosis; 50% recur - Neurological deficits even if pts survive
- Wt loss & exercise within 3mo and may need multiple
• DVLA: if angina occurs at rest, do not procedures
drive (no need to notify DVLA)

(c) qqm / jmsn

Ventricular fibrillation Ventricular tachycardia Bradycardia: peri-arrest Tachycardia: peri-arrest Pacemakers

D: ventricular tachyarrhythmia causing D: broad-complex tachycardia originating D: abnormally slow HR causing haemo- D: ↑HR, generally >100 bpm Temporary pacemakers
unsynchronised and ineffective from ventricular ectopic focus dynamic compromise; defined <50 bpm • Broad complex - used in haemodynamically unstable
contractions of the ventricles ("quiver") • QRS >120ms, rate >100 bpm - Regular: assume VT bradycardia not responding to atropine
• Monomorphic VT (most commonly R: medications, >70yo, recent MI, - Irregular: AF + bundle branch block, - acute anterior MI
R: CAD, acute MI, HOCM, long/short QT, caused by MI) surgery AF with ventricular pre-excitation, TdP - trifascicular block prior to surgery
Brugada, ventricular pre-excitation (e.g. • Polymorphic VT: one subtype is torsade • Narrow complex
WPW), e- imbalance, drugs, infxn de pointes (2/2 prolongation of QT - Regular: SVT Implanted cardioverter defibrillator (ICD)
interval) A: sinus node dysfunction, conduction - Irregular: probably AF (see 01.02)
system disease (including AV block), • Indicated for
A: (see risk factors) / P: anatomical, escape rhythms, AV dissociation, etc - complete AV block
histological ∆ in cardiac tissue (esp Causes of prolonged QT interval: Regular narrow complex tachycardia - Mobitz type II AV block
scarring) due to underlying heart disease, • Congenital = supraventricular tachycardia - persistent AV block after anterior MI
• Drugs - amiodarone, TCAs, fluoxetine, S/smx: dizziness, syncope, fatigue, • = tachycardia not ventricular in origin - symptomatic bradycardias (eg sick
resulting in conductive ∆.
chloroquine, terfenadine, erythromycin exercise intolerance, dyspnea, jugular • QRS <80ms, usually HR 150-220 sinus syndrome)
• Electrolyte abn: hypoCa, hypoK, venous distention (+ a-waves) • Causes: AV nodal re-entry tachy - heart failure
S/Smx: tachycardia, hypotension, hypoMg (AVNRT) or AV re-entry tachy, junctional - drug-resistant tachyarrythmias
(pre)syncope, airway compromise, • Acute MI • Myocarditis Ix: ABG, bloods (TFTs, U&Es, trops), tachycardia, etc • Ventricular pacing and sensing ICDs
impaired consciousness, chest • Hypothermia • SAH 12-lead ECG, Holter monitoring, exercise are most commonly used
discomfort, dyspnea, etc testing or event monitor, echo
Ix: ECG, bloods (U&Es, trops, etc) • Show up in ECG with pacing spike
Ix: ECG, echo, bloods (trops, U&Es)
Ix: ECG, FBC, clotting profile, U&E, TFT, Mx of peri-arrest bradycardia
CXR, TTE, etc • O2 - aim for 94-98% Mx:
→ ECG: wide QRS complex, Mx if unstable
• S/smx: SBP <90, HF, chest pain,
•☝🏻 Atropine boluses to total 3 mg Stable SVT
differentiated from other VTachs by - 500 mcg boluses • Valsava manoeuvre (eg blowing into
syncope, etc empty plastic syringe) Cardiac enzymes
irregularly irregular pattern - CI in pts with heart transplant
• Immediately cardiovert (DC) - treat - If bradycardia 2/2 to βB or CCB, give • Carotid sinus massage
under ALS algorithm glucagon Unstable SVT • Most commonly used: troponin
- If 2/2 to digoxin, call expert help • Adenosine IV - rises 4-6h after start of cardiac
Mx if stable
☝🏻 •✌🏻 Transcutaneous pacing - Rapid IV bolus of 6mg damage
Amiodarone - loading dose then 24h
infusion
✌🏻 Isoprenaline / adrenaline / dopamine - No effect, give 12 mg - peaks at 12-24h

✌🏻
- No effect, give further 18 mg - returns to normal after 7-10d
❗️
- Consider if risk of asystole or no
Mx: DC cardioversion stat ± Lidocaine, procainamide CI in asthmatics - give verapamil
response to atropine • Most useful for reinfarction: CKMB
amiodarone or lidocaine. + ICD if drug therapy fails or if impaired • Electrical cardioversion
- Drug options if pacing unavailable - begins to rise 2-6h
• Long-term: ICD, anti-arrhythmic meds LV function Long term Mx
- Risk factors for asystole: recent - peaks at 16-20h
asystole, Mobitz II AV block, complete • β-blockers • Radio-frequency ablation
Mx of TdP: Mg sulphate - returns to normal after 2-3d
P: ICD results in better outcomes heart block, ventricular pauses >3s
❗️ DO NOT use verapamil
Others (less specific)
Valsava manoeuvre • Myoglobin
Ventricular pre-excitation: Slurring of R wave
• Forced expiration against - begins to rise 1-2h (rises first)
due to abnormal AV conduction pathway,
which activates the ventricles before the
a closed glottis - peaks at 6-8h
normal electrical impulse conducts down the • Can be used to terminate - returns to normal after 1-2d
AV node or Bundle or His. Accessory pathway, episode of supraventri- • CK C - begins to rise 4-8h
e.g. WPW. cular tachycardia or - peaks at 16-24h
normalise middle-ear - returns to normal after 3-4d
pressures • AST - begins to rise 12-24h
- peaks at 36-48h
- returns to normal after 3-4d
• LDH C - begins to rise 24-48h
- peaks at 72h
- returns to normal after 8-10d

diagrams from Wikipedia

01.03 Cardiology – Arrhythmias (VF, VT, bradycardia, tachycardia), Pacemakers, Cardiac enzymes
(c) qqm / jmsn
01.04 Cardiology – ECG, Arrhythmias
Normal range QRS
QRS complex Left bundle branch block (LBBB) Bi-fascicular block Wolff-Parkinson-White syndrome
QRS • PR: 120-200 ms
↳ normal: 80-100 ms • Slow or absent conduction through • RBBB + left anterior or posterior • D: Congenital cardiac condition
LBB → longer time for LV to fully
• QRS: 80-100 ms
• QTc: • Broad complex tachycardia (>100- hemiblock arising from an accessory pathway
Usual settings for 360-440 ms in M 120 ms) – assume to be ventricular depolarise ↳ RBBB + left axis deviation between the atrium and ventricle
ECG: 360-460 ms in F tachycardia until otherwise proven • Causes: acute MI, aortic stenosis, ↳ RBBB + right axis deviation - type A (left-sided pathway)
voltage: 10 mV • Narrow complex tachycardia – hypertension, etc - type B (right-sided)
speed: 25 mm/s
likely supraventricular in origin ↳ a new LBBB is always assumed Tri-fascicular block • R: Ebstein anomaly, other cardiac
ST - atrioventricular nodal re-entry to be an MI until otherwise proven • RBBB + left hemiblock + 3rd defects, HOCM, ?FHx
tachycardia (AVNRT) • "WiLLiaM" V1 V6 degree heart block • A/P: Accessory pathway can lead to
- atrioventricular re-entry - W in V1 and ↳ PassMed says 1st degree heart atrioventricular re-entry tachycardia
tachycardia (AVRT) M in V6 block but LITFL says true trifasci- (AVRT) → can degenerate to AF/VF
- junctional tachycardia R cular block is with 3rd degree heart • S/smx: pt may be asymptomatic, or
PR interval rS block present with palpitations, dizziness,
dyspnea, chest pain, etc
QT interval ST Right bundle branch block (RBBB) • Ix: ECG (short PR interval, δ wave =
ST elevation Left ventricular hypertrophy
• MI (ie STEMI) • Slow or absent conduction through wide QRS with slurred upstroke, LAD/
P RBB → longer time for RV to fully • sum of S wave in V1 + R wave in RAD) ± echo, electrophysiology
↑P wave amplitude 2.5mm
• Pericarditis / myocarditis
↳ diffuse ST elevation + PR depolarise V5 or V6 >40 mm - type A: dominant R wave in V1
• Cor pulmonale • Causes: normal variant (esp with - type B: nope
depression
• Normal variant ("high take off") ↑age), RV hypertrophy, pulmonary Right ventricular hypertrophy • Mx:
Broad, notched (bifid) p waves embolism, MI, etc V1 • Left atrial enlargement - radiofrequency ablation of accessory
• Left ventricular aneurysm V6
- bifid P wave in lead II with duration
- Often most pronounced in lead II • "MaRRoW" pathway - safe and effective
• Prinzmetal angina (coronary artery
- ≈ Left atrial enlargement - M in V1 and >120 ms - medical: sotalol, amiodarone,
spasm) • Right atrial enlargement
• Mitral stenosis W in V6 flecainide
• Takotsubo cardiomyopathy rSR qRs
↳ difficult to differentiate from MI - tall P waves in leads II and V1 which ↳ avoid sotalol in coexistent AF
No P wave – atrial fibrillation 120ms exceed 25 ms
• Subarachnoid haemorrhage (rare) Left axis deviation (LAD)
≈ QRS +ve in lead I Wellen's syndrome
PR ST depression QRS -ve in leads II, III, aVF Hypothermia V4 • = pattern that arises due to high-grade
Prolonged PR interval • MI (ie NSTEMI) • Causes • Bradycardia stenosis in the left anterior descending
↳ >200 ms (5 small squares) • 2/2 abnormal QRS (LVH, LBBB, - left anterior hemiblock • J wave (Osborne wave) – small coronary artery
• Ischaemic heart disease RBBB) - LBBB - inferior MI hump at the end of QRS complex • ECG
• Digoxin toxicity • Digoxin - Wolf-Parkinson-White, where • 1st degree heart block - biphasic or deep T wave inversion in
• Hypokalaemia • Hypokalaemia there is a right-sided accessory • Long QT interval V2-3
• Rheumatic fever • Cardiac syndrome X pathway • Atrial and ventricular arrhythmias - minimal ST elevation
• Aortic root pathology - Hyperkalaemia - no Q waves
• Lyme disease - Congenital: ASD Digoxin
• Sarcoidosis T
T wave changes • Down-sloping ST depression Junctional escape rhythm
• Myotonic dystrophy
• Idiopathic • Athletes
↳ represents ventricular Right axis deviation (RAD) • Flattened / inverted T waves = isolated QRS complexes
repolarisation ≈ QRS -ve in lead I • Short QT interval - usually with rate 40-60 bpm
• T wave "inversion" is normal in aVR QRS +ve in leads II, III, aVF • Arrhythmias, eg AV block, - usually narrow (<120 ms)
Short PR interval and V1 bradycardia - no relationship between QRS
• Wolff-Parkinson-White (δ wave) • Causes
• Peaked T waves - RV hypertrophy complexes and preceding atrial activity
- Hyperkalaemia - left posterior hemiblock Normal variants in athletes • aka junctional rhythm
Atrioventricular blocks - MI - lateral MI • Sinus bradycardia • Arise when rate of supraventricular
• 1st degree heart block • Inverted T waves - cor pulmonale • Junctional escape rhythm impulses is less than impulses arising
- PR >200 ms - MI - pulmonary embolism • First degree heart block from the AV node
• 2nd degree heart block - Digoxin toxicity - WPW, where there is a left-sided • Second degree, Mobitz I
- Type 1 (Mobitz I, Wenckebach): - Subarachnoid haemorrhage accessory pathway
progressively prolonging PR until - Arrhythmogenic right ventricular - normal in infants <1yo
dropped beat occurs cardiomyopathy
- Type 2 (Mobitz II): constant PR - Pulmonary embolism (S1Q3T3)
interval between dropped beats ↳ most commonly presents with Note: QTc = correct QT interval;
• 3rd degree heart block = complete sinus tachycardia estimates the QT interval at a
- dissociation between P waves and - Brugada syndrome standard HR of 60 bpm
QRS complexes
- if arising post MI, think RCA lesion diagrams from Wikipedia

(c) qqm / jmsn

 Long QT syndrome Short QT syndrome Atrial flutter

D: congenital or acquired condition that is D: inheritable condition that is D: a supraventricular tachy-arrhythmia

characterised by a prolonged QT interval characterised by a shortened QT interval characterised by a succession of rapid
– defined as QTc ≤330ms or atrial depolarisation waves
QTc is prolonged if – <360ms and one of the following
> 440ms in men (>2.2 big sq) • Hx of cardiac arrest or syncope R: ↑age, valvular dysfunction, atrial
> 460ms in women (>2.6 big sq) • FHx of sudden cardiac death ≤40yo septal defect, atrial dilation
• FHx of SQTS
Causes of long QT S/smx: • Palpatitations
• Congenital - Jervell-Lange-Neilsen, A: e- imbalances (↑K, ↑Ca), hyper- • Fatigue or lightheadedness
Romano-Ward thermia, acidosis, endocrine disorders • JVP pulsation with rapid flutter or
• Anti-arrythmics: amiodarone, sotalol, cannon waves
class 1a antiarrhythmics
• TCAs, SSRIs (esp citalopram) S/Smx: • lone AF in the absence of
• Antipsychotics, eg haloperidol structural heart disease Ix: ECG – "saw-tooth" appearance best
• Chloroquines • Terfenadine • ventricular arrhythmias and sudden seen in leads II, III, aVF, V1
• Erythromycin • Ondansetron cardiac arrest • 2:1 atrioventricular block is common,
• E- disturbances, eg ↓Ca, ↓K, ↓Mg • ± palpitation, syncope, AF. where ventricular rate is characteris-
• Myocarditis • Hypothermia • May be asmx, picked up on screening tically at 150 bpm
• SAH / big brain bleeds Mean age at Dx is 23yo, more in males
Mx: • similar to that of AF
S/Smx: commonly presents in young Ix: ECG, bloods (K, Mg, Ca). Consider • More sensitive to cardioversion – lower
people with cardiac arrest or Holter monitor, exercise tolerance test, energy levels may be used
unexplained syncope. ECG, genetic testing • Definitive Mx: radiofrequency ablation
• Freq misDx as epilepsy. of the tricuspid valve isthmus
• Cardiac syncope: premonitory smx Mx: mainstay is ICD (although pts may
such as palpitations, CP, dyspnea → get inappropriately shocked due to
syncope (+ pallor, cyanosis) → difficulties in interpreting ECG)
recovery (flushing) ± hydroquinidine (↑QT)
• ❗ Identify trigger (in LQTS1 & 2,
excitement, ↑adrenergic tone; in
LQTS3, rest, bradycardia; in acquired,
drugs, electrolyte imbalance, etc) Brugada syndrome

Ix: ECG, bloods (K, Mg, Ca). Consider D: inherited cardiac disease with a typical
Holter monitor, exercise tolerance test, ECG pattern
ECG, genetic testing Epidemiology: ↑prevalence (≥0.2%; ≥1 in
500) in Iran and Thailand
Mx: ☝🏻lifestyle mod, βB (propranolol or
metaprolol) A: disorder of myocardial Na channels,
• avoid extreme exertion; expert causing variable repolarisation
evaluation, avoid QT-prolonging • characteristic J-point elevation,
drugs, avoid electrolyte imbalance
✌🏻 ICD in pts who have had prev
downward ST in V1-2, "saddle-back"

cardiac arrest + smx despite βB

Mx of TdP: IV Mg sulphate Dx/Ix – ECG
• Most pts are asmx, identified
coincidentally or based on Fhx
P: asmx pts may have normal life
• Na-channel blockers can be used
expectancy.
to provoke and confirm Dx
• Smx + ≥1 syncopal episodes – risk of
• Smx: cardiac arrest, VTach, VF
recurrent syncopal episodes.
• Smx + cardiac arrest – ↑↑ risk; survival
enhanced by βB and ICD Mx: in smx pts, ICD + quinidine or
ablation
diagrams from Wikipedia

01.05 Cardiology – QT syndromes, Brugada syndrome, Atrial flutter

(c) qqm / jmsn
01.06 Cardiology – Valvular disorders, Murmurs, Rheumatic fever, etc

Mitral stenosis Mitral regurgitation Aortic stenosis Aortic regurgitation Murmurs

• Pansystolic ("holosystolic")
- Mitral/tricuspid regurgitation
Aetiology • Rheumatic heart disease (99%) • Rheumatic heart disease
• Infective endocarditis
• Rheumatic heart disease
• Calcified bicuspid valve (50-60yo)
• Rheumatic heart disease
• Infective endocarditis
↳ TR louder during inspiration
- Ventricular septal defect
• Valve prolapse
• Papillary muscle rupture
• Calcified tricuspid valve (≥70yo) • Syphilitic cardiomyopathy
• Bicuspid valve • Rheumatic
↳ harsh murmur
• Ejection systolic
• Marfan syndrome • Hypertension arthritis
- Aortic stenosis
• SLE • Aortic dissection • Ankylosing
- HOCM
• LV dilatation (functional MR) • Marfan syndrome sypondylosis
- Pulmonary stenosis
S/smx • SOB, fatigue • SOB and fatigue • SOB • SOB, fatigue - Atrial septal defect
• Pulmonary oedema, haemoptysis • LV failure – orthopnea, paroxysmal • Syncope / pre-syncope • Palpitations - Tetralogy of Fallot
• Right heart failure nocturnal dyspnoea • Angina • Late systolic
- Mitral valve prolapse
Timing • Mid-diastolic • Pansystolic • Ejection systolic • Early diastolic - Coarctation of the aorta
Position • Apex • Apex • Aortic area • Left lower sternal edge
Manoeuvre • On LHS, on expiration • (none) • (none) • Sitting up, on expiration • Early diastolic
Quality • Rumbling (low-pitched) • Blowing quality • Crescendo-decrescendo • Breath-like (high-pitched) - Aortic regurgitation
Radiation • None • Axilla • Carotid area • None - Pulmonary regurgitation
↳ Graham-Steel murmur; similar to
Associated Opening snap (indicates mitral valve 3rd HS (∵ rapid ventricular filling), 4th HS (∵ poorly compliant ventricle), 3rd HS (∵ rapid ventricular filling), aortic regurgitation murmur
features leaflets are still mobile), tapping apex, AF, thrusting/displaced apex, quiet 1st HS (∵ heaving apex, slow-rising pulse, thrusting/displaced apex, collapsing • Mid-diastolic
loud 1st HS (∵ closure of mitral valve), ↓closure of mitral valve), AF, audible narrow pulse pressure, ejection click, pulse, wide pulse pressure, head - Mitral stenosis
mitral facies, low volume pulse 'click' in valve prolapse quiet 2nd HS if severe (∵ difficult to close bobbing (De Musset's sign), nailbed - Severe aortic regurgitation
aortic valve) pulsation (Quincke's sign) ↳ Austin-Flint murmur
Mx • AF – anticoagulation • Medical: nitrates, diuretics, +ve • Asmx but valvular gradient >40 mmHg • Medical Mx of HF • Continuous machine-like
• Asymptomatic inotropes, intra-aortic balloon pump to + features of LV systolic dysfunction, • If smx or asmx with LV systolic - Patent ductus arteriosus
- monitor with regular echos ↑cardiac output consider surgery dysfunction, surgery indicated
• Symptomatic • HF: ACEI, β-blockers, spironolactone • Smx: ☝🏻 valve replacement
✌🏻
Mnemonics
- percutaneous mitral balloon valvotomy • Surgical: repair if damage is due to balloon – reserved for children (with • RILE: right-sided murmurs best heard
- mitral valve surgery degeneration; otherwise, valve no aortic valve calcification) and adults on inspiration; left-sided best heard on
replacement is indicated not fit for surgery
❗️
expiration
Nitrates CI in aortic stenosis • ASMR: aortic stenosis & mitral regurg
during systole
• ARMS: aortic regurg & mitral stenosis
during diastole
Rheumatic fever S/smx (continued): Pulses
• Minor criteria: ↑ESR/CRP, fever, • Pulsus paradoxus
athralgia, prolonged PR interval - ≥10 mmHg fall in SBP during
D: autoimmune disease usually following
• Dx confirmed if inspiration Heart sounds
Strep pyogenes infxn
- evidence of recent strep infxn and Prosthetic heart valves - seen in cardiac tamponade or • S1 ("lub") – closure of mitral and
- 2 major criteria, or • Biological severe asthma tricuspid valves
P: • type II hypersensitivity thought to - 1 major + 2 minor criteria - usually bovine or porcine origin • Slow-rising: aortic stenosis • S2 ("dub") – closure of aortic and
be caused by molecular mimicry - structural deterioration and • Collapsing: aortic regurg, patent ductus pulmonary valves
• M protein on Strep pyogenes is struc- calcification over time arteriosus, hyperkinetic states (eg
turally similar to myosin → cross-
Ix: strep swabs, strep antibodies / - splitting during inspiration is normal
antigen test, ECG - long term anticoagulation not needed anaemia, thyrotoxicosis) • S3 – caused by rapid ventricular
reactivity; autoimmune response ↳ aspirin long term • Pulsus alternans filling of the ventricle during diastole
against myosin on the heart walls and
Mx: • oral penicillin V
↳ ± warfarin for first 3mo - arterial pulse with alternating strong - normal if <30yo, may persist in some
arterial smooth muscle and weak beats
↳ may prevent rheumatic fever • Mechanical valves
- bileaflet valve most common now - seen in severe LV failure
women ≤50yo

♡
S/smx: "J NES" [major criteria]
• NSAIDs
- low failure rate • Bisferiens pulse ≈ double pulse with
- LV failure (eg dilated cardiomyopathy),
constrictive pericarditis and mitral
- increased risk of thrombosis →
• Tx complications as they occur 2 systolic peaks
• Joints: polyarthritis
♡
• : carditis and valvulitis requires long-term anticoagulation - Seen in mixed aortic valve
disease, sometimes in HOCM
regurgitation
• S4 – caused by atrial contraction
• Nodules (subcutaneous) P: 30-50% of pts with rheumatic fever will with warfarin against a stiff ventricle
• Erythema marginatum develop rheumatic heart disease – >70% ↳ target INR for aortic 3.0, mitral 3.5 • "Jerky" pulse – seen in HOCM - aortic stenosis, HTN, HOCM
• Sydenham's chorea (late) if initial attack severe, or if ≥1 recurrence

(c) qqm / jmsn

 HOCM Hypertrophic obstructive Arrhythmogenic right Dilated cardiomyopathy Chronic heart failure
cardiomyopathy
ventricular cardiomyopathy
D: AD genetic disorder characterised by D: disease of heart muscule character- D: dysfunction of the left ventricle, Mx:
LV hypertrophy without an identifiable D: primary cardiomyopathy characterised ised by enlargement and dilation of one resulting in insufficient delivery of blood ☝🏻 ACEI + β-blocker (eg bisoprolol)
cause. ~1:500 or both of ventricles along with impaired to vital organs. HFpEF (>50%) and - Start one drug at a time
by fibrofatty replacement of the right
ventricular myocardium contractility HFrEF (<40%). ✌🏻 Aldosterone antag (eg eplenerone)
R: FHx of HOCM or sudden cardiac • Autosomal dominant ↳ LVEF ≤40% and systolic dysfunction - Monitor renal function (drugs can
(by definition) NYHA classification: cause hyperK)
✌🏻
death. A/w Friedreich's ataxia, WFW
I. smx do not affect daily activities SGLT2 inhibitor
R: FHx, usually presents in late 20s II. smx occur at moderate effort, slightly 3rd line: (started by specialist)
A/P: most common defect involve (second most common cause of sudden Causes restricting daily activities - Ivabradine – use if sinus rhythm HR
mutation in the gene encoding β-myosin cardiac death in the young after HOCM), • Idiopathic III. smx occur at minimal effort, >75, LVEF <35%
heavy chain protein or myosin-binding M>F (1.6x), intense exercise • Ischaemic heart disease & HTN significantly restricting daily activities - Sacubitril-valsartan (LVEF <35%, must
protein C • A/w Naxos disease (triad of ARVC, • Myocarditis, eg Coxsackie B virus, HIV, IV. delibitating smx at rest have ACEI washout)
• Results in predominantly diastolic palmoplantar keratosis, woolly hair) Chagas disease
- Digoxin – can improve smx, esp useful
dysfunction; left ventricular hypertrophy • Peripartum R: CAD, HTN, ↑chol, DM, smoking,
→ ↓compliance → ↓cardiac output • Iatrogenic, eg doxorubicin radiation, some chemotherapy. FHx.
if coexisting AF
- Hyradalzine and nitrate (esp in Afro-
• Myofibrillar hypertrophy with A: mutations in various genes; 50% pts • Substance abuse, eg alcohol, cocaine
have mutation of several genes which Caribbean pts)
chaotic and disorganised fashion • Inherited, eg Duchenne muscular
myocytes ('disarray') and fibrosis encode components of desmosome dystrophy A/P: HTN, CAD, ↑chol – ↑peripheral - Cardiac resynchronisation therapy
• Infiltrative, eg haemochromatosis, vascular resistance → hypertrophy of • Others: annual influenza vaccine, one-
S/smx: • palpitations sarcoidosis heart to compensate → stressor (e.g. off pneumococcal vaccine
S/smx: can be asmx
• syncope • Thiamine deficiency leading to wet vol overload, arrhythmia, MI) may
• Exertional dyspnea, angina, syncope
• sudden cardiac death beri beri cause heart to decompensation Acute heart failure – Mx
(usually after exercise; 2/2 functional
• Main issue is during diastole - impaired "Pour SOD"
relaxation and/or ↓filling. Impaired
aortic stenosis)
P: • myocardial remodelling → eccentric
• Sudden death (usually 2/2 ventricular • Pour away fluids – fluid restriction
Ix: ECG (ventricular arrhythmia with elasticity or compliance of myocardium
hypertrophy of ventricles → ↓systolic
arrhythmia), HF • Sit them upright
LBBB, T wave inversion in V1-V3,
• Jerky pulse, large 'a' waves, double systolic HF - impaired contraction • Oxygen – target 94-98% sats
epsilon wave ≈ "terminal notch" in QRS dysfunction predominantly
apex beat diastolic HF - impaired filling - CPAP if respiratory failure
complex, see diagram) • Can lead to significant tricuspid and
mitral valve insufficiency → ↓ejection
• Systolic murmurs • Diuretics, eg IV furosemide
- Ejection systolic murmur - ↑ with
☝🏻
• In patients with hypotension or
fraction S/smx: • dyspnea, cough (pink/frothy) ±
Valsava manouvre and ↓ with Mx: sotalol
cardiac wheeze, orthopnea, paroxysmal
cardiogenic shock
squatting • Catheter ablation or ICD to prevent - Ionotropic agents, eg dobutamine
ventricular tachycardia S/smx: nocturnal dyspnea (pt wakes up at night
- pansystolic murmur due to mitral - Vasopressors, eg norepinephrine
• Heart failure s/smx + S3 struggling to breathe),
regurgitation - Mechanical circulatory assistance, eg
• Tricuspid and mitral valve regurgitation • wt loss (cardiac cachexia; may be
diagram from Wikipedia ventricular assist devices
will cause pansystolic murmur masked by water gain)
• Other treatments
Ix: ECG (LVH, deep Q waves, AFib, non- • Peripheral oedema (sacral, pedal)
• Signs of right heart failure: ↑JVP, ankle
- Vasodilators – consider in concomi-
specific signs), echo ("MR SAM ASH" - Ix: CXR – balloon appearance of heart on tant myocardial ischaemia, severe
mitral regurg, systolic anterior motion of CXR. Others as per HF oedema, hepatomegaly
hypertension, aortic regurgitation or
the anterior mitral valve leaflet, mitral regurgitation
asymmetric hypertrophy) Mx → as per HF Ix:☝🏻 NTproBNP (≥400 ng/L = high) - Opiates – not routinely offered
✌🏻 TTEcho w/in 2w (+ estimating EF) • Continue regular medications for HF
Mx: "ABCDE" • Other Ix as appropriate, including - β-blockers – stop only if HR <50, 2nd/
• Amiodarone Takotsubo cardiomyopathy bloods (eg FBC, U&Es), CXR, ECG, etc 3rd degree AV block, or shock
• β-blockers or verapamil • "octopus trap" – transient, apical
ballooning of the myocardium brought CXR: bilat pleural effusions, fluid in interlobar
• Cardioverter defibrillator
about by stress fissures and fluid in septal lines (Kerley B lines)
• Dual chamber pacemaker
• ± Endocarditis prophylaxis • S/smx: CP, features of HF
• Ix: ECG – ST elevation; normal High output heart failure
❗️ Drugs to AVOID: nitrates, ACEIs, coronary angiogram (ie no infarction) Cor pulmonale
= Right heart failure arises from lung
= A normal heart is unable to pump
enough blood to meet metabolic needs
inotropes • Mx: supportive; most pts improve with
disease specifically – COPD, PE, of the body
supportive tx
interstitial lung disease, cystic fibrosis, Eg severe anaemia, pregnancy, Paget's
pulmonary HTN disease, thiamine deficiency

01.07 Cardiology – HOCM, ARVC, Heart failure

(c) qqm / jmsn
01.08 Cardiology – DVT/PE, Infective endocarditis, Pericarditis
Deep vein thrombosis Pulmonary embolism Infective endocarditis Pericarditis Constrictive pericarditis

D: blood clot in a major deep vein, classically D: occlusion in pulmonary vasculature due to D: infection involving the endocardial D: inflammation of the pericardium. D: A form of diastolic heart failure that
in the lower limbs, impairing venous blood thrombus that arises in or travels to the surface of the heart, including valvular > Acute: lasting ≤6w. arises because an inelastic pericardium
flow lungs, most often originating from a deep structures, etc. > Fibrinous vs effusive inhibits cardiac filling
vein.
R: ↑age, recent surgery, immobility >3d, R: prior hx of IE, prosthetic heart valves, R: M>F, 20-50yo, STEMI, cardiac A: similar causes to pericarditis.
previous VTE, cancer, pregnancy, COCP,
HRT, trauma, clotting disorder
R: as per DVT congenital heart disease, heart surgery, cancer, infxn (esp viral), ↳ most common cause is TB
transplant, sources of bacteremia (vasc uraemia, dialysis, autoimmune. • Can also occur following heart surgery
A/P: Virchow's triad (stasis, endothelial A/P: most often, DVT that breaks off and cath, recent dental work, IVDU), etc or mediastinal radiation (M>F 3:1)
damage, hypercoagulopathy). Can lead to gets stuck in the lungs A: 90% idiopathic or viral infxn; 10%
PE if clot embolises A: Strep. viridians, S. aureus, Strep. other. Infxn, autoimmune, 2' immune, P: during healing, granulation tissue
S/Smx based on Well's score heart-related, metabolic, traumatic,
• Risk factors (as for DVT) bovis., Enterococci, Culture -ve HACEK forms. This may contract over time ±
S/Smx based on Well's score
• Clinical s/smx of DVT P: thrombi develop on valvular surfaces neoplastic, drug-related, idiopathic. calcify → constrictive picture
• Risk factors (as above)
• HR >100 • Haemoptysis due to ↑endothelial damage, act as foci P: Inflammation may lead to effusion or
• Localised tenderness along distribution of for bacteria to colonise and grow fibrosis S/smx: • Dyspnoea
venous system Other s/smx: ↑RR (>20), crackles on chest, • Right heart failure: ↑JVP, ascites,
• Entire leg swollen fever, pleuritic chest pain Most common culture -ve causes incl fastidious S/Smx: chest pain (acute, sharp, oedema, hepatomegaly
• Calf swelling ≥3cm larger than other leg organisms (zoonotic agents, fungi), Strep in pts pleuritic/stabbing; relieved by sitting • JVP: prominent x and y descent
• Pitting oedema of affected side Ix & Mx based on PERC & Wells score who have received prior abx forward; may mimic MI but not relieved • Pericardial knock (loud S3)
• Collateral superficial veins • Pulmonary embolism rule-out criteria by GTN), pericardial rub (<33%), fever,
HACEK: Haemophilus, Aggregatibacter (prev • Kussmaul's sign +ve
Ix & Mx based on Well's score
(PERC) – <2% probability of PE if all
Actinobacillus), Cardiobacterium, Eikenella,
myalgia ↳ paradoxical rise in JVP during
criteria ABSENT; if not, do Wells score Kingella inspiration
Wells score ≥2 points Clinical Dx confirmed by 2 of 4:
• Calculate Well's score
(1) proximal leg US within 4h, or characteristic chest pain, pericardial
• Wells score ≥4 points S/Smx: fever, murmur, constitutional Ix: as per acute pericarditis
(2) D-dimer + anticoagulate + scan w/in 24h friction rub, ECG ∆, new/ worsening
• If scan +ve: DVT + anticoagulate
• If scan -ve: D-dimer + anticoagulate
(1) Immediate CTPA, or
(2) Interim DOAC while awaiting CTPA
smx, weakness, arthralgia, HA, dyspnea.
Janeway lesions, Osler nodes, Roth pericardial effusion. ❗ r/o PE. • CXR may show pericardial calcification
- CTPA +ve = PE + anticoagulate spots, splinter haemorrhages
- CTPA -ve → consider proximal leg
• If D-dimer +ve but scan -ve: stop Mx: surgical pericardiectomy is the only
anticoagulating, repeat scan in 1w Ix: ECG - ST elevation &/or PR
vein USS if DVT suspected depression. TTEcho. Bloods. effective tx for chronic constrictive
• If D-dimer -ve and scan -ve: stop Ix: blood cultures (3x 10 mL from pericarditis
- If CTPA contraindicated (eg pregnant, different sites at 30-min intervals), echo, Pericardiocentesis. CXR.
anticoagulating – alternative Dx • If inflammatory process still ongoing, pt
renal impairment), use V/Q scan FBC, CRP, U&E, LFT, urinalysis, ECG
• If 2nd scan +ve: DVT + anticoagulate may respond to NSAIDs or other anti-
• Wells score <4 points Mx: • suspected cardiac tamponade,
• If 2nd scan -ve: alternative Dx inflammatory agents
(1) D-dimer test urgent pericardiocentesis required
☝🏻
Wells score ≤1 point Mx: sepsis pathway if needed, broad
- If D-dimer +ve, treat as per Wells ≥4 • NSAID, PPI, colchicine
(1) D-dimer with result within 4h, or spectrum then adjust according to culture
- If D-dimer -ve, stop anticoagulation, • If present, treat underlying cause
(2) D-dimer + interim anticoagulation results. May need urgent surgery Pericardial rub - "fresh snow" sound best
consider alternative Dx - most 2/2 viral infxn, so no specific tx
• D-dimer -ve: stop anticoagulating, heard left sternal edge leaning forward,
consider alternative Dx Indications for surgery for IE - if bacterial (purulent), IV abx
Other Ix while awaiting results: end-exp. Still heard when holding breath ∵
• D-dimer +ve: treat as per Wells ≥2 • Severe valvular incompetence • Advice pt to avoid strenuous activity
• Aortic abscess (↑PR interval)
• ECG - most commonly showing sinus heart sound not respi-related. Likely need
tachy. S1Q3T3 only in 20%, RBBB and until smx resolve to examine repeatedly.
Anticoagulation • Infxns resistant to abx (* fungal infxn)
• ☝🏻 DOAC (apixaban, rivaroxaban)
RAD may be a/w PE • HF refractory to medical tx
✌🏻 LMWH followed by dabigatran/edoxa-
• CXR - for all pts. Usually normal CXR
unless large PE (wedge-shaped
• Recurrent emboli after abx
P: poorer outcome if large effusion, high
fever, subacute course, failure to
Uraemic pericarditis: tx intensive dialysis.
ban, or LWHM followed by warfarin
P: ↑mortality if elderly and resulting in
opacification) respond Dressler's syndrome: post-MI pericarditis
• Special situations (? inflammatory reaction). Usually 2-4w
• ABG, FBC (including clotting screen) HF. Possible cerebral comp. Surgery a/w
- Cancer: still use DOAC
- Renal impairment: LWMH → warfarin Mx: anticoagulation
↓mortality. post MI Mx as per pericarditis.
- Antiphospholipid syndrome (esp triple • As per DVT Long-haul flights PERC - must all be negative to r/o PE
+ve): LMWH → warfarin • If massive PE + circulatory failure (eg • Slight ↑risk esp on long haul travel
☝🏻
• ≥50yo • HR ≥100 • O2 sats ≤94%
• Length of anticoagulation hypotention), thrombolysis • If no major risk factors for VTE, no • previous DVT/PE
- If provoked, treat for 3mo • Pulmonary embolism severity index special measures required • recent surgery/trauma in past 4w
- If provoked by cancer, length depends (PESI) used to determine who can be • If other risk factors, • haemoptysis
on continued risk (3-6mo) treated as outpatient - wear anti-embolism stockings • unilateral leg swelling • oestrogen use
- If unprovoked, treat for 6mo + may - Takes into account haemodynamic - ? seek medical advice about use of
need Ix to check for causes of DVT stability, comorbidities, etc LMWH
(eg CTTAP to look for cancer) • Repeat PEs: consider IVC filter • No role for aspirin

(c) qqm / jmsn

Cardiac tamponade Antihypertensives Adenosine Antiplatelets LL = lifelong

D: Accumulation of pericardial fluid, ACE inhibitors (-pril) Calcium channel blockers MOA: causes transient heart block 1st line 2nd line
blood, pus or air within the pericardial • Adverse effects • Non-dihydropyridine CCBs: in AV node
space. ❗️ Medical emergency. - dry cough in 15%, 2/2 ↑bradykinin verapamil and diltiazem • α1 agonist at the AV node ACS
or PCI
aspirin (LL)
ticagrelor (12mo)
clopidogrel (LL)
levels – may be intolerable for some • Verapamil • T1/2 of 8-10 s
R: malignancy (esp lung and breast), - Angioedema (may occur up to a year - Adverse effects: HF, constipation, • Used to terminate SVT
❗️ Administer via large-bore
TIA Clopidogrel (LL) aspirin (LL)
aortic dissection, purulent pericarditis, after starting tx) hypotension, bradycardia, flushing
- Hyperkalaemia - DO NOT give with β-blockers or stroke dipyridamole (LL)
heart surgery, TB cannulas due to short half life
- First dose orthostatic hypotension • Diltiazem
PAD Clopidogrel (LL) aspirin (LL)
A: iatrogenic (eg surgery), trauma, • Contraindicated / caution in - Adverse effects: HF, hypotension,
- pregnancy & bfding (teratogenic) bradycardia, ankle swelling • Avoid in asthmatics due to
malignancy, idiopathic possible bronchospasm
- Renovascular disease • Dihydropiridine CCBs Aspirin - MOA: irreversible COX1,2 inhibitor
↳ think esp renal artery stenosis! - eg amlodipine, nifedipine • AE: CP, bronchospasm, transient • Do not use in <16yo due to risk of Reye's
P: ↑pericardial pressure 2/2 - Aortic stenosis - may cause - Affect the peripheral vascular smooth flushing, ↑ventricular rate syndrome (except in Kawasaki disease)
accumulation of fluid in pericardial space hypotension muscle more than heart; do not result • British Society for Haematology recommends
→ if pericardial pressure is greater than - Hereditary idiopathic angioedema in worsening of HF but can cause that aspirin monotherapy can be continued for
intra-chamber pressures, heart will • Monitoring ↑ankle swelling most noncardiac procedures unless bleeding
collapse - U&Es – can cause transient ↑SCr up - Adverse effects: flushing, HA, ankle Amiodarone risk is high – in which case, omit 3d before
to 30% from baseline, transient ↑K up swelling until 7d after operation
S/smx: to 5.5mmol/L - Nifedipine can be used in pregnancy • CABG – continue aspirin
• Beck's triad – hypotension, ↑JVP, - Renal impairment – think about MOA: blocks K ± Na channels
muffled heart sounds undiagnosed bilateral renal artery • very long t1/2 (20-100d)
• Dyspnea, ↑HR, pulsus paradoxus, ❗️ Admin via central veins due to
Thiazide diuretics Clopidogrel, ticagrelor, prasugrel
stenosis • Eg indapamide, chlortalidone • MOA: P2Y12 adenosine diphosphate (ADP)
± Kussmaul's sign thrombophlebitis + loading dose
• MOA: inhibit sodium reabsorption in receptor inhibitor
Angiotensin II blockers (ARBs) kidneys (can result in ↑K loss) • May be less effective if used with PPIs
Ix: ECG, TTE, CXR, bloods (FBC, (-sartan) • Adverse effects: dehydration, - ?best PPI to use with is lansoprazole
Monitoring:
cardiac enzymes) • Generally used where ACE inhibitors orthostatic hypotension, ↓K, ↓Na, • Prior to tx: TFT, LFT, CXR
are not tolerated ↑Ca (and also ↓Ca in urine = hypo-
• Pulsus paradoxus: ↑↑drop in BP • Similar contraindications and cautions calciuria), gout, impaired glucose
• q6mo: TFT, LFT
during inspiration DLVA cardiovascular disorders
with ACE inhibitors tolerance, impotence Adverse effects
• Kussmaul's sign: paradoxical rise in • Rarely can also cause pancreatitis • thyroid dysfunction: both ↑ and ↓
right atrial pressure during • corneal deposits • ACS: 4 weeks off driving
inspiration β-blockers (-olol)
Loop diuretics • pulmonary fibrosis/pneumonitis ↳ 1 week if successfully treated by PCI
• Electrical alternans: QRS complex • Adverse effects: • Angina: driving must cease if smx occur at
• Eg furosemide, bumetanide • liver fibrosis/hepatitis
amplitude changes in alternate - bronchospasm - cold peripheries rest/at the wheel
• MOA: inhibit NaCl reabsorption • peripheral neuropathy
cycles - fatigue - sleep disturbances • Aortic aneurysm ≥6 cm: notify DVLA
• myopathy
- erectile dysfunction in kidneys by inhibiting Na-K-2Cl
cotransporter • photosensitivity ↳ Licensing will be permitted subject to
Mx: urgent pericardiocentesis if pt is • Contraindications / cautions annual review
• Pts with poor renal function may • 'slate-grey' appearance
unstable (needle is inserted into the - Uncontrolled HF • AA ≥ 6.5 cm: pt disqualified from driving
pericardial sac and allows drainage of - Asthma (∵ bronchospasm) require ↑↑dose to ensure sufficient • thrombophlebitis and injection
• CABG: 4 weeks off driving
concentration in renal tubules site reactions
fluid) - Sick sinus syndrome • Catheter ablation for arrhythmia: 2d off
- Concurrent verapamil use – may • Adverse effects: hypotension, ↓Na, • bradycardia
• Heart transplant: do not drive for 6 weeks,
precipitate severe bradycardia ↓K, ↓Mg, ↓Ca, hypochloraemic • lengthens QT interval
no need to notify DVLA
alkalosis, ototoxicity, renal impairment, • HTN: can drive unless tx causes
hyperglycaemia, gout unacceptable AE, no need to notify DVLA
α-blockers
• Not commonly used for HTN ↳ for HGV: no driving if consistently
• Eg doxazosin, tamsulosin Aldosterone antagonists SBP >180 and/or DBP >100
• Adverse effects: orthostatic hypoten- • Eg spironolactone, eplenerone • ICD for sustained ventricular arrhythmia:
sion drowsiness, dyspnea, cough • Sometimes known as potassium- cease driving for 6 months
• Methyldopa – used to control BP in sparing diuretics • ICD for prophylaxis: 1 month off driving
pregnancy • MOA: ↓Na absorption in collecting ↳ HGV: ICD placement – permanent ban
ducts • Pacemaker insertion: 1 week off driving
• Adverse effects: ↑K, gynaecomastia • PCI (elective): 1 week off driving
(less common with eplenerone)

01.09 Cardiology – Cardiac tamponade, DLVA rules, Drugs used in cardiology

(c) qqm / jmsn
01.10 Cardiology / Vascular surgery – Varicose veins, Lower leg ulcers,
Peripheral arterial disease Aortic aneurysm Aortic dissection Varicose veins Lower leg ulcers

D: arterial disease caused by D: permanent pathological dilation of the D: a separation occuring in aortic wall D: Subcutaneous, permanently dilated Venous leg ulcers
atherosclerotic obstruction of arteries aorta. 1.5x expected AP diameter for intima, causing blood flow into a new veins • Located above ankle
outside the heart and brain segment, given pt's sex and body size. false channel composed of the inner and • Usually painless
÷ intermittent claudication, critical limb >3cm. 90% below renal arteries. outer layers of the media R: ↑age, FHx, F>M, ↑number of • Shallow ulcer, undefined borders
ischaemia, & acute limb-threatening pregnancies, DVT, obesity • A/w - Previous DVT - Oedema
ischaemia R: ❗ smoking, FHx, ↑age, M>F R: aneurysms, Marfan, Ehlers-Danlos, - Chronic insufficiency skin changes
• Ix: Dopper US
incidence, F>M rupture, connective bicuspid aortic valve, coarctation, S/smx: • Visibly bulging veins – usually
R: smoking, DM, HTN, ↑cholesterol, tissue disorders. ± hyperlipid, HTN, smoking, FHx, HTN • Mx: Compression banding after r/o
more apparent when standing arterial disease
>40yo, Hx of CAD/stroke/TIA atherosclerosis, etc • Aching, throbbing • Itchy - If no healing in 12w or large ulcer, skin
A: atherosclerosis A/P: intimal tear that extends into the • ± Other signs of chronic insufficiency grafting may be needed
P: fat deposits → clog peripheral arteries A/P: degradation of aortic wall connective media of the aortic wall → blood passes
tissue by enzymes, inflam & immune through the media (antero or retrograde),
creating a false lumen → can cause
Ix: Venous duplex US (retrograde venous Marjolin's ulcer
response, wall stress and genetics flow)
S/smx: occlusion to branches of the aorta • Squamous cell carcinoma
Intermittent claudication • Located at sites of chronic
• Aching or burning in leg muscles during S/Smx: most asmx, picked up on Stanford classification Mx: • Conservative, eg leg elevation, wt inflammation, eg burns
or after walking screening. Palpable pulsatile mass. If A: asc. aorta, prox to L subclavian a loss, regular exercise, graduated
• Predictable distance before smx start, rupture, shock, LOC, pain. B: distal to L subclavian a compression stockings
relieved on stopping DeBakey classification Arterial ulcers
• Referral to vascular surgery if
• Pain not present at rest Ix: Aortic US, contrast CTA to plan for I = A+B II = A II = B • Located on toes and heels
- Significant smx
surgery, bloods (G&S, X-match, clotting, • Painful, with deep punched appearance
🚩
Critical limb ischaemia - Previous bleeding from varicose veins
• Rest pain in foot for ≥2w, ulceration FBC, etc). S/Smx: abrupt severe chest pain, abd • A/w gangrene, peripheral arterial
- Skin changes 2/2 chronic venous
and/or gangrene pain ("tearing") ± syncope. Pt can disease
insufficiency
Acute limb-threatening ischaemia Mx: • stop smoking!! present with shock, HF, cardiac • Ix: low ABPI
- Superficial thrombophlebitis
• ≥1'P's: pale, pulseless, painful, • Ruptured - vascular surgical repair tamponade (Beck's triad: muffled heart - Active or healed venous leg ulcer
paralysed, paraesthetic (numb/sensory (lap repair or endovascular aneurysm sound, hypotension, ↑JVP) • Possible treatments Neuropathic ulcers
changes), perishingly cold repair using stent inserted via femoral ↳ currently under NICE tx can only be • Located on plantar surface of meta-
arteries) Ix: ECG, CXR, bloods. CT for definitive offered if significant smx tarsal head and plantar surface of
Ix: leg pulses ± hand-held Doppler exam, • If stable but ≥5.5cm, or >4cm and Dx. TTE ideally - Endothermal ablation (using radio- hallux
ankle-brachial pressure index (ABPI), growing >1cm/year, urgent ref to frequency or endovenous laser tx) • Esp in diabetics
duplex US, MRI angiography, ECG vascular surgery - Foam sclerotherapy • Ix: r/o other possible causes
Mx: 1. initial resus: O2, fluids, inotropes,
• Surveillance for those not meeting - Surgery: ligation or stripping of veins • Mx: advice pts to wear cushioned
pain control
criteria shoes to reduce callus formation
Mx: • STOP SMOKING 2. monitor vitals
• Mx comorbidities Screening offered to all men in • HR <60, SBP ≤100-120 P: Even if treated, new varicosities likely
• Statin (atorvastatin 80 mg) England – one-off US at 65yo. • IV βB, verapamil or diltiazem will develop over time Pyoderma gangrenosum
+ clopidogrel for all pts + analgesia → CT yearly for 3-4.4cm 3. definitive Mx See 09.02
• Exercise training → CT q3mo for 4.5-5.4 cm • A: emergency surgery Chronic insufficiency skin changes
Severe PAD / Limb-threatening • complicated B: urgent TEVAR or • Telangiectasia
• Acute Mx P: high morbidity for rupture, ↑morbidity open surgery if TEVAR is CI • Reticular veins (dilated, non-palpable,
Ankle-brachial pressure index (ABPI)
- ABCDE + analgesia (eg IV opioids) and mortality a/w surgical intervention. If • uncomplicated B: continue medical subdermal veins ≤3mm)
= ratio of systolic BP in lower leg to that
- IV UFH to prevent thrombus pt survives intervention, low risk of tx, TEVAR w/in 6w if ↑risk for comp • Corona phlebectatica = malleolar flare or
in the arms
ankle flare (fan-shaped pattern of small
enlargement complications 4. chronic aortic dissection (>90d after
veins on the ankle or foot) ↳ in diabetics, may need to do toe-
- Vascular review asap surgery) • Varicose veins brachial pressure index (TBPI)
• Definitive Mx options Leriche syndrome • Mx HR and BP carefully • Atrophie blanche (localised, round areas of • >1.2 – calcified, stiff arteries
- Angioplasty ± stent • D: atheromatous disease of the iliac • Mx risk factors – smoking, chol white, shiny, atrophic skin surrounded by • 0.9-1.2 – normal / acceptable
- Endovascular interventions for short vessels → ↓blood flow to pelvic viscera TEVAR = thoracic endovascular aortic repair
small dilated capillaries) • <0.9 – likely peripheral arterial disease
segment stenosis, aortic iliac ↳ ?subtupe of peripheral arterial • Lipodermatosclerosis (localised chronic
inflammatory and fibrotic condition, esp in
(do not do compression banding)
disease, high-risk pts disease P: left untreated, up to 60% mortality in - <0.5 – severe disease
- Surgical revasc (open): long segment the malleolar region)
• S/smx: (triad) buttock claudication, 24h in type A + rupture • Hyperpigmentation (reddish-brown
lesions (>10cm), multifocal lesions, impotence and no femoral pulses discolouration ≈ "brawny oedema")
lesions of common femoral artery and • Ix: angiography - due to deposition of haemosiderin
purely infrapopliteal disease • Mx: endovascular angioplasty and • Dry, scaling eczema – venous stasis
- Amputation: worst-case option stent insertion dermatitis
• Venous ulcers in gaiter area

(c) qqm / jmsn