Cardiology

Table of Contents
Angina Pectoris.........................................................................................................................2
Acute Coronary Syndrome....................................................................................................... 3
Myocardial Infarction Complications........................................................................................6
Arrhythmias..............................................................................................................................7
Atrial Fibrillation.......................................................................................................................9
Atrial Flutter........................................................................................................................... 10
Heart Failure...........................................................................................................................11
Hypertension..........................................................................................................................13
Rheumatic fever..................................................................................................................... 15
Infective Endocarditis.............................................................................................................15
Pericardial Diseases................................................................................................................17
Diseases of Heart Muscle....................................................................................................... 19
Aortic Stenosis........................................................................................................................21
Aortic Regurgitation............................................................................................................... 22
Mitral Stenosis....................................................................................................................... 23
Mitral Regurgitation............................................................................................................... 23
Right Heart Valve Disease...................................................................................................... 24
Murmurs................................................................................................................................ 25
Drugs...................................................................................................................................... 29

1
Angina Pectoris

Definition:
1. Constricting/heavy discomfort to chest, jaw, neck, shoulders, arms
2. Symptoms brought on by exertion
3. Symptoms relieved within 5 mins by rest or GTN.
All features – typical angina. 2 features – atypical angina. 0-1 features: non-anginal chest pain.
Precipitants – emotion, cold weather, heavy meals. Associated symptoms – faintness, nausea, sweat
Causes: Mainly atheroma. Also – anaemia, coronary A spasm, AS, tachyarrhythmias, HCM
1. Stable angina: Induced by effort, relieved by rest. Good prognosis
2. Unstable angina: Crescendo. Increasing frequency or severity. Occurs on minimal exertion /
at rest. High risk of MI
3. Decubitus angina: Precipitated by lying flat
4. Variant/Prinzmetal: I.e. vasospastic. Coronary A spasm. Pain usually during rest and resolves
rapidly with short-acting nitrates. ECG shows ST segment elevation. Avoid triggers (cocaine,
marijuana, amphetamine). PRN GTN. Very good prognosis.

Investigations
1. ECG: Normal / ST depression and/or flat/inverted T waves. Signs of past MI
2. Bloods: Lipids, HbA1x
3. Echo, exercise ECG, stress echo (exercise/dobutamine) CXR, angiography

Management
1. Lifestyle – stop smoking, exercise, dietary advice, optimise HTN and DM control.
2. Address exacerbating factors e.g. anaemia, tachycardia, thyrotoxicosis.
3. All patients – Aspirin (75mg daily) + statin
4. Symptomatic: Spray/sublingual tabs GTN (to abort angina attacks). If attack does not resolve
after 5mins, take another dose. If it still does not resolve after another 5 mins, ambulance.
a. SE: Headaches, BP.
5. Prophylactic: Beta-blocker or calcium channel blocker (dual if still symptomatic with
monotherapy)
a. If Ca channel blocker as monotherapy: Verapamil or diltiazem
b. If Ca Channel blocker used with beta-blocker: Nifedipine
c. Do not prescribe beta-blockers with verapamil ever - risk of complete heart block
d. If one of the drugs is not tolerated, consider: beta-blockers (e.g. atenolol) long-
acting nitrate (isosorbide mononitrate), ivabradine, nicorandil or ranolazine
6. Revascularisation: When optimal medical therapy is inadequate. PCI (12 months dual
antiplatelet therapy) or CABG (slower recovery but less likely to need repeat
revascularisation)
Note on nitrate tolerance: Many patients taking nitrates develop tolerance and therefore reduced
efficacy. Daily nitrate-free time of 10-14hrs minimises tolerance.

2
Acute Coronary Syndrome

3 presentations:
 ST elevation myocardial infarction (STEMI) - ST elevation + increased cardiac markers
 non-ST elevation myocardial infarction (NSTEMI) - ECG changes (but no elevation) +
increased cardiac markers
 unstable angina (no troponin rises - check twice)

STEMI criteria
 clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent
(> 20 minutes) ECG features in ≥ 2 contiguous leads of:
o 2.5 mm (i.e. ≥ 2.5 small squares) ST elevation in leads V2-3 in men >40yo.
or ≥ 2.0 mm (i.e. ≥ 2 small squares) ST elevation in leads V2-3 in men >40yo
o 1.5 mm ST elevation in V2-3 in women
o 1 mm ST elevation in other leads
o new LBBB (LBBB should be considered new unless there is evidence otherwise)

RFs: Age, male, FH, smoking, DM, HTN, hypercholesterolaemia, obesity, cocaine,  exercise.
Symptoms and signs: Chest pain >20mins (central/left-sided) radiating to jaw or left arm, described
as ‘heavy’ or constricting. Some (diabetics, elderly) may not experience chest pain.
Other symptoms: Dyspnoea, sweating, nausea, vomiting, palpitations
Physical signs: [Pulse, BP, temperature, O2 are often normal or only mildly altered].
Possible findings of complications of ACS (e.g., cardiac failure etc).

Investigations: Most important – ECG and cardiac markers e.g. troponin (esp. T and I)
ECG changes in
ECG changes Coronary artery
a. STEMI: Tall T waves, ST elevation, new LBBB.
Late changes – T wave inversion, Q waves. Anterior V1-V4 LAD
b. NSTEMI: ST depression, T waves, non- Inferior II, III, aVF Right coronary
specific changes. May be normal. Lateral I, V5-6 Left circumflex
Other investigations: CXR, bloods, echo

Management
A commonly taught mnemonic for the treatment of ACS is MONA:
 Morphine (5-10mg IV + metoclopramide 10mg IV)
 Oxygen (only if SaO2 <94%)
 Nitrates (sublingual/IV, now only if in recurrent chest pain – C/I in hypotension)
 Aspirin (300mg)
NSAIDs should be avoided in ACS because they interact poorly with antiplatelet drugs!

a. STEMI
1. ECG
2. IV access + bloods (FBC, U&E, glucose, lipids, troponin)
3. Brief assessment – Hx, examination, CIs to PCI / fibrinolysis

3
 4. Aspirin (300mg) + 2nd antiplatelet agent (ticagrelor 180mg)
Ticagrelor (or prasugrel 60mg if no Hx of stroke/TIA) found to be better than clopidogrel.
5. Morphine 5-10mg IV + anti-emetic (e.g. metoclopramide 10mg IV)
6. PCI available in <120mins – primary PCI
7. Not available – fibrinolysis. Transfer to centre for (a) rescue PCI if fibrinolysis was
unsuccessful or (b) angiography if successful.
GRACE Score
age
b. NSTEMI
heart rate, blood pressure
1. ECG
cardiac (Killip class) and renal
2. Oxygen if <94%
function (serum Cr)
3. Morphine 5-10mg IV + anti-emetic (e.g.
cardiac arrest on
metoclopramide 10mg IV)
presentation
4. Nitrates if in recurrent chest pain
ECG findings
5. Measure troponin and parameters e.g. GRACE score
a. LOW-RISK: Normal ECG, no signs of HF, no troponin levels
recurrence of chest pain, and negative troponin. Ticagrelor + discharge + OP
appointment.
b. HIGH-RISK:
Fondaparinux 2.5mg OD SC (/UFH if immediate angiography planned).
Ticagrelor 180mg PO (/clopidogrel 300mg PO if lower risk) (/prasugrel 60mg OD if
proceeding to PCI)
IV nitrate if pain continues. Maintain SBP >100mgHg.
Oral beta-blocker in high-risk patients (CI: cardiogenic shock, HF, asthma, COPD, heart
block – consider verapamil/diltiazem in these patients).
Angiography.

Percutaneous Coronary Intervention

Contraindications to thrombolysis - SIT ON
If presenting within 12hrs of onset of
HAND
symptoms + can be delivered within 120mins
 Surgery, major and in the last 1 month
of the time when fibrinolysis could otherwise
 Ischaemic stroke in the last 1 year
be given. Use beyond 12hrs of onset may be
 Trauma, major and in the last 1 month (this
appropriate if ongoing ischaemia. If
includes prolonged/traumatic CPR) / TIA
thrombolysis fails – transfer for rescue PCI.
 Ongoing pregnancy (think of the pregnant
Radial access > femoral access.
tummy)
 Non-compressible punctures (<24hrs) e.g.
Fibrinolysis
liver biopsy
Within 12hrs of onset of symptoms if primary
 H = Haemorrhagic stroke, if
PCI cannot be delivered within 120mins.
ever & Hypertension (severe)
If after 90mins of fibrinolysis, ECG still shows
 Aortic dissection
ST elevation, transfer for PCI.
 Neoplasia of the brain
Secondary Prevention  Disorder of bleeding
Beta-blocker, ACE-inhibitor, statin, aspirin, second antiplatelet if appropriate (e.g. clopidogrel).

4
5
Myocardial Infarction Complications

DARTH VADER
Death: Most commonly due to ventricular fibrillation  cardiac arrest. Also, cardiogenic shock, left
ventricular failure.

Aneurysm of the left ventricle: Ischaemic damage weakens myocardium  aneurysm. Persistent ST
elevation and left ventricular failure. Thrombus may form  stroke. Anticoagulate.

Rupture: Of left ventricle. Seen in around 3%. Occurs around 1-2 weeks afterwards. Present with
acute heart failure secondary to cardiac tamponade. Urgent pericardiocentesis and thoracotomy.

Tamponade: Beck’s triad - BP, JVP, muffled heart sounds. Rx: Pericardial aspiration and surgery.

Heart failure: Dysfunctional ventricular myocardium. Rx: Loop diuretics (furosemide), ACE-inhibitors
and beta-blockers.

Valve disease: Mitral regurgitation mainly.

Arrhythmias:
a. Bradyarrhythmias: Sinus bradycardia (inferior Mis), 1 st degree AV block (inferior MI), Mobitz
type I (does not usually require pacing), Mobitz type II (should be paced to avoid sudden
complete AV block), complete AV block (pacemaker), bundle branch block
b. Tachyarrhythmias: Avoid hypokalaemia, hypoxia and acidosis. Sinus tachycardia (treat cause
and add beta-blocker if not CI), SVT, AF, A flutter (cardioversion or rate control), sustained VT
(synchronised DC shock), ventricular fibrillation (80% in first 12hrs. DC shock and consider
ICD)

Dressler’s Syndrome: 2-6 weeks after. AI reaction. Fever + pleuritic pain + pericardial effusion +
ESR. Recurrent pericarditis and effusions. Rx: NSAIDs.

Embolism: From LV mural thrombus. After large anyerior MI, consider anticoagulation with warfarin
for 3 months.

Mitral regurgitation: Commonest with inferoposterior infarction. Presents with pulmonary oedema
and acute hypotension. Rx LVF and consider valve replacement.

Others:
 Pericarditis: Common in the first 48hrs.
 Ventricular septal defect: Usually in the 1st week. In around 1-2% of patients. Acute HF +
pansystolic murmur. Echo is diagnostic. DDx: Acute mitral regurgitation (similar
presentation). Urgent surgical correction needed.

6
7
Arrhythmias

Common, often benign, often intermittent, and occasionally severe.

Causes
 Cardiac: IHD, structural changes, cardiomyopathy, pericarditis, myocarditis, aberrant
conduction pathways
 Non-cardiac: Caffeine, smoking, alcohol, pneumonia, drugs (beta2-agonists, digoxin, L-dopa,
tricyclics, doxorubicin), metabolic imbalance, phaeochromocytoma

Features
Presentation: Palpitations, chest pain, presyncope, syncope, hypotension, pulmonary oedema.
Hx: Detailed Hx of palpitations – precipitating factors, onset/offset, nature, duration, associated
symptoms. Review drug Hx. Ask about medical Hx and FH of cardiac disease / sudden death.
Syncope occurring during exercise is always concerning (e.g. long QT syndrome  SCD).
Tests:
1. Bloods: Incl. Ca2+, Mg2+, glucose, TSH
2. ECG: Signs of IHD, AF, short PR interval (WPW), long QT interval (metabolic imbalance, drugs,
congenital), U waves (hypokalaemia). 24hr ECG monitoring.
3. Echo: Structural heart disease e.g. mitral stenosis, HCM
4. Other tests: Exercise ECG, cardiac catheterisation, electro-physiological studies
Continuous ECG monitoring can be done by telemetry (screens watched by staff), exercise ECG (BP
and ECG monitored during exercise e.g. treadmill), Holter (24hr-7d), loop recorders (record only
when activated, can be implanted under the skin), pacemakers and ICDs.

A) NARROW COMPLEX TACHYCARDIA

Rate >100bpm and QRS complex <120ms.
DDx:
1. Regular rhythm tachycardias – sinus tachycardia, focal atrial tachycardia (P wave
morphology is different to sinus), atrial flutter, atrioventricular re-entry tachycardia
(accessory pathway e.g. WPW syndrome), AV nodal re-entry tachycardia (very common),
junctional tachycardia, bundle branch block, ventricular tachycardia
2. Irregular rhythm – sinus arrhythmia (e.g. with respiration), atrial fibrillation, atrial flutter
with variable block (e.g. 3:1  2:1), multifocal atrial tachycardia (a/w COPD)

Management
1. If compromised- cardiovert
2. Transiently block the AVN if AVNRT/AVRT suspected – vagal manoeuvres (carotid sinus
massage, Valsalva manoeuvre), IV adenosine. If the underlying rhythm is actually atrial in
origin, the blockage will not treat it but it will help in diagnosis and treatment.
3. More intensive treatment is sometimes needed e.g. ablation therapy for accessory pathways

8
 B) BROAD COMPLEX TACHYCARDIA
Rate >100bpm and QRS complex >120ms. If QRS complexes are not clear – VF or asystole.
DDx: Ventricular fibrillation (chaotic), ventricular tachycardia, polymorphic VT (may look like VF), any
cause of narrow complex tachycardias when combined with BBB
Ventricular ectopics are common and may be asymptomatic or described as palpitations or ‘heart
missing a beat’. They are single/in patterns broad QRS complexes. Frequent ectopics (>60/hr) should
prompt testing.

C) BRADYCARDIA
Intermittent episodes can cause recurrent syncope. Seek out reversible causes e.g. hypothyroidism
or medications e.g. beta-blockers. Permanent pacemaker may be needed
Sick sinus syndrome: Sinus node fibrosis, typically in elderly. Dysfunctional sinus node causing either
bradycardia or tachyarrhythmias (e.g. AF, AT). Syncope, life-headedness, palpitations.
Thromboembolism if AF detected. Permanent pacemakers if symptomatic bradycardia.
Some develop tachy-brady syndrome – difficult to treat. Pacing + rate-slowing medications may be
needed.

Jugular venous pulse

As well as providing information on right atrial pressure, the jugular vein waveform may provide
clues to underlying valvular disease. A non-pulsatile JVP is seen in superior vena caval obstruction.
Kussmaul's sign describes a paradoxical rise in JVP during inspiration seen in constrictive pericarditis.
'a' wave = atrial contraction
large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
absent if in atrial fibrillation

Cannon 'a' waves

caused by atrial contractions against a closed tricuspid valve
are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber
ventricular pacing

'c' wave
closure of tricuspid valve
not normally visible

'v' wave
due to passive filling of blood into the atrium against a closed tricuspid valve
giant v waves in tricuspid regurgitation

'x' descent = fall in atrial pressure during

ventricular systole

'y' descent = opening of tricuspid valve

9
Atrial Fibrillation

Commonest sustained cardiac arrhythmia. Present in ~5% of >70-75yrs and ~10% of >80-85yo.
Increased risk of stroke (most imp aspect of treatment!). Can also cause palpitations and inefficient
cardiac function.
Types
 First detected episode (irrespective of whether it is symptomatic or self-terminating)
 Recurrent: Paroxysmal (if terminate spontaneously) or persistent (if not-self terminating,
usually 7days).
 Permanent: Continuous AF which cannot be cardioverted. Rate controlled.

Clinical Features
S&S: Palpitations, dyspnoea, chest pain. Irregular irregular pulse
(Other conditions causing irregular irregular pulse – ventricular ectopics, sinus arrhythmia)

Management
There are two key parts of managing patients with AF: Factors Factors favouring using
 1. Rate/rhythm control: favouring rate rhythm control
 Rate*: Irregular pulse but slowed down to
Older than 65 Younger than 65 years
avoid negative effects on function years Symptomatic
 Rhythm**: Cardioversion. Back into normal History of First presentation
sinus rhythm. ischaemic Lone AF or AF secondary
heart disease to a corrected
 2. Reducing stroke risk: DOACS > warfarin (no
precipitant (e.g. Alcohol)
regular blood tests) e.g. apixaban, dabigatran, Congestive heart failure
rivaroxaban, edoxaban.
*Rate control: 1st line – Beta-blockers, rate-limiting calcium channel blockers. Aim: <90bpm at rest.
If monotherapy fails: Combination therapy with any 2 of – beta-blocker, diltiazem, digoxin.
**Rhythm control: (a) Pharmacological – flecainide 1st line – CI in structural heart disease e.g. MI. In
this case, use amiodarone instead.
(b) Electrical: DC electrical shocks, synchronised to the R wave.
When AF  sinus rhythm – high risk of embolism. Important that there is either (a) short duration of
symptoms (<48hrs) or prior anticoagulation.

a) ACUTE
If adverse signs: ABCDE and DC cardioversion ±
amiodarone.
If stable:
i. <48hrs + no RFs for ischaemic stroke:
Heparinise and cardiovert
(electrical/pharma)
ii. If >48hrs or unsure of onset: Either
rate control (see above) or (TOE or >3
weeks OAC first) rhythm control.
Anticoagulate for at least 4 weeks after CV.

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 b) CHRONIC Risk factor Points
Rate / rhythm control + anticoagulation to decrease stroke
C Congestive heart 1
risk.
failure
If choosing cardioversion: Anticoagulation 4 weeks before
and during the procedure or carry out TOE. H Hypertension 1
Note: If cardioversion fails - consider ablation of the faulty
A2 Age >= 75 years 2
electrical pathways (percutaneously, typically through the
groin) by radiofrequency or cryotherapy. Age 65-74 years 1
For paroxysmal AF: ‘pill in the pocket’ may be used e.g.
sotalol or flecainide PRN. Anticoagulate still. D Diabetes 1

S2 Prior Stroke, TIA or TE 2

Reducing Stroke Risk
Apart from controlling rate/rhythm, anticoagulation V Vascular disease e.g. 1
needed to decrease stroke risk – warfarin or DOAC. IHD, PAD
CHA2DS2-VASc score (AF stroke risk) to determine the
S Sex (female) 1
most
Risk factor Points
appropriate anticoagulation strategy.
Score 0: No H Hypertension 1 treatment
1: Males – consider anticoagulation. Females – no
treatment. A Abnormal renal/liver 1-2
2: Offer AC. S Stroke 1
IMP: Transthoracic echo to exclude valvular
disease – B Bleeding 1 absolute indication for AC, regardless of
score.
L Labile INRs 1
Bleeding risk: HAS-BLED to calculate bleeding risk with
anticoagulation. E Elderly >65yo 1 Balance risks with score above.

D Drugs / alcohol 1-2

Atrial Flutter

Type of SVT – succession of rapid atrial depolarisation waves.

ECG:
 Sawtooth appearance
 Underlying atrial rate ~300/min. ventricular/heart rate dependent on the degree of AV block.
E.g. 2:1 block – ventricular rate 150/min.

Management:
Similar to that of AF but medication less effective.
However, more sensitive to cardioversion so lower energy levels may be used (70-120J)
Radiofrequency ablation of the tricuspid valve isthmus is curative for most patients.

11
Heart Failure

Definition: CO inadequate for body’s requirements

Types:
5. Systolic (EF <40%) e.g. IHD, MI, cardiomyopathy vs
Diastolic (EF >50%) e.g. ventricular hypertrophy,
constrictive pericarditis, tamponade, restrictive
cardiomyopathy, obesity.
6. LVF vs RVF
7. Acute vs chronic
8. Low-output (commonest – see below) vs high-output (rare – normal output not enough to
meet needs) e.g. anaemia, pregnancy, hyperthyroidism, Paget’s disease, AV malformation.
 Excess preload: Mitral regurgitation, fluid overload
 Pump failure: HF, heart block, post-MI, antiarrhythmic drugs, beta-blockers
 Chronic excessive afterload: Aortic stenosis, HTN
Features:
a) LVF: dyspnoea, poor exercise tolerance, orthopnoea, paroxysmal nocturnal dyspnoea, cough
(worse at night, pink/frothy sputum indicates pulmonary oedema), cardiac asthma
(nocturnal cough), nocturia, weight loss (cardiac cachexia – 15% of patients), bibasal
crackles
b) RVF: peripheral oedema, ascites, facial engorgement, epistaxis, JVP, hepatomegaly
Investigations: ECG and BNP (if both normal – HF unlikely). If either +ve  echo (imp for Dx)

Management
1st line: ACE-inhibitor + beta-blocker (together)
 Start with one and then add the next.
 Best beta-blockers: bisoprolol, carvedilol, nebivolol
 Not useful in HFpEF (diastolic)
 Note that ACEi can be substituted for ARB if cough develops.

2nd line: Aldosterone antagonist e.g. spironolactone and eplerenone

 Both ACE-I and aldosterone antagonists cause hyperkalaemia - important to monitor K+

3rd line: Only by a specialist. Options - ivabradine, sacubitril-valsartan, hydralazine, nitrate, digoxin,
cardiac resynchronisation therapy.

Also:
1. Loop diuretics to relieve symptoms e.g. furosemide, bumetanide. Can cause hypokalaemia,
renal impairment. If oedema is refractory - add thiazide.
2. Offer annual influenza vaccine and one-off pneumococcal vaccine (usually one dose but
some patients need a booster every 5yrs).
3. Lifestyle changes - stop smoking, drinking alcohol. Eat less salt. Optimise weight and
nutrition.
4. Treat cause + any exacerbating factors (e.g. anaemia thyroid disease, infection, HTN)

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 5. Avoid exacerbating factors e.g. NSAIDs, verapamil.
Acute Heart Failure
Sudden onset or worsening of symptoms. Symptoms Signs
Decompensated commoner than de novo (66-75%). Breathlessness Cyanosis
De-novo HF causes: Ischaemia, viral myopathy, Reduced exercise Chest signs: bibasal
toxins, valve dysfunction tolerance crackles, wheeze
Decompensated HF precipitants: ACS, hypertensive Oedema Elevated JVP
crisis, acute arrhythmia, valvular disease
Fatigue Displaced apex beat
Presentation: Fluid congestion, weight gain,
orthopnoea, breathlessness. Tachycardia
S3-heart sound
Once stable: Daily weight (aim of decrease weight by 0.5kg/day), repeat CXR, switch IV to oral
Start ACE-I, beta-blocker, spironolactone
Treat cause e.g. AF.

13
Hypertension

Most important RF for premature death and CVD. ~50% of all vascular deaths.
Usually asymptomatic therefore screening is essential.
Don’t rely on a single reading – if high, take another reading and then record the lower one.
Confirm with 24-hr ABPM or 7day HBPM.
Stage Criteria
Stage 1 Clinic BP >= 140/90 mmHg and ABPM/ HBPM average BP >= 135/85 mmHg
Stage 2 Clinic BP >= 160/100 mmHg and ABPM/ HBPM average BP >= 150/95 mmHg
Severe Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 110 mmHg
ABPM - 2 measurements / hour during person’s usual waking hours. Average of 14
measurements.
HBPM – At least twice daily, with 2 measurements each time, 1 min apart. Must be seated.

Secondary Hypertension
5-10% of patients diagnosed with HTN have primary hyperaldosteronism (including Conn’s).
Other (less common) causes:
 Renal disease e.g. glomerulonephritis, pyelonephritis, adult polycystic kidney disease, renal
artery stenosis
 Endocrine e.g. phaeochromocytoma, Cushing’s, Liddle’s, congenital adrenal hyperplasia,
acromegaly
 Drugs e.g. steroids, COCP, NSAIDs, leflunomide
 Others – pregnancy, coarctation of the aorta

Who To Treat
If clinical reading 140/90, use ABPM
or HBPM before starting Rx.
(If 180/110, consider starting
antihypertensive drug Rx immediately).
i) 135/85 – Not hypertensive
ii) 135/85 – Stage 1. Depends*.
iii) 150/95 – Stage 2. Treat all.

*Stage 1 HTN:
Treat if <80yo + any of the following:
- Target organ damage,
established CVD, renal disease, DM, or 10-year CV risk 10% (NICE 2019)

Severe HTN (>180/110)

Admit for specialist assessment if there are:
a. signs of retinal haemorrhage or papilloedema (accelerated HTN) or
b. life-threatening symptoms e.g. new-onset confusion, chest pain, signs of heart failure, or AKI

14
 c. phaeochromocytoma is suspected e.g. labile or postural hypotension, headache, palpitations,
pallor, and diaphoresis.
Urgent investigations for end-organ damage.
Management
Treatment goal: <140/90mmHg. (<130/80mmHg in diabetes, <150/90 if aged above 80yo).
Lifestyle advice! Important:
 Low salt diet - <6g/day (ideally 3g). Reducing salt intake by 6g/day can lower SBP by 10mmHg
 Reduce caffeine intake
 Stop smoking, drink less alcohol, balanced diet, fruits and veggies, exercise, lose weight

Step 1:
 <55yo or any age with DM2: ACE-I or ARB (ARB if ACE-I not tolerated e.g. cough)
 55yo or black African/Caribbean: Calcium channel blocker (bcos the above have reduced
efficacy in these patients).
Step 2:
 In patients of Black African/Caribbean origin taking a CCB, if they require a second agent,
consider ARB in preference to ACE-i.
 (A + C) or (A + D) or (C + A) or (C + D)
Step 3:
 (A + C + D)
Step 4: I.e. Resistant hypertension
 Either add a 4th drug or seek specialist advice. Make sure to discuss adherence and to assess
for postural hypotension.
 if potassium < 4.5 mmol/l add low-dose spironolactone
 if potassium > 4.5 mmol/l add an alpha- or beta-blocker
Patients who fail to respond to step 4 measures should be referred to a specialist.

15
Rheumatic fever

Strep. pyogenes infection (Lancefield group A beta-haemolytic strep) in susceptible individual (2%)
 antibodies  react with heart valves.
Peak incidence: 5-15yo. Tends to recur unless prevented.
Mitral valve (70%) affected most, followed by aortic (40%), tricuspid (10%) and pulmonary (2%).

JONES PEACE Mnemonic

Major Minor
Joints (polyarthritis, hot/swollen joints) Previous rheumatic fever
Heart (carditis, valve damage) ECG with PR prolongated
Nodules (subcutaneous, extensors) Arthralgias
Erythema marginatum (painless) CRP and ESR elevated
Sydenham chorea Elevated temperature

Diagnosis: Hx of recent streptococcal infection + [2 major] / [1 major + 2 minor]

Management
2. Bed rest until CRP normal for 2 weeks
3. Benzylpenicillin IV stat, followed by QDS phenoxymethylpenicillin for 10days (if allergic to
penicillin – erythromycin or azithromycin)
Note: Some patients need lifelong prophylactic antibiotics.
4. Analgesia – aspirin (monitor salicylate level. Toxicity – tinnitus, hyperventilation, metabolic
acidosis) (risk of Reye syndrome in children). Alternative – NSAIDs.
5. Immobilise joints in severe arthritis
6. Haloperidol / diazepam for chorea

Prognosis: 60% with carditis  chronic rheumatic fever.

Acute attacks last ~3 months.
Recurrence: Further streptococcal infections, pregnancy, use of OCP.

Infective Endocarditis

Fever + new murmur = infective endocarditis until proven otherwise

Mortality: 5-50%
a. Acute: 50%. Normal valves. Presents as acute HF ± emboli. Commonest organism: S. aureus
RFs: Skin breaches, renal failure, immunosuppression, DM. Mitral valve most affected.
b. Subacute: Abnormal valves. RFs: Valve disease, IVDU, coarctation, PDA, VSD, prosthetic
valves
Historically, Strep. viridans was commonest cause. Now only accounts for 20% and linked with poor
dental hygiene or dental procedures.

16
S. aureus is now the commonest, particularly in acute cases and IVDUs.
S. epidermidis is common in indwelling lines and commonest 2months post-op.
S. bovis is associated with colorectal cancer. Important to carry out colonoscopy.
Non-infective causes: Libman-Sacks (non-bacterial endocarditis seen in SLE, antiphospholipid
syndrome, malignancy)
Culture may be negative if there was prior antibiotic therapy, or if infecting organism is Coxiella
burnetii, Bartonella, Brucella, HACEK, fungi. These are usually IVDU or immunocompromised
patients.
Note: The following procedures do not require ABX prophylaxis: Dental, gastrointestinal,
genitourinary (incl. childbirth), respiratory tract (incl. bronchoscopy and ENT)

Features
Septic signs: Fever, rigors, night sweats, malaise, weight loss, anaemia, splenomegaly, clubbing
Cardiac: Any new murmurs. PR prolongation ( complete heart block).
Immune complex deposition: Vasculitis may affect any vessel. Roth spots, Osler’s nodes.
Embolic phenomena: Abscesses in organs. Janeway lesions (in skin)
- Bloods: Normochromic normocytic anaemia, neutrophilia, ESR/CRP, RhF +ve
- CXR (cardiomegaly), regular ECGs (heart block), echo (TOE>TTE), CT (emboli)

Prognosis
Poor prognostic factors: S. aureus infection, prosthetic valve (especially early i.e. <60d), culture
negative endocarditis, and low complement levels.
Mortality according to organisms – staph 30%, bowel organisms 15%, streptococci 5%.

Scenario Suggested antibiotic therapy

Initial blind therapy
Native valve endocarditis
caused by staphylococci
Prosthetic valve
endocarditis caused by
staphylococci
Endocarditis caused by
fully-sensitive streptococci
(e.g. viridans)
Endocarditis caused by less
sensitive streptococci
Native valve: amoxicillin, consider adding low-dose gentamicin
If penicillin allergic, MRSA or severe sepsis: vancomycin + low-dose
gentamicin
If prosthetic valve: vancomycin + rifampicin + low-dose gentamicin
Flucloxacillin
If penicillin allergic or MRSA: vancomycin + rifampicin
Flucloxacillin + rifampicin + low-dose gentamicin
If penicillin allergic or MRSA: vancomycin + rifampicin + low-dose
gentamicin
Benzylpenicillin
If penicillin allergic: vancomycin + low-dose gentamicin
Benzylpenicillin + low-dose gentamicin
If penicillin allergic: vancomycin + low-dose gentamicin

Surgery if: HF, valvular obstruction, repeated emboli, fungal IE, persistent bacteraemia, myocardial
abscess, unstable infected prosthetic valve.
50% require surgery. 15% recurrence at 2yrs. 20% hospital mortality.

17
Recommendations: Give clear information about prevention including the importance of good oral
health, symptoms that may indicate IE, risks of invasive procedures e.g. piercings or tattoos.
Pericardial Diseases

Acute Pericarditis
Inflammation of the pericardium – idiopathic or caused by:
 Viruses: e.g. coxsackie, echovirus, EBV, cmv, adenovirus, mumps, varicella, HIV
 Bacteria: e.g. TB—commonest cause worldwide, Lyme disease, Q fever, pneumonia,
rheumatic fever, Staphs, Streps, mycoplasma, legionella, MAI in HIV
 Fungi and parasitic: v rare, usually in immunocompromised
 Autoimmune: systemic autoimmune diseases e.g. SLE, RA; vasculitides e.g. Behcet,
Takayasu; IBD; sarcoid; amyloid; Dressler's
 Drugs: e.g. procainamide, hydralazine, penicillin, isoniazid, chemotherapy
 Metabolic: uraemia, hypothyroidism, anorexia nervosa
 Others: trauma, surgery, malignancy, radiotherapy, MI, chronic heart failure
Features: Central chest pain worse on inspiration / lying flat ± relief by sitting forward (± fever)
Pericardial friction rub. Look for pericardial effusion / cardiac tamponade signs.
Tests: ECG: Concave (saddle-shaped) ST segment elevation and PR depression. May be normal (10%)
Blood tests: FBC, ESR,U&E, cardiac enzymes (NB: troponin in may be raised)
Tests relating to possible aetiology. Cardiomegaly on CXR may indicate pericardial effusion.

Treatment: NSAIDs or aspirin + gastric protection for 1-2 weeks

Colchicine 500mg OD or BD for 3 months to reduce risk of recurrence. Rest until symptoms improve.
Treat the cause. If not improving / AI aetiology: consider steroids (but may increase risk of
recurrence) or other immunosuppressive therapies.

Pericardial effusion
Accumulation of fluid in the pericardial sac (10-50ml).
Causes: Pericarditis, myocardial rupture (haemopericardium – surgical, stab wound, post-MI), aortic
dissection, pericardium filling with pus, malignancy.
Features: Dyspnoea, chest pain, signs of local structures being compressing (e.g. hiccups, nausea,
bronchial breathing at left base i.e. Ewart’s sign). Muffled heart sounds.
Tests: CXR: Enlarged globular heart if effusion >300ml.
ECG: Low-voltage QRS complexes. There may be alternative QRS morphologies (electrical alternans).
Echo: Echo-free complex surrounding the heart.
Rx: Treat the cause. Pericardiocentesis may be diagnostic (suspected bacterial pericarditis) or
therapeutic (cardiac tamponade). Send pericardial fluid for culture, ZN stain, TB culture and cytology.

Constrictive pericarditis
Heart encased in rigid pericardium. Causes often unknown, or due to TB or after pericarditis.
Features: Mainly of right heart failure with JVP (prominent x and y descents), Kussmaul’s sign (JVP
rising paradoxically with inspiration) , soft diffuse apex beat, quiet heart sounds, S3, diatolic
pericardial know, hepato-splenomegaly, ascites, oedema.

18
Tests: CXR: Small heart ± pericardial calcification. CT/MRI – distinguishes from restrictive
cardiomyopathy. Echo.
Rx: Surgical excision (pericardiectomy) is the only definitive treatment. Medical Rx for symptoms.
Cardiac tamponade
Pericardial effusion that raises intrapericardial pressure, reducing ventricular filling and thus
dropping CO. Can lead rapidly to cardiac arrest!
Causes: Dissected aortic aneurysm, trauma, heart surgery, post-MI, pericarditis
Signs: pulse, BP, pulses paradoxus, JVP, Kussmaul’s sign, muffled S1 and S2
Beck’s triad: Falling BP, rising JVP and muffled heart sounds
ECG: Low voltage QRS ± electrical alternans.
Echo is diagnostic: Echo-free zone around the heart ± diastolic collapse of right atrium and ventricle.
Rx: Seek expert help. Urgent pericardiocentesis needed.
Send fluid for culture, ZN stain/TB culture and cytology.

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Diseases of Heart Muscle

Acute myocarditis
Inflammation of myocardium, often
associated with pericardial
inflammation (myopericarditis).
Features: ACS-like symptoms, heart
failure symptoms, palpitations,
tachycardia, soft S1 and S2, gallop.
Consider in young patients presenting with chest pain (± dyspnoea or arrhythmias)
Investigations: Bloods ( inflammatory markers,  cardiac enzymes,  BNP).
On ECG – tachycardia, arrhythmias, ST/T wave changes (e.g. ST elevation, T wave inversion), QT
prolongation, transient AV block.
Viral serology and tests for other likely causes.
Echo: Diastolic dysfunction, regional wall abnormalities. Endomyocardial biopsy is gold standard.
Rx: Treat underlying cause e.g. antibiotics if bacterial cause.
Supportive treatment e.g. of heart failure / arrhythmias.
Avoid exercise – can precipitate arrhythmias.
Complications: Heart failure, arrhythmia (possibly leading to sudden death).
Prognosis: 50% recover within 4 weeks. 12-25% develop DCM and severe heart failure (even years
after apparent recovery).

Dilated Cardiomyopathy
Dilated flabby heart of unknown cause. Prevalence – 0.2%. Commonest cardiomyopathy (90%).
Associations: Idiopathic (commonest), alcohol, BP, chemotherapeutics, haemochromatosis, viral
infection, AI, peri/post-partum, thyrotoxicosis, genetic (1/3rd), myocarditis
Presentation: HF signs, fatigue, dyspnoea, pulmonary oedema, RVF, emboli, AF, VT.
Signs: pulse, BP, JVP, displaced and diffuse apex, systolic murmur, S3 gallop, mitral or tricuspid
regurgitation, pleural effusion, oedema, jaundice, hepatomegaly, ascites.
Tests: BNP. Low Na+ indicates a poor prognosis.
CXR: Cardiomegaly (balloon appearance), pulmonary oedema
ECG: Tachycardia, non-specific T-wave changes, poor R-wave progression
Echo: Globally dilated hypokinetic heart and low ejection fraction
Look for MR, TR, LV mural thrombus.
Rx: Bed rest, diuretics, beta-blockers, ACE-I, anticoagulation, biventricular pacing, ICDs, LVADs,
transplant.

Hypertrophic Obstructive Cardiomyopathy

AD disorder of muscle tissue – defects in the genes encoding contractile proteins. (50% sporadic)
Commonest cause of sudden cardiac death in the young. Prevalence of 1 in 500.
Left ventricle hypertrophy  decreased compliance  decreased CO.
Features: Often asymptomatic. Exertional dyspnoea, angina, syncope (typically after exercise)
Sudden death may be the first manifestation.
Jerky pulse, large ‘a’ waves, double apex beat, ejection systolic murmur ( with Valsalva manoeuvre)

20
Associated with Friedreich’s ataxia and WPW syndrome. Can present at any age.
Echo findings (mnemonic) – MR SAM ASH – mitral regurgitation, systolic anterior motion (of mitral
valve), asymmetric hypertrophy
ECG: Left ventricular hypertrophy, non-specific ST segment, T-wave abnormalities, deep Q waves, AF
MRI, cardiac catheterisation, electrophysiological studies, exercise test, holter monitor
Rx: Beta-blockers or verapamil for symptoms (to reduce ventricular contractility)
Amiodarone for arrhythmias (AF, VT), Anticoagulate for paroxysmal AF or systemic emboli.
Septal myomectomy (surgical / chemical) if severely symptomatic.
Consider implantable defibrillator – use score to assess risk of SCD.
Mortality 6%/yr if <14yo. 2.5%/yr if >14yo.
Poor prognostic factors: Age <14yrs or syncope at presentation. FH of HCM/SCD

Restrictive Cardiomyopathy
Causes: Idiopathic, amyloidosis, haemochromatosis, sarcoidosis, scleroderma
Presentation: Like constrictive pericarditis. Features of RVF predominate.
Diagnosis: Echo, MRI, cardiac catheterisation. Rx the cause.

Cardiac Myxoma
Rare benign cardiac tumour. Prevalence 5/10,000. F:M = 2:1. Usually sporadic but may be familial.
75% occur in the left atrium. Commoner in females.
May mimic infective endocarditis (fever, weight loss, clubbing), or mitral stenosis.
Rx: Excision

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 Aortic Stenosis
Features Classic triad: Angina, syncope and heart failure.
Usually presents as elderly person with chest pain, exertional dyspnoea, or
syncope.
Severe:
 Narrow pulse pressure
 Slow rising pulse
 Delayed ESM
 soft/absent S2
 S4
 thrill
 duration of murmur
 left ventricular hypertrophy or failure

Murmur Ejection systolic murmur - radiates to the carotids. Decreased following Valsalva
manoeuvre.

Causes Causes of aortic stenosis

 degenerative calcification (most common cause in older patients > 65
years)
 bicuspid aortic valve (congenital - most common cause in younger
patients < 65 years)
 William's syndrome (supravalvular aortic stenosis)
 post-rheumatic disease
 sub-valvular: HOCM

Management  if asymptomatic then observe the patient is general rule

 if symptomatic then valve replacement
 if asymptomatic but valvular gradient > 40 mmHg and with
features such as left ventricular systolic dysfunction then consider
surgery
 cardiovascular disease may coexist. For this reason
an angiogram is often done prior to surgery so that the
procedures can be combined
 balloon valvuloplasty is limited to patients with critical aortic
stenosis who are not fit for valve replacement
IMP: Nitrates are CONTRAINDICATED in AS

Note on aortic sclerosis: Senile degeneration of the valve. Ejection systolic murmur but no carotid
radiation and normal pulse and S2. thickened valve without any significant effect on the function of
the valve itself.

22
 Aortic Regurgitation
Features Features
 early diastolic murmur: intensity of the murmur is increased by
the handgrip manoeuvre
 collapsing pulse
 wide pulse pressure
 Quincke's sign (nailbed pulsation)
 De Musset's sign (head bobbing)
 mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of
the anterior mitral valve cusps caused by the regurgitation streams

Murmur Soft, high-pitched, early diastolic decrescendo murmur heard best at the 3rd
intercostal space on the left (Erb's point) on end expiration, with the patient
sitting up and leaning forward.

Causes Acute
 Infective endocarditis
 Ascending aortic dissection
 Chest trauma
Chronic
 Congenital
 CT disorders e.g. Marfan's, Ehler-Danlos syndrome
 Rheumatic fever, rheumatoid arthritis
 Takayasu arteritis
 Seronegative arthritides, osteogenesis imperfecta
 Hypertension

Management  ACE-I to decrease HTN.

 Echo every 6-12months to monitor
 Indications for surgery: Severe AR, enlarging LV, deteriorating LV
function, infective endocarditis refractory to medical therapy.

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 Mitral Stenosis
Features  low volume pulse
 malar flush (due to CO)
 atrial fibrillation (common – due to enlarged LA)
 left atrial enlargement on CXR
 symptoms when <2cm2 (cross-sectional area seen on echo)
 pulmonary hypertension – dyspnoea, haemoptysis, chronic bronchitis-like
picture
 pressure on local structures – dysphagia, hoarseness

Murmur rumbling mid-diastolic murmur (best heard in expiration). Loud S1, opening snap
more severe = longer murmur and opening snap even closer to S2

Causes  rheumatic fever

 rare: carcinoid, prosthetic valve, endocardial fibroelastosis

Management if in AF – rate control + anticoagulate with warfarin (important)

diuretics (preload)
if this fails, balloon valvuloplasty / open mitral valvotomy / valve replacement

Mitral Regurgitation
Features  most asymptomatic
 fatigue, SOB, oedema
 cardiomegaly on CXR, broad P wave on ECG (atrial enlargement)

Murmur Blowing pansystolic murmur, best heard at apex. Radiates to the axilla.
S1 may be quiet (incomplete closure of valve). Severe MR – widely split S2.

Causes  coronary artery disease/post-MI (damage to papillary muscles / chordae)

 mitral valve prolapse (deformed mitral valve)
 infective endocarditis
 rheumatic fever
 congenital

Risk Factors Female, BMI, age, renal dysfunction, prior MI, prior mitral stenosis/valve
prolapse, collage disorders e.g. Marfan’s, Ehlers-Danlos syndrome

Management  If in AF – control rate + anticoagulate.

 Medical: nitrates, diuretics, positive inotropes, intra-aortic balloon pump
 Heart failure: ACE-inhibitors + beta-blockers + spironolactone
 Surgery if severe (repair > replacement)

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Right Heart Valve Disease

Tricuspid Regurgitation
Causes:
 Functional – right ventricular infarction, pulmonary embolism
 Pulmonary hypertension e.g. COPD
 Rheumatic fever, infective endocarditis
 Carcinoid syndrome
 Congenital – e.g. ASD, AV canal, Ebstein’s anomaly
Symptoms: Fatigue, hepatic pain on exertion (dye to hepatic congestion), ascites, oedema.
Signs: Pansystolic murmur; prominent/giant V waves in JVP; left parasternal heave
Pulsatile hepatomegaly, jaundice, ascites
Management:
 Diuretics for systemic congestion + drugs to treat causative condition
 Valve repair or replacement
Tricuspid regurgitation from myocardial dysfunction / dilatation has a mortality of up to 50% at 5yrs

Tricuspid Stenosis
Causes: Rheumatic fever mainly. Also – congenital; infective endocarditis
Symptoms: Fatigue, ascites, oedema
Signs: Giant a wave and slow y descent in JVP; opening snap; early diastolic murmur heard at the left
sternal edge in inspiration. AF can also occur
Treatment: Diuretics + surgical repair

Pulmonary Stenosis
Causes: Usually congenital – Turner syndrome, Noonan syndrome, Williams syndrome, Fallot’s
tetralogy, rubella. Acquired causes – rheumatic fever, carcinoid syndrome.
Symptoms: Dyspnoea, fatigue, oedema, ascites
Signs: Dysmorphic facies in congenital causes. Prominent a wave in JVP; RV heave.
Mild – ejection click, ejection systolic murmur which radiates to the left shoulder, widely split S2.
Severe- Murmur becomes longer and obscures A2. P2 becomes softer.
ECG: RAD, P-pulmonale, RVH, RBBB
CXR: Prominent pulmonary arteries due to post-stenotic dilatation.
Cardiac catheterisation is diagnostic
Rx: Pulmonary valvuloplasty / valvotomy

Pulmonary Regurgitation
Causes: Any cause of pulmonary hypertension.
Signs: Decrescendo murmur in early diastole at the left sternal edge (Graham Steel murmur)

25
Murmurs

Lesion Cardiac cycle Character Breathing Location Radiation

Aortic Systolic Ejection Expiration 2nd intercostal space Carotid
stenosis systolic right sternal edge arteries
Pulmonary Systolic Ejection Inspiration 2nd intercostal space left Left
stenosis systolic sternal edge shoulder/
infraclavicular
Mitral Systolic Pansystolic Expiration Apex Axilla
regurgitation
Tricuspid Systolic Pansystolic Inspiration Left sternal edge
regurgitation
Mitral valve Mid systolic + Expiration Apex
prolapse opening click
Aortic Early diastolic Decrescendo Expiration Left sternal edge (or 2nd Left sternal
regurgitation intercostal space right edge
sternal edge)
Pulmonary Early diastolic Decrescendo Inspiration 2nd intercostal space left
regurgitation sternal edge
Mitral Mid/late Expiration Apex
stenosis diastolic
Tricuspid Mid/late Inspiration Left sternal edge
stenosis diastolic

Innocent murmurs

Ejection Due to turbulent blood flow at the outflow tract of the heart
murmurs
Venous Due to the turbulent blood flow in the great veins returning to the heart. Heard as a
hums continuous blowing noise heard just below the clavicles. Disappears if the child lies
down.
Still's Low-pitched sound heard at the lower left sternal edge. Heard as a buzzing sound
murmur around the apex and varies with posture. AKA vibratory murmur. Commonest
innocent murmur.
Pulmonar soft ejection murmur heard in the second left intercostal space. It is a flow murmur
y flow of a normal pulmonary valve. The increased flow of anaemia, pyrexia and exercise
murmur makes this murmur louder

Characteristics of innocent murmur (7 Ss): Soft, systolic, short duration, sounds normal,
symptomless, special tests normal, standing/sitting (i.e. changes with position)

Physiology of murmurs
 S1: Followed by systole. Caused by closure of the mitral and tricuspid valves (between aorta
and ventricles)
 S2: Followed by diastole. Caused by closure of the aortic and pulmonary valves (out of
ventricles)

26
Left-sided murmurs are commoner (i.e. mitral + aortic vs pulmonary + tricuspid)
There are 4 main areas to auscultate:
 Right 2nd intercostal space - aortic (right upper sternal border)
 Left 2nd intercostal space - pulmonary (left upper sternal border)
 4th intercostal space - tricuspid area
 5th intercostal space at midclavicular line - mitral area (apex)

NOTE:
A. MITRAL and AORTIC: Heard best on EXPIRATION
B. PULMONARY and TRICUSPID: Heard best on INSPIRATION

SYSTOLIC MURMURS

AORTIC STENOSIS
1. S1: Mitral valve closes
2. Systole:
a. For the first milliseconds, the aortic valve is also closed. Then, it opens, but not fully
(because it is stenosed), causing an ejection click.
b. Blood flows out slowly, then more forcefully, then slowly again, causing a crescendo-
decrescendo murmur (diamond-shaped murmur)
3. S2: Aortic valve closes.
4. Diastole: Normal
Radiation: To the neck and the carotids since those are the first few branches of the aorta.

PULMONARY STENOSIS
Essentially the same, but does not radiate to the neck/carotids (instead, to the left shoulder), and is
not heard in the aortic area but the pulmonic area.

MITRAL REGURGITATION
Best heard in the mitral area (apex).

1. S1: Mitral valve closes because pressure in ventricle > pressure in aorta.
2. Systole:
a. For the first milliseconds, the aortic valve is also closed. Additionally, the mitral valve
doesn’t completely close (regurgitation) and therefore blood escapes back into the
atrium, causing a murmur right as S1 occurs (in comparison to aortic stenosis,
whereby the murmur starts slightly after S1).
b. Aortic valve opens but some blood continues to escape into the atrium throughout
all of systole. The sound doesn't change in intensity.
3. Diastole: Normal
Also called a pansystolic/holosystolic murmur - lasts through all of systole. Also called a flat murmur
because the intensity does not change.
Radiation: To the axilla because the blood is pushed from the heart apex back up to the atrium, in
the general direction of the axilla.

TRICUSPID REGURGITATION
Same as mitral regurgitation but on the left side of the heart. It would not radiate to the axilla. It
would be heard best in the tricuspid area.

MITRAL VALVE PROLAPSE

27
The mitral valve billows into the left atrium, causing a click similar to the one in AS.
However is not associated with ejection of blood and therefore is called a non-ejection click.
It is also not in the beginning of systole and therefore is a mid-systolic click.
1. S1: Mitral valve closes (normally)
2. Systole:
a. Left ventricle begins to contract. Pressure builds, and therefore valve billows and
then stops (due to chordae tendinae) causing a mid-systolic click.
b. Since it then does not close normally, some blood starts to flow back into the
atrium, causing a murmur to start after the click, similar to that of mitral
regurgitation (because blood is regurgitating), causing a late systolic murmur.
3. Diastole: Normal
A mid-systolic click is virtually diagnostic for mitral valve prolapse.
Heard best at the apex/mitral area.

DIASTOLIC MURMURS

AORTIC REGURGITATION
1. S2: Closing of aortic valve
2. Diastole:
a. Pressure in the ventricle is initially low, so blood escapes from the aorta back into
the ventricle.
b. As pressure increases in the ventricle, less blood escapes, therefore the murmur
diminishes. This is called an early diastolic murmur - decrescendo shape.
Not heard in the aortic area but at the left sternal border because the blood is flowing in the other
way.

PULMONARY REGURGITATION
Same but heard at the upper left side of the sternum.

MITRAL STENOSIS
1. S2: Closing of aortic valve
2. Diastole:
a. Milliseconds after, the mitral valve opens, but does not open fully due to stenosis. At
the beginning of diastole, there is the most blood passing through from the atrium
to the ventricle (rapid filling) due to the greatest pressure difference.
b. Because the valve is stenotic, the leaflets snap - opening snap (just milliseconds
after S2) similar to ejection click in the systolic murmurs but is called an opening
snap in the diastolic murmurs. The murmur begins and is at highest intensity after
the opening snap, then slows down as pressures become more equal.
c. At the end of diastole, the atrium contracts a bit, causing an upslope in the murmur
at the end - pre-systolic accentuation
Heard in the mitral area (apex).
Described as an opening snap followed by a mid-diastolic rumble.

TRICUSPID STENOSIS
Same but heard in the tricuspid area.

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 EXTRA HEART SOUNDS

1. Systolic clicks: Ejection click (AS) or a non-ejection click (MVP)

2. Opening snap: Mitral stenosis
3. S3: AKA ventricular gallop.
a. Heard best in apex position, specifically when patient is in the lest lateral decubitus
position. Brings the heart closer in position to the stethoscope.
b. S3 is classically a volume-overload condition, heard in early diastole (after S2),
during the rapid filling phase. If there is too much blood, there is tensing of the
chordae tendineae causing the S3 sound.
c. In young patients, it can be normal. In adults, this is usually due to heart disease e.g.
CHF.
4. S4: AKA atrial gallop.
a. Heard best in apex position, specifically when patient is in the lest lateral decubitus
position (as above).
b. S4 is a pressure-overload condition e.g. HTN. Heart is contracting against increased
pressure, causing hypertrophy of the heart concentrically. The ventricle becomes
stiff. The atrium contracts at the end of diastole, causing a heart sound when it
contracts into a very stiff ventricle.
c. Heard at the end of diastole just before the next S1.
d. S4 is always pathological.

Mitral Valve Prolapse

Commonest valvular abnormality. Occurs alone or with:
- ASD, patent ductus arteriosus, cardiomyopathy, Turner’s syndrome, Marfan’s syndrome,
osteogenesis imperfecta, WPW

Symptoms: Usually asymptomatic.

May develop atypical chest pain, palpitations, and autonomic dysfunction symptoms
Signs: Mid-systolic click and/or late systolic murmur

Complications: MR, cerebral emboli, arrhythmias, sudden death

Tests: Echo (diagnostic). ECG – inferior T-wave inversion

Rx: Beta-blockers may help palpitations and chest pain.

Surgery if severe MR

29
Drugs

1. ACE-I
E.g. Perindopril, lisinopril, ramipril, enalapril
First-line hypertensives in young patients. Also used to treat heart failure and diabetic nephropathy.
Less effective in Afro-Caribbean patients.
Side effects: Cough (15% of patients), angioedema, hyperkalaemia, first-dose hypotension.
C/I: Pregnancy and breastfeeding, renovascular disease (may result in renal impairment), aortic
stenosis (hypotension), idiopathic angioedema. Specialist advice if K+ >5.0mmol/L.
Interactions: High-dose diuretic therapy – significantly increased risk of hypotension.
Monitoring: U&Es – a rise in Cr and K+ is expected.

2. ARBs
E.g. valsartan candesartan, losartan, irbesartan,
Generally used when patients do not tolerate ACE-I (cough). Also used for diabetic nephropathy.
Use in caution in patients with renovascular disease.
SEs: Hypotension, hyperkalaemia

3. Thiazide Diuretics
E.g. Bendroflumethiazide, indapamide, chlortalidone
Inhibit sodium reabsorption at the distal convoluted tubule. K+ lost as a result.
Used to treat mild heart failure.
SEs: Dehydration, postural hypotension, hyponatraemia, hypokalaemia, hypercalcaemia, gout.
Rare adverse effects: Thrombocytopenia, agranulocytosis, photosensitivity rash, pancreatitis

4. Direct Renin Inhibitors e.g. Aliskiren.

Relatively new. Adverse effect uncommon but diarrhoea occasionally seen.
Only current role in patients who are intolerant of more established antihypertensive drugs.

5. Beta-Blockers
Indicated for angina, post-MI, heart failure, arrhythmias (AF), HTN, thyrotoxicosis, migraine
prophylaxis, anxiety.
SEs: Bronchospasm, cold peripheries, fatigue, sleep disturbances (nightmares), erectile dysfunction
C/I: Uncontrolled heart failure, asthma, sick sinus syndrome, concurrent verapamil use (may
precipitate severe bradycardia)

6. Calcium Channel Blockers

Verapamil: Angina, HTN, arrhythmias. Highly negatively inotropic. Do not given with beta-blockers!
SEs: Heart failure, constipation, hypotension, bradycardia, flushing.
Diltiazem: Angina, HTN. Caution in HF and in those taking beta-blockers.
SEs: Hypotension, bradycardia, HF, ankle swelling.
Dihydropyridines: E.g. nifedipine, amlodipine, felodipine. Used for HTN, angina, Raynaud’s.
Affect peripheral vascular SM > myocardium therefore do not worsen heat failure but can cause
ankle swelling, flushing and headache.

30