CARDIO Flashcards
Aortic Dissection - Definition
A condition where a tear in the aortic intima allows blood to surge into the aortic wall, causing a split between the inner and outer tunica media, and creating a false lumen. Type A (70%) = ascending aorta, Type B (30%) = descending aorta (distal to L subclavian artery) As the dissection extends, branches of the aorta occlude sequentially, may obstruct subclavian, carotid, coeliac and renal arteries Aortic valve incompetence, inferior MI and cardiac arrest may develop if dissection moves proximally
Aortic Dissection - Aetiology
Degenerative changes in the smooth muscle of the aortic media are the predisposing event.
Common causes and predisposing factors are:
. hypertension;
. aortic atherosclerosis;
. connective tissue disease (e.g. SLE, Marfans, Ehlers–Danlos);
. congenital cardiac abnormalities (e.g. aortic coarctation);
. aortitis (e.g. Takayasus aortitis, tertiary syphilis);
. iatrogenic (e.g. during angiography or angioplasty);
. trauma;
. crack cocaine.
Aortic Dissection - Epidemiology
Most common in males between 40 and 60 years.
EXTRA NOTES:
Pulsus paradoxus = abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is <10mmHg
All patients with Type A thoracic dissection should be considered for surgery
Management = crossmatch 10 units blood, hypotensives, labetolol
Aortic Dissection - History
Sudden central ‘tearing’ pain, may radiate to the back (may mimic an MI).
Aortic dissection can lead to occlusion of the aorta and its branches:
- Carotid obstruction = hemiparesis, dysphasia, blackout.
- Coronary artery obstruction = chest pain (angina or MI).
- Subclavian obstruction = Ataxia, loss of consciousness.
- Anterior spinal artery = paraplegia.
- Coeliac obstruction = severe abdominal pain (ischaemic bowel).
- Renal artery obstruction: Anuria, renal failure.
Aortic Dissection - Exam
Murmur on the back below left scapula, descending to abdomen.
Blood pressure (BP): Hypertension (BP discrepancy between arms of >20 mmHg), wide pulse pressure.
If hypotensive may signify tamponade, check for pulsus paradoxus.
Aortic insufficiency: Collapsing pulse, early diastolic murmur over aortic area.
Unequal arm pulses.
There may be a palpable abdominal mass.
Aortic Dissection- Investigation
Bloods: FBC, cross-match 10 units of blood, U&E (renal function), clotting.
CXR: Widened mediastinum, localized bulge in the aortic arch.
ECG: Often normal. Signs of left ventricular hypertrophy or inferior MI if dissection com-
promises the ostia of the right coronary artery.
CT-thorax: False lumen of dissection can be visualized.
Echocardiography: Transoesophageal is highly specific (TOE). Cardiac catheterization and aortography.
Aortic Regurgitation - Definition & Epidemiology
Reflux of blood from aorta into left ventricle (LV) during diastole. (AR) also called aortic insufficiency.
EPIDEMIOLOGY
Chronic AR often begins in the late 50s, documented most frequently in >80y/o
Aortic Regurgitation- Aetiology
- Aortic valve leaflet abnormalities or damage: Bicuspid aortic valve, infective endocarditis, rheumatic fever, trauma.
- Aortic root/ascending aorta dilation: Systemic hypertension, aortic dissection, aortitis (e.g. syphilis, Takayasus arteritis), arthritides (rheumatoid arthritis, seronegative arthrit- ides), Marfans syndrome, pseudoxanthoma elasticum, Ehlers–Danlos syndrome, osteogenesis imperfecta.
- Reflux of blood into the LV during diastole results in left ventricular dilation and high end-diastolic volume and high Stroke V. The combination of high SV and low end-diastolic pressure in the aorta may explain the collapsing pulse and the wide pulse pressure. In acute AR, the LV cannot adapt to the rapid increase in end-diastolic volume caused by regurgitant blood.
Aortic Regurgitation - History
Chronic AR: initially asymptomatic. Later, symptoms of heart failure: exertional dyspnoea, orthopnoea, fatigue. Occasionally angina.
Severe acute AR: sudden cardiovascular collapse.
Symptoms related to the aetiology, e.g. chest or back pain in patients with aortic dissection.
Aortic Regurgitation - Exam
- Collapsing ‘water-hammer’ pulse and wide pulse pressure
- Thrusting and heaving (volume-loaded) displaced apex beat (hyperdyamic)
- Early diastolic murmur at lower left sternal edge, better heard with patient sitting forward + expiration
- Ejection systolic murmur is often heard because of increased flow across the valve
- Austin-Flint mid-diastolic murmur (severe AR) = over the apex, from turbulent reflux hitting anterior cusp of the mitral valve and causing a physiological mitral stenosis
- Rare signs associated with a hyperdynamic pulse:
- Quincke’s sign = visible pulsations on nail bed
- de Musset’s sign = head nodding in time with pulse
- Becker’s sign = visible pulsations of the pupils and retinal arteries
- Müller’s sign = visible pulsations of the uvula
- Corrigan’s sign = visible pulsations in the neck
- Traube’s sign = Pistol-shot (systolic and diastolic) sounds heard on auscultation of the femoral arteris
Duroziezs sign: A systolic and diastolic bruit heard on partial compression of femoral artery
with a stethoscope.
Rosenbachs sign: Systolic pulsations of the liver.
Gerhards sign: Systolic pulsations of the spleen.
Hills sign: Popliteal cuff systolic pressure exceeding brachial pressure by >60 mmHg.
Aortic Regurgitation - Investigation
CXR: Cardiomegaly. Dilation of the ascending aorta. Signs of pulmonary oedema may be seen with left heart failure.
ECG: May show signs of left ventricular hypertrophy (deep S wave in V1–2, tall R wave in V5–6, inverted T waves in I, aVL, V5–6 and left-axis deviation).
Echocardiogram: 2D echo and M-mode may indicate the underlying cause (e.g. aortic root dilation, bicuspid aortic valve) or the effects of AR (left ventricular dilation/dysfunction and fluttering of the anterior mitral valve leaflet).
Doppler echocardiography for detecting AR and assessing severity.
Cardiac catheterization with angiography: If there is uncertainty about the functional state of the ventricle or the presence of coronary artery disease.
Aortic Stenosis - Definition
Narrowing of the left ventricular outflow at the level of the aortic valve.
Aortic Stenosis - Aetiology
- Stenosis secondary to rheumatic heart disease (commonest worldwide);
- calcification of a congenital bicuspid aortic valve, William’s syndrome
- calcification/degeneration of a tricuspid aortic valve in the elderly, (senile calcification)
Aortic Stenosis - History
Classic triad = angina, syncope and heart failure!
May be asymptomatic initially.
Angina (because of high O2 demand of the hypertrophied ventricles).
Syncope or dizziness on exercise.
Symptoms of heart failure (e.g. dyspnoea).
Aortic Stenosis - Examination
- BP: Narrow pulse pressure.
- Pulse: Slow-rising.
- Palpation: Thrill in the aortic area (if severe). Forceful sustained thrusting undisplaced apex
beat. - Auscultation: Harsh ejection systolic murmur at aortic area, radiating to the carotid artery
and apex. - Second heart sound (A2 component) may be softened or absent (because of
calcification). A bicuspid valve may produce an ejection click. May be an S4 (occurs more often with bicuspid valves)
Distinguish from aortic sclerosis and hypertrophic obstructive cardiomyopathy
(HOCM)
Aortic Stenosis -Investigations
- ECG: Signs of LV hypertrophy (deep S wave in V1–2, tall R wave in V5–6, inverted T waves in I, aVL, V5–6 and left-axis deviation), LBBB, LA enlargement.
- CXR: Post-stenotic enlargement of the ascending aorta, calcification of aortic valve.
- Echocardiogram: Visualizes structural changes of the valves and level of stenosis (valvar, supravalvar or subvalvar). Estimation of aortic valve area and pressure gradient across the
valve in systole and left ventricular function may be assessed. (DIAGNOSTIC)
-Doppler echo = can estimate gradient across valves, severe stenosis if peak gradient ≥ 50mmHg and valve area <1cm2
- Cardiac angiography: Allows differentiation from other causes of angina, and to assess for
concomitant coronary artery disease (50% of patients with severe aortic stenosis have significant coronary artery disease).
Aortic Stenosis- Extra notes
Pulse pressure = difference between systolic and diastolic pressure
Aortic sclerosis = senile degeneration with no left ventricular outflow tract degeneration. The pulse character is normal, a thrill is not palpable and ejection systolic murmur radiates only faintly. S2 normal.
Signs of LVH = deep S wave in V1-2, tall R wave in V5-6, inverted T wave in I, aVL and V5-6, LAD
William’s syndrome = rare neurodevelopmental disorder characterized by a distinctive ‘elfin’ facial appearance, along with a low nasal bridge, unusually cheerful demeanour and ease with strangers, developmental delay coupled with language deficiencies, profound visuo-spatial impairments, supravalvular aortic stenosis and transient high calcium
Atrial Fibrillation - definition
Rapid, chaotic and ineffective atrial electrical conduction. Often subdivided into: ‘permanent’, ‘persistent’ (>7 days and responsive to cardioversion), and ‘paroxysmal’.
EPIDEMIOLOGY
Very common in the elderly, may be paroxysmal
Atrial Fibrillation- Aetiology
There may be no identifiable cause (‘lone’ atrial fibrillation (AF)).
Secondary causes lead to abnormal atrial electrical pathways that result in AF.
Systemic causes: Thyrotoxicosis, hypertension, pneumonia, alcohol.
Heart: Mitral valve disease, ischaemic heart disease, rheumatic heart disease, cardiomyopathy, pericarditis, sick sinus syndrome, atrial myxoma.
Lung: Bronchial carcinoma, pulmonary embolism.
Atrial Fibrillation- Symptoms
Often asymptomatic. Some patients experience palpitations or syncope. Symptoms of the cause of the AF.
Atrial Fibrillation- Examination
Irregularly irregular pulse, difference in apical beat and radial pulse.
Look for thyroid disease and valvular heart disease.
Atrial Fibrillation-Investigations
- ECG: Uneven baseline (fibrillations) with absent P waves, irregular QRS complexes. If there is a saw-tooth baseline, consider if there is atrial flutter.
- Blood: Cardiacenzymes, TFT, lipidprofile, U&E, Mg2, Ca2, (risk of digoxin toxicity high with hypokalaemia, hypomagnesaemia or hypercalcaemia).
- Echocardiogram: To assess for mitral valve disease, left atrial dilation, left ventricular dysfunction or structural abnormalities.
Atrial Fibrillation- Management
Treat any reversible cause (e.g. thyrotoxicosis, chest infection). Specific treatment strategy focuses on:
(1) Rhythm control:
If the AF is >48h from onset, anticoagulate (at least 3–4 weeks) before attempting cardioversion.
- DC cardioversion: Synchronized DC shock (2x 100 J, 1 x 200 J).
- Chemical cardioversion: Flecainide (contraindicated if there is history of ischaemic heart disease) or amiodarone.
- Prophylaxis against AF: Sotalol, amiodarone or flecainide. Also consider providing ‘pill-in-
the-pocket’ strategy for suitable patients.
(2) Rate control = Chronic ‘permanent’ AF: Ventricular rate control with digoxin, verapamil and/or b- blockers. Aim for rate of 90/min..
(3) Stroke risk stratification:
Low-risk patients can be managed with aspirin, and high-risk patients require anticoagulation with warfarin
Risk factors indicating high risk are previous thromboembolic event, age 75 years with hypertension, diabetes or vascular disease, and/or clinical evidence of valve disease, heart failure or impaired left ventricular function.
COMPLICATIONS Thromboembolism, increased with LA enlargement/ LV dysfunction. Heart failure (or worsens existing heart failure), Dilated cardiomyopathy, Angina.
PROGNOSIS
Chronic AF in a diseased heart does not usually return to sinus rhythm.
EXTRA
Atrial myxoma = benign tumour of the heart, found on interatrial septum (left more common than right)
Fleicanide = VG Na+ channel blocker, slowing the upstroke of the cardiac action potential
Amiodarone = K+ channel blocker (main), β-blocker, Ca2+/Na+ channel blocker
Verapamil = VG Ca2+ channel blocker
CHA2DS2VASC = Congestive heart failure, Hypertension (>140/90), Age≥75, Diabetes, Prior stroke/TIA/thromboembolism, vascular disease (PVD, MI), Age 64-75 years, Sex (female)
Cardioversion more likely if: AF recent, <65y/o, underlying cause has been successfully treated
Cardiac Arrest - definition
Acute cessation of cardiac function.
Cardiac Arrest - Aetiology
Classical reversible causes of cardiac arrest are the four Hs and four Ts: Hypoxia Hypothermia Hypovolaemia Hypo- or hyperkalaemia Tamponade Tension pneumothorax Thromboembolism Toxins and other metabolic disorders (drugs, therapeutic agents, sepsis)
Cardiac Arrest- Examination (History too)
Hx - Doesn’t apply
Exam - Unconscious, patient is not breathing, absent carotid pulses.
Cardiac Arrest- Investigations
Cardiac monitor: Classification of the rhythm directs management (see below). Bloods: ABG, U&E, FBC, cross-match, clotting, toxicology screen, glucose.
Cardiac Arrest- Management
Safety: Approach any arrest scene with caution as the cause of the arrest may still pose a threat. Defibrillators and oxygen are hazards. Help should be summoned as soon as possible.
Basic life support: DR ABC
1. If the arrest is witnessed and monitored, consider giving a precordial thump if no
defibrillator immediately available.
2. Clear and maintain airway with head tilt (if no spinal injury), jaw thrust and chin lift.
3. Assess breathing by look, listen and feel.
If not breathing, give two effective breaths immediately.
4. Assess circulation at carotid pulse for 10 s.
If absent, give 30 chest compressions at rate of 100min 1. Continue cycles of 30 compressions for every two breaths.
5. Proceed to advanced life support as soon as possible.
Advanced life support:
1. Attach cardiac monitor and defibrillator.
2. Assess the rhythm:
(A) If pulseless ventricular tachycardia (VT)2 or ventricular fibrillation (VF)3 (‘shockable rhythm’):
- Defibrillate once: 150–360 J biphasic, 360 J monophasic. (Ensure no one is touching
patient or bed when defibrillating.)
- Resume CPR immediately for 2 min, and then return to 2.
- Administer adrenaline (1 mg IV) after second defibrillation and again every 3–5 min.
- If ‘shockable rhythm’ persists after third shock, administer amiodarone 300 mg IV bolus
(or lidocaine).
(B) If pulseless electrical activity (PEA) or asystole:
- CPR for 2 min, and then return to 2.
- Administer adrenaline (1 mg IV) every 3–5 min.
- Atropine (3 mg IV, once only) if asystole or PEA with rate <60 min 1.
(C) During CPR:
- Check electrodes, paddle positions and contacts.
- Secure airway (e.g. attempt endotracheal intubation, high-flow oxygen). Once airway
secure, give continuous compressions and breaths.
- Consider magnesium, bicarbonate, external pacing.
- Stop CPR and check pulse only if change in rhythm or signs of life.
Treatment of reversible causes:
Hypothermia: Warm slowly.
Hypo- or hyperkalaemia: Correction of electrolytes.
Hypovolaemia: IV colloids, crystalloids or blood products.
Tamponade: Pericardiocentesis under xiphisternum up and leftwards.
Tension pneumothorax: Needle into second intercostal space, mid-clavicular line. Thromboembolism: (see Pulmonary embolism, Myocardial infarction).
Toxins: (see drug formulary for antidotes).
COMPLICATIONS Irreversible hypoxic brain damage, death.
P R O G N O S I S Resuscitation is less successful in the arrests that occur outside hospital. Duration of inadequate effective cardiac output is associated with poor prognosis.
Cardiac Failure - Definition
Inability of the cardiac output to meet the bodys demands despite normal venous pressures.
Cardiac Failure - Aetiology
Low output ( low cardiac output):
Left heart failure: Ischaemic heart disease, hypertension, cardiomyopathy, aortic valve
disease, mitral regurgitation.
Right heart failure: Secondary to left heart failure, infarction, cardiomyopathy, pulmonary
hypertension/embolus/valve disease, chronic lung disease, tricuspid regurgitation, con-
strictive pericarditis/pericardial tamponade.
Biventricular failure: Arrhythmia, cardiomyopathy (dilated or restrictive), myocarditis, drug
toxicity.
High output (high demand): Anaemia, beriberi, pregnancy, Pagets disease, hyperthyroidism,
arteriovenous malformation.
Cardiac Failure - Epidemiology
Left: Tachycardia, tachypnoea, displaced apex beat, bilateral basal crackles, third heart sound
(gallop rhythm: rapid ventricular filling), pansystolic murmur (functional mitral
regurgitation).
Acute LVF: Tachypnoea, cyanosis, tachycardia, peripheral shutdown, pulsus alternans, gallop
rhythm, wheeze cardiac asthma, fine crackles throughout the lung.
Right: “ JVP, hepatomegaly, ascites, ankle/sacral pitting, oedema, signs of functional
tricuspid regurgitation (see Tricuspid regurgitation).
Cardiac Failure - History
Left (symptoms caused by pulmonary congestion): Dyspnoea (New York Heart Association classification):
1. no dyspnoea;
2. dyspnoea on ordinary activities;
3. dyspnoea on less than ordinary activities;
4. dyspnoea at rest.
Orthopnoea, paroxysmal nocturnal dyspnoea, fatigue.
Acute LVF: Dyspnoea, wheeze, cough and pink frothy sputum.
Right: Swollen ankles, fatigue, “ weight (resulting from oedema), # exercise tolerance,
anorexia, nausea.
Cardiac Failure -Investigations
Blood: FBC, U&Es, LFTs, CRP, glucose, lipids, TFTs.
In acute LVF: ABG, troponin, brain natriuretic peptide (BNP). “ Plasma BNP suggests the
diagnosis of cardiac failure. A low plasma BNP rules out cardiac failure (90% sensitivity). CXR (in acute LVF): Cardiomegaly (heart >50 % of thoracic width), prominent upper lobe vessels, pleural effusion, interstitial oedema (‘Kerley B lines’), perihilar shadowing (‘bats
wings’), fluid in the fissures.
ECG: May be normal. May have ischaemic changes, arrhythmia, left ventricular hypertrophy
(seen in hypertension).
Echocardiogram: To assess ventricular contraction. If left ventricular ejection fraction (LVEF)
<40%: systolic dysfunction. Diastolic dysfunction: # compliance leading to a restrictive
filling defect.
Swan–Ganz catheter: Allows measurements of right atrial, right ventricular, pulmonary
artery, pulmonary wedge and left ventricular end-diastolic pressures.
Cardiac Failure - Management
Acute LVF: Cardiogenic shock: Severe cardiac failure with low BP requires the use of inotropes (e.g. dopamine, dobutamine) and should be managed in ITU
Pulmonary oedema: Sit up patient, 60–100% O2 and consider CPAP. Other first-line therapies are diamorphine (venodilator and anxiolytic effect), GTN infusion ( decrease preload), IV furo- semide if fluid overloaded (venodilator and later diuretic effect). Monitor BP, respiratory rate, sat. O2, urine output, ECG. Treat the cause, e.g. myocardial infarction, arrhythmia.Chronic LVF: Treat the cause, e.g. hypertension. Treat exacerbating factors, e.g. anaemia. The following drug therapies are evidence-based.1
ACE-inhibitors (e.g. enalapril, perindopril, ramipril): Inhibit intracardiac renin-angiotensin
system which may contribute to myocardial hypertrophy and remodelling. ACE inhibitors
slow progression of the heart failure and improve survival.
b-Blockers (bisprolol or carvedilol): Block the effects of chronically activated sympathetic
system, slow progression of the heart failure and improve survival. The benefits of ACE
inhibitors and b-blockers are additive.
Loop diuretics (e.g. furosemide) and dietary salt restriction to correct fluid overload. Aldosterone antagonists (spironolactone or, if not tolerated, eplerenone) improve survival in
patients with NYHA class III/IV symptoms and on standard therapy. Monitor Kþ (may cause hyperkalaemia). May be used to assist in the management of diuretic-induced hypokalaemia.
Angiotensin receptor blockers (ARB) (e.g. candesartan): May be added in patients with persistent symptoms despite ACE inhibitors and b-blockers. Monitor Kþ (may cause hyperkalaemia).
Hydralazine and a nitrate: May be added in patients (particularly in Afro-Caribbeans) with persistent symptoms despite therapy with an ACE inhibitor and b-blocker.
Digoxin: Positive inotrope, # hospitalization, but does not improve survival.
n-3 polyunsaturated fatty acids: Provide a small beneficial advantage in terms of mortality. Cardiac resynchronization therapy (CRT): Biventricular pacing improves symptoms and
survival in patients with LVEF 35%, cardiac dyssynchrony (QRS>120msec) and moderate to severe symptoms despite optimal medical therapy. Most patients who meet these criteria are also candidates for an implantable cardiac defibrillator (ICD) and receive a combined device.
Avoid drugs that can adversely affect patients with heart failure due to systolic dysfunction, e.g. NSAIDs, non-dihydropyridine calcium channel blockers (i.e. diltiazem and verapamil).
C O M P L I C A T I O N S Respiratory failure, cardiogenic shock, death.
P R O G N O S I S Fifty per cent of patients with severe heart failure die within 2 years.
Cardiomyopathy - definition
Primary disease of the myocardium. Cardiomyopathy may be dilated, hy- pertrophic or restrictive.
Cardiomyopathy - Aetiology
The majority are idiopathic.
Dilated: Post-viral myocarditis, alcohol, drugs (e.g. doxorubicin, cocaine), familial ( 25% of
idiopathic cases, usually autosomal dominant), thyrotoxicosis, haemochromatosis,
peripartum.
Hypertrophic: Up to 50% of cases are genetic (autosomal dominant) with mutations in
b-myosin, troponin T or a-tropomyosin (components of the contractile apparatus). Restrictive: Amyloidosis, sarcoidosis, haemochromatosis.
Cardiomyopathy - History
Dilated: Symptoms of heart failure, arrhythmias, thromboembolism, family history of sudden death.
Hypertrophic: Usually none. Syncope, angina, arrhythmias, family history of sudden death. Restrictive: Dyspnoea, fatigue, arrhythmias, ankle or abdominal swelling.
Enquire about family history of sudden death.
Cardiomyopathy - Examination
Dilated: “ JVP, displaced apex beat, functional mitral and tricuspid regurgitations, third heart sound.
Hypertrophic: Jerky carotid pulse, double apex beat, ejection systolic murmur. Restrictive: “ JVP (Kussmauls sign: further “ on inspiration), palpable apex beat, third heart
sound, ascites, ankle oedema, hepatomegaly.
Cardiomyopathy - Investigations
CXR: May show cardiomegaly, and signs of heart failure.
ECG:
All types: Non-specific ST changes, conduction defects, arrhythmias
Hypertrophic: Left-axis deviation, signs of left ventricular hypertrophy (see Aortic stenosis), Q
waves in inferior and lateral leads.
Restrictive: Low voltage complexes.
Echocardiography:
Dilated: Dilated ventricles with ‘global’ hypokinesia.
Hypertrophic: Ventricular hypertrophy (disproportionate septal involvement)
Restrictive: Non-dilated non-hypertrophied ventricles. Atrial enlargement, preserved systolic
function, diastolic dysfunction, granular or ‘sparkling’ appearance of myocardium in
amyloidosis.
Cardiac catheterization: May be necessary for measurement of pressures. Endomyocardial biopsy: May be helpful in restrictive cardiomyopathy. Pedigree or genetic analysis: Rarely necessary.
Cardiomyopathy - Management
Dilated: Treat heart failure and arrhythmias. Consider implantable cardiac defibrillators (ICD) for recurrent VTs.
Hypertrophic: Treat arrhythmias with drugs, ICD for survivors of sudden death, reduce outflow tract gradients, pacemaker, surgery (e.g. septal myomectomy, septal ablation with ethanol). Screen family members with ECG or echocardiography.
Restrictive: No specific treatment. Manage the underlying cause.
Cardiac transplantation: May be considered in end-stage heart failure in all cardiomyop-
athy types.
C O M P L I C A T I O N S Heart failure, arrhythmias (atrial and ventricular). Dilated and hypertrophic cardiomyopathy: Sudden death and embolism. Hypertrophic: Infective endocarditis.
PROGNOSIS
Dilated: Depends on the aetiology, New York Heart Association functional class and ejection fraction.
Hypertrophic: Ventricular tachyarrhythmias are the major cause of sudden death. Restrictive: Poor prognosis, many die within the first year after diagnosis.
Heart Block - definition
Impairment of the atrioventricular (AV) node impulse conduction, as repre- sented by the interval between P wave and QRS complex.
Heart Block - The 4 different types
“If the R is far from the P then you have first degree,
Longer longer longer drop, then you have Wenchebach,
If some Ps don’t get through then you have Mobitz Type II,
If the Ps and Qs dont agree then you have a third Degree”
First-degree AV block: Prolonged conduction through the AV node.
Second-degree AV block: Mobitz type I (Wenckebach): Progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV
node. The cycle then begins again.
Mobitz type II: Intermittent or regular failure of conduction through AV node. Also defined
by the number of normal conductions per failed or abnormal one (e.g. 2 : 1 or 3 : 1). Third-degree (complete) AV block: No relationship between atrial and ventricular con- traction. Failure of conduction through the AV node leads to a ventricular contraction
generated by a focus of depolarization within the ventricle (ventricular escape).
Heart Block - Aetiology
MI or ischaemic heart disease (most common cause).
Infection (e.g. rheumatic fever, infective endocarditis). Drugs(e.g.digoxin,b-blockers,Ca2þ channelantagonists).
Metabolic (e.g. hyperkalaemia, cholestatic jaundice, hypothermia).
Infiltration of conducting system (e.g. sarcoidosis, cardiac neoplasms, amyloidosis). Degeneration of the conducting system.
Heart Block - History
First degree: Asymptomatic.
Wenckebach: Usually asymptomatic.
Mobitz type II and third-degree block: May cause Stokes–Adams attacks (syncope caused
by ventricular asystole). Other presentations include dizziness, palpitations, chest pain and heart failure.
Heart Block - Examination
ECG
First degree: Prolonged PR interval (>0.2 s)
Mobitz type I (Wenckebach): Progressively prolonged PR interval, culminating in a P wave that is not followed by a QRS. The pattern then begins again.
Mobitz type II: Intermittently a P wave is not followed by a QRS. There may be
a regular pattern of P waves not followed by a QRS (e.g. two
P waves per QRS, indicating 2 : 1 block)
Third degree (complete): No relationship between P waves and QRS complexes. If QRS initiated by focus in the bundle of His, the QRS is narrow. QRS initiated more distally are wide and slow rate ( 30 beats/min).
Look for other signs of cause, e.g. ischaemia.
CXR: Cardiac enlargement, pulmonary oedema.
Blood: TFT, digoxin level, cardiac enzymes, troponin.
Echocardiogram: Wall motion abnormalities, aortic valve disease, vegetations.
Heart Block - Management
MANAGEMENT
Chronic block: Permanent pacemaker (PPM) insertion is recommended in patients with
third-degree heart block, advanced Mobitz type II and symptomatic Mobitz type I. Acute block (e.g. secondary to anterior MI): If associated with clinical deterioration, IV
atropine and consider temporary (external) pacemaker.
C O M P L I C A T I O N S Asystole. Cardiac arrest. Heart failure. Complications of any pacemaker inserted.
P R O G N O S I S Mobitz type II and third-degree block usually indicate serious underlying cardiac disease.
Hypertension - Definition
Defined as systolic BP >140mmHg and/or diastolic BP >85mmHg mea- sured on three separate occasions. Malignant hypertension is defined as BP 200/ 130 mmHg.
Hypertension - Aetiology
Primary:
. Essential or idiopathic hypertension (Commonest, >90% of cases).
Secondary:
. Renal: Renal artery stenosis, chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney disease, chronic renal failure.
. Endocrine: Diabetes mellitus, hyperthyroidism, Cushings syndrome, Conns syndrome, hyperparathyroidism, phaeochromocytoma, congenital adrenal hyperplasia, acromegaly.
. Cardiovascular: Aortic coarctation, “ intravascular volume.
. Drugs: Sympathomimetics, corticosteroids, oral contraceptive pill.
. Pregnancy: Pre-eclampsia.
Hypertension - History
Often asymptomatic.
Symptoms of complications (see Complications).
Symptoms of the cause.
Accelerated or malignant hypertension: Scotomas (visual field loss), blurred vision,
headache, seizures, nausea, vomiting, acute heart failure.
Hypertension - Examination
Measure on two to three different occasions before diagnosing hyper- tension and record lowest reading.
There may be loud second heart sound, fourth heart sound.
Examine for causes, e.g. radiofemoral delay (aortic coarctation), renal artery bruit (renal artery
stenosis). Examine for end-organ damage, e.g. fundoscopy for retinopathy. Keith–Wagner classification of retinopathy:
(I) ‘silver wiring’;
(II) as above, plus arteriovenous nipping;
(III) as above, plus flame haemorrhages and cotton wool exudates;
(IV) as above, plus papilloedema.
Hypertension - Pathology
Fibrotic intimal thickening of the arteries, reduplication of elastic lamina and smooth muscle hypertrophy. Arteriolar wall layers replaced by pink hyaline material with luminal narrowing (hyaline arteriosclerosis).
Hypertension - Investigations
Blood: U&E, glucose, lipids.
Urine dipstick: Blood and protein.
ECG: May show signs of left ventricular hypertrophy (deep S wave in V1–2, tall R wave in V5–6,
inverted T waves in I, aVL, V5–6, left-axis deviation) or ischaemia.
Ambulatory BP monitoring (BP measured throughout the day): Excludes ‘white coat’ hypertension, allows monitoring of treatment response, assesses preservation of noc-
turnal dip.
Others: Especially in patients <35 years or other suspected secondary cases (see relevant
topics).
Hypertension - Management
Assessment and modification of other cardiovascular risk factors. Conservative: Stop smoking, lose weight, decrease alcohol, reduce dietary Na+ .
Investigate for secondary causes: Worthwhile in young patients, malignant hypertension or poor response to treatment.
Medical1: Treatment recommended for systolic BP 160 mmHg and/or diastolic BP 100 mmHg, or if evidence of end-organ damage. Other hypertension patients may still require treatment depending on other cardiac risk factors. Multiple drug therapies often
necessary.
. Thiazide diuretics (e.g. bendrofluamethiazide): Recommended first line, especially in >55-
year-olds or black patients.
. ACE inhibitors (e.g. ramipril) or angiotensin-II antagonist (e.g. losartan): First line in <55-
year-olds, diabetic patients, heart failure or left ventricular dysfunction.
. Ca2 þ channel antagonists (e.g. amlodipine): Recommended first line, especially in >60-
year-olds or black patients.
. b-Blockers (e.g. atenolol): Not preferred initial therapy, but may be considered in younger
patients. Avoid combining with thiazide diuretic to reduce patient risk of developing
diabetes. May increase risk of heart failure.
. a-Blockers (e.g. doxazosin): Fourth-line agent. May be useful for patients with prostatism.
Target BP:
. 140/85 mmHg (non-diabetic);
. 130/80 mmHg (diabetes without proteinuria);
. 125/75 mmHg (diabetes with proteinuria).
Severe hypertension (diastolic BP > 140 mmHg): Atenolol or nifedipine.
Acute malignant hypertension: IV b-blocker, labetolol or hydralazine sodium nitroprus-
side. Avoid very rapid lowering which can cause cerebral infarction.
C O M P L I C A T I O N S Heart failure, coronary artery disease and MI, CVA, peripheral vascular disease, emboli, retinopathy, renal failure, hypertensive encephalopathy, posterior reversible encephalopathy syndrome (PRES), malignant hypertension.
PROGNOSIS Good, if BP controlled. Uncontrolled hypertension linked with increased mortality (6 stroke risk and 3 cardiac death risk). Treatment reduces incidence of renal damage, stroke and heart failure.
Ischaemic Heart Disease - Definition
Characterized by decreased blood supply (ischaemia) to the heart muscle resulting in chest pain (angina pectoris). May present as ‘stable angina’ or ‘acute coronary syndrome’ (ACS).
ACS can be further subdivided into unstable angina (no cardiac injury), non-ST-elevation myocardial infarction (NSTEMI) or ST-elevation MI (STEMI, transmural infarction). MI refers to cardiac muscle necrosis resulting from ischaemia.
Ischaemic Heart Disease - Aetiology
Angina pectoris occurs when myocardial oxygen demand exceeds oxygen supply. The most common cause is atherosclerosis. Other causes of coronary artery narrowing such as spasm (e.g. from cocaine), arteritis and emboli are rare.
MI is caused by sudden occlusion of a coronary artery due to rupture of an atheromatous plaque and thrombus formation.
Atherosclerosis: Endothelial injury is followed by migration of monocytes into subendothe- lial space and differentiation into macrophages. Macrophages accumulate LDL lipids insudated in the subendothelium and become foam cells. They release growth factors, which stimulate smooth muscle proliferation, production of collagen and proteoglycans. This leads to the formation of an atheromatous plaque.
ASSOCIATIONS/RISK FACTORS Male, diabetes mellitus, family history, hypertension, hyperlipidaemia, smoking, previous history.
Ischaemic Heart Disease - History
ACS: Chest pain or discomfort of acute onset. Central heavy tight ‘gripping’ pain that radiates to arms (usually left), neck, jaw or epigastrium. Occurring at rest, “ severity and frequency of previously stable angina.
May be associated with breathlessness, sweating, nausea and vomiting. May be silent in elderly or in patients with diabetes.
Stable angina: Brought on by exertion and relieved by rest.
Ischaemic Heart Disease - Examination
Stable angina: Look for signs of risk factors.
ACS: May have no clinical signs. Pale, sweating, restless, low-grade pyrexia. Check both radial
pulses for aortic dissectio.
Arrhythmias, disturbances of BP. New heart murmurs (e.g. pansystolic murmur of mitral
regurgitation from papillary muscle rupture or ventricular septal defect).
Signs of complications, i.e. acute heart failure, cardiogenic shock (hypotension, cold peripheries, oliguria).
Ischaemic Heart Disease - Investigations : Blood and ECG
Blood: FBC, U&Es, CRP, glucose, lipid profile, cardiac enzymes: CK-MB and troponin-T or I1 (sensitive marker of cardiac injury, “ after 12 h), amylase (pancreatitis may mimic MI), TFTs. AST and LDH “ after 24 and 48 h, respectively; occasionally used only to make retro- spective diagnosis.
ECG:
Unstable angina or NSTEMI: May show ST depression, T-wave inversion (Q waves in these
patients may indicate old MIs).
ST-elevation (Q-wave) MI: Hyperacute T waves, ST elevation (>1 mm in limb leads, >2 mm in
chest leads), new-onset LBBB. Later: T inversion (hours) and Q waves (days).
LOCATION OF INFARCT -
Inferior leads - II, III, aVF
Anterior wall - Septum (V1–V2), apex (V3–V4), anterolateral wall (V5–V6)
Lateral wall - I, aVL
Posterior infarct - Tall R wave and ST depression in V1–V3
Ischaemic Heart Disease - Investigations: Other
CXR: To look for signs of heart failure. Useful to look for differentials (e.g. aortic dissection). Exercise ECG testing (treadmill test)2: To determine prognosis and management. Indications: In patients with troponin-negative ACS, or stable angina with an intermediate or
high pretest probability of coronary heart disease (based on the characteristics of their chest pain, cardiac risk factors, age and gender). Patients should not be on digoxin (associated with a false-positive result).
Positive test: Defined as 1 mm horizontal or downsloping ST-segment depression measured at 80 ms after the end of the QRS complex (sensitivity: 60% and specificity: 90%). Failed test: Failure to achieve at least 85% of the predicted maximal heart rate (220 – age) and
otherwise negative (i.e. absence of chest discomfort or ECG findings). b-Blockers # the
maximal heart rate that is achieved and may be stopped prior to the test.
Resting ECG abnormalities (e.g. preexcitation syndrome, >1mm of ST depression, LBBB or
paced ventricular rhythm) interfere with interpretation.
Radionuclide myocardial perfusion imaging (rMPI): Uses Tc-99m sestamibi or tetro-
fosmin. Can be performed under stress (exercise or pharmacological) or at rest. Stress testing would show low uptake in ischaemic myocardium. Rest testing can be used in patient with ACS, no previous MI but non-diagnostic troponin and ECGs.
Echocardiogram: Measure LVEF (early measurements may be misleading because of myocardial stunning). Exercise (or dobutamine stress) echocardiography may detect inducible wall motion abnormalities.
Pharmacologic stress testing: For patients who cannot exercise or if the exercise test is inconclusive. Pharmacological agents such as dipyridamole, adenosine or dobutamine can be used to induce a tachycardia. Various imaging modalities (e.g. rMPI, echocardi- ography) can be used to detect ischaemic myocardium. Dipyridamole and adenosine are contraindicated in AV block and reactive airway disease.
Cardiac catheterization/angiography: In ACS with positive troponin or TIMI score 5–7, or if high risk on stress testing (using Duke treadmill score based on exercise time, maximum ST-segment deviation and exercise angina).
Coronary calcium scoring using specialized CT (if available): may have a role in outpatients with atypical chest pain or in acute chest pain that is not clearly due to ischaemia (absence of CAC excludes obstructive coronary artery disease).
Ischaemic Heart Disease - Management
Stable angina:
- Minimize cardiac risk factors: Control BP, hyperlipidaemia and diabetes. Provide advice on
smoking, exercise, weight loss and low-fat diet. All patients should receive aspirin (75 mg/ day) unless contraindicated.
- Immediate symptom relief: GTN as a spray or sublingually.
- Long-term treatment: b-Blockers, e.g. atenolol, unless contraindicated (contraindications
include acute heart failure, cardiogenic shock, bradycardia, heart block, asthma), calcium channel blockers (e.g. verapamil, diltiazem), nitrates (e.g. isosorbide dinitrate). Dual therapy may be indicated if monotherapy is ineffective. - Percutaneous coronary intervention (PCI): For localized areas of stenosis, in patients with angina not controlled despite maximal tolerable medical therapy. Restenosis rate is 25% at 6 months but drug-eluting coronary stents # restenosis rates (release an anti-restenotic drug, e.g. sirolimus or paclitaxel).
- Coronary artery bypass graft (CABG): For more severe cases (three-vessel disease). The rates of MI and overall survival are generally similar between PCI and CABG.
Unstable angina/NSTEMI3: - Admit to coronary care unit (CCU), oxygen, IV access, monitor vital signs and serial ECG.
- Analgesia: GTN (initially sublingual, IV infusion if persistent chest pain), morphine sulphate/
diamorphine, antiemetic (metoclopramide). - Aspirin (loading): 300 mg chewed. Maintenance: 75 mg, indefinite.
- Clopidogrel (loading): 300 mg. Maintenance: 75 mg for at least 1 year if troponin positive or
high risk. - Low-molecular-weight heparin (e.g. enoxaparin or dalteparin).
- b-Blocker (e.g. metoprolol) if not contraindicated.
- Glucose–insulin infusion if blood glucose >11 mmol/L.
- Consider glycoprotein (GP) IIb/IIIa inhibitors, e.g. tirofiban (initiated on presentation and
continued for 48–72 h or until PCI) in patients:
. undergoing PCI; or
. at high risk for further cardiac events (troponin positive, TIMI risk score 4, continuing
ischaemia or other high-risk features). - If little improvement, consider urgent angiography revascularization.
STEMI:
- Admit to CCU, oxygen, IV access, monitor vital signs and serial ECG.
- Analgesia: GTN (initially sublingual, IV infusion if persistent chest pain), morphine sulphate/
diamorphine, antiemetic (metoclopramide)
- Aspirin (loading): 300 mg chewed.
Maintenance: 75 mg, indefinite.
- Clopidogrel (loading): 600 mg if patient going to primary PCI, 300 mg if undergoing
thrombolysis and 75 years of age, 75 mg if undergoing thrombolysis and >75 years of
age. Maintenance: 75 mg, for at least 1 year.
- b-Blocker (e.g. metoprolol) if not contraindicated.
- If undergoing primary PCI: IV heparin (plus GP IIb/IIIa inhibitor) or bivalirudin (an
antithrombin). If undergoing thrombolysis with recombinant tissue plasminogen
activator (rtPA): IV heparin.
- Glucose–insulin infusion if blood glucose >11 mmol/L.
- Primary PCI 4 with goal <90 min if available or thrombolysis (see below) with goal of 30 min. - Thrombolysis: Using fibrinolytics such as streptokinase or rtPA (alteplase, reteplase,
tenecteplase) if within 12h of chest pain with ECG changes (ST elevation, new-onset LBBB or posterior infarction) and not contraindicated.5 Rescue PCI: If continued pain or ST elevation after thrombolysis (<50% lower of the initial ST-segment elevation on a follow-up ECG 60–90 min after fibrinolytic therapy).
Secondary Prevention: Antiplatelet agents (aspirin and clopidogrel), ACE inhibitors, b-blockers and statins. Control other risk factors (smoking, diabetes, hypertension). Advice: Not to drive for 1 month following MI. Education by cardiac rehabilitation team:
lifestyle changes (e.g. exercise, stop smoking, changing diet). CABG for patients with left main stem or three-vessel disease.
COMPLICATIONS At risk of MI and other vascular diseases (e.g. stroke, peripheral vascular disease). Cardiac injury can lead secondarily to heart failure and arrhythmias.
Early complications of MI (24–72 h): Death, cardiogenic shock, heart failure, ventricular arrhythmias, heart block, pericarditis, myocardial rupture, thromboembolism.
Late complications of MI: Ventricular wall (or septum) rupture, valvular regurgitation, ventricular aneurysms, tamponade, Dresslers syndrome (pericarditis), thromboembolism.
Ischaemic Heart Disease - Prognosis
ACS: TIMI score (range 0–7) can be used for risk stratification (high scores are associated with high risk of cardiac events within 30 days), consists of:
(1) >65 years;
(2) known coronary artery disease;
(3) aspirin in last 7 days;
(4) severe angina (>2 episodes in 24 h); (5) ST deviation >1 mm;
(6) elevated troponin levels;
(7) >3 coronary artery disease risk factors
(hypertension, hyperlipidaemia, family history, diabetes, smoking).
Killip classification of acute MI:
Class I: no evidence of heart failure.
Class II: mild to moderate heart failure (S3, crepitations
Mitral regurgitation - Definition
Retrograde flow of blood from LV to left atrium during systole.
Mitral regurgitation - Aetiology
Mitral valve damage or dysfunction:
. rheumatic heart disease (most common);
. infective endocarditis;
. mitral valve prolapse (prolapse of mitral valve leaflets into the left atrium during systole);
. papillary muscle rupture or dysfunction (secondary to ischaemic heart disease or
cardiomyopathy);
. chordal rupture and floppy mitral valve associated with connective tissue diseases
(e.g. pseudoxanthoma elasticum1, osteogenesis imperfecta,2 Ehlers–Danlos syndrome, 3 Marfan syndromes, SLE).
Functional mitral regurgitation may be secondary to left ventricular dilation.
Mitral regurgitation - History
Acute MR: May present with symptoms of left ventricular failure.
Chronic MR: May be asymptomatic or present with exertional dyspnoea, palpitations if in AF
and fatigue.
Mitral valve prolapse: Asymptomatic or atypical chest pain or palpitations.
Mitral regurgitation - Examination
Pulse may be normal or irregularly irregular (AF).
Apex beat may be laterally displaced and thrusting (left ventricular dilation).
Pansystolic murmur, loudest at apex, radiating to axilla (palpable as a thrill). S1 is soft; S3 may
be heard (rapid ventricular filling in early diastole).
Signs of left ventricular failure in acute mitral regurgitation.
Mitral valve prolapse: Mid-systolic click and late systolic murmur. The click moves towards
the first heart sound on standing and moves away on lying down.
Mitral regurgitation - Investigation
ECG: Normal or may show AF or broad bifid p wave (p mitrale) indicating delayed activation of left atrium due to left atrial enlargement.
CXR: Acute mitral regurgitation may produce signs of left ventricular failure. Chronic mitral regurgitation shows left atrial enlargement, cardiomegaly (caused by left ventricular dilation) or mitral valve calcification in rheumatic cases.
Echocardiography: Every 6–12 months for moderate–severe MR to assess the LV ejection fraction and end-systolic dimension.
Mitral regurgitation - Management
Surgical: Indicated in patients with chronic MR with symptoms or LV enlargement or dysfunction, pulmonary hypertension, or new-onset AF.
Mitral valve repair: May occasionally be feasible.
Mitral valve replacement: Mechanical valve with lifelong anticoagulation in patients <65 years
with long-standing AF. Bioprosthetic valve in patients with a contraindication to warfarin or 65 years of age (since limited durability of bioprosthetic valve is less of an issue). The choice of valve in patients <65 years who are in sinus rhythm relies on patient preference. Discuss the risks of warfarin compared to the likelihood of repeat valve replacement in the future.
Medical:
Functional MR due to LV dysfunction: ACE inhibitors and/or angiotensin II receptor blockers.
Optimal medical therapy of heart failure. In appropriate patients, CRT.
Mitral valve prolapse and symptomatic patients with primary MR (e.g. rheumatic or myx-
omatous): # systolic pressure (b-blockers, diuretic).
Treatment of atrial fibrillation (See Atrial Fibrillation).
Anticoagulation with warfarin (target INR: 2–3): In patients with AF, history of systemic
embolism or rheumatic mitral valve disease with left atrial thrombus. Antibiotic prophy- laxis is no longer recommended in the absence of prosthetic repair or replacement for those undergoing dental or other invasive procedures.
Advice: Patients with severe MR, LV enlargement, pulmonary hypertension or # left ven- tricular systolic function at rest should not participate in any competitive sports. Patients treated with long-term anticoagulation therapy should not engage in contact sports.
COMPLICATIONS Left atrial enlargement and AF (and resultant systemic embolism), pulmonary oedema, pulmonary hypertension, right heart failure, infective endocarditis.
P R O G N O S I S Prognosis depends on aetiology, severity and state of left ventricular function. Acute mitral regurgitation resulting from rupture of a cusp or papillary muscle has a poor prognosis. Rheumatic mitral regurgitation may slowly deteriorate over 10–20 years.
Mitral Stenosis - Definition
Mitral valve narrowing causing obstruction to blood flow from the left atrium to the ventricle.
Mitral Stenosis - Aetiology
Most common cause is rheumatic heart disease (90%).
Rarer causes are congenital mitral stenosis, SLE, rheumatoid arthritis, endocarditis and atrial
myxoma (rare cardiac tumour).
Mitral Stenosis - History and epidemiology
May be asymptomatic.
Presents with fatigue, shortness of breath on exertion or lying down (orthopnoea). Palpita-
tions (related to AF).
Rare symptoms: Cough, haemoptysis, hoarseness caused by compression of the left
laryngeal nerve by an enlarged left atrium.
Epidemiology:
Incidence is declining in industrialized countries because of declining incidence of rheumatic fever.
Mitral Stenosis - Examination
May have peripheral or facial cyanosis (malar flush).
Pulse: May be ‘thready’ or irregularly irregular (AF).
Palpation: Apex beat is undisplaced and tapping. Parasternal heave (right ventricular
hypertrophy and pulmonary hypertension)
Auscultation: Loud first heart sound with opening snap.
Mid-diastolic murmur (presystolic accentuation if in sinus rhythm). Evidence of pulmonary oedema on lung auscultation (if decompensated).
Mitral Stenosis - Investigations
ECG: May be normal, broad bifid p wave (p mitrale) caused by left atrial hypertrophy, AF or evidence of right ventricular hypertrophy in cases of severe pulmonary hypertension.
CXR: Left atrial enlargement, cardiac enlargement, pulmonary congestion; mitral valve may be calcified in rheumatic cases.
Echocardiography: To assess functional and structural impairments. Transoesophageal gives better valve visualization.
Cardiac catheterization: Measures severity of heart failure.
Mitral Stenosis - Management
Medical: Anticoagulation for AF. Treat dyspnoea and heart failure with diuretics. Antibiotic cover for dental/invasive procedures. Cardioversion of AF may be considered.
Surgical: Mitral valvuloplasty, valvotomy or replacement if severe.
C O M P L I C A T I O N S AF and systemic embolism, pulmonary oedema, pulmonary hyperten-
sion and right heart failure, infective endocarditis.
P R O G N O S I S Significantly worse if pulmonary hypertension or right heart failure develops.
Myocarditis - Definition
Mitral valve narrowing causing obstruction to blood flow from the left atrium to the ventricle.
Myocarditis - Aetiology
Most common cause is rheumatic heart disease (90%).
Rarer causes are congenital mitral stenosis, SLE, rheumatoid arthritis, endocarditis and atrial
myxoma (rare cardiac tumour).
Myocarditis - History
May be asymptomatic.
Presents with fatigue, shortness of breath on exertion or lying down (orthopnoea). Palpita-
tions (related to AF).
Rare symptoms: Cough, haemoptysis, hoarseness caused by compression of the left
laryngeal nerve by an enlarged left atrium.
Myocarditis - Examination
May have peripheral or facial cyanosis (malar flush).
Pulse: May be ‘thready’ or irregularly irregular (AF).
Palpation: Apex beat is undisplaced and tapping. Parasternal heave (right ventricular
hypertrophy and pulmonary hypertension)
Auscultation: Loud first heart sound with opening snap.
Mid-diastolic murmur (presystolic accentuation if in sinus rhythm). Evidence of pulmonary oedema on lung auscultation (if decompensated).
Myocarditis - Investigations
ECG: May be normal, broad bifid p wave (p mitrale) caused by left atrial hypertrophy, AF or evidence of right ventricular hypertrophy in cases of severe pulmonary hypertension.
CXR: Left atrial enlargement, cardiac enlargement, pulmonary congestion; mitral valve may be calcified in rheumatic cases.
Echocardiography: To assess functional and structural impairments. Transoesophageal gives better valve visualization.
Cardiac catheterization: Measures severity of heart failure.
Myocarditis - Management
Medical: Anticoagulation for AF. Treat dyspnoea and heart failure with diuretics. Antibiotic cover for dental/invasive procedures. Cardioversion of AF may be considered.
Surgical: Mitral valvuloplasty, valvotomy or replacement if severe.
C O M P L I C A T I O N S: AF and systemic embolism, pulmonary oedema, pulmonary hyperten-
sion and right heart failure, infective endocarditis.
P R O G N O S I S: Significantly worse if pulmonary hypertension or right heart failure develops.
Pericarditis - Definition
Inflammation of the pericardium, may be acute, subacute or chronic.
Pericarditis - Aetiology
. Idiopathic;
. infective (commonly, coxsackie B, echovirus, mumps virus, streptococci, fungi, staphy-
lococci, TB);
. connective tissue disease (e.g. sarcoid, SLE, scleroderma);
. post-myocardial infarction (24–72 h) in up to 20% of patients;
. Dresslers syndrome (weeks to months after acute MI);
. malignancy (lung, breast, lymphoma, leukaemia, melanoma);
. metabolic (myxoedema, uraemia);
. radiotherapy;
. thoracic surgery;
. drugs (e.g. hydralazine, isoniazid).
Pericarditis - History
Chest pain: Sharp and central, which may radiate to neck or shoulders. Aggravated by coughing, deep inspiration and lying flat. Relieved by sitting forward.
Dyspnoea, nausea.
Pericarditis - Examination
Fever, pericardial friction rub (best heard lower left sternal edge, with patient leaning forward in expiration), heart sounds may be faint in the presence of an effusion. Cardiac tamponade: " JVP, # BP and muffled heart sounds (Becks triad). Tachycardia, pulsus paradoxus (reduced systolic BP by >10 mmHg on inspiration). Constrictive pericarditis (chronic): " JVP with inspiration (Kussmauls sign), pulsus para- doxus, hepatomegaly, ascites, oedema, pericardial knock (rapid ventricular filling), AF.
Pericarditis - Investigations
ECG: Widespread ST elevation that is saddle-shaped.
Echocardiogram: For assessment of pericardial effusion and cardiac function.
Blood: FBC, U&E, ESR, CRP, cardiac enzymes (usually normal). Where appropriate: blood
cultures, ASO titres, ANA, rheumatoid factor, TFT, Mantoux test, viral serology.
CXR: Usually normal (globular heart shadow if >250 mL effusion). Pericardial calcification can
be seen in constrictive pericarditis (best seen on lateral CXR or CT).
Pericarditis - Management
Acute: Cardiac tamponade treated by emergency pericardiocentesis.
Medical: Treat the underlying cause, NSAIDs for relief of pain and fever.
Recurrent: Low-dose steroids, immunosuppressants or colchicine.
Surgical: Surgical excision of the pericardium (pericardiectomy) in constrictive pericarditis.
C O M P L I C A T I O N S Pericardial effusion, cardiac tamponade, cardiac arrythmias.
P R O G N O S I S Depends on underlying cause. Good prognosis in viral cases (recovery within 2 weeks), poor in malignant pericarditis. Pericarditis may be recurrent (particularly in those caused by thoracic surgery).
Pulmonary Hypertension - definition
A consistently increased pulmonary arterial pressure (>20mmHg) under resting conditions.
Pulmonary Hypertension - Aetiology
Primary: Idiopathic.
Secondary: Left heart disease (mitral valve disease, left ventricular failure, left atrial myxoma/
thrombosis), chronic lung disease (COPD), recurrent pulmonary emboli, “ pulmonary blood flow (ASD, VSD, patent ductus arteriosus), connective tissue disease (e.g. SLE, systemic sclerosis), drugs (e.g. amiodarone).
Pulmonary Hypertension - History
Dyspnoea (on exertion), chest pain, syncope, tiredness.
Symptoms of the underlying cause (e.g. chronic cough).
Pulmonary Hypertension - Examination
Increased JVP (Prominent a wave in the JVP waveform).
Palpation: Left parasternal heave (right ventricular hypertrophy).
Auscultation: Loud pulmonary component of S2 (S3/S4 may be heard), an early diastolic
murmur (Graham–Steell murmur) caused by pulmonary regurgitation may be present, if
tricuspid regurgitation develops (large cv wave and pansystolic murmur). Signs of the underlying condition, or right heart failure in severe cases.
Pulmonary Hypertension - Investigations
CXR: Cardiomegaly (right ventricular enlargement, right atrial dilation), prominent main pulmonary arteries (which taper rapidly), signs of the cause (e.g. COPD, calcified mitral valves).
ECG: Right ventricular hypertrophy (right-axis deviation, prominent R wave in V1, T inversion in V1, V2), right atrial enlargement (peaked P wave in II, called ‘P pulmonale’); limb leads exhibit low voltage (R < 5 mm) in COPD.
Echocardiography: To visualize right ventricular hypertrophy or dilation and possible underlying cause.
Lung function tests: To assess for chronic lung disease.
VQ scan: To assess for pulmonary embolism.
Cardiac catheterization: To assess severity, right heart pressures and response to
vasodilators.
High resolution CT-thorax: Images pulmonary arteries and to diagnose lung disease. Lung biopsy: Assesses structural lung changes.
Pulmonary Hypertension - Management
Medical: Treat secondary cause. For primary pulmonary hypertension, consider:
. anticoagulation (warfarin);
. calcium channel antagonists (e.g. verapamil, nifedipine);
. prostacycline analogues (e.g. iloprost);
. endothelial receptor antagonist (bosentan) blocks vasoconstriction, but teratogenic, so only indicated in NYHA III or IV patients;
. phosphodiesterase inhibitor (e.g. sildenafil) promotes pulmonary smooth muscle relax- ation reducing pulmonary hypertension.
Surgical: Heart and lung transplantation may be an option for younger patients.
C O M P L I C A T I O N S Right heart failure, arrhythmias (AF, VT, VF), sudden death.
P R O G N O S I S Chronic and incurable with unpredictable survival rate. Length of survival has improved to up to 15–20 years.
Rheumatic Fever - Definition
An inflammatory multisystem disorder, occurring following group A b-haemolytic streptococci (GAS) infection.
Rheumatic Fever - Aetiology
The pathogenic mechanisms remain incompletely understood. Streptococcal pharyngeal infection is required, and genetic susceptibility may be present. Molecular mimicry is thought to play an important role in the initiation of the tissue injury (antibodies directed against GAS antigens cross-react with host antigens).
Rheumatic Fever - History
2–5 weeks after GAS infection.
General: Fever, malaise, anorexia. Joints: Painful, swollen, # movement/function. Cardiac:
Breathlessness, chest pain, palpitations.
Rheumatic Fever - Examination
Duckett Jones criteria: Positive diagnosis if at least two major criteria, or one major plus two minor criteria are present.
Major criteria:
. Arthritis: Migratory or fleeting polyarthritis with swelling, redness and tenderness of large joints.
. Carditis: New murmur, e.g. Carey Coombs murmur (mid-diastolic murmur due to mitral valvulitis). Pericarditis, pericardial effusion or rub, cardiomegaly, cardiac failure, ECG changes (see Investigations).
. Chorea (Sydenhams): Rapid, involuntary, irregular movements with flowing or dancing quality. May be accompanied by slurred speech. More common in females.
. Nodules: Small firm painless subcutaneous nodules seen on extensor surfaces, joints and tendons.
. Erythema marginatum (20% cases): Transient erythematous rash with raised edges, seen on trunk and proximal limbs. They may form crescent- or ring-shaped patches.
Minor criteria:
. Pyrexia;
. previous rheumatic fever;
. arthralgia (only if arthritis is not present as major criteria);
. recent streptococcal infection (supported by positive throat cultures or increased antistreptolysin O
titre);
. high inflammatory markers (ESR, CRP or WCC);
. high PR and QT intervals on ECG (only if carditis not present as major criteria).
Rheumatic Fever - Investigations
Blood: FBC ( high WCC), ESR/CRP (raised), high or rising antistreptolysin O titre.
Throat swab: Culture for GAS, rapid streptococcal antigen test.
ECG: Saddle-shaped ST elevation and PR segment depression (features of pericarditis),
arrhythmias.
Echocardiogram: Pericardial effusion, myocardial thickening or dysfunction, valvular
dysfunction.
Rheumatic Fever - Management
Strict bed rest: ( 4 weeks) Gradual mobilization with clinical improvement.
Anti-inflammatory drugs: High-dose aspirin or, for more severe carditis, consider corticosteroids.
Antibiotics: Eradicate residual streptococcal infection using oral penicillin V for 10 days. Long-term antibiotics to prevent recurrence is necessary (e.g. long-acting benzathine penicillin G intramuscularly every 4 weeks, switch to oral prophylaxis in young adulthood). Prophylaxis in the setting of carditis should continue usually for 10 years. The risk for GAS exposure and severity of valvular disease should then be reviewed.
Carditis: Treat heart failure if present.
Chorea: May be controlled with diazepam or haloperidol.
Valve surgery: If valvular disease cannot be managed with medical therapy alone.
COMPLICATIONS: Recurrence, may be precipitated by streptococcal infection, more common in patients with residual cardiac damage. Chronic rheumatic valvular disease: scarring, deformation and dysfunction (usually mitral or aortic) after 10–20 years; more common in those with carditis as part of acute rheumatic fever.
P R O G N O S I S: Acute rheumatic fever may last up to 3 months if untreated. , more likely to develop mitral stenosis.
Tricuspid Regurgitation - Definition
Tricuspid regurgitation is backflow of blood from the right ventricle to the right atrium during systole.
Tricuspid Regurgitation - Aetiology
Congenital: Ebstein anomaly (malpositioned tricuspid valve), cleft valve in ostium primum defect.
Functional: Consequence of right ventricular dilation (e.g. in pulmonary hypertension), valve prolapse.
Rheumatic heart disease: Associated with other valvular disease.
Infective endocarditis: Common in IV drug users. Usually staphylococcal.
Other: Carcinoid syndrome, trauma, cirrhosis (long-standing), iatrogenic (e.g. radiotherapy
to the thorax).
Tricuspid Regurgitation - History
Fatigue, breathlessness, palpitations, headaches, nausea, anorexia, epigastric pain made worse by exercise, jaundice, lower limb swelling.
Tricuspid Regurgitation - Examination
Pulse: May be irregularly irregular due to AF (may occur with right atrial enlargement). Inspection: “ JVP with giant v waves which may oscillate the earlobe. This is caused by transmission of right ventricular pressure to the great veins. There may be giant a wave, if the patient is in sinus rhythm.
Palpation: Parasternal heave.
Auscultation: Pansystolic murmur heard best at the lower left sternal edge, louder on
inspiration (Carvallo sign). Loud P2 component of second heart sound. Chest: Pleural effusion. Causes of pulmonary hypertension (e.g. emphysema). Abdomen: Palpable liver (tender, smooth, pulsatile), ascites.
Legs: Pitting oedema.
Tricuspid Regurgitation - Investigations
Blood: FBC, LFT, cardiac enzymes, blood cultures.
ECG: Tall P wave (right atrial hypertrophy) if in sinus rhythm. Changes indicative of other
cardiac disease.
CXR: Right-sided enlargement of cardiac shadow.
Echocardiography: Extent of regurgitation estimated by colour flow Doppler. May be able
to detect tricuspid valve abnormality (e.g. prolapse), right ventricular dilation.
Right heart catheterization: Rarely necessary but may be considered to assess pulmonary
artery pressure.
Tricuspid Regurgitation - Management
Medical: Treat the underlying condition, e.g. infective endocarditis or functional regurgi- tation caused by pulmonary hypertension. Diuretics may be given for fluid retention.
Surgery: Annuloplasty, plication or, rarely, replacement. Repair of the valve only in very severe tricuspid regurgitation, when the required doses of diuretics are large enough to cause metabolic consequences. Surgical removal of the valve may be required to eradicate the source of infection in IV drug users with infective endocarditis.
COMPLICATIONS Heart failure, hepatic fibrosis.
P R O G N O S I S Prognosis varies depending on the underlying cause.
