Cardiology Flashcards
What are the causes of ST elevation?
Myocardial infarction
Pericarditis (saddle-shaped)
Normal variant (high take off)
Left ventricular aneurysm (persistent after MI)
Prinzmetal’s angina (Coronary artery spasm)
Rarely: Subarachnoid Haemorrhage
What are the causes of peaked T waves?
Myocardial ischaemia (Acute ischaemic change) Hyperkalaemia
What are some causes of inverted T waves?
Myocardial ischaemia Digoxin toxicity Subarachnoid haemorrhage (Deep) Arrhymogenic right ventricular cardiomopathy Brugada syndrome.
Causes of a prolonged PR interval?
Idiopathic (athletes) Ischaemic heart disease Digoxin toxicity Hypokalaemia Rheumatic fever Aortic root pathology Lyme disease Sarcoidosis Myotonic dystrophy
What is the criteria defining Stage 1 hypertension?
Clinic BP >140/90mmHg and subsequent ABPM or HBPM average BP >135/85mmHg
What is the criteria defining Stage 2 hypertension?
Clinc BP >160/100mmHg and subsequent ABPM or HBPM average BP >150/95mmHg
What is the criteria defining severe hypertension?
Clinic systolic BP>180mmHg or Clinic diastolic >110mmHg
Describe Atrial Fibrillation, it’s causes, signs and tests, and management
A chaotic irregular atrial rhythm with variable AV response causing an irregularly irregular pulse. May be split into fast and slow AF, Fast AF more than 100bpm, Slow considered less than 60bpm.
Causes: heart failure/ischaemia, IHD, MI, PE, Mitral Valve disease, pneumonia, hyperthyroidism, caffeine, alcohol, hypokalaemia, hypomagnesia
Symptoms: may be none or chest pain, palpitations, dyspnoea, faintness. May be acute, chronic or paroxysmal
Tests: ECG shows absent p waves and irregular QRS complexes. Blood tests; U+E, Troponin, TFTs to look for underlying cause, CXR
Management:
- haemodynamically unstable AF requires immediate DC cardioversion, if prolonged AF (more than 48h) TOE is needed to confirm that there is no evidence of left atrium thrombus.
- Haemodynamically stable, can be rate or rhythm controlled, younger patients or reversible causes should opt for rhythm control, elderly patients with chronic AF should opt for rate control
- Rate control includes beta-blocker (metoprolol, bisoprolol), or rate-limiting Ca-blocker e.g. Verapamil, diltiazem failing this digoxin can be used
- rhythm control, try amiodarone, or sotalol, if persisting for more than 48hr anticoagulation 3wks and cardioversion,
- paroxysmal AF can be dealt with pill in the pocket with flecainide or sotalol.
- Anticoagulation should be initiated in chronic and paroxysmal AF
Describe the CHADS-VASc score
Score of 1 or more consider oral anticoagulation, 2 or more warfarin.
C ongestive cardiac failure H ypertension A ge >75 (2 points) D iabetes S troke (2 points) V ascular disease A ge >65 Sc - Sex catergory female
Describe the HAAS-BLED score
Score of 3 or more indicates high risk of bleeding and alternatives to anticoagulation should be considered
H ypertension A lcohol abuse A bnormal renal or liver function S troke B leeding disorder or previous major bleed L abile INR E lderly >65 D rug abuse
What is a bounding pulse a sign of?
CO2 Retention, liver failure, sepsis
What is a small volume pulse a sign of?
Aortic stenosis, shock, pericardial effusion
What is a collapsing pulse a sign of?
Aortic regurgitation, AV malformation, patent ductus arteriosus
What is a slow rising pulse a sign of?
Aortic stenosis
What is a bisferiens pulse a sign of?
Combined Aortic stenosis and regurgitation
What is pulsus alternans a sign of?
suggests LVF, cardiomyopathy or aortic stenosis
What is a jerky pulse a sign of?
HOCM
What is pulsus paradoxus and what is it a sign of?
Systolic pressure drop in inspiration >10mmHg occurs in severe asthma, constrictive pericarditis or cardiac tamponade.
Describe the 1st heart sound (S1)
S1 represents the closure or mitral (M1) and tricuspid (T1) valves. splitting in inspiration may be heard and is normal.
What is a loud S1 a sign of?
Mitral stenosis
What is a soft S1 a sign of?
occurs if PR interval prolonged or mitral valve incompetent e.g. mitral regurgitation
Describe the 2nd heart sound S2
S2 represents the closure of the aortic (A2) and pulmonary (P2) valves.
What is a soft A2 a sign of?
aortic stenosis
What is a loud P2 a sign of?
Pulmonary hypertension
What is a soft P2 a sign of?
Pulmonary stenosis
Describe the splitting of the second heart sounds under normal and abnormal conditions
In inspiration the sounds are normally split with A2 followed by P2 this is due to the variation of right heart venous return with respiration delaying the pulmonary component.
Wide splitting of the heart sounds occurs in RBBB, pulmonary stenosis, deep inspiration, mitral regurgitation and VSD.
Fixed wide splitting occurs in ASD
Reversed splitting P2 followed by A2 with splitting increasing on expiration occurs in LBBB, aortic stenosis, Patent ductus arteriosus.
Describe the 3rd heart sound
S3 may occur just after S2, it is low pitched and best heard with the bell. S3 is pathological over the age of 30.
What is a loud S3 a sign of?
Mitral regurgitation, VSD, Dilated cardiomyopathy, post MI.
Describe the 4th heart sound
S4 occurs just before S1, always abnormal. it represents atrial contraction against a stiff ventricle i.e. aortic stenosis, HOCM
What is an ejection systolic click a sign of?
heard early in systole with bicuspid aortic valves may be aortic stenosis
What is a mid-systolic click a sign of?
mitral valve prolapse
What is an opening snap a sign of?
precedes the mid-diastolic murmur of mitral and tricuspid regurgitation
What are the causes of an ejection-systolic murmur?
cresendo-decresendo murmur, may be due to aortic stenosis or sclerosis, pulmonary stenosis or HOCM
What are the causes of a pansystolic murmur?
monotoned murmur, and merges with S2. May be due to mitral or tricupsid regurgitation (also soft S1) or VSD.
What are the causes of a late-systolic murmur?
mitral valve prolapse may also have mid-systolic click
What are the causes of an early diastolic murmur?
high pitched murmur occurs in aortic and pulmonary (much rarer cause) regurgitation.
What is a Graham-Steell murmur
A early diastolic murmur due to pulmonary regurgitation because of pulmonary hypertension from a stenotic mitral valve.
What are the causes of a mid-diastolic murmur?
Low pitched and rumbling in nature. the occur in mitral stenosis, rheumatic fever, aortic regurgitation
What is a tapping apex beat a sign of?
Palpable first hearts sound indicative of Mitral Stenosis
What is Corrigan’s sign?
Cartoid pulsation may be seen in Aortic Regurgitation
What is Duroziez’s sign?
In severe Aortic Regurgitation, gradual pressure over the femoral artery leads to a systolic and diastolic bruit. The former heard with the bell of the stethoscope when the proximal femoral artery is compressed and the latter with the distal femoral artery.
What is de Musset’s sign?
Head nodding with each heart beat a sign of Aortic Regurgitation
What is Quincke’s sign?
Capillary pulsations in nail beds a sign of Aortic Regurgitation
What is Traube’s sign?
‘Pistol shot’ sound over femoral arteries a sign of Aortic Regurgitation
What is Austin Flint murmur?
A mid-diastolic murmur due to the fluttering of the anterior mitral valve cusp caused by the regurgitant stream of Aortic Regurgitation.
What are Osler nodes?
Painful pulp infarcts in fingers or toes which together with janeway lesions is pathognomic of IE. Due to immune complex deposition
What are janeway lesions?
Non-tender erythematous, haemorrhagic or pustular spots on the palms or soles, which together with Osler nodes are pathognomic of IE. Due to infective embolic phenomena
Describe bradycardia and its treatment
If asymptomatic and rate greater than 40bpm, no treatment is required. Look for a cause (drugs, sick sinus syndrome, hypothyroidism) and stop any drugs that may be contributing (Beta-blockers, digoxin).
If rate less than 40bpm or patient is symptomatic give atropine 0.6-1.2mg IV up to max of 3mg. If no response, insert a temporary acing wire. If necessary, start an isoprenaline infusion or use external cardiac pacing.
Describe sick-sinus syndrome, its causes, and its management.
Aka Tachy-Brady syndrome, sinus node dysfunction causes bradycardia +/- arrest, sinoatrial block or SVT or AF alternating with bradycardia/asystole.
Causes:
- Intrinsic e.g. Idiopathic Degenerative Fibrosis (Commonest), ischaemia, cardiomyopathy, sarcoidosis, haemochromatosis, congenital abnormalities.
- Extrinsic e.g. Digoxin, beta-blockers, calcium-channel blockers, autonomic dysfunction, hypothyroidism, hyperkalemia
Management:
-Pace if symptomatic
Causes of sinus tachycardia
Rate>100 Causes:
- Anaemia
- Anxiety
- Exercise
- Pain
- Fever
- Sepsis
- hypovolaemia
- Heart failure
- PE
- Pregnacy
- Thyrotoxicosis
- Beriberi
- CO2 retention
- caffeine, adrenaline, nicotine
Define Narrow Complex Tachycardias, the types, and principles of management.
ECG shows rate of >100bpm and QRS complex duration of less than 120ms.
Types:
- sinus tachycardia
- Supraventricular tachycardia
- Atrial fibrillation
- atrial flutter
- multifocal atrial tachycardia
- junctional tachycardia
Management:
- if patient is compromised use DC cardio version
- otherwise identify rhythm and treat accordingly.
- generally vagal manoeuvres (carotid massage, Valsalva) attempted to correct/ unmask rhythm
- if unsuccessful adenosine 6mg IV bolus, if fails try 12mg and another 12mg.
Describe SVT and its management
Narrow complex tachycardia with ECG showing P waves absent or inverted after QRS complex.
Management:
- Vagal manoeuvres (breath-holding, vasalva, carotid massage) are 1st line
- IV adenosine is the drug of choice (6mg bolus)
- If adenosine fails use IV verapamil (5mg over 2mins)
- If drug therapy fails use DC cardioversion
Describe Junctional Tachycardia and its management
Narrow complex tachycardia with ECG showing rate of 150-250bpm, P wave either buried in QRS complex or occurring just after. There are 3 types of junctional tachycardia:
- AV nodal reentry tachycardia
- AV reentry tachycardia
- His bundle tachycardia
Management:
- Try vagal manoeuvres
- IV Adenosine will usually return to sinus rhythm
- If it re-occurs try amiodarone or beta-blocker
- Radiofrequency ablation is more frequently being used in AVRT and symptomatic AVNRT
Describe Wolff-Parkinson-White syndrome, the types, associations, features and management
Caused by congenital accessory conduction pathway between atria and ventricles. May preset as a tachyarrhythmia by the formation of a reentry circuit involving the accessory pathway termed Atrioventricular reentry tachycardias (AVRT).
Types:
- Type A which indicates a left sided accessory pathway, and show a dominant R wave in V1 and tall R waves and inverted T waves in V1-V3 mimicking right ventricular hypertrophy.
- Type B indicates a right sided accessory pathway, there is a dominant S wave in V1 and tall R waves and inverted T waves in inferior leads and V4-V6 mimicking left ventricular hypertrophy.
Associations: HOCM, Mitral valve prolapse, Ebstein’s Anomaly, Thyrotoxicosis, ASD (Ostium Secundum)
Features: Resting ECG shows short PR interval, Wide QRS complex (due to slurred upstroke or delta wave) and ST-T changes in opposite direction of major component of QRS complex
Management:
Refer to cardiologist for electrophysiology and ablation of accessory pathway
WPW with AF needs urgent treatment with DC Cardioversion as it can quickly deteriorate into VF, Digoxin is contradindicated in this scenario.
Define Broad Complex Tachycardia, the differentials and management
ECG shows rate of >100bpm and QRS complexes >120ms. If no clear QRS complexes, it is VF of asystole.
Differential Diagnosis:
- VT includes torsade de pointes
- VF
- SVT with bundle branch block/aberrant conduction
Management:
- if VF or pulseless VT use asynchronised DC shock
- if stable VT give high flow oxygen, obtain IV access, try B-blockers e.g. Sotalol, metoprolol, if fails or known LV Dysfunction try Amiodarone IVI, if fails consider DC shock
Define Torsades de pointes and its management
Looks like VF but is VT with varying axis. it is due to increased QT interval (a SE of antiarrhythmics)
Management:
- magnesium sulphate 2g IV over 10 mins
- look at drug chart for QT prolonging medications (Anti-psychotics)
Describe the Framingham criteria for congestive cardiac failure
Diagnosis of CCF requires the simultaneous presence of at least 2 major criteria or 1 major and 2 minor
Major criteria: •paroxysmal nocturnal dyspnoea •crepitations •S3 gallop •cardiomegaly •increased central venous pressure (>16cmH2O at right atrium) • weight loss >4.5kg in 5 days of treatment •neck vein distension •acute pulmonary oedema •hepatojugular reflux
Minor criteria: •bilateral ankle oedema •dyspnoea on ordinary exertion •tachycardia •nocturnal cough •decreased vital capacity by 1/3 of maximum recorded •hepatomegaly •pleural effusion
Describe the management of chronic heart failure
Conservative: Change lifestyle factors e.g stop smoking, eat less salt, optimise weight and nutrition, Treat exacerbating factors such as anaemia, thyroid disease, infection, hypertension Avoid exacerbating factors such as NSAIDs (cause fluid retention) and verapamil (-ve inotrope)
Pharmacological:
- ACE inhibitors: Consider in all with left ventricular systolic dysfunction, improves symptoms and prolongs life. If cough is a problem an angiotensin receptor blocker may be substituted
- Beta-blockers: e.g. carvedilol decreased mortality in heart failure. Use with caution start low and go slow.
- Diuretics e.g. Frusemide can reduce the risk of death and worsening heart failure.
- Ivabradine can be used it acts by reducing the heart rate via specific inhibition of the funny channel, it is contraindicated in sick-sinus syndrome and should not be used with verapamil or diltiazem
- Spironolactone decreased mortality by 30% when added to conventional therapy. Use in those still symptomatic despite above treatment.
- Digoxin helps symptoms even in those with sinus rhythm and should be considered in those with LVSD HF who have signs or symptoms of heart failure whilst receiving standard therapy or those with concurrent AF
- hydralazine and isosorbide mononitrate symptomatic, not often used now.
Surgical: Symptomatic patients with maximum pharmacological management and LVEF less than 35% may benefit from implantable devices.
- If narrow QRS complex Implantable Cardioverter defibrillators (ICD) may be indicated.
- If broad QRS complex cardiac desynchronisation therapy with defibrillators (CRT-D)
Describe the types of hypertension
Isolated systolic hypertension - the most common form of hypertension in the UK. Affects >50% of over-60s. It results from stiffening of the arteries. Doubles the risk of MI, triples the risk of CVA.
‘Malignant’ or accelerated phase hypertension - refers to a rapid rise in BP leading to vascular damage. Hypertension is usually severe (systolic >200, diastolic >130) + bilateral retinal haemorrhages. Symptoms are common e.g. visual disturbance and headache. It is more common in younger patients and in black patients.
Essential hypertension - cause unknown
Secondary hypertension - due to renal disease, endocrine disease (cushing’s, conn’s, phaeochromocytoma), coarctation, pregnancy, steroids, the pill
Describe the management of hypertension.
Treatment goal: ideally less than 140/90mmHg, less than 130/80mmHg in diabetics, 150/90 if older than 80. Reduce slowly.
Lifestyle changes: stop smoking, low fat diet, reduce alcohol and salt intake, increase excercise and reduce weight if obese.
Drug therapy:
- Monotherapy if older than 55 and/or Afro-carribean 1st line is Ca channel blocker e.g. Amlodopine. Otherwise ACE-i e.g. Ramipril is first line also first in diabetics.
- Dual therapy, both Ca channel blocker and ACE-i
- If this fails add diuretic
- if this fails and potassium less than 4.5mmol/L add spironolactone if K+ high dose diuretic. If further diuretic therapy not tolerated or ineffective consider alpha or beta blocker.
Describe Acute Coronary Syndrome, its risk factors, symptoms, and tests.
ACS includes unstable angina, and evolving MI. MI can be further divided into STEMI or new onset LBBB, and NSTEMI.
Risk factors: age, male, family history, smoking, hypertension, DM, hyperlipidaemia, obesity, sedentary lifestyle, cocaine use.
Symptoms: Acute central chest pain, lasting >20min, often associated with nausea, sweatiness, dyspnoea, palpitations. May present without chest pain e.g. in the elderly or diabetics, in which syncope, pulmonary oedema, epigastric pain, vomiting, post-op hypotension, oliguria, acute confusional state.
Tests: ECG (in 20% ECG may be normal at first repeat ECG!)
-STEMI: Classically hyperacute (tall) t waves, ST elevation or new LBBB, T wave inversion and pathological Q waves follow over hours-days.
-NSTEMI: ST depression, t-wave inversion, non-specific changes.
CXR,Bloods, cardiac enxymes. Troponin elevated after 3-12h of onset if normal 6h after onset chance of missing MI is small.
Describe acute pericarditis, its features, tests and treatment
Inflamation of pericardium it may be idiopathic or secondary due to infection, MI, drugs (procainamide, hydralazine, penicillin, isoniazid), uraemia, RA, SLE, sarcoidosis, radiotherapy.
Features: central chest pain worse on inspiration or lying flat and relieved by sitting forward. A pericardial friction rub may be heard. look for evidence of pericardial effusion or cardiac tamponade. Fever may occur.
Tests: ECG classically shows saddle-shaped ST elevation, but can be normal. Troponin may be raised. Cardiomegaly on CXR may indicate pericardial effusion.
Treatment:
-NSAIDs are first line, ICAP study suggests that Colchicine and Aspirin reduce the risk of recurrent pericarditis.
Describe cardiac tamponade, its causes, signs, and management.
Fluid in the pericardial sac leads to increased pericardial pressure and poor ventricular filling and fall in cardiac output. Beck’s triad, falling BP, rising JVP (distended neck veins), muffled heart sounds. Fast/Echo is diagnostic.
Causes: Trauma (usually penetrating), any cause of pericarditis, aortic dissection, haemodialysis, warfarin, transeptal puncture at cardiac catheterisation, post cardiac biopsy.
Signs: increased PR, decreasing BP, pulsus paradoxus, increased JVP, kussmaul’s sign, muffled heart sounds.
Management:
- ABCDE
- seek expert help
- FAST scan if in ED
- If patient deteriorates consider pericardiocentesis
- If cardiac arrest emergency thoracotomy is needed
- if stable contact cardiothoracic surgeion as effusions need to be drained.
Describe SVC obstruction, its causes, signs and symptoms, investigation, and management
SVC obstruction is not an emergency unless there is tracheal compression with airway compromise.
Causes: malignancy account for >90%, 3/4 of which are lung cancer. rare causes include mediastinal enlargement, thymus malignancy, mediastinal lymphadenopathy (sarcoid, lymphoma).
Signs + symptoms: dyspnoea, orthopnoea, plethora/cyanosis, swollen face and arm, cough, headache, engorged veins.
Investigations: urgent contrast enhanced CT
Management: biopsy if cause unknown, dexamethasone PO 8-16mg/d. Consider balloon venoplasty and SVC stenting for rapid relief of symptoms
Describe Mitral stenosis its causes, symptoms, signs, tests and management
Causes: Rheumatic, congenital, carcinoid, prosthetic valve.
Symptoms: Dyspnoea, fatigue, palpitations, chest pain, systemic emboli, haemoptysis, chronic bronchitis-like picture
Signs: malar flush on cheeks (due to decreased cardiac output), low-volume pulse, AF, tapping non-displaced apex beat (palpable S1). On auscultation, loud S1, opening snap, rumbling mid-diastolic murmur heard best in expiration with the patient on the left side.
Tests: ECG may show AF, P-mitrale, RVH, Progressive RAD. Echo is diagnostic.
Management:
If AF rate control and warfarin.
Diuretics decreased preload and pulmonary venous congestion. May need valve replacement most can be managed with Percutaneous balloon mitral valvotomy unless they have contraindications such as
-Moderate to severe mitral regurgitation
-left atrial thrombus
-heavily calcified mitral Valve
-concomitant coronary artery or other valve disease requiring surgery
In these cases patients should undergo mitral valve replacement.
Describe mitral regurgitation its causes, symptom, signs, tests, and management
Causes: functional (LV dilatation), annular calcification (elderly), rheumatic fever, infective endocarditis, mitral valve prolapse, ruptured chordae tendinae, papillary muscle dysfunction, congenital, connective tissue disorders, cardiomyopathy
Symptoms: dyspnoea, fatigue, palpitation, signs of infective endocarditis
Signs: AF, displaced hyperdynamic apex, RV heave, soft S1, Loud P2 (due to pulmonary hypertension), pansystolic murmur at apex radiating to axilla.
Tests: ECG may show AF +/- P-mitrale, LVH, Echo is diagnostic looking at mitral valve function, degree of LVH, and degree of pulmonary HTN.
Management:
- rate control AF and warfarin
- diuretics improve symptoms
- valve replacement/repair ultimate treatment (metallic valves require INR 3-4)
- mitraclip less invasive, for patients that cannot tolerate open heart surgery, still in research phase
Describe mitral valve prolapse, its symptoms, signs, complications, tests and management.
Most common valvular abnormality (prevalence ~5%), occurs alone or with ASD, patent ductus arteriosus, cardiomyopathy, turner’s syndrome, marfans syndrome, osteogenesis imperfecta, WPW
Symptoms: asymptomatic or atypical chest pain and palpitations.
Signs: mid-diastolic click
Complications: mitral regurgitation, cerebral emboli, arrhythmias, sudden death
Tests: Echo is diagnostic, ECG may show inferior T-wave inversion
Management: beta-blockers may help palpitations and chest pain, surgery needed if progressive to MR
Describe aortic stenosis its causes, symptoms, signs, tests and management
Causes: Senile calcification is the commonest, congeitial (bicuspid valve, williams syndrome), rheumatic heart disease.
Symptoms: The classic triad includes angina, syncope and heart failure. May also have dyspnoea, dizziness, faints
Signs: slow-rising pulse with narrow pulse pressure, heaving non-displaced apex beat, LV heave, aortic thrill, ejection systolic murmur heard best at the base, left sternal edge and aortic area and radiates to the carotids.
Tests: ECG shows P-mitrale, LVH with strain pattern, LAD poor R wave progession LBBB or complete AV block. Echo is diagnostic severe stenosis can be more accurately invgestiaged with cardiac cauterisation and coronary angiography especially if severe (peak gradient over 50mmHg, valve area less than 1cm3, aortic jet velocity is more than 4m/s, Indexed aortic valve area less than 0.6cm2/m2, velocity ratio less than 0.25)
Management:
- Indications for AVR:
- Patients with severe high-gradient AS who have symptoms by history or on exercise testing
- For asymptomatic patients with severe AS and left ventricular ejection fraction less than 50%
- For patients with severe AS when undergoing other cardiac surgery
- For asymptomatic patients with very severe AS and low surgical risk.
- For asymptomatic patients with severe AS and decrease exercise tolerance or fall in systemic blood pressure with exercise
- For symptomatic patients with low-flow/low gradient severe as with reduced LVEF with a low-dose dobutamine stress study that shows aortic velocity over 4.0m/s or mean pressure gradient over 50mmHg with a valve area less than 1.0cm2 at any dobutamine dose.
- For symptomatic normotensive patients with low-flow/low-gradient severe AS with LVEF over 50%, if clinical, haemodynamic and anatomical data support valve obstruction as the most likely cause of symptoms.
- if patients cannot tolerate AVR, Transcatheter Aortic Valve Implantation (TAVI) is an option
Describe aortic regurgitation its causes, symptoms, signs, tests and management
Causes:
- Acute = IE, ascending aortic dissection, chest trauma
- Chronic = congenital, connective tissue disorders, rheumatic fever, takayasu arteritis, RA, SLE, hypertension,
Symptoms: Exertional dyspnoea, orthopnoea, PND, palpitations, angina, syncope, CCF.
Signs: collapsing ‘water-hammer’ pulse, wide pulse pressure, displaced hyperdynamic apex beat.
high pitched early diastolic murmur best heard in expiration with patient sitting forward.
Also corrigan’s sign, de Musset’s sign, duroziez’s sign, quincke’s sign and traube’s sign.
Tests: ECG shows LVH. Echo is diagnostic.
Management:
- Reduce systolic hypertension, ACE-i are helpful.
- surgery should be considered in asymptomatic patients with resting election reaction less than 50% with severe LV Dilatation (LVEDD over 70mm or LVESD over 50mm) and all symptomatic patients
Describe tricuspid regurgitation, its causes symptoms and signs, management
Causes: functional (RV dilatation), rheumatic fever, infective endocarditis (IV drug user), carcinoid syndrome, congenital (e.g. ASD).
Symptoms: Fatigue, hepatic pain on exertion, ascites, oedema. If the cause if LV failure orthopnoea and dyspnoea
Signs: Giant V waves, and prominent y descent in JVP. RV heave, pansystolic murmur heard best at lower sternal edge in inspiration, pulsatile hepatomegaly, jaundice ascites.
Management: Treat underlying cause. Diuretics, ACE-i, valve replacement.
Describe tricuspid stenosis, its causes, symptoms, signs and treatment.
Causes: main cause is rheumatic fever, which almost always occurs with mitral or aortic valve disease. rarer causes congenital, infective endocarditis
Symptoms: fatigue, ascites, oedema
Signs: giant a wave and slow y descent in JVP. opening snap, early diastolic murmur heard best at the left sternal edge in inspiration. AF can also occur.
Treatment is with diuretics and surgical repair.
Describe pulmonary stenosis, its causes, symptoms signs, and treatment
Causes: usually congenital, acquired causes rheumatic fever, carcinoid syndrome.
Symptoms: dyspnoea, fatigue, oedema, ascites
Signs: dysmorphic facies (congenital causes), prominent a wave in JVP, RV heave, in mild stenosis there is an ejection click, ejection systolic murmur which radiates to the left shoulder. widely split S2. in severe stenosis the murmur becomes longer and obscures A2. P2 becomes softer and may be inaudible.
Treatment: pulmonary valvuloplasty or valvotomy
Describe pulmonary regurgitation
It is caused by any cause of pulmonary hypertension. A decrescendo murmur is heard in early diastole at the left sternal edge (known as the graham steell murmur if associated with mitral stenosis and pulmonary hypertension)
Which coronary artery is associated with anteroseptal ECG changes and what leads indicate this?
Anteroseptal = V1-V4
supplied by the left anterior descending artery
Which coronary artery is associated with inferior ECG changes and what leads indicate this?
Inferior = II,III aVF
supplied by the right coronary artery
Which coronary artery is associated with anterolateral ECG changes and what leads indicate this?
anterolateral = V4-6 I aVL
supplied by the left anterior descending artery or left circumflex artery
Which coronary artery is associated with lateral ECG changes and what leads indicate this?
lateral = I, aVL, +/- V5,V6
supplied by the left circumflex artery
Which coronary artery is associated with posterior ECG changes and what leads indicate this?
Posterior = Tall R waves V1 V2
usually supplied by left circumflex also right coronary
Describe Buerger’s test
It is a test for critical ischaemia:
- first lie the patient on the bed
- Elevate legs to 45 degress
- look for palor
- Buerger’s angle is the angle at which the legs go pale
- less than 25 degrees is a sign of critical ischaemia
- sit the patient up hanging legs of the side of the bed
- look for reactive hyperaemia which makes the legs appear dusky red.
What are causes of LBBB?
- Ischaemic Heart Disease
- Hypertension
- Aortic Stenosis
- Cardiomyopathy
- Rarely: Idiopathic fibrosis, digoxin toxicity, hyperkalaemia
Describes the types of heart block, and the management of each
1st degree heart block: prolonged PR
2nd degree mobitz type 1: PR lengthening each successive beat until dropped beat then return to normal
2nd degree mobitz type 2: 2:1, 3:1 missed beat, requires permanent pacing due to risk of progression to complete heart block.
3rd degree complete heart block: no association between p waves nad QRS complex, requires permanent pacing, untreated can lead to asystole and decreased cardiac output.
Describe ECG axis interpretation, its methods, and causes of right and left axis deviation.
The two main methods used to calculate are the quadrant method and isoelectric method. The basic principles are that the axis points roughly in the same direction as positive leads, and opposite in negative leads. In isoelectric leads the axis is +/- 90 degrees from that lead.
Remembering the diagram from frontal leads: Lead I = 0 degrees Lead II = 60 degrees Lead III = 120 degrees Lead aVR = -150 degrees Lead aVL = -30 degrees Lead aVF = 90 degrees
Quadrant method: Look at leads I + aVF. As these leads are perpendicular we are able to roughly place the axis depending on the quadrant. Knowing the upper left quadrant is extreme axis deviation, and bottom left quadrant is RAD, and a normal axis is between 90 and -30. so top right quadrant is either LAD or normal so.
Lead I +ve + Lead aVF +ve = Normal (0-90degrees)
Lead I +ve + Lead aVF -ve = Possible LAD (0 to -90 degrees)
Lead I -ve + Lead aVF +ve = RAD (90-180 degrees)
Lead I -ve + Lead aVF -ve = Indetermine/extreme axis deviation (-90-180degrees)
Isoelectric method allows determination of exact axis by finding the isoelectric lead and using the other leads to determine the exact axis i.e if aVF is isoelectric we know that the axis is 90 +/-90 i.e 0 or 180. If lead I is +ve we know the true axis is 0 if aVR was positive it would be 180.
Causes of RAD:
- Right ventricular hypertrophy
- Right ventricular strain e.g. PE
- Lateral STEMI
- Chronic lung disease e.g. COPD
- Hyperkalaemia
- Sodium channel blockade e.g. TCA poisoning
- WPW syndrome
- Dextrocardia
- ventricular ectopy
- ASD
- Normal paediatric ECG
- Vertical heart e.g. emphysema
Causes of LAD:
- Left ventricular hypertrophy
- LBBB
- Inferior MI
- Ventricular pacing
- WPW syndrome
Extreme axis deviation:
- Ventricular rhythms, CT, AIVR
- Hyperkalaemia
- Severe right ventricular hypertrophy.
Describe pulmonary oedema, its causes, symptoms + signs, management and investigations.
Causes:
- Cardiovascular, usually LVF (post MI or IHD), also valvular heart disease, arrhythmias, malignant hypertension
- ARDS from any cause e.g. trauma, malaria, drugs
- Fluid overload
- Neurogenic e.g. head injury
Symptoms + Signs: Dyspnoea, orthopnoea (e.g. paroxysmal), pink frothy sputum, distressed, pale, sweaty, tachycardic, tachypnoeic, pulsus alternans, raised JVP, fine lung crackles, triple/gallop rhythm, wheeze, sitting up leaning forward.
Management:
- Sit patient upright
- Oxygen 100% if no lung disease
- IV access and ECG, treat any arrhytmias e.g. AF
- Bloods: U+E, troponin, ABG, consider BNP.
- Diamorphine 1.25-5mg IV slowly (caution in liver and COPD)
- Furosemide 40-80mg IV slowly (larger doses needed in renal failure)
- GTN spray 2 puffs SL, or 2 x 0.3mg tablets SL (Dont give if systolic BP less than 90)
- Investigation: CXR, consider ECHO
- If systolic BP greater than 100 start a nitrate infusion e,g, isosorbide dinitrate 2-10mg/h IVI keeping systolic above 90
- If patient worsening consider further dose of furosemide, CPAP or increase nitrate infusion
- if systolic BP less than 90 treat for cardiogenic shock
What is malar flush and what is it a sign of.
Plum-red discolouration of the high chicks classically associated with mitral stenosis due to resulting CO2 retention and its vasodilatory effects.
Describe Peripheral Arterial Disease (PAD), its symptoms, signs, classification, and tests.
PAD occurs due to athersclerosis causing stenosis of arteries. 65% have co-existing cerebral or coronary artery disease.
Symptoms: cramping pain is felt in the calf, thigh or buttocks after walking for a given distance (claudication distance) and relieved by rests. (Calf claudication suggests femoral disease while buttock claudication suggests iliac disease). Ulceration, gangrene and foot pain at rest are the cardinal features of critical ischaemia.
Signs: absent femoral, popliteal or foot pulses, cold white legs, atrophic skin, punched out ulcers (often painful) postural dependent colour change. delayed cap refil
Fontaine classification for PAD: 1 = Asymptomatic 2 = intermittent claudication 3 = ischaemic rest pain 4 = ulceration/gangrene
Tests: Exclide DM, arteritis, do ABPI normal is 1-1.2 PAD = 0.5-0.9 and critical limb ischaemia = less than 0.5. Colour duplex USS is 1st line imaging. If considering intervention e.g. percutaneous transluminal angioplasty, MR/CT angiography is used to assess disease extent and location of stenoses.
Describe Leriche’s syndrome and its symptoms
A syndrome caused by aorto-occlusive disease, commonly due to a saddle embolus ad the aortic bifurcation or stenosis from PAD.
Symptoms: Absent femoral pulse, claudication/wasting of the buttock, a pale cold leg, erectile dysfunction.
Describe Carotid Artery Disease and its management
Accounts for 20% of strokes and TIAs.
Management: Symptomatic patients with ipsilateral stenosis >70% should have carotid endarterectomy within 2 weeks of symptom onset. Carotid endarterectomy is also indicated in those with severe stenosis over 80%
Describe Varicose Veins, it’s signs and symptoms, and treatment
Valves prevent blood from passing from deep to superficial veins. If they become incompetent there is venous hypertension and dilatation of the supervicial veins occurs. Risk factors include prolonged standing, obesity, pregnancy, family history and the Pill. There are 3 main sites:
- lateral lower leg = short saphenous
- Medial leg = long saphenous
- Medial lower leg = calf perforators
Symptoms: ‘my legs are ugly’ pain, cramps, tingling, heaviness, and restless legs.
Signs: oedema, eczema, ulcers, haemosiderin, haemorrhage, phlebitis, atrophie blanche (previous ulcer scar), lipodermatosclerosis.
Treatment:
- Endovascular treatment e.g. radiofrequency abalation, endovenous laser ablation or injection sclerotherapy.
- Surgery stripping
What ECG changes would be seen in a posterior MI?
Horizontal ST depression, tall broad R waves (over 30ms), Upright T waves in v1-v3
Dominant R wave in V2 (R/S ratio over 1)
Upside down appears like a STEMI
Describe Angina Pectoris, symptoms, and management.
Symptoms: Due to myocardial ischaemia and presents as central rightness or heaviness which is brought on by exertion and relieved by rest. Precipitates, stress, cold weather and heavy meals. May slo be associated dyspnoea, nausea, sweatiness, and faintness.
Management:
- modify risk factors e.g. Stop smoking, encourage excercise, weight loss, control hypertension and diabetes.
- aspirin + statin
- sublingual glyceryl trinitrate for acute attacks
- b-blocker or Ca blocker first line
- consider dual therapy if fails
- if unable to tolerate the above dual therapy consider long-acting nitrat, ivabradine, nicorandil, or ranolazine.
- if steal symptomatic refer for PCI or CABG.
Describe Coarctation of the Aorta, its symptoms, investigations and management.
Congenital narrowing of the descending aortas usually occurs just distal to the origin of the left subclavian artery. More common in boys. It is associated with bicuspid aortic valve and turners syndrome. Can lead to heart failure and increased risk of infective endocarditis.
Symptoms: Radiofemoral delay, weak femoral pulse, raised BP scapular bruit, systolic murmur.
Investigations: 4 limb BPs, CT or MRI angiogram, CXR shows rib notching.
Management:
Surgery, or ballon dilatation +/- stenting.
Describe Takotsubo Cardiomyopathy, its symptoms and management.
Stress-induced cardiomyopathy e.g. Patient found out family member dies then develops chest pain and features of heart failure. There is transient apical ballooning of the myocardium.
Symptoms: Chest pain, breathlessness.
Management:
- supportive
- reassure is temporary and reversible
Describe Abdominal Aortic Aneurysm, its symptoms and management.
An artery with dilatation more than 50% of its original diameter has an aneurysm. They are typically caused by atheroma, trauma, infection, connective tissue disorders, or inflammatory disorders (e,g. Takayau’s). All men are screened at 65YRS. 25% of AAA have iliac involvement.
Symptoms: Intermittent or continuous abdominal pain that radiates to the back, iliac fossa ear groins, collapse, an expansive abdominal mass, shock if ruptured. Unruptured my be asymptomatic or present with abdominal pain and the mass.
Management:
Unruptured:
-if small (3-4.4cm) yearly screening, if medium 4.4-5.4cm) screen 3monthly, if large over 5.5cm 2wk referral CT scan and echo aim for operation within 8wks.
Ruptured:
-ABCDE assessment get help from vascular surgeons and anaethetist, dont over treat shock aim sys 70-90 if patient can tolerate.
-do ECG, Bloods, cross-match
-prophylactic Cefuroxime + metronidazole
-straight to theatre.
-Management can be via open repair tube graft or Endovascular Aortic Repair (EVAR).
Describe the different parts of the JVP waveform and possible abnormalities.
JVP provides information on the right atrial pressure but also clues to underlying valvular disease. A non-pulsatile JVP is seen in superior vena caval obstruction. Kussmaul’s sign describes a parodoxical rise in JVP during inspiration seen in constrictive pericarditis.
There are 5 parts to the wave form:
- ‘a’ wave - atrial contraction, it is large if atrial pressure is increased e.g. Tricuspid stenosis, pulmonary stenosis, pulmonary hypertension and it is absent in AF. May have Cannon appearance which is due to atrial contraction against a closed tricuspid valve and is seen in complete heart block
- ‘c’ wave - marks closure of the tricuspid valve and is not normally visible.
- ‘x’ descent - fall in atrial pressure during ventricular systole
- ‘v’ wave - due to passive billing of blood into the atrium against a closed tricuspid valve, giant v waves occur in tricuspid regurgitation
- ‘y’ descent - opening of the tricuspid valve.
What are some causes of a Narrow Pulse Pressure?
Considered narrow if less than 25% of systolic value or 25mmHg.
Causes: AS, Cardiac tamponade, Congestive heart failure, shock.
What are the different P wave morphology and what is Multifocal Atrial Tachycardia?
P-mitrale (bifid p waves) due to left atrial enlargement Classically from mitral stenosis
P-pulmonale (peaked p waves) due to right Atrial enlargement classically due to pulmonary hypertension
Inverted p waves which indicate non-sinus origin
Multifocal atrial tachycardia is a condition most commonly seen with elderly patients with chronic respiratory disease, it is 3 different p wave morphological seen in an ecg trace with tachycardia.
Describe Atrioventricular Reentry Tachycardias (AVRT)
A form of paroxysmal junctional tachycardia. A reentry circuit is formed by the normal conduction system and the accessory pathway resulting in circus movement. It can be further divided into orthodromic and antidromic conduction based on direction of reentry.
AVRT with Orthodromic Conduction: in orthodromic anterograde (towards ventricle) conduction occurs via the AV node with retrograde (away from ventricle) occurring via the accessory pathway. Narrow complex tachycardia with ST segment depression, rate 200-300bpm.
AVRT with Antidromic Conduction: in antidromic anterograde conduction occurs via the accessory pathway with retrograde conduction via the AV node. It is much less common. Rate usually 200-300 bum wide QRS complexes due to abnormal ventricular depolarisation via accessory pathway.
What are U waves?
A small defection immediately following the T wave, usually in the same direction and best seen in leads V2,V3. Prominent U waves are most commonly associated with bradycardia, severe hypokalaemia, but may also be seen in raised ICP, hypothermia, HOCM, LVH, Hypomagnesaemia, hypocalcaemia.
What are J waves?
A positive deflection at the ST segment most commonly associated with hypothermia with the degree of hypothermia correlating to the amplitude of the wave.
Describe fusion beats and capture beats
A fusion beat occurs when a supraventricular and a ventricular impulse coincide to produce a hybrid complex of intermediate width and abnormal morphology.
Capture beats occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.
Both can feature in VT rhythm strips.
Describe Arrhythmogenic Right Ventricular Cardiomyopathy, its symptoms, investigations, and management.
An inherited typically autosomal dominant myocardial disease associated with paroxysmal ventricular arrhythmias and sudden cardiac death. Second most common cause of sudden cardiac death in young after HOCM
Features: Palpitations due to ventricular ectopic beats or sustained VT, syncope or cardiac arrest precipitated by exercise. Family history of sudden cardiac death. ECG may show epsilon wave bunny ear complex between QRS and T wave, Also prolonged s-wave upstroke of 5ms in V1-3, T wave inversion in V1-3
Investigations: Echocardiography, may show dilated hypokinetic right ventricle.
Management:
- low risk patient can use sotalol to suppress ventricular arrhythmias
- High risk patients i.e. History of syncope due to cardiac arrest, recurrent arrhymtias not suppressed by anti-arrhythmic drugs, or FHx of sudden cardiac arrest require urgent insertion of implantable cardioverter-defibrillator
What is electrical alternans on an ECG a sign of?
Alternating voltage of consecutive QRS complexes produced by the heart swinging backwards and forwards within a large fluid-filled pericardium
Therefore a sign of massive pericardial effusion.
What are the causes of prolonged QT interval?
Normally less then 440ms, use formula to calculate corrected QT interval.
Causes:
- Drugs e.g. Amiodarone, TCA’s, many antibiotics, fluconazole, erythromycin, metoclopramide, quinidine, haloperidol, droperidol, methadone, ondansetron, SSRI’s
- Genetic due to cardiac ion channel mutations
- myocardial disease e.g. MI, RF, Complete heart block, cardiomyopathy,
- Metabolic, hypocalcaemia, hypokalaemia, hypomagnesaemia
Describe Wellens’ Syndrome and the different types.
A pattern apparent on ECGs characterised by deeply inverted biphasic T waves in V2-V3 which is highly specific for critical stenosis of the LAD.
Patients may be pain free and have normal/mildly elevated cardiac enzymes, but high risk for extensive anterior wall MI.
There are two types, Type A (25%) with initial positivity and terminal negativity, and Type b (75%) which are deeply and symmetrically inverted. T waves evolve over time from Type A to Type B
What is the criteria for diagnosing LVH on ECG, and some causes.
Sokolov-Lyon criteria: S wave depth in V1 = tallest R wave height in V5-V6 is greater than 35mm, or use both voltage and non-voltage criteria.
Causes: Hypertension (Most common), AS, AR, MR, Coarctation of the aorta, HOCM
Describe Aortic Dissection, its features, types investigations and management.
Features: Blood splits the aortic media with sudden tearing chest pain which may radiate to the back. As the dissection extends, branches of the aorta occlude sequentially leading to hemiplegia (Carotid artery), unequal arm pulses and BP or acute limb ischaemia, paraplegia (anterior spinal artery), and anuria (renal arteries). Aortic valve incompetence, MI, and cardiac arrest may develop if direction move proximally.
Types:
- Type A (70%) dissection involve the ascending aorta, irrespective of the site of the tear
- Type B (30%) does not involve the ascending aorta
Investigations:
-ECG/CXR (Widened mediastinum), CT or TOE
Management:
- Patient with type A should be considered for surgery and require urgent cardiothoracic surgical review
- Type B is less clear and surgery is reserved for directions that are leaking, ruptured or compromising vital organs
- Crossmatch 10units of blood
- Hypotensives to keep systolic at 100-110 labetalol or esmolol by IVI can be useful. (Calcium channel blockers Can be used if b-blockers contraindicated)
Describe Lown-Ganong-Levine syndrome, its features
An accessory pathway bypassing the AV node connecting the left atrium to the His bundle.
Features: Very short PR interval, narrow QRS complexes with no evidence of delta waves (as opposed to WPW).
Management:
- Vagal manoeuvres can terminate
- Avoid alcohol and coffee
- ablation possible
What are the causes of heart failure?
Heart failure can be categorised into left vs right, low-output vs high-output (rare), systolic vs diastolic (EF dependant)
Causes: MI, IHD, HTN, valvular disease, cardiomyopathy, Chronic lung disease, congenital heart defects, peri/myocarditis, alcohol/drug abuse, infection, kidney disease, overactive thyroid gland, anaemia
Describe Atrial Flutter and its management.
A type of Supraventricular tachycardia, cause by a re-entry circuit within the right atrium. Atrial rate runs at about 300bpm, ventricular rate depends on the degree of AV block, the commonest is 2:1 resulting in ventricular rate of 150bpm. Sawtooth baseline best seen in inferior leads.
Management:
- Atrial flutter does not usually cardiovert with vagal manoeuvres or adenosine but these technical can unmask flutter waves
- rate control and DC cardioversion with similar rules to Atrial fibrillation regarding TOE
What is Frank’s sign?
A diagonal ear lobe crease extending from the tragus across the lobule it is a sign of atherosclerosis in cardiovascular disease and/or diabetes
Describe Heyde’s syndrome and it’s symptoms.
A syndrome of gastrointestinal bleeding and IDA, from angiodysplasia in the presence of aortic stenosis. It is caused by the induction of vonWillebrand disease by a depletion of the vWF factor in the blood flowing though the narrowed valvular stenosis. This leads to worsening of intestinal angiodysplasia and more prone to bleeding.
What are some indications for a CABG?
Left main coronary artery stenosis over 50%
Stenosis of proximal LAD and proximal circumflex over 70%
3-vessel disease ins asymptomaic patients or those with mild or stable angina
2-vessel disease with proximal LAD stenosis in patients with poor LV function.
What are the complications of prosthetic heart valves?
Systemic embolism, Infective endocarditis, haemolysis, valve failure (regurgitation), arrhythmias.
Describe Eisenmenger’s syndrome, its features, and management.
The reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension. This occurs when an uncorrected defect leads a to remodelling of the pulmonary vasculature eventually causing obstruction to pulmonary blood and pulmonary hypertension. It is associated with VSD, ASD, PDA.
Features: Murmur may disappear, cyanosis, clubbing, right ventricular failure, haeomptysis, emoblism, polycythaemia, hyperviscosity.
Management:
-heart-lung transplantation.
What is the effect of adenosine with concurrent use of dipyridamole?
Dipyridamole blocks the cellular uptake of adenosine, increasing its concentration at receptors and potentiating its effects.
What is the effect of adenosine wth concurrent use of theophyllines?
Theophylline antagonises adenosine necessitating higher dose
What is pulmonary plethora?
A radio graphic feature of prominent pulmonary vasculature usually due to left to right shunts e.g. ASD, VSD, PDA, or other cardiac abnormalities e.g. Transposition of the great arteries.
What are the four features of tetralogy of fallout?
Pulmonary stenosis
Overriding aorta
Ventricular septal defect
Right ventricular hypertrophy
In an SBA what is ‘tapping apex beat’ usually indicating?
Mitral Stenosis
In an SBA what is ‘canon A waves’ usually indicating?
Complete Heart Block
What are some complications of pacemakers?
Failure to output e.g. Battery failure, lead fracture, oversensing (inhibiting pacing output), MI at lead tip, Metabolic abnormalities e.g. Hyperkalaemia, acidosis, alkalosis
Infection
Pneumothorax
Pericarditis
Erosion of pacer through skin
Venous thrombosis
What are the ECG features of Digoxin treatment?
Down-sloping ST depression (‘reverse tick’)
Flattened/inverted T waves
Short QT interval
Arrhythmias e.g. AV block, Bradycardia (can be sign of toxicity)
Describe Jervell and Lange-Nielsen syndrome.
A type of long QT syndrome associated with severe bilateral sensorineural hearing loss. Autosomal recessive disorder due to an abnormal potassium channel. Two main mutations JLN1 + JLN2
Describe Poor R Wave Progression and its causes.
An ECG finding technically defined as R wave height less than 3mm in V3. S wave starts largest in V1 then progressively decreases in amplitude and R wave increased at around V3 they are isoeletric. Then R wave dominates.
Causes:
- Prior anteroseptal MI
- LVH
- RVH
- Inaccurate lead placement.
- Dilated cardiomyopathy
- Normal Variant
Describe Left Anterior Fasicular Block
Aka left anterior hemiblock. Impulses are conducted to the left ventricle via the left posterior fascicles, which inserts into the inferno-septal wall of the left ventricle along its endocardial surface.
On reaching the left ventricle, the initial electrical vector is therefore directed downwards and rightwards (as excitation spreads outwards from endocardium to epicardium), producing small R waves in the interior leads (II, III, aVF) and small Q waves in the left-sided leads (I, aVL)
The major wave of depolarisation then spreads in an upwards and leftwards direction, producing large positive voltages (Tall R waves) in the left-sided leads and large negative voltages ( depp S waves) in the inferior leads.
THis process takes about 20 milliseconds longer than simultaneous conduction via both fascicles, resulting in a slight widening of the QRS.
The impulse reaches the left-sided leads later than normal, resulting in a increased R wave peak time (the time from onset of the QRS to the peak of the R wave) in aVL.
ECG Criteria for LAFB:
- LAD
- Small Q waves with tall R waves in leads I and aVL
- Small R waves with deep S waves in leads II, III, aVF
- QRS duration normal or slightly prolonged
- Prolonged R wave peak time in aVL more than 45s
- Increased QRS voltage in the limb leads.
Describe Left Posterior Fasciular Block.
Aka Left posterior hemiblock, impulses are conducted to the left ventricle via the left anterior fascicle, which inserts into the upper, lateral wall of the left ventricle along its endocardial surface.
On reaching the ventricle, the initial electrical vector is therefore directed upwards and leftwards (as excitation spreads outwards from endocardium to epicardium), causing small R waves in the lateral leads (I and aVL) and small Q waves in the inferior leads (II, III, aVF).
The major wave of depolarisation then spreads along the free LV wall in a downward and rightward direction, producing large positive voltages (tall R waves) in the inferior leads and large negative voltages (deep S waves) in the lateral leads.
This process takes up to 20 milliseconds longer than simultaneous conduction via both fascicles resulting in a slight widening of the QRS.
The impulse reaches the inferior leads later than normal, resulting in a increased R wave peak time in aVF.
ECG Criteria for Left Posterior Fascicular Block:
- Right Axis Deviation (Over +90 degrees)
- Small R waves with deep S waves in leads I and aVL
- Small Q waves with tall R waves in leads II, III, aVF
- QRS duration normal or slightly prolonged.
- Prolonged R wave peak time in aVF
- No evidence of right ventricular hypertrophy.
- No evidence of any other cause for Right axis deviation
What are the ECG features of hyperkalaemia?
Peak T waves P wave widens and flattens eventually disappear Prolonged PR interval Prolonged QRS Development of Sine wave appearance.
Describe the principles of management of hyperlipidaemia.
Primary Prevention:
- QRISK2 score (unless above 85, T1DM, eGFR less than 60, familial hyperlipidaemia)
- offer treatment to those with QRISK2 over 10%, atorvastatin 20mg ON is first line.
- T1DM - offer atorvastatin if over 40, diagnosed over 10 years or have established nephropathy
- CKD - Offer to all patients increase dose if a greater than 40% reduction in non-HDL cholesterol is not achieved and eGFR. Over 30.
Secondary prevention:
-all patients with CVD should be taking Atorvastatin 80mg ON
Follow-up:
-At 3 months repeat full lipid profile, if non-HDL cholesterol has not fallen by at least 40% then increase dose and promote lifestyle changes. Total fat intake should be less than 30% of energy intake, Saturated fats less than 7% and cholesterol less than 300mg/day. Lose weight, exercise and reduce alcohol and smoking intake.
What is the commonest site for primary cardiac tumours to occur?
Atrial myxoma most common and most common site is left atrium
What are LVH Repolarisation changes?
When the myocardium is abnormally thickened, electrical activity takes longer to traverse throughout the whole heart. This may give rise to a number of associated changes:
- LVH with QRS widening - Appears similar to LBBB.
- LVH with LV Strain i.e ST depression and T wave inversion in Left leads (I, aVL, V5,V6)
- LVH with repolarisation abnormality - these may mimic ischaemic ST changes (ST elevation in V1-V3) typically ST deviation away from the QRS complex with T wave inversion.
What are the associations of Ivabradine and AF
Ivabradine increases the relative risk of AF, it also has been shown not to work in patients with AF.
Describe familial hypercholesteroalaemia, its clinical diagnosis, and management
Familial hypercholesterolaemia is an autosomal dominant condition thought to affect 1 in 500. It results in high levels of LDL cholesterol which if untreated may caused early cardiovascular disease. It is due to a mutation in the gene which encodes the LDL-receptor protein.
Clinical diagnosis based on Simon Broome Criteria:
- In adults Total cholesterol over 7.5mmol/L and LDL-C over 4.9mmol/L, In children TC over 6.7 and LDL-C over 4.0 plus:
- For definite FH, tendon fathoms in patients or 1st degree or 2nd degree relatives or DNA-based evidence of FH
- for possible FH: Family history of myocardial infarction below age 50 years in 2nd degree relative, below age 60 in 1st degree relative, or a family history of raised cholesterol levels.
Management:
- Maximal dose of potent statins are usually required.
- Evolocumab is available as second line agent for those with persistent LDL-C over 5 (or 3.5 with CVD) despite maximal tolerated lipid lowering therapy
Describe Pulmonary Capillary Wedge Pressure and its uses.
PCWP is measured using a balloon tipped Swan-Ganz catheter which is inserted into the pulmonary artery. The pressure measured is similar to that of the left atrium (Normally 6-12mmHg)
One of the main uses of measuring the PCWP is determining whether pulmonary oedema is caused by either heart failure or acute respiratory distress syndrome.
In many modern ITU departments PCWP measurement has been replaced by non-invasive techniques.
What are the ECG features of hypokalaemia?
Increased amplitude and width of the P wave
Prolongation of the PR interval
T wave flattening and inversion
ST Depression
Prominent U waves (Best seen in the precordial leads)
Apparent Long QT due to fusion of the t and U waves = long QU interval.
Later SVT and ventricular ecotopics, VT, VF, Torsades de Pointes
Describe Brugada Syndrome and its ECG features, and management.
Brugada syndrome is a form of inherited cardiovascular disease which may present with sudden cardiac death. It is inherited in an autosomal dominant fashion and has an estimated prevalence of 1:5000-10000. It is more common in Asians.
A large number of variants exist around 20-40% of cases are caused by a mutation in the SCN5A gene which encores the myocardial sodium ion channel protein.
ECG Changes:
- Convex ST segment elevation over 2mm of V1-V3 followed by a negative T wave. (There are two types depending on the T wave which is inverted in type 1 and biphasic in type 2)
- Partial RBBB
- Change may be more apparent following flecainide.
Management is implantable cardioverter-defibrillator
What are the ECG features of a paced rhythm?
Pacing spikes vertical spikes usually 2ms, amplitude depends on position and type of lead.
Atrial Pacing: pacing spike precedes the p wave and p wave morphology appears normal.
Ventricular Pacing: Pacing spike precedes the QRS complex, right ventricular pacing lead placement results in a LBBB QRS morphology, left epicardial pacing lead placement results in a RBBB QRS morphology.
Dual Pacing: All of the above.
Describe Atrial Septal Defects, the features and main types.
Atrial septal defects are the most likely congenital heart defect to be found in adulthood. They carry a significant mortality with 50% of patients being dead at 50yrs. Two types of ASD are recognised, ostium secundnum and osmium primum. Ostium secundum is the most common.
Features: ESM, Fixed splitting of S2, Paradoxical emobili.
Ostium Secundum (70% of ASDs): Associatef with Holt-Oram syndrome (Tri-Phalangeal thumbs) ECG shows RBBB with RAD.
Ostium Primum: Presents earlier than secundum, associated with abnormal AV valves. ECG shows RBB with LAD and prolonged PR interval.
What are the different types of Myocardial Infarction?
Type 1: Spontaneous myocardial infarction related to ischaemia due to a primary coronary event such as plaque eruption and/or fissuring, or dissection.
Type 2: Myocardial infarction secondary to ischaemia due to either decreased supply or increased demand e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension.
Type 3: Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of ischaemia, accompanied by presumably new ST elevation or new LBB or evidence of fresh thrombus in a coronary artery and or at autopsy, but death occurring before blood samples could be obtained or before the appearance of cardiac markers in the blood.
Type 4a: Myocardial infarction associated with PCI.
Type 4b: Myocardial infarction associated with stent thrombosis either at angiography or autopsy.
Type 5: Myocardial infarction associated with CABG.
What are some causes of raised troponin?
Cardiac Causes:
- Type 1 MI
- Type 2 MI
- Cardioversion
- Myocarditis
- Cardiac contusion from trauma
- Heart failure
- Aortic Dissection
- Endomyocardial biopsy
- HOCM
- Aortic Valve disease
- Cardiotoxic drugs
- Tachyarrhythmia
- Bradyarrhythmia
- Cardiac Surgery
- Tako-tsubo cardiomyopathy
- Rhabdomyolysis
- Stenting or angiplasty
- Irukandji syndrome
Non-cardiac causes:
- Renal failure
- PE
- Pulmonary Hypertension
- Sepsis
- Burns
- severe critical illness
- extreme exertion
- amyloidosis or other infiltrative disease
- stroke
- SAH
Describe Myopericarditis, its features, and management
The term myopericarditis indicated a primarily pericarditic syndrome with minor myocardial involvement. On the other hand perimyocarditis indicated a primarily myocarditic syndrome. Acute pericarditis and myocarditis share similar etiologic agents viral infections are the most common causes.
Features:
- Pericarditis: pleuritic chest pain relieved by sitting forward, pericardial friction rub, Saddle ST elevation and PR depression. Pericardial effusion
- Myocarditis: Other ECG abnormalities, depressed LV function, Raised troponin, arrhythmias. Chest pain may mimic MI.
Management:
- similar to pericarditis NSAIDs
- may need management for Heart failure
- better to admit patients with myopericarditis compared to simple acute pericarditis.
Describe multifocal atrial tachycardia and its features
MAT may be defined as a irregular cardiac rhythm caused by at least three different sites in the atria, which may be demonstrated by morphologically distinctive p waves. It is more common in elderly patients with chronic lung disease e.g. COPD.
Management:
- correction of hypoxia and electrolyte disturbance
- rate-limiting calcium channel blockers e.g. Verapamil are ofter used first line.
- Cardioversion and digoxin are NOT useful in management of MAT
What are some risk factors in bradycardia for asytole that may indicate treatment with transvenous pacing?
Complete Heart block with broad complex QRS
Recent Asytole
Mobitz Type II AV Block
Venticular Pause > 3 seconds
What is radionuclide angiography?
Aka Multi-Gated Acquisition Scan. Radionuclide (technetium-99m) is injected intravenously. The patient is placed under a gamma camera. May be performed as a stress tests. It can accurately measure left ventricular ejection fraction. Typically used before and after cardiotoxic drugs are to be used.
Describes Catecholaminergic Polymorphic Ventricular Tachycardia, its features and management.
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a form of inherited cardiac disease associated with sudden cardiac death. It is inherited in an autosomal dominant fashion and has a prevalence of around 1:10000. The most common cause is a defect in the ryanodine receptor (RYR2) which is found in the myocardial sarcoplasmic reticulum.
Features:
- Exercise or emotion induced polymorphic ventricular tachycardia resulting in syncope
- Sudden cardiac death
- Symptoms generally develop before the age of 20.
Management:
- Beta-blockers
- Implantable cardioverter-defibrillator.
What are the causes of a shortened QT interval?
Digoxin, beta blockers, hyperkalaemia, Hypercalcaemia, congenital short QT syndrome
Describe the Cardiac Action potential and its different phases.
Phase 4: Diastole. Resting membrane ptoential. Na/K pump keeps Na Extracellular and K intracellular.
Phase 0: Depolarisation due to activating of Na+ Channels causing influx of Na and positive charge of cell.
Phase 1: Inactivation of Na channels, breif opening of K channels making membrane slightly more negative. Referred to as Notch on the action potential waveform.
Phase 2: Plateau. Potassium continues to leak, whilst L-Type calcium channels (activated by the flow of Na during phase 0) allow movement of calcium into the cell. Ca2+ bind to ryanodine receptors on the sarcoplasmic reticulum. allow flow of calcium out of the sarcoplasmic reticulum. This is responsible for contraction of the heart.
Phase 3: Rapid Replolarization, the L-type Ca2+ channels close, K continues to leak through slow delayed rectifier channels. Rapid K channel rectifiers open. Then ironic pumps restore concentrations back to balanced states pre action potential as in phase 4.
Describe Type I Hyperlipoproteinaemia
aka Hyperchlyomicronaemia is associated with eruptive xanthomas. Mutations in Apolipoprotein C2 cause Hyperlipoproteinaemia Type 1B .
Complications include occlusion of the retinal vein, acute pancreatitis, steatosis, organomegaly and lipaemia retinalis.
Describe Type II Hyperlipoproteinaemia
Associated with xanthoma tendinosum (Nodular swellings of tendons). It is the most common form classified further into types IIa and IIb depending on whether the increase in triglycerides levels occur in addition to those of LDL-cholesterol.
Describe Type III Hyperlipoproteinaemia
Tubeeruptive xanthomas occur due to high numbers of chylomicrons and high levels of Intermediate-density lipoprotein. The most common cause for this form is the apolipoprotein E2/E2 genotype. It is due to cholesterol-rich very-low-density lipoprotein. It is associated with hypercholesterolaemia, hypertriglycerideaemia, a normal concentration of apoplipoprotein B, and two types of skin signs (Palmar xanthomata or orange discolouration of skin creases; tuberoeruptive xanthomata on elbows and knees. It is characterised by the early onset of cardiovascular disease and peripheral vascular disease.
Describe Type IV Hyperlipoproteinaemia
Associated with eruptive xanthomas
Describe Type V Hyperlipoproteinaemia
aka mixed hyperlipoproteinaemia familial or mixed hyperlipidaemia. is very similar to type I but with high levels of VLDL in addition to many chylomicrons. It is also associated with glucose intolerance and hyperuricaemia.
Describe the stages of ECG changes in pericarditis
Stage 1 - Widespread ST elevation and PR depression with reciprocal changes in aVR (occurs in first 2 weeks)
Stage 2 - Normalisation of ST Changes, Generalised T wave flattening (1 to 3 weeks)
Stage 3 - Flattened T waves become inverted (3 - to several weeks)
Stage 4 - ECG returns to normal (After several weeks)
What is the main difference between pravastatin and Simvastatin?
Pravastatin is not metabolised by the P450 3A4 enzyme and as such is better tolerated with other P450-enzyme dependant medications
What are the mutations involved in HOCM?
Autosomal dominant approximately 40% have mutations in beta-myosin heavy chain on chromosome 14, and around 40% involve the myosin-binding protein C gene.
Describe recurrent coronary artery vasospasm, it features and management
aka cardiac syndrome x.
Features: Angina-like pain during rest, particularly in the early hours of the morning, Characteristic ECG changes during exercise testing. Normal Coronary arteries on cardiac catheterisation. Inducible coronary artery spasm during the catheterisation.
Managment:
Nitrates are often effective as are a range of calcium channel antagonists.
What are the common causes of congenital long QT syndrome?
LQT1 (mutation in KCNQ1) a subunit of the slow delayed rectifier potassium channel.
LQT2 (mutation in KCNH2) A subunit of the rapid delayed rectifier potassium channel. These mutations account for 45% of LQTS
LQT3 leads to tachy-arrhythmic episodes during sleep usually triggered by bradycardia. Cardiac pacing is considers, less frequent 7% but more lethal.
LQT7 - Anderson Syndrome extremely rare associated with skeletal abnormalities and periodic episodes of muscle weakness.
What are some prognostic factors of HOCM?
Septal wall thicknesss over 30mm Left ventricular outflow obstruction Family history of sudden death Non sustained ventricular tachycardia on holter monitoring. Syncope.
What is an epsilon wave?
A small positive deflection buried in the end of the QRS complex. It is the characteristic finding in Arrhythmogenic Right Ventricular dysplasia.
What are the ECG changes associated with Arrhythmogenic Right Ventricular Dysplasia ?
- Epsilon wave (Most specific finding seen in 30% of patients)
- T wave inversion in V1-V3
- Prolonged S-wave upstroke of 55ms in V1-V3
- Localised QRS widening of 110ms in v1-v3
- Paroxysmal episodes of ventricular tachycardia with a LBBB morphology
What is the role of Valsartan-Sacubitril in the management of chronic heart failure?
From the Paradigm-HF study, Valsartan-Sacubutril (An angiotensin-neprilysin Inhibitor) has shown to improve mortality in those with chronic heart failure and reduced ejections fraction.
NICE 2016 Recommends its use as an alternative to those already taking a stable dose of ACE or ARB. With NYHA Class II-IV with a left ejection fraction of 35% or less.
Describe Lutembacher’s syndrome
A rare congenital heart defect of bot congenital atrial septal defect and acquired mitral stenosis.
What are the associated features of atrial myxoma?
Finger Clubbing
Normocytic anaemia
Positional murmur
Intracardiac calcification on CXR.
What are the LDL-C targets in statin therapy?
In high risk patient:
- Target LDL-C less than 1.8mmol/l
- OR a reduction of more than 50% in patients with LDL-C between 1.8-3.5
Lower risk patients:
-Target LDL-C of less than 3.0mmol/L
When are premature ventricular ectropics clinically significant?
Occuring frequently (10 or more beats/hour or 6 or more beats /min)
- PVE in bigeminal rhythm
- PVE in short runs of VT
- PVE exhibiting R-on-T phenomenon
- PVE associated with serious organic heart disease such as in the context of MI or LV decompensation
Describe Dressler syndrome, its features, and management.
A secondary form of pericarditis, typically occuring after myocardial injury e.g. Myocardial Infarction. Thought to be due to autoimmune inflammatory reaction to myocardial neo-antigens formed as result of myocardial injury.
Features: Fever, pleuritic chest pain, pericardial effusion occurs 2-3 weeks after MI. Can also occur months later. Very rarely can lead to pericardial tamponade.
Management:
-High dose aspirin 650mg QDS
What is the definition of a shunt and how is it calculated?
The abnormal displacement of blood from one chamber to another:
Shunt = Aorta - Mixed Venous / 98 - Pulmonary Artery
Where mixed venous is the o2 saturation of blood returning to the right side of the heart e.g. IVC/SVC
Describe Prosthetic Valve Thrombosis and its management.
More common in mitral protheses with sub therapeutic anticoagulation can result in shock, pulmonary oedema and hypotension depending on if the thrombus is obstructive.
Management:
- Left sided Valve thrombus with shock require surgery if not available then Fibrinolysis
- right sided valve thrombus are manage with Fibrinolysis
- If Fibrinolysis serial echocardiography should be performed and if inadequate response repeat thrombolysis can be given
What are the indications for Digoxin Antibody?
Haemodynamic instability Life-threatening arrhythmias Serum potassium over 5 in acute toxicity Plasma digoxin level over 12nmol/L Ingestion of more than 10mg in adults and 4mg in children Recurrent bradycardia
Describe Pacemaker syndrome and its management
Iatrogenic disease that represents the clinical consequences of suboptimal AV Synchrony after pacemaker insertion. Usually due to poor synchronisation of atria with single lead paced ventricles
Features:
Feature sof complete heart block, syncope SOB, dizziness,
Management:
-Dual chamber pacemaker.
Describe Intra-Aortic Balloon pump, Its indications, contraindications.
Intra-Aortic Balloon Pump is a device tat aim to improve myocardial oxygenation, increase cardiac output and organ perfusion, with a. Reduction in left ventricular workload, A balloon in the aorta is inflated during diastole to increased coronary perfusion and deflated during systole to decrease afterload.
Indications:
- Cardiogenic Shock
- Post bypass
- Post MI
- Cardiomyopathy
- Severe IHD awaiting surgery to stenting
- Severe acute MR Awaiting surgery
- Prophylactically in high risk patient pre-stenting / Cardiac surgery.
Contraindications:
- Aortic regurgitation
- Aortic Dissection
- Severe aortailiac or PVD
- Aortic Aneurysm
- Prosthetic Aortic tree grafts.
- Local sepsis
- Severe coagulopathy
What is the management of Long QT Syndrome?
In asymptomatic patient beta blockade is appropriate management.
Ina symptomatic patients with QTc over 500 and a specific mutation e.g. KCHN2 or SCN4A, should have ICD considered as well as beta blocker therapy.
Symptomatic patients should be managed with ICD.
What is the significance of assessing Aortic Stenosis in the context of LV dysfunction?
The calculated aortic valve area for patients with severe left ventricular dysfunction can be falsely low because low cardiac output reduces the valve opening forces.
An important method of differentiating between Severe AS with secondary LV dysfunction from those with falsely low AS valve and LV dysfunction is to assess the haemodynamics after increasing the cardiac output by dobutamine infusion during echocardiography or cardiac catheterisation.
Patients with truly severe AS manifest an increase in trans-aortic pressure gradient while the valve surface area remains the same, while those with falsely low calculated valve area manifest an increase in calculated valve surface area. Dobutamine echocardiography can also be use to assess LV Contractile reserve, as patients who have 20% or more increase in stroke volume after dobutamine infusion have. A much better prognosis after surgery compared to those who do no have LV contractile reserve.
What ECG features of Posterior Myocardial Infarction.
Posterior MI is suggested by the following changes in V1-V3:
- Horizontal ST depression
- Tall, Broad R waves
- Upright T waves
- Dominant R waves (R/S Ration >1 )in V2
What is the Simon-Broome Criteria for Diagnosis of Familial Hypercholesterolaemia?
Clinical diagnosis based on Simon Broome Criteria:
In adults Total cholesterol over 7.5mmol/L and LDL-C over 4.9mmol/L, In children TC over 6.7 and LDL-C over 4.0 plus:
- For definite FH, tendon xanthomas in patients or 1st degree or 2nd degree relatives or DNA-based evidence of FH
- for possible FH: Family history of myocardial infarction below age 50 years in 2nd degree relative, below age 60 in 1st degree relative, or a family history of raised cholesterol levels.
Describes Sitosterolaemia and its features
A rare autosomal recessive lipid metabolic disorder, characterised by hyperabsorption and decreased biliary excretion of dietary sterols.
Features: Hypercholesterolaemia, Tendon and Tuberous Xanthomas, Premature Atherosclerosis.
Treatment is to avoid sterols in diet
Describe Benign Early Repolarisation syndrome, its features, and prognosis.
ECG pattern most commonly seen in young heath patients under the age of 50.
Features:
- Widespread concave ST Segment elevation most prominent in the Mid to left precordial leads (V2-V5).
- Notching or slurring at the J-Point
- Prominent concordant T waves.
- The degree of ST Elevation is modest in comparison the the T-wave amplitude (less than 25% of the T wave in V6)
- No reciprocal ST Depression
Prognosis:
-Although benign in the sense of not representing STEMI it is associated with 4-5% risk of developed VT/VF if present in the inferior leads.
Describe Sgarbossa’s criteria’s
For identification of MI in context of LBBB or Paced Rhythm.
1) Concordant ST elevation more than 1mm in leads with a positive QRS. (5 Points)
2) Concordant ST Depression more than 1mm in V1-V3. (3 points)
3) Excessively discordant ST elevation in leads with a negative QRS (AT least 1mm and 25% of the preceding S wave (2 Points)
The original sgarbossas’s criteria 3 points or more meant 90% specificity of MI. Modified changed the last point and any positive point met is specific.
What is persistent ST Elevation indicative of?
Aneurysmal myocardium.
What are the causes of a reduced or absent radial pulse?
Blalock-Tussig Shunt Cervical Rib Subclavian Stenosis Radial Artery Injury Congenitally absent or atretic radial artery Radial Artery harvesting for CABG Arteriovenous fistula Takayasu’s Arteritis Interrupted arch syndromes Coarctation of the aorta with subclavian patch repair
