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1
Q

What are the branches of the left main coronary?

A

Coming from the aorta, passing posterior to the pulmonary artery it then splits to the left anterior descending (alternative name is anterior intraventicular branch) when then gives the diagonal branch. The other main branch is the left circumflex which give the left marginal before continuing posterior.

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2
Q

What are the branches of the right coronary artery?

A

Coming from the aorta it travels in the coronary sulcus under the right auricle then gives the right marginal. It continues posteriorly to give the posterior descending.

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3
Q

What are the common anatomical variations in coronary artery anatomy?

A

Dominance is determined by the supply to the posterior descending artery. 70% right dominant from the RCA, 20% co-dominant and 10% from the LCx

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4
Q

What are the normal pressures during the cardiac cycle?

A

Venous input - 1-3mmHg Right atria - 0-8mmHg peak when end diastolic atrial contraction, small rise when filling in systole Right Ventricle - 15-30/0-8mmHg peak during systole when it equalises/exceeds pulmonary artery Pulmonary artery - 15-30/4-12mmHg maintains a small amount of pressure in diastole due to presence of smooth muscle Pulmonary veins - 1-10mmHg minimal pressure as it flows freely into LA Left atrium - 1-10mmHg similar to RA, peak with end dialstolic contraction Left ventricle - 100-140/3-12mmHg pressures must exceed systemic arterial pressure to open aortic valve

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5
Q

What are the muscle types in the heart?

A

In atrium there is smooth muscle and pectinate muscle In ventricles trabeculae carneae and papillary muscle

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6
Q

What are the causes for myocardial ischaemia?

A
  1. Narrowing/blockage of coronary arteries 2. Increase in demand eg LV hypertrophy, increased CO 3. Decreased O2 carrying capacity eg anaemia, hypotension, hypoxaemia 4. Inability to achieve normal dilatation/regulation - microvascular angina
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7
Q

What are some of the causes of narrowing/blocking of coronary arteries?

A

Atherosclerosis Thrombosis Spasm Embolus Coronary ostial stenosis Coronary arteritis

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8
Q

What are the determinants of myocardial oxygen demand?

A

Heart rate Myocardial contractility Myocardial wall tension (stress)

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9
Q

What are the ECG changes seen in ACS acutely and what do they correlate to?

A

Transient T-wave inversion - nontransmural intramyocardial ischaemia Transient ST-depression - patchy subendocardial ischaemia ST elevation - severe transmural ischaemia

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10
Q

What are the indications for an exercise stress test and when are they positive?

A

Moderate risk chest pain or atypical pain Chest pain during test ST depression greater than 2mm

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11
Q

High risk stable angina features

A

Post-infarct angina

Poor effort tolerance

Ischaemia at low workload

Left main or triple vessel disease

Poor LV function

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12
Q

Medical management of angina

A

GTN Aspirin B Blocker or verapamil/diltiazam Long acting nitrate (isosorbide mononitrate) Ivabradine

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13
Q

What are the available scoring systems for risk stratification for chest pain?

A

TIMI score GRACE score - superior to TIMI score

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14
Q

STEMI criteria

A

ST elevation >2mm in adjacent chest leads (>2.5 for males less than 40 and >1.5 for women) ST elevation >1mm in adjacent limb leads New LBBB

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15
Q

Anatomical localisation of infarct territories

A

Anteroseptal - LAD Anterolateral - Cx Inferior - RCA Posterior - Cx or PDA

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16
Q

Contraindications for thrombolysis for STEMI

A

Risk of bleeding - Active bleeding or bleeding diathesis - Significant head injury or facial trauma in last 3 months - Suspected aortic dissection Risk of intracranial haemorrhage - Any prior ICH - ischaemic stroke in last 3 months - Known intracerebral lesion

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17
Q

Relative contraindications for thrombolysis in STEMI

A

Risk of bleeding: - Anti coagulation - Non-compressible vascular punctures - Recent major surgery - Traumatic or prolonged CPR - Recent internal bleeding - Active peptic ulcer Risk of ICH - Hx of severe poorly controlled HTN - Ischaemic stroke over 3 months ago - Dementia or known intracranial abnormality Pregnancy

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18
Q

Complications of myocardial infarction

A

Heart failure Myocardial rupture and aneurysmal dilation Ventricular septal defect Mitral regurgitation Arrhythmias Heart block Post-MI pericarditis

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19
Q

What are de Winter T-waves?

A

A patterns seen in approx 2% acute LAD occlusions. Usually younger males Tall, prominent, symmetric T waves in the precordial leads Upsloping ST segment depression >1mm at the J-point in the precordial leads Absence of ST elevation in the precordial leads ST segment elevation (0.5mm-1mm) in aVR “Normal” STEMI morphology may precede or follow the deWinter pattern

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20
Q

What is Wellens Syndrome?

A

An ECG pattern which is highly suggestive of critical stenosis of LAD Deeply inverted or biphasic T waves in V2-3 May not be associated with chest pain and may have normal or minimally raised troponin

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21
Q

What is the risk of intracranial haemorrhage from thrombolysis?

A

1%

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22
Q

What are the contraindications for prasugrel?

A

Previous stroke Age greater than 75yr Body weight less than 60Kg

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23
Q

What are the characteristics of a mitral stenosis murmur?

A

mid-diastolic rumbling murmur at the apex Increased on inspiration and lying to left Associated with a loud 1st heart sound and opening snap

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24
Q

What is the normal orifice area of the mitral valve? At what valves does stenosis occur? How is severity determined?

A

Normal 4-6cm2 Symptomatic at less than 2cm2 (1.5cm at rest) Mild >1.5 cm2 Moderate 1.0-1.5cm2 Severe < 1cm2

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25
Q

What is the medical management of MS?

A

Anticoagulation if AF, prior embolic events, LA thrombus

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26
Q

What are the 5 components of the mitral valve?

A

Leaflets (anterior and posterior) Annulus Chordae tendinae Papillary muscles Left ventricle

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27
Q

What are the characteristics of mitral regurgitation murmur?

A

Pansystolic mumur at apex radiating across pericordium and to the axilla Soft or absent 1st heart sounds May have 3rd heart sound Mid-systolic click if mitral valve prolapse Increased with exertion, decreased with valsalva

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28
Q

What is the Bernoulli equation and what is it used for?

A

Change p = 4v2 When an orifice is smaller it requires higher velocity for the same output and the pressure will drop over the orifice Used in echos to calculate pressures

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29
Q

What valves are suitable for a percutaneous balloon valvuloplasty for mitral stenosis?

A

Valve area <1.5cm2 Pliable non-calcified minimal subvalvular fusion

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30
Q

What is the murmur of aortic regurgitation?

A

Early diastolic high pitched murmur, decresendo - gets longer the more severe Increased by leaning forward and expiration May also have a low rumbling end diastolic murmur (Austin flint murmur) May have an ejection systolic murmur at base (Flow murmur)

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31
Q

What are the clinical signs of aortic regurgiation?

A

Water hammer pulse Wide pulse pressure DIsplaced diffuse and forcefull apex beat Early diastolic murmur Quinckes sign - nail abed pulsations De Mussets sign - head bobbing with pulse Duroziez sign - to and from murmur at femorals when distal pressure applied Pistol shot femorals

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32
Q

Indications for surgery in aortic regurgitation

A

Symptomatic severe AR Asymptomatic but EF <50% Asymptomatic but LV dilatation (diastolic >70mm and systolic >50mm) Asymptomatic but having cardiac surgery for another reason

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33
Q

What is the characteristics of an aortic stenosis murmur?

A

Ejection systolic murmur at the base radiating to the carotids. Low pitched. Can radiate down to the apex where it can be confused with mitral stenosis

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34
Q

What is low gradient AS?

A

Where a patient appears to have aortic stenosis based on valve size etc but the gradient across the valve is low. This could be a false AS, ‘classic’ or ‘paradoxical’. Classic is where the EF is not high enough to produce the pressure Paradoxical is when the LV is too small to produce the necessary volume

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35
Q

What are the characteristics of a tricuspid stenosis murmur?

A

Mid-diastolic rumbling murmur heard at the left lower sternal edge Increased on inspiration and strain phase of valsalva Often mistaken for MS

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36
Q

What are the common valvular lesions that occur with tricuspid stenosis?

A

Mitral stenosis secondary to rheumatic heart disease

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37
Q

What are the causes of tricuspid regurgitation?

A

Functional 80% - Cor pumonalae - MI - Trauma Organic 20% - Rheumatic heart disease - Infective endocarditis - Carcinoid syndrome - Ebstein’s anomaly - Congenital abnormalities - Radiation - Endomyocardial fibrosis

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38
Q

When is surgery indicated for tricuspid regurgitation?

A

For severe, symptomatic organic disease If a patient is having surgery for a left sided valvular lesion then repair is recommended - even if functional, asymptomatic or moderate

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39
Q

Aetiology of pericarditis?

A

Infectious Non-infectious Autoimmune/hypersensitivity

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40
Q

What are the causes of a chronic pericardial effusion?

A

TB Hypothyroidism Neoplasm Radiation SLE/RA Mycotic infections Chylopericardium

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41
Q

What are the management options of pericarditis?

A

Colchicine for at least 3 months as per ICAP trial to reduce risk of relapse NSAIDs Treat underlying cause if known Surgical drainage Prednisolone if resistant - may increase recurrence rate

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42
Q

What are the ECG changes that may be seen in pericarditis?

A

ST elevation (over affected area or widespread) PR interval depression T wave inversion

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43
Q

What is Becks triad?

A

Signs of tamponade: - Soft heart sounds - Hypotension - Raised JVP with prominent x descent but absent y

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44
Q

Complications of pericardiocentesis

A

Arrhythmia Damage to coronary artery Bleeding Hypotension if tamponade due to aortic dissection

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45
Q

Likely causes of a haemorrhagic pericardial effusion?

A

TB Neoplasm Renal failure/uraemic Slow leakage from aortic dissection

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46
Q

What are the differential diagnoses for restrictive pericarditis?

A

Restrictive cardiomyopathy Cor pulmonalae Tricuspid stenosis

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47
Q

What are the forms of myocarditis?

A

Fulminant myocarditis Acute myocarditis Chronic active myocarditis Chronic persistent myocarditis

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48
Q

What is Chagas disease?

A

A protozoal infection by T.cruzi transmitted by bug bite. Causes direct damage and a chronic inflammatory process. 5% are symptomatic with acute parasitemia (non-specific, myocarditis or meningoencephalitis) 10-30yrs later develop dilated cardiomyopathy and GI symptoms

49
Q

Where is Chagas disease endemic?

A

South and Central America

50
Q

What are the causes of granulmoatous myocarditis?

A

Sarcoidosis Giant cell myocarditis

51
Q

What is required for a diagnosis of pericarditis?

A

At least 2 of: - typical chest pain - typical ECG changes - Pericardial effusion more than a trivial amount - Pericardial friction rub

52
Q

Where does Atrial Flutter originate from?

A

Around the tricuspid annulus

53
Q

What evidence is there for catheter ablation for AF?

A

Previously no evidence to improve mortality - used for symptoms Castle AF study showed improved mortality and decreased HF hospitalisations for patients with AF and heart failure

54
Q

What medications are available for medical cardioversion?

A

Flecanide Amiodarone Sotalol (inconclusive evidence) Quinidine (inconclusive evidence)

55
Q

What is the risk of IA and IC drugs in atrial flutter?

A

As they do not have AV nodal blocking they can lead to a switch to 1:1 transmission. Other medications for rate control should be used first - b blockers, Ca Channel blockers and digoxin. Amiodarone also does not have this risk

56
Q

What are the ECG findings associated with sick sinus syndrome?

A

Bradycardia Sinus pauses sinus arrest Tachy/brady esp with AF inappropriate response to physiological stimuli

57
Q

What is required for the diagnosis of sick sinus syndrome?

A

There is no definitive criteria or tests ECG changes consistent with SSS with associated symptoms This diagnosis may be aided by ambulatory monitoring or loop recorders

58
Q

What are the forms of supraventricular tachycardia?

A

Atrioventricular nodal re-entry tachycardia (AVNRT) - fast and slow pathway within the AV node which an atrial ectopic may be able to lead to re-entry circuit. Atrioventricular re-entrant tachycardia (AVRT) - accessory pathway or bypass tract allowing electrical connection between the atria and ventricles.

59
Q

What are the longterm treatment options of WPW

A

If asymptomatic - monitor If symptomatic - Catheter ablation 1st line - Medical management 2nd line with flecanide or propafenone (1C drugs), then try b blocker then 1A drugs then amiodarone

60
Q

What is the risk of AF in WPW

A

Risk of transmitted atrial rate to the ventricle especially if transmission prefers the accessory pathway. Do not use medictaions which block the AV node (CCB, B blockers, digoxin, adenosine). Acutely use cardioversion or ibutilide or procainamide

61
Q

What is the management of SVT?

A

If unstable - cardioversion If stable - vagal maneuvers the IV adenosine then IV CCB, B blocker of digoxin

62
Q

What are the ECG findings in WPW?

A

Short PR interval delta wave Widened QRS complexes

63
Q

What is multifocal tachycardia associated with?

A

Drugs - digoxin, theophylline Pulmonary disease Hypokalaemia Hypomagnesaemia Chronic renal failure

64
Q

What are the Aus classifications for hypertension

A

Optimal <120/80 Normal <129/84 High-normal <139/89 Grade 1 (mild) HTN <159/99 Grade 2 (moderate) HTN <179/109 Grade 3 (severe) HTN >180/110 Isolated systolic HTN >140 and <90

65
Q

Pathophysiological changes in hypertension

A
  • Decreased compliance of the vessels - increased resistance - Vascular endothelial dysfunction with decreased NO production - Sclerosis of the glomeruli leading to decreased filtration and activation of RAAS -
66
Q

What are the adrenergic receptors and what are their function?

A

Alpha 1 - Vascular walls - vasoconstriction. Heart Increased contraction Alpha 2 Vascular wall Vasoconstriction Pre-synaptic terminals - negative feedback Beta 1 - Heart increased inotrophy and chronotrophy. Renal - increased renin Beta 2 - vessels vasodilation Alpha receptors more responsive to noradrenaline and beta receptors to adrenaline

67
Q

Causes of systolic hypertension with wide pulse pressure?

A

Decreased vascular compliance Increased cardiac output - Aortic regurgitation - Thyrotoxicosis - Hyperkinetic heart syndrome - Fever - Aterovenous fistula - Patent ductus arteriosus

68
Q

What are the causes for secondary hypertension?

A

Endocrine - Cushings, Acromegaly, Thyroid disease, hyperparathyroidism Adrenal - Conn syndrome, adrenal hyperplasia, pheochromocytoma Renal Cardiovascular - coarctation of aorta Drugs - NSAIDs, OCP, Steroids, Liquorice, MAOI, TCA Neurogenic Other - OSA, eclampsia

69
Q

What are the endocrine causes of hypertension?

A

Excessive renin - Renal artery stenosis, renal disease, renin-secreting tumours Excessive catecholamines - Phaeochromocytoma Excessive GH production - Acromegaly Excessive aldosterone - Adrenal adenoma (Conn’s syndrome) - Adrenal hyperplasia - Dex-suppressible hyperaldosteronism Excessive other mineralcorticoids - Cushings - Tumours producing other mineralcorticoids Exogenous mineralcorticoids - Liquorice

70
Q

What are the changes seen in malignant hypertension?

A

Renal - arteriolar fibrinoid necrosis - renal failure, proteinuria, haematuria CNS - cerebral oedema, haemorrhage - hypertensive encephalopathy Retina - flame haemorrhages, cotton wool spots, hard exudates and papilloedema

71
Q

Investigations for hypertension

A

Urine dipstick, creatinine/albumin ratio UEC Fasting lipids and glucose ECG

72
Q

When should anti-hypertensives be started?

A

If HTN and moderate CVD risk (BP >140/90) If moderate HTN then treatment should be started even with low CVD risk Treat if end-organ damage or high risk condition (stroke, CKD, diabetes, peripheral arterial disease)

73
Q

What lifestyle modifications are recommended for HTN management?

A

Aim BMI 20-25 Aerobic exercise >30min most days Diet - high is fruit and vegetables, low in saturated fat and salt Avoid smoking Increase fish oil intake

74
Q

First line pharmacotherapy for hypertension

A

ACEI/ARB - preferred first line if CKD with microalbumuria Calcium channel blocker Thiazide diuretic *can be combined. Beta blockers not used as first line except when otherwise indicated in ischaemic heart disease or heart failure

75
Q

What are the types of heart block?

A

1st degree - prolonged PR >0.22 sec 2nd degree Mobitz type 1 - Wenckebach with PR prolongation til failed conduction 2nd degree Mobitz type 2 - fixed ratio of block, QRS usually wide 3rd degree - complete heart block with dissociation

76
Q

What drugs can increased HR in an acutely unstable patient?

A

Atropine Adrenaline Isoprenaline

77
Q

What is the definition of sustained VT?

A

>30 seconds of a broad complex tachycardia Non-sustained if greater than 5 beats and less the 30 sec.

78
Q

What is ventricular bigeminy?

A

When ventricular ectopics occur as a pair, they can also occur as a triplet.

79
Q

Longterm management options for VT

A

ICD for primary or secondary prevention Catheter ablation Beta blockers, amiodarone or sotolol to decrease incidence eg frequent shocks

80
Q

What is the genetic basis for Brugada syndrome?

A

A loss in a sodium channel function, 20% are due to a loss of function mutation in the SCN54 gene.

All other genes are association only.

81
Q

What are the strongest indications for a CRT-D

A

Sinus rhythm LBBB with QRS >150ms NYHA class 2 or 3 LVEF <35%

82
Q

What are the common cuases for sudden cardiac death?

A

Brugada syndrome Long QT (congenital or acquired) Catecholaminergic polymorphic VT Idiopathic VT and VF Short QT syndrome Commotio cordis

83
Q

What are the ECG changes in Brugada syndrome/pattern?

A

2 patterns Pseudo-RBBB Coved ST elevation in V1-2 followed by a negative T wave (type 1) Saddle back ST elevation in V1-V2 with an upright or biphasic t wave (type 2) Changes can fluctuate over time. Type 1 can be induced by sodium channel blockers

84
Q

What values indicate prolonged QT interval?

A

Always calculated corrected QT which includes the HR For males >470 milliseconds For females >480 milliseconds

85
Q

What is the treatment for Brugada syndrome?

A

Only treat if type 1 (spontaneous or drug induced) and symptomatic. If family hx of sudden death then treat can do EP study to decide on ICD insertion. ICD If cannot have ICD or frequent shocks trial amiodarone or ablation

86
Q

What are the 5 classes of lipoproteins?

A

Chylomicron VLDL IDL LDL HDL

87
Q

What is a possible cause if TG and HDL both elevated?

A

Alcohol intake

88
Q

What is the lipid profile pattern in Cushings Syndrome?

A

High triglycerdides Low HDL LDL can also be high

89
Q

What is suggestive of familial combined hyperlipidaemia?

A

Mixed dyslipidaemia and family history of dyslipidaemia/premature coronary artery disease

90
Q

What is the genetic basis for familial combined hyperlipidaemia

A

There are no single genes identified and there is no mendalian pattern. It is likely polygenetic

91
Q

What are the lipid targets for secondary prevention?

A

LDL <1.8 HDL >1 TG <2

92
Q

What are the indications lipid lowering?

A

For primary prevention it is based on CVD risk. If greater than 7.5% over 10 years then consider lowering. There is no lipid targets in these patients. Usually only monotherapy unless exceptionally high For secondary prevention all patients should have lipid lowering therapy. There are targets. LDL is the only level to correlate with reduced risk.

93
Q

What is the role for fibrates in lipid lowering?

A

Primary action decreases TG, causes modest HDL rise and has a variable effect on LDL. Used in mixed dyslipidaemia when hypertriglyceridaemia is the predominant factor.

94
Q

What is the 5 year mortality for heart failure?

A

>50%

95
Q

What are the most common causes of heart failure?

A

Ischaemic heart disease Hypertension Dilated cardiomyopathy Others: Other cardiomyopathies Valvular heart disease Congenital Alcohol and drugs inc. chemotherapy Right HF Arrhythmia / tachycardia cardiomyopathy Constrictive pericarditis

96
Q

What beta blockers are used in heart failure?

A

Carvedilol Bisoprolol Long acting metoprolol

97
Q

What is the role for ARNI?

A

An angiotensin receptor blocker and neprilysin inhibitor (sacubitril/valsartan) used when EF <40% and on maximal doses of ACEi, B Blocker, Spironolactone. Replace with the ACEi/ARB

98
Q

What is the role of Ivabradine in heart failure? What is the MOA?

A

Used in patients with EF <35% who are in sinus rhythm with HR >77 despite maximal doses of ACEi and B Blocker or who cannot tolerated B Blocker.

MOA - Slows the sinus node

99
Q

What are the effects of the RAAS system?

A

Designed to increase blood pressure, cardiac output and intravascular volume. - Activation of sympathetics - Na retention and therefore water retention - Vasoconstriction - Stimulation of ADH

100
Q

How do compensatory mechanisms in heart failure lead to further damage?

A

-Direct toxicity of catecholamines -Increased work leads to further damage of myoctes and cardiac remodelling -Increased work worsens ischaemia -Vasoconstriction increases afterload and cardiac workload - Increased preload leads to volume overload and pulmonary HTN - Hyponatraemia due to excessive RAAS and ADH

101
Q

What are the types of cardiomyopathy?

A

Hypertrophic cardiomyopathy

Arrhythmogenic (right) ventricular cardiomyopathy Dilated cardiomyopathy

Primary restrictive non-hypertrophic cardiomyopathy

102
Q

What are the common genetic causes of hypertrophic cardiomyopathy?

A

MYH7 - beta myosin heavy chain

MYBPC3 - myosin binding protin C

HCM is a disease of the sarcomere. These 2 account for approx 50% cases.

103
Q

What are the treatment options for HCM?

A

If symptomatic with heart failure, angina or LVOT obstruction then 1st line is a beta blocker followed by CCB then disopyramide. If they are high risk they should have a ICD If there is significant LVOT obstruction the surgical ablation is recommended.

Primary prevention ICD is based on a score of risk

104
Q

What are the risk factors for sudden death with Hypertrophic cardiomyopathy?

A

There is a risk calculator which incorporates:

Age

Family history of SCD

Unexplained syncope LV outflow gradient

Maximal LV wall thickness

LA diameter

NSVT

Other high risk features: Exercise induced hypotension, Previous cardiac arrest ,or sustained VT

105
Q

What are the histopathological changes in arrhythmogenic ventricular cardiomyopathy?

A

Fatty or fibro-fatty replacement of the ventricular myocytes, Classically right ventricle but LV involved in 75%. Septum is usually spared. This leads to dilatation

106
Q

What is the management of arrhythmogenic ventricular cardiomyopathy?

A

The primary issue is arrythmias rather than heart failure. - ICD for primary or secondary prevention - B blocker for all - Antiarrythmics if ICD shocks - sotolol, flecanide and amiodarone - Radiofrequency ablation for refractory ICD shocks - Generic heart failure treatment if this develops

107
Q

What are the features of a posterior fascicular blocks?

A

Anterior - positive lead 1 (R) and aVL, negative in aVF, II, III (S) Posterior - Negative in lead 1 and aVL, positive in aVF, II , III

108
Q

What is an epsilon wave?

A

Small postive deflection burried at the end of the QRS

Best seen in V1 and V2

Classic of ARVC

109
Q

What are the features of an anterior fascicular block?

A

Anterior - positive lead 1 (R) and aVL, negative in aVF, II, III (S)

110
Q

What are the common genetic mutations in LQT Sydnrome?

A

LQT1 - KCNQ1 on Chromosome 11

LQT2 - KCNQ2 on Chromosome 7

LQT3 - SCN5A (gain of function) on Chromosome 3

111
Q

What is the most common genetic cause of catecholaminergic polymorphic VT?

A

RyR2 mutation - seen in 60-65% patients

* Caused by issues with calcium

112
Q

What is the pathological basis of familial dilated cardiomyopathy?

A

It is a disease of the cytoskeleton. Titin mutations are the most common cause.

113
Q

What are the types of ACS?

A
114
Q

What is VO2?

A

VO2 = CO x C(a-v)O2

Peak VO2 represents exercise tolerence

115
Q

What are the TIMI scoring stages

A
116
Q

What information do the direction of A Flutter waves provide?

A

If positive in V1 and negative in inferior leads then it is a conterclockwise current.

If negative in V1 and positive in inferior leads then it is clockwise.

117
Q

What are the criteria to classify aortic stenosis as severe?

A

Gradient >40mmHg

Area <1cm

Velocity <0.25 DI

118
Q

What are the indications for surgery for aortic stenosis?

A

Severe + symptoms

Severe + EF <50%

Cardiology (1 decks)

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