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Phase 1c: Conditions > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is an aneurysm?

A

A permanent and irreversible dilatation of a blood vessel by at least 50% of the normal expected diameter; it is a true aneurysm if it affects all three muscle layers.

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2
Q

What are the key diagnostic factors for an unruptured abdominal aortic aneurysm?

A

PATIENTS WITH AAA ARE USUALLY ASYMPTOMATIC, UNLESS RUPTURE OCCURS
Presence of risk factors
Pulsatile abdominal mass (uncommon)
Abdominal, flank or back pain

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3
Q

What are the risk factors for AAA?

A

Cigarette smoking
Family history
Increased age

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4
Q

What are the key diagnostic factors for a ruptured abdominal aortic aneurysm?

A

Abdominal, flank, or back pain
Hypotension
Loss of consciousness
Pallor
Abdominal distension
Fever (for infectious AAA)

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5
Q

What investigations are required for AAA?

A

Aortic ultrasound
CT angiography for operative planning
ESR/CRP if infective cause suspected
FBC (possible anaemia if ruptured, leukocytosis if infectious AAA)
Cross match and clotting screen
Blood cultures (infectious AAA)

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6
Q

What is the management plan for unruptured asymptomatic AAA?

A

<3cm: no further action
3-4.4cm: rescan every 12 months
4.5-5.4cm: rescan every 3 months
>5.5cm: refer within 2 weeks to vascular surgery for probably intervention

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7
Q

What is the management plan for unruptured symptomatic AAA?

A

Urgent surgical repair

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8
Q

What is the management plan for ruptured AAA?

A

Urgent surgical repair and resuscitation measures (high mortality)

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9
Q

What are the symptoms and signs of infective endocarditis?

A

Fever/chills
Cardiac murmur (most common is aortic regurgitation)
Night sweats, malaise, fatigue, anorexia, weight loss, myalgias
Arthralgia
Headache
Shortness of breath
Janeway lesions, Osler’s nodes, Roth spots, splinter haemorrhages

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10
Q

What are the investigations for infective endocarditis?

A

Blood culture (3 sets from different venepuncture sites)
Echocardiography (trans-thoracic vs trans-oesophageal - mainly TTE)
FBC (normocytic anaemia, leukocytosis)
CRP (elevated)
Serum U&Es, glucose (urea elevated)
LFT
Urinalysis (microscopic haematuria, proteniuria)
ECG

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11
Q

What is used to diagnose IE?

A

Modified Duke criteria for diagnosis of infective endocarditis: clinical criteria for definite IE requires two major criteria, one major and three minor criteria, or five minor criteria

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12
Q

What are the major criteria for Duke’s?

A

Positive blood cultures for IE typical microbe (2x 12 hours apart)
Echocardiogram showing valvular vegetation/endocardial innvolvement

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13
Q

What are the minor criteria for Duke’s?

A

TIMER acronym
Temperature >38 degrees
Immunological phenomena (Osler’s nodes, Roth spots)
Microbiological evidence (positive blood culture not meeting major criterion)
Embolic phenomenon (conjuctival haemorrhage, Janeway lesions)
Risk factors (congenital heart disease, IV drug users)

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14
Q

How is infective endocarditis treated?

A

Antibiotic therapy
Consider surgery (to remove infected tissue and repair/replace affected valves)

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15
Q

What organism is the most common cause infective endocarditis?

A

S. aureus

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16
Q

Differentiate between a STEMI and an NSTEMI

A

Presentations and symptoms are similar
STEMI is an infarction that extends the entire thickness of the myocardium (complete blockage of artery), whereas NSTEMI is infarction that is limited to the inner layer of the ventricular wall (partial blockage of artery)

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17
Q

Differentiate between an NSTEMI and unstable angina

A

In NSTEMI, troponin levels are elevated
NSTEMI patients may also be clinically unstable (e.g., low blood pressure, shock, left ventricular failure)

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18
Q

What causes ACS?

A

Atherosclerotic plaque may become inflamed and rupture, exposing substances that promote coagulation and promoting a blood clot on top of the clot
Coronary artery embolism
Coronary spasm (cocaine use)
Coronary artery dissection

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19
Q

How does myocardial infarction present?

A

Central crushing chest pain that can radiate to arms, back or jaw
Marked sweating
Nausea and vomiting
Dyspnoea
Fatigue
Shortness of breath
Pallor
Syncope

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20
Q

What are the ECG changes in NSTEMI?

A

ST-depression, T-wave inversion

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21
Q

What are the ECG changes in STEMI?

A

ST-elevation, with reciprocal ST-depression in electrically opposite leads
Location of infarction can be determined by area of ST-elevation

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22
Q

what medication is given for all people with ACS?

A

IV morphine if severe pain
oxygen if sats <94%
nitrates - use in caution if patient is hypotensive
aspirin 300mg

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23
Q

How is STEMI treated?

A

300mg aspirin
PCI if presentation within 12 hours and possible within 120 minutes - with unfractionated heparin
prasugrel if patient not taking anticoagulant - otherwise clopidogre
OTHERWISE, fibrinolysis with antithrombin

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24
Q

How is NSTEMI/unstable treated?

A

fondaparinux
calculate GRACE score
if low risk (<3%): aspirin, ticagrelor (if bleeding risk low)/clopidogrel (if bleeding risk is high)
if high risk (>3%): coronary angiography within 72 hours, PCI, unfractionated heparin

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25
Q

What medication is given for secondary prevention of ACS?

A

ACEi
beta-blocker
dual antiplatelet therapy (aspirin and second antiplatelet) - ticagrelor if low bleeding risk, clopidogrel if high bleeding risk
statin

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26
Q

How is angina treated?

A

Aspirin
Statin
Sublingual GTN spray
1. CCB (verapamil/diltiazem) or beta-blocker
2. Amlodipine and beta-blocker
3. Consider long-acting nitrate (isosorbide mononitrate), ivabradine, nicorandil, ranolazine

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27
Q

What are the key diagnostic factors for aortic stenosis?

A

Exertional dyspnoea
Fatigue
Exertional syncope
Chest pain

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28
Q

What murmurs are heard with aortic stenosis?

A

Ejection systolic murmur heard at the left sternal edge with crescendo-descendo pattern
Murmur radiates to carotid and heard loudest leaning forward on end expiration
S2 diminished and single

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29
Q

What are the risk factors for aortic stenosis?

A

Advanced age
Congenitally bicuspid valve
Rheumatic fever
Chronic kidney disease

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30
Q

What investigations are considered for aortic stenosis?

A

Transthoracic Doppler echocardiogram
ECG (left ventricular hypertrophy, absent Q-waves, atrioventricular block, hemiblock, or bundle branch block)
CXR (may be normal, can show lung pathology)

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31
Q

How is aortic stenosis treated?

A

Balloon valvuloplasty (if not suitable for aortic valve replacement)
Surgical aortic valve replacement (SAVR) for low-risk and <75
Transcatheter aortic valve replacement (TAVI) for >75 and co-morbidities

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32
Q

What are the examination findings of aortic stenosis?

A

Regular, small volume, slow-rising pulse (‘pulsus tardus et parvus’)
Narrow pulse pressure
Apex beat heaving and displaced (LV dysfunction and dilatation)
Ejection systolic murmur

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33
Q

How is clinically stable, symptomatic aortic stenosis treated? (age >80 years)

A

Transcatheter aortic valve replacement
Long-term infective endocarditis antibiotic prophylaxis
Consider long-term anticoagulation and statins

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34
Q

What murmurs are heard with aortic regurgitation?

A

Early decrescendo, high-pitched diastolic murmur heard over aortic area - with patient sitting forwards and in expiration
Corrigan’s pulse (collapsing pulse) heard at carotid
Austin-Flint murmur heard at apex (early diastolic, rumbling murmur)

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35
Q

Describe the presentation of acute aortic regurgitation

A

Early diastolic murmur
Collapsing pulse
Wide pulse pressure
Mid-diastolic Austin-flint murmur in severe AR
Quincke’s sign (nailbed pulsation)
De Musset’s sign (head bobbing)

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36
Q

What are some signs of cardiogenic shock?

A

Pallor and sweating
Mottled extremities
Rapid and faint peripheral pulse
Jugular venous distension
Altered mental status
Urine output <30ml/hour
Severe SOB and tachycardia

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37
Q

Describe the presentation of chronic aortic regurgitation

A

Widened pulse pressure
Fatigue and weakness (progressive LV dysfunction)
Paroxysmal nocturnal dyspnoea (progressive LV dysfunction)

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38
Q

What are the risk factors for aortic regurgitation?

A

Bicuspid aortic valve
Rheumatic fever
Infective endocarditis
Connective tissue disorders, e.g. Ehlers Danlos or Marfan’s

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39
Q

How is aortic regurgitation investigated?

A

ECG
CXR (cardiomegaly)
Echocardiogram (colour Doppler and pulsed-wave Doppler)
Cardiac catheterisation (before surgery)

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40
Q

How is acute AR treated?

A

Ionotropes
Vasodilators
Aortic valve replacement/repair

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41
Q

How is asymptomatic chronic AR treated?

A

If LVEF <55%, aortic valve replacement and vasodilator therapy
If LVEF >55%, reassurance and monitoring

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42
Q

How is symptomatic chronic AR treated?

A

Aortic valve replacement and vasodilator therapy

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43
Q

How does mitral stenosis present?

A

Dyspnoea and orthopnoea
History of rheumatoid fever
Raised JVP
Haemoptysis (if bronchial vein rupture due to increased pulmonary venous pressure)
Hoarseness (enlarged LA compresses left recurrent laryngeal nerve)
Dysphagia (enlarged LA compresses oesophagus)
Peripheral oedema and ascites
Atrial fibrillation (SA node cells irritated as LA dilates)

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44
Q

What murmurs are heard in mitral stenosis?

A

Mid-diastolic, low-pitched rumbling murmur heard in left lateral decubitus position
Loud P2 (pulmonary hypertension)
Loud S1

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45
Q

What are the risk factors for mitral stenosis?

A

Streptococcal infection (rheumatic fever)
Female sex
Amyloidosis
SLE

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46
Q

How is mitral stenosis investigated?

A

ECG (AF, LA enlargement, RV hypertrophy)
CXR
Trans-thoracic echocardiography

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47
Q

How is progressive asymptomatic mitral stenosis treated (valve area >1.5mm2)?

A

No therapy required

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48
Q

How is severe asymptomatic mitral stenosis treated (valve area <1.5mm2)?

A

No therapy generally required, consider balloon valvotomy

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49
Q

How is severe symptomatic mitral stenosis treated (valve area <1.5mm2)?

A

Diuretic (furosemide)
Balloon valvotomy, valve replacement or repair
Consider beta-blocker (atenolol) or ivabradine for rate control

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50
Q

What murmur is heard with mitral regurgitation?

A

Loud pansystolic murmur at the apex radiating into the axilla
Diminished S1 - incomplete closure of the valve
S3 heart sound (left ventricular dysfunction)

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51
Q

How does mitral regurgitation present?

A

Mostly asymptomatic - symptoms due to left-sided heart failure, arrhythmias, pulmonary hypertension
Fatigue
Dyspnoea
Oedema

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52
Q

What are the causes of mitral regurgitation?

A

coronary artery disease or post-MI - damage to papillary muscles or chordae tendinae
mitral valve prolapse
infective endocarditis
rheumatic fever
congenital

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53
Q

what are the symptoms of acute pericarditis?

A

pleuritic chest pain relieved by sitting forwards
non-productive cough, fever, dyspnoea
percardial friction rub

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54
Q

What are the risk factors for pericarditis?

A

Male sex, aged 20-50
Viral infections (e.g. Coxsackie B, mycobacterium tuberculosis)
Dressler syndrome (following an MI)
Uraemic pericarditis (high levels of urea irritate serous pericardium)
Cancers
Autoimmune disorders (RA, SLE)
Mediastinal radiation

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55
Q

What is constrictive pericarditis?

A

When inflammation persists, immune cells initiate fibrosis of the serous pericardium - this makes it hard for ventricles to expand
Therefore, stroke volume decreases and HR increases to compensate

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56
Q

what are the features of constrictive pericarditis?

A

dyspnoea
right sided heart failure - raised JVP, ascites, hepatomegaly, oedema
pericardial knock - loud S3
positive Kussmaul’s sign
pericardial calcification on CXR

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57
Q

How is pericarditis investigated?

A

ECG (saddle-shaped ST elevation, PR depression)
transthoracic echocardiography
ESR and CRP
troponin (elevated troponin indicates myopericarditis)

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58
Q

How is pericarditis treated?

A

NSAID (aspirin or NSAID) and PPI (omeprazole)
Colchicine (to prevent recurrent pericarditis)
Consider corticosteroid - prednisolone, e.g. no infectious cause and contraindication to NSAIDs
IV antibiotics if purulent pericarditis
Consider immunosuppresants (azathioprine) if recurrent disease

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59
Q

How is cardiac tamponade investigated?

A

Echocardiogram (enlarged pericardium or collapsed ventricles) - 1st line
ECG: electrical alternans

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60
Q

What are the characteristics of cardiac tamponade?

A

Raised JVP, hypotension, tachycardia
Kussmaul’s sign (rise in JVP on inspiration)
Muffled heart sounds
Tachypnoea
Pulsus paradoxus - an abnormally large drop in BP during inspiration

61
Q

How is cardiac tamponade treated?

A

Pericardiocentesis

62
Q

What is a sinus rhythm?

A

Regular rhythm, normal P-waves before each QRS complex

63
Q

What can cause sinus tachycardia?

A

Heart needs to compensate for a decrease in stroke volume, e.g. acute heart failure, acute MI, pulmonary embolism
Acceleration of sympathetic nervous system - hyperthyroidism, cocaine or amphetamine use

64
Q

What can cause sinus bradycardia?

A

Hypothyroidism
Anorexia nervosa
Inferior wall MI
Cushing reflex (sign of raised ICP - bradycardia, hypertension, irregular respiration)
Medications: beta blockers, CCBs, opiates

65
Q

How is acute sinus bradycardia treated?

A

IV 500mcg atropine - if unsatisfactory, repeat to a maximum of 3mg
transcutaneous pacing
isoprenaline/adrenaline infusion
if above fails, transvenous pacing

66
Q

How is chronic bradycardia treated?

A

Pacemaker

67
Q

How does paroxysmal supraventricular tachycardia (PSVT) present on ECG?

A

Narrow QRS, absent P-waves, HR 150-200bpm

68
Q

What can cause PSVT?

A

Alcohol, caffeine use, illicit drug use

69
Q

How is PSVT treated?

A

Vagal maneouvres, e.g. carotid massage, Valsalva maneouvre (blow hard against syringe)
NEXT STEP: rate control with IV adenosine (veramapil if contraindication) - 6mg, then 12mg, then 18mg
Direct current cardioversion for unstable patients
Apixaban (DOAC) based on CHA2DS2VASc score

70
Q

When should adenosine be avoided as treatment?

A

If patient has:
asthma
COPD
Heart failure
Heart block
Severe hypotension

71
Q

How is recurrent SVT treated?

A

Medications: beta blockers, CCBs or amiodarone
Radiofrequency ablation

72
Q

What is Wolff-Parkinson White?

A

Extra electrical pathway connecting atria and ventricles (Bundle of Kent) - ventricles are excited earlier than usual

73
Q

How does Wolff-Parkinson White present on ECG?

A

Shortened PR interval (<0.12s), widened QRS complex (>0.12s), delta wave (upwards slurring of QRS complex)

74
Q

How is Wolff-Parkinson White treated?

A

Radiofrequency ablasion of the accessory pathway
Sotalol, amiodarone, fleicanide
Most antiarrhythmic medications contraindication for WPW patients with atrial fibrillation/flutter

75
Q

How does atrial flutter present on ECG?

A

Regular rhythm, atrial HR 250-300bpm, saw-tooth pattern, AV conduction ratio usually 2:1

76
Q

What conditions are associated with atrial flutter?

A

Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis

77
Q

How is atrial flutter treated?

A

Rate/rhythm control with beta blockers or cardioversion
Treat underlying condition
Radiofrequency ablation of re-entrant rhythm
Anticoagulation based on CHA2DS2VASc score

78
Q

How does atrial fibrillation present on ECG?

A

Absent P-waves, irregularly irregular rhythm

79
Q

how is atrial fibrillation treated in haemodynamically unstable patients?

A

DC cardioversion

80
Q

how is atrial fibrillation treated in patients presenting <48 hours?

A

rate or rhythm control
rate: bisoprolol, verapamil, digoxin
rhythm control: beta blocker, amiodarone (particularly if co-existing heart failure?

81
Q

how is atrial fibrillation treated in patients presenting >48 hours or uncertain?

A

rate control: beta blocker, CCB, digoxin

82
Q

What are some causes of chronic left-sided heart failure?

A

Valvular: aortic stenosis, aortic regurgitation, mitral regurgitation
Muscular: ischaemia, cardiomyopathy, arrhythmias, myocarditis
Systemic: hypertension, amyloidosis, drugs (e.g. cocaine, chemo)

83
Q

What are some causes of chronic right-sided heart failure?

A

Valvular: tricuspid regurgitation, pulmonary valve disease
Lungs: pulmonary hypertension, pulmonary embolism, chronic lung disease, e.g. interstitial lung disease, cystic fibrosis

84
Q

What can cause acute HF?

A

Decompensation of chronic HF
Acute coronary syndrome

85
Q

What are the symptoms of left-sided heart failure?

A

Fatigue
Dyspnoea (orthopnoea, paroxysmal nocturnal dyspnoea, exertional dyspnoea)
Nocturnal cough (+/- pink frothy sputum)
S3 gallop
Tachycardia
Fine end-inspiratory crackles at lung base (pulmonary oedema)
Wheeze (cardiac asthma)

86
Q

What are the symptoms of right-sided heart failure?

A

Fatigue
Reduced exercise tolerance
Anorexia
Nausea
Nocturia
Facial swelling
Raised JVP
Ascites, hepatomegaly
Ankle and sacral pitting oedema

87
Q

How is heart failure investigated?

A

CXR (alveolar oedema, Kerley B signs, cardiomegaly, dilated upper lobe vessels, pleural effusion)
Transthoracic echocardiogram with doppler
ECG
BNP
FBC, U&Es, LFTs, TFTs

88
Q

How is chronic heart failure treated? - 1st and 2nd line

A

Lifestyle modifications (annual flu and one-off pneumococcal vaccine, smoking cessation)
Furosemide for symptomatic control
1st line: ACEi (ramipril) and beta-blocker (bisoprolol)
2nd line: spironolactone

89
Q

What is third line treatment for heart failure?

A

Ivabradine if sinus rhythm >170bpm and EF <35%
Sacubitril-valsartan if symptomatic on ACEi or ARB
Digoxin if co-existing AF
CRT if LBBB

90
Q

How is acute heart failure treated?

A

Sit patient upright
60-100% oxygen
IV diamorphine
GTN infusion
IV furosemide

91
Q

What are the symptoms of aortic dissection?

A

Acute onset, severe, tearing chest pain - radiates to back
BP difference between left and right arm
Radial pulse deficit
Syncope
Focal neurological deficit, e.g. limb weakness or paraesthesia
Diastolic murmur
Hypotension and shock if significant blood loss

92
Q

What are the risk factors for aortic dissection?

A

Marfan’s or Ehlers-Danlos
Chronic hypertension
Coarctation of the aorta
CABG
Bicuspid aortic valve
Aortic valve replacement
Age, male, smoking, hyperlipidaemia

93
Q

How is aortic dissection investigated?

A

chest x-ray (widened mediastinum)
CT angiography (investigation of choice)
transoesophageal echocardiogram (unstable patients)

94
Q

How is aortic dissection treated?

A

Beta-blocker to control BP and HR
Opioid analgesia (morphine)
Type A: open surgery
Type B: thoracic endovascular aortic repair

95
Q

What are the shockable cardiac rhythms?

A

Ventricular fibrillation
Pulseless ventricular tachycardia

96
Q

What are the non-shockable cardiac rhythms?

A

Pulseless electrical activity
Asystole

97
Q

How is sudden shockable cardiac arrest treated?

A

Chest compressions (30:2)
Defibrillation (single shock, followed by 2 minutes of CPR)
300 mg amiodarone after 3 shocks
1mg amiodarone after 3rd shock

98
Q

What are the causes of tricuspid regurgitation?

A

Pulmonary hypertension (e.g. COPD)
Right ventricular infarction
Rheumatic heart disease
Ebstein’s anomaly - valve leaflets are too low and sit in ventricle
Infective endocarditis

99
Q

What are the signs of tricuspid regurgitation?

A

Pansystolic murmur
Giant V waves in JVP
Right sided heart failure - distended neck veins, hepatosplenomegaly, peripheral oedema
Left parasternal heave (eccentric right ventricular hypertrophy - blood flows back from atria into ventricle, increasing preload)

100
Q

What are some causes of secondary hypertension?

A

Renal: glomerulonephritis, renal artery stenosis, pyelonephritis
Obesity
Pre-eclampsia/pregnancy
Endocrine: Conn’s, Cushing’s, phaeochromocytoma, acromegaly (also associated with hypokalaemia)

101
Q

How is hypertension managed in patients <55 or with T2DM?

A
  1. ACEi or ARB
  2. ACEi or ARB and thiazide-like diuretic/CCB
  3. ACEi or ARB and thiazide-like diuretic and CCB
  4. If low potassium, add spiranolactone (potassium-sparing diuretic)
    If high potassium, add alpha or beta-blocker
102
Q

How is hypertension investigated?

A

Fundoscopy: hypertensive retinopathy
Urine dipstick and U&Es: renal disease
ECG: LVH or ischaemic heart disease
HbA1C: DM
Lipids: hyperlipidaemia

103
Q

What are the stages of hypertensive retinopathy?

A

Grade 1: silver wiring
Grade 2: AV nipping
Grade 3: flame haemorrhage, cotton wool spots
Grade 4: papilloedema, hard exudates, flame haemorrhage, cotton wool spot

104
Q

How is cardiac tamponade treated?

A

Pericardiocentesis

105
Q

How is angina treated?

A

Aspirin and statin
Sublingual glyceryl trinitrate for attacks
Beta blocker or CCB (veramapil)
Beta blocker and CCB if still symptomatic (amlodipine if dual therapy)

106
Q

What are the symptoms of acute myocarditis?

A

chest pain
dyspnoea
arrhythmias
symptoms of heart failure? - S3 and S4 gallop

107
Q

How is myocarditis investigated?

A

ECG: non-specific ST segment and T wave changes, ? ectopic beats and arrhythmias
Endomyocardial biopsy via cardiac catheterization (GOLD STANDARD)
Troponin: elevated

108
Q

How is myocarditis treated?

A

Address underlying cause and supportive management
? corticosteroids for viral myocarditis

109
Q

How is myocarditis investigated?

A

raised inflammatory markers, cardiac enzymes and BNP
ECG: tachycardia, arrhythmias, ST-elevation and T-wave inversion
echocardiogram

110
Q

How is hypothermia investigated?

A

Core body temperature (mild: 32-35, severe: <32)
ECG: J/Osborne waves (small bump at end of QRS), prolonged QT, QRS, PR, ST elevation
FBC, U&Es: may have hypokalaemia, elevated Hb

111
Q

What are the risk factors for hypothermia?

A

General anaesthesia
Substance abuse
Hypothyroidism
Impaired mental status
Homelessness
Extremes of age

112
Q

What are the symptoms of hypothermia?

A

Shivering
Cold and pale skin
Slurred speech
Tachypnoea, tachycardia and hypertension (if mild)
Respiratory depression, bradycardia and hypothermia (if moderate)
Confusion/ impaired mental state

113
Q

How is hypothermia managed?

A

Passive warming
Securing the airway and monitoring breathing
Warm IV fluids?
Rapid rewarming can lead to shock - avoid heating lamps, hot bath, massaging of limbs, alcohol
Avoid IV drugs

114
Q

What is malignant hyperthermia?

A

A hypermetabolic reaction to anaesthesia

115
Q

What are the symptoms of malignant hyperthermia?

A

Muscle rigidity
Fever
Rhabdomyolysis
Hyperkalaemia
Increased CO2 production, acidosis

116
Q

How is malignant hyperthermia treated?

A

IV dantrolene
Stop triggering agent

117
Q

On ECG, what are leads I, III and aVF?

A

Inferior leads supplied by right coronary artery or left circumflex

118
Q

On ECG, what are leads I, aVL, V5 and V6?

A

Lateral leads supplied by left circumflex artery or diagonal branches of left anterior descending

119
Q

On ECG, what are leads V1-V4?

A

Antero-septal leads supplied by left anterior descending

120
Q

What are the complications of an MI?

A

cardiac arrest due to ventricular fibrillation
cardiogenic shock
chronic heart failure
pericarditis
dressler’s syndrome
left ventricular aneurysm
left ventricular free wall rupture
ventricular septal defect
acute MR (due to ischaemia or rupture of papillary muscle)
tachy- and bradyarrythmias

121
Q

what are the features of dressler’s syndrome?

A

pericarditis 2-6 weeks post-MI
fever, pleuritic chest pain, pericardial effusion, raised ESR

122
Q

what are the features of left ventricular free wall rupture?

A

occurs 1-2 weeks post-MI
acute heart failure secondary to cardiac tamponade
raised JVP, pulsus paradoxus, diminished heart sounds
treated with pericardiocentesis and urgent thoracotomy

123
Q

what are the features of ventricular septal defect?

A

usually occurs in the first week
acute heart failure associated with pansystolic murmur
echocardiogram is diagnostic and will exclude acute MR

124
Q

what are the features of left ventricular aneurysm?

A

persistent ST elevation
left ventricular failure - SOB, bibasal crackles, raised JVP, pulmonary oedema
thrombus may form in aneurysm, so patients are anticoagulated

125
Q

What is S1? when is it soft and loud?

A

closure of mitral and tricuspid valves
soft if long PR or mitral regurgitation
loud in mitral stenosis

126
Q

What is S2? when is it soft?

A

closure of aortic and pulmonary valves
soft in aortic stenosis
splitting during inspiration is normal

127
Q

What is S3?

A

caused by diastolic filling of the ventricle

128
Q

What are the causes of S3?

A

can be considered normal in people <30
left ventricular failure (e.g. dilated cardiomyopathy)
constrictive pericarditis
mitral regurgitation

129
Q

When is S4 heard?

A

aortic stenosis
HOCM
hypertension

130
Q

what is first degree heart block?

A

PR interval >0.2s
asymptomatic first degree heart block is common and does not require treatment

131
Q

what is mobitz type I?

A

progressive prolongation of PR interval until there is a dropped QRS

132
Q

what is mobitz type II?

A

PR interval is constant, but sometimes P wave not followed by QRS

133
Q

what is third degree heart block?

A

no association between P wave and QRS

134
Q

what are the causes of first degree heart block?

A

increased vagal tone (e.g. athletes)
acute inferior MI
electrolyte abnormalities (e.g. hyperkalaemia)
drugs: nonhydropyridine CCBs, beta-blockers, digoxin

135
Q

what are the associations of coarctation of the aorta?

A

Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis

136
Q

what are the features of coarctation of the aorta?

A

infancy: heart failure
adult: hypertension
radio-femoral delay
mid systolic murmur, maximal over the back
apical click from the aortic valve

137
Q

what are the ECG changes in anteroseptal MI?

A

V1-V4
left anterior descending artery

138
Q

what are the ECG changes in inferior MI?

A

II, III and aVF
right coronary artery

139
Q

what are the ECG changes in anterolateral MI?

A

V1-V6, I, aVL
proximal left anterior descending

140
Q

what are the ECG changes in lateral MI?

A

I, aVL, V5, V6
left circumflex artery

141
Q

what are the ECG changes in posterior MI?

A

changes in V1-V3
horizontal ST depression
tall, broad R waves
upright T waves
dominant R wave in V2
ST elevation and Q waves in posterior leads (V7-V9)

142
Q

what are the features of complete heart block?

A

syncope
heart failure
regular bradycardia (30-50 bpm)
wide pulse pressure
JVP: cannon waves in neck
variable intensity of S1

143
Q

what are the causes of high output cardiac failure?

A

anaemia
arteriovenous malformation
Paget’s disease
pregnancy
thyrotoxicosis
thiamine deficiency (wet Beri-Beri)

144
Q

what are the complications of myocarditis?

A

heart failure
arrhythmia
dilated cardiomyopathy

145
Q

what are the causes of dilated cardiomyopathy?

A

idiopathic
myocarditis
ischaemic heart disease
peripartum
hypertension
substance abuse: alcohol, cocaine
inherited
infiltrative: haemochromatosis, sarcoidosis
nutritional, e.g. wet beri beri (thiamine deficiency)

146
Q

what are the features of dilated cardiomyopathy?

A

classic findings of heart failure: dyspnoea, peripheral oedema, raised JVP
displaced apex beat
S3 gallop rhythm
pansystolic murmur - mitral and tricuspid regurgitation
‘balloon appearance’ of the heart on CXR

147
Q

how is familial hypercholesterolaemia inherited?

A

autosomal dominant condition

148
Q

how is familial hypercholesterolaemia investigated?

A

Simon-Broome criteria:
FHx of premature cardiovascular disease
hypercholesterolaemia (>7.5mmol/L in adult)
tendon xanthomata

149
Q

what are the features of HOCM?

A

exertional dyspnoea
angina
syncope
sudden death - due to ventricular arrhythmias, HF
jerky carotid pulse
large ‘a’ waves
double apex beat
ejection systolic and pansystolic murmurs

Phase 1c: Conditions (18 decks)

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