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Year 4 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the atria and ventricles separated by?

A

Annulus fibrosus

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2
Q

Normally, the heart occupies ???% of the trans-thoracic diameter

A

<50%

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3
Q

Which structure form the cardiac silhouette?

A 
Aortic arch
Pulmonary trunk
Left atrial appendage
Left ventricle 
Right atrium
SVC and IVC
Right ventricle
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4
Q

What is the most common cause of angina and acute coronary syndrome, and the most common cause of death worldwide?

A

Coronary artery disease

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5
Q

What is coronary artery disease usually caused by?

A

Atherosclerosis

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6
Q

List 3 causes of coronary artery disease, other than atherosclerosis

A
  1. Vasculitis
  2. Aortitis
  3. Autoimmune connective tissue disease
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7
Q

List the features of an unstable atherosclerotic plaque

A 
Lipid-rich core
Fibrocellular cap
Speckled calcification
Increased inflammatory cells
Few crosslinks
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8
Q

List the risk factors for atherosclerosis

A 
Age
Male
Family history of early-onset coronary artery disease
Smoking
Familial hyperlipidaemia
Hypertension
T2DM
Platelet activation/high plasma fibrinogen
Antiphospholipid antibodies
Inactivity
Obesity/high fat diet
Alcohol
Social deprivation
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9
Q

Describe the classification system for atherosclerosis

A

Type 1 - isolated macrophage foam cells
Type 2 - ‘fatty streak’ of intracellular lipid accumulation
Type 3 - type II changes + small extracellular lipid pools
Type 4 - Atheroma
Type 5 - Fibroatheroma (lipid core with fibrotic layer, or multiple lipid cores with fibrotic layers
Type 6 - complicated fibroatheroma e.g. surface defect, haematoma, haemorrhage, thrombus

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10
Q

What lifestyle advice would you give to help prevent atherosclerosis?

A

Quit smoking
Take regular exercise (20 mins 3x weekly)
Maintain a healthy body weight
Eat a mixed diet rich in fresh fruit and vegetables
Aim to get no more than 10% of energy from saturated fats

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11
Q

What two conditions are considered acute coronary syndromes?

A

Unstable angina

Myocardial infarction

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12
Q

Define unstable angina

A

New-onset or rapidly worsening angina (crescendo angina), angina on minimal exertion or angina at rest in the ABSENCE of myocardial damage

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13
Q

Define myocardial infarction

A

Angina with evidence of myocardial necrosis

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14
Q

What is the most common cause of acute coronary syndromes?

A

Atherosclerosis

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15
Q

Describe the typical clinical features of acute coronary syndrome

A 
Severe, long-lasting tight/heavy/constricting chest pain at rest
Radiation of pain to neck/arms/epigastrium/back
Anxiety/distress
Breathlessness
Nausea/vomiting
Collapse/syncope
Pallor
Sweating
Changes in heart rate
Hypotension
Cold peripheries
Oliguria
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16
Q

Which patients are more likely to experience a ‘silent’ MI?

A

Older patients

Diabetics

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17
Q

What investigations would you perform in a patient presenting with chest pain?

A
  1. History & examination
  2. 12-lead ECG
  3. Serum Troponin I or T
  4. Repeat ECG & Troponin (6-12 hours after presentation)
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18
Q

Describe the changes typically seen in an ECG of a patient with a STEMI?

A
  1. Hyperacute T waves
  2. ST elevation
  3. Progressive loss of R waves
  4. T wave inversion
  5. Q wave development
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19
Q

What ECG pattern would make you think a patient had an old or established infarct?

A

Presence of Q waves and T wave inversion

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20
Q

Describe the changes typically seen in an ECG of a patient with an NSTEMI?

A

ST depression and T-wave changes

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21
Q

Describe the typical pathology of an non-ST acute coronary syndrome

A

Partial occlusion of a major vessel OR

Complete occlusion of a minor vessel

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22
Q

ECG changes in leads V1-6 and aVL would indicate ischaemia in which region?

A

Anterior heart

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23
Q

ECG changes in leads V1-4 would indicate ischaemic in which region?

A

Anteroseptal

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24
Q

ECG changes in leads V4-6 and aVL would indicate ischaemia in which region?

A

Anterolateral

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25
Q

ECG changes in leads II, III and aVF would indicate ischaemia in which region?

A

Inferior

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26
Q

A person with chest pain but no raise in cardiac troponin would be diagnosed with ???

A

Unstable angina

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27
Q

Levels of troponin will increase within ?-? hours, peak at ? hours and may remain elevated for up to ? weeks.

A

Levels of troponin will increase within 3-6 hours, peak at 36 hours and may remain elevated for up to 2 weeks.

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28
Q

What features would indicate that a patient is at high risk of a further cardiac event?

A
  1. Failure of symptoms to settle on medical therapy
  2. Extensive ECG changes
  3. Elevated plasma troponin
  4. Severe pre-existing stable angina
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29
Q

What is the criteria used to diagnose an MI?

A
  1. Detection of a rise and/or fall in cardiac biomarkers with at least 1 value >99th centile upper reference limit with at least one of the following:
    - Symptoms of ischaemia
    - New or presumed new significant ST-T changes or new left bundle branch block
    - Development of pathological Q waves
    Imaging evidence of new loss of viable myocardium or regional wall motion abnormality
    - Identification of intra-coronary thrombus with angiography or post mortem
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30
Q

What is the criteria used for diagnosis of a prior myocardial infarction?

A
  • Pathological Q waves with/without symptoms in the absence of non-ischaemic causes
  • Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract, in the absence of a non ischaemic cause
  • Pathological findings of a prior myocardial infarction
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31
Q

How would you manage a high risk patient presenting with acute coronary syndrome?

A
  1. Early inpatient coronary angiography
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32
Q

How would you manage a low risk patient presenting with acute coronary syndrome?

A
  1. Exercise tolerance test approximately 4 weeks after event
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33
Q

How would you manage a patient presenting with an acute coronary syndrome?

A

Assessment:

  1. History & examination
  2. ECG
  3. Troponin
  4. Oxygen
  5. Morphine
  6. Nitrates
  7. Aspirin
  8. Clopidogrel/Ticagrelor
  9. Metoprolol
  10. PCI (within 120 mins) if STEMI or new bundle branch block + GP IIb/IIIa receptor antagonists
    OR
  11. Thrombolytic therapy IV + fondaparinux OR LMWH
  12. Consider coronary angiography + GP IIb/IIIa receptor antagonists
Long-term management:
Aspirin
Tricagrelor
Fondaparinux/LMWH
Statin
Beta-blocker
ACE inhibitor
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34
Q

List the potential complications of acute coronary syndrome

A
  1. Ventricular fibrillation
  2. Atrial fibrillation
  3. AV block
  4. Recurrent angina
  5. Pericarditis
  6. Dressler’s syndrome
  7. Papillary muscle rupture
  8. Ventricular septal rupture
  9. Ventricular wall rupture
  10. Embolism
  11. Ventricular remodelling
  12. Ventricular aneurysm
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35
Q

How do you minimise the risk of arrhythmias after acute coronary syndrome?

A
  1. Adequate pain relief
  2. Rest
  3. Hypokalemia correction
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36
Q

Describe the Universal Definition of MI

A

Type 1: MI caused by acute atherothromboembolism
Type 2: MI caused by imbalance between myocardial oxygen demand and supply unrelated to atherosclerosis
Type 3: Cardiac death in patients with symptoms suggestive of myocardial ischaemia and presumed new ECG changes before cardiac troponin becomes available
Type 4: MI related to PCI (a) or stenting (b)
Type 5: MI related to CABG

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37
Q

A 54 year old woman presents with central chest pain after having an argument with a neighbour. She is usually well, she is a non-smoker with a history of mild anxiety and depression over many years. On examination she looks well, BP 140/90mmHg and pulse 100/minute. ECG shows T-wave inversion in the anterior chest leads. Plasma troponin is elevated at 100ng/litre (normal <16ng/l). Echocardiogram shows an apical akinetic segment in the left ventricle.

What is the likely diagnosis?
A.    Acute ST elevation myocardial infarction
B.    Acute pulmonary embolism
C.    Takatsubo cardiomyopathy
D.    Coronary artery spasm
E.    Acute pericarditis
A

C Takasubo cardiomyopathy

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38
Q

A 65yr old lady returns to the clinic 1 year following treatment for a type 2 MI. She complains of gradually increasing shortness-of-breath on exertion and when lying down over the past few months. Clinical examination shows only some mild ankle oedema. Following further investigation spirometry and chest X-rays are normal. You are suspicious of heart failure. What of the following would be the most appropriate next investigation?

 A- 	Coronary angiography
 B- 	B- type natriuretic peptide
 C-  	Echocardiogram
 D- 	Troponin 1
 E-  	Holter monitoring
A

C. Echocardiogram (due to previous heart failure). If there has been NO previous heart failure then BNP should be used.

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39
Q

Risk factors for persistent hypertension

A
  • Alcohol excess
  • Smoking
  • High cholesterol
  • Genetics
  • Age
  • Ethnicity e.g. African American, Japanese
  • High salt intake
  • Obesity/lack of exercise
  • Impaired intra-uterine growth
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40
Q

Secondary causes of hypertension

A
  • Renal disease
  • Diabetes
  • Coarctation of the aorta
  • Renal artery stenosis
  • Primary hyperaldosteronism
  • Phaeochromocytoma
  • Acromegaly
  • Hypo/hyperthyroidism
  • Drugs: alcohol, ciclosporin, cocaine, COCP, corticosteroids, erythropoeitn, leflunomide, liquorice, NSAIDs,
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41
Q

How would you manage a patient with a QRISK2 score <10%?

A
  • Lifestyle advice

- Further risk assessment in 5 years

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42
Q

How would you manage patient with a QRISK2 score >10%?

A
  • Atorvostatin 20mg
  • Lifestyle advice
  • Consider testing for familial disorders or secondary causes of hyperlipidaemia
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43
Q

What investigations would you consider in a patient with hypertension?

A
  • Fundoscopy - looking for hypertensive retinopathy
  • Serum cholesterol and HDL cholesterol
  • QRISK2 assessment
  • ECG - assess cardiac function and detect left ventricular hypertrophy
  • Urinalysis - haematuria, urin albumin:creatine ratio
  • Bloods: glucose, U&Es, creatinine, eGFR - exclude adrenal disease, CKD and diabetes
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44
Q

How would you manage a patient <40 with no evidence of organ damage, CVD, renal disease of diabetes with hypertension?

A
  • Consider specialist evaluation of secondary causes of hypertension
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45
Q

How would you manage a patient with hypertension who had signs of papilloedema or retinal haemorrhage, or suspected pheochromocytoma?

A
  • Refer for same-day specialist care
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46
Q

How would you manage a patient with stage 1 hypertension (no other features)?

A

Lifestyle advice

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47
Q

How would you manage a patient under 55 with stage 1 hypertension and one or more of target organ damage/CVD/renal disease/diabetes/QRISK score >20%?

A

1) ACE inhibitor OR ARB OR B-blocker
4) Add a calcium-channel blocker
5) Add a thiazide diuretic

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48
Q

How would you manage a patient <55 with stage 2 hypertension?

A

1) ACE inhibitor OR ARB OR B-blocker
2) Add a calcium channel blocker
3) Add a thiazide diuretic

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49
Q

When would a beta-blocker be indicated as the 1st line treatment in a patient <55 with stage 1 or stage 2 hypertension which required treamtent?

A
  • Younger patients
  • Intolerance to ACEi/ARBs
  • Pregnancy
  • Increased sympathetic drive
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50
Q

How would you manage a patient >55 with stage 1 hypertension and one or more of target organ damage/CVD/renal disease/diabetes/QRISK2 score >20%?

A

1) Calcium channel blocker
2) Thiazide-like diuretic e.g. chlortalidone or indapamide
3) Add an ARB
4) Add low-dose spironolactone OR increase thiazide dose OR add an alpha- or beta-blocker

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51
Q

How would you manage patient >55 with stage 2 hypertension?

A

1) Calcium channel blocker
2) Thiazide-like diuretic e.g. chlortalidone or indapamide
3) Add an ARB
4) Add low-dose spironolactone OR increase thiazide dose OR add an alpha- or beta-blocker

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52
Q

How would you manage an Afro-Carribena patient with stage 2 hypertension

A

1) Calcium channel blocker
2) Thiazide-like diuretic e.g. chlortalidone or indapamide
3) Add an ARB
4) Add low-dose spironolactone OR increase thiazide dose OR add an alpha- or beta-blocker

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53
Q

If a patient presented with a single episode of clinical hypertension, what would your next step be?

A

Ambulatory blood pressure monitoring

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54
Q

Side effects of ACE inhibitors

A
  • Cough
  • Hyperkalemia
  • Angioedema
  • Alopecia
  • Dry mouth
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55
Q

Side effects of ARBs

A
  • Hyperkalemia
  • Abdominal or back pain
  • Diarrhoea
  • Postural hypotension
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56
Q

Side effects of beta-blockers

A
  • Bradycardia

- Hypotension

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57
Q

When are beta-blockers contra-indicated

A
  • Asthma
  • Cardiogenic shock
  • Hypotension
  • Bradycardia
  • Metabolic acidosis
  • Phaeochromocytoma
  • Conduction disorders
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58
Q

Side effects of calcium channel blockers

A
  • Ankle swelling
  • Palpitations
  • Dizziness
  • Flushing
  • Headaches
  • Constipation
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59
Q

When is verapamil contra-indicated?

A
  • Heart failure
  • Oedema
  • Conduction disorders
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60
Q

Side effects of thiazide diuretics

A
  • Gout
  • Hypokalemia
  • Hyponatremia
  • Glucose intolerance/hyperglycaemia
  • Hyperuricaemia
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61
Q

When are thiazide diuretics contra-indicated?

A
  • Addison’s disease
  • Hypercalcemia
  • Hyponatremia
  • Refractory hypokalemia
  • Hyperuricaemia
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62
Q

When should you review a patient with hypertension controlled by lifestyle modification?

A
  • Every 3-4 months until blood pressure is well-controlled or antihypertensive drug is started
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63
Q

When should you review a patient after starting them on an antihypertensive drug?

A

> 4 months after to wait for treatment effects to stabilise

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64
Q

What should an annual blood pressure review entail

A
  • Discussion of lifestyle, symptoms, medication
  • Check BP - recheck on 2-3 occasions if high
  • Check renal function - serum creatinine, electrolytes, eGFR
  • Reassess QRISK2 score
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65
Q

Target blood pressures

A
  • <80: clinical target 140/90; ABPM target <135/85
  • > 80: clinical target <150/90; ABPM target <145/85
  • Diabetics: clinical target <130/90; ABPM target <125/85
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66
Q

Risk factors for infective endocarditis

A
  • Age
  • Rheumatic heart disease
  • Congenital or acquired heart disease e.g. ventricular septal defect, mitral or aortic regurgitation
  • Prosthetic valves
  • IVDU
  • Dental work
  • IV/central lines
  • Cardiac surgery
  • Wound infection with S. epidermis
  • Exposure to farm animals
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67
Q

Main causes of infective endocarditis

A
  • Strep viridans in subacute disease

- Staphylococci - staph aureus, staph epidermis (in IVDU)

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68
Q

Clinical features of acute infective endocarditis

A
  • Severe febrile illness with prominent and changing heart murmurs and petechiae
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69
Q

Clinical features of sub-acute infective endocarditis

A
  • Persistent fever
  • Fatigue
  • Night sweats
  • Weight loss
  • Heart failure symptoms
  • Conduction disorders
  • Splinter haemorrhages
  • Purpura and petechial haemorrhages in the skin, funds and mucous membranes
  • Osler’s nodes
  • Finger clubbing
  • Splenomegaly (and hepatomegaly)
  • Non-visible haematuria
  • Subconjuctival haemorrhage
  • Roth’s spots
  • Poor dentition
  • Loss of peripheral leg pulses
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70
Q

What investigations would you consider in a patient with suspected infective endocarditis?

A

1) Blood cultures - 3-6 discrete sets prior to commencing antibiotics
2) Echocardiogram
3) Bloods - FBC, ESR
4) Urinalysis
5) ECG
6) CXR

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71
Q

Duke’s major criteria for infective endocarditis

A

1) Positive blood culture
- Typical organisms from 2 cultures
- Persistent positive blood cultures taken >12 hours apart
- 3 or more positive cultures taken >1 hour apart

2) Endocardial involvement
- Positive echo findings of vegetations
- New valvular regurgitation

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72
Q

Duke’s minor criteria for infective endocarditis

A
  • Valvular or cardiac abnormality
  • IIVDU
  • Pyrexia >38
  • Embolic phenomenon
  • Vasculitis phenomenon
  • Blood cultures with organism growth not achieving major criteria
  • Suggestive echo findings
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73
Q

What factors of Duke’s criteria would a person have to meet to definitely have infective endocarditis?

A 
2 major criteria 
OR
1 major and 3 minor criteria
OR
5 minor criteria
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74
Q

What factors of Duke’s criteria would a person have to meet to probably have infective endocarditis?

A

1 major and 1 minor criteria
OR
3 minor criteria

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75
Q

How would you manage a patient with infective endocarditis

A
  • Remove any potential source of infection

- Amoxicillin OR vancomycin + gentamicin IV (+ rifampicin if prosthetic valves) for 4-6 weeks minimum

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76
Q

Indications that 2 weeks of antibiotic therapy will be sufficient to treat infective endocarditis

A
  • Native valve infection
  • Minimum inhibitory concentrations <0.125
  • No adverse prognostic factors (heart failure, aortic regurgitation, conduction defect)
  • No evidence of thromboembolic disease
  • No vegetation >5mm diameter
  • Clinical response within 7 days
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77
Q

Indications for surgical debridement and valve replacement in infective endocarditis

A
  • Heart failure due to valve damage
  • Failure of antibiotic therapy
  • Large vegetations on left-side heart valves with echo appearance suggesting high risk of emboli
  • Previous evidence of systemic emboli
  • Abscess formation
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78
Q

Complications of infective endocarditis

A
  • Embolic stroke

- Peripheral arterial embolism

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79
Q

Risk factors for congenital heart disease

A
  • Turner’s syndrome
  • Marfan’s syndrome
  • Down’s syndrome
  • Female (patent ductus arteriosus, atrial septal defect)
  • Male (coarctation of the aorta)
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80
Q

Clinical features of a ventricular septal defect

A
  • Cyanosis
  • Pansystolic murmur loudest over L sternal edge
  • Heart failure
  • Eisenmenger’s syndrome
  • Prominent parasternal pulsation
  • Tacypnoea
  • Undraping of lower ribs on inspiration
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81
Q

Investigations for ventricular septal defect

A

1) Doppler Echo
2) CXR - will show pulmonary congestion
3) ECG - will show bilateral ventricular hypertension

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82
Q

Management of ventricular septal defect

A

1) None
2) Surgical repair
3) Heart-Lung transplant for Eisenmenger’s syndrome

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83
Q

Clinical features of an atrial septal defect

A
  • Often asymptomatic
  • Dyspnoea
  • Chest infections
  • Heart failure
  • AF
  • Wide, fixed splitting of S2
  • Systolic murmus over pulmonary valve area
  • Pulmonary hypertension
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84
Q

Investigations for Atrial septal defect

A

1) Echo - detect defect, will show R ventricular dilation and R ventricular hypertrophy, and pulmonary artery dilation
2) CXR - will show cardiomegaly and pulmonary plethora
3) ECG - will show incomplete RBBB

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85
Q

Management of atrial septal defect

A

1) Closure with cardiac czathetirsation using implantable closing device

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86
Q

Clinical features of patent ductus arteriosus

A
  • Retarded growth and development
  • Dyspnoea
  • Cyanosis
  • ‘Machinery’ murmur in late systole, loudest at left sternal border
  • Thrill
  • Increased pulse volume
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87
Q

Investigations for persistant ductus arteriosus

A

1) CXR - will show pulmonary artery enlargement
2) ECG - will show normal or signs of R ventricular hypertrophy
3) Echo

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88
Q

Management of a patent ductus arteriosus

A

1) Indomethacin or ibuprofen (<1 week of)

2) Cardiac catheterisation with implantable occlusive device

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89
Q

Clinical features of coarctation of the aorta

A
  • Other congenital abnormalities: bicuspid valve, cerebral berry aneurysms
  • Head and neck hypertension
  • Reduced circulation distally
  • Radio-femoral pulse delay
  • Heart failure
  • Headache
  • Leg weakness/cramps
  • Systolic murmur
  • Collateral arteries and bruits
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90
Q

Investigations for coarctation of the aorta

A

1) MRI
2) CXR - will be normal or will show ‘3 sign’
3) ECG - will show L ventricular hypertrophy
4) Echo - will show L ventricular hypertrophy

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91
Q

Management of coarctation of the aorta

A

1) Surgical correction

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92
Q

Clinical features of Tetralogy of Fallot

A
  • Cyanosis (often increasingly on exertion)
  • Apnoea
  • Growth stunting
  • Digit clubbing
  • Polycythaemia
  • Squatting after exertion (Fallot’s sign)
  • Loud ejection systolic murmus loudest in pulmonary area
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93
Q

Investigations for Tetralogy of Fallot

A

1) Echo
2) ECG - will show R ventricular hypertrophy
3) CXR - will show small pulmonary artery, ‘boot-shaped’ hear

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94
Q

Management of tetralogy of Fallot

A

1) Surgical correction

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95
Q

How would you manage a patient with an NSTEMI?

A

1) MONAC
2) Fondaparinux or LMW heparin SC
3) Consider nitrate IV fusion
4) Calculate GRACE score

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96
Q

What does the GRACE score predict

A
  • Risk of in hospital death after ACS
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97
Q

How would you managed a patient with an NSTEMI and a medium-high risk GRACE score?

A

1) Early in-hospital coronary angiography and consider GP IIb/IIIa receipt antagonist IV infusion

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98
Q

What drugs would you start a patient on after an MI?

A
  • Aspirin
  • Clopidogrel/Ticagrelor
  • Fondaparinux/LMWH
  • Statin
  • Beta-blocker
  • ACE inhibitor
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99
Q

How would you manage a patient with a STEMI (presenting within <12 hours)?

A

1) Reperfusion therapy
1a) PCI (if feasible within 120 mins)
1b) Thrombolysis IV + fondaparinux/LMWH (if eligible)
1c) Delayed PCI (if possible)
1d) Fondaparinux/LMWH SC

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100
Q

What investigations would you do in a patient with a suspected arrhythmia?

A

1) ECG

2) Ambulatory or patient-activated ECG

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101
Q

CHA2DSVAS score features

A 
Congestive heart failure 1
Hypertension 1
Age >75 2
Diabetes 1
Stroke or TIA 2
Vascular disease 1
Age 65-74 1
Sex female 1

Maximum = 9
0 points = no anticoagulation
1 point = anticoagulant if male
2+ points = anti coagulate

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102
Q

HAASBLED2 score features

A

Hypertension (>160) 1
Abnromal liver function (cirrhosis, bilirubin >2x upper normal limit, transaminases >3x upper normal limit) 1
Abnormal renal function (creatinine >200) 1
Stroke history 1
Bleeding prior event 1
Elderly >65 1
Drugs - anti platelets or alcohol excess 2

Maximum = 9
Consider careful monitoring if >3

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103
Q

Clinical features of Atrial flutter

A
  • Palpitations
  • Saw tooth pattern on ECG
  • 2:1, 3:1 or 4:1 AV block
104
Q

Management of atrial flutter

A

1) Catheter ablation
2) Beta-blockers
3) Amiodarone
4) Anticoagulation

105
Q

What drug is contra-indicated in atrial flutter?

A

Flecainide

106
Q

Define paroxysmal AF

A

Intermittent episodes which self terminate in 7 days

107
Q

Define persistent AF

A

Prolonged episodes that can be terminated with cardioversion

108
Q

Define permanent AF

A

Prolonged episodes which can’t be terminated

109
Q

Clinical features of AF

A
  • Older people
  • Palpitations
  • Breathlessness
  • Fatigue
  • Asymptomatic
  • Chest pain
  • Heart failure
110
Q

Causes of AF

A
  • Age
  • Alcohol excess
  • Chronic lung disease (hypercapnia)
  • Congential or acquired heart disease
  • PE
  • Chest infection
  • Pericardial disease
  • Cardiomyopathy
  • Hyperthyroidism
  • Hypertension
  • Sepsis
  • Electrical abnormality
111
Q

What investigations would you do in a patient with suspected AF (and what would they show?)

A

1) ECG - normal but irregular QRS complexes, lack of p waves
2) Echo
3) TFTs
4) FBC, U&Es

112
Q

How would you manage a patient in AF who was haemodynamically unstable?

A

1) Urgent DC cardioversion

2) IV amiodarone or digoxin

113
Q

How would you manage a patient with paroxysmal AF?

A

1) Beta blockers

114
Q

How would you manage a patient with persistent AF?

A

Rate control

1) Beta-blocker
2) Verapamil
3) Add Digoxin (in sedentary people)

4) IV flecainide OR amiodarone
5) Cardioversion + amiodarone maintenance

6) Apixaban for 3 weeks before DC cardioversion (unless <48 hours) and 3 months after

115
Q

When is verapamil contra-indicated?

A
  • Management of AF with heart failure
116
Q

When is digoxin contra-indicted?

A
  • Management of AF in active people
117
Q

When is flecainide contra-indicated?

A
  • Atrial flutter

- Coronary artery disease

118
Q

Clinical features of supra ventricular tachycardia

A
  • Triggered by: caffeine, exertion, beta-agonists
  • Rapid, forceful heart beat
  • Palpitations
  • Snycope
  • Chest pain
  • Lightheadedness
  • Breathlessness
  • Polyuria

-ECG: Tachycardia with normal QRS complex, p waves merged into QRS, ST depression

119
Q

Management of an acute (but haemodynamically stable) presentation of supraventricular tachycardia

A

1) ABC
2) Oxygen
3) Carotid sinus pressure or valsalva manoeuvre
4) IV adenosine or verapamil
5) Metoprolol

120
Q

Management of recurrent supraventricular tachycardia

A

1) DC cardioversion

2) Catheter ablation

121
Q

Clinical features of Wolff-Parkinson-White syndrome

A
  • Congenital (presents in children)
  • Palpitations
  • Dizziness
  • Shortness of breath
  • Chest pain
  • Sweating
  • Syncope
  • ECG: shortened PR interval, DELTA WAVES
122
Q

Management of acute but stable Wolff-Parkinson-White syndrome

A

1) Carotid sinus pressure (if narrow complex)
2) IV adenosine
3) Catheter ablation

123
Q

Clinical features of ventricular tachycardia

A
  • History of: acute MI, chronic coronary artery disease, cardiomyopathy
  • Palpitations
  • Dyspnoea
  • Lightheadedness
  • Hypotension
  • Syncope

ECG: Abnormal broad QRS complexes, CAPTURE/FUSION BEATS, extreme left axis deviation

124
Q

Management of acute ventricular tachycardia

A

1) DC cardioversion (if BP <90, haemodynamically unstable)

2) IV amiodarone (first line if haemodynamically stable)

125
Q

Management of recurrent ventricular tachycardia with cardiac comorbidity

A

1) Beta blockers

2) Implantable defibrillation

126
Q

Management of acute haemodynamically unstable WPW syndrome

A

1) DC cardioversion

127
Q

Risk factors for Torsades de Pointe

A
  • Female
  • Flecainide
  • Amiodarone
  • Tricyclic antidepressants
  • Phenothiazines
  • Erythromycin
  • Hypokalemia
  • Hypomagensaemia
  • Hypocalcemia
  • Congenital QT syndrome
  • Bradycardia
128
Q

ECG features of Torsades de Pointes

A
  • Polymorphic VT (corkscrew pattern)
  • Rapid irregular complexes with changing baselines
  • Prolonged QT interval
129
Q

Management of Torsades de Pointes

A

1) Magnesium sulphate
2) Isoprenaline
3) Pacing (if recurrent)

130
Q

Clinical features of ventricular fibrillation

A
  • Loss of consciousness
  • No pulse

ECG: rapid, bizarre and irregular complexes

131
Q

Management of ventricular fibrillation

A

1) ABCDE
2) Defibrillation
3) Implantable defibrillator
4) IV amiodarone or sotalol

132
Q

Clinical features of 1st degree heart block

A

Usually asymptomatic

133
Q

Management of 1st degree heart block

A

Usually none required

134
Q

ECG features of 1st degree heart block

A
  • PR interval prolonged (>0.2seconds)
135
Q

ECG features of 2nd degree heart block Moritz type 1

A
  • Progressive lengthening of the PR intervals which culminate in a dropped beat (Wenckenbach phenomenon(
136
Q

When may 2nd degree heart block be physiological?

A
  • At rest/in sleep of athletic young adults with high vagal tone
137
Q

ECG features of 2nd degree heart block Moritz type 2

A
  • PR interval remains constant but some p waves not conducted
138
Q

ECG features of 3rd degree heart block

A
  • Complete AV dissociation

- Narrow or broad QRS complexes

139
Q

Clinical features of complete AV block

A
  • Slow regular pulse which does not vary with exercise (except in congenital complete AV block)
  • Large pulse volume
  • Cannon waves in the neck
  • Varying intensity of the first heart sound
140
Q

Causes of complete AV block

A
  • Idiopathic fibrosis
  • MI
  • Infective endocarditis
  • Sarcoidosis
  • Chaga’s disease
  • Trauma
  • Drugs e.g. digoxin, beta blockers, calcium antagonists
141
Q

Typical presentation of complete AV block

A
  • Recurrent syncope
  • Stokes-Adams attacks (sudden loss of consciousness that occur without warning and results in collapse)
  • Brief anoxic seizure may occur (pallor and death-like appearance followed by flush)
142
Q

Management of asymptomatic 2nd degree heart block type 2 or 3rd degree heart block

A

1) Permanent pacemaker

143
Q

Management of symptomatic bradycardia associated with AV block

A

1) Permanent pacemaker

144
Q

Management of transient AV block (as a complication of acute inferior MI)

A

1) None required (if patient remains well)
2) IV atropine, repeated if necessary (if symptomatic)
3) Temporary pacemaker

Most cases resolve within 7-10 days

145
Q

Management of 2nd or 3rd degree heart block (as a complication of acute anterior MI)

A

1) IV atropine or IV isoprenaline
2) Temporary pacemaker (if systolic)

Poor prognosis

146
Q

Define a bifascicular block

A

A combination of RBBB and a left anterior or posterior hemiblock

147
Q

Causes of RBBB

A
  • Normal variant in healthy individuals
  • Right ventricular hypertrophy or strain e.g. PE
  • Congenital heart disease e.g. atrial septal defect
  • Coronary artery disease
148
Q

ECG features of RBBB

A
  • Broad QRS complexes (>0.12)
  • ‘M’ shape in leads V1 and V2
  • ‘W’ shape in leads V5 and V6
  • Wide ‘S’ shape in lead 1
149
Q

Causes of LBBB

A
  • Coronary artery disease
  • Hypertension
  • Aortic valve disease
  • Cardiomyopathy

Usually signifies significant underlying heart disease

150
Q

ECG features of LBBB

A
  • Broad QRS complexes (>0.12)
  • ‘W’ shape in leads V1 and V2
  • ‘M’ shape in leads V5 and V6
  • Loss of Q wave or septal vector in lead 1
151
Q

Management of a patient with ventricular incoordination secondary to LBBB

A

1) Cardiac resynchronisation therapy

152
Q

ECG features of Left anterior hemiblock

A
  • Narrow QRS complexes

- Left axis deviation

153
Q

ECG features of left posterior hemiblock

A
  • Narrow QRS complexes

- Right axis deviation

154
Q

How would you manage a patient with normotensive BP in clinic?

A
  • Check BP every 5 years
155
Q

What investigations would you consider in every patient with hypertension?

A
  • Urinalysis (blood, protein, glucose)
  • Bloods - U&Es, creatinine, glucose
  • Cholesterol
  • TFTs
  • 12-lead ECG
156
Q

What investigations would you consider in a patient <40 with hypertension, or someone with resistant hypertension?

A
  • CXR (cardiomegaly, heart failure, coarctation of the aorta)
  • Ambulatory BP
  • Echo (left ventricular hypertrophy)
  • Renal US (renal disease)
  • Renal angiography (renal artery stenosis)
  • Urinary catecholamines (Pheochromocytoma)
  • Urinary cortisol/dexamethasone suppression test (Cushing’s)
  • Plasma renin and aldosterone levels (primary aldosteronism)
157
Q

Clinical features of malignant hypertension

A
  • Very sudden increase in BP
  • Blurred vision
  • Headache
  • Shortness of breath
  • Decrease in urinary output
  • Papilloedema
  • Weakness/tingling in legs
  • Seizures
158
Q

Management of a patient with malignant hypertension

A
  • Controlled reduction of BP to 150/90 in 24 hours using oral hypertensives/IV or IM labetaolol/IV GTN/IM hydrazine or IV sodium nitoprusside
159
Q

Risk factors for aortic aneurysm

A
  • Male
  • Atherosclerosis
  • Marfan’s syndrome
160
Q

Clinical features of aortic aneurysm

A
  • Acute severe chest pain
  • Pain in the central abdomen, back, loin, iliac fossa or groin
  • Aortic regurgiation
  • Compressive symptoms e.g. stridor, hoaresness, superior vena cava syndrome, bowel obstruction and vomiting, oedema and DVT
  • Haemorrhage
161
Q

What investigations would you do in a patient with a suspected aortic aneurysm?

A

1) Ultrasound

2) CT - to provide more accurate information pre-op

162
Q

Management of an asymptomatic aortic aneurysm <5.5.cm diameter

A

Monitoring

163
Q

Management of an asymptomatic aortic aneurysm >5.5cm diameter

A

Open surgical repair OR endovascular repair

164
Q

Management of a ruptured aortic aneurysm

A

Immediate aortic clamping

165
Q

Risk factors for aortic dissection

A
  • Age 60-70
  • Marfan’s syndrome
  • Pregnancy
  • Trauma
  • Male
  • Atherosclerosis
  • Hypertension
  • Aortic coarctation
  • Ehlers’s Danlos syndrome
  • Fibromuscular dysplasia
  • Previous cardiac surgery e.g. CABG, TAVI
  • Cardiac catheterisation
166
Q

Clinical features of aortic regurgitation

A
  • Anterior chest pain and/or intra-scapular back pain
  • Abrupt onset tearing pain
  • Collapse
  • Hypertension
  • Pulse asymmetry
  • Signs of aortic regurgitation
  • MI
  • Stroke
  • Paraplegia
  • Mesenteric ischaemia
  • Renal failure
  • Limb ischaemia
167
Q

What investigations would you do in a patient with a suspected aortic dissection (and what would they show)?

A

1) CT/MRI angiography
2) CXR
- broadening of the upper mediastinum
- distortion of the aortic knuckle
- left sided pleural effusion
3) ECG
- left ventricular hypertrophy
- Acute inferior MI changes
4) Doppler Echo (TOE)
- Aortic regurgitation
- Dilated aortic root
- Flap of the dissection

168
Q

Management of an aortic dissection

A

1) Pain control
2) Antihypertensive treatment
3) Type A - emergency surgical replacement of the ascending aorta
Type B - labetaolol (verapamil/diltiazem if contra-indicated), sodium nitoprusside
4) Percutaneous or minimal access endoluminal repair

169
Q

Causes of aortitis

A
  • Syphilis
  • Takayasu’s disease
  • Reactive arthritis
  • GCA
  • Ankylosing spondylitis
170
Q

Clinical features of Marfan’s syndrome

A
  • Family history (autosomal dominant)
  • Aortic aneurysm/dissection
  • Aortic or mitral regurgitation
  • Skin laxity
  • Joint hypermobility
  • Tall stature and long arms, legs and fingers
  • Scoliosis
  • Pectus excavatum
  • High-arched palate
  • Ocular abnormalities e.g. lens dislocation, retinal detachment
  • Pneumothorax
171
Q

How would you diagnose Marfan’s syndrome

A

1) Clinical examination
2) Genetic testing

3) CXR or Echo to look for aortic dilatation

172
Q

How would you manage someone with Marfan’s syndrome?

A

1) Serial monitoring of the aortic root with Echo - elective surgery if dilatation seen
2) Beta-blockers
3) Avoidance of activities associated with increased cardiac output

173
Q

Clinical features of acute rheumatic fever

A
  • 5-15 year olds
- Strep throat 
2-3 weeks later:
- Fever
- Anorexia
- Lethargy
- Joint pain
- Rashes
- Subcutaneous nodules
- Erythema marginatum
- Pancarditis
- Neurological changes
- Oedema
- Dyspnoea
- Syncope
- Cary Coombs murmur
- Aortic or mitral regurgitation
- Heart block
174
Q

How would you diagnose rheumatic fever?

A

Isolated chorea or pancarditis if other causes have been excluded

Revised Jones criteria - 2+ major criteria OR 2+ minor criteria with evidence of preceding strep infection (only diagnostic criteria in established/prior rheumatic heart disease):
Major Criteria
- Carditis
- Polyarthritis
- Chorea
- Eryhtmea marginatum
- Subcutaneous nodules
Minor criteria
- Fever
- Arthralgia
- Raised ESR/CRP
- Previous rheumatic fever
- Leucocytosis
- 1st degree AV block
175
Q

What investigations would you consider in a patient with suspected rheumatic fever (and what would they show)?

A
  • Bloods (FBC, ESR/CRP) - leucocytosis, raised ESR/CRP
  • Throat culture - group A beta-haemolytic strep
  • Serology - antistreptolysin O antibodies
  • ECG - ST/T wave changes, conduction defects
  • Echo - mitral regurgitation with dilation of mitral annulus and prolapse of anterior mitral leaflet, aortic regurgitation and pericardial effusion
  • CXR - cardiomegaly, pulmonary congestion
176
Q

Management of acute rheumatic fever

A
  • Bed rest
  • Cardiac failure treatment
  • Benzathine Benzylpenicillin IM OR phenoxymethylpenicillin PO for 10 days
  • Consider long term antibiotic prophylaxis
  • Aspirin 60-100mg/kg
  • Prednisolone (if carditis or severe arthritis)
177
Q

Causes of aortic stenosis

A
  • Congenital aortic stenosis
  • Congenital sub/supra-valvular aortic stenosis
  • Calcification and fibrosis of congenitally acquired bicuspid valve
  • Rheumatic aortic stenosis
  • Senile degenerative aortic stenosis
  • Infective endocarditis
178
Q

Clinical features of aortic stenosis

A
  • Asymptomatic
  • Angina
  • Breathlessness
  • Syncope
  • Sudden death
  • Episodes of acute pulmonary oedema/symptoms of heart failure
  • Ejection systolic murmur loudest in aortic area, crescendo-decrescnedo, radiates to carotid radiating to the carotids
  • Soft split S2
  • 4th heart sound
  • Ejection click
  • Slow-rising carotid pulse
  • Thrusting apex beat
  • Narrow pulse pressure
  • Raised JVP
  • Signs of pulmonary venous congestion
179
Q

What investigations would you consider in a patient with aortic stenosis (and what would they show)?

A
  • Doppler echo - severity of stenosis
  • ECG - down-sloping ST segments and T inversion (strain pattern) in lateral leads, left ventricular hypertrophy, LBBB
  • CT/MRI
  • CXR - normal or enlarged left ventricle and dilated aorta
  • Cardiac catheterisation - coronary artery disease
180
Q

Management of aortic stenosis

A

1) TAVI

2) Aortic balloon valvuloplasty (in congenital aortic stenosis)

181
Q

Causes of aortic regurgitation

A
  • Bicuspid valve or disproportionate cusps (congenital)
  • Aortic dissection
  • Rheumatic disease
  • Infective endocarditis
  • Trauma
182
Q

Clinical features of aortic regurgitation

A
  • Palpitations (particularly when laying on left hand side)
  • Breathlessness
  • Paroxysmal nocturnal dyspnoea
  • Peripheral oedema
  • Angina
  • Marfan’s syndrome
  • Large volume or collapsing pulse
  • Low diastolic and increased pulse pressure
  • Bounding peripheral pulses
  • Capillary pulsation in nail bed (Quincke’s sign)
  • Femoral bruit (Duroziez’s sign)
  • Head nodding with pulse (de Musset’s sign)
  • Early diastolic murmur heard at left lower sternal edge with patient leaning forward during held expiration, breath-like murmur
183
Q

What investigations would you consider in a patient with suspected aortic regurgitation (and what would they show)?

A
  • Doppler Echo - dilated left ventricle, hydrodynamic left ventricle, reflux, fluttering anterior mitral valve leaflet
  • Cardiac catheterisation - dilated left ventricle, dilated aortic root, aortic regurgitation
  • Aortography
  • MRI
  • ECG - initially normal –> left ventricular hypertrophy and T wave inversion
  • CXR - cardiac dilatation, features of left heart failure
184
Q

Management of aortic regurgitation

A

1) Treatment of underlying condition e.g. ACE inhibitors + nifedipine
2) Aortic valve replacement with/without aortic root replacement and CABG

185
Q

Causes of mitral stenosis

A
  • Rheumatic heart disease
  • Heavy calcification
  • Congenital heart disease
  • Infective endocarditis
  • SLE
  • Amyloidosis
186
Q

Clinical features of mitral stenosis

A
  • Asymptomatic
  • Malar flush
  • Breathlessness
  • Diminishing exercise tolerance
  • Haemoptysis
  • Fatigue
  • Oedema/ascites
  • Palpitations
  • Cough
  • Chest pain
  • Thromboembolism
  • AF
  • Mitral facies
  • Low pulse volume
  • Loud first heart sound, opening snap
  • Mid diastolic murmur accentuated by exercise heard loudest at the apex with the patient on their left hand side
  • Crepitations
  • Pulmonary oedema
  • Pleural effusions
  • Right ventricular heave
  • Loud S2
187
Q

Complications of mitral stenosis

A
  • AF
  • Pulmonary oedema
  • Pulmonary hypertension
  • Right ventricular hypertrophy and dilatation
  • Tricuspid regurgitation
  • Right heart failure
188
Q

What investigations would you consider in a patient with suspected mitral stenosis (and what would they show)?

A
  • Doppler echo - thickened immobile cusps, reduced valve area, enlarged left atria, reduced rate of diastolic filling of left ventricle, pressure gradient across mitral valve, pulmonary artery pressure
  • Cardiac catheterisation - coronary artery disease, pulmonary artery pressure, mitral stenosis, regurgitation
    ECG - AF, bifed p waves/p mitrale, tall R waves in V1-3 (right ventricular hypertrophy)
  • CXR - enlarged left atrium and appendage, signs of pulmonary congestion
189
Q

Management of mitral stenosis

A

1) Apixaban + digoxin/beta blocker/calcium channel blocker + diuretic
2) Valvuloplasty (with 1-2 yearly follow up)
3) Surgical valvotomy or valve replacement

190
Q

Criteria for a mitral stenosis valvuloplasty

A
  • Significant symptoms
  • Isolated mitral stenosis
  • No/trivial mitral regurgitation
  • Mobile, non-calcified valve/sub-valve apparatus on echo
  • Left atrium free of thrombus
191
Q

Causes of mitral regurgitation

A
  • Papillary muscle after acute MI
  • Infective endocarditis
  • Rupture of chord
  • Rheumatic disease
  • Mitral valve prolapse
  • Left ventricular dilatation
192
Q

Clinical features of mitral regurgitation

A
  • Breathlessness
  • Fatigue
  • Oedema/ascites
  • Palpitations
  • AF
  • Displaced apex beat
  • Apical pansystolic murmur radiating to the axilla
  • Soft S1
  • S3
  • Crepitations
  • Pulmonary oedema
  • Pleural effusions
  • Right ventricular heave
  • Raised JVP
  • Oedema
193
Q

What investigations would you consider in a patient with suspected mitral regurgitation (and what would they show)?

A
  • Doppler echo - valve prolapse
  • ECG - AF, left atrial/ventricular hypertrophy, dynamic left ventricle
  • Cardiac catheterisation - left ventriculography and size of v waves in left atria/pulmonary artery
  • CXR - enlarged left atrium and ventricle, pulmonary venous congestion, pulmonary oedema
194
Q

Management of mitral regurgitation

A

1) Diuretics and vasodilators
- Digoxin and anticoagulants (if in AF)
- ACE inhibitors or ARBs (if hypertensive)
2) Mitral valve replacement

195
Q

Indications for mitral valve replacement in a patient with mitral regurgitation

A
  • Worsening symptoms
  • Progressive cardiomegaly
  • Deteriorating left ventricular function
196
Q

Risk factors for chronic heart failure

A
  • Hypertension
  • Diabetes
  • Obesity
  • Age
  • Renal impairment
  • Lung disease
197
Q

Causes of chronic heart failure

A
  • Ischaemic heart disease
  • Arrhythmia
  • Valvular dysfunction
  • Lifestyle factors
  • Pulmonary disease
  • Idiopathic
  • Infective
  • Infiltrative disease e.g. amyloid
  • Autoimmune disease
  • Inherited/congenital
  • Adverse drug reactions
  • Physiological state
198
Q

Define congestive cardiac failure

A

Both right and left sided heart failure

199
Q

Describe the American Heart Association-American College for Cardiology classification of heart failure

A

A) High risk without structural heart disease
B) Structural heart disease without signs or symptoms
C) Structural heart disease with current or prior symptoms
D) Refractory heart failure requiring specialist intervention

200
Q

Clinical features of chronic heart failure

A

General

  • Peripheral oedema
  • Light-headedness
  • Low mood
  • Lethargy
  • Weight loss

Right-sided failure:

  • Peripheral oedema
  • Elevated JVP
  • Hepatomegaly
  • GI signs

Left-sided failure:

  • Dyspnoea
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Frothy white sputum
  • Cardiomegaly
  • Lung crepitations
  • Gallop rhythm
201
Q

Describe the NYHA classification of heart failure

A

1) No symptoms, normal activity
2) Mild symptoms e.g. breathless on incline
3) Moderate symptoms, comfortable at rest
4) Severe symptoms, breathless at rest

202
Q

What investigations would you consider in a patient with suspected heart failure (and what would they show)?

A

1) BNP (and other bloods)
- FBC - ?anaemia
- U&Es - assess renal function
- LFTs - abnormalities reflect right-heart failure
- TFTs
- Lipids
- Glucose

2) ECG
- Q waves, T wave inversion
- Left ventricular hypertrophy
- Prolonged QRS duration
- Arrhythmia
- Normal ECG makes heart failure unlikely

3) CXR
- Alveolar oedema
- Kerley B lines
- Cardiomegaly
- Dilated pulmonary vessels
- Pleural effusion

4) Echo

  • 6-min walk test
  • Cardiopulmonary exercise testing
  • Coronary angiography
  • Cardiac MRI
203
Q

How would you manage a patient with chronic heart failure?

A

1) Lifestyle modification
- Exercise
- Reduce alcohol
- Smoking cessation
- Salt and water destruction (<1.5L and 6g
- Vaccinations
- Driving advice

If ejection fraction REDUCED

2) ACE inhibitor (or ARB) + Beta-blocker (improve prognosis) + diuretics (symptomatic relief)
3) Add a mineralocorticoid receptor antagonist (improve prognosis), ARB or hydrazine + nitrate
4) Replace ACE inhibitor with sacubitril
5) Cardiac resynchronisation therapy OR implantable defibrillator

If ejection fraction PRESERVED

1) Antihypertensives/diabetic control/weight reduction/lipid control
2) Diuretics + beta blockers

Heart transplant is gold standard treatment in chronic heart failure

204
Q

When is a mineralocorticoid receptor antagonist conta-indicated?

A
  • Renal impairment

- K+ >5

205
Q

When would a heart transplant be CI in a patient with chronic heart failure?

A
  • Elderly patient
  • Renal failure
  • Irreversible pulmonary artery hypertension
  • Non-cardiac severe disease
206
Q

Risk factors for acute heart failure

A
  • Age (70s)
  • Ischaemic heart disease
  • Diabetes
  • CKD
  • COPD
  • AF
207
Q

Clinical features of acute heart failure

A
  • Fatigue
  • Oedema
  • Cough
  • Breathlessness
  • Orthopnoea
  • Tachycardia
  • Increased respiratory rate
  • Hypertension
  • 3rd heart sound/gallop rhythm)
  • Inspiratory crepitations
  • Elevated jugular pressure
  • Peripheral oedema
208
Q

What investigations would you do in a patient with suspected acute heart failure (and what would they show)?

A
  • ECG - non-specific changes
  • CXR - pulmonary oedema
  • Echo
209
Q

How would you manage a patient with acute heart failure?

A
  • Sit patient up
  • Oxygen (if <94%)
  • Stop IV fluids (except in acute right ventricular failure)
  • CPAP
  • Monitor U&Es, urine output and daily weight
  • Restrict fluid intake
  • IV loop diuretics
  • Opiates
  • Vasodilators
  • Inotropic agents
210
Q

Define cardiogenic shock

A

Systolic BP <90 + 1 or more of:

  • Low urine output
  • Poor peripheral perfusion
  • Confusion
  • Serum lactate >2
211
Q

Causes of sudden cardiac death

A
  • Hypertrophic cardiomyopathy
  • Dilated cardiomyopathy
  • Brugada syndrome
  • Long QT syndrome
  • Arrhythmogenic right ventricular cardiomyopathy
212
Q

Clinical features of hypertrophic cardiomyopathy

A
  • Family history (autosomal dominant inheritance with incomplete penetrance and variable expression)
  • Presents in adolescence
  • Chest pain
  • Shortness of breath
  • Palpitations
  • Syncope
  • Diastolic dysfunction
  • Ejection systolic murmur
  • Jerky central pulse
213
Q

How would you diagnose a patient with inherited hypertrophic cardiomyopathy?

A

A maximal ventricle wall thickness >15 mm is required to diagnose HCM.

Investigations may include:

  • ECG (left ventricular hypertrophy, left axis deviation, depolarisation abnormalities)
  • Echo (asymmetrical left ventricular hypertrophy)
  • Cardiac MRI
214
Q

List the screening investigations which should be offered to 1st degree relatives of patients with a hypertrophic cardiomyopathy

A
  • ECG
  • Clinical assessment
  • Echo
  • Genetic testing for known genetic mutations
215
Q

How would you manage a patient with hypertrophic cardiomyopathy?

A

1) Implantation of ICD for patients at risk of sudden cardiac death

If not suitable:

1) Avoidance of competitive and contact sports
2) Beta-blockers or verapamil
3) Add disopyramide (if persistent left ventricle outflow obstruction and symptoms)
4) Surgical myomectomy or alcohol septal ablation

216
Q

Which factors (and how) are assessed to calculate risk of sudden cardiac death in patients with hypertrophic cardiomyopathy?

A
  • Family history of sudden cardiac death
  • Unexplained syncope (1+ episodes in the previous year)
  • Ventricular arrhythmia
  • Maximal left ventricular wall thickness >30mm
  • Abnormal BP response to exercise (no increases of 20-30mmHg)
217
Q

Most common cause of heart failure in the young

A

Dialted cardiomyopathy

218
Q

Causes of dilated cadiomyopathy

A
  • Familial
  • Drugs - anthracyclines, doxorubicin
  • Toxins - alcohol, anabolic steroids
  • Endocrine disorders - hypo/hyperthyroidism, pheochromocytoma, Cushing’s syndrome
  • Post-partum (last month of pregnancy or 5 months after delivery)
  • Tachycardia-induced - persistant atrial/ventricular tachycardia
  • Inflammatory disease - sarcoidosis, vasculitis
  • Infection
  • Haemochromatosis
219
Q

Clinical features of dilated cardiomyopathy

A
  • Breathlessness
  • Chest pain
  • Fatigue
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Peripheral oedema
  • Laterally displaced apex beat
  • 3rd or 4th heart sound
  • Pansystolic murmur
220
Q

What investigations would you consider in a patient with dilated cardiomyopathy (and what would they show)?

A
  • CXR - enlarged cardiac shadow, upper lobe vessel diversion, small pleural effusions
  • Echo
  • ECG - normal or evidence of conduction defects
  • Ambulatory ECG monitoring
  • MRI
221
Q

Management of dilated cardiomyopathy

A

1) ACE inhibitors + beta-blockers
2) Cardiac resynchronisation therapy and implantable defibrillator
3) Pacemaker (if co-existing electrical disorder)

222
Q

Clinical features of Brugada syndrome

A
  • Family history (autosomal dominant inheritance)
  • Asymptomatic
  • Sudden cardiac death
  • Palpitations
  • Syncope
223
Q

How would you make a diagnosis of Brugada syndrome?

A

Characteristic ECG changes (ST elevation and RBBB in leads V1-3) + 1 of:

  • Documented polymorphic ventricular tachycardia or fibrillation
  • Family history of sudden cardiac death
  • Inducible ventricular tachycardia in electrophysiological studies
  • Family members with Brugada syndrome
224
Q

Management of Brugada syndrome

A

Implantable cardioverter defibrillator

225
Q

Clinical features of long QT syndrome

A
  • May be congenital or acquired
  • Triggers: swimming, loud noises
  • Asymptomatic
  • Sudden death (caused by V fib or Torsades de Pointes)
  • Palpitations
  • Syncope
226
Q

How would you diagnose long QT syndrome, and what investigations would you consider in a patient with suspected long QT syndrome?

A
  • Diagnosis is based on abnormally prolonged QT interval on ECG
  • Exercise ECG
  • Signal-averaged ECG
  • Holter-monitor QT interval assessment
  • Adrenaline challenge
227
Q

Management of long QT syndrome

A

1) Lifestyle modification (avoid competitive sports, swimming, loud noises
2) Avoid QT-prolonging drugs
3) Beta-blockers
4) Implantable defibrillator (if recurrent syncope, ventricular tachycardia or cardia arrest)

228
Q

Causes of acute pericarditis

A
  • Trauma
  • Uraemia/renal failure
  • MI
  • Infection (viral or bacterial, usually viral)
  • RA
  • SLE
  • Cardiac surgery
229
Q

Clinical features of acute pericarditis

A
  • Pleuritic chest pain (sharp/stabbing/burning)
  • Pain exacerbated by lying flat or taking deep breaths
  • Pain eased by sitting upright
  • Tachypnoea with shallow, rapid breaths
  • Pericardial rub (heard at lower left sternal edge)
230
Q

What investigations would you consider doing in a patient with suspected acute pericarditis (and what might they show)?

A
  • Bloods (CRP, ESR, WCC, troponin) - elevated inflammatory markers, elevated troponin in myocardial involvement
  • ECG - global concave ‘saddle-shaped’ ST elevation, tall T waves and PR depression
  • CXR - enlarged, globular cardiac silhouette
  • Echo
  • MRI (if myocarditis suspected)
231
Q

Management of idiopathic acute pericarditis

A
  • Reassurance
  • Analgesia
  • NSAIDs
  • Rest
232
Q

Management of recurrent idiopathic pericarditis

A
  • Colchicine
233
Q

Causes of pericardial effusion

A
  • Acute pericarditis
  • Idiopathic
  • MI
  • Trauma
  • Post-cardiac surgery or intervention
  • Aortic dissection
  • Malignancy
  • Renal failure
  • Infection
  • Autoimmune disease e.g. RA, SLE
234
Q

Clinical features of pericardial effusion

A
  • Asymptomatic (small or chronic effusion)
  • Dyspnoea
  • Chest pain
  • Cardiac arrest (if cardiac tamponade)
  • Elevated JVP
  • Hypotension
  • Impalpable apex beat
  • Muffled heart sounds
  • Tachycardia
  • Tachypnoea
  • Pulsus paradoxus (abnormal reduction in pulse volume on inspiration)
  • Kussmaul’s sign (abnormal rise in JVP with inspiration)
235
Q

What investigations would you consider in a patient with suspected pericardial effusion (and what might they show)?

A
  • ECG - small QRS complexes, electrical alternate (electrical cardiac axis changes frequently)
  • CXR - enlarged and globular heart silhouette
  • Echo (confirm diagnosis)
236
Q

Management of pericardial effusion

A

Tamponade: emergency surgical drainage

Small effusion, patient not compromised: diuretics (followed with serial echo until effusion resolved)

237
Q

Causes of cardiac arrest

A
  • Ischaemic heart disease
  • Heart failure
  • Cardiomyopathy
  • Congenital or inherited heart disorders
  • Lung disease
  • PE
  • Haemorrhage
  • Multi-organ failure
238
Q

8 reversible causes of cardiac arrest

A
  • Hypotension (haemorrhage)
  • Hypoxia (lung disease)
  • Hypothermia
  • Hyper or hypokalemia
  • Thromboembolism (PE)
  • Tension pneumothorax
  • Tamponade
  • Toxins
239
Q

How is cardiac arrest diagnosed?

A

An unconscious patient with no palpable pulse and no respiratory effort

240
Q

Shockable rhythms of cardiac arrest

A

1) Ventricular tachycardia

2) Ventricular fibrillation

241
Q

Non-shockable rhythms of cardiac arrest

A

1) Asystole

2) Pulseless electrical activity

242
Q

Management of cardiac arrest

A

CPR (30:2)

Prompt defibrillation in shockable rhythm

243
Q

What should you do during CPR in a cardiac arrest

A
  • Give oxygen
  • Consider advanced airway and capnography
  • Obtain vascular access
  • Give adrenaline every 3-5 mins
  • Correct reversible causes of cardiac arrest
244
Q

What treatment should you give to a patient post-cardiac arrest?

A
  • ABCDE
  • Oxygen and ventilation
  • 12-lead ECG
  • Treat precipitating cause
  • Temperature control/therapeutic hypothermia
245
Q

Which signs would make you think that electrical DC shock is indicated in a patient with a tachycardia?

A
  • Shock (systolic BP <90)
  • Syncope
  • Heart failure
  • Myocardial ischaemia
  • Heart rate >150
246
Q

How would you treat extreme bradycardia with adverse features or risk of asystole?

A

1) IV atropine
2) Repeat IV atropine
3) Isoprenaline
4) Adrenaline
5) Transcutaneous pacing

247
Q

QT-prolonging drugs

A
  • Flecainide
  • Propafenone
  • Amiodarone
  • Sotalol
  • Indapamide
  • Nicardipine
  • Hydroxyzine
  • Terfenadine
  • Clarithromycin
  • Eryhtromycin
  • Ciprofloxacin
  • Ofloxacin
  • Fluconazole
  • Ketoconazole
  • Quetiapine
  • Risperiodone
  • Amitryptilline
  • Citalopram
  • Sumatriptan
  • Salbutamol
  • Opiates
  • Domperidone
248
Q

Causes of cardiac tamponade

A
  • Chest trauma
  • Cardiac surgery
  • Myocardial rupture
  • Malignancy
  • Renal failure
  • Pericarditis
  • Hypothyroidism
249
Q

Clinical features of cardiac tamponade

A
  • Palpitations
  • Anergia
  • Breathlessness
  • Tachycardia
  • Quiet heart sounds
  • Elevated JVP
  • Kussmaul’s sign
  • Pulsus paradoxus
  • Decreased blood pressure
250
Q

Beck’s triad of cardiac tamponade

A

1) Hypotension
2) Quiet heart sounds
3) Raised JVP

251
Q

What investigations would you consider in a patient with suspected cardiac tamponade (and what would they show)?

A
  • ECG - sinus tachycardia, small QRS complexes, electrical alternate
  • CXR - cardiomegaly, globular cardiac silhouette
  • Echo - pericardial effusion with collapsing chambers, abnormally large respiratory swings in the moral and tricuspid flow velocities
252
Q

How would you manage cardiac tamponade?

A

Pericardiocentesis

253
Q

Criteria for diagnosing an MI?

A

Cardiac enzyme rise and fall + 1 or more of:

  • Ischaemic changes
  • ECG changes suggesting new ischaemia
  • New pathological Q waves
  • Loss of myocardium on imaging
  • Identification of an intra-coronary thrombus by angiography or post-mortem
254
Q

Management of a STEMI

A

1) ABCDE
2) Morphine
3) Oxygen (if <94%)
4) Aspirin 300mg PO
5) Nitrates - GTN spray
6) Antiplatelet clopidogrel 300mg PO
7) Reperfusion therapy - Rapid PCI <12 hours of onset from symptoms
OR
Thrombolysis (alteplase) if >12 hours

255
Q

Management of an NSTEMI or unstable angina

A

1) ABCDE
2) Morphine
3) Oxygen (if <94%)
4) Aspirin 300mg PO
5) Nitrates - GTN spray
6) Antiplatelet clopidogrel 300mg PO
7) Reperfusion therapy
- Fondaparinux, LMWH and calculate GRACE score:
8) low risk = maintenance medication and discharge
medium/high risk = angiography or alteplase

256
Q

What maintenance medication would you give to someone after an MI?

A
  • ACE inhibitor (lisinopril)
  • Beta blocker (bisoprolol)
  • Statin (simvastatin)
  • Aspirin 75mg indefinite
  • Clopidogrel (for 6 months)
  • Cardiac rehabilitation
257
Q

Complications of an MI

A

(SPARED)

  • Sudden death
  • Pump failure (heart failure)
  • Arrhythmia (V Fib)
  • Rupture: VSD, cardiac tamponade, papillary muscle rupture
  • Embolism
  • Dresler’s syndrome (pericarditis) 2-6 weeks later

Year 4 (11 decks)

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