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CARDIOVASCULAR Flashcards

1
Q

what are the risk factors associated with the development of AAA?

A
  • Increasing age (typical onset is 65 - 75 years).
  • Male gender (incidence of 5% of men over 60 years).
  • Hypertension.
  • Hyperlipidaemia.
  • Smoking.
  • COPD.
  • Family history of abdominal aortic aneurysm.
  • Coronary, cerebrovascular or peripheral arterial disease.
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2
Q

what are the clinical features of AAA?

A
  • Typically asymptomatic and are found on routine examination or imaging.
  • Non-specific back pain.
  • Expansile and pulsatile abdominal mass may be felt.
  • Dusty discolouration of the digits secondary to emboli.
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3
Q

what are the clinical features of rapid expansion or rupture of AAA?

A
  • Severe epigastric pain radiating to the back
  • Signs of cardiovascular collapse e.g. hypotension and tachycardia
  • Sudden death
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4
Q

How is AAA <5.5cm treated?

A
  • Encourage smoking cessation.
  • Optimisation hypertension medication.
  • Offer a lifelong statin.
  • Offer clopidogrel.
  • Offer regular ultrasound surveillance.
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5
Q

how is AAA of 5.5cm or larger, symptomatic or rapidly enlarging managed?

A
  • Offer open surgical repair with insertion of a Dacron graft if there is no co-pathology, anaesthetic risks, or co-morbidities.
  • Offer a non-surgical endovascular aneurysmal repair (EVAR) with insertion of a stent via the femoral artery, if there is co-pathology, anaesthetic risks, or co-morbidities.
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6
Q

how is ruptured AAA managed?

A
  • Offer open surgical repair in men under 70.

- Offer endovascular aneurysmal repair for men over 70 and women of any age.

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7
Q

what are the risk factors for ACS?

A
  • Smoking
  • Hypertension.
  • Diabetes.
  • Obesity.
  • Hypercholesterolaemia / hyperlipidaemia.
  • Male gender.
  • Previous surgery.
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8
Q

what are the clinical features of ACS?

A
  • Rapid onset pain and lasts longer than 20 minutes.
  • Severe, constricting, and heavy in nature.
  • Referred to the arms, back or jaw.
  • Of new onset or is the result of abrupt deterioration of stable angina with pain occurring frequently with little or no exertion.
  • Dyspnoea due to pulmonary oedema is a sign of complication.
  • Autonomic features including sweating, nausea, vomiting and pallor.
  • Haemodynamic instability, including a systolic blood pressure less than 90 mmHg
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9
Q

how does a STEMIs appearance on ECG change over time?

A
  • ST elevation is the first ECG change.
  • After the first few minutes the T waves become tall, pointed and upright.
  • After the first few hours there is T wave inversion and Q wave development.
  • After a few days, the ST segment returns to normal.
  • After a few weeks the T wave may return upright but the Q wave remains.
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10
Q

what are the ECG features of an anterior wall MI and which artery is affected ?

A
  • ST elevation in leads V2-V4.

- LAD

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11
Q

what are the ECG features of a lateral wall MI and which artery is affected?

A
  • ST elevation in leads I, aVL and V5-V6.

- Circumflex

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12
Q

what are the ECG features of an inferior wall MI and which artery is affected?

A
  • ST elevation in leads II, III and aVF.

- Right coronary artery

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13
Q

what are the ECG features of a posterior wall MI and which artery is affected?

A
  • ST depression in leads V2-V4
  • a tall R wave in V1
  • ST elevation in leads V5-V6
  • Posterior descending .
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14
Q

How should a STEMI be managed initially?

A
  • Oxygen
  • aspirin with ticagrelor (no previous intracerebral haemorrhage or liver disease) or clopidogrel
  • morphine and metoclopramise IV
  • Sublingual GTN followed by IV GTN
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15
Q

which medication should be given to patients undergoing PCI or coronary angiography?

A

-Unfractionated or LMWH

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16
Q

what is the long term management post-MI?

A
  • aspirin 75mg indefinitely, combined with ticagrelor for 12 months
  • ACE inhibitor/ARB
  • Beta-blocker
  • Spironolactone
  • Statin
  • Lifestyle advice and cardiac rehab
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17
Q

what is seen on ECG in NSTEMI?

A
  • T wave inversion of greater than 1 mm in at least two leads corresponding to the site of myocardial damage.
  • There is no ST segment elevation and Q waves do not develop.
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18
Q

what is seen on ECG in unstable angina?

A
  • ST segment depression while the patient has pain

- once the pain has resolved the ECG returns to normal.

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19
Q

how is NSTEMI/unstable angina managed?

A
  • aspirin or ticagrelor
  • unfractionated heparin if coronary angiography to be done within 24 hours of admission
  • if >24 hours, give fondaparinux
  • given oxygen and nitrates
  • Diamorphine and metoclopramide
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20
Q

what is variant angina?

A
  • Prinzmetal angina and vasospastic angina
  • occurs at rest
  • caused by vasospasm of the coronary arteries, rather than an atherosclerotic plaque.
  • It occurs more frequently in women.
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21
Q

what is microvascular angina?

A
  • cardiac syndrome X
  • caused by normal coronary arterial perfusion, but poor perfusion of the microvasculature of cardiac muscles
  • It occurs more frequently in women.
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22
Q

what are the risk factors for angina?

A
  • Smoking.
  • Hypertension.
  • Diabetes.
  • Obesity.
  • Hypercholesterolaemia / hyperlipidaemia.
  • Male gender.
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23
Q

what are the clinical features of angina?

A
  • Constricting and heavy chest pain, or pain in the neck, shoulders, jaws or arms.
  • The pain is precipitated by physical exertion.
  • The pain is relieved by rest or GTN spray within about 5 minutes.
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24
Q

what is seen on ECG in angina?

A
  • can be normal
  • There may be ST depression in stable angina or unstable angina.
  • There may be ST elevation in variant angina.
  • ST elevation, T wave abnormalities, Q waves, and LBBB are suggestive of ischaemia or previous infarction.
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25
Q

what lifestyle advice should be given to patients with angina?

A
  • Smoking cessation.
  • Cardioprotective diet.
  • Increase in physical activity.
  • Limitation of alcohol consumption.
  • Maintenance of a healthy diet.
  • Avoidance of provoking factors such as exertion, stress, or cold exposure.
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26
Q

what symptomatic relief can be given to patients with angina?

A
  • Offer a short-acting nitrate (GTN spray) to use for relief of symptoms while they are waiting for specialist referral.
  • Patients should repeat the dose after 5 minutes if the pain has not gone.
  • Patients should call an ambulance if the pain has not gone 5 minutes after taking a second dose.
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27
Q

what is the long term drug treatment for angina?

A
  • betablocker, verapamil or diltiazem
  • combine beta blocker and nifedipine if poor response
  • Consider dual therapy with a second anti-anginal drug (isosorbide mononitrate, mivabradine, nicorandil, ranolazine) if there is a poor response to initial therapies..
  • Consider triple therapy with a third anti-anginal drug if there is a poor response to dual therapy.
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28
Q

what secondary prevention should be given in angina?

A
  • aspirin 75 mg daily.
  • ACE inhibitors (ramipril) for patients with diabetes.
  • statin (atorvastatin 80 mg).
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29
Q

which patients with angina should be offered revascularisation?

A
  • Whose symptoms are not satisfactorily controlled in patients with optimal medical treatment.
  • In whom angiography has demonstrated left main stem (left anterior descending artery) disease or proximal three-vessel disease.
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30
Q

what are the causes of aortic regurgitation?

A
  • idiopathic
  • ageing
  • syphilis
  • Marfan’s syndrome
  • osteogenesis imperfecta
  • infective endocarditis
  • rheumatic fever
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31
Q

what are the symptoms of aortic regurgitation?

A
  • Dyspnoea.
  • Fatigue.
  • Orthopnoea.
  • Paroxysmal nocturnal dyspnoea
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32
Q

what murmur is heard in aortic regurgitation?

A
  • High pitched early diastolic murmur, best heard at the left sternal edge in the fourth intercostal space with the patient leaning forward and breath held in expiration
  • mid-diastolic Austin flint murmur
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33
Q

how does the pulse appear in aortic regurgitation?

A
  • wide pulse pressure

- collapsing or bounding

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34
Q

which unique signs are seen in aortic regurgitation?

A
  • Quincke’s sign (nail-bed pulsation).
  • De Musset’s sign (head nodding with each heart beat).
  • Duroziez’s sign (murmur heard over the femorals when compressed).
  • Pistol-shot femorals (bang heard on auscultation over femorals).
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35
Q

what is seen on chest x-ray in aortic regurgitation?

A
  • Left ventricular dilatation.
  • Aortic root dilatation.
  • Features of left heart failure.
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36
Q

what is seen on ECG in aortic regurgitation?

A

-Tall R waves in lead V6 and deep S waves in V1 due to left ventricular hypertrophy.

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37
Q

how is aortic regurgitation managed?

A
  • Perform regular review and assessment of asymptomatic aortic stenosis who are unsuitable for surgery.
  • Offer a calcium channel blocker (nifedipine) for symptomatic patients to reduce afterload and degree of regurgitation.
  • Offer an inotrope (dopamine) and a vasodilator (nitroprusside) for an acute exacerbation of aortic regurgitation.
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38
Q

in which patients with aortic regurgitation should valve replacement be offered?

A
  • Symptomatic aortic regurgitation (including an acute exacerbation).
  • Asymptomatic aortic regurgitation with an ejection fraction < 50% or left ventricular dilation.
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39
Q

what are the causes of aortic stenosis?

A
  • age/calcific aortic valve disease

- bicuspid aortic valve

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40
Q

what are the clinical features of aortic stenosis?

A
  • Syncope.
  • Angina.
  • Dyspnoea
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41
Q

what murmur is associated with aortic stenosis?

A
  • Harsh crescendo-decrescendo ejection systolic murmur that radiates into the carotids
  • with soft or inaudible second heart sound
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42
Q

how does the pulse appear in aortic stenosis?

A
  • Slow rising carotid pulse with decreased pulse amplitude

- Narrow pulse pressure.

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43
Q

what is seen on ECG in aortic stenosis?

A
  • Left ventricular hypertrophy (Deep S waves in V1 and tall R waves in V6).
  • Left atrial delay (prolonged P wave in lead II)
  • left ventricular strain (depressed ST segment and T wave inversion in lead I, AVL, V5 and V6).
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44
Q

what is seen on chest x-ray in aortic stenosis?

A
  • Small heart
  • Prominent, dilated ascending aorta
  • Calcified aortic valve
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45
Q

how is aortic stenosis managed?

A
  • Observation is recommended for asymptomatic patients.
  • Perform aortic valve replacement for symptomatic patients or those with a valvular gradient greater than 40 mmHg:
  • Offer long term anticoagulation for patients who have had aortic valve replacement using prosthetic mechanical valves.
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46
Q

what are the risk factors for mitral regurgitation?

A
  • Mitral valve prolapse.
  • History of rheumatic heart disease.
  • Infective endocarditis.
  • history of MI
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47
Q

what are the symptoms of mitral regurgitation?

A
  • Dyspnoea and orthopnoea.
  • Fatigue.
  • Palpitations.
  • Oedema and ascites.
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48
Q

what murmur is associated with mitral regurgitation?

A

-Pan-systolic murmur heard over the apex and radiating to the axilla.

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49
Q

what is seen on chest x-ray in mitral regurgitation?

A
  • A large left atrium

- A large left ventricle.

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50
Q

what is seen on ECG in mitral regurgitation?

A
  • Bifid P waves due to delayed left atrial activation.

- Tall R waves in lead V6 and deep S waves in V1 due to left ventricular hypertrophy.

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51
Q

how is mitral regurgitation managed?

A

-Offer an ACE inhibitor (ramipril) and a beta blocker (atenolol) for patients with minor symptoms and who are not appropriate for surgical intervention to reduce afterload and degree of regurgitation.

  • For patients with atrial fibrillation:
  • –Offer anticoagulants (warfarin) if atrial fibrillation is present, to reduce the risk of systemic embolism.
  • –Offer atenolol, diltiazem or digoxin for ventricular rate control in atrial fibrillation.
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52
Q

which patients with mitral regurgitation should have valve repair or replacement?

A
  • With symptomatic severe mitral regurgitation.
  • Left ventricular ejection fraction less than 30%.
  • Asymptomatic severe mitral regurgitation with preserved left ventricular function and atrial fibrillation or pulmonary hypertension.
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53
Q

what are the causes of mitral stenosis?

A

-rheumatic heart disease

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54
Q

what are the clinical features of mitral stenosis?

A
  • Progressive dyspnoea.
  • Peripheral oedema.
  • Palpitations.
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55
Q

which murmur is associated with mitral stenosis?

A

-Low-pitched, rumbling mid-diastolic murmur heard best in expiration with the bell of the stethoscope held lightly at the apex and the patient lying on their left side

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56
Q

what is seen on chest x-ray in mitral stenosis?

A
  • A large left atrium
  • Distended pulmonary veins
  • Pulmonary oedema
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57
Q

what is seen on ECG in mitral stenosis?

A
  • Bifid P wave due to delayed left atrial activation.
  • Absent P waves, rapid and irregular timing of QRS complexes due to atrial fibrillation
  • Tall R waves in V1 (right axis deviation) due to right ventricular hypertrophy.
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58
Q

how is mitral stenosis managed in patients with minor symptoms?

A

-Offer a loop diuretic (furosemide) to control pulmonary congestion

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59
Q

when should mitral balloon valvotomy be offered in mitral stenosis?

A
  • Severe mitral stenosis with no mitral regurgitation
  • Non-calcified valve on echocardiography.
  • No left atrial thrombus on echocardiography
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60
Q

when should mitral valve replacement be offered in mitral stenosis?

A
  • Severe mitral stenosis and mitral regurgitation.
  • Calcified valve on echocardiography.
  • Left atrial thrombus on echocardiography.
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61
Q

which murmur is associated with pulmonary regurgitation?

A

-High pitched early diastolic decrescendo murmur at the left sternal edge

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62
Q

what are the causes of pulmonary stenosis?

A
  • carcinoid syndrome
  • rheumatic heart disease
  • fallot’s tetralogy
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63
Q

which murmur is associated with pulmonary stenosis?

A

-Harsh mid-systolic ejection murmur, best heard on inspiration, to the left of the sternum in the second intercostal space.

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64
Q

what is seen on chest x-ray in pulmonary stenosis?

A

-Post-stenotic dilatation of the pulmonary trunk.

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65
Q

what is seen on ECG in pulmonary stenosis?

A

-Tall R waves in V1 due to right ventricular hypertrophy.

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66
Q

what are the clinical features of tricuspid stenosis?

A
  • Abdominal pain due to hepatomegaly.
  • Swelling due to ascites.
  • Peripheral oedema.
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67
Q

which murmur is associated with tricuspid stenosis?

A

-Rumbling mid-diastolic murmur heard over the left sternal edge during inspiration.

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68
Q

what is seen on chest x-ray in tricuspid stenosis?

A

-prominent right atrial enlargement.

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69
Q

what is seen on ECG in tricuspid stenosis?

A

-Tall P waves in lead II due to right atrial enlargement

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70
Q

how is tricuspid stenosis managed?

A
  • Offer diuretic therapy.
  • Encourage salt restriction.
  • Offer tricuspid valve replacement where diuretic therapy and salt restriction do not improve the condition.
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71
Q

what murmur is heard in tricuspid regurgitation?

A

-Blowing pansystolic murmur over the left sternal edge on inspiration

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72
Q

how is tricuspid regurgitation managed?

A
  • Offer diuretic and vasodilator therapy.
  • Offer tricuspid valve repair in patients undergoing mitral valve replacement who have tricuspid regurgitation.
  • Offer tricuspid valve replacement if rheumatic damage is severe, or in drug addicts with infective endocarditis.
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73
Q

what are the risk factors for atrial myxoma?

A
  • Female sex.
  • Age 40 - 60 years.
  • Family history of atrial myxoma.
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74
Q

what are the symptoms of atrial myxoma?

A
  • Dyspnoea that can be worse when lying on left side.
  • Syncope.
  • Dizziness.
  • Weight loss.
  • Fatigue.
  • Fever.
  • Pallor.
  • Arthralgia.
  • Raynaud’s phenomenon.
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75
Q

what are the signs of atrial myxoma?

A
  • Loud first heart sound.
  • A tumour plop ‘loud third heart sound produced as the pedunculated tumour comes to an abrupt halt).
  • Mid-diastolic murmur.
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76
Q

how is atrial myxoma diagnosed?

A

-Dense space-occupying lesion.

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77
Q

how is atrial myxoma managed in surgical candidates?

A
  • Perform myxoma resection (atriotomy).
  • Perform adjunct mitral valve repair or replacement.
  • post-op aspirin
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78
Q

how is atrial myxoma managed in non-surgical candidates?

A

-Offer beta blockers, ACE inhibitors and furosemide

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79
Q

what are the causes of AF?

A
  • hypertension
  • coronary artery disease
  • MI
  • rheumatic heart disease
  • cardiomyopathy
  • WPW
  • myocarditis
  • pericarditis
  • thyrotoxicosis
  • electrolyte imbalance
  • alcohol abuse
  • obesity
  • smoking
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80
Q

what are the clinical features of AF?

A
  • Irregular pulse.
  • Breathlessness.
  • Palpitations.
  • Syncope / dizziness.
  • Chest discomfort.
  • Stroke / TIA.
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81
Q

what is seen on ECG in AF?

A
  • Absent P waves
  • F waves
  • Irregularly irregular QRS rhythm
  • Normal QRS complexes.
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82
Q

how is acute AF with haemodynamic instability treated?

A

-emergency electrical cardioversion

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83
Q

how is acute AF in stable patients managed?

A
  • Offer rate control with rhythm control if the onset of AF is less than 48 hours, or rate control if the onset if more than 48 hours or uncertain
  • Offer electrical cardioversion: immediately if the symptoms have occurred for less than 48 hours, the patient start LMWH prior to this

OR

  • After 3 weeks if the symptoms have persisted for longer than 48 hours and the patient is being considered for long term rhythm control. The patient should be fully anticoagulated for 3 weeks and offer rate control as appropriate
  • Offer pharmacological cardioversion (amiodarone or flecainide) as an alternative to electrical cardioversion. Flecainide should be avoided if there is underlying structural or ischaemic heart disease.
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84
Q

how is long term rate control achieved in AF?

A
  • beta blocker or diltiazem
  • digoxin monotherapy
  • combine
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85
Q

how is long term rhythm control achieved in AF?

A
  • pill-in-the-pocket strategy using flecainide or propafenone
  • beta blocker or diltiazem
  • dronderone
  • left atrial catheter ablation
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86
Q

what is seen on ECG in atrial ectopics?

A
  • abnormally shaped P wave

- an early QRS complex.

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87
Q

what is seen on ECG in atrial tachycardia?

A
  • some absent P waves

- a rate of 150 bpm

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88
Q

what is seen on ECG in atrial flutter?

A
  • sawtooth F wave rate of 300/min
  • narrow QRS complexes
  • QRS rate is 150, 100 or 75 bpm if there is 2:1, 3:1 or 4:1 heart block.
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89
Q

how are atrial ectopic beats managed?

A

-treatment is not normally required unless the ectopic beats provoke more significant arrhythmia, when beta blockers are effective.

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90
Q

how is atrial flutter managed?

A
  • Perform emergency electrical cardioversion when there are signs of haemodynamic compromise, such as a systolic blood pressure less than 90 mmHg or a pulse greater than 150 bpm.
  • Provide a beta-blocker (atenolol), diltiazem or verapamil for rate control.
  • Provide cardioversion for conversion to sinus rhythm, the patient should receive oral anticoagulation for at least 3 weeks prior to cardioversion.
  • Provide catheter ablation for treatment of recurrent atrial flutter.
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91
Q

how is atrial tachycardia managed?

A
  • cardioversion
  • beta blockers
  • calcium channel blockers
  • catheter ablation.
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92
Q

define sinus bradycardia

A

pulse rate of less than 50 bpm.

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93
Q

what are the intrinsic causes of bradycardia?

A
  • Acute ischaemia and infarction of the sinus node, as a complication of acute myocardial infarction.
  • Chronic degenerative changes such as fibrosis of the atrium and sinus node (sick sinus syndrome, an idiopathic fibrosis of the sinus node).
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94
Q

what are the extrinsic causes of bradycardia?

A
  • Hypothermia, hypothyroidism, cholestatic jaundice, and raised intracranial pressure.
  • Drug therapy with beta blockers, digitalis and other anti arrhythmic drugs.
  • Neurally mediated syndromes including:
  • –Carotid sinus syndrome.
  • –Vasovagal syncope.
  • –Postural orthostatic tachycardia syndrome (POTS)
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95
Q

what are the clinical features of bradycardia?

A
  • Pulse rate < 50 bpm.
  • Syncope.
  • Fatigue.
  • Exercise intolerance.
  • Shortness of breath.
  • Cannon a-waves in JBP.
  • Jugular venous distension.
  • Increased intracranial pressure.
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96
Q

how is bradycardia managed?

A
  • Administer atropine for haemodynamically unstable patients.
  • Offer permanent pacing for carotid sinus syndrome and sick sinus syndrome.
  • Offer fludrocortisone or midodrine for vasovagal syncope.
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97
Q

what are the reversible causes of cardiac arrest?

A
  • hypoxia
  • hypovolaemia
  • hypo/hyperkalaemia
  • hypothermia
  • acidosis
  • thrombosis
  • toxins
  • tension pneumothorax
  • cardiac tamponade.
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98
Q

what are the risk factors for cardiac arrest?

A
  • Coronary artery disease
  • Left ventricular dysfunction
  • Hypertrophic cardiomyopathy
  • Arrhythmogenic right ventricular dysplasia
  • Long QT syndrome
  • Medical or surgical emergency such as pulmonary embolism or tension pneumothorax
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99
Q

how should cardiac arrest with a shockable rhythm be managed?

A
  • Use 150 J for the first shock and immediately resume CPR for 2 minutes with a ratio of 30:2.
  • If VF or VT persists, repeat this process twice more, for a total of three shocks.
  • Give adrenaline 1 mg IV and amiodarone 300 mg IV and immediately resume CPR with a ratio of 30:2 for 2 minutes.
  • Repeat the sequence and further adrenaline.
  • Start post-resuscitation care if there are signs of return of spontaneous circulation.
  • If there is shockable rhythm in a monitored patient (coronary care unit) give up to three quick successive stacked shocks rather than 1 shock followed by CPR.
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100
Q

how is cardiac arrest with a non-shockable rhythm managed?

A
  • Give adrenaline 1 mg IV and and immediately resume CPR with a ratio of 30:2.
  • Use a laryngeal mask airway (LMA) to secure the patient’s airway. Ventilate the lungs at a rate of 10 breaths per minute and continue chest compressions without pausing ventilation.
  • Continue CPR and give adrenaline 1 mg IV after revert to alternative sequence of CPR.
  • Manage as shockable rhythm if ECG shows signs of VF or VT.
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101
Q

what are the clinical features of hypertrophic cardiomyopathy?

A
  • Many patients are asymptomatic and the condition is detected through family screening.
  • Exertional syncope, angina, and dyspnoea (similar to aortic stenosis).
  • Sudden death.
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102
Q

what are the signs of hypertrophic cardiomyopathy?

A
  • A jerky carotid pulse, which can distinguish it from aortic stenosis.
  • Double apical pulsation.
  • Ejection systolic murmur due to left ventricular outflow obstruction.
  • Pansystolic murmur due to mitral regurgitation secondary to systolic anterior motion.
  • 4th Heart sound if not in AF
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103
Q

what is seen on echo in hypertrophic cardiomyopathy?

A

-asymmetric left ventricular hypertrophy involving the septum

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104
Q

which patients with hypertrophic cardiomyopathy should have an ICD?

A
  • Massive left ventricular hypertrophy greater than 30 mm on echocardiography.
  • Family history of sudden cardiac death below 50 years of age.
  • History of previous cardiac arrest or sustained ventricular tachycardia.
  • Ventricular tachycardia on ambulatory ECG monitoring.
  • Recurrent syncope.
  • Exercise induced hypotension.
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105
Q

how is chest pain and dyspnoea managed in hypertrophic cardiomyopathy?

A
  • beta-blockers and or calcium channel blockers

- Offer disopyramide as an alternative for patients with left ventricular outflow obstruction.

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106
Q

what are the causes of acquired dilated cardiomyopathy?

A
  • myocarditis secondary to Chagas’s disease
  • toxins e.g. alcohol and chemotherapy
  • pregnancy
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107
Q

what are the clinical features of dilated cardiomyopathy?

A
  • Signs and symptoms of heart failure e.g. breathlessness, fluid retention, fatigue, third or fourth heart sounds, raised JVP, hepatomegaly.
  • Palpitations due to arrhythmia.
  • Sudden death.
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108
Q

what is seen on echo in dilated cardiomyopathy?

A
  • Dilatation of the left and right ventricles

- with poor global contraction.

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109
Q

how is dilated cardiomyopathy managed?

A
  • Pharmacological management of heart failure e.g. an ACE inhibitor, a beta blocker, and spironolactone.
  • Offer an ICD in patients with NYHA3/4 grading.
  • Cardiac transplantation for certain patients.
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110
Q

what are the clinical features of arrhythmogenic RV cardiomyopathy?

A
  • Most patients are asymptomatic.
  • Palpitations due to ventricular arrhythmias.
  • Syncope due to reduced cardiac output.
  • Sudden death.
  • Features of right heart failure including peripheral oedema, raised JVP, hepatomegaly, ascites
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111
Q

what are the task force criteria for the diagnosis of arrhythmogenic RV cardiomyopathy?

A
  • Perform cardiac MRI to assess structural abnormalities of the right ventricle .
  • Perform tissue biopsy to demonstrate fibro-fatty replacement of myocytes.
  • Perform ECG shows T wave inversion in V1-V3 and RBBB.
  • Perform ambulatory blood pressure monitoring (ABPM) to demonstrate ventricular tachycardia or ventricular extrasystoles.
  • A family history of ARVC or sudden death.
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112
Q

how is arrhythmogenic RV cardiomyopathy managed?

A
  • Offer a beta blocker for non-life threatening arrhythmias.
  • Offer amiodarone or sotalol for symptomatic arrhythmia.
  • Offer an ICD for life-threatening arrhythmias.
  • Cardiac transplantation is indicated for either intractable arrhythmia or cardiac failure.
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113
Q

what are the clinical features of restrictive cardiomyopathy?

A
  • Dyspnoea and fatigue owing to heart failure.
  • Hepatic enlargement, ascites and oedema owing to heart failure.
  • On examination of the JVP:
  • –Elevated JVP with diastolic collapse (Friedreich’s sign)
  • –Elevation of venous pressure with inspiration (Kussmaul’s sign).
  • –Third and fourth heart sounds.
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114
Q

what is seen on echo in restrictive cardiomyopathy?

A

Impaired ventricular filling

  • tram-lines
  • speckled myocardium in amyloid patients.
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115
Q

how is restrictive cardiomyopathy managed?

A
  • Offer pharmacological management of heart failure e.g. an ACE inhibitor, a beta blocker, and spironolactone.
  • Offer melphalan with prednisolone for primary amyloidosis.
  • Consider liver transplantation in familial amyloidosis.
  • Consider cardiac transplantation in severe cases, usually of idiopathic origin, as there is recurrence after transplantation with amyloidosis
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116
Q

what are the clinical features of coarctation of the aorta?

A
  • Hypertension presenting at young age or resistant to treatment.
  • Diminished lower extremity pulses.
  • Differential upper and lower extremity blood pressure.
  • Ejection systolic murmur at upper sternal edge.
  • Radio-femoral delay, due to blood bypassing the obstruction via collateral walls.
  • Headaches and nosebleeds due to hypertension.
  • Claudication due to poor lower limb perfusion.
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117
Q

what is seen on chest x-ray in coarctation of the aorta?

A
  • Rib notching due to development of enlarged collateral intercostal arteries
  • A ‘3’ sign at the site of coarctation.
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118
Q

what are the clinical features of critical coarctation of the aorta?

A
  • Examination on the first day of life is usually normal.
  • The neonates usually present with acute circulatory collapse at 2 days of age when the duct closes.
  • A sick baby, with severe heart failure
  • Absent femoral pulses
  • Severe metabolic acidosis.
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119
Q

how is critical coarctation of the aorta managed?

A
  • Give a prostaglandin (alprostadil) and oxygen to maintain ductal patency
  • followed by surgical repair.
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120
Q

what is a hypertensive emergency?

A
  • a severely elevated blood pressure (greater than 180/120 mmHg)
  • with new or progressive target organ dysfunction.
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121
Q

what are the complications of malignant hypertension?

A
  • Cardiac failure with left ventricular hypertrophy and dilatation.
  • Blurred vision due to papilloedema and retinal haemorrhages.
  • Haematuria and renal failure due to fibrinoid necrosis of glomeruli.
  • Severe headache and cerebral haemorrhage.
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122
Q

what are the risk factors for a hypertensive emergency?

A
  • Inadequately treated hypertension.
  • Chronic kidney disease.
  • Renal artery stenosis.
  • Renal transplant.
  • Pregnancy.
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123
Q

what are the clinical features of a hypertensive emergency?

A
  • Neurological features include vision changes, dizziness, and headaches.
  • Cardiopulmonary features include shortness of breath, chest pain, raised JVP, third heart sound, peripheral oedema.
  • Haematuria.
  • Oliguria.
  • Nosebleeds.
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124
Q

what is seen on fundoscopy in malignant hypertension?

A
  • Cotton wool spots
  • Hard exudates
  • Papilloedema
  • Engorged veins
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125
Q

how is a hypertensive emergency managed?

A
  • Administer intravenous labetalol if there is malignant hypertension or pre-eclampsia.
  • Administer intravenous glyceryl trinitrate if there is left ventricular failure or pulmonary oedema, or myocardial ischaemia or infarction.
  • Administer intravenous fenoldapam for patients with acute kidney injury.
  • For a hyperadrenergic state:
  • –Offer a benzodiazepine (lorazepam) if there is evidence of sympathomimetic drug use including cocaine and amphetamines.
  • –Offer an alpha blocker (phentolamine) for phaeochromocytoma.
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126
Q

which drugs cause long QT syndrome?

A
  • amiodarone
  • sotalol
  • tricyclic antidepressants
  • SSRIs
  • erythromycin
  • haloperidol
  • ondansetron.
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127
Q

what are the clinical features of LQT1?

A

Syncope during exercise, particularly swimming

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128
Q

what are the clinical features of LQT2?

A
  • Syncope when startled by auditory stimuli, as by a telephone or alarm clock
  • Syncope postpartum.
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129
Q

what are the clinical features of LQT3?

A

-Syncope with rest and bradycardia (typically at night).

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130
Q

How is acquired long QT syndrome managed?

A
  • Stop causative drugs in acquired LQTS.
  • Correct electrolyte abnormalities.
  • The heart rate is maintained with atrial or ventricular pacing
  • Magnesium sulphate 8 mmol (Mg2+) over 10–15 min for acquired long QT
  • Intravenous isoprenaline may be effective when QT prolongation is acquired
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131
Q

how is congenital long QT managed?

A
  • Recommend lifestyle modification including limiting certain sports such as swimming.
  • Offer a beta blocker (nadolol) for low risk patients (QTc < 500 ms and no previous cardiac arrest.
  • Offer an implantable cardioverter defibrillator (ICD) for high risk patients (QTc > 500 ms or previous cardiac arrest), or if beta-blockers are contra-indicated.
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132
Q

how is Marfan’s syndrome inherited?

A

-autosomal dominant

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133
Q

describe the Marfan’s phenotype

A
  • Tall stature.
  • Wide arm span.
  • High arched palate.
  • Arachnodactyly.
  • Pectus excavatum.
  • Pectus carinatum.
  • Scoliosis.
  • Flat feet.
  • Joint hyper-mobility.
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134
Q

what visual system abnormalities are associated with Marfan’s?

A
  • Dislocated eye lens.
  • Myopia or astigmatism.
  • Retinal abnormalities.
  • Glaucoma
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135
Q

what cardiovascular system abnormalities are associated with Marfan’s?

A
  • Aortic valve murmur.
  • Mitral valve murmur.
  • History of spontaneous pneumothorax.
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136
Q

how is aortic root dilation slowed in marfan’s syndrome?

A
  • Offer beta-blocker therapy to slow down the rate of aortic root dilatation.
  • Offer an ACE inhibitor which inhibits TNF-β, which is upregulated in Marfan’s syndrome.
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137
Q

which patients should be offered aortic root replacement in Marfan’s?

A
  • yearly echocardiogram reveals an aortic root diameter measures more than 4.5 to 5 cm.
  • In women of child-bearing age who wish to become pregnant.
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138
Q

what are the causes of myocarditis?

A
  • viral
  • parasitic
  • bacterial
  • fungal
  • Drugs, including alcohol, doxorubicin, methyldopa, penicillins, sulfonamides.
  • Autoimmune conditions, such as systemic lupus erythematosus and rheumatoid arthritis.
  • Complication of infective endocarditis.
  • Drugs causing hypersensitivity, including methyldopa, penicillin and sulfonamides.
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139
Q

what are the clinical features of myocarditis?

A
  • May be asymptomatic.
  • Fever, especially when infectious.
  • Chest pain that is stabbing in nature.
  • Palpitations due to arrhythmia.
  • Dyspnoea and oedema due to congestive cardiac failure.
  • Sudden death.
  • Tachycardia.
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140
Q

what is found on auscultation in myocarditis?

A
  • Soft heart sounds.
  • Prominent third heart sounds.
  • Pericardial friction rub.
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141
Q

how is myocarditis managed?

A
  • Recommend bed rest.
  • Recommend avoidance of athletic activity for 6 months.
  • Offer antibiotics for bacterial causes.
  • Offer γ-interferon for viral causes.
  • Offer ACE inhibitors, beta blockers, spironolactone if evidence of congestive cardiac failure.
  • Offer corticosteroids in giant cell or eosinophilic myocarditis.
  • Offer nifurtimox and benznidazole in Chagas’ disease.
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142
Q

what are the clinical features of acute pericarditis?

A
  • Sharp, constant retrosternal pain that is relieved by sitting forward and worsened by lying down. It may be referred to left shoulder.
  • Pericardiac friction rub, a high pitched stretching sound heard over the left sternal border during expiration.
  • Fever
  • Arthralgia
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143
Q

what are the clinical features of chronic pericarditis?

A
  • Kussmaul’s sign (a paradoxical rise in JVP during inspiration).
  • Ascites, hepatomegaly and peripheral oedema.
  • Dyspnoea, cough, and orthopnoea
  • Fatigue, hypotension, and tachycardia.
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144
Q

what is seen on ECG in pericarditis?

A
  • Global saddle shaped ST elevation in acute pericarditis

- Low voltage QRS complexes and flat T waves in chronic pericarditis.

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145
Q

how is pericarditis managed?

A
  • Offer an NSAID (ibuprofen) plus colchicine as the first line treatment.
  • Perform pericardiocentesis with systemic antibiotics (vancomycin and gentamicin) for patients with purulent pericarditis.
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146
Q

what are the clinical features of cardiac tamponade?

A
  • Beck’s triad - hypotension, muffled heart sounds, and distended jugular veins.
  • Pulsus paradoxus, a drop in blood pressure during inspiration.
  • Dyspnoea.
  • Tachycardia.
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147
Q

what is seen on ECG in cardiac tamponade?

A
  • Low voltage QRS complexes

- Electrical alternans (alteration of QRS amplitude between beats).

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148
Q

how is cardiac tamponade managed?

A
  • Perform pericardiocentesis if there is no haemorrhage, trauma, neoplasm or purulence.
  • Perform surgical drainage (pericardial window) for haemopericardium, trauma, purulent effusion, or neoplastic disease.
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149
Q

what is intermittent claudication?

A

ischaemic leg pain upon walking and relieved by rest.

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150
Q

what is critical limb ischaemia?

A

ischaemic pain at rest, associated with ulceration and gangrene, that may be complicated by sepsis.

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151
Q

what are the risk factors for peripheral arterial disease?

A
  • Smoking.
  • Diabetes.
  • Advancing age.
  • Hypertension.
  • Hypercholesterolaemia.
  • Existing atherosclerotic disease.
  • Chronic kidney disease.
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152
Q

what are the clinical features of acute limb ischaemia?

A
  • Pain.
  • Pulselessness.
  • Pallor.
  • Paralysis.
  • Paraesthesia.
  • Perishingly cold limb.
  • If due to embolus the onset is acute, the limb appears white.
  • If due to thrombosis the onset is more gradual, the leg may not be white.
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153
Q

how is peripheral arterial disease diagnosed using ABPI?

A
  • An ABPI of less than 0.9 indicates peripheral arterial disease.
  • An ABPI of less than 0.5 is associated with severe peripheral arterial disease
  • An ABPI of 0.9 - 1.2 is a normal finding.
  • An ABPI of > 1.2 indicates renal or diabetic disease because the arteries are heavily calcified and incompressible.
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154
Q

how is acute limb ischaemia managed?

A
  • Administer anti-platelet therapy (aspirin 300 mg).
  • Administer intravenous heparin for a target APTT of 2.0 - 3.0.
  • Perform endovascular revascularisation (balloon angioplasty) and intra-arterial thrombolysis (urokinase) if the limb is viable (no significant tissue loss, never damage, or sensory loss).
  • Perform amputation if the limb is not viable (significant tissue loss, never damage, or sensory loss).
155
Q

how is chronic limb ischaemia managed?

A
  • Administer anti-platelet therapy (aspirin 300 mg).
  • Perform endovascular revascularisation (balloon angioplasty) for revascularisation candidates (patient can walk, have a life expectancy of greater than 1 year).
  • Perform amputation if the patient is not a candidate for revascularisation (patient cannot walk, has a life expectancy of less than 1 year).
156
Q

how is intermittent claudication managed?

A
  • Offer anti-platelet therapy (aspirin 300 mg).
  • Offer a supervised exercise programme which involves 2 hours of supervised exercise a week for a 3‐month period, encourage exercise to the point of maximal pain.
  • Refer for consideration of angioplasty when risk modification has been offered and supervised exercise has failed to improve symptoms.
  • Offer naftidrofuryl oxalate or cilostazol where a supervised exercise programme has failed and the patient does not wish to be referred for surgery.
157
Q

what are the causes of postural hypotension?

A
  • Alpha blockers.
  • Diuretics.
  • Diabetes mellitus due to autonomic neuropathy.
  • Tricyclic antidepressants.
  • Hypovolaemia.
  • Amyloidosis.
  • Parkinson’s disease.
158
Q

what are the clinical features of postural hypotension?

A
  • Light-headedness.
  • Syncope.
  • Visual changes.
  • Weakness.
  • Fatigue.
  • Dyspnoea.
159
Q

how is postural hypotension diagnosed?

A

-Systolic blood pressure falls 20 mmHg within three minutes of standing.

160
Q

how is postural hypotension managed?

A
  • Stop causative drugs if appropriate.
  • Offer a mineralocorticoid (fludrocortisone) if the patient has an inadequate response to simple non-pharmacological measures.
  • Offer a short-acting pressor (midodrine) if there is an inadequate reposes to mineralocorticoid therapy.
161
Q

what are the complications associated with occlusion of the aortic branches in aortic dissection?

A
  • Myocardial ischaemia and infarction due to occlusion of the coronary arteries.
  • Stroke due to occlusion of the carotid arteries.
  • Paraplegia due to occlusion of the spinal arteries.
  • Mesenteric infarction with an acute abdomen due to occlusion of the coeliac and superior mesenteric arteries.
  • Acute (typically lower) limb ischaemia due to occlusion of the femoral arteries.
162
Q

what are the risk factors for aortic dissection?

A
  • Hypertension (80% of cases)
  • Aortic atherosclerosis
  • Non-specific aortic aneurysm
  • Aortic coarctation.
  • Collagen disorders (Marfan’s syndrome, Ehler’s Danlors syndrome)
  • Previous aortic surgery
  • Pregnancy (usually third trimester)
  • Trauma.
  • Iatrogenic (cardiac catheterisation)
  • Male gender and increasing age
163
Q

what are the clinical features of aortic dissection?

A
  • Chest pain that is sharp and tearing in nature, that radiates to the back, classically between the shoulder blades.
  • Hypertension.
  • Difference in blood pressure between the 2 arms.
  • Pulse deficit (reduction or absence of upper limb pulses) in type A dissection.
  • Diastolic murmur in type A dissection.
  • Hypotension suggests acute pericardial tamponade and is a grave prognostic indicator.
164
Q

how is aortic dissection diagnosed?

A
  • CT angiography

- Transoesophageal echocardiography

165
Q

how is type A aortic dissection managed?

A
  • Give intravenous labetalol to reduce blood pressure to under 120 mmHg.
  • Perform open surgery (arch replacement).
166
Q

how is type B aortic dissection managed?

A
  • Give intravenous labetalol.
  • Perform open surgery (endovascular stent-graft repair) if there is evidence of complications including vital organ or limb ischaemia. For patients with Type B dissection in whom surgery is not indicated, offer medical management only.
  • Consider verapamil or diltiazem where beta-blockers are contra-indicated.
  • Consider sodium nitroprusside where beta blockers fail to control blood pressure adequately.
167
Q

what are the risk factors for WPW?

A
  • Ebstein’s anomaly.
  • Hypertrophic cardiomyopathy.
  • Mitral valve prolapse.
  • Atrial septal defect.
168
Q

what are the clinical features of WPW?

A
  • Palpitations.
  • Dizziness.
  • Shortness of breath.
  • Chest pain.
  • Atrial fibrillation.
169
Q

What is seen on ECG in WPW?

A
  • Short PR interval
  • Type A WPW: Positive delta wave in all precordial leads with R/S >1 in V1
  • Type B WPW: Negative delta wave in leads V1 and V2
  • Secondary ST-T Wave changes
  • Right axis deviation if left (lead 1 is negative and lead 3 is positive).
170
Q

how is WPW managed?

A
  • Offer accessory pathway catheter ablation as the definitive management.
  • Offer an anti-arrhythmic such as flecainide or propafenone for patients who refuse ablation/are unsuitable for ablation if they have structural or coronary heart disease
  • In patients with structural heart disease, give dofetilide or sotalol
  • Perform DC cardioversion in unstable patients with a systolic blood pressure of less than 90 mmHg.
171
Q

define stage 1 hypertension

A

140/90 mmHg to 159/99 mmHg.

172
Q

define stage 2 hypertension

A

160/100 mmHg to 179/119 mmHg.

173
Q

define stage 3 hypertension

A

180/120 mmHg or higher

174
Q

what are the risk factors for developing hypertension?

A
  • Increasing age.
  • Male gender.
  • Black African and Black Caribbean origin.
  • Social deprivation.
  • Smoking.
  • Excess alcohol consumption.
  • Excess dietary salt.
  • Obesity and lack of physical exercise.
  • Anxiety and emotional stress.
175
Q

what are the complications associated with essential hypertension?

A
  • Heart failure.
  • Coronary artery disease.
  • Peripheral arterial disease.
  • Chronic kidney disease.
  • Intracerebral haemorrhage.
  • Vascular dementia.
  • stroke
  • MI
176
Q

how is essential hypertension diagnosed?

A
  • clinic BP measured in both arms
  • repeat if>140/90
  • ABPM or HBPM
  • Confirm a diagnosis of hypertension in people with a clinic blood pressure of 140/90 mmHg or higher and a ABPM or HBPM daytime average of 135/85 mmHg or higher
177
Q

in which patients with hypertension should anti-hypertensive medication be started?

A
  • Patients with stage 2 hypertension.
  • Patients with stage 1 hypertension with target organ damage, established cardiovascular disease, renal disease, diabetes or a QRISK score > 10%.
178
Q

what is the first step of hypertension management?

A
  • Offer an ACE inhibitor (ramipril) to patients under 55, or who have diabetes or who are not of African or Caribbean origin.
  • Offer a calcium channel blocker (amlodipine) to patients over 55 and people of African or Caribbean origin.
179
Q

what is the second step management of hypertension?

A
  • Add a calcium channel blocker in patients under 55 or who have diabetes or who are not of Afro-Caribbean origin with poorly controlled hypertension (their blood pressure is above 140/90 mmHg).
  • Add an ACE inhibitor in patients over 55 who are not of Afro-Caribbean origin with poorly controlled hypertension (their blood pressure is above 140/90 mmHg).
  • Add an ARB (losartan) in patients over 55 who are of Afro-Caribbean origin with poorly controlled hypertension (their blood pressure is above 140/90 mmHg).
180
Q

what is step 3 of hypertension management?

A

-Offer an ACE inhibitor, calcium channel blocker and a thiazide-like diuretic (indapamide) for all patients in whom hypertension is not controlled by step 2 treatment.

181
Q

how is resistant hypertension managed?

A
  • Offer a mineralocorticoid receptor antagonist (spironolactone) in addition to step 3 treatment to patients with resistant hypertension with a blood potassium level of 4.5 mmol/L or less.
  • Offer an alpha blocker (doxazosin) or a beta blocker (atenolol) in addition to step 3 treatment to patients with resistant hypertension with a blood potassium level of more than 4.5 mmol/L.
182
Q

what is the target blood pressure for patients under 80?

A
  • clinic blood pressure below 140/90 mmHg

- home blood pressure below 135/85 mmHg.

183
Q

what is the target blood pressure for patients over 80?

A
  • clinic blood pressure below 150/90 mmHg.

- home blood pressure below 145/85 mmHg

184
Q

what is first degree AV block?

A

simple prolongation of the PR interval to > 0.22 seconds

185
Q

what is mobitz 1 AV block?

A

progressive PR prolongation until a P wave fails to conduct.

186
Q

what is mobitz 2 AV block?

A
  • AV block Mobitz II occurs when a dropped QRS complex is not preceded by progressive PR interval prolongation
  • Wide QRS
187
Q

what is third degree AV block?

A

all atrial activity fails to conduct to the ventricles.

188
Q

what are the clinical features of AV block?

A
  • Typically asymptomatic.
  • Syncope (Stokes-Adams attacks)
  • Heart rate < 40 bpm.
  • Fatigue.
  • Dyspnoea.
  • Angina.
  • High blood pressure.
  • Cannon A waves (complete heart block)
189
Q

how are 1st degree and mobitz 1 AV block managed?

A
  • Monitoring if asymptomatic.
  • Discontinuation of AV-nodal blocking medications if symptomatic.
  • Dual chamber pacing (1 right atrial and 1 right ventricular lead) with or without an implantable cardioverter-defibrillator (ICD) if severe.
190
Q

how are Mobitz II and third degree AV block managed?

A
  • Digoxin immune Fab if digitalis toxicity.
  • Glucagon if beta-blocker toxicity.
  • Calcium chloride if calcium channel blocker toxicity.
  • Dual chamber pacing with or without an implantable cardioverter-defibrillator (ICD) if severe.
191
Q

what are the causes of RBBB?

A
  • right ventricular hypertrophy
  • coronary artery disease
  • congenital heart disease.
192
Q

what are the causes of LBBB?

A
  • coronary artery disease
  • hypertension
  • aortic valve disease
  • cardiomyopathy.
193
Q

what is heard on auscultation in RBBB?

A

-Wide splitting of the 2nd heart sound

194
Q

what is heard on auscultation in LBBB?

A

-reverse splitting of the second heart sound

195
Q

what is seen on ECG in RBBB?

A
  • tall R waves in V1

- deep S waves in leads V6 and I.

196
Q

what is seen on ECG in LBBB?

A
  • deep S waves in V1

- tall R waves in leads V6 and I.

197
Q

what is seen on ECG in left anterior hemiblock?

A

-left axis deviation (negative QRS deflections in leads II and III)

198
Q

what is seen on ECG in bifascicular block?

A
  • tall R waves in V1 and deep S waves in leads V6 and I

- negative QRS deflections in leads II and III.

199
Q

what is seen on ECG in trifascicular block?

A
  • tall R waves in V1
  • deep S waves in leads V6 and I
  • negative QRS deflections in leads II and III
  • first (incomplete) or third degree (complete) heart block
200
Q

how does left sided heart failure present?

A
  • salt and water retention

- pulmonary congestion and oedema, pleural effusions, and cardiomegaly.

201
Q

how does right sided heart failure present?

A
  • increase in right atrial pressure
  • compounded by salt and water retention
  • causes peripheral oedema
  • hepatomegaly
  • ascites.
202
Q

what are the complications associated with heart failure?

A
  • renal failure
  • impaired liver function
  • hypokalaemia
  • hyponatraemia
  • arrhythmia
  • thromboembolism
203
Q

what are the symptoms of heart failure?

A
  • Dyspnoea on exertion.
  • Dyspnoea at rest.
  • Dyspnoea lying flat (orthopnoea).
  • Nocturnal cough, waking from sleep (paroxysmal nocturnal dyspnoea).
  • Coughing up pink frothy sputum with pulmonary oedema.
  • Fatigue and decreased exercise tolerance.
  • Light headedness or history of syncope.
204
Q

what are the signs of heart failure?

A
  • Signs of fluid retention such as ankle swelling, abdominal swelling.
  • Tachycardia.
  • Third heart sound.
  • Displaced apex beat.
  • Murmurs on auscultation.
  • Hepatomegaly.
  • Raised JVP.
  • Tachypnoea.
  • Basal crepitations.
  • Pleural effusions.
205
Q

what is class 1 of the NYHA?

A
  • No symptoms

- Ordinary physical exercise does not cause limitation.

206
Q

what is class 2 of the NYHA?

A
  • Mild symptoms

- Slight Limitation of ordinary physical activity.

207
Q

what is class 3 of the NYHA?

A
  • Moderate symptoms

- Marked limitation on ordinary physical activity

208
Q

what is class 4 of the NYHA?

A
  • Severe symptoms

- Limitation at rest.

209
Q

when should patients with suspected heart failure be referred for echo with respect to NT-proBNP?

A
  • Urgently refer for specialist assessment and echocardiography within 2 weeks for levels above 2,000 ng/l.
  • Refer for specialist assessment and echocardiography within 6 weeks for levels between 400 and 2,000 ng/l.
210
Q

what factors reduce NT-proBNP levels?

A
  • obesity
  • heart failure medications
  • afro-caribbean
211
Q

what factors increase NT-proBNP levels?

A
  • > 70 years old
  • pulmonary hypertension
  • PE
  • Diabetes mellitus
  • CKD
212
Q

what is seen on chest x-ray in heart failure?

A
  • Alveolar batwing oedema
  • Kerley B lines
  • Cardiomegaly
  • Dilated pulmonary vessels
  • Pleural effusions.
213
Q

how are congestive symptoms treated in chronic heart failure?

A

-furosemide 80mg

214
Q

what is the first line treatment for heart failure with REF?

A
  • ACE inhibitor (ramipril)

- beta blocker (bisoprolol or carvedilol)

215
Q

what is the second line treatment for heart failure with REF?

A
  • an aldosterone antagonist

- with an ACEi and beta-blocker

216
Q

what are the 3rd line treatments for heart failure with REF by a specialist?

A
  • ivabradine or sacubitril valsartan
  • hydralazine and nitrate for afro-caribbean patients
  • digoxin with AF
  • Cardiac resynchronisation, ICD or heart transplant
217
Q

how is acute heart failure managed?

A
  • Administer high flow oxygen in patients with a capillary oxygen saturation of less than 90%.
  • Administer an intravenous loop diuretic (furosemide) for acute pulmonary oedema.
  • Administer a vasodilator (glyceryl trinitrate IV) for patients with a systolic blood pressure greater than 90 mmHg.
  • Administer an inotrope (dobutamine IV) followed by a vasopressor (noradrenaline IV) for patients with a systolic blood pressure less than 90 mmHg.
  • Consider ultrafiltration in patients with confirmed diuretic resistance.
  • Consider left ventricular assist device (LVAD) for advanced heart failure resistant and refractory to maximal medical therapy.
218
Q

what are the clinical features of infective endocarditis?

A
  • Malaise.
  • Pyrexia.
  • New systolic murmur.
  • Haematuria.
  • Petechia.
  • Heart failure.
  • Splenomegaly.
  • Arthralgia.
  • Osler’s nodes
  • Splinter haemorrhages.
  • Janeway lesions.
219
Q

what are the major modified Duke criteria for infective endocarditis?

A
  • Positive blood cultures from two samples taken 12 hours apart.
  • Positive echocardiogram.
  • New valvular regurgitation.
220
Q

what are the minor modified Duke criteria for infective endocarditis?

A
  • Predisposing heart condition or intravenous drug use.
  • Fever greater than 38 degrees Celsius.
  • Vasculitic phenomenon including conjunctival haemorrhages, Janeway’s lesions.
  • Immunological phenomena including glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor.
  • Microbiolgoical evidence including a positive culture or serological test that does not meet major criteria.
  • Echocardiographic evidence that does not meet major criteria.
221
Q

when should urgent surgical valve replacement be performed in infective endocarditis?

A
  • Heart failure due to valve damage.
  • Persistent or uncontrolled infection despite antibiotic therapy.
  • Recurrent embolic episodes despite antibiotic therapy.
  • Pregnancy.
222
Q

how should suspected endocarditis be treated while awaiting culture results be treated?

A
  • amoxicillin

- gentamicin.

223
Q

how should staphylococci endocarditis be treated?

A
  • Offer flucloxacillin + gentamicin for 4 weeks for patients with native valves.
  • Offer flucloxacillin + gentamicin + rifampicin for 6 weeks for patients with prosthetic valves
224
Q

how should streptococcal endocarditis be treated?

A
  • Offer benzylpenicillin for 4 - 6 weeks if fully sensitive.

- Offer benzylpenicillin + rifampicin for 4 - 6 weeks if less sensitive.

225
Q

how should enterococcal endocarditis be treated?

A

-Offer amoxicillin + gentamicin for 4 - 6 weeks.

226
Q

how should HACEK endocarditis be treated?

A

-amoxicillin + gentamicin for 4 - 6 weeks

227
Q

what are the clinical features of an ASD?

A
  • Asymptomatic
  • Recurrent chest infections/wheeze
  • Arrhythmias
228
Q

what is found on examination in ASD?

A
  • An ejection systolic murmur best heard at the upper left sternal edge.
  • A fixed and widely split second heart sound.
  • An apical pansystolic murmur from atrioventricular valve regurgitation with a partial AVSD.
229
Q

what is seen on ECG in secundum ASD?

A
  • right axis deviation

- RBBB.

230
Q

what is seen on ECG in partial AVSD?

A

-superior QRS axis (where QRS axis is negative in AVF)

231
Q

what are the clinical features of a large VSD?

A
  • Failure to thrive.
  • Dyspnoea and heart failure
  • Recurrent pulmonary infections.
232
Q

what are the signs of a large VSD?

A
  • Tachypnoea
  • Tachycardia
  • Soft pansystolic murmur or no murmur
  • Apical mid diastolic murmur from increased flow across the mitral valve
  • Loud pulmonary second sound
233
Q

what are the signs of a small VSD?

A
  • loud pansystolic murmur at the lower left sternal edge

- quiet pulmonary second sound

234
Q

what are the clinical features of PDA?

A
  • Tachypnoea and reduced exercise tolerance.
  • Failure to thrive.
  • Apnoea.
235
Q

what are the signs of PDA?

A
  • A continuous machinery/Gibson murmur beneath the left clavicle
  • collapsing or bounding pulse
236
Q

how is a PDA managed?

A
  • prostaglandin inhibitor (indomethacin) in premature very low birth weight infants.
  • Perform percutaneous catheter device closure in small-to-moderate sized ducts in term infants and children and adults.
  • Perform surgical ligation in large ducts or symptomatic infants too small for device closure.
237
Q

what are the signs of an innocent ejection murmur?

A
  • Soft blowing murmur
  • systolic murmur only, not diastolic
  • Left Sternal edge.
  • Normal heart sounds with no added sounds
  • No parasternal thrill
  • No radiation.
  • During a febrile illness or anaemia, innocent or flow murmurs are often heard because of increased cardiac output.
238
Q

what are the clinical features of hypoplastic left heart syndrome?

A
  • detected antenatally
  • duct-dependent systemic circulation
  • profound acidosis
  • cardiovascular collapse
  • weakness or absence of all peripheral pulses
239
Q

what are the 4 cardinal features of tetralogy of fallot?

A
  • Ventricular septal defect.
  • An enlarged aorta that overrides the defects and receives blood from both the right and left ventricles.
  • Pulmonary valve stenosis.
  • Right ventricular hypertrophy.
240
Q

what are the clinical features of tetralogy of fallot?

A
  • Severe cyanosis.
  • Hyper-cyanotic episodes. The baby is typically crying, and squatting on exertion.
  • Tachypnoea.
  • Clubbing.
241
Q

what murmur can be heard in tetralogy of fallot?

A

harsh ejection systolic murmur at the left sternal edge.

242
Q

what is seen on chest x-ray in tetralogy of fallot?

A
  • Boot-shaped heart

- Right-sided aortic arch

243
Q

how are hyper-cyanotic spells in tetralogy of ballot managed?

A
  • Keeping the infant calm, hold in the parents arms with the knees to the chest.
  • Offer supportive therapy such as oxygen and volume administration.
  • Second line treatment involves administration of an intravenous beta blocker (esmolol or propranolol) which works by decreasing heart rate and prolonging diastolic filling.
  • Third line treatment involves administration of intravenous phenylephrine.
244
Q

what are the clinical features of transposition of the great arteries?

A
  • Profound cyanosis.
  • Presentation is usually on day 2 of life when ductal closure leads to a marked reduction in mixing of the desaturated and saturated blood.
  • Cyanosis will be less severe and presentation delayed if there is more mixing of blood from associated anomalies, e.g. an ASD.
  • Second heart sound is often loud and single.
245
Q

what is seen on chest x-ray in transposition of the great arteries?

A

-‘egg on one side’ appearance of the cardiac shadow

246
Q

how is transposition of the great arteries managed?

A
  • prostaglandin infusion to maintain the latency of the ductus arteriosus.
  • balloon atrial septostomy
  • arterial switch procedure
247
Q

what are the clinical features of supraventricular tachycardias?

A
  • Palpitations which are typically regular and fast, with a sudden onset with a ‘jump’.
  • Polyuria
  • Chest pain.
  • Dyspnoea.
  • Syncope.
248
Q

what is seen on 12 lead ECG in AVNRT?

A
  • no visible P wave

- an inverted P wave immediately before or after a QRS complex.

249
Q

what is seen on 12 lead ECG in AVRT?

A

P wave between the QRS and T wave.

250
Q

how are acute episodes of supraventricular tachycardia managed?

A
  • Perform emergency cardioversion in patients with haemodynamic instability
  • Perform the vagal manoeuvres (Valsava manoeuvre or carotid sinus massage) if the patient is haemodynamically stable
  • Give intravenous adenosine (6 mg)
  • Give an additional 2 doses of intravenous adenosine (12 mg) if there is no response to the 6 mg dose of adenosine, and before considering cardioversion.
  • Give intravenous diltiazem as an alternative treatment to intravenous adenosine in whom it is contraindicated (e.g. asthma).
  • Perform cardioversion in haemodynamically stable patients who respond to neither intravenous adenosine (3 doses) or verapamil.
251
Q

how are recurrent episodes of supraventricular tachycardia prevented?

A
  • Offer a class I anti-arrhythmic agent (flecainide or propafenone) for patients with no additional cardiac disease.
  • Offer a class III anti-arrhythmic agent (sotalol or amiodarone) for patients with coronary artery disease or structural heart disease
  • Catheter ablation.
252
Q

what are the clinical features of ventricular tachyarrhythmias?

A
  • Palpitations
  • Regular fast palpitations in ventricular tachycardia.
  • Dropped or missed beats in ventricular ectopics.
  • Chest pain.
  • Dyspnoea and syncope.
  • Pulseless and unconscious patient in VF
253
Q

what is seen on ECG in ventricular ectopics?

A
  • Absent P wave
  • Early wide QRS complex
  • an abnormal T wave.
254
Q

what is seen on ECG in ventricular tachycardia?

A
  • No P wave

- Broad QRS complex and a rate greater than 160 bpm.

255
Q

what is seen on ECG in brugada syndrome?

A
  • administer flecainide or ajmaline to provoke the classic ECG changes
  • RBBB
  • ST elevation in V1 and V2.
256
Q

what is seen on ECG in torasdes des pointes?

A

QRS complexes alternate in direction.

257
Q

what is seen on ECG in ventricular fibrillation?

A

totally unorganised ECG with no QRS complex.

258
Q

how are ventricular ectopics managed?

A

-beta blockers

259
Q

how are haemodynamically stable patients with ventricular tachycardia managed?

A

IV amiodarone

260
Q

how is pulseless VT or VF managed?

A
  • Perform emergency cardioversion when there are signs of haemodynamic compromise
  • Administer amiodarone for patients who are haemodynamically stable.
  • Refer to a specialist who may provide an implantable cardioverter defibrillator (ICD), in addition to a sotalol or amiodarone in combination with a standard beta-blocker.
261
Q

how is torsades de pointes managed?

A

magnesium sulphate

262
Q

how is brugada syndrome managed?

A

implantable cardioverter defibrillator

263
Q

what are the major manifestations of rheumatic fever according to the revised Jones criteria?

A
  • Carditis e.g. murmurs, cardiomegaly, cardiac failure, pericarditis, myocarditis.
  • Polyarthritis: that is fleeting and affecting large joints
  • Chorea
  • Erythema marginatum
  • Subcutaneous nodules
264
Q

what are the minor manifestations of rheumatic fever according to the revised Jones criteria?

A
  • Fever
  • Arthralgia
  • Raised CRP
  • Leucocytosis
  • First degree AV block
  • Previous rheumatic fever
265
Q

how is rheumatic fever managed?

A
  • Offer oral phenoxymethylpenicillin 500 mg four times daily for 1 week.
  • Erythromycin or clarithromycin is used if the patient is allergic to penicillin
266
Q

what are the risk factors for developing varicose veins?

A
  • Female gender
  • Pregnancy
  • Previous DVT
  • Obesity
  • Family history
  • Occupation with prolonged standing
267
Q

how are varicose veins diagnosed?

A
  • assesses for reversed flow
  • roughly, valve closure time >0.5 second is indicative of reflux, while valve closure time >1.0 second is indicative of reflux in the deep system
268
Q

how are varicose veins managed?

A
  • Offer endothermal ablation and endovenous laser treatment of the long saphenous vein
  • If endothermal ablation is unsuitable, offer ultrasound guided foam scleropathy
  • If ultrasound guided foam scleropathy is unsuitable, offer surgery
269
Q

what are the clinical features of superficial thrombophlebitis?

A
  • painful
  • tender
  • cord-like structure
  • associated redness and swelling.
270
Q

what are the causes of distributive shock?

A
  • sepsis
  • anaphylaxis

-brainstem or spinal injury

271
Q

what are the causes of cariogenic shock?

A
  • myocardial infarction
  • tachyarrhythmias
  • bradyarrhythmias
  • toxic substances
  • non-adherence with salt/fluid intake or medications
  • excessive rise in blood pressure
  • infection
  • acute mechanical causes
272
Q

what are the causes of hypovolaemic shock?

A
  • haemorrhagic causes include gastrointestinal bleeding and trauma
  • Non-haemorrhagic causes include burns and diabetic ketoacidosis.
273
Q

what are the causes of obstructive shock?

A
  • pulmonary embolism
  • cardiac tamponade
  • tension pneumothorax
274
Q

how should suspected shock be assessed initially?

A
  • urgent ABCDE assessment
  • ABG
  • Fluid rests immediately
  • measure temp
  • measure blood glucose
275
Q

what are the diagnostic features of shock?

A
  • hypotension
  • tachycardia
  • poor peripheral perfusion
  • oliguria
  • mental state change
  • fever
  • chest pain
  • dyspnoea
  • hypoxaemia
  • hypothermia
276
Q

what is seen on ABG in shock?

A
  • metabolic acidosis with negative base excess

- raised lactate

277
Q

how should all shock be managed initially?

A
  • airway management
  • give oxygen as required
  • IV fluids e.g. normal saline or hartmann’s
  • give blood products if haemorrhage shock
  • give vasopressor or inotrope if not responding to fluids
  • manage underlying causes
278
Q

how should cardiogenic shock be managed?

A
  • cautious fluid resus
  • IV furosemide
  • vasodilator (GTN)
  • vasopressor and inotrope
279
Q

how should haemorrhagic shock be managed?

A
  • MHP
  • use blood products
  • reverse anti-coagulation
  • IV TXA
  • vasopressor
280
Q

how should obstructive, non-haemorrhagic hypovolaemic or distributive shock be managed?

A
  • treat cause
  • give crystalloids
  • give vasopressors and inotropes
281
Q

what are the causes of acute digoxin toxicity?

A
  • Overdose after suicide attempt
  • Medication dosing error
  • Malicious intent (homicidal poisoning).
282
Q

what are the causes of chronic digoxin toxicity?

A
  • Chronic digoxin over-medication
  • Increased gastrointestinal absorption
  • Decreased renal clearance due to renal insufficiency or drugs
  • Displacement of digoxin from protein-binding sites
  • Conditions that increase susceptibility to digoxin
  • drugs
283
Q

what are the risk factors for developing digoxin toxicity?

A
  • Age >55
  • Decreased renal clearance
  • Hyper/hypokalaemia
  • Hypomagnesaemia
  • Hypercalcaemia
  • Hypothyroidism
  • Use of other drugs e.g. amiodarone, clarithromycin, ciclosporin, itraconazole, propafenone, quinidine, spironolactone, verapamil, diltiazem, ketoconazole, vinblastine, doxorubicin, reserpine and erythromycin
284
Q

what are the clinical features of digoxin toxicity?

A
  • Presence of risk factors
  • Digoxin exposure
  • Nausea, vomiting and diarrhoea
  • Abdominal pain
  • Anorexia
  • Lethargy and weakness
  • Confusion
  • Disturbances of colour vision: tendency to perceive yellow halos (xanthopsia) around objects
  • Blurred vision and diplopia
  • Palpitations
  • Syncope and dyspnoea
  • Arrhythmias
285
Q

how is acute digoxin ingestion with low to moderate toxicity managed?

A
  • 1mg/kg activated charcoal, to a maximum of 4 doses, to be given within 6-8 hours of ingestion
  • Supportive care
286
Q

how is chronic digoxin ingestion with low to moderate toxicity managed?

A

-supportive care

287
Q

when should digoxin immune Fab be given?

A
  • symptomatic bradyarrhythmias
  • ventricular dysrhythmias
  • any patient with digoxin overdose and potassium concentrations >5.0 millimol/L (>5.0 mEq/L
  • acute ingestion of >4 mg in a healthy child (or 0.1 mg/kg)
  • acute ingestion of >10 mg in a healthy adult
  • serum concentration of ≥12.8 nanomol/L ( ≥10 nanograms/mL) 4-6 hours after ingestion (steady state)
  • serum concentration of ≥19.2 nanomol/L (≥15 nanograms/mL) at any time.
288
Q

what are the adverse effects of ACEi?

A
  • Hypotension
  • Persistent dry cough
  • Hyperkalaemia
  • Renal Failure
  • Angiodema (more common in Afro-Caribbean patients)
  • Anaphylactoid reactions.
289
Q

in which patients should ACEi be used cautiously?

A
  • Avoid in renal artery stenosis
  • Avoid in acute kidney injury
  • Caution in pregnancy and breastfeeding
  • Caution in chronic kidney disease.
290
Q

with which other drugs do ACEi interact?

A
  • Increased risk of hyperkalaemia with potassium supplements and potassium sparing diuretics
  • Increased risk of renal failure with NSAIDs
291
Q

what are the adverse effects of ARBs?

A
  • Hypotension
  • Hyperkaleamia
  • Acute renal failure.
292
Q

in which patients should ARBs be used cautiously?

A
  • Avoid in renal artery stenosis
  • Avoid in acute kidney injury
  • Caution in pregnancy and breastfeeding
  • Caution in chronic kidney disease.
293
Q

with which other drugs do ARBs interact?

A
  • Increased risk of hyperkalaemia with potassium supplements and potassium sparing diuretics
  • Increased risk of renal failure with NSAIDs
294
Q

what are the adverse effects of dihydropyridine CCB?

A
  • Ankle swelling
  • Flushing
  • Headache
  • Palpitations.
295
Q

in which patients should dihydropyridine CCBs be used cautiously?

A
  • Avoid in unstable angina

- Avoid in severe aortic stenosis.

296
Q

with which other drugs do dihydropyridine CCBs interact?

A
  • Antihypertensives
  • Statins
  • Antiepileptics
  • Digoxin
  • Theophylline.
297
Q

what are the adverse effects of beta-blockers?

A
  • Fatigue
  • Cold extremities
  • Headache
  • GI disturbances
  • Sleep disturbance and nightmares
  • Impotence in males
298
Q

in which patients should beta-blockers be used cautiously?

A
  • Avoid in asthma due to bronchospasm
  • Avoid in heart block
  • Caution in heart failure
  • Caution in haemodynamic instability
  • Caution in hepatic failure.
299
Q

with which other drugs do beta-blockers interact?

A

Verapamil and diltiazem

300
Q

what are the adverse effects of alpha-adrenoreceptor blockers?

A
  • Postural hypotension
  • Dizziness
  • Syncope.
301
Q

in which patients should alpha-blockers be used cautiously?

A

-Avoid in patients with postural hypotension.

302
Q

with which other drugs do alpha-blockers interact?

A
  • Antihypertensives

- Phosphodiesterase-5 inhibitors.

303
Q

what are the adverse effects of hydralazine?

A
  • Lupus-like syndrome
  • Angina pectoris
  • Headache and flushing,
  • Gastrointestinal disturbances.
304
Q

in which patients should hydralazine be used cautiously?

A
  • Avoid with acute porphyrias
  • Avoid with systemic lupus erythematous
  • Avoid with dissecting aortic aneurysm
  • Caution with cerebrovascular disease
  • Caution with coronary artery disease.
305
Q

what are the adverse effects of loop diuretics?

A
  • Dehydration
  • Hypotension
  • Low electrolyte state
  • Hearing loss and tinnitus as it blocks a Na+K+2Cl- transporter that regulates endolymph composition in the inner ear.
306
Q

where in the nephron do loop diuretics act?

A

-thick ascending limb of the loop of henle

307
Q

in which patients should loop diuretics be used cautiously?

A
  • Avoid in patients with severe hypovolaemia or dehydration
  • Caution in patients with hepatic encephalopathy where hypokalaemia can worsen coma
  • Caution in patients with hypokalaemia and/or hyponatraemia
  • Caution in patients with gout as they inhibit uric acid excretion.
308
Q

with which other drugs do loop diuretics interact?

A
  • Reduced urinary excretion of lithium
  • Reduce urinary excretion of digoxin with increased risk of digoxin toxicity
  • Reduce urinary excretion of aminoglycosides with increased risk of ototoxicity or nephrotoxicity of aminoglycosides.
309
Q

where in the nephron do thiazide diuretics act?

A

-distal convoluted tubule

310
Q

what are the adverse effects of thiazide diuretics?

A
  • Hyponatraemia
  • Hypokalaemia
  • Erectile dysfunction
  • Rarely agranulocytosis
  • Rarely pancreatitis.
311
Q

in which patients should thiazide diuretics be used cautiously?

A
  • Avoid in patient with hypokalaemia and hyponatraemia
  • Avoid in patients with hypercalcaemia
  • Avoid in patients with Addison’s disease
  • Caution in patients with gout due to reduced uric acid excretion.
312
Q

with which other drugs do thiazide diuretics interact?

A
  • Diuretics

- Reduced efficacy by NSAIDs.

313
Q

what are the adverse effects of potassium sparing diuretics?

A
  • GI upset
  • Hypotension
  • Urinary symptoms
  • Electrolyte disturbances.
314
Q

in which patients should potassium sparing diuretics be used cautiously?

A
  • Avoid in severe renal impairment
  • Avoid in hyperkalaemia
  • Avoid in hypovolaemia.
315
Q

with which other drugs do potassium sparing diuretics interact?

A
  • Potassium supplements
  • Aldosterone antagonists
  • Altered renal clearance of digoxin and lithium.
316
Q

what are the adverse effects of adolesterone antagonists?

A
  • Hyperkalaemia, leading to muscle weakness, arrhythmias and cardiac arrest
  • Gynaecomastia as it acts on progesterone and oestrogen receptors
  • Stevens-Johnson syndrome (bullous skin eruption).
317
Q

in which patients should aldosterone antagonists be used cautiously?

A
  • Avoid in patients with renal impairment
  • Avoid in patients with hyperkalaemia
  • Avoid in patients with Addison’s disease (who are aldosterone deficient)
  • Avoid in pregnancy or lactating women as it can cross the placenta.
318
Q

with which other drugs do aldosterone antagonists interact?

A
  • Increased risk of hyperkalaemia with potassium-elevating drugs
  • Increased risk of hyperkalaemia with potassium supplements.
319
Q

what are the adverse effects of calcium gluconate?

A
  • Cardiovascular collapse if administered too fast

- Local tissue damage if given into subcutaneous tissue.

320
Q

what are the adverse effects of nitrates?

A
  • Flushing
  • Headaches
  • Light-headedness
  • Hypotension
  • Tolerance
  • Methaemoglobinaemia in overdose.
321
Q

in which patients should nitrates be used cautiously?

A
  • Avoid in patients with severe aortic stenosis due to risk of cardiovascular collapse
  • Avoid in patients with hypotension.
322
Q

with which drugs do nitrates interact?

A

Phosphodiesterase 5 inhibitors.

323
Q

what are the adverse effects of nicorandil?

A
  • Flushing
  • Dizziness
  • Headache
  • Nausea and Vomiting
  • Hypotension
  • Ulceration of genitals, eyes and skin.
324
Q

in which patients should nicorandil be used cautiously?

A
  • Avoid in patients with poor left ventricular function
  • Avoid in patients with hypotension
  • Avoid in patients with pulmonary oedema.
325
Q

with which drugs do nicorandil interact?

A

Enhanced hypotensive effects with phosphodiesterase 5 inhibitors.

326
Q

what are the adverse effects of digoxin?

A
  • Bradycardia
  • GI disturbance
  • Rash
  • Dizziness
  • Blurred or yellow vision
  • Digoxin toxicity causing a range of life threatening arrhythmia.
327
Q

in which patients should digoxin be used cautiously?

A
  • Avoid in heart block and arrhythmias due to worsening of conduction abnormalities
  • Caution in renal failure as digoxin is eliminated by kidneys
  • Caution in hypokalaemia, hypomagnesaemia and hypercalcaemia due to increased risk of digoxin toxicity.
328
Q

with which drugs do digoxin interact?

A
  • Loop and thiazide diuretics increase risk of digoxin toxicity due to hypokalaemia
  • Amiodarone, calcium channel blockers, spironolactone and quince all increase plasma concentration of digoxin and therefore increase toxicity.
329
Q

what are the adverse effects of class 1 antiarrhythmics?

A
  • Disopyramide causes blurred vision, dry mouth, constipation and urinary retention
  • Lidocaine causes drowsiness, disorientation and convulsions.
330
Q

in which patients should class 1 antiarrhythmics be used cautiously?

A
  • Avoid in bundle branch block
  • Avoid in AV block
  • Avoid in long QT syndrome
  • Caution in atrial flutter
  • Caution in atrial tachycardia
  • Caution in heart failure
  • Caution in myasthenia gravis
  • Caution in prostatic enlargement.
331
Q

what are the adverse effects of class 2 antiarrhythmics?

A
  • Bronchoconstriction
  • Bradycardia
  • Hypotension
  • Hypoglycaemia.
332
Q

in which patients should class 2 antiarrhythmics be used cautiously?

A
  • Avoid in asthma
  • Avoid in heart block
  • Avoid in hypotension
  • Caution in heart failure
  • Caution in COPD
  • Caution in diabetes mellitus
  • Caution in portal hypertension.
333
Q

with which drugs do class 2 antiarrhythmics interact?

A
  • Adrenaline
  • Noradrenaline
  • Amiodarone
  • Diltiazem
  • Ergometrine
  • Flecainide
  • Lidocaine
  • Propafenone
  • Verapamil.
334
Q

what are the adverse effects of amiodarone?

A
  • Torsade de pointes
  • Hypotension
  • Optic neuritis
  • Pneumonitis
  • Hepatitis
  • Photosensitivity
  • Grey discolouration
  • Hyperthyroidism due to its iodine content.
335
Q

in which patients should amiodarone be used cautiously?

A
  • Avoid in patients with severe hypotension
  • Avoid in patients with heart block
  • Avoid in patients with active thyroid disease.
336
Q

with which other drugs does amiodarone interact?

A
  • Increases plasma concentration of digoxin
  • Increases plasma concentration of diltiazem and verapamil
  • Antipsychotics, which prolong QT interval, causing torsade de pointes.
337
Q

what are the adverse effects of sotalol?

A
  • Torsade de pointes
  • Bradycardia
  • Bronchospasm
  • Fatigue
  • Headaches
  • Hyperglycaemia.
338
Q

in which patients should sotalol be used cautiously?

A
  • Avoid in asthma
  • Avoid in cardiogenic shock
  • Avoid in hypotension
  • Avoid in bradycardia
  • Caution in diabetes
  • Caution in first degree AV block.
339
Q

with which drugs does sotalol interact?

A
  • Adrenaline

- Noradrenaline

340
Q

what are the adverse effects of non-dihydropyridine CCBs?

A
  • Constipation
  • Bradycardia
  • Heart block
  • Cardiac failure
  • Hot flushes
  • Headache
  • Ankle oedema.
341
Q

in which patients should non-dihydropyridine CCBs be used cautiously?

A
  • Avoid in patient with AV nodal conduction delay in whom they may provoke complete heart block
  • Avoid in patients with unstable angina as vasodilation causes increase in contractility and tachycardia which increase oxygen demand
  • Avoid in severe aortic stenosis as they may provoke collapse.
  • Caution in patients with poor left ventricular function as they can precipitate or worsen heart failure.
342
Q

with which other drugs do non-dihydropyridine CCBs interact?

A

-beta blockers

343
Q

what are the adverse effects of anti-muscarinincs?

A
  • dry mouth
  • tachycardia
  • urinary retention
  • blurred vision
  • drowsiness
  • confusion.
344
Q

in which patients should anti-muscarinics be used cautiously?

A
  • angle-closure glaucoma

- Caution with arrhythmias

345
Q

with which other drugs do anti-muscarinics interact?

A

-TCAs

346
Q

what are the adverse effects of adenosine?

A
  • Bradycardia and asystole
  • Sinking feeling in chest accompanied by breathlessness and a sense of impending doom
  • Bronchospasm
347
Q

in which patients should adenosine be used cautiously?

A
  • Avoid in hypotension
  • Avoid in coronary ischaemia
  • Avoid in decompensated heart failure
  • Avoid in asthma
  • Caution in COPD
  • Caution in patients who have had a heart transplant.
348
Q

with which other drugs does adenosine interact?

A
  • Dipyridamole blocks cellular uptake of adenosine which prolongs and potentiates its effect
  • Theophylline is a competitive antagonist of adenosine receptors and reduce its effect.
349
Q

what are the adverse effects of statins?

A
  • Headache
  • GI disturbances
  • Muscle ache
  • Myopathy
  • Rhabdomyolysis
  • Rise in ALT.
350
Q

in which patients should statins be used cautiously?

A
  • Caution in hepatic impairment
  • Caution in renal impairment
  • Avoid in pregnancy or with breastfeeding.
351
Q

with which drugs do statins interact?

A

-Reduced metabolism by cytochrome P450 inhibitors such as amiodarone, diltiazem, fluconazole, macrolides.

352
Q

what are the adverse effects of aspirin?

A
  • GI irritation, ulceration and haemorrhage
  • Hypersensitivity reactions including bronchospasm due to overproduction of leukotrienes
  • Tinnitus
353
Q

in which patients should aspirin be used cautiously?

A
  • Avoid in children under 16 years due to risk of Reye’s syndrome
  • Avoid in aspirin hypersensitivity
  • Avoid in third trimester of pregnancy where prostaglandin inhibition may lead to premature closure of ductus arteriosus
  • Caution with peptic ulceration
  • Caution with gout.
354
Q

with which drugs do aspirin interact?

A

Increased risk of bleeding with other anti platelets agents and anticoagulants.

355
Q

what are the adverse effects of clopidogrel?

A
  • Bleeding
  • GI upset including dyspepsia, pain and diarrhoea
  • Thrombocytopenia.
356
Q

in which patients should clopidogrel be used cautiously?

A
  • Avoid in active bleeding
  • Stop 7 days before elective surgery
  • Caution in patients with renal and hepatic impairment.
357
Q

with which other drugs does clopidogrel interact?

A
  • Reduced efficacy with P450 inhibitors including omeprazole, quinolones, erythromycin, antifungals, SSRIs
  • Increased risk of bleeding with anti platelets, anticoagulants or NSAIDs.
358
Q

what are the adverse effects of dipyradimole?

A
  • Headache
  • Flushing
  • Dizziness
  • GI symptoms
  • Increased risk of bleeding
  • Thrombocytopenia.
359
Q

in which patients should dipyradimole be used cautiously?

A
  • Caution in patients with ischaemic heart disease
  • Caution in aortic stenosis
  • Caution in heart failure.
360
Q

with which drugs does dipyradimole interact?

A
  • Increased risk of cardiac arrest with adenosine as it inhibits cellular uptake of adenosine
  • Increased risk of bleeding with anti-platelets and anticoagulants.
361
Q

what are the adverse effects of LMWH?

A
  • Bleeding
  • Injection site reactions
  • Thrombocytopenia.
362
Q

in which patients should LMWH be used with caution?

A
  • Caution with clotting disorders
  • Caution with severe uncontrolled hypertension and renal impairment
  • Caution after surgery or trauma
363
Q

what are the adverse effects of warfarin?

A
  • Bleeding especially in genetically susceptible individuals who have lower CYP2C9 activity
  • Skin necrosis
  • Blue-toe syndrome
  • Liver dysfunction.
364
Q

in which patients should warfarin be used cautiously?

A
  • Avoid in patients at immediate risk of haemorrhage
  • Avoid in pregnancy as it causes fetal malformations
  • Caution in liver disease where patients are less able to metabolise drug and are at risk of over-anticoagulation/bleeding.
365
Q

which factors increase the effect of warfarin?

A
  • drugs that inhibit hepatic drug metabolism (macrolides and azoles)
  • drugs that inhibit the reduction f vitamin K (cephalosporins)
  • drugs that suppress intestinal flora that synthesise vitamin K sulphonamides)
  • drugs that interfere with platelet function
  • liver disease
366
Q

which factors lessen the effect of warfarin?

A
  • drugs that induce hepatic metabolism (aminoglycosides)
  • vitamin K
  • drugs that reduce absorption (cholestyramine)
  • pregnancy
367
Q

what are the adverse effects of factor 2a inhibitors?

A
  • Abnormal hepatic function
  • Haemorrhage
  • Anaemia
  • Gastrointestinal disorders.
368
Q

in which patients should factor 2a inhibitors be used cautiously?

A
  • Avoid with active bleeding
  • Avoid with antiphospholipid syndrome
  • Avoid with prosthetic heart valves
  • Avoid with malignancy
  • Avoid with oesophageal varices
  • Avoid with recent surgery
  • Avoid with peptic ulcer.
369
Q

with which drugs do factor 2a inhibitors interact?

A
  • Carbamazepine
  • Dronaderone
  • Ritonavir
  • St John’s Wart
  • Triazole antifungals.
370
Q

what are the adverse effects of factor Xa inhibitors?

A
  • Haemorrhage
  • Anaemia
  • GI disturbances
  • Headache
  • Hypotension.
371
Q

in which patients should factor Xa inhibitors be used cautiously?

A
  • Avoid with active bleeding
  • Avoid with antiphospholipid syndrome
  • Avoid with prosthetic heart valves
  • Avoid with malignancy
  • Avoid with oesophageal varices
  • Avoid with recent surgery
  • Avoid with peptic ulcer.
372
Q

with which drugs do factor Xa inhibitors interact?

A
  • Carbamazepine
  • Dronaderone
  • Ritonavir
  • St John’s Wart
  • Triazole antifungals.
373
Q

what are the adverse effects of fibrinolytic agents?

A
  • Nausea and Vomiting
  • Bruising at injection site
  • Hypotension
  • Serious bleeding
  • Allergic reaction
  • Cardiogenic shock
  • Cardiac arrest
  • Cerebral oedema
  • Arrhythmias.
374
Q

in which patients should fibrinolytic agents be used cautiously?

A
  • Avoid with recent haemorrhage, trauma or surgery
  • Avoid streptokinase with previous streptokinase treatment as antibodies develop and block its action
  • Intracranial haemorrhage must be excluded with CT.
375
Q

with which drugs do fibrinolytic agents interact?

A
  • Increased risk of haemorrhage with anticoagulants and anti platelet agents
  • Increased risk of anaphylactoid reactions with ACE inhibitors.
376
Q

what are the adverse effects of endothelin receptor antagonists?

A
  • Headaches and flushing
  • Nausea and vomiting
  • Epistaxis and nasal congestion
  • Rarely hepatic disorders and sudden hearing loss.
377
Q

in which patients should endothelin receptor antagonists be used cautiously?

A
  • Avoid in idiopathic pulmonary fibrosis

- Caution in anaemia.

378
Q

what are the adverse effects of adrenaline?

A
  • Hypertension
  • Anxiety
  • Tremor
  • Headache
  • Palpitations
  • Angina
  • Myocardial infarction
  • Arrhythmias.
379
Q

in which patients should adrenaline be given cautiously?

A

-Caution in patients with heart disease

380
Q

with which drugs does adrenaline interact?

A
  • Widespread vasoconstriction with a beta blocker because its vasoconstriction effect is not opposed by β2-mediated vasodilation
  • MAOIs such as phenelzine and tranylcypromine increase risk of hypertensive crisis.
381
Q

what are the adverse effects of dopamine?

A
  • Arrhythmia
  • Tachycardia
  • Anxiety
  • Angina pectoris
  • Tremor
  • Vasoconstriction
  • Vomiting.
382
Q

in which patients should dopamine be used cautiously?

A
  • Avoid with phaeochromocytoma
  • Avoid in with tachyarrhythmia
  • Caution with hypovolaemia
  • Caution with hypertension
  • Caution with hyperthyroidism.
383
Q

what are the adverse of noradrenaline?

A
  • Arrhythmia
  • Hypertension
  • Peripheral ischaemia
  • Dyspnoea
  • Extravastation necrosis
  • Headache
  • Peripheral ischaemia.
384
Q

with which drugs does noradrenaline interact?

A
  • Beta blocker
  • TCA
  • MAO inhibitors.

FINALS (18 decks)

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