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Cardiology Flashcards

1
Q

What are the five big risk factors for the development of cardiovascular disease?

A 
Hypertension. 
Smoking. 
Diabetes mellitus. 
Hypercholesterolaemia. 
Family history.
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2
Q

What is bradycardia?

A

HR < 60bpm

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3
Q

What is tachycardia?

A

HR > 100bpm

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4
Q

ECG interpretation: Presence of P waves.

A

Sinus rhythm.

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5
Q

ECG interpretation: Absence of P waves.

A

Atrial fibrillation.

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6
Q

ECG interpretation: PR interval constant, < 0.2s.

A

No heart block.

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7
Q

ECG interpretation: PR interval constant, > 0.2s.

A

First degree heart block.

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8
Q

ECG interpretation: PR interval increasing, then dropped QRS.

A

Second degree heart block (type 1 / Wenckebach).

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9
Q

ECG interpretation: PR interval constant, then dropped QRS.

A

Second degree heart block (type 2).

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10
Q

ECG interpretation: PR interval random, P waves not associated with QRS.

A

Third degree heart block (complete heart block).

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11
Q

ECG interpretation: QRS < 0.12s.

A

No bundle branch block.

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12
Q

ECG interpretation: QRS > 0.12s.

A

Broad complex.

Bundle branch block.

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13
Q

ECG interpretation: QRS > 0.12s, V1 first deflection down, V6 first deflection up.

A

Left bundle branch block.

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14
Q

ECG interpretation: QRS > 0.12s, V1 first deflection up, V6 first deflection down.

A

Right bundle branch block.

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15
Q

ECG interpretation: ST segment elevated.

A

Infarction.

Pericarditis.

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16
Q

ECG interpretation: ST segment depressed.

A

Ischaemia.
Infarction.
Digoxin treatment.

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17
Q

ECG interpretation: T wave height > two-thirds of QRS height.

A

Hyperkalaemia.

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18
Q

ECG interpretation: T wave inversion.

A

Normal in aVR and V1.
Old infarction.
Left ventricular hypertrophy.

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19
Q

ECG: Which leads have T wave inversion normally?

A

aVR.

V1.

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20
Q

Define atherosclerosis.

A

Plaque accumulation in the arteries of the body.

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21
Q

Describe the mechanism of action of statins.

A

Inhibit the action of HMG-CoA reductase (enzyme in hepatic cholesterol synthesis).

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22
Q

Who should receive a statin?

A

Established cardiovascular disease.

QRISK3 > 10%.

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23
Q

What time of day should patients take a statin?

A

At night (this is when the majority of cholesterol synthesis takes place).

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24
Q

What dose of atorvastatin is used in primary prevention and secondary prevention of cardiovascular disease?

A

Primary - 20mg.

Secondary - 80mg.

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25
Q

How should statin use be managed in pregnancy?

A

Pregnancy is a contraindication to statin use - stop three months before attempting pregnancy.

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26
Q

Define stage 1 hypertension.

A

Clinic blood pressure ≥ 140/90 mmHg.

24hr ABPM average ≥ 135/85 mmHg.

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27
Q

Define stage 2 hypertension.

A

Clinic blood pressure ≥ 160/100 mmHg.

24hr ABPM average ≥ 150/95 mmHg.

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28
Q

Define severe hypertension.

A

Clinic systolic blood pressure ≥ 180 mmHg.

Clinic diastolic blood pressure ≥ 120 mmHg.

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29
Q

What is the difference between primary and secondary hypertension?

A

Primary develops due to complex physiological changes associated with ageing.
Secondary develops as a result of endocrine disease, renal disease, pharmacotherapy (inc. COCP) and pregnancy.

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30
Q

How does hypertension present?

A

Asymptomatic in most cases unless blood pressure is very high.

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31
Q

At what blood pressure do people develop symptoms of hypertension and what are they?

A

≥ 200/120 mmHg including headaches, visual disturbances and seizures.

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32
Q

What is ambulatory blood pressure monitoring?

A

A system that records blood pressure periodically (twice and hour) over a 24hr period - the preferred method for diagnosing hypertension.

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33
Q

It is important to assess someone with newly diagnosed hypertension for end-organ damage. What investigations should be performed?

A 
Fundoscopy (hypertensive retinopathy). 
Urine dipstick (renal disease). 
Urea and electrolytes (renal disease). 
HbA1c (diabetes mellitus).
ECG (LVH, IHD).
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34
Q

What lifestyle changes can be advised for people with hypertension?

A

Improving diet, more physical exercise, losing weight and stopping smoking.

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35
Q

When should pharmacological therapy begin in the management of hypertension?

A

If lifestyle measures fail to control blood pressure and there is evidence of end-organ damage or a QRISK3 of ≥ 10%.

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36
Q

What is first-line pharmacological therapy for hypertension in those under 55 or with T2DM?

A

Angiotensin-converting enzyme inhibitors such as ramipril.

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37
Q

Hypertension: What are side effects of ramipril / ACEi use?

A

Cough, angioedema and hyperkalaemia.

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38
Q

Hypertension: What pharmacological therapy should be used in those aged under 55 or with T2DM if ACEi cannot be tolerated?

A

Angiotensin 2 receptor blockers such as candesartan.

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39
Q

Hypertension: What are side effects of candesartan / ARB use?

A

Hyperkalaemia.

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40
Q

Hypertension: What monitoring is required in the use of ACE inhibitors?

A

Check urea and electrolytes before treatment and one-to-two weeks after starting. As well as after increasing dose.

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41
Q

Hypertension and ACEi: What changes in U&Es should be expected / acceptable?

A

Rise in serum creatinine, acceptable up to 30% from baseline.
Rise in serum potassium, acceptable up to 5.5mmol/l.

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42
Q

What is first-line pharmacological therapy for hypertension in those over 55 without T2DM, or those of Afro-Caribbean heritage with no diabetes mellitus?

A

Calcium channel blockers such as amlodipine.

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43
Q

Hypertension: What are side effects of amlodipine / CCB use?

A

Flushing, ankle swelling and headache.

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44
Q

What is the blood pressure target for people receiving pharmacological therapy?

A

< 80yrs: < 140/90mmHg.

> 80yrs: < 150/90mmHg.

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45
Q

Hypertension: What is second-line pharmacological therapy if first-line fails to control BP?

A

Add a thiazide-like diuretic (indapamide) or ACEi/ARB depending on the pathways.

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46
Q

Hypertension: What are side-effects of thiazide-like diuretic use?

A

Hyponatraemia, hypokalaemia and dehydration.

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47
Q

Hypertension: What is third-line therapy is second-line fails to control BP.

A

Three medications: ACEi/ARB + CCB + thiazide-like diuretic.

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48
Q

Hypertension: What is fourth-line therapy if BP still uncontrolled on triple therapy?

A

If potassium ≤ 4.5 add low-dose spironolactone.

If potassium > 4.5 add alpha-blocker or beta-blocker.

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49
Q

What is malignant hypertension?

A

Severe hypertension (≥180/120mmHg) with symptoms of acute organ injury such as papilloedema, retinal bleeding, headache + nausea, chest pain, haematuria and epistaxis.

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50
Q

Define orthostatic/postural hypotension.

A

Drop in blood pressure > 20/10mmHg within three minutes of standing.

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51
Q

What groups are at risk of orthostatic/postural hypotension?

A

Older people.
Neurodegenerative disease.
Diabetes.
Hypertension.

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52
Q

What are clinical features of orthostatic hypotension?

A

Presyncope (feeling faint) and syncope.

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53
Q

What is the management of orthostatic hypotension?

A

Midodrine (alpha1 agonist).

Fludrocortisone (corticosteroid).

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54
Q

What are the four Ds of postural hypotension with compensatory tachycardia?

A

Deconditioning.
Dysfunctional heart (aortic stenosis).
Dehydration (disease, dialysis, drugs).
Drugs (levodopa, tamsulosin, etc.).

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55
Q

What is angina?

A

Chest pain that usually occurs due to insufficient blood flow to the myocardium (a result of coronary artery narrowing).

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56
Q

What is stable angina?

A

Chest pain that occurs during periods of stress (exercise) when the myocardium becomes ischaemic because oxygen supply cannot meet demand.

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57
Q

What relieves the chest pain associated with stable angina?

A

Rest or GTN spray.

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58
Q

What pharmacotherapy should patients with stable angina receive for immediate symptomatic relief?

A

Sublingual glyceryl trinitrate (GTN) spray PRN.

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59
Q

Stable angina: How often can a patient use a GTN spray during an angina attack?

A

Every 5 minutes. If ongoing for ten minutes call 999.

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60
Q

What pharmacological therapy is given for long-term symptomatic relief of stable angina?

A

Beta-blocker (atenolol) or calcium channel blocker (verapamil, diltiazem).
Or could try long-acting dihydropyridine calcium channel blocker (MR nifedipine).

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61
Q

What pharmacological therapy is offered for long-term symptomatic relief to those suffering from stable angina not controlled on a BB or CCB?

A

Long-acting nitrate (isosorbide mononitrate).

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62
Q

What pharmacological therapy is given for secondary prevention of cardiovascular disease in stable angina?

A

Aspirin 75mg.
Statin 80mg.
ACE inhibitor.

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63
Q

Stable angina management: How should standard-release isosorbide mononitrate be taken?

A

Asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours… to minimise the development of nitrate tolerance.

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64
Q

Stable angina management: What is an alternative to standard-release isosorbide mononitrate that reduces the risk of tolerance developing?

A

Once-daily modified release isosorbide mononitrate.

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65
Q

What is the gold-standard investigation for stable angina?

A

CT coronary angiography reveals stenosed (narrowed) coronary arteries.

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66
Q

What surgical interventions can be offered in the management of stable angina?

A

Percutaneous coronary intervention (PCI).

Coronary artery bypass graft (CABG).

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67
Q

Stable angina: Describe the process of percutaneous coronary intervention.

A

A catheter is inserted into the brachial or femoral artery and guided to the coronary arteries using fluoroscopy… it then involves dilating the blood vessel with a balloon and/or inserting a stent.

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68
Q

Stable angina: Describe the process of coronary artery bypass graft.

A

It involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patients leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis.

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69
Q

Describe the recovery time of CABG vs PCI.

A

CABG have longer recovery and greater complication than PCI.

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70
Q

What is acute coronary syndrome?

A

An umbrella term covering a number of acute presentations in medicine that includes ST-elevation myocardial infarction, non-ST elevation myocardial infarction and unstable angina. The conditions usually result from occlusion of a coronary artery by a thrombus from an atherosclerotic plaque.

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71
Q

What mainly forms a thrombus in arteries?

A

Platelet activation.

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72
Q

What is the most common presenting feature of acute coronary syndrome?

A

Chest pain.

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73
Q

Describe the chest pain associated with acute coronary syndrome.

A

Central/left-sided, may radiate to the jaw or left arm, described as heavy or constricting.

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74
Q

What are clinical features of acute coronary syndrome other than chest pain?

A

Dyspnoea, sweating, nausea and vomiting, pallor and clamminess.

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75
Q

What is the mainstay of investigation in ACS?

A

Twelve-lead ECG.

Serial troponins.

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76
Q

What are troponins?

A

Proteins found in cardiac muscle that are released as a result of myocardial ischaemia.

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77
Q

What is meant by ‘serial’ troponins?

A

Troponins monitored at baseline, six hours and twelve hours after the onset of symptoms.

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78
Q

Are troponins specific for ACS?

A

No - they are also raised in renal failure, sepsis, myocarditis, aortic dissection and pulmonary embolism.

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79
Q

What is the management of all patients with ACS?

A 
Morphine (severe pain only). 
Oxygen (sats < 94% only). 
Nitrates. 
Aspirin 300mg. 
Remember: MONA.
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80
Q

How is STEMI diagnosed?

A

ST elevation or new left bundle branch block on ECG.

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81
Q

How is NSTEMI diagnosed?

A

Raised troponins and/or ST depression, T wave inversion, pathological Q waves.

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82
Q

ACS: What is the diagnosis if troponins are normal and there are no pathological ECG changes?

A

Unstable angina or musculoskeletal pain.

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83
Q

What risk assessment tool can inform the management of ACS?

A

GRACE (Global Registry of Acute Coronary Events).

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84
Q

What GRACE score indicates that patients with ACS should receive coronary angiography within 72 hours?

A

> 3%

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85
Q

What pharmacological therapy is given for acute NSTEMI?

A 
Beta-blocker. 
Aspirin. 
Ticagrelor. 
Morphine. 
Anticoagulant (fondaparinux). 
Nitrates (GTN). 
Remember: BATMAN
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86
Q

Acute NSTEMI management: What alternative can be given to ticagrelor and under what circumstances?

A

Clopidogrel is given in those with a high bleeding risk (i.e. taking an oral anticoagulant).

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87
Q

What is the mechanism of action of fondaparinux?

A

Fondaparinux activates antithrombin III which potentiates the inhibition of coagulation factor Xa.

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88
Q

An anterolateral STEMI will result in ECG changes in which leads?

A

I
aVL
V3-V6

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89
Q

An anterolateral STEMI is associated with occlusion of which coronary artery?

A

Left coronary artery.

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90
Q

An anterior STEMI will result in ECG changes in which leads?

A

V1-V4

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91
Q

An anterior STEMI is associated with occlusion of which coronary artery?

A

Left anterior descending artery.

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92
Q

A lateral STEMI will result in ECG changes in which leads?

A

I
aVL
V5-V6

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93
Q

A lateral STEMI is associated with occlusion of which coronary artery?

A

Left circumflex artery.

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94
Q

An inferior STEMI will result in ECG changes in which leads?

A

II
III
aVF

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95
Q

An inferior STEMI is associated with occlusion of which coronary artery?

A

Right coronary artery.

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96
Q

What is the management of acute STEMI?

A

Percutaneous coronary intervention.

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97
Q

Which patients with acute STEMI should receive percutaneous coronary intervention?

A

Those presenting within twelve hours of symptom onset and if PCI is available within two hours.

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98
Q

Acute STEMI: What is the pharmacological management if PCI is planned?

A

Give dual anti platelet (aspirin + ticagrelor).

Or if at high bleeding risk - clopidogrel.

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99
Q

Acute STEMI: What is the management if PCI unavailable?

A

Thrombolysis (tenecteplase).

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100
Q

How should acute STEMI be monitored following thrombolysis?

A

Aim for 50% resolution in ST elevation on ECG after 90 minutes.

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101
Q

What is secondary prevention pharmacological management following acute STEMI.

A 
Dual-antiplatelet (aspirin, ticagrelor). 
ACEi (ramipril). 
Beta-blocker (bisoprolol). 
Statin (atorvastatin). 
Remember: DABS.
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102
Q

Give six examples of complications resulting from myocardial infarction.

A 
Death. 
Mitral regurgitation. 
Heart failure. 
Arrhythmia. 
Aneurysm. 
Dressler's syndrome.

Remember: DREAD

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103
Q

What memory aid can be used to remember the complications of MI?

A

DREAD.

Death, rupture of heart septum or papillary muscles, oEdema, aneurysm + arrhythmia, Dressler’s syndrome.

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104
Q

Describe the pathophysiology of mitral regurgitation post-MI.

A

Rupture of papillary muscles following infero-posterior myocardial infarction.

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105
Q

Describe the pathophysiology of Dressler’s syndrome post-MI.

A

Localised immune réponse which results in pericarditis two-three weeks post-MI.

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106
Q

What is the presentation of Dressler’s syndrome?

A

Pleuritic chest pain and low grade fever. 2-3 weeks post-MI.

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107
Q

What is heard on auscultation in Dressler’s syndrome?

A

Pericardial rub.

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108
Q

How is a diagnosis of Dressler’s syndrome made?

A 
ECG (global ST elevation, T wave inversion). 
Echocardiogram (pericardial effusion). 
Inflammatory markers (raised CRP, ESR).
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109
Q

What is the management of Dressler’s syndrome?

A

NSAIDs.
If more severe:
Steroids
Pericardiocentesis.

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110
Q

What is bundle branch block?

A

A complete or partial interruption of the electrical pathways inside the wall of the heart between the ventricles.

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111
Q

Describe the pathophysiology of right bundle branch block (RBBB).

A

Delayed electrical conduction to the right ventricle - the right ventricle contracts later and the heart ejects less blood.

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112
Q

What is the cause of RBBB?

A

Often a normal variant… the result of natural degeneration of the conduction system that occurs with age. Can be the result of PE, COPD, cardiomyopathy or heart defect.

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113
Q

What does ECG reveal in RBBB?

A

Widening of the QRS complex (> 0.12s) and a notched morphology of the QRS complex. V1 first deflection up, M morphology. V6 first deflection down, W morphology.

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114
Q

What is the cause of LBBB?

A

Underlying heart disease including myocardial infarction.

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115
Q

What does ECG reveal in LBBB?

A

Widening of the QRS complex (> 0.12s) and a notched morphology of the QRS complex. V1 first deflection down, W morphology. V6 first deflection up, M morphology.

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116
Q

Define heart block.

A

Interruption or delay of electrical conduction in the heart.

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117
Q

How is heart block classified?

A

Where the block occurs: sinoatrial node, atrioventricular node, at/below the bundle of His.

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118
Q

Describe sinoatrial node block.

A

Electrical impulse is delayed or blocked and atrial depolarisation is delayed.

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119
Q

Explain why sinoatrial node block rarely causes severe symptoms.

A

Secondary pacemaker (the atrioventricular node) stimulates a rate of 40-60bpm which is sufficient to retain consciousness in the resting state.

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120
Q

Describe atrioventricular node block.

A

Electrical impulse is delayed or blocked and ventricular depolarisation is delayed or completely blocked.

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121
Q

What are the three types of atrioventricular block?

A

First-degree.
Second-degree (type 1 and 2).
Third-degree.

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122
Q

Describe first-degree AV heart block.

A

Delay, but not disruption, as the electrical signal moves between the atrium and the ventricles through the atrioventricular node.
PR interval > 0.2s on ECG. No dropped or skipped beats.

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123
Q

Describe second-degree AV heart block (type 1 / Wenckebach).

A

Impairment of electrical conduction between the atria and ventricles that results in a failure to conduct an impulse, causing a skipped beat.
Progressive prolongation of PR interval, with resulting dropped beat.

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124
Q

Describe second-degree AV heart block (type 2).

A

Impairment of electrical conduction between the atria and ventricles that results in a failure to conduct an impulse, causing a sudden, unexpected dropped beat.
PR interval is unchanged from beat to beat, with a random skipped beat.

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125
Q

Describe third-degree AV heart block (complete).

A

Complete impairment of conduction between the atria and ventricles.
There is no relationship between P waves and QRS complexes.

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126
Q

What rate do the ventricles contract in complete AV heart block?

A

Ventricles produce their own signal to control rate at approx. 30-40 bpm.

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127
Q

What is the management of second-degree (type 2) and third-degree heart block?

A

Atropine 500 micrograms IV.
Repeat atropine up to 6 times (total 3mg).
Consider noradrenaline.
Consider transcutaneous cardiac pacing.

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128
Q

What is a pacemaker?

A

A device that delivers controlled electrical impulses to specific areas of the heart to restore the normal electrical activity and improve heart function.

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129
Q

What two components make up a pacemaker?

A

A pulse generator.

Pacing leads.

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130
Q

What are three different types of pacemaker?

A

Single-lead chamber pacemaker.
Dual-chamber pacemaker.
Biventricular (triple-chamber) pacemaker.

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131
Q

Describe single-lead chamber pacemaker.

A

Leads in a single chamber - either the right atrium or right ventricle.

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132
Q

Describe dual-chamber pacemaker.

A

Leads in both the right atrium and right ventricle.

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133
Q

Describe biventricular (triple-chamber) pacemakers.

A

Leads in the right atrium, right ventricle and left ventricle.

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134
Q

How can you identify a pacemaker on ECG?

A

Sharp vertical line in all leads either before the P wave (if the lead is in the atria) and/or before the QRS complex (if the lead is in the ventricle).

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135
Q

What is heart failure?

A

Heart is unable to pump sufficiently to maintain blood flow to meet the body’s needs.

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136
Q

What is the clinical presentation of heart failure?

A

Shortness of breath (worse with exercise or lying down), fatigue, peripheral oedema.

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137
Q

What are examination findings in heart failure?

A

Cyanosis, tachycardia, elevated JVP.

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138
Q

What is acute heart failure?

A

Sudden onset or worsening of the symptoms of heart failure.

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139
Q

What are the two types of acute heart failure?

A

De novo acute heart failure (no past history of HF).

Decompensated acute heart failure (background history of HF).

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140
Q

How does right-sided heart failure classically present and why?

A

Peripheral oedema, ascites, hepatosplenomegaly as a result of blood backing up into the systemic circulation.

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141
Q

How does acute left ventricular failure classically present and why?

A

Shortness of breath, productive cough (frothy/pink sputum) as a result of pulmonary oedema.

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142
Q

What are examination findings in acute left ventricular failure?

A

Oxygen desaturation, tachypnoea, tachycardia and bilateral basal crackles on auscultation.

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143
Q

What clinical features may be present in acute left ventricular failure due to underlying cause?

A 
Chest pain (MI). 
Fever/cough (viral infection).
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144
Q

What hormone is useful in the investigation of heart failure?

A

N-terminal pro-B-type natriuretic peptide (NT-proBNP).

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145
Q

Describe the physiological function of NT-proBNP.

A

Hormone produced by the left ventricular myocardium in response to strain. BNP is a vasodilator and diuretic white attempts to reduce strain on the heart.

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146
Q

HF: Interpret raised levels (> 400 ng/L) of NT-proBNP.

A

Supportive of diagnosis of heart failure and indicate further investigation.

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147
Q

HF: Interpret very high levels (> 2000 ng/L) of NT-proBNP.

A

Poor prognosis and requires urgent treatment.

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148
Q

Describe the sensitivity and specificity of NT-proBNP.

A

Sensitive but not specific (raised in renal impairment, tachycardia, pulmonary embolism, COPD).

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149
Q

What are findings on CXR in patients with left ventricular failure?

A 
Alveolar oedema ('bat wings'). 
Kerley B lines. 
Cardiomegaly. 
Dilated upper lobe. 
Pleural effusions. 
Remember ABCDE.
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150
Q

Other than NT-proBNP and CXR… what imaging investigation may be performed in LVF?

A

Echocardiogram.

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151
Q

Echocardiogram: What is normal ejection fraction?

A

50-70%.

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152
Q

Echocardiogram: What is reduced ejection fraction?

A

< 40%.

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153
Q

What is the management of acute left ventricular failure?

A

Stop intravenous fluids.
Sit the patient up.
Give oxygen.
Intravenous loop diuretics (40mg furosemide).

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154
Q

Why does sitting a patient upright improve their symptoms in left ventricular failure?

A

Upright fluid will cover a smaller surface area of lung making the upper zones clear for more efficient gas exchange.

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155
Q

What is chronic heart failure?

A

Impaired left ventricular contraction or left ventricular relaxation that leads to chronic back-pressure of blood trying to flow into and through the left side of the heart.

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156
Q

What are five characteristic clinical features of chronic heart failure?

A 
Shortness of breath worse on exertion. 
Cough. 
Orthopnoea.
Peripheral oedema. 
Paroxysmal nocturnal dyspnoea.
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157
Q

Define orthopnoea.

A

Difficulty breathing when lying down.

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158
Q

What is paroxysmal nocturnal dyspnoea?

A

Episodes of waking at night with a severe attack of shortness of breath and cough. Patients describe feeling suffocated.

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159
Q

Describe the potential mechanisms behind the development of paroxysmal nocturnal dyspnoea.

A

Fluid settles across a larger surface area of the lung when laid flat.
Less responsive respiratory centre during sleep leads to reduced respiratory rate and work of breathing = hypoxia.
Less adrenaline in sleep, myocardium more relaxed = worse cardiac output.

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160
Q

Describe Class I of the New York Heart Association (NYHA) heart failure classification.

A

No symptoms, no limitation.

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161
Q

Describe Class II of the NYHA heart failure classification.

A

Mild symptoms, ordinary physical activity causes breathlessness.

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162
Q

Describe Class III of the NYHA heart failure classification.

A

Moderate symptoms, less than ordinary activity causes breathlessness.

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163
Q

Describe Class IV of the NYHA heart failure classification.

A

Severe symptoms, breathless at rest, increased discomfort with physical activity.

164
Q

Give four examples of causes of chronic heart failure.

A

Ischaemic heart disease.
Valvular heart disease (aortic stenosis).
Hypertension.
Arrhythmias (e.g. AF).

165
Q

What is first-line pharmacological therapy for the treatment of chronic heart failure?

A 
ACE inhibitor (ramipril). 
Beta-blocker (bisoprolol).
166
Q

What is second-line pharmacological therapy for chronic heart failure?

A

Aldosterone antagonist (spironolactone / eplerenone).

167
Q

What pharmacological therapy can be given in chronic heart failure to improve symptoms (but has no effect on mortality)?

A

Furosemide (loop diuretic).

168
Q

What positively inotropic agent can be prescribed in chronic heart failure?

A

Digoxin.

169
Q

What is digoxin and its function?

A

A cardiac glycoside that increases the force of myocardial contraction and reduces conductivity within the AV node.

170
Q

What are clinical features of digoxin toxicity?

A

Anorexia, nausea, vomiting, diarrhoea, malaise, weakness, palpitations, syncope, confusion, hallucinations, blurred vision and arrhythmias.

171
Q

What investigation can be performed in suspected digoxin toxicity?

A

Plasma digoxin concentration - must be measured at least six hours after the last dose of digoxin.

172
Q

Under what circumstances should digoxin dose be reduced?

A

Renal dysfunction (digoxin is renally excreted).

173
Q

What is cor pulmonale?

A

Right-sided heart failure caused by respiratory disease.

174
Q

Describe the pathophysiology of cor pulmonale.

A

Increased pressure and resistance to blood flow in the pulmonary arteries (pulmonary hypertension) results in right ventricular strain.

175
Q

Give five causes of cor pulmonale.

A

COPD, pulmonary embolism, interstitial lung disease, cystic fibrosis and primary pulmonary hypertension.

176
Q

What are the clinical features of bradycardia with haemodynamic compromise?

A

Shock (hypotension, pallor, sweating, clammy extremities, confusion / impaired consciousness), syncope.

177
Q

What is the first-line pharmacological treatment of bradycardia with haemodynamic compromise?

A

Atropine 500 microgram intravenously (repeat up to 6 times, max. 3mg).

178
Q

Describe the mechanism of action of atropine.

A

Antimuscarinic which inhibits the parasympathetic nervous system.

179
Q

What are side effects of atropine use.

A

Pupil dilation, urinary retention, dry eyes, constipation.

180
Q

Give three causes of narrow complex tachyarrhythmias.

A

Atrial fibrillation.
Atrial flutter.
Supraventricular tachycardia.

181
Q

Give two causes of broad complex tachyarrhythmias.

A

Ventricular tachycardia.

SVT with bundle branch block.

182
Q

What is atrial flutter?

A

A form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves due to a re-entrant rhythm.

183
Q

What is the clinical presentation of atrial flutter?

A

Palpitations, light-headedness and shortness of breath.

184
Q

What does ECG reveal in atrial flutter?

A

Narrow complex (< 0.12s), regular tachycardia with ‘sawtooth appearance’.

185
Q

What is the atrial rate in atrial flutter?

A

Often 300bpm.

186
Q

What determines the ventricular rate in atrial flutter (and what is most common)?

A

The degree of AV node block determines the rate. A 2:1 block is most common… resulting in a ventricular rate of 150bpm.

187
Q

What is a supraventricular tachycardia (SVT)?

A

Result of an electrical signal re-entering the atria from the ventricles (tachycardia isn’t ventricular in origin). It is a self-perpetuating loop without an end point.

188
Q

What is the clinical presentation of SVT?

A

Palpitations, light-headedness.

189
Q

What does ECG reveal in SVT?

A

Narrow complex (< 0.12s) tachycardia.

190
Q

What is the first-line management of SVT?

A

Vagal manoeuvres (such as Valsalva or carotid sinus massage).

191
Q

What is second-line management of SVT (after Vagal manoeuvres)?

A

Intravenous 6mg adenosine (or verapamil in asthmatics).

192
Q

Describe the mechanism behind Vagal manoeuvres.

A

They stimulate the parasympathetic nervous system by acting the vagus nerves (stimulating lower heart rate).

193
Q

What are the three main types of SVT?

A

Atrioventricular nodal re-entrant tachycardia (through AV node).
Atrioventricular re-entrant tachycardia (through accessory pathway).
Atrial tachycardia.

194
Q

What is the mechanism of adenosine?

A

Adenosine slows cardiac conduction through the atrioventricular node to reset back to sinus rhythm.

195
Q

How should adenosine be given for management of SVT?

A

6mg as a rapid bolus via a large proximal (antecubital fossa) cannula.

196
Q

What should patients be warned of before giving adenosine?

A

Adenosine can cause a brief period of asystole or bradycardia… warn them they may feel a sense of “impending doom” // dying.

197
Q

What is paroxysmal supraventricular tachycardia?

A

A situation where SVT reoccurs and remits in the same patient over time.

198
Q

What is the long-term management of Paroxysmal supraventricular tachycardia?

A

Beta-blockers, calcium channel blockers, amiodarone.

Radiofrequency ablation.

199
Q

What is Wolff-Parkinson-White (WPW) syndrome?

A

WPW is a condition caused by the presence of a congenital accessory pathway that connects the atria and ventricles (called the Bundle of Kent).

200
Q

What does ECG reveal in Wolff-Parkinson-White syndrome?

A

Delta wave.
QRS prolongation.
Shortened PR interval.

201
Q

ECG: What is a delta wave?

A

Slurred upstroke of QRS (slow rise in the initial part of the QRS complex).

202
Q

What is definitive treatment of Wolff-Parkinson-White syndrome?

A

Radiofrequency ablation.

203
Q

Describe the process of radiofrequency ablation.

A

A catheter is inserted into the femoral veins along with a wire which is guided to the heart under fluoroscopy. The wire is placed against different areas to test the electrical signals… once an abnormal pathway is identified radifrequency ablation is applied to burn the abnormal area (scar tissue doesn’t conduct electricity).

204
Q

What is atrial fibrillation (AF)?

A

A chaotic, irregular atrial tachyarrhythmia that is characterised by fibrillatory waves on ECG.

205
Q

AF: What are fibrillatory waves on ECG?

A

Random oscillations of the baseline.

206
Q

What are causes of AF?

A 
Sepsis. 
Mitral valve stenosis. 
Ischaemic heart disease. 
Thyrotoxicosis. 
Hypertension. 
Remember: Mrs SMITH.
207
Q

What is the difference between paroxysmal and persistent AF?

A

Paroxysmal AF terminates spontaneously (< 7 days, typically < 24 hours).
Persistent AF is continuous and cannot be cardioverted or it is determined that caridoversion is inappropriate.

208
Q

What are the clinical features of AF?

A

Palpitations, shortness of breath, chest pain.

209
Q

Give three causes of an irregularly irregular pulse.

A

Atrial fibrillation.
Ventricular ectopics.
Sinus arrhythmia.

210
Q

How is atrial fibrillation distinguished from other causes of irregularly irregular pulse?

A

ECG.

211
Q

What does ECG reveal in patients with AF?

A

Absent P waves, irregularly irregular QRS complex tachycardia.

212
Q

What is valvular AF?

A

Atrial fibrillation in the presence of moderate-to-severe mitral stenosis or prosthetic heart valve.

213
Q

What are the two stages of AF management?

A

Rate/rhythm control.

Stroke risk reduction.

214
Q

What is the management of a haemodynamically unstable patient with AF?

A

DC cardioversion (give prior sedation).

215
Q

AF: Describe the rate control management approach.

A

Rate control is the predominant management approach in AF and aims to slow the heart rate down (allowing the ventricles to fill) to avoid the negative effects on cardiac function.

216
Q

What pharmacological therapies make up AF rate control?

A

1st: Beta-blocker (atenolol).
2nd: Rate-limiting calcium channel blocker (diltiazem).
3rd: Digoxin (if BB or CCB don’t work and only in sedentary people).

217
Q

AF: Describe the rhythm control management approach.

A

Cardioversion: Aims to get the patient back into and maintain a normal sinus rhythm.

218
Q

When should rhythm control be preferred over rate control in the management of AF (4 things)?

A

Reversible cause for the AF.
AF is new onset (< 48 hours).
AF is causing heart failure.
Patient remains symptomatic despite effective rate control.

219
Q

What are the two options for cardioversion in AF?

A

Pharmacological cardioversion.

Electrical cardioversion.

220
Q

What drugs can be given for pharmacological cardioversion in AF?

A

1st: flecainide.
2nd: amiodarone.

221
Q

AF: How should cardioversion be performed in someone with a short duration of symptoms (< 48 hours)?

A

Heparin is given then cardioversion attempted.

222
Q

AF: How should cardioversion be performed in someone that has been in AF for > 48 hours?

A

Anticoagulation provided for three weeks before cardioversion attempted. Rate control given in the intermediate period.

223
Q

Why do patients require anticoagulation for three weeks before attempted cardioversion in AF?

A

The moment of cardioversion presents the greatest risk of embolism leading to stroke (may mobilise a thrombus from the atrium into the circulation).

224
Q

What scoring system is used for predicting stroke risk in AF patients?

A

CHA2DS2-VASc

225
Q

What are the criteria for the CHA2DS2-VASc risk tool?

A 
Congestive heart failure (1). 
Hypertension (1). 
Age > 75 (1), > 65 (1). 
Diabetes (1). 
Stroke/TIA hx (2). 
Vascular disease (1). 
Sex female (1).
226
Q

How is CHA2DS2-VASc score interpreted?

A

0 - no anticoagulation.
1 - consider anticoagulation in males.
2 - offer anticoagulation.

227
Q

What scoring system is used to assess bleed risk in anti coagulated AF patients?

A

HASBLED.

228
Q

What are the criteria for the HASBLED risk tool?

A 
Hypertension (1). 
Abnormal renal/liver function (2). 
Stroke hx (1). 
Bleeding hx (1). 
Labile INRs (1). 
Elderly (1). 
Drugs or alcohol (2).
229
Q

How is HASBLED score interpreted?

A

≥ 3 is high risk of bleeding.

230
Q

What management approach may be opted for in paroxysmal AF?

A

Pill in the pocket - terminate episodes when they become symptomatic (palpitations, shortness of breath) by taking flecainide.

231
Q

Who is suitable for ‘pill in the pocket’ management in paroxysmal AF?

A

Those who have infrequent episodes and without underlying structural heart disease.

232
Q

What is the mechanism behind warfarin?

A

Vitamin K antagonist. Vitamin K acts as a cofactor in the carboxylation of clotting factors.

233
Q

Vitamin K is involved in the carboxylation in which clotting factors?

A

Factor II
Factor VII
Factor IX
Factor X

234
Q

How is warfarin monitored?

A

INR.

235
Q

What is INR?

A

International normalised ratio - the prothrombin time of the patient compared the prothrombin time of a normal healthy adult.

236
Q

Warfarin: What is the target INR for AF?

A

2.5

237
Q

Warfarin: What is the target INR for VTE?

A

2.5

238
Q

Warfarin: What is the target INR for recurrent VTE?

A

3.5

239
Q

What is the management of someone on warfarin therapy that presents with major bleeding?

A

Stop warfarin.
Give intravenous 5mg vitamin K.
Give prothrombin complex concentrate.

240
Q

What is the management of someone on warfarin therapy that presents with INR > 8.0 and minor bleeding?

A

Stop warfarin.
Give intravenous 1-3g vitamin K.
Restart warfarin when INR < 5.

241
Q

What is the management of someone on warfarin therapy that presents with INR > 8.0 and no bleeding?

A

Stop warfarin.
Give oral vitamin K 1-5mg.
Restart warfarin when INR < 5.

242
Q

What is the management of someone on warfarin therapy that presents with INR 5.0-8.0 and minor bleeding?

A

Stop warfarin.
Give intravenous 1-3g vitamin K.
Restart warfarin when INR < 5.

243
Q

What is the management of someone on warfarin therapy that presents with INR 5.0-8.0 and no bleeding?

A

Omit 1 or 2 doses of warfarin and reduce subsequent maintenance dose.

244
Q

Warfarin: What can induce cP450 and lead to reduced INR?

A 
Phenytoin 
Carbamazepine
Barbituates
Rifampicin 
Alcohol. 
Sulfonylureas / St Johns wart 
Remember: PC BRAS
245
Q

Warfarin: What can inhibit cP450 and lead to raised INR?

A 
Allopurinol
Omeprazole
Disulfiram 
Erythromycin 
Valproate
Isoniazid
Ciprofloxacin 
Ethanol (acute). 
Sulphonamides 
Remember: AO DEVICES
246
Q

What is ventricular tachycardia?

A

A broad-complex tachycardia originating from a ventricular ectopic focus.

247
Q

Why does ventricular tachycardia require urgent treatment?

A

VT has the potential to precipitate into ventricular fibrillation (which results in cardiac arrest).

248
Q

What are the two main types of ventricular tachycardia?

A

Monomorphic ventricular tachycardia (most commonly due to MI).
Polymorphic ventricular tachycardia (such as Torsades de Pointes).

249
Q

What is the management of ventricular tachycardia?

A

Electrical cardioversion.

250
Q

When should electrical cardioversion be performed in a person with VT?

A

Adverse signs e.g. sBP < 90, pulse > 100, chest pain, ischaemia on ECG, heart failure, syncope.

251
Q

How is electrical cardioversion performed in the management of VT?

A

Provide sedation.

Give three synchronised DC shocks.

252
Q

Which electrolytes should be assessed following cardioversion in VT?

A

Potassium.
Magnesium.
Calcium.

253
Q

What medication should be given following electrical cardioversion in VT?

A

Amiodarone 300mg IV over at least 20 minutes.

Then amiodarone 900mg IV over 24 hours.

254
Q

What is long QT?

A

Condition of delayed ventricular repolarisation that can lead to ventricular tachycardia and sudden death.

255
Q

What is a normal QT interval?

A

< 440 ms.

256
Q

What is long QT syndrome?

A

An inherited condition of QT prolongation.

257
Q

Give examples of non-pharmacological causes of QT interval prolongation?

A

Myocardial infarction.
Hypokalaemia.
Hypomagnesaemia.
Hypocalcaemia.

258
Q

Give examples of pharmacological causes of QT interval prolongation?

A 
Methotrexate 
Erythromycin
Terfenadine
Haloperidol
Clarithromycin
Amiodarone
TCAs
SRRIs
Remember: METH CATS
259
Q

What is the management of long QT?

A

Avoid medications that can prolong QT.
Beta-blockers.
Implantable cardioverter defibrillator.

260
Q

What is Torsades de Pointes (TdP)?

A

“Twisting of the points”… a form of polymorphic ventricular tachycardia associated with long QT interval.

261
Q

Describe how a prolonged QT interval can lead to TdP.

A

Prolonged QT = prolonged repolarisation following contraction.
Prolonged repolarisation leads to spontaneous depolarisation in some myocytes.
Depolarisation spreads throughout ventricle and contraction occurs prior to repolarisation.

262
Q

What are causes of Torsades de Pointes?

A 
Hypothermia
Hypothyroidism
Hypocalcaemia
Hypomagnesaemia 
Hypoakalemia
263
Q

What is the management of Torsades de Pointes?

A

Intravenous magnesium sulphate.

Correct underlying cause.

264
Q

What are ventricular topics?

A

Premature ventricular complexes are premature beats caused by random electrical discharges outside the atria.

265
Q

How do ventricular ectopics present?

A

Patients complain of random, brief palpitations.

266
Q

How do ventricular ectopics appear on an ECG?

A

Broad QRS complex, premature to the expected next impulse, often followed by a compensatory pause.

267
Q

What is bigeminy?

A

A type of ventricular ectopic where every other beat is a premature ventricular complex.

268
Q

What is trigeminy?

A

A type of ventricular ectopic where every third beat is a premature ventricular complex.

269
Q

What is the most likely congenital heart defect to be found in adulthood?

A

Atrial septal defect.

270
Q

What is the presentation of atrial septal defect?

A

Fatigue and breathlessness

271
Q

What is heard on auscultation of an atrial septal defect?

A

Ejection systolic murmur (heard loudest on inspiration) with fixed splitting of S2.

272
Q

Explain why fixed splitting of S2 is heard in a patient with atrial septal defect.

A

Blood flows from L atrium to R atrium, more blood in the R atrium means more blood must be pumped out of the R ventricle… pulmonary valve closes later than the aortic valve.

273
Q

What is seen on ECG in a patient with atrial septal defect?

A

RBBB.

274
Q

What valve defect can be heard as a mid-diastolic murmur (louder on expiration) with a loud S1 opening snap.

A

Mitral stenosis

275
Q

What is mitral stenosis?

A

Hardening of the mitral valve (between the L atrium and L ventricle).

276
Q

What features (other than what is heard on auscultation) may present in mitral stenosis?

A 
Low volume pulse. 
Malar flush (plum red discolouration of cheeks).
277
Q

Why do people with mitral stenosis develop malar flush?

A

Back-pressure of blood into pulmonary system causes rise in CO2 and vasodilation.

278
Q

Mitral stenosis can cause what arrhythmia (and why)?

A

Atrial fibrillation - atrial strain results in electrical disruption.

279
Q

What investigations can be performed in the assessment of mitral stenosis?

A

Echocardiography.
ECG.
CXR.

280
Q

What might echocardiography show in mitral stenosis?

A

Reduced cross-sectional area of the mitral valve.

281
Q

What might ECG show in mod-severe mitral stenosis?

A

Broad, notched/bifid P wave - a sign of left atrial enlargement.

282
Q

What might CXR show in mitral stenosis?

A

Left atrial enlargement.

283
Q

What is mitral regurgitation?

A

An incompetent mitral valve allows blood to flow back into the left atrium during ventricular contraction.

284
Q

What causes mitral regurgitation?

A

Idiopathic weakening with age.
Ischaemic heart disease.
Rheumatic heart disease.
Connective tissue disorders (Ehlers Danlos, Marfans).

285
Q

What is heard on auscultation in mitral regurgitation?

A

High-pitched pansystolic murmur (louder on expiration) best heard at the apex with the patient lying on their left.

286
Q

What is heard on auscultation in tricuspid regurgitation?

A

High-pitched pansystolic murmur (louder on inspiration) best heard at the lower left sternal border.

287
Q

What is aortic stenosis?

A

Narrowing of the aortic valve (at the exit of the left ventricle).

288
Q

What is the most common cause of aortic stenos?

A

Age-related calcification (typically present between 65-75 years of age).

289
Q

What are the clinical features of aortic stenosis?

A

Chest pain and exertional syncope.

290
Q

What is heard on auscultation in aortic stenosis?

A

High-pitched ejection systolic murmur that radiates to the carotids.

291
Q

Aortic stenosis leads to the development of…

A

Left ventricular hypertrophy and subsequent failure.

292
Q

When should valve replacement be considered in aortic stenosis?

A

Symptomatic.

Asymptomatic but pressure gradient of > 40mmHg across the aortic valve.

293
Q

What are the two types of prosthetic valve?

A

Biological (bioprosthetic).

Mechanical.

294
Q

What are the advantages/disadvantages of biological heart valves over mechanical valves?

A

Adv: Don’t require long-term anticoagulation.
Dis: Structural deterioration and calcification over time.

295
Q

What are the advantages/disadvantages of mechanical heart valves over biological valves?

A

Adv: Low failure rate.
Dis: Increased risk of thrombosis and require long-term anticoagulation.

296
Q

What is aortic regurgitation?

A

A condition of aortic incompetence whereby blood flows in the reverse direction during ventricular diastole.

297
Q

How does aortic regurgitation present clinically?

A

Palpitations, exertional dyspnoea, orthopnoea and paroxysmal nocturnal dyspnoea.

298
Q

What causes aortic regurgitation?

A

Rheumatic fever, infective endocarditis, connective tissue disease, bicuspid aortic valve.

299
Q

What is found on examination in aortic regurgitation?

A

Collapsing pulse, wide pulse pressure, displaced hyperdynamic apex beat… on auscultation a high-pitched early diastolic murmur.

300
Q

How is aortic regurgitation diagnosed?

A

Echocardiogram.

301
Q

What is the inheritance pattern of hypertrophic obstructive cardiomyopath?

A

Autosomal dominant.

302
Q

What is the pathophysiology of hypertrophic obstructive cardiomyopathy?

A

Disorder of muscle tissue caused by defects in the genes encoding the contractile proteins. Left ventricle hypertrophy results in decreased compliance and decreased cardiac output.

303
Q

What is the most common cause of sudden cardiac death in the young?

A

Hypertrophic obstructive cardiomyopathy (HOCM).

304
Q

How can hypertrophic obstructive cardiomyopathy present?

A

Exertional dyspnoea, angina, syncope or sudden death.

305
Q

What does auscultation of hypertrophic obstructive cardiomyopathy reveal?

A

Ejection systolic murmur loudest at the lower left sternal edge.

306
Q

What does echocardiogram reveal in hypertrophic obstructive cardiomyopathy?

A

Mitral regurgitation.
Systolic anterior motion.
Asymmetric hypertrophy.
Remember: Mr SAM ASH

307
Q

What is the management of HOCM?

A

Amiodarone, beta-blocker/verapamil, cardioverter defibrillator, dual chamber pacemaker and endocarditis prophylaxis.

308
Q

What is the second most common cause of cardiac death in the young?

A

Arrhythmogenic right ventricular dysplasia (ARVD).

309
Q

What is the inheritance pattern of arrhythmogenic right ventricular dysplasia/cardiomytopathy?

A

Autosomal dominant.

310
Q

Describe the pathophysiology of arrhythmogenic right ventricular dysplasia/cardiomyopathy.

A

Replacement of right ventricular myocardium with fatty and fibrofatty tissue.

311
Q

What is the presentation of arrhythmogenic right ventricular dysplasia?

A

Palpitations, syncope and sudden cardiac death.

312
Q

What may ECG reveal in arrhythmogenic right ventricular dysplasia?

A 
T wave inversion (V1-V3). 
Epsilon wave (terminal notch in QRS).
313
Q

How is arrhythmogenic right ventricular dysplasia managed?

A

Sotalol.
Catheter ablation.
Implantable cardioverter-defibrillator.

314
Q

What are causes of dilated cardiomyopathy?

A

Alcohol excess.
Coxsackie B virus.
Wet beriberi (thiamine deficiency).
Doxorubicin (chemo).

315
Q

What is the pathophysiology of dilated caridomyopathy?

A

Dilation of heart chambers, especially left ventricle = systolic dysfunction.

316
Q

What are causes of restrictive cardiomyopathy?

A

Amyloidosis.
Post-radiotherapy.
Loeffler’s endocarditis.

317
Q

When does peripartum cardiomyopathy present?

A

Between the last month of pregnancy and five months post-partum.

318
Q

Which group is at greater risk of developing peripartum cardiomyopathy?

A

Older women.
Greater parity.
Multiple gestations.

319
Q

What is Takotsubo cardiomyopathy?

A

Broken heart syndrome. A cardiomyopathy induced by stressful triggers such as bereavement.

320
Q

What are the clinical features of Takotsubo cardiomyopathy?

A 
Chest pain. 
Heart failure (dyspnoea, oedema).
321
Q

What does echocardiogram reveal in Takotsubo cardiomyopathy?

A

Apical ballooning of the myocardium.

322
Q

What is peripheral arterial disease?

A

Atherosclerosis and subsequent stenosis of arteries (most commonly in the legs).

323
Q

Which arteries are affected in peripheral artery disease (PAD)?

A

Most commonly the arteries in the legs (also arms, neck or kidneys).

324
Q

What is the main clinical feature of peripheral artery disease?

A

Intermittent claudication.

325
Q

PAD: What is intermittent claudication?

A

Muscle pain, ache, cramp that develops on mild exertion and is relieved by rest. Can affect the calf, thigh or buttock.

326
Q

PAD: What is the claudication distance?

A

The distance an individual is able to walk before the onset of pain.

327
Q

What examination findings are present in peripheral arterial disease?

A 
Absent femoral, popliteal or foot pulses. 
Cold legs. 
Atrophic skin changes. 
Skin ulcers. 
Abnormal hair/nail growth.
328
Q

What is the first-line investigation in peripheral arterial disease?

A

Colour duplex ultrasonography.

329
Q

Peripheral arterial disease: What investigation is required before surgical intervention?

A

MR angiography to detail the extent and location of disease as well as the quality of distal vessels.

330
Q

What is the initial management of peripheral arterial disease?

A

Risk factor modification: smoking cessation, blood pressure control, cholesterol control (statin) and antiplatelet. Provide supervised exercise programmes.

331
Q

What surgical intervention can be performed in the management of peripheral arterial disease?

A

Percutaneous transluminal angioplasty (balloon inflated within a narrowed arterial segment).
Arterial reconstruction with bypass graft if distal run-off is good.

332
Q

What is critical limb ischaemia?

A

A complication of peripheral arterial disease that develops when blood flow to the legs becomes severely restricted.

333
Q

What are the clinical features of critical limb ischaemia?

A

Ulceration.
Gangrene.
Foot pain at rest (“burning”).

334
Q

What is acute limb ischaemia?

A

A medical emergency. The result of thrombosis in situ, emboli or graft occlusion.

335
Q

What are the clinical features of acute limb ischaemia?

A

Pale, pulseless, painful, paralysed, parenthetic and perishingly cold.

336
Q

What is the management of acute limb ischaemia?

A

Open surgery or angioplasty.

337
Q

What is Buerger’s disease?

A

Thromboangiitis obliterates (Buerger’s disease) is a small and medium vessel vasculitis that causes thrombus formation.

338
Q

What group of people are most commonly affected by Buerger’s disease?

A

Male aged 25-35 that smokes cigarettes.

339
Q

What is the characteristic presentation of thromboangiitis obliterans?

A

Painful blue discolouration of the fingertips or toes that is worse at night.
May progress to ischaemic ulcers and gangrene.

340
Q

What is gangrene?

A

Death of tissue due to inadequate blood supply.

341
Q

What does angiography reveal in Buerger’s disease?

A

Corkscrew collaterals (collateral vessels which form to bypass the affected arteries).

342
Q

What is the management of Buerger’s disease?

A

Completely stop smoking and don’t use nicotine replacement therapy.

343
Q

Define aneurysm.

A

Artery with dilatation of more than 50% of its original diameter.

344
Q

What causes aneurysms to develop?

A

Atheroma, trauma, infection, connective tissue disorders or inflammatory processes.

345
Q

What is the difference between true and false aneurysms?

A

True aneurysms - abnormal dilatations that involve all layers of the arterial wall.
False aneurysms - involve a collection of blood in the outer layer (adventitia) only.

346
Q

What are common sites of aneurysm?

A

Aorta (infrarenal), iliac arteries, femoral arteries, popliteal arteries.

347
Q

What are complications of aneurysms?

A 
Rupture. 
Thrombosis. 
Embolism. 
Fistulae. 
Pressure/compression on nearby structures.
348
Q

Outline the abdominal aortic aneurysm screening programme in England.

A

All men aged 65 are invited for an ultrasound scan to identify and treat dangerously large aneurysms before rupture.

349
Q

What is an abdominal aortic aneurysm?

A

Aneurysm of the abdominal aorta > 3cm across

350
Q

How are aneurysms monitored?

A

Annual ultrasound.

351
Q

What advice is given to reduce the risk of growth of AAA.

A

Smoking cessation, healthy diet, regular exercise, alcohol moderation.

352
Q

When should people with AAA receive surgical intervention?

A

AAA > 5.5cm

353
Q

What intervention is offered for AAA?

A

Endovascular aneurysm repair (EVAR).

354
Q

What is the presentation of ruptured AAA?

A

Intermittent or continuous abdominal pain, collapse, expansile abdominal mass and shock.

355
Q

What is aortic dissection?

A

Injury to the innermost layer of the aorta allows blood to flow between the layers of the aortic wall, forcing the layers apart.

356
Q

What are the presenting features of aortic dissection?

A

Sudden tearing chest pain that radiates to the back. Vomiting, sweating and light-headedness.

357
Q

How are aortic dissections classified?

A

Type A - involves ascending aorta, arch of the aorta (2/3 cases).
Type B - involves descending aorta distal to left subclavian origin.

358
Q

By what process do the complications of aortic dissection develop?

A

Aortic dissection extends and branches of the aorta occlude sequentially. The dissection can also occlude proximally.

359
Q

What features of aortic dissection may present as a result of branch occlusion?

A

Distal expansion: Hemiplegia (stroke), unequal arm pulses, unequal arm blood pressure, acute limb ischaemia, anuria.
Proximal expansion: murmur (aortic valve incompetence), MI and cardiac arrest.

360
Q

What investigation confirms the diagnosis of aortic dissection?

A

CT angiogram shows a false lumen in the aorta.

361
Q

What is the management of aortic dissection?

A

Control blood pressure with IV labetalol.
Give IV morphine for pain.
Refer for surgery.

362
Q

What surgery is performed for aortic dissection?

A

Type A - open surgery.

Type B - endovascular repair.

363
Q

What is pericarditis?

A

Inflammation of the pericardium.

364
Q

What is the pericardium?

A

Fibroelastic sac that surrounds the heart.

365
Q

What cause pericarditis?

A

Infection (coxsackie, tuberculosis), trauma, post-MI, connective tissue disease, hypothyroidism, malignancy.

366
Q

What are clinical features of pericarditis?

A

Chest pain, fever, non-productive cough, dyspnoea.

367
Q

How may the chest pain in pericarditis be relieved?

A

Sitting forwards.

368
Q

What is found on examination of pericarditis?

A

Tachypnoea, tachycardia, pericardial friction rub on auscultation.

369
Q

What does ECG show in pericarditis?

A

Widespread saddle-shaped ST elevation.

370
Q

What do troponins show in pericarditis?

A

Raised.

371
Q

What is the management of acute pericarditis?

A

Treat underlying cause.

Give ibuprofen.

372
Q

What is constrictive pericarditis?

A

Condition that develops as a result of scarring and loss of elasticity of the pericardial sac… prevents normal filling and thus restricts cardiac output.

373
Q

What is the presentation of constrictive pericarditis?

A

Poor exercise tolerance, exertional dyspnoea. Features of right heart failure (elevated JVP, ascites, oedema, hepatomegaly). Positive Kussmaul’s sign.

374
Q

Constrictive pericarditis: What is Kussmaul’s sign?

A

Paradoxical rise in JVP on inspiration (should fall with inspiration due to reduced pressure in expanding thoracic cavity).

375
Q

What may CXR show in constrictive pericarditis?

A

Pericardial calcification.

376
Q

What is cardiac tamponade?

A

Pericardial effusion raises intrapericardial pressure… reducing ventricular filling and thus restricting cardiac output.

377
Q

What is the diagnostic triad of cardiac tamponade?

A

Low blood pressure.
Raised JVP.
Muffled heart sounds on auscultation.

378
Q

What does ECG show in cardiac tamponade?

A

Electrical alternans (alternation of QRS complex altitude).

379
Q

What is the treatment of cardiac tamponade?

A

Urgent pericardiocentesis.

380
Q

What is infective endocarditis?

A

Endocardial inflammation as a result of microbial infection… typically affecting the heart valves.

381
Q

What are heart valves commonly affected in infective endocarditis?

A

Valves are a source of turbulent blood flow which damages the endocardial lining… thrombi develop on damaged surface and microorganisms attach to thrombi to form vegetations.

382
Q

Assume infective endocarditis in which patients?

A

Fever + new murmur.

383
Q

What pathogen most commonly causes infective endocarditis?

A

Staphylococcus aureus.

384
Q

What are risk factors for infective endocarditis?

A

Skin breaches (dermatitis, intravenous lines, wounds), prosthetic valves, valvular disease, dental problems, renal failure, immunosuppression, diabetes mellitus.

385
Q

In what order are the valves commonly affected in infective endocarditis?

A 
Mitral. 
Aortic. 
Mitral + aortic. 
Tricuspid. 
Pulmonary.
386
Q

What are the clinical features of infective endocarditis?

A

Fever, rigors, night sweats, malaise, weight loss, anaemia, splenomegaly, clubbing.

387
Q

By what mechanism can infective endocarditis damage organs?

A

Vegetations can detach, become septic emboli and then cause abscesses in the relevant organ

388
Q

Give examples of organ damage in infective endocarditis.

A

Skin (Janeway lesions).
Glomerulonephritis.
Roth spots (retinal haemorrhage)
Splinter haemorrhages

389
Q

What criteria are used for diagnosing infective endocarditis?

A

Duke criteria

390
Q

What are the Duke criteria for infective endocarditis?

A

Repeated blood cultures - three sets at different times from different sites.
If negative consider fungal endocarditis.

391
Q

What blood tests may be performed in infective endocarditis (with results).

A

FBC - anaemia, neutrophilia.
ESR - raised.
CRP - raised.
Rheumatoid factor - positive.

392
Q

What imaging can be performed in the investigation of infective endocarditis?

A

Transthoracic echocardiogram may be able to show vegetations > 2mm… transoesophageal echocardiogram is more sensitive.

393
Q

What is the management of infective endocarditis?

A

Intravenous gentamicin.

394
Q

What are varicose veins?

A

Dilated, tortuous, superficial veins that occur secondary to incompetent venous valves.

395
Q

Where do varicose veins most commonly occur?

A

Great saphenous vein.

Small saphenous vein.

396
Q

What are risk factors for varicose veins?

A

Increasing age, female, pregnancy, obesity.

397
Q

What is the presentation of varicose veins?

A

Cosmetic complaints (superficial dilated vessels). Some patients may have aching, throbbing or itching.

398
Q

What are possible complications of varicose veins?

A 
Varicose eczema. 
Hyperpigmentation. 
Hard/tight skin. 
Hypopigmentation. 
Bleeding. 
Superficial thrombophlebitis. 
Venous ulceration.
399
Q

Define syncope.

A

Transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery.

400
Q

Give three causes of reflex syncope.

A

Vasovagal (triggered by emotion, pain or stress).
Situational (triggered by cough, micturition, gastrointestinal causes).
Carotid sinus syncope.

401
Q

What are prodromal symptoms of reflex syncope?

A

Sweating, pallor, nausea + vomiting.

402
Q

What are the causes of orthostatic hypotension?

A 
Venous pooling (after exercise or during pregnancy). 
Post-prandial (after meals). 
Prolonged bed rest (deconditioning).
403
Q

Define shock.

A

Circulatory failure that results in inadequate organ perfusion. sBP < 90mmHg, MAP < 65mmHg.

404
Q

What two factors can contribute to shock?

A 
Cardiac output (inadequate). 
Systemic vascular resistance (inadequate).
405
Q

What is the presentation of shock?

A

Reduced conscious level, agitation, cool peripheries, tachycardia, slow cap refill, tachypnoea, oliguria.

406
Q

What are the three types of shock?

A

Hypovolaemic shock.
Cardiogenic shock.
Septic shock.

407
Q

What are the eight reversible causes of cardiac arrest?

A 
Hypothermia. 
Hypoglycaemia, hypocalcaemia, hypokalaemia, hyperkalaemia. 
Hypoxia. 
Hypovolaemia. 
Thrombosis. 
Tension pneumothorax. 
Tamponade. 
Toxins.

Finals (11 decks)

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