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Phase1c Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is ACS subdivided into?

A

Unstable angina
NSTEMI
STEMI

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2
Q

What is the mechanism of angina pectoris?

A

Increase in myocardial oxygen demand exceeding oxygen supply

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3
Q

What is the most common cause of angina pectoris?

A

Atherosclerosis

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4
Q

What are the other causes of angina?

A

Atherosclerosis
Cocaine-induced coronary spasm
Arteritis
Emboli

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5
Q

What is a myocardial infarction?

A

Sudden occlusion of a coronary artery due to the rupture of an atheromatous plaque and thrombus formation

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6
Q

Which cells migrate into the subendothelial space to form foam cells?

A

Macrophages

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7
Q

How are foam cells formed in atherosclerosis?

A

Macrophages phagocytose oxidised LDL lipid within the subendothelial space to form foam cells

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8
Q

Which growth factors are released from foam cells resulting in the formation of atherosclerotic cells?

A

PDGF and TGF-B

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9
Q

What happens during the rupture of a thin fibrous cap?

A

Prothrombotic components are exposed to platelets and pro-coagulation factors leading to thrombus formation and clinical events

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10
Q

What are the risk factors for ACS?

A 
Male
Diabetes mellitus
FHx
Hypertension
Hyperlipidaemia
Smoking
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11
Q

What is presentation of ACS?

A

Chest pain (acute onset)
Central heavy tight ‘gripping’ pain that radiates to the left arm, jaw or epigastrium
Occurs at rest
Associated with breathlessness, sweating, nausea and vomiting

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12
Q

Where does the chest pain radiate to in angina?

A

Radiates to the left arm, jaw or epigastrium

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13
Q

What is the character of chest pain in angina?

A

Central heavy tight ‘gripping’ pain

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14
Q

What symptoms are associated with angina?

A

Breathlessness, sweating, nausea and vomiting

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15
Q

When is stable angina brought on?

A

On exertion and relieved by rest

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16
Q

How is stable angina resolved?

A

On rest or GTN within 5 minutes

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17
Q

What symptoms are associated with atypical angina?

A

Gastrointestinal discomfort and/or breathlessness and/or nausea

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18
Q

What is Prinzemetal angina?

A

The pain from variant angina is caused by a spasm caused by exposure to cold, smoking or stress

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19
Q

Which murmur is associated as a complication of an MI?

A

Pansystolic murmur due to mitral regurgitation (papillary muscle rupture)

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20
Q

Which cardiac enzymes are profiled in a suspected MI?

A

CK-MB

Troponin-T (remain elevated for 2 weeks)

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21
Q

How long does troponin-T remain elevated for a few hours of cardiac damage?

A

After 2 weeks

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22
Q

What ECG changes are seen in an NSTEMI?

A

ST-depression
T-wave inversion
Q waves reveal previous MIs

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23
Q

Describe the ST-elevation in limb leads (mm)

A

> 1mm

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24
Q

Describe the ST-elevation in chest leads

A

> 2mm

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25
Q

Which leads are associated with an anterior STEMI?

A

V1-V4

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26
Q

Which coronary arteries are associated with an anterior MI?

A

Left coronary artery and left anterior descending artery (LAD)

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27
Q

Which leads are associated with a lateral STEMI?

A

I, aVL, V5 and V6

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28
Q

Which coronary artery is associated with a lateral MI?

A

Left circumflex

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29
Q

Which leads are associated with an inferior STEMI?

A

II, III, AvF

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30
Q

Which leads are associated with a posterior MI?

A

V7-V9

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31
Q

Which leads are associated with a septal MI?

A

v1-v2

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32
Q

What type of ECG is performed in a patient suspected with ACS?

A

Exercise ECG testing

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33
Q

What is the difference between unstable angina and an NSTEMI?

A

Troponin is raised in an NSTEMI

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34
Q

What is the gold standard to detect for coronary stenosis or obstruction?

A

Coronary angiography

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35
Q

What scan i used to detect wall-motion abnormalities and left ventricular function in ACS?

A

Echocardiogram

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36
Q

Which type of echocardiogram is used to assess for an aortic dissection?

A

Transoesophageal echocardiogram

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37
Q

What type of echocardiogram is used to evaluate haemodynamically significant stenoses in ACS?

A

Stress echocardiography

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38
Q

What is the management of stable angina?

A
  • Minimise cardiac risk factors: Control BP, hyperlipidaemia, and diabetes.
  • Advice on smoking, exercise, weight loss and a low-fat diet.
  • All patients to receive aspirin (75mg/day).

-Symptom relief using GTN

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39
Q

What loading dose of aspirin is given in ACS?

A

300mg Aspirin

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40
Q

What is the maintenance dose of aspirin in ACS?

A

75mg

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41
Q

What platelet therapy is administered in ACS?

A

Clopidogrel
ticagrelor
prasugrel

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42
Q

When is prasugrel given in ACS?

A

If the patient is already on a DOAC

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43
Q

What drugs are administered in the long-term for ACS?

A 
Beta-blockers
Calcium channel blockers
Statins
ACEis
Anti-platelet therapy (DAPT)
Nitrates
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44
Q

What is the definitive management of an MI within 12 hours?

A

A percutaneous coronary intervention PCI

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45
Q

When is a CABG indicated in the management of a STEMI?

A

in three-vessel disease

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46
Q

What is the MoA of HMG-CoAi?

A

Lower LDL-C levels and raise HDL levels (Atorvastatin)

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47
Q

How do bile acid sequestrants work?

A

The bile acid sequestrants block enterohepatic circulation of bile acids and increase faecal loss of cholesterol.
• Cholestyramine (Questran, LoCholest, Prevalite)

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48
Q

What is the MoA of CCBs?

A

Relaxes coronary smooth muscle and produces coronary vasodilation which in turns improves myocardial oxygen delivery.
• Amlodipine (Norvasc)

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49
Q

What is the MoA of BBs?

A

Inhibit sympathetic stimulation of the heart, reducing heart rate and contractility; this can decrease myocardial oxygen demand and thus prevent or relieve angina in patients with CAD.

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50
Q

What is Ranolazine?

A

Anti-anginal agents
Relieve ischaemic by reducing myocardial cellular sodium and calcium overload via inhibition of the late sodium current of the cardiac action potential.

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51
Q

What is the first-line management for symptomatic ACS?

A

Short-acting nitrate and 300mg Aspirin

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52
Q

When should a PCI be offered during the symptomatic presentation of ACS?

A

Within 12 hours

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53
Q

What should be offered in the management of ACS if PCI is not available?

A

Fibronlysis

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54
Q

What are the early complications after an MI?

A

• Death, cardiogenic shock, heart failure, ventricular arrhythmias, heart block, pericarditis, myocardial rupture, thromboembolism.

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55
Q

What are the late complications after an MI?

A

• Ventricular wall rupture, valvular regurgitation, ventricular aneurysms, tamponade, Dressler’s syndrome (pericarditis), thromboembolism.

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56
Q

What is aortic regurgitation?

A

Reflux of blood from the aorta into the left ventricle (LV) during diastole. Also known as aortic insufficiency.

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57
Q

What type of pulse is associated with aortic regurgitation?

A

Collapsing pulse and wide pulse pressure

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58
Q

What are the causes of aortic regurgitation?

A

Aetiology
• Aortic valve leaflet abnormalities or damage: Bicuspid aortic valve, infective endocarditis, rheumatic fever, trauma.

Aortic root/ascending aorta dilation:
• Systemic hypertension, aortic dissection, aortitis (syphilis, Takayasu’s arteritis), arthritides, Marfan’s syndrome, Ehrler’s Danlos syndrome, osteogenesis imperfecta.

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59
Q

What is the pathophysiology of aortic regurgitation?

A

Reflux of blood into the left ventricle during diastole  Left ventricular dilation  Increase in end-diastolic volume & stroke volume.
↑ Stroke, volume & low EDV pressure  Collapsing pulse and wide pule pressure.

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60
Q

Which type of murmur is associated with aortic regurgitation?

A

Early diastolic murmur

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61
Q

How are murmurs of aortic regurgitation exaggerated?

A

When the patient is sitting forward and the breath is held in expiration

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62
Q

What is Quincke’s sign?

A

Visible pulsations on the nailbed

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63
Q

What is De Musset’s sign?

A

Head nodding in time with the pulse

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64
Q

What is the presentation of aortic regurgitation?

A

Chronic AR – initially asymptomatic.
• Symptoms of heart failure: Exertional dyspnoea, orthopnoea, fatigue + occasional angina.
• Severe acute AR: Sudden cardiovascular collapse.
Symptoms related to the aetiology: Chest or back pain in patients with aortic dissection.

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65
Q

What are the symptoms of acute heart failure?

A

Exertional dyspnoea, orthopnoea, fatigue + occasional angina.

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66
Q

What is the definitive investigation to confirm aortic regurgitation?

A

Echocardiogram

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67
Q

What is the definitive management of aortic regurgitation?

A

Aortic valve replacement

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68
Q

What is the ejection fraction in aortic regurgitation?

A

EF <50%

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69
Q

What is aortic stenosis?

A

The narrowing of the left ventricular outflow at the level of the aortic valve.

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70
Q

What is the aetiology of aortic stenosis?

A

Aetiology
1) Stenosis secondary to rheumatic disease
2) Calcification of a congenital bicuspid aortic valve – Mechanical stress is distributed between 2 aortic leaflets.
3) Calcification/degeneration of a tricuspid aortic valve in the elderly
The aortic valve is less than 1cm2 in diameter (3-4cm2).

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71
Q

What diameter of the aortic valve to categorise as aortic stenosis?

A

<1cm^2

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72
Q

Which congenital disorder is associated with aortic stenosis?

A

Congenital bicuspid aortic valve

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73
Q

What is the presentation of aortic stenosis?

A

Angina (Increased oxygen demand of the hypertrophied ventricles)

Syncope or dizziness on exercise

symptoms of heart failure (dyspnoea)

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74
Q

What type of anaemia is associated with aortic stenosis?

A

Microangiopathic haemolytic anaemia

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75
Q

How does microangiopathic anaemia occur in aortic stenosis?

A

Damage to erythrocytes being forced through the narrowed aortic valve  Fragmentation into schistocytes  Haemoglobinuria.

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76
Q

Describe the pulse in aortic stenosis

A

Slow rising pulse (Narrow pulse pressure)

Thrill in the aortic area

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77
Q

What murmur is auscultated in aortic stenosis?

A

Ejection systolic murmur at the aortic area

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78
Q

Where does aortic stenosis radiate to?

A

To the carotid arteries

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79
Q

What sound is heard on auscultation due a bicuspid valve?

A

An ejection click

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80
Q

What is the definitive investigation for aortic stenosis?

A 
Transthoracic echocardiography (Including Doppler): 
•	Visualises structural changes of the valves and level of stenosis. 
•	An elevated aortic pressure gradient.
•	Assessment of left ventricular function.
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81
Q

What ECG changes are seen in aortic stenosis?

A

Signs of left ventricular hypertrophy
Absent Q waves
LBBB

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82
Q

What signs are seen on a chest x-ray regarding aortic stenosis?

A

Post-stenotic enlargement of the ascending aorta

Calcification of the aortic valve

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83
Q

What is the definitive management of aortic stenosis?

A

Aortic valve replacement

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84
Q

What option is available if AVR is not possible in aortic stenosis?

A

– Balloon dilation (valvoplasty).

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85
Q

Which type of valve replacement is recommended in patients who are young?

A

Metallic valve

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86
Q

What medical management should be administered alongside an aortic valve replacement?

A

Medical
• Antibiotic prophylaxis against infective endocarditis.
• Long-term anticoagulation for patients with mechanical prosthetics (with a Vitamin-K antagonist). DOACs are not recommended.
• ACEis for TAVR.

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87
Q

What is mitral regurgitation?

A

The mitral valve has two leaflets and consists of chordae tendinea and papillary muscles.
• In mitral regurgitation, during ventricular systole, the blood reflows back through the left ventricle into the left atrium.

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88
Q

What is the most common cause of mitral regurgitation?

A

Rheumatic heart disease and

Mitral valve prolapse (Myxomatous degeneration)

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89
Q

What are the causes of mitral regurgitation?

A
  • Rheumatic heart diseases (most common)
  • Infective endocarditis
  • Mitral valve prolapse
  • Papillary muscle rupture or dysfunction
  • Chordal rupture is associated with connective tissue diseases (osteogenesis imperfecta, Ehrler’s-Danlos syndrome, Marfan syndrome, SLE).
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90
Q

What is the acute presentation of MR?

A

Symptoms of left ventricular failure

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91
Q

What is the chronic presentation of MR?

A

Present with exertional dyspnoea, palpitations

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92
Q

What murmur is heard in mitral regurgitation?

A

Pansystolic murmur that radiates to the axilla

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93
Q

Which heart sound might be heard in mitral regurgitation?

A

S3 due rapid ventricular filling in early diastole

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94
Q

What is the surgical management for mitral valve regurgitation?

A

Mitral valve replacement/Repair

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95
Q

What is the target INR for Warfarin in patients with a mitral valve replacement?

A

INR 2-3

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96
Q

What is mitral valve stenosis?

A

Narrowing causes obstruction to blood flow from the left atrium to the left ventricle

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97
Q

What is the most common cause of mitral stenosis?

A

Rheumatic heart disease

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98
Q

What is the presentation of mitral stenosis?

A

Fatigue
Shortness of breath on exertion or lying down (Orthopnea)

Palpitations (Related to AF)

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99
Q

Malar flush is associated with which valvular pathology?

A

Mitral stenosis

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100
Q

Palpation of the apex beat in mitral stenosis will reveal what?

A

Parasternal heave (Right ventricular hypertrophy and pulmonary hypertension)

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101
Q

Auscultation of a patient with mitral valve stenosis will reveal what?

A

Loud first heart sound with an opening snap

Mid-diastolic murmur

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102
Q

Which type of murmur is associated with mitral stenosis?

A

Mid-diastolic murmur

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103
Q

Which ECG changes are associated with left atrial hypertrophy?

A

Broad bifid P waves

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104
Q

What are the complications of mitral stenosis on the right-side heart?

A

Right ventricular hypertrophy in the cases of severe pulmonary hypertension

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105
Q

What signs are revealed by a Chest X-ray in mitral stenosis?

A

Left atrial enlargement
Cardiac enlargement
Pulmonary congestion
Calcified mitral valve in rheumatic cases

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106
Q

What is the definitive investigation for mitral stenosis?

A

Echocardiography

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107
Q

What investigation measures the severity of heart failure?

A

Cardiac catheterisation

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108
Q

What is the medical management for mitral stenosis?

A

Anticoagulation for atrial fibrillation
Treat dyspnoea and heart failure with diuretics

Antibiotic cover for dental/invasive covers
Cardioversion of AF considered

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109
Q

What is the surgical management for mitral stenosis?

A

Mitral valvuloplasty
Valvotomy
Mitral valve replacement

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110
Q

Define cardiac arrest

A

Acute cessation of cardiac function – a state of circulatory failure due to impaired systolic function.

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111
Q

What are the causes of cardiac arrest?

A 
Hypoxia
Hypothermia
Hypovolaemia
Hypo or hyper-kalaemia
Tamponade
Tension pneumothorax
Thromboembolism 
Toxins
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112
Q

What is the presentation of a cardiac arrest?

A

Patient unconsciousness
Absent breathing
Absent carotid pulse

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113
Q

For a pulseless ventricular tachycardia of ventricular fibrillation, what is the management in cardiac arrest?

A

Shockable rhythm after 30:2 chest compressions-rescue breaths

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114
Q

What drug is administered despite a third shock in cardiac arrest?

A

Amiodarone 300mg IV bolus is lidocaine

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115
Q

What is the management of asystole?

A

CPR for 2 minutes
Administer adrenaline (1mg IV) every 3-5 minutes
atropine

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116
Q

What is the emergency management of tension pnuemothorax?

A

Needle into the 2nd intercostal space, mid-clavicular line

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117
Q

What is tricuspid regurgitation?

A

The backflow of blood from the right ventricle to the right atrium during systole

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118
Q

What are the congenital causes of tricuspid regurgitation?

A

Ebstein anomaly (Mispositioned tricuspid valve)

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119
Q

What are the functional causes of tricuspid regurgitation?

A

Consequence of right ventricular dilation (in pulmonary hypertension)

Valve prolapse

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120
Q

What are the causes of tricuspid regurgitation?

A

Congenital

Functional

Rheumatic heart disease
Infective endocarditis

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121
Q

What is the most likely cause of tricuspid regurgitation?

A

Infective endocarditis

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122
Q

What is the presentation of tricuspid regurgitation?

A 
Fatigue
Breathlessness
Palpitations
Headaches
Nausea
Anorexia
Epigastric pain
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123
Q

What pulse is associated with tricuspid regurgitation?

A

Irregularly irregular due to atrial fibrillation

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124
Q

What examination findings are evident in patients with tricuspid regurgitation?

A

Raised JVP with giant V waves

Parasternal heave

Pansystolic murmur heard best at the lower left sternal edge -louder on inspiration

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125
Q

When is a pansystolic murmur due to TR heard loudest?

A

During inspiration at the lower left sternal edge

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126
Q

What ECG changes are seen in TR?

A

Tall p waves (right atrial hypertrophy)

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127
Q

What is Atrial fibrillation?

A

Atrial fibrillation is characterised by rapid and ineffective atrial electrical conduction at 300-600bpm often subdivided into:
• Permanent
• Persistent (>1 week without self-terminating).
• Paroxysmal (Intermittent <1 week).

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128
Q

What kind of tachycardia is atrial fibrillation?

A

Supraventricular tachycardia caused by a re-entry circuit within the right atrium

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129
Q

What are the causes of Atrial fibrillation?

A 
Heart
•	Mitral valve disease
•	Myocardial infarction (Seen in 22%). 
•	Heart disease
•	Rheumatic heart disease
•	Cardiomyopathy 
•	Ischaemic heart disease
•	Pericarditis 
•	Atrial myxoma

Lung causes
• Bronchial carcinoma
• Pulmonary embolism
• Pneumonia

Other: Caffeine, alcohol, post-operative.

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130
Q

What is the most common conduction ratio of atrial flutter?

A

2:1

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131
Q

What are the symptoms of AF?

A

Often asymptomatic in patients.
• Patients experience palpitations
• Syncope (Cardiac output decreases by 10-20%, as the ventricular filling is ineffective).
• Symptoms of the cause of AF.

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132
Q

What pulse is associated with AF?

A

Irregularly irregular pulse

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133
Q

What is the difference in the apical beat and radial pulse?

A

Apical > radial

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134
Q

What are the ECG changes for AF?

A

Uneven baseline with absent p waves

Irregular intervals between QRS complexes

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135
Q

What are the ECG changes in atrial flutter?

A

Narrow complex tachycardia
Saw tooth appearance
Loss of isoelectric baseline

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136
Q

What are the three steps of management for AF?

A

Rate control - Restores ventricular rate to a normal range
Rhythm control - Restores sinus rhytmn

Anticoagulation

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137
Q

What is the management for acute AF <48 hours that is haemodynamically stable?

A

Synchronised DC cardioversion under sedation

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138
Q

What is the management for acute AF <48 hours (Haemodynamically stable)?

A

Rate control

beta-blockers

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139
Q

What are the signs of haemodynamic instability in AF?

A

rapid pulse (greater than 150 beats per minute) and/or low blood pressure (systolic blood pressure less than 90 mmHg), loss of consciousness, severe dizziness or syncope, ongoing chest pain, or increasing breathlessness.

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140
Q

Which calcium channel blockers are used in the rate control of AF?

A

Diltiazem and verapamil

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141
Q

Why are beta-blockers not prescribed alongside Diltiazem or verapamil?

A

Risk fo bradycardia

Aim for rest rate <90 bpm

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142
Q

If BBs and CBBs are ineffective rate control for AF, what drug can be used?

A

Digoxin

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143
Q

How long should a patient be anti-coagulated for before elective cardioversion?

A

3 weeks using Warfarin

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144
Q

What is the first choice drug for Rhythm control if there is no structural heart disease?

A

Flecainide

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145
Q

In a patient with structural heart disease and AF, what is the drug for Rhytmn control?

A

IV amiodarone

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146
Q

What drug is prescribed for paroxysmal AF?

A

Flecainide or sotalol PRN

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147
Q

Which score is used to assess the risk of stroke in patients with AF?

A

CHA₂DS₂-VASc

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148
Q

What is the CHA₂DS₂-VASc score?

A 
Congestive heart failure = 1
Hypertension = 1
Age (>75) = 2
Diabetes = 1
Stroke = 2
Vascular disease (PVD) =1
Age (65-74) =1
Sex (Female) = 1
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149
Q

When is a DOAC given for AF in a male?

A

1 or more

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150
Q

What is a a DOAC given for AF in a female?

A

2 or more

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151
Q

What is heart block?

A

Heart block is defined as an impairment of the atrioventricular node impulse conduction, as represented by the interval between P waves and the QRS complex.

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152
Q

What is 1st-degree AV block?

A

Prolonged conduction through the AV node

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153
Q

What is the normal PR interval?

A

120-200ms (3-5 squares)

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154
Q

What is the PR interval in 1-st degree AV block?

A

> 200ms

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155
Q

What is 2nd-Degree AV block (Type 1)?

A

Mobitz type 1
-Progressive prolongation of the AV node conduction until one atrial pulse fails to be conducted through the AV node.

  • There is a skipped beat and the cycle begins again
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156
Q

What is Mobitz-Type 2 AV block?

A

Fixed PR interval in duration but not every P wave is followed by a QRS complex

Defined as the number of normal conductions per failed on (2:1, two p waves for each QRS complex)

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157
Q

Describe the PR interval in a Mobitz-Type 2 AV block?

A

Fixed

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158
Q

What is 3rd degree (Complete heart block)?

A

There is no relationship between atrial and ventricular contraction

Failure of conduction through the AV node leads to ventricular contraction generated by a focus of depolarisation within the ventricle

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159
Q

What rhythm is associated with complete heart block?

A

Ventricular escape rhythm

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160
Q

What is the most common metabolic cause for AV block?

A

Hyperkalaemia

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161
Q

What 3 main ECG changes are seen in hyperkalaemia?

A

Tall tented T waves
Flattened P waves
Widened QRS complex
PR prolongation

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162
Q

What is the most common cause of AV block?

A

MI or ischaemic heart disease

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163
Q

What is the presentation of Mobitz Type 2 and 3rd degree heart block?

A

Dizziness, syncope, palpitations, chest pain and heart failure

Adams Attacks

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164
Q

What are Adams Attacks?

A

Syncope caused by ventricular asystole

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165
Q

Which waves are associated with a raised JVP in complete heart block?

A

Cannon A waves

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166
Q

What are cannon A waves?

A

Seen occasionally in the jugular vein due to simultaneous contraction of the atria and ventricles.

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167
Q

What ECG appearances are seen in first-degree AV block?

A

Prolonged PR interval >200ms

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168
Q

What ECG appearances are seen in Mobitz Type 1?

A

Progressive prolongation of the PR interval (Followed by a skipped beat)

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169
Q

What ECG appearances are seen in Mobitz type 2?

A

Intermittent p waves not followed by a QRS complex (regular pattern)
-Fixed PR interval

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170
Q

What ECG appearances are seen in third-degree heart block?

A

No relationship between P waves and QRS complex
If QRS is initiated by focus in the Bundle of His – QRS is narrow.
More distally  Wide and slow rate (~30 beats/min).

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171
Q

What is the management of chronic block?

A

Permanent pacemaker insertion (PPM)

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172
Q

What is the management of acute AV block?

A

IV atropine

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173
Q

What is supraventricular tachycardia?

A

SVT refers to any tachyarrhythmia arising from above the level of the Bundle of His, usually at the atria or the AV node

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174
Q

What kind of tachycardia is associated with an SVT?

A

Narrow Complex tachycardia

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175
Q

What is a normal QRS interval?

A

80 and 100 milliseconds

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176
Q

What is AVNRT and AVRT?

A

Atrioventricular nodal re-entry tachycardia (AVNRT)

Atrioventricular re-entry tachycardia (AVRT)

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177
Q

What is AVNRT?

A

A localised re-entry circuit forms around the AV node - conducts to the ventricles faster than the normal conduction pathway

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178
Q

What is AVRT?

A

Occurs when there is normal AV conduction as well as an accessory pathway being present

Forming a re-entry circuit between atria and ventricles

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179
Q

What is a common form of AVRT?

A

Wolff-Parkinson-white Syndrome

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180
Q

Which accessory pathway is associated with WPWs?

A

Bundle of Kent

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181
Q

What are the risk factors for SVT?

A 
Nicotine
Alcohol
Caffeine
Previous MI
Digoxin toxicity
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182
Q

What is the presentation of SVT?

A
  • Palpitations
  • Light-headedness
  • Polyuria (Due to increased atrial pressure causing ANP release).
  • Abrupt onset and termination of symptoms
  • Other symptoms: Fatigue, chest discomfort, dyspnoea, syncope.
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183
Q

Why is polyuria associated with an SVT?

A

Due to increased atrial pressure causing ANP release

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184
Q

Which heart sound is associated with WPWs?

A

S3 gallop
RV heave
Displaced beat

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185
Q

Which ECG changes are present in AVRT?

A

Delta wave

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186
Q

What ECG appearances are seen in AVNRT?

A

Narrow complex tachycardia
P waves buried in QRS complex
Decreased PR interval

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187
Q

What ECG changes are seen in AVRT?

A

Narrow complex tachycardia
Shortened PR interval
P waves buried in QRS

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188
Q

What investigations are performed in SVT?

A

24 hour ECG monitoring

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189
Q

In a haemodynamically unstable patient what is the management of SVT?

A

DC cardioversion

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190
Q

What is the initial management of SVT, if haemodynamically stable?

A

Vagal manoevures - Valsalva, carotid massage

• Adenosine 6 mg bolus (Can increase to 12 mg)  Contraindicated in asthma as it can cause bronchospasm (Use verapamil).

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191
Q

What drug is administered if vagal manoeuvres fail in acute SVT?

A

6mg bolus Adenosine

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192
Q

What is the definitive management of AVRT?

A

Radiofrequency ablation of the accessory pathway

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193
Q

What is WPWs?

A

A congenital abnormality can result in supraventricular tachycardias that use an accessory pathway (Bundle of Kent).
• Pre-excitation syndrome: Early activation of the ventricles due to impulses bypassing the AV node via the accessory pathway.

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194
Q

Why are there delta waves in WPWs?

A

pre-excitation syndrome

Early activation of the ventricles due to impulses bypassing the AV node via the accessory pathway

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195
Q

What is the presentation of WPWs?

A

Palpitations
Light-headedness
Syncope

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196
Q

What is paroxysmal SVT followed by?

A

Followed by a period of polyuria due to atrial dilation and release of ANP

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197
Q

What are the classical findings in WPSs (ECG)?

A

Short PR interval
Broad QRS complex
Delta-waves

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198
Q

What type of tachycardia is ventricular fibrillation?

A

Irregular broad-complex tachycardia

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199
Q

What is the aetiology of Vfib?

A

Ventricular fibres contract haphazardly causing complete failure of ventricular function due to disorganised electrical activity

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200
Q

What are the risk factors for Vfib?

A
  • Coronary artery disease – most common
  • Atrial fibrillation
  • Hypoxia
  • Ischaemia
  • Pre-excitation syndrome
  • Cardiomyopathy
  • Drugs
  • Electrolyte imbalance
  • Brugada syndrome
  • Long QT-syndrome
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201
Q

What is the presentation of V fib?

A

Chest pain
Fatigue
Palpitations
Cardiac arrest

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202
Q

What are the ECG appearances in V fib?

A

Chaotic irregular deflections of varying amplitude, no identifiable p waves

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203
Q

What investigations are performed in V fib?

A

ECG
Cardiac enzymes- Troponin to identify any recent ischaemic events

Electrolytes - Derangement can cause arrhythmia, including VF

Drug levels and toxicology screen - Anti-arrhytmic can cause arrythmia, as can various recreational drugs

TFTs - Hyperthyroidism

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204
Q

What is the management of Vfib?

A

Requires urgent defibrillation and cardioversion (Non-synchronised DC shock)

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205
Q

What kind of DC shock is administered in VFIB?

A

Non-synchronised DC shock

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206
Q

What may be the chronic management for Vfib?

A

Implantable cardioverter defibrillator (ICD)

Empirical beta-blockers

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207
Q

What are the complications of V fib?

A
  • Ischaemic brain injury due to loss of cardiac output
  • Myocardial injury
  • Post-defibrillation arrhythmias
  • Aspiration pneumonia
  • Skin burns
  • Death
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208
Q

Definition of ventricular tachycardia?

A

A regular broad complex tachycardia, originating from the ventricles

Rate >120bpm

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209
Q

What is the aetiology of vTachy?

A

Electrical impulses arise from a ventricular ectopic focus – an excitable group of cells within the atria/ventricles that cause a premature heartbeat outside the normally functioning circulation.
• Can impair cardiac output – causing hypotension, collapse, and acute cardiac failure.

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210
Q

What are the risk factors of Vtachy?

A
  • Coronary heart disease
  • Structural heart disease
  • Electrolyte deficiencies (Hypokalaemia, hypocalcaemia, hypomagnesaemia)
  • Use of stimulant drugs (Caffeine, cocaine).
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211
Q

What is the presentation of vtachy?

A

Chest pain
Palpitations
Dyspnoea
Syncope

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212
Q

What are the signs of haemodynamic instability in Vtachy?

A
  • Respiratory distress
  • Bibasal crackles
  • Raised JVP
  • Hypotension
  • Anxiety
  • Agitation
  • Lethargy
  • Coma
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213
Q

What are the ECG changes in Vtachy?

A

Rate >100bpm
Broad QRS complexes
AV dissociation

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214
Q

What is the management for Vtachy?

A

Pulseless VT - ALS

+ Unsynchronised DC cardioversion

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215
Q

What is the management for a stable VT?

A

Synchronised DC shock

Amiodarone

216
Q

What drug is used in the management of stable VT?

A

Amiodarone

217
Q

What are the indications of an ICD in VT?

A
  • Sustained VT causing syncope
  • Sustained VT with ejection fraction <35%
  • Previous cardiac arrest due to VT or VF
  • MI complicated by non-sustained VT.
218
Q

What are the complications of VT?

A
  • Congestive cardiac failure
  • Cardiogenic shock
  • VT may deteriorate into VF.
219
Q

What is an aortic dissection?

A

An aortic dissection is characterised by a separation in the aortic wall intima, causing blood flow into a new false lumen

220
Q

What are the two types of aortic dissection?

A

Type A - Ascending Aorta

Type B - Descending Aorta

221
Q

What is a Type A aortic dissection?

A

Ascending Aorta (Most common-70%)

222
Q

What is a type B aortic dissection?

A

Descending aorta (Distal to the left subclavian artery)

223
Q

What is the aetiology of an aortic dissection?

A

An aortic dissection is usually preceded by degenerative changes in the smooth muscle of the aortic media

224
Q

What are the risk factors for aortic dissection?

A
  • Hypertension (Main)
  • Aortic atherosclerosis
  • Connective tissue disease (Marfan’s, Ehler’s Danlos, SLE).
  • Congenital cardiac abnormalities (Coarctation of the aorta).
  • Aortitis
  • Iatrogenic
  • Trauma
  • Crack cocaine
225
Q

Why does aortic dissection cause symptoms?

A

Expansion of the false lumen - obstruction of branches of the aorta

Hypoperfusion of the target organs of these major arteries can give rise to other symptoms

226
Q

What is the main presentation of aortic dissection?

A

Sudden central tearing chest pain radiating to the back (in between the shoulder blades)

227
Q

What symptoms are associated with obstruction of the carotid artery in aortic dissection?

A

Hemiparesis
Dysphasia
Blackout

228
Q

On examination findings what is seen in an aortic dissection?

A

Murmur on the back below the left scapula

Hypertension

Blood pressure difference between the two arms >20mmHg
Wide pulse pressure

229
Q

What is pulsus paradoxus?

A

Abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration

230
Q

What is the first-line imaging for aortic dissection?

A

CT thorax - Reveals false lumen

231
Q

What is the definitive imaging for an aortic dissection?

A

Transoesophageal echocardiogram

232
Q

What would a CXR show in an aortic dissection?

A

Widened mediastinum in acute or chronic dissection

233
Q

What is the management of a haemodynamically unstable aortic dissection?

A

ALS
Supplemental oxygen
IV resus

234
Q

What is the management of a Type A aortic dissection?

A

Beta-blocker (Labetalol) and Endovascular repair

235
Q

What is the 1st line management of a Type B aortic dissection?

A

IV labetalol
Opioid analgesia
Vasodilator (IV sodium nitroprussie)

236
Q

What are the two main types of chronic limb ischaemia?

A

Intermittent claudication

Critical limb ischaemia

237
Q

What is intermittent claudication?

A

Calf pain on exercise - increases muscle demand which cannot be satisfied by supply

Cramping pain in the calf, thigh, or buttock after walking for a given distance

238
Q

When does pain occur in critical limb ischaemia?

A

Pain occurs at rest - most severe manifestation of peripheral vascular disease

239
Q

What are the consequences of critical limb ischaemia?

A

Can lead to tissue loss - gangrene/ulceration

Gangrene - Death of tissue from poor vascular supply

Arterial ulcers - Abnormal breaks in an epithelial surface

240
Q

Define acute limb ischaemia?

A

A sudden decrease in arterial perfusion in a limb due to thrombotic or embolic causes or post-angioplasty

241
Q

What is the treatment for acute limb ischaemia?

A

Medical emergency

-Revascularisation within 4-7 hours

242
Q

When is intermittent claudication relieved?

A

At rest

243
Q

What is claudication distance?

A

Distance walked resulting in cramping pain

244
Q

Which vessel is concerned with calf claudication?

A

Femoral

245
Q

Which vessel is associated with buttock claudication?

A

Iliac

246
Q

What are the features of critical limb ischaemia?

A

Ulcers
Gangrene
Rest pain
Night pain (Relieved by dangling leg over the edge of the bed)

247
Q

What is Leriche Syndrome?

A

Aortoiliac occlusive disease

  • Buttock claudication
  • Impotence (ED)
  • Absent/weak distal pulses
248
Q

What are the 6Ps of acute limb ischaemia?

A 
Pain
Pulseless
Pale
Paralysis
Paraesthesia
Perishingly coLD
249
Q

What are the other symptoms of PVD?

A

Atrophic skin
Hairless
Punched-out ulcers (Painful)
Colour change when raising leg

250
Q

What are the first-line investigations for peripheral vascular disease?

A

Ankle Brachial index (ABI)

251
Q

What ABI parameters are indicative of PAD?

A

0.50-0.90

252
Q

What ABI measurement is associated with critical limb ischaemia?

A

<0.5

253
Q

What is the gold standard investigation for PVD?

A

MRI/CT angiogram

254
Q

What is the first-line management for acute limb ischaemia?

A

Revascularisation

255
Q

What is the management of a non-viable limb in acute limb ischaemia?

A

Amputation

256
Q

What anti-platelet therapy is administered in ALI?

A

Aspirin (75-352mg Orally OD), or clopidogrel

Anticoagulation - UFH Heparin

257
Q

What is the first-line therapy for claudication?

A

Antiplatelet therapy
Exercise therapy
Symptom relief

258
Q

Define arterial ulcer

A

Arterial ulcers are a localised area of damage and breakdown of the skin due to an inadequate arterial blood supply

259
Q

Where are arterial ulcers found?

A

Feet of patients

260
Q

What is the aetiology of arterial ulcers?

A

The ulcers are caused by compromised blood flow to the capillary beds to the lower extremities

261
Q

What are the risk factors fo arterial ulcers?

A 
Coronary heart disease
History of stroke or TIA
Diabetes mellitus
Peripheral arterial disease (Intermittent claudication, critical limb ischaemia)
obesity and immobility
262
Q

What is the presentation of arterial ulcers?

A

Often distal - at the dorsum of the foot or between the toes.

Punched out appearance

Elliptical with clearly defined edges

The ulcer contains grey and granulated tissue

263
Q

What is the appearance of an arterial ulcer?

A

Punched-out

Clearly defined edges

264
Q

When does the pain of arterial ulcers arise?

A

Pain is worse when supine as arterial blood flow is further reduced when supine

Night pain

Pain is relieved by dangling the affected leg off the end of the bed

265
Q

What are the investigations for an arterial ulcer?

A

Duplex ultrasonography of the lower limbs

ABPI

Percutaneous angiography

266
Q

What is the management of arterial ulcers?

A

Revascularisation

267
Q

What are venous ulcers?

A

Large shallow ulcers were predominantly found superior to the medial malleoli

They are caused by incompetent valves in the lower limbs leading to venous stasis and ulceration

268
Q

Where are venous ulcers predominantly found?

A

Superior to the medial malleoli

269
Q

What is the main cause of venous ulcers?

A

Incompetent valves

270
Q

Describe the appearance of venous ulcers

A

Large shallow, relatively painless ulcer with an irregular margin situated superior to the medial malleoli

271
Q

What investigations are performed for venous ulcers?

A

ABPI

272
Q

What is the management for venous ulcers?

A

Graduated compression stockings

273
Q

What is pericarditis?

A

Defined as inflammation of the pericardium

-Characterised clinically by a triad of chest pain, pericardial friction rub and serial ECG changes

274
Q

What are the two layers of the pericardium?

A

Visceral and parietal pericardium

275
Q

What is the visceral layer of the pericardium?

A

Adherent to the myocardium and secretes pericardial fluid

276
Q

What is the parietal pericardium?

A

Composed of collagen fibres with interspersed elastin fibrils (Highly innervated)

277
Q

What is the aetiology of pericarditis?

A
  • Idiopathic
  • Infective
  • Connective tissue disease (Sarcoidosis, SLE, Scleroderma)
  • Post-MI (Within 24-72 hours of MI – occurs in up to 20% of patients).
  • Dressler’s Syndrome – Pericarditis occurring weeks/months after acute MI
  • Malignancy- Lung, breast, lymphoma, leukaemia, melanoma
  • Radiotherapy
  • Thoracic surgery
  • Drugs (Hydralazine, isoniazid)
  • Others: Uraemia, rheumatoid arthritis, myxoedema, trauma
Most common causative organisms
•	Coxsackie B
•	Echovirus
•	Mumps
•	Streptococci
•	Fungi
•	Staphylococci
•	TB
278
Q

Describe the chest pain in pericarditis?

A

Sharp and central , radiating to the neck or shoulders
Worse when coughing or deep inspiration
Relieved by sitting forward
Worse when lying flat

279
Q

When is pericarditis pain worse?

A

Worse on inspiration or coughing

280
Q

When is pericarditis pain relieved?

A

When sitting forward

281
Q

What are the examination findings of pericarditis?

A 
Fever
Pericardial friction rub 
Beck's triad
-Raised JVP
-low blood pressure
-Muffled heart sound
282
Q

What is Beck’s triad?

A
  • Raised JVP
  • low blood pressure
  • Muffled heart sound
283
Q

Where is the pericardial friction rub heard best?

A

Lower left sternal edge with the patient leaning forward

284
Q

What is Kussmaul’s sign?

A

A rise in JVP that occurs during inspiration

285
Q

What are the signs of constrictive pericarditis?

A
  • Kussmaul’s sign – Paradoxical increase in JVP that occurs during inspiration.
  • Pulsus paradoxus
  • Hepatomegaly
  • Ascites
  • Oedema
  • Pericardial knock (Due to rapid ventricular filling) – early diastolic sound.
  • Atrial fibrillation
286
Q

What ECG appearances are seen in pericarditis?

A

Wide-spread Saddle-shaped (concave) ST elevation

Tachycardia

PR depression followed by T wave flattening and inversion

287
Q

What is the acute management of cardiac tamponade?

A

Emergency pericadiocentesis (Aspiration of fluid from pericardial space_

288
Q

What is the medical management for pericarditis?

A

NSAIDs (+Colchicine)

May require PPI protection

289
Q

What is the surgical management for constrictive pericarditis?

A

Pericardiectomy

290
Q

What is constrictive pericarditis?

A

Chronic inflammation of the pericardium with thickening and scarring of the pericardial layers

  • Limits the ability of the heart fo functional normally -encased in a rigid pericardium
291
Q

What is the presentation of constrictive pericarditis?

A

Graduate onset of symptoms

Right heart failure signs

292
Q

what are right heart failure signs?

A
  • Peripheral oedema
  • Raised JVP
  • Kussmaul’s sign
  • Pulsatile hepatomegaly
  • Soft diffuse apex beat
  • Quiet heart sounds, S3
  • Diastolic pericardial knock
  • Splenomegaly
  • Ascites
  • Oedema
293
Q

A CXR in constrictive pericarditis will reveal what?

A

Small heart +/- calcification of the pericardium.

294
Q

What is the definitive management of constrictive pericarditis?

A

Complete pericardiectomy

NSAIDs

295
Q

What is myocarditis?

A

Acute inflammation and necrosis of the cardiac muscle (myocardium)

296
Q

What is the most common cause of myocarditis?

A

Coxsackie B virus

297
Q

What is the presentation of myocarditis?

A

Prodromal flu-like illness with fever, malaise, fatigue and lethargy

Breathlessness (Due to pericardial effusion/myocardial dysfunction)

Palpitations
Sharp chest pain

298
Q

What heart sounds are associated with myocarditis?

A

S4 gallop

Soft S1

299
Q

What is the first-line investigation for myocarditis?

A

ECG

300
Q

What is the definitive investigation for myocarditis?

A

Pericardial fluid drainage
-Measures glucose, protein, cytology, culture and sensitivity

Helps identify the causative organism

301
Q

Which blood test confirms the diagnosis of myocarditis?

A

Troponin I or T

302
Q

Which cardiac enzyme is raised in myocardiits?

A

Troponin

303
Q

What is the management of myocarditis?

A

ACEi
Beta-blockers
Diuretics
Aldosterone antagonists

Steroids and immunosuppressants (Methylpredinsolone)

304
Q

What is an aortic aneurysm?

A

A permanent pathological dilation of the aorta with a diameter of x1.5 or >3cm

305
Q

What is the normal diameter of the aorta?

A

2cm

306
Q

How do unruptured aneurysms occur?

A

Degeneration of elastic lamellae and smooth muscle loss

307
Q

What connective tissue disorders are associated with an aortic aneurysm?

A

Marfan’s syndrome, Ehlers-Danlos syndrome

308
Q

What is the presentation of a ruptured aneurysm?

A

Pain in the abdomen radiating to the back, iliac fossa or groin

pain is sudden/severe

Syncope
Shock

309
Q

On palpation of the abdominal aorta, describe an AAA?

A

Pulsatile and laterally expansile mass on bimanual palpation

310
Q

What is the first-line investigation for an AA?

A

Aortic ultrasound -defined dilation of >1.5x the expected anterior-posterior diameter

311
Q

What imaging modality can identify the site of rupture for an AA?

A

CT contrast

312
Q

What is the management of a ruptured AAA?

A

Urgent surgical repair-EVAR

313
Q

What is Virchow’s triad?

A

Vessel injury, venous stasis and activation of the clotting system

314
Q

What is DVT?

A

DVT is the development of a blood clot in a major deep vein of the leg, thigh, pelvis or abdomen.

315
Q

Where do most blood clots in DVT form?

A

Above or behind the venous valve

316
Q

Which fibrinolytic breakdown product is raised in acute thrombi?

A

D-dimer

317
Q

What are the risk factors for DVT?

A
  • Age
  • COCP (Synthetic oestrogen)
  • Post-surgery
  • Prolonged immobility – Travel history
  • Obesity
  • Pregnancy
  • Dehydration
  • Smoking
  • Polycythaemia
  • Thrombophilia (Protein C deficiency)
  • Malignancy
  • Trauma
  • Past DVT.
318
Q

What is the presentation of DVT?

A 
Swollen limb (calf swelling)
Mild fever
Localised pain along the deep venous system (From groin to the adductor canal and in the popliteal fossa)
319
Q

What are the examination findings for DVT?

A

• Local erythema, warmth and swelling, tenderness
• Measure leg circumference (Increased)
• Varicosities (Swollen/tortuous vessels)
• Skin colour changes
• Mild fever
• Examine for PE – Check RR, pulse oximetry and pulse rate.
N.B: Homan’s sign – Forced passive dorsiflexion of the ankle causes deep calf pain.

320
Q

What is homan’s sign in DVT?

A

Forced passive dosriflexion of the ankle causes deep calf pain

321
Q

Which criteria is used to risk stratify DVT?

A

Well’s Criteria

322
Q

Which scoring threshold of Wells Criteria indicates a D-dimer test?

A

A score <2

323
Q

A raised D-dimer in DVT will indicate what investigation?

A

Duplex USS

324
Q

What is the gold standard investigation for DVT?

A

Doppler Ultrasound (Duplex USS)

325
Q

What are the findings on a Doppler USS for DVT?

A
  • Inability to compress lumen of the vein using an ultrasound transducer
  • Reduced or absent spontaneous flow, lack of respiratory variation, intraluminal echoes or colour flow patency.
326
Q

What is the management of DVT?

A

Low molecular weight heparin

Warfarin INR 2-3

IVC filter

327
Q

What is the prophylaxis for DVT?

A

Graduated compression stockings

328
Q

What is dilated cardiomyopathy?

A

A dilated heart of the unknown cause. Thinning of inner layers of heart chambers, heart muscles stretch and weaken. There is an impairment of contractility (Systolic failure) – left ventricular failure.

329
Q

What type of heart failure is associated with dilated cardiomyopathy?

A

Systolic heart failure

330
Q

What type of heart failure is associated with hypertrophic cardiomyopathy?

A

Diastolic heart failure

331
Q

What is hypertrophic cardiomyopathy?

A

Thickening of the cardiac muscle - impairing compliance

332
Q

What is restrictive cardiomyopathy?

A

The cardiac cells become replaced with abnormal tissue (Scar tissue) – stiffening of ventricular wall  Abnormal filling phase  Impaired compliance and diastolic function.

333
Q

What are the causes of restrictive cardiomyopathy?

A
  • Amyloidosis
  • Sarcoidosis
  • Haemochromatosis
  • Scleroderma
  • Loffler’s eosinophilic endocarditis
  • Endomyocardial fibrosis
334
Q

What are the symptoms associated with hypertrophic cardiomyopathy?

A
  • Usually, asymptomatic
  • Syncope
  • Angina
  • Arrhythmias
  • Dyspnoea
  • Palpitations
  • Family history of sudden cardiac death
335
Q

What are the symptoms associated with dilated cardiomyopathy?

A
  • Raised JVP
  • Displaced apex beat
  • Functional mitral and tricuspid regurgitations
  • Third heart sound
  • Tachycardia
  • Pleural effusion
  • Oedema
  • Jaundice
  • Hepatomegaly
  • Ascites
  • AF
336
Q

What murmur is associated with hypertrophic cardiomyopathy?

A

Ejection systolic murmur

337
Q

What heart sound is associated with hypertrophic cardiomyopathy?

A

S4

338
Q

What is Kussmaul’s sign?

A

Rise in JVP on inspiration due to restricted filling of the ventricles

339
Q

What CXR signs reveal heart failure?

A

Pulmonary oedema

340
Q

What ECG appearances are associated with hypertrophic cardiomyopathy?

A

Left Axis deviation

Signs of left ventricular hypertrophy (Tall R waves)

341
Q

What appearances are revealed on an echocardiogram for dilated cardiomyopathy?

A

Dilated ventricles with global hypokinesia and low ejection fraction

342
Q

What echocardiogram appearance is seen for restrictive cardiomyopathy secondary to amyloidosis?

A

Sparkling appearance

343
Q

What is the management for cardiomyopathy?

A

Treat heart failure and arrythmias

ICD for recurrent VTs

344
Q

What is the definition of systolic heart failure?

A

The inability of the ventricles to contract normally - decreased cardiac output

Ejection fraction <40%

345
Q

What are the main causes of systolic heart failure?

A

IHD, MI, cardiomyopathy

346
Q

What is diastolic heart failure?

A

The inability of the ventricle to relax and fill adequately. - Increased filling pressure (Reduced EDV) - Preserved ejection fraction

347
Q

Acute or decompensated heart failure is associated with what?

A

Pulmonary and peripheral oedema

348
Q

What are the causes of left heart failure?

A
  • Ischaemic heart disease
  • Hypertension
  • Cardiomyopathy
  • Aortic valve disease
  • Mitral regurgitation
349
Q

what are the causes of right heart failure?

A
  • Secondary to left heart failure  Congestive heart failure
  • Infarction
  • Cardiomyopathy
  • Pulmonary hypertension/embolus/valve disease
  • Chronic lung disease
  • Tricuspid regurgitation
350
Q

What are the causes of high-output cardiac failure?

A

• Anaemia, Beriberi, pregnancy, Paget’s disease, Hyperthyroidism, Arteriovenous malformation.

351
Q

What is the presentation of left heart failure?

A 
Left Heart failure – Symptoms caused by pulmonary congestion. 
•	Orthopnoea
•	Paroxysmal nocturnal dyspnoea
•	Fatigue
•	Poor exercise tolerance
•	Nocturnal cough (+/- pink frothy sputum)
•	Wheeze
•	Nocturia
•	Cold peripheries
•	Weight loss
•	Muscle wasting
352
Q

What classification is used to scale Dyspnoea?

A

Dyspnoea (Based on NYHA Classification).
• 1- No dyspnoea
• 2- Dyspnoea on ordinary activities
• 3 – Dyspnoea on less than ordinary activities
• 4 – Dyspnoea at rest.

353
Q

What is the presentation of right heart failure?

A 
Right heart failure – Venous congestion 
•	Swollen ankles 
•	Fatigue
•	Increased weight (Due to oedema)
•	Reduced exercise tolerance
•	Anorexia
•	Nausea
354
Q

What are the examination findings for left heart failure?

A
  • Tachycardia
  • Tachypnoea
  • Displaced apex beat (LV dilatation)
  • Bilateral basal crackles
  • S3 gallop (Caused by rapid ventricular filling)
  • Pansystolic murmur (Due to functional mitral regurgitation)
355
Q

What heart sound is associated with left heart failure?

A

s3 gallop

356
Q

Auscultation of the chest reveals what in acute heart failure?

A

Bilateral basal crackles

357
Q

What are the examination findings for acute left ventricular failure?

A
  • Tachypnoea
  • Cyanosis
  • Tachycardia
  • Peripheral shutdown
  • Gallop rhythm
  • Wheeze
  • Fine crackles throughout lung
  • Pulsus alternans – Arterial pulse waveforms showing alternating strong and weak beats (Sign of left ventricular systolic impairment).
358
Q

What are the examination findings for right heart failure?

A
  • Raised JVP
  • Hepatomegaly
  • Ascites
  • Ankle/sacral pitting oedema
  • Signs of functional tricuspid regurgitation – pulsation in neck and face.
  • Facial engorgement
  • Epistaxis
  • RV heave (Pulmonary hypertension)
359
Q

What are the CXR findings for acute heart failure?

A

Alveolar oedema (Shadowing - Bat’s wings)
Kerley B lines (Interstitial oedema)
Cardiomegaly (Seen in PA film)
Dilated prominent upper lobe vessels (Upper lobe diversion)

Pleural effusion - Blunt costophrenic angles

360
Q

What doe Kerley B lines represent?

A

Interstitial oedema

361
Q

What imaging modality is used to assess ventricular function in heart failure?

A

Echocardiogram

362
Q

What EF is associated with systolic dysfuncgion?

A

EF <40%

363
Q

What investigation is used to measure end-diastolic pressures?

A

Swan-Ganz catheter

364
Q

What is the acute management for heart failure?

A 
Sit the patient up 
60-100% oxygen
Diamorphine
GTN infusion 
IV furosemide
365
Q

What inotropes are given to treat cardiogenic shock?

A

Dobutamine

366
Q

What is the treatment for chronic heart failure?

A

Vasodilators
ACEis ARBS
Diuretics

367
Q

Which diuretic is commonly used in acute heart failure?

A

Furosemide

368
Q

What vasodilators are used in heart failure?

A

Hydralazine and nitrate

369
Q

What aldosterone antagonist is used in acute heart failure?

A

Spironolactone

370
Q

What are the indications for cardiac resynchronisation therapy in acute heart failure?

A

LEF <35% and QRS >120msec

371
Q

What are the adverse effects of beta-blockers?

A

Bradycardia, hypotension, fatigue, dizziness

372
Q

What are the adverse effects of ACEi?

A

Hyperkalaemia, renal impairment, dry cough, light-headedness, fatigue, GI disturbances, angioedema.

373
Q

What are the adverse effects of spironolactone?

A

Hyperkalaemia, renal impairment, gynecomastia, breast tenderness/hair growth in women, changes in libido.

374
Q

What are the adverse effects of hydralazine/nitrate?

A

Headache, palpitation, flushing

375
Q

What is infective endocarditis?

A

Infective endocarditis is an infection involving the endocardial surface of the heart, including the valvular structures, the chordae tendinea, and sites of septal defects

376
Q

What is the most common causative organism for infective endocarditis?

A

Strep Viridian and Bovis

Staph Aureus

377
Q

What is the pathophysiology of infective endocarditis?

A

The mitral and aortic valves are typically affected given that these areas are susceptible to sustained endothelial damage secondary to turbulent flow.
• Platelets and fibrin adhere to the underlying collagen surface to form a prothrombotic milieu.
• Bacteriaemia leads to colonisation of the thrombus, perpetuating further fibrin deposition and platelet aggregation  Infected vegetation.
• Vegetations destroy valve leaflets, invade the myocardium or aortic wall leading to abscess cavities.
• Activation of immune system  Formation of immune complexes  Vasculitis, glomerulonephritis, arthritis.

378
Q

What are the risk factors for infective endocarditis?

A
  • Abnormal valves (Congenital calcification, rheumatic heart disease).
  • Prosthetic heart valves – Can occur during surgery or later
  • Turbulent blood flow (Patent ductus arteriosus)
  • Recent dental work/poor dental hygiene (Source of S. Viridans)
  • Dermatitis
  • IV injections
  • Renal failure
  • Organ transplantation
  • Post-operative wounds.
379
Q

What two symptoms suspect endocarditis?

A

A fever and a new murmur

380
Q

What is the acute course of infective endocarditis?

A

Acute heart failure and emboli

381
Q

What is the presentation of infective endocarditis?

A 
Fever with sweats/chills/rigours (May be relapsing and remitting). 
•	Weight loss
•	Malaise
•	Arthralgia
•	Myalgia 
•	Confusion
•	Skin lesions
•	Ask about recent dental surgery or IV drug use.
382
Q

What is the presentation of infective endocarditis?

A
  • Pyrexia
  • Tachycardia
  • Signs of anaemia
  • Clubbing
  • Splenomegaly
  • Any new murmur or changing the previous murmur.
383
Q

What axial deviation is associated with pulmonary embolism?

A

Right axis deviation

384
Q

What is the most common ECG finding with a pulmonary embolism?

A

Sinus tachycardia

385
Q

What vasculitis changes are associated with infective endocarditis?

A

Roth spots on the retina

Osler’s nodes
Splinter haemorrhages
Janeway Lesions
Glomerulonephritis

386
Q

What are Osler’s nodes?

A

Tender nodules on the finger/toe pads

387
Q

What are roth spots?

A

White centred retinal haemorrhage

388
Q

What are splinter haemorrhages?

A

A longitudinal red-brown haemorrhage under the nail

389
Q

What are Janeway lesions?

A

Irregular non-tender haemorrhaging macules located on the palms (Embolic)

390
Q

How many blood cultures should be taken for the diagnosis of infective endocarditis?

A

Obtain 3 sets of blood cultures from different venipuncture sites taken at 30-minutes prior to antibiotic therapy

391
Q

What is the definitive diagnostic investigation for infective endocarditis?

A

A transoesophageal echocardiogram

392
Q

what does a TOE reveal in IE?

A

Reveals vegetation
Abscess valve perforation
Mobile mass
Dihesnce of the prosthetic valve

393
Q

What criteria is used for the diagnosis of infective endocarditis?

A

Duke’s criteria

394
Q

What are the major criteria for Duke’s?

A

Positive blood cultures for IE- 2 separate

Echocardiogram findings

Coxiella Brunetti infection

395
Q

What are the minor criteria for IE?

A

Predisposing heart condition or IV drug use

Fever over 38

Vascular changes - Janeway lesions, major arterial emboli, septic pulmonary infarcts

Immunological changes - Osler nodes, Roth spots, RF

396
Q

What is the management for IE?

A

Abx for 4-6 weeks

397
Q

What ABx are used for a staph IE?

A
  • Flucloxacillin/Vancomycin

* Gentamicin

398
Q

What is vasovagal syncope?

A

Vasovagal syncope is defined as a loss of consciousness due to a transient decrease in blood flow to the brain caused by excessive vagal damage.

399
Q

What is the most common cause of fainting?

A

Vasovagal syncope

400
Q

What can precipitate vasovagal syncope?

A
  • Emotions: Fear, severe pain, blood phobia

* Orthostatic stress (prolonged standing, hot weather).

401
Q

What is situational syncope?

A

Acute haemorrhage, a cough, a sneeze, gastrointestinal stimulation (swallow, defecation, visceral pain), micturition, post-exercise.

402
Q

What vagal symptoms are associated with vasovagal syncope?

A

sweating, dizziness, light-headedness prior to passing out,

403
Q

What is the presentation of a vasovagal syncope?

A
  • Loss of consciousness lasting a short time
  • Vagal symptoms – sweating, dizziness, light-headedness prior to passing out,
  • Twitching of limbs during the blackout
  • Recovery is normally very quick.
  • Nausea
  • Pallor
404
Q

What investigations are performed in a presentation of vasovagal syncope?

A

12-lead ECG
• Rules out AV block, bradycardia, asystole, long QT, bundle branch block.

Echocardiogram
• Exclude for outflow obstruction

Lying/standing blood pressure – Check for orthostatic hypotension

Fasting blood glucose – Check for DM/hypoglycaemia.

FBC
• Haemoglobin – anaemia

Cardiac enzymes
• Troponin specific for cardiac muscle damage (3-hour delay for TnT to rise). CK-MB levels rise faster and remain elevated for 2-3 days.

D-dimer – Exclude pulmonary embolism

Serum cortisol – Exclude adrenal insufficiency

405
Q

What is the management for vasovagal syncope?

A

Counter-pressure manoeuvre and tilt training

Fludrocortisone for volume-expansion

406
Q

What is an arterial thrombus?

A

An arterial embolism is characterised as a sudden interruption of blood flow to an organ, because of an embolus.

407
Q

What are the risk factors for an arterial thrombus?

A
  • Atrial fibrillation
  • Injury or damage to an artery wall (Atherosclerosis)
  • Conditions that increase blood clotting (thrombophilia)
  • Mitral stenosis
  • Endocarditis
408
Q

What is the presentation of an arterial thrombus?

A
  • Pallor
  • Pulselessness
  • Pain
  • Paraesthesia
  • Perishingly cold
  • Paralysis
Later symptoms
•	Blisters of the skin fed by the affected artery
•	Shedding of skin
•	Skin erosion (ulcer)
•	Tissue necrosis
409
Q

What investigations are performed in an arterial thrombus?

A
  • Angiography of the affected extremity
  • Duplex doppler ultrasound exam
Blood
•	D-dimer
•	Factor VIII assay
•	Isotope study of the affected organ
•	Plasminogen activator inhibitor-1 activity
•	Platelet aggregation test
410
Q

What is the medical management of an arterial thrombus?

A

Anticoagulants – Warfarin or heparin
Thrombolytic therapy – Streptokinase
Anti-platelets - Aspirin or clopidogrel

411
Q

What is gangrene?

A

Gangrene is a complication of necrosis characterised by the decay of body tissues resulting from:
• Ischaemia
• Infection
• Trauma

412
Q

What are the two types of gangrene?

A

Infectious wet gangrene

Ischaemic dry gangrene

413
Q

What is wet gangrene?

A

Tissue death and infection

414
Q

What is dry gangrene?

A

Necrosis in the absence fo an infection and occurs secondary to chronically reduced blood flow

415
Q

What are the main causes of dry gangrene?

A

Atherosclerosis - in association with peripheral arterial disease

Thrombosis - In association with vasculitis and hypercoagulable sate

Vasospasm - In association with cocaine use and Raynaud’s

416
Q

What is Gas gangrene?

A

Subset of necrotising myositis caused by spore-forming Clostridial species.

417
Q

Which bacteria is associated with gas gangrene?

A

spore-forming Clostridial species.

418
Q

What is necrotising fasciitis?

A

A life-threatening infection of deep fascia causing necrosis of subcutaneous tissue.

419
Q

What is the presentation of gangrene?

A

Sudden onset of pain
Discolouration of affected area – Black
- Painful area with an erythematous region around gangrenous tissue (Black because of haemoglobin breakdown products)

420
Q

What are the appearances of wet gangrene?

A

Tissue becomes boggy with associated pus and strong odour caused by the activity of anaerobes

421
Q

What are the appearances of gas gangrene?

A

Spreading infection and destruction of tissues causes overlying oedema, discolouration, and crepitus (due to gas formation by the infection).

422
Q

What is the presentation of necrotising fasciitis?

A
  • Pain – Severe, and out of proportion to the apparent physical signs
  • Predisposing event – trauma, ulcer, surgery
  • Area of erythema and oedema
  • Haemorrhagic blisters may eb present
  • Signs of systemic inflammatory response and sepsis (high/low temperature, tachypnoea, hypotension).
423
Q

What investigations are performed in gangrene?

A

FBC
• WBC >15.4 x 109/L – Leucocytosis
• Haemoglobin <135 g/l

Gas gangrene – Raised serum LDH + X-ray (Gas production).

Blood cultures and wound swab – For infectious gangrene

424
Q

What is the management of necrotising fasciitis?

A

Surgical debridement and local irrigation with bacitracin infused saline

ABx

Surgical emergency

425
Q

What antibiotics are associated with necrotising fasciits?

A

Vancomycin, linezolid and piperacillin

426
Q

What is the management fo gas gangrene?

A
  • Intensive supportive care
  • Surgical debridement (+/- amputation)
  • Intravenous antibiotics
427
Q

What is the management of ischaemic gangrene?

A
  • Intravenous heparin
  • Surgical revascularisation
  • Percutaneous transluminal angioplasty
  • Thrombolytic therapy
428
Q

What is pulmonary hypertension?

A

Pulmonary hypertension is characterised by an elevation in mean arterial pressure, caused by a variety of causes:
• Idiopathic
• Problems affecting the small branches of the pulmonary arteries
• Left ventricular failure
• Lung disease (COPD, interstitial lung disease)
• Thromboses/emboli
N.B: Cor pulmonale is right heart failure caused by chronic pulmonary arterial hypertension.

429
Q

What is the presentation of pulmonary hypertension?

A
  • Progressive breathlessness
  • Weakness/tiredness
  • Exertional dizziness and syncope
  • Late-stage- Oedema and ascites
  • Angina and tachyarrhythmia
  • Cyanosis
430
Q

What signs are associated with pulmonary hypertension?

A
  • Right ventricular heave
  • Loud pulmonary second heart sound (S2)
  • Murmur – Pulmonary regurgitation
  • Tricuspid regurgitation
  • Raised JVP
  • Peripheral oedema
  • Ascites
431
Q

What ECG appearances are associated with pulmonary hypertension?

A

Right ventriocular hypertrophy and strain

432
Q

What is the gold-standard investigation for pulmonary hypertension?

A

Right heart catherisation - directly measure pulmonary pressure and confirm the diagnosis

433
Q

What is management for pulmonary hypertension?

A

Vasodilators

Guanylate cyclase stimulators

434
Q

What ECG changes are associated with hypokalaemia?

A

T wave inversion
ST depression
Prominent U wave

435
Q

What ECG changes are associated with hypocalcaemia?

A

QTc prolongation

436
Q

What ECG changes are associated with hypercalcaemia?

A

J waves, Osborne waves

Shortening of the QTc interval

437
Q

What murmur is associated with HOCM?

A

Systolic ejection murmur

438
Q

What is Brugada Syndrome?

A

Sodium channel-patties

439
Q

What ECG changes are associated with digoxin?

A

Downsloping ST depression
T-wave changes
biphasic and shortened QT interval
PR interval prolongation

Prominent U waves

440
Q

What ECG morphology is associated with digoxin toxicity?

A

“slurred”, “sagging” or “scooped” and resembling either a “reverse tick”, “hockey stick” or even Salvador Dali’s moustache

441
Q

What ECG changes are seen in sick sinus syndrome?

A

Sinus bradycardia
Sinoatrial block
Periods of sinus arest

442
Q

Which cardiac biomarker is suggestive of heart failure?

A

NT-pro-BNP

443
Q

Which cardiac biomarker should be monitored for a reinfarction?

A

Creatine kinase (CK-MB) remains elevated for 3 to 4 days following infarction. Troponin remains elevated for 10 days. This makes CK-MB useful for detecting re-infarction in the window of 4 to 10 days after the initial insult

444
Q

A high-pitched pansystolic murmur heard loudest on inspiration and at the left lower sternal edge is consistent with what valvular defect?

A

Tricuspid regurgitation

445
Q

What murmur is associated with HOCM?

A

Ejection systolic murmur, heard loudest on expiration

446
Q

What murmur is associated with a ventricular septal defect?

A

Ventricular septal defects may also cause a pansystolic murmur at the lower left sternal edge. However, this murmur is harsh, rather than high-pitched, and would not tend to be augmented by inspiration.

447
Q

What type of heart block is associated with athletes?

A

First-degree heart block

448
Q

What is a non-cardioselective beta blocker?

A

Propanolol

449
Q

Which drug can cause Raynaud’s phenomenon?

A

Non-cardioselective betablockes - Propanolol

450
Q

What type of beta-blocker is propanolol?

A

Non-cardioselective

451
Q

What drug is used for treating new-onset AF with a history of asthma?

A

rate-limiting calcium channel blocker.

Diltiazem

452
Q

In acute heart failure which drug improves symptoms but not mortality?

A

Furosemide

453
Q

What ECG changes are seen in LBBB?

A

W in lead V1 and M in V6

454
Q

What ECG changes are seen in RBBB?

A

M in lead V1 and W in v6

455
Q

A new acute LBBB is a sign of what acute condition?

A

STEMI

456
Q

What is the management of bradycardia?

A

IV atropine

457
Q

What is the management of Mobitz-I heart block in a healthy athlete?

A

Reassurance and safety net

458
Q

What ECG appearances are associated with left ventricular hypertrophy?

A

ECG shows–
-large R waves in the left-sided leads (V5, V6) and
-deep S-waves in the right-sided leads (V1, V2).
ST elevation in leads V2-3.

These findings are consistent with left ventricular hypertrophy. Furthermore, there is also T-wave inversion present in leads V5 and V6, known as the left ventricular ‘strain’ pattern.

459
Q

What ECG appearances are associated with a posterior myocardial infarction?

A

Progressive Tall R waves beginning in V1 V2

460
Q

What is an important cause of VT?

A

Hypokalaemia

461
Q

What are the three types of peripheral vascular disease?

A

Acute limb ischaemia
-Sudden decrease in limb perfusion

Intermittent claudication - pain on exertion

Critical limb ischaemia
-Pain at rest

462
Q

In intermittent claudication, when does pain occur?

A

Pain on exertion (Claudication distance)

463
Q

Where does intermittent claudication typically occur in the body?

A

Buttock, Calf or thigh

464
Q

When does critical limb ischaemia occur?

A

Pain at rest

465
Q

What are the RFs for peripheral vascular disease?

A 
Hypertension
Smoking
Elderly 
Male
Hyperlipidaemia
466
Q

What is the presentation of acute limb ischaemia?

A 
Pain 
Pale/pallor
Paraesthesia
Pulselessness
Paralysis
Perishingly cold
467
Q

What are the signs of chronic limb ischaemia?

A 
Hair loss
Numbness in feet/legs
Brittle/slow-growing toenails
Ulcers
Absent pulses
Atrophic skin
468
Q

Which test is used to indicate severe limb ischaemia?

A

Beurger’s test

469
Q

What is Beurger’s test?

A

Lie patient flat on bed and lift leg up to 45 degrees

Limb develops pallor indicates arterial insufficiency
<20 degrees is Beurger’s angle and indicates severe limb ischaemia

patient then swings leg over the bed, reactive hyperaemia is seen due to arteriolar dialtation in response to anaerobic

470
Q

What is the first-line investigation for PVD?

A

Full cardiovascular risk assessment
BP and HR
Bloods (GBC, fasting glucose, lipids)

471
Q

What is the gold-standard investigation for the diagnosis of PVD?

A

Ankle-Brachial pressure index (ABPI)

-Normal range: 0.9-1.2

472
Q

how do you measure ABPI?

A

Measure systolic blood pressure in ankle/brachial

473
Q

What is an abnormal ABPI?

A

<0.9

474
Q

What ABPI parameter is associated with critical limb ischaemia?

A

<0.5

475
Q

What investigation directly visualises the site of stenosis in PVD?

A

Colour duplex ultrasound scan and magnetic resonance angiogram

476
Q

Which syndrome is referred to aortoiliac occlusive disease?

A

Leriche syndrome

477
Q

What are the symptoms of Leriche syndrome?

A

Buttock claudication
Impotence
Absent weak distal pulses

478
Q

What syndrome is characterised as buttock claudication, impotence and absent/weak distal pulses?

A

Leriche syndrome (Aortoiliac occlusive disease)

479
Q

What are the three types of ulcers?

A

Arterial ulcers
Venous ulcers
Neuropathic ulcers

480
Q

What is the appearance of arterial ulcers?

A

Punched out - deeper than venous ulcer

-Distal (Dorsum of the foot and between toes)

  • Well defined edges
  • Pale base -grey granulation tissue
481
Q

What are the signs of an arterial ulcer?

A

Hair loss, shinny and pale skin

Calf muscle wasting

Absent pulses

Night pain

482
Q

At what time of the day are arterial ulcers painful?

A

Night pain

483
Q

What is the appearance of venous ulcers?

A

Large and shallow
-Sloping and less well-defined sides

  • More proximal than AU (gaiter region)
  • Other symptoms. of venous insufficiency (swelling, itching and aching)
484
Q

What are the signs of venous insufficiency?

A
  • Stasis eczema
  • Lipodermatosclerosis (Champagne bottle)
  • Atrophy blanche
  • Hemosiderin deposition
485
Q

What is lipodermatosclerosis?

A

Inflammation of the layer of fat deep to the skin

  • Classic champagne appearance
  • Redness and swelling with tapering around the ankles
486
Q

What is atrophy blanche?

A

Areas of white and shiny skin that is atrophic

-Surrounded by small dilated capillaries

487
Q

What is hemosiderin deposition?

A

Decreased blood flow in the limbs leads to congestion- blood leaks out resulting in discolouration of the skin

488
Q

What is the gold-standard investigation for arterial and venous ulcers?

A

Duplex USS of the lower limbs

489
Q

What is the advantage with using a duplex USS in arterial and venous ulcers?

A

Visualisation and topography of blood flow to identify specific pathological location (Arterial narrowing or valve degeneration)

490
Q

What is the gold-standard investigation for a venous ulcer?

A

Duplex USS of lower limbs and measure surface area of ulcer (To monitor progression)

Swab for infection

Biopsy

491
Q

What investigations are performed in arterial ulcers?

A

Duplex USS of lower limbs
ABPI
Percutaneous angiography

492
Q

What is a Marjolin’s ulcer?

A

A squamous cell carcinoma of the skin, developing from areas of chronic injury and inflammation

493
Q

What is the management for venous ulcers?

A

Graded compression stockings - reduces venous stasis

Debridement and cleaning

ABx

Moisturising cream

494
Q

What is the definition of AAA?

A

Diameter >3cm or 50% larger than normal diameter

495
Q

What are the two forms of true aneursysms?

A

Saccular

Fusiform

496
Q

What is a saccular anerusysm?

A

All three layers are pushed out

497
Q

What is a false anerusysm,?

A

Tear in blood vessel, therefore blood is flowing into the false lumen

498
Q

What are the risk factors for AAA?

A 
Smoking
Male
Connective tissue disorder 
Old age
Hypertension
Inflammatory disorders - pro-aneurysm state
499
Q

What is the screening programme for AAA?

A

Male >65 years

500
Q

What are the signs of unruptured AAA?

A

Usually asymptomatic

Often an incidental finding

May have pain in the back, abdomen or groin

  • Pulsatile and laterally expansile mass on palpation
  • Abdominal bruit
501
Q

What is the presentation of a ruptured AAA?

A

Sudden, severe pain in the back, abdomen and groin

  • Syncope
  • Shock

Pulsatile and laterally expansile mass on palpation

Abdominal bruit

Grey-Turner’s sign (ruptured)

Medical emergency

502
Q

What is the gold-standard investigation for AAA?

A

Abdominal ultrasound - can detect the presence of AAA but not whether it has ruptured or not

-Can measure AA diameter (>3cm)

503
Q

What investigation is used to assess whether an AAA is ruptuted?

A

CT angiogram - visualise blood flow outside the abdominal aorta

MR angiogram - if patient has renal impairment or contrast allergy

504
Q

What is an aortic dissection?

A

A condition where there is a tear in the aortic intima- allowing for blood to flow into a new false channel in between the inner and outer layers of the tunica media

505
Q

What are the two types of aortic dissection?

A

Type A - Ascending

Type B - Descending

506
Q

What are the RFs for aortic dissection?

A 
Male
Connective tissue disorder
Smoking
Hypertension 
Coarctation of the aorta
Cocaine
507
Q

What is the presentation of aortic dissection?

A

Sudden central tearing pain radiating to the back (Interscapular)

  • Symptoms caused by blockages to branches of the aorta:
  • Carotid artery- Blackout and dysphasia
  • Coronary artery - angina
  • Subclavian artery - LOC
  • Renal artery - Anuria, renal failure
508
Q

What are the signs of aortic dissection?

A

Hypertension

Blood pressure difference between two arms

Murmur on the back

Signs of aortic regurgitation
Signs of connective tissue disease

509
Q

Which murmur is associated with aortic dissection?

A

Aortic regurgitation

-Early diastolic murmur

510
Q

What are the four investigations performed in suspected aortic dissection?

A

1- Bloods
2- ECG
3- CXR
4- CT angiogram

511
Q

What is the gold-standard investigation for diagnosing an aortic dissection?

A

CT angiogram

512
Q

What signs are found on a CXR for aortic dissection?

A

Loss of contour of aortic knuckle

Widened mediastinum

Globular heart

513
Q

How do you describe an early-diastolic murmur?

A

Decrescendo murmur

514
Q

What is the definition of varicose veins?

A

Subcutaneous permanently dilated veins >3mm in diameter when measured in a standing position (often the superficial veins of the lower limb)

515
Q

Describe the blood flow in varicose veins?

A

Turbulent- reducing venous return to the heart

516
Q

What are the primary causes of varicose veins?

A

Idiopathic valvular incompetence

517
Q

What are the causes of venous outflow obstruction?

A

Pregnancy
Ascites
Ovarian cysts
Pelvic malignancy

518
Q

What are the secondary causes of varicose veins?

A

DVT
Venous outflow obstruction
AV malformations

519
Q

What are the symptoms of varicose veins?

A

Visible dilation of veins

Leg aching (worse with prolonged standing) 
-Gravity induced

Swelling and itching
Bleeding

520
Q

What are the signs of varicose veins?

A

Veins feel tender or hard

Tap test - tap proximally in the vein and feel thrill in the distal vein

Auscultation for bruits

Trendelenburg test

521
Q

What is the Trendelenburg test in varicose veins?

A

Allow to localise the site of valvular incompetennce

Supine and leg is lifted to empty the veins, tourniquet is applied

-Blood fills veins - if filled quickly - there is incompetence

522
Q

What is the gold-standard investigation for varicose veins?

A

Duplex ultrasound

523
Q

What are the conservative measures for varicose veins?

A

Compression stockings

Lifestyle changes - weight loss, exercise and leg elevation

524
Q

What are the endovascular treatments for varicose veins?

A

Radiofrequency ablation

Endovenous laser ablation

Microinjection scleropathy

525
Q

What is the surgical management for varicose veins?

A

Stripping of the long saphenous veins

Saphenofemoral ligation
Avulsion of varicosities

526
Q

Which vein is most commonly affected in varicose vein?

A

Long saphenous vein

527
Q

What are the complications with varicose vein surgery?

A 
Haemorrhage
Infection
Recurrence
Paraesthesia
Peroneal nerve injury
528
Q

What is gangrene?

A

Tissue necrosis, either wet with superimposed infection, dry or gas gangrene.

529
Q

What bacteria causes gas gangrene?

A

Clostridium perfringens

530
Q

What causes gangrene?

A

Tissue ischaemia and infarction or physical trauma

531
Q

What is the presentation of dry gangrene?

A

Painful black tissue affecting extremities and areas of high pressure

532
Q

Signs and symptoms of DVT?

A

Erythema, warmth, painless, varicosities and swollen limb

533
Q

What is Homan’s signin DVT?

A

Dorsiflex of the ankle causes deep calf pain

534
Q

What criteria is used to for DVT?

A

Well’s criteria

535
Q

What is the first-line investigaiton for DVT?

A

Doppler ultrasound

536
Q

What is the management for DVT?

A

DOACs for 3 months

-Apixaban and rivaroxaban

537
Q

What is the prophylactic treatment for DVT?

A

Compression stocking

Advice physical activity and mobilisation

Phase1c Medicine (11 decks)

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