Cardiology

Question 1

What are the risk factors for atherosclerosis?

Answer 1

• Age
• Smoking
• High serum cholesterol
• Obesity
• Diabetes
• Hypertension
• Family history

Question 2

In which arteries would you be most likely to find atheromatous plaques?

Answer 2

In the peripheral and coronary arteries - LAD, circumflex, RCA

Question 3

Describe in 5 steps the progression of atherosclerosis.

Answer 3

1. Fatty streaks
2. Intermediate lesions
3. Fibrous plaque
4. Plaque rupture
5. Plaque erosion

Question 4

What is the earliest lesion of atherosclerosis? What do they consist of?

Answer 4

• Fatty streaks (appear at a very early age <10 years)
• Consist of aggregations of lipid–laden macrophages and T lymphocytes within the tunica intima

Question 5

What can lesions progress to? What does this contain?

Answer 5

• Intermediate lesion
• Composed of layers of :
• Foam cells
• Vascular smooth muscle cells
• T lymphocytes

Question 6

What can intermediate lesions progress to? What do these contain?

Answer 6

• Fibrous plaques or advanced lesions
• Impedes blood flow
• Prone to rupture
• Covered by dense fibrous cap made of ECM proteins including collagen (strength) and elastin (flexibility) laid down by SMC that overlies lipid core and necrotic debris
• May be calcified
• Contains: smooth muscle cells, macrophages and foam cells and T lymphocytes

Question 7

Describe the process of atherosclerosis.

Answer 7

1. High levels of LDL in the blood. Some deposits in the tunica intima and become oxidised - this activates endothelial cells to attract leukocytes (ENDOTHELIAL CELL DYSFUNCTION)
2. Monocytes etc. are attracted to the site of damage (endothelium) - move to tunica intima (become macrophages)
3. Macrophages take up oxidised lipid to form foam cells (inflammatory response). These foam cells encourage plaque progression by serving as a source of pro inflammatory cytokines. They also promote the migration of smooth muscle cells from the tunica media to the tunica intima and smooth muscle cell proliferation - this causes heightened synthesis of collagen
4. Foam cells die - release lipid contents
5. Fibrous cap maintaining the plaque has to be maintained by resorption and redeposition. However, if the balance is shifted, e.g. in favour of inflammatory conditions we get a plaque rupture. This causes blood coagulation = thrombus = impedes blood flow (occludes vessel)

Question 8

Describe the process of leukocyte recruitment after the endothelial cells have been activated

Answer 8

1. Capture
2. Rolling
3. Slow rolling
4. Adhesion
5. Trans-migration

Question 9

Which histological layer of the artery may be thinned by an atheromatous plaque?

Answer 9

The tunica media

Question 10

What is the treatment for atherosclerosis?

Answer 10

Percutaneous coronary intervention (PCI)

Question 11

What is the major limitation of PCI? How can restenosis be avoided following PCI?

Answer 11

• Restenosis
• Drug eluting stents: anti-proliferative and drugs that inhibit healing

Question 12

What is the key principle behind the pathogenesis of atherosclerosis?

Answer 12

It is an inflammatory process

Question 13

What are the functions of the mitral and aortic valves?

Answer 13

• Mitral valve = lets blood flow the left atrium to the left ventricle
• Aortic valve = opens when the left ventricle squeezes to pump out blood, and closes in between heart beats to keep blood from going backward into the heart

Question 14

Describe aortic stenosis. How common is it?

Answer 14

• A disease where the aortic orifice (aortic opening) is restricted and so the LV can’t eject blood properly in systole = pressure overload
• It is the commonest valvular disease

Question 15

Describe the aetiology of aortic stenosis.

Answer 15

1. Congenital bicuspid aortic valve
2. Rheumatic heart disease
3. Senile calcification of the valve

Question 16

Describe the pathophysiology of aortic stenosis.

Answer 16

Aortic orifice is restricted, e.g. by calcific deposits and so there is a pressure gradient between the LV and the aorta. LV function is initially maintained due to compensatory hypertrophy. Overtime this becomes exhausted = LV failure

Question 17

Give 3 symptoms of aortic stenosis. What is the onset of symptoms associated with?

Answer 17

• SAD:

1. Exertional syncope
2. Angina
3. Exertional dyspnoea
   Onset of symptoms is associated with poor prognosis

Question 18

Give 3 signs of aortic stenosis including the murmur type.

Answer 18

1. Slow rising carotid pulse and decreased pulse amplitude
2. Soft or absent heart sounds (S2) if severe
3. Ejection systolic murmur: <> shape (crescendo-descrendo character)

Question 19

What investigation might you do in someone who you suspect to have aortic stenosis? Which two measurements are obtained?

Answer 19

• Echocardiography - reduced aortic outflow, LVH
• Two measurements are obtained: left ventricular size and function + Doppler derived gradient and valve area
• CXR
• ECG

Question 20

Describe the management for someone with aortic stenosis.

Answer 20

1. Ensure good dental hygiene
2. Consider IE prophylaxis
3. AORTIC VALVE REPLACEMENT or TAVI (Transcatheter Aortic Valve Implantation)

Question 21

Who should be offered an aortic valve replacement?

Answer 21

1. Symptomatic patients with aortic stenosis
2. Any patient with decreasing ejection fraction
3. Any patient undergoing CABG (coronary artery bypass graft) with moderate/severe aortic stenosis

Question 22

What is mitral regurgitation? What is it associated with?

Answer 22

• Backflow of blood from the LV to the LA during systole - LV volume overload
• Associated with ATRIAL FIBRILLATION

Question 23

Describe the aetiology of mitral regurgitation.

Answer 23

1. Papillary muscle rupture
2. Mitral valve prolapse
3. Rheumatic heart disease
4. IE
5. Marfan’s syndrome

Question 24

What is the pathophysiology of mitral regurgitation?

Answer 24

LA enlargement and LVH to maintain BP. Progressive LV volume overload -> dilatation and progressive heart failure

Question 25

Give 3 symptoms of mitral regurgitation.

Answer 25

PEF: 1. Palpitations 2. Exertional dyspnoea 3. Fatigue

Question 26

Give 4 signs of mitral regurgitation including its murmur. In chronic mitral regurgitation, what does the intensity of the murmur correlate with?

Answer 26

1. Pansystolic murmur radiating to left axilla (always there) ADS: 1. Atrial fibrillation 2. Displaced, thrusting apex 3. Soft 1st heart sound + a 3rd heart sound In chronic MR, the intensity of the murmur correlates with disease severity

Question 27

What investigations might you do in someone who you suspect to have mitral regurgitation? What may these show?

Answer 27

1. ECG - may show LA enlargement, atrial fibrillation and LV hypertrophy 2. CXR - LA enlargment 3. Echocardiogram: estimates LA/LV size and function

Question 28

Describe the management of mitral regurgitation.

Answer 28

- Rate control for AF, e.g. beta blockers - Vasodilators, e.g. ACEI - Anticoagulation for AF - Diuretics for fluid overload - IE prophylaxis - If symptomatic = surgery

Question 29

What is aortic regurgitation?

Answer 29

A regurgitant aortic valve means blood leaks back into the LV during diastole due to ineffective aortic cusps

Question 30

What is the aetiology of aortic regurgitation?

Answer 30

1. Bicuspid aortic valve (should be tricuspid) 2. Rheumatic heart disease 3. IE 4. Marfan's syndrome

Question 31

Describe the pathophysiology of aortic regurgitation.

Answer 31

Pressure and volume overload. Compensatory mechanisms - LV dilatation, LVH. Progressive dilation leads to HF

Question 32

Give 3 symptoms of aortic regurgitation.

Answer 32

PAD: - Palpitations - Angina - Dyspnoea

Question 33

Give 4 signs of aortic regurgitation.

Answer 33

1. Wide pulse pressure 2. Water hammer pulse 3. Diastolic blowing murmur 4. Austin flint murmur

Question 34

What investigations might you do in someone who you suspect to have aortic regurgitation?

Answer 34

CXR and echocardiogram

Question 35

Describe the management for someone with aortic regurgitation.

Answer 35

- IE prophylaxis - Vasodilators e.g. ACEI - Regular echocardiograms to monitor progression - Surgery if symptomatic

Question 36

What is mitral stenosis?

Answer 36

Obstruction to LV inflow that prevents proper filling during diastole

Question 37

What is the aetiology of mitral stenosis?

Answer 37

1. Rheumatic heart disease (most common) 2. Congenital 3. Calcification

Question 38

Describe the pathophysiology of mitral stenosis.

Answer 38

1. LA dilation -\> pulmonary congestion (as coming in from the pulmonary vein, reduced emptying) 2. Increased trans-mitral pressures -\> LA enlargement and AF 3. Pulmonary venous hypertension causes RHF symptoms 4. Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure

Question 39

Give 3 symptoms of mitral stenosis.

Answer 39

1. Dyspnoea 2. Haemoptysis (due to pulmonary oedema) 3. Palpitations (AF)

Question 40

Give 5 signs of mitral valve stenosis. What is its murmur?

Answer 40

1. 'a' wave in jugular venous pulsations (due to pulmonary hypertension and right ventricular hypertrophy) 2. Malar flush - pink patches on cheeks due to vasoconstriction 3. Low pitched diastolic murmur 4. Loud S1 5. Tapping apex beat - Murmur = rumbling mid-diastolic murmur with opening snap

Question 41

What investigations might you do in someone who you suspect to have mitral stenosis? What might they show?

Answer 41

1. ECG - atrial fibrillation and LA enlargement 2. CXR - LA enlargement and pulmonary congestion 3. Echocardiogram - GOLD STANDARD. Assess mitral valve mobility, gradient and mitral valve area

Question 42

Describe the management for mitral stenosis.

Answer 42

- If in AF rate control, e.g. beta blockers/CCBs - Anticoagulation if AF - BALLOON VALVULOPLASTY or valve replacement - IE prophylaxis

Question 43

Why does medication not work for mitral and aortic stenosis?

Answer 43

The problem is mechanical and so medical therapy does not prevent progression

Question 44

Explain the shape of the action potential graph.

Answer 44

- 4 = resting potential (-90mV) = due to Na+/K+ ATPase (3 Na+ move out for 2K+ that move into cell) + Na+/K+ leak channels (100 K+ out for every K+ in, but Na+/K+ ATPase much more prominent) - 0 = rapid depolarisation = threshold reached (-70mV), leads to sodium gated fast channels opening. Na+ enters cells + depolarises for +20mV - 1 = partial repolarisation = K+ channels open + K+ leaves cell. Inflow of Na+ stops - 2 = plateau = voltage-gated Ca2+ channels open. Ca2+ moves in + counters K channels. Lasts approx. 200ms. Entry of Ca2+ into cell results in contraction of myocyte. Contraction of cardiac muscle longer than skeletal due to calcium channels that cause plateau. Less duration in atria than ventricles - 3 = repolarisation = K+ outflow and Ca2+ inflow stops until resting potential reached. Closure of Ca2+ channels, opening of more K+ channels

Question 45

What is an ECG? Give a few examples of conditions that we can identify through ECGs.

Answer 45

- The representation of the electrical events of the cardiac cycle - Conditions: arrhythmias, myocardial ischaemia and infarction, pericarditis, electrolyte disturbances

Question 46

What are the main pacemakers of the heart? Which is the dominant pacemaker?

Answer 46

- SA node = dominant pacemaker (60-100 bpm) - AV node = back-up pacemaker (40-60 bpm) - Ventricular cells = back-up pacemaker (20-45 bpm)

Question 47

Starting with the sinoatrial node, where does the electrical impulse travel?

Answer 47

SA node - AV node - Bundle of His - Bundle branches - Purkinje fibres

Question 48

What do the P, QRS and T wave represent?

Answer 48

- P wave = atrial depolarisation (60-80ms) - QRS complex = ventricular depolarisation (100-120ms) - T wave = ventricular repolarisation (120-160ms)

Question 49

What does the PR interval represent? Why is it a bit longer?

Answer 49

- Reflects conduction through the AV node - Accounts for delay that allows time for atria to contract before ventricles contract

Question 50

ECG: how long should the PR interval be?

Answer 50

120-200ms

Question 51

ECG: what is the J point?

Answer 51

Where the QRS complex becomes the ST segment

Question 52

ECG: what is the normal axis of the QRS complex?

Answer 52

-30° -\> +90°

Question 53

How many seconds do the following represent on ECG paper? a) small squares b) large squares

Answer 53

a) 0.04s b) 0.2s

Question 54

What do the ECG leads measure?

Answer 54

The difference in electrical potential between two points

Question 55

How many electrodes does a 12 lead ECG have?

Answer 55

10 electrodes - six on the chest, four on the limbs

Question 56

What are the typical ECG findings for a right axis deviation? What is a right axis deviation associated with?

Answer 56

- Lead III has the most positive deflection and lead I should be negative - Right axis deviation is associated with right ventricular hypertrophy

Question 57

What are the bipolar and unipolar leads?

Answer 57

- Bipolar leads: measure difference in electrical potential between two different points on the body - Unipolar leads: measure difference in electrical potential between one point on the body and a virtual reference point with zero electrical potential, located in the centre of the heart

Question 58

What are the 12 leads of the ECG?

Answer 58

- 3 standard limb leads - 3 augmented limb leads - 6 precordial leads

Question 59

What should the cardiac axis look like in healthy individuals? What should the most positive deflection be in? Why? Where would you see the most negative deflection? Why?

Answer 59

- In healthy individuals, you would expect the cardiac axis to lie between -30°and +90º. The overall direction of electrical activity is therefore towards leads I, II and III. As a result, you see a positive deflection in all these leads, with lead II showing the most positive deflection as it is the most closely aligned to the overall direction of electrical spread - You would expect to see the most negative deflection in aVR. This is due to aVR providing a viewpoint of the heart from the opposite direction

Question 60

What does a positive deflection mean in an ECG? How about a negative deflection? What does the height of a deflection tell us?

Answer 60

- When the electrical activity within the heart travels towards a lead you get a positive deflection - When the electrical activity within the heart travels away from a lead you get a negative deflection - The height of the deflection represents the amount of electrical activity flowing in that direction (i.e. the higher the deflection, the greater the amount of electrical activity flowing towards the lead

Question 61

What are the typical ECG findings for a right axis deviation? What is a right axis deviation associated with?

Answer 61

Lead III has the most positive deflection and lead I should be negative. Right axis deviation is associated with right ventricular hypertrophy

Question 62

What does the cardiac axis tell us? What do we need to determine the cardiac axis? What is the pathway of electrical activity in the heart? What do a positive and negative deflection tell us?

Answer 62

- The cardiac axis gives us an idea of the overall direction of electrical activity - To determine the cardiac axis, you need to look at leads I, II and III - In healthy individuals, the electrical activity of the heart begins at the sinoatrial node then spreads to the atrioventricular (AV) node. It then spreads down the bundle of His and then Purkinje fibres to cause ventricular contraction - Whenever the direction of electrical activity moves towards a lead, a positive deflection is produced - Whenever the direction of electrical activity moves away from a lead a negative deflection is produced

Question 63

What are the typical ECG findings for a left axis deviation? What is it associated with?

Answer 63

- Lead I has the most positive deflection - Leads II and III are negative - Left axis deviation is associated with heart conduction abnormalities

Question 64

Which leads correspond to which view of the heart? What can we infer from these?

Answer 64

- LEARN: - Inferior = II, III, aVF - RCA - Lateral = I, aVL, aVR, V5, V6 - LCx - Anterior = V3, V4 - LAD - Septal = V1, V2 - proximal LAD - Understanding which leads represent which anatomical territory of the heart allows you to localise pathology - For example, if there is ST elevation in leads V3 and V4 it suggests an anterior myocardial infarction (MI). You can then combine this with some anatomical knowledge of the heart’s blood supply, to allow you to work out which artery is likely to be affected (e.g. left anterior descending artery).

Question 65

How do we systematically approach interpreting ECGs?

Answer 65

– Rate – Rhythm – Axis – P, PR, QRS, ST, QT, T

Question 66

ECG: where would you place lead 1 (bipolar)?

Answer 66

From the right arm to the left arm with the positive electrode being at the left arm. At 0°

Question 67

ECG: where would you place lead 2?

Answer 67

From the right arm to the left leg with the positive electrode being at the left leg. At 60°

Question 68

ECG: where would you place lead 3?

Answer 68

From the left arm to the left leg with the positive electrode being at the left leg. At 120°

Question 69

ECG: where would you place lead avF (unipolar)?

Answer 69

From halfway between the left arm and right arm to the left leg with the positive electrode being at the left leg. At 90°

Question 70

ECG: where would you place lead avL?

Answer 70

From halfway between the right arm and left leg to the left arm with the positive electrode being at the left arm. At -30°

Question 71

ECG: where would you place lead avR?

Answer 71

From halfway between the left arm and left leg to the right arm with the positive electrode being at the right arm. At -150°

Question 72

What are the unipolar chest leads?

Answer 72

- V1 = R. of sternum 4th intercostal space - V2 = L. of sternum 4th intercostal space - V3 = Inbetween V2 + V4 - V4 = R. of sternum 5th intercostal space - V5 = 5th intercostal space anterior axillary line - V6 = 5th intercostal space midaxillary line

Question 73

What are Chamberlain's 10 rules of a normal ECG?

Answer 73

ECG RULES: - Rule 1 = PR interval should be 120 to 200 milliseconds or 3 to 5 little squares - Rule 2 = the width of the QRS complex should not exceed 110 ms, less than 3 little squares - Rule 3 = the QRS complex should be dominantly upright in leads I and II - RULE 4 = QRS and T waves tend to have the same general direction in the limb leads - RULE 5 = all waves are negative in lead aVR - RULE 6 = the R wave must grow from V1 to at least V4, the S wave must grow from V1 to at least V3 and disappear in V6 - RULE 7 = the ST segment should start isoelectric except in V1 and V2 where it may be elevated - RULE 8 = the P waves should be upright in I, II, and V2 to V6 - RULE 9 = there should be no Q wave or only a small q less than 0.04 seconds in width in I, II, V2 to V6 - RULE 10 = the T wave must be upright in I, II, V2 to V6

Question 74

What is a P wave like in leads I, II and aVR?

Answer 74

Always positive in leads I + II, always negative in aVR

Question 75

What do P waves look like in right and left atrial enlargement? How about in atrial fibrosis, obesity and hyperkalaemia?

Answer 75

- Right atrial enlargement = tall, pointed P wave (P pulmonale) - Left atrial enlargement = 'M' shaped P wave (P mitrale) - Atrial fibrosis, obesity and hyperkalaemia = low amplitude

Question 76

What can a short PR interval indicate?

Answer 76

WPW (Wolff-Parkinson-White syndrome)

Question 77

What does a long PR interval (\>200ms) indicate?

Answer 77

First degree heart block

Question 78

How long should the QRS complex be? When do we get broad QRS complexes, small QRS complexes and tall QRS complexes?

Answer 78

- \<110ms - Broad QRS = ventricular conduction delay / bundle branch block - Small QRS complexes = obese patient, pericardial effusion, infiltrative cardiac disease - Tall QRS complexes = left ventricular hypertrophy, thin patient

Question 79

In which leads would you expect the QRS complex to be upright in?

Answer 79

Leads I and II

Question 80

In which lead are all waves negative?

Answer 80

aVR

Question 81

In which leads should T waves and P waves be upright?

Answer 81

Leads 1, 2, V2 -\> V6

Question 82

What part of the ECG does the plateau phase of the cardiac action potential coincide with?

Answer 82

QT interval

Question 83

What happens to the QT interval when HR increases?

Answer 83

The QT interval decreases

Question 84

Give 3 signs of abnormal T waves.

Answer 84

1. Symmetrical 2. Tall and peaked (hyperkalaemia) 3. Biphasic (ischaemia or hypokalaemia) or inverted (non-specific but can indicate ischaemia/infarction, hypertrophy, cardiomyopathy)

Question 85

What is the U wave related to? What is their appearance? When are they more prominent?

Answer 85

- The U wave is related to afterdepolarisations which follow repolarisation - U waves are small, round, symmetrical and positive in lead II - More prominent in slower heart rates

Question 86

How do we determine heart rate from an ECG in a regular rhythm? How about in an irregular rhythm?

Answer 86

- Rule of 300: count the number of 'big boxes' between each QRS complex and divide this into 300, e.g. 300/6 = 50bpm - If a patient’s heart rhythm is irregular the first method of heart rate calculation doesn’t work (as the R-R interval differs significantly throughout the ECG). As a result, you need to apply a different method: * Count the number of complexes on the rhythm strip (each rhythm strip is typically 10 seconds long) * Multiply the number of complexes by 6 (giving you the average number of complexes in 1 minute)

Question 87

What does the QRS axis represent? What do QRS axis abnormalities hint at?

Answer 87

- The QRS axis represents the overall direction of the heart's electrical activity - Abnormalities hint at ventricular enlargement and conduction blocks

Question 88

What aspect of the heart is represented by leads 2, 3 and aVF?

Answer 88

The inferior aspect

Question 89

What might ST elevation in leads 2, 3 and aVF suggest?

Answer 89

RCA blockage. These leads show the activity of the inferior aspect of the heart and the RCA supplies the inferior aspect of the heart with blood

Question 90

What is ischaemic heart disease? What is it broken down into? Which condition has ischaemic heart disease as its main cause?

Answer 90

- Ischaemic heart disease (or coronary artery disease) is a condition where the coronary arteries are narrowed or blocked - Broken down into stable angina and acute coronary syndrome - Angina's commonest cause is IHD. This is a symptom of O2 supply/demand mismatch to the heart experienced on **exertion**

Question 91

What is IHD primarily caused by? What happens when a coronary artery is 70-80% sclerosed? Why?

Answer 91

- Primarily caused by atherosclerosis = lipid rich plaques in arterial wall. Inflammatory, progressive process - When 70-80% sclerosed: **exertional** symptoms show: angina. Exertional symptoms only as there is increased oxygen demand on exertion: heart muscle cannot access required oxygen volume due to artery occlusion (due to the atherosclerosis), therefore there is a supply-demand mismatch. Pain occurs: angina

Question 92

What are the modifiable and non-modifiable risk factors for IHD?

Answer 92

- Non modifiable: - Family history - Age - Ethnicity (S. Asian) - Modifiable: - Smoking - Poor nutrition - Sedentary lifestyle - Alcohol - Stress - HTN - Obesity - DM

Question 93

Give 5 possible causes of angina.

Answer 93

1. Narrowed coronary artery = impairment of blood flow, e.g. atherosclerosis 2. Increased distal resistance = LV hypertrophy 3. Reduced O2 carrying capacity, e.g. anaemia 4. Coronary artery spasm 5. Thrombosis

Question 94

Briefly describe the pathophysiology of angina that results from atherosclerosis.

Answer 94

On exertion there is increased O2 demand. Coronary blood flow is obstructed by an atherosclerotic plaque -\> myocardial ischaemia -\> angina

Question 95

Briefly describe the pathophysiology of angina that results from anaemia.

Answer 95

On exertion there is increased O2 demand. In someone with anaemia there is reduced O2 transport -\> myocardial ischaemia -\> angina

Question 96

How do blood vessels try and compensate for increased myocardial demand during exercise?

Answer 96

When myocardial demand increases, e.g. during exercise, microvascular resistance drops and flow increases

Question 97

Why are blood vessels unable to compensate for increased myocardial demand in someone with CV disease?

Answer 97

In CV disease, epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest. When this person exercises, the microvascular resistance can't drop anymore and flow can't increase to meet metabolic demand = angina!

Question 98

What is the typical presentation of someone with IHD? With angina, how do we classify it?

Answer 98

- Central, crushing retrosternal chest pain, radiating into the jaw and typically the left arm - Shortness of breath - Nausea - Sweating - Palpitation - Angina: 1. Constricting discomfort in front of chest, neck, shoulders, jaws or arms 2. Precipitated by physical exertion 3. Relieved by rest/GTN spray ~5 mins - Normal examination - All 3 features: typical angina, 2 features: atypical angina, 1/none: non-anginal pain

Question 99

What are the investigations for IHD?

Answer 99

- ECG: resting and exercise (to induce ischaemia) - Blood tests: HbA1c, FBC, cholesterol profile - Biological markers: troponin, myoglobin etc. - Gold standard angina = CT CORONARY ANGIOGRAPHY

Question 100

How would you describe the chest pain in angina?

Answer 100

Crushing central chest pain. Heavy and tight. The patient will often make a fist shape to describe the pain

Question 101

Give 5 symptoms of angina.

Answer 101

1. Crushing central chest pain 2. The pain is relieved with rest or using a GTN spray 3. The pain is provoked by physical exertion 4. The pain might radiate to the arms, neck or jaw 5. Breathlessness

Question 102

Describe the primary prevention of angina.

Answer 102

1. Risk factor modification 2. Low dose aspirin

Question 103

Describe the secondary prevention of angina.

Answer 103

- Aspirin - Atorvastatin - ACEi - PCI/CABG if extensive disease

Question 104

How do we treat IHD?

Answer 104

BANS: - Beta-blocker, e.g. propanolol - Dual antiplatelet: aspirin and clopidogrel - Nitrate: GTN spray (to abort attacks - Statin: simvastatin

Question 105

What is the symptomatic reflief and long term relief for angina?

Answer 105

- Symptomatic relief = GTN spray - Long term symptomatic relief = beta blocker or CCB

Question 106

Describe the action of beta blockers.

Answer 106

Beta blockers are beta-1 specific. They antagonise sympathetic activation and so are negatively chronotropic and inotropic. Myocardial work is reduced and so is myocardial demand = symptom relief

Question 107

Give 3 side effects of beta blockers.

Answer 107

1. Bradycardia 2. Tiredness 3. Erectile dysfunction

Question 108

When might beta blockers be contraindicated?

Answer 108

They might be contraindicated in someone with asthma or in someone who is bradycardic

Question 109

Describe the action of nitrates.

Answer 109

Nitrates, e.g. GTN spray are venodilators. Venodilators -\> reduced venous return -\> reduced pre-load -\> reduced myocardial work and myocardial demand

Question 110

Describe the action of Ca2+ channel blockers.

Answer 110

Ca2+ blockers are arterodilators -\> reduced BP -\> reduced afterload -\> reduced myocardial demand

Question 111

How does aspirin work?

Answer 111

Aspirin irreversibly inhibits COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced. Caution: Gastric ulcers!

Question 112

What are statins used for?

Answer 112

They reduce the amount of LDL in the blood

Question 113

Give 2 advantages and 1 disadvantage of PCI.

Answer 113

1. Less invasive than CABG 2. Convenient and acceptable 3. High risk of restenosis

Question 114

Give 1 advantage and 2 disadvantages of CABG.

Answer 114

1. Good prognosis after surgery 2. Very invasive 3. Long recovery time

Question 115

Name 3 different types of angina.

Answer 115

1. Stable angina (as we see in IHD) = predictable, happens on exertion 2. Unstable angina (ACS, later) = unexpected, happens during rest + accelerated during sleep. NOT relieved by rest or GTN spray 3. Prinzmetal's angina = sudden, no clear triggers, results from spasms or dysfunctions in coronary artery

Question 116

What are acute coronary syndromes (ACS)?

Answer 116

ACS encompasses a spectrum of acute cardiac conditions including unstable angina, NSTEMI and STEMI

Question 117

What is the common cause of ACS?

Answer 117

Thrombus from an atherosclerotic plaque blocking a coronary artery

Question 118

What are uncommon causes of ACS?

Answer 118

1. Coronary vasospasm 2. Drug abuse 3. Coronary artery dissection

Question 119

Describe unstable angina, NSTEMI and STEMI.

Answer 119

- Unstable angina (ischaemia) - NSTEMI (partial occlusion → subendocardial infarction). Non-ST elevation - STEMI (complete occlusion). ST elevation

Question 120

Describe the differences between stable angina and unstable angina. Include the pathophysiology, ECG and troponin.

Answer 120

- Stable angina: stable atherosclerotic plaque, vessel unable to dilate enough to allow adequate blood flow to meet myocardial demand. Pain upon exertion. Demand ischaemia, no infarct. Normal ECG. Normal troponins - Unstable angina: plaque ruptures and thrombus forms, causing partial occlusion of the vessel. Pain at rest or progresses rapidly over a short period of time. Supply ischaemia, no infarct. Normal, inverted T waves, or ST depression. Normal troponins

Question 121

Describe the differences between NSTEMI and STEMI.

Answer 121

- NSTEMI: the plaque rupture and thrombus formation causes partial occlusion of the vessel that results in injury and infarct to the subendocardial myocardium. Subendocardial infarct. Normal, inverted T waves, or ST depression. Troponin elevated - STEMI: complete occlusion of the blood vessel lumen, resulting in transmural injury and infarct to the myocardium, which is related by ECG changes and a rise in troponins. Transmural infarct. Hyperacute T waves or ST elevation. Troponin elevated. Acute changes = ST elevation or hyperacute T waves, hours/days = T wave inversion, pathological Q waves

Question 122

Why do you see increased serum troponin in NSTEMI and STEMI?

Answer 122

The occluding thrombus causes necrosis of cells and so myocardial damage. Troponin is a sensitive marker for cardiac muscle injury and so is significantly raised in reflection to this

Question 123

What is the presentation of people with ACS?

Answer 123

- Central, constricting chest pain radiating to jaw/arms - Sweating - SOB - \>20 minutes - Unstable angina: pain not relieved by rest or GTN spray - Silent MI: in diabetics

Question 124

Give 3 signs of unstable angina.

Answer 124

1. Cardiac chest pain at rest 2. Cardiac chest pain with crescendo patterns; pain becomes more frequent and easier provoked 3. No significant rise in troponin

Question 125

Give 6 signs/symptoms of MI.

Answer 125

1. Unremitting and usually severe central cardiac chest pain 2. Pain occurs at rest 3. Sweating 4. Breathlessness 5. Nausea/vomiting 6. 1/3 occur in bed at night

Question 126

What investigations would you do on someone you suspect to have ACS?

Answer 126

1. ECG 2. Blood tests; look at serum troponin 3. Coronary angiography 4. Cardiac monitoring for arrhythmias

Question 127

A raised troponin is not specific for ACS. In what other conditions might you see a raised troponin?

Answer 127

1. Gram negative sepsis 2. Pulmonary embolism 3. Myocarditis 4. Heart failure 5. Arrhythmias

Question 128

Describe the initial management for ACS.

Answer 128

1. Get into hospital ASAP - call 999 2. If STEMI, paramedics should call PCI centre for transfer 3. Aspirin 300mg 4. Pain relief e.g. morphine 5. Oxygen if hypoxic 6. Nitrates 7. Clopidogrel

Question 129

Describe the management for STEMI.

Answer 129

- PCI within 120 mins - Fibrinolysis (if PCI not possible in \<120 mins), e.g. alteplase - Clopidogrel or prasugrel and aspirin - Ticagrelor and aspirin

Question 130

Describe the management for NSTEMI/unstable angina.

Answer 130

- BMOAN: beta-blockers, morphine, oxygen, aspirin, nitrate - Use GRACE score to predict 6 month mortality + risk of further cardio events - Fondaparinux - Low risk: ticagrelor (P2Y12 receptor antagonist) and aspirin - Med/high risk: angiography + PCI, prasugrel (P2Y12 receptor antagonist) and aspirin

Question 131

Describe the immediate management for a myocardial infarction.

Answer 131

IMMEDIATE MANAGEMENT: M - Morphine O - Oxygen N - Nitrates (GTN) A - Aspirin (300mg)

Question 132

Describe the secondary prevention for ACS.

Answer 132

- ACEi - Clopidogrel - Aspirin + atorvastatin - Beta blocker

Question 133

What are some complications that can happen post MI?

Answer 133

- Death - Rupture of heart septum/papillary muscles - Oedema (heart failure) - Arrhythmias and aneurysm - Dressler’s syndrome

Question 134

What is the function of P2Y12?

Answer 134

It amplifies platelet activation

Question 135

Give 3 potential side effects of P2Y12 inhibitors.

Answer 135

1. Bleeding 2. Rash 3. GI disturbances

Question 136

What are the 5 classes of risk factors for IHD?

Answer 136

- Clinical risk factors (hypertension, lipids, diabetes) - Lifestyle risk factors (smoking, diet, physical inactivity) - Environmental risk factors (air pollution, chemicals) - Demographic risk factors (age, sex, ethnicity, genetic) - Psychosocial risk factors (behaviour pattern, depression/anxiety, work, social support)

Question 137

What are the layers of the heart wall?

Answer 137

- Endocardium = innermost layer, lines the cavities and valves of the heart - Myocardium = composed of cardiac muscle, responsible for the contractions of the heart - Epicardium = outermost layer of the heart, formed by the visceral layer of the PERICARDIUM. It is composed of connective tissue and fat. The connective tissue secretes a small amount of lubricating fluid into the pericardial cavity

Question 138

What are the two layers of pericardium? How much serous fluid is there between these layers? What is the function of this fluid?

Answer 138

- Visceral and parietal pericardium - 50ml - It acts as a lubricant and so allows smooth movement of the heart inside the pericardium

Question 139

What lies within the pericardium?

Answer 139

Great vessels

Question 140

The pericardial sac has a small reserve volume. What happens if this volume is exceeded? What is Tamponade physiology?

Answer 140

- If this volume is exceeded, the pressure is translated to the cardiac chambers - Tamponade physiology: small amount of volume added to space has dramatic effects on filling but so does removal of a small amount

Question 141

What is pericarditis?

Answer 141

Inflammation of the pericardium with/without effusion

Question 142

What are the causes of pericarditis?

Answer 142

- Infectious: - Viral: coxsackievirus - Bacterial: mycobacterium tuberculosis - Histoplasma spp. (most likely type found in immunocompromised) - Non-infectious: - Trauma (common) and iatrogenic - Autoimmune: rheumatoid arthritis, Sjogren's syndrome, SLE - Secondary metastatic tumours

Question 143

What is the pathophysiology of pericarditis?

Answer 143

- Inflammation of the pericardium (pericardial vascularisation, polymorphonuclear leukocyte infiltration) - This leads to the narrowing of the pericardial space and scarring of the fibrous pericardium - IF UNTREATED, we get a fibrinous reaction = a build up of exudate and adhesions in the pericardial space = PERICARDIAL EFFUSION - Pericardial effusion puts pressure on the cardiac myocytes = cardiac dysfunction. The fluid may be serous or haemorrhagic

Question 144

What are the symptoms of pericarditis?

Answer 144

• Severe chest pain - Sharp, pleuritic, rapid onset - Worse when laying flat + inspiration - Relieved by sitting forward - Radiates to trapezius ridge * Dyspnoea * Cough * Hiccups * Fever * Myalgia

Question 145

What are the signs of pericarditis?

Answer 145

- Pericardial rub friction rub on auscultation - high pitched scratchy sound heard loudest on the midline during inspiration - Tachycardia - Peripheral oedema - Increased JVP - PERICARDIAL EFFUSION: - Bronchial breathing at left base - Muffled heart sounds

Question 146

What are the investigations for pericarditis? What would these show?

Answer 146

- ECG: DIAGNOSTIC * Saddle-shaped ST elevation * PR depression - CXR: • Effusion may cause cardiomegaly - Serum troponin, CRP

Question 147

How do we treat pericarditis?

Answer 147

- NSAIDS with gastric protection: ibuprofen for two weeks, aspirin for two weeks. Colchicine for three months to reduce recurrence risk - Reduce physical activity until symptoms resolve - Treat the cause

Question 148

How do we treat pericardial effusion?

Answer 148

- Treat the cause - Pericardiocentesis

Question 149

What is a cardiac tamponade? What is the pathophysiology? What are the symptoms? What are the investigations? What is the treatement?

Answer 149

- Cardiac tamponade = life threatening condition whereby there is an accumulation of fluid in the pericardial space → compression of the heart chambers → decrease in venous return → decrease in filling in the heart → reducing cardiac output. Major COMPLICATION of pericarditis - Beck’s triad: falling BP, rising JVP, and muffled heart sound. Also pulsus paradoxus (large decrease in stroke volume → systolic blood pressure drops by \> 10mmHg on inspiration) - Investigations: echocardiogram = gold standard - Treatment = pericardiocentesis

Question 150

What is the difference between pericardial effusion and pericardial tamponade?

Answer 150

- Pericardial effusion = happens when pericardial fluid builds up slowly over time, which allows the pericardium to stretch out to accommodate bigger and bigger volumes of fluid without compressing the heart. Over time, it can cause chest pain, shortness of breath, and compression of near structures. Ultimately, if the pressure inside the pericardial cavity increases enough to compress the heart muscle, it may lead to pericardial tamponade. - Pericardial tamponade = when there’s a sudden fluid accumulation, the pericardium has no time to adjust, so even small amounts can cause a dramatic increase of pressure inside the pericardial sac, resulting in acute pericardial tamponade

Question 151

What are the causes of pericardial tamponade?

Answer 151

- Chest trauma, e.g. stab wound or blunt trauma, rupture of the aorta, rupture of the ventricle after a heart attack, or as a complication of cardiac surgery - It can also appear more gradually in individuals with pericardial infection, pericarditis or cancer, due to a progressive build-up of pericardial fluid over time

Question 152

What are the signs of pericardial tamponade?

Answer 152

- Beck's triad: - Low blood pressure - Distension of the jugular veins - Muffled heart sounds

Question 153

What investigations should be done for a pericardial tamponade?

Answer 153

- CXR - enlargement of the heart - Echocardiogram - right-sided chamber collapse during diastole - ECG - low voltage QRS complex

Question 154

How do we manage pericardial tamponade?

Answer 154

Pericardiocentesis

Question 155

You are a junior doctor and see a 26 year old woman who came to A&E complaining of chest pain. She has a past medical history of type 1 diabetes, and has a family history of rheumatoid arthritis. You decide to perform an ECG, and whilst you're placing the leads you notice a widespread rash on the patient's cheeks, neck and chest, which she says gets worse after she's been in the sun. The ECG shows widespread saddle-shaped ST elevation. What is the likely cause of her chest pain? a. STEMI b. Infective Endocarditis c. Prinzmetal Angina d. Pericarditis

Answer 155

D. Pericarditis

Question 156

You are a junior doctor and see a 26 year old woman who came to A&E complaining of chest pain. She has a past medical history of type 1 diabetes, and has a family history of rheumatoid arthritis. You decide to perform an ECG, and whilst you're placing the leads you notice a widespread rash on the patient's cheeks, neck and chest, which she says gets worse after she's been in the sun. The ECG shows widespread saddle-shaped ST elevation. What is the most likely underlying cause? a. Her Type 1 Diabetes Mellitus b. Rheumatoid arthritis c. Systemic Lupus Erythematosus d. Mycobacterium Tuberculosis

Answer 156

C. Systemic Lupus Erythematosus (SLE)

Question 157

What is the definition of heart failure? What happens in order for cardiac output to be maintained? What happens eventually?

Answer 157

- Inability of the heart to deliver blood and thus oxygen at a rate that is commensurate with the requirements of the body. Can result from STRUCTURAL/FUNCTIONAL cardiac disorder that impairs the heart’s ability to function - Compensatory physiological changes occur in order to maintain cardiac output. They are eventually overwhelmed and become pathophysiological: - [sympathetic system activation] BP falls → detected by baroreceptors → sympathetic activation → positively inotropic/chronotropic → CO increases - RAAS system

Question 158

What are the different types of heart failure?

Answer 158

- Acute heart failure = new onset acute or decompensation of chronic - Chronic heart failure = develops/progresses slowly and arterial pressure is well maintained until late - Systolic failure = inability of the ventricle to contract normally - Diastolic failure = inability of the ventricle to relax and fill normally - Left ventricular failure = either systolic or diastolic failure of the left ventricle - Right ventricular failure = either systolic or diastolic failure of the right ventricle

Question 159

What is the aetiology of left sided heart failure?

Answer 159

- Coronary artery disease - Myocardial infarction - Cardiomyopathy - Valvular heart disease - Arrhythmias

Question 160

What is the aetiology of right sided heart failure?

Answer 160

- Right ventricular infarct - Pulmonary hypertension - Pulmonary embolism - COPD - Progression of left sided heart failure - COR PULMONALE (disease of lung/pulmonary vessels → pulmonary hypertension → RV hypertrophy → RHF with venous overload, peripheral oedema, hepatic congestion)

Question 161

What is the aetiology of systolic heart failure?

Answer 161

- ISCHAEMIC HEART DISEASE - Myocardial infection - Cardiomyopathy

Question 162

What is the aetiology of diastolic heart failure?

Answer 162

- Aortic stenosis - Chronic hypertension

Question 163

What is the pathophysiology of heart failure?

Answer 163

- Myocardium fails, so there is a decreased volume of blood ejected. This causes an increase in preload - An increase in ventricular load causes hypertrophy of the myocardium. An increase in the size and number of cells causes an increase in myocardial demand for oxygen. This causes the myocardium to become ischaemic = patchy fibrosis = stiffness and reduced contractibility - Reduced contractibility = increased workload and amount of blood remaining. More force needed to maintain cardiac output = cells become tired = pathological - Increased afterload and preload = increased cardiac work = damage to myocytes = decreased cardiac output = reduced blood flow to kidneys etc. = activates RAAS system and adrenergic pathway. This causes Na2+ and water retention, increased HR and contraction force, and cardiotoxicity

Question 164

What are the symptoms of left sided heart failure? Why?

Answer 164

- 3 cardinal symptoms: SHORTNESS OF BREATH, FATIGUE, ANKLE SWELLING - Exertional dyspnoea - this is because blood backs up to the lungs via pulmonary vein as not pumped around the body - Fatigue - Orthopnoea - Paroxysmal nocturnal - Poor exercise tolerance - Nocturnal cough - Wheeze - Nocturia - Cold peripheries

Question 165

What are the symptoms of right sided heart failure? Why? What is the classifcation for heart failure

Answer 165

- Peripheral OEDEMA (ankle swelling) - this is because blood backs up to the body via the vena cava - ASCITES - RAISED JVP - HEPATOMEGALY - Nausea - Facial engorgement - Epistaxis - Cyanosis - NEW YORK CLASSIFICATION - Hypotension

Question 166

What are the symptoms and signs of heart failure?

Answer 166

SOFA PC: - Shortness of breath - Orthopnoea - Fatigue - Ankle swelling - Pulmonary oedema (due to backflow from decreased CO; produced cough with pink frothy sputum) - Cold peripheries - Raised JVP - End respiratory crackles

Question 167

What are the investigations for heart failure? What is the mnemonic for assessing heart failure through a chest X-ray?

Answer 167

- NT-pro BNP (BRAIN NATRIURETIC PEPTIDE) = a marker of heart failure, released when the myocardial walls are under stress - ECG - Transthoracic ECG: wall motion abnormalities, valvular disease, cardiomyopathies - GOLD STANDARD = ECHOCARDIOGRAPHY - Chest X-ray (ABCDE): – Alveolar oedema (bat wing shadowing) – Kerley B Lines – Cardiomegaly – Dilated upper lobe vessels of lungs – Effusions (pleural)

Question 168

What is the treatment for acute heart failure? What is the treatment for chronic heart failure? Why?

Answer 168

- Acute HF = OMFG: oxygen, morphine, furosemide, GTN spray - Chronic HF: - Lifestyle changes: stop smoking, low salt, weight and nutrition - Medication: - 1st line = ACEIs, e.g. ramipril and BETA BLOCKERS, e.g. bisoprolol - 2nd line = ALDOSTERONE RECEPTOR ANTAGONISTS, e.g. spironolactone - 3rd line = Digoxin - Symptomatic relief: DIURETICS - excretion of water = reduces preload and BP. Loop diuretics (furosemide), thiazide diuretics (bendroflumethiazide), aldosterone antagonists (spironolactone)

Question 169

What is Cor Pulmonale?

Answer 169

Right sided heart failure caused by chronic pulmonary arterial hypertension

Question 170

What are the causes of Cor Pulmonale?

Answer 170

- Chronic lung disease, e.g. COPD - Pulmonary vascular disorders - Neuromuscular and skeletal diseases

Question 171

What are the symptoms of Cor Pulmonale?

Answer 171

- Dyspnoea - Fatigue - Syncope

Question 172

What are the signs of Cor Pulmonale?

Answer 172

- Cyanosis - Tachycardia - Raised JVP - RV heave - Pan-systolic murmur due to tricuspid regurgitation - Hepatomegaly - Oedema

Question 173

What are the investigations for Cor Pulmonale?

Answer 173

- ABG – hypoxia +/- hypercapnia

Question 174

What is the management for Cor Pulmonale?

Answer 174

- TREAT UNDERLYING CAUSE - Give oxygen to treat respiratory failure - Treat cardiac failure the same, e.g. diuretics - Consider venesection if haematocrit \>55 - Consider heart-lung transplantation in young patients

Question 175

A patient with recently diagnosed heart failure comes to your GP practice for a check-up and medication review. He tells you that he has felt a little weaker and more tired than usual recently. His current medications include: Furosemide, Ramipril, Bisoprolol His blood results show: Sodium: 142 (135-145) Potassium: 2.4 (3.5-5.5) 1. Which of the following drugs is the most likely cause of the electrolyte abnormality? a. Furosemide b. Ramipril c. Bisoprolol d. None of the above

Answer 175

A. Furosemide

Question 176

A patient with recently diagnosed heart failure comes to your GP practice for a check-up and medication review. He tells you that he has felt a little weaker and more tired than usual recently. His current medications include: Furosemide, Ramipril, Bisoprolol His blood results show: Sodium: 142 (135-145) Potassium: 2.4 (3.5-5.5) 2. Which of the following diuretics is the most appropriate for this patient? a. Furosemide b. Bendroflumethiazide c. Spironolactone d. Verapamil

Answer 176

C. Spironolactone

Question 177

What is the Tetralogy of Fallot? What is it characterised by?

Answer 177

A congenital heart defect characterised by 4 defects: 1. Ventricular septal defect (a hole allowing blood to flow between the two ventricles) 2. Over-riding aorta (aorta expands to allow blood from both ventricles to enter) 3. RV hypertrophy 4. Pulmonary stenosis (narrowing of the exit of the right ventricle)

Question 178

What is the physiology of Tetralogy of Fallot?

Answer 178

- The stenosis of the RV outflow leads to the RV being at a higher pressure than the left - Therefore deoxygenated blood passes from the RV to the LV

Question 179

Would a baby born with Tetralogy of Fallot be cyanotic?

Answer 179

YES! There is a greater pressure in the RV than the LV and so blood is shunted into the LV -\> CYANOSIS!

Question 180

What are the signs, investigations and treatment of Tetralogy of Fallot?

Answer 180

- Signs: cyanosis, harsh systolic ejection murmur, tachypnoea - Investigations = pulse oximetry, echocardiogram, ECG, CXR - Treatment = surgical repair

Question 181

What is ventricular septal defect? Would a baby born with ventricular septal defect be cyanotic?

Answer 181

- An abnormal connection between the two ventricles - No. There is a higher pressure in the LV than the RV and so blood is shunted from the left to right meaning there is an increased amount of blood going to the lungs; not cyanotic

Question 182

What are the signs of a large VSD? How about a small VSD?

Answer 182

- Moderate-large show exercise intolerance - SOB - Poor weight gain - Harsh systolic murmur - Very high pulmonary blood flow - Usually asymptomatic if small

Question 183

What might VSD lead onto?

Answer 183

Eisenmenger's syndrome

Question 184

What are the investigations and treatment for VSD?

Answer 184

- Investigations: echocardiogram, ECG, CXR - Tx: small asymptomatic = no intervention. Larger + symptoms = consider surgical repair

Question 185

Describe Eisenmenger's syndrome. What is its physiology?

Answer 185

- When shunting through septal defect is from right to left, resulting in deoxygenated blood in the systemic circulation - High pressure pulmonary blood flow damages pulmonary vasculature -\> there is increased resistance to blood flow (pulmonary hypertension) -\> RV pressure increases -\> shunt direction reverses (RV to LV) -\> CYANOSIS!

Question 186

Describe 3 risks associated with Eisenmenger's syndrome.

Answer 186

1. Risk of death 2. Endocarditis 3. Stroke

Question 187

What is atrial septal defect?

Answer 187

An abnormal connection between the two atria; it is fairly common

Question 188

Would a baby born with ASD be cyanotic?

Answer 188

No. There is a higher pressure in the LA than the RA and so blood is shunted from the left to right, therefore not cyanotic

Question 189

What are the signs of ASD?

Answer 189

1. Significant increase in blood flow through the right heart and lungs - pulmonary flow murmur 2. Enlarged pulmonary arteries 3. Right heart dilatation 4. SOBOE 5. Increased chest infection 6. Ejection systolic murmur on auscultation

Question 190

What are the investigations and treatment of ASDs?

Answer 190

- Investigations: echocardiogram, ECG, CXR - Treatments: most close spontaneously, some require corrective closure

Question 191

What is AVSD?

Answer 191

Atrio-ventricular septal defects. Basically a hole in the very centre of the heart. Involves the ventricular septum, the atrial septum, the mitral and tricuspid valves

Question 192

Give 2 clinical signs of AVSD.

Answer 192

1. Breathless 2. Poor feeding and poor weight gain

Question 193

What is a patent ductus arteriosus?

Answer 193

- A patent ductus arteriosus (PDA) occurs when it fails to close - the ductus arteriosus is a vascular foetal structure that connects the pulmonary artery and the aorta and usually closes in the first 48 hours after birth - Persistence of the ductus arteriosus can result in heart failure, increased pulmonary pressures, and endarteritis

Question 194

What are the signs of a patent ductus arteriosus?

Answer 194

- CONTINOUS 'MACHINERY' MURMUR 1. Torrential flow from the aorta to the pulmonary arteries can lead to pulmonary hypertension and RHF 2. Breathless 3. Poor feeding, failure to thrive 4. May be asymptomatic

Question 195

What are the investigations of patent ductus arteriosus?

Answer 195

- Investigations: echocardiogram, ECG, CXR - Treatment: varies. Surgical closure

Question 196

What is the coarctation of the aorta? Describe its pathophysiology.

Answer 196

- Narrowing of the aorta at the site of insertion of the ductus arteriosus - Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing

Question 197

What are the signs of coarctation of aorta?

Answer 197

- RIGHT ARM Hypertension - Differential upper and lower extremity blood pressures - RADIO 'FEMORAL' PULSE - Systolic ejection murmur

Question 198

What are the investigations and treatment for a coarctation of aorta?

Answer 198

- Investigations: ECG, CXR, echocardiogram - Treatment: surgery

Question 199

What do the numbers mean in a blood pressure reading? From which artery is blood pressure usually measured?

Answer 199

- Top number = systolic blood pressure = arterial blood pressure when the heart is contracting - Bottom number = diastolic blood pressure = arterial blood pressure when the heart is relaxing - Usually measured from brachial artery (as if high there then it's probably high elsewhere)

Question 200

What do the terms isolated systolic hypertension and isolated diastolic hypertension mean?

Answer 200

- Isolated systolic hypertension = only systolic pressure raised - Isolated diastolic hypertension = only diastolic pressure raised

Question 201

What are the hospital and non-hospital readings for hypertension (stage 1)?

Answer 201

- BP \>140/90 in clinic = White coat syndrome - BP \>135/85 with ABPM/home readings

Question 202

What are the causes of hypertension?

Answer 202

- 95% idiopathic = Essential hypertension (usually diagnosed by screening of an asymptomatic individual) - 5% underlying cause = Secondary hypertension. ROPE: - Renal disease - Obesity - Pregnancy (pre-eclampsia) - Endocrine (Conn's syndrome)

Question 203

What are the modifiable and non-modifiable risk factors for hypertension?

Answer 203

- Modifiable: - Alcohol intake - Sedentary lifestyle - DM - Sleep apnoea - Smoking - Non-modifiable: - Age (\>65) - FHx - Ethnicity (Afro-Caribbean)

Question 204

On average, by how much does having high blood pressure shorten life?

Answer 204

7 years. Although this depends on onset and severity

Question 205

Name 5 conditions that hypertension is a major risk factor of.

Answer 205

1. MI (IHD) 2. Stroke 3. Heart failure 4. Chronic renal disease 5. Dementia

Question 206

If you gave someone 1 blood pressure tablet by how much would you expect their blood pressure to decrease?

Answer 206

1 tablet = 10mmHg reduction in BP

Question 207

What are the symptoms of different types of hypertension? What are some complications?

Answer 207

- Primary HTN = usually none - Secondary HTN = symptoms relate to underlying cause - Hypertensive crisis = confusion, drowsiness, chest pain, breathlessness

Question 208

What investigations might you do in someone with hypertension?

Answer 208

1. If clinical BP is \>140/90: - Recheck BP on 2-3 occasions over the next few weeks/months - If persistently high, offer 24h ambulatory blood pressure \>135/85 will confirm the diagnosis - If stage 1 diagnosed → do QRISK to decide treatment - If stage 2 diagnosed → start antihypertensive treatment 2. We then need to identify possible causes of secondary hypertension - ECG (cardiovascular complications, e.g old infarction) - Urine ACR (albumin:creatinine ratio): ?proteinuria, dipstick: ?microscopic haematuria, bloods: renal function (GFR), Hb - Hypertensive retinopathy = fundus examination - Others: - HbA1c (DM) - Lipids

Question 209

What are the classifications of the different stages of blood pressure for both clinic BP and ABPM BP? What is the classification for a hypertensive crisis and what is the treatment?

Answer 209

- Clinic BP: - Stage 1 = \>140/90 - Stage 2 = \>160/100 - ABPM BP: - Stage 1 = \>135/85 - Stage 2 = \>150/95 - Stage 3 (hypertensive crisis) = \>180/120. With organ damage, this is known as maligant HTN = medical emergency - SAME DAY ADMISSION AND START ANTIHYPERTENSIVE DRUG IMMEDIATELY

Question 210

What is the treatment for hypertension?

Answer 210

- Lifestyle changes - Hypertension with type 2 diabetes or without T2DM but \<55 and not Afro-Caribbean = ACEi or ARB - Hypertension without T2DM but \>55 or Black-African or Afro-Caribbean (any age) = CCB - May have to include these with thiazide-like diuretics if worse - For diabetics, ACE-i is ALWAYS first line - For black patients, start with CCB as they are not responsive to ACE-i - Give CCB before diuretics, unless evidence of oedema/intolerance - ACE-i are CI in pregnancy/if patient is on general anaesthesia

Question 211

What drugs might you give to someone with hypertension?

Answer 211

- ABCD: A - ACEi, e.g. ramipril or ARB (if they develop a cough with ramirpil), e.g. candesartan B - beta blockers, e.g. bisoprolol C - CCB, e.g. amlodipine D - diuretics, e.g. bendroflumethiazide

Question 212

Give 5 potential side effects of rampiril.

Answer 212

Side effects of ACE inhibitors: 1. Hypotension 2. Acute renal failure 3. Hyperkalaemia 4. Teratogenic 5. Cough, rash, anaphylactoid due to increased kinin production

Question 213

On what receptor does valsartan act?

Answer 213

AT-1, prevents Ang 2 binding

Question 214

Give 4 side effects of valsartan. How about a contraindication?

Answer 214

- Side effects of valsartan: 1. Hypotension 2. Renal dysfunction 3. Hyperkalaemia 4. Rash - Contraindiated in pregnancy!

Question 215

Give 5 side effects of bisoprolol.

Answer 215

Side effects of beta blockers: 1. Hypotension 2. Fatigue 3. Headache 4. Erectile dysfunction 5. Bradycardia

Question 216

Give 3 side effects of amlodipine.

Answer 216

Side effects of dihydropyridines (CCB): 1. Flushing 2. Headache 3. Oedema

Question 217

Give 3 side effects of verapamil.

Answer 217

Side effects due to being negatively chronotropic: 1. Bradycardia 2. AV block Side effects due to being negatively inotropic: 1. Worsening of cardiac failure

Question 218

Give 5 side effects of bendroflumethiazide.

Answer 218

Side effects of diuretics: 1. Hypovolemia 2. Hypotension 3. Reduced K, Na, Mg, Ca 4. Hyperuricaemia -\> gout 5. Erectile dysfunction

Question 219

Why are men more commonly affected by heart failure than women?

Answer 219

Women have 'protective hormones' meaning they are less at risk of developing heart failure

Question 220

What are the compensatory mechanisms in heart failure?

Answer 220

1. Sympathetic system 2. RAAS 3. Natriuretic peptides 4. Ventricular dilation 5. Ventricular hypertrophy

Question 221

Explain how the sympathetic system is compensatory in heart failure and give one disadvantage of sympathetic activation.

Answer 221

The sympathetic system improves ventricular function by increasing HR and contractility = CO maintained. BUT it also causes arteriolar constriction which increases after load and so myocardial work

Question 222

Explain how RAAS is compensatory in heart failure and give one disadvantage of RAAS activation.

Answer 222

Reduced CO leads to reduced renal perfusion; this activates RAAS. There is increased fluid retention and so increased preload. BUT it also causes arteriolar constriction which increases after load and so myocardial work

Question 223

Give 3 properties of natriuretic peptides that make them compensatory in heart failure.

Answer 223

1. Diuretic 2. Hypotensive 3. Vasodilators

Question 224

Give an example of an ACE inhibitor that is commonly used in HF.

Answer 224

Perindopril

Question 225

Name 4 beta blockers that are used in the treatment of heart failure.

Answer 225

1. Metoprolol 2. Bisoprolol 3. Carvedilol 4. Nebivolol

Question 226

What is an arrhythmia? Give a list of common arrhythmias.

Answer 226

- Arrhythmia = an abnormality in cardiac rhythm: - Atrial fibrillation - Atrial flutter - Heart block - Tachycardia - Bradycardia - Prolonged QT - WPW syndrome - BBB

Question 227

What is the definition of tachycardia?

Answer 227

Heart rate \> 100bpm

Question 228

What is atrial tachycardia? How does it appear on an ECG?

Answer 228

- Atrial tachycardia occurs when the electrical signal that controls the heartbeat starts from an unusual location in the upper chambers (atria) and rapidly repeats, causing the atria to beat too quickly - In an ECG we have: - Abnormal P waves - Normal QRS - \>150bpm

Question 229

What is AV nodal re-entrant tachycardia? What is the main symptom? What does it look like on an ECG? How do we treat it?

Answer 229

- Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of paroxysmal supraventricular tachycardia (PSVT) encountered in clinical practice - Main symptom = sudden development of regular rapid palpitations - ECG: - Absent P wave - Normal QRS - Treatment = involves anything blocking the AV node, e.g. carotid sinus massage, Valsalva manoeuvre

Question 230

What is a ventricular tachycardia? How is this different to a supraventricular tachycardia? What does it look like on an ECG?

Answer 230

- It occurs when the ventricles of the heart beat too fast. It is a BROAD-COMPLEX (QRS COMPLEX \>120ms) - A supraventricular tachycardia occurs when the atria beat too fast - ECG: - No P waves - Regular, wide QRS - No T waves

Question 231

Do supraventricular tachycardia's have narrow or broad QRS complexes? Do ventricular tachycardia's have narrow or broad QRS complexes?

Answer 231

- Supraventricular tachycardias are often associated with narrow complexes - Ventricular tachycardias are often associated with broad complexes

Question 232

Give 4 causes of sinus tachycardia.

Answer 232

1. Physiological response to exercise 2. Fever 3. Anaemia 4. Heart failure

Question 233

Name 5 supraventricular tachycardias. What is the first line management in SVT's?

Answer 233

1. Atrial fibrillation 2. Atrial flutter 3. AVRT 4. AV node re-entry tachycardia (AVNRT) 5. Focal atrial tachycardia 1st line management in SVT is ADENOSINE.

Question 234

What is atrial fibrillation? What is its pathophysiology? How does it appear on an ECG?

Answer 234

- Atrial fibrillation = chaotic irregular rhythm with an irregular ventricular rate - IRREGULARLY IRREGULAR - Pathophysiology = continuous rapid activation of the atria with no organised mechanical action - ECG: - No P waves - irregular line - Irregularly irregular QRS

Question 235

What are the causes of atrial fibrillation?

Answer 235

- Idiopathic - Hypertension - Heart failure - Coronary artery disease - Valvular heart disease - Cardiac surgery - Cardiomyopathy - Rheumatic heart disease

Question 236

What are the risk factors for atrial fibrillation?

Answer 236

- Aged 60+ - Diabetes - High BP - Coronary artery disease - Past MI - Structural heart disease

Question 237

What is the clinical presentation of atrial fibrillation?

Answer 237

- Asymptomatic - Palpitations - Dyspnoea - Chest pains - Fatigue - NO P WAVES ON ECG - Rapid/irregular QRS - Apical pulse\>radial

Question 238

How do we treat atrial fibrillation?

Answer 238

- Treat underlying cause, e.g. alcohol, hypertension - Rate control, e.g. BETA BLOCKERS, CCBs - Give a LWMH, e.g. dalteparin to prevent thromboembolism - Restore sinus rhythm = electrical or pharmacological cardioversion - Maintain sinus rhythm, e.g. by using flecainide

Question 239

What is the long term treatment of atrial fibrillation?

Answer 239

Catheter ablation - it targets the triggers of AF

Question 240

The ECG taken from someone with atrial fibrillation shows a fine oscillation of the baseline and absent P waves. Why?

Answer 240

The atria fire a lot, it is chaotic. The AV node and ventricles can't keep up -\> irregularly irregular pulse

Question 241

What score can be used to calculate the risk of stroke in someone with atrial fibrillation?

Answer 241

CHADS2 VASc

Question 242

What does the CHADS2 VASc score take into account?

Answer 242

The CHADS2 VASc score is used to calculate the risk of stroke in patients with atrial fibrillation. It considers: - Congestive heart failure/LV dysfunction - Hypertension - Age \>75 (2) - Diabetes mellitus - Stroke/TIA/thrombo-embolism (2) - Vascular disease - Age 65-74 - Sex category Out of 9 in total. A score \>2 indicates the need for anticoagulation

Question 243

Why does the stroke risk increase in atrial fibrillation?

Answer 243

Stroke risk increase due to static blood in the atria – it pools and it remains still, causing it to clot and embolise

Question 244

What is an atrial flutter? How is it different to atrial fibrillation? What is its pathophysiology? What does it look like on an ECG?

Answer 244

- Atrial flutter = organised atrial rhythm - In atrial fibrillation, the atria beat irregularly. In atrial flutter, the atria beat regularly, but faster than usual and more often than the ventricles - regularly irregular - Pathophysiology: the re-entry mechanism - there is blockage of the normal circuit. Another pathway forms, takes a different course and re-enters the circuit -\> tachycardia - ECG = saw-tooth pattern (F-waves) - DEFINITIVE DIAGNOSIS

Question 245

What are the causes of atrial flutter?

Answer 245

- Idiopathic - Coronary heart disease - Obesity - Hypertension - Heart failure - COPD - Pericarditis

Question 246

What are the risk factors for atrial flutter?

Answer 246

Atrial fibrillation

Question 247

What is the clinical presentation of atrial flutter?

Answer 247

- Palpitations - Breathlessness - Chest pain - Dizziness - Syncope - Fatigue - Sign: narrow QRS and 'sawtooth' flutter waves

Question 248

Describe the ECG pattern taken from someone with atrial flutter.

Answer 248

1. Narrow QRS 2. 'sawtooth' flutter waves

Question 249

What is the treatment for atrial flutter?

Answer 249

- DEFINITIVE = CATHETER ABLATION - Cardioversion - give a LMWH (pharmacological), shock with defibrillator (electrical) - IV Amiodarone - restore sinus rhythm

Question 250

What is the acute management of haemodynamically stable patients with superventricular tachycardia?

Answer 250

1. VALSALVA MANOUEVRE 2. CAROTID SINUS MASSAGE 3. Chemical cardioversion: i. ADENOSINE ii. Alternative to adenosine, e.g. verapamil 4. Direct current (DC) cardioversion

Question 251

What is the definition of bradycardia?

Answer 251

Slow heart rate \<60 bpm

Question 252

What does bradycardia look like on an ECG?

Answer 252

- PR interval between 0.12 and 0.20 seconds - QRS complex \<0.12 seconds

Question 253

What is a bundle branch block? What are the two types?

Answer 253

- Bundle branch block = a block in the conduction of one of the bundle branches, so the ventricles don’t receive impulses at the same time - Right bundle branch block and left bundle branch block

Question 254

What is the pathophysiology of a right bundle branch block? What are the causes?

Answer 254

- Pathophysiology = right bundle doesn’t conduct, so impulse spreads from left ventricle to right, resulting in a late activation of RV - Causes: - Pulmonary embolism - IHD - Atrial Ventricular Septal Defect

Question 255

What is the clinical presentation of right bundle branch block?

Answer 255

- Asymptomatic - Syncope/Presyncope

Question 256

How do we diagnose a right bundle branch block through an ECG?

Answer 256

- MaRRoW (the M and W stand for shapes in V1 and V6, the RR means it's right) - Wide QRS

Question 257

How do we treat a right bundle branch block?

Answer 257

- Pacemaker - CRT - cardiac resynchronisation therapy - Reduce blood pressure

Question 258

What is the pathophysiology of a left bundle branch block? What are the causes of a left bundle branch block?

Answer 258

- Pathophysiology: left bundle doesn’t conduct, so the impulse spreads from right ventricle to left, resulting in a late activation of LV - Causes: - IHD - Aortic valve disease

Question 259

What is the clinical presentation of left bundle branch block?

Answer 259

- Asymptomatic - Syncope/Presyncope

Question 260

How do we diagnose a left bundle branch block from an ECG?

Answer 260

- WiLLiaM (W in V1, LL for left and M in V6) - Wide QRS and notched top - T wave inversion in lateral leads

Question 261

How do we treat left bundle branch block?

Answer 261

- Pacemaker - CRT – cardiac resynchronisation therapy - Reduce blood pressure

Question 262

What is a heart block? What are the different types of heart block?

Answer 262

- Heart block = a block at any level of the conduction system in which conduction seizes - 1st degree heart block, 2nd degree heart block (Mobitz I), 2nd degree heart block (Mobitz II), 2nd degree heart block (2:1), 3rd degree heart block

Question 263

What do the degrees of heart block represent?

Answer 263

How severe the block is, e.g. first degree = delayed but still makes it, PR interval \> 200ms

Question 264

What are the causes of heart block?

Answer 264

- Athletes - Sick sinus syndrome - IHD - esp MI - Acute myocarditis - Drugs - Congenital - Aortic valve calcification - Cardiac surgery/trauma

Question 265

What is first degree heart block? How do people with first degree heart block present? What does first degree heart block look like on an ECG?

Answer 265

- First degree heart block = occurs where there is delayed atrioventricular conduction through the AV node. Despite this, every atrial impulse leads to a ventricular contraction, meaning every p waves results in a QRS complex. On an ECG this presents as a prolonged PR interval - Presentation = asymptomatic - ECG: PR interval \> 200ms

Question 266

What is a second degree heart block?

Answer 266

Second degree heart block is where some of the atrial impulses do not make it through the AV node to the ventricles. This means that there are instances where p waves do not lead to QRS complexes. There are several patterns of second degree heart block

Question 267

What is a second degree heart block (Mobitz I)? How does this show on an ECG?

Answer 267

- Where the atrial imputes becomes gradually weaker until it does not pass through the AV node. After failing to stimulate a ventricular contraction the atrial impulse returns to being strong. This cycle then repeats. - PR interval gradually increases until AV node fails and no QRS complex is seen. The PR interval then returns to normal but progressively becomes longer again until another QRS complex is missed. This cycle repeats itself

Question 268

What is a second degree heart block (Mobitz II)? What does the ECG look like? What is there a risk of?

Answer 268

- This is where there is intermitted failure or interruption of AV conduction - This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes, for example 3 P waves to each QRS complex would be referred to as a 3:1 block. The PR interval remains normal - There is a risk of ASYSTOLE with Mobitz Type 2

Question 269

How would someone with a second degree heart block (Mobitz I) present? What would their ECG look like?

Answer 269

- Presentation: - Light headedness - Dizziness - Syncope - ECG: - Progressive lengthening of PR interval - One non-conducted P wave - Next PR interval is shorter

Question 270

What would the ECG of someone with a second degree heart block (Mobitz II) look like?

Answer 270

- Constant PR - Occasional non-conducted P-waves - Wide QRS

Question 271

What is a second degree heart block (2:1)? What is it caused by? What is the clinical presentation of someone with a second degree heart block (Mobitz II (2:1)) and what would their ECG look like?

Answer 271

- Where there are 2 P waves for each QRS complex. Every second p wave is not a strong enough atrial impulse to stimulate a QRS complex. It can be caused by Mobitz Type 1 or Mobitz Type 2 and it is difficult to tell which - Clinical presentation: - SOB - Postural hypotension - Chest pain - ECG: - Two waves per QRS - Normal consistent PR intervals

Question 272

Describe a third degree heart block. What is there a significant risk of?

Answer 272

- Third degree heart block (complete heart block) = atrial activity fails to conduct to the ventricles. P waves and QRS complexes therefore occur independently (no observable relationship) - Significant risk of asystole

Question 273

What happens in a third degree heart block? What is the clinical presentation of third degree heart block?

Answer 273

- In a third degree heart block, the signal is completely blocked - Clinical presentation = dizziness and blackouts

Question 274

What is the shape of an ECG in a third degree heart block?

Answer 274

- P waves and QRS at different rates (dissociation) - Abnormally shaped QRS

Question 275

What is the treatment for a third degree heart block?

Answer 275

- Permanent pacemaker - IV atropine

Question 276

What are the investigations and treatment for heart block?

Answer 276

- Investigations = ECG - Treatment = cardioversion (give a LWMH, shock with defribrillator), catheter ablation (creates a conduction block), IV amiodarone (restore sinus rhythm)

Question 277

Wolff-Parkinson White syndrome (an accessory pathway syndrome) is a type of arrhythmia. What happens in this syndrome? What is the extra pathway called?

Answer 277

- WPW syndrome is caused by an extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the atrio-ventricular node - The extra pathway that is present in Wolff-Parkinson White Syndrome is often called the Bundle of Ken

Question 278

What does the ECG of some with Wolff-Parkinson-White syndrome look like?

Answer 278

- Pre-excitation: - SHORT PR interval - Wide QRS complex that begins slurred - DELTA WAVE

Question 279

What are the causes of Wolff-Parkinson-White syndrome (an accessory pathway syndrome)?

Answer 279

- Congenital - Hypokalaemia - Hypocalcaemia - Drugs: amiodarone, tricyclic antidepressants - Bradycardia - Acute MI - Diabetes

Question 280

What is the clinical presentation of Wolff-Parkinson-White syndrome?

Answer 280

- Palpitations - Severe dizziness - Dyspnoea - Syncope

Question 281

What is the treatment for Wolff-Parkinson-White syndrome?

Answer 281

- Definitive treatment = RADIOFREQUENCY ABLATION of the accessory pathway - Vagal manoeuvre: breath holding, carotid massage, valsalva manoeuvre - IV adenosine

Question 282

Describe the pathophysiology of focal atrial tachycardia.

Answer 282

Another area of the atrium becomes more autonomic than the sinus node and so sinus node function is taken over -\> focal atrial tachycardia

Question 283

What might you see on an ECG taken from someone with focal atrial tachycardia?

Answer 283

Abnormal P waves appear before a normal QRS

Question 284

What are ectopic beats and what are they caused by? What might the patient complain of?

Answer 284

Very common, generally benign arrhythmias caused by premature discharge. The patient may complain of symptoms of 'skipped beats'

Question 285

What is prolonged QT syndrome? What does the ECG look like?

Answer 285

- Prolonged repolarisation of the muscle cells in the heart after a contraction - The QT interval is greatly increased

Question 286

What are the causes of prolonged QT syndrome?

Answer 286

- Congenital - Hypokalaemia - Hypocalcaemia - Drugs: amiodarone, tricyclic antidepressants - Bradycardia - Acute MI - Diabetes

Question 287

What is the clinical presentation of prolonged QT syndrome? What might it progress to?

Answer 287

- Palpitations - Syncope - May progress to VF (shockable cardiac arrest rhythm)

Question 288

What is the treatment for prolonged QT syndrome?

Answer 288

- Treat underlying cause, e.g. electrolyte management - Defribrillation if VF occurs - If acquired (not congential) = IV isoprenaline

Question 289

What is Torsades de pointes? Who does it occur in? What does its ECG look like?

Answer 289

- Torsades de pointes is a type of polymorphic (multiple shape) ventricular tachycardia - It occurs in people with PROLONGED QT SYNDROME - It looks like normal ventricular tachycardia on an ECG, however there is an appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes progressively get smaller, then larger then smaller and so on

Question 290

A patient presents to A and E following an episode where they lost consciousness. They were alone so are unsure how long they were out for. On questioning, you find out that the episode was preceded by palpitations, dizziness and shortness of breath, and that they have a family history of 'heartbeat problems’. You perform an ECG, which shows a sawtooth pattern. 3. What is the most likely diagnosis? a. Atrial fibrillation b. Atrial flutter c. Mobitz II heart block d. Tachycardia

Answer 290

B. Atrial flutter

Question 291

What is infective endocarditis? Which 2 symptoms/signs signal towards infective endocarditis?

Answer 291

- An infection of the endocardium or vascular endothelium of the heart - Fever + new murmur = infective endocarditis until proven otherwise

Question 292

Which bacteria cause infective endocarditis?

Answer 292

- STAPHYLOCOCCUS AUREUS (most common - IV drug users) - STREPTOCOCCUS VIRIDANS (poor dental health - most common in non-IVDU) - Pseudomonas aeruginosa - Staphylococcus epidermis (prosthetic valves)

Question 293

Based on the bacterial causes of infective endocarditis, in which individuals do we usually find infective endocarditis?

Answer 293

- IV drug users - Immunocompromised patients - People with prosthetic valves - Aortic/mitral valve disease - Poor dental hygiene - Pacemakers - IV Cannula

Question 294

Describe the pathophysiology of infective endocarditis.

Answer 294

- Abnormal cardiac endothelium (damaged by turbulent blood flow, this is why valves are often affected. We get platelet and fibrin deposition and then a thrombus) and organisms in the bloodstream = adherance and growth of organisms to thrombus in affected area - Virulent organisms destroy the valve = valve regurgitation and worsening of heart failure

Question 295

Which area of the heart is usually affected by infective endocarditis? What is the exception?

Answer 295

- Left side of the heart (MITRAL (most common) and aortic valves) - Exception = IV drug users = affects the right side of the heart

Question 296

What are the symptoms and signs of infective endocarditis?

Answer 296

- Symptoms: - Fever - Rigors - Night sweats - Malaise - Weight loss - Signs: - Anaemia - Splenomegaly - Clubbing - New murmur - Sepsis of unknown origin - Embolic events of unknown

Question 297

What are some signs to look out for when investigating infective endocarditis (common exam question)?

Answer 297

- Hands = splinter haemorrhages, Janeway lesions, Osler's nodes - Eyes = Roth spots - Skin = embolic skin lesions, petechiae

Question 298

What are the investigations for infective endocarditis?

Answer 298

- Use Duke Criteria: Major = POSITIVE BLOOD CULTURE, endocardium involved. Minor = FEVER \> 38, predisposition, vascular phenomena (Janeway's lesions etc.), immunological lesions (Osler's nodes etc.), positive blood culture that doesn't meet major criteria. 2 major or 1 major and 2 minor or 5 minor - IN EXAM: TRANSOESOPHAGEAL ECHOCARDIOGRAM = more sensitive, uncomfortable, better at diagnosing - ECG: long PR interval, regular

Question 299

How do we treat infective endocarditis?

Answer 299

- Antibiotics: - FIRST LINE (before organism identified) = FAG: flucloxacillin, ampicillin + gentamicin - If staphylococcus: flucloxacillin, rifampicin + gentamicin - MRSA = VGR: VANCOMYCIN, GENTAMICIN + RIFAMPICIN - Not staphylococcus: benzylpenicillin and gentamycin - Treat any complications, e.g. heart failure, embolism etc. - Surgery: Replace the valve if infection can’t be treated with antibiotics. Remove and replace infected devices. Remove large vegetations at risk of embolising

Question 300

How can we try to prevent infective endocarditis?

Answer 300

Good oral health, no IV drug use, educate surgery patients on symptoms

Question 301

You are the on-call doctor for the cardiology ward, and the dental hospital sends you an urgent referral for a patient who they are treating for gum disease, who has signs of sepsis. The patient is a known intravenous drug user. 6. What diagnosis springs to mind without even seeing the patient? a. Pericarditis b. Infective endocarditis c. NSTEMI d. Rheumatic fever

Answer 301

B. Infective endocarditis

Question 302

You are the on-call doctor for the cardiology ward, and the dental hospital sends you an urgent referral for a patient who they are treating for gum disease, who has signs of sepsis. The patient is a known intravenous drug user. 7. Which of the following signs would help towards your diagnosis a. Splinter haemorrhages b. Roth spots c. Neither d. Both

Answer 302

D. Both

Question 303

You take blood cultures, which show MRSA growth. 8. What antibiotics do you use? a. Rifampicin b. Vancomycin + Rifampicin c. Erythromycin + Vancomycin d. Amoxicillin

Answer 303

B. Vancomycin + Rifampicin

Question 304

What is rheumatic fever? What is it caused by? What is its pathophysiology?

Answer 304

- Autoimmune condition common in developing countries from a Lancefield group A B-haemolytic streptococci (typically STREPTOCOCCUS PYOGENES) - It is caused by ANTIBODIES created against the streptococcus bacteria that also target tissues in the body - Type II hypersensitivity - An antibody from the cell wall cross-reacts with valve tissue which can cause permanent damage to the heart valves

Question 305

What are the symptoms and signs of rheumatic fever?

Answer 305

- Symptoms: - Fever - Arthritis - painful, tender joints - Chest pain - SOB - Fatigue - Chorea - jerky movements - Signs: - Tachycardia - Murmur - dependent on the valve - Pericardial rub - Erythema marginatum - red rash with raised edges and clear centre on trunk, thighs or arms - Prolonged PR interval

Question 306

What are the investigations for rheumatic fever?

Answer 306

- Erythrocyte sedimentation rate (ESR) and CRP - WBC count - Blood cultures - JONES criteria: recent strep. infection and 2 major or 1 major and 2 minor criteria: - Major: - Carditis: tachycardia, murmurs, pericardial rub, cardiomegaly - Arthritis: polyarthritis – usually larger joints - Erythema marginatum – red rash with raised edges and clear center - Sydenham’s chorea – unilateral/bilateral involuntary semi-purposeful movements - Minor: - Fever - Raised ESR/CRP - Arthralgia (as long as no arthritis) - Prolonged PR interval - Previous rheumatic fever

Question 307

How do we treat rheumatic fever?

Answer 307

- Best rest until CRP is normal for 2 weeks consistently - FIRST LINE: Benzylpenicillin IV, then phenoxymethylpenicillin for ten days - Analgesia - aspirin - Haloperidol/Diazepam for chorea

Question 308

Mrs S is a 56-year-old woman who comes to GP complaining of increased fatigue and palpitations. On examination, you hear a pansystolic murmur at the apex that radiates into the axilla. 10. Which pathology causes this murmur? a. Mitral stenosis b. Aortic stenosis c. Mitral regurgitation d. Aortic regurgitation

Answer 308

C. Mitral regurgitation

Question 309

When you ask about previous episodes of palpitations, Mrs S tells you that when she was around 12 and still lived in India, she did experience palpitations, fever and a rash on her torso which she thinks happened around 3 weeks after she had a sore throat. What was the likely cause of her childhood illness? a. Infective endocarditis b. Rheumatic fever c. Scarlet fever d. Hypertension

Answer 309

B. Rheumatic fever

Question 310

What are cardiomyopathies? What are the four types?

Answer 310

- A group of diseases of the myocardium that affect mechanical or electrical function - 4 types: - Hypertrophic - Dilated - Restrictive - Right ventricular arrhythmogenic

Question 311

What is dilated cardiomyopathy? What are the causes?

Answer 311

- Dilated cardiomyopathy = the left ventricle is dilated, with thin muscles, so contracts poorly - Causes: - Ischaemia - Alcohol - Thyroid disorder - Genetic

Question 312

What is the pathophysiology of dilated cardiomyopathy?

Answer 312

- Poorly generated contractile force = progressive dilation of the heart - Diffuse interstitial fibrosis - Systolic dysfunction of the left or both ventricles

Question 313

What are the symptoms and signs of dilated cardiomyopathy?

Answer 313

- Symptoms: - Shortness of breath - Fatigue - Dyspnoea - Signs: - Heart failure - Arrhythmia - Thromboembolism - Increased JVP - Sudden death

Question 314

What are the investigations for dilated cardiomyopathy?

Answer 314

- CXR = cardiac enlargement - ECG = tachycardia, arrhythmia, T-wave changes - Echocardiogram = dilated ventricles

Question 315

What is hypertrophic cardiomyopathy? What are its causes?

Answer 315

- Hypertrophic cardiomyopathy = ventricular hypertrophy, causing the obstruction of the outflow tract - Causes: - Genetic - autosomal dominant - 50% sporadic It is the commonest cause of sudden death in young people

Question 316

What is the pathophysiology of hypertrophic cardiomyopathy?

Answer 316

- Gene mutation for the sarcomere protein - Impaired diastolic filling - Reduced stroke volume - Reduced cardiac output

Question 317

What are the signs and symptoms of hypertrophic cardiomyopathy?

Answer 317

- Symptoms: - Sudden death may be the first symptom - Chest pain/angina - Dyspnoea - Dizziness - Palpitations - Syncope - Signs: - Ejection-systolic murmur - Jerky carotid pulse - Left ventricular outflow obstruction

Question 318

What are the investigations for hypertrophic cardiomyopathy?

Answer 318

- ECG: T wave inversion, deep Q waves - Genetic analysis

Question 319

How do we treat hypertrophic cardiomyopathy?

Answer 319

- Amiodarone - anti-arrhythmic - CCB - verapamil - Beta-blocker - atenolol

Question 320

What is restrictive cardiomyopathy? What are the causes?

Answer 320

- Restrictive cardiomyopathy = scar tissue replaces the normal heart muscle and the ventricles become rigid so don't contract properly - Causes: - Amyloidosis - Idiopathic - Sarcoidosis - End-myocardial fibrosis

Question 321

What is the pathophysiology of restrictive cardiomyopathy?

Answer 321

- Normal/decreased volume in both ventricles - Bi-atrial enlargement - Impaired ventricle filling - Rigid myocardium restricts ventricular filling

Question 322

What are the symptoms and signs of restrictive cardiomyopathy?

Answer 322

- Symptoms: - Dyspnoea - Fatigue - Embolic symptoms - Signs: - Increased JVP, diastolic collapse, elevated on inspiration - Hepatic enlargement - Ascites - Oedema - Third and fourth heart sounds

Question 323

What are the investigations and treatment for restrictive cardiomyopathy?

Answer 323

- Investigations = cardiac catheterisation diagnostic - Treatment = no treatment - poor prognosis

Question 324

What is right ventricular arrhythmogenic cardiomyopathy?

Answer 324

- Arrhythmogenic right ventricular cardiomyopathy is a rare familial disorder that may cause ventricular tachycardia and sudden cardiac death in young, apparently healthy individuals - Progressive loss of myocardium and its replacement by fatty tissue

Question 325

What are the 2 most common presenting complaints for right ventricular arrhythmogenic cardiomyopathy?

Answer 325

- Palpitation - Effort induced syncope

Question 326

How do we manage right ventricular arrhythmogenic cardiomyopathy?

Answer 326

- Implantable cardioverter defribrillator - Beta blockers - Cardiac ablation

Question 327

22 year old presents to the GP saying sometimes he experiences 'his heart racing' and he gets really dizzy. He sometimes gets chest pain during these episodes. His dad and grandad both died in their twenties/thirties, but he doesn't remember what from, and he is scared that he has the same condition. Which of the following differential diagnoses is the most common cause of sudden cardiac death in young people (and the most likely differential)? a. Restrictive cardiomyopathy b. Dilated cardiomyopathy c. Hypertrophic cardiomyopathy d. Pericarditis

Answer 327

C. Hypertrophic cardiomyopathy

Question 328

What is an aneurysm? What is the most common vessel aneurysm? What is the major complication of an anuerysm?

Answer 328

- Aneurysm = weakening of vessel wall followed by dilation due to increased wall stress. True and false - Abdominal Aortic Aneurysm = most common vessel aneurysm - The RUPTURE of the aneurysm is the major complication

Question 329

Describe the pathogenesis of an abdominal aortic aneurysm.

Answer 329

- Inflammation and degeneration of SMC in high-risk patients → loss of structural integrity of the aortic wall → widening of the vessel → mechanical stress (e.g., high blood pressure) acts on weakened wall tissue → dilation and rupture may occur - The aneurysmatic dilatation of the vessel wall may cause disruption of the laminar blood flow and turbulence → possible formation of thrombi in the aneurysm → peripheral thromboembolism

Question 330

What are the risk factors for an abdominal aortic aneurysm?

Answer 330

- Smoking - MAJOR - Family history - Connective tissue disorders - Marfan’s, Ehlers-Danlos - Age - Atherosclerosis - Male

Question 331

What is the clinical presentation of an abdominal aortic aneurysm?

Answer 331

- Patients with unruptured AAAs are usually asymptomatic - Cause symptoms if expanding rapidly: lower back/abdominal pain, hypotension - Usually discovered on routine examinations and imaging. Pulsatile mass on palpation if it is big; bruit on auscultation. Commonly found below the renal arteries (infrarenal)

Question 332

What are the investigations for an abdominal aortic aneurysm?

Answer 332

- 1st line: ULTRASONOGRAPHY - May consider ESR/CRP, FBC

Question 333

How do we manage abdominal aortic aneurysms?

Answer 333

- Patients presenting with a ruptured aneurysm require urgent repair - For patients with symptomatic aortic aneurysms, repair is indicated regardless of diameter - For asymptomatic AAA detected as an incidental finding, surveillance is preferred to repair until the risk of rupture is high. Repair is usually indicated when diameter exceeds 5.5 cm in men or 5.0 cm in women - All MALES at AGE 65

Question 334

What are the complications of an abdominal aortic aneurysm?

Answer 334

- Rupture of AAA = urgent surgery - Thromboembolisms - Fistula formation

Question 335

What is the clinical presentation of a ruptured abdominal aortic aneurysm? What is the treatment?

Answer 335

- Ruptured AAA is the most feared complication of AAA - Presentation: - Acute onset of severe, tearing abdominal pain with radiation to back, flank, groin - Painful pulsatile mass - Hypovolemic shock - Syncope - Nausea, vomiting - Treatment: do NOT waste time with imaging if the presentation seems clear. Treatment is URGENT SURGERY and maintaining haemodynamic stability - EVAR = Endovascular Aneurysmal Repair

Question 336

What is aortic dissection? Who does most commonly occur in? In which blood vessel do most cases occur?

Answer 336

- Aortic dissection is a tear in the intimal layer of the aorta which leads to a collection of blood between the intima and medial layers - Most often occurs in men; 40-60 - 65% of cases in the ascending aorta

Question 337

What is the pathophysiology of aortic dissection?

Answer 337

- Tear in the intimal layer → blood then passes through the media propagating distally or proximally → false lumen - As the dissection propagates, flow through the false lumen can occlude flow through branches of the aorta, including the coronary, brachiocephalic, intercostal, visceral and renal, or iliac vessels 🡪 ischaemia of supplied regions

Question 338

What are the risk factors for aortic dissection?

Answer 338

- Hypertension - most common risk factor - Trauma - Vasculitis - Cocaine use - Connective tissue disorders - cause aortic dissection in younger adults

Question 339

What are the clinical features of aortic dissection?

Answer 339

- Sudden and SEVERE TEARING PAIN in chest radiating to back - Hypotension - ASYMMETRICAL BLOOD PRESSURE - Syncope

Question 340

What are the investigations for aortic dissection?

Answer 340

- ECG - CXR - CT scanning - definitive imaging

Question 341

How do we treat aortic dissection?

Answer 341

- Maintain haemodynamic stability - fluid resuscitation, inotropes, noradrenaline - Opioid analgesia for pain control - Surgical intervention: Endovascular stent-graft repair - Put patient on antihypertensives following surgery and recovery - Type A and Type B (add to this)

Question 342

What is peripheral vascular disease? What is its pathophysiology?

Answer 342

- Peripheral vascular disease = when blood vessels (except those supplying the heart and brain) become narrowed and reduce blood flow, e.g. to arms, legs. POPLITEAL ARTERY IS MOST AFFECTED - FONTAINE CLASSIFICATION (add to this) - Pathophysiology: - Commonly atherosclerosis leading to claudication of vessels - Other (rarer) causes of claudication: aortic coarctation, temporal arteritis, Buerger’s disease

Question 343

What are the risk factors for peripheral vascular disease?

Answer 343

- Smoking - Diabetes - HTN - Sedentary lifestyle - Hyperlipidaemia - History of CAD - Age (\< 40)

Question 344

What is end stage PVD called? How does this present?

Answer 344

- End stage PVD = critical limb ischaemia - 6 P's: - Pain - Parasthesia - Pulselessness - Pallor - Paralysis - Poikilothermia

Question 345

What is the clinical presentation of peripheral vascular disease?

Answer 345

- Pain in lower limbs on exercise, relieved on rest - INTERMITTENT CLAUDICATION - Severe: unremitting pain in foot (esp. at night - HANGS FOOT OUT OF BED) - Leg may be pale, cold, loss of hair, skin changes

Question 346

What are the investigations for PVD? Explain this procedure.

Answer 346

- Ankle Brachial Pressure Index (ABPI): PAD = 0.5-0.9, critical limb ischaemia = \<0.5 - ABPI is doppler ultrasonography = measures ratio of systolic BP at ankle and in arm to provide measure of blood flow at level of ankle, should be 1 - 1st line = COLOUR DUPLEX ULTRASOUND

Question 347

How do we treat PVD?

Answer 347

- Control risk factors: - Smoking cessation - Regular exercise - Weight reduction - BP control, DM control - Statin - Antiplatelet therapy = aspirin/clopidgrel

Question 348

How do we treat critical limb ischaemia?

Answer 348

- How we treat PVD, e.g. controlling risk factors and antiplatelet therapy, PLUS: - Revascularisation, e.g. stenting, angioplasty, bypassing - Amputation if unsuitable

Question 349

What is shock? What are the different types?

Answer 349

- Shock is a life-threatening situation where the body doesn't have enough blood flow, which means cells and tissue don't receive oxygen which can lead to multiple organ failure - Different types: - Cardiogenic - Hypovolaemic - either non-haemorrhagic or haemorrhagic - Septic - Anaphylactic - Neurogenic

Question 350

What is hypovolaemic shock? Describe the two types.

Answer 350

- Hypovolaemic shock = shock induced by a low fluid volume of blood - Non-haemorrhagic = the loss of fluid volume IS NOT from bleeding, e.g sweating + dehydration. So low fluid volume = low blood volume = shock - Haemorrhagic = loss of blood volume from ruptured blood vessels. EDV decreases, so stroke volume decreases, so CO decreases, so blood pressure decreases

Question 351

What are the causes of hypovolaemic shock? What is its pathophysiology?

Answer 351

- Causes: - Low fluid volume - Haemorrhage - Dehydration - Pathophysiology = decreased CO and decreased MAP

Question 352

What is the presentation of hypovolaemic shock?

Answer 352

- Tachypnoea - Weak rapid pulse - Cyanosis - Increased capillary refill time

Question 353

How do we treat hypovolaemic shock?

Answer 353

- ABCDE - Resuscitation (includes CPR, fluids, oxygen) - Fluids - Vasodilators (GTN spray)

Question 354

What is cardiogenic shock? What are its causes? What is its pathophysiology?

Answer 354

- Where there is trauma or obstruction to the heart, therefore it cannot pump enough blood to the body's tissues, e.g. due to myocardial infarction or pericarditis - Causes: pump failure, MI, cardiac arrest - Pathophysiology = decreased CO, decreased MAP

Question 355

What is the presentation of cardiogenic shock?

Answer 355

- Tachycardia + tachypnoea - Decreased urinary output and BP - Cold peripheries - Chest pain

Question 356

How do we treat cardiogenic shock?

Answer 356

- ABCDE - Resuscitation

Question 357

What is septic shock? What are its causes? What is its pathophysiology? How do we treat it?

Answer 357

- Septic shock = when blood pressure drops to a low level after infection - Causes: bacterial toxins - Pathophysiology: blood vessels dilate + increased permeability due to toxins = decreased SVR = decreased BP - BUFALO: blood culture, urine output, fluids, antibiotics, lactate, oxygen

Question 358

What is the presentation of septic shock? How do we treat it?

Answer 358

- Presentation: - Tachycardia - D+V - Decreased UO, O2 and BP - Treatment: - Broad spectrum IV antibiotics - Fluid, O2

Question 359

What is anaphylactic shock? What are its causes? What is its pathophysiology?

Answer 359

- Anaphylactic shock = severe allergic reaction - Causes = bee stings, food allergies, drug allergies, IV contrast - Pathophysiology = histamine release causes vasodilation + increases permeability, therefore fluid can leak out + BP decreases (also there is less oxygent to tissues/organs = ischaemic = necrotic = failure), hypoxia due to bronchoconstriction

Question 360

What is the presentation of anaphylactic shock?

Answer 360

Skin rash, N+V, and a rapid, weak pulse

Question 361

How do we treat an anaphylactic shock?

Answer 361

- Resuscitation - Adrenaline to constrict the blood vessels to retain BP - Anti-histamines to block histamine receptors

Question 362

What are the main causes of neurogenic shock?

Answer 362

- Acute spinal cord injury - Regional anaesthesia

Question 363

What is the clinical presentation of neurogenic shock?

Answer 363

- Unopposed vagal tone causes: - Bradycardia - Vasodilation = decreased SVR = decreased BP = ischaemia, necrosis etc.

Question 364

What is the treatment for neurogenic shock?

Answer 364

- Vasopressors, e.g. dobutamine, epinephrine - IV fluids to stabilise blood volume

Question 365

What is a deep vein thrombosis? What are its risk factors? What are its causes? What is its pathophysiology?

Answer 365

- Deep vein thrombosis = blood clot (thrombus) in the deep veins, usually in the lower leg - Risk factors = smoking, obesity, sitting for long periods of time, prolonged bed rest, injury or surgery - Causes = Virchow's triad: reduced blood flow, blood vessel injury, increased coagulability - Pathophysiology = endothelium damaged = vasoconstriction + platelets adhere = activated by tissue factor + collagen = recruit more + form platelet plug. Coagulation cascade starts when a clotting factor gets proteolytically cleaved, which then causes this clotting factor to proteolytically cleave the next clotting factor. Fibrinogen then gets activated to fibrin, which deposits and polymerises to form a mesh around the platelet plug

Question 366

What are the signs and symptoms of DVT?

Answer 366

- Often asymptomatic - Swelling in the affected leg - Pain in the leg - Red or discoloured skin on the leg - Warmth in the leg - Prominent superficial veins - Unilateral - Positive Wells score, e.g. HR \> 100, haemoptysis

Question 367

What are the investigations for DVT?

Answer 367

- Wells score - \> 2 points = proximal leg USS, \< 2 points = D-dimer - Quantitative D-dimer level - positive D-dimer is not diagnostic (can be positive in cancer, pregnancy, and post-operatively), but a negative D-dimer exclude DVT - Venous ultrasound - Doppler ultrasound - FBC - Urea and creatine - CT/MRI venography

Question 368

How do we treat DVT?

Answer 368

- Anticoagulant (LMWH) if suspected - If diagnosed, anticoagulants (warfarin, rivaroxaban) for 3 months min. - target INR of 2.5 - DOAC - apixaban (note: not with warfarin) - Compression stockings - Inferior Vena Cava Filter Placement - prevents PE

Question 369

What is the major complication of DVT? Explain how this occurs.

Answer 369

Pulmonary embolism - thrombus travels back to heart through vena cava, right atrium, right ventricle, and gets stuck in the pulmonary artery

Question 370

What does a pulmonary embolism usually arise from? What are its rarer causes? What are the risk factors?

Answer 370

- Commonly arises from DVT - Rare causes include sepsis, parasites, fat embolism, neoplastic cells - Risks include: recent surgery, hip/knee replacement, immobility, malignancy, pregnancy, combined contraceptive pill, HRT

Question 371

What are the signs and symptoms of a pulmonary embolism?

Answer 371

- ACUTE ONSET SHORTNESS OF BREATH - Unilateral pleuritic chest pain - Leaning forward to breathe - Tachycardia - Tachypnoea - Haemodynamic instability - pallor, hypotension, shock, collapse - Haemoptysis - Signs of concurrent DVT

Question 372

What are the investigations for a pulmonary embolism?

Answer 372

- COMPUTED TOMOGRAPHIC PULMONARY ANGIOGRAPHY (CPTA)! If Wells score \>4 then immediate CPTA, \<4 = D-dimer - Echocardiography - D-dimer - FBC - ABG - CXR and ECG - look for alternate causes

Question 373

What is the treatment for a pulmonary embolism?

Answer 373

- If PE suspected but unable to investigate, start anticoagulation: APIXABAN (DOAC) or RIVAROXABAN or LMWH - If delay on CTPA give LMWH, e.g. Delteparin - Patient presenting with hypotension and raised JVP = acutely unwell. Offer O2 if \<90%, continuous UNFRACTIONATED HEPARIN and THROMBOLYSIS - senior decision - ALTEPLASE, consider IV fluids - Surgical pulmonary embolectomy - Major complications can occur in pregnant women

Question 374

How does warfarin work? What is warfarin the antagonist of? Why is warfarin difficult to use?

Answer 374

- It produces NON-functional clotting factors 2, 7, 9 and 10 - Vitamin K - Lots of interactions, teratogenic, needs almost constant monitoring

Question 375

What are the main clinical indications of ACE inhibitors? Give some examples of ACE inhibitors.

Answer 375

- Hypertension - Heart failure - Diabetic nephropathy - Examples: ramipril, enalapril, perindopril, trandalopril

Question 376

What are the main side effects of ACE inhibitors?

Answer 376

1. Related to reduced angiotensin II formation a. Hypotension b. Acute renal failure c. Hyperkalaemia d. Teratogenic effects in pregnancy 2. Related to increased kinin production a. Cough b. Rash c. Anaphylactoid reactions

Question 377

What are the main clinical indications of Angiotensin II Receptor Blockers (ARBs)? Give some examples.

Answer 377

- Hypertension - Diabetic nephropathy - Heart failure (when ACE-I contraindicated) - Examples: candesartan, valsartan, losartan, irbesartan, telmisartan

Question 378

What are the main adverse effects of ARBs?

Answer 378

- Symptomatic hypotension (especially volume deplete patients) - Hyperkalaemia - Potential for renal dysfunction - Rash - Angio-oedema

Question 379

What are the main clinical indications of CCBs? Give some examples.

Answer 379

- Hypertension - Ischaemic heart disease (IHD) – angina - Arrhythmia (tachycardia) - Examples: amlodipine, felodipine, lacidipine

Question 380

What are the adverse effects of CCBs?

Answer 380

1. Due to peripheral vasodilatation (mainly dihydropyridines): - Flushing - Headache - Oedema - Palpitations 2. Due to negatively chronotropic effects (mainly verapamil/diltiazem) - Bradycardia - Atrioventricular block 3. Due to negatively inotropic effects (mainly verapamil) - Worsening of cardiac failure 4. Verapamil causes constipation

Question 381

What are the main clinical indications of beta-adrenoreceptor blockers?

Answer 381

- Ischaemic heart disease (IHD) – angina - Heart failure - Arrhythmia - Hypertension - Examples: bisoprolol, atenolol, propanolol

Question 382

What are the main adverse effects of beta blockers?

Answer 382

- Fatigue - Headache - Sleep disturbance/nightmares - Bradycardia - Hypotension - Cold peripheries - Erectile dysfunction

Question 383

What are the main clinical indications of diuretics? What are the four main classes?

Answer 383

- Hypertension - Heart failure - Examples: thiazides and related drugs (distal tubule), loop diuretics (loop of Henle, potassium-sparing diuretics, aldosterone antagonists

Question 384

Give examples of these different classes of diuretics: a) Thiazide and related diuretics b) Loop diuretics c) Potassium-sparing diuretics

Answer 384

a) bendroflumethiazide, hydrochlorothiazide b) furosemide, bumetanide c) spironolactone, amiloride

Question 385

What are the main adverse effects of diuretics?

Answer 385

- Hypovolaemia (mainly loop diuretics) - Hypotension ( “ ) - Hypokalaemia - Hyponatraemia - Hypomagnesaemia - Hypocalcaemia - Hyperuricaemia - gout - Erectile dysfunction (mainly thiazides) - Impaired glucose tolerance ( " )

Question 386

What is the most commonly involved coronary artery in MI? A. RCA B. LAD C. LCA D. PDA

Answer 386

C

Question 387

What is the key complication in the first 24h of an MI? A. Fibrinous pericarditis B. Coronary artery spasm C. Arrhythmia D. Mitral Insufficiency

Answer 387

C

Question 388

48 y.o. woman diagnosed with hypertension. She presents to you with a dry cough that is not getting better despite taking antibiotics. Which medication could be causing her symptoms? A. Amlodipine B. Lisinopril C. Bendroflumethiazide D. Mitral Insufficiency

Answer 388

B

Question 389

45 year old female patient came into the clinic with acute chest pain that is relieved by leaning forward. What is the gold standard investigation? A. ECG B. Chest X-ray C. Echocardiogram D. Blood culture

Answer 389

C

Question 390

A woman presented with dyspnoea, malar flush and new atrial fibrillation. What murmur should you expect from this lady? A. Rumbling mid diastolic murmur with opening snap B. Pansystolic murmur radiating to axilla C. Ejection systolic murmur D. Early diastolic murmur

Answer 390

A

Question 391

Lidocaine is effective in the treatment of ventricular tachycardias because it: ## Footnote 1. Slows conduction in healthy heart tissue 2. Opens sodium channels 3. Blocks sodium channels at rest 4. Blocks the activation gate of the sodium channel 5. Blocks the inactivation gate of the sodium channel

Answer 391

5. Blocks the inactivation gate of the sodium channel

Question 392

Digoxin can be a useful drug in the treatment of supraventricular tachycardias because it: ## Footnote 1. Stimulates the release of acetylcholine from sympathetic nerves 2. Is inotropic 3. Makes the membrane potential more positive releasing acetylcholine from parasympathetic nerves 4. Inhibits calcium channels 5. Stimulates sodium/calcium exchange

Answer 392

3. Makes the membrane potential more positive releasing acetylcholine from parasympathetic nerves

Question 393

Amlodipine and verapamil are both calcium channel blockers, what property makes verapamil the more effective anti-arrhythmic agent? ## Footnote 1. Additional sodium channel blockade 2. Once daily treatment 3. Lack of effect on the calcium channel at rest 4. Blockade of all calcium channel types (L, N & T) 5. Additional potassium channel blockade

Answer 393

3. Lack of effect on the calcium channel at rest

Question 394

Which additional property makes propranolol the most useful beta blocker to help control the arrhythmias which occur immediately following a heart attack? ## Footnote 1. Calcium channel block 2. Potassium channel block 3. Heart block 4. Sodium channel block 5. Parasympathetic activation

Answer 394

4. Sodium channel block

Question 395

In the treatment of heart failure, which transport protein or ion channel is inhibited by the loop diuretic, furosemide? ## Footnote 1. Na/K ATP-ase 2. Epithelial Na channel 3. K channel 4. Na/K/2Cl transporter 5. Na/Cl transporter

Answer 395

4. Na/K/2Cl transporter

Question 396

ACE inhibitors reduce the circulating levels of which adrenal hormone? ## Footnote 1. Aldosterone 2. Adrenaline 3. Cortisone 4. Angiotensin II 5. Atrial Natriuretic Peptide

Answer 396

1. Aldosterone

Question 397

Which drug exerts a direct inotropic effect (+ force of contraction) on heart muscle? ## Footnote 1. Ramipril 2. Furosemide 3. Losartan 4. Digoxin 5. Spironolactone 6. Glyceryl Trinitrate

Answer 397

4. Digoxin

Question 398

In chronic heart failure beta blockers are: ## Footnote 1. Contra-indicated 2. Beneficial by slowing the heart rate 3. Beneficial by depressing the myocardium 4. Beneficial by increasing oxygen demand 5. Effective by blocking reflex sympathetic responses which stress the failing heart

Answer 398

5. Effective by blocking reflex sympathetic responses which stress the failing heart

Question 399

For which CVS drug is BRONCHOSPASM a potential side effect? ## Footnote 1. Morphine 2. Beta blocker 3. Calcium Antagonist 4. Aspirin 5. Nitrate 6. ACE inhibitor

Answer 399

2. Beta blocker

Question 400

For which CVS drug is COUGH a potential side effect? ## Footnote 1. Morphine 2. Beta Blockers 3. Calcium antagonists 4. Aspirin 5. Nitrates 6. ACE inhibitors

Answer 400

6. ACE inhibitors

Question 401

For which CVS drug is TOLERANCE a potential side effect? ## Footnote 1. Bendroflumethazide 2. Beta blockers 3. Calcium antagonist 4. Aspirin 5. Nitrate 6. ACE inhibitor

Answer 401

5. Nitrate

Question 402

Which CVS drug is most likely to induce POSTURAL HYPOTENSION as a potential side effect? ## Footnote 1. Morphine 2. Beta blocker 3. Calcium antagonist 4. Aspirin 5. Nitrate 6. ACE inhibitor

Answer 402

3. Calcium antagonist

Question 403

Doxazosin is an antagonist at which type of peripheral receptor? ## Footnote 1. Alpha-1 adrenoceptor 2. Purine receptor 3. Angiotensin II receptor 4. Vasopressin receptor 5. Beta-1 adrenoceptor 6. Dopamine receptor

Answer 403

1. Alpha-1 adrenoreceptor

Question 404

Atenolol is an antagonist at which type of peripheral receptor? ## Footnote 1. Alpha-1 adrenoceptor 2. Purine receptor 3. Angiotensin II receptor 4. Vasopressin receptor 5. Beta-1 adrenoceptor 6. Dopamine receptor

Answer 404

5. Beta-1 adrenoreceptor

Question 405

The antihypertensive action of lisinopril is due to inhibition of which peripheral enzyme? ## Footnote 1. Kininase II 2. Renin 3. Na/K ATP-ase 4. Angiotensin Converting Enzyme (ACE) 5. DOPA decarboxylase

Answer 405

4. Angiotensin Converting Enzyme (ACE)

Question 406

Which of the following drug side effects is less likely to be seen when treating hypertension with an angiotensin receptor blocker (ARB) rather than an ACE inhibitor? ## Footnote 1. Hyperkalaemia 2. Cough 3. Angioedema 4. Renal failure in the presence bilateral renal stenosis 5. Cold hands/cold feet

Answer 406

2. Cough

Question 407

How do beta-blockers work to relieve the pain from angina pectoris? ## Footnote 1. Reduce O2 demand by slowing the heart rate 2. Reduce O2 demand by reducing myocardial contractility 3. Improve O2 distribution by slowing the heart rate 4. Increase O2 supply by dilating coronary arteries 5. Increase O2 supply by stimulating respiration

Answer 407

1. Reduce O2 demand by slowing the heart rate 2. Reduce O2 demand by reducing myocardial contractility 3. Improve O2 distribution by slowing the heart rate

Question 408

What is the major mechanism by which glyceryl trinitrate can relieve the pain of angina pectoris? ## Footnote 1. Dilatation of veins to reduce the preload on the heart 2. Dilatation of arterioles to reduce the after load on the heart 3. Dilatation of coronary arteries to increase cardiac perfusion 4. Opening of collateral blood vessels to improve cardiac perfusion 5. A positive inotropic effect

Answer 408

1. Dilatation of veins to reduce the preload on the heart

Question 409

Which of the following drugs is likely to be more suitable for the treatment of variant angina due to coronary artery vasospasm? ## Footnote 1. Bumetanide 2. Losartan 3. Isosorbide 4. Amlodipine 5. Glyceryl trintrate

Answer 409

4. Amlodipine

Question 410

Which of the following drugs might be used to reduce atheromatous disease, the underlying cause of angina pectoris? ## Footnote 1. Atenolol 2. Amlodipine 3. Simvastatin 4. Glyceryl trinitrate 5. Enalapril

Answer 410

3. Simvastatin

Question 411

Answer 411

D. Increase heart rate

Question 412

Answer 412

C. Crista terminalis

Question 413

Answer 413

C. Digoxin

Question 414

Answer 414

E. T wave

Question 415

Answer 415

C. Isovolumetric relaxation

Question 416

Answer 416

D. Pericarditis

Question 417

Answer 417

C. Increase cGMP

Question 418

Answer 418

A. Connection between two atria to bypass the pulmonary circulation and foetal lungs

Question 419

Answer 419

D. Left anterior descending (LAD)

Question 420

Answer 420

B. Papillary muscles and/or chordae tendinae

Question 421

Answer 421

B. Vasomotor centre inhibition

Question 422

Answer 422

C. Right coronary

Question 423

Answer 423

B. Morphine, Oxygen, Aspirin 300mg, GTN spray

Question 424

Answer 424

C. 2nd degree AV block (Mobitz Type I)

Answer 425

D. Amlodipine

Question 426

Answer 426

E. All of the above

Question 427

Answer 427

E. Atrial fibrillation

Question 428

Answer 428

B. Can be safely administered with macrolide antibiotics

Question 429

Answer 429

C. Infective endocarditis

Question 430

Answer 430

E. Aortic dissection

Question 431

Complete this table.

Answer 431

Question 432

A 75 year-old male presents with swelling in both of his ankles, a NT-proBNP test comes back raised. What treatment is not indicated in his treatment? A. Ramipril B. Furosemide C. Verapamil D. Carvedilol E. Spironolactone

Answer 432

C. Verapamil

Question 433

What drug should be given for hypertension? a) A 54-year-old Black African male: b) A 75-year-old White female with T2DM: c) A 62-year-old African Caribbean female already being treated with amlodipine and ramipril:

Answer 433

a) A 54-year-old Black African male: amlodipine b) A 75-year-old White female with T2DM: ramipril c) A 62-year-old African Caribbean female already being treated with amlodipine and ramipril: hydrochlorothiazide

Question 434

Which of these is not an effect of ramipril? A. Dilation of vasculature B. Reduction in sympathetic activity C. Renal excretion of Na+ and H2O D. Bradykinin metabolism inhibition E. Exacerbation of hypertension

Answer 434

E. Exacerbation of hypertension

Question 435

Answer 435

C

Question 436

Answer 436

D

Question 437

Answer 437

E

Question 438

Answer 438

C. Hilar haziness is alluding to pleural effusions

Question 439

Answer 439

B

Question 440

Answer 440

B

Question 441

Answer 441

E

Question 442

William is a 54 y.o gentleman presenting to the GP with recurrent chest pain. The pain is intermittent and seems to come more often at night. He describes the pain to be a tightness over his chest. He also has shortness of breath. William has GORD, hypertension and high cholesterol levels. He has a pack history of 20 years. ECG shows ST segment elevation. There is no increase in Troponin. Based on the history, which is the most likely diagnosis? A. Stable angina B. Unstable angina C. Myocardial infarction D. Variant angina E. GORD

Answer 442

D. Variant angina (Prinzmetal's angina)

Question 443

A 23 y.o university student had a sudden loss of consciousness while playing football with his mates. Fortunately, CPR was administered in time and he was saved. A medical student was around and quickly did an examination and found the presence of an ejection systolic murmur. The murmur increases with intensity when standing from a supine position and disappears on squatting. No past medical history. Family history is significant for a brother who died suddenly in his 20s. Based on the above history, what is the underlying cause? A. Aortic stenosis B. Hypertrophic cardiomyopathy C. Acute heart failure D. Vasovagal syncope E. Cardiogenic shock

Answer 443

B. Hypertrophic cardiomyopathy

Question 444

Matthew is a 45 y.o. man coming into the GP for a routine check-up. He denies any past medical history but his blood pressure is raised. He has a 20-pack year history. His has a family history of heart disease for which his dad had an MI at the age of 56. Physical examination is notable for obesity and blood pressure of 150/100mmHg. As the GP, you started him on some medications for hypertension. However 2 weeks later, he starts complaining of swelling in his lower limbs. Which drug is the most likely cause for his problem? A. Amlodipine B. Digoxin C. Enalapril D. Losartan E. Spironolactone

Answer 444

A. Amlodipine

Question 445

A 56 y.o. man presents to the A&E with chest tightness and breathlessness. His symptoms came on 1 hour ago and has not stopped at all. He has an irregularly irregular pulse between 90-110 bpm. He has a past medical history of hypertension and high cholesterol levels. His obs are Temp: 37.00c, RR: 31, PR: 90-110, BP: 80/65mmHg and 02: 96% ECG shows absent p-waves and an irregularly irregular rhythm. Based on the history above, what would your next step in management be? A. Give Flecainide B. Anticoagulate and DC cardioversion C. Anticoagulate and give bisoprolol D. Give amiodarone E. Digoxin and DC cardioversion

Answer 445

B. Anticoagulate and DC cardioversion

Question 446

Alex is brought into the A&E with chest pain. He describes the pain to be crushing in nature and it radiates to his left arm. An ECG revealed ST-segment elevation and raised Troponins. He was treated for myocardial infarction. He was later given several medications for secondary prevention. What is the mechanism of action of aspirin? A. Non-selective inhibitors of COX1 enzymes B. Irreversibly binds to P2Y12 receptors C. Reversibly binds to Factor Xa D. Inhibit HMG CoA reductase E. Irreversibly binds to GP IIb/IIIa receptor sites

Answer 446

A. Non-selective inhibitors of COX-1 enzymes

Question 447

A 30 y.o gentleman comes into the A&E with severe chest pain. He describes himself gardening an hour ago when the pain suddenly came on. Nothing like that has ever happened and he is worried about a heart attack. He has a past medical history of hypertension. Family history is significant for MI of his father at 59 and more cardiovascular events. O/E: Tall and long fingers, sunken chest, high-arched palate, radial-radial delay Based on the above, what is the most likely diagnosis? A. Abdominal aortic aneurysm B. Aortic dissection C. ST-elevation myocardial infarction D. Pulmonary embolism E. Pericarditis

Answer 447

B. Aortic dissection

Question 448

Malcolm is a 76 y.o. gentleman presenting to the A&E with difficulty breathing and chest pain. It came on gradually an hour ago and it is a lot more severe now. The pain is constant and not associated with movement. He has a 50-pack year history. He has lung cancer for which he is on chemo and immunotherapy. His obs are Temp: 37.1oc, RR: 19, PR: 98, BP: 88/65 mmHg and O2: 98%. O/E: Elevated JVP, muffled heart sounds, pulsus paradoxus Based on the most likely diagnosis, what would be the definitive management for this presentation? A. Percutaneous coronary intervention B. Surgical drainage C. Pericardiocentesis D. Colchicine E. Pericardiectomy

Answer 448

B. Surgical drainage

Question 449

Martha is a 73 y.o. woman presenting at the A&E with light headedness, dizziness and sweaty and clammy skin. She looks very pale. She has a history of HF and previous MI. Her BP is 103/66 and RR of 27. She is afebrile (no fever). She has had no recent trauma. Bloods show no signs of anemia. What is the most probable diagnosis? A: Septic Shock B: Hypovolemic Shock C: Cardiogenic Shock D: Neurogenic Shock E: Anaphylactic Shock

Answer 449

C. Cardiogenic shock

Question 450

Joe is a 57 y.o man with BP of 162/88. He has been diagnosed with essential hypertension. He does not like taking Ramipril because of the cough that it gives. What is the best first line drug that he should take for his hypertension? A: Losartan B: Furosemide C: Lisinopril D: Spironolactone E: Amlodipine

Answer 450

E. Amlodipine

Question 451

Mary is a 28 y.o woman of Caucasian heritage. She is 26 weeks pregnant and has been diagnosed with hypertension. Which of these drugs should she NOT take no matter what? 1: Losartan 2: Ramipril 3: Spironolactone 4: Amlodipine 5: Bendroflumethiazide A. 1 and 4 B. 1 and 2 C. 2 D. 2, 3, 4 and 5 E. 1, 2, and 3

Answer 451

B. 1 and 2

Question 452

Michael is a 23 y.o man presenting with pain in the loin when urinating, foul-smelling urine and a fever of 38 degrees Celsius. He also pees with increased frequency and nocturia. While admitted, his fever has gotten much worse to 39 degrees Celsius. His HR is 115, BP of 101/63 and RR of 29. He looks very weak, pale, and clammy. He is barely conscious. What is the appropriate management? 1. Give oxygen 2. Measure urine 3. Give fluids 4. Give IV antibiotics 5. Take blood cultures 6. Measure lactate levels A. 1,3,5,4,2,6 B. 1,5,4,3,2,6 C. 3, 1, 5, 4, 2, 6 D. 1, 3, 4, 5, 2, 6 E. 1, 2, 3, 5, 4, 6

Answer 452

B. 1, 5, 4, 3, 2, 6

Question 453

A 67 y.o. African American man comes to the hospital presenting with dizziness, fatigue and SOB. He feels especially dizzy when suddenly standing up. He has recently acquired a clear productive cough. He has no peripheral swelling. A systolic murmur is heard. What is the most likely diagnosis? A. Mitral stenosis B. Tricuspid Regurgitation C. Pulmonary Stenosis D. Aortic Regurgitation E. Aortic stenosis

Answer 453

E. Aortic stenosis

Question 454

A 67 y.o. African American man comes to the hospital presenting with dizziness, fatigue and SOB. He feels especially dizzy when suddenly standing up. He has recently acquired a clear productive cough. He has no peripheral swelling. A systolic murmur is heard. What is the most likely cause of his diagnosis? A. Calcified aortic valve B. Congenital bicuspid aortic valve C. Myxomatous degeneration D. Endocarditis E. Rheumatic fever

Answer 454

A. Calcified aortic valve

Question 455

Man presents to A+E with sudden shortness of breath, chest pain and hemoptysis. He has felt very weak and has muscle aches for the last couple of days. He has a on examination a systolic murmur at T5 mid-clavicular is found. He has a T of 38, RR of 23, HR of 94 and BP of 112/81. He is determined to have a cardiological cause for his symptoms. A. What is the likely diagnosis? B. What are the gold standard diagnostic investigations need to be done to definitely diagnose this illness?

Answer 455

A. Endocarditis B. 2 separate blood cultures with positive IE microorganisms or 3 positive blood cultures 12 hours apart Echocardiogram positive for IE

Question 456

Patient arrives at A+E with severe dyspnoea and raised jugular vein at each inspiration. He has crushing chest pain that radiates to the the trapezius. He was better when he was sitting and standing but got worse when he was laid onto the bed, he got worse. He has had chills the last few days and is presenting with a fever. On examination his heart sounds are present but muffled. His T is 38.3, HR is 112, RR 26 and BP 106/71. What is the gold standard diagnostic investigation for this illness? A. Blood cultures B. CXR C. ECG D. Echocardiogram E. FBC

Answer 456

C. ECG

Question 457

A 27 y.o. homeless man arrives at A+E with a fever and light headedness. He has been extremely fatigued the last few days and have been lying on the ground the whole time. He has no cough and no headache. On examination, the patient was in extreme pain when his fingers were palpated. There were lesions on his palm and black spots throughout his arm. His teeth were mostly rotten and smelled very bad. He has no history of drug use. What bacteria is the most likely cause of his illness? A. Pseudomonas Aeruginosa B. Strep. Pneuminae C. Strep. Viridans D. Haemophilus Influenza E. Staph Aureus

Answer 457

C. Strep. viridans

Question 458

Josh, a 27 y.o man comes into the clinic. He seems perfectly fine but explains that sometimes he gets headaches, nose bleeds and vision gets a bit blurry. He complains that both his legs usually feel very cold and look pale. His HR is 74, RR 16, and BP was 162/96. What is a likely differential? A. Aortic Regurgitation B. TIA C. Acute limb ischaemia D. Coarction of Aorta E. LVH failure

Answer 458

D. Coarctation of aorta

Question 459

Answer 459

d) Saddle-shaped ST segment

Question 460

Answer 460

d) PR \> 200ms

Question 461

Answer 461

a) Ramipril (ACEi) - this question tricks you because they are Afro-Caribbean (so think amlodipine), but they have T2DM!

Question 462

Answer 462

e) Verapamil (CCB)

Question 463

Answer 463

b) 2nd degree heart block - Mobitz I

Question 464

Answer 464

c) ABPI and duplex ultrasound scan

Question 465

Answer 465

e) Troponin

Question 466

Answer 466

b) Cardioversion with adenosine

Question 467

Answer 467

a) Hyperkalaemia

Question 468

Answer 468

a) Tall tented T-waves

Question 469

Answer 469

d) Blood culture. Infective endocarditis

Question 470

Answer 470

a) Viridans streptococci

Question 471

Answer 471

a) CT angiography. Aortic dissection

Question 472

Answer 472

b) Torsades de pointes

Question 473

Answer 473

e) Right bundle branch block (RBBB). R wave resembles an 'M', slurred S wave represents a 'W'

Question 474

Answer 474

d) Pulmonary embolism

Question 475

Answer 475

c) Ventricular septal defect

Question 476

Answer 476

b) Streptococcus pyogenes

Question 477

Answer 477

c. Metoprolol

Question 478

Answer 478

B. Aortic stenosis

Question 479

Answer 479

D) Atenolol

Question 480

Answer 480

d. Right coronary

Question 481

Answer 481

d. Left ventricular hypertrophy

Question 482

Answer 482

B. Furosemide

Question 483

Answer 483

d) Send directly to A+E

Question 484

Answer 484

b) Factor Xa

Question 485

Answer 485

E. Catheter ablation

Question 486

Answer 486

a) Postural hypotension secondary to medications

Question 487

Answer 487

d) Drug/alcohol use

Question 488

Answer 488

c) Diastolic ventricular dysfunction

Question 489

Answer 489

Question 490

Answer 490

Question 491

Answer 491

Question 492

Answer 492

Question 493

Answer 493