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Phase 2a > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Where do atherosclerotic plaques occur?

A

Peripheral and Coronary arteries.

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2
Q

How are atherosclerotic plaques distributed?

A

Focally distributed - governed by haemodynamic factors (eg. changes in flow or turbulence)

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3
Q

What is neointima?

A

Changes in blood flow altering the phenotype of endothelial cells.

Altered gene expression in endothelial cells, smooth muscle cells, macrophages, and fibroblasts.

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4
Q

What makes up the structure of an atherosclerotic plaque?

A
  • Lipid
  • Necrotic core
  • Connective tissue
  • Fibrous cap
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5
Q

Describe the progression of atherosclerosis.

A
  1. Fatty streak
  2. Intermediate lesions
  3. Fibrous plaques
  4. Plaque rupture
  5. Plaque erosion
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6
Q

Describe the first stage of atherosclerosis - Fatty streak.

A
  • Earliest lesion of atherosclerosis - <10 years
  • Aggregations of lipid-laden macrophages and T lymphocytes within the tunica intima
  • Scavenger receptors take up lipids
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7
Q

Describe the second stage of atherosclerosis - Intermediate lesions.

A
  1. Lesion progresses to comprise layers of:
    - Foam cells (Lipid-laden macrophages)
    - Vascular smooth muscle cells
    - T lymphocytes
    - Adhesion and aggregation of platelets to vessel wall
    - Isolated pools of extracellular lipid
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8
Q

Describe the third stage of atherosclerosis - Fibrous plaques.

A
  • Contains SMCs, macrophages, foam cells, and T-lymphocytes
  • Covered by dense fibrous caps made of ECM proteins including collagen and elastin
  • Impedes blood flow and prone to rupture
  • Often calcified
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9
Q

Describe the fourth stage of atherosclerosis - Plaque rupture.

A
  • Plaque is constantly growing and receding
  • In increased inflammatory conditions the fibrous cap becomes weak and plaque ruptures
  • Exposure of basement membrane, collagen, necrotic tissue and haemorrhage of vessels causes thrombus formation
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10
Q

What is atherosclerosis?

A

An inflammatory process characterised by hardened plaques within the intima of a vessel wall.

Eventually, plaque will either occlude the vessel lumen (restricting blood flow) or rupture (thrombus formation).

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11
Q

Describe the fifth stage of atherosclerosis - Plaque erosion.

A
  • Small early lesions
  • Fibrous cap does not disrupt
  • Luminal surface underneath the clot has less endothelium but more smooth muscle
  • Prominent lipid core
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12
Q

What is Percutaneous Coronary Intervention?

A

A non-surgical procedure that uses a catheter to place a stent into a narrowed blood vessel.

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13
Q

What is Restenosis?

A

The recurrence of abnormal narrowing of an artery or valve after corrective therapy.

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14
Q

What drugs are used to reduce restenosis in patients who have undergone corrective surgery?

A

Taxol and Sirolimus.

These work by reducing SMC proliferation after placement of stent.

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15
Q

How does Aspirin help to treat CHD?

A

It’s an irreversible inhibitor of platelet cyclo-oxygenase.

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16
Q

How does Clopidogrel/Ticagrelor help to treat CHD?

A

They are inhibitors of the stimulatory P2Y12 ADO receptor on platelets.

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17
Q

How do Statins help to treat CHD?

A

Inhibit HMG CoA reductase - reduces cholesterol synthesis.

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18
Q

What inflammation-causing cytokine is targeted using drugs alongside statin therapy?

A

IL-1

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19
Q

What drug therapy is used as an alternative to statins if ineffective or not tolerated?

A

PCSK9 inhibitors.

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20
Q

What are acute coronary syndromes?

A

A spectrum of acute cardiac conditions ranging from unstable angina to varying degrees of MI.

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21
Q

What are the most common causes of Acute Coronary Syndromes?

A

Atherosclerotic rupture and consequential arterial thrombosis.

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22
Q

Name some less common causes of Acute Coronary Syndromes?

A
  • Coronary vasospasm without plaque rupture
  • Drug abuse (amphetamines and cocaine)
  • Spontaneous Coronary Artery Dissection
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23
Q

What is Cardiac Troponin?

A

A protein complex functioning to regulate actin and myosin contraction.

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24
Q

Why is Cardiac Troponin relevant in diagnosing Acute Coronary Syndromes?

A
  • Highly sensitive marker for cardiac muscle injury
  • Not specific for ACS (also increases in conditions that cause stress in myocardium such as PE, sepsis etc)
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25
Q

What is Primary Percutaneous Coronary Intervention (PPCI)?

A
  • Reperfusion injury can occur as a result of opening up the blocked vessel
  • Drug-eluting stent can reduce restenosis
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26
Q

What is the clinical classification of unstable angina?

A
  • Cardiac chest pain at rest or during minimal exertion
  • Severe and of new onset cardiac chest pain
  • Cardiac chest pain with crescendo pattern
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27
Q

How is unstable angina diagnosed?

A
  • History
  • ECG (may present as ST-segment depression, transient ST-elevation, or T-wave inversion)
  • No elevation in troponin = unstable angina not associated with damage to the heart
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28
Q

What are the characteristics of the chest pain associated with myocardial infarction?

A
  • Occurs at rest
  • Unremitting
  • Usually severe, can be mild or absent (silent MI)
  • Associated with autonomic symptoms eg. sweating, breathlessness, nausea and vomiting
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29
Q

What risk factors are associated with MI?

A
  • Old age
  • Diabetes
  • Renal failure
  • Left Ventricular Systolic Dysfunction (LVSD)
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30
Q

What is the process of initial management of MI by ambulance staff?

A
  • If paramedics see presentation of ST-elevation, immediately sent for PPCI
  • Aspirin (300mg) in the ambulance
  • Morphine - reduces pain and myocardial oxygen demand
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31
Q

What is involved in hospital management of MI after diagnosis?

A
  • Bed rest
  • Oxygen therapy (if hypoxic)
  • Pain relief
  • Aspirin (+ P2Y12 inhibitor)
  • Beta-blocker (antianginal therapy)
  • Urgent Percutaneous Coronary Intervention
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32
Q

Name some of the functions of platelets during arterial thrombosis.

A
  • Procoagulant activity (release of thrombin)
  • Dense granule secretion (platelet activation)
  • Alpha granule secretion (coagulation and inflammation)
  • Platelet-fibrin clot
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33
Q

What is the process by which platelets prevent further rupture?

A
  1. Shear flow
  2. Initial adhesion GPIb/VWF
  3. Rolling GPIb/VWF/α2β1/collagen
  4. Stable adhesion activation/aggregation GPVI, GPIIb/IIIa
  5. Platelets are activated by ADP, causing them to change shape, aggregate and seal off the endothelial breach
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34
Q

What combined therapy is used to manage ACS?

A

Asprin, P2Y12 inhibitors and GPIIb/IIIa antagonists.

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35
Q

What is the role of aspirin in treatment of ACS?

A

It prevents collagen-platelet binding through irreversible inactivation of cyclo-oxygenase-1.

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36
Q

What is the role of P2Y12 Inhibitors in the treatment of ACS?

A

They prevent P2Y12 receptor-mediated amplification of platelet activation (P2Y12 is the receptor for ADP).

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37
Q

Give 3 examples of P2Y12 Inhibitors.

A
  1. Clopidogrel
  2. Prasugrel
  3. Ticagrelor
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38
Q

What is the major side effect of P2Y12 inhibitors?

A

Increases risk of bleeding - serious bleeding must subside before administration and risk of thrombosis vs risk of bleeding is monitored.

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39
Q

What is the role of GPIIb/IIIa Antagonists in the treatment of ACS?

A

They prevent amplification of platelet activation by binding to the GPIIb/IIIa complex (receptor for fibrinogen and vWF).

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40
Q

Give 3 examples of GPIIb/IIIa Antagonists.

A
  • Abciximab
  • Tirofiban
  • Eptifibatide
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41
Q

What is the major side effect of GPIIb/IIIa Antagonists?

A

Increased risk of bleeding - used selectively and sparingly.

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42
Q

Why are GPIIb/IIIa Antagonists very useful in STEMI patients undergoing PCI?

A

Cover for delayed absorption of oral P2Y12 Inhibitors occurring due to opiates delaying gastric emptying.

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43
Q

What is the role of anticoagulants used in the treatment of ACS?

A

Targets formation and/or activity of thrombin - inhibiting both fibrin formation and platelet activation.

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44
Q

What anticoagulant is commonly used during Non-STEMI ACS?

A

Fondaparinux is used prior to coronary angiography (safer than heparins as it produces less bleeding).

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45
Q

What anticoagulants are used during PCI?

A

Full dose of anticoagluants, eg:
- Heparin
- Bivalirudin

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46
Q

What is angina?

A

Symptoms of chest pain and shortness of breath caused by the mismatch between oxygen supply and demand occurring as a consequence of restricted blood flow.

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47
Q

Give some causes of oxygen supply reduction associated with Ischaemic Heart Disease.

A
  1. Common:
    - Anaemia
    - Hypoxaemia
  2. Uncommon:
    - Polycythemia
    - Hypothermia
    - Hypovolaemia
    - Hypervolaemia
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48
Q

Give some causes of oxygen demand increase associated with Ischaemic Heart Disease.

A
  1. Common:
    - Hypertension
    - Tachyarrhythmia
    - Valvular heart disease
  2. Uncommon:
    - Hyperthyroidism
    - Hypertrophic cardiomyopathy
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49
Q

What predisposing factors are associated with IHD?

A
  • Age
  • Smoking
  • Family history
  • Diabetes mellitus
  • Hypertension
  • Hyperlipidemia
  • Physical inactivity
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50
Q

What environmental factors often highlight symptoms of Chronic Coronary Syndromes?

A
  • Cold weather
  • Heavy meals (post-prandial angina)
  • Emotional stress
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51
Q

What are the three major physiological factors lending to oxygen mismatch?

A
  • Impairment of blood flow by proximal arterial stenosis (eg. atherosclerosis)
  • Increased distal resistance (eg. left ventricular hypertrophy)
  • Reduced oxygen-carrying capacity of blood (eg.anaemia)
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52
Q

How does Ohm’s Law relate to CCS?

A

F = ∆P/R

Flow = change in pressure gradient / resistance

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53
Q

How does Poisuille’s Law relate to CCS?

A

F ∝ (ΔP x r^4) / ηL

Relationship between flow, pressure and resistance - radius has to fall below 75% before symptoms present.

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54
Q

What is Microvascular Angina?

A

Angina related to stenosis of cardiac microvasculature, not observed on a coronary angiogram.

(Most common in diabetes, LVH and older age)

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55
Q

What is Unstable Angina?

A

Recurrent episodes of angina at rest.

May be the initial presentation of IHD.

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56
Q

What is the most important information when taking a history of a patient with potential IHD?

A
  • Personal details
  • Presenting complaint (discuss pain)
  • Risk factors
  • Past medical history
  • Drug history
  • Family history (first degree relatives under 60)
  • Social history (smoking)
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57
Q

What characteristics of chest pain suggest Ischaemic Cardiac pain?

A
  • Heavy, tight pain
  • Located centrally
  • Provoked by cold weather, big meals or exertion
  • Relieved by rest and GTN spray
  • Associated with SOB
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58
Q

What are some differential diagnoses of chest pain?

A
  • Pericarditis/myocarditis
  • PE/chest infection
  • Aortic dissection
  • GORD
  • Musculoskeletal
  • Psychological
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59
Q

What are the NICE guidelines on diagnosis of CCS?

A
  1. CT Coronary Angiogram (first-line diagnostic test)
  2. Other non-invasive testing
  3. Coronary angiography (when other testing is inconclusive)
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60
Q

What is exercise testing?

A

The patient undertakes mild exercise on a treadmill and an ECG is run simultaneously.

Any abnormalities - the patient is referred to catheterisation lab.

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61
Q

What is a Perfusion/Myoview scan?

A

An IV radio-labelled agent travels to the coronary arteries - areas of darkness signify and blockage.

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62
Q

What is a CT Coronary Angiography?

A

Non-invasive imaging of the coronary arteries used to identify poor blood flow and coronary calcification.

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63
Q

What is a Perfusion MRI?

A

MRI scan used to obtain perfusion maps with different parameters eg. blood volume, blood flow, mean transit time (MTT) and time to peak (TTP)

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64
Q

What is an Invasive Coronary Angiography?

A

Insertion of a catheter tube into a blood vessel (groin, upper thigh or neck) and up to coronary arteries. The catheter is injected with contrast dye to highlight blockages.

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65
Q

What effect do beta-blockers have on the heart?

A

Negative chronotropic (↓ HR) and ionotropic (↓ contractility) effect on the heart - reduces CO and O2 demand.

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66
Q

What are some common side effects of beta-blockers?

A
  • Tiredness
  • Bradycardia
  • Erectile dysfunction
  • Vasoconstriction in extremities
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67
Q

What is the major contraindication of beta-blockers?

A

Severe asthma.

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68
Q

What effect do Nitrates have on the heart?

A

Venous and arteriolar dilation - reduce the preload on the heart and dilate coronary arteries.

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69
Q

Name a common side effect of Nitrates.

A

Headaches.

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70
Q

What effect do Calcium Channel Blockers have on the heart?

A
  • ↓ work - negative chronotropic (↓ HR) and ionotropic (↓ contractility) effects on the heart
  • ↓ O2 demand
  • ↓ afterload
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71
Q

What effect do statins have on the heart?

A

Reduction in LDL synthesis - reduced plaque formation in the coronary arteries.

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72
Q

Give an example of a statin.

A

HMG CoA Reductase Inhibitors.

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73
Q

What effect do ACE Inhibitors have on the heart?

A

Inhibits ACE - decreases BP

Vasodilatory effect due to decreased vasoconstrictor Angiotensin II

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74
Q

Give an example of an ACE Inhibitor.

A

Ramipril.

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75
Q

Define Diastolic Distensibility.

A

The pressure required to fill the ventricle to the same diastolic volume.

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76
Q

What are some consequences of hypertension?

A
  • Stroke (Ischaemic and haemorrhage)
  • MI
  • Heart failure
  • Chronic Renal Disease
  • Cognitive decline
  • Premature death
  • Increases risk of AF
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77
Q

What can be offered to confirm a diagnosis of hypertension?

A

Ambulatory Blood Pressure Monitoring (ABPM) over 24 hours.

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78
Q

Define Stage 1 Hypertension.

A

Clinical = 140/90
Ambulatory = 135/85

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79
Q

Define Stage 2 Hypertension.

A

Clinical = 160/100
Ambulatory = 150/95

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80
Q

Define severe hypertension.

A

Clinical = 180/110

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81
Q

How is Primary Hypertension treated?

A

Lifestyle modification and antihypertensive drug therapy.

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82
Q

Who should be offered antihypertensive drug treatment for hypertension?

A
  1. Individuals aged 80 or younger
  2. Individuals with one or more of the following:
    - Target organ damage
    - Established CVD
    - Renal Disease
    - Diabetes
    - 10 year CVD risk of >20%
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83
Q

Describe the mechanisms of BP control.
(Targets for therapy)

A
  • Cardiac output and peripheral resistance
  • RAAS and Noradrenaline (Sympathetic NS)
  • Local vascular vasoconstrictor and vasodilator mediators
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84
Q

Describe the renin-angiotensin-aldosterone system (RAAS).

A
  1. Kidney receptors detect low BP, renin is released from juxtaglomerular cells
  2. Renin converts angiotensinogen to angiotensin I
  3. ACE from the lungs converts angiotensin I to angiotensin II
  4. Angiotensin II stimulates aldosterone release resulting in increased Na+ and water reabsorption 5. Increased blood volume = Increased BP
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85
Q

Describe how Noradrenaline (sympathetic NS) increases BP.

A
  1. A drop in BP results in the release of noradrenaline, leading to vasoconstriction and increased contractility
  2. Increased peripheral resistance and cardiac output increases BP
  3. Induces renin release (augments RAAS)
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86
Q

Give 4 examples of ACE inhibitors.

A
  • Ramipril
  • Enalapril
  • Perindopril
  • Trandolapril
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87
Q

What are the indications for ACE inhibitors?

A
  • Hypertension
  • Heart failure
  • Diabetic neuropathy
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88
Q

What are the ADRs associated with ACE inhibitors - related to reduced angiotensin II formation?

A
  • Hypotension
  • Acute renal failure (increased renin release)
  • Hyperkalaemia
  • Teratogenic in pregnancy
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89
Q

What are the ADRs associated with ACE inhibitors - related to increased kinins?

A
  • Chronic dry cough
  • Rash
  • Anaphylactoid reaction
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90
Q

Give examples of Angiotensin II Receptor Blockers (ARBs).

A
  • Candesartan
  • Losartan
  • Valsartan
  • Telmisartan
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91
Q

What are the indications of ARBs?

A
  • Hypertension (when ACEi is contradicted)
  • Diabetic neuropathy
  • Heart failure
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92
Q

What ADRs are associated with ARBs?

A
  • Symptomatic hypotension
  • Hyperkalaemia
  • Potential renal dysfunction
  • Rash
  • Angiooedema
  • Teratogenic in pregnancy
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93
Q

What are the indications of Calcium Channel Blockers (CCBs)?

A
  • Hypertension
  • Ischaemic heart disease
  • Arrhythmia
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94
Q

Give examples of Calcium Channel Blockers.

A
  • Dihydropyridines (eg. amlodipine)
  • Phenylalkylamines (eg. verapamil)
  • Benzothiozepines (eg. diltiazem)
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95
Q

What are the actions of Dihydropyridines?

A

Affect vascular smooth muscle - peripheral arterial vasodilators.

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96
Q

What are the actions of Phenylalkylamines?

A
  1. Directly affects the heart
    - Reduces HR (negatively chronotropic) and force of contraction (negatively inotropic).
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97
Q

What are the actions of Benzothiozepines?

A

Intermediate heart and peripheral vascular effects.

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98
Q

What ADRs are associated with CCBs - due to peripheral vasodilation? (Mainly Dihydropyridines)

A
  • Flushing
  • Headache
  • Peripheral oedema
  • Palpitations
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99
Q

What ADRs are associated with CCBs - due to negative chronotropic effect? (Phenylalkylamines and Benzothiozepines)

A
  • Bradycardia
  • Atrioventricular block
  • Postural hypotension
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100
Q

What ADRs are associated with CCBs - due to negative inotropic effect? (Benzothiozepines)

A
  • Worsening of HF
  • Constipation (Verapamil)
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101
Q

Give examples of beta-blockers.

A
  • Bisoprolol
  • Propanolol
  • Atenolol
  • Carvedilol
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102
Q

What are the indications for beta-blockers?

A
  • IHD (angina)
  • Heart failure
  • Arrhythmia
  • Hypertension
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103
Q

Which beta-blockers are B1 sensitive?

A

Metoprolol and Bisoprolol.

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104
Q

Which beta-blockers are non-selective?

A
  • Propanolol
  • Nadolol
  • Carvedilol
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105
Q

What are the ADRs associated with beta-blockers?

A
  • Fatigue
  • Headache
  • Sleep disturbance
  • Bradycardia
  • Hypotension
  • Cold peripheries
  • Erectile dysfunction
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106
Q

How do Diuretics reduce blood pressure?

A

Increased excretion of water, salt and metabolites in urine.

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107
Q

What are the indications for Diuretics?

A
  • Hypertension
  • Heart failure
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108
Q

What are the different classes of Diuretics?

A
  • Thiazide diuretics (act on distal tubule)
  • Loop diuretics (act on ascending loop of henle)
  • Potassium-sparing diuretics (aldosterone antagonists)
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109
Q

Give examples of Diuretics.

A
  • Thiazide diuretics (bendroflumethiazide, hydrochlorothiazide)
  • Loop diuretics (furosemide, bumetanide)
  • Potassium-sparing diuretics (spironolactone, eplerenone)
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110
Q

What are the ADRs associated with Diuretics?

A
  • Hypovolaemia (mainly loop)
  • Hypotension (mainly loop)
  • Hypokalaemia
  • Hyponatraemia
  • Hypomagnesaemia
  • Hypocalcium
  • Hyperuricaemia (gout)
  • Erectile dysfunction (thiazides)
  • Impaired glucose tolerance (thiazides)
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111
Q

What other antihypertensives exist?

A
  1. α1-adrenoceptor blocker (doxazosin)
  2. Centrally acting antihypertensives (moxonidine, methyldopa - can be used in pregnancy)
  3. Direct renin inhibitor: aliskiren
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112
Q

Define Heart Failure.

A

A complex clinical syndrome of signs and symptoms that suggest the efficiency of the heart is impaired.

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113
Q

What are the different types of HF?

A
  • Left ventricular Systolic Dysfunction (most common)
  • Heart Failure with Preserved Ejection Fraction (diastolic failure)
  • Acute/chronic Heart Failure
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114
Q

What is the underlying principle of treatment?

A

Vasodilator therapy via neurohumoral blockade (RAAS-SNS).

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115
Q

What is the symptomatic treatment of congestion?

A

Diuretics (usually loop).

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116
Q

What is the first line treatment involved in disease-influencing neurohumoral blockade therapy?

A

ACE inhibitors and beta-blockers (low dose and slow up-titration).

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117
Q

What are the stages after first-line neurohumoral blockade therapy?

A
  1. Aldosterone antagonists
  2. Aldosterone Receptor antagonist and Neprilysin Inhibitor (ARNIs)
  3. SGLT2 inhibitor

If ACEi intolerant - ARBs

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118
Q

Give some examples of Nitrates.

A
  • Isosorbide mononitrate (tablet)
  • GTN spray
  • GTN infusion (acute/severe angina)
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119
Q

What effect do Nitrates have on the heart?

A
  • Arterial and venous dilators
  • Reduce preload and afterload
  • Lower BP
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120
Q

What effect do Nitrates have on the heart?

A
  • Arterial and venous dilators
  • Reduce preload and afterload
  • Lower BP
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121
Q

What are the indications for Nitrates?

A
  • IHD (angina)
  • Heart failure
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122
Q

What are the ADRs associated with Nitrates?

A
  • Headache
  • GTN spray syncope
  • Potential tolerance to the drug
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123
Q

What are the different types of Cardiac Natriuretic Peptides (CNPs)?

A
  • Atrial natriuretic peptide (ANP) - atria
  • Brain natriuretic peptide (BNP) - ventricles (found in the brain and heart
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124
Q

What causes the physiological release of CNPs?

A
  • Stretching of atrial and ventricular muscle cells
  • Raised atrial or ventricular pressure
  • Volume overload
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125
Q

What effect do CNPs have on renal excretion?

A

Increases renal excretion of sodium (natriuresis) and water (diuresis).

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126
Q

What effect do CNPs have on vascular smooth muscle?

A

Relax vascular smooth muscle of renal glomeruli to preserve filtration pressure in the kidney while still removing Na+.

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127
Q

What effect do CNPs have on the release of other chemical mediators?

A

Reduces aldosterone, angiotensin II, endothelin and ADH release.

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128
Q

What are CNPs a counter-regulatory system to?

A

The renin-angiotensin-aldosterone system (RAAS).

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129
Q

What are Natriuretic Peptides metabolised by?

A

Neutral Endopeptidase (NEP or neprilysin).

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130
Q

How can the inhibition of NP metabolism be used in the treatment of heart failure?

A

NEP inhibition increases levels of NPs.

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131
Q

Give examples of NEP inhibitors.

A
  • Sacubitril (neprilysin inhibitor)
  • Valsartan (ARB)
  • Entresto (combination of the above) - very effective in heart failure
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132
Q

What are the symptoms of Chronic Stable Angina?

A
  • Chest pain (predictable, infrequent and stable)
  • Radiating pain to neck, teeth, jaw and arms
  • Breathlessness
  • Relived by rest or GTN spray
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133
Q

What are the symptoms of Unstable Angina (NSTEMI) chest pain?

A
  • Unpredictable (at rest)
  • Frequent and unstable
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134
Q

What is the nature of STEMI chest pain?

A
  • Unpredictable
  • Pain at rest
  • Persistant
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135
Q

How are patients with chronic stable angina generally treated?

A
  1. Antiplatelet therapy (aspirin, ticagrelor, clopidogrel)
  2. Lipid-lowering therapy (statins)
  3. Short-acting nitrate (GTN spray)
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136
Q

How is frequent angina treated?

A
  1. First line:
    - Beta-blockers or CCBs
  2. Second line:
    - Long-acting nitrates
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137
Q

What are the Class I Anti-arrhythmics?

A

Sodium Channel Blockers:
- 1A: quinidine
- 1B: lidocaine
- 1C: flecainide

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138
Q

What are the Class II Anti-arrhythmics?

A

Beta-blockers:
- Non-selective (eg. propanolol)
- Beta-1 selective (eg. bisoprolol, metoprolol)

139
Q

What are the Class III Anti-arrhythmics?

A

Prolongs action potential (eg. amiodarone and sotalol)

140
Q

What are the Class IV Anti-arrhythmics?

A

Calcium Channel Blockers (only phenylalkylamines and benzothiozepines).

141
Q

Which Anti-arrhythmics involve rate control and which involve rhythm control?

A

Rhythm control = Class I and III
Rate control = Class II and IV

142
Q

What ADRs are associated with Amiodarone?

A
  • Bradycardia
  • Interstitial Lung Disease
  • Hyper- and Hypothyroidism
  • Hepatic dysfunction
  • Photosensitivity
  • Drug interactions
143
Q

What type of drug is Digoxin?

A

Cardiac glycoside.

144
Q

What is the mechanism of action of Digoxin?

A

It inhibits the Na/K pup, causing an increase in Ca2+ inside the cells of the heart.

145
Q

What affect does digoxin have on the heart?

A
  • Bradycardia
  • Slows AV condunction
  • Increased ectopic activity
  • increased force of contraction
146
Q

What are the indications for Digoxin?

A
  • Atrial Fibrillation (reduces ventricular rate response)
  • Severe heart failure (+ve inotropic effect)
147
Q

What ADRs are associated with Digoxin?

A
  • Narrow therapeutic range
  • Nausea
  • Vomiting
  • Diarrhoea
  • Confusion
148
Q

What are the 4 aspects of Tetralogy of Fallot?

A
  1. Ventricular Septal Defect
  2. Pulmonary Stenosis
  3. Hypertrophy of right ventricle
  4. Overriding aorta
149
Q

What is the key issue with Tetralogy of Fallot?

A

Anterior dislocation of the septum below the pulmonary outflow which causes the other issues.

150
Q

What are Fallot spells?

A

A drop in the blood oxygen levels and deep cyanosis.

151
Q

How many babies are born with Tetralogy of Fallot?

A

1 in 1000

10% of all birth defects.

152
Q

What is the treatment for Tetralogy of Fallot?

A

Surgical repair

(Blalock-Thomas-Taussig Shunt or complete repair)

153
Q

What is a Ventricular Septal Defect (VSD)?

A

An abnormal connection between the two ventricles.

154
Q

How common are Ventricular Septal Defects?

A

Most common congenital heart defect (~20%).

Most close spontaneously during childhood.

155
Q

What is the physiology of VSD?

A

High pressure in LV, low pressure in RV - blood flows from left to right.

156
Q

What are the clinical signs of Large VSD?

A
  • Small, breathless, skinny baby
  • Increased resp rate
  • Tachycardia
  • Big heart
  • Murmur
157
Q

What are the clinical signs of Small VSD?

A
  • Loud systolic murmur
  • Thrill (buzzing sensation)
  • Well grown
  • Normal heart size
158
Q

What is Eisenmenger’s Syndrome?

A
  • High pressure pulmonary blood flow
  • Damage to the delicate pulmonary vasculature
  • RV pressure increases, blood moves into LV
  • Patient becomes cyanotic
159
Q

What are Atrial Septal Defects (ASD)?

A

An abnormal connection between the two atria.

Often presents in adulthood (common).

160
Q

What is the physiology of ASD?

A
  • Slightly higher pressure in the LA than RA
  • Shunt is left to right
  • Increased flow into right heart and lungs
161
Q

What are the clinical signs of ASD?

A
  • Pulmonary Flow murmur
  • Fixed split-second heart sound
  • Large heart and pulmonary arteries
162
Q

What are Atrio-Ventricular Septal Defects (AVSD)?

A

Hole in the centre of the heart, involves the ventricular and atrial septum, mitral and tricuspid valves. Can be complete or partial (often associated with Trisomy 21).

163
Q

What is the physiology of AVSD?

A

Instead of two separate AV valves there is one malformed one - usually leaks to some degree.

164
Q

What is Patent Ductus Arteriosus?

A

A continuous “machinery” murmur with a large heart, causes Eisenmenger’s syndrome.

165
Q

How is Patent Ductus Arteriosus treated?

A

Surgical or Percutanous closure.

166
Q

What is Coarctation of the Aorta?

A

Narrowing of the aorta at the site of insertion of the ductus arteriosus.

167
Q

What are the clinical signs of Coarctation of the Aorta?

A
  • Right arm hypertension
  • Bruits over the scapulae and back
  • Murmur
168
Q

What long term problems may be caused by Coarctation of the Aorta?

A
  • Hypertension
  • CAD
  • Subarachnoid haemorrhage
  • Re-coarctation
  • Aneurysm at repair site
169
Q

How is Coarctation of the aorta treated?

A

Surgical or percutaneous repair.

170
Q

What is Bicuspid Aortic Valve (BAV)?

A
  • Normal AV has three cusps
  • Bicuspid AVs are common (1-2% of the population)
171
Q

What is the issue with BAV?

A
  • Can be severely stenotic in infancy/childhood
  • Degenerate/ become regurgitant quicker than normal
  • Less efficient
172
Q

What is Pulmonary Stenosis?

A
  • Narrowing of the outflow of the right ventricle
  • Can be valvar, sub-valvar, supra-valvar or branch
  • 8-12% of all congenital heart defects
173
Q

How is Pulmonary Stenosis treated?

A
  • Balloon valvuloplasty
  • Open valvotomy
  • Open trans-annular patch
  • Shunt
174
Q

What are the two layers the pericardium?

A
  • Serous pericardium
  • Fibrous pericardium
175
Q

Describe the Serous Pericardium.

A
  • Enclosed by fibrous pericardium
  • Divided into two layers (each made up of a single sheet of epithelial cells) - Outer Parietal layer and Internal Visceral layer
176
Q

Describe the Fibrous Pericardium?

A
  • Continuous with the central tendon of the diaphragm
  • 2mm thick layer made of tough connective tissue
177
Q

What is found between the parietal and visceral pericardium?

A

The pericardial cavity - contains 50ml of serous fluid (to minimise friction generated by the heart during contraction)

178
Q

What vessels are contained within the pericardium?

A

Roots of the great vessels:
- Aorta
- Pulmonary artery
- Pulmonary veins
- SVC
- IVC

179
Q

What are the functions of the pericardium?

A
  • Fixes the heart in the mediastinum and limits motion
  • Prevents overfilling of the heart
  • Lubrication
  • Protection from infection (physical barrier)§
180
Q

What is the relevance of the small reserve volume associated with the pericardial sac?

A

The volume of pericardial fluid changes based on the physiological state.

181
Q

What is Cardiac Tamponade?

A

If the volume of serous fluid is exceeded, the pressure is transferred to the cardiac chambers.

The increase in pericardial fluid pressure can prevent the heart from expanding and ventricles from filling sufficiently.

182
Q

What clinical signs are associated with Cardiac Tamponade?

A
  • Reduced intrathoracic pressure during inspiration
  • Increased venous return to the RA (suction due to compression)
  • Increased RA compliance, reducing RA filling
  • Decrease in systolic blood pressure by >10mmHg
183
Q

What is Chronic Pericardial Effusion?

A
  • Chronic accumulation of fluid allowing the adaption of the parietal pericardium
  • Increased compliance reduced the effect on diastolic filling of the chambers
184
Q

Define Acute Pericarditis.

A

An inflammatory pericardial syndrome with or without pericardial effusion.

185
Q

Define Pericardial Effusion.

A

An accumulation of excess fluid in the pericardial cavity.

Pericardial fluid contains blood components such as fibrin, RBCs and WBCs.

186
Q

How is Pericarditis diagnosed?

A
  1. Clinical diagnosis made with two of the following:
    - Chest pain (85-90%)
    - Friction rub (33%)
    - ECG changes (60%)
    - Pericardial effusion (60%)
187
Q

What are the infectious causes of Pericarditis?

A
  1. Viral (most common)
    - Enteroviruses
    - Herpesviruses
    - Adenoviruses
    - Parvovirus B19
  2. Bacterial (rare)
    - Mycobacterium TB
188
Q

What are the non-infectious causes of Pericarditis?

A
  • Autoimmune (most common)
  • Neoplastic
  • Metabolic
  • Traumatic and Iatrogenic
189
Q

Give examples of autoimmune causes of pericarditis.

A
  1. Sjorgen’s syndrome
  2. Rheumatoid arthritis
  3. Scleroderma
  4. Systemic vasculitides
190
Q

Give examples of neoplastic causes of pericarditis.

A

Secondary metastatic tumours - mostly lung and breast cancer and lymphoma.

191
Q

Give examples of metabolic causes of pericarditis.

A

Uraemia and Myxoedema.

192
Q

Give examples of traumatic and iatrogenic caused of pericarditis.

A
  1. Early onset:
    - Direct injury (eg. penetrating thoracic injury)
    - Indirect injury (eg. radiation injury)
  2. Delayed onset:
    - Pericardial injury syndromes (eg. Post-MI)
    - Iatrogenic trauma (eg. Pacemaker lead insertion or PCI)
193
Q

Give examples of other causes of pericarditis.

A
  • Amyloidosis
  • Aortic dissection
  • Pulmonary arterial hypertension
  • Chronic heart failure
194
Q

What is the nature of chest pain associated with pericarditis?

A
  • Severe, sharp and pleuritic
  • No constricting crushing pain (Ischaemic pain)
  • Rapid onset
  • Radiating to arm
  • Relieved by sitting forward
  • Exacerbated by lying down
195
Q

What other clinical presentations are associated with pericarditis?

A
  • Dyspnoea
  • Cough
  • Systemic disturbance (eg. viral symptoms, rash, joint pain)
196
Q

What is a pericardial rub?

A
  • Extra heart sound heard upon auscultation
  • Three components (one systolic, two diastolic)
  • Sound resembles scratching/crushing of snow
  • Audible friction of walls rubbing against each other
197
Q

What are the signs of effusion associated with pericarditis?

A

Pulses Paradoxus - large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration

198
Q

What is Beck’s Triad?

A

Three clinical signs associated with Pericardial Tamponade:
- Hypotension
- Muffled heart sounds
- Raised jugular venous pressure

199
Q

What characteristics of an ECG can be associated with Pericarditis?

A
  • Diffuse ST elevation
  • Concave ST segment
  • Saddle shaped
  • PR depression
200
Q

What blood tests are used to investigate Pericarditis?

A
  • FBC (increased White Cell Count)
  • Erythrocyte Sedimentation Rate (ESR)
  • Troponin
201
Q

Give examples of differential diagnoses related to chest pain.

A
  • Pneumonia
  • PE
  • GORD
  • MI/ischaemia
  • Aortic dissection
  • Pancreatitis
  • Pneumothorax
  • Pneumonia
  • Peritonitis
  • HSV (shingles)
202
Q

How is Pericarditis managed?

A
  • No physical activity until resolution of inflammatory symptoms
  • NSAIDs (ibuprofen or aspirin)
  • Colchicine
203
Q

What pericarditis complications are associated with high risk patients?

A
  • Higher fever
  • Subacute onset
  • Large pericardial onset
  • Cardiac tamponade
  • Lack of response to pain relief
204
Q

What pericarditis complications are associated with low risk patients?

A
  • Myopericarditis
  • Immunosuppression
  • Trauma
205
Q

What is the rate of Acute Pericarditis recurrence?

A

15-30% (Colchicine reduces rate by 50%)

206
Q

What are the different types of Cardiomyopathy?

A
  • Hypertrophic
  • Dilated
  • Arrhythmogenic Right/Left Ventricular
207
Q

What is the usual inheritance pattern for Cardiomyopathy?

A

Autosomal dominant - offspring have a 50% chance of being affected.

208
Q

What is Naxo’s disease?

A

A Recessive condition with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C).

209
Q

What are the histological features of Cardiomyopathy?

A
  • Chaotic arrangement of cells and myofibrils
  • Thicker artery walls
210
Q

What type of mutation causes Hypertrophic Cardiomyopathy?

A

Sarcomeric gene mutations.

211
Q

Describe the pathophysiology of Hypertrophic Cardiomyopathy.

A

Systole is normal but diastole is affected - the heart is unable to relax properly due to thickening of the ventricular walls.

212
Q

What are the symptoms of Hypertrophic Cardiomyopathy?

A
  • Angina
  • Dyspnoea
  • Syncope
213
Q

What ECG abnormalities are associated with Hypertrophic Cardiomyopathy?

A
  • Deep Q waves
  • Large inverted T waves
  • Non-sustained ventricular tachycardia (NSVT)
214
Q

What type of mutation causes Arrhythmogenic Cardiomyopathy?

A

Desmosome gene mutations.

215
Q

What does Arrhythmogenic Cardiomyopathy often present with?

A

Atrial Fibrillation.

216
Q

Describe the pathophysiology of Arrhythmogenic Cardiomyopathy.

A

Desmosome mutations lead to myocytes being pulled apart and ventricular tissue is replaced with fatty fibrous tissue.

217
Q

What is the major clinical sign associated with Arrhythmogenic Cardiomyopathy?

A

Ventricular tachycardia.

218
Q

What ECG abnormalities are associated with Arrhythmogenic Cardiomyopathy?

A
  • Epsilon waves (specifically ARVC)
  • T wave inversion
219
Q

What type of mutation causes Dilated Cardiomyopathy?

A

Cytoskeletal gene mutations.

220
Q

Describe the pathophysiology of Dilated Cardiomyopathy?

A

Ventricular dilation and dysfunction causes poor contractility.

221
Q

What are the symptoms of Dilated Cardiomyopathy?

A
  • Breathlessness
  • Tiredness
  • Oedema
222
Q

What ECG abnormalities are associated with Dilated Cardiomyopathy?

A

Non-specific T wave changes.

223
Q

What are channelopathies?

A

Mutations in genes coding for ion channels.

224
Q

Name the four main channelopathies.

A
  • Long QT syndrome
  • Short QT syndrome
  • Brugada
  • Catecholaminergic polymorphic ventricular tachycardia (CPVT)
225
Q

What is the commonest symptom of channelopathies?

A

Recurrent syncope episodes.

226
Q

What is Brugada Syndrome?

A

A channelopathy caused by a mutation in the cardiac sodium channel gene.

227
Q

What are the symptoms of Brugada Syndrome?

A

Mostly asymptomatic but can cause syncope or sudden cardiac death.

228
Q

What are the common rhythmic abnormalities associated with Brugada Syndrome?

A

Ventricular fibrillation or polymorphic ventricular tachycardia.

229
Q

What ECG abnormalities are associated with Brugada Syndrome?

A

Characteristic ST elevation in chest leads.

230
Q

What is Aortic Stenosis?

A

Narrowing of the aortic valve (normal area = 3-4cm^2)

231
Q

When do symptoms of aortic stenosis present?

A

Valve area 1/4 of normal.

232
Q

What are the 3 types of aortic stenosis?

A
  • Supravalvular
  • Subvalvular
  • Valvular
233
Q

What are the congenital causes of aortic stenosis?

A
  • Congenital aortic stenosis
  • Congenital bicuspid valve
234
Q

What are the acquired causes of aortic stenosis?

A
  • Degenerative calcification
  • Rheumatic heart disease
  • Rare causes
235
Q

When are symptoms first noticed for congenital vs acquired aortic stenosis?

A

Congenital: 30 - 50 years old
Acquired: 70 - 80 years old

236
Q

Describe the pathophysiology of aortic stenosis.

A

Pressure gradient develops between left ventricle and the aorta (increased afterload)

237
Q

What are the compensatory mechanisms in aortic stenosis?

A

LV function initially maintained by compensatory pressure hypertrophy.

If this fails LV function declines.

238
Q

What are the clinical presentations of aortic stenosis?

A
  • Syncope on exertion (15%)
  • Angina (35%)
  • Dyspnoea (50%)
  • Sudden death (rare)
239
Q

What are the physical signs associated with aortic stenosis?

A
  • Pulsus tardus (slow rising carotid pulse)
  • Pulsus parvus (decreased pulse amplitude)
  • Heart sounds (soft/absent 2nd heart sound)
  • Ejection systolic murmur
240
Q

What is the prognosis of aortic stenosis?

A

If with angina: 50% survive for 5 years
If with syncope: 50% survive for 3 years
If with heart failure: mean survival under 2 years

241
Q

How is aortic stenosis graded?

A

Mild - area >1.5cm^2
Moderate - area 1.0-1.5cm^2
Severe - area <1.0cm^2

242
Q

What investigation can assess the severity of aortic stenosis?

A

Echocardiogram:
- LV size and function
- Doppler-derived gradient and valve area

243
Q

What is the general care in the management of aortic stenosis?

A
  • Fastidious dental hygiene
  • Consider infective endocarditis prophylaxis in dental procedures
244
Q

What is the surgical management of aortic stenosis?

A

Valve replacement or definitive treatment.

245
Q

What is the medical management of aortic stenosis?

A

Mechanical problem (a limited role for medication).

Contraindication for vasodilators.

246
Q

What is TAVI?

A

Transcatheter Aortic Valve Implantation.

247
Q

What are the indications for intervention in aortic stenosis?

A
  • Any symptomatic patient with severe aortic stenosis
  • Any patient with decreasing ejection fraction
  • Any patient undergoing CABG with moderate or severe aortic stenosis
248
Q

What is Mitral Regurgitation?

A

The mitral valve does not close properly, allowing for blood to flow backwards from LV to LA.

249
Q

What are the causes of chronic mitral regurgitation?

A
  • Myxomatus degeneration
  • Ischaemic mitral regurgitation
  • Rheumatic heart disease
  • Infective endocarditis
250
Q

What is the pathophysiology of mitral regurgitation?

A

Pure volume overload.

251
Q

What are the compensatory mechanisms in mitral regurgitation?

A
  • Left atrial enlargement
  • Left ventricular hypertrophy
  • Increased contractility
252
Q

WHat are the clinical presentations of mitral regurgitation?

A
  • Pansystolic murmur at apex, radiating to the axilla
  • Exertion dyspnoea
  • Heart failure
253
Q

What are the clinical presentations of mitral regurgitation?

A
  • Pansystolic murmur at apex, radiating to the axilla
  • Exertion dyspnoea
  • Heart failure
254
Q

How long is the compensatory phase of mitral regurgitation?

A

10 to 15 years

255
Q

What caused mortality to increase in patients with mitral regurgitation?

A
  • Symptoms develop
  • Ejection fraction falls to below 60%
256
Q

What is the cause of mortality in patients with mitral regurgitation?

A

Progressive dyspnoea and heart failure.

257
Q

What ECG abnormalities are associated with mitral regurgitation?

A
  • LA enlargement
  • AF
  • LV hypertrophy
258
Q

What do chest X-rays show in mitral regurgitation?

A
  • LA enlargement
  • Central pulmonary artery enlargement
259
Q

What does an echocardiogram show in mitral regurgitation?

A
  • Estimation of LA and LV size and function
  • Valve structure

(Transoesophageal echocardiogram (TOE) most useful)

260
Q

What monitoring is done in mitral regurgitation?

A

Echocardiogram:
- Mild: 2-3 years
- Moderate: 1-2 years
- Severe: 6-12 months

261
Q

What medications can be given in the management of mitral regurgitaiton?

A
  • Vasodilators (eg. ACEi)
  • Rate control for AF (eg. beta-blockers, CCBs)
  • Anticoagulation in AF and flutter
  • Diuretics for fluid overload
262
Q

When is infective endocarditis prophylaxis given in mitral regurgitation?

A
  • Prosthetic valves
  • History of infective endocarditis for dental procedures
263
Q

When is surgery indicated for mitral regurgitation?

A
  1. Any symptoms at rest or exercise
  2. If asymptomatic:
    - Ejection fraction <60%
    - LV end-systolic diameter >45mm
264
Q

What is aortic regurgitation?

A

Leakage of blood into the LV during diastole due to ineffective coaptation of the aortic cusps.

265
Q

What are the causes of aortic regurgitation?

A
  • Bicuspid aortic valve
  • Rheumatic heart disease
  • Infective endocarditis
266
Q

What is the pathophysiology of aortic regurgitation?

A

Combined pressure and volume overload.

267
Q

What are the compensatory mechanisms of aortic regurgitation?

A

LV dilation and hypertrophy.

268
Q

Why can aortic regurgitation lead to heart failure?

A

Progressive LV dilation.

269
Q

What are the clinical presentations of aortic regurgitation?

A
  • Wide pulse pressure
  • Hyperdynamic and displaced apical pulse
270
Q

What can be found on auscultation of aortic regurgitation?

A
  • Diastolic blowing murmur at the left sternal border
  • Austin flint murmur (systolic ejection murmur) at the apex
271
Q

What are the progressive symptoms of aortic regurgitation and when do they present?

A
  • 40 to 50 years
  • Dyspnoea on exertion
  • Palpitations
272
Q

How is a chest X-ray used to evaluate aortic regurgitation?

A
  • Enlarged cardiac silhouette
  • Aortic root enlargement
273
Q

How is an echocardiogram used to evaluate aortic regurgitation?

A
  • AV and aortic root evaluation
  • LV dimensions and function
274
Q

What are the general considerations of aortic regurgitation management?

A

Infective endocarditis prophylaxis.

275
Q

What is the medical management of aortic regurgitation?

A

Vasodilators (ACEi improve stroke volume and reduce regurgitation only if patient is asymptomatic or hypertensive).

276
Q

What is the definitive treatment of aortic regurgitation?

A

Surgical intervention - valve replacement

277
Q

When is atrial regurgitation indicated for surgery?

A
  • Any symptoms at rest or exercise
  • Treat asymptomatic patients if ejection fraction <50% or LV dilated
278
Q

What is mitral stenosis?

A

Obstruction of LV inflow that prevents proper filling in diastole.

279
Q

What is the normal mitral valve area?

A

4-6cm^2

280
Q

What are the causes of mitral stenosis?

A
  • Rheumatic heart disease
  • Infective endocarditis
  • Mitral annular calcification
281
Q

What is the pathophysiology of mitral stenosis?

A
  • Progressive dyspnoea
  • Increased transmitral pressures - LA enlargement and AF
  • RH failure symptoms
  • Haemoptysis
282
Q

What are the clinical presentations of mitral stenosis?

A
  • Prominent ‘a’ wave in jugular venous pulsations
  • Signs of right heart failure (advanced disease)
  • Mitral facies (pink-blue patches on cheeks)
  • Heart sounds
283
Q

What are the heart sounds in mitral stenosis?

A
  • Low-pitched diastolic rumble most prominent at apex
  • Loud opening S1 snap

(Best heard when patient is laying on LHS in expiration)

284
Q

Which heart sounds indicate severe mitral stenosis?

A

Shorter S2 to opening snap interval.

285
Q

What causes mortality in mitral stenosis?

A
  • Progressive pulmonary oedema
  • Infection
  • Thromboembolism
286
Q

How can ECGs evaluate the severity of mitral stenosis?

A

AF and LA enlargement.

287
Q

How can chest X-rays evaluate the severity of mitral stenosis?

A
  • LA enlargement
  • Pulmonary oedema
  • Calcific mitral valve (rare)
288
Q

How can echocardiograms evaluate the severity of mitral stenosis?

A
  • Gold standard diagnostic tool
  • Assess mitral valve mobility, pressure gradient, and mitral valve area
289
Q

How is the mitral stenosis monitored?

A

Serial echocardiography:
- Mild - 3-5 years
- Moderate 1-2 years
- Severe - yearly

290
Q

How can medications be used to manage mitral stenosis?

A
  • Mechanical problem (medication does not prevent progression)
  • Beta-blockers
  • CCBs
  • Digoxin
  • Diuretics
291
Q

What general care should be taken in the management of mitral stenosis?

A

Infective endocarditis prophylaxis for patients with prosthetic valves, or a history of infective endocarditis for dental procedures.

292
Q

What is the best management for mitral stenosis?

A
  • Percutaneous mitral balloon valvotomy
  • Diagnose patients early
293
Q

What is Infective Endocarditis?

A

Infection of the heart valves or other endocardial lined structures within the heart (eg. septal defects, pacemaker leads).

294
Q

What are the different types of Infective Endocarditis?

A
  • Left-sided Native (mitral or aortic)
  • Left-sided Prosthetic (early - within a year, late - after a year)
  • Right-sided IE (rarely prosthetic).
  • Device related (e.g. pacemakers, defibrillators)
295
Q

How does the nature of Infective Endocarditis affect the outcome?

A

Left-sided: More likely to cause thrombo-emboli systematically

Right-sided: More likely to spread to cause a pulmonary embolism

296
Q

What are the risk factors for Infective Endocarditis?

A
  • Having a regurgitant or prosthetic valve
  • If infectious material is introduced into the bloodstream during surgery
  • Individuals who have had IE previously
297
Q

What groups are at increased risk of Infective Endocarditis?

A
  • Elderly
  • IV drug users
  • Individuals with artificial valves
  • Young people with congenital heart diseases
298
Q

What three bacteria are most likely to cause Infective Endocarditis?

A
  • Streptococcus viridans (Group B haemolytic optochin resistant)
  • Staphylococcus aureus
  • Staphylococcus epidermis (coagulase -ve staph)
299
Q

What are the two main sites vegetation adheres to in Infective Endocarditis?

A
  • Atrial surface of AV valves
  • Ventricular surface of SL valves
300
Q

What are the main clinical presentations of Infective Endocarditis?

A
  • Signs of systemic infection (eg. fever and sweats)
  • Embolisation (eg. stroke, PE, MI)
  • Valve dysfunction
301
Q

What are the five main signs associated with Infective Endocarditis?

A
  • Splinter haemorrhages (small blood spots underneath the nail)
  • Osler’s nodes (painful, red, raised lesions found on the hands and feet)
  • Janeway lesions
  • Roth spots (small retinal haemorrhage)
  • Heart murmurs
302
Q

What investigations might be done if Infective Endocarditis is expected?

A
  • Blood cultures
  • Echocardiogram (shows endocardial involvement)
  • Blood samples (raised ESR/CRP)
  • ECG
303
Q

What are the advantages and disadvantages of Trans-Thoracic Echocardiogram?

A
  1. Advantages:
    - Safe
    - Non-invasive
    - No discomfort
  2. Disadvantages
    - Lower quality imaging
304
Q

What are the advantages and disadvantages of Trans-Oesophageal Echocardiography?

A
  1. Advantages:
    - Excellent imaging
  2. Disadvantages:
    - Discomfort
    - Small risk of perforation or aspiration
305
Q

What is the criteria for diagnosis of Infective Endocarditis?

A

Duke’s Criteria: Acombination of major and minor symptoms associated with IE.

  1. Definite:
    - Two major
    - One major and three minor
    - Five minor
  2. Possible:
    - One major and one minor
    - Three minor
306
Q

What are the major and minor signs of Infective Endocarditis according to Duke’s Criteria?

A

Major:
- Positive blood culture
- Echocardiography showing endocardial involvement

Minor:
- Fever
- Pre-disposing factor
- Vascular phenomena
- Immunological problems
- Microbiological evidence

307
Q

How is Infective Endocarditis treated?

A
  • Antimicrobials based on culture
  • Treat complications (eg. arrhythmia, HF etc)
  • Surgery
308
Q

What are the indications for surgery in Infective Endocarditis?

A
  • Antibiotics not working
  • Complications (e.g. aortic root abscess, severe valve damage)
  • Removal of infected devices
  • Valve replacement
  • Removal of large vegetation before they embolise
309
Q

Why is it important to remove large vegetations?

A

To prevent them embolising and causing a stroke, MI etc.

310
Q

What are the normal interval times for each wave on an ECG? (in Milliseconds)

A

PR - 120-200
ST - 270-330
QT - 350-420
QRS - 80-110

311
Q

What do low amplitude P waves suggest?

A
  • AF
  • Obesity
  • Hyeprkalaemia
312
Q

What do high amplitude P waves suggest?

A

Right atrial enlargement.

313
Q

What do broad-notched P waves suggest?

A

Left atrial enlargement.

314
Q

What does a short PR interval suggest?

A
  • Younger patients
  • Pre-excitation eg. Wolf-Parkinson-White syndrome
315
Q

What does a long PR interval suggest?

A

Disorders of the AV node and specialised conducting tissue.

316
Q

What does a broad QRS interval suggest?

A
  • Ventricular conduction delay
  • Pre-excitation
317
Q

What does a small QRS interval suggest?

A
  • Obese patient
  • Pericardial effusion
  • Infiltrative cardiac disease
318
Q

What does a tall QRS interval suggest?

A
  • Left ventricular hypertrophy
  • Thin patient
319
Q

What do “Long QT” or “Short QT” syndromes suggest?

A

Excessively rapid or slow repolarisation - can be arrhythmogenic. (Congenital, drugs or electrolyte disturbances)

320
Q

What does an elevated ST segment suggest?

A
  • Early repolarisation
  • Myocardial infarction
  • Pericarditis/myocarditis
321
Q

What does T wave inversion suggest?

A
  • Ischaemia/infarction
  • Myocardial strain (hypertrophy)
  • Myocardial disease (cardiomyopathy)
322
Q

What are the 5 types of Tachycardia?

A
  • Atrial Fibrillation
  • Atrial Flutter
  • Supraventricular Tachycardia (SVT)
  • Ventricular Tachycardia
  • Ventricular Fibrillation
323
Q

What are the common causes of Bradycardia?

A
  • Conduction tissue fibrosis
  • Ischaemia
  • Inflammation/infiltrative disease
  • Drugs
324
Q

How do Ischaemia and Infarction present on an ECG?

A
  • T wave flattening inversion
  • ST segment depression
  • ST segment elevation
  • Q waves - old infarction
325
Q

What are Ectopic beats?

A
  • Very common
  • Non-sustained beats arising from ectopic regions of atria or ventricles
  • Generally benign
326
Q

What is Atrial Fibrillation?

A
  • Commonest sustained arrhythmia
  • Paroxysmal or persistant
  • Rapid chaotic firing caused loss of mechanical contraction and irregular ventricular response
327
Q

What is the medical treatment for AF?

A
  • Treat underlying cause
  • Rate control (eg. beta-blockers, CCBs)
  • Restore sinus rhythm (eg. cardioversion)
  • Maintain sinus rhythm (eg. amiodarone, flecainide)
328
Q

What is the surgical intervention for AF?

A

Catheter ablation

329
Q

What is a major risk of AF?

A

Stroke due to thrombus formation.

(Risk is calculated with CHA2DS2-VASc score)

330
Q

How is SVT treated?

A
  • Valsalva manouvres
  • Beta-blockers or CCBs
  • Catheter ablation
331
Q

What are Accessory Pathways?

A

Congenital remnant muscle strands between the atrium and ventricle.

Can manifest as pre-excitation or be concealed (normal ECG)

332
Q

What is an “electrical storm”?

A
  • 3 or more sustained episodes of VT or VF
  • High risk/poor prognosis
  • Manage on CCU/ITU
333
Q

How is an electrical storm treated?

A
  • Correct any provoking factors
  • Beta-blockers
  • Sedation
  • Amiodarone
  • Overdrive pacing
  • Catheter ablation
334
Q

What is Heart Failure?

A

An inability of the heart to deliver blood at a rate commensurate with the requirement of the metabolising tissues, despite normal or increased cardiac filling rates.

335
Q

What are the causes of Heart Failure?

A
  • Myocardial dysfunction as a result of IHD (commonest)
  • Hypertension
  • Alcohol excess
  • Cardiomyopathy
  • Valvular
  • Endocardial/Pericardial
336
Q

What are the main phenotypes of Heart Failure?

A
  • HF with reduced ejection fraction (HFrEF)
  • HF with preserved ejection fraction (HRpEF)
337
Q

What are the symptoms of HF?

A
  • Breathlessness
  • Tiredness
  • Cold peripheries
  • Leg swelling
  • Increased weight
338
Q

What are the clinical signs of HF?

A
  • Tachycardia
  • Displaced apex beat
  • Added heart sounds and murmurs
  • Hepatomegaly
  • Peripheral and sacral oedema
  • Ascites
339
Q

What is the New York Heart Association (NYHA) classification?

A

Class I: No limitation (asymptomatic)
Class II: Slight limitation
Class III: Marked limitation
Class IV: Inability to carry out any physical activity without discomfort

340
Q

What is the treatment of HF-PEF?

A
  • Spironolactone in small doses
  • Tafamidis for peripheral neuropathy
341
Q

What is the treatment for HF-REF?

A

1st line: ACEi and beta-blockers
2nd line: ARBs
3rd line: Hydralazine/nitrate combination

342
Q

What lifestyle changes are recommended as treatment for HF?

A
  • Avoid large meals
  • Weight loss
  • Smoking cessation
  • Exercise
  • Vaccination
343
Q

What is the purpose of an ECG of a patient suspected of HF?

A

To ascertain the underlying cause:
- Ischaemia
- LVH
- Hypertension
- Arrhythmia

Phase 2a (11 decks)

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