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Sirpi's Phase 2A Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

betaRisk factors for Atherosclerosis

A

Tobacco Smoking (nicotine damages endothelial cells)
High Serum Cholesterol (LDL)
Obesity
Diabetes
Hypertension

Male - no oestrogen which is cardioprotective.

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2
Q

Where are atherosclerotic plaques more likely to occur?

A

Areas of high turbulence
Bifurcations, aortic arch.

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3
Q

Components of atherosclerotic plaque

A

Lipid, necrotic core, connective tissue, fibrous cap.

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4
Q

What arterial layer can can thin during atherosclerosis?

A

Tunica media

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5
Q

Pathogenesis of atherosclerosis

A

Endothelial cell damage causes increased expression of cell adhesion molecules and increased lipid permeability to lipids such as LDL.
This results in the deposition of inflammatory cells and lipids in the tunica intima.
Inflammatory cytokine release causes more cells to migrate and deposit.
Foam cells that take up these lipids apoptose and spill lipid contents to further enlarge plaque.
Growth factor release such as platelet derived growth factor stimulate proliferation of smooth muscle cells, collagen etc to form the fibrous cap.
The initial enlargement causes microthrombotic events to occur resulting in more and more plaque buildup and arterial stenosis.

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6
Q

What are the stages of atherosclerotic plaque formation?

A

Fatty Streaks
Intermediate Lesions
Advanced Lesions/Fibrous Plaques
Plaque Rupture/Plaque Erosion

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7
Q

What are some cytokines found in atherosclerotic plaques?

A

IL-1,6,8
IFN-gamma

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8
Q

Features of fatty streaks

A

Composed of lipid-laden macrophages & T-cells.
Can occur in people less than 10 years old.

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9
Q

Features of intermediate lesions

A

Presence of smooth muscle cells and platelet aggregation.

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10
Q

Features of advanced lesions

A

Covered by dense fibrous cap
Prone to rupture and calcification

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11
Q

What happens during plaque ruptures?

A

Weakening of fibrous cap can cause plaque ruptures and cause collagen exposure and tissue factor release.

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12
Q

Consequence of plaque rupture?

A

Can result in thrombosis causing stenosis and coronary syndromes.

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13
Q

How is plaque erosion different to plaque rupture?

A

Occurs in earlier stage plaques having a smaller lipid core.
Larger lumen remaining.

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14
Q

What thrombus is formed in plaque erosion?

A

White thrombus

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15
Q

What thrombus is formed in plaque rupture?

A

Red thrombus

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16
Q

Management of coronary atherosclerosis

A

Percutaneous coronary intervention (PCI)

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17
Q

Limitation of PCI

A

Risk of re-stenosis

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18
Q

How can re-stenosis be prevented?

A

Usage of drug eluting stents.

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19
Q

What are coronary artery stents normally made of?

A

Stainless steel.

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20
Q

What is angina?

A

Mismatch of oxygen demand and blood supply causing ischaemia and pain.

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21
Q

What are some ‘low supply’ exacerbating factors of angina?

A

Anaemia
Hypothermia
Hypoxia
Polycythaemia

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22
Q

What are some ‘high demand’ exacerbating factors of angina?

A

Hyperthyroidism
Hypertrophic cardiomyopathy

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23
Q

Causes of myocardial ischaemia?

A

Impairment of blood flow e.g proximal arterial stenosis
Increased distal resistance e.gg left ventricular hypertrophy
Reduced oxygen-carrying capacity of blood e.g anaemia

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24
Q

How much stenosis can occur before presenting symptoms?

A

70% stenosis.

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25
Q

What are the different types of angina?

A

Stable angina
Crescendo angina
Unstable angina
Prinzmental’s angina
Microvascular angina

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26
Q

What is stable angina?

A

Pain upon exertion, not at rest.

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27
Q

What is crescendo angina?

A

Increasing angina over time.

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28
Q

What is unstable angina?

A

Acute onset of pain upon exertion and at rest.

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29
Q

What is prinzmental’s angina?

A

Angina due to coronary artery spasm.

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30
Q

What is microvascular angina?

A

Angina with normal coronary arteries.

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31
Q

Non-modifiable risk factors for atherosclerosis

A

Increasing age
Male gender
Family history

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32
Q

What is the gold standard investigation for angina?

A

CT coronary angiogram

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33
Q

What are other investigations for stable angina?

A

ECG
CT coronary angiography
Stress echo
Exercise testing
Myoview scan

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34
Q

Lifestyle management of stable angina

A

Smoking cessation
Exercise
Low cholesterol diet

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35
Q

First-line pharmacological treatment for stable angina

A

Short-acting nitrates e.g GTN spray.
Beta blockers or CCB if contraindicatred.

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36
Q

Pharmacodynamics of nitrates

A

Cause venodilation to reduce preload.

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37
Q

Pharmacodynacmics of beta blockers

A

Prevent activation of B1 adrenergic receptors causing a negative chronotropic and ionotropic effect.

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38
Q

What other drugs are used to treat stable angina?

A

Calcium channel blockers e.g amlodipine
ACE inhibitors e.g ramipril
Statins e.g atorvastatin
NSAIDs e.g aspirin

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39
Q

Side effects of nitrates

A

Headaches due to sudden hypotension.

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40
Q

Side effects of beta blockers

A

Erectile dysfunction, bradycardia, cold extremities, nightmares, headache, fatigue.

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41
Q

Pharmacodynamics of calcium channel blockers

A

Block L-type calcium channels in cardiac and vascular smooth muscle, lowering BP and causing a negative chronotropic + ionotropic effect.

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42
Q

Side effects of calcium channel blockers

A

Postural hypotension, ankle swelling, flushing

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43
Q

Contraindications of beta blockers

A

Asthmatics, heart block, heart failure, bradycardia, PVD

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44
Q

Pharmacodynamics of aspirin

A

Inhibits cyclo-oxygenase 1
This inhibits prostaglandin and thromboxane A2 production.
Prevents platelet aggregation, is anti inflammatory, antipyretic, analgesic.

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45
Q

Side effects of aspirin

A

Gastric ulcers

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46
Q

Pharmacodynamics of statins

A

Inhibits HMG- CoA reductase, the rate limiting enzyme in cholesterol synthesis pathway.

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47
Q

Pharmacodynamics of ACE inhibitors

A

Inhibits angiotensin converting enzyme which converts angiotensin I to II.
Prevents rise in blood pressure.

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48
Q

Interventional management of stable angina.

A

Percutaenous coronary intervention or coronary artery bypass graft.

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49
Q

What are potential graft sources for CABG?

A

Left internal mammary artery for LAD graft.
Long saphenous vein can be used for RCA graft.

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50
Q

Side effects of statins

A

Headache, dizziness, myalgia.

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51
Q

Side effects of ACE inhibitors

A

Hypotension - over
Acute renal failure due to lack of efferent arteriole constriction to reduce glomerular filtration.
Hyperkalaemia - effect of too little aldosterone due to RAAS.
Teratogenic effects in pregnancy - can cause foetal abnormalities.

ACEi can cause increased bradykinin levels.

Dry cough, rash, anaphylactoid reactions.

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52
Q

What is an acute coronary syndrome?

A

A spectrum of acute cardiac conditions from unstable angina to varying degrees of myocardial infarctions.

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53
Q

Investigation for unstable angina

A

ECG
Serum troponin

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54
Q

What can the ECG show in unstable angina?

A

ST depression
T-wave inversion

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55
Q

What will the serum troponin I levels look like in unstable angina?

A

Non-elevated.

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56
Q

What are the 5 types of myocardial infarction?

A

Type 1: MI with ischaemia (due to primary coronary event e.g atherosclerotic rupture)
Type 2: MI secondary to ischaemia (due to increased oxygen demand e.g anaemia, coronary spasm)
Type 3: Diagnosis of MI in sudden cardiac death.
Type 4a: MI related to PCI
Type 4b: MI related to stent thrombosing
Type 5: MI related to CABG

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57
Q

What are the ECG related classifcations of a myocardial infarction?

A

NSTEMI (non-ST elevated myocardial infarction)
STEMI (ST-elevated myocardial infarction)

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58
Q

Clinical presentation of myocardial infarction

A

Unremitting central chest pain
Usually severe but may be mild/absent.
Can radiate to jaw/shoulder.
Occurs at rest.
Associated with sweating, dyspnoea, nausea, vomiting.
One third occur in bed at night.

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59
Q

Pathophysiology of STEMI

A

Full occlusion causes transmural (full thickness) infarction.

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60
Q

Investigation of STEMI

A

ECG - elevated S-T segment and subsequent pathologic Q-wave formation.
Raised serum troponin and creatinine kinase MB
(CK-MB)

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61
Q

Pathophysiology of NSTEMI

A

Can be caused by partial stenosis of major artery/complete occlusion of minor artery.
Causes partial thickness damage - subendocardial infarct

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62
Q

Pathophysiology of NSTEMI

A

Can be caused by partial stenosis of major artery/complete occlusion of minor artery.
Causes partial thickness damage - subendocardial infarct

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63
Q

Investigation of NSTEMI

A

ECG - ST-segment depression, T-wave inversion.
Raised troponin and CK-MB.

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64
Q

First line management of ACS

A

Loading dose of Aspirin 300mg + P2Y12 inhibitor e.g clopidogrel.
Morphine if in severe pain
Oxygen if hypoxic (<94%)
Nitrates for angina pain relief

If ST elevation/raised troponin, refer for PCI.

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65
Q

What is the clinical significance of troponin?

A

Troponins are involved in cardiac excitation contraction coupling.
They are released into the circualtion during mycardial injury and so are a good blood marker.

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66
Q

What are some non-ACS causes for raised troponin?

A

Gram negative sepsis.
Pulmonary embolism.
Myocarditis.
Heart failure
Arrhythmias.

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67
Q

What is the secondary treatment of ACS?

A

Dual antiplatelet therapy
Glycoprotein II/bIIIa antagonists
Antithrombins

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68
Q

Pharmacodynamics of P2Y12 antagonists.

A

Prevents ADP binding to P2Y12 receptors on platelets, inhibiting further platelet activation and aggregation.

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69
Q

Examples of P2Y12 antagonists

A

Clopidogrel, ticagrelor, prasugrel

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70
Q

Side effects of P2Y12 antagonists.

A

Bleeding.
Rash
Diarrhoea

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71
Q

Pharmacodynamics of glycoprotein IIb/IIIa antagonists

A

Inhibits the action of glycoprotein IIb/IIIa which binds fibrinogen and vWF to facilitate platelet aggregation.

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72
Q

Examples of glycoprotein IIb/IIIa antagonists

A

Abciximab, tirofiban

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73
Q

Side effects of glycoprotein IIb/IIIa antagonists

A

Increased bleeding

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74
Q

What situations are glycoprotein IIb/IIIa antagonists mainly used for?

A

In patients with heavey thrombotic burden undergoing PCI.

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75
Q

What does dual antiplatelet therapy consist of?

A

Aspirin + P2Y12 inhibitor.

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76
Q

Examples of antithrombins

A

Unfractionated heparin, enoxaparin (low molecular weight heparin), bivalirudin, fondaparinux.

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77
Q

Pharmacodynamics of heparin

A

Binds to antithrombin III protein which degrades thrombin in the clotting cascade.

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78
Q

Pharmacodynamics of bivalirudin

A

Direct thrombin inhibitor, binds reversibly to thrombin.

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79
Q

Pharmacodynamics of fondaparinux

A

Selectively binds to antithrombin, increasing its activity in inactivating factor Xa to prevent clotting.

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80
Q

When is fondaparinux usually used?

A

Before coronary angiography in unstable angina/NSTEMI.

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81
Q

Positives of PCI

A

Less invasive
More convenient
Repeatable

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82
Q

Negatives of PCI

A

Re-stenosis risk
Stent thrombosis risk
Not applicable for more complex disease

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83
Q

Positives of CABG

A

Good prognosis after surgery
Can resolve complex pathology.

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84
Q

Negatives of CABG

A

Very invasive.
Longer recovery time
Increased risk of stroke

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85
Q

What is the rate of the SA node?

A

60-100 bpm.

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86
Q

What is the rate of the AV node?

A

40-60 bpm

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87
Q

What is the rate of ventricular cells?

A

20-25 bpm

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88
Q

At what speed are EKGs calibrated?

A

Recorded at speed of 25mm/sec

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89
Q

How are EKGs vertically calibrated?

A

1 mm = 0.1mV

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90
Q

What does a positive deflection mean?

A

Impulse is traveling towards the electrode.

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91
Q

What does 1 small square horizontally mean on an ECG?

A

0.04 sec

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92
Q

What does 1 large square horizontally mean on an ECG?

A

0.20 sec

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93
Q

What does 1 large square vertically mean on an ECG?

A

0.5 mV

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94
Q

What voltage do bipolar leads measure?

A

Voltage between 2 different points on the body

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95
Q

What voltage do unipolar leads measure?

A

Voltage between 1 point on the body and a virtual point with 0 electrical potential located in the center of the heart.

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96
Q

What are the leads in an 12 Lead ECG

A

3 limb leads
6 chest leads
3 augmented leads

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97
Q

Where does lead I of an ECG go?

A

Right arm (-) to left arm (+)

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98
Q

Where does lead 2 of an ECG go?

A

Right arm (-) to left leg (+)

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99
Q

Where does lead 3 of an ECG go?

A

Left arm (-) to left leg (+)

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100
Q

What angle is lead 1 in?

A

0 degrees (right horizontal line)

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101
Q

What angle is lead II in?

A

60 degrees (below 0 degrees)

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102
Q

What angle is lead 3 in?

A

120 degrees (below and left from 0 degrees)

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103
Q

Where is lead aVR placed?

A

Right shoulder

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104
Q

Where is lead aVF placed?

A

Left leg

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105
Q

Where is lead aVL placed?

A

Left arm

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106
Q

Which intercostal space are the V1-V3 chest leads placed in?

A

4th intercostal space.

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107
Q

Which lead is to the right of the sternum?

A

V1

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108
Q

What angle is lead avR

A

-150 degrees (up and left from 0 degrees)

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109
Q

What angle is lead avF

A

90 degrees (perpendicular and below 0 degrees)

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110
Q

What angle is lead avL

A

-30 (up from 0 degrees)

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111
Q

Which ECG leads are unipolar?

A

Augmented and chest leads.

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112
Q

Which ECG leads are bipolar?

A

Limb leads.

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113
Q

What is Einthoven’s triangle?

A

An imaginary triangle formed by all 3 limb leads.

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114
Q

Which intercostal space are the V4-V6 leads placed in?

A

5th intercostal space.

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115
Q

Which leads measure activity of the septum?

A

V1-V2

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116
Q

Which leads measure activity of the anterior portion of the heart?

A

V1-V4

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117
Q

Which leads measure activity of the lateral portion of the heart?

A

V5-V6, I, aVL

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118
Q

Which leads measure activity of the inferior portion of the heart?

A

II, III, avF

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119
Q

What does the P-wave symbolise?

A

Atrial depolarization

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120
Q

In which leads is the P-wave always positive?

A

Leads I, II, V2-V6

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121
Q

What is the expected duration of P-waves?

A

<3 small squares (<0.12 sec)

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122
Q

What is the expected amplitude of P-waves?

A

<3 small squares

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123
Q

Which lead are P-waves best seen in?

A

Lead II

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124
Q

What are tall, pointed P-waves (P-pulmonale) an indication of?

A

Right atrial enlargement.

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125
Q

What are M-shaped, biphasic P-waves (P-mitrale) an indication of?

A

Left atrial enlargement.

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126
Q

In which lead are P-waves commonly biphasic NORMALLY?

A

V1

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127
Q

What is a potential cause for right atrial enlargement?

A

Pulmonary hypertension causing right sided hypertrophy resulting in taller P-waves.

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128
Q

What is indicated by the P-R interval?

A

Time taken between atrial depolarization and ventricular depolarization, time taken for electrical activation to get through AV node.

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129
Q

What is the normal P-R interval duration?

A

0.12-0.20 sec (3-5 little squares)

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130
Q

Cause for short P-R interval

A

Wolff-Parkinson-White syndrome

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131
Q

Cause for long P-R interval

A

First degree heart block.

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132
Q

What does the QRS complex indicate?

A

Ventricular depolarization.

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133
Q

What is the normal duration for a QRS complex?

A

<0.12 sec

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134
Q

How does a pathological Q-wave look?

A

Greater than 1 smal square wide, or greater than 25% amplitude of subsequent R-wave.

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135
Q

In which leads should the QRS complex be dominantly upright?

A

I and II.

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136
Q

In which leads must the R-wave grow?

A

V1-V4.

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137
Q

In which leads must the S-wave grow?

A

V1-V3

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138
Q

In which leads will the S-waves become smaller and finally disappear?

A

V4-V6.

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139
Q

Why do the R-waves grow from V1-V4?

A

Left ventricle depolarization is detected more as you progress from V1-V4.

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140
Q

How would left ventricular hypertrophy look on lead V1?

A

Large S-waves, small R-waves.

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141
Q

How would left ventricular hypertrophy look on lead V6?

A

Large R-waves, small/non-existent S-wave.

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142
Q

How would right ventricular hypertrophy look on lead V1?

A

Dominant R wave

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143
Q

How would right ventricular hypertrophy look on lead V6?

A

Large S-wave.

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144
Q

What does the ST segment indicate?

A

Time between ventricular depolarization and repolarization.

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145
Q

What is the appearance of a normal ST-segment?

A

Flat (isoelectric)

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146
Q

In which leads is there NORMAL ST elevation/depression?

A

V1 & V2.

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147
Q

What is the J-point?

A

The junction point between the QRS complex and ST segment.

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148
Q

What can ST elevation indicate?

A

STEMI
Pericarditis - saddle shaped

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149
Q

What could ST depression indicate?

A

NSTEMI, possible unstable angina.

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150
Q

How does the septum depolarize normally?

A

Left side first then goes to right side of septum.

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151
Q

What causes the R-wave in V1?

A

Septal depolarization. Depolarization from left to right causes the current to approach the lead.

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152
Q

What causes the Q-wave in V6?

A

Left to right septal depolarization causes current to go away from the lead.

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153
Q

Why does V1 have a deep S wave and V6 have a high R-wave?

A

Effect of left ventrcle depolarization is greater so current goes away from V1 and towards V6.

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154
Q

What happens during right bundle branch block?

A

Delayed right ventricular depolarization.

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155
Q

What does delayed right ventricular depolarization cause

A

A second R-wave in V1.

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156
Q

What does right bundle branch block look like on an ECG?

A

M-like QRS in V1 and W-like QRS in V6.

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157
Q

What happens in left bundle branch block?

A

Delayed left ventricular depolarization
Right to left septal depolarization.

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158
Q

What is the appearance of left bundle branch block on an ECG?

A

W-like V1 and M-like V6.

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159
Q

What causes the Q-wave in V1 and the initial R-wave in V6 in left bundle branch block?

A

Right to left septal depolarization.

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160
Q

What causes the R-wave in V1 and the S-wave in V6 during left bundle branch block?

A

Right ventricular depolarization.

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161
Q

What causes the S-wave in V1 and second R-wave in V6 during left bundle branch block?

A

Left ventricular depolarization.

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162
Q

What does the T-wave indicate?

A

Ventricular repolarization.

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163
Q

How are T-waves normally oriented?

A

Same orientation as the QRS complex.

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164
Q

In which leads should T waves be upright?

A

I, II, V2-V6

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165
Q

How should the T wave amplitude be?

A

Less than 2/3 of the R wave.

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166
Q

What are some characeristics of abnormal T-waves?

A

Symmetrical, tall, peaked, inverted.

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167
Q

When can T-wave inversion occur?

A

NSTEMI.

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168
Q

What does the QT interval indicate?

A

Duration of ventricular repolarization and depolarization.

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169
Q

What is the normal duration of the QT interval.

A

0.35-0.45 sec (9-11 small squares)
Should not be more than half of R-R interval.

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170
Q

What happens to the QT interval when heart rate increases?

A

It decreases.

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171
Q

What lead is the QT interval normally measured in?

A

aVL.

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172
Q

What do U waves represent?

A

Afterdepolarizations which occur after repolarization.

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173
Q

What leads are U waves seen in?

A

Lead II.

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174
Q

What is the orientation of U waves?

A

Same as T waves.

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175
Q

When are U waves more prominent?

A

During slower heart rates.

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176
Q

In what lead is all the waves inverted?

A

Lead aVR.

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177
Q

What are the 2 methods used to determine heart rate on an ECG?

A

Rule of 300
10 second rule

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178
Q

What is the rule of 300?

A

Dividing 300 by the number of big squares between 2 QRS complexes.

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179
Q

What is the 10 second rule?

A

Since ECGs are printed for 10 second durations, counting the number of QRS complexes (beats) and multiplying by 6 gives HR.

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180
Q

What is the normal QRS axis range?

A

-30 to 90 degrees.

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181
Q

What is meant by left axis deviation?

A

If the axis is deviated to -30 to -90 degrees.

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182
Q

What is meant by right axis deviation?

A

If the axis is deviated to +90 to +180 degrees.

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183
Q

What are 2 methods of determining the QRS axis?

A

Equiphasic approach
4 quadrant approach

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184
Q

What is the quadrant approach?

A

Look at leads I and avF
Determine if the QRS complex is predominantly positive or negative

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185
Q

What happens if both leads are positive?

A

The QRS axis is normal

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186
Q

What happens if lead I is positive and aVF is negative?

A

There is left axis deviation.

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187
Q

What happens if lead I is negative and aVF is positive?

A

There is right axis deviation.

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188
Q

What happens if both are negative?

A

The axis is indeterminate.

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189
Q

What is the equiphasic approach?

A

Determine limb lead with most equiphasic QRS complex.
Find lead 90 degrees to it.

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190
Q

What is pericarditis?

A

inflammatory pericardial syndrome with or without effusion.

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191
Q

Epidemiology of pericarditis

A

80-90% is idiopathic.
Seasonal with viral trends.

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192
Q

General aetiology of pericarditis

A

Viral infection
Bacterial infection
Malignancy
Autoimmune
Metabolic
Trauma
Iatrogenic
Post-MI

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193
Q

What viruses can cause pericarditis?

A

Coxsackieviruses, enteroviruses, adenoviruses, herpesvirues (EBV, CMV, HHV-6), parvovirus-B09

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194
Q

What bacteria can cause pericarditis?

A

Haemophilus influenzae
Mycobacterium tuberculosis

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195
Q

Metastasis from what cancers commonly causes pericarditis?

A

Lung + breast carcinomas, lymphomas.

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196
Q

What are some autoimmune causes of pericarditis?

A

Rheumatoid arthritis, lupus, sjogren syndrome.

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197
Q

What are some metabolic causes of pericarditis

A

Uraemia, myxoedema

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198
Q

What are some traumatic causes of pericarditis?

A

Penetrating thoracic injury, oesophageal perforation, radiation.

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199
Q

What are some iatrogenic causes of pericarditis?

A

PCI, pacemaker insertion.

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200
Q

Clinical presentation of pericarditis

A

Chest pain
Hiccups - phrenic nerve irritation
Dyspnoea

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201
Q

What is the nature of chest pain for pericarditis?

A

Pleuritic chest pain
Exacerbated when lying down and upon inspiration
Releived when sitting forwards
Radiates to trapezius ridge

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202
Q

What is expected upon examination of a patient with pericarditis?

A

Pericardial rub - crunching sound near 2nd heart sound
Pericardial effusion

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203
Q

What can pericardial effusion result in?

A

Cardiac tamponade.

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204
Q

What is the clinical presentation of cardiac tamponade?

A

Beck’s triad
Pulsus paradoxus

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205
Q

What are the components of Beck’s triad?

A

Hypotension, distended neck veins (elevated JVP), muffled heart sounds.

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206
Q

What is pulsus paradoxus?

A

Normally, fall of systolic BP by <10mmHg during inspiration.
In pulsus paradoxus, this fall is >10mmHg during inspiration.

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207
Q

Investigation of pericarditis

A

ECG,
FBC, ESR, troponin
CXR

208
Q

What does pericarditis show on an ECG?

A

Widespread addle shaped ST-elevation, PR depression

209
Q

What will be expected in the FBC & ESR with pericarditis?

A

Raised leukocytes & ESR.

210
Q

What would a raised troponin in pericarditis suggest?

A

Myopericarditis.

211
Q

What could be seen in a CXR with pericarditis?

A

Cardiac silhouette enlargement could be a sign of pericardial effusion. Needs to be ruled out.

212
Q

Management of pericarditis

A

Sedentary activity until resolution of symptoms and normal ECG/labs.
750-1000mg aspirin/600-800mg ibuprofen TDS 1-2 weeks
Along with Colchine 0.5 mg BD for 3 months.

213
Q

What is colchine?

A

Anti-gout agent which is anti-inflammatory.

214
Q

What are the 4 types of cardiomyopathy?

A

Dilated cardiomyopathy, hypertrophic cardiomyopathy, arrythmogenic cardiomyopathy, restrictive cardiomyopathy.

215
Q

Aetiology of Hypertrophic Cardiomyopathy

A

Mutations in genes encoding for sarcomere proteins.
Myosin binding protein C, B-myosin heavy chain.

216
Q

Pathophysiology of Hypertrophic Cardiomyopathy

A

Primary hypertrophy of the heart.

Causes high ejection fraction

Diastolic dysfunction due to low ventricular compliance.

Mycoyte and myofibril disarray

217
Q

What can be obstruced in hypertrophic cardiomyopathy?

A

Left ventricle outflow tract

218
Q

What causes LVOO in hypertrophic caridomyopathy?

A

Systolic anterior motion of mitral valve
Assymetric septal hypertrophy.

219
Q

Clinical Presentation of Hypertrophic Cardiomyopathy

A

Syncope upon exertion
Angina
Dyspnoea
Palpitations

220
Q

Investigation of Hypertrophic Cardiomyopathy

A

ECG
Echocardiography diagnostic

221
Q

What can an ECG show with HC?

A

T-wave inversion
Ventricular tachycardia
Deep S-waves in V1 and large R-waves in V6 due to LVH.

222
Q

What can an echocardiogram show with hypertrophic cardiomyopathy?

A

Assymetric LV hypertrophy.
Mitral valve anterior systolic motion, vigorously contracting LV.

223
Q

Management of hypertrophic cardiomyopathy

A

Cessation of high-intensity athletics
Use of β-blocker or non-dihydropyridine CCBs (eg, verapamil).
ICD (implantable cardioverter defibrillator) insertion

224
Q

What type of drugs should be avoided with HC?

A

Avoid drugs that decrease preload (eg, diuretics, vasodilators).

225
Q

What are the 2 types of dilated cardiomyopathy?

A

Familial and sporadic

226
Q

Aetiology of familial dilated cardiomyopathy

A

Cytoskeleton proteins mutations such as TTN which codes for titin protein

227
Q

Aetiology of sporadic dilated cardiomyopathy

A

Coxsackievirus
Haemochromatosis
Sarcoidosis
Ischaemia
Cocaine

228
Q

Pathophysiology of Dilated Cardiomyopathy

A

Dilation of ventricular chambers
Causes systolic dysfunction, poor contraction & heart failure.

229
Q

Clinical Presentation of Dilated Cardiomyopathy

A

Heart failure
Arrhythmias
Oedema

230
Q

Investigation of dilated cardiomyopathy

A

ECG
Echocardiogram

231
Q

What can an ECG show with DC?

A

Arrythmias
Sinus tachycardia

232
Q

What can can echocardiogram show with DC?

A

LV + RV dilation (thin walls) with poor contraction.

233
Q

Management of dilated cardiomyopathy

A

Standard heart failure treatment.
Na+ restriction
ACE inhibitors/ARBs,
β-blockers, diuretics, mineralocorticoid
receptor blockers (eg, spironolactone), digoxin

ICD, heart transplant.

234
Q

Aetiology of Arrythmogenic Cardiomyopathy

A

AD mutations in genes coding for desmosomes.

Naxos syndrome, Carvajal’s syndrome (recessive forms)

235
Q

Pathophysiology of Arrhythmogenic Cardiomyopathy

A

Atrophy of mainly right ventricular myocardium.
Replaced by fibrous-fatty tissue.

236
Q

Clinical Presentation of Arrhythmogenic Cardiomyopathy

A

Ventricular arrhythmias
Syncope
Sudden death

237
Q

Investigation of Arrythmogenic Cardiomyopathy

A

ECG

238
Q

What can an ECG show in arrythmogenic cardiomyopathy?

A

Epsilon waves after QRS complex
T-wave inversion in V1-V3 since they look at right ventricle.

239
Q

Management of Arrhythmogenic Cardiomyopathy

A

Beta blockers e.g bisporolol, metoprolol.
K+ channel blockers e.g Amiodarone, sotalol - symptomatic
ICD for refractory, life threatening arrhythmias.

240
Q

Aetiology of restrictive cardiomyopathy

A

Post-radiation fibrosis
Loffler’s endocarditis
Endomyocardial fibrosis
Amyloidosis
Sarcoidosis
Haemochromatosis

241
Q

Pathophysiology of Restrictive Cardiomyopathy

A

Bi-atrial enlargement with decreased ventricular volume.
Impaired ventricular filling (diastole).

242
Q

Clinical Presentation of Restrictive Cardiomyopathy

A

Dyspnoea, Fatigue

243
Q

Examination of Restrictive Cardiomyopathy

A

Freidrich’s sign
Kussmaul’s sign

244
Q

What is Freidrich’s sign?

A

Elevated JVP with diastolic collapse.

245
Q

What is Kussmaul’s sign?

A

Increase in venous pressure upon inspiration

246
Q

Investigation of Restrictive Cardiomyopathy

A

ECG

247
Q

Management of Restrictive Cardiomyopathy

A

Manage the heart failure and potential embolisation

248
Q

What are the inherited arrhythmias?

A

Long QT syndrome
Brugada syndrome
Catecholaminergic Polymorphic VT (CPVT)
Wolff-Parkinsone White syndrome
Progressive conduction disease
Idiopathic ventricular fibrillation

249
Q

Aetiology of inherited arrythmias

A

Channelopathies - mutations in channel proteins.

250
Q

Aetiology of long QT syndrome

A

Caused by mutations of KCNQ1 a potassium channel protein.
Congenital: Romano-Ward syndrome
Jervell and Lange-Nielsen syndrome
Acquired: Hypocalcaemia, Amiodarone, MI.

251
Q

Features of Romano-Ward syndrome

A

Autosomal dominant, no deafness.

252
Q

Features of Jervell and Lange-Nielsen syndrome

A

Autosomal recessive, sensorineural deafness.

253
Q

Pathophysiology of long-QT syndrome

A

Problems with repolarization.

254
Q

Aetiology of Brugada syndrome

A

Autosomal dominant loss of function mutation of Na+ channels.

255
Q

How would Brugada syndrome look on an ECG?

A

Pseudo right bundle branch block and ST-segment elevations in leads V1-V2 on ECG.

256
Q

Aetiology of Marfan’s Syndrome

A

Autosomal dominant FBN1 gene mutation on chromosome 15 affecting fibrillin-1 protein.

257
Q

Pathophysiology of Marfan’s Syndrome

A

FIbrillin-1 is a glycoprotein that forms a sheath around elastin and sequesters TGF-β, a growth factor for connective tissue.
Lack of connective tissue structure and growth.

258
Q

Clinical Presentation of Marfan’s Syndrome

A

Very tall, lanky people
Armspan greater than chest
Chest wall deformity
Tendency to have aortic dilation at the root

259
Q

Why does aortic root dilation occur in Marfan’s syndrome?

A

Because more fibrillin is present there since the energy of ventricular contraction is applied there.

260
Q

What are examples of chest wall deformities that can occur with Marfan’s syndrome?

A

Pectus carinatum (pigeon chest)
Pectus excavatum (deep indentation at and around sternum)

261
Q

Pathophysiology of familial hypercholesterolism

A

Decreased LDL signalling due to cholesterol regulatory protein mutatations.

262
Q

What is an example of a protein that can be mutated to cause familial hypercholestrolism?

A

PCSK9

263
Q

Clinical Presentation of FH

A

Cholesterol deposits in eyes and skin.

264
Q

What is the source of oxygen for a foetus inside a mother’s womb?

A

Placenta

265
Q

What vessels carry oxygenated blood from the placenta?

A

Umbilical veins

266
Q

Where does the umbilical vein lead?

A

Liver

267
Q

What is the foetal shunt present in the liver and what does it do?

A

Ductus venosus, shunts oxygenated blood into the IVC

268
Q

What shunt does the blood from the IVC go to once it reaches the heart?

A

Foramen ovale

269
Q

What does the foramen ovale do?

A

Shunts blood from right to left atrium.

270
Q

What vessel does deoxygenated blood pass through to recieve placental oxygen?

A

Umbilical arteries.

271
Q

What happens to the blood entering the RA from the SVC?

A

2/3 gets shunted to the LA, 1/3 enters the RV

272
Q

What shunt is present at the pulmonary artery?

A

Ductus arteriosus

273
Q

What is the function of the ductus arteriosus?

A

Shunts blood from pulmonary artery into aorta, away from the lungs.

274
Q

What is a ventricular septal defect?

A

Abnormal connection between the two ventricles

275
Q

What type of a shunt is in a VSD?

A

Left to right shunt.

276
Q

Why does blood flow from the left to right ventricle?

A

LV is at higher pressure.

277
Q

What happens as a result of a VSD?

A

Increased pulmonary artery blood pressure.

278
Q

What can happen with a small VSD?

A

Small increase in pulmonary blood flow only
Risk of endocarditis.

279
Q

What can happen with a large VSD?

A

Very high pulmonary blood flow in infancy
Can lead to irreversible pulmonary hypertension due to Eisenmanger’s syndrome.

280
Q

Pathophysiology of Eisenmanger’s syndrome

A

High pressure pulmonary blood flow causes pulmonary vessel remodeling and increased pulmonary resistance.
This causes increase in RV pressure.
At a point, RV pressure can become suprasystemic (>LV).
The shunt direction reverses causing deoxygenated blood to be pumped out.

281
Q

What are some consequences of Eisenmanger’s syndrome

A

Cyanosis
Irreversible pulmonary hypertension.

282
Q

Clinical presentation of a small VSD

A

Asymptomatic
Loud pan-systolic murmur

283
Q

Clinical presentation of a large VSD

A

Small, skinny baby
Can be cyanosed and have signs of clubbing.
Increased respiratory rate
Tachycardia

284
Q

What can be heard upon examination of a baby with a small VSD?

A

Pan-systolic murmur

285
Q

Investigation of large VSD

A

Left heart dilation/cardiomegaly on CXR

Echocardiogram

286
Q

Managment of VSD

A

Surgical repair.

287
Q

What are 3 types of atrial septal defects?

A

Ostium secundum defects
Patent forman ovale
Ostium primum defects

288
Q

What is the shunt direction in ASD?

A

Left to right

289
Q

Pathophysiology of a large ASD

A

Significant increased flow through the right heart and lungs in childhood
Right heart dilation

290
Q

Pathophysiology of a small ASD

A

Only a small increase in blood flow.
No right heart dilation

291
Q

Clinical signs of a large ASD

A

Dyspnoea upon exertion
Increased chest infections

292
Q

Clinical signs of a small ASD

A

Asymptomatic

293
Q

Examination of a large ASD

A

Systolic ejection murmur

Fixed, split S2 due to (delayed closure of PV because more blood has to get out)

294
Q

Investigation of a large ASD

A

X-ray: Large pulmonary arteries and cardiomegaly
Echocardiogram

295
Q

Management of ASD

A

Surgical closure or percutaenous (interventional) closure.
Perctutaneous Mainly for secundum defects.

296
Q

What is a patent ductus arteriosus?

A

When ductus arteriosus remains open.

297
Q

Pathophysiology of PDA

A

Due to increased aortic pressure after birth, some blood flows from aorta to PA during systole.

Can cause increased pulmonary hypertension and lead to Eisenmenger’s syndrome if left untreated.

298
Q

What is the shunt direction in PDA?

A

Left to right shunt

299
Q

Clinical presentation of large PDA

A

Machinery like murmur
Dyspnoea
Central cyanosis (ES)
Toe clubbing (ES)

300
Q

Management of PDA

A

Surgical closure.

301
Q

What genetic condition is associated with atrioventricular septal defects?

A

Trisomy 21.

302
Q

What is an atrioventricular septal defect?

A

Defect that involves the interatrial + invterentricular septum and the tricuspid and mitral valves.

303
Q

Pathophysiology of AVSD

A

Can result in a common atrioventricular valve.
Can result in high pulmonary blood flow.

304
Q

Clinical presentation of a complete AVSD

A

Breathless as neonate
Poor weight gain
Poor feeding

305
Q

Clinical presentation of a partial AVSD

A

Can present in adulthood
Can present as if small ASD/VSD

306
Q

Management of AVSD

A

Needs repair or PA band in infancy

307
Q

What is icoarctation of the aorta and what condition is associated with it?

A

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

Turner’s syndrome

308
Q

Pathophysiology of severe aortic coarctation

A

Complete or almost complete obstruction to aortic flow
Can cause heart failure

Blood gets diverted through aortic arch and upper body.

With age, intercostal arteries enlarge in order to provide collateral aortic circulation.

Associated with bicuspide aortic valve.

309
Q

Clinical presentation of aortic coarctation

A

Higher blood pressure in arms vs legs
Weak pulse and radial-femoral pulse delay in lower extremities.

310
Q

Examination of aortic coarctation

A

Scapular bruit upon auscultation - buzzes heard over scapulae

311
Q

Investigation of aortic coarctation

A

CXR - notched ribs due to dilated intercostal vessels.

CT coronary angiogram

312
Q

Management of aortic coarctation

A

Surgical repair

313
Q

Complications of aortic coarctation

A

Hypertension
Subarachnoid haemhorrage (berry aneurysm)
Re-coarctation
Aneurysm formation and rupture.
Heart failure

314
Q

What is the normal formation of the aortic valve?

A

Tricuspid

315
Q

Pathophysiology of bicuspid aortic valves

A

Bicuspid valves generate turbulence and are not as efficient as tircuspid valves.
They can degenerate faster than normal valves.
Can become regurgitate quicker than normal valves.
Can cause ascending aortic aneurysms

316
Q

What is pulmonary stenosis?

A

Narrowing of the right ventricular outflow tract

317
Q

What are the types of pulmonary stenosis?

A

Valvular, sub valvular and supravalvular.

318
Q

Pathophysiology of severe pulmonary stenosis

A

Right ventricular failure as neonate
Poor pulmonary blood flow
RV hypertrophy
Tricuspid regurgitation

319
Q

Pathophysiology of mild pulmonary stenosis

A

RV hypertrophy mainly

320
Q

Management of pulmonary stenosis

A

Balloon valvuloplasty
Open valvotomy
Open trans-annular patch
Shunt (to bypass the blockage)

321
Q

Aetiology of tetralogy of Fallot

A

Caused by anterosuperior displacement of the
infundibular septum which separates right and left ventricular outflow tracts.

322
Q

Components of tetralogy of Fallot

A

Pulmonary stenosis
Right ventricular hypertrophy (as a response to pulmonary stenosis)
Ventricular septal defect
Overriding aorta

323
Q

Pathophysiology of tetralogy of Fallot

A

Pulmonary stenosis causes suprasystemic RV pressure
Results in RV hypertrophy
There is right-left shunting through the VSD.

324
Q

Clinical presentation of tetralogy of Fallot

A

Early cyanosis of babies.

325
Q

Investigation of tetralogy of Fallot

A

Boot shaped heart on CXR.

326
Q

Management of tetralogy of Fallot

A

Surgery to reopen the RVOT and patching of the VSD.

327
Q

What can cause right to left shunts?

A
  1. Truncus arteriosus (1 vessel)
  2. Transposition (2 switched vessels)
  3. Tricuspid atresia (3 = Tri)
  4. Tetralogy of Fallot (4 = Tetra)
  5. TAPVR (5 letters in the name)
328
Q

What type of shunt can result in Eisenmenger’s syndrome?

A

Untreated left to right shunts.

329
Q

What conditions have left to right shunts?

A

VSD, ASD, PDA

330
Q

What physical activity can be used to relieve cyanosis?

A

Squatting, it increases PVR and reduces efficiency of righ to left shunt.

331
Q

What is a univentricular heart?

A

Heart with only 1 ventricle.

332
Q

Aetiology/risk factors for secondary hypertension

A

ROPE

Renal disese
Obesity
Pregnancy
Endocrine - hyperaldosteronism, cushing’s

High salt diet
Increasing age
Male gender

333
Q

Classification of hypertension

A

No hypertension: <135/85
Stage 1: 135/85
Stage 2:150/95

334
Q

Types of BP measurement methods

A

Office/surgery measurement
Ambulatory measurement
At home self-measurement

335
Q

What is malignant hypertension?

A

Sudden onset of high BP that can cause end organ damage.

336
Q

Clinical presentation of malignant hypertension

A

Retinal haemhorrages.

337
Q

Complications of hypertension

A

Ischaemic heart disease (MI)
Heart failure
Kidney failure/CKD
Stroke
Dementia
PVD

338
Q

Treatment Thresholds for HTN

A

For patients at low CV risk, treatment started if above 160/100 mmHg.

For patients at high CV risk, treatment started if above 140/90 mmHg.

Treatment will be lifelong.

339
Q

Target range for BP treatment

A

Routine : <14/90
Prev. stroke: <130/80
Heavy proteinuria: <130/80
CKD & diabetes: <130/80
Older patients: <150/90

340
Q

Why is the BP threshold for older patients higher?

A

If its too low then increased risk of falling over/collapse.

341
Q

Lifestyle management for hypertension

A

Low salt diet.
Weight decrease.
Increased exercise.
Lower alcohol intake.

342
Q

What is the first-line antihypertensive drug for patients under the age of 55 or diabetic?

A

ACE inhibitors e.g ramipril
OR ARB e.g candesartan

343
Q

What is the first-line antihypertensive drug for non-diabetic patients above the age of 55 or of Afro-Carribean descent?

A

CCB ex. amlodipine, verapamil

344
Q

What is the second line antihypertensive treatment?

A

If ACEi/ARB given first, add CCB.
If CCB given first, add ACEi/ARB

345
Q

What is third line antihypertensive treatment?

A

Addition of a thiazide, ex. benzoflumethiazide, hydrochlorothiazide, indapamide.

346
Q

Reasons for resistant hypertension despite treatment

A

Lack of drug concordance for patients.
Lifestyle changes like increased weight gain, drug usage.
Progression of underlying cause of HTN in secondary HTN.

347
Q

General contraindication for antihypertensives

A

General anaesthesia - anaesthetics can cause hypotension, and antihypertensives can interfere with efforts to raise the BP to normal.

348
Q

Drugs with side effects of increased HTN

A

NSAIDs
SNRI
Corticosteroids
Oestrogen containing oral contraceptives
Stimulants like methylphenidate
Anti anxiety drugs e.g gabapentin
Anti TNFs

349
Q

What are the types of aortic stenosis?

A

Supravalvular
Subvalvular
Valvular

350
Q

Congenital aetiology of aortic stenosis

A

Congenital aortic stenosis
Congenital bicuspide valve

351
Q

Acquired aetiology of aortic stenosis

A

Degenerative calcification
Rheumatic heart disease
Congenital bicuspid valves

352
Q

Pathophysiology of aortic stenosis

A

Increased ESV causes increased LV pressure and afterload.
Causes ventricular hypertrophy as a compensatory mechanism.
Long term stenosis can result in LV failure.
Reduced stroke volume.

353
Q

Clinical Presentation of Aortic Stenosis

A

Exertional syncope
Exertional angina: (increased myocardial oxygen demand; demand/supply mismatch)
Exertional dyspnoea due to heart failure (systolic and diastolic)

354
Q

Examination of aortic stenosis

A

Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus) - slow rising small volume pulse.

Soft or absent second heart sound since valve becomes rigid and doesnt move
S4 gallop due to LVH.
Crescendo-decrescendo jection systolic murmur radiating to carotids.

355
Q

Investigation of aortic stenosis

A

CXR
ECG
Echocardiography

356
Q

What would be expected on an X-ray for aortic stenosis?

A

Dilated ascending aorta

357
Q

What could be seen on an ECG for aortic stenosis

A

ST-segment depression and T-wave inversion for leads orientated towards LV (I, aVL, V5-V6).

358
Q

General management of aortic stenosis

A

Fastidious dental hygiene / care
Consider IE prophylaxis in dental procedures

359
Q

What medication is contraindicated in aortic stenosis?

A

Vasodilators are relatively contraindicated in severe AS

360
Q

Interventional management of aortic stenosis

A

Aortic valve replacement surgery
TAVI – Transcatheter Aortic Valve Implantation

361
Q

What are the indications for interventional treatment of aortic stenosis?

A

Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise)
Any patient with decreasing EF (<50%).
Any patient undergoing CABG
If asymptomatic but adverse features on exercise testing.

362
Q

What is aortic regurgitation?

A

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

363
Q

Aetiology of Aortic Regurgitation

A

Bicuspid aortic valve
Rheumatic fever
Infective endocarditis
Marfan’s syndrome

364
Q

Pathophysiology of Aortic Regurgitation

A

Combined pressure and volume overload

Compensatory Mechanisms: LV dilation, LVH.

Progressive dilation leads to heart failure

365
Q

eExamination of Aortic Regurgitation

A

Early diastolic murmur

Austin flint murmur (apex) - low pitched late diastolic murmur.

Corrigan’s pulse - bounding carotid pulses.

366
Q

Investigation of aortic regurgitation

A

CXR: enlarged cardiac silhouette and aortic root enlargement
ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function (cornerstone for decision making and follow up evaluation)

367
Q

General management of aortic regurgitation

A

Consider IE prophylaxis

368
Q

Medical management of aortic regurgitation

A

Vasodilators (ACEI’s potentially improve stroke volume and reduce regurgitation but indicated only in CCF or HTN

Serial Echocardiograms: to monitor progression.

369
Q

Surgical management of aortic regurgitation

A

Valve replacement

370
Q

Indication for surgery treatment of aortic regurgitation

A

ANY Symptoms at rest or exercise

Asymptomatic treatment if:
EF drops below 50% or LV becomes dilated > 50mm at end systole

371
Q

What is mitral valve stenosis?

A

Obstruction of LV inflow that prevents proper filling during diastole

372
Q

What is the normal mitral valve area?

A

4-6 cm^2

373
Q

At what lower mitral valve area threshold do patients become symptomatic?

A

2 cm^2

374
Q

Aetiolgy of mitral stenosis

A

Rheumatic heart disease
Infective endocarditis
Mitral annular calcification

375
Q

Pathophysiology of Mitral Stenosis

A

To maintain CO, LA pressure is increased causing LA hypertrophy.
Results in PV, PA and RA pressure increasing.
Can cause hemoptysis through bronchial vessel rupturing due to increased pulmonary pressure.

376
Q

Clinical Presentation of Mitral Stenosis

A

Progressive dyspnoea
Malar rash - pink/purple patches on cheeks due to vasoconstriction.
Jugular venous distension
Palpitations

377
Q

Examination of mitral stenosis

A

A wave in venous jugular pulsations.

Low-pitched mid-diastolic rumble most prominent at the apex.
Loud opening S1 snap: heard at the apex when leaflets are still mobile

378
Q

Investigation of Mitral Stenosis

A

ECG: may show atrial fibrillation and LA enlargement
CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV
ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area

379
Q

Medical management of mitral stenosis

A

Serial echocardiography (frequency proportional to severity)

B-blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling

Furosemide for fluid overload

380
Q

Surgical management of mitral stenosis

A

Percutaneous mitral balloon valvotomy.

ANY SYMPTOMATIC Patient with NYHA Class III or IV Symptoms

Asymptomatic moderate or Severe MS with a pliable valve suitable for PMBV

381
Q

What is mitral regurgitation?

A

Backflow of blood from the LV to the LA during systole

382
Q

Aetiology of Mitral Regurgitation

A

Myxomatous degeneration (MVP)
Ischemic heart disease
Rheumatic heart disease
Infective Endocarditis
Marfan’s

383
Q

Pathophysiology of acute mitral regurgitation

A

Regurgitation causes left atrial dilation and pressure.

Can lead to increased PV pressure and pulmonary hypertension /oedema + RVH.

Decreaed EDV causing VH to increase SV to maintain cardiac output.

384
Q

Clinical Presentation of Mitral Regurgitation

A

Exertional dyspnoea/ orthopnea
Fatigue, lethargy

385
Q

Examination of Mitral Regurgitation

A

Pansystolic high-pitched murmur at the apex radiating to the axilla

Prominent S3 (CHF/LA overload)

386
Q

Investigation of Mitral Regurgitation

A

ECG: LV hypertrophy, atrial fibrillation
CXR: LA, LV, PA enlargement.
ECHO: Estimation of LA, LV size and function. Valve structure assessment, papillary muscle rupture.

387
Q

Medical Management of Mitral Regurgitation

A

Rate control for atrial fibrillation with B-blockers, CCB, digoxin
Anticoagulation in atrial fibrillation and flutter
Nitrates / Diuretics in acute MR

Serial echos
I.E prophylaxis.

388
Q

Surgical management of Mitral Regurgitation

A

ANY Symptoms at rest or exercise (repair if feasible)

Asymptomatic:
If EF <60%, LVES Dimension >40mm
If new onset atrial fibrillation/raised PAP >50 mmHg

389
Q

Aetiology/Risk Factors for infective endocarditis

A

Dental procedures/lack of dental hygiene.
Abnormal native valves
Prosthetic valve replacement
Intravenous drug use
Previous history of I.E
GI/GU procedures
Device implantation such as pacemakers, etc.

390
Q

What organism is most likely to cause infection from dental procedures/lack of dental hygiene.

A

S.viridans - a-haemolytic, optochin resistant

391
Q

What organisms are most likely to cause infection from abnormal native valves & prosthetic valve replacement

A

S.aureus, s.epidermidis

392
Q

What organism is most likely to cause infection from IV druge use?

A

S.aureus, pseudomonas aeruginosa, Candida fungi.

393
Q

What organism is most likely to cause infection from GI/GU procedures?

A

Enteroccoci

394
Q

What organism is most likely to cause infection from device implantation?

A

S.aureus, s.epidermidis

395
Q

What side of the heart is most likely to be infected with IV drug use?

A

Right side since circulating blood with infection comes through right atrium.

396
Q

Pathphysiology of infective endocarditis

A

Damaged endocardium promotes platelet and fibrin deposition, which allows organisms to adhere and grow, leading to an infected vegetation.

397
Q

Which valve is ost commonly affected in infective endocarditis?

A

Tricuspid valve

398
Q

Clinical presenetation of infective endocarditis

A

Signs of systemic infection (fever, sweats, etc)
Embolisation: stroke, P.E, osteomyelitis.
Valve dysfunction
Petechiae
Splinter hemorrhages
Osler’s nodes
Janeway lesions
Roth spots on fundoscopy.

399
Q

What are petechiae?

A

Tiny, round spots that appear on the skin as a result of subcutaenous bleeding

400
Q

What are splinter haemhorrages?

A

Thin reddish lines of blood under the nails.

401
Q

What are Osler’s nodes?

A

Small, tender, painful, purple, raised nodules usually found on the fingers and toes.

402
Q

What are Janeway lesions?

A

Painless flat lesions on palms/soles.

403
Q

What ar Roth spots?

A

Retinal haemorrhagic lesions with pale centers

404
Q

What are the 2 major criteria in the modified dukes criteria?

A

Pathogen grown from blood cultures
Evidence of endocarditis on echo, or new valve lea

405
Q

What are the 5 minor criteria in the modified dukes criteria?

A

Predisposing factors
Fever
Vascular phenomena
Immune phenomena
Equivocal blood cultures

406
Q

Investigation of infective endocarditis

A

Blood cultures - raised c-reactive protein.
Echocardiography - visualize vegetation.

407
Q

Management of infective endcarditis

A

Antibiotics to treat the infection
Treating any rhythm issues
Surgery

408
Q

Indications for surgery for infective endocarditis

A

The infection cannot be cured with antibiotics (ie recurs after treatment, or CRP doesn’t fall)
Complications (aortic root abscess, severe valve damage
To remove infected devices (always needed)
To replace valve after infection cured (may be weeks/months/years later
To remove large vegetations before they embolise

409
Q

Complications of infective endocarditis

A

Arrythmias
Pulmonary embolism
Stroke
Cataract

410
Q

What organism can cause cataracts in infective endcoarditis?

A

Candida fungi

411
Q

What can cause P.Es, stroke and cataracts ininfective endocarditis?

A

Vegetation breaking off and floating as an embolus in circulation.

412
Q

What antibiotic treatment would be used for a s.aureus infective endocarditis?

A

Flucloxacillin and gentamicin

413
Q

What antibiotic treatment would be used for a MRSA infective endocarditis?

A

Vancomycin and gentamicin

414
Q

What antibiotic treatment would be used for a s.viridans/s.epidermidis infective endocarditis?

A

Penicillin and gentamicin

415
Q

What antibiotic treatment would be used for a enterococcus infective endocarditis?

A

Amoxicillin and gentamicin

416
Q

Aetiology of atrial fibrillation

A

Hypertension, heart failure, rheumatic heart disease, hyperthyroidism, alcohol intoxication.

417
Q

How would atrial fibrillation present on an ECG?

A

Irregularly irregular atrial rhythm, absent P waves.

418
Q

Pathophysiology of atrial fibrillation

A

Rapid atrial firing results in no mechanical coordination.
Irregula/rapid ventricular response.

419
Q

Management of atrial fibrillation

A

If unstable - DC cardioversion

If stable:

If symptoms < 48 hours, rhythm/rate control
If symptoms >48 hours, rate control + anticoagulation

420
Q

What are the 2 types of cardioversion?

A

Electric and pharmacological (amiodarone, fleicanide)

421
Q

What is the guideline of cardioversion for atrial fibrillation?

A

Immediate cardioversion if presenting within 48 hours.

If presenting after 48 hours - anticoagulate, give beta blockers for 3 weeks then cardioversion.
Done to prevent risk of AF thrombus formation.

422
Q

What drugs could be used for rate control in atrial fibrillation?

A

Calcium channel blockers
Beta blockers
Cardiac glycosides - digoxin

423
Q

What could be done for rhythm control in atrial fibrillation?

A

Amiodarone and fleicanide.

DC cardioversion

424
Q

Pharmacodynamics of class Ia antiarrhythmic drugs

A

Moderate sodium channel blockers

425
Q

Examples of class Ia antiarrhythmic drugs

A

Quinidine, procainamide, disopyramide

426
Q

Pharmacodynamics of class Ib antiarrhythmic drugs

A

Weak sodium channel blockers

427
Q

Examples of class Ib antiarrhythmic drugs

A

Lidocaine, phenytoin

428
Q

Pharmacodynamics of class Ic antiarrhythmic drugs

A

Strong sodium channel blockers

429
Q

Examples of class Ic antiarrhythmic drugs

A

Flecainide, propafenone

430
Q

Pharmacodynamics of class II antiarrhythmic drugs

A

Beta blockers

431
Q

Pharmacodynamics of class III antiarrhythmic drugs

A

Potassium channel blockers

432
Q

Examples of class III antiarrhythmic drugs

A

Amiodarone, sotalol

433
Q

Pharmacodynamics of class IV antiarrhythmic drugs

A

Calcium channel blockers

434
Q

Examples of class III antiarrythmic drugs

A

Verapamil, diltiazem.

435
Q

What score isued to calculate the risk of stroke after atrial fibrillation?

A

CHA2DS2-VASc score

436
Q

If the CHA2DS2-VASc score is >1 or 2, what treatment should be considered?

A

Administratin of direcot oral anticoagulants (DOACs) or warfarin.

437
Q

How would atrial flutter appear on an ECG?

A

Regularly irregular rhythm.
Sawtooth like rhythm between QRS complexes.

438
Q

Pathophysiology of atrial flutter

A

Increased automaticity causes constant atrial firing.

439
Q

Interventional mangement of atrial flutter and atrial fibrillation

A

Catheter ablation

440
Q

Clinical presentation of atrial fibrillation/flutter

A

Palpitations, dyspnoea, fatigue, lightheadedness.

441
Q

What are the 2 types of supraventricular tachycardia?

A

Atrioventricular nodal re-entrant tachycardia (AVNRT)
Atrioventricular re-entrant tachycardia (AVRT)

442
Q

Pathophysiology of AVNRT

A

Slow conduction through AV node but fast conduction when coming back up form the ventricles to AV node.

443
Q

How would AVNRT look on an ECG?

A

Absent P-waves, thin QRS complex.

444
Q

Aetiology of AVRT

A

Accessory pathway (bundle of Kent)

445
Q

Pathophysiology of AVRT

A

Accessory pathway allows bypassing of AV node to cause pre-excitation of ventricles.

446
Q

How would AVRT look on a ECG?

A

Short PR interval
B roader QRS complexes
Slurred beginning of QRS complex known as delta wave.

447
Q

Example of AVRT

A

Wolff-Parkinson-White syndrome

448
Q

Management of supraventricular tachycardias?

A

Vagal manoeuvres
IV adenosine

449
Q

What are examples of vagal maneouvres?

A

Carotid massage
Valsalva manoeuvre

450
Q

Pathophysiology of isolated ectopic atrial beats

A

Origin of beat is not in SAN, can result in early beats being present.

451
Q

How would isolated ectopic atrial beats look on an ECG?

A

Series of normal PQRST complexes with one occassionally having differently shaped P-wave.

452
Q

Aetiology of isolated ectopic atrial beats

A

Secondary to adrenergic drive, so caffiene consumption.

453
Q

Pathophysiology of isolated ectopic ventricular beats

A

Beat origin is outside of the His-Purkinje system and can cause slighly slower but earlier ventricular depolarization.

454
Q

How would an isolated ventricular ectopic beat look on an ECG?

A

Wider QRS, no P wave, between normal QRS complexes.

455
Q

Aetiology of isolated ventricular ectopic beats

A

Underlying heart disease, e.g MI

456
Q

What is ventricular tachycardia?

A

Abnormally fast beating of the ventricles in a regular manner.

457
Q

Pathophysiology of ventricular tachycardia

A

Shortened diastole does not allow for adequarte ventricular filling.

458
Q

How would ventricular tachycardia look on an ECG?

A

Regularly irregular, broad QRS complexes

459
Q

Clinical presentation of ventricular tachycardia

A

Angina, palpitations, dyspnoea.

460
Q

Management of ventricular tachycardia

A

Beta blockers - esmolol
DC cardioversion if still unstable.

461
Q

What is ventricular fibrillation?

A

This involves very rapid and irregular ventricular activation with no cardiac output.

462
Q

How would ventricular fibrillation look on an EG?

A

Disorganized rhythm with no identifiable waves.

463
Q

Pathphysiology of ventricular fibrillation

A

Lack of CO results in patients going into cardiac arrest if left untreated.

464
Q

Management of ventricular fibrillation

A

Electrical defibrillation

465
Q

Aetiology of ventricular fibrillation

A

MI, cardiomyopathy,

466
Q

What is torsades de pointes?

A

Polymorphic ventricular tachycardia.

467
Q

Aetiology of torsades de pointes

A

Drug-induced long QT syndrome

468
Q

How would Torsades de pointes look on an ECG?

A

Shifting sinusoidal waveforms.

469
Q

Management of long QT syndrome and torsades de pointes

A

IV Magnesium sulfate.

470
Q

When would unsynchronized and synchronized DC cardioversion be used?

A

Unsynch: VF, or pulseless

471
Q

What would a first degree heart block look like on an ECG?

A

PR interval >200ms

472
Q

Aetiology of first degree heart block

A

Hypokalaemia, inferior MI, myocarditis

473
Q

What are the classifcations of 2nd degree heart block?

A

Mobitz type 1 and tye 2

474
Q

How would a mobitz type 1 heart block look on an ECG?

A

Progressive lengthening of PR interval until a p wave with no QRS complex.

475
Q

How would a mobitz type 2 heart block look on an ECG?

A

Uniform PR interval with some p waves without QRS complexes.

476
Q

Where would a lesion be for a mobitz type 1 heart block?

A

AV node

477
Q

Where would a lesion be for a mobitz type 2 heart block?

A

Bundle of His

478
Q

Which Mobitz block type has a higher risk of progressing to complete heart block?

A

Mobitz type 2

479
Q

What is third degree heart block?

A

Complete heart block

480
Q

Pathophysiology of third degree heart block

A

Atrial activity does not conduct to ventricles.
Ventricles contract through spontaenous escape rhythm.

Can be caused by RCA infarct since it supplies AV node.

481
Q

How would third degree heart block look on an ECG?

A

Dissocated P waves and QRS complexes. Atrial rate > ventricular rate.

482
Q

Aetiology of Mobitz type 1 block

A

Inferior MI, AV blocking drugs (CCB, BB, digoxin)

483
Q

Aetiology of Mobitz type 2 block

A

Anterior MI, rheumatic fever, lyme disease.

484
Q

Aetiology of third degree heart block

A

Structural heart disease, hypertension, endocarditis.

485
Q

Interventional management for second and third degree heart block

A

Pacemaker insertion

486
Q

Medical management for bradycardia

A

IV atropine 500mg

487
Q

How would hyperkalaemia present in an ECG?

A

Tall, tented T- waves, small P-waves, wide QRS complex.

488
Q

How would hypokalaemia present in an ECG?

A

Small T waves, PR elongation, ST depression,

489
Q

What is an electrical storm?

A

3 more sustained episodes of VF/VT.

490
Q

Management of electrical storm

A

– Correct any provoking factors e.g. electrolyte
(K/Mg), ischaemia, infection, heart failure
– Beta blockers, sedation
– Amiodarone +/- lignocaine

491
Q

What is heart failure?

A

An inability of the heart do deliver blood and O2 at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures.

492
Q

Aetiology of heart failure

A

IHD
Excess alcohol consumption
Dilated cardiomyopathy
Valvular heart disease

493
Q

Types of heart failure

A

Systolic heart failure (heart failure with reduced ejection fraction, EF<40%)
Diastolic heart failure (heart failure with preserved ejection fraction, EF>50%)
Right systolic heart failure

494
Q

Aetiology of heart failure

A
495
Q

Symptoms of heart failure

A

Exertional dyspnoea, orthopnea, fatigue, weight gain, paroxysmal nocturnal dyspnoea, pink frothy sputum.

496
Q

Examination of heart failure

A

Elevated JVP, peripheral oedema, ascites.

497
Q

What would be heard upon auscultation of heart failure?

A

Displaced apex beat, third and fourth heart sounds, bi-basal crackles.

498
Q

What is the NYHA classifcation of heart failure?

A

Class I: No limitation (Asymptomatic)
Class II: Slight limitation (mild HF)
Class III: Marked limitation (Symptomatically moderate HF)
Class IV: Inability to carry out any physical activity without discomfort (symptomatically severe HF)

499
Q

Which clinical presentations are specific to left heart failure?

A

Orthppnoea, paroxysmal nocturnal dyspnoea, pulmonary oedema

500
Q

Which clinical presentations are specific to right heart failure

A

Congestive hepatomegaly, jugular venous distension, peripheral oedema.

501
Q

Management of heart failure

A

Symptomatic - loop diuretic

Guideline:
ACE inhibitor/ARB
Beta blocker
Mineralocorticoid receptor antagonist - spironolactone
SGLT2 inhibitor - osmotic diuresis so reduces preload.

502
Q

Investigation of heart failure

A

FL: Brain natriuretic peptide - elevated in HF
FBC, U + E, LFT, TFT
CXR - ABCDE
ECG
Transthoracic echo - GOLD STANDARD DIAGNOSTIC

503
Q

What are signs of heart failure in a CXR?

A

A: alveolar oedema (perihilar/bat-wing opacification)
B: Kerley B lines (interstitial oedema)
C: cardiomegaly (cardiothoracic ratio >50%) – may be difficult to assess on an AP film
D: dilated upper lobe vessels
E: effusions (i.e. pleural effusions – blunted costophrenic angles with meniscus sign)

504
Q

Clinical presentation of heart blocks

A

Dizziness, syncope, fatigue, dyspnoea.

505
Q

Pharmacodynamics of thiazide like diuretics

A

Inhibits on the NaCl co-transporter in the DCT

506
Q

Examples of thiazide like diuretics

A

Benzoflumethiazide, hydrochlorothiazide, indapamide.

507
Q

Pharmacodynamics of loop diuretics

A

Inhibits the NKCC transporter in the thick ascending loop of henle.

508
Q

Examples of loop diuretics

A

Furosemide, torsemide

509
Q

Examples of potassium-sparing diuretics

A

Spironolactone, eplerenone

510
Q

Side effects of diuretics

A

Hypotension
Hyponatraemia
Hypokalaemia
Raised uric acid - gout

511
Q

Side effects of spironolactone

A

Gynaecomastia

512
Q

What drug options are available for people with resistant hypertension (HTN despite 3 drugs)

A

Beta blockers - not for those on aspirin
Spironolactone

513
Q

Investigation of cardiac tamponade

A

CXR: Cardiomegaly
ECG: Low voltage QRS
Echocardiogram (GS) - late diastolic atrial collapse

514
Q

Management of cardiac tamponade

A

Pericardiocentesis

515
Q

What is the threshold of diagnosis of hypertension in clinic?

A

Over 140/90 mmHg

515
Q

Exmination of HC

A

Ejection systolic murmur- can be due to mitral valve obstruction

S4 sound due to LVH

Sirpi's Phase 2A Medicine (13 decks)

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