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CVS Flashcards

1
Q

What is an ECG?

A

representation of the electrical events of the cardiac cycle

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2
Q

What 6 things can you identify with an ECG?

A
  1. arrhythmias
  2. myocardial ischaemia and infarction
  3. pericarditis
  4. chamber hypertrophy
  5. electrolyte disturbances
  6. drug toxicity (digoxin/ drugs which prolong QT interval)
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3
Q

What is the SA node?

A
  • dominant pacemaker
  • intrinsic rate 60-100bpm
  • fastest depolarising tissue
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4
Q

What is the normal heart rate?

A

60-100bpm

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5
Q

What is the AV node?

A
  • back up pacemaker

- intrinsic rate 40-60 bpm

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6
Q

What are ventricular cells?

A
  • back up pacemaker

- intrinsic rate 20-45bpm

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7
Q

What is the impulse conduction pathway?

A

sinoatrial node - atrioventricular node - bundle of His - bundle branches - purkinje fibres

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8
Q

AV node delay at beginning of a normal ECG trace - how long is it?

A

0.12 - 0.2 s

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9
Q

How long is atrial depolarisation (ECG) ?

A

0.08 - 0.1 s

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10
Q

How long is ventricular depolarisation (ECG)?

A

0.06 - 0.1 s

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11
Q

P wave

A
  • atrial depolarisation

- seen in every lead except aVR

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12
Q

PR interval

A
  • time taken for atria to depolarise and electrical activation to get through AV node
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13
Q

QRS complex

A
  • ventricular depolarisation

- still called QRS even if Q and/or S missing depending on what lead

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14
Q

ST segment

A

interval between depolarisation and repolarisation

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15
Q

T wave

A

ventricular repolarisation

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16
Q

Tachycardia

A

increased heart rate

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17
Q

Bradycardia

A

decreased heart rate

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18
Q

Dextrocardia

A

heart on right side of chest instead of left

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19
Q

Acute anterolateral myocardial infarction

A

ST segments are raised in anterior (V3-V4) and lateral (V5-V6) leads

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20
Q

Acute inferior MI

A

ST segments raised in inferior (II, III, aVF) leads

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21
Q

Can atrial repolarisation be seen on an ECG?

A

No- not usually seen, occurs at same time as QRS complex so hidden

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22
Q

IMPORTANT - ECG paper, value of one small box horizontally?

A

0.04s / 40ms

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23
Q

IMPORTANT - ECG paper, value of one large box horizontally?

A

0.20s

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24
Q

IMPORTANT - ECG paper, value of one large box vertically?

A

0.5mV

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25
Q

Left ventricle definition?

A
  • Palpated in 5th intercostal space and mid clavicular line

- Responsible for apex beat

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26
Q

Stroke volume definition?

A

The volume of blood ejected from each ventricle during systole

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27
Q

Cardiac output definition?

A

The volume of blood each ventricle pumps as a function of time eg litres per min

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28
Q

IMPORTANT - cardiac output equation

A

CO (L/min) = stroke volume (L) x heart rate (bpm)

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29
Q

Total peripheral resistance definition?

A

The total resistance to flow in systemic blood vessels from beginning of aorta to vena cava (arterioles provide most resistance)

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30
Q

Preload definition?

A

The end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions under variable physiologic demand

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31
Q

End diastolic volume definition?

A

How much blood is in the ventricles before it pumps

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32
Q

When veins dilate does this result in an increase or decrease in preload?

A

Decrease in preload - venous return has decreased

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33
Q

Afterload definition

A

The pressure the left ventricle must overcome to eject blood during contraction (dilate arteries = decrease afterload)

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34
Q

Contractility definition

A

force of contraction and change in fibre length - how hard the heart pumps (when muscle contracts myofibrils stay same length but sarcomere shortens - force of heart contraction that is independent of sarcomere length

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35
Q

Elasticity definition

A

myocardial ability to recover normal shape after systolic stress

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36
Q

Diastolic dispensibility definition

A

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

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37
Q

Compliance definition

A

how easily the heart chamber expands when filled with blood volume

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38
Q

Starlings law ?

A

Force of contraction is proportional to the end diastolic length of cardiac muscle fibre - the more ventricle fills harder it contracts

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39
Q

At rest is the cardiac muscle at optimal length?

A

No, force of contraction decreased, inefficient

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40
Q

What happens when there is increased venous return to the heart?

A

increase venous return - increase end diastolic volume - increase preload - increase sarcomere stretch - increase force of contraction - increase stroke volume

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41
Q

What happens to venous return when standing?

A

Decreases venous return due to gravity - cardiac output decreases - drop in blood pressure - stimulating baroreceptors to increase blood pressure

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42
Q

Heart sound S1 ?

A

mitral and tricuspid valve closure

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43
Q

Heart sound S2?

A

aortic and pulmonary valve closure

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44
Q

Heart sound S3?

A
  • in early diastole
  • during rapid ventricular filling
  • normal in children, pregnant women
  • associated with mitral regurgitation and heart failure
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45
Q

Heart sound S4?

A
  • ‘gallop’
  • in late diastole
  • produced by blood being forced into a stiff, hypertrophic ventricle
  • associated with left ventricular hypertrophy
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46
Q

Which coronary arteries commonly develop atheroscleroses?

A
  • right coronary artery
  • left anterior descending
  • circumflex
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47
Q

7 risk factors for atherosclerosis?

A
  • age
  • family history
  • high serum cholesterol
  • tobacco (endothelium erosion)
  • obesity (more pericardial fat, thus increase inflammation)
  • diabetes (hyperglycaemia damages endothelium)
  • hypertension
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48
Q

Distribution of atherosclerotic plaques?

A
  • Peripheral and coronary arteries

- Focal distribution along artery length

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49
Q

An atherosclerotic plaque is a complex lesion of what 4 things?

A
  • lipid
  • necrotic core
  • connective tissue
  • fibrous ‘cap’
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50
Q

2 serious consequences of an atherosclerotic plaque?

A
  • occlude vessel lumen - restriction of blood flow - angina

- rupture - thrombus formation - death

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51
Q

atherosclerosis formation - stage 1

A

initiated by injury to endothelial cells, leads to endothelial dysfunction

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52
Q

Atherosclerosis formation - stage 2

A

chemoattractants released from endothelium to attract leucocytes which accumulate and migrate into vessel wall

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53
Q

What are chemoattractants?

A

Chemicals which attract leucocytes. They are released from the site of injury and a conc gradient is produced

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54
Q

3 inflammatory cytokines found in plaques?

A
  • IL-1 (key one)
  • IL-6
  • IFN-gamma
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55
Q

Atherosclerosis - fatty streaks

A
  • earliest lesion of atherosclerosis
  • appear at very early age (less than 10)
  • aggregations of lipid laden macrophages and T lymphocytes within intimal layer of vessel wall
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56
Q

Atherosclerosis - intermediate lesions

A 
layers of 
lipid laden macrophages (foam cells) 
vascular smooth muscle cells 
T lymphocytes 
(there is adhesion and aggregation of platelets to vessel wall)
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57
Q

Atherosclerosis - fibrous plaques/ advanced lesions

A
  • impede blood flow
  • prone to rupture
  • covered by dense fibrous cap of extracellular matrix proteins - collagen (strength) - elastin (flexibility) laid down by smooth muscle cells that overly lipid core and necrotic debris
  • may be calcified
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58
Q

Atherosclerosis - fibrous plaques/ advanced lesions contain?

A
  • smooth muscle cells
  • macrophages and foam cells
  • T lymphocyte
  • Red cells
  • filled with fibrin
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59
Q

What is a foam cell?

A

lipid laden macrophage

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60
Q

Plaque rupture

A
  • plaque constantly growing and receding
  • fibrous cap needs to be resorbed and redeposited in order to be maintained
  • if balance shifts eg in favour of inflammatory conditions (increase enzyme activity) cap weakens, plaque ruptures
  • basement membrane, collagen, necrotic tissue exposure, haemorrhage of vessel within plaque
  • thrombus formation, vessel occlusion
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61
Q

Angina - definition

A
  • Chest pain or discomfort as a result of reversible myocardial ischaemia
  • Usually implies narrowing one/more coronary arteries
  • Usually exacerbated by exertion and relieved by rest
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62
Q

2 types of angina

A
  • Stable angina - induced by effort, relieved by rest
  • Unstable (crescendo) angina - recent (less 24hrs) onset OR deterioration stable angina (symptoms frequently occurring at rest) OR angina increasing frequency or severity, minimal exertion, at rest - form of acute coronary syndrome
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63
Q

3rd rare type of angina?

A

Prinzmetal’s angina - caused by coronary artery spasm

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64
Q

Angina epidemiology

A

Myocardial ischaemia resulting in angina occurs when mismatch between blood supply and metabolic demand - due to:

  • atheroma/ stenosis coronary arteries
  • valvular disease
  • aortic stenosis
  • arrhythmia
  • anaemia
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65
Q

Most common cause of angina?

A

atheroma/ stenosis of coronary arteries thereby impairing blood flow

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66
Q

What causes the pain in angina?

A

Ischaemic metabolites eg adenosine stimulate nerve endings and produce pain

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67
Q

Is angina more common in men or women?

A

Men

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68
Q

Angina 9 risk factors?

A
  • smoking
  • sedentary lifestyle
  • obesity
  • hypertension
  • diabetes mellitus
  • family history
  • genetics
  • age
  • hypercholesterolaemia
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69
Q

Pathophysiology of angina

A

atherosclerosis developing narrowing of coronary arteries that results in ischaemia and thus pain

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70
Q

pathophysiology of angina - initiation

A
  • endothelial dysfunction/ injury at sites of sheer/ damage –> lipid accumulation at sites impaired endothelial barrier
  • local cellular proliferation, incorporation oxidised lipoproteins
  • mural thrombi on surface - subsequent healing, repeat of cycle
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71
Q

pathophysiology of angina - adaptation

A
  • as plaque progresses to 50% vascular lumen size, vessel no longer compensate by remodelling, becomes narrowed
  • drives variable cell turnover within plaque, new matrix surfaces, degradation matrix
  • may progress to unstable plaque
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72
Q

pathophysiology of angina - clinical stage

A
  • plaque continues encroach upon lumen, risk of haemorrhage/ exposure tissue to HLA-DR antigens, may stimulate T cell accumulation
  • rives inflamm reaction to part of plaque
  • complications:ulceration, fissuring, calcification, aneurysm change
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73
Q

pathophysiology angina - pathophysiological stages - fatty streak

A
  • foam cells

- smooth muscle cells filled with fat

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74
Q

pathophysiology of angina - pathophysiological stages - intimal cell mass

A

collections of muscle cells and connective tissue without lipids - ‘cushions’

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75
Q

pathophysiology of angina - pathophysiological stages - the atheromatous plaque

A
  • distorted endothelial surface with lymphocytes, macrophages, smooth muscle cells, variably complete endothelial surface
  • local necrotic and fatty matter, scattered foam cells
  • evidence local haemorrhage: iron deposition, calcification
  • complicated plaques: calcification, mural thrombus- vulnerable to rupture
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76
Q

what is a complicated plaque?

A

show calcification and mural thrombus (making them vulnerable to rupture)

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77
Q

Angina - complications of plaque rupture

A
  • acute occlusion due to thrombus
  • chronic narrowing vessel lumen with healing of the local thrombus
  • aneurysm change
  • embolism of thrombus/ plaque lipid content
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78
Q

Angina - clinical presentation

A
  • central chest tightness/heaviness
  • provoked by exertion, especially after meal, cold windy weather, anger, excitement
  • relieved by rest/ GTN spray
  • pain may radiate to one/both arms, neck, jaw, teeth
  • dyspnoea (difficult breathing), nausea, sweaty, faintness
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79
Q

Angina scoring

A
  1. Central, tight pain, radiating to arms, jaw, neck
  2. Precipitated by exertion
  3. Relieved by rest, GTN spray
    3/3 typical angina
    2/3 atypical angina
    1/3 non-anginal pain
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80
Q

Angina - differential diagnosis

A
  • pericarditis/myocarditis
  • pulmonary embolism
  • chest infection
  • dissection of aorta
  • GORD
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81
Q

Angina - diagnosis - 5 things

A
  • 12 lead ECG
  • treadmill test/ exercise ECG
  • CT scan calcium scoring
  • SPECT/myoview
  • cardiac catheterisation
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82
Q

angina diagnosis - 12 lea ECG

A
  • often normal
  • may show ST depression
  • flat or inverted T waves
  • look for signs of past MI
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83
Q

angina diagnosis - treadmill test/exercise ECG

A
  • ECG and run on treadmill uphill - trying to induce ischaemia
  • monitor how long able to exercise for
  • ST segment depression - sign of late stage ischaemia
  • unsuitable for many patients cant walk, very unfit, exercise induced bundle branch block in young females
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84
Q

angina diagnosis - CT scan Calcium scoring

A

CT heart, if atherosclerosis calcium will light up white - significant calcium would indicate angina

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85
Q

angina diagnosis - SPECT/myoview

A
  • radio labelled tracer injected into patient
  • taken up by coronary arteries (good blood supply) so will show up here
  • little blood supply - areas will not light up
  • no light up after exercise indicative of myocardial ischaemia
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86
Q

angina - treatment

A
  • modify risk factors (smoking, exercise, weight loss)
  • treat underlying conditions
  • pharmacological
  • revascularisation
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87
Q

What pharmacological interventions can be used to treat angina?

A
  • Aspirin
  • Statins
  • Beta blockers
  • Glyceryl Trinitrate spray
  • Calcium ion channel antagonists
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88
Q

Angina - aspirin

A
  • antiplatelet - inhibits platelet aggregation in coronary arteries - avoiding platelet thrombus
  • to reduce events
  • eg salicylate
  • COX inhibitor - reduced prostaglandin synthesis inc thromboxane A2
  • side effects - gastric ulceration
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89
Q

Angina - statins

A
  • HMG- CoA reductase inhibitors - reduces cholesterol produced by liver
  • reduces events and LDL-cholesterol
  • anti-atherosclerotic
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90
Q

Angina - betablockers

A 
1st line antianginal 
- reduces force of contraction of heart 
- BISOPROLOL, ATENOLOL
- act on B1 receptors in heart as part of adrenergic sympathetic pathway 
B1 - Gs - cAMP to ATP - contraction
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91
Q

angina - what 3 things do betablockers reduce?

A
  • heart rate (negatively chronotropic)
  • left ventricle contractility (negatively inotropic)
  • cardiac output
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92
Q

angina - betablockers - side effects

A
  • tiredness
  • nightmares
  • bradycardia
  • erectile dysfunction
  • cold hands and feet
    DO NOT GIVE in asthma, heart failure/heart block, hypotension, bradyarrhythmias
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93
Q

angina - glyceryl trinitrate spray

A

1st line antianginal
- nitrate that is a venodilator
- dilates systemic veins - reducing venous return to right side of heart
- reduces preload
- thus reduces work of heart and O2 demand
- also dilates coronary arteries
side effect: profuse headache immediately after use

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94
Q

angina - calcium ion channel antagonists/ blockers

A
  • primary arterodilators
  • dilates systemic arteries (BP drop)
  • reduces afterload on heart
  • thus less energy required to produce same cardiac output
  • thus less work on heart and O2 demand
  • VERAPAMIL
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95
Q

angina - revascularisation - 2 types

A

-Percutaneous Coronary Intervention (PCI)
-Coronary artery bypass graft (CABG)
To restore patient coronary artery, increase flow reserve, done mostly when medication fails or when high risk disease identified

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96
Q

angina - PCI

A
  • dilating coronary atheromatous obstructions by inflating balloon within it
  • insert balloon and stent, inflate balloon and remove it, stent persists, keeps artery patent
  • expanding plaque = make artery bigger
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97
Q

angina - PCI pros and cons

A

pros - less invasive, convenient, short recovery, repeatable

cons - risk of stent thrombosis, not good for complex disease

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98
Q

angina - CABG

A
  • left internal mammary artery (LIMA) used to bypass proximal stenosis in LAD artery
  • pros: good prognosis, deals with complex disease
  • cons: invasive, risk of stroke or bleeding, one time treatment, long recovery period
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99
Q

‘Acute coronary syndrome’ umbrella term for what?

A
  • ST elevation myocardial infarction (STEMI)
  • Unstable (crescendo) angina (UA)
  • non ST elevation myocardial infarction (NSTEMI)
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100
Q

What is an ST elevation myocardial infarction?

A
  • complete occlusion of major coronary artery prev affected by atherosclerosis
  • full thickness damage of heart muscle
  • usually diagnose on ECG @ presentation
  • pathological Q wave some time after MI (so aka Q wave infarction)
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101
Q

What is unstable (crescendo) angina (UA) ?

A
  • angina recent onset (less 24hrs) or
  • cardiac chest pain w/ crescendo pattern
  • deterioration in prev stable angina (symptoms freq. occurring at rest)
  • angina increasing frequency or severity, occurs minimal exertion, rest - form of acute coronary syndrome
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102
Q

What is a non ST elevation myocardial infarction?

A
  • complete occlusion minor coronary artery OR partial occlusion of major coronary artery prev affected by atherosclerosis
  • retrospective diagnosis, made after troponin results and sometimes other investigations
  • partial thickness damage of heart muscle
  • non Q wave infarction
  • ST depression and/or T wave inversion
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103
Q

What is the difference between NSTEMI and UA?

A

NSTEMI = an occluding thrombus leads to myocardial necrosis and rise in serum troponin or creatinine kinase-MB (CK-MB)

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104
Q

The 5 types of MI - type 1

A

spontaneous MI with ischaemia due to a primary coronary event eg plaque erosion/rupture, fissuring, dissection

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105
Q

5 types of MI - type 2

A

MI secondary to ischaemia due to increased O2 demand or decreased supply eg coronary spasm, coronary embolism, anaemia, arrhythmias , hypertension, hypotension

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106
Q

5 types of MI - types 3,4,5

A

MI due to sudden cardiac death related to PCI, CABG

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107
Q

How many people per annum have STEMI in UK?

A

5/1000 per annum

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108
Q

Acute coronary syndrome risk factors

A 
Age 
Gender - male 
Family history (IHD/ MI in first degree relative below 55) 
Smoking 
Hypertension 
Diabetes mellitus 
Hyperlipidaemia 
Obesity and sedentary lifestyle
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109
Q

Acute coronary syndrome pathophysiology

A
  • rupture/erosion fibrous cap of coronary artery plaque
  • causes platelet aggregation/adhesion, localised thrombus, vasoconstriction(platelet release serotonin, thromboxane A2), distal thrombus embolisation
  • myocardial ischaemia due to reduction coronary blood flow
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110
Q

Acute coronary syndrome- what 2 things mean increased risk plaque rupture?

A
  • rich lipid pool within plaque

- thin fibrous cap

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111
Q

Acute coronary syndrome - stages of plaque development

A

fatty streak - fibrotic plaque - atherosclerotic plaque - plaque rupture/fissure and thrombosis - MI/ischaemic stroke or critical limb ischaemia or sudden CVS death

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112
Q

Unstable angina - what is the plaque like?

A
  • necrotic centre
  • ulcerated cap
  • thrombus results in PARTIAL occlusion
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113
Q

Myocardial infarction - what is the plaque like?

A
  • necrotic centre

- thrombus results in TOTAL occlusion

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114
Q

Acute coronary syndrome - clinical presentation - unstable angina presentation?

A
  • chest pain, new onset, at rest, crescendo pattern
  • breathlessness
  • pleuritic pain (sharp pain inhale and exhale)
  • indigestion
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115
Q

Clinical presentation acute coronary syndrome?

A

Acute central chest pain more than 20mins

  • sweating
  • nausea and vomiting
  • dyspnoea
  • fatigue
  • shortness of breath
  • palpitations
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116
Q

Clinical presentation acute coronary syndrome?

A
  • without chest pain (silent infarct) (elderly, diabetics)
  • distress, anxiety
  • pallor
  • increased pulse, reduced BP
  • reduced 4th heart sound
  • may be heart failure sings (increase jugular venous pressure)
  • tachycardia/ bradycardia
  • peripheral oedema
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117
Q

Acute coronary syndrome - differential diagnosis?

A
  • angina
  • pericarditis
  • myocarditis
  • aortic dissection
  • pulmonary embolism
  • oesophageal reflux/spasm
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118
Q

Acute coronary syndrome diagnosis tools?

A
  • 12 lead ECG
  • biochemical markers
  • chest X-ray
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119
Q

Acute coronary syndrome - 12 lead ECG

A
  • can be normal
  • ST depression/ T wave inversion (hours/days after NSTEMI) highly suggestive of acute coronary syndrome, esp if associated with anginal chest pain
  • hyperacute (tall) T waves
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120
Q

Acute coronary syndrome - an STEMI on an ECG?

A
  • persistant ST elevation
  • hyperacute (tall) T waves
  • new left BBB pattern
  • pathological Q waves few days after MI
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121
Q

acute coronary syndrome - 4 biochemical markers?

A
  • troponin T
  • troponin I
  • creatinine kinase-MB (CK-MB)
  • myoglobin
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122
Q

acute coronary syndrome - troponin T and I

A
  • T and I most sensitive and specific markers of myocardial necrosis
  • serum levels increase 3-12hrs onset of chest pain, peak 24-48hrs
  • fall back to normal over 5-14days
  • prognostic indicator determine mortality risk define which patients benefit from aggressive medical therapy and early coronary revascularisation
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123
Q

acute coronary syndrome - CK-MB

A
  • marker for myocyte death
  • low accuracy,can be present in normal state, patients significant skeletal muscle damage
  • tests for reinfarction: levels drop back to normal after 36-72hrs
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124
Q

acute coronary syndrome - myoglobin

A
  • elevated v early in MI

- poor specificity: myoglobin present in skeletal muscle

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125
Q

acute coronary syndrome - chest X ray

A

-look for cardiomegaly, pulmonary oedema, widened mediastinum (aortic rupture)

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126
Q

acute coronary syndrome - types of treatment

A
  • pain relief
  • anti-emetic
  • oxygen
  • pharmacological (antiplatelets, BBs, statins, ACEi)
  • coronary revascularisation
  • modify risk factors
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127
Q

acute coronary syndrome - pain relief?

A
  • GTN spray

- IV opioid

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128
Q

acute coronary syndrome - oxygen

A
  • aim for 94-98% saturation

- 88-92% COPD

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129
Q

acute coronary syndrome - antiplatelet therapy - how thrombotic clot forms

A
  • atheromatous plaque rupture = platelets exposed ADP/thromboxane A2/adrenaline/thrombin/collagen tissue factor
  • causes platelet activation/aggregation via IIb/IIIa glycoproteins binding to fibrinogen
  • thrombin enzymatically converts fibrinogen to fibrin(insoluble) forms fibrin mesh over platelet plug, formation thrombotic clot
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130
Q

Examples of 3 antiplatelet drugs

A
  • aspirin
  • P2Y12 inhibitors (oral)
  • glycoprotein IIb/IIIa antagonists (IV)
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131
Q

How does aspirin work?

A

COX-1 inhibitor - blocks formation of thromboxane A2 from thus prevents platelet aggregation

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132
Q

acute coronary syndrome - P2Y12 inhibitors (oral)

A

-inhibit ADP dependant activation IIb/IIIa glycoproteins, preventing amplification response of platelet aggregation
-use if allergic to aspirin
-dual anti-platelet therapy w/ aspirin
-clopidogrel , prasugrel , ticagrelor
side effects:neutropenia, thrombocytopenia, increased risk bleeding
-AVOID if CABG planned

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133
Q

acute coronary syndrome - glycoprotein IIb/IIIa antagonists (IV)

A
  • only IV available
  • used w/ aspirin AND oral P2Y12 inhibitors patients with ACS undergoing PCI
  • increases risk major bleeding
  • abciximab , tirofiban , eptifbatide
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134
Q

acute coronary syndrome - beta blockers (IV and oral)

A
  • avoid with asthma, heart failure, hypotension, bradyarrhythmias
    atenolol (IV then oral)
    metoprolol (IV then oral)
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135
Q

acute coronary syndrome - statins (oral)

A
  • HMG-CoA reductase inhibitors

- simvastatin , pravastatin , atorvastatin

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136
Q

acute coronary syndrome - ACE inhibitors (oral)

A
  • ramipril , lisonopril

- monitor renal function

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137
Q

acute coronary syndrome - coronary revascularisation

A
  • percutaneous coronary intervention (PCI)

- coronary artery bypass graft (CABG) - high risk mortality in high risk groups eg recent MI

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138
Q

acute coronary syndrome - risk factor modification

A
  • stop smoking
  • loose weight , exercise daily
  • healthy diet
  • treat hypertension + diabetes
  • low fat diet with statins
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139
Q

Cardiomyopathy - definition

A

Group of diseases of the myocardium that affect the mechanical or electrical function of the heart

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140
Q

Cardiomyopathy - epidemiology

A
  • in general: inherited genetic conditions, although some acquired ones
  • all carry arrhythmic risk
  • can occur younger ages
  • restrictive cardiomyopathy rare in childhood, poor outcome once symptoms develop
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141
Q

The 4 types of cardiomyopathy?

A
  • hypertrophic
  • dilated
  • restrictive
  • arrhythmogenic right ventricular
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142
Q

cardiomyopathy - 5 risk factors?

A
  • family history
  • hypertension
  • obesity
  • diabetes
  • previous MI
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143
Q

hypertrophic cardiomyopathy - what is it?

A

ventricular hypertrophy/ thickening of the muscle

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144
Q

hypertrophic cardiomyopathy - epidemiology

A
  • quite common, 2nd most common cardiomyopathy
  • 1/500 have it
  • autosomal dominant - familial
  • may present at any age
  • most common cause of sudden cardiac death in the young
  • HCM refers to otherwise unexplained primary cardiac hypertrophy
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145
Q

hypertrophic cardiomyopathy - pathophysiology

A
  • sarcomeric protein gene mutations eg troponin T, B-myosin
  • in absence of hypertension, valvular disease
  • hypertrophic, non-compliant ventricles impair DIASTOLIC filling: reduced stroke volume, reduced cardiac output
  • myofibrillar disarray = conduction is affected
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146
Q

hypertrophic cardiomyopathy - clinical presentation (7)

A
  • hypertrophy of myocardium esp interventricular septum
  • sudden death may be first manifestation
  • chest pain, angina, dysponea, dizziness, palpitations, syncope
  • LV outflow obstruction
  • cardiac arrhythmia
  • ejection systolic murmur
  • jerky carotid pulse
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147
Q

hypertrophic cardiomyopathy - 3 diagnosis tools?

A
  • ECG
  • echocardiogram
  • genetic analysis
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148
Q

hypertrophic cardiomyopathy - ECG

A

ECG: abnormal, LV hypertrophy signs, progressive T wave inversion, deep Q waves

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149
Q

hypertrophic cardiomyopathy - echocardiogram

A

ventricular hypertrophy, small left ventricle cavity

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150
Q

hypertrophic cardiomyopathy - genetic analysis

A

can confirm diagnosis - most cases are autosomal dominant and familial

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151
Q

hypertrophic cardiomyopathy - treatment - 3 drugs

A

AMIODARONE - anti-arrhythmic medication, if at high arrhythmia risk: implantable cardiac defibrillator
CALCIUM CHANNEL BLOCKER- eg verampil
BETA BLOCKER - eg atenolol

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152
Q

Dilated cardiomyopathy - definition

A

Dilated left ventricle (or RV or all 4 chambers) which contracts poorly/ has thin muscle - thus dysfunction

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153
Q

dilated cardiomyopathy - epidemiology

A
  • MOST COMMON cardiomyopathy
  • autosomal dominant - familial
  • caused by: ischaemia, alcohol, thyroid disorder or familial/genetic
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154
Q

dilated cardiomyopathy - pathophysiology

A
  • caused by cytoskeletal gene mutations
  • LV, RV, all 4 chamber dilatation thus dysfunction
  • theory:poorly generated contractile force causes progressive dilatation of heart with some diffuse interstitial fibrosis
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155
Q

dilated cardiomyopathy - clinical presentation

A
  • shortness of breath, fatigue
  • dysponea
  • heart failure (cant contract well)
  • arrhythmias
  • thromboembolism
  • sudden death
  • increased jugular venous pressure
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156
Q

dilated cardiomyopathy - 3 diagnostic tools and what they will show?

A
  • chest X ray (cardiac enlargement)
  • ECG (tachycardia, arrhythmia, non specific T wave changes)
  • echocardiogram (dilated ventricles)
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157
Q

dilated cardiomyopathy - treatment

A

heart failure and atrial fibrilation treated in conventional way

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158
Q

Restrictive cardiomyopathy - epidemiology

A
  • Rare

- Causes: amyloidosis, idiopathic, sarcoidosis, end-myocardial fibrosis

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159
Q

Arrythmogenic right ventricular cardiomyopathy - definition

A

-progressive genetic cardiomyopathy characterised by progressive fatty and fibrous replacement of ventricular myocardium

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160
Q

arrythmogenic right ventricular cardiomyopathy - epidemiology

A
  • cause unknown

- familial form usually autosomal dominant w/ incomplete penetrance but can be recessive

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161
Q

arrtyhmogenic right ventricular cardiomyopathy - pathophysiology

A
  • desmosome gene mutation (normally hold cardiac cells together-cell junctions)
  • RV replaced by fat and fibrous tissue
  • muscle dies, replaced by fat as part of inflammatory process
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162
Q

arrhythmogenic right ventricular cardiomyopathy - clinical presentation

A
  • impairment of holding together of cardiac cells thus conduction issues
  • ARRHYTHMIA most common
  • syncope
  • late stages - maybe signs right heart failure
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163
Q

arrhythmogenic right ventricular cardiomyopathy - diagnosis tools and findings

A
  • ECG: usually normal, may show T wave inversion
  • echocardiogram: maybe normal, advanced disease: RV dilatation
  • genetic testing: gold standard
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164
Q

arrhythmogenic right ventricular cardiomyopathy - treatment

A
  • BETA BLOCKERS eg atenolol for patients non life threatening arrhythmias
  • AMIODARONE for symptomatic arrhythmias
  • occasional cardiac transplant indicated eg cardiac failure, devastating arrhythmia
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165
Q

Structural/ congenital heart defects

A
  • 1% all live births some form cardiac defect
  • minor —- incompatible with life ex utero
  • overall male predominance
  • atrial septal defect, persistant ductus arteriosus more common females
  • usually: misplaced structures, arrest of progression of normal structure development
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166
Q

Causes of congenital heart disease?

A
  • 1 child with defect increases likelihood 2nd child having another defect
  • drugs eg thalidomide, amphetamines,lithium
  • diabetes of mother
  • genetic abnormalities eg familial form ASD, congenital heart block
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167
Q

Maternal prenatal rubella infection associated with which congenital abnormalities?

A
  • persistant ductus arteriosus
  • pulmonary valvular stenosis
  • arterial stenosis
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168
Q

Maternal alcohol misuse associated with which congenital abnormality?

A
  • septal defects
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169
Q

Single genes - what congenital heart defects are associated with Trisomy 21?

A
  • septal valve defects
  • mitral valve defects
  • tricuspid valve defects
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170
Q

Clinical presentation of congenital heart defects

A

should be recognised early as possible (response better the earlier the treatment)

  • central cyanosis
  • pulmonary hypertension
  • clubbing of fingers
  • growth retardation
  • syncope
  • specific problems in adults/adolescents
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171
Q

Clinical presentation congenital heart defects - central cyanosis

A
  • right to left shunting of blood OR
  • complete mixing of systemic+pulmonary blood flow=poorly oxygenated blood entering systemic circulation
  • skin goes blueish
  • Tetralogy of Fallot, Tricuspid atresia
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172
Q

clinical presentation congenital heart defects - pulmonary hypertension

A
  • large left to right shunts
  • persistant raised pulmonary flow = increased pulmonary artery vascular resistance = pulmonary hypertension
  • thickening of pulmonary artery walls in response to high pressure
  • resistance causes RV pressure to increase = REVERSAL OF SHUNT = cyanosis
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173
Q

Eisenmenger’s reaction

A
  • L to R shunt = pulmonary hypertension leading to thickening pulmonary artery walls, increase RV pressure, reversal of initial shunt so now shunt is right to left = cyanosis
  • Eisenmenger’s complex specifically in relation to VSD
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174
Q

Does presence of pulmonary hypertension make prognosis of congenital heart defect better or worse?

A

Significantly worsens the prognosis

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175
Q

congenital heart defects - what leads to clubbing of fingers?

A

associated with prolonged cyanosis

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176
Q

congenital heart defects - what type is associated with growth retardation?

A

common in children with cyanotic heart disease

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177
Q

congenital heart defects - syncope

A
  • presence of severe LV or RV outflow tract obstruction

- exertional syncope associated with keeping central cyanosis, may occur in Fallot’s tetralogy

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178
Q

Congenital heart defects presentation 6 specific common problems in adolescents/adults

A
  • endocarditis (small VSD/bicuspid aortic valve)
  • calcification and stenosis of congenitally deformed valves (bicuspid aortic valve)
  • atrial and ventricular arrhythmias
  • sudden cardiac death
  • right sided heart failure
  • end stage heart failure
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179
Q

congenital heart disease - Bicuspid aortic valve (BAV)

A
  • most common cong heart disease (1-2% live births)
  • can work well at birth (go undetected) but severely stenotic infancy/childhood
  • degenerate quicker and become regurgitant earlier than normal valves
  • predisposed to infective endocarditis
  • intense exercise may accelerate complications - yearly ECGs on affected athletes
180
Q

congenital heart defects- Bicuspid aortic valve - more common in males or females?

181
Q

congenital heart defects - bicuspid aortic valve - what other malformation is it associated with?

A

coarctation and dilation of ascending aorta

182
Q

congenital heart defects - atrial septal defects - epidemiology

A
  • often first diagnosed in adulthood
  • one third of congen heart defects
  • more common in females
  • abnormal connection between 2 atria
183
Q

congenital heart defects - atrial septal defects

A
  • probe can be passed through layers of foramen ovale (primum, secundum) so aka probe patent foramen ovale
  • higher pressure LA, so shunt left to right - so not blue - ACYANOTIC
184
Q

congenital heart defects - atrial septal defects - physiology

A
  • increased flow into right side of heart/lungs
  • untreated=right sided overload, dilatation- RV compliant, easily dilates to accomodate increased pulmonary flow, can cause:
  • RV hypertrophy
  • pulmonary hypertension, Eisenmenger’s
  • +risk infective endocarditis
185
Q

congenital heart defects - atrial septal defects clinical presentation

A
  • dysponea
  • exercise intolerance
  • atrial arrhythmias (artia dilation)
  • pulmonary flow murmur
  • fixed split 2nd heart sound (delayed closure pulmonary valve-more blood has to get out)
186
Q

congenital heart defects - atrial septal defects - chest X ray findings

A
  • large heart

- large pulmonary arteries

187
Q

congenital heart defects - atrial septal defects - ECG findings

A

right bundle branch block (RBBB) due to right ventricle dilatation

188
Q

congenital heart defects - atrial septal defects - echocardiogram findings

A

hypertrophy and dilation of right side of heart and pulmonary arteries

189
Q

congenital heart defects - atrial septal defects - treatment

A
  • surgical closure

- percutaneous (key hole technique)

190
Q

Congenital heart defects - Ventricular septal defects

A
  • abnormal connection between 2 ventricles
  • many close spontaneously during childhood
  • 20% all congen heart defects
  • LV higher pressure: L to R shunt, acyanotic
  • increased blood flow through lungs
191
Q

Congenital heart defects - Ventricular septal defects - clinical presentation of LARGE defects

A
  • pulmonary hypertension (Eisenmenger’s)
  • small breathless skinny baby
  • increased resp rate
  • tachycardia
  • murmur that varies in intensity
  • big heart on chest X ray
192
Q

Congenital heart defects - Ventricular septal defects - clinical presentation of SMALL defects

A
  • large systolic murmur (audible)
  • thrill (buzzing sensation)
  • well grown
  • normal heart rate
  • normal heart size
193
Q

Congenital heart defects - Ventricular septal defects - treatment

A
  • medical initially: many will spontaneously close
  • surgical close
  • small defect = no intervention required
  • prophylactic antibiotics
  • moderate sized lesion: furosemide, ACEi (ramipril) , digoxin may suffice
194
Q

Congenital heart defects - Atrio-ventricular septal defects (AVSD)

A
  • associated with Down’s syndrome
  • hole in very centre of heart
  • involves ventricular and atrial septum, mitral and tricuspid valves
  • can be complete or partial
  • one big malformed AV valve-usually leaks
195
Q

congenital heart defects - AVSD - clinical presentation of complete defect

A
  • neonate breathlessness
  • poor feeding and weight gain
  • torrential pulmonary flow can result in Eisenmenger’s (cyanosis over time)
196
Q

congenital heart defects - AVSD - clinical presentation of partial defect

A
  • can present late adulthood

- presents similar to septal defect eg dysponea, tachycardia, exercise intolerance

197
Q

congenital heart defects - AVSD - treatment

A
  • pulmonary artery banding (if large defect infancy) reduces blood flow to lungs reducing pulmonary hypertension
  • surgical repair challenging
  • partial defect can left alone if no right heart dilatation
198
Q

congenital heart defects - patent ductus arteriosus - epidemiology and definition

A
  • females more than males

- persistant communication proximal left pulmonary artery - descending aorta

199
Q

congenital heart disease - patent ductus arteriosus

A
  • foetal life R heart pressure exceeds left
  • blood R to L through foramen ovale, and pulmonary artery to aorta via ductus arteriosus
  • abnormal L to R shunt (aorta to P artery)
  • pulmonary hypertension
  • right side cardiac failure (+ afterload)
200
Q

congenital heart disease - 2 risk factors for having patent ductus arteriosus?

A

(normally shuts due to decreased pulmonary resistance)
- premature babies
- maternal rubella
(also having it increases risk of infective endocarditis)

201
Q

congenital heart disease - patent ductus arteriosus - clinical presentation

A
  • continuous ‘machinery’ murmurs
  • bounding pulse
  • (large defect)large heart and breathlessness
  • Eisenmenger’s but pink, not clubbed fingers
  • tachycardia
202
Q

congenital heart defects - patent ductus arteriosus - chest X ray

A

-(large shunt) aorta and pumonary arterial system may be prominent

203
Q

congenital heart defects - patent ductus arteriosus - ECG and echocardiogram

A
  • may be left atrial abnormality, left ventricular hypertrophy
  • echo: may show dilated left atrium, left ventricle
204
Q

congenital heart defects - patent ductus arteriosus - treatment

A
  • closed surgically or percutaneously
  • low risk complications
  • venous approach may require AV loop
  • INDOMETACIN (prostaglandin inhibitor) given to stimulate duct closure
205
Q

congenital heart defects - coarctation of the aorta

A

-more males than females
-narrowing of aorta, at or just distal insertion
ductus arteriosus
-net result:narrowing aorta just after arch, excessive blood flow diverted through carotid, subclavian vessels, systemic vascular shunts to supply rest of body (stronger perfusion of upper body)

206
Q

congenital heart defects - coarctation of aorta - what other 4 conditions are associated?

A
  • Turner’s syndrome
  • Berry aneurysms
  • Patent ductus arteriosus
  • Systemic hypertension due to decrease renal perfusion (persists after surgical correction)
207
Q

congenital heart defects - coarctation of aorta clinical presentation

A
  • asymptomatic for many years
  • right arm hypertension
  • bruits (buzzes) over scapulae/back (collateral vessels)
  • murmur
  • headaches, nosebleeds (hypertension)
  • hypertension in upper limbs
  • discrepant blood pressure in upper and lower body (radial before femoral pulse)
208
Q

congenital heart defects - coarctation of aorta long term problems

A

HYPERTENSION

  • early coronary artery disease
  • early strokes
  • sub-arachnoid haemorrhage
209
Q

congenital heart defects - coarctation of aorta - chest X ray, ECG, CT

A

CXR: dilated aorta, indented at side of coarctation
ECG: left ventricular hypertrophy
CT: accurately demonstrate coarctation, quantify flow

210
Q

congenital heart defects - coarctation of aorta - treatment

A
  • surgery
  • balloon dilation (preferred for recoarctation and stenting)
  • risk aneurysm at site of repair
211
Q

congenital heart defects - Tetralogy of Fallot

A

MOST COMMON form cyanotic congenital heart disease

212
Q

congenital heart defects - Tetralogy of Fallot - the 4 things?

A
  • Large MALIGNED ventricular septal defect
  • Overriding aorta
  • RV outflow obstruction (eg due to pulmonary stenosis)
  • RV hypertrophy
213
Q

congenital heart defects - Tetralogy of Fallot - cyanosis

A
  • stenosis of RV outflow (eg pulmonary valve)
  • RV higher pressure than LV
  • so blue blood from RV to LV
  • patients are blue (cyanotic)
214
Q

congenital heart defects - Fallots tetralogy - clinical presentation

A
  • central cyanosis
  • low birth weight and growth
  • dyspnoea on exertion
  • delayed puberty
  • systolic ejection murmurs
  • boot shaped heart on chest X ray
215
Q

congenital heart defects - Fallots tetralogy - treatment

A
  • full surgical during first 2 years life (progressive cardiac debility and cerebral thrombosis risk)
  • often get pulmonary valve regurgitation in adulthood - require redo surgery
216
Q

congenital heart defects - Pulmonary stenosis

A
  • narrowing of outflow of RV
    (can be valvular, subvalvar, supravalvar) (99% valvular)
  • can be severe or mild
217
Q

congenital heart defects - severe pulmonary stenosis

A
  • RV failure as neonate
  • collapse
  • poor pulmonary blood flow
  • RV hypertrophy
  • tricuspid regurgitation
218
Q

congenital heart defects - mild pulmonary stenosis

A
  • well tolerated many years

- RV hypertrophy

219
Q

congenital heart defects - pulmonary stenosis - treatment

A
  • balloon valvoplasty - catheter with balloon through femoral vein- inflate at stenosis to crush (can result in regurgitation)
  • open valvotomy
  • shunt to bypass blockage
220
Q

congenital heart defects - complete transposition of great arteries

A
  • aorta off RV and pulmonary trunk off LV !
  • 2 closed circulations
  • male more common, associated w/ diabetes
  • survival only if communication between 2 circuits
  • most have an ASD, with blood mixing
221
Q

congenital heart defects - complete transposition of great arteries - treatment

A
  • atrial switch operation with good results
222
Q

congenital heart defects - dextrocardia

A
  • heart points to right side chest, rather than left

- associated with severe cardiovascular abnormalities

223
Q

Pericarditis

A
  • pericardium=protective covering of heart
  • outer fibrous pericardial sac
  • inner serous pericardium
224
Q

Pericarditis - layers of pericardium

A

Inner serous pericardium:

  • inner visceral layer - single cell layer adherent to epicardium (myocytes), lines heart and great vessels
  • outer parietal layer - mainly collagen and elastin fibres, no cells, lines fibrous sac
225
Q

Pericarditis - around how much fluid is found in the pericardial sac?

A

50ml serous fluid - lubricant

226
Q

Pericardium - general anatomy

A
  • great vessels lie in pericardium - if proximal/ascending segment aorta ruptures will bleed into pericardial space=tamponade
  • LA mainly outside pericardium
  • promotes cardiac efficiency - limiting dilation, maintaining ventricular compliance, distributing hydrostatic forces
227
Q

Pericarditis - how does pericardium aid atrial filling?

A
  • creating a closed chamber
  • also reduces external friction, barrier against infection + extension of malignancy
  • anatomically fixes heart to sternum, diaphragm, costal cartilages
228
Q

Pericarditis - pericardium is similar to an elastic band

A
  • initially stretchy but stiff at higher tension
  • low tension - small reserve volume
  • volume exceeded-pressure translated to cardiac chambers = pressure on heart
229
Q

Pericarditis - what happens if small amount volume is added into the pericardial space?

A
  • dramatic effects on filling eg cardiac tamponade

- pressure in pericardium is very low

230
Q

Pericarditis - what happens in a chronic pericardial effusion?

A

-pericardium adapts slowly
- lays down elastin and collagen
- becomes more elastic, much slower tamponade (no RA collapse)
- pressure equalises
(entrance fluid making up effusion must be slow)

231
Q

Acute pericarditis

A

Acute inflammation of the pericardium - with or without effusion

232
Q

Acute pericarditis - epidemiology

A
  • most idiopathic
  • most common young, prev healthy patient
  • males more than females
  • adults more than children
233
Q

Acute pericarditis - causes

A
  • infectious (bacterial,viral,fungal)

- non infectious (autoimmune, neoplastic, Dressler’s, traumatic and iatrogenic)

234
Q

Acute pericarditis - infectious causes

A
  • viral (common) : enteroviruses eg echoviruses, adenoviruses
  • bacterial: mycobacterium tuberculosis
  • fungal (very rare) : Histoplasma spp (most likely seen in immunocompromised pt)
235
Q

acute pericarditis - non infectious causes

A
  • autoimmune (Sjorgren’s, rheumatoid arthritis, SLE)
  • neoplastic (secondary metastatic tumor)
  • Dressler’s syndrome - post cardiac injury syndromes
236
Q

acute pericarditis - traumatic and iatrogenic

A
  • early onset (rare) : direct injury/penetrating thoracic injury/ oesophageal perforation or indirect injury/non penetrating thoracic injury/radiation
  • delayed onset (common) : pericardial injury syndromes, iatrogenic trauma eg PCI, pacemaker lead insertion
237
Q

acute pericarditis - pathophysiology

A
  • pericardium becomes acutely inflamed
  • pericardial vascularisation, infiltration polymorphonuclear leucocytes
  • fibrinous reaction freq results in exudate, adhesions within pericardial sac, serous, hemorrhagic effusion may develop
238
Q

acute pericarditis - clinical presentation

A
  • chest pain
  • dysponea
  • cough
  • hiccups (phrenic involvement)
  • pericardial friction rub (auscultation)
  • fever, lymphocytosis (if virus, bacteria)
  • tachycardia
239
Q

acute pericarditis - chest pain

A
  • severe
  • sharp and pleuritic (without constricting, crushing character of ischaemic pain)
  • rapid onset
  • worse on inspiration
  • L anterior chest/epigastrium
  • radiates to arm/ TRAPEZIUS RIDGE (coinnervation phrenic nerve - differs from STEMI)
240
Q

acute pericarditis - differential diagnosis

A
  • MI (most important to rule out)
  • angina
  • pleuritic pain
  • pulmonary infarction
  • pneumonia, GI reflux, peritonitis, aortic dissection
241
Q

acute pericarditis - ECG

A
  • DIAGNOSTIC
  • widespread concave upwards SADDLE SHAPED ST ELEVATION
  • diffuse ST elevation present all leads (in STEMI would be LIMITED to infarcted area)
  • PR depression
242
Q

acute pericarditis - chest X ray

A
  • cardiomegaly in cases of effusion (confirm with echo)
  • often normal in idiopathic
  • pneumonia common with bacterial pericarditis
243
Q

acute pericarditis - FBC

A
  • slight increase white cell count
  • anti neutrophil antibody young females(SLE)
  • elevated troponin suggests myopericarditis
244
Q

acute pericarditis - erythrocyte sedimentation rate/ C reactive protein levels

A

Hight ESR suggests autoimmune

245
Q

acute pericarditis - treatment

A
  • restrict physical activity until resolution of symptoms/ ECG/CRP improvements
  • NSAID or ASPIRIN for 2 weeks
  • COLCHICINE 3 weeks (nausea, diarrhoea )
246
Q

Recurrent or relapsing pericarditis

A
  • 20% acute go on to develop idiopathic relapsing pericarditis
  • 6 weeks weaning off NSAIDs or intermittently
  • first line treatment oral NSAIDs (ibuprofen)
  • Colchicine more effective than aspirin alone
247
Q

Recurrent or relapsing pericarditis - resistant cases

A
  • oral corticosteroids eg prednisolone

- pericardiectomy

248
Q

Pericardial effusion/ cardiac tamponade

A
  • pericardial effusion: collection fluid within potential space serous pericardial sac
  • commonly accompanies acute pericarditis
  • large volume=ventricular filling compromised embarrassment circulation - cardiac tamponade
249
Q

clinical presentation pericardial effusion

A
  • reflect underlying pericarditis
  • soft, distant heart sounds
  • apex beat obscured
  • raised jugular venous pressure
  • dysponea
250
Q

clinical presentation cardiac tamponade

A
  • high pulse but low blood pressure
  • high jugular venous pressure
  • muffled 1st and 2nd heart sounds
  • Kussmaul’s sign
  • pulsus parodoxus
  • reduced cardiac output
251
Q

Kussmauls sign definition

Pulsus parodoxus definition

A
  • rise jugular venous pressure, increased neck vein distention during inspiration
  • exaggeration normal variation pulse pressure with inspiration - drop in systolic BP
252
Q

Pericardial effusion diagnosis

A

CXR: large globular heart
ECG: low voltage QRS complexes, sinus tachycardia
Echo: most useful demonstrating effusion, echo free zone surrounding heart

253
Q

Cardiac tamponade diagnosis

A

CXR: big globular heart
ECG: low voltage QRS
Echo: DIAGNOSTIC, echo free zone around heart, late diastolic collapse RA, early diastolic collapse RV

254
Q

cardiac tamponade diagnosis - Beck’s triad

A
  • falling blood pressure
  • rising jugular venous pressure
  • muffled heart sounds
255
Q

pericardial effusion - treatment

A
  • underlying cause sought and treated
  • most resolve spontaneously
  • may re-accumulate due to malignancy: pericardial fenestration(window allows slow release fluid to surrounding tissues)
256
Q

cardiac tamponade - treatment

A
  • seek expert help
  • urgent drainage via pericardiocentesis
  • fluid sent for Ziehl-Nielsen stain, cytology
257
Q

Constrictive pericarditis

A
  • tuberculosis, bacterial infection, rheumatic heart disease result in pericardium becoming thick, fibrous, calcified
  • cause often unknown, can occur after any pericarditis
258
Q

constrictive pericarditis - pathophysiology

A
  • many cases- no symptoms
  • constrictive pericarditis if so inelastic to interfere w/ diastolic filling
  • changes are chronic - allows time for body to compensate - not as life threatening
259
Q

Constrictive pericarditis vs restrictive cardiomyopathy

A
  • very similar presentation

- constrictive pericarditis treatable - restrictive cardiomyopathy not

260
Q

Constrictive pericarditis - myocardium changes

A
  • later stages of condition

- sub endocardial layers of myocardium may undergo fibrosis, atrophy, calcification

261
Q

constrictive pericarditis - clinical presentation

A
  • Kussmaul’s sign
  • pulsus parodoxus
  • diffuse heart sounds
  • ascites
  • oedema
  • right heart failure signs
  • atrial dilatation
262
Q

constrictive pericarditis - diagnosis

A

CXR: small heart with/without pericardial effusion
ECG: low voltage QRS
Echo: thickened, calcified pericardium, small ventricular cavities w/ normal wall thickness

263
Q

constrictive pericarditis - treatment

A

-complete resection of pericardium (risky, high complication rate)

264
Q

Cardiac failure

A

‘The inability of the heart to deliver blood and thus O2 at a rate commensurate with the requirement of metabolising tissue of the body’

  • syndrome, not diagnosis on own
  • result from any structural/functional cardiac disorder impairs hearts ability to function, meet O2 demands metabolising body
265
Q

Cardiac failure - epidemiology

A

25-50% die within 5yrs diagnosis

  • 1-3% general population
  • 10% among elderly
266
Q

cardiac failure - main causes

A
  • IHD - main cause
  • cardiomyopathy
  • valvular heart disease
  • cor pulmonae
  • hypertension
  • alcohol excess
  • anything increases myocardial work (anaemia,arrhythmias,obesity,hyperthyroidism)
267
Q

cardiac failure - risk factors

A
  • 65 and older
  • african descent
  • men (oestrogen protects IHD)
  • obesity
  • prev had MI
268
Q

Cardiac failure - pathophysiology

A
  • physiological compensatory changes to try maintain CO and peripheral perfusion
  • these mechanisms become overwhelmed as progresses - become pathophysiological = decompensation
  • venous return
  • outflow resistance
  • sympathetic system activation
  • RAAS
269
Q

cardiac failure - pathophysiology - venous return (preload)

A
  • reduction blood volume ejected
  • increase volume left in ventricles
  • increased preload stretched myocardial fibres - Starlings law - contraction force +
  • heart failure, myocardium cannot contract harder in response, CO not maintained
270
Q

cardiac failure - pathophysiology - outflow resistance (afterload) definition

A
  • load/resistance against which ventricles must contract, made up of:
  • pulmonary and systemic resistance
  • physical characteristics vessel walls
  • volume of blood ejected
271
Q

cardiac failure - pathophysiology - outflow resistance (afterload)

A
  • increase afterload, increase end-diastolic volume
  • decrease stroke volume, decrease CO
  • results in increase end diastolic volume, dilatation ventricle, further exacerbates problem of afterload
272
Q

cardiac failure - pathophysiology - sympathetic system activation

A
  • baroreceptors (drop arterial pressure) stimulate sympathetic activation
  • increases SV and HR, increasing CO
  • cardiac failure - chronic symp activation
  • less receptor to act on - effect of symp activation diminished, CO stops increasing in response
273
Q

cardiac failure - pathophysiology - RAAS

A
  • reduced CO, diminished renal perfusion
  • RAAS activated (increase blood volume)
  • so increased preload, stretching of heart, force contraction, SV, CO
  • cardiac myocytes require more energy, more blood - heart failure (IHD) - no increase blood, myocytes die, decrease CO
274
Q

cardiac failure - classification - classes

A
  • systolic vs diastolic

- acute vs chronic

275
Q

cardiac failure - classification - systolic

A
  • inability ventricle contract normally (so decreased CO)

- caused by IHD, MI, cardiomyopathy

276
Q

cardiac failure - classification - diastolic

A
  • inability ventricles relax, fill fully, decrease SV, decrease CO
  • caused by ventricle hypertrophy - less space for blood - decreased CO
  • aortic stenosis increases afterload, decreases CO
277
Q

cardiac failure - classification - acute

A
  • new onset or decompensation chronic heart failure
  • pulmonary and/or peripheral oedema
  • may be signs peripheral hypotension
278
Q

cardiac failure - classification - chronic

A
  • develops slowly

- venous congestion common, arterial pressure well maintained until v late

279
Q

cardiac failure - clinical presentation

A

3 cardinal symptoms: shortness breath, fatigue, ankle swelling (non specific)

  • dyspnoea - esp when lying flat
  • cold peripheries
  • raised jugular venous pressure (JVP)
  • murmurs, displaced apex beat
  • cyanosis
  • hypotension
  • peripheral/pulmonary oedema
  • tachycardia and 3rd and 4th heart sounds
  • ascites and bi-basal crackles
280
Q

cardiac failure - clinical presentation - use of New York Heart Association (NYHA) classification for severity of symptoms:

A
  • Class I: no limitation/asymptomatic, exercise= no dyspnoea, fatigue, palpitation
  • Class II: slight limitation/mild heart failure, comfortable at rest, normal activity= D, F, P Class III: marked limitation/moderate heart failure, comfy at rest, gentle activity=D, F, P
  • Class IV: inability carry out any physical activity without discomfort/ severe heart failure - symptoms at rest
281
Q

cardiac failure - diagnosis

A
  • blood tests
  • chest X ray
  • ECG
  • echo
282
Q

cardiac failure - diagnosis - blood tests

A

Brain natriuretic peptide (BNP)

  • secreted by ventricles response increase myocardial wall stress
  • increased in patients heart failure
  • levels correlate ventricular wall distress, severity heart failure
  • FBC, U+Es, liver biochemistry
283
Q

cardiac failure - diagnosis - chest X ray

A

ACDE

  • Alveolar oedema
  • Cardiomegaly
  • Dilated upper lobe vessels lungs
  • Effusions (pleural)
284
Q

cardiac failure - diagnosis - ECG

A
  • shows underlying cause eg IHD, LVH
  • if ECG and BNP normal,heart failure unlikely
  • if both abnormal, do echocardiogram
285
Q

cardiac failure - diagnosis - echocardiogram

A
  • assess cardiac chamber dimension
  • regional wall motion abnormalities , valvular disease, cardiomyopathies
  • sign of MI
286
Q

cardiac failure - treatment

A
  • lifestyle changes
  • diuretics, ACE inhibitors, beta blockers
  • digoxin, inotropes
  • revascularisation, surgery to repair
  • heart transplant (young people)
  • cardiac resynchronisation
287
Q

cardiac failure treatment - lifestyle changes

A
  • avoid large meals
  • loose weight
  • stop smoking
  • exercise
  • vaccination
288
Q

cardiac failure treatment - diuretics

A
  • reduce preload, decreasing systemic and pulmonary congestion
  • symptomatic relief
  • loop diuretic - furosemide
  • thiazides eg bendroflumethiazide
  • aldosterone antagonsit eg spirolactone
289
Q

cardiac failure treatments - ACE inhibitors

A
  • ramipril, enalipril, captopril
  • cough,hypotension,hyperkalemia,renal dysfunc
  • cough problem - angiotensin receptor blockers
290
Q

cardiac failure treatment - beta blockers

A
  • bisoprolol, nebivolol, carvedilol
  • start low dose, titrate upwards
  • DO NOT GIVE TO ASTHMATICS
291
Q

cardiac failure treatment - revascularisation

A
  • when some viable myocardium remains

- illicit PCI stenting

292
Q

cardiac failure treatment - surgery to repair

A

-mitral valve repair, aortic or mitral valve replacement

293
Q

cardiac failure treatment - resynchronisation

A

-improve coordination of atria and ventricles

294
Q

Clinical example cardiac failure treatment - biventricular failure

A

Shortness of breath = due to right ventricular failure

Leg oedema = due to left ventricular failure

295
Q

Valvular heart diseases - mitral stenosis

A

obstruction of left ventricle inflow - prevents proper filling during diastole
(mitral valve has 2 cusps)

296
Q

valvular heart disease - mitral stenosis epidemiology

A
  • normal 4-6cm2, symptoms less than 2cm2
  • most common cause rheumatic heart disease secondary rheumatic fever from group A beta haemolytic streptococcus infection eg Streptococcus pyogenes
  • more common men
  • prev and inc reducing, reduc rheum heart disease
297
Q

valvular heart disease - mitral stenosis - rheumatic heart disease

A
  • inflammation from rheumatic fever = commissural fusion
  • reduction orifice area (causes characteristic doming seen on echo)
  • years: valve thickening,cusp fusion,calcium deposition,severely narrowed orifice,progressive immobility valve cusps
298
Q

valvular heart disease - mitral stenosis - other causes

A
  • infective endocarditis

- mitral annular calcification

299
Q

valvular heart disease - mitral stenosis - risk factors

A
  • history rheumatic fever

- untreated streptococcus infections

300
Q

valvular heart disease - mitral stenosis - pathophysiology

A

-obstruction flow LA->LV
-maintain CO=LA pressure +, LA hypertrophy, dilatation
-pulmonary venous, pulmonary arterial, right heart pressure increase
+pulmonary cap pressure=pulmonary oedem (particularly when atrial fib occurs)
-alveolar, capillary thickening, reactive pulmonary hypertension ->RV hypertrophy,dilatation, tricuspid regurg

301
Q

valvular heart disease - mitral stenosis - clinical presentation

A
  • symptoms at 2cm2 area
  • several decades after first rheumatic fever
  • progressive dyspnoea (LA dilatation) worse with exercise, fever, tachycardia, pregnancy
  • haemoptysis
  • right heart failure (weakness,fatigue, abdo/lower limb swelling)
302
Q

valvular heart disease - mitral stenosis - clinical presentation -

A
  • atrial fibrillation (LA dilatation) - palpitations
  • systemic emboli(atrial fib)(common cerebral)
  • prominent ‘a’ wave jugular ven pulsations
  • mitral facies/malar flush - bilateral, cyanotic, dusky pink discolouration upper cheeks
303
Q

valvular heart disease - mitral stenosis - heart sounds - what is the murmur like?

A
  • low pitched diastolic (when blood flows over a valve) rumble most prominent at apex
  • patient lying L side, held inspiration
304
Q

valvular heart disease - mitral stenosis - loud opening S1 snap

A
  • at apex when leaflets still mobile
  • abrupt halt leaflet motion early in diastole after rapid initial opening due to fusion leaflet tips
  • MORE immobile, sound decreases
  • more severe stenosis = longer diastolic murmur, closer opening snap to S2
305
Q

valvular heart disease - mitral stenosis - diagnosis

A

CXR: LA enlargement, pulmonary oedema, maybe calcified mitral valve
ECG: atrial fibrillation, left atrial enlargement
Echo: GOLD standard for diagnosis, asses valve mobility, gradient, valve area

306
Q

valvular heart disease - mitral stenosis - 5 treatment options

A

mechanical problem, medical therapy not prevent progression

  • beta blockers
  • digoxin
  • diuretics
  • percutaneous mitral balloon valvotomy
  • mitral valve replacement
307
Q

valvular heart disease - mitral stenosis - pharmacological treatment

A
  • Digoxin and beta blockers eg atenolol - control heart rate, prolong diastole, improved diastolic filling
  • Diuretics for fluid overload eg furosemide
308
Q

valvular heart disease - mitral stenosis purcutaneous balloon valvotomy

A
  • local anaesthetic, catheter to RA via femoral vein
  • puncture interatrial septum, RA to LA
  • balloon inflated across mitral valve, pressure, opens leaflets, increases area
309
Q

valvular heart disease - mitral regurgitation

A
  • backflow blood LV->LA during systole

- mild physiological mitral regurg seen 80% normal individuals

310
Q

valvular heart disease - mitral regurgitation - what is it

A

-abnorms of valve leaflets, chordae tendinae, papillary muscles, LV

311
Q

valvular disease - mitral regurgitation - 6 causes

A
  • myxomatous degeneration (MVP) (weakening chordae tendinae) causing floppy mitral valve that prolapses
  • ischaemic mitral valve
  • rheumatic heart disease
  • infective endocarditis
  • papillary muscle dysfunction/rupture
  • dilated cardiomyopathy
312
Q

valvular disease - mitral regurg - risk factors

A
  • females
  • lower BMI
  • older age
  • renal dysfunction
  • prior MI
313
Q

valvular disease - mitral regurg - pathophysiology

A
  • LA dilatation
  • pure volume overload (leakage blood into LA during systole)
  • compensatory mechanisms: LA enlarge, LV hypertrophy, increased contractility
  • pulmonary hypertension so progressive LA dilatation, RV dysfunction
  • LV volume overload, dilatation, progressive heart failure
314
Q

valvular disease - mitral regurg - clinical presentation

A
  • auscultation (eg pan systolic murmur)
  • exertion dysponea
  • dysponea (pul ven hypertension, LV failure)
  • fatigue and lethargy (CO reduced)
  • palpitations due to increased stroke volume
  • R heart failure symptoms (congestive cardiac failure)
  • heart failure w/ + haemodynamic burden eg pregnancy, infection, atrial fib
315
Q

valvular disease - mitral regurg - natural history

A
  • 10-15yrs compensatory phase
  • once ejection fraction less 60% and/or symptomatic - mortality sharp increase
  • severe has 5% year mortality rate
316
Q

valvular disease - mitral regurg - diagnosis

A

ECG: maybe LA enlargement, atrial fib, LV hypertrophy (severe) but not diagnostic
CXR: LA enlargement, central pulmonary artery enlargement
Echo: estimate LA,LV size and function, valve structure assessment, transoesophageal very helpful

317
Q

valvular disease - mitral regurg - treatment options

A
  • medications
  • serial echocardiography
  • surgery
318
Q

valvular disease - mitral regurg - treatment - medications

A
  • vasodilators eg ACE inhibitors (Ramipril, Hydralazine - smooth muscle relaxer)
  • BBs (atenolol) , Ca channel blockers, digoxin (HR control for atrial fib)
  • anticoagulation (atrial fib, flutter)
  • diuretics - fluid overload - Furosemide
319
Q

valvular disease - mitral regurg - treatment - serial echo

A

mild: 2-3 years
moderate: 1-2 years
severe: 6-12 months

320
Q

valvular disease - mitral regurg - treatment - indications for surgery

A
  • ANY SYMPTOMS at rest or exercise - initiate repair if feasible
  • Asymptomatic: if ejection fraction less than 60%, if new onset atrial fib
321
Q

valvular disease - aortic stenosis

A

narrowing aortic valve resulting in obstruction LV SV leading to symptoms breathlessness, syncope, fatigue, chest pain

322
Q

valvular disease - aortic stenosis - epidemiology

A
  • normal valve area 3-4cm2
  • symptoms: valve area 1/4 normal
  • primarily disease of ageing
  • congenital 2nd most common cause
  • most common valve disease western world
323
Q

valvular disease - aortic stenosis - types

A
  • supravalvular (above valve) eg congen fibrous diaphragm above aortic valve
  • subvalvular (below valve) eg congen fibrous ridge/diaphragm immediatley below aortic valve
  • valvular - MOST COMMONE
324
Q

valvular disease - aortic stenosis - 3 main causes

A
  • calcific aortic valvular disease (CAVD) calcification aortic valve resulting in stenosis- most commonly seen in eldery
  • calcification of congen bicuspid aortic valve (BAV) resulting in stenosis
  • rheumatic heart disease (rare-eradication)
325
Q

valvular disease - aortic stenosis - risk factor

A

-congen bicuspid aortic valve (BAV) (occurs mainly in males) predisposes to stenosis, regurgitation

326
Q

valvular disease - aortic stenosis - pathophysiology

A
  • narrowing=obstructed LV emptying, pressure gradient develops (LV-aorta) = increased afterload
  • so increased LV pressure=LV hypertrophy
  • relative ischaemia LV myocardium=anginas, arrhythmias, LV failure
  • severe on exercise-requires increase CO. BP falls, coronary ischaemia worsens, myocardium fails, arrhythmias develop
327
Q

valvular disease - aortic stenosis - clinical presentation

A

suspect in ANY elderly person with chest pain, exertional dysponea, syncope

  • classic triad
  • sudden death
  • slow rising carotid pulse
  • heart sounds/ murmurs
328
Q

valvular disease - aortic stenosis - clinical presentation - classic triad

A
  • chest pain / angina
  • heart failure (usually after 60) (dysponea on exertion)
  • syncope - usually exertional
329
Q

valvular disease - aortic stenosis - clinical presentation - pulsus tardus and pulsus parvus

A
  • pulsus tardus - slow rising carotid pulse

- pulsus parvus - decreased pulse amplitude

330
Q

valvular disease - aortic stenosis - clinical presentation - heart sounds

A
  • soft or absent 2nd heart sound
  • prominent S4 : LV hypertrophy
  • ejection systolic murmur: crescendo-decrescendo character
  • loudness is not associated with severity
331
Q

valvular disease - aortic stenosis - differential diagnosis

A
  • aortic regurgitation

- subacute bacterial endocarditis

332
Q

valvular disease - aortic stenosis - diagnosis - ECG

A
  • LV hypertrophy
  • LA delay
  • LV ‘strain pattern’ due to ‘pressure overload’ : depressed ST segments, T wave inversion in leads oriented towards LV eg I, AVL, V5, V6 when disease severe
333
Q

valvular disease - aortic stenosis - diagnosis - echo

A
  • LV size and function - LV hypertrophy, dilation, ejection fraction
  • doppler derived gradient and valve area (AVA) - assessment pressure gradient across valve during systole
334
Q

valvular disease - aortic stenosis - diagnosis - CXR

A
  • LV hypertrophy

- calcified aortic valve

335
Q

valvular disease - aortic stenosis - treatment

A
  • rigorous dental hygiene/care (increased IE risk in valvular heart disease) - consider IE prophylaxis in dental procedures
  • mechanical problem so limited role for meds
  • vasodilators CONTRAINDICATED (may trigger hypotension thus syncope)
  • surgical aortic valve replacement
  • transcutaneous aortic valve implementation (TAVI)
336
Q

valvular heart disease - aortic stenosis - treatment - surgical aortic valve replacement indications

A
  • ANY symptomatic patients w/ severe aortic stenosis (inc symptoms with exercise)
  • any patient decreasing ejection fraction
  • any patient undergoing CABG w/ moderate/ severe aortic stenosis
337
Q

valvular heart disease - aortic stenosis - treatment - transcutaneous aortic valve implementation (TAVI)

A
  • minimally invasive
  • catheter up aorta inflate balloon across narrowed valve, crack calcification
  • another catheter, leaves stent with a valve = new aortic valve
338
Q

valvular heart disease - aortic regurgitation

A

-leakage blood into LV from aorta during diastole, due to ineffective coaptation (bringing together) of 3 aortic cusps

339
Q

valvular heart disease - aortic regurgitation - epidemiology

A 
-can associated with aortic stenosis 
main causes: 
-congenital bicuspid aortic valve (BAV) (chronic)
-rheumatic fever (chronic)
-infective endocarditis (acute)
340
Q

valvular heart disease - aortic regurg - risk factors

A
  • SLE (lupus)
  • Marfan’s, Ehlers-Danlos syndromes (connective tissue disorders)
  • aortic dilatation
  • infective endocarditis or aortic dissection
341
Q

valvular heart disease - aortic regurg - pathophysiology

A

(reflux is during diastole)

  • LV dilation and hypertrophy to maintain blood pumped into aorta / net CO
  • progressive dilation = heart failure
  • root aorta supplies coronary arteries via coronary sinus : coronary perfusion decreases
  • LV hypertrophy = cardiac ischaemia
342
Q

valvular heart disease - aortic regurg - clinical presentation

A

chronic regurg - patients remain asymptomatic many years

  • exertional dysponea, palpitations, syncope
  • angina
  • wide pulse pressure
  • apex beat displaced laterally
  • hear sounds/murmurs
  • collapsing water hammer pulse
  • Quincke’s sign, de Musset’s sign, pistol shot femoral
343
Q

valvular heart disease - aortic regurg - heart sounds

A
  • diastolic blowing murmur at the left sternal boarder

- systolic ejection murmur - due to increased flow across aortic valve

344
Q

valvular heart disease - aortic regurg - Quincke’s sign, de Musset’s sign

A

Quincke’s sign - capillary pulsation in the nailbeds

de Musset’s sign - head nodding with each heart beat

345
Q

valvular heart disease - aortic regurg - differential diagnosis

A
  • heart failure
  • infective endocarditis
  • mitral regurgitation
346
Q

valvular heart disease - aortic regurg - echo

A
  • evaluation of aortic valve and aortic route
  • measurement LV dimensions and function
  • cornerstone for decision making, follow up evaluation
347
Q

valvular heart disease - aortic regurg - CXR

A
  • enlarged cardiac silhouette and aortic route enlargement

- LV enlargement

348
Q

valvular heart disease - aortic regurg - ECG

A
  • signs LV hypertrophy : ‘volume overload’
  • tall R waves, deeply inverted T waves in left sided chest leads
  • deep S waves in right sided leads
349
Q

valvular heart disease - aortic regurg - treatment

A
  • IE prophylaxis (any valvular disease)
  • symptomatic/ hypertensive: vasodilators eg ACEi eg Ramipril to improve SV, reduce regurg
  • serial echos to monitor progression
  • surgical valve replacement - if symptoms increasing eg enlarging heart on CXR, echo or ECG deterioration (T wave inversion lateral leads)
350
Q

Infective endocarditis

A
  • an infection of the endocardium or vascular endothelium of the heart
  • known as subacute bacterial endocarditis
351
Q

infective endocarditis - where does it occur?

A
  • valves with conegn or acquired defects (usually left side of heart)
  • right sided IE more common in IV drugusers
  • normal valves with virulent organisms eg Streptococcus pneumoniae, Staphylococcus aureus
  • prosthetic valves, pacemakers
352
Q

infective endocarditis - epidemiology

A
  • more common developing countries
  • elderly / those with prosthetic valves
  • young IV drug users
  • young with congen heart disease
353
Q

infective endocarditis - what caused by?

A
  • Staphylococcus aureus most common (IVDU, diabetes, surgery)
  • Pseudomonas aeruginosa
  • Streptococcus viridans (dental problems) - GRAM POSITIVE, alpha haemolytic, optochin resistant (step mutans, strep sanguis, strep milleri, step oralis)
354
Q

infective endocarditis - risk factors

A
  • IV drug use
  • poor dental hygiene
  • skin and soft tissue infection
  • dental treatment
  • IV cannula
  • cardiac surgery
  • pacemaker
355
Q

infective endocarditis - pathophysiology

A

consequences of

  • presence of organisms in bloodstream
  • abnormal cardiac endothelium (facilitates adherence and growth)
  • bacteraemia (patient specific reasons)
  • associated w/ diagnostic/therapeutic procedures
  • infected vegetation (damaged endocardium promotes platelet, fibrin deposition, organisms adhere and grow)
356
Q

infective endocarditis - pathophysiology - bacteraemia for patient specific reasons

A
  • poor dental hygiene (bacteria tooth plaque - gum disease - bleeding, inflammation - brushing/ dental procedures bacteria enter bloodstream -> heart)
  • IV drug use
  • soft tissue infections
357
Q

infective endocarditis - pathophysiology - associated with diagnostic / therapeutic procedures

A
  • dental treatment
  • intravascular cannulae
  • cardiac surgery
  • permanent pacemakers
358
Q

infective endocarditis - pathophysiology - worsening heart failure

A

virulent organisms destroy valve they are on resulting in regurgitation, worsening heart failure

359
Q

infective endocarditis - clinical presentation - HIGH CLINICAL SUSPICION

A
  • new valve lesion/regurgitant murmur
  • embolic events unknown origin
  • sepsis unknown origin
  • haematuria, glomerulonephritis, suspected renal infarction
  • fever PLUS prosthetic material in heart, IE risk factor eg IVDU, newly developed ventricular arrhythmias/ conduction disturbances
360
Q

infective endocarditis - clinical presentation - general

A

ANY pt w/ heart murmur, fever must exclude

  • headache, confusion, malaise, fever, night sweats (unspecific - often misdiagnosed)
  • finger clubbing
  • Staph aureus -develop v quickly- high fever, feel ill rapidly- other virulent wont feel as ill
  • embolisation of vegetations eg stroke, PE, bone infection, kidney dysfunction, MI
  • arrhythmia, heart failure (valve dysfunction
361
Q

infective endocarditis - clinical manifestations

A
  • splinter haemorrhages (finger nail beds)
  • embolic skin lesions (black skin spots)
  • Osler nodes - tender nodules in digits
  • Janeway lesions- finger haemorrhages, nodules
  • Roth spots - retinal haemorrhages with white or clear centres seen on fundoscopy
  • Petechiae- small red/ purple spots caused by bleeds in skin
362
Q

infective endocarditis - diagnosis

A
  • Duke’s criteria
  • Blood cultures
  • Blood test
  • Urinalysis - haematuria
  • CXR (cardiomegaly)
  • ECG (long PR interval at regular intervals)
  • Echo (TTE vs TOE)
363
Q

infective endocarditis - diagnosis - blood cultures and blood tests

A
  • blood cultures: 3 sets from different sites over 24 hours, take BEFORE antibiotics started, identifies in 75% cases
  • blood tests: CRP, ESR raised, normochromic and normocytic anaemia, neutrophilia
364
Q

infective endocarditis - echo TTE vs TOE

A
  • Transthoracic echo - safe, non invasive, no discomfort, often poor images (low sensitivity), identifies vegetations (2mm+) - neg TTE does not exclude possibility IE
  • Transoesophageal echo - more sensitive, very uncomfy, useful visualising mitral lesions, possible aortic root abscesses - BETTER A DIAGNOSING
365
Q

Infective endocarditis - treatment

A
  • antibiotics (organism specific)
  • treat complications (heart block, arrhythmias, embolism, abscess drainage)
  • surgery
  • prevention (eg good oral health, patient education symptoms may indicate IE)
366
Q

infective endocarditis - treatment - antibiotics

A

4-6 weeks

  • if NOT staphylococcus then Benzylpenicillin (IV penicillin) and Gentamycin
  • If IS staph then Vancomycin and Rifampicin (if MRSA)
367
Q

infective endocarditis - treatment - surgery

A
  • removing valve, replacing with prosthetic one, operate if:
  • if infection cannot be antibiotic cured
  • to remove infected devices
  • to remove large vegetations before they embolise
368
Q

Hypertension (HTN)

A
  • major cause premature vascular disease -> cerebrovascular events, IHD, peripheral vascular disease
  • increases mortality
  • commonest cause cardiac failure, major atherosclerosis, cerebral haemorrhage risk factor
369
Q

Hypertension - epidemiology

A
  • screening vital -often symptomless
  • major risk factor CVD
  • under diagnosed, under treated, poorly controlled in UK
  • prevelant over 35s , more common men
  • less than 140/90 = normotensive
370
Q

Hypertension - stage 1 and stage 2

A
  • Stage 1: more than/ equal to 140/90mmHg clinic BP. Daytime av ABPM/HBPM greater than equal to 135/85mmHg
  • Stage 2: more than/equal to 160/100mmHg clinic BP. Daytime av ABPM/HBPM greater than/ equal to 150/95mmHg
371
Q

Hypertension - severe hypertension

A

-clinic systolic BP greater than/ equal to 180mmHg and/or diastolic greater than/ equal to 110mmHg
(start immediate antihypertensive drugs)

372
Q

Hypertension - essential/primary/idiopathic hypertension

A
  • most cases are essential
  • primary cause unknown - multifactoral: genetic susceptibility, excessive symp nervous system activity, abnormalities Na+/K+ membrane transport, high salt intake, abnormalities in RAAS
373
Q

hypertension - secondary hypertension

A
  • commonly caused renal disease/pregnancy

- possibly endocrine causes, aorta coartication, drug therapy

374
Q

secondary hypertension causes - renal disease

A
  • can be both cause and result of HTN
  • chronic kidney disease commonest cause secondary hypertension, diabetes is most common cause CKD
  • acceleration atherosclerosis, endothelial cell dysfunction (vascular changes induced by hypertension) may cause or exacerbate renal disease
  • chronic glomerulonephritis another potential cause (less common now)
375
Q

secondary hypertension - endocrine causes (tumours are RARE)

A
  • Cushing’s syndrome -hypersecretion corticosteroids (enhcnace adrenalines=vasoconstriction)
  • Conn’s syndrome -adrenal tumor secretes aldosterone
  • Pheochromocytoma - adrenal tumor secretes catecholamines (stimulate alpha and beta adrenergic receptors -vasoconstriction, increased cardiac contractility and HR)
376
Q

secondary hypertension causes -coartication of the aorta

A
  • systemic hypertension commonest features in cortication
  • raised BP detected either arm, not legs
  • femoral pulse delayed relative to radial
  • undetected/untreated die cardiac failure, hypertensive cerebral haemorrhage, dissecting aneurysm
377
Q

secondary hypertension causes - drug therapy

A
  • corticosteroids eg Prednisolone
  • cyclosporin
  • erythropoietin
  • some types oral contraceptive pill
  • antidepressants, antismokings, antiADHDs
  • alcohol, amphetamines, ecstacy, cocaine
378
Q

Hypertension - risk factors

A
  • ageing
  • race (more common in black people)
  • family history
  • overweight and obese, little exercise
  • smoking, too much salt in diet
  • alcohol, diabetes, stress
379
Q

hypertension - pathophysiology

A
  • vascular changes - eg accelerates atherosclerosis
  • heart - major risk factor IHD
  • nervous system - intracerebral haemorrhages (death)
  • kidneys
  • malignant hypertension consequences
380
Q

hypertension pathophysiology - vascular changes

A
  • accelerates atherosclerosis
  • thickening media (muscular arteries)
  • smaller arteries, arterioles esp effected
  • endothelial cell dysfunction associated w/ impaired NO mediated vasodilatation, enhanced secretion vasoconstrictors inc endothelins, prostaglandins
381
Q

hypertension pathophysiology - kidneys

A

HTN can cause or be result of renal disease

-kidney size often reduced, small vessels: intimal thickening medial hypertrophy, numbers sclerotic glomeruli increased

382
Q

hypertension pathophysiology - what is malignant hypertension

A
  • markedly raised diastolic blood pressure, usually over 120mmHg and progressive renal disease
  • quite rare, can occur prev fit individuals, often black males 30s-40s
  • prominent renal vascular changes, usually evidence acute haemorrhage, papilloedema (optic disc swelling: +intracran pressure)
383
Q

hypertension pathophysiology - malignant hypertension consequences

A
  • cardiac failure, LV hypertrophy + dilatation
  • blurred vision (papilloedema, retinal haemorrhages)
  • haematuria, renal failure (fibrinoid necrosis of glomeruli)
  • severe headache, cerebral haemorrhages
384
Q

Hypertension - clinical presentation

A
  • usually ASYMPTOMATIC (except malignant hypertension)

- found on screening

385
Q

Hypertension - diagnosis

A
  • end organ damage eg LV hypertrophy, retinopathy, proteinuria - indicates severity, duration HTN, associated poorer prognosis
  • urinalysis
  • blood tests
  • fundoscopy/opthalmoscopy
  • ECG, echocardiogram
  • 24hr ambulatory BP monitoring
386
Q

Hypertension - diagnostic tests - what are you looking for

A

Urinalysis: protein, albumin:creatinine ratio, haematuria
Blood tests: serum creatinine, eGFR, glucose (assess diabetes risk)
Fundoscopy: retinal haemorrhages, papilloedema
ECG, echo: LV hypertrophy

387
Q

Hypertension - what is the treatment goal BP value?

A

140/90mmHg

388
Q

Hypertension - treatment

A
  • change diet (lots veg, fruits, low fat)
  • regular physical exercise
  • reduce alcohol and salt intake
  • lose weight
  • stop smoking
  • drugs (using NICE ‘ACD’ pathway)
389
Q

Hypertension - pharmacological treatment - NICE guidelines ACD pathway

A
  • under 55: ACEi (ramipril, enalapril) or low cost ARB (candesartan, losartan) if cough
  • over 55 or any age of black/afrocaribbean origin: calcium channel blocker (nifedipine, amlodipine)
  • Step 2: calcium channel blocker AND ACEi/ARB
  • Step 3: add thiazide like diuretic (bendroflumethiazide)
390
Q

Hypertension treatment - beta blockers

A

eg bisoprolol, metoprolol

  • consider in young people esp intolerant ACEi/ ARBs
  • NOT first line treatment
  • if higher dose not tolerated in some patients, consider BBs
391
Q

Acute myocardial infarction - definition and 2 types

A
  • necrosis cardiac tissue (myocyte death) due to prolonged myocardial ischaemia, due to COMPLETE occlusion of artery by thrombus
  • STEMI vs NSTEMI/non Q infarction
392
Q

acute myocardial infarction - STEMI

A
  • COMPLETE occlusion MAJOR coronary artery prev affected by atherosclerosis
  • full thickness damage heart muscle
  • usually diagnosed ECG on presentation
  • tall T waves, ST elevation subsequent pathological Q wave
  • may present new LBBB on ECG
393
Q

acute myocardial infarction - NSTEMI

A
  • complete occlusion minor, or partial occlusion major coronary artery prev affected atherosclerosis
  • partial thickness damage heart muscle
  • RETEROSPECTIVE diagnosis after troponin results, sometimes other investigations
  • ST depression, T wave inversion
394
Q

acute MI - epidemiology

A
  • STEMI most common medical emergency
  • STEMI 5/1000 deaths per annum UK
  • worse prognosis: elderly, those with LV heart failure
395
Q

acute MI - risk factors

A
  • age, being male
  • history premature CHD
  • premature menopause
  • diabetes mellitus, smoking, hypertension
  • hyperlipidaemia, obesity, sedentary lifestyle
  • family history IHD, MI first degree relative below 55
396
Q

acute MI - pathophysiology

A
  • rupture/erosion vulnerable fibrous cap of coronary artery atheromatous plaque
  • platelet aggregation, adhesion, local thrombus, vasoconstriction, distal thrombus embolisation - prolonged complete arterial occlusion - myocardial necrosis within 15-30mins in STEMI
397
Q

acute MI - pathophysiology - specifically STEMI

A
  • subendocardial myocardium initially affected, continued ischaemia, infarct zone extends through myocardium, producing transmural Q wave MI
  • early reperfusion may salvage regions myocardium - reducing future mortality and morbidity
398
Q

acute MI - clinical presentation

A

any severe chest pain more 20 mins - may be MI

  • chest pain
  • breathlessness
  • fatigue
  • distress and anxiety
  • pale, clammy, marked sweating
  • significant hypotension (low BP)
  • bradycardia or tachycardia
399
Q

acute MI - chest pain

A
  • severe central ongoing, more 20mins
  • pain radiate left arm, jaw, neck
  • pain NOT respond sublingual GTN spray - opiate analgesia required
  • substernal pressure, squeezing, aching, burning, sharp pain
  • pain associated with nausea, vomiting, dyspnoea and/or palpitations
400
Q

acute MI - differential diagnosis

A
  • NSTEMI, unstable angina, stable angina
  • pneumonia, pneumothorax, heart failure
  • oesophageal spasm, GORD, acute gastritis
  • pancreatitis, MSK chest pain, PE
  • pericarditis, anxiety attack
401
Q

acute MI - STEMI diagnosis

A
  • diagnosed on presentation
  • ST elevation, tall T waves
  • LBBB
  • T wave inversion and pathological Q waves follow
402
Q

acute MI - NSTEMI diagnosis

A
  • RETEROSPECTIVE diagnosis after troponin etc results

- ST depression, T wave inversion

403
Q

acute MI - diagnosis - ECG

A
  • performed on admission to A+E
  • continuous monitoring required - high likelihood significant cardiac arrhythmias
  • ECG changes confined to leads that face infarction
404
Q

acute MI - evolution STEMI on ECG

A
  • after first few mins: T waves tall, pointed, upright, ST segment elevation
  • after first few hours, T waves invert, R wave voltage decreases, Q waves develop
  • after few days, ST segment normal
  • after weeks or months, T wave may return upright , Q WAVE REMAINS
405
Q

acute MI - diagnosis

A

Troponin I or T increased
Myoglobin increased
Transthoracic echo may help confirm MI - wall motion abnormalities detected early in STEMI

406
Q

acute MI - treatment

A
  • pre hospital (aspirin 300mg chewable, GTN sublingual, morphine)
  • hospital (IV morphine, oxygen if sats below 95% or breathless, BB, P2Y12i - clopidogrel)
  • coronary revascularisation (PCI, CABG)
  • fibrinolysis (enhance breakdown occlusive thromboses acitvation plasminogen-plasmin)
407
Q

acute MI - treatment - coronary revascularisation

A
  • PCI - all patients with acute STEMI who can be transferred primary PCI centre within 120 mins first medical contact. If not, fibrinolysis, transfer PCI centre after infusion
  • CABG
408
Q

acute MI - risk factor modification

A
  • stop smoking
  • lose weight, exercise daily, healthy diet
  • treat hypertension and diabetes
  • low fat diet with statins
409
Q

acute MI - secondary prevention (5)

A
  • statins
  • long term aspirin
  • warfarin if large MI
  • beta blockers
  • ACE inhibitors
410
Q

acute MI - 4 complications of myocardial infarction

A

-sudden death (within hours. ventricle fib)
-arrhythmias (few days. electrical instab,
pump failure, exces symp stimulation)
-persistent pain (12 hours - few days.
myocardial necrosis)
-heart failure (CO insufficient meet body metabolic demands. ventricular dysfunction after muscle necrosis also resulting in arrhythmias)

411
Q

acute MI - 4 complications of myocardial infarction

A
  • mitral incompetence(first few days-later. myocardial scarring preventing valve closure)
  • pericarditis (transmural infarct=inflamm of pericardium, more common STEMI)
  • cardiac rupture (early-result of shearing between mobile, immobile myocardium)
  • ventricular aneurysm (stretching newly formed collagenous scar tissue)
412
Q

acute MI - 8 complications of myocardial infarction

A
  • sudden death
  • pericarditis
  • arrhythmias
  • cardiac rupture
  • ventricular aneurysm
  • persistant pain
  • heart failure
  • mitral incompetence
413
Q

Cardiac arrhythmias

A 
'an abnormality of the cardiac rhythm' 
can cause: sudden death 
syncope 
heart failure 
chest pain 
dizziness 
palpitations 
no symptoms
414
Q

2 main types of cardiac arrhythmias

A

Bradycardia

Tachycardia

415
Q

Bradycardia

A
  • heart rate slow - less than 60bpm (day) less than 50bpm(night)
  • usually asymptomatic unless rate really slow
  • normal in athletes: increased vagal tone thus parasymp activity
416
Q

Tachycardia

A

fast HR - more than 100bpm

  • more symptomatic when arrhythmia is fast and sustained
  • supraventricular tachycardias arise from atria or AV junction
  • ventricular tachycardias arise from ventricles
417
Q

Sinus rhythm (normal) - the pathway

A

SAN - action potention - muscle cells of atria - depolarisation of AVN - slow - interventricular septum - bundle of His - R,L bundle branches - free walls both ventricles - Purkinje cells - ventricular myocardial cells

418
Q

Sinus rhythm (normal)

A
  • SAN @ junction beterrn superior VC and RA
  • action potential travels through gap junctions to get to muscle cells
  • AVN in lower interatrial septum
  • slow spread action potential between AVN, ventricles allows for complete contraction atria before ventricles are excited
419
Q

Sinus node function

A
  • SAN=normal cardiac pacemaker
  • depolarises spontaneously
  • rate SAN discharge modulated by autonomic nervous system, normally parasymp predominates, slowing spontaneous discharge rate
  • increased parasymp tone or decreased symp stimulation produces bradycardia (vice versa to produce tachy)
  • women slightly faster sinus rhythm
420
Q

How is normal sinus rhythm characterised on an ECG?

A

P waves that are upright in leads I and II but inverted in the cavity leads AVR and V1
(and each P wave followed by a QRS complex)

421
Q

Sinus arrhythmia

A
  • fluctuations autonomic tone result in changed sinus discharge rate
  • during inspiration - parasympathetic tone falls, heart rate quickens
  • during expiration - parasympathetic tone increases so heart rate fails
  • this variation is normal esp children and young adults
422
Q

Atrial fibrillation

A

-chaotic irregular atrial rhythm 300-600bpm, AV node respondes intermittently hence an irregular ventricular rate

423
Q

atrial fibrillation - epidemiology

A
  • most common sustained cardiac arrhythmia
  • more males
  • 5-15% patients over 75
  • paroxysmal (self terminating) or persistant (continues without intervention)
424
Q

atrial fibrillation - 5 clinical classifications

A
  • Acute: onset within last 48 hours
  • Paroxysmal: stops spontaneously within 7 days
  • Recurrent: 2 or more episodes
  • Persistent: continues for more than 7 days and not self terminating
  • Permanent
425
Q

atrial fibrillation - causes

A
  • idiopathic (5-10%)
  • Hypertension (most common developed world)
  • Heart failure (most common heart failure)
  • Coronary artery disease
  • Valvular heart disease (esp mitral stenosis)
  • Cardiac surgery (1/3rd patients)
  • Cardiomyopathy (rare cause)
  • Rheumatic heart disease
  • Acute excess alcohol intoxication
  • any condition results in raised atrial pressure, increased atrial mass, atrial fibrosis, inflamm, infiltration of atrium
426
Q

atrial fib - risk factors

A
  • older than 60
  • diabetes
  • hypertension
  • coronary artery disease
  • prior MI
  • structural heart disease (valve problems/ congenital defects)
427
Q

atrial fib - pathophysiology

A
  • maintained by continuous rapid (300-600bpm) activation atria by multiple meandering re-entry wavelets
  • often driven by rapidly depolarising automatic foci, located predom within pulmonary veins
  • atria respond electrically at this rate but there is no coordinated mechanical action - only proportion impulses conducted to ventricles (no unified atrial contraction - atrial spasm)
428
Q

atrial fib - pathophysiology - ventricular response

A
  • depends on rate and regularity atrial activity, esp at entry to AV node and balance between sym and parasymp tone
  • CO drops by 10-20% - ventricles not primed reliably by atria
429
Q

atrial fib and thromboembolic events

A
  • atria spasming = some parts not contracting - causes blood to pool in these parts, remain still - begins to clot = thrombus, easily embolism -> stroke
  • ATRIAL FIB - GIVE BLOOD THINNER EG WARFARIN
430
Q

atrial fib clinical presentation

A
  • symptoms highly variable
  • asymptomatic
  • palpitations
  • dyspnoea and/or chest pain (following onset atrial fib)
  • fatigue
  • apical pulse greater radial rate
  • 1st heart sound variable intensity
431
Q

atrial fib differential diagnosis

A
  • atrial flutter

- supraventricular tachyarrhythmias

432
Q

Atrial fib diagnosis - ECG

A

ABSENT P WAVES

IRREGULAR AND RAPID QRS COMPLEX

433
Q

atrial fib acute management definition

A

when AF is due to acute precipitating event eg alcohol toxicity, chest infection, hyperthyroidism - provoking cause should be treated

434
Q

atrial fib acute management

A
  • cardioversion - conversion to sinus rhythm achieved electrically by DC shock eg defibrillator - give LMW-heparin eg Enoxaparin to minimise thromboembolism risk associated with cardioversion
  • if fails - medically by IV infusion antiarrhythmic drug eg amiodarone
  • Ventricular rate control - drugs that block AV node eg Ca channel blocker, BBs, digoxin, antiarrhythmic drug eg amiodarone
435
Q

atrial fib - long term and stable patient management

A
  • Rate control - AV node slowing agents plus oral anticoagulants - beta blocker - calcium channel blocker - last resort digoxin then amiodarone
  • Rhythm control - advocated for younger, symptomatic, physically active patients - cardioversion to sinus rhythm, use BBs to surpress arrhythmia - can use pharma cardioversion eg Flecainide if no structural heart defect, Amiodarone if is - appropriate anticoagulation with cardioversion
436
Q

CHA2DS2VASc score to calculate stroke risk thus need for anticoagulation

A 
Congestive heart failure (1 point)
Hypertension (1 point) 
Age greater/equal 75 (2 points)
Diabetes mellitus (1 point)
Stroke/TIA/thromboembolism (2 points) 
Vascular disease (aorta, coronary, peripheral arteries) (1 point)
Age 65-74 (1 point)
Sex category female (1 point) 
Score 1 - consider anticoag and or aspirin
Score 2 and above - requires oral anticoag
437
Q

Heart block

A
  • can occur any level in conducting system
  • block in AV node or His bundle results in AV block
  • block lower conducting system produces bundle branch block
438
Q

heart block - AV block - 3 forms?

A
  • first degree AV block
  • second degree AV block
  • third degree AV block
439
Q

heart block - first degree AV block

A
  • simple prolongation PR interval to greater than 0.22s
  • every atrial depolarisation followed by conduction to ventricles but with delay
  • causes: hypokalarmia, myocarditis, inferior MI, AV node blocking drugs eg BBs, Ca channel blockers, digoxin
  • ASYMPTOMATIC - NO TREATMENT
440
Q

heart block - second degree AV block

A
  • some P waves conduct, others do not
  • acute MI may produce it
  • Morbitz I block vs Morbitz II block
441
Q

heart block - second degree AV block - Morbitz I block

A
  • Wenckebach block phenomenon
  • progressive PR interval prolongation until beat is dropped and P wave fails to conduct (excitation completely fails to pass through bundle of his)
  • PR interval before blocked P wave much longer
  • causes: AVN blocking drugs BB, CCB, digoxin - inferior MI
  • causes light headiness, dizziness, syncope
  • does not require pacemaker unless poorly tolerated
442
Q

heart block - second degree AV block - Morbitz II BLOCK

A
  • PR interval constant, QRS interval dropped
  • failure of conduction through His-Purkinje system
  • causes: anterior MI, mitral valve surgery, SLE, lyme disease, rheumatic fever
  • causes shortness of breath, postural hypertension, chest pain
  • high risk developing sudden complete AV block, pacemaker should be inserted
443
Q

heart block - third degree AV block - COMPLETE AV BLOCK

A
  • all atrial activity fails to conduct to ventricles
  • ventricle contractions sustained by spontaneous escape rhythm which originates below the block
  • P waves completely independent of QRS complex
  • causes: structural heart disease (transposition great vessels), IHD (acute MI), hypertension, endocarditis or lyme disease
444
Q

heart block - third degree AV block - complete AV block - Narrow - complex escape rhythms

A
  • QRS complex less than 0.12 seconds
  • implies block originates in His bundle thus region block lies more proximally in AV node
  • recent onset narrow complex AV block with transient causes may respond IV ATROPINE
  • chronic narrow complex AV block requires permanent pacemaker if symptomatic
445
Q

heart block - third degree AV block - complete AV block - broad - complex escape rhythm - B - below His

A
  • QRS complex greater than 0.12 seconds
  • implies block originates below bundle of his thus region of block lies more distally His-Purkinje system
  • dizziness, blackouts
  • permanent pacemaker required - treatment depends on aetiology - IV atropine

Phase 2a (3 decks)

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