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Phase 2a (mine) > Cardio > Flashcards

Cardio Flashcards

1
Q

Define atherosclerosis

A

A degenerative condition of the arteries characterised by a fibrous and lipid rich plaque with variable inflammation, calcification and a tendency to thrombosis

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2
Q

Risk factors for atherosclerosis

A
  • Age
  • Family history
  • Smoking
  • High LDL diet
  • Obesity
  • Sedentary lifestyle
  • Diabetes
  • Hypertension
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3
Q

Which arteries is atherosclerosis most often found in`

A

Coronary and peripheral arteries (focal distribution along artery length)

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4
Q

Virchow’s triad

A

Factors predisposing thrombosis:

  • Change in blood constituents
  • Change in flow (stasis)
  • Change to vessel wall (endothelial injury)
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5
Q

Structure of an atherosclerotic plaque

A
  • Fibrous cap
  • Necrotic core
  • Connective tissue
  • Lipid
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6
Q

Major cell types involved in atherosclerosis

A

Endothelium, macrophages, lymphocytes, smooth muscle cells, platelets

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7
Q

Basic mechanism of atherogenesis

A
  1. Fatty streak formation
  2. Intermediate lesions formed
  3. Fibrous plaques and advanced lesions
  4. Plaque rupture
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8
Q

Describe formation of fatty streaks

A

Endothelial injury and build up of cholesterol within the intima. Monocytes migrate to site of injury and transform into macrophages. These ingest lipids and then die - foam cells.

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9
Q

Components of intermediate lesions

A

Vascular smooth muscle cells, T lymphocytes, adhesion and aggregation of platelets to vessel wall

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10
Q

Fibrous plaque formation

A

Smooth muscles have migrated into the plaque and start secreting elastin and collagen, forming a fibrous plaque round the periphery of the plaque.

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11
Q

Plaque rupture

A

The plaque impedes blood flow causing more turbulence. Fibrous plaque constantly resorbed and redeposited - if balance shifts, cap weakens and may rupture. Thrombosis formation and vessel occlusion

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12
Q

Define mural thrombi

A

Thrombi adhered to vessel wall

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13
Q

Clinical stage of atherosclerosis

A

Plaque occludes vessel, increasing risk of haemorrhage. T cell accumulation stimulated. Inflammatory reaction against plaque contents - complications inc. ulceration, calcification and aneurysm.

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14
Q

Clinical manifestations of atherosclerosis

A

Usually asymptomatic till artery narrowed enough to reduce blood flow to organs so its no longer adequate.

  • Coronary arteries - chest pain/pressure (angina)
  • Brain arteries - TIA, weak arms and legs, slurred speech, temporary vision loss, dropping face muscles
  • Peripheral arteries - peripheral artery disease - leg pain when walking
  • Renal arteries - HTN or kidney failure
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15
Q

Examples of useful inflammation

A
  • Pathogens
  • Parasites
  • Tumours
  • Wound healing
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16
Q

Examples of pathological inflammation

A
  • Atherosclerosis
  • Rheumatoid arthritis
  • IHD
  • Excessive wound healing
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17
Q

Treatment of atherosclerosis

A

PCI (percutaneous coronary intervention)

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18
Q

Biggest limitation of PCI

A

Restenosis

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19
Q

What is done to prevent restenosis after PCI

A

Insertion of drug-eluting stents (anti-proliferative and inhibits healing) - stops the artery narrowing again

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20
Q

Pharmacological interventions for atherosclerosis

A

Aspirin (low dose)
Clopidogrel/ticagrelor
Statins

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21
Q

Drug action of aspirin

A

Irreversible inhibitor of COX1/2 - inhibits thromboxane A2

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22
Q

Drug action of clopidogrel/ticagrelor

A

Inhibits P2Y12 ADP receptor on platelets - stops aggregation

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23
Q

Drug action of statins

A

Inhibits HMG-CoA reductase - in pathway for cholesterol synthesis in the liver

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24
Q

Investigations of heart disease: chest x-ray

A

Snapshot of heart with little detail.

  • Enlarged heart suggests congestive heart failure
  • Pulmonary oedema suggests decompensated HF
  • Globular heart suggests pericardial effusion
  • Shows previous surgeries (metal shows up)
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25
Q

Investigations of heart disease: Echocardiography

A

Ultrasound used to give real time images. Transthoracic (TTC) or Transoesophageal (TOE) at rest, during exercise or with infusion of a pharmacological stressor.

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26
Q

Investigations of heart disease: Cardiac CT

A

Detailed info about cardiac structure and function. CT angiography - contrast enhanced imaging of coronary arteries during single breath hold with low dose radiation.
- Can diagnose stenosis in coronary artery disease with 89% accuracy

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27
Q

CT coronary angiography NPV

A

> 99% - means it’s an effective non-invasive alternative to routine transcatheter coronary artery angiographpy to rule out CAD

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28
Q

Investigations of heart disease: CMR (cardiac magnetic resonance imaging)

A

Radiation free method - characterises cardiac structure and function including viability of myocardium

  • First choice imaging method for diseases that directly affect the myocardium
  • Safe with pacemakers
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29
Q

Investigations of heart disease: Nuclear imaging

A

Perfusion assessed at rest and with exercise/pharmacological stressor.

  • Useful for assessing if myocardium distal to blockage is viable (will stenting or CABG be useful?)
  • If hypoperfusion is fixed at rest, likely to be scar tissue (non-viable)
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30
Q

Define ECG

A

Electrocardiogram - a representation of electrical events of the cardiac cycle. Impulses travelling towards an electrode produce upright positive deflection

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31
Q

ECGs can identify:

A
  • Arrhythmias
  • Myocardial ischaemia and MI
  • Pericarditis
  • Electrolyte disturbances
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32
Q

Standard calibration of an ECG

A

25mm/s

0.1mV/mm

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33
Q

What are the 12 ECG leads

A

6 precordial (chest), 4 limbs (1 neutral)

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34
Q

Common ECG abnormalities: P wave

A
  • Right atrial enlargement (>2.5mm) - P pulmonale
  • Left atrial enlargement (notched M shaped) P mitrale
  • Long PR interval - first degree heart block
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35
Q

Common ECG abnormalities: QRS

A

Generally QRS abnormalities hint at ventricular enlargement or conduction blocks.

  • S wave depth shouldn’t be >30mm
  • Pathological Q wave = >2mm deep and >1mm wide. >25% amplitude of the subsequent R wave
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36
Q

Common ECG abnormalities: ST segment

A

Usually flat - elevation of >1mm pathological

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37
Q

Common ECG abnormalities: T wave

A
  • Should be 1/8
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38
Q

Common ECG abnormalities: QT interval

A

Decreases when HR increases (0.35-0.45s)

Shouldn’t be more than half of the interval between adjacent R waves

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39
Q

Common ECG abnormalities: U waves

A

Small, round, symmetrical positive in lead II, amplitude <2mm. Same direction as T wave

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40
Q

Determining HR

A
  • Regular = 300/number of boxes between adjacent QRS complexes
  • Irregular = count number of beats on ECG and multiply by 6
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41
Q

Quadrant approach for QRS axis

A

lead I and AVF:

  • both positive = normal
  • aVF positive, I negative = RAD
  • aVF negative, I positive = LAD
  • both negative = indeterminate axis
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42
Q

Tachycardia

A

Fast heart rate (>100bpm)

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43
Q

Bradycardia

A

Slow heart rate (<60bpm)

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44
Q

Causes of sinus bradycardia

A
  • Physical fitness
  • Vasovagal attacks
  • Sick sinus syndrome
  • Drugs
  • Hypothyroidism
  • Hypothermia
  • Raised intracranial pressure
  • Cholestasis
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45
Q

Drugs causes bradycardia

A

B-blockers, digoxin, amiodarone

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46
Q

Common causes of AF

A
  • IHD
  • Thyrotoxicosis
  • HTN
  • Obesity
  • HF
  • Alcohol
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47
Q

ST elevation can be a sign of

A
  • Acute MI
  • Prinzmetal’s angina
  • Acute pericarditis
  • Left ventricular aneurysm
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48
Q

ST depression can be a sign of

A
  • Digitoxin toxicity

- Ischaemic heart, angina, NSTEMI, acute posterior MI

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49
Q

T inversion in V1-3

A
  • RBBB

- RV strain

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50
Q

T inversion in V2-5

A
  • Anterior ischaemia
  • HCM (hypertrophic cardiomyopathy)
  • Subarachnoid haemorrhage
  • Lithium
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51
Q

T inversion in V4-6

A
  • Lateral ischaemia
  • LVH
  • LBBB
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52
Q

ECG signs of an MI

A
  • Within hours T wave is peaked and ST elevation
  • Within 24h T wave inverts. ST elevation rarely persists unless left ventricular aneurysm. T wave inversion may or may not persist
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53
Q

ECG signs for PE

A

Sinus tachycardia, RBBB, right ventricular strain pattern

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54
Q

Types of echocardiography

A 
M-mode
Two-dimensional (real time)
3D echocardiography
Doppler and colour-flow echocardiography
Tissue doppler imaging
Transoesophageal echocardiography
Stress echocardiography
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55
Q

M-mode (motion mode) echocardiography

A

A single-dimension image

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56
Q

Two-dimensional (real time) echocardiography

A

2D, fan-shaped image of segment of the heart. Visualising congenital heart disease, LV aneurysm, mural thrombus, LA myxoma, septal defects

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57
Q

Doppler and colour-flow echocardiography

A

Different coloured jets illustrate flow and gradients across valves and septal defects

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58
Q

Tissue doppler imaging

A

Uses Doppler ultrasound to measure velocity of myocardial segments over the cardiac cycle. Useful for assessing longitudinal motion - diagnosis of systolic and diastolic HF

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59
Q

Transoesophageal (TOE) echocardiography

A

More sensitive than transthoracic - transducer nearer the heart. Diagnose aortic dissection, assessing prosthetic valves and finding source of cardiac emboli

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60
Q

Stress echocardiography

A

Evaluates ventricular function, ejection fraction, myocardial thickening and characterises valvular lesions

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61
Q

Uses of echocardiography

A
  1. Quantification of global LV function
  2. Estimating right heart haemodynamics
  3. Valve disease
  4. Congenital heart disease
  5. Endocarditis
  6. Pericardial effusion
  7. Hypertrophy cardiomyopathy
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62
Q

Echocardiography + quantification of global LV function

A

HF may be due to systolic/diastolic ventricular impairment. Echo measure EDV - large = systolic dysfunction small = diastolic dysfunction

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63
Q

Echocardiography + estimating right heart haemodynamics

A

Doppler studies of pulmonary artery flow and tricuspid regurgitation allow evaluation of RV function and pressure

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64
Q

Echocardiography + valve disease

A

Technique of choice for measuring pressure gradients and valve orifice areas in stenotic lesions

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65
Q

Echocardiography + congenital heart disease

A

Presence of lesions and their significance.

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66
Q

Echocardiography + pericardial effusion

A

Best diagnosed by echo - fluid accumulating between posterior pericardium and LV can be detected

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67
Q

Echocardiography + hypertrophic cardiomyopathy

A

Echo shows asymmetrical septal hypertrophy, small LV cavity, dilated left atrium and systolic anterior motion of the mitral valve

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68
Q

Define hypertension

A

Chronic elevation of blood pressure > 140/90 mmHg

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69
Q

Define malignant hypertension

A

Rapid rise in blood pressure leading to vascular damage >160/110 mmHg

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70
Q

Causes of HTN

A

Primary 90% - no known underlying cause

Secondary - 10%

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71
Q

Secondary causes of HTN

A

Endocrine disease
Renal disease
Exogenous agents
Lifestyle

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72
Q

Endocrine disease causing HTN

A
  • Overproduction of aldosterone (Conn’s syndrome)

- Chronic vascular disease - diabetes, Cushing’s, hyperthyroidism

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73
Q

Renal disease causing HTN

A
  • Intrinsic disease (glomerulonephritis, polycystic kidneys)

- Renovascular disease

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74
Q

Exogenous agents causing HTN

A

NSAIDs, combined oral contraceptive, corticosteroids, ciclosporin, cold cures, antidepressants, recreational

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75
Q

Lifestyle factors causing HTN

A

Obesity, excessive salt and alcohol intake, stress, sedentary lifestyle, smoking

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76
Q

Signs and symptoms of HTN

A

Usually asymptomatic. Can sometimes cause headaches

Look for end organ damage (e.g. retinopathy)

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77
Q

Signs and symptoms of malignant HTN

A
  • Bilateral renal haemorrhages
  • Papilloedema
  • Headache and visual disturbance
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78
Q

Investigations for HTN

A
  • 24hr ABPM
  • Fasting glucose + cholesterol (quantify overall risk)
  • ECG or echo (end organ damage)
  • Renal ultrasound/arteriography
  • 24h urinary meta-adrenaline
  • Urinary free cortisol
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79
Q

Complications of HTN

A
  • Cor pulmonale -> right ventricular hypertrophy and dilatation due to pulmonary HTN.
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80
Q

Management of HTN

A
  • Lifestyle changes
  • ACE-i/ARB or CCB
  • ACE-i/ARB and CCB
  • ACE-i/ARB and CCB and thiazide-like diuretic
  • Add spironolactone, beta blockers or alpha blockers
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81
Q

Action and example of ACE-i

A

Inhibits ACE (angiotensin II not made, BP lowered). Ramipril

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82
Q

Action and example of ARB

A

Blocks angiotensin II at peripheral receptors. Candesartan

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83
Q

Action and example of CCB

A

Blocks VG calcium channels in vascular smooth muscle - reduced contraction. Amlodipine

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84
Q

Action and example of thiazide-like diuretic

A

Inhibit sodium reabsorption by DCT, reducing ECF volume. Bendroflumethazide

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85
Q

Define angina

A

Recurrent transient episode of chest pain due to myocardial ischaemia

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86
Q

Types of angina

A
  1. Stable angina - induced by effort, relieved by rest.
  2. Unstable angina (crescendo) - increasing frequency/severity - occurs on minimal exertion/rest. High risk of MI
  3. Decubitis angina- precipitated by lying flat
  4. Prinzmetal angina - causing by coronary artery spasm
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87
Q

Pathology of angina

A
  • Stenosis causes increased resistance within a vessel.
  • In exercise, microvascular resistance falls and increases flow
  • With atherosclerosis, flow cannot meet metabolic demand
  • Myocardial ischaemia
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88
Q

Causes of angina

A

ATHEROSCLEROSIS

  • anaemia
  • coronary artery spasm
  • tachyarrhythmias
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89
Q

RF angina

A 
Non-modifiable
- Gender
- FH
- PMH
- Age
Modifiable
- Smoking
- Diabetes
- HTN
- Hypercholesterolaemia
- Sedentary lifestyle
- Stress
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90
Q

Precipitants of angina

A 
Affects supply
- Anaemia
- Hypoxaemia
- Hypothermia
- Hypovolaemia
- Hypervolaemia
Affects demand
- HTN
- Hyperthyroidism
- Valvular heart disease
- Tachyarrhythmia
- Cold weather
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91
Q

Clinical presentation of angina

A
  1. Contricting/heavy discomfort to the chest, jaw, neck, shoulders, or arms
  2. Symptoms brought on by exertion
  3. Symptoms relieved by rest/GTN spray
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92
Q

Symptoms of angina

A 
Dyspnoea
Nausea
Sweatiness
Faintness
Crushing chest pain (possibly radiating to the jaw)
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93
Q

Differential diagnoses of angina

A
  • Pericarditis
  • Pulmonary embolism
  • Chest infection
  • Dissection of the aorta
  • Gastro-oesophageal reflux/spasm/ulceration
  • Psychological
  • Musculo-skeletal
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94
Q

Investigations for angina

A
  • ECG (often normal)
  • Blood tests (FBC, U%E, TFTs, lipids, HbA1C)
  • Echocardiogram (normal)
  • Chest x-ray
  • Physiological - exercise stress treadmill, stress echo. perfusion MRI
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95
Q

Management of angina

A

Address exacerbating factors (anaemia, tachycardia, thyrotoxicosis) GTN

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96
Q

Primary prevention of angina

A

Reduce risk of CAD and complications

Risk factor modification

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97
Q

Secondary prevention of angina

A
  • Lifestyle changes
  • 75mg daily aspirin
  • ACE-i
  • Address hyperlipidaemia
  • Interventional (PCI and sometimes surgery)
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98
Q

Action and example of beta-blocker

A

Block beta receptors in the sympathetic NS - reduces CO and O2 demand. Bisoprolol

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99
Q

Action and example of nitrates

A

Dilate systemic veins to reduce heart preload on the heart. Isosorbide mononitrate

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100
Q

Action and example of statins

A

Block HMG-CoA reductase - enzyme in cholesterol production pathway. Reduces LDL- cholesterol. Atorvastatin

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101
Q

PCI (percutaneous coronary intervention) in angina

A

Balloon inflated inside a stenosed vessel, opening the lumen. Stent is inserted to reduce chance of restenosis

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102
Q

CABG (coronary artery bypass graft)

A

Internal mammary artery grafted to bypass stenosed vessel

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103
Q

Pros and cons of PCI

A 
Pros
1. Less invasive
2. Convenient
3. Repeatable
4. Acceptable
Cons
1. Risk stent thrombosis
2. Restenosis
3. Can't deal with complex disease
4. Dual antiplatelet therapy
104
Q

Pros and cons of CABG

A 
Pros
1. Good prognosis
2. Deals with complex disease
Cons
1. Invasive
2. Risk of stroke, bleeding
3. Can't do if frail or co-morbid
4. One-time treatment
5. Increased length of stay and recovery time
105
Q

Define acute coronary syndromes

A

Unstable angina and myocardial infarctions. Share common underlying pathology of plaque rupture, thrombosis, and inflammation

106
Q

Rare causes of ACS

A

Coronary vasospasm without plaque rupture, drug abuse, dissection of the coronary artery, thoracic aortic depression

107
Q

RF for ACS

A 
Non-modifiable
- Gender
- FH of IHD
- Age
Modifiable
- Smoking
- Diabetes
- HTN
- Hyperlipidaemia
- Sedentary lifestyle
- Cocaine use
108
Q

Diagnosis of ACS

A
  • Increase in cardiac biomarkers (troponin)
  • Symptoms of ischaemia
  • ECG changes for new ischaemia
  • Pathological Q waves
  • New loss of myocardium
109
Q

Symptoms of ACS

A
  • Acute central crushing chest pain>20min
  • Nausea
  • Sweatiness
  • Dyspnoea
  • Palpitations
  • ACS without chest pain = silent - seen in elderly and diabetics. Pulmonary oedema, syncope, epigastric pain, vomiting
110
Q

Signs of ACS

A
  • Distress
  • Anxiety
  • Pallor
  • Sweatiness
  • 4th heart sound
  • Signs of HF
  • Low grade fever
111
Q

Differential diagnoses of ACS

A
  • Stable angina
  • Pericarditis
  • Myocarditis
  • Takotsubo cardiomyopathy
  • Aortic dissection
112
Q

Investigations for ACS

A
  • ECG - STEMI (tall T waves, ST elevation, T wave inversion and pathological Q waves follow non-specific changes)
  • CXR - cardiomegaly, pulmonary oedema, widened mediastinum
  • Bloods (FBC, U&E, Glucose, lipids, cardiac enzymes - troponin + serial troponins required to differentiate NTEMI from unstable angina)
113
Q

Troponin levels in NSTEMI vs unstable angina

A

Troponin levels raised in NSTEMI, the same in unstable angina

114
Q

3 managements of ACS

A
  1. Symptom control
  2. Modify risk factors
  3. Cardioprotective medications
115
Q

Symptoms control of ACS

A

Relieve chest pain with PRN GTN and opiates

116
Q

Modifying RF of ACS

A
  • STOP SMOKING
  • Treat diabetes, HTN and hyperlipidaemia
  • Mediterranean diet
  • Daily exercise encouraged
  • Mental health flagged to GPs
117
Q

Cardioprotective medications in ACS

A
  1. Dual antiplatelet therapy - aspirin and clopidogrel
  2. Anticoagulants - fondaparinux
  3. Beta-blockers - propanolol (reduce myocardial o2 demand)
  4. ACE-i - patients with LV dysfunction/HTN/diabetes
  5. High dose statin
118
Q

Action and example of anticoagulants

A

Inhibits both fibrin formation and platelet aggregation. Fondaparinux

119
Q

NSTEMI presentation

A

Prolonged ischaemia chest pain on minimal or no exertion. Crescendo pattern. No significant rise in troponin and no ST elevation

120
Q

Subendocardial/patchy infarction

A

Involves the innermost layer and some middle parts of the myocardium but not the epicardium (NSTEMI)

121
Q

Transmural infarction

A

Full thickness of the myocardium

122
Q

Initial management of STEMI

A
  1. Attach ECG (12 lead)
  2. IV access - bloods.
  3. Hx of CVD, RF for IHD
  4. Aspirin 300mg and ticagrelor 180mg
  5. Morphine 5-10mg IV and anti-emetic
  6. STEMI on ECG = primary PCI
123
Q

Treatment of STEMI

A
  1. Aspirin
  2. LMW heparin
  3. Thrombolytic therapy
124
Q

Complications of MI (12)

A
  1. Cardiac arrest
  2. Cardiogenic shock
  3. LV failure
  4. Brady/tachyarrhythmia
  5. RV failure (presents with low CO)
  6. Pericarditis
  7. Systemic embolism
  8. Cardiac tamponade
  9. Mitral regurgitation
  10. Ventricular septal defect
  11. Dressler’s syndrome
  12. LV aneurysm
125
Q

MI related pericarditis

A
  • Central chest pain relieved by sitting forwards
  • ECG - saddle shaped ST elevation
  • NSAIDs
126
Q

MI related systemic embolism

A
  • May arise from LV mural thrombus

- Consider anticoagulation with warfarin for 3 months

127
Q

MI related cardiac tamponade

A
  • Low CO, pulsus paradoxus, muffled heart sounds
  • Echocardiogram used to diagnose
  • Treated by pericardial aspiration, surgery
128
Q

MI related mitral regurgitation

A
  • Presents with pulmonary oedema

- Treated with valve replacement

129
Q

MI related ventricular septal defect

A
  • Presents with pansystolic murmur (extending through entire systolic interval), cardiac failure
  • Diagnosed with echocardiogram
  • Treated with surgery
130
Q

MI related Dressler’s syndrome

A
  • Recurrent pericarditis, pleural effusions, fever, anaemia

- Treatment - NSAIDs if severe

131
Q

Define heart failure

A

Inability of the heart to keep up with demands - failure of the heart to pump blood with normal efficiency so CO is inadequate for body’s requirements. Severe failure causes cardiogenic shock

132
Q

Triggers for hypertrophic response

A
  1. Angiotensin II
  2. ET-1 and insulin-like growth factor 1
  3. TGF-beta
133
Q

Classifications of heart failure

A

Systolic, diastolic, LV, RV

134
Q

Systolic heart failure

A

Inability of the ventricle to contract normally, resulting in low CO. Ejection fraction >40%

135
Q

Causes of systolic HF

A
  1. IHD
  2. MI
  3. Cardiomyopathy
136
Q

Diastolic HF

A

Inability of the ventricles to relax and fill normally, causing increased filling pressures. Typically ejection fraction >50% (HF with preserved EF)

137
Q

Causes of diastolic HF

A
  1. Ventricular hypertrophy
  2. Constrictive pericarditis
  3. Tamponade
  4. Restrictive cardiomyopathy
  5. Obesity
138
Q

LV failure

A

Pulmonary congestion (blood backs up in veins) pressure increases and fluid is pushed into the alveoli ->. overload of the right side

139
Q

Symptoms of LV failure

A
  • Dyspnoea
  • Poor exercise tolerance
  • Fatigue
  • Orthopnoea (SOB lying flat)
  • Paroxysmal nocturnal dyspnoea (SOB at night, awakening from sleep)
  • Nocturnal cough
  • Wheeze
  • Cold peripheries
  • Weight loss
140
Q

RV failure

A

Venous HTN and congestion

141
Q

Causes of RV failure

A
  • LVF
  • Pulmonary stenosis
  • Lung disease
142
Q

Symptoms of RV failure

A
  • Peripheral oedema
  • Ascites
  • Nausea
  • Anorexia
  • Facial engorgement
  • Epistaxis (nose bleed)
143
Q

Define acute HF

A

New-onset acute or decompensation of chronic HF characterised by pulmonary and or peripheral oedema with/without signs of peripheral hypoperfusion

144
Q

Define chronic HF

A

Develops slowly. Venous congestion common but arterial pressure is well maintained until very late

145
Q

Define low-output HF

A

CO is low and fails to increase normally with exertion.

146
Q

Causes of low-output HF

A
  • Excessive pre-load: mitral regurgitation or fluid overload
  • Pump failure - decreased heart rate, negatively inotropic drugs
  • Chronic excessive afterload - aortic stenosis, HTN
147
Q

Define high-output HF

A

Output is normally increased in the face of extremely increased needs. Failure occurs when CO fails to meet these needs

148
Q

Causes of high output HF

A
  • Anaemia
  • Pregnancy
  • Hyperthyroidism
  • Paget’s disease
149
Q

Diagnosis of HF

A
  • Symptoms of HF
  • Objective evidence of cardiac dysfunction at rest
  • Tests: FBC. CXR, ECG, echocardiography
150
Q

Signs of HF

A
  • Cyanosis
  • Decreased BP
  • Narrow pulse pressure
  • Pulsus alternans
  • Displaced apex (LV dilatation)
  • Pulmonary HTN
  • Pink frothy sputum
  • Signs of valve diseases
151
Q

Differential diagnoses of HF

A
  • COPD
  • Emphysema
  • MI
  • PE
  • Pneumonia
152
Q

Management of acute HF

A
  1. Sit upright
  2. High flow O2 if low peripheral capillary o2 saturation
  3. Treat arrhythmias
  4. Investigations while continuing treatment
  5. Diamorphine 1.25-5mg IV slowly
  6. Furosemide 40-80mg IV slowly
  7. GTN spray 2SL puffs
  8. If systolic Bp>100, start nitrate transfusion
  9. If systolic <100 treat as cardiogenic shock and refer to ICU
153
Q

Management of chronic HF

A
  1. Stop smoking, alcohol, reduce salt, optimise weight and nutrition
  2. Treat cause and exacerbating factors (e.g. anaemia)
  3. Annual flu vaccine, one off pneumococcal vaccine
  4. Drugs
154
Q

Pharmacological management of chronic HF

A
  1. Diuretics - furosemide
  2. ACE-i treats LVSD
  3. B-blockers decrease mortality
  4. Mineralocorticoid receptor antagonists (spironolactone)
  5. Digoxin
  6. Vasodilators - hydralazine and isosorbide nitrate
155
Q

Define intractable heart failure

A

Failure that is resistant to further treatment - transfer to palliative care

156
Q

Define valvular heart disease

A

Any disease process involving one of more of the four valves of the heart

157
Q

2 categories of valvular heart disease

A

Congenital and acquired

158
Q

Examples of congenital valvular heart disease

A

Congenital aortic stenosis and congenital bicuspid valve

159
Q

Examples of acquired valvular heart disease

A

Degenerative calcification, rheumatic heart disease, rare causes

160
Q

Examples of mitral valve diseases

A
  1. Mitral regurgitation
  2. Mitral stenosis
  3. Mitral valve prolapse
161
Q

Define mitral regurgitation

A

Backflow through the mitral valve during systole

162
Q

Difference between acute and chronic mitral valve regurgitation

A

Acute results in back up into the lungs, chronic results in dilation as it has had time for adjustment

163
Q

Pathophysiology of mitral valve regurgitation

A

Volume overload. Compensatory mechanisms = left atrial enlargement, LVH and increased contractility.

  • Progressive LA dilation and RV dysfunction due to pulmonary HTN
  • Progressive LV volume overload leads to dilatation and progressive HF
164
Q

Causes of mitral regurgitation

A
  1. Rheumatic fever
  2. Infective endocarditis
  3. Mitral valve prolapse
  4. Ruptured chordae tendinae
  5. Papillary muscle dysfunction
  6. Cardiomyopathy
165
Q

Symptoms of mitral regurgitation

A
  1. Dyspnoea (on exertion)
  2. Pulmonary oedema
  3. Fatigue
  4. Palpitations
166
Q

Signs of mitral regurgitation

A
  1. AF - displaced, hyperdynamic apex
  2. Pansystolic murmur at apex radiating to axilla
  3. The more severe, the larger the LV
167
Q

Investigations of mitral regurgitation

A
  1. ECG - AF, p-mitrale if in sinus rhythm, LA enlargement, LV hypertrophy
  2. CXR - enlarged LA and LV
  3. Mitral valve calcification
  4. Echo - assess LV size, function, MR severity. Cardiac catheterisation to confirm diagnosis
168
Q

Management of mitral valve regurgitation

A
  1. Control of HR if AF (b-blockers)
  2. Anticoagulate with history of AF, embolism, prosthetic valve or additional mitral stenosis
  3. Vasodilators (hydralazine)
  4. Diuretics for fluid overload
  5. Surgery - repair/replacement
169
Q

Define mitral valve prolapse

A

The most common valvular abnormality. Condition in which 2 flaps of the mitral valve do not close smoothly or evenly, but instead bulge upwards into the left atrium

170
Q

Symptoms of mitral prolapse

A
  • Usually asymptomatic

- May develop atypical chest pain, palpitations, autonomic dysfunction symptoms

171
Q

Signs of mitral valve prolapse

A

Mid-systolic click and/or late systolic murmur

172
Q

Complications of mitral valve prolapse

A
  1. Mitral regurgitation
  2. Cerebral emboli
  3. Arrhythmias
  4. Sudden death
173
Q

Investigations for mitral prolapse

A

Echo is diagnostic. ECG may show inferior T wave inversion

174
Q

Treatment of mitral prolapse

A
  • B-blockers may help palpitations and chest pain. Surgery if severe
175
Q

Define mitral stenosis

A

Obstruction of LV inflow that prevents proper filling during diastole due to stenosis of the mitral valave

176
Q

Normal and pathological mitral valve area

A

Normal = 4-6cm2

Pathological< 2cm2

177
Q

Pathophysiology of mitral stenosis

A
  1. Progressive dyspnoea - worse with exercise, fever, tachycardia, pregnancy
  2. Increased trans-mitral pressure - LA enlargement and AF
  3. Right HF symptoms - pulmonary venous HTN
  4. Haemoptysis - due to rupture of bronchial vessels (elevated pulmonary pressure)
178
Q

Causes of mitral stenosis

A
  1. Rheumatic fever
  2. Congenital
  3. Infective endocarditis
  4. Malignant carcinoid
179
Q

Presentation of mitral stenosis

A
  1. Pulmonary HTN - dyspnoea, haemoptysis
  2. Pressure from large LA pressure on local structures - hoarse voice (recurrent laryngeal nerve)
  3. Dysphagia
  4. Bronchial obstruction
  5. Fatigue
  6. Palpitations
  7. Chest pain
180
Q

Signs of mitral valve stenosis

A
  1. Prominent a wave in jugular venous pulsations (due to pulmonary HTN and RV hypertrophy)
  2. Signs of right HF
  3. Mitral facies - severe MS leads to vasoconstriction = pink patches on cheeks
  4. Malar flush on cheeks
  5. Low vol pulse
  6. Low pitch rumbling at the apex
181
Q

Investigation of mitral stenosis

A
  1. ECG - AF and LA enlargement
  2. CXR - LA enlargement and pulmonary congestion
  3. Echo - assess mitral valve mobility, gradient and mitral valve areas
182
Q

Management of mitral stenosis

A
  1. Treat AF
  2. Medication - warfarin, [b-blockers, CCB, digoxin - control HR and prolong diastole], Diuretics reduce fluid overload
  3. Serial echocardiography
  4. Mitral balloon valvotomy
  5. Mitral valve replacement
183
Q

Examples of aortic valve disease

A
  1. Aortic stenosis
  2. Aortic sclerosis
  3. Aortic regurgitation
184
Q

Define aortic valve stenosis

A

Narrowing of the aortic valve opening that restricts blood flow from the left ventricle to the aorta

185
Q

Normal and pathological aortic valve size

A

Normal = 3-4cm2

Pathological < 1/4 normal

186
Q

Types of aortic stenosis

A
  • Supravalvular
  • Subvalvular
  • Valvular
187
Q

Pathophysiology of aortic stenosis

A
  • Pressure gradient develops between LV and aorta
  • LV function initially maintained by compensatory pressure hypertrophy
  • LV function declines as compensation exhausted
188
Q

Causes of aortic stenosis

A
  • Senile calcification (most common)
  • Congenital (bicuspid valve, Williams syndrome)
  • Rheumatic heart disease
189
Q

Presentation of aortic stenosis

A
  • Classic triad of angina, syncope, SOB
  • Extertional dyspnoea
  • Dizziness, faints
  • Systemic emboli (if infective endocarditis)
190
Q

Signs of aortic stenosis

A
  • Slow rising carotid pulse with narrow pulse pressure
  • Heaving, non-displaced apex beat
  • Ejection systolic murmur - crescendo-decrescendo character
191
Q

Investigations of aortic stenosis

A
  • Echo - LV size and function assessed (LVH, dilation, ejection fraction, doppler derived gradient and valve area)
  • Cardiac catheter can access valve gradient, LV function, CAD
  • Pulsus parvus et tardus - weak and late pulse
192
Q

Differential diagnosis of aortic stenosis

A
  1. Hypertrophic cardiomyopathy

2. Aortic sclerosis

193
Q

Management of aortic stenosis

A
  1. Poor prognosis without surgery for symptomatic patients
  2. Valve replacement
  3. Percutaneous valvuloplasty/replacement
  4. TAVI - transcatheter aortic valve implantation
194
Q

Define aortic sclerosis

A

Senile degeneration of the valve. There is an ejection systolic murmur, but no carotid radiation and normal pulse and S2

195
Q

Define aortic regurgitation

A

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

196
Q

Causes of acute aortic regurgitation

A
  1. Infective endocarditis
  2. Ascending aortic dissection
  3. Chest trauma
197
Q

Causes of chronic aortic regurgitation

A
  1. Congenital
  2. Connective tissue disorders (e.g. Marfan’s)
  3. Rheumatic fever
  4. Takayasu arteritis
  5. Rheumatoid arthritis
198
Q

Pathophysiology of aortic regurgitation

A

Combined pressure and volume overload.

- Compensatory mechanisms = LV dilation, LVH, progressive dilation leads to HF

199
Q

Presentation of aortic regurgitation

A
  • Breathlessness
  • Orthopnoea (breathless lying down)
  • Palpitations
  • Diastolic blowing murmur
200
Q

Investigations for aortic regurgitation

A
  1. CXR - enlarged cardiac silhouette and aortic root enlargement
  2. Echo - evaluation of the AV and aortic root with measurement of LV dimensions and function
  3. Cardiac catheterisation to assess severity of lesion, anatomy of aortic root
201
Q

Management of aortic regurgitation

A
  1. Medical - vasodilators
  2. Serial echo to monitor progression
  3. Surgical repair/replacement of valve
202
Q

Examples of tricuspid valve disease

A
  1. Tricuspid regurgitation

2. Tricuspid stenosis

203
Q

Define tricuspid regurgitation

A

A disorder in which the tricuspid valve does not close tight enough. This problem causes blood to flow backward into the RA when the RV contracts

204
Q

Causes of tricuspid regurgitation

A
  1. Rheumatic fever
  2. Infective endocarditis
  3. Carcinoid syndrome
205
Q

Symptoms of tricuspid regurgitation

A
  1. Fatigue
  2. Hepatic pain on exertion
  3. Ascites
  4. Oedema
206
Q

Signs of tricuspid regurgitation

A
  1. Pansystolic murmur
  2. Pulsatile hepatomegaly
  3. Jaundice
207
Q

Management of tricuspid regurgitation

A
  1. Drugs - diuretics for systemic congestion, treat underlying cause
  2. Valve repair/replacement
208
Q

Define tricuspid stenosis

A

Narrowing of the tricuspid valve opening. It restricts blood flow between the upper and lower part of the right side of the heart

209
Q

Causes of tricuspid stenosis

A
  1. Rheumatic fever
  2. Congenital
  3. Infective endocarditis
210
Q

Symptoms of tricuspid stenosis

A
  1. Fatigue
  2. Ascites
  3. Oedema
211
Q

Signs of tricuspid stenosis

A
  1. Opening snap, early diastolic murmur at left sternal edge in inspiration
  2. AF
212
Q

Investigation for tricuspid stenosis

A

Echo

213
Q

Treatment of tricuspid stenosis

A
  1. Diuretics

2. Surgical repair/replacement

214
Q

Define pulmonary stenosis

A

A condition characterised by obstruction to blood flow from the RV to the pulmonary artery. The pulmonary valve leaflets are thickened and fused together along their separation lines

215
Q

Causes of pulmonary stenosis

A
  1. Congenital (e.g. Turner syndrome)

2. Acquired - rheumatic fever and carcinoid syndrome

216
Q

Symptoms of pulmonary stenosis

A
  1. Dyspnoea
  2. Fatigue
  3. Oedema
  4. Ascites
217
Q

Signs of pulmonary stenosis

A
  1. Dysmorphic facies
  2. Ejection click
  3. Ejection systolic murmur
218
Q

Investigations for pulmonary stenosis

A
  1. ECG - p pulmonale, RBBB
  2. CXR - prominent pulmonary arteries (post-stenotic dilatation)
  3. Cardiac catheterisation is diagnostic
219
Q

Treatment of pulmonary stenosis

A

Pulmonary valvuloplasty or valvotomy

220
Q

Define rheumatic fever

A

Pharyngeal infection with Lancefield AB-haemolytic streptococci triggers with rheumatic fever 2-4 weeks later

221
Q

Pathology of rheumatic fever

A

An antibody to the carbohydrate cell wall of the streptococcus cross-reacts with valve tissue and may cause permanent damage to the heart valves

222
Q

Diagnosis of rheumatic fever

A

Must be evidence of recent strep infection plus 2 major criteria or 1 major+2minor

223
Q

Evidence of group A b-haemolytic streptococcal infection

A
  • Positive throat culture
  • Rapid streptococcal antigen test +ve
  • Elevated or rising streptococcal antibody titre
  • Recent scarlet fever
224
Q

Major criteria diagnosis of rheumatic fever

A
  • Carditis (tachycardia, murmurs)
  • Arthritis
  • Subcutaneous nodules
  • Erythema marginatum 3
225
Q

Minor criteria diagnosis of rheumatic fever

A
  • Fever
  • Raised ESR/CRP
  • Arthralgia
226
Q

Management of rheumatic fever

A
  1. Bed rest until CRP normal for 2 weeks
  2. Benzylpenicillin
  3. Analgesia for carditis/arthritis
  4. Immobilise joints in severe arthritis
227
Q

Define infective endocarditis

A

Infection of the heart valves or other endocardial lined structures within the heart (e.g septal defects). Bad infection that showers infectious material around the bloodstream

228
Q

Types of IE

A
  1. Left side native (mitral or aortic)
  2. Left side prosthetic IE
  3. Right side IE
  4. Device related IE (pacemaker/defibrillator)
  5. Prosthetic
229
Q

Causes of IE

A
  1. Have abnormal valve (regurgitant or prosthetic)
  2. Introduce infectious material into the bloodstream or directly onto the heart during surgery
  3. Previous IE
230
Q

Pathology of IE

A
  1. S. aureus gains access in skin via indwelling vascular lines or IV drug abuse
  2. S. viridans access via blood from oropharnyx following tooth brushing or dentistry
  3. Enterococci access blood following instrumentation of bowel or bladder
231
Q

Clinical presentations of IE

A
  1. Left side = fever, valve damage. Right side = fever, chills, pulmonary symptoms (septic emboli)
  2. Systemic infection signs
  3. Embolisation (stroke, pulmonary embolus, MI)
  4. Valve dysfunction (HF arrthymias)
  5. Petechiae (skin lesions)
  6. Splinter haemorrhage
  7. Osler’s nodes (purple node on pulp of digits)
  8. Janeway lesions
  9. Roth spots on fundoscopy
232
Q

Diagnosis of IE

A

Modified Duke critieria (definitive IE = 2M/3m or 1M/5m) M=major m=minor

233
Q

Major criteria of IE

A
  1. Bugs grown from blood cultures

2. Evidence of endocarditis on echo or new valve leak

234
Q

Minor criteria of IE

A
  1. Predisposing factor (e.g IV drug abuse)
  2. Fever
  3. Vascular phenomena (e.g Janeway lesions)
  4. Immune phenomena (e.g Oslar nodes)
  5. Equivocal blood cultures
235
Q

Investigations for IE

A
  1. CXR - cardiomegaly, pulmonary oedema
  2. Regular ECG (look for heart block)
  3. CT (emboli)
  4. Raised CRP
  5. Echo - TOE (-ve result doesnt eliminate)
  6. Blood tests - require long incubation so slow results
236
Q

Treatment of IE

A
  1. Antimicrobials (IV for 6 weeks)
  2. Treat complications
  3. Surgery - indicated if not cured by antibiotics, severe valve damage, remove infected devices, replace valve, remove large vegetations before embolise
237
Q

Complications of IE

A

HF, arrhythmias, heart block, embolisation, stroke

238
Q

Define congenital heart disease

A

General term for a range of birth defects that affect the normal way the heart works. Vary from minor to incompatible with left ex-utero

239
Q

Examples of structural heart defects

A
  1. Ventricular septal
  2. Atrio-ventricular septal
  3. Patent ductus arteriosus
  4. Coarctation of the aorta
  5. Bicuspid aortic valve and aortopathy
  6. Pulmonary stenosis
  7. Eisenmenger syndrome
240
Q

Define Eisenmenger syndrome

A

Any untreated congenital cardiac defect with intracardiac communication that leads to pulmonary HTN, cyanosis, reversal flow

241
Q

Investigations of structural heart defects

A
  1. Echo first line
  2. CT and MR used to provide precise anatomical and functional info
  3. Exercise testing assesses functional capacity
242
Q

What is a ventricular septal defect

A

Abnormal connection between the 2 ventricles

243
Q

Physiology of VSD

A
  • High pressure LV
  • Low pressure RV
  • Blood flows from high to low pressure
  • Increased blood flow through the lungs
244
Q

Causes of VSD

A

Congenital or acquired post-MI

245
Q

Symptoms of VSD

A
  1. Severe HF in infancy
  2. High pulmonary blood flow in infancy
  3. Breathless
  4. Poor feeding
  5. Failure to thrive
246
Q

Signs of VSD

A
  1. Small, breathless, skinny baby
  2. Increased RR
  3. Tachycardia
  4. Enlarged heart on CXR
  5. Murmur varies in intensity
  6. Harsh pansystolic murmur at left sternal edge
247
Q

Complications of VSD

A
  • Pulmonary HTN
  • Eisenmenger’s complex
  • HF from vol overload
248
Q

Pathophysiology of Eisenmenger’s

A
  1. Pulmonary HTN from initial left to right shunt
  2. Damage pulmonary structure
  3. Resistance to blood flow through lungs increases
  4. RV pressure increases
  5. Shunt reverses
  6. De-oxygenated blood enters systemic circulation
  7. Cyanotic
249
Q

Investigations for Eisenmenger’s

A
  1. ECG = normal
  2. CXR = normal heart size, large pulmonary arteries
  3. Cardiac catheter = step up in O2 saturation in RV
250
Q

Treatment of VSD

A
  • Many close spontaneously

- Surgical closure - failed medical therapy, symptomatic, shunt>3:1

251
Q

Physiology of ASD

A
  • Higher pressure in LA
  • Shunt left to right
  • Increased blood flow to right heart and lungs
252
Q

Symptoms of ASD

A
  1. Significant increased blood flow through the right heart and lungs in childhood
  2. Right heart dilatation
  3. SOB on exertion
  4. Increased chest infections
  5. Chest pain
  6. Palpitations
253
Q

Signs of ASD

A
  1. Pulmonary flow murmur
  2. Fixed split-second sound (delayed closure of PV because more blood needs to be let out)
  3. Big pulmonary arteries and heart on CXR
254
Q

Investigations of ASD

A
  1. ECG - RBBB with LAD or RAD

2. CXR - small aortic knuckle, pulmonary plethora, atrial enlargement

255
Q

Complications of ASD

A
  1. Eisenmengers complex

2. Paradoxical emboli

256
Q

Treatment of ASD

A
  1. May close spontaneously

2. Transcatheter closure more common than surgical

Phase 2a (mine) (2 decks)

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