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2A revision > Cardiology > Flashcards

Cardiology Flashcards

1
Q

what is atherosclerosis

A
  • degenerative

- 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 
Tobacco smoking
High serum cholesterol
Obesity 
Diabetes 
Hypertension 
Family history
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3
Q

distribution of atherosclerosis

A
  • peripheral and coronary arteries
  • focal distribution along length
  • changes in blood flow/ turbulence cause artery to develop neointima (new growth)
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4
Q

what does a complex atherosclerotic plaque consist of

A

Lipid
Necrotic core
Connective tissue
Fibrous cap

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5
Q

what are the main cells involved in atherogenesis

A

endothelium, macrophages, smooth muscle cells and platelets

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6
Q

mechanism of development of an atherosclerotic plaque

A
  1. fatty streaks (<10y, lipid laden macrophage and T cells in intimal layer)
  2. intermediate lesions (smooth muscle, Tcells, platelets in vessel wall)
  3. fibrous plaques ( impedes flow, can rupture, more foam cells)
  4. plaque rupture (fibrous cap has to be resorbed and redeposited, shift in balance will cause rupture)
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7
Q

what makes a complicated plaque

A

calcification, mural thrombus, vulnerable plaque

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8
Q

what causes atherosclerosis to develop

A
  1. endothelial dysfunction and injury = lipid accumulation
  2. local cellular proliferation and lipid oxidisation
  3. mural thrombi, vessel healing and cycle repeats
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9
Q

adaptation of atherosclerotic plaques

A
  1. plaque becomes>50% of lumen so vessel can’t compensate by remodelling
  2. narrowing drives cell turnover in plaque
  3. new matrix
  4. may progress to unstable plaque
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10
Q

clinical manifestations of atherosclerosis

A
  • Coronary arteries – chest pain/ pressure (angina)
  • Brain arteries – transient ischaemic attack (TIA)
  • Peripheral arteries – peripheral artery disease
  • Renal arteries – high blood pressure or kidney failure
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11
Q

management of atherosclerosis

A
  • PCI (percutaneous coronary intervention), stop restenosis by using drug eluting stents (anti-proliferative and inhibits healing)
  • aspirin
  • clopidogrel/ ticagrelor (inhibits P2Y12 ADP receptor on platelets)
  • statins (reduce cholesterol synthesis)
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12
Q

investigations for heart disease - CXR

A
  • snapshot of heart in little detail
  • enlarged heart = congestive heart failure
  • Signs of pulmonary oedema = decompensated heart failure
  • globular heart = pericardial effusion
  • Metal wires and valves show up
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13
Q

investigations for heart disease - echocardiography

A
  • US can give real time images of moving heart

- used at rest, during exercise or after use of pharmacological stressor

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14
Q

investigations for heart disease - cardiac CT

A
  • detailed

- CT angiography = contrast used = view coronary arteries = single breath hold and low radiation dose

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15
Q

investigations for heart disease - cardiac MR

A
  • radiation free
  • first choice to look at diseases directly affecting myocardium
  • pacemakers are safe with MR
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16
Q

investigations for heart disease - nuclear imaging

A
  • at rest or stress test

- assesses whether myocardium distal to blockage is viable ( hypoperfusion is reversed at rest)

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17
Q

if an impulse travels towards an electrode in an ECG which way will it deflect

A
  • upwards deflection
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18
Q

what does each section/ wave show in an ECG

A
  • P wave – atrial depolarisation
  • PR interval – atrial depolarisation and delay in AV junction
  • QRS – ventricular depolarisation
  • T wave – ventricular repolarisation
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19
Q

standard calibration of an ECG

A

25mm/s

0.1mV/mm

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20
Q

common p-wave abnormalities

A
  • Right atrial enlargement – tall >2.5mm – P pulmonale
  • Left atrial enlargement – notched (M-shaped) – P mitrale
  • long PR interval = first degree heart block
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21
Q

common QRS complex abnormalities

A

-Depth of the S wave should not excess 30mm
-Pathological Q wave:
>2mm deep and >1mm wide
>25% amplitude of the subsequent R wave

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22
Q

what does abnormalities in the QRS axis suggest

A
  • ventricular enlargement or conduction blocks
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23
Q

common abnormalities of the ST segment

A

ST segment is usually flat (isoelectric), elevation or depression of ST segment by 1mm or more can be pathological

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24
Q

abnormalities in T wave

A
  • Should be at least 1/8 but less than 2/3 of the amplitude of R
  • Abnormal T waves are symmetrical, tall, peaked, biphasic or inverted
  • T wave amplitude rarely exceeds 10mm
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25
Q

abnormalities in QT interval

A
  • decreases when HR increases

- should be 0.35 - 0.45 seconds

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26
Q

abnormalities in U waves

A
  • small, round, symmetrical and positive in lead II, with amplitude <2mm (regular)
  • U wave should be same direction as T wave
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27
Q

what can cause ST elevation

A

Normal variant, acute MI, Prinzmetal’s angina, acute pericarditis, left ventricular aneurysm

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28
Q

what can cause ST depression

A

Normal variant, digitoxin toxicity, ischaemic, angina, NSTEMI, acute posterior MI

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29
Q

what may myocardial infarction look like on ECG

A
  • T wave may become peaked and ST segments may begin to rise

- Within 24h, the T wave inverts. ST elevation rarely persists, unless a left ventricular aneurysm develops

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30
Q

what may a pulmonary embolism look like on ECG

A

sinus tachycardia, RBBB, right ventricular strain pattern

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31
Q

what is hypertension

A
  • Chronic elevation of blood pressure in the arteries.
  • WHO classification: >140/90mmHg.
  • Malignant hypertension: >160/110mmHg (rapid rise causing fibrinoid necrosis of vessels)
  • causes 50% of all vascular deaths
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32
Q

pathology of hypertension

A
  • altered RAAS elevated BP, impaires sympathetic output, causes vasoconstriction
  • normally balanced by atrial natriuretic factor
  • hypertension alters vessel walls by increasing the wall thickness
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33
Q

causes of hypertension

A
  • 90% primary with unknown aetiology

- secondary hypertension

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34
Q

causes of secondary hypertension

A
  • Endocrine disease = overproduction of aldosterone (Conn’s syndrome), Chronic vascular disease
  • renal disease (most common) = intrinsic renal disease, renovascular disease
  • drugs = NSAIDS, COC, corticosteroids, ciclosporin, cold cures, antidepressants, recreational
  • lifestyle = obesity, high salt and alcohol
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35
Q

signs and symptoms of hypertension

A
  • asymptomatic
  • Malignant hypertension = Bilateral renal haemorrhages, Papilledema, Headache and visual disturbance
  • look for causes and end organ damage
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36
Q

tests for hypertension

A
  • 24 hour ambulatory BP monitoring
  • fasting glucose, cholesterol
  • ECG or echo (look for organ damage)
  • special tests (renal US, 24h urinary meta-adrenaline, urinary free cortisol)
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37
Q

complications of hypertension

A
  • cor pulmonale:
  • Right ventricular hypertrophy and dilatation due to pulmonary hypertension
  • Can also be caused by emboli, cystic fibrosis or chronic bronchitis
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38
Q

management of hypertension

A
  • treatment goal <140/90 mmHg - reduce slowly
  • lifestyle changes
  • drugs
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39
Q

calcium antagonists

A

dihydropidines - inhibit the opening of voltage-gated calcium channels in vascular smooth muscle (decrease vasoconstriction)

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40
Q

ACE inhibitors

A

Ramipril and captopril – prevent generation of angiotensin II from angiotensin I.

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41
Q

angiotensin receptor blockers

A

aliskiren (inhibits renin) – block the action of angiotensin II at peripheral angiotensin II receptors

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42
Q

thiazide diuretic

A

Bendroflumethiazide – inhibit sodium reabsorption by the DCT, reducing the ECF volume

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43
Q

drug treatment of hypertension in patients <55 or with T2DM

A
  1. ACEi (angiotensin blocker if not tolerated)
  2. ACEi + CCB or thiazide diuretic
  3. all 3
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44
Q

drug treatment of hypertension in patients >55 or of black African/Caribbean descent

A
  1. CCB
  2. CCB + ACEi (angiotensin blocker if black) or thiazide diuretic
  3. all 3
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45
Q

what is angina pectoris

A

Recurrent transient episodes of chest pain due to myocardial ischaemia

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46
Q

what are the 4 types of angina

A
  • Stable angina: induced by effort, relieved by rest.
  • Unstable angina (crescendo): angina of increasing frequency or severity – occurs on minimal exertion or at rest. high risk of MI.
  • Decubitus angina: precipitated by lying flat.
  • Prinzmetal angina: caused by coronary artery spasm (rare)
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47
Q

pathology of angina

A
  • myocardial ischaemia occurs when myocardial O2 demand outweighs supply
  • artery stenosis increases resistance to flow
  • myocardial ischaemia = pain
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48
Q

causes of angina

A
  • Atheroma

- Rarer = Anaemia, Coronary artery spas, Tachyarrhythmias

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49
Q

modifiable risk factors for angina

A

smoking, diabetes, hypertension, hypercholesterolaemia, sedentary lifestyle, stress

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50
Q

precipitants of angina

A

> affects supply = anaemia, hypoxemia, hypothermia, hypovolaemia, hypervolemia
affects demand = hypertension, hyperthyroidism, valvular heart disease, tachyarrhythmia, cold weather

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51
Q

3 angina history features

A
  1. Constricting/heavy discomfort to the chest, jaw, neck, shoulders or arms
  2. Symptoms brought on by exertion
  3. Symptoms relieved within 5min by rest or GTN spray
    - 3/3 = typical angina, 2/3 atypical, 0/3 not anginal pain
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52
Q

symptoms of angina

A 
Dyspnoea 
Nausea 
Sweatiness 
Faintness
Crushing chest pain
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53
Q

investigations for angina

A
  • ECG (often normal, Twave inversion, BBB)
  • bloods = FBC, U&E, TFTs, lipids, HbA1c
  • echo = normal or signs of previous infarcts
  • CXR
    • stress echo, exercise stress treadmill, perfusion MRI
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54
Q

management of angina

A
  • address exacerbating factors (anaemia, tachycardia, hyperthyroid)
  • GTN (glyceryl trinitrate) spray
  • ambulance if pain doesn’t go 5mins after second dose
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55
Q

primary prevention of angina

A
  • reduce risk of CAD and complications

- risk factor modification

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56
Q

secondary prevention of angina

A
  • lifestyle changes
  • 75mg aspirin daily
  • ACEi if diabetic
  • PCI or surgery (CABG)
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57
Q

what is coronary artery bypass graft surgery (CABG)

A
  • deals with complex disease
  • open heart surgery
  • risk of stroke/bleeding
  • one-time treatment
  • can’t do if frail
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58
Q

what are acute coronary syndromes

A
  • unstable angina, MI

- pathology = plaque rupture, thrombosis, inflammation

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59
Q

what is myocardial infarction

A
  • myocardial cell death, releasing troponin.
  • full thickness necrosis
  • Non-ST-elevation myocardial infarction (NSTEMI)
  • ST-elevation myocardial infarction (STEMI)
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60
Q

modifiable risk factors for acute coronary syndromes

A
  • smoking, diabetes, hypertension, hyperlipidaemia, sedentary lifestyle, cocaine use
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61
Q

diagnosis of acute coronary syndromes

A
  • An increase in cardiac biomarkers (e.g. troponin)
  • Symptoms of ischaemia
  • ECG changes of new ischaemia
  • Development of pathological Q waves
  • New loss of myocardium
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62
Q

symptoms of acute coronary syndromes

A
  • Acute central chest pain lasting >20min
  • Nausea
  • Sweatiness
  • Dyspnoea
  • Palpitations
  • silent ACS = in elderly = syncope, pulmonary oedema, epigastric pain
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63
Q

signs of ACS

A 
Distress 
Anxiety 
Pallor 
Sweatiness 
4th heart sound
Possibly signs of heart failure
Low grade fever
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64
Q

management of ACS

A
  • GTN and opiates for chest pain
  • modify risk factors
  • cardioprotective meds = aspirin, clopidogrel, anticoagulants, beta blocker, ACEi, high dose statin
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65
Q

unstable angina

A
  • severe acute myocardial ischaemia without necrosis
  • at rest or minimal exertion
  • no significant rise in troponin
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66
Q

different types of MI

A
  • Subendocardial/ patchy infarction – involves the innermost layer and some middle parts of the myocardium, but not the epicardium. NSTEMI
  • Transmural infarction – full thickness of the myocardium
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67
Q

initial management of STEMI

A
  1. 12-lead ECG
  2. IV access. Bloods for FBC, U&E, glucose, lipids, troponin
  3. History
  4. Aspirin 300mg and ticagrelor 180mg
  5. Morphine 5-10mg IV +anti-emetic
  6. STEMI on ECG = primary PCI
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68
Q

treatment of MI

A
  • Aspirin – inhibits platelet function
  • LMW heparin
  • Thrombolytic therapy
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69
Q

what is cardiac failure

A
  • heart can’t pump enough = cardiac output is inadequate for the body’s requirements
  • severe cardiac failure causes cardiogenic shock
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70
Q

what happens if the stretch capability of sarcomeres in the myocardium is exceeded

A
  • cardiac contraction force diminishes

- hypertrophic response triggered by angiotensin 2, ET-1, I-LGF1, TGF-beta

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71
Q

systolic failure

A
  • inability of the ventricle to contract normally, resulting in low cardiac output.
  • Ejection fraction <40%.
  • Causes: IHD, MI, Cardiomyopathy
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72
Q

diastolic failure

A
  • inability of the ventricle to relax and fill normally, causing increased filling pressures
  • stiff heart
  • Ventricular hypertrophy, Constrictive pericarditis, Tamponade , Restrictive cardiomyopathy, Obesity
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73
Q

L and R ventricular failure

A
  • L = causes pulmonary congestion then overload of R side

- R = venous hypertension and congestion (leg veins)

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74
Q

acute HF

A

new-onset acute or decompensation of chronic heart failure characterised by pulmonary and/or peripheral oedema with/without signs of peripheral hypoperfusion

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75
Q

chronic HF

A

develops or progresses slowly. Venous congestion is common but arterial pressure is well maintained until very late

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76
Q

diagnosis of HF

A
  • symptoms of failure

- FBC, U&E, CXR, ECG (cause), echo

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77
Q

signs of HF

A 
Cyanosis 
Decreased BP
Narrow pulse pressure
Displaced apex (LV dilatation)
Pulmonary hypertension 
Pink frothy sputum 
Signs of valve diseases
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78
Q

differential diagnoses for HF

A 
COPD
Emphysema 
Myocardial infarction
Pulmonary embolism 
Pneumonia
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79
Q

management to acute HF - emergency

A
  1. sit upright
  2. high flow O2
  3. treat arrhythmias
  4. investigations
  5. Diamorphine 1.25-5mg IV slowly
  6. Furosemide 40-80mg IV slowly
  7. GTN spray 2 SL puffs
  8. If systolic BP 100mmHg, start a nitrate transfusion
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80
Q

management of chronic HF

A
  • manage risk factors
  • treat cause and exacerbating factors (anaemia, infection)
  • flu vaccine
  • pharmacological = diuretics, ACEi, beta-blocker (carvedilol), mineralocorticoid receptor antagonist (spironolactone), digoxin ( helps symptoms), vasodilators (hydralazine and isosorbide nitrate)
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81
Q

2 congenital valvular heart diseases

A

Congenital aortic stenosis

Congenital bicuspid valve

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82
Q

2 acquired valvular heart diseases

A

Degenerative calcification

Rheumatic heart disease

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83
Q

what is mitral regurgitation

A
  • Backflow through the mitral valve during systole.
  • Acute – back up into the lungs
  • Chronic – dilation as it has had time to adjust
  • volume overload
  • compensated by LA enlargement, LVH and increased contractility
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84
Q

causes of mitral valve regurgitation

A 
Rheumatic fever
Infective endocarditis 
Mitral valve prolapse 
Ruptured chordae tendinea 
Papillary muscle dysfunction
Cardiomyopathy
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85
Q

signs and symptoms of mitral regurgitation

A
  • Dyspnoea (exertion), Pulmonary oedema, Fatigue, Palpitations
  • AF, pansystolic murmur, large LV
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86
Q

tests for mitral regurgitation

A
  • ECG = AF, Pmitrale, LA enlargement and LV hypertrophy
  • CXR = mitral valve calcification
  • echo
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87
Q

management of mitral regurgitation

A
  • Beta blocker if fast rate
  • anticoagulant
  • vasodilators - CCB (hydralazine)
  • diuretics improve symptoms
  • replace/ repair valve
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88
Q

what is mitral valve prolapse

A
  • most common valvular abnormality
  • two valve flaps of the mitral valve do not close smoothly or evenly, but instead bulge upwards into the left atrium
  • atypical chest pain, palpitations, and autonomic dysfunction symptoms
  • Mid-systolic click and/or late systolic murmur
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89
Q

complications of mitral valve prolapse

A

Mitral Regurgitation (MR)
Cerebral emboli
Arrhythmias
Sudden death

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90
Q

tests for mitral valve prolapse

A
  • echo = diagnostic
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91
Q

treatment of mitral valve prolapse

A
  • beta blockers help palpitations and pain

- surgery is severe

92
Q

what is mitral stenosis

A
  • Obstruction of LV inflow that prevents proper filling during diastole.
  • Normal mitral valve area 4-6cm2. Symptoms at <2cm2.
  • causes = rheumatic fever, congenital, endocarditis, malignant carcinoid
93
Q

symptoms of mitral stenosis

A
  • Pulmonary hypertension (dyspnoea, haemoptysis)
  • Pressure from large left atrium on local structures causes hoarseness (recurrent laryngeal nerve)
  • Dysphagia
  • Bronchial obstruction
  • Fatigue
  • Palpitations
  • Chest pain
94
Q

signs of mitral stenosis

A
  • Prominent ‘a’ wave in jugular venous pulsations
  • right-sided heart failure
  • Mitral facies – severe MS leads to vasoconstriction: pink patches on cheeks
  • Malar flush on cheeks
  • Low-volume pulse
  • Low pitch rumbling at apex
95
Q

management of mitral stenosis

A
  • rate control
  • warfarin, beta-blocker, CCB, digoxin, diuretics
  • mitral balloon valvotomy
  • mitral valve replacement
96
Q

what is aortic stenosis

A
  • aortic valve narrowing restricts flow from LV to aorta
  • symptoms when area 1/4 of normal (3-4cm2)
  • supravalvular, subvalvular, valvular
  • increases afterload, initially compensated by LVH then function declines
  • causes = calcification, congenital, rheumatic heart disease)
97
Q

classic triad for presentation of aortic stenosis

A

Angina (Chest pain)
Syncope
Breathlessness

98
Q

signs of aortic stenosis

A
  • Slow rising carotid pulse with narrow pulse pressure
  • Heaving, non-displaced apex beat
  • Ejection systolic murmur – crescendo-decrescendo
99
Q

investigations for aortic stenosis

A
  • echo
  • LVH, dilation, ejection fraction
  • cardiac catheter
  • pulsus parvus et tardus (weak and late pulse)
100
Q

management of aortic stenosis

A
  • NEEDS SURGERY
  • valve replacement
  • transcatheter aortic valve implantation
101
Q

what is aortic sclerosis

A

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

102
Q

aortic regurgitation

A
  • Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps.
  • Acute: infective endocarditis, ascending aortic dissection, chest trauma.
  • Chronic: congenital, connective tissue disorders (Marfan’s syndrome), rheumatic fever, Takayasu arteritis, rheumatoid arthritis
  • pressure and volume overload
103
Q

presentation of aortic regurgitation

A

Breathlessness
Orthopnoea (breathless lying down)
Palpitations
Diastolic blowing murmur

104
Q

management of aortic regurgitation

A
  • vasodilators
  • serial echos
  • surgical
105
Q

what is tricuspid regurgitation

A
  • doesn’t close tight enough, backwards flow into RA
  • causes = rheumatic fever, endocarditis, carcinoid syndrome
  • fatigue, hepatic pain, ascites, oedema
106
Q

signs of tricuspid regurgitation

A

Pansystolic murmur
Pulsatile hepatomegaly
Jaundice

107
Q

management of tricuspid regurgitation

A
  • diuretics
  • treat underlying cause
  • valve repair/ replacement
108
Q

what is tricuspid stenosis

A
  • narrowing , restricts blood flow from RA to L
  • causes= rheumatic fever, congenital, endocarditis
  • fatigue, ascites, oedema
109
Q

signs of tricuspid stenosis

A
  • opening snap, early diastolic murmur

- AF

110
Q

treatment of tricuspid stenosis

A
  • diuretics

- surgical repair

111
Q

what is pulmonary stenosis

A
  • obstructs flow from RV to pulmonary artery
  • valve leaflets are thickened and fused together along their separation lines
  • causes = congenital (Turners), rheumatic fever, carcinoid syndrome
  • dyspnoea, fatigue, oedema, ascites
112
Q

signs of pulmonary stenosis

A

Dysmorphic facies
Ejection click
Ejection systolic murmur
- prominent pulmonary arteries (post-stenotic dilation)

113
Q

treatment for pulmonary stenosis

A
  • pulmonary valvuloplasty or valvotomy
114
Q

what is rheumatic fever

A

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

115
Q

pathology of RF

A
  • An antibody to the carbohydrate cell wall of the streptococcus cross-reacts with valve tissue
  • permanent damage to the heart valves
116
Q

diagnosis of RF

A
  • evidence of recent strep infection (Ab test or recent scarlet fever etc) + 2 major or 1 major, 2 minor
  • major = carditis, arthritis, subcut nodules, erythema
  • minor = fever, raised ESR/CRP, arthralgia
117
Q

management of RF

A
  • bed rest until CRP normal (2 weeks)
  • benzylpenicillin
  • analgesia for carditis/ arthritis
118
Q

what is infective endocarditis

A
  • Infection of the heart valve/s or other endocardial lined structures within the heart e.g. septal defects, surgical patches.
  • really bad infection that showers infectious material into bloodstream
119
Q

types of IE

A
  • Left sided native IE (mitral or aortic)
  • Left sided prosthetic IE
  • Right sided IE
  • Device related IE (pacemakers/ defibrillators)
  • Prosthetic
120
Q

causes of IE

A
  • abnormal valve (regurgitant or prosthetic valves are most likely to get infected)
  • bacteria from haematogenous spread or onto heart during surgery
  • had previous IE
121
Q

what infections can cause IE

A
  • s.aureus from skin via indwelling vascular lines or IV drug abuse
  • S.viridans from oropharynx following tooth brushing or dentistry
  • enterococci from instrumentation of the bowel or bladder
122
Q

clinical presentation of IE

A
  • Signs of systemic infection
  • Embolisation
  • Valve dysfunction – HF, arrhythmia
  • Petechiae (skin lesions)
  • Splinter haemorrhages (bruised nails)
  • Osler’s nodes (small, tender, purple nodules on digits)
  • Janeway lesions (non-tender lesions on the fingers, palm or sole)
123
Q

Modified Duke criteria for diagnosis of IE

A
  • 2 major (blood culture growth, endocarditis on echo, or new valve leak)
  • 5 minor (Predisposing factors e.g. IV drug abuse, Fever, Vascular phenomena, Immune phenomena e.g. Osler’s nodes, Equivocal blood cultures)
  • 2 major +3 minor or 1major +5minor
124
Q

investigations for IE

A
  • blood cultures, raised CRP
  • CXR = cardiomegaly, pulmonary oedema
  • CT = emboli
  • ECG
  • Echo = vegetations
125
Q

treatment of IE

A
  • IV antimicrobials for 6 weeks
  • treat complications
  • surgery to remove infected valves or prosthetics
126
Q

what is congenital heart disease

A

general term for a range of birth defects that affect the normal way the heart works
- can be incompatible with ex-utero life

127
Q

what is Eisenmenger syndrome

A

any untreated congenital cardiac defect with intracardiac communication that leads to pulmonary hypertension, cyanosis, reversal of flow

128
Q

physiology of ventricular septal defects

A
  • High pressure LV
  • Low pressure RV
  • Blood flows from high to low pressure chamber (so, not blue)
  • Increased blood flow through the lungs
129
Q

symptoms of ventricular septal defects

A 
Severe heart failure in infancy 
Very high pulmonary blood flow in infancy 
Breathless 
Poor feeding 
Failure to thrive
130
Q

signs of ventricular septal defects

A
  • Small, breathless, skinny baby
  • Tachycardia
  • Big heart on chest X-ray and large pulmonary arteries
  • Murmur varies in intensity
  • Harsh pansystolic murmur heard at left sternal edge
131
Q

complications of septal defects

A

Pulmonary hypertension
Eisenmenger’s complex
Heart failure from volume overload

132
Q

Eisenmenger’s syndrome in ventricular septum defects

A
  1. pulmonary hypertension from L to R shunt
  2. damages pulmonary vasculature
  3. resistance to flow increases in lungs
  4. RV pressure increases
  5. shunt direction reverses
  6. de-oxygenated blood enters systemic circulation
  7. become cyanosed
133
Q

treatment for ventricular septal defects

A
  • may close spontaneously

- surgical closure = shunt > 3:1

134
Q

physiology of atrial septal defect

A
  • Slightly higher pressure in the LA than the RA
  • Shunt is left to right (therefore not blue)
  • Increased flow into right heart and lungs
135
Q

symptoms of atrial septal defect

A
  • Significant increased flow through the right heart and lungs in childhood
  • Right heart dilatation
  • Shortness of breath on exertion
  • Increased chest infections
  • Chest pain
  • Palpitations
136
Q

investigations for atrial septal defect

A
  • CXR = big pulmonary arteries and heart, small aortic knuckle
  • ECG = RBBB with LAD or RAD
137
Q

treatment for atrial septal defects

A
  • may close spontaneously

- close if symptomatic (transcatheter closure > surgical)

138
Q

Atrio-ventricular septal defects

A
  • ventricular septum, atrial septum, mitral and tricuspid valves
  • AV valves become one big one
  • complete defect = torrential pulmonary blood flow causing breathlessness as neonate, needs repair in infancy
  • partial defect = can present in late adulthood, can be left alone if no heart dilation
139
Q

patent ductus arteriosus

A
  • ductus arteriosus fails to close after birth, leaving a vessel connecting the aorta and pulmonary artery
  • Torrential flow from the aorta to the pulmonary arteries in infancy
  • surgical closure under local anaesthetic
140
Q

clinical signs of patent ductus arteriosus

A
  • continuous murmur
  • big heart, breathless
  • Eisenmenger’s syndrome = cyanosed
141
Q

coarctation of the aorta

A

-Congenital narrowing of the descending aorta (usually occurs just distal to the origin of the left subclavian artery – the site of insertion of the ductus arteriosus)

142
Q

what conditions are coarctation of the aorta associated with

A
  • Turner’s syndrome

- bicuspid aortic valve

143
Q

signs of coarctation of the aorta

A 
Radiofemoral delay
Weak femoral pulse
High blood pressure
Cold feet
Scapular bruit
144
Q

investigations for coarctation of the aorta

A
  • CXR= rib notching as blood diverts down intercostal arteries to lower body (dilate and erode rib bone)
145
Q

treatment for coarctation of the aorta

A

surgery

balloon dilatation

146
Q

tetralogy of Fallot

A
  • congenital heart condition with 4 abnormalities
    1. Ventricular septal defect (VSD)
    2. Pulmonary stenosis
    3. Right ventricular hypertrophy
    4. The aorta overrides the VSD, accepting right heart blood
147
Q

physiology of tetralogy of Fallot

A
  • pulmonary stenosis = higher pressure in RV
  • blood from RV to LV
  • patients are blue
148
Q

presentation of tetralogy of Fallot

A
  • cyanotic

- hypoxic spell = becomes restless and agitated

149
Q

investigations for tetralogy of Fallot

A
  • ECG: RV hypertrophy with RBBB.
  • CXR may be normal or show a boot shaped heart (hallmark of TOF)
  • Echo
150
Q

management of tetralogy of Fallot

A

surgery before age 1 = closure of VSD and correction of pulmonary stenosis

151
Q

what is cardiomyopathy

A
  • primary heart muscle diseases
  • often genetic
  • all carry risk of arrhythmias
  • heart doesn’t pump as well
152
Q

what is acute myocarditis

A

-Inflammation of the myocardium - often associated with pericardial inflammation

153
Q

causes of acute myocarditis

A
  • Idiopathic (unknown)
  • Viral, bacterial, protozoan
  • Spirochetes (Lyme disease/ syphilis)
  • Drugs e.g. penicillin
  • Toxins e.g. cocaine, lithium, alcohol, lead, arsenic
  • Immunological e.g. heart transplant rejection
154
Q

symptoms of acute myocarditis

A

ACS-like symptoms
Heart failure symptoms
Palpitations
Tachycardia

155
Q

investigations for acute myocarditis

A

ECG: ST changes and T-wave inversion, atrial arrhythmias
Bloods: CRP, ESR and troponin may be raised
Echo: diastolic dysfunction

156
Q

treatment for acute myocarditis

A
  • supportive
  • treat underlying cause
  • treat arrhythmias and HF
157
Q

what is dilated cardiomyopathy (DCM)

A
  • dilated, flabby heart of unknown cause.
  • Most autosomal dominant, but some recessive and X-linked. Mutations in several genes are recognised – dystrophin, troponin T
  • pathology = poor contractile force leads to dilation of the heart with some interstitial tissue
  • associated with alcohol, high BP, chemotherapeutics, viral infection, autoimmune
158
Q

signs and symptoms of DCM

A
  • fatigue, dyspnoea, pulmonary oedema, RVF, emboli
  • high pulse, low BP, hepatomegaly, mitral/tricuspid regurgitation
  • hyponatraemia indicated a poor prognosis
159
Q

treatment of DCM

A 
Bed rest 
Diuretics 
β-blockers 
Anticoagulation 
Transplantation
160
Q

what is hypertrophic cardiomyopathy (HCM)

A
  • LV outflow tract obstruction from asymmetrical septal hypertrophy.
  • Caused by sarcomeric protein gene mutations – many recognised involving beta-myosin binding protein C, troponin T, titin
161
Q

signs and symptoms of HCM

A
  • Sudden death (troponin T)
  • Cardiac hypertrophy and dysrhythmia (beta-myosin)
  • Angina
  • Dypsnoea
  • Palpitations
  • Dizziness
  • Syncope
162
Q

investigations for HCM

A
  • echo = asymmetrical septal hypertrophy, small LV cavity, dilated LA
  • ECG= Twave inversion, deep Q wave
163
Q

management of HCM

A
  • β-blockers for symptoms
  • Amiodarone for arrhythmias
  • Anticoagulate for systemic emboli
164
Q

what is restrictive cardiomyopathy (RCM)

A
  • Restrictive filling of the ventricles so insufficient pumping
  • causes = idiopathic, amyloidosis, endomyocardial fibrosis
165
Q

presentation of RCM

A
  • Like constrictive pericarditis
  • Features of RVF – hepatomegaly, oedema, ascites
  • do echo and MRI
166
Q

treatment of RCM

A

treat cause

167
Q

what is arrhythmia right ventricular cardiomyopathy

A
  • degenerative
  • progressive dilation of the right ventricle with fibrosis, lymphoid infiltrate and fatty tissue replacement
  • often caused by desmosome gene mutations
168
Q

what is a channelopathy

A
  • Inherited arrhythmia caused by ion channel (K, Na, Ca) protein gene mutations
  • include long QT, short QT, and Brugada syndrome
  • structurally normal
  • recurrent syncope
  • QT prolonging drugs can kill these patients
169
Q

familial hypercholesterolaemia (FH)

A
  • inherited abnormality of cholesterol metabolism (abnormal LDL protein)
  • leads to coronary and other vascular disease
  • aortic aneurysm or dissection
  • AD
  • genetic testing
170
Q

what is pericarditis

A
  • inflammation of the pericardium
  • infections are most common cause along with MI
  • injury to the pericardium causes inflammation
171
Q

presentation of pericarditis

A
  • central chest pain (worse lying flat, better sitting forward)
  • if large may cause breathlessness
172
Q

acute pericarditis

A
  • causes = viruses, bacteria, fungi, autoimmune, drugs, metabolic, others
  • ECG shows concave (saddle-shaped) ST segment elevation and PR depression
  • Blood tests: FBC, ESR, cardiac enzymes, tests related to aetiologies
  • Cardiomegaly on CXR may indicate pericardial effusion
  • CMR and CT may show localised inflammation
  • may hear friction rub
173
Q

treatment of acute pericarditis

A
  • NSAIDs or aspirin with gastric protection
174
Q

constrictive pericarditis

A
  • heart is encased in a rigid pericardium
  • dyspnoea, chest pain, nausea, bronchial breathing
  • CXR = big globular heart
  • ECG = low-voltage QRS complex
  • echo = echo free zone around heart
175
Q

management of constrictive pericarditis

A
  • treat cause
  • pericardiocentesis
  • send fluid for culture and cytology
176
Q

what are some cardiac causes of arrhythmias

A

ischaemic heart disease; structural changes e.g. left atrial dilatation secondary to mitral regurgitation; cardiomyopathy; pericarditis; myocarditis; aberrant conduction pathways

177
Q

what are some non-cardiac causes of arrhythmias

A

caffeine, smoking, alcohol, pneumonia, drugs, metabolic imbalance

178
Q

presentation of arrhythmias

A 
Palpitations 
Chest pain
Presyncope 
Syncope 
Hypotension 
Pulmonary oedema
179
Q

investigations for arrhythmias

A
  • FBC, U&E, glucose, Ca2+, Mg2+
  • ECG: look for signs of IHD, AF, short PR interval, long QT interval, U waves
  • 24h ECG monitoring
  • Echo: look for structural heart disease e.g. mitral stenosis
180
Q

management of arrhythmias

A
  • conservatively (eg. reduce alcohol)
  • medical
  • interventional (pacemakers, ablation, implantable cardioverter defibrillators)
181
Q

sinus tachycardia

A
  • impulses initiated at high frequency

- causes = infection, pain, exercise, anxiety, dehydration

182
Q

focal atrial tachycardia

A
  • group of atrial cells act as a pacemaker, out-pacing the SAN.
  • P-wave morphology is different to sinus.
183
Q

atrial flutter

A

electrical activity circles the atria 300 times per minute, giving a sawtooth baseline. The AVN passes some of these impulses on, resulting in ventricular rates that are factors of 300.

184
Q

junctional tachycardia

A

cells in the AVN become the pacemaker, giving narrow QRS complexes as impulses reach the ventricles through the normal routes; P waves may be inverted and late

185
Q

bundle branch block

A
  • delay or blockage along the pathway that impulses travel
186
Q

ventricular tachycardia

A
  • results from circuits similar to atrial flutter

- QRS is broad with regularly increasing nd decreasing amplitudes (torsades de pointes)

187
Q

what is narrow complex tachycardia

A
  • rate >100 bpm
  • QRS <120ms (narrow because ventricles depolarised via the normal conduction pathway)
  • can be regular or irregular
  • treat underlying rhythm
188
Q

what is broad complex tachycardia

A
  • > 100bpm and QRS complexes >120ms.
  • If no clear QRS complexes, is it VF or asystole
  • differential diagnosis = ventricular tachycardia or fibrillation
  • correct electrolyte problems
189
Q

ventricular extrasystoles

A

palpitations, a thumping sensation, or their heart missing a beat. The pulse may feel irregular if there are frequent ectopics.

190
Q

what is atrial fibrillation

A
  • chaotic, irregular atrial rhythm at 300-600bpm. The AVN responds intermittently, hence an irregular ventricular rhythm.
  • The main risk is embolic stroke.
  • chest pain, palps, dyspnoea, faintness
  • irregularly irregular pulse
  • signs of LVF
191
Q

investigations for atrial fibrillation

A
  • ECG: absent P waves, irregular rapid QRS complexes
  • Blood tests: U&E, cardiac enzymes, thyroid function tests
  • Echo: left atrial enlargement, mitral valve disease, poor LV function, other structural abnormalities
192
Q

management of acute atrial fibrillation

A
  • amiodarone
  • is started >48h ago then bisoprolol
  • correct electrolyte imbalances
193
Q

management of chronic atrial fibrillation

A
  • rate control = beta blocker or CCB
194
Q

causes of atrial flutter

A 
Obesity 
Hypertension 
Excess alcohol
COPD
Heart failure/ CHD
195
Q

management of atrial flutter

A

Amiodarone – anti-arrhythmic drug
Beta blockers - Bisoprolol
LMW Heparin
Catheter ablation

196
Q

first degree heart block

A

PR interval is prolonged and unchanging; no missed beats

197
Q

second degree heart block

A
  • Mobitz I – the PR interval becomes longer and longer until a QRS is missed = Wenckenbach phenomenon
  • Mobitz II – QRSs are regularly missed = dangerous as may develop into complete heart block
  • 3rd degree complete heart block: no impulses are passed from atria to ventricles so P waves and QRSs appear independently of each other. emergency, become bradycardia
198
Q

management of heart block

A

IV atropine

Permanent pacemaker

199
Q

what is Wolff-parkinson-white syndrome

A
  • extra electrical pathway in the heart leading to periods of tachycardia
  • congenital
  • short PR interval, wide QRS complex
  • prone to AF
200
Q

what is an aortic aneurysm

A
  • abnormal bulge that occurs in the wall of the aorta.
  • An artery with a dilatation >50% of its original diameter has an aneurysm
  • true aneurysm = all layers of wall
  • false aneurysm = collection of blood in outer layer only
201
Q

causes of aortic aneurysm

A 
Atheroma 
Trauma 
Infection 
Connective tissue disorders 
Inflammatory
202
Q

common sites for aneurysm

A

Aorta (most common)
Iliac
Femoral
Popliteal arteries

203
Q

clinical presentation of aortic aneurysm

A
  • often asymptomatic (sometimes back pain) until ruptures (abdo pain, collapse, shock)
204
Q

investigations for aortic aneurysm

A

X-ray
Echocardiogram
CT angiography
Ultrasound

205
Q

management of aortic aneurysm

A
  • check ups and monitoring

- surgery (endovascular or open)

206
Q

what is aortic dissection

A
  • tear in aortic wall
  • Blood can flow in between the layers of the blood vessel wall (dissection).
  • This can lead to aortic rupture or decreased blood flow to organs.
  • associated with aortic aneurysms.
207
Q

risk factors for aortic dissection

A
  • Ageing
  • Atherosclerosis
  • Blunt trauma to the chest
  • High blood pressure
  • Bicuspid aortic valve
  • Coarctation (narrowing) of the aorta
208
Q

clinical manifestations of aortic dissection

A
  • Chest Pain – sharp, stabbing, tearing or ripping which radiates to the back
  • Anxiety and feeling of doom
  • Fainting or dizziness
  • Heavy sweating (clammy skin)
  • Nausea and vomiting
  • Pale skin (pallor)
  • Rapid, weak pulse
209
Q

what is the gold standard test for diagnosing aortic dissection

A
  • CT scan of chest
210
Q

management of aortic dissection

A
  • surgical repair
  • lower BP ( beta blockers)
  • pain relief
211
Q

what is peripheral vascular disease

A
  • Occurs due to atherosclerosis causing stenosis of arteries

- restricts blood supply to leg muscles

212
Q

symptoms of peripheral vascular disease

A
  • Cramping pain in the calf, thigh, or buttock after walking for a given distance and relieved by rest
  • Ulceration, gangrene and foot pain at rest
213
Q

signs of peripheral vascular disease

A
  • Absent femoral, popliteal or foot pulses
  • Cold, white legs
  • Atrophic skin
  • Punched out ulcers
  • Buerger’s angle (angle that leg goes pale when raised off the couch)
214
Q

investigations for peripheral vascular diseas

A
  • FBC
  • ECG
  • Ankle-brachial pressure index (ABPI)
  • Colour duplex USS
215
Q

management of peripheral vascular disease

A
  • risk factor modification
  • supervised exercise programmes
  • surgical reconstruction = bypass graft
  • amputation
216
Q

what is shock

A

Circulatory failure resulting in inadequate organ perfusion. Often defined by low BP – systolic <90mmHg, with evidence of tissue hypoperfusion

217
Q

what is cardiogenic shock

A

a state of inadequate tissue perfusion primarily due to cardiac dysfunction

218
Q

causes of cardiogenic shock

A 
Myocardial infarction 
Arrhythmias 
Pulmonary embolus
Tension pneumothorax 
Cardiac tamponade
Myocarditis
Aortic dissection
219
Q

clinical manifestations of cardiogenic shock

A 
Agitation 
Pallor 
Cool peripheries 
Tachycardia 
Slow capillary refill 
Oliguria (abnormally small amounts of urine)
220
Q

investigations for cardiogenic shock

A
  • ECG
  • CXR
  • Echo
  • Monitor –record ECG ever hour until diagnosis
221
Q

management of cardiogenic shock

A
  1. O2
  2. Diamorphine 1.25-5mg IV for pain and anxiety
  3. Investigations and close monitoring
  4. Correct arrhythmias, U&E abnormalities, or acid-base disturbance
  5. Optimize filling pressure
  6. Look for and treat any reversible cause
222
Q

what is cardiac tamponade

A
  • Compression of the heart by an accumulation of fluid in the pericardial sac.
  • Pericardial fluid collects -> intrapericardial pressure rises -> heart cannot fill -> pumping stops
223
Q

what causes cardiac tamponade

A 
Trauma
Lung/breast cancer
Pericarditis 
MI
Bacteria
224
Q

signs of cardiac tamponade

A
  • low BP
  • Muffled heart sounds (Beck’s triad)
  • Echocardiography may be diagnostic
  • CXR: globular heart
225
Q

management of cardiac tamponade

A
  • Pericardiocentesis – quick relief
  • Give oxygen, monitor ECG, set up IV
  • Surgery

2A revision (10 decks)

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