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Phase 2a Resits > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Pathophysiology of IHD

A
  • primarily caused by atherosclerosis
  • when 70-80% sclerosed → exertional symptoms → angina
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2
Q

What is the mechanism of atherosclerotic plaque formation?

A
  1. fatty streaks
  2. intermediate lesions
  3. fibrous plaques of advanced lesions
  4. plaque rupture → infarction
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3
Q

What is an atherosclerotic plaque?

A

complex lesion consisting of:

  • lipid
  • necrotic core
  • connective tissue
  • fibrous cap
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4
Q

What are the major cell types involved in atherogenesis?

A
  • endothelium
  • macrophages
  • smooth muscle cells
  • platelets
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5
Q

What arteries does atherogenesis affect most commonly?

A
  • LAD
  • circumflex
  • RCA
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6
Q

Risk factors of IHD

A
  • family history
  • age
  • South Asian
  • smoking
  • poor nutrition
  • sedentary lifestyle
  • alcohol
  • stress
  • HTN
  • obesity
  • DM
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7
Q

Presentation of angina

A
  • constricting discomfort in front of chest, neck, shoulders, jaw or arms
  • precipitated by physical exertion
  • relieved by rest/GTN spray (5 mins)

normal exam

  • typical angina = all 3
  • atypical angina = 2
  • non anginal pain = 1/none
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8
Q

Investigations for IHD

A
  • ECG usually normal
  • lipid profile → high LDL
  • FBC
  • HbA1c

GOLD STANDARD = CT coronary angiography

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9
Q

Treatment of IHD

A
  • antiplatelet therapy → aspirin/clopidogrel
  • lipid lowering thearpy → statin
  • good hypertensive/glycaemic control
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10
Q

Treatment for angina

A
  • symptomatic relief = GTN spray
  • long term symptomatic relief = beta blocker/CCB
  • secondary prevention = AAA
  • PCI/CABG if extensive damage
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11
Q

What is the secondary prevention for angina?

A

AAA

  • aspirin
  • atorvastatin
  • ACEi
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12
Q

What surgical interventions are available for angina?

A
  • percutaneous coronary intervention
  • coronary artery bypass graft → preferred in patients with diabetes, >65
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13
Q

What is ACS?

A

Acute Coronary Syndrome
- thrombus from an atherosclerotic plaque blocking a coronary artery

  • unstable angina = ischaemia
  • STEMI = complete occlusion
  • NSTEMI = partial occlusion → subendocardial infarction
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14
Q

Presentation of ACS

A
  • central constricting chest pain radiating to jaw/arms
  • sweating
  • SOB
  • >20 mins
  • unstable angina → pain not relieved by rest or GTN spray
  • silent MI → in diabetics
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15
Q

ECG changes in ACS

A

STEMI
- ST segment elevation

NSTEMI/unstable angina

  • ST depression
  • deep T wave inversion
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16
Q

How do you differentiate between unstable angina and NSTEMI?

A
  • unstable angina = troponin normal
  • NSTEMI = troponin abnormal
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17
Q

Immediate management of ACS

A

MONAC

  • morphine
  • oxygen
  • nitrate
  • aspirin
  • clopidogrel
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18
Q

Management of STEMI

A

PCI within 120mins
- clopidogrel/prasugrel and aspirin

Fibrinolysis if not PCI eg alteplase
- ticagrelor and aspirin

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19
Q

Management of NSTEMI/unstable angina

A
  • GRACE score
  • fondaparinux

low risk

  • ticagrelor
  • aspirin

medium/high risk

  • angiography and PCI
  • prasugrel and aspirin
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20
Q

What is the GRACE score?

A
  • assess for PCI in NSTEMI
  • gives 6 month risk of death and repeat MI after having a NSTEMI
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21
Q

Secondary prevention of ACS

A

ACAB

  • ACEi
  • clopidogrel
  • aspirin and atorvastatin
  • beta blocker
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22
Q

What are the post MI complications

A

DREAD

  • death
  • rupture of heart septum/papillary muscles
  • edema (HF)
  • arrhythmias and aneurysms
  • Dressler’s syndrome
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23
Q

Definition of HTN

A
  • >140/90 in clinic (be aware of white coat HTN)
  • >135/85 with ABPM/home readings
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24
Q

Pathophysiology of HTN

A

95% idiopathic = essential HTN
rest = underlying cause → ROPE
- renal disease
- obesity
- pregnancy (pre-eclampsia)
- endocrine (Conns)

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25
Q

Risk factors for HTN

A
  • >65
  • family history
  • Afro-caribbean
  • alcohol intake
  • DM
  • sedentary lifestyle
  • sleep apnoea
  • smoking
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26
Q

Investigations for HTN

A
  1. clinic BP >140/90
  2. offer ABPM or home readings
  3. ABPM >135/95 = diagnosis confirmed
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27
Q

Stages of HTN

A
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28
Q

Further investigations for HTN

A
  • urine ACR, dipstick, bloods
  • ECG
  • hypertensive retinopathy → fundus examination
  • HbA1c
  • lipids
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29
Q

What medications can be used to treat HTN?

A

ABCDA

  • ACEi → ramipril
  • beta blocker → bisoprolol
  • CCB → amlodipine
  • diuretic (thiazide like) → indapamide
  • ARB → candesartan

ARB used instead of ACEi if

  • not tolerated (dry cough)
  • patient is black
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30
Q

When to offer medical management of HTN

A
  • stage 2 HTN
  • <80, stage 1 HTN, QRISK score 10%+, complications
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31
Q

NICE guideline treatment for HTN

A
  1. <55 and non-black = ACEi, >55 or black = CCB
  2. ACEi and CCB, alternative ACEi and D, CCB and D, if black use ARB not ACEi
  3. ACEi and CCB and D
  4. ACEi and CCB and D and additional
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32
Q

Definition of HF

A
  • CO is inadequate for body’s requirement
  • inability of heart to deliver blood and O2 at a rate the body needs to meet demand
  • physiological changes occur to maintain CO
  • eventually overwhelmed and become pathophysiological
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33
Q

Types of HF

A
  • systolic = inability of ventricles to contract normally
  • diastolic = inability of ventricles to relax and fill normally
  • can be left or right ventricular failure
  • acute or chronic HF
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34
Q

Causes of LHF

A
  • coronary artery disease
  • arrhythmias
  • MI
  • cardiomyopathy
  • congenital heart defects
  • valvular heart disease
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35
Q

Causes of RHF

A
  • COPD
  • pulmonary HTN
  • right ventricular infarct
  • cor pulmonale
  • progression of LHF
  • PE
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36
Q

Causes of systolic HF

A
  • IHD
  • MI
  • cardiomyopathy
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37
Q

Causes of diastolic HF

A
  • aortic stenosis
  • chronic HTN
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38
Q

Pathophysiology of HF

A
  1. myocardium fails
  2. decreased volume of blood ejected, increased preload
  3. increased ventricular load causes hypertrophy of myocardium
  4. increase in muscle growth to compensate and pump more blood out
  5. increased myocardial demand for oxygen
  6. myocardium becomes ischaemic → patchy fibrosis → stiffness and reduced contractibility
  7. decreased contractibility = increased workload and amount of blood remaining
  8. more force needed to maintain cardiac output
  9. cells become tired → pathological
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39
Q

How does HF activate RAAS

A
  • increased afterload and preload
  • increased cardiac work
  • damage to myocytes
  • decreased cardiac output
  • activates RAAS and adrenergic pathway
  • Na+ and water retention
  • increased HR and contraction force
  • cardiotoxicity
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40
Q

Common clinical presentation of HF

A
  • SOB
  • fatigue
  • peripheral oedema
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41
Q

Symptoms of LHF

A
  • exertional dyspnoea
  • orthopnoea
  • nocturnal cough
  • wheeze
  • nocturia
  • cold peripheries
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42
Q

Symptoms of RHF

A
  • peripheral oedema
  • ascites
  • facial engorgement
  • epistaxis
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43
Q

Signs of HF

A
  • tachycardia
  • elevated JVP
  • cardiomegaly
  • 3rd/4th heart sounds
  • displaced apex beat
  • bi-basal crackles
  • pleural/peripheral effusion
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44
Q

Investigations for HF

A
  • ECG → may indicate cause
  • BNP
  • chest xray
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45
Q

What is BNP

A
  • brain natriuretic peptide
  • marker of HF
  • released when myocardial walls are under stress
  • levels correlated to ventricular wall stress and HF severity
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46
Q

Chest xray findings in HF

A

ABCDE

  • alveolar oedema
  • B Kerley lines
  • cardiomegaly
  • dilated upper lobe vessels of lungs
  • effusions (pleural)
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47
Q

Treatment of HF

A
  • lifestyle changes
  • diuretics reduce preload and pressure on ventricles → loop/thiazide/aldosterone antagonist
  • ACEi for LV systolic dysfunction
  • beta blocker and spironolactone to decrease mortality
  • digoxin for symptom relief
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48
Q

What is cor pulmonale?

A

right sided HF caused by chronic pulmonary arterial HTN

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49
Q

Causes of cor pulmonale

A
  • chronic lung disease
  • pulmonary vascular disorders
  • neuromuscular and skeletal diseases
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50
Q

Signs and symptoms of cor pulmonale

A
  • cyanosis
  • tachycardia
  • raised JVP
  • RV heave
  • pan systolic murmur
  • hepatomegaly
  • oedema
  • dyspnoea
  • fatigue
  • syncope
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51
Q

Investigations for cor pulmonale

A
  • ABG → hypoxia +/- hypercapnia
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52
Q

Management of cor pulmonale

A
  • treat underlying cause
  • oxygen
  • same treatment as HF
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53
Q

Pathophysiology of PVD

A
  • commonly atherosclerosis → claudication of vessels
  • other causes of claudication = aortic coarctation, temporal arteritis, Burger’s
  • end stage PVD = critical limb ischaemia
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54
Q

Risk factors of PVD

A
  • hyperlipidaemia
  • history of CAD
  • age >40
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55
Q

What are the signs of critical limb ischaemia

A

6 Ps

  • pain
  • paresthesia
  • pulselessness
  • pallor
  • paralysis
  • poikilothermia = perishingly cold
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56
Q

Presentation of PVD

A
  • pain in lower limbs on excercise, relieved on rest = intermittent claudication
  • severe = unremitting pain in foot
  • legs may be pale, bold, loss of hair, skin changes
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57
Q

Investigation for PVD

A
  • ankle brachial pressure index ≤0.90
  • ABPI = doppler ultrasonography
  • should be 1
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58
Q

Treatment for PVD

A

control risk factors - lifestyle changes

antiplatelet therapy

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59
Q

Treatment for critical limb ischaemia

A

as stated plus:

  • revascularisation eg stenting, angioplasty, bypassing
  • amputation if unsuitable
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60
Q

What is pericarditis?

A

inflammation of the pericardium +/- effusion

2 types

  • fibrinous = dry
  • effusive → purulent serous/haemorrhagic
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61
Q

Causes of acute pericarditis

A
  • infection
  • autoimmune → RA, sjogren’s, SLE
  • secondary metastatic tumours
  • traumatic and iatrogenic
  • post cardiac injury
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62
Q

What infections can cause acute pericarditis?

A
  • enteroviruses
  • adenoviruses
  • mycobacterium TB
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63
Q

Pathophysiology of pericarditis

A
  1. inflammation
  2. narrowing of pericardial space and scarring
  3. if untreated, build up of exudate and adhesions in pericardial space → pericardial effusion
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64
Q

Symptoms of pericarditis

A
  • severe chest pain
  • dyspnoea
  • cough
  • hiccups
  • fever
  • myalgia
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65
Q

Signs of pericarditis

A
  • pericardial rub on auscultation
  • tachycardia
  • peripheral oedema
  • increased JVP
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66
Q

Investigations for pericarditis

A

ECG = DIAGNOSTIC

  • saddle shaped ST elevation
  • diffuse ST elevation in all leads
  • PR depression

chest xray → effusion may cause cardiomegaly

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67
Q

What is chest pain like in pericarditis

A
  • sharp, pleuritic, rapid onset
  • worse when laying flat, relieved sitting forwards
  • radiates to trapezius ridge
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68
Q

Treatment for pericarditis

A
  • reduce physical activity until symptoms resole
  • NSAIDs with gastric protection → ibuprofen/aspirin
  • colchicine 3 months
  • treat cause
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69
Q

What is infective endocarditis

A
  • an infection of the endocardium or vascular endothelium of the heart
  • fever and new murmur = infective endocarditis until proven otherwise
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70
Q

What microorganisms cause infective endocarditis

A
  • staph aureus
  • streptococcus viridans
  • strep bovis
  • enterococci
  • coxiella burnetii
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71
Q

Risk factors for infective endocarditis

A
  • IVDU
  • immunocompromised
  • people with prosthetic valves
  • aortic/mitral valve disease
  • poor dental hygiene
  • pacemakers
  • IV cannula
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72
Q

Pathophysiology of infective endocarditis

A
  • abnormal cardiac endothelium and organisms in bloodstream
  • adherence and growth of organisms
  • infective endocarditis
  • LHS of heart = most common side effected
  • RHS affected in IVDU
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73
Q

Symptoms of endocarditis

A
  • fever
  • rigors
  • night sweats
  • malaise
  • weight loss
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74
Q

Signs of endocarditis

A
  • anaemia
  • splenomegaly
  • clubbing
  • new murmurs
  • sepsis
  • embolic events
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75
Q

Typical presentation of endocarditis

A
  • embolic skin lesions
  • petechiae
  • splinter haemorrhages
  • osler nodes
  • janeway lesions
  • roth spots
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76
Q

Investigations for endocarditis

A
  • Duke criteria
  • echo
  • ECG → long PR interval, regular

transoesophageal echo = more sensitive, uncomfortable, better at diagnosing

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77
Q

Treatment for endocarditis

A
  • antibiotics
  • treat any complications
  • surgery
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78
Q

What surgery can be used to treat endocarditis?

A
  • replace valve if infection cannot be treated with Abs
  • remove/replace infected devices
  • remove large vegetations at risk of embolising
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79
Q

Prevention of endocarditis

A
  • good oral health
  • no IV drug use
  • educate surgery patients on symptoms
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80
Q

What is pericardial effusion

A
  • occurs if pericarditis is untreated
  • buildup of exudate in pericardial space
  • puts pressure on cardiac myocytes → cardiac dysfunction
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81
Q

Signs of pericardial effusion

A
  • bronchial breathing at left base
  • muffled heart sounds
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82
Q

Treatment for pericardial effusion

A
  • treat the cause
  • pericardiocentesis

complication = cardiac tamponade

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83
Q

What is cardiac tamponade

A
  • life threatening
  • accumulation of fluid in pericardial space
  • compression of heart chambers
  • decreased venous return and filling of heart
  • reduces cardiac output
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84
Q

Symptoms and signs of cardiac tamponade

A
  • Beck’s triad
  • pulsus paradoxus = large decrease in stroke volume
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85
Q

What is Beck’s triad?

A
  • falling BP
  • rising JVP
  • muffled heart sounds
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86
Q

Investigations for cardiac tamponade

A

GOLD STANDARD = echo

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87
Q

Treatment for cardiac tamponade

A

pericardiocentesis

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88
Q

Murmur in mitral stenosis

A
  • mid-diastolic murmur with opening snap
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89
Q

Symptoms of mitral stenosis

A
  • haemoptysis due to pulmonary oedema
  • palpitations AF
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90
Q

Signs of mitral stenosis

A
  • malar flush
  • tapping apex beat
  • low volume pulse
  • loud S1
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91
Q

Causes of mitral stenosis

A
  • rheumatic heart disease
  • IE
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92
Q

Murmur in mitral regurgitation

A

pansystolic high pitched whistling murmur

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93
Q

Symptoms of mitral regurgitation

A
  • palpitations
  • exertional dyspnoea
  • fatigue
  • weakness
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94
Q

Signs of mitral regurgitation

A
  • AF
  • displaced, thrusting apex
  • soft/absent S1
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95
Q

Causes of mitral regurgitation

A
  • idiopathic
  • IHD
  • rheumatic heart disease
  • EDS, Marfans
96
Q

Complication of mitral regurgitation

A

congestive HF

97
Q

Murmur in aortic stenosis

A

ejection systolic murmur

98
Q

Symptoms of aortic stenosis

A

triad of

  • syncope
  • angina
  • dyspnoea
99
Q

Signs of aortic stenosis

A
  • sustained heaving apex
  • slow rising pulse
  • narrow pulse pressure
  • soft S2 if severe
100
Q

Causes of aortic stenosis

A
  • idiopathic
  • rheumatic heart disease

AS = most common valve defect

101
Q

Murmur in aortic regurgitation

A
  • early diastolic murmur
  • Austin flint murmur at apex
102
Q

Symptoms of aortic regurgitation

A
  • palpitation
  • angina
  • dyspnoea
103
Q

Signs of aortic regurgitation

A
  • water hammer pulse
  • wide pulse pressure
  • displaced apex
  • Corrigan’s pulse → collapsing
104
Q

Causes of aortic regurgitation

A
  • idiopathic
  • EDS, Marfans
105
Q

Treatment for valve defects

A
  • treat symptoms
  • replace defective valve
106
Q

What is VTE?

A
  • venous thromboembolism
  • blood clots develop in circulation
  • due to stagnation of blood and hyper-cogulable states
107
Q

What is a DVT?

A
  • deep vein thrombosis
  • thrombus that develops in the venous circulation
108
Q

What is a PE?

A
  • pulmonary embolism
  • once thrombus develops, it can travel → embolise
  • deep veins → through RHS of heart → lungs → PE
109
Q

What is a complication of VTE?

A
  • if patient has a hole in heart, clot can pass through LHS of heart into systemic circulation
  • causes large stroke
110
Q

Risk factors for VTE

A
  • immobility, long haul travel
  • recent surgery
  • pregnancy
  • hormone therapy with oestrogen → pill, HRT
  • malignancy
  • polycythaemia
  • SLE
  • thrombophilia → antiphospholipid syndrome
111
Q

VTE prophylaxis

A
  • hospital admission → risk assessment for VTE
  • LMW heparin if high risk

contraindicated if active bleeding or existing coagulants

112
Q

Presentation of DVT

A
  • unilateral
  • calf/leg swelling
  • dilated superficial veins
  • calf tenderness
  • oedema
  • colour changes in leg
113
Q

What is a Wells score?

A

predicts risk of patients with symptoms having a DVT/PE

114
Q

Diagnosis of VTE

A

D-dimer

DIAGNOSTIC FOR DVT = doppler US leg

GOLD STANDaRD FOR PE = CT pulmonary angiogram
- V/P scan if contraindicated

115
Q

Initial management of VTE

A
  • anticoagulation
  • catheter directed thrombolysis
116
Q

Long-term anticoagulation in VTE

A

DOAC, warfarin, LMW heparin

  • 3 months if cause reversible
  • 3-6 months if active cancer
117
Q

What is an anuerysm?

A

weakening of vessel wall followed by dilation due to increased wall stress

118
Q

What is the most common vessel aneursym

A

abdominal aortic aneurysm

119
Q

Pathophysiology of aortic aneurysm

A

1 inflammation and degeneration of smooth muscle cells

  1. loss of structural integrity of aortic wall
  2. vessel widens
  3. mechanical stress acts on weakened wall tissue
  4. can lead to dilation or rupture
120
Q

Complication of dilated aneurysm

A

peripheral thromboembolism

121
Q

Risk factors of aortic aneurysm

A
  • SMOKING
  • family history
  • connective tissue disorders
  • age
  • atherosclerosis
  • male
122
Q

Presentation of AAAs

A
  • most are asymptomatic
  • commonly found below renal arteries → infrarenal
  • if big, pulsatile mass on palpation, bruit on auscultation
  • lower back/abdominal pain if expanding rapidly
123
Q

Diagnosis of aortic aneurysms

A
  1. ultrasonography
124
Q

Management of aortic aneurysms

A

symptomatic → repair

asymptomatic

  • surveillance
  • if diameter >5.5cm (m) or >5cm (f) → repair
125
Q

Complications of aortic aneurysms

A
  • rupture of AAA
  • thromboembolism
  • fistula formation
126
Q

Presentation of ruptured AAA

A
  • acute onset of severe, tearing abdominal pain with radiation back, flank, groin
  • painful pulsatile mass
  • hypovolemic shock
  • syncope
  • nausea, vomiting
127
Q

Diagnosis of ruptured AAA

A

clinical to save time

128
Q

Treatment of ruptured AAA

A
  • urgent surgery → endovascular aneurysmal repair
  • maintain haemodynamic stability
129
Q

What is an aortic dissection?

A
  • teat in the intimal layer of aorta
  • leads to collection of blood between intima and medial layers
  • mainly in ascending aorta
130
Q

Pathophysiology of aortic dissection

A
  • tear in intimal layer
  • blood passes through media propagating distally or proximally
  • false lumen
  • can occlude flow through branches of aorta
  • ischaemia of affected regions
131
Q

Risk factors of aortic dissection

A
  • male
  • 40-60
  • HTN → most common
  • trauma
  • vasculitis
  • cocaine use
  • connective tissue disorders in younger adults
132
Q

Clinical features of aortic dissection

A
  • sudden and severe tearing pain in chest radiating to back
  • hypotension
  • asymmetrical BP
  • syncope
133
Q

Diagnosis of aortic dissection

A
  • ECG
  • chest xray
  • CT
134
Q

Management of aortic dissection

A
  • maintain haemodynamic stability
  • opioid analgesia
  • endovascular stent-graft repair
  • antihypertensives post surgery
135
Q

How do you maintain haemodynamic stability

A
  • fluid resuscitation
  • ionotropes
  • noradrenaline
136
Q

What is tetralogy of Fallot?

A
  • large ventricular septal defect
137
Q

Features of tetralogy of Fallot

A
  • overriding aorta
  • RV outflow obstruction
  • RV hypertrophy
138
Q

Investigations for tetralogy of Fallot

A

echo

139
Q

Treatment for tetralogy of Fallot

A

surgical repair

140
Q

What is coarctation of aorta?

A
  • narrowing of aortic arch around ductus arteriosus
  • varied severity
  • associated with Turners syndrome
  • low BP in areas after narrowing
  • high BP in areas before
141
Q

Presentation of coarctation of aorta

A
  • in neonates, weak femoral pulses
  • grey and floppy baby
  • poor feeding
  • tachypnoea
  • left ventricular heave
142
Q

Management of coarctation of aorta

A
  • if severe, prostaglandin E used to keep ductus arteriosus open
  • surgery to correct coarctation and ligate ductus arteriosus
143
Q

What is tachycardia?

A
  • fast hear rate
  • >100bpm
144
Q

What is atrial tachycardia?

A

>150bpm

ECG

  • abnormal P waves
  • normal QRS
145
Q

What is AV nodal re-entrant tachycardia?

A
  • absent P wave
  • normal QRS
146
Q

What is ventricular tachycardia?

A
  • no P waves
  • regular wide QRS
  • no T waves
147
Q

What is bradycardia?

A
  • slow heart rate
  • <60pbm
148
Q

What is atrial fibrillation?

A
  • chaotic irregular rhythm
  • irregular ventricular rate

ECG

  • no P waves
  • irregularly irregular QRS
149
Q

Causes of a fib

A
  • idiopathic
  • HTN
  • HF
  • coronary artery disease
  • vavlular heart disease
  • cardiac surgery
  • cardiomyopathy
  • rheumatic heat disease
150
Q

Pathophysiology of a fib

A
  • continous rapid activation of atria
  • no organised mechanical action
  • 300-600bpm
151
Q

Risk factors for a fib

A
  • 60+
  • diabetes
  • high BP
  • past MI
  • structural heat disease
152
Q

Presentation of a fib

A
  • asymptomatic
  • palpitations
  • dyspnoea
  • chest pain
  • fatigue
  • apical pulse>radial
153
Q

Treatment of a fib

A

cardioversion

  • LMW heparin
  • shock with defib
154
Q

What is atrial flutter?

A
  • organised atrial rhythm
  • rate of 250-250bpm

ECG → saw tooth pattern = DIAGNOSTIC

155
Q

Causes of atrial flutter

A
  • idiopathic
  • coronary heart disease
  • obesity
  • HTN
  • HF
  • COPD
  • pericarditis
156
Q

Risk factors of atrial flutter

A

atrial fibrillation

157
Q

Presentation of atrial flutter

A
  • palpitations
  • breathlessness
  • chest pain
  • dizziness
  • syncope
  • fatigue
158
Q

Treatmen of atrial flutter

A
  • cardioversion
  • catheter ablation → creates conduction block
  • IV amiodarone → restore sinus rhythm
159
Q

What is bundle branch block

A
  • block in conduction of one of the bundle branches
  • ventricles don’t receive impulses at the same time
160
Q

ECG changes in right BBB

A
  • MaRRoW
  • wide QRS

DIAGNOSTIC

161
Q

Causes of right BBB

A
  • PE
  • IHD
  • atrial ventricular septal defect
162
Q

Pathophysiology of right BBB

A
  • right bundle doesn’t conduct
  • impulse spread from LV to RV
  • late activation of RV
163
Q

Presentation of right BBB

A
  • asymptomatic
  • syncope/presyncope
164
Q

Treatment of right BBB

A
  • pacemaker
  • cardiac resynchronisation therapy
  • reduce BP
165
Q

ECG changes in left BBB

A
  • WiLLiaM
  • wide QTS and notched top
  • T wave inversion in lateral leads

DIAGNOSTIC

166
Q

Causes of left BBB

A
  • IHD
  • aortic valve disease
167
Q

Pathophysiology of left BBB

A
  • left bundle doesn’t conduct
  • impulse spreads from RV to LV
  • late activation of LV
168
Q

Presentation of left BBB

A

same as right BBB

169
Q

Treatment of left BBB

A

same as right BBB

170
Q

What is heart block

A

a block at any level of the conduction system in which conduction seizes

171
Q

What are the different types of heart block

A

1st degree

2nd degree

  • Mobitz I
  • Mobitz II

3rd degree

172
Q

1st degree heart block

A
  • PR interval >200ms
  • asymptomatic
173
Q

ECG changes 2nd degree Mobitz I

A
  • progressive lengthening of PR interval
  • one non-conducted P wave
  • next PR interval is shorter
174
Q

Presentation of 2nd degree Mobitz I

A
  • light headedness
  • dizziness
  • syncope
175
Q

ECG changes in 2nd degree Mobitz II

A
  • constant PR
  • occasional non-conducted P waves
  • wide QRS

2: 1
- two waves per QRS
- normal consistent PR intervals

176
Q

Presentation of 2nd degree Mobitz II

A
  • SOB
  • postural hypotension
  • chest pain
177
Q

ECG changes in 3rd degree heart block

A
  • P waves and QRS at different rates → dissociation
  • abnormally shaped QRS
178
Q

Presentation of 3rd degree heart block

A
  • dizziness
  • blackouts
179
Q

Treatment for 3rd degree heart block

A
  • permanent pacemaker
  • IV atropine
180
Q

Causes of heart block

A
  • athletes
  • sick sinus rhythm
  • MI
  • drugs
  • congenital
  • aortic valve calcification
  • cardiac surgery/trauma
181
Q

Treatment for heart block

A
  • cardioversion
  • catheter ablation
  • IV amiodarone
182
Q

What is prolonged QT syndrome?

A

where the QT interval is greatly increased

ECG DIAGNOSTIC

183
Q

Causes of prolonged QT syndrome

A
  • congenital
  • hypokalaemia
  • hypocalcaemia
  • drugs → amiodarone, tricyclic antidepressants
  • bradycardia
  • acute MI
  • diabetes
184
Q

Presentation of prolonged QT syndrome

A
  • syncope
  • palpitations
  • may progress to VF
185
Q

Treatment of prolonged QT syndrome

A
  • cardioversion
  • treat underlying cause
  • if acquired → IV isoprenaline
186
Q

What is Wolff-Parkinson-White syndrome?

A
  • accessory pathway for conduction
  • impulse can travel to AVN but also to ventricle quicker
187
Q

ECG changes in WPW

A

pre-excitation

  • short PR interval
  • wide QRS complex that begins slurred

ECG DIAGNOSTIC

188
Q

Causes of WPW

A

same as prolonged QT syndrome

189
Q

Presentation of WPW

A
  • palpitations
  • severe dizziness
  • dyspnoea
  • syncope
190
Q

Treatment of WPW

A
  • vagal manoeuvre
  • IV adenosine
  • surgery → catheter ablation of pathway
191
Q

What is the vagal manoeuvre?

A
  • breath holding
  • carotid massage
  • valsalva manoeuvre
192
Q

What is rheumatic fever?

A
  • systemic infection common in developing countries
  • from Lancefield group A B-haemolytic streptococci
  • antibody from cell wall cross-reacts with valve tissue → permanent damage to heart valves
193
Q

Symptoms of rheumatic fever

A
  • fever
  • arthritis
  • chest pain
  • SOB
  • fatigue
  • chorea → jerky movements
194
Q

Signs of rheumatic fever

A
  • tachycardia
  • murmur → depends on valve
    pericardial rub
  • erythema marginatum
  • prolonged PR interval
195
Q

Investigations for rheumatic fever

A

Jones criteria

196
Q

Treatment for rheumatic fever

A
  • rest until CRP is normal
  • IV benzylpenicillin then phenoxymethylenicillin for 10 days
  • analgesia
  • haldoperidol/diazepam for chorea
197
Q

Causes of cardiogenic shock

A
  • pump failure
  • MI
  • cardiac arrest
198
Q

Pathophysiology of cardiogenic shock

A
  • decreased CO
  • decreased MAP
199
Q

Presentation of cardiogenic shock

A
  • tachycardia
  • tachypnoea
  • decreased urine output, BP
  • cold peripheries
  • chest pain
200
Q

Treatment for cardiogenic shock

A
  • ABCDE
  • rescucitation
201
Q

Causes of hypovolaemic shock

A
  • low fluid volume
  • haemorrhage
  • dehydration
202
Q

Pathophysiology of hypovolaemic shock

A
  • decreased MAP
  • decreased CO
203
Q

Presentation of hypovolaemic shock

A
  • tachypnoea
  • weak rapid pulse
  • cyanosis
  • increased CRT
204
Q

Treatment of hypovolaemic shock

A
  • ABCDE
  • resuscitation
  • fluids
  • vasodilator GTN
205
Q

Causes of septic shock

A

toxins. inblood

206
Q

Pathophysiology of septic shock

A
  • decreased MAP
  • derangement in physiology
207
Q

Presentation of septic shock

A
  • tachycardia
  • D&V
  • decreased urine output, O2, BP
208
Q

Treatment of septic shock

A
  • broad spectrum IV Abs
  • fluid
  • O2
209
Q

Causes of anaphylactic shock

A

severe allergic reaction

210
Q

Pathophysiology of anaphylactic shock

A
  • histamine release
  • vasodilation
  • hypoxia
211
Q

Treatment for anaphylactic shock

A
  • rescucitation
  • adrenlaine
212
Q

What does resuscitation entail in shock

A
  • CPR
  • fluids
  • O2
213
Q

What is cardiomyopathy?

A

a group of diseases of the myocardium that affect mechanical or electrical function

214
Q

What are the types of cardiomyopathy?

A
  • hypertrophic
  • dilated
  • restricted
215
Q

What is dilated cardiomyopathy?

A

the left ventricle is dilated with thin muscle → contracts poorly

216
Q

Causes of dilated cardiomyopathy

A
  • ischaemia
  • alcohol
  • thyroid disorder
  • genetic
217
Q

Pathophysiology of dilated cardiomyopathy

A
  • poorly generated contractile force → progressive dilation of the heart
  • diffuse interstitial fibrosis
  • systolic dysfunction of left or both ventricles
218
Q

Signs of dilated cardiomyopathy

A
  • HF
  • arrhythmia
  • thromboembolism
  • increased JVP
  • sudden death
219
Q

Symptoms of dilated cardiomyopathy

A
  • SOB
  • fatigue
  • dyspnoea
220
Q

Investigations for dilated cardiomyopathy

A
  • chest xray → cardiac enlargement
  • ECG → tachycardia, arrhythmia, T wave changes
  • echo → dilated ventricles
221
Q

Treatment of dilated cardiomyopathy

A

treat cause

222
Q

What is hypertrophic cardiomyopathy?

A

ventricular hypertrophy → obstruction of outflow tract

223
Q

Causes of hypertrophic cardiomyopathy

A
  • genetic → autosomal dominant
  • 50% sporadic
224
Q

Pathophysiology of hypertrophic cardiomyopathy

A
  • gene mutation for sarcomere protein
  • impaired diastolic filling
  • reduced stroke volume
  • reduced CO
225
Q

Symptoms of hypertrophic cardiomyopathy

A
  • sudden death may be first symptom
  • chest pain/angina
  • dyspnoea
  • dizziness
  • palpitations
  • syncope
226
Q

Signs of hypertrophic cardiomyopathy

A
  • ejection-systolic murmur
  • jerky carotid pulse
  • left ventricular outflow obstruction
227
Q

Investigations for hypertrophic cardiomyopathy

A
  • ECG → T wave inversion, deep Q waves
  • genetic analysis
228
Q

Treatment for hypertrophic cardiomyopathy

A
  • amiodarone → anti-arrhythmic
  • CCB → verapamil
  • beta blocker → atenolol
229
Q

What is restrictive cardiomyopathy?

A

scar tissue replaces normal heart muscle and ventricles become rigid so don’t contract properly

230
Q

Causes of restrictive cardiomyopathy

A
  • amyloidosis
  • idiopathic
  • sarcoidosis
  • end-myocardial fibrosis
231
Q

Symptoms of restrictive cardiomyopathy

A
  • dyspnoea
  • fatigue
  • embolic symptoms
232
Q

Signs of restrictive cardiomyopathy

A
  • increased JVP → diastolic collapse, elevated on inspiration
  • hepatic enlargement
  • ascites
  • oedema
  • 3rd and 4th heart sounds
233
Q

Pathophysiology of restrictive cardiomyopathy

A
  • normal/decreased volume in both ventricles
  • bi-atrial enlargement
  • impaired ventricle filling
  • rigid myocardium restricts ventricular filling
234
Q

Investigations for restrictive cardiomyopathy

A

DIAGNOSTIC = cardiac catheterisation

235
Q

Treatment for restrictive cardiomyopathy

A

no treatment → poor prognosis

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