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2a - SBCS > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Define infective endocarditis (IE)F

A
  • infection of endocardium or vascular endothelium of heart
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2
Q

Difference between early and late prosthetics

A

Early - within 1 year of op
Late - after a year post op

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3
Q

Give 4 risk factors for IE

A
  • Poor dental hygiene
  • young IV drug users
  • young with congenital HD
  • prosthetic valves
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4
Q

Name 3 bacteria that can cause IE

A

staph aureus - drug users
strep viridans - poor dental health
Staph epidermis - prosthetic valve surgery

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5
Q

Explain the pathophysiology of IE

A

Abnormal/ damaged endocardium have increased platelets deposition; bacteria adheres to this and causes vegetations
* typically around valves
* causing regurgitation

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6
Q

Signs and symptoms of IE

A

New regurgitant heart murmur
Fever
Headache and fatigue
Night sweats, malaise
peripheral stigmata

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7
Q

What are the peripheral stigmata of IE

A
  • Osler’s nodes - small tender nodules found on tips of fingers or toes
  • Splinter haemorrhages
  • Roth spots - retinal haemorrhage
  • Janeway lesions - non tender lesions on soles & palm
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8
Q

5 ways in which IE is diagnosed

A
  • ECG - long PR interval
  • Urinalysis - proteinuria and blood
  • Echocardiogram (ECHO) - Detecting vegetation
  • High CRP and ESR
  • Blood cultures: 3 cultures from 3 different sites at different times
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9
Q

What is the scoring system for infective endocarditis

A

Duke’s criteria - definite/possible IE

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10
Q

What are the 2 different echocardiogram (ECHO) methods

A

Transthoracic 2D echo (TTE)
Transoesophageal echo (TOE)

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11
Q

PROS and CONS of TOE

A

TOE more invasive than TTE but has better visualisation sensitivity and specificity

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12
Q

Treatment of IE caused by s.aureus

A

IV Flucloxacillin
or Vancomycin + rifampicin if MRSA

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13
Q

Treatment of IE caused by s.viridans

A

Beta-lactam (e.g. benzylpenicillin, amoxicillin) + gentamicin

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14
Q

How is IE treated if it is unable to be treated by antibiotics

A

Surgery
* remove incompetent valve and replace with prosthetic
* remove large vegetations before they embolise
* replace infected devices

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15
Q

How long are patient’s with IE on antibiotics for

A

4-6 weeks

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16
Q

Complications of IE

A

Heart failure
Aortic root abscess
Sepsis
emboli
Stroke

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17
Q

Define aortic stenosis

A

Narrowing of the aortic valve
Normal valve area is 4cm²
Symptoms occur when area is 1/4th of normal
Systolic murmur

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18
Q

Causes of aortic stenosis (AS)

A

Congenital bicuspid valve
Age-related degenerative calcification

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19
Q

Explain the pathophysiology of AS

A

Narrowing of aortic valve
Decreased SV
Increased after load
increased LV pressure
Compensatory LVH

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20
Q

Presentation of aortic stenosis

A

SAD:
Syncope (collapse, exertional)
Angina (increased myocardial O2 demand)
Dyspnoea (due to heart failure)

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21
Q

Clinical signs of aortic stenosis

A
  • Slow rising pulse and decreased pulse amplitude - severe
  • Prominent S4 due to left ventricular hypertrophy
  • Ejection systolic murmur radiating to carotids - crescendo-decrescendo
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22
Q

How is AS investigated

A

ECG: LVH
ECHO:
* LV size and function: hypertrophy, dilation and ejection fraction
* Aortic valve area (Doppler derived)

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23
Q

Treatment of AS

A

Healthy patient: open repair, valve replacement
At risk patient: TAVI (Transcatheter aortic valve implantation) - less invasive stents

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24
Q

Define aortic regurgitation (AR)

A

Leakage of blood into LV during diastole due to ineffective aortic valve
Diastolic murmur

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25
Q

Causes of AR

A

Congenital Bicuspid aortic valve
Rheumatic heart disease
Infective endocarditis

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26
Q

Clinical signs of aortic regurgitation

A
  • Wide pulse pressure
  • Austin flint murmur - rumbling mid diastolic murmur at apex (severe)
  • Early Diastolic blowing murmur - at left sternal border
  • Collapsing pulse
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27
Q

Give 2 symptoms of aortic regurgitation

A

Exertional dyspnoea
Palpitations

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28
Q

Explain the investigation and diagnosis of AR

A
  • Chest X-ray - enlarged cardiac silhouette and aortic root enlargement
  • ECHO - evaluate AV and aortic root with measurements of LV dimensions
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29
Q

Treatment for AR

A
  • IE prophylaxis
  • Vasodilator - ACEi
  • Surgical valve replacement if appropriate
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30
Q

Define mitral regurgitation

A

Backflow of blood from the LV to the LA during systole due to ineffective mitral valve
*Systolic murmur

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31
Q

State 3 causes of MR

A

Ischaemic MV
Rheumatic HD
Infective endocarditis

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32
Q

Risk factors of MR

A

Low BMI
Congenital HD
Mitral valve prolapse (floppy)
Female

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33
Q

Explain the pathophysiology of MR

A

Regurgitation into the left atrium 🡪 left atrial dilatation 🡪 left atrial enlargement 🡪 LVH (since ventricle needs to put in more effort to pump less blood) 🡪 pulmonary hypertension 🡪 right ventricular dysfunction

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34
Q

Presentation of MR

A

Exertion dyspnoea
Murmur: pansystolic murmur at the apex radiating to axilla
* Soft S1 & Prominent S3
* Chronic MR - intensity correlates with severity
* Displaced apical beat

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35
Q

3 investigations for mitral regurgitation

A

ECG - LA enlargement, AF & LVH with severe MR
Chest Xray - LA enlargement, central pulmonary artery enlargement
ECHO - est LA, LV size and function, Valve structure assessment

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36
Q

What drugs are used to treat MR

A

BB (atenolol), CCB - rate control
ACEi
Nitrates/ diuretics in acute MR

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37
Q

When is surgery for MR undergone

A
  • Any symptoms at rest - valve replacement/repair
  • ejection fraction <60%
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38
Q

Define mitral stenosis

A

Obstruction of LV inflow that prevents proper filling during diastole (diastolic murmur)
Normal MV area: 4-6 cm²
Symptoms begin at areas <2cm²

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39
Q

Causes of m.stenosis

A

Rheumatic heart disease (common)
Infective endocarditis
Mitral valve calcification

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40
Q

Explain the pathophysiology of m.stenosis

A

Thickening and immobility of valve > obstruction of blood flow from right atrium to right ventricle > left atrial pressure increases > LAH > pulmonary venous, arterial and right heart pressures increase > pulmonary oedema > pulmonary HTN > RVH > tricuspid regurgitation

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41
Q

Signs of m.stenosis

A
  • pinkish-purple patches on cheeks
  • prominent a wave in jugular venous pulsations
  • Dyspnoea
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42
Q

Describe the diastolic murmur in mitral stenosis

A

Diastolic murmur:
* low-pitched diastolic rumble most prominent at apex
* heard best with patient lying on left side in held expiration
* intensity of murmur doesn’t correlate with severity of stenosis

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43
Q

Apart from a diastolic murmur, what other heart sounds can be observed in MS

A
  • Loud opening S1 snap: heard at apex when leaflets are still mobile
  • shorter S2 to opening snap interval indicates more severe disease
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44
Q

How is MS diagnosed

A
  • ECG - may show AF and LA enlargement
  • CXR - LA enlargement and pulmonary congestion. Occas calcified MV
    ECHO - Assess MV mobility, gradient and MV area
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45
Q

What drugs may be used in the treatment of MS

A
  • BBs & CCBs which control heart rate
  • Diuretics for fluid overload
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46
Q

Define pericarditis

A

inflammation of the pericardium with or without effusion

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47
Q

What are the types of pericarditis

A

Fibrinous - dry
Effusive (wet):
* Purulent serous exudate - infection/malignancy
* Haemorrhagic exudate - bleeding

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48
Q

Give 4 infectious causes of pericarditis with examples

A
  • Viral (m.common) - CMV, EBV
  • Bacterial - TB (common)
  • Fungal (v.rare)
    • Parasitic (v.rare)
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49
Q

Give 4 non-infectious causes of pericarditis with examples

A
  • Autoimmune (common) - rheumatoid arthritis
  • Neoplastic - 2 metastatic tumours (breast and lung cancer)
  • Traumatic and latrogenic - pericardial injury syndromes (Dressler’s syndrome)
  • Chronic heart failure
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50
Q

What % of pericarditis cases are idiopathic

A

80-90%

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51
Q

Describe the type of chest pain in pericarditis

A
  • Sharp, pleuritic chest pain in left anterior chest/epigastrium
  • Chest pain radiates to trapezius ridge due to co-innervation of phrenic nerve
  • Relieved by sitting forward and exacerbated by lying down
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52
Q

Apart from chest pain, describe other signs and symptoms of pericarditis

A
  • Dyspnoea
  • Hiccups
  • Fever
  • Cough
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53
Q

What is the main differential diagnosis for symptoms of pericarditis

A

Myocardial infarction/ischaemia

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54
Q

Describe the typical results of a clinical exam for pericarditis

A

Clinical exam:
* tachycardia
* pericardial rub - pathognomonic, crunching snow sound
* Signs of effusion

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55
Q

Describe the typical results of an ECG for pericarditis

A
  • Widespread saddle shaped ST elevation
  • PR depression
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56
Q

What may a chest X-ray show in someone with pericarditis show

A
  • Normal in idiopathic
  • Pneumonia common in bacterial
  • Effusion may cause cardiomegaly
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57
Q

Treatment for pericarditis

A
  • NSAIDS: Ibuprofen/ aspirin for 2w
  • Colchicine for 3w - reduce recurrence
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58
Q

What are the possible complications of pericarditis

A
  • Large pericardial effusion can lead to cardiac tamponade
  • myocarditis
  • constrictive pericarditis
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59
Q

Explain how pericardial effusion can lead to cardiac tamponade

A

Accumulation of fluid in pericardial space accompanying pericarditis. Large vol of fluid (enough to impair ventricle filling) = cardiac tamponade

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60
Q

Define cardiac tamponade

A
  • The accumulation of pericardial fluid, blood, pus or air within the pericardial space
  • This creates an increase in intra-pericardial pressure, restricting cardiac filling and decreasing CO
  • Medical emergency
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61
Q

Signs of cardiac tamponade

A
  • Beck’s triad - Hypotension, increased jugular venous pressure, muffled S1 & S2 heart sounds
  • Pulsus paradoxus - fall in sys BP during inspiration
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62
Q

Gold standard investigation for cardiac tamponade

A

ECHO - late diastolic collapse of right atrium

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63
Q

Describe the ECG findings of cardiac tamponade

A

electrical alternans - varying QRS amplitude due to heart bouncing back and fourth in increased fluid

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64
Q

Treatment for cardiac tamponade

A
  • Pericardiocentesis - drain excess fluid using needle and catheter
  • NSAIDs + PPi
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65
Q

Define abdominal aortic aneurysm

A

Permanent dilatation in vessel wall diameter of >50%, which typically means a diameter of >3 cm

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66
Q

Give 5 RFs of AAA

A

Smoking - MAJOR
CT disorders - Marfan’s
Age
Atherosclerosis
Male

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67
Q

Explain the pathophysiology of AAA

A
  • Inflammation and degeneration of smooth and elastic muscle (vascular tunica)
  • Loss of structural integrity of the aortic wall and mechanical stress results in widening of the vessel
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68
Q

Difference between true and pseudoaneurysm

A

True - structural degeneration in all 3 layers of vascular tunica
Pseudo - not all 3 layers

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69
Q

Describe the presentation of AAA

A
  • Usually asymptomatic till rupture
  • If expanding fast: sudden central abdo pain radiating to flank,
  • triad: abdo/back pain, pulsatile abdo mass and hypotension
  • Cullen’s/ grey turners sign
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70
Q

What is the first line investigation for AAA and why

A

Abdo ultrasound
Cheap, easy, sensitive and specific

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71
Q

Where specifically are AAAs usually found

A

Below renal arteries (infrarenal)

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72
Q

Treatment for non-ruptured AAA

A
  • manage RFs - smoking cessation
  • Asymptomatic and < 5.5cm = monitor
  • Symptomatic and >5.5cm or expanding rapidly = surgery
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73
Q

What is the major complication of AAA and how is it treated

A

Rupture of AAA
* Urgent surgery - EVAR (endovascular aneurysmal repair)
* maintain ABCDE and fluids
100% mortality unless treated immediately

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74
Q

Describe the 2 types of surgery that could be done for AAA

A
  • EVAR - stent inserted through fem/iliac a. + less invasive. - more post op comp
  • Open surgery. + fewer Cx, - more invasive
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75
Q

Define aortic dissection

A

Tear in tunica intima of aorta which leads to a collection of blood between the intima and medial layers

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76
Q

Give 5 RFs for AD

A
  • Men aged 50-70
  • Hypertension - most common
  • CT disorder - ehlers danlos
  • Smoking
  • Trauma
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77
Q

Explain the pathophysiology of AD

A
  • Blood dissects media and intima and pools in false lumen
  • Blood can propagate distally or proximally
  • Flow through the false lumen can occlude flow to end organs = organ failure
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78
Q

Signs and symptoms of AD

A
  • Sudden and severe tearing chest pain radiating to back
  • hypotension (linked to cardiac tamponade)
  • Lower limb pain (B)
  • Pulse deficit and diastolic murmur (A)
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79
Q

Describe the Stanford classification of AD

A
  • A - proximal, involves ascending aorta and/ or arch - mc and more severe
  • B - distal, descending thoracic aorta
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80
Q

Explain the diagnosis of AD

A
  • CXR - shows widened mediastinum (>8cm)
  • TOE - classify as A or B, shows intimal flap and false lumen
  • CT (chest, abdo, pelvis) - definitive image
  • ECG - exclude STEMI
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81
Q

What is the surgical treatment for AD

A

A - open repair
B - endovascular aneurysm repair

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82
Q

What is the medical treatment for AD

A
  • Beta blockers, e.g. IV labetalol or CBB if CI (Verapamil)
  • BB and partial alpha blocker - prevents reflex tachycardia & lowers BP
  • Opioid analgesia (morphine)
  • Vasodilator (Na nitroprusside)
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83
Q

Complications of AD

A

Cardiac tamponade
Aortic regurgitation
Pre-renal AKI

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84
Q

Define hypertension

A

Abnormally high BP:
* >140/90 mmHg in clinic
* >135/85 home readings (A)

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85
Q

Types of HTN

A

1) Essential - idiopathic (95%)
2) Known underlying cause (5%)

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86
Q

Causes of HTN

A

‘ROPE’
* Renal disease - CKD
* Obesity
* Pregnancy
* Endocrine - Conn’s (mc) , Cushing’s, phaeochromocytoma
Also: abnormal RAAS

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87
Q

Give 5 modifiable RFs of HTN

A

Sedentary lifestyle
High salt intake
Obesity
Alcohol intake
T2DM

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88
Q

Give 3 non-modifiable risk factors of HTN

A
  • Age >65
  • Family history
  • Afro-caribb ethnicity
  • Obstructive sleep apnoea
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89
Q

Describe the 3 stages of HTN

A

S1) 140/90 or 135/85(A)
S2) 160/100 or 150/95(A)
S3) 180/110 (immediate Tx)

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90
Q

Pathophysiology of HTN

A

Increased RAAS, sympathetic NS and TPR increases BP as BP = CO x TPR

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91
Q

Signs and symptoms of HTN

A

Mostly asymptomatic, found on screening
Malignant HTN:
* heart failure
* Blurred vision
* Headache
* Chest pain
* CKD

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92
Q

Describe the diagnosis of HTN

A
  • Hospital bp reading >140/90mmHg
  • ABPM (ambulatory) for 24h (as you move around) to confirm diagnosis - >135/85
    Organ damage:
  • Fundoscopy - papilloedema
  • Bloods - HbA1C and lipid profile
  • Urinalysis - proteinuria, high albumin = end organ damage
  • ECHO/ ECG - LVH
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93
Q

When are CCB used in first step treatment for HTN

A
  • Black origin
  • > (=) 55
  • No T2DM
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94
Q

When are ACEi (/ARB) used in first step treatment for HTN

A
  • non-black origin
  • <55
  • T2DM
    nb - DM takes precedence i.e. if black + T2DM take ACEi
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95
Q

Describe the 2nd and 3rd step of HTN treatment

A

2) ACEi (e.g. ramipril) / angiotensin 2 receptor blocker + CCB
3) ACEi + CCB + thiazide-like diuretic (e.g. Indapamide)

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96
Q

SEs of ACEi

A
  • Teratogenic effects
  • Acute renal failure
  • Hyperkalaemia
  • Dry cough
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97
Q

Describe the 4th step of HTN treatment

A

ACEi + CCB + TLD + 1/2
* 1 - If k+ >4.5 mmol/L = a/b blocker
* 2 - If k+ < 4.5 = spironolactone (K sparing)

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98
Q

Give some possible complications of HTN

A

Heart failure
Increased IHD risk
CKD
Retinopathy - papilloedema

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99
Q

Define peripheral vascular disease (PVD)

A

Narrowing of peripheral blood vessels
PAD - arterial
Peripheral venous disease

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100
Q

Give 4 RFs of PVD

A

Smoking
>40
Diabetes
HTN

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101
Q

Explain the pathophysiology of PVD

A
  • Least severe: commonly atherosclerosis leading to claudication of vessels
  • Most severe: severe occlusion, blood supply barely adequate to meet metabolic demand = critical limb ischaemia
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102
Q

What are the 6 signs of acute limb ischaemia

A

Pulselessness
Pallor
Pain
Paralysis
Perishing with cold
Paraesthesia - tingling/numbness

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103
Q

What usually causes limb ischaemia

A

Embolic/thrombotic formation at site of critical limb ischaemia lesion

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104
Q

Signs and symptoms of P. venous disease

A
  • red
  • swollen
  • warm
  • Dull, achy, constant pain
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105
Q

Sx of PAD

A

Most patient are asymptomatic
* Intermittent claudication - limp
*Thigh/buttock pain that is quickly relieved on rest

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106
Q

How is PAD investigated

A
  • Ankle brachial pressure index (ABPI): <0.9
  • CT angiogram - stenosis or occlusions
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107
Q

How is peripheral venous disease investigated

A

D-dimer (blood clotting) and doppler ultrasound (blood flow)

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108
Q

How are PVDs treated

A

*ABPI <0.9 = Percutaneous transluminal angioplasty
* Anti-coagulants - heparin
* Anti-platelets - aspirin or clopidogrel

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109
Q

Complications of PAD

A

Acute limb ischaemia -> loss of limb

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110
Q

Complications of PVD

A

pulmonary embolism

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111
Q

What is ischaemic heart disease

A

Term used to describe heart problems caused by narrowed coronary arteries which leads to cardiac myocyte damage due to insufficient blood supply
* MI + angina

112
Q

What is stable angina

A

Chest pain caused by an insufficient blood supply to the myocardium

113
Q

Give 3 characteristics of stable angina

A
  • Central constricting chest pain that may radiate to arms/jaw
  • Brought on by exertion of stress
  • always relieved by rest or GTN (glyceryl trinitrate)
114
Q

6 RFs of angina

A
  • Obesity
  • T2DM
  • HTN
  • Smoking
  • Age
  • Male
115
Q

Explain the pathophysiology of angina

A

Atherosclerosis leads to narrowing of coronary arteries that results in ischaemia

116
Q

Symptoms of angina

A

Nausea
Breathlessness
Sweating

117
Q

Describe the investigations and diagnosis of stable angina

A

1st line = ECG - Normal or ST depression
GS: CT Angiography - stenosed atherosclerotic arteries (70-80% occluded)

118
Q

Treatment for stable angina

A
  • Episodes of chest pain - GTN spray
  • Modify RFs - smoking cessation, exercise, weight loss
  • Asprin 75mg
  • Atrovastatin
  • BB (e.g. propranolol) or CCB (not HF)
  • Revascularisation
119
Q

Describe the 2 types of coronary revascularisation

A
  • PCI (Percutaneous coronary intervention): balloon stent. Less invasive but risk of stenosis
  • CABG (coronary artery bypass graft): bypass graft. Has better prognosis but is more invasive
120
Q

What physical characteristics identifies a patient who’s had a previous CABG

A

A midline sternotomy scar

121
Q

Differential diagnosis for stable angina

A

Pericarditis
Chest infection
GORD

122
Q

What are acute coronary syndromes (ACS)

A

Umbrella term that includes:
* Unstable angina
* ST elevation MI (STEMI)
* Non-ST elevation MI (NSTEMI)

123
Q

What is unstable angina

A

Chest pain that occurs at rest and is not relieved by GTN. Episodes occur more frequently and last longer (>20 mins)

124
Q

What is silent MI and who are they more likely to be seen in

A

May not experience typical chest pain during an ACS. More likely in women and diabetics

125
Q

Additional symptoms of ACS that aren’t seen in stable angina

A
  • Anxiety - Impeding sense of doom
  • Same symptoms but at rest and more severe
  • > 20 mins of symptoms
126
Q

What tests are done to investigate ACS

A

ECG
Troponin
CT coronary angiogram - extent of occlusion

127
Q

How does unstable angina clinically present

A

ECG: normal or may show some ST depression/ T wave inversion
Troponin: normal

128
Q

Clinical presentation of NSTEMI

A
  • ECG: ST depression, pathological Q waves and T wave inversion
  • Troponin: Raised
  • Partial occlusion of major CA or complete occlusion of minor CA
129
Q

Describe findings of ECG, troponin and CT angiography of STEMI

A
  • ECG: ST elevation in leads consistent with an area of ischaemia / new LBBB
  • Raised troponin
  • Complete occlusion of a major coronary artery
130
Q

Treatment for acute STEMI

A

Patient presenting within 12h of onset:
* PCI: If available within 2 hours of medical contact
* Fibrinolytic agent (alteplase): if PCI not available

131
Q

Treatment for acute NSTEMI (batman)

A
  • Beta blockers - bisoprolol
  • Aspirin
  • Ticagrelor - (clopidogrel alternative if high bleeding risk)
  • Morphine
  • Anticoagulant
  • Nitrates - GTN

give 02 if saturation is <94%

132
Q

Describe the GRACE Score

A

Score to assess for PCI in NSTEMI
* Low risk (<5%) = monitor
* High risk (>10%) = immediate angiogram and consider PCI

133
Q

Complications of MI

A
  • Heart failure
  • Death - ventricular fibrillation mc cause (24h)
  • LV free wall rupture
  • Arrhythmia/ aneurysm
  • Dressler’s syndrome - autoimmune-mediated pericarditis occurring 2-6 weeks after a myocardial infarction
134
Q

Define and describe prinzmetal angina

A
  • Chest pain due to coronary vasospasm not vessel atherogenesis
  • Often seen in cocaine users
  • ECG = ST elevation
135
Q

RFs of MI

A

DM
Male
Smoking
HTN
Obesity

136
Q

Define heart failure

A

The inability of the heart to deliver blood and O2 at a satisfactory rate for the tissue’s metabolic requirements
Syndrome not diagnosis

137
Q

State 6 RFs of HF

A
  • IHD - mc
  • HTN
  • > 65
  • Obesity
  • AF
  • DM
138
Q

Define Cor pulmonale

A

Right sided heart failure caused by disease of lungs and/or pulmonary vessels
Right sided hypertrophy

139
Q

Causes of Cor pulmonale

A
  • COPD (mc)
  • Pulm embolism
  • Cystic fibrosis
140
Q

Signs of cor pulmonale

A
  • Hypoxia
  • Shortness of breath
  • Cyanosis
  • peripheral oedema
  • enlarged liver
141
Q

Symptoms of HF

A
  • Breathlessness
  • Tiredness
  • Ankle swelling
  • Increased weight
  • Wheeze
142
Q

Treatment of cor pulmonale

A

Treat underlying cause
Give O2 to treat respiratory failure

143
Q

5 Signs of HF

A
  • Orthopnoea (worse dyspnoea lying flat)
  • Displaced apex beat
  • peripheral and sacral oedema
  • 3rd and 4th heart sounds
  • raised JVP
144
Q

Describe the NY heart association classification for HF

A

Class:
1) No limit on physical activity (asymptomatic)
2) Slight limit (mild HF)
3) Marked limit (symptomatically moderate HF)
4) Inability to carry out physical activity without discomfort (symptomatically severe HF)

145
Q

What is the range of a normal ejection fraction

A

50-70%

146
Q

Describe HF with reduced EF

A

• LV systolic impairment with LVEF <40%
• systolic failure

147
Q

Describe HF with preserved EF

A
  • LVEF>50% with dilatated LA and LVH
  • diastolic failure
  • mc in women
148
Q

Features of right sided HF

A
  • Fluid build up in veins leading to peripheral oedema
  • Increased JVP
  • Hepatomegaly
149
Q

Give one sign specific to left sided HF

A
  • Paroxysmal nocturnal dyspnoea - suddenly waking up at night short of breath
150
Q

Describe the investigations and diagnosis of HF

A
  • Brain natriuretic peptide (BNP): Increases when there is myocardial stress. Correlates with severity of HF
  • ECG - LVH, AF
  • CXR
  • TTE: establish structure and function of LV
  • Hypervolaemic hyponatraemia
151
Q

Describe the chest Xray findings in HF

A

ABCDE
Alveolar batwing oedema
Kerley B lines
Cardiomegaly
Dilated upper lobe vessels
Effusions (pleural)

152
Q

Treatment for HF

A
  • Pharm: ACEi, diuretics (furosemide), BB
  • Surgery: revascularisation, transplant, valve surgery
  • Lifestyle changes
153
Q

Define tachycardia

A

Abnormally high heart rate of >100bpm

154
Q

What are the 4 different types of supraventricular tachycardia

A
  • Atrial fibrillation (AF)
  • Atrial flutter
  • Atrioventricular nodal re-entrant tachycardia (AVNRT)
  • Atrioventricular re-entrant tachycardia (AVRT)
155
Q

Describe the difference between AVRT and AVNRT

A
  • AVRT - when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome)
  • AVNRT - when the re-entry point is back through the AV node
156
Q

Define AF

A

Type of SVT where contraction of the atria is rapid, uncoordinated and irregular

157
Q

Give 6 RFs of AF

A
  • > 60
  • HTN
  • DM
  • valve disease - rheumatic HD
  • HF
  • Coronary artery disease
158
Q

Describe the typical presentation of AF

A
  • Irregularly irregular pulse rate
  • Palpitations
  • Chest pain
  • Shortness of breath
159
Q

Describe the ECG signs of AF

A
  • Irregular and rapid QRS complexes (<120ms)
  • Absent P waves
160
Q

How is acute AF treated

A
  • heparin then DC cardioversion synchronised to R wave
  • IV amiodarone if unsuccessful
  • If >48h give anticoagulants for 3w before cardioversion or rate control: BB (oral bisoprolol) or rate limiting CCB ( IV verapamil)
  • Long-term anticoagulant - apixaban
161
Q

How is paroxysmal or persistent AF treated

A
  • Rate control: BB, rate limiting CCB. IF it falls: digoxin then consider amiodarone
  • Anticoagulants - apixaban
  • DC cardioversion if haemodynamically unstable
162
Q

How is permanent AF treated

A
  • Anticoagulants - apixaban
  • Rate control - propranolol or verapamil
163
Q

Difference between acute and chronic AF

A

To do with the duration
* Acute - less than 48 hours
* Chronic - can be paroxysmal (episodic), persistent (>7 days) or permanent

164
Q

What are some complications of AF

A

HF
Ischaemic stroke

165
Q

Define atrial flutter

A

Abnormal and organised atrial firing
Rate: 250-350bpm

166
Q

Give 3 RFs of atrial flutter

A
  • AF
  • Post surgical scarring of atria
  • Increasing age
167
Q

Explain the pathophysiology of atrial flutter

A

Fast atrial ectopic firing causes atrial spasm

168
Q

3 symptoms of atrial flutter

A
  • Palpitations
  • Breathlessness
  • Fatigue
169
Q

Describe the ECG signs of atrial flutter

A
  • Continuous regular electrical activity mc a saw-tooth pattern
  • Narrow complex tachycardia
170
Q

Which condition is atrial flutter treated the same as

A

AF

171
Q

What is wolff-parkinson white syndrome

A

When an extra electrical pathway exists for impulse conduction
Often hereditary

172
Q

What is the common name of the extra pathway in WPW

A

Bundle of kent

173
Q

Symptoms of WFWs

A

*Dizziness
* Dyspnoea

174
Q

Describe the ECG presentation for WPWs

A
  • Delta waves - slurred upstroke on QRS
  • Short PR interval (<120ms)
  • Wide QRS (>120)
175
Q

Treatment for WPWs

A
  • Valsalva - hold nose, close mouth, exhale hard while straining
  • Rapid atrial pacing
  • Catheter ablation
  • IV Adenosine
  • DC cardioversion
176
Q

Describe long QT syndrome

A
  • Ventricular tachycardia
  • Typically congenital
  • Long QT interval (>480ms)
177
Q

Causes of long QT syndrome

A
  • Hypokalaemia + Hypocalcaemia
  • Drugs - citalopram, amiodarone, macrolides
178
Q

What is torsades de pointes

A

*Polymorphic ventricular tachycardia in patients with prolonged QT
* Stops spontaneously or progresses into ventricular fibrillation

179
Q

ECG characteristics of torsades de pointes

A

Rapid irregular QRS complexes which twist around baseline

180
Q

Describe first degree heart block

A
  • Occurs when there is delayed AV conduction through the AV node
  • Every p wave results in a QRS complex
  • PR interval prolonged (>200ms)
181
Q

3 causes of first degree heart block

A
  • Hypokalaemia
  • Inferior MI
  • drugs - BB, CCB, digoxin (block AV conduction)
182
Q

How is first degree heart block managed

A

Usually asymptomatic and doesn’t require treatment

183
Q

What are the 2 types of 2nd degree heart block

A

Mobitz I and II

184
Q

Describe Mobitz I

A

This is when PR intervals become progressively longer until a p wave is not followed by a QRS complex (dropped)

185
Q

Cause of Mobitz I

A

AV blocking drugs
Inferior MI

186
Q

How is 2nd degree heart block
managed

A

No treatment unless very symptomatic (e.g. fainting) then pacemaker

187
Q

Describe Mobitz II

A

Constant long PR intervals and a random p wave not followed by a QRS complex

188
Q

Causes of Mobitz II

A
  • Anterior MI
  • Rheumatic fever
  • Mitral valve surgery
189
Q

Describe third degree heart block

A

Complete heart block
* atria and ventricles beat independently from each other
* no observable relationship between p waves and QRS complexes

190
Q

Causes of third degree heart block

A
  • structural HD
  • MI
  • Endocarditis
191
Q

Treatment for third degree heart block

A

Permanent pacemaker and IV atropine

192
Q

What are ventricular ectopics

A

Premature ventricular beats caused by random electrical discharges from outside the atria

193
Q

Causes of right bundle branch block (RBBB)

A
  • PE
  • IHD
    *Cor pulmonale
194
Q

Describe the ECG presentation of RBBB

A

MaRRoW:
M: tall late R wave in V1
W: Wide, slurred S wave in V6

195
Q

Explain the pathophys of RBBB

A
  • RB no longer conducts
  • Ventricles don’t contract at same time
  • LV contracts first then activates RV
196
Q

Causes of LBBB

A
  • IHD
  • Aortic valve disease
  • Cardiomyopathy
197
Q

Describe the ECG presentation of LBBB

A

WiLLiaM:
W: Deep S wave in V1
M: tall late R wave in V6

198
Q

Explain the pathophys of LBBB

A

RV contracts first then activates LV

199
Q

Define cardiomyopathy

A

A group of diseases of the myocardium that cause muscular/ conduction defects

200
Q

What are the 3 types of cardiomyopathy

A

Hypertrophic
Dilated
Restricted

201
Q

Define dilated cardiomyopathy

A

MC cardiomyopathy
* dilation of all 4 chambers on the heart
* Contracts poorly due to thin muscle

202
Q

Causes of dilated cardiomyopathy

A
  • IHD
  • Alcohol
  • Genetic
203
Q

Signs and symptoms of dilated cardiomyopathy

A
  • shortness of breath
  • HF - pulm oedema
  • systolic murmur
  • Increase pulse, decrease bp
  • AF
204
Q

Investigations for dilated cardiomyopathy

A
  • ECHO - dilated ventricles
  • ECG - tachycardia, T wave changes
  • Bloods: elevated brain natriuretic peptide
  • CXR - cardiac enlargement
205
Q

Treatment for dilated cardiomyopathy

A

Treat the underlying cause if possible
* BB
* ACEi
* Diuretics if oedema
* Anticoagulation due to increased risk of thromboembolism

206
Q

What is hypertrophic cardiomyopathy

A

Ventricular hypertrophy that causes obstruction of the outflow tract
Mostly LVH

207
Q

Causes of hypertrophic cardiomyopathy

A

Genetic - autosomal dominant
Sporadic

208
Q

Signs and symptoms of hypertrophic cardiomyopathy

A
  • Sudden death (mc cause of sudden death in young people)
  • Palpitations
  • Dyspnoea
  • ejection-systolic murmur - quieter on squatting, louder of valsalva manoeuvre
209
Q

Explain the pathophysiology of hypertrophic cardiomyopathy

A

Gene mutation for sarcomere protein:
* thick non compliant heart = impaired diastolic filling
* reduced CO

210
Q

Describe the diagnosis of hypertrophic cardiomyopathy

A
  • ECG - T wave inversion, deep Q waves
  • ECHO - ventricular hypertrophy
  • Genetic testing
211
Q

Treatment of hypertrophic cardiomyopathy

A

CBB - Verapamil
Amiodarone - anti-arrythmic
BB - atenolol

212
Q

What is restrictive cardiomyopathy

A

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

213
Q

Causes of restrictive cardiomyopathy

A
  • Granulomatous disease: Amyloidosis, Sarcoidosis
  • Idiopathic
  • Post MI fibrosis
214
Q

Signs and symptoms of restrictive cardiomyopathy

A
  • Dyspnoea
  • Oedema
  • 3rd & 4th heart sounds
  • Ascites
215
Q

Investigations for restrictive cardiomyopathy

A
  • Cardiac catheterisation (definitive)
  • ECHO
216
Q

Treatment for restrictive cardiomyopathy

A

Poor prognosis (1y)
No treatment, can consider transplant

217
Q

What is the most common cardiomyopathy in young people

A

Hypertrophic cardiomyopathy

218
Q

Define rheumatic fever

A

Systemic infection from a group A beta-haemolytic streptococci
Common in developing countries

219
Q

Explain the pathophysiology of rheumatic fever

A

Antibody from cell wall cross-reacts with valve tissue which can cause permanent damage to the valves through auto-antibody mediated destruction
* mostly affects MV and typically thickens leaflets = mitral stenosis

220
Q

Signs and symptoms of rheumatic fever

A
  • New pansystolic murmur
  • Erythema marginatum - red rash with raised edges and pale centre
  • Chorea - jerky movements
  • Arthritis
221
Q

Describe the investigation and diagnosis of rheumatic fever

A

Jones criteria - recent strep infection and:
* 2 major (arthritis, chorea) criteria
or
* 1 major (new murmur) and 2 minor (arthralgia, fever ) criteria

222
Q

Treatment for rheumatic fever

A
  • IV Benzylpenicillin then phenoxymethylpenicillin for 10 days
  • Haloperidol/ diazepam for chorea
223
Q

What is deep vein thrombosis

A

thrombus in deep vein of leg

224
Q

Describe the different types of DVT and their severity

A

Below calf:
* minor veins (e.g. ant & post tibial)
* Less concerning and more common
Thigh:
* major veins (e.g. superficial femoral); occlusion may impede distal flow
* Life threatening

225
Q

What is pulmonary embolism

A

This is usually due to DVT embolising and lodging in the pulmonary artery circulation

226
Q

Risk factors for venous thromboembolism (DVT and PE)

A

Venous stasis:
* long flights, recent surgery
Hypercoagulability:
* pregnancy, malignancy, obesity
Endothelial injury:
* Trauma/surgery, smoking

227
Q

Presentation of PE

A
  • Pleuritic chest pain
  • Dyspnoea (+/- blood)
  • Tachycardia
  • Hypotensive
228
Q

Presentation of DVT

A
  • Unilateral swollen calf - typically warm and oedematous
  • Leg turns blue
229
Q

Investigations for PE

A
  • Wells score (>4)
  • D-dimer - size of clot
  • CT pulmonary angiogram (GS) - specific
  • ECG - tachycardia, new RBBB, T wave inversion of ant and inf leads
230
Q

Investigations for DVT

A
  • Wells score (>1)
  • D-dimer
  • Duplex ultrasound (GS)
231
Q

Treatment for massive PE

A

Thrombolysis - injecting fibrinolytic medication (eg. alteplase)

232
Q

Treatment for non-massive PE and DVT

A
  • Anticoagulants - DOAC (Apixaban/ rivaroxaban
  • LMWH if above contraindicated
  • DVT: compression stockings
233
Q

What is a differential diagnosis of DVT

A

Cellulitis
* Skin infection (strep.pyogenes)
* Leukocytosis on blood test
• US to differentiate

234
Q

What is a differential diagnosis of DVT

A

Cellulitis
* Skin infection (strep.pyogenes)
* Leukocytosis on blood test

235
Q

Differential diagnosis of PE

A

Pleural effusion, Pneumothorax and pneumonia all have pleuritic chest pain
* CXR - normal in PE. Diagnostic in others

236
Q

Describe an atrial septal defect
(inc Sx, Dx & Tx)

A
  • Shunting of blood from left to right atria
  • May report dizziness and palpitations
  • Found on ECHO
  • Most close spontaneously otherwise surgical
237
Q

Describe a complication of atrial septal defect

A

Eisenmenger’s syndrome
Pul htn causes reversal of shunt from right to left resulting in deoxygenated blood in the systemic circulation

238
Q

Describe ventricular septal defect
(inc Sx, Dx & Tx)

A
  • Blood shunts from LV to RV
  • small VSD = asymptomatic
  • Large VSD = Exercise intolerance, harsh pansystolic murmur
  • Dx - Found on ECHO
  • Tx - spontaneous closure or surgical
239
Q

What is a patent ductus arteriosus

A

When the ductus arteriosus fails to close after birth
Blood shunts from the aorta to the pulm trunk

240
Q

Describe the Sx, Dx, Tx and Cx of a patent ductus arteriosus

A
  • Sx - failure to thrive, machine like continuous murmur, dyspnoea
  • Dx - ECHO
  • Tx - prostaglandin inhibitors may induce closure or surgery
  • Comp - Eisenmenger’s
241
Q

4 defects found tetralogy of fallot

A
  • Large Ventral septal defect
  • Overriding aorta (misplaced)
  • RV hypertrophy
  • RV outflow obstruction (Pulm stenosis)
242
Q

Sign of tetralogy of fallot

A

Cyanosis due to deoxygenated blood being shunted systemically

243
Q

Investigation and treatment of tetralogy of fallot

A
  • CXR - boot shaped heart
  • Tx- surgical repair within 2y of life
244
Q

What is coarctation of aorta

A
  • Aorta narrow at/just distal to ductus arteriosus
  • Blood is diverted through aortic arch branches = increased perfusion to upper body vs lower
245
Q

Sx, Dx and Tx of coarctation of aorta

A
  • Sx - upper body HTN, leg cramps, cold feet
  • Dx - CXR (dilated intercostal vessels), CT angiogram
  • Tx - surgery or stenting
246
Q

What chromosomal condition is aortic coarctation a common Cx of

A

Turner syndrome - 45 XO, female has a single X chromosome
Sx - short stature, webbed neck, primary amenorrhoea

247
Q

What makes shock a medical emergency

A

It is life threatening due to acute circulation failure
This leads to hypoxia and risk of organ dysfunction

248
Q

What causes hypovolaemic shock

A
  • blood loss - trauma, GI bleed
  • Fluid loss - dehydration
249
Q

Presentation of hypovolaemic shock

A
  • Hypotension
  • Tachycardia
  • Clammy pale skin
  • Confusion
250
Q

Treatment for hypovolaemic shock

A
  • ABCDE
  • IV fluids
251
Q

Causes anaphylactic shock

A
  • Due to type 1 hypersensitivity
  • histamine release causes excess vasodilation and bronchoconstriction
252
Q

Presentation of anaphylactic shock

A
  • Hypotension
  • Tachycardia
  • Puffy face
  • Flushed cheeks
253
Q

Treatment for anaphylactic shock

A

*ABCDE
* IM adrenaline

254
Q

Causes of septic shock

A

Due to uncontrolled bacterial infection in blood

255
Q

Presentation of septic shock

A
  • Fever
  • Tachycardia
  • warm peripheries
  • decreased urine output
256
Q

Treatment of septic shock

A
  • ABCDE
  • Broad spectrum antibiotics
257
Q

Causes of cardiogenic shock

A
  • heart pump failure
  • MI
  • Cardiac tamponade
258
Q

Treatment of cardiogenic shock

A
  • ABCDE
  • treat underlying cause
259
Q

Causes of neurogenic shock

A

spinal cord trauma - disrupted SNS but intact PSNS

260
Q

Presentation of neurogenic shock

A
  • Hypotension
  • Bradycardia
  • Confused
261
Q

Treatment for neurogenic shock

A
  • ABCDE
  • IV atropine
262
Q

What are the 4 key organs at risk of failure from shock

A

Kidney
Lung
Heart
Brain

263
Q

What is syncope

A

Term used to describe temporarily losing consciousness due to disruption of blood flow to the brain
Aka fainting

264
Q

What causes primary syncope

A

Primary (simple fainting)
* extended standing in warm environment
* missed meal
* sudden surprise, pain

265
Q

What causes secondary syncope

A

Secondary (underlying problem)
* hypoglycaemia
* anaemia
* anaphylaxis
Valvular heart disease

266
Q

Signs and symptoms of syncope

A

Hot
Sweaty
Dizzy
Blurry/dark vision
Headache

267
Q

Describe the investigation of syncope

A
  • ECG - assess for arrhythmia and long QT syndrome
  • ECHO - structural HD
  • Bloods - FBC (anaemia), BG (diabetes), Electrolytes (arrhythmias)
268
Q

How is syncope managed

A
  • underlying pathology needs to be managed by appropriate specialist
  • simple fainting usually resolves itself by adulthood
  • reassurance and simple advice - avoid dehydration and skipping meals
269
Q

Which valve disease causes left ventricular dilatation

A

Aortic regurgitation

270
Q

Describe the CHA2DS2-VASc score

A

Tool used for assessing whether patient with AF should have anticoagulants
* Congestive HF
* HTN
* A2 - Age >75
* Diabetes
* S2 - Stroke
* Vascular disease
* Age (65-74)
* Sex (female)

271
Q

3 types of CCB with examples

A
  • Dihydropyridines - e.g. amlodipine, nifedipine
  • Phenylalkylamines - e.g. verapamil
  • Benzothiazepines - e.g. diltiazem
272
Q

MOA of amlodipine

A

Preferentially affect vascular smooth muscle
Peripheral arterial vasodilators

273
Q

MOA of verapamil

A
  • Main effects on heart
  • Negatively chronotropic (rate), negatively inotropic (force)
274
Q

SE of CCB due to vasodilatation

A
  • Flushing
  • Headache
  • Oedema
  • Palpitations
275
Q

SE of CCB due to negatively chronotropic effects

A
  • Bradycardia
  • Atrioventricular block
276
Q

SE of verapamil

A

Constipation

277
Q

SEs of BB

A

Fatigue
Headache
Bradycardia
Hypotension
Erectile dysfunction

2a - SBCS (9 decks)

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