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1
Q

ATHEROSCLEROSIS
What are the constituents of an atheromatous plaque?

A

Lipid core
Necrotic debris
Connective tissue surrounded by foam cells
Fibrous cap
Lymphocytes

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2
Q

ATHEROSCLEROSIS
Describe the process of leukocyte recruitment

A
  1. Capture
  2. Rolling
  3. Slow rolling
  4. Adhesion
  5. Transmigration
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3
Q

ATHEROSCLEROSIS
Describe the 5 steps of progression of atherosclerosis

A
  1. Fatty streaks
  2. Intermediate lesions
  3. Fibrous plaque/advanced lesions
  4. Plaque rupture
  5. Plaque erosion
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4
Q

ATHEROSCLEROSIS
What are the constituents of fibrous plaques?

A

Fibrous cap overlies lipid core and necrotic debris
Smooth muscle cells
Macrophages
Foam cells
T lymphocytes

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5
Q

ANGINA
What investigations might you do in someone you suspect to have angina?

A
  1. ECG - usually normal, sometimes ST depression, flat or inverted T waves
  2. Echocardiography
  3. CT angiography - high NPV and good at excluding disease (gold standard)
  4. Exercise tolerance test - induces ischaemia
  5. Invasive angiogram - tells you FFR (pressure gradient across stenosis)
  6. SPECT - radio labelled tracer taken up by metabolising tissues
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6
Q

ANGINA
Describe the primary prevention for angina

A
  1. Modify risk factors
  2. Treat underlying causes
  3. Low dose aspirin
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7
Q

ANGINA
what is the symptomatic management?

A
  • GTN spray (if pain persists after 5 mins repeat dose, if pain remains after anther 5 mins call ambulance)
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8
Q

ANGINA
what is the long term management?

A
  • 1st line = beta blocker or CCB
  • 2nd line = combination of BB + CCB (nifedipine, or amlodipine)
  • 3rd line = long acting nitrate, ivabradine, nicorandil or ranolazine

all patients should be given aspirin + statin unless contraindicated

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9
Q

PHARMACOLOGY
Describe the action of beta blockers

A

Beta 1 specific
Antagonise sympathetic activation and so are negatively chronotropic and inotropic
Myocardial work is reduced and so is myocardial demand = symptom relief

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10
Q

PHARMACOLOGY
What drugs that might be use in someone with angina or in someone at risk of angina to improve prognosis?

A
  1. Aspirin
  2. Clopidogrel - antiplatelet
  3. Atovostatin - Statin
  4. ACEi - ramipril
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11
Q

ACS
Describe type 1 MI

A

Spontaneous MI with ischaemia due to a primary coronary event
e.g. plaque erosion/rupture, fissuring or dissection

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12
Q

ACS
Describe type 2 MI

A

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

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13
Q

ACS
What might the ECG of someone with unstable angina show?

A

May be normal, or might show T wave inversion and ST depression

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14
Q

ACS
What might the ECG of someone with NSTEMI show?

A

May be normal or might show T wave inversions and ST depression

Might also be R wave regression, ST elevation and biphasic T wave in lead V3

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15
Q

ACS
What might the ECG of someone with STEMI show?

A

ST elevation in the anterolateral leads
After a few hours, T waves inlet and deep, broad, pathological Q waves develop

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16
Q

ACS
A raised troponin is not specific for ACS. In what other conditions might you see a raised troponin?

A
  1. Gram negative sepsis
  2. PE
  3. Myocarditis
  4. Heart failure
  5. Arrhythmias
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17
Q

ACS
Describe the initial management of ACS

A
  • Analgesia - morphine + sublingual GTN
  • Oxygen (if SpO2 > 94%)
  • dual antiplatelets
    - ALL patients = aspirin 300mg
    - if PCI = prasugrel or clopidogrel
    - if fibrinolysis = ticagrelor or clopidogrel

MONA

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18
Q

ACS
What is the overall treatment for STEMI?

A

PCI - if symptom onset within 12 hours and access to PCI within 120 minutes

Thrombolysis e.g. alteplase or tenecteplase - If ineligible for PCI

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19
Q

ACS
Describe the secondary prevention therapy for people after having a STEMI

A
  • lifestyle changes
  • manage CVD risks
  • thrombolysis = 12 months aspirin 75mg + ticagrelor
  • PCI = lifelong aspirin + 12 months ticagrelor/prasugrel
  • ACEi
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20
Q

ACS
Give 5 early complications of MI

A
  • Post MI pericarditis (few days post MI)
  • cardiac arrest (due to VF)
  • heart block
  • cardiogenic shock
  • VSD
  • mitral regurgitation
  • left ventricular wall rupture
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21
Q

DVT
What are the causes of DVT?

A

HYPERCOAGULABILITY
- hereditary e.g. facter V leiden, antiphospholipid syndrome
- acquired e.g. malignancy, chemo, COCP/HRT, pregnancy, obesity

VENOUS STASIS
- immobility e.g. surgery, flights
- polycythaemia

ENDOTHELIAL DAMAGE
- surgery
- catheter (PICC lines)
- trauma
- smoking

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22
Q

DVT
What investigations might be done in order to diagnose a DVT?

A
  1. WELLS score

if WELLS >2 DVT likely
- duplex ultrasound of leg within 4 hours (if not within 4 hrs, offer anticoagulation)
- d-dimer

if WELLS <1 DVT unlikely
- D-dimer with results within 4 hrs (if not within 4hrs offer anticoagulation)
- if D-dimer is raised = duplex USS
- if D-dimer normal = no further Ix

bloods - FBC, U&Es, LFTs, PT + APTT

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23
Q

DVT
What is the treatment for DVT?

A
  • no renal impairment = apixaban/rivaroxaban
  • renal impairment (CrCl<15ml/min) = LMWH or UFH + warfarin for 5 days, then warfarin alone
  • active cancer = consider DOAC or warfarin
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24
Q

DVT
Give 5 risk factors for DVT

A
  • AGE <40
  • IMMOBILITY - surgery, hospitalisation, long-haul travel, bed-bound
  • TRAUMA
  • THROMBOPHILIA
  • MALIGNANCY
  • SMOKING
  • PREGNANCY
  • DRUGS - COCP, HRT, tamoxifen
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25
Q

PE
What investigations might be done to diagnose a patient with PE?

A
  • CXR (typically normal)
  • ECG (sinus tachy, S1Q3T3, RBBB + R axis deviation
  • if WELLS >4 = CTPA (V/Q scan as alternative in severe renal impairment)
  • if WELLS<4 = D-dimer
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26
Q

What is the treatment for a PE?

A

massive PE = thrombolysis e.g. alteplase

non-massive PE =
- no renal impairment = apixaban/rivaroxaban

  • renal impairment (CrCl<15ml/min) = LMWH or UFH + warfarin for 5 days, then warfarin alone
  • active cancer = consider DOAC or warfarin
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27
Q

THROMBUS
How would you describe an arterial thrombus?

A

Platelet rich (a ‘white thrombosis’)

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28
Q

THROMBUS
How would you describe a venous thrombosis?

A

Fibrin rich (a ‘red thrombosis’)

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29
Q

PHARMACOLOGY
How does heparin work?

A

Inhibits thrombin and factor Xa
Indirect thrombin inhibitor - binds to antithrombin and increased its activity

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30
Q

PHARMACOLOGY
How do you monitor heparin?

A

Activated partial thromboplastin time
Aim ratio: 1.8-2.8

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31
Q

PHARMACOLOGY
How does Direct Acting Oral Anticoagulant (DOAC) work?

A

Directly acts on factor 2 (thrombin) or 10
No blood test or monitoring needed just given od or bd

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32
Q

PERICARDITIS
Describe the aetiology of pericarditis

A

IDIOPATHIC
VIRUSES (most common = coxsackie), mumps, EBV, CMV, varicella, HIV

less common
- autoimmune
- TB
- trauma
- uraemia secondary to kidney disease
- post-MI syndrome
- dressler syndrome
- connective tissue disorders
- malignancy
- hypothyroidism

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33
Q

PERICARDITIS
Give 5 symptoms of pericarditis

A
  1. CHEST PAIN - severe, sharp and pleuritic (worse on inspiration/lying flat - relieved by sitting forward)
  2. Dyspnoea
  3. Cough
  4. Hiccups
  5. Skin rash
  6. Fever and myalgia
  7. peripheral oedema
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34
Q

PERICARDITIS
What investigations might you do on someone who you suspect to have pericarditis?

A
  1. ECG - diagnostic
  2. CXR
  3. Bloods - FBC, ESR and CRP, Troponin
  4. Echocardiogram - usually normal, rule out silent pericardial effusion
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35
Q

PERICARDITIS
What might the ECG look like in someone with acute pericarditis?

A
  1. Saddle shaped ST elevation
  2. PR depression
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36
Q

PERICARDITIS
How can acute pericarditis be clinically diagnosed?

A

Patient has to have at least 2 of the following:
1. Chest pain
2. Friction rub
3. ECG changes
4. Pericardial effusion

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37
Q

PERICARDITIS
What is the treatment for pericarditis?

A

idiopathic/viral
- 1st line = NSAIDs + colchicine
- 2nd line = NSAIDs, colchicine + low-dose prednisolone

bacterial
- IV antibiotics + pericardiocentesis with washout, cultures

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38
Q

CARDIAC TAMPONADE
What are the signs of Cardiac tamponade?

A

Beck’s triad:
1. low BP but high HR
2. Increased JVP
3. Quiet S1 and S2

  • Pulsus paradoxus = pulses fade on inspiration
  • Kussmaul’s sign = rise in jugular venous pressure with inspiration
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39
Q

MYOCARDITIS
What can cause myocarditis?

A

most common = coxsackie B

others
Viral infection - coxsackie B, adenovirus, herpes
lyme disease
toxoplasmosis

autoimmune - SLE, dermatomyositis, sarcoidosis

drug-induced - antipsychotics, immunotherapies

hypersensitivity reactions

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40
Q

PVD
what are the treatments for peripheral vascular disease?

A
  • exercise

control risk factors
- stop smoking
- diabetes control
- HTN control
- diet/weight management

  • statin (atorvastatin 80mg)
  • antiplatelet (clopidogrel 75mg)

surgery
- endovascular procedures
- bypass surgery

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41
Q

HEART FAILURE
What are the compensatory mechanisms in heart failure?

A
  1. Sympathetic system
  2. RAAS
  3. Natriuretic peptides
  4. Ventricular dilation
  5. Ventricular hypertrophy
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42
Q

HEART FAILURE
what are the clinical signs of left heart failure?

A
  1. Pulmonary crackles
  2. S3 and S4 and murmurs
  3. Displaced apex beat
  4. Tachycardia
  5. fatigue
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43
Q

HEART FAILURE
what are the clinical features of right HF?

A
  1. Raised JVP
  2. Ascites
  3. peripheral oedema
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44
Q

HEART FAILURE
what is the management for chronic HF?

A

1st line = BB + ACEi (started one at a time)
If ACEi not tolerated, try ARB or hydralazine with nitrate

2nd line = aldosterone antagonist (SPIRONOLACTONE)

3rd line = cardiac resynchronisation therapy (CRT) or ICD insertion, digoxin (particularly in AF) or ivabradine

other options:
- fluid restriction
- loop diuretics (for symptom management)
- annual flu + pneumococcal vaccine

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45
Q

HTN
Describe the pharmacological intervention for someone with hypertension

A

IF <55 OR T2DM
1. ACEi/ARB
2. ACEi/ARB + CCB or ACEi/ARB + thiazide-like diuretic (indapamide)
3. ACEi/ARB + CCB + thiazide-like diuretic
4. if K+<4.5 add spironolactone, if K+>4.5 add alpha/beta-blocker

IF >55 + NO T2DM OR BLACK
1. CCB
2. CCB + ACEi/ARB* or CCB + thiazide like diuretic
3. CCB + ACEi/ARB* + thiazide-like diuretic
4. if K+<4.5 add spironolactone, if K+>4.5 add alpha/beta-blocker

*note ARB is preferred in african-caribbean/black ethnicities

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46
Q

HTN
Write an equation for BP

A

BP = CO x TPR

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47
Q

PHARMACOLOGY
Give 4 functions of angiontensin II

A
  1. Potent vasoconstrictor
  2. Activated sympathetic nervous system - increased NAd
  3. Activates aldosterone - Na+ retention
  4. Vascular growth, hyperplasia and hypertrophy
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48
Q

PHARMACOLOGY
Give 3 ways in which the Sympathetic nervous system (NAd) leads to increased BP

A
  1. Noradrenaline is a vasoconstrictor = increase TPR
  2. NAd has positive chronotropic and inotropic effects
  3. It can cause increase renin release
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49
Q

PHARMACOLOGY
Where in the kidney do thiazide diuretics work?

A

The distal tubule

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50
Q

PHARMACOLOGY
What is the counter regulatory system to RAAS?

A

Atrial Natriuretic Peptide/BNP (ventricular natriuretic peptide) hormones

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51
Q

PHARMACOLOGY
How does digoxin work?

A

Inhibits the Na+/K+ pump therefore making the action potential more positive and ACh is released from parasympathetic nerves

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52
Q

PHARMACOLOGY
How does amiodarone work?

A

Prolongs action potential by delaying depolarisation

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53
Q

PHARMACOLOGY
Name 4 potential effects of amiodarone

A
  1. QT prolongation
  2. Interstitial lung disease
  3. Hypothyroidism
  4. Abnormal liver enzymes
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54
Q

ABNORMAL ECGS
What aspect of the heart is represented by leads II, III and aVF?

A

Inferior aspect

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55
Q

ABNORMAL ECGS
What might ST elevation in leads II, II and aVF suggest?

A

RCA blockage
Leads represent inferior aspect of heart, RCA supplies inferior aspect

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56
Q

ABNORMAL ECGS
Give 3 effects hyperkalaemia on an ECG

A

GO - absent P wave
GO TALL - tall T wave
GO long - prolonged PR
GO wide - wide QRS

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57
Q

ABNORMAL ECGS
Give 2 effects of hypokalaemia on an ECG

A
  1. Flat T waves
  2. QT prolongation
  3. ST depression
  4. Prominent U waves
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58
Q

ABNORMAL ECGS
Give an effect go hypocalcaemia on an ECG

A
  1. QT prolongation
  2. T wave flattening
  3. Narrowed QRS
  4. Prominent U waves
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59
Q

ABNORMAL ECGS
Give an effect of hypercalcaemia on an ECG

A
  1. QT shortening
  2. Tall T wave
  3. No P waves
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60
Q

ATRIAL FIBRILLATION
what are the causes of atrial fibrillation?

A

PIRATES
Pulmonary - PE, COPD
Ischaemic heart disease
Rheumatic heart disease
Anaemia, Alcohol, Advancing age
Thyroid disease (hyperthyroid)
Electrolyte disturbance (hypo/hyperkalaemia)
Sepsis, Sleep apnoea

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61
Q

ATRIAL FIBRILLATION
What does the CHA2DS2 VASc score take into account

A

CHD
HTN
Age (>75) = 2 points
DM
Stroke (previous) = 2 points
Vascular disease
Age 65-74
Sex (female)

Score >1 = anticoagulation

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62
Q

ATRIAL FIBRILLATION
Describe the treatment for atrial fibrillation

A

HAEMODYNAMICALLY UNSTABLE
- 1st line = synchronised DV cardioversion

STABLE
onset <48hrs
- 1st line = rate control (BB or CCB)*
- 2nd line = rhythm control (flecanide or amiodarone)

onset >48hrs
- 1st line = rate control (BB or CCB)* + anticoagulation for at least 3 weeks, then offer rhythm control if appropriate

*consider digoxin 1st line in patients with AF + HF, those who do no exercise or other drugs excluded
avoid CCB in HF
avoid non-selective BB (e.g. propranolol) in asthma

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63
Q

ATRIAL FLUTTER
Describe the ECG pattern taken from someone with atrial flutter

A
  1. Narrow QRS
  2. Saw tooth flutter (F) waves
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64
Q

LONG QT SYNDROME
what are the causes of long QT syndrome?

A
  1. Congenital
  2. hypokalaemia,
  3. hypocalcaemia
  4. Drugs - amiodarone, tricyclic antidepressants
  5. bradycardia
  6. Acute MI
  7. diabetes
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65
Q

HEART BLOCK
Describe a first degree heart block

A

Fixed prolongation of the PR interval due to delayed conduction to the ventricles
- PR interval >0.22s
- asymptomatic

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66
Q

HEART BLOCK
Describe a Mobitz type 1 second degree heart block

A

PR interval gradually increases until AV node fails and no QRS is seen
PR interval returns to normal and the cycle repeats

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67
Q

HEART BLOCK
Describe a Mobitz type 2 second degree heart block

A

Sudden unpredictable loss of AV conduction and so loss of QRS
PR interval is constant but every nth QRS is missing
wide QRS

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68
Q

HEART BLOCK
Describe a third degree heart block

A

Atrial activity fails to conduct to the ventricles
P waves and QRS complexes occur independently
ventricular contractions are maintained by spontaneous escape rhythm originating below the block

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69
Q

HEART BLOCK
What are the treatments for heart blocks?

A

1st = asymptomatic, watch and wait –> atropine
Mobitz 1 = no pacemaker if asymptomatic, pacemaker if symptomatic
Mobitz 2 = pacemaker even if asymptomatic
3rd = transcutaneous pacing followed by permanent pacemaker

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70
Q

HEART BLOCK
what are the causes of heart block?

A

Athletes
Sick sinus syndrome
IHD – esp MI
Acute myocarditis
Drugs
Congenital
Aortic valve calcification
Cardiac surgery/trauma

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71
Q

BUNDLE BRANCH BLOCK
What changes would you see on an ECG from someone with a LBBB?

A

WiLLiaM
slurred S wave in V1 (resembles W)
R wave in V6 (resembles M)

wide QRS with notched top in V6

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72
Q

BUNDLE BRANCH BLOCK
What changes would you see on an ECG from someone with a RBBB?

A

MaRRoW
R wave in V1 (resembles M)
slurred S wave in V6 (resembles W)

wide QRS
RSR pattern in V1

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73
Q

AORTIC STENOSIS
what are the signs of aortic stenosis?

A

MURMUR
- ejection systolic murmur over aortic area
- radiating to carotids and apex
- crescendo-decrescendo
- thrill if severe
- left ventricular heave

ASSOCIATED FEATURES
- diminished S2
- slow rising pulse
- narrow pulse pressure
- S4 heart sound

FEATURES OF HF
- crackles
- raised JVP
- peripheral oedema

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74
Q

AORTIC STENOSIS
What investigation might you do in someone who you suspect to have aortic stenosis?

A

ECG
- L axis deviation
- ST depression
- increased R wave amplitude and S wave depth

TTE (trans-thoracic echo)
- aortic valve are reduced

BLOODs
- BNP raised if HF

CXR
- rule out respiratory pathology

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75
Q

AORTIC STENOSIS
What are the indications for valve replacement

A
  • severe aortic stenosis and symptomatic
  • severe aortic stenosis and asymptomatic but have one of the following
    - heart failure
    - symptoms on exercise testing
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76
Q

MITRAL REGURGITATION
What can cause mitral regurgitation?

A
  1. Myxomatous degeneration (mitral valve prolapse) - most common cause
  2. Ischaemic mitral valve
  3. Rheumatic heart disease
  4. IE
  5. dilating left ventricle
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77
Q

MITRAL REGURGITATION
what are the signs of mitral regurgitation?

A

MURMUR
- Pan-systolic murmur
- Radiates to left axilla
- blowing at apex

  • S3 heart sound
  • Quiet S1
  • displaced apex towards axilla
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78
Q

AORTIC REGURGITATION
What causes aortic regurgitation?

A

acute
- infective endocarditis
- rheumatic fever
- aortic dissection

chronic
- rheumatic disease
- bicuspid aortic valve
- aortic endocarditis

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79
Q

AORTIC REGURGITATION
what are the signs of aortic regurgitation?

A

MURMUR
- early diastolic murmur - decrescendo
- soft, high-pitched

  • collapsing (waterhammer) pulse
  • wide pulse pressure
  • displaced apex

OTHER SIGNS
- austin flint murmur = rumbling mid-diastolic murmur, loudest at apex, suggests severe disease
- corrigans sign = visible distension + collapse of carotid arteries
- millers sign = visible pulsation of uvula
- Quinckes sign = visible pulsations in nail bed when compressed
- De Mussets sign = heartbeat associated with head bobbing
- Traubes sign = pistol shot sound over femoral arteries
- Duroziezs sign = audible systolic + diastolic murmur on compression of femoral artery

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80
Q

AORTIC REGURGITATION
Describe the management for someone with aortic regurgitation

A

MILD - MODERATE
- lifestyle modifications
- ACEi (ramipril)
- Beta-blockers (bisoprolol)

SEVERE DISEASE
- loop diuretic (furosemide)
- aortic valve repair/replacement

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81
Q

MITRAL STENOSIS
Name 3 causes of mitral stenosis

A
  1. Rheumatic heart disease
  2. IE
  3. Mitral annular calcification - rarer
82
Q

MITRAL STENOSIS
what are the symptoms of mitral stenosis?

A
  1. progressive dyspnoea
  2. Haemoptysis (coughing up blood)
  3. palpitations (AF)
  4. chest pain
83
Q

MITRAL STENOSIS
what are the signs of mitral stenosis?

A

rumbling mid-diastolic murmur with opening snap - decrescendo-presystolic crescendo

  1. malar flush
  2. AF
  3. tapping apex beat
  4. low volume pulse
  5. loud snapping S1
84
Q

VALVE DISEASE
In what type of valvular heart disease would you hear a mid-diastolic murmur and a 1st heart sound snap?

A

Mitral stenosis

85
Q

VALVE DISEASE
In what type of valvular heart disease would you hear a pan systolic murmur?

A

Mitral regurgitation

86
Q

VALVE DISEASE
In what type of valvular heart disease would you hear an ejection systolic murmur?

A

Aortic stenosis

87
Q

VALVE DISEASE
In what type of valvular heart disease would you see a wide pulse pressure and hear an early diastolic blowing murmur and systolic ejection murmur?

A

Aortic regurgitation

88
Q

INFECTIVE ENDOCARDITIS
Give the 2 major points in the Duke’s criteria that if presence can confirm a diagnosis of infective endocarditis

A
  1. Two positive blood cultures
  2. Positive echo showing endocardial involvement
89
Q

What investigations might you do in someone who you suspect to have infective endocarditis?

A

BLOODS - raised WCC, neutrophilia, raised CRP + ESR
BLOOD CULTURES - 3 sets, 1 hour apart, ideally before initiating abx
ECHO - to confirm dx
CXR - rule out other causes
ECG
URINALYSIS

90
Q

PULMONARY STENOSIS
How does a patient present with pulmonary stenosis?

A

Right ventricular failure
Collapse
Poor pulmonary blood flow
right ventricular hypertrophy
Tricuspid regurgitation

91
Q

VALVE DISEASE
What are 3 problems with a bicuspid aortic valve?

A
  1. Degenerate quicker than normal valves
  2. Become regurgitant earlier than normal valves
  3. Associated with coarctation and dilation of ascending aorta
92
Q

MITRAL STENOSIS
Why does mitral stenosis cause AF?

A

Increased LA pressure
Stretches myocytes in the atria and irritates pacemaker cells –> AF

93
Q

PERICARDITIS
Give 3 symptoms of Dressler’s syndrome

A
  1. Fever
  2. Chest pain
  3. Pericardial rub
    Occurs 2-10 weeks after MI
94
Q

EQUATIONS
Write an equation for mAP

A

mAP = DP + 1/3PP

95
Q

EQUATIONS
Give the equation for stroke volume

A

SV = EDV - ESV

96
Q

ANEURYSM
Name 3 causes of an aneurysm

A
  1. Atherosclerotic (most common)
  2. Ateriomegaly
  3. Collagen disease - Marfans, vascular Ehlers Danlos
  4. tobacco smoking
97
Q

ANEURYSM
What classifies as an Abdominal aortic aneurysm?

A

> 3 cm
Dilation affects all 3 layers of the vascular tunic

98
Q

COR PULMONALE
what are the causes of cor pulmonale?

A
  • chronic lung disease
  • pulmonary vascular disorders
  • neuromuscular and skeletal diseases
99
Q

COR PULMONALE
what are the signs of cor pulmonale?

A
  • cyanosis
  • tachycardia
  • raised JVP
  • RV heave
  • pan-systolic murmur due to tricuspid regurgitation
  • hepatomegaly
  • oedema
100
Q

COR PULMONALE
what investigations should be undertaken for cor pulmonale?

A

arterial blood gas
- hypoxia
- sometimes shows hypercapnia

101
Q

COR PULMONALE
what is the management for cor pulmonale?

A
  • treat the underlying cause
  • oxygen
  • diuretics
  • venesection if haematocrit >55
  • heart-lung transplant in young patients
102
Q

ATRIAL FLUTTER
what are the causes of atrial flutter?

A

more likely to occur with pulmonary disease:
- COPD
- obstructive sleep apnoea
- PE
- pulmonary hypertension

other causes:
- ischaemic heart disease
- sepsis
- alcohol
- cardiomyopathy
- thyrotoxicosis

103
Q

ATRIAL FLUTTER
what is the management for atrial flutter?

A
  • Cardioversion
    - Give a LMWH
    - Shock with defibrillator
  • Catheter ablation = definitive treatment – creates a conduction block
  • IV Amiodarone – restore sinus rhythm
104
Q

AORTIC DISSECTION
what is an aortic dissection?

A
  • there is a tear in the tunica intima , and blood then splits the vessel wall and dissects through the tunica media .
  • a false lumen is created as the blood in the media layer propagates both proximally and distally. Abnormal flow through this false lumen can occlude flow through the branches of the aorta.
105
Q

AORTIC DISSECTION
what are the risk factors of aortic dissection?

A

Hypertension- most common risk factor
Trauma
Vasculitis
Cocaine use
Connective tissue disorders- Turners + noonans

106
Q

AORTIC DISSECTION
what are the clinical features of aortic dissection?

A

-Sudden and severe tearing pain in chest radiating to back
-Hypotension
-Asymmetrical blood pressure
-Syncope
- Aortic regurgitation, coronary ischaemia, cardiac tamponade
- Peripheral pulses may be absent

107
Q

AORTIC DISSECTION
what are the investigations of aortic dissection?

A

-ECG/cardiac enzymes - rule out MI
-Chest x-ray - widening mediastinum
-CT scanning- definitive imaging
- echo - TTE/TOE
- bloods - FBC, U&Es, group and save, crossmatch

  • gold standard = CT angiography
108
Q

AORTIC DISSECTION
what is the management of aortic dissection?

A

TYPE A
- blood transfusion
- IV labetalol
- urgent surgical repair

TYPE B
- conservative management (bed rest + analgesia)
- IV labetalol
- thoracic endovascular aortic repair (TEVAR)

109
Q

PVD
what are the investigations for peripheral vascular disease?

A

1st line = ankle brachial pressure index (ABPI), duplex ultrasound

< 0.3 = critical ischaemia

ECG
Bloods - FBX, U&E, random glucose/HbA1c, serum cholesterol, lipid profile

110
Q

BUNDLE BRANCH BLOCK
what are the causes of RBBB?

A
  • normal variant (more common with increasing age)
  • right ventricular hypertrophy
  • PE
  • MI
  • Atrial septal defect
  • cardiomyopathy or myocarditis
111
Q

BUNDLE BRANCH BLOCK
what are the causes of LBBB?

A

A new LBBB is always pathological
IHD
Aortic valve disease

112
Q

AORTIC ANEURYSM
what is the clinical presentation of an unruptured abdominal aortic aneurysm?

A
  • often asymptomatic
  • causes symptoms if expanding rapidly
  • pain in abdomen, loin or groin
  • pulsatile abdominal swelling
  • bruit on ascultation
113
Q

AORTIC ANEURYSM
what are the investigations for abdominal aortic aneurysm?

A
  • Abdominal ultrasound – can assess aorta to degree of 3mm
  • CT or MRI angiography scans
114
Q

AORTIC ANEURYSM
what is the management for abdominal aortic aneurysm?

A
  • ruptured = urgent repair (do not wait for imaging)
  • symptomatic = repair indicated regardless of diameter
  • asymptomatic AAA = surveillance until high risk of rupture - 5.5cm in men and 5.0cm in women
115
Q

ENDOCARDITIS
what antibiotics are used for endocarditis?

A

INITIAL BLIND THERAPY
- native valve = amoxicillin (consider gentamicin)
- pen allergy = vancomycin + gentamicin

NATIVE S.AUREUS
- flucloxacillin
- pen allergy = vancomycin + rifampicin

PROSTHETIC VALVE S.AUREUS
- flucloxacillin + rifampicin + gentamicin
- pen allergy = vancomycin + rifampicin + gentamicin

FULLY SENSITIVE STREP (S.VIRIDANS)
- benzylpenicillin
- pen allergy = vancomycin + gentamicin

LESS SENSITIVE STREP
- benzylpenicillin + gentamicin
- pen allergy = vancomycin + gentamicin

116
Q

CARDIAC TAMPONADE
what are the investigations for cardiac tamponade?

A
  • ECG – tachycardia + electrical alternans
  • trans-thoracic echo (TTE) is diagnostic – echo-free space around heart
  • CXR - enlarged heart
  • bloods - inflammatory markers, troponin
117
Q

AORTIC STENOSIS
what murmur is heard with aortic stenosis?

A
  • ejection systolic murmur over aortic area
  • radiating to carotids and apex
  • crescendo-decrescendo
  • thrill if severe
  • left ventricular heave
118
Q

MI ECG
ECG changes in which regions indicates a lateral MI?

A

lead I
aVL
V5
V6

119
Q

MI ECG
ECG changes in which regions indicates an inferior MI?

A

lead II
lead III
aVF

120
Q

MI ECG
ECG changes in which regions indicates a septal MI?

121
Q

MI ECG
ECG changes in lateral regions are caused by which artery in an MI?

A

lateral = circumflex

122
Q

MI ECG
ECG changes in which regions indicates an anterior MI?

123
Q

MI ECG
ECG changes in inferior regions are caused by which artery in an MI?

A

inferior = RCA

124
Q

MI ECG
ECG changes in anterior regions are caused by which artery in an MI?

A

anterior = LAD

125
Q

MI ECG
A blockage in the LAD will cause ECG changes in which regions?

A

anterior - V3, V4
septal - V1, V2

126
Q

MI ECG
A blockage in the RCA will cause ECG changes in which regions?

A

inferior - leads II, III, aVF

127
Q

MI ECG
A blockage in the circumflex artery will cause ECG changes in which regions?

A

lateral - lead I, aVL, V5, V6

128
Q

LONG QT SYNDROME
which abnormal heart rhythm are people with long QT syndrome at risk of developing?

A

torsades de pointes

129
Q

PERCARDITIS
What are the side effects of colchicine?

A

Diarrhoea and nausea

130
Q

ACS
Give 5 late complications of MI

A
  • dresslers syndrome (2-6 weeks post MI)
  • heart failure
  • left ventricular aneurysm
131
Q

DVT
what are the components of the WELLS score?

A
  • active cancer
  • bedridden or recent major surgery
  • calf swelling >3cm compared to other leg
  • superficial veins present (non-varicose)
  • entire leg swollen
  • tenderness along veins
  • pitting oedema of affected leg
  • immobility of affected leg
  • previous DVT
  • alternative diagnosis likely (-2)

all score +1

132
Q

DVT
how do you interpret the results of the WELLS score?

A

> 2 = high risk of DVT/likely
<1 = low risk of DVT/unlikely

133
Q

PE
when would a V/Q scan be used over CTPA?

A
  • patients allergic to contrast
  • severe renal impairment
  • pregnancy
134
Q

PE
what are the components of the WELLs two level score?

A
  • clinical signs + symptoms of DVT (+3)
  • PE is no.1 diagnosis (+3)
  • tachycardia <100 (+1.5)
  • immobilisation for >3 days
  • previous PE/DVT (+1.5)
  • haemoptysis (+1)
  • malignancy with treatment in last 6 months (+1)
135
Q

PE
how long would you offer anticoagulation for?

A
  • provoked = 3 months
  • unprovoked = 6 months
136
Q

CARDIAC TAMPONADE
what are the causes?

A

idiopathic
pericarditis
iatrogenic (cardiothoracic surgery)
malignancy
aortic dissection
rheumatological - SLE, RA, scleroderma

137
Q

CARDIAC TAMPONADE
what are the symptoms?

A
  • shortness of breath
  • chest discomfort
  • peripheral oedema
  • confusion
138
Q

MYOCARDITIS
what are the clinical features?

A

SIGNS
tachycardia
fever
displaced apex beat
S3 gallop
peripheral oedema

SYMPTOMS
chest pain - worse lying flat, improved by sitting forward
shortness of breath
fatigue
syncope
palpitations

139
Q

MYOCARDITIS
what are the investigations?

A
  • ECG (sinus tachy, T wave inversions)
  • serum troponin/CK MB
  • CRP/ESR (may be elevated)
  • echo
140
Q

PVD
what classification is used?

A

fontaine classification for different stages of PVD

141
Q

PVD
what is the site of the disease when the claudication is at the following sites?

  1. unilateral buttock
  2. unilateral thigh
  3. unilateral calf
A

buttock = common iliac

thigh = common femoral

calf = superficial femoral

142
Q

ARTERIAL ULCER
what are the features?

A
  • symmetrical shape
  • well-defined borders
  • punched out appearance
  • loss of hair surrounding (shiny)
  • pale, dry, gangrenous with cool surrounding skin
  • minimal bleeding when knocked/touched
  • painful, particularly at night
143
Q

ARTERIAL ULCER
what are the common locations?

A

lower legs
tops of feet or toes

144
Q

ARTERIAL ULCER
what is the management?

A
  • analgesia
  • wound management (maintain moist environment)

no compression bandages

145
Q

VENOUS ULCERS
where are they most commonly found?

A

around medial and lateral malleolus

146
Q

VENOUS ULCERS
what is the appearance?

A
  • shallow
  • irregular borders
  • oedema, erythema + brown pigment
  • warm skin surrounding
147
Q

VENOUS ULCERS
what is the management?

A
  • lifestyle modifications
  • leg elevation
  • compression bandages
  • emollient use
148
Q

CRITICAL LIMB ISCHAEMIA
how is the pain described?

A

aching pain
at rest
often nocturnal

patients often hang their legs out of the bed to relieve the pain

149
Q

CRITICAL LIMB ISCHAEMIA
what is aortoiliac disease?

A

also known as Leriche syndrome

triad of:
- claudication of buttocks and thighs
- absent or decreased femoral pulses
- erectile dysfunction

150
Q

CRITICAL LIMB ISCHAEMIA

what are the investigations?

A

1st line = duplex USS.

ABPI
0.5-0.9 = claudication
<0.5 = critical limb ischaemia

151
Q

ACUTE LIMB ISCHAEMIA
how can you tell if the cause is embolic or thrombotic?

A

EMBOLIC
- sudden onset
- cardiac history
- arrhythmia (AF)
- cold mottled skin
- clear demarkation

THROMBOTIC
- progressive onset
- no cardiac history
- peripheral artery disease
- no arrhythmias
- cool and cyanotic
- no clear demarkation

152
Q

ACUTE LIMB ISCHAEMIA
what is the classification?

A

rutherford classification

1 = viable
2= threatened
3 = irreversible

153
Q

ACUTE LIMB ISCHAEMIA
what is the management?

A

initially LMWH

based on rutherford classification
I (viable) = catheter-directed thrombolysis/thrombectomy (within 6-24hrs)

IIa = catheter-directed thrombolysis or percutaneous thromboembolectomy

IIb = percutaneous/open thromboembolectomy, bypass surgery

III = amputation

154
Q

HEART FAILURE
what are the causes of HF with reduced ejection fraction (systolic dysfunction)?

A

damage to myocytes e.g. ischaemic heart disease

155
Q

HEART FAILURE
what are the causes of HF with preserved ejection fraction (diastolic dysfunction)?

A

increased ventricular stiffness e.g. HTN

reduced relaxation e.g. constrictive pericarditis

156
Q

ATRIAL FIBRILLATION
which medications are used for rate control?

A

1st line = beta-blocker (bisoprolol) or CCB (diltiazem/verapamil)

consider digoxin 1st line when AF + HF

2nd line = combination therapy with any two
- beta-blocker (bisoprolol)
- diltiazem
- digoxin

157
Q

ATRIAL FIBRILLATION
what medications are used for rhythm control?

A

if no structural/ischaemic heart disease = flecainide or amiodarone

if structural/ischaemic heart disease = amiodarone

158
Q

LONG QT SYNDROME
what is the management?

A

conservative - avoid precipitating factors

beta-blocker (propranolol) to prevent ventricular arrhythmia

ICD may be considered

159
Q

AORTIC STENOSIS
what are the risk factors?

A
  • advancing age
  • congenital bicuspid valve (turners syndrome + coarctation of aorta)
  • rheumatic fever
  • chronic kidney disease
  • HTN
  • Smoking
  • mediastinal radiotherapy
160
Q

MITRAL REGURGITATION
what are the risk factors?

A
  • history of cardiac infection e.g. rheumatic fever, endocarditis
  • cardiac trauma
  • history of ischaemic heart disease e.g. MI
  • congenital heart disease
  • cardiomyopathy
  • HTN
  • structural heart disease
  • dopaminergic drugs e.g. cabergoline, pergolide
161
Q

AORTIC REGURGITATION
what are the risk factors?

A
  • male sex
  • advancing age
  • congenital heart disease
  • bicuspid valve
  • previous rheumatic heart disease
  • previous endocarditis
  • aortic root disorders (marfan, ankylosing spondylitis)
162
Q

MITRAL REGURGITATION
what is the murmur?

A
  • Pan-systolic murmur
  • Radiates to left axilla
  • blowing at apex
163
Q

AORTIC REGURGITATION
what is the murmur?

A
  • early diastolic murmur - decrescendo
  • soft, high-pitched
  • collapsing (waterhammer) pulse
  • wide pulse pressure
  • displaced apex
164
Q

MITRAL STENOSIS
what is the murmur?

A

rumbling mid-diastolic murmur with opening snap - decrescendo-presystolic crescendo

165
Q

INFECTIVE ENDOCARDITIS
which bacteria is associated with IV drug use?

A

staph aureus

166
Q

INFECTIVE ENDOCARDITIS
which bacteria are associated with prosthetic valves?

A

s. aureus
s. epidermidis

167
Q

INFECTIVE ENDOCARDITIS
which bacteria are associated with colon cancer?

A

strep bovis

168
Q

INFECTIVE ENDOCARDITIS
which bacteria is associated with infection of native valves?

A

strep viridans

169
Q

INFECTIVE ENDOCARDITIS
which bacteria is associated with poor dental hygiene and infection following dental procedures?

A

strep viridans

170
Q

INFECTIVE ENDOCARDITIS
what is the minor criteria for Modified Dukes criteria?

A
  • predisposing heart condition or IVDU
  • fever >38
  • immunological phenomenon (glomerulonephritis, osler nodes, roths spots, rheumatoid factor)
  • microbiological evidence not meeting major criteria
  • vascular abnormalities
171
Q

ACS
what is the management of an NSTEMI?

A
  • anticoagulation = fondaparinux to most patients, unfractionated heparin if renal failure
  • use GRACE score to work out if patient requires PCI
172
Q

ACS
what is the grace score?

A

it is used to risk-stratify patients with unstable angina and NSTEMIs

it estimates admission to 6 month mortality

173
Q

AORTIC DISSECTION
what is the classification system for aortic dissections?

A

Stanford
- type A - ascending aorta +/- aortic arch
- type B - descending aorta only

174
Q

HYPERTROPHIC CARDIOMYOPATHY
what are the examination findings?

A
  • ejection systolic murmur at lower left sternal border
  • 4th heart sound
  • thrill at lower left sternal border
175
Q

CARDIOMYOPATHY
what are the different types?

A
  • hypertrophic
  • dilated
  • restrictive
  • arrythmogenic right ventricular
176
Q

CARDIAC ARREST
what are the 4 arrest rhythms?

A
  • pulseless electrical activity (PEA)
  • asystole
  • ventricular fibrillation
  • pulseless ventricular fibrillation
177
Q

CARDIAC ARREST
what are the reversible causes of cardiac arrest?

A

4Hs + 4Ts
- hypoxia
- hypovolaemia
- hypo/hyperkalaemia
- hypothermia

  • thrombosis
  • toxins
  • tension pneumothorax
  • tamponade (cardiac)
178
Q

CARDIAC ARREST
what is the management for all cardiac arrests?

A
  • call for assistance
  • commence CPR 30:2 ratio
  • defib assessment
  • rhythm check every 2 mins
  • treat reversible causes
  • manage airway
179
Q

CARDIAC ARREST
what is the management for shockable rhythms?

A
  • shock ASAP then resume CPR
  • rhythm check
  • give 1mg adrenaline after 3rd shock + after alternating shocks
  • give 300mg amiodarone after 3rd shock + 150mg after 5th shock
180
Q

CARDIAC ARREST
what is the management for non-shockable rhythms?

A
  • no shocks given
  • rhythm check
  • adrenaline 1mg ASAP and after alternating cycles of CPR
181
Q

VARICOSE VEINS
what is the pathophysiology?

A

leaky valves cause retrograde blood flow, resulting in increased pressure on distal valves
superficial veins are thin-walled so cannot withstand increased pressure. This results in dilatation and tortuosity.

182
Q

VARICOSE VEINS
what are the risk factors?

A

genetics/family history
increasing age
female
obesity
pregnancy
history of DVT
prolonged sitting or standing

183
Q

VARICOSE VEINS
what are the investigations?

A

primary
- duplex USS
- ABPI

184
Q

VARICOSE VEINS
what is the management?

A

1st line = endothermal ablation
2nd line = foam sclerotherapy
3rd line = surgery

conservative
- compression hoisery
- lifestyle (wt loss, exercise, leg elevation when resting)

185
Q

ATRIAL FIBRILLATION
what are the risk factors?

A
  • increasing age
  • DM
  • hyperthyroidism
  • HTN
  • congestive heart failure
  • valvular heart disease
  • coronary artery disease
  • dietary + lifestyle (excessive caffeine, alcohol, smoking, medication use (thyroxine or beta-agonists))
186
Q

SVT
what are the risk factors?

A
  • increasing age
  • female
  • hyperthyroidism
  • smoking
  • excessive caffeine or alcohol
  • stress
  • medication (salbutamol, atropine, decongestants)
  • recreational drug use (cocaine, methamphetamines)
187
Q

SVT
what is the management?

A

UNSTABLE
- synchronised DC shock (up to 3 attempts)
- if unsuccessful, 300mg amiodarone IV + repeat shock

STABLE
- 1st line = vagal manoeuvres (Valsalva, carotid sinus massage)
- 2nd line = adenosine 6mg, if unsuccessful give 12mg then 18mg
- 3rd line = verapamil or BB
- long term = catheter ablation

188
Q

SVT
what are the complications?

A
  • syncope
  • congestive heart failure
  • life-threatening arrhythmias
  • sudden death
189
Q

WPW
what are the investigations?

A

12 LEAD ECG
- delta waves (slurred upstroke in QRS)
- short PR interval (<120ms)
- broadened QRS
if a re-entrant circuit has developed, there will be narrow complex tachycardia

BLOODS
- TFTs

IMAGING
- echocardiogram
- cardiac catheterisation

190
Q

WPW
which drugs are contraindicated in WPW syndrome?

A

any drugs that block AVN activity could cause dangerous arrhythmias
- digoxin
- adenosine
- non-dihydropyridine CCBs (verapamil and diltiazem)

191
Q

VENTRICULAR TACHYCARDIA
what are the risk factors?

A
  • electrolyte abnormalities (hypokalaemia, hypomagnesaemia)
  • structural heart disease (previous MI, cardiomyopathies)
  • drugs causing QT prolongation (clarithromycin, erythromycin)
  • inherited channelopathies
192
Q

VENTRICULAR TACHYCARDIA
what is the management of pulsed VT?

A

IF ADVERSE FEATURES PRESENT (HF, MI, shock syncope)
- 1st line = synchronised DC cardioversion (up to 3 attempts)
- 2nd line = amiodarone 300mg IV over 10-20 mins

IF NO ADVERSE FEATURES PRESENT
- 1st line = amiodarone 300mg IV
- 2nd line = synchronised DC cardioversion

if drug therapy fails
- ICD implanted

193
Q

TORSADES DE POINTES
what are the causes?

A
  • congenital
  • antiarrhythmics (amiodarone, sotalol)
  • tricyclic antidepressants
  • antipsychotics
  • chloroquine
  • erythromycin
  • electrolyte abnormalities (hypocalcaemia, hypokalaemia, hypomagnesaemia)
  • myocarditis
  • hypothermia
  • subarachnoid haemorrhage
194
Q

BRADYCARDIA
what are the adverse clinical features for bradycardia?

A
  • shock (hypotension, pallor, sweating, cold, clammy, confusion or impaired consciousness)
  • syncope
  • MI
  • HF
195
Q

BARDYCARDIA
what is the emergency management?

A

LIFE-THREATENING FEATURES
- 1st line = atropine 500 micrograms IV
- if response unsatisfactory repeat 500 micrograms atropine (up to max 3mg), or adrenaline 2-10 micrograms IV,
- arrange transvenous pacing

NO LIFE-THREATENING FEATURES
- if risk of asystole treat as above
- if not at risk of asystole, observe

196
Q

MI COMPLICATIONS
what is the most common cause of death following MI?

A

ventricular fibrillation (cardiac arrest)

197
Q

MI COMPLICATIONS
what type of MI most commonly causes acute mitral regurgitation?

A

infero-posterior MI

198
Q

MI COMPLICATIONS
what is the pathophysiology of acute mitral regurgitation following MI?

A

ischaemia or rupture of papillary muscle

199
Q

MI COMPLICATIONS
how does acute mitral regurgitation after MI present?

A
  • acute hypotension
  • pulmonary oedema
  • early-to-mid systolic murmur
200
Q

MI COMPLICATIONS
how does a ventricular septal defect following MI present?

A

usually occurs in first week following MI
- pansystolic murmur
- acute heart failure

201
Q

MI COMPLICATIONS
how does a left ventricular free wall rupture present?

A

occurs 1-2 weeks after
- acute HF
- cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)

202
Q

MI COMPLICATIONS
which MI region most commonly causes atrioventricular blocks and bradyarrhythmia?

A

inferior MI

MY REVISION - ALL TO DO (21 decks)

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