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Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

How may risk factors be categorised in Atherosclerosis?

Give an example of 3 for each.

A 
NM RFs: 
Older age
Family history
Male
Genetics 
M RFs: 
Smoking
Alcohol consumption
Poor diet (high sugar and trans-fat and reduced fruit and vegetables and omega 3 consumption)
Low exercise
Obesity
Poor sleep
Stress
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2
Q

What decision-making tool may be used to assess the risk that a patient will have a CVI in the next 10 years?

A

QRISK

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3
Q

What is the QRISK threshold to prescribe a statin?

A

> 10%

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4
Q

What monitoring is required for starting a patient on statins in the community?

A

LFTs at 3 months then 12 months

Lipids at 3 months - aim for 40% reduction

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5
Q

What secondary prevention is there for Cardiovascular Disease?

A

Mnemonic: ABS

Aspirin/Antiplatelet 
\+
Beta blocker
\+
Statin
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6
Q

What is the MOA of statins?

A

HMG-CoA reductase inhibitors thus reduce hepatic cholesterol synthesis

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7
Q

What are the side effects of statins?

A

Myopathy…
Myalgia
Myositis
Rhabdomyolysis

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8
Q

Give 3 indications for Statins

A

QRisk > 10%
T1DM + over 40 years/10 years Hx/ Nephropathy
CKD Stage 3a

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9
Q

What is the gold-standard diagnostic investigation for unstable Angina?

A

CT-CA

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10
Q

What is the main difference between stable and unstable angina?

A

Angina is caused by stenosis of the coronary arteries resulting in myocardial ischaemia.

Stable = resolves with rest or GTN within 10 minutes

Unstable = experienced at rest; increases with frequency/severity

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11
Q

What are the clinical features of angina?

A

Constricting pain experienced in the chest +/- typical radiation to the arm/neck/jaw

Precipitated by physical exertion

Relieved by rest or GTN within 5 minutes

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12
Q

How can you grade Angina? Outline the grades.

A

Canadian Cardiovascular Society (CCS)

Grade I = angina with strenuous exercise

Grade II = angina with moderate activities

Grade III = angina with mild exertion (walk up stairs)

Grade IV = angina at rest

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13
Q

What are the criteria for obstructive CAD upon CT-CA?

A

≥70% of stenosis of ≥1 coronary arteries

≥50% stenosis in LAD

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14
Q

For how long after PCI should DAPT be conducted?

A

6 months

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15
Q

What are the indications for CABG?

A

> 50% stenosis of left main stem
70% stenosis of proximal LAD and circumflex
Triple vessel disease

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16
Q

If a patient presents within 12 hours of chest pain, where do you refer them to?

A

RACPC

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17
Q

If a patient presents within 12 hours to 72 hours of chest pain, where do you refer them to?

A

Same day referral to hospital

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18
Q

If a patient presents 3 days following ACS, what do you do regarding management/referral?

A

ECG + Trops

Then decide on further action

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19
Q

Describe the term ACS.

A

Umbrella term for myocardial ischaemia:
Unstable Angina (UA)
NSTEMI
STEMI

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20
Q

What are the types of Myocardial Infarction?

A

5 types based on aetiological mechanism

Type 1 = primary coronary event

Type 2 = oxygen supply/demand mismatch

Type 3 = sudden unexpected cardiac death secondary to myocardial ischaemia

Type 4 = associated with PCI or stent complications

Type 5 = Associated with cardiac injury

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21
Q

Outline the pathophysiology of atherosclerosis.

A

Endothelial dysfunction: LDL accumulate and become oxidised to Ox-LDL

Plaque formation: Macrophages take up Ox-LDL to form lipid laden foam cells and form fatty streaks

Plaque rupture: Chronic inflammation involves cytokines and either stabilisation (fibrous cap) or destabilisation and subsequent rupture (if TNF-a high) resulting in thrombus/embolus

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22
Q

What are the causes of ST elevation?

A 
STEMI 
Pericarditis 
Coronary vasospasm
Bundle branch block 
Ventricular aneurysm
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23
Q

What are the causes of ST depression?

A 
NSTEMI 
Reciprocal change to ST elevation 
Electrolyte imbalances 
Digoxin effects
Bundle branch blocks
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24
Q

What can cause T wave inversion?

A

Myocardial ischaemia

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25
Q

Which leads are anteroseptal territory?

A

V1-V4

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26
Q

Which leads are lateral territory?

A

V5, V6, I, aVL

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27
Q

Which leads are inferior?

A

II, III and aVF

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28
Q

Which leads are posterior?

A

V7-V9

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29
Q

What are the changes in an ECG seen over time in a STEMI?

A

Mins-Hours: Hyperacute T waves

0-12 hours: ST-elevation

1-12 hours: Q-wave development

Days: T wave inversion

Weeks: T wave normalisation and persistent Q waves

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30
Q

What is the gold-standard blood test for investigating myocardial necrosis?

A

Troponin-I/T

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31
Q

Give 5 causes of troponin elevation

A 
Heart Failure 
Hypertensive emergencies 
Myocarditis
Cardiomyopathy 
Coronary Spasm
Renal dysfunction 
Pulmonary Embolism 
Structural Heart Disease
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32
Q

What is the management of acute chest pain suspected to be an ACS?

A

Mnemonic: MONA

Morphine 10mg IV 
\+
Oxygen high flow non-rebreather mask
\+ 
Nitrates sublingual GTN 
\+
Aspirin 300mg STAT
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33
Q

What is the management for a STEMI?

A

Medical: MONA

± within 120 minutes of being diagnosed with ST elevation (within 12 hours of onset of chest pain)
Intervention: PCI

± Unable to be performed within 120 minutes
Medical: Alteplase
+
Arrange transfer to PCI centre (2-24 hours after fibrinolysis)

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34
Q

What may be given in the case of high thrombus burden?

A

GP IIB/IIIA inhibitor such as Tirofiban

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35
Q

What risk stratification tool can be used to guide the management of a patient presenting with chest pain in suspected ACS?

A

GRACE Score = % 6 month mortality risk in patients with NSTMI/UA

Grace score > 1.5% treat with DAPT + Fondaparinux

Grace score (intermediate/high) then treat with PCI

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36
Q

A patient experiences a STEMI. 2 weeks following this, they experience pleuritic chest pain and a low grade fever. O/E there is a pericardial rub heard.

What is your diagnosis?

What is your management?

A

Dressler Syndrome

Tx:
- Medical: NSAIDs
± Severe
- Steroids: Prednisolone

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37
Q

Following a CABG, how soon can a patient drive?

A

4 week

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38
Q

Following insertion of a pacemaker, how soon can someone drive?

A

1 week

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39
Q

How soon after an angioplasty can a patient drive?

A

1 week

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40
Q

If a patient has had sustained ventricular arrhythmia and has an ICD put in, how soon can they drive?

A

6 months

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41
Q

How soon can a patient drive after a successful catheter ablation?

A

2 days off driving

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42
Q

How soon after a heart transplant can a patient drive?

A

6 weeks, do not need to notify DVLA

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43
Q

What are the two types of pericarditis?

A

Acute: Acute-onset chest pain with ECG features

Chronic: >3 months following acute episode

Complications may be: chronic pericardial effusion and constrictive pericarditis

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44
Q

How much fluid is usually present in the pericardial space?

A

20-50mL

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45
Q

What are the 3 functions of the pericardium?

A

Mechanical (limits cardiac dilation; aids ventricular compliance)

Barrier (reduces external friction; barrier)

Anatomical (fixes in position)

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46
Q

What virus commonly causes Pericarditis?

A

Coxsackie B virus

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47
Q

Give 5 causes of pericarditis.

A

Idiopathic

Viral

Bacterial

TB

Systemic disease (e.g. RA, uraemic pericarditis, hypothyroidism or post-myocardial infarction)

Drugs/Radiotherapy

Trauma

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48
Q

What are the features of cardiac tamponade?

A

Muffled heart sounds
Distended JVP
Pulsus paradoxus (reduced BP > 10mmHg during inspiration)
Hypotension

ECG: Saddle-shaped ST elevation; PR depression

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49
Q

How is pericarditis commonly managed?

A

NSAIDs + colchicine

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50
Q

What is the Beck Triad?

A

Hypotension + Muffled Heart Sounds + Raised JVP

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51
Q

What are the complications of pericarditis?

A

Cardiac tamponade

Chronic pericarditis

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52
Q

Muffled heart sounds + Raised JVP + Hypotension are collectively termed?

A

Beck Triad

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53
Q

Give 5 causes of cardiac tamponade.

A 
Trauma 
Tuberculosis 
Malignancy
Iatrogenic 
CT disease 
Radiation
Uraemia 
Post-MI
Aortic dissection 
Bacterial infection
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54
Q

What is the gold-standard investigation to diagnose Cardiac Tamponade?

What may be seen?

A

Echocardiography

Chamber collapse (early diastolic collapse of RV and late diastolic collapse of RA)

Respiratory variation in volume and flow

IVC Plethora (dilation of IVC and reduced diameter during inspiration)

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55
Q

How is cardiac tamponade managed?

A

Intervention: Urgent needle pericardiocentesis

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56
Q

What is the difference between acute and chronic pericarditis?

A

Timeframe

Acute: Initial episode

Chronic: >3 months following initial event

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57
Q

Which cause of pericarditis rarely causes chronic pericarditis?

A

Acute idiopathic pericarditis

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58
Q

What is the gold-standard diagnosis of chronic pericarditis?

A

Echocardiography

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59
Q

How may chronic pericarditis present?

A

Signs of right heart failure

SOB
Peripheral oedema
Abdominal swelling

Raised JVP
Ascites
Hepatomegaly

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60
Q

How is chronic pericarditis managed?

A

Surgery: Pericardiectomy

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61
Q

How may you classify heart failure?

A
  • Acute = Rapid onset of Sx or S/ life-threatening condition requiring urgent care/ acute decompensation of chronic heart failure. E.g.s MI/ Myocarditis/ Acute valvular disease/ Pericardial tamponade
  • Chronic = Progressive cardiac dysfunction due to structural and/or functional cardiac abnormalities. This leads to reduced CO and elevated intracardiac pressure at rest or on stress. Chronic HF is precipitated by conditions affecting the muscles (cardiomyopathy), vessels (IHD), valves (aortic stenosis) or conduction (atria fibrillation)
  • Left = Left ventricle of heart pumps insufficient blood (CO reduced) due to numerous conditions. May lead to RHF due to increased intrathoracic pressure and pulmonary hypertension
  • Right = Right ventricle pumping insufficient blood to lungs (cor pulmonale) which can commonly be due to advanced LHF. Biventricular failure can be referred to as congestive heart failure (CHF). Causes separated into: 2º to pulmonary hypertension; 2º to pulmonary/tricuspid valve pathology or pericardial disease
  • Systolic = reduced left ventricle ejection fraction (LVEF) leading to ventricular dilatation and eccentric remodelling
    Causes: Contractility/ Volume overload/ Pressure overload
  • Diastolic (preserved systolic function) = impaired ventricular relaxation or filling however LVEF is preserved via cardiac remodelling leading to ventricular hypertrophy
    Causes: Reduced expansion/ Increased thickness/ Delayed relaxation/ Increased HR
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62
Q

Give 5 causes of Heart Failure.

A

Think in terms of vascular, valvular, muscular, electrical, output

MI
Hypertension
Vasculitides

Stenosis
Regurgitation

Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Congenital heart disease

Arrhythmias

Hyperthyroid
Septicaemia
Thyrotoxicosis
Anaemia 
Liver failure
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63
Q

Outline the Frank-Starling Law.

A

stretching of cardiac muscle (within physiological limits) will increase the force of contraction

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64
Q

Calculate the MAP.

A

diastolic blood pressure + 1/3rd of the pulse pressure

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65
Q

What factors influence stroke volume?

A

Preload (venous return + filling time)
Afterload (valve function + vascular resistance)
Contractility (muscular function + ANS)

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66
Q

Outline the pathophysiology of heart failure.

A

The heart fails due to numerous reasons which results in a compensatory mechanism to maintain the cardiac output (amount of blood going through the body per minute).

Should demand > supply, decompensation occurs which is pathophysiological

Compensatory mechanisms:
- RAAS: reduced BP thus increased RAAS output, resulting in water retention, oedema, dyspnoea and sodium retention with potassium excretion

  • SNS: reduced BP thus constriction to increase venous return; increase cardiac remodelling and hypertrophy
  • Ventricular dilatation and remodelling: increased EDV leading to greater output however cardiomyocytes remodel which leads to hypertrophy, loss of myocytes and interstitial fibrosis causing contractile failure
  • BNP/ANP: BP high thus natriuresis encouraged
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67
Q

Give some clinical features of HF.

A
  • Dyspnoea: SOBE
  • Orthopnoea
  • Paroxysmal Nocturnal Dyspnoea (PND)
  • Fatigue
  • Tachycardia
  • Raised JVP
  • Cardiomegaly + displaced apex beat
  • S3 or S4 heart sounds
  • Bi-basal lung crackles
  • Pleural effusion
  • Oedema: Ankle; Sacral
  • Ascites
  • Tender hepatomegaly
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68
Q

A patient has a ventricular arrhythmia which required a shock. How long can they not drive for?

A

6 months

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69
Q

How do you manage acute heart failure?

A

Mnemonic: LMNOP

Loop diuretic 
\+
Morphine 
\+
Nitrates (if severe HTN or valvular disease)
\+
Oxygen 
\+
Position (sit forward)

May give…

Inotropes (<85mmHg)
Vasopressors
Mechanical circulatory assistance (Intra-aortic balloon)

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70
Q

What are the criteria for HFpEF?

A

> 50%

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71
Q

What is the criteria for HFrEF?

A

<35-40%

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72
Q

What does R sided heart failure generally give you?

A

Mnemonic: Right = rest of body

Peripheral oedema

Raised JVP

Hepatomegaly

Weight gain

Fluid retention

Cardiac cachexia (anorexia)

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73
Q

What are the general clinical features of Left sided Heart Failure?

A

SOB

Orthopnoea

PND

Bibasal crackles

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74
Q

What is the first line treatment for a patient with Chronic Heart Failure?

A

Mnemonic: ABA

ACEi + ß-blocker ± ARB

No long term reduction in mortality for Diuretic but does give symptomatic alleviation

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75
Q

What effect does Candesartan have on potassium?

A

Hyperkalaemia

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76
Q

What effect does Ramipril have on potassium?

A

Hyperkalaemia

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77
Q

When should you give Ivabradine?

A

Sinus rhythm > 75bpm AND HFrEF <35%

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78
Q

When can you give sacubitril-valsartan?

A

HFrEF <35% when symptomatic on ACEi/ARBs

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79
Q

When can digoxin be used in HF?

A

Symptomatic alleviation due to inotropic effect

Used when co-existant AF

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80
Q

When may hydralazine be used with a nitrate in HF?

A

Afro-Carribean patient

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81
Q

What vaccines should a patient with Heart Failure be offered?

A

Annual Flu Vaccine

One-off Pneumococcal

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82
Q

No symptoms or limitations would be what NYHA classification?

A

I

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83
Q

Mild symptoms and slight limitation of physical activity would be what NYHA classification?

A

II

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84
Q

Moderate symptoms e.g. marked limitation of physical activity would be what NYHA classification?

A

III

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85
Q

Severe symptoms with features at rest would be what NYHA classification?

A

IV

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86
Q

What is the MOA of Digoxin?

A

Reduces AVN conduction to slow ventricular rate in AF/AFlut

Inhibits Na+/K+ ATPase pump to increase force of cardiac muscle contraction

Stimulates vagus nerve

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87
Q

What are the clinical features of Digoxin toxicity?

A

Unwell, lethargic, N/V, anorexia, confusion, xanthopsia, gynaecomastia

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88
Q

What are the precipitating factors for Digoxin toxicity?

A

Increased age

MI

Renal failure

Hypokalaemia

Hypomagnesaemia

Hypercalcaemia

Hypernatraemia

Acidosis

Hypothermia

Hypoalbuminaemia

Hypothyroidism

Drugs: Amiodarone; Quinidine; Verapamil; Diltiazem; Spironolactone; Ciclosporine; Thiazides; Loop diuretics

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89
Q

How do you manage Digoxin toxicity?

A

A-E

Digibind

Correct arrhythmias

Monitor potassium

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90
Q

What are the CXR finds seen in a patient with HF?

A 
Alveolar shadowing
Batwing sign (hilar lymphadenopathy)
Cardiomegaly/Kerley B lines  
Diversion 
Effusion
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91
Q

What would contraindicate Eplerenone in HF treatment?

A

Hyperkalaemia

Hyponatraemia

AKI

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92
Q

How do you initiate ACEi treatment in HF?

A

Ramipril 1.25mg OD

Check U+Es before, repeat in 1-2 weeks

Double dose every 2-4 weeks until symptomatic alleviation achieved

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93
Q

How do you initiate ß-blocker treatment in HF?

A

Bisoprolol 1.25mg OD

Double dose every 4 weeks until target dose achieved

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94
Q

What may contraindicate ß-blockers?

A

Severe asthma

COPD

Pulmonary oedema

Bradycardia

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95
Q

What is the 1st line treatment in a patient with HFpEF?

A

Loop diuretic

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96
Q

Give 3 causes of Cor Pulmonale.

A

COPD

Pulmonary Embolism

Interstitial Lung Disease

Cystic Fibrosis

Primary Pulmonary Hypertension

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97
Q

Describe Cor Pulmonale.

A

RS HF due to respiratory distress which causes increased pressure and resistance in the pulmonary arteries with RV hypertrophy and back pressure to SVC and systemic venous system

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98
Q

Give the clinical features of Cor Pulmonale.

A

Hypoxia
Cyanosis
Raised JVP (due to a back-log of blood in the jugular veins)
Peripheral oedema
Third heart sound
Murmurs (e.g. pan-systolic in tricuspid regurgitation)
Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)

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99
Q

Give 5 causes of Hypertension

A

Vascular: Atherosclerosis; RAS
Idiopathic
Trauma: Psychological; SIADS; DI
Acquired: Diabetes, Pregnancy, Alcoholism, CLD
Metabolic: Renal disease; Hyperaldosteronism (Conn’s); Cushing’s; Nephritic Syndromes
Infective (none)
Neoplasia: Pituitary adenoma; Phaeochromocytoma (adrenal cancer);

Congenital: ASD; VSD; Valvulopathies; Polycythaemia

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100
Q

How much time is given between a seated and standing Blood Pressure reading?

A

3 minutes

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101
Q

What are the criteria for Orthostatic Hypotension?

A

3 minutes apart

> 20mmHg Systolic drop

> 10mmHg Diastolic drop

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102
Q

156/92mmHg is what stage hypertension?

A

Stage 1

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103
Q

164/102mmHg is what stage Hypertension?

A

Stage 2

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104
Q

192/124mmHg is what stage of hypertension?

A

Stage 3

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105
Q

What is the management of Hypertension?

A

Supportive: Low salt diet (<6g/day); reduce caffeine; smoking cessation; exercise; lose weight

± Stage 2 Hypertension/ CKD/ Risk >10%/ Diabetes/ End organ damage

Follow algorithm

Age < 55 years / European/ T2DM = ACEi/ARB

Afro-Carrib = CCB

then follow A + C + D

If potassium is >4.5mmol/L consider alpha/beta blocker

If potassium is <4.5mmol/L consider ARB

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106
Q

Who should be referred to a specialist regarding hypertension?

A

Fail to respond to step 4 measures (resistant hypertension)

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107
Q

What are the clinic BP targets for <80 years?

A

140/90mmHg

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108
Q

What are the HBPM targets for <80 years?

A

135/85mmHg

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109
Q

What are the clinic BP targets for >80 years?

A

150/90mmHg

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110
Q

What are the HBPM targets for >80 years?

A

145/85mmHg

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111
Q

Give 3 causes of aortic regurgitation.

A

Split by valve leaflets or aortic root

Rheumatic heart disease
Infective endocarditis
Connective tissue disease
Bicuspid aortic valve

Aortic dissection
CT disease
Aortitis
Syphilis 
Hypertension 
Spondyloarthropathies
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112
Q

What is the causative pathogen of Rheumatic Heart Disease?

A

GAS

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113
Q

Describe a water hammer pulse?

Give the other name for this.

A

Collapsing pulse due to arm being raised + blood emptying very quickly due to gravity with artery emptying back to heart in diastole which increases preload and cardiac output during aortic regurgitation

Corrigan’s Pulse

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114
Q

What is Quincke’s Sign?

A

Nailbed pulsation

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115
Q

What type of murmur is heart in AR?

A

Early diastolic murmur

Mid-diastolic Austin-Flint murmur in severe AR (partial closure of anterior mitral valve cusps caused by regurgitation streams)

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116
Q

What is de Musset’s sign?

A

Head nodding with heartbeat

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117
Q

What is Muller’s sign in AR?

A

Pulsation of uvula

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118
Q

What is the key diagnostic investigation for AR?

A

Echocardiogram

119
Q

What is the management of chronic AR?

A

Treatment indicated: Significant enlargement / Severe AR / Severe AR + LVEF <50%/ Marfan’s disease with ascending aorta diameter > 50mm

Valve replacement - TAVI or Open surgery

Mechanical vs Bioprosthetic valve replacement

120
Q

Give 5 causes of aortic stenosis.

A

Calcification

Bicuspid aortic valve

William’s Syndrome (supravalvular aortic stenosis)

Rheumatic fever

HOCM (subvalvular)

121
Q

What are the clinical features of AS?

A

Mnemonic: SAD

Syncope
Angina
Dyspnoea

Ejection systolic murmur
Murmur radiates to carotids 
Sustained apex 
Slow rising pulse 
Narrow pulse pressure 
4th heart sound 
Softer S2 (aortic component of second heart sound may become quieter in severe disease as leaflets fail to oppose each other forcefully)
122
Q

What is the management for AS?

A

Asymptomatic = do not treat

Asymptomatic + valvular gradient >40mmHg = consider surgery

Symptomatic = surgery

Valvotomy (open or balloon) or Valve replacement (mechanical vs bioprosthetic)

123
Q

Give 5 causes of MR.

A 
Post-MI 
CAD 
Mitral valve prolapse 
Dilated cardiomyopathy (overfilling) 
Infective endocarditis 
Rheumatic fever 
Congenital 
Medications (ergotamine; bromocriptine; pergolide)
124
Q

What are the clinical features of MR?

A

Asymptomatic

Symptoms will arise due to HF or arrhythmia

Displaced apex beat
Systolic thrill
Pansystolic murmur
S3 heart sound

HF signs: bibasal crackles; peripheral oedema

125
Q

What is the change in P waves in MR and why does this occur?

A

P wave broadened due to atrial enlargement

126
Q

What may be seen on CXR in severe MR?

A

L atrial and ventricular enlargement with double right heart border due to large L atrium

Pulmonary oedema

127
Q

How is MR managed?

A

Acute vs Chronic

Acute 
Supportive: Stabilise
\+
Medical: Nitroprusside/Inotropes/IA balloon pump
± Severe 
Surgery: Valve repair surgery

Chronic:
Medical: ACEi/ß-blocker/ARB
± HFrEF <30%
Surgery: Valve repair; LVAD; Heart transplant

128
Q

Give 3 causes of MS.

A 
Rheumatic feber 
Mucopolysaccharidoses
Carcinoid 
Endocardial fibroelastosis
Fabry's disease 
Radiation 
Mitral annular calcification
Congenital MS (Lutembacher syndrome = ASD + MS)
129
Q

Outline the process of Rheumatic Heart Disease.

A

GAS infection with cross-reactivity of Abs to combat GAS resulting in arthritis and carditis.

130
Q

What is Lutembacher syndrome?

A

ASD + MS

131
Q

What are the clinical features of MS?

A

SOB
CX pain

Irregular pulse

Raised JVP

RV heave (pulmonary heave)
Mid-diastolic murmur
Prominent A wave

Peripheral oedema
Hepatomegaly

132
Q

What is the A wave?

A

RA contracts which creates retrograde pressure thus blood into the IVJ

Mnemonic: A wave is Atrial Contraction wave

133
Q

What is the X descent?

A

RA relaxes thus blood fills RA from SVC

Following C wave, RV contracts which creates space in pericardium for atria to fill again which causes a drop in the IVJ column

134
Q

What is the C wave?

A

RV contracts so blood in the pulmonary artery with temporary rise in the RV projecting tricuspid valve into RA and upward force causing a temporary rise in JVP

Mnemonic: C wave is contraction wave

135
Q

What is the V wave?

A

Relaxation of the RA whilst tricuspid is closed draws blood into the RA

Mnemonic: V wave is venous filling

136
Q

What is the Y descent?

A

Tricuspid valve opens thus blood fills from RA to RV with reduced blood in JVC column

Mnemonic: Y descent as blood descends from RA to RV

137
Q

What are the CXR signs of MS?

A

Double right heart border due to L atrial enlargement

Splayed carina (L main bronchus lifted)

138
Q

How is MS managed?

A

Medical: Anticoagulation (Warfarin)

± Asymptomatic
Supportive: Monitoring with echocardiograms

± Symptomatic
Surgery: Percutaneous mitral balloon valvotomy or Mitral valve replacement

139
Q

What is the most common cause of infective endocarditis?

A

S aureus

140
Q

Infective endocarditis from dental surgery is most likely to be caused by which pathogen?

A. S aureus

B. S viridans

C. S epidermidis

D. S bovis

E. Lupus

A

B

141
Q

Infective endocarditis from IVDU is most likely to be caused by which pathogen?

A. S aureus

B. S viridans

C. S epidermidis

D. S bovis

E. Lupus

A

A

142
Q

Infective endocarditis associated with CRC is most likely to be caused by which pathogen?

A. S aureus

B. S viridans

C. S epidermidis

D. S bovis

E. Lupus

A

D

143
Q

Infective endocarditis from indwelling lines is most likely to be caused by which pathogen?

A. S aureus

B. S viridans

C. S epidermidis

D. S bovis

E. Lupus

A

C

144
Q

Libman-Sacks endocarditis is most likely to be caused by which pathogen?

A. S aureus

B. S viridans

C. S epidermidis

D. S bovis

E. Lupus

A

E

145
Q

Give 3 examples of culture negative infective endocarditis.

A

Prior ABX use

C burnetii

Bartonella

Brucella

HACEK

146
Q

What are the types of infective endocarditis?

A

Based on valve type

NVE: Normal valve

PVE: Early (<1 year) or Late (>1 year)

IVDA Endocarditis: Tricuspid valve (50%)

147
Q

Give 7 RFs for Infective Endocarditis.

A 
Increased age
Male 
IVDU 
Indwelling lines
Recent surgery 
Poor dentition 
Structural heart disease
Valvular heart disease
Previous IE 
Prosthetic heart valves 
Autoimmune conditions 
CRC
Malignancy

Immunosuppressed
Haemodialysis

148
Q

Outline the pathophysiology of Infective Endocarditis.

A

Turbulent blood flow causes endothelial damage thus platelets and fibrin adhere to underlying collagen surface, resulting in a prothrombotic environment.

Bacteraemia (S. aureus) leads to colonisation of thrombus and precipitates additional fibrin deposition, immunological response (mediated by macrophages and neutrophils) and platelet aggregation (‘vegetation’) causing mature infected vegetation. Vegetation causes destruction locally of valves leading to regurgitant murmurs and subsequent congestive cardiac failure.

149
Q

What is the difference between Janeway lesions and Osler nodes?

A

Janeway lesions = painLESS erythematous macules on solar surfaces

Osler nodes = PaiNful violaceous nodules on pads of fingers and toes

150
Q

What are roth spots?

A

Exudative, oedematous haemorrhagic lesions of the retina with a pale centre

151
Q

What criteria is used in the diagnosis of Infective Endocarditis?

A

Duke’s Criteria 2 major or 1 major 3 minor

Major criteria:

  • 2 positive blood cultures
  • Positive echocardiogram finds (vegetation/abscess/valvulopathy)

Minor criteria:

  • IVDU
  • PMHx cardiac condition
  • Fever >38C
  • Vascular phenomenon
  • Immunological phenomena
  • Microbiological evidence
152
Q

How is infective endocarditis managed?

A

Depends on the bacteria isolated

Initial blind therapy: Amoxicillin

S. aureus
Flucloxacillin 12g/day in 4-6 doses over 4-6 wks

MRSA
Vancomycin 30-60mg/kg/day in 2-3 doses over 4-6 weeks

If prosthetic valve
+ Rifampicin + Gentamicin for ≥ 6 weeks

153
Q

How do you treat IE caused by S epidermis?

A

Penicillins for 4-6 wks

154
Q

How do you treat IE caused by a less sensitive streptococci?

A

Benpen + Gentamicin

155
Q

What are the indications for surgery due to IE?

A

Severe valvular incompetence

Aortic abscess

Infections resistant to ABX

Cardiac failure refractory to medical Tx

Recurrent emboli following ABX

156
Q

Where is the aortic valve auscultated?

A

2nd ICS RHS

157
Q

Where is the pulmonary valve heard?

A

2nd ICS LHS

158
Q

Where is the mitral valve heard?

A

5th ICS MCL

159
Q

Where is the tricuspid valve heard best?

A

5th ICS LHS

160
Q

How can you accentuate an aortic murmur?

A

Sit up and lean forward

Expiration

161
Q

How can you accentuate a mitral murmur?

A

LHS and listen with bell of stethoscope

162
Q

How do you accentuate a right sided murmur?

A

Mnemonic: RILE

Right Inspiration

163
Q

How do you accentuate a left sided murmur?

A

Mnemonic: RILE

Left sided expiration

164
Q

How do you characterise a murmur?

A

Timing

Character and grade

Where it is heard loudest

Pitch (diaphragm or bell)

Change with position or dynamic manoeuvres

Radiation

165
Q

How do you grade murmurs?

A

The Levine Scale

Grade 1: Heard by experts

Grade 2: Slight murmur

Grade 3: Moderate, easily heard, no palpable thrill

Grade 4: Loud, palpable thrill

Grade 5: Very loud, palpable thrill

Grade 6: Heard without a stethoscope

166
Q

An ejection systolic murmur is heard which is best heard on expiration.

What is it?

A

Aortic stenosis

167
Q

An ejection systolic murmur is heard which is best heard on inspiration. What is it?

A

Pulmonary stenosis

168
Q

A pansystolic murmur is heard over the apex which radiates to the axilla.

What is it?

A

Mitral regurgitation

169
Q

A pansystolic murmur is heard over the left lower sternal edge. It does not radiate to the axilla. It is best heard on inspiration.

What is it?

A

Tricuspid regurgitation

170
Q

What is Eisenmenger Syndrome?

A

reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension. This occurs when an uncorrected left-to-right leads to remodeling of the pulmonary microvasculature, eventually causing obstruction to pulmonary blood and pulmonary hypertension.

171
Q

An early diastolic murmur is heard on expiration with the patient leaning forward.

What is your diagnosis?

A

Aortic regurgitation

172
Q

A mid-diastolic murmur is heard at the apex with breath held in expiration whilst laying in the left lateral decubitus.

What is your diagnosis?

A

Mitral stenosis

173
Q

A mid-diastolic murmur is heard which is augmented by inspiration.

What is your diagnosis?

A

Tricuspid stenosis

174
Q

What is an Austin-Flint murmur?

A

mid-diastolic rumble seen in severe aortic regurgitation. Its exact aetiology is still debated, but it may be related to vibration of the mitral valve secondary to the regurgitant jet.

175
Q

What is a Graham-Steele murmur?

A

Early diastolic murmur in pulmonary regurgitation which occurs secondary to pulmonary hypertension caused by mitral stenosis

176
Q

Compare and contrast the choices for heart valves.

A

Mechanical:
+ Last longer
+ Lower failure rate

  • Risk of thrombosis
  • Warfarin

Bioprosthetic:
+ Long-term coagulation not needed

  • Structural deterioration
177
Q

What are the types of mechanical heart valve?

A

Tilting disc

St Jude (least risk of thrombus formation)

Starr-Edwards (ball in cage; highest thrombus formation)

178
Q

What proportion of patients undergoing a surgical valve replacement experience infective endocarditis?

A

2.5%

179
Q

What is the INR target range for a patient with a mechanical heart valve?

A

2.5-3.5

180
Q

How may AF be classified?

A

Paroxysmal: Recurrent episodes lasting more than 30 seconds, which terminate spontaneously or within 7 days of intervention

Persistent: AF failing to self-terminate within 7 days; >12 months and it becomes long-standing persistent AF

Permanent: sinus rhythm cannot be restored or maintained and AF accepted in final rhythm

181
Q

Give 5 causes of AF.

A 
Hypertension 
MI
IHD
Valvular disease
Cardiomyopathy 
COPD/Pneumonia/PE 
Hyperthyroidism/DM
Infection
Hypokalaemia/Hypomagnesaemia/Hyponatraemia 
Bronchodilators/Thyroxine 
Alcohol
Excessive caffeine 
Obesity
182
Q

What are the clinical features of AF?

A

Asymptomatic

SOB
Palpitations
Angina
Presyncope

Irregularly irregular pulse
Absent a wave on JVP (≈ atrial contraction)
Tachycardia
Hypotension
HF Features: bibasal crackles, raised JVP and peripheral oedema

183
Q

What risk stratification tool can be used to assess stroke risk in patients with AF?

Outline it.

What is the threshold for anticoagulation?

A

CHADVASc score

CHF
Hypertension 
Age ≥75 (2)
Diabetes
Stroke/TIA/VTE (2)
Vascular disease 
Age 65-74 
Sex category

Score ≥2 = DOAC

If DOAC not suitable or tolerated, offer Warfarin

184
Q

What risk assessment tool can be used in major bleeding?

Outline it.

A

ORBIT Score

Age (75+)
Bleeding Hx (2) 
Coagulation treatment 
Drop in Hb (2) 
eGFR

0-2 = low risk

3 = medium

4-7 = high risk

185
Q

How is AF managed?

A

Establish cause - if any? and Tx cause

THEN

Rate or Rhythm control

Rate control (1st line) 
ß-blocker 
or
CCB
or 
Digoxin (very little physical exercise or co-existent heart failure

Rhythm control
Amiodarone

186
Q

Which patients are suitable for rhythm control in AF?

A

New-onset AF

Identifiable reversible cause

Heart failure (exacerbated by AF)

Associated Atrial Flutter

Rhythm control determined by clinical judgement

187
Q

What are the complications of AF?

A

Heart failure
Tachycardia-induced cardiomyopathy
Ischaemia
Sudden cardiac arrest

Thromboembolic events
Collapse
Bleeding events (anticoagulation)

188
Q

When should rhythm control in AF not be offered?

A

AF has a reversible cause
New-onset AF (<48 hours)
Atrial flutter which is suitable for ablation strategy
Heart failure due to atrial fibrillation
Rhythm control strategy more suitable based on clinical judgement

189
Q

What is the recommended management for patients who have not responded to anti arrhythmic medication in AF?

What impact does this treatment have on the rhythm and the stroke risk?

How long should they be anticoagulated for?

A

Catheter ablation

Use anticoagulation 4 weeks before and during procedure

Note: Controls rhythm but not reduced stroke risk

Therefore if CHADSVASc = 0, 2 months of anticoagulation

If CHADSVASc >1 = long-term anticoagulation recommended

190
Q

What two cell types aid myocardial contraction?

A

Autorhtymic cells (1%): Generate APs to drive contractile cells - these are ‘pacemaker’ cells

Contractile cells (99%): Responsible for myocardial contraction; undergo radical depolarisation driven by auto-rhythmic cells

191
Q

What is the location of the SAN?

A

Junction of SVC and RA (by the right auricle)

192
Q

Where is the AVN located?

A

Base of RA near the septum

193
Q

Outline the phases of the action potential of autorhythmic cells

A

Phase 4 = If channels open thus Na+ in

T-type calcium channels open at -50mV

Phase 0 = L-type calcium channels remain open, continuing depolarisation

Phase 3 = Ik open thus potassium efflux and repolarisation occurs

194
Q

Outline the action potential stages in contractile cardiomyocytes.

A

Phase 4 = Leaky Ik channels allow K+ efflux and keep RMP at -90mV

Phase 0 = Depolarisation via Ina thus sodium channels open and Na+ in

Phase 1 = Ikto (transient) thus K+ efflux

Phase 2 = Plateau phase due to Ical channels open prolonging repolarisation (L-type calcium channels)

Phase 3 = Ik open thus outward movement of K+ to return to -90mV

195
Q

What are the main types of pacemakers?

A

Single-chamber: leads to a single chamber - RA if SAN defunct; RV if AVN defunct

Dual-chamber: Leads in both RA and RV - pacemaker synchronises contractions of both atria and ventricles

Biventricular (triple-chamber): RA, RV and LV - used in patients with heart failure to synchronise contractions in these chambers

Also called Cardiac Resynchronisation Therapy (CRT) pacemakers

Implantable Cardioverter Defibrillators (ICDs): Continually monitor the heart and apply defibrillator shock to Cardioverter patient into sinus rhythm - identify a shockable arrhythmia

196
Q

What are the causes of Cardiomyopathy?

A

Primary: Genetic

Secondary:
Chemotherapy (Doxorubicin) -> Toxicity CM
Infection -> Infective CM
Systemic disease (Amyloidosis/Sarcoidosis) -> Infiltrative/Inflammatory CM
SLE -> Autoimmune CM
Radiation
Malignancy
Alcohol
Diabetes/Acromegaly/Thyrotoxicosis -> Endocrine CM
HH –> Storage CM

Pregnancy -> Peripartum
Stress -> Takotsubo

197
Q

Describe HCM.

A

increased ventricular wall thickness or mass not caused by pathologic loading conditions.

198
Q

Which mutations can cause HCM?

How is it inherited?

A

Myosin heavy chain
Troponin I
Troponin T

Inherited by autosomal dominant

199
Q

What are the potential clinical features of HCM?

A 
Fatigue 
SOB 
Orthopnoea 
Ankle Swelling 
Cx pain 
Pre/syncope 
Palpitations

Heave
Thrill
Ejection systolic murmur
Mid-late systolic murmur (AR)

Potential HF: Raised JVP, crackles, peripheral oedema

200
Q

What is the primary mode of diagnosis of HCM?

What threshold is used?

A

Echocardiography: ≥15mm LV wall thickness

201
Q

What is the management for HCM?

A

ß-blockers reduce outflow tract gradient

Surgery: Septal myomectomy

202
Q

Give 5 causes of dilation cardiomyopathy (DCM).

A

Idiopathic
TTN gene mutation
MYH7 gene mutation
Cardiac: CHD/ Hypertension/ Peripartum cardiomyopathy
MSK: DMD
Infection: Coxsackie B/ Rheumatic Heart Disease/ Chagas disease/ HIV
Autoimmune: Sarcoidosis/ SLE
Toxins: Alcohol; abuse/ Cocaine/ Organic solvents
Malnutrition: Thiamine deficiency/ Selenium deficiency
Radiation

203
Q

What is the management for DCM?

A

Mirrors heart failure thus use the same treatment

ACEi + ß-blocker ± ARB

± Symptoms
Tx symptoms e.g. Diuretics for Oedema

204
Q

A patient has been experiencing SOBE, fatigue, peripheral oedema and PND.

Echocardiography shows non-dilated, non-thickened ventricles with abnormal ventricular filling.

What is your diagnosis?

A

Restrictive cardiomyopathy

205
Q

How is RCM managed?

A

Tx underlying cause
+
Tx symptoms

206
Q

How is Arrhythmogenic Cardiomyopathy managed?

A

ß-blockers
+
ICD

207
Q

What is ARVD?

A

Arrhythmia alongside myocardial structural abnormalities

RV myocardium replaced by fibrofatty tissue due to a mutation of genes encoding hemidesmosomes

208
Q

What ECG abnormality may be seen in ARVD?

A

Epsillon wave with terminal notch in QRS complex

209
Q

What is Naxos disease?

A

Variant of ARVC.

ARVC + Palmoplantar keratosis + Wooly hair

210
Q

The presence of ARVC, palmoplantar keratosis and wooly hair suggests?

A

Naxos disease

211
Q

What is seen on echocardiogram in Takotsubo cardiomyopathy?

A

Transient, apical ballooning whereby hypokinesis of mid and apical segments thus apex balloons but area to base contracts thus appears like the neck of the octopus trap

212
Q

What drugs should be avoided in HOCM?

A

Nitrates
ACEi
Inotropes

213
Q

Discuss the process of cardioversion in AF.

A

Cardioversion may be electrical or pharmacological; subject to onset

Onset < 48 hours
LMWH
+
Cardioversion: Electrical (DC) or Pharmacological (Amiodarone if structural; Flecainide if without)

Onset > 48 hours
LMWH for 3/52 AND continue for 4 weeks after at least
+
Electrical cardioversion: DC

± High risk of cardioversion failure
Amiodarone/Sotalol 4 weeks

214
Q

What are the two shockable rhythms?

A

Ventricular fibrillation

Ventricular tachycardia

215
Q

What are the non-shockable rhythms?

A

PEA (all electrical activity without pulse, except VT or VF)

Asystole (no significant electrical activity)

216
Q

How may you classify arrhythmias?

A

Rate: Bradycardia vs Tachycardia

Site: Supraventricular vs Ventricular

217
Q

What causes a sinus arrhythmia?

A

Respiratory pattern changes e.g. inspiration causes reduction in PSNS thus increase HR

218
Q

What may cause a sinus bradycardia?

A 
ß-blockers
Digoxin
Hypothyroidism 
Hypothermia 
Cholestatic jaundice 
Raised ICP
Vasovagal attacks
Carotid sinus syndrome 
Anorexia
219
Q

How do you treat acute sinus bradycardia?

A

If symptomatic, Atropine

If persistent
Cardiac pacemaker

220
Q

What is the management for a sinus tachycardia?

A

ß-blocker: Bisoprolol

221
Q

How is Atrial Flutter managed?

A 
Rate or Rhythm control 
\+
Anticoagulation 
\+ 
Tx cause
222
Q

What are the treatment steps of managing a stable patient with an SVT?

A 
Valsalva 
±
Carotid sinus massage 
±
Adenosine 
± 
Verapamil (CCB)
±
DC Cardioversion
223
Q

What is the MOA of adenosine?

A

Slows cardiac conduction via AV node to reset back to rhythm

224
Q

How is adenosine administered?

A

Check if patient has asthma/COPD/HF/Heart block/Severe hypotension;
Warn patient of impending doom when injected

Fast IV bolus via grey cannula 6mg then 12mg then 12mg (if no improvement)

225
Q

What is the long term management of a patient with an SVT?

A

Medication: ß-blockers
±
Intervention: Radiofrequency ablation

226
Q

What is WPW Syndrome?

A

Type of SVT that is a AVRT due to an accessory pathway connecting the atria and ventricles (The Bundle of Kent)

227
Q

What ECG changes are seen in WPW Syndrome?

A 
Short PR interval <0.12 seconds 
Wide QRS complex >0.12 
Axis deviation (L if L accessory or R if R accessory)

Delta wave, slow and slurred upstroke on QRS complex

228
Q

What medications may prolong the QT interval?

A

Antipsychotics

SSRIs

ß-blockers

Amiodarone

Macrolide antibiotics

229
Q

Give 5 causes of sinus tachycardia.

A
  • Emotional
  • Exercise
  • Fever
  • Pain
  • Anaemia
  • Heart failure
  • Thyrotoxicosis
  • Acute PE
  • Hypovolemia
  • Drugs (atropine/ catecholamine)
230
Q

At what part of the ECG is DC Electrical cardioversion synchronised to and why?

A

Synchronised to R wave to prevent delivery of a shock during vulnerable period of cardiac repolarisation when ventricular fibrillation can be induced

231
Q

Give 5 causes of ventricular ectopics.

A
  • Anxiety
  • Sympathomimetics
  • ß-agonists
  • Excess caffeine
  • Hypokalaemia
  • Hypomagnesaemia
  • MI
232
Q

What is the management for ventricular ectopics?

A

ß-blockers

233
Q

How may you classify Ventricular Tachycardia?

A

Morphology: Monomorphic vs Polymorphic

Duration: Sustained vs Non-Sustained

234
Q

What are the ECG signs seen in Ventricular Tachycardia?

A

Broad QRS complex

AV dissociation (p wave and QRS complex at different rates)

S wave notching in lead III (Josephson’s sign)

235
Q

What are the clinical features of Jervell-Lange-Nielsen Syndrome?

A

Prolonged QT interval
+
Deafness

236
Q

What are the clinical features of Romano-Ward Syndrome?

A

Prolonged QT interval (congenital)

without deafness

237
Q

Give 5 causes of prolonged QT interval.

A 
Amiodarone 
Sotalol 
TCAs
SSRIs
Chloroquine
Macrolides e.g. Erythromycin 
Electrolyte imbalances: hypokalaemia; hypocalcaemia; hypomagnesaemia
Myocarditis 
MI
Hypothermia 
Subarachnoid haemorrhage

Jervell-Lange-Nielsen Syndrome
Romano-Ward Syndrome

238
Q

How is Ventricular Tachycardia managed?

A

Unstable: Immediate cardioversion

Stable:
Amiodarone (via central line)
Procainamide

If drug therapy fails…
EPS
+
ICD

239
Q

What drug should never be given in VT?

A

Verapamil

240
Q

Exertional syncope following swimming is a feature of which variant of LQT?

A. LQT1

B. LQT2

C. LQT3

D. Sudden Cardiac Death

A

A

241
Q

Syncope following emotional stress is a feature of which variant of LQTS?

A. LQT1

B. LQT2

C. LQT3

D. Sudden Cardiac Death

A

B

242
Q

Cardiac events occurring at night when resting is a feature of which LQTS variant?

A. LQT1

B. LQT2

C. LQT3

D. Sudden Cardiac Death

A

C

243
Q

How is LQTS managed?

A

Avoid precipitants
+
ß-blockers

244
Q

Give 5 causes of Ventricular Fibrillation.

A

4Hs and 4Ts

Hypoxia
Hyperkalaemia
Hypovolaemia
Hypothermia

Thrombosis
Tamponade
Toxins
Tension pneumothorax

245
Q

How do you manage Ventricular Fibrillation?

A

Defibrillator
+
ICD following resuscitation

246
Q

Give 5 causes of LBBB.

A 
MI 
Hypertension 
Idiopathic fibrosis 
Aortic stenosis 
Cardiomyopathy 
Digoxin toxicity
Hyperkalaemia
247
Q

Give 5 causes of RBBB.

A 
RV hypertrophy
Cor pulmonale 
Ischaemic heart disease
PE
Congenital heart disease
Myocarditis
Rheumatic heart disease
Cardiomyopathy 
Idiopathic fibrosis (LLS)
248
Q

What is Ebstein’s anomaly?

A

Low insertion of tricuspid valve thus large atrium and small ventricle = ‘atrialisation of RV’

249
Q

What are the clinical features of Ebstein’s anomaly?

A

Cyanosis
Prominent a wave
Hepatomegaly
Tricuspid regurgitation: pansystolic murmur; worse on inspiration

RBBB

250
Q

What is the mode of inheritance for Brugada syndrome?

A

Autosomal Dominant

251
Q

What gene mutation is predominantly responsible for Brugada syndrome?

A

SCN5A

252
Q

What are the ECG changes observed in Brugada syndrome?

A

Convex ST segment elevation >2mm in V1-V3 AND negative T wave

Partial RBBB

253
Q

What is the management of Brugada syndrome?

A

ICD

254
Q

What is a bifascicular block?

A

Combination of RBBB or LBBB with anterior or posterior hemiblock

255
Q

What classification system can be used for anti arrhythmic drugs?

A

Vaughan-Williams

256
Q

What V-W class of drug is Disopyramide?

A

1a

257
Q

What V-W class of drug is Lignocaine?

A

1b

258
Q

What V-W class of drug is Bisoprolol?

A

2

259
Q

What V-W class of drug is Amiodarone?

A

Class 3

260
Q

What is the MOA of Amiodarone?

A

Blocks KCN thus increases refractory period

261
Q

What is the MOA of Flecainide?

A

NaCN blocker thus reduces rate of firing and Na+ influx

262
Q

What is the MOA of Verapamil?

A

Block CCN therefore reduce conduction

263
Q

Which biochemical marker gives the most accurate reflection of an MI in the last 5 days?

A

CK-MB (up to 5 days)

Trop-I (up to 10 days)

264
Q

What is the eponymous term for Costochondritis?

A

Tietze Syndrome

265
Q

What is the MOA of aspirin?

A

COX-i thus prevent TXA2 production and inhibits platelet aggregation to stop clots

266
Q

What is the MOA of Apixaban?

A

Factor X inhibitor thus stops clotting

267
Q

What is the MOA of bisoprolol?

A

Antagonist of ß-adreoceptor thus antagonises SNS

268
Q

Give 3 side effects of beta blockers?

A

Bronchoconstriction

Vasoconstriction

Lethargy

Hyperkalaemia

Erectile dysfunction

Loss of joie de vivre

Nightmares

Headaches

269
Q

When should you consider stopping ACEi?

A

sCr >20%

Angiooedema

Cough

eGFR drops markedly

270
Q

What is the MOA of Furosemide?

A

Loop diuretic - inhibiting Na/2Cl/K cotransporter thus increases loss of water and electrolytes

271
Q

What are the side effects of CCBs?

A

Ankle oedema
Flushes
Headaches
Gingival hypertrophy

272
Q

What is the MOA of Digoxin?

A

Inhibits Na+/K+ pump

Vagal nerve discharge

273
Q

What ECG sign may be seen in Digoxin toxicity?

A

Reverse tick sign

ST depression with rapid upstroke back to isoelectric line

274
Q

What is the MOA of Flecainide?

A

Sodium channel blocker

Class I anti-arrhythmia drug

Useful in AF and SVT with accessory pathways

275
Q

What are the contraindications for Flecainide?

A

Structural heart disease
Post-MI infarction
Sinus node dysfunction
Atrial flutter

276
Q

What are the side effects of Flecainide?

A

Negatively inotropic
Bradycardia
Oral paraesthesia
Visual disturbances

277
Q

What is the MOA of Amiodarone?

A

Class III anti-arrhythmia drug blocking potassium channels to inhibit repolarisation thus prolongs AP

278
Q

What are the adverse effects of Amiodarone?

A 
Slate-gray appearance
Corneal deposits
Thyroid derangement (hypo and hyper) 
Pulmonary fibrosis/pneumonitis 
Liver fibrosis/hepatitis 
Thrombophlebitis 
Bradycardia
QT interval prolongation
279
Q

What is the MOA of statins?

A

HMG-CoA reductase inhibitors thus reduces cholesterol synthesis

Increased LDL-r expression by hepatocytes thus reduced LDL concentration in blood

280
Q

What are the potential side effects of Statins?

A 
Abdo discomfort
Muscle aches 
Myositis 
Raised CK 
Raised transaminases
281
Q

What types of angina are there?

A

Stable

Prinzmetal angina

Decubitus

Unstable

282
Q

What is the management of angina?

A

Investigate with CT coronary angiography
Do other tests too…FBC; U+Es; LFTs; TFTs; Troponin; HbA1c; ECG

Acute: Morphine + Oxygen + Aspirin + Nitrates

Ongoing
Beta blockers or CCB (rate-limiting) 
Nitrates 
RF modification 
Aspirin 75mg 
Statins 
ACEi (if diabetic or HTN) - or CCBs if needed
283
Q

What are the criteria for a STEMI?

A

> 20mins of ECG features in ≥2 contiguous leads showing:
2.5mm ST elevation in leads V2-V3 in men under 40 or 2.0mm ST elevation in V2-V3 in men over 40

1.5mm ST elevation in V2-V3 in women

1mm ST elevation in other leads

New LBBB criteria

284
Q

How is a GRACE score calculated?

A 
Age 
BP
Cardiac: ECG findings, Troponin, HR
Disability: cardiac arrest? 
eGFR: Renal function
285
Q

What are the potential complications of an MI?

A

Cardiac arrest
Cardiogenic shock
Bradyarrhythmia

Tachyarrhythmia

Pericarditis 
Cardiac tamponade 
Mitral regurgitation 
VSD
LV aneurysm

Dressler syndrome

286
Q

What is bigeminy?

A

normal QRS followed by ventricular ectopic beat with compensatory pause and repeat

287
Q

Outline the Orbit score.

A

Mnemonic: ABCDE

Age (75+)
Bleeding Hx 
Coagulation 
Dick? (M or F) 
eGFR
288
Q

Outline the treatment steps for Hypertension.

A

<55 y/o or DM give ACEi/ARB

> 55y/o or Afro-Carrib give CCB

Add the other

Add a diuretic

[K+] > 4.5 = alpha blocker//beta blocker

[K+] < 4.5 = spironolactone

Beta Blocker

289
Q

When should you treat in Hypertension?

A

HBPM >135/85mmHg AND 1 of following: end-organ damage; CVD disease; 10-year CV risk >10%

HBPM >150/95mmHg regardless of age

290
Q

What is the most common valve affected in IVDU for endocarditis? Explain why.

A

Tricuspid valve - this is the first valve receiving venous blood

291
Q

What is the most common valvulopathy associated with PCKD?

A

Mitral prolapse/regurgitation

292
Q

When might you prescribe nitrates in heart failure?

A

MI
AR or MS
Hypertension

293
Q

What are the target saturations in a patient with hypoxia in HF?

A

94-98%

294
Q

List 5 causes of VT.

A

Congenital: Jervell-Lange-Nielsen Syndrome (with deafness); Romano-Ward Syndrome

Drugs: Macrolides; Amiodarone; Sotalol; TCAs; SSRIs

Electrolytes: Hypocalcemia; Hypokalaemia; Hypomagnesaemia

SAH; Myocarditis

Hypothermia

Medicine (18 decks)

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