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Year 4 Semester 2 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is normal heart rhythm called?

A

Sinus rhythm

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2
Q

What causes sinus arrhythmias?

A

Changes in the autonomic NS

Due to the rate of respiration

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3
Q

Pathological causes of sinus bradycardia?

A 
MI- inferior affecting the R coronary artery
Sick sinus syndrome
Hypothermia
Hypothyroidism
Cholestatic jaundice
Raised ICP
Drugs: b-blockers, digoxin, verapamil
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4
Q

Management of symptomatic sinus bradycardia?

A

IC atropine

Think about a pacemaker if persistent

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5
Q

Pathological causes of sinus tachycardia?

A 
Anxiety
Fear
Anaemia
Heart failure
Thyrotoxicosis
Phaechromocytoma
Drugs: b-agonists (bronchodilators)
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6
Q

What is sick sinus syndrome?

A

Fibrosis and degenerative changes/ischaemia of the SA node

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7
Q

Which arrhythmias can sick sinus syndrome cause?

A 
Sinus bradycardia
Sinoatrial block
Paroxysmal atrial fibrillation
Paroxysmal atrial tachycardia
Atrioventricular block
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8
Q

Presentation of sick sinus syndrome?

A

Palpitations
Dizzy spells
Syncope

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9
Q

Types of atrial tachycardias?

A

Atrial ectopic beats
Atrial tachycardia
Atrial flutter
Atrial fibrillation

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10
Q

Presentation of atrial ectopic beats?

A

Usually asymptomatic

May feel like a skipped/missed beat

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11
Q

ECG of atrial ectopic beats?

A

Premature but normal QRS complex

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12
Q

When and how do you treat atrial ectopic beats?

A

If intrusive beats

B-blockers

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13
Q

Causes of atrial tachycardia?

A

Increased atrial automaticity
Sinoatrial disease
Digoxin toxicity

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14
Q

Management of atrial tachycardia?

A

B-blockers, anti-arrhythmic drugs

Catheter ablation if due to an ectopic site

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15
Q

Cause of atrial flutter?

A

Large re-entry circuit usually in the RA

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16
Q

What is happening in atrial flutter?

A

The atrium are contracting very quickly -> atrial rate about 300/min
Not all of these atrial beats are conducted to the ventricles -> tachycardia
All the atrial beats can be conducted in young people -> heart rate up to 300/min
Conduction of atrial beats is often 2:1 or 3:1 or 4:1 -> 150, 100, 75 bpm heart rate

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17
Q

ECG of atrial flutter?

A

Sawtooth flutter waves

More atrial sawtooth waves than QRS complexes

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18
Q

Management of atrial flutter?

A

Rate limitation: digoxin, b-blockers, verapamil to control the ventricular rate
Direct current cardioversion or IV amiodarone can restore sinus rhythm
Catheter ablation very effective for those with persistent symptoms

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19
Q

Pathology of atrial fibrillation?

A

Abnormal autonomic firing and presence of multiple interacting re-entry circuits
Initiate by ectopic beats (usually from the pulmonary veins)
Maintained by re-entry in the atria

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20
Q

ECG in atrial fibrillation?

A

Irregularly irregular
No P waves
Narrow complex

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21
Q

Types of atrial fibrillation?

A

Paroxysmal: intermittent, will self terminate
Persistent: prolonged episodes terminated by electrical/chemical cardioversion
Permanent

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22
Q

Causes of atrial fibrillation?

A 
CHD
Valvular heart disease: especially mitral valve disease
Hypertension
Sinoatrial disease
Hyperthyroidism
Alcohol
Cardiomyopathy
Congenital heart disease
Chest infection
Pulmonary embolism
Pericardial disease
Idiopathic
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23
Q

Presentation of atrial fibrillation?

A

Palpitation
Dyspnoea
Fatigue
Asymptomatic

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24
Q

How do you measure stroke risk for non-valvular atrial fibrillation?

A

CHA2DS2-VASc score

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25
Q

Management of atrial fibrillation?

A

Treat ant acute condition
Rhythm control: electrical cardioversion/pharmacological cardioversion with anticoagulation, catheter ablation
Rate control: digoxin, b-blockers, rate limiting calcium antagonists
Oral anticoagulation to prevent VTE

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26
Q

Types of supraventricular tachycardias?

A 
Atrial fibrillation
Atrial flutter
Sinus tachycardia
Wolff-Parkinson-White syndrome
Atrioventricular nodal re-entrant tachycardia (AVNRT)
Can occur with a bundle branch block
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27
Q

ECG of supraventricular tachycardias?

A

Narrow complex tachycardia

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28
Q

Presentation of AVNRT?

A 
Rapid, very forceful, regular heart beat
Chest discomfort
Light-headedness
Dyspnoea
Polyuria due to release of ANP
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29
Q

Management of supraventricular tachycardia?

A

Vagal manoeuvres: carotid sinus pressure, valsalva manoeuvre
Adenosine/verapamil to restore sinus rhythms
Catheter ablation if recurrent

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30
Q

Wolff-Parkinson-White syndrome on ECG?

A

Delta waves
Narrow complex
Tachycardia

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31
Q

How do ventricular arrhythmias often present?

A

As cardiac arrest

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32
Q

Pathology of ventricular ectopic beats?

A

Rapid and simultaneous activation of the ventricles

Ectopic beats produce low stroke volume -> irregular pulse with weak/missed beats

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33
Q

ECG for ventricular ectopic beats?

A

Broad complexes

Random broad and deep complexes

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34
Q

When and how do you treat ventricular ectopic beats?

A

If highly symptomatic
B-blockers
Catheter ablation

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35
Q

When do people get ventricular ectopic beats?

A

Older age
During an acute MI
Heart failure
Digoxin toxicity

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36
Q

When do ventricular tachycardias occur?

A

Acute MI
Chronic coronary artery disease
Cardiomyopathy
Extensive ventricular disease

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37
Q

ECG in ventricular tachycardia?

A

Tachycardia
Broad, abnormal complexes
Left axis deviation

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38
Q

Presentation of ventricular tachycardia?

A

Palpitation

Symptoms of low cardiac output

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39
Q

Management of ventricular tachycardia?

A

Restore sinus rhythm:
Synchronised DC cardioversion if unstable
IV amiodarone
Correct abnormal electrolytes

Prophylaxis:
B-blockers
Implantable cardiac defibrillator
Surgery or catheter ablation

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40
Q

What is Torsades de pointes?

A

A ventricular tachycardia

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41
Q

ECG of Torsades de pointes?

A 
Tachycardia
Polymorphic
Broad complexes
Complexes oscillating
Non-sustained
Repetitive
Prolonged QT (often when in sinus rhythm)
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42
Q

Management of Torsades de pointes?

A

Treat underlying cause
IV magnesium sulphate
B-blockers to prevent syncope
Defibrillation implantation: extreme QT prolongation, at risk patients

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43
Q

ECG in ventricular fibrillation?

A

Tachycardia

Rapid, bizarre and irregular ventricular complexes

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44
Q

Management of ventricular fibrillation?

A

As soon as possible

Defibrillation to induce sinus rhythm and normal cardiac output

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45
Q

Differentials for a regular broad complex tachycardia?

A

Ventricular tachycardia

Any cause of a narrow tachycardia + bundle branch block or metabolic broadening of the QRS complex

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46
Q

Differentials for an irregular broad complex tachycardia?

A

Torsades de pointes

Any cause of a narrow tachycardia + bundle branch block or metabolic broadening of the QRS complex

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47
Q

Differentials for a regular narrow complex tachycardia?

A

Sinoventricular tachycardia
Sinus tachycardia
Atrial flutter

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48
Q

Differentials fro an irregular narrow complex tachycardia?

A

Atrial fibrillation

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49
Q

What makes a tachycardia unstable?

A

Shock
Syncope
Myocardial ischaemia
Heart failure

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50
Q

Management of an unstable tachycardia?

A

Synchronised DC shock
Amiodarone 300 mg IV over 10-20 mins
Repeat shock
Amiodarone 900 mg over 24 hours

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51
Q

Types of atrioventricular heart block?

A

First degree
Second degree: Mobitz type I and Mobitz type II
Third degree/complete

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52
Q

What is first degree AV heart block?

A

AV conduction is delayed

All atrial impulses reach the ventricle

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53
Q

ECG of first degree AV heart block?

A

Bradycardia

Prolonged PR interval

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54
Q

Pathology of second degree AV heart block?

A

Some impulses from the atria fail to conduct to the ventricles -> dropped beat

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55
Q

ECG of Mobitz type I second degree AV heart block?

A

Bradycardia
Progressively lengthening successive PR intervals
Leads to a dropped beat
Cycle then repeats

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56
Q

ECG of Mobitz type II second degree AV heart block?

A

Bradycardia
PR intervals are constant
Some P waves are not conducted to the ventricles

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57
Q

Pathology of third degree/complete heart block?

A

Complete failure of the AV conduction

Atria and ventricles beat independently

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58
Q

ECG of third degree/complete heart block?

A

Bradycardia

Does not vary with exercise

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59
Q

Clinical features of third degree/complete heart block?

A

Bradycardia
Large volume pulse
Cannon waves in the neck
Intensity of S1 varies due to loss of AV synchrony

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60
Q

Management of third degree/complete heart block?

A

Pacemaker

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61
Q

What is a Stokes-Adam attack?

A

Episodes of ventricular asystole

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62
Q

Clinical features of a Stokes-Adam attack?

A 
Sudden LOC
Brief anoxic seizure
Pallor/death like appearance
Characteristic flush when heart starts to beat again
Rapid recovery
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63
Q

Causes of right bundle branch block?

A

Normal variant
Right ventricular hypertrophy
Congenital heart disease
Coronary artery disease

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64
Q

Causes of left bundle branch block?

A

Coronary heart disease
Hypertension
Aortic valve disease
Cardiomyopathy

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65
Q

Pathology of a bundle branch block?

A

Block in the bundle branches
Depolarisation has to go slower through the myocardium
Delayed conduction into the ventricles

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66
Q

ECG of bundle branch block?

A

Broad QRS complex

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67
Q

ECG of a left bundle branch block?

A

WiLLiaM

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68
Q

ECG of a right bundle branch block?

A

MaRRoW

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69
Q

What is cardiac arrest?

A

Sudden and complete loss of cardiac output due to:
Asystole- VT, VF
Loss of mechanical cardiac contraction

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70
Q

Causes of cardiac arrest?

A

Coronary artery disease

VF or VT- often in the first few hours of a MI

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71
Q

Presentation of a cardiac arrest?

A

Unconscious
Pulseless
Breathing may take some time to stop completely
Death

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72
Q

How does ventricular tachycardia cause cardiac arrest?

A

When the ventricular rate is so high that effective mechanical contraction and relaxation doesn’t occur

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73
Q

What is asystole?

A

When there is no contraction due to no electrical activity in the ventricles

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74
Q

Management of asystole?

A

Precordial thump
External cardiac massage
IV atropine or adrenaline
Permanent pacemaker implantation

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75
Q

What is pulseless electrical activity?

A

When there is no effective cardiac output despite the presence of organised electrical activity

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76
Q

Causes of pulseless electrical activity?

A 
Hypovolaemia
Cardiac tamponade
Tension pneumothorax
Hypoxia
Hypokalaemia
Hyperkalaemia
Metabolic causes
Toxins
Thrombosis: coronary or pulmonary
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77
Q

Causes of sudden cardiac death?

A

Coronary artery disease- 85%
Myocardial ischaemia
Acute MI
Prior MI with myocardial scarring

Structural heart disease- 10%
Aortic stenosis
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Arrhythmogenic right ventricular dysplasia
Congenital heart disease
Non-structural heart disease- 5%
Long QT syndrome
Brugada syndrome
Wolff-Parkinson-White syndrome
Adverse drug reaction
Severe electrolyte abnormalities
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78
Q

Baseline hypertension values?

A

140/90

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79
Q

Types of hypertension?

A

Essential- 95%

Secondary- 5%

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80
Q

Lifestyle management for hypertension?

A 
Lose weight
Ideal BMI
Reduce alcohol
Diet low in: salt, saturated fat
Diet high in: fruit, vegetables, oily fish
Exercise
Smoking cessation
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81
Q

When to manage hypertension with drugs?

A

Severe hypertension (>180/>110)
Confirmed stage 2 hypertension (160/100)
Stage 1 hypertension (140/90) if target organ damage/disease, diabetes, 10 year CVD risk > 20%

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82
Q

Drug management for hypertension?

A

Stage 1:
> 55 years or black -> amlodipine (CCB)
< 55 years -> lisinopril (ACEi)

Stage 2:
Amlodipine + lisinopril

Stage 3:
Amlodipine + lisinopril + thiazide diuretic

Stage 4:
Amlodipine + lisinopril + thiazide diuretic + spironolactone

Stage 5:
Specialist referral

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83
Q

Which is the bad lipid to have?

A

LDL

Cholesterol

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84
Q

Management of hyperlipidaemia and hypercholestrolaemia?

A

Statin therapy- atorvastatin
Ezetimibe
Alirocumab

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85
Q

What is the pathological process causing atherosclerosis?

A

Progressive inflammation

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86
Q

Risk factors for atherosclerosis?

A 
Age
Sex
Fix
Smoking
Hypertension
Hypercholestrolaemia
Diabetes mellitus
Haemostatic factors- platelet activation, high plasma fibrinogen concentration, antiphospholipid antibodies
Physical inactivity
Obesity
Alcohol
Deficits of fruit, vegetables
Polyunsaturated fats
Social deprevation
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87
Q

Management of atherosclerosis?

A

Lifestyle advice
Statin therapy
Blood pressure optimisation
Anticoagulation if evidence of vascular disease

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88
Q

Causes of coronary artery disease?

A

Atheroma (most common)
Aortitis
Polyarteritis
Connective tissue disorders

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89
Q

Manifestations of coronary artery disease?

A 
Stable angina
Unstable angina
Myocardial infarction
Heart failure
Arrhythmia
Sudden death
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90
Q

What is acute coronary syndrome?

A

Unstable angina

Myocardial infarction

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91
Q

What is angina?

A

Symptomatic reversible myocardial ischaemia

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92
Q

Causes of angina?

A

Atheroma (main)
Rare: anaemia, coronary artery spasm, aortic stenosis, hypertrophic obstructive cardiomyopathy, arteritis/small vessel disease

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93
Q

Triggers of angina?

A

Exertion
Emotion
Cold weather
Heavy meals

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94
Q

Clinical features of angina?

A

Constricting/heavy discomfort to the chest, jaw, neck, shoulders, arms
Symptoms bought on by exertion
Symptoms reversed by 5 min rest or GTN

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95
Q

Catagories of angina?

A

Typical angina- all 3 features
Atypical angina- 2 features
Non-Anginas chest pain- 0/1 features

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96
Q

Types of angina?

A

Stable angina
Unstable angina
Decubitis angina: when lying flat
Variant angina: due to coronary artery spasm

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97
Q

What is the clinical difference between unstable angina and a NSTEMI?

A

NSTEMI has troponin changes

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98
Q

Investigations in angina?

A

Examination
ECG
Bloods: FBC, U&Es, TFTs, lipids, HbA1c, cardiac enzymes

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99
Q

Management of angina?

A

Treat any exacerbating factors: anaemia, tachycardia, thyrotoxicosis

Secondary prevention of CV disease:
Lifestyle factors
Optimise hypertension and diabetes control
Antiplatelet therapy- 75 mg aspirin
Statin therapy
Consider ACEi

PRN symptomatic relief:
GTN spray or sublingual tablets

Anti-anginal medication:
B-blocker- atenolol
Calcium antagonist- amlodipine
Long acting nitrates- isosorbide mononitrate
Ivabradine (reduce HR and not affect BP)
Ranolazine
Nocorandil

Revascularisation if needed: PCI, CABG

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100
Q

What does PCI stand for?

A

Percutaneous coronary intervention

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101
Q

What does CABG stand for?

A

Coronary artery bypass graft?

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102
Q

Pathology of a myocardial infarction?

A

Myocardial necrosis due to acute occlusion of a coronary artery due to plaque rupture or erosion with superimposed thrombosis

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103
Q

Types of myocardial infarction?

A

STEMI

NSTEMI

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104
Q

What is a STEMI?

A

Acute coronary syndrome with ST elevation or new onset LBBB

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105
Q

What is a NSTEMI?

A

Troponin positive acute coronary syndrome without ST elevation

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106
Q

Symptoms of a myocardial infarction?

A 
Chest pain: central, acute onset, severe, prolonged, radiation
Nausea
Vomiting
Sweatiness
Dyspnoea
Palpitations
Collapse/syncope
Anxiety
Fear of impending death
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107
Q

Signs of a myocardial infarction?

A

Sympathetic activation: pallor, sweating, tachycardia
Vagal activation: vomiting, bradycardia
Impaired myocardial function: hypotension, oliguria, cold peripheries, narrow pulse pressure, raised JVP, third heart sound, quiet first heart sound, diffuse apical impulse, lung crepitations
Tissue damage: fever
Complications e.g. mitral regurgitation, pericarditis

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108
Q

Investigations for a myocardial infarction?

A

ECG
Bloods: FBC, U&Es, glucose, lipid, cardiac enzymes
Chest x-ray
Echocardiography

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109
Q

Diagnosis of a myocardial infarction?

A

Detection of a rise/fall of cardiac biomarker values and:
Symptoms OR new/presumed significant ST or T wave changes OR development of pathological Q waves OR imaging evidence of new loss of viable myocardium OR identification of an intra-coronary thrombus by angiography or post mortem

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110
Q

Management of a STEMI?

A 
Aspirin 300 mg
Ticagrelor 180 mg
Morphine 
Anti-emetic
Primary PCI within 2 hours
If not available in 2 hours -> fibrinolysis
111
Q

Contraindications for PCI?

A

Active internal bleeding
Previous subarachnoid or intracerebral haemorrhage
Uncontrolled hypertension
Recent surgery within a month
Recent trauma
High probability of an active peptic ulcer
Pregnancy

112
Q

Management of a NSTEMI?

A

High flow oxygen
Analgesia
Nitrates
Aspirin 300 mg
High risk patients: fondaparinux, another antiplatelet, IV nitrate, oral b-blocker
Low risk (more likely an unstable angina): monitor

113
Q

Secondary prevention of myocardial infarction?

A 
Smoking cessation
Diet
Statin therapy
Optimise blood pressure
Optimise diabetes
Aspirin and clopidogrel
B-blockers
Coronary revascularisation
Implantable cardiac defibrillator
114
Q

Complications of myocardial infarction?

A 
Arrhythmias
Cardiac arrest
Ischaemia
Acute circulatory failure
Pericarditis
Mechanical defaults
Embolism
Impaired ventricular function, remodelling and ventricular aneurysm
Cardiac tamponade
115
Q

What is heart failure?

A

When the heart cannot maintain adequate output for the body’s requirements

116
Q

What is cardiac output determined by?

A

Preload
Afterload
Myocardial contractility

117
Q

Clinical features of left heart failure?

A 
Rised JVP
Pulmonary oedema
Cardiomegaly
Pleural effusions
Pitting oedema
118
Q

Clinical features of right heart failure?

A

Raised JVP
Hepatomegaly
Ascites
Severe peripheral pitting oedema

119
Q

Systolic heart failure?

A

Inability of the ventricle to contract normally -> reduced cardiac output
Ejection fraction < 40%

120
Q

Causes of systolic heart failure?

A

Ischaemic heart disease
Myocardial infarction
Cardiomyopathy

121
Q

Diastolic heart failure?

A

Inability of the ventricle to relax and fill normally -> increased filling pressure
Ejection fraction > 50%

122
Q

Causes of diastolic heart failure?

A 
Ventricular hypertrophy
Constrictive pericarditis
Cardiac tamponade
Restrictive cardiomyopathy
Obesity
123
Q

How to assess severity of heart failure?

A

New York classification of heart failure

124
Q

Management of acute heart failure?

A 
Sit the patient upright
High flow oxygen
IV access
ECG monitoring
Treat any arrhythmias
Diamorphine IV
Furosemide IV
GTN spray or SL tablets
Nitrate infusion if BP > 100
Treat as cariogenic shock if BP < 100
125
Q

Management of chronic heart failure?

A 
Lifestyle
Treat cause
Treat exacerbating factors
Avoid exacerbating factors
Annual flu vaccine and one-off pneumococcal vaccine
Diuretics (loop)
ACEi (ARB if a cough)
B-blockers
Mineralocorticoid receptor antagonists
Digoxine
Vasodilators
Implantable cardiac defibrillator
Coronary revascularisation
Heart transplant
Ventricular assist devices (VADs)
126
Q

Causes of peripheral arterial disease?

A

Atheroma is the main cause

127
Q

Risk factors for peripheral arterial disease?

A

Smoking
Diabetes mellitus
Hyperlipidaemia
Hypertension

128
Q

Clinical features of peripheral arterial disease?

A

Cerebral: TIA, amaurosis fugal, vertobrobasilar insufficiency
Renal: hypertension, renal failure
Mesenteric arteries: mesenteric angina, acute intestinal ischaemia
Limbs: intermittent claudication, critical limb ischaemia, acute limb ischaemia

129
Q

What happens if the onset of peripheral arterial disease is slow?

A

Collaterals will develop

130
Q

Clinical features of limb peripheral arterial disease?

A 
Reduced/absent pulses
Bruits
Reduced skin temperature
Pallor on elevation
Rubor on dependency
Superficial veins that fill sluggishly and empty on minimal elevation
Muscle-wasting
Dry/thin/brittle skin and nails
Hair loss
Ankle-brachial pressure index (ABPI) < 1
131
Q

What is intermittent claudication?

A

Ischaemic pain affecting the legs on exertion

132
Q

Management of intermittent claudication?

A

Smoking cessation
Regular exercise
Antiplatelet agent
Cholesterol reduction: diet, statin therapy
Diagnose and treat diabetes if present
Diagnose and treat other conditions e.g. hypertension, anaemia, heart failure

133
Q

What is critical limb ischaemia?

A

Rest (night) pain requiring opiate analgesia and/or tissue loss for > 2 weeks
ABPI < 0.5

134
Q

Causes of acute limb ischaemia?

A

Thrombotic occlusion of a pre-existing stenotic arterial segment
Thromboembolism
Trauma
Iatrogenic

135
Q

Clinical features of acute lumbar ischaemia?

A 
Pain
Pallor
Pulselessness
Perishing cold
Paraesthesia
Paralysis
136
Q

Management of acute limb ischaemia?

A

Discuss with vascular surgeon
IV heparin
If due to thrombosis: IV heparin, anti platelet agents, high-dose statins, IV fluids, correct anaemia, oxygen, sometimes prostaglandins
If due to embolism: revascularisation, surgical embolectomy, local thrombolysis
Irreversible ischaemia: early amputation, palliative care

137
Q

What is an aortic aneurysm?

A

Abnormal dilation of the aortic lumen

138
Q

Locations of aortic aneurysm?

A

Abdominal
Dilated thoracic e.g. Marfan’s
Saccular thoracic e.g. atheromatous, syphilitic

139
Q

Types of aortic aneurysm?

A 
Non-specific
Marfan's syndrome
Aortitis
Thoracic aortic aneurysms
Abdominal aortic aneurysms
140
Q

Who gets abdominal aortic aneurysms?

A

Male

Older

141
Q

Presentation of abdominal aortic aneurysms?

A 
Incidental
Pain
Thromboembolic complications
Compression of surrounding structures: bowel obstruction, vomiting, oedema, DVT
Rupture
142
Q

Investigations for an abdominal aortic aneurysm?

A

Ultrasound

CT

143
Q

Management of an abdominal aortic aneurysm?

A

Surgical repair- open or endovascular aneurysm repair (EVAR)

144
Q

What is aortic dissection?

A

When the wall of the aorta is damaged and it splits creating a false lumen and true lumen

145
Q

Types of aortic dissection?

A

Type A

Type B

146
Q

What is a type A aortic dissection?

A

In the aortic arch and proximal descending aorta

High risk of rupture

147
Q

What is a type B aortic dissection?

A

In the descending aorta

Lower risk of rupture

148
Q

Risk factors for aortic dissection?

A 
Hypertension
Aortic atherosclerosis
Aortic coarctation
Collagen disorders
Fibromuscular displasia
Previous aortic surgery
Pregnancy
Trauma
Iatrogenic
149
Q

Clinical features of aortic dissection?

A

Tearing chest pain
Collapse
Hypertension (unless a major haemorrhage)
Asymmetry of brachial, carotid or femoral pulses

150
Q

Investigations for aortic dissection?

A 
Chest x-ray
ECG
Dopple echocardiography
Transoesophageal echocardiography
CT and MRI angiography
151
Q

Management of aortic dissection?

A

Analgesia
Anti-hypertensives
Type A -> emergency surgery to replace the ascending aorta
Type B -> treat medically with B-blockers

152
Q

What is the pathology of varicose veins?

A

Valves in the veins are incompetent so blood can pass from the deep to superficial veins -> venous hypertension, dilation of the superficial veins

153
Q

Risk factors for varicose veins?

A 
Prolonged standing
Obesity
Pregnancy
FHx
Contraceptive pill
154
Q

Symptoms of varicose veins?

A 
Pain
Cramps
Tingling
Heaviness
Restless legs
155
Q

Signs of varicose veins?

A 
Oedema
Eczema
Ulcers
Haemosiderin
Haemorrhage
Phlebitis
Atrophie blanche
Lipodermatosclerosis
156
Q

How to do a venous examination for varicose veins?

A 
Inspection
Palpation
Tap test
Auscultation
Soppler
Trendelenburg's test
157
Q

Management of varicose veins?

A 
Avoid prolonged standing
Elevate legs where possible
Support stockings
Weight loss
Regular walks
Radiofrequency ablation/endovenous laser ablation/surgery
158
Q

Pathology of acute rheumatic fever?

A

Immune mediated delayed response to a group A streptococci infection

159
Q

Clinical features of acute rheumatic fever?

A 
Sydenham's chorea
Prior sore throat
Carditis
Dyspnoea
Syncope
Pericarditis
Carey Coombs murmur
Aortic/mitral regurgitation
Heart block
Subcutaneous nodules
Flitting polyarthritis and arthralgia
Oedema
Erythma marginatum
160
Q

Criteria used to diagnose acute rheumatic fever?

A

Jones criteria

161
Q

Management of acute rheumatic fever?

A 
Benzylpenicillin
Bed rest until CRP is normal
Supportive therapy
Aspirin to control inflammatory symptoms
Haloperidol or diazepam for chorea
162
Q

How many people who are affected by rheumatic fever with carditis develop chronic valvular disease?

A

At least 50%

163
Q

What is the most common valve affected by rheumatic fever?

A

Mitral valve > aortic > tricuspid > pulmonary

164
Q

What is the pathology of chronic valvular disease following rheumatic fever?

A

Progressive fibrosis

Once the valve is damaged -> altered haemodynamic stresses perpetuate and extend the damage

165
Q

Causes of mitral stenosis?

A

Usually rheumatic fever
Calcification (older people)
Rare form of congenital mitral stenosis

166
Q

Pathology of mitral stenosis?

A

Reduced blood flow from left atrium to ventricle
Left atrium pressure rises
Pulmonary venous congestion and dyspnoea
Dilation and hypertrophy of the left atrium
Heart rate increases to drive left ventricle filling
Shorter diastole where the mitral valve is open
Further rise in atrial pressure
Situations needing increased cardiac output (exercise, pregnancy) -> higher left atrium pressure

167
Q

What conditions can result from pathological changes in mitral stenosis?

A

Atrial fibrillation due to progressive dilation of the left atrium
Pulmonary hypertension due to rise in left atrial pressure

168
Q

Pathological effects of mitral stenosis?

A

Pulmonary congestion
Right heart failure
Low cardiac output
Atrial fibrillation

169
Q

Symptoms of mitral stenosis?

A 
Dyspnoea
Fatigue
Oedema
Ascites
Palpitations
Haemoptysis
Cough
Chest pain
Thromboembolic complications
170
Q

Signs of mitral stenosis?

A 
Atrial fibrillation
Mitral facies
Loud first heart sound
Mid-diastolic murmur (bell at apex)
Crepitations
Pulmonary oedema
Effusions
Right ventricular heave
Loud P2 (pulmonary hypertension)
171
Q

Investigations for mitral stenosis?

A

ECG: right ventricular hypertrophy (tall R waves in V1-V3)
Chest x-ray: dilated LA, signs of pulmonary venous congestion
Echocardigraphy: thick immobile cusps, reduced valve area, enlarged LA, reduced rate of diastolic filling of LV
Doppler
Cardiac catheterisation

172
Q

Management of mitral stenosis?

A 
Rate control if in AF
Anticoagulation
Diuretics (pulmonary congestion)
Balloon valvuoplasty or valve replacement
Yearly follow ups as stenosis can recur
173
Q

Causes of mitral regurgitation?

A

Rheumatic disease
Mitral valve prolapse
Dilation of the left ventricle and mitral valve ring e.g. coronary artery disease, cardiomyopathy
Damage to valve cusps and chord e.g. rheumatic heart disease, endocarditis
Ischaemia/infarction of the papillary muscle
Myocardial infarction
Following mitral valvotomy/valvuoplasty

174
Q

Pathology of chronic mitral regurgitation

A

Gradual dilation of the left atrium with little increase in pressure -> few symptoms
Left ventricle slowly dilates too and ventricle and atrium pressures increase very gradually

175
Q

Does acute mitral regurgitation cause symptoms?

A

Yes

176
Q

Pathological processes in mitral regurgitation?

A 
Pulmonary venous congestion
Low cardiac output
Atrial fibrillation
Increased stroke volume
Right heart failure
177
Q

Symptoms of mitral regurgitation?

A 
Dyspnoea
Fatigue
Palpitation
Oedema
Ascites
178
Q

Signs of mitral regurgitation?

A

Atrial fibrillation/flutter
Cardiomegaly
Apical pansstolic murmur
Soft S1
Apical S3
Signs of pulmonary venous congestion- crepitations, pulmonary oedema, effusions
Signs of pulmonary hypertension and right heart failure

179
Q

Investigations for mitral regurgitation?

A

ECG: left atrium and ventricle hypertrophy
Chest x-ray: enlarged left atrium and ventricle, pulmonary venous congestion, pulmonary oedema
Echocardiography: dilated left atrium and ventricle, dynamic left ventricle, structural abnormalities e.g. prolapse
Doppler: detects and quantifies regurgitation
Cardiac catheterisation

180
Q

Management of mitral regurgitation?

A 
Rate control if fast AF
Anti-coagulate if AF
Diuretics for symptoms
Anti-hypertensives
Regular review
Valve replacement/repair if: worsening symptoms, progressive cardiomegaly, echocardiographic evidence of deteriorating left ventricle function
181
Q

Causes of aortic stenosis?

A

Infants/children/adolescents:
Congenital aortic stenosis
Congenital subvalvular aortic stenosis
Congenital supravalvular aortic stenosis

Young adults/middle aged:
Calcification and fibrosis of congenitally bicuspid aortic valve
Rheumatic aortic stenosis

Middle aged/elderly:
Senile degenerative aortic stenosis
Calcification of bicuspid valve
Rheumatic aortic stenosis

182
Q

Pathology of aortic stenosis?

A

Left ventricle hypertrophies and coronary blood flow may be inadequate here
Fixed outflow obstruction limits increase in cardiac output required on exercise
Pulmonary oedema

183
Q

Symptoms of aortic stenosis?

A 
Exertional dyspnoea
Exertional syncope
Angina
Sudden death
Episodes of acute pulmonary oedema
184
Q

Signs of aortic stenosis?

A 
Ejection systolic murmur
Slow rising carotid pulse
Thrusting apex beat
Narrow pulse pressure
Signs of pulmonary venous congestion e.g. crepitations
185
Q

Investigations for aortic stenosis?

A

ECG: left ventricular hypertrophy, LBBB
Chest x-ray: normal, enlarged left ventricle, dilated ascending aorta, calcified valve
Echocardiography: calcified valve, hypertrophied left ventricle
Doppler: severity, associated aortic regurgitation
Cardiac catheterisation: CHD

186
Q

When do you manage aortic stenosis?

A

When it become symptomatic

187
Q

Management for aortic stenosis?

A

Prompt

Aortic valve replacement: surgery or TAVI

188
Q

Causes of aortic regurgitation?

A

Congenital: bicuspid valve or disproportionate cusps
Acquired: rheumatic disease, infective endocarditis, trauma, aortic dilation

189
Q

Signs of aortic regurgitation?

A 
Large volume pulse
Collapsing pulse
Low diastolic pressure
Increased pulse pressure
Bounding peripheral pulses
Carotid pulsation (Corrigan's sign)
Capillary visual pulsation (Quincke's sign)
Femoral bruit (Duroziez's sign)
Pistol shot over femoral arteries (Traube's sign)
Head nodding (de Musset's sign)
Early diastolic murmur
Austin Flint murmur
Displaced, heaving apex beat
Pre-systolic impulse
Fourth heart sound
Crepitations
190
Q

Investigations for aortic regurgitation?

A

ECG: later LV hypertrophy, T wave inversion
Chest x-ray: cardiac dilation, aortic dilation, features of left heart failure
Echocardiography: dilated LV, hyper dynamic LV, reflux, fluttering anterior mitral leaflet
Cardiac catheterisation: dilated LV, aortic regurgitation, dilated aortic root

191
Q

Management of aortic regurgitation?

A

ACE inhibitors
Echocardiogram every 6-12 months
Surgery if: severe enlarged ascending aorta, increasing symptoms, enlarging LV, deteriorating LV function, IE

192
Q

Causes of tricuspid stenosis?

A

Rheumatic fever

193
Q

Symptoms of tricuspid stenosis?

A

Hepatic discomfort

Peripheral oedema

194
Q

Signs of tricuspid stenosis?

A 
Raised JVP
Hepatomegaly
Ascites
Peripheral pitting oedema
Mid-diastolic murmur
195
Q

Investigations for tricuspid stenosis?

A

Echocardiography with doppler

196
Q

Management of tricuspid stenosis?

A

Diuretics

Valve repair

197
Q

Causes of tricuspid regurgitation?

A 
Rheumatic heart disease
Endocarditis
Ebstein's congenital anomaly
Right ventricle dilation due to chronic left heart failure
Right ventricular infarction
Pulmonary hypertension
198
Q

Symptoms of tricuspid regurgitation?

A 
Usually non-specific
Fatigue
Oedema
Hepatic enlargement
Hepatic pain on exertion
Ascites
199
Q

Signs of tricuspid regurgitation?

A 
Giant wave in the JVP
Pansystolic murmur at left sternal edge
Pulsatile liver
Right ventricular heave
Ascites
200
Q

Investigations for tricuspid regurgitation?

A

Echocardiography: dilated RV, thickened valve leaflets (rheumatic), vegetations (endocarditis)

201
Q

Management of tricuspid regurgitation?

A

Correct the cause of right ventricular overload
Diuretic and vasodilator in congestive cardiac failure
Tricuspid valve replacement if rheumatic damage

202
Q

What is infective endocarditis?

A

Microbial infection of a heart valve, lining of a cardiac chamber/blood vessel or congenital abnormality

203
Q

Causes of infective endocarditis?

A

Bacterial
Fungal
Other: SLE, malignancy

204
Q

Risk factors for infective endocarditis?

A 
Skin breaches
Renal failure
Immunosuppression
Diabetes mellitus
Aortic or mitral valve disease
Tricuspid valves in IVDU
Coarctation
Patent ductus arteriosis
Ventricular septal defects
Prosthetic valve
205
Q

Clinical features of infective endocarditis?

A

Septic signs of infection: fever, riggers, night sweats, malaise, weight loss, anaemia, splenomegaly, clubbing
Cardiac lesion: new murmur, change in murmur
Immune complex deposition: vasculitis, microscopic haematuria, glomerulonephritis, AKI, Roth spots, splinter haemorrhages, Osler’s nodes
Embolic signs: abscesses in organ (Janeway lesions on skin)

206
Q

Investigations for infective endocarditis?

A 
Bloods: FBC, U&amp;Es, CRP, ESR, WCC
Blood culture
Urinalysis
Echocardiography
ECG
Chest x-ray
207
Q

When do you have to presume something is endocarditis?

A

Fever + new murmur

Unless proven otherwise

208
Q

Criteria for diagnosing infective endocarditis?

A

Duke criteria

2 major or 1 major +3 minor or 5 minor

209
Q

Management of infective endocarditis?

A

Antibiotic therapy
Surgery, if: heart failure, valvular obstruction, repeated emboli, fungal IE, persistent bacteraemia, myocardial abscess, unstable infected prosthetic valve

210
Q

Causes of congenital heart disease?

A

Maternal rubella infection
Maternal alcohol misuse
Maternal lupus erythematosus
Genetic/chromosomal abnormalities

211
Q

Clinical features of congenital heart disease at birth/neonatal?

A

Cyanosis

Heart failure

212
Q

Clinical features of congenital heart disease in infancy/childhood?

A 
Cyanosis
Heart failure
Arrhythmia
Murmur
Failure to thrive
213
Q

Clinical features of congenital heart disease in adolescence/adulthood?

A 
Heart failure
Murmur
Arrhythmia
Cyanosis
Hypertension
Late consequences of previous cardiac surgery
214
Q

Congenital heart disease causes of central cyanosis and digital clubbing?

A

Neonate: transposition of the great arteries

Older children: severe pulmonary stenosis or pulmonary vascular disease

215
Q

Congenital heart disease causes of growth retardation?

A

Large left-to-right shunts

216
Q

Congenital heart disease causes of syncope?

A

Due to arrhythmias

217
Q

What causes pulmonary hypertension in congenital heart disease?

A

When the pulmonary flow is persistently raised (left-to-right shunt) -> increased pulmonary resistance -> pulmonary hypertension

218
Q

What is Eisenmenger’s syndrome?

A

When a shunt reverses in severe pulmonary hypertension

219
Q

What is persistent ductus arteriosus?

A

When the hole between the aorta and pulmonary artery remains open

220
Q

Clinical features of persistent ductus arteriosus?

A

Retarded growth and development
Cardiac failure -> dyspnoea
Continuous murmur maximal in second left intercostal space
Thrill
Increased pulse volume
Eisenmenger’s syndrome: murmur quieter/only in systole/disappear

221
Q

Management of persistent ductus arteriosus?

A

Neonatal period: prostaglandin synthetase inhibitor
Closed by an implantable occlusive device at cardiac catheterisation
If impaired lung perfusion: keep ductus open with prostaglandin treatment

222
Q

What is coarctation of the aorta?

A

Narrowing of the aorta in the region where the ductus arteriosus joins

223
Q

Clinical features of coarctation of the aorta?

A

Cardiac failure in the newborn
Headache
Leg weakness and cramps
Upper body hypertension and normal/hypotension in lower body
Femoral pulses are weak and delayed (compared to radial)
Ejection click and systolic murmur in aortic region
Collateral formation -> bruits

224
Q

Investigations for coarctation of the aorta?

A

Chest x-ray: changes appear later on
MRI (best imaging here)
ECG: LV hypertrophy
Echocardiography: LV hypertrophy

225
Q

Management of coarctation of the aorta?

A

Surgical correction
Stenosis can re-occur with growth -> balloon dilation and stunting
Long term follow up

226
Q

What is atrial septal defect?

A

Hole between the two atria
Blood shunts from the left atrium to the right atrium
More blood going through the right side of the heart -> enlargement of right heart and pulmonary arteries

227
Q

Clinical features of atrial septal defect?

A 
Most are aysmptomatic
Dyspnoea
Chest infections
Cardiac failure
Arrhythmias: especially AF
228
Q

Investigations for atrial septal defect?

A

Chest x-ray: enlargement of heart and pulmonary artery
ECG: incomplete RBBB
Echocardiography: defect, RV dilation, RV hypertrophy, pulmonary artery dilation
Transoesophageal echocardiography

229
Q

Management of atrial septal defect?

A

Surgical closure at cardiac catheterisation with an implantable closure device

230
Q

When not to surgically close an atrial septal defect?

A

Pulmonary hypertension, shunt reversal

231
Q

What is a ventricular septal defect?

A

Hole between the two ventricles

Either congenital or acquired (post MI etc.)

232
Q

Clinical features of a ventricular septal defect?

A

Pansystolic murmur

Cardiac failure in infants

233
Q

Investigations for ventricular septal defect?

A

Chest x-ray
ECG: bilateral ventricular hypertrophy
Doppler echocardiography: to predict which smaller defects might close spontaneously

234
Q

Management of ventricular septal defect?

A

Small -> no treatment
Infant cardiac failure: digoxin, diuretics
Persistent failure -> surgical repair (not in Eisenmenger’s)
Eisenmenger’s syndrome: heart-lung transplant

235
Q

What is Tetralogy of Fallot?

A 
Combination of:
Pulmonary stenosis
Overriding aorta
Ventricular septal defect
Right ventricular hypertrophy
Causes high RV pressure and right-to-left shunting through septal defect
236
Q

Clinical features of Tetralogy of Fallot?

A 
Cyanosis
Stunted growth
Digital clubbing
Polycythaemia
Faloot's sign
Loud ejection systolic murmur in the pulmonary area
237
Q

Investigations for Tetralogy of Fallot?

A

ECG: RV hypertrophy

Chest x-ray: small pulmonary artery, boot shaped heart

238
Q

Management of Tetralogy of Fallot?

A

Surgical correction of pulmonary stenosis
Surgical closure of ventricular septal defect
Follow up
Implantable defibrillation sometimes needed in adulthood

239
Q

Effects of cardiac surgery in adulthood?

A

Correction of coarctation -> hypertension
Mustard repair of great vessel transposition -> RV failure
Atrial surgery -> atrial arrhythmias
Ventricle scars -> ventricular arrhythmias

240
Q

What is cardiomyopathy?

A

Disease of the myocardium

241
Q

Causes of cardiomyopathy?

A

Inherited
Infective
Toxic
Idiopathic

242
Q

Types of cardiomyopathy?

A

Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Arrhythmic right ventricular cardiomyopathy

243
Q

What is dilated cardiomyopathy?

A

Dilation and impaired contraction of the left ventricle and often the right ventricle
Valve rings are dilated -> mitral and tricuspid incompetence

244
Q

Causes of dilated cardiomyopathy?

A 
Alcohol
Hypertension
Chemotherapeutics
Haemochromatosis
Peri- or post-partum
Thyrotoxicosis
Congenital
Late autoimmune react to viral myocarditis
245
Q

Symptoms of dilated cardiomyopathy?

A 
Heart failure
Asymptomatic
Sporadic chest pain
Fatigue
Dyspnoea
246
Q

Signs of dilated cardiomyopathy?

A 
Tachycardia
Hypotension
Raised JVP
Displaced and diffuse apex beat
S3 gallop
Mitral/tricuspid regurgitation
Pleural effusion
Oedema
Jaundice
Hepatomegaly
Ascites
247
Q

Investigations for dilated cardiomyopathy?

A

ECG
Echocardiography
Cardiac MRI

248
Q

Management of dilated cardiomyopathy?

A 
Bed rest
Control heart failure
B-blockers
ACE inhibitors
Anti-coagulation
Biventricular pacing
Cardiac transplantation
249
Q

What is hypertrophic cardiomyopathy?

A

Left ventricular hypertrophy

Left ventricular outflow obstruction

250
Q

Cause of hypertrophic cardiomyopathy?

A

Autosomal dominant inheritance

251
Q

Symptoms of hypertrophic cardiomyopathy?

A

Angina on effort
Dyspnoea on effort
Syncope on effort
Sudden death

252
Q

Signs of hypertrophic cardiomyopathy?

A 
Jerky pulse
Palpable left ventricular hypertrophy
Double impulse at apex
Mid-systolic murmur at the base
Pansystolic murmur at the apex
253
Q

Investigations for hypertrophic cardiomyopathy?

A

ECG: LV hypertrophy, progressive T wave inversion, deep Q waves, AF, WPW syndrome, ventricular ectopics, VT
Echocardiography: asymmetrical septal hypertrophy, small LV cavity with hyper contractile properties, mid-systolic closure of aortic valve, systolic anterior movement of mitral valve
MRI
Cardiac catheterisation: assess severity, CAD, mitral regurgitation
Exercise test

254
Q

What helps stratify risk and severity in hypertrophic cardiomyopathy?

A

Cardiac catheterisation

Exercise test

255
Q

Management of hypertrophic cardiomyopathy?

A 
B-blockers or verapamil for symptoms
Amiodarone for arrhythmias
Anti-coagulation for paroxysmal AF or systemic emboli
Septal myomectomy
Implantable defibrillator
256
Q

What is restrictive cardiomyopathy?

A

When ventricular filling is impaired as the ventricles are too stiff -> high atrial pressures, atrial hypertrophy/dilation, AF

257
Q

Causes of restrictive cardiomyopathy?

A 
Amyloidosis
Idiopathic
Haemochomatosis
Sarcoidosis
Scleroderma
Löffler's eosinophilic endocarditis
Endomyocardial fibrosis
258
Q

Clinical features of restrictive cardiomyopathy?

A 
Like constrictive pericarditis
Right heart failure
Raised JVP
Hepatomegaly
Ascites
Oedema
259
Q

Investigations for restrictive cardiomyopathy?

A

Echocardiography
MRI
Cardiac catheterisation

260
Q

Management of restrictive cardiomyopathy?

A

Treat the underlying cause

261
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A

When areas of right ventricular myocardium are replaced with fibrous and fatty tissue

262
Q

Risks of arrhythmogenic right ventricular cardiomyopathy?

A

Ventricular arrhythmias
Sudden death
Right sided heart failure

263
Q

Investigations for arrhythmogenic right ventricular cardiomyopathy?

A

ECG: slightly broad QRS, inverted T waves in right precordial leads
MRI

264
Q

Management of arrhythmogenic right ventricular cardiomyopathy?

A

Implantable cardiac defibrillator

265
Q

What is pericarditis?

A

Inflammation of the pericardium

266
Q

Causes of pericarditis?

A

Idiopathic
Secondary to: viruses, bacteria, fungi, autoimmune systemic diseases, drugs, metabolic, trauma, surgery, malignancy, radiotherapy

267
Q

Clinical features of pericarditis?

A

Central chest pain worse on inspiration/lying flat
Pain may be relieved sitting forward
Pericardial friction rub
Evidence of pericardial effusion: dyspnoea, chest pain, local structures being compressed, bronchial breathing at left base, muffled heart signs
Evidence of cardiac tamponade: tachycardia, hypotension, pulses paradoxes, raised JVP, Kussmaul’s sign, muffled heart signs
Fever

268
Q

Investigations for pericarditis?

A

ECG: concave (saddle shaped) ST segment elevation
Bloods: FBC, U&Es, ESR, cardiac enzymes
Chest x-ray: cardiomegaly
Echocardiography: if you suspect an effusion

269
Q

Management of pericarditis?

A

NSAIDs or aspirin with gastric protection
Colchicine
Rest
Treat the cause
Treat pericardial effusion/cardiac tamponade

270
Q

What is constrictive pericarditis?

A

When the heart is encased in a rigid pericardium

271
Q

Causes of constrictive pericarditis?

A

Idiopathic
TB
After any pericarditis

272
Q

Clinical features of constrictive pericarditis?

A 
Similar to right heart failure
Raised JVP
Kussmaul's sign
Soft, diffuse apex beat
Quiet heart sounds
D3
Diastolic pericardial knock
Hepatosplenomegaly
Ascites
Oedema
273
Q

Investigations for constrictive pericarditis?

A

Chest x-ray: small heart, pericardial calcification
CT/MRI: to distinguish form restrictive cardiomyopathy
Echocardiography
Cardiac catheterisation

274
Q

Management of constrictive pericarditis?

A

Surgical excision

Year 4 Semester 2 (3 decks)

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