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Final Year > Cardiology > Flashcards

Cardiology Flashcards

1
Q

How does a pacemaker work?

A

Delivers controlled electrical impulses to specific areas of the heart to restore normal electrical activity and improve heart function

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2
Q

How long do pacemakers last?

A

Battery lasts approx. 5y

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3
Q

What are CI with pacemakers?

A

Diathermy in surgery, tens machines, mri scans

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4
Q

List indications for a pacemaker

A

Symptomatic bradycardia, mobitz type 2 av block, 3rd degree heart block (risk of asystole), severe heart failure (use biventricular pacemakers), HCOM

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5
Q

Describe single chamber pacemakers

A

Leads in a single chamber– In RA if av conduction normal and issue in sino atrial node
-In RV if AV conduction abnormal

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6
Q

Describe dual chamber pacemakers

A

Leads in RA and RV– Synchronises conduction

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7
Q

Describe biventricular/triple chamber/CRT pacemakers

A

Leads in RA, RV and LV
Used in HF

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8
Q

Describe ICDs

A

Continuously monitor heart and can give shock to cardiovert patient if in VF/VT

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9
Q

Describe ECG changes with pacemakers

A

Pacemaker intervention = Sharp vertical line on all leads on the trace
Line before each P wave = Lead in atria
Line before QRS complex = Lead in ventricles

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10
Q

What is cor pulmonale?

A

Right sided HF Caused by respiratory disease

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11
Q

What is the pathophysiology of cor pulmonale?

A

Increased pressure in arteries (pulmonary HTN) results in right heart not pumping blood out of ventricle into PA– Back pressure in RA, vena cava, and systemic venous system

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12
Q

What are the causes of cor pulmonale?

A

COPD most common, PE, ILD, CF, primary pulmonary HTN

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13
Q

Outline presentation of cor pulmonale

A

Early– Asymptomatic or SOB
Peripheral oedema, increased breathlessness on exertion, syncope, chest pain

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14
Q

What are the signs of cor pulmonale on examination?

A

Hypoxia, cyanosis, raised JVP, peripheral oedema, 3rd heart sound, pansystolic murmur (tricuspid regurgitation), hepatomegaly (pulsatile in tricuspid regurgitation)

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15
Q

Outline management of cor pulmonale

A

Treat symptoms and underlying cause
Long term oxygen therapy

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16
Q

Outline prognosis of cor pulmonale

A

Poor unless reversible underlying cause

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17
Q

What is an arrhythmia?

A

Abnormal heart rhythm resulting from interruption to normal electrical signal that coordinate contraction of heart muscle

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18
Q

List the shockable rhythms

A

Ventricular tachycardia
Ventricular fibrillation

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19
Q

List the non-shockable rhythms

A

PEA
Asystole

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20
Q

How to manage unstable tachycardia

A

Consider 3 stacked shocks
Consider amiodarone infusion

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21
Q

What are the types of stable tachycardia?

A

Narrow complex or broad complex

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22
Q

What is a narrow complex tachycardia?

A

QRS complex less than 0.12s duration
Af, atrial flutter, SVT

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23
Q

How do you manage AF?

A

Rate control– BB, CCB (Diltiazam)
Rhythm control

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24
Q

How do you manage atrial flutter?

A

BB

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25
Q

How do you manage SVT?

A

Vagal manoeuvres
Adenosine

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26
Q

What is a broad complex tachycardia?

A

QRS complex greater than 0.12s

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27
Q

How do you manage ventricular tachycardia or a tachycardia trace you are unsure of?

A

Amiodarone infusion

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28
Q

How do you manage an SVT with bundle branch block?

A

Vagal manoeuvres and adenosine

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29
Q

What is atrial flutter?

A

Electrical activity passes through atrial flutter as re-entrant rhythm
Extra electrical pathway in atria
Atrial contraction at 300bpm
Signal goes into ventricles every second lap due to long refractory period of av node causing ventricular contraction of 150bpm

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30
Q

What is the ECG characteristic of atrial flutter?

A

Sawtooth appearance
P wave after p wave

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31
Q

Which conditions are associated with atrial flutter?

A

Hypertension
IHD
Cardiomyopathy
Thyrotoxicosis

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32
Q

What is the management of atrial flutter?

A

Rate control (BB)
Rhythm control (cardioversion)
Anticoagulation using CHA2DS2-VASc
Radio frequency ablation can be a permanent solution

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33
Q

What is a prolonged QT interval?

A

Start of QRS complex to end of t wave
Men— More than 440ms
Women— More than 460ms

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34
Q

What is the pathophysiology of a prolonged QT interval?

A

Represents prolonged repolarisation of the myocyte after a contraction
Results in spontaneous depolarisation in some muscle cells= Afterdepolarisations= Spread throughout the ventricles causing contraction before proper repolarisation
Torsades de pointes= When this leads to recurrent contractions without normal repolarisation

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35
Q

What is Torsades de pointes?

A

Polymorphic VT
Height of QRS complex gets progressively smaller then larger

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36
Q

What is the progression of TdP?

A

Terminates spontaneously and reverts to sinus rhythm
Or
Progresses to VT and potentially CA

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37
Q

What are the causes of prolonged QT?

A

Long QT syndrome (inherited)
Meds- Antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide ABs
Electrolytes- Hypokalaemia, hypomagnesaemia, hypocalcaemia

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38
Q

Outline management of prolonged QT interval

A

Stop meds that prolong QT interval
Correct electrolytes
BBs
Pacemakers/implantable cardioverter defibrillators

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39
Q

Outline Acute management of TdP

A

Correct underlying cause
Magnesium infusion
Defibrillation if VT

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40
Q

What are Ventricular ectopics?

A

Premature ventricular beats caused by random electrical discharges outside the atria

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41
Q

What is a key characteristic of Ventricular ectopics?

A

Patients complain of random extra or missed beat
Common at all ages and in healthy patients
More common if pre-existing heart conditions (IHD or HF)

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42
Q

What do Ventricular ectopics look like on ECG?

A

Isolated, random, abnormal, broad QRS complexes on otherwise normal ECG

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43
Q

What is bigeminy?

A

When every other beat is a Ventricular ectopic

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44
Q

What does a bigeminy ECG look like?

A

Normal beat, followed immediately by an ectopic beat, then normal beat, then ectopic, etc…

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45
Q

What is repolarisation?

A

Recovery period before muscle cells are ready to depolarise again

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46
Q

What is depolarisation?

A

Electrical process that leads to heart contraction

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47
Q

What is 1st degree heart block?

A

Delayed conduction through the AV node- Every P wave is followed by a QRS complex
PR interval >0.2s

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48
Q

Outline Mobitz type 1 (Wenckebach phenomenon) heart block

A

Conduction through AV node takes progressively longer until it finally fails, then resets and starts again
Increasing PR interval until a P wave not followed by QRS complex
PR interval returns to normal, cycle repeats

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49
Q

Outline Mobitz type 2 heart block

A

Intermittent failure of conduction through AV node, with absence of QRS complex
Absence of QRS complexes following P waves
Set ratio of p waves to QRS complexes
PR interval normal
Risk of asystole

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50
Q

Outline 3rd degree heart block

A

Complete heart block
No relationship between the P waves and QRS complexes
Significant risk of asystole

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51
Q

List causes of Bradycardia

A

BBs
Heart block
Sick sinus syndrome

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52
Q

What is sick sinus syndrome?

A

Conditions that cause dysfunction in sino Atrial node
Caused by- Idiopathic degenerative fibrosis of sinoatrial node
Results in- Sinus bradycardia, sinus arrhythmia, prolonged pauses

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53
Q

What is asystole?

A

Absence of electrical activity in heart

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54
Q

What increases risk of asystole?

A

Mobitz type 2
3rd degree heart block
Previous asystole
Ventricular pauses longer than 3s

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55
Q

Outline management of asystole

A

IV atropine
Inotropes (adrenaline)
Temporary cardiac pacing
Permanent implantable pacemaker

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56
Q

What are the options for temporary cardiac pacing?

A

Transcutaneous (pads on chest)
Transvenous (catheter through vein to stimulate heart directly)

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57
Q

How does atropine work?

A

Antimuscarinic
Inhibits parasympathetic nervous system

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58
Q

What are the side effects of antimuscarinic medication?

A

Pupil dilation
Dry mouth
Urinary retention
Constipation

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59
Q

What is supraventricular tachycardia?

A

Abnormal electrical signals from above the ventricles cause a fast heart rate

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60
Q

Outline the pathophysiology of SVT

A

Electrical signals start in sinoatrial node (hearts pacemaker)- Located between SVC and RA
Signal travels through right and left atrium causing atria to contract
Travels through AV node causing ventricles to contract
SVT- Electrical signal re-enters atria from the ventricles
Self-perpetuating electrical loop- Results in narrow complex tachycardia

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61
Q

What is paroxysmal SVT?

A

SVT reoccurs and remits in same patient over time

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62
Q

List the types of narrow complex tachycardia

A

Sinus tachycardia
SVT
AF
Atrial flutter

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63
Q

What are the characteristics of AF on an ECG?

A

Absent p waves
Narrow QRS complex tachycardia
Irregularly irregular ventricular rhythm

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64
Q

What are the ECG characteristics of SVT?

A

QRS complex followed immediately by a T wave, then a QRS complex, then a T wave, etc
P waves often buried in T waves so can’t see them
Regular rhythm

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65
Q

How do you distinguish SVT from sinus tachycardia?

A

SVT- Abrupt onset, very regular pattern w/o variability, can have no apparent cause
Sinus tachycardia- Gradual onset, more variability in rate, usually has an explanation (pain or fever)

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66
Q

Which differential is important to consider in patients with tachycardia and wide QRS complexes?

A

SVT with a bundle branch block

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67
Q

What are the 3 main types of SVT?

A

Atrioventricular nodal re-entrant tachycardia- Re-entrant point is back through AV node (most common)
Atrioventricular re-entrant tachycardia- Re-entrant point is accessory pathway between atria and ventricles (Wolff-Parkinson-White syndrome)
Atrial tachycardia- Electrical signal originates in atria somewhere other than the sino atrial node

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68
Q

What is Wolff-Parkinson-White syndrome?

A

Caused by extra electrical pathway connecting atria and ventricles
Pre-excitation syndrome
Additional pathway allows bypassing of AV node
Might not cause symptoms or may cause SVT

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69
Q

What are the ECG changes in Wolff-Parkinson White syndrome?

A

Short PR interval
Wide QRS complex
Delta wave

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70
Q

What is a delta wave?

A

Slurred upstroke in QRS complex caused by electricity prematurely entering ventricles through accessory pathway

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71
Q

What is the definitive treatment for Wolff-Parkinson-White syndrome?

A

Radiofrequency ablation of accessory pathway

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72
Q

What is a cause of a polymorphic wide complex tachycardia?

A

Combination of AF/Atrial flutter with WPW
Chaotic atrial electrical activity can pass through accessory pathway into ventricles
LIFE-THREATENING EMERGENCY- HR can raise >200bpm and progress to VF and cardiac arrest

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73
Q

What can increase the risk of VF and cardiac arrest in polymorphic wide complex tachycardia?

A

Anti-arrhythmic meds- BBs, CCBs, digoxin, adenosine)- Reduce conduction through AV node and promote conduction through accessory pathway- CI in WPW that develop AF or flutter

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74
Q

Outline Acute management of tachycardia without life-threatening features

A

Continuous ECG monitoring
1. Vagal manoeuvres
2. Adenosine
3. Verapamil or beta blocker
4. Synchronised DC cardioversion

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75
Q

What are the life-threatening features of tachycardia?

A

Loss of consciousness (syncope)
Heart muscle ischaemia (chest pain)
Shock or severe HF

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76
Q

Outline treatment of life-threatening tachycardia

A

Synchronised DC cardioversion under sedation or general anaesthesia
IV amiodarone added if initial DC shocks unsuccessful

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77
Q

What is the management of WPWs with atrial arrhythmias?

A

Procainamide or electrical cardioversion if unstable

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78
Q

Why should adenosine, verapamil and BBs not be used to treat WPWs with atrial arrhythmias?

A

Blocks the AV node, promoting conduction of atrial rhythm through accessory pathway into ventricles, causing potentially life threatening ventricular rhythms

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79
Q

Outline vagal manoeuvres

A

Used to treat tachycardias
Stimulate vagus nerve, increasing activity in parasympathetic nervous system
Slows conduction of electrical activity in heart, terminating SVT

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80
Q

How does the valsalva manoeuvre work?

A

Treat SVT
Increases intrathoracic pressure
Patients blows hard against resistance

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81
Q

How does a carotid sinus massage work?

A

Treats SVT
Stimulate baroreceptors in carotid sinus
Avoid in patients with carotid artery stenosis

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82
Q

What is the diving reflex?

A

Used to treat SVT
Briefly submerge patient’s face in cold water

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83
Q

Outline the MoA of adenosine

A

Slows cardiac conduction, primarily through AV node
Interrupts AV node or accessory pathway during SVT And resets it to sinus rhythm

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84
Q

How should you give adenosine for SVT?

A

Rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway for a short period
Often causes brief asystole/bradycardia
Short half life so metabolises quickly and stops having effect

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85
Q

Which patients should adenosine not be given to?

A

Asthma
COPD
HF
Heart block
Severe hypotension
Potential atrial arrhythmia with underlying pre-excitation

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86
Q

Outline synchronised DC cardioversion

A

Used for SVT
Electric shock applied to heart to restore normal sinus rhythm
Synchronised with ventricular contraction at R wave
Used in patients with a pulse to avoid shocking the T wave which can result in VF and cardiac arrest

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87
Q

Outline management of paroxysmal SVT

A

Long term BBs, CCBs, or amiodarone
Radiofrequency ablation

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88
Q

What is Radiofrequency ablation?

A

Catheter ablation in a Cath lab
General anaesthetic or sedation
Catheter inserted into femoral vein and fed through venous system under xray guidance to heart
Catheter tests electrical signals in different areas of the heart and identifies abnormal patterns
Radiofrequency ablation burns abnormal areas and leaves scar tissue that doesn’t conduct electrical activity

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89
Q

What are the effects of AF?

A

Irregularly irregular ventricular contractions
Tachycardia
HF due to impaired filling of ventricles during diastole
Increased risk of stroke

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90
Q

Outline pathophysiology of AF

A

Sinoatrial node produces disorganised electrical activity
Causes contraction of atria to become uncoordinated, rapid and irregular
Chaotic electrical activity overrides regular activity from SA node
Passes through ventricles causing irregularly irregular ventricular contraction

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91
Q

How can AF increase risk of a stroke?

A

Uncoordinated atrial activity can cause blood to stagnate in atria, forming a thrombus
Thrombus in LA May travel to Brian NS cause Ischaemic stroke

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92
Q

What are the most common causes of AF?

A

S-epsis
M-itral valve pathology (stenosis or regurgitation)
I-schaemic heart disease
T-hyrotoxicosis
H-TN
Alcohol and caffeine

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93
Q

Outline presentation of AF

A

Asymptomatic
Palpitations
SOB
Dizziness or syncope
Symptoms of associated conditions- Stroke, sepsis, thyrotoxicosis

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94
Q

What are the differential diagnoses for an irregularly irregular pulse and how can you differentiate between them?

A

Atrial fibrillation
Ventricular ectopics- Disappear when HR above a certain threshold

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95
Q

Which investigations are done for AF?

A

ECG
Echo- Valvular heart disease, HF, planned cardioversion

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96
Q

What is paroxysmal AF and how is it managed?

A

AF that reoccurs and spontaneously resolves back to sinus rhythm
If normal ECG- 24h ambulatory ECG, cardiac event recorder lasting 1-2 wks

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97
Q

What is valvular AF?

A

AF with significant mitral stenosis or a mechanical heart valve

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98
Q

Outline rate control for AF

A

Aims to get the heart rate <100bpm and extend time during diastole for ventricles to fill with blood

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99
Q

When is rhythm control offered to patients?

A

Reversible cause
New onset AF (within last 48h)
HF caused by AF
Symptoms despite being affective key rate controlled

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100
Q

Which drugs are given for rate control in AF?

A

BBs (atenolol or bisoprolol)
CCB (Diltiazem or verapamil)- Not preferable in HF
Digoxin- Only in sedentary people with persistent AF, requires monitoring and risk of toxicity

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101
Q

What are the options for rhythm control of AF?

A

Cardioversion
Long-term rhythm control using medications

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102
Q

When is immediate cardioversion used?

A

If AF is either:
Present for <48h or causing life-threatening haemodynamic instability

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103
Q

What are the 2 options for immediate cardioversion?

A

Pharmacological- Flecainide, amiodarone
Electrical- Defib

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104
Q

When is delayed cardioversion used?

A

If AF has been present for >48h and they are stable
Patient should be anticoagulated for >3wks before delayed cardioversion

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105
Q

Outline long term rhythm control

A

1st line- BBs
2nd line- Dronedarone
Amiodarone if HF or left ventricular dysfunction

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106
Q

Outline management of paroxysmal AF

A

‘Pill in the pocket’- Flecainide
Must have infrequent episodes w/o structural heart disease
Increased risk of converting AF into atrial flutter

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107
Q

What are the ablation options for AF?

A

Left atrial ablation
Atrioventricular node ablation and a permanent pacemaker

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108
Q

Which anticoagulation should be offered to AF patients?

A

DOACs
Warfarin

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109
Q

What is the MoA of apixaban, edoxaban and rivaroxaban?

A

Direct factor Xa inhibitor

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110
Q

What is the MoA of dabigatran?

A

Direct thrombin inhibitor

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111
Q

What is the antidote to apixaban and rivaroxaban?

A

Andexanet alfa

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112
Q

What is the antidote to dabigatran?

A

Idarucizumab

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113
Q

What is the MoA of warfarin?

A

Vitamin K antagonist
Vit K is important for functioning of several clotting factors
Warfarin blocks Vit K and prolongs prothrombin time= Longer clotting time

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114
Q

What does INR measure?

A

Assesses how anticoagulated the patient is by warfarin
Calculates patient’s prothrombin time compared with PTT of average healthy adult

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115
Q

How do you interpret INR?

A

1= Normal PTT
2= PTT twice that of an average healthy adult

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116
Q

What is the target INR for an AF patient on warfarin?

A

2-3

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117
Q

What is the TTR in regards to INR?

A

Time in Therapeutic Range
Percentage of time that INR is in the target range
If too low- Increased stroke risk
If too high- Increased bleeding risk

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118
Q

What does INR stand for?

A

International normalised ratio

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119
Q

What does the metabolism of warfarin involve?

A

Cytochrome P450 system in the liver
Interacts with other drugs- Inc. ABs

120
Q

Which foods affect INR?

A

Foods that contain Vit K- Leafy green veg
Foods that affect P450- Cranberry juice, alcohol

121
Q

What is the reversing agent of warfarin?

A

Vit K

122
Q

What is the CHA2DS2-VASc tool used for?

A

Whether a patient with AF should start anticoagulation
Higher score= Higher risk of stroke or TIA

123
Q

Outline the CHA2DS2-VASc tool

A

C- Congestive HF
H- HTN
A2- Age>75 (scores 2)
D- Diabetes
S- Stroke/previous TIA (scores 2)
V- Vascular disease
A- Age 65-74
S- Sex (female)

0= No anticoagulation
1= Consider anticoagulation in men (women automatically score 1)
2+= Offer anticoagulation

124
Q

What is the ORBIT score?

A

Used to assess major bleeding risk in patients with AF taking anticoagulation

125
Q

Outline the scoring system of the ORBIT score

A

O- Older age (>75y)
R- Renal impairment (GFR<60)
B- Bleeding previously (history of GI or IC bleeding)
I- Iron (low Hb or haematocrit)
T- Taking antiplatelet meds

126
Q

What is a left atrial appendage occlusion?

A

Option for patients with CIs to anticoagulation and high stroke risk
Left atrial appendage= Most common site for thrombus to form
Insert catheter into femoral vein into RA and puncturing septum between atria to access LA and place a plug

127
Q

What is HCOM?

A

Hypertrophic obstructive cardiomyopathy
LV hypertrophic, with thickening of muscle
Asymmetrically affects septum of the heart, blocks flow of blood out of LV

128
Q

What risks are associated with HCOM?

A

HF
MI
Arrhythmias
Sudden cardiac death

129
Q

What is the inheritance of HCOM?

A

Autosomal dominant

130
Q

Outline the presentation of HCOM

A

Mostly asymptomatic
SOB
Fatigue
Dizziness
Syncope
Chest pain
Palpitations
Severe- Symptoms of HF (cough, SOB, orthopnoea, paroxysmal noctural dyspnoea, oedema)

131
Q

Outline examination findings of HCOM

A

Ejection systolic murmur at lower left sternal border
4th heart sound
Thrill at lower left sternal border

132
Q

Outline investigations of HCOM

A

ECG- LV hypertrophy
Chest xray- Normal or may show signs of pulmonary oedema
ECHO or Cardiac MRI- Establish diagnosis
Genetic testing

133
Q

Outline management of HCOM

A

BBs
Surgical myectomy (remove part of heart muscle to relieve obstruction)
Alcohol septal ablation
Implantable cardioverter defibrillator
Heart transplant
Avoid intense exercise/heavy lifting/dehydration
Avoid ACE-i and nitrates

134
Q

What is dilated cardiomyopathy?

A

Heart muscle becomes thin and dilated
Can be genetic or secondary to other conditions (eg: Myocarditis)

135
Q

What is alcohol-induced cardiomyopathy?

A

Type of dilated cardiomyopathy

136
Q

What is restrictive cardiomyopathy?

A

Heart becomes rigid and stiff, causing impaired ventricular filling during diastole

137
Q

What is arrhythmogenic cardiomyopathy?

A

Genetic
Heart muscle progressively replaced with fibrofatty tissue
Becomes prone to ventricular arrhythmias
Notable cause of sudden cardiac death in young people

138
Q

What is Takotsubo cardiomyopathy?

A

Rapid onset of LV dysfunction and weakness
Follows severe emotional stress
Broken heart syndrome
Resolves spontaneously with time

139
Q

What is infective endocarditis?

A

Infection of endothelium of the heart
Most commonly affects heart valves

140
Q

List the risk factors for infective endocarditis

A

IV drug use
Structural heart pathology (valvular HD, CHD, HCOM, prosthetic heart valves, ICD)
CKD (particularly on dialysis)
Immunocompromised
History of infective endocarditis

141
Q

What is the most common cause of infective endocarditis?

A

*Staph aureus
Strep viridans
Enterococcus

142
Q

Outline presentation of infective endocarditis?

A

Non-specific symptoms of infection:
Fever
Fatigue
Night sweats
Muscle aches
Anorexia (loss of appetite)

143
Q

What are the examination findings of infective endocarditis?

A

New/changing heart murmur
Splinter haemorrhages
Petechiae (small, non-blanching red/brown spots) on trunk/limbs/or mucosa/conjunctiva
Janeway lesions (painless red flat macules on palms of hands and soles of feet)
Osler’s nodes (tender red/purple nodules on pads of fingers and toes)
Roth spots (haemorrhages on retina)
Splenomegaly and finger clubbing in long standing disease

144
Q

Outline investigations of infective endocarditis

A

Blood cultures before starting ABs
Echo (TOE is more sensitive)— Vegetations May be seen on the valves

145
Q

How is a diagnosis of HF established?

A

Clinical assessment
NT-proBNP
ECG
ECHO
Bloods- Anaemia, renal function, thyroid, liver, lipids, diabetes
Chest X-ray and lung pathology

146
Q

What is the Modified Duke Criteria?

A

Diagnosing of infective endocarditis
One major plus 3 minor criteria
Five minor criteria

147
Q

What are the major modified duke criteria?

A
  • Persistently positive blood cultures
  • Specific imaging findings (vegetation seen o
148
Q

What are the minor modified duke criteria?

A
  • Predisposition (eg: IV drug use or heart valve pathology)
  • Fever >38 degree C
  • Vascular phenomena (eg: Splenic infarction, ICH, Janeway lesions)
  • Immunological phenomena (eg: Osler’s nodes, Roth spots, glomerulonephritis)
  • Microbiological phenomena (positive cultures not qualifying as major criteria)
149
Q

Outline management of infective endocarditis

A

IV broad-spectrum ABs (eg: Amoxicillin and optional gentamicin)- Continue for 4wks with native heart valves or 6wks with prosthetic heart valves

150
Q

What are the key complications of infective endocarditis?

A

Heart valve damage, causing regurgitation
Heart failure
Infective and non-infective emboli (causing abscesses, strokes and splenic infarction)
Glomerulonephritis, causing renal impairment

151
Q

What is the prognosis of infective endocarditis?

A

High mortality rate

152
Q

What is the difference between bio prosthetic versus mechanical?

A

Bioprosthetic- Lifespan of 10y
Mechanical- 20y but require lifelong warfarin with INR 2.5-3.5

153
Q

List gram-positive cocci

A

Staph
Strep
Entero

154
Q

What are the major complications of mechanical heart valves?

A
  • Thrombus formation
  • Infective endocarditis
  • Haemolysis causing anaemia
155
Q

What is a TAVI?

A

Transcatheter Aortic Valve Implantation
Treatment for severe aortic stenosis
Insert catheter into femoral artery and implant bioprosthetic valve

156
Q

What is the 1st HS?

A

S1
Closing of AV valves (tricuspid and mitral) at start of systolic contraction of ventricles

157
Q

What is the 2nd HS?

A

Closing of semilunar valves (pulmonary and aortic) once systolic contraction is complete

158
Q

What is the 3rd HS?

A

Heard 0.1s after 2nd HS
Rapid ventricular filling causing chordae tendinae to pull to full length and twang
Gallop rhythm
Normal in 15-40y
Older = Can indicate HF as ventricles and chordae are stiff and weak

159
Q

What is the 4th HS?

A

Heard directly before S1
Always abnormal and rare
Indicates stiff or hypertrophic ventricle
Caused by turbulent flow from atria contracting against non-compliant ventricle

160
Q

What is Erb’s point?

A

3rd intercostal space on left sternal border
Best for listening to heart sounds (S1 and S2)

161
Q

Which manoeuvres can be used to emphasise murmurs?

A

Mitral stenosis- Patient on left
Aortic regurgitation- Lean forward and hold exhalation

162
Q

Outline the mneumonic used to assess murmurs

A

S- Site- Where is the murmur loudest?
C- Character- Soft/blowing/crescendo/decrescendo/crescendo-decrescedo
R- Radiation- Over carotids (aortic stenosis), over left axilla (mitral regurgitation)
I- Intensity- What grade is the murmur?
P- Pitch- High/low/rumbling
T- Timing- Systolic or diastolic

163
Q

Outline grades of murmurs

A

1- Difficult to hear
2- Quiet
3- Easy to hear
4- Easy to hear with palpable thrill
5- Audible with stethoscope barely touching chest
6- Audible with stethoscope off chest

164
Q

Which valvular heart diseases cause hypertrophy?

A

Mitral stenosis- LA hypertrophy
Aortic stenosis- LV hypertrophy

165
Q

Which valvular heart diseases cause dilatation?

A

Mitral regurgitation- LA dilatation
Aortic regurgitation- LV dilatation

166
Q

What are the signs of pulmonary stenosis?

A

Ejection systolic murmur loudest in pulmonary area with deep inspiration
Wide split 2nd HS (LV empties quicker than RV)
Thrill in pulmonary area on palpation
Raised JVP with giant a waves (RA contracts against hypertrophic RV)
Peripheral oedema
Ascites

167
Q

What is the pathophysiology of pulmonary stenosis?

A

Congenital

168
Q

What conditions is pulmonary stenosis linked with?

A

Noonan syndrome
ToF

169
Q

What are the signs of tricuspid regurgitation?

A

Blood flows back from RV to RA during systolic contraction of RV
Pan systolic murmur
Split 2nd HS due to pulmonary valve closing earlier than aortic valve (RV empties quicker than LV)
Thrill in tricuspid area on palpation
Raise JVP with giant C-V waves
Pulsatile liver
Peripheral oedema
Ascites

170
Q

What are the causes of tricuspid regurgitation?

A

Pressure due to L sided HF or pulmonary HTN
Infective endocarditis
Rheumatic heart disease
Carcinoid syndrome
Ebstein’s anomaly
Marfan syndrome

171
Q

What are the signs of aortic stenosis?

A

Ejection systolic, high pitched murmur due to high velocity through aortic valve
Crescendo-decrescendo
Radiates to carotids
Thrill in aortic area on palpation
Slow rising pulse
Narrow pulse pressure
Exertional syncope

172
Q

What are the causes of aortic stenosis?

A

Idiopathic age-related calcification
Bicuspid aortic valve
Rheumatic heart disease

173
Q

What are the signs of aortic regurgitation?

A

Early diastolic, soft murmur
Heard at apex
Rumbling
Thrill in aortic area on palpation
Collapsing pulse
Wide pulse pressure
HF and pulmonary oedema

174
Q

What are the causes of aortic regurgitation?

A

Idiopathic age-related weakness
Bicuspid aortic valve
Ehlers-Danlos syndrome and Marfan syndrome

175
Q

What are the signs of mitral stenosis?

A

Mid-diastolic, low pitched rumbling
Loud S1 (thick valves require large systolic force to shut)
Tapping apex beat
Malar flush
AF

176
Q

What is the physiology causing a malar flush?

A

Back pressure of blood into pulmonary system, causing a rise in CO2 and vasodilation

177
Q

What are the causes of mitral stenosis?

A

Rheumatic heart disease
Infective endocarditis

178
Q

What are the signs of mitral regurgitation?

A

Reduced ejection fraction
Congestive HF
Pan-systolic, high pitched whistling
Radiates to left axilla
Potential 3rd HS
Thrill in mitral area on palpation
HF and pulmonary oedema
AF

179
Q

What are the causes of mitral regurgitation?

A

Idiopathic weakening of valve with age
Ischaemic heart disease
Infective endocarditis
Rheumatic heart disease
Ehlers-Danlos or Marfans

180
Q

What causes impaired LV function?

A

Chronic backlog of blood waiting to flow through left side of heart
LA, pulmonary veins and lungs have increased volume and pressure of blood
Start to leak fluid and can’t reabsorb excess = Pulmonary oedema

181
Q

What is ejection fraction?

A

Percentage of blood in LV squeezed out with each ventricular contraction
>50 = Normal

182
Q

What is HF with reduced ejection fraction?

A

Ejection fraction <50%

183
Q

What is HF with preserved ejection fraction?

A

Clinical features of HF with ejection fraction >50%
Result of diastolic dysfunction- Issue with LV filling with blood during diastole

184
Q

What are the causes of HF?

A

Ischaemic heart disease
Valvular heart disease (aortic stenosis)
HTN
Arrhythmias (AF)
Cardiomyopathy

185
Q

Outline the presentation of HF

A

Breathlessness (worse on exertion)
Cough (frothy pink sputum)
Orthopnoea (ask about pillows)
Paroxysmal nocturnal Dyspnoea
Peripheral oedema
Fatigue

186
Q

What are the signs of HF on examination?

A

Tachycardia
Tachypnoea
HTN
Murmurs
3rd heart sound
Bilateral basal crackles
Raised JVP
Peripheral oedema

187
Q

What is paroxysmal nocturnal dyspnoa?

A

Sudden waking at night with severe attack of SOB, cough, and wheeze

188
Q

What is the New York Heart Association Classification?

A

Assesses severity of HF:
Class 1- No limitation on activity
Class 2- Comfortable at rest but symptomatic with ordinary activities
Class 3- Comfortable at rest but symptomatic with activity
Class 4- Symptomatic at rest

189
Q

What is the use of NT-proBNP in HF?

A

400-2000ng/l = Have ECHO within 6wks
>2000ng/l = Have ECHO within 2wks

190
Q

Which vaccinations are required in HF patients?

A

Flu
Covid
Pneumococcal

191
Q

What is the medical management of chronic HF?

A

A- ACE inhibitor (ramipril)
B- BB (bisoprolol)
A- Aldosterone antagonist if symptoms not controlled with A and B (spironolactone/eplerenone)
L- Loop diuretic (furosemide/bumetanide)

192
Q

What can you use instead of an ACE-I if not tolerated?

A

ARB- Candesartan
Avoid ACE-is in valvular heart disease

193
Q

When are aldosterone antagonists used in HF?

A

Reduced EF
Symptoms not controlled with ACE-I and BB

194
Q

Which HF meds require monitoring of U&Es and why?

A

Diuretics
ACE-is
Aldosterone antagonists
All can cause electrolyte disturbances
ACE-is and aldosterone antagonists can cause hyperkalaemia

195
Q

What are the additional specialist meds for HF?

A

SGLT2 inhibitor (dpagliflozin)
Sacubitril with Valsartan
Ivabradine
Hydralazine with nitrate
Digoxin

196
Q

What surgical interventions can be used for HF?

A

ICD- Used if previous VT or VF
Cardiac resynchronisation therapy (CRT)- Used if EF<35%- Involves biventricular pacemakers
Heart transplant

197
Q

What is acute LV failure?

A

Acute event results in LV unable to more blood efficiently through left side of heart and into systemic circulation

198
Q

What is cardiac output?

A

Volume of blood ejected by heart per minute
CO = SV x HR

199
Q

What is stroke volume?

A

Volume of blood ejected each beat

200
Q

What is the cardiac cause of pulmonary oedema?

A

Backlog of blood waiting in LA, pulmonary veins and lungs = Increased volume and pressure of blood= Leak fluid and can’t reabsorb excess from surrounding tissues

201
Q

What is pulmonary oedema?

A

Lung tissue and alveoli filled with interstitial fluid
Interferes with normal gas exchange= SOB and reduced O2 sats

202
Q

What are the triggers of acute LV failure?

A

Often result of decompensated chronic HF
Iatrogenic (aggressive IV fluids in frail elderly with impaired LV function)
MI
Arrhythmias
Sepsis
Hypertensive emergency (acute, severe increase in BP)

203
Q

How do you treat an 85y patient with CKD and aortic stenosis who has been given 2l fluid over 4h and starts to drop O2 sats?

A

IV furosemide

204
Q

Outline presentation of Acute LVF

A

Acute SOB exacerbated by lying flat and improves sitting up
Looking unwell
Cough with frothy white/pink sputum

205
Q

What are the signs of Acute LVF on examination?

A

Raised RR
Reduced O2 sats
Tachycardia
3rd heart sound
Bilateral basal crackles
Hypotension if severe- Cardiogenic shock

206
Q

What are the signs of R sided HF?

A

Raised JVP
Peripheral oedema

207
Q

What investigations are required for Acute LVF?

A

Clinical assessment
ECG
Bloods- Anaemia, infection, kidney function, BNP, troponin (if suspect MI)
ABG
Chest X-ray
ECHO

208
Q

What does a raised BNP suggest?

A

Hormone released from heart ventricles when myocardium stretched beyond normal range
Raised BNP indicates heart overloaded
Sensitive but not specific= Can be positive due to other causes

209
Q

What is the role of BNP?

A

To relax smooth muscle in blood vessels to reduce systemic vascular resistance= Easier for heart to pump blood
Acts in kidneys as diuretic to promote water excretion in urine= Reduces circulating volume

210
Q

What are the causes of raised BNP?

A

Tachycardia
Sepsis
PE
Renal impairment
Acute LVF
COPD

211
Q

What may be seen on a chest X-ray of Acute LVF?

A

Cardiomegaly
Upper lobe venous diversion- When standing erect lower lobe veins usually contain more blood and upper remain small- In Acute LVF back pressure means upper lobes fill with blood and become engorged = Increased prominence and diameter of upper lobe vessels on CXR
Fluid leaking from oedematous lung tissue= Bilateral pleural effusions, fluid in interlobar fissures, fluid in septal (Kerley) lines

212
Q

Outline basic management of Acute LVF

A

S- Sit up
O- Oxygen
D- Diuretics
I- IV fluids stopped
U- Underlying causes identified and treated
M- Monitor fluid balance

213
Q

What are the specialist management options for Acute LVF?

A

IV opiates (morphine)- Vasodilator
IV nitrates- Vasodilator (consider in every HTN or ACS)
Inotropes (dobutamine)- Improves contractility and cardiac output
Vasopressors (noradrenaline)- Improves BP- Vasoconstricts= Increases SVR and MAP
NIV
Invasive ventilation

214
Q

How do positive inotropes work?

A

Increase contractility of heart
Increase CO and Mean arterial pressure
Used in Acute HF, recent MI, or following heart surgery

215
Q

How do vasopressors work?

A

Cause vasoconstriction
Increase SVR and MAP

216
Q

What is pericarditis?

A

Inflammation of pericardium (membrane surrounding heart)

217
Q

What are the most common causes of pericarditis?

A

Idiopathic
Viral

218
Q

Outline the presentation of pericarditis

A

Chest pain- Sharp, central, worse on inspiration (pleuritic), worse lying down, better sitting forward
Low grade fever

219
Q

What is pleuritic chest pain?

A

Worse on inspiration

220
Q

Outline the pathophysiology of pericarditis

A

Membrane surrounds heart is pericardium or pericardial sac- Has 2 layers with <50mls fluid between providing lubrication allowing beat without too much friction
Potential space between 2 layers is pericardial cavity

221
Q

What are the causes of pericarditis?

A

Idiopathic
Infection (TB, HIV, Coxsackie, EBV)
AI and inflammatory (SLE, RA)
Injury to pericardium (after MI/open heart surgery/trauma)
Uraemia secondary to renal impairment
Cancer
Medications (methotrexate)

222
Q

What is a pericardial effusion?

A

Potential space of pericardial cavity fills with fluid
Creates inward pressure on heart= Difficult to expand during diastole (filling of heart)

223
Q

What is a pericardial tamponade?

A

Pericardial effusion large enough to raise intra-pericardial pressure
Increased pressure squeezes heart and affects ability to function
Reduces heart filling during diastole, decreasing CO during systole

224
Q

What is a key examination finding in pericarditis?

A

Pericardial friction rub on auscultation
Rubbing/scratching sound occurring alongside heart sounds

225
Q

Outline investigations of pericarditis

A

Bloods- Riased inflammatory markers (WBC, CRP, ESR)
ECG- Saddle-shaped ST-elevation, PR depression
ECHO

226
Q

Outline management of pericarditis

A

NSAIDs- Aspirin or ibuprofen
Colchicine long term (3mths)
2nd line- Steroids if associated with inflammatory conditions or recurrent
Pericardiocentesis if fluid around heart

227
Q

What is the prognosis of pericarditis?

A

Most resolve within a month
Can be recurrent
Some cases chronic

228
Q

What is atherosclerosis?

A

Fatty deposits in artery walls
Hardening or stiffening of blood vessel walls
Affects medium and large arteries
Caused by chronic inflammation and activation of immune system in artery wall

229
Q

What can be the result of plaques in the arteries?

A

Stiffening
Stenosis
Rupture

230
Q

What is the result of stiffening of the arteries in atherosclerosis?

A

HTN
Heart strain

231
Q

What is the result of stenosis in atherosclerosis?

A

Reduced blood flow

232
Q

What is the result of plaque rupture in atherosclerosis?

A

Creates thrombus that blocks distal vessel and causes ischaemia

233
Q

What is acute coronary syndrome?

A

Coronary artery becomes blocked

234
Q

What are the modifiable risk factors for cardiovascular disease?

A

Raised cholesterol
Smoking
Alcohol consumption
Poor diet
Lack of exercise
Obesity
Poor sleep
Stress

235
Q

What are the non-modifiable risk factors for cardiovascular disease?

A

Older age
Family history
Male

236
Q

What are the complications of atherosclerosis?

A

Angina
MI
TIA
Strokes
Peripheral artery disease
Chronic mesenteric ischaemia

237
Q

What is the dietary advice for cardiovascular disease?

A

Reduced sugar
Whole grain
5 a day
2 a week fish
4 and week of legumes/seeds/nuts

238
Q

What is the exercise advise for cardiovascular disease?

A

Aerobic activity 150mins moderate or 75mins vigorous/wk
Strength training 2d a week

239
Q

What is a QRISK3 score?

A

Estimate of % risk of stroke or MI in next 10y
When >10% offer a statin (20mg atorvastatin at night)

240
Q

When is atorvastatin offered as primary prevention for cardiovascular disease?

A

CKD (eGFR <60ml/min/1.73m2)
T1D for >10y or over 40y
QRSIK3 >10%

241
Q

What is the role of statins?

A

Reduce cholesterol production in liver by inhibiting HMG CoA reductase

242
Q

What monitoring is required on statins?

A

Lipids at 3mths
LFTs at 3mths and 12mths
Statins can cause transient rise in ALT and AST in first few weeks

243
Q

List some rare and significant SEs of statins

A

Myopathy (muscle weakness and pain)
Rhabdomyolysis (muscle damage- Check creatine kinase if muscle pain)
T2D
Haemorrhaging stroke

244
Q

Which medications interact with statins?

A

Macrolide antibiotics- Stop taking statin whilst taking erythromycin or Clarithromycin

245
Q

Which drugs apart from statins lower cholesterol?

A

Ezetimibe (inhibits absorption of cholesterol in intestine)
PCSK9 inhibitors (evolocumab or alirocumab)

246
Q

Outline secondary prevention of CVD

A

A- Antiplatelet (aspirin, clopidogrel, ticagrelor)
A- Atorvastatin 80mg
A- Atenolol (or bisoprolol)
A- ACE-I

247
Q

What is the medical prevention treatment following an MI?

A

Aspirin 75mg/d indefinitely
Clopidogrel/ticagrelor 12mths

248
Q

What is the anti platelet of choice following peripheral arterial disease or an Ischaemic stroke?

A

Clopidogrel

249
Q

What is the Inheritance of familial hypercholesterolaemia?

A

Autosomal dominant

250
Q

What are the criteria used for a clinical diagnosis of familial hypercholesterolaemia?

A

FH premature CVD (<60y)
Very high cholesterol (>7.5mmol/L)
Tendon Xanthomata (hard nodules in tendons containing cholesterol on back of hand or Achilles)

251
Q

What is the management of familial hypercholesterolaemia?

A

Genetic testing
Statins

252
Q

What is angina caused by?

A

Atherosclerosis affecting coronary arteries, narrowing lumen and reducing blood flow to myocardium

253
Q

What is stable angina?

A

Symptoms come on with exertion and are relieved by rest
High demand = Insufficient supply of blood = Symptoms of angina

254
Q

What is unstable angina?

A

Type of ACS
Symptoms not relieved by rest

255
Q

What investigations are required for angina?

A

Physical examination (heart sounds, signs of HF, BP and BMI)
ECG
FBC (anaemia)
U&Es (required before starting ACE-I
LFTs (required before starting statin)
Lipid profile
TFTs
HbA1c
Cardiac stress testing- Assess heart function during exertion
CT coronary angiogram
Invasive coronary angiography

256
Q

Outline medical management for immediate symptomatic relief of stable angina

A

GTN when symptoms start (causes vasodilation)
2nd dose after 5mins if symptoms remain
3rd dose after 5mins if symptoms remain
Ambulance after further 5mins if symptoms remain

257
Q

Outline medical management for long term symptomatic relief of stable angina

A

BB (bisoprolol)
CCB (Diltiazem or verapamil- Avoid both in HF with reduced ejection fraction)
Specialist- Long acting nitrates (isosorbide mononitrate), ivabradine, nicorandil, ranolazine

258
Q

What are the side effects of GTN?

A

Headaches
Dizziness

259
Q

What are the medications used for secondary prevention of stable angina?

A

A- Aspirin 75mg once/d
A- Atorvastatin 80mg once daily
A- ACE-I if diabetes/HTN/CKD/HF
A- Already on BB for symptomatic relief

260
Q

Which surgical interventions are used for stable angina?

A

Percutaneous coronary intervention (PCI)- Insert catheter into brachial/femoral artery to coronary arteries, dilate a balloon and stent
Coronary artery bypass graft (CABG)- Offered in severe stenosis, midline sternotomy- Graft from saphenous vein, internal thoracic artery or radial artery

261
Q

What are the pros and cons of PCI over CABG?

A

Faster recovery
Lower rate of strokes
Higher rate of revascularisation (further procedures)

262
Q

What is Acute coronary syndrome?

A

Result of thrombus from atherosclerosic plaque blocking a coronary artery
If formed in fast flowing artery = Mainly formed of platelets

263
Q

What are the 3 types of ACS?

A

Unstable angina
STEMI
NSTEMI

264
Q

Which coronary arteries branch from the aorta?

A

Right coronary artery
Left coronary artery

265
Q

What does the right coronary artery supply?

A

Curves around right side of heart
RA
RV
Inferior aspect of LV
Posterior septal area

266
Q

What does the left coronary artery become?

A

Circumflex artery
Left anterior descending

267
Q

What does the circumflex artery supply?

A

Curves around top, left and back of heart
LA
Posterior aspect of left ventricle

268
Q

What does the left anterior descending artery supply?

A

Travels down middle of heart
Anterior aspect of LV
Anterior aspect of septum

269
Q

Outline presentation of ACS

A

Central constricting chest pain
Pain radiating to jaw or arms
Nausea and vomiting
Sweating and clamminess
Feeling of impending doom
SOB
Palpitations
Symptoms continue at rest for >15mins

270
Q

What is a silent MI?

A

Patient doesn’t experience typical chest pain during acute ACS
Patients with diabetes at greater risk

271
Q

What are the ECG changes in an acute STEMI?

A

ST segment elevation
New LBBB

272
Q

What are the ECG changes in a new NSTEMI?

A

ST segment depression
T wave inversion

273
Q

What do pathological Q waves suggest in ACS?

A

Deep infarction involving full thickness of heart muscle and typically appear >6h after onset of symptoms

274
Q

Which heart area does the LCA supply and which ECG leads does it correlate with?

A

Anterolateral
I, aVL, V3-V6

275
Q

Which area of the heart does LAD correlate with and which ECG leads?

A

Anterior
V1-V4

276
Q

Which area of the heart does circumflex correlate with and which ECG leads?

A

Lateral
I, aVL, V5-V6

277
Q

Which area of the heart does RCA correlate with and which ECG leads?

A

Inferior
II, III, aVF

278
Q

What is troponin?

A

Protein in cardiac muscle (myocardium) and skeletal muscle
Rise in troponin is consistent with myocardial ischaemia

279
Q

When is troponin used to diagnose an MI?

A

In NSTEMI, not STEMI

280
Q

How do you diagnose NSTEMI based of troponin?

A

High troponin/rising troponin in context of suspected ACS

281
Q

What are the causes of raised troponin?

A

MI
CKD
Sepsis
Myocarditis
Aortic dissection
PE

282
Q

What investigations are required to confirm ACS?

A

ECG
Troponin
Baseline bloods- FBC, U&Es, LFTs, lipids, glucose
Chest X-ray
ECHO- Assess LV function

283
Q

When is unstable angina diagnosed if symptoms suggest ACS?

A

Normal ECG
Troponin normal
Other ECG changes (ST depression or T wave inversion)

284
Q

What is the initial management of ACS?

A

Aspirin 300mg
IV morphine if required + Metoclopramide
Nitrate (GTN)

285
Q

Outline management of a STEMI

A

PCI if available within 2h of presenting
Thrombolysis if PCI not available within 2h

286
Q

Which medications are given in preparation for PCI?

A

Aspirin and prasugrel

287
Q

What is thrombolysis?

A

Dissolving the clot using a fibrinolytic agent- Streptokinase, alteplase, tenecteplase

288
Q

Outline medical management of NSTEMI

A

B- Base decision about angiography and PCI on GRACE score
A- Aspirin 300mg stat dose
T- Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if angiography)
M- Morphine
A- Antithrombin therapy with fondaparinux
N- Nitrate (GTN)

289
Q

What is Dressler’s syndrome?

A

Post-MI syndrome
Occurs 2-3wks after acute MI
Caused by localised immune response resulting in inflammation of pericardium (pericarditis)

290
Q

Outline presentation of Dressler’s syndrome

A

Pleuritic chest pain
Low grade fever
Pericardial rub on auscultation (rubbing/scratching sound alongside heart sounds)
Can cause pericardial effusion and rarely pericardial tamponade

291
Q

How is Dressler’s syndrome diagnosed?

A

ECG- Global ST elevation and T wave inversion
ECHO- Pericardial effusion
Raised inflammatory markers (CRP and ESR)

292
Q

How is Dressler’s syndrome managed?

A

NSAIDs (ibuprofen or aspirin)
Steroids if severe (prednisolone)
Pericardiocentesis if required

293
Q

List the complications of MI

A

D- Death
R- Rupture of heart septum or papillary muscles
E- oEdema (HF)
A- Arrhythmia and Aneurysm
D- Dressler’s syndrome

294
Q

What is the GRACE score?

A

Gives 6mth probability of death after NSTEMI

295
Q

Outline secondary management of ACS

A

Aspirin once daily indefinitely
Antipalatelet (ticagrelor or clopidogrel) for 12mths
Atorvastatin 80mg once daily
ACE-is (ramipril)
Atenolol or Bisoprolol
Aldosterone antagonist if clinical HF (epleronone 50mg once daily)

296
Q

What is the risk associated with ACE-is and aldosterone antagonists that needs to be monitored?

A

Renal function to monitor for Hyperkalaemia

Final Year (14 decks)

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