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CARD - 1 > Passmedicine - Cardiology > Flashcards

Passmedicine - Cardiology Flashcards

1
Q

Define syncope

A

Transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous recovery

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2
Q

What are the three types of syncope?

A

Reflex syncope (neurally mediated)

Orthostatic syncope

Cardiac syncope

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3
Q

What are the types of reflex syncope?

A

Vasovagal
Situational
Carotid sinus syncope

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4
Q

What triggers vasovagal syncope?

A

Emotion
Pain
Stress

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5
Q

What is vasovagal syncope otherwise known as?

A

Fainting

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6
Q

What things may cause situational syncope?

A

Cough
Micturition
GI

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7
Q

What are the types of orthostatic syncope?

A

Primary automatic failure - PD, LBD
Secondary automatic failure - e.g. diabetic neuropathy, amyloidosis, uraemia
Drug induced - diuretics, alcohol, vasodilators
Volume depletion - haemorrhage, diarrhoea

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8
Q

What things may cause a cardiac syncope?

A

Arrhythmias - bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular)
Structural - valvular, MI, hypertrophic obstructive cardiomyopathy
PE

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9
Q

How do you examine someone presenting with syncope?

A 
CV Ex
Postural BP readings - symptomatic fall in systolic BP >20 or diastolic >10 or decrease in systolic BP <90 is diagnostic 
ECG
Carotid sinus massage
Tilt table tet
24h ECG
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10
Q

What does carotid artery sinus massage involve?

A

Massaging the carotid artery for 5 seconds to stimulate the baroreceptors and parasympathetic nervous system –> increased vaal tone + affects SA and AV node –> decreased BP and HR

If baroreceptor is hypersensitive response is exaggerated

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11
Q

What are the two types of exaggerated responses that can occur after a carotid sinus massage?

A

Cardioinhibitory - ventricular pause of >3s

Vasodepressive - fall in SBP >50mmHg

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12
Q

What is long QT syndrome?

A

An inherited condition associated with delayed repolarisation of the ventricles

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13
Q

What can long QT syndrome lead to?

A

VT/torsade de pointes can lead to collapse/sudden death

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14
Q

What are the most common variants of long QT syndrome? What causes them?

A

LQT1 and 2 - caused by defects in alpha subunit of the slow delayed rectifier potassium channel

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15
Q

What is a normal correct QT interval?

A

<430ms in males

<450ms in females

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16
Q

What are congenital causes of a long QT interval?

A

Jervell-Lange Neilsen syndrome (deafness)

Romano-Ward syndrome (no deafness)

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17
Q

What are drug causes of a long QT interval?

A 
Amiodarone, sotalol, class 1a antiarrhythmics 
TCAs, SSRIs (esp citalopram)
Methadone
Chloroquine
Terfenadine
Erythromycin
Haloperidol
Ondansteron
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18
Q

What other things can cause a long QT?

A 
Electrolytes - hypocalcaemia, hypokalaemia, hypomagnaemia
Acute MI 
Myocarditis
Hypothermia
SAH
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19
Q

What is LQT1 usually associated with?

A

Exertional syncope, often swimming

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20
Q

What is LQT2 usually associated with?

A

Syncope often following emotional stress, exercise or auditory stimuli

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21
Q

What is LQT3 associated with?

A

Events often occur at night/rest

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22
Q

What is the management of long QT syndrome?

A

Avoid drugs that prolong the QT interval + other precipitants, e.g. strenuous exercise
Beta blockers
Implantable cardioverter defibs if high risk

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23
Q

What are the characteristic exam features of MI?

A

Heavy, central chest pain, radiates to L arm/neck
N, sweating
RFs for cardiovascular dx
Elderly/DM may experience no pain

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24
Q

What are the characteristic exam features of pneumothorax?

A

Hx of asthma, Marfans etc.

Sudden SoB, pleuritic chest pain

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25
Q

What are the characteristic exam features of PE?

A

Sudden SoB, pleuritic chest pain
Calf swelling/pain
Current COC user, malignancy

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26
Q

What are the characteristic exam features of pericarditis?

A

Sharp pain relieved by sitting forwards

May be pleuritic in nature

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27
Q

What are the characteristic exam features of dissecting aortic aneurysm?

A

Tearing chest pain radiating to back

Unequal upper limb BP

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28
Q

What are the characteristic exam features of GORD?

A

Burning retrosternal pain

Regurg/dysphagia

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29
Q

What are the characteristic exam features of MSK chest pain

A

Worse on movement and palpation

May be precipitated by coughing/trauma

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30
Q

What causes aortic dissection?

A

Flap/filling defect within aortic intima –> blood tracks into medial layer and splits tissues creating a false lumen

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31
Q

Where does aortic dissection most commonly occur?

A

In ascending aorta

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32
Q

Who is aortic dissection most common in?

A

Afrocarribean males 50-70y

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33
Q

How does aortic dissection classically present?

A

Tearing intrascapular pain (similar to MI pain)

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34
Q

What is the classification of aortic dissection?

A

Stanford (A = proximal origin, B = distal to L subclavian)

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35
Q

How can aortic dissection be diagnosed?

A

CXR showing widening mediastinum

Confirmed usually with CT angiography

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36
Q

How can you diagnose perforated peptic ulcer?

A

Erect CXR - shows small amounts of free intra-abdominal air

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37
Q

How is perforated peptic ulcer managed?

A

Laparotomy (small –> excised and overlaid with omental patch, large –> partial gastrectomy)

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38
Q

What is Boerhaaves syndrome?

A

Spontaneous rupture of the oesophagus that occurs due to repeated vomiting

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39
Q

How is Boerhaaves syndrome diagnosed?

A

CT contrast swallow

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40
Q

How is Boerhaaves syndrome managed?

A

Thoracotomy and lavage
If <12h –> repair
>12h –> insert T tube to create a controlled fistula between oesophagus and skin

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41
Q

What are features of complete heart block?

A 
syncope
heart failure
regular bradycardia (30-50 bpm)
wide pulse pressure
JVP: cannon waves in neck
variable intensity of S1
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42
Q

What are the types of heart block?

A 
1st degree
2nd degree (Mobitz 1 and 2) 
3rd degree (complete)
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43
Q

What is 1st degree heart block?

A

PR interval >0.2s

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44
Q

What is 2nd degree heart block (Mobitz 1)?

A

Progressive prolongation of the PR interval until a dropped beat occurs

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45
Q

What is 2nd degree heart block (Mobitz 2)?

A

PR interval is constant but P wave is often not followed by a QRS complex

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46
Q

What is 3rd degree heart block?

A

No associated between P waves and QRS complexes

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47
Q

What is coarctation of the aorta?

A

Congenital narrowing of the descending aorta

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48
Q

What are features of coarctation of the aorta?

A 
Infancy - heart failure
Adult - HTN
Radio-femoral delay
Midsystolic murmur, maximal over back 
Apical click from aortic valve
Notching at inferior border of ribs (due to collateral vessels)
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49
Q

What things are associated with coarctation of the aorta?

A

Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis

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50
Q

What are SEs of ACEis?

A

Cough
Andioedema
Hyperkalaemia
First dose hypotension

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51
Q

What is thought to cause the cough associated with ACEis?

A

Increased bradykinin levels

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52
Q

What are CIs for ACEis?

A 
Pregnancy, breastfeeding
Renovascular disease
Aortic stenosis (leads to hypotension)
Seek specialist advice is K >=5mmol/L
Avoid in those on high dose diuretics (hypotension)
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53
Q

What parameters should be checked before starting someone on ACEis?

A

U+E

Acceptable changes are increase in serum Cr up to 30% from baseline + increase in K up to 5.5mmol/L

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54
Q

What are complications of MI?

A 
Cardiac arrest (usually due to VF)
Cardiogenic shock
Chronic heart failure
Tachyarrhythmias
Bradyarrhythmias
Pericarditis
Left ventricular aneurysm
Left ventricular free wall rupture
VSD
Acute MR
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55
Q

What causes cardiogenic shock post MI?

A

If large part of ventricular myocardium is damage –> decreased ejection systolic fracture

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56
Q

How is cardiogenic shock post-MI treated?

A

Inotropic support and/or intra-aortic balloon pump

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57
Q

What can cause chronic heart failure post-MI?

A

Ventricular myocardial damage

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58
Q

How is chronic heart failure post-MI treated?

A

Loop diuretics, e.g. furosemide

ACEi/Bblockers

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59
Q

AV block is more common following which kind of MI?

A

Inferior MI

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60
Q

Pericarditis in the first ____ following a ______ MI is common.

A

48 hours

Transmural

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61
Q

How does pericarditis post-MI present?

A

Pain worse on lying flat
Pericardial rub
Pericardial effusion on echo

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62
Q

What is Dressler’s syndrome?

A

Syndrome that occurs 2-6w post Mi
Thought to be autoimmune reaction against antigenic proteins formed as the myocardium recovers

Get fever, pleuritic pain, pericardial effusion, raised ESR

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63
Q

How is Dressler’s syndrome managed?

A

NSAIDs

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64
Q

How can LV aneurysm occur after an MI?

A

Ischaemic damage weakens myocardium

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65
Q

What is LV aneurysm post MI typically associated with?

A

Persistent ST elevation and LV failure

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66
Q

What are patients who get LV aneurysm more at risk of?

A

Thrombus and therefore stroke

Must anticoagulate them

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67
Q

When does LV free wall rupture tend to occur post-MI? How do patients present?

A

1-2 weeks

Heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds

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68
Q

How is LV free wall rupture managed?

A

Urgent pericardiocentesis

Thoracotomy

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69
Q

When does VSD tend to occur post-MI and how does it present?

A

1st week

Acute heart failure + pansystolic murmur

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70
Q

How is VSD post-MI diagnosed?

A

Echocardiogram

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71
Q

How is VSD post-MI managed?

A

Surgery

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72
Q

With what kind of MI is MR most common?

A

Inferio-posterior

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73
Q

What causes MR post-MI?

A

Ischaemia/rupture of papillary muscle

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74
Q

What are features of MR post-MI?

A

Acute hypotension and pulmonary oedema

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75
Q

How is MR post-MI managed?

A

Vasodilator therapy, surgery often req.

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76
Q

What is the strongest RF for developing IE?

A

Prev episode IE

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77
Q

What is the most commonly affected valve in those with no RF for IE?

A

Mitral valve

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78
Q

What are RFs for IE?

A 
Rheumatic valve disease
Prosthetic valves
Congenital heart defects
IVDU
Recent piercings
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79
Q

What valve is usually affected in IE in IVDAs?

A

Tricuspid

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80
Q

What is the most common cause of IE?

A

Staph aureus (was strep viridians)

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81
Q

What is the most common cause of IE in IDVAs?

A

Staph aureus

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82
Q

What is the most common cause of IE in those with prosthetic valves?

A

For first 2 months after surgery - staph epidermis, thereafter staph aureus

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83
Q

What is strep viridians IE associated with?

A

Poor dental hygiene

Following a dental procedure

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84
Q

What are non-infective causes of IE?

A

SLE (Libman-Sacks)

Malignancy - marantic endocarditis

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85
Q

What are culture negative causes of IE?

A 
Prior antibiotics
Coxiella burnetii
Bartonella
Brucella
HACEK - haemophilus, actinobacillus, cardiobacterium, eikenella, kingella
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86
Q

The vast majority of IE are caused by what three organisms?

A

Strep viridians
Staph aureus
Staph epidermis

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87
Q

What are rare causes of IE?

A 
Enterococcus
Strep bovis
Candida 
HACEK group
Coxiella burnetii
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88
Q

Acute endocarditis is most commonly caused by what organism?

A

Staph

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89
Q

What is subacute IE most commonly caused by?

A

Strep

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90
Q

What is the empirical antibiotic therapy for IE?

A

Native valve - amoxicillian + gentamicin
NVE + severe sepsis, penicillin allergy/suspected MRSA - vancomycin + gentamicin
NVE with sepsis + RF for gram negative infection - vancomycin + meropenem
Prosthetic valve endocarditis - vancomycin, gentamicin, rifampicin

Once blood culture results available - give specific therapy
Treatment usually 4-6w IV

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91
Q

What criteria is used for diagnosing IE?

A

Modified Duke

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92
Q

How can IE be diagnosed using Duke’s criteria?

A

Pathological criteria positive or
2 major criteria or
1 major and 3 minor or
5 minor

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93
Q

What is the pathological duke criteria?

A

Positive histology/microbiology of pathological material obtained at autopsy/cardiac surgery

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94
Q

What are the major duke criteria?

A

Positive blood cultures

  • 2 +ve showing typical IE organisms, e.g. HACEK or strep viridians
  • persistent bacteraemia from 2 blood cultures taken >12h apart/3+ +ve blood cultures where the pathogen is less specific, e.g. staph aureus, staph epidermis…
  • Positive serology for coxiella burnetii, bartonella spp or chlamydia psittaci
  • Positive molecular assays for specific gene targets

Evidence of endocardial involvement

  • +ve echo (oscilating structures, abscess formation, new valvular regurg, dehisence of prosthetic valves) or
  • New valvular regurg
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95
Q

What are the minor Duke criteria?

A

predisposing heart condition or intravenous drug use
microbiological evidence does not meet major criteria
fever > 38ºC
vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots

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96
Q

What is the following scoring system used for:

CHA2DS2VASc?

A

Determine need for anticoagulation in AF

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97
Q

What is the following scoring system used for:

ABCD2?

A

Prognostic scoring for risk stratifying patients with suspected TIA

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98
Q

What is the following scoring system used for:

NYHA?

A

Heart failure severity

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99
Q

What is the following scoring system used for:

DAS28?

A

Disease activity in RA

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100
Q

What is the following scoring system used for:

Child-Pugh?

A

Severity of liver cirrhosis

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101
Q

What is the following scoring system used for:

Wells score?

A

Risk of DVT

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102
Q

What is the following scoring system used for:

MMSE?

A

Cognitive impairment

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103
Q

What is the following scoring system used for:

HAD?

A

Hospital anxiety and depression scale

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104
Q

What is the following scoring system used for:

PHQ-9?

A

Patient health questionnaire - assess severity of depression symptoms

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105
Q

What is the following scoring system used for:

GAD-7?

A

Screening tool and measure for GAD

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106
Q

What is the following scoring system used for:

SCOFF?

A

Detect eating disorders and aid treatment

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107
Q

What is the following scoring system used for:
AUDIT
CAGE
FAST

A

Alcohol screening tools

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108
Q

What is the following scoring system used for:

CURB-65?

A

Prognosis of pt with pneumonia

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109
Q

What is the following scoring system used for:

IPSS?

A

International prostate symptom score

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110
Q

What is the following scoring system used for:

Gleason score?

A

Prognosis in prostate cancer

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111
Q

What is the following scoring system used for:

APGAR?

A

Assess health of newborn immediately after birth

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112
Q

What is the following scoring system used for:

Bishop?

A

Whether induction of labour will be req.

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113
Q

What is the following scoring system used for:

Waterlow?

A

Risk of developing a pressure sore

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114
Q

What is the following scoring system used for:

FRAX?

A

10 year risk of developing osteoporosis related fragility fracture

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115
Q

What is the following scoring system used for:

Ranson criteria?

A

Pancreatitis

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116
Q

What is the following scoring system used for:

MUST?

A

Malnutrition

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117
Q

What are features of inhaled FB?

A

Cough
Stridor
SoB

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118
Q

Where are inhaled FBs most likely to be found?

A

R main bronchus

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119
Q

What drugs have been proven to improve mortality in HF patients?

A

ACEi
Spironolactone
Beta blockesr
Hydralazine with nitrates

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120
Q

What is the first line management for all patients with HF?

A

ACEi and beta blocker (start 1 at a time)

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121
Q

What is the second line treatment of heart failure?

A

Aldosterone antagonist, ARB/hyralazine in combination with a nitrate

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122
Q

If symptoms of HF persistent despite 1st and 2nd line treatment what should be considered?

A

Cardiac resynchonisation therapy or digoxin or ivabradine (ivabradine only if pt already on aldosterone antagonist, ACEi, bblocker + HR >75 + LVF <35%)

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123
Q

What treatment should be given for fluid overload in HF?

A

Diuretics

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124
Q

What vaccinations should those with HF be offered?

A

Annual flu

One off pneumococcal

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125
Q

What beta blockers are licensed in the UK to treat HF?

A

Bisoprolol, carvedilol, nebivolol

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126
Q

What other drug can be used in those with HF with reduced ejection fraction who are still symptomatic on ACEi or ARBs?

A

Sacubitril-valsartan

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127
Q

What is p. mitrale?

A

Bifid P wave due atrial hypertrophy/strain (e.g. in mitral stenosis)

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128
Q

In which condition is increased P wave amplitude classically seen?

A

Cor pulmonale

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129
Q

What is the most likely congenital heart defect to be found in adulthood?

A

ASD

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130
Q

What are the two types of ASD?

A

Ostium secundum

Ostium primum

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131
Q

What are features of ASDs?

A

Ejection systolic murmur, fixed splitting of S2

Embolism may pass from venous system to L side of heart –> stroke

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132
Q

What syndrome is ostium secundum associated with?

A

Holt-Oram syndrome (tripharyngeal thumbs)

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133
Q

What do you see on ECG with ostium secundum?

A

RBBB with RAD

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134
Q

What is ostium primum associated with?

A

Abnormal AV valves

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135
Q

What do you see on ECG with ostium primum?

A

RBBB with LAD and prolonged PR interval

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136
Q

What is involved in adult life support?

A

Chest compressions + ventilations (30:2)
Defibrillation
VF/VT cardiac arrest - 1mg adrenaline (then given every 3-5 minutes)

If cardiac arrest witness in monitored patient give up to 3 quick successive shocks rather than 1 shock followed by CPR

Asystole/pulseless electrical activity - 1mg adrenaline followed by 2 min CPR prior to reassessment of rhythm

Successful resus –> O2 to reach sats of 94-98%

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137
Q

What are reversible causes of cardiac arrest?

A 
The Hs - 
Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
The Ts - 
Thrombosis (pulmonary/coronary)
Tension pneumothorax
Tamponade (cardiac) 
Toxins
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138
Q

How is ivabradine work?

A

Reduces HR by acting on Lf ion current which is highly expressed in the SA node

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139
Q

What AEs are associated with ivabradine?

A

Visual effects, esp. luminous phenomena
Headache
Bradycardia, heart block

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140
Q

What does complete heart block following an Mi indicate?

A

Right coronary artery lesion (as AV node is supplied by branch of right coronary (posterior interventricular artery))

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141
Q

What is the investigation of choice in suspected PE in renal impairment?

A

VQ scan

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142
Q

What are adverse signs in bradycardia that indicate haemodynamic compromise and the need for treatment?

A

Shock - hypotension (SBP <90), pallor sweating, cold, clammy extremities, confusion, impaired consciousness
Syncope
MI
Heart failure

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143
Q

What is given for bradycardia if there are adverse signs?

A

Atropine 500mcg IV

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144
Q

If atrophine fails to treat bradycardia what can be given?

A

Atropine up to max 3mg
Transcutaneous pacing
Isoprenaline/adrenaline infusion titrated to response

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145
Q

What are risk factors for asystole (so that even if there is an okay response to atropine, specialist help should be sought to determine need for transvenous pacing)?

A

Complete heart block with broad QRS complex
Recent asystole
Mobitz type II AV block
Ventricular pause >3s

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146
Q

Define stage I HTN

A

Clinic BP >=140/90 + ABPM daytime average/HBPM average >=135/85

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147
Q

Define stage II HTN

A

Clinic BP >=160/100, ABPM daytime average/HBPM average BP >=150/95

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148
Q

Define severe HTN

A

Clinic systolic BP >=180 or clinic diastolic BP >=110

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149
Q

What lifestyle advice should be given to those with HTN?

A

Low salt diet (<6g/day)
Reduced caffeine intake
Stop smoking, drink less, balanced diet, wt loss

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150
Q

When should you treat stage I HTN?

A

If <80 + any of: target organ damage, established CV disease, renal disease, DM or 10 year CV risk equivalent to 10% or more

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151
Q

When should stage II HTN be treated?

A

Always

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152
Q

What age should you consider referring if they develop HTN?

A

<40

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153
Q

What are step 1 treatments for HTN in those who are <55 or have T2DM?

A

ACEi/ARB

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154
Q

What are step 1 treatments for HTN in those who are >55 or afrocaribbean?

A

CCB

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155
Q

What are step 2 treatments for HTN?

A

Already on ACEi/ARB –> add CCB/thiazide type diuretic

If already on CCB –> add ACEi/ARB (ARB if afrocarribbean)

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156
Q

What are step 3 treatments for HTN?

A

Add other drug they’re not on - so on ACEi/ARB + CCB + thiazide type diuretic

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157
Q

What are step 4 treatments for HTN?

A

NB step 4 = resistant HTN
Confirm elevated BP, assess for postural hypotension, discuss adherence

If K <4.5 - add low dose spironoloactone
If K>4.5 - add alpha/beta blocker

if this fails –> refer to specialist

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158
Q

What is the BP target for someone with HTN who is <80?

A

Clinic - 140/90

ABPM/HBPM - 135/85

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159
Q

What is the BP target for someone with HTN who is >80?

A

Clinic - 150/90

ABPM/HBPM - 145/85

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160
Q

What is paroxysmal SVT?

A

Sudden onset of narrow complex tachycardia, typically AV nodal re-entry tachycardia

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161
Q

What is involved in the acute management of SVT?

A

Vagal manoeuvres - valsalva, carotid sinus massage
IV adenosine 6mg –> 12mg –> 12mg (CI in asthmatics, alt: verpamil)
Electrical cardioversion

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162
Q

What is used to prevent episodes of SVT?

A

Beta blockers

Radio-frequency ablation

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163
Q

How do statins work?

A

Inhibit HMG-CoA reductase (the rate limiting step in hepatic cholesterol synthesis)

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164
Q

What adverse effects are associated with statins?

A

Myopathy

Liver impairment

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165
Q

What are CIs for statins?

A

Macrolides
Pregnancy
Prev ICH

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166
Q

Who should recieve statins?

A

Those with established CV disease
10 year Cv risk >10%
T1 diabetics who were diagnosed >10 years ago or are aged over 40 or have established neprhopathy

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167
Q

when should statins be taken?

A

At night (this is when most of cholesterol synthesis takes place)

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168
Q

What is the currently recommended statin for primary prevention?

A

Atrovastatin 20mg

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169
Q

What is the currently recommended statin for secondary prevention?

A

Atrovastatin 80mg

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170
Q

What monitoring should be done for those on amiodarone?

A

TFT, LFT, UE, CXR prior to treatment

TFT, LFT every 6 months

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171
Q

What is VT?

A

A broad complex tachycardia originating from a ventricular ectopic focus

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172
Q

Why does VT require urgent treatment?

A

It can cause VF

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173
Q

What are the two main types of VT?

A

Monomorphic - commonly caused by MI

Polymorphic - subtype of polymorphic is torsade de pointes which is precipitated by prolongation of the QT interval

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174
Q

How is VT managed?

A

Patient has adverse signs (SBP <90, chest pain, heart failure) –> immediate cardioversion)
If none of these –> antiarrhythmic (fail –> electrical cardioversion can be used)

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175
Q

What drugs can be used to treat VT?

A

Amiodarone (through central line)
Lidocaine (caution in LV impairment)
Procainamide

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176
Q

What drug must you AVOID in VT?

A

Verapamil

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177
Q

If drug therapy fails in VT what are treatment options?

A

Electrophysiology study

Implantable cardioverted defibrillator (particularly in patients with LV impairment)

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178
Q

What is the most common important cause of VT clinically?

A

Hypokalaemia (followed by hypomagnesaemia)

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179
Q

What is the DeBakey classification of aortic dissection?

A

Type 1 - originates in ascending aorta, propagates to at least the arch and possibly beyond it
Type 2 - originates in and is confined to the ascending aorta
Type 3 - originates in descending aorta

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180
Q

How is type A aortic dissection managed?

A

Surgery

Maintain target SBP 100-120

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181
Q

How is type B aortic dissection managed?

A

Conservative
Bed rest
Reduced BP (IV labetalol)

182
Q

What are complications of a backward tear in aortic dissection?

A

Aortic incompetence/regurg

MI - inferior pattern often seen due to R coronary involvement

183
Q

What complications of a forward tear are often seen in aortic dissection?

A

Unequal arm pulses and BP
Stroke
Renal failure

184
Q

What agents have proven efficiacy in the pharmacological cardioversion of AF?

A 
Amiodarone
Flecanide (if no structural heart disease)
185
Q

What are less effective agents used in pharmacological cardioversion in AF?

A 
Beta blockers
CCB
Digoxin
Disopyramide
Procainamide
186
Q

What are common SEs of amiodarone?

A 
Bradycardia
Hyper/hypothyroidism
Pulmonary fibrosis/pneumonitis
Liver fibrosis/hepatitis
Jaundice
Taste disturbance
Persistent slate grey appearance
Raised serum transaminases
Nausea
Constipation
187
Q

What are the two situations cardioversion should be used in AF?

A

Electrical cardioversion as an emergency if the patient is haemodynamically unstable
Electrical/pharmacological cardioversion as an elective procedure where rhythm control strategy is preferred

188
Q

What is the approach to AF management?

A

Rate or rhythm control if onset of arrhythmia less than 48h

Rate control only if >48h since onset/uncertain

189
Q

How is AF onset <48h managed?

A 
Give heparin, if RF for ischaemic stroke - lifelong oral anticoagulation 
Otherwise cardiovert (DC/pharmacological - amiodarone if structural heart disease or flecainide/amiodarone if no structural heart disease)

Following DC cardioversion if AF is confirmed as being <48h - further anticoagulation unnecessary

190
Q

How is AF onset >48h ago managed?

A

Anticoagulation required for 3 weeks prior to cardioversion OR TOE to exclude left atrial appendage thrombus (if excluded can heparinise patient and cardiovert immediately)

191
Q

If you are cardioverting after 3 weeks of anticoagulation for AF, is DC or pharmacological cardioversion recommended?

192
Q

If there is a high risk of cardioversion failure in AF (e.g. prev failure/AF recurrence)?

A

Have at least 4 weeks amiodarone or sotalol prior to DC cardioversion

193
Q

Following DC cardioversion should patients be anticoagulation?

A

Yes, for at least 4 weeks (unless done <48h of onset)

194
Q

What monitoring should be done for those on statins?

A

LFTs at baseline, 3 months and 12 months

195
Q

What is the first line test for chronic heart failure?

A

N-terminal pro-B-type natriuretic peptide (NT-proBNP)

196
Q

How should NT-proBNP be interpreted?

A

If levels high - arrange specialist assessment (incl. TTE) within 2 weeks
If levels raised arrange specialist assessment (incl. TTE) within 6 weeks

197
Q

What is BNP?

A

A hormone produced mainly in the left ventricular myocardium in response to strain

198
Q

Very high levels of what hormone are associated with poor prognosis in heart failure?

199
Q

What factors increase BNP levels?

A 
LV hypertrophy
Ischaemia
Tachycardia
RV overload
Hypoaemia
GFR <60
Sepsis
COPD
DM
Age >70
Liver cirrhosis
200
Q

What factors lower BNP levels?

A 
Obesity
Diuretics
ACEi
Betablockers
ARBs
Aldosterone antagonists
201
Q

How is major bleeding in a patient on warfarin managed?

A

Stop warfarin
Give IV vit K 5mg
Prothrombin complex concentrate (or FFP if not available)

202
Q

How is minor bleeding with INR >8 in a warfarin patient managed?

A

Stop warfarin
IV vit K 1-3mg
Repeat dose of vit K if INR still too high after 24h
Restart warfarin when INR <5

203
Q

How is INR >8 and no bleeding managed in a warfarin patient?

A

Stop warfarin
Give vit K 1-5mg by mouth (using IV prep orally)
Repeat if INR still too high after 24h
Restart when INR <5

204
Q

How should INR 5-8 in a warfarin patient who has a minor bleed be managed?

A

Stop warfarin
Give IV vit K 1-3mg
Restart when INR <5

205
Q

How should INR 5-8 with no bleeding in a warfarin patient be managed?

A

Withhold 1-2 doses of warfarin

Reduce subsequent maintenance dose

206
Q

Patients on warfarin have reduced levels of what clotting factors?

A

X, IX, VII, II

207
Q

What is the management of orthostatic hypotension?

A

Education + lifestyle changes, e.g. adequate hydration
Discontinuation of vasoactive drugs, e.g. anti-HTNs, nitrates…
If symptoms persist, consider compression garments, fludrocortisone, midodrine, counter pressure manoeuvres and head tilt sleeping

208
Q

What is postural hypotension?

A

Fall in systolic BP of >20mmHg on standing

209
Q

What are causes of postural hypotension?

A

Hypovolaemia
Autonomic dysfunction - DM, PD
Drugs - diuretics, antiHTN, Ldopa, phenothiazines, antidepressants, sedatives
Alcohol

210
Q

What is the most important thing in managing AF?

A

Reducing risk of stroke

211
Q

What are the types of AF?

A 
First detected 
Recurrent episodes 
Paroxysmal 
Persistent 
Permanent
212
Q

What is recurrent AF?

A

If there are 2 or more episodes of AF

213
Q

What is paroxysmal AF?

A

AF that self-terminates (episodes tend to last less than 7 days)

214
Q

What is persistent AF?

A

Arrhythmias that do not self-terminate

215
Q

What is permanent AF?

A

Continuous AF that cannot be cardioverted or attempts to do are deemed inappropriate - treat with rate control/anticoagulation

216
Q

What are features of AF?

A

Palpitations
SoB
Chest pain
Irreg irreg pulse

217
Q

What investigation is key to a diagnosis of AF?

218
Q

What are the two paths of treating AF?

A

Rate control - reduce rate to avoid negative effects on cardiac function
Rhythm control - try to make normal sinus rhythm return

219
Q

NICE advocate using a rate control strategy to treat AF except in what situations?

A

Coexistent heart failure
First onset AF
Or an obvious reversible cause

220
Q

What drugs are used first line for rate control in AF?

A

Beta blocker

Rate limiting CCB, e.g. diltiazem

221
Q

What is second line rate control for AF?

A

Combination therapy with 2 of:

  • Beta blocker
  • Diltiazem
  • Digoxin
222
Q

When is the highest risk for embolism leading to a stroke in AF?

A

When a patient switches from AF to sinus rhythm

223
Q

What is CHA2DS2-VASc score?

A 
C = congestive heart failure 1
H = hypertension 1
A2 = age >75 -2, age 65-74 - 1
D = diabetes
S = prior stroke/TIA 2
V = vascular disease, incl IHD/PAD 1
S = sex (female)
224
Q

What CHA2DS2VASc score does not require any treatment?

225
Q

What CHA2DS2VASc score should prompt consideration of treatment?

A

1
Males - consider anticoagulation
1 - females - no treatment

226
Q

What CHA2DS2VASc score definitely requires treatment?

A

2+ - give anticoagulants

227
Q

What anticoagulation should be given for prevention of stroke in AF?

A

NOACs or warfarin

228
Q

What is bifasicular block?

A

RBBB + left anterior or posterior hemiblock, e.g. RBBB with left axis deviation

229
Q

What is trifasicular block?

A

Features of bifasicular heart block + 1st degree heart block

230
Q

What are SEs of betablockers?

A 
Bronchospasm
Cold peripheries
Fatigue
Sleep disturbances, incl. nightmares
Erectile dysfunction
Reduced hypoglycaemia awareness
231
Q

What are CIs of beta blockers?

A

Uncontrolled heart failure
Asthma
Sick sinus syndrome
Concurrent verapamil use - may precipitate severe bradycardia

232
Q

What is torsade de pointes?

A

Form of polymorphic VT associated with a long QT interval

233
Q

How is torsade de pointes managed?

A

IV Mg Sulphate

234
Q

How does pericarditis present?

A

Pleuritic chest pain relieved by sitting forward
Non-productive cough, SoB, flu like symptoms
Pericardial rub
Tachypnoea, tachycardia

235
Q

What can cause pericarditis?

A 
Viral infections (Coxsackie)
TB
Uraemia (fibrinous pericarditis) 
Trauma
Post-MI, Dressler's
Connective tissue dx
Hypothyroidism
Malignancy
236
Q

What changes do you see on ECG in pericarditis?

A

Saddle shaped ST elevation

PR depression

237
Q

All patients with suspected acute pericarditis should have what investigation?

238
Q

How is pericarditis managed?

A

Treat underlying cause

Combo of NSAIDs and colchicine 1st line for idiopathic/viral pericarditis

239
Q

How do thiazide diuretics work?

A

Inhibit Na resorption at DCT by blocking thiazide sensitive NaCl symporter

240
Q

What thiazides are recommended for HTN?

A

Indapamide or chlortalidone

241
Q

What are common AEs of thiazide diuretics?

A 
Dehydration
Postural hypotension 
Hyponatraemia, hypokalaemia, hypercalcaemia
Gout
Impaired glucose tolerance
Impotence
242
Q

What are rare SEs associated with thiazide diuretics?

A

Thrombocytopenia
Agranulocytosis
Photosensitivity rash
Pancreatitis

243
Q

Peri-arrest tachycardias should be classified as being stable or unstable based on the presence of what signs?

A

Shock - hypotension (SBP <90), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
Syncope
MI
Heart failure

244
Q

If adverse signs are present in a tachyarrhythmia how is it managed?

A

Synchronised DC shocks

Then treatment is based on whether QRS is narrow or broad and whether rhythm is regular or not

245
Q

How is regular broad-complex tachycardia managed?

A

Assume VT - give loading dose of amiodarone followed by 24h infusion

246
Q

How is irregular broad-complex tachycardia managed?

A
  1. AF with bundle branch block - treat as for narrow complex tachycardia
  2. Polymorphic VT - IV magnesium
247
Q

How is regular narrow complex tachycardia managed?

A

Vagal manoeuvres followed by IV adenosine, if unsuccessful consider diagnosis of atrial flutter and give rate control

248
Q

How is irregular narrow complex tachycardia manaed?

A

Probably AF
<48h cardiovert
Rate control + anticoagulation

249
Q

What are signs of mild airway obstruction?

A

Able to respond to ‘are you choking’

Able to breath, cough and speak

250
Q

What are signs of severe airway obstruction?

A

Unable to respond to ‘are you choking’

Unable to breath, wheezing, attempts at coughing are silent, victim may be unconscious

251
Q

How is mild airway obstruction managed?

A

Encourage pt to cough

252
Q

How is severe airway obstruction where the patient is conscious managed?

A

5 back blows
If unsuccessful 5 abdominal thrusts
Repeat

253
Q

How is severe airway obstruction where the patient is unconscious managed?

A

Call ambulance

Start CPR

254
Q

What are common things that should prompt you to reconsider putting someone on warfarin?

A

Hx falls
Old age
Alcohol xs

255
Q

What score can be used to help decide if we should put someone on warfarin based on their bleeding risk?

A

HASBLED

HTN (uncontrolled SBP >160) - 1
Abnormal renal/liver function - 1 each
S - stroke hx - 1
B - bleeding, hx of bleeding, tendency to bleed
L - liable INR -1
E - elderly (>65) - 1
D - drugs prediposing to bleeding (antiplatelet, NSAID or alcohol use (>8 drinks/week) - 1 each

Score >=3 = high risk of bleeding

256
Q

What ECG changes occur in acute MI?

A

Hyperacute t waves often first sign (only last a few mins)
ST elevation
T waves invert within first 24h (lasts days - months)
Pathological Q waves develop after several hours/days (persistent indefinitely)

257
Q

What is NYHA class I?

A

No symptoms

No limitation: ordinary physical exercise does not cause undue fatigue, SoB or palpitations

258
Q

What is NYHA class II?

A

Mild symptoms

Slight limitation of physical activity: comfortable at rest but ordinary activity –> fatigue, palpitations, SoB

259
Q

What is NYHA class III?

A

Moderate symptoms

Marked limitation of physical activity - comfortable at rest but less than ordinary activity –> symptoms

260
Q

What is NYHA class IV?

A

Severe symptoms

Unable to carry out any physical activity without discomfort, symptoms even at rest

261
Q

What are AEs of adenosine?

A

Chest pain
Bronchospasm
Transient flushing
Can enhance conduction down accessory pathways –> increased ventricular rate (e.g. WPW syndrome)

262
Q

How is adenosine given?

A

Ideally infused via a large calibre cannula due to its short halflife

263
Q

How does adenosine work?

A

Causes transient heart block in AV node

264
Q

In which group of patients should adenosine be avoided?

A

Asthmatics (bronchospasm)

265
Q

Where are the changes in a posterior MI?

A

V1-2

Also see tall R waves

266
Q

What artery is affected in a posterior MI?

A

Usually left circumflex, also right coronary

267
Q

What drug is CI in aortic stenosis?

A

Nitrates due to risk of profound hypotension

268
Q

What is Eisenmenger’s syndrome?

A

Reversal of a L to R shunt in a congenital heart defect due to pulmonary hypertension

269
Q

What is Eisenmenger’s syndrome associated with?

270
Q

What are features of Eisenmenger’s syndrome?

A 
original murmur may disappear
cyanosis
clubbing
right ventricular failure
haemoptysis, embolism
271
Q

How is Eisenmenger’s syndrome managed?

A

Heart lung transplantation is req

272
Q

What can cause constrictive pericarditis?

A

Any cause of pericarditis

Esp TB or recent cardiac surgery

273
Q

What are features of constrictive pericarditis?

A 
SoB
Right heart failure (elevated JVP, ascites, oedema, hepatomegaly)
JVP shows prominent x and y descent
Pericardial knock (loud S3)
Kussmaul sign is +ve
274
Q

What is commonly seen on CXR in constrictive pericarditis?

A

Pericardial calcification

275
Q

What is kussmauls sign?

A

A raised JVP that increases with inspiration

276
Q

What is Buerger’s disease?

A

A small and medium vessel vasculitis that is strongly associated with smoking

277
Q

What are features of Buerger’s disease?

A

Extremity ischaemia (intermittent claudication, ischaemic ulcers)
Superficial thrombophlebitis
Raynaud’s phenomenon

278
Q

What are possible causes of palpitations?

A

Arrhythmias
Stress
Increased awareness of normal heart beat/stress

279
Q

What are first line investigations for palpitations?

A

12 lead ECG
TFTs (thyrotoxicosis can precipitate AF)
UE (e.g. to rule out hypokalaemia)
FBC

280
Q

If all the first line investigations for palpitations are normal what can be done next?

A 
Holter monitoring (continuously records ECG from 2-3 leads, usually done for 24h)
Pt keeps sympto diary
281
Q

If no symptoms are found on holter monitor and symptoms continue, what investigations can be done for palpitations?

A

External loop recorder

Implantable loop recorder

282
Q

What are ECG features of hypokalaemia?

A 
U waves
Small/absent T waves
Prolonged PR interval 
ST depression
Long QT
283
Q

What is hypertrophic obstructive cardiomyopathy?

A

An AD disorder of muscle tissue caused by defects in genes encoding contracile proteins

284
Q

HOCM is the most common cause of what in young people?

A

Sudden cardiac death

285
Q

What does the most common defect in HOCM involve?

A

A mutation in the gene encoding b-myosin heavy chain protein or myosin-binding protein C –> predominantly diastolic dysfunction

286
Q

What is HOCM characterised by on biopsy?

A

Myofibrillar hypertrophy and chaotic and disorganised myocytes and fibrosis

287
Q

How does HOCM present?

A

Often asymptomatic
Exertional SoB
Angina
Syncope (typically following exercise - due to hypertrophy of ventricular septum –> AS)
Sudden death (due to ventricular arrhythmias)
Jerky pulse, large ‘a’ waves, double apex beat
Ejection systolic murmur (increases with valsalva, decreases on squatting)

HOCM –> mitral valve closure impairment –> regurg

288
Q

What is HOCM associated with?

A

Friedreich’s ataxia

WPW

289
Q

What are common echo findings in HOCM?

A

MR SAM ASH
Mitral regurg
Systolic anterior motion of the anterior mitral valve leaflet
Asymmetric hypertrophy

290
Q

What do you see on ECG in HOCM?

A

L ventricular hypertrophy
Non-specific ST segment and T wave abnormalities, progressive T wave inversion
Deep Q waves
AF sometimes seen

291
Q

What are the two types of HTN?

A

Primary/essential

Secondary

292
Q

What are secondary causes of HTN?

A 
GN
Chronic pyelonephritis
APCK
Renal artery stenosis
Primary hyperaldosteronism
Phaeochromocytoma
Cushing's
Liddles syndrome
Congenital adrenal hyperplasia
Acromegaly
Glucocorticoids
NSAIDs
Pregnancy
Coarctation of the aorta
COC
293
Q

What 3 things are essential to check when newly diagnosing someone with HTN?

A

Fundoscopy - check for hypertensive retinopathy

Urine dipstick - check for renal disease (cause/consequence)

ECG - check for LV hypertrophy/IHD

Others to consider - UE (renal dx), HbA1c, lipids

294
Q

What are SEs of CCBs?

A

Flushing
Ankle swelling
Headache

295
Q

What do ARBs typically end in?

296
Q

What is malignant hypertension?

A

Very severe hypertension (>=180/120) with evidence of acute organ damage

297
Q

What are signs and symptoms of malignant hypertension?

A

Papilloedema (must be present before a diagnosis of malignant hypertension can be made)
Retinal bleeding
Increased cranial pressure causing headache and nausea
Chest pain due to increased workload on the heart
Haematuria due to kidney failure
Nosebleeds which are difficult to stop

298
Q

What is the BP target for someone with T1DM?

299
Q

What is the BP target for someone with T2DM?

A

Intervene if BP 135/85 unless they have albuminuria/2+ features of metabolic syndrome - then intervene if 130/80

300
Q

Why are ACEi first line for hypertension in DM?

A

They have a renoprotective effect in DM

301
Q

What should afrocarribbean diabetic patients have to treat their HTN?

A

AEi + TZD/CCB

302
Q

Why should beta blockers be avoided in diabetics?

A

Can cause insulin resistance, impair insulin secretion + alter autonomic response to hypoglycaemia

303
Q

What is acute heart failure?

A

Sudden onset or worsening symptoms of heart failure

304
Q

What is AHF without pre-existing heart failure called?

A

De-novo AHF

305
Q

Which of decompensated and de-novo AFH is more common?

A

Decompensated

306
Q

What causes AHF?

A

Reduced cardiac output that results from functional/structural abnormality

307
Q

What causes de-novo heart failure?

A

Increased cardiac filling pressures and myocardial dysfunction usually due to ischaemia –> reduced cardiac output + hypoperfusion
Can cause pulmonary oedema

Less common causes - viral myopathy, toxins, valve dysfunction

308
Q

What are the most common precipitating causes of decompensated AHF?

A

ACS
Hypertensive crisis
Acute arrhythmia
Valvular disease

309
Q

How are AHF patients generally categorised?

A

With/without fluid congestion

With/without hypoperfusion

310
Q

What are symptoms of AHF?

A

Breathlessness
Reduced exercise tolerance
Oedema
Fatigue

311
Q

What are signs of AHF?

A 
Cyanosis
Tachycardia
Elevated JVP
Displaced apex beat
Chest signs - classically bibasal crackles, wheeze
S3 heart sound
312
Q

How is BP affected in AHF?

A

Normal/elevatd usually

313
Q

What is involved in the diagnostic workup of AHF?

A

Blood tests - check for underlying abnormality, e.g. anaemia, abnormal electrolytes, infection
CXR - findings incl. pulmonary venous congestion, interstitial oedema, cardiomegaly
Echo - pericardial effusion/cardiac tamponade
BNP - raised levels indicate myocardial damage and support diagnosis

314
Q

What ECG changes are associated with hypothermia?

A 
bradycardia
'J' wave - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias
315
Q

When digoxin first line for rate control in AF?

A

If the patient has co-existing heart failure

316
Q

What favours rate control in AF?

A

Older than 5

Hx IHD

317
Q

What factors favour rhythm control in AF?

A 
<65
Symptomatic 
First presentation 
Lone AF or AF secondary to a corrected precipitant (e.g. alcohol)
Congestive heart failure
318
Q

When is catheter ablation used in AF?

A

For those who have not responded to or wish to avoid antiarrhythmic medication

319
Q

What is the aim of catheter ablation in the treatment of AF?

A

To ablate the faulty electrical pathways causing the AF (usually due to aberrant electrical activity between the pulmonary veins and left atrium)

320
Q

How is catheter ablation performed?

A

Percutaneously usually via the groin

Can be done via radiofrequency/cryotherapy

321
Q

What are the guidelines re anticoagulation for catheter ablation?

A

Use 4 weeks before and during the procedure
Does not reduce stroke risk even if patients remain in rhythm so if CHA2DS2VASc >1 still req. long term anticoagulation
(if score 0 - 2 months anticoagulation)

322
Q

What are complications of catheter ablation?

A

Cardiac tamponade
Stroke
Pulmonary valve stenosis

323
Q

What is the pulmonary artery occlusion pressure an indirect measure of?

A

Left atrial pressure + thus the filling pressure of the heart

324
Q

What are key points to remember about arrhythmogenic right ventricular dysplasia?

A

Genetic AD condition
RV myocardium replaced by fatty + fibrofatty tissue
50% pts have mutation of one of the several genes which encodes the components of the desmosome
ECG abnormalities in V1-3, typically T wave inversion
Epilson wave found in 50%

325
Q

What are classic causes of dilated cardiomyopathy?

A

Alcohol
Coxsackie B virus
Wet beri beri
Doxorubicin

326
Q

What are classic causes of restrictive cardiomyopathy?

A

Amyloidosis
Post-radiotherapy
Loefflers endocarditis

327
Q

When does peripartum cardiomyopathy typically develop?

A

Last month of pregnancy - 5months post-partum

328
Q

Who is peripartum cardiomyopathy more common in?

A

Older women
Greater parity
Multiple gestations

329
Q

What is takotsubo cardiomyopathy?

A

Stress induced cardiomyopathy, e.g. pt just found out family member died and develops chest pain and feature of heart failure
Transient, apical ballooning of myocardium

330
Q

What infections can cause a cardiomyopathy?

A

Coxsackie B

Chagas

331
Q

What are infiltrative causes of cardiomyopathy?

A

Amyloidosis

332
Q

What are storage causes of cardiomyopathy?

A

Haemachromatosis

333
Q

What are toxic causes of cardiomyopathy?

A

Doxorubicin

Alcoholic cardiomyopathy

334
Q

What are inflammatory causes of cardiomyopathy?

A

Sarcoidosis

335
Q

What are endocrine causes of cardiomyopathy?

A

DM
Thyrotoxicosis
Acromegaly

336
Q

What are neuromuscular causes of cardiomyopathy?

A

Friedreich’s ataxia
Duchenne-Becker muscular dystrophy
Myotonic dystrophy

337
Q

What nutritional deficiency can cause cardiomyopathy?

338
Q

What is an autoimmune cause of cardiomyopathy?

339
Q

What are features of a dilated cardiomyopathy?

A

Four chamber dilatation and systolic dysfunction

340
Q

What is Wolff-Parkinson White syndrome?

A

A condition caused by a congenital accessory conducting pathway between the atria and ventricles –> AVRT

As accessory pathway does not slow conduction AF can degenerate into VF

341
Q

What are ECG features of WPW?

A

Short PR interval
Wide QRS with slurred upstroke (delta wave)
Left axis deviation if R sided accessory pathway
Right axis deviation if left sided accessory pathway

342
Q

How can you differentiate between WPW type A and B?

A

Type A - left sided - dominant R wave in V1

Type B - right sided - no dominant R wave in V1

343
Q

What is WPW associated with?

A 
HOCM
Mitral valve prolapse
Ebstein's anomaly
Thyrotoxicosis
Secundum ASD
344
Q

What is the definitive management of WPW?

A

Radiofrequency ablation of accessory pathway

345
Q

What medical therapies can be used for WPW?

A

Sotalol (only if no AF), amiodarone, flecanide

346
Q

What every day activities may contribute to orthostatic hypotension?

A

After meals
Venous pooling during exercise
Prolonged bed rest (deconditioning)

347
Q

What are the three main SEs of GTN spray?

A

Hypotension
Headache
Tachycardia

348
Q

What is the most important risk factor for aortic dissection?

349
Q

What are associations with aortic dissection?

A 
Trauma
Bicuspid aortic valve
Marfans, EDS
Turners, Noonans
Pregnancy
Syphillis
350
Q

What are the clinical features of aortic dissection?

A

Tearing chest pain, radiates to back
AR
Hypertension
If coronary arteries involved –> angina
Spinal artery involvement –> paraplegia
Distal aorta involvement –> limb ischaemia

351
Q

Patients with heart failure and a reduced LVEF should be given what as first line treatment?

A

A beta blocker and an ACE inhibitor

352
Q

What is normal LVEF?

353
Q

What are the two types of chronic heart failure?

A

Impaired left ventricular contraction (systolic heart failure)

Impaired left ventricular relaxation (diastolic heart failure)

354
Q

What does left ventricular failure lead to?

A

Back up of blood into the lungs

355
Q

What are key features of chronic heart failure?

A 
Breathlessness (worse on exertion)
Cough (frothy white/pink sputum)
Orthopnoea 
PND
Peripheral oedema
356
Q

What is PND?

A

Suddenly wakening up at night with acute SoB and cough

357
Q

What are causes of chronic heart failure?

A

IHD
Valvular heart disease (e.g. aortic stenosis)
HTN
Arrhythmias, AF

358
Q

How is chronic heart failure managed?

A 
Check BNP (urgent referral if BNP >2000)
Medical and surgical treatment
359
Q

What is key to remember about treating someone with heart failure who has valvular disease?

A

Avoid ACEi use until a specialist can see the patient

360
Q

What should be offered to any patient with BP >=140/90mmHg?

A

ABPM or HBPM to confirm diagnosis

361
Q

In which hypertensive patients is one reading of HTN enough for immediate treatment?

A

If BP >=180/110mmHg

If signs of papilloedema/retinal haemorrhages –> same day assessment by specialist

362
Q

What are common clinic signs in PE?

A

Tachypnoea
Crackles
Tachycardia
Fever

363
Q

What should all patients presenting with PE have done?

A

Hx, Ex, CXR (to exclude other pathologies)

364
Q

What scoring system is used to determine likelihood of a PE?

A

Clinical signs and symptoms of DVT - 3
Alternative diagnosis is less likely than PE - 3
HR >100
Immobilisation >3 days/surgery in last 4 weeks - 1.5
Prev DVT/PE - 1.5
Haemopytsis - 1
Malignancy (on treatment or treated in last 6 months or palliative) - 1

365
Q

If well’s score is ___ or more, PE is likely.

366
Q

If PE is likely what is your management?

A

Arrange urgent CTPA (if delay give therapeutic anticoagulation (DOAC) in interim

367
Q

If PE is unlikely what is your management?

A

D-dimer
If +ve –> CTPA
-ve –> consider alt diagnosis

368
Q

What are the classic ECG signs seen in PE?

A

Large S wave in lead I, large Q wave in lead III and inverted T wave in lead III

Most common finding is sinus tachycardia

RBBB and R axis deviation also associated with PE

369
Q

What must you consider in cardiac arrest before calling time of death?

A

The 8 reversible causes of cardiac arrest (hypothermia, hypoxia, hypovolaemia, hypokalaemia, hyperkalaemia, hypoglycaemia, tension pneumothorax, toxins, tamponade, thrombosis)

370
Q

What should all patients be offered post-MI?

A

Dual antiplatelet therapy (aspirin + second antiplatelet)
ACEi
Beta blocker
Statin

371
Q

When can sexual activity resume after an MI?

A

4 weeks

Only use PDE5 inhibitor 6 months after an MI

372
Q

What are the second antiplatelets of choice in secondary prevention fo MI?

A

Ticagrelor + prasugrel
Post-ACS medically managed - ticagrelor (stop after 12m) + aspirin

Post-PCI: prasugrel/ticagrelor (stop after 12m) + aspirin

373
Q

When might aldosterone antagonists be used after an MI?

A

In those who had an acute MI and who have symptoms/signs of heart failure and LV systolic dysfunction

374
Q

When are nitrates contraindiated in ACS management?

A

In hypotension (<90mmHg)
Bradycardia (<50bpm)
Recent PDE5 inhibitors

375
Q

When should type 1 diabetics be offered statins?

A

Age >40
DM for >10 years
Established neprhopathy
Other CV risk factors, e.g. HTN, obesity

Give atrovastatin 20mg

376
Q

How can you distinguish between unstable angina and NSTEMI?

A

Serial troponin tests (rises in NSTEMI, does not rise in unstable angina)

377
Q

In which situations are patients with long QT given implantable cardioverted defibrillators?

A

High risk situations only, e.g. if QTc >500ms or prev. episodes of cardiac arrest

378
Q

How do you measure the QT interval?

A

From start of Q to end of T wave

379
Q

What does a long QT interval mean?

A

QRS = ventricular depol
T wave = ventricular repol

Long QT = some of heart cells taking longer to repolarise

380
Q

What kindof channels do class 1A antiarrythmics block?

381
Q

What kind of channels do class II antiarrythmics block?

382
Q

In what % of cases do VSDs spontaneously close?

383
Q

What are congenital VSDs associated with?

A

Downs
Edwards
Patau syndrome

384
Q

What is the classic murmur heard in VSD?

A

Pan systolic murmur which is louder in smaller defects

Louder P2

385
Q

What are complications of VSD?

A 
Aortic regurg
IE
Eisenmenger's complex
R heart failure
Pulmonary hypertension
386
Q

The majority of VSDs are caused by a defect in the muscular region/membranous region of the ventricular septum?

A

Membranous

387
Q

What is NT-proBNP?

A

Inactive prohormone of BNP that is released from left ventricle in response to strain and acts to increase renal excretion of water and sodium, and relax smooth muscle –> vasodilation

388
Q

What may a diagnosis of new LBBB point toward?

A

Diagnosis of ACS

389
Q

Define postural hypotension?

A

Fall in SBP >20mmHg on standing (or DBP >10mmHg or drop in SBP below 90mmHg)

390
Q

What are causes of postural hypotension?

A

Hypovolaemia
Autonomic dysfunction - PD, DM (HR does not respond appropriately)
Drugs - antidepressants, antihypertensives, Ldopa, phenothiazines, sedatives
Alcohol

391
Q

What is the mechanism of action of warfarin?

A

Inhibits epoxide reductase preventing reduction of vit K to its active hydroquinone form prevents formation of factors II, VII, IX, X) and protien C

392
Q

What is the target INR for someone who has had a VTE?

A

2.5

If recurrent 3.5

393
Q

What is the target INR for someone on warfarin for AF?

394
Q

What factors may potentiate warfarin?

A

Liver disease
P450 enzyme inhibitors, e.g. amiodarone, ciprofloxacin
Cranberry juice
Drugs which displace warfarin from plasma albumin, e.g. NSAIDs
Drugs which inhibit platelet function, e.g. NSAIDs

395
Q

What SEs are associated with warfarin?

A

Haemorrhage
Teratogenic
Skin necrosis
Purple toes

396
Q

What is the mechanism of action of dipyridamole?

A

Inhibits phosphodiesterase and decreases cellular uptake of adenosine

397
Q

What is preload?

A

Amount of blood entering ventricles at end of diastole (increased pre-load increases contraction = frank startling mechanism)

398
Q

What is afterload?

A

Force cardiomyocytes must overcome to pump blood out of the ventricle

399
Q

What does the heart look with in hypertrophic cardiomyopathy?

A

Left ventricular hypertrophy with no chamber dilation

400
Q

What is the most common mutation in hypertrophic cardiomyopathy?

A

Myosin heavy chain

401
Q

What are causes of hypertrophic cardiomyopathy?

A

Chronic hypertension –> increased afterload –> LV hypertrophy
Aortic stenosis
Inherited

402
Q

What are the two types of hypertrophic cardiomyopathy?

A

Obstructive - LV hypertrophy + interventricular septal hypertrophy (blocks outflow through aorta)

Non-obstructive type - LV hypertrophy (reduced EDV —> reduced SV –> reduced CO)

403
Q

How does LV ejection fraction differ between obstructive and non-obstructive hypertrophic cardiomyopathy?

A

In obstructive the interventricular septum thickening blocks outflow –> reduced ejection systolic fraction

Normal in non-obstructive as outflow is not blocked

404
Q

What kind of pulse is sometimes associated with HOCM?

A

Bisferiens pulse

405
Q

An inferior MI and AR murmur points towards what?

A

Ascending aortic dissection

406
Q

Following a TIA or stroke, what should be given to AF patients?

A

Warfarin/direct thrombin/factor Xa inhibitor

Start after 2 weeks in absence of haemorrhage

407
Q

In general, how long is warfarin stopped before surgery?

A

5 days and once the INR is <1.5

408
Q

When may warfarin be resumed after surgery?

A

On evening/next day after surgery

409
Q

How is acute heart failure managed?

A 
Oxygen 
IV loop diuretics
Opiates
Vasodilators
Inotropic agents
CPAP
Ultrafiltration 
Mechanical circulatory assistance, e.g. intra-aortic balloon counterpulsation/ventricular assist devices
Consider stopping beta blockers
410
Q

What is Takotsubo cardiomyopathy?

A

Non-ischaemic cardiomyopathy associated with transient, apical ballooning of the myocardium
Can be triggered by stress

411
Q

What are features of Takotsubo cardiomyopathy?

A

Chest pain
Features of heart failure
ST elevation

412
Q

What are considered acceptable changes in UE and creatinine after starting an ACEi?

A

Increase in serum Cr up to 30% from baseline

Increase in K up to 5.5mmol/l

413
Q

Do NICE recommend routine antibiotic prophylaxis for those at risk of infective endocarditis undergoing dental and other procedures?

414
Q

After starting an ACE inhibitor, significant renal impairment may occur in the the patient has what?

A

Undiagnosed bilateral renal artery stenosis

415
Q

How is systolic hypertension managed?

A

In same way as essential hypertension

416
Q

What is the advice re VTE related to travel?

A

No major risk factors - no prophylaxis req
Major risk factors - compression stockings
If risk very high - consider delaying flight or LMWH

417
Q

When should CPAP be considered in those who have acute heart failure?

A

Considered for those not responding to treatment

418
Q

What are features of chronic heart failure?

A 
SoB
Cough 
Orthopnoea
PND
Cardiac wheeze
Anorexia
Bibasal crackles on Ex
419
Q

What are signs of R heart failure?

A

Raised JVP
Ankle oedema
Hepatomegaly

420
Q

Is atropine recommended for asystole/pulseless electrical activity?

421
Q

What is the mechanism of action of loop diuretics?

A

Inhibit Na-K-Cl cotransporter on thick ascending limb of loop of henle

422
Q

What are SEs of loop duretics?

A 
hypotension
hyponatraemia
hypokalaemia, hypomagnesaemia
hypochloraemic alkalosis
ototoxicity
hypocalcaemia
renal impairment (from dehydration + direct toxic effect)
hyperglycaemia (less common than with thiazides)
gout
423
Q

What are features of Takayasu’s arteritis?

A 
Systemic features, malaise, headache
Unequal BP in upper limbs
Carotid bruit
Intermittent claudication 
AR
Seen in young Asian females classically
424
Q

When should treatment with statins be discontinued?

A

If serum transaminases rise to and persist 3x upper limit of reference range

425
Q

How are pulseless electrical activity and asystole managed?

A

These are non-shockable rhythms and are therefore unresponsive to defib
give 1mg IV adrenaline and CPR
Can give adrenaline 1mg every 3-5m during alternate 2-min loops of CPR

426
Q

What are the criteira for urgent valvular replacement in IE?

A

Severe congestive cardiac failure
Overwhelming sepsis
Recurrent embolic episodes despite antibiotics
Pregnancy

427
Q

What clotting test does warfarin affect?

428
Q

What is teh most common ECG finding in hypercalcaemia?

A

Shorted QT interval

429
Q

How long should you not drive for after an MI?

430
Q

Do patients who have had catheter ablation for AF still require long-term anticoagulation?

A

Yes, as per their CHADSVASC

431
Q

What signs do you see on ECG in digoxin toxicity?

A

Down sloping ST depression
Flattened/inverted T waves
Short QT interval
Arrhythmias, e.g. AV blocl, bradycardia

432
Q

What is the most common cause of secondary hypertension?

A

Primary aldosteronism

433
Q

What is atrial flutter?

A

A form of SVT characterised by succession of rapid atrial depolarisation waves

434
Q

What are the ECG findings in atrial flutter?

A

Sawtooth appearance
Underlying atrial rate often about 300/min
Flutter waves may be visible following carotid sinus massage/adenosine

435
Q

How is atrial flutter managed?

A

Similar to AF

436
Q

What is curative in most patients with atrial flutter?

A

Radiofrequency ablation of tricuspid valve isthmus

437
Q

What is the most common form of cardiomyopathy?

A

Dilated (DCM)

438
Q

What are causes of DCM?

A

idiopathic: the most common cause
myocarditis: e.g. Coxsackie B, HIV, diphtheria, Chagas disease
ischaemic heart disease
peripartum
hypertension
iatrogenic: e.g. doxorubicin
substance abuse: e.g. alcohol, cocaine
inherited: either a familial genetic predisposition to DCM or a specific syndrome e.g. Duchenne muscular dystrophy
around a third of patients with DCM are thought to have a genetic predisposition
a large number of heterogeneous defects have been identified
the majority of defects are inherited in an autosomal dominant fashion although other patterns of inheritance are seen
infiltrative e.g. haemochromatosis, sarcoidosis

439
Q

What is the pathophysiology of DCM?

A

Dilated heart leading to predominantly systolic dysfunction

Eccentric hypertrophy seen (sarcomeres added in series)

440
Q

What are features of DCM?

A

Heart failure
Systolic murmur
S3
Balloon appearance of heart on CXR

441
Q

What is the grading of murmurs?

A

Grade 1 - very faint, frequently overlooked
Grade 2 - slight murmur
Grade 3 - moderate murmur, without palpable thrill
Grade 4 - loud murmur with palpable thrill
Grade 5 - very loud murmur with extremely palpable thrill
Grade 6 - extremely loud murmur, can be heard wo stethoscope touching chest wall

442
Q

What is the half life of adenosine?

A

10 seconds

443
Q

Can warfarin be used when breast feeding?

444
Q

What should be given to patients on warfarin who are going for emergency surgery?

A

If surgery can wait 6-8h: 5mg vit K IV

If surgery cant wait - 25-50 units/kg four factor prothrombin complex

445
Q

When is thrombolysis given first line for PE?

A

Massive PE with circulatory failure

446
Q

Define mild hypothermia

447
Q

Define moderate/severe hypothermia

448
Q

What are general RFs for hypothermia?

A 
GA
Substance abuse
Hypothyroidism
Impaired mental status
Homelessness
extremes of age
449
Q

What are signs of hypothermia?

A

Shivering
Cold pale skin
Slurred speech
Tachycardia, tachypnoea, hypertension if mild
Resp depression, bradycardia and hypothermia if moderate

450
Q

What are investigations for hypothermia?

A 
Temperature 
12 lead ECG 
FBC, serum electrolytes
BG
ABG
Coagulation factors
CXR
451
Q

How should hypothermia causing cardiac arrest be managed?

A

Chest compressions but withhold shocks until patients temp >30

CARD - 1 (28 decks)

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