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Year 4 Final > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the management of a major bleed while on warfarin?

A

Stop warfarin
Give IV vit K 5mg and prothrombin complex concentrate

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2
Q

What antibiotics should statins bet stopped on?

A

Macrolides

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3
Q

If a patient is on monotherapy for angina and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs:

A

a long-acting nitrate
ivabradine
nicorandil
ranolazine

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4
Q

Adverse effects of thiazide diuretics

A

Dehydration
Postural hypothension
Hyponatremia, hypokalaemia, hypercalcaemia
Gout
Impaired glucose tolerance
Impotence

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5
Q

When is arenaline used in cardiac arrest

A

Non shockable rhythm or if in shockable rhythm but 3 unsuccessful shocks

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6
Q

What score must be calculated in patients with an NSTEMI?

A

GRACE score
If above 3% do a coronary angiography within 72 hours

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7
Q

Management if Wells score more than 4

A

Immediate CTPA or interim anticoagulation whist awaiting CTPA

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8
Q

MI complication that presents with acute HF secondary to a cardiac tamponade?

A

Left ventricular free wall rupture

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9
Q

Management of acute stroke in the absence of haemorrhage?

A

Anticoagulation therapy should be commenced after 2 weeks. Antiplatelet therapy should be given in the intervening period. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed

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10
Q

Side effects of beta blockers?

A

bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction

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11
Q

Cytochrome p450 and warfarin

A

Inhibitors of the cytochrome P450 system leads to accumulation of warfarin and causes the INR to increase.

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12
Q

How can constrictive pericarditis be differentiated from cardiac tamponade

A

Cardiac tamponade has pulsus paradoxus (an abnormally large drop in BP during inspiration)
Constrive pericarditis has Kussmaul’s sign

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13
Q

What is third degree heart block?

A

No association between the P waves and the QRS complexes

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14
Q

What is Buerger’s disease?

A

Small and medium vessel vasculitis that is strongly associated with smoking.

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15
Q

Pneumonic for hypertension medication in over 55?

A

Old people like CATs
Calcium blocker
ACE/ARB
Thiazide-like diuretic

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16
Q

What is Dressler’s syndrome?

A

Autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain,

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17
Q

When does acute mitral regurgitation happen post MI?

A

More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle.

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18
Q

Immediate treatment of bradychardia?

A

500mg atropine

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19
Q

What is eisenmenger’s syndrome?

A

reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension

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20
Q

What is malignant hypertension?

A

severe hypertension and bilateral retinal hemorrhages and exudates

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21
Q

Causes of LBBB

A

Heart issues

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22
Q

Causes of LBBB

A

Heart issues

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23
Q

Causes of RBBB

A

Lung things

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24
Q

What shoudl you think when you see a global T wave inversion?

A

Think non cardiac causes of abnormal ECG

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25
Q

Kussmals sign?

A

JVP increasing with inspiration

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26
Q

Most specific ECG change for pericarditis?

A

PR depression

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27
Q

What is bifasicular block?

A

combination of RBBB with left anterior or posterior hemiblock

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28
Q

What is trifasicular block

A

combination of RBBB with left anterior or posterior hemiblock and first degree heart block

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29
Q

What is Wolff Parkinson White syndrome?

A

caused by a congenital accessory conducting pathway between the atria and ventricles leading to a atrioventricular re-entry tachycardia

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30
Q

Possible ECG features of WPW?

A

short PR interval
wide QRS complexes with a slurred upstroke - ‘delta wave’
left axis deviation if right-sided accessory pathway*
right axis deviation if left-sided accessory pathway*

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31
Q

What should be started following a TIA?

A

anticoagulation for AF should start immediately once imaging has excluded haemorrhage

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32
Q

Main ECG abnormality in hypercalcaemia?

A

Shortening of the QT interval

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33
Q

What is Wellen’s syndrome

A

ECG pattern that is typically caused by high-grade stenosis in the left anterior descending coronary artery.

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34
Q

Treatment of torsades de points?

A

IV magnesium sulfate

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35
Q

What foods should patients taking warfarin avoid?

A

Foods high in Vitamin K

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36
Q

Acute management of SVT

A

Vagal manoeuvres
IV adenosine (6mg, 12mg, 18mg)
Electrical cardioversion

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37
Q

Contraindication to statins?

A

Macrolides
Pregnancy

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38
Q

In ACS when should nitrates not be used>?

A

If the patient is hypotensive

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39
Q

Inheritance pattern of hypertrophic obstriuctive cardiomyopathy

A

Autosomal domainant

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40
Q

What is arrhythmogenic right ventricular cardiomyopatjhy?

A

Autosomal domiannt condition where the right ventricular myocardium is replaced by fatty and fibrofatty tissue

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41
Q

ECG chnges of arrhythmogenic right ventricular cardiomyopathy?

A

T wave inversion in leads V1-3V3 without the presence of a RBBB

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42
Q

What is Wellen’s syndrom?

A

ECG pattern that is typically caused by high grade stenosis in the left anterior descending coronary artery

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43
Q

ECG features of Wellen’s syndrome?

A

Biphasic or deep T wave inversion in V2-3
Minimal STEMI
No Q waves

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44
Q

What is BNP?

A

hormone produced mainly by the left ventricular myocardium in response to strain.

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45
Q

What kind of medication is indapamide?

A

Thiazide like diuretic

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46
Q

ACS inital drug therapy

A

MONA
Morphine if severe pain
Oxygen if sats below 94
Nitrates- If ongoing chest pain
Aspirin 300mg

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47
Q

Side effects of warfarin

A

Haemorrhage
Teratogenuc
Skin necrosis
Purple toes

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48
Q

Rate control in AF

A

BB
CCB
Digoxin

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49
Q

What medication reverses efffecgs of dabigatran?

A

Idarucixumab

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50
Q

What is arrhythmogenic right ventirvcular cardiomyopathy?

A

Inherited cardiovascular disease which may present sith sudden cardiac death

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51
Q

ECG abnormalities in arrhythmogenic right ventricular cardiomyopathy?

A

V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex

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52
Q

When is pulsus paradoxus found?

A

Severe asthm
Cardac tamponade

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53
Q

Investigations for takyusa arteritis?

A

vascular imaging of the arterial tree is required to make a diagnosis of Takayasu’s arteritis
either magnetic resonance angiography (MRA) or CT angiography (CTA)

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54
Q

Why would hypertrophic obstructive cardiomyopathy cause sudden death most commonly?

A

Ventricular arrhythmias

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55
Q

Features of hypercalcaemia?

A

‘bones, stones, groans and psychic moans’
corneal calcification
shortened QT interval on ECG
hypertension

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56
Q

First line for HF?

A

Ace-I and BB

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57
Q

What valve is most commonly affeted in IE?

A

Tricuspid valve

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58
Q

What is takotsubo cardiomyopathy?

A

Type of non-ischaemic cardiomyopathy associated with a transient, apical ballooning of the myocardium. It may be triggered by stress.

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59
Q

Most common cause of mitral stenosis?

A

Rheumatic fever

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60
Q

What are features of aortic regurgitiation?

A

early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
collapsing pulse
wide pulse pressure
Quincke’s sign (nailbed pulsation)
De Musset’s sign (head bobbing)
mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams

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61
Q

Mneumonic for mumurs louder on inspiration and expiration?

A

RILE
Right inspiration
Left expiration

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62
Q

Mneumonic for minor criteria for Duke’s

A

FIVEMP
F - Fever
I - Immunological phenomena (Oslers, nodes, Roth spots, GN, Rh Factor)
V - Vascular phenomena (arterial embolisation, mycotic aneurism, Janeway lesions)
E - Echocardiographic evidence not meeting dukes
M - Microbiological evidence not meeting dukes
P - Predisposition

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63
Q

Presentation of left ventricular free wall rupture?

A

Acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds).

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64
Q

Best first line for 45 YO male for hypertension but he has renovascular disease?

A

Amlodipine (CCB)

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65
Q

Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillation

A

amiodarone
flecainide (if no structural heart disease)
others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone

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66
Q

What things are mitral valve prolapse associated with?

A

congenital heart disease: PDA, ASD
cardiomyopathy
Turner’s syndrome
Marfan’s syndrome, Fragile X
osteogenesis imperfecta
pseudoxanthoma elasticum
Wolff-Parkinson White syndrome
long-QT syndrome
Ehlers-Danlos Syndrome
polycystic kidney disease

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67
Q

How long should CPR be continued after giving a thrombolytic drug?

A

60-90 minutes

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68
Q

ECG findings in PE?

A

the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’. However, this change is seen in no more than 20% of patients
right bundle branch block and right axis deviation are also associated with PE
sinus tachycardia may also be seen

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69
Q

First line for over 55 but got diabetes?

A

AceI or ARB

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70
Q

Co-administration of sacubitril (a neprilysin inhibitor) with an ACE inhibitor can cause what?

A

otentiates the levels of plasma bradykinin as they both inhibit bradykinin degradation, resulting in a higher risk of angioedema. In order to reduce this risk a 36 hour washout period is required to prevent the accumulation of bradykinin.

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71
Q

BP drop that can be used to diagnose orthostatic hypotension?

A

there is a drop in SBP of at least 20 mmHg and/or a drop in DBP of at least 10 mmHg after 3 minutes of standing

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72
Q

Pathophysiology of hypertrophic obstructive cardiomyopathy?

A

the most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C

results in predominantly diastolic dysfunction
left ventricle hypertrophy → decreased compliance → decreased cardiac output

characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes (‘disarray’) and fibrosis on biopsy

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73
Q

What is hypertrophic obstructive cardiomyopathy associated with?

A

Friedreich’s ataxia
Wolff-Parkinson White

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74
Q

Side effects of Ace-i

A

cough- occurs in around 15% of patients and may occur up to a year after starting treatment. thought to be due to increased bradykinin levels
angioedema: may occur up to a year after starting treatment
hyperkalaemia
first-dose hypotension: more common in patients taking diuretics

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75
Q

How long are provoked PEs treated for?

A

3 months

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76
Q

Beck’s triad?

A

hypotension
raised JVP
muffled heart sounds

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77
Q

What medication should not be used in VT?

A

Verapamil

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78
Q

Why does a narrow pulse pressure occur?

A

happens when your heart isn’t pumping enough blood, which is seen in heart failure and certain heart valve diseases

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79
Q

What type of arrhythmia is long QT associated with?

A

Torsades

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80
Q

ECG findings in PE?

A

the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’. However, this change is seen in no more than 20% of patients
right bundle branch block and right axis deviation are also associated with PE
sinus tachycardia may also be seen

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81
Q

Adverse effects of nicorandil?

A

headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration

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82
Q

What is S4?

A

results from the contraction of the atria pushing blood into a stiff or hypertrophic ventricle, indicating failure of the left ventricle

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83
Q

What is a stroke-Adams attack?

A

Collapse without warning, associated with loss of consciousness for a few seconds[1]. Typically, complete (third-degree) heart block is seen on the ECG during an attack (but other ECG abnormalities such as tachy-brady syndrome have been reported

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84
Q

How can dabigatran effects be reversed?

A

Idarucizumab

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85
Q

Post Mi mneumonic

A

DABS
Dual antiplatelet therapy
AceI
BB
Statin

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86
Q

What is Wellen’s syndrome?

A

ECG pattern that is typically caused by high-grade stenosis in the left anterior descending coronary artery.

The patient’s pain may have resolved at the time of presentation and cardiac enzymes may be normal/minimally elevated.

ECG features
biphasic or deep T wave inversion in V2-3
minimal ST elevation
no Q waves

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87
Q

First line for bradycardia?

A

Atropine

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88
Q

Who should statins be given to QRISK score wise?

A

People with a 10 year cardiovascular risk over 10%

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89
Q

Features of an aortic regurgitation murmur?

A

Early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
Collapsing pulse
Wide pulse pressure
Quincke’s sign (nailbed pulsation)
De Musset’s sign (head bobbing)
Mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams

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90
Q

First line for angina pectoris?

A

Beta blocker of CCB

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91
Q

Adverse effects of thiazide diuretics?

A

dehydration
postural hypotension
hyponatraemia, hypokalaemia, hypercalcaemia*
gout
impaired glucose tolerance
impotence

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92
Q

Anteroseptal ECG changes and which coronary artery?

A

V1-V4
LAD

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93
Q

Inferior ECG changes and coronary artery?

A

II, III, aVF
RCA

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94
Q

Anterolateral ECG changes and coronary artery?

A

V1-V6, I, aVL
Proximal LAD

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95
Q

Lateral ECG changes and coronary artery

A

I, aVL, plus/minus V5-6
Left circumflex

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96
Q

Posterior ECG changes and coronary artery

A

Changes in. V1-3
Reciprocal changes of STEMI are seen:
Horizontal ST depression
Tall, broad R waves
Upright T waves
Dominant R wave in V2

Usually left circumfle, also RCA

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97
Q

How many seconds is 1 small square on an ECG?

A

0.04 seconds

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98
Q

How many seconds is 5 small squares on an ECG?

A

0.2 seconds

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99
Q

How many seconds is 5 large squares on an ECG?

A

1 second

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100
Q

Axis of p wave morphology

A

Upright in leads I and II. Inverted in aVR

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101
Q

Duration of a normal P wave

A

Less than 0.12s

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102
Q

What is the P wave morphology in V1?

A

Biphasic- Positive and negative deflections

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103
Q

What are the part of the P wave

A

First half is right depolarisation and secocnd part is left

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104
Q

What are the part of the P wave

A

First half is right depolarisation and secocnd part is left

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105
Q

What does the Q wave represent?

A

Normal left to right depolarisation of the interventricular septum

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106
Q

Pathological Q waves

A

More than 40 ms wide
More than 2mm deep
More than 25& of depth of QRS complex
Seen in leads V1-3

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107
Q

When should the loss of Q waves be considered abnormal

A

If in leads V5-6
This is most commonly due to LBBB

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108
Q

What are the 3 key R wave abnormalities?

A

Dominant R wae in V1
Dominant R wave in aVR
Poor R wave progreession

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109
Q

What leads are T waves upright?

A

All except aVR and V1

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110
Q

When are peaked T waves commonly seen?

A

Hyperkalaemia

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111
Q

When are broad, asymmetrically peaked T waves often seen?

A

In early stages of a STEMI

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112
Q

T wave inversion due to MI in contigous leads based on the anatomical location of the area of ischaemia/infarction
Inferior-
Lateral-
Anterior-

A

Inferior = II, III, aVF
Lateral = I, aVL, V5-6
Anterior = V2-6

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113
Q

In LBBB where is the T-wave inversion?

A

I, aVL and V5-6

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114
Q

In right bundle branch block where is the T wave inversion?

A

Right precordial leads in V1-3

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115
Q

Where do you get T wave inversion in LVH?

A

I, aVL an V5-6

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116
Q

Where do you get T wave inversion in RVH

A

Right precodial leas in V1-3 and also in the inferior leads (II,III and AVF)

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117
Q

Causes of biphasic T waves?

A

MI and hypokalaemia

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118
Q

What does a T phase due to ischaemia look like?

A

T waves goes up then down

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119
Q

What does a T wave due to hypokalaemia do?

A

T waves goes down then up

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120
Q

What is Wellens syndrome?

A

Wellens Syndrome is a clinical syndrome characterised by biphasic or deeply inverted T waves in V2-3, plus a history of recent chest pain now resolved. It is highly specific for critical stenosis of the left anterior descending artery (LAD)

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121
Q

Causes of prominent U waves?

A

Bradychardia and severe hypokalaemia

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122
Q

What is a J wave?

A

positive deflection seen at the J point in precordial and true limb leads. It is most commonly associated with hypothermia. These changes will appear as a reciprocal, negative deflection in aVR and V1.

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123
Q

What is the J point?

A

Point where the QRS complex joins the ST segment. It represents the approximate end of depolarization and the beginning of repolarization as determined by the surface ECG. There is an overlap of around 10ms.

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124
Q

What is a delta wave?

A

Slurred upstroke in the QRS complex. It relates to pre-excitation of the ventricles, and therefore often causes an associated shortening of the PR interval. It is most commonly associated with pre-excitation syndromes such as WPW.

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125
Q

What should you give to patients on warfarin undergoing emergency surgery?

A

Four factor prothrombin complex concentreate

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126
Q

GRACE score

A

age
heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels

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127
Q

Which patients with NSTEMI/unstable angina should have coronary angiography (with follow-on PCI if necessary)?

A

immediate: patient who are clinically unstable (e.g. hypotensive)
within 72 hours: patients with a GRACE score > 3% i.e. those at intermediate, high or highest risk
coronary angiography should also be considered for patients if ischaemia is subsequently experienced after admission

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128
Q

Mneumonic for rheumatic fever?

A

JONES
Joints
O (shaped as heart) pancarditis
N odules (subcutaneous)
E rythema marginatum
S ydenham chorea

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129
Q

What should you do when INR 5-8?

A

INR 5.0-8.0 (minor bleeding) - stop warfarin, give intravenous vitamin K 1-3mg, restart when INR < 5.0

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130
Q

SVT adenosine protocol?

A

Adenosine 6mg, then 12, then 18

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131
Q

Second line preference for hyprtension in afro caribbean?

A

ARB

132
Q

What should be done following a TIA?

A

Anticoagulation should be started immediately

133
Q

When should anticoagulation be started post ischaemic stroke

A

After 2 weeks

134
Q

When should anticoagulation be started post ischaemic stroke

A

After 2 weeks

135
Q

What is seen on an ECG in cardiac tamponade?

A

Electrical alternans

136
Q

ECG findings with digoxin?

A

down-sloping ST depression (‘reverse tick’, ‘scooped out’)
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia

137
Q

ECG findings with digoxin?

A

down-sloping ST depression (‘reverse tick’, ‘scooped out’)
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia

138
Q

Drug delivery in ALS?

A

IV access should be attempted and is first-line
if IV access cannot be achieved then drugs should be given via the intraosseous route (IO)
delivery of drugs via a tracheal tube is no longer recommended

139
Q

Frist line for hypertension if have T2DM?

A

Acei or ARB

140
Q

What is S3 caused by?

A

Diastolic filling of the ventricle
Heard in LVF, Constructuve pericarditis and MR
Normal if lesss than 30

141
Q

Angina management

A

Aspirin and a statin
GTN spray
BB or CCB first line
If CCB first line give verapamil or dilitazem
If used in combination with BB then use a longer-acting dihydropine (amlodipine, modified release nifedipine

142
Q

Drugs that pologn QT interval?

A

amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
methadone
chloroquine
terfenadine**
erythromycin
haloperidol
ondanestron

143
Q

Drugs that pologn QT interval?

A

amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
methadone
chloroquine
terfenadine**
erythromycin
haloperidol
ondanestron

144
Q

Side effects of ivabradine?

A

visual effects, particular luminous phenomena, are common
headache
bradycardia, heart block

145
Q

What does stanford B aortic dissection mean?

A

Site of dissection is in the descending aorta

146
Q

What is Buerger’s disease

A

Small and medium vessel vasculitis that is strongly associated with smoking

147
Q

Features of Buerger’s disease?

A

extremity ischaemia
intermittent claudication
ischaemic ulcers
superficial thrombophlebitis
Raynaud’s phenomenon

148
Q

What should be first line in peri-arrest tachycardian if have adevrse signs?

A

Synchronised DC shcok

149
Q

What should be first line in peri-arrest tachycardian if have adevrse signs?

A

Synchronised DC shcok

150
Q

How does a left ventricular aneurysm present?

A

Angina (chest pain or pressure).
Edema (fluid retention).
Fatigue.
Heart palpitations.
Shortness of breath.
Stroke (due to a blood clot which may form in the aneurysm).
Persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

151
Q

Main angina drugs mneumonic

A

Coronaries need blood
CCB
Nitrates/nicronadil
BB

152
Q

The Mackler triad for Boerhaave syndrome

A

vomiting, thoracic pain, subcutaneous emphysema. It commonly presents in middle aged men with a background of alcohol abuse.

153
Q

What is Boerhaaves syndrome?

A

Spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting.
The rupture is usually distally sited and on the left side.

154
Q

Contraindications of statins?

A

macrolides (e.g. erythromycin, clarithromycin) are an important interaction. Statins should be stopped until patients complete the course
pregnancy

155
Q

Guidelines of amiodaroine in ALS?

A

amiodarone 300 mg should be given to patients who are in VF/pulseless VT after 3 shocks have been administered.
a further dose of amiodarone 150 mg should be given to patients who are in VF/pulseless VT after 5 shocks have been administered
lidocaine used as an alternative if amiodarone is not available or a local decision has been made to use lidocaine instead

156
Q

How long do you have after STEMI identified to do PCI?

A

120 MINUTES

157
Q

What is coarctation of the aorta?

A

congenital narrowing of the descending aorta.

158
Q

Features of coarctation of the aorta?

A

infancy: heart failure
adult: hypertension
radio-femoral delay
mid systolic murmur, maximal over back
apical click from the aortic valve
notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children

159
Q

What is added in hypertension if patient already on Acei, CCB and a standard dose thiazide diuretic and potassium more than 4.,5?

A

Alpha or beta blocker
Beta blocker cotnraindicated in asthma

160
Q

The following ECG changes are considered normal variants in an athlete:

A

sinus bradycardia
junctional rhythm
first degree heart block
Mobitz type 1 (Wenckebach phenomenon)

161
Q

Shocking when hypothermia. iscausing cardiac arrest?

A

defibrillation is less effective and only 3 shocks should be administered before the patient is rewarmed to 30 degrees centigrade

162
Q

The main ECG abnormality seen with hypercalcaemia

A

Shortening. ofthe QT interval

163
Q

Amiodarone useful mneumonic?

A

Am-3-odarone - Classs III anti-arrhytmic, 300mg IV in cardiac arrest after 3rd shock

164
Q

Adverse effects of amiodarone use?

A

thyroid dysfunction: both hypothyroidism and hyper-thyroidism
corneal deposits
pulmonary fibrosis/pneumonitis
liver fibrosis/hepatitis
peripheral neuropathy, myopathy
photosensitivity
‘slate-grey’ appearance
thrombophlebitis and injection site reactions
bradycardia
lengths QT interval

165
Q

What coronary artery is associated with complete heart block?

A

Right coronary artery

166
Q

What coronary artery is associated with complete heart block?

A

Right coronary artery

167
Q

Wells score more than 4 but CTPA negative?

A

Do a proximal leg US

168
Q

Ejection systolic murmurs louder on inspiration?

A

pulmonary stenosis
atrial septal defect

169
Q

Side effects oif beta blockers?

A

bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction

170
Q

Management of torsades des pointes?

A

Magnesium sulphate

171
Q

What is Sydenham’s chorea

A

Late complication of rheumatic fever

172
Q

What drug should not be used in VT?

A

Veramapril

173
Q

Rate control medications in AF?

A

BB, CCBs, digoxin

174
Q

What is atrioventricular block more common following?

A

Inferior MIs

175
Q

What to give if intracranial haemorrhage on Warfarin?

A

IV vitamin K 5mg and prothrombin complex

176
Q

First line for definite diagnosis of a PE?

A

CTPA

177
Q

What is used to reduce risk of sudden cardiac death in HOCM?

A

Implantable carioverter-defibrillator

178
Q

Following an ACS, all patients should be offered what medications?

A

Dual anti platelet therapy, Ace-I, BB and a statin

179
Q

When should beta blockers be stopped in acute HF?

A

heart rate < 50/min, second or third degree AV block, or shock

180
Q

ECG results in myocarditis?

A

Tachycardia, arruthmias, ST/T wave changes including STEMI and T wave inversion

181
Q

What are ECG findings of hypokalaemia?

A

U waves
* small or absent T waves (occasionally inversion)
* prolong PR interval
* ST depression
* long QT

182
Q

Contraindications to ace inhibitors?

A
  • pregnancyand breastfeeding - avoid
  • renovascular disease- may result in renal impairment
  • aortic stenosis- may result in hypotension
  • hereditary of idiopathic angioedema
  • specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L
183
Q

Side effects of ace-i?

A
  • cough
    • occurs in around 15% of patients and may occur up to a year after starting treatment
    • thought to be due toincreased bradykinin levels
  • angioedema: may occur up to a year after starting treatment
  • hyperkalaemia
  • first-dose hypotension: more common in patients taking diuretics
184
Q

Adverse effects of thiazide diuretics

A
  • dehydration
  • postural hypotension
  • hyponatraemia,hypokalaemia,hypercalcaemia*
  • gout
  • impaired glucose tolerance
  • impotence
185
Q

Action of thiazide diuretics?

A

work byinhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl−symporter. Potassium is lost as a result of more sodium reaching the collecting ducts.

186
Q

What is kussmaul’s sign?

A

JVP doesn’t fall with inspiration. Likely occurs due to obstruction to RV outflow that prevents the forward passage of the augmented volume of blood entering the right atrium and ventricle with inspiration, thus elevating JVP and right atrial pressures

187
Q

Anticoagulants an antiplatelets in Secondary prevention of stable cardiovascular disease with an indication for an anticoagulant?

A
  • normally in this situation, all patients are recommended to be prescribed an antiplatelet
  • if an indication for anticoagulant exists (for example atrial fibrillation) it is indicated thatanticoagulant monotherapy is given without the addition of antiplatelets
188
Q

Contraindications to thrombolysis: Mneumonic

A

ABC SHIP
Aortic dissection
Bleeding
Coag disorders
Stroke <3 months
Hypertension (severe)
Intracranial neoplasm/injury
Pregnancy

189
Q

Management of aortic dissection of descending aorta?

A

IV labetalol

190
Q

First line management of acute perciarditis?

A

NSAIDs and colchicine

191
Q

Examples of early diastolic murmurs?

A
  • aortic regurgitation(high-pitched and ‘blowing’ in character)
  • Graham-Steel murmur (pulmonary regurgitation, again high-pitched and ‘blowing’ in character)
192
Q

What is a left ventricular aneurysm typically associated with?

A

Persistent ST elevation and left ventricular failure

193
Q

When should thrombolytic drugs be used in ALS?

A

If PE is suspected

194
Q

Management of NSTEMI?

A

Aspirin 300mg. Fondaparinux if no immediate PCI planned

195
Q

What statin dose should be given following a cardiovascular event for secondary prevention?

A

Atorvastatin 80mg

196
Q

What medication for angina pectoris do patients sometimes develop tolerance to?

A

Standard release isobride mononitrate

197
Q

Mechanism of action of adenosine?

A
  • causes transientheart blockin the AV node
  • agonist of the A1 receptor in the atrioventricular node, which inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux
  • adenosine has avery short half-life of about 8-10 seconds
198
Q

Adverse effects of adenosine?

A
  • chest pain
  • bronchospasm
  • transient flushing
  • can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
199
Q

What is Beck’s triad and when is it used?

A

Cardiac tamponade- Hypotension, raised JVP, muffled heart sounds

200
Q

What should be done if patient still has persistent MI following fibrinolysis?

A

PCI

201
Q

What do patients with bradycardia and signs of shock require?

A

Atropine as first line

202
Q

Best investigation for aortic dissection?

A

CT angiography

203
Q

Causes of LBBB?

A
  • myocardial infarction
    • diagnosing a myocardial infarction for patients withexistingLBBB is difficult
    • rhe Sgarbossa criteria can help with this - please see the link for more details
  • hypertension
  • aortic stenosis
  • cardiomyopathy
  • rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
204
Q

What to do if strong suspicion of PE but delay in scan?

A

Prescribe rivoroxaban whilst awaiting further investigation

205
Q

Congenital causes of a prolonged QT?

A

Jerrell-Lange-Nielsen syndrome and ramano ward syndrome

206
Q

Drugs causing a prolonged QT?

A

amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, fluoxetine
chloroquine
terfenadine
erythromyci

207
Q

Contraindications to beta blockers?

A

uncontrolled heart failure
* asthma
* sick sinus syndrome
* concurrent verapamil use: may precipitate severe bradycardia

208
Q

Common adverse effects of indapamide

A
  • dehydration
  • postural hypotension
  • hyponatraemia, hypokalaemia, hypercalcaemia*
  • gout
  • impaired glucose tolerance
  • impotence
209
Q

What is bifasicular block

A

RBBB wirh left anterior or posterior hemiblock- look up hemiblocks

210
Q

NSTEMI Anriplarelet choice

A

Ticagreloe id not high risk bleeding
Clopidogrel if high risk bleeding

211
Q

What kind of diuretic is furosemide and how does it work?

A

loop diuretics that act by inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl

212
Q

What does increased P wave amplitude suggest?

A

Cor pulmonale

213
Q

What does broad, notched P waves represent?

A

Often most pronounced In Lead II. Sign of left atrial enlargement, classically due to mitral stenosis

214
Q

Action of thiazide diuretics?

A

work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter. Potassium is lost as a result of more sodium reaching the collecting ducts.

215
Q

What is the action of thrombolyric drugs?

A

activate plasminogen to form plasmin. This in turn degrades fibrin and help breaks up thrombi.

216
Q

First line therapy for heart failure?

A

Ace inhibitors and a beta blocker

217
Q

What is malignant hypertension?

A

BP extremely high and potential life threatening symptoms indicative of acute impairment of one or more organs systems

218
Q

Anticoagulation If patient has a stroke or TIA choice?

A

Warfarin or direct rhrombin or factor Xa inhibitor

219
Q

If less than 48 hours since start of AF?

A

Rate or rhythm control

220
Q

If more rhan 48 hours since onset or uncertain since start of AF management?

A

Rate control. Consider long term rhythm control. Delay cardio version until 3 weeks of anticoagulantion

221
Q

Rate control should be first line in AF except in:

A

patients wirh reversible cause, HF causing AF, AF who is considered suitable for an ablation strategy

222
Q

Best aortic dissection investigation In patients who are too risky to take to CT scanner?

A

Trans oesophageal echocardiography

223
Q

What to do if INR less than 2 and recent PE?

A

ImcreSe dose of warfarin and start LMWH as a immediate anticoagulantion agent

224
Q

Causes of acute presentation due to aortic regurgitation?

A

IE or aortic dissection

225
Q

When is a CTPA contraindication in patients with suspected PE?

A

When there is renal impairment or allergy to contract media. Do a V/Q scan instead

226
Q

Drugs that reduce INR mnemonic?

A

PC BRAS
P Phenytoin
C Carbamazepine
B Barbituates
R Rifampicin
A Alcohol (chronic use)
S Sulphonylureas

227
Q

Drugs that increase INR mneumonic?

A

O-Devices
O Omperazole
D Disulfiram
E Erythromycin
V Valproate
I Isoniazid
C Cimetidine + Ciprofloxacin
E Ethanol (Acutely)
S Sulphonamides

228
Q

Most common cause of IE in IVDU?

A

Staph aureus

229
Q

ECG changes for thrombolysis or percutaneous intervention:

A

T elevation of > 2mm (2 small squares) in 2 or more consecutive anterior leads (V1-V6) OR

ST elevation of greater than 1mm (1 small square) in greater than 2 consecutive inferior leads (II, III, avF, avL) OR

New Left bundle branch block

230
Q

INR range if VTE despite taking warfarin?

A

3-4

231
Q

ECG finding in cardiac tampomade?

A

Electrical alternans. This is consecutive normally-conducted QRS complexes that alternate in height due to heart swinging back and forth in fluid filled pericardium

232
Q

ECG findings of hypokalaemia?

A

U waves
* small or absent T waves (occasionally inversion)
* prolong PR interval
* ST depression
* long QT

233
Q

Most common cause of endocarditis if less than 2 months post valve surgery?

A

Staphylococcus epidermisis

234
Q

What is preferred over DOACs for patients with mechanical heart valves

A

Warfarin

235
Q

Ace inhibitor side effects mneumonic?

A

ACE I
Angioeswma, cough, elevated potassium and 1st dose hypotension

236
Q

For patient African origin what is second line for hypertension after CCB?

A

ARB

237
Q

Second line for heart failure after ace inhibitor and beta blocker?

A

Aldosterone antagonist

238
Q

ECG features In digoxin?

A
  • down-sloping ST depression (‘reverse tick’, ‘scooped out’)
  • flattened/inverted T waves
  • short QT interval
  • arrhythmias e.g. AV block, bradycardia
239
Q

Angina pectoris first line?

A

BB or CCB. If CCB used as first line use a rate limiting one. If used in combination with a beta blocker use a long acting dihydropuridine CCB

240
Q

What May rise after starting an ace inhibitor?

A

Serum creatinine and potassium. So u and es should be checked before treatment is initiated and after increasing dose

241
Q

Drugs if patient on mono therapy for angina pecforis but can’t tolerate the other first line medication too?

A

Long acting nitrate, ivabaradine, niceonadio or ranolazine

242
Q

HypOtheramia memory aid?

A

Jesus Quist it’s bloody freezing J-Waves
QT interval - prolonged
Irregular Rhythm
Bradycardia
First Degree Heart Block

243
Q

Features of an atrial septal defect?

A
  • ejection systolic murmur, fixed splitting of S2
  • embolism may pass from venous system to left side of heart causing a stroke
244
Q

First cardiac enzyme to rise in MI?

A

Myoglobin

245
Q

What cardiac enzyme is useful to look at in reinfarction?

A

CK-MB as it usually returns to normal after 2-3 days

246
Q

What is the target of adalimumab, infliximab, etanercept

A

TNF alpha inhibitor

247
Q

Uses of Adalimumab
Infliximab
Etanercept?

A

Crohns disease and rheumatoid disease

248
Q

Target of bevacizumab?

A

Anti VEGF

249
Q

Uses of bevacizumab

A

Colorectal cancer
Renal
Gioblastoma

250
Q

Target of transtuzumab

A

HER receptor

251
Q

Uses of transtuzumab

A

Breast ancer

252
Q

Target of imatibib

A

Tyrosine kinase inhibitor

253
Q

Target of basiliximab

A

IL2 binding site

254
Q

Use of basiliximab?

A

Renal transplants

255
Q

Target of cetuximab

A

Epidermal growth factor inhibitor

256
Q

Uses of cetuximab?

A

EGF positive colorectal cancers

257
Q

When in AF should rhythm control be offered over rate control?

A

When the AF has a reversible cause

258
Q

Management of major bleed if on warfarin?

A

Stop warfarin
Give intravenous vitamin K 5mg
Prothrombin complex concentrate - if not available then FFP*

259
Q

Causes of aortic regurgitation not due to aortic root disease?

A

bicuspid aortic valve (affects both the valves and the aortic root)
spondylarthropathies (e.g. ankylosing spondylitis)
hypertension
syphilis
Marfan’s, Ehler-Danlos syndrome

260
Q

What kind of MI can cause an AV block after?

A

Inferior MI

261
Q

Contraindication ot statins?

A

macrolides (e.g. erythromycin, clarithromycin) are an important interaction. Statins should be stopped until patients complete the course
pregnancy

262
Q

Difference between anticoagulants and antiplatelets?

A

Clotting in arterial system is mainly platelet-driven (activated when in contact with damaged endothelium/atheroma). Clotting in venous system /AF is due to blood stasis, not due to damaged endothelium, and is therefore mostly clotting-factor driven.

263
Q

Hypokalaemia ECG memory aid?

A

U have no Pot and no T, but a long PR and a long QT

264
Q

What is Eisenmenger’s syndrome?

A

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

265
Q

Memory aid for warfarin, INR and bleeding?

A

No bleeding
5-8 you delay
>8 you give PO vitamin K

minor bleed
regardless of INR give IV 1-3mg (with INR>8 you can repeat dose but tomato tomato its the same in my head)

Major bleed
regardless of INR give IV 5 + FFP

266
Q

Features of aortic regurgitiation?

A

early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
collapsing pulse
wide pulse pressure
Quincke’s sign (nailbed pulsation)
De Musset’s sign (head bobbing)
mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams

267
Q

Featues of acute MR secondary to MI?

A

ischaemia or rupture of the papillary muscle. Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.

268
Q

Mneumonic for mumurs?

A

ARD - Aortic regurg (Diastolic)
ASS - Aortic Stenosis (Systolic)
MRS - Mitral regurg (systolic)
MSD - Mitral stenosis (Diastolic)

269
Q

Eponymous signs of aortic regurgitation:

A

Corrigan’s - exaggerated carotid pulse
Quinke’s - nailbed pulsation
De Musset’s - head nodding
Duroziez’s - diastolic femoral murmur
Traube’s - ‘pistol shot’ femorals

270
Q

How long to contrinue anticoagulation ater DC cardioersion?

A

Lifwlong

271
Q

Rhythm control medications in AF?

A

beta-blockers
dronedarone: second-line in patients following cardioversion
amiodarone: particularly if coexisting heart failure

272
Q

Rate control medications in AF?

A

BB
CBB
Digoxin

273
Q

First line for bradycardia if need treatment?

A

Atropine 500mcg

If there is an unsatisfactory response the following interventions may be used:
atropine, up to a maximum of 3mg
transcutaneous pacing
isoprenaline/adrenaline infusion titrated to response

Specialist help should be sought for consideration of transvenous pacing if there is no response to the above measures.

274
Q

Adulty tachycardia resus guidlines

A
275
Q

if the cardiac arrested is witnessed in a monitored patient (e.g. in a coronary care unit) then the 2015 guidelines recommend what in terms of shock?

A

if the cardiac arrested is witnessed in a monitored patient (e.g. in a coronary care unit) then the 2015 guidelines recommend

276
Q

The vast majority of cases of bacterial endocarditis are what?

A

Gram positive cocci

277
Q

Infective endocarditis - indications for surgery:

A

severe valvular incompetence
aortic abscess (often indicated by a lengthening PR interval)
infections resistant to antibiotics/fungal infections
cardiac failure refractory to standard medical treatment
recurrent emboli after antibiotic therapy

278
Q

HF referral BNP investigations levels?

A

if levels are ‘high’ arrange specialist assessment (including transthoracic echocardiography) within 2 weeks
if levels are ‘raised’ arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks

279
Q

What is fondaparinux?

A

Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa. It is given subcutaneously.

280
Q

P450 Inhibitors second mneumonic

A

ASS-ZOLES
A ? Antibiotics: Ciprofloxacin, Erythromycin, Isoniazid
S ? SSRIs: Fluoxetine, Sertraline
S ? Sodium Valproate
- Zoles ? Omeprazole, Ketoconazole, Fluconazole

281
Q

What is Takotsubo cardiomyopathy?

A

Broken heart syndrome’ and ‘Takotsubo apical ballooning syndrome’ describes a cardiomyopathy induced by severe stressful triggers (e.g. emotional upset). It is commoner in women. In this scenario, we assume that the patient is in bereavement which precipitated the stress cardiomyopathy.

Takotsubo is a Japanese word that describes an octopus trap; this is used to describe the appearance of the heart on left ventriculogram, CMR or echocardiogram. This apical ballooning appearance occurs due to severe hypokinesis of the mid and apical segments with preservation of activity of the basal segments. In simple terms, the bottom of the heart (the apex) does not contract and therefore appears to balloon out. However, the area closer to the top (the base) continues to contract (creating the neck of the octopus trap).

282
Q

If non shockable rhythms when should you give adrenaline?

A

Immediatrly then every 2 cycles

283
Q

Best insertion site for primary PCI?

A

Radial access

284
Q

What is an alternative treatment to long-term anticoagulation for atrial fibrillation and can be considered if patients do not want to be on long-term medication

A

Left atrial appengage closure, surgically preventing clots from entering the blood stream

285
Q

Broad complex tachycardia following a myocardial infarction is almost always due to what?

A

VT

286
Q

wHAT DOEs PE cause in terms of an ABG?

A

hyperventilation, causing a drop in arterial carbonic dioxide partial pressure and thus alkalosis.

287
Q

sIGN OF A PACEMAKER ON AN ECG?

A

long straight lines preceding QRS complexes - these are pacing spikes delivered by a pacemaker to stimulate contraction of the heart

288
Q

What is electrical cardiovaersion synchronised to?

A

R wave

289
Q

Reduce mortality in HF?

A

Bisoprolol and cardevilol

290
Q

Well’s scre features

A
291
Q

STEMI ECG criteria - ≥ 2 contiguous leads of:

A

2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men < 40 years, or ≥ 2.0 mm ST elevation in leads V2-3 in men > 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads
new LBBB

292
Q

Inital drug therapy for ACS?

A

Aspirin
Oxygen if sats lesss than 94
Morphine if severe pain
Nitrates

293
Q

Management of NSTEMI?

A
294
Q

Features in a GRACE score

A

age
heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels

295
Q

mANAGEMENT OF a STEMI?

A
296
Q

What to give if patient if patietn having PCI for STEMI management?

A

if patient is having PCI then prasugrel is given in addition to aspirin. If patient is on an anticoagulant then clopidogrel used instead

297
Q

First line for bradycardia?

A

Atropine 500mg

298
Q

If patients treated with PCI for MI are experiencing pain or haemodynamic instability post PCI do what?

A

urgent coronary artery bypass graft (CABG) is recommended

299
Q

Management of torsades des pointes?

A

IV magnesium sulohate

300
Q

Murmurs scale?

A

The Levine Scale:
Grade 1 - Very faint murmur, 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. Can be heard with stethoscope edge
Grade 6 - Extremely loud murmur - can be heard without stethoscope touching the chest wall

301
Q

Adverse effects of thiazide diruetics

A

dehydration
postural hypotension
hyponatraemia, hypokalaemia, hypercalcaemia*
gout
impaired glucose tolerance
impotence

302
Q

What is electrical alternans?

A

alternating QRS amplitudes in any or all leads on an electrocardiogram (ECG) with no additional evident changes in conduction pathways of the heart. This rhythm is typically associated with pericardial effusion from fluid surrounding the heart.

303
Q

Example of a non-cardioselective beta blockers

A

Propanolol

304
Q

What is cardiogenic shock?

A

If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock. This is difficult to treat. Other causes of cardiogenic shock include the ‘mechanical’ complications such as left ventricular free wall rupture as listed below. Patients may require inotropic support and/or an intra-aortic balloon pump.

305
Q

What is a left ventricular aneurysm?

A

The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.
forms when a section of the heart muscle in the left ventricle (the chamber of the heart that pumps blood to the body) stretches and become very thin.

306
Q

The ratio of T-wave to QRS amplitude can help what?

A

Differentiate between an LV aneurysm and STEMI. If the T-wave/QRS ratio is <0.36 in all precordial leads, an LV aneurysm is more likely, which is the case here.
T-waves have a relatively small amplitude in comparison to the QRS complex (unlike the hyperacute T-waves of acute STEMI)

307
Q

Drugs to avoid in HOCM?

A

nitrates
ACE-inhibitors
inotropes

308
Q

mANAgement of HOCM?

A

Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*

309
Q

ECG findings of HOCM?

A

left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
atrial fibrillation may occasionally be seen

310
Q

What is the Killip class?

A

system used to stratify risk post myocardial infarction

311
Q

Investigations for myocardtditis?

A

bloods
↑ inflammatory markers in 99%
↑ cardiac enzymes
↑ BNP
ECG
tachycardia
arrhythmias
ST/T wave changes including ST-segment elevation and T wave inversion

312
Q

what score would justify the prescription of a statin?

A

Statins should be given to patients with a 10-year cardiovascular risk >= 10%

313
Q

ORBIT SCORE?

A

O - old: 75 or older
R - reduced Hb/Hct/Iron (anaemia)
B - bleeding history
I - insufficient renal function (GFR <60mg/dL/1.73m2)
T - treatment with antiplatelet

1, 2, 2, 1, 1

314
Q

What age should you definitely treat stage 1 hypertension?

A

Less than 80

315
Q

PAILS mneumonic for reciprocal changes?

A

PAILS stands for P-posterior A-anterior I-inferior L-lateral S-septal.

ST elevations in these leads most commonly create�reciprocal�ST depressions in the corresponding leads of the next letter in the mnemonic.

316
Q

Secondary management of MI - CRABS

A

Clopidogrel
Ramipril
Aspirin
Beta-blocker
Statin

317
Q

Nicronadol major side effect?

A

lcers that can occur anywhere along the gastrointestinal tract. They are refractory to treatment and most only respond to withdrawal of treatment. Patients with diverticular disease are at particular risk of bowel perforation during nicorandil treatment, hence the British National Formulary advises caution in its use in this population.

318
Q

Bundle branch block help aid that is not William Marrow

A

If QRS is broad look at V1:
If QRS predominantly negative then its a LBBB
If QRS predominantly positive then its a RBBB
So much more reliable than William marrow as it doesn’t rely on you looking at the shape of the QRS

319
Q

Anticoagulation should be considered for the following

A

Men: CHA2DS2-VASC >= 1
Women CHA2DS2-VASC >= 2

320
Q

What kind of drugs is bumetanide?

A

Loop diuretic

321
Q

Contraindcations to beta blockers?

A

uncontrolled heart failure
asthma
sick sinus syndrome
concurrent verapamil use: may precipitate severe bradycardia

322
Q

Major criteria forn rheumatic fever?

A

erythema marginatum
Sydenham’s chorea: this is often a late feature
polyarthritis
carditis and valvulitis (eg, pancarditis)
The latest iteration of the Jones criteria (published in 2015) state that rheumatic carditis cannot be based on pericarditis or myocarditis alone and that there must be evidence of endocarditis (the clinical correlate of which is valvulitis which manifests as a regurgitant murmur)
subcutaneous nodules

323
Q

Why can’t bisoprolol and verapamil be prescibed together?

A

Increases risk of complete hearrtt block

324
Q

Why can’t bisoprolol and verapamil be prescibed together?

A

Increases risk of complete hearrtt block

325
Q

Why can’t bisoprolol and verapamil be prescibed together?

A

Increases risk of complete hearrtt block

Year 4 Final (39 decks)

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