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FINALS- random flashcards per system > cardiology > Flashcards

cardiology Flashcards

1
Q

bloods taken in infective endocarditis

A

3 separate blood cultures 6 hours apart

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2
Q

management of aortic dissection

A

Analgesia (e.g., morphine) is required to manage the pain.

Blood pressure and heart rate need to be well controlled to reduce the stress on the aortic walls. This usually involves beta-blockers.

Surgical intervention from the vascular team will depend on the type of aortic dissection

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3
Q

presentation of mitral stenosis

A

mid-diastolic murmur loudest over the apex and accentuated with the patient in a left lateral position.

It commonly causes atrial fibrillation (secondary to left atrial enlargement) which may result in embolic sequelae (e.g. stroke, TIA, mesenteric ischaemia).

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4
Q

mechanism of action of thiazide diuretics

A

Thiazide diuretics work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter

THIAZIDES=
HYPOKALAEMIA
HYPONATRAEMIA
HYPERGYLCAEMIA
HYPERCALCAEMIA

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5
Q

first and second line management of HF

A

1st- ACE + BB

2nd- aldosterone antagonist (spironolactone)

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6
Q

features of pericarditis

A

chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include non-productive cough, dyspnoea and flu-like symptoms
pericardial rub
tachypnoea
tachycardia

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7
Q

ECG changes-pericarditis

A

the changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
‘saddle-shaped’ ST elevation
PR depression: most specific ECG marker for pericarditis

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8
Q

pericarditis- management

A

NSAIDs + colchicine

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9
Q

posterior MI presentation on ECG

A

ST DEPRESSION V1-V3

tall R waves V1-V3

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10
Q

Hypokalaemia- ECG presentation

A

U waves on ECG

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11
Q

ACE inhibitors- contraindications

A

pregnancy and breastfeeding - avoid
renovascular disease - may result in renal impairment
aortic stenosis - may result in hypotension

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12
Q

SE’s of ACE inhibitors

A

cough
angioedema
hyperkalaemia

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13
Q

what is Becks triad and what is it seen in?

A

hypotension + muffled (distant) heart sounds + elevated JVP- seen in cardiac tamponade

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14
Q

medication causes of long-QT syndrome

A

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

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15
Q

ECG changes (MI)= anteroseptal

  • leads changes are seen in
  • artery affected
A

V1-V4

LAD

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16
Q

ECG changes (MI)= inferior

  • leads changes are seen in
  • artery affected
A

II, III, avf

RCA

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17
Q

ECG changes (MI)= anterolateral

  • leads changes are seen in
  • artery affecteD
A

V4-V6, I, Avl

LAD/ left circumflex

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18
Q

ECG changes (MI)= lateral

  • leads changes are seen in
  • artery affected
A

I, AVL +/- V5/V6

left circumflex

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19
Q

ECG changes (MI)= posterior

  • leads changes are seen in
  • artery affected
A

V1-V3

left circumflex/ RCA

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20
Q

Aortic regurgitation- murmur heard

A

early or mid/late diastolic

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21
Q

first-line therapy for anticoagulation in patients with atrial fibrillation

A

DOACs (apixaban)

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22
Q

what is pulsus paradoxus and what does it commonly occur in

A

abnormally large drop in blood pressure during inspiration, recognisable by the radial pulse disappearance during inspiration

seen in cardiac tamponade, severe asthma and pericardial constriction

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23
Q

management of an SVT

A

vagal manoeuvres:
Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
carotid sinus massage

intravenous adenosine
rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
contraindicated in asthmatics - verapamil is a preferable option

electrical cardioversion

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24
Q

When is spironolactone safe to add in hypertension management?

A

only be recommended if the potassium was below 4.5mmol/l

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25
Q

second line management of hypertension in afro-carribeans (after CCB)

A

one of the changes in the 2019 update to the NICE guidelines on hypertension is that an angiotensin II receptor blocker (ARB) be considered in preference to an angiotensin-converting enzyme inhibitor (ACE inhibitor) in patients of black African/Caribbean family origin.

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26
Q

Causative organisms of infective endocarditis (normally and 2 months post-valve surgery)

A

Staphylococcus aureus
Staphylococcus epidermidis if < 2 months post valve surgery

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27
Q

slow rising pulse

A

aortic stenosis

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28
Q

collapsing pulse

A

aortic valve incompetence/regurgitation.

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29
Q

bounding pulse

A

sepsis/ hyperglycaemia

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30
Q

RBBB- presentation on ECG

A

The ECG changes in RBBB include QRS prolongation (>120ms), an additional R wave in lead V1 and a wide slurred S wave in lead V6. These changes are commonly referred to as producing an ‘M-shaped’ QRS complex in lead V1 and a ‘W-shaped’ QRS complex in lead V6. It is useful to recall the ECG changes in bundle branch blocks using the phrase ‘WiLLiaM MaRRoW’ in which the first and last letters of each word refer to the morphology of the QRS in leads V1 and V6 respectively, with the middle letter indicating left (L) or right (R) bundle branch block

31
Q

ECG- first degree heart block

A

long PR (>200ms)

32
Q

ECG- second degree heart block (mobitz 1)

A

progressive PR lengthening followed by a dropped p wave

33
Q

ECG- second degree heart block (mobitz 2)

A

intermittent non-conducted P waves without the gradual lengthening of the PR interval seen in type I

34
Q

What is Dresslers syndrome and how does it present?

A

a pericarditis that occurs in about 4% of patients post-MI. People typically present 2–4 weeks after an MI with a self-limiting febrile illness accompanied by pericardial or pleural pain. Pericarditis is evidenced by a characteristic ‘saddle-shaped’ ST elevation that is widespread on most leads.

35
Q

management of Wenckebach phenomenon (mobitz 1)

A

atropine 500 mcg IV

36
Q

atrial flutter- ECG

A

sawtooth baseline

37
Q

what is an atrial myxoma and how does it present?

A

benign tumour most commonly occurring in the left atrium. It can present with the triad of mitral valve obstruction, systemic embolisation and constitutional symptoms such as breathlessness, weight loss and fever

most common primary cardiac tumour

38
Q

if a patient has been in AF for more than 48 hours- what is the management?

A

Because more than 48 hours have elapsed since the onset of symptoms, cardioversion would risk thrombus embolisation from the left atrial appendage. Instead, several weeks of oral anticoagulation would be required before cardioversion

39
Q

when does left ventricular free wall rupture occur and what is the management?

A

occurs around 1-2 weeks post MI

. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.

40
Q

inheritance of HOCM

A

AD

41
Q

presentation of HOCM

A

exertional dyspnoea
angina
syncope
typically following exercise

due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis

sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure

jerky pulse, large ‘a’ waves, double apex beat
ejection systolic murmur

increases with Valsalva manoeuvre and decreases on squatting

hypertrophic cardiomyopathy may impair mitral valve closure, thus causing regurgitation

42
Q

What 2 conditions is HOCM associated with?

A

WPW
Friedreich’s ataxia

43
Q

management of HOCM

A

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

44
Q

what is Takotsubo CM

A

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

‘Broken heart’

45
Q

management of Takotsubo CM

A

supportive

46
Q

what medications must be avoided in HOCM and why?

A

ACEi

can reduce afterload- which may worsen the left ventricular outflow tract gradient

47
Q

most common cause of death in HOCM

A

ventricular arrythmia

48
Q

causes of dilated CM

A

idiopathic: the most common cause
myocarditis
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
the majority of defects are inherited in an autosomal dominant fashion
infiltrative e.g. haemochromatosis, sarcoidosis

49
Q

Pathophysiology of DCM

A

dilated heart leading to predominately systolic dysfunction
all 4 chambers are dilated, but the left ventricle more so than right ventricle
eccentric hypertrophy (sarcomeres added in series) is seen

50
Q

Investigative features of DCM

A

classic findings of heart failure
systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
S3
‘balloon’ appearance of the heart on the chest x-ray

51
Q

what is Arrhythmogenic right ventricular dysplasia/ myopathy?

A

type of primary cardiomyopathy

Right ventricular myocardium is replaced by fatty and fibrofatty tissue
Around 50% of patients have a mutation of one of the several genes which encode components of desmosome

52
Q

causes of restrictive cardiomyopathy

A

amyloidosis
post-radiotherapy
Loeffler’s endocarditis

53
Q

mitral regurgitation murmur

A

A pansystolic murmur is associated with mitral regurgitation.

54
Q

aortic regurgitation murmur

A

Aortic regurgitation typically causes an early diastolic murmur

55
Q

aortic stenosis murmur

A

An ejection systolic murmur is associated with aortic stenosis

56
Q

PDA murmur

A

A continuous ‘machinery’ murmur is associated with a patent ductus arteriosus.

57
Q

mitral stenosis murmur

A

A late diastolic murmur is associated with mitral stenosis.

58
Q

statin dosing- primary and secondary prevention

A

atorvastatin 20mg for primary prevention, 80mg for secondary prevention

59
Q

AF- electric cardioversion- which part of the cycle does it affect?

A

Electrical cardioversion is synchronised to the R wave to prevent delivery of a shock during the vulnerable period of cardiac repolarisation when ventricular fibrillation can be induced.

60
Q

what anticoagulant is used in patients with mechanical heart valves?

A

Warfarin is still used in preference to DOACs for patients with mechanical heart valves

61
Q

monitoring of statins

A

LFT’s at baseline, 3 months and 12 months

62
Q

what is De Mussets sign and what is it indicative of?

A

De Musset’s sign (head bobbing) is a clinical sign of aortic regurgitation

63
Q

What valvular pathology is Marfans associated with?

A

aortic regurgitation

64
Q

side effects of GTN

A

hypotension, headache, tachycardia

65
Q

infective endocarditis- criteria used

A

modified dukes

66
Q

bradycardia and shock- management

A

500micrograms of atropine (repeated up to max 3mg)

67
Q

causes of torsades de pointes

A

hypo: Ca, Mg, K

macrolides, ciprofloxacin

SSRI, TCA, neuroleptics

68
Q

management of peripheral arterial disease

A

antiplatelet + statin

69
Q

diagnostic criteria for orthostatic hypertension

A

systolic drop in >20

systolic bp drops below 90 (regardless of drop itself)

diastolic drop of 10 + symptoms

70
Q

in what murmur is head bobbing seen?

A

Involuntary head nodding - patients rhythmically nodding their head in synchrony to their heartbeat is known as de Musset’s sign which can be caused by aortic regurgitation.

71
Q

signs of mitral stenosis

A

dyspnoea
↑ left atrail pressure → pulmonary venous hypertension
haemoptysis
due to pulmonary pressures and vascular congestion
may range from pink frothy sputum to sudden haemorrhage secondary to rupture of thin walled and dilated bronchial veins
mid-late diastolic murmur (best heard in expiration)
loud S1, opening snap
low volume pulse
malar flush
atrial fibrillation
secondary to ↑ left atrail pressure → left atrial enlargement

72
Q

side effects of the use of adenosine in an SVT

A

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

73
Q

what medications are used within PCI treatment

A

PCI treatment would include the administration of prasugrel, unfractionated heparin and a bailout glycoprotein IIb/IIIa inhibitor

FINALS- random flashcards per system (16 decks)

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