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MRCP Part 1 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

In HOCM what echo finding is associated with poor prognosis?

A

HOCM - poor prognostic factor on echo = septal wall thickness of > 3cm

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2
Q

In HOCM what are the poor prognostic factors?

A

syncope
family history of sudden death
young age at presentation
non-sustained ventricular tachycardia on 24 or 48-hour Holter monitoring
abnormal blood pressure changes on exercise

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3
Q

Which patients are considered unstable in the mx of tachyarrhythmias?

A

shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
syncope
myocardial ischaemia
heart failure

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4
Q

What is the algorithm for mx of tachyarrhythmias?

A
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5
Q

What are the actions of NT-pro BNP?

A

vasodilator: can decrease cardiac afterload
diuretic and natriuretic
suppresses both sympathetic tone and the renin-angiotensin-aldosterone system

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6
Q

What are the clinical uses of NT-pro BNP?

A

Diagnosing patients with acute dyspnoea
a low concentration of BNP(< 100pg/ml) makes a diagnosis of heart failure unlikely, but raised levels should prompt further investigation to confirm the diagnosis
NICE currently recommends BNP as a helpful test to rule out a diagnosis of heart failure

Prognosis in patients with chronic heart failure
initial evidence suggests BNP is an extremely useful marker of prognosis

Guiding treatment in patients with chronic heart failure
effective treatment lowers BNP levels

Screening for cardiac dysfunction
not currently recommended for population screening

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7
Q

What is PAH?

A

Pulmonary arterial hypertension (PAH) may be defined as a resting mean pulmonary artery pressure of >= 20 mmH

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8
Q

What are the features of PAH?

A

progressive exertional dyspnoea is the classical presentation
other possible features include exertional syncope, exertional chest pain and peripheral oedema
cyanosis
clinical signs:
right ventricular heave: indicating right ventricular hypertrophy or dilatation
loud P2: early in the disease reflects increased pulmonary artery pressure and may be accompanied by a palpable P2 in severe cases. With advanced PAH there may be right ventricular failure leading to a soft S2
raised JVP with prominent ‘a’ waves: reflects increased resistance to right atrial emptying due to elevated right ventricular end-diastolic pressure
tricuspid regurgitation

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9
Q

What is the mx of PAH?

A

Management should first involve treating any underlying conditions, for example with anticoagulants or oxygen. Following this, it has now been shown that acute vasodilator testing is central to deciding on the appropriate management strategy. Acute vasodilator testing aims to decide which patients show a significant fall in pulmonary arterial pressure following the administration of vasodilators such as intravenous epoprostenol or inhaled nitric oxide.

If there is a positive response to acute vasodilator testing (a minority of patients)
oral calcium channel blockers

If there is a negative response to acute vasodilator testing (the vast majority of patients)
prostacyclin analogues: treprostinil, iloprost
endothelin receptor antagonists
non-selective: bosentan
selective antagonist of endothelin receptor A: ambrisentan
phosphodiesterase inhibitors: sildenafil

Patients with progressive symptoms should be considered for a heart-lung transplant.

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10
Q

What is the BP classification according to NICE?

A
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11
Q

What is the algorithm for managing hypertension?

A
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12
Q

Complete heart block following an MI, which artery is affected?

A

RCA

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13
Q

What are the 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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14
Q

What are the glycoproteins IIb/IIIa inhibitors?

A

abciximab
eptifibatide
tirofiban

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15
Q

How do Glp IIb/IIIa inhibitors work?

A

works by inhibiting platelet aggregation. It does this by binding to the GP IIb/IIIa receptors on the surface of platelets, preventing fibrinogen from binding to these receptors and thus blocking platelet aggregation. This reduces thrombus formation in the coronary arteries and improves blood flow, making it an effective treatment for acute coronary syndrome

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16
Q

Drugs which cause torsades de pointes affect which channel in the heart?

A

Potassium channels

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17
Q

What are the causes of torsades de pointes?

A

congenital
Jervell-Lange-Nielsen syndrome
Romano-Ward syndrome
antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants
antipsychotics
chloroquine
terfenadine
erythromycin
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
myocarditis
hypothermia
subarachnoid haemorrhage

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18
Q

What are the features of severe AS?

A

narrow pulse pressure
slow rising pulse
delayed ESM
soft/absent S2
S4
thrill
duration of murmur
left ventricular hypertrophy or failure

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19
Q

What are the causes of AS?

A

degenerative calcification (most common cause in older patients > 65 years)
bicuspid aortic valve (most common cause in younger patients < 65 years)
William’s syndrome (supravalvular aortic stenosis)
post-rheumatic disease
subvalvular: HOCM

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20
Q

What is the mx of AS?

A

if asymptomatic then observe the patient is a general rule
if symptomatic then valve replacement
if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
options for aortic valve replacement (AVR) include:
surgical AVR is the treatment of choice for young, low/medium operative risk patients. Cardiovascular disease may coexist. For this reason, an angiogram is often done prior to surgery so that the procedures can be combined
transcatheter AVR (TAVR) is used for patients with a high operative risk
balloon valvuloplasty
may be used in children with no aortic valve calcification
in adults limited to patients with critical aortic stenosis who are not fit for valve replacement

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21
Q

What is a PDA?

A

a form of congenital heart defect
generally classed as ‘acyanotic’. However, uncorrected can eventually result in late cyanosis in the lower extremities, termed differential cyanosis
connection between the pulmonary trunk and descending aorta
usually, the ductus arteriosus closes with the first breaths due to increased pulmonary flow which enhances prostaglandins clearance
more common in premature babies, born at high altitude or maternal rubella infection in the first trimester

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22
Q

What are the clinical features of a PDA?

A

left subclavicular thrill
continuous ‘machinery’ murmur
large volume, bounding, collapsing pulse
wide pulse pressure
heaving apex beat

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23
Q

What is the mx of a PDA?

A

indomethacin or ibuprofen
given to the neonate
inhibits prostaglandin synthesis
closes the connection in the majority of cases
if associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair

24
Q

What are the normal physiological changes in BP in pregnant women?

A

blood pressure usually falls in the first trimester (particularly the diastolic), and continues to fall until 20-24 weeks
after this time the blood pressure usually increases to pre-pregnancy levels by term

25
Q

What is the definition of hypertension in pregnancy?

A

Hypertension in pregnancy in usually defined as:
systolic > 140 mmHg or diastolic > 90 mmHg
or an increase above booking readings of > 30 mmHg systolic or > 15 mmHg diastolic

26
Q

What are the different types of hypertension ?

A
27
Q

What is the mx of hypertension in pregnancy?

A

Management
oral labetalol is now first-line following the 2010 NICE guidelines
oral nifedipine (e.g. if asthmatic) and hydralazine

28
Q

What are the different types of AF?

A

first detected episode (irrespective of whether it is symptomatic or self-terminating)

recurrent episodes, when a patient has 2 or more episodes of AF. If episodes of AF terminate spontaneously then the term paroxysmal AF is used. Such episodes last less than 7 days (typically < 24 hours).

If the arrhythmia is not self-terminating then the term persistent AF is used. Such episodes usually last greater than 7 days

In permanent AF there is continuous atrial fibrillation which cannot be cardioverted or if attempts to do so are deemed inappropriate. Treatment goals are therefore rate control and anticoagulation if appropriate

29
Q

What are the RF for infective endocarditis?

A

The strongest risk factor for developing infective endocarditis is a previous episode of endocarditis. The following types of patients are affected:
previously normal valves (50%, typically acute presentation)
the mitral valve is most commonly affected
rheumatic valve disease (30%)
prosthetic valves
congenital heart defects
intravenous drug users (IVDUs)
e.g. typically causing tricuspid lesion)
others: recent piercings

30
Q

What are the causes of S. aureus IE?

A

now the most common cause of infective endocarditis
particularly common in acute presentation and IVDUs

31
Q

What are the causes of viridian IE?

A

historically Streptococcus viridans was the most common cause of infective endocarditis. This is no longer the case, except in developing countries
technically Streptococcus viridans is a pseudotaxonomic term, referring to viridans streptococci, rather than a particular organism. The two most notable viridans streptococci are Streptococcus mitis and Streptococcus sanguinis
they are both commonly found in the mouth and in particular dental plaque so endocarditis caused by these organisms is linked with poor dental hygiene or following a dental procedure

32
Q

What are the causes of coagulase negative staph IE (like Staph epidermis)?

A

commonly colonize indwelling lines and are the most cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination.

after 2 months the spectrum of organisms which cause endocarditis return to normal (i.e. Staphylococcus aureus is the most common cause)

33
Q

What are the causes/associations of strep bovis IE?

A

associated with colorectal cancer
the subtype Streptococcus gallolyticus is most linked with colorectal cancer

34
Q

What are the non-infective causes/associations of non-infective IE?

A

systemic lupus erythematosus (Libman-Sacks)
malignancy: marantic endocarditis

35
Q

What are the causes of culture negative IE?

A

prior antibiotic therapy
Coxiella burnetii
Bartonella
Brucella
HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

36
Q

What electrolyte abnormalities cause long QT?

A

hypokalaemia, hypocalcaemia and hypomagnesaemia.

37
Q

What are the causes of long QT syndrome?

A
38
Q

What is the mx of long QT syndrome?

A

avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise)
beta-blockers***
implantable cardioverter defibrillators in high risk cases

*the usual mechanism by which drugs prolong the QT interval is blockage of potassium channels. See the link for more details

**a non-sedating antihistamine and classic cause of prolonged QT in a patient, especially if also taking P450 enzyme inhibitor, e.g. Patient with a cold takes terfenadine and erythromycin at the same time

***note sotalol may exacerbate long QT syndrome

39
Q

Inherited long QT + sensorineural deafness?

A

Jervell and Lange-Nielsen syndrome

40
Q

What are the signs of tricuspid regurgitation?

A

pan-systolic murmur
prominent/giant V waves in JVP
pulsatile hepatomegaly
left parasternal heave

41
Q

What are the causes of TR?

A

right ventricular infarction
pulmonary hypertension e.g. COPD
rheumatic heart disease
infective endocarditis (especially intravenous drug users)
Ebstein’s anomaly
carcinoid syndrome

42
Q

What is the action of BNP?

A

vasodilator: can decrease cardiac afterload
diuretic and natriuretic
suppresses both sympathetic tone and the renin-angiotensin-aldosterone system

43
Q

What are the clinical uses of BNP?

A

Diagnosing patients with acute dyspnoea
a low concentration of BNP(< 100pg/ml) makes a diagnosis of heart failure unlikely, but raised levels should prompt further investigation to confirm the diagnosis
NICE currently recommends BNP as a helpful test to rule out a diagnosis of heart failure

Prognosis in patients with chronic heart failure
initial evidence suggests BNP is an extremely useful marker of prognosis

Guiding treatment in patients with chronic heart failure
effective treatment lowers BNP levels

Screening for cardiac dysfunction
not currently recommended for population screening

44
Q

What is the mx of a patient with major bleeding (variceal or intracranial haemorrhage) + on warfarin

A

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

45
Q

What is the mx of INR > 8 with minor bleeding and on warfarin?

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Repeat dose of vitamin K if INR still too high after 24 hours
Restart warfarin when INR < 5.0

46
Q

What is the mx of INR > 8 with no bleeding and on warfarin?

A

Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0

47
Q

What is the mx of INR 5 - 8 with minor bleeding and on warfarin?

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR < 5.0

48
Q

What is the mx of INR 5 -8 with no bleeding and on warfarin?

A

Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose

49
Q

Which signs are most commonly seen in a PE?

A

The relative frequency of common clinical signs is shown below:
Tachypnea (respiratory rate >20/min) - 96%
Crackles - 58%
Tachycardia (heart rate >100/min) - 44%
Fever (temperature >37.8°C) - 43%

50
Q

What is the PERC?

A
51
Q

What is the 2-level Wells score?

A
52
Q

If the 2-level Wells score is > 4 what is the next step?

A

arrange an immediate computed tomography pulmonary angiogram (CTPA)
If there is a delay in getting the CTPA then interim therapeutic anticoagulation should be given until the scan is performed.
interim therapeutic anticoagulation used to mean giving low-molecular-weight heparin
NICE updated their guidance in 2020. They now recommend using an anticoagulant that can be continued if the result is positive.
this means normally a direct oral anticoagulant (DOAC) such as apixaban or rivaroxaban
if the CTPA is positive then a PE is diagnosed
if the CTPA is negative then consider a proximal leg vein ultrasound scan if DVT is suspected

53
Q

If the 2-level Wells score is <4 what is the next step?

A

arranged a D-dimer test
if positive arrange an immediate computed tomography pulmonary angiogram (CTPA). If there is a delay in getting the CTPA then give interim therapeutic anticoagulation until the scan is performed
if negative then PE is unlikely - stop anticoagulation and consider an alternative diagnosis

54
Q

What are the cut-offs for high, raised, and normal BNPs?

A
55
Q

How do you interpret BNP tests?

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

56
Q

Which factors increase BNP?

A
57
Q
A

MRCP Part 1 (3 decks)

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