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cardiology Flashcards

(73 cards)

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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
second line management of hypertension in afro-carribeans (after CCB)
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.
26
Causative organisms of infective endocarditis (normally and 2 months post-valve surgery)
Staphylococcus aureus Staphylococcus epidermidis if < 2 months post valve surgery
27
slow rising pulse
aortic stenosis
28
collapsing pulse
aortic valve incompetence/regurgitation.
29
bounding pulse
sepsis/ hyperglycaemia
30
RBBB- presentation on ECG
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
ECG- first degree heart block
long PR (>200ms)
32
ECG- second degree heart block (mobitz 1)
progressive PR lengthening followed by a dropped p wave
33
ECG- second degree heart block (mobitz 2)
intermittent non-conducted P waves without the gradual lengthening of the PR interval seen in type I
34
What is Dresslers syndrome and how does it present?
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
management of Wenckebach phenomenon (mobitz 1)
atropine 500 mcg IV
36
atrial flutter- ECG
sawtooth baseline
37
what is an atrial myxoma and how does it present?
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
if a patient has been in AF for more than 48 hours- what is the management?
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
when does left ventricular free wall rupture occur and what is the management?
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
inheritance of HOCM
AD
41
presentation of HOCM
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
What 2 conditions is HOCM associated with?
WPW Friedreich's ataxia
43
management of HOCM
Amiodarone Beta-blockers or verapamil for symptoms Cardioverter defibrillator Dual chamber pacemaker Endocarditis prophylaxis*
44
what is Takotsubo CM
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
management of Takotsubo CM
supportive
46
what medications must be avoided in HOCM and why?
ACEi can reduce afterload- which may worsen the left ventricular outflow tract gradient
47
most common cause of death in HOCM
ventricular arrythmia
48
causes of dilated CM
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
Pathophysiology of DCM
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
Investigative features of DCM
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
what is Arrhythmogenic right ventricular dysplasia/ myopathy?
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
causes of restrictive cardiomyopathy
amyloidosis post-radiotherapy Loeffler's endocarditis
53
mitral regurgitation murmur
A pansystolic murmur is associated with mitral regurgitation.
54
aortic regurgitation murmur
Aortic regurgitation typically causes an early diastolic murmur
55
aortic stenosis murmur
An ejection systolic murmur is associated with aortic stenosis
56
PDA murmur
A continuous 'machinery' murmur is associated with a patent ductus arteriosus.
57
mitral stenosis murmur
A late diastolic murmur is associated with mitral stenosis.
58
statin dosing- primary and secondary prevention
atorvastatin 20mg for primary prevention, 80mg for secondary prevention
59
AF- electric cardioversion- which part of the cycle does it affect?
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
what anticoagulant is used in patients with mechanical heart valves?
Warfarin is still used in preference to DOACs for patients with mechanical heart valves
61
monitoring of statins
LFT's at baseline, 3 months and 12 months
62
what is De Mussets sign and what is it indicative of?
De Musset's sign (head bobbing) is a clinical sign of aortic regurgitation
63
What valvular pathology is Marfans associated with?
aortic regurgitation
64
side effects of GTN
hypotension, headache, tachycardia
65
infective endocarditis- criteria used
modified dukes
66
bradycardia and shock- management
500micrograms of atropine (repeated up to max 3mg)
67
causes of torsades de pointes
hypo: Ca, Mg, K macrolides, ciprofloxacin SSRI, TCA, neuroleptics
68
management of peripheral arterial disease
antiplatelet + statin
69
diagnostic criteria for orthostatic hypertension
systolic drop in >20 systolic bp drops below 90 (regardless of drop itself) diastolic drop of 10 + symptoms
70
in what murmur is head bobbing seen?
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
signs of mitral stenosis
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
side effects of the use of adenosine in an SVT
chest pain bronchospasm transient flushing can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
73
what medications are used within PCI treatment
PCI treatment would include the administration of prasugrel, unfractionated heparin and a bailout glycoprotein IIb/IIIa inhibitor

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