Cardiology Flashcards

1
Q

What is S4 heart sound and which part of the ECG does this sound coincide with?

A

S4 heart sound is caused by atrial contraction against a stiff ventricle occurring just before the S1 sound. It may be heard in aortic stenosis, hypertrophic cardiomyopathy or HTN.
It coincides with the P wave on the ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes S3 - 3rd heart sound?

A

caused by diastolic filling of the ventricle
considered normal if < 30 years old (may persist in women up to 50 years old)
heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the first line investigation for stable angina?

A

Contrast-enhanced CT coronary angiogram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how is anginal chest pain defined?

A
  1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
  2. precipitated by physical exertion
  3. relieved by rest or GTN in about 5 minutes
    patients with all 3 features have typical angina
    patients with 2 of the above features have atypical angina
    patients with 1 or none of the above features have non-anginal chest pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how is stable angina managed?

A

aspirin + statin
GTN
Beta blocker or CCB as first line
If CCB used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used
If CCB in combo with BB then use a longer-acting dihydropyridine calcium channel blocker (e.g. amlodipine, modified-release nifedipine)
If monotherapy does not work then add in the other
Then consider adding in a long actin nitrate, ivabradine nicorandil, ranolazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is Arrhythmogenic right ventricular cardiomyopathy?

A

a form of inherited cardiovascular disease which may present with syncope or sudden cardiac death. It is generally regarded as the second most common cause of sudden cardiac death in the young after hypertrophic cardiomyopathy.

Pathophysiology
inherited in an autosomal dominant pattern with variable expression
the 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the JVP wave form

A

a’ wave = atrial contraction
large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
absent if in atrial fibrillation

Cannon ‘a’ waves
caused by atrial contractions against a closed tricuspid valve
are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing

‘c’ wave
closure of tricuspid valve
not normally visible

‘v’ wave
due to passive filling of blood into the atrium against a closed tricuspid valve
giant v waves in tricuspid regurgitation

‘x’ descent = fall in atrial pressure during ventricular systole

‘y’ descent = opening of tricuspid valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does arrhythmogenic right ventricular cardiomyopathy present?

A

palpitations
syncope
sudden cardiac death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What investigations for Arrhythmogenic right ventricular cardiomyopathy and what do they show?

A

ECG abnormalities in 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
echo changes are often subtle in the early stages but may show an enlarged, hypokinetic right ventricle with a thin free wall
magnetic resonance imaging is useful to show fibrofatty tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

WHat is the management of arrhythmogenic right ventricular cardiomyopathy ?

A

drugs: sotalol is the most widely used antiarrhythmic
catheter ablation to prevent ventricular tachycardia
implantable cardioverter-defibrillator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

WHat is Naxos disease?

A

an autosomal recessive variant of ARVC
a triad of ARVC, palmoplantar keratosis, and woolly hair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what murmur is heard in ASD?

A

Ejection systolic murmur heard louder on inspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what causes ejection systolic murmurs

A

louder on expiration
aortic stenosis
hypertrophic obstructive cardiomyopathy

louder on inspiration
pulmonary stenosis
atrial septal defect

also: tetralogy of Fallot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What causes pansystolic murmur

A

mitral/tricuspid regurgitation (high-pitched and ‘blowing’ in character)
tricuspid regurgitation becomes louder during inspiration, unlike mitral reguritation
during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole

ventricular septal defect (‘harsh’ in character)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what causes a late systolic murmur

A

mitral valve prolapse
coarctation of aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what causes early diastolic murmur

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes mid-late diastolic murmur?

A

mitral stenosis (‘rumbling’ in character)
Austin-Flint murmur (severe aortic regurgitation, again is ‘rumbling’ in character)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what causes a continuous machine-like murmur?

A

patent ductus arteriosus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how is DVT/PE investigated in pregnancy?

A

Suspected DVT - USS Doppler
PE - if DVT also suspected the USS doppler, if just PE - then the decision to perform a V/Q or CTPA should be taken at a local level after discussion with the patient and radiologist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the treatment of prinzmetal angina?

A

dihydropyridine calcium channel blocker
Felodipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is SVT managed and prevented?

A

Acute management
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

Prevention of episodes
beta-blockers
radio-frequency ablation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is given for SVT prevention in pregnancy?

A

Metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is pulmonary capillary wedge pressure?

A

Pulmonary capillary wedge pressure (PCWP) is measured using a balloon tipped Swan-Ganz catheter which is inserted into the pulmonary artery. The pressure measured is similar to that of the left atrium (normally 6-12 mmHg).

One of the main uses of measuring the PCWP is determining whether pulmonary oedema is caused by either heart failure or acute respiratory distress syndrome.

In many modern ITU departments PCWP measurement has been replaced by non-invasive techniques.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

why is an asymmetric dosing regimen of isosorbide mononitrate recommended?

A

An asymmetric dosing regimen would involve taking the morning dose as normal, then taking the second dose in the early afternoon. This allows a sufficiently long nitrate-free period and helps reduce tolerance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the mechanism of action of amiodarone?

A

he main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the monitoring requirements of amiodarone?

A

TFT, LFT, U&E, CXR prior to treatment
TFT, LFT every 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

where do thiazide/thiazide like diuretics act?

A

inhibits sodium reabsorption by blocking the Na+-Clˆ’ symporter at the beginning of the distal convoluted tubule
Potassium is lost as a result of more sodium reaching the collecting ducts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the common adverse effects of thiazide/thiazide like diuretics?

A

dehydration
postural hypotension
hypokalaemia - due to increased delivery of sodium to the distal part of the distal convoluted tubule → increased sodium reabsorption in exchange for potassium and hydrogen ions
hyponatraemia
hypercalcaemia
the flip side of this is hypocalciuria, which may be useful in reducing the incidence of renal stones
gout
impaired glucose tolerance
impotence

Rare adverse effects
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

where do loop diuretics act?

A

Loop diuretics (furosemide, bumetanide) act by inhibiting the Na+/K+/2Cl- cotransporter in the thick ascending limb of the loop of Henle. This causes loss of water along with sodium chloride, potassium, calcium, and hydrogen ions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the are the adverse effects of loop diuretics?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is pulmonary artery hypertension defined as?

A

defined as a resting mean pulmonary artery pressure of >= 20 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are the features of pulmonary artery hypertension?

A

progressive exertional dyspnoea is the classical presentation
other possible features include exertional syncope, exertional chest pain and peripheral oedema
cyanosis
right ventricular heave, loud P2, raised JVP with prominent ‘a’ waves, tricuspid regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How is pulmonary artery hypertension managed?

A

Treat underlying conditions
Following this - acute vasodilator testing is central to deciding on the appropriate management strategy.
If there is a positive response - oral calcium channel blockers

If there is a negative response:
prostacyclin analogues: treprostinil, iloprost

endothelin receptor antagonists
non-selective: bosentan
selective antagonist of endothelin receptor A: ambrisentan

phosphodiesterase inhibitors: sildenafil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is acute vasodilator testing?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the causes of pericarditis?

A

viral infections (Coxsackie)
tuberculosis
uraemia
post-myocardial infarction
early (1-3 days): fibrinous pericarditis
late (weeks to months): autoimmune pericarditis (Dressler’s syndrome)
radiotherapy
connective tissue disease
systemic lupus erythematosus
rheumatoid arthritis
hypothyroidism
malignancy
lung cancer
breast cancer
trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are the features of pericarditis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what would ECG show in 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

WHat are the investigations in pericarditis?

A

ECG
all patients with suspected acute pericarditis should have transthoracic echocardiography
bloods
inflammatory markers
troponin: around 30% of patients may have an elevated troponin - this indicates possible myopericarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the management of pericarditis?

A

treat underlying cause
avoid strenuous physical activity until resolution of symptoms
NSAIDs and colchicine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

when should pericarditis be managed in the hospital?

A

patients who have high-risk features such as fever > 38°C or elevated troponin should be managed as an inpatient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What happens to BP in pregnancy?

A

Falls in first half of pregnancy before rising to pre-pregnancy levels before term. During a healthy pregnancy, blood pressure will typically fall during the first half of pregnancy due to systemic vasodilation and increased blood volume. The systolic pressure tends to drop by 5-10 mmHg and the diastolic by as much as 10-15 mmHg. This decrease reaches its nadir between the mid-second and early third trimester, after which it gradually rises back towards baseline prepregnancy levels just before term.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the management of hypertension in pregnancy?

A

Labetalol
oral nifedipine labetalol is contraindicated

43
Q

what are the poor prognostic factors in infective endocarditis?

A

Staphylococcus aureus infection (see below)
prosthetic valve (especially ‘early’, acquired during surgery)
culture negative endocarditis
low complement levels

44
Q

what bacteria has the highest mortality in IE?

A

staphylococci - 30%

45
Q

why are ACEi contraindicated in HOCM with left ventricular outflow tract obstruction

A

. ACE inhibitors can reduce afterload which may worsen the LVOT gradient

46
Q

What are the characteristic signs of HOCM on echo

A

mitral regurgitation, systolic anterior motion of the anterior mitral valve leaflet, asymmetric hypertrophy

47
Q

How is HOCM inherited

A

AD

48
Q

How is HOCM managed

A

ABCDE

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

49
Q

drugs to avoid in HOCM?

A

nitrates
ACE-inhibitors
inotropes

50
Q

what is the pathophysiology of HOCM ?

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

51
Q

What are the features of HOCM

A

exertional dyspnoea
angina
syncope - typically following exercise
sudden death
jerky pulse, large a waves, double apex beat
systolic murmurs
ejection systolic murmur: due to left ventricular outflow tract obstruction. Increases with Valsalva manoeuvre and decreases on squatting
pansystolic murmur: due to systolic anterior motion of the mitral valve → mitral regurgitation

52
Q

What are the ECG findings in HOCM

A

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

53
Q

how long do you treat unprovoked PE for?

A

6 months

54
Q

what is the mechanism of action of statins?

A

Statins inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.

55
Q

What are the adverse effects of statins

A

myopathy (myalgia, myositis, rhabdomyolysis, and asymptomatic raised creatine kinase)
Liver impairment
there is some evidence that statins may increase the risk of intracerebral haemorrhage in patients who’ve previously had a stroke. This effect is not seen in primary prevention. For this reason the Royal College of Physicians recommend avoiding statins in patients with a history of intracerebral haemorrhage

56
Q

WHat increases the risk of statin-induced myopathy?

A

Risks factors for myopathy include advanced age, female sex, low body mass index and presence of multisystem disease such as diabetes mellitus. Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)

57
Q

What are contraindications to statins

A

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

58
Q

what conditions are associated with mitral valve prolapse?

A

coarr ngenital heart disease: PDA, ASD
cardiomyopathy
Turner’s syndrome
Marfan’s syndrome, Fragile X
hapseudoxanthoma elasticum
Wolff-Parkinson White syndrome
long-QT syndrome
Ehlers-Danlos Syndrome
polycystic kidney disease

59
Q

what are the fetures of mitral prolapse?

A

patients may complain of atypical chest pain or palpitations
mid-systolic click (occurs later if patient squatting)
late systolic murmur (longer if patient standing)
complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death

60
Q

what are the features of aortic regurgitation

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

61
Q

what are the side effects of ACEi

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

62
Q

what are the cautions and contraindications when using ACEi

A

pregnancy and breastfeeding - avoid
renovascular disease - significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis
aortic stenosis - may result in hypotension
patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day) - significantly increases the risk of hypotension
hereditary or idiopathic angioedema

63
Q

what is patent ductus arteriosus?

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

64
Q

what are the features of PDA?

A

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

65
Q

what is the management of 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

66
Q

what is Tirofiban?

A

Tirofiban is a glycoprotein (GP) IIb/IIIa receptor antagonist that 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.

67
Q

what is the mechanism of action of ACEi?

A

inhibits the conversion angiotensin I to angiotensin II
→ decrease in angiotensin II levels → to vasodilation and reduced blood pressure
→ decrease in angiotensin II levels → reduced stimulation for aldosterone release → decrease in sodium and water retention by the kidneys

68
Q

what is the renoprotective mechanism of ACEi?

A

angiotensin II constricts the efferent glomerular arterioles
ACE inhibitors therefore lead to dilation of the efferent arterioles → reduced glomerular capillary pressure → decreased mechanical stress on the delicate filtration barriers of the glomeruli
this is particularly important in diabetic nephropathy
ACE inhibitors are activated by phase 1 metabolism in the liver

69
Q

how do you manage patients taking warfarin who need emergency?

A

If surgery can wait for 6-8 hours - give 5 mg vitamin K IV
If surgery can’t wait - 25-50 units/kg four-factor prothrombin complex
The guidance is to stop warfarin before elective or emergency surgery, so options 3 and 5 are incorrect
Because this is emergency surgery, reversal of anticoagulation is necessary so option 2 is incorrect

70
Q

what is the mechanism of action of warfarin?

A

mechanical heart valves
target INR depends on the valve type and location
mitral valves generally require a higher INR than aortic valves.
second-line after DOACs:
venous thromboembolism: target INR = 2.5, if recurrent 3.5
atrial fibrillation, target INR = 2.5

71
Q

what are the features of ASD

A

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

72
Q

what are the types of ASD

A

Ostium secundum (70% of ASDs)
associated with Holt-Oram syndrome (tri-phalangeal thumbs)
ECG: RBBB with RAD

Ostium primum
present earlier than ostium secundum defects
associated with abnormal AV valves
ECG: RBBB with LAD, prolonged PR interval

73
Q

why should verapamil not be used in VT ?

A

Verapamil should be avoided in this patient as it is contraindicated in VT due to the risk of causing significant hypotension, ventricular fibrillation and cardiac arrest. However, verapamil can be used safely in the management of supraventricular tachycardia (SVT).

74
Q

what are the drugs routinely used in VT?

A

amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide

75
Q

which coronary artery is most likely to be affected if a patient presents with heart block post MI

A

The atrioventricular node is supplied by the posterior interventricular artery, which in the majority of patients is a branch of the right coronary artery. In the remainder of patients the posterior interventricular artery is supplied by the left circumflex artery.

76
Q

what are the causes of palmar xanthoma?

A

remnant hyperlipidaemia
may less commonly be seen in familial hypercholesterolaemia

77
Q

what is eruptive xanthoma?

A

Eruptive xanthoma are due to high triglyceride levels and present as multiple red/yellow vesicles on the extensor surfaces (e.g. elbows, knees)

78
Q

what are the causes of eruptive xanthoma?

A

familial hypertriglyceridaemia
lipoprotein lipase deficiency

79
Q

what are the causes of Tendon xanthoma, tuberous xanthoma, xanthelasma?

A

familial hypercholesterolaemia
remnant hyperlipidaemia

80
Q

what are the clinical features of aortic stenosis?

A

chest pain
SOB
syncope/presyncope
murmur

81
Q

what are the features of severe aortic stenosis?

A

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

82
Q

what are the causes of aortic stenosis?

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

83
Q

how is aortic stenosis managed ?

A

if asymptomatic - observation
symptomatic - valve replacement
asymptomatic - but valvular gradient > 40 then consider surgery

84
Q

what ate the complications of bicuspid aortic valve

A

aortic stenosis/regurgitation as above
higher risk for aortic dissection and aneurysm formation of the ascending aorta

84
Q

what congenital heart defect is associated with bicuspid aortic valve ?

A

coarctation of the aorta

85
Q

what are the indications for ICD?

A

long QT syndrome
hypertrophic obstructive cardiomyopathy
previous cardiac arrest due to VT/VF
previous myocardial infarction with non-sustained VT on 24 hr monitoring, inducible VT on electrophysiology testing and ejection fraction < 35%
Brugada syndrome

86
Q

what are the causes of prolonged PR interval?

A

idiopathic
ischaemic heart disease
digoxin toxicity
hypokalaemia*
rheumatic fever
aortic root pathology e.g. abscess secondary to endocarditis
Lyme disease
sarcoidosis
myotonic dystrophy

87
Q

what are the features of aortic regurgitation?

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

88
Q

what are causes of aortic regurgitation
?

A

rheumatic fever
calcified valve disease
connective tissue diseases e.g. rheumatoid arthritis/SLE
Bicuspid aortic valve
spondyarthropathies
HTN
Syphlis
marfams

Acute causes - IE, aortic dissection

89
Q

what is the most specific marker of pericarditis on ECG?

A

PR depression

Sadly shaped ST elevation is also seen but not as a specific marker as PR depression

90
Q

what are the clinical features of pericarditis?

A

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

91
Q

what are the signs of tricuspid regurgitation?

A

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

92
Q

what is the PERC criteria?

A

Pulmonary embolism rule-out criteria (PERC

Age > 50
HR > 110
O2 <94
previous DVT/PE
recent surgery/trauma in the last 4 weeks
haemoptysis
unilateral leg swelling
oestrogen use

if all of the above are negative the post test probably of PE is < 2%

93
Q

what are the causes of tricuspid regurgitation ?

A

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

94
Q

what are the reversible causes of cardiac arrest?

A

Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia

Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade - cardiac
Toxins

95
Q

when is adenosine used?

A

used in haemodynamically stable patients with a narrow complex tachycardia

96
Q

when is amioderone given in an arrest?

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

96
Q

when is adrenaline given in an arrest?

A

adrenaline 1 mg as soon as possible for non-shockable rhythms
during a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted after the third shock
repeat adrenaline 1mg every 3-5 minutes whilst ALS continues

97
Q

what are the causes of IE?

A

staph aureus - most common, especially in IVDU
Strep viridian - linked with poor dental hygiene
coagulase-negative staph - caused by lines, common in patients post valve replacement
strep bovis - colorectal cancer
non-infective 0 SLE (Libman sacks), malignancy - mar antic endocarditis

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

98
Q

what ECG changes are commonly seen in athletes?

A

first degree AV block
Incomplete RBBB
isolated QRS voltage criteria for left ventricular hypertrophy

98
Q

what does an ECG show in LBBB?

A

in LBBB there is a ‘W’ in V1 and a ‘M’ in V6

99
Q

what does an ECG show in RBBB ?

A

in RBBB there is a ‘M’ in V1 and a ‘W’ in V6

100
Q

what are the causes of LBBB?

A

LBBB is always pathological
causes include:
myocardial infarction
diagnosing a myocardial infarction for patients with existing LBBB 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

101
Q

what form of step is most associated with colorectal cancer?

A

Streptococcus gallolyticus is the subtype of Streptococcus bovis most linked with colorectal cancer

102
Q

What are the radioactive substances used in nuclear cardiac imaging?

A

thallium
technetium (99mTc) sestamibi: a coordination complex of the radioisotope technetium-99m with the ligand methoxyisobutyl isonitrile (MIBI), used in ‘MIBI’ or cardiac Single Photon Emission Computed Tomography (SPECT) scans
fluorodeoxyglucose (FDG): used in Positron Emission Tomography (PET) scans
radionuclide (technetium-99m) is injected intravenously- multigated acquisition scan - radionuclide angiography

102
Q
A