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Aisha > Dunedin-Cardiology > Flashcards

Dunedin-Cardiology Flashcards

1
Q

How does a vagal manoeuvre help with SVT?

A

Block the AV node

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2
Q

What is the MOA of adenosine?

A

ultimately causes AV node block
Acts on A1 receptors on heart- SA and AV nodes
A2 coronary vasodilation

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3
Q

What is a relative contraindication for adenosine?

A

asthma

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4
Q

What are short RP tachycardia vs long RP tachycardia?

A

short RP tachycardia: AVRT, AVNRT
Long RP tachycardia: sinus tachycardia, focal atrial tachycardia

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5
Q

What type of circuit is atrial flutter?

A

macro re-entrant circuit
typically in right atrium around tricuspid annulus
90% counter-clockwise
10% clockwise

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6
Q

Why should you avoid flecainide in atrial flutter?

A

slows conduction velocity within flutter circuit, relatively minimal effect on AV nodal conduction

if using it, should use with AV nodal blocking agent such as b-blocker to prevent 1:1 conduction

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6
Q

Describe the CHA2DS2-VA score

A

note, new score has taken out the sex guidelines

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7
Q

List DOACS and their target

A

Dabigatran- thrombin inhibitor (reversible idarucizumab), renal cleared, p-glycoprotein substrate

Rivaroxoban- Factor Xa inhibitor (reversible andexanet alfa, prothrombin complex partial reversal), primarily hepatic clearance, some renal, metabolised CYP3A4, p-glycoprotein substrate

Apixaban- Factor Xa inhibitor (reversible adexanet alpha), primarily hepatic/biliary clearance, metabolised by CYP3A4, p-glycoprotein substrate

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8
Q

DOAC metabolism interactions

A
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9
Q

What did the LEGACY Trial suggest?

A

BMI >27 should loose weight (10% of body weight) if have AF
Also managing sleep apnoea

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10
Q

What are some complications for ablation of AF?

A

tamponade > CVA/TIA > PV stenosis > phrenic palsy >atrial oesophageal fistula

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11
Q

What is a bifascicular block?

A

RBBB + block of anterior (LAD) or posterior (RAD) fascicle of left bundle; or LBBB

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12
Q

What is a trifascicular block?

A

bifascicular block + PR prolongation (ie. AV node)

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13
Q

What are indications for CRT?

A

Heart failure
ideally SR
LBBB QRS >150ms
LVEF <35%

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14
Q

What is left bundle branch area (deep septal) pacing?

A

pacing in the left bundle region
thought to be superior

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15
Q

How to treat fascicular VT? “Normal heart” VT Of left ventricle

A

verapamil, ablation

ECG- tachy, ‘narrow’ RBBB mimicry and LAD

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16
Q

What is the most common cause of sudden cardiac death in athletes?

A

hypertrophic cardiomyopathy

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17
Q

What are indications for ICD?

A

Resuscitated VT/VF cardiac arrest not due to reversible cause

Ventricular tachycardia - sustained or symptomatic , not ablatable, associated with:
- severe compromise or
- failed anti-arrhythmias, or
- LVEF <40%

Hereditary cardiac conditions at high risk of sudden cardiac death: hypertrophic cardiomyopathy, long QT syndrome, arrhythmogenic cardiomyopathy, brigade syndrome

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18
Q

What gene gives highest risk in dilated cardiomyopathy?

A

LMNA gene mutation

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19
Q

Describe congenital long QT syndromes

A
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20
Q

Describe arrhythmias and their type of circuit

A

Focal atrial tachycardia –> ectopic atrial focus

Atrial flutter –> intra-atrial macro re-entry circuit

Atrial fibrillation –> multiple small atrial re-entry circuits pulmonary veins

VT –> macro re-entry around myocardial infarct

AVNRT –> re-entrant circuit within or around AV node

WPW –> re-entrant circuit within accessory pathway

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21
Q

What is ejection fraction?

A

stroke volume/ end-diastolic volume

Stroke volume: end diastolic- end systolic

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22
Q

On echocardiography what is a normal global strain?

A

More negative is better

abnormal if > -16%
usual < -18%
young people < -20%

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23
Q

What is the indication for cardiac MRI?

A

infiltrative disease
fairy disease
inflammatory disease (myocarditis)
LV non-compaction
amyloid
sarcoidosis
iron overload/haemochromatosis

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24
Q

How to treat cardiac amyloid?

A

CyBorDex chemotherapy x3

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25
Q

What are the types of amyloid that affect the heart?

A

AL amyloid, TTR (transthyretin amyloidosis)

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26
Q

What are investigations in cardiac amyloidosis?

A

free light chain ratio 51
IgG free kappa light chain paraprotein 6g/L
bone marrow- 8% plasma cells with amyloid infiltration

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27
Q

What is E/A reversal?

A

Indicates diastolic dysfunction

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28
Q

What is a normal LV wall thickness?

A

<11mm

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29
Q

What are some factors that indicate HEFpEF

A
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30
Q

When to do bone scintigraphy in heart failure?

A

in patients with suspected ATTR-related cardiac amyloidosis

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31
Q

What investigations for cardiac amyloid?

A

*serum free light-chain assay
*serum and urine protein electrophoresis with immunofixation
* 99mTc-PYP, DPD, or HMDP scintigraphy with SPECT

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31
Q

Who should be investigated for cardiac amyloid?

A

Heart failure and wall thickness >12mm
AND Age >65 OR “red flag”

Red flag:
- polyneuropathy
- dysautonomia
- skin bruising
- macroglossia
- deafness
- bilateral carpal tunnel
- ruptured biceps tendon
- lumbar spinal stenosis
- vitreous deposits
- family history
- renal insufficiency/proteinuria

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32
Q

What is high-gradient AS?

A

VMax >4m/s
pressure gradient >40mmHg
valve area <1

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33
Q

What is a high CT aortic valve calcium score?

A

Men: >3000
Women: >1600

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33
Q

What is a simplified Bernoulli pressure for RV pressure?

A

4xV^2

34
Q

What tricuspid regurgitation suggests PH?

A

Tricuspid regurgitation velocity >2.9m/s

35
Q

What is normal, intermediate, or high right atrial pressure?

A

Normal <5mmHg
Intermediate 5-10mmHg
high >10mmgHg

36
Q

Indication for aortic valve replacement in asymptomatic patients?

A

1) Severe aortic stenosis
2) systolic LV dysfunction (LVEF <50%)
3) demonstrable symptoms on exercise testing
4) Very severe, progression, elevated BNP

37
Q

TAVI vs surgical?

A

TAVI recommended in >75 years or high risk or unsuitable for surgery

SAVR if younger and low risk for surgery

38
Q

Severity of mitral stenosis

A
39
Q

Management of mitral stenosis?

A

percutaneous mitral comissurotomy or mitral valve surgery in symptomatic patients

40
Q

Management of mitral regurgitation

A

PRIMARY MITRAL REGURGITATION
1) surgery for symptomatic patients
2) surgery is ASYMPTOMATIC patients with LV dysfunction (LVESD >40 and /or LVEF <60%)

SECONDARY MR
1) Medical therapy: angiotensin receptor blocker/neprilysin inhibitor, CRT, SGLT2
2) if no improvement, workup to valve intervention eg transcatheter edge-to- edge repair (TEER)

41
Q

In heart failure with reduced systolic function, which has least mortality benefit?

A

angiotensin receptor blocker

42
Q

In acute heart failure, what is the role of continuous infusion furosemide?

A

continuous infusion Frusemide same outcome as 12hr bolus IV dose.

High Dose (2.5 x usual dose) not significantly different to low dose (usual oral dose).

43
Q

What is the MOA of ARNI?

A

Degrades vasoactive peptides, including natriuretic peptides,
bradykinin, and adrenomedullin

44
Q

What happens to eGFR when starting SGLT2?

A

Initially eGFR falls by 5ml/min, albuminuria falls 30-40% but then improved

45
Q

How does spironolactone cause gynaecomastia?

A

Spironolactone – inhibits testosterone binding to androgren receptor in breast tissue, less common with Eplerenone, not with Finerenone

46
Q

Which agents in heart failure improve all cause mortality?

A

1) BB, MRA, ARNI
2) ACEI, SGLT2
3) ARB, vericguat

47
Q

What is the MOA of digoxin?

A

Inhibition of Na+-K+ATPase, –> increase in contractility, benefit thought to be positive ionotropic action

48
Q

What are the symptoms of digoxin toxicity?

A

life threatening arrhythmias, end organ dysfunction, hyperkalaemia

48
Q

What electrolytes can contribute towards digoxin toxicity?

A

hypokalaemia, hypomagnesaemia, hypothyroidism

49
Q

What drugs increase serum levels of digoxin toxicity?

A

– Clarithromycin, erythromycin,
Itraconazole
– Amiodarone, Verapamil, Quinidine
– Cyclosporine

50
Q

What is the MOA of ivabradine?

A

Inhibition of If channel in the sinus node

slows heart rate in sinus rhythm

51
Q

Describe LV pressure volume loops in systolic and diastolic dysfunction

A

note in diastolic dysfunction end systolic pressure is high

52
Q

What are echo signs of HFpEF?

A

E/E’ >13
left atrial volume index (LAVI) >30ml/m

53
Q

If someone has mildly reduced-preserved ejection fraction, what drugs should you use?

A

SGLT2 + ARNI + BB + MRA
BB less important

54
Q

What is the role for semaglutide in heart failure?

A

use in BMI >30, improves outcomes and also improved BNP

55
Q

When to use fenerenone in HF?

A

When EF <60%

56
Q

What is the role of plasminogen activator inhibitor-1 in predicting cardiovascular disease?

A

it predicts cardiovascular disease

57
Q

Lipid management to improve cardiovascular risk

A

simvastatin +/- ezetimibe

58
Q

What is Incilsiran?

A

interferes with production of PCSK9, interferes with double-strand RNA- not enough evidence

58
Q

What can reduce lipoprotein (a)?

A

PCSK9

note that statins will increase Lp(a) but due to reduction in LDL-C improve outcomes

59
Q

First line investigations for suspected coronary cardiac syndromes?

A
60
Q

What to do in a patient with LBBB and possible coronary artery disease?

A
61
Q

LDL targets in someone with coronary disease

A

<1.4 and a >50% reduction in LDL.C baseline

62
Q

What is the role of revascularisation in stable angina?

A

dont do it

63
Q

In someone with stable coronary disease, with AF, what should you do?

A

stop anti platelet and start anti-thrombotic agent.

64
Q

Anti-platlets vs anti-thrombotics in Coronary syndromes

A

Aspirin is enough
clopidogrel is the same

warfarin is as good as aspirin but more bleeds

rivaroxoban 5mg BD as effective as aspirin (but more bleeds)

65
Q

Management of pain syndromes with normal coronary arteries?

A

CCB

66
Q

What is the best timing for PPCI?

A

within 120min

if its going to take >90 min, give fibrinolysis and then send to intervention

67
Q

What is the most preferred fibrinolytic in STEMI?

A

*tenecteplase

*Alteplase is good but needs infusion
*reteplase is double bolus
*streptokinase is least effective

68
Q

What is the MOA of several anti-platelet therapy

A

Ticagrelor: REVERSIBLY binds to P2Y12 receptors. NOT a pro-drug.

Clopidogrel: IRREVERSIBLY binds to P2Y12 receptors. is a pro-drug and needs to go through the liver.

Tirofiban, eptifibatide: GP IIb-IIIa inhibitors

Aspirin: IRREVERSIBLY inhibits cyclooxygenase-1 (COX-1), blocking thromboxane A2 (TXA2) production, reducing platelet aggregation.

69
Q

What is the most common type of atrial septal defects?

A

Secundum ASDs

70
Q

Types of atrial septal defects?

A
70
Q

What are some post-repair complications for coarctation of the aorta

A

Post surgical repair dilation / risk of dissection

71
Q

What is the clinical signs of a coarctation of the aorta

A

*Loud continuous murmur, especially over L chest
*Quiet ‘hum’ due to collateral flow

72
Q

How does an ECHO for coarctation of the aorta look?

A
73
Q

What are risk factors for tetralogy of Fallott?

A

maternal alcohol consumption, smoking, and DM

74
Q

What is the main complication after a tetralogy of fallot

A

progressive pulmonary regurgitation, RV dilation and impairment and arrhythmias

75
Q

Echo flow for tetralogy of fallot

A
76
Q

What characterises tetrology of fallot

A
77
Q

How common is transposition of the great arteries?

A

3% of congenital heart disease

78
Q

What is the optimal treatment of D-TGA?

A

arterial switch operation at birth

79
Q

What is the difference between D-TGA and L-TGA?

A

D-TGA is where the aorta arises from RV and the PA from the LV but the ventricles are in the usual position

L-TGA is rarer and more complex with the aorta arising from the RV and the PA from the LV with the ventricles also reverses

80
Q

What is a Mustard repair?

A

repair previously with an atrial baffle

81
Q

What is Fontan circulation?

A

Its a palliative procedure used in HLHS (hypo plastic left heart syndrome), tricuspid/pulmonary atresia/ mitral atresia

82
Q
A

Aisha (33 decks)

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