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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

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34
Q

What tricuspid regurgitation suggests PH?

A

Tricuspid regurgitation velocity >2.9m/s

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35
Q

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

A

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

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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

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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

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38
Q

Severity of mitral stenosis

A
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39
Q

Management of mitral stenosis?

A

percutaneous mitral comissurotomy or mitral valve surgery in symptomatic patients

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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

Which of the following is most suggestive of a non-cardiogenic cause of pulmonary oedema?
A) Normal left ventricular function on echocardiogram
B) Normal pulmonary capillary wedge pressure
C) Normal troponin
D) Clinical signs of sepsis
E) Evidence of pulmonary oedema on CXR

A

B) Normal pulmonary capillary wedge pressure

83
Q

Describe the cardiac electrical potential

A
84
Q

Describe the inheritance of hypertrophic cardiomyopathy

A

autosomal dominant
mutations of genes of the thick and thin contractile myofilaments of the sarcomere

85
Q

What is involved in the diagnosis of hypertrophic cardiomyopathy?

A

*Increased LV thickness
*one or more LV regional walls
* >15mm
* ASH
* SAM- lengthened MV leaflets
*LVOT gradient: dynamic
*histology
- hypertrophic cardiac myocyte
- chaotic and disordered architecture
* abnormal intramural arteries- medial thickness

86
Q

Describe HCM and its relation to Valsalva

A

Gets louder with valsalva

87
Q

Management of HOCM

A

ICD for secondary prevention
ICD for primary prevention if
- family history of SCD, <50 years close relative
- wall thickness equal or more than 30mm
- unexplained syncope
- LVEF < 50%
- LV apical aneurysm
- extensive LGE. equal or more than 15%
- NSVT on 24-48 hours of amb monitoring
- NSVT more than 3, more than 10 beats, or more than 200bpm

NO ROLE FOR ANTI-ARRHYTMIC agents

Drugs: B-blockers, verapamil, disopyramide with AV block, myosin inhibitors (mavecamten)

Surgical myectomy

Alcohol spatial ablation

dual chamber pacing

treat AF regardless of CHADSVASC

88
Q

With the histology of arrhythmogenic RV cardiomyopathy (ARVC)?

A

fibrofatty replacement of myocytes
50% biventricular

89
Q

Describe genetics of arrhythmogenic RV cardiomyopathy (ARVC)

A

mutation in desmosomal gene
significant allelic heterogeneity

90
Q

Management of ARVC

A
  • avoid strenuous activity
  • anti-arrhythmic (won’t prevent sudden cardiac death)
  • B-blockers
  • ICD
  • Catheter ablation
  • treat heart failure
91
Q

What is LV non-compaction?

A

morphological trait shared by cardiomyopathies, channelopathies and congenital heart disease

Ratio of trabeculated to compact myocardium >2.3 on echo or CMR in end diastole

Ratio of mass of non-computed to compact myocardium >20%

note: increased risk of thromboembolism

92
Q

What is tachycardia induced cardiomyopathy?

A

due to incessant or increased frequency of
- atrial tachycardia- AF, SVT
- junctional tachycardia
- very frequent VEBs
- recurrent NSVT

93
Q

What are risk factors for peripartum cardiomyopathy?

A

older women
multiple fetuses
genetic
uncover underlying CM

94
Q

Describe the management of peripartum cardiomyopathy

A

pre-partum: ACEI, ARB, eplerenone contraindicated

metoprolol rather than carvedilol

spironolactone later in pregnancy

loop diuretics with caution

95
Q

Describe the pattern of heart failure depending on the type of cardiac amyloidosis

A

AL- rapidly progressive HF, biventricular, predominately RHF

Angina- amyloid infiltration of small coronary vessels

Postural syncope: autonomic dysfunction, mutant TTR

96
Q

Describe keys in physical exam that point towards cardiac amyloidosis

A

Absence of S4- despite stiff ventricle due to atrial systolic dysfunction from infiltration

Periorbital purpura- pathognomic of AL

Peripheral and autonomic neuropathy- mutant TTR

macroglossia
cachexia
heavy proteinuria

97
Q

What is the ECG and echo findings in cardiac amyloidosis

A

ECG: low voltage, first degree and higher degree heart block, Q waves V1-3

Echo: small LV size, increased RV and LV wall thickness, increased echogenicity, increased LV filling pressure, severely increased regional longitudinal dysfunction

98
Q

How to investigate cardiac amyloidosis?

A

Cardiac MRI- biventricular thickening with normal cavity size, atrial septal thickening, late gadolinium enhancement

DPP (technetium pyro phosphate) scan
- TTR amyloidosis

Monoclonal gammopathy (free kappa and lambda light chain)- AL

Subcutaneous fat pad aspiration

endomyocardial biopsy

99
Q

What is the management of amyloid cardiomyopathy?

A

Treat heart failure: ACEI and diuretics, NOT b-blockers or CCB

AL –> chemotherapy

ATTR –> Tafamidis

Liver and cardiac transplation for mutant TTE

steroids, methotrexate, anti-TNF antibodies, manage arrhythmias

100
Q

What is the mechanism of hypercalcaemia in sarcoid?

A

activation of Vitamin D by macrophages

101
Q
A

Aisha (47 decks)

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