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Cardio Flashcards

1
Q

Why do you give AV node blockers with flecanide when cardioverting AF?

A

Flecanide organises AF into macro circulations and often leads to flutter. It also increases the capacity of the AV node to conduct so can lead to 1:1 conduction of flutter i.e HR 300bpm–> VF. B-blocker prevents this.

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2
Q

What is target HR in majority of patients wqith AF?

A

<110bpm - the fewer agents necessary the better. Inc risk of complete HB + PPM requirement with increased number of agents

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3
Q

When is AF ablation indicated?

A

For symptomatic AF refractory to medications, and AF with heart failure, doesn’t improve outcomes or need for anticoag

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4
Q

What effect does pulmonary vein isolation have on AF patients with heart failuer?

A

Marked reduction in CHF hospitalisation and all cause mortality.
No benefit shown in people without CHF in ablation vs drug therapy however

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5
Q

What associations should you make if young patient wiyth AF? (19-30y/o)

A

Structural heart disease ( HOCM) and chanellopathies (e.g brugada)

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6
Q

Where does the electrical circuit run in A flutter?

A

in the RA, around the tricuspid ishthmus

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7
Q

What is the treatment for flutter?

A

Ablation - at the tricuspid isthmus
Anticoag same as for AF
Beware of 1:1 conduction with flecanide

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8
Q

In what situations is warfarin used over NOAC for AF anticoagulation?

A

Mechanical heart valves, and rheumatic valvular heart disease. - excess of thrombotic AND bleeding events seen.

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9
Q

If there are retrograde P waves after QRS whatdoes this indicate?

A

AV node re-entrant tachycardia - normal beat down fast pathway, ectopic beat conducted down slow (but short refractory time) pathway and back up fast pathway.

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10
Q

If there is broad complex tachycardia with irregular R-R intervals what is the underlying rhythm ( looks like VT)

A

Need to think about AF with conduction down an accessory pathway . VT is regular!

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11
Q

What features mean a broad complex tachy is definitely VT?

A

AV dissociation, fusion and capure beats

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12
Q

Is patients with non-ischaemic cardiomyopathy, which benefit from CRT device?

A

Broad complex QRS - >120ms ~ 10% risk reduction.
No role for antiarthmis other than b-clockers. No evidence for narrow QRS

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13
Q

What patients with ischaemic heart disease benefit from ICD?

A

Post MI B-blockers reduce VT and sudden cardiac death by 30%
Patients with LVEF <35% more than 40 days post acute MI

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14
Q

what are the common HOCM ECG findings?

A

infrolateral TWI +/- Q waves (in 90%)

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15
Q

What factors are taken in HCM risk of SCD stratification?

A

Age, max LV wall thickness, Left atrial size, max LVOT gradient, fam hx SCD, non-sustained VT, unexplained syncope.
If risk <3-4 % not recommend defib > than than - ICD

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16
Q

What is the screening for someone who has a 1st degree relative with HOCM?

A

if can identify gene then genetic screening ( 50-60% have identifieable gene).
Otherwise annual ECG + ECHO age 11-20, 2-3 yearly age 21-30, and 3-5 yearly >31.

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17
Q

What genes commonly cause Long QT? (AD inheritance)

A

KCNQ1, KCH2, SCN5A ( LQT1-3)

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18
Q

What are the characteristics of the 3 LQT syndromes

A

LQT1 - normal but long - tri by exercise/emotional stress
LQT2 - biphasic T wave -trig by emotion/ loud noises
LQT3 - late peaking T wave - trig in sleep/loud noises

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19
Q

What is the greatest risk of developing arrythmia in LQT?

A

QTc >500

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20
Q

What is treatment for long QT?

A

B-blockers, ICD for high risk

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21
Q

What are the ECG changes for brugada syndrome?

A

Septal downslping ST elevation - may be elicited with flecanide challence. (v1-V3)

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22
Q

What is the inheritence of brugada?

A

AD

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23
Q

“Imapaired longitudinal strain with apical sparing” on myocardial strain indicates what? ( bullseye pattern)

A

Cardiac amyloid

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24
Q

What are indications for cardiac MRI?

A

Assessment of suspected infiltrative disease - Fabry disease, myocarditis, amyloid, sarcoidosis, haemochromatosis. Should be considetred in dilated cardiomyopathy to determine if ischanemic or non-ischaemic

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25
What is fabry disease?
It is glycosphingolipid metabolic pathway that results in lysosomal accumulation of globotriaosylceramide (Gb3). Cardiac manifestations: left ventricular hypertrophy (LVH), aortic and mitral regurgitation, conduction defects, coronary artery disease, hypertension, and aortic root dilation
26
What are : - Increased extracellular volume - Abnormal gadolinum kinetics - Late gadolinium enhancement typical features of?
Cardiac Amyloid
27
What amyloid affects the heart more?
TTR (transtheyretin) amyloid. Protein misfolding leading to dissociated monomores which aggregate and form amyloid fibrils. Fibrils deposit in the myocardium
28
What happens in the L) heart during diastole?
Mitral valve open, passive filling, then atrial contraction for active filling. Passive filling on dopler represented by E wave and active/atrial contraction filling represented by A wave
29
What is the echo doppler findings with normal diastolic function?
Dominant E wave. - passive filling
30
What is the echo doppler findings with mild diastolic function?
E/A wave reversal; - most filling by active atrial contraction. Pseudonormal in Moderate and restrictive pattern in severe
31
What do you use a bone scintigraphy for in cardiology?
Will have cardiac uptake in cardiac amyloid
32
What are indications to investiate for cardiac amyloid?
Heart failure with wall thickness >12mm AND age >65 or a red flag symptom (polyneuropathy, dysautonomia, skin bruisin macroglosia, renal failure, family history ect)
33
What is tafamidis?
Used to treat TTR cardiac amyloidosis - stabilises TTR monomers.
34
in What patients is a TOE contraindicated?
Eosophageal abnormalities - tumour, stricture, fistula, perforation, active UGIB, perforated bowel, unstable C-spine, uncooperative pt. relative contraindication: Barrets, active oesophagitis, neck immobility, coagulopathy, high grade oesophageal varices or active peptic ulcer disease
35
Why is TOE better than TTE in infective endocarditis?
higher SPECIFICITY ( tests that are negative are truely negative)
36
What is Libman-sacks endocarditis?
Non-infective mitral vegetations, seen in Lupus and APS, myeloproliferative disorders
37
How long after cardioversion do patients need to have anticoagulation?
Min 4 weeks to prevent thrombus formation in the cardiac stunning phase post DCCV
38
What are indicaytions for intervention in severe AS?
Asymptomatic patients with EF <50%, asymptomatic patients with symptoms on exercising, Sustained fall in BP >20mmHg during exercise, LVEF <55% without other cause
39
Which patients with severe AS should have intervention?
Symptomatic patient, asymp with EF <55%, asymptomatic but symptoms with exercise.
40
Which patients should have valver replace vs TAVI
TAVI - >75y/o, high risk (Euro score II >8%) or unsuitable for surgery SAVR: <75y/o, low risk, or can't do AVI
41
When do you use Baloon aortic valvotomy?
In patients with severe AS requiring intervention as a bridge to SAVR or TAVI in haemodynamically unstable patients
42
Which valve disease should have intervention even only at moderate impairment?
Mitral stenosis ( Valve area 1-1.5cm)
43
What are the cut offs for mitral valve stenosis?
MILD: Valv area: >1.5cm^2, mean gradient <5, PASP <30 MOD: Area: 1-1.5, Gradient 5-10, PASP 30-50 SEV: Area <1, Mean grad > 10, PASP >50
44
What patients with asymptomatic MR should have surgery?
Severe primary MR with EF <60, >40
45
What is primary vs secondary MR?
Primary - valve problem Secondary - something else pulling valve apparet ( e.g scarred chordae, dilated LV, dilated atrium)
46
What interventions are helpful for secondary MR?
Maximise medical therapy then mitra clip - transcatheter edge to edge repair - reduces grade of MR and shown to have improved outcomes in severe MR
47
What ECHO findins are unusual in MR?
Would expect EF to be higher than usualy BECAUSe blood is ejected out both valves
48
What gene leads to bicuspid aortic valve and what is the inheritance?
AD with variable penetrance, NOTCH1 gene mutation
49
What are cut offs for AS?
Mild = 1.5-2 Mod = Valve area 1 -1.5cm2 Mean Gradient 20-40mmHg Severe = Valve area <1cm2 Mean gradient >40mmHg Jet velocity >4m/sec
50
What is the most common valvular disease?
AS - degenerative calciofic in most, bicuspid aortic valve, Rheumatic HD and radiation other causes
51
What is low flow low gradient severe AS?
Low flow - from LV dysfunction or altered haemodynamics ( e.g UGIB) will have lower gradients, but aortic avlve area can still be <1cm2
52
How is valve area calculated?
Using LVOT and velocity - error in tese will alter AVA
53
What are causes of acute severe AR?
Aortic dissection, endocarditis, trauma
54
What does the ductus arteriosis connect?
Connects the pulmonary artery ( deoxygenated blood going to lungs) to the aorta
55
What type of defect is a PFO?
ASD
56
What shunt is created with a parent ductus arteriosus?
L-> R shunt, blood moves from aorta to pulmonary artery
57
What is a congenital bicuspid valve associated with?
Aortic coarctation
58
What is ebsteins anomaly?
ABN tricuspid valve that sits deeper into the ventricle, abn RV. Ass with WPW,
59
What is truncus arteriosus?
When the aorta and the pulmonary artery don't seperate properly so you have a dilated aortic root that leads to one large vessel draining th heart
60
When do you do CRT device?
Biventricular pacing with cardiac resynchronisation therapy is considered a class I indication in patients with an ejection fraction of less than 35%, left bundle branch block with a QRS greater than 150 ms and sinus rhythm, NYHA class 2-4 on maximum medical therapy.
61
What is PCKS9?
When expressed it causes removal of LDL-receptor on hepatocytes. LDL-receptor removes LDL from the blood normally, so removal of this from the hepatocyte surface leads to increased LDL in the blood.
62
What meds are PCKS9 inhibitors ?
Alirocumab, evolocumab - reduce lipids by 60%, reduce MACE by 15%
63
What is the target of statins?
Inhibition of HMG-CoA (hydroxymethylglutaryl-coenzyme A) reductase
64
What does HMG CoA reductase do?
Converts -3-hydroxy-3- methylglutaryl coenzyme A to mevalonate, a precursor of cholesterol.
65
What is the MoA of Aspirin?
COX 1 (and 2) inhibitor
66
What is the MoA of clopidogrel?
Its is metabolised by CYP2C19 into its active form that irreversibly binds to P2Y12 ADP receptors on platelets.
67
What is the MoA of ticagrelor?
binds reversibly and non-competitively to the P2Y12 ADP receptor on platelets
68
What is the FFR? What is a significant FFR value?
Fractional flow reserve - determines if a coonary lesions is functionally significant. Ischaemia = FFR <0.8
69
What is prasgrel, when cant it be used?
Antiplatelet med - irreversible antagonist of the ADP P2Y12 receptor. Increased bleeding in people wt <60kg, previous stroke and age >75 so don't use in that group.
70
Where do loop diuretics act?
Thick ascending loop of henle - reduce reabsorption by inhibition of NA-K-Cl cotransporter
71
Where does acetazolamide work?
Proximal tubuut - added to loop in acute CHF for faster diuresis
72
Where do thiazides act?
Inhibit Na-Cl transporter in the distal tubule
73
What do ARNIs do?
Degrades vasoactive peptices, including natriuretic peptide, bradykinin, adrenomedullin. LCZ696 neprilysin inhibitor
74
Where to SGLT2 inhibitors work?
Proximal tubule
75
What is the MoA of digoxin?
N-K-ATPase inhibitor - increases contractility
76
What are features of digoxin toxicity?
Hypokalaemia, hypomagnasaemia, hypothyroidism. Levels increased by CPY3A4 inhibitors (Macrolides, itraconazole
77
What is the MoA and function of ivasbridine?
a selective inhibitor of the sinus node cardiac pacemaker If, lowers heart rate so reducing cardiac workload and myocardial oxygen demand.
78
What cardiac devices do you use in CHF after medical optimisation and when?
LVEF <35% and QRS <130ms - ICD implantation LVEF <35, SR and QRS >130 - CRT-D implantation
79
What is inclisiran?
silences RNA Downregulates PCSK9 expression so LDL-R last longer No clinical events outcome data yet
80
What is Bempedoic acid?
Blocks ATP citrate lyase (enzyme in cholesterol production upstream from HMGCoA) No expressed in muslces so may reduce myalgia. Increased Gout and uric acid with this drug
81
What is ANGPLT3 ?
Anti-cholesterol in development
82
Do PCSK9 inhibitors decude risk of death?
Reduction in MI, Odyssey showed reduction in mortality also
83
What are the key proteins that are inhibited to lower cholesterol?
ATP citrate lyase ANGPLT3 HMGCoA reductase PCSK9
84
What is APOC3?
PArt of triclyceride - trials underway to block this to reduce Triglycerides
85
What are the characteristics of coronary lesions that correlate with MACE?
Plaque burden >70% Thin Cap fibroatheroma Minimum lumen area <4mm2
86
In stable coronary aretery disease should you stent coronary lesions? Stable angina
No, increased events and no change in outcomes.
87
What is the benefit of CTCA?
Associated with a lower rate of invasive catheterisation without obstructive CAD. Higher absolute rate of invasive catheterisation but in those patients who actually NEED stents. CCA viable alternative to stress testing
88
What is the coronary calcium score used for?
Can identify individuals at risk that would not be detected by traditional risk factors. Recommended for those at intermediate risk - bc if already high risk - treat as high risk, if already low risk - treat as low risk
89
What is agatston score?
The score that comes out after low dose CT to count the conorary calcium score
90
How do you calculate FFR?
FFR= Distal coronary pressure / Aortic pressure
91
which is better stenting based on angiogram or FFR?
FFR - reduced MR and death at 1 year by 35%
92
What is the commonest drug used to induce hyperaemia for FFR?
Adenosine
93
What is the difference between prasugrel and ticagrelor if they both bind to P2Y12 ADP receptor?
Presugrel - irreversibkly binds, ticagrelor, reversibly binds
94
What is the mechanism of action of ticagrelor mediated dyspnoea and ventricular pauses?
Increased endogenous adenosine
95
Why is radial access better than femoral in cath lab?
Associated with decreased death and easier to control bleeding complications
96
Should patients with out of hospital cardiac arrest have immediate angiography or delayed angiography?
No advantage to immediate catheterisation vs stabilisation and doing it a few days later
97
Should baloon pumps be inserted for cardiogenic shock post MI?
No - no evidence for improved outcomes with this .
98
Should you treat bystander lesions at PCI as well as the culprit lesions in acute MI?
Yes, preventative PCI reduced death from cardiac causes, non-fatal MI, refractory angina in setting of ACS
99
When should you NOT treat non-culprit lesions with PCI?
Stable coronary disease AND STEMI with multivessel disease and cardiogenic shock
100
Which patients with multivessel disease would PCI be acceptable in place of CABG?
Patient with low SYNTAX score without diabetes
101
What intervention for revascularisation is better for left main stenosis?
CABG better than PCI for death, MI, stroke
102
Is there a benefit to CABG in patients with CAD and heart failure with LVEF <35%?
10 year survival benefit for patients with CABG + Optimal medical therapy
103
How do you test for low flow low gradient severe as?
Low dose dobutamine stress echo - if the mean gradient doesnt change with this then not low flow low gradietn severe AS
104
What medical management should be given to patients who have Marfans syndrome and AR?
B-blockers have a role in reducing the shear sress and aortic growth rate and should be considered before and after surgery
105
What is the medical therapy for AR?
None if no HTN If HTN - aim BP <140mmHg
106
What is the cause and timing of acute mitral regurgitation?
Classically spontaneous chrotae tendinae or papillary muscle ruptue secondary to MI. Occurs 2-7 days post infarct ( commonly after inferior infarct)
107
Why is acute MR important?
HD changes are more severe than chronic MR because the heart doesn't have time to adapt to changes leading to cardiogenic shock + APO
108
What intervention is used as a bridge to surgery in acute MR?
Intraaortic balloon counterpulsation or ECMO
109
What population of patients requiring anticoagulation (for AF, thrombus, embolic event ect) are NOACs contraindicated?
Rheumatic heart disease! (and mechanical valve replacements)
110
What valvular disease leads to AF?
Mitral stenosis
111
What malignancy is associated with tricuspid valve disease?
Carcinoid ( usually only ones that invade the liver) release vasoactive substances that have paraneoplastic effects on cardiac tissue.
112
What are the findings of carcinoid heart disease?
Endocardial plaques of fibrous tissue. This results in distortion of the valves leading to stenosis or regurg or both. R > L
113
What inv is used to diagnose carcinoid heart disease?
24 hour urine 5HIAA - elevated in cardiac disease

FRACP Exam (15 decks)

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