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Cardiology Flashcards

1
Q

CHA2DS2VASC score for non-valvular AF?

A 
CCF
HT
Age >= 75
DM
Stroke/TIA/Thromboembolism
Vascular disease
Age 65-74
Female
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2
Q

Indications for heart transplantation?

A

Include deteriorating cardiac function and a prognosis of less than 1 year to live
Dilated cardiomyopathy
Ischaemic cardiomyopathy
Congenital heart disease for which no conventional therapy exists or for which conventional therapy has failed
Ejection fraction less than 20%
Intractable angina or malignant cardiac arrhythmias for which conventional therapy has been exhausted
Pulmonary vascular resistance of less than 2 wood units
Age younger than 65 y
Ability to comply with medical follow up care

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3
Q

What are the CI for heart transplantation?

A

Age > 65 y, evaluated on individual basis
Fixed pulmonary vascular resistance of > 4 Wood Units
Active systemic infection
Active systemic diseases such as collagen vascular disease or sickle cell disease
Active malignancy - pts with a 3-5 yr disease free interval may be considered depending on tumour type and evaluating program
An ongoing Hx of substance abuse
Psychosocial instability
Inability to comply with medical FU

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4
Q

What is the culprit artery with the following ST elevation ECG changes?

A

II, III, aVF - inferior - RCA or LCx
I, aVL, V5, V6 - Lateral - LCX
V7, 8, 9 - Posterior descending (PDA) of the RCA or LCx
V1,2,3,4,5,6, I, aVL - anteroseptal with lateral extension - LCA

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5
Q

In pts with ACS, the addition of which medication with moderate-intensity statin therapy is associated with a reduction in CVS mortality?

A

Ezetimibe

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6
Q

In contrast nephropathy, when does the creatinine return to baseline?

A

within 7 days

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7
Q

What are the post cardiac catherisation causes of acute renal failure?

A

Renal athero-embolism - persistent renal failure after 7 days
Contrast nephropathy

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8
Q

What factor confers the worst prognosis in a patient with cardiomyopathy?

A

Mitral regurgitation - usually associated with HOCM, sudden cause of cardiac death in young ppl

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9
Q

What superior advantage does apixiban have over warfarin?

A

Greater reduction in rates of stroke or systemic embolism with lower rates of bleeding- ARISTOTLE study 2011

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10
Q

What are the features of CHB?

A 
Syncope
HF
Regular bradycardia 30-50 bp
Wide pulse pressure
JVP cannon waves in neck
Variable intensity of S1
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11
Q

What does the a, x, c, v and y represent in the JVP?

A 
a = atrial contraction
x = fall in atrial pressure during ventricular systole
c = closure of tricuspid valve
v = volume filling
y = opening of tricuspid valve
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12
Q

What is the recommended daily salt intake that is proven to be beneficial in reducing CVS events?

A

3-6 g/d PURE study NEJM 2014

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13
Q

What are the examination findings in mitral stenosis?

A 
Reduced arterial pulse volume
Prominent a wave in JVP. Absent in F
Prominanet v wave seoncardy to TR
Rigt ventricular heave
Palpable S2
loud S1
late diastolic murmur in mild MS, early diastolic murmur in severe MS
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14
Q

What are the specific signs of severe MS?

A

Mitral facies
prominent V wave in the JVP
Right ventricle lift
early opening snap following S2
loud pulmonary component of the seance heart sound
early diastolic murmur (murmur diminished in Ispiration, augments with expiration)

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15
Q

What are the sounds when pulmonary HT is present?

A

Pulmonary ejection sound
holosystoic murmur of TR heard best along the right sternal border which increases with inspiration
Graham Steel murmur of Pul regard best heard at the base

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16
Q

What are the continuous wave doppler findings in mitral regurgitation?

A 
Dominant E wave (positive wave above the line before QRS)
Restrictive flow pattern
High velocity E wave 
Small A wave
E/A ratio is increased
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17
Q

What is the continuous wave doppler findings in aortic stenosis?

A

Negative wave form after QRS

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18
Q

What is the continuous wave doppler findings in mitral stenosis?

A

Negative wave form before QRS complex

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19
Q

What is the continuous wave doppler findings in aortic regurg?

A

Positive wave form after QRS complex

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20
Q

What are the indications for intervention for the Mx of Mitral stenosis?

A

Mod to severe MS

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21
Q

What is the main indication for intervention in asymptomatic patent with mitral stenosis?

A

Mod to severe MS and pulmonary HT (PAP > 50 mmHg at rest or > 60 mmHg with exercise)

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22
Q

When is Sx indicated in mitral valve repair?

A

Among patients who are symptomatic(NYHA class III-IV) if:
1) Percutaneous mitral balloon valvotomy is not available.
2) PMBV is contraindicated because of moderate to severe MR or of left atrial thrombus that persists despite anticoagulation.
3) Mitral valve morphology is not favourable for PMBV in patients with acceptable operative risk.
Symptomatic patients who also have moderate to severe MR.

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23
Q

What are the CI to percutaneous mitral balloon valvotomy?

A

1) Mitral valve area >1.5cm2
2) Left atrial thrombus
3) Moderate to severe MR
4) Severe or bicommissural calcification
5) Absence of commisural fusion
6) Severe concomitant aortic valve disease,or severe combined tricuspid stenosis and regurgitation.
7) Concomitant CAD requiring bypass surgery.

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24
Q

What type of murmurs are heard during early, mid, pan and late systole?

A

Early systolic- MR, TR, VSD
Midsystolic ejection- Aortic stenosis, Aortic sclerosis.
Holo/Pansystolic – MR, TR, VSD
Late systolic- Mitral valve prolapse, Tricuspid valve prolapse

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25
Q

What type of murmurs are heard during early, mid and late diastole?

A

Early diastolic – AR, PR
Mid-diastolic- MS, TS, Atrial myxoma
Late diastolic- MS, TS, Atrial myxoma, Complete heart block.

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26
Q

Which artery is most commonly affected in a pt with an ascending aortic dissection presenting with an AMI?

A

RCA

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27
Q

What anti-coagulation therapy is recommended for patients with a CHA2DS2-VASC score between 0-1 and >2?

A

0-1 aspirin

> 2 warfarin, dabigatran (RE-LY), Rivaroxiban (ROCKET-AF), Apixaban (ARISTOTLE)

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28
Q

MOA of Tirofiban?

A

Reversible non peptide recepor antagonist against Glycoprotein IIB/IIIA

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29
Q

How do you treat hypotension in the setting of a right ventricular infraction?

A

Fluid loading

Nitrates are CI

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30
Q

What is the most common mutation in patients with HCM?

A

cardiac beta-myosin heavy chain gene on chromosome 14

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31
Q

What are the sign of cardiac toxicity with flecainide?

A

Prolonged PR interval
Widening QRS
Heart failure
Torsades de pointes

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32
Q

What are the indications for ICD placement in a patient with HOCM?

A

ICD placement is indicated if any ONE of the major risk factors are present:

1) Left ventricular wall thickness >30 mm
2) Family history of premature sudden cardiac death
3) Previous cardiac arrest/ventricular tachycardia
4) Previous episodes of documented non-sustained VT (>3 beats, rate >120 bpm)
5) Unexplained syncope

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33
Q

When is it safe for non cardiac invasive procedure post stent insertion for a bare metal stent vs drug eluting stent?

A

Bare metal > 6 weeks

Drug eluting > 1y

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34
Q

What is the cause of dyspnoea, haemoptysis, hoarseness in MS?

A

Elevation in left atrial pressure leading to reduced lung compliance
Haemoptysis due to increased pulmonary pressure and vascular congestion
Hoarseness due to compression of recurrent laryngeal nerve

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35
Q

What is the MOA of spironolactone?

A

K sparng loop diuretic

AMdrogen receptor antagonist and may cause feminisation side effects such as gynaecomastia

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36
Q

What is the MOA of eplerenone?

A

Selective aldosterone antagonist without antiandrgenic effects
Reduce mortality in the immediate 314 days post MI period in patients with LV systolic dysfunction and symptoms of H

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37
Q

MOA Digoxin?

A

Reduces sympathetic flow
Inhibits Sodium-Potassium ATPase
Reduce renin secretion
Sensitize cardiopulmonary baroreceptors

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38
Q

Why are CCB Diltiazem ad Verapamil CI in pots with systolic HF?

A

non-dihydropyridine CCB that have direct negative inotropic properties

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39
Q

Which drugs should be avoided in HF?

A
  • anti-arrhythmic agents (apart from beta-blockers and amiodarone)
  • non-dihydropyridine calcium-channel blockers (verapamil, diltiazem)
  • tricyclic antidepressants
  • non-steroidal anti-infl ammatory drugs and COX-2 inhibitors
  • clozapine
  • metformin and thiazolidinediones(pioglitazone, rosiglitazone)
  • corticosteroids (glucocorticoids and mineralocorticoids)
  • tumour necrosis factor antagonist biologicals.
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40
Q

What is the MOA of abciximab?

A

Glycoprotein IIb/IIIa receptor antagonsit

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41
Q

All anti platelets are irreversible. T/F

A

False, Tirofiban is reversible

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42
Q

Which drug reduces the incidence of major cardiovascular events in pts with elevated CRP without hyperlipidaemia?

A

Atorvastatin

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43
Q

What are the indications for a biventricular pacemaker defibrillator?

A

1) NYHA class III or IV heart failure,
2) ejection fraction less than or equal to 35%
3) QRS width greater than 120 msec.

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44
Q

What are the indications for a permanent pacemaker insertion?

A

Symptomatic sinus node dysfunction
Acquired AV block in adults, Mobitz II or 3rd degree HB (symptomatic/asymptomatic)
Chronic bifasicular block- Mobitz II, intermittent 3rd degree HB or alternating BBB
Persistent and symptomatic 2nd or 3rd degree AV block and associated BBB after STEMI.
Symptomatic Hypersensitive carotid sinus syndrome and neurocardiogenic syncope
Persistent inappropriate or symptomatic bradycardia not expected to resolve after cardiac transplantation

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45
Q

What is the indication of a permanent pacemaker insertion following an STEMI?

A

Persistent/Transient 2nd degree AV block or 3rd degree block and associated BBB

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46
Q

What are the benefits of cardio resynchronisation?

A

1) Improvement in 6 minute walking distance
2) Improvement in quality of life
3) Improvement in VO2 max
4) Improvement in hospitalization for heart failure
5) Reduction in NYHA class score
6) Decreased mortality

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47
Q

Which variable carries the greatest impact on the AR of a CVS event in the CVS risk table?

A

Age

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48
Q

What is the MOA of aspirin?

A

Irreversibly inhibits COX1 and COX2 enzymes thereby suppressing the production of prostaglandins and thromboxanes

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49
Q

What is the mechanism of action of clopidogrel?

A

Clopidogrel works by blocking the ADP receptor thereby preventng the activation of GP IIb/IIIa receptor complex. Other ADP receptor blocker includes: Ticagrelor (reversible) Prasugrel.

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50
Q

What is the mechanism of action of Bivalirudin?

A

Reversible direct thrombin inhibitor
. It cleaves fibrinogen into fibrin monomers, activates Factor V, VIII, and XIII, allowing fibrin to develop a covalently cross-linked framework which stabilizes the thrombus

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51
Q

List the direct thrombin inhibitors

A

Argatroban
Bivalirudin
Hirudin

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52
Q

MOA of Fondaparinux?

A

synthetic pentasaccharide Factor Xa inhibitor

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53
Q

List the Factor Xa inhibitors

A

Apixaban
Enoxaparin
Fondaparinux
Rivaroxaban

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54
Q

What is the mechanism of action of enoxaparin(LMWH)?

A

Potentiates action of anti-thrombin III and also inhibits factor Xa.

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55
Q

Which drug prevented the development of symptomatic CHF and lowered the risk of both hospitalisation for, and death from, CHF in pts with asymptomatic LV dysfunction LVEF

A

Enalapril 10 mg BD

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56
Q

Which medication has been proven to reduce the subsequent development of CHF in patients with preserved ventricular function in the early post MI period?

A

BB
Limited data exist on the use of beta-blockers to prevent progression to symptomatic CHF in patients with asymptomatic LV dysfunction not associated with MI.

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57
Q

In patients with systolic LV dysfunction, which medication should be started regardless if patient is symptomatic or not?

A

All patients with systolic LV dysfunction, whether symptomatic or asymptomatic, should be commenced on ACE inhibitors with every effort made to up-titrate to the dose shown to be of benefit in major trials

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58
Q

What is the mechanism of action of carvedilol?

A

Beta-1, Beta-2 and alpha-1 antagonist.

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59
Q

MOA of metoprolol?

A

beta-1 selective antagonist

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60
Q

In patients with severe aortic stenosis who are not candidates for surgical replacement of the aortic valve, which treatment significantly reduces mortality?

A

TAVI (NEJM 2010)

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61
Q

Where is the location of the AMI in (V1, V2), (V3, 4), (V5,6,I and aVL)?

A

Septal
Anterior
Lateral MI

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62
Q

What are the ECG changes in aVR with pericarditis?

A

PR elevation and ST depression

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63
Q

In patients with severe aortic stenosis who are not candidates for surgical replacement of the aortic valve, which of the following treatment significantly reduces mortality?

A

TAVI

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64
Q

What are the ECG changes in Lown-Ganong-Levin syndrome?

A

PR interval

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65
Q

What is the Tx of Torsades?

A

1) Correct underlying cause.ie: electrolyte disturbance
2) Magnesium sulphate
3) Consider overdrive pacing or isoproterenol infusion
4) Consider DC cardioversion if hemodynamically unstable

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66
Q

Which anti-arrhythmic drugs should be avoided in Torsades?

A

1) class IA agents (eg, quinidine, procainamide, disopyramide),
2) class IC agents (eg,flecainide)
3) class III agents (eg, sotalol, amiodarone).

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67
Q

In 2nd degree HB type1 (prolonged PR interval until drop- Wenkerbach), where is the location of the block?

A

Above the AV node

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68
Q

What is the next line of investigation for a pt with atypical chest paun and LBBB on resting ECG?

A

Stress echo

BBB makes EST difficult to interpret

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69
Q

What factor contributes the greatest population risk for MI?

A

Interheart Study
Dyslipidaemia 49%
Smoking 36%
Psychosocial factors 33%

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70
Q

Which patients have poorer outcomes in STEMI vs NSTEMI?

A

NSTEMI
OPERA registry in France 2151 pts
In hospital mortality similar 4.6 (STEMI) vs 4.3 (NSTEMI) and 1 yr mortality was 9.0% in STEMI vs 11.6% in NSTEMI

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71
Q

Does a LBBB constitue a +ve EST?

A

No, is a function of conduction - system capacity not ischaemia

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72
Q

What are the CI for an EST?

A

LBBB
Severe HOCM
Asever AS
Recent MI (304d)
Unstable angina with recent rest pain or increased symptoms
Untreated life threatening cardiac arrhythmia
Advanced AV block
Uncontrolled systemic HT (>220/120)
Acute systemic illness e.g. PE/aortic dissection
Unable to perform test

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73
Q

Is TAVI superior to medical therapy in inoperable patients with severe AS?

A

Yes

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74
Q

Transapical vs Transfemoral TAVI. Which has better outcome?

A

Transfemoral TAVI

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75
Q

In elderly patients eligible for a TAVI or surgical AVR, TAVI has non-inferior outcomes over the first 2 years? T/F

A

true

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76
Q

What is the Tx of choice for a bicuspid aortic valve?

A

Sx

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77
Q

Elderly lady with syncopal episodes. ECG- PR interval prolonged, RBBB and LAD (trifasicular block). Where is the pathology in the heart? Tx?

A

AV and Purkinje fibres
Pacemaker
Dual chamber if in sinus rhythm

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78
Q

Implantable cardioverter defibrillator (ICD) devices should be considered in patients with HF who fulfil which criteria?

A

LVEF =40 days post MI and NYHA class II or III

NON-ICM (non ischaemic cardiomyopathy) LVEF =40 days post MI and NYHA class I

NSVT due to prior MI, LVEF

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79
Q

What is the Tx for a bicuspid valve with RF i.e. aortic root > 50 mm?

A

Aortic root replacement.

No indication for valve replacement

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80
Q 
Young male with syncope while running and several episodes of pre syncope during high intensity sports. 
Dx
Mean presentation
Pathophys
Next Ix?
A

Catecholaminergic polymorphic VT

6-10 y, 75% before 20y

Path:
AD
Ryanodine receptor (RyR2) 60-75%
CASQ

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81
Q

Non-commercial driver suffers cardiac arrest. When can they drive?

A

Not for at least 6 months following a cardiac arrest.

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82
Q

Truck driver suffers cardiac arrest and ICD implanted. When can he drive a commercial vehicle again?

A

He can no longer hold a commercial vehicle licence if ICD implanted.
Otherwise cannot drive for 6 months after a cardiac arrest. Reversible cause has to be identified and recurrence unlikely and there are minimal symptoms related to driving upon review.

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83
Q

Truck driver with HF and EF

A

Cannot hold a commercial licence again

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84
Q

Pt inferolateral NSTEM and drug eluting stent inserted. When can she drive a non-commercial vehicle?

A

2 weeks

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85
Q

Pt with non commercial licence post CABG. When can they drive?

A

Not for at least 4 weeks after CABG

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86
Q

Pt with commercial licence post CABG. When can they drive?

A

> 3 months after CABG, Exercise tolerance >=90% of age/sex predicted according to Bruce protocol and no evidence of ischaemia on exercise ECG (40%, minimal symptoms and minimal residual musculoskeletal pain after Sx

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87
Q

Pt with non commercial licence post ICD implantation. When can they drive?

A

Unfit to drive if ICD implanted for ventricular arrhythmias
Conditional licence may be considered if:
- ICD implanted for an episode of cardiac arrest and person asymptomatic for 6 moths OR
- ICD prophylactically implanted for at least 2 weeks AND
- there are minimal symptoms.

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88
Q

Pt with commercial licence post ICD implantation. When can they drive?

A

Not fit to hold a conditional or unconditional licence

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89
Q

When can a pt drive private vehicle after a ICD generator change?

A

> 2 weeks after generator change

> 4 weeks after ICD therapy associated with symptoms of haemodynamic compromise

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90
Q

What is the most appropriate age to commence the Framingham CVS risk assessment for Indigenous vs. general population?

A

35 y in Indigenous

45 y in caucasians

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91
Q

What are the CI to ticagrelor?

A

Hx of intracranial bleed
acitive pathological bleed e.g. PU, intracranial haemorrhage
severe hepatic impairment
Hypersensativity t ticagrelor

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92
Q

MOA ticagrelor?

A

P2Y12 antagonsit
Caution with strong inhibitors of CYP3A4 -> may increase bleeding
Irreversibly binds to platelt P2Y12 receptor and inhibits platelet aggregation for the life of the platelet.

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93
Q

CI to thrombolysis in STEMI?

A

Risk of bleeding

  • active bleeding or bleeding diathesis
  • significant closed head trauma
  • suspected aortic dissection

Risk of intracranial haemorrhage
- any prior intracranial haemorrhage
- ischaemic stroke within 3 months
- known structural cerebral vascular lesion e.g.
AV malformation
- known malignant intracranial neoplasm
- intracranial or intraspinal Sx within the past 2 months

94
Q

What is the most important RF for coronary stent thrombosis?

A
  • interruption of dual anti-platelet therapy within 6 weeks of implantation, Significant P value when Clopidogrel stopped
95
Q

What are the indications for ICD in CHF?

A
  • survived cardiac arrest resulting from VF/VT not due to a transient or reversible cause
  • spontaneous sustained VT in association with structural CHD
    LVEF
96
Q

Indications for cardiac resynchronisation therapy i.e. biventricular pacemaker in CHF?

A

Class I:
LVEF =150 AND
NYHA II, III or ambulatory IV on GDMT (medical Tx)

Class IIa:
LVEF =120, NYHA II, III or ambulatory IV on GDMT

LVEF =150, NYHA III/ambulatory IV on GDMT

97
Q

Which ARB has the most evidence behind its use in HF?

A

Candesartan

98
Q

What is the 5 year survival after cardiac transplant?

A

75%

99
Q

Which NOAC is superior to warfarin in the Mx of non-valvular AF in reducing the risk of stroke and systemic immobilisation?

A

Apixiban has mortality benefit

Rivaroxiban is non inferior, non superior

100
Q

What are the definite indications for cardiac transplant?

A

Persitent NYHA Class IV symtpoms

Volume of O2 consumed per minute at maximal exercise (VO2 max)

101
Q

What were the outcomes of the RE-LY study of Dabigatran vs warfarin for non valvular AF and >=1 RF for stroke?

A

150 mg of Dabigaran was associated with lower rates of stroke and systemic embolism but similar rate of bleeding
110 mg of Dabigatran was associated with similar rates of stroke and systemic embolism and lower rates of bleeding

102
Q

What was the outcome of the ROCKET study of Rivaroxiban vs warfarin in non valvular AF and >=1 RF for stroke?

A

Rivaroxiban was non inferior ro warfarin for prevention of stroke or systemic embolism
There was no significant difference in major and clinically relevant non-major bleeding between the 2 groups
Intracranial and fatal bleeding occurred less frequently in the rivaroxaban group

103
Q

What was the outcome of the ARISTOTLE study of Apixaban vs warfarin in non valvular AF and >=1 RF for stroke?

A

Prevented stroke = mortality benefit

104
Q

T/F. Higher dose dabigatran and apixiban are superior to warfarin?

A

True

105
Q

When do you treat AF with anticoagulant?

A

If valvular AF or CHA2DS2VASc 1 = NOAC

If CHA2DS2VASc >=2 then NOAC or VKA

106
Q

What is the Tx for Brugada syndrome?

A

BB
ICD if syncope or FHx of SCD
Quinidine if recurrent ICD shocks

107
Q

What is Familial hypocalciuric hypercalcaemia? Clinical presentation and Ix findings?

A 
AD condition caused by mutation of calcium sensing receptor 
Clinical:
Asymptomatic hypercalcaemia
may suffer from recurrent episodes of renal stones
Ix:
High serum Ca
High PTH
Urine Ca normal
108
Q

When is PCI indicated?

A

> 70% stenosis

109
Q

Which medication has the best CV benefit in pt with angina and

A

ACEI and BB

110
Q

What is Repetitive monomorphic VT? Pathophys, Clin, Ix, Tx?

A 
Characterised by VT bought on by exercise due to right ventricular outflow obstruction.
AKA RV tachycardia, catecholamine-sensitive VT, adenosine-sensitive VT, and exercise-induced VT.
Path:
RV tachycardias arise from the septal aspect of the RVOT
Clin:
Dizziness while exercising
periods of pulselessness
Ix:
RMVT rate 140-180 bpm
ECG
LBBB
inferior axis
Tx:
1st line: BB/CCB
2nd line: RFA
111
Q

Familial hypercholesterolaemia. Genetic mutation, clinical presentation, Ix findings?

A

Defects in apoliprotein B and apo E receptor genes resulting in the decrease in the number of LDL receptors.
Heterozygous = 50% LDL receptors -> 2x normal LDL levels
Homozygous = no functional LDL receptors

Clinical:
Tendon Xanthoma
LDL: apo B ratio 1.4 in normal)
FX of premature CHD

Ix:
Heterozygous = 50% LDL receptors -> 2x normal LDL levels
Homozygous = no functional LDL receptors

112
Q

Familial combined hyperlipidaemia. Genetic mutation, Ix findings?

A

Increased production of both apo B100 and VLDL.
Most common cause of lactescent plasma)

Ix
increased LDL and VLDL (Hyperchol and Hypertrig)

113
Q

Familial hypertriglyceridaemia (Type IV hyperlipoproteinemia). Genetic mutation, clinical presentation, Ix findings?

A

AD disorder associated with moderate elevations of serum triglyceride concentration.
Heterozygous for inactivating mutations of the LPL gene.

Clinical:
Obesity
Hyperglycaemia
HT
Hyperuricaemia

Ix:
Elevated triglycerides
Low serum HDL-C (hypoalphalipoproteinemia)

Lipoprotein lipase deficiency:
Characterised by high triglycerides but low levels of HDL and LDL

114
Q

Familial hypoalphaliproteinemia. Genetic mutation, clinical presentation, Ix findings?

A

AD disorder associated with mutations in gene for pa AL resulting in isolated low HDL.

115
Q

Acquired cases of hypercholesterolaemia?

A

Oestrogen replacement -> fall in LDL-C -> elevated triglycerides
Hypothyroidism

116
Q

Mx of asymptomatic vs. symptomatic pts with carotid stenosis of 70%?

A

Asymptomatic:
Carotid endarterctomy beneficial for pts with carotid stenosis 60-99%. However degree is not as great as for symptomatic stenosis.
CEA suggested for medically stable men who have a life expectancy of >5 y
Tx with aspirin recommended for all patients who are having a CEA. Aspirin should be started prior to Sx and continued for 3 months after Sx

Symptomatic
CEA recommended.
Carotid artery angioplasty and stenting is an alternative to carotid endarterectomy for the Tx of patient with carotid arthersclerotic disease, particularly in patient considered to be poor candidates for Sx.

117
Q

Which antihypertensive is beneficial in GOUT?

A

Losartan - has uricosuric effects and may be a good alternative antihypertensive agent

118
Q

What is Tetrology of Fallot characterised by? Commonest post operative complication of TOF?

A 
Large VSD
Over riding aorta
RVOT obstruction/pulmonary stenosis
RV hypertrophy
Post operative complciation is pulmonary valve incompetence. May require re-intervention
119
Q

Which NSAID has the least cardiovascular adverse effects?

A

Naproxen

Lowest risk of MI and stroke compare to other non selective NSAIDs

120
Q

What Ix is most useful in assessing symptomatic response to CRT?

A

Echo useful in optimising AV delay

121
Q

Signs and symptoms of a RCA infarct?

A 
Chest pain
Raised JVP
S3 gallop
Chest clear to auscultation
Hypotensive
ECG: ST elevation V1-4 and V4-6
122
Q

What is the greatest disadvantage of coronary stenting compared to CABG?

A

Post procedural AF
At one year and longer, CABG and PCI appear to have similar rates of combined end point of death from any cause, MI, stroke.
CABG is associated with a significantly higher incidence of adverse in hospital outcomes including death, MI and stroke.
PCI with stunting is associated with a higher incidence of target vessel revascularisation at long term follow.

123
Q

What is the most common complication in patients who have had a tetralogy of Fallot deficit corrected successfully during childhood?

A

Pulmonary regurgitation with associated RV enlargement
Residual RVOT
RV dysfunction
Aortic root dilatation
Aortic valve insufficiency
Arrhythmias including atrial tachycardia and VT

124
Q

MOA of adrenaline?

A

Increases arterial BP and coronary perfusion during CPR via alpha 1 adrenoreceptor agonist effects.
Low dose increases CO by beta adrenergic effects (inotropic and chronotropic)

125
Q

When to chose a BMS over a DES?

A

Compliance is likely to be problematic for 12 months of dual anti-plt
Those known to be at higher risk for bleeding

126
Q

What drugs are used in DES?

A

Sirolimus - macrocytic triene ab, inhibits proliferation of smooth muscle cells and other cell types seen with restenosis after PCI
Paclitaxel - interferes with the function of the microtubules during cell division. Reduces smooth muscle proliferation.

127
Q

What is the benefit of drug eluting stent over over BMS?

A

Inhibition of in stent neointimal hyperplasia

128
Q

In a patient with aortic stenosis, what portends a bad prognosis?

A

Without Sx, the mean survival depends on clinical presentation:
Impaired LV function -> heart failure in 2 years
Syncope in 3 years
Angina in 5 years

129
Q

Pt with ischaemic cardiomyopathy and EF 30% presents with decompensated HF and pulmonary oedema. He is in AF, assuming this is paroxysmal. What drug should be used to treat AF?

A

Rate control preferable to rhythm control - BB initial therapy e.g. metoprolol
Rhythm control drug of choice is amiodarone.
Felcainide is associated with increased risk of proarrhythmias and risk for sudden cardiac death and shouldn’t be used in CCF.
Verapamil can exacerbate HF symptoms.
Lignocaine used in serious ventricular arrhythmias and isn’t indicated for AF. May worsen HF.

130
Q

IE. Most common infections for native valve infection? Tx for each?

A

1st- S. aureus, poor outcomes
Tx- Fluclox in MSSA, Vanc in MRSA. can add gentamicin for empiric therapy but does not alter outcome.

2nd - Strep viridans
Tx - Benpen + Gent. If resistant then van + gent.

3rd - enterococci, least virulent
Tx- Benpen + Gent

HACEK (gram -ve), slow growing in culture
Tx - Ceftriaxone

131
Q

What is the advantage of cardiac resynchronisation over implanted defib?

A

Improved symptoms
CRT does not reduce arrhythmias.
CRT and defib reduces cardiac mortality.
CRT reduces mortality, improves symptoms and hospitilisations.
CRT improves systolic function and reverses ventricular remodelling and decreases MR.

132
Q

What is the most common symptoms in myocarditis? Most common organism?

A

Chest pain, 35%

Enterovirus due to easy access through coxsackie adenoviral receptor

133
Q

MOA of dihydropyridine CCB?

A

Block inward current of Ca into cells in vascular smooth muscle, myocardium and cardiac conducting system via L-type calcium channels.
Dihydropyridines mainly act on arteriolar smooth muscle to reduce peripheral vascular resistance and BP. Have minimal effects on myocardial cells.
e.g. amlodipine, felodipine, lercanidipine, nifedipine.

134
Q

MOA of non-dihydropyridines CCB?

A

Non-dihydro (D&V) act on cardiac and ateriolar smooth muscle to reduce cardiac contractility, HR and conduction. V has a greater effect. D has greater affect on arteriolar smooth muscles than V.

135
Q

Dig toxicity. Level that is toxic? Clinical? Tx?

A

> 2.0 associated with systemic effects.

Acute OD- If

136
Q

What factors do statins reduce the cholesterol profile?

A

LDL, 30-64% reduction - Atorvastatin most potent
Triglycerides, 14-33% - gemfibrozil good for lowering triglycerides and raising HDL level
Mild increase of HDL to 10%

137
Q

Most common organism causing prosthetic heat value IE?

A

Staph aureus

> 12months is Strep (includes viridans group)

138
Q 
What Abx choice is recommended for IE prophylaxis in:
Dental 
GI, GU
Skin
Penicillin allergy
A

Dental - Amoxicillin 2 g PO 30 min before procedure
GI, GU - Ampicillin or amoxicillin
Skin - cephalosporins
Penicillin allergy or worried about MRSA - Clindamycin or Vancomycin

139
Q

HT: Tx for general population >= 60 years. Non black vs. black? If not at goal BP, next step?

A

Non black = ACEI/ARB/CCB or thiazide diuretic or combination
black = CCB or thiazide diuretic or both
Use single medication 1st, then add another. Increase doses to max if goal not achieved.
If goal still not achieved with above, add BB, aldosterone antagonist or others and refer

140
Q

HT: Tx population with DM or CKD. All ages.

A

All races: CKD present, no DM = ACE/ARB or in combination with other drug classes
Diabetes present, no CKD = follow Tx as for nonblack vs. blacks.
Non black = ACEI/ARB/CCB or thiazide diuretic or combination
black = CCB or thiazide diuretic or both
Use single medication 1st, then add another. Increase doses to max if goal not achieved.
If goal still not achieved with above, add BB, aldosterone antagonist or others and refer

141
Q

Types of Long QT, Clinical, RF, Tx?

A

QTc > 460 ms in females
QTc > 440 in males
Long QT 1 - K defect, not enough. Associated with swimming, exercise
Long QT 2 - K defect, too much, associated with arm clocks, post partum
Long QT 3 - Na channel mutation

Clinical:
syncope related to polymorphic VT

RF:
QT> 500 ms
Hx of sudden cardiac arrest
recent syncope

Tx
BB

Cardiodefib indicated if:
QTc > 500
recurrent syncope while on BB
Cardiac arrest

142
Q

Catecholaminergic polymorphic VT. Epid, Clinical, Ix, Tx?

A

Epid

143
Q

Arrhyhthmogenic right ventricular cardiomyopathy/dysplasia. What, Clinical, Ix, Tx?

A

Characterised by a disease of the desmosome that leads to fibrofatty infiltration of the myocardium

Clinical presentation
heralded by a syncopal episode secondary to monomorphic ventricular tachycardia originating from the RV

Ix
ECG
T wave insertions in leads V1-3 with an epsilon wave (high freq signal at end of QRS)
Echo - moderate RV dysfunction and enlargement
Cardiac MRI
dilatation and akinesia of RV outflow tract
Continuous ambulatory ECG monitoring demonstrating VT or >500 PVCs in a 24 hr period
loop event recorder

Tx
Medications
BB and class III anti-arrhythmic e.g. stall can be used to reduce the incidence of VT or reduce ICD shocks. Not to be used in place of ICD.
Implantable defibrillator if syncopal episode
if multiple ICD shocks, intra-cardiac ablation can be used as adjunct for VT
discourage competitive sports -> 5 fold increased risk of sudden death.

144
Q

Which part of myocardium is most vulnerable to ischaemia?

A

Subendocardium

Small vessels which enter the myocardium are contracted during systole and hence the area is prone to ischaemia.

145
Q

Wolf Parkinson White.
Ix
ECG
Tx? CI?

A

ECG:

Short PR interval

146
Q

Pregnancy is CI in which cardiac conditions?

A

PAH

LVEF 40 mm

147
Q

Tx for HOCM?

Drugs to avoid

A

BB, verapamil if stable
Cardiovert if HD unstable

Avoid GTN as will make pt HT due to decreased preload
Inotropic drugs worsen outflow tract obstruction

148
Q

Where is the hypertrophy is HOCM?

A

Most common is septal hypertrophy
Can be diffuse
Diastolic dysfunction
Exercise exacerbates symptoms as already under filled and more under filled with tachycardia

GENETIC DEFECT IS IN THE CARIAC MYSOIN GENES

149
Q

Criteria for LVH?

A

S wave depth (V1) + tallest R wave height in V5-6. > 3.5 (=3.5 squares)

150
Q

ECG changes for LV strain?

A 
LV strain (due to L hypertrophy, HT most common cause)
- ST depression and inverted T wave
151
Q

ECG changes for HOCM

A

LVH - S wave depth (V1) + tallest R wave height in V5-6. > 3.5 (=3.5 squares)

Other features:
High voltage
Q waves in inferolateral leads = septal hypertrophy

152
Q

What is the most common cardiac tumour?

A

Atrial myxoma, left sided 80%

Malignant cardiac tumours are freq sarcomas

153
Q

What is Eissenmenger syndrome?

A

Right to left shunt.
Often a result of pulmonary HT e.g. unrepaired VSD

Greatest risk of cardiac complication during pregnancy.

154
Q

What are the stress exercise ECG changes predictive of CAD?

A

ST elevation greater than 1 mm in aVR - indicates left main disease or triple vessel disease
(reciprocal change sin lateral ischaemia)
Indicates need for bypass
Magnitude of elevation in aVR correlates with mortality

155
Q

How do you differentiate between pericarditis and left main disease on ECG?

A

In pericarditis ECG will demonstrate PR elevation and ST depression

156
Q

Prominent v wave suggest?

A

Tricuspid regurg

V wave presents tricuspid valve closure.
Atrial venous filling. Occurs at the same time as ventricular contraction.

157
Q

JVP. Large a wave suggest? Cannon a wave suggest? Absent a wave?

A

Large a wave:
tricuspid stenosis
Right heart failure
Pulmonary hypertension

Cannon a wave:
Atrial flutter
Premature atrial rhythm (or tachycardia)
third degree heart block

Absent a wave:
AF

158
Q

What is Kussmaul’s sign?

A 
JVP rises with inspiration, drops with expiration.
Due to: 
Pericardial effusion
Constrictive pericarditis
Pericardial tamponade
159
Q

Sign of RVH on CXR?

A

LV Apex is tipped upwards

Prominent ventricle on left side on CXR

160
Q

Most specific sign of HOCM on echo is?

A

A ratio of septal to posterior wall thickness of greater than 1.3:1.0

161
Q

Criteria for pre-ecclampsia?

A

BP > 140 and proteinuria at 20 weeks of pregnancy

162
Q

Most common complication of cardiac catherisation?

A

Arterial false aneurysm

163
Q

Smoking lowers BP. T/F

A

False.
Reducing EtOH lowers BP.

Lower BP pressure values have been observed after chronic smoking cessation.
However, HT smokers are more likely to develop malignant or renal HT.

164
Q

Drinking EtOH doubles your risk of HT. T/F

A

True

165
Q

What is the Tx for WPW?

A

Amiodarone (if in doubt and concerned of VT)
Flecanide
Cardiovert in unstable

DO NOT use BB or Verapmil as block AV and make conduction go through the accessory pathway.

166
Q

Describe the sounds of Korotkoff in BP measurement?

A

ICuff is inflated above the patien’t SBP and blood flow completely occluded therefore no sounds

Pressure dropped to equal that of patinet’s SBP, 1st sound heard

AS the pressure drops, thumping sounds can be heard as long as pressure in cuff is between systolic and diastolic pressures.

When the pressure falls below diastolic blood, no sounds heard

167
Q

Most common AE of Clopidogel?

A

Rash 6^
GI bleeding 2%
Neutropenia 1 in 2000

168
Q

What Wellen’s syndrome? Risk associated? Tx?

A

ECG manifestation of critical LAD coronary artery stenosis in pts with unstable angina

ECG:
Biphasic or deeply inverted T waves in V1-4 highly specific for a proximal LAD occlusion
Pts may be asymptomatic with minimal elevation of cardiac enzymes.

High risk for anterior wall MI within the next 2-3 weeks.

Tx:
PCI within 48 hrs
Medical Mx ineffective

169
Q

What cardiac mumur is Noonan’s syndrome associated with?

A

Pulmonary stenosis

170
Q 
Takotsubo:
Presentation
Ix
Mx
Prognosis
A

Presentation:
Chest pain
Dyspnoea

Ix:
Anormal ECG (STE, SDD, TWI)
Echo- apical ballooning
Coronaries ok
LV gram apical ballooning
Trops elevated

Mx:
HF Tx
BB

Prognosis:
Majority recover however not benign
Small risk of cardiogenic shock, death.

171
Q

What is the MOA of proprotein convertase subtilisin-kexin type 9 inhibitors (PCSK-9).
Indication?

A

A fully humanised monoclonal antibody that acts by inactivation of PCSK-9 resulting in decreased LDL receptor degradation and increasing the recirculation of the LDL receptor to the surface of hepatocytes and lowers LDL cholesterol.

Indication:
Hypercholesterolaemia

172
Q

Describe an austin flint murmur?

A

Occurs in AR with Austin flint murmur

Mid diastolic murmur to presystolic

Caused by vibrations in the mitral valve leaflets esp anterior leaflet oscillating between the AR jet and the diastolic blood flow from the LA.

Similar to MS murmur = diastolic murmur with opening snap and prominent S1

173
Q

What are the clinical features of constrictive pericarditis?

A 
Raised JVP with Kussmaul's sign
Pulses paradoxus is uncommon (more with tamponade)
Ascites and peripheral oedema
Prominent X and Y descents on JVP
Tamponade has absent y descent
174
Q

What are the causes of constrictive pericarditis?

A 
Idiopathic
Chronic pericarditis
Tb
Neoplastic
Post mediastinal irradiation
CTD
Post cardiac Sx
175
Q

What is the pathophys of AF?

A

Atrial ectopic beats arising from the muscle sleeve of the pulmonary veins.

Pulmonary vein-LA junction and an enlarged LA harbouring fibrosis and inflammation serve as a substrate for sustaining AF.

AF itself leads to elctrophyisological remodelling -> shortening refractory period -> increased risk of FA

176
Q

Arrhythmogenic Right ventricular cardiomyopathy/dysplasia.
What
Presentation
ECG

A

Characterised by a disease of the desmosome that leads to fibrofatty infiltration of the myocardium

Presentation:
heralded by a syncopal episode secondary to monomorphic ventricular tachycardia originating from the RV

ECG:
T wave inversions in leads V1-3 with an epsilon wave (high freq signal at end of QRS)
T wave inversions V2-3
Prolonged QRS V1-3
RBBB - complete or incomplete

Echo: moderate RV dysfunction and enlargement
Continuous ambulatory demonstrating VT or >500 PVCs in a 24 hr period
Cardiac MRI: dilatation and akinesia of RV outflow tract

Tx:
BB
Class III antiarrhythics - K channel blockers
ICD if syncope
Intracardiac ablation if multiple shocks
177
Q

Brugada syndrome:
Pathophys
ECG
Tx

A

AD condition due to Na channel defect.
More common in Asian males

ECG:
RRR with >2mm ST elevation (tomb stone)
If presents with a type 2 picture, try and bring out type 1 with flecainide challenge.
If positive then genetic testing for pt and family

Tx:
BB
ICD if hx of SCD, syncope or VT while taking BB
AVOID drugs that prolong QT interval
- Sotalol, haloperidol, erythromycin
Tx for reccurent ICD discharges?
- Quinidine, class 1 anti-arrhythmic
178
Q

Pt with mechanical aortic and mitral valve on warfarin 3 mg. Presents at 8 weeks gestation. Advise her to?

What are the Tx options for the 1st, 2nd and 3rd trimester?

What is the delivery plan?

A

Continue warfarin.
Warfarin has lowest risk of thrombosis.

1st semester:
If low dose warfarin 5 mg, LMWH with anti-Xa monitoring or
IV UFH with APTT monitoring.

Warfarin is recommended in the 2nd and 3rd trimester.

Delivery plan:
Cease warfarin at 35 weeks and admit for IVUF

179
Q

What is the risk of warfarin embryopathy in the 1st, 2nd and 3rd trimester?

A

Risk of warfarin embryopathy in 1st trimester

- warfarin 5 mg = 8%

180
Q

What are the indications for emergency surgery in patients with left sided native valve Infective endocarditis?

A

Heart failure:
- aortic or mitral valve IE with severe acute regurg or obstruction causing refractory pulmonary oedema or cardiogenic shock (emergency)
Aortic ot mitral vlave IE with fistula into a cradiac chamber or pericardium causing refractory pulmonary oedema or shock (emergency)

Uncontrolled infection:
Infection caused by fungi or MDR organism e.g. P. aeuruginosa and other gram -ve bacilli (urgent)
Persistent fever and positive BC for >5-7d (Urgent)

Prevention of embolism:
Aortic or mitral valve IE with vegetation 15 mm. Sx may be performed in a procedure preserving the native valve is feasible.

181
Q

Pt has had out of hospital arrest. 1 shcok and 2 doses of adrenaline given. Further round of CPR and rhythm shows asystole. Next step?

A

Adrenaline 1 mg as nonshockable rhythm

If shockable, amiodarone 300 mg after 3rd shock

182
Q

IHD. How is Fractional flow reserve performed? Cut off for ischaemia?

A

A physiological index of blood flow reduction caused by coronary stenosis.
Calculated by measuring the pressure gradient across that stenosis during reactive hyperaemia.
Values of 0.75 = ischaemia

183
Q

CRT therapy in a pt with HF and narrow QRS complex. What will happen?

A

CRT will increase mortality. No indicated in HF narrow QRS complex.

184
Q

Ivabradine:
MOA
Indications
AE

A

Ivabradine inhibits a If channels regulating the interval between depolarisations of the sinoatrial (SA) node. It reduces heart rate (by about 10 beats/minute) which in turn lowers cardiac workload and myocardial oxygen demand

Indications:
Stable angina with HR > 70 bpm and SR
Chronic HF with HR > 77 bpm and SR as an adjunct to BB
Be careful with cyp inhibitors, prolong clearance of ivabradine.
Avoid with CCB.

AE:
Visual disturbance
- goes away
- advise pt to stop driving however continue ivabradine
Bradycardia
- reduce dose
185
Q

Heart failure Mx?

A 
1st line - ACEI/ARB (candesartan)
BB 1st line with ACEI/ARB. Evidence for:
- Bisoprolol
- Carvedilol
- Metoprolol XL/CR
- Nebivolol
Add diuretic - spironolactone or eplerenone

Above drugs reduced mortality, increased EF, reduced hospitalisation, improved symptoms.

186
Q

In the Mx of refractory heart failure i.e. optimal medications and unable to tolerate nitrates due to hypotension. Next step?

A

Doubutamine can be considered.

May increase mortality.

187
Q

Levosimendan.
MOA
Indication

A

sensitises cardiac myofilaments to calcium, producing an inotropic effect; vasodilator

Indication:
Acutely decompensated severe chronic heart failure
Not marketed in Australia but available through SAS.

188
Q

Dobutamine.
MOA
Indication
AE

A

Intotropic agent, a sympathomimetics.
Sympathomimetics partially or completely mimic the agonistic actions of noradrenaline or adrenaline on the alpha and/or beta adrenoreceptors.

Indication:
Inotropic support in acute heart failure, cardiogenic and septic shock

AE:
tachycardia, excessive increase in BP, ventricular ectopic activity

189
Q

Which parameter best predicts a benefit from cardiac resynchronisation therapy?

A

QRS> 150
- strongest evidence for CRT
Can still perform CRT without a LBBB if QRS > 150
Other

190
Q

Which drugs prolong QT?

A

Abx:
macrolides
moxiflox

Antifungals:
Fluconazole
Ketoconazole

Antivirals:
Nelfinavir

Antimalarials:
Chrloroquine
mefloquine

Anaesthetics:
Halothane

Antiarrhythmics:
Amiodarone
Sotalol
Disopyramide
Procainamide
Quinidine

Antidepressants:
TCA
Dothiepin
Doxepin

Antipsychotics:
Risperidone
Fluphenazine
Haloperidol
Clozapine
Ziprasidone
Droperidol
Pimozidole

Antihistamines:
Terfenadine
Astemizole

Others:
Cisapride

191
Q

What is the preferred method: on pump vs. off pump CABG?

A

On pump, traditional method.

192
Q

Most likely complication post stenting of coronary artery wit drug eluting stent?

A

Coronary artery narrowing at another site.
DES (sirolimus or pacitaxel)
- less early stent thrombosis and reduction in the rate of repeat revascularsiation
- increased rate of very late stent thrombsois cw BMS
- risk of death and MI were similar to BMS

Highest risk of stent thrombosis in the first 30 days.

193
Q

Primary PCI is done only for STEMI. T/F

A

True.

In NSTEMI can perform early stent to LAD.

194
Q

Aspirin, clopidogrel and warfarin is the preferred Tx in apt with a drug eluting stent, AF and presents with a STEMI. T/F

A

True.

If bleeding risk high, reduce therapy to 1 month.
If not high, then minimum of 6 months of triple therapy.

195
Q

Which valve defect is most commonly associated with IE?

A

Mitral valve prolapse

196
Q

Indication for a dobutamine stress echocardiography?

A

If pt is unable to exercise.
Mimics the effects of exercise.

Determines the degree of known heart valve disease.
E.g. In Aortic stenosis, to determine if CO and Aortic valve gradient increases in response to dobutamine..

197
Q

What is the best indication for CABG over PCI in multi vessel disease?

A

Diabetets

Studies showed:
Increased recurrent angina and repeat revascularisation with PCI
Increased risk of stroke with CABG

198
Q

Stroke and fever = … until proven otherwise

A

Endocarditis

199
Q

Duke Criteria for Dx of IE.

A

2 major OR
1 major and 3 minor OR
5 minor

Major:

  1. Micro
    - typical bugs in 2 bottles
    - persistently +ve BC with unusual organisms
  2. Endocardial involvement
    - echo: oscillating mass, abscess, new partial dehiscence of prosthetic valve
  3. Positive serology or culture ofr C. burnetti

Minor:

  1. Predisposition e.g. heart condition or IVDU
  2. fever > 38
  3. Vascular phenomena e.g. arterial embolism, septic pulmonary infarct, janeway lesion, mycotic aneurysm, intracranial haemorrhage
  4. Immunological phenomena e.g. glomerulonephritis, oslers nodes, roth spots
  5. Suggestive microbiology
200
Q

Infective endocarditits: Empirical Tx

Native valve vs. prosthetic valve and pacemaker lead

A

Native valve:
Gentamicin + Benpen + fluclox

If hypersensitivity to penicillins use Gent + Van + Cefalotin or Cephazolin
If immediate hypersensitivity ti penicillins use Gent + Vanc

Prosthetic valve:
Gent + Fluclox + Vanc

If hypersensitive to penicillins,
Gent + Vanc + Cefalotin or Cephazolin
If immediate hypersensitivity,
Gent + Van

201
Q

Infective endocarditis: Empiric Tx for suspected MRSA

A

Gent + Fluclox + Vanc

202
Q

Respiratory tract procedures in pts with cardiac condition requiring endocarditis prophylaxis?

A
  1. Invasive ear/nose/throat or resp tract procedure to treat an established infection e.g. drainage of abscess
    - abx to viridans group strep (bepen + gent) and staph aureus (fluclox)
  2. Tonsillectomy and/or adenoidectomy
    - amoxicillin/ampicillin
    - cephalex or cephazolin if hypersensitivity
    - clindamycin if immediate hypersensitivity

Abx delivered before Sx

203
Q

genitourinary and GIT procedures in pts with cardiac condition requiring endocarditis prophylaxis?

A
  1. Suspected or confirmed GU or intra-abdominal infection regardless of whether a procedure is involved
  2. GU or GIT procedure where surgical antibiotic proph is routinely indicated

Abx therapy should be directed at enterococci

  • amoxy/ampi
  • vanc or teicoplanin if hypersensitive

Abx before procedure

204
Q

Dental procedures in pts with cardiac condition requiring endocarditis prophylaxis?

A
  1. Extraction
  2. Periodontal procedures involving Sx, subgingival scaling and root planning
  3. replanting avulsed teeth
  4. Other Sx procedure e.g. apicoectomy

Abx

  • amoxy/amp
  • cephalexin or cephazolin if hypersensitive (T-cell mediated)
  • clindamycin if immediate hypersensitivity (IgE)
205
Q

Which cardiac conditions require IE prophylaxis?

A
  1. Prosthetic cardiac valve or prothetic material used for cardiac valve repair
  2. Previous IE
  3. Congenital HD only if it involves:
    - unrepaired cyanotic defects, including palliative shunts and conuits
    - completely repaired defects with prosthetic material or devices, whether placed by Sx or catheter intervention, during the first 6 months after the procedure.
    - repaired defects with residual defects at or adjacent to the site of a prothestic patch or device
  4. RHD in high risk pts
206
Q

Mx of culture negative endocarditis.

Ix and choice of abx?

A 
Test for unusual pathogens 
- fastidious gram +ve cocci
Bartonella species
Coxiella burnetii (q fever)
Tropheryma whipplei (Whipple disease)
Brucella species
Fungi
legionella

Can perform 16s ribosomal RNA sequencing of valve tissue to provide a specific Dx if pt is requiring cardiac Sx.

If pathogen is not identified, treat for 4-6 weeks
- benpen + gent as for enterococcal endocarditis
Q fever requires a longer course
Bartonella - doxy + gent or rifam ( azithro is for non-endocarditis Tx)

207
Q

Tx of IE caused by HACEK (oral gram -ve species) group?

A 
H. parainfluenza
Aggregatibacter sp
Cardiobacterium sp
Eikenella corrodens
Kingella sp

HACEK group are fastidious and may produce betalactamase enzymes.

Ceftriaxone or
Cefotaxime

208
Q

Measurement of what factor most reliably differentiates between noncardiogenic and cardiogenic pulmonary oedema?

A

Left ventricular end diastolic volume

209
Q

Exercise stress test. Goals expected to reach for following parameters:
Maxiumum HR
Systolic BP

A

Maximum HR 80% age predicted = good result
(measured by Patient’s age - 220).

Systolic BP - increase by at keast 10 mmHg

Diastolic BP - can increase or decrease by 10 mmHg.

210
Q

What are the physiological changes with exercise?

A

Oxygen extraction increases by 3 fold.
Peripheral resistance decreases
SBP and HR increase
Modest increase i PAP, PCWP and Right atrial pressure (these are not limiting determinant of peak exercise capacity in healthy individuals)

211
Q

Ejection click associated with?

A

Ear;y systolic sounds
Stenotic aortic of pulmonary valve
Dilated aorta or pulmonary artery

212
Q

Which lowers BP, alcohol or smoking cessation?

A

Alcohol cessation

213
Q

How can you differentiate a cardiac tamponade from constrictive pericarditis?

A

Cardiac tamponade has ABSENT y descent (opening of tricuspid valve)

214
Q

Cardiac defect. Which has the greatest risk of cardiac complication during pregnancy?

A

Eissenmenger syndrome

- R-L shunt

215
Q

What medication is recommended pre op to reduce risk of peri-op cardiac event in pt with T2DM and obesity?

A

BB e.g. metop

216
Q

What is the annual risk of stroke in pts with untreated AF?

A

5%

217
Q

Pt with angina on exertion. What will angioplasty and stenting improve?

A

Improve angina symptoms.

218
Q

How can you distinguish between familial combined hyperlipidaemia and familial triglyceridaemia?

A

Measure apoliprotein B level which is elevated in
familial combined hyperlipidaemia.

familial combined hyperlipidaemia

  • defect in overproduction of apoliprotein and LDL -> elevated cholesterol and triglycerides
  • associated with premature CVD

familial triglyceridaemia

  • not associated with CVS
  • isolated high triglycerides
219
Q

Echo findings of severe AR for Sx?

A

Asymptomatic:
LVEF 70 mm
LVES diameter > 50 mm (or >25 mm/m2 BSA)

Symptomatic:
Sx

Enlargement of ascending aorta:
Sx

220
Q

Mx:
SVT (HD stable narrow complex tachycardia including AVNRT)?

Ventricular tachycardia (monomorphic VT)

A 
SVT:
Vagal manoeuvres PLUS
IV adenosine 
If no improvement, 2nd line
-BB, ND CCB

Ventricular tachycardia (monomorphic VT):
IV amiodarone bolus followed by infusion.
Other anti-arrhythmics are:
Procainamide
Lidocaine

221
Q

Standard dose Adenosine is CI in?

A

2nd or 3rd degree HB
SSS without a pacemaker
Heart transplant

Use low dose

222
Q

AF Mx:

Tx in symptomatic vs. asymptomatic

A

symptomatic:
Cardiovert after TOE

Asymptomatic
Medical Tx with BB.
Can add dig if not well controlled (esp if pt has HF, is hyptoensive). Can’t increase BB as hypotensive and CCB will exacerbate HF.

223
Q

What do the following suggest?
SBP difference of at least 15 mm Hg between the L and R arm.

Pulses paradoxus

Tricuspid valve insufficiency

Pulses alterans

Radiofemoral pulse delay

A

SBP difference of at least 15 mm Hg between the L and R arm.
- coronary subclaian steal syndrome (veterbrobasilar insufficiency and anterior perfusion defect)

Pulses paradoxus

  • tamponade
  • decrease in SBP on inspiration

Tricuspid valve insufficiency
- large V wave

Pulses alterans

  • severe LV systolic dysfunction
  • a beat to beat variation

Radiofemoral pulse delay
- aortic co-artation

224
Q

Examples of P2Y12 inhibitors?

A

Clopidogrel
prasugrul
- CI in stroke due to bleeding
- avoid in pts >75y, previous stroke or TIA and weight

225
Q

Examples of Glycoprotein IIb/IIIa inhibitors?

Indications?

A

Tirofiban
Eptifibatide
Abxicimab (made from Fab fragments of Ig)

Indication:
reserved for pts who have undergone PCI

226
Q

Indications for ICD post MI vs. post PCI or CABG?

A

Post MI:

If ongoing LVEF

227
Q

Test to order if you suspect CAD in a pt with an uninterpretable ECG?

A

Myocardial perfusion scan (aka exercise nuclear test)

228
Q

Doppler US is most useful for the Dx of?

A

To determine flow velocity within a structure, in this case the heart or great vessels. Thus, it is most useful for determining abnormal flow or flow limitation. Specifically, it is useful in defining valvular regurgitation or stenosis, cardiac output when combined with the cross-sectional area, and diastolic filling of the ventricle. Heart failure with preserved ejection fraction is associated with impaired left ventricle relaxation in early diastole and subsequently there is reduced early transmitral flow compared to normal individuals.

2D echo is better fro pericardial effusion, cardiac mass and LVEF calculation.

229
Q

Splitting of second heart sound. Causes for:
Reversed splitting S2
Wide splitting S2
Fixed splitting

A

Normal physiology is P2 follows A2. Splitting increases with inspiration.

Reversed (paradoxical) splitting S2 (P2 precedes A2 during expiration due to delay of A2)
- AS
-HOCM
LBBB
R ventriucular pacing

Wide splitting S2

  • accentuation of physiological pattern
  • delayed pulmonic valve closure (RBBB, pul stenosis, pul HTN)
  • early AV closure (severe mitral regurg)

Fixed splitting

  • ASD
  • No respiration variation
  • Asymptomatic until 3rd/4th decade
  • may lead to pul HTN and eissenmengers
230
Q

Where are the cardiac: baroreceptors

A

Barorceptors
Aortic arch:
-transmits via vagus nerve to solitary nucelus of the medulla
- responds to increase and decrease in BP

Carotid bodies:

  • tranmits vis glossopharyngeal nerve to soliatry nucleu sof the medulla
  • responds to increase and decrease in BP
231
Q

Where are the cardiac: chemoreceptor

A

Peripheral in carotid bodies and arotic arch

- responds to decrease PO2

MK (28 decks)

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