Cardiology notes Flashcards

1
Q

Give some ddx for chest pain, SOB, heart failure signs?

A
  • ACS (can cause heart block causing acute heart failure and acute pulmonary edema)
  • Aortic stenosis
  • Cardiomyopathies (4 types: HOCM, restrictive cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy)
  • Aortic dissection (medical emergency)
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2
Q

How may pulmonary embolism present with chest pain, SOB, heart failure symptoms?
What CXR features may be seen?

A
  • There is decreased perfusion causing V/Q mismatch
  • Acts on right heart which causes right heart failure –> obstructive shock
  • CXR is mostly normal as hard to find oligemic fields
  • May have Hamptons hump, wedge infarct
  • Dilated pulmonary trunk, enlarged hilum
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3
Q

How may aortic dissection result in acute heart failure and acute pulmonary edema?

A
  • Type A ascending aortic dissection may extend into the aortic root and detach the aortic valve leaflets causing aortic regurgitation (severe)
  • Can extend into the main coronary arteries (RCA affected more commonly –> presents with ST elevation in inferior leads)
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4
Q

What symptoms of aortic stenosis are relevant to the patients prognosis?

A
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5
Q

What portion of the heart is affected in Takotsubo cardiomyopathy?

A

Takotsubo = octopus in japanese
* Mid and apical contraction impaired
* Basal has normal contraction

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6
Q

What are the Ix and why are they done for chest pain, SOB, heart failure symptoms?
What would you expect?

A
  • CBC: anemia (CKD, anemia of chronic disease, post gastrectomy (Fe def anemia patient)), leukocytosis (common triggering factor of exacerbation), reactive thrombocytosis (chronic Fe iron deficiency)
  • LRFT: if CKD will ahve high creatinine, urea and low eGFR
  • Clotting profile (may need anticoagulants if undergoing operation): INR, aPTT
  • Cardiac profile: myoglobin, CKMB, cTnT, cTnI
  • BNP, anti pro BNP (end terminal peptide so more specific. BNP is an atrial neutritic peptide (released when there is atrial stretch –> indicates volume status. When there is increase in BNP means there is high volume overload). Good prognostic indicator if low anti pro BNP level
  • Lactate levels: elevated (as less oxygen and patient in shock so in lactic acidosis)
  • ABG: suspect hypoxia, or CO2 retention (if fatigued) if acidotic more stress on the heart
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7
Q

In patient with chest pain, SOB, heart failure symptoms what are the main 2 types of MI that can occur?
What are the 5 types of MI?

A

In critical illness, it is most likely type 2 MI
Type 2 MI: MI due to oxygen supply. demand mismatch without acute coronary obstruction)
Increased demand causes: thyrotoxicosis, pregnancy, large AVN shunt
Decreased supply: systemic hypoperfusion = common cause (aortic stenosis), coronary artery vasospasm, coronary artery dissection

Type 1: MI due to coronary artery plaque rupture/erosion
Type 2: MI due to imbalance in oxygen supply/demand without evidence of coronary plaque rupture
Type 3: cardiac death with symptoms suggestive of myocardial ischemia (death before biomarkers could be obtained), or mycoardial ischemia detected by autopsy exam
Type 4: MI related to previous coronary interventin. 4a: after PCI, 4b: due to stent/scaffold thrombosis, 4c: due to restenosis (where CKMB is used as cTnI stays elevated for up 10 days)
Type 5: MI associated with CABG

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8
Q

What is the managent of patient with chest pain, SOB and heart failure symptoms with aortic stenosis?

A

ABCDE (always resuscitation and stabilize first)
Decongest the patient first prior to any surgical consideration

Management of acute pulmonary edema: fluid and salt restriction, IV lasix, acetozolamide, check urine sodium (check natriuresis)
Haemodynamically sunstable: inotropes are not ideal but used as bridging therapy as it increases myocardial oxygen demand (use IV dobutamine/dopamine)

Surgical management
Balloon aortic valvuloplasty (briding to definitive surgery) as it will improve the AVA (aortic valve area). However complications include acute aortic regurgitation (cannot control where the crack occurs and valve already impaired in AS). Contraindications to BAV when patient already has baseline AR (has high chance of progressing to severe AR which is much worse than AS)
Valvular replacement (definitive): surgical AVR for low/intermediate surgical risk (young patients) however transcatheter AV implantation (TAVI) originally only for high surgical patietns is being slowly phased into medium and low risk patients.

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9
Q

What is surgical management of MR?

A

Transcatheter repair clip of mitral valve (clip the leaflets together)
TMVR: transapical approach (done by surgery), percutaneous= more common (femoral vein, RA than transeptal puncture –> left atrium). Normally the ASD is well tolerated so iatrogenic ASD is left behind.

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10
Q

What are the indications for closure of ASD?

A

Concept: if it will lead to right heart failure (right atrial/ ventricular dilatation) –> must operate before it progresses to Eisenmenger syndrome

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11
Q

What are the ix that must be done prior to doing TAVI in aortic stenosis?

A
  • CT scan of aorta, iliac and femoral arteries (vascular insuffciency that prevents catheter access)
  • CT angiogram (done with contrast even with renal impairment as it is urgent
  • After doing repair there will be increased blood supply to the kidneys improving renal outcome
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12
Q

What can be causes of anemia in post gastrectomy, CKD, aortic stenosis patient?

A
  • CKD (reduced EPO)
  • Anemia of chronic disease
  • Heyde disease: triad of aortic stenosis, GI angiodysplasia (postulated that AS changes vasculature of the gut), acquired type 2a vWF –> once AS is fixed –> angiodysplasia disappears
  • MAHA (if prosthetic)
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13
Q

What simple test can be done to confirm AR?

A
  • Measure BP –> wide pulse pressure (low diastolic pressure due to blood run off)
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14
Q

What are the surgical options for aortic stenosis?

A

Old school: balloon valvuloplasty (disadv: can crack the calcified valve and cause aortic regurgitation –> can only use small balloon)

TAVI/TAVR preferred (but can only be used for degenerative causes of AS as the calcification causes better adherence of valve to the wall): lasts for 10-15 years (bioprosthetic valve)
Out of pocket payment (300k) but can apply for funding via HA.

If younger patient: can do mechanical heart valve replacement (lasts longer but requires lifelong anticoagulant) –> open heart surgery that is fully funded by HA.

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15
Q

What are the options for TAVR (transcatheter aortic valve replacement)?

A

Self expanding valve: navitor (abott) TAVI system, Evolut Pro
Balloon expanding valve: Sapien XT (Edwards lifesciences)

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16
Q

Who are the younger individuals who may be affected by aortic stenosis?

A
  • Bicuspid aortic valve
  • Rheumatic heart disease (however more commonly affecting mitral valve)
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17
Q

How to manage symptomatic ASD?
What must be given after procedure?

A

Transcatheter closure of atrial septal defect: goes from IVC –> RA –> LA
Fill up balloon in the LA side than pull out through ASD which covers the defect. Then inflate the other balloon in the RA which closes defect.
* Takes 3 months for epitheliazation

Given antiplatelets for 6 months (given SD) to prevent clot formation for turbulent flow

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18
Q

How can ASD present?

A

Mostly will be congenital and will be left to right shunt (due to higher left heart pressure over the right side) –> will present with leg swelling

Rarer: eisenmenger syndrome (as it takes a long time to develop) –> pulmonary hypertension, volume overload causing right to left shunt –> will present with pulmonary edema

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19
Q

What is the management of moderate to severe MR?

A
  • Mitraclip (2nd most common valvular replacement after TAVI)
  • Clips the posterior and anterior leaflet which forms 2 orifices. This is considered repair. (cannot do replacement with current technology as attachment sites is not firm enough)

consideration: more clips inserted (restrict forward flow) which may induce mitral stenosis
Real time USG to measure gradient (try to adust clip)

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20
Q

What can mitraclip be used for?

A
  • Degenerative prolapse
  • Secondary MR/functional MR in the setting of normal mitral leaflet morphology (annulus keeps enlarging, pulling the valves apart) which is normally due to atrial (left atrial dilatation) or ventricular dilatation (cardiomyopathic diseases)
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21
Q

What is the gold standard treatment for moderate/severe MS?
Why is TMVR not feasible (such as in TAVR) with current technology?

A

Balloon valvuloplasty (improves pressure gradient but can cause MR)
If concomitant MS and MR: dont do balloon valvuloplasty (can induce severe MR)

TMVR cannot be done as in TAVR as the annulus in mitral valve is very compliant. Valve cant be held well in comparison to aortic valve which is rigid.

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22
Q

Mx of severe tricuspid regurgitation?

A

Tric valve: transcatheter bicaval valves system

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23
Q

What is the role of ventricular pacing (VC) and ventricular sensing (VS) in pacemaker?

A

Used to monitor how much ventricular control is self regulated vs pacemaker regulated. Will dictate consumption of battery.

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24
Q

Can you have 40 year old presenting with symptoms of ASD?

A

Can be symptomatic from childhood to adulthood –> then due to aging there is degeneration and heart starts to dilate manifesting the symptoms

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25
Q

What are the rare causes of acquired ASD?
What commonly causes VSD in adults?

A

Acquired ASD: endocarditis, MI, iatrogenic ASD (from valve replacement procedures)

If there is acquired septal defect: most common is VSD from MI

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26
Q

Benefits of self expandible valves over balloon expanding valves for TAVR?

A

If calcified valve balloon expanding valve places more stress on the calcification and has higher risk of plaque rupture
Self expandible has lower risk of plaque rupture. It partially blocks the coronary vessels (longer valve): harder to manipulate if there is CAD requiring intervention.

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27
Q

What devices for left atrial appendage occlusion?
What drugs must be used after operation?
What alternative is there and why is it not done?

A
  • Watchman Boston
  • Amulet abott
    After operation: can stop warfarin after 3 months, can stop aspirin after 6 months (unless indicated)
    USG, TEE to decide what shape and configuration to plug the hole.

Anticoagulants has same efficacy as LAAO (but with more side effects)
These methods reduces chance of thromboembolic stroke (removes local effect of producing thrombus) but does not reduce chance of ischemic stroke.

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28
Q

What drug coverage after TAVI needed?

A

DAPT 3 months post TAVI
Than aspirin monotherapy

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29
Q

What is the anticoagulants given for valvular and non valvular AF?

A

AF should be given NOAC 1st line
Other valvular issues with AF can give NOAC

Only medium/severe MS with AF –> requires warfarin. Doing LAAO would not help in patient with severe MS with AF as thrombus formation is from the whole left atrium.

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30
Q

What drugs may be needed for heart failure patient?

A
  • Eplerenone (K+ sparing diuretic): same MOA as spironolactone but less AE but also more expensive
  • Furosemide is an extra (if patient has foot edema)
  • Entresto (ACEI and ARB): newer generation drug
  • Dapagliflozin (heart failure: SGLT2 inhibitor)
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31
Q

What needs to be counselled when using warfarin as an anticoagulant?
What is the target INR?

A
  • Warfarin requires monitoring of INR, diet control (antagonizes vit K (downstream clotting factors) –> requires a stable vit K intake so that INR will not fluctuate due to diet. Dosage changes all the time -> will adjust if INR is too low or high
  • Target INR is 2-3
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32
Q

What anticoagulant for non valvular AF?

A
  • 1st line is NOAC (superior to warfarin: less stroke, less bleeding. But higher risk of GI bleed): rivaroxaban (highest GI bleed risk) –> can take etoxiban
  • 2nd line is warfarn
  • Alternative is left atrial appendage occlusion if non valvular AF (most thrombus formation is here due to stasis of blood). It is non inferior to warfarin. Currently undergoing trial to see if efficacy is comparible to NOAC. If it is in the future LAAO may be 1st line as no associated bleeding risk and decreased risk of ischemic stroke.
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33
Q

What is done for Mx of AF?

A

Rate control for everyone
Rhythm control (improve overall cardiovascular mortality): K channel blockers: amiodarone (cardioversion and maintenance), dronedarone (maintenance)

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34
Q

When is ablation done for AF?
What are the 2 types available?

A
  • Catheter pulmonary vein isolation: indicated in patients wit symptomatic paroxysmal/ persistent/long standing persistent AF who are refractory or intolerant to 1 class I or class 3 antiarrhythmic drugs when a rhythm control strategy is desired.
    Primary trigger for most episodes of AF involves electrical discarhge within 1 or pulmonary veins. Principle goal is to isolate the pulmonary veins so that these discharges do not activate the atrial tissue.
    2 main types of energy source for catheter ablation include RFA and cryoballoon (cryothermal) ablation.
    Most common pulmonary vein isolation is circumferential pulmonary vein isolation.
  • Surgical ablation (open heart surgery): indicated in select patients underoing cardiac surgery for another indication such as valvular replacement or CABG. Aim to create a maze of functional myocardium within the atrium that allows for propogatation of atrial depolarization while reducing the likelihood that the wavefront would promote microentry

Theoretically can do pulmonary vein isolation and ablation at the same time.

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34
Q

Indications for repair of MR?

A

Dilated LV and AF
Impaired systolic dysfunction

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35
Q

What are structural and functional tests for cardiac function?

A

Structural tests
* Coronary CT angiogram (non invasive)
* Coronary angiography (invasive: requires catheterization)

Functional tests
* Thallium scan (huge radiation risk)
* MRI scan (more time consuming)

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36
Q

CAD and angina management?

A
  • B blocker/ CCB for 1st line
  • 2nd line: BB +CCB
  • 3rd line: nitrates, ivabradine
  • PCI for refractory PCI symptoms: in stable angina PCI is not proven to improve mortality

STEMI PCI is free
NSTEMI PCI may require subsidy

36
Q

What is the cholesterol target?
What are the treatment options?
Target level after initiating treatment?

A
  • Cholesterol target: <1.4
  • 1st line is statins: should be at least 50% reduction from baseline
  • 2nd line: ezetimibe (NPC1L1 inhibitor –> binds to enterocytes –> dereases absorption of cholesterol at gut –> decreased in blood stream)
  • 3rd line: PCSK9 inhibitor: evolocumba, alirocumab
  • 4th line: small interfering RNA (inclisiran)
  • 5th line: ACL inhibitors (bempedoic acid)
37
Q

What are ACEI complications?

A
  • Hypotension
  • HyperK (fatal)
  • Angioedema
  • Cough (due to bradycardia)
  • If on ACEI cannot use ARNI (heart failure): neprilysin
38
Q

Patient has syncope during food, 2 reasons?

A
  • Vagal system stimulated during swallowing
  • If full stomach –> splanchnic vasodilation –> blood pooling in stomach –> relative hypotension –> prone to orthostatic hypotension
39
Q

What is 1st line Mx of vasovagal syncope?

A
  • Cross legs, cross arms, lie down, drink water (if pure vasovagal syncoep: drink 3L of water and high salt intake (not advised in older patients)
  • Compressive stockings
  • Metoprolol (B1 blocker: cardiac selective): useful in some (but not clinically shown to be effective
40
Q

If it is tachycardia related cardiomyopathy what is prognosis?
What about alcohol related?

A

If tachycardia controlled than after a few days will have improvement
If alcohol related cardiomyopathy: B1 (thiamine) deficiency –> if quit alcohol and have vit b1 –> will recover

41
Q

What are red flag syncope situations?

A

Below 2 must be pathological
* Excercise induced syncope
* Supine syncope (cannot be orthostatic or vasovagal)
Cardiac symptoms before syncope

42
Q

What is Mx of AF?

A

Will do cardioversion for AF in 1st year (aim for sinus rhythm).

Rate control (ABCD medication: B blocker most effective (metoprolol, B1 selective)
Digoxin preferred drug only in patients with HFrEF (does not have negative inotropic effects)
Rhythm control: amiodarone (class 3 AAC)

If long standing AF: rate control with BB (metoprolol). If ejection fraction <35% than will offer ablation and permanent single chamber ventricular pacemaker insertion.

43
Q

Complications of MI

A
  • Structural: MR, VSD, pericardial effusion / cardiac tamponade
  • Rhythm: bradyarrhythmia (bradycardia, conduction block, BBB), tachyarrhythmia (AF, VT, VF)
  • Heart failure
  • Cardiogenic shock
44
Q

MR caused by AMI mechanism

A
  • Inferior MI
  • Ischemia of papillary muscles
45
Q

post AMI experiences bradyarrhythmia, which part of heart is affected?
Patient experiences SOB after the procedure? What is underlying cause?

A
  • RCA territory i.e. inferior part
  • Left heart failure/cardiogenic shock
46
Q

AMI
What artery commonly blocked? leads?
What other area affected? leads?
AMI how to manage?

A
  • LAD, anterior leads (V1-6)
  • Inferior: lead II, III, aVF
  • PCI
47
Q

After AMI mx what detection and treatment of complications?

A

Arrhythmia
* Bradycardia
AV block: 1st degree and mobitz type 1 2nd degree: conservative. Mobitz type 2 2nd deegree or 3rd degree: pacing

  • Tachycarrhythmia
    PSVT
    Atrial flutter/fib: digoxin, amiodarone

Pump failure
RV dysfunction (consider swan ganz catheter to monitor PCWP
LV dysfunction: vasodilators (esp ACEI) if BP OK
Inotropic agents

Mechanical complications
* VSD, mitral regurgitation
* Observe if stable (repair later), emergency cardiac catheterization and repair if unstable

Pericarditis (dressler syndrome): high dose aspirin, NSAID e.g. indomethacine. Others: colchicine, paracetamol

48
Q

What auscultation in acute MI complications?

A

Signs of AHF.
* Left HF: displaced and thrusting apex beat, S3, basal crepitations
* Right HF: ankle edema, raised JVP, hepatomegaly
* Signs of arrhythmia: pulse rhythm, rate and character
* Signs of mechanical complications: new onset PSM (papillary rupture=MR, septal rupture= VSD). muffled heart sound –> cardiac tamponade (hypotension and tachycardiac)
* Pericardial rub (grating sound of the friction of heart against the pericardium) due to underlying pericarditis

49
Q

How to mx post MI patient long term?

A
  • B blocker: metoprolol (cardiac selective –> helps prevent dilatation of the heart when infarcted)
  • Aspirin
  • ACEI (esp for large anterior MI, impaired LV systolic dysfunction): lisinopril (reduces cardiac remodelling)
  • Angiotensin receptor blocker: captopril
  • Statins

Life style: weight reduction, monitor lipid levels, BP control, BG control

50
Q

Why do 24 hour monitoring in irregular pulse?

A

Paroxysmal AF

51
Q

Mx of AF

A
  • Correct underlying causes: hypoxia, electrolyte disorders, sepsis, thyrotoxicosis
  • Rate control (always): diltiazem
  • Rhythm control: amiodarone. For persistent AF, anticoagulate for 3 weeks before conversion and continue for 4 weeks after
  • Anticoag: UFH with maintenance of aPTT 1.5-2x control or LMWH. Long term anticoag with warfarin with maintenance of PT 2-3x control

Prevention of recurrence: class 1a, 1c, sotaolol, amiodarone or dronedarone

52
Q

Mx of Torsade de pointes?

A

Always correct underlying cause in acquired LQTS e.g. electrolytes (hypoK, hypoCa, hypoMg), stop medications

  • Defibrillation if haemodynamically unstbale
  • IV MgSO4 as 1st line therapy (even if Mg is normal)
  • Transvenous overdrive pacing (induce tachycardia so patient wont have R on T phenemenon)
53
Q

What organ can be affected when using amiodarone?

A

Thyroid: TFT (can cause thyroid storm)

54
Q

What to check for diagnosing DM?

A

Symptomatic: random glucose >11.1
Asymptomatic
OGTT: fasting glucose >7, 2 hour glucose >11.1
HbA1c >6.5%

55
Q

PCI management before and after

A

Before PCI
* Antiischemia: nitrate (C/I if RV involved). B blocker (if no containdications), morphine (best avoided since it reduces intestinal absorption of antiplatelets)
* DAPT initiated: aspirin and ticagrelor (superior to clopidogrel)
* Anticoagulation (no need to continue after PCI): enoxaparin

Post PCI
* Statin therapy (high dose) in statin naive, PCSK 9inhibitor if non statin naive
* BB (reduces cardiac workload, remodelling)
* ACEI (reduces remodelling, indicated for poor LVEF, HF, DM, HT, anterior STEMI)

56
Q

Patient present with chest pain and SOB what needs to be excluded apart from MI? How to differentiate?

A

Aortic dissection: excruciating pain radiating to back, radioradial felay
Tension pneumothorax: deviated trachea, reduces AE, hyperresonance on percission
Pulmonary embolism: history of leg pain

Ix
ECG
CXR: cardiomegaly and pulmonary edema if AFH in IHD, widened mediastinum in aortic dissection, wedge infarction in PE
CTPA, duplex ultrasound leg vein: pulmonary embolism

57
Q

Features of PE in ECG

A
  • Sinus tachycardia (most common)
  • Right ventricular strain pattern: ST depression and T wave inversion in right precordial leads (V1-3, often extending to V4) and inferior leads (II, III, aVF)
  • Right axis deviation
  • RBBB
  • Dominant R wave in V1 (acute RV dilatation)
  • P Pulmonale (right atrial dilatation
  • S1Q3T3 (only in massive PE)
58
Q

Target for lipid control?

A

<1.8mmol/L –> aggressive lipid control in the presence of established CAD or CAD equivalent

59
Q

How would you look out for dressler syndrome?

A
  • Usually occurs 2-3 weeks after MI
  • Symptom: chest pain better sitting up and worse supine
  • PE: pericardial rub
  • ECG: diffuse concave up ST elevation
  • Echocardiogram: pericardial effusion
60
Q

Causes of MI at young age

A
  • HOCM
  • Familial hyperlipidemia (accelerated atherosclerosis)
  • Cocaine (coronary artery spasm)
  • Anomalous origin of coronary arteries
  • Coronary aneurysm (history of Kawaski disease)
  • Hypercoaguability: nephrotic syndrome, APLS, proteinC/protein S deficiency
61
Q

How can AF and hypertension cause HF?

A
  • AF can cause HF due to overlying rapid ventricular rate and in turn cause tachycardia induced cardiomyopathy. It might worsen HF due to irregular stroke volume and reduced LV filling (atrial contraction contributes 20%) in the setting of diastolic HF
  • HT causes increased afterload –> LVH –> diastolic dysfunction
62
Q

Types of HF?
Frank starling Law?

A

Left vs right, HFpEF vs HFrEF, low output vs high output

Increase in myocyte length increases contractility until a certain point which further myocyte stretch reduces contractility
Therefore increases in ventricular volume increases contractility and stroke volume, until a certain point where further increase in volume leads to a reduction in stroke volume.

63
Q

Causes of aortic regurgitation?

A
  • Rheumatic heart disease
  • Congenital: marfans syndrome, congenital bicuspid valve
  • Seronegative arthritis: ankylosing spondylitis, psoriatic arthritis, reactive arthritis, arthritis associated with IBD
  • Syphilis (primary is genital ulcers)
  • Infective endocarditis
64
Q

Indications for implantable cardioverter device in heart failure?

A
  • Poor LVEF despite optical medical tehrapy: in symptomatic HF (Class 2-3) and LVEF <35% despite >3 months of optimal medical therapy, provided they are expected to survive >1 years with good functional status
  • Previous episode of ventricular arrhyhtmia: secondary prevention in HF who have recovered from a ventricular arrhythmia causing haemodynamic instability, who are expected to survive >1 year with good functional status
65
Q

Mechanism of MR post MI?

A
  • Inferior MI can cause papillary muscle dysfunction or even rupture leading to functional MR
  • Post MI heart failure and LV dilatation can also lead to functional MR
66
Q

When is antibiotic prophylaxis indicated for mechanical heart valve?

A
  • Prior to dental procedures
  • Prosthetic cardiac valve/prosthetic valvular repeair
  • Previous IE
  • Congenital heart disease: unrepaired cyanotic CHD, including those with palliative shunts (BT shunt) and conduits.
  • Cardiac transplant recipients (immunocompromised) who develop cardiac valvulopathy
67
Q

Patient on warfarin after CVA, what precautions?

A
  • Seek medical advise if notice GI bleefing (fresh, melena), haematuria (INR may be too high and need adjustment)
  • Drug-drug interaction (inhibiting warfarin breakdown): commonly prescribed drugs by GP include NSAID, antihistamine, antibiotics (macrolide, septrin, flagyl)
  • Drug food interaction: if change to low vit K diet can cause overdose (vit K found in green vegetable). Avoid alcohol, grapefruit, cranberry
68
Q

What are the causes of bradycardia?

A

Drug:
Parasympathomimetics - acetylcholine, acetylcholineesterase inhibitors
Sympatholytics - beta-blockers, methyldopa
Opioids and sedatives
Cimetidine (H2 antagonist)
Digitalis
Non-DHP CCB (diltiazem, verapamil)
Ivabradine
Amiodarone
Lithium
Chemotherapeutic agents - thalidomide, lenalidomide, paclitaxel
Intrinsic Cardiac causes :
Sick sinus syndrome
AV block (e.g. from AMI)

Electrolytes (e.g. HyperK)
Endocrine (e.g. Hypothyroid)
Others - increased ICP, anorexia nervosa, certain infections (e.g. typhoid fever)

69
Q

Can MI cause bradycardia?

A

Yes due to RCA occlusion and therefore ischemia to SA and AVN
Or transient bradycardia due to excessive vagal activity (which calso causes the nausea and diaphoresis)

70
Q

How to manage first presentation of AF?

A

Identify and manage underlying cause (IHD, thyrotoxicosis, valvular heart fdisease)
Stroke prevention: anticoag with NOAC (enoxaparin) vs warfarin (if MS AF/mechanical heart valve)

Rate control (often sufficeint to control symptoms of AF): class 2 AAD: BB, class 4 AAD non DHP CCB (verapamil, diltiazem)
Rhythm control (cardioversion): all patients with new onset AF should have at least 1 attempt at cardioversion to sinus rhythm.
Cardioversion in stable patients with AF >2 days should start oral anticoagulation 3 weeks before cardioversion before cardioversion and continue for 4 weeks after and indefinitely if indicated. For early cardioversion, TEE to rule out left atrial thrombi to allow immedaite cardioversion.
Class 1AAD: flecainide, propafenone. Class 3 AAD: amiodarone
2nd line is catheter ablation (pulmonary vein isolation as most irregular signals originate from here)
Can also consider left atrial appendage occlusion (trial phase: similar efficacy to NOACs)

71
Q

AE of amiodarone?

Hence not used for chronic rhythm control due to irreversible AE

A
  • Pulmonary toxicity: interstitial lung disease, dyspnea, dry cough
  • Thyroid dysfunction (hyper or hypo)
  • Cardiac: long QT syndrome
  • Hepatotoxicity
  • Eyes: vortex keratopathy/corneal microdeposits
  • Derm: photosensitivity, blue grey discoloration
72
Q

What are some causes of syncope?

A
  • Cardiac: mechanical (AS), arrhythmia
  • Neurocardiogenic: vasovagal, carotid hypersensitivity
  • Postural hypotension
73
Q

Types of heart block and cause?

A

1st degree: prolongation of PR interval >200ms
2nd degree: type 1 (progressive prolongation of PR interval culminating in a non conducted P wave), type 2 (intermittent non conducted P wave)
3rd degree: complete AV dissociation with junctional/ventriculara escapes

Etiology
* Degenerative (most common)
* IHD: coduction disturbed in both stable CAD and acute coronary syndrome (RCA infarct with SAN and AVN)
* Cardiomyopathy: HOCM, infiltrative cardiomyopathy
* Myocarditis: ARF, viruses
* Congenital heart disease: neonatal lupus, large primum ASD or large AVSD

Increased risk of death from HF, sudden cardiac death (lethal ventricular arrhythmias: does not happen in SSS)
Asymptomatic patients with type 2 2nd degree AV block and 3rd degree AV block require pacemaker to improve dx

74
Q

In uncontrolled hypertension what PE and Mx to do?

A

history and PE to assess for end organ damage: mental status, palpate bilateral pulses for aortic dissection
Ix to look for end organ damage
* Eyes: fundoscopy (flame shaped hemorrhage, papilledema)
* Brain: CT/MRI brain (stroke)
* Cardiovascular: ECG, cardiac biomarkers (troponin, CKMB), CXR, echocardiography
* Kidney: urine dipstix, urine ACR, microscopy for RBC, WBC and casts (acute hypertensive nephrosclerosis), RFT (AKI)
* Microangiopathic haemolytic anemia: CBC, clotting profile

Labetolol: combined beta and alpha blocker, achieve more rapid lowering of BP
Nitroprusside: both an arterial and venous vasodilator, effective in reducing BP

AE of nitroprusside: cyanide toxicity (palpitation, abd pain, confusion, psychosis, weakness, lactic acidosis

75
Q

Define postural hypotension

A

Sustained drop in systolic BP>20mmHg, diastolic BP>10mmHg within 3 minutes of active standing
Also measure BP at 1 and 5 minutes of standing to detect early and delayed postural hypotension

76
Q

Causes of poorly contorlled hypertension

A
  • A: apnea
  • B: bad kidney (CKD, PKD), bruit (renal artery stenosis)
  • C: coarctation of aorta
  • D: drugs (NSAID, COX2 inhibitor, steroids and immunosuppressants, estrogen)
  • Endocrine (phaeochromocytoma, hyperaldosteronism, cushing syndrome, hyper/hypothyroidism, hyperparathyroidism)
77
Q

AE of antihypertensives

A
  • ACEI: hyperK, angioedema, dry cough
  • BB: bradycardia, postural hypotension, bronchoconstriction
  • CCB: postural hypotension, peripheral edmea
  • Diuretics: postural hypotension, hypoK, hypoNa, hypoMg, hyperuricemia (precipitate gout)
78
Q

How does NSAID cause renal impairment?

A
  • Haemodynamically mediated: inhibits PG production –> afferent arteriole vasoconstriction resulting in reduced GFR thus prerenal AKI and also acute tubular necrosis due to ischemia
  • Immune mediated: acute interstitial nephritis
79
Q

How to dx IE?
Antibiotics?
Cause for kidney failure in IE?

A

Duke criteria:
Persistent bacteremia demonstrates 2 positive blood cultures 12 hours apart from 2 different sites
New murmur/ vegatation on valve
Minor: fever, vascular phenemonon (roth spots etc)

Ampicillin + cloxacillin + gentamicin
Vanco + gentamicin if PCN allergic

Prereneal: septic emboli causing renal infarction, acute HF
Renal
GN: immune complex deposition –> MPGN
ATN: aminoglycosides
AIN: penicillins

80
Q

Cause of post transplant lymphoproliferative disease?

A
  • Due to EBV infected latent B cells which can be from donor or recipient in solid organ transplant, but in HSCT, more likely from donor since the BM graft is depleted of T cell to prevent GVHD
  • After transplant when px is on immunosuppressan,t T cell suppressed so these latent EBV infected B cells can proliferate
  • PTLD can be early, polymorphic, monomorphic
  • Early resembles infectious mononucleosis
  • Polymorphic is when there is evidence of malignancy but not yet B/T/NK cell lymphoma
  • Monomorphic is when there is B/T/NK cell lymphoma
81
Q

What cardiac device used in severe HF?
How to differentiate betwen pacemaker and ICD on CXR?

A

In implantable cardioverter defibrillator a lead is only present in right ventricle. Also has radiodense coil to deliver shock for life threatening arrhythmia.

In heart failure cardiac resynchronization therapy (CRT)/pacing is biventricular to coordinate both the right ventricle and left ventricle contraction –> lead present in both LV and RV. (there is no radiodense coil) Can also be biventricular in RA and RV instead.

82
Q

Apart from statin what other lipid lowering agents?

A

PCSK9 inhibitor (evolocumab): PCSK9 binds to LDL receptors which stops LDL being removed from blood. Therefore by inhibiting –> more LDL removal
Ezetimibe (cholesterol absorption inhibitor)
Resins: increases excretion of bile acids in the jejunum and ileum to increase conversion of cholesterol to bile acids inthe liver. Increased LDL receptors in the liver
Fibrates: enhances lipoprotein lipase activity to increase clearance of VLDL. Increased FA oxidation. Increased plasma HDL.
Niacin: inhibit hormone sensitive lipase in adipose tissue, enhance lipoprotein lipase in adipose tissue.

83
Q

Common flora in oral cavity

A

Related to infective endocarditis
Streptococcus viridans
HACEK group
* Haemophilus aphrophilus
* Actinobacillus
* Cardiobacterium hominis
* Eikenella corrodens
* Kingella kingae

84
Q

Cx of metallic valve

A
  • Paravalvular leak: small central jet of regurgitation is normal in mechanical valve
  • Obstruction from thrombosis or pannus
  • Infective endocarditis, valvular abscess
  • Embolization: highest risk in 1st 90 days
  • Bleeding from anticoagulation
  • Structural failure: rare in metallic heart stent –> more common in bioprosthetic valve

Anticoagulation for mitral valve more important than AVR

85
Q

What drug added on top of statin?

A

Ezetimibe (cholesterol absorption inhibitor): inhibits NPC1L1 at the intestinal brush border (reduction in delivery of cholesterol to the liver)

PCSK9i is not used as combination therapy but to replace statin: PCSK9 is a proprotein convertase which is involved in the degradation of LDL receptors in the liver (causing decreased uptake of LDL by the liver). This antibody reduces the degradation of LDL receptors and increases clearance of LDL cholesterol.

86
Q

Indications for ICD

A
  • secondary prevention of sudden cardiac death in patients with prior sustained ventricular tachycardia and ventricular fibrillation, or resuscitated SCD thought to be due to VT/VF
  • Patients with episodes of spontaneous sustained VT in the presence of heart disease (ischemic, valvular, hypertrophic, dilated or infiltrative cardiomyopathies)
  • Patients on guideline-directed medical therapy who have high risk of SCD (patients with a prior MI and LVEF ≤30 percent, heart failure who also have intraventricular conduction delay > 120ms- Combined ICD and biventricular pacing)
87
Q

Pacemaker indication

A

High-degree heart block such as Morbitz type 2 and complete AV dissociation (complete heart block), sick sinus syndrome

88
Q

What is heard in ASD auscultation?

A
  • Split S2, widened on inspiration (exacerbates right sided murmur as increases venous return)
  • Ejection systolic murmur (flow murmur due to increased blood from LA –> RA –> RV than into pulmonary artery)
89
Q

What basic test to do in AR?

A

BP: wide pulse pressure

Collapsing pulse, quinckes sign, de musset sign

90
Q

What AE and B blockers and mechanism?

A
  • Bradycardia: BB inhibit B1 adrenergic receptors leading to decrease in HR
  • Hypotension: Blocking B1 receptors also has negative inotropic effect decreasing myocardial contraction. These 2 factors decreases cardiac output which can lead to hypotension
  • Decreased PEFR: as inhibits B2 receptors on bronchial smooth muscles causing bronchoconstriction
  • Hypothermia: due to decreased cardiac output, (as well if B2 agonist activity such as in carvediolol causes vasodilation further causing temperature loss)