Cardiology Flashcards

1
Q

Why is radial access superior to femoral access for PCI?

A

all cause mortalitiy
MI
Stroke
non-CABG related bleeding

NO DATA on contrast induced nephropathy

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2
Q

Jugular venous pressures

A

a = atrial contraction
c = closure of the tricuspid valve
x-decent: fall in atrial pressure during ventricular systole
v = passive filling of atrium
large v in tricuspid regurgitation
y-decent: opening of the tricuspid valve

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3
Q

Contraindications for balloon valvulotomy for MS

A

Mitral valve area >1.5cm2
Left atrial thrombus
Mod to severe MR
Severe or bicommissural calcification
Absence of commisural fusion
Severe concomitant AV disease or severe combined TS or TR
Concomitant CAD requiring bypass surgery

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4
Q

Murmurs and respiration

A

rIght is louder with inspiration

lEft is louder with Expiration

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5
Q

CABG vs PCI

A

patients with left main stem disease and low-intermediate anatomic complexity PCI with 2nd gen DES is non-inferior to CABG with respect to death, stroke or MI at 3 years

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6
Q

GRACE score

A

risk with NSTEMI
>140 is high risk and would benefit from early intervention

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7
Q

STEMI and early PCI

A

associated with reduction in death, reinfarction, recurrent ischaemia, CHF, or cardiogenic shock at 30days

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8
Q

features of complete heart block

A

syncope
heart failure
regular bradycardia
wide pulse pressure
cannon wave in neck
variable intensity of S1

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9
Q

Exam finding in Mitral stenosis

A
  • reduced arterial pulse volume
  • prominent ‘a’ wave in JVP, absent in AF
  • prominent ‘v’ wave secondary to TR
  • right ventricular heave
  • palpable S2
  • loud S1
  • late diastolic in mild MS, becomes early in severe disease
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10
Q

Exam finding in Mitral stenosis

A
  • reduced arterial pulse volume
  • prominent ‘a’ wave in JVP, absent in AF
  • prominent ‘v’ wave secondary to TR
  • right ventricular heave
  • palpable S2
  • loud S1
  • late diastolic in mild MS, becomes early in severe disease

SEVERE:
- mitral facies
- prominent V
- RV lift
- early opening snap following S2
- loud pulm component of S2

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11
Q

ECG features of pericardial tamponade

A
  • low voltage
  • electrical alternans
  • PR segment depression
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12
Q

Posterior infarcts usually accompany which STEMI

A

Inferior/Lateral
Isolated posterior infarct is uncommon

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13
Q

Indications for PPM

PPM = permanent pacemaker

A
  1. Symptomatic sinus node dysfunction
  2. Acquired AV blocks in adults - Mobitz Type 2 or CHB
  3. Chronic bifascicular block: Mobitz Type 2 or intermittent CHB or alternating BBB
  4. Persistent and symptomatic 2nd or 3rd degree AV block after STEMI
  5. Symptomatic hypersensitive carotid sinus syndrome and neurocardiogenic syncope
  6. Persistent inappropriate or symptomatic bradycarida
  7. Sustained pause dependent VT with or without QT prolongation
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14
Q

Antiarrhythmic to avoid in Torsades

Class

A

1A: Quinidine, procainamide, disopyramide
1c: Flecainide
3: Sotalol, Amiodarone

Class I - Sodium-channel blockers.
Class II - Beta-blockers.
Class III - Potassium-channel blockers.
Class IV - Calcium-channel blockers.
Miscellaneous - adenosine. - electrolyte supplement (magnesium and potassium salts) - digitalis compounds (cardiac glycosides)

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15
Q

Which drugs increase digoxin level?

A
  1. Clarithromycin, erythromycin, azole
  2. Amiodarone, Verapamil, quinidine
  3. Cyclosporin

  1. inhibit P-glycoprotein in the kidney
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16
Q

What is a Hill sign and what is it associated with

A

Popliteal BP exceeds brachial BP by >60mmHg, associated with AR

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17
Q

Digoxin

A

Digoxin – Never first line only after B Blocker and CCB failed
Steady state is achieved after 5x T1/2 – approx. 7-10 days
Serum levels 0.5 - 0.9 ng CHF and 0.5 – 2ng in AF

Digoxin Effect

Reverse tick or sagging ST segment
Also inverted, flattened or biphasics T waves
U waves
Prolonged PR
Short QTc

Digoxin Toxicity

Clinical features include:
Gastrointestinal: Nausea, vomiting and abdominal pain (usually less prominent than with acute toxicity)
Cardiovascular: Bradycardias (1st, 2nd or 3rd degree blocks, AF with a rate <60), increased automaticity (ventricular ectopic beats, bigeminy, SVT with AV block, ventricular tachycardia) and hypotension.
CNS: Lethargy and confusion
Visual: Decreased visual acuity, yellow halos (xanthopsia) – more in chronic toxicity

Mechanism:
Direct
inhibition of Na/K ATPase on the cell surface
-> increased intracellular Na+ and increased extracellular K+
-> increased intracellular Ca2+ due to Na+/Ca2+ antiporter
-> calcium-mediated ionotropy and increased automaticity, as well as negative dromotropy due to decreased intracellular K+
Indirect
increased vagal tone (vagomimetic effect)
Toxicokinetics
Absorption – good oral absorption with oral bioavailability of 80% and peak levels at 6 hours
Distribution – 30% protein bound, Vd 10L/kg (higher in the elderly and obese)
Metabolism – minimal hepatic metabolism
Elimination – 60% renal, t ½ of 30-40 h, longer in renal failure

**Treatment: **
Digoxin immune FAB (Digibind)
Atropine for AV block and lignocaine for tachyarrthmias
Supportive therapy – treat losses, AKI and hyperkalemia

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18
Q

Ivabradine

A

Inhibits funny potassium channels in the AVN
Pt need to be in SR, EF less than 30% HR more than 70
SE: bradycardia, HTN, dizziness, AF and visual disturbances (phosphenes = flashes of light), assoc with TdP when taken with other QT prolonging drugs.

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19
Q

Frusemide

A

Ascending LoH
NKCC2
Pharmakokinetics
Onset of action – 30-60 mins
Bioavailibility – 40-70%
Elimination T1/2 – 2 hours
Excretion – renal 66% biliary 33% (check)
Metabolism – liver 10% (glucoronidation) and kidney

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20
Q

Perhexillene is metabolised by CYP2D6

A

Perhexiline is a coronary vasodilator used especially for angina of effort. It may cause neuropathy and hepatitis.

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21
Q

U-wave

A

Normal: <25% of Twave
Can appear when HR <65
Prominent U wave is seen in bradycardia and severe hypoklaemia

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22
Q

Diuretic resistance?

A

Delayed absorption of the diuretic
Reduced secretion of the diuretic into the tubular lumen
Compensatory retention of sodium after the effective period of the diuretic.
Hypertrophy and hyperplasia of epithelial cells of the distal convoluted tubule. (distal to the ascending L-oH)

23
Q

Bare metal stent and minor GI bleed on DAPT

A

After a bare metal stent, dual antiplatelet therapy (DAPT) needs to be continued for minimum of 30 days. Without antiplatelet therapy during this period, the incidence of in-stent thrombosis and death can be as high as 86%. Therefore all attempts should be made to continue DAPT if possible.
In non- life threatening GI bleeding, concurrent anti-ulcer treatment (PPI and endoscopic management) should be performed alongside dual anti-platelet therapy. This patient is considered non life threatening because he is haemodynamically stable and not requiring transfusion.
If the bleed is life threatening, stopping the aspirin initially and then clopidogrel can be considered for a duration of 48 hours.

24
Q

Aortic dissecton and BP/HR control

A

Aim SBP 100-120 and HR <60 BPM. Intravenous beta blockers (eg, propranolol, labetalol) are typically used as initial anti-impulse therapy. Blood pressure should be maintained at as low a level in this range as can be achieved without compromising mentation or urine output. Intravenous sodium nitroprusside can be added if the systolic blood pressure remains above 100 mmHg. Nitroprusside should not be used without beta blockade, since vasodilation induces reflex activation of the sympathetic nervous system, leading to enhanced ventricular contraction and aortic shear stress. Direct vasodilators, such as hydralazine, should be avoided since they increase aortic wall shear stress.

25
Q

CREST and beta blockers

A

can worsen raynauds

26
Q

Tunrer’s and associated CV abnormalities

A

Elongated transverse aortic arch – 40-50%
Bicuspid aortic valve – 15-30% (although this is actually the risk of aortic valve abnormalities in total which is mainly Bicuspid aortic valve)
Coarctation of Aorta – up to 17%
Ventricular Septal Defect 1-4%
Atrial Septal Defect 1-2%

27
Q

Indication for surgery in ASD

A

This lady has an atrial septal defect. Indications for surgery include presence of symptoms (particularly orthodexia platypnoea), evidence of RV failure with a Qp/Qs>1.5/1, the presence of a paradoxical embolism in a patient less than 60 years old with other causes of stroke being excluded.
The presence of severe pulmonary hypertension and/or Eisenmenger syndrome contraindicates surgery as at this point it is too late.

28
Q

Pt presenting with acute SOB and you find severe AR (no dissection - which medication to use whilst awaiting surgery and which to avoid?

A

Nitroprusside or dobutamine - to allow foward flow
Avoid beta blocker as it may take way compensatory tachycardia –> hypotension

29
Q

PCSK9 deficiency: good or bad? why?

A

Good
results in less LDL-R breakdown, thus more LDL-R on surface –> reduce circulating LDL

30
Q

AAA

A
  • smoking cessation represents the single most effective nonsurgical intervention to reduce the risk of aneurysm-related complications and/or death.
31
Q

ASD: primum

A

Both ostium primum and secondum are associated with RBBB, with primum having left axis deviation typically where as secondum is associated with right axis deviation. Ostium primum defects tend to occur low down in the AV septum and therefore can affect the function of the anterior leaflet of the mitral valve causing mitral regurgitation

32
Q

Limitations of stress ECHO

A
  • Limitations include false positives due to a hypertensive response during exercise
  • false negatives in patients with single vessel disease
  • the potential of rapid resolution of ischaemia prior to image acquisition post exercise.
33
Q

BNP and certain people/conditions

A

Natriuretic peptide levels are elevated in some patients with non-heart failure conditions such as coronary heart disease, valvular heart disease, pulmonary hypertension, and sepsis. Obese patients tend to have lower plasma BNP and NT-proBNP concentrations than nonobese patients. The other options listed above may elevate BNP in the absence of heart failure.

34
Q

ARNI

A

Sacubitril is a pro-drug
NT-ProBNP should be used to monitor rather than BNP

SE:hypotension, hyperkalemia, cough, dizziness, and renal failure. Angioedema is a less frequent adverse effect but may be life threatening.

Should not use in pregnancy

35
Q

Most significant RF for Acute MI

A

LDL level –> Smoking –> psychosocial stressors –> abdominal obesity –> reduced exercise

36
Q

Can you use Prasugrel in medically managed MI?

A

No

37
Q

To stent bystander or not?

A
  1. There is evidence of benefit for revascularisation of non culprit lesions in ST elevation myocardial infarction.
  2. Currently there is insufficient evidence suggesting that staged PCI vs index PCI is inferior/superior therefore the current recommendation is to do the intervention prior to discharge.
  3. The caveat to this is with patients who present with cardiogenic shock, culprit vessel only PCI is preferred over multi vessel PCI due to poorer outcomes with the latter
38
Q

MS

A
  • In nearly all cases, MS is caused by rheumatic involvement of the mitral valve
  • Atrial fibrillation is often the first trigger of symptoms in asymptomatic patients
  • Death from MS is due to progressive right-sided heart failure and/or pulmonary edema in over 60 percent of cases
39
Q

TAVI vs SAVR complications

A

TAVI is generally associated with lower rates of major bleeding and atrial fibrillation,
- but higher rates of short-term aortic valve reintervention, pacemaker requirement, and paravalvular aortic regurgitation compared to SAVR.

40
Q

How to calculate PVR?

unit is WU

A

(PAP-PAWP)/Qp

41
Q

Qp/Qs >1.5 is an indication for what?

A

Suggestive of RV failure –> one of the indication for ASD closure

42
Q

Absolute CI for thrombolysis in STEMI:

A
  • History of ANY intracranial haemorrhage
  • Ischaemic stroke <3MONTHS
  • cerebral vascular malformation or a primary or metastatic intracranial malignancy
  • symptoms suggestive of aortic dissection
  • Significant closed-head or facial trauma within the preceding 3 MONTHS
  • A bleeding diathesis or active bleeding, with the exception of menses; thrombolytic therapy may increase the risk of moderate bleeding, which is offset by the benefits of thrombolysis
43
Q

PFO and RF for recurrent related strokes

A
  • large PFO
  • large/spontaneous R->L shunt
  • greater PFO flap mobility
  • prominent Eustachian valve or Chiari network
  • presence of an ASA (atrial septal aneurysm)
44
Q

How long should you continue OAC post cardioversion for AF?

A

4 weeks, due to risk of AF recurrence

45
Q

How is RVSP calculated?

A

RVSP is calculated using RA + 4V^2 where RA is the right atrial pressure and V is the tricuspid jet velocity. 4+ 9x4 = 40

46
Q

Success of cardioversion for AF is inversely proportional to:

A

Duration of AF and size of LA

47
Q

TB vs amyloid heart disease:

A

how to differentiate between constrictive pericarditis (TB) and restrictive cardiomyopathy (amyloidosis). The most important distinguishing factor is the finding of ventricular interdepenence on ECHO in patients with constrictive pericarditis: In patients with constrictive disease a deep inspiration causes a rise in RV pressure which causes a decrease in the LV pressure.
Low voltage and raised right atrial pressures are present in both. E’ is a measure of relaxation velocity- this is low in restrictive cardiomyopathy and high in constrictive cardiomyopathy

48
Q

When not to use prasugrel?

A

Age >75
Weight <60
Prev. history of stroke

49
Q

Do ionotropes improve mortality in cardiogenic shock secondary to decom. HF?

A

No

50
Q

Stress ECHO

A

non-invasice assessment of pan-cardiac status
- quatification of capacity
- detection of myocardial ischaemia via RWMA’s
- Causes of dyspnoea
- Predictor of outcome: ischaemia, HF

Ideally tredmill, but if you can’t then dobutamine.

51
Q

Iscahemic cascade

A

Metabolic abnormalities (ATP)
Relaxation disturbances
Contractile disturbances
RWMA
ECG abnormalities
Angina symptoms

52
Q

Diastolic stress test

A

Calculate E/e’ at rest and post-exercise

In normal pt - the ratio remains the same (7-8). but if you have diastolic dysfunction then it will increase > 12 post exercise

positive diastolic stress test is associated with poor survival and HF admission

But if you had a ratio >12 at rest, and similar post exercise you had similar outcomes to those with negative study

53
Q

Indication for TOE

A
  1. Endocarditis
    - Staph: ABE - leaves abscess, valve distruction, large vegetation and embolic phenomenon, perforations
    - Strep etc: SBE: indolent. Vegetation without abscess or deep tissue destruction
  2. Cardioversion
    - TOE cardioversion has a stroke risk of 0.6%, which is the same as the conventional method of waiting 4 weeks on anticoagulation
54
Q

LAA closure: watchman

A

for AF