Cardiology

Question 1

Secondary prevention MI

Answer 1

DAPT: aspirin + ticagreolor for 12 months if ACS, choice of ticagrelor or prasugrel if PCI, ACEi, BB, statin

Question 2

Orthostatic hypotension tx

Answer 2

Fludrocortisone and midodrine

Question 3

NSTEMI
: mx, mortality risk.

Answer 3

Aspirin, fondaparinux if no immediate PCI
Mortality risk: GRACE- age, ECG, troponin, renal function, CA, BP, HR
If <3%, ticagrelor. Otherwise, PCI, give prasugrel/ticag

Question 4

Chronic HF Mx

Answer 4

1st line: ACEi/BB(Bisoprolol, Carvedilol)
2nd line Aldosterone antagonist(Spironolactone, Eplerenone)-monitor K as ACEi and spiro cause high K. Also, SGLT2 inhibitors- dapagliflozin, empagliflozin- increase urinary glucose excretion
3rd line: involve a specialist for
-Ivabradine(SR, HR>75+ EF<35%)
-Sacubitril-valsartan( EF <35%+ Symptoms despite ACEi/ARB)
-Digoxin( if coexistent AF)
- Hydralazine+Nitrate( in Afro-Caribbean)
-Cardiac resynchronization therapy( Widened QRS e.g. LBBB)

Question 5

Acute mitral regurgitation cause + presentation

Answer 5

Infero-posterior infarction. Acute hypotension/plmonary oedema. Systolic murmur

Question 6

Aortic stenosis features

Answer 6

Narrow pulse pressure
ejection systolic, louder on expiration

Question 7

NSTEMI identified, aspirin given, 6-month mortality low (<3%)

Answer 7

Conservative management - give ticagrelor

Question 8

Dresslers syndrome

Answer 8

2-6wks post MI, low grade fever, pleuritic CP, pericardial effusion, pericardial rub, raised ESR. Tx NSAIDs, sometimes steroids, pericardiocentesis if significant pericardial effusion to remove the fluid around the heart . (ECG global ST elevation, T wave inversion)

Question 9

Aortic dissection features

Answer 9

Severe tearing CP, unequal BP in arms, false lumen on CT, widened mediastinum on CXR

Question 10

a patient is noted to have a new early-to-mid systolic murmur 10 days after being admitted for a myocardial infarction

Answer 10

Ischaemia of the papillary muscle

Question 11

Left ventricular free rupture presentation

Answer 11

sudden heart failure, raised JVP, pulsus parodoxus, recent MI

Question 12

Mitral stenosis

Answer 12

mid-late diastolic, rumbling, malar flush, P mitrale on ECG -representing left atrial hypertrophy/strain

Question 13

Aortic regurgitation

Answer 13

early diastolic, high pitched, blowing, collapsing pulse, Quinckes sign (nailbed), de mussets (head bobbing)

Question 14

Beck’s triad

Answer 14

hypotension, raised JVP, muffled HS, electrical alternans on ecg: ACUTE CARDIAC TAMPONADE

Question 15

Use of statin for primary prevention of CVD

Answer 15

20mg atorvastatin
-reduce cholesterol production in liver-inhibits HMG CoA reductase
-check lipids 3/12 after
-LFTs after 3/12 and at 12/12
-offered if QRISK>10%/ T1DM for 10 yrs/ CKD pts

Question 16

Statin interaction with which abx

Answer 16

macrolides- clarithromycin, erythromycin

Question 17

pericarditis ix

Answer 17

raised inflammatory markers
ECG: Widespread concave/saddle shaped ST elevation, PR depression (most specific marker)

Question 18

Mx acute pericarditis

Answer 18

Mx: admit if fever>38/high troponin. NSAIDs + colchicine.

Question 19

signs o/e acute HF

Answer 19

Raised respiratory rate
Reduced oxygen saturations
Tachycardia (fast heart rate)
3rd heart sound
Bilateral basal crackles (sounding “wet”) on auscultation of the lungs
Hypotension in severe cases (cardiogenic shock)

Question 20

R HF

Answer 20

1) Raised jugular venous pressure (JVP), caused by a backlog on the right side of the heart, leading to an engorged internal jugular vein in the neck
2) Peripheral oedema of the ankles, legs and sacrum

Question 21

acute LVF presentation

Answer 21

acute SoB (improves sitting up) , frothy sputum, looks unwell, type 1 RF (low O2, normal CO2)

Question 22

causes of high BNP

Answer 22

HF, renal impairment, PE, tachycardia/sepsis, COPD

Question 23

effects of LVF on the lungs

Answer 23

In the lungs LV failure will lead to dilatation of pulmonary vessels, leakage of fluid into the interstitium and the pleural space and finally into the alveoli resulting in pulmonary edema.

Question 24

risk factors for infective endocarditis

Answer 24

Intravenous drug use
Structural heart pathology (see below)
Chronic kidney disease (particularly on dialysis)
Immunocompromised (e.g., cancer, HIV or immunosuppressive medications)
History of infective endocarditis
Structural pathology- valvular heart disease, congenital HD, hypertrophic cardiomyopathy, prosthetic valves, implantable cardiac devices

Question 25

Modified Duke criteria

Answer 25

Major criteria are:

Persistently positive blood cultures (typical bacteria on multiple cultures)
Specific imaging findings (e.g., a vegetation seen on the echocardiogram)

Minor criteria are:

Predisposition (e.g., IV drug use or heart valve pathology)
Fever above 38°C
Vascular phenomena (e.g., splenic infarction, intracranial haemorrhage and Janeway lesions)
Immunological phenomena (e.g., Osler’s nodes, Roth spots and glomerulonephritis)
Microbiological phenomena (e.g., positive cultures not qualifying as a major criterion)

Require 1 major+3 minor, or 5 minor to diagnose IE.

Question 26

duration tx for IE

Answer 26

4/52 native heart valve
6/52 for prosthetic heart valve

Question 27

HOCM management

Answer 27

beta blockers
heart surgery: myectomy, heart transplant
implantable cardioverter defibrillator

Question 28

what to avoid in HOCM

Answer 28

ACEi and nitrates: can worsen the left ventricular outflow tract obstruction
avoid heavy lifting/intense exercise/dehydration

Question 29

When is nitrate tolerance seen

Answer 29

With standard release isosorbide mononitrate: with continuous use- diminished response to nitrates, and so 10-12hr nitrate-free interval recommended. Modified release has been designed to overcome this problem - avoids continuous exposure to nitrates hence minimising risk of developing tolerance.