Questions

Question 1

Anticoagulation post CABG

Question 2

Aortic Stenosis - Severe Criteria

Answer 2

Mean pressure gradient >40 mmHg, a peak aortic velocity >4 m/s, and an aortic valve area (AVA) ≤ 1 cm2

Question 3

MINOCA causes

Answer 3

intrinsic (microvascular spasm, Takotsubo syndrome and coronary embolization) and extrinsic (myocarditis)

Question 4

Loud S1

Answer 4

MV or TV open long -> shuts forcefully

MS
increased HR

Question 5

Fourth heart sound (S4) causes

1. Sounds like
2. Physiology
3. Causes
   a. Left sided
   b. Right sided

Answer 5

Kentucky
Atria contracting against a stiff ventricle ‘decreased ventricular compliance’

Causes of a left-sided S4 include left ventricular hypertrophy or impaired diastolic relaxation (especially infiltrative cardiomyopathies and ischemic heart disease).

Causes of a right-sided S4 include right ventricular hypertrophy, pulmonary hypertension, and pulmonic stenosis.

Question 6

S3

Answer 6

1. Tennesee
2. Rapid ventricular filling
3. Physiologic causes: pregnancy, healthy children, and young adults.
4. Pathologic causes: myocardial infarction, decreased ventricular contractility (increased end-diastolic volume in patients with systolic heart failure) due to any cause (see Heart Failure), or ventricular volume overload (eg, due to regurgitant valvular lesions).

Question 6

AAA surveillance

Answer 6

3.0-3.9 cm - 24 months
4.0-4.5 - 12 months
4.6 - 5.0 6 months
>5.0 3 months

Question 7

When to repair AAA

Answer 7

Men ≥ 5.5 cm, Women ≥5.0 cm

Question 8

Anthracyclines

1. Mechanism of action and how it damages the heart
2. Name 2 anthracyclines

Answer 8

Inhibition of Topoisomerase 2α in cancer cells, and their toxicity is largely through inhibition of Top 2β in cardiac myocytes.
2. Doxorubicin + idarubicin

Question 9

Patient factors for risk of cardiomyopathy

Answer 9

Lifetime cumualtive dose, age less than 18 or 65, female gender, renal failure, radiotherapy ivolving the heart, carbonyl reductase gene polymoprhisms, and carrier status for haemochromatosis

Question 10

Low gradient AS
1. Clinical definition
2. `true aortic stenosis vs pseudoaortic stenosis

Answer 10

1. Valve area <1.0 cm2 with transvalvular pressure gradient less than 30 mmHg.
2. True aortic stenosis - severe stenotic lesion results in an excessive afterload and reduced LVEF. Pseudostenosis - patients have low transvalvular pressure gradient because of combination of moderate AS and low cardiac output.

Question 11

Anticoagulation post TAVI

Answer 11

DAPT for 3-6 months, aspirin life long.

Question 12

CHADSVASC

Answer 12

CHA₂DS₂-VASc Score

2
Risk of ischemic stroke 2.2%

Risk of stroke/TIA/systemic embolism 2.9%

3

Risk of ischemic stroke 3.2%

Risk of stroke/TIA/systemic embolism 4.6%

Question 13

4 acoustic views on TTE

Answer 13

Question 14

Label the parasternal long axis view of the heart

Answer 14

Question 15

Label the parasternal short axis (aortic valve level)

Answer 15

Question 16

Label the parasternal short axis (mitral valve level)

Answer 16

Question 17

What is this view called

Answer 17

Apical 4 chamber

Question 18

What is this view called

Answer 18

Subcostal 4 chamber

Question 19

HCM mutation

Answer 19

cardiac myosin binding proteinC gene are most common, accounting for up to half of the mutations identified. Mutations in the cardiac beta-myosin heavy chain gene are second in frequency, being present in 25 to 40 percent of patients

Question 20

Mitral valve repair indications (MR)

Answer 20

Symptomatic patients with LVEF >30%
Asymptomatic patients with LV dysfunction (LVESD ≥45 mm and/or LVEF ≤60%)
Asymptomatic patients with preserved LV function and new onset of atrial fibrillation or pulmonary hypertension (systolic pulmonary pressure at rest >50 mmHg).
Asymptomatic patients with preserved LV function, high likelihood of durable repair, low surgical risk, and flail leaflet and LVESD ≥40 mm.

Question 21

HOCM ICD Indications

Answer 21

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

Question 22

In-stent thrombosis risk factors

Answer 22

Question 23

HCM Echo findings

Answer 23

HOCM is asymmetric septal hypertrophy (ASH), which refers to the thickening of the wall that separates the two lower chambers of the heart (the ventricles). Typically, there is LV hypertrophy, often with the septum more than 1.3 times thicker compared to the posterior LV free wall.

Question 24

Lown-Ganong-Levine 1. What is it 2. What ECG findings do you get

Answer 24

abnormal electrical connection between the atria and ventricles. However, in LGL, the accessory pathway (the abnormal connection) is located in the bundle of James, ECG findings: short PR interval and possibly a delta wave, which can help to distinguish this condition from other cardiac arrhythmias.

Question 25

Mean pressure gradient calculated in Echo

Answer 25

Area under curve

Question 26

Pressure gradient calculated in Echo

Answer 26

4x max velocity squard (y axis in m/s)

Question 27

patients with diabetes aged 40-75 years with LDL-C ≥3.8 mmol/L and a 10-year ASCVD risk ≥7.5% should be treated with high-intensity statin therapy to reduce LDL-C by ____

Answer 27

≥50%

Question 28

How does CPAP reduce in pulmonary oedema

Answer 28

1. Reduces preload by reducing venous return by increasing intrathoracic pressure 2. the prevention of alveolar collapse at end expiration 3. decreased left ventricular afterload.

Question 29

Brugada Types

Answer 29

Type 1: Coved ST segment in V1 and V2, with TWI Type 2: Downsloping ST segment elevation in V1 and V2, with upright T wave Type 3: Brugada type 3: can be the morphology of either type 1 or type 2, but with <2mm of ST segment elevation.

Question 30

HOCM medical management

Question 31

DeBakey classification of aortic dissection

Answer 31

Type I: Dissection tear originates in the ascending aorta and propagates distally to include the aortic arch and typically the descending aorta ● Type II: Dissection tear is confined only to the ascending aorta ● Type III: Dissection tear originates in the descending thoracic aorta and propagates most often distally

Question 32

NYHA Classification

Question 33

Which medication to avoid in aortic dissection

Answer 33

Increased aortic wall stress: In acute aortic dissection, there is already significant stress on the weakened aortic wall. Hydralazine can cause reflex tachycardia and increase cardiac output, which can further increase aortic wall stress and lead to aortic rupture. Reflex sympathetic stimulation: Hydralazine can cause reflex sympathetic stimulation, which can increase heart rate and blood pressure. This can increase aortic wall stress and worsen the dissection. Delayed diagnosis: Hydralazine can mask the symptoms of acute aortic dissection, making it difficult to diagnose the condition in a timely manner. This can lead to a delay in treatment, which can be life-threatening in patients with acute aortic dissection. Alternative therapies: There are other medications that can be used to treat hypertension in patients with acute aortic dissection, such as beta-blockers and calcium channel blockers. These medications are less likely to increase aortic wall stress and are preferred in this patient population.

Question 34

Which medications to use in aortic dissection

Answer 34

Beta-blockers: These medications are the first-line therapy for blood pressure control in acute aortic dissection. They work by reducing heart rate and myocardial contractility, which decreases the force of the blood flowing through the aorta. Intravenous beta-blockers such as labetalol or esmolol are usually preferred. Sodium nitroprusside: This medication is a potent vasodilator that can rapidly lower blood pressure in acute aortic dissection. It works by relaxing the smooth muscle in the blood vessels, which reduces peripheral vascular resistance and decreases the force of the blood flowing through the aorta. Nicardipine: This medication is a calcium channel blocker that can be used as an alternative to sodium nitroprusside. It works by relaxing the smooth muscle in the blood vessels, which reduces peripheral vascular resistance and decreases the force of the blood flowing through the aorta.

Question 35

Treatment of high grade Barett's oesophagus

Answer 35

hermal ablative therapy, such as radiofrequency ablation (RFA), is currently the most appropriate and commonly recommended management for high-grade dysplasia in Barrett’s esophagus. RFA involves the use of heat to destroy the dysplastic cells without damaging the underlying structures. It has a high success rate in eradicating dysplasia and preventing progression to cancer, with a favorable safety profile. Surgical resection, such as esophagectomy, is a definitive treatment that may be considered for high-grade dysplasia, especially if there are areas that are not amenable to endoscopic treatment or if there is evidence of early invasive cancer. However, it is associated with significant morbidity and mortality and is usually reserved for cases where endoscopic therapies are not feasible or have failed.