Cardiology Flashcards

1
Q

Which valvular abnormality is a mid diastolic murmur?

A

Mitral stenosis.

Mid-late diastolic murmur (best heard in expiration)
loud S1

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1
Q

Features of cardiac syndrome X?

A
  • Angina-like chest pain on exertion
  • ST depression on exercise stress test
  • but normal coronary arteries on angiography
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2
Q

continuous ‘machinery’ murmur?

A

Patent ductus arteriosus.

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3
Q

Mechanism of action of ACE inhibitors?

A

Inhibits the conversion angiotensin I to angiotensin II
→ decrease in angiotensin II levels → to vasodilation and reduced blood pressure
→ decrease in angiotensin II levels → reduced stimulation for aldosterone release → decrease in sodium and water retention by the kidneys.

Renoprotective mechanism:
angiotensin II constricts the efferent glomerular arterioles.
ACE inhibitors therefore lead to DILATION of the EFFERENT arterioles → reduced glomerular capillary pressure → decreased mechanical stress on the delicate filtration barriers of the glomeruli

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4
Q

Side effect of ACE-inhibitors?

A
  • Cough
    occurs in around 15% of patients and may occur up to a year after starting treatment
    thought to be due to increased bradykinin levels
  • Angioedema: may occur up to a year after starting treatment
  • Hyperkalaemia
  • First-dose hypotension: more common in patients taking diuretics
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5
Q

Cause of JVP irregular cannon wave?

A

Complete heart block.

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6
Q

Causes of JVP regular cannon wave?

A
  • Ventricular tachycardia (with 1:1 ventricular-atrial conduction)
  • Atrio-ventricular nodal re-entry tachycardia (AVNRT)
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7
Q

Feature of Aortic regurgitation?

A

Early diastolic murmur.

  • Collapsing pulse
  • Wide pulse pressure
  • Quincke’s sign (nailbed pulsation)
  • De Musset’s sign (head bobbing)
  • Mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
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8
Q

How does BNP help heart failure?

A
  1. Decreases cardiac afterload.
    - Diuretic and natriuretic
    - Suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
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9
Q

What can cause a DVT to lead to a stroke?

A

Patent foramen ovale (hole between left atrium and right atrium) may allow embolus (e.g. from DVT) to pass from right side of the heart to the left side leading to a stroke - ‘a paradoxical embolus’.

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10
Q

Mainstay of treatment for pulmonary arterial hypertension? (PAH)

A

If there is a negative response to acute vasodilator testing (the vast majority of patients):

  1. Prostacyclin analogues: Treprostinil, Iloprost
  2. Endothelin receptor antagonists: Bosentan, Ambrisentan
  3. Phosphodiesterase inhibitors: Sildenafil

If there is a positive response to acute vasodilator testing (a minority of patients)
- Oral calcium channel blockers

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11
Q

Features of WPW on ECG?

A

WPW syndrome is caused by a congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VF.

  • Short PR interval
  • Wide QRS complexes with a slurred upstroke - ‘Delta Wave’
  • Left axis deviation if right-sided accessory pathway
    (in the majority of cases, or in a question without qualification, WPW syndrome is associated with left axis deviation)
  • Right axis deviation if left-sided accessory pathway
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12
Q

Management of WPW syndrome?

A

Definitive treatment: radiofrequency ablation of the accessory pathway.

Medical therapy: Sotalol***, Amiodarone, Flecainide

(Sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation)

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13
Q

What is Eisenmenger’s syndrome?

A

Eisenmenger’s syndrome describes the reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension. This occurs when an uncorrected left-to-right leads to remodeling of the pulmonary microvasculature, eventually causing obstruction to pulmonary blood and pulmonary hypertension.

Features:
- Original murmur may disappear
- Cyanosis
- Clubbing
- Right ventricular failure
- Haemoptysis, embolism

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14
Q

What is the drug management for chronic heart failure?

A
  1. The first-line treatment for all patients is both an ACE-inhibitor and a beta-blocker.

(ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with preserved ejection fraction).

  1. The standard second-line treatment is an aldosterone antagonist (mineralocorticoid receptor antagonists). Examples include spironolactone and eplerenone.

increasing role for SGLT-2 inhibitors in the management of heart failure with a reduced ejection fraction.
They reduce glucose reabsorption and increase urinary glucose excretion. (canagliflozin, dapagliflozin and empagliflozin)

  1. Third-line treatment should be initiated by a specialist. Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy.
  • Offer annual influenza vaccine
  • Offer one-off pneumococcal vaccine
    adults usually require just one dose but those with asplenia, splenic dysfunction or chronic kidney disease need a booster every 5 years.
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15
Q

Most common organism for infective endocarditis in IVDU?

A

Staphylococcus aureus is commonly associated with infective endocarditis amongst IVDU.

Typically causing tricuspid lesions.

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16
Q

Most common organism involved in prosthetic valve endocarditis?

A

Staphylococcus epidermidis
commonly colonize indwelling lines and are the most cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination.

After 2 months the spectrum of organisms which cause endocarditis return to normal (i.e. Staphylococcus aureus is the most common cause)

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17
Q

Treatment for eclampsia?

A

Magnesium sulphate is used to both prevent seizures in patients with severe pre-eclampsia and treat seizures once they develop.

  • In eclampsia an IV bolus of 4g over 5-10 minutes should be given followed by an infusion of 1g / hour.
  • Urine output, reflexes, respiratory rate and oxygen saturations should be monitored during treatment
    respiratory depression can occur: calcium gluconate is the first-line treatment for magnesium sulphate induced respiratory depression.

Monitoring reflexes, particularly deep tendon reflexes (DTR), and respiratory rate are crucial during magnesium administration. Loss of DTRs may indicate magnesium toxicity, which can lead to muscle weakness, respiratory depression, and even respiratory arrest if not addressed promptly. Similarly, monitoring the patient’s respiratory rate is essential as a decreasing rate can be an early sign of magnesium toxicity.

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18
Q

Drug for Torsades de pointes?

A

Torsades de pointes is a specific form of polymorphic ventricular tachycardia, characterized by a twisting QRS complex around the isoelectric baseline.

It can be precipitated by various factors, including electrolyte imbalances, medications, and underlying cardiac conditions.

Intravenous magnesium sulphate is the first-line treatment for torsades de pointes especially when the patient is hemodynamically stable (normal BP and no signs of HF).

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19
Q

How long for DAPT following placement of a drug-eluting stent?

A

12 months of dual antiplatelet therapy after placement of a drug-eluting stent (DES).

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20
Q

Initial blind therapy for infective endocarditis including native and prosthetic valves?

A
  • Native valve:
    Amoxicillin, consider adding Gentamicin.
  • If penicillin allergic, MRSA or severe sepsis:
    Vancomycin + Gentamicin
  • If prosthetic valve:
    Vancomycin + Rifampicin + Gentamicin
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21
Q

Classic features of cardiac tamponade?

A

Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure.

Classical features - Beck’s triad:
1. Hypotension
2. Raised JVP
3. Muffled heart sounds

  • Dyspnoea
  • Tachycardia
  • An absent Y descent on the JVP - this is due to the limited right ventricular filling
  • Pulsus paradoxus - an abnormally large drop in BP during inspiration
  • ECG: electrical alternans

Management:
Urgent pericardiocentesis

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22
Q

What are the indications for ICDs?

A

Implantable cardiac defibrillators (ICDs) are used to prevent sudden cardiac death in patients at risk of life-threatening ventricular arrhythmias.

  • Long QT syndrome
  • HOCM
  • Previous cardiac arrest due to VT/VF
  • Previous myocardial infarction with non-sustained VT on 24 hr monitoring, inducible VT on electrophysiology testing and ejection fraction < 35%
  • Brugada syndrome
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23
Q

Adverse effects of thiazide like diuretics?

A

Thiazide diuretics work by inhibiting sodium reabsorption at the proximal part of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter.

Common adverse effects:
- Dehydration
- Postural hypotension
- Hypokalaemia: increased delivery of sodium to the distal part of the distal convoluted tubule → increased sodium reabsorption in exchange for potassium and hydrogen ions
- Hyponatraemia
- Hypercalcaemia: the flip side of this is hypocalciuria, which may be useful in reducing the incidence of renal stones.
- Gout
- Impaired glucose tolerance
- Impotence

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24
Q

Which condition is growing Streptococcus bovis and
the subtype Streptococcus gallolyticus most linked with in infective endocarditis?

A

Streptococcus bovis is associated with colorectal cancer.
the subtype Streptococcus gallolyticus is most linked with colorectal cancer.

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25
Q

Drug Mx for multifocal atrial tachycardia (MAT)?

A

Multifocal atrial tachycardia (MAT) may be defined as a irregular cardiac rhythm caused by at least three different sites in the atria, which may be demonstrated by morphologically distinctive P waves. It is more common in elderly patients with chronic lung disease, for example COPD.

Management:
- Rate-limiting calcium channel blockers are often used first-line (e.g Verapamil)

26
Q

Which medication is used for pharmacological cardioversion in patient’s presenting with AF onset <48 hours?

A

Flecainide or Amiodarone in those without structural heart disease.

Amiodarone if structural heart disease.

27
Q

Persistent ST-segment elevation in the absence of chest pain following a recent myocardial infarction (MI) are most consistent with a diagnosis of what?

A

Left ventricular aneurysm.

The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

28
Q

ECG changes seen in pericarditis?

A

Features of pericarditis:
- chest pain: may be pleuritic. Is often relieved by sitting forwards
- other symptoms include a non-productive cough, dyspnoea and flu-like symptoms
- pericardial rub

The ECG changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events.

  1. ‘Saddle-shaped’ ST elevation (Concave)
  2. PR depression: most specific ECG marker for pericarditis

troponin: around 30% of patients may have an elevated troponin - this indicates possible myopericarditis

29
Q

Drug management for pericarditis?

A

A combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis.

  • until symptom resolution and normalisation of inflammatory markers (usually 1-2 weeks) followed by tapering of dose recommended over
30
Q

Brugada syndrome caused by mutation in which gene?

A

Brugada syndrome is a form of inherited cardiovascular disease with may present with sudden cardiac death. It is inherited in an autosomal dominant fashion.

  • Mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein.
31
Q

Which drugs need to be avoided in HOCM?

A

Nitrates
ACE-inhibitors
Inotropes

All agents that reduce the preload or afterload, including nitrates. If used they may worsen the outflow tract obstruction.

32
Q

Anticoagulation for patients with bioprosthetic valves?

A

Long-term anticoagulation not usually needed.
Warfarin may be given for the first 3 months depending on patient factors.
Low-dose aspirin is given long-term.

33
Q

Anticoagulation for patients with mechanical valves?

A

Major disadvantage is the increased risk of thrombosis meaning long-term anticoagulation is needed.

Warfarin is still used in preference to DOACs for patients with mechanical heart valves.

Aspirin is only normally given in addition if there is an additional indication, e.g. ischaemic heart disease.

Target INR:
Aortic: 3.0
Mitral: 3.5

34
Q

Management for rate control in AF?

A

Agents used to control rate in patients with atrial fibrillation:

  1. Beta-blockers
    (a common contraindication for beta-blockers is asthma)
  2. Calcium channel blockers (diltiazem)
  3. Digoxin
35
Q

Management for PDA?

A

Indomethacin or ibuprofen given to the neonate.
- inhibits prostaglandin synthesis
- closes the connection in the majority of cases

36
Q

Reversal agent for Dabigatran?

A

Idarucizumab.

Dabigatran is an oral anticoagulant that works by being a direct thrombin inhibitor.

37
Q

Drug management for stable angina?

A
  • All patients should receive aspirin and a statin in the absence of any contraindication.
  • Sublingual glyceryl trinitrate to abort angina attacks.
  1. Either a Beta-blocker or a Calcium Channel Blocker first-line.

If CCB is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used.

if used in combination with a beta-blocker then use a longer-acting dihydropyridine calcium channel blocker (e.g. amlodipine, modified-release nifedipine).

Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block).

if a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa.

  • If a patient is on monotherapy and cannot tolerate the addition of a CCB or a beta-blocker then consider one of the following drugs:
  • Long-acting nitrate
  • Ivabradine
  • Nicorandil
  • Ranolazine
38
Q

Abx mangement for prosthetic valve endocarditis caused by staphylococci?

A

Flucloxacillin + Rifampicin + Gentamicin

39
Q

Pharmacological management for HTN in pregnancy?

A
  1. Oral Labetalol is now first-line
  2. Oral Nifedipine (e.g. if asthmatic) and hydralazine.
40
Q

Pharmacological Mx for STEMI?

A
  1. Aspirin
  2. Ticagrelor (higher bleeding risk)
    / Prasugrel (If pt going for PCI)
  3. Unfractionated heparin is usually given for patients who’re are going to have a PCI.
41
Q

Medication for thrombolysis in STEMI?

A

Thrombolysis should be performed in patients without access to primary PCI.

Tenecteplase is easier to administer and has been shown to have non-inferior efficacy to Alteplase with a similar adverse effect profile.

An ECG should be performed 90 minutes following thrombolysis to assess whether there has been a greater than 50% resolution in the ST elevation:
- if there has not been adequate resolution then rescue PCI is superior to repeat thrombolysis.
- For patients successfully treated with thrombolysis PCI has been shown to be beneficial.

42
Q

Which heart murmur is seen in Ebstein’s anomaly?

A

Tricuspid regurgitation:
pansystolic murmur, worse on inspiration.

Ebstein’s anomaly is a congenital heart defect characterised by low insertion of the tricuspid valve resulting in a large atrium and small ventricle.

Associations:
- Patent Foramen Ovale or atrial septal defect is seen in at least 80% of patients, resulting in a shunt between the right and left atria.
- Wolff-Parkinson White syndrome

43
Q

Mx in patients on warfarin with major bleeding?

A
  1. Stop warfarin
  2. Give intravenous vitamin K 5mg
  3. Prothrombin complex concentrate - if not available then FFP*
44
Q

Mx in patient with INR >8 with no bleeding?

A
  1. Stop warfarin
  2. Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
  3. Repeat dose of vitamin K if INR still too high after 24 hours
  4. Restart when INR < 5.0
45
Q

Mechanism of action of Tirofiban?

A

Glycoprotein IIb/IIIa receptor antagonist.

Examples include Tirofiban, eptifibatide.

Used in NSTEMI where GRACE score is intermediate risk >3%, a glycoprotein inhibitor is started prior to angiography within 96 hours.

46
Q

Management for SVT?

A
  1. Vagal manoeuvres:
    - Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
    - Carotid sinus massage
  2. Intravenous adenosine
    - Rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
    - Contraindicated in asthmatics - verapamil is a preferable option
  3. Electrical cardioversion
47
Q

Inferior coronary territory is supplied by which artery?

A

Inferior = II, III, aVF

Right coronary artery.

48
Q

Lateral coronary territory is supplied by which artery?

A

Lateral = I, aVL, V5, V6

Left Circumflex.

49
Q

Mechanism of action of bumetanide?

A

Furosemide and bumetanide are loop diuretics that act by inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl.

50
Q

Adverse effects of loop diuretics?

A
  • Hypotension
  • Hyponatraemia
  • Hypokalaemia, Hypomagnesaemia
    Hypochloraemic alkalosis
  • Ototoxicity
  • Hypocalcaemia
  • Renal impairment (from dehydration + direct toxic effect)
  • Hyperglycaemia (less common than with thiazides)
  • Gout
51
Q

When starting a patient on ACE-inhibitor what is the acceptable level of creatinine on rechecking the blood tests?

A

Monitoring: Acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l.

52
Q

Cause for persistent ST elevation following recent MI , no chest pain in patient who has had recent STEMI?

A

Left ventricular aneurysm.

The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

53
Q

What is the main ECG abnormality seen in Hypercalcaemia?

A

Shortening of QT interval.

54
Q

What are the indications for a temporary pacemaker?

A
  • Symptomatic/haemodynamically unstable bradycardia, not responding to atropine.
  • Post-ANTERIOR MI: type 2 or complete heart block. Post-INFERIOR MI complete heart block is common and can be managed conservatively if asymptomatic and haemodynamically stable.
  • Trifascicular block prior to surgery
55
Q

How long should patients be anticoagulated following electrical cardioversion for AF?

A

Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence.

56
Q

What ECG features are seen in hypokalaemia?

A
  1. U waves
  2. Small or absent T waves (occasionally inversion)
  3. Prolong PR interval
  4. ST depression
  5. Long QT
57
Q

Criteria for commencing on sacubitril-valsartan?

A

Criteria: left ventricular fraction <35%
is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs.
- should be initiated following ACEi or ARB wash-out period

58
Q

In SVT, adenosine should not be given in patients with a history of what medical condition?

A

Adenosine is contraindicated in asthma.

Verapamil should be given instead.

59
Q

Features of TOF?

A

TOF: PROVE

P Pulmonary Stenosis
R Right Ventricular hypetrophy
O Overriding Aorta
V Ventricular septal defect
E Eisenmengers

60
Q

MI with complete heart block is seen due to occlusion of which artery?

A

Right coronary artery.

Inferior MI can present with bradycardia and complete heart block.

61
Q

What ECG finding is specific to pericarditis?

A

PR depression.

62
Q

Which Abx is important to avoid giving in patients with Long QT syndrome?

A

Erythromycin.

Erythromycin is a macrolide antibiotic that has been associated with cardiotoxicity, specifically QT interval prolongation and ventricular arrhythmias such as torsades de pointes.