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Cardiology Flashcards

1
Q

What lifestyle advice can be given to patients in management of hypertension?

A

Lifestyle advice should not be forgotten and is frequently tested in exams:

  1. A low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in the UK consumes around 8-12g/day of salt. A recent BMJ paper* showed that lowering salt intake can have a significant effect on blood pressure. For example, reducing salt intake by 6g/day can lower systolic blood pressure by 10mmHg.
  2. Caffeine intake should be reduced
  3. The other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weight.
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2
Q

What is the blood pressure target for clinic BP in those below 80 years old and those above 80 years old?

A

Age < 80 years: 140/90 mmHg

Age > 80 years: 150/90 mmHg

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3
Q

How do we determine which patients with high BP are offered drug treatment?

A

First clinic reading of BP is >140/90 mmHg. Then offer ABPM/HBPM. Then based on the reading;

  1. ABPM/HBPM <135/85 mmHg
    - Not hypertensive. Monitor.
  2. ABPM/HBPM >= 135/85 mmHg (Stage 1 hypertension)
    - Treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 10% or greater
  3. ABPM/HBPM >= 150/95 mmHg (Stage 2 hypertension)
    offer drug treatment regardless of age
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4
Q

What is the step by step approach for pharmacological management of hypertension?

A
  1. Step 1 treatment:
    - Patients < 55-years-old OR a background of T2DM: ACE inhibitor or an Angiotensin receptor blocker (ACE-i or ARB): (A)
  • ARBs should be used where ACE inhibitors are not tolerated (ex: due to a cough)
  • Patients >= 55-years-old OR of black African or African–Caribbean origin: Calcium channel blocker (C)
  • ACE inhibitors have reduced efficacy in patients of black African or African–Caribbean origin are therefore not used first-line
  1. Step 2 treatment:
    - If already taking an ACE-i or ARB add a Calcium channel blocker OR a thiazide-like Diuretic.
  • If already taking a Calcium channel blocker add an ACE-i or ARB.
  • For patients of black African or African–Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an ARB in preference to an ACE inhibitor
    (A + C) or (A + D)
  1. Step 3 treatment:
    - Add a third drug to make, i.e.:
    - if already taking an (A + C) then add a D
    - if already (A + D) then add a C
    (A + C + D)
  2. Step 4 treatment:
    - NICE define step 4 as resistant hypertension and suggest either adding a 4th drug or seeking specialist advice.

First, check for:

  • confirm elevated clinic BP with ABPM or HBPM
  • assess for postural hypotension.
  • discuss adherence

If potassium < 4.5 mmol/l add low-dose Spironolactone
If potassium > 4.5 mmol/l add an Alpha- or Beta-blocker

Patients who fail to respond to step 4 measures should be referred to a specialist.

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5
Q

Which valve is comonly affected in infective endocarditis?

A

The strongest risk factor for developing infective endocarditis is a previous episode of endocarditis. The following types of patients are affected:

  • Previously normal valves (50%, typically acute presentation)
  • the mitral valve is most commonly affected
  • Rheumatic valve disease (30%)
  • Rrosthetic valves
  • Congenital heart defects
  • Intravenous drug users (IVDUs, e.g. typically causing tricuspid lesion)
  • Others: recent piercings

Causes:

Staphylococcus aureus is now the most common cause of infective endocarditis. Staphylococcus aureus is also particularly common in acute presentation and IVDUs

Streptococcus viridans was the most common cause of infective endocarditis in developing countries.

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.

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6
Q

What are the medications offered to patients following a myocardial infarction for secondary prevention?

A

Management of patients following a myocardial infarction:

All patients should be offered the following drugs:

  1. Dual antiplatelet therapy (aspirin plus a second antiplatelet agent)
  2. ACE inhibitor
  3. Beta-blocker
  4. Statin

Most patients who’ve had an acute coronary syndrome are now given dual antiplatelet therapy (DAPT). Clopidogrel was previously the second antiplatelet of choice. Now Ticagrelor and Prasugrel (also ADP-receptor inhibitors) are more widely used.

The NICE Clinical Knowledge Summaries now recommend:
- Post acute coronary syndrome (medically managed): add Ticagrelor to Aspirin, stop ticagrelor after 12 months.

  • Post percutaneous coronary intervention: add Prasugrel or Ticagrelor to Aspirin, stop the second antiplatelet after 12 months.
  • This 12 month period may be altered for people at a high-risk of bleeding or those who at high-risk of further ischaemic events
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7
Q

What is the first line blood test needed in patients with suspected heart failure?

A

All patients with suspected chronic heart failure should have an NT‑proBNP test first-line.

Measure serum natriuretic peptides (B-type natriuretic peptide [BNP] or N-terminal pro-B-type natriuretic peptide [NTproBNP]) in patients with suspected heart failure without previous MI.

Interpreting the test:

  • If levels are ‘high’ arrange specialist assessment (including transthoracic echocardiography) within 2 weeks.
  • If levels are ‘raised’ arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks.

B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain. Very high levels are associated with a poor prognosis.

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8
Q

How to differentiate left and right bundle branch block?

A

One of the most common ways to remember the difference between LBBB and RBBB is WiLLiaM MaRRoW.

in LBBB there is a ‘W’ in V1 and a ‘M’ in V6 = WiLLiaM
in RBBB there is a ‘M’ in V1 and a ‘W’ in V6 = MaRRoW

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9
Q

What are some causes of Right Bundle Branch Block?

A

Causes of RBBB:

  • normal variant - more common with increasing age
  • Right ventricular hypertrophy
  • Chronically increased right ventricular pressure - e.g. Cor Pulmonale
  • pulmonary embolism
  • myocardial infarction
  • atrial septal defect (ostium secundum)
  • cardiomyopathy or myocarditis
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10
Q

What is the target INR for venous thromboembolism? What if recurrent venous thromboembolism?

A

Indications for Warfarin:

  • Venous thromboembolism: target INR = 2.5, if recurrent 3.5
  • Atrial fibrillation, target INR = 2.5
  • Mechanical heart valves, target INR depends on the valve type and location. Mitral valves generally require a higher INR than aortic valves.

Patients on warfarin are monitored using the INR (international normalised ration), the ratio of the prothrombin time for the patient over the normal prothrombin time. Warfarin has a long half-life and achieving a stable INR may take several days.

Side-effects

  • Haemorrhage
  • Teratogenic, although can be used in breastfeeding mothers
  • Skin necrosis: when warfarin is first started biosynthesis of protein C is reduced. This results in a temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration. Thrombosis may occur in venules leading to skin necrosis
  • Purple toes
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11
Q

How is aortic dissection classified into type A or type B?

A

Pathophysiology
- Tear in the tunica intima of the wall of the aorta.

Associations:

  • Hypertension: the most important risk factor
  • Trauma
  • Bicuspid aortic valve
  • Collagens: Marfan’s syndrome, Ehlers-Danlos syndrome
  • Turner’s and Noonan’s syndrome
  • pregnancy
  • syphilis

Features:

  • Chest pain: typically severe, radiates through to the back and ‘tearing’ in nature!
  • Aortic regurgitation
  • Hypertension
  • other features may result from the involvement of specific arteries. For example coronary arteries → angina, spinal arteries → paraplegia, distal aorta → limb ischaemia
  • the majority of patients have no or non-specific ECG changes. In a minority of patients, ST-segment elevation may be seen in the inferior leads

Stanford Classification
Type A - Ascending aorta, 2/3 of cases
Type B - Descending aorta, distal to left subclavian origin, 1/3 of cases

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12
Q

What is the management for supraventricular tachycardia?

A

Whilst strictly speaking the term supraventricular tachycardia (SVT) refers to any tachycardia that is not ventricular in origin the term is generally used in the context of paroxysmal SVT. Episodes are characterised by the sudden onset of a narrow complex tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.

Acute management with no adverse signs (e.g. shock, myocardial ischaemia):

  1. Vagal manoeuvres: e.g. Valsalva manoeuvre, Carotid sinus massage
  2. Intravenous adenosine 6mg → 12mg → 12mg: contraindicated in asthmatics - Verapamil is a preferable option
  3. Electrical cardioversion

Prevention of episodes:

  • beta-blockers
  • radio-frequency ablation
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13
Q

What are some adverse effects of statins? Which drug is statin contraindicated with?

A

Adverse effects:

  • Myopathy: includes myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase.
  • Liver impairment: the 2014 NICE guidelines recommend checking LFTs at baseline, 3 months and 12 months. Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range.
  • There is some evidence that statins may increase the risk of intracerebral haemorrhage in patients who’ve previously had a stroke. This effect is not seen in primary prevention. For this reason it is recommended to avoid statins in patients with a history of intracerebral haemorrhage.

Contraindications:

  • Macrolides! (e.g. erythromycin, clarithromycin) are an important interaction. Statins should be stopped until patients complete the course (statin induced myopathy)
  • Pregnancy

Statins should be taken at night as this is when the majority of cholesterol synthesis takes place.

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14
Q

What is the recommended statin dose for primary and secondary prevention of cardiovascular disease?

A

Primary Prevention:

  • 10-year cardiovascular risk >= 10% OR most type 1 diabetics OR CKD if eGFR <60)
  • ATORVASTATIN 20mg for primary prevention.

Secondary Prevention:

  • Known people with established cardiovascular disease (stroke, TIA, ischaemic heart disease, peripheral arterial disease)
  • ATORVASTATIN 80mg for secondary prevention
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15
Q

What are the ECG changes seen in Pericarditis?

A

Features:

  • Chest pain: may be pleuritic. Is often relieved by sitting forwards! exacerbated when lying flat or inhaling deep breaths.
  • Other symptoms include non-productive cough, dyspnoea and flu-like symptoms
  • Fever
  • Pericardial rub
  • Tachypnoea
  • Tachycardia

Causes:

  • Viral infections (Coxsackie)
  • Tuberculosis
  • Uraemia (causes ‘fibrinous’ pericarditis)
  • Trauma
  • Post-myocardial infarction, Dressler’s syndrome
  • Connective tissue disease
  • Hypothyroidism
  • Malignancy

Investigations:
- ECG changes
the changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
- ‘Saddle-shaped’ ST elevation
- PR depression: most specific ECG marker for pericarditis
- All patients with suspected acute pericarditis should have transthoracic echocardiography

Management:

  • Treat the underlying cause
  • A combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis
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16
Q

What are some of the adverse effects of loop diuretics? (Furosemide, 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.

Indications:

  • Heart failure: both acute (usually intravenously) and chronic (usually orally)
  • Resistant hypertension, particularly in patients with renal impairment

Adverse effects:

  • hypotension
  • hyponatraemia
  • hypokalaemia, hypomagnesaemia
  • hypochloraemic alkalosis
  • ototoxicity
  • hypocalcaemia
  • renal impairment (from dehydration + direct toxic effect)
  • hyperglycaemia (less common than with thiazides)
  • gout
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17
Q

Briefly, what is the immediate management for suspected ACS?

A

Immediate management of suspected acute coronary syndrome (ACS):

  1. Glyceryl trinitrate
  2. Aspirin 300mg. NICE do not recommend giving other antiplatelet agents (i.e. Clopidogrel) outside of hospital
  3. Do not routinely give oxygen, only give if sats < 94%*
  4. Perform an ECG as soon as possible but do not delay transfer to hospital. A normal ECG does not exclude ACS

Referral:

  • Current chest pain or chest pain in the last 12 hours with an abnormal ECG: Emergency Admission
  • Chest pain 12-72 hours ago: refer to hospital the same-day for assessment
  • Chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action
  • Do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to:
  • people with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98%
  • people with COPD who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available
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18
Q

What are the three characteristics of typical angine?

A

NICE define anginal pain as the following:

  1. Constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
  2. Precipitated by physical exertion
  3. Relieved by rest or GTN in about 5 minutes
  • Patients with all 3 features have typical angina
  • Patients with 2 of the above features have atypical angina
  • Patients with 1 or none of the above features have non-anginal chest pain
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19
Q

What are the 4Hs and 4Ts of reversible causes of cardiac arrest?

A

Reversible causes of cardiac arrest:

  • Hypoxia
  • Hypovolaemia
  • Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
  • Hypothermia
  • Thrombosis (coronary or pulmonary)
  • Tension pneumothorax
  • Tamponade – cardiac
  • Toxins
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20
Q

What are the different types of heart block?

A

First degree heart block
- PR interval > 0.2 seconds

Second degree heart block

  • Type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs
  • Type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex
Third degree (complete) heart block
- There is no association between the P waves and QRS complexes
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21
Q

What is a first degree heart block?

A

The PR interval is prolonged and unchanging; no missed beats.

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22
Q

What is second degree heart block Mobitz type 1?

A

The PR interval becomes longer and longer until a QRS is missed, the pattern then resets. This is Weckenback phenomenoon.

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23
Q

What is second degree heart block Mobitz type 2?

A

QRSs are regularly missed. This is a dangerous rhythm as it may progress to complete heart block.

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24
Q

What is third degree complete heart block?

A

No impulses are passed from atria to ventricles so P waves and QRSs appear independently of each other. The patient becomes very bradycardic and may develop haemodynamic compromise.

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25
Q

What factors favour a rate control strategy for atrial fibrillation?

A
  • Older than 65 years

- History of ischaemic heart disease

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26
Q

What factors favour a rhythm control strategy for atrial fibrillation?

A
  • Younger than 65 years
  • Symptomatic
  • First presentation
  • Lone AF or AF secondary to a corrected precipitant (e.g. Alcohol)
  • Congestive heart failure
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27
Q

Briefly, what are the class of drugs used for rate control in AF?

A
  1. Beta-blockers
    - a common contraindication for beta-blockers is asthma
  2. Calcium channel blockers
  3. Digoxin
    - not considered first-line anymore as they are less effective at controlling the heart rate during exercise
    - however, they are the preferred choice if the patient has coexistent heart failure
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28
Q

Briefly, what are the class of drugs used for rhythm control in AF?

A
  1. Sotalol
  2. Amiodarone
  3. Flecainide
  4. Others (less commonly used in UK): disopyramide, dofetilide, procainamide, propafenone, quinidine
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29
Q

Which condition are these pulses seen in?

Pulsus paradoxus
Slow-rising/plateau
Collapsing
Pulsus alternans

A

Pulsus paradoxus:

  • Greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration
  • Severe asthma, cardiac tamponade

Slow-rising/plateau
- aortic stenosis

Collapsing

  • Aortic regurgitation
  • Patent ductus arteriosus
  • hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)

Pulsus alternans
- When the upstroke of the pulse alternates between strong and weak. It indicates systolic dysfunction and is seen in patients with heart failure (severe LVF).

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30
Q

What is the main effect of nitrates and what are the indicated for?

A

Nitrates are a group of drugs which have vasodilating effects. The main indications for their use is in the management of angina and the acute treatment of heart failure. Sublingual glyceryl trinitrate is the most common drug used in patients with ischaemic heart disease to relieve angina attacks.

In angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand.

Side-effects:

  • Hypotension
  • Tachycardia
  • Headaches
  • Flushing
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31
Q

All patients with STEMI should be given..?

A

Myocardial infarction: STEMI management

In the absence of contraindications, all patients should be given:

  1. Aspirin
  2. P2Y12-receptor antagonist. Clopidogrel was the first P2Y12-receptor antagonist to be widely used but now Ticagrelor is often favoured as studies have shown improved outcomes compared to clopidogrel, but at the expense of slightly higher rates of bleeding. They also recommend that Prasugrel (another P2Y12-receptor antagonist) could be considered if the patient is going to have a percutaneous coronary intervention
  3. Unfractionated heparin is usually given for patients who’re are going to have a PCI. Alternatives include low-molecular weight heparin

Primary percutaneous coronary intervention (PCI) has emerged as the gold-standard treatment for STEMI but is not available in all centres. Thrombolysis should be performed in patients without access to primary PCI

With regards to thrombolysis:

  • Tissue plasminogen activator (tPA) has been shown to offer clear mortality benefits over streptokinase
  • 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. The optimal timing of this is still under investigation
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32
Q

Examples of thrombolytic drugs?

A

Alteplase
Tenecteplase
Streptokinase

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33
Q

What changes are seen on ECG in STEMI?

A

Acute myocardial infarction (MI):

  1. Hyperacute T waves are often the first sign of MI but often only persists for a few minutes.
  2. ST elevation may then develop.
  3. The T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months.
  4. Pathological Q waves develop after several hours to days. This change usually persists indefinitely

A posterior MI causes ST depression not elevation on a 12-lead ECG.

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34
Q

What are the classes for NYHA for heart failure?

A

The New York Heart Association (NYHA) classification is widely used to classify the severity of heart failure:

NYHA Class I
no symptoms
no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations

NYHA Class II
mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

NYHA Class III
moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

NYHA Class IV
severe symptoms
unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

35
Q

What is the drugs of choice for management of stable angina?

A

Medication:

  1. All patients should receive aspirin and a statin in the absence of any contraindication.
  2. Sublingual glyceryl trinitrate to abort angina attacks.
  3. NICE recommend using either a Beta-Blocker or a Calcium Channel Blocker first-line based on ‘comorbidities, contraindications and the person’s preference’.
  4. If a calcium channel blocker 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 long-acting dihydropyridine calcium-channel blocker (e.g. modified-release Nifedipine). Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block).
  5. If there is a poor response to initial treatment then medication should be increased to the maximum tolerated dose.
  6. If a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa.
  7. If a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs: a long-acting nitrate, ivabradine, nicorandil or ranolazine.
  8. if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG
36
Q

What murmur is classically heard in Aortic Stenosis? Where does it radiate to?

A
  • An ejection systolic murmur (ESM) is classically seen in aortic stenosis.
  • Classically radiates to the carotids
  • this is decreased following the Valsalva manoeuvre
  • chest pain
  • dyspnoea
  • syncope

Causes of aortic stenosis:

  • Degenerative calcification (most common cause in older patients > 65 years)
  • Bicuspid aortic valve (most common cause in younger patients < 65 years)
  • William’s syndrome (supravalvular aortic stenosis)
  • post-rheumatic disease
  • subvalvular: HOCM

Management

  • if asymptomatic then observe the patient is general rule
  • if symptomatic then valve replacement
  • if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
37
Q

What is the HAS-BLED score used for?

A

HAS-BLED is a scoring system developed to assess 1-year risk of major bleeding in patients taking anticoagulants for atrial fibrillation.

38
Q

Management of NSTEMI?

A

All patients should receive:

  • Aspirin 300mg
  • Nitrates or morphine to relieve chest pain if required

Whilst it is common that non-hypoxic patients receive oxygen therapy there is little evidence to support this approach. The 2008 British Thoracic Society oxygen therapy guidelines advise not giving oxygen unless the patient is hypoxic.

  • Antithrombin treatment. FONDAPARINUX should be offered to patients who are not at a high risk of bleeding and who are not having angiography within the next 24 hours. If angiography is likely within 24 hours or a patients creatinine is > 265 µmol/l unfractionated heparin should be given.
  • Ticagrelor and prasugrel are now the preferred second antiplatelet instead of clopidogrel. PRASUGREL is generally favoured if the patient is going to have a percutaneous coronary intervention. They should generally be given to all patients and continued for 12 months, although this may vary according to bleeding and ischaemic risk.
  • Intravenous glycoprotein IIb/IIIa receptor antagonists (eptifibatide or tirofiban) should be given to patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital admission.
  • Coronary angiography should be considered within 96 hours of first admission to hospital to patients who have a predicted 6-month mortality above 3.0%. It should also be performed as soon as possible in patients who are clinically unstable.
39
Q

What drugs are offered to patients with AF that require anticoagulation?

A

The CHA2DS2-VASc score, are clinical prediction rules for estimating the risk of stroke in patients with AF. Such a score is used to determine whether or not treatment is required with anticoagulation therapy or antiplatelet therapy, since AF can cause stasis of blood in the upper heart chambers, leading to the formation of a mural thrombus that can cause a stroke.

A high score corresponds to a greater risk of stroke, while a low score corresponds to a lower risk of stroke.

Score 1 Males: Consider anticoagulation
Females: No treatment (this is because their score of 1 is only reached due to their gender)

2 or more: Offer anticoagulation

NICE recommend that we offer patients a choice of anticoagulation, including Warfarin and the novel oral anticoagulants (NOACs).

40
Q

What is the management for chronic heart failure?

A

Whilst loop diuretics play an important role in managing fluid overload it should be remembered that no long-term reduction in mortality has been demonstrated for loop diuretics such as furosemide.

  1. The first-line treatment for all patients is both an ACE-inhibitor and a beta-blocker.
    - Generally, one drug should be started at a time. NICE advise that clinical judgement is used when determining which one to start first.
    - Beta-blockers licensed to treat heart failure in the UK include bisoprolol, carvedilol, and nebivolol.
    ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with preserved ejection fraction
  2. Second-line treatment is an aldosterone antagonist
    these are sometimes referred to as mineralocorticoid receptor antagonists. Examples include Spironolactone and Eplerenone
    - it should be remember that both ACE inhibitors (which the patient is likely to already be on) and aldosterone antagonists both cause hyperkalaemia - therefore potassium should be monitored
  3. Third-line treatment should be initiated by a specialist. Options include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy
    ivabradine.

Other treatments:

  • Offer annual influenza vaccine
  • Offer one-off pneumococcal vaccine
41
Q

What antiplatelet is given for ACS and for what duration?

A

Antiplatelets Summary of latest Guidance:

Acute coronary syndrome (medically treated)
1st line: Aspirin (lifelong) & Ticagrelor (12 months)
2nd line: If aspirin CI, Clopidogrel (lifelong)

Percutaneous coronary intervention

1st: Aspirin (lifelong) & Prasurgrel OR Ticagrelor (12 months)
2nd: If aspirin CI, Clopidogrel (lifelong)

TIA
1st line: Clopidogrel (lifelong)
2nd line: Aspirin (lifelong) & dipyridamole (lifelong)

Ischaemic stroke
1st line: Clopidogrel (lifelong)
2nd line: Aspirin (lifelong) & dipyridamole (lifelong)

Peripheral arterial disease
1st line: Clopidogrel (lifelong)
2nd line: Asprin (lifelong)

42
Q

When is a patient in AF cardioverted?

A

There are two scenarios where cardioversion may be used in atrial fibrillation:

  1. Electrical cardioversion as an emergency if the patient is haemodynamically unstable (shock)
  2. Electrical or pharmacological cardioversion as an elective procedure where a rhythm control strategy is preferred.
43
Q

ECG changes in V1 - V4 correspond to which territory and which coronary artery?

A

Anteroseptal: V1-V4

Left anterior descending artery

44
Q

ECG changes in II, III, aVF correspond to which territory and which coronary artery?

A

Inferior: II, III, aVF

Right coronary artery

45
Q

ECG changes in V6, I, aVL correspond to which territory and which coronary artery?

A

Anterolateral: V4-6, I, aVL

Left anterior descending or left circumflex artery

46
Q

What is the antihypertensive of choice in diabetics?

A

ACE inhibitors eg. ramipril should be used first-line for treating hypertension in diabetics, exceptions to this are people of Afro-Caribbean origin and women for whom there is a possibility of becoming pregnant. ACE-inhibitors are first-line in diabetics regardless of age eventhough >55 years! ACE inhibitors are used first-line in diabetics due to their renoprotective effect.

47
Q

Beta blockers should not be combined with which drug?

A

Beta-blockers should not be combined with non-dihydropyridine Verapamil (CCB) and Diltiazem as it can potentially cause profound bradycardia and asystole.

48
Q

What will the blood gas show in pulmonary embolism?

A

Pulmonary embolism causes hyperventilation, causing a drop in arterial carbonic dioxide partial pressure and thus respiratory alkalosis.

49
Q

If a a 2-level PE Wells score is less than 4 and is therefore unlikely, what test should be performed?

A

If a PE is ‘unlikely’ (4 points or less) arranged a D-dimer test.

D-dimer is a very sensitive, but non-specific marker for PE, meaning it is more useful when it is negative than when it is positive and it is therefore used in ruling out PE in patients where there is little clinical likelihood. If the D-dimer comes back positive in this patient, she should then receive a CTPA to look for PE.

50
Q

A continuous machine-like murmur is heard in which condition?

A

Patent ductus arteriosus

51
Q

An ejection systolic murmur is heard in which condition?

A

Aortic stenosis

  • pulmonary stenosis, HOCM
  • atrial septal defect, tetralogy of Fallot
52
Q

A holosystolic (pansystolic) murmur is heard in which condition?

A

Mitral/tricuspid Regurgitation (high-pitched and ‘blowing’ in character)

ventricular septal defect (‘harsh’ in character)

53
Q

A late systolic murmur is heard in which condition?

A

Mitral valve prolapse

coarctation of aorta

54
Q

An early diastolic murmur is heard in which condition?

A

Aortic regurgitation (high-pitched and ‘blowing’ in character)

Graham-Steel murmur (pulmonary regurgitation, again high-pitched and ‘blowing’ in character)

55
Q

A Mid-late diastolic murmur is heard in which condition?

A

Mitral stenosis (‘rumbling’ in character)

Austin-Flint murmur (severe aortic regurgitation, again is ‘rumbling’ in character)

56
Q

List the major criteria for rheumatic fever?

A

Major criteria:

  • Erythema marginatum
  • Sydenham’s chorea: this is often a late feature
  • Polyarthritis
  • Carditis and valvulitis (eg, pancarditis)*
  • Subcutaneous nodules

JONES CAFEPAL MNEMONIC

Joint involvement
O looks like heart = myocarditis
Nodules, subcutaneous
Erythema marginatum
Sydenham's chorea

Minor criteria:

  • raised ESR or CRP
  • pyrexia
  • arthralgia (not if arthritis a major criteria)
  • prolonged PR interval

Rheumatic fever develops following an immunological reaction to recent (2-6 weeks ago) Streptococcus pyogenes infection.

Diagnosis is based on evidence of recent streptococcal infection accompanied by:

  • 2 major criteria
  • 1 major with 2 minor criteria

Evidence of recent streptococcal infection:

  • raised or rising streptococci antibodies,
  • positive throat swab
  • positive rapid group A streptococcal antigen test
57
Q

How do you manage a patient on warfarin that has major bleeding?

A
  • Stop warfarin
  • Give intravenous vitamin K 5mg
  • Prothrombin complex concentrate - if not available then FFP
58
Q

How do you manage a patient on warfarin that has INR >8 and minor bleeding?

A
  • Stop warfarin
  • Give intravenous vitamin K 1-3mg
  • Repeat dose of vitamin K if INR still too high after 24 hours
  • Restart warfarin when INR < 5.0
59
Q

How do you manage a patient on warfarin that has INR >8 and no bleeding?

A
  • Stop warfarin
  • Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
  • Repeat dose of vitamin K if INR still too high after 24 hours
  • Restart when INR < 5.0
60
Q

How do you manage a patient on warfarin that has INR 5 -8 and minor bleeding?

A
  • Stop warfarin
  • Give intravenous vitamin K 1-3mg
  • Restart when INR < 5.0
61
Q

How do you manage a patient on warfarin that has INR 5 -8 and no bleeding?

A
  • Withhold 1 or 2 doses of warfarin

- Reduce subsequent maintenance dose

62
Q

What is the gold standard intervention for STEMI?

A

Primary percutaneous coronary intervention is the gold-standard treatment for ST-elevation myocardial infarction but is not available in all centres. Thrombolysis should be performed in patients without access to primary PCI.

With regards to thrombolysis:
- Tenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profile

63
Q

What is the management of patients in acute heart failure?

A

Management options in acute heart failure include:

  • Oxygen
  • IV loop diuretics
  • Opiates
  • Vasodilators
  • Inotropic agents

A patient who has failed medical management of pulmonary oedema with severe dyspnoea should be considered for CPAP

  • CPAP
  • Ultrafiltration
  • Mechanical circulatory assistance: e.g. intra-aortic balloon counterpulsation or ventricular assist devices
64
Q

When is Warfarin usually stopped before elective surgery?

A

In general, warfarin is usually stopped 5 days before planned surgery, and once the person’s international normalized ration (INR) is less than 1.5 surgery can go ahead. Warfarin is usually resumed at the normal dose on the evening of surgery or the next day if haemostasis is adequate.

65
Q

Which antihypertensive has a side effect of gout?

A

Gout is a common side effect of thiazide diuretics. Thiazide diuretics reduce uric acid excretion from the kidneys causing hyperuricaemia.

66
Q

What are the symptoms and signs of heart failure?

A

Symptoms

  • Breathlessness
  • Reduced exercise tolerance
  • Oedema
  • Fatigue

Signs

  • Cyanosis
  • Tachycardia
  • Elevated JVP
  • Displaced apex beat
  • Chest signs: classically bibasal crackles but may also cause a wheeze
  • S3-heart sound

The diagnostic workup for patients with AHF includes:

  1. Blood tests – this is to look for any underlying abnormality such as anaemia, abnormal electrolytes or infection.
  2. Chest X-ray – findings include pulmonary venous congestion, interstitial oedema and cardiomegaly
  3. Echocardiogram – this will identify pericardial effusion and cardiac tamponade
  4. B-type natriuretic peptide – raised levels (>100mg/litre) indicate myocardial damage and are supportive of the diagnosis.
67
Q

Where is BNP produced?

A

B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain.

Whilst heart failure is the most obvious cause of raised BNP levels any cause of left ventricular dysfunction such as myocardial ischaemia or valvular disease may raise levels. Raised levels may also be seen due to reduced excretion in patients with chronic kidney disease. Factors which reduce BNP levels include treatment with ACE inhibitors, angiotensin-2 receptor blockers and diuretics.

Clinical uses of BNP:

  1. Diagnosing patients with acute dyspnoea
    - A low concentration of BNP(< 100pg/ml) makes a diagnosis of heart failure unlikely, but raised levels should prompt further investigation to confirm the diagnosis.
    - NICE currently recommends BNP as a helpful test to rule out a diagnosis of heart failure.
  2. Prognosis in patients with chronic heart failure
    initial evidence suggests BNP is an extremely useful marker of prognosis.
  3. Guiding treatment in patients with chronic heart failure, effective treatment lowers BNP level.
68
Q

What is first degree heart block?

A

First-degree heart block

  • PR interval > 0.2 seconds
  • Asymptomatic first-degree heart block is relatively common and does not need treatment
69
Q

What is second-degree heart block

A

Second-degree heart block

  • Type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs
  • Type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex
70
Q

What is third-degree heart block?

A

Third-degree (complete) heart block

  • There is no association between the P waves and QRS complexes
71
Q

Which drugs are commonly used for pharmacological cardioversion of AF?

A

Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillation:

  1. Amiodarone
  2. Flecainide (if no structural heart disease)
  3. others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone

If pharmacological cardioversion has been agreed on clinical and resource grounds for new-onset atrial fibrillation, offer:

  • Flecainide or amiodarone if there is no evidence of structural or ischaemic heart disease or
    Amiodarone if there is evidence of structural heart disease.
72
Q

What are the ECG features seen in hypokalaemia?

A

ECG features of hypokalaemia:

  • U waves!
  • small or absent T waves (occasionally inversion)
  • prolong PR interval
  • ST depression
  • long QT
73
Q

What are 3 side effects of ACEi?

A

Side-effects:

  1. 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
  2. Angioedema: may occur up to a year after starting treatment
  3. Hyperkalaemia
  4. First-dose hypotension: more common in patients taking diuretics
74
Q

Which medications are used for rate control in AF?

A

Agents used to control rate in patients with atrial fibrillation:

Beta-blockers
- a common contraindication for beta-blockers is asthma

Calcium channel blockers

Digoxin

  • not considered first-line anymore as they are less effective at controlling the heart rate during exercise
  • however, they are the preferred choice if the patient has coexistent heart failure
75
Q

What is the correct ratio of chest compressions to ventilation?

A

Ratio of chest compressions to ventilation is 30:2

76
Q

What is the difference between crossmatching and group and save?

A

A crossmatch indicates that you will be giving the patient blood, whereas a group and save only saves the patient’s blood type for future reference and future blood transfusions. In this case, you need blood now, thus a crossmatch is the better option.

77
Q

What is the management for someone choking based on mild airway obstruction and severe airway obstruction?

A

Mild airway obstruction:

Response to question ‘Are you choking?’
- victim speaks and answers yes
Victim is able to speak, cough, and breathe

Severe airway obstruction

Response to question ‘Are you choking?’

  • victim unable to speak
  • victim may respond by nodding
  • victim unable to breathe
  • breathing sounds wheezy
  • attempts at coughing are silent
  • victim may be unconscious

If mild airway obstruction
- encourage the patient to cough

If severe airway obstruction and is conscious:

  • give up to 5 back-blows
  • if unsuccessful give up to 5 abdominal thrusts
  • if unsuccessful continue the above cycle

If unconscious

  • call for an ambulance
  • start cardiopulmonary resuscitation (CPR)
78
Q

What investigations are done for palpitations?

A

First-line investigations include:

  • 12-lead ECG: this will only capture the heart rhythm for a few seconds and hence is likely to miss episodic arrhythmias. However, other abnormalities linked to the underlying arrhythmia (for example a prolonged QT interval or PR interval, or changes suggesting recent myocardial ischaemia) may be seen.
  • Thyroid function tests: thyrotoxicosis may precipitate atrial fibrillation and other arrhythmias
  • Urea and electrolytes: looking for disturbances such as a low potassium
  • Full blood count

First-line investigations are often normal in patients complaining of palpitations. The next step is to exclude an episode arrhythmia.

The most common investigation is Holter monitoring

If no abnormality is found on the Holter monitor, and symptoms continue, other options include:

  • external loop recorder
  • implantable loop recorder
79
Q

When is PCI offered to patients in management of STEMI?

A

Offer primary PCI to all patients presenting within 12h of symptom onset with a STEMI who either are at or can be transferred to a primary PCI centre within 120 minutes of first medical contact.

If this is not possible patients should receive thrombolysis and be transferred to a primary PCI centre after the infusion for either rescue PCI (if there is residual ST elevation) or angiography (if successful).

Example: A patient who presents with a STEMI to a small DGH which does not have facilities for PCI. If they cannot be transferred to a larger hospital for PCI within 120 minutes then fibrinolysis should be given. If the patient’s ECG taken 90 minutes after fibrinolysis failed to show resolution of the ST elevation then they would then require transfer for rescue PCI.

80
Q

Management of STEMI briefly.

A

Management of STEMI:

MONAT

  1. Intravenous Morphine + IV anti-emetic, Metoclopramide to help relieve symptoms.
  2. Sublingual glyceryl trinitrate. Routine use now not recmmended in acute setting unless patient hypertensive or in acute LVF. Useful as anti-anginal in chronic/stable patients.
  3. Oxygen should only be given if the oxygen saturations are < 94%.
  4. Aspirin 300mg PO should be given to all patients (unless contraindicated).
  5. Second antiplatelet, Ticagrelor. (alternative; Prasugrel, clopidogrel)
    - If thrombolysis required because >2h then tissue plasminogen activator, Tenectaplase IV.
81
Q

Causes of atrial fibrillation?

A

PIRATES MNEMONIC

Pulmonary: PE, COPD
Iatrogenic
Rheumatic heart: Mitral regurgitation 
Atherosclerotic: CAD, MI
Thyroid: Hyperthyroid
Endocarditis
Sick sinus syndrome
82
Q

What are the causes of a narrow pulse pressure?

A

Narrow pulse pressure: less than 25 mmHg of difference between the systolic and diastolic blood pressure. Causes include:

  • Aortic stenosis
  • Congestive heart failure
  • Cardiac tamponade
83
Q

Causes of wide pulse pressure?

A

Wide pulse pressure: more than 100 mmHg of difference between systolic and diastolic blood pressure. Causes include aortic regurgitation and aortic dissection.

Medicine (21 decks)

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