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BNF Topics > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are the 4 classes of anti-arrhythmic drugs?

A

Class 1 - Membrane stabilising drugs (Na+ blockers) - Rhythm Control

Class 2 - Beta-blockers - Rate Control

Class 3 - K+ channel blockers - Rhythm Control

Class 4 - calcium-channel blockers (rate-limiting) - Rate Control

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2
Q

Give examples of Class 1 anti-arrhythmic drugs.

A

Rhythm Control

  • Disopyramide
  • Lidocaine
  • Flecainide / Propafenone (CI in asthma / severe COPD, avoid in structural / ischaemic heart disease)
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3
Q

Give examples of Class 2 anti-arrhythmic drugs.

A

Rate Control

  • Bisoprolol
  • Propranolol
  • Esmolol
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4
Q

Give examples of Class 3 anti-arrhythmic drugs.

A

Rhythm Control

  • Amiodarone - 4 weeks before and 12 months after electrical cardioversion to increase success.
  • Sotalol
  • Dronedarone
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5
Q

Give examples of Class 4 anti-arrhythmic drugs.

A

Rate-Control

  • Verapamil
  • Diltiazem
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6
Q

Give examples of other anti-arrhythmic drugs.

A
  • Adenosine

- Digoxin - effective in sedentary patients with non-paroxysmal AF and in patients with associative CHF.

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7
Q

What is AF?

A

Abnormal, disorganised electrical signals fired causing the atria to fibrilate (quiver) resulting in a rapid and irregular heartbeat.

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8
Q

What are the symptoms of AF?

A
  • Heart palpitations
  • Dizziness
  • SOB
  • Tiredness
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9
Q

What are the complications of AF?

A
  • Stroke

- HF

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10
Q

What are the types of AF?

A
  • Paroxysmal - episodes stop within 48 hours without treatment.
  • Persistent - episodes last >7 days.
  • Permanent - present all the time.
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11
Q

What is cardioversion?

A

Cardioversion is procedure which restores sinus rhythm. It uses a defibrillator device.

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12
Q

How is acute, new onset AF managed?

A

If the patient has life-threatening haemodynamic instability:
- Use electrical cardioversion.

If the patient does NOT have life-threatening haemodynamic stability:

  • <48 hours of symptoms - rate or rhythm control (cardioversion OR amiodarone / flecainide).
  • > 48 hours of symptoms - rate control (verapamil / beta-blocker).
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13
Q

Outline the pharmacological management of AF.

A
  • 1st-Line: Beta-blockers (not sotalol) / rate-limiting CCB / digoxin for rate control.1

Use monotherapy, then dual therapy, then consider rhythm control.

  • 2nd-Line: Rhythm control using Class 1/3 anti-arrhythmic.
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14
Q

What needs to be assessed in patients who have AF?

A

Risk of thromboembolic stroke and the risk of bleeding.

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15
Q

How is risk of thromboembolic stroke assessed for patients with AF?

A

CHA2DS2VASc Score

C = CHF / LVSD (Yes = 1)
H = HTN (Yes = 1)
A2 = Age 75+ (2)
D = Diabetes Mellitus (Yes = 1)
S2 = Stroke / TIA / VTE Hx (Yes = 2)
V = Vascular Disease (Yes = 1)
A = Age 65-74 (1)
Sc = Sex category (female = 1, male = 0)

Anticoagulation is indicated if score = 2+.

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16
Q

How is bleeding risk assessed for patients with AF?

A

HAS-BLED Score

H = HTN, >160mmHg systolic (1)
A = Abnormal liver / renal function (1)
S = Stroke Hx (1)
B = Bleeding Hx / predisposition (1)
L = Labile INR (1)
E = Elderly >65 (1)
D = Drugs, antiplatelet or NSAID use (1)
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17
Q

When should anticoagulation be given in patients with AF?

A

If the risk of thromboembolic stroke > risk of bleeding.

AND

CHA2DS2VASc score = 2+.

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18
Q

What is the choice of anticoagulant for AF?

A

New-onset AF = parenteral anticoagulant

Diagnosed AF = Warfarin / DOAC

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19
Q

What is ventricular tachycardia (VT)?

A

Quick, abnormal HR.

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20
Q

How is ventricular tachycardia managed?

A
  • Pulseless = immediate defibrilation and CPR
  • Unstable sustained VT = direct current cardioversion. If failed, IV amiodarone and repeat cardioversion.
  • Stable sustained VT = IV anti-arrhythmic (preferably amiodarone)
  • Non-sustained VT = beta-blocker
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21
Q

How is Torsades de pointes managed?

A

Magnesium sulfate.

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22
Q

What causes Torsades de pointes?

A
  • Drugs that cause QT interval prolongation..
  • HypOkalaemia.
  • Bradycardia.
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23
Q

What is paroxysmal supraventricular tachycardia?

A

A type of supraventricular tachycardia, named for its intermittent episodes of abrupt onset and termination. Often people have no symptoms but may include palpitations, feeling lightheaded, sweating, shortness of breath, and chest pain.

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24
Q

How is paroxysmal supraventricular tachycardia managed?

A
  1. Reflex vagal nerve stimulation.
  2. IV adenosine (CI in COPD / asthma).
  3. IV verapamil.

If the patient is haemodynamically unstable, cardioversion is required.

If there are recurrent episodes, catheter ablation or other anti-arrhythmics may be used.

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25
Q

What is the initial loading dose of amiodarone?

A 
200mg TDS for 7/7
THEN
200mg BD for 7/7
THEN 
200mg OD maintenance
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26
Q

Side-effects of amiodarone.

A

Eyes:

  • Corneal micro-deposits - advise patients it may cause night-time glares when driving.
  • Blindness - advise patient to stop taking if vision becomes impaired.

Skin:
- Phototoxicity - burning and erythema
- Slate-grey skin on light-exposed areas.
Advise patient to shield skin from light and use a high SPF for months after stopping.

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27
Q

What monitoring is required with amiodarone use?

A
  • Annual eye test
  • Chest x-ray before treatment
  • LFTs every 6 months
  • TFTs before treatment and every 6 months
  • BP and ECG (causes hypotension and bradycardia)
  • U&E’s (causes hypOkalaemia)
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28
Q

What is the half-life of amiodarone?

A

50 days.

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29
Q

Interactions of amiodarone.

A

Increased plasma amiodarone concentration
- Grapefruit juice (enzyme inhibitor)

Amiodarone is an enzyme inhibitor - increases plasma concentration of

  • Warfarin
  • Phenytoin
  • Digoxin (half dose)

Increased risk of myopathy
- Statins

Bradycardia, AV block and myocardial depression
- Anti-arrhythmics

QT prolongations

  • Quinolones
  • Macrolides
  • TCA’s
  • SSRI’s
  • Lithium
  • Quinine
  • Hydroxychloroquine
  • Anti-malarials
  • Antipsychotics

Due to half-life, there’s a danger of interactions for nearly 2 months after stopping.

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30
Q

What is the target plasma concentration of digoxin?

When should blood be taken to test levels?

A

1-2 mcg/L

Samples should be taken 6 hours following the previous dose of digoxin.

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31
Q

How does digoxin work?

A

Increases the force of myocardial contraction (positive inotrope).

Reduces conductivity in the AV node (negative chronotrope).

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32
Q

What monitoring is required for digoxin use?

A

Regular monitoring is not required during maintenance unless toxicity is suspected OR in renal impairment.

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33
Q

True or False - Digoxin does not require a loading dose.

A

False - loading doses are required due to long half-life of digoxin.

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34
Q

What is the maintenance dose of digoxin?

A

AF = 125-250mcg OD

Worsening / Severe HF (sinus) = 62.5-125mcg OD

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35
Q

What is the difference between bioavailability in different preparations of digoxin?

A

Elixir = 75%

Tablet = 90%

IV = 100%

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36
Q

What are the signs of digoxin toxicity?

A

SLOW & SICK

  • Bradycardia / heart block
  • N&V, diarrhoea and abdominal pain
  • Blurred or yellow vision
  • Confusion or delirium
  • Rash
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37
Q

When are patients at risk of developing digoxin toxicity?

A
  • HypOkalaemia
  • HypOmagnaesaemia
  • HypERcalcaemia
  • Hypoxia
  • Renal impairment
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38
Q

How is digoxin toxicity managed?

A
  • Withdraw digoxin use.
  • Correct electrolyte imbalances.
  • Digoxin-specific antibody (used in life-threatening ventricular arrhythmias unresponsive to atropine).
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39
Q

Digoxin interactions.

A

HypOkalaemia predisposes to toxicity:

  • Diuretics
  • Beta-2 agonists
  • Steroids
  • Theophylline
Increased plasma digoxin concentration = toxicity
- Amiodarone (half digoxin dose)
- Rate-limiting CCB
-Macrolides
- Ciclosporin
These drugs are enzyme inhibitors.

Decreased plasma digoxin concentration = subtherapeutic
- St. John’s Wort
- Rifampacin
These drugs are enzyme inducers.

Reduced renal excretion = toxicity

  • NSAIDs
  • ACE-i / ARB’s
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40
Q

Pneumonic to remember digoxin interactions?

A

CRASED

C = CCB
R = Rifampicin
A = Amiodarone
S = St. John's Wort
E = Erythromycin
D = Diuretics`
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41
Q

What are the 2 types of VTE?

A

1) Deep Vein Thrombosis - a blood clot occurring within a deep vein, usually in calf.
2) Pulmonary Embolism - detachment of a blood clot which travels to the lungs and blocks the pulmonary artery.

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42
Q

What are the risk factors for developing VTE?

A
  • Immobility
  • Obesity
  • Malignant disease
  • Age >60
  • Personal Hx of VTE
  • HRT / COC use
  • Pregnancy
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43
Q

What do you have to compare to VTE risk to assess whether VTE prophylaxis is required?

A

Bleeding risk:

  • Thrombocytopenia
  • Acute stroke
  • Bleeding disorders (acquired or inherited)
  • Anticoagulant use
  • Systolic HTN
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44
Q

What types of VTE prophylaxis are available?

A

1) Mechanical, e.g. compression stockings. FLOWTRONS.

2) Pharmacological - for high VTE risk. This may be using parenteral anticoagulants or DOACs.

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45
Q

How long is VTE prophylaxis required?

A

Depending on the indication:

  • General surgery = 5-7 days, or until sufficiently mobile.
  • Major cancer surgery in abdomen/pelvis - 28 days
  • Knee/Hip surgery - extended duration
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46
Q

What comprises VTE treatment?

A
  • LMBH / unfractioned heparin for at least 5 days and until INR >2 for at least 24 hours.
  • Start oral anticoagulant at the same time (usually warfarin).
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47
Q

What treatment should be used for VTE in pregnancy?

Why?

A

LMWH preferred due to lower risk of osteoporosis and heparin-induced thrombocytopenia. Stopped at labor.

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48
Q

How does heparin work?

A

Unfractioned heparin activates antithrombin.

LMWH inactivate factor Xa.

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49
Q

What LMWH are available?

A
  • Tinzaparin
  • Enoxaparin
  • Dalteparin
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50
Q

When would unfractioned heparin be preferred to LMWH’s?

A
  • High risk of bleeding

- Renal impairment

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51
Q

What needs to be monitored with heparin use?

A

APTT

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52
Q

What are the side-effects of heparin & LMWH’s?

A
  • Hemorrhage - withdraw use and if rapid reversal required, give protamine.
  • HypERkalaemia - inhibits aldosterone secretion. Monitor.
  • Osteoporosis.
  • Heparin-induced thrombocytopenia - occurs after 5-10 days. Shows as 30% reduction in platelets, skin allergy and thrombosis.
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53
Q

What other parenteral anticoagulants are available?

A
  • Heparinoid - used in thrombophlebitis, bruising and haematoma.
  • Argatroban - use for anticoagulation in patients with heparin-induced thrombocytopenia.
  • Hirudin
  • Heparin flushes - used to maintain patency of peripheral and central catheters.
  • Epoprostenol
  • Fondaparinux - used for patients unable to use animal products.
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54
Q

What is the mechanism of action of warfarin?

A

Antagonises the action of Vitamin K in blood clotting.

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55
Q

How long does it take for warfarin to work?

A

48-72 hours.

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56
Q

What is the initiation dose of warfarin?

A

5mg initially and monitored every 1-2 days.

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57
Q

What is the usual maintenance dose of warfarin?

A

3-9mg OD taken at the same time each day.

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58
Q

What monitoring is required with warfarin treatment?

A

INR every 3 months once stable.

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59
Q

What should the target INR be?

A

Depends on indication:

  1. 5 - VTE, AF, MI, Cardioversion, Bioprosthetic mitral valve
  2. 5 - Recurrent VTE
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60
Q

Important warfarin interactions.

A

Changes in INR:
- Direct-acting antivirals for chronic hepatitis C treatment

Increased risk of bleeding:
- Miconazole. Closely monitor if miconazole prescribed.

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61
Q

Warfarin side-effects.

A
  • Bleeding, e.g. node bleeds <10mins, bleeding gums, bruising.
  • Calciphylaxis (painful skin rash). Consider stopping if diagnosed. Increased risk in end-stage renal disease.
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62
Q

What is used to reverse the effects of warfarin in a major bleed?

A

Vitamin K (phytomenadione)

+

Dried prothrombin complex / Fresh Frozen Plasma

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63
Q

What should you do if a patient’s INR is 5.0-8.0 with no bleeding?

A
  • Withhold 1-2 doses.
  • Reduce maintenance dose.
  • Measure INR after 2-3 days.
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64
Q

What should you do if a patient’s INR is 5.0-8.0 with minor bleeding?

A
  • Omit warfarin.
  • IV Vitamin K.
  • Repeat if INR still high after 24 hours.
  • Restart warfarin when INR<5.0.
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65
Q

What should you do if a patient’s INR is >8.0 with no bleeding?

A
  • Omit warfarin.
  • IV Vitamin K.
  • Repeat if INR still high after 24 hours.
  • Restart warfarin when INR<5.0.
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66
Q

What should you do if a patient’s INR is >8.0 with minor bleeding?

A
  • Omit warfarin.
  • IV Vitamin K.
  • Repeat if INR still high after 24 hours.
  • Restart warfarin when INR<5.0.
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67
Q

When should warfarin be held before surgery?

A

Elective:

  • Stop 5 days before surgery.
  • Give oral Vitamin K for 1 day if INR>1.5.
  • Restart warfarin on evening or next day.

Emergency:

  • Delay surgery for 16-12 hours.
  • Delay not possible, give IV Vitamin K and dried prothrombin complex.

If high risk of VTE:
- If VTE in last 3 months, AF with previous stroke/TIA or mechanical valve, bridge therapy with LMWH (treatment dose) and stop 24 hours before surgery.

High risk of bleeding:
- Start LMWH 48 hours after surgery.

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68
Q

Which DOAC works by directly inhibiting thrombin?

A

Dabigatran.

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69
Q

Which DOAC’s work by directly inhibiting factor Xa?

A
  • Apixaban
  • Edoxaban
  • Rivaroxaban
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70
Q

What are the 2 types of stroke?

A

1) Ischaemic - blood clot obstructs blood supply to the brain.
2) Haemorrhagic - weak blood vessel in the brain bursts.

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71
Q

What is the long-term management of a TIA?

A

MR dipyridamole & aspirin & statin (irrespective of serum cholesterol)

Treat any HTN

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72
Q

What is the long-term management of an ischaemic stoke?

A

Clopidogrel & statin (irrespective of serum cholesterol)

In an AF-related stroke, review for an anticoagulant.

Treat any HTN.

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73
Q

How do antiplatelet drugs work?

A

Decrease platelet aggregation and inhibit thrombus formation in the arterial circulation.

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74
Q

Name the antiplatelet drugs.

A
  • Low-dose aspirin
  • Clopidogrel
  • Dipyridamole
  • Cangrelor
  • Prasugrel
  • Ticagrelor

The following are glycoprotein IIa/b inhibitors:

  • Abciximab
  • Eptifibatide
  • Tirofiban
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75
Q

Outline the HTN treatment pathway.

A

Aged < 55 years
Stage 1:
- ACEi / ARB
- If CI or not tolerated, use beta-blocker.

Stage 2:

  • Add CCB
  • If high-risk of HF or CCB CI or not tolerated, TLD.

Stage 3:
- ACEi/ARB + CCB + TLD

Stage 4:

  • Low-dose spironolactone / high-dose TLD if K>4.5.
  • If other diuretics are CI or ineffective, add alpha/beta-blocker.

Aged >55 / Afro-Carbbiean origin
Stage 1:
- CCB
- If high-risk of HF or CCB CI or not tolerated, TLD.

Stage 2:
- Add ACEi/ARB. ARB’s preferred in Afro-Caribbean patients.

Stage 3 & 4 as in those aged <55.

76
Q

What is considered ‘normal’ BP?

A

120/80 mmHg

77
Q

What are the stages of HTN?

A

Stage 1 = 140/90mmHg
Offer lifestyle advice. Only treat if patients are under 80 and have target organ damage, CVD or a CVD risk >20%, renal disease or diabetes.

Stage 2 = 160/100 mmHg. Treat all patients.

Stage 3 = >180 systolic > 110 diastolic.

78
Q

What are the clinic BP targets?

A

Under 80:

  • <140/90
  • <130/80 in CVD / diabetes with kidney, eye or cerebrovascular disease.

Over 80:
- <150/90

Renal disease:

  • <140/90
  • <130/80 in CKD, diabetes, proteinuria >1g/24 hours.

Diabetic:

  • <140/80
  • <130/80 if complications with kidney, eye or cerebrovascular disease.

Pregnancy:

  • <150/100 for chronic HTN
  • <140/90 - chronic HTN and if target organ damage or given birth.
79
Q

What medications are commonly used to treat gestational HTN?

A

1st-Line: Labetalol

Methyldopa (stopped 2 days after birth).

MR Nifedipine (unlicensed).

80
Q

How do ACEi’s work?

A

Inhibit the conversion of angiotensin I to II.

They also inhibit the breakdown of bradykinin.

81
Q

How do ARB’s work?

A

Block the angiotensin receptor preventing the action of angiotensin II.

They do not breakdown bradykinin.

82
Q

Name the common ACEi’s.

A
  • Enalapril
  • Lisinopril
  • Perindopril (30-60mins before food)
  • Ramipril

All are taken OD (except captopril - BD) with first dose taken at bedtime.

83
Q

Name the common ARB’s.

A
  • Candesartan
  • Irbesartan
  • Losartan
  • Telmisartan
  • Valsartan
84
Q

Side-effects of ACEi’s.

A
  • Persistent dry cough - ARB’s can be given as an alternative.
  • HypERkalaemia - higher risk in renal impairment and diabetes.
  • Angioedema
  • Nephorotoxic in AKI and reduces eGFR via efferent arteriole dilation.
  • Hepatic effects - cholestatic jaundice and hepatic failure. Stop if liver transaminases 3x normal, or jaundice occurs.
  • Oral ulcers
  • Taste disturbance
  • HypOglycaemia
85
Q

True or False - ACEi’s are safe to use in pregnancy.

A

False - they should be avoided.

86
Q

Important interactions for ACEi’s.

A

HypERkalaemia:

  • Aliskeren
  • ARB’s
  • K-sparing diuretics / aldosterone antagonists

Nephrotoxicity
- NSAIDs

87
Q

Why can ARB’s be given to patients who experience a dry cough with ACEi’s?

A

ARB’s do not break down bradykinin as ACEi’s do (which causes the cough).

88
Q

What are the centrally-acting anti-hypertensives?

A
  • Methyldopa - side-effects= drowsiness.
  • Clonidine - side-effects = flushing.
  • Moxonidine
89
Q

What are the vasodilator anti-hypertensives?

A
  • Hydroxyzine - side-effects=fluid retention and tachycardia.
  • Minoxidil - side-effects=tachycardia, fluid retention and increased cardiac output.
90
Q

What are the alpha-blockers used in HTN?

A
  • Doxazosin
  • Prazosin
  • Terazosin
  • Indoramin
91
Q

How do beta-blockers work?

A

Block the beta-adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas and liver.

92
Q

What are the 4 types of beta-blockers?

A

1) Intrinsic sympathomimetic activity. They result in less bradycardia and less coldness of the extremities.
2) Water-soluble. They’re less likely to cross the BBB and therefore cause less nightmares and sleep disturbances.
3) Cardio-selective. They cause less bronchospasm and are the ones that should be used in patients with well-controlled asthma (if no other choice available).
4) Intrinsically long duration of action allowing for once-daily dosing.

93
Q

Pneumonic to remember beta-blockers with intrinsic sympathomimetic activity.

A

PACO

P = Pindolol
A = Acebutol
C = Celiprolol
O = Oxprenolol
94
Q

Pneumonic to remember water-soluble beta-blockers.

A

CANS

C = Celiprolol
A = Atenolol
N = Nadolol
S = Sotalol
95
Q

Pneumonic to remember cardio-selective beta-blockers.

A

Be A MAN

Be = Bisoprolol
A = Atenolol
M = Metoprolol
A = Acebutol
N = Nebivolol
96
Q

Pneumonic to remember beta-blockers with intrinsic long duration of action.

A

BACoN

B = Bisoprolol
A = Atenolol
Co = Celiprolol
N = Nadolol
97
Q

Side-effects of beta-blockers.

A
  • Bradycardia & hypOtension

- HypERglycaemia / hypOglycaemia. Masks signs of hypO’s.

98
Q

In what patients are beta-blockers CI?

A
  • Asthma - causes bronchospasm.
  • Worsening unstable HF.
  • 2nd/3rd degree heart block.
  • Severe hypotension and bradycardia.
99
Q

Important beta-blocker interactions.

A

Asystole and hypOtension:
- Verapamil injection

HypERglycaemia
- TLD (avoid in diabetes / high risk of diabetes)

100
Q

How do CCB’s work?

A

Block calcium channels to reduce the force of contraction, conductivity and vascular tone.

101
Q

What are the 2 types of CCB? Give examples of each type.

A 
Dihydropyridine CCB:
Cause vasodilation. These include:
- Amlodipine
- Felodipine
- Lacidipine
- Lercanidipine
- Nifedipine (maintained by brand)

Rate-limiting CCB: Avoided in HF. These include:

  • Verapamil
  • Diltiazem
102
Q

Important interactions for CCB.

A

Increased CCB concentration:

- Grapefruit juice (avoid).

103
Q

What is phaechromocytoma?

A

A rare tumor of adrenal gland tissue. It results in the release of too much adrenaline and noradrenaline that control HR, metabolism, and BP.

104
Q

What drugs are used to manage HTN caused by phaechromocytoma?

A

Beta-blocker + phenoxybenzamine (alpha-blocker).

105
Q

How do vasoconstrictor sympathomimetics work?

Give examples.

A

Raise BP transiently by acting on alpha-adrenergic receptors to constrict peripheral blood vessels.

  • Noradrenaline
  • Phenylephrine
106
Q

What are the side-effects of vasoconstrictor sympathomimetics?

A

Reduced perfusion to vital organs.

107
Q

What are the symptoms of HF?

A
  • Dyspnoea during activity or at rest.
  • Exercise intolerance / fatigue.
  • Oedema - pulmonary (resulting in breathlessness) and peripheral (resulting in swollen ankles and legs).
108
Q

Outline the NICE Guidelines for treatment of Chronic HF.

A

Stage 1:
ACEi/ARB + Beta-blocker
- ARB licensed for HF = candesartan / valsartan
- For mild-moderate HF aged >70 = nebivolol
- For all grades of LVSD = bisoprolol / carvedilol.
Alternatives include hydralazine + isosorbide dinitrate (specialist use)

Stage 2:
Add Spironolactone.
- Eplerenone may be used after acute MI with LVSD or mild HF.
Alternatives inclue:
- Hydralazine+ isosorbide dinitrate (especially in Afro-Caribbean)
- ARB (only with ACEi if no other option)
- Entresto (sacubutril + valsartan) if LVEF<35% and taking stable dose of ACEi/ARB.

Stage 3:
Add Ivabridine for patients in sinus rhythm and HR>75bpm.
OR
Add digoxin for worsening or severe HF (doesn’t reduce mortality).

109
Q

What treatment should be given to patients with HF with fluid overload?

A
  • Add on loop diuretics.

- Add on thiazide diuretics in mild HF (if eGFR>30ml/min).

110
Q

What is hyperlipidaemia?

A

High levels of cholesterol, triglycerides or both.

111
Q

When is primary prevention required?

A
  • Type 1 diabetes
  • Type 2 diabetes if CVD risk >10%
  • QRISK score > 10%
  • CKD or albuminuria
  • Familial hypercholesterolaemia
  • > 85 to reduce the risk of non-fatal MI
112
Q

When is secondary prevention required?

A

In established CVD

113
Q

What is the diagnostic level for diagnosis of hyperlipiaemia?

A

Total cholesterol >6mmol/L

114
Q

What are the target cholesterol levels for healthy adults?

A

Total Cholesterol = <5mmol/L

LDL = <3mmol/L

HDL = >1mmol/L

Triglycerides = <1.7mmol/L

115
Q

What are the target cholesterol levels for high risk adults?

A

Total Cholesterol = <4mmol/L

LDL = <2mmol/L

HDL = >1mmol/L

Triglycerides = <1.7mmol/L

116
Q

What can cause hyperlipidaemia?

A

Drugs:

  • Antipsychotics
  • Immunosuppressants
  • Corticosteroids
  • Antiretroviral

Conditions:

  • HypOthyroidism
  • Liver / kidney disease
  • Diabetes
  • Family Hx of high cholesterol
  • Lifestyle factors: smoking, excess alcohol consumption, obesity and poor fatty diet.
117
Q

What are the different classes of lipid-regulating drugs?

Give examples.

A

Statins

  • Atorvastatin
  • Pravastatin
  • Simvastatin

Fibrates

  • Bezafibrate
  • Ciprofibrate
  • Fenofibrate

Ezetimibe

Bile Acid Sequestrants

  • Colesevelam
  • Colestyramine

Nicotinic Acid Group
- Nicotinic Acid

118
Q

What is the mechanism of action of statins?

A

Reduces LDL synthesis by the live via inhibition of HMG-CoA reductase (indirectly reducing triglycerides and increasing HDL).

119
Q

Which statins must be taken at night?

Why?

A
  • Pravastatin
  • Simvastatin
  • Fluvastatin (excluding MR)

They should be taken at night as they have shorter durations of action than atorvastatin and rosuvastatin. Cholesterol synthesis is greater at night therefore enhancing their effect.

120
Q

When are high-intensity statins use?

A

To prevent CVD.

121
Q

What are the doses of high-intensity statins?

A

Atorvastatin - choice of statin

  • Primary prevention = 20mg OD
  • Secondary prevention = 80mg OD

Rosuvastatin = 10mg OD

Simvastatin = 80mg OD
- MHRA warning surrounding risk of myopathy. Only give if high risk of CV complications or severe hypercholesterolemia and treatment goals not achieved at lower doses.

122
Q

What is the 1st-line treatment for hyperlipidaemia?

A

Statins.

For hypercholesterolemia, if statins are CI or not tolerated, ezetimibe should be used.

For moderate hypertriglyceridaemia, if statins are CI or not tolerated, fibrates may be used.

In severe hyperlipidaemia, ezetimibe may be used in conjunction with statins. If triglycerides are still high after LDL reduced, add a fibrate or nicotinic acid.

123
Q

What should be considered before starting statin therapy for hyperlipidaemia?

A

Secondary causes of dyslipidaemia.

124
Q

Side-effects of statins.

A

Myopathy, myositis and rhabdomyolysis
- Patients should be counselled to report tender, weak or painful muscles.

Interstitial lung disease
- Patients should be counselled to report SOB, cough and weight loss.

Diabetes
- Statins can raise HbA1c or blood glucose levels.

125
Q

In which patients is there a higher risk of muscle toxicity when taking a statin?

A
  • Personal or family Hx or muscle disorder.
  • High alcohol intake.
  • Renal impairment.
  • HypOthyroidism.

Increased risk of myopathy with concomitant use of ezetimibe or fibrates.

126
Q

What monitoring is required for patients taking statins?

A
  • Baseline lipid profile
  • Renal function
  • Thyroid function
  • HbA1c if at high risk of developing diabetes
  • Monitor for severe muscle symptoms and discontinue.
  • Creatine kinase should be measured in symptoms of muscle pain. Discontinue if levels 5x normal. If levels return to normal and symptoms resolve, statin can be reintroduced at lower dose / alternative statin used and monitor.
  • LFTs - discontinue if transaminases 3x normal.
127
Q

Important interactions of statins.

A

Increased statin levels = increased myopathy risk:

  • Amiodarone
  • Grapefruit juice
  • CCB’s
  • Imidazole/triazole antifungals

Macrolide antibiotics
- Counsel patients to stop taking statin until antibiotic course is completed.

Fusidic Acid (PO):
- Restart statin 7 days after last dose.
128
Q

What dose adjustments are required for statins due to interactions?

A

Simvastatin:

  • Max 10mg OD with fibrate.
  • Max 20mg OD with amiodarone / amlodipine / diltiazem / verapamil.

Atrovastatin:
- Max 10mg OD with ciclosporin.

Rosuvastatin
- Initially 5mg, max 20mg OD with clopidogrel.

129
Q

True or False - Statins are teratogenic.

A

True - effective contraception during and 1 month after stopping treatment is required.

Statins should be stopped 3 months before conceiving and restarted after breastfeeding has finished.

130
Q

What is the mechanism of action of ezetimibe?

A

Reduces blood cholesterol by inhibiting the absorption of cholesterol by the small intestine.

131
Q

What is the mechanism of action of fibrates?

A

Lowes blood triglyceride levels by reducing the liver’s production of VLDL (the triglyceride-carrying particle that circulates in the blood) and by speeding up the removal of triglycerides from the blood.

132
Q

What is the mechanism of action of bile acid sequestrants?

A

They bind and sequester bile acids.

Cholesterol is used by the body to make bile acids, thereby reducing the amount of LDL circulating.

133
Q

Important interactions of bile acid sequestrants.

A

Impaired absorption of fat-soluble vitamins.

- Take other drugs 1 hour before or 4 hours after.

134
Q

What types of nitrates are available?

A
  • Short-acting

- Long-acting

135
Q

Give examples of short-acting nitrates.

A
  • Glyceryl trinitrate

- Isosorbide dinitrate (S/L)

136
Q

Give examples of long-acting nitrates.

A
  • MR Isosorbide dinitrate

- Isosorbide mononitrate

137
Q

What are short-acting nitrates used for?

A

Acute angina attacks.

138
Q

What are long-acting nitrates used for?

A

Long-term prophylaxis of angina.

139
Q

What medications (excluding nitrates) are used for the long-term prophylaxis of angina?

A
  • Beta-blockers
  • CCB’s
  • Ivabradine
  • Ranolazine
  • Nicorandil
140
Q

How does GTN work?

A

It’s converted to nitric oxide, a short-acting vasodilator, improving blood supply.

141
Q

What formulations of GTN are available?

A

Sublingual tablet and sublingual spray.

142
Q

How long does the effect of GTN last?

A

20-30 minutes.

143
Q

When would long-term prophylaxis of angina be indicated (based on GTN use)?

A

If GTN is used more than x2 a week.

144
Q

What are the storage requirements for GTN sublingual tablets?

A

Kept in a special container which expires 8 weeks after opening.

145
Q

When should patients use GTN?

A

PRN / before angina-inducing activities.

146
Q

How should patients use GTN?

A

Sitting down (to prevent dizziness).

147
Q

How many doses of GTN should patients use before calling 999 (if pain persists)?

A

Max. 3 doses 5 minutes apart.

148
Q

What is the treatment guideline for angina prophylaxis?

A

1st-Line: Beta-blocker / CCB (e.g. diltiazem).
2nd-Line: Beta-blocker + dihydrophyridine CCB

If either or both of 2nd-line are CI, add/use a vasodilator:

  • Long-acting nitrate
  • Ivabradine (if normal sinus rhythm)
  • Ranolazine
  • Nicorandil (risk of ulcer complications)
149
Q

What is the mechanism of action of nitrates?

A

Potent vasodilators and reduce venous return and cardiac output.

150
Q

When does nitrate tolerance develop?

A

With use of long-acting preparations or transdermal patches.

151
Q

How is nitrate tolerance avoided?

A

Limit blood nitrate concentrations for 4-12 hours a day by either:

1) Leaving patches off for 8-12 hours (overnight).
2) Taking 2nd dose of MR ISDN / ISMN after 8 hours, not 12 hours.
3) Take MR ISMN OD.

152
Q

What are the side-effects of nitrates?

A

Vasodilation: flushing, throbbing headache, dizziness, postural hypotension, tachycardia, dyspepsia & heartburn.

153
Q

Why should abrupt withdrawal of nitrates be avoided?

A

Worsens angina symptoms.

154
Q

What are the acute coronary syndromes.

A
  • Myocardial infarction: NSTEMI & STEMI

- Unstable angina

155
Q

What should be given for acute treatment of ACS?

A

1) Oxygen if patient is hypoxic.
2) GTN / IV ISDN for ischaemic pain. IV diamorphine/morphine with metoclopramide may be used for pain relief.
3) Reperfusion with aspirin 300mg + clopidogrel 300mg.
3) Prevent re-occlusion and embolisation with a parenteral anticoagulant.

156
Q

What is the long-term management post-MI?

A

SAAB:

S = Statin (secondary prevention dose)

A = ACEi/ARB

A = Aspirin indefinitely

B = Beta-bloker

157
Q

If used as part of DAPT following MI, how long should clopidogrel be continued for?

A

NSTEMI / Angina = 12 months

STEMI = 4 weeks

158
Q

When may you use clopidogrel indefinitely instead of aspirin post-MI?

A
  • If aspirin is CI or not tolerated.

- If the patient has had a PCI and also has an indication requiring anticoagulation.

159
Q

When may you use prasugrel or ticagrelor as part of DAPT following MI?

A

If the patient has had a PCI.

160
Q

True or False - Ticagrelor can be used with aspirin as part of DAPT post-MI instead of clopidogrel.

If so, when can it be used?

A

True.

It can be used if patients are at high risk of a further event - it should only be stopped when clinically indicated, or at a maximum of 3 years.

161
Q

What thrombolytic medications are available?

When can they be used?

A

Thrombolysis can be used to break down a thrombus post-MI or during an ischaemic stroke:

  • Streptokinase - within 12 hours of MI onset.
  • Alteplase - within 6-12 hours of MI onset, or within 4.5hours of stroke onset.
  • Reteplase - not really used.
  • Tenecteplase - within 6 hours of MI onset.
162
Q

How often should IV adrenaline be given for patients in cardiac arrest?

Why is it used?

A

Every 3-5 minutes.

It’s a sympathomimetic ionotrope use for cardiogenic shock.

163
Q

What should be given to a patient in cardiac arrest if there is ventricular fibrillation present?

A

IV amiodarone

164
Q

What class of drugs is used to relieve oedema?

A

Diuretics

165
Q

When should diuretics be taken? Why?

A

In the morning to avoid sleep disruption (from waking to urinate).

166
Q

How do diuretics work in general?

A

They increase urine output by the kidneys, i.e. promote diuresis by inhibiting sodium reabsorption at different parts of the nephron.

167
Q

How do loop diuretics work?

What is their onset and duration of action.

A

Inhibit the Na/Cl co-transporter in the ascending Loop of Henle.

They have a 1 hour onset and 6 hour duration of action.

168
Q

Give examples of loop diuretics.

In what conditions can they be used?

A
  • Bumetanide (most potent) - resistant HTN
  • Torasemide (musculoskeletal pain) - - resistant HTN
  • Furosemide - - resistant HTN & HF
169
Q

What are the main side-effects of loop diuretics?

A
  • Ototoxicity
  • Acute urinary retention (therefore cautioned in BPH)
  • Hyperglycaemia (caution with use in diabetes)
  • Hyperuricaemia (displayed with furosemide use - caution in gout)
  • HypO K / Na / Cl / Mg (alcoholic cirrhosis)
  • HypER Ca
170
Q

How do thiazide-like diuretics work?

What is their onset and duration of action?

A

Inhibit the Na/Cl co-transporter in the distal convoluted tube.

They have a 1-2 hour onset and 12-24 duration of action.

171
Q

Give examples of thiazide-like diuretics.

In what conditions can they be used?

A
  • Bendroflumethiazide - HF and HTN
  • Indapamide (causes less hypERglycaemia) - HTN
  • Metolazone - HTN & HF
172
Q

What are the main side-effects of thiazide-like diuretics?

A
  • GI disturbances
  • Impotence
  • High LDL / triglycerides
  • Hyperglycaemia (caution with use in diabetes)
  • Hyperuricaemia (displayed with furosemide use - caution in gout)
  • HypO K / Na / Cl / Mg (alcoholic cirrhosis)
  • HypER Ca
173
Q

When are thiazide-like diuretics ineffective?

A

If eGFR<30ml/min (except metolazone).

174
Q

How do potassium-sparing diuretics work?

A

Promote diuresis without the loss of potassium by inhibiting the sodium channels in the distal convoluted tubule. They are weak diuretics used in conjunction with loop/thiazide-like diuretics.

175
Q

Give examples of potassium-sparing diuretics.

A
  • Triamterene (can cause blue urine)

- Amiloride

176
Q

What are the main side-effects of potassium-sparing diuretics?

A

HypERkalaemia.

177
Q

How do aldosterone antagonist diuretics work?

A

Inhibits aldosterone (which causes sodium reabsorption via the Na/K/H co-transporter). Less K & H ions are exchanged fro sodium and are therefore lost to the urine.

178
Q

Give examples of aldosterone antagonist diuretics.

A
  • Spironolactone

- Eplerenone

179
Q

What are the main side-effects of spironolactone?

A
  • Gynaecomastia, benign breast tumours and menstrual disturbances
  • Hypertrichosis
  • Change in libido
  • HypERkalaemia, hypERuraemic, hypOnatraemia
180
Q

What does the MHRA warning around the use of aldosterone antagonists and ACEi/ARB’s suggest?

A

When used in HF, there’s a potential risk of fatal/severe hypERkalamia. Monitoring of U&E’s is essential.

181
Q

How do osmotic diuretics work?

A

Inhibit sodium and water reabsorption by increasing the osmolarity of blood and renal filtrate. They act on the water permeable parts of the nephron: proximal convoluted tubule and the descending limb of the Loop of Henle.

182
Q

Give an example of an osmotic diuretic.

When can it be used?

A

Mannitol - used in cerebral oedema and high ICP.

183
Q

What is peripheral vascular disease (PVD)?

What are the 2 types?

A

A slow and progressive circulation disorder caused by narrowing, blockage, or spasms of any blood vessel outside of the heart including the arteries, veins, or lymphatic vessels.

The 2 types are:

1) Occlusive
2) Vasospastic

184
Q

What is used to treat occlusive PVD?

A

Aspirin 75mg OD + statin (secondary prevention dose)

185
Q

What is used to treat vasospastic PVD?

A

Stopping smoking and avoid exposure to cold.

For Raynaud’s syndrome - nifedipine.

BNF Topics (11 decks)

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