Angina Flashcards

1
Q

Stable angina

Sub-lingual GTN- Mechanism of action

A
  • Nitrates are converted to NO
  • NO increases cGMP synthesis and reduces Intracellular Ca2+ in vascular smooth muscle= relaxation and vasodilation
  • This reduces cardiac work and myocardial oxygen demand by improving perfusion to cardiac muscle
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2
Q

GTN spray- Adverse effects

A
  • Flushing
  • Headache
  • Hypotension
  • Tolerance
  • Don’t use overnight- increase side effects (NOT needed)
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3
Q

GTN- Contraindications

A
  • Severe Aortic Stenosis- cause cardiovascular collapse
    • This is because the heart is unable to increase cardiac output sufficiently through the narrow valve area to maintain pressure
  • Haemodynamic instability
  • Hypotension
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4
Q

GTN- important interactions

A
  • Phosphodiesterase inhibitors (Sildenafil)
    • because of the enhanced hypotensive effect
  • Anti-HTN- use with caution
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5
Q

GTN- Communication

A
  • Explain that you are prescribing a nitrate to relieve chest pain and or breathlessness
  • May develop a headache when starting but should go
  • Better at preventing than terminating angina pain, take before tasks that can bring on angina
  • Because of postural Hypotension- it is a good idea to advise them to sit down and rest before and 5 minutes after taking GTN spray
  • Tolerance can occur- make sure there is a nitrate free period every day during a time of inactivity (overnight)
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6
Q

Beta blockers

A

See atrial fibrillation

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7
Q

Calcium channel blockers

Common indications

A
  1. All Calcium channel blockers can be used to control symptoms in people with stable angina, BB are the main alternative
  2. Amlodipine is used for HTN
  3. Diltiazem and verapamil are used to control cardiac rate in people with supraventricular arrhythmias including supraventricular tachycardia, atrial flutter and AF
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8
Q

Calcium channel blockers

MOA

A
  • CCB decrease Ca2+ entry into vascular and cardiac cells, reducing the intracellular calcium concentration
  • This causes relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure
  • In the heart, CCB reduce Myocardial contractility
  • Suppression cardiac conduction, particularly across the AV node, slowing ventricular rate
  • Reduced cardiac rate, contractility and afterload reduce myocardial oxygen demand preventing angina
  • CCB can broadly be divided into two classes. Dihydropyridines, including amlodipine and nifedipine, is relatively selective for the vasculature, whereas non-dihydropyridines are more selective for the heart. Of the non-dihydropyridines, verapamil is the most cardioselective, whereas diltiazem also has some effects on the vessels.
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9
Q

CCB

Warnings

A
  • Poor left ventricular function as they worsen HF
  • AV nodal conduction delay in whom they may provoke complete heart block
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10
Q

CCB

Interactions

A
  • Non-dihydropyridine- should not be prescribed with a BB as both classes are negatively inotropic and chronotropic and together may cause HF, bradycardia and asystole
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11
Q

CCB

Communication

A
  • MR and SR should be swallowed whole and not crushed or chewed
  • Common side effects- ankle oedema
    *
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12
Q

CCB

Monitoring

A
  • Treatment efficacy can be judged by regular BP monitoring for HTN, enquiry about chest pain for angina and by pulse rate from examination or ECG
  • A 24-hour tape can be performed to review arrhythmias
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13
Q

Nicorandil

Common indications

A
  • For prevention and treatment of chest pain in people with stable angina
  • First choice treatments for stable angina are BB and CCB
  • These may be used if the other drugs can not be tolerated
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14
Q

Nicorandil

MOA

A
  • Nicorandil causes both arterial and venous vasodilation through its action as a nitrate (see nitrate) and by activating K-ATP channels
  • Efflux of K through K/ATPase channels leads to hyperpolarisation of the cell membrane and subsequent inactivation of voltage-gated Ca2+ channels
  • The net effect is a decrease in free intracellular calcium
  • As Ca is required for smooth muscle contraction, relaxation and vasodilation occur
  • The effect of this is to reduce cardiac preload and systematic and coronary vascular resistance
  • This improves myocardial perfusion and decreases myocardial work as well as oxygen demand
  • Clinically, this reduces the frequency and severity of angina attacks
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15
Q

Nicorandil

Warnings

A
  • You should not prescribe nicorandil for patients with poor:
    • Poor Left ventricular function
    • Hypotension
    • Pulmonary oedema
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16
Q

Nicorandil
Interactions

A
  • As with nitrates, the hypotensive side effects of nicorandil are significantly enhanced by phosphodiesterase inhibitors
  • They should not be prescribed together
17
Q

Nicorandil

Communication

A
  • Reduce attacks of chest pain
  • Warn patient not to drive or use heavy machinary until angia symptoms are controlled and side effects of nicorandil, including dizziness and hypotension have settled
18
Q

Ranalozine

Indications

A
  • Adjunctive therapy in the treatment of stable angina in patient inadequately controlled by first-line antianginal therapies
19
Q

Ranolazine

MOA

A
  • Largely unknown
  • Some antianginal effect is by inhibition of the late sodium current in cardiac cells
  • This reduces intracellular sodium accumulation and consequently decreases intracellular calcium overload
  • Reduction in cellular calcium overload is expected to improve myocardial relaxation and thereby decrease left ventricular diastolic stiffness
  • Also significantly shortens QTc interval
20
Q

Ranolazine

Warnings

A
  • Contraindicated in
    • Hypersensitivity
    • Severe renal impairment (<30mL/min)
    • Moderate-severe hepatic impairment
  • Cautioned in
    • Elderly
    • Low body weight (<60kg)
    • Patients with moderate to severe CHF
21
Q

Ranolazine

Adverse effects

A

*

22
Q

Ranolazine

Interactions

A
  • CYP inhibitors (Azoles, Clarithromycin, Diltiazem, Ciclosporin, Verapamil, Grapefruit)
  • CYP inducers (Rifampicin, CBZ, Phenytoin, STW, Phenobarbital)
  • Digoxin- increase in dig concentration meaning levels should be monitored on initiation and termination of treatment
  • Statin- Increase statin concentration, increase risk of rhabdo
  • Ciclosporin, sirolimus, tacrolimus-
23
Q

Ivabradine

Indications

A
  • Treatment of angina in patients in normal sinus rhythm
  • Mild to severe chronic HF
24
Q

Ivabradine

MOA

A
  • Pure HR lowering agent
  • Selective and specific inhibition of cardiac pacemaker If current that controls the spontaneous diastolic depolarisation in the sinus node and regulates HR
  • Cardiac effects are specific to the sinus node
  • Ivabradine can also interact with the retinal Ih which resembles cardiac If
  • Patients can get phosphenes- described as transient enhanced brightness in a limited area of the visual field
  • NB- reduce cardiac work, O2 consumption, No inotropic effect
25
Q

Ivabradine

Warnings- contraindications

A
  • Hypersensitivity
  • Resting HR <70 bpm
  • Cardiogenic shock
  • Acute MI
  • Severe Hypotension (<90/50mmHg)
  • Severe hepatic dysfunction
  • Sino-atrial block
  • Unstable angina
  • CYP inhibitors
  • Pregnancy/breastfeeding
  • HF
26
Q

Ivabradine

Cautions

A
  • AF
  • Other arrhythmias
  • Elderly
  • Stop if no symptom improvement in angina
  • hypotension
  • Retinitis pigmentosa
  • Intraventricular conduction defects
27
Q

Ivabradine

Adverse effects

A
  • Tranient luminous phenomena (Phosphenes) - NB- counsel around driving
  • Bradycardia
  • AV block
  • Different arrhythmias
  • Uncontrolled `BP
    *
28
Q

Ivabradine

Interactions

A
  • QT prolonging medicinal products
  • CYP inhibitors
  • CYP inducers
  • Verapamil/Diltiazem- contra-indicated
29
Q

Ivabradine

Monitoring

A
  • ECG- AF
  • HR
  • BP
  • Monitor for visual disturbances
30
Q
A