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Cardiovascular drugs Flashcards

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1
Q

Drugs which reduce ventricular dimension

A

Nitrovasodilators e.g. glyceryl nitrate, isosorbide mononitrate, amyl nitrate.

These relax smooth muscle and preferentially affect veins. Leads to increase in venous capacitance with small falls in arteriolar resistance. This reduces the heart size

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2
Q

Drugs given to reduce arterial pressure

A

Ca2+ channel blockers: Nifedipine, Diltiazem, Verapamil

Work by reducing Ca2+ influx through VG-Ca2+ channels in peripheral vasculature. Leads to relaxation of resistance vessels and a fall in TPR.

Heart has to pump against a lower pressure so the work of the heart is reduced.

Ca2+ channel antagonists also prevent calcium entry in coronary vessels and may prevent vaso-spasm

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3
Q

Drugs given to reduce heart rate

A

Beta blockers - slow the heart rate and attenuate increase in heart rate in respone to exercise and stress

Ivabradine - slows the heart by inhibiting If ion channels in the SA node but does not affect contractility of ventricles. Used in patients intolerant of beta blockers

Ca2+ channel blockers - slow the heart rate by reducing Ca2+ entry into pacemaker cells.

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4
Q

Name three inotropic drugs

A

Adrenaline / Noradrenaline: Directly stimulates ß1-adrenergic receptors

Sympathomimetics (e.g. Dobutamine): Directly stimulates ß1-adrenergic receptors

Phosphodiesterase inhibitors (e.g. Milrinone): Inhibit breakdown of cAMP, increasing intracellular cAMP levels
Also cause vasodilation of peripheral arterioles

Digoxin: Inhibits Na+-K+ ATPase, reducing removal of Ca2+ from cell by Na+/Ca+ exchanger, increasing Ca2+ storage in sarcoplasmic reticulum. On the next contraction there is increased Ca2+ released into cell from SR.

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5
Q

Management of stable angina

A

Acute attacks - GTN

Long term -
First line: beta blocker or calcium channel blocker

If not tolerated: Long acting nitrate, ivabradine, nicorandil, ranolazine

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6
Q

Treatment for unstable angina

A

Antiplatelt treatment asap. Aspirin (clopidogrel 2nd line)

Antithrombin treatment: Heparin or direct thrombin inhibitor

Nitrates

Oxygen if evidence of hypoxia

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7
Q

Treatment of a patient with NSTEMI

A

Pain relief: morphine, anti-emetic

Aspirin: to reduce risk of further clot formation

Rapid transfer to hospital - treat as MI

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8
Q

Treatment immediately following MI

A

Rapid admission to coronary care unit

Early clot-busting treatment (PTCA, thrombolysis)

Aspirin (anti-platelet)

Beta blockers

Prevent thrombo-embolism

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9
Q

Treatment for acute heart failure

A

Morphine IV

Oxygen

Nitrates (IV GTN)

Inotropes (dolbutamine, milrinone)

Diuretics (furosemide)

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10
Q

Nice guidelines for the mangement of HF

A

HF with preserved ejection fraction - manage comorbidites e.g. high bp, heart disease, diabetes

HF with ventricular dysfunction: Offer ACEi and beta-blockers. If symptoms persist add aldosterone antagonist, hydralazine with nitrates. If symtoms persist consider digoxin.

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11
Q

Name four broad classes of drugs used in the treatment of heart failure

A

Vasodilator drugs

Positive inotropes

Beta blockers

ACE inhibitors/ARBs

Aldosterone antagonists

Diuretics

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12
Q

Drug interventions to prevent recurrent MI

A

anti-platelet treatment - prevent clotting (Clopidogrel/Aspirin or warfarin)

ACE-inhibitors/ARBs - reduce fluid retention

Beta blockers - reduce heart rate, reduce blood pressure

Statins - reduce cholesterol

Lifestyle interventions: Diet, weight reduction, stop smoking

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13
Q

Main groups of drugs used to lower blood pressure

A
  • Diuretics
  • Beta-adrenoceptor blockers
  • Calcium channel blockers
  • Angiotensin converting enzyme (ACE) inhibitors
  • Angiotensin receptor blockers
  • Alpha-adrenoceptor blockers
  • Direct renin inhibitors
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14
Q

Name 3 clot-busting drugs

A

Streptokinase

urokinase

tPA

reteplase

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15
Q

beta-blockers mechanism of action

A

reduce exercise-induced rise in heart rate and recides cardiac contractlily.

This resudes systolic BP and myocardial O2 demand

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16
Q

Side effects of beta blockers

A

Bronchospasm

Bradycardia and hypotension

Hyperkalemia

Sexual dysfunction (males)

Heart block

Cold peripheries (acts of b3Rs)

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17
Q

Name 4 beta blockers

A

Atenalol

Propanlol

Bisoprolol

Labetalol

Sotalol

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18
Q

Use of beta blockers in hypertension

A

Atenolol: cardioselective (b1)
Propanolol: non-selective (b1,b2)

Decrease cardiac output and prevent fatal arrhythmias, heart attack and stroke. Also blocks adrenal system (sympathetic innervation direct to adrenal gland)

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19
Q

Why are beta blockers used in heart failure

A

Bisoprolol, carvedilol

Beta blockers reduce the contractility of the heart and reduce heart rate by blocking the sympathic nervous system. This redues the work of the heart which is benefical in heart failure.

Not to be used in acute HF.

Side effects: bradycardia, hypotension, bronchospasm, impotence

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20
Q

Indications for beta-blockers

A

Angina

Arrythmias

Hypertension

heart failure (bisoprolol, carvedilol)

Prophylaxis post-MI

Migraine prophylaxis

Thyrotoxicosis

Anxiety

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21
Q

Classification of blood pressure in adults

A

Normal: 120-140 systolic, 80-90 diastolic

Mild: 140-150 systolic, 90-100 diastolic

Moderate: 160-180 systolic, 100-110 diastolic

Severe: >180 systolic, >120 diastolic

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22
Q

Use of beta-blockers as anti-arrythmics

A

Attenuate effect of sympathetic system. Can be used with digoxin to control ventricular response in AF.

Also used in management of SVT

Esmolol

Sotalol

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23
Q

Cardioselective beta-blockers

A

Atenolol

Bisoprolol

Nebivolol

Reduced bronchospasm with these drugs

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24
Q

Mechanism of nitrovasodilators

A

Broken down or metabolised to nitric oxide in endothelial cells. This activates guanylate cyclase in vascular smooth muscle to cause an increase in cGMP, reducing [Ca}i and causing vascular relaxation.

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25
Administration or nitrates in angia
GTN: given sublingually, when swallowed undergoes extensive first pass metabolism in the liver and is inactive. When sucked it is rapidly absorbed in the buccal mucosa into the systemic circulation. Action within 1-2mins that lasts for 15-20mins Isosorbide mononitrate: sublingual or oral. Isosorbide DI-nitrate is converted to mononitrate in the liver by first pass metabolism. Long acting drugs that last for several hours. Some patients may develop tolerance rapidly
26
Side effects of nitrovasodilators
Vascular headaches as a result of dilation of the muscular intracranial arteries. Reflex tachycardia in response to vasodilation which offsets some of the benefit of the drugs. Postural hypotension Potential for dilating sites of atheroma leading to further reduction in coronary circulation Prolonged exposure to nitrates results in tolerance. vsmc becomes resistant to dilator effects and following withdrawal may result in abnormal constriction.
27
Preparations of GTN
Short-acting tablets/sprays Parenteral (nitrocine, nitronal, GTN) Transdermal (minitran, deponit)
28
Nicorandil mechanism of action
Drugs that open K-ATP channels in vascular smooth muscle. This hyperpolarises the cell, closing Ca2+ channels. Low Ca2+ causes vessel relaxation. More targeted towards arteries and arterioles which have a higher smooth musle tone. May also cause headaches, flushing and dizziness. Used in conjuction with beta blockers to limit reflex tachycardia
29
Ranolazine
Used to treat angina Blocks late inward sodium currents in cardiomyocytes. In ischemic myocardium, late inward sodium currents contribute to an elevation in [Na]i which increases [Ca]i via the Na/Ca exchanger. Ca2+ overload in ishemic cells leads to impaired relaxation and compresses microcirculation in the walls of the ventricle. Coronary blood flow is reduced and ischemia worsens. Blocking late inward sodium currents reduces Ca levels, therefore stress on the heart and improves coronary flow.
30
Chemical classes of calcium channel blockers
Dihydropyridines: nifedipine, amlodipine (arterioselective - vascular effects, relaxes arteries and increases excretion of Na+ and water but increases HR) Benzothiazepine: diltiazem (cardioselective, relaxes arteries, decreases HR and SV) Phenylalkalamine: verapamil (cardioselective, relaxes arteries, decreases HR and SV)
31
Cardioselective calcium channel blockers
Verapamil and diltiazem Side effects: Heart failure Heart block Peripheral oedema Constipation Facial flushing, headaches
32
Calcium channel blockers mechanism of action
Block L-type Ca2+ channels to reduce Ca2+ influx into cells. Causes: vascular smooth muscle relaxation decreased myocardial force generation decreased heart rate natriuresis & diuresis
33
Side effects of Ca2+ channel blockers
Heart: Bradycardia, Oedema, Heart failure, Arterial pressure: Flushing, headaches, ankle swelling, reflex tachycardia (nifedipine only), hypotension
34
Clinical use of Ca2+ channel blockers
Hypertension SVT (verapamil, diltaizem) Angina prophylaxis Raynaud's (dihydropyridines) Cluster headaches
35
Side effects of dihydropyridines
Marked facial flushing Headaches Peripheral oedema Polyuria (exacerbate prostatism)
36
Action of cardiac glycosides e.g. digoxin
Blocks the Na+/K+-ATPase. Results in increased intracellular Na+ Ca2+ exchanged for Na+ via exchanger Less Ca2+ is removed from the cell because the exchanger is inhibited by the concentration gradient This increases contraction
37
Contraindications for clot-busting drugs
Previous harmorrhagic stroke Recent major surgery Peptic ulceration/internal bleeding Oesophageal varices Pregnancy Any stroke within 6 months
38
Risks of using streptokinase
Re-perfusion arrhythmia Development of neutralising antibodies (no re-use after 1 year of treatment) Allergic reaction Not to be used if patient has had recent streptococcal infection.
39
Vasodilator drugs used in heart failure
Nitrates e.g. isosorbide mononitrate: Relxaes smooth muscles in veins and arteries Reduces CVP and afterload. Can be used acutely to treat pulmonary oedema and acuteHF (IV GTN) Side effects - hypotension, dizziness, headaches, flushing Hydralazine: unknown mechanism. Dilates arteries and arterioles to reduce afterload. Given comined with ISMN. Side effects - tachycardia and lupus-like syndrome hydralazine + nitrates particularly given to afro-caribbeans with HF.
40
Positive inotropes used in heart failure
b1-agonists (Dolbutamine IV): used in acute management of HF. Side effects - increases myocardial O2 demand, tachycardia, hypertension, arrhythmia, headache PDE inhibitors (Milronone IV): inhibits cAMP breadown, potentiation sympathetic effects. used in short term management. Side effects: hypotension, ventricular tachycardia, headache Cardiac glycosides (Digoxin): inhibits Na+/K+ATPase to increase [Ca2+]i store. Contraindication: hypokalemia. Side effects: **yellow-green halos,** gynaecomastia, arrhythmias All increase force of contraction of the heartto increase CO. None recommended as routine treatment.
41
ACE inhibitors used in heart failure
ACEi: ramipril. Blocks formation of angiotensin II. Reduces vascular resistance, restores tissue perfusion, reduces afterload, reduces aldosterone production. Side effects: **dry cough,** hypotension, hyperkalemia ARB: losartan. Inhibits action of angiotensin II. Same effects as ACEi. Side effects: hypotension, renal impairment, hyperkalemia, angioedema
42
Diuretics used in heart failure
Diuretics used to treat the symptoms of HF but no evidence treatment prolongs life. Loop diuretics: furosemide. Inhibits luminal Na+/K+/Cl- transporter in the thick ascending limb of the loop of Henle. Increases water excretion. Early venodilator effect which reduces preload (useful in pulmonary oedema). Side effects: Low K+ and Na+, hypotension, dehydration Thiazide diuretics: bendroflumethiazide. Inhibits Na+/Cl- cotransporter in the DCT to increase Na+ and water excretion. Side effects: Low K+, low Ca2+, hypotension, dehydration
43
Aldosterone antagonists used in heart failure
Spironolactone: Blocks action of aldosterone at DCT o increase Na+ and water exretion. Very effective if combined with ACEi/ARB. Side effects: gynaeocomastia, hyperkalemia, hypernatremia Eplerenone: Often used for post-MI heart failure.
44
When is digoxin used in the treatment of heart failure
Treatment for cadiac failure with atrial fibrillation or severe congestive heart failure not responding to initial medical treatment. ## Footnote Digoxin (cardiac glycoside) increases the force of contraction by inhibiting the Na/K-ATPase. This increases [Na]i and reduces the amount of Ca2+ pumped out of the cell. As [Ca2+]i increases force of contraction increases. Loss of [K+]i reduces the membrane potenial, slowing cardiac conduction and increasing the refractory period at the AV node.
45
Toxic effects of cardiac glycosides
Raised [Ca2+]i can result in arrhythmias, ectopic beats followed by VT or VF. AV block may produce nausea, vomitng and confusion.
46
Why should digoxin not be given with loop diuretics?
Digoxin is a competitive inhibitor of K+, act on the same site at the Na+/K+ pump. If extracellular K+ is high, digoxin will be less effective, low K+ enhances effects. Loop diuretics cause a reduction in plasma K+ levels and therefore potentiates it's effects (lack of competition). Leads to loss of K+ and arrhythmias.
47
Diuretics used in hypertension
Thiazides, loop diuretics, K+-sparing diuretics
48
Use of thiazides in hypertension
Thiazides are the most powerful anti-hypertensives (e.g. bendroflumethiazide). Preferred as they are weak and long acting. They act at the DCT and inhibit the Na/Cl co-transporer in the luminal membrane. Increased Na+ and water is excreted and K+ secretion is increased. Reduced blood volume reduces filling of the heart Adverse effects: hypokalemia (muscle weakness), hyponatremia (causes confusion) hyperuricaemia (gout), raised glucose and cholesterol
49
K+-sparing diuretics in hypertension
Produce mild diuresis and cause excretion of 2-3% sodium. Used in combination with other drugs, useful in excess aldosterone. Contraindicated in renal patients * Spironolactone: aldosterone antagonist. Competitive antagonist of receptor and reduces Na+ absorption and therefore K+ and H+ secretion * Triamterene and Amiloride: Ep Na+ channel blocker. Block Na+ reabsorption by principal cells, reducing membrane potential and reducing K+ secretion. Decreased H+ secretion. Side effects: High K+ and low Na+ Interact with ACEi to increase hyperkalemia. Aldosterone similar to oestrogen, causes gynaecomastia.
50
Adverse effects of angiotensin II
Excess Ang II stimulates NADPH oxidase to produce superoxide Superoxide is a potent oxygen free radical Oxidation by superoxide impairs protein & DNA function Superoxide also inactivates nitric oxide:
51
Action of ACEi
Inhibit the formation of angiotensin II, also inhibit the breakdown of bradykinin (vasodilator) Side effects: Dry cough Angioedema Hyperkalemia Contraindicated in asthmatics
52
Why are ACEi and ARBs contraindicated in renal artery stenosis?
Patients with bilateral renal artery stenosis may experience renal failure if ARBs are administered. The reason is that the elevated circulating and intrarenal angiotensin II in this condition constricts the efferent arteriole more than the afferent arteriole within the kidney, which helps to maintain glomerular capillary pressure and filtration. Removing this constriction by blocking angiotensin II receptors on the efferent arteriole can cause an abrupt fall in glomerular filtration rate.
53
Action of ARBs
Receptor antagonists that block type 1 angiotensin II (AT1) receptors on blood vessels and other tissues such as the heart. These receptors are coupled to the Gq-protein and IP3 signal transduction pathway that stimulates vascular smooth muscle contraction
54
Alpha-adrenoreceptor blockers
α1-adrenoceptor antagonists cause vasodilation by blocking the binding of norepinephrine to the smooth muscle receptors. Non-selective α1 and α2-adrenoceptor antagonists block postjunctional α1 and α2-adrenoceptors, which causes vasodilation. Alpha-blockers dilate both arteries and veins because both vessel types are innervated by sympathetic adrenergic nerves; however, the vasodilator effect is more pronounced in the arterial resistance vessels.
55
Class 1 anti-arrhythmic drugs
Block Na+ channels 1a: Block open channels. Delay depoarisation. Lengthens action potential e.g. quinidine 1b: Blocks Na+ channels in actively depolarising cells. Action potential is shortened. e.g. lignocaine 1c: Slow depoarisation and conduction speed. No change in duration of the action potential e.g. flecainide
56
Class 2 anti-arrhythmics
Block beta-adrenoreceptors Act on SA node to block the pacemaker potential. Slows the heart rate. Also reduce force of contractions by reducing [Ca]i i. e. Used in atrial fibrillation e. g. bisoprolol, propanolol
57
Class 3 anti-arrhythmic drugs
Block K+ channels. Delay repolarisation, action potential prolonged e.g. Amiodarone
58
Class 4 anti-arrhythmic drugs
Block Ca2+ channels. Myocytes: Reduce amplitude of the action potential and shorten the plateau phase. Force of contraction reduced (negatively inotropic) Pacemaker cells: reduces rate of firing e.g. Verpamil
59
Treatment of SVTs
Adenosine Verapamil Amiodarone Flecanide
60
Action of atropine on the heart
Speeds up the heart rate Blocks muscarinic Ach receptors in the SA and AV node. Reduces parasympathetic effects, so the heart beats faster. side effects: dry mouth, urinary retention, dilated pupils
61
Main contraindication for verapamil
Do not give with beta-blockers. Risk of hypotension and asystole
62
Treatment of ventricular arrhythmias
IV lidocaine in VT (if patient haemodynamically stable) Also use amiodarone, flecanide
63
Dobutamine
Inotropic sympathomimetic Acts on b1R in cardiac muscle to increase cotnracility, little effect on rate. Used in treatment of shock Other sympathetomimetics - dopaine, dopexamine

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