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1

alpha blockers

a -adrenoceptor antagonists ( alpha blockers)


EXAMPLES
Doxazosin, prazosin, tamsulosin, alfuzosin


MECHANISMOFACTION
Inhibit a1 -adrenoceptors in arterioles, thereby reducing tone of vascular smooth muscle and reducing total peripheral resistance. Inhibition of a 1 -adreno- ceptors in periurethral prostatic stroma results in relaxation of internal urethral sphincter and some relief of obstructive urinary symptoms in males.

INDICATIONS
.

  1. Hypertension (i.e. doxazosin, particularly in resistant cases as part of polytherapy)
  2. Benign prostatic hyperplasia


CAUTIONS AND CONTRA-INDICATIONS
Caution in patients with a susceptibility to heart failure

SIDE-EFFECTS

  1. Dizziness
  2. Postural hypotension
  3. Weakness and fatigue
  4. Reflex tachycardia
  5. Headache
  6. Dry mouth
  7. Ejaculatory failure

METABOLISM AND HALF-LIFE
Variable – e.g. doxazosin (t ½ 22h) extensively metabo-
lised by liver; alfuzosin (t ½ 3–5h) partially metabolised.
MONITORING
May cause severe first-dose hypotension therefore need to start at low dose
and warn patient of side-effects.
DRUG INTERACTIONS
Enhanced hypotensive effect with antihypertensives and alcohol


IMPORTANT POINTS
.
Centrally acting a2 -adrenoceptor agonists (e.g. clonidine, alpha-methyldopa) also have an
antihypertensive effect (mediated via suppression of the vasomotor centre in the brain).
These agents are rarely used due to infrequent but potentially severe adverse effects (alpha-
methyldopa may cause hepatitis BUT is safe in pregnancy)

2

Adenosine

Stimulates A1 receptors of cardiac cells influencing adenosine-sensitive-K+channels and cAMP production. Causes prolonged AVN conduction.

INDICATIONS

  1. Rapid reversal of SVT to sinus rhythm
  2. SVT with aberrant conduction

CAUTIONS AND CONTRA_INDICATIONS

  1. 2nd and 3rd degree AV block
  2. Sick sinus syndrome
  3. Prolonged QT syndrome
  4. Severe hypotension
  5. Decompensated HF
  6. Asthma

SIDE EFFECTS

  1. Chest tightness
  2. Dyspnoea
  3. Bronchospasm
  4. Nausea
  5. Severe Brady
  6. Light-headedness

3

Aldosterone antagonists

Spironolactone, eplerenone

Antagonist of intracellular aldosterone receptors in renal tubules. Indirectly reduces activity of Na+/K+ ATPase >> reduces K+ loss and increases Na+ loss

INDICATIONS

  1. Congestive HF
  2. Oedema and ascieties in liver disease
  3. Post-MI Heart failure
  4. Nephrotic syndrome
  5. Primary hyperaldosteronism (Conn's)

 

SIDE EFFECTS

  1. Hyperkalemia
  2. GI disturbance
  3. Anti-androgenic effects

4

AMIODARONE

Inhibits Na+/K+ATPases in myocardium. Prolongs action potentials and refractory period, slows AVN conduction and SAN function

INDICATIONS

  1. paroxysmal SVT
  2. Nodal and ventricular tachy
  3. Atrial fibrillation and flutter
  4. VF
  5. Tahyarrhythmias associated with WPW?? NOOO

 

CAUTIONS

  1. THyroid dysfunction
  2. Sinus brady
  3. Sinus block

SIDE EFFECTS

  1. Photosensitive rash
  2. Skin discolouration
  3. Brady
  4. Thyroid function disturbance
  5. Corneal deposits
  6. Pulmonary fibrosis
  7. Torsades de pointes

5

ACEI

Ramipril, lisinopril, perindopril

 

MECHANISMOFACTION

Inhibit angiotensin-converting enzyme, preventing the conver- sion of  angiotensin I to angiotensin II.This prevents angiotensin II-mediated effects(arteriolar constriction and aldosterone release) resulting in reduced afterload and reduced circulating volume, thereby reducing BP.


INDICATIONS
.

  1. Hypertension
  2. Heart failure (result in improved survival in LV dysfunction)
  3. Prophylaxis of further cardiovascular events post-MI
  4. Diabetic nephropathy (lisinopril - results in reduced progression of disease)
  5. Patients at high cardiovascular risk (ramipril)

CAUTIONS AND CONTRA-INDICATIONS
.

  1. Hypersensitivity to ACEIs
  2. Pregnancy
  3. Renal artery stenosis (reversal of angiotensin II-mediated constriction of efferent arterioleresults in reduced GFR)
  4. Caution in peripheral vascular disease as this may be associated with  undiagnosed renalartery stenosis

SIDE-EFFECTS
.

  1. Persistent dry cough
  2. Hypotension (may get severe first-dose hypotension)
  3. Renal impairment
  4. Hyperkalaemia
  5. Angioedema (rare)

MONITORING
Monitor U&Es for renal impairment prior to and 1–2 weeks after commencing treatment.Once stable on therapy U&Es must be checked at least annually. Careful clinical monitoring is required when used in severe heart failure.


DRUG INTERACTIONS
.

  1. Risk of profound first-dose hypotension with loop diuretics and enhanced hypotensive effect with other antihypertensive agents
  2. Increased risk of renal impairment with NSAIDs .
  3. Enhanced hypoglycaemic effect of insulin, metformin and sulfonylureas
  4. Effects are antagonised by corticosteroids

IMPORTAN TPOINTS
.
ACEIs/ARBs are less effective in African–Caribbean patients due to ACE polymorphisms

6

ANTIMUSCARINICS

ATROPINE, hysocine, procyclidine

They block Muscarinic receptors (ACh antagonists)

MECHANISMOFACTION
Antimuscarinics act as competitive antagonists of A Choneffector cells by blocking specific muscarinic receptors (e.g. atropine blocks cardiac M 2 receptors).
Their therapeutic action stems mainly from inhibition of smooth muscle contraction and
glandular tissue innervated by postganglionic cholinergic neurones.

INDICATIONS

  1. Bradycardia (atropine)
  2. Mydriasis and cycloplegia
  3. Parkinsonism (procyclidine)
  4. Symptomatic relief of GI or GU muscle spasm (hyoscine)
  5. Urinary incontinence (see Oxybutynin, p.97)

CAUTIONS AND CONTRA-INDICATIONS

  1. Myasthenia gravis
  2. Paralytic ileus
  3. Pyloric stenosis
  4. Prostatic enlargement


SIDE-EFFECTS

  1. Constipation
  2. Urinary retention
  3. Dry mouth
  4. Blurred vision
  5. Drowsiness

METABOLISMANDHALF-LIFE
Highlyvariable–t ½  foratropine is 2–4h and it is metabolised by the liver to inactive metabolites; t ½ for hyoscine is 5h;t ½ for procyclidine is 12h
MONITORING
Administration of atropine requires cardiac and blood pressure monitoring.
DRUGINTERACTIONS

Increased sedative effect when hyoscine given with alcohol


IMPORTANT POINTS

Hyoscine may be used for GI colic and excessive respiratory secretions in end-of-lifecare .It is also used to reduce respiratory secretions during anaesthesia

Atropine is used as part of the Resuscitation Council UK guidelines for symptomatic
bradycardia and in cardiac arrests when pulseless electrical activity is below 60 complexes
per min

7


Beta blockers

Atenolol, propranolol, bisoprolol, carvedilol, sotalol (mixed class II/III actions), labetalol (can be used IV for hypertension and in pregnancy), nebivolol


MECHANISMOFACTION
Block activation of b -adrenoceptors (predominantly
mediated through b 1 antagonism) thereby reducing exertionally-induced rise in heart rate and reducing cardiac contractility. This reduces systolic BP and myocardial O 2 demand.


INDICATIONS
.

  1. Angina
  2. Arrhythmias
  3. Hypertension
  4. Heart failure (bisoprolol and carvedilol only)
  5. Prophylaxis post-MI
  6. Migraine prophylaxis
  7. Thyrotoxicosis
  8. Anxiety

CAUTIONSANDCONTRA-INDICATIONS
.

  1. Asthma
  2. Uncontrolled heart failure
  3. Bradycardia, sick sinus syndrome, second or third degree heart block
  4. Hypotension/cardiogenic shock
  5. Severe peripheral arterial disease

SIDE-EFFECTS
.

  1. Bronchospasm
  2. Fatigue
  3. Cold peripheries
  4. Bradycardia and hypotension
  5. Sleep disturbances
  6. Reduced glucose tolerance
  7. Hyperkalaemia
  8. Sexual dysfunction in males
  9. Dizziness and headache
  10. Heart block

DRUG INTERACTIONS
.

  1. Enhanced hypotensive effects with antihypertensives and alcohol
  2. Hypotensive effect antagonised by NSAIDs, steroids and oestrogens
  3. May mask warning signs of hypoglycaemia in diabetics
  4. Increased risk of AV block and heart failure with verapamil and diltiazem


IMPORTANTPOINTS
.

  1. Cardioselectivity: atenolol, bisoprolol and nebivolol have less effect on b 2 receptors and therefore reduced bronchospasm
  2. Lipid solubility: atenolol and sotalol are most water-soluble therefore less able to cross blood–brain barrier resulting in less sleep disturbance
  3. Half-life: atenolol, bisoprololandcarvedilol havelongerdurationofactionhenceonly needto be taken once daily

8

IONOTROPIC SYMPATHOMIMETICS

Adrenaline, dopamine, dobutamine, isoprenaline

MECHANISMOFACTION
Actions vary depending on which receptors are stimulated.
Adrenaline acts on a -(peripheral vasculature) and b -adrenoceptors (myocardium),producing positive inotropic and chronotropic effects.

Low-dose dopamine and dobutamine stimulate b
1 -adrenoceptors in the myocardium, predominantly increasing contractility.


INDICATIONS

  1. Cardiogenic shock
  2. Septic shock
  3. Acute hypotension
  4. Cardiac arrest (adrenaline)


CAUTIONS AND CONTRA-INDICATIONS
.

  1. Phaechromocytoma (dopamine)
  2. Atrial and ventricular tachyarrhythmias (dobutamine)

SIDE-EFFECTS
.

  1. Nausea and vomiting
  2. Hypotension/hypertension
  3. Peripheral vasoconstriction
  4. Tachycardia


MONITORING
Continuous cardiac monitoring in a high-dependency area is required.
Monitoring of oxygen saturation, urine output and renal function is also necessary

DRUGINTERACTIONS
.
Adrenaline should not be used with other sympathomimetic agents due to the additive effect
Hypertensive crisis when given in combination with MAOIs
Hypertension and reflex bradycardia when given in combination with b-blockers


IMPORTANT POINTS
.
In patients with septic or haemorrhagic shock, volume must be replaced (though this may
worsen cardiogenic shock), after which sympathomimetics may be required to improve
cardiac output
.
Often used in the intensive care setting to maintain perfusion to vital organs
.
Adrenaline is used as part of the Resuscitation Council UK guidelines

9

Vasoconstrictor sympathomimetics

Noradrenaline, ephdrine, phenylephrine

 

Stimulate peripheral alpha adrenoreceptors, causing vasoconstiriction and increased both SBP and DBP

 

10

Ca2+ blockers

EXAMPLES
Dihydropyridines (nifedipine, amlodipine, felodipine),

diltiazem, verapamil


MECHANISM OF ACTION
Block L-type Ca 2+
channels to reduce influx of Ca2 + into cells and
thereby reduce contraction of myocytes. Dihydropyridines are highly vascular selective and cause peripheral and coronary vasodilatation. Verapamil and diltiazem are less selective and act directly on cardiac tissue to reduce cardiac contractility and slow conduction at the AV node.


INDICATIONS
1. Hypertension
2. SVT (verapamil and diltiazem)
3. Prophylaxis of angina
4. Raynaud’s phenomenon (dihydropyridines only)
5. Cluster headache prophylaxis (verapamil)

CAUTIONS AND CONTRA-INDICATIONS
1. Cardiogenic shock or hypotension
2. LVF (verapamil and diltiazem)
3. Second or third degree heart block (verapamil and diltiazem)
4. Bradycardia (verapamil and diltiazem)
5. Unstable angina (dihydropyridines)

SIDE-EFFECTS
1. Bradycardia (verapamil and diltiazem)
2. Reflex tachycardia (dihydropyridines)
3. Hypotension
4. Vasodilatory effects (flushing, headache, ankle swelling, palpitations)
5. Constipation (verapamil)
6. Heart failure (verapamil)

METABOLISM AND HALF-LIFE
All extensively metabolised in liver. for dihydropyridines is highly variable.

MONITORING
No specific drug monitoring required.

DRUG INTERACTIONS
Enhanced hypotensive effects with antihypertensives and alcohol
IncreasedriskofAVblock,bradycardia,severehypotensionandheartfailureifverapamilor
diltiazem are given with b blockers
Plasma concentration of some CCBs are increased by grapefruit juice

IMPORTANT POINTS
Verapamil and diltiazem are Vaughan Williams class IV anti-arrhythmics
Vascularselectivity of different CCBs is explained by voltage dependence; dihydropyridines are inactive at the hyperpolarised membrane potentials of the myocardium during diastole. Verapamil and diltiazem are less voltage dependent and hence less selective

 

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