Treatment
of Heart Failure: ABCDE
ACE
inhibitors
Beta-blockers
Calcium
channel blockers
Diuretics
Endothelin-converting
enzyme inhibitors
ACE inhibitors- for the treatment of hypertension & congestive
heart failure. inhibit angiotensin-converting enzyme (a component of the blood
pressure-regulating renin-angiotensin
system), thereby decreasing the tension of blood vessels and blood volume, thus lowering
blood pressure. perindopril, captopril, enalapril, lisinopril, and ramipril.
Sulfhydryl-containing
agents
- Captopril -the first ACE inhibitor
- Zofenopril
Dicarboxylate-containing
agents
- Enalapril
- Ramipril )
- Quinapril
- Perindopril
- Lisinopril
- Benazepril
- Imidapril
- Trandolapril
Phosphonate-containing
agents
- Fosinopril
Use-
- Acute myocardial infarction (MI, heart attack)
- Cardiac failure (left ventricular systolic dysfunction)
- Renal complications of diabetes mellitus (Diabetic nephropathy)
Adverse effects- hypotension, cough, hyperkalemia, headache, dizziness, fatigue, nausea, and renal impairment.
Contraindications-
- Previous angioedema associated with ACE inhibitor therapy
- Renal artery stenosis (bilateral or unilateral with a solitary functioning kidney)
- Hypersensitivity to ACE inhibitors
Beta-blockers- target the beta receptor. Beta
receptors are found on cells of the heart
muscles, smooth
muscles, airways, arteries, kidneys, and other tissues that are part
of the sympathetic nervous system and lead to stress responses,
especially when they are stimulated by epinephrine (adrenaline).
Beta blockers block the action of endogenous catecholamines epinephrine
(adrenaline) and norepinephrine
(noradrenaline) in particular, on β-adrenergic
receptors, part of the sympathetic nervous system, which mediates the fight-or-flight
response. Three types of beta receptors are known, designated β1,
β2 and β3 receptors.
β1-adrenergic receptors are located mainly in the
heart and in the kidneys.
β2-adrenergic receptors are located mainly in the
lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and
skeletal muscle.
β3-adrenergic receptors are located in fat cells.
Nonselective agents
- Alprenolol
- Bucindolol
- Carteolol
- Carvedilol
- Labetalol
- Nadolol
- Oxprenolol
- Penbutolol
- Pindolol
- Propranolol
- Sotalol
- Timolol
- Eucommia bark (herb)
β1-selective
agents
Also known as cardioselective
- Acebutolol
- Atenolol
- Betaxolol
- Bisoprolol
- Celiprolol
- Esmolol[49]
- Metoprolol
- Nebivolol (also increases nitric oxide release for vasodilation)
β2-selective
agents
- Butaxamine (weak α-adrenergic agonist activity): No common clinical applications, but used in experiments.
- ICI-118,551: Highly selective β2-adrenergic receptor antagonist—no known clinical applications, but used in experiments due to its strong receptor specificity.
β3-selective
agents
- SR 59230A (has additional α-blocking activity): Used in experiments.
Uses-
- Angina pectoris
- Atrial fibrillation
- Cardiac arrhythmia
- Congestive heart failure
- Essential tremor
- Glaucoma
- Hypertension
- Migraine prophylaxis
- Mitral valve prolapse
- Myocardial infarction
- Phaeochromocytoma, in conjunction with α-blocker
- Postural orthostatic tachycardia syndrome
- Symptomatic control (tachycardia, tremor) in anxiety and hyperthyroidism
- Theophylline overdose
Adverse
drug reactions
nausea, diarrhea, bronchospasm, dyspnea, cold extremities,
exacerbation of Raynaud's
syndrome, bradycardia,
hypotension, heart failure, heart block, fatigue,
dizziness, alopecia (hair loss),
abnormal vision, hallucinations,
insomnia, nightmares, sexual
dysfunction, erectile
dysfunction and/or alteration of glucose and lipid metabolism.
Contraindications-They should also be avoided in patients with a history of cocaine use or in cocaine-induced tachycardia.
Calcium channel
blockers- antihypertensive
drugs. Calcium channel blockers (CCBs)are also frequently used to
alter heart rate, to prevent cerebral
vasospasm, and to reduce chest pain caused by angina pectoris.
CCBs used as medications primarily have three
effects:
- by acting on vascular smooth muscle they reduce contraction of the arteries and cause an increase in arterial diameter, a phenomenon called vasodilation (CCBs do not work on venous smooth muscle)
- by acting on cardiac muscles (myocardium), they reduce the force of contraction of the heart
- by slowing down the conduction of electrical activity within the heart, they slow down the heart beat.
Dihydropyridine
Dihydropyridine calcium channel blockers are derived from the molecule dihydropyridine and often used to reduce systemic vascular
resistance and arterial pressure. Dihydropyridine calcium channel blockers can
worsen proteinuria in patients with nephropathy.Amlodipine Nifedipine
Side
effects of these drugs may include but are not limited to:
- Dizziness, headache, redness in the face
- Fluid buildup in the legs and ankle edema
- Rapid heart rate
- Slow heart rate
- Constipation
- Gingival overgrowth
Non-dihydropyridine
Phenylalkylamine
Phenylalkylamine calcium channel blockers are relatively selective for myocardium,
reduce myocardial oxygen demand and reverse coronary vasospasm, and are often
used to treat angina.
- Verapamil
- Gallopamil
- Fendiline
Benzothiazepine
Diltiazem (also used experimentally to prevent migraine)
Ziconotide
Ziconotide, a peptide compound derived from the omega-conotoxin, is a selective N-type calcium channel
blocker that has potent analgesic properties that are equivalent
to approximate 1,000 times that of morphine.
Toxicity
Caution should be taken when using verapamil
with a Beta blocker due to the risk of severe bradycardia. If unsuccessful, ventricular pacing should be
used
Diuretics- diuretics are used to treat heart failure, liver cirrhosis, hypertension and certain kidney diseases. Some diuretics, such as acetazolamide, help to make the urine
more alkaline and are helpful in increasing excretion of substances
such as aspirin in cases of overdose or poisoning.
Adverse effects
The
main adverse effects of diuretics are hypovolemia, hypokalemia, hyperkalemia, hyponatremia, metabolic alkalosis, metabolic acidosis and hyperuricemia.
|
Adverse effect
|
Diuretics
|
Symptoms
|
|
metabolic alkalosis
|
|
|
|
metabolic acidosis
|
|
|
|
Hypovolemia
|
|
|
|
hyponatremia
|
|
|
|
hypokalemia
|
|
|
|
hyperuricemia
|
|
|
|
Hyperkalemia
|
|
|
|
hypercalcemia
|
|
|
|
Examples
|
Mechanism
|
Location (numbered in distance along
nephron)
|
|
|
–
|
ethanol, water
|
Inhibits
vasopressin secretion
|
1.
|
|
Xanthines
|
caffeine, theophylline, theobromine
|
Inhibits
reabsorption of Na+, increase glomerular filtration rate
|
1.
tubules
|
|
Thiazides
|
bendroflumethiazide, hydrochlorothiazide
|
Inhibits
reabsorption by Na+/Cl-
symporter
|
4.
distal convoluted tubules
|
|
Potassium-sparing diuretics
|
amiloride, spironolactone, eplerenone, triamterene, potassium canrenoate.
|
Inhibition
of Na+/K+ exchanger:
Spironolactone inhibits aldosterone action, Amiloride inhibits epithelial sodium channels
|
5.
cortical collecting ducts
|
|
Osmotic diuretics
|
glucose (especially in uncontrolled diabetes), mannitol
|
Promotes
osmotic diuresis
|
2.
proximal tubule, descending limb
|
|
Na-H exchanger antagonists
|
Promotes
Na+ excretion
|
||
|
Loop diuretics
|
bumetanide, ethacrynic acid, furosemide, torsemide
|
Inhibits
the Na-K-2Cl symporter
|
3.
medullary thick ascending limb
|
|
Carbonic anhydrase inhibitors
|
acetazolamide, dorzolamide
|
Inhibits
H+ secretion, resultant promotion of Na+ and K+
excretion
|
2:
proximal tubule
|
|
Arginine vasopressin
receptor 2 antagonists |
amphotericin B, lithium citrate
|
Inhibits
vasopressin's action
|
5.
collecting duct
|
|
Aquaretics
|
Increases
blood flow in kidneys
|
||
|
Acidifying salts
|
CaCl2,
NH4Cl
|
1.
|
No comments:
Post a Comment