Anti-angina & anti-hypertensive

drugs
By
Zubair
 Objectives
• Discuss the main classes of drugs that are
used for treating AP.
• Discuss the nursing care for anti-anginal and
anti-hypertensive drugs.
• Discuss the pharmacological management of
hypertension and hypertensive crisis.
• Calculate the drug dosage accurately while
administering oral and parenteral medications
 Drugs for Angina Pectoris
• Angina
I. Prevention of myocardial infarction (mi) and
death
II. Prevention of myocardial ischemia and
anginal pain
• Organic nitrates (eg, nitroglycerin),
• Beta blockers (eg, propranolol)
• Calcium channel blockers (eg, verapamil).
 Organic nitrates
Nitroglycerin:
• Nitroglycerin has been used to treat angina
since 1879.
• The drug is effective, fast acting, and
inexpensive.
• Remains the drug of choice for relieving acute
anginal attacks
 Nitroglycerin
Vasodilator Actions:
• Acts directly on vascular smooth muscle (VSM)
to promote vasodilation
Stable Angina:
• Decreases the pain of exertional angina
Variant Angina:
• Acts by relaxing or preventing spasm in
coronary arteries
 Nitroglycerin
Adverse Effects:
• Headache
• Orthostatic Hypotension
• Reflex Tachycardia
 Nitroglycerin
Pharmacokinetics:
• Highly lipid soluble and crosses membranes
with ease
Metabolism:
• Nitroglycerin undergoes rapid inactivation by
hepatic enzymes
• Plasma half-life of only 5 to 7 minutes.
• When administered orally, most of each dose is
destroyed on its first pass through the liver.
 Nitroglycerin
Drug Interactions:
• Hypotensive Drugs
• Phosphodiesterase Type 5 Inhibitors
• Beta Blockers, Verapamil, and Diltiazem
Organic Nitrates: Time Course of Action
Organic Nitrates: Trade Names and Dosages
Mechanisms of Antianginal Action
 Nursing interventions
• History of allergy
• Blood pressure
• Pulse rates
• Respiratory rate
• Weight
• Inspection of the extremities for edema
• Auscultation of the lung
• Assess for the side effects of medications
Anti-hypertensive drugs
 Renin–angiotensin–aldosterone system

Renin: Releases due to

• Stenosis of the renal arteries,
• Reduced systemic blood pressure
• Reduced plasma volume (brought on by
dehydration, hemorrhage, or chronic sodium
depletion)
 Renin–angiotensin–aldosterone system

• Suppressed by

• Blood pressure
• Blood volume
• Plasma sodium

Aldosterone
 ACE Inhibitors
• Benazepril LOTENSIN
• Captopril CAPOTEN
• Enalapril VASOTEC
• Fosinopril MONOPRIL
• Lisinopril PRINIVIL, ZESTRIL
• Moexipril UNIVASC
• Quinapril ACCUPRIL
• PerindoprilACEON
• Ramipril ALTACE
• TrandolaprilMAVIK
 ACE Inhibitors (Cont)
MOA:
• Reduce peripheral vascular resistance
• Block the enzyme ACE
• Decrease the secretion of aldosterone
• ACE inhibitors decrease angiotensin II
 ACE Inhibitors (Cont)
Therapeutic uses:
• Hypertension
• Myocardial infarction
• First-line agents for systolic dysfunction
• Regression of left ventricular hypertrophy
• Prevention of ventricular remodeling
• Heart failure
• Hypertensive patients with kidney disease
• For coronary artery disease.
 ACE Inhibitors (Cont)
Adverse Effects:
• Dry cough, rash, fever, altered taste,
• Hypotension
• Angioedema
• Hyperkalemia
• Fetal malformations
 ACE Inhibitors (Cont)
Drug Interactions:
• Diuretics
• Antihypertensive Agents
• Drugs That Raise Potassium Levels
• Lithium toxicity
Drug Dosages
 Angiotensin II Receptor Blockers
• ARBs block access of angiotensin II to its
receptors in blood vessels, the adrenals, and
all other tissues (Lehen, Richard 2007)
• Don’t increase the bradykinin
• Do not promote cough
 Renin Inhibitor
• Selective renin inhibitor, (aliskiren)

• Aliskiren directly inhibits renin and, thus, acts

earlier in the renin–angiotensin–aldosterone
system than ACE inhibitors or ARBs
• Should not be routinely combined with an ACE
inhibitor or ARB
Calcium Channel Blocker & Beta
Blockers
 Diuretics
A diuretic is a drug that increases the rate of urine flow.
The goal of most diuretic therapy is to reverse
abnormal fluid retention by the body.
Excretion of excess fluid is particularly desirable in the
following conditions:
● HTN.
● Heart failure.
● Kidney failure.
● Liver failure or cirrhosis.
● Pulmonary edema.
 Classification of Diuretics
I. High-ceiling (loop) diuretics (eg, furosemide)
II. Thiazide diuretics (eg, hydrochlorothiazide)
III. Osmotic diuretics (eg, mannitol)
IV. Potassium-sparing diuretics
 High-ceiling (loop) diuretics
Bumetanide, furosemide, torsemide, and
ethacrynic acid
• Diuretic action on the ascending limb of the
loop of Henle
• Produce copious amounts of urine.
• Furosemide is the most commonly used
 Mechanism of action
• Drugs in this class act by blocking the
reabsorption of Na and Cl in the loop of Henle
• Cause large amounts of fluid to be excreted by
the kidney in a very short time
 Therapeutic uses
• Pulmonary edema and acute/chronic
peripheral edema caused from heart failure or
renal impairment.
• Useful in emergency situations such as acute
pulmonary edema.
• Hypercalcemia,
• Hyperkalemia
 Pharmacokinetics
• Administered orally or parenterally.
• Their duration of action is relatively brief (2 t 4
hours),
• Secreted into urine.
 Adverse effects
Ototoxicity:
• Reversible or permanent hearing loss may occur
particularly when used in conjunction with other
ototoxic
• Ethacrynic acid is the most likely to cause deafness.
• Vertigo
Hyperuricemia
• Elevation of plasma uric acid
• cause or exacerbate gouty attacks
 Adverse effects (Cont)
Hyponatremia, Hypochloremia, and
Dehydration
• Can produce excessive loss of sodium,
chloride, and water
Hypotension
• Loss of volume
• Relaxation of venous smooth muscle
 Adverse effects (Cont)
Hypokalemia
• Potassium is lost through increased secretion
in the distal nephron
 Drug Interactions of Furosemide
• Digoxin
• Ototoxic Drugs
• Lithium
• Antihypertensive Agents
 Thiazide diuretics
Effects similar to those of the loop diuretics. Like
the loop diuretics, thiazides increase renal
excretion of sodium, chloride, potassium, and
water
Hydrochlorothiazide is the most widely used
thiazide diuretic
 Mechanism of Action
• Act mainly in the cortical region of the
ascending loop of Henle and
• The distal convoluted tubule to decrease the
reabsorption of Na+
• They have a lesser effect in the proximal
tubule. As a result, these drugs increase the
concentration of Na+ and Cl− in the tubular
fluid
 Therapeutic Uses
Hypertension
Heart failure
• Reducing extracellular volume
Hypercalciuria
• Inhibit urinary Ca2+ excretion.
 Pharmacokinetics
• The drugs are effective orally. Most thiazides
take 1 to 3 weeks to produce a stable
reduction in blood pressure
• Exhibit a prolonged half-life.
• All thiazides are secreted by the kidney
 Adverse effects
Potassium depletion
• Hypokalemia
Hyponatremia
Hyperuricemia
Volume depletion
Hypercalcemia
 Potassium-sparing diuretics
• They produce a modest increase in urine
production.
• They produce a substantial decrease in
potassium excretion

I. Aldosterone antagonists
II. Nonaldosterone antagonists
 Spironolactone
MOA:
• Block the action of aldosterone
• Retention of potassium and excretion of
sodium
 Therapeutic Uses
spironolactone
• Diuretic
• Secondary hyperaldosteronism
• Heart failure
• Ascites
 Pharmacokinetics
• Oral administration
• Extensively metabolized and converted to
several active metabolites
 Adverse effects
• Spironolactone can cause gastric upset.
• Induce gynecomastia in male patients and
menstrual irregularities in female patients.
• Hyperkalemia
• Nausea
• Lethargy
• Mental confusion
 Osmotic diuretics (eg, mannitol)
Mannitol
a simple six-carbon sugar
• It is freely filtered at the glomerulus
• It undergoes minimal reabsorption.
• It is not metabolized to a significant degree.
• It is pharmacologically inert
 MOA
• Creat an osmotic force that inhibits passive
reabsorption of water
• Degree of diuresis produced is directly related
to the concentration of mannitol
• No significant effect on the excretion of
potassium and other electrolytes
 Therapeutic Uses
• Renal Failure
• Reduction of Intracranial Pressure
• Reduction of Intraocular Pressure
 Adverse Effects
• Edema
• Headache
• Nausea and vomiting.
• Fluid and electrolyte imbalance
 Nursing Interventions
• Obtain a complete health history including
• Evaluate appropriate laboratory findings,
electrolytes (especially potassium level),
glucose, liver and renal function studies, and
lipid profiles.
• Obtain baseline weight, vital signs
• Assess for edema
• Assess for adverse effect
 Reference
• Bullock, S., & Manias, E. (2013). Fundamentals of
pharmacology.
• Howland, R. D., Mycek, M. J., Harvey, R. A., Champe, P. C., &
Mycek, M. J. (2006).Pharmacology. Philadelphia: Lippincott
Williams & Wilkins.
• Lehne, R. A. (2007). Pharmacology for nursing care. St. Louis,
MO: Saunders Elsevier.
• Neal, M. J. (2009). Medical pharmacology at a glance.
Chichester, UK: Wiley-Blackwell.
• Whalen, K., & Finkel, R. (2012). Lippincott Illustrated Reviews:
Pharmacology Sixth Edition (6th ed.). philadelphia: wolter
kluwer.
• Thank You