Week 3 Study Guide
Chapter 16: Drugs Affecting the Cardiovascular and Renal Systems
ACEIs, ARBs and Direct Renin Inhibitors: Act on the RAA system to reduce pressure by decreasing
sodium and water retention, decreasing vasoconstriction, and increasing vasodilation.
ACEI: PRILs
• MOAs: Improve oxygenation to heart muscle and decrease inappropriate remodeling of the heart
muscle after MI or with HF. Decrease production of ATII and Aldosterone.
• Indications: Hypertension. Young, white, DM, MI, or HF. AA=increased angioedema.
• Absolute contraindications: Bilateral renal artery stenosis, angioedema, pregnancy
• Precautions: impaired renal function, hypovolemic and hyponatremic states. Hyperkalemia,
hepatic impairments
• Monitoring: BP, weight, fluid status, renal function, potassium, WBC for neutropenia.
• Adverse drug reactions: Angioedema. Hypotension (dizzy, HA, fatigue). Dry hacking cough within
first week of therapy. Rash, photosensitivity.
• Drug interactions: Diuretics should be stopped for 2-3 days before starting meds. Increase doses
in 1-2 weeks intervals. NSAIDS interact. No salt substitutes.
ARBSs: ARTANs
• MOAs: Block ATII receptor. Do not affect cardiac output and do not produce tachycardia.
• Indications: Hypertension. Young, white, DM, MI, or HF. AA=increased angioedema.
• Absolute contraindications: Bilateral renal artery stenosis, angioedema, pregnancy
• Precautions: Impaired renal function, hypovolemic, hyponatremic states. Hyperkalemia, hepatic
impairments
• Monitoring: BP, weight, fluid status, renal function, potassium,
• Adverse drug reactions: Hypotension (dizzy, HA, fatigue).
• Drug interactions: Losartan lowered by P450. NSAIDS interact. No salt substitutes.
DRI: Aliskiren.
• MOAs: Directly impact renin levels with ATI and ATII reductions.
• Indications: Hypertension. Young, white, DM, MI, or HF. AA=increased angioedema.
• Absolute contraindications: Bilateral renal artery stenosis, angioedema, pregnancy
• Precautions: Impaired renal function, hypovolemic and hyponatremic states, hyperkalemia,
hepatic impairments.
• Monitoring: BP, weight, fluid status, renal function, potassium,
• Adverse drug reactions: Angioedema. Hypotension (dizzy, HA, fatigue). Sometimes produce
cough.
• Drug interactions: CYP3A4. NSAIDS interact. No salt substitutes.
CCBs:
• MOA: Block the L-type calcium channel. Relax arterial smooth muscle=reduces afterload, with
limited effect on preload. Reduces contractility (Neg inotrope) Decrease in SA-AV node
conduction.
, • Indications: HTN, angina, tachyarrhythmia. Unlabeled: migraine, Raynaud’s, cardiomyopathy,
esophageal spasm.
• Precautions: See below
• Contraindications: Verapamil/Diltiazem avoided in HF=bradycardia. Type 1 CCB=EF<40% and
early after MI. Dihydropyradines should be avoided for patients with peripheral edema. Can
cause tachycardia in unstable angina. Preg Category C, do not use with breastfeeding.
• Adverse drug reactions: (Hypotension) Dizzy, HA, syncope. Leads to HF with congestion, SOB,
cough and palpitations. HF worse with Verapamil, diltiazem and nifedipine. GI symptoms. Sexual
dysfunction, Gynecomastia, hyperglycemia, photosensitivity.
• Drug interactions: Alcohol, nitrates, quinidine, other HTN meds may lower BP even more.
NSAIDS decrease effect. Digoxin. Grapefruit juice=CYP3A4
• Differences between Type 1 CCB and dihydropyridines:
o Type 1: diphenylalkylamine and benzothiazepine based. (Cardizem, Verapamil)
o Type 2: diphydropyridine based. Greater vasodilation. Do not affect conduction through
the AV node. (Amlodipine, Felodipine, Nicardipine, Nifedipine)
o Diltiazem is good to lower HR, and improves coronary artery filling time and myocardial
oxygen supply. Verapamil has more potent negative inotropic effects, and slows AV nodal
conduction.
o
• Patient education: Same time of the day. Food interactions. No exercise in hot weather.
• Short acting vs long acting CCB:
o Short acting: More adverse drug reactions. They cause vasodilation, tachycardia, and
peripheral pooling of blood.
• Side effects: Hypotension, bradycardia,
Cardiac Glycosides: Digoxin. Strong and highly selective inhibitors of the sodium-K+-ATP ase
system: The “sodium pump.” The preferential binding of CGs to ATPase, occurs following
phosphorylation of the alpha subunit of the enzyme. Extracellular potassium promotes
dephosphorization of the enzyme and decreases the affinity of the enzyme for the CG. This may explain
why increased extracellular potassium reverses some of the toxic effects of these drugs.
• Indications: HTN, HF.
• MOA: Decreases automaticity and conduction velocity (neg dromotropism) throught the AV node
via central vagal stimulation and facilitation of muscarinic transmission at the cardiac muscle cell.
Effect all smooth excitable tissues, including smooth muscle and CNS.
• Adverse drug reactions:
• Contraindications: Severe Renal Impairment, AV blocks and uncontrolled Ventricular arrhythmias
because of their action on the AV node. IHSS.
• Cautions: Electrolyte abnormalities: K=, Ca+, Mag+. Category C=Pregnancy.
• Toxicity: Greater than 2ng/ml. Tachycardia. Treat with K+, Lidocaine, Atropine. Digibind is
expensive.
• Drug and potassium, calcium and Mg interactions: Any drug that may cause HypoK, HyperCa+,
or HypoMag+ can increase the risk of toxicity.
• Monitoring: Digoxin levels. Watch other drugs.
• Patient education: High fiber meal may decrease absorption. Take at same time each day. If one
dose is missed, but remembered within 12 hours, take it. High Potassium Diet. Separate milk by
one hour.
• Clinical pearls: Should not be used unless clear evidence of severe chronic systolic dysfunction
or A fib. Digoxin should not be discontinued unless a reversible cause of HF has been completely
Chapter 16: Drugs Affecting the Cardiovascular and Renal Systems
ACEIs, ARBs and Direct Renin Inhibitors: Act on the RAA system to reduce pressure by decreasing
sodium and water retention, decreasing vasoconstriction, and increasing vasodilation.
ACEI: PRILs
• MOAs: Improve oxygenation to heart muscle and decrease inappropriate remodeling of the heart
muscle after MI or with HF. Decrease production of ATII and Aldosterone.
• Indications: Hypertension. Young, white, DM, MI, or HF. AA=increased angioedema.
• Absolute contraindications: Bilateral renal artery stenosis, angioedema, pregnancy
• Precautions: impaired renal function, hypovolemic and hyponatremic states. Hyperkalemia,
hepatic impairments
• Monitoring: BP, weight, fluid status, renal function, potassium, WBC for neutropenia.
• Adverse drug reactions: Angioedema. Hypotension (dizzy, HA, fatigue). Dry hacking cough within
first week of therapy. Rash, photosensitivity.
• Drug interactions: Diuretics should be stopped for 2-3 days before starting meds. Increase doses
in 1-2 weeks intervals. NSAIDS interact. No salt substitutes.
ARBSs: ARTANs
• MOAs: Block ATII receptor. Do not affect cardiac output and do not produce tachycardia.
• Indications: Hypertension. Young, white, DM, MI, or HF. AA=increased angioedema.
• Absolute contraindications: Bilateral renal artery stenosis, angioedema, pregnancy
• Precautions: Impaired renal function, hypovolemic, hyponatremic states. Hyperkalemia, hepatic
impairments
• Monitoring: BP, weight, fluid status, renal function, potassium,
• Adverse drug reactions: Hypotension (dizzy, HA, fatigue).
• Drug interactions: Losartan lowered by P450. NSAIDS interact. No salt substitutes.
DRI: Aliskiren.
• MOAs: Directly impact renin levels with ATI and ATII reductions.
• Indications: Hypertension. Young, white, DM, MI, or HF. AA=increased angioedema.
• Absolute contraindications: Bilateral renal artery stenosis, angioedema, pregnancy
• Precautions: Impaired renal function, hypovolemic and hyponatremic states, hyperkalemia,
hepatic impairments.
• Monitoring: BP, weight, fluid status, renal function, potassium,
• Adverse drug reactions: Angioedema. Hypotension (dizzy, HA, fatigue). Sometimes produce
cough.
• Drug interactions: CYP3A4. NSAIDS interact. No salt substitutes.
CCBs:
• MOA: Block the L-type calcium channel. Relax arterial smooth muscle=reduces afterload, with
limited effect on preload. Reduces contractility (Neg inotrope) Decrease in SA-AV node
conduction.
, • Indications: HTN, angina, tachyarrhythmia. Unlabeled: migraine, Raynaud’s, cardiomyopathy,
esophageal spasm.
• Precautions: See below
• Contraindications: Verapamil/Diltiazem avoided in HF=bradycardia. Type 1 CCB=EF<40% and
early after MI. Dihydropyradines should be avoided for patients with peripheral edema. Can
cause tachycardia in unstable angina. Preg Category C, do not use with breastfeeding.
• Adverse drug reactions: (Hypotension) Dizzy, HA, syncope. Leads to HF with congestion, SOB,
cough and palpitations. HF worse with Verapamil, diltiazem and nifedipine. GI symptoms. Sexual
dysfunction, Gynecomastia, hyperglycemia, photosensitivity.
• Drug interactions: Alcohol, nitrates, quinidine, other HTN meds may lower BP even more.
NSAIDS decrease effect. Digoxin. Grapefruit juice=CYP3A4
• Differences between Type 1 CCB and dihydropyridines:
o Type 1: diphenylalkylamine and benzothiazepine based. (Cardizem, Verapamil)
o Type 2: diphydropyridine based. Greater vasodilation. Do not affect conduction through
the AV node. (Amlodipine, Felodipine, Nicardipine, Nifedipine)
o Diltiazem is good to lower HR, and improves coronary artery filling time and myocardial
oxygen supply. Verapamil has more potent negative inotropic effects, and slows AV nodal
conduction.
o
• Patient education: Same time of the day. Food interactions. No exercise in hot weather.
• Short acting vs long acting CCB:
o Short acting: More adverse drug reactions. They cause vasodilation, tachycardia, and
peripheral pooling of blood.
• Side effects: Hypotension, bradycardia,
Cardiac Glycosides: Digoxin. Strong and highly selective inhibitors of the sodium-K+-ATP ase
system: The “sodium pump.” The preferential binding of CGs to ATPase, occurs following
phosphorylation of the alpha subunit of the enzyme. Extracellular potassium promotes
dephosphorization of the enzyme and decreases the affinity of the enzyme for the CG. This may explain
why increased extracellular potassium reverses some of the toxic effects of these drugs.
• Indications: HTN, HF.
• MOA: Decreases automaticity and conduction velocity (neg dromotropism) throught the AV node
via central vagal stimulation and facilitation of muscarinic transmission at the cardiac muscle cell.
Effect all smooth excitable tissues, including smooth muscle and CNS.
• Adverse drug reactions:
• Contraindications: Severe Renal Impairment, AV blocks and uncontrolled Ventricular arrhythmias
because of their action on the AV node. IHSS.
• Cautions: Electrolyte abnormalities: K=, Ca+, Mag+. Category C=Pregnancy.
• Toxicity: Greater than 2ng/ml. Tachycardia. Treat with K+, Lidocaine, Atropine. Digibind is
expensive.
• Drug and potassium, calcium and Mg interactions: Any drug that may cause HypoK, HyperCa+,
or HypoMag+ can increase the risk of toxicity.
• Monitoring: Digoxin levels. Watch other drugs.
• Patient education: High fiber meal may decrease absorption. Take at same time each day. If one
dose is missed, but remembered within 12 hours, take it. High Potassium Diet. Separate milk by
one hour.
• Clinical pearls: Should not be used unless clear evidence of severe chronic systolic dysfunction
or A fib. Digoxin should not be discontinued unless a reversible cause of HF has been completely
