CVS Drugs Week 2 and 3 Flashcards
what are the 2 major forms of heart failure?
a) HF with left ventricular systolic dysfunction
b) Diastolic HF
What is heart failure?
Progressive disease, characterized by ventricular dysfunction, reduced CO, insufficient tissue perfusion, fluid retention.
What are the causes of HF?
Chronic hypertension and myocardial infraction.
What is cardiac remodeling?
In the inital phase, heart tries to compensate by remodeling itself. This puts more stress on the heart, and decreases the CO progressively.
what is cardiac dilation?
Result of increased venous pressure and reduced contractile force. Basically, the heart is dilating because of the fluid.
What is digoxin?
A cardiac glycoside. Effects the mechanical and electrical properties of the heart.
How does digoxin affect the heart?
Exerts a positive inotropic action on the heart. Increases the ventricular contraction, increasing CO.
What is the MA for digoxin?
Inhibits sodium potassium-ATPase. Increases Ca, which augments contractile force by facilitating the interaction of myocardial contractile proteins (actin and myosin).
Why is the relationship b/w potassium and inotropic action important for digoxin?
K+ competes with digoxin to bind to the enzyme. When K+ levels are low, digoxin binding increases. When K+ levels are high, thereapeutic effect is decreased.
What are the consequences of an increased CO (digoxin)?
a) sympathetic tone declines
b) urine production increases
c) renin release declines
What are the hemodynamic benefits to digoxin?
CO improves, HR decreases, heart size declines, constriction of arterioles and veins, water retention reverses, decreased blood volume, peripheral and pulmonary edema decreases, water weight is lost.
What are the neurohormonal benefits of digoxin in HF?
Inhibit renin release by decreasing Na absorption. Can decrease sympathetic outflow to CNS.
What electrical effects on the heart does digoxin have?
Digoxin can alter electrical activity in noncontractile tissue, and ventricular muscle. Can alter automaticity, refractionriness, and impulse conduction.
What are the cardiac adverse effects of digoxin?
Dysrythmias!!
What are some predisposing factors to dysrhythmias happening when taking digoxin?
Hypokalemia, elevate digoxin levels, heart disease.
What are some noncardiac adverse effects?
Anorexia, nausea vomiting- causes by simulation of the chemoreceptor trigger zone of medulla. Fatigue, visual disturbances also common.
What are some important drug interactions for digoxin?
Diuretics- loss of K
ACE inhibitors and ARBs- increase K levels
Sympathomimetics- increase hr and force
Quinidine- causes plasma levels of digoxin to rise
Verapamil- Ca channel blocker.
What are statins?
HMG-CoA inhibitors. Most effective drug for lowering LDL and total cholesterol. Lower risk of HF, MI, sudden death.
What are the beneficial actions of statins?
- Lower LDL cholesterol
- Elevate HDL cholesterol
- Reduce triglyceride levels.
What is the MA of statins?
Depends on increasing the number of LDL receptors on hepatocytes. -
Inhibits hepatic HMG-CoA reductase. This decreases cholesterol production.
what are the therapeutic uses for statins?
- hypercholesterolemia
- Primary/secondary prevention of CV events
- Primary prevention in peeps with normal LDL levels
- Post MI therapy
- Diabetes
When do you administer a statin?
AT NIGHT.
What statins are excreted in the urine?
Lovastatin, pitavastatin, pravastatin, simvastatin.
What statins are metabolized by CYP3A4?
Atorvastatin, lovastatin, simvastatin.
What are adverse effects of statins?
AE are uncommon, but some pts experience headache, rash, cramps, memory loss, GI problems. Usually transient.
What is myopathy/rhabdomyolysis and statins?
Statins can injure muscle tissue. AE include muscle aches, tenderness, weakness. Rhabdomyolysis is muscle disintegration or dissolution.
What are some important drug interactions for statins?
W/ other lipid lowering drugs, drugs that inhibit CYP3A4.
What is angina pectoris?
Chest pain.
What are the 3 forms of angina?
a) Chronic stable angina
b) Variant angina
c) Unstable angina
What is the treatment strategy for angina?
a) Increase cardiac oxygen supply.
b) Decrease O2 demand
What do nitrates do for stable angina?
Decrease O2 demand by dilating veins, which decreases preload.
What do nitrates do for variant angina?
increase O2 supply by relaxing coronary vasospasm. Does not reduce O2 supply.
What is nitroglycerin?
Acts on vascular smooth muscle to promote vasodilation. Acts on veins.
What are the AE of nitro?
Headache, orthostatic hypotension,
reflex tachycardia.
What are some important drug interactions for nitro?
Hypotensive drugs, BB, Verapamil, Diltiazem.
How can you administer nitro?
PO, IV, sublingual, translingual, transdermal, topical,
What is important to know about discontinuing nitro?
Stop slowly, abrupt discontinuation may cause vasospasm.
What are the therapeutic uses of nitro?
Acute therapy of angina, sustained therapy of angina, intravenous therapy.
What does the RAAS system do?
Regulates BP, blood volume, fluid and electrolyte balances.
How does the RAAS system exert its effects?
Angiotensin 2 and aldosterone.
What are the actions of angiotensin 2?
Vasoconstriction, release of aldosterone, alteration of cardiac and vascular structure.
How does angiotensin 2 cause vasoconstriction?
Acts on sympathetic neurons to promote NE, acts on adrenal medulla to promote epi, acts on CNS to increase sympathetic outflow to blood vessels.
How does angiotensin release aldosterone?
Acts on adrenal cortex to promote synthesis and secretion of aldosterone.
How does angiotensin 2 alter cardiac and vascular structure?
Can cause hypertrophy and remodeling in the heart.
What are the actions of aldosterone?
Regulating blood volume and blood pressure, pathologic cardiovascular effects.
Explain the formation of angiotensin 2.
Renin catalyzes the formation of angiotensin 1.
What causes renin release?
Decreased BP, blood volume, plasma Na content, reduced renal perfusion pressure.
Why may reduced renal perfusion occur?
a) Stenosis of renal arteries
b) Reduced systemic BP
c) reduced plasma volume.
What is renin secretion inhibited by?
Elevated BP, blood volume, and plasma sodium content.
What is ACE?
Angiotensin Converting Enzyme (Kinase II).
Converts angiotensin 1 to angiotensin 2.
How do ACE inhibitors produce their effects?
a) Reducing levels of angiotensin
b) Increase levels of bradykinin.
What does reducing levels of angiotensin 2 by ACE inhibitors do?
a) Dilate blood vessels
b) reduce blood volume
c) Prevent/reverse pathologic changes in heart and blood vessels mediated by angiotensin 2 and aldosterone.
How are ACE inhibitors administered?
Orally, except enalaprilat.
What are prodrugs?
Drugs that have to undergo conversion to their active form. Except for lisinopril.
How are ACE inhibitors excreted?
Kidneys.
What are the therapeutic indications for ACE inhibitors?
- Hypertension
- Heart Failure
- Myocardial Infraction
- Diabetic and -Nondiabetic Nephropathy
- Prevention of MI, Stroke, and Death in pts at high cardiovascular risk
- Diabetic Retinopathy
What are the adverse effects of ACE inhibitors?
First-Dose Hypotension, Cough, Hyperkalemia, Renal Failure, Fetal Injury, Angioedema.
What is angioedema?
Fatal reaction that develops in 1% of patients. Symptoms- increased giant wheals, edema of tongue, glottis, lips, eyes, and phayrnx.
What are important drug interactions with ACE inhibitors?
- Diuretics
- Antihypertensive Agents
- Drugs that raise potassium levels
- Lithium
- NSAIDs
CAPTOPRIL (side effects of ACE inhibitors)
Cough/C1 esterase deficiency Angioedema/Agranulocytosis Proteinuria/Potassium Excess Taste change Orthostatic hypotension Pregnancy Renal Artery stenosis Increase renin Leukopenia/Liver toxicity
What is cardiac dilation the result of?
Combo of increased venous pressure and reduced contractile force.
What are the consequences of increased sympathetic tone?
- Increased HR
- Increased contractility
- Increased venous tone
- Increased arteriolar tone
