NU 578 UNIT 3 EXAM
Treatment of CHF
Digoxin (increases cardiac contractility), diuretics (increases NA and H2O excretion),
ACEI (decreases BP and BV), Vasodilators (decreases BP), dobutamine and
dopamine and PDE inhibitors (increase ventricular contractility)
Digoxin
class: cardiac glycoside
increases myocardial contractile force and increases cardiac output
has a positive inotropic effect by inhibiting sodium potassium tump (this increases
Calcium into cell).
decreases HR
decreases AV nodal conduction
USED FOR HF AND DYSRHYTHMIAS
Digoxin toxicity
warn patients about dig induced dysrhythmias and instruct to take meds exactly as
prescribed. toxicity symptoms are altered hr or rhythm, visual or gi disturbances
(nausea, anorexia, vomiting, fatigue, blurred vision, yellow tinge to vision). toxicity is
made much worse by hypokalemia or anything that decreases digoxin clearance.
-Treatment: d/c digoxin, correct potassium, administer digibind
,Digoxin pharmacokinetics
good PO absorption but capsules are better than tablets. Don’t switch forms once
prescribed. Dosage is based on lean body weight and is really excreted. Therapeutic
levels are 0.5-0.8ng/ml.
-half life is 1.5 days. 6 days required to reach plateau and 6 days to eliminate.
Digoxin drug interactions
Antacids: decease absorption
diuretics: cause hypokalemia and increase toxicity
quinidine: displaces dig from tissues and decreases excretion
amiodarone: increases concentration of dig
verapamil: increase plasma levels of dig
sympathomimetics: increases chance of arrythmias
How do ACEI work in CHF?
inhibitor of ACE decreases angiotensin II, decreases total peripheral resistance, and
decreases blood volume. decreased aldosterone decreases TPR and BV.
-Block the production of angiotensin II, decrease the release of aldosterone, and
suppress degradation of kinins. arteriolar dilation improves blood flow in kidneys,
venous dilation reduces venous pressure, edema, preload, and suppression of
, aldosterone release enhances excretion of sodium and water . contribute to cardiac
remodeling!!! prolong life. not in acute decompensated HF. excreted by kidneys
FIRST LINE TREATMENT IN CHF!!!!
ACEI side effects
cough, increased potassium, dizziness, angioedema, hypotension. can cause renal
failure in patients with bilateral renal artery stenosis. use with caution in patients
taking potassium supplements or k sparing diuretics, neutropenia
-DDI: diuretics can intensify hypotension, antihypertensive agents can increase
powered bp, risk of hyperkalemia with k sparing diuretics and k supplements, NSaids
and Lithium decrease effects of ACEI
-BBW: can cause fetal injury in pregnancy.
Lisinopril
ACE inhibitor that is given in active form
decreases TPR, Na and H2O load by inhibiting ACE.
block angiotensin II, decreases BO and salt and water retention.
longer 1/2 life. q day dosing. causes first dose syncope, dizziness, GI SE
-approved for MI, HTN, heart failure.
Angiotensin 2 receptor blockers
Treatment of CHF
Digoxin (increases cardiac contractility), diuretics (increases NA and H2O excretion),
ACEI (decreases BP and BV), Vasodilators (decreases BP), dobutamine and
dopamine and PDE inhibitors (increase ventricular contractility)
Digoxin
class: cardiac glycoside
increases myocardial contractile force and increases cardiac output
has a positive inotropic effect by inhibiting sodium potassium tump (this increases
Calcium into cell).
decreases HR
decreases AV nodal conduction
USED FOR HF AND DYSRHYTHMIAS
Digoxin toxicity
warn patients about dig induced dysrhythmias and instruct to take meds exactly as
prescribed. toxicity symptoms are altered hr or rhythm, visual or gi disturbances
(nausea, anorexia, vomiting, fatigue, blurred vision, yellow tinge to vision). toxicity is
made much worse by hypokalemia or anything that decreases digoxin clearance.
-Treatment: d/c digoxin, correct potassium, administer digibind
,Digoxin pharmacokinetics
good PO absorption but capsules are better than tablets. Don’t switch forms once
prescribed. Dosage is based on lean body weight and is really excreted. Therapeutic
levels are 0.5-0.8ng/ml.
-half life is 1.5 days. 6 days required to reach plateau and 6 days to eliminate.
Digoxin drug interactions
Antacids: decease absorption
diuretics: cause hypokalemia and increase toxicity
quinidine: displaces dig from tissues and decreases excretion
amiodarone: increases concentration of dig
verapamil: increase plasma levels of dig
sympathomimetics: increases chance of arrythmias
How do ACEI work in CHF?
inhibitor of ACE decreases angiotensin II, decreases total peripheral resistance, and
decreases blood volume. decreased aldosterone decreases TPR and BV.
-Block the production of angiotensin II, decrease the release of aldosterone, and
suppress degradation of kinins. arteriolar dilation improves blood flow in kidneys,
venous dilation reduces venous pressure, edema, preload, and suppression of
, aldosterone release enhances excretion of sodium and water . contribute to cardiac
remodeling!!! prolong life. not in acute decompensated HF. excreted by kidneys
FIRST LINE TREATMENT IN CHF!!!!
ACEI side effects
cough, increased potassium, dizziness, angioedema, hypotension. can cause renal
failure in patients with bilateral renal artery stenosis. use with caution in patients
taking potassium supplements or k sparing diuretics, neutropenia
-DDI: diuretics can intensify hypotension, antihypertensive agents can increase
powered bp, risk of hyperkalemia with k sparing diuretics and k supplements, NSaids
and Lithium decrease effects of ACEI
-BBW: can cause fetal injury in pregnancy.
Lisinopril
ACE inhibitor that is given in active form
decreases TPR, Na and H2O load by inhibiting ACE.
block angiotensin II, decreases BO and salt and water retention.
longer 1/2 life. q day dosing. causes first dose syncope, dizziness, GI SE
-approved for MI, HTN, heart failure.
Angiotensin 2 receptor blockers
