NU 578 - Unit 3 Questions with 100% Correct
Answers
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,
vomitting, 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 arrthymias
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
approved for hypertension, heart failure, diabetic nephropathhy, MI, prevention of MI and
stroke
They block the action of angiotensin 2. cause dilation of the arterioles, prevent cardiac
structure change, increase renal excretion of sodium and water. DO NOT INHIBIT KINASE
II and do not increase levels of bradykinin in the lungs. have lower risk for cough.
Answers
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,
vomitting, 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 arrthymias
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
approved for hypertension, heart failure, diabetic nephropathhy, MI, prevention of MI and
stroke
They block the action of angiotensin 2. cause dilation of the arterioles, prevent cardiac
structure change, increase renal excretion of sodium and water. DO NOT INHIBIT KINASE
II and do not increase levels of bradykinin in the lungs. have lower risk for cough.
