Cardiac Medications

5 classes of HTN drugs
diuretics, CCB, ACE inhibitors, adrenergic agents, direct-acting vasodilators
Diuretics (MOA)
MOA: reduce blood volume, increase urine output, first line therapy for HTN
diuretics (SE)
SE: dehydration and hypovolemia
diuretics (RN)
RN: watch for orthostatic hypotension, dizziness, fainting, monitoring lab work Na, K, daily weights intake and output, s/s heart failure (lung sounds), safety, s/s of edema, can increase toxicity of lithium and digoxin, photosensitivity
potassium-sparing diuretics (MOA)
MOA: blacks sodium reabsorption in the distal renal tubule
potassium-sparing diuretics (CI)
CI: renal insuffiency, hyperkalemia, pregnant or lactating women, careful use with gout or kidney stones, can increase K if taken with supplements or ACE inhibitors
potassium sparing diuretics (RN)
RN: CBC for agranulocytosis, report fever, rash, and sore throat, uric acid levels, restrict use of salt substitutes & sports drinks
potassium sparing diuretics (SE)
SE: gynecomastia, testicular atrophy, hirsutism,
thiazide diuretics (MOA)
MOA: inhibit sodium reabsorption in ascending loop of henle and early distal tubules, decrease reabsorption of Na--> Na excreted by kidneys --> blood volume decreased
thiazide diuretics
if used initially decrease mortality
thiazide diuretics (SE)
SE: uric acid levels increase (gout patients), hyperlipidemia, hypercalcemia, may increase blood sugar, increase risk for dig and lithium toxicity, increase loss of K when taken with steroids, decrease effects of antidiabetic agents due to hyperglycemia
loop diuretics (MOA)
MOA: inhibit reabsorption of sodium and water in proximal portion of ascending loop of Henle, activate renal porstaglandins, dilation of blood vessels, reduce preload and central venous pressure
loop diuretics (SE)
SE: ototoxic, increase glucose and uric acid levles, severe potassium loss, hypovolemia, increase lithium and dig toxicity, decrease K when used with steroids, decrease effects of anticoagulants, avoid nephrotoxic meds
loop diuretics (RN)
RN: report changes in hearing, vomiting, anorexia, twitching, monitor chemistry labwork, diet rich in potassium
calcium channel blockers (MOA)
MOA: block calcium into vascular smooth muscle, prevent contractions using vasodilation, increase cardiac output, BP decreases, less oxygenation utilization by the heart
calcium channel blocker
useful for elderly and african americans with HTN
calcium channel blocker (SE)
SE: dizziness, facial flushing, peripheral edema, reflex tachycardia, immediately report: chest pain, SOB (sings of CHF), increases digoxin levels, increases serum levels with H2 antagonists, potentiate warfarin
calcium channel blockers
negative chronotropic and negative inotropic
calcium channel blockers (RN)
RN: taper off drug, grapefruit enhances absorption, alcohol potentiate vasodilation- syncope, smoking causes vasoconstriction, monitor hepatic/renal studies, monitor EKG< position to decrease peripheral edema, K level, monitor HR and B/P
ACE inhibitor (MOA) {HTN}
MOA: blocks effects of angiotensin II, lowers peripheral resistance, decreases blood volume, prevents breakdown of bradykinin (potent vasodilator), decrease in vascular tone, decrase in NA and H20 reabsorption {HTN}
ACE inhibitors {HTN}
first line therapy for HF, reduces development of severe heart failure after MI {HTN}
ACE inhibitors (SE) {HTN}
SE: postural hypotension, first dose syncope, angioedema, infections (neutropenia), persistent, dry cough, hyperkalemia {HTN}
ACE inhibitors (CI) {HTN}
CI: pregnancy, lactation, history of angioedema, HF patients taking K-sparing diuretics, renal insufficiency, african americans (increased angioedema) {HTN}
ACE inhibitors (RN) {HTN}
RN: take first dose lying down, monitor labs, hepatic/renal studies, monitor for dehydration or fluid overload, watch for s/s infections, patient safety, no potassium supplements {HTN}
angiotensin II receptor antagonists (MOA)
MOA: blockade of angiotensin II receptors after being formed, vasodilation and suppression of aldosterone, arteriolar dilation, increased sodium excretion
angiotensin II receptor antagonists (RN)
RN: renal function tests, for hypotension elevate feel, lay down, patient safety, with/without meals, no potassium supplements, watch for s/s URIs
angiotensin II receptor antagonists (SE)
SE: orthostatic hypotension, upper repspiratory infections
alpha1 adrenergic blockers (MOA)
MOA: block alpha1 receptors in arterioles, dilation of both arterioles and veins, decrease peripheral resistance of arterioles
alpha1 adrenergic blockers (tx)
alpha1 adrenergic blockers (SE)
SE: orthostatic hypotension, first dose syncope, dizziness, n/v, bradycardia, dry mouth, decreased libido and impotence, blurred vision, tinnitus, epitaxis, edema
alpha1 adrenergic blockers (RN)
RN: fall precautions, vital signs and LOC, assess incomplete bladder emptying
alpha2 adrenergic agonists
used when other drugs don't work
alpha2 adrenergic agonists (MOA)
MOA: act on alpha2 receptors in brainstem, aldomet becomes a "false" transmitter to brain, cause inhibition of SNS, BP reduced
alpha2 adrenergic agonists (MOA)
MOA: stimultaes alpha adrenergic receptors in cardiovascular control center of brain, dilation of both arterioles and veins, decrease BP
alpha2 adrenergic agonists (SE)
SE: CNS depression, sedation, sexual dysfunction, orthostatic hpotension, abrupt clonidine withidrawal can cause rebound HTN, constipation, edema, wt. gain, dry mouth, methyldopa may cause hepatotoxicity
alpha2 adrenergic agonists (RN)
RN: baseline vitals, monitor q30 min during initial therapy, recommend last dose at hs (b/c of sedentary effect), daily weight (report gain of >4 lb/wk)
sympatholytics/beta adrenergics (MOA)
blck effects of sympathetic nervous system, decrease contractility by blocking receptors on heart conduction system and myocardium
sympatholytics/beta adrenergics
negative inotropic and negative chronotropics
beta blockers (MOA)
MOA: decrease cardiac workload and ease symptoms of angina, slow conduction through myocardium and treats some dysrhythmias
beta blockers (tx)
tx: heart failure, migraines, HTN
beta1 blockers (major action)
action: cause decreased heart rate, contractility, reduce myocardial oxygen demand
beta2 blockers (major action)
action: bronchoconstriction
beta blockers (SE)
SE: bradycardia, bronchoconstriction, clinical depression, heart block, fatiuge and activity intolerance, hypoglycemia, drowsiness, sedation, weight gain, pulmonary edema
beta-blockers (RN)
RN: vital sings, breath sounds (pulmonary edema), monitor hypoglycemia, assess LOC, intake and output
direct acting vasodilators (MOA)
MOA: act directly to relax blood vessels and lower blood pressure, some work on arterioles, some on veins, used in emergency situations
direct acting vasodilators (SE)
SE: reflex tachycarida, increase myocardial contractions- exacerbate angina, lupus-like syndrome, edema/wt. gain -fluid retention, priapism, (hypertrichosis-minoxidil)
direct acting vasodilators (RN)
RN: for aggressive life-threatening HTN, lower BP instantaneously with IV drip, given only in ICU setting, vital signs/orthostatic vitals, daily weights (call for >5lb gain/wk) chemistry and renal function labs, dizziness, taper off medications
ACE inhibitors (MOA) {HF}
MOA: lower peripheral resistance, reduce blood volume, enhance secretion of Na and H2O, diminish afterload, increase cardiac output, dilate veins returning blood to the heart, decrease preload, reduce peripheral edema, decrease workload of the heart {HF}
ACE inhibitors {HF}
drugs of choice in HF- decrease mortality
ACE inhibitor (RN) {HF}
RN: baseline serum/urine protein, BUN, CR, glucose, CBC< K, and NA levels, first dose syncope with HF patient, report s/s infection, bruising, bleeding, hold for neutrophils <1000/mm3 {HF}
ACE inhibitor (CI) {HF}
CI: pregnancy, angioedema, orthostatic hypotension, alter taste, dry persisting cough {HF}
diuretics (MOA) {HF}
MOA: increase urine flow, reduce blood volume, edma, and pulmonary congestion, reduce cardiac workload {HF}
diuretics (RN) {HF}
RN: baseline vitals, tests for renal disorders, watch for s/s side effects, monitor for chemistry imbalances (K levels, I&O, hypovolemia), monitor sodium intake, report weight loss >2 lb/week, report fatigue and muscle cramping, change positions slowly {HF}
diuretics (CI) {HF}
CI: renal dysfunction, fluid/electrolyte depletion, hepatic coma, pregnancy and lactation, caution: hepatic cirrhosis, nephrotic syndrome & elderly {HF}
beta-blockers (MOA) {HF}
MOA: reduce cardiac workload, decrease afterload, negative inotropic effect, slow heart rate, reduce blood pressure {HF}
beta-blockers (SE) {HF}
SE: bradycardia, mask s/s of hypoglycemia, hepatic toxicity, monitor for worsening of s/s HF
beta-blockers (CI) {HF}
CI: decompensated heart failure, chronic obstructive pulmonary disease (COPD), bradycardia, heart block, pregnant/lactating, Caution: diabetics, peripheral vascular disease, hepatic impairment, elderly {HF}
beta-blockers (RN) {HF}
RN: monitor BP and pulse (hold if P<60, SBP<100), do not stop taking drug abruptly, diabetics will have changes in blood sugar levels, monitor LFT's, CALL MD: s/s worsening HF, SOB/dyspnea, edema of feet and ankles, chest pain, fainting, slow irregular HR, weight gain
direct acting vasodilators (MOA) {HF}
MOA: decrease preload and myocardial O2 demand
direct acting vasodilators {HF}
only given if unable to tolerate ACE inhibitors {HF}
direct acting vasodilators (RN) {HF}
RN: monitor vitals, check effectiveness of medication, for aggressive life-threatening HTN, lower BP instantaneously with IV drip, given only in ICU setting, vital signs/orthostatic vitals, daily weights (call for >5lb gain/wk) chemistry and renal function labs, dizziness, taper off medications {HF}
cardiac glycosides (MOA) {HF}
MOA: positive inotropic action, negative chronotropic action {HF}
digoxin/cardiac glycosides (MOA) (HF)
MOA: increase in myocardial contractility, slows heart rate, improves cardiac output (HF)
used for advance HF in combo rx
digoxin/cardiac glycosides (SE) {HF}
SE: dysrhythmias, tachycardia, bradycardia, PVCs, AV block, fatigue, drowsiness, dizziness, anorexia, nausea (first sign of adult toxicity), vomiting, colored vision, halo vision, flickering lights {HF}
0.8 ng/ml - 2.0 ng/ml
therapeutic digoxin level
digoxin/cardiac glycosides (CI) {HF}
CI: pregnant women, Caution: elderly, renal insuff, MI {HF}
digoxin toxicity (s/s)
s/s: n/v, diarrhea, visual illusions - yellow green halos, blind spots, blurred vision/diplopia
digoxin/cardiac glycosides (RN) {HF}
RN: provide potassium rich diet, vital signs, telemetry, monitor EKG for rate and rhythm changes during digitalization, draw dig levels q8h after last dose, BUN & Cr., hold for hypokalemia, check apical HR for 1 full minute- hold for <60 bpm, report immediately s/s of toxicity or dig level >2.0 ng/ml, wear ID bracelet, given antacids and antidiarrheals 2 hours after, avoid herbal supplement- purple and white floxglove, give at same time each day, daily weight, restrict salt intake, restrict alcohol and smoking, potassium supplements or diet K rich to prevent hypokalemia {HF}
phosphodiesterase inhibitors (MOA) {HF}
MOA: bolck enzyme phosphodiesterase in cardiac and smooth muscle, increase amount of calcium for myocardial contraction, positive inotropic response, vasodilation, cardiac output increased {HF}
phosphodiesterase inhibitors
used for short term control of HF (2-3 day therapy), can become toxic with long term use, used when ACE inhibitors or cardiac glycosides ineffective
phosphodiesterase inhibitors (SE) {HF}
SE: ventricular dysrhythmias, exacerbate hypokalemia, severe hypotension {HF}
phosphodiesterase inhibitors (RN) {HF}
RN: baseline vitals, report immediately: irregular fast heartbeat, pain or swelling at IV site, temp of 101 or greater, increase of angina, continuous telemetry of EKG monitoring