Exam 4: Cardiac (HF, ACS, dysrhythmias, shock, TGL)

Question 1

Therapeutic goals for HF

Answer 1

Correct sodium and water retention and volume overload (diuretics)

block negative compensatory mechanisms (RAAS - ACEi, ARBs, DRIs, ARNIs)

Reduce inotopic, chronotropic, dromotropic workload of heart (BB, CCB)

Control precipitating and complicating factors -> lifestyle

Question 2

Furosemide

Answer 2

Loop diuretic

SOA: ascending limb of the Loop of Henle -> potent and rapid

ADRs: all diuretics ADRs (Hypovolemia, hypotension, change in pH-Acid Base Imbalance, electrolyte imbalances, sleep disturbances, Hyperglycemia, Cholesterol levels: ↑ LDL ↓ HDL, Hyperuricemia (gout)) + OTOTOXICITY

Indic.: rapid or continued mobilization of fluid, IV for emergent or urgent diuretic needs (significant edema, HTN)

Interactions: all diuretics inter. + ototoxic drugs

Nursing Implications: K+ rich foods, changes to hearing/balance, orthostatics, daily weights, insulin, take in the morning

Question 3

Hydrochlorothiazide (HCTZ)

Answer 3

Thiazide diuretic

**dependent on GFR (renal function is necessary)

SOA: early distal tube of nephron (moderate reabsorption, less than loop)

ADRs: all diuretics ADRs (Hypovolemia, hypotension, change in pH-Acid Base Imbalance, electrolyte imbalances, sleep disturbances, Hyperglycemia, Cholesterol levels: ↑ LDL ↓ HDL, Hyperuricemia (gout)) + HYPERCALCEMIA

Indic.: mild/mod. HTN, edema, postmenopausal osteoporosis (reabsorb Ca+)

Contras: hypersensitivity (SJS), renal disease

Nursing Implications: K+ rich foods, orthostatics, daily weights, insulin, take in the morning

Question 4

Spironolactone/eplerenone

Answer 4

Potassium sparing diuretic (aldosterone antagonist -> also included in RAAS agents)

MOA: blocks action of aldosterone in the distal tubule; K+ retention

SOA: late distal tube of nephron (weak diuretic)

ADRs: HYPERKALEMIA + ENDOCRINE EFFECTS

Indic.: HTN, edema, HF, hyperaldosteronism, hormonal acne/PCOS, hypokalemia (used with other antihypertensives to counteract K+ loss)

Contras: hypersensitivity, hyperkalemia, anuria, AKI

Nursing Implications: monitor for K+ (salt substitutes and no supplements)

Question 5

Captopril/lisinopril/enalapril

Answer 5

-pril
MOA: angiotensin converting enzyme inhibitors (ACEis) -> block vasoconstriction and fluid retention

ADRs: persistent cough, first dose hypotension, angioedema, hyperkalemia, fetal harm

Indic.: HTN, HF, diabetic & non- DM nephropathy, MI (reduce rate of cardiac remodeling)

Contras: renal failure

Interactions: other HTN, lithium, NSAIDs, ^K+ drugs

Nursing Implications: monitor first dose, hyperkalemia warnings and diet restrictions

Question 6

Losartan

Answer 6

-sartan
MOA: Angiotensin II Receptor Blockers (ARBs) -> similar to ACEis

ADRs: first dose hypotension, angioedema, fetal harm

Indic.: HTN, HF, diabetic & non- DM nephropathy, MI

Contras: renal failure

Nursing Implications: monitor first dose

Question 7

Sacubitril/valsartan

Answer 7

Angiotensin Receptor Neprilysin Inhibitor (ARNI)
(Entresto)

MOA:
Sacubitril - increase release of natriuretic peptides
Valsartan - ARB -> suppress neg effects from RAAS

ADRs: angioedema, hypotension, and some hyperkalemia, decreased GFR, fetal harm (all related to ARB)

Risks: low BP issues and renal stenosis

Question 8

Aliskiren

Answer 8

MOA: direct renin inhibitor -> blocks entire RAAS

ADRs: less hyperkalemia, cough, and angioedema, BUT same fetal danger and some GI upset

Contras: pt w/ DM also taking ACEis or ARBs -> cause renal impairment

Question 9

Carvedilol/Bisoprolol/SR metoprolol

Answer 9

guidelines just indicate these over the other BB specifically for HF

MOA: improve CO by reduce workload from SNS stim (dec. HR & BP, dec. dsyrythmias)

Start low and slow, not used alone (w/ACEi, ARB, ARNI, or diuretic)

ADRs: Fluid retention worsening HF(?), CNS fatigue, hypotension, bradycardia or heart block, may worsen HF in acute decompensated situation

Question 10

Dapagliflozin/empaglifozin

Answer 10

(Jardiance)
SGLT-2 Inhibitors -> “-aglifozin”

MOA: blocks SLGT2 to increase glucose excretion via urine. More glucose in nephron -> H2O follows higher concentration to increase diuresis

not first line, but would add on later
typically used in DM but also now in HF (pt doesn’t have to be diabetic)

ADRs: more UTIs and genital infections, increased UOP, orthostatic hypotension, hypoglycemia (dizzy, lightheaded)

ADD PIC FROM SLIDES

Question 11

Ivabradine

Answer 11

MOA: Blocks channels responsible for cardiac pacemaking (i.e.: SA Node) (dec. conduction, but not contractility)

Useful for patients who need additional beta blockade (on BBlkrs and HR is still >70) or those who have a contraindication to a beta blocker

ADRs: cardiac changes, hypotension, fetal danger

Question 12

BiDil

Answer 12

Isosorbide Dinitrate plus Hydralazine

MOA: venous and direct acting arteriole vasodilation

BiDil is indicated as an alternative to ACEis and ARBs (contras or GFR too low) and in black pts w/HF

ADR: Hypotension, reflex tachycardia

Question 13

Digoxin

Answer 13

used only as a 2nd line for HF when exhausted all other options and sometimes when there is a dysrythmia too

MOA: inhibits the enzyme Na+K+-ATPase to increase intracellular calcium in myocytes
positive inotrope -> increase contractility to improve CO

**Toxic - direct relationship to potassium levels (hypokalemia = increased risk for dig tox)
Narrow Therapeutic Range (0.5-0.8 ng/mL)

ADRs: GI upset and yellow/green visual disturbances (early warning signs) -> later: arrhythmias, bradycardia, ECG changes, AV/SV blocks, anorexia, N/V/D, fatigue

Implications: teach pt early signs, check apical 1 min and need recent K+ value, be very careful with diuretics, corticosteroids and other K+ lowering drugs

Question 14

Digoxin interactions

Answer 14

Diuretics - hypokalemia

ACEis - increases likelihood of dig tox

Sympathomimetics (dobutamine) - increase risk of dysrythmias

Question 15

Dobutamine

Answer 15

sympathomimetic - acts on beta1 only in heart

Used: HF & Shock

IV dobutamine - rescue med for severe, acute HF, short action

catecholamine

improves LVEF and improves kidney function through improved perfusion

Question 16

Dopamine

Answer 16

sympathomimetic

Used: HF & Shock

activates beta1 and dopamine receptors (alpha1 at high doses)

catecholamine

continuous IV for short-term rescue of severe, acute HF

ADR: DYSRHYTHMIAS!!!

Question 17

Milrinone

Answer 17

PDE3 Inhibitor

MOA: ^cAMP -> increases contractility and leads to vasodilation (“ino-dilator”)

continuous IV and only short-term for severe HF

Question 18

Drugs to avoid in HF

Answer 18

Antidysrhythmics -> Can cause worsening of HF

Amiodarone: has been shown not to decrease survival

Calcium Channel Blockers: most increase risk of CV events

NSAIDS: promote Na+ and peripheral vasoconstriction

Question 19

Nitroglycerin

Answer 19

MOA: vasodilates the arteries and veins -> decreases venous return (preload) and less volume in ventricles (workload)
**does not dilate atherosclerotic coronary arteries - instead pain relief comes from venous dilation

ADR: orthostatic hypotension, HA, tachy, flushing

Interactions: PDE5 Inhibitor (viagra) * look at safety alert life-threatening vasodilation

short term - sublingual or transligual spray (acute anginal attacks)

Question 20

Isosobide dinitrate

Answer 20

long acting nitrate - SR oral

high dose due to first pass effect and admin on fixed schedule

may be instructed to have “drug-free” time by removing for 8 -12 hours

Question 21

Metoprolol/atenolol/propanolol

Answer 21

1st line for prevention of angina by decreasing O2 demand of myocardium

Question 22

Nifedipine/amlodipine

Answer 22

Dihydropyridines - CCB

MOA: selective to calcium block in arterioles **can relax coronary vasospasm

ADRs: severe reflex tachy

Indic.: angina, HTN, Prophylaxis for vascular headaches

Nursing Implications: assess HR before dose

Question 23

Diltiazem/verapamil

Answer 23

Non-dihydropyridines

MOA: blocks calcium channels in heart and arterioles **can relax coronary vasospasm

Indic.: angina, HTN, supraventricular dysrhythmias (fib/flutter, SV tach)

Contras: use w/ caution w/ pts bradycardia, HF or AV block

Nursing Implications: no grapefruit**, interacts with Digoxin (toxicity)

Question 24

Ranolazine

Answer 24

Newest class of antianginal agents…preventative for angina
Clinical trials showed a reduction in anginal episodes and an increase in activity tolerance

MOA: Reduces accumulation of sodium and calcium in myocardial cells -> heart uses energy more efficiently
(exact mechanism is not understood)

ADRs: Prolonged QT interval, multiple drug interactions
Combined with other agents for angina – nitrates, BBlkrs, etc.

Question 25

Atropine

Answer 25

Antiarrhythmic (anticholinergic)

IV treats sinus bradycardia and heart block (also antidote for cholinergic OD)

MOA: Blocks acteylcholine at muscarinic receptors (inc HR, dec secretions)

Contras: Glaucoma, hemorrhage, tachy secondary to cardiac insufficiency (MI), BPH

ADRs: anticholinergic effects

Nursing implications: BEERS -> strict I&Os for elderly and check for constipation, VS & ECG during admin

Question 26

Drugs for sinus tach

Answer 26

Bisoprolol and metoprolol succinate
Verapamil and diltiazem

both lower heart rate and decrease workload of the heart

Question 27

Drugs for AFib/flutter

Answer 27

Propranolol
Sotalol
Acebutalol -> cardioselective, IV, immediate rescue
Esmolol (class II Beta blockers) -> cardioselective and PO for PVCs

Verapamil -> SVT/Afib/flutter

Question 28

Drugs for sustained SV Tach

Answer 28

Beta blockers, calcium channel blockers, adenosine

Question 29

Adenosine

Answer 29

1st line for paroxysmal SVT

IV administration (antecubital or above) -> immediate onset -> half life is < 10 seconds

Given as a rapid 1 – 2 second IV bolus
Follow each administration with 20mL rapid saline flush to ensure injection reaches the systemic circulation
Followed by a 1 – 5 second period of asystole

Nursing implications: Monitor ECG continuously - prolongs PR Interval, monitor blood pressure (lay pt flat) and respiratory status closely

ADRs may occur, but due to the 10 second half-life they are typically self-limiting - SOB, hyperventilation, facial flushing

Question 30

Amiodarone

Answer 30

Potassium Channel Blocker w/ long half life

broad spectrum dysrythmia med = both atrial and ventricles
used for acute and long-term suppression
PO & IV

ADRs:
** Pulmonary Toxicity - (fibrosis, pneumonitis)
**Cardiotoxicity (worsen dysrythmia, bradycardia, AV block
Liver & thyroid Toxicity
** Ophthalmic effects (Optic neuropathy and neuritis)
Toxicity in Pregnancy/Breast Feeding
** Dermatologic Effects - even indoors -> gray/blue skin w/sun exposure
**Contraindicated in severe Heart Blocks
** Drug interactions: many

Nursing implications: extremely long half life (25 – 110 days following PO), effects and toxicity for weeks or months after drug is withdrawn, no grapefruit juice, pt cannot miss a dose

Question 31

Lidocaine

Answer 31

Group 1 B Sodium Channel Blocker
IV for dysrythmias (no PO - first pass)

only ventricular dysrythmias

ADRs: CNS effects can occur (drowsy, slurred, confusion, paresthesias, tremors)
Toxic: convulsions, cardiac arrest

Nursing implications: BP and ECG should be monitored
Equipment for resuscitation should be available

**never give IV Lido+Epi

Question 32

Procainamide/quinidine

Answer 32

Class 1A Sodium Channel Blocker

Broad spectrum (atria & vent)
last choice -> toxic
IV/IM no longer PO

ADRs: Confusion and psychosis, SLE like syndrome, severe immunologic reactions, blood dyscrasias (neutropenia & thrombocytopenia), cardiotoxicity

Nursing implications: Weekly CBC because of the blood dyscrasias.

Question 33

Epinephrine/norepi

Answer 33

adrenergic agonist

Alpha 1 - vasoconstrict (BP)
Beta 1 - heart contractility (HR)
Beta 2 - bronchodilation & ^BGL

catacholamine, so no PO

ADR: HTN, angina, necrosis from extravasation, ^BGL, dysrythmias

Question 34

Atorvastatin/simvastatin

Answer 34

HMG-CoA Reductase Inhibitors
1st line for lipid lowering
-statin

MOA: inhibits cholesterol production
Reduce LDL levels by 25 – 60%, based on dose; Reduce triglyceride levels; Raise HDL levels

Indications: Hypercholesterolemia, MI, angina, CVA, DM

Nursing implications: take in the evening and if stop abruptly, hyperlipidemia comes back quickly
blocks in the liver

Simvastatin prescribed if need to lower LDL by 40%
Atorvastatin for pts with renal impairment

ADRs: HA, Fatigue, fetal harm (need birth control), liver dysfunction, myopathy/rhabdo

Nursing implications: Birth control, liver labs, caution w/ alcoholics, teach about muscle weakness and monitor CK levels

Question 35

Coleserleam

Answer 35

Bile Acid Sequestrant (adjunct to statin)

Reduces LDL Cholesterol

MOA: Binds to bile acids to prevent its intestinal absorption
» serum bile acids become depleted.
Body responds to the decrease in serum bile acids by converting cholesterol to bile acids
Result: Lowering serum cholesterol

ADRs: Expect GI adverse effects (constipation chief complaint, abdominal pain, bloating, flatus, steatorrhea)

Question 36

Ezetimibe

Answer 36

Selective Cholesterol Absorption Inhibitors (adjunct to statins or monotherapy)

(Zetia)
blocks absorption of lipids (dietary cholesterol) in the small intestine -> reducing plasma levels of LDL, total cholesterol and TG

No GI adverse effects and oes not significantly reduce clinical risk of atherosclerosis

Question 37

Gemfibrozil

Answer 37

MOA: Most effective at decreasing triglycerides (VLDL)
Also raises HDL and only minor effect on LDL

3rd line drug due to ADRs:
Rash, GI disturbances, gallstones, myopathy, can lead to rhabdomyolysis w/ Statins, liver toxicity

Interactions: Increase risk of bleeding w/ Warfarin

Question 38

Alirocumab/evolocumab

Answer 38

Monoclonal Antibodies
SQ

Indications: High LDL

Pts with atherosclerotic concerns or familial hypercholesterolemia
MOA: block the PCSK9 Enzyme which normally blocks the LDL Receptors -> LDL cannot be taken up by the liver
If we block the enzyme, LDL is removed from the bloodstream and taken up by the liver

ADR: severe hypersensitivity, immunogenicity
Triggers unwanted antibody reaction…immune response