Drugs For Cardio Flashcards Preview

Pharmocology > Drugs For Cardio > Flashcards

Flashcards in Drugs For Cardio Deck (56):


QRS - ventricular repolarization
ST - ventricular depolarization
P - atrial depolarization



Abnormal impulse formation or conduction in the myocardium
Vary in severity from being basically undetectable to life-threatening
Use EKG to diagnose
Some can lead to stroke or heart failure


Goals of therapy for dysrhytmias
(Use of antidysrhythmic drugs)

Prevent or terminate
**carry potential to worked or create new dysrhythmias
Typically reserved for symptomatic dysrhythmias or ones that cannot be controlled by other means


Ectopic Foci
Ectopic pacemaker

Impulse originating outside of normal conduction system


Drug Class I

Sodium Channel Blockers
(Procainamide and lidocaine)
Largest group or antidysrhythmics
Subgroups ABC differentiated by speed of binding and dissociation from receptor sites
Similar to local anesthetic as (think lidocaine)
Frequent ECGs should be obtained due to potential to worsen//cause new


Drug Class II

Beta-adrenergic blockers
(Propranolol and metoprolol)
Slow HR and decrease conduction of velocity through AV node can suppressed several types of dysrhythmias
Typically used to treat ATRIAL DYSRHYTHMIAS


Drug Class III

Potassium channel blockers
(Amiodarone and sotalol)
Prolong refractory period which stabilizes the dysrhythmia.
Refractory period is the resting periods that occurs after depolarization in which a cell cannot initiate another action potential
Produces slowing of HR
Can worsen dysrhythmias


Drug Class IV

Calcium channel blockers
(Verapamil and diltiazem)
Stabilize dysrhythmias be decreasing automaticity at SA node, slowing conduction velocity through the AV node and prolonging the refractory period.
Generally well tolerated


Miscellaneous Drugs

Digoxin and adenosine



*most commonly used
Thera: Antidysrhythmic
Pharm: Potassium Channel Blocker
Indications: Treatment of life threatening ventricular dysrhythmias, treatment of atrial dysrhythmias (off-label)
MOA: Prolongs action potential and refractory period slowing the HR. Decreases peripheral vascular resistance through vasodilation
Adverse: Worsens dysrhythmias, pulmonary toxicity, bradycardia, hypotension, N/V, dizziness, fatigue, blue discoloration of skin, increased liver enzymes, effect on thyroid function, photosensitivity, tremors, blurry vision
Interactions: Multiple drug interactions, increases drug levels of digoxin, warfrin and carvedilol.
Nursing: Requires losing dose, ECG monitoring if IV, monitor HR and BR, assess for pulmonary toxicity, monitor liver and thyroid function, AVOID GRAPEFRUIT juice. Can be given PO or IV, has prolonged half life and is Preg Cat D



Decreases automaticity of SA node and slows conduction through AV node. Used to atrial dysrhythmias. Narrow therapeutic window and many interactions with other medications. May Cause yellowing of vision



Administered by IV (rapid IV push) to decrease automaticity of SA node and slow conduction of AV node. Used to terminate atrial dysrhythmias or slow conduction (to determine underlying rhythm). Duration of action if 15 seconds


Nursing implications for Antidysrhythmic Drugs

Educate client about side effect and monitoring pulse.
Do not discontinue medication even if feeling ill
ECG monitoring while in hospital for changes in HR or rhythm
Monitor BP
Factors that may increase risk of dysrhythmias:
Electrolyte disturbances (esp K+ and Mg)
Decreased O2 levels
Monitor fluid status for signs of HF



"Strangling of the chest"
Reduced BP causes ischemia to the heart muscle.
Stable: Most common, >70% stenosis, causes common artery to work harder and cannot meet demands of heart muscle
Unstable: pain during exercise or stress, doesnt go away. Heart tissue is alive but ischemic
Vasospastic: may/may not have atherosclerosis. Ischemia from coronary artery vasospasm.




Volume of blood in the ventricles at the end of diastole


After load


Resistance left ventricle must over come to circulate blood



Relax both arterial and venous smooth muscle (a little stronger at venous system), reduces workload of the heart, dilates coronary arteries
Examples: Isosorbide and nitroglycerine (come in both SA and LA)
Short Acting: Given sublingual to stop acute angina attack
Long Acting: Given PO or transdermal to decrease frequency and severity of attacks
Adverse: Hypotension, dizziness, headache, flushing of face, reflex tachycardia, can develop tolerance.
*need to have nitrate free period to avoid tolerance*
DO NOT USE with viagra, Levitra and Cialis may cause life threatening hypotension and cardio collapse


Administration of nitroglycerine.

1 tablet sublingual
No relief after 5 minutes, give 2nd dose
No relief after 5 minutes, give 3rd dose
No relief after 3 doses, CALL EMS


Beta Blockers

Block Beta receptor site resulting in reduced workload by slowing heart rate and reducing contractility which in turn decreases BP and myocardial O2 demand. Negative inotropic effect
Indications: HTN, HF, arrhythmias, MI mortality (8 hours), prophylaxis for angina
Adverse: Bradycardia, hypotension, dizziness, fatigue, decreased sexual ability, depression, worsening heart failure symptoms, bronchoconstriction
Education: Rise slowly (orthostatic htn), DO NOT stop taking suddenly. Check pulse daily (<60 report), Check BP daily (<90/60 report)
Implications: monitor HR and BP, may mask symptoms of hyperglycemia (think diabetics), avoid in patients with asthma
Black box for patients with CAD - do not stop taking abruptly


Calcium Channel Blockers

Inhibit transport of Ca+ into myocardial cells, relax arteriolar smooth muscle (decreases workload/inhibits muscular contraction), dilate coronary arteries (relaxation of arteriolar vasculature and a reduction in BP)
Reduce myocardial O2 demand by lowering BP and HR (CCB classes vary in ability to affect HR)
Typically NOT first drug for HTN
African Americans tend to respond more favorably to CCBs
3 different sub-classes that differ in ability to treat HTN, angina and arrhythmia
Adverse: hypotension, bradycardia, HF symptoms, headache, fatigue, arrhythmias
END IN PINE (amlodipine, felodipine, nicardipine, nifedipine) except DILTIAZEM and VERAPAMIL


Goals for treating MI

Early diagnoses and treatment to reduce mycardial ischemia and damage, relieve pain, reduce mortality & long term disability
1. Restore blood supply
2. Reduce myocardial O2 demand
3. Control prevent dysrhythmias
4. Reduce post MI mortality
5. Manage pain/anxiety
6. Prevent enlargement of clots



EX: reteplase, alteplase, tenecteplase (END IN -plase)
Dissolve clots obstructing coronary arteries to restore perfusion to myocardium. Followed by anticoagulant therapy to prevent additional clots.
Administer within 12 of initial symptoms
Narrow margin of safety
Adverse: hemorrhage, hypotension
Used when MI patient cannot make it to CATH lab.
Contraindications: previous inter-cranial hemorrhage, recent ischemic stroke (<3 mos), recent internal bleeding, recent intercranial surgery/spinal surgery, recent major surgery/trauma/prolonged CPR, severe and uncontrolled hypertensions (SBP >180)


Nursing considerations with Thrombolytics

Administer through dedicated IV line
Frequent vitals (15-30 min during infusion)
Hourly neurological checks (inter-cranial bleeding)
Monitor for bleeding
Client on bed rest
Monitor ECG and for arrhythmias


Anti-platelet/Anticoagulant for MI

Aspirin (325mg) given ASAP when MI is suspected then daily (81mg)
Other: clopidogrel (placid), eptifibatide (Integrilin) and heparin


ACE Inhibitors

Reduce MI mortality is started w/in 24 hours
Inhibit angiotensin 1 from turning into angiotensin 2. Inhibits RAAS system.
Dilated arteries and decrease blood volume)
Used for HF, MI and HTN
No Angina



Stopping of blood flow; it is a complex balance that attempts to maintain a balance between blood and fluidity coagulation



Starts 24-48 hours after clot formation and continues until clot is dissolved


Tissue Plasminogen Activator (tPA)

Enzyme secreted by blood vessels located near the clot. TPA converts plasminogen to plain which digests fibrin strands ultimately dissolving the clot



Used to prevent the formation of clots. Increase normal clotting time. Used primarily to prevent clot formation in VEINS
Usually started IV or SQ then switched to PO
Adverse: bleeding
Reversal agents: Protamine sulfate for heparin. Vitamin K or FFP reverses warfarin
Examples: heparin, warfarin, enoxaparin, bivalirudin


Anti-platelet agents/drugs

Inhibit platelet aggregation. Primarily used to prevent clot formation in arteries
Monitor signs and symptoms of bleeding
Classes: aspirin (ASA), adenosine diphosphate (ADP) receptor blockers (clopidogrel/placid, ticlodipine/Ticlid), glycoprotein (GP) IIb/IIIa receptor blockers (abciximab/REOPro)
*antiplatelet effect lasts the life of the platelet
Active bleeding is contraindication



Action is opposite of anticoagulants-- Promote formation of clots. Inhibit removal of fibrin. Speed clot formation and shorten bleeding time
Most often used to prevent excessive bleeding after surgery or in clients with systemic clotting disorders (oncology and open heart patients)
EX: aminocaproic acid (Amicar), topical thrombin, trade amid acid (Lysteda)



Thera class: anticoagulant
Pharm class: Indirect thrombin inhibitor
Indications: Prevent formation of clots, often prophylactically
MOA: binding of heparin to antithrombin III blocks clotting through the inactivation of Factor X and inhibition of prothrombin conversation to thrombin.
Adverse: Bleeding, heparin induced. Thrombocytopenia (platelet counts drops day over day)
Indications: Administered SQ, or IV, monitor for bleeding, monitor platelets, monitor PTT goal 1.5-2.5 x normal range (if informal is 35 we want 60-70)
Protamine sulfate if antidote
Half life is 1 hour (for IV)
Black box: paralysis can result when used with epidurals/spinal hematoma


Low Molecular Weight Heparins

Enoxaparin (Lovonox) and dalteparin
Indications: prophylaxis and treatment of DVT and PE, Unstable angina/non-Q-wave MI
MOA; binds to antithrombin and accelerates its ability to inhibit factor Xa preventing growth of thrombi
Adverse: Bleeding, bruising at invention site
Implications: DO NOT EXPEL AIR BUBBLE when SQ. Generally no lab monitoring, discontinue 24 hours prior to surgery. Protamine sulfate is antidote.
*LMWH is replacing UFH due to better SQ absorption, longer half life, less frequent dosing and lower risk of HIT and osteoporosis



Thera class: Anticoagulant
Pharm Class: Vitamin K antagonist
Indications: Prevent formation of clots and can be used prophylactically. Chronic AFib often take at home.
MOA: block generation of VitK thereby inhibiting the synthesis of VItK dependent clotting factors
Adverse: Bleeding, skin necrosis (rare)
Implications: give at same time each day (usually 5pm), takes several days to reach max effect (overlaps with heparin therapy - start heparin IV then warfarin for 3-4 days until it fully kicks in). Monitor PT/INR (goal is INR 2-3), bleeding precautions, contraindicated in pregnancy. MULTIPLE DRUG & DRUG/DIET INTERACTIONS (avoid too much VitK). Be consistent



Elevation in arterial blood pressure
Systolic >140
DIastolic >90
Treatment based off guidelines developed but JNC-8
Need multiple BP readings to diagnose HTN
Untreated can lead to: stroke, MI, HF, renal damage, vision loss


Blood Pressure

Cardiac output, Peripheral vascular resistance, Blood volume are regulated by baroreflexes (located in the aortic arch and carotid sinuses sense drop in BP and signal NS) and the Renin-Angiotension-Aldosterone System (RAAS)



Kidneys sense a drop in BP and drop in sodium in renal tubules OR stimulation of the SNS and respond by releasing renin. Renin converts angiotensinogen to angiotensin I. Angiotensin I converted by ACE to angiotensin II (potent vasoconstrictor) and Angiotensin II stimulates the release of aldosterone which causes sodium reabsorption leading to increased blood volume


ACE Inhibitors

Reduce blood pressure by inhibiting RAAS (dilating arteries and decreasing BV).
Decreases preload and afterload, can stop or slow cardiac remodeling
Excellent choice for diabetics as they also slow the progression of kidney failure
Prevent death after MI
End in PRIL (lisinopril, catopril, enalapril)



Prinivil, Zestril
Thera: Drug for HTN, HF and MI prevention
Pharm: ACE inhibitor
Indications: HTN, HF and acute MI
MOA: prevents conversion of angiotensin 1 to angiotensin 2 thereby decreasing vasoconstriction and aldosterone secretion. Excreting out Na+ and retaining K+
Adverse: Orthostatic hypotension, dizziness, headache, ANGIOEDEMA, PERSISTANT DRY COUGH, renal impairment, hyperkalemia
Implications: discontinue if pregnant or planning, patient education, avoid high Na+ and K+ foods, first does phenomenon, monitor renal function and K+


Angiotensin Receptor Blocker

Block the binding of angiotensin 2 to angiotensin receptors
Similar MOA as ACE
Similar adverse effect as ACE but with less dry cough and angioedema
ENDS IN SARTAN (valsartan, losartan, candle sartan, irbesartan)



Thera: antihypertensive, Antianginal, anti arrhythmic
Pharm: Calcium Channel Blocker
Indications: HTN, angina, tachyarrhythmias
MOA: blocks transport of calcium into myocardial and vascular smooth muscle cells
Contraindications: heart block.shock
Adverse: hypotension, bradycardia, heart failure symptoms, headache, fatigue, N/V, arrhythmias
Implications: Monitor HR,BP,ECG (prior and during), administered PO or IV


Second Line Treatments for HTN

Beta adrenergic blockers (antagonists)
Alpha 1 adrenergic blockers (antagonists)
Alpha 2 adrenergic agonists

Aldosterone antagonists
Renin inhibitors

Direct vasodilators


First Lien Treatments for HTN

Thiazides Diuretics
ACE Inhibitors

African Americans first line is thiazides and CCBs as they have poor response to ACE and ARB


Selective vs Nonselective BB

Nonselective - block both beta 1 and beta 2 receptors

Selective - block only beta 1 receptors.
I.e. No bronchoconstriction.
May lose the feature at higher doses


Alpha 1 Adrenergic Blockers

Indications: HTN, benign prostatic hypertrophy (BPH)
MOA: blocking the A1 adrenergic receptors results in vasodilation and relaxation of smooth muscles in prostate and bladder
Adverse: orthostatic hypotension, dizziness/drowsiness, headache, First Dose phenomenon (take around bedtime)
Implications: Take at night to avoid dizziness/drowsiness, rise slowly when getting up
Examples: doxazosin, prazosin, terazosin


Alpha 2 Adrenergic Agonists

Indication: HTN
MOA: stimulating A2 receptors results in decreased sympathetic responsive from CNS causing vasodilation and decreased BP
Adverse: depressed CNS, dizziness, drowsiness, orthostatic hypotension
Implications: Do not stop abruptly (rebound HTN, withdrawal), rotate patch site weekly.
Example: clonidine


Renin inhibitors

MOA: directly inhibits renin. Works earlier in the RAAS than ACE and ARBs
Adverse: diarrhea, renal impairment, headache, dizziness, cough (less likely than ACE), flu-like symptoms
Implications: Similar as ACE and ARBS, contraindicated during pregnancy
Examples: aliskiren



*Adverse effects and dosing regimen prevents it from being first line treatment
Indications: HTN crisis (>180/120), during or post-cardiac surgery
MOA: Directly causes relaxations of arteriolar smooth muscles leading to vasodilation and decreased peripheral resistance = lowers BP
Adverse: reflex tachycardia which could precipitate angina, MI or HF
Na+ and H2O retention, flushing headache, N/V, cyanide and thiocyanate toxicity
Implications: Adminicatered as IV continuous infusion, rapid onset and short half life, monitor BP, HR, monitor for cyanide/thiocyanate toxicity, transition to oral therapy ASAP, dont bring them down too quickly b/c organs are used to high pressure
Effects minimized by concomitant use of a diuretic and BB
Examples: hydralazine (I/PO), minoxidil, nitroprusside (life threatening htn), isosobide dinitrate (HF)


Inotropic drugs

Affect contractility
Positive inatropes increase force
Negative inatropes decrease force


Chronotropic drugs

Affect HR
Positive increase HR
Negative decrease HR


Cardiac Remdeling

Blood backs up in left ventricle causes ventricle to enlarge and attempt to work harder to compensate. This changes the size and shape and structure over time and cardiac cell are injured or die.


Pharm therapy for HF

Reduce preload (less BV in ventricles)
Reduce BP (reducing afterload)
Inhibit RAAS and stimulation of SNS

First line:
ACE and diuretics (must had decent BP)
Second line:
Cardiac glycoside, beta blockers, vasodilators, phosphodiesterase inhibitors (typically combo)


Cardiac GLycoside

Thera: inatropes, antiarrythmic
Pharm: cardiac glycoside
Indications: HF, AFib, atrial flutter
MOA: Increase intracellur calcium leading to positive inotropic effect
Adverse: bradycardia, arrhythmias, fatigue, N/V, blurred yellow vision (toxicity)
Implications: loading dose followed by daily maintenance, monitor drug levels, check apical pulse for one minute before administering.
Digibind is antidote



Thera: antihypertensive, drug for HF
Pharm: Beta Blocker
Indications: HTN, HF, MI
MOA; blocks stimulation of B1,B2 and A1 receptors. Leading it decreased HR and BP
Adverse: dizziness, fatigue, depression, bradycardia, ED, HF, bronchospasms, hyperglycemia
*very cautious with asthma b/c non-selective*
Implications: monitor BP,HR, weight, signs of worsening HF, glucose levels, client education



Thera: Inotrope
Pharm: Phosphodiesterase inhibitor
Indications: a true decompensated HF
MOA: blocking of phosphodiesterase enzyme leads to increased cardiac contractility (pos inotropic) and vasodilation (decrease preload and afterload) leading to increased cardiac output
Adverse: hypotension, arrhythmia s, angina
Implications: continuous IV, short half life, monitor BP ECG


Human B-Type Natriuretic Peptides

BNP is secreted by ventricles in response to fluid overload
Caused natriuretic effect (increase Na+) and inhibits RAAS
Hypotension is common adverse effect so do not administer if SBP <90
Mesiritide is vasodilator identical to BNP