Drugs For Cardio

Question 1

EKG/ECG

Answer 1

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

Question 2

Dysrhythmias

Arrhythmia

Answer 2

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

Question 3

Goals of therapy for dysrhytmias

Use of antidysrhythmic drugs

Answer 3

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

Question 4

Ectopic Foci

Ectopic pacemaker

Answer 4

Impulse originating outside of normal conduction system

Question 5

Drug Class I

Answer 5

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

Question 6

Drug Class II

Answer 6

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

Question 7

Drug Class III

Answer 7

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

Question 8

Drug Class IV

Answer 8

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

Question 9

Miscellaneous Drugs

Answer 9

Digoxin and adenosine

Question 10

Amiodarone

Cordarone

Answer 10

*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

Question 11

Digoxin

Answer 11

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

Question 12

Adenosine

Answer 12

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

Question 13

Nursing implications for Antidysrhythmic Drugs

Answer 13

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

Question 14

Angina

Answer 14

“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.

Question 15

Preload

Answer 15

Stretch

Volume of blood in the ventricles at the end of diastole

Question 16

After load

Answer 16

Resistance

Resistance left ventricle must over come to circulate blood

Question 17

Nitrates

Answer 17

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

Question 18

Administration of nitroglycerine.

Answer 18

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

Question 19

Beta Blockers

Answer 19

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

Question 20

Calcium Channel Blockers

Answer 20

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

Question 21

Goals for treating MI

Answer 21

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

Question 22

Thrombolytics

Answer 22

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)

Question 23

Nursing considerations with Thrombolytics

Answer 23

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

Question 24

Anti-platelet/Anticoagulant for MI

Answer 24

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

Question 25

ACE Inhibitors

Answer 25

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

Question 26

Hemeostatics

Answer 26

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

Question 27

Fibrinolysis

Answer 27

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

Question 28

Tissue Plasminogen Activator (tPA)

Answer 28

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

Question 29

Anticoagulants

Answer 29

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

Question 30

Anti-platelet agents/drugs

Answer 30

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

Question 31

Hemostatics

Answer 31

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)

Question 32

Heparin

Answer 32

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

Question 33

Low Molecular Weight Heparins | LMWH

Answer 33

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

Question 34

Warfarin | Coumadin

Answer 34

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

Question 35

Hypertension

Answer 35

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

Question 36

Blood Pressure

Answer 36

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)

Question 37

RAAS

Answer 37

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

Question 38

ACE Inhibitors

Answer 38

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)

Question 39

Lisinopril

Answer 39

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+

Question 40

Angiotensin Receptor Blocker | ARBs

Answer 40

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)

Question 41

Diltiazem

Answer 41

Cardizem 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

Question 42

Second Line Treatments for HTN

Answer 42

Beta adrenergic blockers (antagonists) Alpha 1 adrenergic blockers (antagonists) Alpha 2 adrenergic agonists Aldosterone antagonists Renin inhibitors Direct vasodilators

Question 43

First Lien Treatments for HTN

Answer 43

Thiazides Diuretics CCB's ACE Inhibitors ARBs African Americans first line is thiazides and CCBs as they have poor response to ACE and ARB

Question 44

Selective vs Nonselective BB

Answer 44

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

Question 45

Alpha 1 Adrenergic Blockers

Answer 45

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 END IN AZOSIN

Question 46

Alpha 2 Adrenergic Agonists

Answer 46

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

Question 47

Renin inhibitors

Answer 47

Indications:HTN 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

Question 48

Vasodilators

Answer 48

*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)

Question 49

Inotropic drugs

Answer 49

Affect contractility Positive inatropes increase force Negative inatropes decrease force

Question 50

Chronotropic drugs

Answer 50

Affect HR Positive increase HR Negative decrease HR

Question 51

Cardiac Remdeling

Answer 51

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.

Question 52

Pharm therapy for HF

Answer 52

``` 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)

Question 53

Cardiac GLycoside | Digoxin

Answer 53

Digoxin 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

Question 54

carvedilol

Answer 54

Coreg 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

Question 55

Milrinone

Answer 55

Primacor 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

Question 56

Human B-Type Natriuretic Peptides | BNP

Answer 56

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