CARDIAC Part I & II- CAD, CHF, Arrythmias Flashcards

Question

Newer Antianginal

Answer 1

Ranolazine (Ranexa) – Approved in first line chronic angina – Decreases late sodium current; decreases intracellular calcium overload – Has no effect on HR, BP, and helps prolong exercise – Safe to use with erectile dysfunction drugs – Dose is 500mg BID – Caution in patients with QT Prolongation (antiarhythmics)- however, there is a decrease in V. arrhymias when used after acute coronary syndrome – Decreased a fib – Caution in significant liver and renal disease

Answer 2

``` Recommended by American College of Physicians ( Snow et. al. 2004). – For chronic stable angina – Prevent MI or death – Reduce symptoms – VAMC (2003) in diabetics and LVD ```

Answer 3

``` Recommended for use in CAD – Diabetes with HTN – LV systolic dysfunction – When patients are intolerant of ACEI – Can be added to ACEI Rx in uncontrolled HTN, or insufficient vasodilation ```

Answer 4

Act by affecting the renin-angiotensinaldosterone (RAA) system to lower blood pressure • Improve oxygenation to the heart muscle • Decrease inappropriate remodeling of heart muscle after an MI, or heart failure • ARBS have similar effect in treating HTN and Heart failure ACEI & ARBS • Work by inhibiting ACE activity • Decrease angiotensin II and aldosterone production • AII- stimulates sm. muscle contractions; – Increased blood pressure – Increases intravascular volume ( stim. Of aldosterone) – Alters glomerular function • AII causes remodeling leading to hypertrophy and fibrosis of cardiac tissue after ischemic injury in response to persistent afterload – primary mechanism in Heart Failure

Answer 5

ACEIs affect MOS (myocardial O2 supply) and MOD (myocardial O2 Demand) • Inhibition of A II decreases PVR (peripheral vascular resistance), decreasing MOD. • Decreases thickening of coronary arteries, therefore, increasing MOS • Decreases thickening of ventricular walls= MOD • Because they decrease aldosterone, they decrease sodium and water retention; decreasing ECF (extracellular fluid volume), and preload • ACEI are recommended by American College of Physicians in chronic stable angina

Answer 6

start low and go slow • Captropril: Heart failure; dose 6.25 - 25mg TID, increase to 50mg TID • Enalapril: Heart failure: start at 2.5mg daily and increase to 40mg daily • Lininopril: heart failure: 5mg daily, maximal dose 20mg

Answer 7

These agents reduce remodeling • An underlying cause of HF is chronic HTN: both are effective treatments • ACEIs are the cornerstone for treatment in Heart Failure, in all the guidelines (Flather et. al, 2000; Hunt et al, 2005; ICSI, 2004; National Collaborating Center for Chronic Conditions, 2003). – Improve symptoms – Decrease morbidity, increase life expectancy – Only set of drugs that address all of the physiologic causes of HF, they helpful in patients with ventricular dysfunction who have no symptoms – All patients with LVD should be on an ACEI

Answer 8

Additive hypotensive effect with diuretics • Acute alcohol, nitrates, phenothiazides, other antihypertensives • Hyperkalemia can occur with concurrent use of potassium supplements, cyclosporin and potassium-sparing diuretics • Antihypertensive response is diminished with NSAIDS

Answer 9

``` Bilateral renal artery stenosis • Angioedema: occurs in .2% – Is life threatening and if occurs, can not switch to another agent in the same category – Seen with ACEI not ARBs • Pregnancy; category C in 1st trimester, and Category X in 2nd and 3rd . • Hyperkalemia • Hepatic impairment ```

Answer 10

``` Reactions are usually mild and transient • Cough; can change to another drug from same class: ARBs do not cause cough • Hypotension: dizziness, headaches, fatigue, postural hypotension • Rash: most common with Captopril, not ARBs ```

Answer 11

``` • With no intrinsic sympathominimetic activity (ISA) recommended as initial Rx – With or without previous MI – Decrease MOD – Drug of choice for exertional angina (ACC/AHA, all classes) – Main goal is to prevent recurrence of MI in patients with CAD – In patients who have resting tachycardia (hyperthyroidism) Beta Blockers in CAD • Decreased sympathetic nervous system stimulation – Reduced cardiac workload by decreasing HR and contractility by blocking beta1 receptors; decrease afterload .Used for angina prevention. – Decreased activation of reninangiotensin-aldosterone •Used post-myocardial infarction Beta Blockers in CAD • Slowed Heart Rate – ➔ Increased diastolic filling time • → Increased coronary perfusion • → Increased O2 supply – ➔ Decreased myocardial workload • → Decreased myocardial O2 consumption • → Decreased O2 demand ```

Answer 12

``` Atenolol (Tenormin) • Metoprolol (Lopressor, Toprol XL) – Best BB for asthma patients • Nadolol (Corgard) • Propanolol (Inderal) ```

Answer 13

Check resting HR and exercise HR. HR 50-60 is usually good evidence of beta blockade exertional HR should be

Answer 14

Use cautiously with asthmatics, sick sinus syndrome, 2nd & 3rd degree heart block, diabetes – Metoprolol is best for asthmatics

Answer 15

``` Dizziness, lightheadedness – Fatigue, nightmares, – Heartburn, constipation, diarrhea – Sudden weight gain – Sexual dysfunction ```

Answer 16

``` Report dizziness, light-headedness, faintness with position changes – Orthostasis • Do not discontinue suddenly! – Beta blocker withdrawal syndrome •Tachycardia, CHF •Increased platelet aggregation ```

Answer 17

Contraindicated in patients with severe | reactive airway disease

Answer 18

Most cost effective Beta blocker is atenolol | (Tenormin), twice day dosing

Answer 19

``` Kaiser guidelines (2006) recommend in patients with LV systolic dysfunction stages I-IV ```

Answer 20

Calcium is crucial in the excitation-contraction of muscles; in electrical excitation and myocardial relaxation. • There are 3 types of voltage channels that Ca uses to enter cells- L-type, N-type, T-type • L-type channels are predominant in cardiac and smooth muscle- these are what CCB mostly block • In cardiac conduction, CCBs close calcium channels (not all of them!) to decrease heart rate Calcium Channel Blockers • Cardiac muscle is highly dependent on calcium influx during each action potential for normal function. – Impulse generation in the SA node, and conduction in the AV node- slow response or calcium dependent action potentials • Are all reduced or blocked by CCB’s – Excitation-concentration coupling in cardiac cells requires calcium influx • CCB’s reduce contractility (dose dependent). Decrease CO. • Ultimately reduce O2 requirement.

Answer 21

``` Calcium Channel Blockers • Multiple Indications: – Angina – HTN – Selected tachyarrhythmias • Unlabeled Indication: – Migraine headache prophylaxis – Raynaud’s syndrome – Cardiomyopathy – Esophageal spasm Used for stable and unstable angina • Indications •Vasospastic (variant, Prinzmetal) angina: relax coronary artery vasospasm •First choice in patients who don’t tolerate nitrates and if beta blockers are contraindicated – Relax peripheral arterioles, reduce afterload & cardiac O2 demands ```

Answer 22

``` Type 1 Nondihydropyridines – Verapamil (Calan) – Diltiazem (Cardizem) • Type 2 (Dihydropyridines) – Amlodipine (Norvasc) – Nifedipine (Procardia) – Nicardipine (Cardene) – Felodipine (Plendil) ```

Answer 23

``` Decrease myocardial oxygen demand by: There are 3 receptors – Choice of CCB is dependent on how the channel is opened. – Dilation of peripheral vessels (Types 1 and 2), primarily arteriolar dilation •Reduced afterload (reduced PVR) – Depression of cardiac contractility- (Type 1) – Depression of heart rate - (Type 1) •Depression of automaticity and conduction through the SA and AV nodes Calcium Channel Blockers - Actions in CAD • Increase myocardial oxygen supply by: •Causing coronary vasodilation and preventing vasospasm (Types I and II) – Improve blood supply to both ischemic and non-ischemic tissue •Enhancing diastolic relaxation of the left ventricle (Type I) – improved filling of the coronary arteries ```

Answer 24

Dihydropyridine-based work to increase reflex in sympathetic tone, to overcome negative inotropic effects – Reduction in afterload, but little effect on preload – Slow recovery channel – Do not affect rate of recovery through channels – Do not affect conduction through AV node.

Answer 25

Affects opening of calcium channels – Decreases rate of recovery, thus causing depression of the AV nodal conduction- this is the basis of treating supraventricular tachcardia – Has a direct negative inotropic effect. • Veraparmil has strongest effect and should avoided in CHF, it can worsen the disorder – Type I receptor

Answer 26

IN GENERAL: Not drug of choice immediately after MI. exception is Diltiazem: reduces mortality in Q-wave MI if EF is > 40 %. • Otherwise contraindicated due to negative inotropic and bradycardia • Patients with SA, AV node disturbances or SBP

Answer 27

– Exert strong peripheral vasodilation – Should be avoided in patients with peripheral edema, can result in pooling and reflex tachycardia – Contraindicated in unstable angina, can cause tachycardia – If necessary in the above situations, a long acting preparation is recommended.

Answer 28

``` CCBs vasodilate arterioles, but in areas of ischemia, arterioles may already be maximally dilated. Dilation of arterioles in non-ischemic tissues then draws blood away from ischemic areas → infarct of ischemic areas ```

Answer 29

``` Well absorbed • Significant 1st pass effect • Highly protein bound • Excreted urine • Use cautiously in liver disease ```

Answer 30

Nitrate plus calcium channel blocker – For patients who are poor candidates for beta blockers • Calcium channel blocker (amlodipine) and beta blocker – Additive effect in decreasing cardiac workload, BP • Calcium channel blocker (amlodipine), beta blocker, nitrate

Answer 31

``` • Nifedipine: reflex tachycardia*, ? Increased mortality if MI or angina • Verapamil: constipation • All: flushing, HA, dizziness, gingival hyperplasia, edema » *reflex tachycardia: BP goes down, baroreceptors sense decr. BP & HR increases ```

Answer 32

Inhibits synthesis of thromboxane A2, in the production of platelets. • Recommended after Heart attack – Stable or unstable angina – During a heart attack – Recommended dose is between 81mg to 162.5 mg/daily

Answer 33

Combination treatment can be more beneficial than single agent drugs • Adequately reduce MOD, using lower doses and decreasing side effects. • Lower doses reduce risk of hypotension • Nifedipine and Amodipine ( dihydropyridine CCB), are examples • Combinations of B blockers and Nitrates are safe, cost effective • Verapamil and Ditiazem should not be used together as they can potentiate HF and bradycardia – Combinations of long acting nitrates and CCB’s not used, as SE panel is additive

Answer 34

Focus on PREVENTION of MI – Dietary management – Aspirin – Statins- aim to decrease LDL to

Answer 35

``` Prolong clotting time, stabilize thrombi – Heparin: inhibits anti-thrombin III • IV, SQ, LMWH – Warfarin (Coumadin): inhibits hepatic synthesis of coagulation factors ```

Answer 36

Monitor platelets for heparin induced thrombocyopemia (HIT) – HIT=antibody reaction against heparin – platelet complexes causing thrombosis and precipitous drop in platelets • Risk of DVT, PE, MI, stroke • Nursing implications: monitor CBC/diff, PT/PTT. Stop heparin if necessary. • Rx=lepirudan or argatroban • Antidote heparin OD= protamine sulfate IV

Answer 37

``` Shorter molecule than unfractionated heparin – Inactivate factor Xa – Enoxaparin (Lovenox), dalteparin (Fragmin), tinzaparin ( Innohep) – Used for prevention/rx. DVT, PE, MI – SQ abdomen QD-BID depending ```

Answer 38

Fondaparinus ( Arixtra) | • Rivaoxaban (Xarelto)

Answer 39

``` PT/INR • Antidote: Vitamin K – Reverses risk bleeding associated with warfarin (Coumadin) – May be given IV, IM, SQ,PO ```

Answer 40

Glycoprotein IIb/IIIa receptor blockers 2. Adenosine diphosphate receptor blockers 3. ASA – Binds irreversibly to cyclooxygenase in platelets and inhibits platelet aggregation Glycoprotein IIb/IIIa receptor blockers – Inhibit enzyme necessary for platelet aggregation – Used if patient having an MI, stroke, PTCA – IV use only

Answer 41

Used to dissolve blood clots – t-PA (Activase now most commonly used – History very important as contraindicated recent surgery, trauma, childbirth, GI bleed, thrombocytopenia

Answer 42

Complex clinical syndrome, that includes any structural or functional cardiac disorder altering cardiac output, resulting in inadequate supply of the oxygen demands of the body • A number of abnormalities – CAD, underlying cause in about 2/3 of individuals – Left ventricular dsyfunction, (systolic heart failure) • progressive

Answer 43

``` Systolic Dysfunction – Often acute; following an MI – Decreased force generated to eject blood from the ventricles •Other causes: nonischemic cardiomyopathy, alcohol and drug that affect the myocardium, conditions that = vol overload Types of HF, cont. • Diastolic Dysfunction – Inadequate relaxation and loss of muscle fiber, with resulting loss of elasticity – Slower filling rates – Elevated diastolic pressures, decreased cardiac output – May have normal EF – Causes: • Uncontrolled HTN, hypothyroidism, hypertrophic and ischemic cardiomyopathy, elderly • Highest rate in elderly women, > 70 ```

Answer 44

New York Heart Association (NYHA); classified based on symptoms: See handout • Four Classes • SYMPTOMS: – Based on Left vs Right ventricular failure – Lung symptoms (congestion) ,are usually LVF – Body-focused, edema, are usually RVF

Answer 45

``` Improvement of symptoms • Reduction in mortality • Reduction in morbidity – Decrease overload, either preload and/or afterload. – Improve contractility – Decrease heart rate ```

Answer 46

Stage A: At risk for HF but without structural heart disease for sx of HF – HTN, CAD, DM – Patients using cardiotoxins, FH of cardiomyopathy – TREAT: • HTN, smoking cessation, Rx lipid disorder, regular exercise, discourage ETOH, and illicit drug use • Treat with ACEI- Captopril 6.25mg, only short acting ACEI ,can be d/c’d if renal issues, otherwise go to longer acting ACEI (go to ARB if not tolerated)

Answer 47

(structural heart disease, without symptoms or HF) • Previous MI • LV systolic dysfunction • Asymptomatic valvular disease • Treatment: – Utilize all Rx measures for Stage A – ACI I, in appropriate patients- moderate increase in EF, decrease LV end diastolic pressures, improve myocardial metabolism, only drug that addresses all pathophys causes, (Contraindicated in pregnancy and renal artery stenosis. – ACEI useful in reducing HF Stage B, (continued) • Beta Blockers and ACEI are superior both as monotherapy and in combination • Beta Blockers- in appropriate patients; MI prophylaxis – Unless contraindicated should be given in all patients with recent MI, and LV dysfunction – Added to ACEI – Recommended for all patients who have not had MI and reduced EF of = 40% – Careful use in acute MI as these agents can cause acute decompensation Stage B, (cont.) • Beta Blockers: – Increase life expectancy in HF with LV dysfunction – 3 BB with strongest evidence • Bisoprolol • Metoprolol 12.5mg qd, up to 200mg qd • Cavedilol- this one is alpha1, BB starting dose: 3.125mg BID,titrated up to 25mg to 50mg BID max

Answer 48

``` Stage C (development of symptoms of HF) Known structural heart disease • Shortness of breath, and fatigue, reduced exercise tolerance • TREATMENT: – All measures used for Stage A – Diuretics – ACEI – Beta Blockers – Digitalis – Sodium reduced diets Stage C Treatment • Digoxin: Cardiac Glycoside; indicated in HF and Afib. • Doses -125mg - .375mg/daily • Inhibits sodium-potassium ATPase, increasing intracellular Na resulting in increased intracellular Ca -> + inotropic action: which reduces sympathetic response and reninangiotensin, system output, thereby reducing the heart rate ```

Answer 49

Stage D-refractory symptoms of HF at Rest • Patients with marked symptoms at rest, despite maximal therapies- frequent hospitalizations, not safely d/c without specialized interventions • TREATMENT: – All measures in A,B, C – Mechanical assist devices, implantable pacers, defib – Continuous IV inotropic infusions for palpitations – hospice

Answer 50

• Contraindicated: hypersensitivity, Vfib • Precautions: elderly, Av block, weight loss, – Hypokalemia, hypocalemia, hypomagesemia – Need a diet high in K, mg – Hyperthyroidism-may be resistent – Renal impairment – Side effects: N,V, Dizziness, mental disorders (halos, green/yellow), cardiac dysrhythmia, ischemia, SA block, vasoconstriction, thrombocytopenia

Answer 51

Absorption: well absorbed orally- however taking with high bran/fiber, inhibits absorption and should be taken ½ hour ac. • Taking with antibiotics can increase bioavailability= toxicity • Metabolized and excreted largely unchanged in the kidneys, ½ life is 36 to 48 hours and longer in the elderly • Pregnancy C

Answer 52

Automaticity - Able to initiate an impulse spontaneously and continuously 2. Contractility - Ability to respond mechanically to an impulse 3. Conductivity - Ability to transmit an impulse along a membrane in an orderly manner 4. Excitability - Ability to be electrically stimulated

Answer 53

Sympathetic - β1 adrenergic receptors (norepi and epi) - Speed up HR Parasympathetic - Vagus nerve - Slow HR

Answer 54

Class I: Sodium-Channel Blockers * Class II: Beta-Blockers * Class III: Potassium-Channel Blockers * Class IV: Calcium-Channel Blockers • Miscellaneous: Electrolytes (Mg and K+), adenosine, digitalis compounds (cardiac glycosides), atropine (muscarinic receptor antagonists)

Answer 55

Reduce the rate and magnitude of depolarization by blocking sodium channels is a decrease in conduction velocity in non-nodal tissue (atrial and ventricular muscle, Purkinje conducting system). • Blocking sodium channels reduces the velocity of action potential transmission within the heart (reduced conduction velocity; negative dromotropy) • Anticholinergic actions - Inhibit vagal activity -> increase in sinoatrial rate and atrioventricular conduction -> offset the direct effects of the drugs on

Answer 56

Slow pacemaker and decrease conduction velocity. Also increase action potential duration and effective refractory period of non-pacemaker cells

Answer 57

Blocking potassium channels slows repolarization and increased the effective refractory period * Increase QT interval * Effective for re-entry mechanism arrhythmias

Answer 58

Block calcium entry into cell • Decrease firing rate of aberrant sites • Decrease conduction velocity and prolong repolarization, esp. at the AVN.

Answer 59

Muscarinic receptor antagonists • Block vagus nerve (parasympathetic system)

Answer 60

• Class I: Greatest risk for proarrhythmia, especially in patients with structural heart disease (coronary heart disease and/or left ventricular dysfunction) • Class II: beta blockers, except sotalol (also has class III properties). No tachyarrhythmic or proarrhythmic effects but can cause bradycardia. • Class III: Prolong repolarization and pose the specific risk of torsades des pointes ventricular tachycardia. Proarrhythmic Risks • Depending upon the medication selected and other patient-specific factors, initiation of therapy may need to be done with patient hospitalized for observation. • Dofetilide and Sotalol labelings specify inpatient initiation. • Flecainide, propafenone, dronedarone, and amiodarone can generally be initiated on an out-patient basis in appropriate patients.

Answer 61

Is the arrhythmia causing symptoms or could it? * Does the arrhythmia pose a risk to the patient? * Which arrhythmia is present? * Does the arrhythmia require emergent cardioversion? * Does the patient require urgent hospitalization? • Is specialist consultation required, and if so, how urgently? • Should anticoagulation and/or other medical therapy be started?

Answer 62

Specialist Consultation RECOMMENDED when considering initiation of antiarrhythmic Rx. • Must be very familiar with assessing risks. Strong knowledge required of baseline ECG characteristics, structural heart conditions, therapeutic dosing and levels, drug-drug interactions, and other med side effect considerations.

Answer 63

Brand name: Coumadin • Category: Vitamin K antagonist (II, VII, IX, X) Risk vs. Benefit • Reduction in Thromboembolic Events - >80% risk reduction for non-valvular AFa - 60-79% risk reduction for prosthetic heart valves as compared to antiplatelet regimensa • Increased Risk of Hemorrhagic Events - 6% per year (RR 3.4; 95% CI 3.0-3.9)b aHirsh, J., Fuster, V., Ansell, J., & Halperin, J. L. (2003). American heart association/American college of cardiology foundation guide to warfarin therapy. Circulation, 107(12), 1692-1711. bOake, N., Fergusson, D. A., Forster, A. J., & van Walraven, C. (2007). Frequency of adverse events in patients with poor anticoagulation: A meta-analysis. CMAJ: Canadian Medical Association Journal = Journal De L'Association Medicale Canadienne, 176(11), 1589-1594. Warfarin The anticoagulant effect of warfarin is mediated through inhibition of vitamin K- dependent coagulation factors, including clotting factors II, VII, IX, and X. (Proteins C and S) Valentine, K. A. & Hull, R. D. (2009). Therapeutic use of warfarin. UpToDate Online. Last literature review version 18.1 Warfarin (cont.) • Warfarin is rapidly absorbed in the GI tract, circulates bound to plasma proteins, and has a half-life of 36 to 42 hoursa • Warfarin is a racemic mixture of S and R enantiomers, and the more potent S form of the drug is metabolized primarily by the hepatic CYP2C9 systemb a(Hirsh, Fuster, Ansell, & Halperin, 2003) b(Valentine & Hull, 2009) Warfarin (cont.) • Variable amounts of dietary intake of vitamin K will have an effect on warfarin dosing, as will alterations in vitamin-K producing intestinal flora • Because warfarin is strongly protein-bound and only the non-protein-bound fraction is biologically active, any substance that binds to albumin may displace warfarin from its albumin binding sites and increase its biological activity

Answer 64

The prothrombin time (PT) responds to reduction of 3 of the 4 vitamin K-dependent procoagulant clotting factors that are reduced by warfarin and is therefore a surrogate marker of the anticoagulation effect exhibited by the therapy. • The International Normalized Ratio (INR) is the ratio of an individual’s prothrombin time to a control sample, raised to the power of the International Sensitivity Index. Thus, the INR is a standardized value for a patient’s clotting time͘ Limitations of Testing • Variable half-lives of clotting factors - Factor II (prothrombin): half-life approx. 60 to 72 hours • Long half-life of medication - Anticoagulation effect half-life 40 to 70 hours • Non-steady state conditions

Answer 65

AF/AFL • CHADS2 • CHA2DS2 VASc Mechanical Valve DVT PE Prophylaxis

Answer 66

Goal Ranges - 2.5 (2-3) or 3.0 (2.5-3.5)

Answer 67

Brand name: Pradaxa • Category: Thrombin Inhibitor • Major Trial: RE-LY Dabigatran Indications/Dosing: • Non-valvular AF: 150 mg PO bid - Renal: CrCl 15-30: 75 mg bid Pharmacodynamics/kinetics: No CYP450. Primarly excreted urine. Half-life 12-17 hrs aPTT provides an approximation of anticoagulant effect Ecarin clotting time (ECT) more specific measure of effect

Answer 68

Brand name: Xarelto • Category: Factor Xa Inhibitor • Major trial: ROCKET AF Rivaroxaban Indications/Dosing: • Non-valvular AF: 20 mg PO qd - give with evening meal - Renal: CrCl 15-50: 15 mg qd • DVT prophylaxis: 10 mg PO qd x 35 days (hip replacement) or x12 days (knee replacement) Pharmacodynamics/kinetics: CYP450: 2J2, 3A4/5, excreted urine 66% - 36% unchanged. Half-life 5- 9 hrs (longer in elderly)

Answer 69

Brand name: Eliquis • Category: Factor Xa Inhibitor • Major trial: ARISTOTLE Apixaban Indications/Dosing: • Non-valvular AF: Oral: 5 mg twice daily unless patient has any 2 of the following: ge ≥80 years, body weight ≤60 kg, or serum creatinine ≥1͘5 mg/dL, then reduce dose to 2.5 mg twice daily. Pharmacodynamics/kinetics: * Onset: 3-4 hours * Protein binding: ~87% • Metabolism: Hepatic predominantly via CYP3A4/5 and to a lesser extent via CYP1A2, 2C8, 2C9, 2C19, and 2J2 to inactive metabolites; * Bioavailability: ~50% * Half-life elimination: 2.5 mg dose (repeated oral administration): ~8 hours; 5 mg single dose: ~15 hours (Frost, 2012) • Time to peak: 3-4 hours • Excretion: Urine (~27% as parent drug); feces (~25% of dose recovered as metabolites)

Answer 70

ASA alone * ASA + Clopidogrel * ACTIVE A and W trial data * It should be kept in mind that as dual antiplatelet therapy and oral anticoagulation have similar bleeding risks, a patient who would not be a candidate for oral anticoagulation because of bleeding risk is also not a candidate for dual antiplatelet therapy.