Cardiovascular Drugs Study Notes

Anti-hypertensive Drugs

• Hypertension Definition (JNC-8):
  • Aged 60 or older: Systolic Blood Pressure (SBP) > 150 mm Hg or Diastolic Blood Pressure (DBP) > 90 mm Hg.
  • Younger than 60, or those with chronic kidney disease/diabetes: SBP > 140 and DBP > 90.
  • Hypertension as a major risk factor for Coronary Artery Disease (CAD) and Cardiovascular Disease (CVD).
• Blood Pressure (BP) Calculation: BP = Cardiac Output (CO) × Systemic Vascular Resistance (SVR).
• Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-8):
  • Initial treatment for non-African Americans: thiazide diuretic, calcium channel blocker, ACE inhibitor, or ARB.
  • Initial treatment for African Americans: thiazide diuretic or calcium channel blocker.
  • If target BP isn't reached within one month, increase the initial medication dosage or add a second medication.
• Individualized drug therapy is crucial.
• Seven main drug categories to treat hypertension:
  • Angiotensin-converting enzyme (ACE) inhibitors
  • Angiotensin II receptor blockers (ARBs)
  • Beta blockers
  • Calcium channel blockers (CCBs)
  • Diuretics (first-line treatment)
  • Vasodilators
  • Adrenergic drugs, including direct renin inhibitors
• African-American patients generally respond better to CCB + Diuretic combinations.

Angiotensin-Converting Enzyme (ACE) Inhibitors

• Large group of safe and effective drugs (currently 10 ACE inhibitors).
• Often used as first-line drugs for Heart Failure (HF) and hypertension.
• May be combined with a thiazide diuretic or CCB.
• Mechanism of Action (MOA): Inhibit Angiotensin-Converting Enzyme (ACE).
• Suffix: "PRIL".
• Renin-Angiotensin-Aldosterone System (RAAS):
  • Renin converts Angiotensinogen to Angiotensin I.
  • ACE converts Angiotensin I to Angiotensin II.
  • Angiotensin II causes systemic vasoconstriction, aldosterone release, ADH (pituitary) release, and stimulates thirst (hypothalamus).
  • Aldosterone leads to sodium/water retention and reduced baroreflex sensitivity.
• Examples: Captopril (Capoten), Benazepril (Lotensin), Enalapril (Vasotec), Fosinopril (Monopril), Lisinopril (Prinivil), Perindopril (Aceon), Quinapril (Accupril), Ramipril (Altace), Trandolapril (Mavik).
• Primary Effects:
  • Cardiovascular and renal protection.
  • Reduce BP by decreasing SVR.
  • HF: Prevent sodium and water resorption by inhibiting aldosterone secretion, leading to diuresis.
    • Decreases blood volume and return to the heart.
    • Decreases preload (left ventricular end-diastolic volume).
    • Decreases the workload of the heart
• Cardioprotective Effects:
  • Decrease SVR and preload.
  • Prevent complications after MI, such as ventricular remodeling (left ventricular hypertrophy).
  • Decrease morbidity and mortality in HF patients.
  • Drugs of choice for hypertensive patients with HF.
• Renal Protective Effects:
  • Reduce glomerular filtration pressure.
  • Cardiovascular drugs of choice for patients with diabetes.
  • Reduce proteinuria.
  • Standard therapy to prevent progression of diabetic nephropathy.
• Indications:
  • Hypertension.
  • HF (alone or with diuretics/other drugs).
  • Slow progression of left ventricular hypertrophy after MI (cardioprotective).
  • Renal protective effects in diabetic patients.
• Adverse Effects:
  • First-dose orthostatic hypotension: Monitor blood pressure for 2 hours after initiation.
    • May need to stop diuretics temporarily 2-3 days prior to starting ACE inhibitor.
  • Rash, mood changes, impaired taste (dysgeusia).
  • Hyperkalemia.
  • Dry, nonproductive cough (reversible upon discontinuation).
  • Angioedema: rare but potentially fatal.
• Considerations:
  • Captopril (Capoten):
    • Uses: Prevention of ventricular remodeling after MI; reduce the risk of HF after MI.
    • Shortest half-life, administered multiple times daily.
    • Not a prodrug, so effective in patients with liver disease.
  • Enalapril (Vasotec):
    • Available in both oral and parenteral forms.
    • Oral form is a prodrug.
    • Improves patient survival after MI.
• Laboratory Values:
  • Can cause renal impairment, monitor serum creatinine.
  • Can cause hyperkalemia, monitor potassium levels.

Angiotensin II Receptor Blockers (ARBs)

• Referred to as angiotensin II blockers.
• Well-tolerated.
• Do not cause a dry cough like ACE inhibitors.
• Suffix: “sartan”.
• Mechanism of Action:
  • Affect primarily vascular smooth muscle and adrenal gland.
  • Selectively block binding of Angiotensin II to type 1 Angiotensin II receptors in tissues.
  • Block vasoconstriction and aldosterone secretion.
  • Potent vasodilators, decreasing systemic vascular resistance (afterload); helpful in HF.
• Examples: Losartan (Cozaar), Eprosartan (Teveten), Valsartan (Diovan), Irbesartan (Avapro), Candesartan (Atacand), Olmesartan (Benicar), Telmisartan (Micardis), Azilsartan (Edarbi).
• Comparison to ACE Inhibitors:
  • Equally effective for hypertension.
  • Both are well-tolerated, but ARBs are less likely to cause dry cough and hyperkalemia.
  • Evidence suggests ARBs are better tolerated and associated with lower mortality after MI.
• Indications:
  • Hypertension.
  • Adjunctive drugs for HF.
  • Used alone or with diuretics.
• Adverse Effects:
  • Hypotension.
  • Hyperkalemia and cough (less likely than with ACE inhibitors).
  • Angioedema: swelling of tongue/pharynx (treat with epinephrine, discontinue medication).
• Considerations:
  • Losartan (Cozaar):
    • Beneficial in patients with hypertension and HF.
    • Use with caution in renal/hepatic dysfunction and renal artery stenosis.
    • Not safe for breastfeeding women, avoid in pregnancy.

Beta Blockers

• Mechanism of Action:
  • Block beta1 receptors on the heart.
  • Decrease heart rate, myocardial oxygen demand, and increase oxygen delivery.
  • Decrease myocardial contractility, conserving energy.
• Examples: Propranolol, metoprolol, and atenolol.
• Indications:
  • Angina, antihypertensive, cardiac dysrhythmias, cardioprotective effects (especially after MI).
  • Some used for migraine headaches, essential tremors, and stage fright.
• Contraindications:
  • Systolic HF, serious conduction disturbances.
  • Caution: bronchial asthma (beta2 blockade can cause bronchoconstriction).
  • Diabetes mellitus (can mask hypoglycemia-induced tachycardia).
  • Peripheral vascular disease (may compromise blood flow).
• Adverse Effects:
  • Hypotension, bradycardia.
  • Bronchospasm/wheezing.
  • Reduced renin secretion.
  • Mask signs of hypoglycemia.
  • May cause hyperlipidemia, impotence.
  • Long-term use reduces peripheral vascular resistance.
• Considerations:
  • Nebivolol (Bystolic):
    • Uses: Hypertension and HF.
    • Less sexual dysfunction.
    • Do not stop abruptly; taper over 1-2 weeks.

Dual-Action Alpha1 and Beta Receptor Blockers

• Labetalol and carvedilol: Dual antihypertensive effects: reduction in heart rate (beta1 blockade) and vasodilation (alpha1 blockade).
• Carvedilol (Coreg):
  • Widely used and well-tolerated.
  • Uses: Hypertension, mild to moderate HF (with digoxin, diuretics, ACE inhibitors).
  • Contraindications: Drug allergy, cardiogenic shock, severe bradycardia/HF, bronchospastic conditions (asthma), conduction system problems.

Calcium Channel Blockers (CCBs)

• Mechanism of Action:
  • Cause coronary artery vasodilation and peripheral arterial vasodilation (decreasing SVR).
  • Reduce the workload of the heart.
  • Affect dysrhythmias by depressing automaticity and conduction through SA and AV nodes.
  • Results in decreased peripheral smooth muscle tone, SVR, BP, and myocardial oxygen demand.
• Examples: Nifedipine, Verapamil, Diltiazem, Amlodipine, Felodipine, Nimodipine, Nicardipine.
• Indications:
  • Angina, hypertension (amlodipine).
  • Dysrhythmias.
  • Migraine headaches.
  • Preterm labor (nifedipine), Raynaud’s disease
  • Prevent cerebral artery spasms after subarachnoid hemorrhage (nimodipine).
• Contraindications:
  • Known drug allergy, acute MI, second- or third-degree AV block (unless pacemaker is present), hypotension.
• Adverse Effects:
  • Constipation (primarily verapamil).
  • Reflex tachycardia, orthostatic hypotension, peripheral edema.
  • Suppression of cardiac function (verapamil, diltiazem).
• Interactions:
  • Grapefruit juice can lead to toxicity.
  • Acute toxicity: hypotension, bradycardia, AV block, dysrhythmia.

Diuretics

• First-line antihypertensives (JNC 8 guidelines).
• Decrease plasma and extracellular fluid volumes.
• Results:
  • Decreased preload, CO, and total peripheral resistance.
• Overall effect: Decreased workload of the heart and decreased BP.
• Thiazide diuretics are most commonly used for hypertension.
• Loop Diuretics (Furosemide):
  • Adverse effects: electrolyte imbalance, ototoxicity, hypotension, dehydration, increased LDL and triglycerides.
  • Drug Interactions: Digoxin, Lithium, Aminoglycosides (ototoxicity), NSAIDs.
  • Monitor ECG if potassium drops below normal and notify provider.
  • Take medication first thing in the morning.
• Thiazide Diuretics:
  • Adverse effects: electrolyte imbalance, dehydration, hypotension, hyperuricemia, hyperglycemia.
  • First-line treatment for hypertension.
  • Take medication first thing in the morning.
• Potassium-sparing Diuretics (Aldosterone antagonists):
  • Examples: Spironolactone, Eplerenone.
  • Adverse effects: hyperkalemia, endocrine effects (hirsutism, irregular menstrual cycle, gynecomastia, deepened voice), drowsiness, and metabolic acidosis.
  • Avoid salt substitutes containing potassium.

Vasodilators

• Examples: Diazoxide (Hyperstat), Hydralazine (Apresoline), Minoxidil (Rogaine), Nitroprusside (Nitropress).
  • BiDil (isosorbide dinitrate/hydralazine): for HF treatment in African-American patients.
  • Injectable hydralazine: hypertensive emergencies.
  • Minoxidil: hair regrowth.
• Mechanism of Action: Directly relax arteriolar/venous smooth muscle.
  • Results in decreased SVR, afterload, and peripheral vasodilation.
• Indications:
  • Treatment of hypertension, often in combination with other drugs.
  • Sodium nitroprusside and IV diazoxide are for hypertensive emergencies.
• Adverse Effects:
  • Hydralazine: dizziness, headache, anxiety, tachycardia, edema, dyspnea, nausea, vomiting, diarrhea, hepatitis, SLE, vitamin B6 deficiency, rash.
  • Minoxidil: T-wave changes, pericardial effusion/tamponade, angina, breast tenderness, rash, thrombocytopenia.
  • Sodium nitroprusside: bradycardia, decreased platelet aggregation, rash, hypothyroidism, hypotension, methemoglobinemia, cyanide toxicity (rare).

Centrally Acting Adrenergic Drugs

• Clonidine and methyldopa: stimulate alpha2-adrenergic receptors in the brain.
  • Decrease sympathetic outflow from the CNS due to decreased norepinephrine production, resulting in decreased BP.
  • Not typically first-line drugs due to adverse effects (orthostatic hypotension, fatigue, dizziness).
  • Adjunct drugs for hypertension after other drugs have failed; used with other antihypertensives, such as diuretics.
• Clonidine:
  • Used primarily to decrease blood pressure; also for opioid withdrawal management.
  • Available in oral and topical patch forms.
  • Do not stop abruptly (rebound hypertension).

Peripherally Acting Alpha1 Blockers

• Doxazosin, prazosin, and terazosin: block alpha1-adrenergic receptors.
  • When alpha1-adrenergic receptors are blocked, BP is decreased.
  • Dilate arteries and veins.
  • Increase urinary flow rates and decrease outflow obstruction in the bladder neck and urethra.
  • Use: Benign Prostatic Hyperplasia (BPH).
  • Tamsulosin (Flomax) – solely indicated for BPH.

Miscellaneous Antihypertensive Drugs

• Eplerenone (Inspra):
  • Selective aldosterone blocker.
  • Reduces BP by blocking aldosterone action at receptors in the kidney, heart, blood vessels, and brain.
  • Indications: routine treatment of hypertension and for post-MI HF.
  • Contraindicated in high serum potassium levels (above 5.6 mEq/L).

Nursing Implications (Antihypertensives)

• Obtain thorough health history and physical examination.
• Assess for contraindications and conditions requiring cautious use.
• Educate patients about adhering to dosing schedules and not missing doses.
• Monitor BP during therapy; instruct patients to keep a journal of regular BP checks.
• Instruct patients not to stop drugs abruptly (rebound hypertensive crisis, stroke).
• Give oral forms with meals for gradual and effective absorption.
• Encourage patients to watch their diet, stress level, weight, and alcohol intake.
• Instruct patients to avoid smoking and high-sodium foods.
• Encourage supervised exercise.
• Teach patients to change positions slowly to avoid postural hypotension/syncope.
• Instruct patients to report unusual shortness of breath, difficulty breathing, swelling, weight changes, chest pain, palpitations, excessive fatigue.
• Inform male patients about the possibility of impotence.
• Instruct patients to contact physicians immediately for serious adverse effects or if dose adjustments are needed.
• Hot tubs, showers, hot weather, prolonged sitting/standing, exercise, and alcohol may aggravate low BP, leading to fainting/injury; patients should sit/lie down until symptoms subside.
• Patients should not take other medications, including OTC drugs, without physician approval.
• Educate patients about lifestyle changes (weight loss, stress management, supervised exercise, dietary measures).
• Monitor for adverse and toxic effects.
• Monitor for therapeutic effects.

Antianginal Drugs

• Angina Pectoris Definition: Chest pain due to insufficient oxygen and nutrients in the blood to meet the heart's demands.
  • Heart muscle “aches”.
  • The heart requires a large supply of oxygen to meet demands.
• Ischemic Heart Disease:
  • Poor blood supply to the heart muscle.
  • Causes: Atherosclerosis and Coronary Artery Disease.
• Myocardial Infarction (MI):
  • Necrosis (death) of cardiac tissue.
  • Can be disabling or fatal.
• Types of Angina:
  • Chronic stable angina (classic/effort angina): predictable.
  • Unstable angina (preinfarction/crescendo angina): unpredictable.
  • Vasospastic angina (Prinzmetal/variant angina).
• Therapeutic Objectives:
  • Minimize the frequency and decrease duration/intensity of attacks.
  • Improve patient's functional capacity with minimal adverse effects.
  • Prevent or delay MI.
• Drug Classes:
  • Nitrates or nitrites.
  • Beta blockers.
  • Calcium channel blockers (CCBs).

Nitrates and Nitrites

• Available Forms:
  • Sublingual, chewable tablets, oral capsules/tablets, IV solutions, transdermal patches, ointments, translingual sprays.
    • Sublingual, IV, transdermal patches and translingual sprays bypass the liver and the first-pass effect.
• Examples: Nitroglycerin (rapid and long-acting), Isosorbide dinitrate (rapid and long-acting), Isosorbide mononitrate (primarily long-acting).
• Mechanism of Action and Drug Effects:
  • Cause vasodilation due to relaxation of smooth muscles.
  • Potent dilating effect on coronary arteries.
  • Result: Increased oxygen supply to ischemic myocardial tissue.
  • Used for prevention and treatment of angina.
• Indications:
  • Treat stable, unstable, and vasospastic angina.
  • Rapid-acting forms (sublingual tablets, IV infusion): treat acute anginal attacks.
  • Long-acting forms: prevent anginal episodes.
• Contraindications:
  • Known drug allergy, severe anemia, closed-angle glaucoma, hypotension, severe head injury.
  • Use of erectile dysfunction drugs (sildenafil, tadalafil, vardenafil).
• Adverse Effects:
  • Headaches (usually diminish with continued use).
  • Reflex tachycardia, postural hypotension.
  • Skin irritation with topical application.
  • Tolerance may develop (prevented by nitrate-free period).
    • Transdermal forms: remove patch at bedtime for 8 hours, then apply a new one in the morning.
• Isosorbide dinitrate (Isordil):
  • Organic nitrate, available in rapid-acting sublingual tablets, immediate-release tablets, and long-acting oral dosage forms.
  • Produces more consistent, steady, therapeutic response.
• Nitroglycerin:
  • Prototypical nitrate, the most important drug in treating ischemic heart conditions (angina).
  • Large first-pass effect with oral forms.
  • Routes: PO, SL, metered-dose aerosol (under the tongue), IV, topical.
  • IV form: BP control in perioperative hypertension, treatment of HF, ischemic pain, pulmonary edema associated with acute MI, hypertensive emergencies.

Beta Blockers (Antianginal)

• Mainstay in treating several cardiovascular diseases (angina, MI, hypertension, dysrhythmias).
• Reduce mortality rate after MI and in treating angina.
• Mechanism of Action:
  • After an MI, high levels of circulating catecholamines irritate the heart, causing imbalance and dysrhythmias.
  • Beta blockers block the harmful effects of catecholamines, improving survival after MI.

Calcium Channel Blockers (CCBs) for Chronic Stable Angina

• Examples: Amlodipine, Nicardipine, Nifedipine, Verapamil, Diltiazem.

Miscellaneous Antianginal Drug

• Ranolazine (Ranexa):
  • Mechanism of action is unknown, but thought to lowers myocardial oxygen demand
  • Prolongs QT interval on ECG.
  • Reserved for patients who have failed other antianginal drug therapy.
  • Contraindications: pre-existing QT prolongation, hepatic impairment, taking other QT-prolonging drugs.
  • Drug interactions:
    • Grapefruit juice, macrolide antibiotics, azole antifungals, some CCBs: increase ranolazine levels, possibly leading to Torsades de Pointes.
    • Quinidine and Sotalol: prolong QT interval.
    • Can increase levels of digoxin and simvastatin.

Nursing Implications (Antianginal)

• Encourage patients to limit caffeine intake.
• Patients should report: blurred vision, persistent headache, dry mouth, edema, fainting episodes, a weight gain of 2 lb in 1 day or 5 lb in 1 week, pulse rate less than 60 beats/min, dyspnea.
• Teach patients to change positions slowly to avoid postural BP changes.
• Encourage patients to keep a record of their anginal attacks, including precipitating factors, number of pills taken, and therapeutic effects.
• Nitroglycerin Instructions:
  • Instruct proper technique for sublingual nitroglycerin for anginal pain; never chew or swallow the sublingual form.
  • Burning sensation with sublingual forms indicates drug potency.
  • Keep a fresh supply on hand; potency is lost ~3 months after opening.
  • Store medications in an airtight, dark glass bottle with a metal cap and no cotton filler.
  • Instruct in proper application of nitrate topical ointments and transdermal forms, including site rotation and removal of old medication.
  • To reduce tolerance, remove topical forms at bedtime and apply a new dose in the morning (nitrate-free period).
  • Take as-needed nitrates at the first hint of anginal pain.
  • Monitor vital signs frequently during acute exacerbations of angina and IV administration.
  • If experiencing chest pain, lie down to prevent dizziness/fainting.
  • If anginal pain occurs:
    • Stop activity, sit/lie down, and take a sublingual tablet.
    • If no relief in 5 minutes, call 911 and take a second sublingual tablet.
    • If still no relief in another 5 minutes, take a third sublingual tablet.
    • Do not try to drive to the hospital.
  • IV nitroglycerin requires special non-PVC tubing and bags.
  • Discard parenteral solution that is blue, green, or dark red.
• Beta Blocker Instructions:
  • Monitor pulse rates daily and report any rate lower than 60 beats/min or symptoms of relative bradycardia.
  • Report dizziness or fainting.
  • Never abruptly discontinue medication.
  • Medications are for long-term prevention of angina, not immediate relief.
• CCB Instructions:
  • Constipation is a common problem; instruct patients to take in adequate fluids and eat high-fiber foods.
• General Instructions:
  • Monitor for adverse reactions: allergic reactions, headache, lightheadedness, hypotension, dizziness.
  • Monitor for therapeutic effects: relief of angina, decreased BP, or both.

Heart Failure (HF) Drugs

• Definition: The heart is unable to pump blood in sufficient amounts to meet the body's metabolic needs.
• Symptoms depend on the affected cardiac area:
  • Common: dyspnea, fatigue, fluid retention and/or pulmonary edema.
  • “Left-sided” HF: pulmonary edema, coughing, shortness of breath, and dyspnea.
  • “Right-sided” HF: systemic venous congestion, pedal edema, jugular venous distension, ascites, and hepatic congestion.
• Causes:
  • Myocardial infarction (MI), coronary artery disease, cardiomyopathy, valvular insufficiency, atrial fibrillation, infection, tamponade, ischemia, pulmonary hypertension, systemic hypertension, outflow obstruction, hypervolemia, congenital abnormalities, anemia, thyroid disease, infection, diabetes.
• Drug Therapy for Heart Failure:
  • Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), angiotensin receptor-neprilysin inhibitors (ARNIs), beta blockers, aldosterone antagonists, diuretics, sinoatrial modulators, phosphodiesterase Inhibitors (PDIs), cardiac glycosides.
• Drugs of Choice for Early Treatment:
  • Focus on reducing effects of the renin-angiotensin-aldosterone system and the sympathetic nervous system.
    • ACE inhibitors (lisinopril, enalapril, captopril).
    • ARBs (valsartan, candesartan, losartan).
  • Certain beta blockers (metoprolol, carvedilol).
• Additional Drugs:
  • Loop diuretics (furosemide): reduce symptoms of HF due to fluid overload.
  • Aldosterone inhibitors (spironolactone, eplerenone): added as HF progresses.
  • Digoxin: added after the above drugs are used; Reduces, but does not eliminate symptoms.
  • Dobutamine: positive inotropic drug.
  • Hydralazine/isosorbide dinitrate (BiDil): approved for use in Blacks.

Angiotensin Receptor-Neprilysin Inhibitors (ARNI)

• Combination drug: ARB and neprilysin inhibitor (Valsartan/sacubitril (Entresto)).
• New class for management of heart failure with reduced ejection fraction.
• Common adverse effects: hypotension, hyperkalemia, increased serum creatinine.
• Not for use in pregnancy.
• Several drug interactions, including ACEIs and NSAIDs.

Aldosterone Antagonists (Heart Failure)

• Useful in severe stages of HF.
• Action: Block aldosterone, which causes retention of sodium and water, leading to edema that can worsen HF.
• Examples: Spironolactone (Aldactone) and Eplerenone (Inspra).
  • Spironolactone: potassium-sparing diuretic and aldosterone antagonist, reduces symptoms of HF.
  • Eplerenone: selective aldosterone blocker, blocks aldosterone at receptors in the kidney, heart, blood vessels, and brain

Ivabradine (Corlanor)

• Sinoatrial node modulator: results in reduced heart rate.
• Used in stable, symptomatic HF with ejection fraction of 35% or less.
• Risk of atrial fibrillation, bradycardia, and conduction disturbances.
• Avoid grapefruit juice.

Phosphodiesterase Inhibitors (PDIs)

• Mechanism of Action:
  • Inhibit the enzyme phosphodiesterase, leading to increased calcium for myocardial muscle contraction.
• Inodilators (inotropics and dilators).
• Short-term management of HF for patients in the intensive care unit (ICU).
• Milrinone (injectable form only).
  • Adverse effects: cardiac dysrhythmias, headache, hypokalemia, tremor, thrombocytopenia, elevated liver enzyme levels.
  • Interactions: diuretics (additive hypotensive effects) and digoxin (additive inotropic effects).

Cardiac Glycosides

• One of the oldest groups of cardiac drugs.
• No longer used as first-line treatment; Reduces, but does not eliminate symptoms.
• Digoxin is the prototype.
• Used in HF and to control ventricular response to atrial fibrillation.
• Mechanism of Action:
  • Increase myocardial contractility (positive inotropic effect without increased oxygen consumption).
  • Negative chronotropic effect (reduced heart rate).
  • Negative dromotropic effect (decreased automaticity at SA node, decreased AV nodal conduction).

Cardiac Glycosides: Adverse Effects:

• Digoxin (Lanoxin):
  • Very narrow therapeutic window (0.5 to 2 ng/mL).
  • Low potassium levels increase toxicity; Hypomagnesemia and Hypercalcemia can also increase risk of toxicity.
  • Electrolyte levels must be monitored.
  • Cardiovascular: dysrhythmias, including bradycardia or tachycardia.
  • Central nervous system: headaches, fatigue, malaise, confusion, convulsions.
  • Eyes: colored vision (seeing green, yellow, purple), halo vision, flickering lights.
  • Gastrointestinal: anorexia, nausea, vomiting, diarrhea.
• Digoxin Toxicity:
  • Digoxin immune Fab (Digibind) therapy indications:
    • Hyperkalemia (serum potassium greater than 5 mEq/L) in a digitalis-toxic patient.
    • Life-threatening cardiac dysrhythmias.
    • Life-threatening digoxin overdose.
• Conditions That Predispose to Digoxin Toxicity:
  • Hypokalemia, Hypercalcemia, Hypomagnesemia, Use of cardiac pacemaker, Hepatic dysfunction, Dysrhythmias, Hypothyroid, respiratory, or renal disease, Advanced age.

Nursing Implications (Heart Failure)

• Assess:
  • History, drug allergies, and contraindications.
  • Clinical parameters, including: BP, Apical pulse (for 1 full minute), Heart/breath sounds, Weight/input/output measures, ECG, Serum labs (potassium, sodium, magnesium, calcium, renal/liver function).
• Before giving digoxin/beta blockers, count apical pulse for 1 full minute.
  • If apical pulse is less than 60 or greater than 100 beats/min: Hold dose and notify prescriber.
• Interventions:
  • Hold dose and notify prescriber if the patient experiences signs or symptoms of digoxin toxicity.
    • Anorexia, nausea, vomiting, diarrhea.
    • Visual disturbances (blurred vision, seeing green or yellow halos around objects).
  • Avoid giving digoxin with high-fiber foods.
  • Patients should immediately report a weight gain of 2 lb or more in 1 day or 5 lb or more in 1 week.
  • Use an infusion pump for nesiritide or milrinone.
  • Monitor input and output, heart rate/rhythm, BP, daily weights, respirations.
• Monitor for therapeutic effects:
  • Increased urinary output.
  • Decreased edema, shortness of breath, dyspnea, crackles, fatigue.
  • Resolution of paroxysmal nocturnal dyspnea.
  • Improved peripheral pulses, skin color, temperature.
• Monitor for adverse effects.

Antidysrhythmic Drugs

• Dysrhythmia Definition: Any deviation from the normal rhythm of the heart.
• Arrhythmia Definition: "No rhythm," implying asystole.
  • Terms dysrhythmia and arrhythmia are used interchangeably with the term arrhythmia being most commonly used.
• Antidysrhythmics: Used for the treatment and prevention of disturbances in cardiac rhythm.
• Dysrhythmia Development: Can develop after MI, cardiac surgery, or as a result of CAD; Requires treatment with antidysrhythmic drug or nonpharmacological therapies.
• Common Dysrhythmias:
  • Supraventricular dysrhythmias: originate above the ventricles in the SA or AV node or atrial myocardium.
  • Ventricular dysrhythmias: originate below the AV node in the His-Purkinje system or ventricular myocardium.
  • Ectopic foci: outside the conduction system.
  • Conduction blocks: disruption of impulse conduction between the atria and ventricles.
  • Examples: Atrial fibrillation, AV nodal reentrant tachycardia (AVNRT)/Paroxysmal supraventricular tachycardia (PSVT), Varying degrees of AV block, Premature ventricular contractions (PVCs), Ventricular fibrillation, Ventricular tachycardia.
• Antidysrhythmic Drugs Categorization:
  • Categorized according to where and how they affect cardiac cells.
  • Vaughan Williams classification: based on the electrophysiologic effect of particular drugs on the action potential.
• Vaughan Williams Classification: Mechanism of Action and Indications:
  • Class I: Fast sodium channel blockers; Divided into Ia, Ib, and Ic drugs according to effects.
    • Class Ia: procainamide, quinidine, and disopyramide; Block sodium (fast) channels; Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions, ventricular tachycardia, Wolff-Parkinson-White syndrome.
    • Class Ib: phenytoin, lidocaine; Block sodium channels; Lidocaine is used for ventricular dysrhythmias only; Phenytoin is used for atrial and ventricular tachydysrhythmias caused by digitalis toxicity or long QT syndrome.
    • Class Ic: flecainide, propafenone; Block sodium channels (more pronounced effect); Used for severe ventricular dysrhythmias; May be used in atrial fibrillation or flutter, Wolff-Parkinson-White syndrome, supraventricular tachycardia dysrhythmias.
  • Class II: beta blockers; Reduce or block sympathetic nervous system stimulation, thus reducing transmission of impulses in the heart’s conduction system; General myocardial depressants for both supraventricular and ventricular dysrhythmias; Also used as antianginal and antihypertensive drugs; some used for heart failure.
  • Class III: amiodarone, dronedarone, dofetilide, sotalol, ibutilide; Potassium channel blockers; Used for dysrhythmias that are difficult to treat, such as life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter that is resistant to other drugs.
  • Class IV: Calcium channel blockers; Inhibit slow-channel (calcium-dependent) pathways; Reduce AV node conduction; Used for paroxysmal supraventricular tachycardia (PSVT); rate control for atrial fibrillation and flutter.
• Contraindications to Antidysrhythmic Drugs:
  • Known drug allergy; Second- or third-degree AV block, bundle branch block, cardiogenic shock, sick sinus syndrome, other ECG changes (depending on the clinical judgment of a cardiologist); Other antidysrhythmic drugs.
• Antidysrhythmics: Adverse Effects:
  • ALL antidysrhythmics can cause dysrhythmias!
  • Hypersensitivity reactions, nausea, vomiting, diarrhea, dizziness, headache, blurred vision, prolongation of the QT interval.
• Antidysrhythmics: Drug Interactions:
  • Coumadin: monitor international normalized ratio (INR).
  • Grapefruit juice: amiodarone, disopyramide, and quinidine.
• Amiodarone (Cordarone, Pacerone):
  • Class III, blocks both alpha- and beta-adrenergic receptors of the sympathetic nervous system.
  • Uses: One of the most effective antidysrhythmic drugs for controlling supraventricular and ventricular dysrhythmias.
  • Indications: management of sustained ventricular tachycardia, ventricular fibrillation, and nonsustained ventricular tachycardia.
  • Drug of choice for ventricular dysrhythmias according to the Advanced Cardiac Life Support guidelines.
  • Adverse effects: corneal microdeposits (may cause visual halos, photophobia, and dry eyes), photosensitivity, pulmonary toxicity.
  • Drug interactions: digoxin and warfarin.
  • Contraindications: hypersensitivity, severe sinus bradycardia or second- or third-degree heart block.

Unclassified Antidysrhythmic

• Adenosine (Adenocard):
  • Slows conduction through the AV node.
  • Used to convert PSVT to sinus rhythm.
  • Very short half-life (less than 10 seconds).
  • Administered as fast intravenous (IV) push.
  • May cause asystole for a few seconds.
  • Other adverse effects are minimal.

Nursing Implications (Antidysrhythmic Drugs)

• Obtain a thorough drug and medical history.
• Assess for conditions that may be contraindications for use of specific drugs.
• Measure baseline blood pressure (BP), pulse, input and output, and cardiac rhythm.
• Measure serum potassium levels before initiating therapy