Heart Failure Meds and Anticoagulants
Heart Failure Medications and Anticoagulants
Heart Failure Medications: These include ACE inhibitors, beta-blockers, diuretics, and aldosterone antagonists, which help manage symptoms and improve heart function.
Anticoagulants: Medications such as warfarin, heparin, rivaroxaban, and apixaban are used to prevent blood clots, particularly in patients with atrial fibrillation or those at high risk for thromboembolic events.
Heart Failure Overview
Definition: Inability of heart to meet circulatory needs.
Compensatory mechanisms increase cardiac output (CO).
Over time, weakened heart is unable to maintain CO.
Compensation can exacerbate heart failure (HF).
Fluid backs up, leading to decreased oxygenation of tissues.
Decreased quality of the hearts ability to pump adequately.
Compensatory mechanism: decreased quality of heart pump results in tachycardia, further decreasing CO and increasing myocardial oxygen demand.
Causes of Heart Failure
Coronary Artery Disease: Most common cause 19 out of 20 times, often leading to myocardial infraction (MI).
Hypertension: Contributes significantly to HF.
Valvular Disease: Affects heart function.
Cardiomyopathy: Disease of heart muscle leading to heart failure.
Signs and Symptoms of Heart Failure
Left-Sided Heart Failure
Orthopnea: Difficulty breathing when lying flat.
Anxiety: Secondary to shortness of breath (SHOB).
Tachycardia: Increased heart rate to compensate.
Weak Pulses: Indicating decreased cardiac output.
Cough: Fluid backing up into lungs.
Right-Sided Heart Failure
Jugular Venous Distension (JVD): Observed when not lying flat.
Hepatomegaly: Liver enlargement due to fluid back-up.
Edema: Fluid retention in body tissues.
Nocturia: Increased urination at night due to fluid dynamics.
Exertional Dyspnea: Shortness of breath on exertion.
Blood will back up into the body
Drug Treatment for Heart Failure
Primary goal: Reduce workload on heart and/or improve heart's ability to increase output.
Beta Blockers reduce rate and force of heart contractions, resulting in less oxygen demand needs.
Diuretics help reduce fluid build up
Nitrates and ACE Inhibitors help decrease after-load and cardiac remodeling
Reduces peripheral vascular pooling and optimizes cardiac function
Drug Classes
Beta Blockers: -lol’s
Reduce heart rate and force of contractions, lowering oxygen demand.
Examples: Metoprolol, Atenolol, Propranolol.
Block beta-1 receptors, leading to decreased heart workload.
What happens when Beta 1 receptors are stimulated? Heart rate increases
What happens when Beta 1 receptors are blocked? Heart rate is decreased, leading to decreased heart workload.
Monitor heart rate (HR) and blood pressure (BP) before administration.
Beta Blockers may cause bronchospasms
IMPORTANT!! Masks signs and symptoms of hypoglycemia, blocking the parasympathetic stress response
Some beta blockers are also attached to beta 2 receptors (lungs), leading to bronchoconstriction.
Parameters: Check HR and BP before administration, monitor blood sugar and watch for s/s of hypoglycemic shock
ACE Inhibitors: -pril’s
Examples: Lisinopril, Captopril.
Block angiotensin II to reduce afterload and decrease cardiac remodeling.
If ACE’s are not tolerated, ARB’s can be used instead.
Less vasoconstriction with ACE inhibitors
Primarily used as anti-hypertensives and it beneficial to patients with HF
Reduces cardiac after-load and cardiac remodeling with long term use
<40% Ejection Fraction (EF) indicates that patient will be recommended for a ACE Inhibitor.
Parameters: Check BP before administration.
Diuretics:
Reduce fluid overload and improve symptoms (covered separately).
Digoxin (Cardiotonics)
Cardiac glycoside that increases force of contraction (positive inotrope) and decreases heart rate (negative chronotrope).
Positive Inotrope: medications that increase the force of heart contractions (ex. digoxin, dobutamine, norepinephrine, epinephrine.)
Negative Inotrope: medications that decrease the force of heart muscle (myocardial) contraction. (ex. beta blockers, calcium channel blockers such as amlodipine, anti- arrhythmic, nitrates, and digoxin if given in high doses.)
Parameters: Check apical pulse for 60 seconds before administration.
Narrow therapeutic range: 0.5-0.8 mg/mL
Lowers BP and HR
Prolongs diastolic filling time, giving the heart more time to fill up with blood
1/3 contracting and 2/3 relaxing and filling up.
Will increase renal perfusion, increases the force of contraction, while decreasing the heart rate
Monitor for digoxin toxicity: dysrhythmias, nausea and vomiting, halo vision, anorexia, visual disturbances, etc.
Digoxin interacts with many herbals such as St. John’s wort and ginseng
IMPORTANT!! Digoxin competes with potassium for binding sites
Low K+ = hypokalemic, increased digoxin effects
High digoxin levels = will cause lethal arrhythmias
Digoxin can be oral or IV route
Antidote: Digibind
Digoxin dosing: 200-500 mcg (0.2-0.5 mg)
What should be monitored when taking Digoxin?
Serum potassium levels to avoid hypokalemia along with digoxin serum levels to avoid toxicity
Heart rate and rhythm to detect arrhythmias
Sign of digoxin toxicity
Newer Medications (Heart Squeezers)
Dobutamine: A beta-1 agonist, improving cardiac output and lowering BP.
Postitive Inotrope
Promotes peripheral vasodilation
Gives the heart a stronger squeeze, increasing force of contractions
Lowers BP
Milrinone: A phosphodiesterase inhibitor, enhancing cardiac function and decreasing after-load.
Increases cardiac output while decreasing after-load
Has vasodilating properties
Positive Inotrope
PDI- potentially driver impairing
Ivabradine: An HCN blocker that lowers heart rate without affecting contractility.
prolongs diastole filling time
HCN Blocker = Hyperpolarization-activated cyclic nucleotide-gated channel blocker that selectively inhibits the funny current in pacemaker cells.
SGLT2 Inhibitors (e.g., Dapagliflozin): Promote fluid and sugar excretion.
Excretes sugar anf fluid
Tells the kidneys to let go of the sugar and gets rid of fluid, lowers blood sugar.
Assessing Heart Failure Drug Therapy
What do we monitor?
Heart Rate (HR) and Blood Pressure (BP)
Level of consciousness (LOC)
Exertion tolerance
Urine output (UOP)
Capillary refill and peripheral pulses
Skin warmth/temperature
Lung sounds and daily weights
Electrolytes and Brain Natriuretic Peptide (BNP) levels
Improved functional status, is the drug therapy and interventions working?
Anticoagulants Overview
Antiplatelets:
Examples: Aspirin, Clopidogrel (Plavix).
Stop platelets from aggregating (sticking together); used primarily for arterial clots.
Avoids clots in the arteries, especially in the heart
Does NOT affect the clotting cascade
Often prescribed together, used for dual antiplatelet therapy
Should not affect platelet levels
Indications:
Thrombosis prophylaxis (preventing the formation of blood clots)
Thrombolytics:
Examples: Urokinase, Alteplase.
Used to dissolve existing clots; high risk of bleeding.
Can cause uncontrolled bleeding
Patient needs to be screened extremely carefully in order yo be placed on these
Not commonly used
Dissolving a clot is much riskier. Therefore, careful consideration of the patient's medical history and current medications is essential before initiation.
IMPORTANT!! Too risky to be used for DVT
Indications:
Thrombolysis (PE, MI, CVA)
Anticoagulants:
Indicated for prevention of blood clots, e.g., in DVT, PE, atrial fibrillation.
Treatment involves parenteral drugs like heparin, enoxaparin (lovenox), warfarin, apixaban (eliquis), and dabigatran (pradaxa).
Will interrupt some aspect of the clotting cascade
Are all used to prevent the development of blood clots
Heparin
Administered subcutaneously or IV.
Can also be administered in the abdomen (subq), avoiding the 2” around the umbilicus
Indications:
DVT Prophylaxis (most common)
Treatment of PE and DVT
Prevention of thrombus in atrial fibrillation
Prevention of clotting in transported blood products
Prevent formation of clots
Used in high clot situations
Used in some DIC (disseminated intravascular coagulation) cases
Monitor Partial Thromboplastin Time (PTT), aiming for specific therapeutic ranges.
What is the normal clotting time? 25-35 seconds
What the the clotting time expected when on Heparin? Generally 60-100 seconds
NOT used for SQ administration, ONLY for IV Heparin
PTT = IV Heparin
Highly titratable
Protamine Sulfate: reverses heparin, can be given for overdose or if patient needs to have surgery or if an unexpected situation happens.
Parental use only
Platelet count lab: checked when on Heparin at least every 3 days
Heparin can cause low platelet count (thrombocytopenia)
30-90 minute half life
Risk of complications, including bleeding and HIT ( heparin induced thrombocytopenia.)
Low Molecular Weight Heparin (LMWH)
Example: Enoxaparin (Lovenox).
Similar to heparin
Less frequent dosing than heparin, half life is 6 times for than heparin
Sometimes can be sent home for long term use
Comes in prefilled syringes, leave in the air bubble it goes in last
Goes in the abdomen, ALWAYS SQ
Indications:
DVT and for some post op patients
More expensive, longer half-life, and can be given at home post-surgery.
Warfarin
Oral anticoagulant, requiring monitoring of INR (ideal range typically 2-3).
Many drug interactions, vitamin K is essential in management.
Takes 3-4 days to see therapeutic levels
Used for long term anticoagulation
What is the normal INR Level? Should be 1
What is the expected INR level when on Warfarin? 2-3 or 2.5-3.5
INR = Warfarin
Newer Oral Anticoagulants
Apixaban, Dabigatran have more rapid onset and less monitoring requirements along wtih less lab test monitoring.
Important Considerations
Patient Monitoring:
Signs of active bleeding or upcoming invasive procedures are critical to hold these medications
Contextualize anticoagulation therapy in relation to patient’s overall health and treatment plan.
Additional Resources
Heart Failure readings: Pages 211-241 for background; pages 255-256 for nursing process; pages 265-271 for digoxin and nitrates; pages 288-302 for anticoagulants.