Heart Failure, Dysrhythmias, and Coagulation Therapy Pharmacology

Pathophysiology of Heart Failure (HF)

• The Heart's Primary Function: The number one job of the heart is to pump blood throughout the body.

• Compensatory Mechanisms: When cardiac output ($CO$) drops, the body attempts to compensate, which initially helps but becomes harmful over time.

  • Renin-Angiotensin System (RAS) Activation: Helpful in the short term to increase fluid retention; however, chronic activation stresses the heart and eventually makes the condition worse.

  • Cardiac Remodeling: Chronic stress and over-activation of compensatory systems actually change the physical shape of the heart.

• Sympathetic Nervous System (SNS) Activation: The "fight or flight" system releases norepinephrine ($NE$) and epinephrine ($Epi$). This causes vasoconstriction to increase blood pressure, but long-term activation is detrimental to the heart.

Goals of Heart Failure Treatment

• Increase Contractility (Inotropy): Enhancing the force of the heart's contraction. This is likened to squeezing a water-filled sponge to maximize cardiac output.

• Decrease Preload: Reducing the amount of blood ready to enter the heart with each beat. This makes the workload manageable, compared to giving the heart "one question at a time" instead of $50$.

• Decrease Afterload: Reducing the force the heart must overcome to push blood out into the systemic circulation.

Heart Failure Patient Education

• Dietary Restrictions: Low sodium diet is essential. Patients must avoid canned or processed foods.

• Fluid and Weight Monitoring:

  • Patients must report weight gains of $1\text{--}2\,lbs$ in a single day or $3\text{--}5\,lbs$ in a seven-day period.

  • Proper Weighing Technique: Weigh at the same time every day, on the same scale, in the morning after urinating, and while naked (as clothes affect weight).

• DASH Diet: Patients are encouraged to follow the Dietary Approaches to Stop Hypertension (DASH) diet.

• Salt Substitutes: Patients must avoid salt substitutes because they are typically made with potassium, which can be dangerous. Instead, the use of herb-based seasonings like "Mrs. Dash" is recommended.

Heart Failure Medications

ACE Inhibitors

• Role: The cornerstone of heart failure therapy; every HF patient should be on one unless contraindicated.

• Mechanism: Reduces both afterload and preload to help the heart pump more efficiently.

• Patient Education: Patients should NOT stop taking the medication once their blood pressure stabilizes or they feel better. Feeling better is a sign the drug is working.

• Monitoring: Monitor blood pressure and kidney function labs ($BUN$ and $Creatinine$), especially in those with chronic kidney disease ($CKD$).

• Risks: Hyperkalemia (high potassium). These drugs are also teratogenic (dangerous in pregnancy).

Milrinone (Rescue Drug)

• Classification: Phosphodiesterase-3 (PDE) inhibitor.

• Mechanism: Increases contractility and cardiac output.

• Administration: IV only; strictly for short-term use ($\le 72\,hours$). Used for acute decompensated heart failure.

• PDE Monitoring Acronym:

  • P: Potassium levels.

  • D: Duration (limited time).

  • E: EKG (continuous monitoring).

• Adverse Effects: Hypotension and dysrhythmias. If the patient reports chest pain or palpitations, or exhibits an irregular rhythm, the nurse should stop or slow the infusion and notify the provider.

• Weight-Based Dosing: It is a weight-based drug; the patient's weight must be verified to program the IV pump accurately.

• Therapeutic Effectiveness: Successful treatment is evidenced by improved perfusion to vital organs. A key indicator is increased urine output (reduced anuria or oliguria) as kidneys become happier.

Beta Blockers ("LOLs")

• Role: Key in both heart failure management and treating dysrhythmias.

• Mechanism: Decrease heart rate to reduce myocardial oxygen demand.

• Hold Parameters: Hold the medication if the heart rate is < 60\,bpm.

• Diabetes Warning: Beta blockers can mask the symptoms of hypoglycemia (tachycardia, shakiness, sweating). A diabetic patient may drop unconscious without recognizing symptoms because the sympathetic response is blocked.

• Respiratory Warning: Non-selective beta blockers can trigger bronchospasms. Nurses must assess for asthma, COPD, or wheezing before administration.

• Abrupt Cessation: Do not stop abruptly; this can cause rebound hypertension or angina.

Diuretics (Spironolactone, Loops, Thiazides)

• Goal: Reduce fluid overload (preload) to decrease strain on the heart.

• Effectiveness Indicators: Decreased peripheral edema, diminished lung crackles, stable blood pressure, and increased urine output.

• Potassium Differences:

  • Loop and Thiazide Diuretics: Potassium-wasting; can cause hypokalemia.

  • Spironolactone: Potassium-sparing; can cause hyperkalemia.

• IV Administration: IV loop diuretics (e.g., Furosemide) must be given slowly to prevent ototoxicity (ear damage, mnemonic: "loop" sounds like "hoop" earrings).

Vasodilators (Hydralazine, Nitrates)

• Mechanism: Decrease afterload and the workload of the heart.

• Side Effects: Headache and hypotension. Headheads are considered normal (due to vessel dilation) and do not require a provider call unless severe.

• Education: Do not chew tablets. Monitor blood pressure before and after administration. Rise slowly from a sitting or lying position to prevent falls from orthostatic hypotension.

Cholesterol Management

• Pathophysiology: High cholesterol leads to plaques in arteries (atherosclerosis), causing narrowing and potential blockages. These plaques can break off and cause a stroke (brain), heart attack (heart), or pulmonary embolism (lungs).

• Lab Targets:

  • Total Cholesterol: < 200\,mg/dL.

  • LDL (Lousy/Bad): < 100\,mg/dL.

  • HDL (Happy/Good): > 60\,mg/dL.

  • Triglycerides: < 150\,mg/dL.

Statins (HMG-CoA Reductase Inhibitors)

• Mechanism: Inhibits the enzyme in the liver that produces cholesterol.

• Timing: Take at night because the liver produces the most cholesterol during sleep.

• Avoid: Grapefruit juice.

• Serious Adverse Effect: Rhabdomyolysis (muscle breakdown). Signs include muscle pain and dark urine (due to myoglobin, a dark byproduct of muscle breakdown, clogging the kidneys).

• Labs: Monitor $CK$ (Creatine Kinase) for muscle breakdown and liver enzymes ($AST$ and $ALT$).

Fibric Acid Derivatives (Gemfibrozil)

• Primary Goal: Lowering triglycerides and increasing $HDL$.

• Risks: Liver and muscle toxicity (similar to statins).

• Specific Warning: Can cause gallstones. Patients should monitor for Right Upper Quadrant (RUQ) pain.

Cholesterol Absorption Inhibitors (Ezetimibe)

• Side Effects: Think of the name sounding like a sneeze; it can cause nasopharyngitis and upper respiratory infections ($URIs$).

Dysrhythmia Medications

Digoxin

• Classification: Inotrope and Anti-dysrhythmic ("twofer").

• Mechanism: Increases contractility (HF) and slows the heart rate (Dysrhythmias).

• Assessment: Check the apical pulse with a stethoscope and digital watch for one full minute ($60\,seconds$). Do not cut corners.

• Hold Parameter: Hold if heart rate is < 60\,bpm.

• Toxicity: Includes nausea, vomiting, and visual changes (yellow-green halos).

• Potassium Interaction: Hypokalemia increases the risk of Digoxin toxicity.

• ATP Mnemonic:

  • A: Apical pulse.

  • T: Toxicity signs.

  • P: Potassium levels.

Potassium Channel Blockers (Amiodarone)

• Usage: For complex atrial and ventricular dysrhythmias ($Afib$, $Vtach$, $Vfib$).

• Labs: Monitor potassium and magnesium levels (they often rise or fall together).

• Half-life: Exceptionally long, up to $50\,days$.

• Toxicities:

  • Pulmonary Toxicity: Fever, shortness of breath, cough, and infiltrates on X-ray.

  • Photosensitivity: Skin sensitivity to sunlight; use sunscreen.

  • Thyroid: Can cause thyroid changes over time.

  • Pregnancy: Highly teratogenic; use birth control.

Sodium Channel Blockers (Lidocaine)

• Usage: Ventricular dysrhythmias ONLY ($Vtach$, $Vfib$).

• Toxicity: Neurotoxicity/CNS toxicity. Symptoms include dizziness, confusion, vertigo, and blurred vision.

• Mnemonic: "Cain and Abel" — Cain hit Abel in the head (CNS).

Calcium Channel Blockers (Verapamil, Diltiazem)

• Usage: Atrial dysrhythmias ONLY ($Afib$, $Aflutter$).

• Avoid: Grapefruit juice.

• Monitoring: Since these are not the "-dipines," you must check both heart rate and blood pressure.

Adenosine

• Usage: Supraventricular Tachycardia (SVT).

• Mechanism: Slows the heart rate so significantly that it causes a brief period of asystole (heart stop) to allow the rhythm to reset.

• Half-life: Extremely short ($3\text{--}10\,seconds$).

• Administration: Must be "slammed" (fast IV push) while the patient is lying down.

• Patient Education: Warn the patient they will feel extreme pressure or a "kick in the heart."

Coagulation Therapy

• General Adverse Effect: Bleeding. Signs include black tarry stools, hypotension, bleeding gums, hematuria, ecchymosis, petechiae, decreased level of consciousness ($LOC$), and "coffee ground" emesis.

Anti-platelets (Clopidogrel, Aspirin)

• Clopidogrel: Used after stent placement or for Peripheral Arterial Disease (PAD). PAD is described as a "heart attack in the legs" causing intermittent claudication (leg pain while walking).

• Education: Stop medication $7\,days$ before surgery.

Warfarin (Vitamin K Antagonist)

• Mechanism: Interferes with Vitamin K to thin blood.

• Monitoring: Monitor $INR$. Therapeutic sweet spot is $2\text{--}3$. (Normal person without treatment = $1$).

• Antidote: Vitamin K.

• Patient Education:

  • Maintain a consistent intake of Vitamin K-rich leafy greens (spinach, kale, broccoli). Do not suddenly stop or increase intake.

  • Avoid antibiotics and "G" herbs (Garlic, Ginkgo) as they interact.

  • Use an electric razor and soft toothbrush.

  • Teratogenic; not for use in pregnancy.

Heparin and Enoxaparin (Lovenox)

• Administration: IV or Subcutaneous.

• Monitoring: Monitor $PTT$. (Mnemonic: lower case "t's" in $ptt$ look like an "H" for Heparin).

• Antidote: Protamine Sulfate (resembling a "Harry Potter" spell).

Direct Oral Anti-coagulants (DOACs)

• Drugs: Rivaroxaban, Dabigatran.

• Benefits: No lab monitoring required; fewer drug-to-drug interactions; short half-life ($1\,day$). They are more expensive.

• Antidotes:

  • Rivaroxaban: Andexanet Alfa (both have "XA").

  • Dabigatran: Idarucizumab.

Thrombolytics (Alteplase/TPA)

• Role: "Clot busters" that end in "-teplase."

• Usage: IV only for acute ischemic stroke.

• Contraindications: Recent surgery or trauma.

• "Cathflo": The brand name for Alteplase used to restore patency to occluded central lines.

Questions & Discussion

• Q: What is the most dangerous side effect of Lisinopril (an ACE inhibitor)?

• A: Angioedema. It causes swelling of the face, lips, tongue, and throat, leading to airway obstruction (marked by hoarseness or inspiratory stridor). This is a medical emergency; stop the drug and give Epinephrine.

• Q: How do you know if an anti-coagulant is effective?

• A: The goal is prevention. It is effective if the patient does NOT have a stroke or forms no new clots.

• Q: How do you know if Amiodarone is effective for Afib?

• A: The heart rate will decrease (e.g., from $150\,bpm$ down to $90\,bpm$) and the rhythm may convert back to sinus or show less ectopy ($PACs$, $PVCs$).