NLE Cardiovascular Nursing — Heart Failure and Cardiac DysrhythmiasCheat Sheet

Common values

Important facts

• HF compensatory mechanisms initially: sympathetic nervous system (↑ HR, contractility), renin-angiotensin-aldosterone system (↑ sodium/water retention), and ventricular hypertrophy/dilation
• These mechanisms eventually become MALADAPTIVE: ↑ afterload, fluid overload, ventricular remodeling worsen HF — rationale for blocking these systems with ACE-I, ARBs, beta-blockers
• Leading cause of HF is coronary artery disease; second most common is chronic hypertension
• HF affects 1-2% of population; mortality highest in systolic HF
• Compensation eventually fails, leading to acute decompensation and emergency presentation

Key definitions

Diagrams to know

• Starling curve showing relationship between ventricular filling pressure and cardiac output
• Sympathetic nervous system cascade in HF compensation
• Renin-angiotensin-aldosterone system activation pathway

Important facts

• LEFT HF manifestations all relate to PULMONARY CONGESTION (behind failing LV)
• Dyspnea, orthopnea, PND = classic triad for left HF assessment
• Crackles (rales) heard on auscultation indicate fluid in alveoli (pulmonary edema)
• Pink or blood-tinged frothy sputum = hallmark of acute pulmonary edema; fluid mixes with air and blood
• S3 gallop (ventricular gallop) = early diastolic sound indicating rapid ventricular filling in HF
• Fatigue from decreased cardiac output and tissue hypoxia
• Cough is often mistaken for respiratory disease but is a cardinal sign of left HF

Key definitions

Diagrams to know

• Left ventricle backward fluid flow into pulmonary circulation
• Progressive fluid accumulation in alveoli stages
• Lung auscultation zones for crackle detection

Common values

Important facts

• RIGHT HF manifestations all relate to SYSTEMIC VENOUS CONGESTION (behind failing RV)
• Most common cause of right HF is LEFT HF (pulmonary hypertension damages RV over time)
• Peripheral and dependent edema = fluid settles in lowest gravity areas (ankles, sacrum if bedridden)
• Weight gain is often from fluid retention, not actual tissue growth (rapid 1-2 kg gains in days)
• Anorexia, nausea, abdominal discomfort = GI congestion from hepatomegaly
• JVD, peripheral edema, hepatomegaly form classic triad for right HF assessment
• Cor pulmonale = chronic RV failure from chronic lung disease (COPD, pulmonary hypertension)

Key definitions

Diagrams to know

• Right ventricle backward fluid flow into systemic circulation
• JVD measurement technique (45° position, measure above sternal angle)
• Dependent edema pattern in ambulatory vs bedridden patients

Important facts

• ACUTE pulmonary edema is life-threatening EMERGENCY — patients can deteriorate rapidly
• Presentation: severe dyspnea, anxiety, pink frothy sputum, orthopnea, restlessness from hypoxia
• Auscultation findings: bilateral crackles (usually from bases upward), possibly wheezes, diminished breath sounds
• Vital signs: tachypnea (RR >30), tachycardia, elevated BP, hypoxia (O2 sat <90%)
• Chest X-ray shows infiltrates in classic 'butterfly' or perihilar pattern
• Most common cause: acute MI, hypertensive crisis, acute valvular disease, or decompensation of chronic HF

Key definitions

Diagrams to know

• Stages of fluid accumulation: interstitial edema → alveolar flooding
• Pink frothy sputum pathophysiology diagram
• Bilateral crackles progression from bases upward

Common values

Important facts

• LMNOP priority order for acute pulmonary edema:
• L = Positioning: HIGH FOWLER'S position with legs DEPENDENT (reduces venous return, improves oxygenation)
• M = Morphine: IV morphine to reduce anxiety, preload, and work of breathing
• N = Nitrates/Nitroprusside: vasodilators to reduce preload and afterload
• O = Oxygen: high-flow O2 via non-rebreather mask; prepare for CPAP/BiPAP if needed
• P = Pharmacotherapy: IV loop diuretic (furosemide) to remove fluid RAPIDLY
• POSITION is PRIORITY #1 — high Fowler's immediately improves breathing mechanics
• Continuous monitoring: O2 sat, respiratory status, vital signs, heart sounds, I&O
• Be ready for intubation/mechanical ventilation if respiratory status worsens
• Loop diuretics (furosemide) given IV because absorption unreliable in acute HF
• Morphine IV: also has anxiolytic effect which reduces sympathetic discharge and workload
• Nitrates work within minutes to reduce preload; vasodilators reduce afterload
• May need continuous positive airway pressure (CPAP) or BiPAP to avoid intubation

Diagrams to know

• Acute pulmonary edema management flowchart
• Position progression: supine → semi-Fowler's → high Fowler's effect on lung expansion

Common values

Important facts

• DAILY WEIGHT is cornerstone of HF self-management and primary nursing assessment
• Critical thresholds: 1 kg gain in 24 hours OR 2.5 kg gain in 1 week = reportable
• Instruct patient to weigh at same time, place, and day (e.g., every morning after toilet, before breakfast)
• Use same scale for consistency; sudden unexplained weight loss may indicate poor intake
• Monitor intake and output: aim for negative fluid balance in HF (output > intake)
• Fluid restriction typically 1.5-2 L/day in HF; teach patient fluid limits include soups, ice cream, etc.
• Sodium restriction typically less than 2 g/day; teach label reading and low-sodium cooking
• Position in semi- to high-Fowler's for comfort and to aid breathing
• Auscultate lung sounds EVERY SHIFT — new crackles indicate fluid accumulation
• Assess peripheral edema daily (grade 1-4+) and note pitting vs non-pitting
• Monitor for signs of pulmonary edema: orthopnea, PND, increased dyspnea, crackles
• Activity: balance rest with graduated ambulation (sitting → standing → walking) to prevent deconditioning
• Sleep in semi-Fowler's or with HOB elevated; provide extra pillows
• Monitor vital signs: HR, BP, RR; report persistently low BP (may need to hold diuretics/vasodilators)
• Check for medication adherence — many HF exacerbations from non-adherence
• Encourage low-sodium diet; teach reading nutrition labels (sodium in unexpected places: breads, canned foods, processed meats)

Key definitions

Diagrams to know

• Daily weight tracking chart and decision tree (when to report)
• Fluid restriction teaching poster (1.5-2 L distributed throughout day)
• Edema grading scale (0 to 4+) with visual examples

Common values

Important facts

• ALWAYS assess BOTH ECG rhythm AND patient hemodynamic response (BP, mental status, symptoms)
• Hemodynamically STABLE: patient alert, BP normal, no chest pain or syncope → may observe and treat if symptomatic
• Hemodynamically UNSTABLE: hypotension, altered consciousness, chest pain, syncope → EMERGENCY treatment
• Rate: bradycardia <60 bpm, normal 60-100 bpm, tachycardia >100 bpm
• Rhythm: regular (consistent intervals) vs irregular (variable intervals)
• P waves: must identify (normal, abnormal, absent, buried in QRS or T wave)
• QRS duration: narrow (<0.12 sec = supraventricular origin) vs wide (≥0.12 sec = ventricular origin)
• PR interval: measure to assess AV conduction (normal 0.12-0.20 sec)
• Shockable rhythms: VF, pulseless VT → defibrillation
• Non-shockable rhythms: asystole, PEA → CPR, epinephrine (NO defibrillation)

Key definitions

Diagrams to know

• ECG strip analysis algorithm (P wave, QRS, T wave identification)
• Dysrhythmia classification by origin (supraventricular vs ventricular)
• Heart rate calculation from ECG (6-second strip method, small box method)

Common values

Important facts

• SINUS BRADYCARDIA: Treat ONLY if SYMPTOMATIC (dizziness, hypotension, syncope, chest pain)
• - Asymptomatic bradycardia in athletes = normal, no treatment
• - Symptomatic bradycardia: atropine IV 0.5-1 mg; may need pacemaker
• SINUS TACHYCARDIA: Address UNDERLYING CAUSE, not the rhythm itself
• - Causes: pain, fever, anxiety, hypovolemia, hyperthyroidism, infection, decompensated HF
• ATRIAL FIBRILLATION: Most common CHRONIC dysrhythmia; major stroke risk
• - Characteristics: IRREGULARLY IRREGULAR rhythm, NO P waves, fibrillation waves visible
• - ANTICOAGULATION IS ESSENTIAL to prevent thromboembolic stroke (warfarin or DOAC)
• - Rate control: beta-blockers (metoprolol, atenolol), calcium channel blockers (diltiazem, verapamil), digoxin
• - Rhythm control: antiarrhythmics (amiodarone); consider cardioversion if recent onset (<48 hrs)
• - CHA2DS2-VASc score guides anticoagulation decision
• ATRIAL FLUTTER: Less common than AFib; has characteristic SAWTOOTH pattern
• - Usually regular ventricular rate (2:1 or 3:1 AV conduction block)
• - Treatment: rate control with beta-blockers or calcium channel blockers; may need cardioversion
• VENTRICULAR TACHYCARDIA: Most dangerous of sustained dysrhythmias; can degenerate to VF
• - With pulse + hemodynamically UNSTABLE (hypotension, altered mental status): SYNCHRONIZED CARDIOVERSION
• - With pulse + hemodynamically STABLE: IV amiodarone or procainamide; prepare for cardioversion
• - Pulseless VT: treat as cardiac arrest → IMMEDIATE CPR + DEFIBRILLATION + epinephrine
• VENTRICULAR FIBRILLATION: LETHAL — immediate CPR and DEFIBRILLATION are only treatment
• - No pulse, no perfusion, requires immediate intervention
• - Outcome depends on time to defibrillation ('golden period' is first 4-6 minutes)
• ASYSTOLE: Non-shockable rhythm; CPR + epinephrine 1 mg IV push q 3-5 min
• - Defibrillation is INEFFECTIVE — do NOT shock asystole
• - Consider causes: hypoxia, hypokalemia, hypothermia, toxins, tension pneumothorax (H's and T's)

Key definitions

Diagrams to know

• Sinus bradycardia ECG strip: slow, regular rhythm
• Sinus tachycardia ECG strip: fast, regular rhythm
• Atrial fibrillation ECG strip: irregularly irregular with no P waves
• Atrial flutter ECG strip: sawtooth pattern between QRS complexes
• Ventricular tachycardia ECG strip: wide QRS complexes at rapid rate
• Ventricular fibrillation ECG strip: chaotic, disorganized waveforms
• Asystole ECG strip: flatline with no activity

Common values

Important facts

• DEFIBRILLATION: Used for pulseless VT and VF (arrest rhythms)
• - UNSYNCHRONIZED shock delivered IMMEDIATELY
• - Goal: convert chaotic rhythm to organized rhythm (or asystole)
• - Energy: 120-200 J biphasic, repeat at same or higher energy
• - No need to check rhythm or wait — patient has no pulse
• SYNCHRONIZED CARDIOVERSION: Used for unstable but perfusing rhythms
• - AFib with rapid rate + hypotension
• - SVT with hypotension
• - Atrial flutter with hypotension
• - VT with pulse + hypotension or altered mental status
• - Synchronized to R wave; NEVER to T wave (can precipitate VF)
• - MUST sedate conscious patient (midazolam, propofol) before cardioversion
• - Energy: 50-100 J initial; increase if unsuccessful
• KEY DIFFERENCE: VT/VF pulseless → DEFIBRILLATION (unsynchronized, immediate); VT/other rhythm with pulse but unstable → CARDIOVERSION (synchronized, after sedation)

Key definitions

Diagrams to know

• Decision algorithm: Pulseless vs perfusing → defibrillation vs cardioversion
• Synchronization window: QRS complex timing for cardioversion

Common values

Important facts

• INDICATIONS for pacemaker: symptomatic bradycardia, complete heart block, sick sinus syndrome, certain AV blocks
• TEMPORARY pacemakers: transcutaneous (non-invasive) or transvenous (central line); used acutely
• PERMANENT pacemakers: implanted subcutaneously, usually left anterior chest wall below clavicle
• POST-IMPLANTATION NURSING CARE:
• - Limit arm movement on paced side for 4-6 weeks to prevent lead dislodgement
• - Keep surgical site clean and dry; watch for infection signs
• - No lifting >5 lbs with paced arm; avoid heavy activities
• - ECG monitoring to assess pacing adequacy and rhythm
• ONGOING MONITORING:
• - Assess ECG for FAILURE TO CAPTURE (spike not followed by QRS) → urgent
• - Assess ECG for FAILURE TO SENSE (inappropriate firing) → urgent
• - Monitor patient's apical pulse daily; should be at or above set rate (usually 60-70 bpm)
• - Report if pulse below set rate, dizziness, syncope, palpitations, or hiccups (diaphragm pacing)
• PATIENT TEACHING:
• - Check pulse daily for 60 seconds; report if slower than set rate
• - Carry pacemaker identification card at all times
• - AVOID MRI unless device is MRI-conditional; most other imaging safe
• - AVOID strong electromagnetic fields: arc welding, high-voltage electrical work, strong magnets
• - Household appliances mostly safe: microwave, TV, cell phone (keep 6 inches away), airport security (notify staff)
• - Report signs of infection at incision: fever, redness, warmth, drainage, swelling
• - Do NOT allow shoulder/arm on paced side to be abducted or reach above shoulder
• - Keep follow-up appointments for device checks (usually every 3-6 months)
• - Pacemaker battery life typically 5-10 years; eventually requires replacement

Key definitions

Diagrams to know

• Pacemaker placement anatomy (left anterior chest, subclavicular)
• ECG interpretation: normal paced beat (spike + QRS), failure to capture, failure to sense
• Arm movement restrictions post-implantation

Formulas

Common values

Important facts

• DIGOXIN MECHANISM: Increases myocardial contractility (positive inotrope); slows AV nodal conduction (negative chronotrope used for AFib rate control)
• THERAPEUTIC LEVEL: 0.5–2.0 ng/mL
• TOXICITY THRESHOLD: >2.0 ng/mL (but may occur at therapeutic level with hypokalemia)
• ADMINISTRATION SAFETY — CRITICAL:
• - TAKE APICAL PULSE FOR FULL 60 SECONDS BEFORE EVERY DOSE
• - HOLD digoxin and notify provider if apical rate <60 bpm in adults (or <90-110 in infants)
• - If pulse rate meets holding criteria, do NOT give dose — risk of severe bradycardia
• HYPOKALEMIA IS THE MAJOR RISK FACTOR for digoxin toxicity:
• - Low K+ increases cellular uptake of digoxin and increases myocardial sensitivity
• - Monitor K+ level closely, especially in patients on loop/thiazide diuretics
• - Normal K+: 3.5-5.0 mEq/L; give K+ supplements if <3.5 mEq/L
• SIGNS OF DIGOXIN TOXICITY:
• - GI: anorexia, nausea, vomiting, diarrhea (early signs)
• - Visual: YELLOW-GREEN HALOS around lights, blurred vision, photophobia (pathognomonic)
• - Cardiac: bradycardia, all types of dysrhythmias (PACs, PVCs, AV blocks, VT)
• - CNS: confusion, hallucinations, weakness, dizziness
• - Most common early sign is nausea/anorexia; most characteristic is yellow-green halos
• DRUG INTERACTIONS — Increase toxicity risk:
• - Diuretics (cause hypokalemia)
• - NSAIDs (decrease digoxin clearance)
• - Calcium channel blockers, beta-blockers (increase digoxin level)
• - Amiodarone, quinidine (increase digoxin level)
• ANTIDOTE: Digoxin immune Fab (Digibind) — used for severe toxicity
• MONITORING:
• - Check digoxin level 5-7 days after initiation (takes time to reach steady state)
• - Monitor K+, Cr, BUN regularly (renal disease increases digoxin accumulation)
• - Assess for toxicity signs at every patient encounter

Key definitions

Diagrams to know

• Digoxin mechanism: contractility and AV conduction effects
• Hypokalemia-digoxin toxicity relationship diagram
• Apical pulse assessment technique

Common values

Important facts

• LOOP DIURETICS: Most potent; used for acute HF, pulmonary edema, severe fluid overload
• - Examples: furosemide (Lasix), torsemide (Demadex), bumetanide (Bumex)
• - Mechanism: Block Na-K-2Cl cotransporter in loop of Henle → massive fluid loss
• - IV administration: Onset 5-15 min; peak 1-2 hours; duration 6-8 hours
• - PO administration: Slower onset (1 hour); use in chronic management
• - IV furosemide must be infused SLOWLY to prevent ototoxicity (hearing loss)
• THIAZIDE DIURETICS: Moderate strength; used for mild HF and chronic hypertension
• - Examples: hydrochlorothiazide (HCTZ), chlorthalidone
• - Mechanism: Inhibit NaCl reabsorption in distal convoluted tubule
• - Less potent than loop diuretics; better for maintenance therapy
• COMMON ADVERSE EFFECTS (both loop and thiazide):
• - HYPOKALEMIA (low K+): Loss of potassium → weakness, dysrhythmias, digoxin toxicity risk
• - Hyponatremia: Loss of sodium
• - Dehydration: Volume depletion → hypotension, dizziness, syncope
• - Hyperglycemia: Thiazides impair glucose metabolism
• - Hyperuricemia: Increased uric acid (gout risk)
• - Ototoxicity: Especially with IV furosemide given rapidly
• MONITORING:
• - Monitor I&O; expect increased output
• - Monitor daily weight (should decrease)
• - Check electrolytes weekly (K+, Na+, Cl-) and renal function (Cr, BUN)
• - Monitor for dehydration signs: dizziness, orthostatic hypotension, dry mouth
• - Monitor for hypokalemia signs: weakness, muscle cramps, dysrhythmias
• - Monitor BP; diuretics cause hypotension
• PATIENT TEACHING:
• - Take in morning to avoid nighttime diuresis and sleep disruption
• - Eat potassium-rich foods (bananas, oranges, potatoes, spinach) if on loop/thiazide
• - Monitor for weakness, muscle cramps, dizziness
• - Do not skip doses; consistent use prevents fluid reaccumulation
• - Rise slowly from sitting/lying to prevent orthostatic hypotension

Key definitions

Diagrams to know

• Nephron anatomy showing loop of Henle and distal convoluted tubule sites of action
• Fluid and electrolyte losses with loop vs thiazide diuretics
• Monitoring timeline for diuretic effects

Common values

Important facts

• SPIRONOLACTONE (Aldactone): Most commonly used potassium-sparing diuretic in HF
• - Mechanism: Aldosterone antagonist; blocks aldosterone effects in collecting duct
• - Effects: Mild diuresis, sodium loss, POTASSIUM RETENTION
• - Special benefit: Improves survival in systolic HF and post-MI (clinical trial evidence)
• - Usual dose: 12.5-25 mg daily in HF
• AMILORIDE (Midamor): Another potassium-sparing option; epithelial sodium channel blocker
• - Similar effects to spironolactone but different mechanism
• - Used less commonly than spironolactone
• OTHER POTASSIUM-SPARING: Triamterene (Dyrenium) — less common
• MAJOR CONCERN: HYPERKALEMIA (high potassium)
• - Risk is much greater than hypokalemia with potassium-sparers
• - Dangerous dysrhythmias if K+ >5.5 mEq/L
• - Patients with renal impairment at higher risk
• CONTRAINDICATIONS and CAUTIONS:
• - Renal disease (Cr >1.5 or GFR <30): risk of dangerous hyperkalemia
• - Do NOT combine with ACE inhibitors or ARBs (all retain K+ — compounded risk)
• - Do NOT use with potassium supplements or salt substitutes (contain K+)
• MONITORING — CRITICAL:
• - Check K+ level BEFORE starting spironolactone, then 1 week after, then monthly
• - Check BUN/Cr (renal function) regularly; high Cr increases hyperkalemia risk
• - Patient education: AVOID salt substitutes (contain K+); avoid excessive K+-rich foods if K+ trending up
• - If K+ >5.5 mEq/L: hold spironolactone, notify provider; may need potassium-lowering treatment
• ADVANTAGES in HF:
• - Mild diuretic effect helps with fluid overload
• - DRAMATIC survival benefit in systolic HF (Class II recommendation)
• - Aldosterone blockade reduces cardiac remodeling and fibrosis
• - Avoids need for separate potassium supplementation with loop/thiazide diuretics

Key definitions

Diagrams to know

• Aldosterone mechanism in collecting duct: spironolactone blockade effect
• Hyperkalemia danger: K+ levels and cardiac effects
• Combination therapy: loop diuretic + potassium-sparer balance

Common values

Important facts

• ACE INHIBITORS — First-line HF therapy:
• - Reduce afterload (lower blood pressure)
• - Prevent ventricular remodeling (reduce cardiac fibrosis)
• - Improve survival in systolic HF
• - Examples: lisinopril, enalapril, ramipril, perindopril
• - MAJOR SIDE EFFECT: DRY COUGH (10-20% of patients) from bradykinin accumulation — not dangerous but may require switching
• - Other side effects: hyperkalemia (blocks aldosterone), hypotension, angioedema (rare but serious — stop immediately)
• - Monitoring: Check BP, K+, Cr before starting and regularly; watch for persistent dry cough
• ARBs — Alternative to ACE-I:
• - Similar benefits to ACE-I for HF reduction and survival
• - Do NOT cause dry cough (main advantage over ACE-I)
• - Examples: losartan, valsartan, irbesartan, candesartan
• - Side effects: hyperkalemia, hypotension (less pronounced than ACE-I)
• - Use when ACE-I cause dry cough or if ACE-I intolerance
• - NOTE: Do NOT combine ACE-I + ARB (compounded hyperkalemia risk); choose one class
• BETA-BLOCKERS — Essential HF therapy:
• - Three proven to improve survival in systolic HF: carvedilol, metoprolol XL, bisoprolol
• - MUST start LOW and titrate GRADUALLY (weeks to months) to target dose
• - Mechanism: Reduce sympathetic overdrive; slow remodeling; improve contractility paradoxically with time
• - Carvedilol: non-selective beta + alpha blocker; best survival data
• - Metoprolol XL: selective beta-1 blocker; controlled-release
• - Bisoprolol: highly selective beta-1 blocker
• - Side effects: bradycardia, hypotension, fatigue, sexual dysfunction, bronchospasm (caution in asthma/COPD)
• CRITICAL SAFETY POINTS:
• - HOLD ACE-I, ARB, beta-blocker if systolic BP <90 mmHg or HR <50-60 bpm
• - Do NOT stop beta-blockers abruptly (risk of rebound tachycardia, MI, arrhythmias) — taper slowly
• - Monitor BP and HR at each visit; titrate doses up gradually if tolerated
• - Monitor K+ and Cr (especially with ACE-I/ARB); renal patients need dose adjustment
• PATIENT TEACHING:
• - Take as directed; do not skip doses
• - Rise slowly from lying to prevent dizziness (orthostatic hypotension)
• - Report persistent dry cough (ACE-I), dizziness, syncope, swelling of face/lips (angioedema)
• - Do NOT stop beta-blockers abruptly — can cause dangerous rebound effects

Key definitions

Diagrams to know

• Renin-angiotensin-aldosterone system (RAAS) and ACE-I/ARB blockade sites
• Sympathetic nervous system and beta-blocker effects
• Mechanism comparison: ACE-I vs ARB vs Beta-blocker

Common values

Important facts

• NITRATES — Mechanism and benefits:
• - Release nitric oxide → smooth muscle relaxation → venous dilation
• - Reduce preload (less blood returning to heart) → relieves pulmonary and systemic congestion
• - Improve symptoms rapidly (10-20 minutes)
• - Examples: isosorbide dinitrate (Isordil), isosorbide mononitrate (Imdur), nitroglycerin
• - Survival benefit in HF is modest; mainly used for symptom relief
• NITRATE SIDE EFFECTS and PRECAUTIONS:
• - HEADACHE (very common — tolerance develops in 1-2 weeks)
• - Hypotension and orthostatic dizziness — check BP before giving
• - HOLD if systolic BP <90 mmHg
• - Reflex tachycardia in some patients
• - ABSOLUTE CONTRAINDICATION: Do NOT use with phosphodiesterase inhibitors (sildenafil, tadalafil) — severe hypotension risk
• NITRATE TOLERANCE:
• - Develops with continuous exposure (usually after 24-48 hours of continuous nitrate)
• - Solution: Nitrate-free interval of 10-14 hours daily (give doses in morning/afternoon, skip evening)
• - Example dosing: isosorbide dinitrate 10 mg at 8 AM, 2 PM, skip 8 PM dose
• HYDRALAZINE — Direct-acting vasodilator:
• - Reduces afterload (lowers blood pressure) → improves cardiac output
• - Less venous dilation than nitrates; more arterial dilation
• - ALWAYS combined with nitrate (nitrate + hydralazine = synergistic benefit)
• - Special indication: Hydralazine + nitrate combination superior to other agents in African-American HF patients (BIDIL study)
• - Doses: Hydralazine 37.5 mg TID + isosorbide dinitrate 20 mg TID
• HYDRALAZINE SIDE EFFECTS:
• - Lupus-like syndrome (especially at high doses >200 mg/day)
• - Tachycardia and palpitations (reflex sympathetic response)
• - Headache, dizziness, hypotension
• COMBINATION THERAPY — Nitrate + Hydralazine:
• - Proven to improve survival in systolic HF, especially African-American population
• - May be alternative when ACE-I/ARB contraindicated or intolerant
• - Example: isosorbide dinitrate 10 mg TID + hydralazine 25-50 mg TID
• MONITORING:
• - Check BP before administration; hold if SBP <90 mmHg
• - Monitor for dizziness and orthostatic hypotension
• - Patient counseling: Rise slowly from sitting/lying
• - Assess symptom improvement (dyspnea, orthopnea, exercise tolerance)

Key definitions

Diagrams to know

• Nitrate mechanism: nitric oxide pathway and vascular smooth muscle relaxation
• Preload and afterload reduction effects of nitrates and hydralazine
• Nitrate tolerance and nitrate-free interval strategy

Common values

Important facts

• AMIODARONE — Most powerful antiarrhythmic:
• - Class III agent: blocks potassium channels; prolongs action potential and refractory period
• - Effective for: atrial fibrillation, atrial flutter, VT, VF, SVT
• - IV use: acute setting (VT, hemodynamically unstable AFib); onset 15-30 minutes, peak 1 hour
• - PO use: chronic suppression of dysrhythmias; loading required (800 mg-1.6 g/day × 1-3 weeks), then maintenance 200-400 mg/day
• AMIODARONE SIDE EFFECTS — SIGNIFICANT:
• - Pulmonary toxicity: interstitial pneumonitis, fibrosis (1-5% patients); can be fatal if unrecognized
• - Thyroid dysfunction: hypo- or hyperthyroidism (15-25% patients) from high iodine content
• - QT prolongation: risk of torsades de pointes (especially if K+ low or other QT-prolonging drugs)
• - Hepatotoxicity: monitor LFTs regularly
• - Photosensitivity: bluish skin discoloration with sun exposure; teach sunscreen use
• - CNS: tremor, ataxia, neuropathy
• - GI: nausea, anorexia
• MONITORING FOR AMIODARONE:
• - Baseline: Chest X-ray, PFTs (pulmonary function), TSH, LFTs, K+, Mg2+, ECG (QT interval)
• - Ongoing: Repeat Chest X-ray, PFTs every 6-12 months; TSH q 6 months; LFTs q 6 months
• - ECG: Lengthen QT interval expected; excessive prolongation increases torsades risk
• - Symptoms: shortness of breath (may indicate pulmonary toxicity), fatigue, tremor
• OTHER ANTIARRHYTHMICS:
• - Procainamide (Class IA): less commonly used due to side effects
• - Sotalol (Class III): beta-blocker with antiarrhythmic property; risk of QT prolongation
• - Propafenone (Class IC): used for AFib; risk of proarrhythmia
• ANTIARRHYTHMIC DRUGS AND ELECTROLYTES:
• - Hypokalemia (K+ <3.5) and hypomagnesemia (Mg2+ <2) INCREASE dysrhythmia risk
• - Especially dangerous with Class III agents (prolong QT) — maintain normal K+ and Mg2+
• - Check K+, Mg2+ regularly; supplement if low

Key definitions

Diagrams to know

• Action potential and Class III antiarrhythmic mechanism (potassium channel blockade)
• QT prolongation and torsades de pointes risk
• Amiodarone toxicity monitoring timeline

Common values

Important facts

• ATRIAL FIBRILLATION STROKE RISK:
• - Loss of atrial 'kick' → blood stasis in atria → thrombus formation
• - AFib patients have 4-5x HIGHER stroke risk than normal population
• - Strokes from AFib tend to be MORE SEVERE than other causes
• ANTICOAGULATION IS ESSENTIAL in AFib:
• - All patients with AFib and CHA2DS2-VASc ≥1 (male) or ≥2 (female) should receive anticoagulation
• - Stroke reduction: 60-70% with warfarin; similar with DOACs
• WARFARIN (Coumadin) — Traditional therapy:
• - Mechanism: Inhibits vitamin K-dependent factors (II, VII, IX, X); takes 3-5 days for effect
• - INR monitoring: Target INR 2-3 for AFib
• - INR <2: Subtherapeutic (under-anticoagulated, stroke risk)
• - INR 2-3: Therapeutic range (optimal balance)
• - INR >3: Bleeding risk increases
• - Frequent INR checks: initially weekly, then monthly once stable
• - Many drug interactions: NSAIDs, antibiotics, antifungals affect INR
• - Diet consistency: vitamin K-rich foods (spinach, broccoli, kale) affect INR; patient must maintain consistent intake
• DIRECT ORAL ANTICOAGULANTS (DOACs) — Newer agents:
• - Examples: apixaban (Eliquat), rivaroxaban (Xarelto), dabigatran (Pradaxa), edoxaban (Savaysa)
• - Advantages over warfarin:
• - No INR monitoring
• - Fixed dosing (more convenient)
• - Fewer food/drug interactions
• - Faster onset/offset (hours vs days)
• - Disadvantages:
• - More expensive than warfarin
• - Irreversible anticoagulation (no reversal agent for some)
• - Renal dosing adjustments for some agents
• ANTICOAGULATION PRECAUTIONS:
• - Monitor for bleeding: bruising, blood in stool/urine, nosebleeds, hemoptysis
• - Teach fall prevention (high bleeding risk with anticoagulation)
• - Patient education: do NOT skip doses; do NOT stop abruptly (clot risk)
• - NSAIDs increase bleeding risk with anticoagulants; avoid or use cautiously
• - Instruct on when to seek help: severe bleeding, signs of stroke (sudden weakness, speech difficulty)
• BRIDGING THERAPY:
• - When warfarin started, takes days to therapeutic; use heparin bridge (IV or SC) initially
• - Once INR ≥2 × 24 hours, can stop heparin and continue warfarin

Key definitions

Diagrams to know

• CHA2DS2-VASc scoring and stroke risk stratification
• INR therapeutic window and warfarin dosing adjustment logic
• Coagulation cascade and warfarin mechanism (factors II, VII, IX, X blockade)