NLE Cardiovascular Nursing — Heart Failure and Cardiac DysrhythmiasCheat Sheet

Common Values

Section Title

Heart Failure Fundamentals

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

Section Title

Left-Sided Heart Failure (Left HF)

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

Section Title

Right-Sided Heart Failure (Right HF)

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

Section Title

Acute Pulmonary Edema

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

Section Title

Acute Pulmonary Edema — Nursing Interventions (LMNOP Mnemonic)

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

Section Title

Chronic Heart Failure Management

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

Section Title

Cardiac Dysrhythmias — Assessment Principles

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

Section Title

Common Dysrhythmias — Identification & Management

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

Section Title

Defibrillation vs Synchronized Cardioversion

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

Section Title

Pacemakers — Indications & Nursing Care

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

Section Title

Digoxin (Lanoxin) — Cardiac Glycoside

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

Section Title

Loop & Thiazide Diuretics

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

Section Title

Potassium-Sparing Diuretics

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

Section Title

ACE Inhibitors, ARBs, & Beta-Blockers

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

Section Title

Nitrates & Vasodilators

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

Section Title

Antiarrhythmic Agents

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

Section Title

Anticoagulation in Atrial Fibrillation

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)

Item

LEFT-sided HF = LUNGS (dyspnea, orthopnea, crackles, pink frothy sputum); RIGHT-sided HF = REST of body (peripheral edema, JVD, hepatomegaly, ascites). This distinction is CRITICAL on NLE.

Why Important

Most common exam questions test ability to differentiate clinical presentations. Wrong answer = wrong diagnosis and wrong management.

Item

DIGOXIN: Always take APICAL PULSE for FULL 60 SECONDS before every dose. HOLD if <60 bpm. Therapeutic level 0.5-2.0 ng/mL. HYPOKALEMIA potentiates toxicity. Yellow-green halos = classic toxicity sign.

Why Important

Digoxin is high-yield for NLE. Students often miss the apical pulse assessment rule and hypokalemia connection, leading to missed toxicity.

Item

ACUTE PULMONARY EDEMA = EMERGENCY. Priority: HIGH FOWLER'S position → O2 → IV furosemide → morphine → nitrates. MNEMONIC: LMNOP (if using). Position is PRIORITY #1.

Why Important

High-yield emergency scenario. Correct sequencing of interventions separates excellent nurses from average ones on exams.

Item

DAILY WEIGHT in HF: Gain of 1 kg in 24 hours OR 2.5 kg in 1 week = REPORTABLE. Same time, same scale each day. This is THE cornerstone of HF self-management.

Why Important

Often tested as patient teaching point. Many students don't remember the specific threshold amounts.

Item

ATRIAL FIBRILLATION: IRREGULARLY IRREGULAR rhythm, NO P waves, requires ANTICOAGULATION (warfarin INR 2-3 or DOAC) to prevent stroke. Rate control with beta-blockers, calcium channel blockers, or digoxin.

Why Important

AFib is the most common chronic dysrhythmia tested. Anticoagulation requirement is critical safety knowledge. CHA2DS2-VASc scoring guides decisions.

Item

DEFIBRILLATION: Unsynchronized shock for pulseless VT and VF (ARREST rhythms). SYNCHRONIZED CARDIOVERSION: Timed shock for unstable but perfusing rhythms (AFib with RVR, stable VT). These are EASILY confused on exams.

Why Important

High-yield distinction. Students commonly mix these up. Correct identification determines appropriate life-saving intervention.

Item

LOOP & THIAZIDE diuretics cause HYPOKALEMIA. POTASSIUM-SPARING diuretics (spironolactone) cause HYPERKALEMIA. Spironolactone improves HF survival but requires K+ monitoring. Do NOT combine with ACE-I/ARB (compounded hyperkalemia).

Why Important

Critical electrolyte management concept. Hypokalemia increases digoxin toxicity risk and dysrhythmias. Students often miss the drug interaction warnings.

Item

BETA-BLOCKERS in HF: Start LOW, titrate GRADUALLY (weeks to months). Do NOT stop abruptly (rebound effect). HOLD if HR <50-60 or SBP <90. Three proven to improve survival: carvedilol, metoprolol XL, bisoprolol.

Why Important

Safety-critical. Abrupt discontinuation is dangerous. Slow titration principle is often tested. Students rush titration timelines on exams.

Item

PACEMAKER PROBLEMS: Failure to capture = spike visible but no QRS (urgent). Failure to sense = pacer fires during patient's own beats (urgent). Teach daily pulse check; report if below set rate. Limit arm movement 4-6 weeks post-implant.

Why Important

Pacemaker complications are high-yield. Assessment skills and patient teaching are commonly tested. Many students miss the specific post-implant precautions.

Item

WARFARIN INR TARGET for AFib = 2.0-3.0. INR <2 = under-anticoagulated (stroke risk). INR >3 = bleeding risk. DOACs (apixaban, rivaroxaban) require NO INR monitoring. Do NOT combine warfarin + DOAC. Teach bleeding precautions.

Why Important

Anticoagulation is critical for AFib stroke prevention. INR interpretation is commonly tested. DOAC vs warfarin choice is increasingly important with newer agents.

Tip

When you see 'pulmonary edema' or 'crackles' in a question, think LEFT-SIDED HF. When you see 'JVD' or 'hepatomegaly', think RIGHT-SIDED HF. This simple mental shortcut eliminates wrong answers fast.

Timing

Perfect for the 30-minute review before exam. Builds pattern recognition.

Tip

For digoxin questions, ALWAYS look for: (1) apical pulse check, (2) hypokalemia as toxicity risk, (3) yellow-green halos as pathognomonic sign. If the question mentions any of these, anticoagulation is likely correct answer.

Timing

Digoxin appears in almost every NLE exam. This tip helps you recognize the concept being tested.

Tip

On dysrhythmia questions, ask yourself: Does patient have a pulse? If NO → arrest rhythm (VF, pulseless VT) → DEFIBRILLATION (unsynchronized). If YES but unstable → CARDIOVERSION (synchronized). This flowchart decision eliminates 50% wrong answers.

Timing

Dysrhythmia management is heavily tested. This decision tree is faster than memorizing each rhythm.

Tip

For any HF management question, remember the RAAS blockers (ACE-I, ARB) and sympathetic blockers (beta-blockers) are ALWAYS part of the answer. If neither is mentioned in a management plan, it's likely WRONG.

Timing

HF pharmacology dominates the exam. This pattern recognition saves time on complex questions.

Tip

If a question involves AFib, anticoagulation is THE critical nursing intervention. Don't get distracted by rate control drugs — the STROKE RISK is what makes anticoagulation non-negotiable. Students often pick rhythm control when anticoagulation is the priority.

Timing

AFib is heavily tested. This refocuses attention on the most important safety issue.

Rows

Columns

• Feature
• Left-Sided HF (LEFT = LUNGS)
• Right-Sided HF (RIGHT = REST of body)

Table Title

Left-Sided HF vs Right-Sided HF

Rows

Columns

• Parameter
• Therapeutic Range
• Toxic Range
• Clinical Significance

Table Title

Digoxin Therapeutic vs Toxic Levels

Rows

Columns

• Feature
• Loop Diuretics (Furosemide)
• Thiazide (HCTZ)
• Potassium-Sparing (Spironolactone)

Table Title

Loop Diuretics vs Thiazide Diuretics vs Potassium-Sparing

Rows

Columns

• Feature
• Defibrillation
• Synchronized Cardioversion

Table Title

Defibrillation vs Synchronized Cardioversion

Rows

Columns

• Dysrhythmia
• Rate
• Rhythm
• P Waves
• QRS
• KEY FEATURE

Table Title

Dysrhythmia Recognition at a Glance

Rows

Columns

• Feature
• ACE Inhibitors (Lisinopril, Enalapril)
• ARBs (Valsartan, Losartan)
• Beta-Blockers (Carvedilol, Metoprolol)

Table Title

ACE Inhibitor vs ARB vs Beta-Blocker in HF