NLE Cardiovascular Nursing — Heart Failure and Cardiac DysrhythmiasRevision Notes

Formulas

Exam Tips

• NLE FAVORITE: The echocardiogram measures ejection fraction — it is the most definitive test for HF type.
• BNP > 100 pg/mL = think HF in any dyspneic patient scenario.
• Drugs that BLOCK compensatory mechanisms (ACE-I, beta-blockers, spironolactone) are the cornerstone of HF treatment — know their mechanisms.
• Philippine context: Hypertension is the #1 cause of HF in the Philippines — PhilPEN addresses this at the RHU/barangay health center level.

Key Points

• Heart failure (HF) is a clinical syndrome where the heart CANNOT pump enough blood to meet the body's metabolic demands.
• Common causes in the Philippine setting include hypertension (HTN), coronary artery disease (CAD), myocardial infarction (MI), rheumatic heart disease (valvular), and cardiomyopathy.
• The DOH PhilPEN (Philippine Package of Essential NCD Interventions) program at the primary-care level targets HTN and NCD control to prevent HF progression.
• Compensatory mechanisms are initially helpful but become MALADAPTIVE over time.
• Three main compensatory mechanisms: (1) Sympathetic Nervous System (SNS) activation — increases heart rate (HR) and contractility; (2) Renin-Angiotensin-Aldosterone System (RAAS) — causes Na+ and water retention, increasing preload; (3) Ventricular hypertrophy and dilation — the heart muscle thickens and enlarges to pump harder.
• Maladaptive effects: increased afterload, fluid overload, ventricular remodeling — all WORSEN the failure.
• HF drugs (ACE inhibitors, beta-blockers, spironolactone) work by BLOCKING these compensatory systems.
• Ejection Fraction (EF): Normal is 55–70%; reduced EF (<40%) = HFrEF (systolic HF); preserved EF (≥50%) = HFpEF (diastolic HF).

Definitions

Section Title

Heart Failure: Pathophysiology and Compensatory Mechanisms

Common Mistakes

• Confusing PRELOAD and AFTERLOAD: Remember — PRELOAD is what fills the heart BEFORE contraction (volume); AFTERLOAD is the resistance the heart pumps AGAINST during contraction (pressure).
• Thinking compensatory mechanisms are always beneficial — they eventually WORSEN heart failure (maladaptive).
• Forgetting that RAAS activation causes both Na+ AND water retention, not just sodium.
• Mixing up HFrEF (reduced EF, systolic dysfunction) and HFpEF (preserved EF, diastolic dysfunction) — NLE may distinguish these.

Exam Tips

• NLE MEMORY TRICK: L for Left = L for Lungs (pulmonary signs); R for Right = R for Rest of body (systemic signs).
• If the NLE scenario describes 'frothy, pink-tinged sputum with crackles' — this is LEFT HF / pulmonary edema.
• If the NLE scenario describes 'swollen ankles, JVD, enlarged liver, weight gain' — this is RIGHT HF.
• Nursing priority based on Maslow: BREATHING problems (left HF) take priority over FLUID issues (right HF).
• S3 gallop = decreased cardiac output = hallmark of LEFT HF = NLE favorite.

Key Points

• MEMORY TRICK: Left = Lungs; Right = Rest of the body (systemic).
• LEFT-SIDED HF: Blood backs up into the PULMONARY circulation (lungs) because the left ventricle cannot pump forward effectively.
• RIGHT-SIDED HF: Blood backs up into the SYSTEMIC venous circulation because the right ventricle cannot pump blood into the pulmonary artery. The most common cause of right HF is LEFT HF.
• Most patients eventually develop BIVENTRICULAR failure (both sides).
• NANDA Nursing Diagnoses for HF: Decreased Cardiac Output; Excess Fluid Volume; Impaired Gas Exchange; Activity Intolerance; Deficient Knowledge.
• Maslow Priority: Oxygenation and hemodynamic stability are ALWAYS the highest priority (physiologic/safety needs first).
• LEFT HF key signs: Dyspnea on exertion → orthopnea → paroxysmal nocturnal dyspnea (PND) → pulmonary edema. Crackles (rales) on auscultation. Frothy, pink (blood-tinged) sputum. S3 gallop (hallmark of left HF). Tachycardia, fatigue, restlessness from hypoxia.
• RIGHT HF key signs: Peripheral and dependent edema (ankles, sacrum). Weight gain. Jugular venous distention (JVD). Hepatomegaly (enlarged liver) and ascites. Anorexia, nausea from GI congestion. Right upper quadrant discomfort.
• Orthopnea: breathlessness when lying flat — patient needs 2 or more pillows to sleep; documented as '2-pillow orthopnea.'
• Paroxysmal Nocturnal Dyspnea (PND): sudden awakening from sleep with severe shortness of breath — caused by redistribution of fluid when patient lies down at night.

Definitions

Section Title

Left-Sided vs. Right-Sided Heart Failure: Clinical Manifestations

Common Mistakes

• Forgetting to assess the SACRAL area for edema in bedridden patients — dependent edema shifts to the sacrum, not the ankles, when the patient is lying down.
• Attributing ALL respiratory symptoms to left HF without considering biventricular failure.
• Confusing S3 (normal in young adults but pathological in adults >40 = HF) with S4 (associated with hypertension and reduced ventricular compliance).
• Forgetting that the most common cause of RIGHT-sided HF is LEFT-sided HF — always think of it as a continuum.
• Missing that anorexia and nausea in RIGHT HF are due to GI/hepatic CONGESTION, not a GI disease.

Exam Tips

• NLE PRIORITY: In pulmonary edema, the FIRST nursing action is ALWAYS positioning — HIGH FOWLER'S with legs dangling. Then oxygen, then medications.
• Remember LMNOP: Legs dependent → Morphine → Nitrates → Oxygen → Pump (furosemide).
• Furosemide IV has a DUAL action in pulmonary edema: (1) venodilation within minutes (rapid preload reduction before diuresis starts), then (2) diuresis to remove fluid.
• NLE SCENARIO CLUE: 'Patient woke up at 3 AM, cannot breathe, using multiple pillows, frothy pink sputum' = ACUTE PULMONARY EDEMA = HIGH FOWLER'S + O2 + IV furosemide.
• In the Philippine hospital setting (DOH hospitals), always document and report the emergency response per hospital protocol as required under RA 9173 standards of nursing practice.

Key Points

• Acute pulmonary edema is a MEDICAL EMERGENCY — fluid rapidly floods the alveoli, impeding gas exchange. It is usually caused by ACUTE DECOMPENSATED LEFT HF.
• Clinical picture: Severe, sudden dyspnea; extreme anxiety ('air hunger'); pink, frothy sputum; crackles throughout ALL lung fields; tachypnea; hypoxia (SpO2 dropping rapidly); diaphoresis; cyanosis.
• PRIORITY NURSING INTERVENTION: Position the patient in HIGH FOWLER'S (90°) with LEGS DEPENDENT (feet dangling off bed). This REDUCES venous return (preload) to the heart and lungs and improves breathing mechanics.
• Why legs DEPENDENT? It traps blood in the lower extremities through gravity, reducing the amount of fluid returning to the overloaded pulmonary circulation.
• MNEMONIC: 'LMNOP' for acute pulmonary edema management: L = Legs dependent / High Fowler's; M = Morphine IV (reduces anxiety, preload, dyspnea); N = Nitrates (vasodilators, reduce preload/afterload); O = Oxygen (high-flow, prepare for NIV/BiPAP); P = Pump (IV Loop diuretic — furosemide).
• Furosemide (Lasix) IV — given IV for IMMEDIATE action (onset within 5–15 minutes); causes rapid diuresis to remove excess fluid.
• Morphine — reduces the sensation of breathlessness, decreases anxiety (which worsens O2 consumption), and causes mild vasodilation (reduces preload). MONITOR for respiratory depression.
• Nitrates (NTG) — powerful venodilators that RAPIDLY reduce preload; given sublingually, IV drip, or as spray. Hold if systolic BP < 90 mmHg.
• Continuous monitoring: SpO2, RR, HR, BP, cardiac rhythm, urine output, and mental status.
• NANDA Priority Nursing Diagnosis: Impaired Gas Exchange related to alveolar-capillary membrane changes (fluid in alveoli).

Definitions

Section Title

Acute Pulmonary Edema: Emergency Nursing Management

Common Mistakes

• Positioning the patient SUPINE or SEMI-RECUMBENT instead of HIGH FOWLER'S with legs DEPENDENT — this is a critical error.
• Giving furosemide PO (oral) instead of IV in acute pulmonary edema — IV is required for rapid onset.
• Forgetting to CHECK systolic BP BEFORE giving nitrates — do NOT give if SBP < 90 mmHg.
• Forgetting to monitor for RESPIRATORY DEPRESSION after giving morphine.
• Treating the numbers (ECG rhythm) rather than the PATIENT — always assess hemodynamics first.

Exam Tips

• NLE CRITICAL: Weight gain of 1 kg/day or 2.5 kg/week = call the doctor. This number is tested repeatedly on the board exam.
• Patient teaching about digoxin: check APICAL pulse for 1 full minute BEFORE each dose; hold if <60 bpm; report nausea, visual changes, slow pulse.
• Salt substitutes contain POTASSIUM — warn patients on ACE inhibitors or spironolactone to avoid them (hyperkalemia risk).
• The nursing diagnosis 'Deficient Knowledge' related to HF self-management is commonly paired with patient teaching scenarios in NLE.
• Philippine context: PhilPEN and the Malasakit Program support NCD management; as a nurse under RA 9173, you are responsible for health education as an independent nursing function.

Key Points

• DAILY WEIGHT MONITORING is the cornerstone of HF self-management. Weigh at the SAME TIME each day, after urinating, before eating, on the SAME scale, wearing the SAME type of clothing.
• REPORT immediately: Weight gain of 1 kg (about 2 lbs) in 1 DAY or 2.5 kg (about 5 lbs) in 1 WEEK — this signals fluid retention (decompensation).
• Sodium restriction: Typically 2,000–3,000 mg Na per day (low-sodium diet). Avoid processed foods, canned goods, bagoong, patis, toyo, instant noodles — common Filipino dietary challenges.
• Fluid restriction: Usually 1.5–2 liters per day if ordered. Teach patient to measure fluid intake including all soups, ice cream, and gelatin.
• Position: Semi-Fowler's to High Fowler's during rest and sleep to ease breathing.
• Activity: Balance rest and activity. Cardiac rehabilitation and graded exercise as tolerated. Avoid activity after meals (increases cardiac demand).
• Monitor I&O (intake and output) every shift; monitor daily weight; auscultate lung sounds every shift for crackles; assess peripheral edema (grade 0–4+).
• NANDA Nursing Diagnoses for Chronic HF: Decreased Cardiac Output; Excess Fluid Volume; Activity Intolerance; Ineffective Health Management; Deficient Knowledge (Patient Teaching).
• Teach patient: Medication compliance (never skip digoxin without checking pulse; never stop beta-blockers abruptly); signs of worsening HF; when to call the doctor; pulse-taking technique before digoxin.
• Follow-up care: Reinforce compliance with clinic visits, laboratory monitoring (electrolytes, BNP, creatinine), and weight logs.

Definitions

Section Title

Chronic Heart Failure: Nursing Management and Patient Teaching

Common Mistakes

• Teaching the patient to weigh themselves at different times of day — this gives inaccurate trending.
• Forgetting to specify 'same scale, same clothing, after first void in the morning' in patient teaching.
• Allowing the patient to use salt substitutes — most contain POTASSIUM CHLORIDE which can cause hyperkalemia especially in patients on spironolactone or ACE inhibitors.
• Restricting sodium without also educating about HIDDEN sodium sources (canned goods, instant noodles, processed meats) common in Filipino diets.
• Not teaching the patient to check the APICAL PULSE before taking digoxin — a key medication safety teaching point.

Exam Tips

• NLE FORMULA: Patient assessment FIRST → Check pulse → Check BP → Then decide on intervention.
• ARREST RHYTHMS (no pulse): VF, Pulseless VT → CPR + DEFIBRILLATE (shockable). Asystole, PEA → CPR + EPINEPHRINE (not shockable).
• AFib = irregularly irregular + no P waves + stroke risk = ANTICOAGULATION is mandatory.
• REMEMBER: Defibrillation = D for Disorganized (VF/pulseless VT). Cardioversion = C for Controlled timing (synchronized).
• For NLE scenarios involving the nurse's FIRST action in cardiac arrest: Call for help / activate emergency response → Start CPR → Attach AED/defibrillator → Defibrillate if shockable.

Key Points

• A dysrhythmia is any disturbance in the RATE, RHYTHM, or CONDUCTION of the heartbeat.
• MOST IMPORTANT RULE: Always assess the PATIENT first — not just the ECG. Ask: Is the patient conscious? Do they have a pulse? Are they hemodynamically stable (BP, mental status)?
• SINUS BRADYCARDIA: Regular rhythm, rate <60 bpm. P waves present. PR interval normal. Treat only if SYMPTOMATIC (dizziness, hypotension, syncope). Drug: ATROPINE 0.5 mg IV. May need a PACEMAKER if refractory.
• SINUS TACHYCARDIA: Regular rhythm, rate >100 bpm. P waves present. Treat the UNDERLYING CAUSE (pain, fever, hypovolemia, anxiety, anemia) — NOT the rhythm itself.
• ATRIAL FIBRILLATION (AFib): IRREGULARLY IRREGULAR rhythm. NO discernible P waves (replaced by chaotic 'f' waves). Ventricular response is irregular. Most common CHRONIC dysrhythmia. Risk: THROMBUS formation in left atrium → STROKE (embolic). Management: Anticoagulation (warfarin or DOAC) + Rate control (beta-blockers, CCB, digoxin). May need rhythm control (cardioversion or amiodarone).
• ATRIAL FLUTTER: Rapid, regular atrial activity at 250–350 bpm. Classic SAWTOOTH flutter waves (F waves). Ventricular rate is regular (2:1, 3:1, or 4:1 conduction ratio). Also has stroke risk — anticoagulation needed.
• VENTRICULAR TACHYCARDIA (VT): 3 or more consecutive PVCs (premature ventricular contractions). WIDE, bizarre QRS complexes at >100 bpm. NO normal P waves associated. TWO types: (1) VT WITH PULSE but unstable → SYNCHRONIZED CARDIOVERSION; (2) PULSELESS VT → CPR + IMMEDIATE DEFIBRILLATION (treat as cardiac arrest).
• VENTRICULAR FIBRILLATION (VF): Completely chaotic, disorganized ventricular electrical activity. NO effective cardiac output. Wavy, irregular baseline — NO recognizable QRS, P waves, or T waves. LETHAL arrest rhythm. Priority: Immediate CPR + DEFIBRILLATION. Call for crash cart.
• ASYSTOLE: 'Flatline' — complete absence of electrical activity. NOT SHOCKABLE (defibrillation will not help). Treat with CPR + EPINEPHRINE IV every 3–5 minutes. Look for reversible causes (Hs and Ts).
• PVCs (Premature Ventricular Contractions): Early, wide, bizarre QRS without preceding P wave, followed by a COMPENSATORY PAUSE. Occasional PVCs in healthy adults may be normal. Concerning when: more than 6/minute, multifocal, bigeminal, R-on-T phenomenon (risk of VF).
• HEART BLOCK (3rd Degree / Complete): P waves and QRS have NO relationship. Atria and ventricles beat INDEPENDENTLY. SYMPTOMATIC — needs a PACEMAKER.

Definitions

Section Title

Cardiac Dysrhythmias: Recognition and Management

Common Mistakes

• Treating the RHYTHM on the monitor rather than the PATIENT — always assess the patient's pulse, BP, and consciousness first.
• Using DEFIBRILLATION for asystole — asystole is NOT shockable. Use CPR and epinephrine.
• Confusing defibrillation (unsynchronized, for arrest rhythms) with cardioversion (synchronized, for unstable perfusing rhythms).
• Thinking ALL bradycardia needs atropine — treat ONLY if symptomatic (hypotension, syncope, chest pain).
• Thinking sinus tachycardia is treated with antidysrhythmic drugs — treat the underlying CAUSE, not the rate.
• Missing that PULSELESS VT is treated the same as VF — CPR + immediate defibrillation.

Exam Tips

• NLE QUESTION TYPE: 'The nurse notices pacemaker spikes on the ECG not followed by QRS complexes' = FAILURE TO CAPTURE → Assess the patient, report to physician.
• Hiccups after pacemaker insertion = LEAD DISPLACEMENT into diaphragm → Medical emergency, notify physician.
• Patient teaching priority: Check pulse DAILY; carry ID card; avoid arc welding and MRI (unless MRI-conditional); tell all health providers.
• Under RA 9173, the nurse is responsible for safe monitoring and patient teaching for pacemaker patients — this is both an independent and collaborative nursing function.
• Temporary transcutaneous pacing (external pads) = EMERGENCY bridge; transvenous = ICU setting; permanent = surgically implanted for chronic conditions.

Key Points

• A pacemaker delivers electrical impulses to stimulate myocardial depolarization when the heart's natural conduction system fails.
• INDICATIONS: Symptomatic bradycardia, complete heart block (3rd degree), sick sinus syndrome, and asystole.
• TYPES: (1) TEMPORARY pacemakers — Transcutaneous (external pads on chest, used in emergencies) or Transvenous (electrode catheter via subclavian/jugular vein to right ventricle, used in ICU/CCU); (2) PERMANENT pacemakers — surgically implanted device under the skin, usually below the LEFT clavicle.
• On ECG, a pacemaker spike (vertical line) should IMMEDIATELY precede each paced QRS complex (ventricular pacing) or P wave (atrial pacing).
• FAILURE TO CAPTURE: Pacemaker spike visible on ECG but NOT followed by a QRS complex. The myocardium is not responding to the electrical stimulus. Causes: lead displacement, battery depletion, inflammation at the lead tip.
• FAILURE TO SENSE: The pacemaker does NOT detect the patient's own heartbeats and fires inappropriately (competing with the patient's own rhythm). This is dangerous — can trigger VF (R-on-T).
• FAILURE TO FIRE (OUTPUT FAILURE): No pacemaker spike when one is expected. Causes: battery failure, lead fracture, loose connections.
• After PERMANENT pacemaker implantation nursing care: Monitor incision site for signs of infection; limit movement of the IPSILATERAL arm (same side as implant) for 48–72 hours to prevent lead dislodgement; semi-Fowler's position; continuous cardiac monitoring; assess for hiccups (diaphragmatic stimulation = lead displacement into diaphragm).
• PATIENT TEACHING after permanent pacemaker: Check pulse DAILY (wrist or carotid); report pulse below the set rate, dizziness, syncope, hiccups; carry a pacemaker ID card at all times; avoid strong electromagnetic fields (arc welding, MRI unless MRI-conditional); most household appliances are SAFE (microwave ovens, cell phones if kept >15–20 cm from the device); tell all healthcare providers (dentists, surgeons) about the pacemaker; medical alert bracelet recommended.
• MRI compatibility: MOST older pacemakers are NOT MRI-compatible. Newer MRI-conditional devices are safe under specific conditions. Always verify BEFORE any MRI procedure.

Definitions

Section Title

Pacemakers: Types, Indications, and Nursing Care

Common Mistakes

• Restricting movement of the WRONG arm — limit the arm on the SAME SIDE as the pacemaker implant (usually left subclavicular region).
• Telling patients that ALL electromagnetic sources are dangerous — most household appliances (microwaves, cell phones) are SAFE at normal distances.
• Forgetting to check for HICCUPS after pacemaker insertion — hiccups indicate lead displacement into the diaphragm.
• Not knowing the DIFFERENCE between failure to capture, failure to sense, and failure to fire — NLE may describe an ECG tracing and ask you to identify the problem.
• Forgetting to teach the patient to carry a PACEMAKER ID CARD — especially important in the Philippine context for emergency medical situations.

Exam Tips

• NLE CRITICAL: Digoxin apical pulse <60 bpm = HOLD the drug + notify the physician = ALWAYS.
• Digoxin toxicity = anorexia (FIRST sign) + nausea + YELLOW-GREEN HALOS (visual disturbances) + bradycardia + dysrhythmias → Antidote: DIGOXIN IMMUNE FAB.
• HYPOKALEMIA + DIGOXIN = DANGER — monitor K+ in ALL patients on both loop diuretics AND digoxin.
• DIURETIC MEMORY AID: Loop and Thiazide = LOSE Potassium (hypokalemia). Spironolactone = KEEPS Potassium (hyperkalemia). 'K-SPARING = K-KEEPING'.
• ACE inhibitor cough → switch to ARB. ACE inhibitor angioedema → STOP IMMEDIATELY, switch to ARB.
• Beta-blockers in HF: 'START LOW, GO SLOW' — never start at high doses; never stop abruptly.
• Amiodarone side effects = PATTCH: Pulmonary toxicity, Arrhythmias (pro-arrhythmic), Thyroid dysfunction, Torsades (QT prolongation), Corneal deposits, Hepatotoxicity/photosensitivity.

Key Points

• DIGOXIN (Cardiac Glycoside): Positive INOTROPE (increases contractility) + Negative CHRONOTROPE (slows HR). Uses: HF with reduced EF; rate control in AFib.
• DIGOXIN THERAPEUTIC LEVEL: 0.5–2 ng/mL. Toxicity occurs >2 ng/mL.
• BEFORE EVERY DOSE of digoxin: Take APICAL PULSE for ONE FULL MINUTE. HOLD and notify the physician if HR <60 bpm in adults (or <90–110 in infants/children).
• DIGOXIN TOXICITY SIGNS: Anorexia (FIRST sign), nausea, vomiting, VISUAL DISTURBANCES (yellow-green halos around lights, blurred vision), bradycardia, and dysrhythmias (PVCs, heart block).
• HYPOKALEMIA POTENTIATES DIGOXIN TOXICITY — when potassium is low, digoxin binds more avidly to the Na-K-ATPase pump → increased toxicity risk. Monitor K+ closely especially in patients on loop diuretics.
• ANTIDOTE for digoxin toxicity: DIGOXIN IMMUNE FAB (Digibind).
• LOOP DIURETICS (Furosemide/Lasix): Most potent; used for acute and chronic fluid overload. Side effects: HYPOKALEMIA, hyponatremia, ototoxicity (with rapid IV push or high doses), dehydration. Monitor K+ and urine output. Give IV furosemide SLOWLY to prevent ototoxicity.
• THIAZIDE DIURETICS (Hydrochlorothiazide/HCTZ): For mild HF and hypertension. Also cause HYPOKALEMIA. Less potent than loop diuretics.
• POTASSIUM-SPARING DIURETICS (Spironolactone/Aldactone): Aldosterone antagonist. Improves HF SURVIVAL (RALES trial). Risk: HYPERKALEMIA. Avoid KCl supplements and salt substitutes (potassium chloride) in patients on spironolactone. Monitor K+.
• ACE INHIBITORS (Enalapril, Lisinopril, Captopril): Reduce afterload and prevent remodeling. Side effects: Dry persistent cough (most common), HYPERKALEMIA, hypotension (first-dose), ANGIOEDEMA (rare but dangerous — discontinue immediately). Monitor K+ and BUN/creatinine.
• ARBs (Losartan, Valsartan): Same mechanism as ACE-I but block the Ang-II receptor. Alternative when ACE-I causes cough. Same hyperkalemia risk. NO cough side effect.
• BETA-BLOCKERS (Carvedilol, Metoprolol succinate, Bisoprolol): Improve long-term HF SURVIVAL. Start at low doses, titrate slowly. Side effects: Bradycardia, hypotension, fatigue, bronchospasm (avoid in asthma). HOLD if HR <60 bpm or BP is low. NEVER STOP ABRUPTLY — rebound tachycardia and angina may occur.
• NITRATES (Isosorbide Dinitrate, Nitroglycerin): Venodilators — reduce PRELOAD. Used in HF and angina. Combined with hydralazine, they improve HF survival in ACE-I intolerant patients. Side effects: HEADACHE (most common), orthostatic hypotension. Hold if SBP <90 mmHg. Tolerance develops with continuous use — provide nitrate-free interval.
• HYDRALAZINE (Apresoline): Arterial vasodilator — reduces AFTERLOAD. Used with nitrates in HF. Side effect: Reflex tachycardia, lupus-like syndrome with long-term use.
• AMIODARONE: Broad-spectrum antidysrhythmic used for AFib, VT, VF. MONITOR for: Pulmonary toxicity (most serious), thyroid dysfunction (both hypo and hyperthyroidism), hepatotoxicity, corneal microdeposits (vision changes), skin photosensitivity, QT prolongation. Sun protection teaching required.
• ANTICOAGULANTS (Warfarin, DOACs — Apixaban, Rivaroxaban, Dabigatran): Required in AFib to prevent EMBOLIC STROKE. Warfarin: Monitor INR (target 2.0–3.0); many drug and food interactions; antidote = Vitamin K (or FFP for emergencies). DOACs: Fewer interactions, no routine INR monitoring needed.
• IV POSITIVE INOTROPES (Dobutamine, Milrinone): Used in ACUTE DECOMPENSATED HF in ICU/CCU. Improve contractility and cardiac output. Given IV drip, require continuous cardiac monitoring. Dobutamine: beta-1 agonist. Milrinone: phosphodiesterase inhibitor.
• NEVER combine rate-slowing drugs (e.g., digoxin + beta-blocker, or digoxin + diltiazem) without CLOSE monitoring for dangerous bradycardia.

Definitions

Section Title

Cardiac Pharmacology: Key Drugs for Heart Failure and Dysrhythmias

Common Mistakes

• Forgetting to take the APICAL PULSE (not radial) before digoxin — apical pulse is used because it accounts for pulse deficit.
• Holding digoxin based on RADIAL pulse instead of the APICAL pulse — use the APICAL pulse over the apex of the heart.
• Not connecting hypokalemia (from loop diuretics) to increased digoxin toxicity risk — these two are frequently combined in NLE scenarios.
• Giving potassium supplements or salt substitutes to a patient on SPIRONOLACTONE — this can cause life-threatening hyperkalemia.
• Stopping beta-blockers ABRUPTLY — this causes rebound sympathetic activation: sudden tachycardia, hypertension, and potential MI or angina.
• Giving nitrates to a patient with SBP <90 mmHg — will cause severe hypotension.
• Not knowing the antidote for digoxin toxicity = DIGOXIN IMMUNE FAB (Digibind) — this is a classic NLE question.