HF and dysrhythmias

HF

Structural/functional heart abnormality → impaired pumping and/or filling → ↓ cardiac output and/or ↑ filling pressures → poor perfusion and fluid congestion.

HF Common causes

CAD/MI, hypertension, valve disease, cardiomyopathy, dysrhythmias.

Left-sided HF:

blood backs up into pulmonary circulation → dyspnea, orthopnea, crackles, hypoxemia, pulmonary edema.

Right-sided HF:

Blood backs up into systemic venous circulation → JVD, hepatomegaly, dependent edema, ascites.

HFrEF: EF ≤40%;

impaired ventricular contraction (systolic dysfunction).

HFpEF: EF ≥50%;

preserved EF but elevated filling pressures, often impaired relaxation.

HFmrEF: EF

41–49%

Compensation becomes harmful

↓ cardiac output activates SNS → tachycardia + vasoconstriction + ↑ workload. Renal hypoperfusion activates RAAS → Na+/water retention + vasoconstriction + fibrosis. Long-term activation increases preload/afterload and ventricular remodeling → worsening HF. BNP/NT-proBNP rise with cardiac wall stretch.FH

HF Signs/symptoms

Exertional dyspnea, orthopnea, nocturnal dyspnea, fatigue, weight gain, crackles, JVD, edema, S3, low SpO2, poor perfusion.

Diagnostics:

• Echo: EF, chambers, valves.

• ECG: dysrhythmias.

• CXR: cardiomegaly, pulmonary congestion/edema, pleural effusion.

• BNP <100 pg/mL or NT-proBNP <300 pg/mL makes acute HF less likely.

• Monitor creatinine/eGFR, K+, Na+.

Red flags:

Acute pulmonary edema, hypotension, confusion, ↓ urine output.

HF treatment goals:

1.Reduce mortality/hospitalizations and slow progression.

1. Relieve congestion, dyspnea, edema.

2. Maintain cardiac output and tissue perfusion.

Four foundational HFrEF drug groups:

1. ARNI (sacubitril/valsartan) OR ACE inhibitor/ARB.

2. Evidence-based beta blocker.

3. Mineralocorticoid receptor antagonist (spironolactone/eplerenone).

4. SGLT2 inhibitor (dapagliflozin/empagliflozin).
   Add loop diuretic for symptomatic fluid retention.

ARNI/ACEI/ARB, evidence-based beta blocker, MRA, SGLT2 inhibito

= improve long-term outcomes in HFrEF.

Loop diuretics

relieve congestion; not a proven mortality benefit.

Dobutamine/milrinone

short-term support in selected severe low-output HF; not routine long-term treatmen

HF nursing priorities:

• Daily weights, I&O, edema, lung sounds.

• Monitor BP, HR, mental status, urine output, perfusion.

• Monitor K+, renal function, and medication effects.

• Report weight gain of 2–3 lb in 24 hours or 5 lb in one week.

• Avoid NSAIDs unless approved; they may worsen fluid retention and kidney function.

• Do not initiate/increase beta blockers during cardiogenic shock or severe hemodynamic instability.

• Teach medication adherence and when to report worsening symptoms.

Stenosis

valve does not open fully → obstructed forward flow/pressure overload.

Regurgitation

valve does not close fully → backward flow/volume overload.

Echo with Doppler

is the primary valve assessment.

Severe symptomatic valve disease

• may need repair/replacement, not medication alone.

Severe aortic stenosis

monitor dyspnea, angina, syncope; avoid dehydration/over-diuresis and sudden hypotension.

Mitral stenosis

manage AF and anticoagulation when indicated.

Valve infection

→ vegetations → valve damage/embolization. Signs: fever, new/changing murmur, systemic illness.

• Obtain blood cultures before antibiotics when feasible; echo assesses valves.

• Treat with prolonged IV antibiotics; surgery if complications.

• Report new neurologic deficits or poor perfusion immediately.

Pericarditis:

• Sharp pleuritic chest pain worse lying flat, better leaning forward; friction rub ± fever.

• ECG: diffuse ST elevation and PR depression.

• Echo checks for pericardial effusion.

• Uncomplicated cases: NSAIDs + colchicine; treat underlying cause.

• Hypotension + JVD + muffled heart sounds or shock may indicate tamponade → emergency

Myocarditis:

infection/immune response → myocardial inflammation → impaired contraction/electrical stability.

• Chest pain, palpitations, dyspnea, dysrhythmias; severe cases may cause cardiogenic shock.

• Tests: troponin, ECG, echo, cardiac MRI.

• Cause-specific/supportive care; manage HF and dysrhythmias.

• Avoid strenuous exercise during active disease until cardiology clearance.

Cardiomyopathy:

• Dilated: enlarged, weak ventricle → systolic dysfunction/HFrEF.

• Hypertrophic: thickened myocardium → impaired filling; possible LV outflow obstruction.

• Restrictive: stiff ventricles → impaired filling/elevated venous pressures.

Normal conduction

SA node → atria/P wave → AV node (delays impulse for filling) → His bundle → bundle branches → Purkinje fibers → ventricles/QRS.

Automaticity:

generates impulse.

Excitability:

responds to impulse.

Conductivity

passes impulse.

Contractility

contracts.

Refractoriness:

• : temporarily cannot respond again.

Na+ enters →

depolarization.

K+ leaves →

repolarization.

Ca2+ enters →

• contraction.

Mg2+

• helps stabilize rhythm.

Normal sinus rhythm

regular, 60–100 bpm, P before each QRS, PR 0.12–0.20 sec, QRS 0.06–0.10 sec.

PR >0.20 sec with every P conducted =

first-degree AV block.

QRS ≥0.12 sec =

wide QRS.

Nursing approach:

Assess pulse, BP, symptoms, mental status, perfusion → identify ECG rhythm → determine stability → intervene according to rhythm and patient → reassess. Treat the patient, not just the monitor.

Sinus tachycardia:

regular >100 bpm, normal P/PR/QRS. Causes: fever, pain, anxiety, dehydration, hypoxia, stimulants. Treat the cause; assess BP, perfusion, O2. No cardioversion for sinus tachycardia itself.

Sinus bradycardia

regular <60 bpm, normal conduction. Causes include beta blockers, CCBs, digoxin, ischemia, increased vagal tone. Asymptomatic: monitor/treat cause. Symptomatic: atropine; if ineffective, pacing and/or dopamine/epinephrine infusion per protocol.

Atrial fibrillation (AF):

irregularly irregular; no distinct P waves. Atria quiver → reduced effective contraction, embolic stroke risk, possible ↓ cardiac output with RVR. Stable: rate control + assess anticoagulation. Unstable: synchronized cardioversion.

Atrial flutter:

sawtooth F waves; rapid atrial rate; ventricular rate often ~150 with 2:1 block. Stroke risk; management similar to AF.

AF/flutter with RVR

slides list IV metoprolol or diltiazem when appropriate. Avoid AV-nodal blockers in pre-excited AF/WPW; avoid IV diltiazem in HFrEF.

SVT/PSVT

regular 150–250 bpm, sudden onset/termination, P waves often hidden. Stable: vagal maneuvers → adenosine. Unstable: synchronized cardioversion. Recurrent cases may need ablation.

AV BLOCKS First-degree:

PR >0.20 sec, constant; every P conducts. Usually monitor/correct cause.

AVB Mobitz I/Wenckebach:

R progressively lengthens, then a QRS drops. Stable: monitor/correct cause; symptomatic treatment may include atropine.

AVB Mobitz II

constant PR with sudden dropped QRS. Apply pacing pads; urgent pacing evaluation. Unstable: transcutaneous pacing; atropine often ineffective.

AVB Third-degree/complete block:

P waves and QRS independent; slow escape rhythm. Urgent pacemaker evaluation; unstable → immediate transcutaneous pacing and prepare transvenous pacing. If atropine ineffective or while arranging pacing: dopamine or epinephrine infusion may be used per protocol.

PAC:

arly, different-shaped P wave with narrow QRS. Often monitor and correct triggers (stress, caffeine, stimulants, illness, electrolyte changes).

PVC:

• early wide QRS ≥0.12 sec, no preceding P. Assess ischemia/heart disease; correct hypoxia/electrolyte problems/triggers. Frequent or symptomatic PVCs may require further evaluation or beta blocker\

VT:

usually regular wide-complex tachycardia; pulse determines treatment

Pulseless VT

CPR + immediate defibrillation; epinephrine; amiodarone or lidocaine for refractory rhythm.

VT with pulse, stable:

expert consultation; may use procainamide or amiodarone with ECG/BP monitoring.

VT with pulse, unstable:

synchronized cardioversion for regular monomorphic VT.

Torsades de pointes:

• polymorphic VT with prolonged QT; associated with low K+/Mg2+, QT-prolonging drugs, congenital long QT, bradycardia. Give magnesium; correct K+/Mg2+ and stop QT-prolonging drugs. Sustained/unstable torsades → unsynchronized defibrillation.

VF:

chaotic ventricular activity, no effective cardiac output. Immediate CPR + defibrillation; epinephrine; amiodarone or lidocaine for refractory VF.

Asystole

• no ventricular electrical activity. Nonshockable → CPR + epinephrine; treat reversible causes; NO defibrillation.

PEA

• organized electrical rhythm but no pulse. Nonshockable → CPR + epinephrine; treat Hs & Ts; NO defibrillation.

Hs & Ts for PEA/reversible causes:

Hs: hypovolemia, hypoxia, hydrogen ion/acidosis, hypo-/hyperkalemia, hypothermia.

Ts: tension pneumothorax, tamponade, toxins, pulmonary thrombosis, coronary thrombosis.

Electrical/other treatment:

• Synchronized cardioversion: selected unstable tachyarrhythmias with a pulse.

• Defibrillation: VF, pulseless VT, and sustained polymorphic VT requiring shock.

• Pacemaker: bradyarrhythmias/conduction block.

• ICD: dangerous ventricular rhythms.

• Catheter ablation: selected recurrent abnormal rhythms.

• AF: assess need for anticoagulation to reduce stroke risk.

Class IA: procainamide; 

Na+ block, prolongs repolarization → QRS/QT prolongation.

Class IB: lidocaine; 

Na+ block, suppresses ventricular arrhythmias.

Class IC: flecainide;

strong Na+ block → marked conduction slowing/QRS widening.

Class II:

metoprolol; beta blocker → slows SA rate and AV conduction.

Class III: 

amiodarone; K+ channel effects → prolongs repolarization/refractoriness.

Class IV: 

diltiazem; non-DHP CCB → slows AV node.

Other: 

adenosine causes transient AV block; digoxin slows AV conduction; magnesium treats torsades; atropine treats symptomatic bradycardia.

Sacubitril/valsartan (ARNI)

Preferred foundational therapy for symptomatic chronic HFrEF; increases natriuretic peptide effects and blocks angiotensin II

ADR -Hypotension, hyperkalemia, renal impairment, angioedema; monitor BP, K⁺, kidney function. Wait 36 hours after ACE inhibitor before starting

Lisinopril (ACEI)

HFrEF alternative; ↓ angiotensin II/aldosterone → ↓ vasoconstriction and fluid retention

Cough, hyperkalemia, angioedema, hypotension; monitor BP, K⁺, kidneys

Valsartan (ARB)

HFrEF alternative when ACEI not tolerated and ARNI not feasible; blocks angiotensin II

Hyperkalemia, hypotension, renal impairment; monitor BP, K⁺, kidneys

Carvedilol, metoprolol succinate, bisoprolol (beta blockers)

Foundational HFrEF therapy; block chronic SNS stimulation → ↓ workload/remodeling and improve survival

Bradycardia, hypotension; monitor HR/BP. Don't initiate or increase during cardiogenic shock/severe instability

Spironolactone, eplerenone (MRAs)

HFrEF foundational therapy; block aldosterone → ↓ Na⁺ retention and cardiac remodeling

Hyperkalemia, renal impairment; monitor K⁺ and kidney function

Dapagliflozin, empagliflozin (SGLT2 inhibitors)

HFrEF foundational therapy; increase urinary glucose/Na⁺ excretion and provide cardiorenal protection

Monitor renal function, volume status, and treatment response; slide lists these as foundational HF drugs

Furosemide (loop diuretic

Relieves fluid overload, edema, and dyspnea by increasing Na⁺/water excretion

Monitor daily weight, I&O, BP, electrolytes, kidney function; relieves symptoms but isn't listed as a mortality-benefit drug

Hydralazine + isosorbide dinitrate

Selected HFrEF patients; hydralazine ↓ afterload, nitrate ↓ preload

Headache, dizziness, hypotension, reflex tachycardia; hydralazine can cause lupus-like syndrome. Avoid nitrates with PDE-5 inhibitors

Digoxin (cardiac glycoside)

Selected symptomatic HFrEF; also controls ventricular rate in AF; increases contractility and slows AV conduction

Nausea, anorexia, visual changes, bradycardia, dysrhythmias. Check apical pulse; monitor K⁺, Mg²⁺, kidney function and levels as indicated. Low K⁺ increases toxicity risk

Dobutamine (IV beta-1 agonist)

Short-term support in selected acute low-output HF/cardiogenic shock; increases contractility and cardiac output

Tachycardia, dysrhythmias, ischemia, BP changes; continuous ECG/BP monitoring and infusion pump

Milrinone (IV PDE3 inhibitor)

Short-term support for severe low-output decompensated HF; increases contractility and causes vasodilation

Ventricular dysrhythmias, hypotension; monitor ECG, BP, kidneys, K⁺/Mg²⁺. Renal dysfunction can cause accumulation

IV antibiotics

Infective endocarditis; treat valve infection

Obtain blood cultures before antibiotics when feasible; prolonged IV treatment, monitor fever, cultures, perfusion, neurologic status, and HF symptoms

NSAIDs + colchicine

Treat most uncomplicated pericarditis

Monitor chest pain and response; assess for effusion/tamponade signs. The slides do not list specific doses

Atropine

Symptomatic bradycardia; increases HR by reducing vagal effects

Monitor HR, ECG, BP, and perfusion; may be ineffective in Mobitz II or complete heart block

Adenosine

Stable regular narrow-complex SVT; briefly blocks AV-node conduction

Flushing, chest pressure, dyspnea, brief AV block/asystole. Rapid IV push + immediate flush; continuous ECG and resuscitation readiness

Metoprolol (Class II beta blocker)

AF/flutter rate control; selected SVT; slows HR and AV conduction

Bradycardia, hypotension, fatigue, AV block. Check HR/BP; avoid in cardiogenic shock, severe bradycardia, or high-grade block without pacing

Diltiazem (Class IV non-DHP CCB)

AF/flutter with RVR and selected SVT; slows AV-node conduction

Bradycardia, hypotension, AV block, edema. Avoid in HFrEF with systolic dysfunction and pre-excited AF/WPW

Digoxin (cardiac glycoside)

Selected HFrEF and AF rate control; increases contractility and slows AV conduction

Nausea, anorexia, visual changes, dysrhythmias. Check apical pulse for 1 minute; monitor K⁺, renal function, and levels. Hypokalemia increases toxicity

Amiodarone (Class III)

Shock-refractory VF/pulseless VT; selected VT and AF

Pulmonary, thyroid, and liver toxicity; bradycardia, hypotension, QT prolongation. Monitor ECG/BP; long-term therapy requires thyroid, liver, and pulmonary monitoring

Lidocaine (Class IB)

Alternative for refractory VF/pulseless VT; selected ventricular arrhythmias

Confusion, tremor, seizures, bradycardia, hypotension. Monitor ECG and neurologic status

Procainamide (Class IA

Selected stable wide-QRS tachycardia with a pulse

Hypotension, QRS widening, QT prolongation/torsades, drug-induced lupus. Continuous ECG/BP monitoring; stop infusion for significant hypotension or QRS widening per protocol

Flecainide (Class IC)

Selected AF/SVT rhythm control in patients without significant structural heart disease

Proarrhythmia, QRS widening, dizziness, AV block. Avoid in structural/ischemic heart disease; monitor ECG

Magnesium sulfate

Torsades de pointes (polymorphic VT with prolonged QT)

Flushing, hypotension; toxicity can cause loss of reflexes and respiratory depression. Monitor ECG, BP, RR, renal function, Mg²⁺ and K

Epinephrine

Cardiac arrest: VF, pulseless VT, asystole, PEA; also infusion for selected bradycardia when atropine fails

Monitor ECG, BP and response; for arrest, slides list 1 mg IV/IO every 3–5 minutes

Dopamine infusion

Selected symptomatic bradycardia when atropine fails; may support HR/BP

Monitor ECG, BP, perfusion and response

Digoxin immune Fab (DigiFab

Antidote for life-threatening digoxin toxicity, especially severe dysrhythmias

Monitor rhythm and clinical response

Stable SVT

Vagal maneuvers → adenosine

Unstable tachyarrhythmia with a pulse

Synchronized cardioversion when appropriate for the rhythm

Symptomatic bradycardia

Atropine; if ineffective, pacing and/or dopamine/epinephrine infusion

Mobitz II or complete heart block

Pacing evaluation; unstable patients need immediate transcutaneous pacing