ECG

EKG LAB N240

Cardiac Conduction & Dysrhythmias

  • Dysrhythmias: Disorders of formation or conduction of electrical impulses in the heart.

  • Affected by electrolytes: Sodium (Na), Potassium (K), and Calcium affect heart function.

  • Depolarization: The phase of contraction.

  • Repolarization: The phase of relaxation.

  • Autonomic Nervous System:

    • Sympathetic: Fight or flight response; increases heart rate (HR), constricts blood vessels.

    • Parasympathetic: Slows heart rate, causes vasodilation of vessels.

Cardiac Impulse Characteristics

  • Automaticity: Ability to initiate an electrical impulse; all cardiac muscle has this property (SA node should be the strongest and quickest).

    • Atrial fibrillation (Afib) caused by faster responses outside of the SA node.

    • Ventricular fibrillation (Vfib) caused by stronger impulses in ventricles.

  • Excitability: Ability to respond to an electrical impulse.

  • Conductivity: Ability to transmit electrical impulses from one cell to another.

Heart Node Functions

  • SA Node: 60-100 bpm.

  • AV Node: 40-60 bpm.

  • Bundle of His to Purkinje Fibers: 20-40 bpm.

  • Firing order: SA Node → AV Node → Bundle of His → Purkinje Fibers.

EKG Waveform Components

  • Components include:

    • R, P, P-R interval, S-T interval, Q, S, Q-T interval.

QRS Variations Analysis

  • Variations in QRS patterns:

    • R, R, R

    • Q, QS, S

ST Segment Abnormalities

  • ST Segment: Various forms include:

    • Isoelectric

    • Elevated

    • Depressed

Q Waves Post Myocardial Infarction (MI)

  • Q waves observed after inferior MI.

  • Lead locations: II, III, AVF.

Arrhythmias: Pathophysiology

  • Prompt assessment of abnormal cardiac rhythm and patient's response is critical.

  • Origin Disturbances:

    • Sinus, atrial, ventricular, junctional (AV node).

  • Rate Disturbances: Brady and tachyarrhythmias.

  • Conduction Disturbances: Heart blocks.

Arrhythmia Interpretation Process

  • Steps to interpret:

    • Determine rate.

    • Determine rhythm.

    • Check if P wave is uniform and precedes each QRS.

    • Ensure QRS duration is < 0.12 sec.

    • Confirm 1:1 P to QRS relationship.

    • Ensure P-R interval is consistent and < 0.20 sec.

Determining Heart Rate

  • Calculate number of R to R intervals in a 6-second interval and multiply by 10 to get rate per minute.

  • A 6-second interval equals 30 large boxes on EKG.

Assessment of Cardiac Rhythm

  • Use a 6-second interval to assess and interpret rhythm components:

    • QRS, T, P waves.

ECG Interpretation Analysis

  • Questions revolving around the specific rhythm depicted in the ECG.

Arrhythmias/Dysrhythmias Etiologies

  • Factors that can cause:

    • Cardiac conditions (MI, CHF, hypertrophy).

    • Hypoxia/ischemia.

    • Acid/base, electrolyte imbalances.

    • Drugs, alcohol, caffeine.

    • Emotional stress.

    • Metabolic conditions (e.g., hyperthyroidism).

    • Connective tissue disorders.

Sinus Rhythm

  • Basis of normal heart rhythm and dynamics.

Sinus Bradycardia

  • Important to determine if the patient is symptomatic or asymptomatic.

Sinus Bradycardia Clinical Associations

  • Occurs in response to:

    • Carotid sinus massage.

    • Hypothermia.

    • Increased vagal tone.

    • Administration of parasympathomimetic drugs.

  • Disease states include:

    • Hypothyroidism.

    • Increased intracranial pressure.

    • Obstructive jaundice.

    • Inferior wall MI (R coronary artery occluded).

Sinus Bradycardia Significance & Treatment

  • Significance: May cause hypotension with decreased cardiac output leading to syncope, angina.

  • Treatment Options:

    • Atropine administration.

    • Potential need for a pacemaker.

    • Addressing the underlying cause (Mnemonic: All Dogs Eat Pie = Atropine, Dopamine, Epinephrine, Pacemaker).

Decreased Cardiac Output (CO)

  • Considerations:

    • Signs & symptoms of decreased CO.

    • Assessments required by the RN.

    • Information needed to report to the provider.

    • Nursing interventions to implement.

    • Collaborative interventions may be necessary.

Sinus Tachycardia

  • Overview of significant implications and physiological response to increased HR.

Sinus Tachycardia Clinical Associations

  • Associated with physiological stressors:

    • Exercise, hypotension, hypovolemia, myocardial ischemia, CHF, anxiety, pain, anemia, fever, hyperthyroidism, hypoxia.

Sinus Tachycardia Treatment

  • Treatment determined by underlying causes:

    • Focus on the cause; beta-adrenergic blockers may be employed to reduce HR and myocardial oxygen consumption.

Sinus Tachycardia Significance

  • Decreased filling time leads to decreased CO; symptoms may include dizziness and hypotension.

  • Increased myocardial oxygen consumption commonly follows elevated HR, contributing to angina or increased infarct size in acute MI patients.

Atrial Fibrillation

  • Characterized by absence of P wave due to atrial vibration.

  • Causes:

    • Cardiomyopathy, pericarditis, hyperthyroidism, HTN, valvular disease, obesity, diabetes, chronic kidney disease, recent cardiac procedures, coronary artery disease.

  • Complication: Loss of CO leading to thromboembolic events.

  • Treatment Strategies: Medications, ablation, cardioversion.

Atrial Flutter

  • A dysrhythmia produced by a pacemaker cell other than SA node; absence of P waves results.

Premature Ventricular Contractions (PVCs)

  • Characteristics: Wide and atypical QRS complexes that occur prematurely from within the ventricles.

PVCs Causes and Treatments

  • Causes:

    • Hypoxia, MI, cardiomyopathy, electrolyte imbalance, excessive stimulant intake, hypertension, recreational drug use.

  • Treatment:

    • Based on signs and symptoms; if symptomatic, correct the underlying cause; antiarrhythmic therapy used rarely.

PVCs Characteristics

  • Conduction originating from ectopic focus in ventricles; premature QRS complex appearance (wide, unusual beats).

  • Terminology:

    • Unifocal: One ectopic source.

    • Multifocal: Multiple ectopic sources, varied PVC configurations.

    • Bigeminy: Every other beat is a PVC.

    • Trigeminy: Every third beat is a PVC.

    • Couplets: Two PVCs in succession.

    • Triplets: Three PVCs consecutively.

Multifocal PVCs Analysis

  • Assessment of various forms in PVCs (Lead II).

    • Group beats, couplets, ventricular tachycardia, bigeminy, trigeminy.

PVCs Clinical Associations

  • Associated with any condition causing myocardial ischemia; includes stimulants, hypokalemia, exercise, MI, mitral valve prolapse.

PVCs Significance

  • Generally benign in a normal heart; in heart disease, PVCs could reduce CO and precipitate angina and heart failure.

  • Indicates ventricular irritability in ischemic heart disease or acute MI.

  • Possible occurrence in reperfusion arrhythmias following thrombolytic therapy or coronary intervention.

PVCs Treatment

  • Focus on correction of underlying causes.

  • Hemodynamic status assessment is vital for determining drug therapy requirements (e.g., Amiodarone, Lidocaine, Beta-blockers, Procainamide).

Ventricular Tachycardia (VT)

  • Significant for being life-threatening.

  • Seen in patients without heart disease history.

  • May result in severe decrease in CO, leading to pulmonary edema, shock, or compromised brain circulation.

Ventricular Tachycardia Causes & Treatment

  • Causes:

    • Hypovolemia, hypoxia, acidosis, electrolyte imbalances (hypo/hyperkalemia), toxins, cardiac tamponade, MI, pulmonary embolism.

  • Treatment Options:

    • Begin chest compressions immediately.

    • Defibrillation and medications are key interventions.

VT Treatment Based on Pulse Status

  • For Pulse Palpable VT:

    • If nonsustained and patient is hemodynamically stable, treat with IV Amiodarone, Procainamide, or Lidocaine.

    • Synchronized cardioversion when drug therapy fails and patient is responsive.

  • For VT without a Pulse:

    • Treat as ventricular fibrillation; rapid defibrillation is required.

Ventricular Fibrillation (VF)

  • Severe derangement of heart rhythm characterized by irregular ECG patterns.

  • No effective contraction or cardiac output occurs.

  • Outcomes include unconsciousness, absence of pulse, apnea, and seizures.

  • If untreated, the patient may die.

VF Treatment Protocol

  • Immediate initiation of CPR and ACLS required, along with drug therapy and defibrillation.

  • Associated with sudden cardiac death due to arrhythmia.

Ventricular Tachycardia & Fibrillation References

  • Medscape resource: Images from ECG monitoring for VT/VF interpretation and management strategies.

Asystole

  • Considerations and management protocols for asystolic events in clinical practice.

Pacemaker Overview

  • Discussion on atrial and ventricular pacing mechanisms.

Failure to Capture

  • Diagnostic criteria and response strategies for failure to capture in pacing.

CPR-BLS Technique Illustration

  • The procedure for chin lift and bag-and-mask technique for ventilating patients needing CPR.

Defibrillation vs. Cardioversion

  • Explanation and illustration of the differences in technique between defibrillation in VT without a pulse and synchronized cardioversion with a pulse.

Defibrillation Protocol Summary

  • Detailed documentation for pre-and post-shock protocols, with specifics on patient identifiers and timing.

Cardioversion Considerations

  • Synchronization importance for effective cardioversion; differences in rhythms treated.

Key Reminders

  • A dysrhythmia reducing CO will produce symptoms.

  • Identify the dysrhythmia for treatment: Drugs, CPR, cardioversion, defibrillation, or pacemaker application.

  • Correct electrolyte abnormalities; provide supportive care; and monitor vital signs and tissue perfusion closely.