1.ECG Workshop: PART ONE Kathleen Brownrigg, BSc, RN, MScN July 2011

2. Cardiac cycle = Cardiac outputFilling + Contraction = Cardiac CycleSystoleDiastole Lub Dub 3. Cardiac Cycle 4. Mechanical Activity of the HeartDiastole Systole Semilunar valves open Atrioventricular Valves closed 5. Cardiac outputCO = HR X SVThe amount of blood ejected Affected by: The amount of bloodfrom the heart per minute. -Physical factors ejected from theNormal (adults)= 4-6L/min -Nervous systemheart with eachNormal (children) = -Environment contraction.-ElectrolytesAffected by:ectPRELOAD AFTERLOAD CONTRACTILITY 6. Preload Frank Starlings Law of Degree of fiber stretch as a resultof a quantity of blood placed onthe Heart the muscle prior to contraction. The more diastolic volume orfibre stretch at end diastole, thegreater the force of the nextcontraction during systole Measured by LVEDP - leftventricular end diastolic pressure- prior to systole (max. full) Normal value 6-12 mmHgAbility of the muscle fibers to stretch The > stretch = > contractilityaccording to incoming volume. If preload increases so does C.O. 7. AfterloadThe resistance to which the ventricles must overcome to eject blood.Resistance to blood flow as it leaves the ventriclesSVR on the Lt sidePVR on the RT side As resistance , stroke volume 8. ContractilityThe ability of the myofibrils to shorten in length and produce a contraction.Not measured directlyFactors that affect contractility: PRELOAD AFTERLOAD DRUGS CARDIAC OXYGENATION FUNCTIONAL MYOCARDIUM 9. Electrical Activity of the Heart 10. The HeartELECTRICAL PROPERTIES MECHANICAL PROPERTIESAUTOMATICITYCONTRACTILITYCONDUCTIVITY CARDIAC OUTPUT BP Perfusion (capillary refill) EXCITABILITYLOC Pulses ECG 11. Conduction System of the Heart 12. Intra- and extracellular ion concentrations (mmol/L)Element Ion Extracellular Intracellular Ratio SodiumNa+135 - 14510 14:1 PotassiumK+ 3.5 - 5.0155 1:30ChlorideCl-95 - 11010 - 20 4:1 CalciumCa2+ 210-42 x 104:1Although intracellular Ca2+ content is about 2 mM, most of this is bound or sequestered in intracellular organelles(mitochondria and sarcoplasmic reticulum). 13. MyocardialContractile Action Potential 14. Myocardial Contractile Cell:Action Potential Phase 0: Depolarization phase, Na+ channels open andrapid influx of Na+ into cells Phase 1: Repolarization phase (brief) cause byinactivating Na+ influx and activation of outward K +current. Phase 2: Plateau phase cause by slow inward Ca++current and decreased K+ efflux. Phase 3: Rapid repolarization to resting potential dueto outward K+ current Phase 4: Resting membrane potential, Na+ moves outof cell and K+ moves into cell via an active pump(Na+/K+ pump) 15. Summary of Electrical Pathway Distinct ion channels drive the depolarization andrepolarization of cardiac cells during actionpotential. Na+ channels (dominant in cardiac cells)depolarize quickly, but Ca++ channels (dominantin the SA and AV nodes) depolarize slowly. The cell cannot respond to stimuli during therefractory period, except late in phase 3 when itcan respond to strong stimuli. The cell can respond again when it is completelyrepolarized. 16. Linking Conductionto the Cardiac CyclePressure (mmHg)Aortic blood flow(L/min) Ventricular volume (mL) Heart soundsVenous pulse Electrocardiogram 17. ECG Cycle 18. The Principals of Cardiac Monitoring 19. ECG Waves and IntervalsP wave: the sequential activation (depolarization) of the right and left atriaQRS complex: right and left ventricular depolarization (normally theventricles are activated simultaneously)ST-T wave: ventricular repolarization U wave: origin for this wave is not clear - but probably represents"afterdepolarizations" in the ventriclesPR interval: time interval from onset of atrial depolarization (P wave) toonset of ventricular depolarization (QRS complex)QRS duration: duration of ventricular muscle depolarizationQT interval: duration of ventricular depolarization and repolarizationRR interval: duration of ventricular cardiac cycle (an indicator ofventricular rate)PP interval: duration of atrial cycle (an indicator of atrial rate) 20. 1. Impulse from sinus node2. Depolarization of the atria3. Depolarization of the A-V node4. Repolarization of the atria5. Depolarization of ventricles6. Activated state of ventricles immediately after depolarization7. Repolarization of ventricles8. After-potentials following repolarization of ventricles 21. ECG Waves and Intervals 22. Monitoring Leads 23. Basic Rhythm Interpretation Use a systematic approach A consistent method will help enhance yourassessment, confidence and comfort level. At CDH, we will use a 10-Step Method toRhythm Analysis 24. 10-Step Method1. Assess your patient (A, B, C, Ds)2. Assess the heart rate (ventricular & atrial)3. Evaluate the regularity of the rhythm4. Assess the P waves5. Evaluate the PR Interval6. Assess the P:QRS ration7. Evaluate the QRS complex8. Assess the ST segment9. Identify the rhythm10. Determine the clinical significance 25. Mechanisms of Arrhythmias Abnormal Impulse Formation Depressed automaticity: bradycardia or escape beats Increased automaticity: premature beats, tachycardia Depolarization and triggered activity: ectopic firing Abnormal Impulse Formation Block or delay Re-entry tachycardias (Wolff-Parkinson-White/WPW,A. flutter, A. fib 26. Goals of Antiarrhythmic Drugs Restore synchrony to myocardial contraction Suppress abnormal rhythms Reduce heart rate to maintain cardiac output As a bridge to ICD, radio-frequency ablation Match the drugs mechanism of action to thetype of arrhythmia 27. Vaughn-Williams Classification of Antiarrhythmics Class I: Sodium Channel Blockers Ia: Prolong refractory period Ib: No change or shorten the refractory period Ic: Prolongation of the refractory period Class II: Beta-adrenergic Receptor Blockers Class III: Potassium Channel Blockers Prolong action potential duration & refractoriness Class IV: Calcium Channel Blockers Others: Digoxin, Adenosine, Magnesium 28. Questions and Comments Questions and Comments