Mechanical Activity of the Heart Diastole Systole Semilunar valves open Atrioventricular Valves closed
Cardiac output CO = 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 system heart with eachNormal (children) = -Environment contraction. -Electrolytes Affected by: …ect… PRELOAD AFTERLOAD CONTRACTILITY
Preload• Frank Starling’s Law of Degree of fiber stretch as a result of a quantity of blood placed on the Heart the muscle prior to contraction. The more diastolic volume or fibre stretch at end diastole, the greater the force of the next contraction during systole Measured by LVEDP - left ventricular 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.
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
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
Electrical Activity of the Heart
The HeartELECTRICAL PROPERTIES MECHANICAL PROPERTIES AUTOMATICITY CONTRACTILITY CONDUCTIVITY CARDIAC OUTPUT BP Perfusion (capillary refill) EXCITABILITY LOC Pulses ECG
Conduction System of the Heart
Intra- and extracellular ion concentrations (mmol/L) Element Ion Extracellular Intracellular Ratio Sodium Na+ 135 - 145 10 14:1 Potassium K+ 3.5 - 5.0 155 1:30 Chloride Cl- 95 - 110 10 - 20 4:1 Calcium Ca2+ 2 10-4 2 x 104:1Although intracellular Ca2+ content is about 2 mM, most of this is bound or sequestered in intracellular organelles (mitochondria and sarcoplasmic reticulum).
MyocardialContractile Action Potential
Myocardial Contractile Cell: Action Potential• Phase 0: Depolarization phase, Na+ channels open and rapid influx of Na+ into cells• Phase 1: Repolarization phase (brief) cause by inactivating 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 due to outward K+ current• Phase 4: Resting membrane potential, Na+ moves out of cell and K+ moves into cell via an active pump (Na+/K+ pump)
Summary of Electrical Pathway• Distinct ion channels drive the depolarization and repolarization of cardiac cells during action potential.• Na+ channels (dominant in cardiac cells) depolarize quickly, but Ca++ channels (dominant in the SA and AV nodes) depolarize slowly.• The cell cannot respond to stimuli during the refractory period, except late in phase 3 when it can respond to strong stimuli.• The cell can respond again when it is completely repolarized.
Linking Conduction to the Cardiac CyclePressure (mmHg)Aortic blood flow(L/min) Ventricular volume (mL) Heart soundsVenous pulse Electrocardiogram
The Principals of Cardiac Monitoring
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)
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
ECG Waves and Intervals
Basic Rhythm Interpretation• Use a systematic approach• A consistent method will help enhance your assessment, confidence and comfort level.• At CDH, we will use a 10-Step Method to Rhythm Analysis
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
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
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 the type of arrhythmia
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