Electrophysiology of heart
Download as PPTX, PDF222 likes83,276 views
This document provides information on cardiac physiology and electrocardiography (ECG). It discusses the action potential in cardiac muscle, the specialized conductive system of the heart including the sinoatrial node, atrioventricular node and Purkinje fibers. It also describes the normal components of an ECG including the P wave, QRS complex and T wave. The document outlines the standard 12-lead ECG and provides details on how to correctly report ECG findings.
Electrophysiology of heart
- 2. Physiology of cardiac muscle • Introduction • Action potential in cardiac muscle • Pacemaker potential • Conductive system of heart ECG • History • What is ECG? • Characterstics of normal ECG • ECG paper • ECG leads • How to report an ECG? • Individual waves and intervals of ECG and their abnormalities • AHA Guidelines for ECG CONTENTS
- 3. PHYSIOLOGY OF CARDIAC MUSCLE
- 4. Three Major type of cardiac muscle fiber:- Atrial muscle Ventricular muscle Specialized excitatory and conductive muscle fibers INTRODUCTION
- 5. Atrial and ventricular muscle contract in a same way as skeletal muscle but the duration of contraction is longer The specialized excitatory and conductive fibers • Contract feebly because they contain few contractile fibrils • Exhibit automatic rhythmical electrical discharge in the form of action potentials
- 6. CARDIAC MUSCLE AS SYNCYTIUM INTERCALATED DISC
- 7. Intercalated discs are cell membranes that separate individual cardiac muscle cells from one another. At each intercalated disc there are communicating gap junctions that allow rapid diffusion of ions so that action potentials travel easily from one cardiac muscle cell to the next
- 8. Myocardial fibers have a resting membrane potential of −90 mV The action potential of single cardiac muscle cells is characterized by • Rapid depolarization (phase 0) • Initial rapid repolarization (phase 1) • Plateau (phase 2) • Slow repolarization process (phase 3) • Resting membrane potential (phase 4) ACTION POTENTIAL IN CARDIAC MUSCLE 0
- 9. Phase 0 (rapid depolarization) External stimulus to excitable tissue opens the voltage gated sodium ion channels sodium ions enter the cells down their electrochemical gradient intracellular movement of sodium ion depolarizes the membrane increases the membrane conductance to sodium ion displaces the membrane potential to +30mV
- 10. Phase 1 (early repolarization) • Following phase 0, the membrane repolarizes rapidly and transiently to almost 0 mV because of the inactivation of sodium ion channel and simultaneous transient increases in outward potassium currents Phase 2 (plateau) • Membrane potential remains approximately 0 mV for a relatively prolonged duration • A balance between slow inward Ca2+ and outward K+ currents mediates the plateau phase of the action potential.
- 11. Phase 3 (repolarization) • Inactivation of Ca2+ channels and a simultaneous increase in outward K+ current through K+ channels produces a net outward movement of positive charge and repolarization of the membrane Phase 4 (resting membrane potential) • The membrane potential of ventricular myocytes remains at the resting membrane potential until the cell is stimulated again
- 12. The types of action potential in the heart can be separated into two categories: (1) fast-response action potentials, which are found in the His-Purkinje system and atrial or ventricular cardiomyocytes (2) slow- response action potentials, which are found in the pacemaker cells in the SA and AV nodes
- 13. • Two types of action potential in the heart:- (1) fast-response action potentials:- His-Purkinje system and atrial or ventricular muscle (2) slow- response action potentials:- pacemaker cells in the SA and AV nodes
- 14. PACEMAKER POTENTIAL • Ik:- K+ current • Ih:- Funny current/’f’channel • ICaT:- Transient Ca2+ channel • ICaL:-Long lasting Ca2+ channel
- 17. Specialized Excitatory and Conductive System of the Heart
- 18. A. SA NODE • The sinus node/ sinoatrial node is located in the superior posterolateral wall of the right atrium immediately below and lateral to the opening of the superior vena cava • The sinus nodal fibers connect directly with the atrial muscle fibers so that any action potential that begins in the sinus node spreads immediately into the atrial muscle wall
- 19. Mechanism of Sinus Nodal Rhythmicity • Resting membrane potential is -55mV. At this -55mV,the fast sodium ion channel closes but slow sodium and calcium channels remain open and there by causing action potential Self-Excitation of Sinus Nodal Fibers • The inherent leakiness of the sinus nodal fibers to sodium and calcium ions causes their self-excitation Automatic Electrical Rhythmicity of the Sinus Fibers • Because of self excitation, sinus fibers has automatic rhythmical discharge and contraction
- 21. B. INTERNODAL PATHWAYS • Anterior (Bachmann) • Middle(Wenckebach) • Posterior(Thorel) internodal pathways
- 22. C. AV NODE • The A-V node is located in the posterior wall of the right atrium immediately behind the tricuspid valve
- 23. D.PURKINJE FIBERS • Velocity of conduction is 1 to 4m/sec • The ends of the Purkinje fibers penetrate about one third of the way into the muscle mass and finally become continuous with the cardiac muscle fibers • Once the impulse reaches the ends of the Purkinje fibers, it is transmitted through the ventricular muscle mass by the ventricular muscle fibers themselves. The velocity of transmission is now only 0.3 to 0.5 m/sec, one sixth that in the Purkinje fibers.
- 24. TRANSMISSION OF CARDIAC IMPULSE THROUGH THE HEART
- 25. SA Node 0.05m/sec Atrial pathways 1m/sec AV Node 0.05m/sec Bundle of his 1m/sec Purkinje fibers 4m/sec Ventricular muscle 1m/sec CONDUCTION SPEEDS IN CARDIAC TISSUES
- 27. HISTORY 1842- Italian scientist Carlo Matteucci realizes that electricity is associated with heart 1876- Irish scientist Marey analyzes electrical pattern of frog’s heart 1887- The first electrocardiogram (ECG) from the intact human heart was recorded with a mercury capillary electrometer by Augustus Waller . The tracings were poor and exhibited only 2 distorted deflections
- 28. Willem Einthoven (1860-1927) was awarded the Nobel Prize in 1924 in physiology and medicine, "for the discovery of the mechanism of the electrocardiogram."
- 30. WHAT IS ECG? • Electrocardiogram/ECG/EKG is the graphical representation of electrical events of heart • Each event has a distinctive waveform • When the cardiac impulse passes through the heart, electrical current also spreads from the heart into the adjacent tissues surrounding the heart
- 32. • The normal electrocardiogram is composed of a P wave, a QRS complex, and a T wave. • The P wave is caused by electrical potentials generated when the atria depolarize before atrial contraction begins. • The QRS complex is caused by potentials generated when the ventricles depolarize before contraction, that is, as the depolarization wave spreads through the ventricles. • Therefore, both the P wave and the components of the QRS complex are depolarization waves.
- 33. • J point is the point where QRS complex ends • The T wave is caused by potentials generated as the ventricles recover from the state of depolarization • In some ECGs an extra wave can be seen on the end of the T wave, and this is called a U wave. It represent repolarization of the papillary muscles. • If a U wave follows a normally shaped T wave, it can be assumed to be normal. If it follows a flattened T wave , it may be pathological
- 34. THE ECG PAPER ECG Machines runs at a standard rate of 25mm/s and use paper with standard-sized squares Horizontally, one large box=0.2 sec and one small box=0.04 sec Vertically, one large box=0.5mV
- 35. ELECTROCARDIOGRAPHIC LEADS • Electrocardiographic leads measures the electrical potential between the two points Bipolar leads:- electrocardiogram is recorded from two electrodes located on different sides of the heart Unipolar leads:- one point on the body and a virtual reference point with zero electrical potential located in the center of heart
- 36. The standard ECG has 12 leads:- 1.Three standard limb leads(Bipolar) 2.Three Augmented limb leads(unipolar) 3.Six chest/precordial leads(unipolar)
- 38. For heart with normal ECG and mean cardiac axis of +60, the standard limb leads will appear as:-
- 39. Einthoven's Law Einthoven's law states that if the electrical potentials of any two of the three bipolar limb electrocardiographic leads are known at any given instant, the third one can be determined mathematically by simply summing the first two Lead I + Lead III= Lead II
- 42. For heart with normal ECG and mean cardiac axis of +60, the augmented limb leads will appear as:-
- 43. ECG pattern recorded by six standard leads
- 46. V1 : Over 4th intercostal space near right sternal margin V2 : Over 4th intercostal space near left sternal margin V3 : In between V2 and V4 V4 : Over left 5th intercostal space on the mid clavicular line V5 : Over left 5th intercostal space on the anterior axillary line V6 : Over left 5th intercostal space on the mid axillary line.
- 49. • Lead I, aVL,V5,V6:- lateral wall • Lead II,III,aVF:-Inferior wall • Lead V1,V2:- Septal • Lead V3,V4:- Anterior wall ANATOMIC GROUPS
- 50. HOW TO REPORT AN ECG? The description should always be in the sequence:- 1 Rhythm, Rate 2 Conduction intervals 3 Cardiac axis 4 A description of the QRS complexes 5 A description of the ST segments and T waves
- 51. 1. Rhythm, Rate • The word ‘rhythm’ is used to refer to the part of the heart which is controlling the activation sequence. The normal heart rhythm, with electrical activation beginning in the SA node, is called ‘sinus rhythm’ • If the intervals between QRS complexes (R-R intervals) are consistent, ventricular rhythm is regular. If intervals between P waves (P-P intervals) are consistent, the atrial rhythm is regular
- 52. • If the rhythm is regular, Rate= 300 Number of large squares between R-R interval OR Rate= 1500 Number of small squares between R-R interval • If the rhythm is irregular, count the number of QRS complexes in a 6-second segment and multiply by 10. Rates below 60 indicate bradycardia; those above 100 indicate tachycardia.
- 56. 3. CARDIAC AXIS • Leads VR and II look at the heart from opposite directions. When seen from the front, the depolarization wave normally spreads through the ventricles from 11 o’clock to 5 o’clock, so the deflections in lead VR are normally mainly downward (negative) and in lead II mainly upward (positive) • The average direction of spread of the depolarization wave through the ventricles as seen from the front is called the ‘cardiac axis’
- 60. 4. Shape of QRS complexes
- 64. P WAVE Always positive in lead I and II Always negative in lead aVR <3 small square in duration <2.5 small square in amplitute May be biphasic in lead V1 Best seen in lead II
- 65. Abnormalities of P Wave 1. Right atrial enlargement:- Tall(>2.5mm), Pointed P wave(‘P Pulmonale’)
- 66. 2. Left atrial enlargement:- Notched/bifid (‘M’ shaped) P wave (‘P Mitrale’) in limb leads
- 70. P-Q or P-R Interval • The time between the beginning of the P wave and the beginning of the QRS complex is the interval between the beginning of electrical excitation of the atria and the beginning of excitation of the ventricles. This period is called the P-Q interval. • The normal P-R interval is 3-5 small squares/120- 220ms (Often this interval is called the P-R interval because the Q wave is likely to be absent.)
- 72. Second degree heart block(Wenckebach/mobitz type 1) showing progresssive lengthening of the PR interval, one non conducted P wave, next conducted beat has a shorter PR interval than the preceding conducted beat
- 74. QRS Complexes • The duration of the QRS complex shows how long excitation takes to spread through the ventricles. • The QRS complex duration is normally 120ms (3 small squares) or less, but any abnormality of conduction takes longer, and causes widened QRS complexes
- 75. QRS in LVH and RVH
- 76. • Sinus Rhythm, rate 63/min • RAD ( deep S wave in lead I) • Dominant R wave in lead V1 • Inverted T wave in lead II,III,VF and V1-V3 • Flat T wave in V4-V6 SEVERE RVH
- 77. LVH Sinus rhythm,rate 83/min Normal axis Tall R wave in V5-V6 and deep S waves in V1-V2 Inverted T waves in lead I, aVL and V5-V6
- 78. Left Ventricular Hypertrophy SOKOLOW & LYON Criteria S wave in V1 and R wave in V5 or V6 >35mm R wave of 11 to 13mm (1.1 to 1.3 mV) or more in lead aVL is another sign of LVH
- 80. THE ORIGIN OF Q WAVES • Small (septal) ‘Q’ waves in the left ventricular leads result from depolarization of the septum from left to right • Q wave greater than one small square in width and at least 2mm deep therefore indicate a myocardial infarction and the lead in which the Q wave appears give some indication of the part of the heart that has been damaged
- 82. J point • J point is the junction between the termination of QRS complex and beginning of ST segment • A positive deflection at the J point is termed a J wave (Osborn wave) and is characteristically seen with hypothermia
- 83. OSBORNE WAVE
- 84. ST Segment • ST segment lies between the QRS complex and the T wave • Should be isoelectric, indicates plateau portion of ventricular action potential • Normal duration= 0.32 sec • Elevation of the ST segment is an indication of acute myocardial injury, usually due either to a recent infarction • or to pericarditis • Horizontal depression of the ST segment, associated with an upright T wave, is usually a sign of ischemia as opposed to infarction
- 85. • To be considered significant elevation or depression , the ST segment must deviate 1mm below or above the baseline in at least 2 or more correlating leads
- 87. T Wave • Positive deflection (above baseline<5mm) • Should appear rounded and symmetrical • Should be atleast 1/8th but less than 2/3rd of the amplitude of R wave • Positive in all standard bipolar limb leads ( caused by repolarization of the apex and outer surfaces of the ventricles ahead of the interventricular surfaces) • Normally inverted in lead aVR and V1
- 88. • Elevated T wave:- positive deflection >5mm Tall, pointed(tented) wave in hyperkalemia or myocardial injury • T wave inversion is seen in the following circumstances: 1.Ischemia 2.Ventricular hypertrophy 3.Bundle branch block 4.Digoxin treatment.
- 91. ‘U’ Wave • Indicates:- late repolarization of the Purkinje fibers long action potential of midmyocardial M cells delayed repolarization in areas of the ventricle that undergo late mechanical relaxation. • < 0.1 mV in amplitude • normally has the same polarity as the preceding T wave • largest in the leads V1 and V2 • most often seen at slow heart rates
- 92. QT INTERVAL • Total duration of depolarization and repolarization • Contraction of the ventricle lasts from the beginning of the Q wave (or R wave, if the Q wave is absent) to the end of the T wave. This interval is called Q-T interval and is about 0.35 second. • The corrected interval (QTc) can be calculated using Bazett’s formula: QTc = QT ÷(square root of R–R interval) • AHA/ACC:- QTc= QT+1.75(HR - 60)
- 93. • A QTc interval longer than 450 ms is considred to be abnormal. • Whatever its cause, a corrected QT interval of 500 ms or longer can predispose to paroxysmal ventricular tachycardia of a particular type called ‘torsade de pointes’, which can cause either symptoms typical of paroxysmal tachycardia or sudden death
- 98. REFERENCES 1. Guyton & Hall: Textbook of Medical Physiology, 12e 2. Ganong’s Review of Medical Physiology , 25TH ed 3. Harrison’s principles of internal medicine, 19th ed 4. The ECG Made Easy, John R. Hampton, 8th ed 5. Braunwald’s Heart disease, 9th ed 6. Becker, Daniel E. “Fundamentals of Electrocardiography Interpretation.” Anesthesia Progress 53.2 (2006) 7. Miller’s Anesthesia 8th edition