The document discusses cardiac muscle and the cardiac cycle. It provides details on: - Cardiac muscle histology and action potential, including ion channels involved - The cardiac cycle and components such as atrial systole, ventricular ejection, and filling phases - How the cardiac cycle is coordinated by the conduction system and regulated by the autonomic nervous system - Key concepts like the Frank-Starling law of the heart and factors affecting cardiac performance

1. Heart Physiology Department of Physiology SKZMDC

4. Cardiac Muscle Cardiac Muscle Atrial muscle Ventricular muscle Specialized excitatory & conductive muscle fibers Cardiac Muscle as a Syncytium Intercalated disc “communicating” junctions (gap junctions) - totally free diffusion of ions Atrial syncytium Ventricular syncytium

5. Cardiac Muscle - Histology

8. Cardiac Muscle Action Potential Depolarization Fast Na + channels Plateau Slow Ca ++ channels Slow to open Slow to close After depol. cardiac muscle membrane permeability to K + decreases Ca ++ thus pumped in – excitation-contraction coupling Repolarization Slow K + channels Refractory Periods 0.25 - 0.3 sec (Absolute) Corresponds to plateau 0.05 sec (Relative)

9. AP Comparison

10. Cardiac Muscle Action Potential

11. Cardiac Muscle Action Potential

12. Problem A drug is found to partially inactivate fast sodium channels. Q: How would this drug alter the action potential in a ventricular myocyte? Q: How would the drug alter conduction velocity within the ventricle?

13. Cardiac Cycle Cardiac events occurring from beginning of one heartbeat to the beginning of the next beat Each cycle – INITIATED by SA node Spontaneous generation of AP in SA node AP travels through both atria Through A-V bundle into the ventricles AV node delay (more than 0.1 second) Hence atria contract ahead of ventricles Diastole and Systole Period of relaxation – Diastole Heart fills with blood Period of contraction – Systole Ejection of blood

14. Cardiac Cycle - Components ECG is the event marker 1. Atrial Systole Follows P wave (electric activation of atria) Contributes to ventricular filling Forms the ‘ a wave ’ in the venous pulse curve Ventricular filling by atrial systole – 4 th heart sound (not audible in normal adults) 2. Isovolumetric contraction of Ventricle Occurs after QRS wave (electric activation of ventricles) Ventricular P raised above atrial P: AV valves close ( 1 st heart sound ) Split in 1 st heart sound may occur (since mitral valve closes b/f tricuspid) Ventricular P rises – NO CHANGE IN VOLUME Aortic valve is closed

15. Cardiac Cycle - Components 3. Rapid Ventricular Ejection Ventricular P reaches its max. When it b/c greater than aortic P – aortic valve opens Rapid ejection of blood takes place Ventricular volume decreases rapidly Atrial filling begins Onset of “T wave” (ventricular repolarization) – marks end of vent. contraction & ejection 4. Reduced Ventricular Ejection Slower ejection of blood from ventricles Ventricle P decreases Aortic P decreases (runoff of blood from large arteries into smaller arteries) Atrial filling continues

16. Cardiac Cycle - Components 5. Isovolumetric Ventricular Relaxation Ventricle replorization is complete (end of “T wave”) Aortic valve closes (followed by pulmonic valve) 2 nd heart sound Splitting occurs during inspiration AV valves remain closed mostly during this phase Ventricle P drops rapidly Ventricle volume remains CONSTANT – all valves are closed Incisura When ventricle P b/c < atrial P – mitral valve opens 6. Rapid Ventricular Filling Post-mitral valve opening – rapid filling of ventricles occurs Aortic P continues to decrease – more run-off of blood 3 rd heart sound (due to rapid flow from atria to ventricles Normally heard in children Abnormal in adults 7. Reduced Ventricular Filling (Diastasis) Longest phase of cardiac cycle Ventricular filling slows down Diastasis time period depends on heart rate!

19. Cardiac Cycle End-diastolic volume (130 ml) End-systolic volume (50 ml) Stroke volume (70 to 90 ml - @ rest) Ejection fraction % of end-diastolic ventricular volume that is ejected with each stroke Is about 65% Valuable index of ventricular function Preload Afterload

20. Cardiac Chamber Pressures

21. Overall Length-tension relationship: Heart during diastole (preload ‘formation’) It is the study of effects of cardiac muscle stretch on tension produced in the muscle during diastole & systole Force-velocity relationship: Ventricular function with regards to afterload Side point: Heart after it starts systole , follows: Isometeric dynamics – IVC Isotonic dynamics – Ejection Isometeric dynamics – IVR

22. Length (L) –Tension (T) Curve Isolated Cardiac Muscle

23. Length (L) –Tension (T) Curve – Skeletal M Fiber

25. Pressure (‘T’) – Volume (‘L’) Curve – Whole Heart PV loops: Depict cardiac cycle Show effects of Preload, afterload & inotropic state on cardiac pumping ability (SV)

27. Regulation of Heart Pumping (1) INTRINSIC cardiac regulation of pumping in response to changes in volume of blood flowing into the heart ( Frank-Starling Law ) (2) Control of heart rate and strength of heart pumping by ANS

28. Frank-Starling Law “ Volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole” Underlying principle Length-tension relationship in cardiac muscle fibers SV & CO correlate directly with EDV EDV correlates with VR CO = VR (FS Law ensures this) Cardiac muscle normally operates only on the ascending limb of the systolic curve

29. Explanation of FS Law

30. Concept of Contractility Inherent cardiac M Ca++ based ability – INOTROPISM Modified by ANS, catecholamines Loading situations of the heart Preload Stretch-induced enhancement in contraction More overlapping of thick & thin filaments More Ca ++ sensitivity of troponin C More Ca ++ release from SR After load

31. Heart Control by ANS Sympathetic NE via action on Beta-1 receptors Positive CHRONOTROPIC Increased HR (increase Phase-4 depolarization) Positive IONOTROPIC Increased force of contraction (increased inward Ca++ current during plateau + increases the ability of SR Ca++ pump) Positive DROMOTROPIC Increased conduction velocity through AV node (increased inward Ca++ current) Decreased PR interval Positive BATHMOTROPIC Increased excitability of myocardium

32. Heart Control by ANS Parasympathetic SA node, atria & AV node have supply, ventricles don’t! Ach via muscarinic receptors Negative chronotropic Decreasing phase-4 depolarizations Negative dromotropic Negative ionotropic Vagal escape

33. Determinants of Performance of Heart as a Pump 4 factors: ‘ Loading’ conditions of the cardiac muscle (1) Preload , or the initial length to which the muscle is stretched prior to contraction (2) Afterload , or all the forces against which cardiac muscle must contract to generate pressure and shorten ‘ Extrinsic’ factors (3) Contractility , or inotropic state (4) Inotropic effect of increased heart rate (beats/min)

36. S-A Nodal Action Potential I ca L (long-lasting) I ca T (transient) Firing potential: -40 mv Hyperpolarization

37. Cardiac Impulse Initiated in SA node Spreads radially into atrial muscle mostly @ 0.3 m/sec Atrial conduction is done via bands of fibres Anterior Middle Posterior Arrives at AV node after 0.03 sec AV delay of 0.13 sec occurs 0.09 in bundle 0.04 in bundle of HIS Reason for delay? Benefit of delay? Total delay at this point is 0.16 sec

38. Cardiac Impulse After AV node Velocity is maximum Bundle of HIS – 1 m/sec Purkinje system – 4 m/sec From the top of septum – via purkinje system – all of ventricle – 0.06 – 0.1 sec Total duration: 0.22 sec Parts that are last depolarized Posterobasal portion of left ventricle Pulmonary conus Upper most part of septum

40. Normal ECG ECG is produced only when current flows through the heart and this occurs only when the heart is partially depolarized/polarized

41. Normal ECG P wave Atria depolarize before contraction 0.08 - 0.10 sec QRS complex Ventricles depolarize before contraction 0.06 – 0.10 sec T wave Ventricles repolarize Atrial T wave is obscured by QRS Duration normally not taken U wave Inconstant finding Slow repolarization of papillary muscles

42. Normal ECG PR interval – 0.16 sec Time b/w beginning of P wave and beginning of QRS complex Interval between the beginning of electrical excitation of the atria and the beginning of excitation of the ventricles Prolonged: Vagal stimulation, AV block Shortened: Accelerated AV conduction, sympathetic stimulation ST interval (QT minus QRS) – 0.32 sec Ventricular repolarization Q-T interval – 0.2-0.40 sec Ventricular depolarization and ventricular repolarization Corresponds to AP duration Prolonged: ventricular extrasystole

43. Dipole The electric dipole consists of two equal and opposite charges, +q and –q , separated by a distance d Dipole vector : Vector whose magnitude is equal to the dipole moment [voltage] and that points from –ve charge to + one Direction of dipole is from –ve towards +ve

44. A wave of depolarization heading toward the +ve electrode is recorded as a +ve voltage Represents Atrial & Vent. Depol . A wave of repolarization moving away from a +ve electrode produces a +ve voltage difference T-wave (Vent. Repol.) A wave of repolarization moving toward a +ve electrode produces a –ve voltage deflection Atrial Repol.

45. Mean Electrical Vector/s Individual waves of depol. – electrical vectors Summation of electrical vectors at any instance – mean electrical vector (MEV) Direction of MEV determines its polarity & magnitude*

46. Mean Electrical Axis 1-4 are individual MEVs during ventricle depol. Give rise to QRS 1-4 summed up in time: Mean Electrical Axis It is the average ventricle depolarization vector over time Deviation is clinically imp*

47. Rules of ECG Interpretation 1. A wave of depolarization traveling toward a +ve electrode results in a +ve deflection in ECG [Corollary: A wave of depolarization traveling away from a positive electrode results in a negative deflection.] 2. A wave of repolarization traveling toward a +ve electrode results in a -ve deflection [Corollary: A wave of repolarization traveling away from a positive electrode results in a positive deflection.]

48. Rules of ECG Interpretation 3. A wave of depolarization or repolarization oriented perpendicular to an electrode axis has no net deflection. 4. The instantaneous amplitude of the measured potentials depends upon the orientation of the +ve electrode relative to the mean electrical vector

49. Rules of ECG Interpretation 5. Voltage amplitude (+ve or -ve) is directly related to the mass of tissue undergoing depolarization or repolarization

50. ECG Written Competition 2011 “ Vectors in ECG” Based on supplimental material.doc uploaded on: Physiologylectures @ hotmail.com (facebook or slideshare.com) Reward : Top written essay: ECG Cup + Box of (delicious) chocolates 1 st runner up: Certificate + Single chocolate bar 2 nd runner up: Certificate + Candy bag Assignments are to be turned in by 30 th April No late submissions will be entertained Assignments HAVE to be Original The department may ask a student to defend his/her essay in verbal Simple copy/paste submissions are discouraged

51. ECG Leads Recorded by placing an array of electrodes at specific locations on the body surface Electrodes are placed on: Each arm & leg 6 electrodes placed on chest Three basic types of ECG leads are recorded by these electrodes: Standard limb leads (Bipolar) Augmented limb leads (Unipolar) Chest leads (Unipolar)

52. ECG Standard Limb Leads: Einthoven’s Triangle Einthoven’s triangle Wave of depolar. - toward left arm - +ve deflection (lead I*) Wave of depolar. - away from left arm - deflection is –ve Wave of depolar. - toward left leg - +ve deflection (leads II and III)

53. Standard Limb Leads: Normal ECGs

54. ECG Standard Limb Leads: Axial Reference System Wave of depolar. oriented @ 60º produces greatest +ve deflection in lead II Wave of depolar. Oriented @ 90º produces equally +ve deflections in both leads II & III

55. ECG Augmented Limb Leads aV L (+ve on left arm; -ve rest*) aV R (+ve on right arm; -ve rest*) aV F (+ve on left leg; -ve rest*) Standard + Augmented = 6 limb leads of ECG

56. ECG Chest Leads V1 – V6 V1 overlies right ventricular free wall, V6 overlies left ventricular lateral wall

57. Cardiac Arrhythmias & ECG Five things to be read: Rate Rhythm Axis Hypertrophy Infarction Cardiac arrhythmias reflect disturbances in: Impulse initiation (S-A nodal cause/ectopic focus) Impulse propagation (conduction blocks/re-entry rhythm) Normal sinus rhythm (NSR) Normal heart Each heart beat originates in S-A node

58. Cardiac Arrhythmias & ECG Abnormal sinus rhythms Sinus Tachycardia Rate change is gradual Fast HR – more than 100 beats/min Causes: increased body temperature, sympathetic stimulation of heart or toxic conditions of heart Sinus Bradycardia Rate change is gradual Slow HR – less than 60 beats/min Bradycardia in athletes Sick sinus syndrome Excessively sensitive baroreceptors Mild external pressure on neck – strong vagal stimulation – heart may stop!

60. Cardiac Arrhythmias & ECG Heart Blocks Sinoatrial block Blockage of impulse before entry into atrial muscle Disappearance of P waves AV block Conditions decreasing rate of impulse conduction/complete block: Ischemia Compression Inflammation Extreme vagal stimulation

61. AV BLOCKS First Degree Block Delay in conduction from atria PR interval increases to > 0.2 sec Second Degree Block PR interval increases to 0.25 – 0.45 sec – some APs pass through, some don’t! “ Dropped beats ” – P wave present, no QRS 2:1, 3:2, 3:1 rhythms Mobitz-I : Repeated sequence of beats in which PR interval lengthens progressively until a ventricular beat is dropped (also called Wenckebach Phenomenon ) Mobitz-II : Prolongation of PR interval is constant , but there are some P waves which are not followed by QRS

62. AV BLOCKS Third Degree Block - Complete AV block Serious conduction abnormality at AV node No conduction of impulses Ventricles establish their own rhythm P waves dissociate from QRS complexes

63. AV BLOCKS - ECG

64. Stokes-Adam Syndrome Ventricular escape AV block “comes and goes” Occurs in borderline ischemia of conductive system Block duration: secs to weeks (or longer) Ventricles ‘escape’ after a delay of 5-30 secs (overdrive suppression) Clinically Patients faint due to lack of blood supply to brain Recovers due to ventricular escape Repeated fainting spells (Stokes-Adams Syndrome)

65. Wolff-Parkinson-White Syndrome Accessory pathway b/w atria & ventricles Ordinarily, no functional abnormality AV node + Bundle of Kent Bundle of Kent conducts faster than AV node Excites one ventricle early – circus movement Paroxysmal atrial tachycardia ECG Short P-R interval Prolonged QRS (slurred upstroke)

66. ECTOPIC PACEMAKERS Ectopic foci may become pacemakers when: Their own rhythmicity becomes enhanced Rhythmicity of the higher-order pacemakers becomes depressed All conduction pathways b/w ectopic focus & those regions with greater rhythmicity become blocked May be safety net – when higher pacemaker fail May cause problems – when fires in presence of normal pacemaker Sporadic rhythm disturbances, such as premature depolarizations/beats – atrial/nodal/ventricular beats Continuous rhythm disturbances cause atrial/nodal/ventricular paroxysmal tachycardias

67. Premature Contractions Contraction of the heart b/f normal contraction would have been expected Also called extrasystole/premature beat/ectopic beat Types: Premature Atrial Contractions A-V Nodal or A-V Bundle Premature Contractions Premature Ventricular Contractions

68. Premature Contractions Causes: Local areas of ischemia Small calcified plaques pressing against adjacent cardiac muscle - irritation Toxic irritation of (caused by drugs, nicotine, or caffeine): A-V node Purkinje system Myocardium

69. Atrial PC P wave of this beat occurred too soon P-R interval is shortened Indicating ectopic origin of the beat to be in atria near A-V node Compensatory pause Interval between premature contraction & next succeeding contraction is slightly prolonged* Pulse Deficit

70. A-V Nodal/Bundle PC P wave is missing Instead, the P wave is superimposed onto the QRS-T complex*

71. Ventricular PC QRS complex is usually considerably prolonged QRS complex has a high voltage T wave inverts

72. RE-ENTRY PHENOMENON Three conditions necessary for re-entry: The impulse loop becomes longer Dilated hearts Conduction velocity is decreased Blockage of Purkinje fibres Ischemia of muscles High blood K + Relative refractory period of the reentered region must be shorter than the propagation time around the loop

73. Ventricular Fibrillation Most serious arrhythmia If not stopped within 1-3 mins – fatal Phenomenon of Re-entry “Circus Movements” Causes Sudden electric shock of the heart (moderate voltage) Ischemia of Part of myocardium Part of conductive system Both ECG Bizarre Coarse irregular waves Treatment Strong high voltage AC

74. Atrial Fibrillation Similar to V-Fib Due to enlargement of atria secondary to valvular disease ECG: No P waves QRS, T waves present Irregular ventricular rhythm Due to irregular atrial impulses

75. Atrial Flutter

76. Myocardial Infarction & ECG Ischemia changes myocardial properties Become irreversible – death of myocardial fibers – infarction! ECG can detect these changes Three main changes in infarcted area: Rapid repolarization – C.o.I. out of infarct - ST segment elevation Decreased RMP - C.o.I. into infarct - ST segment elevation Delayed depolarization – C.o.I. out of infarct - ST segment elevation

77. ECG Changes in MI - Timeline Very early pattern (hrs after infarction) ST segment elevation – in leads facing infarct ST segment depression – in reciprocal leads Late pattern (many hrs – few days) Deep & wide Q waves appear Normal Q wave: <1/3 of R wave (height), 0.02 sec (wide) Deep/wide Q wave: > 1/3 of R wave, > 0.03 sec Q waves: “ Window effect ”

78. ECG Changes in MI - Timeline Late established pattern (many days – weeks) Q waves, QS complexes persist ST segment – isoelectric T waves – invert – segments that had ST elevation T waves – tall – segments that had ST depression This pattern may persist for the patient’s life Very late pattern (months to years) Abnormal Q waves, QS complexes persist T wave normalizes

79. ECF K + and ECG Hypokalemia +/- 3.5 mEq/L ST depression Prominent U wave +/- 2.5 mEq/L PR interval prolonged ST depression T wave inverts Prominent U wave Hyperkalemia +/- 7.0 mEq/L Tall slender, peaked T waves present +/- 8.5 mEq/L No evidence of atrial activity QRS – broad and slurred QRS interval – wide T waves remain tall, slender Further increase in K+ - ventricular tachycardia or fibrillation

81. Revision