Cardiac Electrical Physiology PDF

ELECTROCARDIOVASCULAR PHYSIOLOGY Dr. Samantha Solecki, DC, MS Instructor, Biology Thinker. Learner. Motivator. Lover of Anatomy & Physiology [email protected] © 2019 Pearson Education, Inc. 1 Learning Objectives *Acquired from the Human Anatomy and Physiolog...

ELECTROCARDIOVASCULAR PHYSIOLOGY Dr. Samantha Solecki, DC, MS Instructor, Biology Thinker. Learner. Motivator. Lover of Anatomy & Physiology [email protected] © 2019 Pearson Education, Inc. 1 Learning Objectives *Acquired from the Human Anatomy and Physiology Society (HAPS) with personal additions 2  Describe the major functions of the cardiovascular system.  List the phases of the cardiac muscle action potential and explain the ion movements that occur in each phase.  Contrast the way action potentials are generated in cardiac pacemaker cells, in cardiac contractile cells and in skeletal muscle cells.  Explain the significance of the plateau phase in the action potential of a cardiac contractile cell.  Compare and contrast cardiac muscle contraction and skeletal muscle contraction.  Compare and contrast the role of nerves in the depolarization of cardiac pacemaker cells, ventricular contractile cells and skeletal muscle cells.  With respect to the conduction system of the heart:  List the parts of the conduction system and explain how the system functions.  Define automaticity and explain why the SA node normally paces the heart.  Explain how the cardiac conduction system produces efficient pumping of blood.  Describe the role of the autonomic nervous system in the regulation of cardiac function.  With respect to the electrocardiogram (EKG or ECG):  Identify the waveforms in a normal ECG.  Relate the waveforms to atrial and ventricular depolarization and repolarization and to the activity of the conduction system. 3 4  5 Heart Physiology: Electrical Events  Heart depolarizes and contracts without nervous system stimulation  Rhythm can be altered by autonomic nervous system  6 Heart Physiology: Setting the Basic Rhythm  Coordinated heartbeat is a function of  Presence of gap junctions  Intrinsic cardiac conduction system  Network of noncontractile (autorhythmic) cells  Initiate and distribute impulses  coordinated depolarization and contraction of heart Pacemaker (Autorhythmic) 7 Cells – Intrinsic Innervation  Have unstable resting membrane potentials (pacemaker potentials or prepotentials) due to opening of slow Na+ channels  Continuously depolarize  At threshold, Ca2+ channels open  Explosive Ca2+ influx produces the rising phase of the action potential  Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channels  8 Action Potential Initiation by Pacemaker Cells  Three parts of action potential:  Pacemaker potential  Repolarization closes K+ channels and opens slow Na+ channels  ion imbalance   Depolarization  Ca2+ channels open  huge influx  rising phase of action potential  Repolarization  K+ channels open  efflux of K+ Figure 18.14 Pacemaker and action potentials of pacemaker cells in the heart. Slide 4 9 1 Pacemaker potential This slow depolarization is due to both opening of Na+ channels and closing of K+ channels. Notice that the membrane potential is Action Threshold Membrane potential (mV) +10 never a flat line. potential 0 2 Depolarization The action –10 potential begins when the 2 2 pacemaker potential reaches –20 threshold. Depolarization is due –30 3 3 to Ca2+ influx through Ca2+ –40 channels. –50 1 3 Repolarization is due to Ca2+ 1 –60 Pacemaker channels inactivating and potential K+ channels opening. This allows –70 K+ efflux, which brings the membrane potential back to its Time (ms) most negative voltage.  1 0 Sequence of Excitation  Cardiac pacemaker cells pass impulses, in order, across heart in ~220 ms  Sinoatrial node   Atrioventricular node   Atrioventricular bundle   Right and left bundle branches   Subendocardial conducting network (Purkinje fibers) 1 1  1 2 Heart Physiology: Sequence of Excitation  Sinoatrial (SA) node  Pacemaker of heart in right atrial wall  Depolarizes faster than rest of myocardium  Generates impulses about 75X/minute (sinus rhythm)  Inherent rate of 100X/minute tempered by extrinsic factors  Impulse spreads across atria, and to AV node  1 3 Heart Physiology: Sequence of Excitation  Atrioventricular (AV) node  In inferior interatrial septum  Delays impulses approximately 0.1 second  Because fibers are smaller diameter, have fewer gap junctions  Allows atrial contraction prior to ventricular contraction  Inherent rate of 50X/minute in absence of SA node input  1 4 Heart Physiology: Sequence of Excitation  Atrioventricular (AV) bundle (bundle of His)  In superior interventricular septum  Only electrical connection between atria and ventricles  Atria and ventricles not connected via gap junctions  Right and left bundle branches  Two pathways in interventricular septum  Carry impulses toward apex of heart  1 5 Heart Physiology: Sequence of Excitation  Subendocardial conducting network  Complete pathway through interventricular septum into apex and ventricular walls  More elaborate on left side of heart  AV bundle and subendocardial conducting network depolarize 30X/minute in absence of AV node input  Ventricular contraction immediately follows from apex toward atria Figure 18.15a Intrinsic cardiac conduction system and action potential succession during one heartbeat. Slide 1 Superior vena cava Right atrium 1 1 The sinoatrial (SA) node (pacemaker) 6 generates impulses. Internodal pathway 2 The impulses Left atrium pause (0.1 s) at the atrioventricular (AV) node. 3 The Subendocardial atrioventricular conducting (AV) bundle network connects the atria (Purkinje fibers) to the ventricles. 4 The bundle branches conduct the impulses Inter- through the ventricular interventricular septum. septum 5 The subendocardial conducting network depolarizes the contractile cells of both ventricles. Anatomy of the intrinsic conduction system showing the sequence of electrical excitation  1 7 Action Potentials of Contractile Cardiac Muscle Cells  Contractile muscle fibers make up bulk of heart and are responsible for pumping action  Different from skeletal muscle contraction; cardiac muscle action potentials have plateau  Steps involved in AP: 1.Depolarization opens fast voltage-gated Na+ channels; Na+ enters cell  Positive feedback influx of Na+ causes rising phase of AP (from 90 mV to +30 mV)  1 8 Action Potentials of Contractile Cardiac Muscle Cells 2. Depolarization by Na+ also opens slow Ca2+ channels  At 30 mV, Na+ channels close, but slow Ca2+ channels remain open, prolonging depolarization  Seen as a plateau 3. After about 200 ms, slow Ca2+ channels are closed, and voltage-gated K+ channels are open 2.Rapid efflux of K+ repolarizes cell to RMP 3. Ca2+ is pumped both back into SR and out of cell into extracellular space  1 9 Action Potentials of Contractile Cardiac Muscle Cells  Difference between contractile muscle fiber and skeletal muscle fiber contractions  AP in skeletal muscle lasts 1–2 ms; in cardiac muscle it lasts 200 ms  Contraction in skeletal muscle lasts 15–100 ms; in cardiac contraction lasts over 200 ms  Benefit of longer AP and contraction:  Sustained contraction ensures efficient ejection of blood  Longer refractory period prevents tetanic contractions Figure 18.13 The action potential of contractile cardiac muscle cells. Slide 4 2 0 Action potential 1 Depolarization is due to Na+ 20 influx through fast voltage-gated Na+ Membrane potential (mV) Plateau channels. A positive feedback cycle 0 2 Tension rapidly opens many Na+ channels, development reversing the membrane potential. Channel inactivation ends this phase. Tension (g) –20 (contraction) 1 3 2 Plateau phase is due to Ca2+ –40 influx through slow Ca2+ channels. This keeps the cell depolarized –60 because few K+ channels are open. Absolute refractory 3 Repolarization is due to Ca2+ –80 period channels inactivating and K+ channels opening. This allows K+ 0 150 300 efflux, which brings the membrane Time (ms) potential back to its resting voltage.  2 1 Cardiac Muscle Contraction  Three similarities with skeletal muscle:  Depolarization opens few voltage-gated fast Na+ channels in sarcolemma   Reversal of membrane potential from –90 mV to +30 mV  Brief; Na channels close rapidly  Depolarization wave down T tubules  SR to release Ca2+   Excitation-contraction coupling occurs  Ca2+ binds troponin  filaments slide  2 2 Cardiac Muscle Contraction  Differences from skeletal muscle:  ~1% of cells have automaticity (autorhythmicity)  Do not need nervous system stimulation  Can depolarize entire heart  All cardiomyocytes contract as unit, or none do  Long absolute refractory period (250 ms)  Prevents tetanic contractions  Depolarization wave also opens slow Ca2+ channels in sarcolemma  SR to release its Ca2+  Ca2+ surge prolongs the depolarization phase (plateau)  2 3 Cardiac Muscle Contraction  More differences  Action potential and contractile phase last much longer  Allow blood ejection from heart  Repolarization result of inactivation of Ca 2+ channels and opening of voltage-gated K+ channels  Ca2+ pumped back to SR and extracellularly Figure 18.15b Intrinsic cardiac conduction system and action potential succession during one heartbeat. Pacemaker potential 2 4 SA node Atrial muscle AV node Pacemaker Ventricular potential muscle Plateau 0 100 200 300 400 Milliseconds Comparison of action potential shape at various locations  2 5 Energy Requirements  Cardiac muscle  Has many mitochondria  Great dependence on aerobic respiration  Little anaerobic respiration ability  Readily switches fuel source for respiration  Even uses lactic acid from skeletal muscles  2 6 Homeostatic Imbalance  Ischemic cells  anaerobic respiration  lactic acid   High H+ concentration  high Ca2+ concentration   Mitochondrial damage  decreased ATP production   Gap junctions close  fatal arrhythmias  2 7 Homeostatic Imbalances  Defects in intrinsic conduction system may cause  Arrhythmias - irregular heart rhythms  Uncoordinated atrial and ventricular contractions  Fibrillation - rapid, irregular contractions; useless for pumping blood  circulation ceases  brain death  Defibrillation to treat  2 8 Review...  List the similarities of cardiac muscle to skeletal muscle.  Identify the differences between cardiac muscle and skeletal muscle.  What is meant by autorhythmic?  Name the pacemakers in the heart.  List the spread of depolarization in the heart.  2 9 Extrinsic Innervation of the Heart  Heartbeat modified by ANS via cardiac centers in medulla oblongata  Sympathetic   rate and force  Parasympathetic   rate  Cardioacceleratory center – sympathetic – affects SA, AV nodes, heart muscle, coronary arteries  Cardioinhibitory center – parasympathetic – inhibits SA and AV nodes via vagus nerves Figure 18.16 Autonomic innervation of the heart. The vagus nerve Dorsal motor nucleus (parasympathetic) of vagus decreases heart rate. Cardioinhibitory 3 center 0 Cardioaccele- Medulla oblongata ratory center Sympathetic trunk ganglion Thoracic spinal cord Sympathetic trunk Sympathetic cardiac nerves increase heart rate and force of contraction. AV node SA node Parasympathetic fibers Sympathetic fibers Interneurons THE ECG 31  3 2 Electrocardiography  Electrocardiograph can detect electrical currents generated by heart  Electrocardiogram (ECG or EKG) is a graphic recording of electrical activity  Composite of all action potentials at given time; not a tracing of a single AP  Electrodes are placed at various points on body to measure voltage differences  12 lead ECG is most typical  3 3 Electrocardiography  Main features:  P wave: depolarization of SA node and atria  QRS complex: ventricular depolarization and atrial repolarization  T wave: ventricular repolarization  P-R interval: beginning of atrial excitation to beginning of ventricular excitation  S-T segment: entire ventricular myocardium depolarized  Q-T interval: beginning of ventricular depolarization through ventricular repolarization  3 4 Electrocardiography  Electrocardiogram (ECG or EKG)  Composite of all action potentials generated by nodal and contractile cells at given time  Three waves:  P wave – depolarization SA node  atria  QRS complex - ventricular depolarization and atrial repolarization  T wave - ventricular repolarization Figure 18.17 An electrocardiogram (ECG) tracing. 3 5 Sinoatrial node Atrioventricular node QRS complex R Ventricular depolarization Atrial Ventricular depolarization repolarization P T Q P-R S-T Interval Segment S Q-T Interval 0 0.2 0.4 0.6 0.8 Time (s) Figure 18.18 The sequence of depolarization and repolarization of the heart related to the deflection Slide 2 waves of an ECG tracing. SA node R 3 Depolarization Repolarization 6 P T Q S 1 Atrial depolarization, initiated by the SA node, causes the P wave. Figure 18.18 The sequence of depolarization and repolarization of the heart related to the deflection Slide 3 waves of an ECG tracing. SA node R 3 Depolarization Repolarization 7 P T Q S 1 Atrial depolarization, initiated by the SA node, causes the P wave. AV node R P T Q S 2 With atrial depolarization complete, the impulse is delayed at the AV node. Figure 18.18 The sequence of depolarization and repolarization of the heart related to the deflection Slide 4 waves of an ECG tracing. SA node R 3 Depolarization Repolarization 8 P T Q S 1 Atrial depolarization, initiated by the SA node, causes the P wave. AV node R P T Q S 2 With atrial depolarization complete, the impulse is delayed at the AV node. R P T Q S 3 Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs. Figure 18.18 The sequence of depolarization and repolarization of the heart related to the deflection Slide 5 waves of an ECG tracing. 3 Depolarization R 9 Repolarization P T Q S 4 Ventricular depolarization is complete. Figure 18.18 The sequence of depolarization and repolarization of the heart related to the deflection Slide 6 waves of an ECG tracing. 4 Depolarization R 0 Repolarization P T Q S 4 Ventricular depolarization is complete. R P T Q S 5 Ventricular repolarization begins at apex, causing the T wave. Figure 18.18 The sequence of depolarization and repolarization of the heart related to the deflection Slide 7 waves of an ECG tracing. 4 Depolarization R 1 Repolarization P T Q S 4 Ventricular depolarization is complete. R P T Q S 5 Ventricular repolarization begins at apex, causing the T wave. R P T Q S 6 Ventricular repolarization is complete. Figure 18.18 The sequence of depolarization and repolarization of the heart related to the deflection Slide 8 waves of an ECG tracing. 4 SA node R R 2 P T P T Q S Q S 1 Atrial depolarization, initiated by 4 Ventricular depolarization is the SA node, causes the P wave. complete. R AV node R P T P T Q Q S S 2 With atrial depolarization 5 Ventricular repolarization complete, the impulse is delayed at begins at apex, causing the T wave. the AV node. R R P T P T Q Q S S 6 Ventricular repolarization is 3 Ventricular depolarization begins at complete. apex, causing the QRS complex. Atrial repolarization occurs. Depolarization Repolarization  4 3 Heart Sounds  Two sounds (lub-dup) associated with closing of heart valves  First as AV valves close; beginning of systole  Second as SL valves close; beginning of ventricular diastole  Pause indicates heart relaxation  Heart murmurs - abnormal heart sounds; usually indicate incompetent or stenotic valves  4 4 Homeostatic Imbalances  Tachycardia - abnormally fast heart rate (>100 beats/min)  If persistent, may lead to fibrillation  Bradycardia - heart rate slower than 60 beats/min  May result in grossly inadequate blood circulation in nonathletes  May be desirable result of endurance training  4 5 Review...  S1 is caused by?  The P wave on the ECG is due to?  Analyze the events that correlate with QRS complex on the ECG.