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Cardio-Vascular System Dr Sethu Ngubane [email protected] Copyright © The McGra...

Cardio-Vascular System Dr Sethu Ngubane [email protected] Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. ELECTRICAL ACTIVITY OF THE HEART AND THE ELECTROCARDIOGRAM  Introduction Cardiac muscle cells are interconnected by gap junctions called intercalated discs. Once stimulation is applied, the impulse flows from cell to cell. The area of the heart that contracts from one stimulation event is called a myocardium or functional syncytium. The atria and ventricles are separated electrically by the fibrous skeleton. 3  Automatic rhythmicity of the sinus fibres The sino atrial node (SA node) exhibits the greatest degree of self excitation and inherent discharge rate For this reason the SA node is the pacemaker of the heart  Electrical Activity of the Heart Automaticity – automatic nature of the heartbeat Sinoatrial node (SA node) - “pacemaker”; located in right atrium AV node and Purkinje fibers are secondary pacemakers of ectopic pacemakers; slower rate than the “sinus rhythm” 6  Conducting tissues of the heart a. Action potentials spread via intercalated discs (gap junctions). b.SA node to AV node to stimulate atrial contraction c. AV node at base of right atrium and bundle of His (a collection of heart muscle cells specialized for electrical conduction) conduct stimulation to ventricles. d.In the interventricular septum, the bundle of His divides into right and left bundle branches. e. Branch bundles become Purkinje fibers, which stimulate ventricular contraction. 7  Self excitation of nodal fibres Na+ ions naturally tend to leak into sinus nodal fibres- multiple membrane channels Membrane potential rises to a threshold voltage of -40 millivolts the Ca+ Na+ channels open Ca+ and Na+ rapidly enter leading to the action potential. It is this inherent leakiness to Na+ that causes their self excitation Mechanism of SA node rhythmicity Pacemaker & Action Potentials 1 repolarization 3 Na 1 Na Ca Na connexons Na Ca 2 K K Ca K K Cardiac cell 10 SA Node Ca  Pacemaker potential cont: d. Pacemaker cells in the sinoatrial node depolarize spontaneously, but the rate at which they do so can be modulated: 1) Sympathetic activity: Epinephrine and norepinephrine * +chronotropic and ionotropic effects- + chronotropic effects- increases rate of SA node discharge= cardiac cell contraction + ionotropic- increase in force of cardiac contraction +Dromotropic- increased conduction velocity The above effects will be MAINLY via B receptors B1 formal normal cardiac function B2 during heart failure- because B1 receptors become down regulated during heart failure 2.) Parasympathetic neurons secrete acetylcholine, which opens K+ channels to slow the heart rate. Also, the muscarinic receptors are involved in causing negative chronotropic, dromotropic and inotropic effects 11  The potential of the SA fibre between discharges is -55 to -60 millivolts The potential of the ventricular fibre between discharges is -85 to -90 millivolts The reason for this difference is the that the sinus fibres are naturally leaky to sodium ions  Action Potentials in Cardiac Muscle Resting membrane potential of cardiac muscle is -85 to - 90 millivolts Ventricular membrane potential moves from -85 to +20 millivolts (overshoot potential) The plateau phase in cardiac muscle 3-15 times the duration of the plateau phase of skeletal muscle Action Potential in a Myocardial Cell Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. + 20 L type Ca2+ channels In (slow) 0 – 20 T type Millivolts channels Ca2+ – 40 K+ Out – 60 Na+ In – 80 – 100 0 50 100 150 200 250 300 350 400 14 Milliseconds  Reason for prolonged action potential  Skeletal muscle-Fast sodium channels in skeletal muscle open causing depolarization in 10 000ths of a sec after which they close and repolarization occurs  Cardiac muscle fast sodium channels as well as slow calcium Sodium channels (slow calcium-sodium channels T TYPE calcium channels) open  The L-TYPE calcium-sodium channels open slower but remain opened for longer. Both sodium and calcium flow in for a prolonged period causing the extended plateau phase  The calcium that enters the muscle is also instrumental in muscle contractility Opening of K channels Lead to repolarization  Reason for prolonged action potential Secondly onset of the AP decreases the muscle permeability to potassium by about 5 fold Decreased potassium permeability decreases the outflux of potassium ions during the AP and prevents early recovery The cessation of calcium and sodium influx into the muscle is followed by increased potassium membrane permeability which returns the muscle to its resting potential  Excitation-contraction Coupling a. Ca2+-stimulated Ca2+ release b. Action potentials conducted along the sarcolemma and T tubules, open voltage-gated Ca2+ channels c. Ca2+ diffuses into cells and stimulates the opening of calcium release channels of the SR d. Ca2+ (mostly from SR) binds to troponin to stimulate contraction e. These events occur at signaling complexes on the sarcolemma where it is close to the SR 17 Contraction of cardiac muscle AP cardiac muscle T-Tubules Sarcoplasmic reticulum Ca 2+ Ca 2+ Rayonodin Muscle sarcoplasm Rec type 2 RYR2 Ca 2+ diffuse into myofibrils and promotes sliding of actin myosin filaments along each other causing contraction CVS 2015 19  Repolarization a. Ca2+ concentration in cytoplasm reduced by active transport back into the SR and extrusion of Ca2+ through the plasma membrane by the Na+-Ca2+ exchanger b.Myocardium relaxes 20 Differences in the conduction of the AP in cardiac muscle vs skeletal muscle cont.. In cardiac muscle large amounts of Ca2+ diffuse into the sarcoplasm from the T-tubules- without this the cardiac muscle will not contract fully The sarcoplasmic reticulum of cardiac muscle-less developed than skeletal muscle but: T tubule diameter in cardiac muscle – 5 times that of skeletal muscle and 25 times greater volume  Electrocardiogram (ECG or EKG) The electrocardiograph records the electrical activity of the heart by picking up the movement of ions in body tissues in response to this activity. a.Does not record action potentials, but results from waves of depolarization b.Does not record contraction or relaxation, but the electrical events leading to contraction and relaxation 22 Electrocardiogram waves and intervals a. P wave - atrial depolarization b.P-Q interval – atrial systole c. QRS wave - ventricular depolarization d.S-T segment - plateau phase, ventricular systole e.T wave - ventricular repolarization 23 ECG trace 24 Examples of using an ECG to pickup on electrolyte abnormalities that impact cardiac function Hyperkalaemia is defined as a serum potassium level of > 5.2 mmol/L. ECG changes generally do not manifest until there is a moderate degree of hyperkalaemia (≥ 6.0 mmol/L). The earliest manifestation of hyperkalaemia is an increase in T wave amplitude. In hyperkalaemia, the T wave is “pulled upwards”, creating tall “tented” T waves, and stretching the remainder of the ECG to cause P wave flattening, PR prolongation, and QRS widening Hypokalaemia creates the illusion that the T wave is “pushed down”, with resultant T- wave flattening/inversion, ST depression, and prominent U waves 25  Electrocardiograph leads a. Bipolar limb leads record voltage between electrodes placed on wrists and legs. 1)Lead I: between right arm and right leg 2)Lead II: between right arm and left leg 3)Lead III: between left arm and left leg 26  Electrocardiograph leads cont: b.Unipolar leads record voltage between a single electrode on the body and one built into the machine (ground). 1) Limb leads go on the right arm (AVR), left arm (AVL), and left leg (AVF). 2) There are six chest leads. CVS 2015 27 Electrocardiograph Leads CVS 2015 28  Electrocardiograph Leads Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Right arm Left arm RA I LA II III LL 1 2 6 3 4 5 Left leg 29  ECG and Heart Sounds a.“Lub” occurs after the QRS wave as the AV valves close b.“Dub” occurs at the beginning of the T wave as the SL valves close 30 ECG, Pressures and Heart Sounds 31  Heart Arrhythmias Detected by ECG Abnormal heart rhythms a. Bradycardia: slow heart rate, below 60 bpm b. Tachycardia: fast heart rate, above 100 bpm c. These heart rhythms are normal if the person is active, but not normal at rest. d. Abnormal tachycardia can occur due to drugs or fast ectopic pacemakers. 32  Heart Arrhythmias cont: e.Ventricular tachycardia occurs when pacemakers in the ventricles make them contract out of synch with the atria. f. This condition is very dangerous and can lead to ventricular fibrillation and sudden death. 33  Flutter and Fibrillation a. Flutter: extremely fast (200−300 bpm) but coordinated contractions b.Fibrillation: uncoordinated pumping between the atria and ventricles 34  Arrhythmias Detected by ECG Tachycardia at rest 60-78 BPM----100 BPM Bradycardia at rest Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Sinus bradycardia Ventricular tachycardia (a) Sinus tachycardia (b) Ventricular fibrillation 35  Types of Fibrillation a. Atrial fibrillation: 1) Can result from atrial flutter 2) Atrial muscles cannot effectively contract. 3) AV node can’t keep pace with speed of atrial contractions, but some stimulation is passed on. 4) Only reduces cardiac output by 15% 5) Associated with increased risk of thrombi, stroke, and heart failure 36  Types of Fibrillation cont: b.Ventricular fibrillation 1) Ventricles can’t pump blood, and victim dies without CPR and/or electrical defibrillation to reset the heart rhythm. 2) Caused by circus rhythms – continuous cycling of electrical waves 3) Refractory period prevented 4) Sudden death progresses from ventricular tachycardia, through ventricular fibrillation, ending in astole (straight- line ECG) 37  AV Node Block a. Damage to the AV node can be seen in changes in the P-R interval of an ECG. b. First degree: Impulse conduction exceeds 0.2 secs. c. Second degree: Not every electrical wave can pass to ventricles d. Third degree/complete: No stimulation gets through. A pacemaker in the Purkinje fibers takes over, but this is slow (20−40 bpm). 38  AV Node Block Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. QRS QRS P P T T First-degree AV block R R R R R P P P P P P P P P P QS T QST QS T QS T QS T Second-degree AV block QRS T QRS T QRS T QRS T P P P P P P P P P P P 39 Third-degree AV block