cardiac1w2009out - Cardiac physiology “Physiology of the...

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Unformatted text preview: Cardiac physiology “Physiology of the heart” – review the anatomy of the heart review • • • name 3 great vessels name the 4 chambers name the 4 valves Fig. 18-12a, Martini • heart contains 2 functionally important types of cells – non-contractile cells • ‘autorhythmic’ • __________ of cardiac tissue • generates and conducts electrical impulses within the heart heart – “____________________________” – contractile cells • • • _________ of cardiac tissue “myocardium” causes pumping of blood upon contraction • pacemaker activity of cardiac autorhythmic cells – due primarily to unstable membrane potential due to sodium ‘leak’ channels (_____) – What other ion conductances cause these membrane potential changes? Martini, Fig. 18-12b • ion movements and ion channels during ion cardiac autorhythmic cell action potentials cardiac Silverthorn, Fig. 14-15 b,c • Identification of currents and channels in Identification cardiac autorhythmic cells cardiac – ____ = allows Na+ ions to pass into cell, causing depolarization of cell to threshold causing • pacemaker potential; never at rest – ICa= voltage-gated Ca++ channels cause rapid depolarization depolarization no voltage gated Na channels in cardiac • can neural input alter the rate of autorhythmic can cells’ action potential generation? cells’ – YES – this controls the heart rate this controls • sympathetic and parasympathetic neural sympathetic control of heart rate control – acts on receptors on the _______________ cells acts _______________ • in SA node Sympathetic stimulation increases heart rate Silverthorn, Fig. 14-16a (see also Fig. 18-22, Martini) • Sympathetic stimulation of autorhythmic cells – norepinephrine (sympathetic neurons) norepinephrine (sympathetic – epinephrine (adrenal medulla) epinephrine (adrenal – binds to β 1 adrenergic receptors on autorhythmic binds cells cells • metabotropic β 1 adrenergic receptor activated metabotropic receptor causes rise in ________, alters ____ and I currents parasympathetic stimulation decreases heart rate Silverthorn, Fig. 14-16b (see also Fig. 18-22, Martini) • parasympathetic stimulation of autorhythmic cells – acetylcholine released by vagus nerve – binds to muscarinic acetylcholine receptors (mAchRs) on binds autorhythmic cells autorhythmic • metabotropic mAchR on autorhythmic cells activated metabotropic on – causes activation of ______________ signaling causes cascade cascade • causes increased opening of _______ channels and also causes decreases ________ channel permeability decreases – cell ___________________ and depolarizes more cell slowly slowly – increased time interval between action potentials • causes heart to contract more slowly • How do action potential impulses generated by cardiac How autorhythmic cells spread throughout the heart? autorhythmic – action potentials propagate along conducting system – this is needed for temporal regulation of contractile events this temporal in regions of heart in • timing of the impulse conduction through the heart: – allows the contraction of atria, filling of ventricles before allows ventricular contraction ventricular – depolarizing action potential spreads first through depolarizing conducting system, then through myocardia in each area conducting – atria contract completely before ventricles • contractile myocardial cells – __________ of heart tissue – Contracts in 3 dimensions-how? • Presence of intercalated disks connects all myocardial cells into a syncitial sheet Martini, Fig. 18-5a Structure of myocardial cells Martini, Fig. 18-5b • Specializations of _______________________ – gap junctions connect cells to each other electrically – Z-lines bind to opposing cell membranes – desmosomes (tight cell connections) • intercalated discs allow cells to branch and form intercalated sheets and contract together (coordinately) sheets • Structure within a contractile myocardial cell – next slide Specialized myocardial cell structure Fig. 8-20c, Martini • myocardial cell action potential – this causes the myocardial cells to contract – note differences from that of autorhythmic cells: • ion channels used • time course of action potential • tissue needs to be stimulated plateau Fig. 14-13, Silverthorn • myocardial action potentials • • • • • • • Fig. 14-13, Silverthorn __Na+__ channels open, rapid depolarization (0) __Na+__ (0) At peak, Na+ channels close, fast K+ channels open (1) (1) __Ca++ channels open, plateau of action __Ca++ potential; fast K+ channels close (2) potential; (2) Ca+ + channels close, slower K+ channels open (3) (3) repolarization complete, slower K+ channels close (4) (4) What do these action potentials cause? • Contraction: excitation-contraction coupling – See next figure Fig. 14-11, Silverthorn • myocardium excitation-contraction coupling • similar to skeletal muscle • Fig. 14-11, Silverthorn The process: 1) action potential causes opening of voltagegated Ca++ channels in T-tubules 2) Ca++ flows into cell, down electrochemical gradient gradient 3) entry of Ca++ triggers release of more Ca++ 3) from sarcoplasmic reticulum from supplies 90-95% of Ca for contraction supplies of 7) Ca++–ATPase pump removes Ca++ from 7) sarcoplasm into the sarcoplasmic reticulum sarcoplasm 8) some Ca++ eliminated from cell via a Ca++-Na+ co-transporter co-transporter uses the Na gradient to supply energy to • note short A. P. refractory period in skeletal muscle – this allows summation (addition of contraction upon contraction until tetnus is reahed) • note prolonged A.P. refractory period in myocardium – prevents Summation – muscle contraction complete before A.P. refractory period ends Martini, Fig. 18-15b • skeletal vs. cardiac muscle contraction – cardiac muscle absolute refractory period for action cardiac potential longer than cardiac cell contraction potential • prevents the myocardial tissue from Summating prevents Summating contractions contractions • this prevents fatigue, tetanic contractions – a heart that is in a tetanic contraction no longer heart serves as a pump! serves – • What links autorhythmic and contractile cells? – conducting system • review previous lecture • function of conducting system – controls depolarization across myocardium – disruption of pathway disrupts normal heart cycle • Heart cycle: – One complete contraction (systole) and relaxation and (Diastole) period • autorhythmic cells cause the contractile autorhythmic myocardium cells to depolarize and propagate action potentials action – electrical activity precedes mechanical contraction • How does the electrical signal from autorhythmic How cells propagate across the myocardium? cells – conducting fibers allow more rapid action potential conducting propagation than through myocardium itself propagation – know the order, timing of events in the pathway – Fig. 18-13, Martini Martini, Fig. 18-13 Martini, Fig. 18-13 • Why does the SA node “drive” the heart rate? Why (because its faster) (because – autorhythmic action potentials occur at a frequency autorhythmic of ~70/minute of – other ‘nodes’ have much slower rates • A-V node, at about 50 action potentials/minute A-V action • Purkinje fibers, about 35 action potentials/minute Purkinje action – Disruption of this conduction pathway can occur • “complete heart block” – atria contract at ~70 beats/minute – ventricles contract at ~35 beats/minute » means that the Purkinje fiber cells are ‘driving’ means the ventricular rate in these cases the • How can the spread of electrical activity across the How electrical myocardium be detected? myocardium • Electrocardiogram (EKG) – this is not a recording of the muscle contraction this is – mechanical activity can only be inferred from the EKG mechanical inferred • contraction of myocardium (systole) contraction • relaxation of myocardium (diastole) relaxation (diastole) – recorded through the use of monitoring electrodes recorded • ‘leads’ – use from 4 to 18 leads to monitor electrical activity of use the heart the Normal electrocardiogram (identify and infer cardiac cycle events listed) Figure 18-14b, Martini Cardiac events and the EKG Cardiac • • • • • P wave: depolarization of atria wave: depolarization QRS complex: depolarization of the ventricles QRS depolarization T wave: repolarization of ventricles wave: repolarization _P-R segment: atrial contraction _P-R atrial R wave to end of T wave: ventricular contraction Cardiac cycle Cardiac 1) atrial systole atrial Atrial contraction forces more blood into Atrial ventricles ventricles 20% more blood filling in ventricle due to atrial 20% contraction contraction 1) atrial systole ends; atrial diastole begins atrial About 100 time elapse 1) ventricular systole begins 1) AV valves closed shut-first “heart sound” o “lub” o caused by increase in ventricular pressure “isovolumetric contraction” pressure increased but no blood ejected atrial cells repolarize (atrial diastole) 1) ventricular ejection 1) “isotonic contraction” semilunar valves opened blood ejected into pulmonary and aortic trunks amount of blood ejected is the stroke volume amount stroke (_70-80_) (_70-80_) peripheral blood pressure rises to ~120 mm Hg pressure in ventricle begins to fall at end of pressure period period end systolic volume (ESV) amount of blood left in ventricle at end of amount systole systole 1) ventricular diastole (early) 1) ventricular begins ~375 msec into heart cycle relaxation phase of ventricular cycle pressure falls, causes semi-lunar valves to close Heart sound number 2 “dubb” small rise in pressure occurs due to recoil of aorta “dicrotic notch” ventricular diastole lasts through atrial systole 1) late ventricular diastole 1) late ventricles fill passively as relaxation proceeds blood flows through atria to get into ventricles end-diastolic volume (EDV) amount of blood left in ventricle at end of diastole _____________130 ml are relaxed _____________130 are peripheral blood pressure falls to ~80 mm Hg majority of 900 msec spent in this period Fig. 18-16, Martini • Left ventricular Left pressure and volume changes that occur during the cardiac cycle cycle • Silverthorn, Silverthorn, Fig. 14-25 Fig. • Wiggers diagram Wiggers diagram – Relates electrical events of heart cycle to the Relates mechanical, pressure, and sound changes that occur during a cardiac cycle occur – Fig. 18-17, Martini Mitral valve • Heart sounds – sound 1: mitral (A-V) valve closes sound mitral – sound 2: aortic semilunar valve closes sound aortic – sound 3: rushing of blood into ventricles sound rushing – sound 4: atrial contraction (blood rushing in sound to atria) to – Sounds only produced when valves close Sounds close • Valve opening is quiet • Sounds 1 and 2 – Fig. 18-18b, Martini Mitral valve Mitral valve • Heart valve defects – Mitral valve prolapse • • • leakage of blood during ventricular systole creates extra sounds: “ murmurs” creates murmurs” murmurs could also be due to extra atrial murmurs contractions contractions – any abnormal heart sound is a murmur • Cardiac arrhythmias – alteration in the periods of the heart cycle, as alteration recorded by an EKG recorded – _bradycardia • abnormally slow heart rate – _tachycardia • abnormally fast heart rate ...
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