Electrical system of the heart Purkinje fibers Bundle of His Sinoatrial node Atrioventricular node 3 possible Pacemakers – Primary – Sinoatrial node, Secondary – Atrioventricular node Tertiary – Purkinje fibers
Pacemaker activity <ul><li>Spontaneous time-dependent depolarization leading to action potentials </li></ul><ul><li>Pacemaker with highest frequency sets the heart rate. </li></ul><ul><ul><li>SA node – 60 b/min – smallest electrical region in the heart, sum of 3 ion channels produces pacemaker (ca, k, f) </li></ul></ul><ul><ul><li>AV node – 40 b/min – can take over for SA node, pacemaker determined by same three channels as SA node. </li></ul></ul><ul><ul><li>Purkinje fibers – slow – 20 b/min – unreliable pacemaker, but great conducting system, pacemaker determined by ‘f’ channels only. </li></ul></ul>
I Na+ rapid depolarizing (non-nodal) I K+ repolarizing (all myocytes) I Ca+ depolarizing (nodal AP and myocyte contraction) I f “ funny channel” or HCN Pacemaker current (activated during hyperpolarization) H yperpolarization activated C yclic N ucleotide gated channel Na + /K + (activated during depolarization) MAJOR MYOCYTE ION CHANNELS Which channel is absent in SA and AV node? Absent in ventricular myocytes? Read- Table 20-1
intracellular extracellular (interstitial fluid) [Na+] 10 mM [K+] 120mM [Ca+] .0001 mM [Na+] 145 mM [K+] 4.5 mM [Ca+] 1.0 mM Intra and extracellular ion concentrations [A - ] protein 4 mM [A - ] protein 0 mM [Cl-] 116 mM [Cl-] 20 mM Resting membrane potential ~ -(60-80) mV
Ventricular action potential 5 Phases 0 – upstroke of AP I ca+ – slow I ca+/ I na+ - fast 1 – rapid repolarization I k+ – activation I ca+/ I na+ - inactivation 2 – plateau phase I ca+/ I na+ - activated 3 – repolarization I k+ 4 – diastolic potential I k+ I ca+ I f Produce pacemaker activity SA/AV node, purkinje use I f Phase 1 and 2 not present in SA/AV node
Comparison of slow nodal and fast non-nodal cardiac action potentials
Another comparison of slow nodal and fast non-nodal cardiac action potentials
Effective and relative refractory periods ERP RRP ERP due to inactivated Na and Ca channels, once they begin to recover the RRP begins.
Velocity of electrical conduction Purkinje fibers Bundle of His Sinoatrial node Atrioventricular node (0.05 m/s) (0.05 m/s) (1 m/s) (1 m/s) (4 m/s) Functionally, how might the speeds be important?
<ul><li>Decrease RATE </li></ul><ul><li>of depolarization </li></ul><ul><li>(more time to reach threshold) </li></ul>2. Decrease maximum diastolic potential . (more time to reach threshold) 3. Increase threshold potential . (more time to reach threshold) Decrease in I f activity Increase in I k activity Decrease in I ca activity Parasympathetic vagal release of acetylcholine Mechanisms for altering heart rate or rate of nodal depolarization Read about catecholamines p. 493
Pharmacological manipulation of ion channels and heart rate and conduction velocity activity. Potassium channel blockers – Increase AP duration and ERF (phase 3) Calcium channel blockers – L-type Ca, slows rate in SA and AV node Sodium channel blockers – Reduce phase 0 and slope of depolarization
Calcium channel blockers Decrease entry of calcium and delay the depolarization of SA and AV nodal cells. Used for: Angina Hypertension Arrhythmias Dihydropyridine class and Verapamil
Potassium channel blockers -Slow repolarization and therefore extends the Effective Refractory Period. -Extends the “Q-T interval” on the electrocardiogram (lecture Part II) -Helpful in preventing tachyarrhythmias from re-entry mechanisms (lecture Part II).
Sodium channel blockers -Slow the rate and magnitude of depolarization in non-nodal cells -Used to treat tachycardia -Extends the Effective Refractory Period
Beta blockers -Prevent calcium entry into the cell - Decrease HR, conduction velocity, strength of contraction. -Used to treat many CVS conditions: -Hypertension (inhibit renin) -Angina/myocardial infarction - Arrhythmias (slows rate of depol.)
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