This document discusses the anatomy and physiology of the heart. It describes the layers of the pericardium, the phases of the cardiac action potential including depolarization and repolarization, the differences in action potentials between pacemaker and muscle cells, and the refractory period of cardiac cells. Specifically, it outlines the roles of sodium, calcium, and potassium ion channels in generating and regulating the cardiac action potential.

1. Anatomy and Physiology of Heart
Lilly, LS. 2016. Patophysiology of
Heart Disease. 6th Ed. Wolter Kluwer

2. • REFERENSI :
• Lilly, LS. 2016. Patophysiology of Heart
Disease. 6th Ed. Wolter Kluwer

3. PERI
CARDIUM

4. Pericardium
• Consists of two layers: a strong outer fibrous
layer and an inner serosal layer.
• The inner serosal layer adheres to the external
wall of the heart and is called the visceral
pericardium.
• The visceral pericardium reflects back on
itself and lines the outer fibrous layer, forming
the parietal pericardium.

6. ACTION
POTENTIAL

7. Transmembrane Cardiac Ionic Current
Lilly, LS. 2016. Patophysiology of Heart Disease. 6th Ed. Wolter Kluwer

8. Myocyte action potential (AP)
• Phase 0 :
– Depolarisasi, influks dari ion Na
– Potential : until – 70 mV  into positive voltage range
• Phase 1 :
– Partial repolarization, transient outward ion K (ITo)
– Potential : returns to 0 mV
• Phase 2 :
– Slow influx Ca, eflux ion K. The plateu phase. (Iks)
• Phase 3 :
– Final phase repolarization : Largely eflux of ion K.(Ikr)
• Phase 4 :
– Resting potential : - 90mV, maintained by rectifier K channels
Lilly, LS. 2016. Patophysiology of Heart Disease. 6th Ed. Wolter Kluwer

9. Lilly, LS. 2016. Patophysiology of Heart Disease. 6th Ed. Wolter Kluwer

10. Phase 0
• Na and Ca channels are closed.
• Entry of ion Na into the cell 
transmembrane potential less negative 
threshold potential – 70 mV.
• Entry of ion Na through inward rectifier
channels.
• Prominent influx Na ( I-Na rectifier)  rapid
upstroke  rapid early depolarization.
Lilly, LS. 2016. Patophysiology of Heart Disease. 6th Ed. Wolter Kluwer

11. Phase 1
• Returns the membrane into approx 0 mV
• Responsible current : I to : the outward flow of
K ions.
• Through : transiently activated potassium
channels.
Lilly, LS. 2016. Patophysiology of Heart Disease. 6th Ed. Wolter Kluwer

12. Phase 2
• Long plateu phase : mediated outward K+ and
competition with inward Ca++  zero net
current
• Inward Ca++ through L-type specific channels
• Inward Ca++ start when potential membrane -
40 mV.
• Ca channel inactivaed  eflux K+ exceed 
phase 3 begins
Lilly, LS. 2016. Patophysiology of Heart Disease. 6th Ed. Wolter Kluwer

13. Phase 3
• Final phase of repolarization
• Returns transmembrane voltage to – 90 mV
• Outward K+ >> other cations
• To preserve transmembrane ionic
concentration gradient :
– Ca++ removed by sarcolemal NaCa exchanger
– Corrective Na K mediated by Na K ATPase
Lilly, LS. 2016. Patophysiology of Heart Disease. 6th Ed. Wolter Kluwer

14. Phase 4
• Represents the resting membrane potential in
cardiac myocytes.
• Phase a set of potassium membrane channels
are open, while other ionic channels are
essentially impermeable to flow.
• Resting cardiac transmembrane potential is
primarily determined by the equilibrium
potential of potassium, at approximately −91
mV

15. Pacemaker cell
• Certain heart cell initiated depolarization through
pacemaker cell and some with provokation
neighboring cells.
• AP of pacemaker is different of muscle cell of
ventricle.
• Maximum negative voltage pacemaker : - 60 mV
 phase 4 not flat : spontaneous gradual
depolarization ec different type Na channel
• Action potential relying on Ca inlfux.
• Repolarization by K+ eflux.
Lilly, LS. 2016. Patophysiology of Heart Disease. 6th Ed. Wolter Kluwer

16. Action Potential Pacemaker Cell
• Phase 4
• Phase 0
• Repolarization
Lilly, LS. 2016. Patophysiology of Heart Disease. 6th Ed. Wolter Kluwer

17. Action Potential of Pacemaker Cell
• Phase 4 :
– Is characterized by gradual, spontaneous
depolarization owing to the pacemaker current (I-f)
 start threshold – 60 mV to – 40 mV.
• Phase 0 :
– Start from – 40 mV. Less rapid than nonpacemaker cell
 influx Ca through slow calcium channel.
• Repolarization :
– Inactivation of calcium channels  K efflux through
potassium channel (I-Ks dan I-Kr)
Lilly, LS. 2016. Patophysiology of Heart Disease. 6th Ed. Wolter Kluwer

18. Refractory Period
• Cardiac muscle : prolong action potential and
prolong refractory period (allow ventricle to
relax and refill)
• Refractory period atrial is shorter than that of
ventricular muscle cell.
• Degree of refractoriness : percentage of Na
channels from inactive  reopening 
response to next depolarization.
Lilly, LS. 2016. Patophysiology of Heart Disease. 6th Ed. Wolter Kluwer

19. Refractory Period
• Absolute refractory period  cell completely
unexcitable to new stimulation
• Effective refractoriness : absolute refractory
period + short interval of phase 3.
• Relative refractoriness : stimulation  low
action potential  some Na inactivated
• Short supranormal period  low stimuli 
conduct action potential