The cardiac cycle consists of two phases: diastole and systole. During diastole, the heart relaxes and chambers fill with blood. During systole, the heart contracts and blood is ejected. The heart's conduction system coordinates this cycle, initiating each beat from the sinoatrial node and conducting the impulse through the atrioventricular node and Purkinje fibers. Regulation occurs through the Frank-Starling mechanism and autonomic nervous system, with sympathetic stimulation increasing heart rate and contractility and parasympathetic stimulation decreasing heart rate.

1. The Cardiac
Cycle

2. Cardiac Cycle
 The extrinsic nerve supply coming from the nervous system serves
to modify and control the intrinsic beating established by the heart
(1) a relaxation phase (diastole) during which the chambers of the heart
are filled with blood
(2) a contraction phase (systole) during which blood is ejected from the
heart

3. Heart Conduction System
 4 basic components
(1) sinoatrial node (SA node)
 small mass of specialised cardiac muscle situated in the
superior aspect of the right atrium, lying along the
anterolateral margin of this chamber between the orifice
of the superior vena cava and the auricle.
 characterised by the property of automatic self-
excitation and it initiates each beat of the heart.
 pacemaker of the heart.
(2) inter-nodal fibre bundles
 Interspersed among the atrial muscle fibres which
conduct the action potential to the atrioventricular (AV)
node with a greater velocity (approximately 1.0 meter
per second) than ordinary atrial muscle.

4. Heart Conduction System
(3) atrioventricular node (AV node)
 The AV node is located in the right atrium near the lower part of the
interatrial septurn. Here there is a short delay (approximately 0.1
second) in transmission of the impulse to the ventricles.
 This permits the atria to complete their contraction and empty their
blood into the ventricles before the ventricles contract.

5. Heart Conduction System
(4) atrioventricular bundle
 After the AV node, the action potential enters
specialised muscle fibres called Purkinje fibres which
are grouped into a mass termed the atrioventricular
(AV) bundle, or the bundle of His
 The Purkinje fibres are very large and conduct the
action potential at about six times the velocity of
ordinary cardiac muscle (i.e., 1.5 to 4.0 m/s).
 Thus the Purkinje fibres permit a very rapid and
simultaneous distribution of the impulse throughout
the muscular walls of both ventricles.

6. Heart Conduction System

7. Action Potentials in Cardiac Muscle
 Resting membrane potential of cardiac muscle is -85 to -
95 mV
 Action potential is 105 mV
 Membranes remained polarized for 0.2s (atria) and 0.3
(ventricles)
 At the start of the action potential, fast Na+ channels
open; at the same time the slower Ca++ -Na+ channels
that maintain the plateau after the spike
 On the other hand, the plateau is also due to the
decrease in the permeability of K+ ions

8. Action Potentials in Cardiac Muscle
How does Ca++ promote cardiac muscle contraction?
 As AP spreads into the cardiac mm. fiber along the T-tubules
 longitudinal sacroplasmic tubules release Ca++  promote
the sliding of the actin and myosin filaments along one
another to cause mm contraction
 T-tubules in cardiac mm contains larger amounts of Ca++ that
are released during AP than in skeletal mm
 T-tubules open directly into the extracellular fluid in cardiac
mm
 At the end of the plateau of AP, Ca++ stops flowing into the
mm fiber and pumped back into the sarcoplasmic reticulum
and T-tubules – end of contraction

12. Atrial Pressure Waves
 Atria function as Primer Pumps for the ventricles
 a wave – caused by atrial contraction
 c wave – occurs during ventricular contraction
 v wave – caused by in-filling of the atria from venous return

13. Diastole
 Beginning of diastole, isovolemic relaxation,
caused by ventricular relaxation, occurs  vent.
press. < atrial press.  A-V valves open
 Higher press. in atria pushes blood into
ventricles
 Period of rapid filling of the ventricles (during
first 3rd of diastole)
 Atrial contraction (last 3rd of diastole) contributes
25% of filling of the ventricle

14. Systole
 Vent. contraction occurs  A-V valves close
 No outflow of blood occurs during the first 0.2-0.3s of
ventricular contraction (period of isovolumic contraction)
 Left vent. press. > aortic press. (80mmHg) & right vent.
press. > pulm. aa. press.(8mmHg)  aortic and pulm.
valves open  ventricular outflow occurs (period of
ejection)
 Most ejection occurs in the 1st part of this period (period
of rapid ejection)
 Aortic press. slightly exceed the vent. press. (period of
slow ejection)
 Vent. press. < aortic and pulm. aa. press  aortic valves
and pulmonary valves close at this time

15. Ejection Fraction
 End of diastole, volume in each ventricle is 110-120mL – end-
diastolic volume
 Amount of blood ejected with each beat is called the stroke volume
(70mL)
 Remaining volume in the ventricle at the end of systole is 40-50mL –
end systolic volume
 Ejection Fraction – dividing stroke vol (SV) by the end-diastolic (60%)

17.  Phase I – Period of Filling
 LV volume increases from end-systolic volume (45ml)
to the end-diastolic volume (115ml)
 Phase II – Period of Isovolumic Contraction
 Intraventricular pressure increases to the level of the
aortic diastolic pressure (80mmHg)
 Phase III – Period of Ejection
 Increased systolic pressure due to additional
ventricular contraction, and ventricular volume
decreases by 70ml (stroke volume)
 Phase IV – Period of Isovolumic Relaxation
 Ventricular volume remains at 45ml but
intraventricular pressure decreases to its diastolic
pressure level

18. Regulation of Heart Pumping
1. Frank-Starling Mechanism
 When venous return of blood increases, the heart muscle
stretches more, and will pump with a greater force of contraction.
 Within physiological limits, the heart pumps all the blood that
comes to it without allowing excess accumulation of blood in the
veins.

19. Regulation of Heart Pumping
2. Autonomic Nervous System
 Sympathetic stimulation can increase CO 2-3x by:
1. Increasing the heart rate
2. Increasing the force of contraction of heart muscles
 Parasympathetic stimulation only affects the atria and can
decrease heart rate dramatically and the force of contraction of
the ventricles slightly

20. Regulation of Heart Pumping
 Other factors
1. Extracellular electrolyte concentrations
1. Extra Potassium in ECF causes the heart to
become flaccid and reduces heart rate
2. Excessive Calcium in ECF causes the heart to
go into spastic contraction