80 or more of blood passively flows into ventricles

80% or more of blood passively flows into ventricles (inertia and low pressure gradient)
o atrial systole occurs near end, delivering the remaining 20% (less at rest – 5%)
o end diastolic volume (EDV): volume of blood in each ventricle immediately before starting
ventricular systole
 Ventricular systole (and atrial diastole)
o Atria relax and ventricles begin to contract
o Rising ventricular pressure results in closing of AV valves
o Isovolumetric contraction phase (all valves are closed)
o In ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the SL
valves open
o End Systolic Volume (ESV): Volume of blood remaining in each ventricle

 Isovolumetric relaxation happens at the start of atrial and ventricular diastole
o Ventricles relax
o Backflow of blood in aorta and pulmonary trunk closes SL valves and causes dicrotic not
(brief rise in aortic pressure)
 LOOK AT DIAGRAM ****
Cardiac Output (CO)
 Volume of blood pumped by each ventricle in one minute
o L/blood/min
 CO= heart rate (HR) x stroke volume (SV)
o HR= number of beats per minute
o SV= volume of blood pumped out by a ventricle with each beat
 At rest
o CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)  5.25 L/min
 Most adults = 5-6 L per circuit
o Maximal CO is 4-5 times resting CO in nonathletic people
o Maximal CO may reach 35 L/min in trained athletes
Regulation of Stroke Volume
 SV= EDV-ESV
 Three main factors affect SV
o Preload : EDV venous return
o Contractility : muscular effort affected by chemical agents
o Afterload : arterial blood pressure (systemic)
 Preload: degree of stretch of cardiac muscle cells before they contract (Frank-Starling law of the
heart )
o Moderate stretch- increase contraction effort by the heart
o Cardiac muscle exhibits a length tension relationship
o At rest cardiac muscle cells are shorter than optimal length
o Increase venous return
o Increased venous return distends (stretches) the ventricles and increases contraction force
 Contractility : contractile strength at a given muscle length, independent of muscle stretch and EDV
 Positive inotropic agents increase contractility
o Increased Ca 2+ influx due to sympathetic stimulation via epinephrine/norepinephrine
o Secondary hormone actions (thyroxine)
 Negative inotropic agents decrease contractility (reduce Ca
++
levels)
o Acidosis
o Calcium channel blockers (propranolol)
 Reduce stroke volume
 LOOK AT DIAGRAM ****
Regulation of Stroke Volume
 Afterload : pressure that must be overcome for ventricles to eject blood
 Hypertension increases afterload, resulting in increased ESV and reduced SV
o This increases the chronic workload of the as happens with heart valve disease
o Best conditions promote abnormal ventricular hypertrophy

Regulation of heart rate (autonomic nervous system)
 Positive chronotropic factors increase heart rate
o Sympathetic division
o accelerator nerve
 non-epinephrine
 SA node
 Negative chronotropic factors decrease heart rate
o parasympathetic division
 vagus nerve
 acetylcholine
 adrenal gland
 epinephrine
 Ventricle pressure 0 mm Hg
