80 or more of blood passively flows into ventricles inertia and low pressure

80 or more of blood passively flows into ventricles

This preview shows page 2 - 5 out of 42 pages.

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
Image of page 2
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
Image of page 3
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
Image of page 4
Image of page 5

You've reached the end of your free preview.

Want to read all 42 pages?

  • Fall '17
  • LINDA SALICE
  •  Volume of blood

  • Left Quote Icon

    Student Picture

  • Left Quote Icon

    Student Picture

  • Left Quote Icon

    Student Picture