Stroke Volume, Heart Rate, and Cardiac Output

Stroke Volume

• Stroke volume is defined as the amount of blood pumped out of the ventricle during each contraction.

• Formula for calculating stroke volume:
  $Stroke Volume = End Diastolic Volume - End Systolic Volume$

  • End Diastolic Volume: Amount of blood in the ventricle at the end of diastole (when it's full, before contraction).
  • End Systolic Volume: Amount of blood remaining in the ventricle after contraction.
  • The ventricle never completely empties, so there's always some blood left after contraction.

• Three factors determine stroke volume:

  • Preload
  • Contractility
  • Afterload

Preload

• Preload refers to the ability of the ventricular muscle to stretch during diastole.

• During diastole, the ventricle fills with blood from the atria, causing it to stretch.

• The more blood that enters the ventricle, the greater the stretch and the greater the preload.

• Increased preload leads to a greater amount of blood that can be pumped out, resulting in increased stroke volume and cardiac output.

Contractility

• Contractility is the force produced by the heart muscle during contraction.

• Cardiac muscle cells contract to pump blood out of the heart.

Afterload

• Afterload is the pressure the ventricle must overcome to eject blood.

• It represents the resistance to blood flow in the systemic circulation.

• Increased resistance (afterload) reduces the amount of blood pumped out, decreasing stroke volume.

Factors Affecting Preload, Contractility, and Afterload

• Venous Return:
  • Increased venous return increases preload and end diastolic volume.
  • Decreased venous return decreases preload and end diastolic volume.
• Sympathetic Stimulation:
  • Increases contractility via hormones like epinephrine (adrenaline) and norepinephrine (noradrenaline).
• Parasympathetic Stimulation:
  • Decreases activity; opposes sympathetic effects.
• Vasoconstriction and Vasodilation:
  • Affect afterload

Heart Rate

• Heart rate is the number of times the heart contracts per minute, measured in beats per minute (bpm).

• Controlled by:

  • Autonomic nervous system
  • Hormones (adrenaline, thyroxine)
  • Intracellular ions (calcium, potassium)
  • Other factors (age, gender, exercise, body temperature)

• Calcium influx is crucial for heart muscle contraction, similar to action potentials.

• Young children have faster heart rates than older adults.

• Heart rate increases during exercise due to increased demand for oxygen and nutrients in skeletal muscles.

Cardiac Output

• Cardiac output is the amount of blood pumped out of the ventricle per minute.
  $Cardiac Output = Heart Rate \times Stroke Volume$

• Changes in heart rate or stroke volume affect cardiac output.

  • Increased heart rate increases cardiac output.
  • Increased stroke volume increases cardiac output.
  • Decreased stroke volume decreases cardiac output.

Autonomic Nervous System Regulation of Cardiac Output

• The autonomic nervous system regulates cardiac output mainly through heart rate control.

• Two divisions:

  • Sympathetic: Speeds things up (fight or flight).
  • Parasympathetic (vagal): Slows things down.

• Sympathetic Nervous System:

  • Activated by emotions or physical stressors.
  • Increases heart rate via adrenaline.

• Parasympathetic Nervous System:

  • Slows down heart rate via acetylcholine.

• Vagal Tone:

  • Balance between sympathetic and parasympathetic activity during relaxation.
  • The parasympathetic system has a dominant inhibitory influence.

Heart Rate and Blood Pressure

Impact of Autonomic Activity on Cardiac Output

• Increased sympathetic activity increases venous return and end diastolic volume.

• This increases stroke volume, leading to increased cardiac output.

• Fight or flight response (increased sympathetic activity) increases contractility and heart rate, resulting in higher cardiac output.

• Decreased parasympathetic activity further increases heart rate and cardiac output.