Formulas

• Cardiac Output:

  • Volume of blood pumped by each ventricle in 1 minute
  • CO = heart rate (HR) × stroke volume (SV)
  • HR = number of beats per minute
  • SV = volume of blood pumped out by one ventricle with each beat
  • Normal: 5.25 L/min
• • Cardiac output: amount of blood pumped out by each ventricle in 1 minute
  • Equals heart rate (HR) times stroke volume (SV)
• • Stroke volume: volume of blood pumped out by one ventricle with each beat
  • Correlates with force of contraction 
• • At rest: CO (ml/min) = HR (75 beats/min) × SV (70 ml/beat) = 5.25 L/min
• • Maximal CO is 4–5 times resting CO in non athletic people (20–25 L/min)
  • Maximal CO may reach 35 L/min in trained athletes
• • Cardiac reserve: difference between resting and maximal CO
  • CO changes (increases/decreases) if either or both SV or HR is changed
• • CO is affected by factors leading to:
  • Regulation of stroke volume
  • Regulation of heart rates
• Mathematically: SV = EDV − ESV
• • EDV is affected by length of ventricular diastole and venous pressure (~120 ml/beat)
  • ESV is affected by arterial BP and force of ventricular contraction (~50 ml/beat)

  Normal SV = 120 ml − 50 ml = 70 ml/beat
• • Three main factors that affect SV:
  • Preload
  • Contractility
  • Afterload
• • Preload: degree to which cardiac muscle cells are stretched just before they contract
  • Changes in preload cause changes in SV
  • Affects EDV
  • Relationship between preload and SV called Frank-Starling law of the heart
• • Cardiac muscle exhibits a length-tension relationship
  • At rest, cardiac muscle cells are shorter than optimal length; leads to dramatic increase in contractile force
• • Most important factor in preload stretching of cardiac muscle is venous return—amount of blood returning to heart
  • Slow heartbeat and exercise increase venous return 
  • Increased venous return distends (stretches) ventricles and increases contraction force
• • Contractile strength at given muscle length
  • Independent of muscle stretch and EDV
• • Increased contractility lowers ESV; caused by:
  • Sympathetic epinephrine release stimulates increased Ca2+ influx, leading to more cross bridge formations
  • Positive inotropic agents increase contractility

  Thyroxine, glucagon, epinephrine, digitalis, high extracellular Ca2+
• • Decreased by negative inotropic agents

  Acidosis (excess H+), increased extracellular K+, calcium channel blockers
• • Afterload is pressure that ventricles must overcome to eject blood
  • Back pressure from arterial blood pushing on SL valves is major pressure
  • Aortic pressure is around 80 mm Hg
  • Pulmonary trunk pressure is around 10 mm Hg
• Hypertension increases afterload, resulting in increased ESV and reduced SV
• If SV decreases as a result of decreased blood volume or weakened heart, CO can be maintained by increasing HR and contractility