Heart and Circulation

The aim of this page is to act like a "virtual handout". It is not a complete overview of the subject, but it should help you to direct your reading and discussions. Any of the standard texts in your reading list will help you to make sense of this subject. You might also like to check my ECG web page.

These pages are © David Taylor/The University of Liverpool, 2003.

Pacemaker activity

Cardiac Action Potentials

Interaction

Cardiac Output

Factors affecting stroke volume

Preload

Starling’s Law

Contractility-"Inotropic effect"

Afterload

Heart Rate

Control

Pressure

Volume

Chemicals

Local Blood Flow (kidney)

Hormones

Overview

• The blood is pumped from the left ventricle
• around the body to the right atrium
• and passes into the right ventricle
• From the right ventricle
• the blood is pumped around the lungs
  • lower pressure
• to the left atrium
• and then it passes to the left ventricle

Pacemaker activity

• The rhythm of the pump is provided by the pacemaker activity of some specialized muscle cells in the wall of the right atrium - the sinoatrial node

Cardiac Action Potentials

• The most obvious thing is that they last longer than those in ordinary muscle
• This is partly due to the plateau (arrow) due to an inward Ca²⁺ current

No Tetanus

• the action potentials last so long there is no possibility of tetanus

Control

• is both intrinsic and extrinsic

• The heart contracts more strongly when it is full of blood

• The force of contraction is proportional to the initial fibre length

• The sympathetic system
  • increase in the rate and force of contraction largely through increasing the permeability of cardiac muscle cells to Ca²⁺
• The parasympathetic system
  • decrease in the rate of contraction by slowing the pre-potential of the pacemaker cells.
• changes in heart rate are called chronotropic changes
• changes in the force of contraction are called inotropic changes

Interaction

• extrinsic and intrinsic systems interact

Cardiac Output

• Heart rate x stroke volume

Factors affecting stroke volume

Preload

• increased end-diastolic volume stretches the heart
• cardiac muscles stretch and contract more forcefully
  • Frank-Starling Law of the heart

Starling’s Law

Contractility-"Inotropic effect"

• increase available intracellular Ca²⁺
• increase number of actinomyosin binding sites
• increase force of contraction
• positive inotropic agents are
  • sympathetic stimulation
  • catecholamines
  • glucagon
  • thyroid hormones
  • increased extracellular Ca²⁺

Afterload

• decreased arterial blood pressure during diastole
• decreased afterload
• semilunar valves open sooner when blood pressure in pulmonary artery & aorta is lower
• afterload is due to
  • blood pressure
  • viscosity of blood
  • elasticity of arteries

Heart Rate

• Nervous system
  • increased sympathetic
  • decreased parasympathetic
• Chemicals
  • catecholamines
  • thyroid hormones
  • moderate Ca²⁺ increase
• Other factors
  • age
  • gender
  • "fitness"
  • body temperature

Control

Pressure

• Sensed by baroreceptors
  • in carotid arteries and aortic arch
• an increase in pressure causes a decrease in sympathetic activity
• a decrease in pressure causes an increase in sympathetic activity

Volume

• Sensed by atrial volume receptors

  an increase in volume

• causes a decrease in ADH secretion
• and an increase in ANF secretion

Chemicals

• increases sympathetic activity

Local Blood Flow (kidney)

Hormones

• Angiotensin II is a vasoconstrictor
• Aldosterone increases vascular sensitivity to Angiotensin II
• ADH (anti-diuretic hormone) increases water reabsorption
• ANF decreases sodium reabsorption

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