Mechanical Properties of

Cardiac Muscle

Dr Shimaa Magdy
• The primary function of the heart is to pump blood through repeating
sequences of contraction and relaxation.

• Heart contraction is called (systole) and relaxation is called (diastole).

• Atrial systole occurs before ventricular systole.

• Contraction of cardiac myocyte is preceded by action potential.

➢ How action potential is converted to contraction of cardiac myocyte ?
1. Membrane depolarization leads to opening of Ca++ channels present in
sarcolemma. This leads to entry of small amount of Ca++ inside the
myocyte. This increases Ca++ concentration in local region just inside the
sarcolemma.
2. This Ca++ is sensed by calcium release channel in the sarcoendoplasmic
reticulum (“ryanodine receptor RyR”). This triggers the release of large
amount of Ca++ from the sarcoplasmic reticulum “Calcium-induced
Calcium release”.
3. Ca++ binds to Troponin-C and starts the steps of interaction between actin
and myosin leading to contraction as described for skeletal muscle.
4. As the action potential ends, Ca++ release decreases.
5. Relaxation starts when calcium concentration in the cytoplasm decreases.
This leads to inhibition of interaction between actin & myosin and subsequent
relaxation.
6. Calcium is removed from the cytoplasm by :
Sarco-endoplasmic reticulum actively reuptakes Ca++ by ATP-dependent
calcium pump known as sarco-endoplasmic reticulum calcium ATPase
(SERCA)
• Ca++ plays a main role in determining the force with which the cardiac
myocyte contracts (contractility or inotropic state).
• Under normal resting conditions Ca++ release inside the myocyte is not
maximal.
• If more Ca++ is available in the cytoplasm, cardiac myocyte contracts with
greater force i.e. has higher contractility (positive inotropic state).
• If less Ca++ is available lower contractility is observed (negative inotropic
state).
Regulation of Contractility (inotropic state) of cardiac
myocytes:
A- Positive inotropic mechanisms:
1- Stimulation of beta- adrenergic receptors
(catecholamines or sympathetic stimulation).
2- Increased extracellular Ca++ concentration →increase Ca++ entry in myocytes
3- Drugs:
a. Digitalis: this drug inhibits Na+-K+ ATPase in sarcolemma. This causes an
increase in Na+ concentration inside the myocyte. The Na+-Ca++ exchanger will
move 3Na+ out and brings 1Ca++ in →more Ca++ will be available inside the
myocytes.
b. Xanthines (caffeine).
B- Negative Inotropic Mechanisms:

1- Hypoxia of the myocytes.

This is usually due to insufficient blood supply
(ischemia) to cardiac muscle. Hypoxia inhibits ATP production which is the
source of energy for muscle contraction.
2- Activation of muscarinic receptors by acetylcholine released by
parasympathetic vagal nerve stimulation.
3- Drugs:
a. Calcium channel blockers inhibit Ca++ channels and decrease Ca++ inside
the myocyte.
b. Anesthetic drugs.
• Cardiac muscle cannot be tetanized.
WHY?

• As cardiac muscle has plateau phase

which prolongs the duration of action
potential and so prolongs the
duration of absolute refractory
period , so the heart can begin
contraction and start its relaxation
before responding to any other
stimulus whatever its strength.
 Cardiac Output
• is the volume of blood pumped by each ventricle per minute.
Average normal value for CO in adults is about 5 liters/minute.
• Cardiac output increases in the following conditions:
1- Physical exercise (up to 700%).
2- Anxiety and excitement (up to 100%).
3- After meals (30%).
4- High environmental temperature.
5- Pregnancy.
• Cardiac output decreases in the following conditions:
1- Standing from supine position (30%)
2- Rapid cardiac arrhythmias and many other heart diseases.
 Determinants of Cardiac output
• With each heart beat, each ventricle ejects a volume of blood (stroke volume
SV).
• This stroke volume, multiplied by the number of beats/minute (heart rate HR)
equals the CO:
• Cardiac output is determined therefore by:
a. Heart rate.
b. Stroke volume.

CO = SV X HR
 Stroke volume (SV):
• It is the volume pumped by each ventricle per beat (during each systole). It
is about 70 ml/beat.
• Stroke volume is the difference between end-diastolic volume (EDV( and end
systolic volume (ESV).
• Stroke volume = EDV-ESV
• Stroke volume = 135 ml - 65 ml= 70 ml
• Cardiac output (CO) = stroke volume x heart rate (number of beats per
minute)
• CO= 70 X 70 = 4900 ml/min
= about 5 L/min
• So if I want to increase cardiac output, I will increase heart rate or , and
increase stroke volume.
• And if I want to decrease cardiac output, I will decrease heart rate or , and
decrease stroke volume.
• Sympathetic stimulation to the heart increases heart rate( +ve chronotropy)
and increases force of contraction (+ve inotropy) so increase stroke volume →
increases cardiac output.
• Parasympathetic stimulation to the heart decreases heart rate only (-ve
chronotropy) as it supplies atria only → decreases cardiac output.
 What is the effect of increasing arterial blood pressure on
cardiac output?
• Arterial blood pressure: is the pressure in the large arteries. It is the
pressure that the heart pumps the blood against it.
• It ranges between 120/80.
• Co is decreased when the aortic pressure is markedly increased, as it
decreases the velocity of shortening during contraction and this decreases
the stroke volume.
• Thus Co is inversely proportional to arterial blood pressure.
 Ejection fraction (EF)
• Ejection fraction = Stroke volume / End diastolic volume
• End diastolic volume: is the volume of blood in the ventricles after filling of
blood just before ventricular contraction.
• Ejection fraction It is the fraction of the EDV that is ejected with each beat.
• Ejection fraction is normally greater than 55%.
• Ejection fraction is used clinically as an index of contractility.
• Increasing inotropy increases EF, whereas decreasing inotropy decreases EF.
Low ejection fraction indicates heart failure.
Venous circulation
• Venous return is the volume of blood that flows back to the heart per minute.
• Under normal steady conditions, venous return is equal to cardiac output
(5 L/min).
• Skeletal muscle contraction and competent valves helps venous return against
gravity because it allow blood flow in one direction toward the heart and
prevent its retrograde flow.
• Incompetent valves called varicose veins which
makes the flow of blood in the veins slow.
• ?? What is the danger of varicose veins???