Lec2: Contractility

Contractility: ability of the cardiac muscle to contract. It's the strength of

contraction at any given end-diastolic volume
Inotropism: effect of various factors on contractility (Neural, Drugs, …).
• Positive (+ve) inotropic effect: increase in myocardial contractility
(sympathetic stimulation).
• Negative (-ve) inotropic effect: decrease in myocardial contractility.
Excitation – Contraction Coupling:
It's the process by which depolarization of cardiac muscle produces mechanical
contraction. It occurs in 3 stages:
The First Stage: (Produces the contraction of cardiac nuscle)
1. Depolarization of myocardial cell stimulates opening of Ca2+ channels in the
T -tubule membrane and sarcolema (dCa+2).
2. dCa+2 acts as a signal for the opening of Ca2+ channels in SR to release large
amount of activator Ca+2 from its cisternae.
3. Ca2+ binds to troponin C of actin allowing the myosin to interact with actin
and causes contraction
The Second Stage: (Produces the relaxation: Ca2+ decreases to its resting level,
so the actin-myosin interactions stops & produces relaxation) this occurs
through:
1- Ca+2 is pumped back into the SR by an ATP-dependent Ca+2 pump
2- Ca+2 is transported out of the cell by Na+ - Ca+2 exchanger
3- Ca2+ binds to intracellular buffering protein (Calmodulin)
The Third Stage: Ca+2 release process is recovered before the next contraction
Factors Affecting the Performance of the cardiac muscle
1- The preload (the resting muscle length)
2- The afterload (the load after start of contraction)
3- The state of contraction (inotropic state)
4- The frequency of contraction
Preload (venous return)
• Preload: It is the amount of blood coming into the heart from superior and
inferior vena cava; i.e., venous return (VR) to LV through LA.
• The extent of filling is referred to as the preload because it is the work load imposed on
the heart before contraction begins. Therefore, the heart is stretched when more blood is
pouring in it.
• It is the load that determines the initial length of the resting ventricular muscle
fiber before contraction.
• The main determinant of cardiac muscle fiber length is the degree of diastolic filling.
• A stronger contraction squeezes out more blood, thus as more blood is returned to the
heart and the end diastolic volume increases, the heart automatically pumps out a
correspondingly larger stroke volume.
Afterload
• Afterload is the resistance that the ventricles have to overcome to pump out the blood
through the aorta (Tension at which, the load is lifted) (End-Systolic Pressure)
• It is the load that the ventricular muscle faces when it begins to contract = Aortic Pressure
= aortic impedance.
• Afterload is determined by:
1. Aortic pressure (systolic pressure).
2. Arterial wall rigidity (arteriosclerosis).
3. Blood viscosity (polycythemia).
Frank-Starling Law:
- This law states that “within physiological limits, a ↑ in the resting (diastolic) fiber length
→ ↑ in the force of myocardial contraction”.
- In other words, when the diastolic volume [diastolic fiber length] of the heart is
increased, the heart responds with a more forceful contraction.
- i.e. the returned blood to heart will distend the ventricles so the ventricles will produce
more powerful contraction to pump the returned blood.
- The Frank-Starling Law of the Heart describes the:
• intrinsic relationship between end-diastolic volume and stoke volume.
• effect of increased work load on cardiac output.
Notes:
- Preload can be represented by EDV (End Diastolic Volume) & Afterload can be
represented by ESV (End Systolic Volume)
- The EDV depends on venous return
- Increased Preload leads to increased systolic volume (SV) because:
SV = EDV – ESV
Heart rate & myocardial contractility
The heart rate refers to the ventricular rate of beating per minute. Normally, it averages 72
beats/minute (range 60-100 beats/minute).
• An increase in the frequency of stimulation causes a proportional increase in the force of
contraction. increased Heart rate = increase in the number of depolarization (Ca+2 influx …
contraction).
• tachycardia exerts a +ve inotropic effect.
• bradycardia exerts a -ve inotropic action.
Neural factors & Cardiac Contractility
1- Parasympathetic control: 2- Sympathetic control:
The vagal stimulation causes: Stimulation of the sympathetic nerves to
the heart causes:
• ↓ HR [Negative chronotropic effect]. • ↑ HR [positive chronotropic effect].
• ↓ in the force of atrial contraction • ↑ force of myocardial contraction
[negative inotropic effect]. [positive inotropic effect].
• ↓ in the AVN conduction velocity. • ↑ in AVN conduction velocity.

Exert a negative inotropic effect Exert a positive inotropic effect by

increasing; Cyclic-AMP in the cardiac
muscle fibers which activate Ca+2 channels
inducing more Ca+2 influx from the ECF
Effect of temperature on cardiac contractility:
• A moderate rise of the body temperature strengthens cardiac contractility.
• Excessive rise of the body temperature (e.g. in fever) decreases contractility.
• Hypothermia also decreases cardiac contractility.
Effect of Sodium & Calcium on contractility
Mineral High Low
Sodium Hypernatraemia: exerts negative Hyponatraemia: exerts positive inotropic
inotropic effect effect.
Calcium Hypercalcaemia: exerts a positive Hypocalcaemia: has a little
inotropic effect (or no) negative inotropic effect
Potassium Hyperkalaemia: has a negative Hypokalaemia: Has a positive inotropic
inotropic effect effect.