properties of cardiac muscle

Cardiovascular Physiology

Properties of the Cardiac Muscle

Properties of the cardiac muscle:

I. Excitability

II. Conductivity

III. Contractility

IV. Rhythmicity

Properties of the cardiac Muscle

I. Excitability (Irritability)

I. Excitability (Irritability):= the ability of cardiac ms to respond to adequate

stimuli by generating an action potential followed by a mechanical contraction.

■ The mechanical response consists of contraction (systole) & relaxation (diastole).

■ Cardiac ms begins to contract few milliseconds after the AP begins, & continues to contract until few milliseconds after the AP ends.

■ Duration of contraction:

0.2 sec in arial muscle, &

0.3 sec in ventricular muscle.

Relation between the action potential & the mechanical response

■ Diastole begins at the end of the plateau.

■ 2nd rapid repolarization is completed at about the middle of diastole.

Relation between the action potential & the mechanical response (continued)

Action potential of different types of cardiac muscle

Action potential of ventricular muscle■ Ventricular ms has a RMP of –90 mV. ( –85 to –95mV).

■ The trans-membranous AP overshoots to a potential of ( +20mV).

AP of ventricular muscle (continued)

Phase 0 = Rapid depolarization.

Phase 1 = Rapid repolarization/ 1st rapid repolarization.

Phase 2 = A plateau.

Phase 3 = Slow repolarization/

2nd rapid repolarization.

Phase 4 = Complete repolarization.

■ Trans-membranous AP of ventricular ms is characterized by presence of 5 phases.

Phase 0 = Rapid depolarization. ■ op fast Na+ channels Na+ influx.

Phase 1 = Rapid repolarization/ 1st rapid repolarization. ■ cls Na+ channels, K+ permeability, w Cl- influx.

Phase 2 = A plateau. ■ op slow Ca2+ channels (slow Ca2+ Na+ channels) Ca2+

influx, w slow op K+ channels.

Phase 3 = Slow repolarization/ 2nd rapid repolarization. ■ cls slow Ca2+ channels, w K+ permeability K+ efflux.

Phase 4 = Complete repolarization.

■ actv Na+ K+ pump 2K+ in/ 3Na+ out.

AP of ventricular muscle (continued) 0

1

2

3

4

Excitability changes during the action potential:

■ Passes through 3 periods:

1. Absolute refractory period (ARP)

2. Relative refractory period (RRP)

3. Dangerous period (supranormal period)

Refractory Periods

1. Absolute refractory period (ARP):

■ The excitability of cardiac ms is completely lost during this period, i.e. doesn’t respond to 2nd stimulus.

■ V. longV. long.

■ Occupies the whole period of systole.

■ Corresponds to the period of depolarization (phase 0), & the first 2 phases of repolarization.

■ Ht can’t be tetanized (continuous contraction), as its ARP occupies the whole contraction phase.

■ The excitability of cardiac ms is partially recovered during this period, i.e. stronger stimuli than normal are required to excite the ms.

■ Occupies the time of diastole.

■ Corresponds to the 3rd phase of repolarization.

■ Can be affected by the HR, temp., bacterial toxins, vagal stimulation, sympathetic stimulation & drugs.

2. Relative Refractory Period (RRP):

■ The excitability of cardiac ms is supranormal just at the end of the AP, i.e. weaker stimuli than normal can excite the ms.

■ ? result in ventricular fibrillation.

3. Dangerous Period (Supranormal):

1. Cardiac innervation.

2. Effect of ions concentration in ECF.

3. Physical factors.

4. Blood flow.

5. Chemical factors (drugs).

Factors affecting myocardial excitability:

1. Cardiac Innervation: ■ Sympathetic NS excitability.

■ Parasympathetic NS (vagus) excitability.

2. Effect of ions concentration in ECF: ■ Ca2+ excitability.

■ K+ excitability.

3. Physical factors: ■ temperature excitability.

■ temperature excitability.

Factors affecting myocardial excitability (continued)

4. Blood flow:

■ Insufficient bl flow to cardiac ms excitability &

myocardial metabolism for 3 reasons:

(1) lack of O2,

(2) excess accumulation of CO2, &

(3) lack of sufficient food nutrients.

5. Chemical factors (drugs): ■ Digitalis excitability.

Factors affecting myocardial excitability (continued)


II. Conductivity

II. Conductivity:

= the ability of cardiac ms fibers to conduct the cardiac impulses that are initiated in the SA-node (the pacemaker of the heart).

■ The impulse is conducted:

1st Atrial spread ■ from SA-node conductive tissue ventricles.

2nd Ventricular spread ■ from apex of the heart base, via Purkinje fibers to the endocardial surface of ventricles.

The direction of the impulse:

The direction of the impulse (continued)

N.B. LBB starts before RBB, as LV wall is thicker so the impulse

needs more enough time to reach. Accordingly both ventricles

will contract together.

Conduction of Impulse

■ APs from SA node spread quickly at rate of 0.8 - 1.0 m/sec.

■ Time delay occurs as impulses pass through AV node. Slow conduction of 0.03 – 0.05 m/sec.

■ Impulse conduction as spread to Purkinje fibers at a velocity of 5.0 m/sec. Ventricular contraction begins 0.1–0.2 sec. after

contraction of the atria.

The conduction velocities of the impulse:

SA-node 0.05 m/sec. AV-node 0.01 m/sec. … (slowest) Bundle of His 1.00 m/sec. Purkinje fibers 4.00 m/sec. …. (fastest) Atrial & Ventricular muscles 0.3 to 0.4 m/sec.

The conduction velocities (continued)

■ The slowest conduction velocity in AV-node:

■ because it has few no. of intercalated discs. ■ Importance: to allow sufficient time for ventricles to be filled w bl before they contract.

■ The fastest Conduction velocity in Purkinje fibers:

■ Importance: to allow the 2 ventricles to contract at the same time simultaneously.




4. Blood flow.


Factors affecting myocardial conductivity:

1. Cardiac Innervation: ■ Sympathetic NS conductivity.

■ Parasympathetic NS (vagus) conductivity.

2. Effect of ions concentration in ECF: ■ Ca2+ conductivity.

■ K+ conductivity.

3. Physical factors: ■ temperature conductivity.

■ temperature conductivity.

Factors affecting myocardial conductivity (continued)

4. Blood flow:

■ Insufficient bl flow to cardiac ms conductivity &

myocardial metabolism for 3 reasons: (1) lack of O2,

(2) excess accumulation of CO2, &

(3) lack of sufficient food nutrients.

5. Chemical factors (drugs): ■ Digitalis conductivity.

Factors affecting myocardial conductivity (continued)


III. Contractility

III. Contractility:

= the ability of the cardiac muscle to convert

chemical energy into mechanical work.

Contractility (continued)

♥ Myocardial fibers have ‘Functional syncytium’ &

NOT ‘anatomical syncytium’, because they present in contact but NOT in continuity.

♥ Strength of myocardial contraction determines the

heart pumping power.

♥ Mechanism of contraction depends on the contractile

filaments, which contain the protein molecules (actin

& myosin).

Excitation-Contraction Coupling in Heart Muscle

= is the mechanism by which AP causes myofibrils of cardiac ms to contract.

♥ When AP passes over cardiac ms membrane, AP also spread to interior of cardiac ms fiber along membranes of transverse (T) tubules.

♥ Depolarization of myocardial cell stimulates opening of Ca2+ channels in sarcolema. Ca2+ diffuses down gradient into cell through T tubules.

Stimulates opening of Ca2+-release channels in SR.

Ca2+ binds to troponin & stimulates contraction (same mechanisms as in skeletal ms).

Excitation-Contraction Coupling (continued)

♥ At the end of plateau of cardiac AP, i.e. during

repolarization,

■ Ca2+ in sarcoplasm is rapidly & actively transported

& pumped out of the cell via a Na+- Ca2+- exchanger,

back into both SR & T tubules.

■ Resulting in cessation of the contraction until new

AP occurs.

Excitation-Contraction Coupling (continued)


2. Oxygen supply.

3. Calcium & potassium ions concentration in ECF.


5. Hormonal & chemical factors (drugs).

6. Mechanical factors.

Factors affecting myocardial contractility: (Inotropic effectors)

1. Cardiac Innervation: ■ Sympathetic NS force of contraction.

■ Parasympathetic NS (vagus) atrial force of contraction w no significant effect on ventricular ms.

Factors affecting myocardial contractility (continued)

2. Oxygen supply: ■ Hypoxia contractility.

3. Calcium & potassium ions concentration in ECF:

■ Ca2+ contractility. ■ K+ contractility.

4. Physical factors: ■ Warming contractility. ■ Cooling contractility.


5. Hormonal & chemical factors (drugs):

■ +ve inotropics: (Adrenaline, noradrenaline, alkalosis, digitalis, Ca2+, caffieen,…)

■ -ve inotropics: (Acetylcholine, acidosis, ether, chloroform, some bacterial toxins (e.g. diphtheria toxins), K+, …)


6. Mechanical factors:

a. Cardiac ms. obeys ‘all or none law’:

i.e. minimal or threshold stimuli lead to maximal

cardiac contraction, because cardiac ms. behaves as

a syncytium.


b. Cardiac ms. can’t be stimulated while it is contracted, because its excitability during contraction is zero due to long ARP, so it can’t be tetanized.

c. Cardiac ms. can perform both isometric & isotonic types of contractions.


d. Starling’s law of the heart:

■ “Length-tension relationship” ‘Within limits, the greater the initial length of the fiber, the stronger will be the force of its contraction; However, overstretching the fiber as in heart failure its power of contractility decreases’

i.e. within limits, the power of contraction is directly proportional to the initial length of the ms.

■ Cardiac ms accommodates itself (up to certain limit) to the changes in venous return.


e. Cardiac ms shows staircase phenomenon (gradation),

if providing all other conditions kept constant.

i.e. if an isolated heart is stimulated by successive

equal & effective stimuli, the 1st few contractions

show a gradual in the magnitude of contraction.



IV. Rhythmicity (Automaticity)

IV. Rhythmicity (automaticity):

= the ability of cardiac ms to contract in a regular

constant manner w/out nerve supply.

♥ It’s myogenic in origin (i.e. not neurogenic).

♥ Its initiated by the ‘pacemaker’ of the ht, the

SA- node.

The pacemaker of the heart:

= the SA- node.

♥ Contains the P- cells, which are probably the

actual pacemaker cells.

♥ Has the fastest rhythm (rate of discharge) of all

parts of the heart, 90 impulses/min. its fibers have an unstable RMP.

♥ Has spontaneous (w/out stimulation) depolarization,

up to firing level.

?

Pacemaker potential:

♥ Its RMP is ( -60 mV).

♥ Pacemaker tissue is characterized by unstable

membrane potential, Prepotential. ?

-6

Pacemaker Prepotential:♥ Due to gradual state of depolarization:

■ Steady in K+ permeability ( K+ efflux), leading to intracellular negativity. ■ Causing spontaneous leakage of membrane to Na+ w/out stimulation. (-60 mV to -55 mV). ■ Which causes op of voltage gated transient Ca2+ channels, leading to some Ca2+ influx. (-40 mV).

?

-6

Pacemaker Action potential (AP)

♥ Pacemaker Depolarization:

Opening of long lasting (fast) Ca2+ channels. More Ca2+ influx till reaching the potential, i.e. firing

level point leading to depolarization.

Opening of VG Na+ channels ? also contribute to the upshoot phase of the AP.

-6

Pacemaker Action potential (AP) (continued)

♥ Pacemaker Repolarization: Opening of VG K+ channels.

K+ diffuses outward (efflux), … (so +vity will go out of cell).

♥ Pacemaker Hyperpolarization: ■ excessive K+ effllux,

(This will lead to hardship of K+ efflux in 2nd depolarization).

Ectopic pacemaker: Pacemaker other than SA node:

If APs from SA node are prevented from reaching these areas, these cells will generate pacemaker potentials.

-6

-6 K+ out

Ca2+ inT Ca2+ L Ca2+

L Ca2+ K+ out

K+ out

Na+ in

Ca2+

in





Factors affecting myocardial rhythmicity (chronotropic effectors):

a. Sympathetic stimuli:

Tachycardia, by spontaneous depolarization of SA- node.

How? ■ SA- node membrane permeability to K+ less K+ efflux. ■ membrane permeability to Ca2+ more Ca2+ influx.

■ As a result, the slope of depolarization , causing rate of SA- node firing & HR.

Factors affecting myocardial rhythmicity:

1. Cardiac Innervation:

b. Parasympathetic stimuli (vagus):

Bradycardia, by spontaneous depolarization of

SA- node. How? ■ SA- node membrane permeability to K+ more K+ efflux.

■ membrane permeability to Ca2+ less Ca2+ influx.

■ As a result, the prepotential slope , causing rate of SA- node firing & HR.

Factors affecting myocardial rhythmicity:1. Cardiac Innervation (continued)

a. K+ ions: ■ If in ECF rhythmicity.

■ If in ECF rhythmicity.

(? stop heart in diastole)

b. Na+ ions: ■ If in ECF innitiate rhythmicity, but can’t maintain it.


2. Effect of ion concentrations in ECF:

a. Warming: rhythmicity.

b. Cooling: rhythmicity.

c. Exercise: HR as a result of sympathetic n.

stimulation & vagal inhibition to

SA- node.

d. Endurance-trained athletes: Resting bradycardia

due to high vagal activity.


3. Physical factors:

a. Thyroid hormones & catecholamines:

rhythmicity.

b. Ach:

rhythmicity.

c. Hypoxia:

rhythmicity.


4. Chemical factors (drugs):

Remember:

■ Intrinsic rhythmicity of denervated SA- node is 90

impulses/min, while that of AV- node is 60

impulses/min.

■ However, vagal tone controls SA- node to become 70

impulses/min, & AV- node to 40 impulses/min.

■ If SA- node activity is depressed by a disease, AV-

node takes over & becomes the pacemaker instead,

leading to bradycardia.

properties of cardiac muscle

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