Cardiac contractility

Kiran Goushika

Cardiac Electrophysiology

Cardiac Contractility

The science of elucidating ,diagnosing, and treating electrical activities of heart.

Actions potentials◦ SA node◦ Cardiac muscle

(atria, ventricles & Purkinje fibers)

Channels◦ Ca2+ channel◦ β-adrenergic receptor◦ Na+/K+-ATPase

0 mV0 mV

-70 mV-70 mV

-50 mV-50 mV

Phase 0Phase 0

Phase 3Phase 3

Phase 4Phase 4 Phase 4Phase 4

Ca2+

Pacemaker of the heart Unstable resting potential◦ Exhibits automaticity◦ AV node & His-Purkinje system are latent pacemakers

Phase 1 & 2 are not present in pacemaker action potentials

Resting PotentialResting Potential-90 mV-90 mV

0 mV0 mV

+30 mV+30 mV

-70 mV-70 mV

Phase 0Phase 0 Phase 1Phase 1 Phase 2Phase 2

Phase 3Phase 3

Phase 4Phase 4

Ca2+

Na+/K+ ATPase

3 Na3 Na++

2 K2 K++

Representative Cardiac CellRepresentative Cardiac Cell

NaNa++ channel channelNaNa++ channel channelVoltage dependentVoltage dependentL-typeL-type CaCa2+2+ channel channelVoltage dependentVoltage dependentL-typeL-type CaCa2+2+ channel channel NaNa++/K/K++ ATPase ATPaseNaNa++/K/K++ ATPase ATPase

NaNa++/Ca/Ca2+2+ exchanger exchangerNaNa++/Ca/Ca2+2+ exchanger exchanger

SR (Mitochondria)SR (Mitochondria)

Heart muscleHeart muscleHeart muscleHeart muscle

KK++ channel(s) channel(s)KK++ channel(s) channel(s)

Na+/Ca2+ Antiporter

Ryanodine receptorRyanodine receptorRyanodine receptorRyanodine receptor

3 Na3 Na++

CaCa2+2+

ββ-adrenergic receptor-adrenergic receptorββ-adrenergic receptor-adrenergic receptor

The intrinsic ability of heart to contract

Intrinsic ability of cardiac muscle

Also called ‘inotropism’ or ‘inotropy’

Related to the intracellular [Ca2+]

Inotropic agents◦ positive: increase contractility◦ negative: decrease contractility

Chronotropy◦ rate of contraction◦ also affected by intracellular [Ca2+]

Dromotropy◦ rate of impulse conduction◦ noted particularly at AV node

Increased intracellular [Ca2+]◦ increased heart rate◦ cardiac glycosides (e.g. digoxin)

Stimulation of β1-adrenergic receptor◦ sympathomimetic agents◦ catecholamines

Ca2+ entry through L-type channels in T tubules triggers larger release of Ca2+ from sarcoplasmic reticulum◦ Ca2+ induced Ca2+ release leads to cross-bridge

cycling and contraction

3 Na3 Na++

2 K2 K++

Cell ElectrophysiologyCell Electrophysiology

SR (Mitochondria)SR (Mitochondria)

CaCa2+2+

Phase 2Phase 2

CaCa2+2+

CaCa2+2+

CaCa2+2+

CaCa2+2+

CaCa2+2+

CaCa2+2+

CaCa2+2+

3 Na3 Na++

CaCa2+2+

ATRIAL MUSCLE

VENTRICULAR MUSCLE

SPECIALISES EXCITATORY &CONDUCTIVE MUSCLE FIBERS

Interconnected by intercalated discs and form functional syncytia

Within intercalated discs – two kinds of membrane junctions◦ Desmosomes◦ Gap junctions

Exhibit branching Adjacent cardiac cells are

joined end to end by specialized structures known as intercalated discs

Within intercalated discs there are two types of junctions◦ Desmosomes◦ Gap junctions..allow action

potential to spread from one cell to adjacent cells.

Heart function as syncytiumwhen one cardiac cell undergoes an action potential, the electrical impulse spreads to all other cells that are joined by gap junctions so they become excited and contract as a single functional syncytium.

Atrial syncytium and ventricular syncytium

Autorhythmicity: The ability to initiate a heart beat continuously and regularly without external stimulation

Excitability: The ability to respond to a stimulus of adequate strength and duration (i.e. threshold or more) by generating a propagated action potential

Conductivity: The ability to conduct excitation through the cardiac tissue

Contractility: The ability to contract in response to stimulation

Definition: the ability of the heart to initiate its beat continuously and regularly without external stimulation

myogenic (independent of nerve supply)

due to the specialized excitatory & conductive system of the heart

↓ intrinsic ability of self-excitation (waves of depolarization) ↓ cardiac impulses

Autorythmic cells do not have stable resting membrane potential (RMP)

Natural leakiness to Na & Ca→ spontaneous and gradual depolarization

Unstable resting membrane potential (= pacemaker potential)

Gradual depolarization reaches threshold (-40 mv) → spontaneous AP generation

SITE RATE(Time/minu

te)SA Node 100

AV Node 40-60

AV bundle, bundle AV bundle, bundle branches,& Purkinje branches,& Purkinje fibrfibreses

20-35

SA node acts as heart pacemaker because it has the fastest rate of generating action potentialNerve impulses from autonomic nervous system and hormones modify the timing and strength of each heart beat but do not establish the fundamental rhythm.

Definition: The ability of cardiac muscle to respond to a stimulus of adequate strength & duration by generating an AP

AP initiated by SA node→travels along conductive pathway→ excites atrial & ventricular muscle fibres

Long refractory period (250 msec) compared to skeletal muscle (3msec)

During this period membrane is refractory to further stimulation until contraction is over.

It lasts longer than muscle contraction, prevents tetanus

Gives time to heart to relax after each contraction, prevent fatigue

It allows time for the heart chambers to fill during diastole before next contraction

AP in skeletal muscle : 1-5 msecAP in cardiac muscle :200 -300 msec

Definition: ability of cardiac muscle to contract in response to stimulation

Similar to that in Similar to that in skeletal musclesskeletal muscles

Definition: property by which excitation is conducted through the cardiac tissue

Cardiac impulse originates at SA node Action potential spreads throughout right and left atria Impulse passes from atria into ventricles through AV

node (only point of electrical contact between chambers) Action potential briefly delayed at AV node (ensures

atrial contraction precedes ventricular contraction to allow complete ventricular filling)

Impulse travels rapidly down interventricular septum by means of bundle of His

Impulse rapidly disperses throughout myocardium by means of Purkinje fibers

Rest of ventricular cells activated by cell-to-cell spread of impulse through gap junctions

PROFESSOR: Maka