ELECTRICAL ACTIVITY OF THE HEART Heart Anatomy Its size is equal to your fist Location Superior surface of diaphragm Left of the midline Anterior to the vertebral column, posterior to the sternum Coverings of the Heart: Anatomy Pericardium – a double-walled sac around the heart composed of: A superficial fibrous pericardium A deep two-layer serous pericardium The parietal layer lines the internal surface of the fibrous pericardium The visceral layer or epicardium lines the surface of the heart They are separated by the fluid-filled pericardial cavity Heart Wall Epicardium – visceral layer of the serous pericardium Myocardium – cardiac muscle layer forming the bulk of the heart Fibrous skeleton of the heart – crisscrossing, interlacing layer of connective tissue Endocardium – endothelial layer of the inner myocardial surface Myocardial Thickness and Function Thickness of myocardium varies according to the function of the chamber Atria are thin walled, deliver blood to adjacent ventricles Ventricle walls are much thicker and stronger right ventricle supplies blood to the lungs (little flow resistance) left ventricle wall is the thickest to supply systemic circulation THE MYOCARDIUM Two specialized types of cardiac muscle cells: Each of these 2 types of cells has a distinctive action potential. Cardiac cells contract without Nervous Stimulation. CARDIAC MUSCLE Contracti le 99% Autorryth mic 1%
Transcript
ELECTRICAL ACTIVITY OF THE HEART
Heart Anatomy
Its size is equal to your fist
Location
Superior surface of diaphragm Left of the midline Anterior to the vertebral column,
posterior to the sternum
Coverings of the Heart: Anatomy
Pericardium – a double-walled sac around the heart composed of:
A superficial fibrous pericardium A deep two-layer serous
pericardium The parietal layer lines the internal surface of the fibrous pericardium The visceral layer or epicardium lines the surface of the heart They are separated by the fluid-filled pericardial cavity
Heart Wall
Epicardium – visceral layer of the serous pericardium Myocardium – cardiac muscle layer forming the bulk of the heart Fibrous skeleton of the heart – crisscrossing, interlacing layer of connective tissue Endocardium – endothelial layer of the inner myocardial surface
Myocardial Thickness and Function
Thickness of myocardium varies according to the function of the chamber
Atria are thin walled, deliver blood to adjacent ventricles
Ventricle walls are much thicker and stronger
right ventricle supplies blood to the lungs (little flow resistance) left ventricle wall is the thickest to supply systemic circulation
THE MYOCARDIUM
Two specialized types of cardiac muscle cells: Each of these 2 types of cells has a distinctive action potential.
Cardiac cells contract without Nervous Stimulation.
Cardiac muscle, like skeletal muscle & neurons, is an excitable tissue with the ability to generate action potential.
Most cardiac muscle is contractile (99%), but about 1% of the myocardial cells are specialized to generate action potentials spontaneously. These cells are responsible for a unique property of the heart: its ability to contract without any outside signal.
The heart can contract without an outside signal because the signal for contraction is myogenic, originating within the heart itself.
The heart contracts, or beats, rhythmically as a result of action potentials that it generates by itself, a property called auto rhythmicity (auto means “self”).
The signal for myocardial contraction comes NOT from the nervous system but from specialized myocardial cells also called auto rhythmic cells.
CARDIAC MUSCLE
Contractile99%
Autorrythmic 1%
These cells are also called pacemaker cells because they set the rate of the heart beat.
Electrical Activity Of The Heart
Myocardial Auto rhythmic cells (1%) – These cells are smaller and contain few contractile fibers or organelles. Because they do not have organized sarcomeres, they do not contribute to the contractile force of the heart.
Myocardial Contractile cells (99%) - Contractile cells which include most of the heart muscle called Atrial muscle and Ventricular muscle. These cells contract and are also known as the Working Myocardium.
Action Potential of the Auto-rythmic cardiac cells
The auto rhythmic cells do not have a stable resting membrane potential like the nerve and the skeletal muscles.
Instead they have an unstable membrane potential that starts at – 60mv and slowly drifts upwards towards threshold.
Because the membrane potential never rests at a constant value, it is called a Pacemaker Potential rather than a resting membrane potential.
What causes the membrane potentials of these cells to be unstable?
Auto rhythmic cells contain channels different from other excitable cells.
When cell membrane potential is at -60mv, channels are permeable to both Na and K.
This leads to Na influx and K efflux.
The net influx of positive charges slowly depolarizes the auto rhythmic cells. This leads to opening of Calcium channels.
This moves the cell more towards threshold. When threshold is reached, many Calcium channels open leading to the Depolarization phase.
IONIC BASIS OF ACTION POTENTIAL OF AUTORRYTHMIC CELLS
Phase 1: Pacemaker Potential:
Opening of voltage-gated Sodium channels called Funny channels (If or f channels ).
Closure of voltage-gated Potassium channels.
Opening of Voltage-gated Transient-type Calcium (T-type Ca2+ channels) channels .
Phase 2: The Rising Phase or Depolarization:
Opening of Long-lasting voltage-gated Calcium channels (L-type Ca2+ channels).
Large influx of Calcium.
Phase 3: The Falling Phase or Repolarization:
Opening of voltage-gated Potassium channels
Closing of L-type Ca channels.
Potassium Efflux.
ACTION POTENTIAL OF A CONTRACTILE MYOCARDIAL CELL:A TYPICAL VENTRICULAR CELL
Unlike the membranes of the autorrythmic cells, the membrane of the contractile cells remain essentially at rest at about -90mv until excited by electrical activity propagated by the pacemaker cells.
Depolarization
Opening of fast voltage-gated Na+ channels. Rapid Influx of Sodium ions leading to rapid depolarization.
Small Repolarization
Opening of a subclass of Potassium channels which are fast channels. Rapid Potassium Efflux.
Plateau phase
250 msec duration (while it is only 1msec in neuron) Opening of the L-type voltage-gated slow Calcium channels & Closure of the Fast K+ channels. Large Calcium influx K+ Efflux is very small as K+ permeability decreases & only few K channels are open.
Repolarization
Opening of the typical, slow, voltage-gated Potassium channels. Closure of the L-type, voltage-gated Calcium channels. Calcium Influx STOPS Potassium Efflux takes place.
Summary of Action Potential of a Myocardial Contractile Cell
Cardiac Muscle Branching cells One or two nuclei per cell Striated Involuntary Medium speed contractions
Excitation-Contraction Coupling and Relaxation of Cardiac Muscle
How are cardiac contractions started? Cardiac conduction system
Specialized muscle cells “pace” the rest of the heart; cells contain less actin and myosin, are thin and pale microscopically
Sinoatrial (SA) node; pace of about 65 bpm
Internodal pathways connect SA node to atrioventricular (AV) node
AV node could act as a secondary pacemaker; auto-rhythmic at about 55 bpm
Bundle of His
Left and right bundle branches
Purkinje fibers; also auto-rhythmic at about 45 bpm
All conduction fibers are connected to muscle fibers through gap junctions
Action Potentials (APs)
APs are the electrical signals that we have been discussing. Before going to the action potential one should know membrane potential, Na+, K+, and Ca2+ channels, Na+/K+ ATPase
New material will be APs in the SA node and ventricles.
Sinoatrial Node
Pacemaker of the heart.
Flattened ellipsoid strip of cells on the right atrium.
No contractile filaments.
Electrically connected to atrium.
Sinoatrial Node Action Potential
Phase 4: slow depolarization due to Na+ and Ca2+ leak until threshold. Note fast Na+ channels are inactive at -60 to -40 mV.
Phase 0: at threshold, Ca2+ channels open.
Phase 3: As in nerves, K+ channels open during repolarization.
Finally, note the slow rise and fall of the SA AP compared to that of the nerve AP, and the rhythmic firing.
AV Node and Bundle Delays AP from reaching the ventricles, allowing the atria to empty blood into ventricles before the ventricles contract.
Purkinje Fibres Receives the AP from the AV bundle and rapidly transmits the impulse through the ventricles.
Impulses in Ventricles
At the termination of the Purkinje fibres, the impulse rapidly travels through the ventricle muscle fibres via gap junctions, from the inside (endocardium) to the outside (epicardium).
The rapid propagation of the cardiac impulse through the Purkinje fibers and ventricles is important for an effective contraction.
Ventricular AP
Phase 4: resting membrane potential near the K+ equilibrium potential.
Phase 0: depolarizing impulse activates fast Na+ channels and inactivates K+
channels.
Phase 1: Transient opening of K+ channels and Na+ channels begin to close.
Phase 2: Ca2+ channels are open, key difference between nerve AP.
Phase 3: repolarization, Ca2+ inactivate and K+ channels open.
Refractory period: Na+ channels are inactive until membrane is repolarized.
Sequence of Excitation
Electrocardiography (EKG) Examines how Depolarization occurs in the HeartAction potential vs electrocardiogram
Normal ECGP wave: occurs at beginning of atrial contraction
QRS complex : occurs at beginning of ventricular contraction
T wave : occurs at during ventrical repolarization
Einthoven’s triangle
ECG examines how depolarization events occur in the heart
If a wavefront of depolarization travels towards the electrode attached to the + input terminal of the ECG amplifier and away from the electrode attached to the - terminal, a positive deflection will result.
If the waveform travels away from the + terminal lead towards the - terminal, a negative going deflection will be seen.
If the waveform is travelling in a direction perpendicular to the line joining the sites where the two leads are placed, no deflection or a biphasic deflection will be produced.
ECG measures the voltage changes as an impulse propagates through the heart
The electrical activity of the heart originates in the sino-atrial node. The impulse then rapidly spreads through the right atrium to the atrioventricular node. (It also spreads through the atrial muscle directly from the right atrium to the left atrium.) This generates the P-wave
The first area of the ventricular muscle to be activated is the interventricular septum, which activates from left to right. This generates the Q-wave
Next the bulk of the muscle of both ventricles gets activated, with the endocardial surface being activated before the epicardial surface. This generates the R-wave
A few small areas of the ventricles are activated at a rather late stage. This generates the S-wave
Finally, the ventricular muscle repolarizes. This generates the T-wave
Since the direction of atrial depolarization is almost exactly parallel to the axis of lead II (which is from RA to LL), a positive deflection (P wave) would result in that lead.
Since the ventricular muscle is much thicker in the left than in the right ventricle, the summated depolarization of the two ventricles is downwards and toward the left leg: this produces again a positive deflection (R-wave) in lead II, since the depolarization vector is in the same direction as the lead II axis.
Septal depolarization moves from left to right, the depolarization vector is directed towards the - electrode of lead II (RA), and therefore a negative deflection (Q-wave) is produced.
Electrocardiography
Time intervals in an ECG
P-Q or P-R interval: time from beginning of atrial contraction to beginning of ventricular depolaeization
Q-T interval : time of ventricular contraction
R-R interval: used to determine rate of heartbeat ( reciprocal of R-R interval)
