Origin and conduction of cardiac impulse (tbc)

The electrical signals that control the heart are generated within the heart itself. It is capable of functioning rhythmically without any external stimuli. This is called the auto rhythmic nature of the heart.

Pacemaker cells in the SA node

Upper right atrium; at the junction of the Superior vena cava and the opening of the right atrium.

A heart controlled by the impulses generated by the Sino atrial (SA) node is said to be in sinus rhythm.

No

1. Pacemaker potential- slow depolarisation of a membrane till the threshold.
2. Once the threshold is reached, it triggers the rising phase of action potential through depolarisation.
3. Falling phase of action potential through repolarisation.

The pacemaker potential is the first step in the generation of an action potential in the SA node. It is the slow depolarisation of the membrane potential till the threshold. It is caused by:-

1. Funny current- depolarising cation current due to the slow influx of Na+ ions through HCN channels.
2. Decreased K+ ion efflux
3. Ca 2+ ion influx

Once the threshold is reached via slow depolarisation, the rising phase of action potential is caused by:-

1. Opening of L type voltage gated Ca 2+ ion channels
2. This results in Ca 2+ influx.

Once the depolarisation reaches the peak, there is the falling phase of the action potential that is caused by:-

1. Inactivation of the L type voltage gated Ca 2+ ion channels.
2. Activation of K+ ion channels resulting in K+ ion efflux. This causes the repolarisation of the pacemaker cells.

The AV node is located at the base of the right atrium just above the junction of the atria and ventricles.

The AV node is a small bundle of specialised cardiac cells. The AV node cells are small in diameter and has a slow conduction velocity.

The AV node is the only point of electrical contact between the atria and the ventricles.

1. From SA node to AV node- cell to cell conduction through gap junctions across the atria (there are also other internodal pathways).
2. Delay of conduction in the AV node- allows the atrium to complete contraction
3. AV node spreads action potential to ventricles rapidly through Bundle of His (left and right) and Purkinje fibres.
4. Cell to cell conduction of impulses in the ventricular muscles.

There is a resting membrane potential at -90 mV.

1. Rising phase of action potential- depolarisation
2. Plateau phase- The membrane potential is maintained near the peak of action potential for a few hundred milliseconds.
3. Falling phase of action potential- repolarisation. Then it returns to the resting membrane potential.

The resting potential remains at -90 mV until the excitation.

1. It is the depolarisation of the membrane potential caused by the fast Na+ influx.
2. This rapidly reverses the membrane potential from -90 mV to +20 mV. This is known as Phase 0 of action potential in the contractile cardiac muscle cells.

The membrane potential is maintained near the peak of action potential for few hundred milliseconds causing the plateau phase of action potential. The plateau phase is due to:-

1. Closure of Na+ ion channels and transient K+ efflux. (Phase 1)
2. Influx of Ca 2+ (L-type Ca 2+ channels)- Phase 2

The Phases 1 and 2 make the plateau phase of action potential.

The falling phase of the action potential through repolarisation is caused by:-

1. Inactivation of Ca 2+ channels and activation of K+ channels.
2. This results in K+ efflux This is the Phase 3 of the action potential in contractile myocytes.

Resting membrane potential at -90 mV

The ECG is a record of depolarisation and repolarisation cycle of cardiac muscle obtained from skin surface. -The wave of depolarisation and repolarisation moves across the heart and sets up electrical currents which can be detected by surface electrodes.

Atrial depolarisation

Ventricular depolarisation (masks atrial repolarisation)

Ventricular repolarisation

AV node delay

Ventricular systole

Diastole

Although the heart is auto rhythmic in nature and the SA node generates impulses, the autonomic nervous system modifies the heart rate.

1. Sympathetic stimulation- increases heart rate.
2. Parasympathetic stimulation- decreases heart rate Their roles are reciprocal in nature.

The vagus nerve is the parasympathetic supply to the SA node of the heart. In resting conditions, the vagal tone dominates. It slows down the intrinsic heart rate from 100 bpm to 70 bpm (normal heart rate).

60-100 bpm

Resting heart rate lower than 60

Resting heart rate above 100 bpm

The vagus nerve supplies to the SA and the AV node in the heart.

1. It slows down the rate of firing from the SA node
2. It increases the AV node delay The neurotransmitter is acetylcholine acting through the muscarinic M2 receptors.

1. The pacemaker potential takes longer to reach the threshold. Thus, the slope of pacemaker potential decreases.
2. The frequency of AP decreases.
3. Negative chonotropic effect

The cardiac sympathetic nerves supply the SA node, AV node and the myocardium.

1. The sympathetic stimulation increases rate of firing from the SA node
2. Decreases AV nodal delay
3. Increases force of contraction. Noradrenaline is the neurotransmitter working through the beta 1 adrenoreceptors.

1. Slope of pacemaker potential decreases
2. Pacemaker potential reaches threshold quicker
3. Frequency of action potential increases. This causes a positive chronotropic effect.

It is caused by the regular arrangement of contractile proteins.

The cardiac myocytes are electrically coupled by gap junctions.

1. These are protein channels which form low resistance communication pathways between neighbouring myocytes.
2. They ensure that each impulse reaches all cardiac myocytes through the all-or-none law of the heart.

The desmosomes within the intercalated discs provide mechanical adhesion between adjacent cardiac cells. They ensure that the tension developed by one cell is transmitted on to the next.

Each muscle fibre (cell) contains many myofibrils- contractile units of muscle. The myofibrils have alternating segments of thick and thin protein filaments. (a) Actin (thin filaments): lighter appearance (b) Myosin (thick filaments): darker appearance.

• Within each myofibril, actin and myosin are arranged into sarcomeres.

Myofibrils consist of sarcomeres- the main contractile unit of the muscle fibre. They have alternating segments of thick and thin filaments protein filaments. Actin (thin)- lighter appearance; Myosin (thick)- darker appearance

Muscle tension is produced by sliding of actin filaments on myosin filaments. The sliding filaments theory is the explanation how muscle shortens and produces force.

1. Muscle fibre relaxed due to troponin-tropomyosin complex covering the cross bridge binding site.
2. Muscle fibre excitation caused by ventricular action potential generation (fast response).
3. L type voltage gated Ca 2+ ion channels open allowing influx of Ca ions into the cytoplasm.
4. This causes Calcium induced Calcium release (CICR) by the sarcoplasmic reticulum in the myocytes.
5. Ca 2+ ions binds with the troponin- causing a conformational change to the myosin binding site- cross bridge occurs.
6. Binding of actin/myosin cross bridge triggers power stroke pulling the actin filament (thin) close during contraction (systole).
7. After contraction has occurred and the action potential has passed, Ca 2+ influx ceases due to the ion channels closing. The Ca ions need to be sequestered back to the sarcoplasmic reticulum via ATP use. This allows heart to relax- diastole.

Period following an AP in which it is not possible to produce another AP in the heart. AP is action potential.

1. During the plateau phase of ventricular action potential, the Na+ channels are in the depolarized closed state - not available for opening
2. During the descending phase (repolarizing) of the AP the K+ channels are open, and the membrane cannot be depolarised.

The long refractory period prevents generation of tetanic contraction - protective function

The volume of blood ejected by each ventricle per heart beat. Contraction of the ventricular muscle ejects the stroke volume.

SV= End Diastolic Volume (EDV)- End Systolic Volume (ESV)

It is regulated by extrinsic and intrinsic mechanisms. Intrinsic= within the heart muscle itself. Extrinsic= nervous and hormonal control.

The volume of each blood within each ventricle at the end of diastole. - Determined by the venous return to the heart

The volume of blood pumped by each ventricle per minute. CO = Stroke Volume x Heart Rate - If we regulate SV and HR, we will regulate SO

5 litres/min

The diastolic length/stretch of myocardial fibres - Determined by EDV (end diastolic volume)

The force against which the ventricle contracts to eject blood during systole. - Determined by the MAP in the aorta, which is influenced by SVR