The heart as an electrical pump Flashcards

1
Q

What are the internal components of myocytes?

A

Composed of myofibrils containing myofilaments (actin and myosin).

Myofilaments are interdigitated which forms sarcomeres that are responsible for contraction.

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2
Q

How do myocytes function as a syncytium?

A

Myocytes are arranged into a syncytium of cells that branch and interdigitate providing both mechanical and electrical interconnection between the myocytes.

This coupling results in a low threshold all or nothing response with rapid propagation of electrical activity.

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3
Q

What are the characteristics of sinoatrial cells that allow them to carry out their role of pacemaker?

A

1) No true resting potential

2) Generation of regular and spontaneous action potentials

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4
Q

What is a sarcomere?

A

The region of myofibril between two Z lines comprised of interdigitated thick (myosin) and thin (actin) myofilaments which slide along each other to shorten the muscle during contraction.

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5
Q

What factors can modify the activity of sinoatrial cells?

A
Autonomic Nerves
Hormones 
Drugs
Ions
Hypoxia 
Ischemia
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6
Q

What is the role of the sinoatrial node?

A

Pacemaker of the heart
Source of action potentials that drive cardiac contractions (that then travel through the atrium to the atrioventricular node)

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7
Q

How are action potentials generated in the SAN?

A

1) Pre-potential - slow influx of Na+ ions into the cell until threshold is reached
2) Depolarisation - rapid influx of Ca2+ ions
3) Repolarisation - outflux of K+ ions (membrane returns to resting potential of -60mV)

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8
Q

How are action potentials formed in the cardiac myocyte?

A

1) Influx of Na+ from adjacent action potential
2) Voltage-gated ion channels open causing rapid depolarisation
3) Membrane potential approx. +30mV - Na+ channels close, K+ channels open and slow Ca2+ channels open
4) Plateau - slow Ca2+ channels close at end of plateau when membrane potential is approx. 0mV
5) Repolarisation (outflux of K+ ions ongoing)
6) K+ channels close when membrane potential is approx. -90mV
7) Na/K channels return Na to extracellular fluid and K to intracellular fluid

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9
Q

What is a refractory period?

A

Period immediately following action potential where a nerve or muscle is unresponsive to further stimulation (i.e. can not generate another action potential)

Nb. cardiac muscles have relatively long refractory period compared to skeletal muscles

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10
Q

What is action potential propagation?

A

Change in potential difference across the cell surface in which an action potential is reached thus modifying adjacent membrane by cytosolic ion influx - occurs in opposite direction to refractory zone meaning action potentials can only travel in one direction.

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11
Q

What features of the conduction system allow for coordinated contraction?

A

2 myocardial syncytia (atrial and ventricular) separated by the AVN.
AVN causes a delay in conduction which allows for a coordinated contraction

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12
Q

What is the mechanism of excitation-contraction coupling?

A

1) Excitation - action potential originates in pacemaker cells and passes along membrane of myocyte syncytium and enters the cell via the T tubule system
2) Coupling - membrane depolarisation initiates the release of calcium into the sarcoplasm from T tubules, sarcoplasmic reticulum and cell membrane
3) Contraction - increase in intracellular calcium facilitates process of contraction

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13
Q

How does actin-myosin activation allow for cardiac muscle contraction?

A

1) Calcium binds to troponin on Actin filament
2) Binding causes Tropomysin to move, revealing actin binding site for myosin heads
3) ATP bound and hydrolysed by ATPase in the myosin head, providing energy
4) ATP hydrolysis drives the repeated cycle of interaction between myosin heads and actin
5) During each cycle, conformational changes in myosin result in the movement of myosin heads along actin filaments resulting in shortening of muscle fibre

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14
Q

What is the role of calcium in muscle contraction?

A

Influx of calcium activates troponin molecules which initiates contraction cycle (the higher the calcium concentration, the greater the activation of troponin)

Calcium flow reversed at end of cycle which stops actin-myosin interaction and relaxes muscles

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15
Q

What are the 4 phases of the cardiac cycle?

A
  1. Filling phase
  2. Isovolumetric contraction
  3. Outflow phase
  4. Isovolumetric relaxation
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16
Q

What occurs during phase 1 (filling) of the cardiac cycle?

A

Higher pressure in atria means atrioventricular valves are open.
Diastole (atria and ventricles relaxed) - ventricles fill with blood from the vena cava and pulmonary veins (via the atria).
Atrial systole - contraction of atria causes extra blood flow into ventricles making pressure in ventricles higher than the atria - causes atrioventricular valves to close

[Atrial systole = p wave on ECG]

17
Q

What occurs during phase 2 (isovolumetric contraction) of the cardiac cycle?

A

Both sets (atrioventricular and semilunar) of valves are closed so no blood can leave ventricles meaning that when systole begins and ventricles begin to contract opening the pressure increases massively ready to eject blood into the aorta and pulmonary trunk

[Ventricular systole = QRS complex on ECG]

18
Q

What occurs during phase 3 (outflow) of the cardiac cycle?

A
Semilunar valves (aortic and pulmonary) open once ventricular pressure is greater than that of the aorta and pulmonary trunk 
Ventricles begin to relax causing decrease in pressure compared to the aorta - this causes valves to close

[ventricular repolarisation = T wave on ECG]

19
Q

What occurs during phase 4 (isovolumetric relaxation) of the cardiac cycle?

A

Ventricles relax further reducing pressure so that the atrioventricular valves open
Ventricles then start to fill again and cycle repeats

20
Q

What types of valve disease can occur in the heart?

A

Stenosis

Regurgitation

21
Q

How does valve stenosis affect the heart?

A

Causes ventricular flow obstruction and fixed cardiac output which places a pressure load on the ventricle

22
Q

How does the heart compensate for a valve stenosis?

A

Ventricular hypertrophy

23
Q

How does regurgitation affect the heart?

A

Increased volume load

24
Q

How does the heart compensate for valvular regurgitation?

A

Increased sarcomere length and cavity volume
Increased stroke volume
Eccentric hypertrophy to compensate for wall stress