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Cardiac Innervation Myocardial Infarction Notes

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Semester 2 Case 5: The Faint Heart


How is heartbeat controlled? And how is the heart innervated?

[1] Two

types of cardiac muscle are involved in a normal heartbeat - Conducting system: controls & coordinates heartbeat, Contractile cells: produce powerful contractions that propel blood. Cardiac muscle tissue contracts on its own, in the absence of neural or hormonal stimulation - known as automaticity or autorhythmicity.

Conducting system: Sinoatrial node: Embedded in posterior wall of right atrium near the entrance of the superior vena cava. Contains pacemaker cells. Area of fastest spontaneous depolarisation, and so because it reaches threshold first, it establishes the heart rate. (80-100 per minute without hormonal or neural influence.) Atrioventricular node: Sits within the floor of the right atrium near the opening of the coronary sinus. Nodal cells are smaller in diameter than conducting cells, and connections between nodal cells are less efficient at relaying the impulse, which allows for a 100ms delay so that the atria contract before the ventricles do. Brought to threshold by impulse from SA node, as this is quicker than via prepotential. (40-60 per minute without impulses from SA node eg. Due to damage of atrial pathways or to the SA node.) Conducting cells: Interconnect the 2 nodes & distribute the contractile stimulus throughout the myocardium. Found in intermodal pathways in atria from the SA node to AV node. The ventricular conducting cells include the AV bundle and bundle branches, & the Purkinje fibres. Most cells of conducting system are smaller than contractile cells and contain very few myofibrils. However, Purkinje cells are much larger in diameter and so conduct action potentials more quickly than other conducting cells. The membranes of conducting cells of the SA and AV nodes cannot maintain a stable resting potential. After each repolarisation, the membrane gradually drifts towards threshold. This gradual depolarisation = prepotential or pacemaker potential. It takes roughly 50ms for an action potential to travel from the SA node to the AV node along intermodal pathways. Conducting cells pass stimulus to contractile cells of both atria, and the action potential spreads across the atrial surfaces by cell-to-cell contact. The stimulus only affects the atria because the fibrous skeleton isolates the atrial myocardium from the ventricular myocardium. After the delay at the AV node, the impulse is conducted along the interventricular bundle and the bundle branches to the Purkinje fibres and the papillary muscles. The Purkinje fibres then distribute the impulse to the ventricular myocardium, and ventricular contraction begins.

Maximum AV node impulse conductivity = 230bpm = Maximum heart rate. This can only be exceeded if the conducting system has been damaged or stimulated by drugs. The connection between the AV node and AV bundle is the only electrical connection between the atria and ventricles. Impulse enters AV bundle ?Travels to the interventricular septum ?Enters right and left bundle branches ?Conduct impulse to Purkinje fibres ?Through the moderator band ? To the papillary muscles. Left bundle branch is much larger than the right as it supplies the massive left ventricle. Both branches extend toward the apex of the heart, turn, and fan out deep to the endocardial surface. Because the bundle branches deliver the impulse across the moderator band to the papillary muscles directly, rather than via Purkinje fibres, the papillary muscles begin contracting before the rest of the ventricular musculature. Contraction of papillary mucles ?Tenses chordae tendinae ?keeping AV valves shut.

Contractile cells: Make up most of the atrial and ventricular walls. ~99% of muscle cells in the heart (cardiomyocytes). Purkinje fibres distribute stimulus to the contractile cells.
[2] Structure: Each cell has a single nucleus, but many mitochondria. Can be branched or not. The myocytes attach end-to-end via intercalated discs. Intercalated discs: Contain 3 functional "zones": Gap junctions, desmosomes, and fascia adherens. Gap junctions transmit ionic currents from one cell to the next. They're made up of 6 connexin sub-units, which form a hollow tube called the connexon. The connexon spans the intercellular gap enabling the myocardium to act as an electrically continuous sheet and all myocytes to be activated simultaneously. Desmosomes 'glue' cells together. Glycoproteins called cadherins span the gap between cell membranes, and desmin forms the intermediate filaments.

Sarcolemma = Membrane surrounding cardiomyocyte. Mitochondria = Provide ready supply of ATP to maintain contraction. Contractile proteins = Actin and myosin. Sarcomere = The essential contractile unit of a cardiomyocyte. Z line = A dark thin protein band to which actin filaments are attached, marking boundary between adjacent sarcomeres. A band = Dark staining zone where actin and myosin overlap. H zone = A region in the A band where only myosin is present. I band = Light zone composed mainly of actin filaments.

T tubules = Invaginations of the cell membrane which run, and rapidly transmit the electrical stimulus, into the interior of the cell. This ensures the entire depth of the cell is activated synchronously, even though it's the external membrane that relays the signal to contract.

Action Potential in Cardiomyocytes

Resting potential of a ventricular contractile cell = -90mV (Atrial cell = -80mV, same principles apply). An action potential begins when the membrane of the ventricular muscle cell is brought to threshold, usually at about -75mV. Threshold is normally reached next to an intercalated disc. Typical stimulus is excitation of an adjacent muscle cell. Once threshold has been reached: 1) Rapid depolarisation: At threshold, voltage-gated Na+ channels open. Na+ influx depolarises the membrane and triggers the opening of more Na+ channels - positive feedback response. These are called fast channels because they open quickly and only for a few milliseconds. 2) Plateau: When transmembrane potential peaks at +30mV, the voltage-gated Na+
channels close, and Ca2+ channels open. These are called slow calcium channels because they open slowly and remain open for a relatively long period. These pump calcium into the sarcoplasm, whilst Na+ is actively pumped out. Transmembrane potential remains near 0mV for an extended period. Plateau decreases slightly due to some leakage of K+, although most potassium channels remain closed. A plateau is not present in skeletal muscle fibre. 3) Repolarisation: Slow calcium channels begin closing, and slow potassium channels begin opening. K+ rushes out of the cell, and net result is a period of rapid repolarisation that restores the resting potential. Intracellular Ca2+ is absorbed by the sarcoplasmic reticulum or pumped out of the cell. The refractory period is the time after an action potential when the membrane will not respond normally to a second stimulus. The absolute refractory period is when the

membrane cannot respond at all, and lasts 200ms, spanning the duration of the plateau and the initial period of repolarisation. This is due to Na+ channels either being open or closed and inactivated. This is followed by the relative refractory period, which lasts for 50ms. Na +
channels are closed but may open in response to a stronger-than-normal stimulus. Summation is not possible in cardiac muscle.

Role of Calcium in Cardiac Contractions Contraction is produced by an action potential causing an increase in the concentration of Ca2+ around the myofibrils. This pathway is called excitation-contraction coupling. This occurs in 2 steps: 1) 20% of calcium needed for contraction comes from calcium entering the cell membrane during the plateau phase of the action potential. 2) The arrival of this extracellular Ca2+ triggers the release of additional Ca2+ from reserves in the sarcoplasmic reticulum. Therefore, cardiac muscle tissue is highly sensitive to changes in the Ca2+ concentration of extracellular fluid. Actin = Made up of 2 helical strands of globular actin molecules (G actin)which twist around each other. Each molecule of G actin has an ATP molecule attached. The whole assembly of actin molecules is called F-actin (fibrous actin). Actin filaments consist of F-actin and also 2 accessory proteins; tropomyosin and troponin. Tropomyosin forms 2 helical strands which are wrapped around the F-actin, and it switches on and off the contraction mechanism. Troponin is a globular protein which binds to calcium ions and to tropomyosin. Myosin = Made up of a long rod-shaped region called a myosin rod, with myosin globular heads at intervals along the filament. The heads attach to actin filaments during contraction. When the muscle is at rest, tropomyosin blocks the site to which myosin attaches. Actin is in the 'off' position. When Ca2+ is released, they bind to cTnC (cardiac troponin C, causing troponin and the tropomyosin that it's attached to, to move away from the myosin binding site. The actin is now in the 'on' position. Actin is then able to bind to myosin by forming a cross bridge. When excitation of the muscle by nerve impulses ceases, Ca2+ ions are pumped by active transport back into the sarcoplasmic reticulum by a calcium pump located in the sarcolemma. This also requires ATP. The muscle then relaxes. In the heart, the strength of contraction is regulated by varying the intracellular Ca2+
concentration during activation of the cells, or by altering the sensitivity of the myofilaments to Ca2+.

Autonomic Innervation The heart receives dual innervation. Acetylcholine released by postganglionic fibers of the parasympathetic division causes a reduction in heart rate. Whereas, noradrenaline released by varicosities of the sympathetic division accelerates heart rate. Because autonomic tone is present, small amounts of both of these neurotransmitters are released continuously. However, under resting conditions parasympathetic innervations dominates, which is why the resting heart rate is below 80-100bpm.


Why does cardiac pain spread to the left arm?

[3] The

heart is insensitive to touch, cutting, cold, and heat; however, ischaemia and the accumulation of metabolic products stimulate pain endings in the myocardium. The afferent pain fibers run centrally in the middle and inferior cervical branches and especially in the thoracic cardiac branches of the sympathetic trunk. The axons of these primary sensory neurons enter spinal cord segments T1-T4/T5, especially on the left side. Cardiac referred pain is where noxious stimuli originating in the heart are perceived by a person as pain arising from a superficial part of the body - eg. the skin on the left upper limb. Often, the lateral cutaneous branches of the 2nd and 3rd intercostals nerves join or overlap in their distribution with the medial cutaneous nerve of the arm. Consequently, cardiac pain is referred to the upper limb because T1-T3 are also common to the visceral afferent terminations for the coronary arteries.

What is an ECG?
An electrocardiogram detects the electrical activity of the heart. It may be used in the case of; chest pains, shortness of breath, abnormal heart rhythm, loss of consciousness, and collapse. The atria are smaller than the ventricles, so the wave produced on ECG for the atria is smaller than for the ventricles.

QRS waves collectively form the QRS complex. Rules of QRS complex:
- First deflection downwards = Q wave.
- Upward deflection = R wave.
- Any deflection below the baseline following the R wave = S wave. P-R interval = Time taken for excitation to spread through atria and ventricles. R-R interval = Time for one cardiac cycle. QRS duration = Time for excitation to spread through the ventricles. Electrical signals from the heart are detected through electrodes at the body surface. The patient must lie very still, and there must be good electrical contact between the skin and electrodes.

ECG Chest Leads

V1 & V2 = Right ventricle. V3 & V4 = Ventricular septum. V5 & V6 = Anterior & Lateral wall of left ventricle.

ECG Limb Leads

Example ECGs Sinus Rhythm (normal):

Sinus Arrhythmia:

Atrial fibrillation:

- No 'P' waves on ECG.
- Irregularly irregular pulse.
- Danger of clot formation. Ventricular fibrillation:Fatal. Patient loses consciousness.

- QRS complex of normal shape.
- Atria not beating in harmony.
- Common causes: Myocardial ischaemia, MI.

- No recognisable ECG pattern.
- Advanced Life Support needed.

How is cholesterol transported and used in the body?
All animal cell membranes contain the steroid, cholesterol. Cholesterol serves as:
- Waterproofing for the epidermis.
- Lipid component of all cell membranes.
- A key constituent of bile.
- Precursor of several steroid hormones.
- Precursor of Vitamin D3.

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