Cardiac Mechanics Flashcards

1
Q

What prompts myocyte contraction and how is it different to skeletal muscle?

A

Contraction prompted when an electrical event induces calcium influx and release leading to contraction. The rise and fall in calcium levels is known as calcium transience. Electrical event couples to contractile event and hence system known as excitation-contraction coupling. Contractility of cardiac muscle relies on external calcium influx whereas skeletal muscle relies on internal calcium stores in sarcoplasmic reticulum.

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2
Q

Describe single ventricular cell structure

A

Ventricular cells 100 μm long and 15 μm wide. T-tubules (transverse tubules) are finger-like invaginations of the cell surface. T-tubule openings are up to 200 nm in diameter. Spaced (approx. 2 μm apart) so that a T-tubule lies alongside each Z-line of every myofibril. Carry surface depolarisation deep into the cell to allow synchronous activation and contraction.

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3
Q

Describe composition of a single ventricular cell

A

Myofibrils make up 46% of cell and are contractile part of cell. Mitochondria makes up 36% of cell. SR makes up 4% of cell. Nucleus makes up 2% of cell.

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4
Q

Describe process of excitation-contraction coupling

A
  1. Surface depolarisation occurs and travels deep into tissue through T-tubules.
  2. LTCC senses this depolarisation and undergoes a confirmational change, allowing calcium to enter the cell.
  3. Calcium from outside the cell enters the cell, moving down its concentration gradient, into the cytosol.
    This calcium can either directly bind to the myofibrils or, as is its main purpose, bind to SR calcium release channels.
  4. SR calcium release channels are ligand operated and open up in response to calcium binding to them. Once calcium binds to them, calcium efflux from SR occurs and cytosol Ca concentrations increase. These then bind to the troponin on myofibrils and cause contraction.
  5. Calcium then actively transported into the SR by SR ATPase and stored – brings about relaxation. The calcium that entered from T-tubule effluxed by sodium/calcium exchanger in T-tubule membrane which uses energy of sodium moving into cell down conc grad to remove calcium from cell. Hence, in steady state, there is neither a gain nor loss of calcium from cell as amount removed is equal to amount allowed in.
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5
Q

Describe relationship between force production and intracellular Ca2+

A

A sigmoidal relationship exists between force produced and cytoplasmic calcium concentration. The amount of calcium that influxes into a cell can be controlled and so amount of force produced can also be altered. In some scenarios, such as if a sympathetic response occurs, some proteins within the myocyte can undergo phosphorylation to increase calcium influx.

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6
Q

Describe the length-tension relation in cardiac muscle

A

Active force production is a result of cross-bridge production and muscle length determines amount of force produced. Greater the muscle length, greater the active force produced but proportional increase in passive force with increasing length. This is because cardiac muscle cells and tissues have a degree of elasticity and so when stretched, will tend to recoil a little.

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7
Q

What are the differences in how skeletal muscle responds to increasing length compared to cardiac muscle?

A

Cardiac muscle more resistant to stretch and less compliant than skeletal muscle due to properties of its extracellular matrix and cytoskeleton. Hence, greater passive force produced when cardiac muscle increases in length whereas skeletal muscle doesn’t produce much passive force.

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8
Q

How does force produced by muscle change with muscle length?

A

In cardiac muscle, with muscle length, passive force also increases by a significant and proportional amount. Total force is the sum of the active and passive elements. However, past a certain optimum length, active force decreases by a large amount and so does total force. Only ascending limb of the relation is important for cardiac muscle as cardiac muscle can’t overstretch as it is contained within the pericardial sac.

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9
Q

What are the 2 forms of contraction the heart uses?

A

Isometric and isotonic. Isometric contraction occurs when muscle fibres do not change length but pressures increase in both ventricles. Isotonic contraction occurs when shortening of fibres happens and blood is ejected from ventricles.

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10
Q

What is preload and afterload?

A

Preload is the weight that stretches muscle before it is stimulated to contract. Afterload is when the muscle actually contracts against the weight - this is when weight and resistance become apparent.

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11
Q

What type of contraction is used in preload and afterload?

A

Preload involves isomteric contraction as ventricles stretch, filling with blood during diastole. Force increases as preload increases up to a certain point, beyond which force decreases as preload increases. Afterload uses isotonic contraction.

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12
Q

What are in-vivo correlates of preload?

A

As blood fills the heart during diastole, it stretches the resting ventricular walls. This stretch (filling) determines the preload on the ventricles before ejection. Preload is dependent on venous return. Measures of preload include end-diastolic volume, end-diastolic pressure and right atrial pressure.

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13
Q

What are in vivo correlates of afterload?

A

Afterload is the load against which the left ventricle ejects blood after opening of the aortic valve. Any increase in afterload decreases the amount of isotonic shortening that occurs and decreases the velocity of shortening. Measures of afterload include diastolic blood pressure.

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14
Q

What is the Frank-Starling relationship and what is a consequence of it?

A

Increased diastolic fibre length increases ventricular contraction. Hence, ventricles pump greater stroke volume so that, at equilibrium, cardiac output exactly balances the augmented venous return.

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15
Q

What are the causes of the Frank-Starling relationship?

A

Two potential causes. The first is, at shorter lengths than optimal the actin filaments overlap on themselves so reducing the number of myosin cross bridges that can be made. The second is that there are changes in the Ca2+ sensitivity of the myofilaments. Mechanism still unclear but 2 proposed theories.

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16
Q

What are the proposed theories for change in Ca2+ sensitivity of myofilaments?

A

The first is, at longer sarcomere lengths the affinity of TnC for Ca2+ is increased due to conformational change in protein. This means less Ca2+ required for same amount of force at longer length. The second is that with stretch the spacing between myosin and actin filaments (so-called “lattice spacing”) decreases. With decreasing myofilament lattice spacing, the probability of forming strong binding cross-bridges increases and so this produces more force for the same amount of activating calcium.

17
Q

What is the definition of stroke work?

A

Work done by heart to eject blood under pressure into aorta and pulmonary artery.

18
Q

What is the equation for stroke work?

A

volume of blood ejected during each stroke (SV) multiplied by the pressure at which the blood is ejected (P). Preload and afterload greatly influence stroke volume. Cardiac structure greatly affects pressure.

19
Q

What is the law of LaPlace?

A

When the pressure within a cylinder is held constant, the tension on its walls increases with increasing radius. Hence, derived equation is:
Wall tension = Pressure in vessel x Radius of vessel
Incorporating wall thickness, this can be amended to:
T= (PxR)/h

20
Q

How does the law of LaPlace influence structure of the heart?

A

Radius of curvature of walls of LV less than that of RV allowing LV to generate higher pressures with similar wall stress.