Cardiac Myocyte and Cardiac electrophysiology Flashcards

(49 cards)

1
Q

Where is the heart located?

A

Thoracic cavity medial to the lungs,posterior to breastbone

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2
Q

What are the three layers of the heart?

A

Epicardium
Myocardium
Endocardium

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3
Q

What is the epicardium?

A

Thin layer of serous membrane that helps protect and lubricate the outside of the heart

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4
Q

What is the myocardium?

A

Muscular middle layer of heart
contains cardiac muscle tissue
Makes up thickness of the heart and is responsible for pumping blood

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5
Q

What is the endocardium?

A

Simple Squamous endothelium layer that lines inside of the heart.
Stops blood from sticking inside the heart (which could cause blood clots)

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6
Q

What are the 4 chambers of the heart?

A

Right Atrium
Right Ventricle
Left Atrium
Left Ventricle

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7
Q

What is the role of the atria?

A

Receiving chambers of the heart
Connected to veins that carry blood to the heart

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8
Q

What is the role of the Ventricles?

A

Larger, stronger pumping chambers that send blood out the heart through the arteries

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9
Q

Why is the right side ventricle myocardium thinner than the left?

A

Sends blood to the nearby lungs compared to whole body

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10
Q

What is the role of the heart (atrioventricular) valves?

A

Prevent blood flowing back (regurgitating)
Located in the middle of atrium and ventricles

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11
Q

Which valve is in between the right atrium and ventricle?

A

Tricuspid valves (three flaps)

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12
Q

Which valve is in between the left atrium and ventricle?

A

Mitral valve/bicuspid valve

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13
Q

What controls the valves (connected to them?)

A

Chordae Tendineae

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14
Q

What are the semilunar valves?

A

Named after their crescent moon shaped cusps
Located between ventricles and arteries that carry blood away from heart

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15
Q

Right side semilunar valve?

A

Pulmonary Valve
Prevents backflow from pulmonary trunk into ventricles

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16
Q

Left side semilunar valve?

A

Aortic valve
prevents aorta sending blood back

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17
Q

How do they close?

A

They are smaller- no chordae tendineae
Rely on blood pressure to snap shut
Are cup shaped

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18
Q

Blood flow through heart

A

(superior+inferior) Vena Cava—> right atrium—-> tricuspid valve—-> right ventricle—-> pulmonary semilunar valve—-> pulmonary trunk—-> lungs—–> Pulmonary vein—-> left atrium—-> bicuspid valve—–> left ventricle—-> aortic semi lunar valve—-> aorta—–> whole body

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19
Q

What is the sinoatrial node?

A

Pacemaker cells located in the upper wall of the right atrium, at junction where superior vena cava enters

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20
Q

How are they special?

A

They have natural automaticity- generate their own impulses

21
Q

What is the Atrioventricular node?

A

Where the electrical impulses that have spread across the atria converge
Located near the AV septum (near openings of coronary sinus)

22
Q

How is the AV node special?

A

Delays impulses by 120 ms to ensure atria can completely eject blood into ventricles before ventricular systole

23
Q

What is the AV bundle?

A

(Bundle of His) continuation of the specialised tissue of the AV node
transmits electrical impulse from AV node to Purkinje fibre in ventricles

24
Q

How does it (AV Bundle) split?

A

Goes down membranous part of intraventricular septum
divides into right bundle branch and left bundle branch

25
What are the purkinje fibres?
Sub endocardial plexus of conduction cells Lots of glycogen lots of gap junctions Transmit cardiac action potentials from AV bundle to Myocardium of ventricles
26
What does this allow for?
Coordinated Ventricular contraction (systole) Moves blood from ventricles to leaving blood vessels
27
What overrides the intrinsic AV node and purkinje fibre pacemaker activity?
SA node
28
Sequence of electrical events?
SA----> Atrial contraction--->AV node signal delay----> Bundle of his conduction----> His and purkinje fibre signal spread---> ventricular systole
29
Pacemaker potential
Occurs at end of one action potential and just before start of next Slow depolarisation of pacemaker cells (SA) towards depolarisation called a funny current (or IF)
30
How is pacemaker potential achieved?
Activation of HCN channels (Hyper Polarisation activated cyclic nucleotide gated channels) Allow Na+ entry into cells-ensures slow depolarisation Channels activated at membrane potentials more negative than -50mV
31
Action potential in SA node
Once HCN has brought membrane potential to -40mV, Ca2+ voltage gated channels open Produces faster rate of depolarisation for positive membrane depolarisation HCN channels inactivate At peak of actionpotential, Ca2+ channels inactivate-K+ channels open
32
What effect does opening k+ channels have?
Movement of K+ causes repolarisation
33
What is different in the SA node actional potential?
Opening of CA 2+ channels are not sustained- no plateau so action potential is triangular in shape
34
What are gap junctions?
Regulated pores that exist between cardiac myocytes Made of connexins which form a unit called connexon
35
Where are connexons embedded?
Plasma membrane of adjacent cells located at either end of cell at region of intercalated disks Connecting connexons allows for cytosol of two cells to mix
36
Allowing cytosol to mix freely is helpful because?
Ions easily pass from cell to cell-electrically coupled
37
What does electric coupling ensure?
Synchronised heart activity large electrochemical gradient lots of passive diffusion Unidirectional spread of action potential
38
What makes cardiac action potential different from other action potential?
Duration is longer (200-400 ms) Calcium ions play a large role in depolarization Calcium influx prolongs duration of action potential
39
Phase 4 in non pacemaker cells
Phase 4- true resting membrane potential (-90mV) due to potassium channels being open (positive K+ leaves cell making membrane potential) (Fast sodium channel and slow l type calcium channel closed)
40
Phase 0 in non pacemaker
Rapidly depolarised to around -70 Due to increase in fast sodium channel Potassium channels close Conductance changes move membrane potential away from EK (negative) to equilibrium potential for sodium
41
Phase 1-Notch
Transient opening og K+ channels rapidly repolarise cell. Set membrane potential of plateau phase More K+: more repolarisation-plateau at lower voltages Less K+: less repolarisation- plateau at higher voltages
42
Phase 2 of non pacemaker cells
L-Type Ca 2+ channels in t tubules penetrating cell Channels close to Sarcoplasmic reticulum Ca 2+ entering them bind to ryanodine receptor Calcium induced calcium release Essential for excitation contraction coupling of cell Ca binds to troponin C causing muscle contraction
43
Phase 3 non pacemaker
As Ca2+ channels close, K+ channels repolarise the cell-driving membrane potetial towards equillibrium K Membrane potential more negative
44
Cardiac Myocyte
specialized muscle cell myocyte-> myofibril-> myofilaments Have sarcomeres within it
45
cardiac excitation-contraction coupling
1)Action potentials traveling along the sarcolemma and down into the transverse tubule (T-tubule) system depolarize the cell membrane. 2) Voltage-sensitive dihydropyridine (DHP) receptors (L-type calcium channels) open to permit calcium entry into the cell during phase 2 of the action potential. 3)Calcium influx triggers a subsequent release of calcium that is stored in the sarcoplasmic reticulum (SR) through calcium-release channels ("ryanodine receptors"), and increases intracellular calcium concentration from about 10-7 to 10-5 M 4) Free calcium binds to troponin-C (TN-C) that is part of the regulatory complex attached to the thin filaments. When calcium binds to the TN-C, this induces a conformational change in the regulatory complex such that troponin-I (TN-I) exposes a site on the actin molecule that is able to bind to the myosin ATPase located on the myosin head. This binding results in ATP hydrolysis that supplies energy for a conformational change to occur in the actin-myosin complex. The result of these changes is a movement ("ratcheting") between the myosin heads and the actin, such that the actin and myosin filaments slide past each other thereby shortening the sarcomere length. Ratcheting cycles occur as long as the cytosolic calcium remains elevated 5) At the end of phase 2, calcium entry into the cell slows and calcium is sequestered by the SR by an ATP-dependent calcium pump (SERCA, sarco-endoplasmic reticulum calcium-ATPase), thus lowering the cytosolic calcium concentration and removing calcium from the TN-C. To a quantitatively smaller extent, cytosolic calcium is transported out of the cell by the sodium-calcium-exchange pump. Unbinding of calcium from TN-C induces a conformational change in the troponin complex leading, once again, to TN-I inhibition of the actin binding site. At the end of the cycle, a new ATP binds to the myosin head, displacing the ADP, and the initial sarcomere length is restored.
46
Cardiac Muscle
Long branching cells Less abundant SR Gap junctions and intercalated discs Myogenic Plateaud action potential 25-40% of cell volume
47
What is chronotrophy?
Rate the heart beats
48
Through which receptor does the parasympathetic system act to influence the heart
M2 ACHR
49
Which of these is not an action of the sympathetic nervous system (SNS) (fight or flight) on the heart?
Reduce AV delay