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Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Abnormal heart sounds
Normal heart sounds
Changes in pressure-volume loops
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Law of Laplace
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Cardiac conduction velocity
Electrical conduction in the heart
ECG normal sinus rhythm
ECG QRS transition
ECG rate and rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Control of blood flow circulation
Microcirculation and Starling forces
Blood pressure, blood flow, and resistance
Compliance of blood vessels
Laminar flow and Reynolds number
Pressures in the cardiovascular system
Resistance to blood flow
Action potentials in myocytes
Action potentials in pacemaker cells
Cardiac excitation-contraction coupling
Excitability and refractory periods
Cardiac excitation-contraction coupling is the relationship between electrical signals in the form of action potentials, and mechanical changes in the heart muscle cells, called cardiomyocytes, that causes them to contract.
Let’s start by looking at the structure of a cardiomyocyte. Cardiomyocytes have branches, and have intercalated disks along their edges which have small holes called gap junctions that allow ions to flow from one cardiomyocyte to the next. When a cardiomyocyte depolarizes, ions like calcium move from that cell into a neighboring cell, and these ions trigger depolarization to happen in that cell. This is what makes cardiomyocytes part of a “functional syncytium,” they’re like a little community of cells intimately working together. In addition, cardiomyocytes stay physically attached to one another through proteins called desmosomes, which are like staples that hold the cells together when they’re contracting. Another feature of cardiomyocytes are passageways called transverse tubules, or T-tubules. T-tubules are extensions of the outside environment. They increase the surface area of the cardiomyocyte and they look like the letter T, so it’s easy to remember their name. Think of a large walk-through aquarium: you can walk through tunnels and look at the sea creatures all around you, but you’re not in the water with them. Finally, there’s the sarcoplasmic reticulum, which is an organelle that stores intracellular calcium, the calcium that is sequestered inside the cell.
When a depolarization wavefront hits a cardiomyocyte, a few calcium ions flow through gap junctions, and if a threshold membrane potential is reached, then sodium channels start to open up. If there’s a depolarization, then ions start to move across the cell membrane, and that’s where the T-tubules play a key role. During the part of the cardiomyocyte action potential when calcium ions flow into the cell, the presence of T-tubules helps bring calcium deep into the cell. Once this extracellular calcium gets inside, it binds to the ryanodine receptors on the sarcoplasmic reticulum, which releases even more calcium into the cell - a process called calcium-induced calcium release. The calcium helps activate two contractile proteins, actin and myosin, which are called myofilaments, and are ultimately responsible for cell contraction, and that’s the key moment when the chemical signal is converted into a mechanical signal.
Cardiac excitation-contraction coupling is the process by which an electrical signal generated by the sinoatrial node (the heart's natural pacemaker) is converted into a mechanical force that makes the heart contract. It occurs in a series of events that include:
Excitation: The process by which an electrical signal causes calcium ions to enter the cell.
Calcium is released from the sarcoplasmic reticulum.
Myofilament activation: The released calcium ions bind to troponin C, which causes tropomyosin to move out of the way and expose binding sites on actin for myosin heads. With the help of ATP, the myosin heads then attach to the actin filaments and slide them past each other, shortening the sarcomere (the basic unit of muscle contraction) and leading to cardiac muscle contraction.
Relaxation: The calcium ions are removed from the cytosol by the sarcoplasmic reticulum, and tropomyosin returns to its position blocking the binding sites on actin. This prevents further interaction between myosin and actin, and the muscle relaxes.
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