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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
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More than a century ago, two physiologists, Otto Frank and Ernest Starling discovered that as the heart gets filled up with more blood during diastole, it contracts harder and pumps out more blood during systole. So they came up with the Frank Starling Law to explain this relationship.
To understand this relationship, let’s zoom into the wall of the ventricles. The bulk of these walls is made up of short, branched cardiac muscle cells packed one next to the other. Zooming in further, if we look inside the muscle cells, we see bundles of myofibrils, or long chains of sarcomeres. The sarcomere is the smallest structure in the muscle that is capable of contracting so it's considered the basic contractile unit of the muscle. The sarcomere has two Z discs that form its boundary and a M line in the middle. Attached to the Z disc are thin filaments made of actin protein. These actin filaments have structural polarity which means both ends of the filament look different. We can think of it like an arrow with the pointed end being the “minus end,” pointing towards the M line, and the tail end being the “plus end,” attached to the Z disc. Just like an arrow, the actin filament can only move in one direction: the direction it’s pointed at. Attached to the M line are the myosin filaments which are thick bundles of myosin proteins with two globular heads. During a muscle contraction, the myosin heads grabs onto the actin filaments, and pull them towards the M line which brings the two Z discs closer together.
Overall, the amount of tension developed, or the force of muscle contraction during systole, depends on the number of myosin heads that bind to actin. And this number directly depends on the length of the overlapping section between actin and myosin filaments. The length of the overlapping section depends on the overall length of the sarcomere. And the length of the sarcomere depends on how much blood fills the ventricle during diastole - because that affects how stretched out the overall muscle wall and each sarcomere within it end up being. This relationship is known as the cardiac length-tension relationship and it can be shown by this graph, with the sarcomere length or the ventricular end- diastolic volume on the x axis and the tension or pressure developed within the ventricle, during their contraction, or systole, on the y axis.
So let’s imagine that the ventricles are mostly empty, with almost no blood in them. This would mean that there’s nothing stretching the muscles in the ventricular wall, so the length of sarcomeres are really short. At this length, the two Z discs are pulled close to each and there’s not much room for further contraction. Furthermore, the actin filaments from each side of the sarcomere crosses the M line and overlap. Since actin can be pulled only in one direction- towards the midline, myosin has to attach and pull the actin filament with the right structural polarity: the one pointing in the same direction as that the myosin pulls. So, when the actin filaments overlap, myosin is prevented from binding to its own actin filament by the actin filament from the other side with the wrong polarity. As a result, very few myosin- actin attachments are made and the cells can contract only very weakly during systole. On the graph, we can see near the point of origin, the short length of myocardial fibers corresponds with a low contractile force.
The Frank-Starling mechanism is a physiological principle that explains how the heart responds to changes in venous return. Increases in venous return cause the heart's chambers to fill with more blood, which then causes the heart to stretch and contract more forcefully, and pump more blood out to the rest of the body. The Frank-Starling mechanism is named after physiologist Otto Frank and anatomist Ernest Starling, who first described it in 1899.
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