Manual of Equine Anesthesia and Analgesia. Группа авторов

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rich blood from the lungs is delivered to the left atrium via pulmonary veins.

       Ventricles

       The primary function is to pump blood into the high‐pressure systemic (left ventricle) and low‐pressure pulmonary (right ventricle) circulations.

       As described by the Law of LaPlace (see Table 3.1), the thick‐walled, conical left ventricle is better suited for high‐pressure pumping than the thin‐walled, flattened right ventricle.

Name of Law Formula Formula components Application
LaPlace T = P x R T = TensionP = pressureR = radius For any given pressure, the tension developed by the wall of the ventricle increases as the radius of the cylinder increases.
The left ventricle has a much greater radius than the right ventricle and thus is able to develop greater tension (or force).(LV = left ventricle; RV = right ventricle)
Ohm's Q=∆P/R Q = blood flow∆P = the pressure difference (P1‐P2) between the two ends of the vessel.R = resistance Blood flow is directly proportional to pressure difference and inversely proportional to resistance.
Thus, the difference in pressure between the two ends of the vessel determines the rate of flow and not the absolute pressure in the vessel.
Poiseuille’s Q=π∆Pr4 / 8ηl Q = blood flow∆P = the pressure gradientr = the radius of the vesselη = the viscosity of the bloodl = the length of the vesselπ relates to the vessel radius Blood flow is directly proportional to the 4th power of the radius of the vessel as long as the flow is laminar.Slight changes in the diameter of a vessel cause tremendous changes in flow because blood flowing in the middle of the vessel flows freely, whereas blood at the periphery flows slowly because of friction caused by the endothelium of the vessel wall. In a small vessel, a large percentage of the blood is in contact with the vessel wall so the rapidly flowing central stream of blood is absent.
Changes in vessel diameter greatly influence blood flow (Q).
Starling's None None Within physiological limits, stretched cardiac muscle (and other forms of striated muscle like skeletal muscle) will contract with greater force.
The force of contraction of the cardiac muscle is proportional to its initial length.When the diastolic filling of the heart is increased or decreased with a given volume, the displacement of the heart increases or decreases with this volume.Excessive stretch can result in decreased contractility.

       Atrio‐ventricular valves

       They connect atria and ventricles.

       Tricuspid valve is between the right atrium and right ventricle.

       Mitral valve is between the left atrium and left ventricle.

       Semilunar valves

       They connect ventricles to the outflow tracts.

       Aortic valve is between the left ventricle and aorta.

       Pulmonary valve is between the right ventricle and pulmonary artery.

      B Structural or “skeletal” components of the heart

       Myocardium – muscle layer (striated muscle) of atria and ventricles.

       Endocardium – internal lining of the heart chambers, valves and blood vessels.

       Epicardium – external lining of the myocardium, continuous with pericardium; secretes pericardial fluid.

      C Neural input to the heart

       Atria are highly innervated by sympathetic and parasympathetic fibers.Controls heart rate (HR) and contractility.Parasympathetic fibers – decrease rate and contractility.Sympathetic fibers – increase HR and contractility.

       Ventricles are primarily innervated by sympathetic fibers.They continually discharge to maintain a strength of ventricular contraction 20–25% greater than what would occur with no sympathetic input.

      II Cardiac contractions

      A Initiation

       Unlike most physiologic systems, neither the autonomic nor motor neurons are necessary for initiating cardiac contractions.

       The heart can continue beating in the absence of outside neural control because the cells of the specialized electrical conducting system of the heart are capable of automatic rhythmical depolarization or “self‐excitation.” This is due to:Cell membranes that are “leaky” or permeable to sodium ions.Increased permeability to potassium and calcium ions also plays a role in the spontaneous depolarization of the pacemaker cells.A resting cell membrane potential that is not adequately negative to keep sodium channels closed.The resting membrane potential of cardiac conducting cells is −60 to −70 millivolts (mV) and that of the SA node is −55 to −60 mV (compared to −90 mV for other cell membranes).

       Sinoatrial (SA node)Has the fastest rate of spontaneous depolarization and is the pacemaker.Located at the junction of the cranial vena cava and the right auricle.

       Atrioventricular (AV) nodeSlows the rate of impulse transmission as it conducts impulses from the atria to the ventricles.

       Internodal

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