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This flow is turbulent rather than streamlined and generates sounds called Korotkoff sounds, which can be heard through the stethoscope. When the cuff pressure begins to fall below the systolic pressure in the artery, blood begins to flow to the arm through the partially collapsed artery. The pressure in the cuff is then released slowly.
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The cuff is placed on the upper arm and inflated to stop arterial blood flow to the arm from the brachial artery the high pressure in the cuff collapses the artery. Ventricular pressure continues to fall and once it has fallen below that in the atria, the AV valves open and ventricular filling begins again.īlood pressure is estimated using a stethoscope and a blood pressure cuff connected to a mercury sphygmomanometer. As the ventricular muscle relaxes, pressures in the ventricles fall below those in the aorta and pulmonary artery, and the aortic and pulmonary valves close. Finally, when the pressure in the left ventricle exceeds that in the aorta (and the pressure in the right ventricle exceeds that in the pulmonary artery), the aortic and pulmonary valves open and blood is ejected into the aorta and pulmonary arteries. This is the so-called isovolumic phase of ventricular contraction. But, until the pressure in the left ventricle exceeds that in the aorta (and pressure in the right ventricle exceeds that in the pulmonary artery), the volume of the ventricles can not change. Initially, as the ventricles begin to contract, the pressure in them rises and exceeds that in the atria. Atrial contraction is followed by contraction of the ventricles (ventricular systole). Filling of the ventricles is completed when the atria contract (atrial systole). Oxygenated blood from the lungs enters the left atrium and flows into the left ventricle through its open AV valve. Deoxygenated blood from the periphery enters the right atrium and flows into the right ventricle through its open atrioventricular (AV) valve. Ventricular contraction then pumps blood from the heart into circulation.ĭuring ventricular diastole, blood returns to the heart. The action potential, following the AV nodal delay, then spreads rapidly through the AV bundle and Purkinje fibers to excite both ventricles. This AV nodal delay allows for both atria to contract in unison, emptying their remaining blood content into the ventricles prior to ventricular contraction. Upon reaching the AV node, electrical transmission to the ventricles is delayed about 100 msec. The only electrical connection between the atria and the ventricles is the atrioventricular (AV) node.
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Once an action potential is generated by cardiac autorhythmic cells, the depolarizing potential is rapidly transmitted through both atria via gap functions and the interatrial conductive pathway, as well as to the secondary pacemaker of the heart, the atrioventricular node, along the internodal conductive pathway. The specialized cardiac muscle fibers of the sinoatrial (SA) node rhythmically produce action potentials (AP) that spread through the muscle fibers of the atria.