Heart

• The heart, approximately the size of a fist, is located in the mediastinum between the second rib and the fifth intercostal space, on the superior surface of the diaphragm, two-thirds to the left of the midsternal line, and anterior to the vertebral column, posterior to the sternum.
• The heart is enclosed in a pericardium, a double-walled sac.
• Atrial fibrillation occurs when the atria beat irregularly and often too fast.
• Atrial fibrillation is a condition where the heart beats irregularly and often too fast.
• The point of maximal intensity (PMI) is located in the diaphragm.
• The heart has a superficial fibrous pericardium that protects, anchors, and prevents overfilling.
• The heart has a deep two-layered serous pericardium, with the parietal layer lining the internal surface of the fibrous pericardium and the visceral layer (epicardium) on the external surface of the heart, separated by a fluid-filled pericardial cavity that decreases friction.
• The myocardium consists of spiral bundles of cardiac muscle cells and a fibrous skeleton of the heart, a crisscrossing, interlacing layer of connective tissue that anchors cardiac muscle fibers, supports great vessels and valves, and limits the spread of action potentials to specific paths.
• The endocardium is continuous with the endothelial lining of blood vessels, the innermost layer of the heart's walls.
• Atria contract, forcing additional blood into ventricles.
• Desmosomes resist cellular separation and cell disruption, contribute to the stability of the cells and tissue, and provide cellular support of cardiac muscle from pulling apart during contraction.
• Intercalated discs are junctions between cells that anchor cardiac cells and contribute to the stability of the cells and tissue.
• A gap junction or nexus is a junction that allows different molecules and ions, mostly small intracellular signaling molecules (intracellular mediators), to pass freely between cells.
• As ventricles relax and intraventricular pressure falls, blood flows back from arteries, filling the cusps of semilunar valves and forcing them to close.
• Desmosomes prevent cells from separating during contraction and contribute to the stability of the cells and tissue.
• Atrioventricular valves close.
• Pulmonary trunk
• Ventricles contract, forcing blood against atrioventricular valve cusps.
• Semilunar valves closed.
• The five most important kinds of cell junctions are: tight junctions, adherens junctions, desmosomes, hemidesmosomes, and gap junctions.
• Blood returning to the heart fills atria, putting pressure against atrioventricular valves; atrioventricular valves are forced open.
• As ventricles contract and intraventricular pressure rises, blood is pushed up against semilunar valves, forcing them open.
• Papillary muscles contract and chordae tendineae tighten, preventing valve flaps from everting into atria.
• The heart muscle behaves as a functional syncytium.
• As ventricles fill, atrioventricular valve flaps hang limply into ventricles.
• Semilunar valves open.
• Gap junctions allow ions to pass; electrically couple adjacent cells and dictate the speed and direction of cardiac conduction.
• Cardiac reserve is the ratio between the maximum cardiac output a person can achieve and the cardiac output at rest.
• The sympathetic nervous system is activated by emotional or physical stressors, causing norepinephrine to cause the pacemaker to fire more rapidly and increasing contractility.
• The heart at rest exhibits vagal tone (parasympathetic).
• Three main factors affect stroke volume: preload, contractility, and afterload.
• Blood pressure in the aorta is 120mm Hg and in the pulmonary trunk is 30mm Hg.
• Isovolumetric relaxation occurs in early diastole, causing the ventricles to relax and closing the dicrotic notch.
• Differences in ventricle wall thickness allow the heart to push the same amount of blood with more force from the left ventricle.
• Maximal CO may reach 35 L/min in trained athletes.
• Atrial (Bainbridge) reflex is a sympathetic reflex initiated by increased venous return, stimulating the SA node and atrial stretch receptors.
• Venous return increases during slow heartbeat and exercise, increasing venous return and distending (stretching) the ventricles, which increases contraction force.
• Cardiac Output (CO) is the volume of blood pumped by each ventricle in one minute, calculated as heart rate (HR) x stroke volume (SV).
• Regulation of the cardiac output is calculated as CO = HR X SV.
• Hormones such as epinephrine from the adrenal medulla enhance heart rate and contractility, while thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine.