Term
| Heart Contraction and Relaxation - the Cardiac Cycle |
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Definition
| Nearly all the pumping action of the heart is due to ventricular contraction. The heart function so that blood rushes from the veins through the open atria and on into the ventricles. The atria then contract, and force a litle more blood into the ventricles. The atria relax, then the ventricles contract vigorously, forcing the blood into the pulmonary and systemic circuits. Finally, ventricles relax, and the cycle is repeated. |
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Term
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Definition
| The sequental and synchcronized contraction (systole) and relaxation (diastole) of the atria and ventricles, along with opening and closing of properly functioning valves allows the heart to propel blood to all areas of the body - quickly and repeatedly throughout our lives. |
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Term
| Synchronization of the heart Beat Sinoatrial node (or S-A node) |
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Definition
| Although the heart consists of two pumps, the atria and ventricles are under a common control mechanism that regulates and synchronizes their contraction (systole) and relaxation (diastole) during the cardiac cycle. These chambers beat in response to electrical signals generated by rhythmic depolarization of a special region in the posterior wall of the right atrium below the opening of the superior vena cava. The region is often called the pacemaker, also known by its name, Sinoatrial node |
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Term
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Definition
| the atria and ventricles are relaxed. This state is called diastole. The mitral and tricuspid valves (the A-V valves) are wide opened, the aortic and pulmonary semilunar valves are closed. The pressure in the venae cavae and atria is slightly higher than in the ventricles. Therefore, blood rushes from the venae cavae into the atria and on into the ventricles. About 70% of the ventricular filling occurs during this phase. |
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Term
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Definition
| the atria contract, forcing the remaining 30% of the blood into the ventricles. The atria then relax, a stage known as atrial diastole. |
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Term
| Stage 3. Isovolumic ventricular contraction |
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Definition
| This is the first phase of ventricular systole. When the ventricles contract, pressure rises in their interiors and exceeds the pressure in the atria. This causes the A-V valves to close, which occurs passively in response to the pressure differential. As the ventricles contract, the papillary contract, pulling on and tensing the chordae tendineae. this prevents the A-V valves from turning inside out into the atria. The ventricles continue to contract with all four valves closed, raising the pressure still more. |
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Term
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Definition
| pressure in the ventricles reaches the point where it exceeds the pressure in the pulmonary arteries and aorta The semilunar valves open passively, and blood is ejected from the ventricles into the pulmonary and systemic circuits, at first rapidly, then at a reduced rate. As blood is ejected, the pressure in the ventricles starts to fall, an effect that is accentuated when the ventricles cease to contract and enter the phase known as ventricular diastole. |
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Term
| Stage 5. Isovolumic relaxation |
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Definition
| pressure in the ventricles drops below the pressures in the pulmonary arteries and the aorta. the result is that the semilunar valves to close passively. The pressure in the continues to fall. At this stage, all four valves are closed |
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Term
| Stage 6. Onset of filling |
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Definition
| once the pressure in the ventricles falls below the pressure in the atria, the A-V open, allowing blood to rush into them and on into the relaxed ventricles. Filling with blood is at first rapid, then its rate is reduced. This phase of reduced filling is sometimes called diastasis |
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Term
| Blood Pressure: Sphygmomanometer manometer systolic pressure |
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Definition
| Consists of a inflatable bag contained in an inextensible cuff. The cuff is wrapped around the arm (occasionallly the thigh), and inflated to a pressure somewhat in excess of arterial systolic pressure. This pressure is determined by a measureing device called a manometer. The pressure is then released slowly. When the pressure falls just below the systolic level, small spurts of blood escape through the brachial artery. They either be detected by palpating the radial artery at the wrist, or by listening with a stethoscope applied to the skin of the antecubital space over the brachial artery. This latter method is called auscultation. The sounds that are first heard are called Korotkoff sounds. The Korotkoff sounds disappear once the cuff pressure drops below diastolic pressure. |
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Term
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Definition
| occurs at the onset of ventricular systole. It is due to the closure of the A-V valves (the mitral and tricuspid valves) and the tensing of the chordae tendineae. The mitral valve closes slightly ahead of the tricuspid valve, generating two components to S(1) that are called M(1) and T(1) |
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Term
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Definition
| occurs when the semilunar valves close, and marks the end of ventricular systole. The aortic valve closes slightly ahead of the pulmonic valve, generating two components to S(2) that are called A(2) and P(2) |
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Term
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Definition
| are abnormal sounds that may be heard during ventricular systole or diastole. |
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Term
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Definition
| A systolic murmur can occur when the tricuspid or mitral valves do not close properly during systole. This causes blood to regurgitate into the corresponding atrium during ventricular systole and during isovolumic ventricular relaxation, a time when A-V valves should be tightly closed. |
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Term
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Definition
| can occur when the aortic or pulmonic valves do not close properly. This allows blood to regurgitate into the ventricles during ventricular diastole, a time when the aortic and pulmonic valves should be tightly closed |
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Term
| Source of Energy for Cardiac Muscle |
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Definition
| In cardiac muscle, fatty acids are the preferred source of energy Cardiac muscle also uses lactic acid as an energy source (it converts it to pyruvic acid). This is very useful, because during heavy exercise, skeletal muscle produces large amounts of lactic acid, ad some of this is utilized by he heart. The glycogen stored in cardiac muscle is primarily used as a reserve. It can be mobilized by sympathetic stimulation of the heart. |
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Term
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Definition
| end diastolic volume - end systolic volume |
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Term
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Definition
| systolic aortic pressure - diastolic aortic pressure |
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Term
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Definition
| diastolic aortic pressure + 1/3 pulse pressure |
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Term
| Total peripheral resistance |
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Definition
| mean blood pressure / cardiac output |
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Term
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Definition
| heart rate x stoke volume |
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Term
| Mean arterial (blood) pressure = |
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Definition
| total peripheral resistance x cardiac output |
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Term
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Definition
| stroke volume/ end diastolic volume a low ejection fraction (e.g. 0.4) indicates that the heart is pumping inefficiently and may be failing. |
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Term
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Definition
| is the amount of blood pumped by the blood per minute. Therefore it is a very important index of the function of the heart. During a heart attack, for example, there is usually a drop in the cadiac output |
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Term
| Factors that determinates of cardiac output |
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Definition
| preload afterload heart rate myocardial contractility |
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Term
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Definition
| the amount of blood returning to the heart (end diastolic volume) (inflow) |
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Term
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Definition
| the resistance to ejection of blood from the ventricles (outflow) |
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Term
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Definition
| strength of cardiac muscle contraction |
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Term
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Definition
| the more that returns to the heart while the heart is in diastole, the greater will be the filling of the ventricles, the greater will be their end-diastolic voulume. this means that their walls will be stretched. The volume or stretching factor is called the PRE-LOAD, because it is a load applied to the heart before the ventricles contract. An increase in preload increases the force of contraction and increases the stroke volume. Muscles fibers that are stretched (provided the stretching is not excessive) contract more forcefully |
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Term
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Definition
| the resistance to ejection of blood from the ventricles is called the AFTERLOAD, because it is a load that occurs after the ventricles have started to contract. |
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Term
| For the left ventricle, the resistance to ejection (afterload) is affected by the: |
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Definition
| Pressure in the aorta Total peripheral resistance Pathological changes |
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Term
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Definition
| the higher the pressure, the higher the resistance, and the tougher it is for the heart to pump against it (like pumping up a bicycle tire) |
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Term
| Toral peripheral resistance |
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Definition
| determined by the arteriole diameters, and therefore by vasoconstriction (like blowing through a narrow tube compared with a wide tube |
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Term
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Definition
| that lead to a narrowing (stenosis) of the aortic valce or narrowing (stenosis) of the aorta itself - the effect is similar to an increase in total peripheral resistance |
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Term
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Definition
| Since cardiac outpur is the heart rate multiplied by the stoke volume, any factor that changes the heart rate is likely to change the cardiac output. The heart rate doubles during exercise (from 60 to 120 beats per minute). However, the cardiac output more that doubles because of an increased stroke volume, and goes up from 5.52 liters per minute to 13.74 per minute |
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Term
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Definition
| is the force of contraction of the cardiac muscle at a given fiber length Myocardial contractility does not change during the operation of Starling’s law of the Heart, which is the result of increased force of contraction when the fibers increase in length during streching |
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Term
| Myocardial contractility is increased by number of factors |
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Definition
1 Norepinephrine and epinephrine (increase the heart rate as well)
2 Increased extracellular calcium.
3. Digitalis, which increases intracellular calcium. |
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Term
| Heart: Sympathetic Branch |
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Definition
| The heart is innervated by postganglionic sympathetic nerve that release the neurotransmitter norepinephrine, which binds to Beta-adrenergic receptors in the myocardial cell membranes |
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Term
| Sympathetic stimulation acts on two regions of the heart: |
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Definition
1. Sinus node, causing the hate to increase
2. Cardiac muscle of the ventricles (and of the atria), causing it to increase its contractile force. An increase in contractile force is spoken of as an increase in myocardial contractily. An increase of myocardial contractility will usually increase the the stroke volume, because the end-systolic volume is diminished by the more forceful systole of the ventricles. this will increase cardiac output |
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Term
| Parasympathetic Branch: Heart |
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Definition
| parasympathetic nerve fibers from the left and right vegus (X) nerves innervate mainly the sinus and A-V nodes (not the ventricular myocardium), and cause the heart to beast more slowly The preganglionic parasympathetic nerve ending release acetylcholine, which binds to nicotinic receptors on postganglionic (intramural) neurons found in the heart. these postganglionic neurons also release acetylcholine, which binds to muscarinic receptors on the membranes of the pacemaker cells. |
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Term
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Definition
| block muscarinic receptors (acetylcholine) |
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Term
| Vasomotor center or cardiac center |
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Definition
| Cental control of the heart is primarily from a region of the medulla. Output from this center controls both sympathetic outflow to the heart and the flow nerve impulses down the vagus nerve. In turn, the vasomotor center is under higher control from many areas of the brain, including the hypothalamus, reticular from of the brain stem, and the limbic system. |
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Term
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Definition
| 1) Accelerates heart rate (SA node) 2) Increases force of contraction of the ventricular myocardium. 3) Norepinephrine is released at sympathetic nerve terminals and acts on Beta-adrenergic receptors in the pacemaker cells of the sinoatrial node and on cardiac muscle cells of the ventricles. 4) Action of norepinephrine (and epinephrine) on the heart is blocked by Beta-blockers |
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Term
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Definition
1) Slows heart rate (SA node)
2) Does not alter force of contraction of ventricles because it doesn’t innervate them
3) Acetylcholine is released at parasympathetic nerve terminals and acts on nicotinic receptors on intramural neurons which also release acetylcholine, which binds to muscarinic receceptors in the pacemaker cells of SA node.
4) Muscarinic receptors are blocked by atropine |
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