Glossary

= HHP621= = = =Definitions=
 * afterload**The amount of tension a muscle must build up before it can start to contract. For the heart, this is dependent on the aortic pressure. Before the ventricle can start to move blood through the aortic valve the pressure in the ventricle must equal that in the aorta.


 * aldosterone**Aldosterone is secreted by the zona glomerulosa of the adrenal gland. It causes the body to retain sodium and secrete potassium. It effects the distal tubule and collecting ducts of the kidney. It also effects the sweat and saliva glands. Its secretion is stimulated by...
 * ACTH adrenocorticotropic hormone.
 * angiotensin II.
 * elevated blood potassium levels.


 * angina pectoris**A suffocating pain (angina) of the chest (pectoris). Angina is a result of the oxygen demands of the heart not being met. This can be caused by increased oxygen demand or by decreased oxygen supply.


 * angina -- stable** Also known as angina of effort, this angina is caused when the demands of the heart increase (due to exercise or some other event) and the oxygen supply is unable to increase with it. The underlying cause is a narrowing of the blood vessels due to atherosclerosis.
 * Therapy.** Beta-blockers, calcium channel blockers, and organonitrates can be used. Beta-blockers are generally used to control the patient's blood pressure, with the organonitrates being used to alleviate specific attacks. Combined therapy with calcium channel blockers, or calcium channel blocker therapy by itself might be used depending on the indications and contraindications a given patient presents with and how they respond to therapy.


 * angina -- unstable** This is the most serious form of angina and can indicate an imminent myocardial infarction. Its onset is unpredictable and frequent. Vasospasm may contribute to the condition. Also small embolisms getting caught in the already atherosclerotic coronary vessels might be the underlying cause.
 * Therapy.** Drug treatment is similar to exercise induced angina. Beta-blockers, calcium channel blockers and organonitrates can all be effective. If there is a vasospastic component, beta-blockers should not be used. Heparin, aspirin, and surgical procedures (cardiac bypass or angioplasty) might be indicated.


 * angina -- variant** Also known as vasospastic or Prinzmetal's angina, it is caused by vasospasm of coronary vessels, causing a reduction in blood and oxygen supply to the heart. Atherosclerotic plaques may or may not be involved.
 * Therapy.** Vasodilators (i.e. nitrates and calcium channel blockers) should be used to treat this type of angina. Beta-blockers can actually //cause// vasospasm and are therefore contraindicated.


 * angiotensin** Angiotensin I is converted from angiotensinogen by renin. Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE).Angiotensin II is the active form. Its actions are...
 * vasoconstriction.
 * stimulates release of aldosterone.
 * stimulates release of ADH.
 * stimulates thirst.


 * angiotensin-converting enzyme (ACE)** ACE converts angiotensin I to a biologically active form, angiotensin II. ACE is found in epithelial cells. Since the first major capillary bed the blood goes through after leaving the kidney is the lungs, most of the conversion takes place in the lungs epithelium. ACE inhibitors are used to combat hypertension.


 * aortic arch** The part of the aorta that connects the ascending(just as it leaves the heart) with the descending aorta. It is significant for two major reasons.
 * The major vessels to the head and arms branch off the aortic arch.
 * Baroreceptors and chemoreceptors are located on the aortic arch.


 * arteriole** Microscopic blood vessels that connect the smallest arteries with the capillary beds. The arterioles together with the smaller arteries make up the resistance vessels.


 * asystole** absence (a) of contraction (systole). Asystole is when the heart has stopped beating. This is different than fibrillation where the heart is still contracting, but not in a coordinated fashion.


 * atrial naturetic hormone/factor/peptide (atriopeptin)**Released by the atria in response to elevated blood pressure, ANH works to suppress aldosterone, and ADH. It also causes vasodilation. The net result is a decrease in blood pressure.


 * atrioventricular (AV) node** Specialized conduction tissue found in the right atrium. In a healthy heart the AV node is the only electrical connection between the atria and ventricles. By having a relatively slow conduction rate, the AV node allows the atria to empty more blood into the ventricles before they contract.


 * atrium, atria(pl)** The upper chambers of the heart. Blood returning to the heart is stored in the atria before being ejected into the [|**ventricles**]


 * baroreceptor reflex** Baroreceptors, found in the arch|aortic arch and sinus|carotid sinuses, sense changes in blood pressure. As blood pressure goes up, the baroreceptors are stimulated and they deliver a higher rate of impulses to the centers|vasomotor centers of the brain. This causes a reduction in [|tone|sympathetic tone] and a stimulation of tone|vagal tone. As a result, there is a reduction in heart rate, cardiac contractility, and vasodilationof blood vessels throughout the body which all contribute to lower blood pressure.

If blood pressure goes down, baroreceptors reduce their rate of firing, causing the opposite effect. The baroreceptor reflex is more sensitive to rapidly changing pressure (standing up, or sitting down) than to a constantly elevated or depressed pressure. Baroreceptors will adapt to long term increased or decreased blood pressure.


 * bradycardia** Slow (brady) heart (cardia). Bradycardia is an abnormally slow heart rate (less than 50 bpm for an adult).

Veins have a much higher capacitance than arteries. This allows them to be a reservoir for blood. Many vasodilator drugs reduce cardiac preload by increasing venous capacitance. See also compliance.
 * capacitance vessels** The capacitance of a vessel is a measure of how easily it stretches.
 * capacitance=change in volume/change in pressure.**


 * cardiac index** cardiac index=output|cardiac output/body surface area. This is a normalizing technique used to compare cardiac outputs of different sized people (for adults average=3 liter/min/meter^2).


 * cardiac output** The amount of blood per a minute that the heart pumps.
 * cardiac output (CO) = volume|stroke volume(SV) x heart rate.**


 * carotid sinus** A pocket found in the carotid artery at the bifurcation of its internal and external branches in the neck. Baroreceptors and chemoreceptors which monitor the blood are found here.


 * chronotropic effect** Chrono- is a prefix that refers to time. Chronotropic effects are ones that change the heart rate (i.e. the time between p waves). See also dromotropic effect.

OR
 * compliance** The compliance or capacitanceof a vessel is a measure of its stiffness.
 * compliance = change in volume / change in pressure.**
 * compliance = change in length / change in tension.**


 * congestive heart failure (CHF)** A condition when the heart, for what ever reason, cannot meet the demands of the body. The body compensates in three major ways.
 * Increased sympathetic tone.
 * Increased sodium and water retention.
 * Myocardial hypertrophy.


 * contractility or inotropy** Contractility refers to how strongly the heart contracts. The contractility or inotropic state of the heart is largely controlled by the sympathetic autonomic nervous system and is related to the concentration of intracellular calcium ion in cardica myoctes. Sympathetic tone increases the strength of contraction, as does heart rate. See inotropic effect.


 * coronary insufficiency** The right and left coronary arteries supply blood to the heart. Flow is considered insufficient if it cannot meet the needs of the heart. See ischemia.


 * cyclic nucleotide phosphodiesterase (PDE)** Enzymes which take cyclic nucleotides (cAMP, cGMP) and convert them to simple nucleotides. cAMP is an important secondary messenger. Stimulation of Beta receptors produces cAMP. Clinically PDE is important because drugs that can block PDE can prolong the effects of cAMP. PDE inhibitors are used in the treatment of CHF.


 * diastole** The period of the cardiac cycle when the ventricles are relaxed. It begins approximately with the opening of the AV valves and ends with their closing. It is during diastole that the ventricles fill with blood.


 * dromotropic effect** Dromo- is a prefix that refers to speed. Dromotropic effects are ones that change the amount of time it takes the heart to complete one beat (i.e the p-t interval). see also chronotropic effect.


 * ectopic** An adjective referring to an event or tissue occurring at a place other than its normal location. Ectopic heart beats are generated from an impulse originating some other place than the SA node.


 * edema** The accumulation of extra fluid in tissues. The tissue looks puffy and if pressed with a finger will hold the indentation after the finger is removed. In CHF when the body starts to retain water to raise the blood pressure, edema can often result. Pulmonary edema (excessive fluid in the lung tissue) can also result.

Ejection fraction = stroke volume/ end-diastolic volume.
 * ejection fraction** The fraction of the volume|end-diastolic volume that is pushed into the aorta during [|systole.]


 * electrocardiogram (ECG, EKG)** This is a tracing over time of the electrical potential between two points on the surface of the body caused by a beating heart. The electrocardiogram reflects the contractile activity of the heart muscle and can be used to identify a variety of cardiac dysfunctions including arrhythmias, infarctions, and hypertrophy.


 * end-diastolic pressure (EDP)** The amount of pressure in the ventricle found at the end of diastole. This pressure equals the pressure found in the atrium, and is a measure of preload on the heart.


 * end-diastolic volume (EDV)** The amount of blood found in the ventricle at the end of diastole. This is the greatest amount of blood found in the ventricle during the cardiac cycle. Since EDV is determined by [|EDP], it is a measure of preload on the heart.


 * end-systolic pressure (ESP)** The hydrostatic pressure in the ventricle at the end of systole


 * end-systolic volume (ESV)** The amount of blood left in the ventricle at the end of systole. This is the smallest volume of blood in the ventricle during the cardiac cycle.


 * fibrillation** A nonsynchronous contraction of muscle tissue, with individual cells firing at their own rate. Fibrillation can be isolated to the atria or the ventricles. Ventricle fibrillation is not compatible with life. A heart in fibrillation has been described as looking and feeling like a "bag of worms".


 * flutter** An extremely fast heart beat (200 -350 bpm) usually occurring only in the atria. Flutter is different than fibrillation in that flutter is a coordinated beat.


 * Frank-Starling relationship** One of the mechanisms by which the heart can increase cardiac output. The heart muscle intrinsically increases its strength of contraction when its fibers are stretched. A plot of tension generated as a function of fiber length volume|(EDV) is known as a Frank-Starling curve. Myocardial fiber stretch is increased by an increase in venous return (preload).


 * hemostasis** Blood (hemo) stopping of flow (stasis). The termination of bleeding due to clotting and [|vasoconstriction.]


 * His bundle (bundle of His)** The bundle of His or AV bundle is the part of the Purkinje system that connects directly to the AV node. It later breaks into two separate tracks (right and left bundle branches).


 * hypokalemia** Low potassium levels in the blood. This can be caused by excessive secretion of [|aldosterone] which promotes the excretion of potassium in the urine, sweat and saliva. When potassium levels drop to about half the normal levels muscle, weakness results.


 * infarction** The death of tissue due to a lack of blood flow. A myocardial infarction is death of part of the heart muscle caused by an obstruction of a coronary artery.


 * inotropic effect/state** Ino- is a prefix that refers to muscle. Inotropic effects are ones that change the strength of contraction of the heart muscle.


 * ischemia** Reduced (isch) blood (emia). A condition of inadequate blood flow to a tissue. Ischemia to the heart can cause angina, and if present long enough, infarction.

In heart failure as the heart increases in size (i.e. increased fiber length, increased diameter) to take advantage of the Frank-Starling relationship to increase cardiac output, the tension in the walls of the heart is also increased according to the Laplace relationship.
 * Laplace relationship** Relationship between the tension on the walls of a container, the pressure inside the container, and the diameter of the container.
 * Tension = Diameter x Pressure.**


 * mean arterial pressure (MAP)** the average blood pressure throughout the cardiac cycle. Because the blood pressure tends to stay closer to the diastolic pressure for most of the cardiac cycle the number is a little less than the average of the diastolic and systolic pressures. For the average adult MAP = 100 mmHg.


 * nitric oxide (NO)** A potent vasodilator, NO is released by endothelial cells, signaling smooth muscle cells to relax. Nitrates and nitrites mediate their pharmacological effects by releasing NO.


 * Ohm's law** A fundamental relationship between resistance (R), pressure (P), and flow (Q) that is applicable to the flow of electrons or blood flow.
 * P = Q x R.**


 * orthostatic hypotension** A fall in blood pressure upon standing, which causes symptoms such as dizziness, lightheadedness, dimming or tunnelling of vision, and pain or discomfort in the back of the head and neck.


 * parasympathetic tone** "Feed or breed" response. This is virtually synonymous with vagal tone. The parasympathetic system slows the heart rate, reduces contractility of the myocardium, increases airway resistance and increases gastric motility and secretion.


 * paroxysmal** Referring to an attack or condition of sudden onset. Paroxysmal tachycardia is a sudden (two to five seconds) increase in heart rate.


 * perfusion** The movement of blood throughout a tissue. If the body's tissues are not well perfused with blood they will not function properly or will die. If the lungs are not properly perfused, proper gas exchange cannot take place; the body will retain carbon dioxide and be unable to renew its stores of oxygen.


 * preload** The amount of tension on a muscle before it begins to contract. The preload of the heart is determined by the end-diastolic volume.


 * Purkinje system** The Purkinje fibers are specialized conducting cells found in the ventricular septum of the heart. They transmit the impulse from the AV node to the myocardium. They are organized in such a way as to mediate a smooth contraction that wrings the blood from the apex out toward the base of the heart.


 * renin** A protease released by the kidney that cleaves angiotensinogen to angiotensin I. Angiotensin I breakdown products mediate responses that elevate blood volume and pressure. Renin release is stimulated by:
 * sympathetic tone
 * low blood flow and pressure in the kidney
 * low sodium in the urine.


 * resistance vessels** The greatest control over total peripheral resistance is had by the smallest arteries and the arterioles. These vessels also control how much blood is dispensed to each capillary bed. The smooth muscle tone in these vessels is controlled by sympathetic innervation and local metabolic needs of tissue. See vasoconstriction..


 * sarcolemma (SL)** The cell membrane of a muscle cell. Like the cell membrane of nerves, the sarcolemma is able to conduct action potentials.


 * sarcoplasmic reticulum (SR)** The endoplasmic reticulum of muscle cells. The SR plays an essential role in linking excitation with contraction. Calcium ions are stored in the SR; it is the release of this calcium that allows contraction.


 * sinoatrial (SA) node** Specialized myocardial tissue found in the upper wall of the right atrium. The SA node is the pace maker of the heart. Although other tissues in the heart have intrinsic pacemaker abilities, in a healthy heart the SA node fires at the fastest rate, thereby driving the other tissues.


 * sinus rhythm** In the normal heart, heart rate is under the control of the SA node and is said to be in sinus rhythm. Conduction blocks or an ectopic source of impulses can remove the heart from normal sinus rhythm.


 * stroke volume (SV)** The amount of blood pushed into the aorta with each beat of the heart.

This is a measure of how much energy is converted to work by the heart. The left ventricle does significantly more work than the right due to the greater pressure it pumps against.
 * stroke work (SW)****stroke work (SW) = [|Mean pressure] x [|volume|stroke volume.]**


 * sympathetic tone**"Fight or flight" response. The sympathetic system prepares the body for action.
 * increased heart rate.
 * increased contractility.
 * increased blood pressure.
 * blood flow increased to skeletal muscle.
 * blood flow decreased to viscera.
 * release of catecholamines by adrenal gland.
 * retention of sodium and water (secretion of renin from the kidney)
 * relaxation of bronchiolar smooth muscle.

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 * syncope** Temporary loss of consciousness due to reduced blood flow to the brain. A common symptom of cardiac arrhthymias.

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 * systole** The part of the cardiac cycle when the ventricles are contracting. Systole begins with the closing of the AV valves and ends with their opening.


 * tachycardia** Fast (tachy) heart (cardia). An abnormally fast heart rate.


 * total peripheral resistance (TPR)** This is the resistance of the systemic circulation. law|Ohm`s law]] describes the relationship between TPR, [|MAP] and [|output|CO].
 * TPR = (mean aortic pressure - mean right atrial pressure) / [|output|cardiac output]**.


 * vagal tone** Vagal tone is virtually synonymous with parasympathetic tone in regards to the heart. Stimulation of the vagus causes a decreased heart rate, which in turn causes a drop in blood pressure.

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 * vasoconstriction** The effects of vasoconstriction (or the constriction of a vessel) are best understood if the following relationship is remembered. Resistance through a vessel is inversely proportional to the fourth power of the radius. Simply put, a small decrease in the radius of a vessel can cause a marked decrease in flow or increase in pressure or both.


 * vasodilation** Also known as vasodilatation. It is caused by relaxing the smooth muscle around a vessel, allowing it to increase in diameter. See [|vasoconstriction.]


 * vasomotor centers** Located in the medulla and lower part of the pons, the vasomotor centers control the autonomic nervous system. The vasomotor centers receive inputs from a variety of sources including baroreceptors, chemoreceptors, and higher brain centers. These inputs are integrated and the activities of the sympathetic and parasympathetic nervous system are adjusted to maintain adequate blood flow to the brain and other essential organs of the body.


 * vasopressin** Also known as antidiuretic hormone (ADH) or arginine vasopressin (AVP). ADH is secreted by the posterior pituitary and acts on the collecting ducts of the kidneys to cause them to reabsorb water, thereby concentrating the urine. ADH is also a vasoconstrictor. Its overall effect is to increase blood volume and raise blood pressure. Its secretion is stimulated by...
 * osmoreceptors in the CNS (low osmolarity causes secretion)
 * low blood pressure as sensed by the [|baroreceptors.]
 * [|angiotensin II.]


 * venous tone** The relative state of constriction of the venous bed of the body. The veins of the body play an important role in [|cardiac preload] and are also the major [|reservoir] for blood in the body. Changes in venous tone have large effects on both cardiac preload and circulating blood volume.


 * ventricle** The two lower chambers of the heart. These two chambers are responsible for sending blood out into the circulation. The left ventricle pumps blood into the systemic circulation and the right ventricle pumps blood into the pulmonary circulation.


 * Wolff-Parkinson-White syndrome** A conduction disorder of the heart where electrical pathways other than the [|node|AV nodal system] connect the atria with the ventricles. This type of disorder can lead to reentrant arrhythmias.