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cone-shaped, hollow, muscular organ weighing about 300g in mediastinum, left of midline, between 3rd & 6th intercostal cartilage function: supplying oxygenated blood to all cells of the body through 60,000 miles of blood vessels and returning deoxygenated blood to the lungs |
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all muscle tissue contracts in response to a(n) ____ stimulus or impulse. Cardiac muscle is unique; not only can it respond to a(n) _____ impulse, it also has ____ that can generate their own electrical impulses. |
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electrical electrical pacemaker cells |
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Four primary characteristics of cardiac cells |
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Conductivity: ability of cardiac cells to receive an electrcal stimuls and then conduct it to other cardiac cells Contractility: ability of cardiac cells to shorten, causing cardiac muscle contraction in response to an electrical stimulus (to eject the blood) Automaticity: ability of cardiac pacemaker cells to generate their own electrical impulses (SA node-normal conduction starts here, AV node, bundle of his/purkinje fibers) Excitability: irritability; ability of cardiac cells to respond to an electrical stimulus; when a cardiac cell is highly excitable, less stimulus is required to cause contraction
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a property of all tissue cells; K+ is on the inside of the cell and Na+ is on the outside; muscle is relaxed and cardiac cells are ready to receive an electrical impulse |
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the phase of contraction; myocardial cells are conducting an electrical impulse through the muscle causing the heart to contract (heartbeat); as the electrical impulse moves through the cells, K+ leaves the cells and Na+ enters. While in this state, the cardiac cells are fully depolarized. They cannot respond to any further electrical impulses until they have repolarized. |
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the recovery phase; the cells are returning to a ready state, however, all cells are not repolarized at the same time. So, some cardiac cells are able to conduct an electrical impulse sooner than others. After the electrical impulse has passed through the cells, K+ reenters the cell and Na+ leaves. |
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the time between the end of a contraction and reutrn of the cardiac cells to the ready state. While the cells are recovering, the atria and ventricles are refilling with blood and preparing to contract again. |
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the two phases of the refractory period |
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Definition
Absolute refractory period: cardiac cells have not completed repolarization and cannot be stimulated to conduct an electrical impulse and contract again (depolarize); period from the beginning of the QRS complex through about the first 1/3 of the T wave Relative refractory period: cardiac cells have repolarized to the point that some cells can again be stimulated to depolarize, if the stiumus is strong enough. If these cells are stimulated during this period, they could conduct the electrical impulse in an abnormal pattern. The period from the end of the absolute refractory period to the end of the T wave (vulnerable). |
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heart rate is under the control of the autonomic NS (symp/parasymp divisons); involuntary but can be modified with drugs cardiac centers in the brainstem in the medulla oblongata (sends APs) |
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via efferent (adrenergic) fibers to the heart, accelerates the heart rate and strengthens the force of contraction through the effects of circulation catecholamines- norepinephrine and epinephrine fight or flight |
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binds with BETA 1 adrenergic receptors of the heart, increasing the rate of impulse generation and the strength of contraction during systole binds with ALPHA 1 adrenergic receptors in the coronary arteries causing vasocontriction |
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binds with BETA 2, BETA 1, and ALPHA 1 adrenergic receptors BETA 1 - stimulate the heart ALPHA 1- constricts certain blood vessels BETA 2- dilutes certain blood vessels and causes bronchodilation |
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Definition
via the efferent (cholinergic) vagus nerve, when vagal stimulation occurs, the neurotransmitter ACETYLCHOLINE is released at the juntion of the nerve and the myocardium; it slows the heart rate by inhibiting impulse formation and electrical conduction in the heart |
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Definition
specialized nerve tissue in the internal carotid arteries and the aorta are responsible for activation of the vagus nerve e.g. when stimulated upon stretch, such as occurs in HTN, these receptors activate the vagus nerve to decrease HR & AV conduction (accommodate to change in pos'n so fainting doesn't occur in orthostatic HTN) |
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Definition
pressure the blood exerts on the blood vessels walls, i.e., the arteries, capillaries, and veins differs in the vessels - it is greatest in the arteries and falls as blood moves into the capillaries and veins generated by the left ventricle during contraction/systole arterial pressure is composed of the systolic and diastolic pressures |
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max pressure generated by the left ventricle during contraction (systole) |
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pressure exerted on the artery walls during relaxation of the diastolic phase of the cardiac cycle |
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difference between SBP and DBP |
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BP is lowest at birth and increases with age as the vessels lose their _____ and therefore more pressure is required to pump blood through them. |
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BP is maintained by the interplay of four systems: |
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Renal Endocrine Neurologic Cardiovascular |
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produces and stores a proteolytic enzyme-RENIN- that is being released into the bloodstream in response to a decrease in BP in the circ. system, renin reacts w/ a substrate formed in the liver, and inactive peptide-angiotensinogen, to form ANGIOTENSIN I Angiotensin I is converted to ANGIOTENSIN II by the enzyme Angiotensin Converting Enzyme (ACE) found in highest quantities in the lungs Angiotensin II is a powerful vasoconstrictor which then constricts blood vessels in order to elevate the BP directly Angiotensin II stimulates the adrenal cortext to release ALDOSTERONE, a mineralocorticoid, increasig the reabs. of Na+ in the kidney which increases blood vol. and elevates BP indirectly |
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Renin-Angiotensin system is thought of as being responsible for the ____ control of BP. |
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posterior pituitary is also stimulated by a decrease in BP; it increases its release of ANTIDIURETIC HORMONE (ADH) or VASOPRESSIN Aldosterone and ADH increase the reabs. of Na and H20, increasing blood vol. (decreased urine release leads to increased circulating vol) |
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responds to a fall in BP by stimulating the sympathetic NS this causes peripheral vasoconstriction and increased HR and stroke vol, which leads to an increase in CO (b/c CO = SV x HR) NS also responds to messages from the pressure sensitive baroreceptors in the aortic arch and carotids low pressure messages from baroreceptors elevate BP. In the heart, BETA receptor stimulation will cause increased contractility and HR; in the blood vessels, ALPHA receptors are stimulated causing vasoconstriction |
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Sympathetic NS regulation of BP is thought of as ____ control. |
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volume of blood ejected from the heart in unit time (usually min) ~5 L CO = SV x HR |
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volume of blood ejected with each beat ~70 cc/beat |
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number of beats/min 60-90 beats/min is average |
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Blood Pressure BP = ________ |
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pressure the blood exerts on the blood vessels walls BP = CO x PVR |
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force against which the left ventricle must contract to eject blood arterial pressure, arterial resistance (narrow diameter = higher pressure) |
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amount of blood going into the heart (amt the heart has to eject) |
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Types of chemical effects on the heart (3) |
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Definition
Inotropic Chronotropic Dromotropic |
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Inotropic effects on the heart |
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Definition
affect the strength of myocardial contraction (strength leads to increased CO) pos. inotropic effects = pts with pump failure respond to drugs with this action |
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Chronotropic effects on the heart |
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Definition
affect the rate of myocardial contraction by altering the rate of impulse formation at the SA node pos chronotropic effect = pts w/ bradyarrhythmias respond to increased cardiac rate neg chronotropic effect = pts w/ tachyarrhythmias respond to decreased cardiac rate |
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Dromotropic effects on the heart |
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affect the conduction of electrical impulses through the myocardium (through AV node) pos dromotropic effect = pts w/ heart blocks respond to increased AV conducdtivity neg dromotropic effect = pts w/ conduction disorders such as atrial fibrillation resond to decreased/blocked conduction |
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Term
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Definition
persistant elevation of SBP > 140mmHg or DBP > 90 mmHg at least 3 times on 2 different occasions Isolated systolic HTN (ISH): persistant elevated SBP w/ normal DBP (more damage from systolic; treated as drastically as HTN w/ both elevated primary HTN: 95% of people, genetic secondary HTN: neurological problems, etc |
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Definition
Imbalances symp. NS hyperactivity: increased HR leads to decreased CO, which increases BP renin-angiotensin system malfuntion: feedback loops may not work properly allowing for higher circulation levels of renin, leading to HTN sodium balance problems & salt sensitivity: inability to normally excrete Na via the kidneys and/or abnormal electrolyte transport, resulting in disturbance in the systolic Ca/Na balance and vasoconstricition age, AA heritage, DM, low renin levels often predict salt sensitivity causes: increased Na intake, heredity, ETOH intake, smoking, obesity **usually multifactorial |
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Etiology of secondary HTN: |
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Definition
second most common reason for office visits int he US and for use of prescription drugs approx. 50 million Americans affected about 32% AA popl'n, 23% of white and Mexican-American popl'n |
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Complications of Hypertension (8) |
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Definition
-Cardiovascular Disease: HTN is the major risk factor; more common than smoking, diabetes, etc.; increase in risk as BP rises above 110/75 mmHg -Heart Failure: increased risk at all ages -Left Ventricular Hypertrophy: common w/ HTN; associated w/ enhanced incidence of HF,ventricular arrhythmias, death following MI, sudden cardiac death -Stroke (CVA): most common/important risk factor -Intracerebral Hemorrhage: most important risk factor -Chronic Renal Insufficiancy & End stage Renal Disease -Retinopathy: caused by long term, uncontrolled HTN -Acute, Life-Threatening Emergency: hypertensive encephalopathy
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often none; "silent killer" b/c don't realize that damage is being done until it's too late and irreversible |
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Major Cardiovascular Disease risk factors: |
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HTN obesity (BMI > 30 kg/m) dyslipidemia diabetes mellitus smoking physical inactivity microalbuminuria age (>55 for men, >65 for women) family history of premature CVD |
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Lifestyle Modification Recommendations |
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Definition
weight reduction: 5-20mmHg SBP reduction DASH eating plan: 8-14 mmHg Dietary sodium reduction: 2-8 mmHg Aerobic physical activity: 4-9 mmHg Moderation in alcohol consumption: 2-4 mmHg one drug decreases one side by 5-10 mmHg, so this can lead to a large # of drugs if lifestyle cannot be modified
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