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37 Cards in this Set
- Front
- Back
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Acute Coronary Syndrome
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-ACS term used to describe pt who have clinical symptoms compatible with acute myocardial ischemia
-includes unstable angina and acute MI |
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Classification of Angina
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-stable angina- chronic stable angina or exertional angina, pain occurs with physical exertion, relieved by rest or nitro
-unstable angina- pre-infarction angina, occurs while at rest, it is a type of ACS and requires immediate treatment because the pt is at increased for AMI variant angina: -prinzmetal angina, vasospastic angina -is a form of unstable angina -occurs at rest, often between midnight and 8am -is the result coronary artery spasm -pt have severe coronary atherosclerosis of at least one major coronary artery -the spasm occurs very near the area of blockage |
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Anterior left ventricle and Septal MI
IBAP |
-left coronary artery LCA divides into the left anterior descending and left circumflex artery
-LAD supplies oxygenated blood to the (I)nterventricular septum; (B)undle branches/ventricular conducting tissue; (A)nterior wall of the left ventricle; (P)apillary muscles and mitral valve -Anterior wall and Septum MI result from occlusion of the LAD -pt are at risk for heart failure, pulmonary edema, cardiogenic shock if the BB/ventricular conducting tissue are involved in the MI process and failure of the left ventricle to pump blood. -increased risk on intraventricular conduction disturbances, BBB and fascicular blocks -VI differentiates RBBB, QRS width of 120ms indicates BBB -I B A P; (I)nterventricular septum, (B)undle Branches, (A)nterior wall, (P)apillary muscles |
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Bundle branch blocks
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-a block of one of the fascicles of the bundle branch system can be caused by MI, congenital defects, or ischemic tissue
-BBB represent an increased risk for developing complete heart block -at risk for sudden death when associated with an MI due to the proximal occlusion of the LAD coronary artery -the impulse coming down from the AV node travels down the bundles and reaches the blocked tissue on one side -the impulse stops on that side and the other proceeds to depolarize as normal -the depolarization eventually works across to the blocked side, causing a delayed depolarization -if depolarization of the ventricles is longer than 0.12sec or 120ms, then it is a BBB -a left BBB has a higher mortality rate, -V1 differentiates BBB -find and circle J point, draw a line back toward the direction of the terminal deflection -shade the triangle, if it points up it is a RBBB, if it points down it is a LBBB |
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BBB cont
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-as conduction through one bundle is blocked, the impulse travels along the unaffected bundle and activates one ventricle normally
-the impulse is delayed in reaching the other ventricle because it travels outside of the normal conducting fibers -the right and left ventricle are thus depolarized sequentially instead of simultaneously -the abnormal activation produces a wide QRS complex, representing the inc time it takes for ventricular depolarization -a RBBB alters the configuration of the QRS complex in V1 and V2 -normally these leads have a small single peaked R wave and a deep S wave -with a RBBB depolarization of the right ventricle is delayed, and the ECG pattern changes, evidenced by an RSR configuration in V1 -whenever ventricular depolarization is abnormal, so is ventricular repolarization. -as a result, ST segment and T wave abnormalities may be seen in leads V1 and V2 for pt with a RBBB -a LBBB changes the QRS complex pattern in V5 and V6 -like RBBB, the ST segments and T waves may be abnormal in leads V5 and V6 when the pt has a LBBB -BBB signifies underlying disease of the intraventricular conduction system -a new onset LBBB in conjunction with an acute MI is associated with a higher mortality rate |
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lateral left ventricle
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-left coronary artery divides into the left circumflex artery and LAD
-Lateral MI results from occlusion of the left circumflex artery -LCA is the source of blood supply to the SA node in about 50% of population -pt at risk for dysrhythmias associated with dysfunction of the SA or AV nodes |
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Inferior left ventricle
IRAP |
-results from occlusion of the right coronary artery
-RCA supplies inferior wall and right ventricle -RCA gives off to the posterior descending artery PDA and supplies the posterior wall of left ventricle -also source of blood supply to the SA node is 50% of the population -AV node supply is about 90% -pt are risk for dysrhythmias related to altered function of the SA and AV nodes -associated with bradycardia and AV blocks -IRAP: (I)nferior MI; (R)ight ventricle MI; (A)V node dysrhythmias; (P)osterior MI |
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Right ventricular MI
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-right coronary artery disease causing an inferior MI is likely to be associated with concomitant right ventricular involvement
-RCA supplies inferior wall and right ventricle -may experience significant hemodynamic compromise due to biventricular dysfunction -associated dysrhythmias involve SA and AV node dysfunction -RCA supplies blood to the AV node in about 90% of population -when damaged, the right ventricle can dramatically affect the blood available for the left ventricle to pump, thus preload is reduced. -the cardio sys can compensate for reduction in preload by increasing peripheral vascular resistance through vasoconstriction -Patientis will require fluids in larger quantities to restore adequate preload and BP -Right ventricular leads include V1R-V6R |
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Posterior MI
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-Posterior leads V1-V4 can be reciprocal findings of posterior wall ischemia, and should demonstrate a mirror test of ST elevation and pathological Q wave formation
-ST segment depression with or without large R waves in leads: V1, V2, V3 -inverted T waves may also be present -Posterior MI is rarely seen alone, usually component of a multiple site infarction, including Inferior MI -the Right Coronary Artery (RCA) or the Left Circumflex Artery (LCA) is occluded |
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Type of infarction
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-in most pt with ST segment elevation, a Q wave ultimately develops
-the term Q wave MI is used to describe the type of MI they experience -ST segment elevation without Q wave is termed non-Q wave MI -pt who present without ST segment elevations are diagnosed with either unstable angina or a non-ST segment elevation MI (NSTEMI) -Q wave is the initial downward deflection of the QRS complex -A Q wave is not present on the normal ECG -presence of significant Q waves indicates an MI |
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Ischemia, Infarction
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-when a coronary artery becomes about 70% occluded and oxygen demand exceeds oxygen supply, myocardial ischemia may result
-ischemia- local deficiency of blood supply -if the ischemic state is not corrected, injury to the myocardium may occur -eventually, if adequate blood flow to the myocardium is not restored, an MI may result -ischemia and injury are reversible processes, however, infarction is not reversible -infarction- is a localized area of tissue that is dying or dead, having been deprived of its blood supply because of an obstruction |
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Ischemia
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-myocardial ischemia results in T wave inversion or ST segment depression
-ischemia and injury are reversible processes, however, infarction is not reversible -ischemia- local deficiency of blood supply -infarction- is a localized area of tissue that is dying or dead, having been deprived of its blood supply because of an obstruction -the inverted T wave of ischemia is symmetrical, relatively narrow, and pointed -an asymmetrical inversion of the T wave usually does not indicate ischemia, it may signify ventricular hypertrophy or BBB -ST segment depressions of 1-2mm or more for a duration of 0.08 seconds may indicate myocardial ischemia |
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injury
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-like ischemia, myocardial injury is a reversible process if interventions are instituted rapidly
-on ECG, the hallmark of acute myocardial injury is the presence of ST segment elevation |
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Infarction
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-prolonged ischemia is caused by an imbalance between oxygen supply and oxygen demand causes MI
-the prolonged ischemia causes irreversible cell damage and muscle death when myocardial injury persists, and MI is the result -infarction- is a localized area of tissue that is dying or dead, having been deprived of its blood supply because of an obstruction -the earliest stage of a MI id the T wave becomes tall and narrow -referred to as hyperacute -next the ST segments elevate -reciprocal changes are most likely to be seen at the onset of infarction -the last stage in the ECG evolution of an MI is the development of Q waves -Q waves represent the flow of electrical forces toward the septum -small narrow Q waves may be seen in the normal ECG -Q waves compatible with an MI are usually 0.04 seconds or more in width or one fourth to one third the height of the R wave -Q waves indicative of infarction usually develop within several hours of the onset of the infarction -may not appear until 24-48hrs after -Q waves do not disappear and therefore always provide ECG evidence of a previous MI -abnormal Q waves accompanied by ST segment elevation indicate an AMI -abnormal Q waves accompanied by a normal ST segment indicates a previous MI |
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CK-MB
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-when heart muscle is damaged, CK is released into the blood
-becomes abnormal within 6-8hrs -peaks within 12hrs -isoenzyme of CK are measured to determine if the CK came from the heart (CK-MB) |
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Myoglobin
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-is an oxygen binding protein found in skeletal and cardiac muscle
-myoglobin release from ischemic muscle occurs earlier than the release of CK -serum level of myoglobin can be detected soon after the onset of symptoms -it elevates within 1-2hrs of AMI -elevated myoglobin level is not specific for the diagnosis of MI |
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Troponin
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-is highly specific for cardiac muscle
-levels rise in about 3hrs, peak at 14-18hrs |
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QT Interval
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-the QT interval represents the time from the start of depolarization of the ventricles to the end of ventricular repolarization
-this is functionally the refractory period -it is measured from the start of the QRS complex to the end of the T wave -some meds can prolong the QT interval -amiodarone, procainamide, haloperidol, erythromycin, and TCAs -acute inc in QT interval can be associated with an inc risk of syncope and sudden death from torsade de pointes type V-tach |
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Nitro infusion
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-is a mainstay of therapy
-reduces preload and relieves cardiac stress -potent vasodilator that affects primarily the venous system -direct smooth muscle relaxation of the coronary arteries, improves coronary blood flow and increasing myocardial oxygen supply -dec myocardial oxygen demand by reducing preload -Nitro gtt 50mg/250ml D5W -Infuse 10mcg/min inc q 5min by 10mcg/min |
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MS
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-is indicated for pt whose symptoms are not relieved after 3 SL nitro or whose symptoms recur with adequate anti-ischemic therapy
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Beta blockers
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-beta receptors have beta1 or beta2
-heart has mostly beta1 (beta1 - 1 heart) -activation of beta1 receptors in the SA node by norepi results in depolarization of the SA node and inc HR -may be used to decrease myocardial oxygen consumption by reduction myocardial contractility, sinus node rate, and AV node conduction -the reduction in myocardial contractility reduces the work of the heart and decreases myocardial oxygen demand -the slowing of the heart rate helps to increase the time for diastolic filling, thus improving blood flow to the coronary arteries -IV lopressor 5mg q 5min x3 |
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CCB
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-may be beneficial for the pt with unstable angina
-decrease myocardial oxygen demand by decreasing afterload, contractility, and HR -verapamil or diltiazem can be used as second or third choice therapy after the initiation of nitrates and BB -arterial vasospasm results primarily from prolonged smooth muscle contraction -Calcium ions regulate contraction in smooth and cardiac muscle -CCB inhibit the movement of Ca ions across myocardial and vascular smooth muscle -this leads to decreased myocardial contractility and decreased myocardial oxygen demand -CCB also improve coronary blood flow via direct smooth muscle relaxation -they also cause peripheral vasodilation from direct smooth muscle relaxation |
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Heparin
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-anticoagulation agent that inhibits reactions that lead to the clotting of blood and formation of fibrin clots by blocking the conversion of prothrombin to thrombin and fibrinogen to fibrin
-Dose- loading dose ranges from 5000-7500 units IVP -maintenance infusion is based on PTT levels -dose is usually 1000-2000u/hr or 20K-40K units over 24 hours -Heparin comes in 25,000u/250ml, 100u/ml -ASA should be administered asap concurrently -Lovenox- low molecular weight heparin that has antithrombotic properties, for ACS 1mg/kg sq, prn q 12hrs |
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Thrombolytic therapy
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-Fibrinolytics work by converting plasminogen to the natural fibrinolytic agent plasmin
-Plasmin lyses a clot by breaking down the fibrinogen and fibrin contained in a clot. -With the thrombus dissolved, blood flow through the vessel is restored -thrombolytic drugs lyse coronary thrombi by converting plasminogen to plasmin -Tissue plasminogen activator- is a protein involved in the breakdown of blood clots, as an enzyme it catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown -thrombolytic therapy provides maximal benefit if given within the first 3hrs after the onset of symptoms -in addition to the thrombolytic agent, the person should receive heparin and ASA -commonly seen reperfusion dysrhythmias include an accelerated idioventricular rhythm, v-tach, and AV heart block -t-PA may be manufactured using recombinant technology, and referred to recombinant tissue plasminogen activator (r-tPA) -recombinant tissue plasminogen activator (r-tPA)- includes activase (alteplase), retavase (retaplase), TNKase (tenecteplase) -A major risk of this therapy is intracerebral hemorrhage -stop antiplatelet agents and heparin if serious bleeding occurs -Activase, (t-PA) at 0.9mg/kg is administered as 10% of the total dose as a bolus over 1-2 minutes, with the remainder infused over 60min -Retavase, 10units IV x 2, 2nd dose given 30min after 1st -TNkase, <60Kg=30mg; 60-69kg=35mg; 70-79kg=40mg; 80-89kg=45mg; >90kg=50mg |
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Percutaneous transluminal coronary angioplasty
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-PTCA is an effective alternative to reestablish blood flow to ischemic myocardium
-It is the technique of mechanically widening a narrowed or obstructed blood vessel, typically as a result of atherosclerosis. -An empty and collapsed balloon on a guide wire, known as a balloon catheter, is passed into the narrowed locations and then inflated to a fixed size using water pressures some 75 to 500 times normal blood pressure (6 to 20 atmospheres). -The balloon crushes the fatty deposits, so opening up the blood vessel to improved flow, and the balloon is then collapsed and withdrawn. |
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Valves
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-Mitral on left and tricuspid and right are between the atria and ventricles and are called atrioventricular valves
-Semilunar include pulmonic and aortic vavles -The 5th intercostals space, mid-clavicular line on the left side is the point of auscultation for the mitral valve, also called point of maximal impule (PMI); A murmur heard at this point identifies the mitral valve is involved. -During diastole the mitral valve should be opening, as the blood flows from the lt atrium to lt ventricle -A stenotic mitral valve will cause a murmur during the opening phase. -LAD also supplies the papillary muscles of the mitral valve |
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Mitral regurgitation
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-Is the abnormal leaking of blood through the mitral valve, from the left ventricle into the left atrium of the heart
-The mitral component of the first heart sound is usually soft and is followed by a pansystolic murmur which is high pitched and extends, as the name suggests, the whole of systole -The murmur usually radiates to the axilla -Patients may also have a third heart sound (S3) heard closely after S2 -Will be heard at same location but heard during systole -S3 also associated with left ventricular failure -Regurgitation is associated with closing of mitral valve |
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Mitral Stenosis
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-Characterized by the narrowing of the orifice of the mitral valve of the heart
-Is associated with opening -The first heart sound is unusually loud and may be palpable (tapping apex beat) because of increased force in closing the mitral valve -If pulmonary hypertension secondary to mitral stenosis is severe, the P2 (pulmonic) component of the second heart sound (S2) will become loud. |
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A&P
Autonomic Nervous System |
-contains sympathetic and parasympathetic
-acetylcholine is the neurotransmitter synthesized by all autonomic neurons both SNS and PNS -when an action potential is conducted down the axon, acetylcholine is released into the synapse between the axon terminals -alpha receptors have alpha1 or alpha 2 receptors -beta receptors have beta1 or beta2 -heart has mostly beta1 (beta1 - 1 heart) -smooth muscles of the arteries and veins have mostly alpha1 and alpha2 receptors (A for Arteries & A for Alpha) -the SNS innervates organs with alpha1, alpha2, and beta1 receptors and norepi activates these receptors to changes - |
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A&P
Autonomic Nervous System cont |
-activation of beta1 receptors in the SA node by norepi results in depolarization of the SA node and inc HR
-activation of alpha1 and alpha2 receptors in the arteries results in inc contraction by arteriolar smooth muscle and an inc BP -beta2 (beta2 - 2 lungs) receptors are not innervated by SNS and norepi does not bind or activate beta2 receptors -epinephrine is powerful stimulator of beta2 receptors, which it reaches through the blood stream after being secreted by the adrenal medulla -dilation of bronchiolar smooth muscle or dilation of blood vessels in skeletal muscles are important effects of beta2 receptors that are mediated by circulating epinephrine rather than norepi. (beta2 - 2 lungs) -while Alpha 1 receptors mediate vasoconstriction, Beta 2 receptors induce vasodilation in vascular smooth muscle -the SNS and PNS are antagonistic -the SNS inc the rate of firing of the SA node and inc the speed of conduction in the AV node of the heart, the PNS does the opposite -blood vessels are not innervated by the PNS |
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Action potential
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-an action potential is simply an electrical current that travels down an axon of a neuron
-an action potential can only occur when opposite charges exist on two sides of a cell membrane -an action potential is a brief reversal of that charge which moves down the axon -neurons use Na and K to create membrane polarity -when a neuron is resting (not transmitting an electrical message), Na and K ions move down their concentration gradients through their membrane channels to opposite sides of the membrane -meanwhile, a specialized pump located in the membrane maintains the concentration gradient by using energy to force Na and K back to the sides they came from - |
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Resting potential
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-the outside concentration of Na is higher than inside the cell
-while the inside concentration of K is higher than outside the cell -the Na-K pump works constantly to ensure that more pos ions remain outside the cell than inside the cell -the outside of the neuron is positive when compared to the inside, and called resting potential |
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Depolarization
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-the first step in sending a signal (action potential) is called depolarization
-depolarization is when the inside of the cell becomes positive and the outside is more negative -when the K channel is closed Na rushes in and causes the cell interior to become more positive -this depolarizes that region of the membrane -when the Na influx changes the polarity, the electrical change opens the previously closed Ca channels in the myocardial cell membrane -once opened, these channels permit the influx of Ca -the entry of Ca, together with the continued entry of Na, is responsible for the remainder of the depolarization, which continues until the polarity of the extracellular side equals |
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Repolarization
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-is the returning of the cell to the resting potential
-the inside of the cell will become more negative - -when the Na channel is closed and the K channel is opened, K flows out of the cell and restores pos charge outside the cell -the Na-K pump is responsible for restoring the original concentrations of Na and K to the resting potential |
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Regulation of HR
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-cardiac rate is under autonomic and adrenal catecholamine influence
-parasympathetic and sympathetic fibers innervate the SA and AV nodes -parasympathetic stimulation releases acetylcholine and decreases the rate of depolarization, and slowing HR -sympathetic stimulation causes the release of norepinephrine, inc the rate of depolarization and inc HR -the adrenal medulla also releases norepi and epi into the bloodstream, these catecholamines act on the heart in the same way as sympathetic stimulation - |
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Regulation of HR cont
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-in the aortic reflex, a rise in arterial BP stimulates aortic and carotid sinus baroreceptors to fire sensory impulses to the cardioregulatory center in the medulla
-the result is an inc in parasympathetic stimulation or a dec in sympathetic stimulation to the heart -the dec in heart rate results in a dec output which can dec arterial BP |
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ECG paper
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-the paper consists of horizontal and vertical lines, each 1mm apart
-horizontal lines denote time -each small square measured horizontally is equal to 0.04 sec (0.04 x 5 = 0.2) -a large square, (five small squares) equals to 0.2 sec -most ECG paper is marked by vertical slash marks across the top of bottom -the distance between two vertical markings represents 3 seconds, the distance between 6 seconds is used for rate calc -5 large squares x 0.2 sec = 1 sec -15 large squares x 0.2 sec = 3 sec -30 large squares x 0.2 sec = 6 sec -to determine the ventricular rate, count the number of QRS complexes in a 6 sec strip and multiply by 10 |
