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37 Cards in this Set

  • Front
  • Back
Acute Coronary Syndrome
-ACS term used to describe pt who have clinical symptoms compatible with acute myocardial ischemia
-includes unstable angina and acute MI
Classification of Angina
-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
Anterior left ventricle and Septal MI
-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
Bundle branch blocks
-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
BBB cont
-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
lateral left ventricle
-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
Inferior left ventricle
-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
Right ventricular MI
-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
Posterior MI
-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
Type of infarction
-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
Ischemia, Infarction
-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
-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
-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
-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
-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)
-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
-is highly specific for cardiac muscle
-levels rise in about 3hrs, peak at 14-18hrs
QT Interval
-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
Nitro infusion
-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
-is indicated for pt whose symptoms are not relieved after 3 SL nitro or whose symptoms recur with adequate anti-ischemic therapy
Beta blockers
-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
-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
-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
Thrombolytic therapy
-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
Percutaneous transluminal coronary angioplasty
-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.
-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
Mitral regurgitation
-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
Mitral Stenosis
-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.
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
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
Action potential
-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
Resting potential
-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
-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
-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
Regulation of HR
-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
Regulation of HR cont
-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
ECG paper
-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