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2011-11-03 22:20:01

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  1. What are the components of the cardiac conduction system?
    • Sinoatrial (SA) node
    • Atrioventricular (AV) junctional area
    • Bundle branch system
  2. What is the sinoatrial (SA) node?
    • Natural pacemaker
    • Located close to the surface of the right atrium near its junction with superior vena cava
    • Primary pacemaker
    • Rate 60-100 bpm
    • Has greatest degree of automaticity
    • Impulses move directly through atrial muscle and lead to atrial depolarization, which is reflected in a P wave on a ECG
  3. What is the atrioventricular (AV) junctional area?
    • Consists of a transitional cell zone, the AV node, and the bundle of His
    • Lies just beneath the R atrial endocardium, btwn the tricuspid valve and the ostium of the coronary sinus
    • T-cells cause impulses to slow down or be delayed in the AV node before proceeding to the ventricles
    • Delay is reflected in the PR segment on the ECG
    • The slow conduction allows the atria to contract and the ventricles to fill
    • Contraction is known as "atrial kick" and contributes to additional blood volume for a greater CO
  4. What is the bundle of His?
    • Connects with the distal portion of the AV node and continues through intraventricular septum
    • Extends as a right bundle branch down the right side of intraventricular septum to the apex of the right ventricle
    • On the left side, it extends as a left bundle branch, which further divides
  5. What are the Purkinjie fibers?
    • At ends of both R and L bundle branch systems are the Purkinjie fibers
    • Interweaving network located on the endocardial surface of both ventricles, from apex to base
    • Fibers then partially penetrate into the myocardium
    • Makes up the bundle of Hiis, bundle branches and terminal Purkinjie fibers
    • Responsible for rapid conduction of electrical impulses throughut the ventricles, leading to ventricular depolarization and the subsequent ventricular muscle contraction
    • When SA and AV nodes fail, can initiate impulses at a rate of 20-40 bpm
  6. What are the valves of the heart?
    • Atrioventricular valve
    • Tricuspid valve
    • Mitral valve
    • Semilunar valve
    • Pulmonic valve
    • Aortic Valve
  7. What is the atrioventricular valve?
    • Separates atria from the ventricles
    • Control blood flow btwn atria and ventricles
  8. What is the tricuspid valve?
    • Located btwn the right atrium and the right ventricle
    • Has three leaflets
  9. What is the mitral valve?
    • Located bten the left atrium and left ventricle
    • Has two leaflets
  10. What are the leaflets of the AV valves?
    • Connected to the papillary muscles by the chordae tendinae to prevent backflow
    • S1, the first heart sound, is heard when AV valves close
  11. What are the semilunar valves?
    • Pulmonic valve
    • Aortic valve
    • Separate the cardiac chambers from the great vessels
    • Control blood flow out of the cardiac chambers
    • Each valve has three cusps that prevent backflow
    • S2, the second heart sound, is heard when the semilunar valves close
  12. What is the pulmonic valve?
    • Located btwn the right ventricle and the pulmonic artery
    • Unoxygenated blood flows through this valve to the lungs
  13. What is the aortic valve?
    • Located btwn the left ventricle and the aorta
    • Oxygenated blood is pumped from the heart through this valve into systemic circulation
  14. Blood flow
    • Blood flows from the body into the R atrium and from the lungs into the L atrium
    • With atrial contraction, the blood is pumped from the atria into the ventricles
    • With ventricular contraction, the blood is pumped from the R ventricle into the pulmonary artery and lungs, and from the L ventricle into the aorta and the arterial circulation
  15. Right heart circulation- deoxygenated blood
    Venous syatem -> right atrium -> right ventricle -> lungs for oxygenation via pulmonary artery
  16. Left heart circulation- oxygenated blood
    Lungs via pulmonary veins -> left atrium -> left ventricle -> aorta -> systemic circulation for tissue perfusion
  17. Coronary vessels
    • Right main coronary artery
    • Left main coronary artery
    • 2 main branches-
    • Circumflex coronary artery
    • Left anterior descending coronary artery
  18. Right coronary artery
    • Supplies:
    • R atrium, R ventricle, inferior L ventricle, posterior septum, SA node
  19. Left coronary artery
    • 2 main branches
    • LAD: descends toward anterior wall and apex of L ventricle, supplies portions of L ventricle, ventricular septum, chordae tendinae, papillary muscle, to lesser extent R ventricle
    • Circumflex: descends toward lateral wall of L ventricle and apex, supplies L atria, lateral and posterior surfaces of L ventricle, sometimes portions of intraventricular septum
  20. Coronary vessel blood flow
    • 75% of coronary blood flow occurs during diastole
    • Need diastolic pressure of 60 to maintain adequate flow to the heart muscle
    • Flow increases with activity and sympathetic stimulation
  21. What is the P wave?
    A deflection representing atrial depolarization
  22. What is the PR segment?
    • The isoelectric line from the end of the P wave to the beginning of the QRS complex, when the impulse is traveling through the AV node, where it is delayed
    • It then travels through the ventricular conduction system to the Purkinjie fibers
  23. What is the PR interval?
    • Measured from the beginning of the P wave to the end of the PR segment
    • Represents the time required for atrial depolarization as well as the impulse delay in the AV node and the travel time to the Purkinjie fibers
    • Normally measures from 0.12 to 0.20 sec (5 small blocks)
  24. what is the QRS complex?
    • Represents ventricular depolarization
    • Q wave is the first negative deflection
    • It's small and it represents septal depolarization
    • When Q wave is abnormally present it represents myocardial necrosis (cell death)
    • The R wave is the first positive deflection-may be small, large, or absent
    • The S wave is a negative deflection following the R wave
  25. What is the QRS duration?
    • Represents the time required for depolarization of both ventricles
    • Measured from the beginning of QRS complex to the J point (the junction where the QRS complex ends and the ST segment begins)
    • Normally measures from 0.04-0.10 sec (up to three small blocks)
  26. What is the ST segment?
    • Normally an isoelectric line and represents early ventricular repolarization
    • Occurs from the J point to the beginning of the T wave
    • Length varies with changes in HR, administration of meds, and electrolyte disturbances
    • Normally not elevated more than 1mm or depressed more than 0.5mm from baseline
    • Its amplitude is measured at a point 1.5 - 2mm after the J point
    • ST elevation or depression can be caused by myocardial injury, ischemia or infarction, conduction abnormalities, or the administration of meds
  27. What is the T wave?
    • Follows the ST segment and represents ventricular repolarization
    • Usually positive, rounded, and slightly asymmetric
    • If an ectopic stimulus excites the ventricles it may cause ventricular irritability, lethal dysrhythmias, possible cardiac arrest in the vulnerable heart-known as the R-on-T phenomenon
    • Waves may become tall and peaked, inverted (negative), or flat as a result of myocardial ischemia, potassium or calcium imbalances, meds, or ANS effects
  28. What is the U wave?
    • When present, follows the T wave and may result from slow repolarization of ventricular Purkinjie fibers
    • Of the same polarity as the T wave, although it is generally smaller
    • Abnormal wave may suggest an electrolyte abnormality (particularly hypokalemia) or other disturbance
    • Correct ID is important so that it is not mistaken for a P wave
  29. What is the QT interval?
    • Represents the total time required for ventricular depolarization and repolarization
    • Is meaured from the beginning of the QRS complex to the end of the T wave
    • Interval varies with age, gender, and changes in HR, lengthening with slower HR and shortening with faster rates
    • May be prolonged by certain meds, electrolyte disturbences, Prinzmetal's angina, or subarachnoid hemorrhage
    • Prolonged QT may lead to unique type of ventricular tachycardia called torsades de pointes
  30. What is artifact?
    • Interference seen on the monitor or rhythm strip, which may look like a wandering or fuzzy baseline
    • May be caused by pt mvmnt, loose or defective electrodes, improper grounding, faulty ECG equip, such as broken wires or cables
    • Some artifact can mimic lethal dysrhythmias like v tach or v fib
    • Assess pt to differentiate artifact from lethal rhythms
  31. ECG rhythm analysis
    • Determine heart rate
    • Determine heart rhythm
    • Analyze P waves
    • Measure PR interval
    • Measure QRS duration
    • Interpret the rhythm
  32. Normal rhythms
    • Normal sinus rhythm (NSR)
    • Sinus arrythmia
  33. What is NSR?
    • Rate: a/v rates of 60-100bpm
    • Rhythm: a/v rhythms regular
    • P waves: present, consistent configuration, one P wave before each QRS complex
    • PR interval: 0.12-0.20 sec and constant
    • QRS duration: 0.04-0.10 sec and constant
  34. What is sinus arrhythmia?
    • Variant of NSR
    • All the characteristics of NSR except for its irregularity
    • Rate: a/v rates btwn 60-100bpm
    • Rhythm: a/v rhythms are irregular, with shortest PP or RR interval varying at least 0.12sec from the longest PP or RR interval
    • P waves: one P wave before ea QRS complex, consistent configuration
    • PR interval: normal, constant
    • QRS duration: normal, constant
  35. What are dysrhythmias?
    • Any disorder of the heartbeat
    • Result from:
    • A disturbance in the relationship btwn electrical conductivity and the mechanical response of the myocardium
    • A disturbance in impulse formation (either from an abnormal rate or from an ectopic focus)
    • A disturbance in impulse conduction (delays and blocks)
    • The combination of several mechanisms
  36. What are tachydysrhythmias?
    • HR > 100bpm
    • Major concern in adult pt with coronary artery disease (CAD)
    • Coronary artery blood flow occurs mostly during diastole when the aortic valve is closed and is determined by diastolic time and BP in the root of the aorta
    • They shorten the time and therefore the coronary perfusion time (the amount of time available for blood to flow through the coronary arteries to the myocardium)
    • Initially increases CO and BP; however, a continued rise in HR decreases the ventricular filling time because of a shortened diiastole , decreasing the stroke volume. Consequently, CO and BP will begin to decrease, reducing aortic pressure and therefore coronary perfusion pressure
    • Increase the work of the heart, increasing myocardial oxygen demand
    • Pt may have: palpitations, chest discomfort, restlessness/anxiety, pale/cool skin, syncope from hypotension
    • This may lead to heart failure
    • Presenting symptoms are: dyspnea, lung crackles, distended neck veins, fatigue, and weakness
  37. What are bradydysrhythmias?
    • HR < 60bpm
    • Myocardial oxygen demand is reduced from the slow HR, which can be beneficial
    • Coronary perfusion time may be adequate because of prolonged diastole, which is desireable
    • Coronary perfusion pressure may decrease if HR is too slow to provide adequate CO and BP; this is a serious consequence
    • Pt may tolerate this well if BP is adequate
    • If BP not adequate, symptomatic bradydysrhythmias may lead to myocardial ischemia or infarction, dysrhythmias, hypotension, and HF
  38. What are premature complexes?
    • Early rhythm complexes
    • Occur when cardiac cell/cell group, other than SA node, becomes irritable and fires an impulse before the next sinus impulse is produced
    • The ectopic focus (abnormal focus) may be generated by atrial, junctional, or ventricular tissue
    • After the premature complex,there is a pause prior to the next normal complex, creating an irregularity in the rhythm
    • Pt may/may not feel palpitations or a skipping of the heartbeat
    • If premature complexes, esp ventricular, become more frequent, the pt may experience symptoms of decreased CO
  39. What is bigeminy?
    When normal complexes and premature complexes occur alternately in a repetitive two-beat pattern, with a pause after each premature complex so that complexes occur in pairs
  40. What is trigeminy?
    A repeated thee-beat pattern, usually occuring as two sequential normal complexes followed by a premature complex and a pause, with same pattern repeating itself in triplets
  41. What is quadrigeminy?
    A repeated four-beat pattern, usually occuring as three sequential normal complexes followed by a premature complex and a pause, with same pattern repeating itself in a four-beat pattern
  42. What are escape complexes/rhythms?
    • Occur when SA node fails to discharge or is blocked or when a sinus impulse fails to depolarize the ventricles because of an AV nodal block
    • Serve as secondary or escape pacemaker and are seen just after a pause
    • May originate from AV junctional or ventricular tissue
    • They stop when the SA or AV node can function normally
    • If pauses are followed by escape beats or rhythms, pts may feel light-headed, dizzy, or faint during the pause
  43. Classification of dysrhythmias?
    • Classified according to site of origin
    • Sites include SA node, atrial tissue, AV node, junctional tissue, and ventricular tissue
    • May be caused by a disturbance in impulse formation or by conduction delays or blocks
  44. What is sinus tachycardia?
    • SNS stimulation or vagal inhibition results in an increased rate of SA node discharge, which increases HR
    • SA node discharge > 100bpm
    • Sinus tach initially increases CO and BP
    • Continued increases in HR decrease cardiac perfusion time, diastlic filling time, and coronary perfusion pressure while increasing myocardial oxygen demand
    • Drugs such as catecholamines, atropine, caffeine, alcohol, nicotine, aminophylline, and thyroid meds may increase HR
    • Sinus tach may be a compensatory response to decreased CO or BP as occurs with hypovolemic shock, MI, infection, and HF
    • Assess for fatigue, weakness, SOB, orthopnea, neck vein distention, decreased oxygen saturation, and
    • decreased BP
    • Assess for restlessness and anxiety from decreased cerebral perfusion
    • Assess for decreased urine output from impaired renal perfusion
    • ECG pattern may show T-wave inversion or ST-segment elevation or depression in response to myocardial ischemia
  45. What is sinus bradycardia?
    • Excessive vagal stimulation (PNS) to heart causes decreased rate of sinus node discharge
    • This stimulus slows HR and decreases speed of conduction through heart
    • Sinus node discharge < 60bpm
    • Increases coronary perfusion timeMay decrease coronary perrfusion pressure
    • Myocardial oxygen demand is decreased
    • Excessive vagal stimulation may result from carotid sinus massage, vomiting, suctioning, valsalva maneuvers, occular pressure, or pain
    • Sinus brady may also result from hypoxia, inferior wall MI, admin of drugs such as beta-blockers, calcium channel blockers, and digitalis
    • Assess pt for syncope, dizziness/weakness, confusion, hypotension, diaphoresis, SOB, ventricular ectopy (superficial beats), anginal pain
  46. What is an atrial dysrhythmia?
    • The focus of impulse generation shifts away from the sinus node to the atrial tissue, which acts as an ectopic pacemaker for one or more beats
    • The shift changes the direction of atrial depolarization, resulting in a P wave shape that differs from normal P waves
    • Most common are premature atrial complexes, supraventricular tachycardia, atrial flutter, and atrial fibrillation
  47. What are premature atrial complexes?
    • Occurs when atrial tissue becomes irritable
    • This ectopic focus fires an impulse before the next sinus impulse is due
    • The premature P wave may not always be visible because it can be hidden in the preceeding T wave
    • A PAC is usually followed by a pause
    • Causes of atrial irritability iclude stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine, alcohol, drugs such as catecholamines, sympathomimetics, amphetamines, digitalis, or anesthetic agents
    • PACs can also result from myocardial ischemia, hypermetabolic states, electrolyte imbalance or atrial stretch
  48. What is supraventricular tachycardia?
    • Involves rapid stimulation of atrial tissue at a rate of 100-280bpm
    • P waves may not be visible because they are imbedded in the preceeding T wave
    • Usually due to a re-entry mechanism in which one impulse circulates repeatedly throughout the atrial pathway, restimulating the atrial tissue at a rapid rate
    • Assess for palpitations, CP, weakness, fatigue, SOB, nervousness, anxiety, hypotension, syncope
    • Cardiovascular deterioration may occur if the rate does not sustain adequate BP
  49. What is atrial fibrillation?
    • The most common dysrhythmia
    • Multiple rapid impulses from many atrail foci depolarize the atria in a totally disorganized manner at a rate of 350-600 times per minute
    • Results in a chaotic rhythm with no clear P waves, no atrial contractions, loss of atrial kick, and an irregular ventricular response
    • Often the ventricles beat with a rapid rate in response to the num,erous atrial impulses
    • Heart dilation and blood pooling in the atria can lead to thrombus formation
    • Rapid and irregular ventricular rate decreases ventricular filling and reduces CO, futher impairing the heart's perfusion ability
    • Because of loss of atrial kick, pt is at greater risk fo inadequate CO
    • Assess pt for fatigue, weakness, SOB, distended neck veins, dizziness, decreased exercise tolerance, anxiety, syncope, palpitations, chest discomfort/pain, hypotension
  50. What is atrial flutter?
    • Rapid atrial depolarization occuring at a rate of 250-350 times per min
    • The AV node blocks the number of impulses that reach the ventricles as a protective mechanism
    • May be caused by rheumatic or ischemic heart disease, HF, AV valve disease, pre-excitation syndromes, septal defects, pulmonary emboli, thyrotoxicosis, alcoholism, or pericarditis
    • Assess pt for palpitations, weakness, fatigue, SOB, nervousness, anxiety, syncope, angina, evidence of HF, shock
  51. What are junctional dysrhythmias?
    • Nodal cells in the AV junctional area can generate electrical impulses and are therefore secondary or latent pacemaker cells
    • Hane a slower rate of dicscharge, usually 40 to 60bpm, and are usually suppressed
    • Rhythms are most commonly temporary, and pts usually remain stable
  52. What are ventricular dysrhythmias?
    • Ventricles have the fewest nodal cells and are the slowest pacemaker
    • Irritable ventricular cells may generate electrical impulses and fire prematurely
    • The impulse originates in and depolarizes one ventricle first and then spreads to depolarize the other, the resulting QRS complex is wide, measuring > 0.12sec