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Cardio > exam 1 lecture 5 > Flashcards

exam 1 lecture 5 Flashcards

1
Q

interpretation of ECG, Rate

A

R-R interval gives ventricular rate, P-P interval gives atrial rate, should be the same EXCEPT in AV block

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2
Q

rhythm

A

are interval the same, regular, irregular

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3
Q

conduction and repolarization, P-R interval

A

time of conduction through AV node, bundle of His and bundle branches. P-R interval less than .12 seconds indicates first degree AV block

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4
Q

WPW and LGL

A

see a short P-R interval

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5
Q

Width of QSR complex

A

time ventricles take to depolarize. Broadened in bundle branch block and pre-excitation condition like WPW syndrome

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6
Q

Q-T interval

A

time ventricles take to repolarize. QT is shorter in fast heart rates and longer in LQTS. should be less than half preceding RR interval at resting rate

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7
Q

U waves

A

usually associated with depressed ST segments and low amplitude T waves

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8
Q

normal sinus rhythm

A

QRS after each P wave, P-R interval is typically .12-.2 seconds, R-R interval is regular about .6-1 seconds apart, each beat is looks exactly like any other beat

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9
Q

dysrhthmias and other changes in ECG

A

supraventricular dysrhythmias accessory pathway-> originate in sinus, atrial or junctional

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10
Q

myocardial hypertrophy

A

atrial or ventricular

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11
Q

dysrythmias

A

ventricular or conduction blocks, repolarization phenomena (long QT), myocardial ischemia infraction: STEMI and non-STEMI

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12
Q

Sinus node Supraventricular dysrhythmias

A

sinus tachycardia, sinus bradycardia, sinus arrhythmia, sinus arrest, wandering pacemaker

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13
Q

atrial supraventricular dys

A

premature atrial contraction (PAC), paroxysmal atrial tachycardia, atrial flutter, atrial fibrillation. There is also junctional (A-V nodal) supraventricular dys.

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14
Q

ventricular dyshythmias

A

premature ventricular contractions, paroxysmal ventricular tachycardia, ventricular tachyacrdia, torsade de pointes, ventricular fibrillation

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15
Q

Sinus node: Sinus tachycardia

A

rate 101-160 beats/min. QRS: normal, conduction: P-R normal, rhythm: usually regular. Pulse pressure may be reduced because of a lower stroke volume and decreased time for peripheral (diastolic) runoff, increased diastolic pressure. Include: increased circulating catecholamines and sympathetic stimulation, possibly as a result of stress, anxiety, hypoxia

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16
Q

Sinus node: sinus bradycardia

A

is less 60 beats/minutes at rest (R-R interval) Rate: 40-59 bpm, QRS: normal, Conduction: P-R normal or slightly increased at slower rates, Rhythm: regular or slightly irregular. PP may be increased due to a larger stroke volume (systolic pressure is elevated) and increased time for peripheral runoff diastolic pressure. Often seen as normal variation in trained long distance runners, during sleep, or in response to parasympathetic stimulation during vagal maneuvers

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17
Q

Sinus node: Sinus arrhythmia

A

normal variaton of sinus rhythm, often a vagal tone effect, associated with inspiration and expiration, common in children. rate: 45-10 bmp, QRS normal, P-R normal, rhythm regularly irregular

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18
Q

Sinus node: sinus arrest

A

failure of pacemaker cells Rate: normal, P wave: normal, QRS: normal, Rhythm: basically irregular, length of the pause is not multiple of sinus interval

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19
Q

sinus node: wandering pacemaker

A

varying rhythm in which the P wave may vary in direction. P-R interval may vary, the cause may be inflamed and irritated atrial tissue or digitalis toxicity, which can be cause DAD due to elevated intracellular calcium. rate: variable, P wave:variable, QRS: normal, conduction: P-R interval according to site of pacemaker Rhythm: irregular

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20
Q

Atrial: premature atrial contraction

A

atrial ectopic focus. P-wave usually has different morphology from a normal sinus P-wave because it originates from an ectopic pacemaker, sometimes is obscured Rate: variable, normal or accelerated. P-wave: from normal sinus P wave because originate from an ectopic pacemaker QRS:normal. conduction: ectopic beats may have a different P-R interval from sinus beats, often shortened. Rhythm: PAC’s occur prematurely in cycle. systolic pressure following a PAC is often reduced, reflecting reduced filling time of ventricles

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21
Q

PAC

A

normally in non diseased heart, sometimes from alcohol, smoking, caffeine, gastric overload, CHF, ischemia and COPD.

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22
Q

Atrial: Paroxysmal atrial tachycardia (PAT), or paroxysmal supraventricular tachycardia

A

associated by a premature atrial contraction due to an ectopic focus in atria or AV node. Can also originate from re-entry. Last a few seconds or minutes.manifest by a sudden train of very rapid heart beats. QRS-T region of ECG usually appears normal, but P-wave may be missing, inverted or obscured in preceding T wave

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23
Q

PAT

A

not usually possible to determine actual pacemaker site in this condition, PAT often called paroxysmal supraventricular tachycardia (PSVT)

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24
Q

PAT or (PSVT)

A

ca be caused by a lot of caffeine, nicotine, alcohol, during anxiety attacks. can be stopped by Valsalva maneuver, or by carotid sinus massage, both these increase parasympathetic which slow down SA and AV nodes

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25
Q

PSVT and WPW

A

in men below 30, PSVT may occur with WPW, reduced ventricular filling time, MAP is usually reduced during PAT

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26
Q

Atrial: atrial flutter

A

atrial rates of 250-350 bmp.caused by Macro-reentry. Can be a fixed ratio of flutter waves to QRS but not always. Coordinated circus movement around opening of vena cavae or tricuspid valve. rate: 250-350, ventricular rate: 150-175, P wave: NOT PRESENT. QRS: normal. Conduction: 2;1 atrial/ventricular is most common. rhythm: regular

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27
Q

atrial fibrillation

A

can be caused by any disease process that increases atrial size, decreases conduction velocity, decreases refractory period duration, caused by MICRO REENTRY loops. No P wave. QRS normal. irregularly irregular

28
Q

junctional (AV nodal)

A

SA node has failed, and AV node has taken over. P wave is INVERTED preceding QRS because of retrograde conduction into the atria

29
Q

how to distinguish junctional from atrial firbrillation

A

P wave, NO P wave in atrial fibrillation

30
Q

Idioventricular rhythm

A

failure of both sinus and AV nodes, originates in perkinje fibers. QRS widened.

31
Q

cannon a-waves

A

atria contract during or after onset of ventricular contraction. RA is contracting against a closed triscuspid vavle (also seen in 3rd degree AV block). Ventricular filling reduced. reduced cardiac output

32
Q

premature ventricular contractions (PVC)

A

due to one or more ectopic foci in ventricles, the have WIDE QRS waves with NO PRECEDING P WAVES. reduced pulse pressure (less time to fill)

33
Q

multifocal PVC

A

PVC that originate from different ectopic foci. can be in pairs or triplets

34
Q

Bigeminy

A

PVC follows every normal QRS

35
Q

R on T event

A

T waves defines ventricular repolarization phase, and during this vulnerable period of repolarization dispersion a depolarizing pulse from PVC may take a circuitous route that avoids refractory regions,can lead to reentry rhythms or circus movements-> ventricular tachycardia or fibrillation

36
Q

Paroxysmal ventricular tachycardia or ventricular tachycardia (VT)

A

sudden rapid ventricular beat, often precipitated by a PVC that occurs during vulnerable period, creating MACRO REENTRY

37
Q

VT

A

can be life threatening because ventricles don’t have time to fill properly, leading to reduction in cardiac output, fainting, or MI. Also can lead to ventricular fibrillation

38
Q

torsade de pointes

A

polymorphic ventricular tachycardia. Caused by hyperkalemia and long QT syndrome. macro-reentry circuit

39
Q

ventricular fibrillation

A

micro-reentry circuits. cardiac output drops to zero. (ECG electric storm)

40
Q

common cordis

A

precordial blow to chest, wall (puck or fist to chest), young athletes without chest protection

41
Q

risk window

A

during the period of repolarization dispersion just before the peak of t wave

42
Q

myocardial hypertrophy

A

caused by pressure or volume overload

43
Q

atrial hypertrophy: right atrial hypertrophy

A

Tall peaked P waves in inferior leads: II, III and aVF. Caused by tricuspid valve disease, pulmonary valve disease, or pulmonary hypertension

44
Q

left atrial hypertrophy

A

Two peaked P wave in lead I, often called P mitrale because main cause is disease of mitral valve

45
Q

causes of rightventricular hypertrophy

A

pulmonary valve stenosis, tricuspid insufficiency, pulmonary hypertension, ventricular septal defect, tetraolgy of Fallot

46
Q

RVH

A

tall R wave in lead V1 and isoelectric lead at V4-V6

47
Q

Left ventricular hypertrophy

A

mitral valve regurgitation, aortic valve stenosis or regurgitation, systemic hypertension

48
Q

AV Block, first degree

A

P-R interval is .2 seconds (only characteristic)

49
Q

Second degree

A

P waves are not always followed by a QRS, sometimes QRS dropped

50
Q

Second degree: Mobitz Type 1 (Wenckebach) (3:1)

A

P-R interval gets longer and longer until a QRS is dropped, then cycle begins again. side of block almost always AV node, or junction between atrium and AV node

51
Q

Second degree: Mobitz type 2 (2:1)

A

P-R interval are normal, but a QRS is periodically dropped without warning, block us usually lower than Mobitz I

52
Q

Third degree block

A

total heart block, AV dissociation and ventricles and atria beat independently of another. No association between P or QRS waves

53
Q

Stokes-Andes syndrome

A

3rd degree block be associated with prolonged ventricular standstill until ventricular or junctional focus begins to fire, cardiac arrest is prolonged and cerebral ischemia and syncope

54
Q

bundle branch block: left bundle branch block

A

common in heart disease. wide R waves in 1, aVL or V, may be deep wide S waves in V1-V4

55
Q

right bundle branch block

A

wide S waves in lead I. Two superimposed R waves may be visible in precordial leads. V1 mainly looks at right heart, the second R will get smaller and R larger as move through leads V2-V6

56
Q

Long QT syndrome, congenital long QT syndrome

A

risk of sudden death from torsade de pointes leading to ventricular fibrillation can be as high as 50%. 7 mutations in genes have been identified. Mutations have been in: sodium channels, potassium channels, ankyrin B, L-type calcium channel (timothy syndrome)

57
Q

acquired Long QT syndrome

A

electrolyte imbalance: long St with delayed onset of T wave is seen in hypocalcemia. T wave is typically tall, narrow and pointed

58
Q

other causes of long-QT

A

alcoholism, slow heart rates, percarditis, left ventricular hypertrophy, hypothermia, CNS disorders, quinidine, procainamide, tricyclic antidepressants, diispyramide, amiodarone, phenthiazine and cocaine. Some specifically block cardiac potassium channels

59
Q

prolongation of period of depolarizatin

A

CAN RESULT IN EAD’S-> INITIATE TORSADE DE POINTES

60
Q

coronary artery disease CAD

A

result atherosclerosis, development of arterial lesions that can lead to narrowing of the lumen and to thrombotic events that can obstruct the lumen completely. can restrict blood to part of myocardium and can lead to angina pain on exertion-> pain dies away when exercise stops-> stable angina

61
Q

acute coronary syndrome

A

results from disruption of previously nonsevere lesion leading to stenosis or blockage of culprit vessels and acute myocardial ischemia. Divided into STEMI or non-STEMI, unstable angina (UA).

62
Q

stable angina versus UA

A

UA not triggered by certain level activity

63
Q

ACS-STEMI

A

prolonged UA, full thickness of ventricular wall usually involved

64
Q

ACS-NSTEMI

A

severe coronary artery narrowing, elevation of cardiac biomarkers (troponins or Ck-MB), in absence of ST elevation. MI usually occurs in subendocardial region. Result usually subendocardial ischemia and ST depression coupled with US

65
Q

patient in ED presenting with ischemic-type chest discomfort

A

12 lead ECG is critical component of management

66
Q

Prinzmetal’s variant angina

A

transient vasospasm of coronary vessels, triggered by substances released from an atherosclerotic plaque. non-infraction, transiet ST segment elevations coinciding with transient periods of anignal pain

67
Q

STEMI sequence

A

culprit atery can often be deduced from leads in which ST elevation is observed.

Cardio (8 decks)

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