exam 1 lecture 5 Flashcards
interpretation of ECG, Rate
R-R interval gives ventricular rate, P-P interval gives atrial rate, should be the same EXCEPT in AV block
rhythm
are interval the same, regular, irregular
conduction and repolarization, P-R interval
time of conduction through AV node, bundle of His and bundle branches. P-R interval less than .12 seconds indicates first degree AV block
WPW and LGL
see a short P-R interval
Width of QSR complex
time ventricles take to depolarize. Broadened in bundle branch block and pre-excitation condition like WPW syndrome
Q-T interval
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
U waves
usually associated with depressed ST segments and low amplitude T waves
normal sinus rhythm
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
dysrhthmias and other changes in ECG
supraventricular dysrhythmias accessory pathway-> originate in sinus, atrial or junctional
myocardial hypertrophy
atrial or ventricular
dysrythmias
ventricular or conduction blocks, repolarization phenomena (long QT), myocardial ischemia infraction: STEMI and non-STEMI
Sinus node Supraventricular dysrhythmias
sinus tachycardia, sinus bradycardia, sinus arrhythmia, sinus arrest, wandering pacemaker
atrial supraventricular dys
premature atrial contraction (PAC), paroxysmal atrial tachycardia, atrial flutter, atrial fibrillation. There is also junctional (A-V nodal) supraventricular dys.
ventricular dyshythmias
premature ventricular contractions, paroxysmal ventricular tachycardia, ventricular tachyacrdia, torsade de pointes, ventricular fibrillation
Sinus node: Sinus tachycardia
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
Sinus node: sinus bradycardia
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
Sinus node: Sinus arrhythmia
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
Sinus node: sinus arrest
failure of pacemaker cells Rate: normal, P wave: normal, QRS: normal, Rhythm: basically irregular, length of the pause is not multiple of sinus interval
sinus node: wandering pacemaker
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
Atrial: premature atrial contraction
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
PAC
normally in non diseased heart, sometimes from alcohol, smoking, caffeine, gastric overload, CHF, ischemia and COPD.
Atrial: Paroxysmal atrial tachycardia (PAT), or paroxysmal supraventricular tachycardia
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
PAT
not usually possible to determine actual pacemaker site in this condition, PAT often called paroxysmal supraventricular tachycardia (PSVT)
PAT or (PSVT)
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
PSVT and WPW
in men below 30, PSVT may occur with WPW, reduced ventricular filling time, MAP is usually reduced during PAT
Atrial: atrial flutter
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
atrial fibrillation
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
junctional (AV nodal)
SA node has failed, and AV node has taken over. P wave is INVERTED preceding QRS because of retrograde conduction into the atria
how to distinguish junctional from atrial firbrillation
P wave, NO P wave in atrial fibrillation
Idioventricular rhythm
failure of both sinus and AV nodes, originates in perkinje fibers. QRS widened.
cannon a-waves
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
premature ventricular contractions (PVC)
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)
multifocal PVC
PVC that originate from different ectopic foci. can be in pairs or triplets
Bigeminy
PVC follows every normal QRS
R on T event
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
Paroxysmal ventricular tachycardia or ventricular tachycardia (VT)
sudden rapid ventricular beat, often precipitated by a PVC that occurs during vulnerable period, creating MACRO REENTRY
VT
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
torsade de pointes
polymorphic ventricular tachycardia. Caused by hyperkalemia and long QT syndrome. macro-reentry circuit
ventricular fibrillation
micro-reentry circuits. cardiac output drops to zero. (ECG electric storm)
common cordis
precordial blow to chest, wall (puck or fist to chest), young athletes without chest protection
risk window
during the period of repolarization dispersion just before the peak of t wave
myocardial hypertrophy
caused by pressure or volume overload
atrial hypertrophy: right atrial hypertrophy
Tall peaked P waves in inferior leads: II, III and aVF. Caused by tricuspid valve disease, pulmonary valve disease, or pulmonary hypertension
left atrial hypertrophy
Two peaked P wave in lead I, often called P mitrale because main cause is disease of mitral valve
causes of rightventricular hypertrophy
pulmonary valve stenosis, tricuspid insufficiency, pulmonary hypertension, ventricular septal defect, tetraolgy of Fallot
RVH
tall R wave in lead V1 and isoelectric lead at V4-V6
Left ventricular hypertrophy
mitral valve regurgitation, aortic valve stenosis or regurgitation, systemic hypertension
AV Block, first degree
P-R interval is .2 seconds (only characteristic)
Second degree
P waves are not always followed by a QRS, sometimes QRS dropped
Second degree: Mobitz Type 1 (Wenckebach) (3:1)
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
Second degree: Mobitz type 2 (2:1)
P-R interval are normal, but a QRS is periodically dropped without warning, block us usually lower than Mobitz I
Third degree block
total heart block, AV dissociation and ventricles and atria beat independently of another. No association between P or QRS waves
Stokes-Andes syndrome
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
bundle branch block: left bundle branch block
common in heart disease. wide R waves in 1, aVL or V, may be deep wide S waves in V1-V4
right bundle branch block
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
Long QT syndrome, congenital long QT syndrome
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)
acquired Long QT syndrome
electrolyte imbalance: long St with delayed onset of T wave is seen in hypocalcemia. T wave is typically tall, narrow and pointed
other causes of long-QT
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
prolongation of period of depolarizatin
CAN RESULT IN EAD’S-> INITIATE TORSADE DE POINTES
coronary artery disease CAD
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
acute coronary syndrome
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).
stable angina versus UA
UA not triggered by certain level activity
ACS-STEMI
prolonged UA, full thickness of ventricular wall usually involved
ACS-NSTEMI
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
patient in ED presenting with ischemic-type chest discomfort
12 lead ECG is critical component of management
Prinzmetal’s variant angina
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
STEMI sequence
culprit atery can often be deduced from leads in which ST elevation is observed.
