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131 Cards in this Set
- Front
- Back
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During CPR, maintain ventilator breaths at _____ a minute
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12-15
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During pause in CPR, assess for signs of circulation for no greater than ____ seconds
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10
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When can you continue chest compressions during CPR and not pause for respirations?
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when an advanced airway has been placed
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CPR performed correctly provides ___ % of normal cardiac output
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20%
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Identification and treatment of cause of cardiac arrest is especially important when the rhythm is ____
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PEA
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precordial thump, when to use?
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witnessed VF or pulseless VT
or VT with pulse only if defribrillator nearby (may deteriorate) |
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Most defibrillators automatically reset to synchronized or nonsynchronized mode?
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non synchronized (for codes) or if rhythm deteriorates post cardioversion
If cardioverting,must reset this each time |
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successful defibrillation is less likely if any of the following are present (6)
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hypoxia
severe acidosis alkalosis local ionic imbalance ischemia Long VF duration |
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Procedure to follow when giving drugs during code
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Give in central line if available
flush with 20 ml NS post elevate extremity if given peripheral |
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pharmacologic agents for cerebral resuscitation post arrest (5)
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osmotics (mannitol) to increase cortical circulation
Ca. channel blockers to prevent cerebral vasospasm anticonvulsants muscle paralytics to decr. cerebral O2 demand Steroids to reduce cerebral edema |
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Brugada syndrome
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main cause of sudden unexplained death (esp. southeast asia/japanese)
ST segment elevation V1-2 & R. BBB sudden death from VT/VF |
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"holiday heart"
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syndrome caused by excessive alcohol consumption
may cause dysrhythmias usually SVT |
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define enhanced automaticity
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pacemaker cells firing rate increases above inherent rate
(resting membrane potential is less negative, increasing chance of depolarization) |
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causes of enhanced automaticity (9)
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hypoxia
hypercapnia ischemia, infarction hypokalemia, hypocalcemia catecholamines hyperthermia dignitalis toxicity stretching of heart muscle |
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What is the cause of MOST atrial, junctional and ventricular ectopic beats (and most VTs!)
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enhanced automaticity of pacemaker cells
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define depressed automaticity
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resting membrane potential is more negative, decreasing chance of depolarization
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causes of depressed automaticity (6)
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vagal stimulation
hyperkalemia hypercalcemia decreased catecholamines hypothermia beta blockers |
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what is an afterdepolarization?
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an abnormal electrical impulse that occurs during or after repolarization of an action potential.
If its strong enough to reach threshold, a triggered beat occurs. May be early or late. |
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what is main cause of early afterdepolarization?
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prolonged QT (aka prolonged repolarization)
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Causes of sinus bradycardia (10)
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athletic heart
sleep vagal stimulation MI (inferior/posterior) fiberodegenerative SA node changes (aka sick sinus syndrome) increased ICP hypothermia hypothyroid cervical/mediastinal tumor drug effects: digitalis, beta blockers, opiates etc. |
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treatment of sinus bradycardia if symptomatic (2)
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atropine
transcutaneous pacing |
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Causes of sinus tachycardia (13)
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stress, fear, anxiety, pain
exercise hypovolemia/hypervolemia shock hypoxia fever anemia hyperthyroidism MI (anterior) fibrodegenerative changes (sick sinus) HF PE Drug effect (epi, dopamine etc) |
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sinus tachycardia should be controlled in patients who also have _______
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heart disease
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Treatment for symptomatic sinus tachycardia
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treat cause! (anxiety, pain, fever, hypovolemia, HF etc)
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Causes of sinus block (sinus exit block) (5)
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fibrodegenerative changes of SA node
ischemia of SA node (MI) vagal stimulation inflammatory heart disease (i.e. myocarditis) Drug toxicity: dig |
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Causes of sinus arrest (5)
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fibrodegenerative changes
ischemia SA node (MI) vagal stimulation electrolyte imbalance (K, mag) drug toxicity: dig |
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Causes of PAC's (10)
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increased sympathetic stimulation (stress, pain, fear)
exercise inflammatory heart disease myocardial ischemia valvular heart disease HF electrolyte imbalance hypoxia drug effect: caffeine, nicotine, ETOH drug toxicity: dig |
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How frequent do PAC's have to be to be considered significant?
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> 6 / minute
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wandering atrial pacemaker causes (3)
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vagal stimulation
sinus bradycardia dig toxicity |
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causes of atrial fibrillation
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HF
cardiomyopathy MI (esp. anterior) Valvular heart disease hyperthyroidisim HTN after cardiotomy (incision in heart) pulmonary HTN WPW syndrome Drug effect: ETOH |
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What the heck is WPW (Wolff Parkinson White) syndrome?
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WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.
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How long does patient have to be in A-fib for anticoags to be needed before trying to convert to NSR?
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48 hrs
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Causes of atrial flutter (10)
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HF
MI valvular heart disease HTN after cardiotomy Pulm. HTN hyperthyroidism drug effect: ETOH drug tox: dig |
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Causes of PJC's (6)
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MI (esp, inferior)
HF Valvular heart disease hypoxia drug effect: nicotine, caffeine, ETOH drug tox: dig |
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Causes of Jxnl escape rhythm (8)
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vagal stimulation
SA block complete AV block MI valvular heart disease hypoxia after cardiotomy drug tox: dig |
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Treatment for Jxnl escape rhythm
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treat failure of SA node
atropine pacer may be needed |
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Causes of accelerated jxnl rhythm (9)
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vagal stimulation
SA block complete AV block MI reperfusion of myocardium hypoxia inflammatory heart disease after cardiotomy drug tox: dig |
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inflammatory heart disease (3 types based on location)
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myocarditis
endocarditis pericarditis |
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treatment for accelerated jxnl rhythm
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treat failure of SA node
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Causes of Jnxl tachycardia (5)
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MI
reperfusion of myocardium inflammatory heart disease after cardiotomy drug tox: dig |
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treatment for Jxnl tachycardia
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treat cause
vagal stimulation adenosine amiodarone beta blockers/Ca ch. blockers (if normal LV fxn!) |
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Causes of 1st degree AV block (9)
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normal variation
MI conduction system fibrosis inflammatory heart disease vagal stimulation after cardiotomy myocardial contusion (bruise) hyperkalemia drug tox: dig, beta blockers, Ca.Ch. blockers |
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What do you need to be worried about when patient is in 1st degree AV block?
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progression to 2nd degree. Just observe for now.
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Causes of 2nd degree Mobitz I (wenckebach) block (6)
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MI (inferior/posterior)
conduction system fibrosis inflammatory heart disease after cardiotomy myocardial contusion drug tox: dig, beta block, ca. ch. blockers |
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treatment for Mobitz I
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usually none
monitor for progression of block atropine if rate slow and patient symptomatic |
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Causes of 2nd degree Mobitz II block (7)
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MI (anterior)
HTN valvular heart disease conduction system fibrosis inflammatory heart disease after cardiotomy myocardial contusion |
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Where does block in Mobitz II occur?
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bundle of His, which accounts for slightly widened QRS
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treatment Mobitz II
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atropine (not always helpful though)
prophylactic use of pacemaker |
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Causes of Third degree AV block (8)
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MI
conduction system fibrosis inflammatory heart disease after cardiotomy myocardial contusion hypoxia electrolyte imbalance: potassium drug tox: dig |
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In 3rd degree block, if no ______ rhythm is established, the patient has ventricular ________.
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escape, asystole
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Treatment 3rd degree AV block
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observe for hypoperfusion (esp. if inferior MI with jxnl escape rhythm)
atropine (doesn't always help though) pacemaker (esp. if anterior MI, inferior with V escape rhythm) |
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Causes of L. BBB (3)
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MI (anterior)
fibrodegenerative changes after cardiotomy |
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what type of bundle branch block is most serious?
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bifasicular block more serious than R. BBB especially in presence of acute MI
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How many bundle branches are there?
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3 (2 on left, one on right)
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treatment for LBBB
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new LBBB in acute MI may be treated with prophylactic pacemaker, esp. if an AV nodal block is also present
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Causes of R. BBB (5)
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MI (anterior/inferior)
fibrodegenerative changes after cardiotomy PA catheter insertion! acute PE |
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Any treatment for R. BBB?
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Nope. Just monitor closely for development of L. BBB
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Causes of PVC's (10)
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Increased SNS
MI reperfusion of myocardium HF ventricular aneurysm cardiomyopathy hypoxia acidosis electrolyte imbalance: potassium, calcium, mag drug tox: dig |
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When are PVC's concerning/significant?
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When frequent (> 6/minute)
bigeminal multifocal R on T phenomenon couplets runs (3 or more in a row) |
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PVC's treatment
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treat cause (oxygen, electrolytes)
If frequent, Amio, lidocaine, beta blockers |
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Causes of monomorphic VT (11)
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MI
reperfusion of myocardium ventricular aneurysm cardiomyopathy valvular heart disease after cardiotomy R on T PVC hypoxia acidosis electrolyte imbalance: hypokalemia Drug tox: dig |
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Treatment of monomorphic VT
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treat cause
normal LV: amio, lidocaine, procain Impaired LV: amio, lidocaine, cardioversion IF symptomatic: immediate cardioversion If pulseless: defib, epi etc. CODE! |
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Causes of polymorphic VT (i.e. Torsades) (10)
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antidysrhythmic drugs (Class IA, Class III-Amio)
Tricyclic antidepressants Phenothiazines organic insecticides electrolyte imbalance (hypoK, hypomag, hypocalcemia) Congenital Long QT syndrome or Brugada syndrome Marked bradycardia hypothermia subarachnoid hemorrhage |
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how to prevent polymorphic VT
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Prevent by monitoring QT closely, hold drugs that prolong QT interval
...and treat cause |
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Causes of Vfib (9)
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MI
R on T PVC electric shock Brugada syndrome drowning hypothermia hypoxia drug tox: dig dying heart :( |
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Vfib is lethal within ____ minutes
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4-6 minutes
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treatment Vfib
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Code time baby!
immediate defibrillation, CPR, epi etc. |
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Causes of idioventricular rhythm (5)
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vagal stimulation
failure of higher pacemakers (i.e. ischemia, fibrosis etc) MI third degree AV block drug tox: dig |
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treatment idioventricular rhythm
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accelerate higher pacemakers with atropine
pacemaker If pulseless...code! |
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Causes of accelerated idioventricular rhythm (4)
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failure of higher pacemakers
MI reperfusion of myocardium drug tox: dig |
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Causes of asystole (9)
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vagal stimulation
MI third degree AV block anaphylaxis drug overdosage hypoxia acidosis shock dying heart :( |
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Define reentry (heart conduction)
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an impulse travels through an area of the myocardium and depolarizes it but then reenters the same area to depolarize it again
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requirements for reentry to occur
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an available circuit: esp. where conduction velocity is abnormally slow
an area of slowed conduction/unidirectional block |
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Reentry is caused by (4)
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some ectopy
some VTs some SVTs WPW syndrome |
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Lown-Ganong-Levine syndrome
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an accessory pathway caused by AV nodal bypass tract, small AV node, fibers through node that don't have the built in delay feature
Causes: short PR, tachydysrhythmias |
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Kent bundle
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bypasses the AV node, present in WPW syndrome
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delta wave
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slurring of first portion of QRS, aka upstroke from P wave over to R wave
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Mahaim fibers
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caused by nodoventricular or fasciculoventricular fibers
causes: short PR, wide QRS, tachydysrhythmias |
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aberrant conduction
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cardiac conduction through pathways not normally conducting cardiac impulses, particularly through ventricular tissue.
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Aberrant conduction occurs most often when...(3)
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rate is rapid
PACs are very premature There are changes in cycle length (i.e. afib |
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How do we differentiate between ectopy and aberrancy?
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QRS complex morphology is how.
Aberrancy QRS 0.12 -0.14 ectopy QRS > 0.14 |
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Which is more common and more serious: ectopy or aberrancy?
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ectopy (and aberrancy is no more serious than the supraventricular mechanism that caused it)
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contraindications to cardioversion (5)
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tachydysrhythmias that result from dig toxicity
nonsustained tachydysrhythmias long standing AF AF with normal/slow V rate multifocal A tach |
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Synchronized cardioversion: how many joules?
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25-200 J
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Vaughan-Williams antidysrhythmia Classification System: IA effect
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blocks sodium influx (depresses rate of depolarization)
prolongs repolarization & action potential duration negative inotrope prolongs QT and QRS complex |
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Antidysrhythmia Class IA examples
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Procainamide
Quinidine Disopyramide |
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Antidysrhythmia Class IB effects
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blocks sodium influx during phase O, which depresses rate of depolarization
shortens repolarization & action potential duration suppresses ventricular automaticity in ischemic tissue |
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Antidsrhythmia IB examples
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Lidocaine
Phenytoin (dilantin) |
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Antidysrhythimia Class IC effects
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blocks sodium influx, which depresses rate of depolarization
does not change repolarization and action potential duration has proarrhythmogenic potential |
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antidysrhythmia class IC examples
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Flecainade
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Antidysrhythmias Class II effects
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depresses SA node automaticity
increases refractory period of atrial and AV jxnl tissue to slow conduction shortens action potential duration inhibits sympathetic activity |
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Antidysrhythmia Class II examples
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Beta blockers (propranolol, esmolol)
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Antidysrhythmia Class III effects
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blocks potassium movement during phase III
increases action potential duration prolongs effective refractory period |
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Antidysrhythmia Class III examples
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Amio
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Antidysrhythmia Class IV effects
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blocks calcium movement during phase II
depresses automaticity in the SA & AV nodes prolongs the conduction time in the AV jxn and increases the refractory period at the AV jxn negative inotrope |
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How does adenosine work?
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blocks reentry mechanism
shortens action potential of atrial tisssue with little/no effect on action potential of ventricle prolongs AV nodal refractory period decreases SA node automaticity and slows sinus rate |
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How does atropine work?
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blocks parasympathetic nervous system effects to increase SA node firing rate and improve AV nodal conduction
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How does Digitalis work?
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slows conduction through AV node and prolongs AV nodal refractory period
decreases SA node automaticity and slows sinus rate |
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In the presence of AMI, which of the heart blocks would indicate transvenous pacing?
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Any symptomatic blocks OR...
anterior MI: second degree AV block Mobitz II Inferior MI: Third degree with Jxnl escape rhythm if symptomatic Any Third degree block with ventricular escape rhythm |
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asynchronous pacing
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also called "fixed rate"
ignores intrinsic activity of heart rare today! |
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synchronous pacing
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"demand" pacing
pacer delivers stimulus only when intrinsic pacemaker fails |
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Pacemaker code: what is first letter? what is second letter?
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chamber paced (O,A, V, D)
chamber sensed (O, A, V, D) |
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Pacemaker code: what is third letter? What is fourth?
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response to sensing (O, T=triggered, I=inhibited, D=dual)
programmability rate modulation (0, P=simple programmable, M= multiprogrammable, C= communicating, R=rate modulation) |
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Pacemaker code: what is the 5th letter?
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antitachyarrhythmia functions
0=none P= pacing S= shock D=dual |
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Interventions if pacer fails to sense
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position patient on left side (or to whatever position sensing was last seen)
make sure pacer is NOT set on asynchronous increase sensitivity check connections |
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Interventions if pacer fails to capture
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position patient on L side (or last position when it was capturing)
increase mA replace battery correct metabolic/electrolyte imbalance |
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When do we use a magnet with pacemakers?
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To turn off AICD
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What causes organ ischemia in hypertensive crisis?
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platelet aggregation, intravascular coagulation, arteriolar spasm and edema
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Target organs most likely to be damaged in hypertensive crisis are (4)
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heart
kidney brain retina |
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How fast can you safely decrease BP in hypertensive crisis?
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reduce MAP by at most 20-25% during first 2 hours because too fast can cause neuro damage by decreasing cerebral perfusion pressure (CPP)
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Peripheral arterial disease
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partial/total occlusion of an artery by atherosclerosis/arteriosclerosis
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arteriosclerosis
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fibrosis/calcification of arteries
usually occurs with aging |
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What part of arteries do most significant occlusions occur?
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bifurcations
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Arterial occlusion with pain at rest signifies that artery is (what)% occluded?
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90-95%
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objective s/s of peripheral artery disease (of terminal aorta/iliac)
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cool lower extremities
hair loss lower extremities decr./absent femoral/iliac pulses |
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objective s/s of peripheral artery disease (of femoral and popliteal arteries)
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decreased sensation/paresthesia of lower extremities
lower extremity hair loss coolness LE's nonhealing ulcers toes/trauma points |
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endarderectomy
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plaque is surgically seperated from arterial wall and removed
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acute arterial occlusion
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acute complete occlusion of an artery by thrombosis in an already narrowed artery, embolism or trauma
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How can trauma cause acute arterial occlusion?
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compression of artery from swelling such as compartment syndrome in a fracture
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What are the signs of acute arterial occlusion?
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the 6 P's
pain pallor pulselessness paresis/paralysis paresthesia polar (cold) |
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Is there still a peripheral pulse in acute arterial occlusion?
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Yes or no. If yes it is diminished
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aortic aneurysm
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permanent localized dilation of aorta with an increase of at least 1.5 times its normal diameter
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pathophysiology of aortic aneurysm
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elastin provides elasticity to vessels while collagen provides strength. It is thought that elastin destruction is the triggering event of aneurysm formation.
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What leads to aortic aneurysm dissection?
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hematoma formation in the medial layer causes longitudinal seperation of the layers of the aorta
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a false aortic aneurysm vs. true
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false = does not involev all layers of artery (i.e. in arterial cannulation)
true= involves all layers |
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When does aneurysm become symptomatic?
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usually when dissection or rupture occurs
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carotid arterial stenosis
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atherosclerotic plaque accumulate at the bifurcation of the internal and external carotid arteries
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Indication for surgical repair of carotid arterial stenosis
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occlusion of 70% or greater of internal carotid or mild stroke in past 6 months
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What is one inpatient cause of myocardial contusion?
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vigorous CPR
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What happens in cardiac tamponade?
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fluid or blood accumulates in the pericardial space (50 ml-2L can cause depending on how fast/slow), intrapericardial pressures get high and heart can't fill during diastole
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Beck's triad
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hypotension
distended neck veins muffled heart sounds |
