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critical care test 3

QuestionAnswer
count the numbers of QRS complexes on a 6-second rhythm strip and multiply by 10. the least accurate of all the methods 6-second strip method
there are 300 big blocks every minute, so count the number of big blocks between consecutive QRS complexes an divide that number into 300. the fastest method the memory method
count the number of little blocks between QRS complexes and divide into 1,500, since there are 1,500 little blocks in one minute the little block method
is concerned with the spacing of the QRS complexes rhythm regularity
this in which the R-R intervals vary by only one or two little blocks. the QRS complexes usually look alike regular
regular rhythm that is interrupted by either premature beats or pause regular but interrupted
are those that arrive early, before the next normal beat is due premature beats
this is which the R-R intervals vary, not just because of premature beats or pauses, but because the rhythm is intrinsically chaotic irregular
calculate the heart rate by choosing any two successive QRS complexes and using the little block or memory method to calculate HR for regular rhythms
calculate the mean rate by using the 6-second strip method, and then calculate the heart rate range using the little block or memory method to calculate HR for irregular rhythms
ignore the premature beats and calculate the heart rate, using the little block or memory method, on an interrupted part of the strip to calculate HR for rhythms that are regular but interrupted by premature beats
calculate the heart rate range slowest to fastest, along with the mean rate to calculate HR for rhythms that are regular but interrupted by pause
the normal rhythm originating from he sinus node is called normal sinus
heart rate for normal sinus 60-100
in normal sinus p waves should be upright, rounded and "married" to the QRS complexes
PR interval in normal sinus 0.12-0.20 seconds
ORS interval in normal sinus <0.12 seconds
heart rates that are too slow or too fast can cause symptoms of decreased cardiac output
the criteria that must be met for the rhythm to be sinus in origin 1) upright matching P waves followed by a QRS 2) PR intervals constant 3) heart rate less than or equal to 160 at rest
the width and deflection of the QRS complex is irrelevant in determining whether a rhythm originates in the sinus node
sinus rhythm is the normal rhythm
heart rate of sinus rhythm 60-100
regularity of sinus rhythm regular
p waves of sinus rhythm upright in most leads, on P to each QRS, same shape, P-P interval in regular
PR interval in sinus rhythm 0.12-0.20 seconds
QRS interval in sinus rhythm <0.12 seconds
slower than normal rhythm from the sinus node sinus bradycardia
heart rate in sinus brady <60
regularity in sinus brady regular
p waves in sinus brady upright in most leads, one P to each QRS, same shape, P-P interval regular
PR interval in sinus brady 0.12-0.20 seconds
QRS interval in sinus brady <0.12 seconds
causes of sinus brady vagal stimulation, MI, hypoxia, digitalis toxicity, other med side effects
is sinus brady common in athletes yes
adverse effect of sinus brady decreased cardiac output
treatment for sinus brady none unless patient is symptomatic. atropine, pacemaker, epinephrine, dopamine, O2
the sinus node fires at a heart rate faster than normal sinus tachycardia
heart rate in sinus tach 101-160
regularity of sinus tach regular
p waves in sinus tach upright in most leads, one P to each QRS, same shape, P-P interval regular
PR interval in sinus tach 0.12-0.20 seconds
QRS interval in sinus tach <0.12 seconds
causes of sinus tach atropine or bronchodilators, emotional upset, PE, MI, CHF, fever, inhibition of vagus nerve, hypoxia, thyrotoxicosis
adverse effects of sinus tach decreased cardiac output
treatment for sinus tach treat the cause, beta-blockers, O2
the criteria that must be met for it to be atrial in origin 1) matching upright Ps, atrial rate >160 2) No Ps at all 3) P waves of > or = 3 different shapes 4) premature abnormal P wave 5) Heart rate > or = 130, rhythm regular, P waves not discernible
are premature beats that are fired out by irritable atrial tissue before the next sinus beat is due premature atrial complexes (PAC)
heart rate with a PAC can occur at any rate
regularity with a PAC regular but interrupted (by the PAC)
p waves with PAC shaped differently from sinus P waves, premature P waves of PACs may be hidden in T wave on preceding beat.
PR interval with PAC 0.12-0.20 seconds
QRS interval with PAC <0.12 seconds. QRS will be absent after a nonconducted PAC
the most common cause of an unexplained pause is a nonconducted PAC
causes of PAC Medications ( stimulants, caffeine, bronchodilators), tobacco, hypoxia, heart disease
are occasional PACs normal yes
adverse effects of PACs frequent PACs can be an early sign of impending heart failure or impending a-tach or a-fib, usually no ill effects from occasional PACs
treatment for PACs usually none needed. omit caffeine, tobacco, and other stimulants. can give digitalis, CCB, or beta blockers to treat if needed. treat HF if present. O2
s rhythm that results when one irritable atrial focus fires out regular impulses at a rate so rapid that a fluttery pattern in produced instead of P waves atrial flutter
heart rate of atrial flutter atrial rate of 250-350, ventricular rate depends on the conduction ratio
regularity of atrial flutter regular if the conduction ratio if constant; irregular is the conduction ratio varies; can look regular but interrupted at times
p waves in atrial flutter no p waves present; flutter waves are present instead
PR interval in atrial flutter PR is not measured, since there are no real P waves
QRS interval in atrial flutter <0.12 seconds
cause of atrial flutter almost always implies heart disease; PE, valvular heart disease, thyrotoxicosis, or lung disease
adverse effects of atrial flutter can be well tolerated at normal heart rates; decreased cardiac output
treatment of atrial flutter digitalis, CCB, beta blockers, adenosine, and carotid sinus massage. electrical cardioversion can be done if meds are ineffective or the patient is unstable
hundreds of atrial impluses from different locations all fire at the same time atrial fibrillation
heart rate with a-fib atrial rate is 350-700; ventricular rate varies
regularity of a-fib irregularly irregular; completely unpredictable
p waves with a-fib no p waves are present; fibrillatory waves are present instead
PR interval with a-fib since there are no p waves, there is no PR interval
QRS interval with a-fib <0.12 seconds
causes of a-fib MI, lung disease, valvular heart disease, hyperthyroidism
adverse effects of a-fib decreased cardiac output; blood clots which can result in MI, strokes, or blood clots in the lung
treatment for a-fib depends on duration of a-fib; if < 48 hrs the goal is to convert back to sinus. digitalis, CCB, beta blockers amiodorone, or electrical cardioversion; >48 hrs goal is to control heart rate. anticoagulants, cardioversion is delayed, heparin IV, TEE, O2
is a catchall tern given to tachycardias that are superventricular; that is they originate above the ventricles in either sinus node, the atrium, or the AV junction, but whose exact origin cannot be identified because P waves are not discernible supraventricular tachycardia (SVT)
heart rate in SVT about 130 or higher (usually >150)
regularity in SVT regular
p waves in SVT not discernible
PR interval in SVT PR cannot be measured since P waves cannot be positively identified
QRS interval in SVT <0.12 seconds
causes of SVT the atria becomes hyper; medications (stimulants, caffeine, bronchodilators), tobacco, hypoxia, heart disease
adverse effects with SVT decreased cardiac output
treatment for SVT adenosine, digitalis, ibutilide, CCB, beta blockers, O2, elective cardioversion can also be done if the patient is unstable
premature beats that originate in irritable ventricular tissue before the next sinus beat is due premature ventricular complexes (PVC)
heart rate in PVC can occur at any rate
regularity in PVC regular but interrupted
p waves in PVC usually not seen
PR interval with PVC PR not applicable
QRS interval with pVC >0.12 seconds; wide and bizarre in shape
t wave with PVC slopes off in the opposite direction to the QRS
causes of PVCs heart disease, hypokalemia, and hypoxia are the big three reasons; low blood mag levels, stimulants, caffeine, stress or aniexty
adverse effects with PVCs occasional PVCs are of no concern; frequent PVCs can progress to lethal arrhythmias such as v-tach or v-fib
treatment for PVCs occasional PVCs dont require treatment; frequent PVCs, treat the cause. O2, amiodarone, antiarrhythmias are used to treat both atrial and ventricular arrhythmias; frequent PVCs with bradycardia treat with atropine
PVCs that come from a single focus all look alike unifocal PVCs
PVCs from different foci look different multifocal PVCs
two consecutive PVCs are called a couplet
if every other beat is a PVC, its called ventricular bigeminy
if every third beat is a PVC, its called ventricular trigeminy
if every fourth beat is a PVC, its called ventricular quadrigeminy
an irregular rhythm in which the severely impaired heart is only able to "cough out" an occasional beat from its only remaining pacemaker, the ventricle agonal rhythm
heart rate with agonal rhythm <20; although a occasional beat might some in at a slightly higher rate
regularity of agonal rhythm irregular
p waves of agonal rhythm none
PR intervals with agonal rhythm not applicable
QRS intervals with agonal rhythm >0.12 seconds; wide and bizarre
t wave with agonal rhythm slopes off in the opposite directions to the QRS
the cause of agonal rhythm the patient is dying, usually from profound cardiac or other damage or from hypoxia
adverse effects of agonal rhythm profound shock, unconsciousness, death is left untreated
treatment for agonal rhythm CPR, epinephrine and/or vasopressin, atropine, O2
an irritable ventricular focus has usurped the sinus node to become the pacemaker and is firing very rapidly ventricular tachycardia
heart rate in v-tach >100
regularity in v-tach usually regular but can be a little irregular at times
p waves in v-tach usually none seen, but dissociated from the QRS if present
PR intervals in v-tach variable PR if even present
QRS intervals in v-tach >0.12 seconds; wide and bizarre
t wave in vtach slopes off in the opposite direction to the QRS
causes of v tach heart disease, hypokalemia, hypoxia, low blood mag levels, stimulants, caffeine, stress or anxiety
adverse effects of vtach profound shock, unconsciousness, and death
treatment for vtach amiodarone or lidocaine IV is pt is stable; electric shock to the heart is pt is unstable or pulseless; treat cause (low K, mag, or O2 levels); CPR is pulseless
a form of polymorphic ventricular tachycardia that is recognized primarily by its classic shape-it oscillates around an axis, with the QRS complexes pointing up, then becoming smaller, then rotating around until they point down torsades de pointes
heart rate with torsades >200
regularity of torsades regular or irregular
p waves of torsades none seen
PR interval with torsades not applicable
QRS interval with torsades >0.12 seconds; wide and bizarre; before torsades QT will be prolonged
t wave with torsades opposite the QRS, but may not be seen due to rapidity of the rhythm
causes of torsades antiarrhythmic meds such as quinidine, procainamide, or amiodarone.. otherwise same causes as vtach
adverse effects of torsades cardiac arrest
treatment for torsades IV mag, electrical cardioversion or defilbrillation may be needed. O2
hundreds of impulses in the ventricle are firing, each depolarizing its own little piece of territory; as a result the ventricles wiggle instead of contract ventricular fibrillation
heart rate with v-fib cannot be counted
regularity with vfib none detectable
p waves with vfib none
intervals with vfib no PR or QRS
t wave with vfib none
causes of vfib drowning, drug overdoses, accidental electrical shock, and same as vtach
adverse effects of vfib profound cardiovascular collapse
treatment of vfib immediate defibrillation, epinephrine, CPR, amiodarone, lidocaine, O2
flat line EKG, every one of the heart's pacemakers has failed asystole
heart rate with asystole 0
regularity with asystole none
p waves with asystole none
intervals with asystole no PR or QRS
t wave with asystol none
causes of asystole profound cardiac or other body system damage, hypoxia
adverse effects death
treatment for asystole atropine, epinephrine and/or vasopressin, CPR, O2
prolonged PR interval that results from a delay in the AV node's conduction of sinus impulses to the ventricle first degree AV block
heart rate with first degree block can occur at any rate
regularity with first degree block depends on the underlying rhythm
p waves with first degree block upright, matching; one P wave for each QRS
PR intervals with first degree block prolonged >0.20, constant
QRS intervals with first degree block <0.12 seconds
cause of first degree block AV node ischemia, digitalis toxicity, SE of other meds (BB, CCB)
adverse effects of first degree block causes no symptoms
treatment of first degree block remove any meds causing it; treat the cause
occurs when the AV node becomes progressively weaker and less able to conduct the sinus impulses until finally it is unable to send the impulse down to the ventricle at all resulting in PR intervals grow progressively longer until there is a Pwave w/o QRS second degree AV block (wenckebach)
heart rate with wenckebach atrial rate usually 60-100; ventricular rate less than atrial rate due to nonconducted beats
regularity with wenckebach usually irregular; can look regular but interrupted at times
p waves with wenckebach normal sinus P waves. All Ps except the blocked P are followed by QRS, P-P interval regular
PR interval in wenckebach PR gradually prolongs until a QRS is dropped
QRS interval in wenckebach <0.12 seconds
cause of wenckebach MI, digitalis toxicity, med SE
adverse effects of wenckebach usually no ill effects, watch for worsening block
treatment for wenckebach watch for transcutaneous pacing with signs of decreased cardiac output. atropine if pacemaker is not immediately available. cautious observation
a block caused by an intermittent block at the AV node or the bundle branches, preventing some sinus impulses from getting to the ventricles Mobitz II second degree AV block
heart rate with mobitz II atrial rate usually 60-100; ventricular rate is less than atrial rate due to dropped beats
regularity with mobitz II may be regular, irregular, or regular but interrupted
P waves with mobitz II normal sinus P wave, all Ps except the blocked Ps have a QRS behind them, P-P interval regular
PR interval with mobitz II constant on the conducted beats
QRS interval with mobitz II <0.12 seconds at AV node; >0.12 seconds at bundle branches
causes of mobitz II MI, conduction system lesion, med side effect, hypoxia
adverse effects with mobitz II decreased cardiac output, progress to third degree block
treatment for mobitz II immediate transcutaneous pacing, O2, atropine or epinephrine (narrow QRS-atropine) (wide QRS-epinephrine)
the sinus node sends out its impulses as usual but none of them ever gets to the ventricles because there is a complete block at the AV node or the bundle branches third degree AV block
heart rate with third degree block atrial rate is usually 60-100; ventricular rate usually 20-60
regularity of third degree block regular
p waves with third degree block normal sinus p waves, P-P interval is regular, may be hidden inside QRS complexes or T waves, not associated with QRS complexes
PR intervals with third degree block varies
QRS intervals with third degree block <0.12 seconds or >0.12 seconds depending on location of block
causes of third degree block MI, conduction system lesion, med SE, hypoxia
adverse effects of third degree block decreased cardiac output
treatment for third degree block transcutaneous pacing is indicated is pt is symptomatic, atropine, epinephrine, or dopamine, O2
Created by: 605946556