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139 Cards in this Set
- Front
- Back
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how does the sympathetic nervous system control the heart
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cardioacceleratory reflex; release of epi and norepi which accelerates firing of SA node, increases contractility and increases conduction through AV node
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how does the parasympathetic nervous system control the heart
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cardioinhibitor reflex via vagus nerve; releases acetylcholine which slows the firing of the SA node, decreases contractility and slows conduction through the AV node
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chronotropic effect
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rate increase or decrease
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inotropic effect
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contractility increase or decrease
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dromotropic effect
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AV node conduction increase or decrease
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automaticity
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ability to spontaneously produce electrical impulse; specific to pacemaker cells
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excitability
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ability of cardiac cells to react to a stimulus
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conductivity
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ability to receive an impulse and transfer to other cardiac cells
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where are the pacemaker cells located in our heart
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SA node, AV node and purkinje fibers
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if the SA node is setting the heart rate it will normally be
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60-100bpm
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if the AV node is setting the heart rate it will normally be
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40-60bpm
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if the purkinje fibers are setting the heart rate it will normally be
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20-40bpm
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ectopic response area
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area of the heart that is irritated and it generates a beat
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drugs that alter conductivity
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digitalis, beta blockers, ca channel blockers, amiodarone, atropine
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contractility
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ability of cardiac cells to shorten and cause contraction
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extensibility
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ability of cardiac cells to stretch and lengthen
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explain starlings law
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the more we stretch the ventricle (Fill it up), the stronger the contraction and the higher the stroke volume
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what is the normal charge for cardiac cells
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positive charge EXTRAcellular and negative charge INTRAcellular
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which electrolyte initiates the first phase of depolarization and where is it located
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sodium; extracellular
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which electrolyte initiates the second phase of depolarization and where is it located
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calcium; extracellular
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what is the response to the action of calcium during depolarization
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INTRAcellular potassium moves out of the cell
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what is depolarization
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spread of electrical impulse through heart
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what is repolarization
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heart returns to resting state
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how much time is measured in the small squares of EKG paper
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.04 seconds
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how much time is measured in the big squares of EKG paper
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0.2
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the vertical lines of the EKG paper measure
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amplitude of the waveform
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two types of EKG monitoring
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hardwire: 3, 5 or 12 lead; telemetry: 3 or 5 lead
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5 lead monitoring is aka
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limb lead monitoring
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how do you position the leads in a 5 lead monitor
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RA: white; LA: black; LL: red; RL: green; chest lead is brown
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5 lead monitors generate how many views of the heart and how are they labeled
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6 views; I, II, III and aVr, aVl and aVf
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when looking at the EKG we generally look from lead #
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2
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the p wave represents
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atrial depolarization (contraction of the atrium)
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the QRS compled represents
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ventricular depolarization (contraction of the ventricle)
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normal size for QRS
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0.11 secs or < 3 small squares
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a p wave should go in what direction
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positive
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when is a Q wave significant
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when it is 1/3 the height of the R wave; current cannot go through infarcted tissue
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the T wave represents
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ventricular repolarization (relaxation)
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what does the PR interval represent
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SA and AV node function; point of atrial activation up to ventricular activation; basically conduction from SA node to AV node
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what does the QT interval represent
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ventricular depolarization to repolarization
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normal QT interval
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0.2-0.4 seconds; 1-2 large squares
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normal PR interval
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0.12-0.20 seconds (<1 large square)
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if the PR interval is bigger than 1 large square this indicates
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SLOW conduction
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absolute refractory period
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from the Q wave to the peak of the T wave; cells CANNOT be depolarized (contracted)
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relative refractory period
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from the peak of the T wave to the isoelectric line; cells can be depolarized (contracted) with a strong stimulus (R on T phenomenon)
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supernormal refractory period
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where T wave meets isoelectric line; cells will respond to weak stimulus; doesn't mess with the overall rhythm
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ST segment
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from beginning of S wave to beginning of T wave
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what can the ST segment show us?
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myocardial status
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T wave inversion indicates
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ischemia; not getting enough O2
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ST depression indicates
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injury; result of ischemia; reversible
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ST elevation indicates
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infarction
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5 steps of strip analysis
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1)check regularity of R waves 2)calc HR 3)identify P waves and if assoc with QRS 4)measure PR interval 5) measure QRS complex
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identifying P waves and assoc them with QRS complexes shows us what
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atria are working
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how do we determine the atrial HR from a strip
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P wave to P wave
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how do we determine the ventricular HR from a strip
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R wave to R wave
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how do we calculate the HR
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1500/ number of small squares
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how can we ESTIMATE the HR
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count big squares
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normal estimated HR is
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3-5 big squares
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a slow ESTIMATED HR is
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more than 5 big squares
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a fast ESTIMATED HR is
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less than 3 big squares
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sinus bradycardia is characterized by
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regular rhythm; HR 40-60; normal everything else
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sinus bradycardia can be the result of
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normal for some people; inferior wall MI, vagal stimulation, meds
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treatment of choice for symptomatic bradycardia
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atropine
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sinus tachycardia is characterized by
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regular rhythm; HR 100-180; normal everything else
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sinus tachycardia can be caused by
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excitement, stress, fever, hypovolemia, hypoxia, pain; this is a compensatory response
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how do we treat sinus tachycardia
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treat the cause not the rate
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supraventricular tachycardia is characterized by
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no p wave; regular rhythm; HR 140-250
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a narrow QRS complex indicates that it came from where
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above the ventricle: hopefully AV node
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a wide QRS complex such as in PVCs come from where
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at the ventricle; below the AV node
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SVT or atrial tachycardia results in
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decreased cardiac output and increased oxygen demand
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how do we treat SVT
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treat the rate! Hemodynamically unstable: synchronized cardioversion at 50-100 joules; STABLE= vagal maneuver, adenosine or CCB, BB or digitalis
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how do we determine if someone is hemodynamically stable
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systolic BP is above 90
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what does a PAC or PJC look like on a strip
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much like a regular QRS comples just comes earlier than expected rhythmic beat; usually a long pause after to allow SA node to reset
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definitive sign of atrial flutter
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sawtooth pattern
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strip characteristics of atrial flutter
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irregular R waves; atrial rate 250-400; QRS is narrow; P wave with QRS becomes sawtooth pattern
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how do we determine the ratio of sawtooth waves
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how many sawtooth compared to QRS complexes
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atrial flutter results in
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reduced atrial kick and reduced cardiac output
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how do we treat atrial flutter
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control the ventricular rate; if unstable, cardiovert; if stable, CCB, BB, digitalis, adenosine or overdrive pacing
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what are some possible secondary complications of atrial flutter
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embolic stroke
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why is it important to know when the atrial flutter began
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if < 48 hours we can cardiovert or give amiodarone; if > 48 hours we need to anticoagulate first to prevent throwing clots
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how do we permanently eliminate atrial flutter
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ectopic atrial focus ablation
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how does the atrial fibrillation strip look different from the atrial flutter strip
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irregular beats are smaller faster waves whereas flutter has sawtooth appearance
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atrial fibrillation results in
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loss of atrial kick and reduced cardiac output
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how do we treat atrial fibrillation
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control the ventricular rate; if unstable, cardiovert; if stable, CCB, BB, digitalis, adenosine or overdrive pacing
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why do we need to control the ventricular rate
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they generate the pulse so when they are going to fast they aren't filling and aren't perfusing the body = little to no pulse
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secondary complication of atrial fibrillation
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embolic stroke
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RVR
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rapid ventricular response; ventricular rate is greater than 100
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how can we distinguish a 1st degree heart block
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prolonged PR interval; > 1 large square
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what does 1st degree heart block mean
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delayed conduction through the AV node
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how do we treat 1st degree heart block
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usually benign; normal sinus with prolonged PR; it can be indicative of underlying condition such as hyperkalemia, inferior wall MI or be caused by a med so look at big picture
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how do we distinguish a 2nd degree heart block type 1
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the R wave intermittently drops a QRS complex; generally a pattern to it; the PR interval will progressively lengthen then QRS will drop
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how do we treat 2nd degree heart block type 1
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usually benign; can be caused by inferior wall MI or certain meds so look at big picture
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how do we distinguish a 2nd degree heart block type 2
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the R wave intermittently drops a QRS complex; no pattern to dropped beat; PR interval can be normal or prolonged
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2nd degree heart block type 2 is usually assoc with
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anterior MI; usually not med related
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if we do not treat 2nd degree heart block type 2 it will progress to
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3rd degree AV block or ventricular standstill
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how do we treat 2nd degree AV block type 2
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needs a pacemaker; if hypotensive, dopamine or epi; if still then transcutaneous pacing
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what does 3rd degree AV block look like
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regular rhythm; P wave is disassociated with QRS complex; there is no measurable PR interval bc P waves are all over
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what does the QRS look like in 3rd degree AV block
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if junctional they will be narrow; if ventricular they will be wide
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what is happening in the heart during 3rd degree AV block
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atria and ventricles are beating independently of each other; no electrical movement through AV node
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causes of 3rd degree AV block
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inferior or anterior MI, meds
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how do we treat 3rd degree AV block
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needs a permanent pacemaker; if hypotensive, dopamine or epi; if remains hypotensive, immediate transcutaneous pacing
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in 3rd degree AV block which med do we exercise caution with
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atropine
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how do we treat asystole
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CPR! No shocking, give epi or atropine
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describe the appearance of a bundle branch block
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QRS is wide, will be notched (2 complexes)
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a bundle branch block can be assoc with
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anterior wall MI (left side); left fascicular block (anterior)
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how do we treat bundle branch blocks
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like an acute anterior MI
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where do PVCs originate
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in an area of the left or right ventricle
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what does a PVC look like
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has a wide and bizzare shape
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when do we treat a PVC
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most don’t require treatment but if >6/min, post MI or unstable treat with lidocaine
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what do we need to check if PVCs are present
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pulse; some perfuse and some don't; so HR may show 80 and perfusion may only be at 40
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ventricular tachycardia
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4 or more PVCs that usually don't perfuse\
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how do we treat ventricular tachycardia
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pulseless: treat as Vfib and debibrillate at 200-360 joules; if stable give amiodarone, lidocaine, or procainamide (use one!) then cardioversion if needed
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why is ventricular tachycardia so serious
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no perfusion occurring; can convert to ventricular fibrillation rapidly
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describe polymorphic v tach
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nonuniform; appears to twist around isoelectric line; cardioversion and meds usually not effective
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what is the common name for polymorphic v tach
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torsades de pointes
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how do we treat torsades de pointes
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mag sulfate; then underlying cause
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dose for mag sulfate
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1-2g IVPB over 10 mins
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what does v fib look like
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no discernible complexes
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if you have a pulse during v fib what do you do
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check the monitor, lead wires and patches; pt should not have one if truly in v fib
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how do we treat v fib
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defibrillate at 200-360 joules; BLS-CPR; check pulse/rhythm; meds, ACLS
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what does asystole look like
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ventricular standstill; may still see P waves
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leads I and aVl show what view of the heart
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left ventricle; lateral area
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leads II, III and aVf show what view of the heart
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right ventricle; inferior area
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leads V1 and V2 show us
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septal area of the heart, edge of sternal border
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leads V3 and V4 show us
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anterior area, midclavicular line (V4)
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leads V5 and V6 show us
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lateral area (V6-mid axillary)
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what is axis deviation
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the normal axis is lead II but heart will shift in the direction of the problem so a different lead will become the axis
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how do we know which lead is the axis
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talles R waves; how much is above the isoelectric line
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purpose of a pacemaker
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control heart rate when conduction is compromised
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single chamber pacemaker
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paces either the atria or the ventricle
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dual chamber pacemaker
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paces both the atria and ventricle
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typers of pacemakers
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permanent or temporary
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types of permanent pacemakers
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implanted, PPM perm pacemaker, AICD automated internal cardioverter defibrillator
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types of temporary pacemakers
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transcutaneous, transvenous, epicardial
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describe the 5 letter system for pacemaker settings
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1) chamber being paced 2) chamber being sensed 3) pacemaker response to a heartbeat 4) rate regulation 5) indicates pulse generator has multisite capabilities
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in what ways can a pacemaker respond to a heartbeat
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I-inhibited: won't fire when heartbeat is sensed: T-triggered: when atrial beat is sensed, pacemaker delivers current to ventricle; D-dual response: inhibited and triggered; O-no response: pacer is set to pace and not sense, fixed or asynchronous
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most commonly what system is used for pacing code
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3 letter
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most common complication of pacemaker insertion
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dislodged electrode
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things pt needs to do after pacemaker insertion
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restrict motion of transvenous point of entry; teach not to raise affected extremity above shoulder level for 2 weeks; tape pacer wires to chest wall
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what does hiccuping, rhythmic chest wall or diaphragmatic twitching indicate in pacemaker pt
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pacer wire is dislodged or perforated the myocardium
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