Ch 3 EKG Book Notes

Torsade de Pointes

--"twisting of the points" --unique form of tachycardia that is seen in patients with prolonged QT intervals which can occur from 1. congenital 2. various electrolyte disturbances 3. an acute MI 4. medicines --a prolonged QT interval is usually the result of prolonged ventriculae repolarization --a PVC falling within the prolonged T wave can cause this

what does a wide QRS complex imply

-->0.12 sec --implies that the origin of the ventricular depolarization is within the ventricles themselves (the myocardium) therefore it spreads much more slowly; conduction does NOT follow the most efficient pathway, so the QRS complex is wide

what does a narrow normal QRS complex imply

--a narrow normal QRS complex= <0.12 seconds --implies that ventricular depolarization is proceeding along the usual pathways, which is the most efficient means of conduction, requiring the least amount of time, so the QRS complex has a short duration (narrow) --indicates the origin of the rhythm must be at or above the AV node

Ventricular Fibrillation

--a preterminal event (seen almost soley in dying hearts) --most frequently encounterd in adults who experience sudden death --there are no true QRS complexes --the heart generates no cardiac output

Ventricular Tachycardia

--a run of three or more consecutive PVCs --rate is usually between 120 and 200 beats per minute --unlike PSVT, may be slightly irregular --if this is sustained, its an emergency --may be Uniform 1.healed infarctions (scarred myocardium provides the substrate for the reentrant ventricular tachycardia) --OR may be Polymorphic 1.acute coronary ischemia 2. infarction 3. profound electrolyte disurbance 4. conditions causing prolongation of the QT interval

Multifocal Atrial Tachycardia (MAT)

--an irregular rhythm occurring at a rate of 100-200 beats per minute --results from the random firing of several different ectopic atrial foci --common in patients with severe lung disease --rarely requires treatment, carotid massage has NO EFFECT ON IT --irregular rhythm --easily identifiable p waves BUT the p waves will vary in shape and the interval between the p wave and QRS complex will vary in size --in order to diagnose MAT you need to identify atleast 3 differnt p-wave morphologies --if the rate is less than 100 bpm= WANDERING ATRIAL PACEMAKER; can be seen in normal healthy hearts --in wandering atrial pacemaker, at least 3 different p wave morphologies can be seen BUT there will be at least two or three beats of each p wave morphology before the site moves on and creates the next morphology

Atrial Flutter

--atrial activation is regular but rapid -p waves appear at a rate of 250-350 bpm --most commonly generated by reentrant circuit that runs around the annulus of the tricuspid valve**** --atrial depolarization occurs at such a rapid rate that discrete P wave separated by a flat baseline are not seen; instead, the baseline continually rises and falls, producing so called flutter-waves -prominently seen in Lead II and III (saw-toothed pattern) --bc the av node cannot handle the extraordinary number of atrial impulses bombarding it (it doesnt have time to repolarize in time)so therefore not all of the atrial impulses that pass through theAV node generate the QRS complex --the ones that just bump into a refactory node= AV BLOCK

Atrial Fibrillation

--atrial activity is completely chaotic --AV node may be bombarded by more than 500 impulses per minute --multiple reentrant circuits in totally unpredictable fashion --no true p wave can be seen --av node only allows occassional impulses to pass through at variable rate which generates an IRREGULARLY IRREGULAR VENTRICULAR RATE between 120 and 180 bpm ***This irregularly irregular appearance of QRS complexes in the absence of discrete P waves is key to identifying atrial fibrillation --carotid massage may slow ventricular rate in afib but it is rarely used --causes (same as A flutter ie hypertensive heart dieseae, metabolic syndrome, mitral valve disease, coronary artery disease) but also ACUTE precipitants such as 1. PE (when one or more arteries in the lung get a blood clot) 2. Thyrotoxicosis 3. Pericarditis 4. Obstructive Sleep Apnea --symptoms same as Aflutter or NO SYMPTOMS AT ALL --patients with persistant Afib are at risk for: systemic embolization --the chambers of the heart shake instead of contract and this is where blood clots can form and break off (embolize) and travel to other parts of the body to cause stroke or vascular occlusion elsewhere pg 134-135 treatment plans (stuff about anticoagulation)

Programmed Electrical Stimulation (EPS)

--expensive and invasive but has great value to choose the right meds to go on --the arrhythmia is induced with intracardiac electrodes, tiny catheters are inserted through peropheral veins or arteries and are then advanced to various locations within the chambers of the heart; the BUNDLE OF HIS is recorded --successful in managing patients who have recurrent ventricular tachycardia or who have experienced an episode of sudden death --uses cather ablation (also used to treat Stones niece)

sinus exit block

--failure of sinus depolarization to be transmitted out of the node and into the atria --the same result as a sinus arrest: a straight line on the EKG --sinus arrest= failure of the sinus mechanism to deliver its current in to the surrounding tissue

Holter monitor aka ambulatory monitor

--how the ultimate rhythm strip is provided --a portable EKG machine with a memory --a patient wears it for 24 or 48 hrs or longer --used when the suspected arrhythmia is an INFREQUENT occurrence and is therefore unlikely to be captured on a random 12 lead EKG --the patient is to write down exact time when he or she feels discomfort so that it can be compared to the strip

Paroxysmal supraventricular tachycardia (PSVT)

--in medicine, paroxysm means a sudden violent attack --absolutely regular rhythm --rate between 150 and 250 bpm --its onset is sudden, usually initiated by a premature supraventricular beat (atrial or junctional) --termination is abrupt --it can occur in healthy people, may be no underlying cardiac disease --presentation: palpitations, shortness of breath, dizziness, (rarely) syncope --cause: alcohol, coffee, sheer excitement --the most common type: AV nodal reentrant tachycardia= driven by a reentrant circuit looping within the AV node --this can be identified by a pseudo-R' in the QRS complex of Lead V1 which represents the retrograde p wave --retrograde p waves can also be seen in Leads II and III

What would carotid massage do to an AV Block

--it may increase the degree of block ( ie 3:1 or 4:1) --bc atrial flutter originates above the AV node, carotid massage will not result in termination of the rhythm ******

how can you diagnose and terminate a PSVT

--massaging the carotid artery --baroreceptors where the common carotid artery bifurcates: when the BP rises, the baroreceptors cause reflex responses from the brain to be sent along the vagus nerve to the heart; vagal input decreases the rate at which the sinus node fires, and more importantly, slows conduction through the AV node --if you apply outside pressure to this, the baroreceptors will still fire to do this bc they don't know how the increase pressure is getting there they just know it its and is bad --so carotid massage will: 1. interrupt the reentrant circuit and thereby terminate the arrhythmia 2. or slow the arrhythmia so that the presence or absence of p waves can be more easily determined and the arrhythmia diagnosed

in what type of patients could a sinus arrhythmia be diminished

--may be causes by diminished autonomic feedback to the sinus node --seen in patients with 1. diabetes mellitus (which can overtime cause autonomic neuropathy) 2.aging 3. obesity 4. patients with long standing hypertension

how does a reentry loop occur

--normally any two adjacent regions of cardiac function conduct current equally well --however, if conduction at one point (B) is temporarily slowed, the current passing down A can then turn back and conduct in a retrograde fashion through B and establish a reentry loop --retrograde= moving backward

Paroxysmal Atrial Tachycardia (PAT)

--regular rhythm with a rate of 100 to 200 beats per minute --can result either from: 1. the enhanced automaticity of an ectopic atrial focus--displays a warm up and cool downtime in which the rhtym appears irregular; much more common 2. a reentrant circuit within the atria--starts abruptly with an atrial premature beat; aka "atypical atrial flutter" --can be caused by digitalis toxicity --carotid massage has no effect

ectopic rhythms

--the electrical activity originates from a focus other than the sinus node --abnormal rhythms that arise from elsewhere than the sinus node

junctional escape

--the most common of the available escape mechanisms --depolarization originates near the AV node and the usual pattern of atrial depolarization does not occur --a normal P wave is NOT seen --a RETROGRADE p wave may be seen= representing atrial depolarization moving Backward from the AV node into the atria --the mean electrical axis of this retrograde P wave is reversed 180 degrees from the the normal P wave --changes in Leads 1. Lead II (it used to be upright but now the retrograde p wave is INVERTED) 2. Lead aVR (it used to be inverted but now the retrograde p wave is UPRIGHT)

Premature Ventricular Contractions (PVC)

--the most common ventricular arrhythmia **THE QRS complex of a PVC appears wide and bizarre becuase ventricular depolarization does not follow the normal ventricular conduction pathway*** (the QRS complex must be at least 0.12 in the majority of leads except that one place with the premature contraction) --a PVC is usually followed by a prolonged compensatory pause before the next beat appears Interpolated PVC= less common, when a PVC occurs between two normally conducted beats without a compensatory pause --if a PVC is isolated, its normal --if a PVC is shown in a patient with an acute MI its bad bc this can trigger 1. ventricular tachycardia or 2. ventricular fibrillation (which are both life threatening) Bigeminy=if the ratio is one normal sinus beat to one PVC Trigeminy= two normal sinus beats for every one PVC

event monitor

--when a holter monitor doesnt work --worn by the patient and turned on by the patient when he or she feels palpitations --records only 3-5 mins of a rhythm strip

What is the one common circumstance in which supraventricular beats can produce wide QRS complexes?

--when a supraventricular beat is conducted aberrantly through the ventricles, producing a wide, bizarre looking QRS complex that is indistinguishable from a PVC --a premature atrial impulse can occur before the right purkinje fibers have repolarized meaning they are in refractory period so when the signal gets passed down it cant get passed to the right bundle so instead of the right ventricle becoming depolarized via the normal route, instead the electrical conduction goes more into the left bundle and the right ventricle can only become depolarized by the cells of left ventricle that have already been depolarized by the left bundle; this makes for a bizarre QRS complex see pg 147

which questions is responsible for making the distinction between an arrhythmia with a ventricular or supraventricular (atrial or junctional) origin

1 (p waves present) and 2 (size of QRS complexes)

The 4 Questions in order to spot a Nonsinus Arrhythmia

1. Are Normal P waves Present? 2. Are the QRS Complexes Narrow or Wide? 3. What is the Relationship Between the P waves and the QRS Complexes? 4. Is the Rhythm Regular or Irregular?

The 5 types of Sustained Supraventricular (ie Atrial, basically any tachycardia that dont originate in the ventricles) Arrhythmias--These are all Reetrant ones? (or atleast 1, and 2 are)

1. Paroxysmal supraventricular tachycardia (PSVT) aka Av odal reentrant tachycardia 2. atrial flutter 3. atrial fibrillation 4. multifocal atrial tachycardia (MAT) 5. paroxysmal atrial tachycardia (PAT) aka ectopic atrial tachycardia

a wide QRS complex can signify what 2 things

1. a beat originating within the ventricles 2. a supraventricular beat conducted aberrantly see pgs 148-151 to learn how to differentiate between the 2: 1. clinical clues 2. electrocardiographic clues 3. ashman phenomenon

the 5 basic types of Arrhythmias

1. arrhythmia of sinus origin 2. ectopic rhythm 3. reentrant arrhythmia 4. conduction block 5. preexcitation syndromes

different types of nonsinus pacemakers

1. atrial pacemaker= usually discharge at a rate of 60 to 75 beats per minute 2. junctional pacemaker= pacemaker cells located near the AV node that typically discharge at 40 to 60 beats per minute---JUNCTIONAL ESCAPE IS THE MOST COMMON 3. Ventricular pacemaker cells= usually discharge at 30 -45 beats per minute

if both the holter monitor and event monitor dont work

1. cell phone based telemetry in home up to 4 weeks 2. surgically implanted event recorder under the skin, rates trigger the recorder or the patient activates it themself

how to determine a heart rate from an EKG

1. count the large boxes between R waves then divide 300 by this 2. count the small boxes between R waves then divide 1500 by this

the 2 main causes of nonsinus arrhythmias

1. ectopic rhythms 2. reentrant rhythms

When to worry about PVCs

1. frequent PVCs 2. Runs of consecutive PVCs, esp three or more in a row 3. multiform PVCs in which the PVCs vary in their site of origin and hence their appearance 4. PVCs falling on the T wave of the previous beat, called the "R-on-T" phenomenon. The T wave is a vulnerable period in the cardiac cycle and a PVC falling there is more likely to set of ventricular tachycardia 5. any PVC occuring in the setting of an acute MI

common conditions associated with atrial flutter

1. hypertension 2. obesity 3. diabetes mellitus 4. electrolyte imbalances 5. alcohol intoxication 6. drug abuse, cocaine, amphetamines, 7. thyrotoxicosis 8. various underlying cardiac conditions both congenital (atrial septic defect) and acquired (rheumatic valvular disease, coronary artery disease, congestive heart disease)

what can rapid arryhthmias cause (Symptoms)

1. increase in the oxygen demands of the myocardium 2. angina (chest pain)

what are they symptoms of decreased cardiac output which can occur when the arrhytmia compromises the cardiac function

1. light-headedness 2. syncope ( a sudden faint)

who can have sinus tachycardia

1. patients with congestive heart failure (a chronic condition in which the heart cannot pump blood as well as it should) 2. patients with severe lung disease 3. can be the only presenting sign of hyperthyroidism in the elderly

types of arrhythmias of sinus origin

1. sinus tachycardia= if heart rate increases above 100 bpm 2. sinus bradycardia= if heart rate slows below 60 bpm 3. sinus arrhythmia= totally normal; rhythm that appears in all respects to be normal sinus rhythm except that it is slightly irregular; reflects the variation in heart rate that accompanies inspiration and expiration 4. sinus arrest= occurs when the SA node stops firing 5. asystole= a flat line without any electrical activity (patient will die unless other myocardial cell such as AV node takes over and OVERDRIVES the other pacemaker cells by delivering waves of depolarization before the other ones get a chance to); when other myocardial cells take over, this is called ESCAPE BEATS 6. nonsinus pacemakers

who can have sinus bradycardia

1. the most common rhythm disturbance seen in the early stages of an acute myocardial infarction 2. in healthy individuals, enhanced vagal tone which can cause fainting

on horizontal axis of EKG, 1mm= ?

1mm= 1 small box= 0.4 sec

the most common AV Block

2:1 meaning that for every two visible flutter waves, one passes through the AV node to generate a QRS complex and the other doesnt

on horizontal axis of EKG, 5 big boxes=?

5 big boxes= 1 second

on horizontal axis of EKG, 5mm=?

5mm= 1 big box= 0.2 sec

difference between A flutter and A fib

Aflutter= a single constant reentrant circuit Afib= multiple unpredictable reetrant circuits **Afib is much more common

What causes arrythmias

H=Hypoxia I=Iscehmia and Irritability S=Sympathetic Stimulation D=Drugs E=Electrolyte Disturbance B=Bradycardia S=Stretch

causes of left ventricular hypertrophy

High blood pressure, or hypertension, is the most frequent cause of left ventricular hypertrophy (LVH). Stenosis of the aortic valve - a condition in which, for a variety of reasons, this heart valve cannot open fully - is another common cause of LVH. Hypertrophic cardiomyopathy (a disease previously known as idiopathic hypertrophic subaortic stenosis or IHSS), and the ongoing use of cocaine round out the list of most common causes of LVH. Hypertrophic cardiomyopathy is a genetic disease related to weakness of the individual muscle fibers of the heart. These fibers need to work harder to pump blood and become thickened over time. Hypertrophic cardiomyopathy occurs in 1 in 500 people and is the most common cardiac cause of sudden death in young athletes.

what is the stable of the arrhythmia diagnosis and treatment

Holter monitor

what does it mean if there are normal p waves with an ABNORMAL axis

MAY POSSIBLY reflect retrograde activation of the atria from impulses originating below the sinus node from other atrial focus or from within the AV node or the ventricles, from the current flowing backward into the atria through the AV node or through an accessory pathway

How to distinguish between Supraventricular Arrhythmias and Ventricular Arrhythmias

Supraventricular Arrhythmias= associated with narrow QRS complex Ventricular Arrhytmias= associated with WIDE QRS complex

causes of right ventricular hypertrophy

The most common causes of right ventricle hypertrophy (RVH) are diseases that damage the lung like emphysema and cystic fibrosis. These diseases destroy blood vessels in the lung, causing increased pressure in the remaining vessels. Conditions that decrease oxygen levels, such as chronic bronchitis and sleep apnea, also lead to RVH. Stenosis of the pulmonic heart valve, repeated blood clots to the lungs (chronic pulmonary embolism), and primary pulmonary hypertension are a few of the remaining causes of RVH.

Accelerated Idioventricular Rhythm

a benign rhythm that s sometimes seen during an acute infarction or during the early hours following reperfusion after an occluded coronary artery has been opened --rhythm occuring 50 to 100 beats per minute

enhanced automaticity represents what

a disorder of IMPULSE FORMATION --ie new impulses that are formed elsewhere than the sinus node take over the heart

reentry represents what

a disorder of IMPULSE TRANSMISSION

Hypoxia

a myocardium deprived of oxygen is an irritable myocardium. Pulmonary disorders, whether severe chronic lung disease or acute pulmonary embolus are major precipitants of cardiac arrhythmias

Bradycardia

a very slow heart rate seems to predispose to arrhythmias. one could include the bradytachycardia syndrome (also called the sick sinus syndrome) in this category

palpitations

an awareness of ones own heart beat: perhaps described as intermittent accelerations or decelerations of their heart beat, or a sustained rapid heartbeat that may be regular or irregular

arrythmia

any disturbance in the rate, regularity, site of origin, or conduction of the cardiac electrical impulse

myocardial infarction

blockage of blood flow to the heart muscle; heart muscle affected from lack of blood supply

external defibrillator

can deliver defibrillation shocks that may be lifesaving

the sudden onset of an arrythmia in a patient with underlying cardiac disease can also precipitate what

congestive heart failure

what does the axis of the p waves (flutter waves) in atrial flutter depend on?

depends on whether the reentrant circuit rotates counterclockwise ( most common) which will produce negative sawtooth deflections in the inferior leads or clockwise (positive deflections int he inferior leads) around the tricuspid valve

what does ectopic rhythms arise from

enhanced automaticity= caused by a) digitalis toxicity (a certain drug that is actually for a heart condition that people take too much of) b) beta adrenergic (relax muscles of the airways) stimulation from inhaler used to treat asthma and COPD **looks like it really arises from medicines

Sympathetic Stimulation

enhanced sympathetic tone from any cause (ie hyperthyroidism, congestive heart failure, nervousness, exercise) can elicit arrhtymias

Stretch

enlargement and hypertrophy of the atria and ventricles can produce arrhythmias. this is one way in which congestive heart failure (a chronic condition in which the heart doesnt pump blood the way it should), cardiomyopathies (heart muscle disease) and valvular disease can cause arrhythmias

Electrolyte Disturbance

hypokalemia (blood potassium too low) is notorious for its ability to induce arrhythmias, but imbalances of calcium and magnesium can also be responsible

how are EKGs helpful

it shows conditions that predispose to malignant arrythmias and sudden death

Drugs

many drugs can cause arrhythmias, especially anti- arrhythmic drugs such as quinidine

Ischemia and Irritability

myocardial infarctions (a blockage of blood flow to the heart), angina (even without the actual death of myocardial cells that occurs with infarction) and myocarditis (an inflammation of the heart muscle often caused by routine viral infections) can induce or precipitate an arrhythmia

if there is a lack of correlation between the P waves and the QRS complexes

the atria and ventricles depolarize and contract independenly of each other= AV DISSOCIATION

a) whats the difference between a junctional premature beat and a junctional escape beat? b) the same

premature beat= occurs EARLY escape beat= occurs LATE, following a PROLONGED PAUSE when the sinus node has failed to fire; it establishes a sustained junctional rhythm b) they are conducted normally to the ventricles so QRS is narrow pg 125

The 5 Types of Ventricular Arrhythmias

rhythm disturbances arising below the AV node 1. Premature Ventricular Contractions 2. Ventricular Tachycardia 3. Ventricular Fibrillation 4. Accelerated Idioventricular Rhythm 5. Torsade de Pointes

Atrial Premature Beats/contractions

single ectopic supraventricular beats that can originate in the ATRIA --the premature p wave will look different than the other ones on the EKG --distinguished by: 1. the contour of the P wave= (p wave is shaped differently than the other p waves on the ekg) pg 124 2. the timing of the beat= it comes too early --does not indicate cardiac disease, does not require treatment, they can initiate more sustained arrhythmias though

Junctional Premature Beats

single ectopic supraventricular beats that can originate in the vicinity of the AV node --there will be an ABSENT P WAVE (or sometimes a retrograde one) --does not indicate cardiac disease, does not require treatment, they can initiate more sustained arrhythmias though

what can be the first clinical manifestation of an arrhytmia

sudden death when they are in the midst of an acute myocardial infarction

what does it mean if the p waves are normal (normal size, normal axis)

the arrhythmia (OR RHYTHM???) is almost certainly within the atria--?? how would i know this

Supraventricular Arrhythmias

the arrhythmias that originate in the atria or the AV node

preexcitation syndromes

the electrical activity follows accessory conduction pathways that bypass the normal ones, providing an electrical shortcut, or short circuit

arrhythmias of sinus origin

the electrical activity follows the usual conduction pathways we have already outlined, but it is too fast, too slow, or irregular

reentrant arrhythmias

the electrical activity is trapped within an electrical racetrack whose shape and boundaries are determined by various anatomic or electrical myocardial configurations; they can occur anywhere in the heart

conduction blocks

the electrical activity originates in the sinus node and follows the usual pathways but encounters unexpected bocks and delays

normal sinus rhythm

the everyday cardiac rhythm

what does it mean if the p wave and QRS complex correlate in the usual one-to-one fashion with a single p wave preceding each QRS complex

the rhythm almost certainly has a sinus or other atrial origin

what does it mean if there are no p waves present

the rhythm(??) must have originated BELOW the atria, in the AV node or ventricles

Implantable Defibrillators

when EPS guided drug therapies or catheter ablation techniques are successful standard protection for people with life threatening arrhythmias surgically impnated under the skin, when it senses a dangerous arrythmia it delivers an electric shock to the heart through an electrode that rests in the right ventricle

hypokalemia

when the bloods potassium levels are too low--can cause arrhythmias Lower potassium levels in the extracellular space cause hyperpolarization of the resting membrane potential. bc if its low potassium outside the cell, more potassium from inside the cell will leave making the cell even more negative---takes more time/energy/positive charge to reach threshold --results in ST depression bc doesnt easily return to isoelectric state?

how can you tell the difference between PAT and PSVT?

you really cant unless you the warm ups of PAT, and unless yu do a carotid massage (it will slow/terminate PSVT but has no effect of PAT)