Exam 3 Flashcards
Bundle branch block BBB
Caused by a block of conduction in the right or left bundle branch (comprised of left and right anterior fascicle) delaying depolarization to the ventricle that it supplies with the stimulus not conducted to both ventricles at the same time as the bundle branch that is blocked cannot proceed through its normal conduction system, but is normal till it hits the spot, so it creeps slowly to the surrounding muscle via cell-to-cell conduction, which is slow and chaotic creating wide, bizare VPC (aberrantly conducted from inception) conducted beat than the specialized bundle branch. after the delay it proceed rapidly below the block however the delay in the black bundle branch allows the unblocked ventricle to begin the polarizing before the blocked ventricle causing two joined QRSs appearing as a widened QRS with two peaks with R and R’ with the R’ being the delayed depolarization of the blocked ventricle end it is greater than 0.12 seconds Best to check them leads where QRS amplitude is minimal to get the correct timing of the tracing If BBB look at lead to V1 and V2 for the right chest leads and V5 in V6 for the left chest leads for the R to R prime. Because with BBB the ventricles do not be polarized simultaneously there are two separate right and left ventricular vectors. BBBB caused by idiopathic degeneration of conduction fibers, ischemic heart disease of atrial septum and small area of infarction.
Right bundle branch block
First notice widened QRS then R to Rprime configuration for RBBB left ventricle D polarizes punctually in our represent left ventricular depolarization in our prime represents delayed right ventricular depolarization Appears as bunny ears in chest lead V1 & V2 also appears as slurred S wave in leads I V5, and V6 can be sharp, conical, curved
RBBB has a normal origin and is only delayed in the terminal portion of the complexes. You can therefore diagnose LVH by the normal criteria. RVH, however, cannot be diagnosed.
Left bundle branch block
Left ventricular depolarization is delayed so right ventricle D polarizes punctually within our and our prime represents delayed left ventricular depolarization Appears notched or a flattened peak with two tiny points in V5 or V6. Also has ST depressions below isoelectric line and inverted T waves in I, AVL, V5 and V6. Left bundle branch has two subdivisions or fascicles and blocks of these fascicles are called hemi blocks. Causes of LBBB are widespread myocardial disease, degenerative disease of conduction system, ischemic heart diseases, and caused by Left ventricular hypertrophy.
In LBBB, it is not possible to diagnose LVH or RVH. This is because the complexes are conducted aberrantly for the most part; the true size of the complexes, if the block were not present, cannot be calculated.
Most LBBBs have a normal axis or left axis.
Bundle branch block tachycardia
if a patient with a bundle branch block develops a supra ventricular tachycardia the rapid succession of white and QRSs may imitate ventricular tachycardia. During ventricular depolarization and just afterward up to the peak of the T-wave any additional stimulus cannot depolarize the ventricles they are refractory to a premature stimulus. However the left and right bundle branch refractory period or not identical so with SVT one bundle branch is receptive to stimulation before the other at a certain critical rapid rate one bundle branch conduct before the other producing non-simultaneous depolarization of the ventricles this rate dependent bundle branch block produces a tachycardia with wide QRSs imitating ventricular tachycardia.
Incomplete bundle branch block
Sometimes you will see in R to R prime In a QRS of normal duration. If QRS < 0.12 but RSR’ present, we can call this “incomplete” BBB or “right/left ventricular conduction delay.”
third-degree AV block
Simultaneous right bundle branch block and left bundle branch block prevents depolarization from reaching the ventricles
Intermittent Mobitz seconddegree AV block
Block of one bundle branch with intermittent block of the other produces intermittent to complete AV block or intermittent Mobitz. Right bundle branch block plus intermittent left bundle branch block will record as continuous right bundle branch block patterns the QRS is with intermittent episodes of complete AV block or P waves without a QRS response and vice versa. This may worsen eventually becoming a constant complete AV block in flash is an important warning sign that eventually it will need an artificial pacemaker to dry the ventricles at a normal rate
Imitators of intermittent Mobitz
Wenckebach, non-conducted premature atrial beat, transient sinus block.
Axis
The direction of movement of depolarization spreads throughout the heart to stimulate the myocardium to contract using a vector to show the direction.
- Sum total of electrical events in heart
- Has magnitude and direction (vector)
- Affected by changes in amount of current
- Hypertrophy -Infarction
- Affected by changes in direction of current
- Retrograde conduction
the normal axis is -30 to 105 degrees or 0-90 degrees
Normal ventricular depolarization
Occurs simultaneously as well as contraction represented by the QRS complex beginning at the endocardium that lines both ventricles proceeding towards the outside surface or epicardium via the. Per Kenji fibers in all areas at once at great speed. When adding up the vectors considering direction and magnitude there is a mean QRS vector or the general direction of ventricular depolarization beginning at the AV node usually pointing towards downward to the left because the left ventricle is thicker and larger having greater magnitude
Axis circle
Position of mean QRS factor described in degrees within a circle in the frontal plane with the limb leads used to determine the position of the vector the center of the circle being the AV node in the vector normally. Is downward into the patients left between zero and 90° positive. Normal is -30-105 degrees. The lower half of the circle is positive degrees and the upper half is negative degrees.
Direction of heart
The heart displacement means that the mean QRS vector is displaced in the same direction with the AV node always the center if rotated towards the right mean QRS vector is to the right common in tall slender individuals Or vertical heart. Obese people have diaphragms that are pushed up because of abdominal pressure including the heart so the mean QRS vector points towards the patients left Or horizontal heart
Hyper trophied heart
With hyper trophy or in large meant of one ventricle the greater depolarization activity of the hyper trophy side displaces the mean QRS factor toward that side with more in larger vectors
Infarctions affect on vectors
In mile cardio infarction the necrotic or dead area of the heart that has lost its blood supply does not be polarized meaning we on impose vectors from the other side draw the mean QRS vector away from the infarct
Importance of mean QRS vector
Gives us valuable information on the position of the heart insight into ventricular hypertrophy and infarction with mean QRS vector pointing towards ventricular high to hyper trophy and away from mile cardio infarction
Lead one significance in axis determination
Lead one left arm with a positive electrode right arm with the negative electrode passing directly through the center of the sphere or is being old with the left-hand side of the sphere being positive in the right half negative. As deep polarization waves of positive charges move towards positive electrode there is a positive deflection. If the QRS complex is positive or mainly operate and lee won the mean QRS factor is pointing somewhere to the patients left half or positive half of the sphere it has normal or left axis deviation. If the QRS is Mainly negative the vector points to the patient’s right side or Right axis deviation
Lateral leads
One and AVL Both positive towards the left hand
Inferior leads
2, 3 and AVF Positive towards the ground
Lead AVF importance in determining access
Makes the electrode on the left foot positive with the lower half of the sphere being positive the center of the sphere being the AV node in the top of the sphere being negative. If the QRS has an upward direction or is positive than the mean QRS vector points downward toward the lead. If there is a Negative QRS complex in this lead then the mean QRS vector Points upward into the negative half of the severe pointing away from the positive electrode on the left foot
Discovering the quadrants using lead one and AVF
Look to see if tracing of I is up or down and point thumb in that direction. For AVF see if it is up or down and if two thumbs up it is normal. If I is up and AVF is down then it is left axis deviation. AVF up and I down RAD. If both down extreme
If the QRS is positive and lead one and AVF vector points downward to the patients left which is the normal access range. Anytime the QRS complex is negative in need one there is right axis deviation. When the vector points upward into the patients right this is extreme right extubation. If the QRS is positive and lead one and negative and lead ABF there is left axis deviation. If the vector points are poured from the AV node into the patients left this is the left axis deviation. If vector points to patients right side right axis deviation. If vector point downward to patient left it is in the normal range
Iso electric QRS significance
When depolarization moves in a direction perpendicular to the orientation of a lead with minimal deflection. Recording equal magnitude of both upward or positive and negative or downward deflection or the same voltage. Therefore the lead that is isoelectric indicates that being mean QRS vector is perpendicular to that lead. Electrical Vector is perpendicular to the axis so equal components of the current are toward the positive and negative ends of the axis yielding a QRS complex with the upward deflection and downward deflection of equal magnitude.
If vector is exactly isoelectric, it will fall directly on isoelectric lead. If that occurs:
Go back to ECG. Look at complexes found in isoelectric lead.
ë If +, vector points in direction of positive pole.
î If –, vector points in direction of negative pole
P wave Vector location
P wave vector points a downward toward a positive electrode on the patients left foot or inferior leads 2 three and AVF Being upright in those leads. P wave vector also points leftward for the positive electrode on the patients left arm or at least one and a VL producing generally operate P waves in those leads. And inverted P-wave in any of those leads means it is a P prime depolarizing upwards from a low atrial focus or retrograde atrial depolarization moving upward from the AV node. Most PB C’s emanate from peripheral focus in a ventricular wall depolarizing the ventricles in a general bottom up direction so they are mostly negative in the inferior and lateral limb leads where the QRS Is usually upward.
V2 significance In the horizontal plane QRS Vector
V2 always positive fourth enter space to the left of the sternum just anterior to the AV node. The front half of the body is positive in the back half is negative with the center of the sphere still the AV node. Normally the QRS and lead V2 is negative or moving away from the electrode with the mean QRS vector pointing backward Because of the posterior position of the thick left ventricle. Allowing us to best determine anterior and posterior infarction as it projects through the anterior wall of the left ventricle as well as the posterior wall
Atrial enlargement
The P-wave will give signs. Atria dilate more than hyper trophy use V one As it is directly over atria providing best information and is usually positive. Presents as die phasic or both positive and negative.
Right atrial hyper trophy
If the initial component of a di phasic P-wave (Diphasic- goes up as well as going down. If both sides equal it is fine. If first up part bigger than down part is right atrial enlargement don’t need to have P pulmonalas as well as diphasic P wave could be either or in leads II, II, AVF). Lead V1 Is larger then the right atria is a large especially if it is larger than 2.5 mm. Increased amplitude due to increased current required by the hypertrophied muscle
Chronic obstructive pulmonary disease (COPD)
Pulmonary emboli
Pulmonary hypertension
Mitral, tricuspid (Tricuspid insufficiency, Tricuspid stenosis), or pulmonary valve disease
Right atrial enlargement (from afib) could have right atrial deviation or right ventricular hypertrophy.
RVH
RAD
–More likely due to the RVH
Atrialectopyor dysrhythmia
Left atrial hyper trophy
If the terminal portion of a die phasic P-wave in V1 is large and wide and is usually negative. P-waves of increased duration due to increased time required by the hypertrophied muscle with wide terminal component or double humped P wave . Abnormal conduction toward the negative pole of V1 in the horizontal plane
With my toaster gnosis or narrowed mitral valve opening causing left atrial enlargement or systemic hypertension are both causes. Enlargement occurs when the muscle dilates in order to compensate for the additional blood volume.
Severe systemic hypertension
Aortic or mitral valve disease
Restrictive cardiomyopathy
Left ventricle failure
Anything that obstructs forward flow
Thick, stiff LV
Valvulardisease
–Mitral insufficiency
–Mitral stenosis
Right ventricular hypertrophy
Large R wave in V1 >S wave can be pointed down (–Result of adding energy generated by initial QRS vector to larger vector generated by enlarged RV). Wall of right ventricle is very thick so there is much more positive depolarization towards the positive V1 Electrode. With the QRS to be more positive and taller than usual and the S wave smaller than the R wave. The large R-wave gets progressively smaller from Vone to V4 From the right to the left chest leads. Causing right axis deviation in the frontal plane and right word rotation of the mean QRS vector.
RVH: Enlargement usually seen in RV pressure overload due to:
–Pulmonary hypertension
–Multiple pulmonary emboli
–Primary pulmonary hypertension
–Scarring
Valvulardisease
–Pulmonic insufficiency
–Pulmonic stenosis
COPD
Pulmonary hypertension
Pulmonary emboli
VSD
associated w/ RAD and RAE
Left ventricular hypertrophy
The left ventricle wall is very thick causing great QRS deflections in the chest leads it causing exaggerated amplitude in height and depth in chest leads. Normally the S wave in V1 is deep but with ventricular hypertrophy even more depolarization is going down word to the patients left away from that electrode causing it to be deeper. With left axis deviation and the vector displaced in a leftward direction in the horizontal plane. A tall R wave in lead V5. V5 is over the left ventricle with increased depolarization going towards it when it is in large causing more positive depolarization producing a tall R-wave. The depth of the S wave in V1 plus the height of R in V5 if more than 35 mm is also a sign. T-wave may show characteristic inversion asymmetry with long and gradual downslope and rapid return to isoelectric making it a symmetrical checking for in V5 and B6.
–Outflow problem, pressure overload develops when ventricle has to pump harder against resistance such as:
High arterial blood pressure
Stenosedaortic valve
–Volume or dilation problem, volume overload can occur when a valve is leaking blood back into the heart after it was pumped out, such as aortic valve insufficiency or mitral valve regurgitation.
–Aortic insufficiency
–Aortic stenosis
–Mitral insufficiency
hypertension
larger left ventricle pushes the heart forward, closer to the electrodes, producing a larger complex.
Tall and touching. Down part in V1 at it to up part in V5 or V6.
Always have to go look at lead I and 3 have to have equal 25.
Need to have one to call LVH
ST-T wave abnormalities
LAE
LAD
Ventricularectopyor dysrhythmia (v-tach)
Ventricular strain
Ventricular hypertrophy may be associated with a strain pattern causing the ST segment to become depressed and humped. Strain is against resistance from a narrowed valve or hypertension causing it to become hyper trophy to compensate
Brugada syndrome
Right bundle branch block with ST elevation in leads V1 V2 in V3 and they are susceptible to deadly arrhythmias. The treatment is in implantation of an ICD implantable cardioverter defibrillator
Diffeentialon inside versus outside and can triggerarryhtmiaor concern.
Digitalis effect
Causes a gradual downward curve of the ST segment similar to a mustache with the lowest portion of the segment depressed below the baseline. To find observe a lead with no Demonstrable S wav, Downward portion of our wave gradually seconds as it curves down into the ST segment which is usually depressed. The downward limb of the R with has a gentle carving slob that gradually blends into the depressed ST segment. Excess digitalis tends to cause AV slowing of depolarization through the AV node and can cause rate dependent AV blocks and can even induce sinus blocks. Premature atrial beats are the earliest warning signs of elevated levels of digitalis as atrial automaticity foci are very effective Sensors. Low serum potassium can enhance the toxicity of digitalis producing undesirable signs of toxicity. This Toxicity can produce a trail and junctional tacky arrhythmias, PVCs, ventricular bigeminy and trigeminy, ventricular tachycardia, and ventricular fibrillation. Marked digitalis toxicity not only affects the very sensitive atrial and unctional automaticity foci But can impact the ventricular foci causing them to fire multiple discharges that can initiate dangerous ventricular tachyarrhythmias. Has a parasympathetic affect can be used for therapy with certain doses with a sinus rhythm digitalis slows The SA node pacing right. Conduction through the AV node is slowed and digitalis also inhibits the AV node’s receptive Ness to multiple stimuli allowing fewer stimuli to reach the ventricles which is necessary for us to do in someone with atrial flutter and fibrillation in order to permit a more physiological and efficient ventricular response rate
- Shortened QT interval (the high intracellular calcium levels tends to inhibits Ca2+channels for less depolarization in phase 2 and encourages the Ca2+-dependent enhancement of K channels for more rapid repolarization in phase 3)
- Characteristic down-sloping ST depression (with alterations in the slopes of phase 2 and 3 of the ventricular AP, as mentioned above)
- Disruption of sodium pump will disrupt membrane potentials and hence help to trigger a variety of arrhythmias (e.g., with afterpolarizationsthat reach threshold)
- Digitalis binds to the K+side of the sodium pump, so that hypokalemiacan worsen digitalis toxicity
High intercellularcalcium, getting potassium channels firing to rapidly repolarize forming scooped out pattern. Firing off all over place more positive on outside w/ greater risk of arrythmia, binding to potassium side if someone hypokalemic on diurheticsso peed out potassium making digitalis toxicity dig and diarrhetics.
Binds to external surface of sodium pump, so Na+buildup in cell and more Na+/Ca2+exchange
Autonomic influences with ↑vagal tone (variety of ways, ultimately stemming from sodium pump blockade, e.g., hypersensitivity of carotid sinus)
Quinidine affects
Causes widening of the P-wave and widening and notching of the QRS complex. ST depression with a prolonged QT and usually has the presence of u waves representing delayed repolarization of the ventricular conduction system. Quinta dine retards depolarization and repolarization through the atrial and ventricular myocardium due to its affects on sodium and potassium channels. w/ differential along thicknesses of ventricular myocardium deeloping Can cause torsades de points
Blocks voltage gated potassium channels getting prolonged QT,
Frontal Plane
Letters are positive ends of leads. Leads positive and negative are polarity for each lead.
II, III, AVF positive on bottom
AVR, AVL positive on top
I positive on right side negative on left side
Sum at certain point is pointing in this or that direction should all be going towards the left ventricle. If pointing up, down, or other side not normal.
axis deviation
relative deviation vs. absolute deviation
- Less than 30 degrees of deviation from normal, likely to be physiologic
- Abnormal usually > 30 degrees of deviation from normal range
- Relative deviation is more than ~ 90 degree change from one ‘normal’ value to another ‘normal’ value
(for example, an axis of -5 degrees and +90 degrees in the same patient)
•Absolute deviation is when the mean axis falls outside of the normal range -30 to 105
Left axis deviation and its causes
0 to 90 is left axis deviation LAD normal
0 to -90 is still LAD
Causes:
Toward hypertrophy away from infarction
- Left ventricular hypertrophy- 50% of time, Left side pumping hard to get it out of aorta. More muscle mass and current in that direction shifting to left side.
- Right ventricular infarction- Current cannot travel through dead muscle no place for current to travel so no current to right shifting to left
Mental retardation- cushingsyndrome. Exoskeletaondoesn’tform well changing conduction left axis deviaiton, ventricular and atrial septaldefect as well as mitral.
Pneumothroaxheart pushed to other side of body. SOB weight loss- lung cancer. If axis changes car accident- pneumothorax
Lvieron right- normal
Liver on left- sinus inversus
- LBBB
- Abdominal tumor
- High Diaphragm
- Pregnancy
- Obesity
Right axis deviation
90-180 right axis deviation opposite things cause it than LAD
- Young patients
- Thin patients
- Dextrocardia- heart on opposite side of body
- Right ventricular hypertrophy
- Left ventricular infarction
- RBBB
- Emphysema flattens diaphragm
Midline liver- changes venous return to heart diminished impossible to catheterize heart.
COPD- low voltage QRS differentiate pericardial effusion, obesity, and hyperthyroidism.
Pulmonary embolism- acute strain on right ventricle for right axis deviation.
•Pulmonary infarcts/emboli
positive and negative vectors
Positive vector will be taller or more positive
Negative vector will appear deeper or more
negative
- A lead is considered positive if it is even a tiny bit more positive than negative.
- A lead is considered negative if it is even a tiny bit more negative than positive.
Bundle Branches
come from bundle of his to the two bundle branches forming the right and left bundle branch (left anterior and posterior fasicle)
abnormal amplitudes
Criteria for abnormally small complex:
decreased Voltage in all limb leads <5 mm
decreased Waves <10 mm high in precordials
- A thin person with an effusion will have larger precordial leads than a more robust person with an effusion.
- In a heavier person, you have to contend with the effusion and the size of the body wall between the heart and the electrode.
P pulmonale
P-pulmonaleis a peaked, teepee-shaped P wave that is more than 2.5 mm high in the limb leads. It is most commonly found in leads II and III.
This is the classic finding for severe right atrial enlargement.
When a peaked P wave is less than 2.5 mm high, it is not associated with atrial enlargement.
P-mitrale
Is > 0.12 sec in limb leads (I and II)
Notched (M-shaped)
A classic but uncommon finding in severe left atrial enlargement (LAE)
P-mitrales an M-shaped P wave in the limb leads that is greater than 0.12 seconds.
The notching is caused by prolonged conduction times required to transmit the impulse through the enlarged left atrium.
Notching can also be found in P waves less than 0.12 seconds wide, but may not be associated with LAE.
hypokalemia
- Makes membrane potential more negative.
- Also generates problems with prolonged repolarization, including:
- Low amplitude T waves
- Prominent U waves(normal U waves are ventricular afterpolarizations, but many abnormal “U” waves are altered/interrupted T waves)
hyperkalemia
- Makes membrane potential less negative.
- Also generates problems with excessive depolarization of cardiac tissue, and repolarizationat a less negative level, including:
- Peaked T waves
- Flattened/lost P waves
- Widening of QRSàrisk of ventricular defibrillation
sine wave degenerate to erratic uncoordinated depolarization of VFIB
hypocalcemia
- Delay of repolarization (less calcium coming in, less “triggering” of repolarization), so…
- QT prolongation with ↑ ST
Hypocalcemia- not calcium rushing in as vigorously not strong postiviecharge keeping it high to stimulate increasing opening of potassium channels so repolarization prolonged wont stay positive long in creating plateau.
hypercalcemia
- Increases in the rate of ventricular repolarization, so…
- QT shortened, as ↓ ST
Amount of calcium keeps equilibrium potential in positive area enhancing potassium conduction across membrane to drive it back down to the level closer to potassium normally is.
Hypercalcemia- voltage gated potassium channels to compensate w/ rapid repolarization
pulmonary embolism
Tachycardia, “S1,Q3, inverted T3”, ST depression in II, T wave inversion in V1-4, all classically associated with pulmonary embolism (think increased right heart afterload)
