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CV 2 Exam 1 > Dubin book > Flashcards

Dubin book Flashcards

1
Q

P wave represents

A

atrial deploarization and contraction (contraction does take longer than the p wave shows).

Blood goes through the AV valves. (mitral and tricuspid)

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2
Q

The AV valves

A

The mitral and tricuspid (AV) valves lie between the atria and the ventricles, thereby acting to electrically insulated the ventricles from the atria

Tricuspid is on the right side.

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3
Q

The AV node

A

is the sole pathway to conduct the depolarization stimulus through the fibrous AV valves to the ventricles.

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4
Q

the timing of the contractions

A

both atria contract simultaneously, and also both ventricles contract together.

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5
Q

what is the part after the P wave on the EKG?

A

It takes a little time for the blood to flow through the valves into the ventricles, hence the necessary pause that produces a short piece of flat baseline after each P wave on the EKG.

At the AV node, depolarization slows down; slow conduction through the AV node is carried by calcium ions.

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6
Q

what happens after slow depolarization of the AV node?

A

depolarization shoots rapidly through the His Bundle and the Bundle branches and their subdivisions, so depolarization is quickly distributed to the myocytes of the ventricles.

Purkinje fibers use fast-moving Na+ ions for the conduction of depolarization

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7
Q

The ST segment is normally… and represents…

A

horizontal, flat, and most importantly, level with other areas of the baseline. If the ST segment is elevated or depressed beyond the normal baseline level, this is usually a sign of serious pathology that may indicate imminent problems.

It represents the plateau (initial) phase of ventricular repolarization.

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8
Q

The T wave represents

A

the final, “rapid” phase of ventricular repolarization, which occurs quickly and effectively.

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9
Q

Repolarization of the ventricles is accomplished by what ions leaving the myocytes?

A

K+

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10
Q

Ventricular systole is marked on the ekg how?

A

it begins with the QRS and persists until the end of the T wave.

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11
Q

The QT interval is a good indicator of

A

repolarization of the ventricles. Patients with hereditary long qt interval syndromes are vulnerable to dangerous or even deadly rapid ventricular rhythms.

The QT interval is usually less than half of the R-to-R interval.

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12
Q

The roles of ions

A

Calcium ions cause myocyte contraction
Potassium ion outflow causes repolarization of the myocytes
Sodium ion movement produces cell-to-cell conduction of depolarization in the heart, except the AV Node, which depends on the (slow) movement of Calcium ions.

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13
Q

EKG paper

A

little squares are 1 mm and represent .04 seconds

big squares are made up of 5 little ones = .2 seconds

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14
Q

The height (magnitude) of waves is a measure of

A

voltage

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15
Q

positive and negative deflections

A

positive deflections are upward on the EKG, negatives are downward.

When a wave of stimulation (depolarization) advances toward a positive skin electrode, this produces a positive deflection.

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16
Q

The leads of an EKG

A

6 limb leads: I, II, III, AVR, AVF and AVL. The R means “right arm positive,” F is left Foot, and L is Left Arm.
The AV leads are also called “unipolar.”

The limb leads are in the “frontal” plane.

6 chest leads (= precordial leads) in the horizontal plane. The point of intersection is the AV Node.
V1 and V2 are the right chest leads, V5 and V6 are the left chest leads
V3 and V4 are oriented over the area of the interventricular septum.

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17
Q

Sympathetic system on the heart

A

activates cardiac Beta 1 adrenergic receptors.

increases rate of SA Node pacing, rate of conduction, force of contraction and irritability of foci.

Norepinephrine does this, and epinephrine from the adrenal gland does it even more forcefully.

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18
Q

Parasympathetic system on the heart

A

Ach decreases the rate of SA node pacing, the rate of conduction, the force of contraction, nd the irritability of atrial and junctional foci.

“vagal” stimulation.

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19
Q

Autonomic control of blood flow and blood pressure

A

alpha 1 adrenergic receptors constrict arteries

cholinergic receptors dilate arteries

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20
Q

Merciful syncope

A

Severe pain may induce a reflex parasympathetic response that causes syncope

Slowing of SA node –> bradycardia and dilated arteries –> hypotension

Also called “vaso-vagal syncope”

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21
Q

Vagal maneuver

A

carotid sinus massage or induced gagging

inhibits irritable focus (atrial or AV jucntional) –> supraventricular tachycardia converts to sinus rhythm.

Also inhibits AV node (increases refractoriness) –> diagnostic aid with 2:1 AV block or atrial flutter

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22
Q

sympathetic response to standing

A

constriction of peripheral arteries to prevent distal blood pooling AND stimulate sinus pacing. (communicated by baroreceptors)

orthostatic hypotension is caused by failure of these compensatory sympathetic mechanisms upon standing.

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23
Q

Neurocardiogenic syncope

A

In some elderly patients, prolonged standing stimulates sinus pacing but vasoconstriction fails –> transient tachycardia with poor cardiac volume -> stimulates left ventricular stretch receptors (mechanoreceptors)–> paradoxical parasympathetic reflex:
- bradicardia and hypotension –> syncope

Head Up Tilt (HUT) test confirms diagnosis

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24
Q

THe 5 steps of reading an EKG

A

Rate: 300, 150, 100, 75, 60, 50

Rhythm: P before QRS, QRS after each P
PR intervals (for AV Blocks)
QRS interval (for BBB)
If Axis Deviation, rule out hemiblock

Axis: QRS above or below baseline for Axis Quadrant (for normal vs. R or L axis deviation
For Axis in degrees, find isoelectric QRS in a limb lead of Axis Quadrant using the Axis in Degrees chart.
Axis rotation in the horizontal plane: find transitional (isoelectric) QRS.

Hypertrophy: Check V1 (P wave for atrial hypertrophy, R wave for Right Ventricular Hypertrophy, S wave depth in V1 + R wave height in V5 for left ventricular hypertrophy)

Infarction: scan all leads for Q waves, inverted T waves, ST segment elevation or depression. Find the location of the pathology (in th e left ventricle) and then identify the occluded coronary artery.

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25
Q

Normal sinus rhythm

A

60-100 beats per minute.

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26
Q

The heart’s normal pacemaker

A

SA Node. Located in the upper-posterior wall of the right atrium.

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27
Q

Sinus rhythm slower than 60 bpm

A

sinus bradycardia. Often results from parasympathetic excess. (conditioned athletes at rest)

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28
Q

Sinus rhythm faster than 100 bpm

A

sinus tachycardia. Exercise can cause this, for example.

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29
Q

automaticity foci (= ectopic foci)

A

focal areas of automaticity in the heart that are potential pacemakers capable of pacing in emergency situations. Normally electrically silent.

Atrial automaticity foci (within the atrial conduction system)

Junctional automaticity foci (in the AV junction)

Ventricular automaticity foci (in the purkinje fibers)

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30
Q

Pacing rates of automaticity foci

A

Atrial: 60-80

Junctional: 40-60

Ventricular: 20-40

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31
Q

overdrive suppression

A

The SA Node overdrive-suppresses all foci (since they have a slower inherent pacing rate)

Each ectopic focus will overdrive -suppress all lower (slower) foci, eliminating any competition.

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32
Q

Idioventricular rhythm

A

occurs if all pacemaking centers above the bundle of His ectopic focus have failed OR if there is a complete block of conduction below the AV node that prevents any pacing stimulus above it from reaching the ventricle.

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33
Q

Count the large boxes for rate

A

300, 150, 100

75, 60, 50

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34
Q

For bradycardia, check rate by…

A

looking at the 3-second marks. 2 of these is 6 seconds, multiply the numer of waves by 10.

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35
Q

respiration and sinus rhythm

A

The slight increase in heart rate during inspiration is due to sympathetic stimulation of the SA node, and the slight decrease during expiration– parasympathetic inhibition of hte SA node. This is normal.

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36
Q

Three conduction pathways from the SA node to the AV node

A

Anterior, middle and posterior internodal tracts.

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37
Q

Bachmann’s bundle

A

originates in the SA node and distributes depolarization to the left atrium.

this does not record on the EKG, but depolarization of the atrial mycoardium produces a P wave.

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38
Q

coronary sinus

A

the heart’s own venous drainage empties into the right atrium via the coronary sinus

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39
Q

U wave

A

purkinje fibers take longer to repolarize than the ventricular repolarization. The final phase of purkinje repolarization may record a small hump, the U wave, on EKG.

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40
Q

Irregular rhythms usually caused by multiple, active automaticity sites

A

Wandering pacemaker
multifocal atrial tachycardia
atrial fibrillation

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41
Q

irregular rhythms

A

lack a constant duration between paced cycles.

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42
Q

entrance block

A

when any incoming depolarization is blocked, and ectopic foci cannot be overdrive-suppressed while their own automaticity is still conducted to surrounding tissue. When an automaticity focus has entrance block, it is said to be parasystolic.

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43
Q

Wandering pacemaker

A

irregular ventricular rhythm.
P’ wave shape varies
atrial rate less than 100

irregular rhythm produced by the pacemaker activity wandering from the SA node to nearby atrial automaticity foci. –> cycle length variation and variation in the shape of the P’ waves.

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44
Q

Multifocal atrial tachycardia

A

p’ wave shape varies
atrial rate exceeds 100
irregular ventricular rhythm.

often seen in COPD. heart rate over 100 per minute with P’ waves of various shapes, since 3 or more atrial foci are involved.

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45
Q

Atrial fibrillation

A

continuous chaotic atrial spikes (no real P waves0
irregular ventricular rhythm.

Caused by the continuous rapid-firing of multiple atrial automaticity foci. No impulse depolarizes the atria completely, and only an occasional, random atrial depolarization reaches the AV node to be conducted to the ventricles; this produces an irregular ventricular (QRS) rhythm.

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46
Q

Escape Rhythm

A

an automaticity focus escapes overdrive suppression to pace at its inherent rate:
- atrial escape rhythm
junctional escape rhythm
ventricular escape rhythm

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47
Q

Escape Beat

A

an automaticity focus transiently escapes overdrive suppression to emit one beat:
atrial escape beat
junctional escape beat
ventricular escape beat

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48
Q

Atrial escape rhythm

A

with sinus arrest, an atrial focus quickly escapes overdrive suppression to become the dominant pacemaker at its inherent rate.

P waves will look different than before.

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49
Q

Junctional escape rhythm.

A

absent regular pacing stimulie from above, an automaticity focus in the AV juction may escape overdrive suppression to become an active pacemaker producing a junctional escape rhythm in its inherent range: 40-60 per minute.

Mainly conducts to ventricles, producing a series of lone QRS complexes. But can cause retrograde atrial depolarization–> inverted P’.

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50
Q

downward displacement of the pacemaker

A

total failure of hte SA node and all automaticity foci above the ventricles is a rare and grave condition. In extremis, a ventricular focus escapes to become the active ventricular pacemaker in a final attempt to sustain life.

blood flow is often so slow as to –> syncope, “Stokes-Adams Syndrome.”

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51
Q

what does a burst of parasympathetic activity do?

A

depresses the SA node (producing a pause) and also depresses the atrial and junctional foci, which leaves only the ventricular foci to respond to the pause. So a ventricular automaticity focus escapes overdrive suppression and discharges, depolarizing the ventricles, producing an enormous ventricular complex.

This is usually transient.

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52
Q

premature beat

A

an irritable focus spontaneously fires a single stimulus:
premature atrial beat
premature junctional beat
premature ventricular beat

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53
Q

Atrial and junctional foci become irritable because of

A

adrenaline (epinephrine)
increased sympathetic stimulation
presence of caffeine, amphetamines, cocaine, or other beta 1 receptor stimulants
excess digitalis, some toxins, occasionally ethanol
hyperthyroidism (direct stimulation plus heart oversensitive to adrenergic stimulants)
stretch … and to some extent, low O2

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54
Q

a VERY irritable atrial or junctional focus

A

may fire a series of rapid pacing impulses to become the dominant pacemaker, overdrive-suppressing all automaticity centers.

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55
Q

the giveaway of a premature atrial beat

A

a PAB records as a P’. The P’ may be difficult to detect when it’s hiding on the peak of a T wave; the giveaway is a too-tall T, taller than the other T waves in the same lead.

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56
Q

when does an active automaticity center reset the pace?

A

when it reaches the dominant (active) center of automaticity. If it doesn’t, then the dominant center will continue with its original pace.

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57
Q

premature atrial beat with aberrent ventricular conduction

A

the ventricular conduction system is usually receptive to being depolarized by a Premature Atrial Beat, but one bundle branch may not have completely RE polarized when the other is receptive. This produces a slightly widened QRS for that premature cycle only.

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58
Q

Non-conducted premature atrial beat

A

a PAB may be unable to depolarize the AV node if it is not fully repolarized and still refractory to an extra stimulus. This records as a too-early, unusual P’ wave that has no ventricular QRS-T response.

this DOES depolarize the SA node, which resets its pacemaking one cycle length after the premature stimulus.

this harmless, but dangerous-looking, span of empty baseline has the sinister appearance of a “some-kind-of-block” but is not.

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59
Q

Atrial bigeminy

A

Occasionally, an irritable automaticity focus fires a premature atrial beat (P’) that couples to the end of a normal cycle, and repeats this process by coupling a PAB to the end of each successive normal cycle. This is Atrial Bigeminy.

60
Q

if you see a premature QRS complex that is slightly widened, consider…

A

it may be due to a premature junctional (or premature atrial) beat with aberrant ventricular conduction.

61
Q

aberrent ventricular conduction

A

With a premature junctional beat, one bundle branch may repolarize slower than the other, so the too-early depolarization from a JB may conduct through one bundle branch, but the impulse is temporarily delayed in the other, still refractory, bundle branch (usually the right). So instead of depolarizing simultaneously, one ventricle depolarizes punctually and the other is delayed, producing a slightly widened QRS complex typical of a PJB (premature junctional beat) with aberrant ventricular conduction.

62
Q

A ventricular focus can be made irritable by

A

Low O2- airway obstruction, absence of air, air with poor O2 content, minimal blood oxygenation in lungs, reduced CO, poor to absent coronary blood supply

hypokalemia

pathology- mitral valve prolapse, stretch, myocarditis, etc.

also some B1 adrenergic stimulants.

63
Q

Premature Ventricular Complex

A

an irritable ventricular focus may suddenly fire a stimulus and produce a PVC on EKG.

They occur early in the cycle. Easily recognized by their great width adn enormous amplitude, they are usually opposite the polarity of normal QRSs.

Most likely cause is hypoxia.

64
Q

frequent unifocal PVCs

A

usually indicate poor oxygenation of a single ventricular focus– often because the blood supply to that focus is diminished. Remember, six PVCs per minute is pathological. Don’t ignore this patient!

65
Q

Ventricular parasystole

A

is produced by a ventricular automaticity focus that suffers from entrance block but is NOT irritable. The parasystolic focus is not vulnerable to overdrive suppression, so it paces at its inherent rate, and the ventricular complexes that it generates poke through the dominant sinus rhythm.

When you see PVCs that appear to be coupled to a long series of normal cycles, you should suspect ventricular parasystole

66
Q

a run of three or more pVCs in rapid succession

A

is really a run of Ventricular Tachycardia. If it lasts longer than 30 seconds, it is called sustained VT.

67
Q

Multifocal PVCs

A

severe cardiac hypoxia can cause multifocal PVCs- a desperation measure produced by multiple, exceptionally irritable (hypoxic) ventricular foci. Each focus produces its own unique, identifiable PVC every time it fires.

Each irritable focus produces its own distinctive PVC.

Danger!

68
Q

Mitral valve prolapse

A

causes PVCs, including runs of VT and multifocal PVCs, yet it is considered a benign condition. With MVP the mitral valve is “floppy” and billows into the left atrium during ventricular systole.

the traction on the papillary muscles may cause localized stretch and ischemia, irritating adjacent ventricular automaticity foci.

69
Q

R on T phenomenon

A

If a PVC falls on a T wave, particularly in situations of hypoxia or low serum potassium, it occurs during a “ulnerable period” and dangerous arrhythmias may result.

70
Q

Tachy-arrhythmias

A

rapid rhythms originating in very irritable automaticity foci.

Paroxysmal : 150-250
Flutter: 250-350
Fibrillation: 350-450

71
Q

paroxysmal means

A

sudden

72
Q

why is sinus tachycardia not paroxysmal?

A

Sinus tachycardia is the SA node’s gradual response to exercise, excitement, etc. Although its rate of pacing may eventually become quite rapid, sinus tachycardia is neither sudden nor does it originate in an automaticity focus, so by definition, iti is NOT a tachycardia.

73
Q

paroxysmal atrial tachycardia with AV block

A

has more than one P’ wave spike for every QRS response. Suspect digitalis excess or toxicity; atrial foci are very sensitive to the irritating effects of digitalis preparations.

Excess digitalis can provoke an atrial focus into such an irritable state that it suddnly paces rapidly. At the same time, digitalis markedly inhibits the AV node, so that only every second stimulus conducts to the ventricles (every other atrial stimulus is blocked in the digitalis-inhibited AV node)

74
Q

paroxysmal junctional tachycardia

A

is caused by the sudden rapid pacing of a very irritable automaticity focus in the AV junction. The junctional focus may suddenly initiate tachycardia pacing, because of marked irritability induced by stimulants and/or by a well-timed premature beat from another focus.

75
Q

AV Nodal Re-entry

A

Another type of junctional tachycardia is AV Nodal Reentry tachycardia. In theory, a continuous reentry circuit devleops (which includes the AV node and the lower atria) and rapidly paces the atria and ventricles.

76
Q

Supraventricular tachycardia

A

is a general term, which includes both paroxysmal atrial tachycardia (PAT) and paroxysmal junctional tachycardia (PJT)

77
Q

PVT

A

Paroxysmal ventricular tachycardia is produced by a very irritable ventricular atuomaticity focus that paces in the 150-250 per minute range. It has a characteristic patttern of enormous, consecutive PVC-like complexes.

78
Q

What convirms PVT over SVT?

A

The presence of “captures” or “fusions– a blending on EKG of a normal QRS with a PCV-like complex– could only happen in VT, not SVT.

79
Q

Distinguishing Wide QRS complex SVT from VT

A

The patient with VT is most llikely elerly and suffering from diminished oronary blood flow, reducing the oxygen supplyl to the ventricular foci.

Signs of AV dissociation (presence of fusions or captures) or Extreme R.A.D. is characteristic of VT.

80
Q

Torsades de Points

A

is a peculiar form of very rapid ventricular rhythm caused by low potassium, medications that block potassium channels, or congenital abnormalities (long QT syndrome) all of which lengthen the QT segment. The rate is a variable 250-350 per minute, usually in brief episodes.

81
Q

Atrial flutter

A

originates in an atrial automaticity focus. The rapid succession of identical, back-to-back atrial depolarization waves, “flutter” waves, suggest a reentry origin to some experts.

250-350 bpm

The AV node has a long refractory period, so only one in a series of flutter waves conducts to the ventricles.

82
Q

Ventricular flutter

A

is produced by a single ventricular automaticity focus firing at an exceptionally rapid rate of 250-350 per minute. It produces a rapid series of smooth sine-waves of similar amplitude.

83
Q

Fibrillation

A

is a totally erratic rhythm caused by continuous, rapid rate discharges from numerous automaticity foci in either the atria or in the ventricles.

84
Q

Atrial fibrillation

A

is caused by many irritable parasystolic atrial foci (with entrance block) firing at rapid rates, producing an exceedingly rapid, erratic atrial rhythm. Th atrial “rate” is 350-450 per minute.

Depolarizations from foci near the AV node conduct to the ventricles, producing very irregular ventricular rhythm.

85
Q

Ventricular fibrillation

A

is cause by rapid-rate discharges from many irritable, parasystolic ventricular automaticity foci, producing an erratic, rapid twiching of the ventricles (250-450 per minute)

each one depolarizes only a small area of ventricle. –> rapid, ineffective twitching

looks like a “bag of worms”

Requires CPR and defibrillation!

86
Q

Wolf-Parkinson White Sundrome

A

an abnormal, accessory AV conduction pathway, the bundle of Kent, can “short circuit” the (usual) delay of ventricular conduction in the AV node. This prematurely depolarizes (“pre-excitess”) a portion of the ventricles (producing a delta wave on EKG) just before normal ventricular depolarization begins.

The delta wave creates the illlusion of a “shortened” PR interval and “lengthened” QRS. The delta wave actually records the depolarization of an area of ventricular pre-excitation.

87
Q

Lown-Ganong-Levine syndrome

A

the AV node is bypassed by an extension of hte Anterior Internodal Tract. Absent the conduction delay in the AV node, this “James bundle” conducts atrial depolarizations directly to the His Bunle without delay. This can pose a serious problem with rapid atrial arrhythmias like atrial flutter.

88
Q

Blocks

A

retard or prevent the conduction of depolarization; they can occur in the SA node, the AV node, or in the larger divisions of the ventricular conduction system.

89
Q

Sinus block

A

an unhealthy SA node (sinus node) may temporarily fail to pace for at least one cycle; this is Sinus Block. Then the SA node resumes pacing. Notice that the missed cycle has no P wave; a very important feature.

90
Q

Sick Sinus Syndrome

A

is a wastebasket of arrhythmias caused by SA node dysfunction associated with unresponsive supraventricular (atrial and junctional) automaticity foci, which are also dysfunctional and can’t employ their normal escape mechanism to assume pacing responsibility.

often in elderly with heart disease

usually characterized by marked sinus bradycardia, but without normal escape mechanisms of atrial and junctional foci.

young athletes can appear to have this, due to parasympathetic hyperactivity at rest.

91
Q

AV blocks

A

either retard or eliminate (or both!) conduction from teh atria to the ventricles.

1st, 2nd Wenckebach and Mobitz) and 3rd degree

92
Q

First degree AV block

A

prolongs AV node conduction.

prolongs the PR interval. Should be less than one large square, which is less than .2 seconds.

93
Q

2nd degree AV Blocks

A

allow some atrial depolarizations to conduct to the ventricles, while some are blocked, leaving lone P waves without associated QRS.

2 types:

Wenckebach- a block of the AV Node. produce a series of cycles with progressive blocking of AV node conduction (longer distance from P to QRS) until the final P wave is totally blocked in the AV node, eliminating the QRS response. Each repeating wenckebach series has a consistent P:QRS ratio.
- PR is long, QRS is normal

Mobitz: a block of the Purkinje fiber bundles. Usually produce a series of cycles consisting of one normal P-QRS-T cycle preceded by a series of paced P waves that fail to conduct through the AV node (no QRS response). Each repeating mobitz series has a consistent P:QRS ratio. 2:1 or 3:1 Ps and Ps with QRS
- PR is normal, often QRS is widened

94
Q

3rd degree AV block

A

complete 3rd degree AV block is a total block of conduction to the ventricles, so atrial depolarizations are NOT conducted to the ventricles. Therefore, an automaticity focuse below the complete block escapes to pace the ventricles at its inherent rate.

95
Q

Downward Displacement of the Pacemaker

A

the absence of atrial activity with wide complex bradycardia indicates that neither the SA node nor supraventricular foci are viable enough to apce the atria. This failure of all automaticity centers above the ventricles, called “downward displacement of the pacemaker,” usually carries an unfavorable progrnosis. Make certain that the flat baseline is not due to atrial fibrillation.

Extremely high serum K+ concentrations can severely depress the SA Nodea nd supraventricular foci, producing the same EKG findings. Hyperkalemia can cause cardiac asystole, a form or cardiac arrest.

96
Q

Bundle Branch Block

A

ordinarily both ventricles are depolarized simultaneously. But with bundle branch block, the unblocked bundle branch conducts normally, while depollarization in the blocked bundle branch has to creep slowly through the surrounding muscle (shich conducts more slowly than the specialized bundle branch) to stimulate the bundle branch below the block. After the delay, depolarization proceeds rapidly again elow the block. However, the delay in the blocked bundle branch allows the unblocked ventricle to begin depolarizing before the blocked ventricle.

Looks like two mountain peaks on QRS

97
Q

Right bundle branch block

A

creates R1 and R1 on leads V1 and V2.

98
Q

Left bundle branch block

A

produces R and R’ in V5 and V6, although not as distinctly separate as the Rs in RBBB

99
Q

Depolarization is an advancing wave of

A

Na+ ions

100
Q

myocardial infarction

A

in MI there is a necrotic area of the heart that has lost its blood supply and does not depolarize. The unopposed vectors from the other side draw the mean qrs vector away from the infaarct.

101
Q

mean QRS vector and pathology

A

points toward ventricular hypertrophy and away from infarction

102
Q

If the R is far from P

A

then you have a first degree

103
Q

longer, longer, longer, drop

A

then you have a Wenckebach

104
Q

if some Ps do not get through

A

then you have a Mobitz II

105
Q

If Ps and Qs do not agree

A

then you have a third degree

106
Q

atrial hypertrophy looks like?

A

diphasic P wave in lead 1

if the first part is larger, then it’s right atrial enlargement. If the terminal portion is large and wwide, it’s Left atrial enlargement.

107
Q

what do we see in lead one with right ventricular hypertrophy?

A

a large R wave.

108
Q

in left ventricular hypertrophy there is a very talll…

A

R wave in lead V5

109
Q

how to sum up if L ventricular hypertrophy is present

A

add the depth of the S wave in V1 to the height of the R wave in V5. If it’s more than 35 mm, then you have Left Ventricular Hypertrophy

110
Q

characteristic T wave that accompanies Left Ventricular Hypertophy

A

inversion with asymmetry

check v5 and v6, they are right over the ventricle

111
Q

Ventricular strain is characterized by depression of the

A

ST segment

112
Q

Ischemia is characterized by

A

inverted T waves. Symmetrical.

113
Q

elevation of the ST segment means

A

injury. (acute/ recent)

It is the earliest sign of an infarction to record on EKG, but can also be a sign of ventricular aneurysm or pericarditis.

114
Q

pericarditis

A

the ST segment is elevated and usually flat or concave. THe entire T wave may be elevated off the baseline.

115
Q

a subendocardial infarction (does not extend through the full thickness of the left ventricular wall) will…

A

depress the ST segment.

116
Q

ST segment depression

A

could be from subendocardial infarction, a positive stres test, or digitalis with weird flattened look.

117
Q

what do significant Q waves mean?

A

diagnostic for infarction (area of necrosis)

118
Q

how to identify a lateral infarction

A

AVL and I (L I) will show a Q wave (through the void of the necrotic infarct)

119
Q

what will we see in an inferior infarction?

A

negative Q wave in the inferior leads, II, III and AVF

120
Q

what do we see in a posterior infarction?

A

a large R wave in V1 and V2 because that is what an inverted Q wave would look like

121
Q

What happens to the ST segment in anterior and posterior infarctions?

A

in anterior– elevated in the chest leads

in posterior- depression in V1 and V2

122
Q

four general locations in the left ventricle where infarctions commonly occur

A

Posterior (large R in V1, V2, maybe Q in V6)

lateral- Q in I, AVL

Inferior- Q in II, III, AVF

Anterior- Q in V1, V2, V3 or V4

123
Q

2 coronary arteries

A

left and right

124
Q

branches of the left coronary artery

A

circumflex

descending

125
Q

Where does the right coronary artery go?

A

curves around the right ventricle

126
Q

a lateral infarction is caused by

A

an occlusion of the circumflex branch of the Left Coronary Artery

127
Q

An anterior infarction is due to

A

an occlusion of the anterior descending branch of the LCA

128
Q

true posterior infarctions

A

are generally caused by an occlusion of the right coronary artery or one of its branches

The RCA proides blood to SA node, AV node, and His Bundle

129
Q

inferior infarctions

A

are caused by an occluded terminal branch of either the RCA or LCA, depending on which one is dominant RCA more common.

130
Q

Hemiblocks

A

commonly occur with infarction and an associated diminshed blood supply to one of the 2 divisions of the left Bundle Branch.

The are blocks of either the anterior or teh posterior division of the LBB

131
Q

Anterior hemiblock

A

LAD (left axis deviations)- usually assoc with an MI or othe rheart disease
normal or slightly widened QRS
Q1S3

132
Q

pure anterior hemiblock vs. in association with other blocks of the BUndle Branch system

A

pure: QRS is widened only .1 to .12 sec

with others– more

133
Q

Posterior hemiblock

A

RAD - usually assoc. with an MI or other heart disease

normal or slightly widened QRS

S1Q3

134
Q

Brugada Syndrome

A

RBBB with ST elevation in V1, V2, and V3

susceptible to deadly arrhythmias

135
Q

Wellens Syndrome

A

marked T wave inversion in V2 and V3

- ant. descending coronary stenosis

136
Q

Long QT syndrome

A

QT interval more than 1/2 of the cardiac cycle

- predisposed to ventricular arrhythmias

137
Q

COPD

A

often produces low voltage amplitude in all leads, and there is usually Right Axis Deviation

usually some degree of right ventricular hypertrophy

Also, multifocal atrial tachycardia often seen.

138
Q

Pulmonary embolus

A

large S in I, ST depression in II, large Q in III with T wave inversion

tendency toward RAD

139
Q

Hyperkalemia

A

P wave flattens down, QRS widens, T wave becomes peaked

140
Q

Hypokalemia

A

T wave becomes flat and a U wave appears

Think of the T wave as a Tent for Potassium ions. It gets bigger in Hyperkalemia and smaller in hypokalemia

hypokalemia can lead to torsades de pointes, and enhances the toxic effects of digitalis excess

141
Q

Calcium’s effects on the EKG

A

Hyper Ca++ shortens the QT

Hypocalcemia prolongs it

142
Q

digitalis effects on EKG

A

adds a Salvador Dali mustache– a gradual downward curve of the ST segment.

143
Q

Quinidine effects

A

retards depolariztion and repolarization

causes widening of P and QRS, often with ST depression and prolonged QT and U waves

144
Q

pacemakers

A

emit regular pacing stimuli, which record on the EKG as a narrow vertical spike

145
Q

Transplant patients

A

have 2 SA nodes, each producing p waves. The native P wave’s signals don’t cross the stuture line.

CV 2 Exam 1 (3 decks)

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