Ch. 27 & 28 Flashcards

Cardiac Output and Tissue Perfusion

1
Q

automaticity (define in regards to specialized myocardial cells)

A

pacing function

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2
Q

excitability (define in regards to specialized myocardial cells)

A

response of non-pacemaker cells

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3
Q

conductivity (define in regards to specialized myocardial cells)

A

sends the stimuli from cell to cell

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4
Q

contractility (define in regards to specialized myocardial cells)

A

muscles response to the stimuli

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5
Q

cardiac conduction system: flow of electricity

A

SA node to AV junction to Bundle of HIS to Purkinje fibers

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6
Q

Sinoatrial (SA) node

A
  • electrical impulses 60-100 beats/min
  • P wave on the ECG
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7
Q

what is the P wave on the ECG?

A

P wave means that the electricity is coming from the SA node
- atrial depolarization

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8
Q

Atrioventricular (AV) junction

A
  • PR segment on ECG (electricity slows down)
  • contraction known as “atrial kick”
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9
Q

what is the PR segment on the ECG?

A

the AV junction
- 0.12 - 0.20

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10
Q

what is the “atrial kick?”

A

the AV junction

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11
Q

Bundle of His is comprised of

A
  • right bundle branch system
  • left bundle branch system
  • Purkinje Fibers
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12
Q

Bundle of His: right bundle branch system

A

carries electricity to the right side of the heart

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13
Q

Bundle of His: left bundle branch system

A

carries electricity to the left side of the heart

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14
Q

lead placement: continuous EKG monitoring v. 12 lead EKG monitoring

A
  • the number of wires
  • wires pick up electrical impulses going through the heart
  • more info from the 12 lead vs the bedside monitor
  • bedside monitor will not diagnose heart attack
  • chest pain = 12 lead monitor
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15
Q

hard-wired monitoring *

A

electrodes and lead wires are attached directly to the patient
- impulses are transmitted directly from the patient to the monitor

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16
Q

telemetry monitoring

A
  • 3 lead or 5 lead
  • continuous monitoring, in real time
  • to always keep eyes on the patient
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17
Q

nursing responsibility with EKGs *

A
  • ensure correct placement
  • prepare patient
  • set up machine
  • monitoring the ECG
  • interpret the strip/give to MD to interpret
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18
Q

12 lead EKG

A
  • starts at 4th ICS (sternal border)
  • placement matters
  • 12 different angles of the heart
  • GOLD STANDARD for EKG rhythms/picking up heart problems (in rhythm)
  • use for dx of something, then put it away
  • snapshot of information
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19
Q

duration is measured in __

A

fraction of second
on a graph: 1 small square is 1 mm/0.04 seconds; 1 large square is 5mm/0.2 seconds

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20
Q

amplitude is measured in __

A

millivolts (mV)
on a graph: 1 small square is 0.1 mV; 1 large square is 0.5mV

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21
Q

configuration (define in regards to reading an EKG)

A

the shape and appearance of a wave

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22
Q

atrial depolarization occurs during the

A

P wave
- electricity is firing from atrium- SA node (action)

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23
Q

ventricular depolarization occurs during the

A

QRS complex
- ventricle is deploying (action)
- 1-3 tiny squares

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24
Q

early ventricular repolarization occurs during the

A

ST wave
- should almost be flat on graph (flat to isometric line)
- if bump, could mean heart attack

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25
Q

ventricular repolarization occurs during the

A

T wave
“the reset”

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26
Q

U wave

A

late ventricular repolarization

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27
Q

ventricular depolarization and repolarization occurs during the

A

QT interval

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28
Q

normal ECG

A

depol (P wave)
depol (QRS interval)
repol (T wave)
- is it regular or irregular, fast or slow? are all the parts there: pqrst?

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29
Q

ECG rhythm analysis includes (how do you read an ECG)

A
  • determine heart rate
  • determine heart rhythm: is the distance between complexes consistent
  • analyze P waves
  • measure PR interval
  • measure QRS duration
  • interpret rhythm
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30
Q

determining 6 second strip

A
  • count R waves (the QRS complexes) in 6 seconds
  • multiply by 10
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31
Q

determining rate can be measured by (methods)

A
  • beat to beat measurement: R-R or P-P
  • rule of 300
  • 6 second strip
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32
Q

determining rate: rule of 300

A
  • 300, 150, 100, 75, 60, 50
  • find R wave that falls on bolded line, start counting down at next bolded line until next R wave (gives estimate if only have a little bit of strip, less than 6 sec)

don’t really need to know:
- count number of large boxes between R to R (if small boxes, count them and each one is 0.2). ~ ie. 5 big boxes + 2 small boxes is 5.4.
- divide 300 by the number of boxes
- may be a range if irregular
- normal is 60-100

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33
Q

regular rhythm

A
  • P wave before each QRS (atria drives the rate)
  • PR interval is consistent**
  • if no P wave before each QRS, determine the cause
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34
Q

what may cause no P wave before a QRS interval?

A
  • heart block (if the PR interval is very wide)
  • junctional
  • atrial arrhythmia
  • ventricular arrhythmia (wide QRS)
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35
Q

irregular rhythm: regularly irregular

A

premature complexes
- bigeminy
- trigeminy

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36
Q

bigeminy *

A

when normal complexes and premature complexes occur alternately in a repetitive two-beat pattern, with a pause occurring after each premature complex, so complexes occur in pairs

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37
Q

trigeminy *

A

repeated three-beat pattern, usually occurring as two sequential normal complexes followed by a premature complex and a pause, with the same pattern repeating itself in triplets

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38
Q

irregular rhythm: irregularly irregular

A
  • atrial fibrillation
  • premature beats
  • paced beats
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39
Q

atrial fibrillation

A

350-650 beats/min (slow to rapid V)
irregular rhythm
P wave fibrillatory (fine to course)
PR interval: N/A
QRS < 0.12 seconds

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40
Q

premature beats *

A

extra heartbeat that occurs when the heart contracts before it should
- for example, PVCs, PACs

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41
Q

paced beats *

A

an ECG finding that is shown during the cardiac rhythm, controlled by an electrical impulse from an artificial cardiac pacemaker

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42
Q

normal sinus rhythm: rate

A

atrial and ventricular rates of 60-100 beats/min

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43
Q

normal sinus rhythm: rhythm

A

atrial and ventricular rhythms regular
- the space between each R wave is consistent

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44
Q

normal sinus rhythm: P waves

A
  • present
  • consistent configuration
  • one P wave before each QRS complex
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45
Q

normal sinus rhythm: PR interval

A

0.12 to 0.20 second and constant

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46
Q

normal sinus rhythm: QRS duration

A

0.06 to 0.10 second and constant (< 0.12 second)

47
Q

types of dysrhythmias

A
  • tachydysrhythmias
  • bradydysrhythmias
  • premature complexes
  • repetitive rhythm complexes
48
Q

tachydysrhythmias (sinus tachy)

A

rate > 100, < 150
regular rhythm
P wave identical, before each QRS
PR interval is 0.12 to 0.20 second
QRS < 0.12 second

49
Q

bradydysrhythmias (sinus brady)

A

rate < 60
regular rhythm
P wave identical, before each QRS
PR interval is 0.12 to 0.20 second
QRS < 0.12 second

50
Q

repetitive rhythm complexes

A
  • bigeminy (in pairs)
  • trigeminy (in triples)
  • quadrigeminy (in quadruplets)
51
Q

causes of sinus tachycardia

A
  • blood loss
  • dehydration
  • exercise
  • pain
  • caffeine
52
Q

symptoms of sinus tachycardia

A
  • heart rate over 100 bpm; p wave present
53
Q

treatment of sinus tachycardia

A
  • treat the underlying problem before throwing cardiac meds at the patient
  • ie dehydration: hydrate patient IV fluids; exercise a lot: relax; pain: give pain meds
54
Q

causes of sinus bradycardia

A
  • could be marathon runner (which in this case would most likely not be concern if this is their regular HR)
  • hyperkalemia
  • beta blocks, CCB, digoxin
  • cardiac ischemia
55
Q

treatment of sinus bradycardia

A

medicine vs Edison

medicine- atropine: pick up the pace
- given IV, does not get mixed with anything, push, works immediately/picks up in real time

Edison- pacemaker: transcutaneous: temporary, pacemaker pulse generator: permanent

55
Q

symptoms of sinus bradycardia

A
  • fatigue
  • dizziness
  • SOB
  • foggy mentation
  • low BP
56
Q

types of pacemakers

A
  • can be temporary or permanent
  • temporary pacemakers can be invasive or noninvasive
  • temporary: transcutaneous
  • permanent: put into body surgically/cut into patient at bedside
  • pacer spikes will be shown between the p wave and QRS- this means that the pacemaker is working
57
Q

examples of atrial dysrhythmias

A
  • premature atrial contractions
  • supraventricular tachycardia
  • atrial fibrillation
  • atrial flutter
58
Q

premature atrial contractions (PACs)

A

ectopic focus of atrial tissue fires an impulse before next sinus impulse is due
- p wave is funky looking, rhythm is irregular
- don’t really do anything for this; reduce stress or decrease caffeine intake; not really a medical intervention

  • not a rhythm; ie “in sinus rhythm with PACs”
59
Q

premature atrial contractions (PACs) are caused by

A
  • stress
  • fatigue
  • anxiety
  • infection
  • inflammation
  • caffeine
  • nicotine
  • alcohol
  • certain drugs
60
Q

supraventricular tachycardia (SVT) definition/sx

A
  • supra: electrical impulse is coming from above the ventricle not necessarily from the SA node though
  • rapid stimulation of atrial tissue occurs at rate of 100-280 beats/min with mean of 170 beats/min (adult)
  • sx: chest pain, SOB, dizzy mentation
61
Q

supraventricular tachycardia (SVT) treatment

A

medicine vs Edison

medicine- give adenosine: slow it down; stops the heart for 6 sec (causes asystole, with idea that the heart will come back in regular sinus rhythm)
- push very fast, through large IV close to the heart, need second nurse
- can be repeated a couple times if necessary

Edison- synchronized cardioversion: monitor controls when electrical shock happens; put pads on patient and put synchronized on monitor- shock is delivered at specific time in cardiac cycle, less electricity delivered so patient will not go into asystole

62
Q

atrial tachycardia

A

140-250 bpm
regular rhythm
P wave is abnormal, before each QRS but difficult to see
PR interval < 0.20 second
QRS interval < 0.12 second

63
Q

pathophysiology of atrial fibrillation

A

chaotic rhythm (always irregular)
no clear P wave (looks like a bunch of waves, a bunch of foki firing)
irregular ventricular response

64
Q

causes of atrial fibrillation

A
  • incidence increases with age
  • associated with atrial fibrosis and loss of muscle mass
  • common in heart disease (HTN, HF, CAD)
65
Q

most common dysrhythmia

A

atrial fibrillation
- increases with age

66
Q

cardiac output can decrease by ___ % with atrial fibrillation

A

20-30%

67
Q

a fib puts a person at high risk for ___

A

stroke (BIG stroke risk)
- blood is sitting in the atrium, forms clot, clot is shot out of heart

68
Q

atrial fibrillation treatment

A
  • monitoring bleeding (pt probably on blood thinners)
  • looking at coag studies
  • give lovenox (low molecular weight heparin)
  • beta blocker could be used

medicine vs Edison

medicine- CCB is 1st line med: diltiazem (slows rhythm down); give as IV bolus first, push through IV, then hang a bag for small drip dose (*watch blood pressure, it will tank) *give this slowly, little bit then check BP, little more check BP again

Edison- cardioversion: if patient is talking, has rhythm and pulse

69
Q

a fib: assessment

A
  • signs of poor perfusion: SOB, hypotension, poor mentation
  • anxiety
  • 12 lead ECG
  • present with SOB
  • patients can live in chronic a-fib
  • probably on blood thinner: bleeding risk
  • worry about bleeding risk
70
Q

a fib: analysis

A
  • potential for embolus formation
  • potential for heart failure
71
Q

a fib: response

A
  • preventing embolus formation
  • preventing heart failure
72
Q

a fib: patient-centered collaborative care

A
  • risk for stroke
  • antidysrhythmic drugs
  • cardioversion
  • percutaneous radiofrequency catheter ablation
  • bi-ventricular pacing
  • maze procedure
73
Q

digoxin: watch out for

A
  • narrow therapeutic range; need to take blood levels
  • watch for hypokalemia, visual disturbances (halo around lights), fatigue, anorexia, arrhythmias
74
Q

digoxin

A

old med
anti-irrhythmic drug
older patient with chronic a-fib

take apical HR for 1 min; hold if HR < 60 bpm
dig toxicity: patient sees halos around light

75
Q

atrial flutter

A
  • rapid atrial depolarization occurring at a rate of 250-350 times per minute
  • looks like saw tooth on strip

220-430 bpm, <300 bpm (V)
regular or variable rhythm
P wave sawtoothed appearance
PR interval: N/A
QRS < 0.12 second

76
Q

ventricular dysrhythmias vs atrial dysrhythmias

A

ventricular are more life-threatening
- they will kill you
- not good cardiac output, cant live long if big part of heart is not perfusing well

77
Q

What is happening during ventricular dysrhythmias?

A

left ventricle is not pumping oxygenated blood through the body to perfuse vital organs and other tissues

78
Q

premature ventricular complexes

A

a result of increased irritability of ventricular cells- early ventricular complexes followed by a pause

  • wide QRS interval, not obvious P wave
79
Q

ventricular tachycardia

A
  • repetitive firing of an irritable ventricular ectopic focus
  • usually at a rate of 140-180 bpm
  • big wide complexes, no P waves

**always check a pulse FIRST- this determines treatment

80
Q

managing cardiac arrest

A
  • cardiopulmonary resuscitation (CPR)
  • defibrillation
  • cooling
  • catheterization
81
Q

managing cardiac arrest: cardiopulmonary resuscitation

A
  • advanced cardiac life support
  • C-A-B
82
Q

managing cardiac arrest: defibrillation

A

asynchronous countershock depolarizes a critical mass of myocardium simultaneously to stop the re-entry circuit and allow the sinus node to regain control of the heart

83
Q

managing cardiac arrest: cooling *

A

therapeutic hypothermia is a treatment for unconscious cardiac arrest survivors that involves lowering their body temperature to reduce brain damage and increase chances of recovery

84
Q

managing cardiac arrest: catheterization *

A

cardiac catheterization lab- used for patients who have experienced out of hospital cardiac arrest (OHCA)
- provides a setting for resuscitation and stabilization, and can be especially useful for treating OHCA caused by coronary artery disease

85
Q

cardioversion (define)

A

synchronized countershock that may be performed in emergencies for unstable ventricular or supraventricular tachydysrhythmias or electively for stable tachydysrhythmias that are resistant to medical therapies

86
Q

cardioversion (broken down/simple)

A
  • elective procedure
  • client awake and frequently sedated
  • synchronized with QRS
  • 50-200 joules
  • EKG monitor
  • consent form
87
Q

defibrillation (broken down/simple)

A
  • emergency
  • v-fib/ v-tach without a pulse
  • no cardiac output
  • begin with 200 joules, up to 360 joules
  • client unconscious
  • EKG monitor

if its v fib we defib

88
Q

ventricular fibrillation aka v fib is a result of

A

result of electrical chaos in the ventricles- cardiac arrest
- looks like a bunch of squiggles on EKG strip

89
Q

ventricular asystole aka ventricular standstill is

A

the complete absence of any ventricular rhythm- cardiac arrest; “dying heart”

  • flat line accompanied by a ventricular blip (big wide QRS)
90
Q

ventricular asystole treatment

A

medicine vs Edison

medicine- epinephrine (adrenaline to start the heart)

NO Edison- do not defibrillate/shock them; not shockable rhythm

Do CPR; determine if there is an underlying cause to attempt to reverse it (ie electrolyte imbalance)

91
Q

managing dysrhythmias is determined by

A
  • depends on the rhythm
  • first step is to identify rhythm
  • too slow –> speed up
  • too fast –> slow down, may need to interrupt cardiac cycle for this to occur
92
Q

non-surgical management of dysthymias is

A
  • antidysrhythmic agents
  • other drugs
  • drugs used during cardiac arrest
  • vagal maneuvers - carotid sinus massage, vagal reflex
93
Q

automated external defibrillation

A
  • allows for earlier defibrillation
  • when used, there is a greater chance of successful rhythm conversion and patient survival
94
Q

implantable cardioverter/defibrillator

A
  • indicated for patients who have experienced one or more episodes of spontaneous sustained VT or VF not caused by MI
  • transvenous and subcutaneous types
  • wearable cardioverter/defibrillator (WCD)
95
Q

what is a wearable cardioverter/defibrillator (WCD)?

A

an external vest-like device worn 24 hours/day except when showering/bathing

96
Q

sinus tachycardia

A

heart rate: >100 bpm
rhythm: regular
P wave: present before each QRS
PR interval: 0.12-0.2 sec
QRS: < 0.12 sec

97
Q

sinus bradycardia

A

heart rate: < 60 bpm
rhythm: regular
P wave: present before each QRS
PR interval: 0.12-0.2 sec
QRS: < 0.12 sec

98
Q

which is worse: PAC or PVC?

A

PVC will kill you faster than PAC
- if multiple PVCs happen in a row we are concerned: electrolyte imbalance
- a few in a minute not really concerning: caffeine, anxiety

99
Q

paroxysmal supraventricular tachycardia rhythm is

A
  • is intermittent, terminated suddenly with or without intervention (means that it comes and goes)
100
Q

ventricular beats are narrow or wide

A

wide

101
Q

vagal manuever

A

non-invasive way to stimulate the vagus nerve; does not always work

  • carotid massage
  • bear down like trying to have BM
  • blow in straw and block end of it
102
Q

atrial flutter interventions/precautions

A

same as a-fib! *watch bleeding risk/bld thinners, watch BP w/ diltiazem

medicine- CCB is 1st line med: diltiazem (slows rhythm down); give as IV bolus first, push through IV, then hang a bag for small drip dose (*watch blood pressure, it will tank) *give this slowly, little bit then check BP, little more check BP again

Edison- cardioversion: if patient is talking, has rhythm and pulse

103
Q

unifocal PVCs vs multifocal PVCs

A

identical shapes (one funky spot shooting) vs a single PVC is labeled isolated

multifocal is more worrisome; two different funky spots shooting

104
Q

PVC treatments

A

TREAT THE CAUSE
- if patient has low oxygen: give O2
- electrolyte imbalance: fix imbalance (ie give potassium)
- heart attack: do 12 lead EKG

105
Q

v-tach sx

A

EMERGENCY
- not talking
- SOB
- chest pain
- syncope/fainting
- palpitations/fluttering

106
Q

v-tach with a pulse treatment

A

cardioversion

107
Q

v-tach without a pulse treatment

A

no pulse = cardiac arrest
- defibrillate and CPR
- give epinephrine, IV push, don’t mix with anything

  • in a perfect world, defibrillate the patient first
  • defibrillation can fix the problem, CPR buys time
108
Q

v tach without a pulse is the same treatment as

A

v-fib (v-fib will never have a pulse)

  • both get defibrillated and CPR, epinephrine
109
Q

a fib treatment (“A” drug)

A

anti-irrhythmic drug: amioderone

110
Q

managing dysrhythmia (treatments)

A

too slow: atropine, pacing
too fast: adenosine, cardioversion

111
Q

non-surgical management of dysrhythmias

A
  • antidysrhythmic meds: amioderone (can go home on pill), cholesterol meds, blood thinners
  • vagal manuevers: carotid massage, vagal stimulation
112
Q

implantable defibrillator is for patients with

A

for patients with chronic V tach or V fib