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Complex care > EKG > Flashcards

EKG Flashcards

1
Q

Order of electrical conductivity

A
  1. sa node
  2. Av node
  3. bundle of his
  4. R and L bundle branches
  5. purkinje fibers
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2
Q

relative refractory phase

A
  • where cardiac gradually recover their excitability
  • cardiac muscles will respond to STRONG stimuli
  • peak to the end of the T wave
  • vulnerable stage
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3
Q

absolute refractory phase

A
  • beginning of depolarization until the fiber can accept another action potential
  • cardiac muscle cannot be depolarized by any stimuli
  • beginning of the QRS to the peak of the T wave
  • as long as it takes for the heart to contract is the length of this phase
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4
Q

time measurement of an ECG

A
  • represents the time it takes for an electrical impulse to pass through a part of the heart
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5
Q

box sizes

A
  • tiny box = 0.04 (5 small will equal one large)

- large box = 0.20

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6
Q

What does the p wave represent

A
  • atrial depolarization

- comes before the QRS

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7
Q

PR interval: normal length

A
  • 0.12 - .20
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8
Q

What does the PR interval represent

A

the time it takes the original impulse to leave the SA node and travel through the AV node
-tells us how the AV node is functioning

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9
Q

Why does there need to be a delay at the av node

A
  • allows the atria and the ventricles to contract separately from the ventricles
  • allows for atrial kick which helps CO
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10
Q

What does the QRS interval represent

A
  • ventricular repolarization
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11
Q

what is the normal length for the QRS interval

A
  • less than 0.12 seconds
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12
Q

What does the ST segment represent

A
  • time btwn completion of ventricular depolarization and beginning of ventricular repolarization
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13
Q

what is a normal ST segment length

A

isoelectric (not elevated or depressed)

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14
Q

what does an elevated ST mean

A
  • represents myocardial injury/ infarction (irreversible damage)
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15
Q

what does an depression ST mean

A
  • represents myocardial ischemia (reversible)
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16
Q

T wave representation and what does it mean when it is inverted

A
  • ventricular repolarization

- inverted t wave represents any condition that interferes with normal repolarization (ischemia or injury)

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17
Q

What does the QT interval mean

A
  • total duration of combined depolarization and repolarization
  • from the beginning of the QRS wave to the end of the T wave
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18
Q

what is normal length of QT

A
  • 0.34-0.43
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19
Q

what is a regular rhythm

A
  • distance between the r waves doesn’t vary more than 3 boxes
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20
Q

what is an regularly irregular rhythm

A
  • if the pattern can be recognized and predicted for the r waves
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21
Q

What is a irregularly irregular rhythm

A
  • if it has no pattern and has no patterns of regularity
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22
Q

Step one:

A
  • figure out the rhythm

- ventricular (count the R x 10) and atrial (count the P x 10) the same

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23
Q

Step two

A
  • calculate HR

- ventricular (count the R x 10) and atrial (count the P x 10) the same

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24
Q

Step 3

A
  • look at the P wave
  • are they present?
  • are they all the same shape?
  • is there one p wave for every QRS
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25
Q

Step 4

A
  • measure the PR interval
  • is there consistent PR interval?
  • is the measurement normal for PR interval (0.12-0.20)
  • is the PR interval measurable?
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26
Q

Step 5

A
  • measure the QRS
  • do they all look the same?
  • is the measurement normal (less than 0.12)
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27
Q

Normal sinus rhythm

A
  • HR: 60-100
  • regular rhythm
  • p wave: 1:1
  • PRI: normal
  • QRS: normal
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28
Q

Sinus bradycardia (SB)

A
  • increased ventricular filling due to firing too slow
  • HR: less than 50-60 bpm
  • rhythm: regular
  • p wave: 1:1
  • PRI: normal
  • QRS: normal
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29
Q

cause of SB

A
  • variation in athletes
  • meds
  • MI
  • vagal stimulation
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30
Q

TX for SB

A
  • tx only if symptoms of decreased CO ( SOB, hypotension, angina)
  • treat the underlying cause
  • if s/s of poor perfusion: give atropine
  • if atropine is ineffective: transcutaneous pacing, dopamine infusion or epinephrine infusion
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31
Q

Sinus tachycardia (ST)

A
  • decreased ventricular filling due to firing too fast
  • HR: > 100 bpm
  • rhythm: regular
  • P wave: 1:1
  • PRI: normal
  • QRS: normal
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32
Q

cause of ST

A
  • blood loss
  • fever
  • anxiety
  • meds
  • coffee
  • hypovolemia
  • external influences
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33
Q

TX of ST

A
  • tx only when symptoms present (SOB, hypotension, angina, altered mental status)
  • TX underlying cause since brought on by external factors
  • stable: diltiazem (ca channel blocker), inderal (B blocker), or vagal maneuvers
34
Q

General Atrial Dysrhythmias

A
  • p waves differ in configuration for atrial dys.
  • AV node replaces the SA node as the gatekeeper (pacemaker)
  • the atrial pacemaking sites replace the SA node as pace maker
  • conduction pathway is the same through the AV node and it acts as the gatekeeper to control how many impulses reach the ventricles
  • protective mechanism
35
Q

What is most concerning about atrial fib and flutter

A
  • risk for thrombi formation and low CO
  • thrombi can form due to the incomplete emptying of the atrium since the AV node is acting as the gatekeeper
  • low CO due to: loss of atrial kick, ventricular rate is too fast or too slow, one or both
36
Q

what is atrial flutter

A
  • rapid discharge of one single ectopic foci causing the atria to contract but not all impulses make it to the ventricles causing a protective block at the AV node
  • atrial kick becomes compromised by the multiple atrial contractions each time the ventricles contract so CO is affected
37
Q

what happens if too many impulses get through the AV node

A
  • the ventricles will respond, the pt will have symptoms due to the increased HR, decreased ventricular filling time, and resulting in low CO
38
Q

what happens if too little impulses get through the AV node

A
  • the pt will have symptoms of low CO
39
Q

Atrial flutter

A
  • Atrial rate: 250-350 Ventricular rate: 75-150 –> if vent is less than 100= controlled
  • rhythm: regular or irregular
  • p wave: saw tooth pattern- called F waves
  • PRI: not measurable
  • QRS: NORMAL
40
Q

causes of A flutter

A
  • disease (cardiomyopathy, Coronary heart disease, vulvular disease, HTN
41
Q

tx for A flutter

A
  • treat underlying cause
  • reduce fast HR
  • reduce risk of stroke
  • convert to or maintaining NSR
  • difference between if they are stable or not
42
Q

Atrial flutter when Pt is unstable

A
  • synchronized cardioversion
43
Q

atrial flutter if Stable

A
  • look for cause, may not need tx
44
Q

Atrial flutter and stable but has high ventricular rate or some symptoms

A
  • slow vent rate with meds (diltiazem or verapamil, inderel, digoxin
  • then restore NSR with chemical or electrical cardioversion
45
Q

cardioversion

A
  • giving electrical shock so the SA node can take over

- load with amioderone 150 mg IVP slowly (over 10 minutes) before

46
Q

steps for synchronized cardioversion

A
  • needs to be delivered to heart during R wave
  • shock 50-360 J
  • Use defib in sync mode
  • is do it when in the T wave then VT or VF could happen
  • done with sedation and analgesics
47
Q

anticoagulation prior to cardioversion

A
  • based on TEE
  • If stable w/out clots: cardioversion
  • if stable w/clots: send home on anticoag like coumadin or lovenox or heparin before cardioversion occurs
  • if unstable (with or without clots): immediate cardioversion and don’t give amioderone prior
48
Q

Atrial flutter and anticoags

A
  • ppl with chronic a flutter will be on anticoag therapy for ever (warfarin or aspirin)
49
Q

what is A fib?

A
  • rapid discharge of multiple atrial ectopic foci; each electrical impulse results in depolarization of a small part of the myocardium and not the entire atrium
  • the atria cannot contract effectively and empty into the ventricles
  • the atria are twitching
  • AV node will randomly conduct the impulse to the ventricles
50
Q

Atrial fib

A
  • atrial rate: 350-600 –> irregular and not measured normally ventricular rate: irregular at 100-150 –> less than 100 = controlled
  • rhythm: irregularly irregular
  • p wave: f waves (squiggly and cant tell P wave)
  • PRI: not measurable
  • QRS: normal
51
Q

causes of A fib

A
  • a flutter, high alcohol intake, idiopathic, COPD, cardiac valve disease, CHF
52
Q

Tx for A fib

A
  • treat underlying cause
  • reduce fast HR
  • reduce risk of stroke
  • convert to or maintaining NSR
  • difference between if they are stable or not
53
Q

what is a first degree AV block

A
  • delay in normal conduction of the impulse from the atria to the ventricles
  • p wave for every QRS but the PRI is long
  • could lead to other blocks but usually not a big deal and dont worry about
54
Q

First degree Av block

A
  • constant prolonged PRI
  • rate: normal
  • rhythm: regular
  • P wave: 1:1
  • PRI: constant greater than .20
  • QRS: normal
55
Q

causes of first degree AV block

A
  • athletes and children

- lesions along the conduction pathway, MI, myocarditis

56
Q

TX for first degree

A
  • monitor pt and tolerance
  • monitor for progression to 2ND
  • no tx if tolerating
57
Q

second degree AV block type 1

A
  • progressively long PRI and not p wave for every QRS
  • prolonged
  • Atrial: normal Ventricular: normal but slower than atrial
  • rhythm: regularly irregular
  • P wave: normal
  • PRI: progressively lengthens until QRS is dropped
  • QRS: normal, wide, dropped
58
Q

Causes of 2nd degree type 1 AV block

A
  • ischemia
59
Q

TX of 2nd deg type 1 AV block

A
  • monitor for tolerance
  • monitor for progression to third degree (but rare and normally stable)
  • No tx if handling well
  • if symptoms: atropine or temporary pacer
60
Q

Second degree type 2 av block

A
  • PR interval constant AND no P for every QRS
  • P wave is unconducted without proceeding prolongation of the PR interval ( PR intervals are all the same size and some QRS can be dropped)
  • Atrial rate: normal Ventricular: normal but slower than atrial
  • rhythm: irregular
  • P wave: normal
  • PRI: constant
  • QRS: normal, wide, or dropped
61
Q

causes of second degree type 2 AV block

A
  • ischemia, heart disease
62
Q

TX of second degree type 2 AV block

A
  • atropine may be tried but will probably increase demand on heart by increasing atrial rate
  • pacemaker
63
Q

Third degree AV block

A
  • complete absence of conduction between atrial and ventricles
  • atria and vents beat independently
  • no impulses get through the AV node
  • atrial: may or may not be normal ventricular: may or may not be normal (usually 40)
  • rhythm: regular
  • P wave: normal, may not be associated with a QRS
  • PR interval: not measured, changes randomly
  • QRS: normal or wide
  • no consistant PRI and p wave may be all over the place
64
Q

causes of 3rd degree AV block

A
  • ischemia, heart disease
65
Q

tx of 3rd degree AV block

A
  • follow symptomatic SB algorithm (if signs and symptoms showing do atropine)
  • early pacemaker application
66
Q

what is Premature ventricular Contractions

A
  • QRS will look wide and bizzarre ( > 0.12)

- premature QRS complex due to ectopic foci causing an impulse to start in the ventricle before next sinus impulse

67
Q

PVC

A
  • rate: any rate
  • Rhythm: irregular
  • P wave: none
  • QRS: WIDE AND BIZZARRE - NOT EVERY ONE HAS TO BE THIS
68
Q

Sinus rhythym with bigeminy of PVC

A
  • every other beat is going to be upside down
69
Q

couplet Vent tachy

A
  • there will 2 QRS in a row that are tall
70
Q

ventricular trigeminy

A
  • every 3rd beat is upside down and looks like a fish hook
71
Q

when do PVC need TX

A
  • occur frequently ( > 6/min)
  • occur on every other beat (bigeminy)
  • strike on T wave of proceeding beat (R- on T pattern)
  • originate from more than one focus (multifocal)
  • occur in consecutive fashion (couplets, triplets)
  • occur after MI
72
Q

Causes of PVC

A
  • with or without cardiac disease
  • hypoxia
  • ventricular irritability
  • caffeine intake
73
Q

Tx FOR PVC

A
  • look for cause
  • monitor pt for tolerance
  • consider amioderone 150 mg
74
Q

V tach

A
  • originates suddenly from very irritable ectopic foci
  • ventricles take over as pacemaker
  • run of 3 or more PVC’s with rate greater than 100= VT
  • Rate: vent- 150-250 atrial: un measurable
  • rhythm: regular
  • P wave and PRI: not present
  • QRS: wide and bizzare (all will look the same)- tall and a lot in a row
75
Q

cause of V tach

A
  • with or without cardiac disease
  • cardiomyopathy
  • electrolyte imbalance
76
Q

tx of v tach

A
  1. with pulse and stable:
    - medically manage- IV, O2, ECG, echo, cariology consult. load with amioderone and prepare for immediate cardioversion
  2. without pulse: treat like V fib (dfib)
77
Q

V fib

A
  • ventricles quivering, no effective CO or contractions occurring
  • always fatal unless treated
  • caused by ischemia and infarction, heart disease
  • will convert to a-systole within few minutes
  • TX: CRP, defib (see pulseless VT/VF)
  • small squiggly line with no obvious QRS
78
Q

Causes of PEA

A
  • absence of detectable pulse despite evidence of electrical activity
  • H’s and T’s ( hypovolemia, hypoxia, acidosis, hyper or hypo K+, hypoglycemia, hypothermia, drug overdose, cardiac tamponode, pneumothorax, thrombosis
79
Q

tx of PEA

A
  • P-E begin BLS
  • P= search for probable cause, push fluids
  • E= epi or vasopressin
  • not condusive to shock
80
Q

Asystole

A
  • total absence of ventricular electrical activity
  • TX: look for cause, early intubation, epi, don’t attempt to shock, prognosis is poor but exceptions include hypothermia and electrocution
81
Q

What is cardiac output and what are implications when compromised

A

CO: HR x SV (volume of blood heart pumps per minute
Implications: SOB, angina, hypotension, altered mental status

82
Q

When is the use of an ICD warranted?

A
  • when the pt survived VT OR VF, or sudden cardiac death
  • experienced syncope with VT/VF
  • at high risk for VT/VF after cardiac surgery and cannot tolerate meds or ablation
  • prophylactically in pt with ischemic and idiopathic cardiomyopathy with EF 30% or below for prevention of sudden death due to ventricular arrythimias

Complex care (9 decks)

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