<3 dysrhyms - patho E3 Flashcards

1
Q

what do cardiac muscle cells do

A

1) automaticity
2) excitability
3) conductivity
4) contractility

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2
Q

atrial depolarization

A

“the squeeze during systole”
P wave (little bump) caused by the SA node

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3
Q

delay at AV node

A

PR segment

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4
Q

ventricular depolarization

A

“the squeeze during diastole”
QRS complex (big peak) caused by AV node

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5
Q

ventricular repolarization

A

“filling the tank”
T wave

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6
Q

no electrical activity

A

isoelectric line

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7
Q

what are responsible for the left ventricular contractions

A

bundle of his & purkinje fibers

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8
Q

PR interval

A

-beginning of the P wave to the tip of R
-interval: 0.12-0.20 seconds

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9
Q

QRS

A

-narrow
- less than 0.12 sec

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10
Q

sinus rhythm

A

-rate: 60-100
-rhythm: regular
-P wave: up & round before every QRS
-PR: 0.12-0.20 sec
-QRS: <0.12 sec

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11
Q

sinus arrhythmia

A

-a degree of variability in the heart rate
-a normal rhythm
-no changes to CO
-rate: 60 to 100
-PR: 0.12-0.20 sec
-QRS: <0.12 sec
**common in younger pop & associated w/ respiration or autonomic nervous system fluctuations

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12
Q

what causes dysrhythmias: inappropriate automaticity

A

a cell initiates action potentials when it isn’t supposed to
examples: myocardial ischemia & electrolyte imbalance

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13
Q

what causes dysrhythmias: triggered activity

A

an extra impulse is generated during or just after depolarization
ex: digoxin toxicity, SNS stim, genetics

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14
Q

what causes dysrhythmias: re entry

A

cardiac impulse in one part of the heart continues to depolarize after the main impulse has finished
ex: myocardial ischemia & electrolyte imbalance

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15
Q

sinus brady

A

-originates in the SA node
-regular rhythm
-PR: 0.12-0.20 sec
-QRS: <0.12 sec
-rate: <60

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16
Q

causes of sinus brady

A

-hyperK
-vagal response
-digoxin toxicity
-late hypoxia
-medications (betas, CCB, & amiodarone)
-MI

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17
Q

clinical manifestations of sinus brady

A

-lightheaded/dizzy
-easily fatigued
-syncope
-dyspnea
-chest pain/discomfort
-confusion

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18
Q

anytime you see an abnormal rhythm, what do you do first (unless lethal rhythm)

A

assess patient to see if the are symptomatic or not
ex: fit people can live at a lower HR

19
Q

treatment of sinus brady

A

-atropine (anticholingeric)
-pace maker

20
Q

sinus tach

A

-originates in SA node
-rhythm: regular
-PR: 0.12-0.20 sec
-QRS: <0.12 sec
-rate: 100-150

21
Q

causes of sinus tach

A

-exercise, pain, strong emotions
-fever
-fluid volume deficit
-medications
-substances
-early hypoxia

22
Q

treatment for sinus tach

A

hypovol = fluids
fever = antipyretics
pain = analgesics
if a heart thing = beta blockers

23
Q

paroxysmal supraventricular tachycardia (PSVT)

A

-originates in the AV node, above the ventricles
-rate:150-250
-usually no P wave or will be abnormal
-QRS: <0.12 sec
-will begin & end suddenly “my heart is racing”
-

24
Q

PSVT causes

A

over exertion
emotional stress
stimulants
digitalis toxicity
rheumatic heart disease
CAD
WPW (wolff parkinson white diease)
right sided heart failure

25
Q

PSVT clinical signs & symptoms

A

palpitations
chest pain
fatigue
lightheadedness / dizzy
dyspnea
decreased CO

26
Q

Premature Atrial Contractions (PACs)

A

-early P waves that usually look a little different, usually no consequence but if frequent indicates that a pt is at high (usually afib) risk for dysrhythmias
-PR: 0.12-0.20 sec
-QRS: <0.12 sec

27
Q

what to do if you see a patient in PACs

A

check electrolytes
may need O2

28
Q

atrial flutter

A

-originates in the AV, overrides the SA node
-caused by reentry impulse that is repetitive & cyclic so regular artial rhythm w/ an atrial rate of >250 bmps
- ventricular rate is slower & QRS doesn’t follow every P wave (Ps look like a sawtooth)

29
Q

causes of atrial flutter

A

CHD, cardiomyopathy, heart valve disease, inflammation, high BP, lung disease, electrolytes

30
Q

a fibrillation

A

-multiple irritable sports in the atria
-irregularly irregular (both atrial & ventricular)
-HR: 100-175
-no easily seen P wave or T wave
-r to r are not evenly spaced

31
Q

a fib clinical manifestations (& flutter)

A

-palpitations
-heart racing
-fatigue
-dizziness
-chest discomfort
-SOB
~asym

32
Q

what is our main question with afib

A

is it rate controlled?
idk losing mass amount of cardiac output so their rate is more important then rthymn

33
Q

A.fib causes

A

-electrolyte imbalance
-hypoxia
-CAD

34
Q

A.fib complications

A

-decreased CO
-heart failure
-embolus that can lead to stroke

35
Q

treatment of A.fib & A.flutter

A

-rate control w/ beta blockers, CCB, digitalis, & amiodarone
-prevent stroke w/ anticoags & anti platelets

36
Q

premature ventricular contractions (PVCs)

A

-contraction coming from an ectopic focus in the ventricles no atrial contraction
-it comes earlier than the QRS should come & doesn’t follow a normal rhythm or P wave
-wide and distorted in shape compared to normal QRS

37
Q

causes of PVCs

A

stimulants
electrolytes
hypoxia
fever
exercise
emotional stress
CVD
to fix treat cause

38
Q

V. tach

A

-consists of 3 or more PVCs together (counts in beats “12 beat run of v. tact”)
-ectopic focus within the ventricles takes controls and fires repeatedly -> no atrial contractions occurring no p wave
-seriously decrease CO
-HR between 150-200

39
Q

Vtach is what type of rhythm

A

a deadly rhythm
full hands on deck, things need to happen and fast

40
Q

V.tach is associated w/

A

MI, CAD, sign electrolyte abnorms, heart failure, drug toxicity & other bad things

41
Q

how to treat V.tach

A

-ACLS -> depends on pulse, patient will be symptomatic very quickly unless it converts back to other rhythm
-may need anti dysrhythmic like beta or CCB
-electrolytes replacement

42
Q

will you have a pulse w/ V.tach

A

some will, some wont but eventually everyone will lose a pulse
if no pulse, begin CPR immediately

43
Q

V.FIb

A

irregular waveforms of varying shapes and sizes (the ventricles are just quivering)
No cardiac output

44
Q

what to do if you see your patient in A.fib

A

check pulse and immediately start cpr