<3 dysrhyms - patho E3 Flashcards by Stef Sis

what do cardiac muscle cells do

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

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atrial depolarization

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

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delay at AV node

PR segment

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ventricular depolarization

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

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ventricular repolarization

“filling the tank”
T wave

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no electrical activity

isoelectric line

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what are responsible for the left ventricular contractions

bundle of his & purkinje fibers

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PR interval

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

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QRS

-narrow
- less than 0.12 sec

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sinus rhythm

-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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sinus arrhythmia

-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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what causes dysrhythmias: inappropriate automaticity

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

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what causes dysrhythmias: triggered activity

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

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what causes dysrhythmias: re entry

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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sinus brady

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

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causes of sinus brady

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

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clinical manifestations of sinus brady

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

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

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

treatment of sinus brady

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-atropine (anticholingeric)
-pace maker

sinus tach

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

causes of sinus tach

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

treatment for sinus tach

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

paroxysmal supraventricular tachycardia (PSVT)

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-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”
-

PSVT causes

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

PSVT clinical signs & symptoms

palpitations chest pain fatigue lightheadedness / dizzy dyspnea **decreased CO**

Premature Atrial Contractions (PACs)

-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

what to do if you see a patient in PACs

check electrolytes may need O2

atrial flutter

-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)

causes of atrial flutter

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

a fibrillation

-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

a fib clinical manifestations (& flutter)

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

what is our main question with afib

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

A.fib causes

-electrolyte imbalance -hypoxia -CAD

A.fib complications

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

treatment of A.fib & A.flutter

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

premature ventricular contractions (PVCs)

-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**

causes of PVCs

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

V. tach

-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**

Vtach is what type of rhythm

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

V.tach is associated w/

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

how to treat V.tach

-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

will you have a pulse w/ V.tach

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

V.FIb

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

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

check pulse and immediately start cpr

<3 dysrhyms - patho E3 Flashcards

(44 cards)