midterm updated Flashcards
sinus arrhythmia:
conduction prob-
none present. no potential
originate at SA node, but firing is variable. Related to resp pattern. HR increases when PT breaths in (from changes in intrathoracic pressure)
rate is firing irreg but conduction of impulse is normal
sinus arrhythmia:
cause
not associated with being a problem. occasional type associated with heart disease
R-R interval irreg by resp pattern
sinus arrhythmia:
implication O2 sup and demand
not a problem
sinus arrhythmia:
interventions
document but no intervention required unless HR <60
sinus arrhythmia:
rate-
rhythm-
P-wave-
rate - reg
rhythm- irreg
P wave norm
Sinus Brady:
conduction prob
SA node normal path of conduction atria to vents
Sinus Brady:
cause
athlete, dig, BB
slower = increased vent filling time = better coronary perfusion time = decreased myocardial consumption
Sinus Brady:
implication O2 sup and demand
decreased HR = decreased CO. need to assess PT to see if signs
Sinus Brady:
Intervention
If signs of decreased CO then intervene
Atropine or temp pacemaker
Sinus Brady:
rate-
rhythm-
P wave-
rate < 60
rhythm - reg
P wave +
Sinus arrest/ Pause
conduction prob
when SA node fires NP. When it doesnt fire = problem
lacks a P-QRS-T
pause/arrest can cause rate to be too slow
If pause long. back up pacemaker in junction or vents take over.
Sinus arrest/ Pause
cause
depression from automaticity of SA node
hypoxia hypothermia, drug toxicity, vagal stimulation, electrolyte imbalance, infection/myocarditis, ischemia to conduction system
Sinus arrest/ Pause
implication O2 sup and demand
If transient - NP. The backup pacemakers will kick in
If protective pacemaker doesnt take over then act quick
Sinus arrest/ Pause
intervention
Symptom support
Atropine
temp pacemaker
Sinus arrest/ Pause
rate
rhythm
P wave
rate norm
rhythm- irreg. underlying could be reg
P wave +
Sinoatrial Block
conduction prob
Primary SA node. Period of time when impulses are prevented from depolarizing atrial tissue and there is a block in conduction to atria and vents
Sinoatrial Block
cause
Ischemia
Sinoatrial Block
implication O2 sup and demand
If the block is a long enough period of time can cause signif impact on CO. HR would decrease if prolonged and decrease CO
Sinoatrial Block
intervention
assess CO impact
atropine
temp external pacemaker
Sinoatrial Block
rate
rhythm
P wave
rate normal
rhythm irreg but can be underlying reg
P wave +
Sinus Tacky
Conduction
SA node fast > 100
< 180
Sinus Tacky
cause
exercise exertion stimulant fever anemia hypovolemia CHF PE myocardial ischemia
Sinus Tacky
Implications O2 sup and dem
Healthy - NP
increased HR = increased myocardial consumption = further ischemia.
shortens diastolic filling time = decreased preload and SV = decreased CO
decreased coronary artery perfusion time = decreased O2 supply to heart muscle = decreased contractility = decreased CO
Sinus Tacky
interventions
determine impact. correct cause and deal with symptoms
BB
Sinus Tacky
rate
rhythm
P wave
rate > 100 and < 180
rhythm- reg
P wave +
Premature Atrial Contractions (PAC’s)
conduction
site of impulse is both SA node and atrial tissue
**premature impulses in atrial tissue not the SA node = ectopic P focus
when ectopic impulses fire faster than SA node
Premature Atrial Contractions (PAC’s)
cause
alcohol
caffeine
tobacco
narcotics **
dig toxicity, hypoxia, electrolyte imbalance, heart disease (HF can cause atrial tissue to stretch = PAC
Premature Atrial Contractions (PAC’s)
Implications O2 sup and dem
Heathy = NP
If heart disease then increased HR = increased demand
could convert to A.fib A.flutter
Premature Atrial Contractions (PAC’s)
Intervention
treat the causes:
pain, hypovolemic, myocardial ischemia, CHF
document, notify MRP
Premature Atrial Contractions (PAC’s)
rate
rhythm
P wave
rate normal
underlying regular
P wave +, but looks different bc it doesnt fire from SA node. They dont always look the same, vary depend on where they come from
QRS normal
atrial tissue doesnt like to fire faster than?
But can fire at?
150-180
250-300
which is related to resp pattern?
sinus arrhythmia
which drugs slow HR?
amiodarone, digoxin, BB. adenosine,
vagal maneuver, electrical
which drugs increase HR and conduction?
Atropine
pacemaker
what is the difference between sinus arrest and sinus pause?
arrest gap between QRS = > 3 sec
pause gap between QRS = < 3 sec
what is the difference between sinus pause/arrest and sinus block?
pause/arrest = SA node does not generate impulse. There is no P when starts back up. backup can take over or a P is terminated by normal sinus beat.
sinus block = SA node does generate an impulse but blocked from entering atria. multiple QRS missing
Atrial tachy
conduction
Atrial tissue - irritable atrial ectopic focus robs SA node of its power
> 180 BMP (110-250)
Atrial tachy
cause
heart disease: ischemic and valvular
tissue hypoxia
dig toxicity
cor pulmonale
resp failure d/t atrial distension
Atrial tachy
Implication O2 sup and dem
increased HR = increased consumption = increased ischemia = tissue damage
short diastolic filling = decreased CO and decreased coronary perfusion = decreased O2 supply
increased demand
no P wave= no atrial kick = decreased preload, and CO
possible clot formation
Atrial tachy
Intervention
assess PT. depend on degree of compromise
Decreased BP, chest pain, SOB, dizzy, palpatations
medication interventions: BB, CCB
electrical/cardioversion- to attempt to terminate cardiac dysrhythmia
Atrial tachy
rate
rhythm
P waves
rate > 180 (150-250)
rhythm reg
P waves - might not be able to see them. BC they travel diff pathway than those coming from SA node. BC atrial and vent depolarization fast, P wave blurred in QRS or T wave.
normal QRS (vent tachy is very wide QRS)
Paroysmal atrial tachy
sudden onset and abrupt cessation (short lived)
Atrial Flutter
conduction
irritable ectopic atrial focus. 250-350 BPM
rapid reg rate of atrial depolarization. The AV junction protects (blocks) the vents from rapid rate of fire (<150/min) d/t long refractory period (rest) that prevents conduction of all impulses from atria. Less QRS complexes
Called physiologic AV block
can be: atria 240 BPM, vents 78 BPM
Atrial flutter 3:1 block
Atrial Flutter
cause
heart disease ischemic or valvular, hypoxia
dig tox
cor pulmonale
resp failure
Atrial Flutter
implication O2 sup and dem
depends on PT and how long they can tolerate
No P wave = Loss atrial kick = loss 20-30 % CO
= decreased preload and decreased CO
possible clot formation
Atrial Flutter
Intervention
assess PT. depend on degree of compromise
Decreased BP, chest pain, SOB, dizzy, palpatations
medication interventions: BB, CCB, amiodarone*
electrical/cardioversion- to attempt to terminate cardiac dysrhythmia (if dramatic)
Atrial Flutter
rate
rhythm
P wave
rate 250-350 atrial, vent variable give reange**
rhythm- atrial reg, vent mostly reg
P wave - flutter (saw tooth)
PR/T/QT - NA
Amiodarone
A,fib/A.flutter
Atropine
bradycardia/ sinoatrial block
what is SVT?
supraventricular tachycardia – Or Atrial tachy
how do you know if it’s controlled or uncontrolled A.Flutter? or A. fib
controlled = HR vent response <100 BPM
uncontrolled = HR vent response > 100 BPM
Atrial Fibrillation
conduction
site of impulse formation is the atrial tissue
wavy baseline is from multiple ectopic pacemaker sites generating impulses at a very fast and irregular rate> 350 BPM
Atrial kick lost
Ventricles are irreg but AV junction cause AV block to protect against v. rapid vent rate in A.fib
Atrial Fibrillation
cause
heart disease ischemic or valvular, hypoxia
dig tox
cor pulmonale
resp failure
Atrial Fibrillation
Implications O2 sup and demand
loss atrial kick and rapid vent response can seriously impact preload.
potential clot formation in atria
Atrial Fibrillation
intervention
assess PT. depend on degree of compromise
Decreased BP, chest pain, SOB, dizzy, palpitations
medication interventions: BB, CCB, amiodarone*
electrical/cardioversion- to attempt to terminate cardiac dysrhythmia (if dramatic)
Atrial Fibrillation
rate
rhythm
P wave
QRS
rate 300-500, vent variable
rhythm- vent usually irreg
P wave - fibrillary waves , cant ID P waves
QRS - usually normal appearance
what are the two characteristics of A.Fib?
- the baseline is wavy and chaotic looking
- the ventricular response is always grossly irregular
what does it mean for CO to have an uncontrolled vent rate in A.fib/flutter
higher rate allows for less time for vents to fill = decreased preload and CO
