Dysrhythmia Interpretation Flashcards
Automaticity
creates an electrical impulse
Excitability
ability to respond to outside stimulus
Conductivity
receives an impulse and conducts it to an adjacent cell
Contractility
shortening of fibers in response to impulses
Polarized
resting membrane potential (movement of ions across a membrane)
Depolarization
Sodium goes in, Potassium goes out
electrical activation of cell caused by influx of sodium into cell while potassium exits
Repolarization
Potassium back in, Sodium back out
return of cell to resting state caused by re-entry of potassium into cell while sodium exits
Effective or absolute refractory period
Refractory Period
- phase in which cells are incapable of depolarizing
Relative Refractory period
phase in which cells require stronger-than-normal stimulus to depolarize
Pacemaker Sites
SA node, AV node, Bundle of HIS, Purkinje Fibers
Cardiac Cycle
Atrial depolarization (blood drains into ventricles) -> atrial contraction (atrial kick) -> AV node (impulse delayed ventricles fill) -> impulse moves through the common Bundle of HIS (divides into left and right branches) -> purkinje fibers (ventricular contraction)
Electrocardiogram (EKG)
looking at electrical activity of the heart viewed as “leads”
picked up by sensors placed on the skin (electrodes)
waves on the ECG correlate with the electrical activity conducted to the atria and ventricles
P wave
atrial depolarization
looking at where it leaves the baseline and returns back
want to know if there is a P wave present
QRS Complex
should be
T Wave
ventricular depolarization
Follows QRS complex and is usually in the same direction; coming back to resting state
*Atrial depolarization also occurs but is not visible on the EKG because it occurs at the same time at QRS
PR Interval
0.12 to 0.20 seconds
measured from beginning of P waves to the beginning of the QRS complex
represents time needed for sinus node stimulation, atrial depolarization and conduction through the AV node before ventricular depolarization
ST Segment
represents early ventricular depolarization
End of QRS complex to the beginning of the T wave
normally isoelectric
QT Interval
total time for ventricular depolarization and depolarization
Beginning of the QRS complex to the end of the T wave
varies w/ HR, gender, age and lead
Prolonged: can lead to lethal dysrhythmia Torsades de points
Sinus Tachycardia Intervention
Assessment; worry about perfusion
Want to address underlying causes: fever, pain, hypoxia, CHF, hypovolemia, dehydration, anxiety, drugs
continue to monitor
Six Second Method/Rule of 10
number of complete QRS complexes in 6 seconds of strip multiply by 10 and get the heart rate
ex: 9 QRS complex X 10 seconds = 90HR
Normal Sinus Rhythm
Rate: 60-100bpm Rhythm: atrial and ventricular regular P Waves: uniform, upright, one preceding each QRS PR Interval: 0.12-0.2 seconds QRS: 0.10 seconds or less
Sinus Tachycardia
Rate: usually 100-160bpm Rhythm: atrial and ventricular regular P waves: uniform, upright, one preceding each QRS PR Interval: 0.12-0.2 seconds QRS: 0.10 seconds or less
Sinus Bradycardia
Rate: less than 60 bpm Rhythm: atrial and ventricular regular P waves: uniform, upright, one preceding each QRS PR interval: 0.12-0.2 seconds QRS: 0.10 seconds or less
Vagal Stimulation
bearing down, coughing, sneezing
Atrial Dysrhythmias
impulse originates from somewhere other than the SA node in the atria
premature atrial depolarization
ex: SVT, AFIB, Aflutter
Supraventricular Tachycardia aka SVT
varied group of dysrhytmias that originates above the AV node with a heart rate greater than 150
can include: ST, atrial tachycardia (afib/aflutter); AV nodal reentrant tachycardia, AV reentrant tachycardia
Atrial Tachycardia
an SVT
originates usually from an irritable site in the atria and overrides the SA node
looks similar to ST but P waves differ in shape
going very fast, don’t really know what it is; don’t know underlying rhythm
Atrial Tachycardia Interventions
assess pt, ABS, oxygen, IV access, vagal maneuvers
Adenosine, calcium channel blockers and beta blockers to slow ventricular rate, consider cardioversion if rhythm is resistant to drugs; cardioversion seldom stops AT’s
ablation
Atrial Fibrillation
involves several reentry circuits within the atria; the four pulmonary veins that drain into the left atria are a trigger site
Assess, ABS, **Research is finding that staying out of Afib may be an unattainable goal!
Rhythm Conversion for Afib
convert the afib to sinus with using pharmacological or electrical cardioversion (rhythm control) and anti coagulate if the person has been in Afib for greater than 3days
patient may require long term drug therapy to maintain sinus rhythm (amiodarone, dofetilide, ilbutilide)
Rate Control for Afib
control the VENTRICULAR response rate using antidysrhythmic drugs and anticoagulation
ex: calcium channel blockers, beta blockers, digoxin
may leave pt in a fib and control ventricular to slow number of impulses that contract the ventricles
Atrial flutter intervention and Tx
assess pt; ABC
causes: reentry circular pathway
Tx: electrical cardioversion, atrial overdrive pacing, pharmacological cardioverson: ibutilide; radiofrequency catheter ablation
always check BP
Premature Ventricular Complexes intervention and tx
assess pt, ABC
Assess underlying problem: hypoxia, digitalis toxicity, acid-bace imbalance, MI, electrolyte imbalance, HF, AMI, increased sympathetic tone, stimulants
**Seen with low K
Tx: O2, IV therapy, correct underlying imbalance
Ventricular Tachycardia intervention and causes
Assess pt and ABCs
Causes: ACS; cardiomyopathy, tricyclic overdose; digoxin toxicity, valvular heart disease, cocaine abuse, MVP, acid-base imbalances, trauma
Ventricular Tachycardia Tx
pulseless VT: Defibrillate!!!**
Unstable VT w/ a HR of 150 or more: oxygen, IV access, ventricular antiarrhythmics, sedation (if wake and time permits) electrical therapy
stable VT w/ HR less than 150 and a BP: use drugs such as amiodarone, beta blockers, lidocaine, or overdrive pacing
determine cause
pt’s who have had sustained VT are at risk of sudden cardiac death
therapy is aimed at preventing a recurrence
Ventricular Fibrillation Intervention and Causes and TX
Assess pt and ABCs
Causes: VT is the most common precursor of Vfib!!
increases sympathetic nervous system activity; vagal stimulation; electrolyte imbalance; antiarrhythmics and other meds; electrocution; ACS; HF
Tx: CPR, defibrillation, meds, supportive measures (airway, correct imbalances)
Asystole intervention and causes
Check second lead; O2, IV, consider pacing, meds, termination
underlying causes: (H&Ts)
H’s: hypovolemia, hypoxia, H+ (acidosis), hypokalemia, hyperkalemia, hypotherma
T’s: toxins, tamponade (cardiac), tension pneumothorax, thrombosis (pulmonary, coronary)
Pulseless Electrical Activity causes
H and T’s
H’s: hypovolemia, hypoxia, H+ (acidosis), Hypokalemia, hyperkalemia, hypothermia
T’s: toxins, tamponade (cardiac), tension pneumothorax, thrombosis (pulmonary, coronary)
start giving them fluid back if hypovolemia like 18 gauge run them in
1st degree AV block
assess pt and continue to monitor for increase block
causes: may be normal; ischemia or injury to AV node; rheumatic heart disease; hyperkalemia, AMI; increased vagal tone
2nd Degree AVB Type 1 Mobitz Type 1, Wenkebach
intervention: assess and continue to monitor for increased block
caused by a conduction delay within the AV node
patients are usually asymptomatic
if symptomatic: give O2, IV, Atropine, transcutaneous pacing
2nd Degree AVB Type ll, Mobitz Type ll
Intervention: assess and continue to monitor for increased block
caused by a conduction delay lower in the conduction system: bundle of HIS, bundle branches
treatment depends on ventricular response rate; if response is slow prepare for pacing
atropine will increase discharge from SA node but fewer impulses are conducted through the AV node further decreasing the ventricular rate
3rd Degree AVB
assess and monitor
ventricular response will determine pt presentation
O2, IV, atropine, transcutaneous pacemaker
may require a permanent pacemaker depending on cause of rhythm
