Conduction Disturbances/Dysrhythmias Flashcards
Properties of Cardiac Cells
automaticity: ability to initiate an impulse spontaneously and continuously
excitability: ability to be electrically stimulated
conductivity: ability to transmit an impulse along a membrane in an orderly manner
contractility: ability to respond mechanically to an impulse
3 Main Components of Functions of the Heart
- Electrical
- Plumbing (cardiac vessels, whether they are occluded)
- Pump itself (heart failure, cardiac myopathy, dilated cardiac myopathy, hypertrophy, etc.)
Intrinsic Rates of the Conduction System
SA node: 60-100 times/min
AV node: 40-60 times/min
Bundle of His and Purkinje Fibers: 20-40 times/min
Phases of Action
0: rapid depolarization and corresponds with ventricular contraction
1, 2, and 3: repolarization
4: complete repolarization and corresponds to diastole
Telemetry Monitoring
the observation of a pt’s HR and rhythm to rapidly dx ischemia or infarction
Methods to calculate HR from ECG
when the rhythm is regular:
- count the number of QRS complexes in 1 min
- count number of R-R intervals in 6 seconds and x 10
- count the number of small squares between one R-R interval, divide by 1500
- count the number of large squares between one R-R interval, divide by 300
Waveforms
P wave: impulse through atrium causing atrial depolarization (when SA node fires and contracts atrium)
QRS complex: time taken for depolarization of both ventricles
ST segment: end of the QRS complex to the T wave, the time between ventricular depolarization and repolarization.
STEMI
ST elevation myocardial infarction
Depressions and T-wave inversion on ECG
usually caused by toxicity of drugs (usually digoxin toxicity) and electrolyte imbalance (high or low - K, Mg, Na, Ca)
Artifact on ECG
can occur if:
- leads and electrodes are not firmly placed (hair, old conduction gel)
- there is muscle activity (shivering, seizures, hiccups, brushing teeth, strong respiratory/muscle movement, etc.)
- electrical interference from an outside source
Questions to Ask Self when Assessing Cardiac Rhythms
- Note the P wave. Is it upright or inverted? Is there one for every QRS complex?
- Evaluate the atrial rhythm. Is it regular or irregular?
- Calculate the atrial rate.
- Measure the duration of the PR interval. Is it normal duration or prolonged.?
- Evaluate the ventricular rhythm. Is it regular or irregular?
- Calculate the ventricular rate.
- Measure the duration of the QRS complex. Is it normal duration or prolonged?
- Assess the ST segment. Is it isoelectric, elevated, or depressed?
- Measure the duration of the QT interval Is it normal duration or prolonged?
- note the T wave. Is it upright or inverted?
Cardiac Stress Test (Things to Know as Nurse)
- not NPO, need light and good breakfast (need calories and sugar for exercise)
- ensure sugars are at a good level
- hold beta blockers for the day so HR can elevate
- hold all caffeine (b/c unnecessarily raises HR)
Things that stop Cardiac Stress Test
- chest pain
- EKG changes
*SOB does not stop test b/c you’re expected to have SOB when exercising
Normal Sinus Rhythm
Rate: 60-100 bpm
Rhythm: P-P interval regular, R-R interval regular
P waves: positive (upright), one precedes each QRS complex, P waves look alike.
PR interval: 0.12-0.20 second and consistent from beat to beat
QRS duration: 0.10 second or less an intraventricular conduction delay exists
Sinus Bradycardia
Rate: less than 60 bpm
Rhythm: P-P interval regular, R-R interval regular
P waves: positive (upright), one precedes each QRS complex, P waves look alike.
PR interval: 0.12-0.20 second and consistent from beat to beat
QRS duration: 0.10 second or less an intraventricular conduction delay exists
Symptomatic v. Asymptomatic Bradycardia
symptomatic bradycardia: requires intervention
-may be experiencing SOB, dizziness, lightheadedness, decreased LOC d/t heart not keeping up with CO and demand
asymptomatic bradycardia: no intervention necessary, just monitor
Tx for Symptomatic Bradycardia
- Atropine (first line drug)
- Temporary Pacemaker (transcutaneous or transvenous)
- Permanent Pacemaker
Transcutaneous v. Transveous Pacemaker
transcutaneous: patch goes right on skin
transvenous: used after open heart surgery when bypass is used. Heart is irritable d/t bypass and may need assistance for 2-3 days post surgery until it gets in groove again.
Sinus Tachycardia
Rate: 101-180 bpm
Rhythm: P-P interval regular, R-R interval regular
P waves: positive (upright), one precedes each QRS complex, P waves look alike. At fast rates it may be hard to tell the difference between a P wave and a T wave.
PR interval: 0.12-0.20 second (may shorten with faster rates) and consistent from beat to beat
QRS duration: 0.10 second or less an in traventricular conduction delay exists
Causes of Tachycardia
pain exercise fever anemia dehydration anxiety sepsis heart failure MI PE stimulant use
Tx of Sinus Tachycardia
Tx underlying cause:
antipyretic (for fever) analgesics (for pain) fluids (for dehydration) avoiding caffeine or nicotine relaxation techniques (for anxiety)
PSVT
Rate: 100-300 bpm
Rhythm: regular or slightly irregular
P waves: often hidden in the preceding T wave, but if seen, it may have an abnormal shape
PR interval: may be shortened or normal
QRS complex: usually normal
- need to tx b/c heart cannot sustain a rate that high for very long and will stop
- Sx: SOB b.c CO is down d/t high HR
- CO = HR x SV (ex. when HR is 200 bpm, SV decreases b/c it’s shortened, not enough time for ventricles to fill and move blood forward)
Tx of PSVT
- Vagal Maneuvers if pt is awake and able to follow commands (cough, hold breath, bear down like having a BM)
* children: cold to face to stimulate vagus nerve b/c they can’t follow these commands - Adenosine: slows rate of SA node, slows conduction time through the AV node to reset heart.
- first dose = 6mg via large IV closest to heart, push as fast as possible, follow with immediate flush (adenosine has short half life, need to get med to heart ASAP).
- in EKG you see heart beating quickly, then momentary pause.
- ensure good IV access and pads in place in case heart does not start again so you can immediately defibrillate
Synchronized Cardioversion
shock delivered on the R wave of the electrical activity of heart using lower energy levels than with defibrillation
machine picks up pts rhythm and knows wen to shock
Preparing Pt for Cardioversion
- Informed consent required
- NPO b/c they get sedating meds
- Recent ECG
- 18g IV w/ fluids (large bore)
- O2 b/c they are getting sedation
- Sedation
Premature Atrial Contraction (PACs)
premature heartbeats originating in the atria
Rate: usually 60-100 bpm
Rhythm: irregular
P waves: abnormal shape
PR interval: normal
QRS complex: normal (usually)
- PACs and PVC aka “line jumpers” b/c they are outlying electrical activity that originate outside the normal conduction system
- called ectopic foci (electrical activity that occurs outside normal conduction system)
PVC
premature heartbeats originating in the ventricles
Atrial Fibrillation
Rate: atrial: 350-600bpm
ventricular: >or< 100bpm
Rhythm: irregular
P waves: fibrillatory
PR interval: not measurable
QRS complex: normal (usually)
- no definable P waves b/c there is no contraction. SA node is out of commission, resulting in no P waves (atria are just quivering)
- Pt is on anticoagulants to prevent PEs
Atrial Fibrillation w/ Rapid Ventricular Respons (RVR)
atria chambers fibrillate resulting in rapid and irregular pumping of blood through the heart
in some cases of aFib, the fibrillation of the atria causes the ventricles to beat too fast which is called RVR.
Atrial Flutter (ECG)
Rate: atrial: 250-350 bpm, ventricular: >or< 100bpm
Rhythm: atrial: regular, ventricular: may be regular or irregular
P wave: flutter (F) waves (sawtooth pattern) more flutter waves than QRS complexes; may occur in a 2:1, 3:1, 4:1, etc. pattern
PR interval: not measurable
QRS complex: normal (usually)
S/Sx of Atrial Fib/Flutter
palpitations
weakness
dizziness
SOB
d/t 20% loss of CO from atria not contracting properly and not squeezing the blood into the ventricles
Tx for Atrial Fib/Flutter
medications:
- calcium channel blockers (slow HR, specifically the ventricular rate)
- beta blockers
- antiarrhythmic
- antiplatelet aggregators
- anticoagulants
synchronized cardioversion
cardiac ablation
Cardiac Ablation
procedure to scar or destroy tissue in your heart that’s allowing incorrect electrical signals to cause an abnormal heart rhythm
diagnostic catheters are threaded through blood vessels to the heart where they are used to map the heart’s electrical signals
Heart Blocks
aka conduction delay
can be born with it or have “acquired heart block”
causes:
- surgeries that affect the heart’s electrical system
- changes in your genes
- MI
- heart issues like clogged arteries, inflammation of the heart muscle, and heart failure
- muscle disorders or other diseases
- some meds (can try to change doseage or Rx to fix)
First Degree Heart Block (ECG)
Rate: 60-100 bpm
Rhythm: regular
P wave: normal
PR interval: >0.20 seconds
QRS complex: normal
*Pt in normal sinus rhythm but PR interval is greater than 0.2 seconds.
totally fine if pt is asymptomatic
Heart Block Clinical Manifestations
usually w/ first degree and sometimes w/ second degree pts are asymptomatic
most common s/sx d/t decrease CO:
- bradycardia
- hypotension
- syncope
- chest pain
- dizziness
- dyspnea
Tx of Heart Block
*same as for symptomatic bradycardia
- atropine
- transcutaneous pacemaker
- permanent pacemaker
Third-Degree Heart Block (ECG)
Rate: atrial: 60-100 bpm, ventricular: 20-40 bpm
Rhythm: atrial: regular but may appear irregular d/t P waves hidden in the QRS complex
P wave: normal, but no connection with the QRS complex
PR interval: variable
QRS complex: normal or widened, no relationship w/ P waves
Third-Degree Heart Block
can lead to lethal rhythms
atrium and ventricles are doing their own thing, not working together anymore
no perfusion occurring to the body or heart
emergency situation requiring immediate medical attention
call 911 for any:
- cardiac arrest
- dizziness
- fainting
- new, severe tiredness
- irregular heartbeat or new palpitations
Tx of Third-Degree Heart Block
permanent pacemaker
need to get them to cath lab ASAP, do transcutaneous pacemaking in interim
Pt Teaching for Pacemaker
- know what kind of pacemaker you have
- let all health care providers know about pacemaker
- wear medical alert bracelet or necklace
- stay away from electrical devices w/ strong magnetic fields (get pat down at airport, don’t go through x-ray machine)
- it’s ok to be active w/ Dr.’s approval, but don’t do contact sports like football or ice hockey
- get pacemaker checked regularly to ensure it’s working well
- pacemaker batteries have shelf-life of 5 years, need to replace every 5-7 years
Permanent Pacemaker
pacemaker’s power source is implanted subcutaneously over the pectoral muscle on the pt’s non-dominant side
Single-chambered Pacemaker v. Dual-chambered Pacemaker
single-chambered: either working on atrium OR ventricles
dual-chambered: working in both atrium AND ventricles
*atrial spike before P wave and then ventricular spike then QRS complex
Atrial Pacemaker
atrial pacing:
pacing system with lead attached to right atrium designed to correct abnormalities in SA node
on ECG: can see pacer spike just before P wave, which is how you know they’re being atrial paced
Ventricular Pacemaker
ventricular pacing: pacing system w/ a lead attached in the right ventricle
on ECG: can see pacer spike then QRS complex
QRS complex is inverted in pt’s w/ pacemakers.
In normal sinus rhythm, conduction system is working from SA node and is moving downward, so when it moves down you have normal QRS complex.
B/c conduction is being stimulated and started at the bottom of the ventricle (tip of pacemaker is sitting at bottom of ventricle), so energy is moving up through the heart instead of down and as a result of that you will see a reciprocal deflection of the QRS complex (it’s moving in the opposite direction), which is why pacemaker QRS complexes look this way.
Failure to Capture
ventricles did not contract after pacemaker spike meaning something is wrong with pacemaker and it needs to be tweaked/fine-tuned
Failure to Sense
pacemaker should sense when heart is going to fire on its own and sit back and not fire
failure to sense = pacemaker doesn’t sense this and fires regardless
a malfunction of the pacemaker that needs to be addressed
Types of PVCs
unifocal: PVCs look alike meaning they’re coming from same foci
multifocal: PVCs look differently meaning they’re coming from different foci
ventricular bigeminy: every other beat/complex is a PVC
ventricular trigeminy: every third complex is a PVC
couplet: two PVCs together
Ventricular Tachycardia (ECG)
Rate: 150-250 bpm
Rhythm: regular or irregular
P waves: occurring independently of the QRS complex, and usually buried in the QRS complex
PR interval: not measurable
QRS complex: distorted
Tx of Ventricular Tachycardia
depends on if pt has pulse or not
if they have a pulse, try meds and synchronized cardioversion
if they don’t have a pulse, defibrillation
Causes of Ventricular Tachycardia
CAD, cardio myopathy, congenital disorder
Types of Ventricular Fibrillation
- course
- fine
*no pulse with either
need to do CPR and defibrillate right away
Asystole
aka ventricular standstill
non-shockable rhythm
need to do CPR and give meds until pulse returns
PEA
pulseless electrical activity
electrical activity on ECG but there is no mechanical activity of the ventricles and pt has no pulse
poor prognosis unless the underlying cause can be identified and quickly corrected.
Causes of PEA
6 H’s:
- hypovolemia
- hypoxia
- hydrogen ion (acidosis)
- hypo/hyperkalemia
- hypoglycemia
- hypothermia
5 T’s:
- toxins (poisons/ODs)
- tamponade (cardiac)
- tension pneumothorax
- thrombosis (coronary. or pulmonary)
- trauma
SCD
sudden cardiac death
death from cardiac causes
most often from ventricular dysrhythmias, specifically ventricular tachycardia or fibrillation
Implantable Cardioverter-Defibrillator (ICD)
device that senses when pt is going into lethal rhythm and defibrillates the pt
Ischemia v. Injury v. Infarction
Ischemia: reduction of myocardial oxygen for less than 20 min. Damage is reversible. In ECG, you see changes in T wave.
Injury: persistence of oxygen deficiency for more than 20 min. Damage is reversible. Injury is characterized by ST segment abnormalities.
Infarction: Persistence of oxygen deficiency for more than two hours. Damage is irreversible. Infarction is characterized by pathological Q waves on the ECG. Scarring occurs which leads to conduction delay.
