EKG Flashcards
Adequate perfusion requires the heart to generate sufficient
cardiac output to distribute blood to the body tissues
Dysrhythmias can directly
decrease CO by changing stroke volume and heart rate
Tachycardia from a fever an decrease _____ and cause
CO; cause hypotension
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
Contractibility
ability to respond mechanically to an impulse
What are the 4 properties of enabling the heart’s conduction system?
Automaticity
Excitability
Conductivity
Contractibility
Conduction System of the Heart purpose
sends signals to each part of the heart contracting and relaxing = control blood flow through your heart and to the rest of your body
What is the order of a normal cardiac impulse?
- Sinoatrial (SA) node signals the atrial myocardium and causes the atrium to contract
- Atrioventricular (AV) node
- Bundle of His
- Bundles Branches
- Purkinje fibers impulses the ventricles
SA node is located in the
upper right atrium
Dysrhythmias result from disorders of what
impulse formation, conduction of impulses, or both
Which node is considered the pacemaker of the heart
SA node
SA node spontaneously fires how many times in a minute?
60-100 times a minute
What is the secondary pace maker
AV node automatically at its intrinsic rate
The AV node starts at a rate of
40-60 times per minute
The Bundle of His, Bundle Branches, and Purkinje fibers start at a rate of
20-40 times per minute
When the 2nd pacemaker starts firing more rapidly than the SA node, this causes?
Triggers early/late beats resulting in dysrhythmia replacing the normal sinus rhythm
Autonomic nervous system controls
Parasympathetic and sympathetic nervous systems
- rate of impulse formation
- speed of conduction
- strength of cardiac contraction
Parasympathetic Nervous System affects on the heart
decrease rate of SA node
slows impulse conduction of AV node
- pupils shrink
- slow, deep breaths, heart slows, gut active
Calm parachute
Sympathetic Nervous System affects on the heart
increase SA node
increase conduction of AV node
increase cardiac contractility
- pupils expand
- fast and shallow breaths
- heart pumps faster
- gut inactive
What components of the autonomic nervous system that affect the heart?
vagus nerve fibers of both parasym. / and sympathetic nervous systems
Stimulation of the vagus nerve causes
decrease rate of the SA node and slowed impulse conduction of the AV node
Stimulation of the sympathetic nerves increases what in conduction
increases SA node, AV impulse conduction and
cardiac contractility
Telemetry
observation of a patient’s HR and rhythm at a site distant from the patient.
- Centralized monitoring (Nurse and technician)
- Advanced Alarm Systems (Detect dysrhythmias, ischemia, or MI from a different location)
All telemetry patients should be assessed for
s/s of hemodynamic instability
Where do the 5 cardiac telemetry wires be placed?
Below right clavicle
- RA white
Below left clavicle
- LA black
Left lower rib cage
- LL red
Right lower rib cage
- RL green
Chest lead position
- MCL brown
not on bony prominences
The P wave represents*
SA node sending out an electrical impulse and represents atrial depolarization/contraction
QRS Complex represents
ventricular depolarization / contraction**.
In what way do the ventricles contract the heart?
endocardial to the epicardial (in - out)
What does it mean if the QRS Complex is wider than normal?
impulse started in the ventricles but there was a block delaying the impulse from completely contracting the heart
T and U waves represent
a resting spot for the heart to refill with blood
1 large square on an ECG is how long
0.20 seconds
How many large squares does it take to reach a full minute of ECG?
300
The time of an ECG is measured on what line
horizontal axis
The voltage of an ECG is measured on what line
vertical axis
Each small square is ____ mm and represents
1 mm = 0.04 seconds
10mm = ____ mVolt
1
The top lines on an ECG in bold mark what
3 seconds
How do you calculate HR on an ECG?
number of QRS coplexes in 1 minute
- QRS coplex in 6 seconds times 10 ~ HR in one minute
R wave is
first upward (positve) wave of the QRS complex
How do you determine regularity of a rhythm?
couning boxes btw waveforms (P wave to P wave or QRS to QRS
Marching out the rhythm =
determines early or late and hiding within another waveform
If the spaces between the waveforms are not equal =
irregular
How dod you determine if the pateint is hemodynamically stable?
BP
NH
RR
O2 Sat
cap refill
After determining the dysrhythmia is present, what is the priority?
determine the cause
- fever
- electrolyte
Treat the _______, not the monitor!
patient
- could be normal for them
- lead is off
What pulses are best to determine a pulse before starting CPR?
Carotid
Femoral
What should be assessed during a cardiac rhythm?
P wave (consistency, inverted)
P-R interval (prolonged)
Ventricular rate and rhythm (regular)
QRS complex (prolonged)
ST segment (flat, elevated. depressed)
Q-T interval
T wave (inverted)
Elongation of >0.2 PR interval means
slow conduction and heart block
What is artifact caused by?
leads and electrodes not secure
muscle activity (shivering)
electrical interference
Artifiact is
distortion of the baseline and waveforms seen on the ECG
What should the nurse do when she sees artifact?
check the patient not the rhythm
check connections in the equipment
replace electrodes
conductive gel
remove interference
Normal sinus rhythm rate
60-100 bpm
What starts normal sinus rhythm?
SA node and follows normal conduction pathways
- P wave - QRS complex (normal shape and duration
Sinus bradycardia
< 60 bpm with regular rhythm
Sinus bradycardia is normal for what type of people
aerobically trained athletes (runners)
people sleeping
Beta blockers
hypothyroidism
ask questions about why it could be so low
Sinus bradycardia can occur in response to
parasympathetic nervous system
carotid sinus massage
Valsalva manuever
hypothermia
increase intraocular pressure
vagal stimulation
Beta blockers, Calcium channel blockers
Common diseases associated with sinus bradycardia
hypothyroidism
increase intracranial pressure
hypoglycemia
inferior MI
S/S of Bradycardia
Hypotension
Pale, cool skin
Weakness
Angina
Dizziness or syncope
Confusion or disorientation
Shortness of breath
Tx for Bradycardia
Atropine
Pacemaker
Stop offending drugs (Hold, DC, or lower dose)
Symptomatic bradycardia is
a HR that is less than 60 beats/minute and is inadequate for the patient’s condition, causing the patient to experience symptoms
Atropine is what type of drug
anticholinergic (pt with symptoms)
Atropine for bradycardia (with symptoms) is
temporary fix and need to find a source
A patient’s cardiac rhythm is sinus bradycardia with a heart rate of 34 beats/minute. If the bradycardia is symptomatic, the nurse would expect the patient to exhibit
- Palpitations.
- Hypertension.
- Warm, flushed skin.
- Shortness of breath.
- Shortness of breath.
Rational : Signs of symptomatic bradycardia include pale, cool skin, hypotension, weakness, dizziness or syncope, confusion or disorientation, and shortness of breath.
Sinus Tachycardia is
normal sinus rhythm 101-180 bpm
Sinus tachycardia is associated with what physiologic and psychologic stressors including
exercise
fever
pain
hypotension
hypovolemia
anemia
hypoxia
hypoglycemia
MI
HF
hyperthyoidism
anxiety
fear
What drugs can cause sinus tachycardia?
epinephrine (EpiPen), norepinephrine (Levophed), atropine (AtroPen),
caffeine,
theophylline (Theo-Dur), or hydralazine (Apresoline).
over-the-counter cold remedies have active ingredients (e.g., pseudoephedrine [Sudafed])
Will fluid bolus’ help tachycardia patients?
yes
Tachycardia s/s
depends on tolerance of the increased HR
Dizziness
Dyspnea
Hypotension - low CO
Angina in patients with CAD
Tx of Tachycardia
Guided by cause (e.g., treat pain)
Vagal maneuver – bearing down and take a deep breath, cough hard,
- NO ICE WATER ON THE FACE OR JUGULAR RUB as that is only for HCPs
β-adrenergic blockers (metoprolol)
PSVT means
Paroxymal Supravntricular Tachycardia
PSVT is caused by
ectopic focus anywhere above the bifurcation of the bundle of His. Identification of the ectopic focus is often difficult even with a 12-lead ECG as it requires recording the dysrhythmia as it starts
PSVT on EKG
absent P wave the faster it gets
- hidden in preceding T wave
- QRS interval is normal
PSVT bpm
151-220 (regular or slightly irregular)
PSVT occurs due to
reexcitation of the atria when there is a one-way block
- PAC
Paroxysmal refers to
abrupt onset and ending
Paroxymal SVT followed by
brief period of asystole
PSVT is associated with
overexertion
emotional stress
deep inspiration
caffeine and tobacco
rheumatic heart disease
dig toxicity
CAD
cor pulmonale
S/S of PSVT
HR is 150–220 beats/minute (add for clarification)
HR > 180 leads to decreased cardiac output and stroke volume
Hypotension
Dyspnea
Angina
PSVT with HR > 180 leads to
decreased CO and stroke volume
PSVT with HR > 180 s/s
Hypotension
Dyspnea
Angina
PSVT Tx
Vagal stimulation
IV adenosine (1st)
IV β-adrenergic blockers (sotalol)
Calcium channel blockers (diltiazeem and amiodarone)
Amiodarone
DC cardioversion
What are common vagal stimulation manuevers tx for PSVT?
Valsalva, coughing, and or (Singing, Humming, and Gargling)
-carotid massageonly a doctor should perform this one.
Adenosine’s half life is
short (10 seconds)
If vagal stimulation and drug therapy are ineffective for a PSVT and the patient becomes hemodynamically unstable, what should be used?
direct current cardioversion
Adenosine is what type of drug
antidysrhythmic
Adenosine for dx purpose can be used to
myocardial perfusion stress imaging study (vasodilator)
Adenosine for tx is used to
antidysrythmic for AVTs
- gives the heart a break for the SA node to take back control
When giving adenosine you should tell the patient about feeling
chest pressure after the medication is given
- injection in antecubital space close to the heart
How should adenosine be given?
IV rapid (1-2 secs)
follow with 20mL flush rapid
stop cock setup
What is the half-life of adenosine?
2-3 seconds
If the patient given adenosine has asystole after delivery what should the nurse do?
continue to monitor as asystole is normal
What equipment should a patient receiving adenosine have?
BP cuff
12 lead
cardiac monitor
defibrillator or AID ready
What should you assess for on a patient receiving adenosine?
flushing, dizziness, chest pain, or palpitation
What are the doses for adenosine?
6 mg
12 mg
Stop after the second, HCP can continue
- Cardioversion
Atrial flutter is a
atrial tachydysrhythmia identified by recurring, regular, sawtooth-shaped flutter waves that originate from a single ectopic/misfire focus in the right atrium or, less commonly, the left atrium
Atrial flutter means
atria is not emptying
Atrial flutter rates bpm
200-350
The ventricular rate of atrial flutter will vary based on
conduction ratio
2:1
The ventricular rate bpm in atrial flutter
150 bpm
In atrial flutter, the atrial and ventricular rythms are regular/irregular.
regular
Atrial flutter on EKG
P-R interval not measurable
QRS normal
**AV node delay signal to the atria - some AV block in fixed ratio
If the atrial flutter is not hemodynamically stable then what s/s or hx is seen?
cardiac hx
medications
chest pain
SOB
sweat
Atrial flutter is typically associated with
chronic lung disease, PE, cor pulmonale
cardiomyopathy
hyperthyoidism
HTN
CAD
mitral valve disorders
What drugs can cause atrial flutter?
digoxin
quinidine
epinephrine
Patients with atrial flutter have an increased risk of stroke because
risk of thrombus formation in the atria from the stasis of blood
What is given to atrial flutter patients as a preventative of stroke
Warfarin
Tx of Atrial Flutter
Pharmacologic agent – anti-dysrhythmic
Electrical cardioversion
Radiofrequency ablation
The primary goal in treatment of atrial flutter is to
slow the ventricular response by increasing AV block
What drugs are used to slow down ventricular response in atrial flutter
Calcium channel and beta blockers
What is used to convert atrial flutter to sinus?
antidyrhythmic
- ibutilide [Corvert]
- amiodarone
- flecainide [Tambocor]
- dronedarone [Multaq]
If the patient is hemodynamically unstable with atrial flutter or they elect to have it, what can be used
electrical cardioversion
What is the treatment of choice for atrial flutter?
radiofrequency ablation
- catheter in the r. atrium
- low voltage and high frequency
- tissue is destroyed and normal sinus rhythm restored
Atrial fibrillation causes the CO to
decrease = risk of stroke
Atrial fibrillation results in
decrease in CO because of ineffective atrial contractions (loss of atrial kick) and/or a rapid ventricular response
When the blood is stasis during a fib. =
clots form
- pass into the brain causing a stroke
Paroxymal
spontaneous brief
Persistent lasts for
7 days +
A fib occurs in ___% of 65 + patients
6; increases with age
A fib occurs in what diseases
underlying heart disease, such as CAD, rheumatic heart disease, cardiomyopathy, hypertensive heart disease, HF, and pericarditis
Outside sources can cause a fib
acutely with thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte disturbances, stress, and cardiac surgery
A fib is charcterized as
total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction
Atrial rate during a fib
350-600 bpm
P waves in a fib
chaotic, fibrillatory waves
The ventricular rate of a fib is
irregular
The ventricular rate of someone with a fib with controlled ventricular response?
60-100 bpm
Atrial fibrillaion with rapid ventricular response rate is
> 100 bpm (uncontrolled)
Tx for a fib.
slow the ventricular response by increasing AV block
Drugs to control ventricular rate and/or convert to sinus rhythm (amiodarone and ibutilide most common)
Electrical cardioversion (see about pain meds before)
Anticoagulation – Warfarin
Radiofrequency ablation – cath lab
Maze procedure with cryoablation
The goal of a fib tx is to
decrease in ventricular repsonse <100 bpm
prevent stroke
conversion to sinus
What drugs are used for ventricular rate control in a fib patients?
calcium channel blockers
beta blockers
digoxin
dronedarone
What drugs are most common for chemical cardioversion?
amiodarone and ibutilide
If a patient is in atrial fibrillation for longer than 48 hours, what is needed?
anticogulation therapy with warfarin for 3-4 weeks before cardioversion
- clots dislodge = stroke
For patients with drug-refractory atrial fibrillation or who do not respond to electrical conversion what is used?
radiofrequency catheter ablation (similar to the procedure for atrial flutter) and the Maze procedure are further options.
The Maze procedure is a surgical intervention that
stops atrial fibrillation by interrupting the ectopic electrical signals that are responsible for the dysrhythmia. Incisions are made in both atria, and cryoablation (cold therapy) is used to stop the formation and conduction of these signals and restore normal sinus rhythm.
If the pateint has a fib start with
electrical cardioversion then drugs
If the patient has a SVT, start with
drugs then go to electrical cardioversion
PVCs are known as
mide, bizarre, QRS
PVC is a
contraction coming from an ectopic focus in the ventricles. It is the premature (early) occurrence of a QRS complex.
Multifocal means
different in shape PVCs
Unifocal PVC
PVCs remain the same
Ventricular bigeminy
every other beat is PVC
Ventricular trigeminy
every third beat is PVC
Couplet PVC
two consecutive PVCs
Ventricular tachycardia occurs when how many PVCS consecutive
3+
R-on-T phenomenon occurs
PVC falls on the T wave of a preceding beat. This is especially dangerous because the PVC is firing during the relative refractory phase of ventricular repolarization
Excitability of the cardiac cells increase during
PVC - evolve into vent tachy or fibrillation
PVC rhythm
irregular
- P wave rarely visible (lost in QRS)
Retrograde conduction
P wave is inside the ectopic beat
- QRS distorted, prolonged, weird
- T - large and opposite direction of QRS
If a hemodynamically stable patient has PVC, then
leave them alone
What should you use to treat a patient having numerous PVCs
lidocaine
PVCs are associated with
stimulants
electrolyte imbalances
hypoxia
fever
exercise
emotional stress
heart disease (MI, mitral valve prolapse, HF, and CAD)
PVC patients need to be assessed for
apical-radial pulse deficit
Tx for PVCs
Correct cause (O2 - hypoxia, replacement)
assess hemodynamic state
Antidysrhythmics - beta blockers, procainamide or amiodarone
What are stimulants for PVCs?
caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol, and digoxin
If a heart disease patient gets PVCs, then what will develop?
reduce the CO and lead to angina and HF depending on the frequency.
Because PVCs in CAD or acute MI indicate ventricular irritability, assess the patient’s physiologic response to PVCs. Obtain the patient’s apical-radial pulse rate, since PVCs often do not generate a sufficient ventricular contraction to result in a peripheral pulse. This can lead to a pulse deficit.
Ventricular Tachycardia is
3+ PVCs (Tombstones)
Ventricular rate of V Tach
150-250 bpm
AV ____________ may be present, with P waves occurring independently of the QRS complex IN V.Tach
dissociation
When V Tach is seen, what should you immediately do?
Start CPR when unconscious, if they are still alert it won’t last long so start large bore IV and calmly send you to cath lab
Polymorphic V Tach =
Torsades de Pointes
Torsades de Pointes means
twisting of the points
Torsades de Pointes is a deficit of
magnesium
With Torsades de Pointes, the nurse can give mag if
they know the mag level
Tx for Torsades de Pointe
code, CPR AND, defibrillate them
Mag if know level
Ventricular Tachycardia pacemaker
ectopic foci (ventricles take over)
V Tach is considered life-threatening due to
decreased CO and the possibility of deterioration to ventricular fibrillation
- low perfusion = hypoxic = unconscious
VT can quickly develop into
v fib
V Tach is associated with
heart disease (MI, CAD, significant electrolyte imbalances, cardiomyopathy, mitral valve prolapse, long QT syndrome)
electrolyte imbalances
drugs toxicity
CNS disorder
Sustained Vtach causes
decrease in CO because of decreased ventricular diastolic filling times and loss of atrial contraction
Sustained V tach results in
hypotension, pulmonary edema, decreased cerebral blood flow, and cardiopulmonary arrest
Unstable V tach
pulseless
Stable V Tach
pulse
Stable V tach tx
VT with pulse (stable) treated with antidysrhythmics or cardioversion
- IV procainamide, sotalol, or amiodarone
Unstable V tach Tx
CPR and rapid defibrillation
vasopressors (epinephrine) antidyrhthymic (amiodarone)
If the VT is polymorphic with a normal baseline Q-T interval, any one of the following drugs is used:
β-adrenergic blockers, amiodarone, procainamide, or sotalol.
Polymorphic VT with a prolonged baseline Q-T interval is treated with
IV magnesium, isoproterenol, phenytoin (Dilantin), or antitachycardia pacing
dofetilide does what to QT interval
prolongs
V fib is a
severe derangement of the heart rhythm characterized on ECG by irregular waveforms of varying shapes and amplitude
V fib is firings of
multiple ectopic foci in the ventricle. Mechanically the ventricle is simply “quivering,” with no effective contraction, and consequently no CO occurs
chaotic squiggles
In v fib, what is the heart rate
not measurable
V fib is associated with
MI, ischemia, disease states in the heart (HF and cardiomyopathy), procedures (cardiac pacing and catheterization)
- coronary reperfusion after thrombolytic therapy
- electric shock, hypoxemia, acidosis, drug toxicity
V fib patients are usually
unresponsive, pulseless, and apneic state.
Tx for v fib
with immediate CPR and ACLS
Defibrillation ACLS
Drug therapy (epinephrine, vasopressin)**
A patient in the coronary care unit develops ventricular fibrillation. The first action the nurse should take is to
Perform defibrillation.
Initiate cardiopulmonary resuscitation.
Prepare for synchronized cardioversion.
Administer IV antidysrhythmic drugs per protocol.
Initiate cardiopulmonary resuscitation.
Rationale: Immediate treatment for ventricular fibrillation is the initiation of Cardiopulmonary resuscitation, followed by the use of defibrillation and definitive drug therapy according to advanced cardiac life support guidelines.
Asystole represents
total absence of ventricular electrical activity
- no depolarization = no contractions
Asystole patients are found
unresponsive, pulseless, and apneic
With asystole patients check the rhythms in
all leads
Tx of Asystole
Treat with immediate CPR and ACLS measures
- do not defibrillate
Epinephrine and/or vasopressin
Intubation
Poor prognosis
- take a pulse, cap refill, O2, BP, lead check, start CPR
Asystole result in
advanced cardiac disease, severe conduction disturbance, or end-stage HF
- prolonged arrest usually not able to be resuscitated
PEA
Electrical activity can be observed on the ECG, but no mechanical activity of the ventricles is evident, and the patient has no pulse
PEA has no
mechanical movement of the heart
- poor prognosis unless cause is tx
The most common causes of PEA
Hs and Ts
Hypovolemia,
hypoxia,
Hydrogen ion (metabolic acidosis)
hyper/hypokalemia,
hypoglycemia,
hypothermia
Toxins (e.g., drug overdose),
cardiac tamponade,
thrombosis (e.g., MI, pulmonary embolus),
tension pneumothorax
trauma.
Treatment for PEA
CPR followed by intubation and IV epinephrine
Treatment is directed toward correction of the underlying cause
DO NOT SHOCK to not knock the electrical system
ALWAYS touch the patient to confirm
Third-Degree AV Heart Block
complete heart block, constitutes one form of AV dissociation in which no impulses from the atria are conducted to the ventricles
Third-Degree AV Heart Block is caused by what in the heart
atria are stimulated and contract independently of the ventricles. The ventricular rhythm is an escape rhythm, and the ectopic pacemaker may be above or below the bifurcation of the bundle of His.
Cardiac output is depleting and the P waves do not fit together
Third-Degree AV Heart Block
- atrial rate AV
40-60 bpm
Third-Degree AV Heart Block
- Purkinje fibers rate
20-40 bpm
Third-Degree AV Heart Block is associated with
severe heart disease (CAD, MI, myocarditis, cardiomyopathy, some systemic diseases (amyloidosis, scleroderma, certain drugs (digoxin, β-adrenergic blockers, and calcium channel blockers)
Third-Degree AV Heart Block usually results in
decreased CO
Third-Degree AV Heart Block leads to
syncope, HF, shock
- severe bradycardia to periods of asystole
Third-Degree AV Heart Block Tx
symptomatic - permanent trancutaneous pacemaker ASAP
Temporary Tx for Third-Degree AV Heart Block
atropine, dopamine (Intropin), and epinephrine is a temporary measure to increase HR and support blood pressure until temporary pacing is started. Patients will need a permanent pacemaker as soon as possible.
Isoelectric line is
flat and represents those normal times in the cardiac cycle when the ECG is not recording any electrical activity in the heart
St-segment elevation associated with
myocardial injury (STEMI)
- Q wave is prolonged
- R is elevated and prolonged
- tx cath lab within 90 minutes
ST segment depression and T inversion is in a
NSTEMI
- tx medically
Biphasmic Defibrillation joules
120-200 J
Monophasmic Defibrillation joules
360 J
After the first shock of defibrillation,
start CPR immediately beginning with chest compressions.
- give it time to go back to rhythm
Cardioversion needs to
sync with Q waves for shock
Cardiac Pacemaker
electronic device used to pace the heart when the normal conduction pathway is damaged
- control heart rate with compromised conduction
Single chamber pacemaker
either atria or ventricles
Dual chmaber pacemaker
paces both atrium and ventricles
Capture measn
electrical charge produces atrial or ventricular contraction
Sensed
recognize spontaneous atrial or ventricular activity
Permanent Pacemaker is
implanted
Temporary Pacemaker
power source outside the body
- transvenous, epicrdial, trancutaneous
Trancutaneous Pacemakers
noninvasive, temporary procedure used until a transvenous pacemaker is inserted or until more definitive therapy is available
Where do you place the pads for defibrillation?
R upper part of chest and L lower part of chest with the heart in the middle to transfer energy
If anterior and posterior pads are available do those
Failure to senseoccurs
pacemaker fails to recognize spontaneous atrial or ventricular activity, and it fires inappropriately. This can result in the pacemaker firing during the excitable period of the cardiac cycle, resulting in VT. Failure to sense is caused by fibrosis around the tip of the pacing lead, battery failure, sensing set too high, or dislodgment of the electrode.
Failure to capture
when the electrical charge to the myocardium is insufficient to produce atrial or ventricular contraction. This can result in serious bradycardia or asystole. Failure to capture is caused by pacer lead damage, battery failure, dislodgment of the electrode, electrical charge set too low, or fibrosis at the electrode tip.
What are the lethal dysrhythmias?
Vtach
Vfib
Asystole
3 degree Heart Block
What are shockable rhythms?
V tach and v Fib
Rhythms that can cardiovert
SVT
Afib
Aflutter
