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Dysrhythmias- Lewis Ch 35
Terms in this set (72)
What can dysrhythmias cause?
A direct decrease in cardiac output by changing stroke volume and heart rate.
Where does a normal electrical impulse start?
Sinoatrial node (SA node) in the upper right atrium near the entrance to the vena cava
Describe the conduction of electricity in the heart
Impulse starts in the SA node
--> spreads over the atrial myocardium via the interatrial and internodal pathways
--> impulse then spreads to the atrioventricular node (AV) through the bundle of His
--> down the left and right Purkinje fibers, which then transmit the impulse to the ventricles
What does the autonomic nervous system control? What does it affect in the heart?
rate of impulse formation, speed of conduction, and strength of cardiac contraction
The parts of the autonomic p=NS that affect the heart rate are the vagus nerve fibers of the parasympathetic NS and the nerve fibers of the parasympathetic NS
What happens when you stimulate the vagus nerve?
Slows the firing of the SA node and Slows the impulse conduction of the AV node
What happens when you stimulate the sympathetic nerves?
Increases SA node firing, AV node impulse conduction, and cardiac CONTRACTILITY.
What are the four properties of heart cells?
1. AUTOMATICITY: ability to initiate an impulse spontaneously
2. EXCITABILITY: Ability to be electrically excited
3. CONDUCTIVITY: ability to transmit an impulse along a membrane in an orderly manner
CONTRACTILITY: Ability to respond mechanically to an impulse
Within the cell, there is a high concentration of ___ and low concentration of ___
Otside the cell, a high concentration of ___ and a low concentration of ___
high potassium, low sodium within the cell
high sodium and low potassium outside the cell
What happens during depolarization?
Sodium moves rapidly into the cell
On an ECG, one small square represents ____
one large square represents ___
Normally, the ___ is the natural pacemaker of the heart
Which areas of the heart have cells with automaticity (ability to transmit an impulse) (5)
1. SA node
3. AV node
4. bundle of His
5. Purkinje fibers
What are the ECG Intervals (3) and their durations?
PR Interval: 0.12-0.20
QRS Interval: <0.12
QT Interval: 0.34-0.43
Describe or draw were the intervals start and stop?
P wave is what action?
Source of possible variation
Problem in conduction within Atria
What does the PR interval represent?
What problems can it represent?
-->Time taken for impulse to spread through the atria, AV node, bundle of His --> all leading up to ventricular contraction
Problems in conduction in AV node, bundle of His, or bundle branches
0.12-0.20, Measured from beginning of p-wave to beginning of QRS complex
QRS complex is what action?
Source of possible variation
MI may result in pathologic Q wave that is wide and deep
<0.03 (Q wave duration)
QRS interval represents?
Source of possible variation
Represents time taken for contraction of both ventricles
Problem in conduction in bundle branches or in ventricles
<0.12, Measured from beginning of QRS complex.
Source of possible variation
Measured from beginning of QRS complex to end of T wave
Representes the time taken for entire electrical depolarization and repolarization of ventricles
Normal adult women have slightly longer QT intervals than men
Oroblems usually affect repolarization - drugs, electrolytes, changes in heart rate
Source of possible variation
Measured from the S wave of the QRS complex to the beginning of the T wave
Represents the time between ventricular depolarization and repolarization (systole and diastole)
Should be isoelectric (flat)
Elevation or depression caused by ischemia, infarction, or injury
Describe a normal sinus rhythm
1) Rate: 60-100 bpm
2) P waves precede each QRS complex (atrial depolarization)
3) P-R interval between atrial and ventricular repolarization
4) QRS: ventricular depolarization
5) T wave: ventricular repolarization, rhythm: regular
Normal sinus rhythm implies that cardiac electrical activity is normal
SA node fires at a rate <60 bmp, rhythm is regular
Causes patient to have symptoms of inadequate perfusion (fatigue, dizziness, chest pain, syncope)
What drugs can cause sinus bradycardia?
Beta-adrenergic blockers and calcium channel blockers
Treatment of sinus bradycardia
- Stop Drugs (which lower HR rate)
- If Atropine is ineffective, transcutaneous pacing or dopamine or epinephrine
The discharge rate from the SA node increases because of vagal inhibition or sympathetic stimulation
HR 101-180 bmp and rhythm is regular
Dizziness, dyspnea, hypotension because of decreased CO
Treatment of sinus tachycardia in stable and unstable patients, Non-Rx & Rx
Stable: Vagal maneuvers, pain management
Meds: Beta blockers, Calcium channel blockers, Adenosine
Beta blockers MOA?
Cause the heart to beat slowly with less force by blocking the hormone epinephrine or adrenalin
Adenosine mechanism of action?
Slows conduction through the AV node
Calcium channel blockers are medications used to lower blood pressure. They work by preventing calcium from entering the cells of the heart and arteries. Calcium causes the heart and arteries to squeeze (contract) more strongly. By blocking calcium, calcium channel blockers allow blood vessels to relax and open.
Blocks parasympathetic [PARACHUTE=SLOW] hormone acetylcholine receptors.
Thus increases HR
1. Explain that the pt may feel chest pressure
2. Injection close to the heart as possible (antecubital)
3. Give IV dose rapidly
4. Brief period of Asystole is common
Premture atrial contraction (PAC)
A contraction starting from an ectopic focus in the atrium (somewhere other than the SA node) sooner than the next expected sinus beat
Creates a distorted p wave
PAC's can be no biggy in healthy patients, but in patients with heart disease, may warn of more serious dysrhythmias, such as SVT
Withdrawal from caffeine, epinephrine, dopamine.
Beta-blockers can be used to decrease PACs
Paroxymal Supraventricular Tachycardia (SVT or PSVT)
A dysrhythmia starting in an ectopic focus anywhere above the bifurcation of the bundle of His
Hypotension, dyspnea, angina
***Photo SVT with rapid Adenosine IV push
ECG characteristics of SVT
HR is 151-220 bpm
Rhythm is regular
P wave may have an abnormal shape or be hidden in the preceding T wave
Has to be regular, narrow, and have no p wave
What is the drug of choice for SVT?
- administer it
rapidly over 1-2 secs
flush after w/ NS
as close to heart as possible
Given to patients that are STABLE
Atrial flutter ECG characteristics
Atrial rate 200-350 bpm, ventricular rate ~150 bpm
What are the complications of Atrial flutter?
Patients are at a high risk for stroke because clots can form in the atria from stasis of blood
An atrial tachydysrhythmia identified by recurring, regular, sawtooth-shaped flutter waves that originate from a single ectopic focus in the right atrium, less commonly, can occur in left atrium.
total disorganization of atrial electrical activity because of multiple ectopic foci
chaotic fibrillatory waves replace the p waves
rhythm is usually IRREGULAR
If a patient is in atrial fibrillation for longer than 48 hours, ____ therapy is needed
anticoagulation - warfarin (require routine INR lab)
Alternatives that do NOT require routine lab tests are: dabigatran, apixaban, rivaroxaban
What do you need to monitor with Warfarin?
First degree AV block
every impulse is conducted to the ventricles, but duration of AV conduction is prolonged
The PR interval is prolonged (>0.20 second)
Everything else is normal
Patients are usually Asymptomatic
Second degree AV block type 1
gradual lengthening of the PR interval until an atrial impulse is not conducted and a QRS complex is blocked
Drugs that cause second degree type 1 AV block
Treatment for second degree AB block type 1
Atropine (to increase HR)
Second degree AV block, type 2
A P wave is non-conducted without progressive PR lengthening
This usually occurs when a block in one of the bundle branches is present
Which is more serious, second degree AV block type 1 or 2?
A certain number of impulses from the SA node are not conducted to the ventricles
Atrial rhythm may be regular, but the ventricular rate is IRREGULAR
Third degree AV block (complete heart block)
Impulses and contractions in Atria and Ventricles happen independently of each other.
No impulses from the atria are conducted to the ventricles . The atria are stimulated and contract independently of the ventricles
Treatment of third degree heart block
Drugs such as dopamine and epinephrine are an interim measure to increase HR and support BP until temporary pacing is started
Atropine is NOT effective
premature ventricular contraction (PVC)
a ventricular contraction preceding the normal impulse initiated by the SA node (pacemaker)
A PVC is wide and distorted in shape compared with a QRS complex
PVCs from a unifocal source:
PVCs from a multifocal source:
unifocal: look the same
multifocal: appear different from one another
When every other beat is premature and the QRS is wide and bizarre, this is called:
When every third beat is a PVC it is called
PVCs are associated with
-stimulants such as caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol, and digoxin
-electrolyte imbalances, hypoxia, fever, exercise, and emotional stress
-MI, mitral valve prolapse, HF, cardiomyopathy, and CAD
A run of three or more PVCs defines
Ventricular tachycardia occurs when
-an ectopic focus or foci fire repeatedly and the ventricle takes control as the pacemaker
V-tach ECG characteristics
Ventricular rate is 150-250 beats/minute. Rhythm may be regular or irregular.
Atrioventricular (AV) dissociation may be present with P waves occurring independently of the QRS complex.
The atria may be depolarized by the ventricles in a retrograde fashion.
The P wave is usually buried in the QRS complex, and the PR interval is not measurable.
The QRS complex is distorted in appearance and wide (>0.12 seconds in duration).
Treatment of V-tach
IV magnesium (to
Cardioversion is used if drug therapy is ineffective
Why do you give epinephrine during a code?
Epinephrine increases arterial blood pressure and coronary perfusion during CPR via alpha-1-adrenoceptor agonist effects.
Why do you give magnesium during a code?
Magnesium sulfate is effective as an anticonvulsant and an antiarrhythmic.
t is used to treat polymorphic ventricular tachycardia with a pulse.
It is only recommended for use in cardiac arrest if Torsades de pointes or suspected hypomagnesemia is present.
Why do you give sodium bicarb during a code?
Because of concerns regarding the deleterious effects of acidosis, clinicians have used bicarbonates as buffer to offset the high acid production, in an attempt to help the body restore normal homeostasis in cardiac arrest.
A severe derangement of the heart rhythm characterized on ECG by irregular waveforms of varying shapes and amplitude.
This represents firing of multiple ectopic foci in the ventricle. Ventricle is just 'quivering'
Causes of Vfib? (5)
- May occur with coronary reperfusion after thrombolytic therapy
- Electric shock
Pulseless Electrical Activity (PEA)
A situation in which organized electrical activity is seen on the ECG, but there is no mechanical heart activity and the patient has no pulse
Common causes of PEA
What is a prodysrhythic drug? Examples?
Antidysrhythmic drugs that can cause life-threatening dysrhymias similar to those for which they are treating
Before giving antidysrhythmic drugs, the nurse should
1. complete a full physical assessment/health history/ medication history
2. Obtain a baseline ECG
3. Asess vital signs, heart/lung sounds
4. Observe for signs of decrease CO
5. Review labs on electrolytes
What do sodium channel blockers do?
Decrease impulse conduction in the atria, ventricles, and His-Purkinje system
Lidocaine and phenytoin belong to the class of:
How does this affect action potential?
Sodium channel blockers
It can terminate ventricular dysrhythmias
How do beta blockers affect the action potential of the heart?
Decrease automaticity of the SA nod, slows impulse conduction in the AV node, and reduces atrial and ventricular contractility
How do potassium channel blockers affect the action potential of the heart?
They delay repolarization, resulting in prolonged duration of action potential and refractory period
How do Calcium channel blocker affect the action potential of the heart?
Delay repolarization, delay AV node conduction, reduce myocardial contractility
Patient teaching for Implantable Cardioverter-Defibrillator (ICD)
1. Avoid direct blows to the ICD site
2. Avoid large magnets and strong electromagnetic fields
3. Do not have an MRI unless the ICD is approved
4. Tell security before travel to avoid magnets
5. Do not stand near antitheft dectors
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