Ch 36: Care of Pts with Dysrhthmias Flashcards
12 lead ECG placement
See pic Tale 36-1
Cardiac conduction
Sinoatrial SA node is the primary pacemaker. travels thru atrium to the AV node (reflected in the P wave). Leads to the AV node and the bundle of His. This causes a delay before moving to ventricle (reflected in the PR segment). It allows atria to contract and ventricles to fill. Continues thru the L & R bundle branches. The L branch divides even further. End in Purkinje fibers which cause ventricular contraction.
P wave
Represents atrial depolarization. They have a consistent shape if the electrical pulse is coming from the SA node.
60-100 bpm
PR segment
isoelectric line from end of P to beginning of QRS complex, when the impulse is traveling thru the AV node where it is delayed. Allows the atria to contract and the ventricles to fill
PR interval
Beginning of P wave to the end of the PR segment. Depolarization plus impulse delay and time to travel to the purkinje fibers. Normal is 0.12 to 0.2 seconds (5 small blocks)
QRS complex
ventricular depolarization. Shape depends on the lead selected.
Q wave: 1st negative deflection and is not seen in all leads. It is small and represents initial ventricular septal depolarization. If it is abnormally present it represents necrosis
R wave: 1st positive deflection (small large or absent, depending on lead)
S wave: negative deflection following the R wave and is not present in all leads
QRS duration
time required for depolarization of both ventricles. beginning of QRS complex to the J point (where QRS ends and ST segment begins). Normal is .04 -.10 (3 small blocks)
ST segment
Isoelectric line that represents early ventricular repolarization. It is from the J point to the beginning of the T wave. It varies with changes in the heart rate, medications, and electrolyte disturbances. It is normally not elevated more than 1mm or depressed less than 0.5mm. Elevation or depression can be caused by myocardial injury, ischemia or infarction, conduction abnormalities, or medications
T wave
Represents ventricular repolarization. Usually positive, rounded, and slightly asymmetric.
U wave
when present It may result from slow repolarization of the ventricular Purkinje fibers. Same polorization as the T-wave but usually smaller. It’s not seen in all leads. It is common in V3. An abnormality may suggest hypokalemia or other imbalance.
Possibly request a potassium level and be care not to mistake it for a P wave
QT interval
The total time required for ventricular depolarization and repolarization. From the beginning of the QRS complex to the end of the T-wave. It varies with age, gender, and changes with heart rate. Prolonged QT interval can lead to ventricular tachycardia called torsades de pointes
Up to .40 is nomal
Artifact
An interference seen on the rhythm strip or monitor which looks like a wandering or fuzzy baseline. It can be caused by movement, loose or defected electrodes, improper grounding, faulty equipment. It can mimic lethal dysrhythmias or ventricular fibrillation.
ECG components
see pic Fig 36-5
ECG rhythm analysis
- Determine the heart rate
300 / # big blocks between 2 R wave
Count backward 300, 150, 100, 75, 60, 50, 43, 37, 33, 30
#QRS complexes in 6 seconds x 10 (use if irregular) - Determine the heart rhythm
Regular, irregular, regularly irregular, occasionally irregular, irregular irregular
Atrial rhythm: Count P-Pwaves, regular if varies less than 3 small blocks
Ventricular rhythm: RR intervals - Analyze the P waves
Ask : are P waves present, occurring regular, one for each QRS complex, Smooth rounded and upright or inverted, do they all look same? - Measure the PR interval
beginning of P wave to end of PR interval; 0.12-0.2 sec is normal, constant throughout - Measure the QRS duration
beginning of QRS to the j point; 0.04-0.10 sec, constant - Interpret the rhythm
ECG graph paper
1 small block = .04 sec
5 small blocks = 1 large block = .20 sec
5 large blocks = 1 sec
30 large blocks = 6 sec
Time is horizontal
Amplitude is vertical
Normal Sinus Rhythm
originates from the SA node
Rate: 60-100
Rhythm: atrial and ventricular are regular
P waves: present, consistent, one before each QRS
PR interval 0.12 - 0.2 sec and constant
QRS duration: 0.04-0.10 sec and constant
Sinus arrhythmia
variant of NSR, from changes during breathing. HR increases slightly during inspiration and decreases slightly during exhalation. All same as normal NSR except that PP and RR intervals vary with the difference between the shortest and longest intervals >0.12 sec
Can be caused by digitalis or morphine.
Dysrhythmia/arrhythmia
Results from
- a disturbance in the relationship between the electrical conductivity in the mechanical response of the myocardium.
- A disturbance of impulse formation either from abnormal rate or from ectopic focus.
- A disturbance in impulse conduction such as delays and blocks.
- The combination of several mechanisms. They have no clinical manifestations but can have serious consequences
Key features of sustained tachy dysrhythmias and Brady dysrhythmias
Chest discomfort, pressure, pain which may radiate to the jaw back or arm.
Restlessness, anxiety, nervousness, confusion. Dizziness, syncope.
Palpitations with tachy.
Changes and pulse rate and rhythm. Pulse deficit.
Shortness of breath and dyspnea, tachypnea, pulmonary crackles, orthopnea
S3 s4 heart sounds
Jugular venous distention. Weakness, fatigue, pill cool skin, diaphoresis, nausea and vomiting, decreased urine output, delayed capillary refill, hypotension
Tachydysrhythmias
> 100bpm, all ECG components remain normal
They shorten the diastolic time and coronary perfusion time. Initially cardiac output and blood pressure is increased. As it continues, stroke volume is decreased and cardiac output and blood pressure begin to decrease, decreasing perfusion pressure. Increased work of the heart increases oxygen demand. Symptoms include palpitations, chest discomfort, restlessness and anxiety, pale cool skin, syncope from hypotension.
Bradydysrhythmias
<60bpm. All ECG opponents same
Myocardial oxygen demand is reduced which can be beneficial.
Coronary perfusion time may be adequate because of a prolonged diastole which is desirable.
Coronary perfusion pressure may decrease if heart is too slow which can be a serious consequence.
It can be tolerated if blood pressure is adequate.
Premature complexes
When a cell group other than that SA node fires an impulse before the next sinus impulse is generated. There is a pause before the next normal complex, which creates an irregularity in the rhythm. They may feel palpitations of the heart or be unaware. If they become more frequent the patient can experience decreased cardiac output.
Bigeminy: occurs in a repetitive 2 beat pattern
Trigeminy: 3 beat pattern, 2 normals followed by a premature and a pause
Quadrigeminy: 4 beat pattern, 3 norms followed by premature and a pause
Sinus tachycardia causes
Heart rate can increase in response to sympathetic stimulation due to physical activity, anxiety, pain, stress, fear, fever, anemia, hypoxemia, hypothyroidism, pulmonary embolism. Meds such as catecholamines, atropine, caffeine, alcohol, nicotine, aminophylline, thyroid medications.
Increases in response to decreased cardiac output or blood pressure, hypovolemic shock, myocardial infarction, infection, and heart failure. They can be asymptomatic or symptomatic.
Treat angina with oxygen, rest, nitroglycerin or morphine, IV diuretics, volume replacement, antipyretics, antibiotics. Beta-adrenergic blocking agents may be prescribed.
Sinus bradycardia causes
Excessive vagal stimulation from carotid sinus massage, vomiting, suctioning, Valsalva maneuver, ocular pressure, or pain can cause this. It can result from hypoxia, administration of drugs such as beta adrenergic blocking agents, calcium channel blockers, and digitalis.
Assess for: Syncope, dizziness and weakness, confusion, hypotension, diaphoresis, shortness of breath, ventricular ectopy, anginal pain.
Treat with atropine and oxygen. Possible volume replacement. Excessive atropine could cause tachycardia and myocardial ischemia.
Atrial dysrhythmias
shows as a p wave that differs in shape
Most common are premature atrial complexes, supraventricular tachycardia, atrial flutter, and atrial fibrillation
Premature atrial complexes PAC
Atrial tissue becomes irritable which fires and impulse before the next sinus impulse is due. The premature P-wave may not clearly be visible in can be hidden by T-wave. It is usually followed by a pause. Causes include stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine, alcohol, and meds; myocardial ischemia, hypermetabolic states, electrolyte imbalance, or atrial stretch. Usually no symptoms except possible palpitations. Treat the cause.
Supraventricular Tachycardia SVT
Rapid stimulation of atrial tissue at a rate of 100 to 280 bpm in adults. P waves may not be visible because they may be embedded in the preceding T-wave. It can result in angina, heart failure, and cardiogenic shock if not treated. The preferred treatment for recurrent SVT is radiofrequency catheter ablation. Vagal stimulation my be performed by a doc but is usually temporary. Give O2 and administer meds to slow ventricular rate. Cardioversion may regain rhythm.
Atrial fibrilation
The most common seen in clinical practice
Leads to heart failure and stroke.
Risk factors: HTN, DM, male, CHF, valvular disease
Episodes caused by: alcohol, heart surgery, electrocution, MI, pericarditis, myocarditis, pulmonary embolism
Treat the underlying cause usually fixes it
ECG: Chaotic rhythm with no clear P waves, no atrial contractions, irregular ventricular response. Looks limeade wavy baseline
Atria quiver. Heart dilation and blood pooling in atria can lead to thrombus and pulmonary embolism, cardiac output is decreased.
Meds: antidysrhythmics such as calcium channel blockers, amiodarone, Anticoagulants
Cardioversion (anticoagulant for 6 wks prior), A TEE transesophageal echocardiogram to make sure there are not any clots before. Always shock on the R wave
Radiofrequency catheter ablation creates a scar to block abnormal pathways. May require a pacemaker
Atrial Flutter
rapid atrial depolarization at rate of 250-350 times per min.
ECG: saw tooth wave
Caused by: rheumatic or ischemic heart disease, HF, AV valve disease, pre-excitation, septal defects, pulmonary emboli, thyrotoxicosis, alcoholism, pericarditis
If ventricular rate is normal, pt may be asymptomatic.
Administer O2, and meds to slow the rapid beat
If severe, cardioversion
Ventricular dysrhythmias
results in a widened, odd shaped QRS complex >0.12 sec.
Idioventricular rhythm (ventricular escape rhythm)
ventricular nodes pace the cells at less than 40 beats/min. If Pwaves are seen, they are independent if the QRS
rhythm in a dying heart. Pulseless electrical activity. No palpable pulse. Pt is hypotensive and in shock. Assess ABC, LOC, and O2. Begin CPR and ACLS may be started.
Common causes are hypovolemia, hypoxia, acidosis, potassium imbalance, hypothermia, drug overdose, tension pneumothorax, coronary or pulmonary thrombosis, cardiac tamponade
Premature ventricular complexes
PVCs are common and their frequency increases with age. You can occur with ischemia, chronic card failure, chronic hypoxemia, chronic airway limitation, anemia, hypokalemia, or hypo magnesium.
Postmenopausal women find that caffeine causes palpitations and PVCs.
The result of an increased irritability of ventricular cells, early ventricular complexes followed by a pause
Ventricular Tachycardia VT “V tach”
140-180 beats/min. Usually lethal
Intermittent or sustained (longer than 30 sec)
P waves seldom seen if sustained
In cardiac arrest, VT is the rhythm before deterioration to VFib
Can cause cardiac arrest
If stable, give O2, 12 lead ECG, meds, possible cardioversion.
If unstable treat same as ventricular fibrillation
Slower rates are better tolerated. In some patients, VT causes cardiac arrest. Assess ABCs, level of consciousness and O2
Ventricular Fibrillation VF “V Fib”
LIFE THREATENING
ventricular contraction cannot occur, no recognizable ECG deflections, no CO, no pulse, no perfusion, Fatal if not corrected n 3-5 minutes
Pt becomes faint, looses consciousness, pulseless, apneic, no BP, no heart sounds, resp and metabolic acidosis, seizures, pupils become fixed and dilated, skin cold and mottled, > death
It may be the first manifestation of coronary artery disease. It can occur with hypokalemia, hypo magnesium, hemorrhage, antidysrhythmic therapy, rapid supraventricular tachycardia, shock, surgery, or trauma.
Trt: Defibrillate immediately according to ACLS guidelines, CPR if no defibrillator is available. CPR if shock does not work.
Ventricular Asystole
complete absence of electrical rhythm, pt in full cardiac arrest, ECG may only have possible P waves, but is usually flat. Usually from myocardial hypoxemia, severe hyperkalemia and acidosis. If P wave is seen it is probably from severe ventricular conduction block.
Treatment: CPR, assess another ECG lead to make sure in is not VF, do not shock asystole. Give O2, epi, and atropine. Follow ACLS guidelines
Atrioventricular AV blocks
The SA node functions and atria functions normally. The AV node is delayed or blocked > QRS complexes delayed or blocked
1st degree: all sinus impluses eventually reach the ventricles. (Prolonged PR interval, don’t treat, it’s asymptomatic)
2nd degree: only some reach (need a pacemaker)
3rd degree/complete heart block: none of them. Bradycardia, pacemaker, usually confused and lightheaded
differentiated by PR intervals
Bundle Branch Blocks BBB
Delay or block in the bundle of His. Usually a sinus rhythm. Temporary or permanent.
Bunny ears in the QRS
Vagal maneuvers
induce vagal stimulation and slowing of the AV and SA nodes. Used to treat Supraventricular tachydysrythmias. Include carotid sinus massage and Valsalva maneuvers. May cause rebound tachycardia or severe bradycardia.
Carotid Sinus massage: doc massaged over one carotid artery for a few seconds while observing for rhythm change. Not common and resusctiation equipment needs to be on hand.
Vagal reflux: instruct pt to bear down.
Vagal stimulation can be accidentally done while suctioning trach, enemas, rectal temps, gagging, constipation, straining during BM, tight collars, raising arms above head.
Temporary Pacing
provides timed electrical stimulus to the heart (nonsurgical). On demand or at a fixed rate. Invasive or noninvasive
capture is seen on ECG (artifact-spike followed by P wave or QRS complex) indicated the pacemaker was successful
Common complications from noninvasive include discomfort from muscle stimulation, skin irritation, diaphoresis.
Invasive complications: infection, hematoma, ectopic complexes, loss of capture, under or over sensing, electromagnetic interference, stimulation of chest wall or diaphragm. Always wear rubber gloves when touching wires.
Assess vitals on the R side of the body.
Cardioversion
withhold digoxin for 48 hrs
anticoagulants for 4-6 weeks prior if elective
usually conscious, give a short acting anesthetic agent for sedation
One electrode to the left of the precordium, in the other on the right next to the sternum. Set the defibrillator in synchronized mode so it is not discharged during the T-wave.
Do not use oxygen while shocking
Nursing care: maintain airway, O2, assess vitals and LOC, administer antidysrythmic meds, monitor for dysrythmias, asses for burns from electrodes, emotional support, document
radio frequency catheter ablation
invasive, destroys the irritable focus. Must undergo studies and mapping procedures to ID the area. Possibility of destroying the normal conduction system and therefore may require a pacemaker.
Torsades de pointes
A type of ventricular tachycardia that is related to a prolonged QT interval. Just treated with magnesium sulfate.
Noninvasive temporary pacing
It is accomplished through the application of two large external electrodes. The generator emits electrical pulses which are transmitted through the electrodes been transcutaneously to stimulate ventricular depolarization when the patient’s heart rate is slower than the rate set on the pacemaker. It is used as an emergency measure to provide demand ventricular pacing in a profoundly Brady cardiac or asystolic patient.
Lost the skin with soap and water, do not read or apply alcohol. One on upper chest to the right of the Sterling and one over the apex of the heart. Displaced breast tissue. Just the pacing rate.
Complications of CPR
Rib fractures, sternum fracture, costochondral separation, lacerations of the liver and spleen, pneumothorax, hemothorax, cardiac tamponade, lung contusions, fat emboli
Defibrillation
Early defibrillation is critical in resolving pulseless the Vtach or VFib. The earlier the defibrillation, the better the chance of survival. Resume CPR immediately after the shock and continue for five cycles or two minutes. Reassess and shock if needed.
Permanent pacemaker
Treats complete heart block. Battery lasts 10 yrs. Pacemaker checks are done at regular intervals and can be done over the telephone.
No heavy lifting, do not lift arms above the head, give them an ID card, wear a bracelet, caution in magnetic field, keep cell phone 6 inches away, no MRIs,
Keep a diary and record your poults for one full minute at the same time each day. Know the rate your pacemaker is set and call if your rate is lower. Antitheft devices in stores could cause problems just move away. Enform airport personnel. Stay away from arcwelding equipment. Report difficulty breathing, dizziness, fainting, chest pain, weight gain, prolonged hiccuping.
Cardiac conduction rates
SA node 60-100 bpm, seen in Pwave
