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Temporary pacing
- 1. Temporary Pacemakers- SICU’s 101 Primer
- 13. TEMPORARY PACING DEFINITIONS (from AACN procedure manual for Critical Care, 5 th edition, 2005, pg.325)
- 28. Medtronic 5388 Temporary Pacemaker *The following slides are courtesy of Medtronics*
Notes de l'éditeur
- When a patient has extreme bradycardia, the ventricle will try to compensate with ventricular escape beats.
- We supplement our OHS patients to increase atrial kick/ cardiac output.
- Bradydysrhythmias include: idioventricular, junctional, slow atrial fibrillation, agonal for example.
- Long QT syndromes would include Torsades de pointes. Medication toxicity would include quinidine, some tricyclic antidepressants, phenotiazines, Haldol, digoxin.
- Transcutaneous pacing is another alternative. Is used emergently because it is more easily applied (anterior/posterior) and does not require venous cannulation. It is painful and requires some pain medication and sedation. Our Zoll defibrillators have a transcutaneous pacing mode. Requires more energy and this does create pain. Higher incidence of undesired pacing of chest wall and body muscles. Stimulation of diaphragm causes hiccups. Epicardial pacing wires: Wires are placed on the right atrium and ventricle. Left ventricle is not used because it is inaccessible through deep pulmonary vein and artery.
- Our main focus is on chambers paced, sensed, and response to sensing (I-III). Position IV and V refer more to permanent pacers and AICDs.
- Used to treat symptomatic bradycardia (and transient decrease in HR) and to allow administration of medications (Beta-blockers) and to increase cardiac output/atrial kick.
- Slow atrial fibrillation, back-up pacing, sinus node dysfunction, idioventricular
- Avoids competition between pacemaker-initiated beats and the patient’s on intrinsic rhythm. 2 nd degree type I (Wenckebach) and 2 nd degree type II and complete heart block that is symptomatic. New BBB with transient CHB. Sinus node dysfunction, alternating BBB and junctional.
- Asynchronous pacing in presence of intrinsic rhythm may result in R on T phenomenon which may lead to a lethal dysrhthmia. Only us in absence of an intrinsic rhythm.
- Also known as failure of pulse generation. Mechanical failure of pacemaker to generate impulse. Represented by absence of pacer spike.
- EMI= electomechanical interference
- Heart fails to respond to the pacemaker stimulus. Represented by an absence of a complex after spike.
- #1. Evidenced by appropriate HR, proper sensing, and proper capture. #2 evidenced by b/p > 90, MAP>60, A&O, and no syncope or ischemia. No lightheadedness,faintess, dizziness or confusion. #3 use paper tape to anchor wires/leads to abdomen. Hypafix or clear tape is to sticky. Harder to get wires loose.
- May be changing are site care in near future. Maryellen will hopefully be taking to practice in February.
- Failure of pacemaker to sense properly causes competition between pacemaker initiated impulses and the patient’s intrinsic cardiac rhythm. Pacemaker oversensing causes the pacemaker to be inappropriately inhibited. Failure to capture myocardium. Stimulation of the diaphragm causes hiccupping. May be related to pacing the phrenic nerve, perforation, wire dislodgement, or excessively high pacemaker MA setting. Ventricular dysrhythmias occur from manipulation of lead within the cardiac chamber. Pneumo/ hemothorax, myocardial perforation, air embolism and cardiac tamponade may occur during insertion of pacemaker and electrode placement.
- Do they have a pulse? Are they in PEA related to acidosis, hypoxia or electrolyte imbalance? This will affect the level of energy required to pace. Do they have fibrotic tissue around tip of catheter which will affect the ability of the patient to capture even with an increased MA? 2. Do you need to change MA or sensitivity? If fail to capture or pace, are they acidotic or need a new battery? Do we need to initiate asynchronous pacing or change to emergent transcutaneous pacing?