6. DEFINITION:
A CARDIAC PACEMAKER IS AN ELECTRONIC DEVICE,
THAT DELIERS, DIRECT ELECTRICAL STIMULATION TO
STIMULATE THE MYOCARDIUM TO DEPOLARIZE,
INITIATING A MECHANICAL CONTRACTION.
THE PACEMAKER INITIATES AND MAINTAINS THE HEART
RATE WHEN THE HEART’S NATURAL PACEMAKER IS
UNABLE TO DO SO.
7. TYPES OF PACEMAKERS:
PERMANENT PACEMAKERS:
SURGICALLY PLACED
LEADS ARE PLACED TRANVENOUSLY, IN APPROPRIATE CHAMBER
OF THE HEART, AND THEN ANCHORED TO THE ENDOCARDIUM
PULSE GENERATOR PLACE IN A POCKET IN THE SUBCUTANEOUS
TISSUE UNDER THE CLAVICLE OR ABDOMEN.
MOSTLY USED FOR LONG-TERM , PATIENTS WITH CHRONIC HEART
CONDITIONS.
9. METHODS OF PLACEMENT OF A
TEMPORARY PACEMAKER:
TRANSVENOUS PACEMAKERS:
INSERTED TRANSVENOUSLY( USUALLY
SUBCLAVIAN, INTERNAL JUGULAR,
ANTECUBITAL OR FEMORAL), INTO THE
RIGHT VENTRICLE( OR RIGHT ATRIUM)
AND RIGHT VENTRICLE FOR DUAL-
CHAMBER PACING. AND THEN ATTACHED
TO AN EXTERNAL PULSE GENERATOR.
PROCEDURE DONE BEDSIDE OR UNDER
FLUROSCOPY.
10. EPICARDIAC PACEMAKERS:
IN THIS CASE, THE WIRES ARE
ATTACHED TO THE ENDOCARDIUM,
AND ARE BROUGHT OUT THROUGH
A SURGICAL INCISION IN THE
THORAX.
THESE WIRES ARE CONNECTED TO
AN EXTERNAL PULSE GENERATOR.
COMMONLY SEEN AFTER CARDIAC
SURGERY.
12. TRANSCUTANEOUS PACING:
NON- INVASIVE, MULTIFUNCTIONAL, ELECTRODE PADS ARE PLACED.
PLACEMENT: ANTERIOR- POSTERIORLY, ANTERIOR- LATERALLY
MULTIFUNCTIONAL ELECRODE PADS ARE THEN CONNECTED TO AN
EXTERNAL SOURCE( DEFIBRILLATOR WITH PACING ABILITY).
THE EXTERNAL IMPULSE FLOWS THROUGH THE ELECTRODE PADS
AND SUBCUTANEOUS SKIN TO THE HEART.
THUS PACING THE HEART.
13. TRANSTHORACIC PACING:
PLACED IN EMERGENCY, VIAA
LONG NEEDLE, USING A
SUBXYPHOID APPROACH.
THE WIRE IS THEN PLACED
DIRECTLY INTO THE RIGHT
VENTRICLE.
14. BIVENTRICULAR PACEMAKERS:
ALSO KNOWN AS CARDIAC RESYNCHRONIZATION.
USED TO TREAT MODERATE TO SEVERE HEART FAILURE AS A RESULT
OF LEFT VENTRICULAR DYSSYNCHRONY.
INTRAVENTRICULAR CONDUCTION DEFECTS RESULT IN AN
UNCORDINATED CONTRACTION OF THE LEFT AND RIGHT
VENTRICLE, WHICH CAUSES A WIDE QRS COMPLEX AND IS
ASSOCIATED WITH WORSENING HEART FAILURE AND MORTALITY.
BIVENTRICULAR PACEMAKERS CAN INCORPORATE IMPLANTABLE
CARDIO-VERTER DEFIBRILLATORS OR CAN BE USED ALONE.
18. PULSE GENERATOR:
IT CONSISTS OF A CIRCUITRY AND BATTERIES.
IN A PPI, IT IS ENCAPSULATED IN A METAL BOX, EMBEDDED UNDER THE
SKIN.
THE BOX PROTECTS THE GENERATOR FROM ELECTROMAGNETIC
INTERFERENCE AND TRAUMA.
PPI USE LITHIUM BATTRIES. LIFE SPAN= 8-12 YRS.
IN A TPM, THE GENERATOR IS A SMALL BOX WITH DIALS FOR
PROGRAMMING.TRANSCUTANEOUS PACING SYSTEMS, USE EXTERNAL
SOURCE LIKE DEFIBRILLATOR WITH PACING ACTIVITY.
TPM USE BATTERIES WHICH NEED REPLACEMENT AS PER THE USE OF THE
DEVICE.
TRANSCUTANEOUS SYSTEMS USE RECHARGEABLE BATTERY CIRCUITRY.
20. TYPES OF PACEMAKER LEADS:
SINGLE CHAMBER PACEMAKER:
1 LEAD, EITHER IN ATRIAL OR
VENTRICULAR CHAMBER.
SENSING AND PACING FUNCTIONS
ARE CONFINED TO THE CHAMBER
WHERE THE LEAD IS PLACED.
21. CONTD..
DUAL- CHAMBER PACEMAKER:
2 LEADS
ONE LEAD IN ATRIUM, OTHER IN
VENTRICLE.
PACING AND SENSING OCCUR IN
BOTH HEART CHAMBERS, MIMICKING
THE PHYSIOLOGICAL PACING.
23. CONTD..
IN SINGLE RIGHT VENTRICLE PACING, THERE IS SLIGHT DELAY OF THE
LEFT VENTRICLE CONTRACTING, AS THE ELECTRICAL IMPULSE BEGINS IN
THE RIGHT VENTRICLE AND MOVES IN THE LEFT VENTRICLE, GIVING A
LEFT BUNDLE BRANCH BLOCK APPEARANCE.
BY PACING BOTH VENTRICLES AT THE SAME TIME,THE PACEMAKER CAN
RESYNCHRONIZE THE HEART.
24. CONTD..
APPROACH:
LEADS MAY BE INSERTED VIAA VEIN, INTO THE RT. ATRIUM/ RT.
VENTRICLE, OR DIRECT PENETRATION INTO THE CHEST WALLAND
ATTACHED TO THE LT. VENTRICLE OR RT. ATRIUM.
FIXATION DEVICE:
LOCATED AT THE END OF THE PACEMAKER LEAD, ALLOW FOR
SECURE ATTACHMENT TO THE HEART, REDUCING THE POSSIBILITY OF
LEAD DISLODGEMENT.
TEMPORARY LEADS:
CONNECTED TO EXTERNAL PULSE GENERATOR AND
PROTRUDEFROM THE INCISION.PERMANENT LEADS ARE CONNECTED
TO PULSE GENERATOR IMPLANTED UNDER THE SKIN.
25. INDICATIONS:
SYMPTOMATIC BRADYDYSRTHYTHMIAS.
SINUS BRADYCARDIA DUE TO DRUG THERAPY.
HEART BLOCK
HYPERSENSITIVE CAROTID SINUS SYNDROME AND NEUROCARDIOGENIC
SYNCOPE.
PROPHYLAXIS( PRIOR CARDIAC SX, POST ACUTE MI)
DIAGNOSTIC TESTS:
CARDIAC CATHETERIZATION
PTCA/ STRESS TEST/ PRIOR TO PERMANENT PACING
TACHYDYSRHYTHMIAS( SVT, VT)
26. FUNCTIONS OF A PACEMAKER:
CARDIAC PACING STIMULATES EITHER THE ATRIUM, VENTRICLE OR
BOTHIN SEQUENCE, AND INITIATES ELECTRICAL DEPOLARIZATION AND
CARDIAC CONTRACTIONS.
CARDIAC CONTRACTIONS ARE EVEDENCED ON THE ECG BY THE
PRESENCE OF “A SPIKE”, OR “PACING ARTIFACT”.
27. PACING FUNCTIONS:
1. ATRIAL PACING:
DIRECT STIMULATION OF THE RT.
ATRIUM, PRODUCING A “SPIKE” ON
THE ECG PRECEDING A P WAVE.
28. 2. VENTRICULAR PACING:
DIRECT STIMULATION TO OF THE
RIGHT OR LEFT VENTRICLE
PRODUCING A “SIPKE”, ON THE ECG
PRECEEDING A QRS COMPLEX.
29. 3. AV PACING:
DIRECT STIMULATION TO THE RIGHT
ATRIUM, AND EITHER VENTRICLE IN
SEQUENCE; MIMICS NORNAL
CARDIAC CONDUCTION, ALLOWING
THE ATRIA TO CONTRACT
BEFORETHE VENTRICLES TO
INCREASE CARDIAC OUTPUT.
30. SENSING FUNCTIONS:
CARDIAC PACEMAKERS SENSE THE INTRINSIC CARDIAC ACTIVITY.
1. DEMAND:
ABILITY TO “ SENSE” INTRINSIC CARDIAC ACTIVITY AND DELIVER A PACING
STIMULUS ONLY IF THE HEART RATE FALLS BELOW THE PRESET RATE.
2. FIXED:
NO ABILITY TO “SENSE” INTRINSIC CARDIAC ACTIVITY. THE PACEMAKER CANT “”
WITH THE HEARTS NATURAL ACTIVITY AND CONTINOUSLY DE LIVERS ASYNCHRONIZE
PACING STIMULUS AT A PRESET RATE.
3. TRIGGERED:
ACTIVITY TO DELIVER PACING STIMULI IN A RESPONSE TO “ SENSING” A
CARDIAC EVENT.
31. CONTD..
1. “SEES”---ATRIAL ACTIVITY AND DELIVERS A PACING SPIKE TO THE VENTRICL
AFTER AN APPROPRIATE DELAY(0.16 SEC).
2. MAINTAIN AV SYNCHRONY AND INCREASE HEART RATE BASED ON INCREASES
IN THE BODY DEMANDS,THAT OCCUR DURING EXERCISE OR DURING STRESS.
3. “PHYSIOLOGICAL” SENSORSARE BEING DEVELOPED AS ALTERNATIVES TO
“TRIGGER” A VENTRICULAR RESPONSE BECAUSE MANY PATIENTS HAVE ATRIAL
DYSFUNCTION.
4. “ SENSOR- DRIVEN” RATE RESPONSIVE PACEMAKERS DO NOT SENSE ATRIAL
ACTIVITY, A TRIGGERED VENTRICULAR BEAT OCCURS WHEN THE PACEMAKER
SENSES EITHER INCREASE IN MUSCLE ACTIVITY, TEMPERATURE, O2
UTILIZATION,OR CHANGES IN BLOOD PH.
32. CAPTURE FUNCTIONS:
THE PACEMAKERS ABILITY TO GENERATE A RESPONSE FROM THE HEART
(CONTRACTION), AFTER ELECTRICAL STIMULATION IS REFFERED TO AS
CAPTURE.
CAPTURE IS DETERMINED BY THE STRENGTH OF THE ELECTRICAL
STIMULUS, MEASURED IN mA, THE AMOUNT OF TIME THE STIMULUS IS
APPLIED T THE HEART AND BY CONTACT OF THE DISTAL TIP OF THE
PACING LEAD TO THE MYOCARDIAL TISSUE.
(A) ELECTRICAL: INDICATED BY A P WAVE OR QRS FOLLOWED BY A
PACEMAKER SPIKE.
(B) MECHANICAL: PALPABLE PULSE CORRESPONDING TO THE ELECTRIC
EVENT.
34. PACEMAKER CODES:
THE INTESOCIETY COMMISSION FOR HEART DISEASE(ICHD) HAS
ESTABLISHED A 5- LETTER CODE TO DESCRIBE THE NORMAL FUNCTIONIN
OF THE PACE MAKER
35.
36. COMPLICATIONS:
1. ASYSTOLE FOLLOWING ABRUPT CESSATION OF PACING.
2. ACCELARATION OF EXISTING TACCHYCARDIABOR FIBRILLATION.
3. DISCONNECTION OF LEAD SYSTEM.
4. BREACH IN THE LEAD SYSTEM– THUS CAUSING LOSS OF CAPTURE OR
SENSING---- CAUSING FIBRILLATION--- PERICARDITIS.
37. RESEARCH:
Johns Hopkins heart researchers are unravelling the mystery of how a
modified pacemaker used to treat many patients with heart failure, known
as cardiac resynchronization therapy (CRT), is able to strengthen the heart
muscle while making it beat in a coordinated fashion.
The researchers also identified an enzyme that mimics this effect of CRT
without use of the device.
By studying isolated muscle tissue and muscle cells, they examined the
relationship between contraction and the calcium that triggers it. In the
hearts that beat out of sync, force from the muscle cells and the level of
calcium needed to generate contractions were very much reduced. CRT
improved contraction force more than calcium, and this led to the
discovery that CRT had increased the sensitivity of the muscle to calcium.
38. CONTD..
Working with heart muscle and isolated cells from the same animal
models, the researchers found that the enzyme turned out to be GSK-3
beta, which was able to convert the behavior of muscle cells from a heart
that was beating out of sync to what looked like heart cells that had
received CRT, essentially mimicking the effect of CRT.
GSK-3 beta was inactive in muscle from a failing and dyssynchronous
heart, it was reactivated by CRT. When that happened, the enzyme altered
the motor proteins so that they generated greater force using the same
amount of calcium- based activation.
Nearly all existing medications for heart failure increase heart contraction
by enhancing levels of calcium available to muscle cells, but over time,
these higher levels can be toxic to the heart.
39. RESEARCH 2:
. In a study published in 2011, Kass and colleagues also showed that CRT
enables heart muscle to respond to hormones, such as adrenaline, which
stimulates pumping ability, in a similar way to what happens during
exercise.
40. ASSIGNMENT:
“A”
TACHYDYSRHYTHMIA
DISCONNECTION OF LEAD
INTERSOCIETY COMMISSION FOR
HEART DISEASE.
ONE LEAD IN RA, RV LV
SPIKE ON ECG PRECEEDING QRS
COMPLEX
5mA
“B”
BIVENTRICULAR PACEMAKER
OUTPUT OF TEMPORARY
PACEMAKER
SVT AND VT
COMPLICATION OF PACEMAKER
PACEMAKER CODES
VENTRICULAR PACING.
TRIGGER FUNCTION
41. BIBLIOGRAPHY:
NETTINA M. SANDRA, LIPPINCOTT MANUAL OF NURSING PRACTICE, 10TH
EDITION, WOLTERS KLUWER (INDIA), PVT LTD, NEW DELHI, 2014, PG NO:
248-256.
BLACK M. JOYCE, HAWKS HOKANSON JANE, MEDICAL- SURGICAL
NURSING: CLINICAL MANAGEMENT OF POSITIVE OUTCOME, 7TH EDITION,
SAUNDERS ELSEIVER PUBLICATIONS, NEW DELHI, 2005, PG NO: 1548-
1559.
SCHEETZ LINDA, EDITOR, CRITICAL CARE NURSING SECRETS, NEW JERSEY,
MOSBY, 2006, PG NO:28-34.
JACOB ANNAMMA, EDITOR, CRITICAL CARE PROCEDURE: THE ART OF
NURSING PRACTICE, 2ND EDITION, NEW DELHI, JAYPEE BROTHERS
MEDICAL PUBLISHERS, 2010, PG NO: 381-386.
INTERNET SOURCES: www.emedicine.Medscape.com
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