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Pejcingi Zemres

The document discusses transcutaneous and transvenous cardiac pacing techniques, detailing electrode placement, pacing thresholds, and the importance of proper catheter positioning for effective pacing. It highlights the complications associated with both methods, including risks of arrhythmias, myocardial perforation, and thromboembolic events. The success rates of pacing vary based on the urgency of the situation and the patient's condition, with higher success rates observed in early intervention scenarios.

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0% found this document useful (0 votes)
13 views52 pages

Pejcingi Zemres

The document discusses transcutaneous and transvenous cardiac pacing techniques, detailing electrode placement, pacing thresholds, and the importance of proper catheter positioning for effective pacing. It highlights the complications associated with both methods, including risks of arrhythmias, myocardial perforation, and thromboembolic events. The success rates of pacing vary based on the urgency of the situation and the patient's condition, with higher success rates observed in early intervention scenarios.

Uploaded by

cwpqcnmgh2
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPT, PDF, TXT or read online on Scribd
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Pejsingu i zemres

TRANSCUTANEOUS CARDIAC
PACING
 To initiate transcutaneous pacing, the patch
electrodes are secured anteriorly and
posteriorly to the chest wall.
 For effective capture, it is essential that the
anterior chest electrode be of negative
polarity.
 Thresholds may be unobtainable or intolerably
painful if the negative electrode is placed
posteriorly.The anterior (negative) electrode
can be centered over the palpable cardiac
apex, or over the chest lead V3 position along
the left sternal border
The posterior (positive) electrode is centered at the level of the
inferior aspect of the scapula between the spine and either the
right or left scapula, but it is equally effective when positioned on
the anterior right chest
 Placement directly over the scapula or spine
may increase the pacing threshold. Before
electrode placement, the skin should be
thoroughly cleaned with alcohol to remove salt
deposits and skin debris, which contribute to
patient discomfort and/or elevate pacing
thresholds. Excessive body hair beneath the
electrode interface raises transthoracic and
impedance.
 Transcutaneous pacing generators are usually
incorporated into external defibrillator units.
These units provide up to 200mA of current
and use a rectangular or truncated exponential
pulse waveform of 20 to 40 milliseconds
duration. The long pulse widths permit the
lowest pacing thresholds while minimizing the
stimulation of skeletal muscle and cutaneous
nerves.
 In emergency bradyasystolic situations,
transcutaneous pacing should be initiated at
maximal current output to ensure ventricular
capture. Chest compressions may be performed
directly over the electrodes without disruption of
pacing or danger to medical personnel.
 Cardiac capture is suggested by the
appearance of depolarization artifacts following
the pacing stimuli, but capture must be
confirmed by palpation of a pulse
 Once capture is documented, the current may
be decreased gradually until loss of capture
defines the pacing current threshold.
 In conscious patients, transcutaneous pacing
is begun at rates slightly faster than the native
rhythm and at minimal current output. The
current is gradually increased until cardiac
capture is documented or until intolerable
discomfort develops. The final current output is
left at or slightly (5 to 10mA) above threshold
 The current output that produces
intolerable pain is highly variable among
individuals; however, the majority of
patients can be paced at manageable
levels of discomfort.
 Electrophysiologically, transcutaneous pacing
affects ventricular pacing in humans.
Retrograde activation of the atria may occur.
Intracardiac, electrocardiographic, and
pressure monitoring during transcutaneous
pacing have shown the right ventricle to be the
site of earliest myocardial activation.
Theoretically, this follows from the proximity of
the right ventricle to the anterior (negative)
electrode
 The incidence of ventricular capture with transcutaneous
pacing is greatly influenced by the setting in which it is
used.
 In healthy subjects, the ability to capture and tolerate
transcutaneous pacing is high, ranging from 50% to
100%.
 Clinically, success rates appear to be highest when
transcutaneous pacing is used prophylactically or early
(within 5 minutes) in the course of bradycardic arrests.5
In these situations, success rates may exceed 90%.5
 In emergency situations, the success of transcutaneous
pacing is lower, but ranges from 10% to 93%
A variety of causes may contribute
to failure of transcutaneous pacing.
TRANSVENOUS PACING
 The technique permits reliable atrial and/or ventricular
pacing, a feature unique to this modality.
 Once initiated,pacing is generally stable and extremely
well tolerated.
 The bipolar electrodes are most commonly used for
temporary pacing, and a variety of pacing leads are
available. These catheters are typically 3 to 6F in
diameter, use platinum-coated electrodes, and are
constructed of flexible plastic
 These leads have been used for prolonged pacing up
to 32 days and permit ambulatory temporary pacing
 Temporary pacing generators are typically
constant-current output devices.These
generators are designed to function against
loads of 300 to 1000 ohms.The stimulus pulse
width is usually 1 to 2 milliseconds.Temporary
pacing generators typically feature adjustable
rates (30 to 180 pulses per minute [ppm]),
sensitivity (0.1 mV-asynchronous), and current
output (0.1 to 20mA).
 Decisions regarding the site of venous
access for pacing should take into
consideration the urgency to initiate
pacing, desired lead stability, need to
avoid specific complications, and
anticipated duration of pacing.
 Proper catheter position is most easily
and rapidly obtained from the right
internal jugular approach.
 This site and the left subclavian route
are the sites of choice during emergencu
situations,
 Catheter stability is maximized by use of
the internal jugular or subclavian routes;
it is most problematic with peripheral
sites, especially brachial, because of
movement of the extremities.
 The peripheral routes do, however, permit greatest
control of bleeding complications and avoid
pneumothorax and inadvertent puncture of the carotid
or subclavian arteries.
 Femoral venous pacing carries the greatest risks of
thrombosis, phlebitis, and infection, thus necessitating
site changes every 24 hours.
 Temporary pacing for extended periods is best
tolerated and least complicated by using the internal
jugular or subclavian routes; however, subclavian
access may preclude immediate use of this vein for
permanent pacing if it is needed.
 Once venous access is obtained, the catheter
may be directed to the desired intracardiac
position by electrocardiographic,
echocardiographic, or, ideally, fluoroscopic
guidance.
 Optimal pacing thresholds and lead stability
are usually achieved in the right ventricular
apex and right atrial appendage.
 An external defibrillator should always be
present during catheter manipulation.
 For placement in the right ventricular
apex, non-floating catheters usually
require formation and rotation of a loop
in the atrium under fluoroscopy but may
advance directly across the tricuspid
valve by deflecting off the tricuspid
annulus
Inferior vena
cava aproach
 When fluoroscopy is unavailable or
mpractical, electrocardiographic guidance is
possible using flow-directed balloon-tipped
catheters or semirigid catheters.
 While advancing these leads, the distal
electrode is connected to lead V1 of a
standard ECG recorder.
 Balloon-tipped catheters are inflated in
the central circulation.The catheter
location is known from the characteristic
unipolar electrograms recorded in each
chamber.
 Balloon-tipped catheters are deflated
upon entry into the ventricle to avoid
displacement into the pulmonary artery.
Large ventricular
electrograms (≥6mV) with ST
segment elevation
(injury pattern) signal contact
with ventricular endocardium.
 Echocardiographic guidance of catheter
position is possible by filling the balloon of
flow-directed catheters with echogenic fluid.
 In asystole, a semi-floating catheter is
advanced during asynchronous pacing at
maximal output until ventricular capture is
documented by ECG monitoring or palpation
of a pulse. Flow-directed catheters provide the
shortest insertion times
 Once positioned, the electrodes are
connected to the pacing generator
 During emergency situations, pacing is
initiated asynchronously, at maximal
outputs. Following capture, current
output is reduced until loss of capture
defines the pacing threshold.
 During non-emergency situations, pacing is begun at
low outputs in the demand mode at rates slightly
above (10 ppm) the intrinsic heart rate. Current is
increased until capture is achieved.
 Optimal ventricular and atrial pacing thresholds are
less than 1.0mA.
 Pacemaker output is maintained at three to five times
threshold to compensate for subsequent threshold
elevations due to inflammation and edema at the
electrode-tissue interface, physiologic alterations, or
pharmacologic interventions.
Seting the sensing
 Sensing threshold in the demand mode is determined
by setting the pacemaker rate below the intrinsic heart
rate, then reducing sensitivity (increasing the value of
the millivolt scale) until pacing output occurs.
 Sensing thresholds should be greater than 6mV and
1mV for the ventricle and atrium, respectively.
 Sensitivity is maintained at 25% to 50% of the sensing
threshold.AV intervals between 100 and 200
milliseconds are usually optimal during AV sequential
pacing. Small changes in the AV interval can
significantly influence hemodynamics in some patients.
 After initiation of ventricular pacing, the
position of the catheter should be confirmed by
anteroposterior and lateral chest radiograph
and electrocardiography.
 On the anteroposterior chest radiograph, a
catheter tip in the right ventricular apex should
cross to the left of the spine near the lateral
cardiac border and point slightly inferiorly. On
lateral projections, the catheter tip should be
directed anteriorly only a few centimeters
posterior to the sternum.
 Electrocardiographically paced QRS complexes originating from the right
ventricular apex should demonstrate left bundle branch block morphology
with a superior axis.
 A right bundle branch block pattern during temporary ventricular pacing
usually indicates coronary sinus pacing or lead perforation into the left
ventricle or pericardial space.
 Rarely, apical pacing can produce a pattern of right bundle branch block due
to preferential activation of the interventricular septum or delayed activation
of the right ventricle.
 In this situation, the QRS axis maintains a left superior orientation and the
precordial transition occurs by lead V3.
 Once it is in a satisfactory position, the
lead is sutured securely to the skin,
covered with a protective dressing, and
examined daily for infection.
 The generator is affixed to the patient or
bed with its controls shielded from
inadvertent manipulation. Threshold
testing and paced 12-lead ECGs should
be performed daily.
 For most emergency and prophylactic pacing
situations, single-chamber ventricular pacing is
preferred.
 Temporary atrial pacing is restricted to those
patients with primarily sinus node dysfunction,
absence of atrial dysrhythmias, and intact AV
nodal function, as documented by 1:1AV
conduction at rates of 125ppm.
 The instability of atrial leads and unpredictable
effects of autonomic tone and ischemia on AV
nodal conduction frequently preclude its use
 Although patients without underlying cardiac
disease usually demonstrate similar
hemodynamic responses to atrial and
ventricular pacing, the maintenance of AV
synchrony through atrial or dual-chamber
pacing is beneficial in patients with left
ventricular systolic and/or diastolic
dysfunction. In these patients,AV sequential
pacing may augment cardiac output by 20% to
30% over ventricular pacing alone,
 Initiating and sustaining myocardial capture depends
on obtaining a stable catheter position, the viability of
the paced myocardial tissue, and the electrical
integrity of the pacing system.
 With fluoroscopy, a satisfactory catheter position
should be obtainable in virtually all patients.
 The reported incidence of ventricular capture without
fluoroscopy using flow-directed or semi-floating
catheters ranges from 30% to 90%.
 Capture is least likely during emergency situations,
especially during asystole, without fluoroscopy.
 Ventricular capture is adversely affected by hypoxia,
myocardial ischemia, acidosis, alkalosis, marked
hyperglycemia, and hypercapnia.
 Electrode contact with previously infarcted or fibrotic
myocardium may also prevent capture. Pharmacologic
interventions such as administration of type Ia and Ic
antiarrhythmics, hypertonic saline, glucose and
 insulin, and mineralocorticoids may also increase
entricular capture thresholds by up to 60%.
 Conversely, thresholds may be decreased by
epinephrine, ephedrine, glucocorticoids, and
hyperkalemia.
complication
 The complications of transvenous pacing are related
to acquisition of venous access, intravascular catheter
manipulation, and maintenance of an intravascular
foreign body. In large series, the reported incidence of
clinical complications ranges from virtually zero for
prophylactic pacemaker insertion in the catheterization
laboratory42 to 20% of cases in coronary intensive
care units.
 Complications tend to be more common with brachial
or femoral pacing sites.
 Arterial trauma, air embolism, or pneumothorax may
complicate 1% to 2% of insertions.
 Significant bleeding may be seen in 4% of patients.
VT or VF induced by catheter manipulation

 One of the most common complications of temporary


pacing is the induction of ventricular tachycardia or
fibrillation. Non-sustained ventricular tachycardia is
most common during catheter manipulation (3% to
10% incidence) and is usually terminated by withdrawal
of the catheter.
 Ventricular tachyarrhythmias are more common in the
setting of myocardial ischemia, acute infarction,
hypoxia, general anesthesia, vagal stimulation, drug
toxicity, and catecholamine administration and during
coronary artery catheterization.
 Ventricular fibrillation may complicate up to 14% of
acute myocardial infarctions requiring temporary
pacemaker insertion. Supraventricular tachycardias
may result from catheter manipulation within the
atrium.
Myocardial perforation
 Myocardial perforation may complicate
temporary pacing in 2% to 20% of cases and
is probably underdiagnosed clinically.
Perforation is more common with brachial or
femoral catheters.
 Loss of pacing or sensing,changes in paced
QRS morphology, and diaphragmatic or
skeletal muscle pacing are the most common
manifestations; however, perforation to
intracardiac and extracardiac locations can be
clinically silent.
 Penetration into the myocardium may occur in
up to 30% of patients and is suggested by
ventricular arrhythmias with the same
morphology as paced complexes.
 Perforation of the interventricular septum is
usually hemodynamically inconsequential;
however, extracardiac migration of the
catheter can produce pericardial tamponade in
approximately 1% of perforations.
 Pericarditis may be seen in 5% of patients
with perforated temporary pacing catheters.
 In the absence of hemodynamically significant
pericardial effusion, myocardial perforation is
managed by catheter withdrawal until effective
capture is restored.
 Careful patient monitoring follows.
 Unipolar electrograms recorded from the
catheter tip will demonstrate a pathognomonic
transition from R wave to S wave morphology
with ST elevation upon withdrawal from
extracardiac to intracardiac locations, thereby
confirming the diagnosis.
Thromboembolic events
 Thromboembolic events from temporary pacing appear
to be more frequent than are clinically
recognized.Venograms or ultrasound in patients with
femoral pacing catheters reveal evidence of femoral
venous thrombosis in up to 39% of the patients despite
their receiving subcutaneous or systemic heparin.
 Of the patients with thrombosis, 60% may have
evidence of pulmonary emboli on ventilation perfusion
scans.
 Thrombosis is rarely suspected clinically.
 The incidence of thrombosis with other pacing sites has
not been systematically studied. Systemic
anticoagulation with femoral pacing may reduce but
does not eliminate venous thrombosis
Setting the pacemaker
 Set to 70/min or 10/min above patient’s ventricular
rate.
 Set a pulse of 3V (or follow manufacturer’s
instructions); at this voltage should capture ventricle
so that each pacing spike is followed by a QRS
complex. Determine voltage threshold by gradually
turning down voltage until capture is lost (usually 0.7-
1.0V) and usually set pacemaker to deliver pulse of at
least twice threshold.
 Check sensing by setting pacemaker rate at 10-20/min
<spontaneous ventricular rate and check ECG and
pulse generator for pacing inhibition.
 Normally set sensitivity to maximum.
Setting the pacemaker
 Common problems:
 No spikes seen and no output: usually due
to failure of battery or generator or loose
connection. Otherwise, oversensing cured
by reducing sensitivity or going to fixed rate
pacing.
 Spikes seen but no capture: often a loose
connection but may be due to exit block
causing a high threshold. Check position of
pacing wire and consider repositioning.
Inserting pacing wire

 Preparation:
 Ensure that a defibrillator and other
resuscitation equipment are immediately
accessible.
 The procedure requires strict aseptic

technique, using a mask, gown and gloves.


 ECG monitoring is required but the ECG leads

should be off the chest


Inserting pacing wire

 Cannulate right subclavian, right internal


jugular or right femoral vein using
Seldinger technique of guidewire and
dilators to place sheath of correct size to
allow passage of pacing wire.
 Mould the tip of the electrode to give a
20-30° curve for correct positioning in
the heart..
Inserting pacing wire
 Advance electrode under ultrasound or
fluoroscopic guidance until it lies vertically in
the right atrium with its tip pointing towards the
free wall on the right side.
 Rotate wire between index finger and thumb
such that it points towards the patient’s left
side, advance wire steadily through the
tricuspid valve and along the floor of the right
ventricle to the apex
Inserting pacing wire
 Common problems:
 Wire does not cross the tricuspid valve: continue advancing
wire into right atrium until it catches on the wall and forms a
large loop. If it passes into the IVC or SVC, pull back and
push forward again until it does catch. With large loop in
place, rotate wire until its tip flips through into the ventricle.
 A wire appears to be in correct position but will not capture
ventricle at acceptable output: fluoroscopy shows electrode
tip is directed upwards towards left shoulder and directed
posteriorly rather than anteriorly.
 Cannot obtain satisfactory pacing, withdraw wire into right
atrium and repeat attempt to cross tricuspid valve.
 Difficulty in positioning wire at apex of right ventricle: pass tip
of wire into right ventricular outflow tract and gently withdraw
while rotating between index finger and thumb. When tip is at
a downwards angle, advance towards apex.

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