2019 Flashcards

1
Q

Conclusions for the article “Echocardiographic phenotype of canine
dilated cardiomyopathy differs based on
diet type”

A

Dietary-associated DCM occurs with some GF diets and can improve with nutritional management, including diet change. The role of taurine supplementation, even without deficiency, is uncertain.

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2
Q

Diferentials diagnosis for DCM phenotipe

A

can result from numerous etiologies including genetic mutations, infections, toxins, and nutritional
imbalances

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3
Q

Echocardiographic phenotype of canine
dilated cardiomyopathy differs based on
diet type CONCLUSIONS

A

Dietary-associated DCM occurs with some GF diets and can improve with nutritional management, including diet change. The role of taurine supplementation, even without deficiency, is uncertain

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4
Q

DCM predisposition

A

Dogs, male, large-breed dogs with certain breed predilections including Doberman Pinschers, Great Danes, and Irish Wolf- hounds

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5
Q

The hallmark findings of DCM

A

Ventricular dilation and impaired contractility in the absence of primary valvular or vascular diseases

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6
Q

Nutritional causes of DCM

A

Taurina and carnitina

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7
Q

Nutrient toxicities associated with DCM

A

Iron and cobalt

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8
Q
Conclusions: Association between atrial fibrillation and
right-sided manifestations of congestive
heart failure in dogs with degenerative
mitral valve disease or dilated
cardiomyopathy
A

Dogs with AF are more likely to manifest R-CHF than dogs without AF.
Cavitary effusions are an expected finding in approximately three-quarters of dogs
with AF and CHF secondary to either DCM or DMVD

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9
Q

The strongest predictor of R-CHF

A

AF

Atrial fibrillation and right-sided congestive heart failure

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10
Q

Conditions associated with R-CHF in the article “Atrial fibrillation and right-sided congestive heart failure”

A

The presence of AF, diagnosis of DCM, and moderate
to severe tricuspid regurgitation were associated with R-CHF in multivariate analysis
(Atrial fibrillation and right-sided congestive heart failure)

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11
Q

The most common underlying

heart diseases associated with AF

A

dilated cardiomyopathy (DCM) and degenerative
mitral valve disease (DMVD). These diseases lead to both structural and electrical
remodeling of the atria that provide a profibrillatory substrate for initiation and propagation
of AF
(Atrial fibrillation and right-sided congestive heart failure)

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12
Q

Hemodynamic consequences of AF

A

Decreased diastolic filling time and loss of
atrial contraction, both of which result in
decreased cardiac output and increased atrial
filling pressures. Because of these negative hemodynamic effects, onset of AF in patients
with underlying structural heart disease is often
accompanied by cardiac decompensation and
congestive heart failure (CHF).
(Atrial fibrillation and right-sided congestive heart failure)

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13
Q

Proportions of dogs with AF that have CHF

A

63% - 100% of dogs with AF have concurrent
CHF
(Atrial fibrillation and right-sided congestive heart failure)

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14
Q

What is predominant in the case of DCM? R or L CHF?

A

L-CHF

Atrial fibrillation and right-sided congestive heart failure

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15
Q

Variables predictive of AF and R-CHF

A

The only variables that remained significantly associated with AF in multivariate analysis were heart rate and body weight
(Atrial fibrillation and right-sided congestive heart failure)

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16
Q

variables were significantly associated with R-CHF in univariate logistic regression

A

Variables that remained significant in multivariate analysis were presence of AF, diagnosis of DCM, and moderate-to-severe TR
(Atrial fibrillation and right-sided congestive heart failure)

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17
Q

DMVD dogs differed from DCM dogs in number of clinical and echocardiographic variables that reflect the distinct signalment and pathophysiology associated with each heart disease….

A

Compared with dogs with DMVD, dogs with
DCM were younger, larger, and more likely to be
male; had higher heart rates and more ventricular
arrhythmias; and demonstrated less dramatic LA
dilation.
(Atrial fibrillation and right-sided congestive heart failure)

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18
Q

Why R-CHF is most frequently in case of AF than L_CHF?

A

a possible explanation for increased prevalence of
R-CHF in dogs with AF and left-sided structural
heart disease is that AF causes an acute increase in
RA pressure that is more hemodynamically significant than the pressure increase within an
already volume overloaded and dilated LA. It is theoretically possible that at
extremely high heart rates, LA pressure quickly
rises to critical levels; whereas at the more modest
tachycardia typical of AF (mean 218 beats per
minute in this study), the effects on RA pressure
are more clinically relevant.
(Atrial fibrillation and right-sided congestive heart failure)

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19
Q

Clinical and echocardiographic variables predictive of AF

A

AF was more common in dogs with DCM than those with DMVD.
Within disease subgroups, dogs with AF had higher body weight than dogs without AF.
the only significant predictors
of AF in multivariate analysis were higher body
weight and higher heart rate. It is not surprising
that dogs with AF had higher heart rates than those
with underlying sinus rhythm, reflecting the
pathologically elevated heart rates associated
with this tachyarrhythmia.
(Atrial fibrillation and right-sided congestive heart failure)

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20
Q

Conclusions: Anatomical anomalies and variations of
main thoracic vessels in dogs: a computed
tomography study

A

Major anatomical variations or anomalies of the main great thoracic
vessels in dogs without congenital cardiac disease were rare. An aberrant retroesophageal right subclavian artery was the most common anomaly found. Three slight
variations of common carotid artery branching were identified. These findings
might be of relevance for surgical or catheterization procedures.

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21
Q

The main great thoracic vessels in dogs

A

ascending aorta, the aortic arch and the
descending aorta, the brachiocephalic trunk, subclavian arteries and veins, common carotid arteries, internal thoracic arteries and veins, axillary
artery and vein, superficial cervical artery and
vein, vertebral arteries and veins, the costocervical trunk, pulmonary arteries and veins, the
cranial vena cava and the post-hepatic caudal
vena cava and azygos veins

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22
Q

Clasification of arterial and venous vascular anomalies

A

Sistemic, pulmonary or coronary

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23
Q

the most important vascular

malformation in veterinary medicine

A

PDA

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24
Q

Concept: Vascular

anomalies

A

Vascular anomalies are considered those that may be associated with clinical symptoms.

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25
Q

Concept: anatomical variations

A

those alterations which do not lead to symptoms

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26
Q

The most

frequently reported anatomical variations of the venous vasculature

A

the presence of a persistent

left cranial vena cava (PLCVC)

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27
Q

The two configurations of left cranial vena cava

described in dogs

A

complete (where the
PLCVC receives blood from veins cranial to the
heart) or incomplete PLCVC (where the proximal
portion of the PLCVC receives a vein which drains
from the left costocervicalevertebral trunk)

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28
Q

The technique for vascular evaluation

A

CT

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29
Q

Description of the aberrant right subclavian artery

A

In all ARSA cases, the right subclavian artery branched
directly from the aortic arch and passed dorsally
to the oesophagus, forming an incomplete vascular ring around the oesophagus.

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30
Q

Predisposition for ARSA

A

No association
was identified between the presence of ARSA and
sex, brachycephalic breed or weight groups

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31
Q

Most comun Type of carotid artery branching

A

Type I

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32
Q

Retro-oesophageal right subclavian

artery

A

An ARSA, the right subclavian artery arises directly from the aortic arch and passes dorsal to the oesophagus. This forms an incomplete vascular ring
anomaly, where the oesophagus was mildly compressed between the vessel dorsally and the trachea ventrally, but it is not enough to cause clinical signs such as obstruction or dysphagia

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33
Q

Dysphagia lusoria

A

Dysphagia secondary to extrinsic esophageal compression by an aberrant right subclavian artery

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34
Q

Predisposition PLCVC

A

Shih Tzus and one Pekingese , and dogs under 10 kg and 5 kg

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35
Q

There is association of carotid anatomy type and different breed morphotype (brachycephalic versus non-brachycephalic breeds) ?

A

No showed (Asymptomatic vascular anomalies in dogs)

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36
Q
Conclusions: Quantitative assessment of two- and
three-dimensional transthoracic and
two-dimensional transesophageal
echocardiography, computed
tomography, and magnetic resonance
imaging in normal canine hearts
A

Measurements of LV, RV, and RA volumes via 3D TTE and LA volume and
LV EF assessed by CTA compared best with CMR. Three-dimensional echocardiography had lower interrater and intrarater CV compared with 2D TTE.

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37
Q
Results: Quantitative assessment of two- and
three-dimensional transthoracic and
two-dimensional transesophageal
echocardiography, computed
tomography, and magnetic resonance
imaging in normal canine hearts
A

No clinically relevant differences in LV volume were detected between CMR
and all modalities. Importantly, 3D TTE had the lowest CV (6.45%), correlated with
(rs ¼ 0.62, p ¼ 0.01), and had the highest overlap in distribution with CMR (OVL >80%). Left ventricular EF and LA size via CTA compared best with CMR and RV and RA
volumes were best estimated by 3D TTE. Assessment of LV and LA volumes via 3D
TTE had moderate repeatability (15e21%) compared with LV M-mode measurements
and 2D LA-to-aortic ratio (<10%), respectively. For LV size, interrater CV for 3D
TTE (19.4%) was lower than 2D TTE (23.1%).

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38
Q

Number of specialized SAN conduction pathways that preferentially conduct electrical activation to atrial tissues

A

5

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39
Q

Measure of the sino atrial node in dogs

A

11-29 mm long and 2-5 mm wide

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40
Q

Intrinsic HR in the Sino Atrial Node in dogs

A

60-140 bpm

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41
Q

Localization of the ‘leading pacemaker’ site, or the first site of SAN activation

A

the central part of the SAN

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42
Q

Factors afected sino atrail node conduction

A

sympathetic and parasympathetic agonists, antiarrhythmic drugs, and naturally occurring metabolites including adenosine

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43
Q

The most common rhythm disturbances that

require pacing to either alleviate clinical signs or prolong survival

A

Advanced second-degree and third-degree atrioventricular blocks, sick sinus syndrome, persistent atrial standstill, and vasovagal syncope

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44
Q

the pathogen that most commonly

causes acute myocarditis and AVB in dogs

A

enteric coronavirus

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45
Q

gold standard for in vivo diagnosis of myocarditis

A

Endoiocardial biopsie and increased serum concentrations of cTnI and cardiac troponin T are considered reliable to confirm the diagnosis

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46
Q

Patogens described as cause of myocarditis in cats

A

Toxoplasma gondii , Bartonella henselae , Streptococcus canis , and Borrelia burgdorferi

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47
Q

The occurrence of sudden cardiac

death among the population of dogs with AVB

A

42.7 %

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48
Q

the occurrence of sudden death in dogs with second and third-degree AVB

A

40.6% and 32.8%, respectively. From the diagnosis, 24% of dogs die within 30 days and 40% of dogs die within six months

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49
Q

association between age and sudden death

A

no demostrated in veterinary

50
Q

AVB and prognosis with drugs treatment

A

On the other hand, a
negative association between terbutaline or
methylxanthine administration (or both) and
duration of survival has been reported

51
Q

alterations of the SA node in case of SSS

A

These changes include total or subtotal destruction of the SA node, areas of nodalatrial discontinuity, inflammatory or degenerative
changes in the nerves and ganglias surrounding the
SA node, and pathological changes in the atrial
wall

52
Q

The molecular basis for some forms of congenital SSS

A

a recessive disorder of a human heart voltage-gated sodium channel

53
Q

Predisposition for dogs dogs

affected by SSS/SND

A

older, females are overrepresented, and Miniature schnauzers, West
Highland white terriers, and Cocker spaniels are
considered predisposed breeds

54
Q

The cardiopathologic findings observed in elderly dogs with myxomatous mitral valve disease in the sinus node (can predisposes to SSS)

A

significant changes, such as extensive
damage of the SA node with depletion of the nodal
cells and increase of fibrous or fibro-fatty tissue,
interrupted contiguity between the SA node and
the surrounding atrial myocardium, and interstitial
fibrosis of the left and right atrial walls

55
Q

Prognosis in dogs with SSS and PM

A

In agreement with human medicine data, there
is no evidence that cardiac pacing prolongs survival
in dogs with sinus node disease. In one study,
survival times did not differ between symptomatic
and asymptomatic dogs or between dogs that
received PM implantation and dogs that were
medically treated (theophylline, propantheline,
hyoscyamine, terbutaline)

56
Q

Cause of death in dogs with SSS

A

In dogs, the most
common cause of death in the SSS population is
euthanasia for non-cardiacerelated disease, even
though several reported non-cardiacerelated
causes could have been exacerbated by low cardiac output, causing poor peripheral perfusion

57
Q

Prognosis in case of SSS

A

The prognosis of SSS in dogs is usually good, although development of congestive heart failure does not appear to be mitigated by PM implantation

58
Q

Causes of perssitent atrial standstill

A

PAS has been described to occur in conjunction with a number of muscular dystrophy disorders and with amyloidosis and myocarditis . In dogs, although neuromuscular disease, long-standing cardiac disease, and myocarditis have been proposed as cause of PAS, this rhythm disturbance is generally attributed to atrial myopathy.

59
Q

Atrial myopathy

A

Atrial myopathy is characterized by progressive loss of atrial myocardium, with loss of the ability to conduct
impulses, histological findings of myocardial necrosis, infiltration of inflammatory cells, and
replacement fibrosis. Both the atrial myocardium
and the conduction system are affected

60
Q

causes of temporary atrial standstill

A

can be secondary to digitalis toxicity, quinidine toxicity,
myocardial infarction, hyperkalemia, hypoxia, and
hypothermia

61
Q

Breeds predisposes to PAS

A

most commonly been reported in English springer spaniels and Labrador retrievers

62
Q

Prognosis in cases of PAs

A

It has been initially suggested that dogs with PAS
have a poor prognosis, despite PM implantation. The median survival time of PAS
dogs was reported to be approximately 28 months
after pacing, indicating that these animals can be
expected to survive a similar amount of time to
dogs affects by other bradyarrhythmias .
However, of the dogs with PAS that died, 64% suffered a cardiac-related death , which appears
to be a relatively high incidence compared with
other bradyarrhythmias, where it varies from 22%
to 60% . Despite the high incidence of
cardiac-related death in PAS dogs, no difference in
survival times was noted between cardiac and noncardiac causes of death

63
Q

causes of intermittent symptomatic

bradyarrhythmias

A

intermittent/paroxysmal AVB, some forms of SND, such as tachycardiaebradycardia syndrome, and disturbance ofthe autonomic nervous system, such as vasovagal
sinus arrest or AVB

64
Q

Clinical presentation of AVB

A

The most commonly reported clinical sign is transient loss of consciousness, which occurs in 23%e77% of dogs, followed by weakness and exercise intolerance (14%e
48%), lethargy (23%e26%), vomiting and diarrhea
(11%e23%), and signs of congestive heart failure
(3%e10%). In about 4% of cases, no clinical signs
are reported. Congestive heart failure
signs, such as ascites or pulmonary edema, can be
present due to several myocardial changes induced
during sustained abnormal AV activation and
decreased heart rate

65
Q

third-degree AVB in cats

A

Clinical signs are present in the majority of cats
with third-degree AVB, although around one-third
of cats with third-degree AVB had their arrhythmia
diagnosed as an incidental finding . If present,
clinical signs are consistent with transient loss of
consciousness or related to congestive heart
failure.

66
Q

In Human in the case of 2º AVB, when it is assumed that the site of conduction failure is above the bifurcation of the bundle of His?

A

second-degree AVB with normal QRS duration, and it is

defined as type A.

67
Q

type B second-degree AVB

A

When there is a wide QRS complex and the
site of block is assumed to be below the bundle
branch bifurcation.

68
Q

When the second-degree AVB is named

advanced

A

When more than one P wave are block

69
Q

When we have a trifascicular block

A

Trifascicular block occurs
when the right and left bundle branches are
alternately interrupted due to infranodal disease
or when a bifascicular block accompanies a nodal
block with evidence of AV conduction disturbance

70
Q

Diagnosis of persistent atrail standstil

A

Electrocardiographic findings of PAS are absent
P waves and idioventricular escape rhythm with
normal serum potassium concentration

71
Q

survival times after PM implantation in case of PAS

A

it appears that dogs with PAS have similar survival

times than in cases of other bradiarrhythmias

72
Q

In human, contraindication for singlechamber atrial pacing

A

A Wenckebach point of <120 beats per minute in

humans is considered a contraindication for singlechamber atrial pacing

73
Q

contraindications to physiologic VDD PMs

A

dogs that present an atrial rate <70 beats per
minute and a negative atropine response test
(<25% increase of sinus rate 20e30 min post
0.04 mg/kg atropine SQ injection). Other contraindications to
physiologic VDD PMs are represented by AVB complicated by AF or supraventricular tachycardia.

74
Q

statistically significant benefit in
survival times in dogs that received a physiologic
VDD PM compared with dogs that received a nonphysiologic VVI PM

A

recent retrospective study
demonstrated no statistically significant benefit in
survival times in dogs that received a physiologic
VDD PM compared with dogs that received a nonphysiologic VVI PM

75
Q

PM. Pacing thresholds

A

Pacing thresholds have been shown to be lower
in the acute setting, and chronic pacing thresholds
typically rise over time.

76
Q

The conductor wires are an alloy of

A

nickel, cobalt, chromium, and molybdenum. MP-35N (SPS

Technologies, Cleveland)

77
Q

Hoe appeared abrasion the abrasion of the insulation material, exposing the conductors, and cause lead failure

A

with a low lead impedance measurement

(short circuit) during pacemaker interrogation

78
Q

Electrode tips materials

A
  Platinum iridium
  Elgiloy e cobalt, iron, chromium, molybdenum,
nickel, and manganese
  Platinized platinum e platinum coated with
platinized titanium
  Vitreous or pyrolytic carbon
  Titanium
  Titanium oxide
  Iridium oxideecoated titanium
  Titanium nitride
79
Q

The design of actual pacemakers

A

incorporates a
sensing circuit, a logic circuit, and an output circuit,
with the ability to communicate with a pacemaker
programmer and a remote-monitoring device

80
Q

The output circuit of the pacemaker

A

consists of two basic factors: voltage and duration. The former is the programmed voltage, and the latter is the pulse width of the delivered pacing pulse.

81
Q

The

largest component of the output circuit in the PM

A

The battery

82
Q

The battery longevity can roughly be calculated

A
Usable battery capacity   1.2 amp hours.
Pacer current drain   20 microamps.
Hours in 1 year   8760.
[1,200,000 microamps (hrs)]/20
microamps   60,000 h.
60,000 h/8760   6.849 years.
The energy delivered plays a significant role in
longevity. The energy equation is
(E   V2   t)/R.
where V   output voltage, t   pulse width of
pacing pulse, and R   resistance. The energy (E)
delivered is expressed in micro Joules.
83
Q

Some PM devices begin to turn off certain

functions when appeared the replacement indicator or elective replacement time

A

rate response and automatic threshold

testing

84
Q

Historically, non-MRI conditional

devices would be contraindicated for scanning.

A

However, several studies have shown that
patients with these devices can safely have an MRI
(non-thoracic) at 1.5 T

85
Q

Devices are typically labeled as Magnetic resonance
imaging (MRI) compatible, conditional, or
non-MRI conditional.

A

Devices labeled as compatible
are safe for whole-body scans without regard
to the patient positioning. Devices labeled as
conditional are safe for scans with proper programming
and generally not for scanning the
implant area. Typically, the recommendation is for
scans at 1.5 T or less.

86
Q

leads problems

A

conductor
wires can break, and insulation can
degrade, exposing the conductors. Tying
down the suture sleeve on the lead too tight can
cause a crush phenomenon, damaging the conductor
wires and causing the lead to fail.

87
Q

sutures used for securing the lead wires to the

fascia

A

are non-absorbable 2-0 Ticron or 2-0 Silk

88
Q

Consequences of damaging the insulation at the implant

A

it can expose the
conductor wire, causing a short circuit. This results
in very low impedance values and can cause rapid
battery depletion because of a damaged lead.

89
Q

Consecuences of not tightening the setscrew enough

A

will cause high impedance (open circuit) and loss

of pacing

90
Q

External defibrillation in the case of PM

A

External defibrillation is generally safe, and the
pads (or paddles) should be placed as far away
from the device as possible but still give a good
vector for defibrillation. Energy from the external
defibrillator can be coupled into the device,
causing major component failure. Sometimes, this
results in a reset (or backup) mode within the
pacemaker which can generally be reset with the
programmer, and other times, it can be a terminal
condition resulting in no output.

91
Q

Pacemaker parameters

A

Setting of output parameters (pulse amplitude
and pulse width)
  Sensitivity parameter settings
  Impedance (component and system including
patient interface)

92
Q

Ohm’s law

A

V  = IR.where
V   the voltage or the force which drives the
current
I   the current, described as the flow of electrons
past a certain point measured in
milliamperes
R   the resistance (impedance) or opposition to
flow of electrical current expressed in Ohms (U).

93
Q

Relationship between impedance and current

A

Impedance and current have an inverse relationship.

94
Q

Resistance versus impedance

A

Resistance and impedance are both expressed in Ohms;
however, the two differ in that resistance is the
opposition to current flow in a direct current circuit,
whereas impedance describes the resistance
to current flow in an alternating current circuit.
The terms are often used interchangeably when
describing current flow in pacing circuits

95
Q

Range of normal impedance values

A

Impedance values typically range from 300 to

1200 U.

96
Q

Impedance of <200 U

A

A low impedance measurement (<200 U) indicates

a short circuit, usually from an insulation breach.

97
Q

Impedance >2000 U

A

An unusually high impedance measurement
(>2,000 U) indicates an open circuit, typically
caused by a conductor fracture.

98
Q

The capture threshold

A
is the minimum
amount of energy delivered by the device to
consistently depolarize (capture) the myocardium.
99
Q

The capture threshold increased or decreased with the time

A

Thresholds are typically low at the initial implant
and generally rise over time as the leads become
chronic [18]. Typically, the output voltage to the
lead(s) can be decreased to twice the pacing
threshold 90 days after implant. At this point, the
leads are generally considered to be chronic.

100
Q

Acceptable pacing thresholds for canines

A

Acceptable pacing thresholds for canines are
<1.5 V for an acute implant and <2.5 V for a
chronically implanted system.

101
Q

the capture safety margin or

threshold safety margin

A

A generally accepted
tenet is that the device should be programmed
to twice the pacing threshold.

102
Q

Loss of capture

A

Loss of capture occurs
when the output pulse from the pacemaker is of
insufficient amplitude to capture the heart (loss of
capture)

103
Q

the output parameters

A

pulse amplitude and pulse width

104
Q

The strength-duration curve

A

The strength-duration curve is particularly
useful because the chronaxie shows the combination
of pulse width and pulse amplitude (voltage
and duration) that uses the least energy to reliably
capture the heart.

105
Q

Rheobase

A

The lowest voltage threshold at an infinitely wide pulse width

106
Q

Chronaxie Point

A

The width point a twice the rheobase

107
Q

Sensing (PM)

A

Sensing refers to the capability of the device to

detect intrinsic cardiac activity

108
Q

Unipolar sensing

A

Unipolar sensing refers to the use
of the pacemaker itself and the tip of the pacing lead as the antenna for sensing. This results in a
larger signal and is more likely to sense myopotentials
and could possibly cause oversensing. The
possibility of pacemaker inhibition to the sensing
of extraneous signals is more likely in a unipolar
sensing circuit.

109
Q

bipolar sensing circuit

A

A bipolar sensing circuit uses a
much smaller antenna than the unipolar because the anode and cathode are incorporated into pacing lead and is less likely to oversense extraneous signals. The
height, or amplitude, of the smaller signal is then
amplified and measured by the device.

110
Q

Sensing program in the PM

A

An acceptable intrinsicmeasured atrial signal is>1mV,
whereas an acceptable measured ventricular signal
would be>10mVfor the typical canine implant. The
typical safety margin is 2:1. For example, an atrial
signal of 1 mV would require the atrial sensitivity to
be programmed to .5 mV. In contrast to the pacing
threshold which is two times the capture thresholds,
the sensing circuit is just the opposite. A smaller
value is programmed to make the device more sensitive.
In this case, the sensitivity should be programmed
to at least themeasured intrinsic signal.

111
Q

Pacing modes. Chamber I

A

It indicates the chamber (or
chambers) paced. If only one chamber is paced,
the designation would be either A or V, and if both chambers are paced, the designation would be D.
O indicates that no chamber is paced. A manufacturer
code of ‘S’ in this position indicates single
chamber is paced (atrial or ventricular).

112
Q

Pacing modes. Chamber II

A

Position II indicates the chamber (or chambers)
sensed. If only one chamber is sensed, the designation
would be A or V, and if both chambers are
sensed, the designation would be D. O indicates
that no chamber is sensed. A manufacturer code of
‘S’ in this position indicates that single chamber is
sensed (atrial or ventricular).

113
Q

Pacing modes. Chamber III

A

Position III indicates
the mode of response to sensing. Triggered means
the device will pace when an intrinsic signal is
sensed. Inhibit means the pacing output will be
withheld when an intrinsic signal is sensed. D indicates
that the device can both trigger and inhibit in
response to intrinsic signals. O indicates that there
is no response (neither triggered nor inhibited) to
sensed intrinsic signals. Essentially, this is committed
pacing.

114
Q

Pacing modes. Chamber IV

A

Position IV indicates other programmable
functions of the device. Rate modulation
allows the device to change its pacing rate based on
physiologic need such as increased activity. Communicating indicates that the device can transmit
and receive information regarding diagnostics or
programming. Multiprogrammable means that
greater than three parameters are programmable.
All pacemakers today are multiprogrammable. P
indicates simple programmable, limiting the functions
to three or less. It would be rare to see any of
these types of devices in operation today.

115
Q

Pacing modes. Chamber V

A

Position V is reserved for antitachycardia functions. This
would indicate that the device can rapidly pace a
tachycardic rhythm, shock a tachycardic rhythm, or
both. Most cardiac defibrillators utilize the ‘D’
designation in this position.

116
Q

How work Dual chamber systems

A

Dual chamber systems with a single lead that
allows for atrial synchronous ventricular-inhibited
pacing use one pacing lead that incorporates both
a pacing electrode within the right ventricle and a
floating atrial electrode within the intra-atrial
portion of the ventricular lead to sense P waves
propagated through the blood. These
native P waves are sensed by the pacemaker, and
then after an appropriately programmed atrioventricular
delay, the system delivers a ventricular
pacing impulse.

117
Q

Testing the pacemaker lead

A

These parameters include sensed P wave
amplitude (if implanting an RA lead), sensed R
wave amplitude (for ventricular leads), current of
injury, lead impedance, and threshold testing.

118
Q

Sense P wave

A

In our experience, most
leads within the right auricular appendage or RA
septum sense P waves that are between 3 and
3.5 mV.

119
Q

Sense R wave

A

Generally, an appropriately
placed RVA pacing lead will measure/sense
an R wave that is at least 10 mV (and usually
higher). With RV septal/groove placement of
leads, the R wave amplitude will be much smaller
than that with RVA leads. Acceptable R wave
amplitude in these locations is 4e5 mV because of
the perpendicular alignment of the dipoles and
also because there is less muscle and vector in this
plane.

120
Q

LV leads sensing

A

LV leads will generally sense larger amplitude
R waves than RVA leads. In our population of
dogs with implanted LV leads that were stable long
term, we have seen R wave amplitudes of
15e20 mV

121
Q

ST segment elevation on the intracardiac

electrogram during PM implantation

A

Both passive- and active-fixation leads are initially
traumatic to the myocardium when implanted
and can temporarily cause increased pacing
threshold. The magnitude of this current of injury
can be assessed with a PSA and is characterized as
prolongation of the atrial or ventricular depolarization
and ST segment elevation on the intracardiac
electrogram

122
Q

The current of injury

A

The current of injury indicated by an increase in the duration of the intracardiac electrogram (msec) and
the magnitude of ST segment elevation (mV) can be used to assess the adequacy of active-fixation at the time of lead
implantation.