Kursk State Medical University

Department of Propaedeutics of
Internal Diseases

Arrhythmias
Arrhythmias
Definition: A disorder of heart beat (disturbance of
rate, rhythm or both) - derangement of hearts
conduction system, not of heart structure
Analization: ECG wave forms
Named according to site of origin of impulse and
mechanism of conduction involved
4 possible sites of arrhythmias origin

Ex: arrhythmia originated in SA node & slow in rate
sinus bradycardia
Properties of cardiac muscle

Automaticity - generation of impulses
Excitability - ability of a myocardial cell to
respond to a stimulus
Conductivity - ability of the muscle to
move an impulse from cell to cell
Contractility - muscle contraction with
stimulation
Norm: impulses originated in SA node
hearts pacemaker
Arrhythmia from SA node
Sinus bradycardia:
vagus stimulation, digitalis intoxication,
increased intracranial pressure, myocardial
infarction, in highly trained athletes, in severe
pain, on medication (propranolol, reserpine,
methyldopa), in hypoendocrine states
(myxedema, Addisons disease,
panhypopituitarism), anorexia nervosa,
hypothermia, surgical damage to SA node
Sinus bradycardia

Rate: 40-60 beats per minute
P waves: Precede each QRS complex; PR interval
normal
QRS complex: Usually normal
Conduction: Usually normal
Rhythm: Regular
Sinus tachycardia:
fever, acute blood loss, anemia, shock,
exercise, congestive heart failure, pain,
hypermetabolic states, anxiety,
sympathomimetic or parasympatholytic
drugs
Sinus tachycardia

Rate: 100 - 180 beats per minute
P waves: Precede each QRS complex; may be buried
in the preceding T wave; PR interval normal
QRS complex: Usually normal
Conduction: Usually normal
Rhythm: Regular

Sinus arrhythmia
Variations of vagus tone (respiratory
arrhythmia)
in children, adolescents (juvenile)
Reconvalescents from infections
CNS diseases
Irregular pulse & cardiac rate
ECG: varying RR intervals
Ectopic arrhythmias

Premature atrial contractions
(atrial extrasystole):
caffeine, alcohol, nicotine, stretched atrial
myocardium, stress or anxiety,
hypokalemia, atrial ischemia, injury,
infarction or hypermetabolic states
Mechanism: a) increased myocardium
excitability
b) re-entry
Ventricular extrasystole
Patient with extrasystole can feel their heart missing a beat ( escape
beat ) and a subsequent strong stroke
Auscultation reveals its premature contraction with a specific loud 1
st

sound ( small diastolic filling of ventricles )
Extrasystoles can be easily revealed by feeling the pulse : a
premature weaker pulse wave and a subsequent long pause a
characteristic
If extrasystoles follows immediately a regular contraction, the left
ventricle may be filled with blood very poorly and the pressure inside
it may be so small that the aortic valve would not open during the
extrasystolic contraction and blood will not be ejected into the aorta
The pulse wave on the radial artery will not be then detectable (
missing pulse )
Premature atrial contraction

Rate: 60 - 100 beats per minute
P waves: Usually different from normal P waves. PR interval varies
from the PR intervals of impulses originating in the SA node.
QRS complex: normal
Rhythm: Regular, except when the PACs occur.
PQRS - early in the cycle
Not complete compensatory pause (< 2 RR intervals)
Atrial extrasystole
Frequent in normal hearts (after heavy smoking,
strong tea / coffe), hormonal disoders
(thyrotoxicosis, menopause), intoxications,
electrolyte metabolism disorders
Complaints: the heart skipped a beat, missing
a beat (escape) with a subsequent strong
stroke.
Irregular Pulse( weak wave subsequent strong
stroke). Pulse deficit may exist.
Loud F1
Paroxysmal atrial tachycardia
Paroxysmal atrial tachycardia (PAT) is characterized by
abrupt onset and abrupt cessation.
It may be triggered by emotion, tobacco, caffeine,
fatigue, sympathomimetic drugs, or alcohol.
Paroxysmal atrial tachycardia is not usually associated
with organic heart disease.
The rapid rate may produce angina due to decreased
coronary artery filling. Cardiac output is reduced and
heart failure may occur. The patient frequently does not
tolerate this rhythm for long periods.
Characteristics of paroxysmal
atrial tachycardia:
ECG of Paroxysmal atrial tachycardia

Rate: 150 to 250 beats per minute
P waves: Ectopic and distorted as compared with normal P wave; may be
found in preceding T wave; PR interval shortened (less than 0.12 sec)
QRS complex: Usually normal, but may be distorted if aberrant conduction is
present
Conduction: Usually normal
Rhythm: Regular


The patient may not be aware of PAT.
Clinical picture
Strong palpitation, discomfort in the chest, weakness
Skin turns pale and cyanosis if attack persist
Swelling and pulsation of neck veins due to atria
contraction before ventricular systole ends which causes
ejection of blood back to the vein
Auscultation reveals decrease diastolic pause, whose
length near that of systolic one and the heart rhythm
become foetal/pendulum
Pulse is rhythmic, very fast and small
Arterial pressure may fall
Symptoms of cardiac insufficiency if an attacks persists

Atrial flutter
Atrial flutter occurs when an atrial focus captured
the heart rhythm and discharges impulses at a
rate between 250 and 400 time per minute.
An important characteristic of the dysrhythmia is
that a therapeutic block occurs at the AV node,
which prevents some impulse transmission.
Conduction of the impulse through the heart is
otherwise normal, so the QRS complex is
unaffected.
This is an important feature of this dysrhythmia,
as the 1:1 conduction of atrial impulses firing at
250 to 400 times per minute would result in
ventricular fibrillation, a life threatening
dysrhythmia.
Characteristics of atrial flutter:
ECG of atrial flutter

Rate: Atrial rate between 250 and 400 beats per minute
Rhythm: Regular or irregular, depending on kind of block (e.g.
2:1, 3:1 or a combination)
P wave: Not present, instead it is replaced by a saw-toothed
pattern that is produced by the rapid firing of the atrial focus.
These waves are referred to as F waves
QRS complex: Normal configuration and normal conduction
time
T wave: Present but may be obscured by flutter waves
Clinical picture
Complains of palpitation
Tachycardia that doesnt depend on
posture of patient, exercise of physic
strain, since the SA node does not
function as pacemaker
Heart contraction are arrhythmic with
varying conduction of Aschoff-Tawara
node

Atrial fibrillation
Atrial fibrillation (disorganized and
uncoordinated twitching of atrial
musculature) is usually associated with
atherosclerotic heart disease, valvular
heart disease, chronic heart failure,
thyrotoxicosis, cor pulmonale, or
congenital heart disease.
Characteristics of atrial
fibrillation:
ECG of atrial fibrillation

Rate: An atrial rate of 350 to 600 beats per minute; ventricular
response usually 120 to 200 beats per minute.
P waves: No discernible P waves; irregular undulation, termed
fibrillatory or F waves is seen, PR interval cannot be measured.
Conduction: Usually normal through the ventricles. Characterized
by an irregular ventricular response, because the AV node does not
respond to the rapid atrial rate. Impulses that are transmitted cause
the ventricles to respond irregularly.
Rhythm: Irregular and usually rapid, unless controlled. Irregularity of
rhythm is due to concealed conduction within the AV node.
Atrial fibrillation
A rapid ventricular response reduces the
time for ventricular filling and hence the
stroke volume.
The atrial kick, which is 25% to 30% of the
cardiac output, is also lost.
Congestive heart failure frequently follows.
There is usually a pulse deficit, the
numeric difference between apical and
radical pulse rates.
Clinical picture
May occur as permenant symptom or in attacks of
tachyarrhythmia
Bradyarrhythmia may cause no subjective symptoms
Tachyarrhythmia characterized by palpitation
Heart contraction is irregular
Variation in length of diastole account for variations in
ventricular filling and hence in the intensity of heart
sounds
Pulse is arrhytmic, waves vary in height ( irregular pulse
) and pulse deficit often develops in frequent heart
contractions
Dysrhythmias originating in the
ventricular muscle
Premature ventricular contraction

Premature ventricular contractions (PVCs) are the result of increased
automaticity of the ventricular muscle cells.
It can be due to digitalis toxicity, hypoxia, hypokalemia, fever, acidosis,
exercise, or increased circulating catecholamines.
Usually patient feels a palpitating sensation but has no other complaints.
The concern, however, lies in the fact that these premature contractions
may lead to more serious ventricular dysrhythmias.
In patients with acute myocardial infarction, PVCs are considered serious
precauses of ventricular tachycardia and ventricular fibrillation when they :
1) Occur in increasing number, more than 6 per minute
2) Are multi focal or originates from several areas in the heart
3) Occur in pairs or triplets
4) Occur in the vulnerable phase of conduction
The T wave represents the period when the heart is most likely to respond
to any stray beat and be excited in dysrhythmic manner. This phase of T
wave conduction is said to be the vulnerable phase.
Characteristics of premature
ventricular contraction:
ECG of premature ventricular contraction

Rate: 60 to 100 beats per minute
P wave: Will not be present because impulse originates in the
ventricles
QRS complex: Usually wide and bizzard. Usually longer then 0.1 sec in
duration. May have the same focus in the ventricles or may have a
wide variety of configurations if occurring from multiply foci in the
ventricles.
Conduction: Occasionally retrograde through the junctional tissue and
atria
Rhythm: Irregular when the premature beat occurs
Ventricular bigeminy
Ventricular bigeminy is frequently
associated with digitalis excess, coronary
artery disease, acute MI, and chronic heart
failure.
The term bigeminy refers to a condition in
which every other beat is premature.
Characteristics of ventricular
bigeminy:
ECG of ventricular bigeminy

Rate: May occur at any rate, but rate us usually less than 90 beats per minute
P waves: The same as described for premature ventricular contraction; may be hidden
within the QRS complex
QRS complex: Every other beat in a premature ventricular contraction with a wide,
bizarre QRS complex and a complete compensatory pause.
Conduction: The sinus beats are conducted from the sinus node in a normal fashion, but
alternating premature ventricular contractions start in the ventricles and may have
retrograde conduction through the junctional tissue and atria.
Rhythm: Irregular
If the ectopic beats occur every third beat, this is termed trigeminy; every fourth beat,
quadrigeminy.
Ventricular tachycardia
This dysrhythmia is cause by increased
myocardial irritability, as are premature
ventricular contractions.
It is usually associated with coronary artery
disease and may precede ventricular fibrillation.
Ventricular tachycardia is extremely dangerous
and should be considered an emergency.
The patient is generally aware of this rapid
rhythm and is quite anxious.
Characteristics of ventricular tachycardia
and accelerated ventricular rhythm:
ECG of ventricular tachycardia

Rate: 120 to 200 beats per minute
P waves: Usually buries in the QRS complex; if seen, they do not necessarily
fall in the normal pattern with the QRS. The ventricular contractions are
dissociated from the atrial contractions.
QRS complex: Have the same configurations as those of a premature
ventricular contraction- wide and bizarre, with T waves in the opposite
direction. A ventricular beat may fuse with a normal QRS, resulting in a fusion
beat.
Conduction: Originates in the ventricle, with possible retrograde conduction to
the junctional tissue and atria.
Rhythm: Usually regular, but irregular ventricular tachycardia is also seen.
Ventricular fibrillation
Ventricular fibrillation is a rapid, ineffective
quivering of the ventricles.
With this dysrhythmia there is no audible
heartbeat, no palpable pulse, and no
respiration. This pattern is so grossly
irregular it can be hardly mistaken for
another type of dysrhythmia.
Characteristics of ventricular
fibrillation:
ECG of ventricular fibrillation with defibrillation

Rate: Rapid, uncoordinated, ineffective.
P waves: Not seen
QRS complex: Rapid, irregular undulation without specific pattern (multifocal).
The ventricles have only a quivering motion.
Conduction: Foci are located in the ventricles, but so many foci are firing at
one time that there is no organized conduction; no ventricular contractions
occur.
Rhythm: Extremely irregular and uncoordinated, without specific pattern.
Diagnosis
Electrophysiologic studies
Electrophysiologic studies (EPSs) allow the physician to
induce the troubling dysrhythmias in a controlled
environment.
Catheters containing electrodes in the distal portion are
placed within the heart. Stimulation of these electrode-
containing catheters induces dysrhythmias.
Once a dysrhythmia is induced, different medications are
administered to determine which is the most effective in
suppressing the dysrhythmia.
EPS is a new technology; the long term benefit to the
patient remains to be determined.
Electrocardiogram
The ECG pattern is analyzed for the presence of
dysrhythmia.
Medical management
Dysrhythmias are most commonly treated
with medication therapy.
In situations in which medications alone
are not adequate, certain adjunctive
mechanical therapies are available.
The most common are elective
cardioversion, defibrillation and
pacemakers.
Cardioversion
Definition
Cardioversion is the use of electricity to
terminate dysrhythmias that have QRS
complexes. It is usually an elective
procedure.
Steps of treatment
The patient is alert and informed consent is obtained.
The patient is usually given diazepam (valium) intravenously before
cardioversion to promote anesthesia, and is usually intubated after being
anesthetized. The amount of voltage used varied from 25 to 400 watt-
seconds. Digoxin is usually withheld for 48 hours before cardioversion to
prevent postcardioversion dysrhythmias.
The synchronizer is turned on. The defibrillator is synchronized with a
cardiac monitor so that an electrical impulse is discharged during ventricular
depolarization (the QRS complex).
If not synchronized, the defibrillator could discharge during the vulnerable
period (T wave), resulting in ventricular tachycardia or fibrillation.
There is no discernible QRS in ventricular fibrillation; the synchronizer is
programmed to sense the QRSs. If the synchronizer is left on , the machine
will not fire as it waits to respond to a QRS.
If ventricular fibrillation occurs after cardioversion, the defibrillator must be
recharged immediately, the synchronizer turned off, and defibrillation
repeated.
After use, the defibrillator must be turned off to prevent accidental discharge
of the paddles.
Oxygen flow should be stopped during cardioversion, if possible, to avoid
the hazard of fire.
Indications
Indications of a successful response are
conversion to sinus rhythm, strong peripheral
pulses, and adequate blood pressure.
Airway patency should be maintained, and the
patients state of consciousness assessed.
Vital signs should be monitored and recorded
until the patient is stabilized.
ECG monitoring is required during and after
cardioverion; therefore, these patients are in a
critical care environment.
Steps of treatment
The mechanical system consists of a pulse generator,
two rate sensing leads, and two leads through which
electrical shock can be delivered directly to the
myocardium.
This is an invasive device that is implanted by
thoracotomy under surgical conditions.
The rate-sensing leads are designed to response to two
criteria: a rate change and an altered length of isoelectric
line segments.
When a dysrhythmia occurs, the rate sensors take 5 to
10 seconds to sense the dysrhythmia and another 5 to 7
seconds to charge the capacitors to deliver electrical
shock to revert the rhythm. The device can deliver up to
3 shocks if necessary.
The use of the ICD does not eliminate the need to
antidysrhythmic medication therapy. Medication is
administered in conjunction with this technology.
Complications
The primary complications associated with the ICD are pulmonary in
origin.
The 2 most common complications are pulmonary dysfunctions
secondary to the thoracotomy required for insertion of the ICD and
surgical infections.
There are lesser complications associated with the technical
aspects of the equipment such as premature battery depletion or
fractured lead.

The implantable cardioverter-defibrillator mechanical system
consists of a generator, two rate-sensing electrodes and two
epicardial patches
Nursing interventions
The nursing interventions for the patient with an ICD
occur throughout 3 phases: preoperative,
postoperative and predischarge.

Preoperative phase: Requires management of acute
episode of life-threatening dysrhythmias in addition to
providing the patient and family with explanations
regarding the implantation of the ICD
Postoperative phase: Involves astute observation of
the patient and his responses to his new technology.
Predischarge phase: Involves more teaching and is
vitality important to the patients ability to live
independently.
Nursing process
The patient with a dysrhythmia
Assessment
The assessment of the patient with cardiac dysrhythmias is
accomplished through patient history and physical and psychosocial
assessments.
A major focus of assessment is the dysrhythmia and the effect is
having on cardiac output (heart rate [HR] x stroke volume [SV]).
When cardiac output is reduced, optimum oxygenation to the tissues
and vital organs is diminished. The diminished oxygenation
produces the signs associated with dysrhythmias.
A patient history is conducted to determine the past or present
existence of syncope, light headedness, dizziness, fatigue, chest
discomfort, and palpitations. Any one of there signs can be present
when cardiac output is decreasing.
Physical Assessment
Its conducted to confirm the data obtained from the
patient history and to observe for signs of diminished
cardiac output.
The nurses attention is directed toward the skin, which
can be pale and cool.
Signs of fluid retention, such as neck vein distention and
crackles and wheezes in the lungs are observed.
The pulse is assessed apically and peripherally for rate
and rhythm. The presence or absence of a pulse deficit
is noted.
The heart is auscultated for extra sounds, especially S3
and S4, which reflect a reduced compliance of the
myocardium seen in reduced cardiac output.
Blood pressure is measured and pulse pressure is
determined. A declining pulse pressure indicates
reduced cardiac output.
Nursing diagnoses
Based on the assessment data, major diagnose of the
patient may include:
Decreased cardiac output related to slow or rapid rate
dysrhythmia.
Anxiety related to fear of the unknown.
Knowledge deficit about the disease and its treatment.

Planning and implementation
Goals

Maintenance of cardiac output
Minimization of anxiety
Attainment of knowledge of dysrhythmia and its
treatment
Nursing interventions
Maintenance of cardiac output
Cardiac output is best protected by controlling
episodes of dysrhythmia.
Administration of medications is managed carefully
so that constant serum blood level of the
medication is maintained at all times.
Frequent rhythm strips are analyzed to track the
dysrhythmia and prevent its deterioration into a
more malignant dysrhythmia. Ex: (premature
ventricular contractions are aggressively managed
before they become ventricular tachycardia).
Rest is promoted for the patient so that myocardial
oxygen needs are reduced
Minimization of anxiety
The relationship between a dysrhythmia and cardiac
output is explained to the patient so that he understands
the rationale for his medical regiment.
In particular, the relationship between myocardial oxygen
demands and the subsequent effect on cardiac output is
stressed.
During episodes of dysrhythmia, the nurse maintains a
calm and reassuring attitude; this forces a trusting
relationship with the patient and assist in reducing
anxiety
Attainment of knowledge of dysrhythmia and its
treatment
In terms the patient can understand and without unduly
frightening the patient, information specific to his circumstances
is explained.
The importance of maintaining therapeutic serum levels of
antidysrhythmic medication is explained instead of his statement
such as, always take your medications at a regular time each
day.
Evaluation

Expected outcomes:


1) Cardiac output is maintained.
a) Demonstrate minimal numbers of dysrhythmia
b) Demonstrate blood pressure and pulse within normal parameters
without wide variations
2) Anxiety is minimized
a) Expresses a positive attitude about living with the dysrhythmia.
b) Expresses confidence in knowing what to do in case of emergency
3) Attainment of knowledge of dysrhythmia and its treatment
a) Explain his dysrhythmia and its effect on cardiac output
b) Articulates rationale for medication regiment and explains need for
therapeutic serum level of the medication
c) States actions to take in event of an emergency.
Conduction abnormalities
First degree AV block

Definition
Its usually associated with organic heart
disease and maybe due to the effect of
digitalis.
It is seen frequently with inferior wall
myocardial infarctions
Characteristics of first degree
AV block:
ECG of first degree heart block
Rate: Variable, usually 60 to 100 beats per minute.
P waves: Precede each QRS complex. The PR interval is greater than 0.20 seconds in
duration
QRS complex: Follows each P wave, usually normal.
Conduction: Delayed conduction, usually anywhere between the junctional tissue and the
Purkinje network, produces a prolonged PR interval. Ventricular conduction is usually
normal.
Rhythm: Usually regular
This dysrhythmia is important because it may lead to more serious forms of heart block.
Its often a warning signal.
Therefore, the patient should be monitored closely for any advancing block.
Clinical picture
Cannot be detected clinically except that
splitting of the 1
st
sound may sometimes
detected by auscultation ( splitting of the
atrial component )
Second degree AV block
Definition
Its caused also by organic disease, and
MI, or digitalis intoxication.
This type of block results in a reduced
heart rate and usually reduced cardiac
output. (cardiac output = stroke volume x
heart rate)
Characteristics of second degree heart block:
ECG of second degree heart block

Rate: 30 to 55 beat per minute. The atrial maybe two, three or four times faster
than the ventricular rate.
P waves: There are two, three or four P waves for each QRS complex. The PR
interval of the conducted beat is usually normal in duration.
QRS complex: Usually normal.
Conduction: One or more of the impulses are not conducted to the ventricles.
Rhythm: Usually slow and regular. When an irregularity is present, it is due to
the fact that the block is varying from 2:1 to 3:1 or to some other combination
Clinical picture
Periodically missing ventricular contractions, and
hence missing pulse beats which correspond to
Samoilov-Wenckebach period
If each 3
rd
or 4
th
beat is missing, the pulse is
irregular and resembles trigeminy or
quadrigeminy with early extrasystoles and pulse
deficit
If heart rhythm slows down significantly the
patient complains of giddiness, everything going
black before his eyes and transient loss of
consciousness due to anemia of the brain
Third degree AV block
Definition

Its also associated with organic heart
disease, digitalis toxicity, and MI.
The heart rate may be markedly
decreased, resulting in a decrease in
perfusion to vital organs, such as the
brain, heart, kidneys, lungs and skin.
Characteristics of third degree AV block:
Origin: Impulses originate in the SA node, but are not conducted to the Purkinje fibers.
They are completely blocked. An escape rhythm from either the junctional or the
ventricular are therefore takes over as the pacemaker.
Rate: Atrial rate, 60 to 100 beats per minute; ventricular rate, 40 to 60 beats per minute
if the escape rhythm originated in the junction, 20 to 40 beats per minute if the escape
rhythm originated in the ventricle.
P waves: The P waves originating from the SA node are seen regularly throughout the
rhythm, but they have not association with the QRS complexes.
QRS complex: If the escape rhythm originated in the junction, the QRS complexes
have a normal supraventricular configuration, but have no association with the P
waves. QRS complexes occur regularly. If the escape rhythm originated in the
ventricle, the QRS complex is longer than 0.10 second in duration, and is usually road
and slurred. These QRS complexes have the same configuration as the QRS complex
of premature ventricular contraction.
Conduction: The SA node is firing, and P waves can be seen. They are all blocked
and not conducted to the ventricles. Escape rhythms originating in the junction are
usually conducted normally through the ventricles. Escape rhythms from the ventricles
are ectopic with aberrant configuration.
Rhythm: Usually slow but regular.
ECG of third degree heart block
Clinical picture
The heart rate in persistent complete heart block may be
sufficiently high ( 40-50 beats per min ) but the patient
may be unaware of the disease for a long time
Examination reveals slow, rhythmic and full pulse
The heart sound are dulled but a loud S1 ( pistol shot )
may be heard periodically
During an attack the patient loses consciousness, falls,
general epileptiform, convulsions develop, the respiration
becomes deep, the skin pallid, pulse slow or even
impalpable
Ventricular Asystole
Definition

In ventricular asystole there are not QRS
complexes. There is no heartbeat, no
palpable pulse and no respiration.
Characteristics of ventricular asystole:
ECG of ventricular asystole

Rate: None
P waves: May be visible, but they do not conduct
through the AV and ventricles.
QRS complexes: None
Conduction: Possibly, through the atria only.
Rhythm: None
Normal conduction pathway
The impulse travels from the sinus node
through the atria to the AV node or
junction, which also includes the bundle of
His. The impulse is delayed in time at the
AV node to allow the ventricles to fill with
blood. From the AV node the impulse
travels very quickly through the bundle
branches, terminating in the Purkinje fibers
of the ventricular walls to initiate systole.
The cycle then begins again.
Autonomic nervous system
The heart is under the control of the autonomic nervous
system, which consists of sympathetic and
parasympathetic fibers. The sympathetic system is also
referred to as adrenergic. Thus, stimulation of the
sympathetic system accelerates heart rate, raises blood
pressure and enhances the force of myocardial
contraction. Parasympathetic stimulation, conversely,
slows the heart rate, lowers blood pressure, and reduces
the force of contraction.
Manipulation of the autonomic nervous system forms the
foundation for much of the medication therapy in
dysrhythmia control (e.g. Beta-adrenergic blockers).
Treatment of sinus bradycardia
If slow heart rate is causing significant
hemodynamic changes with resultant syncope,
angina, or ectopic dysrhythmias, then treatment
is directed towards increasing the heart rate.
If decrease in heart rate is due to vagal
stimulation such as bearing down during
defecation or vomiting, attempts are made to
prevent further vagal stimulation.
If patient has digitalis intoxication, digitalis is
withheld.
Drug of choice in treating sinus bradycardia is
atrophine. Atrophine blocks vagal stimulation thus
allowing a normal rate to occur.
Sinus tachycardia
All aspects of sinus tachycardia are the same as those of
normal sinus rhythm, except for the rate.
Carotid sinus pressure, applied to one side at a time,
may be effective in slowing the rate temporarily, and
thereby help to rule out other dysrhythmias.
As heart rate increases, diastolic filling time decreases,
resulting in reduced cardiac output and subsequent
symptoms of syncope, fainting and low blood pressure.
If the rapid rate persists and the heart is unable to
compensate for the decreased ventricular filling, the
patient may develop acute pulmonary edema
Treatment
Treatment of sinus tachycardia is usually
directed at abolishing the cause.
Propanolol (inderal) may be used if rapid
reduction of rate is necessary. Propanolol
blocks the effect of adrenergic fibers, thus
slowing the rate.
Treatment paroxysmal atrial
tachycardia:
Treatment is directed toward eliminating the cause and
decreasing the heart rate.
Morphine may slow the rate without further treatment.
Carotid sinus pressure, applied to one side of at a time,
slows the rate or stops the attack and is usually more
effective after the digitalis or vasopressors.
The use of vasopressors has a reflex effect on the
carotid sinus by elevating the blood pressure and thus
slowing the heart rate.
Short acting digitalis preparations may be used.
Propranolol may be tried if digitalis is unsuccessful.
Quinidine may be effective, or the calcium channel
blocker verapamil (Calan) can be used.
Cardioversion may be necessary if the patient does not
tolerate the fast heart
Treatment atrial flutter
The accepted treatment for atrial flutter is a
digitalis preparation.
This enhances the block at the AV node, thus
slowing he rate.
Quinidine also may be given to suppress the
ectopic atrial focus.
The concomitant use of digitalis and quinidune
usually reverts the dysrhythmia to sinus rhythm.
Other drug therapies that are useful are calcium
channel and beta adrenergic blockers.
If drug therapy is unsuccessful, atrial flutter often
will respond to electrical cardioversion.
Treatment
The treatment for ventricular bigeminy is
the same as for the premature ventricular
contractions. Because the underlying
cause of ventricular bigeminy is frequently
digitalis toxicity, this should be ruled out or
treated if present.
Ventricular bigeminy caused by digitalis
toxicity is treated with phenytoin (Dilantin).
Treatment Atrial fibrillation
Treatment is directed toward decreasing the atrial
irritability and decreasing the rate of the ventricular
response.
In patients with chronic and atrial fibrillation,
anticoagulant therapy may be used to prevent
thromboemboli from forming in the atria.
At times mixture of atrial flutter and atrial fibrillation is
seen, sometimes called atrial flutter-fibrillation or coarse
atrial fibrillation.
Medications of choice to treat atrial fibrillation are similar
to those used in the treatment of PAT.
A digitalis preparation is used to slow the heart rate and
an antidysrhythmic such as quinidine is used to suppress
the dysrhythmia.
Treatment ventricular
contraction
To decrease the myocardia irritability, the
cause must be determined and if possible,
corrected.
An antidysrhythmic drug may be used for
immediate and possibly long term therapy.
Drug most commonly used in acute care is
lidocaine, for long term therapy
procainamide (pronestyl) or quinidine
maybe effective.
Treatment ventricular tachycardia
The patients tolerance or lack of tolerance
for this rapid rhythm will dictate the
therapy to be given.
The cause of the myocardial irritability
must be determined and corrected, if
possible.
Antidysrhythmic drugs may be used.
Cardioversion may be indicated if the
reduction in cardiac output is marked.
Treatment ventricular fibrillation
Immediate treatment is defibrillation.
Defibrillation
Definition
Defibrillation is asynchronous cardioversion that is used
in an emergency situation.
Its use is usually confined to the treatment of ventricular
fibrillation where there is not organized cardiac rhythm.
Defibrillation completely depolarizes all the myocardial
cells at once, allowing the sinus node to recapture its
role as the pacemaker.
The electrical voltage required to defibrillate the heart is
much greater than that usually required for
cardioversion.
The following are some key points to
remember in assisting with defibrillation or
cardioversion:
Use a good conducting agent
between the skin and the paddles,
such as saline pads or electrode
paste.
Position the paddles so as to
create an effective arc.
Exert 20 to 25 pounds of pressure
on each paddle to ensure good
skin contact.
Practice safety by being certain no
one is touching the bed or patient
when the paddles are discharged.
In the case of ventricular
fibrillation, cardiopulmonary
resuscitation (CPR) is initiated and
continued until mechanical
defibrillation is available.

One method of paddle placement in
cardioversion


If defibrillation has been unsuccessful, cardiopulmonary resuscitation is
resumed immediately.
Epinephrine may be used if the pattern of ventricular fibrillation is fine; that
is, no undulating waveform is discernible. Epinephrine may make the
fibrillation coarser and thus easier to convert with defibrillation.
Sodium bicarbonate is prescribed to reverse the acidosis cause by lack of
respiratory exchange.
Epinephrine and sodium bicarbonate are incompatible when mixed together
and much be administered separately.
Blood pressure is supported using vasopressors.
At no time during resuscitation should the external cardiac massage and the
assisted ventilation be stopped for longer than 5 seconds.


Diagram of very fine fibrillatory waves of ventricular fibrillation
A) can sometimes be coarsened into a more distinct fibrillatory pattern
B) by administration of epinephrine
Implantable cardioverter
defibrillator
Definition
The implantable cardioverter defibrillator (ICD) is a
device that detects and terminates life-threatening
episodes of ventricular tachycardia or ventricular
fibrillation in patients deemed at high risk.
The patients at high risk are those who have survived
sudden cardiac death, who have sustained ventricular
tachycardia, or who have syncope secondary to
ventricular tachycardia.
Many of these patients are unresponsive to medications
or surgical ablation of irritable myocardial tissue. This is
the population of patients most suitable for ICD.
Treatment second degree heart block:
Its directed towards increasing the heart
rate to maintain a normal cardiac output.
Digitalis toxicity should be ruled out and
myocardial depressant medications
withheld.
Treatment third degree AV block
Its directed toward increasing perfusion to
vital organs.
The insertion of a temporary transvenous
pacemaker is the acceptable treatment.
A permanent pacemaker may be
necessary if the block is persistent.
Treatment ventricular asystole
Cardiopulmonary resuscitation (CPR) is
necessary to keep the patient alive.
To decrease any vagal stimuli, atropine is
administered intravenously.
Epinephrine (intracardiac) should be
administered and repeated at 5-minute intervals.
Sodium bicarbonate may be given intravenously.
Insertion of a transthoracic or transvenous
pacemaker may be necessary.
Pacemaker therapy
Definitions and indications for use


A pacemaker is an electric device that provides repetitive electrical
stimuli to the heart muscle for the control of heart rate.
It initiates and maintains the heart rate when the natural pacemakers
of the heart are unable to do so.
Pacemakers are generally used when a patient has a conduction
disturbance of the forerunner of a conduction disturbance that
causes failure or cardiac output.
Pacemakers can be temporary or permanent.
Permanent pacemakers are used most commonly for irreversible
complete heart block; temporary pacemakers are used as adjunctive
therapy to support patients who have had heart block after
myocardial infarction or open heart surgery.
In some cases a pacemaker can also be used to control
tachydysrhythmias that otherwise do not response to medication
therapy.
Pacemaker design
Pacemakers consist of 2 components:
The electronic pulse generator, which contains the
circuitry and batteries that generate the electrical
stimulus
The pacemaker electrodes (also called leads or wires),
which transmit the pacemaker impulses to the heart

The stimuli from the pacemaker travel through a flexible catheter
electrode that is threaded through a vein into the right ventricle
or introduced by direct penetration of the chest wall.
The pulse generator is usually implanted in a subcutaneous
pocket in the pectoral or axillary region; sometimes abdominal
site is selected.
Types of pacemakers
The most commonly used pacemaker is the demand
(synchronous; noncompetitive) pacemaker, which is set for a
specific rate and stimulates the heart when normal ventricular
depolarization does not occur. It functions only when the natural
heart rate goes below a certain level.
The fixed rate pacemaker (asynchronous; competitive)
stimulates the ventricle at a preset constant rate that is
independent of the patients rhythm. It is used infrequently, usually
in patients with complete and unvarying heart block.

ECG of synchronized pacemaker rhythm. Arrows indicate
presence of sensed pacing spike
Temporary pacemaker systems
Temporary pacing is usually an emergency procedure and permits
the observation of the effects of pacing on heart function so that
optimum pacing rate for the patient can be selected before a
permanent pacemaker is implanted.
It is used in patients who have suffered myocardial infarction
complicated by heart block, in patients with cardiac arrest with
bradycardia and asystole, or in selected postoperative cardiac
surgery patients.
Temporary pacing may be done for hours, days, or weeks and is
continued until the patient improves or a permanent pacemaker is
implanted.
Temporary pacing may be carried out either by an endocardial
(transvenous) approach or by the transthoracic approach to the
myocardium.
The transvenous electrode is passed under fluoroscopic guidance
through any peripheral vein (antecubital, brachial, jugular,
subclavian, femoral) and the catheter tip is positioned in the apex of
the right ventricle.
Complications
The most common complication occur
during pacemaker insertion is ventricular
dysrhythmia.
Cardiac perforation occurs rarely. A
defibrillator should be immediately
available.
Permanent pacemaker system
For permanent pacing the endocardial lead is passed transvenously into the
right ventricle, and the pulse generator is implanted within the body
underneath the skin below the right or left pectoral region or below the
clavicle.
This is termed an endocardial or transvenous inplant.

Implanted tranvenous pacing electrode and pacemaker generator
Procedure
This procedure is usually performed under local
anesthesia.
Another method of permanent pacing is the
implantation of the pulse generator in the
abdominal wall.
The electrode is passed transthoracically to the
myocardium, where it is sutured in place.
This method, termed an epicardial or myocardial
implant, a thoracotomy is required to provide
access to the heart.
Atrioventricular pacemaker
(physiological pacemakers)
Definition

AV pacemakers are the safe and effective
pacemaker therapy for many complex cardiac
problems.
They are considered highly desirable because
they can be programmed to mimic the patients
own intrinsic cardiac function; hence they are
referred to as physiological pacemakers.
Details about common practice

Because of the sophistication of these AV pacemakers, a universal code has been
adopted to provide a means of safe communication about their function.
The coding is referred to as the ICHD code because it is sanctioned by the
intersociety commission for heart disease. The complete consist of 5 letters, but only
3 are used in common practice.
The 1st letter of code always describes the chamber being paced, that is, the
chamber containing the pacing electrode. The possible letter characters for these
code are A (atrium), B (ventricle) or D (dual or meaning both A and B).
The 2nd letter describes the chamber being sensed by the pacemaker generator.
Information sensed is dispatched to the generator for interpretation and action by the
generator. The possible letter characters are once again A (atrium), B (ventricle), and
D (dual).
The 3rd letter of the code always describes the type of resonance exhibited by the
pacemaker.
There are 5 characters used to describe this response, but of the 5 only 2 is in
common use: I (inhibitory) and T (triggered).
Inhibitory response means that the response of the pacemaker is controlled by the
activity of the patients own heart; that is, the pacemaker will not function when the
patients heart beats.
In contrast triggered response means that the pacemaker will trigger a response
based on intrinsic heart activity.
Example of ICHD coded pacemaker in DVI:
D- both the atrium and the ventricle have a pacing electrode in place
V- the pacemaker is sensing the activity of the ventricle only
I- the pacemakers stimulating is being inhibited by the activity of the patients
ventricle
Complications
They are associated with pacemakers relate to:
Their presence within the body
Improper functioning

The following complications may arise from the presence of
pacemaker:
Local infection (sepsis or hematoma formation) may
occur at the site of venous cut down or subcutaneous
pacemaker placement.
Dysrhythmias- ventricular ectopic activity may follow
irritation of the ventricular wall by the electrode.
Perforation of the myocardium or right ventricle by the
catheter may occur.
Abrupt loss of pacing caused by high ventricular
threshold
Pacemaker malfunction
It can arise from the failure in one or more components
of the pacing system.
The majority of pulse generator failures are from
depletion of the power supply that is battery supply.
Patient should be informed that the battery cells are
sealed in the pulse generator. When it is time for battery
change, a new incision is made over old incision.
The old pulse generator is removed and the new unit is
connected to the existing leads and reimplanted in the
existing pocket.
Complications of malfunction of pacemaker

Fracture or dislocation of the electrodes and
electronic failure
Malfunction can also occur with exposure to
electromagnetic fields. Electromagnetic fields are
produced by equipments such as microwave ovens,
MRI equipment and metal detectors.

Diagnosis of complications

Diagnosis of these complications is made by ECG
analysis. Manipulation of the electrodes or replacement
of the pacemaker generator maybe necessary
Pacemaker surveillance

Pacemaker clinics have been established to monitor and to test
pulse generators for warning of impending pacemaker system
failure.
Testing of pacemaker pulse amplitude and duration and analysis of
pulse contour require amplification equipment.
With special equipment, lead fracture and insulation disruption can
be detected.
A 12-lead ECG is performed during each patients visit to clinic.
Another method to follow up is evaluation by tanstelephone
monitoring of the transmission of the generators pulse rate.
By means of special equipment the sound tone of the patients
pacemaker is transmitted over the telephone to a receiving system
at a pacemakers clinic.
The sounds are converted into an electronic signal and permanently
recorded on an ECG strip.
The pacemaker rate and other data concerning pacemakers
function are obtained and evaluated by a cardiologist.
This simplifies the diagnosis of a failing generator, provides
reassurance and improves the management of the person who is
physically remote from the pacemaker testing facilities.
Pacemaker development
Activity response pacemaker

A pacemaker that will alter cardiac rate in
response to changes in activity is being
investigated.
The preliminary designs depend on parameters
such as physical activities, acid base changes
and oxygen saturation instead of depending on
sinus node function.
This pacemaker will be capable of improving
cardiac output during exercise