Heart Block

heart block
lack of synchronization in the contractions of the upper and the lower chambers of the heart--the
atria and the ventricles. The lack of synchronization may range from a slight delay in the
ventricular contractions to total heart block, a complete lack of synchronization between the atria
and the ventricles. A characteristic of heart block is that the ventricles contract more slowly than
the atria. Heart block is caused by disease of some portion of the pathway over which the
contractive impulse travels through the heart. The condition is treated by increasing the rate
of impulses that regulate ventricular contractions; this can be done by administering
drugs or by implanting an artificial pacemaker, a device that regulates heart action by means
of minute electric shocks.
Atrioventricular node mechanisms
Normally, the impulse for ventricular contraction arises from a focus in the atria, passes through
the atrioventricular node and bundle of His, which delay progression, and then excites ventricular
activity. This mechanism may not operate properly in various pathological states. In some
instances, more rapidly firing (i.e., impulse-emitting) tissue in the atrioventricular node may
initiate the ventricular activity, supplanting the normal atrial focus and resulting in tachycardia,
called nodal tachycardia because of the part played by the atrioventricular node. More frequently,
the abnormal mechanism is one of delay or obstruction in progression of the impulse, creating
"heart block," a lack of synchronization between atria and ventricles; there may be varying degrees
of severity. In first-degree heart block, there is merely a short delay over the normal conduction
time from the atrium to the ventricle. This condition does not result in clinical manifestation but is
detected electrocardiographically by a longer than normal period of time between the P wave,
which is associated with atrial activity, and the QRS complex, which is associated with ventricular
excitation.
In a more severe (second-degree) form, the impulse may travel relatively normally through the
conduction system, but some beats are blocked. Alternate beats may be blocked, resulting in what
is known as a two-to-one heart block, or the ratio may be three-to-one, four-to-one, etc. The
degree of blockage of conduction may be influenced by stimulation from outside the heart, such as
from the carotid sinus or the central nervous system, and is dependent in part on drug action. (The
carotid arteries are the principal arteries to the head. The carotid sinus, located at the fork where
the common carotid divides into the external and internal carotid arteries, is an important structure
for monitoring and regulating blood pressure.)
The conduction system below the atrioventricular node divides into two major branches, to the two
ventricles, and, therefore, blockage of impulse transmission in either of these is termed right or left
bundle branch block. This condition is identified by electrocardiographic changes and is most
frequently associated with organic heart disease, though it may occur rarely in normal individuals.
The most severe form of heart block, complete heart block, is characterized by total dissociation of
atrial activity and ventricular activity. In this situation, atrial activity usually continues at a normal
or higher than normal rate. Independently the ventricle establishes its own rate, usually slower
than normal, but in some instances within the normal range. If the latter is the case, the difficulty
is without major consequence on the circulation. More frequently, however, it is at a slower rate,
and there may be some resultant inadequacy of the circulation. This condition is usually associated
with forms of organic heart disease, and the slowness of the rate may precipitate congestive heart
failure or other manifestations. It may be treated by the use of drugs or electrical pacemakers to
increase the rate of ventricular activity.
At times, the degree of heart block or its occurrence may be variable and erratic. This condition
may result in considerable pauses in left-ventricular depolarization and contraction, the basic
mechanism that precipitates the Adams-Stokes syndrome, which leads to occasional episodes of
unconsciousness. (The syndrome is named for the Irish physicians Robert Adams and William
Stokes, whose descriptions of the disease are celebrated.)
Cardiac pacemakers
The normal rhythm of the heart is generated by spontaneous electrical activity in cells in an area of
the heart called the sinoatrial node. The electrical activity is usually at a rate of about 70 beats per
minute at rest and is transmitted to the pumping chambers of the heart, the atria, and the
ventricles through a specialized conducting system. The electrical activity causes contraction of the
heart muscle, which results in a detectable pulse at the wrist and elsewhere. Disease of the sinus
node (sick sinus syndrome) or the conducting system (heart block) can cause an abnormally slow
rhythm of the heart; because blood supply to the brain is inadequate, severe disease can cause
loss of consciousness. This occurs if there is no heartbeat for about six seconds.
A pacemaker is a device that artificially stimulates the heart when the abnormal electrical activity is
absent. A pacemaker comprises a pulse generator connected to the heart by wire or electrode. The
pulse generator has a battery power source and electronic circuitry that can generate an artificial
stimulus at a predetermined rate. It can also detect normal activity of the heart so that the
artificial stimulus is only discharged when the natural activity is absent. In this way the pacemaker
functions on demand, inserting an artificial beat as required.
The pulse generator is usually placed under the skin over the right or left chest and has enough
power to last several years. The electrode is passed from the pulse generator along a vein and is
connected to either the atrium or ventricle, depending on whether the underlying problem is sick
sinus syndrome or heart block. In many models the performance of the pacemaker can be altered
by using radio frequency signals to alter its programmed settings. Some pacemakers may last up
to 15 years and can be reused; the most common lifetime is seven years.
Inotropic agents
Inotropic agents are drugs that influence the force of contraction of cardiac muscle, thereby
tending to affect the cardiac output. Drugs have a positive inotropic effect if they increase the force
of contraction of the heart. The most important group of inotropic agents is the cardiac glycosides,
substances that occur in the leaves of the foxglove (Digitalis purpurea) and other plants.
Although they have been used for many purposes throughout the centuries the effectiveness of
cardiac glycosides in heart disease was established in 1785 by an English physician, William
Withering, who successfully used an extract of foxglove leaves to treat heart failure. Many closely
related glycosides with similar pharmacological actions are found in various plants, but they differ
in ease of absorption from the gastrointestinal tract and in duration of action. The two compounds
most often used therapeutically are digoxin and digitoxin.
The most useful effect of cardiac glycosides is their ability to increase the force of contraction of
cardiac muscle. They have, however, several additional effects, most of which are
disadvantageous. These include a tendency to block conduction of the electrical impulse that
causes contraction as it passes from the atria to the ventricles of the heart (heart block). Cardiac
glycosides also have a tendency to produce an abnormal cardiac rhythm by causing electrical
impulses to be generated at points in the heart other than the normal pacemaker region, the cells
that rhythmically maintain the heartbeat. These irregular impulses result in ectopic heartbeats that
are out of sequence with the normal cardiac rhythm. Occasional ectopic beats are harmless, but if
this process continues to a complete disorganization of the cardiac rhythm (ventricular fibrillation),
the pumping action of the heart is stopped, causing death within minutes unless resuscitation is
carried out. Because the margin of safety between the therapeutic and the toxic doses of
glycosides is relatively narrow, they must be used carefully.
Cardiac glycosides are believed to increase the force of cardiac muscle contraction by binding to
and inhibiting the action of a membrane enzyme that extrudes sodium ions from the cell interior.
Inhibiting the free flow of sodium ions from the interior of the cell across the membrane to the
exterior of the cell causes the intracellular sodium concentration to rise. The interior of the cell then
becomes depolarized, or electrically less negative than normal with respect to the exterior of the
cell. Because the cell is able to exchange sodium ions within the cell for calcium ions outside it,
there is a secondary rise in intracellular calcium. This subsequently increases the force of
contraction, since intracellular calcium ions are responsible for initiating the shortening of muscle
cells.
The disturbances of rhythm that may be caused by cardiac glycosides result partly from the
depolarization and partly from the increase in intracellular calcium. Because these rhythm
disturbances are caused by the same underlying mechanism that causes the beneficial effect, there
is no likelihood of finding a cardiac glycoside with a significantly better margin of safety. Apart from
their cardiac actions, these glycosides tend to cause nausea and loss of appetite. Because digoxin
and digitoxin have long plasma half-lives (two and seven days, respectively), they are liable to
accumulate in the body. Treatment with either of these drugs must involve careful monitoring to
avoid the adverse effects that may result from their slow buildup in the body.
The second type of inotropic agent that increases the force of cardiac muscle contraction includes
epinephrine and norepinephrine. In addition to affecting the force of contraction, however, they
also increase the heart rate. This, and the fact that they are quickly metabolized by the body and
act only for a few minutes, means that they are not useful inotropic agents.
The third type of inotropic agent that acts as a cardiac stimulant is the caffeine-related series of
drugs represented by theophylline. Its action, like that of epinephrine, depends on an increase in
the intracellular concentration of cyclic adenosine 3',5'-monophosphate, which indirectly increases
the influx of calcium ions into the cells, thereby increasing the force of contraction of cardiac
muscle.
pacemaker
electronic cardiac-support device that produces rhythmic electrical impulses that take over the
regulation of the heartbeat in patients with certain types of heart disease.
A healthy human heart contains its own electrical conducting system capable of controlling both the
rate and the order of cardiac contractions. Electrical impulses are generated at the sinoatrial node
in the right atrium, one of the chambers of the heart. They then pass through the muscles of both
atria to trigger the contraction of those two chambers, which forces blood into the ventricles. The
wave of atrial electrical activity activates a second patch of conductive tissue, the atrioventricular
node, initiating a second discharge along an assembly of conductive fibres called the bundle of His,
which induces the contraction of the ventricles. When electrical conduction through this system is
interrupted, as is the case in a number of diseases including congestive heart failure and as an
aftereffect of heart surgery, the condition is called heart block. An artificial pacemaker may be
employed temporarily until normal conduction returns, or permanently to overcome the block.
In temporary pacing, a miniature electrode attached to fine wires is introduced into the heart
through a vein, usually in the arm. The pacing device, an electric generator, remains outside the
body and produces regular pulses of electric charge to maintain the heartbeat. In permanent
pacing, the electrode may again be passed into the heart through a vein or it may be surgically
implanted on the heart's surface; in either case the electrode is generally located in the right
ventricle. The electric generator is placed just beneath the skin, usually in a surgically created
pocket below the collarbone.
The first pacemakers were of a type called asynchronous, or fixed, and they generated regular
discharges that overrode the natural pacemaker. The rate of asynchronous pacemakers may be set
at the factory or may be altered by the physician, but once set they will continue to generate an
electric pulse at regular intervals. Most are set at 70 to 75 beats per minute. More recent devices
are synchronous, or demand, pacemakers that trigger heart contractions only when the normal
beat is interrupted. Most pacemakers of this type are designed to generate a pulse when the
natural heart rate falls below 68 to 72 beats per minute. These instruments have a sensing
electrode that detects the atrial impulse.
Once in place, the electrode and wires of the pacemaker usually require almost no further
attention. The power source of the implanted pulse generator, however, requires replacement at
regular intervals, generally every four to five years. Most current pacemakers use batteries as a
power source, but there has been some exploration of generators energized by radioactive isotopes
such as plutonium-238.
Heart block
From Wikipedia, the free encyclopedia.
A heart block denotes a disease in the electrical system of the heart. This is opposed to
coronary artery disease, which is disease of the blood vessels of the heart. While
coronary artery disease can cause angina (chest pain) or myocardial infarction (heart
attack), heart block can cause lightheadedness, syncope (passing out), and palpitations.
Contents
[hide]
 1 Types of heart block
o 1.1 Types of SA nodal blocks
o 1.2 Types of AV nodal blocks
o 1.3 Types of infrahisian block
 2 Related topics
 3 External links
[edit]
Types of heart block
A heart block can be a blockage at any level of the electrical conduction system of the heart.
Blocks that occur within the sinoatrial node (SA node) are described as SA nodal blocks.
Blocks that occur within the atrioventricular node (AV node) are described as AV nodal
blocks. Blocks that occur below the AV node are known as infra-Hisian blocks (named after
the bundle of His). Clinically speaking, most of the important heart blocks are AV nodal
blocks and infrahisian blocks.
[edit]
Types of SA nodal blocks
The SA nodal blocks rarely give symptoms. This is because if an individual had complete
block at this level of the conduction system (which is uncommon), the secondary pacemaker
of the heart would be at the AV node, which would fire at 40 to 60 beats a minute, which is
enough to retain consciousness in the resting state.
Types of SA nodal blocks include:
 SA node Wenckebach (Mobitz I)

 SA node Mobitz II
 SA node exit block
In addition to the above blocks, the SA node can be suppressed by any other arrhythmia that
reaches it. This includes retrograde conduction from the ventricles, ectopic atrial beats, atrial
fibrillation, and atrial flutter.
The difference between SA node block and SA node suppression is that in SA node block an
electrical impulse is generated by the SA node that doesn't conduct to the ventricles. In SA
node suppression, on the other hand, the SA node doesn't generate an electrical impulse
because it is reset by the electrical impulse that enters the SA node.
[edit]
Types of AV nodal blocks
There are four basic types of AV nodal block:
 First degree heart block

 Second degree heart block
o Type 1 second degree heart block (Mobitz I) (also known as Wenckeback
phenomenon)
 Third degree heart block (Complete heart block)
[edit]
Types of infrahisian block
Infrahisian block describes block of the distal conduction system. Types of infrahisian block
include:
 Type 2 second degree heart block (Mobitz II)

 Left bundle branch block
o Left anterior hemiblock
o Left posterior hemiblock
 Right bundle branch block
Of these types of infrahisian block, Mobitz II heart block is considered most important
because of the possible progression to complete heart block.
Related topics
 Electrical conduction system of the heart
o Sinoatrial node (SA node)
o Atrioventricular node (AV node)
 First degree heart block
 Second degree heart block
 Trifascicular heart block
 Third degree heart block (Complete heart block)
 Left bundle branch block
o Left anterior hemiblock
o Left posterior hemiblock
 Right bundle branch block
 Lev's disease
[edit]
External links
 "heartblock.blogspot.com - Living with Heart Block and a Pacemaker"
First degree heart block is a disease of the electrical conduction system of the
heart.
In first degree heart block, the disease is almost always at the level of the atrioventricular
node (AV node).
In normal individuals, the AV node slows the conduction of electrical impulse through the
heart. This is manifest on a surface EKG as the PR interval. The normal PR interval is from
120 ms to 200 ms in length.
In first degree heart block, the diseased AV node conducts the electrical activity slower. This
is seen as a PR interval greater than 200 ms in length on the surface EKG.
Isolated first degree heart block has no clinical consequences. There are no symptoms or signs
associated with it, and there is no danger of progression to complete heart block.
In a subset of individuals with the triad of first degree heart block, right bundle branch block,
and either left anterior or left posterior fascicular block (known as trifascicular heart block)
may be at an increased risk of progression to complete heart block.
Second degree heart block

Second degree heart block is a disease of the electrical conduction system of the heart.
If this term is used without a qualifier, it is usually assumed to be regarding disease of the
atrioventricular node (AV node). However it is possible to have a second degree heart block
involving the sinoatrial node (SA node) as well.
There are two distinct types of second degree heart block, called type 1 and type 2. The
distinction is made between them because type 1 second degree heart block is considered a
more benign entity than type 2 second degree heart block.
[edit]
Type 1 Second degree heart block
Type 1 Second degree heart block, also known as Mobitz I heart block or Wenckebach
phenomenon, is a disease of the AV node.
Mobitz I heart block is characterized by progressive prolongation of the PR interval on the

electrocardiogram (EKG) on consecutive beats followed by a blocked beat (dropped QRS
complex). After the dropped QRS complex, the PR interval resets and the cycle repeats.
One of the baseline assumptions when determining if an individual has Mobitz I heart block is
that the sinus rhythm has to be regular. If the sinus rhythm is not regular, there could be
alternative explanations as to why the P wave wasn't followed by a QRS complex.
[edit]
Type 2 Second degree heart block
Type 2 Second degree heart block, also known as Mobitz II heart block is a disease of the
distal conduction system. This is also known as Infrahisian block because the level of block
is below the bundle of His.
Mobitz II heart block is characterized on a surface ECG by a fixed PR interval with a dropped
QRS complex after a certain number of P waves. For instance, for every 4 P waves, there are
only 3 QRS complexes. Since there is no lengthening of the PR interval, the PR interval does
not reset after the dropped QRS complex.
Third degree heart block

Third degree heart block, also known as complete heart block, is a disease of the electrical
system of the heart, in which the impulse generated in the top half of the heart (typically the
SA node in the right atrium) does not propagate to the left or right ventricles.
Due to the blocked rhythm, an accessory pacemaker below the level of the block typically
will activate the ventricles. Since this accessory pacemaker activates independently of the
impulse generated at the SA node, two independent rhythms can be noted on the
electrocardiogram (EKG). One rhythm, generated from the SA node, will activate the atria
and create the p wave on the EKG. The second rhythm, generated from the accessory
pacemaker, will activate the ventricles and produce the QRS complex on the EKG.
The hallmark of complete heart block is no apparent relationship between p waves and QRS
complexes on the EKG.
[edit]
Etiology
Many conditions can cause third degree heart block. Progressive degeneration of the electrical
conduction system of the heart can lead to third degree heart block. This may be preceded by
second degree heart block, particularly Mobitz II heart block.
An acute myocardial infarction (heart attack), may also lead to third degree heart block. This
may be due to damage to the AV node, preventing impulse propagation distal to that portion
of the conduction system, or it may be due to damage of the distal conduction system.
An inferior wall myocardial infarction may cause damage to the AV node, causing third
degree heart block. In this case, the damage is usually transitory, and the AV node may
recover. Studies have shown that third degree heart block in the setting of an inferior wall
myocardial infarction typically resolves within 2 weeks.
An anterior wall myocardial infarction may damage the distal conduction system of the heart,
causing third degree heart block. This is typically extensive, permanent damage to the
conduction system, necessitating a permanent pacemaker to be placed.
Heart
For other uses, see Heart (disambiguation).
The heart and lungs (from an older edition of Gray's Anatomy)
The heart (Latin cor) is a hollow, muscular organ that pumps blood through the blood vessels
by repeated, rhythmic contractions. The term cardiac means "related to the heart", from the
Greek kardia (καρδια) for "heart".
Contents
[hide]
 1 The human heart
o 1.1 Structure
o 1.2 The cardiac cycle
 1.2.1 Regulation of the cardiac cycle
o 1.3 Diseases and treatments
o 1.4 First Aid
 2 The hearts of other animals
o 2.1 Structure
o 2.2 Heartbeat
o 2.3 Food use
 3 As an icon
 4 See also
 5 External links
[edit]
The human heart

[edit]
Structure
In the human body, the heart is normally situated slightly to the left of the middle of the
thorax, underneath the sternum (breastbone). It is enclosed by a sac known as the pericardium
and is surrounded by the lungs. In normal adults, it weighs 250-350 g, but in extremely
diseased hearts can weigh up to 1000 g. It consists of four chambers, the two upper atria
(singular: atrium) and the two lower ventricles.
A septum, divides the right atrium and ventricle from the left atrium and ventricle, preventing
blood from passing between them. Valves between the atria and ventricles (atrioventricular
valves) maintain coordinated unidirectional flow of blood from the atria to the ventricles.
The function of the right side of the heart is to collect deoxygenated blood from the body and
pump it into the lungs so that carbon dioxide can be dropped off and oxygen picked up. The
left side collects oxygenated blood from the lungs and pumps it out to the body. On both
sides, the lower ventricles are thicker than the upper atria.
Anterior (frontal) view of the opened heart. White arrows indicate normal blood flow. (SVG
version)
Oxygen-depleted or deoxygenated blood from the body enters the right atrium through two
great veins, the superior vena cava which drains the upper part of the body and the inferior
vena cava that drains the lower part. The blood then passes through the tricuspid valve to the
right ventricle. The right ventricle pumps the deoxygenated blood to the lungs, through the
pulmonary artery. In the lungs gaseous exchange takes places and the blood releases carbon
dioxide into the lung cavity and picks up oxygen. The oxygenated blood then flows through
pulmonary veins to the left atrium. From the left atrium this newly oxygenated blood passes
through the mitral valve to enter the left ventricle. The left ventricle then pumps the blood
through the aorta to the entire body. Even the lung takes some blood supply from the aorta via
bronchial arteries.
The left ventricle is much more muscular (1.3 - 1.5 cm thick) than the right (0.3 - 0.5 cm
thick) as it has to pump blood around the entire body, which involves exerting a considerable
force to overcome the vascular pressure. As the right ventricle needs to pump blood only to
the lungs, it requires less muscle.
Even though the ventricles lie below the atria, the two vessels through which the blood exits
the heart (the pulmonary artery and the aorta) leave the heart at its top side.
The contractile nature of the heart is due to the presence of cardiac muscle in its wall which
can work continuously without fatigue. The heart wall is made of three distinct layers. The
first is the outer epicardium which is composed of a layer of flattened epithelial cells and
connective tissue. Beneath this is a much thicker myocardium made up of cardiac muscle. The
endocardium is a further layer of flattened epithelial cells and connective tissue which lines
the chambers of the heart.
The blood supply to the heart itself is supplied by the left and right coronary arteries, which
branch off from the aorta.
[edit]
The cardiac cycle

See main page cardiac cycle
Atrial systole
Ventricular systole
The function of the heart is to pump blood around the body. Every single beat of the heart
involves a sequence of events known as the cardiac cycle, which consists of three major
stages: atrial systole, ventricular systole and complete cardiac diastole. The atrial systole
consists of the contraction of the atria and the corresponding influx of blood into the
ventricles. Once the blood has fully left the atria, the atrioventricular valves, which are
situated between the atria and ventricular chambers, close. This prevents any backflow into
the atria. It is the closing of the valves that produces the familiar beating sounds of the heart,
commonly referred to as the "lub-dub" sound.
The ventricular systole consists of the contraction of the ventricles and flow of blood into the
circulatory system. Again, once all the blood empties from the ventricles, the pulmonary and
aortic semilunar valves close. Finally complete cardiac diastole involves relaxation of the
atria and ventricles in preparation for refilling with circulating blood.
[edit]
Regulation of the cardiac cycle
Cardiac muscle is myogenic, which means that it is self-exciting. This is in contrast with
skeletal muscle, which requires either conscious or reflex nervous stimuli. The heart's
rhythmic contractions occur spontaneously, although the frequency or heart rate can be
changed by nervous or hormonal influences such as exercise or the perception of danger.
The rhythmic sequence of contractions is coordinated by the sinoatrial and atrioventricular

nodes. The sinoatrial node, often known as the cardiac pacemaker, is located in the upper
wall of the right atrium and is responsible for the wave of electrical stimulation (See action
potential) that initiates atria contraction. Once the wave reaches the atrioventricular node,
situated in the lower right atrium, it is conducted through the bundles of His and causes
contraction of the ventricles. The time taken for the wave to reach this node from the
sinoatrial nerve creates a delay between contraction of the two chambers and ensures that
each contraction is coordinated simultaneously throughout all of the heart. In the event of
severe pathology, the Purkinje fibers can also act as a pacemaker; this is usually not the case
because their rate of spontaneous firing is considerably lower than that of the other
pacemakers and hence is overridden.
[edit]
Diseases and treatments
The study of diseases of the heart is known as cardiology. Important diseases of the heart
include:
 Coronary heart disease is the lack of oxygen supply to the heart muscle; it can cause
severe pain and discomfort known as Angina.
 A heart attack occurs when heart muscle cells die because blood circulation to a part
of the heart is interrupted.
 Congestive heart failure is the gradual loss of pumping power of the heart.
 Endocarditis and myocarditis are inflammations of the heart.
 Cardiac arrhythmia is an irregularity in the heartbeat. It is sometimes treated by
implanting an artificial pacemaker
 Congenital heart defects.
If a coronary artery is blocked or narrowed, the problem spot can be bypassed with coronary
artery bypass surgery or it can be widened with angioplasty.
Beta blockers are drugs that lower the heart rate and blood pressure and reduce the heart's
oxygen requirements. Nitroglycerin and other compounds that give off nitric oxide are used to
treat heart disease as they cause the dilation of coronary vessels.
At Groote Schuur Hospital in Cape Town, South Africa, 53-year-old Lewis Washkansky on
December 3, 1967 became the first human to receive a heart transplant (however he died 18
days later from double pneumonia). The transplant team was headed by Christiaan Barnard.
See also: Cardiology diagnostic tests and procedures
[edit]
First Aid
See cardiac arrest for emergencies involving the heart

If a person is encountered in cardiac arrest (no heartbeat), cardio-pulmonary resuscitation
(i.e., CPR) should be started.
[edit]
The hearts of other animals

[edit]
Structure
The structure of the heart of other mammals is quite similar to that of humans, with four
chambers. Birds also have a four-chambered heart; however, it is thought that this evolved
independently of that of mammals. Amphibians have a three-chambered heart. Reptilia also
have a three-chambered heart, except for crocodilians (which have four). Fish have a single
circulation system and a heart with two chambers. The hearts of arthropods and mollusks have
a single chamber.
[edit]
Heartbeat
Smaller animals have faster heartbeats. This is evident within a species as well, as the young
beat their hearts faster than the adults. Gray Whale beats 9 times per minute, Harbour Seal 10
when diving, 140 when on land, elephant 25, human 70, sparrow 500, shrew 600, and
hummingbird 1,200 when hovering.
The earthworm has a series of multiple primitive hearts.
[edit]
Food use
The hearts of cattle, sheep, pigs and certain fowl are consumed as food in many countries.
They are counted among offal, but being a muscle, the taste of heart is much more like regular
meat than that of other offal. It resembles venison in structure and taste.
The conducting system of the heart showing the source of the electrical
impulses (P, QRS complex, and T waves) produced on a normal
electrocardiogram.
http://www.wrongdiagnosis.com/h/heart_block/intro.htm
Introduction: Heart block
Heart block: Failure of the heart's normal rhythm controls leading to arrhythmia
Heart block: Heart block is a condition in which the electrical signal cannot travel normally
down the special pathways to the ventricles. For example, the signal from the atria to the
ventricle may be (1) delayed, but each one conducted; (2) delayed with only some getting
through; or (3) completely interrupted. If there is no conduction, the beat generally originates
from the ventricles and is very slow. 1
Symptoms of Heart block
General information about symptoms of Heart block: The symptom information on this
page attempts to provide a list of some possible symptoms of Heart block. This symptom
information has been gathered from various sources, may not be fully accurate, and may not
be the full list of symptoms of Heart block. Furthermore, symptoms of Heart block may vary
on an individual basis for each patient. Only your doctor can provide adequate diagnosis of
symptoms and whether they are indeed symptoms of Heart block.
List of symptoms of Heart block: The list of symptoms mentioned in various sources for
Heart block includes:
 Slow heartbeat
 Irregular heartbeat
 Arrhythmias
 Blackouts (Stokes Adams syndrome)
 Symptoms of severe case:
o Breathlessness
o Breathlessness with exertion
o Breathlessness caused by fever
o Dizziness
o Weakness
o Fainting
o Fatigue
o Heart failure - see also symptoms of heart failure
More symptoms of Heart block: In addition to the above information, to get a full picture of
the possible symptoms of this condition and its related conditions, it may be necessary to
examine symptoms that may be caused by complications of Heart block, underlying causes of
Heart block, associated conditions for Heart block, risk factors for Heart block, or other
related conditions.
Medical articles on symptoms: These general reference articles may be of interest:
 Symptoms of the Silent Killer Diseases

 Symptoms and Medical Malpractice
Misdiagnosis of Heart block

About misdiagnosis: When checking for a misdiagnosis of Heart block or confirming a
diagnosis of Heart block, it is useful to consider what other medical conditions might be
possible misdiagnoses or other alternative conditions relevant to diagnosis. These alternate
diagnoses of Heart block may already have been considered by your doctor or may need to be
considered as possible alternative diagnoses or candidates for misdiagnosis of Heart block.
For a general overview of misdiagnosis issues for all diseases, see Overview of Misdiagnosis.
Alternative diagnoses list for Heart block: For a diagnosis of Heart block, the following list
of conditions have been mentioned in sources as possible alternative diagnoses to consider
during the diagnostic process for Heart block:
 Normal athlete - first degree mild heart block may be a normal rhythm for very
fit people.
Misdiagnosis cases for Heart block: No cases available yet.

Last revision: May 29, 2003
Misdiagnosis of Underlying Causes of Heart block

About underlying conditions: With a diagnosis of Heart block, it is important to consider
whether there is an underlying condition causing Heart block. These are other medical
conditions that may possibly cause Heart block. For general information on this form of
misdiagnosis, see Underlying Condition Misdiagnosis or Overview of Misdiagnosis.
Underlying conditions list: The list of possible underlying conditions mentioned in various
sources for Heart block includes:
 Heart attack
 Coronary artery disease
 Sinus node disease
 Congenital heart defect
 Myocarditis
 Coronary thrombosis (see Heart symptoms)
 Cardiomyopathy
 Heart valve disease
 Rheumatic fever
Heart block as a complication: Other conditions that might have Heart block as a
complication might be potential underlying conditions. The list of conditions listing Heart
block as a complication includes:
 Endocarditis
Heart block as a symptom: Conditions listing Heart block as a symptom may also be
potential underlying conditions:
 Endocarditis
 Rheumatic heart disease
Treatments for Heart block
Treatment list for Heart block: The list of treatments mentioned in various sources for
Heart block includes the following list. Always seek professional medical advice about any
treatment or change in treatment plans.
 Hospitalization
 Artificial pacemaker
 Treatment of any underlying cause
Basic Summary for Heart block
Main name of condition: Heart block
What is Heart block?

Brief description of Heart block: Failure of the heart's normal rhythm controls leading to
arrhythmia
Parent types of Heart block: Heart conditions
Organs Affected by Heart block: heart
Types of Heart block: First-degree heart block, Second-degree heart block, Third-degree
heart block
Who gets Heart block?

Patient Profile for Heart block: Usually older adults but younger age possible.
What causes Heart block?

Causes of Heart block: see causes of Heart block
Risk factors for Heart block: see risk factors for Heart block
What are the symptoms of Heart block?

Symptoms of Heart block: see symptoms of Heart block
How is it treated?
Treatments for Heart block: see treatments for Heart block
Risk factor list: The list of risk factors mentioned for Heart block in various sources
includes:
 Aging
 Atherosclerosis
 Diabetes
 Hypertension
 Electrolyte imbalance
 Heart disease
 Smoking
 Poor diet
 High-salt diet
 High cholesterol diet
 Stress
 Poor fitness
 Inactivity
http://www.emedicine.com/EMERG/topic233.htm
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Heart Block, First Degree
Last Updated: September 27, 2002 Email to a Colleague
Synonyms and related keywords: atrioventricular block, first-degree atrioventricular block,
AV block, first-degree AV block
AUTHOR INFORMATION Section 1 of 8
Author Information Introduction Clinical Differentials Workup Treatment Follow-up Bibliography
Author: David FM Brown, MD, Instructor, Department of Medicine, Division of Emergency

Medicine, Harvard Medical School; Associate Chief, Department of Emergency Medicine,
Massachusetts General Hospital
David FM Brown, MD, is a member of the following medical societies: Society for Academic
Emergency Medicine
Editor(s): Theodore Gaeta, DO, MPH, Residency Director, Clinical Associate Professor of
Emergency Medicine in Medicine, Department of Emergency Medicine, New York
Methodist Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor,
eMedicine; Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of
Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine,
The Sir Mortimer B Davis-Jewish General Hospital; John Halamka, MD, Chief Information
Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of
Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of
Medicine, Harvard Medical School; and Scott H Plantz, MD, FAAEM, Research Director,
Assistant Professor, Department of Emergency Medicine, Mount Sinai School of Medicine
Disclosure
INTRODUCTION Section 2 of 8
Background: First-degree heart block, or first-degree atrioventricular (AV) block, is a

condition that results in prolongation of the PR interval on electrocardiogram (ECG) to >0.20
seconds. The PR interval is defined as the time from the initial deflection of the P wave from
the baseline to the beginning of the QRS complex. A normal PR interval is from 0.12-0.20
seconds.
Pathophysiology: Electrophysiological studies have shown that first-degree heart block may
be due to conduction delay in the AV node, in the His-Purkinje system, or a combination of
the two. AV nodal dysfunction accounts for the majority of cases. However, in the subset of
patients with first-degree heart block and bundle-branch block, conduction delay in the His-
Purkinje system is the more likely cause.
Frequency:
 In the US: Prevalence in the young adult population ranges from 0.65-1.1%. Higher
prevalences are reported in studies of trained athletes (8.7%) and medical students
(8%). The incidence is 1.13 per 1000 persons.
Mortality/Morbidity: Morbidity and mortality rates from heart disease appear to be

unaffected by the presence of first-degree block.
CLINICAL Section 3 of 8
History:
 Patients may have a past history of heart disease, including myocardial infarction (MI)
or myocarditis.
 Patients may be highly conditioned athletes with a high degree of vagal tone or they
may be on medications that slow conduction through the AV node.
Physical: First-degree heart block is generally an incidental finding noted on ECG without
any particular associated signs.
Causes:
 The following are the most common causes of first-degree heart block:
o Intrinsic AV nodal disease
o Enhanced vagal tone
o Acute MI, particularly acute inferior MI
o Myocarditis
o Electrolyte disturbances
o Drugs
 The drugs that most commonly cause first-degree heart block are those that increase
the refractory time of the AV node, thereby slowing AV conduction. These drugs
include the following:
o Calcium channel blockers

o Beta-blockers
o Digitalis glycosides
Rate this Article

Heart Block, Second Degree
Last Updated: March 10, 2004 Email to a Colleague
Synonyms and related keywords: atrioventricular block, second-degree atrioventricular
block, AV block, A-V block, second-degree AV block, second-degree A-V block, Mobitz I,
Mobitz I heart block, Mobitz I atrioventricular block, Mobitz I AV block, Mobitz I A-V
block, Mobitz II, Mobitz II heart block, Mobitz II atrioventricular block, Mobitz II AV block,
Mobitz II A-V block
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Bibliography

Emergency Medicine
Disclosure
Background: Second-degree heart block or second-degree atrioventricular (AV) block refers

to a disorder of the cardiac conduction system in which some P waves fail to conduct to the
ventricle and to generate a QRS complex. Second-degree AV block comprises 2 types,
Mobitz I and Mobitz II.
Mobitz I AV block, or Wenckebach block, is characterized by progressive prolongation of the
PR interval causing progressive R-R interval shortening until a P wave fails to conduct to the
ventricle.
Mobitz II AV block is characterized by sudden unexpected blocked P waves without variation

or prolongation of the PR interval.
Pathophysiology: Mobitz I (Wenckebach) block is caused by conduction delay in the AV

node in 72% of patients and by conduction delay in the His-Purkinje system in the other 28%.
A narrow QRS complex makes the site of delay even more likely to be the AV node.
Wenckebach block with a wide QRS complex may be due to AV nodal or infranodal
conduction delay.
Electrophysiological studies have proved that Mobitz II block is due to an infranodal His-
Purkinje system conduction delay. It generally is associated with a wide QRS complex, except
in some patients whose delays are localized within the bundle of His.
Frequency:
 In the US: The prevalence of second-degree heart block in young adults is reported to
be 0.003%. Higher rates (2.4%) are observed in trained athletes undergoing routine
ECG.
Mortality/Morbidity:
 Most investigators believe that Mobitz I block localized to the AV node is not
significantly associated with morbidity or death in the absence of organic heart
disease. Type I block localized to the His-Purkinje system has the same risks as type II
block.
 Mobitz II block carries a high risk of progression to complete heart block, often with
associated cardiovascular collapse.
History:
 Mobitz I (Wenckebach) block
o Most patients are asymptomatic.
o Patients may experience dizziness, lightheadedness, or syncope, but these are

uncommon.
o Patients may have symptoms of myocardial ischemia or myocarditis.
o Patients may have a history of organic heart disease.
 Mobitz II block
o Patients may be asymptomatic but are more likely to present with dizziness,
lightheadedness, or syncope.
o Patients may have symptoms of myocardial ischemia or a history of organic

heart disease.
Physical:
 Patients may have an irregular heart rate, and often accompanying bradycardia, but the
examination is otherwise generally unremarkable.
 Symptomatic patients may have signs of hypoperfusion, including hypotension and

altered mental status.
 Patients with concomitant myocardial infarction (MI) may exhibit signs related to
acute MI.
Causes:
 Mobitz I block can be caused by acute inferior MI, states of vagal stimulation or
enhanced vagal tone, or toxicity relating to digitalis, beta-blockers, or calcium channel
blockers.
 Mobitz II block most commonly is caused by acute MI (anterior or inferior).
Lab Studies:
 Serum electrolytes may be checked, and a digoxin level is indicated for patients on
digoxin.
 Cardiac enzyme studies are indicated for any patient with suspected myocardial
ischemia, especially those with type II block.
Imaging Studies:
 Routine imaging studies are not required, although a chest radiograph may be
appropriate for those with signs and symptoms of myocardial ischemia.
Other Tests:
 Follow-up ECGs and cardiac monitoring are appropriate.
TREATMENT Section 6 of 9
Prehospital Care:
 Second-degree heart block requires no specific prehospital therapy, unless the patient
is symptomatic from a resulting bradycardia.
 Follow standard advanced cardiac life support (ACLS) guidelines in bradycardic

patients, including the use of atropine and transcutaneous pacing.
Emergency Department Care:
o No specific ED therapy is required.

o Treat patients who have associated myocardial ischemia with appropriate anti-
ischemic medications.
o Withhold AV nodal agents.

o Treat patients who have symptomatic bradycardia with atropine and
transcutaneous pacing per standard ACLS guidelines.
o Use caution in administering atropine to a patient with suspected acute MI,

because atropine has been reported to precipitate ventricular tachycardia or
ventricular fibrillation in this situation.
 Mobitz II block
o More aggressive ED therapy is required.

o Withhold AV nodal agents and initiate anti-ischemic therapy when
appropriate.
o Apply and test transcutaneous pacing patches, even in asymptomatic patients;

patients with Mobitz II block have a propensity for progression to complete
heart block.
o Urgent cardiology consultation is indicated in patients with symptoms and

those in whom transcutaneous pacing is tested unsuccessfully; these patients
may require placement of a temporary transvenous pacing wire.
o Some experts recommend transvenous pacing in all patients with new type II
block, although this practice varies from institution to institution.
o Patients with unstable cardiac signs also may be treated with atropine, although
this is much less likely to be successful in Mobitz II block. Use caution in
administering atropine in the setting of a suspected acute MI.
o Patients with unstable cardiac signs for whom cardiology consultation is not
available in a timely fashion should undergo temporary transvenous pacing
wire placement in the ED.
o Obtain a chest radiograph to confirm placement of the transvenous pacing wire
and exclude complications of the procedure, including pneumothorax and
hemothorax.
Consultations:
 Mobitz I block
o Cardiology consultation is indicated for symptomatic patients or those with

concomitant myocardial ischemia.
o Cardiology consultation also may be useful in asymptomatic patients in stable

condition, particularly with regard to disposition decisions.
 Mobitz II block: Cardiology consultation is indicated for all of these patients,

regardless of symptoms.
The goal is to improve conduction through the AV node by reducing vagal tone via
atropine-induced receptor blockade. This is effective only if the site of block is the AV node.
For patients with infranodal second-degree heart block, atropine generally is ineffective.
Drug Category: Anticholinergic -- Drug therapy in second-degree heart block is aimed at

vagolysis; atropine is the only currently available agent.
Atropine (Atropair, Atropine-Care, Isopto) -- Enhances sinus

node automaticity. In addition, blocks effects of acetylcholine
Drug Name at AV node, thereby decreasing refractory time and speeding
conduction through AV node. Insufficient doses may cause
paradoxical effects, further slowing heart rate.
0.5-1 mg rapid IV push q3-5min; not to exceed 0.04 mg/kg
Adult Dose Also may be given via endotracheal tube, although its
absorption may be unreliable
0.02 mg/kg IV push; minimum dose 0.1 mg; single dose not
to exceed 0.5 mg (child), 1 mg (adolescent); total dose not to
Pediatric Dose exceed 1 mg (child), 2 mg (adolescent)
Also may be given via endotracheal tube, although its
absorption may be unreliable
Absolute: None
Relative: Documented hypersensitivity; documented
sensitivity to belladonna alkaloids or related products;
concomitant acute MI/ischemia, thyrotoxicosis, narrow-angle
Contraindications
glaucoma, or tachycardia; Down syndrome or brain damage
in children because they may show hyperreactive response to
topical atropine; coronary heart disease; congestive heart
failure; cardiac arrhythmias; hypertension
Interactions Other anticholinergics have additive effects; may increase
pharmacologic effects of atenolol and digoxin; may decrease
antipsychotic effects of phenothiazines; tricyclic
antidepressants with anticholinergic activity may increase
effects
Pregnancy C - Safety for use during pregnancy has not been established.
Avoid in Down syndrome and/or children with brain damage
to prevent hyperreactive response; avoid also in coronary
heart disease, tachycardia, congestive heart failure, cardiac
Precautions arrhythmias, and hypertension; caution in peritonitis,
ulcerative colitis, hepatic disease, and hiatal hernia with
reflux esophagitis; in prostatic hypertrophy or prostatism,
may cause dysuria, necessitating catheterization
FOLLOW-UP Section 8 of 9
Further Inpatient Care:
o Admit patient with symptoms of bradycardia or with concomitant acute

myocardial ischemia.
o Admission should be to a unit that has telemetry monitoring and available

transcutaneous pacing capabilities.
 Mobitz II block
o Admit all patients to a unit with monitored beds.
o Transcutaneous and transvenous pacing capabilities should be available.
o The admitting cardiologist should determine whether permanent pacemaker

implantation is necessary.
Further Outpatient Care:
 Patients who are discharged from the ED with Wenckebach block should have prompt
follow-up with a primary care physician or cardiologist.
Complications:
 The most important complication of second-degree heart block is progression to
complete heart block with associated cardiovascular collapse.
 Progression to complete heart block is seen much more commonly with Mobitz II
block than with Wenckebach block.
Prognosis:
 Wenckebach block carries a good prognosis with appropriate follow-up and treatment.
 Mobitz II block is a more dangerous entity, as it progresses more frequently to

complete heart block and cardiovascular collapse. It also commonly is associated with
acute MI and its attendant risks.
Rate this Article

Heart Block, Third Degree
Last Updated: September 27, 2002 Email to a Colleague
Synonyms and related keywords: atrioventricular block, AV block, third-degree
atrioventricular block, third-degree AV block, complete heart block
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

Emergency Medicine
Disclosure
Background: Third-degree heart block, also referred to as third-degree atrioventricular (AV)
block or complete heart block, is a disorder of the cardiac conduction system with complete
absence of AV conduction. No P waves conduct to the ventricle, and AV dissociation is
complete. The ventricular escape mechanism may originate anywhere from the AV node to
the bundle branch-Purkinje system. Not all patients with AV dissociation have complete heart
block. For example, patients with accelerated junctional rhythms that are faster than their
native sinus rates have AV dissociation but not complete heart block, because no AV
conduction disorder is present.
Pathophysiology: Third-degree heart block is caused by conduction block at the level of the
AV node, the His bundle, or the bundle branch-Purkinje system. Block below the His bundle
accounts for the majority of cases (approximately 61%). Block within the AV node accounts
for 21%, and block within the His bundle represents 14-18%.
Duration of the escape QRS complex depends on the site of the block and the site of the
escape rhythm pacemaker. Pacemakers above the His bundle produce a narrow QRS complex
escape rhythm, while those at or below the His bundle produce a wide QRS complex. When
the block is at the level of the AV node, the escape rhythm generally arises from a junctional
pacemaker with a rate of 45-60 beats per minute. Such patients frequently are
hemodynamically stable, and their heart rates increase in response to exercise and atropine.
When the block is below the AV node, the escape rhythm arises from the His bundle or the
bundle branch-Purkinje system at rates less than 45 beats per minute. These patients generally
are hemodynamically unstable, and their heart rates are unresponsive to exercise and atropine.
Mortality/Morbidity: Patients with complete heart block frequently are hemodynamically

unstable. This may lead to cardiovascular collapse, syncope, and death.
History:
 Patients may be asymptomatic or may have minimal symptoms related to

hypoperfusion, including the following:
o Fatigue
o Dizziness
o Impaired exercise tolerance
 Symptoms are more likely to be minimal in patients with narrow complex escape
rhythms.
 More commonly, patients are profoundly symptomatic, especially when the escape
rhythm is wide and slow.
 Symptoms may include the following:
o Syncope (Stokes-Adams attack)
o Confusion
o Sudden death
 Patients also may have associated symptoms of acute myocardial infarction (MI).
 Patients may have a prior history of organic heart disease or be on medications that
affect AV nodal conduction, including the following:
o Beta-blockers
o Calcium channel blockers
o Digitalis glycosides
Physical:
 The physical examination will be notable for bradycardia, which may be profound.
 Symptomatic patients will have signs of hypoperfusion, including the following:
o Hypotension
o Altered mental status
o Lethargy
 Congestive heart failure may be present.
 In patients with concomitant MI, signs of acute MI may be evident on examination.
 Regularized atrial fibrillation is the classic sign of complete heart block due to digitalis
toxicity. The rhythm is regularized because of the junctional escape rhythm.
Causes: Third-degree heart block may be congenital or acquired.
 Congenital block usually occurs at the level of the AV node.
 Acquired block at the AV node is due to the following:
o Acute inferior MI
o Profound hypervagotonicity
o Drug intoxications (eg, digitalis, beta-blockers, calcium channel blockers)
 Infranodal block most commonly is caused by acute anterior MI. This may require
emergency pacing.
 Other causes of third-degree heart block
o Metabolic disturbances
o Cardiomyopathies
DIFFERENTIALS Section 4 of 10
Cardiomyopathy, Dilated
Cardiomyopathy, Restrictive
Heart Block, First Degree
Heart Block, Second Degree
Myocardial Infarction
Myocarditis
Myopathies
WORKUP Section 5 of 10
Lab Studies:
 Cardiac enzymes are indicated to rule out MI.
 Check serum electrolytes in addition to a digoxin level when appropriate.
Imaging Studies:
 Obtain a chest radiograph to evaluate for pulmonary edema.
Other Tests:
 Perform initial and follow-up ECGs, which are necessary to make the diagnosis and to
monitor response to therapy.
Procedures:
 Temporary pacemaker insertion through a central venous introducer may be required

in a subset of hemodynamically unstable patients who do not respond to less invasive
therapy.
TREATMENT Section 6 of 10
Prehospital Care:
 Asymptomatic patients: Rapidly transport to the nearest available facility, applying

advanced life support (ALS) with continuous cardiac monitoring as needed.
 Symptomatic patients: Transcutaneous pacing is the treatment of choice.
 Administer oxygen.
 Establish intravenous access.
 Avoid maneuvers likely to increase vagal tone (ie, Valsalva, painful stimuli).
 Atropine can be administered (cautiously, if acute MI is the underlying cause) but is
likely to be ineffective unless the escape QRS complex is narrow.
Emergency Department Care:
 In the ED, continue the treatment initiated in the prehospital setting, which includes
the following:
o Oxygen administration
o Continuous cardiac monitoring
o Frequent blood pressure measurements
 Establish secure large-bore intravenous access.
 Withhold AV nodal agents and deliver anti-ischemic therapy where appropriate.
 Apply and test transcutaneous pacing patches for all patients with third-degree heart
block.
 Hemodynamically stable patients in whom pacing can be established transcutaneously

can be admitted to a telemetry unit. They may undergo elective placement of a
permanent pacemaker at the discretion of the cardiologist.
 Symptomatic patients and those in whom transcutaneous pacing is tested
unsuccessfully should have urgent cardiac consultation for the placement of a
temporary transvenous pacing wire.
 Hemodynamically unstable patients may be treated with atropine, although this will be
ineffective in patients with a wide complex escape rhythm. Use caution in
administering atropine in the setting of a suspected acute MI, as the resulting vagolysis
leads to unopposed sympathetic stimulation, causing increased ventricular irritability
and, potentially, ventricular tachycardia (VT)/ventricular fibrillation (VF).
 Hemodynamically unstable patients for whom timely cardiology consultation is

unavailable should undergo temporary transvenous pacemaker insertion in the ED by
the ED physician.
 Obtain a chest radiograph to confirm placement and exclude complications of
transvenous pacemaker insertion, including pneumothorax and hemothorax.
Consultations:
 Cardiology consultation is indicated for all patients with third-degree heart block.
 The consultation is urgent in patients with concomitant acute MI, wide complex
escape rhythms, or symptoms of hypoperfusion.
http://www.med.umich.edu/1libr/heart/rate04.htm
Heart Rate and Rhythym

Heart Block
What is heart block?
Heart block is a disorder of the heartbeat. It occurs when the contractions of the
upper chambers of the heart, called atria (AY-tree-ah), fail to coordinate with the
contractions of the ventricles, or the heart's lower chambers. This interrupts the
passage of impulses from the atria to the ventricles. There are various degrees of
heart block. In first-degree block, the passage of impulses is delayed and there are
no symptoms. In second-degree heart block, some of the atrial impulses fail to reach
the ventricles that can cause the pulse to become irregular. In third-degree block,
known as complete heart block, no atrial impulses reach the ventricles and the flow
of oxygenated blood to the brain and the rest of the body is insufficient. Fainting or
convulsions may result.
What causes heart block and how is it treated?
Heart block may be caused by coronary artery disease, inflammation of the heart
muscle, rheumatic fever, or overdose of certain heart drugs. Treatment depends on
the degree of heart block experienced. Some cases need no treatment while others
require medication or an artificial pacemakers.
http://www.americanheart.org/presenter.jhtml?identifier=4611
Heart Block
The heart has four chambers. The top two are called the atria. The bottom two are called the
ventricles.
The heart's "natural" pacemaker is called the sinoatrial (SA) node or sinus node. It's a small
mass of specialized cells in the heart's right atrium. It produces electrical impulses that make
your heart beat. For your heart to beat properly, the signal must travel from the SA node down
a specific path to reach the ventricles. As the signal goes from the atria to the ventricles, it
passes through specialized conducting tissue called the atrioventricular (A'tre-o-ven-TRIK'u-
ler) (AV) node.
On an electrocardiogram (e-lek"tro-KAR'de-o-gram) (ECG), a portion of the graph called the

P wave shows the impulse passing through the atria. Another portion of the graph, the QRS
wave, shows the impulse passing through the ventricles. As long as the impulse is transmitted
normally, the heart pumps and beats at a regular pace.
What is heart block?
Sometimes the signal from the heart's upper to lower chambers is impaired or doesn't
transmit. This is "heart block" or "AV block." This does not mean that the blood flow or
blood vessels are blocked.
Heart block is classified according to the level of impairment -- first-degree heart block,
second-degree heart block or third-degree (complete) heart block.
What is first-degree heart block?
First-degree heart block, or first-degree AV block, is when the electrical impulse moves
through the AV node more slowly than normal. The time it takes for the impulse to get from
the atria to the ventricles (the PR interval) should be less than about 0.2 seconds. If it takes
longer than this, it's called first-degree heart block.
Heart rate and rhythm are normal, and there may be nothing wrong with the heart.
Certain heart medicines such as digitalis (DIJ'ih-TAL'is) can slow conduction of the impulse
from the atria to the ventricles and cause first-degree AV block. Also, well-trained athletes
may have it.
Generally, no treatment is necessary for first-degree heart block.

What is second-degree heart block?
In this condition, some signals from the atria don't reach the ventricles. This causes "dropped
beats." On an ECG, the P wave isn't followed by the QRS wave, because the ventricles
weren't activated. There are two types:
 Type I second-degree heart block, or Mobitz Type I, or Wenckebach's AV block.

Electrical impulses are delayed more and more with each heartbeat until a beat is
skipped. This condition is not too serious but sometimes causes dizziness and/or other
symptoms.
 Type II second-degree heart block, or Mobitz Type II. This is less common than
Type I but generally more serious. Because electrical impulses can't reach the
ventricles, an abnormally slow heartbeat may result. In some cases a pacemaker is
needed.
What is third-degree or complete heart block?
Complete heart block (complete AV block) means that the heart's electrical signal doesn't pass
from the upper to the lower chambers. When this occurs, an independent pacemaker in the
lower chambers takes over. The ventricles can contract and pump blood, but at a slower rate
than that of the atrial pacemaker.
These impulses are called functional or ventricular scope beats. They're usually very slow and
can't generate the signals needed to maintain full functioning of the heart muscle. On the
ECG, there's no normal relationship between the P and the QRS waves.
Complete heart block is most often caused in adults by heart disease or as a side effect of drug
toxicity. Heart block also can be present at -- or even before -- birth. (This is called congenital
heart block.) It also may result from an injury to the electrical conduction system during heart
surgery. Complete heart block may be a medical emergency with potentially severe symptoms
and a serious risk of cardiac arrest (sudden cardiac death). If a pacemaker can't be implanted
immediately, a temporary pacemaker might be used to keep the heart pumping until surgery
can be performed.
http://www.nhsdirect.nhs.uk/en.asp?TopicID=232
Introduction
Heart block is a condition where the heart beats
irregularly or much more slowly than normal.
Sometimes the heart may even stop for up to 20
seconds. It is caused by a delay or disruption of the
electrical signals that usually control the heartbeat.
A healthy heart in an averagely fit person beats

between 60 and 80 times a minute. A heartbeat is
when the muscles of the heart contract and push
blood around the body. These muscle contractions
are controlled by electrical signals that travel
between the heart’s upper chambers (the atria) and
lower chambers (the ventricles).
If these electrical impulses are delayed or sometimes

stopped (partial heart block), then the heart may not
beat regularly. If the electrical signals are stopped
completely (complete heart block), then the heart
will only beat around 40 times a minute.
Heart block reduces the heart’s efficiency in pushing

blood around the body. This means that the muscles
and brain may not be getting enough oxygen for
them to work properly.
Diagnosis
Heart block is usually diagnosed by a doctor by recognising the symptoms in the light of the
patient’s age and medical history. An electrocardiogram (ECG) test is needed to be sure of
the diagnosis.
Symptoms
The main symptoms of heart block are a slow or irregular heartbeat. Symptoms can also
include:
 shortness of breath
 palpitations (when you notice the irregular heartbeat)
 fainting or light-headedness
 discomfort or pain in the chest.
Heart block usually happens to older people with a history of heart disease or smoking.
If left untreated, heart block can lead to a stroke and heart failure
Treatment
The long-term treatment for heart block is to fit a ‘pacemaker’. This is a small, battery-driven
device that sends out electrical signals to keep the heartbeat regular.
Modern pacemakers are very sophisticated and some can be set to produce an electrical
impulse only when one is needed. Some can even tell when the heart stops beating and
produce a small electric shock to restart it. (Older pacemakers used to produce the electrical
signal at a constant rate and this limited the patient’s physical activity.)
Before having a permanent pacemaker, some patients might need a temporary ‘pacing wire’.
The pacing wire does a similar job to a pacemaker (sending electrical signals to regulate the
heartbeat) but is inserted through a vein in the chest or groin area.
Sometimes no treatment is recommended. This may be when patients are elderly and the
symptoms are very minor, or where people have other medical conditions that would make
the operation to fit a pacemaker too dangerous.
Causes
Heart block is caused by damage to the tissue that passes the electrical signals through the
heart. This usually happens to older people who have had a heart disease such as:
 cardiomyopathy (disease of heart muscle)

 Coronary thrombosis (sudden blockage in the heart blood vessels)
 myocarditis (inflammation of the muscle in the wall of the heart)
 valvular heart disease (disease of the heart valves).
Sudden complete heart block (either temporary or permanent) can also happen after a heart
operation or following a heart attack.
Heart block may also be caused by problems that have been there from birth (congenital heart
block).
http://www.tmg.org.yu/v281207.htm
Prikaz bolesnika
Overdrive pace marker u akutnom trovanju propranololom - prikaz

slučaja
Overdrive pace maker in propranolol - induced poisoning - case
report
Slađana Anđelić
Gradski zavod za hitnu medicinsku pomoć, Beograd
Sažetak:
Beta-adrenergički blokatori primenjuju se u lečenju hipertenzije, angine pectoris,
tahidizritmije i predoziranju teofilinom. Pacijenti sa simptomatskim overdozama beta-
adrenergičkih antagonista su hipotenzivni i bradikardični. Smanjenje funkcije SA čvora
dovodi do sinusne bradikardije ili sinusnog aresta. Oštećenje atrioventrikularnog sprovodjenja
se odlikuje produženim PR intervalom ili kompletnim AV blokom. Indikacije za privremenu
elektrostimulaciju srca su sinusna bradikardija i kompletni AV blok koji ne reaguju na i.v.
terapiju atropinom. Prikazujemo slučaj 65-godišnje pacijentkinje predozirane propranololom.
Pri pregledu je bila somnolentna, dizartrična, eupnoična sa teškom hipotenzijom. Na
uradjenom EKG-u registruje se sinusna bradikardija frekvence 29/min sa kompletnim AV
blokom, koji nisu reagovali na i.v. primenu atropina. Kao terapija izbora bila je neophodna
primena privremene elektrostimulacije srca.
Ključne reči: Beta-blokatori, Propranolol, Bradikardija, Kompletni AV blok, Privremeni
pejsmejker
Summary:
Beta-adrenergic antagonist are used in the treatment of hypertension, angina, tachy-
dysrhythmias and theophylline overdoses. Patients with symptomatic beta-adrenergic
antagonist overdose are hypotensive and bradycardic. Decreased SA node functions results in
sinus bradycardia or sinus arrest. Impaired atrioventricular conductions is manifested as
prolonged PR interval or complete AV block. The indication for overdrive pacing was
symptomatic bradicardia and complete AV block, not responding to i.v. atropine. We present
a case of 65-years old women with propranolol poisoning. At the reception she was
somnolent, disartric, eupnoic, with severe hypotension. There was a 29/min sinus bradicardia
on ECG, with an complete AV block, not responding to i.v. atropin. In that case overdrive
pacing is an optimal therapeutical option.
Key words: Beta-antagonist, Propranolol, Bradicardia, Complete AV block, Overdrive
Pacing
Uvod
Lekovi mogu prouzrokovati simptomatske bradikardije sa poremećajem ritma kod kojih je

nekada neophodna primena privremene elektrostimulacije srca. Trovanja beta blokatorima ne
retko (1, 2) dovode do teške pa i fatalne kardiovaskularne depresije, sa ozbiljnim
poremećajima srčanog ritma, kardiogenim šokom, respiratornim depresijama, konvulzijama i
komom (3,4). Pacijent je u stanju vitalne ugroženosti što se ne objašnjava samo beta
blokadom već i mehanizmima centralne kardio i respiratorne toksičnosti, poremećajem
homeostaze kalcijuma i efektom stabilizacije ćelijske membrane. Neki od ovih agenasa, kao
propranolol, su "neselektivni" sa istim afinitetom za beta1 i beta2 receptore, i visoko
liposolubilni. Klasični nalazi u situacijama njegovog predoziranja su bradikardija, AV blok i
hipotenzija, praćeni neurološkom i plućnom simptomatologijom (1).
Klinička prezentacija predoziranja propranololom obuhvata: kardijalne efekte: sinusna
bradikardija, AV blok i hipotenzija, neurološke efekte: izmenjen mentalni status, od
delirijuma do kome i konvulzije čija su preteča poremećaji sprovodjenja u srcu, plućne efekte:
bronhospazam, nestabilni dijabetes (hipoglikemijska reakcija) i Renalna i hepatična
disfunkcija.
Laboratorijska procena kvalitativnog i kvantitativnog nivoa propranolola u inicijalnom
lečenju nisu dostupni. Vodiči za interpretaciju dijagnoze trovanja na terenu su indirektni
parametri za efekte beta-blokatora kroz EKG zapis ili EKG monitoring. Kongestija, posebno
sa blokatorima Ca-kanala, dovodi do toksičnosti u kojoj su beta-blokeri "dirigenti" ispoljene
kliničke slike (5).
TERAPIJA obuhvata opšte i specifične (antidotske) mere.
A. OPŠTE MERE su: mere kardiopulmonalne reanimacije, lavaža želuca (ne provocirati
povraćanje), primena aktivnog uglja i nadoknada tečnosti. Eksperti savetuju upotrebu
atropina, pre gastrične lavaže, za prevenciju povišenog vagalnog tonusa koji pogoršava
kardiodepresiju. Konvulzije su posledica liposolubilnosti propranolola ili sekundarnih efekata
(hipoksija, hipoglikemija). Kupiraju se diazepamom.
B. SPECIFIČNE MERE I ANTIDOTI su fokus lečenja. Za prevladavanje kardijalnih efekata
beta-blokade koji su glavni razlog letalnog ishoda, neophodni su atropin, kateholamini i
glukagon. Lek prve linije za savladavanje bradikardije i hipotenzije kod predoziranja beta-
blokatora je glukagon koji povećava miokardni c-AMP, inotropni i hronotropni efekat
mehanizmima koji su nezavisni od beta-receptora. Pojačava kontraktilnost miokarda, srčanu
frekvencu i AV sprovodjenje. Po potrebi ponavljati bolus-dozu od 5 mg svakih 15-30 minuta
ili primeniti i.v infuziju 1-5 mg/h sve do 10 mg/h za teška trovanja. U ozbiljnim ingestijama,
ukupna doza je 30 mg ili više. Kod simptomatske bradikardije, inicijalno lečenje započeti
atropinom u početku 0.5 mg i.v sa ponavljanjem do kumulativne doze od 3 mg. I
kateholamini dobutamin, epinefrin, dopamin mogu biti neophodni. Predlaže se spora
i.v.infuzija dopaminom 3-20µg/kg/min u lečenju bradikardije i hipotenzije. Renalna doza
dopamina se može koristiti s ciljem da se održi renalna perfuzija. Inhibitori fosfodiesteraze
(aminofilin) pomažu u održavanju nivoa intracelularnog c-AMP-a i pojačanju kontraktilnosti
miokarda. Ako postoji srčani blok visokog stepena a nema odgovora na farmakološku terapiju
neophodan je pacemaker (6). Primenjuje se transvenska ventrikularna privremena
elektrostimulacija srca. Kao pristupni put za plasiranje pejsmejkerske elektrode koriste se
velike vene (najčešće v.jugularis int.dex.) (7). Česte su novonastale sinkope kao posledica
sekundarnih efekata: hipoksije, hipoglikemije i hipotenzije. U ovakvim stanjima
elektromehanička podrška privremenim pejsmejkerom jedina je efikasna terapijska mera.
Indikacije za privremenu elektrostimulaciju su: bradikardija uzrokovana lekom (frekvenca
manja od 45/min), i/ili AV blok teškog stepena, praćena hipotenzijom (sistolni krvni pritisak
manji od 90 mmHg) i simptomima i znacima poremećenog hemodinamskog stanja (sinkopa,
srčana insuficijencija, bol u grudima, poremećen mentalni status i dr.), a koja ne reaguju na
atropin. Zaključak da su ove manifestacije uzrokovane propranololom, donosi se na osnovu
podataka da je bolesnik uzimao ovaj lek, utvrdjivanjem njegove koncentracije u serumu, na
osnovu prolaznosti poremećaja provodjenja po obustavi leka i isključivanjem drugih uzroka.
Pacijenti koji su ingestirali preparate sa usporenim oslobadjanjem ili su životno ugroženi
moraju biti hospitalizovni.
Prikaz slučaja
Pacijentkinja u dobi od 42 god., predaje poziv Službi hitne medicinske pomoći zbog povrede
desnog ramena. Anamnestički opisuje dve epizode sinkope: jednu par sati a drugu dvadesetak
minuta pre dolaska ekipe Hitne pomoći, kada i zadobija lakšu povredu. Dugogodišnji je
hipertoničar, koji nerado posećuje lekare, pa je poslednjih desetak dana samoinicijativno zbog
učestalih bolova u grudima, koristila iz kućne apoteke, staru zalihu leka propranolol (ukupno i
do 300 mg dnevno). Pri pregledu je lako somnolentna, verbalno komunikativna ali konfuzna,
nesigurna pri hodu, afebrilna, eupnoična, acijanotična, anikterična, orošena hladnim znojem.
Glava palpatorno bez bolnih tačaka. Zenice kružne i jednake sa reakcijom na svetlost i
akomodaciju. Neurološki bez znakova lateralizacije. Srčana radnja bradikardična do 32/min,
tonovi mukli, tenzija nemerljiva. Na EKG-u: bradikardija do 29/min i AV blok IIIo (Sl.1.).
Auskultatorno, na plućima vezikularno disanje. Abdomen mek, palpatorno bolno neosetljiv.
Jetra i slezina u fiziološkim granicama. Sem hematoma na desnom ramenu, ekstremiteti bez
otoka i deformiteta. Nakon pregleda pacijentinji je plasirana i.v. braunila putem koje je
ordinirana terapija. Nakon 2 miligrama atropina data u i.v. bolusu, uspostavljena je frekvenca
od 32/min, ali se evidentira epi napad po tipu grand mal (kupiran sa 5 mg diazepama i.v.) sa
respiratornim arestom, zbog čega je odmah intubirana, nakon čega suficijentno i spontano
diše. Arterijski krvni pritisak i dalje ispod 70/0 mmHg te je uključena i.v.infuzija 200 mg
dopamina u 500 ml 5% glukoze brzinom 10µg/kg/min = 35 kapi/min. Pacijentkinja je u
pratnji lekara i medicinskog tehničara prebačena do bolnice. Zbog teške kardiodepresije u
Prijemnoj ambulanti je plasiran overdrive pace maker. Nakon uspostavljanja ritma
pejsmejkera, u toku hospitalizacije pritisak se normalizuje, da bi tek četvrtog dana nakon
normalizovanja frekvencije bila prekinuta elektrostimulacija. Normalan EKG zapis se beleži
tek desetog dana od trovanja.
Zaključak
Beta blokatori, pored nesumljive terapijske efikasnosti, imaju veliki potencijal u izazivanju
kardiodepresije, hipotenzije i bradikardije. Terapija trovanja je suportivna i simptomatska.
Privremeni kardijalni pejsing je ne samo apsolutna indikacija kod kardionestabilnih pacijenata
već i efikasna mera lečenja.
Literatura
1. Zipes D.P.: Management of cardiac arrhythmias, pharmacological, elektrical and
surgical techniques. In: Braunwald E. (ed): Heart disease. A textbook of
cardiovascular medicine. Philadelphia, Saunders,1997: 593-639.
2. Ramoska E.A., Spiller H.A., Winter M. A I year evaluation of beta blocker overdoses:
Toxicity and treatment. Ann Emerg Med, 1993; 22:196.
3. Browning RG, Merigian KS: Acute beta blocker poisoning. Top Emerg med 1993; 15:
1-14
Reith DM, Dawson AH, Epid D.: Relative toxicity of beta blockers in overdose. J
Toxicol Clin Toxicol 1996; 34(3): 273-8.
4. Harby K, Kucharski K, Tuck S, Vasquez J.: Beta blockers and performance anxiety in
musicians: frequently asked questions. Larry Krantz Flute,1997; 1-6.
5. Mukherjee D.: Temporary transvenous pacing. In: Topol E.J. (ed): Manual of
cardiovascular Medicine. Philadelphia, Lippincott Williams&Wilkins 2000; 666-9.
6. Keim S.: Temporary pacing. In: Uretsky B.F. (ed): Cardiac catheterization: concepts,
Techniques and applications. Boston, Blackwell Scientific 1997; 618-29.
Adresa autora:
Anđelić Slađana
Pariske Komune 61/132
11000 Beograd
e-mail: pekos@yubc.net
Rad je primljen: 26. 12. 2002.

Rad je prihvaćen: 15. 01. 2003.
PROPRANOLOL tablete 40 mg
GENERIČKO IME
propranolol
PAKOVANJE
50 tableta od 40 mg
SASTAV
1 tableta sadrži:
propranolol-hidrohlorida 40 mg
DEJSTVO
PROPRANOLOL je kompetitivni antagonist beta-adrenergičkog receptora, bez ispoljavanja

selektivnog delovanja prema podklasama beta-1 i beta-2. On ne poseduje unutrašnju aktivnost
kao neki drugi beta-blokatori, ali pokazuje stabilišuće delovanje na ćelijsku membranu.
Njegov najvažniji efekat je zaštita srca od ekscesivne simpatičke stimulacije psihičkog ili
fizičkog porekla.
Propranolol-hidrohlorid smanjuje srčanu frekvenciju, snagu srčane kontrakcije, minutni
volumen srca, ukupni srčani rad, pa prema tome smanjuje i potrebu za kiseonikom.
Propranolol-hidrohlorid dovodi do blagog i postepenog snižavanja krvnog pritiska u bolesnika
sa esencijalnom i renalnom hipertenzijom.
TERAPIJSKE INDIKACIJE
Arterijska hipertenzija, angina pektoris, neki oblici disritmije srca, dugotrajna profilaksa posle
infarkta miokarda, hipertrofična opstruktivna kardiomiopatija, profilaksa migrene, esencijalni
tremor, razna anksiozna stanja, feohromocitom, kao adjuvans za lečenje od tireotoksikoze i
tireotoksične krize, glaukom i profilaksa krvarenja iz gornjeg dela gastrointestinalnog trakta u
bolesnika sa portnom hipertenzijom i ezofagealnim variksima.
DOZIRANJE I NAČIN PRIMENE
Arterijska hipertenzija
Početna doza od 80 mg dva puta dnevno može se, po potrebi, postepeno povećavati u
nedeljnim intervalima do uobičajene dnevne doze od 160 do 320 mg. Kombinacija sa
diureticima ili nekim drugim antihipertenzivom je moguća.
Angina pektoris, anksioznost, migrena i esencijalni tremor
Početna doza od 40 mg 2-3 puta dnevno može se postepeno povećavati za 40 mg u nedeljnim
intervalima do postizanja željenog odgovora. Kod anksioznosti, migrene i esencijalnog
tremora dobar efekat se postiže sa dozom od 80 do 160 mg dnevno, a kod angine pektoris sa
dozom od 120 - 240 mg dnevno.
Dugotrajna profilaksa posle infarkta miokarda
Terapiju treba početi između 5. i 21. dana posle preležanog infarkta miokarda, dozom od 40
mg 4 puta dnevno. Posle 2-3 dana, nastaviti sa 80 mg 2 puta dnevno.
Feohromocitom
60 mg dnevno sa alfa-blokatorima, u toku 3 dana pre operacije, ili 30 mg dnevno u
neoperacionim slučajevima.
Aritmije, kardiomiopatije i tireotoksikoza
Dozom od 10-40 mg 3-4 puta dnevno postiže se željeni odgovor.
Portna hipertenzija i glaukom
Minimalna dnevna doza je 80 mg, a maksimalna dnevna doza je 320 mg.
Tablete PROPRANOLOLA se uzimaju pre jela.
NEŽELJENI EFEKTI
Hladni ekstremiteti, muka, nesanica, malaksalost i dijareja obično su prolaznog karaktera i

nestaju posle prestanka uzimanja leka. U pojedinim slučajevima zabeleženi su purpura i suve
oči, trombocitopenija, eritematozni raš, parestezije ruku i simptomi vezani za CNS,
uključujući i halucinacije. Učestalost ovih pojava je mala i simptomi se uglavnom povlače sa
prestankom upotrebe leka.
U retkim slučajevima, kada se usled nepodnošljivosti javi znatnija bradikardija i hipotenzija,
terapija se prekida i, ukoliko je potrebno, pristupa se lečenju kao pri prekoračenju doze.
Ukoliko se prekorači doza, bradikardiju sanirati intravenskom primenom 1-2 mg atropina ili,
ako je potrebno, primeniti bolus dozu glukagona od 10 mg i.v. ili i.v. infuziju glukagona 1-10
mg/h, zavisno od reakcije pacijenta. Ako je neophodno, treba primeniti i stimulatore beta-
adrenergičkih receptora, izoprenalin u dozi od 25 mcg i.v. ili orciprenalin u dozi od 0,5 mg
i.v.
Pri ponovnom uvođjenju PROPRANOLOLA u terapiju, lečenje započeti malim dozama uz
njihovo postepeno povećavanje.
KONTRAINDIKACIJE
- Srčani blok II i III stepena,

- kardiogeni šok,
- pacijenti sa bronhospazmom u anamnezi i opstruktivnom bolešću pluća,
- posle duže dijete,
- metabolička acidoza (u dijabetičara).
UPOZORENJE
Naročitu pažnju treba posvetiti bolesnicima čija je srčana rezerva mala. Simptome slabljenja
kontraktilnosti miokarda treba suzbiti primenom digitalisa i diuretika.
Jedna od farmakoloških osobina PROPRANOLOLA je negativno hronotropno delovanje.
Frekvencija manja od 55 do 50 udara u minuti ukazuje da se doza ne sme povećavati. U
bolesnika sa ishemijskom srčanom bolešću lečenje beta-blokatorima ne sme se naglo
prekinuti, već doze PROPRANOLOLA treba postepeno smanjivati.
Nepoželjna je primena propranolola u opstruktivnim oboljenjima perifernih arterija.
Propranolol, kao i drugi beta-blokatori, maskira tahikardiju u hipoglikemiji. Takođe, kod
insulin-zavisnih dijabetičara propranolol može da produži hipoglikemijski odgovor na insulin.
Preporučuje se prekid terapije blokatorima beta-adrenergičkih receptora pre hirurške
intervencije. Ukoliko to nije moguće potrebna je opreznost pri primeni anestetika kao što su:
etar, ciklopropan i trihloretilen i, ukoliko se javi dominacija vagusa, dati intravenski 1-2 mg
atropina.
Propranolol ne treba davati u trudnoći i dojiljama, osim kada je njegova primena neophodna.
Nema dokaza o teratogenosti propranolola.
INTERAKCIJE
Ako se PROPRANOLOL primenjuje sa klonidinom, treba nastaviti lečenje klonidinom

nekoliko dana posle prekidanja terapije PROPRANOLOLOM.
Propranolol može potencirati negativno inotropno dejstvo antiaritmika, naročito prenilamina i
verapamila, pa ih ne treba kombinovati.
Delovanje drugih depresora miokarda kao što su halotan, ciklopropan, etar, naročito
antiaritmika hinidina, prokainamida, lidokaina, fenitoina i kalcijumskih antagonista može biti
pojačano istovremenom primenom sa propranololom.
NAČIN IZDAVANJA
Lek se može izdavati samo uz lekarski recept.
NAČIN ČUVANJA
Čuvati na temperaturi do 25°C, zaštićeno od svetlosti i vlage.

Čuvati van domašaja dece.
ROK UPOTREBE
5 godina
Lek se ne sme koristiti posle isteka roka upotrebe označenog na pakovanju.
EKG - elektrokardiogram
Ovaj tekst ne želi i sigurno ne može nadomjestiti sve knjige i tekstove koji su
pisani o EKG-u, ali može razjasniti neke osnovne pojmove, oblike, načela i
mehanizme nastanka otisaka crne tinte na milimetarskom papiru koje nazivamo
EKG ili elektrokardiogram.
Definicija
Elektrokardiogram je grafički zapis električnih potencijala nastalih u srcu. EKG je jedna od
najstarijih dijagnostičkih metoda u kardiologiji, koja do danas ne samo da nije izgubila na
važnosti (dolaskom novijih metoda), već postaje sve raširenija i praktički nezamjenjiva u
dijagnostici mnogih srčanih (ali i drugih) bolesti.
Anatomija i fiziologija
Da bi razumjeli logiku EKG-a moramo biti upućeni u strukturu provodnog sustava srca i
mehanizam nastanka izbijanja i provođenja električnih impulsa.
Tri komponente imaju ulogu u nastanku električnog impulsa koji se širi kroz srce:
1. predvodnički dio - obično u sinusnom atrijskom čvoru koji se nalazi u desnoj pretklijetci
(atriju). Odavde počinje električni impuls.
2. provodni dio - srčane stanice s karakteristikom brzog provođenja električnog impulsa.
Sastoji se od internodalnih putova (spajaju sinusno atrijski čvor s atrioventrikulskim čvorom),
atrioventrikulskog čvora (električni spoj između pretklijetki i klijetki) te Hisova snopa koji se
grana na lijevu i desnu granu, podražujući na taj način lijevu i desnu klijetku (ventrikul).
3. tkivo srčanog mišića koje se kao reakcija na putujući električni podražaj skraćuje i na taj
način dovodi do srčane kontrakcije.
Upravo ovaj posljednji korak (kontrakcija srčanog mišića, ali i relaksacija) stvara dovoljno
velik električni potencijal koji možemo zamijetiti i registrirati vanjskim mjerenjem, odnosno
EKG-om.
Uređaj
Elektrokardiogram se snima pomoću uređaja kojeg zovemo elektrokardiograf.
Da bi se bioelektrični potencijala kojeg stvara srčani mišić, svojom kontrakcijom i
relaksacijom, mogao registrirati potrebno ga je elektronski pojačati. Princip rada
elektrokardiografskog uređaja je da žica koja se nalazi u elektromagnetskom polju oscilira
kada kroz nju teče struja koja je odraz srčane električne aktivnosti. Žica koja oscilira na svom
vrhu ima pisaljku na tintu ili se oscilacije snimaju na fotografski papir. EKG se obično snima
na papiru podijeljenom u polja veličine 1mm2. Kako se papir u uređaju kreće brzinom od
najčešće 25mm/s jedan milimetar odgovara vremenskom periodu od 0,04s dok razmak
između dvije podebljane linije iznosi 5mm ili 0,20s.
Standardni EKG snima 12 odvoda koji predstavljaju razlike električnih potencijala između
pojedinih elektroda postavljenih na površinu tijela. Snimaju se tri standardna (I, II, III), tri
unipolarna (aVR, aVL, aVF) i šest prekordijalnih (V1 - V6) odvoda.
Izgled normalnog EKG-a

Normalni EKG ima karakteristične valove i zupce koji se označavaju abecedno slovima
počevši od slova P a završavaju sa slovom U.
P-val predstavlja depolarizaciju atrija (pretklijetke).
QRS-kompleks ocrtava depolarizacjiu ventrikula (klijetke).
ST-segment je dio krivulje između kraja QRS i početka T-vala a predstavlja trajanje
depolariziranog stanja ventrikula.
T-val označava repolarizaciju ventrikula.
U-val označava period u kojem je klijetka najpodražljivija.
Slika: Izgled normalnog EKG-a
Izgled normalnog EKG-a nije univerzalan, mnogi vanjski utjecaji mogu imati utjecaja na
izgled EKG-a. Strah, hiperventilacija, pušenje, pijenje hladne tekućine i uzimanje različitih
lijekova mogu bitno promijeniti izgled EKG-a kod zdrave osobe. Upravo iz ovog razloga bilo
kakvu dijagnozu srčanih bolesti nije moguće donijeti na temelju samog EKG-a. Ipak ukoliko
se EKG promatra unutar kliničke slike, fizikalnog statusa bolesnika i ostalih dijagnostičkih
pretraga, dobiveni podaci mogu biti krucijalni.
Na što obratiti pažnju kada gledamo EKG?

Nakon prvog pogleda na EKG najčešće smo zbunjeni izgledom valova i zubaca. Iz ovog
razloga ali i zbog mogućnosti da nam neka bitna promjena EKG-a promakne najbolje je pri
promatranju biti metodičan.
1. Frekvencija - određuje se tako da se 300 podjeli sa brojem velikih kvadratića u jednom R-R
intervalu.
2. Ritam - normalno su razmaci između pojedinih R-ova jednaki. Ovo nije slučaj ukoliko
postoje poremećaji srčanog ritma kao atrijska fibrilacija, atrijska undulacija, ekstrasistole, itd.
3. Električna osovina - srednja električna os je zbroj svih pojedinih ventrikulnih električnih
sila pri depolarizaciji. Normalno leži između -30 i +90 stupnjeva (nulta linija je usmjerena
prema lijevom ramenu). Električna os može biti u lijevoj (manje od -30o) i desnoj (više od
+90o) devijaciji.
4. P-val - normalno se nalazi ispred svakog QRS-kompleksa. Nedostaje kod atrijske
fibrilacije, nodalnog ritma, itd. P-val može biti i promijenjena izgleda: dvostruki vrh, izrazito
uzdignut, itd.
5. PR-interval - od starta P-vala do početka QRS-kompleksa, normalnog trajanja između 0,12
i 0,20s. Duži PR-interval govori za smetnje atrioventrikulnog provođenja, kraći PR-interval
može biti posljedica brzog provođenja kroz akcesorne putove provođenja (Wolff-Parkinson-
White sindrom).
6. QRS-kompleks - normalno traje manje od 0,12s (tri mala kvadratića), ukoliko je produžen
moguć je defekt ventrikularnog provođenja (blokovi grana Hisova snopa). Visok QRS
sugerira hipertrofiju ventrikula. Normalan Q-zubac je uži od 0,04s i manji od 1/3 visine
cjelokupnog QRS-a, ukoliko je veći od tih vrijednosti patološki je znak i najčešće označava
preboljeli infarkt miokarda.
7. QT-interval - od starta QRS-a do kraja T-vala, trajanje mu varira ovisno u frekvenciji.
Produžen je kod raznih stanja kao: infarkt miokarda, bradikardija, elektrolitni poremećaji,
utjecaj lijekova, itd.
8. ST-segment - obično u izoelektričnoj liniji, elevacija ili depresija ST spojnice govori za
infarkt ili ishemiju.
9. T-val - patološki ukoliko je obrnut (vrh prema dole) u I, II, i V4 - V6 odvodima. Visok i
špicast T-val nalazimo kod povišene koncentracije kalija u plazmi, a nizak spušten u niskoj
koncentraciji kalija u plazmi.
Abnormalnosti u EKG-u
1. sinusna tahikardija - sinusni ritam brži od 100/min, mogu je uzrokovati emocije, napor, bol,
infekcije, zatajenje srca, plućna embolija, perikarditis, hipertireoza, kofein, nikotin, itd.
2. sinusna bradikardija - sinusni ritam sporiji od 60/min, uzroci: dobra fizička kondicija,
sindrom bolesnog sinusnog čvora, infarkt miokarda, lijekovi (npr. beta-blokatori), hipotireoza,
itd.
3. atrijska fibrilacija - apsolutno nepravilan srčani ritam, s nedostatkom P-valova ali s
postojanjem tzv. F-valova visoke frekvencije (350 - 600/min). Uzroci: ishemična bolest srca,
hipertireoza, mitralna stenoza, alkohol, itd.
4. atrioventrikulski blokovi - zapreke provođenja električnog impulsa iz atrija u ventrikul.
Postoje tri stupnja ovisno o težini poremećaja provođenja, karakterizirani su produljenjem
PR-intervala ili potpunom nepovezanošću P-valova i ventrikulskih kompleksa (QRS).
5. elevacija (podizanje) ST-segmenta - uzroci: akutni infarkt miokarda, Prinzmetalova angina,
aneurizma lijevog ventrikula, akutni perikarditis.
6. depresija (spuštanje) ST-segmenta - uzroci: ishemija, predoziranje digitalisom.
7. inverzija T-valova - normalna pojava u nekim odvodima, ostali uzroci: ishemija,
hipertrofija lijevog ventrikula, plućna embolija, poremećaji intraventrikularnog provođenja,
itd.
8. ventrikularna hipertrofija - nema jednog sigurnog pokazatelja, već je potrebno uzeti u obzir
položaj električne osi, izgled QRS-kompleksa, i položaj ST-segmenta. Suspektna hipertrofija
lijevog ventrikula ukoliko je R-zubac u V6 veći od 25mm ili ukoliko je zbroj R-zupca u V6 i
S-zupca u V1 veći od 35mm. Suspektna je hipertrofija desnog ventrikula kada je dominantan
R-zubac u V1, obrnuti T-valovi u V1 - V3, i duboki S-zubac u V6.
Atrijski septalni defekt

Što je atrijski septalni defekt?
Atrijski septalni defekt (ASD) je najčešća prirođena srčana greška. "Defekt" je
posljedica nepotpunog zatvaranja zida između dvije srčanih pretklijetki. Banalno
rečeno, to je rupa u srcu na mjestu gdje rupe ne bi trebalo biti. ASD često ne
izaziva nikakve simptome sve do odrasle dobi, a ukoliko se ne prepozna može
izazvati niz komplikacija. Učestalost je 0.2-0.6 na 1000 djece.
Nazivlje
Latinski naziv: Defectus septi atriorum cordis
Engleski nazivi: coronary sinus atrial septal defect, coronary sinus ASD, unroofed coronary
sinus
Građa srca
Srce ima 4 šupljine: dvije pretklijetke i dvije klijetke. U medicini se često koristi izraz
"desno" i "lijevo" srce. Desno srce je desna pretklijetka i klijetka; u desnu pretklijetku dolazi
venska krv iz tijela koja se kroz desnu klijetku pumpa u pluća. Krv iz desnog srca u pluća
vodi plućna arterija (u njoj se nalazi venska krv, a zove se arterija zato jer je pravilo da su sve
krvne žile koje idu od srca prema periferiji "arterije").
U plućima se krv rješava ugljik-dioksida, a opskrbljuje kisikom. Takva pročišćena krv je sad
arterijska te iz pluća dolazi u lijevu pretklijetku plućnim venama (iako sadrže arterijsku krv
zovu se vene jer dolaze s �periferije� u srce). Iz lijeve pretklijetke arterijska krv dalje ide u
lijevu klijetku pa u aortu koja je nosi u cijelo tijelo. Budući lijevo srce pumpa arterijsku krv u
cijelo tijelo (a desno srce vensku krv samo u pluća), u lijevom srcu su tlakovi triput veči i
njegove stijenke su deblje.
Latinski naziv za pretklijetku je atrium (mi gaobino zovemo atrij), klijetka je ventriculus
(ventrikul), a "zid" koji dijeli desno i lijevo srce (srčana pregrada) naziva se septum. Zbog
postojanja septuma nema kontakta između dvije pretklijetke i dvije klijetke, inače bi doslo do
miješanja venske i arterijske krvi.
Između pretklijetke i klijetke se nalazi suženje (ventil ili lat. valvula) sa zaliscima (zalistak se
na latinski zove cuspis). Zalisci spriječavaju vraćanje krvi iz klijetke u pretklijetku. U desnom
srcu se nalaze tri takva zaliska pa se valvula naziva "trikuspidalna valvula" ili valvula s tri
kuspisa. U lijevom srcu su između pretklijetke i klijetke dva zaliska pa je to bikuspidalna (ili
mitralna jer slici na biskupovu mitru) valvula.
Zalisci se također nalaze na izlazu iz klijetki u plućnu arteriju i aortu.
Ako se zbog bilo kojeg razloga krv vraća nazad kroz valvulu u pretklijetku to se naziva
insuficijencija valvule. Riječ insuficijencija dolazi od latinske riječi za "nedovoljno". Dakle,
valvula je nedovoljno funkcionalna da bi spriječila vraćanje krvi natrag.
Ukoliko zbog poremečaja srce treba obaviti veći rad nego sto je normalno, srčane stijenke se
zadebljavaju.
Dvije faze rada srca su sistola i dijastola. Sistola je ispumpavanje, a dijastola punjenje krvlju.
Embrionalni razvoj
Pregrađivanje srčanih pretklijetki počinje u petom tjednu trudnoće. Najprije nastaje primarna
pregrada (septum primum), a nakon toga sekundarna (septum secundum).
Prema klasičnom modelu razvoja srca, process počinje kad se tanka membrana (septum
primum) počinje oblikovati na stražnjem i gornjem zidu atrija. Membrana raste te se napokon
spoji s tkivom endokardija (unutrašnjost srca). Dok membana raste između nje i
endokardijalnih jastučića postoji otvor, primarno ušče (ostium primum), koji se zatvori kad se
ove dvije strukture spoje. Prije nego se ostium primum posve zatvori, u primarnoj pregradi se
stvori mali otvor, sekundarno ušče (ostium secundum). Krajem petog tjedna embrionalnog
života počinje druga faza razvoja kad se u atriju počinje oblikovati sekundarna pregrada. Ova
membrana također raste prema endokardijalnim jastučićima i prekriva sekundarno ušče.
Sekundarna pregrada ostaje nepotpuna. Ovalni otvor (fossa ovalis; foramen ovale) je otvor
koji ostaje nakon sto završi rast sekundarne pregrade.
Završna faza procesa počinje kad gornji dio sekundarne pregrade počinje popadati te napokon
posve nestane. Potpuno oblikovana pretklijetka sada ima dvije pregrade, obje nepotpune, koje
se preklapaju. Gornji dio sekundarne pregrade prekriva sekundarno ušče te oblikuje
jednosmjerni ventil koji dozvoljava desno-lijevi protok krvi u fetusa.
Sve dok je dijete u maternici, između dvije pretklijetke postoji ovaj ovalni otvor koji skreće
krv iz desnog u lijevo srce. Na ovaj način se spriječava odlazak velike količine krvi u pluća
koja se još ne koriste. U fetalnom razdoblju je tlak u desnoj pretklijetki veći nego u lijevoj što
pospješuje tok krvi kroz ovalni otvor. Pri porodu dijete napravi prvi udah, rasire se pluća,
snizuje tlak u desnom srcu i zatvara ovalni otvor. U prosječno 70% osoba nakon rođenja se
spajaju primarni i sekundarni spetum te nastaje jedinstvena, cjelovita pregrada. Nepotpuno
zatvaranje pregrade uzrokuje nastanak atrijskog septalnog defekta.
Razvoj poremečaja
Funkcija srca i tijela postojanjem ASD-a nije pogođena dok je fetus još u maternici, uglavnom
zbog toga sto nerođeno dijete ne koristi pluća (iz majčine krvi dobija sav potreban kisik i
hranu) pa se veliki dio krvi kanalizira drugim putevima u tjelesnu cirkulaciju. Fetalni krvotok
se razlikuje od krvotoka odraslih.
Nakon rođenja se počinju koristiti pluća i normalno znatno poraste protok krvi u plućnom
krvotoku i tlak u lijevom srcu. Bez obzira na smještaj defekta srčane pregrade među
pretklijetkama, poremečaj koji posljedično nastaje je otprilike jednak.
Ako postoji mali ASD, tlak u lijevoj pretklijetki ostaje veći nego u desnoj pa krv iz lijevog
srca kroz šupljinu prelazi u desno. Tlakovi u lijevom i desnom srcu te količina krvi koja
prolazi kroz otvor ovisi o veličini defekta te relativnoj rastezljivosti desnog i lijevog srca.
Lijevo-desni protok krvi (engl. shunt) nastaje prvenstveno u kasnoj sistoli te ranoj dijastoli te
se nešto pojačava tijekom atrijske sistole.
Čak i kad su tlakovi u lijevoj i desnoj pretklijetki jednaki, krv kroz otvor svejedno teče u
lijevo-desnom smjeru jer je desno srce popustljivije.
Ne samo sto abnormalni protok krvi vraća arterijsku krv iz lijevo u desno srce te ponovo u
pluća, već ovaj povećan volumen krvi znatno opterećuje desno srce i pluća koji sad moraju
vise raditi. Nastaje tzv. beskorisni krug � određena količina krvi se vraća iz lijevog atrija u
desni atrij, otkud ide u desnu klijetku, plućnu arteriju, u pluća pa u lijevi atrij otkud se
ponovno vraća u desni atrij. Plućni protok krvi zna biti osam puta veći nego protok u cijelom
tijelu, ali u mladih odraslih osoba bez simptoma češće je 2-5 puta veći. Zbog ovog viska krvi
desno srce vise radi pa se povećava i zadebljava kako bi uspjelo sve ispumpati u pluća.
Proširenje desnog srca vidljivo je na rendgenskim i ultrazvučnim snimkama. Zbog povećanog
volumena i tlaka krvi u desnom srcu proširuje se i plućna arterija te arterije u samim plućima
koje se ponekad opažaju na rendgenskim snimkama.
Preopterećenje volumenom u desnoj strani srca obično se godinama dobro podnosi.
Eventualni razvoj bolesti plućnih krvnih žila signalizira nastup povećanog krvnog tlaka u
plućima (plućna hipertenzija) čija je posljedica Eisenmengerov sindrom: zatajene desnog srca
te promjena smjera protoka krvi kroz ASD. Zbog povišenog tlaka u plućima, krv sad iz desne
pretklijetke teče u lijevu.
Razvoj plućne hipertenzije ovisi o veličini i trajanju abnormalnog protoka krvi kroz ASD te o
nepoznatim individualnim čimbenicima. Plućna hipertenzija je opisana i kod pacijenata nakon
kirurškog zatvaranja srčanog defekta koji su u vrijeme operacije imali uredan protok krvi kroz
pluća, ali ovakvi su slučajevi vrlo rijetki.
Rizični čimbenici
Nisu utvrdjeni nikakvi rizični faktori od strane roditelja ili lijekovi/otrovi uzimani u trudnoći
koji bi bili povezani s nastankom ove bolesti.
Tipovi ASD
Pretklijetka ima vise dijelova i ovisno o tome gdje se defekt nalazi razlikuje se nekoliko
tipova: secundum, primum, sinus venosus (sinus coronarius), otvoreni foramen ovale te
familijarni ASD.
Secundum ASD
Defekti u području ovalnog otvora (šupljine između pretklijetki koja postoji dok je dijete još u
maternici) nazivaju se tip secundum. Posljedica je nedovoljnog rasta sekundarne srčane
pregrade ili pretjerane razgradnje primarne pregrade. Češći je kod ženskog spola te čini 70%
svih ASD-a. Kod 70% pacijenata s ovim tipom nalazi se još jedna srčana greška � prolaps
mitralne valvule (ventila između lijeve pretklijetke i klijetke). Rijetka kombinacija ASD i
mitralne stenoze (suženja), posljedica reumatske upale zalistaka, naziva se Lutembacherov
sindrom.
Primum ASD
Nastaje jer se primarna pregrada ne spaja s endokardijem; ostavlja defekt na bazi pregrade
između pretklijetki koji je obično velik. Tipično je povezan s rascjepom prednjeg mitralnog
zaliska, ali u većini slučajeva trikuspidalna valvula nije zahvaćena.
Potpuni defekt ovog dijela endokardija javlja se kad je u isto vrijeme prisutan i ventrikulski
septalni defekt (defekt pregrade između srčane klijetki).
Sinus coronarius ASD

Sinus coronarius (koronarni džep) ili sinus venosus (venski džep) je latinski naziv za strukturu
koja prima najveći dio venske krvi iz samog srca i prazni se u desnu pretklijetku.
ASD koronarnog sinusa nastaje kao posljedica abnormalnog umetanja gornje šuplje vene koja
se nalazi iznad atrijske pregrade. Abnormalna komunikacija među pretklijetkama tada nastaje
unutar �usta� gornje šuplje vene te se nalazi izvan područja ovalnog otvora.
Desne pljucne vene, ovisno o smještaju defekta, mogu biti usmjerene u desnu pretklijetku
umjesto u lijevu. Vene unutar pluća također mogu biti posve izmještene te umetnute u donju
šuplju venu. �Scimitar znak� opisuje sjenu na rentgenogramu grudnog kosa koja nastaje
zbog umetanja plućne vene u donju šuplju venu (scimitar je zakrivljena azijska sablja).
Familijarni ASD
Iako je većinom ASD izoliran kod jedne osobe, ponekad postoji obiteljska povijest ove greške
ili drugih prirođenih srčanih pogrešaka. Jedno istraživanje triju obitelji kod kojih se ASD
pojavio u tri generacije otkrilo je autosomno dominantnu prirodu nasljeđivanja kod jedne
obitelji ASD gen je bio smješten na 5p kromosomu. Ekspresija je ipak varijabilna i greška se
ne javlja kod svih potomaka.
Kliničke manifestacije familijarnog ASD mogu uključivati druge abnormalnosti srca i krvnih
žila poput atrijske septalne aneurizme, aortne stenoze, perzistentne lijeve gornje šuplje vene.
Mutacije na genu NKX2.5 transkripcijskog faktora povezane su s progresivnim
atrioventrikularnim blokom i složenom prirođenom bolesti srca.
Otvoreni foramen ovale

Građa ovalnog otvora omogućuje desno-lijevi protok krvi među pretklijetkama tijekom
fetalnog života te se zatvara nakon poroda. Međutim, porast tlaka u lijevom atriju i rastezanje
rubova otvora može uzrokovati protok krvi kroz njega. Ovo nije defekt u pravom smislu jer
ne nedostaje tkivo srčane pregrade. Klinički značaj otvorenog ovalnog otvora jest mogućnost
izazivanja paradoksne embolije i moždanog udara. Ako je većeg promjera ( 4 mm) ili ako
kroz njega prolazi veća količina krvi u desno srce, smatra se klinički značajnim.
Zapaža se kod prosječno 30% populacije. Može biti obiteljska osobina.
Simptomi
Procjenjuje se kako će većina bolesnika čiji ASD ima značajan protok kroz defekt (ako je
plućni nasuprot tjelesnom protoku veći od 2:1) imati simptome do 40. godine.
Mali defekti u djetinjstvu ne uzrokuju nikakve simptome pa se cesto niti ne dijagnosticiraju.
Srednji pa i veliki defekti također cesto ne uzrokuju simptome pa se znaju dijagnosticirati tek
u kasnom djetinjstvu ili u odrasloj dobi. Kad je ASD jedina srčana greška (nema abnormalnih
rupa niti suženja u drugim dijelovima srca) abnormalni protok krvi iz lijeve u desnu
pretklijetku se povećava s dobi te se javljaju simptomi zatajenja srca. Nastup i težina
simptoma razlikuju se kod pojedinih pacijenata. Simptomi poput nepodnošenja tjelesnog
napora mogu se javiti u drugom desetljeću života, a ponekad nekoliko desetljeća kasnije.
Bolest srca
Poremećaj srčanog ritma (atrijska aritmija) najčešće je prvi simptom kod odraslih. Aritmije se
češće javljaju s porastom dobi i plućnog arterijskog tlaka. Simptomi koje uzrokuje ASD mogu
biti blagi i zanemareni. Pacijenti kod kojih se u odrasloj dobi usputno otkrije ASD nakon
operacije često kažu kako mnogo bolje podnose tjelesni napor. Zatajenje lijeve srčane klijetke
je rijetko, ali se može javiti nakon dugogodišnjeg nekompliciranog ASD. Uzrok ove
komplikacije je nepoznat.
Ukoliko je prisutan povišen krvni tlak u cijelom tijelu (sustavna hipertenzija), to može
pogoršati promjene protoka krvotoka. Lijeva klijetka se može povećati (hipertrofija) sto može
povećati lijevo-desni protok kroz otvor, doprinijeti kasnom razvoju plućne hipertenzije i
zatajenja desnog srca.
Moždani udar
Pacijenti s ASD kod kojih krv kroz defekt ponekad ili uvijak teče u desno-lijevom smjeru
mogu razviti moždani udar (odumiranje stanica središnjeg živčanog sustava zbog prekida
cirkulacije krvi) zbog paradoksne embolije.
Paradoksna embolija
Embolija je začepljenje krvne žile različitim masama koje se zajedničkim imenom nazivaju
embolus. Embolus je masa poput mjehura zraka, slobodnog krvnog ugruška, kapljica masti
itd. koja putuje kroz krvne žile te se zaustavlja i začepi krvnu žilu kad ona postane preuska da
bi prošla dalje. Kad se začepi krvna žila, dio tkiva koji se njome hrani umire. Paradoks je
naziv za nešto neobjašnjivo, proturječno ili naizgled nemoguće/neistinito.
Embolus koji nastaje u venskom sustavu venama dolazi u desno srce i otud može ići samo u
pluća, tu se zaustavlja i uzrokovati plućnu emboliju. Ukoliko postoji defekt srčane pregrade,
taj embolus može prijeći u lijevo srce koje ga izbacuje u arterijsku cirkulaciju. Embolus dalje
putuje arterijama te začepi jednu od njih. Budući prvi ogranci aorte iza srca vode krv u glavu,
embolus nerijetko začepi krvne žile mozga.
Embolus je najčešće krvni ugrušak koji nastaje u venama noge ili zdjelice. Proširene vene
cesto su ishodiste ugrušaka pa ih je potrebno redovito liječiti i kontrolirati.
Migrene
Učestalost migrenoznih glavobolja češća je kod bolesnika s desno-lijevim protokom kroz
srčani defekt. Mehanizam povezanosti defekta s migrenom nije dovoljno objašnjen.
Eisenmengerov sindrom
Plućna hipertenzija kod osoba s ASD je rijetka; javlja se u manje od 10% odraslih u vrijeme
postavljanja dijagnoze. Pacijenti koji imaju ASD tipa koronarnog sinusa imaju veći arterijski
krvni tlak i otpor te plućnu hipertenziju razvijaju u ranijoj dobi kad se usporede s pacijentima
koji imaju druge oblike ASD.
Eisenmengerov sindrom nastaje kad razvoj nepovratne (neizlječive) plućne hipertenzije
promjeni smjer protoka kroz defekt. Krv sada teče iz desne u lijevu pretklijetku. Krv iz desne
pretklijetke je venska krv sto znaci da se sad u arterijama nalazi velika količina venske krvi
bez kisika sto uzrokuje plavu boju koze i sluznica (cijanoza) te niz posljedica zbog manjka
kisika. Iako je Eisenmengerov sindrom opisan kod djece s ASD, mnogo je češći kad postoji
ventrikulski septalni defekt (VSD) kod kojeg se defekt nalazi između klijetki. Kad nastane
Eisenmengerov sindrom prognoza je losa; očekivano trajanje života nakon toga je manje od
tri godine. Smatra se kako je plućna hipertenzija u ovom slučaju posljedica bolesti krvnih žila
koja nastaje zbog promjena uzrokovanih dugotrajno povećanim protokom krvi. Kod ovih se
osoba u plućnim žilama cesto nalaze mali ugrušci pa se preporučuje terapija lijekovima protiv
zgrušavanja.
Posljedice Eisenmengerova sindroma su nepodnošenje čak i blagog tjelesnog napora,
poremećaji srčanog ritma, visok rizik od paradoksne embolije, nakupine gnoja u mozgu
(cerebralni apsces) i iznenadna smrt. Cijanoza zbog velike količine venske krvi u arterijama
uzrokuje zadebljanje krajeva prstiju (batičasti prsti), povećanje broja krvnih stanica
(policitemija), zatajenje organa poput bubrega te ponekad mentalna oštećenja.
Trudnoća se dobro podnosi ako trudnoća ima nekomplicirani ASD, a kad pacijentica s
Eisenmengerovim sindromom zatrudni preporučuje se obaviti pobacaj.
U rijetkim slučajevima desno-lijevi protok krvi kroz ASD može uzrokovati cijanozu bez
prisutnosti plućne hipertenzije. Tada obično postoji nekakva neoubičajena osobitost građe
srca koja usmjerava vensku krv u lijevo srce protiv gradijenta tlaka. Prolazni, kratkotrajni,
desno-lijevi protok može nastati tijekom grčevitog plaća, kašljanja, kihanja i određenih dišnih
manevara.
Dijagnoza
Dijagnoza se postavlja pregledom, eventualnim postojanjem simptoma, rendgenskom
snimkom srca i pluća, elektrokardiografijom (EKG) i ultrazvukom (ehokardiografija) srca.
Magnetska rezonancija (MR) se preporučuje kad je ASD dio složenih srčanih poremećaja.
Holter monitor (24 satno mjerenje EKGa) preporučuje se kod postojanja poremećaja srčanog
ritma (aritmija) te kod novo-dijagnosticiranih odraslih pacijenata prije operacije.
Kateterizacija srca nije nužna za dijagnozu, ali može biti potrebna kako bi se procijenila
dinamika srčanog protoka.
Liječenje
ASD ne dovodi obavezno niti cesto do nastupa plućne hipertenzije pa se cesto postavlja
pitanje je li kirurška terapija uopće potrebna.
Smrtnost tijekom kirurškog zatvaranja ASD-a u nekim se centrima približava nuli, a
dugotrajno preživljavanje nakon operacije slično je preživljavanju kontrolnih zdravih osoba.
Kirurški rezultati su ohrabrujući i kod osoba nakon dobi od 50 ili 60 godina. Ipak se
preporučuje obaviti raniji zahvat ako se postavi dijagnoza. Jedno je istraživanje pokazalo kako
pacijenti koji se operiraju prije 5. godine kasnije bolje podnose tjelesni napor nego pacijenti
koji su kasnije operirani bez obzira na usporedivi tlak plućnog krvotoka. Niz istraživanja
pokazuje korist od kirurškog zahvata.
Budući je poremećaj srčanog ritma u pretklijetkama najčešći simptom kod odraslih i pojačava
mu se učestalost s dobi, istraživao se utjecaj kirurškog zahvata na pojavu aritmija. Rezultati su
pokazali kako se smanjuje učestalost atrijske ondulacije, ali ne i atrijske fibrilacije, vjerojatno
zbog nepovratnih čimbenika koji uzrokuju nastanak aritmija.
Kirurška terapija
Prednji pristup (desni anterolateralni submamarni subpektoralni) korišten je za liječenje ASD
s dobrim rezultatima, osobito kod ženskog spola. Ipak, minimalno invazivni direktni pristup
uz desni rub prsne kosti ili otvaranjem njenog gornjeg dijela može se učinkovito izvesti kod
svih odraslih bez obzira na tip ASDa. Koriste se dakronske ili perikardijalne (napravljene od
osrčja) �zakrpe�.
Tijekom operacije potrebno je testirati električnu aktivnost srca ultrazvukom kroz jednjak
(transezofagealna ehokardiografija, TEE) kako bi se provjerila učinkovitost zatvaranja ASD te
isključila mogućnost vraćanja krvi kroz srčane zaliske ili druge srčane greške.
Gubitak krvi tijekom i nakon operacije je minimalan pa transfuzija obično nije potrebna.
Komplikacije nakon operacije su rijetke, a uključuju srčani udar, stvaranje ugrušaka i
začepljenje niza krvnih žila, infekciju, krvarenje, poremećaj zgrušavanja krvi, poremećaj
ritma srca, nakupljanje tekućine u osrčju, smrt.
Nakon operacije većina pacijenata je dobrog stanja dugo vremena. Preživljenje je nakon
zahvata općenito slično kao kod opće populacije. Nakon zahvata je potrebno provesti
određene terapijske rezime kako bi se spriječile komplikacije:
- terapija lijekovima protiv zgrušavanja (antikoagulansi) primjenjuje se kod odraslih tijekom
nekoliko mjeseci nakon zatvaranja ASDa zbog velike učestalosti atrijske fibrilacije nakon
operacije
- dugotrajne povremene kontrole potrebne su zbog mogućeg kasnog nastupa aritmija i
moždanog udara, osobito kad se zahvat obavi u odrasloj dobi. Veći rizik imaju pacijenti koji
su aritmije imali prije operacije. Djeca također imaju određeni rizik od aritmija; istraživanjem
je pokazano kako 67% djece ima poremećaje ritma, ali svega 3% treba terapiju zbog toga.
- TEE (ultrazvučno snimanje kroz jednjak) provjerava uspješnost zatvaranja defekta te prati
očekivano smanjenje desnog srca i tlaka u plućima
- zahvatom se mogu poremetiti specijalizirani čvorovi u srcu koji stvaraju i provode električne
impulse; mali broj pacijenata zbog toga će kasnije trebati elektrostimulator (pacemaker)
Perkutano zatvaranje
Zatvaranje defekta preko koze (perkutano) alternativa je kirurškom zatvaranju kod pacijenata
s pogodnom građom.. Za ovu neoperativnu intervenciju pogodni su pacijenti sa secundum
tipom ASDa. Od ovih defekata 40% ih je za ovaj postupak preveliko ili preblizu gornjoj
šupljoj veni. Idealan defekt za perkutano zatvaranje je manji od 13 mm u promjeru s rubom
tkiva oko defekta od najmanje 5 mm.
Intervencija se obavlja u općoj anesteziji pod kontrolom ultrazvučne sonde postavljene u
jednjak. Sredstva za perkutano zatvaranje su proteze koje se u srce uvode kroz kateter (tanka
plastična cijev) provučen kroz krvne žile. Obično su oblika diska ili kišobrana te se proizvode
u nekoliko veličina. Kad se pomoću ultrazvuka proteza namjesti u defekt, oslobađa se
kontroliranim pokretima s nosaca (koji omogućuje ponovno vraćanje proteze na nosac
ukoliko nakon oslobađanja proteza nije na dobrom mjestu). Proteza se nakon oslobađanja
obično siri i pričvršćuje za rubove otvora. Uvođenje više od jednog sredstva za zatvaranje
višestrukih defekata smatra se sigurno i učinkovito.
Nakon 24 sata obavljaju se detaljna snimanja prsnog kosa i srca; ako sve izgleda uredno
pacijentu se nakon otpuštanja propisuje terapija lijekovima protiv zgrušavanja tijekom 6
mjeseci. Intervencija prosječno traje 100 minuta.
U SAD su 2001. odobreni uređaji pod nazivom Amplatzer Septal Occluder i Cardio-Seal
Septal Occlusion System za ovaj zahvat Provode se istraživanja i drugih sredstava za
perkutano zatvaranje ASDa (Button device, Angel wings, Atrial septal defect occlusion
system).
Komplikacije su rijetke. Moguća je iznenadna smrt tijekom postavljanja proteze kateterom,
lose postavljanje proteze, poremećaj srčanog ritma, embolija, srčani blok, izljev krvi u osrčje
(perikardijalna efuzija), rascjep preponskih krvnih žila, hematom u preponi).
Iako su podaci o perkutanom zatvaranju ograničeni, dosadašnje studije pokazuju kako su
rezultati usporedivi ili bolji od kirurškog liječenja, ali je učestalost komplikacija manja i
boravak u bolnici kraci.
Profilaksa endokarditisa
Endokarditis je upala unutarnjeg sloja srčanog tkiva. Prema trenutno važećim smjernicama
izolirani ASD je povezan s vrlo malim rizikom od endokarditisa pa se ne preporučuje
preventivna terapija antibioticima. Može se propisati ako postoje druge srčane greške koje su
povezane s mnogo većim rizikom.
Prehrana
Bolesnicima s ASD nije potrebna nikakva posebna prehrana.
Bavljenje sportom
Bolesnici kojima nije obavljen kirurški zahvat i koji nemaju povišen krvni tlak u plućima
(plućna hipertenzija) mogu sudjelovati u svim sportovima.
Ako postoji plućna hipertenzija preporučuju se samo sportovi tipa kuglanja ili golfa.
Natjecateljski sportovi mogu se ograničiti jedino kod pacijenata kod kojih je tjelesni napor
povezan s nastankom značajnih poremećaja ritma srca.
Pacijenti se mogu baviti svim mogućim sportovima 6 mjeseci nakon uspješne operacije ASD-
a.
Prognoza
Ukoliko je ASD jedina srčana greška pobol i smrtnost su vrlo niski, a prognoza vrlo dobra.
Veličina defekta i količina krvi koja iz lijevog srca prolazi u desno određuju postojanje i
težinu simptoma. Ako je ASD jedina srčana greška, većina djece nema nikakve simptome.
Ako se ne bi obavio kirurški zahvat u dobi od 20-30 godina bi mogle početi smetnje poput
poremećaja srčanog ritma, kronično preopterećenje desnog srca, javljanje paradoksnih
ugrušaka i nastanak povišenog tlaka u plućima (plućna hipertenzija) zbog preopterećenja
krvlju.
Prognoza je općenito izvrsna kad se defekti kirurški izliječe u djetinjstvu ili adolescenciji te
ako nema plućne hipertenzije.
Normalna frekvencija srca ide u rasponu od 60-100(a ne do 80)
Broj VES( ventrikularnih ekstrasistola ili receno srpski-preskakanja) koje se registruju za
24h(holterom) raste sa starenjem. Smatra se da do 100 VES za osobe do 40 godina starosti a
do 200 VES za starije osobe za 24 sata moze biti uobicajeni nalaz. Multiformne i VES u paru
se takodje mogu naci kod zdravih osoba.
Stanje nervnog sistema umnogome utice na porast broja prepoznatih poremecaja srcanog
ritma.
Aritmije i nesvestice
• Već dugo se lečim zbog nepravilnog rada srca. Pet godina čak. U više mahova sam imao i
gubitak svesti. Šta se to dešava sa mnom? Inače sam vitalan i osećam se kao zdrav.
(Aca Stakić, Miloševo)
Nesvestica predstavlja značajan simptom koji zahteva pravovremeno i stručno ispitivanje.
Postoje mnogobrojni uzroci gubitka svesti. Lekar najpre mora razgraničiti da li su nesvestice
kardiovaskularnog ili neurološkog porekla. Poremećaj svesti prouzrokovan neurološkim
oboljenjem (zbog moždanih ili živčanih poremećaja) često je udružen sa vrtoglavicom,
mukom, glavoboljom...
Vi ste naveli da se lečite od nepravilnog rada srca. Poremećaji srčanog ritma ili aritmije
predstavljaju vrlo česte uzroke nesvestice.
Postoje dva potpuno različita oblika aritmija: prvi se manifestuje ubrzanim radom srca
(tahikardije), a drugi usporenim pulsom (bradikardije), tako da je lečenje za svakog bolesnika
individualno, a sprovodi se tek posle detaljnog ispitivanja. Uzroci poremećaja ritma su veoma
različiti i mogu biti potpuno bezazleni, odnosno javljaju se kod zdravih ljudi, posle
prekomernog uzimanja kafe, alkohola i strasnih pušača, ali aritmije mogu biti i prvi znak
nekog težeg oboljenja srca (zapaljenja srčanog mišića ili ishemijske bolesti srca, koja se
manifestuje kao angina pektoris ili infarkt).
S obzirom na to da Vi više godina imate povremene gubitke svesti i verifikovanu aritmiju, a

navodite da i dalje ne znate od čega bolujete, predlažemo Vam kvalifikovano kardiološko
ispitivanje radi utvrđivanja prave prirode i težine tegoba, da bi se potom odredio adekvatan
način lečenja. Najjednostavniji test za utvrđivanje aritmije je elektrokardiogram (često se
naziva EKG). Njime se mogu ustanoviti neke, ali ne i sve vrste aritmija. Sigurno je da Vaš
kardiološki pregled mora obuhvatiti i kontinuirano (dvadesetčetvoročasovno ) snimanje
elektrokardiograma posebnim monitorom (holter monitorom), koji predstavlja mali portabilni
kasetofon, sličan vokmenu. Na njemu postoji i malo dugme koje se pritisne kada bolesnik
oseti neki značajan simptom (prekid u radu srca, vrtoglavicu, nesvesticu i slično). Tokom
nošenja ovog monitora vodi se detaljan dnevnik u kome se navode svi važni događaji koji su
se desili na dan pregleda.
Predlažemo da uradite i ultrazvučni pregled srca (ehokardiografiju), za procenu funkcije

srčanog mišića i zaliska, kao i test opterećenja na biciklu ili pokretnoj traci (ergometriju),
kojom se utvrđuje postojanje potencijalne pektoralne angine.
Ponekada je neophodno uraditi i elektrofiziološko ispitivanje. Ova procedura uključuje

kateterizaciju srca iz velike vene noge (femoralne vene) preko koje se plasiraju kateteri u srce
i ispituje pravilnost sprovođenjem impulsa. Ovo ispitivanje je korisno radi utvrđivanja rizika
od potencijalno opasnih aritmija.
Pored kardiološkog pregleda potrebna je konsultacija i neurologija.
Docent dr sc. med. Žarko Vučinić, kardiolog

Heart Block

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heart block

Atrioventricular node mechanisms

Types of heart block

Types of SA nodal blocks

Types of SA nodal blocks include:

 SA node Wenckebach (Mobitz I)

Types of AV nodal blocks

There are four basic types of AV nodal block:

 First degree heart block

Types of infrahisian block

 Type 2 second degree heart block (Mobitz II)

Second degree heart block

Mobitz I heart block is characterized by progressive prolongation of the PR interval on the

Type 2 Second degree heart block

Third degree heart block

For other uses, see Heart (disambiguation).

The heart and lungs (from an older edition of Gray's Anatomy)

The human heart

The cardiac cycle

Regulation of the cardiac cycle

The rhythmic sequence of contractions is coordinated by the sinoatrial and atrioventricular

Diseases and treatments

See also: Cardiology diagnostic tests and procedures

See cardiac arrest for emergencies involving the heart

The hearts of other animals

The earthworm has a series of multiple primitive hearts.

Introduction: Heart block

Symptoms of Heart block

Medical articles on symptoms: These general reference articles may be of interest:

 Symptoms of the Silent Killer Diseases

Misdiagnosis of Heart block

Misdiagnosis cases for Heart block: No cases available yet.

Misdiagnosis of Underlying Causes of Heart block

Treatments for Heart block

Basic Summary for Heart block

Main name of condition: Heart block

What is Heart block?

Who gets Heart block?

What causes Heart block?

What are the symptoms of Heart block?

Author Information Introduction Clinical Differentials Workup Treatment Follow-up Bibliography

Author: David FM Brown, MD, Instructor, Department of Medicine, Division of Emergency

Author Information Introduction Clinical Differentials Workup Treatment Follow-up Bibliography

Background: First-degree heart block, or first-degree atrioventricular (AV) block, is a

Mortality/Morbidity: Morbidity and mortality rates from heart disease appear to be

Author Information Introduction Clinical Differentials Workup Treatment Follow-up Bibliography

o Intrinsic AV nodal disease

o Enhanced vagal tone

o Acute MI, particularly acute inferior MI

o Calcium channel blockers

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Author: David FM Brown, MD, Instructor, Department of Medicine, Division of Emergency

Background: Second-degree heart block or second-degree atrioventricular (AV) block refers

Mobitz II AV block is characterized by sudden unexpected blocked P waves without variation

Pathophysiology: Mobitz I (Wenckebach) block is caused by conduction delay in the AV

 Mobitz I (Wenckebach) block

o Most patients are asymptomatic.

o Patients may experience dizziness, lightheadedness, or syncope, but these are

o Patients may have a history of organic heart disease.

o Patients may have symptoms of myocardial ischemia or a history of organic

 Symptomatic patients may have signs of hypoperfusion, including hypotension and

 Mobitz II block most commonly is caused by acute MI (anterior or inferior).

 Follow-up ECGs and cardiac monitoring are appropriate.