I21 ST elevation (STEMI) and non-ST elevation (NSTEMI) myocardial infarction Introduction Acute coronary syndrome (ACS) can be divided into subgroups of ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina. ACS carries significant morbidity and mortality and the prompt diagnosis, and appropriate treatment is essential. STEMI diagnosis and management are discussed elsewhere. NSTEMI and Unstable angina are very similar, with NSTEMI having positive cardiac biomarkers. The presentation, diagnosis, and management of NSTEMI are discussed below.[1][2][3] Go to:Etiology The etiology of NSTEMI varies as there are several potential causes. Go to:Epidemiology The median age at the time of presentation for ACS in the United States is 68 years. Males outnumber females by a 3:2 ratio. The incidence of ACS in the United States is over 780,000, and of those, approximately 70% will have NSTEMI. Go to:Pathophysiology ACSs are simply a mismatch in the myocardial oxygen demand and myocardial oxygen consumption. While the cause of this mismatch in STEMI is nearly always coronary plaque rupture resulting thrombosis formation occluding a coronary artery, there are several potential causes of this mismatch in NSTEMI. There may be a flow-limiting condition such as a stable plaque, vasospasm as in Prinzmetal angina, coronary embolism, or coronary arteritis. Non-coronary injury to the heart such as cardiac contusion, myocarditis, or presence of cardiotoxic substances can also produce NSTEMI. Finally, conditions relatively unrelated to the coronary arteries or myocardium itself such as hypotension, hypertension, tachycardia, aortic stenosis, and pulmonary embolism lead to NSTEMI because the increased oxygen demand cannot be met.[4][5] Go to:History and Physical The “typical†presentation of NSTEMI is a pressure-like substernal pain, occurring at rest or with minimal exertion. The pain generally lasts more than 10 minutes and may radiate to either arm, the neck, or the jaw. The pain may be associated with dyspnea, nausea or vomiting, syncope, fatigue, or diaphoresis. Sudden onset of unexplained dyspnea with or without associated symptoms is also a common presentation. Risk factors for ACS include male sex, older age, family history of coronary artery disease, diabetes, personal history of coronary artery disease, and renal insufficiency. Atypical symptoms may include a stabbing or pleuritic pain, epigastric or abdominal pain, indigestion, and isolated dyspnea. While all patients presenting with ACS are more likely to present with typical symptoms than atypical symptoms, the likelihood of atypical presentations increases with age over 75, women and those with diabetes, renal insufficiency, and dementia. Physical Exam for ACS and NSTEMI is often nonspecific. Clues such as back pain with aortic dissection or pericardial friction rub with pericarditis may point to an alternative diagnosis for a patient’s chest pain, but no such exam finding exists that indicates ACS as the most likely diagnosis. Signs of heart failure should increase concern for ACS but are, again, nonspecific findings.[6][7][8] Go to:Evaluation
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I21 ST elevation (STEMI) and non-ST elevation (NSTEMI) myocardial infarction
Introduction Acute coronary syndrome (ACS) can be divided into subgroups of ST-segment elevation
myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable
angina. ACS carries significant morbidity and mortality and the prompt diagnosis, and appropriate
treatment is essential. STEMI diagnosis and management are discussed elsewhere. NSTEMI and
Unstable angina are very similar, with NSTEMI having positive cardiac biomarkers. The presentation,
diagnosis, and management of NSTEMI are discussed below.[1][2][3]
Go to:Etiology
The etiology of NSTEMI varies as there are several potential causes.
Go to:Epidemiology
The median age at the time of presentation for ACS in the United States is 68 years. Males outnumber
females by a 3:2 ratio. The incidence of ACS in the United States is over 780,000, and of those,
approximately 70% will have NSTEMI.
Go to:Pathophysiology
ACSs are simply a mismatch in the myocardial oxygen demand and myocardial oxygen consumption.
While the cause of this mismatch in STEMI is nearly always coronary plaque rupture resulting
thrombosis formation occluding a coronary artery, there are several potential causes of this mismatch in
NSTEMI. There may be a flow-limiting condition such as a stable plaque, vasospasm as in Prinzmetal
angina, coronary embolism, or coronary arteritis. Non-coronary injury to the heart such as cardiac
contusion, myocarditis, or presence of cardiotoxic substances can also produce NSTEMI. Finally,
conditions relatively unrelated to the coronary arteries or myocardium itself such as hypotension,
hypertension, tachycardia, aortic stenosis, and pulmonary embolism lead to NSTEMI because the
increased oxygen demand cannot be met.[4][5]
Go to:History and Physical
The “typical� presentation of NSTEMI is a pressure-like substernal pain, occurring at rest or with
minimal exertion. The pain generally lasts more than 10 minutes and may radiate to either arm, the
neck, or the jaw. The pain may be associated with dyspnea, nausea or vomiting, syncope, fatigue, or
diaphoresis. Sudden onset of unexplained dyspnea with or without associated symptoms is also a
common presentation. Risk factors for ACS include male sex, older age, family history of coronary artery
disease, diabetes, personal history of coronary artery disease, and renal insufficiency. Atypical
symptoms may include a stabbing or pleuritic pain, epigastric or abdominal pain, indigestion, and
isolated dyspnea. While all patients presenting with ACS are more likely to present with typical
symptoms than atypical symptoms, the likelihood of atypical presentations increases with age over 75,
women and those with diabetes, renal insufficiency, and dementia.
Physical Exam for ACS and NSTEMI is often nonspecific. Clues such as back pain with aortic dissection or
pericardial friction rub with pericarditis may point to an alternative diagnosis for a patient’s chest
pain, but no such exam finding exists that indicates ACS as the most likely diagnosis. Signs of heart
failure should increase concern for ACS but are, again, nonspecific findings.[6][7][8]
Go to:Evaluation
History, ECG, and cardiac biomarkers are the mainstays in the evaluation. An ECG should be performed
as soon as possible in patients presenting with chest pain or those with a concern for ACS. A normal ECG
does not exclude ACS and NSTEMI. ST elevation or anterior ST depression should be considered a STEMI
until proven otherwise and treated as such. Findings suggestive of NSTEMI include transient ST
elevation, ST depression, or new T wave inversions. ECG should be repeated at predetermined intervals
or if symptoms return.
Cardiac troponin is the cardiac biomarker of choice. Troponin is more specific and more sensitive than
other biomarkers and becomes elevated relatively early in the disease process. While contemporary
cardiac troponin may not be elevated within the first 2 to 4 hours after symptom onset, newer high
sensitivity troponin assays have detectable elevations much earlier. It is also true that the amount of
troponin released, and therefore the time to elevation, is proportional with infarct size, so it is unlikely
to have a negative initial troponin with larger infarcts. Regardless of infarct size, most patients with true
ischemia will have elevations in troponin within 6 hours, and negative troponins at this point effectively
rule out infarct in most patients. Most assays use a cutoff value of greater than a 99th percentile as a
positive test. In older, contemporary troponin assays, no detectable troponin is reported in most healthy
individuals without the disease. Newer high sensitivity troponin assays often will report a normal
detectable range in healthy individuals without the disease.
Several tools and scores have been developed to assist in the workup of ACS. These tools must be used
with caution and in the appropriate context as none have been definitively
I24 Other acute ischemic heart diseases
What is ischemic heart disease? It's the term given to heart problems caused by narrowed heart
arteries. When arteries are narrowed, less blood and oxygen reaches the heart muscle. This is also called
coronary artery disease and coronary heart disease.
I44.0 Atrioventricular block, first degree
First-degree atrioventricular block (AV block), is a disease of the electrical conduction system of the
heart in which the PR interval is lengthened beyond 0.20 seconds.
In first-degree AV block, the impulse conducting from atria to ventricles through the atrioventricular
node (AV node) is delayed and travels slower than normal. It has a prevalence in the normal (young
adult) population of 0.65-1.1% and the incidence is 0.13 per 1000 persons.
I44.4 Left anterior fascicular block
Left anterior fascicular block (LAFB) is an abnormal condition of the left ventricle of the heart, related to,
but distinguished from, left bundle branch block (LBBB). It is caused by only the anterior half of the left
bundle branch being defective. It is manifested on the ECG by left axis deviation
I44.7 Left bundle-branch block, unspecified
Left bundle branch block (LBBB) is a cardiac conduction abnormality seen on the electrocardiogram
(ECG). In this condition, activation of the left ventricle of the heart is delayed, which causes the left
ventricle to contract later than the right ventricle.
ECG characteristics of a typical LBBB showing wide QRS complexes with abnormal morphology in leads
V1 and V6.
I45.1 Other and unspecified right bundle-branch block
During a right bundle branch block, the right ventricle is not directly activated by impulses travelling
through the right bundle branch. The left ventricle however, is still normally activated by the left bundle
branch.
I48 Atrial fibrillation and flutter
Atrial fibrillation (AF), not to be confused with atrial flutter, is the term used to describe an irregular or
abnormal heart rate. While AF and atrial flutter are similar, AF has more serious health implications such
as an increased risk of having a stroke or a blood clot (thrombosis).
The resting heart rate of someone without AF is usually between 60 and 100 beats per minute1 but
this number is usually over 100 beats per minute in AF.
It is usually the result of an underlying condition such as hypertension (high blood pressure) or having
an overactive thyroid but may develop for no known reason. In this circumstance, the person is said to
have ‘lone atrial fibrillation’. AF can affect people at any age but is rare in children and is more common
in the elderly populatio
I45.6 Pre-excitation syndrome
Pre-excitation syndrome is an abnormal heart rhythm in which the ventricles of the heart become
depolarized too early, which leads to their partial premature contraction.
I45.81 Long QT syndrome
Long QT syndrome (LQTS) is a condition which affects repolarization of the heart after a heartbeat. It
results in an increased risk of an irregular heartbeat which can result in palpitations, fainting, drowning,
or sudden death. These episodes can be triggered by exercise or stress. Other associated symptoms may
include hearing loss.
Long QT syndrome may be present at birth or develop later in life. The inherited form may occur by
itself or as part of larger genetic disorder. Onset later in life may result from certain medications, low
blood potassium, low blood calcium, or heart failure. Medications that are implicated include certain
antiarrhythmic, antibiotics, and antipsychotics. Diagnosis is based on an electrocardiogram (EKG) finding
a corrected QT interval of greater than 440 to 500 milliseconds together with clinical findings.
I45.9 Conduction disorder, unspecified
Arrhythmias and conduction disorders are caused by abnormalities in the generation or conduction of
these electrical impulses or both. Any heart disorder, including congenital abnormalities of structure (eg,
accessory atrioventricular connection) or function (eg, hereditary ion channelopathies), can disturb
rhythm.
R00 Tachycardia, unspecified
Tachycardia is a common type of heart rhythm disorder (arrhythmia) in which the heart beats faster
than normal while at rest. It's normal for your heart rate to rise during exercise or as a physiological
response to stress, trauma or illness (sinus tachycardia). But in tachycardia (tak-ih-KAHR-dee-uh), the
heart beats faster than normal in the upper or lower chambers of the heart or both while at rest. Your
heart rate is controlled by electrical signals sent across heart tissues. Tachycardia occurs when an
abnormality in the heart produces rapid electrical signals that quicken the heart rate, which is normally
about 60 to 100 beats a minute at rest. In some cases, tachycardia may cause no symptoms or
complications. But if left untreated, tachycardia can disrupt normal heart function and lead to serious
complications, including:
Heart failure
Stroke
Sudden cardiac arrest or death
Treatments, such as drugs, medical procedures or surgery, may help control a rapid heartbeat or
manage other conditions contributing to tachycardia.
R00.1 Bradycardia, unspecified
Bradycardia is a condition typically defined wherein an individual has a resting heart rate of under 60
beats per minute (BPM) in adults.Bradycardia typically does not cause symptoms until the rate drops
below 50 BPM. When symptomatic, it may cause fatigue, weakness, dizziness, sweating, and at very low
rates, fainting
During sleep, a slow heartbeat with rates around 40–50 BPM is common, and is considered normal.
Highly trained athletes may also have athletic heart syndrome, a very slow resting heart rate that occurs
as a sport adaptation and helps prevent tachycardia during training.
The term "relative bradycardia" is used to refer to a heart rate that, although not actually below 60
BPM, is still considered too slow for the individual's current medical condition.
R94.31 Abnormal electrocardiogram
Because an EKG measures so many different aspects of the heart’s function, abnormal results can signify
several issues. These include:
1. Defects or abnormalities in the heart’s shape and size: An abnormal EKG can signal that one or more
aspects of the heart’s walls are larger than another. This can signal that the heart is working harder than
normal to pump blood.
2. Electrolyte imbalances: Electrolytes are electricity-conducting particles in the body that help keep
the heart muscle beating in rhythm. Potassium, calcium, and magnesium are electrolytes. If your
electrolytes are imbalanced, you may have an abnormal EKG reading.
3. Heart attack or ischemia: During a heart attack, blood flow in the heart is affected and heart tissue
can begin to lose oxygen and die. This tissue will not conduct electricity as well, which can cause an
abnormal EKG. Ischemia, or lack of blood flow, may also cause an abnormal EKG.
4. Heart rate abnormalities: A typical human heart rate is between 60 and 100 beats per minute
(bpm). An EKG can determine if the heart is beating too fast or too slow.
5. Heart rhythm abnormalities: A heart typically beats in a steady rhythm. An EKG can reveal if the
heart is beating out of rhythm or sequence.
6. Medication side effects: Taking certain medications can impact a heart’s rate and rhythm.
Sometimes, medications given to improve the heart’s rhythm can have the reverse effect and cause
arrhythmias. Examples of medications that affect heart rhythm include beta-blockers, sodium channel
blockers, and calcium channel blockers. Learn more about arrhythmia drugs.
1.11 Q wave MI major Q waves with or without ST-T abnormalities Q wave on the
electrocardiogram (ECG) is an initially negative deflection of the QRS complex. Technically, a Q wave
indicates that the net direction of early ventricular depolarization (QRS) electrical forces projects toward
the negative pole of the lead axis in question.A non-Q wave myocardial infarction refers to a myocardial
infarction that does not result in a Q wave on the 12-lead ECG once the infarction is completed. ...
Instead, acute coronary syndromes are classified as unstable angina, non-ST elevation myocardial
infarction and ST elevation myocardial infarction.
1.12 Q wave MI major Q waves with or without ST-T abnormalities
Coming soon...
1.21 Possible Q wave MI moderate Q waves without ST-T abnormalities
Moderate risk of ischemc injury / possible Q wave MI:
Q >= 30 ms and ST deviation > 0.20 mV (minor Q waves with STT abnormalities)
Q >= 40 ms and ST deviation < 0.20mV (moderate Q waves without STT abnormalities)
1.22 Possible Q wave MI moderate Q waves without ST-T abnormalities
The T wave is the most labile wave in the ECG. T wave changes including low-amplitude T waves and
abnormally inverted T waves may be the result of many cardiac and non-cardiac conditions. The normal
T wave is usually in the same direction as the QRS except in the right precordial leads (see V2 below).
Also, the normal T wave is asymmetric with the first half moving more slowly than the second half. In
the normal ECG (see below) the T wave is always upright in leads I, II, V3-6, and always inverted in lead
aVR. The other leads are variable depending on the direction of the QRS and the age of the patient.
1.31 Minor Q waves without ST-T abnormalities
In general, T wave changes are very non-specific. They can occur with hyperventilation, anxiety, drinking
hot or cold beverages, and positional changes. Dramatic T wave inversions are often seen in the athletic
heart syndrome (a constellation of findings not associated with any pathology), and the dramatic T wave
inversions associated with CNS events are very rare. Hyperkalemia (hyperpotassemia) can cause tall,
peaked T waves. Hypokalemia and ischemia can cause low amplitude or inverted T waves.
1.41 Supraventricular tachycardia, rate 130 cpm
Supraventricular tachycardia (SVT) is an abnormally fast heart rhythm arising from improper electrical
activity in the upper part of the heart. There are four main types: atrial fibrillation, paroxysmal
supraventricular tachycardia (PSVT), atrial flutter, and Wolff–Parkinson–White syndrome. Symptoms
may include palpitations, feeling faint, sweating, shortness of breath, or chest pain.
They start from either the atria or atrioventricular node. They are generally due to one of two
mechanisms: re-entry or increased automaticity. The other type of fast heart rhythm is ventricular
arrhythmias—rapid rhythms that start within the ventricle. Diagnosis is typically by electrocardiogram
(ECG), holter monitor, or event monitor. Blood tests may be done to rule out specific underlying causes
such as hyperthyroidism or electrolyte abnormalities.
1.42 Supraventricular tachycardia, rate 130 cpm
Supraventricular tachycardia (SVT) is an abnormally fast heart rhythm arising from improper electrical
activity in the upper part of the heart. There are four main types: atrial fibrillation, paroxysmal
supraventricular tachycardia (PSVT), atrial flutter, and Wolff–Parkinson–White syndrome. Symptoms
may include palpitations, feeling faint, sweating, shortness of breath, or chest pain.
They start from either the atria or atrioventricular node. They are generally due to one of two
mechanisms: re-entry or increased automaticity. The other type of fast heart rhythm is ventricular
arrhythmias—rapid rhythms that start within the ventricle. Diagnosis is typically by electrocardiogram
(ECG), holter monitor, or event monitor. Blood tests may be done to rule out specific underlying causes
such as hyperthyroidism or electrolyte abnormalities.
2.1 First-degree AV block (AVB1)
First-degree atrioventricular block (AV block), is a disease of the electrical conduction system of the
heart in which the PR interval is lengthened beyond 0.20 seconds.In first-degree AV block, the impulse
conducting from atria to ventricles through the atrioventricular node (AV node) is delayed and travels
slower than normal. It has a prevalence in the normal (young adult) population of 0.65-1.1% and the
incidence is 0.13 per 1000 persons.In normal individuals, the AV node slows the conduction of electrical
impulse through the heart. This is manifest on a surface electrocardiogram (ECG) as the PR interval. The
normal PR interval is from 120 ms to 200 ms in length. This is measured from the initial deflection of the
P wave to the beginning of the QRS complex.In first-degree heart block, the diseased AV node conducts
the electrical activity more slowly. This is seen as a PR interval greater than 200 ms in length on the
surface ECG. It is usually an incidental finding on a routine ECG.
3.1 Left ventricular hypertrophy without ST-T
Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your heart's
main pumping chamber (left ventricle). Left ventricular hypertrophy can develop in response to some
factor — such as high blood pressure or a heart condition — that causes the left ventricle to work
harder.
3.1 Left bundle branch block without ECG evidence of myocardial infarction (MI)
Left bundle branch block (LBBB) is a common electrocardiographic (ECG) abnormality seen in patients
whose normal cardiac conduction down both anterior and posterior left fascicles of the His-Purkinje
system is compromised. Although LBBB is often associated with significant heart disease and is often the
result of myocardial injury, strain or hypertrophy, it can also be seen in patients without any particular
clinical disease. In isolation the presence of LBBB does not lend itself to any specific clinical concern, nor
does it affect prognosis. However, in the proper clinical context, LBBB can of great consequence and
importance, especially in patients presenting with acute chest pain, syncope and in those suffering from
heart failure with reduced ejection fraction (HFrEF).
3.11 Left bundle branch block with possible MI
Patients with a suspected myocardial infarction (MI) in the setting of a left bundle branch block (LBBB)
present a unique diagnostic and therapeutic challenge to the clinician. A diagnosis of MI with
electrocardiogram (ECG) is especially difficult in the setting of LBBB because of the characteristic ECG
changes caused by altered ventricular depolarization. The Sgarbossa criteria1 were first introduced over
20 years ago to improve the diagnostic accuracy for MI in the presence of LBBB; others have
subsequently modified the criteria to improve sensitivity.2 Here we review the pathophysiology of LBBB
in MI, discuss current guidelines, and highlight evolving paradigms for the diagnosis and treatment of
suspected MI in patients with LBBB.
3.2 Right bundle branch block without ECG evidence of MI
A right bundle branch block (RBBB) is a heart block in the right bundle branch of the electrical
conduction system.During a right bundle branch block, the right ventricle is not directly activated by
impulses travelling through the right bundle branch. The left ventricle however, is still normally
activated by the left bundle branch. These impulses are then able to travel through the myocardium of
the left ventricle to the right ventricle and depolarize the right ventricle this way. As conduction through
the myocardium is slower than conduction through the Bundle of His-Purkinje fibres, the QRS complex is
seen to be widened. The QRS complex often shows an extra deflection that reflects the rapid
depolarisation of the left ventricle followed by the slower depolarisation of the right ventricle.It is seen
in healthy individuals in about 1.5-3%.
3.21 Right bundle branch block with possible MI
A right bundle branch block (RBBB) is a heart block in the right bundle branch of the electrical
conduction system. During a right bundle branch block, the right ventricle is not directly activated by
impulses travelling through the right bundle branch.
3.3 Indeterminate ventricular conduction delay without ECG evidence of MI
In general, “conduction delay” refers to a slight widening of the QRS complex, especially in the
right precordial leads (leads V1, V2, and V3); it is sometimes also called incomplete right bundle branch
block. The most common cause of this is just being a normal variant, in other words, there is nothing
wrong with the heart. There are, however, some patients who have enlargement of the right heart as a
cause for this, such as having an atrial septal defect resulting in enlargement of the right ventricle or
perhaps partial anomalous pulmonary venous drainage of some of the pulmonary veins return to the
right side instead of the left side. Sometimes medications can cause conduction delay because of
indirect effects on the heart and generally that is considered safe. Finally, there are some individuals
where conduction delay may represent conduction system disease, but this is very uncommon.
3.31 Indeterminate ventricular conduction delay with possible MI
Coming soon...
3.41 Borderline delay of right ventricular excitation
Right ventricular hypertrophy (RVH) is a condition defined by an abnormal enlargement of the cardiac
muscle surrounding the right ventricle. The right ventricle is one of the four chambers of the heart. It is
located towards the lower-end of the heart and it receives blood from the right atrium and pumps blood
into the lungs.Since RVH is an enlargement of muscle it arises when the muscle is required to work
harder. Therefore, the main causes of RVH are pathologies of systems related to the right ventricle such
as the pulmonary artery, the tricuspid valve or the airways.RVH can be benign and have little impact on
day-to-day life or it can lead to conditions such as heart failure, which has a poor prognosis
3.42 Borderline delay of left ventricular excitation
Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your heart's
main pumping chamber (left ventricle). Left ventricular hypertrophy can develop in response to some
factor — such as high blood pressure or a heart condition — that causes the left ventricle to work
harder.
4.11 Marginal prolongation of ventricular repolarization
Ventricular repolarization is a complex electrical phenomenon which represents a crucial stage in
electrical cardiac activity. It is expressed on the surface electrocardiogram by the interval between the
start of the QRS complex and the end of the T wave or U wave (QT). Several physiological, pathological
and iatrogenic factors can influence ventricular repolarization. It has been demonstrated that small
perturbations in this process can be a potential trigger of malignant arrhythmias, therefore the analysis
of ventricular repolarization represents an interesting tool to implement risk stratification of arrhythmic
events in different clinical settings. The aim of this review is to critically revise the traditional methods of
static analysis of ventricular repolarization as well as those for dynamic evaluation, their prognostic
significance and the possible application in daily clinical practice.
4.11 Left ventricular hypertrophy with ST-T ST abnormalities without Q waves
Ventricular repolarization is a complex electrical phenomenon which represents a crucial stage
in electrical cardiac activity. It is expressed on the surface electrocardiogram by the interval between the
start of the QRS complex and the end of the T wave or U wave (QT). Several physiological, pathological
and iatrogenic factors can influence ventricular repolarization. It has been demonstrated that small
perturbations in this process can be a potential trigger of malignant arrhythmias, therefore the analysis
of ventricular repolarization represents an interesting tool to implement risk stratification of arrhythmic
events in different clinical settings. The aim of this review is to critically revise the traditional methods of
static analysis of ventricular repolarization as well as those for dynamic evaluation, their prognostic
significance and the possible application in daily clinical practice.
4.12 Significant prolongation of ventricular repolarization
Ventricular depolarization (activation) is depicted by the QRS complex, whereas ventricular
repolarization is defined by the interval from the beginning of the QRS complex to the end of the T- or
U-wave. On the surface ECG, ventricular repolarization components include the J-wave, ST-segment, and
T- and U-waves.
4.12 Left ventricular hypertrophy with ST-T ST abnormalities without Q waves
Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your heart's
main pumping chamber (left ventricle). Left ventricular hypertrophy can develop in response to some
factor — such as high blood pressure or a heart condition — that causes the left ventricle to work
harder.
4.2 Left ventricular hypertrophy with ST-T ST abnormalities without Q waves
Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your heart's
main pumping chamber (left ventricle). Left ventricular hypertrophy can develop in response to some
factor ” such as high blood pressure or a heart condition ” that causes the left ventricle to work harder.
4.3 Minor ST-T abnormalities
The specificity of ST-T and U wave abnormalities is provided more by the clinical circumstances in which
the ECG changes are found than by the particular changes themselves. Thus the term, nonspecific ST-T
wave abnormalities, is frequently used when the clinical data are not available to correlate with the ECG
findings. This does not mean that the ECG changes are unimportant! It is the responsibility of the
clinician providing care for the patient to ascertain the importance of the ECG findings.
4.4 Minor ST-T abnormalities
The specificity of ST-T and U wave abnormalities is provided more by the clinical circumstances in which
the ECG changes are found than by the particular changes themselves. Thus the term, nonspecific ST-T
wave abnormalities, is frequently used when the clinical data are not available to correlate with the ECG
findings. This does not mean that the ECG changes are unimportant! It is the responsibility of the
clinician providing care for the patient to ascertain the importance of the ECG findings.
5.1 Q wave MI major Q waves with or without ST-T abnormalities
Coming soon...
5.1 T-wave abnormalities without Q waves Possible Q wave MI minor Q waves with ST-T
abnormalities Q wave MI moderate Q waves with ST-T abnormalities
Coming soon...
5.2 Q wave MI moderate Q waves with ST-T abnormalities
Coming soon...
5.2 Left ventricular hypertrophy with ST-T T-wave abnormalities without Q waves Possible Q wave
MI minor Q waves with ST-T abnormalities Q wave MI moderate Q waves with ST-T abnormalities
Coming soon...
5.3 Possible Q wave MI moderate Q waves without ST-T abnormalities
Coming soon...
5.3 Minor ST-T abnormalities
Coming soon...
5.4 Minor ST-T abnormalities
The specificity of ST-T and U wave abnormalities is provided more by the clinical circumstances in which
the ECG changes are found than by the particular changes themselves. Thus the term, nonspecific ST-T
wave abnormalities, is frequently used when the clinical data are not available to correlate with the ECG
findings. This does not mean that the ECG changes are unimportant! It is the responsibility of the
clinician providing care for the patient to ascertain the importance of the ECG findings.
5.4 Possible Q wave MI minor Q waves with ST-T abnormalities
Coming soon...
5.5 ST abnormalities without Q waves
The ST-T configuration in the electrocardiogram of patients with left ventricular hypertrophy is said to
have a typical pattern of ST depression together with asymmetrical T wave inversion (the so-called left
ventricular strain pattern). However, many patients with left ventricular hypertrophy may also have
ischaemic heart disease. To revise the electrocardiographic criteria for left ventricular hypertrophy the
ST-T configuration in patients with left ventricular hypertrophy documented by echocardiography and
with normal coronary arteries was assessed.
5.6 T-wave abnormalities without Q waves
T wave abnormalities on resting ECG should be given special attention and correlated with
clinical information. Risk factors for major Q/QS patterns need not be the same as traditional risk factors
for clinically recognized CHD. High lipoprotein (a) levels may be a stronger risk factor for silent
myocardial infarction (MI) compared to clinically recognized MI.
5.7 Minor Q waves without ST-T abnormalities
Coming soon...
5.8 Minor ST-T abnormalities
Persistent, minor, nonspecific ST-T abnormalities are associated with increased long-term risk of
mortality to MI, CHD, CVD, and all causes; the higher the frequency of occurrence of minor ST-T
abnormalities, the greater the risk.
6.3 First-degree AV block (AVB1)
First-degree atrioventricular block (AV block), is a disease of the electrical conduction system of the
heart in which the PR interval is lengthened beyond 0.20 seconds.In first-degree AV block, the impulse
conducting from atria to ventricles through the atrioventricular node (AV node) is delayed and travels
slower than normal. It has a prevalence in the normal (young adult) population of 0.65-1.1% and the
incidence is 0.13 per 1000 persons.
6.41 QRS duration 120 ms Ventricular preexcitation pattern (WPW)
The diagnosis of WPW typically occurs via ECG. The pathognomonic ECG findings in WPW are
the delta wave, characterized by a slurred upstroke in the QRS complex and a short PR interval 120 ms
(Figure 1). Depolarization of the ventricles via the accessory pathway contributes to QRS durations
longer than 120 ms. The location and refractory period of the accessory pathway may diminish the
prominence of the delta wave, making the diagnosis more challenging in some cases. ECG findings
associated with a subtle WPW pattern include left-axis deviation, abnormal Q waves in leads V5 and V6,
ST-segment depression, and T-wave changes. An intermittent WPW pattern on ECG (ie, a delta wave
present on every other QRS complex) is considered low risk for ventricular arrhythmia.
6.5 Short P-R interval
A short A-V conduction time, whether present with normal or with abnormal QRS complex, is associated
with an increased incidence of paroxysmal rapid heart action. There are a considerable number of
patients who have a short P-R interval, normal QRS complex and bouts of tachycardia. They are usually
females, in middle life, devoid of organic heart disease and exhibit a snapping apical first heart sound.
They do not demonstrate any of the features of anomalous A-V conduction. Evidence is presented
suggesting the operation of endocrine and autonomic nervous system factors in the genesis both of the