Post on 28-Jul-2020
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
short P-R interval and the tachycardia.
6.6 Intermittent aberrant atrioventricular conduction
Aberrant ventricular conduction definition: It is a term applied to alterations in QRS contour of
supraventricular beats resulting from impulse transmition during periods of physiologic refractoriness
and/or depressed conductivity.
7.11 Left bundle branch block without ECG evidence of myocardial infarction (MI) QRS duration 120
ms
Coming soon...
7.21 Right bundle branch block without ECG evidence of MI Right bundle branch block with possible
MI QRS duration 120 ms
Coming soon...
7.4 Indeterminate ventricular conduction delay without ECG evidence of MI QRS duration 120 m
Coming soon...
7.6 Left posterior fascicular block (LPFB) Borderline delay of left ventricular excitation
Coming soon...
7.7 Left anterior fascicular block (LAFB)
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.
8.7 Sinus Tachycardia (ST)
Sinus tachycardia (also colloquially known as sinus tach or sinus tachy) is a sinus rhythm with an
elevated rate of impulses, defined as a rate greater than 100 beats/min (bpm) in an average adult. The
normal resting heart rate in the average male adult ranges from 60–100 bpm and women 60-90bpm.
Note that the normal heart rate varies with age, with infants having normal heart rate of 110–150
bpm, in contrast to the elderly, who have slower normals.
8.8 Sinus Bradycardia (SB)
Sinus bradycardia is a sinus rhythm with a rate that is lower than normal. In humans,
bradycardia is generally defined to be a rate of under 60 beats per minute.
9.1 Low QRS amplitude
The QRS is said to be low voltage when: The amplitudes of all the QRS complexes in the limb
leads are 5 mm; or. The amplitudes of all the QRS complexes in the precordial leads are 10 mm.
9.2 InfarctionIschemia
Ischemia: not enough blood (=oxygen) supply to whatever was ischemic, usually the heart muscle, but
can also be a limb, intestine, kidney, spleen etc. , but ischemic tissue isnt dead (yet), if oxygen needs can
be lowered the symptoms go away, e.g. patients having angina pectoris (ischemic heart pain) during
exertion, which goes away after stopping exertion. Infarction: tissue that has died because of not getting
enough oxygen containing blood: heart infarction AKA myocardial infarction, brain infarction, lung
infarction, spleen infarction, kidney infarction, bowel infarction, placental infarction.
9.5 T-wave amplitude 12 mm
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
HR Heart rate
Heart rate is the speed of the heartbeat;measured by the number of contractions (beats) of the heart
per minute (bpm). The heart rate can vary according to the body's physical needs, including the need to
absorb oxygen and excrete carbon dioxide. It is usually equal or close to the pulse measured at any
peripheral point. Activities that can provoke change include physical exercise, sleep, anxiety, stress,
illness, and ingestion of drugs.
The American Heart Association states the normal resting adult human heart rate is 60–100 bpm.
Tachycardia is a fast heart rate, defined as above 100 bpm at rest. Bradycardia is a slow heart rate,
defined as below 60 bpm at rest. During sleep a slow heartbeat with rates around 40–50 bpm is
common and is considered normal. When the heart is not beating in a regular pattern, this is referred to
as an arrhythmia. Abnormalities of heart rate sometimes indicate disease.
HI Health index
Health index is a number based on scientific calculations from 1 (low index) to 100 (high index). It grows
or decreases in real time and depends on changes in the parameters of your body, emotional well-being
and lifestyle. The health index is similar to the stock quote of a stock, but only in the role of a stock in
real time is your health and well-being.
SI Stress index
The stress index reflects the degree of stress on the body.
Stress is a response of the human body to an overstrain, negative emotions, or simply to monotonous
bustle.
During stress, the human body produces the hormone adrenaline, which makes you look for a way out.
Stress in small quantities is needed by everyone, as it makes you think, to seek a way out of the
problem.
But severe stress affects health. Immunity decreases and a number of diseases develop (cardiovascular,
gastrointestinal, etc.).
BMI Body mass index
The body mass index (BMI) or Quetelet index is a value derived from the mass (weight) and height of a
person. The BMI is defined as the body mass divided by the square of the body height, and is universally
expressed in units of kg/m2, resulting from mass in kilograms and height in metres.
The BMI may also be determined using a table or chart which displays BMI as a function of mass and
height using contour lines or colours for different BMI categories, and which may use other units of
measurement (converted to metric units for the calculation).
The BMI is a convenient rule of thumb used to broadly categorize a person as underweight, normal
weight, overweight, or obese based on tissue mass (muscle, fat, and bone) and height. That
categorization is the subject of some debate about where on the BMI scale the dividing lines between
categories should be placed. Commonly accepted BMI ranges are underweight: under 18.5 kg/m2,
normal weight: 18.5 to 25, overweight: 25 to 30, obese: over 30.
BMIs under 20.0 and over 25.0 have been associated with higher all-cause mortality, increasing risk with
distance from the 20.0-25.0 range. The prevalence of overweight and obesity is the highest in the
Americas and lowest in South East Asia. The prevalence of overweight and obesity in high income and
upper middle income countries is more than double that of low and lower middle income countries.
BMr Basal metabolic rate
Basal metabolic rate (BMR) is the rate of energy expenditure per unit time by endothermic animals at
rest. It is reported in energy units per unit time ranging from watt (joule/second) to ml O2/min or joule
per hour per kg body mass J/(h•kg). Proper measurement requires a strict set of criteria be met. These
criteria include being in a physically and psychologically undisturbed state, in a thermally neutral
environment, while in the post-absorptive state (i.e., not actively digesting food). In bradymetabolic
animals, such as fish and reptiles, the equivalent term standard metabolic rate (SMR) is used. It follows
the same criteria as BMR, but requires the documentation of the temperature at which the metabolic
rate was measured. This makes BMR a variant of standard metabolic rate measurement that excludes
the temperature data, a practice that has led to problems in defining "standard" rates of metabolism for
many mammals.
Metabolism comprises the processes that the body needs to function. Basal metabolic rate is the
amount of energy per unit time that a person needs to keep the body functioning at rest. Some of those
processes are breathing, blood circulation, controlling body temperature, cell growth, brain and nerve
function, and contraction of muscles. Basal metabolic rate (BMR) affects the rate that a person burns
calories and ultimately whether that individual maintains, gains, or loses weight. The basal metabolic
rate accounts for about 60 to 75% of the daily calorie expenditure by individuals. It is influenced by
several factors. BMR typically declines by 1–2% per decade after age 20, mostly due to loss of fat-free
mass, although the variability between individuals is high.
Ee Energy Expenditure
Energy expenditure is the amount of energy (or calories) that a person needs to carry out a physical
function such as breathing, circulating blood, digesting food, or physical movement. Your total daily
energy expenditure (TDEE) is the total number of calories you burn each day. To prevent weight gain,
energy intake or calorie intake must be balanced with energy expenditure.
SBP Systolic blood pressure
The upper number - systolic blood pressure, shows the pressure in the arteries at the time when the
heart contracts and pushes blood into the arteries, it depends on the strength of the contraction of the
heart, the resistance of the walls of blood vessels, and the number of contractions per unit of time.
Blood pressure is one of the most important parameters characterizing the work of the circulatory
system. Blood pressure is determined by the volume of blood pumped per unit of time by the heart and
the resistance of the vascular bed. Since the blood moves under the influence of the pressure gradient
in the vessels created by the heart, the greatest pressure of the blood will be at the exit of the blood
from the heart (in the left ventricle), a little less pressure will be in the arteries, even lower in the
capillaries, and the lowest in the veins and at the entrance heart (in the right atrium).
DBP Diastolic blood pressure
The bottom number - diastolic blood pressure, shows the pressure in the arteries at the time of
relaxation of the heart muscle. This is the minimum pressure in the arteries, it reflects the resistance of
peripheral vessels. As the blood moves along the vascular channel, the amplitude of blood pressure
fluctuations decreases, the venous and capillary pressure depend little on the phase of the cardiac cycle.
Blood pressure is one of the most important parameters characterizing the work of the circulatory
system. Blood pressure is determined by the volume of blood pumped per unit of time by the heart and
the resistance of the vascular bed. Since the blood moves under the influence of the pressure gradient
in the vessels created by the heart, the greatest pressure of the blood will be at the exit of the blood
from the heart (in the left ventricle), a little less pressure will be in the arteries, even lower in the
capillaries, and the lowest in the veins and at the entrance heart (in the right atrium).
HGB Hemoglobin (HGB)
Hemoglobin (American English) or haemoglobin (British English), abbreviated Hb or Hgb, is the iron-
containing oxygen-transport metalloprotein in the red blood cells (erythrocytes) of almost all
vertebrates (the exception being the fish family Channichthyidae) as well as the tissues of some
invertebrates. Haemoglobin in blood carries oxygen from the lungs or gills to the rest of the body (i.e.
the tissues). There it releases the oxygen to permit aerobic respiration to provide energy to power the
functions of the organism in the process called metabolism. A healthy individual has 12 to 20 grams of
haemoglobin in every 100 ml of blood.In mammals, the protein makes up about 96% of the red blood
cells' dry content (by weight), and around 35% of the total content (including water).
Haemoglobin has an oxygen-binding capacity of 1.34 mL O2 per gram, which increases the total blood
oxygen capacity seventy-fold compared to dissolved oxygen in blood. The mammalian hemoglobin
molecule can bind (carry) up to four oxygen molecules.
Hemoglobin is involved in the transport of other gases: It carries some of the body's respiratory carbon
dioxide (about 20–25% of the total[9]) as carbaminohemoglobin, in which CO2 is bound to the heme
protein. The molecule also carries the important regulatory molecule nitric oxide bound to a globin
protein thiol group, releasing it at the same time as oxygen.Haemoglobin is also found outside red blood
cells and their progenitor lines. Other cells that contain haemoglobin include the A9 dopaminergic
neurons in the substantia nigra, macrophages, alveolar cells, lungs, retinal pigment epithelium,
hepatocytes, mesangial cells in the kidney, endometrial cells, cervical cells and vaginal epithelial cells. In
these tissues, haemoglobin has a non-oxygen-carrying function as an antioxidant and a regulator of iron
metabolism.
Excessive glucose in one's blood can attach to hemoglobin and raise the level of hemoglobin
A1c.Haemoglobin and haemoglobin-like molecules are also found in many invertebrates, fungi, and
plants. In these organisms, haemoglobins may carry oxygen, or they may act to transport and regulate
other small molecules and ions such as carbon dioxide, nitric oxide, hydrogen sulfide and sulfide. A
variant of the molecule, called leghaemoglobin, is used to scavenge oxygen away from anaerobic
systems, such as the nitrogen-fixing nodules of leguminous plants, before the oxygen can poison
(deactivate) the system.
Hct Hematocrit
The hematocrit (Ht or HCT), also known by several other names, is a blood test that measures
the volume percentage (vol%) of red blood cells (RBC) in blood. The measurement depends on the
number and size of red bloods cells. It is normally 40.7% to 50.3% for men and 36.1% to 44.3% for
women. It is a part of a person's complete blood count results, along with hemoglobin concentration,
white blood cell count, and platelet count. Because the purpose of red blood cells is to transfer oxygen
from the lungs to body tissues, a blood sample's hematocrit—the red blood cell volume percentage—
can become a point of reference of its capability of delivering oxygen. Hematocrit levels that are too
high or too low can indicate a blood disorder, dehydration, or other medical conditions. An abnormally
low hematocrit may suggest anemia, a decrease in the total amount of red blood cells, while an
abnormally high hematocrit is called polycythemia. Both are potentially life-threatening disorders.
Plt Platelets
Platelets, also called thrombocytes, are a component of blood whose function (along with the
coagulation factors) is to react to bleeding from blood vessel injury by clumping, thereby initiating a
blood clot. Platelets have no cell nucleus: they are fragments of cytoplasm that are derived from the
megakaryocytes of the bone marrow, and then enter the circulation. Circulating unactivated platelets
are biconvex discoid (lens-shaped) structures,:117–18 2–3 µm in greatest diameter. Activated platelets
have cell membrane projections covering their surface. Platelets are found only in mammals, whereas in
other animals (e.g. birds, amphibians) thrombocytes circulate as intact mononuclear cells.
On a stained blood smear, platelets appear as dark purple spots, about 20% the diameter of red blood
cells. The smear is used to examine platelets for size, shape, qualitative number, and clumping. The ratio
of platelets to red blood cells in a healthy adult ranges from 1:10 to 1:20. One major function of
platelets is to contribute to hemostasis: the process of stopping bleeding at the site of interrupted
endothelium. They gather at the site and unless the interruption is physically too large, they plug the
hole. First, platelets attach to substances outside the interrupted endothelium: adhesion. Second, they
change shape, turn on receptors and secrete chemical messengers: activation. Third, they connect to
each other through receptor bridges: aggregation. Formation of this platelet plug (primary hemostasis)
is associated with activation of the coagulation cascade with resultant fibrin deposition and linking
(secondary hemostasis). These processes may overlap: the spectrum is from a predominantly platelet
plug, or "white clot" to a predominantly fibrin, or "red clot" or the more typical mixture. Some would
add the subsequent retraction and platelet inhibition as fourth and fifth steps to the completion of the
process and still others a sixth step wound repair. Platelets also participate in both innate and adaptive
intravascular immune responses.
Rbc Red blood cells
Red blood cells, also known as RBCs, red cells, red blood corpuscles, haematids, erythroid cells or
erythrocytes (from Greek erythros for "red" and kytos for "hollow vessel", with -cyte translated as "cell"
in modern usage), are the most common type of blood cell and the vertebrate's principal means of
delivering oxygen (O2) to the body tissues” via blood flow through the circulatory system. RBCs take up
oxygen in the lungs, or gills of fish, and release it into tissues while squeezing through the body's
capillaries.
The cytoplasm of erythrocytes is rich in hemoglobin, an iron-containing biomolecule that can bind
oxygen and is responsible for the red color of the cells and the blood. The cell membrane is composed of
proteins and lipids, and this structure provides properties essential for physiological cell function such as
deformability and stability while traversing the circulatory system and specifically the capillary
network.In humans, mature red blood cells are flexible and oval biconcave disks. They lack a cell nucleus
and most organelles, in order to accommodate maximum space for hemoglobin; they can be viewed as
sacks of hemoglobin, with a plasma membrane as the sack. Approximately 2.4 million new erythrocytes
are produced per second in human adults. The cells develop in the bone marrow and circulate for about
100–120 days in the body before their components are recycled by macrophages. Each circulation
takes about 60 seconds (one minute). Approximately a quarter of the cells in the human body are red
blood cells. Nearly half of the blood's volume (40% to 45%) is red blood cells.
Packed red blood cells (pRBC) are red blood cells that have been donated, processed, and stored in a
blood bank for blood transfusion.
WBCs White blood cells
White blood cells (also called leukocytes or leucocytes and abbreviated as WBCs) are the cells of the
immune system that are involved in protecting the body against both infectious disease and foreign
invaders. All white blood cells are produced and derived from multipotent cells in the bone marrow
known as hematopoietic stem cells. Leukocytes are found throughout the body, including the blood and
lymphatic system.
All white blood cells have nuclei, which distinguishes them from the other blood cells, the anucleated
red blood cells (RBCs) and platelets. Types of white blood cells can be classified in standard ways. Two
pairs of broadest categories classify them either by structure (granulocytes or agranulocytes) or by cell
lineage (myeloid cells or lymphoid cells). These broadest categories can be further divided into the five
main types: neutrophils, eosinophils (acidophiles), basophils, lymphocytes, and monocytes. These types
are distinguished by their physical and functional characteristics. Monocytes and neutrophils are
phagocytic. Further subtypes can be classified; for example, among lymphocytes, there are B cells, T
cells, and NK cells.
The number of leukocytes in the blood is often an indicator of disease, and thus the white blood cell
count is an important subset of the complete blood count. The normal white cell count is usually
between 4 × 109/L and 1.1 × 1010/L. In the US, this is usually expressed as 4,000 to 11,000 white
blood cells per microliter of blood. White blood cells make up approximately 1% of the total blood
volume in a healthy adult, making them substantially less numerous than the red blood cells at 40% to
45%. However, this 1% of the blood makes a large difference to health, because immunity depends on
it. An increase in the number of leukocytes over the upper limits is called leukocytosis. It is normal when
it is part of healthy immune responses, which happen frequently. It is occasionally abnormal, when it is
neoplastic or autoimmune in origin. A decrease below the lower limit is called leukopenia. This indicates
a weakened immune system.
SDNN Standard deviation of the normal-to-normal intervals
The Standard Normal curve, shown here, has mean 0 and standard deviation 1. If a dataset follows a
normal distribution, then about 68% of the observations will fall within of the mean , which in this case
is with the interval (-1,1). About 95% of the observations will fall within 2 standard deviations of the
mean, which is the interval (-2,2) for the standard normal, and about 99.7% of the observations will fall
within 3 standard deviations of the mean, which corresponds to the interval (-3,3) in this case. Although
it may appear as if a normal distribution does not include any values beyond a certain interval, the
density is actually positive for all values, . Data from any normal distribution may be transformed into
data following the standard normal distribution by subtracting the mean and dividing by the standard
deviation .
ARP index Index of adequacy of the regulatory processes
Coming soon...
AR index Autonomic rate index
Coming soon...
AB index Autonomic balance index
Coming soon...
SER index Normalized index of summary effect of regulation
Coming soon...
ASER index Conditional index of activity of the sympathetic element of regulation
Coming soon...
FCS index The most probable level of functioning of cardiovascular system
Coming soon...
MARI Maximum amplitude of regulatory influences
Coming soon...
TINN Triangular interpolation of the normal-to-normal interval of a histogram
Coming soon...
HRVti HRV triangular index
HRV Triangular Index. The HTI is a geometric measure based on 24 h recordings which calculates the
integral of the density of the RR interval histogram divided by its height.
sdHR Deviation of heart rate
Recent clinical studies have proposed standard deviation of heart rate as a diagnostic tool for
the outcome of cardiac infarction. Mathematical analysis of heart rate variability shows that heart rate is
influenced by different frequency components derived from different parts of the autonomous nervous
system. In the experimental part of this study, we investigated the possibility of calculating a variable
describing the parasympathetic branch of the autonomous nervous system exclusively.
Heart rate was found to be lower at rest (65.9 +/- 9.7 beats per minute) than during dynamometry (72.8
+/- 10.4 beats per minute, P < .001).
pNN50 The number of cardiac intervals with a difference of more than 50 ms,
The percentage of difference between adjacent NN intervals differing by more than 50 ms
MeanRR Mean RR-interval
The interval from the peak of one QRS complex to the peak of the next as shown on an
electrocardiogram. It is used to assess the ventricular rate.
MinRR Min RR-interval Minimum R-R interval (100 bpm = 3 squares)
MaxRR Max RR-interval
Maximum R-R interval (60 bpm = 5 squares)
SD1 Poincare plot, SD1
SD1: dispersion (standard deviation) of points perpendicular to the axis of line of identity.
SD2 Poincare plot, SD2
SD2: dispersion (standard deviation) of points along the axis of line of identity
DFA1 Detrended fluctuation analysis, alpha1
Coming soon...
DFA2 Detrended fluctuation analysis, alpha2
Coming soon...
nLF Normalized LF
The normalized spectral heart rate variability (HRV) measures low-frequency (LF)nu and high-frequency
(HF)nu are frequently used in contemporary sleep research studies to quantify modulation of the
sympathetic and parasympathetic branches of the autonomic nervous system. The purpose of this
tutorial and methodologic critique is to concisely demonstrate the structural algebraic redundancy
inherent in the normalized spectral HRV measures with respect to each other, and also with respect to
the well-known HRV index of sympathovagal balance, LF:HF ratio. The statistical problems and
interpretational paradoxes related to the mathematical definitions of LFnu and HFnu are briefly
outlined. Examples of use of normalized spectral HRV measures in recent articles from the sleep-
relevant research literature are critically reviewed. LFnu, HFnu, and LF:HF ratio should be considered
equivalent carriers of information about sympathovagal balance
nHF Normalized HF
The normalized spectral heart rate variability (HRV) measures low-frequency (LF)nu and high-frequency
(HF)nu are frequently used in contemporary sleep research studies to quantify modulation of the
sympathetic and parasympathetic branches of the autonomic nervous system. The purpose of this
tutorial and methodologic critique is to concisely demonstrate the structural algebraic redundancy
inherent in the normalized spectral HRV measures with respect to each other, and also with respect to
the well-known HRV index of sympathovagal balance, LF:HF ratio. The statistical problems and
interpretational paradoxes related to the mathematical definitions of LFnu and HFnu are briefly
outlined. Examples of use of normalized spectral HRV measures in recent articles from the sleep-
relevant research literature are critically reviewed. LFnu, HFnu, and LF:HF ratio should be considered
equivalent carriers of information about sympathovagal balance.
LFHF LFHF Ratio
To evaluate the high-frequency component (HF) of the heart rhythm, a recording of about 1 min is
needed, whereas for the analysis of the low-frequency component (LF), 2 minutes of recording are
required. For an objective assessment of the very low-frequency component of HRV (VLF), the recording
time must be at least 5 minutes. Therefore, for the standardization of studies of HRV with short
recordings, a preferred recording duration of 5 minutes was chosen.
VLF Power in very low frequency range
To evaluate the high-frequency component (HF) of the heart rhythm, a recording of about 1 min
is needed, whereas for the analysis of the low-frequency component (LF), 2 minutes of recording are
required. For an objective assessment of the very low-frequency component of HRV (VLF), the recording
time must be at least 5 minutes. Therefore, for the standardization of studies of HRV with short
recordings, a preferred recording duration of 5 minutes was chosen.
LF Power in low frequency range
The activity of the ANS divisions was differentiated using spectral analysis — the following HRV
frequency values were determined: the power of the low-frequency spectrum (0.05“0.15 Hz) - LF, which
mainly reflects the activity of the sympathetic ANS
HF Power in high frequency range
The activity of the ANS divisions was differentiated using spectral analysis — the following HRV
frequency values were determined: the power of the high-frequency spectrum (0.15“0.40 Hz) - HF,
reflecting the influence of the parasympathetic division of the ANS
TP Power in whole frequency range
Coming soon...
TG Triglycerides (TG)
A triglyceride (TG) is an ester derived from glycerol and three fatty acids (from tri- and
glyceride). Triglycerides are the main constituents of body fat in humans and other vertebrates, as well
as vegetable fat. They are also present in the blood to enable the bidirectional transference of adipose
fat and blood glucose from the liver, and are a major component of human skin oils.
There are many different types of triglyceride, with the main division between saturated and
unsaturated types. Saturated fats are "saturated" with hydrogen — all available places where hydrogen
atoms could be bonded to carbon atoms are occupied. These have a higher melting point and are more
likely to be solid at room temperature. Unsaturated fats have double bonds between some of the
carbon atoms, reducing the number of places where hydrogen atoms can bond to carbon atoms. These
have a lower melting point and are more likely to be liquid at room temperature.
LDL-C Low-density lipoproteins
Low-density lipoprotein (LDL) is one of the five major groups of lipoprotein which transport all fat
molecules around the body in the extracellular water. These groups, from least dense, compared to
surrounding water (largest particles) to most dense (smallest particles), are chylomicrons (aka ULDL by
the overall density naming convention), very low-density lipoprotein (VLDL), intermediate-density
lipoprotein (IDL), low-density lipoprotein and high-density lipoprotein (HDL). LDL delivers fat molecules
to the cells and can drive the progression of atherosclerosis if they become oxidized within the walls of
arteries.It is important to note that LDL is not "bad cholesterol". It is an essential transport system for
lipids the human body needs to survive, including cholesterol. There is both "large" and "small" particle
LDL, and while only small is associated with cholesterol-related issues, neither is "bad". Even "small" LDL
is necessary to conduct nutrients to vessels that "large" LDL can't reach.
HDL-C High-density lipoproteins (HDL-C)
High-density lipoprotein (HDL) is one of the five major groups of lipoproteins. Lipoproteins are complex
particles composed of multiple proteins which transport all fat molecules (lipids) around the body within
the water outside cells. They are typically composed of 80“100 proteins per particle (organized by one,
two or three ApoA; more as the particles enlarge picking up and carrying more fat molecules) and
transporting up to hundreds of fat molecules per particle.
CHOL Cholesterol
Cholesterol (from the Ancient Greek chole- (bile) and stereos (solid), followed by the chemical
suffix -ol for an alcohol) is an organic molecule. It is a sterol (or modified steroid), a type of lipid.
Cholesterol is biosynthesized by all animal cells and is an essential structural component of animal cell
membranes.
Cholesterol also serves as a precursor for the biosynthesis of steroid hormones, bile acid and vitamin
D. Cholesterol is the principal sterol synthesized by all animals. In vertebrates, hepatic cells typically
produce the greatest amounts. It is absent among prokaryotes (bacteria and archaea), although there
are some exceptions, such as Mycoplasma, which require cholesterol for growth.
François Poulletier de la Salle first identified cholesterol in solid form in gallstones in 1769. However, it
was not until 1815 that chemist Michel Eugène Chevreul named the compound "cholesterine".
BCI Blood carbohydrate index
Coming soon...
RRI RR interval
This connection depends on tracking small changes (milliseconds) in the intervals between successive
heartbeats (Fig 1), also called "RR intervals". This is different from heart rate, which just averages the
number of beats per minute.
PW P-wave
The P wave on the ECG represents atrial depolarization, which results in atrial contraction, or atrial
systole.
PRs PR segment
The PR segment is the flat line between the end of the P-wave and the start of the QRS complex.
The PR segment reflects the time delay between atrial and ventricular activation.
The PR segment also serves as the baseline (reference line or isoelectric line) of the ECG curve. The
amplitude of any deflection/wave is measured by using the PR segment as the baseline.
PRi PR interval
In electrocardiography, the PR interval is the period, measured in milliseconds, that extends from the
beginning of the P wave (the onset of atrial depolarization) until the beginning of the QRS complex (the
onset of ventricular depolarization); it is normally between 120 and 200ms in duration. The PR interval is
sometimes termed the PQ interval.
QRSc QRS complex
The QRS complex is a name for the combination of three of the graphical deflections seen on a
typical electrocardiogram (EKG or ECG). It is usually the central and most visually obvious part of the
tracing; in other words, it's the main spike seen on an ECG line. It corresponds to the depolarization of
the right and left ventricles of the human heart and contraction of the large ventricular muscles.
In adults, the QRS complex normally lasts 0.06“0.10 s; in children and during physical activity, it may be
shorter. The Q, R, and S waves occur in rapid succession, do not all appear in all leads, and reflect a
single event and thus are usually considered together. A Q wave is any downward deflection
immediately following the P wave. An R wave follows as an upward deflection, and the S wave is any
downward deflection after the R wave. The T wave follows the S wave, and in some cases, an additional
U wave follows the T wave.
QTi QT interval
The QT interval is a measurement made on an electrocardiogram used to assess some of the
electrical properties of the heart. It is calculated as the time from the start of the Q wave to the end of
the T wave, and approximates to the time taken from when the cardiac ventricles start to contract to
when they finish relaxing. An abnormally long or abnormally short QT interval is associated with an
increased risk of developing abnormal heart rhythms and sudden cardiac death. Abnormalities in the QT
interval can be caused by genetic conditions such as Long QT syndrome, by certain medications such as
sotalol, by disturbances in the concentrations of certain salts within the blood such as hypokalaemia, or
by hormonal imbalances such as hypothyroidism.
STs ST segment
In electrocardiography, the ST segment connects the QRS complex and the T wave and has a
duration of 0.005 to 0.150 sec (5 to 150 ms).It starts at the J point (junction between the QRS complex
and ST segment) and ends at the beginning of the T wave. However, since it is usually difficult to
determine exactly where the ST segment ends and the T wave begins, the relationship between the ST
segment and T wave should be examined together. The typical ST segment duration is usually around
0.08 sec (80 ms). It should be essentially level with the PR and TP segments.The ST segment represents
the isoelectric period when the ventricles are in between depolarization and repolarization.
STi ST interval
Coming soon...
Tw T-wave
In electrocardiography, the T wave represents the repolarization of the ventricles. The interval from the
beginning of the QRS complex to the apex of the T wave is referred to as the absolute refractory period.
The last half of the T wave is referred to as the relative refractory period or vulnerable period. The T
wave contains more information than the QT interval. The T wave can be described by its symmetry,
skewness, slope of ascending and descending limbs, amplitude and subintervals like the Tpeak “Tend
interval.
In most leads, the T wave is positive. This is due to the repolarization of the membrane. During ventricle
contraction (QRS complex), the heart depolarizes. Repolarization of the ventricle happens in the
opposite direction of depolarization and is negative current, signifying the relaxation of the cardiac
muscle of the ventricles. This double negative of direction and charge is why the T wave is positive;
although the cell becomes more negatively charged, the net effect is in the positive direction, and the
ECG reports this as a positive spike. However, a negative T wave is normal in lead aVR. Lead V1 may
have a T wave with positive, negative, or biphasic where positive is followed by negative, or vice versa.
In addition, it is not uncommon to have an isolated negative T wave in lead III, aVL, or aVF. A periodic
beat-to-beat variation in the amplitude or shape of the T wave may be termed T wave alternans.
MTw Morphology of T-wave
T-wave morphology analysis (TMA) quantifies irregularities of ventricular repolarization based on
singular value decomposition of the 12-lead electrocardiogram (ECG). Furthermore, TMA is useful for
risk stratification of patients with myocardial infarction (MI), although gender differences in TMA and
the relationship between TMA and heart diseases are unknown. The aim of this study was to evaluate
the significance of TMA in healthy individuals and patients with heart diseases.
QTc QTc interval
The corrected QT interval (QTc) estimates the QT interval at a standard heart rate of 60 bpm.
This allows comparison of QT values over time at different heart rates and improves detection of
patients at increased risk of arrhythmias.
There are multiple formulas used to estimate QTc (see below). It is not clear which formula is the
most useful.
Bazett formula: QTC = QT / √ RR
Fridericia formula: QTC = QT / RR 1/3
Framingham formula: QTC = QT + 0.154 (1 – RR)
Hodges formula: QTC = QT + 1.75 (heart rate – 60)
Note: The RR interval is given in seconds (RR interval = 60 / heart rate).
K Potassium (K)
Potassium is a chemical element with the symbol K and atomic number 19. Potassium is a
silvery-white metal that is soft enough to be cut with a knife with little force. Potassium metal reacts
rapidly with atmospheric oxygen to form flaky white potassium peroxide in only seconds of exposure. It
was first isolated from potash, the ashes of plants, from which its name derives. In the periodic table,
potassium is one of the alkali metals, all of which have a single valence electron in the outer electron
shell, that is easily removed to create an ion with a positive charge – a cation, that combines with
anions to form salts. Potassium in nature occurs only in ionic salts. Elemental potassium reacts
vigorously with water, generating sufficient heat to ignite hydrogen emitted in the reaction, and burning
with a lilac-colored flame. It is found dissolved in sea water (which is 0.04% potassium by weight), and
occurs in many minerals such as orthoclase, a common constituent of granites and other igneous rocks.
Na Sodium (Na)
Sodium is a chemical element with the symbol Na (from Latin natrium) and atomic number 11. It is a
soft, silvery-white, highly reactive metal. Sodium is an alkali metal, being in group 1 of the periodic table,
because it has a single electron in its outer shell, which it readily donates, creating a positively charged
ion—the Na+ cation. Its only stable isotope is 23Na. The free metal does not occur in nature, and must
be prepared from compounds. Sodium is the sixth most abundant element in the Earth's crust and exists
in numerous minerals such as feldspars, sodalite, and rock salt (NaCl). Many salts of sodium are highly
water-soluble: sodium ions have been leached by the action of water from the Earth's minerals over
eons, and thus sodium and chlorine are the most common dissolved elements by weight in the oceans.
Ca Calcium (Ca)
Calcium is a chemical element with the symbol Ca and atomic number 20. As an alkaline earth metal,
calcium is a reactive metal that forms a dark oxide-nitride layer when exposed to air. Its physical and
chemical properties are most similar to its heavier homologues strontium and barium. It is the fifth most
abundant element in Earth's crust and the third most abundant metal, after iron and aluminium. The
most common calcium compound on Earth is calcium carbonate, found in limestone and the fossilised
remnants of early sea life; gypsum, anhydrite, fluorite, and apatite are also sources of calcium. The
name derives from Latin calx "lime", which was obtained from heating limestone.