Cardiac biomarker and ecg diagnosis

1. Cardiac Biomarker
&
ECG Diagnosis
BY-: PRATYASHA
PARIPURNA

2. CARDIAC
BIOMARKER

3. Biomarker
Biomarkers are biological measures of a biological state. By
definition, a biomarker is "a characteristic that is objectively
measured and evaluated as an indicator of normal biological
processes, pathogenic processes or pharmacological
responses to a therapeutic intervention.
In medicine, a biomarker is a measurable indicator of the
severity or presence of some disease state. More generally a
biomarker is anything that can be used as an indicator of a
particular disease state or some other physiological state of
an organism.

4. Cardiac biomarkers
Cardiac biomarkers are substances that are released into the
blood when the heart is damaged or stressed. Measurements
of these biomarkers are used to help diagnose acute coronary
syndrome (ACS) and cardiac ischemia, conditions associated
with insufficient blood flow to the heart.
A cardiac enzyme test is a tool used by doctors to determine if
someone is having or has already had a heart attack. This test
checks for levels of enzymes that are released by the heart
muscle when it is injured, such as during a heart attack.

5. HISTORY OF
CARDIAC
BIOMARKERS
1954 - SGOT (AST)
1955 - LDH
1960 - CPK
1972 - CPK isoforms by Electrophoresis
1975 - CK - MB by immune inhibition
1975 - Myoglobin
1985 - CK - MB Mass immunoassay
1989 - Troponin T
1992 - Troponin I

6. Applications
of
measurement
Measuring cardiac biomarkers can be a step toward making a
diagnosis for a condition.
Whereas cardiac imaging often confirms a diagnosis, simpler and
less expensive cardiac biomarker measurements can advise a
physician whether more complicated or invasive procedures are
warranted.
In many cases medical societies advise doctors to make
biomarker measurements an initial testing strategy especially for
patients at low risk of cardiac death.

7. CLASSIFICATION
OF CARDIAC
BIOMARKERS
Biomarkers of myocardial injury
-markers of myocardial necrosis
-markers of myocardial ischemia
Biomarkers of haemodynamic stress
Inflammatory and prognostic Biomarkers

8. Types of
cardiac
markers
Troponin
CPK-MB
Lactate dehydrogenase
Aspartate transaminase
Myoglobin
Human serum albumin
Ventricular natriuretic peptide
Glycogen phosphorylase isoenzyme BB

9. Troponin
Troponin, or the troponin complex, is a complex of three
regulatory proteins .
The most sensitive and specific test for myocardial damage.
Because it has increased specificity compared with CK-MB,
troponin is composed of 3 proteins- Troponin C, Cardiac
troponin I, and Cardiac troponin T. Troponin I especially has a
high affinity for myocardial injury.

10. TROPONIN
Troponin is released during MI from the cytosolic pool of the
myocytes. Its subsequent release is prolonged with
degradation of actin and myosin filaments. Isoforms of the
protein, T and I, are specific to myocardium.
Differential diagnosis of troponin elevation includes acute
infarction, severe pulmonary embolism causing acute right
heart overload, heart failure, myocarditis.
Troponins can also calculate infarct size but the peak must
be measured in the 3rd day.
After myocyte injury, troponin is released in 2–4 hours and
persists for up to 7 days. Normal value are- Troponin I <0.3
ng/ml and Troponin T <0.2 ng/ml

11. CPK-MB test
The CPK-MB test is a cardiac marker used to assist diagnoses of an
acute myocardial infarction.
It measures the blood level of CK-MB (creatine kinase myocardial
band), the bound combination of two variants (isoenzymes CKM
and CKB) of the enzyme phosphocreatine kinase.
It is relatively specific when skeletal muscle damage is not present.
The CK-MB isoform of creatine kinase is expressed in heart muscle.
It resides in the cytosol and facilitates movement of high energy
phosphates into and out of mitochondria. Since it has a short
duration, it cannot be used for late diagnosis of acute MI but can
be used to suggest infarct extension if levels rise again. This is
usually back to normal within 2–3 days. Normal range- 2-6ng/ml

12. Lactate
dehydrogenase
Lactate dehydrogenase (LDH or LD) is an enzyme found in nearly
all living cells. LDH catalyses the conversion of lactate to
pyruvate and back, as it converts NAD+ to NADH and back. A
dehydrogenase is an enzyme that transfers a hydride from one
molecule to another.
Lactate dehydrogenase catalyses the conversion of pyruvate to
lactate. LDH-1 isozyme is normally found in the heart muscle and
LDH-2 is found predominantly in blood serum. A high LDH-1 level
to LDH-2 suggest MI. LDH levels are also high in tissue
breakdown or homolysis. It can mean cancer, meningitis,
encephalitis, or HIV. This is usually back to normal 10–14 days.

13. Aspartate transaminase
Aspartate transaminase (AST) or aspartate aminotransferase,
also known as AspAT/ASAT/AAT or (serum) glutamic oxaloacetic
transaminase (GOT, SGOT), is a pyridoxal phosphate (PLP)-
dependent transaminase enzyme.
AST catalyses the reversible transfer of an α-amino group
between aspartate and glutamate and, as such, is an important
enzyme in amino acid metabolism. AST is found in the liver,
heart, skeletal muscle, kidneys, brain, and red blood cells.
Serum AST level, serum ALT (alanine transaminase) level, and
their ratio (AST/ALT ratio) are commonly measured clinically as
biomarkers for liver health.

14. Myoglobin
Myoglobin (symbol Mb or MB) is an iron- and oxygen-binding
protein found in the skeletal muscle tissue of vertebrates in
general and in almost all mammals.
Myoglobin is used less than the other markers. Myoglobin is
the primary oxygen-carrying pigment of muscle tissue. It is
high when muscle tissue is damaged but it lacks specificity. It
has the advantage of responding very rapidly,[8] rising and
falling earlier than CK-MB or troponin. It also has been used
in assessing reperfusion after thrombolysis.

15. Human
serum
albumin
Human serum albumin is the serum albumin found in human
blood. It is the most abundant protein in human blood plasma; it
constitutes about half of serum protein. It is produced in the
liver. It is soluble in water, and it is monomeric.
Human albumin solution (HSA) is available for medical use,
usually at concentrations of 5–25%.
Human albumin is often used to replace lost fluid and help
restore blood volume in trauma, burns and surgery patients.
There is no strong medical evidence that albumin administration
(compared to saline) saves lives for people who have
hypovolaemia or for those who are critically ill due to burns or
hypoalbuminaemia.[16] It is also not known if there are people
who are critically ill that may benefit from albumin.

16. Ventricular
natriuretic
peptide
Ventricular natriuretic peptide or brain natriuretic peptide
(BNP), also known as B-type natriuretic peptide, is a
hormone secreted by cardiomyocytes in the heart ventricles
in response to stretching caused by increased ventricular
blood volume.
This is increased in patients with heart failure. It has been
approved as a marker for acute congestive heart failure. Pt
with < 80 have a much higher rate of symptom-free survival
within a year. Generally, pt with CHF will have > 100.

17. Glycogen
phosphorylase
isoenzyme BB
Glycogen phosphorylase isoenzyme BB (abbreviation: GPBB) is
an isoenzyme of glycogen phosphorylase. This isoform of the
enzyme exists in cardiac (heart) and brain tissue.
The enzyme is one of the "new cardiac markers" which are
discussed to improve early diagnosis in acute coronary
syndrome. A rapid rise in blood levels can be seen in myocardial
infarction and unstable angina

18. Approximate peak

20. Limitations
Depending on the marker, it can take between 2 and 24 hours
for the level to increase in the blood.
Additionally, determining the levels of cardiac markers in the
laboratory - like many other lab measurements - takes
substantial time.
Cardiac markers are therefore not useful in diagnosing a
myocardial infarction in the acute phase.
The clinical presentation and results from an ECG are more
appropriate in the acute situation.

21. BIOMARKERS OF
MYOCARDIAL ISCHEMIA

22. Heart-type
fatty acid
binding
protein (H-
FABP)
H-FABP is a sensitive biomarker for myocardial infarction[11][12]
and can be detected in the blood within one to three hours of
the pain.
The diagnostic potential of the biomarker H-FABP for heart
injury.
H-FABP is 20 times more specific to cardiac muscle than
myoglobin, it is found at 10-fold lower levels in skeletal muscle
than heart muscle and the amounts in the kidney, liver and small
intestine are even lower again.
A study by Pulse the negative predictive value (NPV) of H-FABP
was an impressive 100%its Positive predictive value was 41%
which was greater than that of both cTnT (29%) and NT-proBNP
(19%)The myoglobin/heart FABP ratio has been used to
differentiate between heart muscle and skeletal muscle injury.

23. BIOMARKERS OF
HAEMODYNAMIC
STRESS

24. Natriuretic
peptides
The natriuretic peptides (NP) are a group of structurally similar
but genetically distinct peptides.
NPs are identified as regulatory diuretic-natriuretic substances
responsible for salt and water homeostasis lowers blood
pressure.
ANP and related peptides are used as biomarkers for
cardiovascular diseases such as stroke, coronary artery disease,
myocardial infarction and heart failure
A specific ANP precursor called mid-regional pro-atrial
natriuretic peptide (MRproANP) is a highly sensitive biomarker in
heart failure.
MRproANP levels below 120 pmol/L can be used to effectively
rule out acute heart failure

25. INFLAMMATORY
AND
PROGNOSTIC
BIOMARKERS
C-reactive protein
Myeloperoxidase
Homocysteine

26. C- REACTIVE
PROTEIN
CRP is considered as a serum biomarker in patients undergoing
acute inflammatory response (2–4).
The elevation in baseline CRP level was shown to be useful to
gauge chronic inflammation and tissue damage resulting from
excessive inflammation or failure of the initial inflammatory
response

27. Myeloperoxidase
Myeloperoxidase (MPO) is a peroxidase enzyme that in humans
is encoded by the MPO gene on chromosome 17.
MPO is most abundantly expressed in neutrophil granulocytes (a
subtype of white blood cells), and produces hypohalous acids to
carry out their antimicrobial activity.
MPO leads to oxidized LDL cholesterol
Oxidized LDL is phagocytosed by macrophages producing foam
cells.
MPO leads to the consumption of nitric oxidation.
Vasoconstriction and endothelial dysfunction MPO can cause
endothelial denuding and superficial platelet aggregation

28. Homocysteine
Intermediary amino acid formed by the conversion of
methionine to cysteine.
Moderate hyper homo cysteinemia occurs in 5- 7% of the
population recognized as an independent risk factor for the
development of atherosclerotic vascular disease and venous
thrombosis.
Can result from genetic defects, drugs, vitamin deficiencies

29. Biomarkers
for Diagnosis
The diagnosis of heart failure in a patient presenting with
breathlessness for the first time is often difficult, and biomarkers
— along with other investigations — can contribute to diagnosis.
Echocardiography is a useful component of diagnosis, but in the
acute setting it may not always be possible to obtain an
echocardiogram, particularly out of hours.
The natriuretic peptides are the most extensively studied and
used biomarkers in heart failure. As a result of myocardial
stretch, the B-type natriuretic peptide (BNP) gene is activated
and prohormone proBNP1–108 is produced.
. Atrial natriuretic peptide (ANP) as rapid clearance and is less
consistent as a diagnostic marker and hence is not used
routinely. However, newer assays have been developed that
measure the precursor hormone of ANP, mid-regional proANP
(MR-proANP). MR-proANP is more stable, giving more reliable
results, and has therefore been identified as a reliable marker.

30. Biomarkers for Prognosis
The natriuretic peptides again are the most extensively
investigated biomarker for assessing prognosis of patients with
heart failure — both in the acute setting as well as for patients with
chronic heart failure seen in the office setting.
It has been shown that at baseline, the higher the BNP, the worse
the prognosis, with patients having almost a five-fold greater
mortality between the highest and lowest tertials.
In patients admitted with heart failure, the risk of readmission and
death is high if the discharge BNP is not lower than the admission
value. Many of the large heart failure studies have also examined
the role of biomarkers in prognosis.

31. CONCLUSION
The use of biomarkers in the management of patients with heart
failure has increased tremendously over the past few years.
Currently the natriuretic peptides are the most commonly used
biomarker and help in the diagnosis and prognostication of
patients with heart failure.
Their role in the monitoring of treatment is still debatable,
although it seems reasonable that patients have their natriuretic
peptide values checked at discharge.
There are many new biomarkers currently under investigation.
The results are promising and they evaluate different aspects of
the heart failure spectrum. At present they appear to have a
synergistic role along with the natriuretic peptides — both in
terms of diagnosis and determination of prognosis.

32. ECG DIAGNOSIS

33. ECG
An electrocardiogram (ECG or EKG) records the electrical signal
from your heart to check for different heart conditions.
Electrodes are placed on your chest to record your heart's
electrical signals, which cause your heart to beat. The signals are
shown as waves on an attached computer monitor or printer.

34. Why might I need an electrocardiogram?
To look for the cause of
chest pain
To evaluate problems which
may be heart-related, such
as severe tiredness,
shortness of breath,
dizziness, or fainting
To identify irregular
heartbeats
To help determine the
overall health of the heart
before procedures such as
surgery; or after treatment
for conditions such as a
heart attack .
To see how an implanted
pacemaker is working
To determine how well
certain heart medicines are
working
To get a baseline tracing of
the heart's function during a
physical exam;

35. What are the risks
of an
electrocardiogram?
An electrocardiogram (ECG) is a quick, easy way to assess the
heart's function. Risks associated with ECG are minimal and rare.
You will not feel anything during the ECG, but it may be
uncomfortable when the sticky electrodes are taken off. If the
electrode patches are left on too long they may cause tissue
breakdown or skin irritation.

36. Conditions affect result of
ECG.
Obesity
Pregnancy
Fluid build up in the abdomen (ascites)
Anatomical considerations,
Movement during the test
Exercise or smoking before the test
Certain medicines
Electrolyte imbalances.

37. THE
APPLICATION
AREAS OF
ECG
DIAGNOSIS
1.The electric axis of the
heart
2.Heart rate monitoring
3.Arrhythmias
1. Supraventricular
arrhythmias
2. Ventricular
arrhythmias
4.Disorders in the activation
sequence
1. Atrioventricular
conduction defects
(blocks)
2. Bundle-branch block
3. Wolff-Parkinson-
White syndrome
5.Increase in wall thickness
or size of the atria and
ventricles
1. Atrial enlargement
(hypertrophy)
2. Ventricular
enlargement
(hypertrophy)

38. 6.Myocardial ischemia and infarction
◦ Ischemia
Infarction.
7. Drug Effect
Digitalis
◦ Quinidine
8.Electrolyte imbalance
◦ Potassium
◦ Calcium
9.Carditis
◦ Pericarditis
◦ Myocarditis
10.Pacemaker monitoring

39. Application
areas of ECG
diagnosis.

40. DETERMINATION
OF THE ELECTRIC
AXIS OF THE
HEART
The concept of the electric axis of the heart usually denotes
the average direction of the electric activity throughout
ventricular (or sometimes atrial) activation.
The term mean vector is frequently used instead of
"electric axis." The direction of the electric axis may also
denote the instantaneous direction of the electric heart
vector. This is shown in vectorcardiography as a function of
time.
The normal range of the electric axis lies between +30° and
-110° in the frontal plane and between +30° and -30° in the
transverse plane.

41. ELECTRIC
AXIS OF
HEART
The direction of the electric axis may be approximated from the 12-lead ECG
by finding the lead in the frontal plane, where the QRS-complex has largest
positive deflection.
The direction of the electric axis is in the direction of this lead vector. The
result can be checked by observing that the QRS-complex is symmetrically
biphasic in the lead that is normal to the electric axis.
Deviation of the electric axis to the right is an indication of increased electric
activity in the right ventricle due to increased right ventricular mass.
This is usually a consequence of chronic obstructive lung disease, pulmonary
emboli, certain types of congenital heart disease, or other disorders causing
severe pulmonary hypertension and pulmonale.
Deviation of the electric axis to the left is an indication of increased electric
activity in the left ventricle due to increased left ventricular mass.
This is usually a consequence of hypertension, aortic stenosis, ischemic heart
disease, or some intraventricular conduction defect.

42. CARDIAC
RHYTHM
DIAGNOSIS

43. Differentiating
the P-, QRS-
and T-waves
Because of the anatomical difference of the atria and the
ventricles, their sequential activation, depolarization, and
repolarization produce clearly differentiable deflections. This
may be possible even when they do not follow one another in
the correct sequence: P-QRS-T.
Identification of the normal QRS-complex from the P- and T-
waves does not create difficulties because it has a characteristic
waveform and dominating amplitude. This amplitude is about 1
mV in a normal heart and can be much greater in ventricular
hypertrophy. The normal duration of the QRS is 0.08-0.09 s.
If the heart does not exhibit atrial hypertrophy, the P-wave has
an amplitude of about 0.1 mV and duration of 0.1 s. For the T-
wave both of these numbers are about double. The T-wave can
be differentiated from the P-wave by observing that the T-wave
follows the QRS-complex after about 0.2 s.

44. Supraventricular
arrhythmias
Cardiac rhythms may be divided into two categories:
supraventricular (above the ventricles) and ventricular rhythms.
The origin of supraventricular rhythms (a single pulse or a
continuous rhythm) is in the atria or AV junction, and the
activation proceeds to the ventricles along the conduction
system in a normal way.

45. TYPES OF
SUPRAVENTRI
CULAR
1. Normal sinus rhythm
2. Sinus bradycardia
3. Sinus tachycardia
4 . Sinus arrhythmia
5. Non sinus atrial rhythm
6. Atrial flutter
7 Atrial fibrillation
8. Wandering pacemaker
9. Paroxysmal atrial tachycardia (PAT)
10. Junctional rhythm

46. Normal sinus rhythm- Normal sinus rhythm is the rhythm of a
healthy normal heart, where the sinus node triggers the cardiac
activation. This is easily diagnosed by noting that the three
deflections, P-QRS-T, follow in this order and are differentiable.
Sinus bradycardia- A sinus rhythm of less than 60/min is called
sinus bradycardia. This may be a consequence of increased vagal
or parasympathetic tone.
Sinus tachycardia- A sinus rhythm of higher than 100/min is
called sinus tachycardia. It occurs most often as a physiological
response to physical exercise or psychical stress, but may also
result from congestive heart failure.
Sinus arrhythmia- If the sinus rhythm is irregular such that the
longest PP- or RR-interval exceeds the shortest interval by 0.16
s, the situation is called sinus arrhythmia. This situation is very
common in all age groups. This arrhythmia is so common in
young people that it is not considered a heart disease. One
origin for the sinus arrhythmia may be the vagus nerve which
mediates respiration as well as heart rhythm.

47. Non sinus atrial rhythm- The origin of atrial contraction may
be located somewhere else in the atria other than the sinus
node. If it is located close to the AV node, the atrial
depolarization occurs in a direction that is opposite the normal
one. An obvious consequence is that in the ECG the P-wave .
Wandering pacemaker- The origin of the atrial contraction
may also vary or wander. Consequently, the P-waves will vary in
polarity, and the PQ-interval will also vary.
Paroxysmal atrial tachycardia (PAT)- Paroxysmal atrial
tachycardia (PAT) describes the condition when the P-waves are
a result of a re-entrant activation front (circus movement) in
the atria, usually involving the AV node. This leads to a high rate
of activation, usually between 160 and 220/min. In the ECG the
P-wave is regularly followed by the QRS-complex. The
isoelectric baseline may be seen between the T-wave and the
next P-wave.

48. Atrial flutter- when the heart rate is sufficiently elevated so that the
isoelectric interval between the end of T and beginning of P disappears, the
arrhythmia is called atrial flutter. The origin is also believed to involve a re-
entrant atrial pathway. The frequency of these fluctuations is between 220
and 300/min. The av-node and, thereafter, the ventricles are generally
activated by every second or every third atrial impulse
Atrial fibrillation- the activation in the atria may also be fully irregular and
chaotic, producing irregular fluctuations in the baseline. A consequence is
that the ventricular rate is rapid and irregular, though the QRS contour is
usually normal.
Junctional rhythm- if the heart rate is slow (40-55/min), the qrs-complex is
normal, the p-waves are possibly not seen, then the origin of the cardiac
rhythm is in the av node. Because the origin is in the junction between atria
and ventricles, this is called junctional rhythm.

49. Ventricular arrhythmias
In ventricular arrhythmias ventricular activation does not
originate from the AV node and/or does not proceed in the
ventricles in a normal way. If the activation proceeds to the
ventricles along the conduction system, the inner walls of the
ventricles are activated almost simultaneously and the
activation front proceeds mainly radially toward the outer
walls. As a result, the QRS-complex is of relatively short
duration.

50. TYPES OF VENTRICULAR ARRYTHMIAS
Premature ventricular contraction
Idioventricular rhythm
Ventricular tachycardia
Ventricular fibrillation
Pacer rhythm

51. Premature ventricular contraction- A premature ventricular contraction is
one that occurs abnormally early. If its origin is in the atrium or in the AV
node, it has a supraventricular origin. The complex produced by this
supraventricular arrhythmia lasts less than 0.1 s. If the origin is in the
ventricular muscle, the QRS-complex has a very abnormal form and lasts
longer than 0.1 s. Usually the P-wave is not associated with it.
Idioventricular rhythm- If the ventricles are continuously activated by a
ventricular focus whose rhythm is under 40/min, the rhythm is called
idioventricular rhythm. The ventricular activity may also be formed from
short (less than 20 s) bursts of ventricular activity at higher rates (between
40 and 120/min).
Ventricular tachycardia- A rhythm of ventricular origin may also be a
consequence of a slower conduction in ischemic ventricular muscle that
leads to circular activation (re-entry). The result is activation of the
ventricular muscle at a high rate (over 120/min), causing rapid, bizarre, and
wide QRS-complexes; the arrythmia is called ventricular tachycardia. As
noted, ventricular tachycardia is often a consequence of ischemia and
myocardial infarction.

52. Ventricular fibrillation- When ventricular depolarization occurs
chaotically, the situation is called ventricular fibrillation. This is
reflected in the ECG, which demonstrates coarse irregular
undulations without QRS-complexes. The cause of fibrillation is
the establishment of multiple re-entry loops usually involving
diseased heart muscle. In this arrhythmia the contraction of the
ventricular muscle is also irregular and is ineffective at pumping
blood.
Pacer rhythm- A ventricular rhythm originating from a cardiac
pacemaker is associated with wide QRS-complexes because the
pacing electrode is (usually) located in the right ventricle and
activation does not involve the conduction system. In pacer
rhythm the ventricular contraction is usually preceded by a
clearly visible pacer impulse spike. The pacer rhythm is usually
set to 72/min..

53. DISORDERS
IN THE
ACTIVATION
SEQUENCE
Atrioventricular conduction variations-
P-waves always precede the QRS-complex with
a PR-interval of 0.12-0.2 s, the AV conduction is
normal and a sinus rhythm is diagnosed.
If the PR-interval is fixed but shorter than
normal, either the origin of the impulse is
closer to the ventricles or the atrioventricular
conduction is utilizing an (abnormal) bypass
tract leading to pre-excitation of the ventricles

54. Types
First-degree
atrioventricular
block
Second-degree
atrioventricular
block
Third-degree
atrioventricular
block

55. Bundle-
branch block
Bundle-branch block denotes a conduction defect in either of
the bundle-branches or in either fascicle of the left bundle-
branch.
If the two bundle-branches exhibit a block simultaneously, the
progress of activation from the atria to the ventricles is
completely inhibited; this is regarded as third-degree
atrioventricular block (see the previous section).
The consequence of left or right bundle-branch block is that
activation of the ventricle must await initiation by the opposite
ventricle.
2 types Of BUNDLE BRANCH BLOCK-:
-Right bundle-branch block
-Left bundle-branch block

56. Wolff-Parkinson-White
syndrome
One cause for a broad QRS-complex that exceeds over 0.12 s,
may be the Wolff-Parkinson-White syndrome (WPW syndrome).
In the WPW syndrome the QRS-complex initially exhibits an
early upstroke called the delta wave. The interval from the P-
wave to the R spike is normal, but the early ventricular
excitation forming the delta wave shortens the PQ-time.
This activates part of the ventricular muscle before normal
activation reaches it via the conduction system (after a delay in
the AV junction). The process is called pre-excitation, and the
resulting ECG depends on the specific location of the accessory
pathway.

57. INCREASE IN
WALL
THICKNESS OR
SIZE OF ATRIA
AND
VENTRICLES
Atrial and ventricular muscles react to physical stress in the
same way as skeletal muscles: The muscles enlarge with
increased amount of exercise.
Pressure overload is a consequence of increased resistance
in the outflow tract of the particular compartment
concerned (e.g., aortic stenosis). Volume overload means
that either the outflow valve or the inflow valve of the
compartment is incompetent, thus necessitating a larger
stroke volume as compensation for the regurgitant backflow.

58. TYPES
Arterial hypertrophy types-:
1 .Right atrial hypertrophy
2 .Left atrial hypertrophy
Ventricular hypertrophy types-:
1 . Right ventricular hypertrophy
2 . Left ventricular hypertrophy

59. Arterial
hypertrophy
Right atrial hypertrophy
Right atrial hypertrophy is a consequence of right atrial overload.
This may be a result of tricuspid valve disease (stenosis or insufficiency), pulmonary valve
disease, or pulmonary hypertension (increased pulmonary blood pressure In right atrial
hypertrophy the electrical force due to the enlarged right atrium is larger.
This electrical force is oriented mainly in the direction of lead II but also in leads aVF and
III. In all of these leads an unusually large (i.e., 0.25 mV) P-wave is seen.
Left atrial hypertrophy
Left atrial hypertrophy is a consequence of left atrial overload. This may be a result of
mitral valve disease (stenosis or insufficiency), aortic valve disease, or hypertension in the
systemic circulation.
In left atrial hypertrophy the electrical impulse due to the enlarged left atrium is
strengthened. This electrical impulse is directed mainly along lead I or opposite to the
direction of lead V1lead I these phases have the same polarities and in lead V1 the
opposite polarities.
This typical P-wave form is called the mitral P-wave. The specific diagnostic criterion for
left atrial hypertrophy is the terminal portion of the P-wave in V1, having a duration 0.04
s and negative amplitude 0.1 mV..

60. Ventricular
hypertrophy
Right ventricular hypertrophy
Right ventricular hypertrophy is a consequence of right ventricular overload. This is
caused by pulmonary valve stenosis, tricuspid insufficiency, or pulmonary
hypertension (see above). Also many congenital cardiac abnormalities, such as a
ventricular septal defect, may cause right ventricular overload.
Right ventricular hypertrophy increases the ventricular electrical forces directed to
the right ventricle - that is, to the right and front. This is seen in lead V1 as a tall R-
wave of 0.7 mV.
Left ventricular hypertrophy
Left ventricular hypertrophy is a consequence of left ventricular overload. It arises
from mitral valve disease, aortic valve disease, or systemic hypertension. Left
ventricular hypertrophy may also be a consequence of obstructive hypertrophic
cardiomyopathy, which is a sickness of the cardiac muscle cells.
Left ventricular hypertrophy increases the ventricular electric forces directed to the
left ventricle - that is, to the left and posteriorly. Evidence of this is seen in lead I as
a tall R-wave and in lead III as a tall S-wave (2.5 mV). Also a tall S-wave is seen in
precordial leads V1 and V2 and a tall R-wave in leads V5 and V6, (3.5 mV).

61. Heart problems
diagnosed by
ECG
Some of the various heart problems that can be diagnosed
by ECG include:
1. enlargement of the heart
2. congenital heart defects
3. abnormal rhythm (arrhythmia)
4. poor blood supply to the heart
5. abnormal position of the heart
6. heart inflammation – pericarditis or myocarditis
7. disturbances of the heart’s conducting system
8. imbalances in the blood chemicals (electrolytes) that
control heart activity
9. previous heart attacks.

62. MYOCARDIAL
ISCHEMIA
AND
INFARCTION
If a coronary artery is occluded, the transport of oxygen to the
cardiac muscle is decreased, causing an oxygen debt in the
muscle, which is called ischemia. Ischemia causes changes in the
resting potential and in the repolarization of the muscle cells,
which is seen as changes in the T-wave. If the oxygen transport is
terminated in a certain area, the heart muscle dies in that
region. This is called an infarction.
An infarct area is electrically silent since it has lost its excitability.
With this principle it is possible to locate the infarction. (Of
course, the infarct region also affects the activation sequence
and the volume conductor so the outcome is more complicated.

63. CONCLUSIONS
This interpretation, or final conclusion, is the starting point
for treatment of the patient.
Examples of conclusions are:
"Sinus tachycardia with ST elevation, likely caused by acute
myocardial infarction"
"Supraventricular tachycardia of 200 beats per minute caused
by an AV nodal re-entry"
"Previous infarction combined with an acute lateral
myocardial infarction with widening of the QRS complexes"
"Normal ECG"

64. THANK YOU