Cardiac Function Tests

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CARDIAC FUNCTION & DISORDERS

DORICE BERKOH
DORICE BERKOH
DEPT. OF MEDIAL LABORATORY SCIENCE
DEPT. OF MEDICAL LABORATORY
UENR-SUNYANI
SCIENCE
UENR-SUNYANI.
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A BRIEF LOOK AT THE CARDIOVASCULAR SYSTEM

 Cardiovascular system entails:

 The heart; muscular pump

 Blood; fluid connective tissue

 Blood vessels; arteries, capillaries and veins

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 Arteries carry blood away from the heart to the capillaries

 Blood flows back to the heart through the veins

 When blood travels away from the heart, there is a decrease in blood pressure

 Arterial branches of the aorta supply oxygenated blood to all parts of the body

 Deoxygenated blood is transported from organs via veins. Veins unite to form the

vena cava which returns blood to the heart

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STRUCTURE & FUNCTION OF THE HEART

 Heart divided into 4 chambers; two atria and 2 ventricles

 Right atrium receives deoxygenated blood from all parts of the body via the

vena cavae

 Deoxygenated blood enters the right ventricle before leaving the heart through

the pulmonary artery

 Pulmonary artery divides into 2 branches, each leading to a lung

 Oxygenated blood returns to the heart through the pulmonary veins


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 Main function of the heart is to maintain continuous flow and circulation of blood

 Left ventricle pumps blood all around the body due to its more muscular and

thicker walls

 Right ventricle pumps blood only to the lungs

 There are valves between the atria and ventricles which prevent the backflow of

blood and ensure that blood flows in one direction through the heart

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CARDIAC FUNCTION

 At each contraction, the right ventricle pumps some volume of blood through the

pulmonary artery as the left ventricle pumps through the aorta

 Heart rate (pulse) is the number of heart beats per minute

 Stroke volume is the volume of blood expelled by each ventricle on contraction

while cardiac output is the volume of blood pumped out of a ventricle per minute

CO = HR x SV

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PULSE, HEALTH INDICATOR

 If an individual is fit, the quantity of muscle present in the heart wall is greater

and more efficient than that of an individual who is unfit

 Fit persons have a lower pulse than an unfit person (fit person’s heart is larger

and stronger)

 Fit individuals have a greater stoke volume and their heart do no not need to

contract too often to pump an equal volume of blood round the body

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CARDIAC FUNCTION TESTS

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A LIL HUMOUR

 “ If you want to know whether a patient with suspected or real CHD is ok for

non-cardiac surgery, take the patient, the surgeon and the anesthesiologist in
the night before the surgery and have them all walk up a flight of stairs. If
everybody made it, you’re good to go.”
-Functional capacity trumps everything else.

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BIOCHEMICAL MARKERS OF CARDIAC FUNCTION

 Aspartate aminotransferase (AST)

 Lactate dehydrogenase and its isoenzyme LDH1

 Creatine kinase (CK-MB)

 Myoglobin

 Cardiac troponin

 C-reactive Protein (inflammation marker)

 Cardiac natriuretic peptide


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BIOMARKERS AND TISSUE DAMAGE
 Changes in concentration can be a signal to tissue injury

 Tissue may find itself under abnormal stress due to injury from disease and

may respond by increasing the amount of biomarker produced as a corrective


response

 Increased amounts may leak into the bloodstream which can then be measured

 Biomarkers may also act as biological messengers –send messages to other

parts of the body when tissue is stressed


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CARDIAC DISEASE
 Occurs as a result of blockage of blood vessels supplying oxygen to the heart

muscle

 In tisues where the need for oxygen exceeds the rate at which it can be supplied,

ischaemia occurs

 Prolonged ischaemia results in irreversible cell damage and cell death known as

infarction, followed by cellular breakdown and necrosis

 In the heart muscle, ishaemia occurs when an artery supplying blood to an area of

cardiac muscle becomes partially/totally blocked


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 Myocardial infarction (MI) and Acute Myocardial Infarction (AMI) are associated

with cardiac pain and death of cardiac tissue

 In some patients, esp diabetics, myocardial infarction can be “silent”. Ie occurs

without pain

 Angina simply means heart pain without damage to heart muscles. Angina occurs in

two forms:

 Stable angina: cardiac pain occurs predictably and gradually. Can be controlled by

medication or rest

 Unstable angina: pain is unpredictable and not relieved partially by drugs or rest
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ELECTROCARDIOGRAM (ECG)
 An electric signal is sent to the muscle fibres of the heart in a well-defined sequence

 This coordinates the contraction of the individual heart muscle fibres

 Muscles of the atria contract, then as they relax, the muscular walls of the ventricles

begin their contraction

 The ECG is a record of the sequence of these electrical events

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 Ischaemic heart muscles cannot conduct the electrical impulses properly-

causes the area of ischaemic attack to short circuit

 Cardiac muscles fibres contract separately and independently

 If not treated immediately, patient can die

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CARDIAC TROPONINS
 Troponin is a complex of 3 proteins (Troponin I, Troponin T and Troponin C)

 They regulate contraction of heart muscle. Ca2+ binds to troponin to initiate

contraction. There are skeletal and cardiac isoforms

 Damage to cardiac muscles cause an increase in cardiac troponin in the blood

 Cardiac troponin is the most sensitive marker of cardiac function cardiac

troponin assays are able to detect patients with AMI who otherwise could not
be detected with CK and CK-MB

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CARDIAC TROPONIN T AND CARDIAC TROPONIN I

 Up to 80% of patients with acute MI will have elevated Troponin levels within

2-3 hrs of reporting to the hospital compared to 6-9 hrs or more with CK-MB
and other cardiac markers. Troponin can stay elevated for weeks

 Assays for cTnT and cTnI have become the gold standards for detecting

myocardial necrosis because they are highly specific to cardiac damage but cTI
is used more often.

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CREATINE KINASE
 Activities increase in circulation due to leakage from muscle tissues. This

means its activity is affected by muscle mass and composition

 Men have higher CK activities than women. CK activities also influenced by

ethnicity or race. Eg: CK levels higher in Afro-Carribeans than Caucasians

 Activities begin to rise 4-6 hrs following an AMI and peaks at 12-24 hrs

 Assaying for the individual isoenzymes of CK can help distinguish damage to

heart muscles from skeletal muscle damage


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 Measuring CK-MB activity is a more sensitive marker of AMI, especially if

there has been damage to skeletal muscle

 CK-MB begins to rise earlier than overall CK levels and peaks 21 hrs after an

MI

 High CK-MB/total CK ratio more likely to be related to cardiac injury than

skeletal

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MYOGLOBIN
 Found in the cytoplasm and released within 2-3 hours of an AMI and peaks

after 12 hours

 It is released when muscle is damaged and it is also nonspecific.

 Because it is also found in skeletal muscle, it also stands at a disadvantage like

CK in assessing MI

 An absence of it is useful to rule out an MI and rises earlier than Troponin and

CK-MB

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ASPARTATE AMINOTRANSFERASE (AST)

 AST activities begin to rise abt 12 hrs after an MI and reaches a peak at 36 hrs

 Comes back to normal values after 60 hrs (roughly 2½ days)

 AST was the first enzyme used as a biomarker. However, since the year 2000,

it is no longer recommended as a good marker for AMI

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LACTATE DEHYDROGENASE
 Activities begin to rise at 36 hrs after an infarction and is detectable for up to

72 hours

 Can be used to detect an AMI in patients whose symptoms occurred more

than 24 hrs previously

 The LDH1 isoenzyme is more specific to the heart. Its levels begin to rise

within 12-24 hours after infarction


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NOTE

 MI is defined by the detection in the rise and/or fall of biomarkers (preferably Troponin)

with one value above the upper reference limit

 In addition patient must show symptoms of ischaemia, new or presumed new significant

ST segment-T wave changes (new ST-T changes), development of Q waves in an ECG

 Evidence of new loss of viable myocardium or new regional wall motion abnormality,

or identification of an intracoronary thrombus by autopsy or angiography

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 When a patient reports with suspected acute coronary syndrome (ACS),

1. Perform ECG and measure cTnT or cTnI


2. If ECG shows ST elevation, the diagnosis is presumed to be ST-Elevation
Myocardial Infarction (STEMI) and patient will receive a thrombolytic drug
or taken to the cardiac catheterization lab
3. Confirm diagnosis , measure cTnT or cTnI 10-12 hrs after patient arrives at
hospital
4. For diagnosis of AMI, in addition to ECG, cTnT or cTnI should be measured
6-8hrs after patient is brought to the hospital
5. Normal troponin levels after 12-24 hrs excludes an AMI

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NATRIURETIC PEPTIDES

 Series of ring-shaped molecules that promote increased loss of sodium and

water by the kidneys. Can be used to diagnose both acute and chronic heart
failure

 4 main types: atrial, B type(BNP), C and D type natriuretic peptides

 B type natriuretic peptide produced by both atria and ventricles of the heart and

produced constantly by cardiac muscle cells

 Increases when the heart is stretched owing to volume overload. Most common

cause is heart failure (heart fails to pump blood to meet body’s needs)
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CARDIAC BIOMARKERS IN HEART FAILURE

 Congestive heart failure (CHF) most common cause


of heart failure
 Monitor using
 B-type natriuretic peptide (BNP) or NT-proBNP
 Troponins (steady elevation)

 BNP assays can be done on most immunoassay


analyzers. Important to separate specimen from
cells within 4 hours after draw and the plasma
(EDTA) refrigerated

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MARKERS OF CHD RISK
 C-reactive Protein

 Inflammation plays an important role in the development and

progression of atherosclerosis and CHD. CRP is used clinically to


evaluate CVD risk. It is a non-specific marker of acute
inflammation

 Predicts mortality and cardiac complications in persons with acute

coronary disease

 High levels are suggestive of a worse prognosis in patients with

acute coronary syndromes


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 Homocysteine

 Sulphur-containing amino acid derived from dietary protein. It is formed in plasma

from the removal of a methyl group from Methionine

 High levels of plasma homocysteine implicated in the onset of CVD (> 100 μmol/L

or >13.5 mg/L)

 Mild elevations also reported to be associated with risk of CVD

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MARKERS OF PULMONARY EMBOLISM
 D-dimer testing

 D-dimer is a product of plasmin-mediated fibrin degradation

 Presence in bloodstream is indicative of current or recent

coagulation or fibrinolysis

 Abnormal levels are detected in 90% of patients with PE

 Possible use of troponins and BNP tests. Elevated troponin

measurement in patients with PE may not be useful in


determining their short-term mortality outcome.

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CASE STUDY
 A 56-year-old man was admitted to the hospital with a 6-hr history of central
crushing chest pain that went into his left arm and neck. An ECG showed
elevation of the ST segments in the chest leads. His Troponin value on
admission was < 10ng/L and one measured 6 hours later was 1500 ng/L
(reference range < 50 ng/L)

a) Do you think this man was having an MI?


b) Should you wait for the second troponin results taken 6 hrs after admission to
hospital before starting treatment?
c) What is the role of the 2nd Troponin measurement in this patient?
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END OF LECTURE

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