LABORATORY STUDIES OF CARDIAC DISORDERS

KRISHNA INSTITUTE OF
NURSING SCIENCES KARAD
SUBJECT:- MEDICAL SURGICAL NURSING
TOPIC:- LABORATORY STUDIES OF CARDIAC
DISORDERS
PRESENTED BY:-
MS.POOJA MHALATKAR
2ND YEAR MSC(N)

INTRODUCTION
Diagnostic investigations in cardiology are methods of
identifying heart conditions associated with
unhealthy, pathologic, heart function.
TYPES:-
 INVASIVE
 NON INVASIVE
A variety of noninvasive and invasive laboratory and
diagnostic tests are used to evaluate and monitor
the cardiovascular system.

BLOOD SPECIMEN COLLECTION
Collection of blood specimens is a process that involves
three phases:- patient preparation, collection of the blood
sample, and interpretations of results.
1) CK-MB:-
immunochemical process using monoclonal antibodies that
measures this cardiospecific enzyme. concentrations > 5%
of total creatine kinase (CK) are highly indicative of MI.
serum levels increase within 4-6 hour after MI.
NORMAL VALUE:- 0-4 U/L.

2) CARDIAC SEPCIFIC TROPONINS:-
Contractile proteins that are released following MI.
Both troponin T and troponin I are highly specific to
cardiac tissue.
NORMAL:- Troponin T (cTnT):<0.1ng/mL
NORMAL:- Troponin I (cTnI):< 0.4ng/mL

3) MYOGLOBIN:-
 Low molecular weight protein that is 99-100%
sensitive for myocardial injury.
 Serum concentrations rise 30-60 minutes after MI.
 cleared from the circulation rapidly and most
diagnostic if measured within 1 day of onset of chest
pain.
NORMAL:- Normal <92 ng/ML (men)
< 76ng/mL (women)

4) C-REACTIVE PROTEIN:-
Marker of inflammation that can predict risk of cardiac
diseases and cardiac events, even in patients with
normal lipid values.
NORMAL:- <1 mg/L
Moderate risk:-1-3mg/L
High risk:- > 3 mg/L

5) HOMOCYSTEINE:-
 Amino acid produced during protein catabolism that
has been identified as a risk factor for cardiovascular
dis eases.
 It is postulated that homocysteine causes damage to
the endothelium or has a role in formation of thrombi.

Hyperhomocysteinemia resulting from dietary
deficiencies is treated with folic acid B6 and B12
supplements.
NORMAL VALUES:- Optimal <12 mol/L
Moderate risk 12-15 mol/L
High risk:->15 mol/L

6) BETA TYPE NATRIURETIC PEPTIDE:-
peptide that causes natriuresis. Elevation indicates
presence of heart failure and distinguishes cardiac
versus respiratory causes of dyspnea.
Normal:-< 100pg/mL
7) CHOLESTEROL:-
cholesterol is a blood lipid. Elevated cholesterol is
considered a risk factor for atherosclerotic heart
diseases. Level can be measured at anytime of the day
in a nonfasting state.

Triglyceride levels and lipoproteins, should done in
fasting state for at least 12 hours (except for water)
is necessary, and no alcohol intake is allowed for 24 hrs
before testing.
Normal:- 140-200mg/DL
(3.62-5.17 mmol/L)
8) TRIGLYCERIDES:-
Triglycerides are mixtures of fatty acids. Elevation are
associated with cardiovascular diseases.
NORMAL:- 40-190 mg/dL)
(0.45-2.15mmol/L)

9) LIPOPROTEINS:-
Electrophoresis is done to separate lipoproteins into
HDL, LDL and VLDL and chylomicrons.
There are marked day to day fluctuations in serum
lipid levels.
More than one determination is needed for accurate
diagnosis and treatment.
Risk for cardiac diseases is assessed by dividing the
total cholesterol level by the HDL level.
Target values are < 5 for men and <4.4 for women.

PATIENT PREPARATION
 Adequate preparation of the patient and their
family involves education.
 Frequently, proper specimen collection and
interpretation requires compliance with instructions
about food or fluids restrictions, taking or
withholding medications, and meeting criteria for
proper timing of the blood sample.
 When the blood sample is taken, patients should
receive an explaination about what tests are being
drawn, why they have been ordered, and when
results will be available.

CONT…..
 If the sample is being obtained by venipuncture,
arterial puncture, or vascular port access,
preparation of the patient includes a reminder
about pain during the procedure and the importance
of complying with instructions to maintain a certain
position.

BLOOD SAMPLE
COLLECTION
1) When blood is withdrawn from the
body, its eventually clots.
• The fluids that separates from the clot
is called SERUM.
• Plasma, from unclotted blood, contains
fibrinogen, which is eventually converted
to fibrin.
• Most blood tests are done on serum, and
therefore require use of a tube that
allows blood to clot.

2) RED-TOP TUBES contains no additives, they are
used for chemistries, drug monitoring, serology and
blood typing.
3) GREEN TOP TUBES contains heparin as the
anticoagulant and can be used for chemistries, arterial
blood gases and hormone levels.
4) GRAY-TOP TUBES contains sodium floride,
prevents glycolysis and may be used to test blood
glucose in its vivo.

5) BLUE TOP TUBES used for coagulation studies contains
citrate.
6) LAVENDER TOP TUBES which contain
ethylenediaminetetra acetic acid (EDTA) are usually used for
hematology.

When multiple blood samples are drawn at the same
collection time,the preferred order is as follows:
tubes with no preservative (red-top); tubes with mild
anticoagulations (green, gray, blue) lavender top tubes
should be collected last.
 Blood for coagulations studies should never be drawn
first because tissue injury can initiated the clotting
process and result in falsely low levels of coagulations
factors.

Specimens in tubes with additives should be rotated
gently to mix the anticoagulant with the blood. They
should never be shaken.

HEMOLYSIS
 Hemolysis refers to the lysis of red blood cells.
Hemolysis may also occur as a result of improper
sample collection technique or specimen transport.
 specimens may be hemolyzed if they are collected
from poorly flowing venipuncture.
 Greater hemolysis occurs with the use of a large
bore needle than with a small bore needle.
 Failure to dry alcohol from the venipuncture site
also results in hemolysis.

 Blood should usually never be forcibly withdrawn
from the venipuncture, nor should it be forcibly
entered into the collection tube by pushing on the
syringe barrel to fill faster.
 Hemolysis increases the laboratory values of lactate
dehydrogenase (LDH), asparate aminotransferase
(AST or SGOT), and phosphorus, as well as potassium,
magnesium and calcium.

INTERPRETATION OF RESULTS
The specimen collected must be sent to the lab as
soon as possible for accurate results. Specimens that
are left to stand unprocessed often yield inaccurate
results.

CARDIAC MARKERS
1) When myocardiac cells are injured. They release
their contents, including enzymes and other proteins,
into the circulation.
2) These biochemical markers are useful in the
diagnosis of myocardial injury and necrosis.
3) The enzyme characteristic of cardiac injury are
creatine kinase (CK), lactate dehydrogenase (LDH), and
serum aspartate aminotransferase (AST), formerly
called serum glutamic-oxaloacetic transaminase
(SGOT).

4) Because these enzymes are found in a variety of
body tissues, they can be elevated as a result of injury
to the muscles, liver, brain and other organs. LDL and
AST levels are no longer used as markers of myocardial
injury.
5) CK is present in heart muscles, skeletal muscle, and
brain tissue. CK-MM is found primarily in the skeletal
muscle, and CK-BB is found in the brain and nervous
tissue.

6) CK-MB elevation is specific for myocardial tissue
injury. CK-MB levels rise 4 to 6 hours after symptoms
onset, peak in 18 to 24 hours, and return to baseline
within 3 days after myocardial infarction (MI).

CARDIAC SPECIFIC TROPONIN
 It is a myocardial muscle protein released into
circulation after injury.
 There are two subtypes, cardiac specific troponin T
(cTnT) and cardiac specific troponin I (cTnI), that
are specific for myocardial tissue.

 Normally there is no circulating troponin, so a rise
in its level is diagnostic of myocardial injury.
 cTnT and cTnI are detectable within 1 hour of
myocardial injury, have high specificity at 3 to 6
hours following the onset of symptoms, and reach
peak levels within 12 hours.

MYOGLOBIN
• It is a low molecular weight heme protein found in
cardiac and skeletal muscle.
• Myoglobin elevation is a sensitive indicator of early
myocardial injury, and serum elevations occur within 1
hour after injury.
• its clinical value is limited due to nonspecificity of
myoglobin for MI and its brief presence following
infarction.

SERUM LIPIDS
Serum lipids consists of triglycerides, cholesterol
and phospholipids, they circulate in the blood bound
to protein.
Thus they are often referred to as lipoproteins.
 triglycerides are the main storage form of lipids
and constitute approximately 95% of fatty tissue.
 cholesterol, a structural component of cell
membranes and plasma lipoproteins, is a precursor of
corticosteroids, sex hormones, and bile salts.

In addition to being absorbed from food in the
gastrointestinal tract, cholesterol can also be
synthesized in the liver.
phospholips contain glycerol, fatty acids, phosphates,
and a nitrogenous compound.
Although formed in most cells, phospholipids usually
enter the circulation as lipoproteins synthesized by
the liver.
Apoproteins are water soluble proteins that combine
with most lipids to form lipoproteins.

Different classes of lipoproteins contain varying
amounts of the naturally occurring lipids. These include
the following:-
 CHYLOMICRONS:-
Primarily exogenous triglycerides from dietary fat.
 LOW DENSITY LIPOPROTEINS (LDLs):-
Mostly cholesterol with moderate amounts of
phospholipids.

 HIGH- DENSITY LIPOPROTEIN (HDLs):-
About one half protein and one half phospholipids and
cholesterol.
 VERY LOW DENSITY LIPOPROTEINS (VLDLs):-
Primarily endogenous triglycerides with moderate
amounts of phospholipids and cholesterol.

A lipid profile test usually consists of cholesterol,
triglyceride, LDL and HDL measurements.
An elevation in LDL level has a strong and direct
association with CAD; an increased HDL level has been
associated with a decreased risk of CAD.
 High levels of HDLs serve a protective role by
mobilizing cholesterol from tissues.
 increased triglyceride levels are also linked to the
progression of CAD.

Although the association between elevated serum
cholesterol levels and CAD exists, determination of
total cholesterol level alone is not sufficient for an
assessment of coronary risk.
A risk assessment for CAD is determined by
comparing the total cholesterol to HDL ratio, HDL and
LDL ratio overtime.
 This combination provides more information than
either values alone.

The patient must fast for 12 to 14 hours before the
blood draw to eliminate the effects of a recent meal.
A specimen should not be drawn if the patient is
having acute stress.
RATIOS:-
HDL/LDL=0.33-0.4 ( normal value) if the value
increases, risk of CAD decreases.
Total cholesterol/HDL=3-4 ( normal value) if the value
increases, risk of CAD increases.

LDL/HDL= 3-4 (Normal value) if the value increases,
risk of CAD increases.
APOLIPOPROTEINS
Plasma levels of apolipoproteins A-1 (apo A-1) ( the
major HDL protein) and apolipoproteins B ( apo B) (
the major LDL protein) may be better predictors of
CAD than HDLs or LDLs.

Measurements of these lipoproteins may replace
cholesterol lipoprotein derterminations in assessing
the risk of CAD but Typically are used for patients
with unknown coronary artery diseases, suspected
familial hypercholesterolemia, or other lipid disorders.
 Apolipoprotein B (134mg/dL normal value) is being
assessed for its role as a risk factor for CAD.
Increased levels of apolipoprotein B have been
associated with the progression of atherosclerosis.

In addition, apolipoprotein B has been found to have
thrombogenic properties that increase the risk of clot
formation at the site of intravascular lesions.
 Apolipoprotein A (120mg/DL normal value): If the
value increases risk of CAD is decreases, if the value
decreases the risk of CAD increases.

LIPOPROTEIN- ASSOCIATED PHOSPHOLIPASE A2
Lipoprotein associated phospholipase A2 (LP-PLA2) is
an enzyme made by microphages.
LP-LPA, promotes vascular inflammation through the
hydrolysis of oxidized LDLs within the intima of blood
vessels, thus contributing directly to the development
of atherosclerosis.
Elevated levels of Lp-PLA2 are indicative of the
vascular inflammation that is associated with the
formation of plaque within the arteries.

C-REACTIVE PROTEIN
CRP is a protein produced by the liver during periods of
acute inflammation. It is emerging as an independent
risk factor for CAD and a predictor of cardiac events.
HOMOCYSTEINE
• Hcy is an amino acid that is produced during protein
catabolism.
• Elevated Hcy levels can be either hereditary or
acquired from dietary deficiencies of B6-B12 or
folate.

• Elevated levels of Hcy have been linked to an
increased risk of a first cardiac event.
• they have also been identified as a predictor of CAD,
STROKE, and thromboembolism even in the presence
of normal lipid levels.
• It is recommended that Hcy testing be performed in
those patients with a familial predisposition for early
cardiovascular diseases.

CARDIAC NATRIURETIC PEPTIDE MARKERS
 There are three natriuretic peptides: Atrial
natriuretic peptide (ANP) originates in the atrium,
beta-type natriuretic peptide (BNP) in the ventricles,
and C- type natriuretic peptide in endothelial and renal
epithelial cells.
 BNP has emerged as the marker of choice for
distinguishing a cardiac or respiratory cause of
dyspnea.
 When ventricle DBP increases(e.g heart failure), BNP
is released and serves to increase natriuresis.

HEMATOLOGICAL STUDIES
COMPLETE BLOOD COUNT
The complete blood count (CBC) involves several
laboratory tests, each of which serves to assess the
three major blood cells formed in the bone marrow.
Although the status of each cell type is important,
the entire system may be disrupted.

HEMOGLOBIN:-
Measurement of gas carrying capacity of RBC.
WOMEN:- 12-16g/dl (120-160g/L)
Men:- 13.5g/dL (135-180g/L)
HEMATOCRIT (Hct):-
Measure of packed cell volume of RBCs
Women:- 38-47% (0.38-0.47)
Men:- 40-54% (0.40-0.54)

TOTAL RBC COUNT:-
Count of total number of circulating RBCs
Women:- 4-5*10/ul(4-5*10/L)
Men:- 4.5*10/ul(4.5-6*10/L)
WBC COUNT:-
Measurement of total number of leucocytes
4000-11000/uL(4-11*10/L)

WBC DIFFERENTIAL:-
Determination of whether each kind of WBC is present
in proper proportion.
Neutrophils:-50-70%
Eosinophils:- 2-4%
Basophils:-0-2%
Lymphocytes:-20-40%
Monocytes:-4-8%

PLATELET COUNT:-
Measurement of number of platelets available to
maintain platelet clotting functions
150,000-400,000/uL
(150-400*10/L)
By diseases, as well as by treatment of diseases. When
the entire CBC is suppressed, a condition termed
pancytopenia (marked decrease in the number of RBCs,
WBCs and platelets) exists. In such cases the patient
needs care directed towards the management of
anemia, infection and hemorrhage.

RED BLOOD CELLS
Normal values of some RBC tests are reported separately
for men and women because normal values are based on
body mass and men usually have larger body mass than
women.
The hemoglobin (HB) value is reduced in cases of anemia,
hemorrhage, and states of hemodilution , such as those
that occur when the fluid volume is excessive.
Increases in hemoglobin are found in polycythemia or in
states of hemoconcentration, which can develop from
volume depletion.

The hematocrit (hct) value is determined by spinning
blood in a centrifuge, which causes RBCs and plasma to
separate.
The RBCs being the heavier elements, settle to the
bottom.
The hematocrit value represents the percentage of
RBcs compared with the total blood volume.
Reductions and elevations of hematocrit value are
seen in the same conditions that raise and lower
hemoglobin value.
 The hematocrit value generally is three times the
hemoglobin value.

 However, total RBC count is not always reliable in
determining the adequacy of RBC function.
Coonsequently, other data, such as hemoglobin ,
hemocrit, and RBC indices, must also be evaluated.
the RBC count is altered by the same conditions that
raise and lower the hemoglobin and hematocrit values.

 RBC indices are special indicators that reflect RBC
volume, color, and hemoglobin saturation.
 these parameters may provide insight into the causes
of anemia.
The shape and appearance of cells is called
morphology.
Cell morphology can provide clues to the presence of
specific diseases states.

The shape and appearance of cells is called
morphology. Cell morphology can provide clues to the
presence of specific diseases states.
Examples of RBC morphologies that may be reported
include Dohl bodies, Heinz bodies, anistocytes,
Schistocytes, and sickled cells.

WHITE BLOOD CELLS
The white count provides two
different sets of information.
 The first is a total count of
WBCs in 1 mL of peripheral
blood.
 Elevations in WBC count over
11,000uL are associated with
infection, inflammation, tissue
injury or death, and
malignancies (e.g leukemia,
lymphoma).

 Although the degree of WBC elevation does not
necessarily predict the severity of illness, it can
provide clues to the etiology.
 Certain types of leukemias are more likely to
produce extremely high WBC counts (e.g. greater than
25,000/ul).
 A total WBC count less than 4000/uL (leukopenia) is
associated with bone marrow depression, severe or
chronic illness, and/ or some types of leukemia.

 The second aspect of the WBC count, the
differential count, measures the percentage of each
type of leukocyte.
 The information from the WBC differential provides
valuable clues in determining the cause of illness.
 An important concept related to neutrophil counts is
shift to the left.
 When infections are severe, more granulocytes are
released from the bone marrow as a compensatory
mechanisms.

 To meet the increased demand, many young,
immature polymorphonuclear neutrophils (bands) are
released into circulation.
 The usual laboratory procedure is to report the
WBCs in order of maturity, with the less mature
forms on the side of the written report.
Consequently, the existence of many immature cells is
termed a “shift to the left.”

PLATELET COUNT
The platelet count is the number of platelets per
microliter of blood.
Normal platelet counts are between 150,000 and
400,000/uL counts below 100,000/UL signify a
condition termed thrombocytopenia. Bleeding may
occur with thrombocytopenia.
 Spontaneous hemorrhage is possible once platelet
counts fall below 20,000/uL.

Thrombocytosis is defined as excessive platelets, a
disorder that occurs with inflammation and some
malignant disorder. The most likely complication
related to thrombocytosis is excessive clotting.

ERTHROCYTE SEDIMENTATION RATE
The erythrocyte sedimentation rate (ESR)
measures the speed at which anticoagulant
erythrocytes settle in along, narrow tube.
The speed depends on the size of the clumps into
which the cells aggregate in the presence of blood
fibrinogen.
The ESR is a nonspecific indicator of inflammatory
diseases.

It may be elevated in MI and bacterial endocarditis,
it is usually low in CHF.
 Although many factors affect the ESR and it is
considered a test with neither diseases nor organ
specificity, it is usually test in differentiating the pain
of pericarditis and Dressler’s syndrome from angina
pain.
 The degree of increase of the ESR does not
correlate with severity or prognosis.
 Normal value of ESR for male is 15-20 mm/h and
female is 25-30mm/h by westergren method and
wintrobe method.

COAGULATION STUDIES
PLATELET COUNT
Platelets are elements of the blood that promote
coagulation and are produced by the bone marrow.
 They contribute to blood clotting by clumping or
sticking to rough surfaces and injured sites.
 The average life span of a platelet is 7 to 9.

platelet counts are useful for monitoring the course
of a diseases or treatment.
 Thrombocytopenia (low platelet count) is a common
cause of abnormal bledding.
 There is a serious risk of hemorrhage when the
platelet count is less than 50,000/mm and a
spontaneous bleed may occur when platelets are less
than 20,000/mm.
 Bleeding due to thrombocytopenia is characterized
by petechiae, bleeding from the gums or tongue or
epistaxis.

Specific conditions that cause a decrease in platelets
include hemorrhage, hypersplenism, leukemia,
prosthetic heart valves, DIC, lupus, hemolytic anemia,
and infection.
 Medications that decrease the platelet count include
Acetaminophen, aspirin, chemotherapy, histamine
blocking agents, hydralazine, indomethacin, quindine,
and thiazide diuretics.

PROTHROMBIN TIME
 The PT is used to evaluate the extrinsic system and
common pathway in the clotting mechanism.
 specifically, it measures the activity of prothrombin,
fibrinogen. Prothrombin is synthesized by the liver.
 PT may be prolonged in heart failure, vitamin K
deficiency, liver diseases, bile duct obstruction,
coumarin ingestion, DIC, massive blood transfusion,
salicylate intoxication, and alcohol use.

 severe liver damage may prolong PT.
 Drugs that may prolong PT include some antibiotics,
allopurinol, cimetidine, warfarin, heparin, quinidine, and
aspirin.
 Decreased PT is seen in thrombophlebitis, MI, and
pulmonary embolus.
Medication that may decrease PT include digitalis
preparations diuretics, diphenhydramine and
metaproterenol.

ARTERIAL BLOOD GAS ANALYSIS
An arterial blood gas (ABG) is a blood test that is
performed using blood from an artery.
it involves puncturing an artery with a needle and
syringe and drawing a small volume of blood.
The most common puncture site is the radial
artery at the wrist, but sometimes the femoral
artery in the groin or other sites are used.

The blood can also be drawn from an arterial
catheter.
 ( ABG) analysis is used to measure the partial
pressures of oxygen (Pao2) and carbondioxide (Paco2)
and the pH of an arterial sample.
 Oxygen content, oxygen saturation(sao2) and
bicarbonate (HCo3) values are also measured.
 A blood sample for ABC analysis may be drawn by
percutaneous arterial puncture or from an arterial
line.

PURPOSES
To evaluate gas exchange in the lungs.
 To assess integrity of the ventilator control
system.
 To determine the acid base level of the blood.
 To monitor respiratory therapy.

CONTRAINDICATIONS
Allen test (collateral circulation test) here nurse
compresses the radial and ulnar arteries
simultaneously and asks the patient to make a fist,
causing the hand to blanch.
 After the patient open the fist, the nurse releases
the pressure on the ulnar artery while maintaining
pressure on the radial artery.
 The patients hand will turn pink if the ulnar artery is
patent.

Negative allen test is indicative of inadequate blood
supply to the hand and suggest the need to select
another extremity as the site for puncture.
 Arterial puncture should not be performed through a
lesion or through or distal to a surgical shunt( e.g as in
a dialysis patient.
 A coagulation or medium to high dose anticoagulation
therapy ( e.g heparin or Coumadin, streptokinase and
tissue plasminogen activator but not necessarily
aspirin.

COMPLICATIONS
 Bleeding.
 Hematoma.
 Arterial thrombosis.
 Air or clotted blood emboli.
 Trauma to the blood vessel.
 Pain.
 Arterial occlusion.

INTERPRETATION OF ABG VALUES
ACID-BASE BALANCE
The pH is a measurement of the acidity or alkalinity
of the blood.
 It is inversely proportional to the number of
hydrogen ions (H*) in the blood.
 The more H* present, the lower the pH will be.
 Likewise, the fewer H*present, the higher the PH
will be.

The pH of a solution on a scale from 1 ( very acidic) to
14 ( very alkalotic).
 A liquid with a pH of 7, such as water, is neutral (
neither acidic nor alkalotic.)
 The normal blood PH range is 7.35 to 7.45.
 In order for normal metabolism to take place, the
body must maintain this narrow range at all times.
 When the pH is below 7.35, the blood is said to be
acidic.

Change in body system functions that occur in an
acidic state include a decrease in the force of cardiac
contractions, a decrease in the vascular response to
catecholamines, and a diminished response to the
effects and actions of certain medications.
 When pH is above 7.45, the blood is said to be
alkalotic.
 An alkalotic state interferes with tissue oxygenation
and normal neurogical and muscular functioning.

 Significant changes in the blood PH above 7.8 or
below 6.8 will interfere with cellular functioning and
if uncorrected, will lead to death.
 So how is the body able to self regulate acid base
balance in order to maintain pH within the normal
range.
 It is accomplished using delicate buffer mechanisms
between the respiratory and renal systems.
1 7 14
Acidic Neutral Alklotic

RESPIRATORY (LUNGS) BUFFER RESPONSE
• A normal by product of cellular metabolism is
carbondioxide (co2).
• CO2 is carried in the blood to the lungs, where excess
co2 combines with water (H2o) to form carbonic acid
(H2CO3).
• The blood PH will change according to the level of
carbonic acid present.

This triggers the lungs to either increase or decrease
the rate and depth of ventilation until the appropriate
amount of co2 has been re-established.
 Activation of the lungs to compensate for an
imbalance starts to occur within 1 to 3 minutes.

THE RENAL (METABOLIC) BUFFER
RESPONSE
 In an effort to maintain the PH of the blood within
its normal range, the kidneys excrete or retain
bicarbonate (HCO3).
 As the blood PH decreases, the kidneys will
compensate by retaining HCO3 and as the pH rises,
the kidneys excrete HCO3 through the urine.

 Although the kidneys provide an excellent means of
regulating acid base balance , the system may take
from hours to days to correct the imbalance.
 When respiratory and renal systems are working
together, they are able to keep the blood PH balanced
by maintaining 1 part acid to 20 parts base.

ACID BASE DISORDERS
1) RESPIRATORY ACIDOSIS
a) Respiratory acidosis is defined as a PH than 7.35
with a paco2 greater than 45mmHg.
b) Acidosis is caused by an accumulation of co2 which
combines with water in the body to produce a
carbonic acid, thus, lowering the PH of the blood.

RESPIRATORY ALKALOSIS
a) Respiratory alkalosis is defined as a pH greater
than 7.45 with a paco2 less than 35mmHg.
b) Any conditions that causes hyperventilation can
result in respiratory alkalosis.

METABOLIC ACIDOSIS
a) Metabolic acidosis is defined as a bicarbonate level
of less than 22mEq/L with a pH of less than 7.35.
b) Metabolic acidosis is caused by either a deficit of
base in the bloodstream or an excess of acids, or
other than cO2

METABOLIC ALKALOSIS
a) Metabolic alkalosis is defined as a bicarbonate level
greater than 26mEq/ liter with a PH greater than
7.45.
b) Either an excess of base or loss of acid within the
body can cause metabolic alkalosis.
c) Excess base occurs ingestion of antaacids, excess
use of bicarbonate , or use of lactate in dialysis.

d) Metabolic alkalosis is one of the most difficult acid
base imbalances to treat.
e) Bicarbonate excretion through the kidneys can be
stimulated with drugs such as acetazolamide (Diamox),
but resolution of the imbalance will be slow.
f) In severe cases, IV administration of acids may be
used.

HEMODYNAMIC MONITORING
Hemodynamic monitoring refers to the measurement of
pressure, flow and oxygenation within the cardiovascular
system.
Commonly measured values includes direct arterial
pressure, pulmonary artery pressure, central venous
pressure (CVP), pulmonary artery wedge pressure
(PAWP), cardiac output/index, stroke volume /index, and
oxygen saturation of the hemoglobin of arterial blood
(saO2).

PRINCIPLES OF INVASIVE PRESSURE
MONITORING
REFERENCING OF INVASIVE PRESSURE
MONITORING
Referencing and zeroing
To accurately measure the pressure, equipment must be
referenced and zero balanced to the environment and
dynamic response characteristics optimized.

REFERENCING
1) It means positioning the tranducer so that zero
reference point is at the level of the atria of the heart.
2) The stopcock nearest the transducer is usually the zero
reference for the transducer.
3) To place this level with the atria, the nurse uses an
external landmark, the phlebostatic axis.

4) To identify the phlebostatic axis two imaginary lines
are drawn with the patient supine.
5) The first line, a horizontal line, is drawn through the
midchest, half between the outermost anterior and
posterior surfaces.
6) The second line, a vertical line is drawn through the
fourth intercoastal space at the sternum.

7) The phlebostatic axis is the intersection of the two
imaginary line.
8) Once the phlebostatic axis is identified, it should be
marked on the patients chest with a permanent marker.
9) The port of stopcock nearest the transducer must
be positioned level with the phlebostatic axis.

10) It is recommended that the transducer be taped on
the patients chest at the phlebostatic axis or mounted
on a bedside pole.

ZEROING
 It confirms that when pressure within the system is
zero.
 This is accomplished by opening the reference
stopcock to room air ( off to the patient) and
observing the monitor for a reading zero.
 transducers in current use are disposable and have
little zero drift.

 Zeroing the transducer is recommended during initial
set-up, immediately after insertion of the arterial
line, when the transducer has been disconnected From
the pressure cable or the pressure cable has been
disconnected from the monitor, and when the
accuracy of the measurements is questioned, and it
should be done according to the manufacturer’s
guidelines.

NURSING MANAGEMENT
 Asessment of hemodynamic status requires
integration of data from many sources and trending of
the data overtime.
 Through, basic nursing observations provide
important clues about the patients hemodynamic
status.
 The nurse should begin by obtaining baseline data
regarding the patients general appearance, level of
consciousness, skin colour and temperature

Vital signs, peripheral pulses, and urine output.
 Does the patient appear tired, weak, exhausted?
There may be too little cardiac reserve to sustain
even minimum activity.
 Pallor, cool skin, and diminished pulses may indicate
decrease CO.
 Changes in mental clarity may reflect problems with
cerebral perfusion or oxygenation.

 Monitoring urine output reflects the adequacy of
perfusion to the kidneys
 The patient will diminished perfusion to the GI tract
may develop hypoactive or absent bowel sounds.
 If the patients is bleeding and developing shock,
blood pressure might initially be relatively stable, yet
the patient may become increasingly pale and cool
from peripheral vasoconstriction.

 Conversely, the patient experiencing septic shock
may remain warm and pink yet develops tachycardia
and blood pressure instability.
 Although heart rates of 100 beats per minute are
common among stressed, compromised, critically ill
patients, sustained tachycardia greatly increases
myocardial oxygen demand and may result in
diminished CO.

ELECTROCARDIOGRAM
ECG waves:-
1) P wave:- First seen wave, small, upright (positive)
wave indicating atrial depolarization (0.1 sec)
2) QRS COMPLEX:- Represents ventricular
depolarization.
3) Q wave:- First negative wave, R wave: first
positive wave ( note R wave cannot be negative in
any leads),

S wave: First negative after positive R wave and the
duration of QRS complex is (0.08 to 0.1 s).
4) T wave:- Rounded upright (positive) wave following
QRS complex indicating ventricular repolarization
(0.2s).
5) U wave:- small rounded, upright (positive) wave
following T wave repolarization of purkinje muscles

6) Q-T interval:- Measured from beginning of QRS
complex to end of T wave it represents the total
ventricular activity and the duration is 0.4-0.42s.
7) P-R interval :- Distance beginning of P wave and
beginning of QRS complex indicating the duration of
deporization wave travelling from the atria to
ventricles its duration is 0.12-0.2 s.
8) S-T segment:- Measured as a distance between S
wave and beginning of T wave and represents the time

between the ventricular depolarization and beginning of
ventricular repolarization its duration is 0.08s.

VELOCITY OF CONDUCTION OF
IMPULSES
1) Atrial muscle fibres- 0.3m/s
2) Intercode fibres- 1m/s
3) AV node- 0.05 m/s
4) Bundle of HIS- 0.12 m/s
5) Purkinje fibres- 4m/s
6) Ventricular muscle fibres- 0.5m/s

CARDIAC ACTION POTENTIAL
RAPID DEPOLARIZATION
1) Due to rapid opening of Na channels.
2) Duration:- 2 millisecond
3) Amplitude: +20mv

PLATEAU
1) Due to slow and prolonged opening of calcium
channels
2) Duration 200 and 300 millisecond atrial and
ventricular respectively.

SLOW REPOLARIZATION
Due to closure of calcium channels and openings of
potassium channels. Lasts for 50 miliseconds.

BASIC ELECTROCARDIOGRAPHY
1) The ECG is the graphical record of the electrical
activity of the heart.
2) The spread of the electrical impulses through the
heart produces weak electrical currents through the
entire body, which can be detected and amplified by
the ECG machine and recorded on calibrated graph
paper.

3) The grid on the paper consists of a series of small and
large boxes, both horizontally and vertically ; horizontally
boxes measures time, and vertical boxes measures voltage.
4) Each small box horizontally is equal to 0.04 second, and
large box horizontally is equal to 0.20 second.
5) On the vertical axis, each small box measures 1mm and
is equal to 0.1 mV; each large box measures 5mm and is
equal to 0.5 mV

THE 12 LEAD ELECTROCARDIOGRAM
1) The standard 12 lead ECG consists of 4 standard
limb leads that record electrical activity in the
frontal plane traveling up-down and right/ left in
the heart; and 6 precordial leads that records
electricity activity in the horizontal plane-
travelling anterior/ posterior and right/left.
2) limb leads are recorded by electrodes placed on
the arms and legs, whereas precordial (chest) leads

are recorded by electrodes placed on the chest.
1) BIPOLAR LEADS:-
A bipolar leads has a positive pole and a negative
pole, with each contributing equally to the recording.
Lead 1, 2,3 are bipolar limb leads.

2) UNIPOLAR LEADS
A unipolar lead has one positive pole and a reference
pole in the center of the chest that is algebraically
determined by the ECG machine.
The reference pole represents the center of the
electrical field of the heart and has a zero potential,
so only the positive pole of a unipolar lead contributes
to the tracing.
 Unipolar leads are aVR, aVL, aVF these are also
called as augmented limb leads.

These augmented leads are produced when the current
flows from right arm (aVR), left arm (aVL) and left leg
(aVF) respectively to the center of the heart. The
chest leads V1 to V6 are also called as unipolar leads.
3) RIGHT CHEST AND POSTERIOR LEADS
Additional leads can be recorded on the right chest or
posterior thorax to gain additional information about
ventricular or posterior infarction or right ventricular
hypertrophy (RVH).

AXIS DETERMINATION :-
Generally, for the axis determination perpendicular
leads are taken into account
 Lead 1 and aVF are perpendicular leads.
 Lead 2 and aVL are perpendicular leads.
 Lead 3 and aVR are perpendicular leads.

EXERCISE TESTING
1) Exercise testing is a widely used, noninvasive
procedure that provides diagnostic, prognostic, and
functional information for a wide spectrum of
patients with cardiovascular, pulmonary and other
disorders.
2) Exercise test are used to assess a patients ability
to tolerate increased physical activity while
electrocardiographic, hemodynamic, and symptomatic
responses are monitored in a controlled environment.

3) Exercise test can produce abnormalities that are not
present at rest, the most important of which are
manifestation of myocardial ischemia, including ST
segment changes on the electrocardiogram, symptoms,
and electricity instability.

INDICATIONS
1) Physiologic response of post MI and post
revascularization patients to exercise.
2) Functional capacity for the purpose of exercise
prescription.
3) Exercise capacity for the purpose of work
classification (disability evaluation) and risk
stratification (prognosis).
4) The efficacy of medical, surgical, or pharmacologic
treatment.

5) The presence and severity of arrhythmias.
6) Preoperative physiologic status.
7) Intermittent claudication.

CONTRAINDICATIONS
1) A recent change in the resting electrocardiogram
suggesting infarction or other acute cardiac event.
2) Recent complicated myocardial infarction.
3) Unstable angina.
4) Uncontrolled ventricular arrhythmia.
5) Uncontrolled atrial arrhythmia that comprises
cardiac function.

6) Third degree atrioventricular heart block without
pacemaker.
7) Acute congestive heart failure.
8) Severe aortic stenosis.
9) Suspected or known dissecting aneurysm.
10) Active or suspected myocarditis or pericarditis.
11) Recent systemic or pulmonary embolus.
12) Acute infections.
13) Significant emotional distress (psychosis).

PREPARATION FOR
ELECTROCARDIOGRAM
1) Skin should be prepared to decrease the resistance
at the skin electrode interface and thus improve
the signal to noise ratio.
2) After removing hair from the general areas of
placement, each site should be vigorously rubbed
with an alcohol pad to remove skin oil.
3) The skin should be abraded using a product designed
further to reduce resistance by removing the
superficial layers of skin.

4) Finally, each electrode should be carefully placed in
the proper location to ensure good skin contact with
both the conducting gel and adhesive surfaces of the
electrode.

ECHOCARDIOGRAPHY
 Electrocardiography is the evaluation of cardiac
structures and function utilizing images produced by
ultrasound energy.
 Electrocardiography can be done in two dimensions
(2-D), three dimensions (3-D) and can be performed
from the chest wall, from the esophagus.

DOPPLER
1) When an ultrasound beam with known frequency
(f) is transmitted to the heart, it is reflected by
red blood cells.
2) The frequency of the reflected ultrasound waves
(f1) increases when the red blood cells are moving
toward the source of ultrasound and decreases when
the red blood cells are moving away.

3) The difference in frequency between transmitted
sound and reflected sound is called as frequency shift
or Doppler shift ( f1-f0).
MODES
PULSED WAVE DOPPLER
Pulsed wave Doppler is location specific. A single crystal
sends a short burst of ultrasound at a pulse repetition
frequency and receives sound beams reflected from
moving red blood cells from a specified location.

Thus, the maximal frequency shift that pulsed wave
Doppler can measure is half the pulse repetition
frequency, called the Nyquist frequency.
CONTINUOUS WAVE DOPPLER
1) In continuous wave Doppler, the transducer
ultrasound waves and receives the reflected ultrasound
waves continuously with the use of two separate
crystals.

2) Therefore, the maximal frequency shift and velocity
recorded with continuous wave.
3) Doppler are not limited by the pulse repetition
frequency or Nyquist phenomenon.

COLOUR DOPPLER
Colour Doppler codes for the direction of ultrasound
shift, eg red indicating blood moving towards the
transducer, blue indicating blood moving away from
the tranducer. This enables to localize the site and
direction of abnormal blood flow.(eg valve
regurgitation).

NORMAL ECHOCARDIOGRAPHIC VALUES
Ventricular and Atrial dimensions (ID, internal
dimensions)
 LVIDd (end diastole): 3.5-5.6 cm
 LVIDs (end systole):1.9-4.0 cm
 Posterior LV wall thickness: 0.7-1.1 cm ( at end
diastole).
 RVID (end diastole): 0.7-2.6 cm.

 Posterior LV wall excursion (amplitude): 0.8-1.2cm
 Interventricular septal thickness: 0.7-1.2 cm
 LAID ( end systole): 2.0-4.0cm
 Ratio of septum to posterior wall thickness= 1.3:1
AORTA AND AORTIC VALVE
 Aortic root internal diameter:2.0-4.0cm.
 Aortic valve opening: 1.6-2.6cm.

MITRAL VALVE:-
E-P slope (closure rate): 70-150cm/s.
E point to septal distance: 0-5mm.
D-E distance: 20-30mm.
VENTRICULAR FUNCTION:-
Ejection fraction: 50-85%
Fractional shortening: 30-45%

CARDIAC CATHERIZATION
Cardiac catheterization is widely used for diagnostic
evaluation and therapeutic intervention in the
management of patients with cardiac diseases.
The nurse’s role in precatheterization teaching and
intracatheterization and postcatheterization care is
important.

INDICATIONS
1) Unstable angina/ACS, refactory to medical
therapy or with high/ imtermediate risk features.
2) Suspected Prinzmetal’s angina
3) As a plan to proceed with primary PCI for ST
elevation MI.
4) Cardiogenic shock owing to acute MI.
5) Recurrent ischemia after ST elevation MI.

6) Persistent chest pain after fibrinloysis,.
7) Abnormal stress test after fibrinolysis.
8) Abnormal stress test with high risk features.
9) Sudden cardiac death or ventricular arrhythmia with
no obvious cause.
10) Congestive heart failure with angina or ischemia.
11) Suspected stent thrombosis.
12) Recurrent angina within 9 months of PCI.
13) Before repair of a mechanical complications of MI.

CONTRAINDICATIONS
1) Acute gastrointestinal bleeding
2) Severe hypokalemia
3) Uncorrected digitalis toxicity
4) Acute stroke
5) Acute renal failure or severe chronic non dialysis
dependent kidney diseases.
6) Severe anemia
7) Uncooperative patient.

CATHETERIZATION APPROACH
1) Cardiac catheterization is usually accomplished by
percutaneous methods ( the seldinger technique).
2) Direct exposure of the vein and the artery (sones
technique) may be also used.
3) The percutaneous method is used for the femoral
artery and vein; direct exposure is used for the
brachial artery and basilica vein.

4) All chambers and vessels may be cannulated using
either approach, and both approaches have high degree
of safety.

VENTRICULOGRAPHY
• Ventriculography is performed to evaluate valve
structure or function, to define ventricular anatomy,
and to evaluate ventricular function.
• Ventriculography is accomplished by spacifying the
ventricular cavity with contrast medium and filming
ventricular motion.

COMPLICATIONS
1) Arrhythmias
2) Thrombosis
3) Embolism
4) Stroke
5) Myocardial infarction
6) Hemorrhage
7) Contrast reactions.

CORONARY ARTERIOGRAM
TECHNIQUES
Percutaneous Approach/ Judkins Technique
In this technique catheter is guided over a guide wire
through the distal aortic arch to the coronary ostia,
the guide is withdrawn, and the catheter is placed
with contrast medium.

The judkins left catheter is preshaped to allow entry
into the left coronary ostium from the femoral
approach with minimal catheter manipulation.
 The judkins right catheter is shaped to permit entry
into the right coronary artery (RCA) with a small
amount of rotational (clockwise) catheter manipulation
from any vascular approach.

CARDIAC ELECTROPHYSIOLOGY
PROCEDURES
1) The cardiac electrophysiology (EP) procedures
include both diagnostic testing and interventional
treatment procedures.
2) In general, diagnostic EP studies are performed to
determine an arrhythmia diagnosis or EP mechanism
of a known arrhythmia.
3) Interventional or therapeutic EP studies include
endocardial catheter ablation and surgical procedures

For both supraventricular and ventricular arrhythmias.
4) The placement of implantable cardioverter-
defibrillations for management of ventricular
tachycardia (VT) and ventricular fibrillation (VF) is
also an interventional EP procedure.

INDICATIONS
1) Sustained ventricular tachycardia or cardia arrest
occurring in the absence of acute myocardial
infarction, antiarrhythmia drug toxicity, or
electrolyte imbalance, particularly when baseline
ventricular ectopic frequency is too low to permit
assessment of anti arrhythmic drug by
electrocardiographic monitoring.

2) Wide QRS tachycardia of uncertain etiology.
3) Evaluation of a device for the detection and
electrical termination of tachycardia.
4) Second degree atrioventricular block in which the
level of block is uncertain.

COMPLICATIONS
1) Cardiac perforation
2) Cardiac tamponade
3) Arrhythmias
4) Venous thrombosis
5) Pulmonary embolism
6) Pericardial efusion
7) Infection

INTERVENTIONAL
ELECTROPHYSIOLOGY AND
CATHETER ABLATION
This interventional procedure includes both a
diagnostic EP study and catheter ablation. The
mechanism of the arrhythmias is confirmed during
the first part of the procedure, and the ablation
takes place during the second part.

INDICATIONS
1) Atrioventricular nodal reentrant tachycardia.
2) Atrioventricular reentrant tachycardia
3) Atrial fibrillation or flutter
4) Atrial arrhythmias
5) Ventricular tachycardia

BIBLIOGRAPHY
P.Hariprasath, “Textbook of Cardiovascular &
Thoracic Nursing”, First Edition 2016, Jaypee
Borthers Medical Publishers (P) Ltd, page no. 523-
532
Javed Ansari, Davinder Kalir;”Text Book of Medical
Surgical Nursing- I” Part A, Published by PV Books,
2015 edition, Pageno. 17 – 19.

Suzanne C. Smelter, Brenda Bare, “Brunner and
Suddarth’s Textbook of Medical Surgical Nursing”,
10th edition, published by Lippincott Williams and
Wilkins, page no.
Janice L Hinkle, Kerry H Cheever,” Brunner and
Suddarth’s Textbook of Medical Surgical Nursing”,
volume 1, 13th edition, published by, Wolters Kluwer,
New Delhi, page no.29-31.

LABORATORY STUDIES OF CARDIAC DISORDERS

LABORATORY STUDIES OF CARDIAC DISORDERS

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