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LABORATORY TESTS AND RESULTS:

BLOOD IMMUNO CHEMISTRY

(October 13, 2016)

Test Result Reference range

Troponin I 0.01ng/mL <0.01ng/mL

SIGNIFICANCE:

Troponin I The cardiac troponin complex is a basic component of the

myocardium that is involved in the contraction of the myocardial muscle.
POSITIVE LEVEL of troponin is considered a virtually diagnostic of acute M.I.

SERUM TEST

(October 13, 2016)

Test Result Reference range

Sodium 122.1mmol/L 135-145 mmol/L

Potassium 4.54mmol/L 3.5-5.5

Chloride 87.5mmol/L 98-107

Creatinine 90umol/L 49-90

BUN 6.3mmol/L 2.1-7.1

SIGNIFICANCE:

Sodium Decreased sodium due to inadequate sodium intake, diuretic therapy

(Furosemide), vomited for 3 days PTA and 4x vomited during admission.

Chloride Decreased chloride may result from low sodium and K+ levels due to
prolonged vomiting (Vomited 3days PTA, 4x vomited during admission.
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HEMATOLOGY TEST

(October 13, 2016)

Test Result Reference range

Hemoglobin 100g/L 120-150g/L

Hematocrit 0.32u/L 0.37-0.47

RBC 3.5x10^9g/L 4.2-5.4

WBC 11.5 4.8-10.8

Neutrophils 0.77 0.43-0.65

Lymphocytes 0.15 0.20-0.45

Monocytes 0.07 0.05-0.12

Eosinophils 0.01 0.01-0.03

Basophils 0.00 0.00-0.03

MCV 91Fl 81-99Fl

MCH 31pg 27-31pg

MCHC 339g/L 320-360g/L

Platelet 298x10^9/L 150-450x10^9/L

SIGNIFICANCE:

Hemoglobin Decreased hemoglobin due to hemolysis, or RBC destruction

caused by blood vessel injury (Hypertension) and presence of Diabetes,
rheumatoid arthritis and old age can also be a reason.

Hematocrit Decreased hematocrit due to hemolysis, or RBC destruction

caused by blood vessel injury (Hypertension) and presence of Diabetes,
rheumatoid arthritis and old age can also be a reason.
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RBC Decreased RBC due to hemolysis, or RBC destruction caused by blood

vessel injury (Hypertension) and presence of Diabetes, rheumatoid arthritis and
old age can also be a reason.

WBC Increased WBC in people with myocardial infarction, and rheumatoid

arthritis. Increased level signals the presence of inflammation in blood vessels
which is involved in hardening and clogging arteries.

Neutrophil Increased neutrophil due to emotional and physical stress and

rheumatoid arthritis.

Lymphocytes Decreased lymphocyte due to rheumatoid arthritis and

nutritional deficiency.

BLOOD CHEMISTRY

(October 14, 2016)

Test Result Reference range

Total Cholesterol 5.50mmol/L <3.6-5.7

Triglyceride 1.52mmol/L 0.002.26mmol/L

HDL-Cholesterol 0.71 mmol/L 0.85-2.38 mmol/L

HDL Ratio 7.75 mmol/L 2.94-4.62 mmol/L

LDL Cholesterol 4.10 mmol/L 1.66-3.89 mmol/L

VLDL Cholesterol 0.69 mmol/L 0.00-1.03 mmol/L

FBS 5.5 mmol/L 3.9-5.8 mmol/L

SIGNIFICANCE:

HDL cholesterol Decreased due to stress and recent illness, obesity and lack of
exercise.

HDL Ratio Increased ratio means at risk for heart disease.

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LDL Cholesterol Increased due to DM, lack of exercise, obesity and unhealthy
diet ; increase saturated fat and trans-fat can result to increase LDL

URINALYSIS

(October 14, 2016)

Result Reference range

Color Straw

Clarity Clear

Chem Examination

pH 8.5 4.5 8.0

Specific gravity 1.005 1.005 -1.030

Leukocyte (-) <trace

Blood (-) <trace

Nitrate (-) <trace

Protein (-) <trace

Urobilinogen normal

Ketone (-) <trace

Bilirubin (-) <trace

Ascorbic acid (-) <trace

Microscopic/urine flow cytometry examination

Test Result Reference range

Pus cells 1/uL 0-17/uL

Red cells 1/uL 0-11/uL

Non squamous epithelial <1/uL

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cell

Bacteria 3/uL 0-278/uL

CBG MONITORING

DATE TIME RESULT

10 13 16 10 AM 169 mg/dL

10 16 16 5am ----------

11am 94mg/dL

10 18 16 11am ----------

Increased blood glucose signifies recent acute illness (myocardial infarction),

and patient is diabetic.

ELECTROCARDIOGRAPHY

(October 13, 2016 @ 9:15 AM)

(October 13, 2016 @ 7:00 PM)

 57

(October 14, 2016 @ 5:39 AM)

(October 16, 2016 @ 11:47 AM)

SIGNIFICANCE:

Sinus rhythm; Normal axis; Antero-lateral wall infarction

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ANATOMY AND PHYSIOLOGY:

CARDIOVASCULAR SYSTEM

*FUNCTIONS OF THE HEART

Generates blood pressure

Routing blood

Ensuring one-way blood

Regulating blood supply

*LAYERS OF THE HEART

ENDOCARDIUM

Innermost layer

Endothilial tissues

Lines the inner chambers and heart valves

MYOCARDIUM

Middle layer
Striated muscle fibers
Contracting muscle

EPICARDIUM

Outer surface

Encased by parietal pericardium

- Tough loose-fitting

- Fibrous outer membrane

- Attached anteriorly to the lower half of the sternum

2 UPPER COLLECTING ATRIA

2 LOWER PUMPING VENTRICLES

Right Atrium
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o Receives deoxygenated systemic blood via superior and

inferior vena cava

Right Ventricle

o receives blood from atrium via tricuspid valve

o Pump blood to the lungs (pulmonary circulation)

Left Atrium

o Receives oxygenated blood from the lungs

Left Ventricle

o Receives blood from the atrium via mitral valve

o Largest , most muscular chamber

o Pumps against high resistance into the systemic circulation

Tricuspid Valves

Prevent backflow from the right ventricle to right atrium

Bicuspid/Mitral Valve

Prevent backflow from the left ventricle to left atrium

Pulmonary Semilunar Valve

Prevent backflow from pulmonary artery to right ventricle.

Aortic Semilunar Valve

Prevent backflow from aorta to left ventricle.

Coronary Arteries

Supply blood to Heart

Right Common Artery

Perfuse Right Atrium, Right Ventricle, inferior portion of Left Ventricle

and posterior Septal Wall

SA node and AV node

Left Common Artery

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Supplied blood to anterior wall of Left Ventricular septum

Apex of Left Ventricle

Left Anterior Descending Artery

- Supplies blood to Left Atrium , Lateral and Posterior surface of Left

Ventricle

- Posterior Interventricular Septum

- Sometime supplies SA and AV node

- Circumflex Artery

SA Node

- Pacemaker node

- Initiates heartbeat by generating an electrical impulse

AV Node

Normal pathway for impulses originating in atria to be conducted to

ventricles

Posterior pacemaker

Bundle of His, Bundle Branches, Purkinje Fibers

Rapidly transmit cardiac action potentials to enable synchronous

contraction of ventricles.

Action potential originates in the SA node and travel across the wall
of the atrium from the SA node to the AV node.
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Action potential passes through the AV node and along AV bundle

which extends from the AV node, through the fibrous skeleton, into
the interventricular septum.

AV bundle divides into right and left bundle branches, the action
potentials descend to the apex of each ventricle along the bundle
branches.

Action potentials are carried by the Purkinje fibers from the bundle
branches to the ventricular walls.

CARDIAC CYCLE

Atrial Systole

Depolarization of the SA node spreads through the atria by

internodal pathways.

P wave on ECG

Contraction and pressure generation due to Ca+ entry.

atrial kick blood propelled by the atria to the ventricle.

Ventricular Systole

Depolarization on the ventricles spread by the Bundle branches

and Purkinje fibers

QRS complex on ECG

Ca+ entry and contraction occurs

Isovolumic phase

Ventricles contract

Closes the AV valves

First sound heard (S1)

Ventricular Diastole

Ventricles relax

Semilunar valve close

Second heart sound (S2)

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Isovolumic relaxation

AV valve remains closed

AV valves open

Ventricular filling

*CARDIAC OUTPUT AND INDEX

Cardiac Output

Volume of blood ejected per min. by rhythmic ventricular

contraction

140 ml blood each ventricle

Cardiac Index

2.5 -4 L/min./m

140 ml blood each ventricle

Stroke Volume

Volume of blood ejected per beat.

Preload

Myocardial fiber length of the ventricle at end diastole.

Determined by EDV

Inc. when inc. EDV

Afterload

Resistance to left ventricular ejection.

Amount of pressure required by the LV to open the aortic valve

during systole.

Contractile State

Vigor of contraction generated by the myocardium regardless of its

blood volume.

Normal HR :

120-160 beats/min.
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Sinus tachycardia

>160 beats/min.

Sinus bradycardia

<120 beats/min.

BLOOD SUPPLY

Blood that has passed through the lungs and picked up oxygen is called
oxygenated blood, and blood that has passed through the tissues and
released some of its oxygen is deoxygenated blood.

The major route takes deoxygenated blood to the lungs, where it is

oxygenated.

The deoxygenated blood flows through pulmonary arteries to pulmonary

capillaries, becomes oxygenated and returns to the heart through
pulmonary vein.
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PROGNOSIS:

A further MI may happen sometime in the future. This is more likely if the
coronary arteries are badly affected with atheroma, or further build up of
atheroma continues. If the risk of this is thought to be high then surgery may be
advised to bypass or widen severely narrowed coronary arteries by further
angioplastic procedures with stenting.
The most crucial time is during the first day or so. If no complications arise,
and you are well after a couple weeks, then you have a good chance of
making a full recovery. A main objective then is to get back into normal life, and
to minimise the risk of a further MI.

The morbidity and mortality of myocardial infarction (MI) result from arrhythmias,
cardiac rupture, heart failure, valve insufficiency, and embolization.

Arrhythmias include ventricular tachyarrhythmias, which are the most common

cause of sudden death, especially early after infarction, and various degrees of
heart block.

Cardiac rupture occurs in approximately 5% of patients, has a high mortality,

and is increased in frequency in patients experiencing their first infarct,
hypertensive patients, and women.

The risk of heart failure is proportional to the size of the infarct and the presence
of papillary muscle necrosis. The size of infarct may be significantly decreased
with prompt reperfusion after the first symptoms, either by thrombolytic
treatment or by percutaneous intervention. Stem cell treatment is an
investigative approach to minimizing myocardial infarct size.

Infarction or rupture of the posteromedial papillary muscle causes acute mitral

insufficiency, which greatly worsens cardiac output and which may be treated
surgically. The improvement in prognosis that has occurred in the last decade is
due to early treatment with thrombolytic agents and reperfusion.

Mural thrombosis over the area of infarction may result in embolization and
concomitant stroke but is decreased in incidence with anticoagulation therapy.
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RECOMMENDATIONS:

This report summarizes key recommendations from the clinical group for
the patient herself to keep, including: (1) A nutritious and adequate diet
with minimal consumption of fats and sugar; (2) Appropriate exercise as
tolerated at least 3 times a week; (3) Cessation of alcohol beverage
drinking; (4) Religious compliance to the medication therapy; (5) Follow-
up check up as instructed; and (6) Prompt consultation for early
management during ill-effects.
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