CWU Medicine

8/2/2019 CWU Medicine

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PATIENT INITIALS: Mr KAMARUDDIN ABD RAHMAN

R/N: 40480

SEX: Male

WARD: 4C

AGE: 45 years old

OCCUPATION: Retiree from Tesco Manager

MARITAL STATUS: Married

ETHNIC GROUP: MalAY

DATE OF ADMISSION: 25th

MARCH 2012

DATE OF CLERKING: 25th

MARCH 2012

HISTORY TAKEN FROM: Patient and his wife

RELIABILITY: Good

PRESENTING COMPLAINT(s)

Mr Kamaruddin, 45 years old Malay gentleman known case of hypertension

was admitted to Selayang Hospital on 25th

March 2012 with complained of

sudden onset of chest pain 1 hour prior to admission.

HISTORY OF PRESENTING COMPLAINT(s)

Patient was last well until 8.30 am at morning when he developed sudden

onset of chest pain that was centrally located, occur at rest, radiated to left arm,

described as pressure in nature, associated with profuse sweating, palpitations,

nausea, vomiting dyspnea, and pedal edema. The chest pain described as severe

chest pain with score 8/10 and continuous for more than 30 minutes. There was no

aggravating and relieving factor. Regarding dyspnea, it was occur immediately

after having the chest pain.

On further questioning, this is not the first time he was having the chest pain.

he was having multiple attack since August last year. His doctor has prescribes

him sublingual GTN and instructed him to take the medication when he was

having heart attack. He will having the pain when he tries to do a physical

activity, and he is emotionally unstable. He also has reduced effort tolerance. He

only can walk up to 200 meters or climbing 1 flight stairs before having shortness


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of breath. He also cannot lie flat because it also will cause him having shortness of

breath. He needs to use 3 pillows to sleep. Her wife mention that he often wakes

up in the middle of night to catch his breath. He also noticed that he has swelling

on his leg when he was having heart attacks. Besides that, he also has productive

cough with white sputum, however, he did not notice any blood tinged in the

sputum. He was advice to reduce fluid intakes to 800ml but he rarely follow the

instruction unless when his wife is at home.

SYSTEMIC REVIEW

SYSTEMS REVIEW

GENERAL No fever, no loss of weight, no loss of appetite

HEMATOLOGIC No bruises, no pallor, no bleeding

RESPIRATORY Besides dyspnea and cough, he does not has any

respiratory sypmtoms.

GASTROINTESTINAL No abdominal pain, no diarrhea or constipation, no

melena, no hematemesis

GENITOURINARY No dysuria, no hematuria, no nocturia, no polyuria , urine

was normal

CENTRAL NERVOUS

SYSTEM

No headache, no vertigo, no loss of consciousness, no

blurred vision, no loss of memory, no fits

MUSCULOSKELETAL No rashes, No muscle pain, no abnormal movement, no

gross deformity, no joint swelling, no joint pain.

ENT No epistaxis, no runny nose, no ear discharge, no sore

throat

ENDOCRINE No tremors, no heat or cold intolerance, no polyphagia

PAST MEDICAL / SURGICAL HISTORY

This was the second admission. His first admission was at August 2011 due to

heart attack. He has undergone angiogram at UiTM sungai Buloh at December

2011.

He had been diagnosed with hypertension since 15 years ago when doing

medical checkup at KKSB. He follow up at clinic hospital sungai buloh and

prescribes with prerindopril, carvedilol and furosemide. He claimed to comply to


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his medication. he also was diagnosed with hyperlipidemia and was prescribes

with simvastatin. He also was diagnosed with hemorrhoid grade 3 and peptic

ulcer disease.

He never had undergone any surgery before.

DRUG HISTORY

T Perindopril 4mg OD.

Sublingual GTN PRN

T Aspirin 75mg OD

T Furosemide 40mg OD

T simvastatin 20 mg ON

T carvedilol 6.25mg BD

T Hemo Rid OD.

ALLERGIES

He is allergic to EES.

DIETARY HISTORY

He ate three times daily. His foods are rich of carbohydrate and fat. during

breakfast he usually takes roti canai. During lunch and dinner, he takes rice with

malay diet. He did not follow fluid restriction that doctor advice.

FAMILY HISTORY

His father has passed away because of old age. His mother is still alive, with

history of hypertension and heart disease. He is theforth out of 5 siblings. His

elder brother also has hypertension and heart disease. Other siblings is alive and

well.

SOCIAL HISTORY

He is married and blessed with 3 daughters and 2 stepchild. He lived in kota

damansara with his family. Previously he works as manager at Tesco, currently he

is not working because of his disease. Her wife is the breadwinner. She is

businesswoman. The total family income is RM2000 per month. He is a heavy


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smoker since 15 years ago. He smokes for 20 cigarettes per day. Since having

heart attack august last year, he reduce smoking up to 5 sticks per day. He did not

consume any alcohol and not elicit illegal drugs.

SUMMARY

Mr Kamaruddin, 45 years old malay gentleman known case of hypertension,

and previous heart attack was admitted to hospital sungai buloh with the chief

complaint of chest pain 1 hour prior to admission. The pain was sudden onset

crushing in nature, radiated to left arm, associated with profuse sweating, palpitation,

dyspnea, orthopnea, PND, and leg swelling.


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PHYSICAL EXAMINATION

General examination

Anthropometry :

Height: 175 cm

Weight: 72.6 kg

BMI: 23.7

Vital signs :

Blood pressure : 132/80 mm/Hg

Pulse rate : 100 beat per minute, regular rhythm and

normal volume.

Respiratory rate : 30 breaths per minute

Temperature : 370C

General condition

He was lying comfortably on the bed with one pillow. He was alert,

conscious, and well orientated to time, place and people surrounding him. He

was on respiratory distress with evidence of using accessory muscle to breath.

His palm was warm, moist, not pale and no palmar erythema. Capillary

refill less than 2 seconds and no abnormality noted over the nails such as

clubbing, koilonychia, leuconychia and splincter hemorrhage.

On examination of the neck, the jugular venous pressure was not raise.

There was no carotid bruits.

His conjunctivae were pink and no discolouration over the sclera. There

was also no xanthelasma and corneal ulcus. His hydrational status was good

by the evidence of moist lips and mucous membrane. His nutritional was good

by the evidence of no muscle wasting noted. He was not cyanosed centrally

and peripherally. He has good dental hygiene.

On the examination of cervical lymph node, there was no lymph node

enlargement.

On examination of the leg, he has pitting edema up to mid tibia. On

examination of peripheral pulses, radial, brachial, carotid, femoral, popliteal,

and pedal pulses were are present bilaterally.


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Systemic examination

i. Cardiovascular System

On examination of precordium, on inspection, the chest shape looked

normal. No visible dilated vein, visible pulsation, scar, abnormal pigmentation

or spider naevi.

On palpation, apex beat situated at the sixth intercostal space at

anterior axillary over the left chest. No parasternal heave or thrill palpable.

On auscultation, there was dual rhythm of heart sound and no murmur

heard over the four regions of the cardiac valves.

Impression: evidence of cardiomegaly.

ii. Respiratory System

There was no chest wall deformity such as pectus excavatum or pectus

carinatum. Chest wall moves symmetrically with respiration. There was no

abnormal dilated vein, no visible pulsation, no scar or abnormal pigmentation

over the anterior part and the posterior part of the chest. No spider naevi

noted.

Trachea was centrally located. Apex beat situated at the fifth

intercostal space at midclavicular line over the left chest. Chest expansion

equal bilaterally anteriorly and posteriorly. Vocal fremitus was normal and

equal bilaterally anteriorly and posteriorly.

There was no abnormal dullness over the lung area anteriorly and

posteriorly. Upper border of the liver was at the fifth intercostals space and

there was a normal cardiac dullness over the left lung area.

Vesicular breath sounds heard over the anterior and the posterior chest

bilaterally. Air entry was equal on both sides and there was bilateral

crepitation on inspiration lower zone of lungs.

Impression: bibasal crepitation indicates pulmonary edema.

iii. Abdominal examination

The abdomen was not distended and moves symmetrically with

respiration. The umbilicus was centrally located and inverted. There were no


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scar, no visible dilated veins, no visible peristalsis, no visible pulsation, no

abnormal pigmentation, and no swelling of the penis and scrotum. No caput

medusa noted.

On soft palpation, the abdomen was soft and non tender. No guarding

or rigidity noted. On deep palpation, liver and spleen were not palpable. No

other masses palpable. Kidneys were not ballotable.

On percussion, there was no ascites evidenced by shifting dullness and

fluid thrill were negative.

On auscultation, bowel sounds heard with normal intensity and no

bruit heard.

Hernial orifices were intact bilaterally.

Impression: No abnormality detected.

iv. Central Nervous System

General inspection

He was alert, conscious and well orientated to time, place and

person. He recognized people well. He looked calm and not in state

of depression. He answered questions accordingly. He can read and

write well.

Cranial nerves

(a)Olfactory

He has no problem with smelling.

(b)Optic

He was wearing spectacles. Not complaining of blurred

vision with spectacles. Color vision tested from pictures in

Hutchisons Clinical Method and it was normal. Visual fields

were normal. Pupillary size, equality, reflex and

accommodation were normal and equal bilaterally.

Funduscopy was not done.

(c)Occulomotor, Trochlear, Abducens

No ptosis or strabismus noted. Eye movements were

normal and equal bilaterally.

(d)Trigerminal


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Sensation over the ophthalmic, mandibular and

maxillary division of trigerminal nerve were normal. Corneal

reflex was normal and equal bilaterally. Tests for motor

function of trigerminal nerve such as clench teeth, open or

close mouth against resistance, and jaw jerk were normal.

(e)Facial

Face was symmetry bilaterally. Wrinkling of forehead,

close eyes tight, blow cheeks and show teeth were normal. He

had not complained of any abnormal taste or abnormal

loudness over one of the ear.

(f) Vestibulocochlear

No abnormal discharge from the ear. Rinnes and

Webers test was not performed.

(g)Glossopharyngeal, Vagus

Uvula placed at the normal position and not deviated.

No hoarseness of voice noted.

(h)Accessory

He was able to shrug shoulder and turn head to against

resistant.

(i) Hypoglossal

No tongue deviation, no wasting or fasciculation noted.

Normal power for tongue.

Peripheral nervous system :

Upper limb

(i) Motor

1. Inspection- There were normal muscle bulk, posture and

skin. No abnormal movements or fasciculation noted.

2. Tone - There was normal tone and equal bilaterally.

3. Power - Muscle power was 5/5.

4. Coordination - Coordination was normal.

5. Reflexes - Reflexes were normal and present bilaterally.

(ii)Sensory


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There were normal sensations of pain, propioception and light

touch.

Lower Limb

i) Motor

1. Inspection- There were normal muscle bulk, posture and

skin. No abnormal movements or fasciculation noted.

2. Tone- There was normal tone and equal bilaterally.

3. Power- Muscle power was 5/5.

4. Coordination - Coordination was normal.

5. Reflexes - Reflexes were normal and present bilaterally. No

ankle clonus elicited.

ii) Sensory

There were normal sensations of pain, proprioception and light

touch. Gait is stable and steady

Impression: No abnormality detected

SUMMARY

Mr Kamaruddin, 45 years old malay gentleman known case of hypertension,

and previous heart attack was admitted to hospital sungai buloh with the chief

complaint of chest pain 1 hour prior to admission. The pain was sudden onset

crushing in nature, radiated to left arm, associated with profuse sweating, palpitation,

dyspnea, orthopnea, PND, and leg swelling. He has family history of heart disease.

On physical examination, he was on respiratory distress with 30 breath per

minutes, the apex beat was displaced to 6th

intercostal space at midclavicular line. On

auscultation of lungs, there was bibasal crepitation.


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PROVISIONAL DIAGNOSIS

1) Acute Myocardial Infarction

Risk Factor : Gender male, age >45 years old, heavy smoker

Long standing hypertension

Does not control his diet

Sudden onset of chest pain for more than an 30 minutes duration.

Chest pain described as pricking in nature

Associated symptoms : profused sweating, palpitations, nausea,

vomiting.

2)

Left ventricular heart failure Long standing history of hypertension

Does not follow fluid restriction

Poor exercise tolerance

Orthopnea and PND.

Basal crepitation on both lungs.

DIFFERENTIAL DIAGNOSIS

1) Aortic dissection

Pros :

Sudden onset of severe and central chest pain

Associated symptoms : Profuse sweating and palpitations

Long standing hypertension and diabetes mellitus

First presentation

Cons :

Not radiate to back

Not exaggerated by inspiration

No dyspnea

The chest pain not described as tearing in nature


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2) Pericarditis

Pros :

Sudden onset of severe and central chest pain

During examination, patient complained of chest pain that worsen on

inspiration.

Cons :

No history of fever

Pain usually stabbing and sharp pain in nature

Pain not exaggerated by lying flat and also not relieved by bending

forward.

4) Acute Gastritis

Pros :

Sudden onset of central chest pain

Patient had diagnosed with gastritis on medication.

Cons :

Chest pain described as severe, pricking in nature and not radiate to

back.

No other symptoms such as belching, bloating, feeling of fullness or

burning.

5) Pulmonary embolism

Pros

Sudden onset chest pain

Dyspnea

Long standing hypertension

Multiple episode of heart attack may cause complication


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Cons

Patient does not have clotting disorder.

The pain is not sharp stabbing pain

Patient does not have history of prolonged immobilization and limb

trauma

He is not hypoxic.

INVESTIGATIONS

General investigations (to assess patient general condition)i) Full blood count (taken on 22 Feb)

Content Value(mmol/L) Normal value (mmol/L) Interpretation

WBC 9.00 x 109

4.513.5 x 109

Normal

RBC 4.49 x 109

45.4 x 109

Normal

RBC Distribution Width 69.5 30 - 100 Normal

Hemoglobin 12.1 g/dL 11.514.5 g/dL Normal

Hematocrit 42.1 % 37 %45 % NormalMean Cell Hb 26.1 2430 Normal

Mean Cell Volume 80.5 7692 Normal

Mean Cell Hb Conc. 32.4 2833 Normal

Platelet 232 x 109

150400 x 109

Normal


ii)

Electrolytes (taken on 22 Feb)To assess level of potassium as the patient has an episode of vomiting.

Content Value(mmol/L) Normal value

(mmol/L)

Interpretation

Urea 4.6 1.76.4 Normal

Sodium 138.7 135150 Normal

Potassium 4.15 3.5 -5 Normal

Creatinine 72 4488 Normal


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Impression: No abnormality detected.

iii) Liver Function Test ( taken on 22 Feb)

Content Value(mmol/L) Normal value (mmol/L) Interpretation

Total Protein 77 6687 g/L Normal

Albumin 45 3550 Normal

Total Bilirubin 7 < 20 Normal

Alkaline Phosphatase 70 53141 Normal

Alanine Transaminase 30 < 33 Normal

Impression : No abnormality detected.

iv) Inorganic chemistry (taken on 22Feb)

Content Value(mmol/L) Normal value

(mmol/L)

Interpretation

Calcium 2.23 2.12.6 Normal

Phosphate 1.28 0.81.45 Normal

Magnesium 0.78 0.651.2 Normal


v) Fasting Blood Glucose

Taken on 22 Feb 2012 : 10.5 mmol/L

Impression : He was hyperglycemic.

vi) Coagulation Profile (taken on 22 Feb)

Content Value Normal value Interpretation

Prothrombin time 10.4 1013 Normal

Activated Partial Thrombin

Time

26.6 2032.4 Normal


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INR 0.9 1 - 2 Normal

Impression : No abnormality detected.

vii) Serial cardiac profileContent 24/2 (mmol/L) 25/2 (mmol/L) Normal value (iU/L)

Creatine Kinase 100 (N) 845 60-400 iU/L

CKMB 3.0 (N) 3.2 2.5-3

Aspartate transaminase 30 (N) 70 5-35

Lactate Dehydrogenase 60 (High) 73 70-250

Impression : Significantly increases at all the cardiac enzymes at day 2

admission.

rate : 100 bpm

rhythm : sinus tachycardia

axis : normal axis

no ischemic changes

intermintent ventricular ectopic

pathological Q wave at lead III


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Chest x-ray

this is PA view of chest x-ray Mr. Kamaruddin Abdul Rahman

there is cardiomegaly with evidence of cardiothoracic ration more than 50%

bilateral haziness all over the lung

alveolar oedema ( Bats wings appearance)

impression : features of fluid overload.


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FINAL DIAGNOSIS

1) Acute coronary syndrome

2) Decompensated CCF secondary to non compliance to fluid restriction.

PRINCIPLE OF MANAGEMENT

In ED

Oxygen by nasal prongs 3L/m

Captopril 25mg stat

IV furosemide 40 mg stat

CBD

Strict I/O chart

Aspirin 300mg stat

IV morphine 2.5mg stat

Fondaparinux 2.5mg stat

Clopidogrel 300mg stat

Sublingual GTN 1/1 PRN

Venous access for FBC, Cardiac enzyme, renal profile

In Ward

Current medication

o iv frusemide 40mg tds

o carvedilol 6.25mg od

o simvastatin 20mg odo omeprazole 20mg od

o aspirin 75mg od

plan

o reduce frusemide to 40mg bd

o withhod carvedilol

o start arixtra 2.5mg od--day 2,given stat dose at ED

o start amlodipine 5mg od

o s/l GTN PRN

o daily RP

o slow K 1 TAB OD


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Discussion

For this patient, Mr Kamaruddin, 45 years old malay gentleman with known case

of hypertension and was admitted to Selayang Hospital on 22nd

February 2012

with complained of sudden onset of chest pain on the day of admission associated

with profused sweating and palpitations at rest. He also has features of left

ventricular heart failure.

From the classical symptoms and findings in clinical examination, most probably

patient had underlying cardiac pathology. Thus, i would like to discuss about :

the blood supply and physiology of the normal heart.

Acute Coronary Syndrome(ACS) - definition, epidemiology,

classification, risk factors, pathophysiology, classical symptoms, how to

differentiate one another, investigation

Management of ACS- medical therapy and surgical intervention

Heart Failure - definition, etiology, criteria to diagnosed heart failure,

history and examination, management

The Blood Supply & Physiology of the Heart

The diagram above shows the coronary arterial supply of the myocardium.


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Coronary Arteries Area of Blood SuppliesRight Coronary Artery Right Atrium & Ventricle, Superior part

of left ventricle and Posterior septal wall

Circumflex Artery Left Atrium, Lateral and Posterior part of

Left Ventricle

Left Anterior Descending Artery Anterior and Inferior part of Left

Ventricle, Anterior septal wall

What is the function of coronary arteries?

They supply blood flow to the heart, and when functioning normally, they ensureadequate oxygenation of the myocardium at all levels of cardiac activity. It is

important for cardiac cycle, which involves diastolic and systolic function so that

heart able to pump blood to the surrounding tissues and also pump blood into the

pulmonary circulation. Constriction and dilation of the coronary arteries regulate by

local regulatory mechanism that ensure the amount of blood flow to the myocardium

matches the amount of oxygen delivered to the myocardium with the

myocardial demand for oxygen. Diagram below shows the cardiac blood flow during

systolic and diastolic phase.

Acute Coronary Syndrome (ACS)

ACS is a clinical spectrum of ischemic heart disease. Depending upon the degree and

acuteness of coronary occlusion, it is ranging from


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a) Unstable angina (UA)

b) Non-ST elevation myocardial infarction (NSTEMI)

c) ST elevation myocardial infarction (STEMI)

Epidemiology Of ACS

According to 2011 Latest Edition CPG Management Of UA/ NSTEMI, Acute

Coronary Syndrome incidence is 141/100,000 population per year , inpatient

mortality rate is approximately 7% . Based on the National Cardiovascular Disease

Database 2008,to study the risk factors for ACS, below are the results :

Ratio of men to women = 3:1

Mean age 59 years old

BMI greater than 23 (75%)

Dyslipidaemia (33% )

Hypertension(23%)

Diabetes (36%)

Active smokers (33%), while 24% quit smoking over one month previously.

Coronary disease (64%)

Other co-morbidities were

- heart failure (8%)

- chronic renal disease or failure (7%)

- cerebrovascular disease (4%)

- chronic lung disease (4%)

- peripheral vascular disease (1%)

- 2% of patients did NOT have any of the co-morbidities or risk factors

According to this patient, the risk factors are :

male gender

age > 45 years old

long standing hypertension and diabetes

an active smoker


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environmental issue - he works as manager, thus predispose to stress at long-

hour of working and lack of rest

Pathophysiology of ACS

Clinical Features of ACS

Symptoms :

1) CHEST PAINindistinguishable from STEMI/NSTEMI

TYPICAL - Retrosternal, Severe, crushing, squeezing, or pressing

in nature lasting more than 30 minutes.

Radiate to the jaw or down the left upper limb

May occur at rest or on exertion made worse by

exertion

2) Associated with profuse sweating, palpitations

3) Nausea and vomiting

4) Shortness of breath.

5) ATYPICAL symptoms - unexplained nausea and vomiting, weakness,

dizziness, lightheadness, syncope

- for elderly and diabetic - dyspnoea and atypical chest

pain

6) Positive Past Medical History

Atherosclerotic plaqueformation

Atherosclerotic plaque rupture, fissure or ulceration withsuperimposed thrombosis and coronary vasospasm

aetiology -unclear. Possible causes include inflammation,infection, uncontrolled blood pressure and smoking

present as UA, NSTEMI or STEMI - depending on the acuteness,degree of occlusion and the presence of collaterals


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previous hx of ischemic heart disease, percutaneous coronary intervention (PCI) or

coronary artery bypass surgery (CABG)

Physical Signs :

Sign of sympathetic activation: pallor,sweating, tachycardia

Sign of vagal activation : vomitting, bradycardia

Sign of impaired myocardial infarction:

Hypotension

olyguria

cold peripheries

narrow pulse presssure

raised JVP

3rd heart sound heard, quiet 1st

heart sound, diffuse apical impulse

lung crepitations

Sign of tissue damage: fever

Sign of complication : e.g mitral regurgitation , pericarditis

The recurrent symptoms patient had might be due to spread of infarction to

other sides of myocardial muscle as a result of old infarction and without

reperfusion.

Investigations

In order to differentiate between each types of acute coronary syndrome ie.unstable

angina, STEMI and NSTEMI correspond to patient's presentation and findings, we

had to make diagnosis for determine the possible and best treatment for this

patient.Thus investigation needed are :

1) ECG

2) Cardiac Biomarkers


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Diagram shows algorithm for management of unstable angina, NSTEMI and STEMI.

1)Electrocardiography/ECG (after 10 minutes arrival)UA/NSTEMI :

Dynamic ST/T changes

ST depression > 0.5 mm in 2 or more contiguous leads

T-wave inversiondeep symmetrical T-wave inversion

STEMI:

Dynamic ST/T changes

New onset ST-segment elevation of 0.1 mV in leads of V4 to V6 and/or

0.2 mV in leads V1 to V3 T-wave inversiondeep symmetrical T-wave inversion


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2) Cardiac Biomarkers

Cardiac troponins (cTnT and cTnI)

Creatine kinase-Myocardial Band (CK-MB)

Creatine kinase (CK)

Myoglobin

Lactate Dehydrogenase (LDH)

TIME COURSE of ELEVATION of Serum Cardiac Biomarkers after STEMI

The graph above shows the kinetic profiles of cardiac markers following ST elevation

myocardial infarction. These profiles are schematic and do not differentiate between

patients with early reperfusion and those with persistent occlusion of the infarct

related artery. When there is early reperfusion, cardiac marker concentrations rise

more rapidly, peak earlier and at a higher value, and return to the reference range

more rapidly.

LOCATION LEADS FINDINGS

ANTEROSEPTAL V1V3 ST elevation, Q wave

EXTENSIVE ANTERIOR V1V6 ST elevation, Q wave

POSTERIOR V7V8 T elevation, Q wavePOSTERIOR V1V2 ST depression, Tall R wave

ANTEROLATERAL I, aVL, V5V6 ST elevation, Q wave

INFERIOR II, III, aVF ST elevation, Q wave


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How to differentiate between unstable angina and acute Myocardial infarction?

CHARACTERISTIC STEMI NSTEMI

PATHOGENESIS Total occlusion of coronary

artery

Subtotal occlusion of coronary

artery

ECG DYNAMIC CHANGES -dynamic ST/T changes-T-wave Inversion

-ST elevation

-dynamic ST/T changes-T-wave inversion

-ST depression

CARDIAC BIOMARKERS -Troponin, CK and CK-MB

increase

-Troponin increase

-CK and CK-MB normal (10-20%)

Treatment for Acute MI

Can be divided into medical therapy, reperfusion and surgical therapy :

Treatment is aimed at the following:

Restoration of the balance between the oxygen supply and demand to prevent

further ischemia

Pain relief

Prevention and treatment of complications

List of medication given :

1 tablet of 300mg aspirinchew and swallow

1 tablet of 0.5mg GTN administered sublingually

Set up the oxygen via nasal prong / face mask (2-4L/min)

Set up for IV access large bore needle14G

Pain relief with IV morphine 3-5 mg slowly

Antiemetic also administered (10mg Metoclopramide IV slow infusion)

Tab Metoprolol - 15 mg IV 1 then 200 mg/day PO in divided doses

Captopril - 6.25 mg tid titrated to 50 mg tid

Simvastatin 40 mg ON

Assessment for reperfusion strategy :

Time from symptom onset to first medical contact

Time delay to PCI (time from hospital arrival to balloon dilatationdoor to

balloon time)

Time to hospital fibrinolysis (time from hospital arrival to administration offibrinolytic therapydoor to needle time)


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Contraindications to fibrinolytic therapy

High risk patients

How to decide whether fibrinolytic therapy or primary PCI?

Early and prompt reperfusion is crucial as TIME LOST isequivalent to

MYOCARDIUM LOST

fibrinolytic therapy -main reperfusion strategy

primary PCI is the preferred strategy in cases of

fibrinolytic therapy is contraindicated

in high-risk patients

- Late presentation (3-12hrs)

High risk patients criteria :

Large infarcts

Anterior infarcts

Cardiogenic shock

Elderly patient

Post revascularization (post CABG and post PCI)

Post infarct angina

Treatment in ED, he was put on nasal prone of oxygen 3L/min. His BP on admission

was 159/95mmHg. After ECG and other blood tests was done, then he was given IV-

Streptokinase 1.5 mega units in 100 mls of Normal saline. Medications given were IV

Morphine,Aspirin,Plavix,Metoprolol,Captopril,Simvastatin. In ward, they did serial

ECG and CE, vital signs close monitoring. Medication continued and added drugs

were Tab Metformin and Isordil.


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HEART FAILURE

1.definition

Heart failure is a clinical syndrome characterized by symptoms of breathlessness and

fatigue, with signs of fluid retention and supported by objective evidence of cardiac

dysfunction (systolic and/or diastolic). The severity of the symptoms may be graded

according to the New York Heart Association (NYHA) Functional Class. (Appendix

1) These symptoms may fluctuate in severity with time and may completely disappear

following therapy.

2. pathophysiology

Heart failure is due to the inability of the heart to pump blood at a rate to meet the

needs of various organs of the body or its ability to do so only at high filling

pressures. It may be the result of any disorder of the endocardium, myocardium,

pericardium or great vessels although commonly, it is due to myocardial dysfunction.

Myocardial contractility is most often reduced resulting in Left Ventricular (LV)

systolic dysfunction. Occasionally, however, myocardial contractility may be

preserved and LV systolic function is normal, the HF being due to diastolic

dysfunction. Commonly, LV systolic dysfunction is associated with some degree of

diastolic dysfunction.

2.1 Heart Failure due to LV systolic dysfunction

In LV systolic dysfunction, cardiac output is reduced due to depressed myocardial

contractility. This initiates a complex pathophysiological process which includes

haemodynamic alterations and structural changes within the myocardium and

vasculature. Activation of neuro- hormones such as catecholamines and the renin-

angiotensin-aldosterone system play a pivotal role in this process.

2.2 Heart Failure with Preserved LV systolic function

Up to 50% of patients presenting with heart failure have normal or near normal


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systolic function with predominantly diastolic dysfunction11. Diastolic dysfunction

leads to impaired LV filling due to diminished relaxation (during early diastole) and /

or reduced compliance (early to late diastole) leading to elevated filling pressures.

These haemodynamic changes lead to clinical symptoms and signs similar to those of

LV systolic dysfunction.

Many different classifications of HF have been used to emphasize some aspects of the

condition: right vs left vs biventricular heart failure, forward vs backward failure, low

output vs high output heart failure, volume overload vs pressure overload, acute vs

chronic heart failure, systolic vs diastolic HF. For practical purposes, it may be

sufficient to classify HF into acute heart failure (AHF) and chronic heart failure

(CHF).

Acute Heart Failure is defined as rapid onset of symptoms and signs of HF due to an

acute deterioration of cardiac function. Chronic Heart Failure is the chronic state

when patients have stable symptoms. In these patients an acute precipitating or

aggravating factor(s) may cause acute cardiac decompensation.

Etiology

Heart failure is not a complete diagnosis by itself. It is important to identify the

underlying disease and the precipitating cause(s), if present. Although systolic and

diastolic dysfunction are separate pathophysiological entities, they often share

common aetiologies.

The most common underlying causes of HF in adults are:

Coronary heart disease Hypertension

Slightly less common causes include:

Idiopathic dilated cardiomyopathy

Valvular heart disease Diabetic cardiomyopathy

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Other causes of HF include: Congenital heart disease Cor pulmonale Pericardial disease: constrictive pericarditis, cardiac tamponade

Hypertrophic cardiomyopathy Viral myocarditis Acute rheumatic fever Toxic: Alcohol, adriamycin, cyclophosphamide Endocrine and metabolic

disorders: thyroid disease, acromegaly,

Diagnostic criteria

New York Heart Association Classification

This classification is symptom-based and has primarily been used as shorthand to

describe functional limitations. Heart failure symptoms may progress from one class

to the next in a given patient, but can also follow the path in reverse; for example, a

patient with NYHA class IV symptoms might have quick improvement to class III

with diuretic therapy alone.

Class I: Mild. No limitation of physical activity. Ordinary physical activity

does not cause undue fatigue, palpitations, or dyspnoea.

Class II: Mild. Slight limitation of physical activity. Comfortable at rest, but

ordinary physical activity results in fatigue, palpitations, or dyspnoea.

Class III: Moderate. Marked limitation of physical activity. Comfortable at

rest, but gentle activity causes fatigue, palpitations, or dyspnoea.

Class IV: Unable to carry out any physical activity without discomfort.

Symptoms of cardiac insufficiency at rest. If any physical activity is

undertaken, discomfort is increased.

For this patient, he is classified in class III


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History and examination

We need to assess the presence of risk factor in patient. The important key for risk

factor include history of MI; diabetes mellitus; dyslipidemia; old age; male gender;

hypertension family history of heart failure. For this patient, he has long history of

dyslipidemia, hypertension, and multiple history of heart attack since august

2011, family history of heart failure which is his mother and his elder brother .

As for the symptom, he also complaint of dyspnea. Dyspnea is the most common

symptom of left-sided heart failure. May occur with exertion (NYHA II or III) or, in

more severe cases, at rest (NYHA IV). This is considered a minor criterion for the

diagnosis of heart failure (Framingham criteria). JVP for this patient also increase.

A major Framingham criterion for the diagnosis of heart failure. Besides that, he also

has evidence of cardiomegally, which is a major Framingham criterion for the

diagnosis of heart failure. Left ventricular dilation or hypertrophy are common

findings. He also has orthopnea and PND. Orthopnoea worsens immediately after

lying down, because of a sudden increase in venous return (i.e., pre-load). Paroxysmal

nocturnal dyspnoea occurs several hours after the patient lies down to sleep; it results

from the central re-distribution of extravascular fluid that progressively increases the

venous return.

Investigations

For all patients, initial investigations should include ECG, CXR, transthoracic

echocardiogram, and baseline haematology and blood chemistry, including CBC,

serum electrolytes (including calcium and magnesium), serum urea and creatinine,

LFTs, and B-type natriuretic peptide (BNP)/N-terminal pro-brain natriuretic peptide

(NT-pro-BNP) levels. Blood glucose, thyroid function tests and blood lipids are

useful to assess for commonly associated comorbid disease.

Subsequent investigations that help in assessing severity of heart failure and

functional status include standard exercise stress testing (bicycle or treadmill),

cardiopulmonary exercise testing (CPX) with VO2max, 6-minute walking test

exercise, right heart catheterisation, and endomyocardial biopsy. Based on clinical

history, HIV screening and measurement of iron levels and fasting transferrin

saturation to screen for haemochromatosis may also be performed. For this patient,


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ECG, Cardiac Marker and chest Xray has shown positive findings of diagnosing

left ventricular heart failure.

Algorithm for the diagnosis of Heart Failure or LV dysfunction


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Treatment approach

Goals of treatment of chronic CHF are to:

Alleviate symptoms

Delay progression

Reduce mortality.

Lifestyle changes

The success of pharmacological therapy is strongly related to, and greatly enhanced

by, encouraging the patient and his/her family to participate in various

complementary non-pharmacological management strategies. These mainly include

lifestyle changes, dietary and nutritional modifications, exercise training, and health

maintenance.

Initial drug treatments

ACE inhibitors or beta-blockers may be used as first-line treatment. Both are equally

important in terms of survival benefit. It has not been shown that starting with an

ACE inhibitor is better than starting with a beta-blocker, but in practice most

physicians start an ACE inhibitor first; the origin of this practice is historical, as the

benefits of ACE inhibitors were demonstrated 10 years before those of beta-blockers.

If a patient cannot tolerate target doses of both an ACE inhibitor and a beta-blocker

when these drugs are co-administered, it is preferable to co-administer lower doses of

both drugs than to reach the target dose in one class and not be able to initiate the

other.

ACE inhibitors have been shown to decrease the morbidity and mortality associated

with heart failure, and should be given to all patients with left venticular (LV)

dysfunction, symptomatic or otherwise, unless there is a contra-indication or prior

intolerance to therapy.


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Beta-blockers have also been shown to decrease the morbidity and mortality

associated with heart failure. They are initiated at low doses and titrated to target

dosages. Although side effects can include bradycardia, worsening of reactive airway

disease, and worsening heart failure, these can often be avoided by careful patient

selection, dose titration, and close monitoring. Clinical improvement may be delayed

and may take 2 to 3 months to become apparent. However, long-term treatment with

beta-blockers can lessen the symptoms of heart failure and improve clinical status.

Angiotensin-II receptor blockers can now be considered a reasonable alternative to

ACE inhibitors in all patients with preserved or decreased left ventricular ejection

fraction (LVEF) who are intolerant of ACE inhibitors because of cough or angio-

oedema. Experience with these drugs in controlled clinical trials of patients with heart

failure is considerably less than that with ACE inhibitors. Nevertheless, valsartan and

candesartan have demonstrated benefit by reducing hospitalisations and mortality. In

patients with evidence of LV dysfunction early after MI, angiotensin-II receptor

blockers may be no more effective than ACE inhibitors and may be no better

tolerated. The combination of an ACE inhibitor and an angiotensin-II receptor blocker

may produce more reduction of LV size and may reduce the need for hospitalisation

than either agent alone, although whether or not combination therapy further reduces

mortality remains unclear. As an alternative to ACE inhibitors, angiotensin-II receptor

blockers should be initiated in patients early post-infarct, but caution should be used

in patients in cardiogenic shock or with marginal renal output.

Concomitant administration of an ACE inhibitor, a beta-blocker, and an angiotensin-

II receptor blocker should be used with great caution and perhaps initiated only in

hospital under continuous blood pressure and renal function monitoring, since it may

provoke life-threatening hypotension and acute renal insufficiency. The CHARM trial

showed that this combination may confer added benefit with acceptable risk, but

further studies are required. The routine combined use of all three inhibitors of the

renin-angiotensin system cannot be recommended at present.

The addition of a combination of hydralazine and a nitrate is reasonable for patients

with reduced LVEF who are already taking an ACE inhibitor and beta-blocker for

symptomatic heart failure and who have persistent symptoms (class IIa), and has

demonstrated benefit in black patients with heart failure. The combined use of


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hydralazine and isosorbide dinitrate may be also be considered as a therapeutic option

in patients who are intolerant of ACE inhibitors. This combination may be a useful

alternative in patients intolerant to both ACE inhibitors and angiotensin-II receptor

blockers.

Digoxin for patients with heart failure

Digoxin can be beneficial in patients with current or prior symptoms of heart failure

or reduced LVEF, especially those with atrial fibrillation. When added to ACE

inhibitors, beta-blockers, and diuretics, digoxin can reduce symptoms, prevent

hospitalisation, control rhythm, and enhance exercise tolerance, although it has not

been shown to reduce all-cause mortality. Digoxin should not be used in patients withlow ejection fraction (EF) who are in sinus rhythm and who have no history of heart

failure symptoms because, in this population, the risk of harm is not balanced by any

known benefit.

Aldosterone antagonists in moderate-to-severe heart failure

Aldosterone antagonists decrease the morbidity and mortality associated with

symptomatic chronic heart failure and should be used in early post-MI patients with

LV dysfunction and/or moderate-to-severe heart failure (NYHA III or IV).

Aldosterone antagonists should be initiated after titration of standard medical therapy.

Spironolactone and eplerenone can both cause hyperkalaemia, and precautions should

be taken to minimise the risk. In the EPHESUS trial, the addition of eplerenone to

standard care did not increase the risk of hyperkalemia when potassium was regularly

monitored.

Diuretics for fluid retention

Diuretics should be considered for patients who have evidence of, or a prior history

of, fluid retention. Diuretics should generally be combined with an ACE inhibitor and

a beta-blocker. Diuretics interfere with the sodium retention of heart failure by

inhibiting the re-absorption of sodium or chloride at specific sites in the renal tubules.

Bumetanide, furosemide, and torasemide (loop diuretics) act at the loop of Henle,

whereas thiazides, metolazone, and potassium-sparing agents (e.g., spironolactone)
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act in the distal portion of the tubule. These two classes of diuretics differ in their

pharmacological actions. The loop diuretics increase excretion of up to 20% to 25%

of the filtered load of sodium, enhance free-water clearance, and maintain their

efficacy unless renal function is severely impaired. In contrast, the thiazide diuretics

increase the fractional excretion of sodium to only 5% to 10% of the filtered load,

tend to decrease free-water clearance, and lose their effectiveness in patients with

impaired renal function (creatinine clearance less than 40 mL/minute). Consequently,

the loop diuretics have emerged as the preferred diuretic agents for use in most

patients with heart failure; however, thiazide diuretics may be preferred in patients

with hypertension, heart failure, and mild fluid retention because they confer more

persistent antihypertensive effects.

Heart transplant and medical devices

Cardiac transplantation is currently the only established surgical approach, but it is

available to fewer than 2500 patients in the US each year. Current indications for

cardiac transplantation focus on the identification of patients with severe functional

impairment, dependence on IV inotropic agents, recurrent life-threatening ventricular

arrhythmias, or angina that is refractory to all currently available treatments.

Implantable defibrillators have been shown to decrease mortality in patients with

heart failure, both ischaemic and non-ischaemic. The SCD-Heft trial enrolled patients

who had LV dysfunction and no prior history of syncope or sustained ventricular

tachycardia, and included patients with a prior MI and no prior CAD. Use of

implantable defibrillators led to a 23% relative mortality risk reduction at 5 years.

It has been estimated that one quarter to one third of patients with heart failure haveleft bundle-branch block: that is, manifest a QRS duration greater than 120

ms.Patients with heart failure who have left bundle-branch block, known as

ventricular dyssynchrony, have a poorer prognosis than those without left bundle-

branch block. Studies have shown that, in these patients, cardiac re-synchronisation

therapy (CRT) decreases hospitalisation and, when combined with an implantable

defibrillator, significantly reduces mortality.In patients who have conduction delay

and LV dysfunction, biventricular pacemakers have been shown to improve exercise

tolerance and quality of life while decreasing morbidity and mortality. The CArdiac
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REsynchronisation-Heart Failure study (CARE-HF) randomised patients with a

widened QRS, LVEF of 35% or less, and persistent moderate or severe symptoms of

heart failure despite pharmacological therapy, to implantation of a CRT device or not.

The main study observed substantial benefits on morbidity and mortality that

persisted or increased with longer follow-up. Reduction in mortality was due to fewer

deaths from heart failure and from reduced sudden death. Based on those studies, the

ACC/AHA guidelines recommend that patients with LVEF of 35% or less, sinus

rhythm, NYHA III or IV symptoms despite recommended optimal medical therapy,

and a QRS of 120 ms or longer should receive CRT unless contra-indicated.


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NAME OF STUDENT:

AZIZI BIN ABD RAHMAN (2008402216)

DATE : 26

th

MARCH 2012

COMMENTS ON CASE WRITE-UP

_____________________________________________________________________

_____________________________________________________________________

_____________________________________________________________________

_____________________________________________________________________

_____________________________________________________________________

_____________________________________________________________________

_____________________________________________________________________

_____________________________________________________________________

______________________

GRADE: ______________________

NAME OF TUTOR:

SIGNATURE: _______________________ DATE:

_______________________


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CASE WRITE-UP

CONFIDENTIAL

NAME OF STUDENT : AZIZI BIN ABD RAHMAN

YEAR OF STUDY : 4

MATRIC NO : 2008402216

SESSION : 2011/2012

POSTING : MEDICINE

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