cwu medicine
TRANSCRIPT
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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
Impression: No abnormality detected
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
Impression: No abnormality detected
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