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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

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 GENERAL HEMATOLOGIC RESPIRATORY REVIEW No fever, no loss of weight, no loss of appetite No bruises, no pallor, no bleeding 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 No headache, no vertigo, no loss of consciousness, no SYSTEM 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

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

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.


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.


General examination Anthropometry : Height: Weight: BMI: 175 cm 72.6 kg 23.7

Vital signs : Blood pressure Pulse rate normal volume. Respiratory rate Temperature : 30 breaths per minute : 370C : 132/80 mm/Hg : 100 beat per minute, regular rhythm and

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.

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

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 were size, equality, and equal reflex and




Funduscopy was not done. (c) Occulomotor, Trochlear, Abducens No ptosis or strabismus noted. Eye movements were normal and equal bilaterally. (d) Trigerminal

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

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


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.

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.


1) Aortic dissection Pros : Cons : Not radiate to back Not exaggerated by inspiration No dyspnea The chest pain not described as tearing in nature Sudden onset of severe and central chest pain Associated symptoms : Profuse sweating and palpitations Long standing hypertension and diabetes mellitus First presentation

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

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 WBC RBC RBC Distribution Width Hemoglobin Hematocrit Mean Cell Hb Mean Cell Volume Mean Cell Hb Conc. Platelet Value(mmol/L) 9.00 x 109 4.49 x 109 69.5 12.1 g/dL 42.1 % 26.1 80.5 32.4 232 x 10

Normal value (mmol/L) 4.5 13.5 x 109 4 5.4 x 109 30 - 100 11.5 14.5 g/dL 37 % 45 % 24 30 76 92 28 33 150 400 x 10

Interpretation Normal Normal Normal Normal Normal Normal Normal Normal 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) Urea Sodium Potassium Creatinine 4.6 138.7 4.15 72 1.7 6.4 135 150 3.5 -5 44 88 Normal Normal Normal Normal Interpretation

Impression: No abnormality detected.

iii) Liver Function Test ( taken on 22 Feb) Content Total Protein Albumin Total Bilirubin Alkaline Phosphatase Alanine Transaminase Value(mmol/L) 77 45 7 70 30 Normal value (mmol/L) 66 87 g/L 35 50 < 20 53 141 < 33 Interpretation Normal Normal Normal Normal Normal

Impression : No abnormality detected.


Inorganic chemistry (taken on 22Feb) Value(mmol/L) Normal value (mmol/L) 2.1 2.6 0.8 1.45 0.65 1.2 Interpretation


Calcium Phosphate Magnesium

2.23 1.28 0.78

Normal Normal Normal

Impression: No abnormality detected


Fasting Blood Glucose Taken on 22 Feb 2012 : 10.5 mmol/L Impression : He was hyperglycemic.


Coagulation Profile (taken on 22 Feb) Value 10.4 Thrombin 26.6 Normal value 10 13 20 32.4 Interpretation Normal Normal

Content Prothrombin time Activated Time Partial





Impression : No abnormality detected. vii) Content Creatine Kinase CKMB Aspartate transaminase Lactate Dehydrogenase Serial cardiac profile 24/2 (mmol/L) 100 (N) 3.0 (N) 30 (N) 60 (High) 25/2 (mmol/L) 845 3.2 70 73 Normal value (iU/L) 60-400 iU/L 2.5-3 5-35 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

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.

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 o o o o plan o o o o o o o iv frusemide 40mg tds carvedilol 6.25mg od simvastatin 20mg od omeprazole 20mg od aspirin 75mg od reduce frusemide to 40mg bd withhod carvedilol start arixtra 2.5mg od--day 2,given stat dose at ED start amlodipine 5mg od s/l GTN PRN daily RP slow K 1 TAB OD

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.

Coronary Arteries Right Coronary Artery Circumflex Artery Left Anterior Descending Artery

Area of Blood Supplies Right Atrium & Ventricle, Superior part of left ventricle and Posterior septal wall Left Atrium, Lateral and Posterior part of Left Ventricle 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 ensure adequate 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

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

environmental issue - he works as manager, thus predispose to stress at longhour of working and lack of rest

Pathophysiology of ACS Atherosclerotic plaque formation

Atherosclerotic plaque rupture, fissure or ulceration with superimposed 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
Clinical Features of ACS Symptoms : 1) CHEST PAIN indistinguishable 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

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

Diagram shows algorithm for management of unstable angina, NSTEMI and STEMI. 1) Electrocardiography/ECG (after 10 minutes arrival)


Dynamic ST/T changes ST depression > 0.5 mm in 2 or more contiguous leads T-wave inversion deep 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 inversion deep symmetrical T-wave inversion


LEADS V1 V3 V1 V6 V7 V8 V1 V2 I, aVL, V5 V6 II, III, aVF

FINDINGS ST elevation, Q wave ST elevation, Q wave T elevation, Q wave ST depression, Tall R wave ST elevation, Q wave ST elevation, Q wave

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.

How to differentiate between unstable angina and acute Myocardial infarction? CHARACTERISTIC PATHOGENESIS ECG DYNAMIC CHANGES CARDIAC BIOMARKERS STEMI Total occlusion of coronary artery -dynamic ST/T changes -T-wave Inversion -ST elevation -Troponin, CK and CK-MB increase NSTEMI Subtotal occlusion of coronary artery -dynamic ST/T changes -T-wave inversion -ST depression -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 aspirin chew 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 dilatation door to balloon time) Time to hospital fibrinolysis (time from hospital arrival to administration of fibrinolytic therapy door to needle time)

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 is equivalent 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 IVStreptokinase 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.


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 reninangiotensin-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

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

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

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,

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

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.

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 angiooedema. 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 angiotensinII 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

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 with low 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)

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 have left 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 bundlebranch 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

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.



DATE : 26th MARCH 2012


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: AZIZI BIN ABD RAHMAN : 4 : 2008402216 : 2011/2012 : MEDICINE