A STUDY of HYPONATREMIA AS a PROGNOSTIC INDICATOR in ACUTE MYOCARDIAL INFARCTION a Dissertation Submitted to the TAMILNADU DR. M

A STUDY OF HYPONATREMIA AS A PROGNOSTIC INDICATOR IN ACUTE

MYOCARDIAL INFARCTION

A Dissertation Submitted to

THE TAMILNADU DR. M.G.R MEDICAL UNIVERSITY

CHENNAI

REGISTRATION NUMBER: 201711710

In Partial Fulfillment of the requirement for the

Award of the Degree of

M.D. (GENERAL MEDICINE) - BRANCH – I

MAY 2020

CERTIFICATE FROM THE DEAN

This is to certify that the dissertation entitled “A STUDY OF HYPONATREMIA AS A

PROGNOSTIC INDICATOR IN ACUTE MYOCARDIAL INFARCTION” is the bonafide work of Dr. N.C. VIVEK ANAND in partial fulfilment of the University regulations of The Tamilnadu Dr. M.G.R Medical University, Chennai, for the award of degree of Doctor Of Medicine (M.D) Branch- I -General Medicine under my direct supervision and guidance , during the academic period of 2017 - 2020

Prof.Dr. R. BALAJI NATHAN M.D.,

Dean,

Kanyakumari Government Medical College,

Asaripallam.-629201

CERTIFICATE FROM THE HOD

This is to certify that the dissertation entitled “A STUDY OF HYPONATREMIA AS A

PROGNOSTIC INDICATOR IN ACUTE MYOCARDIAL INFARCTION” is the bonafide work of Dr. N.C.VIVEK ANAND in partial fulfilment of the University regulations of The Tamilnadu Dr. M.G.R Medical University, Chennai, for the award of degree of Doctor Of Medicine (M.D) Branch- I -General Medicine under my direct supervision and guidance , during the academic period 0f 2017 – 2020.

Prof.Dr. PRINCE SREEKUMAR PIUS , M.D.,

HEAD OF DEPARTMENT, DEPT. OF MEDICINE,

Kanyakumari Government Medical College,

Asaripallam-629201.

CERTIFICATE FROM THE GUIDE

This is to certify that the dissertation entitled “A STUDY OF HYPONATREMIA AS A

PROF.Dr. SANKAR, M.D.,

DEPT. OF MEDICINE,

Kanyakumari Government Medical College,

Asaripallam.

DECLARATION

I, Dr. N.C. VIVEK ANAND, hereby declare that, I carried out this work entitled “A

STUDY OF HYPONATREMIA AS A PROGNOSTIC INDICATOR IN ACUTE

MYOCARDIAL INFARCTION” at Kanyakumari Government Medical College

Hospital, Asaripallam, under the guidance of Professor .Dr. PRINCE SREEKUMAR

PIUS M.D., Professor of Medicine, I also declare that this bonafide work has not been submitted in part or full by me or any others for any award, degree or diploma to any other University or Board either in India or abroad.

This is submitted to The Tamilnadu Dr. M.G.R Medical University, Chennai, in partial fulfilment of the University rules and regulations for the award of degree of Doctor of

Medicine (M.D) Branch- I-General Medicine.

Place: Asaripallam

Date:

Dr. N.C. VIVEK ANAND

ACKNOWLEDGEMENTS

I would like to express my sincere gratitude to Prof. Dr. R. BALAJI NATHAN, M.D.,

Dean, Kanyakumari Government Medical College, for having permitted me conduct this study and to use the hospital facilities at Kanyakumari Government Medical College

Hospital, Asaripallam.

I am greatly indebted to my beloved teacher Prof.Dr. PRINCE SREEKUMAR PIUS,

M.D., Professor and Head, Department of Medicine for allowing me to do this study in the Department of Medicine. I also express my sincere thanks to him for giving me proper guidance, protocol and immense help and encouragement in conducting this study.

I express my gratitude to Dr. SANKAR M.D., Assosciate professor, Department of

Medicine who immensely helped me in conducting this study.

I express my sincere and heartfelt gratitude to Dr. A. SRIVIDHYA., Dr. AMALAN

CHRISTUDAS, Dr. JOHN VINOJ, Dr. BRINDA DAVIS, Dr. PREETHI SHAHILA

Assistant professors in the Department of Medicine for their encouragement, kind guidance, constant support and cooperation in evaluating the patients.

I thank the Members, Secretary and Chairman of the Institutional Ethical committee,

Kanyakumari Government College hospital, Asaripallam.

I thank all the paramedical staff and other staff of the Kanyakumari Government Medical

College Hospital for all their help and cooperation in conducting this study.

I thank all my colleagues and friends for their constant encouragement and valuable criticism.

I am extremely thankful to all my family members for their continuous support. Above all I thank God Almighty for his immense blessings.

Last, but not least, my profound gratitude to all the patients, to whom I owe everything because this venture would not have been possible without them.

ETHICAL COMMITTEE APPROVAL

ANTI PLAGIARISM RECEIPT

CERTIFICATE

This is to certify that this dissertation work titled “ A STUDY OF HYPONATREMIA

AS A PROGNOSTIC INDICATOR IN ACUTE MYOCARDIAL INFARCTION” of the candidate Dr. N.C.VIVEK ANAND with registration number 201711710 for the award of M.D in the branch of GENERAL MEDICINE. I personally verified the urkund .com website for the plagiarism check. I found that the uploaded thesis file contains from the introduction to conclusion pages and the result shows 2 percentage of plagiarism in the dissertation

Guide & Supervisor sign with seal.

LIST OF ABBREVIATION

ACS – Acute Coronary Syndrome LV – Left Ventricle

ACE – Angiotensin Converting Enzyme MI – Myocardial infarction

AMI- Acute Myocardial Infarction NSTEMI – Non ST Elevation MI

ASMI – Anteroseptal Myocardial Infarction ODS –Osmotic Demyelination Syndrome

ALMI – Anterolateral Myocardial Infarction PCI – Percutaneous Coronary Intervention

ARF – Acute Renal Failure PTCA –Percutaneous transluminal

AV –Atrio Ventricular coronary angiogram

AWMI – Anterior Wall Myocardial Infarction RCA Right Coronary Artery

ATP – Adenosine Tri Phosphate STEMI – ST Elevation MI

AVP- Arginine Vasopressin SVC – Superior Vena Cava

CAD- Coronary Artery Disease TIMI – Thrombolysis in MI

CPK – Creatine Phosphokinase UA – Unstable Angina

CK-MB – Creatinine Kinase-MB WHO – World Health Organisation

CRP – C reactive protein

CSW –Cerebral Salt Wasting

CVA – Cerebro Vascular Accident

DM – Diabetes Mellitus

ECG- Electrocardiogram

EF – Election Fraction

GFR – Glomerular Filtration Rate

HT – Hypertension

LCA – Left Coronary Artery

LBBB – Left Bundle Branch Block

LVSD –Left Ventricular Systolic Dysfunction

CONTENTS S.No CONTENTS PAGE NO

1 INTRODUCTION 14

2 AIM OF THE STUDY 15

3 REVIEW OF LITERATURE 16

4 MATERIALS AND METHODS 69

5 STATISTICAL ANALYSIS 71

6 OBSERVATION AND RESULTS 72

7 DISCUSSION 86

8 CONCLUSION 93

9 BIBLIOGRAPHY 94

10 PROFORMA 99

11 MASTER CHART 113

12 ETHICAL COMMITTEE APPROVAL 8

13 ANTI PLAGIARISM RECEIPT 10

INTRODUCTION

EPIDEMIOLOGY:

Coronary artery disease is one of the most common cause of morbidity and mortality in both low income countries and developed countries. In the year 2012, globally27 cardiovascular diseases led to more than 17.5 million deaths. About 80% of these deaths occurred in low income/ middle income countries. According to WHO report in 2014,age adjusted cardiovascular disease mortality in India were 349 and 265 per 1,00,000 deaths in men and women respectively .The prevalence of CAD increased for past 30 years as per studies conducted in both rural and urban india1.

NSSO Survey (National Statistical Survey Organisation) in its 16th survey

(2004 to 2005) said that a total of 3,90,313 subjects evaluated .The prevalence of CAD

,found to be 7% in urban and 3% in rural population.

Hyponatremia is one of the common electrolyte disorder11 . In case of heart failure it is the main predisposing factor for cardiovascular mortality. Hyponatremia most frequently found after MI,which is due to neurohumoral activation22 seen in acute STEMI &HF

AIMS OF THE STUDY

1. To study the effect of hyponatremia in acute myocardial infarction.

2. To study the association between severity of hyonatremia and ejection fraction,

outcome in myocardial infarction.

3. To predict the importance of hyponatremia in acute Myocardial Infarction and

assess the significance of hyponatremia as an independent factor in predicting

short term mortality.

Review of literature

ANATOMY OF HEART:5

. Location

. Superior surface of diaphragm

. Left of the midline

. Anterior to the vertebral column, posterior to the sternum

. COVERINGS OFHEART:5

Pericardium – a double-walled sac around the heart composed of:

1. A superficial fibrous pericardium

2. A deep two-layer serous pericardium

a. The parietal layer lines the internal surface of the fibrous

pericardium

b. The visceral layer or epicardium lines the surface of the heart

c. They are separated by the fluid-filled pericardial cavity

. The Function of the Pericardium:5

1. Protects and anchors the heart

2. Prevents overfilling of the heart with blood

3. Allows for the heart to work in a relatively friction-free environment

ANTERIOR VIEW:

POSTERIOR VIEW:

ATRIA OF THE HEART:5

. Atria are the receiving chambers of the heart, Right atrium receives from superior

vena cava, inferior venae cava and coronary sinus whereas left atrium from

pulmonary veins

. Each atrium has a protruding auricle

. Pectinate muscles mark atrial walls

VENTRICLES OF THE HEART:

. Ventricles are the discharging chambers of the heart, Right ventricle pumps the

blood into pulmonary artery , while left ventricle pumps into the aorta

. Papillary muscles and trabeculae carneae muscles mark ventricular walls

FRONTAL SECTION:

Superior border5 – Right atrium,left atrium and great vessels forms the superior border.

Inferior border – Right and Left ventricles form the inferior border.

Right border – is slightly convex andlong, formed by right atrium and ventricle above and below respectively, it is in line with SVC.

Left border – major portion of left border is formed by left ventricle and smaller by left auricle.

Ligamentum arteriosum- It extends from the origin of left pulmonary artery and aortic arch.

Pulmonary artery: It divides into left and right branch inferior to aortic arch.Right branch passes below the arch.The branches are parallel and superior to the vein.

Arch of aorta- gets arched into 2 planes,superiorly and to theleft, the pulmonary artery bifurcates below it.

Azygos vein- begins from the abdomen and arches over the right pulmonary vessels and drains into superior vena cava.

Pulmonary veins- both left and right drains into left atrium.

BLOOD SUPPLY OF HEART:5

ARTERIAL SUPPLY OF HEART5

 Heart is supplied by coronary arteries

 Anatomically coronary arteries are not end arteries but functionally they behave

as end arteries.

 Coronary is vasa vasorum of ascending aorta.

AORTIC SINUSES

 Aortic sinuses – 1 Anteriorly & 2 Posteriorly.

 Anterior – Right coronary artery

 Posterior – no branch in the right side

 Left – Left coronary artery

COURSE OF RIGHT CORONARY ARTERY

 Passes forwards and to the right between pulmonary trunk and right auricle and

then downwards and to the right in anterior atrioventricular groove and winds

round the inferior border to reach the diaphragmatic surface of the heart.

 Passes upwards to left in posterior part of atrioventricular groove & reach crux of

heart ends by anastomosing with circumflex branch of left coronary artery

BRANCHES OF RCA5

 From 1st part

 Ventricular rami:

• Right conus artery

• Right anterior ventricular rami(3-4)

• Largest - right marginal artery

 Atrial rami: 3 groups

• Anterior, lateral and posterior groups

• One of this is sino – atrial nodal artery

From 2nd part:

 Right posterior ventricular rami forms the diaphragmatic surface of right ventricle

whereas Posterior interventricular branch forms diaphragmatic surface of right

and left ventricle

 Septal rami – undergo inverted loop and forms AV nodal artery which supplies

atrio - ventricular node.

 Right posterior atrial rami supplies the right and left atrium

AREA OF DISTRIBUTION OF RCA

• Right atrium

• Greater part of right ventricle

• Small part of left ventricle adjoining inter ventricular groove

• Posterior part of interventricular septum

• Conducting system of heart in 40%

From the left posterior aortic sinus of the ascending aorta, left coronary artery originates

COURSE OF LEFT CORONARY ARTERY

 Passes forwards and to the left between pulmonary trunk and left auricle, divides

into anterior interventricular artery & circumflex artery.

 Anterior interventricular artery which is the continuation of LCA descends in the

anterior interventricular groove upto the apex then winds round incisura apices

cordis ends on the inferior surface by anastomosing with Posterior interventricular

artery (RCA)

 Circumflex artery passes to the left in the left atrio ventricular groove and winds

round the left border of heart and occupies the posterior part of atrio ventricular

groove and ends by anastomosing with RCA .

BRANCHES OF LCA

 Anterior interventricular artery

 Circumflex artery

BRANCHES OF ANTERIOR INTERVENTRICULAR ARTERY

 Anterior ventricular rami to the right and left

 Right ventricular rami - Left conus artery

 Left ventricular rami - large Diagonal artery

 Septal rami

BRANCHES OF CIRCUMFLEX ARTERY

 Atrial & ventricular rami to the left and right atrium

 Sino-atrial nodal artery[in 35% people]

 Left marginal artery

 Circumflex artery continues as Posterior interventricular artery [in 10% people]

 Atrial branch communicates with similar branch of RCA (Kugels artery)

AREA OF DISTRIBUTION OF LCA5

Left atrium, most of left ventricle nearby the posterior interventricular groove, minor region of right ventricle near the anterior interventricular groove, part of left branch of atrioventricular bundle& anterior part of interventricular septum.

CARDIAC DOMINANCE

Posterior interventricular artery –arises from RCA- right dominance.

Posterior interventricular artery – arises from LCA- left dominance

MYOCARDIAL INFARCTION:1

CLASSIFICATION OF MYOCARDIAL INFARCTION:16

TYPE 1: Spontaneous Myocardial infarction.

TYPE 2:MI due to an Ischemic imbalance.

TYPE 3:MI resulting in death when biomarkers values are unavailable.

TYPE 4a: MI related to percutaneous coronary intervention (PCI).

TYPE 4b:MI related to stent thrombosis.

TYPE 5: MI related to Coronary Artery Bypass Graft

CORONARY RISK FACTORS FOR ASIAN INDIANS1

NON MODIFIABLE

 Increasing age  Male gender  Family history  Origin – ethnic

MODIFIABLE:

 Smoking  High blood pressure  hypercholesterolemia  Diabetes mellitus  Obesity and metabolic syndrome  Psychological stress  High calorie high fat diet  Physical inactivity.

PATHOPHYSIOLOGY OF MI:6

Endothelial injury and dysfunction

Increased vascular permeability,

Leucocyte adhesion and thrombosis

Accumulation of lipoproteins in vessel wall

(LDL and its oxidized form)

Monocyte adhesion to endothelium

This migrates to intima and transformation

Into macrophages and foam cells

Platelet adhesion

Factors are released from activated platelets,

Macrophages, vascular wall

Smooth muscle cell recruitment from tunica media

smooth muscle cell proliferation and

recruitment of T cells

lipid accumulation both extracellularly and

within cells(macrophages and smooth muscle cell)

This forms the atheromatous plaque6 which undergoes acute change and leads to

Intraplaque haemorrhage, erosion or ulceration, rupture or fissuring.

Mediators are released from platelets which leads to Vasospasm within minutes, thrombus expand & complete to occlude the vessel lumen. This leads to Myocardial

Infarction.

Time of onset of key events in Ischemic cardiac myocytes:

EVENTS TIME

 Onset of ATP depletion within seconds

 Loss of contractility <2 mins

 ATP reduced

To 50% of normal 10 mins

To 10% of normal 40 mins

 Irreversible cell injury 20 40 mins

 Microvascular injury >1 hr

SIZE OF THE INFARCTION:

 Infarction involving all 3 layers of the myocardium is called as

transmural infarction

 It leads to both Systolic and diastolic dysfunction

 Smaller infarct: hypokinesia

 Larger infarct : akinesia

LOCATION OF INFARCTION:2

Myocardial infarction of the heart can be located

1) anterior,

2) septal,

3) lateral,

4) inferior and

5) posterior walls of the left ventricle.

UA vs NSTEMI vs STEMI14

Unstable Angina NSTEMI STEMI

Pathology Non occlusive Non Complete thrombotic

occlusive thrombus occlusion thrombus

ECG changes Non specific ST ST elevation

ECG depression+/-

T inversion

Cardiac Normal Cardiac Elevated Elevated Cardiac biomarkers Cardiac Biomarkers Biomarkers Biomarkers

Treatment LOADING DOSE LOADING DOSE strategy (Antiplatelets, Statins) (Antiplatelets, Statins)

Anticoagulants Anticoagulants

Fibrinolysis contraindicated Immediate Fibrinolysis/

PPCI

Clinical approach to ACS

• History

• Clinical examination

• Electrocardiography

• Cardiac enzymes

• Echocardiography

DIAGNOSTIC TESTS:1

ELECTROCARDIOGRAM2

 An Electrocardiogram identifies the location of infarction . T-wave inversion or ST segment depression in ecg suggests myocardial ischaemia.  The inverted T wave in ischemia is symmetrical, narrow, whereas asymmetrical T wave inversion seen in hypertrophy of the heart.  Depression of ST segment more than or equal to 1 to 2 mm or more in contiguous limb or chest leads respectively indicate myocardial ischemia INJURY  It starts from the subendocardial layer of the heart and moves towards the epicardium.. it should be stopped early to avoid a transmural infarction.  In ECG, the characteristic change of acute myocardial injury is the presence of ST segment elevation.  In STEMI, the ST segments elevation is seen in the leads of injured myocardium. The elevation has a downward concavity or coving shape which merges with the T wave21

INFARCTION

If the myocardial injury is not treated earlier. Acute STEMI occurs,

There are five phases of ECG changes in stemi2

1 .HYPERACUTE T WAVES

2 . HYPERACUTE T WAVES WITH ST ELEVATION

3 . DIMUNITION OF SIZE OF R WAVES

4 . DEVELOPMENT OF PATHOLOGICAL Q WAVES

5 . INVERSION OF T WAVES

ST elevation >1 mm in any two or more contiguous limb or chest leads. ST segment is measured at the J point. It is the junction between the terminal portion of QRS and the beginning of ST segment . T-P segment is the baseline to which the ST segment is compared

NEW ONSET LBBB:2

The presence of LBBB in ECG cover changes in STEMI. If the LBBB is new or if there is no previous ECG to substantiate LBBB with symptoms of acute myocardial ischaemia it is an indication to thrombolyse. There is a criteria to detect

STEMI in LBBB namely sgarbossa

PATTERNS OF ST ELEVATION:2

1 . coved or convex upwards

2 . horizontal or plateau

3 . oblique resembling a ski-slope

4 . tomb stone st segment is at the same level with R wave

4 . concave

Reciprocal ST depression in one of the important characteristics of STEMI which differentiates it from other causes of st elevation2

 Take ECG early: Target first Medical Contact to ECG time < 10 minutes

 Initial ECG not diagnostic  Repeat ECG after 15 and 30 minutes interval.

 Ask for any earlier ECG: Comparison and identify early or subtle ECG changes

Criteria for ST changes in ECG

ST Elevation :

 ST elevation of ≥0.1 mV in two contiguous leads (except V2-V3) at the J point

 Leads V2-V3 it should be atleast ≥0.2 mV in men ≥40 years and ≥0.25 mV in

men <40 years and ≥0.15 mV in women

ANTERIOR WALL MI:

INFERIOR WALL MI:

RIGHT VENTRICULAR INFARCTION :

ST DEPRESSION or NSTEMI1 occurs when there is incomplete occlusion of the vessel leading to reduced blood flow leading to myocardial necrosis it is differentiated from UA by elevation of cardiac biomarkers

Cardiac biomarkers are elevated if there is myocardial necrosis which is not seen in

UNSTABLE ANGINA

ECG changes include horizontal or down sloping ST depression ≥0.05 mV in two contiguous leads or T-wave inversion ≥0.1 mV in two contiguous leads.

Echocardiography in ACS:25

Normal LV wall motion

GLOBAL LV HYPOKINESIA:

RWMA IN INFERIOR WALL MI:

RWMA IN ANTERIOR WALL MI:

Laboratory Tests

CARDIAC BIOMARKERS1

1 . Myoglobin

2 . CPK / CKMB

3 . Troponin T and I

Myoglobin elevates within 1 to 2 hours , peaks in about 3 to 15 hours one of the earliest marker but it is also seen in skeletal muscle it is not confirmatory. Creatine kinase has two isoforms CK-MB 1 and CK –MB 2 in acute MI CK-MB2 level rises more than the other isoforms it elevates within 4- 8 hrs , peaks in about 12 to 28 hours and normalises after 48 to 72 hours.1 Troponin I rises in three hours peaks within 14 to 18 hours and persistently elevated for about 5 to 7 days, Troponin T rises in three to five hours and remains for about 10 to 14 days .cardiac specific troponins have amino acid sequences different from the skeletal muscle forms of these proteins. These are now the preferred biomarkers

NOVEL CARDIAC BIOMARKERS:25

I) BIOMARKERS OF MYOCARDIAL INJURY:

 Cardiac Troponin

 High sensitivity cardiac Troponin (hs crn)

 Heart type fatty acid binding protein.

II) BIOMARKERS OF INFLAMMATION:

 High sensitivity CRP

 Growth differentiation factor

 Fibrinogen

 Uric acid.

III) BIOMARKERS OF PLAQUE INSTABILITY OR RUPTURE:

 Pregnancy Assosiated PlasmaProtein A (PAPP A)

 Myeloperoxidase(MPO)

 Matrix Metalloproteinase (MMPs)

IV) BIOMARKERS OF PLATELET ACTIVATION:

 Lipoprotein associated phospholipase A2

 SecretoryPhospholipase A2

 Soluble CD40 ligands.

V) BIOMARKERS OF NEUROHUMORAL ACTIVATION:

 Copeptin

 Midregional pro adreno medullin

VI) BIOMARKERS OF MYOCARDIAL DYFUNCTION ON STRESS:

 Natriuretic peptides.

 ST 2

 Endothelin I

 Galectin 3

 Neurgulin 1

RELEASE OF CARDIAC MARKERS AFTER MYOCARDIAL INFARCTION:

MANAGEMENT:1

EARLY MANAGEMENT

After the diagnosis of myocardial infarction treatment includes

1 . control of cardiac discomfort

2 . rapid identificationof patients who are candidates for urgent reperfusion

3 . triage of lower risk patients to appropriate location in hospital

4 . avoid inappropriate discharge

Treatment includes bed rest , supplemental oxygen 2-4L/min, sublingual

nitroglycerine upto 3 doses 0.4 mg at every 5 min interval & morphine.

 Loading dose :

 Aspirin 300 mg (Chewable non–enteric-coated)

 Clopidogrel 300 mg (if age <75 yrs), 75 mg (if age >75yrs)

 Atorvastatin 80 mg or Rosuvastatin 40 mg

 Reperfusion is the cornerstone of STEMI Management

 Reperfusion should be instituted at the earliest in all patients

 Early reperfusion saves more lives

The most effective therapy is Primary PCI

Reperfusion is assessed using TIMI flow grade1

 TIMI 0 – Absence of any antegrade flow beyond a coronary occlusion

 TIMI 1- flow crosses beyond the occlusion , but filling of distal coronary bed

incomplete

 TIMI 2 – flow is delayed or sluggish , distal bed is completely filled

 TIMI 3 – flow is normal, with distal coronary bed is completely filled

Modes of Reperfusion

1. Thrombolysis

2. Primary Per-cutaneous Intervention

3. Pharmaco-invasive Strategy

THROMBOLYTIC THERAPHY:14

 Thrombolytic drug given lyses coronary thrombi by converting plasminogen to

plasmin and provides maximal benefit when given within the first 3 hours after the

onset of symptoms Significant benefit is obtained if therapy is given up to 12

hours after onset of symptoms.

Contraindications1

ABSOLUTE C.I RELATIVE C.I

1.Prior hemorrhagic stroke at any time; 1. Severe uncontrolled hypertension on

other strokes presentation (blood pressure >180/110

or cerebrovascular events within 1 year mm Hg)

2.Known intracranial neoplasm 2.History of prior cerebrovascular

3.Active internal bleeding (excluding accident

menses) 3.Current use of anticoagulants in

4.Suspected aortic dissection therapeutic doses (international

normalized ratio [INR] ≥2:3); known

bleeding diathesis

4.Recent trauma (within 2–4 weeks),

including head trauma

or traumatic or prolonged (>10 minutes)

cardiopulmonary resuscitation (CPR) or

major surgery (<3 weeks)

5.Noncompressible vascular punctures

6.Recent (within 2–4 weeks) internal

bleeding

7.For streptokinase/anistreplase: prior

exposure (especially within 5 days to 2

years) or prior allergic reaction

8.Pregnancy

9.Active peptic ulcer

THROMBOLYTIC AGENTS:14

• Streptokinase:

– 1.5 million units intravenous infusion over 60 minutes

– Can cause allergic reactions / hypotension

– Avoid reuse within 5 days to 6 months [lesser efficacy / more allergic

reactions]

• Tenecteplase: [TNK]14

Single bolus injection adjusted to weight.

< 60 Kg 60-69 kg 70-79 Kg 80-89 Kg > 90 kg

30 mg 35 mg 40 mg 45 mg 50 mg

– UFH: Given in a dose of 60 units / kg IV bolus [ maximum dose of 4000U]

before TNK and 12 U/kg/ hr infusion of UFH [ maximum dose of 1000U /

hr] after TNK

– Enoxaparin: Given at a dose of 30 mg IV bolus before TNK and enoxaparin

1mg/kg bid 15 minutes after TNK.

 RETEPLASE:

– Double Bolus of 10 U + 10 U IV injections given 30 minutes apart

Adjunctive Antithrombotic Therapy to Support Reperfusion with thrombolysis

Unfractionated Heparin 21

• IV bolus of 60 units/kg upto maximum of 4000 units followed by an infusion of

12 units/kg/ hr to a maximum, 1000 units initially adjusted to maintain the APTT

at 1.5-2.0 times control for 48 hr or until revascularization

Enoxaparin: 14

• Age < 75 yr: 30-mg IV bolus followed in 15 by 1 mg/kg after 15 mins

subcutaneously for every 12 hr (maximum, 100 mg for the first 2 doses)

• Age ≥ 75 yr: no bolus dose to be given, 0.75 mg/kg subcutaneously every 12 hr

(maximum, 75 mg for the first 2 doses)

SUCESSFUL LYSIS:1

ECG criteria:

ST segment resolution of more than 50%in ECG taken 90 minutes of after thrombolysis.

Accelerated idioventricular rhythm seen in cardiac monitor

CLINICAL CRITERIA: Improvement of chest pain & hemodynamic status.

FAILED LYSIS:

ECG CRITERIA:

ST segment resolution <50% in the ecg taken 90 mins after fibrinolysis.

CLINICAL CRITERIA:

No significant improvement of chest pain and hemodynamis status.

PRIMARY PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY:

PTCA1 was introduced by Andreas gruentzig in 1977 which is an alternative to

CABG , there are two types of stents , it is of 3 types primary , rescue and urgent PCI

BARE METAL STENT

DRUG ELUTING STENTS – which slowly release antiproliferative agents drugs

used are paclitaxel, sirolimus, everolimus, biolimus3,4

Successful procedure , stenosis is reduced to less than 20% of diameter narrowing

COMPLICATIONS:3

1. Death ( 0.1 – 0.3% of elective cases)

2. Large myocardial infarction

3. Stroke

4. Stent thrombosis

In order to avoid complications prior to procedurepatients are given loading dose of antiplatelets , and after procedure dual antiplatelet therapy is given for a period of six months to 1year

 Continue Dual Antiplatelet Therapy for at least 1 year period

 Aspirin 150 mg daily ,Clopidogrel: 75 mg daily or Prasugrel: 10 mg daily or

Ticagrelor: 90 mg twice a day

 Avoid prasugrel if

 Weight < 60 kg

 Age > 75 years

 H/o bleeding or CVA

Beta blockers1 should be started with 24 hrs unless otherwise contraindicated, acute i.v beta blockers improves myocardial oxygen demand mismatch , reduces the pain , reduces the size of the infarct, reduces the occurrence of arrhythmias.

ACE inhibitors1 reduces the mortality and morbidity in acute STEMI , patients who are benefitted includes high risk patients like elderly, who have anterior myocardial infarction, reduced LV function, short term benefits also seen in stable patients, it prevents the ventricular remodelling effectively, prior to its administration contraindications are to be checked

In patients with progressive heart failure, pulmonary edema and cardiogenic shock the hemodynamic status of the patients is monitored using pulmonary artery catheter

OTHER DIAGNOSTIC TESTS include echocardiogram , stress testing (i) exercise stress

(ii) drug stress test using dobutamine and results are interpreted in a monitor, coronary angiogram, radionuclide imaging.

COMPLICATIONS:

Mechanical Complications1 Electrical Complications

 Ventricular septal rupture  Ventricular fibrillation

 Left ventricular free wall rupture  Ventricular tachycardia

 Papillary muscle rupture with acute  Supraventricular tachydysrhythmias

mitral regurgitation  Bradyarrhythmias

 Atrioventricular block (first, second,

or third degree)

OTHERS:

 Systolic & diastolic dysfunction

 LV aneurysm

 Recurrent chest pain

 thromboembolism

NOT ALL ST ELEVATION ARE ACUTE MI:2

Electrolyte abnormality (Hyperkalemia)

Left Bundle Branch Block

Early repolarisation syndrome

Left Ventricular Hypertrophy

ARRYTHMIA,Aneurysm of LV,Aortic dissection

Takotsuba disease,Traumatic brain injury,

Infarct,Injury,Inflammation

Osborn waves (hypothermis or hypercalcemia)

Coronary vasospasm

HYPONATREMIA11

Hyponatremia is defined as plasma Na+ levels less than 135 mEq/L10. it is commonly seen in hospitalized patients around 22%

PATHOPHYSIOLOGY:11

Response of arginine vasopressin differs in patients with hyponatremia as a function of their extracellular fluid volume

It is of three types

1. hypovolemic

2. euvolemic

3. hypervolemic

Hyponatremia is clinically an important entity because

SEVERITY:.

3MILD : serum sodium concentration130 135mmol/L

MODERATE: serum sodium concentration 125 129mmol/L

PROFOUND: serum sodium concentration <125 mmol/L

Acute hyponatremia11 is seen documented less than 48 hrs causes include iatrogenic like colonoscopy preparation, hypotonic fluids with cause of increased vasopressin, post operative premenopausal women, glycine irrigation in TURP surgery

CHRONIC: documented as lasting >48 hr or duration cannot be classified.

CLINICAL FEATURES:

MILD MODERATE SEVERE

Anorexia Personality changes Drowsiness

Headache Muscle cramps Diminished reflexes

Nausea Confusion Convulsions

Vomiting Ataxia Coma

Lethargy Muscular weakness Death

DIAGNOSTIC APPROACH:1

TREATMENT OF HYPONATREMIA:11

There are three important things to be looked into before going into treatment

1. presence of symptoms determines the urgent need for treatment

2. chronic hyponatremia if treated rapidly are at increased risk of osmotic

demyelination syndrome

3. response to treatment like isotonic and hypertonic saline , AVP antagonists are

highly unpredictable and serial monitoring is needed.

Mainstay of treatment is based on the cause, which includes

Fluid restriction based on electrolyte free water excretion calculated by urine to

plasma electrolyte ratio

Hypokalemia should be corrected

Patients with SIADH are given a combined therapy of oral furosemide 20 mg and oral

salt tablets , if there is no response to treatment demeclocycline is given

Other drugs are tolvaptan and conivaptan

• Na deficit = 0.6 x body weight x (target plasma Na+ cocncentration –

starting plasma Na+ concentration)1

RAPID CORRECTION if there is acute severe hyponatremia to prevent brain swelling or symptomatic hyponatremia to alleviate symptoms

Rate of correction should be slow in chronic hyponatremia to avoid ODS, the target rates should be lowered in patients at risk of ODS like hypokalemia and alcoholics23

If the plasma sodium is overcorrected desmopressin , free water , 5% dextrose to be given

SIADH Vs CEREBRAL SALT WASTING:

SIADH CSW

Serum Na ↓ ↓

ECF volume Normal ↓

Urinary sodium ↑ ↑↑

Urine osmolality ↑ ↑

Urine volume N or ↑ ↑

Serum urate ↓ Normal or ↓

Urine urate ↑ Normal or ↓

INDICATIONS FOR 3% NACL:

• hyponatremia with symptoms& acute severe cases

NEUROHUMORAL ACTIVATION AFTER MYOCARDIAL INFARCTION:22

Acute myocardial infarction is followed by several metabolic changes in patients. Plasma

Insulin levels falls initially then return back to normal , plasma concentration of glucose, catecholamines, glycerol, cortisol and cyclic AMP increases following MI.

According to the study if the sodium level is found to be< 130mEq/L in patients admitted in coronary care unit then the mortality is found to be higher.7

Due to sudden development of left ventricular dysfunction or pain ,stress and nausea, or administration of diuretics in acute myocardial damage there is non osmotic release of vasopressin.9

It is the common cause of hyponatremia in adults. serum osmolality in these patients does not correlate with level of vasopressin, even other hormones19 renin or norepinephrine also rises along with vasopressin, this proves importance of non osmotic mechanism involvement.

Arterial underfilling due to carotid baroreceptors in addition to increased messenger RNA expression in hypothalamus are found to be the reason for non osmotic release of vasopressin.

The Vasopressin regulated water is up regulated in collecting duct in patients with heart failure due to renal effect of the hormone.

Renin angiotensin system is then activated & catecholamine19 production is increased in patients with myocardial infarction which further aggravates hyponatremia.

The decline in renal water excretion due to the above factors reduces GFR and there is delivery of tubular fluid to diluting segment of nephron.

The ventricular remodelling occurs after the acute MI leads to sudden death due to arrhythmia & ventricular dysfunction, remodelling leads to ventricular enlargement leading to heart failure & sudden death due to pump failure.

A STUDY OF HYPONATREMIA AS A PROGNOSTIC INDICATOR IN ACUTE

MYOCARDIAL INFARCTION

MATERIALS AND METHODS

100 patients admitted to the ICCU and Department of Internal Medicine, KGMC,

Asaripallam between March 2019 to September 2019 with Acute Myocardial Infarction

(STEMI ) were studied in a prospective manner.

STUDY DESIGN: PROSPECTIVE COMPARATIVE STUDY

Patients were grouped into two

GROUP 1: Normal Sodium levels

GROUP 2: Serum Sodium less than 135mEq/L

STUDY PARTICIPANTS:

INCLUSION CRITERIA

1. All adult cases of acute myocardial infarction (STEMI) as per the above definition;

EXCLUSION CRITERIA

 Any history of rheumatic heart disease

 Infective endocarditis

 Cardiomyopathy

 Old MI

 clinical conditions which causes syndrome inappropriate of ADH secretion

 patients with renal failure ( ARF and CRF )

 Acute and chronic liver failure

 Acute gastroenteritis

 Malignancy

 Adrenal insufficiency

 Hypertensive patients on diuretics

 patients with other electrolyte abnormalities

Patients who fulfilled the above Inclusion criteria and not with any of the above

Exclusion criteria were included as a participant.

METHODS:

All patients were taken 12 lead ECG, right sided and posterior leads were taken for

Inferior wall MI.

Study data will be collected by detailed history, clinical examination, and daily serum electrolytes and ECHO

MEASUREMENT OF SERUM SODIUM:

serum Sodium concentration was determined by using an Ion selective electrode auto analyzer (Roche OMNIC). Hyponatremia is defined as sodium levels less than

135mEq/L.

STUDY PROTOCOL:

Approval for this study was obtained from the Research and Ethical committee Of

Kanyakumari Medical college.Written and Informed consent obtained from all patients.

Data retrieved from patients by direct Interrogation and examination.

STASTICAL ANALYSIS:

All the data were analysed with SPSS software (version 21.0)

Variables are compared using

PEARSON CHI SQUARE TEST

INDEPENDENT SAMPLE T TEST

OBSERVATION AND RESULTS

TABLE NO1 AGE DISTRIBUTION OF CASES

AGE Group

<40 41-50 51-60 >61 Total

Group Na>135 3 9 11 27 50

Control Na<135 3 7 24 16 50

Total 6 16 35 43 100

GRAPH 1 AGE DISTRIBUTION

30 27 24 25

20 16 15

11 Frequency 10 9 7

5 3 3

0 <40 41-50 51-60 >61 Na>135 Na<135

In our study majority of cases were in age group of > 61.Minimum age was

30,Maximum age was 80.

SEX DISTRIBUTION OF CASES

TABLE 2 SEX DISTRIBUTION OF CASES

SEX

Male Female Total

Group Control Na>135 31 19 50

Na<135 31 19 50

Total 62 38 100

In our study 62% were males and 38% were females. Males are more prone for ischaemic heart diseases.

GRAPH 2 SEX DISTRIBUTION OF CASES

35 31 31 30 25 19 19 20 15 Frequency 10 5 0 Male Female Na>135 Na<135

RISK FACTORS

TABLE 3 SHOWING DISTRIBUTION AMONG DIABETES MELLITUS

No Yes Total

Group Control Na>135 32 18 50

Na<135 26 24 50

Total 58 42 100

GRAPH 3 SHOWING DISTRIBUTION AMONG DIABETES MELLITUS

35 32 30 26 24 25 18 20

15 Frequency 10

0 No Yes Na>135 Na<135

TABLE 4 SHOWING DISTRIBUTION AMONG HYPERTENSION

No Yes Total

Group Control Na>135 27 23 50

Na<135 22 28 50

Total 49 51 100

GRAPH 4: SHOWING DISTRIBUTION AMONG HYPERTENSION:

120

100 100

49 51 50 Frequency 40 27 28 27 22 23 23 20

0 No Yes Na>135 Na<135 Group Control Total

SHOWING DISTRIBUTION AMONG SMOKERS:

SMOKING

No Yes Total

Group Control Na>135 29 21 50

Na<135 26 24 50

Total 55 45 100

GRAPH SHOWING DISTRIBUTION AMONG SMOKERS:

35 29 30 26 24 25 21 20 15

Frequency 10 5 0 No Yes Na>135 Na<135

48% were Diabetic, 56% were Hypertensive, 48% were Smokers among patients who presented with Hyponatremia on admission. Among patients who had normal sodium levels only 36% were Diabetic, 46% were Hypertensive,42% were smokers. The proportion of Diabetic, Smokers, hypertensives were more among patients with

Hyponatremia.

TABLE 4 SHOWING TYPE OF STEMI

DIAGNOSIS

ALMI ASMI AWMI IPWMI IRVMI IWMI Total P value

Group Na>135 2 4 31 2 2 9 50

Control Na<135 2 3 36 1 0 8 50 0.714

Total 4 7 67 3 2 17 100

GRAPH 4 SHOWING DISTRIBUTION OF TYPE OF STEMI

35 29 30 26 24 25 21 20

15 Frequency

0 No Yes Na>135 Na<135

In our study , Anterior wall MI predominated followed closely by Inferior wall

Myocardial Infarction.

TABLE 5 :EJECTION FRACTION:

Std.

Group Control N Mean Deviation P value

EF Na>135 50 53.42 7.76 <0.0001 Na<135 50 45.96 10.13

<50 >51 Total P value

Group Na>135 8 42 50

Control Na<135 33 17 50 <0.0001

Total 41 59 100

GRAPH 5: EJECTION FRACTION

45 42 40 33 35

20 17 Frequency 15 8 10

0 <50 Na>135 Na<135 >51

The Ejection Fraction was lower among patients presented with hyponatremia/ developed hyponatremia within 72 hrs was compared with patients with normal sodium levels which was found to be statiscally significant (p<0.0001)

TABLE 6 : SHOWING KILLIP CLASSIFICATION:

KILLIP CLASS

I II III IV Total P value

Group Na>135 38 9 3 0 50

Control Na<135 31 11 7 1 50 0.319

Total 69 20 10 1 100

KILLIP CLASS P value III IV

Na>135 3 0 Group Control Na<135 7 1 0.319

Total 10 1

GRAPH 6:SHOWING KILLIP CLASS

40 38 35 31 30 25 20 15 Frequency 9 11 7 10 3 5 0 1 0 I II III IV Na>135 Na<135

Killip class I is found in 38(76%) patients in normal sodium levels compared to 31(62%) in hyponatremia groups, class II 9(18%) patients compared to 11 (22%) patients in hyponatremia, class III is seen in 3(6%) patients compared to 7(14%) patients in hyponatremic patients and class IV seen in only one patients with hyponatrmia whose sodium level is <130 so lower the serum sodium levels higher the killip class

TABLE 7:SHOWING INHOSPITAL COMPLICATIONS:

IN HOSPITAL COMPLICATIONS

ACUTE P

2*HB MR CCF CHB PE Vfib VT Total value

Group Na>135 0 1 0 0 2 0 0 3

Control Na<135 2 1 2 2 1 1 1 10 0.377

Total 2 2 2 2 3 1 1 13

GRAPH 6:SHOWING INHOSPITAL COMPLICATION:

3 2 2 2 2 2

2 1 1 1 1 1

1 Frequency 1

0 2*HB ACUTE CCF CHB PE Vfib 7.00 MR Na>135 Na<135

The hospital complications were more among patients with hyponatremia.

TABLE 7 :SHOWING OUTCOME:

OUTCOME

A D Total P value

Group Na>135 41 9 50

Control Na<135 31 19 50 0.026

Total 72 28 100

GRAPH 7:GRAPH SHOWING OUTCOME:

35 30 30 25 20 15

Frequency 10 9 10 5 1 0 A D Na>135 Na<135

The patients who developed hyponatremia had higher percentage of mortality than the patient with normal sodium.

TABLE 8:TABLE SHOWING FOLLOWUP PERIOD

FOLLOWUP PERIOD

Acute

Nil lvf ccf Chb PE Total P value

Group Na>135 46 1 1 1 1 50

Control Na<135 45 2 0 2 1 50 0.795

Total 91 3 1 3 2 100

GRAPH 8:FOLLOWUP PERIOD

50 46 45 45 40 35 30 25

20 Frequency 15 10 2 2 1 5 1 1 1 1 0 Nil Acute lvf ccf chb PE Na>135 Na<135

P value

STEMI 0.714

EJECTION FRACTION <0.0001

KILLIP CLASS 0.319

IN HOSPITAL COMPLICATIONS 0.377

OUTCOME 0.026

FOLLOW UP 0.795

DISCUSSION

In acute MI, hyponatremia - a marker that incorporates different prognostic values, including hemodynamic alterations, severe LVSD based on the extent of neurohormonal activation. 19

Goldberg A66 et al12 had studied 1047 patients with acute STEMI, without any past history of cardiac disease. It was found that hyponatremia on admission or early development of hyponatremia associated with higher % of short term mortality.

AGE DISTRIBUTION IN MYOCARDIAL INFARCTION

In our study 100 pateints with acute ST elevation MI, mean age was found to be 52.4 ±

12.8 .Majority of the cases were in the age group of >61years . In the study conducted by

Aziz M et al , the mean age was found to be 57.28±6. In Goldberg”s13 study the mean age group was 61±12. Indians are prone to develop MI at an early age

SEX DISTRIBUTION IN MYOCARDIAL INFARCTION

In our study, 62% were males and 38% were females. Similar results were found in a studies conducted by Goldberg12 A66 et al, Aziz M et al. These studies shows males are more prone to develop Myocardial Infarction.

RISK FACTORS IN MYOCARDIAL INFARCTION

In our study 45 patients were smokers, 51 were hypertensive and 42 were diabetic. Killip and Norris et al 68in the Framingham heart study said that diabetes and smoking increases the risk of death in MI. In GISS-2 trial69, out of 11483 hypertensive MI patients,3306 patients died. Our study reveals that Diabetes, smoking and Hypertension are important risk factors in predicting the prognosis and determining mortality.

HYPONATREMIA IN ASSOCIATION WITH AGE

Patients with hyponatremia on admission belonged to a higher age (51-60) mean age (56 plus or minus 4) when compared to patients with normal sodium levels who belonged to younger age (40-50) and >61 groups. 50 – 60 more common group with hyponatremia and higher mortality. In the study conducted by Goldberg A, Hammerman H et al,13 mean age group among patients with normal sodium levels was 61±13 and hypontremia individuals was 63±13.

HYPONATREMIA IN ASSOCIATION WITH SEX

Males constituted majority of the cases in acute MI .There were 31 males(62%) in both patients with normal sodium levels and hyponatremia. The higher male ratio may be due to number of females were less in the study. Similar results were also found in Goldberg

A , Hammerman H et al13,Aziz M et al “s study.

HYPONATREMIA IN ASSOSIATION WITH DIABETES,SMOKING AND

HYPERTENSION.

Among patients with normal sodium levels 36% were diabetic, 42% were smokers and

46% were hypertensive.In patients who presented with hyponatremia on 48% were diabetic,48% were smokers,56% were hypertensive. Thus hyponatremia was more common among those with diabetes, smokers, and hypertensive individuals.This is in accordance to the studies conducted by Goldberg A , Hammerman H et al13, Aziz M et al,Hilis et al., and sangumani etal15 study in Madurai medical college in jebmh

HYPONATREMIA IN ASSOSIATION WITH ANTERIOR WALL INFARCTION

The incidence of anterior wall MI among patients with normal sodium levels and hyponatremia are 31(62%) and 36(72%)respectively. It is higher than the results of golberg”s study which was 37% and ,49% respectively. Studies by Krumholz et al35,Hillis et al also showed, hyponatremia was common in anterior wall infarction.

The study conducted by sangumani etal15 from Madurai Medical college showed that

Anterior wall MI had greater incidence of Hyponatremia when compared to Inferior wall

MI.

HYPONATREMIA IN ASSOSIATION WITH KILLIP CLASS :

31(62%) of patients with hyponatremia belonged to killip class I and 11(22 %) belonged to killip class II and (7)14 % belonged to class III (1)2% belong to killip class IV. Killip class III and IV found more in patients with hyponatremia than normal sodium group.

Our results were similar to the studies done by Hillis et al , Kerry Lee and Eric J Topol et al, and Goldberg A et el.13

HYPONATREMIA IN ASSOSIATION WITH EJECTION FRACTION

The mean ejection fraction was lower in patients who presented with hyponatremia

(mean EF 45.96) compared to those patients with normal sodium levels(mean EF

53.42%) which is found to be statistically significant(<0.0001). Our results were similar with the study conducted by Goldberg A ,Hammerman H et al12, were the mean EF in patients with normal sodium levels , hyponatremia during admission and hyponatremia within 72 hours were 47%,42% and 42% respectively.

Sangumani et al15 also showed the same results.

HYPONATREMIA IN ASSOSIATION WITH MORTALITY

The overall mortality rate in our study was 28(28%).Mortality among patients with normal sodium levels was 9(18 %) ,mortality with hyponatremia was 19(38%), which is statistically significant(0.026).

In study done by Goldberg et al,12 the mortality rate was 10% . Mortality among patients with normal sodium levels were 6.2%.With hyponatremia on admission mortality were

20 %, with hyponatremia within 72 hours mortality were 17 % . In comparsion with above study, our study had higher mortality in patients with hyponatremia on admission and within 72 hours than the mortality in patients with normal sodium levels

In study done by Sidhnath singh from Ranchi University says that serum sodium was stastically significant in determining mortality.

RELATIONSHIP BETWEEN SEVERITY OF HYPONATREMIA AND

MORTALITY

11 patients had a sodium level of <130meq/l and out of which 10 patient died .In comparison with other studies by Rahman et al Goldber A, Aziz M et al and our study had a higher mortality rate.

From our study it is found that patients with hyponatremia were males belonging to a

,had smoking history, diabetes,hypertension, , lower ejection fraction and anterior infarction . This is in accordance to the studies conducted by Aziz M et al ,Goldberg

A,Hammerman H et al,.

It was found that serum sodium levels was statistically significant in determining mortality

This is compared to 39 patients with sodium values >130mEq/L out of which 9 deaths.

This shows that more severe the hyponatremia more poorer the prognosis. Thus sodium can be used as an independent marker and predictor of morbidity and mortality.

CONCLUSION:

1. STEMI occurs earlier among Asians.

2. Smoking, Diabetes, Hypertension and hypercholesterolemia are the major risk

factors in acute Myocardial Infarction.

3. Hyponatremia (i.e. sodium levels < 135 mEq/l) on admission or within 72 hrs have

poor prognosis.

4. More severe the Hyponatremia and more poorer the prognosis.

5. Low sodium levels are more common among males and those with other risk

factors.

6. Anterior wall MI patients are more prone for Hyponatremia and lower ejection

fraction than those with normal sodium levels.

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A STUDY OF HYPONATREMIA AS A PROGNOSTIC INDICATOR IN ACUTE

MYOCARDIAL INFARCTION

PROFORMA

NAME: IP. NO:

AGE: DOA:

SEX: DOD:

OCCUPATION:

RELIGION:

MARITAL STATUS:

ADDRESS:

TELEPHONE NO:

STATUS AT DISCHARGE:

PRESENTING COMPLAINTS:

I. HISTORY OF PRESENTING ILLNESS:

A. CHEST PAIN:

 Site: Precordial/ Restrosternal Epigastric/ Shoulder/ Neck

 Time of onset:

 Nature: Squeezing/ Crushing/ Compressive/ Tightness

 Radiation: Arm/ Back/ Epigastric/ Neck

 Frequency:

 Severity

 Aggravating Factor:

 Relieving Factor:

 Associated sweating:

B. BREATHLESSNESS:

 Onset: Sudden/ Gradual

 Grade: I/II/III/IV

 H/O Orthopnea: Yes/ No

 Wheeze: Present/ Absent

 H/O PND: Yes/No

Associated symptoms

100

C. COUGH

Onset: acute insidious

 Productive/ Non Productive

 Sputum: Quantity

Quality

 Colour

 Postural Variation

 Haemoptysis: Yes/ NO

D. PALPITATION

 Onset: Acute/ Insidious

 Duration

 Nature: intermittent/ continuous

 Aggravating Factors: Exertion/ Excitement

 Relieving Factors

E. PRESYNCOPE/ SYNCOPE

 Related to exertion : Yes

 Postural relation : Erect Supine

 Frequency : Isolated Frequent

 Loss of consciousness : Yes No

101

 Others

F. SWELLING OF LEGS/ FACE

 Onset: Acute/ Insidious

 Duration:

 Associated with pain: yes/ No

 Diurnal Variation: Yes /No

G. NAUSEA /VOMITING

H. MISCELLANEOUS Present Absent

 General weakness/ Fatigue

 Altered sensorium

 Oliguria

 Convulsion

 Others

II. PAST HISTORY

 Past history : Present/Absent

 Duration

 Treatment

 IHD –Angina

 Infarction

102

 Hypertension

 Diabetes

 Rheumatic

 Syphilis

 vascular heart disease

 TIA/ Stroke

 Any other

III. PERSONAL HISTORY

1. Diet Vegetarian Mixed

2. Sleep Sound Disturbed

3. Appetite Good Decreased

4. Bladder Normal Polyuria/

Anuria/Dysuria

5. Bowel Normal Constipated/Loose stools

6. Menstrual history Normal /Irregular

Postmenopausal

103

7. Habits a) Smoking : Duration b) Alcohol : Duration

Type

Quantity c) Tobacco Chewing: Duration

Quantity d) History of exposure to STD: Present/ Absent

IV. GENERAL PHYSICAL EXAMINATION

1) Built Well/Moderate Poor

2) Nourishment Obese/Average Poor

3) Emotional state Calm/Anxious Restless

4) Pallor Present/ Absent

5) Cyanosis Present/ Absent

6) Icterus Present/ Absent

7) Clubbing Present/ Absent

104

8) Pedal oedema Present/ Absent

9) Lymphadenopathy Present/ Absent

10) Extremities Warm/ Cold

V. VITAL SIGNS

-Pulse

-Blood pressure

-Respiratory rate

-Temperature

VI. SYSTEMIC EXAMINATION

CVS EXAMINATION

1) Pulse

-Rate

-Rhythm

-Volume

-Character

-Condition of Vessel Wall

105

-Radio Femoral Delay

2) JVP –Normal /Raised

A. INSPECTION

Precordium Normal/Bulged

Apical impulse Visible / Non Visible

Other pulsation

B. PALPATION

Apical impulse Location, Character

Palpable Heart Sounds

Thrills Apex

Parasternal area

Any other

C. PERCUSSION

Cardiomegaly

Pericardial effusion

106

D. AUSCULTATION

Heart sounds

S3/S4 Present/ Absent

Murmur

Timing/Location/Character/Radiation/Grade

Pericardial rub

Basal crepitations

Others

KILLIP CLASS:

RESPIRATORY SYSTEM:

PER ABDOMEN:

CENTRAL NERVOUS SYSTEM

107

INVESTIGATIONS

I. BLOOD

HAEMOGLOBIN gm/dl

NEUTROPHILS %

LYMPHOCYTES %

EOSINOPHILS %

BASOPHILS %

MONOCYTES %

ESR %

CARDIAC ENZYMES: CPK-MB IU/L

108

II.URINE

ALBUMIN

SUGAR

MICROSCOPY

III.BIOCHEMISTRY

RBS mg/dl

SODIUM LEVELS ON ADMISSION mEq/L

-AFTER 24 HRS mEq/L

-AFTER 48 HRS mEq/L

-AFTER 72 HRS mEq/L

TOTAL CHOLESTEROL mg/dl

HDL CHOLESTROL mg/dl

LDL CHOLESTROL mg/dl

VLDL CHOLESTROL mg/dl

TRIGLYCERIDE mg/dl

109

IV.ELECTROCARDIOGRAPHY

V.ECHOCARDIOGRAPHY

EJECTION FRACTION

CONCLUSIONS

OTHER RELEVANT INVESTIGATIONS

DIAGNOSIS

IN HOSPITAL COMPLICATIONS

CCF/LVF

Cardiogenic shock

Arrhythmias

Thromboembolism

Pericarditis

Rupture of Interventricular septum

Rupture of papillary muscle

Aneurysm

Any other

FOLLOW UP UPTO 30 DAYS

110

CONSENT FORM:

111

112

MASTER CHART

FOLLOWUP PERIOD FOLLOWUP

OUTCOME

IN HOSPITAL COMPLICATIONSIN HOSPITAL

DIAGNOSIS

KILLIP CLASS KILLIP

LDL

S.CHOLESTROL

S.CREATININE

BLOOD UREA BLOOD

RBS

DBP

SBP

SODIUM AT 72SODIUMHRS AT

SODIUM AT 48SODIUMHRS AT

SODIUM AT 24SODIUMHRS AT

SODIUMADMISSIONON

PRIOR CADPRIOR

PRIOR DIURETIC THERAPHY DIURETIC PRIOR

SMOKING

SEX SEX

AGE AGE

NAME

S NOS 1 VELAMMAL 54 F N Y N N N 53 134 133 133 132 150 100 142 25 1 168 117 1 AWMI A . 2 RAJAN 54 M N N Y N N 58 133 134 132 132 110 70 128 27 0.9 192 119 1 AWMI A 3 RAGU 75 M Y Y Y N N 34 129 128 126 129 130 74 86 32 1.3 234 152 3 ALMI CCF D 4 REBECCA 62 F N N N N N 63 137 136 133 132 134 72 132 26 0.8 158 96 2 IWMI A acute lvf 5 SIMONE 72 M Y N Y N N 44 132 133 131 132 120 74 186 27 0.9 188 104 1 IWMI D 6 RAJAMMAL 70 F Y Y N N N 49 134 134 132 133 160 100 152 25 0.7 204 86 1 ASMI A 7 RAJA 43 M N Y Y N N 42 133 130 131 132 140 90 98 33 1.2 232 112 2 AWMI D 8 SATHISH 42 M N Y Y N N 48 136 133 134 133 142 80 126 32 1 176 99 1 AWMI A 9 MARY 55 F N N N N N 60 133 134 132 131 118 76 156 25 0.9 198 115 1 AWMI A 10 SENTHIL 60 M Y Y Y N N 51 129 127 128 127 154 90 220 36 1.6 247 145 2 IWMI CHB D 11 SORNAM 50 F N Y N N N 47 132 134 133 133 140 100 84 29 0.9 242 98 1 AWMI A 12 CHARLES 74 M Y N Y N N 33 129 130 130 128 90 60 212 37 1.5 204 108 3 AWMI D 13 ARUNACHALAM 53 M N Y Y N N 54 137 134 133 134 150 90 136 35 1.3 188 117 1 ASMI A 14 LAILA 54 F N N N N N 59 134 133 133 132 130 74 128 22 0.8 252 158 1 AWMI A 15 SELVARAJ 63 M Y Y N N N 39 131 132 131 133 156 94 310 28 0.9 189 120 1 AWMI D 16 SEKARAN 59 M Y Y Y N N 29 136 133 131 133 132 84 98 27 0.9 212 131 3 AWMI D 17 SAROJA 57 F Y N N N N 52 135 133 134 134 110 70 262 25 0.7 168 86 1 IWMI 2*HB A CHB 18 SREEMATHI 70 F N N N N N 46 133 133 131 132 126 74 114 33 1.1 175 103 1 AWMI A 19 NABIN CHANDRA 53 M N Y Y N N 43 132 131 130 131 132 86 78 23 0.9 194 111 1 AWMI D 20 SELVARAJ 42 M Y N N N N 57 134 132 133 134 100 60 154 26 0.8 246 136 1 AWMI A 21 DURAISAMY 67 M Y Y Y N N 45 136 134 134 133 124 88 186 32 1.2 204 106 1 AWMI A 22 CHELLAMMAL 80 F N N N N N 30 127 129 128 128 86 58 76 23 0.7 278 146 4 IWMI CHB D 23 MUPPANDARI 60 F N N N N N 67 135 132 132 133 104 70 150 33 1.3 214 135 1 ALMI A 24 AMALDAS 60 M Y Y Y N N 42 128 128 127 129 106 60 216 29 0.8 155 94 3 AWMI Vfib D 25 DHARMARAJ 40 M N Y Y N N 43 134 131 130 132 164 110 122 30 1 246 135 1 AWMI A 26 LILLI 60 F N N N N N 55 137 134 133 134 130 76 98 27 0.7 232 147 1 AWMI A 27 SUNDARRAJ 72 M Y Y Y N N 31 129 129 131 130 144 78 286 25 0.8 147 117 2 ASMI PE A 28 GANAPATHY 51 M N Y N N N 28 128 129 126 129 100 60 146 37 1.7 226 142 2 AWMI D 29 SER SELIN 57 F Y N N N N 47 133 134 132 132 108 72 134 35 1.3 142 92 1 AWMI A 30 MUTHU 47 M Y N Y N N 62 136 134 133 132 110 76 208 29 1.2 178 110 2 IWMI 2*HB A 31 MERCY RANI 52 F Y Y N N N 38 131 134 133 133 120 70 198 28 0.8 225 141 2 AWMI D 32 MUTHURAJ 58 M Y Y Y N N 52 133 132 132 134 154 102 234 29 0.7 221 110 1 AWMI A 33 NESAIYAN 75 M N Y Y N N 43 137 134 133 132 140 98 126 23 0.9 202 114 1 AWMI A 34 NAGARAJAN 48 M N N N N N 36 130 132 131 130 104 76 106 35 1.2 156 117 2 AWMI D 35 VASANTHI 51 F Y N N N N 44 135 133 133 134 116 78 188 37 1.6 214 106 1 AWMI A 36 MAHADEVAN 34 M N Y N N N 56 131 132 134 133 132 76 102 33 1 221 122 3 AWMI A 37 GUNASEKAR 55 M Y Y Y N N 48 131 131 132 134 154 98 176 36 1.3 140 89 1 AWMI A acute lvf 38 CHELLATHANGAM58 F Y N N N N 32 130 131 130 132 102 74 244 33 1.4 265 144 1 AWMI D 39 ANANDHAKUMAR40 M N Y Y N N 49 135 134 131 130 160 100 84 30 1.2 247 133 1 IWMI acute mr D 40 CHELLATHAI 65 F N N N N N 44 134 133 133 132 120 84 112 25 0.7 146 97 1 AWMI A 41 SUBBULAKSHMI 55 F Y Y N N N 54 138 134 134 132 140 86 190 36 1.4 188 93 2 IWMI A CHB 42 THANGARAJ 63 M N N Y N N 29 126 129 129 128 90 60 68 27 0.9 292 160 3 AWMI VT D 43 MUTHAIYAN 56 M N Y N N N 33 134 131 130 130 100 76 106 33 1.5 194 117 2 IPWMI D 44 POOMANI 70 M Y N Y N N 46 135 133 133 134 130 80 204 38 1.4 168 89 1 AWMI A 45 MURUGAN 58 M Y Y N N N 57 137 134 133 134 148 88 193 33 1.2 205 126 2 AWMI D 46 VASANTHA 51 F N Y N N N 48 132 133 134 132 142 94 134 34 1 204 132 1 AWMI A PE 47 YESUVADIYAN 80 M N N Y N N 41 136 134 133 131 126 78 146 32 0.9 176 97 1 AWMI A 48 KASTHURI 66 F Y Y N N N 48 133 134 133 132 130 80 236 23 0.8 224 109 1 AWMI A 49 KANTHAIYA 47 M N N Y N N 59 137 134 133 134 110 78 104 35 1.2 165 92 1 AWMI A 50 DURAIRAJ 58 M Y Y Y N N 30 126 129 129 127 108 76 142 34 1 225 103 3 AWMI CCF D

113

S NOS NAME AGE SEX DM HT SMOKING THERAPHY DIURETIC PRIOR CADPRIOR EF SODIUMADMISSIONON 24SODIUMHRS AT 48SODIUMHRS AT 72SODIUMHRS AT SBP DBP RBS UREA BLOOD S.CREATININE S.CHOLESTROL LDL CLASS KILLIP DIAGNOSIS COMPLICATIONSIN HOSPITAL OUTCOME PERIOD FOLLOWUP 1 BAGAVATHIYAMMAL55 F Y Y N N N 30 135 137 137 135 140 100 118 35 0.9 234 141 II ALMI PE D . 2 AVUDAIYAPPAN 65 M N N Y N N 50 137 140 136 138 120 70 130 36 0.8 130 86 I AWMI A 3 THANGAM 71 F Y N N N N 52 138 136 138 138 110 74 250 40 0.9 170 112 I AWMI A acute lvf 4 SRIDHARAN 31 M N Y Y N N 54 140 142 141 140 150 100 132 42 1 180 124 I IWMI A 5 MANIKANDAN 30 M Y N Y N N 60 138 136 138 138 106 68 240 40 1.1 150 92 I AWMI A 6 MEENA 61 F Y Y N N N 62 138 136 135 136 130 90 98 42 1.3 130 89 I AWMI A 7 RAMASAMY 65 M Y Y Y N N 32 138 140 136 138 160 96 88 40 0.9 220 137 III ALMI D 8 MEENA 67 F N Y N N N 55 137 141 138 139 110 90 100 44 0.8 120 78 I IPWMI A 9 MURUGAN 60 M Y N Y N N 57 137 138 138 136 100 60 220 38 0.6 140 87 I IWMI A 10 MANI 60 M Y N Y N N 38 138 137 138 137 104 68 110 38 0.7 150 93 I AWMI D 11 MANGAL RANI 66 F N Y N N N 56 137 136 138 135 100 60 113 40 1.2 220 126 I AWMI A ccf 12 ISRAVEL 49 M Y Y N N N 60 140 142 142 144 108 56 254 44 1.4 230 141 I AWMI PE A 13 MADATHI 53 F N Y N N N 64 137 138 137 138 110 68 116 42 1.1 130 84 I AWMI A 14 RAJAMANI 65 F Y Y N N N 52 138 138 138 137 122 70 227 36 0.8 120 93 II AWMI D 15 PAULDURAI 65 M Y N Y N N 66 137 136 138 137 100 70 218 38 0.6 220 116 I IPWMI A 16 SUBRAMANIAM 48 M Y N Y N N 62 138 140 138 137 106 72 129 40 0.5 250 156 I AWMI A 17 THANGAMMAL 68 F N N N N N 54 139 138 142 140 102 74 134 44 0.8 230 131 I ASMI A 18 GOPALAN 50 M Y Y N N N 56 139 138 136 138 166 102 124 40 0.9 150 108 I IRVMI A chb 19 NAGULAN 42 M Y Y N N N 56 138 137 138 139 118 70 130 42 0.8 170 105 I AWMI A 20 THANGABAI 62 F Y N N N N 57 139 138 138 137 140 76 234 44 0.9 200 99 I AWMI A 21 MANI 60 M Y N N N N 58 138 138 138 139 128 74 95 40 0.7 240 128 II IRVMI A 22 MUTHAIYA 72 M Y N N N N 48 139 137 138 139 100 60 240 38 0.9 250 144 I ASMI D 23 SUBBAIYAH 66 M N Y N N N 54 137 139 138 137 100 78 103 38 1 230 87 I AWMI A 24 CHRISTI AMALA 67 F N Y N N N 34 136 138 138 137 120 78 108 36 1.2 190 76 II AWMI D 25 RAJA 64 M N Y N N N 54 138 137 138 139 110 72 106 36 1.3 160 88 I IWMI A 26 GNANAMMAL 50 F N N N N N 30 140 139 138 139 118 68 104 37 1.4 180 126 I IWMI ACUTE MRD 27 MABEL 80 M N N Y N N 52 138 141 140 142 108 70 102 38 1.2 150 84 I IWMI A 28 CHELLAIYAN 63 M N N Y N N 56 140 138 140 138 120 74 104 37 1.6 220 151 I AWMI A 29 ASAYAN 60 M N Y N N N 54 140 136 137 138 130 70 98 38 1.2 170 95 I AWMI A 30 LALITHA 49 F N Y N N N 54 138 138 137 136 116 68 140 40 0.8 210 134 II AWMI A PE 31 YASOTHA 70 F N Y N N N 56 138 136 137 138 130 80 170 38 0.9 180 103 I AWMI A 32 RAJ 64 M N Y N N N 55 139 138 139 137 116 74 140 36 1.2 230 143 I AWMI A 33 PANI PITCHAI 65 M N N Y N N 56 137 139 138 138 132 72 119 38 1.4 140 86 I ASMI A 34 RASALAN 65 M N N Y N N 58 139 139 140 140 128 68 130 40 1.3 150 90 I AWMI A 35 VELUSAMY 62 M N N Y N N 57 139 138 136 138 134 70 126 38 1.2 220 114 I AWMI A 36 RAJA 47 M N N Y N N 54 136 136 138 139 124 68 130 39 1.4 210 97 I IWMI A 37 BALUSAMY 50 M N N Y N N 55 137 135 136 135 126 78 122 36 1.3 160 95 I IWMI A 38 RAGINI 37 F N N N N N 57 138 137 138 136 114 76 120 37 1.6 170 102 I ASMI A 39 RAJAMANI 65 M N N Y N N 56 139 138 137 137 130 74 122 38 1.3 190 122 II AWMI A 40 BALAKRISHNAN 50 M N N Y N N 57 138 136 136 138 108 80 106 38 1.1 160 91 I AWMI A 41 LAKSHMI 67 F Y N N N N 55 139 137 137 139 110 78 211 39 1 180 119 I AWMI A 42 MERCILLINE 56 F N Y N N N 52 137 138 137 138 140 82 104 38 1 170 94 II AWMI A 43 CHELLAPPAN 59 M N Y Y N N 50 138 140 138 137 122 70 105 40 0.9 230 138 I IWMI D 44 MURUGAN 61 M N Y Y N N 57 140 138 139 139 110 72 104 38 0.9 190 99 I AWMI A 45 PUSHPARANI 52 F N N N N N 56 137 137 137 138 134 80 102 36 0.8 240 127 I AWMI A 46 AMBIGA 68 F N N N N N 55 138 136 136 136 136 78 104 37 1.2 160 85 II AWMI A 47 PONNUMUTHU 62 M N N N N N 58 142 137 140 137 128 74 102 44 1.1 250 147 III AWMI A 48 SASIKUMAR 54 M Y N Y N N 56 139 139 138 138 118 72 100 46 1 150 82 II AWMI A 49 PUSHPAM 71 F N Y N N N 52 138 139 139 139 134 68 99 44 1.3 200 97 I AWMI A 50 DENNIS 56 M N Y Y N N 52 139 138 140 138 106 60 94 43 1.2 160 102 III IWMI D

114