STANDARD TREATMENT GUIDELINES

CARDIOLOGY

DEPARTMENT OF HEALTH AND FAMILY WELFARE

GOVERNMENT OF KERALA
STANDARD TREATMENT GUIDELINES IN
CARDIOLOGY

Two sections
Section I

Evaluation and management of patients presenting with

Acute coronary syndrome in secondary and tertiary
care hospitals

Section II

Evaluation and management of heart failure

Committee for Development of Standard Treatment
Guidelines
Convener for STG in Cardiology

Dr. Cibu Mathew, Additional Professor of Cardiology, Medical College,

Thrissur

Members of the Expert committee who reviewed the guidelines.

1. Dr. A. George Koshy, Professor of Cardiology, Medical College,

Trivandrum
2. Dr. K. Sivaprasad, Professor and HOD of Cardiology, Medical
College, Alappuzha
3. Dr. Sajeev C.G., Professor and HOD of Cardiology, Medical
College, Kozhikkode
4. Dr. Raju George, Professor and HOD of Cardiology, Medical
College, Ernakulam
5. Dr. N. Sudhayakumar, Professor & HOD of Cardiology,
Travancore Medical College, Kollam
6. Dr. K. Venugopal, Professor & HOD of Cardiology, Pushapagiri
Institute of Medical Sciences and Research centre, Thiruvalla
7. Dr. Karunadas C.P., Additional Professor of Cardiology, Medical
College, Thrissur, CSI Kerala Chapter secretary

External Expert

Dr. G.Justin Paul, Professor of Cardiology, Madras Medical College,

Chennai

“Driven by the inspiration drawn from Shri Rajeev Sadanandan IAS,

Additional Chief Secretary , Department of Health and Family Welfare, Government
of Kerala, the process of preparation of Standard Treatment Guidelines (STG) was
initiated by the Director of Medical Education Dr Remla Beevi. A.The process of
developing and finalizing the STG’s were coordinated by Dr.Sreekumari. K. Joint
Director Medical education and Dr.Suma T K, Professor of Medicine and ably
supported by a dedicated team of experts, including external faculty”.
TABLE OF CONTENTS

Message by Chief Minister 11

Message by Health Minister 13
Foreword by Additional Chief Secretary 15

Section-1 19
Evaluation and management of patients presenting with Acute
coronary syndrome in secondary and tertiary care hospitals
1. Scope 19
2. Abbreviations 20
3. Diagnosis, investigations and risk stratification
of acute coronary syndrome(ACS) 21
3.1 Introduction 21
3.2 Definitions 21
3.2.1 Definitions of Health care setting 21
3.2.2 Acute coronary syndrome 21
4. Assessment in suspected cases of ACS 24
4.1 History 24
4.2 Physical examination 27
4.3 Investigations 28
4.3.1 Electrocardiogram 28
4.3.2 Biomarkers 32
4.3.3 Lab investigations 35
4.3.4 Others 35
5. Early risk stratification 36
5.1 TIMI score for UA/NSTEMI 38
5.2 TIMI score for STEMI 37
6. Management plan for ACS in secondary care 38
6.1 General measures 40
6.2 Specific treatment of ACS 41
 6.2.1 Antiplatelets 41
6.2.2. Statin 41
6.2.3 Nitrates 41
6.2.4 Reperfusion therapy 42
6.2.5 Antithrombotics 43
6.2.6 Beta blockers 44
6.2.7 Other medications 45
6.3 Referral to tertiary care centre for PCI 45
6.4 Monitoring and follow up 46
6.5 Check list for secondary care 47
7. Management plan for ACS in tertiary care 48
7.1 General care 48
7.2 Specific care 48
7.2.1 Antiplatelets 48
7.2.2 Reperfusion therapy 49
7.2.3 Antithrombotics 51
7.2.4 PCI in NSTEMI/UA 51
7.3 Monitoring and follow up 52
7.4 Check list for ACS management in tertiary care 52
8. Facilities to be available in hospitals managing ACS 53
9. Algorithm 54
10. References. 55
Section 2
Evaluation and management of heart failure 59
1. Scope 59
2. Abbreviations 60
3. Evaluation of heart failure 61
3.1 Introduction 61
3.2 Definition 61
3.3 Diagnosis 61
3.3.1. History 61
 3.3.2. Physical examination 62
3.3.3. Investigations 62
3.3.4. Risk stratification 64
4. Management of heart failure 65
4.1 Introduction 65
4.2 Definition and classification 65
4.3Treatment 66
4.3.1 General measures 66
4.3.2 Specific treatment 67
4.3.3 Follow up 70
4.3.4 Advanced investigations 71
4.3.5 Special modes of treatment 71
4.3.6 Heart failure with preserved EF 72
5. Acute decompensated heart failure 72
5.1 Definition and classification 72
5.2 Symptoms and signs 73
5.3 Investigations 73
5.4 Management 74
5.5 Management algorithm 76
6. References 77
 Message

Pinarayi Vijayan Secretariat

Chief Minister Thiruvananthapuram

The Government is taking many initiatives to ensure providing quality

health care to all. Out of the five missions launched by the Government, the
Aardram mission is primarily focussed to improve Primary Health Care to
provide standard health care facilities to people at grassroots. This initiative is
complemented by strategic investment for the improvement of infrastructure in
secondary and tertiary health care institutions to provide quality health care
services.
I am happy to note that the Department of Health is also taking
initiatives to bring standardization in treatment for various disciplines like
Cardiology, Critical care, Diabetes Mellitus, Cancer Care, etc. It is a noteworthy
initiative to improve the qualitative aspects of the health service delivery. I
appreciate the efforts taken by the experts from Government sector and private
sector from Kerala and also the subject experts from outside the state. I am
hopeful that the introduction of standard guidelines for diagnosis and
treatment will ensure better quality and consistency in health care.
I wish all the success to this endeavour.

Pinarayi Vijayan
Chief Minister

11
Message

13
 Foreword

Patient care has moved away from management by an

individual based on personal knowledge and skill to an evidence
based, team managed operation. Decisions are reviewed more
rigorously post facto and their alignment verified with standard
practice. With the mode of payment for care moving from out of
pocket payments to third party payers there will be a demand for
rigorous documentation and evidence of having conformed to
standard practice. When analysis of big data and machine learning
becomes the norm it will require a standard set of procedures to act
as the baseline from which to measure deviations and differences in
impact.
To meet the requirement of these developments in the field
of medicine, it is necessary to have explicit, objectively verifiable set
of standard operating procedures. They have to be prepared based
on international guidelines with the highest acceptance, but have to
be modified to suit local knowledge and practice, so that there is
local ownership. Government of Kerala has been trying to get the
guidelines prepared for some time now. I would like to thank and
congratulate Dr. Sreekumari, Joint Director of Medical Education
and Dr. T.K.Suma, Professor of Medicine, T.D. Medical College,
Alappuzha who took on the task of preparing standard treatment
guidelines and completed it through a long, consultative process. I
also thank the conveners of the different thematic groups who
coordinated the work in their field as well as the innumerable
number of participants, in government and private sector, who
contributed their effort and knowledge to improve the guidelines.
Professional associations have also contributed in their fields. Their
efforts have resulted in a product they and Kerala can be proud of.
Treatment guidelines cannot be static if they are to remain
relevant. They must be updated based on new knowledge and the

15
 experience of treatment based on these guidelines. To do this the
group which prepared the guidelines has to remain active and have
a system for collecting data on the results of practice based on
these guidelines. I hope such an activity is institutionalised and
periodic revisions of the guidelines are prepared and published.

I wish that these guidelines contribute to raising the quality of

patient care in Kerala.

Rajeev Sadanandan IAS

Addl Chief Secretary
Health & Family Welfare
Department

16
Section I
 Section I
STANDARD TREATMENT GUIDELINES - CARDIOLOGY

Section I
Evaluation and management of patients presenting with
Acute coronary syndrome in secondary and tertiary care
hospitals

1. Scope
Population
Adults more than 18 years of age
Key clinical issues covered:
Definition, clinical features, investigations, risk stratification and
management of acute coronary syndromes
Clinical issues that will not be covered:
Management of non-cardiac causes of chest pain, methods of coronary
intervention, cardiopulmonary resuscitation and management of heart
failure. The following are only a guide and always the clinician has to
exercise own judgment and clinical experience.
Health care setting:
Secondary and tertiary health care, as defined later
Outcome:
Early diagnosis and management of acute coronary syndrome, early
reperfusion in STEMI, prevention of cardiac arrest and mortality.

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2. Abbreviations.
ACLS Advanced Cardiac Life Support
ACS Acute Coronary Syndrome
CAD Coronary Artery Disease
CAG Coronary Angiogram
CKMB Creatine Phosphokinase MB fraction
CPR Cardiopulmonary Resuscitation
CVA Cerebrovascular Accident
CVD Cardiovascular Disease
ECG Electrocardiogram
ED Emergency Department.
GFR Glomerular Filtration Rate
LBBB Left Bundle Branch Block
LMWH Low Molecular Weight Heparin
MI Myocardial Infarction
MR Mitral Regurgitation
NSTEACS Non ST Elevation Acute Coronary Syndrome
NSTEMI Non ST Elevation Myocardial Infarction
PCI Percutaneous Coronary Intervention
PTCA Percutanoeus Transluminal Angioplasty.
RBBB Right Bundle Branch Block
RBS Random Blood Sugar.
STEACS ST Elevation Acute Coronary Syndrome
STEMI ST Slevation Myocardial Infarction
UA Unstable Angina
UFH Un-fractionated Heparin
VSR Ventricular Septal Rupture.

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3. Diagnosis, investigations and risk stratification of acute

coronary syndrome (ACS)
3.1. Introduction
Chest pain due to myocardial ischemia can be life threatening and early
diagnosis and appropriate management is needed to reduce mortality and morbidity.
Detailed history, physical examination and investigations are useful in diagnosis and
proper management. History of cardiac pain, typical electrocardiographic (ECG)
changes and rise and fall of biomarkers like cardiac troponin or creatine
phosphokinase MB fraction (CKMB) are the most important tools to diagnose acute
coronary syndrome (ACS).
3.2. Definitions
3.2.1 Health care setting. For the purpose of this guideline we define the level of
health care setting for acute coronary syndrome (ACS) management as follows.
· Primary care setup is a hospital where a basic qualification doctor is
available; ECG can be done but has no facility to manage ACS as inpatient.
· Secondary care setup is a hospital where ECG, cardiac Troponin and basic
blood investigations are available and medical management including
thrombolysis can be done but cathlab based interventional management is
not possible.
· Tertiary care setup is a hospital where there is facility to manage ACS both
medically and by cathlab based interventional management.
3.2.2 Acute Coronary syndrome refers to clinical situations that are compatible
with acute myocardial ischemia. They classically present with ischemic cardiac pain
or angina, though atypical symptoms (like abdominal discomfort or dyspnoea) or
even 'silent' ischemia (where there may not be a significant symptom) can occur.
ECG changes of myocardial ischemia/infarction or biomarker elevation may or may
not be present at presentation, but usually become evident over a period of time.
ACS consists of myocardial infarction (MI) and unstable angina (UA). Cardiac
ischemia without development of myocardial infarction is called unstable angina.
Presentation of UA can be one among the following, angina at rest, a new onset effort
angina, or rapid worsening of the preexisting effort angina. In UA, cardiac ischemic
biomarkers will not be elevated to the range diagnostic of myocardial infarction (MI).
Acute myocardial infarction is defined as a rise and/or fall of cardiac

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biomarker values [preferably cardiac troponin (cTn)] with at least one value above
the 99th percentile (or upper reference limit of normal) and with at least one of the
following:
· Symptoms of ischaemia.
· New or presumed new significant ST-segment–T wave changes (ST-T
changes) or new left bundle branch block (LBBB).
· Development of pathological Q waves in the ECG.
· Imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality.
· identification of an intracoronary thrombus by angiography

In studies of disease prevalence by the World Health Organization (WHO)

myocardial infarction was defined by a combination of two of three characteristics:
typical symptoms, biomarker elevation and a typical ECG pattern. This definition
seems to be suitable in context to applicability compared to the Universal definition
of myocardial infarction.

Cardiac pain of ischemic nature for less than 20

Stable minutes, only on effort, relieved by rest, no
effort angina hemodynamic changes, no recent worsening
Symptoms in severity
due to Cardiac pain of ischemic nature at rest/ or new
cardiac onset effort angina/ or effort angina with recent
ischemia Acute worsening/ or prolonged cardiac pain/ or cardiac
coronary ischemic symptoms with hemodynamic
Syndrome disturbance (like pulmonary congestion,
hypotension) or with persistent ECG changes or
cardiac biomarker positivity

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Acute coronary syndrome

ST elevation in ECG No ST elevation in ECG

ST elevation ACS Non ST elevation ACS

Cardiac Biomarkers Cardiac Biomarkers

elevated not elevated
(*Biomarker takes
time to rise)

NSTEMI Unstable Angina

ST elevations ACS vs Non ST elevation ACS

l ST elevation ACS have essentially ST segment elevation in the ECG, of
>0.1 mV (or > 1 mm in normal standardization) in two contiguous leads
(except V2 V3, where the elevation should be >2mm in males >40 years,
>2.5mm in males < 40 years and >1.5 mm in females). ST segment
elevation is measured at the J point. J point is the junction of QRS and ST
segment. Non-ST elevation ACS is diagnosed in a patient having ACS
but the ECG diagnostic criteria for ST elevation are not satisfied. It
comprises of unstable angina (UA) and Non ST Elevation myocardial
infarction (NSTEMI). In the very early phase of ACS, biomarker
elevation need not be present and hence it is impossible to distinguish
between NSTEMI and UA. Hence they are grouped as NSTEMI/UA
initially and further classified into NSTEMI or UA once the disease
evolves.

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4. Assessment in suspected cases of ACS

4.1 History
Among unselected patients presenting with acute chest pain to the
emergency department of tertiary care center, 5–10% have STEMI, 15–20%
NSTEMI, 10% unstable angina, 15% other cardiac conditions and 50% have non-
cardiac diseases. The background risk of the patient to develop atherosclerotic event
and the description of the pain are very important in the early evaluation of acute
chest pain.
Typical ischemic chest pain is characterized by a retrosternal sensation of
pressure or heaviness ('angina') radiating classically to the left arm (less frequently to
both arms or to the right arm), neck or jaw, which may be intermittent (usually lasting
several minutes) or lasting for more than 30 minutes. Though right arm radiation is
less frequent, radiation to right arm and lower jaw is more specific for cardiac pain
(Fig 1). Cardiac pain lasting for more than 30 minutes is more likely to result in
myocardial infarction than short duration pain and hence short episode of pain is
provisionally considered as angina and longer duration as myocardial infarction.
Additional symptoms such as sweating, nausea, abdominal pain, dyspnoea and
syncope may be present. Exacerbation of symptoms by physical exertion and relief
with rest favours cardiac ischemic pain. Relief of symptoms after nitrate
administration is suggestive but not specific for cardiac pain.

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Other presentations. Acute pulmonary oedema or cardiac arrest can be presenting

symptom of ACS. In patients with longstanding diabetes mellitus, silent myocardial
infarction (infarction without significant symptoms) can occur.
Atypical presentations of ACS include
· Epigastric pain
· Indigestion-like symptoms
· Isolated dyspnoea
· Fatigue
· Syncope.

Atypical pain or ischemic symptoms are more often observed in the elderly, in
diabetic patients, in women and in patients with chronic renal disease and
dementia. Ischemia can present with syncope, dyspnoea or abdominal pain
without chest pain. Hence in high risk patients presenting with atypical symptoms,
due care should be given to exclude ACS.

The following pain descriptions are not suggestive of myocardial ischemia.

· Pleuritic type pain, sharp or knife-like pain occurring on respiratory

movements or cough
· Primary or sole location of discomfort in the middle or lower abdominal
region
· Pain that can be localized with tip of one finger
· Pain reproduced with movement or palpation of the chest wall or arms
· Constant pain that persists for many days
· Very brief episodes of pain that last a few seconds or less
· Pain that radiates into the lower extremities

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Causes of chest pain other than due to cardiac ischemia

Associated with heartburn, regurgitation, and dysphagia

Gastro-oesophageal
and bad taste in the mouth. Relation with food and
reflux disease(GERD)
sometimes relief with upright posture is seen
May be associated with fever and tachycardia. Pain can
increase on movement. Pericardial rub may be heard.
Global ST elevation (almost all leads showing ST
Pericarditis
elevation except in aVR and V1) in ECG with
PR segment depression is suggestive of pericarditis.
Echo cardiogram shows pericardial effusion.
Pain increases on inspiration, may have associated
Pleurisy cough, fever and evidence of respiratory tract infection.
A pleural rub may be heard
Small pulmonary embolism can produce pleuritic chest
pain. Massive embolism presents with hypotension or
Pulmonary embolism syncope and may be confused with ACS. Pulmonary
embolism should be suspected in patients at high risk
of deep venous thrombosis like those having
prolonged limb immobilization.
Acute chest or back pain and a difference in the pulse
volume in the upper extremities suggest possibility of
acute thoracic aortic dissection. In dissection of aorta
Dissection of aorta
the pain may be tearing in type and can have maximum
intensity to start with, in contrast to myocardial
ischemia where pain builds up
Musculoskeletal causes are very common and can be
due to trauma, isolated musculoskeletal pain or
costochondritis. Cervical spondylosis can produce
Musculoskeletal chest pain and shoulder pain. Stinging character of
pain, pain that is reproducible on palpation and
movement/ respiration and localized muscle tension
suggest musculoskeletal pain.
Abdominal examination and associated symptoms may
give a clue. Cholecystitis can produce pain in right
Acute cholecystitis/ hypochondrum with radiation to right shoulder and
pancreatitis minor ECG change like T inversion. In pancreatitis pain
radiates to back and may be lesser on sitting and
bending forward.

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It is important to identify clinical circumstances that may precipitate or

exacerbate ACS, such as anaemia, infection, fever and metabolic or thyroid
disorders. Every patient suspected of having acute coronary syndrome should be
asked for history of bleeding, for example melena. Identify conditions which puts
patient at higher risk for bleeding like bleeding diathesis, use of oral anticoagulants or
recent surgery or trauma. This is because ACS management essentially involves
aggressive antithrombotic therapy.
4.2 Physical examination.
The first step in clinical evaluation is to identify any life-threatening situation
with a view to preventing death. Rapidly evaluate for signs of high risk. Look for
evidences of
· Shock - hypotension, feeble pulse, cold and clammy extremities
· Acute heart failure – dyspnea or orthopnea, tachycardia and tachypnoea
rd
with bi-basal lung crepitation, 3 heart sound and desaturation
· Arrhythmia - very high or low heart rate especially with rhythm irregularity.
Shock, acute heart failure and arrhythmia need urgent intervention. In case of no
features needing urgent intervention continue to do a quick but focused physical
examination.

l A fast but focused physical examination is to be done when ACS is suspected.

In stable patients a complete physical examination is to be done.
l Is the patient in distress, sweating, dyspnoeic, pale /or cold? Hypotension,
acute pulmonary oedema, bradycardia or tachycardia may be the reason and
are indications for immediate emergency care.
l Look for anemia which may the primary reason for cardiac ischemia.
l Pulse- rate, volume and pulse asymmetry are very important. Tachycardia and
irregular rhythm are suggestive of arrhythmia.
l Both high blood pressure and hypotension are important. If there is pulse
asymmetry and aortic dissection is suspected, blood pressure should be
evaluated in lower limbs also.
l Respiratory rate and oxygen saturation by pulse oximetry may be measured in
all patients whenever possible.

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In the focused physical examination one has to look for anemia, evaluate the
pulse (in all limbs) including rate, rhythm, volume and pulse symmetry, check blood
pressure (BP) both systolic and diastolic (in all limbs when there is pulse asymmetry
which will give a clue to dissection of aorta), respiratory rate, saturation by pulse
oximetry, JVP and heart sounds including 3rd and 4th heart sound. Auscultate for
systolic murmur (which can be due to mitral regurgitation/ ventricular septal rupture)
and pericardial rub. Look for evidence of atherosclerotic cardiovascular disease like
stroke, peripheral vascular disease and carotid bruit. A respiratory system evaluation
for pneumothorax or plueral effusion and an abdominal examination for possible
diseases like cholecystitis/pancreatitis is to be done in quick time. Vital signs can be
used to determine subsequent evaluation and cause of chest pain. For example,
hypoxemia increases suspicion for pulmonary or cardiac etiologies of chest pain,
while fever raises suspicion for infection.
4.3 Investigations
4.3.1 Electrocardiogram
A 12 lead ECG is mandatory, if the history is suggestive of cardiac ischemia. It
is preferable to obtain V3R and V4R recordings also. The resting 12-lead ECG may
be obtained as early as possible and preferably within 10 minutes of the
patient's arrival. Initial ECG can be normal even in acute MI and a normal early ECG
does not exclude ACS, if the history is suggestive of ACS. Repeat ECG may show
ischemic changes. When clinical presentation is suggestive of ACS and initial ECG is
normal, ECG may be repeated after ½ an hour and at 4 hour interval if the patient is
not having continuing symptom or more frequently at ½ hour interval, if the patient
has symptoms of continuing cardiac ischemia.
l Look for ischemic changes like ST elevation, ST depression, T inversions,
or pathological Q waves (width of Q wave equal to or more than 40 msec-
or 1mm). New ECG changes like significant ST shift and T inversion and
evolving ECG changes are highly suggestive of ACS. (Fig 2 & 3)
l Very tall T may occur before ST elevates and may be the first change in MI.
T inversion of cardiac ischemia is typically symmetric and arrow shaped.

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l Combination of ST elevation localized to an arterial territory (indicative

changes) and ST depression in oppositely placed leads (reciprocal
changes) is highly suggestive of MI. ST elevation can be used to localise
the culprit artery.

l Right ventricular myocardial infarction (RVMI) is diagnosed when there is

ST elevation in V3R and V4R in patients with inferior wall MI (Fig 4). ST
elevation in right sided chest leads and JVP elevation usually normalizes
early and hence recording of the right sided chest leads at presentation is
important to diagnose RVMI.

l Special leads V7 V8 V9 may be recorded to look for ST elevation in posterior

wall MI

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STEMI - naming based on the leads showing ST elevation

l Anterior ST elevation in Chest leads
l Inferior ST elevation in 2,3,aVF
l Lateral ST elevation in I, aVL, V5,V6
l Posterior ST elevation in V7,V8,V9 & ST depression chest leads
l RV ST elevation in right sided chest leads

l Asymmetric low amplitude (<3 mm) T inversions may occur at times in

precordial and inferior leads in normal young people, especially in obese
females and do not suggest ischemia. T inversion can occur in many non
cardiac conditions also.
l Rate and rhythm-look for presence of tachy or brady arrhythmias. Identify
bundle branch block which will have wide QRS (>120 millisec or >3 mm in
normal paper speed). Atrioventricular block including PR interval
prolongation are to be identified.
l Normal ECG does not exclude ACS in a patient with high likelihood
presentation and serial ECG evaluation is very important to look at
evolving changes.
l Apart from making diagnosis, ECG is useful for risk stratification. It also
gives clues to the diagnosis of other conditions like pulmonary embolism
(Right axis deviation; T inversion in V1 to V3; S1,Q3,T3; RBBB), or
pericarditis (diffuse concave upward ST elevation in most leads, no
reciprocal ST depression, PR segment depression).
l Q wave is the first and negative deflection in QRS. Leads I, aVL, V5 and V6
normally show a physiological q wave which is narrow. Q wave seen in
evolved myocardial infarction is wider (> 40 m.sec - 1mm in standard
ECG) and deeper (more than 2 mm. or > 25 % or R wave height).(Fig 5)

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l Examples of some arrhythmias are given below. Atrial fibrillation (Fig. 6)

will have absence of P wave, presence of fibrillary waves and irregularly
irregular RR interval.

l In complete heart block (Fig. 7) there will be dissociation of P and QRS

waves and regularly occurring P at a faster rate than regularly occurring
QRS. Compete heart block is more common in inferior wall MI.

l Ventricular tachycardia is regular tachycardia with wide QRS (>120 msec or

3 mm in regular ECG) and presence of atrioventricular dissociation (P and
Q R S o c c u r r i n g i n d e p e n d e n t l y ) . ( F i g 8 . )

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l Presence of RBBB in anterior wall STEMI (Fig 8) is highly suggestive of

block in the proximal left coronary vessel and hence indicates poor
outcome. ST elevation in aVR and V1 are also suggestive of proximal left
coronary occlusion. When there is ST elevation in V3R and V4R in inferior
wall STEMI, RV MI is also present and outcome can be worse than isolated
inferior wall MI.

4.3.2 Biomarkers
Measurement of a biomarker of cardiomyocyte injury is to be done in all
patients with suspected ACS whenever facility permits. Cardiac troponins are more
sensitive and specific markers of cardiomyocyte injury than creatine kinase (CK),
creatine kinase MB isoenzyme (CK-MB) and myoglobin and hence cardiac troponin I
or T is preferred and should be available in all secondary or tertiary care hospitals.
Elevation of cardiac troponin above the 99th percentile or the upper reference limit
indicates MI. Troponin starts rising by 4-6 hours (Fig. 10) after chest pain. If the first
value is negative, troponin can be repeated after six hours in cases of continuing pain
or after 24 hours to rule out ACS.

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Cardiac troponin may take

hours to become elevated
(biomarker blind period).
Therefore very early
treatment is not based on
troponin elevation

Figure 10. Pattern of rise and fall of troponin & CKMB in acute MI.
Cardiac troponins can remain elevated for 7-10 days after myocardial
infarction. CK-MB shows a more rapid decline and normalize by 24-48 hours after
MI and may provide added value for the timing of myocardial injury and the
detection of early re-infarction compared to troponin. CK-MB is useful in renal
disease where troponin can be elevated.
High sensitivity troponin (hs-Trop) can accurately measure smaller
quantities of troponin and hence is useful in early rule in and rule out of MI. Rule
out and rule in algorithms for MI using hs-Trop are available. However this is not
to be used to decide reperfusion strategy in STEMI. The following is a modified
chart for decision making in suspected case of ACS. Upper limit of normal (ULN)
th
is the 99 percentile of value in healthy controls. Both hs- Trop I and hs-Trop T
can be used. A value of hs-cTnT>14 ng/l is considered elevated. However ULN
Value can vary with the method/manufacturer and hence is to be modified
accordingly.

Time of Hs-Trop Rule in ACS Rule out ACS Observe

Clinical probability high Pain free, low clinical Intermediate clinical

and probability probability
+ + +
Hs- Trop value more values of Hs –Trop Rise of troponins in
0 hour / 3 hour than the Upper limit of
normal at 0 hour or at less than ULN at serial testing but not
3 hours, with a rise of both 0 hour and 3 reaching the
more than 1 value hour diagnostic value.
between two tests

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Causes of troponin elevation other than MI. Elevated Cardiac troponins do

not always mean ACS. Elevated levels of cardiac troponins can occur several
conditions other than ACS and hence troponin elevation should be always analysed
on the background of clinical presentation.

Causes of Troponin elevation other than ACS.

· Renal dysfunction.
· Myocardial injury other than due to ACS, as in the case of myo-
carditis, myocardial contusion, DC shock given for cardioversion or
defibrillation
· Left ventricular strain from congestive heart failure
· Hypertensive crisis
· Right ventricular strain from pulmonary embolism or other causes of
acute pulmonary hypertension
· Severe sepsis
· Stress cardiomyopathy
· Acute stroke
· Extreme exercise

From the clinical presentation the likelihood of CAD can be classified as low,
intermediate or high.

Feature High likelihood Low likelihood Intermediate likelihood

Chest or left arm pain or Chest or left arm pain Probable ischemic
discomfort is the chief or discomfort as chief symptoms in absence
History symptom and similar to symptom in of any of the
prior documented Age >70, Male sex, intermediate likelihood
angina, occurring in Diabetes mellitus characteristic
known CAD including
MI + +
+ Absence of high Absence of high or
Any of the following likelihood features and intermediate likelihood
presence of any of the features but may have
following any of the following

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Feature High likelihood Low likelihood Intermediate likelihood

Transient MR murmur Chest pain reproduced

Extra cardiac vascular
Examination Pulmonary edema or
rales disease by palpation

New or presumably
new, transient ST Fixed Q waves T flattening or inversion
segment elevation ST depression 0.05 to <0.1mV in leads with
ECG
(>0.1mV) or T inversion 0.1 mV or T inversion dominant R waves or
in multiple precordial >0.1mV normal ECG
leads

Cardiac Elevated Cardiac

Troponin I or T, or Normal Normal
markers CKMB

4.3.3 Lab investigations

Blood tests to be done in all cases at presentation
· Hemogram
· Serum creatinine and blood urea
· Blood sugar.
Other lab tests
· Liver function test, urinalysis, serum electrolytes, lipid profile, fasting
blood sugar/post prandial blood sugar, PT-INR etc. may be done as
per the clinical situation. For those needing coronary angiography
(CAG), screening for markers of viral infection HBs Ag, HCV and HIV
may also be done.
· Blood Gas evaluation may be done if available in cases of dyspnoea
and shock.
4.3.4 Other investigations
Echo cardiogram
Early evaluation with 2D echocardiography, Doppler and Color Doppler may
be done in cases of clinical ventricular dysfunction or hemodynamic disturbance.
Echo may be done electively in stable cases. Estimation of left ventricular (LV)
function is useful to prognosticate. Echo identifies ventricular wall motion

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abnormality, hypertrophy, abnormality of the valves, pericardial effusion or

thrombus, dissection of aorta and may give clue to concomitant diseases.
Mechanical complications like acute mitral regurgitation, ventricular septal rupture
or free wall rupture can be diagnosed with Echo. In patients with dyspnoea,
presence of lung comets or multiple B lines on the chest ultasonography is highly
suggestive of pulmonary oedema. (see chapter on heart failure)
Chest X-ray is not routinely needed in the acute setting of every ACS but will
be useful in patients with dyspnea / desaturation. It is also useful to detect
pneumonia, pneumothorax, rib fractures or other thoracic disorders. CT and
pulmonary angiogram is useful in suspected case of pulmonary embolism and
dissection of aorta.

History Points Risk of Cardiac events by 14 days

Age 65 years 1 Death/ MI/

Risk score Death or MI
Three or more risk revascularization
factors for coronary
0-1 3% 5%
artery disease (CAD)
(family history of CAD, 1 2 3% 8%
hypertension,
hypercholesterolemia, 3 5% 13%
diabetes mellitus,
tobacco use) 4 7% 20%
Known CAD (coronary 5 12% 26%
1
stenosis >50%)
Aspirin use in the past 6-7 19% 41%
1
7 days
Presentation Points
Severe angina
(≥2 episodes in 1
24 hours)

ST deviation ≥0.5 mm 1
Elevated cardiac
marker level 1

RISK SCORE Total 0-7

TIMI score for “NSTEMI”

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5. Early risk stratification

Patients with ACS must be evaluated rapidly in order to identify those at risk of
life-threatening arrhythmias and therefore needing close surveillance. All patients
with ACS need monitoring. Those having continuing pain and high risk ACS need
continuous ECG and monitoring of the vitals in an ICU. There are several scoring
systems to assess the risk of ACS like TIMI risk scores and Killips classification..
5.1 UA/NSTEMI. The TIMI risk score in NSTEMI uses seven variables in an additive
way. A low TIMI score <3 usually indicates a low risk and a TIMI score > 3 indicates
intermediate or high risk. Decision on medical management or early invasive
management can be done based on the risk.
5.2 STEMI. Since early reperfusion therapy is to be done in STEMI presenting in
window period, risk scoring is not that important compared to NSTEMI in deciding
various strategies in early management. TIMI scoring for STEMI has 8 variables and
Killips class is one among them.
TIMI Score for STEMI. The table gives the variables assessed and the chart
gives the risk for the score.

History Points
Age
65-74 2
75 3
Mortality at 30 Days (%)

40
DM/HTN or agina 1 35.9
35
Examination
30 26.8
SPB 100 3 25 23.4
HR 100 2 20
16.1
Killip class-II-IV 2 15 12.4
Weight 67 1 10 7.3
Presentation 5 4.4
1.6 2.2
0.8
Anterior STEMI of LBBB 1 0
Time to treatment 4 hours 1 Risk score:0 1 2 3 4 5 6 7 8 8

Risk Score 0-14 % at risk: 12% 22% 16% 16% 14% 9% 6% 3% 2% 1%

(Only 1% of patients with STEMI are at high risk with >8 score and 50% have
score of 2 or less with a low risk)

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Killip class is a very simple tool for risk stratifying. 'Killip class' is based on clinical
features at admission, and has independent prognostic value, with Class I at very
low risk and Class IV at very high risk.
Killip class in STEMI
Class I No signs of heart failure
Class II S3, elevated JVP, rales less than half of posterior lung fields
Class III Overt pulmonary edema
Class IV Cardiogenic shock

The following are very high risk features in any ACS

· Cardiogenic shock
· Acute heart failure
· Life-threatening arrhythmias or cardiac arrest
· Recurrent or ongoing chest pain refractory to medical
treatment
· Mechanical complications of MI
· Mecurrent dynamic ST-T wave changes, particularly with
intermittent ST-elevation

6. Management of ACS in secondary care setting.

Once acute coronary syndrome is diagnosed, early, rapid and aggressive
management is to be instituted. Immediate management of any life threatening
emergency like hypotension / shock / pulmonary oedema / arrhythmia should be
done. The specific management essentially consists of administration of
antiplatelets, antithrombotics like heparin, opening of the occluded vessel by
reperfusion strategies, high dose statins, hypertension/diabetes management and
management of complications like arrhythmia and heart failure.

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All patients with ACS should receive the following initially.

· Aspirin 300 mg, to be chewed
· Clopidogrel 300 mg in patients below 75 years, (75 mg above 75
years of age)
· High dose atorvastatin (40 or 80 mg).
· Secure an IV line as soon as diagnosis is made
All STEMI patients presenting within 12 hours to be considered for
reperfusion therapy. Referral to tertiary care center for angioplasty may be
considered if angioplasty can be done within120 minutes of diagnosis of
STEMI after contacting the tertiary care centre regarding feasibility. If delay
of more than 120 minutes expected from STEMI diagnosis to PCI,
thrombolyse without delay (start in 10 minutes), if there are no
contraindication to thrombolysis.
Thrombolysis is for STEMI only and is not to be given in UA/NSTEMI
Antithrombotics, like heparin are to be given in UA/NSTEMI and post
thrombolysis in STEMI
Other medications based on need
· Nitrates- Sublingual nitrate/IV nitrate may be given to patients
with pain if the BP is >100mm of Hg systolic
· Beta-blockers like metoprolol 50 mg orally may be given in
selected cases of STEMI, if the patient has tachycardia and high
blood pressure with no features of heart failure. In all
UA/NSTEMI, early initiation of metoprolol may be done if there is
no contraindication.
· Oxygen administration is to be considered when the patient is
dyspnoeic and having desaturation.
ACE-I and aldosterone receptor blocker are indicated in STEMI and
LV dysfunction and for hypertension management

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6.1 General measures

· With a quick evaluation identify presence of any life threatening situations like
shock, significant tachy or brady arrhythmia and pulmonary edema. If any of
the above is present, appropriate management for that may be given.
· All cases of STEMI and high risk UA/NSTEMI should have an IV line secured.
In case of hypotension, volume supplementation by IV infusion and pressor
support may be initiated. Many patients with hypotension will be hypovolemic
and unless volume is corrected, the BP will not stabilize.

Hypotension in ACS
· Hypovolemia- significant fluid loss can occur due to sweating
and vomiting- volume correction needed
· Massive myocardial damage- early reperfusion and inotropes
· Arrhythmia like atrial fibrillation or ventricular tachycardia- DC
shock may be needed.
· Bezold-Jarisch reflex- seen in inferior wall MI associated with
significant bradycardia and hypotension - atropine and IV
fluids to be given
· Drug induced. Many drugs like nitrate, betablocker, and
streptokinase can produce hypotension. Adjust the drug dose
· Mechanical complications like ventricular septal rupture/
pericardial tamponade

.· Oxygen administration is to be considered when the patient is dyspnoeic

and having desaturation. Administer oxygen, at 2-4 L/min, to maintain
oxygen saturation > 90%. Routine administration of oxygen in stable patients
is not needed.

· In patients whose ischemic symptoms are not relieved by nitrates and beta-
blockers, small dose of morphine (dose of 2-3 mg i.v. with promethazine 12.5
mg) can be useful if there is no hypotension. There is a concern that morphine
may reduce the effectiveness of anti-platelets and hence is to be used in
select patients having significant pain or pulmonary oedema.

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6.2 Specific treatment of ACS.

6.2.1 Antiplatelets. In all cases of ACS, administer aspirin 300 mg (to chew)
immediatley( if not administered earlier), followed by 75-150 mg daily unless there is
a contraindication for aspirin use. Second antiplatelet agent, a P2Y12 inhibitor,
clopidogrel is to be given in addition to aspirin. (other drugs like ticagrelor or prasugrel
are prefered over clopidogrel in patients being managed with percutaneous coronary
intervention).
· Dose of clopidogrel is 300 mg loading given orally in patients <75 years of age
and 75 mg in pateints > 75 years of age, when non invasive (medical)
management is planned. (The loading dose for clopidogrel in case of
angioplasty is 600 mg orally). Clopidogrel maintanance dose is 75mg orally
daily.
6.2.2 Statin. High dose statin like atorvastatin 40-80 mg or rosuvastatin 20 -40 mg (in
older people above 75 yrs half the dose) is to be given stat at admission and may be
continued daily in all patients unless there is a contraindication. The dose of statin is
not dependent on lipid level in the ACS setting and hence fasting lipd profile is not
needed to initiate high dose statin.
6.2.3 Nitrates are useful in reducing pain and ischemic symptms by reducing preload
(venodilation) and by coronary artery dilation. it also reduces the pulmonary
congestion. It is useful in reducing the BP in hypertensive states. It may be given
orally/sublingually or intravenously till the pain subsides and if the BP is >100mm of
Hg systolic or till the BP is controlled in patients with high BP.
· Sublingual administration of 5 mg of isosorbide dintrate (or nitroglycerine)
followed by repeat dose at 15 minutes interval may be given before i.v. line is
established.
· Intravenous adminstration should be under careful blood pressure
monitoring. The Starting dose of nitroglycerine (NTG) is 10 mcg /min. by i.v.
infusion and the dose should be titrated upwards by 10mcg/min every 15-30
minutes, until symptoms are relieved, unless side effects (notably headache
or hypotension) occur.
· In hypertensive patients NTG is given till the mean arterial blood pressure is
reduced by at least 25%.
· Nitrates are contraindicated in cases of right ventricular MI and in hypotension

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and sildenafil or other phospho diesterase - 5 (PDE-5) inhibitor use. Right

ventricular MI is to be expected in all cases of inferior wall MI especially when
there is hypotension.
6.2.4 Reperfusion therapy
Reperfusion therapy is to be considered urgently in all STEMI patients and are of two
types.
· pharmacological - thrombolysis or fibrinolysis
· mechanical - Percutaneous coronary Intervention (PCI).
Window period-Reperfusion is indicated if a STEMI patient presents within the
window period of 12 hours after the onset of pain and should be given as early as
possible. In cases of continuing ischemia, shock or LV failure PCI may be done after
12 hours also. Routine PCI after 48 hours is to be avoided.
Which method of reperfusion?. Reperfusion by angioplasty is prefered over
thrombolysis if the procedure can be done within 120 minutes of diagnosis of STEMI
by referring to a tertiary care centre. If angioplasty is not possible within in 120
minutes from diagnosis of STEMI (various reasons are delay in decision making and
delay in transportation to another centre), thrombolysis is the reperfusion strategy.
Thrombolytic therapy. It is indicated in STEMI patients presenting within 12 hours
of onset of pain, when there are no contraindications. In NSTEMI/UA thrombolysis
is contraindicated. There are absolute and relative contraindications to
thrombolysis in STEMI.

Absolute contrindication for thrombolysis Relative contraindication for

thrombolysis
Previous intracranial bleed Oral anticoagulant therapy
Ischemic stroke in 6 months Transient ischemic attack in last 6 months
CNS neoplasms or AV malformation Pregnancy or within one week postpartum
Refractory hypertension of >180 mm Hg.
GI bleed in one month systolic or >110 distolic.
Advanced liver disease or active
Known active bleeding disrder
peptic ulcer

Aortic dissection Infective endocarditis

Noncompressible punctures in Prolonged resuscitation
last 24 hours

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Thrombolytic agents. Fibrin specific agents like tenecteplase or reteplase are

prefered over streptokinase. Streptokinase is not fibrin-specific, requires to be given
as an infusion over one hour and may be associated with hypersensitivity reactions.
Previous streptokinase administration can result in antibody formation and repeat
administration is to be avoided especially within 6 months of previous use.
Tenecteplase has the advantage of being fibrin-specific, can be given as a bolus
dose, and has a lower incidence of hypersensitivity reactions. Reperfusion is better
with tenecteplase compared to streptokinase. Advantage of streptokinase is that is is
very cheap compared to tenecteplase. Doses of individual lytic agents are given
below. Those getting fibrin specific lytic agents should be given heparin or
enoxaparin also(dose given below). Fondaparinux is an antithrombotic option
after Streptokinase (dose 2.5 mg i.v. followed by 2.5mg/day/s.c)

Fibrinolytic agent Dose

Streptokinase 1.5 million units as an infusion over 30-60 minutes

Reteplase 10 units + 10 units iv bolus given 10 minuts apart

Single IV bolus
30 mg if <60 kg body weight
35 mg if 60 to <70 kg body weight
40 mg if 70 to <80 kg body weight
45 mg if 80 to <90 kg body weight
50 mg if > 90 kg body weight
Tenecteplase Half the dose in > 75 years of age
(co-therapy with parenteral anticoaglation with
enoxaparin or heparin infusion is to be given, till PCI
is performed or if PCI not done for the duration of the
hospital stay for minimum of 48 hours and maximum
8 days - dose detailed below)

6.2.5 Antithrombotics (heparin, enoxaparin or fondaparinux )

· Antithrombotics are indicated in all cases of STEMI with thrombolysis and in
all cases of NSTEMI/UA until PCI is done, or till hospital discharge, for
maximum 8 days.
· Dose of antithrombotic is given in the table. Most commonly used low
molecular weight heparin (LMWH) is enoxaparin.
· LMWH should not be given in patients with eGFR <15mL/min and here UFH
is preferred.

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Antithrombotic agent Dose

i.v. bolus of 60–70 IU/kg up to a maximum of 5000

IU, followed by an infusion of 12 -16IU/kg/h up to a
maximum of 1000 IU/h, aPTT target 50–75 sec or
Unfractionated heparin
1.5– 2.5 times the upper limit of normal.

Post thrombolysis, loading 30mg i.v. followed 15

minutes later by 1 mg/kg s/c twice daily. >75 years
of age, avoid bolus and 0.75 mg/kg per dose s/c
twice a day
Enoxaparin In NSTEMI/UA, loading dose not to be given given.
Daily dose same.
When the eGFR is 15-30 mL/mt reduce to 1mg/kg
once a day

Fondaparinux 2.5 mg iv bolus followd by 2.5 mg s/c daily for

maximum 8 days.

6.2.6 Beta-blockers (BB) reduce myocardial oxygen consumption by lowering heart

rate, BP and myocardial contractility and produce 13% relative risk reduction of
mortality in the first week following MI. BB are more useful in patients with tachycardia
and hypertension. Oral metoprolol may be considered in all cases of UA/NSTEMI in
the absence of contraindications. I.V. metoprolol is selectively used in acute phase of
STEMI, only if there is tachycardia and hypertension. After acute phase is over, BB
may be started by 24 hours, if not already started. BB (carvedilol, metoprolol
succinate or bisoprolol) is indicated in patients with reduced LV systolic function (see
the chapter on management of heart failure).
Contraindication for initiating betablocker
· signs of heart failure-(in heart failure start at low dose, once congestive
symptoms are controlled)
· systolic BP <100 mmHg
· heart rate <60 beats/min
· PR interval > 0.24 sec, second or third degree heart block
· active asthma or COPD- relative contraindication

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Dose of oral metoprolol is 25-50 mg 12 hourly, titrated up to 100 mg every 12 hour

based on BP and HR. In select cases with high BP and tachycardia, if there is no
evidence of heart failure, i.v. metoprolol may be given at a dose of 5mg, to be
followed by two more doses of 5mg at 5 minute interval, to a maximum of 15 mg,
provided heart rate > 60/mt and BP > 100 mm Hg systolic. I.V. metoprolol is to be
followed by oral metoprolol 50 mg within 6 hours. When there is LV dysfunction,
preferred drugs are carvedilol, bisoprolol or metoprolol succinate to be started at low
dose and stepped up gradually.
6.2.7 Other medications
· ACE-I and aldoserone receptor blocker in cases of STEMI may be started by
24 hours if there is no hypotension or elevated serum creatinine. ACE-I and
Aldosterone receptor blockers are indicated in LV dysfunction both in STEMI
or NSTEMI.
· Calcium channel blockers like diltiazem and verapamil are to be avoided in
cases of STEMI, and when there are features of heart failure. In NSTEMI/UA
with no features of heart failure and not tolerating BB due to wheeze,
diltiazem or verapamil may be considered as they reduce heart rate and have
antianginal action. Amlodipine may be used for hypertension control as add
on therapy in the continuing treatment of MI.
6.3 Referral to tertiary care for PCI
In STEMI.
· Primary angioplasty (angioplasty as the primary mode of reperfusion in
STEMI) is prefered over thrombolysis if the angioplasty can be done within
120 minutes of STEMI diagnosis. If the time limit can be met, patient may be
immediatley refered to a tertiary care center, preferably after contacting the
center to which patient is being refered to. Referal also should consider the
clincial situation and risk of transportation and should be done after
discussing with the patient/relatives regarding various issues in
transportation.
· Angioplasty after thrombolysis may be considered in some situations. They
are
£ Rescue PCI. Whenever there is evidence of failed thrombolysis
rescue angioplasty may be considered after discussing with the

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patient and relatives. Failed thrombolysis is diagnosed when the

patient after lytic therapy has continuing ischemia, hemodynamic or
electriclal instabillity and absence of ST resolution by atleast 50% in
the ECG taken at 60-90 minutes after starting lysis.
£ Early CAG after fibrinolysis followed by PCI of culprit vessel. In
cases of stable patients after lysis, a CAG may be considered within 2
to 24 hours after thrombolysis.

When considering referal for angioplasty, the centre to which patient is

being refered to should be contacted and the feasibilty of angioplasty in
120 minutes from diagnosis of STEMI assessed and if angioplasty in
time limit is not possible, thrombolysis may be initiated in the secondary
care centre. When decided to give thrombolytic therapy, it should be
initiated in 10 minutes.

In NSTEMI/UA. Early PCI may be done in high risk cases of NSTEMI/UA and
patient may be refered to tertiary care after the early management. In very low risk
cases of NSTEMI/UA initial medical management is ideal. Use TIMI score or look at
high risk features discussed in risk stratification.
Details to be included in the referral letter when sending to tertiary care
centre. All referred patients may be given a letter with a provisional clinical diagnosis
along with ECG and other investigation reports. Drugs given and time of
administration are to be mentioned. A copy of the check list can be useful during
referral.
6.4. Monitoring and follow up.
All high risk cases of ACS should be monitored for a period of 24 hours or till
they are stable, preferably in the ICU. Rehabilitation and continuation of the drug
therapy are important. Early in-hospital rehabilitation and lifestyle modification are to
be instituted. Advise regading healthy lifestyle and smoking cessation should be
given.

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6.5. Check list for management of ACS in secondary care

Name ……………….age…………sex………weight…….time of presentation………………

Mark appropriately- Yes/No/ select option by circling /or write comment

Clinical evaluation

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7. Management plan for ACS in Tertiary care.

Tertiary care centre for ACS is defined as a centre capable of doing cath lab based
interventions for management of acute coronary syndrome, including primary
angioplasty, in addition to having facility for medical management. The basic
management plan in a tertairy care centre is essentially same as described for
secondary care and points in relation to PCI is discussed in this chapter. Three
categories of patients with acute coronary syndrome come to tertiary care.
1. Patients directly coming to tertiary care centre
2. Refered from a primary or secondary care setup after receiving basic treatment
with antiplatelet and statins.
2. Patients who have received thrombolysis in a secondary care and refered for
angioplasty.
7.1 Management strategy in general
· After a quick clinical evaluation and necessary investigations, make
diagnosis and risk stratify (see previous discussions). If ACS is diagnosed,
basic management is same as the management in secondary care. General
care, identification and management of complications like heart failure,
arrhythmia and hypotension are to be done without delay. Dual antiplatelets,
high dose statins and antithrombotics are to be given in all patients unless
contraindicated. Use of drugs like nitrates, ACE-I, BB are as discussed in
chapter 2 under secondary care. (See management algorhithm also)
· Send blood sample for hemogram, RBS, S. creatinine and screening for viral
markers (for HIV, hetatitis B and C) immediately. Other blood investigations
depending on the clinical status may be done but less urgently.
· A quick echocardiographic assessment may be done before being taken up
for PCI, either in the ED or in the cathlab. However echocardiography should
not delay PCI. Elective and complete echocardiogram may be done in all
patients during the hospital course.
7.2 Specific management consideration in tertiary care
7.2.1 Antiplatelets. Aspirin 300 mg (to be chewed) is to be administered to all unless
there is specific contraindication. Second antiplatelet is also to be given. Ticagrelor or
prasugrel are prefered over clopidogrel in patients being managed with
percutaneous coronary intervention (PCI). Clopidogrel is prefered in patients to be

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thrombolysed.
· Dose of ticagrelor is 180 mg loading followed by 90 mg 12 hourly. For
PCI in ACS, in case the patient is already on clopidogrel, if needed,
clopidogrel can be switched over to ticagrelor with a loading dose of
180 mg (but not to prasugrel).
· Dose of prasugrel is 60 mg loading followed by 10 mg daily. Prasugrel
is contraindicated in patients to be taken up for CABG and in patients
with prior stroke/transient ischaemic attack (TIA). It is generally not
recommended in patients >75 years of age or with low bodyweight
(<60 kg). Prasugrel is not a good choice if patient is already on
clopidogrel or ticagrelor.
· Dose of Clopidogrel is 300 mg loading given orally in patients <75
years of age and 75 mg in pateints > 75 years of age, when non
invasive (medical) management is planned. The loading dose for
clopidogrel in case of angioplasty is 600 mg orally. Clopidogrel
maintanance dose is 75mg orally daily.
· If the patient has already received adequate dose of antiplatelet from
the referal centre, it need not be repeated.
7.2.2 Reperfusion therapy.
· Decide on the mode of reperfusion strategy as early as possibe.
· In all STEMI patients presenting in window period of 12 hours from
onset of pain, primary angioplasty is the prefered method of
reperfusion if it can be done in 120 minutes from the point of STEMI
diagnosis. Once decided to do PCI, wire crossing of the occluded
vessel may be done within 60 minutes.
· In a patient refered from another centre for primary or rescue
angioplasty, do a quick assessement and if PCI option is considered
appropriate, shift to cathlab for PCI with minimum possible delay.
· In patients with STEMI, reperfusion with PCI may be considered after
12 hours if the patient is having continuing symptoms or
hemodynamic instability.
· Routine PCI after 48 hours of STEMI is not recommended.

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· If primary angioplasty is not possible in time frame within 120 minutes

of STEMI diagnosis (eg. nonavailability of cathlab for timely
intervention due to various reasons), if there are relative
contraindications for PCI or if the patient and relatives do not want or
cannot afford invasive management with angioplasty, thrombolysis
may be administered without delay (if there is no contraindication to
lysis).
Percutaneous coronary intervention. Different terminologies are used in
angioplasty in STEMI
· Primary PCI is the term used when angioplasty is the first method of
reperfusion in acute STEMI.
· Rescue PCI. Whenever there is evidence of failed thrombolysis
rescue angioplasty is to be considered after discussing with the
patient and relatives. Failed thrombolysis is diagnosed when after
lytic therapy, if there is continuing ischemia, hemodynamic or
electriclal instabillity and absence of ST resolution of at least 50% in
the ECG taken at 60-90 minutes after starting lysis.
· Early CAG within 2- 24 hours of lysis after fibrinolysis and PCI of
infarct related artery may be considered if significant lesion is
present in culprit vessel especially in high risk cases.
· Pharmaco invasive strategy. Routine PCI 2-24 hours after
successful thrombolysis and rescue PCI in case of failed
thormbolysis are called pharmaco invasive strategy.
Thrombolytic therapy. It is indicated in STEMI patients presenting in 12
hours of onset of pain, when there are no contraindications. In NSTEMI/UA
thrombolysis is not to be given. In STEMI, when there is a delay of >120 minutes
for PCI, immediate fibrinolysis is to be done, if there is no contraindication.
Time to reperfusion. Time to reperfusion should be minimised to the lowest in all
cases of STEMI. Steps to reduce this are
· Early diagnosis. ECG to be done as early as possible, preferably in 10
minutes.
· Quick decision making on reperfusion strategy after discussing the
options with patient and relatives.

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· Consider a shift directly to cathlab from ED to prevent time delay,

when primary angioplasty is decided.
· Thrombolytic therapy may be initiated in ED itself, when thrombolysis
is the reperfusion strategy
7.2.3 Antithrombotics
· Antithrombotic (heparin, enoxaparin or bivaluridine) is to be
given in all cases of PCI at the time of intervention but need not be
continued after PCI unless there are high risk features for
thrombosis and embolism, like atrial fibrillation (AF) or left
ventricular (LV) clot. Heparin is the prefered antithrombotic.
· Antithrombotics are to be given in patients going for medical
management both in STEMI and NSTEACS. Dose and drugs is
discussed along with management in secondary care.
· Antithrombotic agents used in PCI are un-fractionated heparin (UFH),
low molecular weight heparin (LMWH- like enoxaparin) and
bivalirudin. Dose of UFH in PCI is weight-adjusted administration
with an initial bolus of 70-100 IU/kg in case of no GPIIb/IIIa
administration and 60-70 IU/kg in case of GPIIb/IIIa co-therapy,
under ACT monitoring.
· Fondaparinux is not to be used in angioplasty

Antithrombotic agent Dose With PCI

Initial bolus of 70-100 IU/kg in case of no GPIIb/IIIa

Unfractionated heparin administration and 60-70 IU/kg in case of GPIIb/IIIa
co-therapy, under ACT monitoring

Enoxaparin 0.5 mg/KG iv bolus

In heparin iduced thrombocytopenia. 0.75mg/kg iv
Bivaluridine followed by 1.75mg/kg/hour infusion for maximum
of 4 hours

7.2.4 PCI in NSTEMI/UA. PCI is indicated in higher risk cases of NSTEMI/UA and
may be considered urgent or elective as per the risk at presentation. In very low risk
cases of NSTEMI/UA early medical management is ideal.

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7.3 Monitoring and follow up.

All high risk cases of ACS should be monitored for a period of 24 hours or till
they are stable, preferably in the ICU. All patients who had PCI should be followed up
with s. creatinine estimation. Care of arterial access site and observation for any
bleeding are important. Early inhospital rehabilitation and lifestyle modification are to
be instituted. Advise regading healthy lifestyle and smoking cessation should be
given.

7.4. Check list for early management of ACS in tertiary care centre

Name ……………….age…………sex……………weight…………….time of presentation………………

Mark appropriately- Yes/No/ select option /or write comment

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8. Facilities to be available in hospitals for ACS care.

· Every health care centre should have a functioning ECG machine available
24 hours a day. Health workers at these centers should be trained to interpret
the ECG so that treatment can be initiated without delay.
· Finger pulse oximeter to assess saturation to be available in all hospitals
· Blood investigations like hemogram, S.creatinine, RBS in all hospitals.
· High sensitivity troponin evaluation in tertiary care. Regular troponin in
secondary care.
· A handheld echo machine/portable echo machine is desirable in the ED or
ICU in tertiary care centre. Every emergency care physician should be
trained in basic echocardiogram to assess LV function, valve dysfunction
and regional wall motion abnormalities, to look for pericardial effusion and to
look for lung comets of pulmonary oedema (see chapter on heart failure).
· Facility to do angioplasty (tertiary care) and thrombolyse (tertiary care and
secondary care) including facility for continuous monitoring of ECG and
vitals and availability of defibrillator.
· It is useful to have risk calculators/ drug dose calculator/drip calculator in the
smart phone of the healthcare provider and several algorithms/apps
available in the internet may be downloaded to help in decision making

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9. Management Algorithm for ACS in ED

Shock

management

onset of pain

option Lysis preferred

Thrombolyse

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10. References

1. Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD,
Writing Group on the Joint ESC/ACCF/AHA/WHF Task Force for the
Universal Definition of Myocardial Infarction-Third universal definition of
myocardial infarction. Eur Heart J 2012;33(20):2551–2567.
2. 2017 ESC Guidelines for the management of acutemyocardial infarction in
patients presenting with ST-segment elevation The Task Force for the
management of acute myocardial infarction in patients presenting with ST-
segment elevation, European Heart Journal (2017) 00, 1–66
3. 2015 ESC Guidelines for the management of acute coronary syndromes in
patients presenting without persistent ST-segment elevation Task Force for
the Management of Acute Coronary Syndromes in Patients Presenting
without Persistent ST-Segment Elevation of the European Society of
Cardiology (ESC), European Heart Journal (2016) 37, 267–315.
4. Clinical Management Guidelines for Coronary Artery Disease for National
Programme for Prevention and Control of Diabetes, Cardiovascular
Disease and Stroke Partners, developed by Department of Cardiology and
Community Medicine, Post Graduate Institute of Medical education and
Research, Chandigarh, India.
5. Guidelines for the management of cardiovascular diseases in india, Part 1,
Ministry of Health & Family Welfare Govt. of India, New Delhi.
6. Antman E.M, Cohen M., Bernink et al, The TIMI Risk Score for Unstable
Angina/Non–ST Elevation MIA Method for Prognostication and Therapeutic
Decision Making, JAMA. 2000;284(7):835-842.
7. Morrow D.A, Antman E.M., Charlesworth A., Cairns R., Murphy S.A., de
Lemos J.A., et al., TIMI Risk Score for ST-Elevation Myocardial Infarction: A
Convenient, Bedside, Clinical Score for Risk Assessment at Presentation-
An Intravenous n PA for Treatment of Infarcting Myocardium Early II Trial
Substudy: Circulation. 2000;102:2031-2037

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Section II

Evaluation and management of heart failure

1. Scope

Population
Adults more than 18 years of age; not applicable to paediatric population

Key clinical issues covered:

Evaluation of heart failure
Management of Heart Failure
Acute decompensated heart failure

Clinical issues not covered:

Detailed description of drugs and interventions

Health care setting:

Secondary and tertiary health care, patient presenting in the outpatient
department or emergency department

Outcome:
Early diagnosis of heart failure with appropriate management and reduction in
mortality and morbidity.

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2. Abbreviations

ACEI Angiotensin Converting Enzyme Inhibitor

ADHF Acute Decompensated Heart Failure
ARB Angiotensin receptor blocker
ARNI Angiotensin Receptor Blocker Neprilysn Inhibitor
BB Beta Blocker
CAD Coronary Artery Disease
CBC Complete Blood Count
COPD Chronic Obstructive Pulmonary Diseases
CVD Cardiovascular Disease
DCM Dilated Cardiomyopathy
ECG Electrocardiogram
EF Ejection fraction
HCM Hypertrophic Cardiomyopathy
HF Heart Failure
HFrEF Heart Failure with Reduced Ejection Fraction
HFpEF Heart Failure with Preserved Ejection Fraction
IHD Ischemic Heart Disease
LVD Left Ventricular Dysfunction
MI Myocardial Infarction
NP Natriuretic Peptide
OMT Optimal Medical Therapy
PND Paroxysmal Nocturnal Dyspnoea

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3. Evaluation of Heart Failure

3.1. Introduction
Patients with heart failure (HF) present with various symptoms and signs.
The predominant symptom of heart failure is dyspnoea. Dyspnoea can occur in other
conditions, the commonest being chronic obstructive pulmonary disease (COPD).
Similarly the major sign of HF, oedema, can be caused by many other conditions
especially renal failure. It is important to diagnose HF early and to start appropriate
treatment as the short term and long term mortality of HF are high.
3.2. Definition
HF is defined as a clinical condition in which the heart is unable to pump
blood to meet the requirements of the body or is able to do so at increased
filling pressures. In other words the cardiac output is decreased or there is
elevation of venous pressures.
3.3 Diagnosis of heart failure
3. 3. 1. History
Typical symptoms of heart failure include
i. Dyspnea
ii. Orthopnea
iii. Paroxysmal nocturnal dyspnea
iv. Reduced exercise tolerance
v. Fatigue
vi. Edema
Dyspnoea, one of the typical symptoms of HF, can also be due to respiratory
system diseases. The pointers to a cardiac cause are new onset of dyspnoea with no
previous history of wheezing or other respiratory symptoms and the presence of
paroxysmal nocturnal dyspnoea (PND). Patients having PND wake up from sleep 1-
2 hours after going to bed with intense breathlessness which makes them sit up or
even go out of the room to get air. The dyspnoea subsides in about half an hour after
which the patient will have a comfortable sleep with no recurrence in the same night.
It may be associated with cough with pink frothy sputum. COPD patients also can
have nocturnal dyspnoea. Here the exacerbation occurs in the early morning
hours(3 am - 4 am).HF can also present with less typical symptoms like nocturnal

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cough, wheezing, bloated feeling, loss of appetite, other gastrointestinal symptoms

and confusion (especially in the elderly).
When eliciting history, any underlying cause for HF and any precipitating factor
leading to acute worsening have to be looked into. Underlying causes include
coronary artery disease, hypertension, valvular heart diseases and the use of cardio
toxic medications or radiation. Precipitating factors include anaemia, infection and
thyrotoxicosis, intake of drugs retaining salt and water(e.g. NSAIDs) and stoppage of
drugs given as treatment for HF.
3. 3. 2. Physical examination
The following signs can be present
i. Cold extremities
ii. Peripheral edema (ankle, sacral, scrotal)
iii. Tachypnea
iv. Tachycardia
v. Irregular pulse
vi. Narrow pulse pressure
vii. Elevated jugular venous pressure
viii. Cardiomegaly
ix. Third heart sound (gallop rhythm if there is tachycardia)
x. Murmur
xi. Hepatomegaly
xii. Ascites
xiii. Pulmonary crepitations
xiv. Signs of pleural effusion
xv. Cachexia
3.3. 3. Investigations
I. Blood
Complete blood count, blood sugar, blood urea, serum creatinine, sodium,
potassium, magnesium, thyroid function tests and liver function tests are indicated in
all HF patients.

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Anemia is a common precipitating factor and needs further evaluation including

peripheral smear, serum iron, ferritin and transferrin saturations. Peripheral smear
showing microcytic hypochromic anemia indicates iron deficiency while macrocytic
anemia indicates vitamin B12 deficiency. Elevated WBC count can be a clue to
infection. HF as well as the drugs used to treat HF can lead to renal function
derangement. Hence renal function tests are to be closely monitored especially in
those getting parenteral therapy for HF. HF therapy can lead to electrolyte imbalance
and frequent monitoring is needed. As both hyper and hypothyroidism can lead to or
precipitate HF, thyroid function tests should be done.
ii. Chest X-ray
Features of HF include cardiomegaly, prominence of upper lobe vessels,
interstitial edema and pleural effusion. X-ray can give a clue about underlying
valvular heart disease. However it may be normal especially in recent onset HF. It is
also useful to diagnose respiratory diseases like COPD, pneumonia or
pneumothorax.
iii. ECG
An abnormal ECG increases the likelihood of HF but has low specificity.
Abnormalities on the ECG may provide information on etiology (e.g. myocardial
infarction). ECG can help in diagnosing chamber enlargement, arrhythmias and
electrolyte abnormalities.
iv. Echocardiogram
Following parameters are to assessed
Ø LA
Ø LV size especially LV end systolic diameter
Ø Ejection fraction to assess the systolic function
Ø E/A reversal on mitral Doppler to assess diastolic dysfunction
Ø RWMA- Regional wall motion abnormality
Ø Left ventricular hypertrophy
Ø Pulmonary artery pressure
Ø Right ventricular function
Ø Inferior venecava – more than 21 mm in diameter and not collapsing
by 50% on sniffing indicates fluid overload

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v. Natriuretic peptide (NP) levels can be assessed in selected cases- It is

useful if the diagnosis is in doubt or to prognosticate in diagnosed heart
failure or to assess response to therapy. BNP or NT-pro BNP can be
used. Values less than 35 pg/ml for BNP and 125pg/ml for NT-pro BNP
rules out HF.
vi. Lung ultrasound is useful in acute of heart failure to distinguish between
exacerbation of COPD and acute pulmonary oedema. This is done by
keeping an ultrasound probe in the intercostal spaces and looking for
comet-tail artefact. ( In the figure below first picture is of a normal person or
person with COPD and second picture shows comet tail artefact
suggestive of pulmonary oedema)
.

3.3.4. Risk stratification

Assess the symptomatic status of patient by NYHA class

No limitation of physical activity. Ordinary physical

NYHA Class I activity does not cause undue fatigue, palpitation,
dyspnoea or angina
Slight limitation of physical activity. Comfortable at
NYHA Class II rest. Ordinary physical activity results in fatigue,
palpitation, dyspnoea, or angina
Marked limitation of physical activity. Comfortable at
NYHA Class III rest. Less than ordinary activity causes fatigue,
palpitation, dyspnoea or angina
Unable to carry on any physical activity without
NYHA Class IV discomfort. Symptoms of heart failure may be
present at rest.

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High risk indicators

Ø NYHA Class III/IV
Ø Hypotension
Ø EF <35%
Ø Severe pulmonary artery hypertension
Ø Renal failure
Ø Electrolyte imbalance
Ø RV Dysfunction
4. Management of Heart Failure
4.1. Introduction
The aims of treatment are to control the HF, stabilise the cardiac status,
correct the precipitating factors, prevent progression of the disease and if possible
correct the underlying cause. The main stay of treatment is medical in majority of
patients so that drug therapy should be optimal with periodic stepping up or
stepping down of the dose of medications. Other modes of therapy like cath lab
based intervention, devices or surgery may be required in selected patients.
4.2. Classification of HF
Classification is done based on the left ventricular function (LV ejection
fraction) assessed by echocardiogram.

Hf with reduced EF HF with preserved

Features EF (HFpEF)
(HFrEF)
Symptoms + +
Signs + +

LVEF < 40% >50%

None needed Elevated natriuretic

peptides and one of the
Other Criteria following needed
·LV diastolic dysfunction
·Structural heart disease

LVEF in the range of 40–49% is called as HF with mid-range EF. Generally it is

grouped along with HF with reduced EF for treatment purpose

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.4.3.Treatment
4.3.1. General measures

v NYHA Class I and II Patients can be managed as outpatients

1. Assess all the drugs patient is taking and make necessary changes- non-
steroid anti-inflammatory drugs, steroids and pioglitazone should be
stopped.
2. Salt restriction – less than 4 gm per day
3. Fluid restriction to 1.2-1.5 litres per day
4. Oral furosemide40 mg once or twice daily (daily weight recording is useful to
assess the fluid restriction and dose of diuretic especially in severe cases)
5. If BP is more than 100 mm of Hg systolic, start angiotensin converting
enzyme inhibitorsACE-I). Any one of the ACE Inhibitors may be chosen.
Enalapril 2.5 mg twice daily is a good choice for initiation and titration. If ACE-
I are not tolerated due to cough, angiotensin receptor blocker (ARB) can be
considered (see tables 1 & 2 for details)
6. Beta blocker (BB)is to be considered after careful evaluation if there are no
contraindications like bradycardia, hypotension or wheeze(see table 3 for
details)
v NYHA Class III/IV are to be managed as In patients
1. Hospitalise the patient and as mentioned above check the drugs patient is
taking
2. Propped up position as needed.
3. Oxygen inhalation if O2 saturation<90%
4. Record heart rate, BP, respiratory rate and oxygen saturation by pulse
oxymeter twice daily
5. Weight recording daily- plan to lose at least 0.5 kg per day with proper
treatment
6. Salt restriction
7. Fluid restriction- 1.2 -1.5 litres daily (including all liquid foods like tea, coffee,
kanji and drinking water). This amounts to six or seven glasses of 200 ml.
8. Blood investigations to be routinely monitored during hospital stay include

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Hb, serum levels of creatinine, sodium and potassium

9. Avoid NSAIDs, pioglitazone, systemic steroids and other drugs causing fluid
retention
10. Drugs for diabetes, hypertension, COPD or for management of CAD should
be continued
4. 3.2. Specific treatment
· Start drugs at low doses
· Titrate up to maximum tolerated dose or maximum recommended
dose
· Watch for side effects and make drug change or dose reduction
· Therapy given below has to be modified based on the clinical status of
patient
· First two days
1. Parenteral diuretics (oral absorption may be erratic due to gut wall edema) -
Inj. Furosemide 40 -80mg i.v. 8thhourly or 12th hourly
Furosemide i.v. infusion of 5-10 mg/hr for 24 hours is an alternative if venous
congestion is gross
2. I.V Inotropes- In extremely dyspnoeic patients a short period- 24 to 48
hours- of inotropic support can be helpful. I.V dobutamine can be given as
infusion at a dose of 5 microgram/kg/min and can be increased up to 20
microgram/kg/min
3. ACEI- if systolic BP is more than 100 mm of Hg and there is no renal failure or
hyperkalemia. Eg: Tab. enalapril 2.5 mg twice daily can be started. (See
Table 1 for doses and other ACEI)
4. ARB- if ACEI intolerant(See Table 2 for doses)
5. Spironolactone- 25 mg once daily. Watch for hyperkalemia
· Days 3 to 5- Clinically Improved Patient
1. Change to oral diuretics
2. Start BB- carvedilol 3.125 mg twice daily (See Table 3 for doses and other
Beta blockers)
3. Step up ACEI
4. Advise ambulation- walk slowly for short distance in the ward- gradually

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increase
5. Discharge by 5 days - Schedule review at 2 to 3 weeks with the following
investigations- Hb, Serum levels of creatinine, sodium and potassium

· Days 3 to 5- Clinically Not Improved Patient

1. Do not start beta blockers
2. Check for compliance to drugs , salt and fluid restriction
3. Add a second diuretic if sodium and potassium are normal. Add metolazone
2.5 mg once daily. Can be stepped up if needed with monitoring of
electrolytes
4. Digoxin 0.125 mg once daily may be started( Watch for side effects)

5. Consider new drugs

· Day 5-7- Clinically not improved- Resistant Heart Failure

Consider referral to a specialised centre for special investigations and advanced

modes of management (see section 5)

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Table 1. ACE Inhibitors

Drug Starting Dose Target dose

Enalapril 2.5 mg twice daily orally 20 mg twice daily

Ramipril 1.25 mg twice daily orally 5 mg twice daily
Lisinopril 2.5 mg oncedaily orally 20mg once daily

Table 2. ARBs

Drug Starting Dose Target dose

Losartan 25mg once daily orally 100mg once daily

Valsartan 40mg twice daily orally 160mg twice daily

Table 3- Beta Blockers

Drug Starting Dose Target dose

Carvedilol 3.125 mg twice daily orally 25mg twice daily

Metoprolol succinate
(CR/XL) 12.5 mg once daily orally 100-200 mg once daily
(sustained release only
to be used)
Bisoprolol 1.25mg once daily 10mg once daily

· New Drugs
1. Ivabradine slows heart rate if the patient is in sinus rhythm. Ivabradine is not
to be used in atrial fibrillation. Starting dose is 5 mg twice daily and can be
stepped up to 7.5 mg twice daily if needed to control heart rate in patients in
whom BB cannot be started or are not tolerated or when the heart rate cannot
be brought down below 70/min with BB alone.
2. ARNI is ARB (valsartan) combined with neprilysn inhibitor
(Sacubitril).Natriuretic peptides naturally promote diuresis and are degraded
by neprilysn. Thus neprilysn inhibitor raises levels of peptides and induces
diuresis. When introducing ARNI, if the patient is already on ACEI, stop ACEI
and start ARNI only after 36 hours. If the patient is on ARB, it can be directly

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switched over to ARNI without waiting period.

3. Tolvaptan: To be considered in cases with hyponatremia and fluid overload
for a short term use. Better to use for in-patients only with careful monitoring of
electrolytes.
4.3.3. Follow UP
v First review- 2 weeks after discharge
a) See investigation results- Hb, S. creatinine, sodium and potassium and
take corrective steps.
b) Reduce diuretics if no fluid overload
c) Step up enalapril if BP is more than 100 mm of Hg
d) step up carvedilol if heart rate is high and BP is more than 100 mm of Hg
e) Consider H Influenza and pneumococcal vaccination in cases with
repeated hospitalization
v Second review- 1 month after first review
a) Do investigations as in previous step and correct if needed
b) Try to step up ACEI and BB depending on BP and heart rate
v Long term follow up
a) Reduce diuretics to minimum possible dose or stop
b) Continue ACEI and BB at maximum tolerated/ maximum recommended
dose
v Problems during follow up
a) Dry cough: Can be due to ACEI - change to ARB if sleep is disturbed
b) Cramps: Electrolyte imbalance due to diuretics. Correct by oral
supplementation and by reducing diuretics
c) Painful gynaecomastia- due to spironolactone or digoxin. Try changing to
eplerenone
d) Anemia: Evaluate for the type and cause and correct appropriately.
Consider IV Iron in selected cases( ferric carboxy maltose)

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4.3.4. Advanced Investigations

1. Trans esophageal Echocardiogram (TEE) –Consider in cases of poor
trans thoracic window, prosthetic valve malfunction and suspected
infective endocarditis
2. Coronary angiography(CAG)- In patients with previous history of IHD,
having angina pectoris or ECG and Echo evidence of CAD (after
stabilizing the CHF)
3. SPECT-(Single Photon Emission Computerized Tomography)-to
look for viability of myocardium prior to revascularization
4. Cardiac Magnetic Resonance Imaging (CMR)-to rule out suspected
inflammatory / infiltrative conditions or cardiomyopathy
4.3.5. Special modes of treatment
1. Implantable cardioverter defibrillator (ICD) -to be considered in HF
patients who have survived a cardiac arrest. Can be considered in
patients with symptomatic HF with LVEF ≤ 35% despite ≥ 3 months of
OMT.
2. Cardiac resynchronization therapy (CRT) -For HF patients who
continue to be symptomatic despite OMT and in sinus rhythm with QRS
morphology of LBBB type and QRS duration more of than 150
milliseconds
3. Mechanical circulatory support (Left Ventricular Assist Devices
LVAD)-can be considered in HF patients as a bridge to transplant. It
can be considered in patients with severe symptoms for last 2 months
despite optimal medical and device therapy if LVEF <25%, and there are
≥3 HF hospitalizations in last 1 year
4. Cardiac Transplantation-May be considered for end-stage HF patient
with severe symptoms, a poor prognosis, and no remaining alternative
treatment options. Patient should be motivated, well informed, and
emotionally stable and capable of complying with the intensive treatment
required postoperatively

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4. 3.6. Heart failure with preserved EF

Clinical presentation can be similar to patients with heart failure with reduced
EF. Management is mainly control of basic diseases like hypertension, CAD,
diabetes mellitus etc. Symptomatic management with diuretics to reduce congestion
and management of arrhythmia like atrial fibrillation is indicated. Diuretic use has to
be judicious.
5. Acute Decompensated Heart Failure (ADHF)
5.1 Definition and classification
ADHF is the rapid onset or acute worsening of symptoms and signs of heart
failure. It requires urgent evaluation and treatment as it is a life threatening
emergency. ADHF may present as a first occurrence (20% cases) or, more
frequently, as a consequence of acute decompensation in chronic HF patients (80%
cases). In ADHF the symptoms can be of congestion (systemic and or pulmonary-
the WET cases) or of low cardiac output (the DRY cases).There can be four
different classes of patients.
1. Wet and warm : congestion with normal cardiac output
2. Wet and cold : congestion with low cardiac output
3. Dry and cold : no congestion but low cardiac output
4. Dry and warm : no congestion and normal cardiac output

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5.2 Symptoms and signs

Congestion - Systemic /
Pulmonary Low cardiac output

Dyspnoea at rest Fatigue

Orthopnoea Decreased urine output
Paroxysmal nocturnal Altered mental status
Symptoms dyspnoea Nausea/ vomiting
Leg edema
Early satiety
Abdominal distension
Bloating
Cool extremities
Edema
Low volume pulse
Tachypnea
Hypotension
Signs Tachycardia
Altered mental status
Low oxygen saturation
Worsening renal function
Elevated jugular venous
pressure
Basal lung crepitations

5.3 Investigations( Similar to Chronic Heart Failure)

1. X-ray Chest: Confirms pulmonary congestion(may even show the typical

bat's wing appearance of pulmonary edema) and excludes respiratory
causes
2. ECG : Assess rhythm and any ongoing ischemia
3. Natriuretic Peptides: Plasma BNP levels less than 100 pg/ml or NT- Pro
BNP less than 300 pg/ml excludes AHF (Cut off values are higher in the
acute setting)
4. Echocardiogram: Limited bedside Echo can assess LV function by noting
the ejection fraction, systemic congestion by noting. Inferior venecaval
distension more than 21 mm and pulmonary congestion by noting comet
sign on lungs. Echo also helps to differentiate acute HF from conditions like
pulmonary embolism, cardiac tamponade, exacerbation of COPD
5. Lung Ultrasound: Look for comet tail artefacts in lung fields which are
specific for acute pulmonary edema.

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Acute pulmonary edema

5.4.Management
a) Identify the cause or precipitating factor of AHF and correct it. It may
be high blood pressure, arrhythmia, acute ischemia, infection or
drugs
b) Oxygen can be given to all patients to relieve dyspnoea. Non-
invasive and even invasive ventilation can be given if oxygen
saturation remains persistently low.
c) Intravenous Diuretics- Furosemide can be given IV. Dose can be
decided based on blood pressure. If systolic BP is above 90 mm of
Hg, 40-60 mg furosemide can be given. If BP is lower than 90 mm of
Hg smaller doses 20- 40 mg can be given.
d) Intravenous vasodilators: Are to be given if blood pressure is high.
The agents used are Nitroglycerin- start with 20 micro gram /min; can
go up to 400 microgram/min
Nitroprusside- start with 10 micro gram /min; can go up to 350
microgram/min
e) Intravenous inotropes: are to be given if BP is low and there are signs
of hypo perfusion. The agents used are
Dopamine: 5-10 micro gm/kg/min can increase to 10-15 micro
gm/kg/min
Dobutamine: 5-10 micro gm/kg/min can increase to 10-20 micro
gm/kg/min
Milrinone: bolus 50 micro gm/kg followed by 0.125 – 0.75 micro

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gm/kg/min
Levosimendan: loading dose of 6-12microgm/kg followed by 0.05 –
0.2 microgm/kg/min as infusion
f. Adjustment of pre-existing drugs
i. ACEI/ARB- can be continued in most cases. Temporary
withdrawal or reduction in dose may be needed in case of severe
symptomatic hypotension or creatinine rise
ii. Beta Blockers : Can be withheld if patient has pulmonary edema
iii. Mineralocorticoid antagonists : With hold if creatinine is more
than 2.5 mg/dl or potassium more than 5.5 meq/L
iv. Digoxin can be started if not already being given
If not improving
Ultra filtration: can be tried if diuretics are not producing adequate
response
LV assist devices
Look for any unidentified underlying cause
Refer to a dedicated heart failure team

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Presence of congestion

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6. References
1. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic
heart failure - European Heart Journal (2016) 37, 2129–2200
2. An Official American Thoracic Society Statement :Update on the
Mechanisms, Assessment, and Management of dyspnea- American journal
of respiratory and critical care medicine Vol 185: 2012
3. Frese T, Sobeck C, Herrmann K, Sandholzer H: Dyspnea as thereason for
encounter in general practice. J Clin Med Res 2011; 3:239–46.
4. Wang CS, FitzGerald J, Schulzer M, Mak E, Ayas NT: Does thisdyspnoeic
patient in the emergency department have congestive heart failure? JAMA
2005; 294: 1944–56.
5. Nomenclature and Criteria for Diagnosis of Diseases of the Heart and Great
th
Vessels (Little, Brown & Co).-9 edition
6. Roberts E, Ludman AJ, et al The diagnostic accuracy of the natriuretic
peptides in heart failure: systematic review and diagnostic meta-analysis in
the acute care setting. BMJ 2015;350:h910.55.
7. Maisel A, Mueller C, Braunwald E. ET AL State of the art: using natriuretic
peptide levels in clinical practice. Eur J Heart Fail 2008; 10:824–839.
8. Braunwalds Text Book of Cardiology 14th Edition
th
9. Hurst Text Book of Cardiology- 14 Edition
10. Cardiological Society of India Update 2015- Heart Failure
11. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for
the management of heart failure, Circulation April 28,2017

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Department Of Health And Family Welfare
Government Of Kerala
Annexe II, Secretariat
Thiruvananthapuram
Kerala-695001
February 2021

Kerala HEALT H