Assess Chest Pain

CLINICAL DECISION
MAKING TOOLKIT
Instant guidance
for diagnosis, risk management
and treatment
2018 edition

The
Clinical Decision Making
Toolkit is produced by the Acute Cardiovascular
Care Association (ACCA), developed and distributed
through an educational grant from AstraZeneca.
AstraZeneca was not involved in the development
of this publication and in no way influenced its content.

ISBN: 978-2-9537898-7-4
The Acute Cardiovascular Care Association
Clinical Decision-Making
TOOLKIT
Héctor Bueno, M.D., PhD., FESC
Editor in Chief
Pascal Vranckx, M.D., PhD
Associate Editor

The ACCA Toolkit is available
through different platforms:
•
Printed booklet, available at congresses
where ESC-ACCA is represented
•
Web-based pdf file downloadable at:
www.escardio.org/ACCA
•
Mobile application for smartphones/tablets
available in both Apple Googleplay stores
Héctor Bueno
M.D., PhD., FESC
Editor in Chief
The best care of patients with acute cardiovascular syndromes
relies not only on specialists but also on systems of care that
involve many non-cardiologists. Several of these syndromes
require immediate diagnosis and decisions on treatment,
some of them life-saving. Critical decisions must often be
made quickly by professionals with different backgrounds
and levels of expertise with limited resources. This poses a
significant clinical challenge.
Against this background, the ACCA Clinical Decision-
Making Toolkit was created as a comprehensive resource
encompassing all aspects of acute cardiovascular care but
structured as an easy-to-use instrument in environments
where initial acute cardiovascular care is typically initiated.
Comprehensive tables, clear diagrams and algorithms, based
on the ESC clinical practice guidelines as well as in clinical
experience should provide diagnostic and therapeutic
guidance at a glance.
This 2018 Edition of the Clinical Decision Making Toolkit
has been updated with the 2016 and 2017 ESC Guidelines,
a chapter on secondary prevention was added and the chapter
on acute heart failure benefited a major update. However, it
does not replace textbooks and other sources of information
that need to be consulted to reach an optimal management
of these patients.
II
Preface

7 DAYS F R O M C A R D I A C E V E N T
U N T I L P A T I E N T S T A B I L I S A T I O N
ICCU
INTENSIVE
CARDIAC
CARE UNIT
CCU
CORONARY
CARE UNIT
PRE-HOSPITAL CARE
GENERAL
HOSPITAL
EMERGENCY ROOM
CARDIAC ARREST, STEMI, ACS, AHF,
CARDIOGENIC SHOCK, ARRHYTHMIAS,
VASCULAR SYNDROMES

List of Authors �� VI
CHAPTER 1: KEY SYMPTOMS
Chest Pain - M. Lettino, F. Schiele �� P. 2
Dyspnea - C. Müller �� P. 9
Syncope - R. Sutton �� P. 16
CHAPTER 2: ACUTE CORONARY SYNDROMES
General concepts - H. Bueno �� P. 24
Non ST-segment elevation ACS - H. Bueno �� P. 29
STEMI - P. Vranckx, B. Ibañez �� P. 34
CHAPTER 3: SECONDARY PREVENTION AFTER ACS
General secondary prevention strategies and lipid lowering - H. Bueno, S. Halvorsen �� P. 38
Antithrombotic treatment - F. Costa, S. Halvorsen �� P. 41
CHAPTER 4: ACUTE HEART FAILURE
Wet-and-warm heart failure patient - V.P. Harjola, O. Miró �� P. 52
Cardiogenic shock (wet-and-cold) - P. Vranckx, U. Zeymer �� P. 61
IV
Contents

CHAPTER 5: CARDIAC ARREST AND CPR - N. Nikolaou, L. Bossaert �� P. 71
CHAPTER 6: RHYTHM DISTURBANCES
Supraventricular tachycardias and atrial fibrillation - J. Brugada �� P. 80
Ventricular tachycardias - M. Santini, C. Lavalle, S. Lanzara �� P. 84
Bradyarrhythmias - B. Gorenek �� P. 87
CHAPTER 7: ACUTE VASCULAR SYNDROMES
Acute aortic syndromes - A. Evangelista �� P. 92
Acute pulmonary embolism - A. Torbicki �� P. 102
CHAPTER 8: ACUTE MYOCARDIAL/PERICARDIAL SYNDROMES
Acute myocarditis - A. Keren, A. Caforio �� P. 112
Acute pericarditis and cardiac tamponade - C. Vrints, S. Price �� P. 117
CHAPTER 9: DRUGS IN ACUTE CARDIOVASCULAR CARE - A. de Lorenzo �� P. 121
Abbreviations �� P. 191
References and copyright acknowledgments �� P. 199
V
Contents (Cont.)

Leo Bossaert
Department of Medicine, University and University Hospital Antwerp, Antwerp,
Belgium
Josep Brugada
Department of Cardiology, Hospital Clinic Universitat de Barcelona, Barcelona, Spain
Héctor Bueno
Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC),
and Department of Cardiology, Hospital Universitario 12 de Octubre, Madrid, Spain
Alida Caforio
Department of Cardiology, Padua University Medical School, Padua, Italy
Francesco Costa
Cardiovascular institute, Hospital Clínic, University of Barcelona, Barcelona, Spain
Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy
Artur Evangelista
Department of Cardiology, Hospital Universitario Vall d’Hebrón, Barcelona, Spain
Bulent Gorenek
Department of Cardiology, Eskisehir Osmangazy University, Eskisehir, Turkey
Sigrun Halvorsen
Department of Cardiology, Oslo University Hospital Ulleval and University of Oslo, Oslo, Norway
Veli-Pekka Harjola
Division of Emergency Medicine, Department of Emergency Care and Services, Helsinki
University Hospital, Finland
Borja Ibañez
Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC),
and Department of Cardiology, University Hospital Fundación Jiménez Díaz, Madrid, Spain
Andre Keren
Heart Failure and Heart Muscle Disease Centre, Hadassah University Hospital,
Jerusalem, Israel
VI
List of Authors

Stefania Lanzara
Department of Emergency, Ospedale Madre Giuseppina Vannini, Rome, Italy
Carlo Lavalle
Department of Cardiology, Ospedale San Filippo Neri, Rome Italy
Maddalena Lettino
Clinical Cardiology Unit, IRCCS Istituto Clinico Humanitas, Milano, Italy
Ana de Lorenzo
Pharmacy Department, Hospital General Universitario Gregorio Marañón, Madrid, Spain
Òscar Miró
Emergency Department, Hospital Clínic, University of Barcelona, Barcelona, Catalonia, Spain
Christian Müller
Department of Cardiology, University Hospital Basel, Basel,Switzerland
Nikolaos Nikolaou
Departement of Cardiology, Konstantopouleio General Hospital, Athens, Greece
Susanna Price
Consultant Cardiologist Intensivist, Royal Brompton Hospital, London, United Kingdom
Massimo Santini
Department of Cardiology, Ospedale San Filippo Neri, Rome, Italy
François Schiele
Department of Cardiology, University Hospital Jean-Minjoz, Besancon, France
Richard Sutton
Department of Cardiology, National Heart and Lung Institute Imperial College,
London, United Kingdom
Adam Torbicki
Department of Pulmonary Circulation and Thromboembolic Diseases, Centre of
Postgraduate Medical Education, ECZ Otwock, Poland
Pascal Vranckx
Department of Cardiology and Critical Care Medicine, Hartcentrum Hasselt, Hasselt, Belgium
Christiaan Vrints
Department of Cardiology, Antwerp University Hospital, Edegem, Belgium
Uwe Zeymer
Department of Cardiology, Herzzentrum Klinikum Ludwigshafen, Ludwigshafen, Germany
VII
List of Authors (Cont.)

CHAPTER 1
KEY SYMPTOMS
1.1 CHEST PAIN �� p.2
M. Lettino, F. Schiele
1.2 DYSPNEA �� p.9
C. Müller
1.3 SYNCOPE �� p.16
R. Sutton
P.1
1

1. Presentation
2. ECG
3. Troponin
4. Diagnosis
Reference: Roffi et al. Eur Heart J 2015; eurheartj.ehv320.
Low likelihood
of Acute Coronary Syndrome
High likelihood
of Acute Coronary Syndrome
Noncardiac
Other
Cardiac
UA STEMI
NSTEMI
P.2
1.1
Initial assessment of patients with CHEST PAIN

First call for
chest pain Higher death risk / probability for ACS Lower death risk / probability for ACS
Arguments
for vital risk
•
Cardiorespiratory arrest, syncope/
loss of consciousness, neurological defect
• Dyspnea (see chapter 1.2 page 9)
•
Arrhythmias – tachycardia
• Normal consciousness
• Normal breathing
•
Normal heart rhythm
Context, CV risk Age 40 years, previous CV disease
(MI, stroke, PE), modifiable CV risk factors
(smoker, HTN, hypercholesterolemia, diabetes),
chronic CV treatment
•
Age 40 years,
•
No previous CV disease
•
No CV risk factors
• No chronic treatment
Chest Pain Medial/lateral thoracic pain, intense,
with dyspnea
•
Depends on position/palpation/
movements
•
Variable intensity, short duration (1 min)
• Hyperthermia
Cardiac
Ischemic
Pain
Retro-sternal, constriction, jaw/cervical/arm/back
irradiation, spontaneous, prolonged 20 min +
dyspnea, sweating, lightheadedness, nausea
•
Lateral, abdominal irradiation
•
No neuro-vegetative symptoms
P.3
1.1
Factors to be considered in the evaluation
after the first call for CHEST PAIN

No
Yes
Likelihood of ACS
High probability for ACS Low probability for ACS
Emergency transport
with trained medical team
Emergency care:
Resuscitation, hemodynamic or
rhythm restoration (see chapter 5)
APPROACH AFTER FIRST CALL FOR OUT-OF-HOSPITAL CHEST PAIN
VITAL RISK? (see chapter 1.1 page 3)
P.4
1.1
Approach after first call for out-of-hospital CHEST PAIN

ECG, decision for reperfusion,
antithrombotics, immediate
transport to ED/CPU/ICCU/Cathlab
(see chapter 2)
Emergency transport
Emergency transport
with trained medical team
Hospital admission
to the ED/CPU
Cardiology
ward
Non-cardiology
ward
Discharge after
prolonged observation
P.5
1.1

First medical contact Higher death risk / probability for ACS Lower death risk / probability for ACS
Hemodynamic,
respiratory, neurological
distress
•
Cardiopulmonary arrest, hypotension, tachycardia,
shock
•
Dyspnea, hypoxemia, lung rales (Killip class 2)
•
ECG: ST-segment deviation
•
Normal consciousness, no motion defects
•
Normal HR and BP
•
Normal breathing and SpO2,
no loss of pulse
Probability for ACS •
Context, typical symptoms consistent
with myocardial ischemia
• ECG changes
• Hs cTn
•
No CV risk, atypical symptoms,
normal ECG
•
Negative hs cTn only if onset of pain
3 hours (see chapter 2.1 page 24)
STEMI NSTE-ACS
Uncertain diagnosis
(see chapter 2.1 page 24)
ECG criteria for STEMI
ST depression or normal ECG
Normal ECG (repeat 12-lead ECG
recording if symptoms persist/recur)
Other ST-segment abnormalities
Type of reperfusion
Time assessment
•
Primary PCI or thrombolysis? Primary PCI if delay
120 min (preferably 90 min)
or 60 min if onset of pain 120 min
Consider age, anterior wall location
•
Relevant times: Symptom onset, first medical
contact (FMC). FMC → ECG/diagnosis; FMC → PCI;
FMC → thrombolysis
•
Primary PCI between 12-48 hours
in patients with ongoing ischemia,
symptoms or clinical/haemodynamic
or electrical instability
•
No reperfusion if delay 12 hours
and stable, asymptomatic, without
ST-segment elevation
P.6
1.1
Factors to be considered in the evaluation
during the first medical contact for CHEST PAIN

Yes
Resuscitation, hemodynamic
or respiratory support
(see chapters 4 5)
Type of reperfusion (primary PCI or fibrinolysis)
Record times (symptom onset, FMC)
High probability Low probability
No
FIRST MEDICAL CONTACT IN PATIENTS WITH CHEST PAIN (HOME-AMBULANCE)
Hemodynamic, respiratory or neurological distress?
ST-segment elevation
ECG 10 min → ACS ?
No ST-segment elevation but
other ECG changes or persistent pain
Suspect ACS
Uncertain diagnosis
No antithrombotic treatment
Transfer to a proximity centre
(with or without cath-lab)
Start recommended medical therapy
(including antithrombotic drugs)
Transfer to a centre with cath-lab
Non cardiovascular disease?
• Sepsis
• Acute respiratory distress
• GI disease, bleeding, others
Acute cardiovascular disease other than ACS?
• Acute aortic syndrome (see chapter 7)
• Pulmonary embolism (see chapter 7)
• Acute pericarditis (see chapter 8)
• Acute heart failure (see chapter 4)
P.7
1.1
First medical contact in patients with CHEST PAIN (home-ambulance)

• Diagnosis of NSTE-ACS (see chapter 2)
• Acute aortic syndrome (see chapter 7)
• Acute pulmonary embolism (see chapter 7)
• Acute pericarditis (see chapter 8)
• Acute heart failure (see chapter 4)
• Aortic stenosis, hyperthrophic cardiomyopathy
• Acute gastro-oesophageal disease
• Acute pleuro-pulmonary disease
• Acute psychogenic disorders
Repeat clinical and ECG examination
Laboratory: cTn, renal function, Hb,
D-dimers
Imaging: TTE, CT scan
Diagnostic coronary angiography
Yes No
Yes No
MANAGEMENT OF PATIENTS WITH CHEST PAIN (EMERGENCY ROOM)
STEMI,
NSTE-ACS with persistent pain,
Hemodynamic distress
No direct transfer to cath-lab
→ ED, Chest Pain Unit,
cardiology ward, other wards
Other CVD
or No ACS
Resuscitation, hemodynamic
or respiratory support
(see chapters 4 5)
Direct transfer to cath-lab
Complicated NSTEMI
STEMI (see chapter 2)
Hemodynamic, respiratory or neurological distress?
P.8
1.1
Management of patients with CHEST PAIN (emergency room)

DYSPNEA: DIFERENTIAL DIAGNOSIS
50% have ≥2 diagnoses, which may result in acute respiratory failure*!
• ECG • Chest X-ray • Blood count • cTn
• BNP • Venous BG • D-dimers if suspicion of PE
Basic measures
• BP, HR, respiratory rate, SpO2 temperature
• Start oxygen to target SpO2 94-98%
• Start i.v. line monitor patient
Criteria for transfer to ICU
(despite treatment for 30 minutes)
• Respiratory rate 35/min
• SpO2 85%
• SBP 90 mmHg
• HR 120 bpm
Investigations:
Acute heart
failure
Acute coronary
syndrome
Exacerbated COPD
or other chronic
lung disease
Other causes, including
• Asthma
• Severe sepsis
• Tumor
• Pneumothorax
• Pleural effusion/ascites
• Anxiety disorder
• Anemia
• Bronchitis
• Metabolic acidosis
• Neurologic disease
Pneumonia Pulmonary
embolism
* Defined as ≥1 criterion:
• Respiratory rate ≥25/min
• PaO2 ≤75 mmHg
• SpO2 ≤92% in ambient air
• PaCO2 ≥45 mmHg with arterial pH ≤7.35
Reference: Ray P et al. Acute respiratory failure in the elderly: etiology, emergency diagnosis and prognosis. Critical Care (2006); 10 (3):R82.
P.9
1.2
DYSPNEA: Diferential diagnosis

BASIC WORK-UP
• Positioning Keep head of bed elevated above level of legs
• Oxygen Up to 12 l/min via rebreather mask, titrate oxygen saturation to 94%
• Nitroglycerin 1-2 SL tablets or 2-3 patches 10 mg (1st
choice). In pulmonary edema with severe shortness
of breath: NTG drip 0.05% (100 mg in 200 ml)
- Start with 25 µg/min = 3 ml/h, check BP after 5 and 10 min
- Increase dose by 25 µg/min at a time as long as SBP 90 mmHg
- Additional BP check 5 and 10 min after each increase in dosing
- Check BP every 20 min once a steady drip rate is reached
• Furosemide 40-120 mg i.v. (adjust based on kidney function and clinical findings; monitor creatinine)
• Morphine 2 mg i.v. (preceeded by 10 mg i.v. metoclopramide PRN) if patient is in severe dyspnoea
• Consider digoxin 0.5 (-1.0) mg i.v. in patients with atrial fibrillation
• Anticoagulation Therapeutic dosing in ACS and atrial fibrillation: Enoxaparin 1 mg/kg body weight as 1st
dose
• Chest X-ray (lung ultrasound)
• Echocardiogram
During admission (earlier if decompensated
aortic stenosis or endocarditis are suspected)
• Coronary angiography
Emergent in patients with ACS; delayed in
patients with suspected coronary artery disease
• Immediate 12-lead ECG, cardiac monitor, BP, respiratory rate,
pulse oximetry
• Clinical findings
Most commonly: lower extremity edema, jugular venous
distension,rales,workupforunderlyingcardiacdiseaseandtriggers
• Laboratory findings
Complete blood count, chemistries, cardiac enzymes, BNP,
TSH, ABG as needed
P.10
1.2
DYSPNEA: Acute heart failure (see chapter 4.1)

Reference: Ware L B and Matthay M A. Acute Pulmonary Edema. New Engl J Med (2005); 353:2788-2796.
Unstable after 30 minutes
CCU/ICU transfer Ward transfer
Stable after 30 minutes
P.11
1.2

Priorities: 1. Vital signs 2. Diagnostic screening dependent upon clinical stratification
Hemodynamically unstable Hemodynamically stable
Initiate transfer to ICU
Immediate TTE (if available)
Result
inconclusive
→ CT-angio
Right
ventricular
dysfunction
Wells criteria for PE:
Score
• Clinical signs and symptoms of
deep vein thrombosis (DVT) + 3.0
• No alternative diagnosis (or alternative
diagnosis less likely than PE) + 3.0
• Heart rate 100/min + 1.5
• Immobilization or operation within
the last 4 weeks + 1.5
• Previous DVT or PE + 1.5
• Hemoptysis + 1.0
• Malignant tumor with treatment within the
last 6 months or palliative care + 1.0
ABG, ECG, chest X-ray plus clinical assessment of PE probability (risk factors) plus monitoring
P.12
1.2
DYSPNEA: Acute pulmonary embolism (see chapter 7.2)

Copyright: Stein PD, Woodard PK, Weg JG, et al. Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II investigators.
Am J Med (2006); 119:1048–55. - Goldhaber SZ. Pulmonary embolism. Lancet (2004); 363 (9417) 1295-1305. - Agnelli G and Becattini C. Acute Pulmonary
Embolism. New Engl J Med (2010); 363:266-274.
Intermediate
probability
Total score 2-6
High
probability
Total score 6
Low
probability
Total score 2
Outpatient management possible?
→ Risk stratification
PE confirmed: Treatment
(see chapter 7.2)
(see chapter 7.2)
P.13
1.2

DYSPNEA: COPD EXACERBATION
• Verify diagnosis (DD: PE, acute heart failure, pneumothorax)
• Oxygen administration → SpO2 target 88-92% (Beware of carbonarcosis: ABC after 1 h)
Definition:
Known COPD and/or • Progressive dyspnea and/or
• Change in quantitiy and color of sputum and/or
• Heavy coughing
• COPD classification
(GOLD)
• Etiology
• Hospitalisation indicated?
• Follow-up
• Evaluate ICU criteria
• NIV indicated?
• Laboratory findings: Blood count, coagulation, ProCT, perhaps BNP, D-Dimers
• Chest X-ray; ECG (exclusion of differential diagnoses)
• Sputum cultures (always in case of hospitalisation or previous
outpatient antibiotic treatment)
• Oxygen therapy 2-(4) l; target saturation 90%
• Salbutamol/ipratropium inhalations ≥4-6 x/d, if needed long-term inhalation
• Systemic steroids prednisone 0.5 mg/kg of body weight for 5 days
• Antibiotic treatment should be considered; always indicated in stage Gold IV
• Physiotherapy
• History, clinical examination (blood pressure, pulse, oxygen saturation, vigilance)
Copyright: Leuppi JD et al. JAMA. 2013 Jun 5; 309(21):2223-31.
P.14
1.2
DYSPNEA: COPD exacerbation

DYSPNEA: COMMUNITY-ACQUIRED PNEUMONIA
Objective: diagnostics, risk stratification empirical immediate treatment 2(-4) hours
Definition
Complications
• Chest X-ray if dyspnea cough
• Laboratory workup clinical chemistry; BGA; procalcitonin
• Sputum if patient admitted
• Blood cultures (2x2) if patient admitted
• Legionella antigen (urine) if Legionellosis suspected
• Pneumococcus antigen (urine) if no other pathogen isolated
Risk stratification → manageable on an outpatient basis?
- Pneumonia Severity Index
- CURB-65
• Treatment; procalcitonin guided treatment
• Consider outpatient treatment where PSI I-III or CURB65 0 or 1
• Minimum 5-day course of treatment and afebrile for 48-72h, 7-10 days,
14 days where intracellular organisms (e.g. Legionella) are present
Copyrights:MandellLAetal.InfectiousDiseasesSocietyofAmerica/AmericanThoracicSocietyconsensusguidelinesonthemanagementofcommunity-acquired
pneumonia in adults. Clin Infect Dis. (2007); 44 Suppl 2:S27-72. - Halm EA and Teirstein AS. Management of Community-Acquired Pneumonia New Engl J Med
(2002);347:2039-2045.-WoodheadMetal.GuidelinesforthemanagementofadultlowerrespiratorytractinfectionsERJDecember1,(2005);26(6)1138-1180.
P.15
1.2
DYSPNEA: Community-acquired pneumonia

Syncope is a transient loss of consciousness due to global cerebral hypoperfusion (usually, itself due to
period of low blood pressure) characterised by rapid onset, short duration, spontaneous and complete recovery.
The differentiation between syncope and non-syncopal conditions with real or apparent LOC can be achieved
in most cases with a detailed clinical history but sometimes can be extremely difficult. The following
questions should be answered:
•
Was LOC complete?
•
Was LOC transient with rapid onset and short duration?
•
Did the patient recover spontaneously, completely and without sequelae?
•
Did the patient lose postural tone?
If the answers to these questions are positive, the episode has a high likelihood of being syncope. If the answer to
one or more of these questions is negative, exclude other forms of LOC before proceeding with syncope evaluation.
Loss of Consciousness?
TLOC
Trauma Not Trauma
• Accidental • Fall
• Other abnormal mental state
No
No
Yes
Yes
• Coma
• Intoxication
• Metabolic disturbance
• Aborted sudden death
Transient, rapid onset,
short time, self-terminating
Syncope Epilepsy Psychogenic
Reference: Sutton R. Clinical classification of syncope. - Prog Cardiovasc Dis. (2013); 55(4):339-44.
P.16
1.3
SYNCOPE: Assessment of patients
with transient loss of conscioussness (TLOC)

Vasovagal syncope is diagnosed if syncope is precipitated by emotional distress or orthostatic stress
and is associated with typical prodrome.
Situational syncope is diagnosed if syncope occurs during or immediately after specific triggers.
Orthostatic syncope is diagnosed when it occurs after standing up and there is documentation
of orthostatic hypotension.
Arrhythmia related syncope is diagnosed by ECG when there is:
•
Persistent sinus bradycardia 40 bpm in awake or repetitive sinoatrial block or sinus pauses 3 s
•
Mobitz II 2nd
or 3rd
degree AV block
•
Alternating left and right BBB
•
VT or rapid paroxysmal SVT
•
Non-sustained episodes of polymorphic VT and long or short QT interval
•
Pacemaker or ICD malfunction with cardiac pauses
Cardiac ischemia related syncope is diagnosed when syncope presents with ECG evidence of acute ischemia
with or without myocardial infarction.
Cardiovascular syncope is diagnosed when syncope presents in patients with prolapsing atrial myxoma, severe
aortic stenosis, pulmonary hypertension, pulmonary embolus or acute aortic dissection.
Reference: Moya A et al. Eur Heart J(2009) 30, 2631–2671 (1).
P.17
1.3
SYNCOPE: Diagnostic criteria (1)
Diagnostic criteria with initial evaluation

Patients with suspected syncope presenting to ED or clinic
“Uncertain” or unexplained syncope Certain diagnosis of syncope
Risk stratification
High risk Intermediate risk Low risk
Observation Unit
Home if stable,
Admit to hospital
if evidence of high risk
Home
Outpatient SMU
referral
Outpatient SMU for diagnosis, treatment
and follow-up as appropriate
Hospital admission
Inpatient SMU
Initiate therapy
Inpatient SMU, outpatient SMU or
personal physician as appropriate
Copyright: Sutton R, Brignole M, Benditt DG. Key challenges in the current management of syncope. Nat Rev Cardiol. (2012 ); (10):590-8.
Once syncope is considered to be the likely diagnosis, risk stratification is required to determine further management. P.18
1.3
SYNCOPE: Evaluation and risk stratification of patients
with suspected syncope

Carotid sinus massage Orthostatic Hypotension
Indications
•
CSM is indicated in patients 40 years with syncope
of unknown aetiology after initial evaluation;
•
CSM should be avoided in patients with previous MI,
TIA or stroke within the past 3 months and in
patients with carotid bruits (except if carotid Doppler
studies excluded significant stenosis)
Recommendations: Active standing Indications
•
Manual intermittent determination with
sphygmomanometer of BP supine and, when OH
is suspected, during active standing for 3 min is
indicated as initial evaluation;
•
Continuous beat-to-beat non-invasive pressure
measurement may be helpful in cases of doubt
Diagnostic criteria
•
CSM is diagnostic if syncope is reproduced in presence
of asystole longer than 3 s and/or a fall in systolic
BP 50 mmHg
Diagnostic criteria
•
The test is diagnostic when there is a symptomatic
fall in systolic BP from baseline value ≥20 mmHg
or diastolic BP ≥10 mmHg or a decrease in systolic BP
to 90 mmHg;
•
The test should be considered diagnostic when there
is an asymptomatic fall in systolic BP from baseline
value ≥20 mmHg or diastolic BP 10 mmHg
or a decrease in systolic BP to 90 mmHg
Reference: Moya A et al. Eur Heart J(2009) 30; 2631–2671 (2).
P.19
1.3
SYNCOPE: Diagnostic criteria (2)
Diagnostic criteria with provocation maneuvers

Treatment of reflex syncope Treatment of orthostatic hypotension
•
Explanation of the diagnosis, provision of reassurance and explanation
of risk of recurrence are in all patients
•
Isometric PCM are indicated in patients with prodrome
•
Cardiac pacing should be considered in patients with dominant
cardioinhibitory CSS
•
Cardiac pacing should be considered in patients with frequent recurrent reflex
syncope, age 40 years and documented spontaneous cardioinhibitory response
during monitoring
•
Midodrine may be indicated in patients with VVS refractory to lifestyle measures
•
Tilt training may be useful for education of patients but long-term benefit depends
on compliance
•
Cardiac pacing may be indicated in patients with tilt-induced cardioinhibitory
response with recurrent frequent unpredictable syncope and age 40 after
alternative therapy has failed
•
Triggers or situations inducing syncope must be avoided as much as possible
•
Hypotensive drugs must be modified or discontinued
•
Cardiac pacing is not indicated in the absence of a documented cardioinhibitory
reflex
•
Beta-adrenergic blocking drugs are not indicated
•
Fluid consumption and salt in the diet should be increased
•
Adequate hydration and salt
intake must be maintained
•
Midodrine should be administered
as adjunctive therapy if needed
•
Fludrocortisone should be
administered as adjunctive
therapy if needed
•
PCM may be indicated
•
Abdominal binders and/or support
stockings to reduce venous
pooling may be indicated
•
Head-up tilt sleeping (10°)
to increase fluid volume
may be indicated
•
Triggers or situations inducing
syncope must be avoided
as much as possible
•
Hypotensive drugs administered
for concomitant conditions must
be discontinued or reduced
Copyright: Moya A et al. Eur Heart J(2009) 30; 2631–2671 (3).
P.20
1.3
Treatment according to type of SYNCOPE (1)

Treatment of arrhythmic syncope
Cardiac Pacing
•
Pacing is indicated in patients with sinus node disease in
whom syncope is demonstrated to be due to sinus arrest
(symptom-ECG correlation) without a correctable cause
•
Pacing is indicated in sinus node disease patients with
syncope and abnormal CSNRT
•
Pacing is indicated in sinus node disease patients with
syncope and asymptomatic pauses 3 sec. (with possible
exceptions of young trained persons, during sleep and in
medicated patients)
•
Pacing is indicated in patients with syncope and 2nd
degree
Mobitz II, advanced or complete AV block
•
Pacing is indicated in patients with syncope,
BBB and positive EPS
•
Pacing should be considered in patients with unexplained
syncope and BBB
•
Pacing may be indicated in patients with unexplained
syncope and sinus node disease with persistent sinus
bradycardia itself asymptomatic
•
Pacing is not indicated in patients with unexplained syncope
without evidence of any conduction disturbance
Catheter ablation
•

Catheter ablation is indicated in patients with symptom/
arrhythmia ECG correlation in both SVT and VT in the
absence of structural heart disease
(with exception of atrial fibrillation)
•

Catheter ablation may be indicated in patients with syncope
due to the onset of rapid atrial fibrillation
Antiarrhythmic drug therapy
•

Antiarrhythmic drug therapy, including rate control drugs,
is indicated in patients with syncope due to onset of rapid
atrial fibrillation
•

Drug therapy should be considered in patients with
symptom/ arrhythmia ECG correlation in both SVT and VT
when catheter ablation cannot be undertaken or has failed
Implantable Cardioverter Defibrillator (ICD)
•

ICD is indicated in patients with documented VT
and structural heart disease
•

ICD is indicated when sustained monomorphic VT is induced
at EPS in patients with previous myocardial infarction
•

ICD should be considered in patients with documented VT
and inherited cardiomyopathies or channelopathies
Copyright: Moya A et al. Eur Heart J(2009) 30; 2631–2671 (4).
P.21
1.3
Treatment according to type of SYNCOPE (2)

CHAPTER 2
ACUTE CORONARY SYNDROMES
2.1 GENERAL CONCEPTS �� p.24
H. Bueno
2.2
NON ST-SEGMENT ELEVATION ACS �� p.29
H. Bueno
2.3 ST-SEGMENT ELEVATION MI (STEMI) �� p.35
P. Vranckx, B. Ibañez
2

hs-cTnULN
hs-cTnULN
ACUTE CORONARY SYNDROMES: DIAGNOSIS
CHEST PAIN
or symptoms sugestive of myocardial ischemia
ECG
ST elevation
(persistent)
Repolarization not interpretable
(i.e. LBBB, pacemaker...)
ST/T abnormalities Normal ECG
STEMI
Pain resolves with
nitroglycerin 1st hsTn
NSTEMI Unstable Angina
Work-up
differential diagnoses
Pain onset 6 h
Pain onset 6 h
Re-test hs-cTn (3h later)
See next page for 1 h rule-in rule-out algorithm
hs-cTn
no change
∆ hs-cTn
(1 value ULN)
hs-cTn x5 ULN
or
clinical
diagnosis
clear
Potential
noncardiac
causes for
abnormal Tn
Consider
STEMI
Yes
No
References: Roffi M. Eur Heart J 2016; 37:267-315.
Ibañez B. Eur Heart J 2018; 39:119-177.
P.24
2.1
ACUTE CORONARY SYNDROMES: Diagnosis (1)

Suspected NSTEMI
Other
0h≥D ng/l
or
≥
Observe
Rule-out Rule-in
hs-cTnT (Elecsys)*
hs-cTnl (Architect)*
hs-cTnl (DimensionVista)*
0-1h E ng/l
0hA ng/l
0hB ng/l
and
0-1hCng/l
A
5
2
0,5
B
12
5
5
C
3
2
2
D
52
52
107
E
5
6
19
or
or
•
NSTEMI can be ruled-out at presentation, if hs-cTn concentration is very low
•
NSTEMI can be ruled out by the combination of low baseline levels and the lack of a relevant increase within 1 h
•
NSTEMI is highly likely if initial hs-cTn concentration is at least moderately elevated or hs-cTn concentrations
show a clear rise within the first hour
Reference: Roffi M. Eur Heart J 2016; 37:267-315.
*Cut-off levels are assay-specific.
P.25
2.1
ACUTE CORONARY SYNDROMES: Diagnosis (2)
0-1 H Rule-in rule out test for NSTEMI

Causes of chest pain
Not related to ACS
Causes of troponin elevation
Not related to ACS
Primary cardiovascular
•
Acute pericarditis, pericardial effusion
• Acute myocarditis
•
Severe hypertensive crisis
•
Stress cardiomyopathy (Tako-Tsubo syndrome)
•
Hypertrophic cardiomyopathy, aortic stenosis
•
Severe acute heart failure
•
Acute aortic syndrome (dissection, hematoma)
•
Pulmonary embolism, pulmonary infarction
• Cardiac contusion
Primary cardiovascular
• Acute myo(peri)carditis
•
•
Pulmonary edema or severe congestive heart failure
•
Stress cardiomyopathy (Tako-Tsubo syndrome)
•
Post- tachy- or bradyarrhythmias
•
Cardiac contusion or cardiac procedures
(ablation, cardioversion, or endomyocardial biopsy)
•
Aortic dissection, aortic valve disease or hypertrophic cardiomyopathy
•
Pulmonary embolism, severe pulmonary hypertension
Primary non-cardiovascular
•
Oesophageal spasm, oesophagitis, Gastro
Esophageal Reflux (GER)
•
Peptic ulcer disease, cholecystitis, pancreatitis
•
Pneumonia, bronchitis, asthma attack
•
Pleuritis, pleural effusion, pneumothorax
•
Pulmonary embolism, severe pulmonary
hypertension
• Thoracic trauma
•
Costochondritis, rib fracture
•
Cervical / thoracic vertebral or discal damage
• Herpes Zoster
Primary non-cardiovascular
•
Renal dysfunction (acute or chronic)
•
Critical illness (sepsis, repiratory failure…)
•
Acute neurological damage (i.e. stroke, subarachnoid hemorrhage)
•
Severe burns (affecting 30% of body surface area)
• Rhabdomyolysis
•
Drug toxicity (chemotherapy with adriamycin, 5-fluorouracil,
herceptin, snake venoms…)
•
Inflammatory or degenerative muscle diseases
• Hypothyroidism
•
Infiltrative diseases (amyloidosis, hemochromatosis, sarcoidosis)
• Scleroderma
P.26
2.1
ACUTE CORONARY SYNDROMES: Differential diagnosis (1)

ST-segment elevation Negative T waves
Fixed
• LV aneurysm
•
LBBB, WPW, hypertrophic cardiomyopathy, LVH
• Pacemaker stimulation
•
Early repolarisation (elevated J-point)
Dynamic
•
Acute (myo)pericarditis
•
Pulmonary embolism
•
Electrolyte disturbances (hyperkalemia)
•
Acute brain damage (stroke, subarachnoid haemorrhage)
•
Tako Tsubo syndrome
•
Normal variants, i.e. women
(right precordial leads),
children, teenagers
•
Evolutive changes post
myocardial infarction
•
Chronic ischemic heart disease
• Acute (myo)pericarditis,
cardiomyopathies
•
BBB, LVH, WPW
• Post-tachycardia or
pacemaker stimulation
•
Metabolic or ionic disturbances
ST-segment depression Prominent T waves
Fixed
•
Abnormal QRS (LBBB, WPW, pacemaker stimulation…)
•
LVH, hypertrophic cardiomyopathy
•
Chronic ischemic heart disease
•
Normal variants, i.e.
early repolarisation
•
Metabolic or ionic disturbances
(i.e. hyperkalemia)
•
Acute neurological damage
(stroke, subarachnoid haemorrhage)
Dynamic
•
Acute (myo)pericarditis
•
Acute pulmonary hypertension
•
Electrolyte disturbances (hyperkalemia)
•
Intermitent LBBB, WPW, pacing
•
Post-tachycardia / cardioversion
•
• Drug effects (digoxin)
• Shock, pancreatitis
• Hyperventilation
• Tako Tsubo syndrome
P.27
2.1
ACUTE CORONARY SYNDROMES: Differential diagnosis (2)
Causes of repolarisation abnormalities in the ECG not related to ACS

2
ECG
(10 min)
3
Diagnosis /
Risk assessment
4
Medical
Treatment
5
Invasive
Strategy
STEMI (see chapter 2.3)
Thrombolysis
for STEMI if
primary PCI not
timely available
Primary
PCI
1
Clinical
Evaluation
NSTE ACS
(see chapter 2.2)
ACS unclear
(Rule out ACS) (see chapter 1.1)
No ACS
Chest Pain Unit
• Clinical presentation
(BP, HR)
• ECG presentation
• Past history
• Ischemic risk
(i.e. GRACE, TIMI scores)
• Bleeding risk
(i.e. CRUSADE score)
• Additional information
(labs, imaging...) optional
Anti-ischemic
therapy
Antiplatelet
therapy
Anticoagulation
Emergent
2 hours
Urgent
2-24 hours
Early
24-72 hours
No /
Elective
Quality of
chest pain
Clinical
context
Probability
of CAD
Physical
examination
GENERAL APPROACH TO THE PATIENT WITH CHEST PAIN / SUSPECTED ACS
ECG
Rule out noncardiac causes
P.28
2.1
GENERAL APPROACH
to the patient with chest pain/suspected ACS

Ischemic risk
GRACE risk score TIMI risk score
Predictive Factors
• Age
• HR*
• SBP*
• Creatinine (mg/dl)*
• Killip class*
• Cardiac arrest*
• ST-segment deviation
•
Elevated cardiac markers
Outcomes
In-hospital, 6-month,
1-year and 3-year mortality
1-year death/MI
Predictive Factors
•
Age 65 years
•
At least 3 risk factors for CAD
•
Significant (50%) coronary stenosis
•
ST deviation
•
Severe anginal symptoms (2 events in last 24h)
•
Use of aspirin in last 7 days
•
Elevated serum cardiac markers
Outcome
All-cause mortality/new
or recurrent MI/severe
recurrent ischemia requiring
urgent revascularisation at
14 days
* At admission.
50
40
30
20
10
0
70 90 110 130 150 170 190 210
GRACE Risk Score
Probability of all-cause mortality from
hopital discharge to 6 months (%)
50
40
30
20
10
0
0-1 2 3 4 5 =6
TIMI Risk Score
Risk of 14 days events (%)
Risk calculation
http://www.gracescore.org/WebSite/WebVersion.aspx
Risk calculation
http://www.timi.org/index.php?page=calculators
P.29
2.2
NON ST-SEGMENT ELEVATION ACS: Risk stratification (1)

Bleeding risk
CRUSADE risk score
Predictive Factors
• Sex
• HR*
• SBP*
• Creatinine (mg/dl)*
• Baseline hematocrit*
• GFR: Cockcroft-Gault*
• Diabetes
•
Prior vascular disease
•
Signs of congestive heart failure*
Outcome
In-hospital major bleeding
Copyrights: Eagle KA et al. A validated prediction model for all forms of acute coronary syndrome: estimating the risk of 6-month post-discharge death
in an international registry. JAMA. (2004); 291(22):2727-33. - Antman EM, et al. The TIMI risk score for unstable angina/non-ST elevation MI: A method
for prognostication and therapeutic decision making. JAMA. (2000); 284(7):835-42. - Subherwal S, et al Baseline risk of major bleeding in non-ST-segment-
elevation myocardial infarction: the CRUSADE (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation
of the ACC/AHA Guidelines) Bleeding Score. Circulation (2009); 119(14):1873-82.
* At admission.
50
40
30
20
10
0
0 20 40 60 80 100
CRUSADE Bleeding Score
Probability of in-hospital major bleeding(%)
Risk calculation
www.crusadebleedingscore.org
P.30
2.2
NON ST-SEGMENT ELEVATION ACS: Risk stratification (2)

Initial treatment*
• Nitrates
• Morphine
• Oxygen (if SpO2 90%)
One of the following:
• Fondaparinux
• Enoxaparin
• UFH
• Bivalirudin
Aspirin + one of:
• Ticagrelor
• Prasugrel
• Clopidogrel
Optionally:
• GP IIb/IIIa inhibitors
• Cangrelor
• Nitrates
• Beta-blockers
• Calcium antagonists
• Statins
• ACE inh. (or ARB)
• Aldosterone inhibitors
Pharmacological
treatment*
Anti ischemic
treatment
Antithrombotic
therapy
Anticoagulation Antiplatelets
PCI
CABG
Other preventive
therapies
Myocardial
revascularisation
*
For more information on individual drug doses and indications,
SEE CHAPTER3 SECONDARY PREVENTION AFTER ACS CHAPTER9 DRUGS USED IN ACUTE CARDIOVASCULAR CARE
P.31
2.2
NON ST-SEGMENT ELEVATION ACS: Treatment (1)
General overview

Very-high-risk
criteria
• Haemodynamic instability or cardiogenic shock
• Recurrent or ongoing chest pain refractory to medical treatment
• Life-threatening arrhythmias or cardiac arrest
• Mechanical complications of MI
• Acute heart failure
• Recurrent dynamic ST-T wave changes, particularly with intermittent ST-elevation
High-risk criteria • Rise or fall in cardiac troponin compatible with MI
• Dynamic ST- or T-wave changes (symptomatic or silent)
• GRACE score 140
Intermediate-risk
criteria
• Diabetes mellitus
• Renal insufficienty (eGFR 60 ml/min/1.73 m2
)
• LVEF 40% or congestive heart failure
• Early post-infarction angina
• Prior PCI
• Prior CABG
• GRACE risk score 109 and 140
Low-risk criteria • Any characteristics not mentioned above
P.32
2.2
Risk criteria mandating invasive strategy in NSTE-ACS

Symptoms Onset
PCI centre
Very high
Immediate
Invasive (2 hr)
Early invasive
(24 hr)
Invasive
(72 hr)
High
Intermediate
Immediate transfer to PCI centre
Same-day transfer
Transfer
Transfer optional
Risk
stratification
Therapeutic
strategy
Low
EMS or Non–PCI centre
First medical contact NSTE-ACS diagnosis
Very high
High
Intermediate
Low
Non-invasive
testing if appropriate
P.33
2.2
Timing and strategy for invasive management

0
24 hours
10 min
90 min
2 hours
Strategy
clock ECG STEMI diagnosis
Time to PCI?
≤120min
Primary PCI
strategy
Fibrinolysis
strategya
Bolus of
fibrinolyticb
Transfer
to PCI centre
Meet reperfusion
criteria?
No Yes
Routine PCI strategy
Rescue
PCI
120min
Alert transfer
to PCI centre
Wire crossing
(reperfusion)
≥120min
60-90min
Reference: Ibañez B. Eur Heart J 2018; 39:119-177.
STEMI Treatment (1):
Reperfusion strategy
a
If fibrinolysis is contra-indicated, direct for primary PCI strategy regardless of time to PCI.
b
10 min is the maximum target delay time from STEMI diagnosis to fibrinolytic bolus administration, however, it should be given as soon as
possible after STEMI diagnosis (after ruling out contra-indications).
P.34
2.3

Aspirin
Loading
Prasugrel or ticagrelor loading
(clopidogrel as alternative)
Aspirin
maintenance
Prasugrel or ticagrelor maintenance
(clopidogrel as alternative)
Oxygen when SpO2 90%
High dose statin
(e.g. atorvastatin 80 mg or rosuvastatin 40 mg)
Oral β-blocker
ACE inhibitor
Mineralocorticoid receptor antagonist
(if LVEF 40% and heart failure)
i.v. Beta-blocker
i.v. Opioids/tranquilizer
DURING PCI: radial access, UFH (enoxaparin/bivalirudin as alternatives)
STEMI
diagnosis
Wire crossing
(reperfusion)
Hospital
Admission
Hospital
Discharge
P.35
2.3
Medical management of patients treated with primary PCI

Aspirin
loading
Clopidogrel
loading
Fibrinolysis bolus Enoxaparin
Aspirin
maintenance
Clopidogrel
maintenance
Oxygen when SpO2 90%
i.v. Opioids/tranquilizer
High dose statin
(e.g. atorvastatin 80 mg or rosuvastatin 40 mg)
Oral β-blocker
ACE inhibitor
Mineralocorticoid receptor antagonist
(if LVEF 40% and heart failure)
STEMI
diagnosis
Hospital
Admission
Hospital
Discharge
10min
Coronary angiography ± PCI
(2-24h)
P.36
2.3
Medical management of patients treated with fibrinolysis

CHAPTER 3
SECONDARY PREVENTION
AFTER ACS
3.1 GENERAL SECONDARY PREVENTION STRATEGIES
AND LIPID LOWERING �� p.38
H. Bueno, S. Halvorsen
3.2 ANTITHROMBOTIC TREATMENT �� p.41
F. Costa, S. Halvorsen
P.37
3

Acute Coronary Syndrome
Antithrombotic
therapy
Aspirin + P2Y12
inhibitor
(12 months)
Lipid
lowering
High intensity
statin therapy
BP/LVD/
HF control
ACEI / ARB*,
Beta-blockers*,
MRA*
Glucose
control
Metformin
Insulin*
Hospitalization
• Risk factor control (e.g.
weight control, smoking cessation,
blood pressure and lipid control)
• Diet/nutritional counseling
• Physical activity counseling/
excercise training
• Psychosocial management,
sex advice
• Vocational advice
Plan and schedule
Cardiac Rehabilitation
Education
and counselling
Cardioprotective drugs
in secondary prevention
1- Acute care
• Drug therapy
• Coronary revascularisation
2- Cardiovascular risk assessment (e.g. concealed and uncontrolled risk factors)
3- Initiate secondary prevention and set treatment goals
Cardiac
Rehabilitation
programme
P.38
3.1
SECONDARY PREVENTION STRATEGIES after ACS

Re-evaluate lifestyle, control of risk factors, psychosocial factors and adherance to therapy
Adjustment of secondary prevention therapies. Consider polypill, if needed
Consider adding
Ezetimibe*
PCSK9 inhibitor*
Consider
dose adjustment
Consider ARNI*
Consider
SGLT2 inhibitor*
GLP-1 agonists*
Reinforce education
Psychosocial support
After Discharge
After 12 months
consider*:
Ticagrelor
60 mg bid
Anticoagulation?**
Reference modified from Cortés-Beringola A. Eur J Prev Cardiol 2017; 24(3 suppl): 22-28.
* When individually indicated and without specific contraindications. - ** Rivaroxaban 2.5 mg bid pending approval for indication in chronic CAD.
P.39
3.1

Potential strategies to optimize secondary prevention therapy after ACS
•
Participation in a comprehensive, multi-disciplinary cardiac
rehabilitation programme after hospital discharge
•
Coordination with primary care provider
(and other specilaists) in therapeutic plan and objectives
•
Re-check and reinforce advise on all lifestyle changes
(diet, physical activity, smoking cessation…) during follow-up visits
•
Check and optimise doses of all indicated secondary prevention drugs
•
Use of specialist support, nicotine replacement therapies, varenicline,
and/or bupropion individually or in combination
for patients who do not quit or restart smoking
•
Use of ezetimibe and/or a PCSK9 inhibitor in patients
who remain at high risk with LDL-cholesterol 70 mg/dl despite
apropriate diet and maximally tolerated doses of statins
•
Use of a polypill or combination therapy in patients
with suboptimal adherence to drug therapy
P.40
3.1
After ACS: POTENTIAL STRATEGIES
TO OPTIMIZE SECONDARY PREVENTION THERAPY

PCI
Stable CAD
DES/BMS or DCB BRS DES/BMS or DCB
High Bleeding Risk
6mo DAPT
Class I A1
1mo DAPT Class IIb C
3mo DAPT Class IIa B
≥12mo DAPT
Class IIa C
12mo DAPT
Class I A
6mo DAPT
Class IIa B
12mo DAPT
Class IIb B
DAPT 6mo
Class IIb A
High Bleeding Risk
ACS
No
1mo
3mo
6mo
12mo
30mo
Yes No
or
Yes
A C
A C
A C
A C
2
A P A T
or
A C
3
A C
A P A T
or A C
4
A P
A T
A T
Treatment
indication
Device used
Time
A = Aspirin C = Clopidogrel P = Prasugrel T = Tricagrelor
Reference: Valgimigli M, et al. Eur Heart J. 2018; 39:213-260.
P.41
3.2
ANTITHROMBOTIC TREATMENT:
Dual antiplatelet therapy duration in patients with ACS (1)

Medical Treatment Alone
Stable CAD ACS
No indication
for DAPT unless
concomitant or
prior indication
overrides
Stable CAD
No indication
for DAPT unless
concomitant or
prior indication
overrides
12mo DAPT
Class I C
6mo DAPT
Class IIa C
12moDAPT
Class IIb C
High Bleeding Risk
CABG
No
1mo
3mo
6mo
12mo
30mo
Yes
ACS
High Bleeding Risk
No Yes
Time
or
A C
3
A C
A P A T
or
A C
A P
A T
A T
12mo DAPT
Class I C
1mo DAPT
Class IIa C
12moDAPT
Class IIb C
or
A C
3
A C
A T
or A C
A T
Treatment
indication
Device used
A = Aspirin C = Clopidogrel P = Prasugrel T = Tricagrelor
Reference: Valgimigli M, et al. Eur Heart J. 2018; 39:213-260.
P.42
3.2
Dual antiplatelet therapy duration in patients with ACS (2)

CLOPIDOGREL
Ticagrelor LD (180 mg)
24h after last prasugrel dose
Prasugrel LD (60 mg)
24h after last ticagrelor dose
P
r
a
s
u
g
r
e
l
L
D
(
6
0
m
g
)
i
r
r
e
s
p
e
c
t
i
c
e
o
f
p
r
i
o
r
c
l
o
p
i
d
o
g
r
e
l
t
i
m
i
n
g
a
n
d
d
o
s
i
n
g
C
l
o
p
i
d
o
g
r
e
l
L
D
(
6
0
0
m
g
)
2
4
h
a
f
t
e
r
l
a
s
t
p
r
a
s
u
g
r
e
l
d
o
s
e
T
i
c
a
g
r
e
l
o
r
L
D
(
1
8
0
m
g
)
i
r
r
e
s
p
e
c
t
i
c
e
o
f
p
r
i
o
r
c
l
o
p
i
d
o
g
r
e
l
t
i
m
i
n
g
a
n
d
d
o
s
i
n
g
C
l
o
p
i
d
o
g
r
e
l
L
D
(
6
0
0
m
g
)
2
4
h
a
f
t
e
r
l
a
s
t
t
i
c
a
g
r
e
l
o
r
d
o
s
e
ACCUTE SETTING
ALWAYS RELOAD
PRASUGREL TICAGRELOR
Reference: Valgimigli M, et al. Eur Heart J. 2018;39:213-260.
P.43
3.2
Switching between P2Y12 inhibitors for DAPT after ACS (1)

Ticagrelor LD (90 mg b.i.d.)
24h after last prasugrel dose
Prasugrel LD (60 mg)
24h after last ticagrelor dose
P
r
a
s
u
g
r
e
l
M
D
(
1
0
m
g
q
.
d
.
)
2
4
h
a
f
t
e
r
l
a
s
t
c
l
o
p
i
d
o
g
r
e
l
d
o
s
e
C
l
o
p
i
d
o
g
r
e
l
M
D
(
7
5
m
g
q
.
d
.
)
2
4
h
a
f
t
e
r
l
a
s
t
p
r
a
s
u
g
r
e
l
d
o
s
e
T
r
i
c
a
g
r
e
l
o
r
M
D
(
9
0
m
g
b
.
i
.
d
.
)
2
4
h
a
f
t
e
r
l
a
s
t
c
l
o
p
i
d
o
g
r
e
l
d
o
s
e
C
l
o
p
i
d
o
g
r
e
l
L
D
(
6
0
0
m
g
)
2
4
h
a
f
t
e
r
l
a
s
t
t
i
c
a
g
r
e
l
o
r
d
o
s
e
CLOPIDOGREL
CHRONIC
SETTING
PRASUGREL TICAGRELOR
Reference: Valgimigli M, et al. Eur Heart J. 2018;39:213-260.
P.44
3.2
Switching between P2Y12 inhibitors for DAPT after ACS (2)

P.45
3.2
Risk scores validated for DAPT duration decision-making
PRECISE-DAPT score DAPT score
Time of use At the time of coronary stenting After 12 months of uneventful DAPT
DAPT duration
strategies assessed
Short DAPT (3-6 months)
vs. Standard/long DAPT (12-24 monts)
Standard DAPT (12 months)
vs. Long DAPT (30 months)
Score calculation
HB
Age
≥75
65 to 75
65
Cigarette smoking
Diabetes mellitus
MI at presentation
Prior PCI or prior MI
Paclitaxel-eluting stent
Stent diameter 3 mm
CHF or LVEF 30%
Vein graft stent
— 2 pt
— 1 pt
0 pt
+ 1 pt
+ 1 pt
+ 1 pt
+ 1 pt
+ 1 pt
+ 1 pt
+ 2 pt
+ 2 pt
WBC
Age
CrCl
Prior
Bleeding
Score
Points
Score range 0 to 100 points — 2 to 10 points
Decision making
cut-off
Score ≥25 → Short DAPT
Score 25 → Standard/long DAPT
Score ≥2 → Long DAPT
Score 2 → Standard DAPT
Electronic calculator www.precisedaptscore.com www.daptstudy.org

DUAL THERAPY strategy:
TRIPLE THERAPY strategy:
STEP
2:
Treatment
type
STEP
3:
Treatment
duration
STEP
1:
Patient
risk
assessment
BRIR
DUAL (12 mo.) OAC alone
OAC alone
OAC alone
TRIPLE (for 1 mo.)
TRIPLE (up to 6 mo.)
DUAL
(up to 12 mo.)
DUAL (up to 12 mo.)
BRIR
• NOAC* (preferable)
- Apixaban 5 mg b.i.d. (reduce to 2.5 mg b.i.d.(1)
- Dabigatran 110 mg b.i.d. (preferable while on DAPT)
or 150 mg b.i.d.
- Edoxaban 60 mg q.d. (reduce to 30 mg q.d.(2)
- Rivaroxaban 20 mg q.d. (reduce to 15 mg q.d.(3)
or 15 mg
(may be considered DAPT/SAPT)
or
• VKA dose ajusted: consider maintaining INR in the lower
part of the recommended target range (e.g. 2.0-2.5 for AF
and MV in aortic position, 2.5-3.0 for MV in mitral position)
OAC:
• Clopidogrel 75 mg q.d.
(preferable)*
or
• Aspirin 75-100 mg q.d.
SAPT:
• Clopidogrel 75 mg q.d.
and
• Aspirin 75-100 mg q.d.
DAPT:
• HIGH RISK OF BLEEDING?
High HAS-BLED: Hypertension, abnormal liver/renal function, prior stroke, bleeding diathesis, labile INR if on VKA, age 65, drugs
(e.g. NSAIDs or antiplatelets), alcohol abuse, ABC score: Age, Biomarkers (GDF-15, hs cTnT, Hb) and Clinical history of prior bleeding
• HIGH RISK OF RECURRENT CORONARY ISCHEMIC EVENTS?
ACS at presentation, prior ST, stenting of last remaining vessel, CrCL 60 ml/min, ≥3 stents implanted or lesions treated,
bifurcation with 2 stents, overall stentlengh 60 mm, treatment of CTO
TRIPLE
THERAPY
(If High BR Low IR)
(If High BR High IR)
or
(If Low BR High IR)
DUAL
THERAPY
Reference adapted from Valgimigli M et al. Eur Heart J. 2018;39:213-260.
*
In case of
selecting
dual therapy
immediately after
stent implantation
clopidogrel should
be selected as
single antiplatelet
agent. Aspirin
should however
be administered
at the time of the
intervention.
(1)
Age ≥80 years,
body weight ≤60 kg
or serum creatinine
level ≥1.5 mg/dL.
(2)
CrCl of
30–50 ml/min,
body weight
≤60 kg,
concomitant use
of verapamil,
quinidine or
dronedarone.
(3)
CrCl30-49 ml/min.
P.46
3.2
ANTITHROMBOTIC TREATMENT in patients with concomitant
indication for DAPT and chronic oral anticoagulation (1)

SURGERY
Minimal delay for P2Y12 interruption Days after surgery
CLOPIDOGREL
PRASUGREL
TICAGRELOR
CLOPIDOGREL
PRASUGREL(2)
TICAGRELOR(2)
ASPIRIN(1)
//••••••9••••••8••••••7••••••6••••••5••••••4••••••3••••••2••••••1•••••• 0••••••••••••••••••1-4
STOP
STOP
STOP
= Expected average platelet function recovery
(1)
Decision to stop aspirin throughout surgery should be made on a single case basis taking into account the surgical bleeding risk
(2)
In patients not requiring OAC
Reference: Valgimigli et al. Eur Heart J.2018; 39:213-260.
P.47
3.2
Management of DAPT after ACS in patients
with indication for surgery

LIFE-THREATENING BLEEDING
e.g. massive overt genitourinary,
respiratory or upper/lower
gastrointestinal bleeding,
active intracranial, spinal
or intraocular haemorrhage,
or any bleeding
STOP ALL ANTITHROMBOTIC MEDICATIONS
and reverse OAC. Once bleeding has ceased, re-evaluate the need
for DAPT or SAPT, preferably with the P2Y12 inhibitor
especially in case of upper GI bleeding
CONTINUE DAPT a
, CONTINUE OAC c
CONTINUE DAPT, CONTINUE OAC Consider skipping one single next pill
CONSIDER STOPPING DAPT
and continue with SAPT, preferably with the P2Y12 inhibitor
especially in case of upper GI bleeding. Once bleeding has ceased,
re-evaluate the need for DAPT or SAPTa
CONSIDER STOPPING OAC
or even reversal until bleeding is controlled, unless prohibitive thrombotic risk
(i.e. mechanical heart valve in mitral position, cardiac assist device )b-c-d
Reinitiate treatment within one week if clinically indicated.
If Bleeding persist despite treatment, or treatment is not possible
CONSIDER STOPPING ALL ANTITHROMBOTIC MEDICATIONS
CONSIDER STOPPING DAPT
and continue with SAPT, preferably with the P2Y12 inhibitorespecially in case
of upper GI bleeding Reinitiate DAPT as soon as deemed safea
CONSIDER STOPPING OAC
or even reversal until bleeding is controlled, unless very high thrombotic risk
(i.e. mechanical heart valves, cardiac assist device, CHA2DS2-VASc ≥4 ).b-c-d
Reinitiate treatment within one week if clinically indicated.
SEVERE BLEEDING
e.g. severe genitourinary,
respiratory or upper/lower
gastrointestinal bleeding
MODERATE BLEEDING
e.g. genitourinary, respiratory
or upper/lower gastrointestinal
bleeding with significant blood
loss or requiring transfusion
MILD BLEEDING
e.g. not self resolving epistaxis,
moderate conjunctival bleeding,
genitourinary or upper/lower
gastrointestinal bleeding
without significant blood loss,
mild haemoptysis
TRIVIAL BLEEDING e.g. skin bruising or ecchimosis,
self-resolving epistaxis, minimal conjunctival bleeding
ANTITHROMBOTIC TREATMENT
MANAGEMENT DURING BLEEDING
Active bleeding and unstable hemodynamic
putting patient’s life immediately at risk?
Hospitalization required? Hb loss 5 g/dl
Hb loss 5 g/dl
Significant blood loss (3 g/dl) ?
Requires medical intervention
or further evaluation?
Yes
Yes
Yes
Yes
No
No
No
No
Reference: Valgimigli et al. Eur Heart J.2018; 39:213-260.
a
Consider shortening DAPT duration or switching to less potent P2Y12 inhibitor (i.e. from ticagrelor/prasugrel to clopidogrel), especially if recurrent bleeding occurs
b
Reinitiate treatment within one week if clinically indicated. For Vitamin-K antagonist consider a target INR of 2.0-2.5 unless overriding indication (i.e. mechanical
heart valves or cardiac assist device) for NOAC consider the lowest effective dose. - c
In case of triple therapy consider downgrading to dual therapy, preferably with
clopidogrel and OAC. - d
If patients on dual therapy, consider stopping antiplatelet therapy if deemed safe.
P.48
3.2
Management of acute bleeding after ACS

Acute upper GI haemorrhage in patient using antiplatelet agent(s) (APT)
Upper GI endoscopy demonstrates a nonvariceal source of bleeding (e.g. peptic ucler bleed)
High risk endoscopic stigmata identified
(Forrest classification* Ia, Ib, IIa, IIb)
APT used for secondary prophylaxis
(known cardiovascular disease)
Patients on low dose ASA alone
•Resumelow-loseASAbyday3followingindexendoscopy
• Second-look endoscopy at the discretion
of the endoscopist may be considered
Paptients on dual antiplatelet therapy (DAPT)
• Continue low dose ASA without interruption
• Early cardiology consultation for recommendation
of second resumption/ continuation of second APT
• Second-look endoscopy at the discretion of the
endoscopoist may be considered
APT used for secondary prophylaxis
(known cardiovascular disease)
Patients on low dose ASA alone
•Continue low-dose ASA without interruption
Paptients on dual antiplatelet therapy (DAPT)
• Continue DAPT without interruption
Low risk endoscopic stigmata identified
(Forrest classification* IIc, III)
*The Forrest classification in defined as follows: Ia spuring
hemorrhage, Ib oozing hemorrhage, IIa nonbleeding visible
vessel, IIb an adherent clot, IIc flat pigmented spot, and III clean
base ucler.
Reference: Halvorsen et al. Eur Heart J 2017; 38: 1455-62.
P.49
3.2
Management of antiplatelet therapy after acute GI bleeding

CHAPTER 4
ACUTE HEART FAILURE
4.1 WET-AND-WARM HEART FAILURE PATIENT �� p.52
V.P. Harjola, O. Miró
4.2 CARDIOGENIC SHOCK (WET-AND-COLD) �� p.61
P. Vranckx, U. Zeymer
4

Reference: Ponikowski P et al. Eur J Heart Fail. 2016; 18(8):891-975. DOI: 10.1002/ejhf.592.
WARM-DRY WARM-WET
COLD-DRY COLD-WET
HYPOPERFUSION (+)
Cold sweaty extremities, Oliguria,
Mental confusion, Dizziness,
Narrow pulse pressure
HYPOPERFUSION (-)
CONGESTION (-) CONGESTION (+)
Pulmonary congestion, orthopnoea/paroxismal,
nocturnal dyspnoea, peripheral (bilateral) oedema,
jugular venous dilatation, congested hepatomegaly,
gut congestion, ascites, hepatojugular reflux
Clinical profiles of patients with acute heart failure
based on the presence/absence of congestion and/or hypoperfusion
Hypoperfusion is not synonymous with hypotension, but often hypoperfusion is accompanied by hypotension.
P.52
4.1
Clinical profiles of patients with acute heart failure

Reference: McMurray JJ et al. Eur Heart J (2012); 33:1787-847.
Ponikowski P et al. Eur J Heart Fail. 2016; 18:891-975.
1 Symptoms: Dyspnea (on effort or at rest)/
breathlessness, fatigue, orthopnea, cough,
weight gain/ankle swelling.
2 Signs: Tachypnea, tachycardia, low or normal blood
pressure, raised jugular venous pressure,
3rd
/4th
heart sound, rales, oedema, intolerance
of the supine position.
3
Cardiovascular risk profile: Older age, HTN, diabetes,
smoking, dyslipidemia, family history, history of CVD.
4
Precipitants/causes that need urgent management
(CHAMP): Acute coronary syndrome. Hypertensive
emergency. Rapid arrhythmias or severe
bradyarrhythmia/conduction disturbance. Mechanical
causes. Pulmonary embolism.
5 Differential diagnosis: Exacerbated pulmonary disease,
pneumonia, pulmonary embolism, pneumothorax,
acute respiratory distress syndrome, (severe) anaemia,
hyperventilation (metabolic acidosis), sepsis/septic
shock, redistributive/hypovolemic shock.
FACTORS TRIGGERING ACUTE HEART FAILURE
•
Acute coronary syndrome
•
Tachyarrhythmia (e.g. atrial fibrillation, ventricular tachycardia)
•
Excessive rise in blood pressure
•
Infection (e.g. pneumonia, infective endocarditis, sepsis).
•
Non-adherence with salt/fluid intake or medications
•
Toxic substances (alcohol, recreational drugs)
•
Drugs (e.g. NSAIDs, corticosteroids, negative inotropic
substances, cardiotoxic chemotherapeutics)
•
Exacerbation of chronic obstructive pulmonary disease
• Pulmonary embolism
•
Surgery and perioperative complications
•
Increased sympathetic drive, stress-related cardiomyopathy
•
Metabolic/hormonal derangements (e.g. thyroid dysfunction,
diabetic ketosis, adrenal dysfunction, pregnancy and
peripartum related abnormalities)
• Cerebrovascular insult
•
Acute mechanical cause : myocardial rupture complicating
ACS (free wall rupture, ventricular septal defect, acute
mitral regurgitation), chest trauma or cardiac intervention,
acute native or prosthetic valve incompetence secondary
to endocarditis, aortic dissection or thrombosis
P.53
4.1
ACUTE HEART FAILURE: Diagnosis and causes (2)

Reference: Ponikowski P et al. Eur J Heart Fail. 2016; 18(8): 891-975. DOI: 10.1002/ejhf.592.
Patient with suspected AHF
1. Cardiogenic shock ?
Urgent phase after
first medical contact
Immediate stabilization
and transfer to ICU/CCU
Immediate initiation
of specific treatement
Indentification of acute aeticology :
C = Acute Coronary syndrome
H = Hypertension emergency
A = Arrhythmia
M = Acute Mechanical cause
P = Pulmonary embolism
Diagnostic work-up to confirm AHF
Clinical evaluation to select optimal management
Immediate phase
(initial 60-120 minutes)
Circulatory support
• pharmacological
• mechanical
Ventilatory support
• oxygen
• non-invasive positive
pressure ventilation (CPAP, BiPAP)
• mechanical ventilation
2. Respiratory failure ?
Yes
No
No
No
Yes
Yes
P.54
4.1
Initial management of a patient with ACUTE HEART FAILURE

After
60-90 min
In hospital
Pre-hospital or
emergency room
Reference adapted from Mebazaa A et al. Eur J Heart Fail. (2015); 17:544-58.
Conventional oxygen therapy
Conventional
oxygen therapy
Intolerance
Weaning
CPAP
CPAP
FAILURE
PS-PEEP
SUCCESS
SIGNIFICANT HYPERCAPNIA
AND ACIDOSIS
NORMAL pH
AND pCO2
Intubation
Intubation
RESPIRATORY DISTRESS?
SpO2 90%, RR25,
Work of breathing, orthopnea
PERSISTENT RESPIRATORY DISTRESS?
Upright position
No Yes
Yes
Venous/Arterial blood gases
No
Room air
P.55
4.1
ACUTE HEART FAILURE: Airway (A) and breathing (B)
Oxygen therapy and ventilatory support in acute heart failure

INSTRUMENTATION INVESTIGATIONS:
Intravenous line (peripheral/central) and BP monitoring (arterial line in shock
and severe ventilatory/gas-exchange disturbances)
Laboratory measures
• Cardiac markers (troponin, BNP/NT-proBNP/MR-proANP)
•
Complete blood count, electrolytes, creatinine, urea, glucose,
inflammation, TSH
•
Consider arterial or venous blood gases, lactate, D-dimer
(suspicion of acute pulmonary embolism)
Standard 12-lead ECG
• Rhythm, rate, conduction times?
• Signs of ischemia/myocardial infarction? Hypertrophy?
Echocardiography
a) Immediately in haemodynamically unstable patients
b)
Within 48 hours when cardiac structure and function are either not known or
may have changed since previous studies
Ventricular function (systolic and diastolic)? Estimated left-and right-side filling
pressures? Lung ultrasound? Presence of valve dysfunction (severe stenosis/
insufficiency)? Pericardial tamponade?
ACTIONS:
Rule in/out
acute heart failure
as cause of symptoms
and signs
Determine
clinical profile
Start as soon as
possible treatment of
both heart failure and
the factors identified
as triggers
Establish cause
C - CIRCULATION*
HR (bradycardia [60/min], normal [60-100/min], tachycardia [100/min]), rhythm (regular, irregular), SBP (very low
[90 mmHg], low, normal [110-140 mmHg], high [140 mmHg]), and elevated jugular pressure should be checked.
P.56
4.1
ACUTE HEART FAILURE: Initial diagnosis (CDE)

References: Mebazaa A et al. Intensive Care Med. (2016); 42(2):147-63; Mueller C et al. Eur Heart J Acute Cardiovasc Care. (2017); 6(1):81-6.
D – DISABILITY DUE TO NEUROLOGICAL DETERIORATION
•
Normal consiousness/altered mental status?
Measurement of mental state with AVPU (alert, visual, pain or unresponsive)
or Glasgow
•
Coma Scale: EMV score 8 Consider endotracheal intubation and mechanical ventilation
•
Anxiety, severe dyspnea? Consider cautious administration of morphine 2 mg i.v. bolus,
preceded by antiemetic as needed
E – EXPOSURE EXAMINATION
• Temperature/fever: central and peripheral
• Weight
• Skin/extremities: circulation (e.g. capilary refill), color
•
Urinary output (0.5 ml/kg/hr) Consider inserting indwelling catheter;
the benefits should outweigh the risks of infection and long-term complications
P.57
4.1

Patient with AHF
Bedside assessment to identify haemodynamic profiles
DRY patient
WET patient
No
(5% of all AHF patients)
Yes
(95% of all AHF patients)
Yes No
Yes
No
PRESENCE OF CONGESTIONa
?
ADEQUATE PERIPHERAL PERFUSION?
DRY and COLD
Hypoperfused, hypovolemic
DRY and WARM
Adequately perfused
≈ Compensated
Consider fluid challenge
Consider inotropic agent if still hypoperfused
Adjust oral therapy
WET and WARM
patient (typically elevated
or normal systolic blood
pressure)
P.58
4.1
ACUTE HEART FAILURE: Management of patients with acute heart
failure based on clinical profile during an early phase

WET and COLD patient
Systolic blood pressure 90 mmHg
Yes No
• Inotropic agent
• Consider vasopressor
in refractory cases
• Diuretic
(when perfusion corrected)
• Consider machanical circulatory
support if no response to drugs
• Vasodilators
• Diuretics
• Consider inotropic agent
In refractory cases
• Vasodilator
• Diuretic
• Diuretic
• Vasodilator
• Ultrafiltration
(consider if diuretic resistance)
Vascular type-fluid
redistribution
Hypertension predominates
Cardiac type-fluid
accumulation
Congestion predominates
a
Symptoms/signs of congestion: orthopnoea, paroxysmal nocturnal dyspnoea, breathlessness, bi-basilar rales, abnormal blood pressure response to the
Valsalva maneuver (left-sided); symptoms of gut congestion, jugular venous distension, hepatojugular reflux, hepatomegaly, ascites, and peripheral
oedema (right-sided).
SEE CHAPTER 9 DRUGS USED IN ACUTE CARDIOVASCULAR CARE
Reference: Ponikowski P et al. Eur J Heart Fail. 2016; 18(8):891-975. DOI: 10.1002/ejhf.592.
P.59
4.1

No acute heart failure
MONITORING
Dyspnea (VAS, RR), BP, SpO2, HR and
rhythm, urine output, peripheral perfusion
REASSESSMENT
Clinical, biological and psychosocial parameters by trained nurses
Observation unit (24h)
Discharge home
Ward (cardiology, internal
medicine, geriatrics)
Rehabilitation
program
Visit to cardiologist
1-2 weeks
Palliative care
hospitals
ICU/CCU
Confirmed acute heart failure
DIAGNOSTIC TESTS
OBSERVATION
UP
TO
120
min
ADMISSION/DISCHARGE
Risk stratification: ensure patient
is at low risk before direct discharge
Risk stratification: ensure patient
is at low risk before direct discharge
TREATMENT OBJECTIVES to prevent organ dysfunction:
Improve symptoms, maintain SBP 90 mmHg and peripheral
perfusion, mantain SpO2 90% (see table in pages 63-64)
Reference adapted from Mebazaa A et al. Eur J Heart Fail. (2015); 17: 544-58 and Miró Ò et al. Ann Intern Med (2017); 167:698-705.
P.60
4.1
ACUTE HEART FAILURE: Management of acute heart failure

Normotension/
Hypertension
Hypotension Low heart rate Potassium Renal impairment
100 90
mmHg
90
mmHg
60
≥50 bpm
50 bpm ≤3.5
mmol/L
5.5
mmol/L
Cr 2.5,
eGFR 30
Cr 2.5,
eGFR 30
ACE-I/ARB Review/
increase
Reduce/
stop
Stop No
change
No
change
Review/
increase
Stop Review Stop
Beta-blocker No change Reduce/
stop
Stop Reduce Stop No
change
No
change
No
change
No
change
MRA No change No
change
Stop No
change
No
change
Review/
increase
Stop Reduce Stop
Diuretics Increase Reduce Stop No
change
No
change
Review/
No
change
Review/
increase
No
change
Review
Sacubitril/
Valsartan
Review/
increase
Stop Stop No
change
No
change
Review/
increase
Stop Review Stop
Reference adapted from Mebazaa A et al. Eur J Heart Fail. (2015); 17(6):544-58.
Management of oral therapy in AHF in the first 48 hours P.61
ACUTE HEART FAILURE: Treatment (C) and preventive measures 4.0
4.1

Normotension/
Hypertension
Hypotension Low heart rate Potassium Renal impairment
100 90
mmHg
90
mmHg
60
≥50 bpm
50 bpm ≤3.5
mmol/L
5.5
mmol/L
Cr 2.5,
eGFR 30
Cr 2.5,
eGFR 30
Other
vasodilators
(nitrates)
Increase Reduce/
stop
Stop No
change
No
change
No
change
No
change
No
change
No
change
Other heart rate
slowing drugs
(amiodarone,
non-dihydropyridine
CCB, ivabradine)
Review Reduce/
stop
Stop Reduce/
stop
Stop Review/
stop(*)
No
change
No
change
No
change
Thrombosis prophylaxis should be started in patients not anticoagulated.
(*) Amiodarone.
Management of oral therapy in AHF in the first 48 hours
Reference adapted from Mebazaa A et al. Eur J Heart Fail. (2015); 17(6):544-58.
P.62
ACUTEHEARTFAILURE:Treatment(C)andpreventivemeasures(Cont.) 4.1

Hemodynamic criteria to define cardiogenic shock
•
Systolic blood pressure 80 to 90 mmHg
or mean arterial pressure 30 mmHg lower than baseline
•
Severe reduction in cardiac index:
1.8 l/min/m2
without support
or 2.0 to 2.2 l/min/m2
with support
•
Adequate or elevated filling pressure:
Left ventricular end-diastolic pressure 18 mmHg
or Right atrial pressure 10 to 15 mmHg
Clinical condition defined as the inability of the heart to deliver an adequate amount of blood
to the tissues to meet resting metabolic demands as a result of impairment of its pumping function.
Cardiogenic shock is equal to wet-cold phenotype. The clinical signs of hypoperfusion are listed in page 65.
In addition, blood lactate is typically elevated above 2 mmol/L.
P.63
4.2
CARDIOGENIC SHOCK: Definition

LV pump failure is the primary insult in most forms of CS, but other parts of the circulatory system
contribute to shock with inadequate compensation or additional defects P.64
4.2
CARDIOGENIC SHOCK: Causes

This protocol should be initiated as soon as cardiogenic shock/end organ hypoperfusion is recognised
and should not be delayed pending intensive care admission.
EARLY TRIAGE MONITORING
Start high flow O2
Establish i.v. access
• Age: 65–74, ≥75
• Heart rate 100 beats per minute
• Systolic blood pressure 100 mmHg
• Proportional pulse pressure ≤25 % (CI 2.2 l/min/m2
)
• Orthopnea (PCWP 22 mmHg)
• Tachypnea (20/min), 30/min (!)
• Killip class IV
•
Clinical symptoms of tissue hypoperfusion/hypoxia:
- cool extremities - decreasedurineoutput(urineoutput40
ml/h)
- decreased capillary refill or mottling - alteration in mental status
INITIAL RESUSCITATION
•
Arterial and a central venous
catheterization with a catheter
capable of measuring central venous
oxygen saturation
•
Standard transthoracic
echocardiogram to assess left (and
right) ventricular function and for
the detection of potential mechanical
complications following MI
•
Early coronary angiography in
specialized myocardial intervention
centre when signs and/or symptoms
of ongoing myocardial ischemia
(e.g. ST-segment elevation myocardial
infarction).
• CORRECT: hypoglycemia hypocalcemia,
• TREAT: sustaned arrhythmias: brady- or tachycardia
•
Isotonic saline-fluid challenge - 200-300 ml
over 30 min period to achieve a central venous pressure of 8 to 12 mmHg
or until perfusion improves (with a maximum of 500 ml)
•
CONSIDER NIMV for comfort (fatigue, distress) or as needed:
- To correct acidosis - To correct hypoxemia
• INOTROPIC SUPPORT (dobutamine, levosimendan and/or vasopressor support)
TREATMENT GOALS
• a mean arterial pressure of 60 mmHg or above,
• a mean pulmonary artery wedge pressure of 18 mmHg or below,
• a central venous pressure of 8 to 12 mmHg,
• a urinary output of 0,5 ml or more per hour per kilogram of body weight
• an arterial pH of 7.3 to 7.5
•
a central venous saturation (ScvO2) ≥70% (provided SpO2 ≥93%
and Hb level ≥9 g/dl)
In persistent drug-resistant cardiogenic shock,
consider mechanical circulatory support
0 min
5 min
15 min
60 min
EMERGENCY
DEPARTMENT
CARDIAC
INTENSIVE
CARE
UNIT
P.65
4.2
CARDIOGENIC SHOCK: Initial triage and management

Ventilator mode
Tidal Volume goal
Plateau Pressure goal
Anticipated PEEP levels
Ventilator rate and pH goal
Inspiration: Expiration time
Oxygenation goal:
• PaO2
• SpO2
Pressure assist/control
Reduce tidal volume to 6-8 ml/kg lean body weight
≤30 cm H2O
5-10 cm H2O
12-20, adjusted to achieve a pH ≥7.30 if possible
1:1 to 1:2
50-80 mmHg
90%
Predicted body weight calculation:
• Male: 50 + 0.91 (height in cm - 152.4)
• Female: 45.5 + 0.91 (height in cm - 152.4)
Some patients with CS will require increased PEEP to attain functional residual capacity and maintain oxygenation,
and peak pressures above 30 cm H2O to attain effective tidal volumes of 6-8 ml/kg with adequate CO2 removal.
For more informations on individual drug doses and indications:
P.66
4.2
CARDIOGENIC SHOCK: Treatment and ventilator procedures

CARDIOGENIC SHOCK: MANAGEMENT FOLLOWING STEMI
Assess volume status
Treat sustained arrhythmias: brady - or tachy -
Consider mechanical ventilation for comfort (during PCI) and/or as needed:
• to correct acidosis
• to correct hypoxemia
Inotropic support (dobutamine and/or vasopressor support)
Signs (ST-segment elevation or new LBBB)
and/or clinical symptoms of ongoing
myocardial ischemia
Early coronary angiography
± Pulmonary artery catheter
± IABP in selected patients
in a specialised Myocardial
Intervention Centre
PCI ± stenting
of the culprit lesion
CABG
+ correct mechanical complications
Pump failure
RV, LV, both
Short-term
mechanical
circulatory
support
Aortic
dissection
Pericardial
tamponade
• Acute severe mitral valve regurgitation
• Ventricular septum rupture
• Severe aortic/mitral valve stenosis
Operating theater ± coronary angiography
Emergency echocardiography
± Tissue doppler imaging
± Color flow imaging
No
NSTEACS,
Delayed CS
Yes
P.67
4.2
CARDIOGENIC SHOCK: management following STEMI

72-hrs
2-weeks
1-month ...
Left ventricular support BiVentricular support
Partial support
IABP Impella 2.5 Tandem-
heart
Impella 5.0 Implantable
ECMO
Levitronix
Full support
Level of support
Pulmonary support
P.68
4.2
CARDIOGENIC SHOCK:
Mechanical circulatory support, basic characteristics

Different systems for mechanical circulatory support are available to the medical community.
The available devices differ in terms of the insertion procedure, mechanical properties, and
mode of action. A minimal flow rate of 70 ml/kg/min, representing a cardiac index of at least
2.5 L/m2
, is generally required to provide adequate organ perfusion. This flow is the sum
of the mechanical circulatory support output and the remaining function of the heart.
The SAVE-score may be a tool to predict survival for patients receiving ECMO for refractory
cardiogenic shock
Type Support Access
Intra-aortic balloon
pump
Balloon
counterpulsation
Pulsatile flow 0.5 L Arterial: 7.5 French
Impella Recover
LP 2.5
CP
LP 5.0
Axial flow Continuous flow
2.5 L
4.0 L
5.0 L
Arterial: 12 French
Arterial: 14 French
Arterial: 21 French
Tandemheart
Centrifugal flow
5.0 L
Continuous flow
5.0 L
Venous: 21 French
Arterial: 15-17 French
Venous: 15-29 French
Arterial: 15-29 French
Cardiohelp
(www.save-score.com).
P.69
4.2

Monsieurs KG, et al. European Resuscitation Council Guidelines for Resuscitation 2015. Section 1
Executive Summary. Resuscitation 2015; 95C:1-80, DOI:10.1016/j.resuscitation.2015.07.038
CHAPTER 5
CARDIAC ARREST AND
CARDIOPULMONARY RESUSCITATION
N. Nikolaou, L. Bossaert
5
THE CHAIN OF SURVIVAL
P.71

OUT OF HOSPITAL CARDIAC ARREST:
ASSESSMENT OF A COLLAPSED VICTIM AND INITIAL TREATMENT
VICTIM COLLAPSES
Victim responds
Victim unresponsive
Leave victim as found
Find out what is wrong
Reassess victim regularly
Shout for help
Open airway
Assess breathing
Not breathing normally
Call for an ambulance
Start CPR 30:2
Send or go for an AED
As soon as AED arrives
Start AED,
listen to and follow voice prompts
AED Assesses rhythm
AED not available
30 chest compressions:
2 rescue breaths
Breathing normally
Put victim in recovery position
and call for an ambulance
Approach safely
Check response
P.72
5
OUT OF HOSPITAL CARDIAC ARREST:
Assessment of a collapsed victim and initial treatment

Continue until victim starts to wake up: to move, open eyes, and breathe normally
No shock advised
Immediately resume
CPR 30:2 for 2 min
Shock advised
1 shock
Immediately resume
CPR 30:2 for 2 min
P.73
5

IN-HOSPITAL CARDIAC ARREST:
ASSESSMENT OF A COLLAPSED VICTIM AND INITIAL TREATMENT
Collapsed/sick patient
Shout for HELP assess patient
Yes
No
Assess ABCDE
Recognise treat
oxygen; monitoring, i.v. access
Call resuscitation
team
CPR 30:2
with oxygen and airway adjuncts
Signs of life?
P.74
5
Assessment of a collapsed victim and initial treatment

Call resuscitation team
if appropriate
Apply pads/monitor
Attempt defibrillation
if appropriate
Handover to resuscitation team
Advanced Life Support
when resuscitation team arrives
P.75
5

IN-HOSPITAL CARDIAC ARREST: ADVANCED LIFE SUPPORT
Unresponsive
and not breathing
normally ?
Assess
rhythm
CPR 30:2
Attach defibrillator/monitor
Minimise interruptions
Call resuscitation
team
Shockable
(VF/Pulseless VT)
Non-shockable
(PEA/Asystole)
P.76
5
IN-HOSPITAL CARDIAC ARREST: Advanced life support

DURING CPR
• Ensure high-quality
chest compressions
• Minimise interruptions
to compressions
• Give Oxygen
• Use waveform capnography
• Continuous chest compressions
when advanced airway in place
• Vascular access (intravenous,
intraosseous)
• Give adrenaline every 3-5 min
• Give amiodarone after 3 shocks
• Correct reversible causes
REVERSIBLE CAUSES
• Hypoxia
• Hypovolaemia
• Hypo-/hyperkalaemia/metabolic
• Hypothermia
• Thrombosis
• Tamponade - cardiac
• Toxins
• Tension pneumothorax
1 Shock
Return of
spontaneous circulation
IMMEDIATE POST
CARDIAC
ARREST TREATMENT
Immediately resume:
CPR for 2 min
Minimise interruptions
Immediately resume:
CPR for 2 min
Minimise interruptions • Use ABCDE approach
• Aim for SaO2 94-98%
• Aim for normal PaCO2
• 12-lead ECG
• Treat precipitating cause
• Temperature control /
Therapeutic hypothermia
CONSIDER
• Ultrasound imaging
• Mechanical chest
compressions to facilitate
transfer/treatment
• Coronary angiography
and PCI
• Extracorporeal CPR
P.77
5

Give adrenaline and amiodarone
after 3rd
shock
Adrenaline: 1 mg i.v.
(10 ml 1:10,000 or 1 ml 1:1000)
repeated every 3-5 min
(alternate loops)
given without interrupting
chest compressions
Amiodarone
300 mg bolus i.v.
Second bolus dose of 150 mg i.v.
if VF/VT persists
followed by infusion of
900 mg over 24 h
Adrenaline: 1mg i.v. (10 ml 1:10,000 or 1 ml 1:1000)
given as soon as circulatory access is obtained
Repeat every 3-5 min (alternate loops)
Give without interrupting chest compressions
IN-HOSPITAL CARDIAC ARREST: DRUG THERAPY DURING ADVANCED LIFE SUPPORT
Cardiac Arrest
Non-shockable
rhythm
Shockable rhythm
(VF, pulseless VT)
P.78
5
Drug therapy during advanced life support

CHAPTER 6
RHYTHM DISTURBANCES
6.1 SUPRAVENTRICULAR TACHYCARDIAS AND ATRIAL FIBRILLATION �� p.80
J. Brugada
6.2 VENTRICULAR TACHYCARDIAS �� p.84
M. Santini, C. Lavalle, S. Lanzara
6.3 BRADYARRHYTHMIAS �� p.87
B. Gorenek
6

QRS morphology similar to QRS morphology
in sinus rhythm?
QRS morphology similar to QRS morphology
in sinus rhythm?
YES
QRS complex
120 msec
Supraventr.
Tachycardia
QRS complex
120 msec
Supraventr.
Tachycardia
+ BBB
QRS complex
120 msec
QRS complex
120 msec
Fascicular
Tachycardia
or SVT with
aberrant
conduction
Ventricular
Tachycardia
or SVT with
aberrant
conduction
QRS complex
120 msec
QRS complex
120 msec
AF
conducting
over AVN
AF + BBB
or
AF + WPW
AF
+
WPW
Irregular
Ventricular
Tachycardia
Variable QRS
morphology
NO YES NO
TACHYARRHYTHMIAS: DIAGNOSTIC CRITERIA
Tachycardia
100 beats/min
Irregular
Regular
P.80
6.1
TACHYARRHYTHMIAS: Diagnostic criteria

• Concordant precordial pattern
(all leads + or all leads –)
• No RS pattern in precordial leads
• RS pattern with beginning
of R wave to nadir
of S wave 100 msec
Consider
SVT using
the AV node
(AVNRT, AVNT)
Atrial flutter
or atrial
tachycardia
Ventricular
Tachycardia
Ventricular
Tachycardia
Ventricular
Tachycardia
Consider
Sinus tachycardia
or non proper
administration
of adenosine
(too slow, insufficient
dose, etc)
Typical
morphology
in V1 V6
More As
than Vs
More Vs
than As
Wide
QRS complex
Narrow
QRS complex
Regular tachycardia
Vagal maneuvers
or
i.v. adenosine
No change
Tachycardia
terminates
AV relation
changes
P.81
6.1
TACHYARRHYTHMIAS: Diagnostic maneuvers

Hemodynamically
non-stable
Immediate electrical
cardioversion
No termination
Hemodynamically
stable
Vagal maneuvers
and/or i.v. Adenosine
Less than 48 hours
since initiation
AND
hemodynamically stable
Cardioversion
Electrical or pharmacological
using oral or i.v. flecainide
(only in normal heart)
or i.v. vernakalant
Anticoagulation
is initiated using i.v. heparine
Hemodynamically non-stable
Cardioversion
If no cardioversion
is considered: rate control
using betablockers or
calcium antagonists,
together with proper
anticoagulation, if required
Narrow QRS
complex tachycardia
Reconsider diagnosis:
sinus tachycardia,
atrial tachycardia
If no evidence:
Intravenous verapamil
Wide QRS
complex tachycardia
Reconsider the diagnosis of
Ventricular Tachycardia even
if hemodynamically stable
Do not administer
verapimil
More than 48 hours OR
unknown time of initiation,
AND
Patient chronically anticoagulated
OR
a TEE showing no thrombus
Electrical or pharmacological Cardioversion
Termination
TACHYARRHYTHMIAS: THERAPEUTIC ALGORITHMS (1)
Regular Supraventricular Tachycardias
with or without bundle branch block
Irregular and narrow QRS complex
Tachycardia
Hemodynamically
non-stable
cardioversion
No termination
Hemodynamically
stable
Vagal maneuvers
and/or i.v. Adenosine
Less than 48 hours
since initiation
AND
Cardioversion
or i.v. vernakalant
Anticoagulation
is initiated using i.v. heparine
Hemodynamically non-stable
Cardioversion
If no cardioversion
is considered: rate control
using betablockers or
calcium antagonists,
together with proper
anticoagulation, if required
Narrow QRS
complex tachycardia
Reconsider diagnosis:
sinus tachycardia,
atrial tachycardia
If no evidence:
Intravenous verapamil
Wide QRS
complex tachycardia
Reconsider the diagnosis of
Ventricular Tachycardia even
if hemodynamically stable
Do not administer
verapimil
More than 48 hours OR
unknown time of initiation,
AND
Patient chronically anticoagulated
OR
a TEE showing no thrombus
Electrical or pharmacological Cardioversion
Termination
Regular Supraventricular Tachycardias
with or without bundle branch block
Irregular and narrow QRS complex
Tachycardia
P.82
6.1
TACHYARRHYTHMIAS: Therapeutic algorithms (1)

Hemodynamically
non-stable
Cardioversion
If no cardioversion is considered:
rate control using betablockers or
calcium antagonists (only if VT and
AF+WPW is excluded), together
with proper anticoagulation
if required
Less than 48 hours since initiation
AND
Cardioversion
electrical or pharmacological
or i.v. amiodarone
Anticoagulation
is initiated using i.v. heparin
More than 48 hours
or unknown initiation,
AND
patient chronically anticoagulated
or a TEE showing no thrombus
Cardioversion
Irregular and wide QRS complex Tachycardia
P.83
6.1
TACHYARRHYTHMIAS: Therapeutic algorithms (2)

VENTRICULAR TACHYCARDIAS: DIFERENTIAL DIAGNOSIS OF WIDE QRS TACHYCARDIA
EKG signs of atrio-ventricular dissociation
Random P waves unrelated to QRS complexes
Capture beats / fusion beats / second degree V-A block
1st
Step
2nd
Step
3rd
Step
Concordant pattern in precordial leads
No RS morphology in any of the precordial leads
An interval 100 ms from the beginning of the
QRS complex to the nadir of S in a precordial lead
Morphology in precordial leads Morphology
in aVR lead
Yes
Yes
Yes
No
No
No
VT
P.84
6.2
VENTRICULAR TACHYSCARDIAS:
Diferential diagnosis of wide QRS tachyscardias

RBBB morphology LBBB morphology Initial R wave
Initial R wave
or q 40 msec
V1: qR, R, R’
V6: rS,QS
V1: rsR’, RSR’
V6: qRs
Aberrant conduction
V6: R V1: rS; R 30 ms,
S nadir 60 ms,
notching of the
S wave
V6: qR, QS
Yes
No
No
No
No
Yes
Yes
Yes
Notch in the
descending
Q wave limb
Vi/Vt ≤1
VT
Aberrant conduction
VT
P.85
6.2

MANAGEMENT OF WIDE QRS TACHYCARDIAS
Hemodynamic Tolerance
Stable
Regular rhythm
Irregular rhythm
Vagal maneuver
and/or
i.v. adenosine (push)
Differential Diagnosis
Interruption or
slow down HR
Yes
Yes
No
No
Differential
Diagnosis
(see chapter 6.1
page 81)
SVT
AF with aberrant
ventricular conduction
• β-blockers
• i.v.
• Verapamil or diltazem
Pre excited AF
• Class 1 AADs
Polymorphic VT
• Amiodarone
Amiodarone 150 mg i.v.
(can be repeated up to
a maximum dose of 2.2 g in 24 h)
Synchronised cardioversion
With pulse
Pulseless
Non-stable
• Sedation
or analgesia
• Synchronised
cardioversion
100 to 200 J
(monophasic)
or 50-100 J
(biphasic)
ACLS Resuscitation algorithm
• Immediate high- energy
defibrillation (200 J biphasic
or 360 monophasic)
• Resume CPR and continue
according to the ACLS algorithm
Drugs used in the ACLS algorithm
• Epinephrine 1 mg i.v./i.o.
(repeat every 3-5 min)
• Vasopressin 40 i.v./i.o.
• Amiodarone 300 mg i.v./i.o.
once then consider an additional
150 mg i.v./i.o. dose
• Lidocaine 1-1.5 mg/kg first dose
then 0.5-0-75 mg/kg i.v./i.o.
for max 3 doses or 3 mg/kg
• Magnesium loading dose 1-2 gr
i.v./i.o. for torsade des pointes
P.86
6.2
Management of wide QRS TACHYSCARDIAS

Sinus node dysfunction Atrioventricular (AV) blocks
• Sinus bradycardia: It is a rhythm that originates
from the sinus node and has a rate of under 60 beats
per minute
•
Sinoatrial exit block: The depolarisations that occur in
the sinus node cannot leave the node towards the atria
• Sinus arrest: Sinus pause or arrest is defined as the
transient absence of sinus P waves
on the ECG
•
First degree AV block: Atrioventricular impulse
transmission is delayed, resulting in a PR interval
longer than 200 msec
•
Second degree AV block: Mobitz type I (Wenckebach
block): Progressive PR interval prolongation, which
precedes a nonconducted P wave
•
Second degree AV block: Mobitz type II: PR interval
remains unchanged prior to a P wave that suddenly fails
to conduct to the ventricles
•
Third degree (complete) AV block:
No atrial impulses reach the ventricle
P.87
6.3
BRADYARRHYTHMIAS: Definitions and diagnosis

•
Rule out and treat any underlying causes of bradyarrhythmia
•
Treat symptomatic patients only
Temporary transvenous pacing
Be Careful!
•

Complications are common!
•

Shall not be used routinely
•

Use only as a last resource when chronotropic drugs are insufficient
•

Every effort should be made to implant a permanent pacemaker
as soon as possible, if the indications are established.
Indications limited to:
•

High-degree AV block without escape rhythm
•

Life threatening bradyarrhythmias, such as those that occur during interventional
procedures, in acute settings such as acute myocardial infarction, drug toxicity.
P.88
6.3
BRADYARRHYTHMIAS: Treatment (1)

Permanent pacemaker is indicated in the following settings:
•

Documented symptomatic bradycardia, including frequent sinus pauses that produce symptoms
•

Symptomatic chronotropic incompetence
•

Symptomatic sinus bradycardia that results from required drug therapy for medical conditions
Permanent pacemaker is not recommended in the following settings:
•

Asymptomatic patients
•

Patients for whom the symptoms suggestive of bradycardia
have been clearly documented to occur in the absence of bradycardia
•

Symptomatic bradycardia due to nonessential drug therapy
P.89
6.3
Pacemaker therapies in sinus node dysfunction

Permanent pacemaker therapy is indicated in the following settings regardless of associated symptoms:
•

Third-degree AV block
•

Advanced second-degree AV block
•

Symptomatic Mobitz I or Mobitz II second-degree AV block
•

Mobitz II second-degree AV block with a wide QRS or chronic bifascicular block
•

Exercise-induced second- or third-degree AV block
•

Neuromuscular diseases with third- or second-degree AV block
•

Third- or second-degree (Mobitz I or II) AV block after catheter ablation or valve surgery
when block is not expected to resolve
Permanent pacemaker is not recommended in the following settings:
•

Asymptomatic patients
•

Patients for whom the symptoms suggestive of bradycardia have been clearly documented
to occur in the absence of bradycardia
•

Symptomatic bradycardia due to nonessential drug therapy
P.90
6.3
Pacemaker therapies in atrioventricular blocks

CHAPTER 7
ACUTE VASCULAR SYNDROMES
7.1 ACUTE AORTIC SYNDROMES �� p.92
A. Evangelista
7.2 ACUTE PULMONARY EMBOLISM �� p.102
A. Torbicki
7

Classic aortic dissection
Separation of the aorta media with presence
of extraluminal blood within the layers of the aortic wall.
The intimal flap divides the aorta into two lumina, the true and the false
Penetrating aortic ulcer (PAU)
Atherosclerotic lesion penetrates
the internal elastic lamina of the aorta wall
Aortic aneurysm rupture
(contained or not contained)
Intramural hematoma (IMH)
Aortic wall hematoma with no entry tear
and no two-lumen flow
P.92
7.1
ACUTE AORTIC SYNDROMES: Concept and classification (1)
Types of presentation

DeBakey’s Classification
•
Type I and Type II dissections both originate in the ascending aorta
In type I, the dissection extends distally to the descending aorta
In type II, it is confined to the ascending aorta
•
Type III dissections originate in the descending aorta
Stanford Classification
•
Type A includes all dissections involving the ascending
aorta regardless of entry site location
•
Type B dissections include all those distal to the
brachiocephalic trunk, sparing the ascending aorta
Time course
•
Acute: 14 days
•
Subacute: 15-90 days
•
Chronic: 90 days
Copyright: Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and management: Part II: therapeutic management and follow-up.
Circulation (2003); 108(6),772-778.
Adapted with permission from Nienaber CA, Eagle KA,
Circulation 2003;108(6):772-778. All rights reserved.
De Bakey
Stanford
Type I
Type A
Type II
Type A
Type III
Type B
P.93
7.1
ACUTE AORTIC SYNDROMES: Concept and classification (2)
Anatomic classification and time course

SYMPTOMS AND SIGNS
SUGGESTIVE OF AAS
•
Abrupt and severe chest/back pain with
maximum intensity at onset
• Pulse/pressure deficit
- Peripheral or visceral ischemia
- Neurological deficit
•
Widened mediastinum on chest X -ray
•
Risk factors for dissection
• Other
- Acute aortic regurgitation
- Pericardial effusion
- Hemomediastinum/hemothorax
DIFFERENTIAL DIAGNOSIS
•
Acute coronary syndrome
(with/without ST-segment elevation)
•
Aortic regurgitation without dissection
•
Aortic aneurysms without dissection
• Musculoskeletal pain
• Pericarditis
• Pleuritis
• Mediastinal tumours
• Pulmonary embolism
• Cholecystitis
•
Atherosclerosis or cholesterol embolism
P.94
7.1
ACUTE AORTIC SYNDROME:
Clinical suspicion and differential diagnosis

Copyright: Hiratzka et al. 2010 Guidelines on Thoracic Aortic Disease. Circulation. (2010) ; 121: page-310 (fig 25 step 2).
Consider acute aortic dissection in all patients presenting with:
• Chest, back or abdominal pain
• Syncope
• Symptoms consistent with perfusion deficit
(central nervous system, visceral myocardial or limb ischemia)
Pre-test risk assessment for acute aortic dissection
• Marfan’s syndrome
• Connective tissue disease
• Family history of aortic disease
• Aortic valve disease
• Thoracic aortic aneurysm
• Perfusion deficit:
- Pulse deficit
- SBP differential
- Focal neurological deficit
• Aortic regurgitation murmur
• Hypotension or shock
Chest, back or abdominal pain
described as:
Abrupt at onset, severe in intensity,
and ripping/sharp or stabbing quality
High-risk conditions High-risk pain features High-risk exam features
P.95
7.1
General approach to the patient
with suspected ACUTE AORTIC SYNDROME

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