toolkit v2 copy

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A Reg ister ed Br anch of th e ESC

AcuteCardiovascularCare Association

ACUTE CARDIOVASCULAR CARE ASSOCIATION

T O O LK ITCLINICAL DECISION-MAKING

SECOND EDITION


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Preface

The best care of patients with acute cardiovascular syndromes relies not only on specialists but also onsystems 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 wdifferent backgrounds and levels of expertise with limited resources. This poses a signi cant clinical challenge.Against this background, theACCA Clinical Decision-Making Toolkit was created as a comprehensive resourceencompassing all aspects of acute cardiovascular care but structured as an easy-to-use instrument in environmentwhere initial acute cardiovascular care is typically initiated. Comprehensive tables, clear diagrams and algorithbased on the ESC clinical practice guidelines as well as in clinical experience should provide diagnostic and therapeuguidance at a glance.

The Second Edition of the ACCA Toolkit has been updated with the 2014 and 2015 ESC Guidelines , and enriched wita new chapter with up-to-date coverage of drugs most frequently used in acute cardiovascular care. However, it doesnot replace textbooks and other sources of information that need to be consulted to reach an optimal management of

these patients.

The ACCA Toolkit is available through different platforms:Printed booklet, available at congresses where ESC-ACCA is represented

Web-based pdf le downloadable at www.escardio.org/ACCAMobile application for smartphones/tablets available in both Apple & Googleplay stores

Héctor Bueno, M.D., PhD., FESC, FAHAEditor in Chief

II


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List of Authors• 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 Department of Cardiology, Hospital Universitario 12 de Octubre and Centro Nacional de

Investigaciones Cardiovasculares, Madrid, Spain

• Alida Caforio Department of Cardiology, Padua University Medical School, Padua, Italy • Peter Clemmensen Department of Cardiology, Rigshospitalet Copenhagen University, Copenhagen, Denmark • Artur Evangelista Department of Cardiology, Hospital Universitario Vall d’Hebrón, Barcelona, Spain• Gerasimos Filippatos Department of Cardiology, Attikon University Hospital, Athens, Greece• Bulent Gorenek Department of Cardiology, Eskisehir Osmangazy University, Eskisehir, Turkey • Andre Keren Heart Failure and Heart Muscle Disease Center, Hadassah University Hospital, Jerusalem, Israel• 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• 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• Iwan C.C. van der Horst Department of Critical Care. University Medical Center Groningen, Groningen, The Netherlands• Pascal Vranckx Department of Cardiology and Critical Care Medicine, Hartcentrum Hasselt, Hasselt, Belgium• Christiaan Vrints Department of Cardiology, Antwerp University Hospital, Edegem, Belgium• Doron Zahger Department of Cardiology, Soroka Univ, Medical Center, Beer Sheva, Israel• Uwe Zeymer Department of Cardiology, Herzzentrum Klinikum Ludwigshafen, Ludwigshafen, Germany

IV


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CHAPTER 1: KEY SYMPTOMS

1.1 CHEST PAIN ...................................................................................................................................... p.2M. Lettino, F. Schiele

1.2 DYSPNEA .............................................................................................................................................. p.9C. Müller

1.3 SYNCOPE ........................................................................................................................................... p.16R. Sutton

p.1

1


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1. Presentation

2. ECG

3. Troponin

4. Diagnosis

STEMI = ST-elevation m ocardial infarction; NSTEMI = non-ST-elevation m ocardial infarction; UA = unstable angina.Reference: Rof et Al. Eur Heart J 2015;eurheartj.ehv320

Low Likelihood High Likelihood

NoncardiacOther

CardiacUA STEMINSTEMI

p.2

Initial assessment of patients with CHEST PAIN 1.1


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First call forchest pain Higher risk / probability Lower risk / probability

Argumentsfor vital risk

• Cardiorespirator arrest, s ncope / loss ofconsciousness, neurological defect

• D spnea• Nausea – vomiting• Arrh thmias – tach cardia

• Normal consciousness• Normal breathing (see chapter 1.1

page 9)• Normal heart rh thm

Context, CV risk Age > 40 years, previous CV disease(MI, stroke, PE), modi able CV risk factors(smoker, HTN, h percholesterolemia, diabetes),chronic CV treatment

• Age < 40 ears,• 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 intensit , short duration ( 20 min+ dyspnea, sweating, lightheadedness, nausea

• Lateral, abdominal irradiation• No neuro-vegetative s mptoms

p.3

Factors to be considered in the evaluationafter the rst call for CHEST PAIN 1.1


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First medicalcontact

Higher risk / probability Lower risk / probability

Hemodynamic,respiratory,neurologicaldistress

• Cardiopulmonar arrest, h potension,tachycardia, shock

• D spnea, h poxemia, 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 forACS

• Context, t pical s mptoms consistent withmyocardial ischemia

• ECG changes• Bedside Tn

• No CV risk, at pical s mptoms, normalECG

• Negative bedside Tn onl if onset of pain>6 hours (see chapter 2.1 page 24)

STEMI NSTEACSUncertaindiagnosis (seechapter 2.1 page 24)

• ECG criteria for STEMI(see chapter 2.3page 35)

• ST depression or normal ECG• Normal ECG→ Repeat 12-lead ECG recording

• Other ST-segment abnormalities notrelated to STEMI(see chapter 2.3)

Type ofreperfusion

Time assessment

• Primary PCI or thrombolysis? PrimaryPCI if dela


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50% have ≥ 2 diagnoses, which may result in acute respiratory failure*!

• ECg • Chest X-ray • Blood count • Tn • 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

Criteri a for transfer to I CU

(despite treatment for 30 minutes) • Respiratory rate >35/min • SBP


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BASIC WORK-UP

• Immediate 12-lead ECG, cardiac monitor, BP, respiratoryrate, pulse oximetry • Clinical findings Most commonl : lower extremit edema, jugular venous distension,

rales; work up for underl ing cardiac disease and triggers• Laboratory findings Complete blood count, chemistries, cardiac enz mes, BNP, TSH,

ABG as needed

• Chest X-ray (lung ultrasound)• Echocardiogram During admission (earlier if decompensated aortic

stenosis or endocarditis are suspected)• Coronary angiography Emergent in patients with ACS; dela ed in patients with suspected coronar arter disease

• Positioning Keep head of bed elevated above level of legs• Ox gen Up to 12 L/min via non-rebreather, titrate ox gen saturation to 95%• Nitrogl cerin 1-2 SL tablets or 2-3 patches 10 mg (1st choice). In pulmonar edema with severe shortness of breath:

NTG drip 0.05% (100 mg in 200 ml) - Start with 25µ g/min = 3 ml/h, check BP after 5 and 10 min - Increase dose per SHO/attending recommendations b 25µ g/min at a time as long as SBP >90 mmHg - Additional BP check 5 and 10 min after each increase in dosing

- Check BP ever 20 min once a stead drip rate is reached• Furosemide 40-120 mg i.v. (adjust based on kidne function and clinical findings; monitor creatinine)• Morphine 2 mg i.v. (preceeded b 10 mg i.v. metoclopramide PRN)• 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 bod weight as 1st dose

p.10

DYSPNEA: Acute heart failure (see chapter 3.1) 1.2


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Reference: Ware L B and Mattha M A. Acute Pulmonar Edema. New Engl J Med (2005); 353:2788-2796.

Unstable after 30 minutes

CCU/ICU transfer Ward transfer

Stable after 30 minutes

p.11p.11

1.2


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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 criteriaNIV indicated?

Laboratory findings: Blood count, coagulation, ProCT, perhaps BNP, D-DimersChest X-ray; ECG (exclusion of differential diagnoses)Sputum cultures (always in case of hospitalisation or previous outpatient antibiotictreatment)

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 daysAntibiotic treatment should be considered; always indicated in stage Gold IVPhysiotherapy

History, clinical examination (blood pressure, pulse, oxygen saturation, vigilance)

Cop right: Leuppi JD e t al. JAMA . 2013 Jun 5;309(21):2223-31.

p.14p.14

DYSPNEA: COPD exacerbation 1.2


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Objective: diagnostics, risk stratification & empirical immediate treatment


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S ncope is a transient loss of consciousness due to global cerebral h poperfusion (usuall , itself due to a periodof low blood pressure) characterised b rapid onset, short duration, spontaneous and complete recover .

The differentiation between s ncope and non-s ncopal conditions with real or apparent LOC can be achieved in most cawith adetailed clinical history but sometimes can be extremel dif cult. The following questions should be answere• Was LOC complete?• Was LOC transient with rapid onset and short duration?• Did the patient recover spontaneousl , completel 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 s ncope. If the answer to oor more of these questions is negative, exclude other forms of LOC before proceeding with s ncope evaluation.

Loss of Consciousness?

TLOCTrauma Not Trauma

• Accidental • Fall• Other abnormal mental state

No

Noyes

yes

• Coma• Intoxication

• Metabolic disturbance• Aborted sudden death

Transient, rapid onset,short time, self-terminating

S ncope Epileps Ps chogenicReference: Sutton R. Clinical classi cation of s ncope. - Prog Cardiovasc Dis. (2013) ; 55(4):339-44.

p.16

SYNCOPE: Assessment of patientswith transient loss of conscioussness (TLOC) 1.3


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Vasovagal syncope is diagnosed if s ncope is precipitated b emotional distress or orthostatic stressand is associated with typical prodrome.

Situational syncope is diagnosed if s ncope occurs during or immediatel after speci c triggers.

Orthostatic syncope is diagnosed when it occurs after standing up and there is documentationof orthostatic hypotension.

Arrhythmia related syncope is diagnosed b ECG when there is:• Persistent sinus brad cardia 3 s

• Mobitz II 2nd or 3rd degree AV block• Alternating left and right BBB• VT or rapid parox smal SVT• Non-sustained episodes of pol morphic 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 ischemiawith or without myocardial infarction.

Cardiovascular syncope is diagnosed when syncope presents in patients with prolapsing atrial myxoma, severeaortic stenosis, pulmonar h pertension, pulmonar embolus or acute aortic dissection.

Reference: Mo a A e t al. Eur Hear t J(2009) 30, 2631–2671 (1).

p.17p.17

SYNCOPE: Dia nostic criteria (1)Diagnostic criteria with initial evaluation 1.3


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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 UnitHome if stable,

Admit to hospitalif evidence of high risk

HomeOutpatient SMU

referral

Outpatient SMUfor diagnosis, treatment

and follow-up as appropriateHospital admission

Inpatient SMU

Initiate therapyInpatient SMU, outpatient SMU orpersonal physician as appropriate

Cop right: Sutton R, Brignole M, Benditt DG. Ke challenges in the current management of s ncope. Nat Rev Cardiol. (2012 );(10):590-8.

Once s ncope is considered to be the likel diagnosis, risk strati cation is required to determine further management.p.18p.18

SYNCOPE: E aluation and risk strati cation of patients with suspected syncope1.3


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Carotid sinus massage Orthostatic Hypotension

Indications• CSM is indicated in patients >40 ears with s ncope of unknown

aetiology after initial evaluation;• CSM should be avoided in patients with previous MI,

TIA or stroke within the past 3 months and inpatients with carotid bruits (except if carotid Doppler

studies excluded signi cant stenosis)

Recommendations: Active standing Indications• Manual intermittent determination with sph gmomanometer

of BP supine and, when OH is suspected, during activestanding for 3 min is indicated as initial evaluation;

• Continuous beat-to-beat non-invasive pressure measurement ma be helpful in cases of doubt

Diagnostic criteria• CSM is diagnostic if s ncope is reproduced in

presence of as stole longer than 3 s and/or a fall ins stolic BP >50 mmHg

Diagnostic criteria• The test is diagnostic when there is a s mptomatic fall in

s stolic BP from baseline value≥20 mmHg or diastolicBP≥10 mmHg or a decrease in s stolic BP to 10 mmHg or a decrease in systolic BPto


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Treatment of re ex syncopeTreatment of orthostatic

hypotension

• Explanation of the diagnosis, provision of reassurance and explanationof risk of recurrence are in all patients

• Isometric PCM are indicated in patients with prodrome• Cardiac pacing should be considered in patients with dominant cardioinhibitor CSS• Cardiac pacing should be considered in patients with frequent recurrent re ex s ncope,

age > 40 ears and documented spontaneous cardioinhibitor response during monitoring• Midodrine ma be indicated in patients with VVS refractor to lifest le measures

• Tilt training ma be useful for education of patients but long-term bene t dependson compliance

• Cardiac pacing ma be indicated in patients with tilt-inducedcardioinhibitor response with recurrent frequent unpredictablesyncope and age > 40 after alternative therapy has failed

• Triggers or situations inducing s ncope must be avoided as much as possible• H potensive drugs must be modi ed or discontinued• Cardiac pacing is not indicated in the absence of a documented

cardioinhibitor re ex• Beta-adrenergic blocking drugs are not indicated• Fluid consumption and salt in the diet should be increased

• Adequate h dration and salt intakemust be maintained

• Midodrine should be administered asadjunctive therap if needed

• Fludrocortisone should be administeredas adjunctive therap if needed

• PCM ma be indicated

• Abdominal binders and/or supportstockings to reduce venous pooling maybe indicated

• Head-up tilt sleeping (>10°) to increaseuid volume ma be indicated

• Triggers or situations inducing s ncopemust be avoided as much as possible

• H potensive drugs administered forconcomitant conditions must bediscontinued or reduced

Cop right: Mo a A et al . Eur Heart J(2009) 30, 2631–2671 (3).

p.20p.20

Treatment according to type of SYNCOPE (1) 1.01.3


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Treatment of arrhythmic syncope

Cardiac Pacing• Pacing is indicated in patients with sinus node disease in whoms ncope is demonstrated to be due to sinus arrest (s mptom-ECG correlation) without a correctable cause

• Pacing is indicated in sinus node disease patients with s ncopeand abnormal CSNRT

• Pacing is indicated in sinus node disease patients with s ncopeand as mptomatic pauses > 3 sec. (with possible exceptions of

young trained persons, during sleep and in medicated patients)• Pacing is indicated in patients with s ncope and 2nd degree

Mobitz II, advanced or complete AV block • Pacing is indicated in patients with s ncope, BBB and positive EPS• Pacing should be considered in patients with unexplained

syncope and BBB• Pacing ma be indicated in patients with unexplained s ncope

and sinus node disease with persistent sinus brad cardia itselfasymptomatic

• Pacing is not indicated in patients with unexplained s ncopewithout evidence of an conduction disturbance

Catheter ablation• Catheter ablation is indicated in patients with s mptom/ arrh thmia ECG correlation in both SVT and VT in the absenceof structural heart disease (with exception of atrial brillation)

• Catheter ablation ma be indicated in patients with s ncope dueto the onset of rapid atrial brillation

Antiarrhythmic drug therapy • Antiarrhythmic drug therapy, including rate control drugs, is indicated

in patients with s ncope due to onset of rapid atrial brillation• Drug therap should be considered in patients with s mptom/

arrh thmia ECG correlation in both SVT and VT when catheterablation cannot be undertaken or has failed

Implantable Cardio erter De brillator (ICD)• ICD is indicated in patients with documented VT and structural

heart disease

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

• ICD should be considered in patients with documented VT andinherited cardiomyopathies or channelopathies

Cop right: Mo a A et al . Eur Heart J(2009) 30, 2631–2671 (4).

p.21p.21

Treatment according to type of SYNCOPE (2) 1.3


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p.22


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CHAPTER 2: ACUTE CORONARYSYNDROMES

2.1 GENERAL CONCEPTS ........................................................................................................ p.24H. Bueno

2.2 NON ST-SEGMENT ELEVATION ACS .............................................................. p.29H. Bueno

2.3 ST-SEGMENT ELEVATION MI (STEMI) .......................................................... p.35D. Zahger, P. Clemmensen

p.23

2


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hs-cTn ULN

CHEST PAINor symptoms sugestive of myocardial ischemia

ECG

ST elevation

(persistent)LBBB ST/T abnormalities Normal ECG

STEMI

Pain resolves withnitroglycerin 1st hsTn

NSTEMI Unstable AnginaWork-up

differential diagnoses

Pain onset >6hPain onset ULN)

hs-cTn>x5 ULN

orclinical

diagnosis clear

Potentialnoncardiac

causes forabnormal Tn

ConsiderSTEMI

Yes

No

Reference: Rof M. Eur Heart J 2015;eurheartj.ehv320

p.24

ACUTE CORONARY SYNDROMES: Dia nosis (1) 2.1


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Suspected NSTEMI

Other0h ≥ D ng/l

or0-1h ≥ E ng/l

ObserveRule-out Rule-in

0hor

< B ng/land

0-1h < Cng/l

A B C D E

hs-cTnT (Elecsys)* 5 12 3 52 5

hs-cTnl (Architect)* 2 5 2 52 6

hs-cTnl (Dimension Vista)* 0.5 5 2 107 19

0h < A ng/l

• NSTEMI can be ruled-out at presentation, if hs-cTn concentration is ver low• NSTEMI can be ruled out b the combination of low baseline levels and the lack of a relevant increase within 1 h• NSTEMI is highl likel if initial hs-cTn concentration is at least moderatel elevated or hs-cTn concentrations

a clear rise within the rst hourReference: Rof M. Eur Heart J 2015;eurheartj.ehv320

*Cut-off levels are assa -speci c.

p.25

ACUTE CORONARY SYNDROMES: Dia nosis (2)0-1 H Rule-in & rule out test for NSTEMI 2.1


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Causes of chest painNot related to ACS

Causes of troponin elevationNot related to ACS

Primary cardiovascular

• Acute pericarditis, pericardial effusion• Acute m ocarditis• Severe h pertensive crisis• Stress cardiom opath (Tako-Tsubo s ndrome)• H pertrophic cardiom opath , aortic stenosis• Severe acute heart failure• Acute aortic s ndrome (dissection, hematoma)• Pulmonar embolism, pulmonar infarction

• Cardiac contusion

Primary cardiovascular

• Acute m o(peri)carditis• Severe h pertensive crisis• Pulmonar edema or severe congestive heart failure• Stress cardiom opath (Tako-Tsubo s ndrome)• Post- tach - or brad arrh thmias• Cardiac contusion or cardiac procedures (ablation, cardioversion, or

endom ocardial biops )• Aortic dissection, aortic valve disease or h pertrophic cardiom opath

• Pulmonar embolism, severe pulmonar h pertensionPrimary non-cardio ascular• Oesophageal spasm, oesophagitis, Gastro

Esophageal Re ux (GER)• Peptic ulcer disease, cholec stitis, pancreatitis• Pneumonia, bronchitis, asthma attack • Pleuritis, pleural effusion, pneumothorax• Pulmonar embolism, severe pulmonar

hypertension• Thoracic trauma• Costochondritis, rib fracture• Cervical / thoracic vertebral or discal damage• Herpes Zoster

Primary non-cardio ascular• Renal d sfunction (acute or chronic)• Critical illness (sepsis, repirator failure…)• Acute neurological damage (i.e. stroke, subarachnoid hemorrhage)• Severe burns (affecting >30% of bod surface area)• Rhabdom ol sis• Drug toxicit (chemotherap with adriam cin, 5- uorouracil,

herceptin, snake venoms…)• In ammator or degenerative muscle diseases• H poth roidism• In ltrative diseases (am loidosis, hemochromatosis, sarcoidosis)• Scleroderma

p.26

ACUTE CORONARY SYNDROMES: Differential dia nosis (1)2.1


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ST-se ment ele ation Negative T waves

Fixed• LV aneur sm• LBBB, WPW, h pertrophic cardiom opath , LVH• Pacemaker stimulation• Earl repolarisation (elevated J-point)Dynamic• Acute (m o)pericarditis• Pulmonar embolism• Electrol te disturbances (h perkalemia)• Acute brain damage (stroke, subarachnoid haemorrhage)• Tako Tsubo s ndrome

• Normal variants, i.e. women (rightprecordial leads), children, teenagers• Evolutive changes post m ocardialinfarction

• Chronic ischemic heart disease• Acute (m o)pericarditis, cardiom opathies• BBB, LVH, WPW• Post-tach cardia or pacemaker stimulation• Metabolic or ionic disturbances

ST-se ment depression Prominent T waves

Fixed• Abnormal QRS (LBBB, WPW, pacemaker stimulation…)• LVH, h pertrophic cardiom opath• Chronic ischemic heart diseaseDynamic• Acute (m o)pericarditis • Severe h pertensive crisis• Acute pulmonar h pertension • Drug effects (digoxin)• Electrol te disturbances (h perkalemia) • Shock, pancreatitis• Intermitent LBBB, WPW, pacing • H perventilation• Post-tach cardia / cardioversion • Tako Tsubo s ndrome

• Normal variants, i.e. earl repolarisation• Metabolic or ionic disturbances

(i.e. hyperkalemia)• Acute neurological damage(stroke, subarachnoid haemorrhage)

p.27

ACUTE CORONARY SYNDROMES: Differential dia nosis (2)Causes of repolarisation abnormalities in the ECG not related to ACS 2.1


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2ECG

(


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Ischemic risk

Grace risk score Timi risk scorePredictive Factors• Age• HR*• SBP*• Creatinine (mg/dl)*• Killip class*• Cardiac arrest*

• ST-segment deviation• Elevated cardiac markers

OutcomesIn-hospital, 6-month,1-year and 3-year mortality1- ear death/MI

Predictive Factors• Age 65 ears• At least 3 risk factors for CAD• Signi cant (>50%) coronar stenosis• ST deviation• Severe anginal s mptoms (>2 events in last 24 h)• Use of aspirin in last 7 da s

• Elevated serum cardiac markers

OutcomeAll-cause mortalit / newor recurrent MI / severerecurrent ischemia requiringurgent revascularisation at14 days

≤

* At admission.

p.29

NON ST-SEgMENT ELEvATION ACS: Risk strati cation (1) 2.2


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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*

OutcomeIn-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 registr JAMA. (2004) ;291(22):2727-33.

Antman EM, et a l. 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 m ocardial infarction: the CRUSADE (Can Rapid risk s trati cation of Unstable angina patients SADverse outcomes with Earl implementation of the ACC/AHA Guidelines) Bleeding Score. Circulation (2009) ;119(14):1873-82.

* At admission.

p.30

NON ST-SEgMENT ELEvATION ACS: Risk strati cation (2) 2.2


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Initial treatment*

• Nitrates• Morphine• Oxygen (if SatO2 < 95%)

One of the following: • Fondaparinux • Enoxaparin

• UFH • Bivalirudin

Aspirin + one of: • Ticagrelor • Prasugrel

• ClopidogrelOptionally: • GP IIb/IIIa inhibitors • Cangrelor

• Nitrates• Beta-blockers• Calcium antagonists

• Statins• ACE inh. (or ARB)• Aldosterone inhibitors

Pharmacologicaltreatment*

Anti ischemictreatment

Antithrombotictherapy

Anticoagulation Antiplatelets

PCICABG

Other preventivetherapies

Myocardialrevascularisation

For more information on individual drug dosesand indications, See chapter 8: Use of drugs inAcute Cardiovascular Care .

p.31

NON ST-SEgMENT ELEvATION ACS: Treatment (1)General overview 2.2

NON ST SE MENT ELE ATION ACS T (2)


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NSTE-ACS patients with non-valvular atrial fibrillation

PCI

Low to intermediate(e.g. HAS-BLED = 0–2)

Triple

therapy

High(e.g. HAS-BLED ≥ 3)

Triple or dualtherapy a

Dualtherapy b

Dualtherapy b

Dualtherapy b

0

4 weeks

6 months

12 months

Lifelong

Oral anticoagulat ion (VKA or NOACs) Aspirin 75–100 mg dai ly Clopidogrel 75 mg dailyO

Monotherapy cO

A C

O A C

O C or A

O C or A

O C or A

O A C

Medically managed / CABGManagement strategy

Bleeding risk

T i m e

f r o m

P C I / A C S

CHA2DS2-VASc = Cardiac failure, H pertension, Age≥ 75[2 points], Diabetes, Stroke [2 points] – Vascular disease,Age 65–74, Sex categor .

a Dual therapy with oral anticoagulation and clopidogrel maybe considered in selected patients (low ischaemic risk).

b Aspirin as an alternative to clopidogrel ma be considered in patients on dual therapy (i.e., oral anticoagulation plussingle antiplatelet); triple therap ma be considered up to12 months in patients at ver high risk for ischaemic events.

c Dual therapy with oral anticoagulation and one antiplateletagent (aspirin or clopidogrel) be ond one ear ma beconsidered in patients at very high risk of coronary events.

d In patients undergoing coronary stenting, dual antiplatelettherap ma be an alternative to triple or a combinationof anticoagulants and single antiplatelet therapy if theCHA2DS2-VASc score is 1 (males) or 2 (females).

Reference: Eur Heart J 2015;eurheartj.ehv320- Figure 5.

p.32

NON ST-SEgMENT ELEvATION ACS: Treatment (2)Antithrombotic strate ies in patients with NSTE-ACS and non- al ular atrial brillation 2.2

NON ST SE MENT ELE ATION ACS T t t (3)


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very-hi h-riskcriteria

• Haemod namic instabilit or cardiogenic shock • Recurrent or ongoing chest pain refractor to medical treatment

• Life-threatening arrh thmias or cardiac arrest• Mechanical complications of MI• Acute heart failure• Recurrent d namic ST-T wave changes, particularl with intermittent ST-elevation

Hi h-risk criteria • Rise or fall in cardiac troponin compatible with MI• D namic ST- or T-wave changes (s mptomatic or silent)• GRACE score >140

Intermediate-risk criteria

• Diabetes mellitus• Renal insuf cient (eGFR


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Symptoms Onset

First medical contact NSTE-ACS diagnosis

PCI center

Very high

ImmediateInvasive(


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STEMI: Treatment (2)


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Pre hospital PCI CCU/ICCU MedicationTitration Day 2-7

Reference: Steg G et al. Eur Heart J. (2012);33:2569-619(7).Pre-hospital management of patients with chest pain and/or d spnoea of cardiac origin. A position paper of the Acute Cardiovascular Care Association (ACCA)of the ESC - European He art Journa l: Acute Cardiovascular Care August 27, 2015 2048872615604119.

Acetylicsalisylic Acid 300 mgHeparin 70 IU/kg

Bivalirudinor GPI: Epti batide Tiro ban AbxicimabFollow local in-lab instruction / dosing

Metoprolol 25 mg x 2or carvedilol 3,25 mg x 2or bisoprolol 2,5 mg x 2

Atorvastatin 80 mg x 1

or Rosuvastatin 40 mg x 1

Acet licsalis lic Acid 75 mg x 1Ticagrelor 90 mg x 2or Prasugrel 10/5 mg x 1or Clopidogrel 75 mg x 1

Metoprolol 200mg x 1or carvedilol 25 mg x 2or bisoprolol 5 mg x 2or Ca-antagonist(see chapter 2.2)

Start ACE-i or ARB in DM, LVSD, CHF, or to control BPAldosterone RBStart or continue anti-diabetic medication

Ticagrelor 180 mgor Prasugrel 60 mg or Clopidogrel 600 mg

p.37

2.3STEMI: Treatment (2)

Primary PCI - First 24 hours and days 2-7

For more information on individual drug doses and indications, See chapter 8: Use of drugs in

Acute Cardiovascular Care .


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p.38

2.3


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CHAPTER 3: ACUTE HEART FAILURE

3.1 HEART FAILURE AND PULMONARY OEDEMA ................................. p.40I.C.C. van der Horst, G. Filippatos

3.2 CARDIOGENIC SHOCK ..................................................................................................... p.52P. Vranckx, U. Zeymer

3

p.39

ACUTE HEART FAILURE Di i d (I) 3 1


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Rapid onset of,or worseningof symptoms

and signsof heart failure*

Cardiovascular risk profile *

Precipitating factors *

Precipitating factors *

High likelihood of acute heart failure *

Intermediate to highlikelihood of

acute heart failure *

Intermediate likelihoodof acute heart failure *

History of heart failure

Yes

No

Yes

20-40%

60-80%

Yes

No

No

Rule outdifferentialdiagnosis *

* (See page 41) .

ACUTE HEART FAILURE : Dia nosis and causes (I) 3.1

p.40

ACUTE HEART FAILURE Di i d (2) 3 1


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1• Symptoms: D spnea (on effort or at rest)/breathlessness, fatigue, orthopnea, cough, weight gain/ankle swelling2• Si ns: Tach pnea, tach cardia, low or normal blood pressure, raised jugular venous pressure, 3rd/4th

heart sound, rales, oedema, intolerance of the supine position3• Cardio ascular risk pro le: Older age, HTN, diabetes, smoking, d slipidemia, famil histor , histor of CVD4• Precipitatin factors: M ocardial ischemia, rh thm disturbances, medication (NSAID, negative inotropic agents)

infection, noncompliance5• Differential diagnosis: Exacerbated pulmonar disease, pneumonia, pulmonar embolism, pneumothorax,

acute respirator distress s ndrome, (severe) anaemia, h perventilation (acidosis), sepsis/septic shock, redistributive/hypovolemic shock

6• Likelihood: Depending on the site off presentation the underlying cause of acute heart failure is likely to differ.Cardiologists see more often worsening heart failure and physicians at the Emergency Department more often seepatients with preserved systolic left ventricular function

MAIN CAUSES OF ACUTE HEART FAILURE• Coronar arter disease • Congenital heart disease • Pleural effusion• H pertension • Arrh thmia (tach -, brad -) • Anxiet disorder

• Cardiom opath (familial, acquired) • Conduction disorder (blocks) • Neurologic disease• Valvular heart disease • Volume overload (renal, iatrogenic)• Peri-/endocardial disease • Tumor

Reference: McMurra JJ et al, Eur Heart J (2012) ;33(14):1787-847 (19).

ACUTE HEART FAILURE : Dia nosis and causes (2) 3.1

p.41

SUSPECTED ACUTE HEART FAILURE 3 1


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SEVERITY SCORE(excluding shock)Respiratory distress

RR > 25/min,SpO2


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RESUSCITATION AREA/CCU/ICUTo stabilize vital signs (echo if needed) and/or

immediate non-invasive ventilation(see chapter 3.1 page 44)

DIAGNOSTIC TESTS• ECG• Laboratory tests

(see chapter 3.1 page 44)• Echo (lung, heart)• Chest X-ray

IV THERAPY• See chapter 3.1 page 47

Yes

No

I N I T I A L 3 0 - 6

0 M I N

Algorithm for the management of acute hear t failure. Depicted from Mebazaa A et al. Eur J Heart Fail. (2015);17(6):544-58.

3.1

p.43

ACUTE HEART FAILURE: Initial diagnosis and treatment3 1


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AB Sufficient oxygenation(SpO2>90%)

Sufficient ventilation(pCO290%)

OXYGEN* (+ oropharyngeal airway [Guedel/Mayo]/nasopharyngeal airway and upright position)

Oxygen * + Positive End-Expiratory Pressure (PEEP) 5-7.5 mmHg

Nasal: 1 ltr = FiO2 22%, 2 ltr = 25%, 3 ltr = 27%, 4 ltr = 30%, 5 ltr = 35%Mask: 2 ltr = FiO2 25%, 4 ltr = 30%, 6 ltr = 40%, 7 ltr = 45%, >8 ltr = 50%Mask + reservoir: 6 ltr = FiO2 60%, 7 ltr = 70%, 8 ltr = 80%, 10 ltr = 90%Venturimask**: 24% = FiO2 24%, 35% = 35%, 40% = 40%, 60% = 50%

Yes

Yes

Yes

~5 minutes to reassess

~15 minutes to reassess

No

No

No

Start CONTINUOUS POSITIVEAIRWAY PRESSURE (CPAP)

Airway (A) & Breathin (B) 3.1

p.44

3 1


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* Goal SpO2 94-98%. ** Use the prede ned liters of ox gen. When using higher ows the FiO2 will drop.*** For a patient with COPD, a pCO2 of 45-50 mmHg ma be optimal. Aim for a normal pH.**** Consider if the above fails or when patient is fatigued.

Start NON-INVASIVE VENTILATION (NIV)(positive pressure, bilevel) + PEEP 5-10 mmHg

Consider ENDOTRACHEAL INTUBATION (ETT)****

Get support on time

C

Sufficient oxygenation (SpO 2>90%)

Oxygen * + PEEP 5-10 mmHg + Ventilatory Support (pressure support)

YesNo

3.1

p.45

ACUTE HEART FAILURE : Initial dia nosis (CDE) 3.1


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References: Mebazaa A et al. Intensive Care Med. (2015) Sep 14. [Epub ahead of print]; Mueller C et al. Eur Heart J Acute Cardiovasc Care. (2015) Jun 29.

C - CIRCULATION * HR (brad cardia [100/min]), rh thm (regular, irregular), SBP (ver low[140 mmHg]), and elevated jugular pressure should be checked

INSTRUMENTATION & INvESTIgATIONS:Consider intravenous (central) & arterial line (BP monitoring)

Laboratory measures • Cardiac markers (troponin, (BNP/NT-proBNP, MR-proANP)

• Complete blood count, electrol tes, creatinine, urea, glucose, in ammation, TSH Standard 12-lead ECg • Venous blood gases, D-dimer (suspicion of acute pulmonar embolism)

• Rh thm, rate, conduction times? • Signs of ischemia/m ocardial infarction? H pertroph ?

Echocardiography

• Ventricular function (s stolic and diastolic)? • Presence of valve d sfunction (severe stenosis/insuf cienc )? • Pericardial effusion/tamponade?

ACTIONS:Rule in/out diagnosis of acute heart

failure as diagnosis for symptomsand signsEstablish cause of diseaseDetermine severity of diseaseStart treatment as soon as possible,i.e. both heart failure and the factors identi ed as triggers

D – DISABILITY DUE TO NEUROLOGICAL DETERIORATION Normal consiousness/altered mental status? Measurement of mental state with AVPU (alert, visual, pain or unresponsive) Glasgow

Coma Scale: EMV score


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1 Inotropic drugs• Dobutamine 2.5 μg/kg/min • Milrinone bolus 25 μg/kg in10-20 min,

continuous 0.375 μg/kg/min2 Vasopressor i.v.

• Norepinephrine 0.2 μg/kg/min3 Diuretics i.v.

• Furosemide 20-40 mg bolus, continuous 100 mg/6 h

4 Consider hypertonicsaline + diuretic

5 Consider mechanicalcirculatory support

1 Diuretics i.v.• Furosemide 20-40 mg bolus,

continuous 100 mg/6 h*

2 Inotropic drugs• Dobutamine continuous 2.5 μg/kg/min • Milrinone bolus 25 μg/kg in 10-20 min, continuous 0.375 μg/kg/min

• Levosimendan bolus 12 μg/kg in10 min, continuous 0.1 μg/kg/min

3 Consider to start ACE-I/ARB, beta-blocker, MRA.

*See Chapter 8: use of drugs inacute Cardiovascular Care .(See table page 50-51)

1 Vasodilators• Nitrogl cerine spra 400 μg sublingual, repeat ~5-10 min

• Nitrogl cerine i.v. continuousl ~10 μg/min, increase ~5 μg/min

• Nitroprusside 0.3 μg/kg/minincrease to 5 microg/kg/min

2 Diuretics i.v.• Furosemide 20-40 mg bolus, continuous 100 mg/6 h

3 Consider to start ACE-I/ARB, beta-blocker, MRA.

*See Chapter 8: use of drugs in acuteCardiovascular Care .(See table page 50-51)

Low cardiac output60%

No

No

Yes

Yes

C: Circulatory failure/shock 110 mmHg?

* Use higher dose in patients on chonic diuretic treatment for HF (i.e. 2.5 times normal dose).

CU U : t a t eat e t (C) v t e apy

p.47


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ACUTE HEART FAILURE: Treatment (C) and pre enti e measures 3.1


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Normotension/

Hypertension

Hypotension Low Heart rate Potassium Renal

impairment85 mmHg 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 changeReview/increase

Stop Reduce Stop

Diuretics Increase Reduce Stop No change No changeReview/ No change

Review/ increase

No change Review

CCB, calcium channel blockers (mg/dL); Cr, creatinine blood level (mg/dL); eGFR, estimated glomerular ltration rate ml/min/1.73 m2; MRA, mineralocorticoid receptor antago(*) amiodarone. - Depicted from Mebazaa A et al. Eur J Heart Fail. (2015);17(6):544-58.

Mana ement of oral therapy in AHF in the rst 48 hours p.50

3.1ACUTE HEART FAILURE: Treatment (C) and pre enti e measures (Cont.)


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CCB, calcium channel blockers (mg/dL); Cr, creatinine blood level (mg/dL); eGFR, estimated glomerular ltration rate ml/min/1.73 m2; MRA, mineralocorticoid receptor antago(*) amiodarone. - Depicted from Mebazaa A et al. Eur J Heart Fail. (2015);17(6):544-58.

Thrombosis proph laxis should be started in patients not anticoagulated (enoxaparin 1 mg/kg as rst dose)Maintain an adequate nutritional status with a nutritional support of 20-25 kcal/kg/da within the rst 48 hours

Normotension/

Hypertension

Hypotension Low Heart rate Potassium Renal

impairment85 mmHg 2.5,

eGFR < 30

Othervasodilators(Nitrates)

Increase Reduce/stop

Stop No change No change Nochange

No change No change No change

Other heartrate slowingdrugs(amiodarone,CCB,Ivabradine)

Review Reduce/stop

Stop Reduce/stop

Stop Review/stop (*)

No change No change No change

Mana ement of oral therapy in AHF in the rst 48 hours p.51

CARDIOGENIC SHOCK: De nition 3.2


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Clinical condition de ned as the inabilit of the heart to deliver an adequate amount of blood to thetissues to meet resting metabolic demands as a result of impairment of its pumping function.

Hemodynamic criteria to de ne cardio enic shock

• S stolic blood pressure


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LV pump f ailure is the primar insult in most forms of CS, but other parts of the circulator s stemcontribute to shock with inadequate compensation or additional defects. p.53

This protocol should be initiated as soon as cardiogenic shock/end organ h poperfusion is recognisedCARDIOGENIC SHOCK: Initial triage and management

3.2


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This protocol should be initiated as soon as cardiogenic shock/end organ h poperfusion is recognisedand should not be dela ed pending intensive care admission.

In persistent dru -resistant cardi ogenic shock,consider mechanical circulatory support

EARLY TRIAgE & MONITORINgStart high ow O2 Establish i.v. access

• Age: 65–74,≥75• Heart rate >100 beats per minute• S stolic blood pressure 20/min), >30/min (!)• Killip class II-IV• Clinical s mptoms of tissue h poperfusion/h poxia:

- cool extremities, - decreased urine output (urine output


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Ventilator modeTidal Volume goalPlateau Pressure goalAnticipated PEEP levelsVentilator rate and pH goalInspiration: Expiration timeOxygenation goal: • PaO2 • SpO2

Pressure assist/controlReduce tidal volume to 6-8 ml/kg lean bod weight≤ 30 cm H2O5-10 cm H2O12-20, adjusted to achieve a pH≥ 7.30 if possible1:1 to 1:2

50-80 mmHg> 90%

Predicted bod 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 capacit and maintain ox genationand peak pressures above 30 cm H2O to attain effective tidal volumes of 6-8ml/kg with adequate CO2 removal.

*See Chapter 8: Use of drugs in Acute Cardiovascular Care.

For more informations on individual drug doses and indications:p.55

CARDIOGENIC SHOCK: Management following STEMI 3.2


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Assess volume statusTreat sustained arrhythmias: brady- or tachy-Consider mechanical ventilation for comfort (during PCI) and/or as needed: • to correct acidosis • to correct h poxemiaInotropic support (dobutamine and/or vasopressor support)

Signs (ST-segment elevation or new LBBB)and/or clinical s mptoms of ongoing

myocardial ischemia

Emergenc echocardiograph Tissue doppler imaging± Color flow imaging

No

NSTEACS,Delayed CS

Yes

p.56

Earl coronar angiograph Pump failurep

o r t Aortic dissection• Acute severe mitral

3.2


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± Pulmonary artery catheter IABP in selected patients

in a specialised M ocardial InterventionCenter

PCI ± stentingof the culprit lesion

CABG+ correct mechanical complications

RV, LV, both

S h o r t - t e r m

m e c h a n

i c a l c i r c u

l a t o r y s u p p

Pericardial tamponade valve regurgitation• Ventricular septum

rupture• Severe aortic/mitral

valve stenosis

Operating theater coronar angiograph

p.57

CARDIOGENIC SHOCK:Mechanical circulatory support, basic characteristics 3.2


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72-hrs

2-weeks

1-month . . .

Left ventricular support BiVentricular support

Partial support

IABP Impella 2,5 Tandem-heart

Impella 5,0 ImplantableECMOLevitronix

Full support

Level of support

Pulmonary support

p.58

Type Support Access 3.2

59


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Different s stems for mechanical circulator support are available to the medical communit .The available devices differ in terms of the insertion procedure, mechanical properties, andmode of action. A minimal ow rate of 70 ml/kg/min, representing a cardiac index of at least2.5 L/m², is generall required to provide adequate organ perfusion. This ow is the sum of

the mechanical circulatory support output and the remaining function of the heart.The SAVE-score ma be a tool to predict survival for patients receiving ECMO forrefractory cardiogenic shock ( ).

Intra-aorticballoon pump

Ballooncounterpulsation

Pulsatile ow


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p.60

CHAPTER 4: CARDIAC ARRESTp 61

4


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AND CARDIOPULMONARY RESUSCITATION

THE CHAIN OF SURVIVAL

Monsieurs KG, et al. European Resuscitation Council Guidelines for Resuscit ation 2015. Section 1.Executive Summar . Resuscitation 2015; 95C:1-80, DOI:10.1016/j.resuscitation.2015.07.038

p.61

p 62

4OUT OF HOSPITAL CARDIAC ARREST:

Assessment of a collapsed victim and initial treatment


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VICTIM COLLAPSES

Victim respondsVictim unresponsive

Leave victim as foundFind out what is wrong

Reassess victim regularlyShout for helpOpen airway

Assess breathing

Not breathing normally

Call for an ambulanceStart 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 positionand call for an ambulance

Approach safely Check response

p.62

p 63

4


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Continue until victim starts to wake up: to move, open eyes, and breathe normally

No shock advised

Immediately resumeCPR 30:2 for 2 min

Shock advised

1 shock

Immediately resumeCPR 30:2 for 2 min

p.63

p 64

4IN-HOSPITAL CARDIAC ARREST :

Assessment of a collapsed victim and initial treatment


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Collapsed/sick patient

Shout for HELP & assess patient

YesNo

Assess ABCDERecognise & treat

oxygen; monitoring, i.v. access

Call resuscitationteam

CPR 30:2with oxygen and airway adjuncts

Signs of life?

p.64

Call resuscitation teamApply pads/monitor p.65

4


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Call resuscitation teamif appropriate

Apply pads/monitorAttempt defibrillation

if appropriate

Handover to resuscitation teamAdvanced Life Supportwhen resuscitation team arrives

p.65

p.66

4IN-HOSPITAL CARDIAC ARREST: Advanced life support


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Unresponsiveand not breathing

normally ?

Assessrhythm

CPR 30:2Attach defibrillator/monitor

Minimise interruptions

Call resuscitationteam

Shockable(VF/Pulseless VT)

Non-shockable(PEA/Asystole)

p.66

1 Shock Return of spontaneous circulation

p.67

4


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DURING CPR• Ensure high-qualit chest compressions• Minimise interruptions to

compressions• Give Ox gen• Use waveform capnograph• Continuous chest compressions when

advanced airwa in place• Vascular access (intravenous,

intraosseous)• Give adrenaline ever 3-5 min• Give amiodarone after 3 shocks• Correct reversible causes

REVERSIBLE CAUSES• H poxia• H povolaemia

• H po-/h perkalaemia/metabolic• H pothermia

• Thrombosis• Tamponade - cardiac• Toxins• Tension pneumothorax

IMMEDIATE POST

CARDIAC

ARREST TREATMENT

Immediately resume:

CPR for 2 minMinimise interruptions

Immediately resume:

CPR for 2 minMinimise interruptions

• Use ABCDE approach• Aim for SaO2 94-98%• Aim for normal PaCO2• 12-lead ECG• Treat precipitating cause• Temperature control / Therapeutic h pothermia

CONSIDER• Ultrasound imaging• Mechanical chest

compressions to facilitatetransfer/treatment

• Coronar angiograph and PCI• Extracorporeal CPR

p

p.68

4IN-HOSPITAL CARDIAC ARREST: Drug therapy during advanced life support


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Give adrenaline and amiodaroneafter 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

Amiodarone300 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

Cardiac Arrest

Non-shockablerhythm

Shockable rhythm(VF, pulseless VT)

p

p.69

5


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CHAPTER 5: RHYTHM DISTURBANCES

5.1 SUPRAVENTRICULAR TACHYCARDIASAND ATRIAL FIBRILLATION .............................................................................................. p.70

J. Brugada

5.2 VENTRICULAR TACHYCARDIAS ......................................................................... p.74M. Santini, C. Lavalle, S. Lanzara

5.3 BRADYARRHYTHMIAS .................................................................................................... p.77B. Gorenek

TACHYARRHYTHMIAS: Diagnostic criteria5.1

Tachycardia100 b / i

p.70


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QRS morphology similar to QRS morphologyin sinus rhythm?

QRS morphology similar to QRS morphologyin sinus rhythm?

YES

QRS complex120 msec

Supraventr.Tachycardia

+ BBB

QRS complex120 msec

FascicularTachycardia

or SVT withaberrantconduction

(see chapter 5.3page 77)

VentricularTachycardia

or SVT withaberrantconduction(see chapter 5.2

page 76)

QRS complex120 msec

AFconducting

over AVN

AF + BBBor

AF + WPW

AF+

WPW

IrregularVentricular

Tachycardia

Variable QRSmorphology

NO YES NO

> 100 beats/minute

IrregularRegular

Regular tach cardia p.71

TACHYARRHYTHMIAS: Diagnostic maneuvers5.1


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• Concordant precordial pattern (all leads + or all leads –)• No RS pattern in precordial leads• RS pattern with beginningof R wave to nadirof S wave


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Hemodynamicallynon-stable

Immediate electricalcardioversion

No termination

Hemodynamicallystable

Vagal maneuversand/or i.v. Adenosine

Less than 48 hours since initiationAND

hemodynamically stable

CardioversionElectrical or pharmacological

using oral or i.v.flecainide(only in normal heart)or i.v.vernakalant

Anticoagulationis initiated using i.v. heparine

Hemodynamically non-stable

Immediate electricalCardioversion

If no cardioversion is considered:rate control usingbetablockers

or calcium antagonists ,together with properanticoagulation ,

if required

Narrow QRScomplex tachycardia

Reconsider diagnosis:sinus tachycardia, atrial tachycardia

If no evidence:Intravenous verapamil

Wide QRScomplex tachycardia

Reconsider the diagnosis ofVentricular Tachycardia even

if hemodynamically stable

Do not administerverapimil

More than 48 hours ORunknown time of initiation,

ANDPatient chronically anticoagulated

ORa TEE showing no thrombus

Electrical or pharmacologicalCardioversion

Termination

with or without bundle branch block Tachycardia

p.73

TACHYARRHYTHMIAS: Therapeutic al orithms (2) 5.1


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Hemodynamicallynon-stable

Immediate electricalCardioversion

If no cardioversion is considered:rate control using betablockers orcalcium antagonists (only if VT andAF+WPW is excluded), together

with proper anticoagulationif required

Less than 48 hours since initiationAND

hemodynamically stable

Cardioversionelectrical or pharmacological

using oral or i.v.flecainide(only in normal heart)or i.v.amiodarone

Anticoagulationis initiated using i.v. heparin

More than 48 hoursor unknown initiation,

ANDpatient chronically anticoagulatedor a TEE showing no thrombus

Electrical or pharmacologicalCardioversion

Irregular and wide QRS complex Tachycardia

p.74

VENTRICULAR TACHYSCARDIAS:Diferential diagnosis of wide QRS tachyscardias 5.2


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EKG signs of atrio-ventricular dissociation

Random P waves unrelated to QRS complexesCapture beats / fusion beats / second degree V-A block

1st Step

2nd Step

3rd Step

Concordant pattern in precordial leadsNo RS morphology in any of the precordial leads

An interval >100 ms from the beginning of theQRS 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

RBBB morphology LBBB morphology Initial R waveYes p.75

5.2


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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

No

No

No

Yes

Yes

Yes

Notch in thedescending

Q wave limb

Vi/Vt ≤ 1VT

Aberrant conduction

VT

Hemodynamic Tolerance p.76

Management of wide QRS TACHYSCARDIAS5.2


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Stable

Regular rhythmIrregular rhythm

Vagal maneuverand/or

i.v. adenosine (push)

Differential Diagnosis• Sedation or analgesia

• Synchronised cardioversion100 to 200 J (monophasic)

or 50-100 J (biphasic)

ACLS Resuscitation algorithm• Immediatehigh- energy defibrillation (200J biphasic or 360 monophasic)• Resume CPR and continue

according to the ACLS algorithm

Dru s used in the ACLSalgorithm• Epinephrine 1 mg i.v./i.o. (repeat every 3-5min)• 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• Ma nesium loading dose 1-2 gr

i.v./i.o. for torsade des pointes

Interruption orslow down HR

Yes

YesNo

No

DifferentialDiagnosis

(see chapter 5.1page 73)

SvT

AF with aberrantentricular 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 amaximum dose of 2.2 g in 24 h)

Synchronised cardio ersion

With pulsePulseless

Non-stable


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• Rule out and treat an underl ing causes of brad arrh thmiap.78

BRADYARRHYTHMIAS: Treatment (1)5.3


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• Treat s mptomatic patients onl

Temporary transvenous pacing

Be Careful! • Complications are common! • Shall not be used routinel • Use onl as a last resource when chronotropic drugs are insuf cient • Ever 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 rh thm • Life threatening brad arrh thmias, such as those that occur during interventional

procedures, in acute settings such as acute myocardial infarction, drug toxicity.

For more information on individual drug doses and indications, See chapter 8: Use ofdrugs in Acute Cardiovascular Care .

p.79

BRADYARRHYTHMIAS: Treatment (2)Pacemaker therapies in sinus node dysfunction 5.3


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Permanent pacemaker is indicated in the following settings:

• Documented s mptomatic brad cardia, including frequent sinus pauses that produce s mptoms • S mptomatic chronotropic incompetence • S mptomatic sinus brad cardia that results from required drug therap for medical conditions

Permanent pacemaker is not recommended in the following settings:

• As mptomatic patients • Patients for whom the s mptoms suggestive of brad cardia have been clearl documented to occur

in the absence of brad cardia • S mptomatic brad cardia due to nonessential drug therap

p.80

BRADYARRHYTHMIAS: Treatment (3)Pacemaker therapies in atrioventricular blocks 5.3


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Permanent pacemaker therapy is indicated in the following settings regardless ofassociated symptoms:

• Third-degree AV block • Advanced second-degree AV block • S mptomatic 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 surger when blockis not expected to resolve

Permanent pacemaker is not recommended in the following settings:

• As mptomatic patients • Patients for whom the s mptoms suggestive of brad cardia have been clearl documented to occur

in the absence of brad cardia • S mptomatic brad cardia due to nonessential drug therap

TITRETITRETITRE

6

p.81


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CHAPTER 6: ACUTE VASCULAR SYNDROMES

6.1 ACUTE AORTIC SYNDROMES ................................................................................. p.82A. Evangelista

6.2 ACUTE PULMONARY EMBOLISM ....................................................................... p.92A. Torbicki

ACUTE AORTIC SYNDROMES: Concept and classi cation (1)Types of presentation 6.1

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Classic aortic dissectionSeparation of the aorta media with presence

of extraluminal blood within the la ers of the aortic wall.The intimal ap divides the aorta into two lumina, the true and the false

Penetratin 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 tearand no two-lumen ow


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ACUTE AORTIC SYNDROME: Clinical suspicionand differential diagnosis 6.1

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SYMPTOMS AND SIGNSSUGGESTIVE OF AAS

• Abrupt and severe chest/back pain with maximum intensity at onset• Pulse/pressure de cit - Peripheral or visceral ischemia - Neurological de cit• Widened mediastinum on chest X -ra• Risk factors for dissection• Other - Acute aortic regurgitation - Pericardial effusion - Hemomediastinum/hemothorax

DIFFERENTIAL DIAGNOSIS

• Acute coronar s ndrome(with/without ST-segment elevation)

• Aortic regurgitation without dissection• Aortic aneur sms without dissection• Musculoskeletal pain• Pericarditis• Pleuritis• Mediastinal tumours• Pulmonar embolism• Cholec stitis• Atherosclerosis or cholesterol embolism

Consider acute aortic dissection in all patients presenting with:

General approach to the patient with suspectedACUTE AORTIC SYNDROME 6.1

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Cop right: Hiratzka et al. 2010 Guidelines on Thoracic Aortic Disease. Circulation. (2010) ;121: page-310 ( g 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• Connecti e tissue disease• Family history of aortic disease• Aortic al e disease• Thoracic aortic aneurysm

• Perfusion deficit: - Pulse deficit - SBP differential - Focal neurological deficit• Aortic re ur itation murmur• Hypotension or shock

Chest, back or abdominal paindescribed as:

Abrupt at onset, severe in intensity,and ripping/sharp or stabbing quality

Hi h-risk conditions Hi h-risk pain features Hi h-risk exam features

Laboratory tests required for patientswith ACUTE AORTIC dissection 6.1

Laboratory tests To detect signs of:

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Laboratory tests To detect signs of:

Red blood cell count Blood loss, bleeding, anaemia

White blood cell count Infection, in ammation (SIRS*)

C-reactive protein In ammator response

ProCalcitonin Differential diagnosis between SIRS* and sepsis

Creatine kinase Reperfusion injur , rhabdom ol sis

TroponinIorT Myocardial ischaemia, myocardial infarction

D-dimer Aortic dissection, pulmonar embolism, thrombosisCreatinine Renal failure (existing or developing)

Aspartate transaminase/alanine aminotransferase

Liver ischaemia, liver disease

Lactate Bowel ischaemia, metabolic disorder

Glucose Diabetes mellitus

Blood gases Metabolic disorder, ox genation

*SIRS = s stemic in ammator response s ndrome.

Reference: Eur Heart J 2014;eurheartj.ehu281.

ACUTE CHEST PAIN6.1

Medical history + clinic al examination + ECG STEMI a : see ESC guidelines 169

HAEMODYNAMIC STATEUNSTABLE STABLE

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High probability (score 2-3)or typical chest pain

HAEMODYNAMIC STATEUNSTABLE

Low probability (score 0-1)TTE + TOE/CT°

STABLE

AASconfirmed

AASexcludedConsideralternatediagnosis

D-dimers d,e + TTE + Chest X-ray TTE

Consideralternatediagnosis

No argumentfor AD

Signsof AD

Widenedmedia-

stinum

DefiniteType A -AD c

Inconclusive

Refer on emergencyto surgical team andpre-operative TOE

CT (or TOE)

AASconfirmed

Consideralternatediagnosisrepeat CT

if necessaryAAS

confirmedConsideralternatediagnosis

CT (MRI or TOE) b

a STEMI can be associated with AAS in rare cases.b Pending local availabilit , patient characteristics, and

physician experience.c Proof of t pe-A AD b the presence of ap, aorticregurgitation, and/or pericardial effusion.

d Preferabl point-of-care, otherwise classical.e Also troponin to detect non–ST-segment elevation

myocardial infarction.

Flowchart for decision-making based on pre-test sensitivit of acute aortic s ndrome.Reference: Eur Heart J 2014;eurheartj.ehu281

Details required from ima in in ACUTE AORTIC dissection 6.1

Aortic dissection • Visualization of intimal ap• Extent of the disease according to the aortic anatomic segmentation• Identi cation of the false and true lumens (if present)

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• Identi cation of the false and true lumens (if present)• Localization of entr and re-entr tears (if present)• Identi cation of antegrade and/or retrograde aortic dissection• Identi cation grading, and mechanism of aortic valve regurgitation• Involvement of side branches• Detection of malperfusion (low ow or no ow)• Detection of organ ischaemia (brain, m ocardium, bowels, kidne s, etc.)• Detection of pericardial effusion and its severit• Detection and extent of pleural effusion• Detection of peri-aortic bleeding• Signs of mediastinal bleeding

Intramuralhaematoma

• Localization and extent of aortic wall thickening• Co-existence of atheromatous disease (calcium shift)• Presence of small intimal tears

Penetratingaortic ulcer

• Localization of the lesion (length and depth)• Co-existence of intramural haematoma• Involvement of the peri-aortic tissue and bleeding• Thickness of the residual wall

In all cases • Co-existence of other aortic lesions: aneur sms, plaques, signs of in ammator disease, etc.

ACUTE AORTIC DISSECTION

ACUTE AORTIC SYNDROMES MANAGEMENT: General approach 6.1

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Type A(Ascending aorta

involvement)

Type B(No ascending

aorta involvement)

Uncomplicated

Medicaltreatment

Open Surgerywith/without

EndovascularTherapy

EndovascularTherapy or

Open Surgery (TEVAR*)

Complicated(malperfusion,

rupture)

*TEVAR Thoracic Endovascular Aortic Repair.

1 • Detailedmedical history and completephysical examination (when possible)

ACUTE AORTIC SYNDROMES: Initial management 6.1

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y p p y ( p )

2 • Standard 12-lead ECg: Rule-out ACS, documentation of myocardial ischemia

3 • Intravenous line, blood sample (CK, Tn, m oglobin, white blood count, D-dimer,hematocrit, LDH)

4 • Monitoring: HR and BP

5 • Pain relief (morphine sulphate)(see chapter 3)

6 • Noninvasive imaging (see previous page)

7 • Transfer to ICU

For more information on individual drug doses and indications, See chapter 8: Use of drugs inAcute Cardiovascular Care .

TYPE A ACUTE AORTIC DISSECTION TYPE B ACUTE AORTIC DISSECTION

ACUTE AORTIC SYNDROMES: Surgical management 6.1

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URGENT SURGERY (80 ears

Definitive diagnosis

COMPLICATEDdefined as:

b clinical presentation and imaging

• Impending rupture• Malperfusion

• Refractor HTN • SBP


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Shock / h potension?

Shock / h potension?

Diagnostic algorithmas for suspected not high-risk PE

Diagnosticalgorithm

as for suspected nothigh-risk PE

Intermediate risk

Yes

PE con rmed

Consider furtherrisk strati caiton

PESI Class III-IVor sPESI≥ I

PESI Class I-IIor sPESI =0

PE con rmed

No

RV function (echo or CT)a

Laborator testingb

Both positive One positiveor both negative

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6.2Intermediate-high risk Low risk c

A/C; monitoring Consider early

Intermediate-low risk High-risk


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A/C; monitoringconsider rescue

reperfusiond

HospitalizationA/Ce

Consider earlydischarge and

home treatmentif feasiblef

Primaryreperfusion

Reference: Eur Heart J 2014;35:3033-3073.

a If echocardiograph has alread been performed during diagnostic work-up for PE and detected RV d sfunction, or if the CT alread performed for diagnostic work–upshown RV enlargement (RV/LV (left ventricular) ratio≥0.9, a cardiac troponin test should be performed except for cases in which primar reperfusion is not a therapeuticoption (e.g. due to severe comorbidit or limited life expectanc of the patient).

b Markers of m ocardial injur (e.g. elevated cardiac troponin I or T concentrations in plasma), or of heart failure as a result of (right) ventricular d sfunction(elevated natriuretic peptide concentrations in plasma). If a laborator test for a cardiac biomarker has alread been performed during initial diagnostic work-up (e.g. in

chest pain unit) and was positive, then an echocardiogram should be considered to assess RV function, or RV size should be (re)assessed on CT.c Patients in the PESI Class I-II, or with sPESI of 0, and elevated cardiac biomarkers or signs of RV d sfunction on imaging tests, are also to be classi ed into the interme

low risk categor . This might appl to situations in which imaging or biomarker results become available before calculation of the clinical severit index. These patients probabl no candidates for home treatment.

d Thrombol sis, if (and as soon as) clinical signs of haemod namic decompensation appear; surgical pulmonar embolectom or percutaneous catheter-directed treatmenma be considered as alternative options to s stemic thrombol sis, particularl if the bleeding risk is high.

e Monitoring should be considered for patients with con rmed PE and a positive troponin test, even if there is no evidence of RV d sfunction on echocardiograph or CT.

f The simpli ed version of the PESI has not been validated in prospective home treatment trials; inclusion criteria other than the PESI were used in two single-armed(non-randomized) management studies.

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ACUTE PULMONARY EMBOLISM: Diagnosis 6.2

CARDIOVASCULARSymptoms/Signs

RESPIRATORYSymptoms/Signs


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including but not limited to:

Shock? orSBP 40 mmHg?

persisting > 15 min, otherwise unexplained

including but not limited to:

YES NO

Dyspnea

• Chest pain (angina)• S ncope• Tach cardia• ECG changes• NT-proBNP• Troponin

• Chest pain (pleural)• Pleural effusion• Tach pnea• Hemopt sis• H poxemia• Atelectasis

Suspectacute

PE

Management algorithmfor UNSTABLE patients Management algorithmfor initially STABLE patients

Reference: IACC Textbook (2015) chapter 66 Pulmonar embolism - page 638 - gure 66.1

Management algorithm for unstable patients withsuspected ACUTE PULMONARY EMBOLISM 6.2

CT angiography immediately availableand patient stabilisedNo Yes

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and patient stabilised

Primary PA reperfusion

Primary PA reperfusion not justified

patient stabilised

No further diagnostictests feasible

Right heart,pulmonary artery or

venous thrombi?

Echocardiography (bedside)

CT *Angio

RV pressure overload

CUS

No Yes

Yes

Yes positive

negative

No

TEE

Search for other causes


* Consider also pulmonary angiography if unstablepatient in hemodynamic lab.

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ACUTE PE: Management strategy for initially unstable patientswith con rmed hi h risk pulmonary embolism 6.2


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Shock orhypotension YES

Contraindicationsfor thrombolysis

No Relative Absolute

Primary PAreperfusion

strategy

Thrombolysis

Low- dose/transcatheterthrombolysis/

clot fragmetation

Surgical orPercutaneous catheter

embolectomy (a ailability/experience)

Supportivetreatment

i.v. UFH, STABILISE SYSTEMIC BLOOD PRESSURE,CORRECT HYPOXEMIA

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Management algorithm for initially stable patients withsuspected ACUTE PULMONARY EMBOLISM 6.2

Asses clinical (pre-test) probalility


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Low or intermediate

“PE unlikely“

positive

negative D-dimer

CT angiography

negative positive negative

Confirm by CUSV/Q scan or angiography

positive

CT angiography

CUS

CUSpositive

High or

“PE likely“

Anticoagulation

not justified

Anticoagulation

required

Anticoagulation

not justified

Anticoagulation

required


p.98

Suggested management strategy for initially stable patientswith (non-hi h risk) con rmed 6.2


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Markers for

myocardial injury Positive Positive Negative

Markers for RV overload Positive Positive Negative

Clinical risk assessmentscore (PESI)

Positive (class III-V) Positive (class III-V) Negative (class I-II)

Suggested initialanticoagulation

UFH i.v /LMWH s.c.LMWH/Fonda/

apixaban/ rivaroxabanapixaban/rivaroxaban

STRATEGYMonitorin (ICU) *

rescue thrombolysisHospitalisation **

(telemonitorin )Early

discharge ***

* When all markers are positive. ** When at least one marker is positive. *** When all markers are negative.

Pharmacological treatment:

For more information on individual drug doses and indications, See chapter 8: Use of drugs inAcute Cardiovascular Care .

p.99

PULMONARY EMBOLISM: Pharmacological treatment 6.2Key dru s for initial treatment of patients with con rmed PE

For more information on individual drug doses and indications See chapter 8: Use of


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U n s

t a b l e

Alteplase (rtPA) (intravenous) 100 mg/2 h or0.6 mg/kg/15 min (max 50 mg)

Urokinase (intravenous) 3 million IU over 2 h

Streptokinase (intravenous) 1.5 million IU over 2 h

Unfractionated heparin (intravenous) 80 IU/kg bolus + 18 IU/kg/h

S t a b

l e

Enoxaparine (subcutaneous) 1.0 mg/kgBID or 1.5 mg/kg QD

Tinzaparin (subcutaneous) 175 U/kg QD

Fondaparinux (subcutaneous) 7.5 mg (50-100 Kg of bod weight)5 mg for patients 100 kg

Rivaroxaban (oral) 15 mgBID(for 3 weeks, then 20 mg QD)

Apixaban (oral) 10mg bid (for 7 da s, than 5mg bid)

For more information on individual drug doses and indications, See chapter 8: Use ofdrugs in Acute Cardiovascular Care .

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6.2


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Chapter 5RHYTHM DISTURBANCES

CHAPTER 7ACUTE M OCARDIAL /

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7


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5.1 Supraventricular tach cardias and atrial brillation

5.2 Ventricular tach cardias

5.3 Brad arrh thmias

CHAPTER 7: ACUTE MyOCARDIAL /PERICARDIAL SYNDROMES

7.1 ACUTE MYOCARDITIS .................................................................................................... p.102

A. Keren, A. Caforio

7.2 ACUTE PERICARDITISAND CARDIAC TAMPONADE .......................................................................................... p.107C. Vrints, S. Price

MYOCARDITIS (WHO /ISFC): Inflammatory disease of the myocardium diagnosed by established histological,immunological and immunohistochemical criteria.

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ACUTE MYOCARDITIS: De nition and causes 7.1


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CAUSES OF MYOCARDITIS

INFECTIOUS TOXICIMMUNE-MEDIATED

• Viral• Bacterial• Spirochaetal• Fungal• Protozoal• Parasitic

• Rickettsial

• Drugs• Heav Metals• Hormones, e.g. catecholamines(Pheochromoc toma)

• Ph sical agents

• Allergens: Tetanus toxoid, vaccines,serum sickness, Drugs

• Alloantigens: Heart transplant rejection• Autoantigens: Infection-negative lymphocytic,

infection-negative giant cell, associated with autoimmune or

immune oriented disorders

Clinical presentationswith or without ancillary ndin s Diagnostic criteria

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ACUTE MYOCARDITIS: Dia nostic criteria (1)Diagnostic criteria for clinically suspected myocarditis 7.1


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Reference: Caforio ALP et al. Eur Heart J. (2013) Jul 3 (15).

• Acute chest pain (pericarditic or pseudo-ischemic )

• New-onset (da s up to 3 months) or worsening d spnea or fatigue, with or without left/right heart failure signs

• Palpitation, unexplained arrh thmia s mptoms, s ncope, aborted sudden cardiac death

• Unexplained cardiogenic shock and/or pulmonaroedema

I. ECG/Holter/stress test features: Newl abnormal ECG and/or

Holter and/or stress testing, an of the following:• I to III degree atrioventricular block, or bundle branch block,ST/T wave changes (ST elevation or non ST elevation, T wave inversion),

• Sinus arrest, ventricular tach cardia or brillation and as stole, atrial brillation, frequent premature beats, supraventricular tach cardia

• Reduced R wave height, intraventricular conduction dela (widened QRS complex), abnormal Q waves, low voltage

II. Myocardiocytolysis markers: Elevated TnT/TnI

III. Functional/structural abnormalities on echocardiography • New, otherwise unexplained LV and/or RV structure and function

abnormalit (including incidental nding in apparentl as mptomaticsubjects): regional wall motion or global s stolic or diastolic functionabnormalit , with or without ventricular dilatation, with or withoutincreased wall thickness, with or without pericardial effusion, with orwithout endocavitar thrombi

IV. Tissue characterisation by CMR:Edema and/or LGE of classical m ocarditic pattern

Ancillary ndin s which support

the clinical suspicion of myocarditis• Fever≥38.0°C within the preceding 30 da s• A respirator or gastrointestinal infection• Previous clinicall suspected or biops proven

myocarditis• Peri-partum period• Personal and/or famil histor of allergic asthma• Other t pes of allerg• Extra-cardiac autoimmune disease• Toxic agents• Famil histor of dilated cardiom opath , m ocarditis

One or more of the clinical presentations shown in the Diagnostic Criteria*

with or without Ancillary Features*

AND

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ACUTE MYOCARDITIS: Dia nostic criteria (2) Acute myocarditis should be clinically suspected in the presence of: 7.1


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AND

One or more Diagnostic Criteria from different categories (I to IV)*

OR

when the patient is asymptomatic, two or more diagnostic criteria from different categories (I to IV)*

in the absence of:1) angiographicall detectable coronar arter disease

2) known pre-existing cardiovascular disease or extra-cardiac causes that could explain the s ndrome(e.g. valve disease, congenital heart disease, hyperthyroidism, etc.)

Suspicion is hi her with hi her number of ful lled criteria *

Endom ocardial biops is necessar to: 1) con rm the diagnosis of clinicall suspected m ocarditis, 3) identif the t pe and aetiolog of in ammation, and 2) provide the basis for safe immunosuppression

(in virus negative cases).*See chapter 7.1 page 101.Reference: Caforio ALP et al. Eur Heart J. (2013) Jul 3 (16).

History, Physycal examination; ECG; Echocardiogram; Laboratory tests(Troponin, CRP, ESR, blood cell count, BNP); CMR; If available, serum cardiac autoantibodies

p.105

ACUTE MYOCARDITIS: Diagnostic and management protocol 7.1


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Hemodynamically stablePreserved LV function

No eosinophiliaNo significant rhythm orconduction disturbances

Not associated withsystemic immune disease*

General supportive therapy

General supportive therapyImmunosuppression if

unresponsive and virus negative EMB

Hemodynamically unstable,decreased LV function, cardiogenic shock

Pharmacological and, if needed,mechanical circulatory support (ECMO, LVAD/Bi-VAD,

bridge to heart transplant or to recovery)

Lymphocytic Giant cell, eosinophilic,sarcoidosis (acute decompensation)

Immunosuppressionif infection-negative EMB

Clinically suspected myocarditis

Consider coronary angiography and EMB

No coronary artery disease

*If myocarditis is associated with systemic immunedisease exacerbation, therap overlaps with treatmentof the background disease (usuall immunosuppression).

p.106

Management of patientswith life-threatenin ACUTE MYOCARDITIS 7.1


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• Patients with a life-threatening presentation should be sent to specialised units with capabilit for hemod namic monitoring, cardiac catheterisation and expertise in endom ocardial biops .

• In patients with hemod namic instabilit amechanical cardio-pulmonary assist de ice ma be needed as a bridge to recover or to heart transplantation.

• Heart transplant should be deferred in the acute phase, because recover ma occur, but can be consideredfor hemod namicall unstable m ocarditis patients, including those with giant cell m ocarditis, if optimal pharmacological support and mechanical assistance cannot stabilise the patient

• ICD implantation for complex arrh thmias should be deferred until resolution of the acute episode, with possibleuse of a lifevest during the recovery period.

Reference: Caforio ALP et al. Eur Heart J. 2013 Jul 3 (18).

DIAGNOSIS ( ≥ 2 of the following):

• Chest pain (pleuritic) var ing with position

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ACUTE PERICARDITIS: Diagnosis 7.2


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Chest pain (pleuritic) var ing with position• Pericardial friction rub• T pical ECG changes (PR depression and/or diffuse concave ST-segment elevation)• Echocardiograph : new pericardial effusion

yes

Myopericarditis if:

TroponinEchocardiograph : LV-function

Acute

pericarditis

Equivocal or no

Considercardiac

MRI

Dela edenhancementpericardium

Consideralternativediagnoses

Acute pericarditis

High-risk features?Other causesMost frequent cause:Viral pericarditis

p.108

ACUTE PERICARDITIS: Management7.2


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g • Fever >38°C • Subacute onset • Anticoagulated • Trauma • Immunocompromised • Hypotension • Jugular venous distension • Large effusion

• Post cardiac injury syndrome• Post cardiac surgery• Post MI: Dressler syndrome• Uremic• Neoplastic• Collagen vascular diseases (e.g. SLE)• Bacterial• Tuberculous

Yes

Hospital admissionStable

Ibuprofen + colchicineFurther testing for underlying etiology

Tamponade?

Pericardiocentesis

No

Outpatient treatment

Aspirin 800 mg orIbuprofen 600 mg BID - 2 weeks

If persisting or recurrent chest pain :Addcolchicine 2.0 mg BID for 24 hours,followed by 0.5 to 1.0 mg BID for 6 monthsAvoid corticosteroids !

Tamponade ?

Echocardiography

Physical examination• Distended neck veins• Shock • Pulsus parado us

Cardiac catheterizationEarly

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