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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
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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
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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
p.87
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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
p.93
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.
p.94
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
Reference: IACC Textbook (2015) chapter 66 Pulmonar embolism - page 639 - gure 66.2
* Consider also pulmonary angiography if unstablepatient in hemodynamic lab.
p.96
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
p.97
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
Reference: IACC Textbook (2015) chapter 66 Pulmonar embolism - page 640 - gure 66.3
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 .
p.100
6.2
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Chapter 5RHYTHM DISTURBANCES
CHAPTER 7ACUTE M OCARDIAL /
p.101
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.
p.102
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
p.103
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
p.104
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
p.107
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