chest pain, acute coronary syndrome, pulmonary embolism...
TRANSCRIPT
Chest pain, Acute coronary syndrome,
Pulmonary embolism, Aortic dissection
Dr. Szabó Zoltán
Definitions
• Acute coronary syndrome is defined as myocardial ischemia due to myocardial infarction (NSTEMI or STEMI) or unstable angina
• Unstable angina is defined as angina at rest, new onset exertional angina (<2 months), recent acceleration of angina (<2 months), or post revascularization angina
Pathophysiology of ACS
• Plaque rupture and subsequent formation of thrombus – this can be either occlusive or non-occlusive (STEMI, NSTEMI, USA)
• Vasospasm such as that seen in Prinzmetal’s angina, cocaine use (STEMI, NSTEMI, USA)
• Progression of obstructive coronary atherosclerotic disease
• In-stent thrombosis (early post PCI) • In-stent restenosis (late post PCI • Poor surgical technique (post CABG)
Pathophysiology of ACS
• Acute coronary syndromes can also be due to secondary causes • Thyrotoxicosis
• Anemia
• Tachycardia
• Hypotension
• Hypoxemia
• Aterial inflammation (infection, arteritis)
Epidemiology
In 2013, Hungary: 34 062 pts suffering from malignancy
31447 pts suffering from ischemic heart disease
Death due to acute myocardial infarction: 10 160 (decreasing)
Improving tendency
Reperfusion
Thrombolysis
PCI
Medical treatment:
ACEI
BB
Platelet aggregation inhibitors (aspirin, clopidogrel, ticlopidin)
Heparin
Statins
Pathophysiology
STEMI: Occlusive thrombus
NSTEMI: Unstable plaque
Non occlusive thrombus
It may worsen and lead to total occlusion
May be complicated with coronary spasm, due to inflammatory respons
Risk factors
• atherosclerosis,
• dyslipidaemia,
• diabetes mellitus (type 2),
• hypertension,
• smoking
• The combination of risk factors can contribute to a significant worsening of the disease
Cardiovascular risk factors
x1.6 x4
x3
x6
x16
x4.5 x9
Hypertension
(SBP >195 Hgmm)
Cholesterol (>8.5 mmol/L) Smoking
Poulter N et al., 1993
Diagnostic tools
• 12-lead ECG
• Echocardiography
• Stress test
• Holter ECG
• Event recorder
• Myocardial scintigraphy
• Coronary CT
• Coronarography
• Electrophysiological testing
Diagnosis
• Clinical symptoms • Chest pain • Heart failure • Circulatory shock
• Electrocardiography • ST segment abnormalities • Acute left bundle branch block
• Laboratory parameters • cTroponin • CK • other (myoglobin, GOT, LDH, BNP, hs CRP)
• Echocardiography • Negative predictive value
Angina Pectoris
• Episode of chest pain or pressure due to insufficient artery flow of oxygenated blood.
• Myocardial 02 demand exceeds 02 supply. CAD is the most common cause.
• One coronary artery branch becomes completely occluded; therefore, 02 is not perfused to the myocardium, resulting in transient ischemia and subsequent retrosternal pain.
Angina Pectoris
Precipitating Factors: Warning Sign for MI
Clinical Signs & Symptoms: do not occur until lumen is 75% narrowed. Sternal pain: mild to severe. May be described as heavy, squeezing, pressing, burning, crushing or aching. Onset sudden or gradual. May radiate to L. shoulder and arm. Radiates less commonly to R. shoulder, neck, jaw. Pt may have weakness/numbness of wrist, arm, hands. pain usually short duration and relieved by removal precipitating factors,rest or NTG. Can be
gradual (CAD) or sudden(vasospasm) Associated Symptoms: dyspnea, N & V, tachycardia, palpitations, fatigue, diaphoresis,
pallor, weakness, syncope, factors
Types of Angina
• Stable: There is a stable pattern of onset, duration and intensity of sx, pain is triggered by a predictable degree of exertion or emotion. • Variant Angina (Prinzmetal's)
Cyclical, may occur at rest. Ventricular arrhythmia, brady arrhythmia and conduction disturbances occur. Syncope associated with arrhythmia may occur • Nocturnal Angina only at night. Possible associated with REM sleep. • Unstable Angina AKA Pre infarction angina Pain is more intense, lasts longer
Angina equivalent symptoms
• Fatigue • Dyspnea • Palpitation
Physical examination
• Inspection • Fear
• Dyspnea
• Sweating
• Jaundice
• Xanthomas, xanthelasmas
• Distension of the jugular veins
• Cyanosis
• Edema
• Abnormal pulses
Diagnosis
• Clinical symptoms • Chest pain • Heart failure • Circulatory shock
• Electrocardiography • ST segment abnormalities • Acute left bundle branch block
• Laboratory parameters • cTroponin • CK • other (myoglobin, GOT, LDH, BNP, hs CRP)
• Echocardiography • Negative predictive value
AMI és elektrokardiográfia
Elevation •1mm •V1-3 2 mms Depression
•Horizontal
•Ascending
•Descending
Anterior STEMI
Inferior STEMI
Anteroseptal STEMI
Posterior STEMI
Lateral STEMI
Left Bundle Branch Block
• QRS>120 msec
• V1-2 depolarization is dominantely negative
• I, aVL: pozitive depolarization
• Secondary ST changes
• Discordant T waves
Diagnosis
• Clinical symptoms • Chest pain • Heart failure • Circulatory shock
• Electrocardiography • ST segment abnormalities • Acute left bundle branch block
• Laboratory parameters • cTroponin • CK • other (myoglobin, GOT, LDH, BNP, hs CRP)
• Echocardiography • Negative predictive value
Diagnosztika
Az említett diagnosztikus kritériumokon alapul
1. Necroenzimemelkedés: Troponin I v. T
vagy CK-MB
+ egy az alábbiak közül
2. Típusos tünetek
patológiás Q-hullám kialakulása
ST-eleváció ( >20 perc) vagy depresszió
coronariaintervenció
A fizikális vizsgálatnak kicsi a jelentősége, aspecifikus: tachycardia, néha inferior AMI-ban bradycardia, hypotonia, S4 hang.
Szövődményei: pericarditis (napok): dörzszörej
septumruptúra, papilláris izom dysfunkció-ruptúra: systolés zörej, sokk, pulmonális pangás
Járulékos vizsgálatok: echocardiographia, mellkas rtg
Troponin
Diagnosis
• Clinical symptoms • Chest pain • Heart failure • Circulatory shock
• Electrocardiography • ST segment abnormalities • Acute left bundle branch block
• Laboratory parameters • cTroponin • CK • other (myoglobin, GOT, LDH, BNP, hs CRP)
• Echocardiography • Negative predictive value
AMI-Echocardiographia
Reperfusion therapy-STEMI
Reperfúziós therapy is indicated within 12 hours from the beginning
of chest pain, furtheromere in the case of ST elevation and novel
LBBB
PCI Thrombolysis
Fibrinolysis (tPA) alteplase, tenecteplase
Absolute Contraindications to Thrombolysis
• Any previous history of hemorrhagic stroke
• History of stroke, dementia, or central nervous system damage within 1 year
• Head trauma or brain surgery within 6 months
• Known intracranial neoplasm
• Suspected aortic dissection
• Internal bleeding within 6 weeks
• Active bleeding or known bleeding disorder
• Major surgery, trauma, or bleeding within 3 weeks
• Traumatic cardiopulmonary resuscitation within 3 weeks
Relative Contraindications to Thrombolysis
• Oral anticoagulant therapy
• Acute pancreatitis
• Pregnancy or within 1 week postpartum
• Active peptic ulceration
• Transient ischemic attack within 6 months
• Dementia
• Infective endocarditis
• Active cavitating pulmonary tuberculosis
• Advanced liver disease
• Intracardiac thrombi
• Uncontrolled hypertension (systolic blood pressure >180 mm Hg, diastolic blood pressure >110 mm Hg)
• Puncture of noncompressible blood vessel within 2 weeks
Date of download:
1/21/2014
Copyright © The American College of Cardiology.
All rights reserved. J Am Coll Cardiol. 2010;55(2):102-110. doi:10.1016/j.jacc.2009.08.007
PCI vs. Thrombolysis
PCI
Primary Percutaneous Coronaria Intervention
A primer PCI-t minél gyorsabban javasolt elvégezni, megcélozva, hogy
az első orvosi kontaktus – balloon időt 120 percen belül tartsuk,
illetve 2 ó-n belüli nagy (ált. anterior) STEMI esetében 90 percen belül.
Egyébként fibrinolízis a választandó terápia!
Nem javasolt: panaszmentes betegnél 24 ó után (lezajlott AMI)
Coronarography
PCI: guide wire, ballon catheters, stents
Mguard stent
Drugs
• ASA
• NTG (consider MSO4 if pain not relieved)
• Beta Blocker
• Heparin/LMWH
• ACE-I
• +/-Clopidogrel (based on possibility of CABG)
• IIBIIIA
• Statin
• Activate the Cath Lab!!!
Treatment of ACS; Aspirin
• Aspirin is an antiplatelet agent that initiates the irreversible inhibition of cyclooxygenase, thereby preventing platelet production of thromboxane A2 and decreasing platelet aggregation
• Administration of ASA in ACS reduces cardiac endpoints
ACC/AHA Guidelines for Aspirin Therapy
• Aspirin should be given in a dose of 75-325 mg/day to all patients with ACS unless there is a contraindication (in which case, clopidogrel should be given)
Nitrates
1. Nitrates decrease myocardial 02 demand via peripheral vasodilation and reverse coronary artery spasm thus
increase 02 supply to myocardial tissue.
2. Understanding how Nitrates Work: peripheral vasodilation results in: -decreased 02 demand -decreased venous return to heart -decreased ventricular filling which results in decreased wall
tension and thus
-decreased 02 demand
NTG Forms
• SL (Nitromint)
• Lingual Sprays - similar to SL in use (Nitrolingual)
• Sustained release capsules/tablets (Nitromint retard)
• Transdermal Patch (Nitro-Dur)
• IV (Nitro-Pohl)
ACC/AHA Guidelines for Heparin Therapy
• All patients with acute coronary syndromes should be treated with a combination of ASA (325 mg/day) and heparin (bolus followed by continuous infusion with goal of PTT 1-2.5X control) or ASA and low molecular weight heparin unless one of the drugs is contraindicated
Peiotropic effects of statins
Renin Angiotensin Aldosterone System
Beta Blockers
100
90
80
60
70
50
24 0 20 16 12 8 4 28
Placebo
Carvedilol
months
N = 2289
III-IV NYHA
NEJM 2001;344:1651
Survival %
Beta blocker
p=0.00014
35% RR
COPERNICUS study
NEJM 1996; 334: 1349-55
Carvedilol
(n=696)
Placebo
(n=398)
Risk reduction 65%
p<0.001
0 50 100 150 200 250 300 350 400
1.0
0.9
0.8
0.7
0.6
Béta-blocker
0.7
0.8
0.9
1.0
Survival %
Days
NYHA I-II
US-CARVEDILOL
Diuretics
Aldactone
Placebo
survival
1.0
0.9
0.8
0.7
0.6
0.5
0 6 12 18 24 30 36
months
p < 0.0001
Decrease in mortality
N = 1663
NYHA III-IV
Follow up time: 2 yrs
30 % reduction in mortality
NEJM 1999;341:709
Spironolactone
RALES study
Acute Angina Treatment
Goal: Enhance 02 supply to myocardium:
M- Morphine for pain O- Oxygen 4-6L as ordered N- NTG sublingual, repeat q5 minutes x3 A- Aspirin to prevent platelet aggregation
Differential diagnosis
Pulmonary Embolism
PE
• 2/3 patients remained undiagnosed
• mortality rate up to 30% if untreated due to recurrent embolization primarily and 2 8 % mortality if well treated
• Often occurring as a terminal event with comorbid disease
• Originate primarily from deep venous system of lower extremities
• Ilio femoral thrombi and pelvic veins appear to be the most clinically recognized source Ilio-
• Air , amniotic fluid and fat emboli are rarer causes air
• 67% of proximal DVTs,
• 77% of pelvic veins
• 38–51% of all DVT cases
Virchow’s triad
Risk factors for deep venous thromboembolism
Endothelial injury
Stasis
Hypercoagulation status
The last 2 components predominate in venous thrombosis thromboembolism
PE classification
• Massive PE: haemodinamic unstability (hypotension <90/40 mmHg, shock)
• Submassive PE: normális blood pressure, right ventricular dysfunction
• Non-massive PE: other
Provoking factors
• Malignancies • obesity, • pregnancy • labour • Long term immobilisation, • anticoncipients, • smoking • steroids, • trauma, • surgery • antiphospholipid syndrome, • stroke, • chronic circulatory diseases
Symptoms • Chest pain 88%,
• dyspnea 84%,
• pleuritis,
• cyanosis,
• cough 53%,
• hemoptysis 30%,
• syncope 13%,
• fever,
• Tachypnea, tachycardia,
• Distension of the jugular veins,
• phlebitis,
• edema,
• sweating,
• confusion
• shock
Clinical features
Most PE are small, and infarcts are usually associated with small PE
Small embolism may produce dyspnea , pleuritic chest pain , and
occasionally hemoptysis dyspnea, pain,
Epidemiology
• Third most important factor for cardiovascular death
• Incidence: 50-100/100.000 inhabitants/year
• 65-75% not clarified /25-30% fatális/
• Hungary: 20.000 cases/year, 3000 death/year
1. Huisman M. V., Buller H. R., ten Cate J. W., et al.: Unexpected high prevalence of silent pulmonary embolism in patients with deep venous thrombosis, Chest, 1989; 95:498–502. 2. Goldhaber SZ, Visani L, De Rosa M.: Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet 1999; 353: 1386–9. 3. Konstantinides S., Geibel A. et al.: Association between thrombolytic treatment and the prognosis of hemodynamic stable patients with major pulmonary embolism, Circ., 1997; 96: 882–888. 4. Stein P. D., Henry J. W.: Prevalence of acute pulmonary embolism among patients in a general hospital and at autopsy, Chest, 1995;108:978–981. 5. Stein P. D., Kalpesh C. P., Neeraj K. K., et al.: Estimated incidence of acute pulmonary embolism in a community/teaching general hospital, Chest, 2002; 121: 802–805. 6. Magyar Thrombosis és Haemostasis Társaság: A thromboemboliák megelőzése és kezelése. Magyar konszenzus nyilatkozat 1998. Gyógyszereink 1995/5 Supplementum.
Diagnosis Depends on patient’s hemodynamic status
• Anamnesis
risk factors
previous data
current complaints
• Physical examination
• ECG
• Echocardiography • TTE, TEE – signs of right ventricular pressure overload
• Laboratory tests • Blood gas analysis • D-dimer, • Troponin, • BNP
• Hemodynamic measurements: CVP, pulmonary wedge pressure
• Angiography – „gold standard”
• Scintigraphy
Chest X-ray
• Atelectasis or a pulmonary parenchymal abnormality is the most frequent radiographic abnormalities
• Westermark’s sign
• Hampton’s hump
• massive PE acute phase 100 % negative!!
X ray
ECG - S1Q3
ECG-Uncomplete RBBB
ECG-P pulmonale
Massive PE
Echocardiography
• Basic diagnostic tool
• In the case of shock and/or resuscitation echocardiography is the first diagnostic method to choose.
TTE- views
TTE- right ventricular dilation
TI
Right ventricular systolic pressure
IVC
Systolic D-sign - pressure overload
Intracardial (transit) thrombus
Torbicki A et al: Right heart trombi in pulmonary embolism: results from the international Coperative Pulmonary Embolism Registry. J Am Coll Cardiol 2003, 41:2245
Paradoxical embolisation
TEE-central thrombus
Elevated right ventricular afterload
Kreit WJ. The impact of right ventricular dysfunction on the prognosis and therapy of normotensive patients with pulmonary embolism. Chest 2004, 125(4)
D-dimer
• Sensitivity >90%
• Specificity 40-68%
• Normal d-dimer excludes pulmonary embolism
• Negative predictive value!
• <500 ng/mL (ELISA) - cut off
• GFR <60 decreases its diagnostic value
Kearon C et al: An evaluation of d-dimer in the diagnosis of pulmonary embolism: a randomized trial. Ann Intern Med 1998, 129:1006
Le gal G et al: value of d-dimer testing for the exclusion of pulmonary embolism in ptients with previous venous thromboembolism. Arch Intern Med 2006, 166:176
BNP, NT-proBNP
• Predictor of right ventricular dysfunction
• Predicts mortality
• >90 pg/mL (within 4 hours) • Predicts poor outcome
• <50 pg/mL • 95 % of patients with favorable outcome
Cavallazi et al: Natriuretic peptides in acute pulmonary embolism: a systematic review. Intensive Care Med 2008, 34:2147
Troponine
• Together with BNP diagnostic value is increased • TnT >0.07 ug/mL + NT-proBNP>600 ng/mL
Becattini C et al: Prognostic value of troponins in acute pulmonary embolism: a meta-analysis. Circulation, 2007, 116:427
Other non specific findings
• Nonspecific: leukocytosis , ESR elevation, LDH, SGOT elevation with normal bilirubin leukocytosis,
• CK, CK MB or Troponin I should be checked to rule out AMI CK-Troponin-
• ABG usually revealed hypoxemia, hypocapnia , with respiratory alkalosis hypocapnia,
• Respiratory collapse and hypotension due to massive pulmonary embolus may reveal combined respiratory and metabolic acidosis
CT angio
• Its sensitivity is 86-96 %, specificity is between 92-98 %.
Beigelman C, Chartrand-Lefebvre C, Howarth N, et al.: Pitfalls in Diagnosis of Embolism with Helical CT Angiography. AJR 1998; 171:579–585. Holbert JM, Costello P, Federle MP., Role of spiral computed tomography in the diagnosis of pulmonary embolism in the emergency department, Ann Emerg Med. 1999; 33:520–8. Review. Reid JH, Murchison JT. Acute right ventricular dilatation: a new helical CT sign of massive pulmonary embolism. Clinical Radiology 1998; 53:694–698.
Ventilation-Perfusion scans
• It remains one of the first line investigations of possible PE • It should be performed in all clinically stable patients
Ventilation-perfusion mismatch
Pulmonary angiography
• It has the highest sensitivity and specificity,
• Gold standard of the diagnosis of PE
Risk stratification
Thrombolytics
• Streptokinase
• Urokinase
• Alteplase: 10 mg 1-2 min. , 90 mg/2 h.
• Tenecteplase: 0,5 mg/kg, max. 50 mg.
+ heparin /UFH, LMWH/
Thrombolysis vs. heparin
Heparin
• Na-heparin • 5000–10 000 IU loading dose, continued with iv infusion: 1250 IU/hour (min.
32 000, max. 60 000 IU/24 hrs). • APTT (1,5–2,5- fold increase)
• LMWH • non massive PE • Twice daily, 100 IU/kg 12 hrs
• Duration • min. 4–5 days, • May be finished when oral anticoagualnt reached its effective INR value
Gould, Dembitzer AD, Doyle RL, et al.: Low molecular weight heparins compared with unfractionated heparin for the treatment of acute deep venous thrombosis: a metaanalysis of randomized controlled trials. Ann Intern Med 1999, 13: 800–809. Meyer G, Brenot F, Pacouret G, et al.: Subcutaneous low-molecular-weight heparin Fragmin versus intravenous unfractionated heparin in the treatment of acute non massive pulmonary embolism¨an open randomized pilot study. Thromb Haemost 1995, 74: 1432–1435. Simonneau G, Sors H, Charbonnier B, et al for the THESEE Study Group. A comparison of low-molecular-weight heparin with unfractionated heparin for acute pulmonary embolism. N Engl J Med 1997;337: 663–669. The COLUMBUS Investigators. Low-molecular-weight heparin in the treatment of patients with venous thromboembolism. N Engl J Med 1997;337: 657–662. .
Coumarin
• At least three months • Proxymal DVT
• At least 6 months • Idiopathic DVT, Leiden-mutation (Heterozygous),
• At least 12 months or till the end of life • proxymal DVT, • Recurrent DVT • AT-III-deficiency • Homozygous Leiden-mutation • anticardiolipin antibody, • PC-, PS-defect, • severe postthrombotic syndrome
Agnelli G, Prandoni P, Santamaria MG, et al.: The WARFARIN Optimal Duration Italian Trial Investigators: Three months versus one year of oral anticoagulant therapy for idiopathic deep venous thrombosis. N Engl J Med, 2001, 345: 165–169. Ansell J, Hirsh J, Dalen J, et al.: Managing Oral Anticoagulant Therapy. Chest 2001;119: 22S–38S. Hirch J, Warkentin TE, Sheughnessy SG, Anand SS, Halperin JL, Raschke R, Granger C, Ohman EM, Dalen JE: Heparin and low-molecular-weight heparin. Mechnism of action, Pharmacokinetics, Dosing, Monitoring, Efficacy, and Safety. Chest 2001; 119: 64S–94S. Hirsch J, Raschke R, Waekentis TE, et al.: Heparin: mechanism of action, pharmacokinetics, dosing, consideration, monitoring, efficacy and safety. Chest 1995; 108:258–275. Kearon C, Gent M, Hirsh J, et al.: A comparison of three months of anticoagulation with extended anticoagulation for a first episode of idiopathic venous thromboembolism. N Engl J Med 1999; 340: 901–7.
When to anticoagulate?
Interventional radiology
If
- thrombolysis contraindicated
- Thrombolysis ineffective
- No time for thrombolysis
Surgical treatment
• Invasive embolectomy
• Vena cava filter
If
- Thrombolysis contraindicated
Complex management
• Oxygenation
• Bronchodilators,
• Sedatives
• Prevention of stress ulcer formation
• Arrhythmia management
• Resuscitation
• Management of consequences
• Post resuscitation care
Aortic dissection
• Stanford A, B
• DeBakey I, II, III
Symptoms, emergency care
Management
Thank you for the attention!