chest pain, acute coronary syndrome, pulmonary embolism...

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!