Cardiovascular emergencies. 05/March/2014 László Rudas Szeged

Transcription

1 Cardiovascular emergencies 05/March/2014 László Rudas Szeged

2 Acute chest pain Acute heart failure Sudden cardiac death

3 Acute chest pain What is the etiology?

4 Chest pain signals emergency: - ACS - Pulmonary embolism - Aortic dissection - Boerhaave syndrome A notorious confounder: - Pericarditis

5 Acute Coronary Syndrome (25-30%) Acute chest pain

6 Unstable angina AMI Ischemic death of The myocytes Acute Coronary Syndromes

7 Thygesen K Circulation. 2012;126: Infarction means ischemic myocardial necrosis spontaneous No plaque rupture occures

8 Signs & Symptomes Abnormal findings -ST-, T abnormalities Troponin positivity -LBBB Required, but not sufficient -Pathological Q for the diagnosis by itself -Wall motion abnormalities -Loss of myocardium by imaging -Coronary thrombosis(angiography, autopsy)

9 Universal definition of myocardial infarction, 2012 Type 1 Plaque rupture & thrombus formation. Type 2 O2 demand and/or O2 supply related myocardial infarction. Type 3 Sudden cardiac death 4/a típus PCI-relates MI. 4/b típus Stent-thrombosis induced MI. 5. típus CABG-surgery related MI. -Tünetek - EKG mozgás - Troponinok Thygesen K Circulation. 2012;126:

10 Propagation thrombus Intraluminal thrombus Intra-plaque thrombus Ruptured plaque

11 ECG findings compatible with STEMI: ST-segment elevation measured at the J point, should be found in two contiguous leads and be 0.25 mv in men below the age of 40 years, 0.2 mv in men over the age of 40 years, or 0.15 mv in women in leads V2 V3 and/or 0.1 mv in other leads in the absence of left ventricular (LV) hypertrophy or left bundle branch block (LBBB) New, or presumably new LBBB

12 Thombstone sign

13

14 True posterior infarction

15

16 ST-elevation in avr

17 Left main coronary stenosis or significant tripple vessel disease

18 Benefit of reperfusion Effectivity of reperfusion therapy? Time to reperfusion? Myocardium salvage Hours after the onset of STEMI

19 STEMI 2012

20 STEMI 2012

21 STEMI 2012

22 STEMI 2012

23 Natural course of the disease 30 day outcome ST +ST ST ST T inversion p incidence 15% 28% 35% 23% AMI at presentation 87% 81% 47% 31% < death 6.8% 5.0% 5.0% 1.8% <0.001 reinfarction 6.9% 5.1% 6.7% 4.3% <0.001 GUSTO II.b patients

24 The NSTE ACS is a dangerous entity

25 Immediate invasive strategy is recommended: -Recurring / continuous chest pain, signs of ischemy -ST changes at the time of pain -Chest pain with heatr failure, galopp sounds or mitral regurgiitation -Haemodynamical instability -Sustained VT

26 Severe, recurring or continuous angina, marked ST-changes, hemodnamical instability or major arrhythmia occure in 2-15% of NSTEMI cases.

27 Risk-stratification

28 The TIMI risk score TIMI Score Calculation (1 point for each): - Age >= 65 - Aspirin use in the last 7 days (patient experiences chest pain despite ASA use) - At least 2 angina episodes within the last 24hrs - ST changes of at least 0.5mm on admission ECG - Elevated serum cardiac biomarkers - Known Coronary Artery Disease (CAD) (coronary stenosis >= 50%) -At least 3 risk factors for CAD -Hypertension -> 140/90 or on antihypertensives, -Cigarette smoking, -HDL < 40, -Diabetes, -Family history of premature CAD (CAD in male first-degree relative, or father less than 55, or female first-degree relative or mother less than 65). Antman EM et al. JAMA 2000;284:

29 The TIMI Risk Score: Based on the data of the TIMI 11/B study Composite end-points (death-ami-recurring angina) % / /7 Sisk Score Antman EM et al. JAMA 2000;284:

30 The GRACE score

31 A confounding presentation

32

33 - Flu-like symptoms - Sharp, ( stabbing ) inspiratory chest pain -Eased by sitting up, or leaning forward

34

35 Pericardial tamponade

36

37 -Low cardiac output -Collapting cardiac chambers -Paradox pulse - Swinging heart

38

39 Volume Pressure ventricle

40

41 paradox pulse, and equalization of RA and pericardial pressures Jeremias A & Brown DL Cardiac intensive care 2010, p283

42 Flow paradoxes Tricuspidal inflow fluctuation >80% Dudzinsky DM Curr Probl Cardiol 2012.

43 Massive Pulmonary Embolism

44 Pulmonary embolism PE remains an underdiagnosed and lethal entity Fatal PE diagnosed PE (one third of the suspected) Suspected PE Ryu JH Mayo Clin Proc 1998;73:

45 50%

46 2-, or more lobes

47 Patophysiology

48 What force brings the blood back to the heart? Cardiac output? Right atria What Is the pressure gradient?

49 Venous Capillary pressure 8 mmhg Right atria pressure 0 mmhg

50 The right heart is vulnerable!

51 Poiseuille s law Wood KE, Chest 2002;121:

52 Wood KE, Chest 2002;121:

53 I. II. III. Wood KE, Chest 2002;121:

54 Classification of PE into prognostic categories by the European Society of Cardiology and American Heart Association (Circulation 2011;123(16): ) I. High-risk (massive) PE (20%), defined as PE in the presence of: a. Arterial hypotension (systolic blood pressure <90 mm Hg or a decrease of >40 mm Hg) for more than 15 minutes or requiring inotropic support b. Cardiogenic shock (oliguria, lactic acidosis, cool extremities, or altered level of consciousness) c. Circulatory collapse, in patients with syncope or undergoing CPR

55 Classification of PE into prognostic categories by the European Society of Cardiology and American Heart Association (Circulation 2011;123(16): ) II. Intermediate-risk (submassive) PE (32%) Defined as PE with a systolic blood pressure greater than 90mmHg but echocardiographic evidence of RV dysfunction or pulmonary hypertension, or the presence of increased markers of myocardial injury (such as troponin)

56 Classification of PE into prognostic categories by the European Society of Cardiology and American Heart Association (Circulation 2011;123(16): ) II. Low-risk (nonmassive) PE (48%) Defined as PE with a systolic blood pressure greater than 90 mm Hg and no evidence of RV dysfunction, pulmonary hypertension, or increased markers of myocardial injury.

57 Diagnostics

58 The Wells Score

59 Presentation of major pulmonary embolism Wood KE, Chest 2002;121:

60 Harrigan RA, Jones K BMJ 2002;324:

61 Diagnostic value of chest Xray in acute pulmonary embolism Elliott CG Chest 2002,118: 33-38

62 Acute vs chronic right ventricular overload Cor pulmonale/ recurrent PE Pulmonary embolism/ RV infarct hypertrophied RV - > mm normal inspiratory collapse of the IVC minimal inspiratory collapse of the IVC minimal septal shift characteristic septal shift D sign Wood KE, Chest 2002;121:

63

64 Contrast-enhanced CTPA axial images showing (A) a large saddle embolus at the pulmonary artery bifurcation (arrow) with extension into both the left and right pulmonary arteries. (B) evidence of right heartstrain shown by enlarged right heart chambers, an RV/LV ratio greater than 1.5, and displacement of the interventricularseptum.

65 Agnelli G. N Engl J Med 2010;363:266-74

66 Pulmonary embolism: haemodynamics In patients without prior CPD, cardiac output (CO) is characteristically normal or elevated despite substantial obstruction. A sympathetic response that augments inotropic/chronotropic responses and venoconstriction is the responsible mechanism. A decrease in CO is unusual without at least 50% obstruction. Wood KE, Chest 2002;121:

67 Pulmonary embolism: right heart haemodynamics Pulmonary artery (PA) hypertension begins to manifest only when 25-30% of the pulmonary vascular bed is obstructed. (Normal mpap=20mmhg.) Wood KE, Chest 2002;121:

68 Pulmonary embolism: right heart haemodynamics Despite massive embolic obstruction of 50%, patients without prior CPD are unable to generate an mpap of 40 mmhg, which appears to be the maximal pressure that a healthy ventricle can generate. mpap values of 40 mmhg represent either the baseline underlying CPD or the cumulative effects of multiple embolic events over a greater period of time, allowing for RV hypertrophy. Wood KE, Chest 2002;121:

69 Pulmonary embolism: right heart haemodynamics RAP elevation is unusual until mpap is 30 mmhg, and obstruction exceeds 35-40%. Elevation of RAP reflects the compensatory use of the Frank-Starling mechanism. Wood KE, Chest 2002;121:

70 Pulmonary embolism: right heart haemodynamics patients with prior CPD Patients with prior CPD characteristically manifest a greater degree of cardiovascular impairment with a lesser degree of pulmonary vascular obstruction. Massive obstruction of 50% is uncommonly reported in this population; - they often do not survive to be studied. Wood KE, Chest 2002;121: