CARDIOGENIC SHOCK Antonio Pesenti Università degli Studi di Milano Bicocca Azienda Ospedaliera San Gerardo Monza (MI)
Primary myocardial dysfunction resulting in the inability of the heart to mantain an adeuqte cardiac output (CO) with subsequent compromising of metabolic requirements From: Civetta et al (eds) Critical Care
DEFINITION (1) Decreased cardiac output Evidence of tissue hypoxia Adequate intravascular volume
DEFINITION (2) Reduced CI ( < 2.2 l/min/ m2) Sustained hypotension ( BP < 90 mmhg or drop > 30 mmhg for > 30 min) WP > 15 mmhg
DEFINITION (3) Poor tissue perfusion ( cold clammy skin, altered sensorium, oligo-anuria) Hypotension Jugular vein fillings, rales
CARDIOGENIC SHOCK Clinical Recognition In the SHOCK trial: 64% of pts : Hypotension; Ineffective CO ( tachycardia, altered mentation, oliguria, cold periphery Pulmonary congestion Menon V, et al. J Am Coll Cardiol 2000;36:1071 6.
CARDIOGENIC SHOCK Clinical Recognition In the SHOCK trial: 28% of pts : Hypotension Hypoperfusion No pulmonary congestion ( silent lung) WP 21.5 + 6.7 mmhg Menon V, et al. J Am Coll Cardiol 2000;36:1071 6.
GUSTO I study: 30 days mortality model importance of subjective signs Altered sensorium Dying OR = 1.68 Cold Clammy Skin Dying OR = 1.68 Oliguria Dying OR = 2.25 Independently of objective hemodynamics From Hasdai D, et al. Cardiogenic shock complicating acute myocardial infarction: predictors of death. Am Heart J 1999;138:21 31.
Causes (1) Systolic dysfunction (decreased contractility): Ischemia/Myocardial Infarction Global hypoxemia Myocarditis (viral, autoimmune, parasitic) Cardiomyopathies (hypertrophic, amyloid) Myocardial depressant drugs (eg, beta-blockers blockers, calcium channel blockers, antiarrhythmics, propofol, anthracycline) Myocardial contusion Intrinsic Depression (eg( eg, hypoxia, acidosis, hypocalcemia, hypophosphatemia)
Causes (2) Diastolic dysfunction (increased myocardial stiffness) Ischemia Ventricular hypertrophy Restrictive cardiomyopathy Consequence of prolonged hypovolemic or septic shock Ventricular interdependence External compression by pericardial tamponade
Causes (3) Greatly increased afterload Aortic stenosis Hypertrophic cardiomyopathy Dynamic aortic outflow tract obstruction Coarctation of the aorta Malignant hypertension
Causes (4) Valvular or structural abnormality Mitral stenosis Endocarditis Mitral aortic regurgitation Obstruction due to atrial myxoma or thrombus Papillary muscle dysfunction or rupture Ruptured septum or free wall Arrhythmias
Main Cause Miocardial Infarction (MI) Cardiogenic Shock Complicates 4.2-7.2 % of the MIs Leading cause of death (mortality( rate 50%) Usually develops for losses of tissue mass greater than 40 %
(N Engl J Med 1999;340:1162-8.)
AnnInternMed. 1999;131:47-59.
Loss of myocardial contractility CO Blood pressure Adrenergic response Inotropism HR Arterial tone Venous tone Myocardial VO 2 Afterload Preload Myocardial perfusion Ventricular Worsening in myocardial ischemia
Preload does not help 10 Cardiac Output (l/min) 8 6 4 2 Normal Depressed contractility 5 1 10 5 20 25 30 35 Wedge Pressure (mmhg)
In the lungs Preload Diastolic Function Splancnic perfusion Atrial pressure H 2 O retention Pulmonary vasculature congestion Worsening of hypoxaemia
Challenging the paradigm LV EF approx 30% Average SVR not elevated ( wide range) SIRS obviuos Survivors class I CHF status From the SHOCK study
Influence of inflammatory response From: Circulation 2003; 107: 2998-3002
Role of systemic inflammation A substantial number of patients die with a normalized CI in absence of obvious infection (22.5%) Release of mediators secundary to gut hypoperfusion? Chest 2003, 124:1885-1891 1891
Left ventricle always guilty? SHOCK Registry: In 49 of 993 patients (5%) the shock was caused by right heart infarction Mortality not different in the right vs left ventricular shock J Am Coll Cardiol 2003, 341:1273-79 79
Causes of RV failure Right heart infarction Acute Cor Pulmonale Massive Pulmonary embolism Acute Respiratory Distress Syndrome
The RV failure Loss of myocardial contractility CO RV Volume PAP RV Pressure LV preload WP! Tricuspid insufficency Venous district and splanchnic congestion Hypoxaemia Int Care Med 2004, 30:185-96
Hemodynamic patterns during shock BP HR CO CVP Hypovolemic shock Cardiogenic shock Left Ventricular MI Or Nl WP Right Ventricular MI Or Nl Extracardiac Obstructive Pericardial Tamponade Equalized Massive Pumonary Embolism Or Nl Septic/Anaphilactic shock Or Nl shock Or Nl Or Nl
CARDIOGENIC SHOCK Therapy Immediate resuscitation Early definition of coronary anatomy Early revascularization
CARDIOGENIC SHOCK Immediate resuscitation Pressure: dopamine noradrenaline dobutamine Monitor ECG, defibrillators and drugs available ( 33% of SHOCK trial had CPR, VT, or VF) Oxygen, CPAP, CPPV Aspirin, heparin Fibrinolitics if PCI > 90-120 min IABP
Circulation 2003: 107: 2998 CARDIOGENIC SHOCK Early definition of coronary anatomy
Circulation 2003: 107: 2998 CARDIOGENIC SHOCK Early revascularization
Intraaortic Balloon Counterpulsation BMJ 2003;326:1450-1452
Intraaortic Balloon Counterpulsation BMJ 2003;326:1450-1452
Intraaortic Balloon Counterpulsation BMJ 2003;326:1450-1452
Mortality rate after MI (N Engl J Med 1999;340:1162-8.) Better drugs?
Patients with cardiogenic shock complicating MI Medical Therapy - Thrombolitic therapy - Intraaortic balloon counterpulsation Revasculatization - Angioplasty/Bypass surgery - Intraaortic balloon counterpulsation
Conclusions At 30 days there was no significant overall benefit of early revascularization for patients with myocardial infarction who had cardiogenic shock due to left ventricular dysfunction. However, early revascularization resulted in lower mortality from all causes at six months.
The current strategy Cardiogenic shock : commonest cause of death in AMI. -thrombolysis can be attempted with inotropic support or augmentation of blood pressure with the intra-aortic balloon pump - greatest mortality benefit seen after urgent coronary angiography and revascularisation BMJ 2003;326:1450-1452
CARDIOGENIC SHOCK VAD LVAD ECMO Et al
Rossi F et al J.Thorac Cardiovasc Surg 100:914:1990
Healing the heart with ventricular assist devices therapy Reversal of left ventricular remodeling: reduction of LV size, improved contractility, regression of myocyte hypertrophy Molecular remodeling: apoptosis regulation, improved calcium exchange