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CARDIOGENIC SHOCK:

CARDIOGENIC SHOCK Mary W. Lieh-Lai, MD Critical Care Medicine Children’s Hospital of Michigan/ Wayne State University School of Medicine

Cardiogenic Shock:

Cardiogenic Shock Pump Failure Ductal dependent lesions Myocardial failure myocarditis cardiomyopathy electrolyte abnormalities ischemia Restrictive: Tamponade Abnormalities in heart rate

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PHYSIOLOGIC PRINCIPLES Frank-Starling Phenomenon Cardiac Output Oxygen delivery and utilization

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Frank-Starling Phenomenon End-Diastolic Pressure Stroke Volume “In the normal heart, the diastolic volume (preload) is the principal force that governs the strength of ventricular contraction.” Otto Frank and Ernest Starling

Cardiogenic Shock:

Cardiogenic Shock Cardiac output is inadequate to meet tissue demands Phases: Early, compensated Late, uncompensated Symptomatology varies Hypotension and bradycardia are late signs

C.O. = Stroke volume x Heart rate:

C.O. = Stroke volume x Heart rate Stroke volume: Preload Myocardial contractility Afterload: systemic and pulmonary resistance blood viscosity Heart Rate Bradycardia Sustained tachycardia

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OXYGEN DELIVERY DO 2 = Q X CaO 2 DO 2 = Q X (1.34 X Hb X SaO 2 ) X 10 Q = cardiac output CaO 2 = arterial oxygen content Normal DO 2 : 520-570 ml/min/m 2 Oxygen extraction ratio = (SaO 2 -SvO 2 /SaO 2 ) X 100 Normal O 2 ER = 20-30%

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OXYGEN EXTRACTION VO 2 = Q x Hb X 13.4 X (SaO 2 - SvO 2 ) Arterial Inflow (Q) capillary O 2 O 2 O 2 O 2 O 2 O 2 O 2 Venous Outflow (Q) C ell O 2 (Adapted from the ICU Book by P. Marino)

Ductal Dependent Lesions:

Systemic blood flow is through the PDA When PDA closes, systemic blood flow drops Coarctation of the aorta Check pulses: compare brachial and femoral pulses Femoral pulses weaker than brachial or non-palpable Hypoplastic left heart syndrome Gray and cold baby with overall poor perfusion Prostaglandin infusion Ductal Dependent Lesions

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DUCTAL DEPENDENT LESIONS COARCTATION OF THE AORTA

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DUCTAL DEPENDENT LESIONS

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PROSTAGLANDIN E1 INFUSION Dose: 0.05 – 0.2 mcg/kg/minute Adverse effects: hypotension apnea fever

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CARDIOVASCULAR SUPPORT Ductal Dependent Lesion Assure ventilation and oxygenation Correct metabolic acidosis Prostaglandin E1 Other inotropic support: dopamine epinephrine dobutamine Treat complications: DIC, hypoglycemia

Acute Myocarditis - Definition:

Acute Myocarditis - Definition A process characterized by inflammatory infiltrates of the myocardium, with necrosis and/or degeneration of myocytes which is very different from the ischemic damage observed in ischemic heart disease.

CAUSES OF MYOCARDITIS:

CAUSES OF MYOCARDITIS Infectious: Viral: adenovirus (2&5), enterovirus, CMV, RSV Bacterial: meningococcus, TB, Legionella, Leptospira Rickettsial Protozoal: T. cruzi Non-infectious: toxic, drugs, hypersensitivity/ autoimmune

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Brown-stained Coxsackie virus in infected myocytes Negative control

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Acute Viral Myocarditis Heart Failure Complete Recovery No Symptoms Chronic Dilated Cardiomyopathy Dysrhythmias/ Conduction Disorders Sudden Death Clinical Presentation of Myocarditis

PATHOPHYSIOLOGY OF MYOCARDITIS THE DOMINO EFFECT:

PATHOPHYSIOLOGY OF MYOCARDITIS THE DOMINO EFFECT Viral Infection Inflammation and Injury Decreased Myocardial Contractility Heart Enlarges:  LVEDV  Cardiac Output  Sympathetic Tone CHF  LAP Pulm. edema Scarring Dysrhythmias

Ischemic Heart Disease in Children:

Ischemic Heart Disease in Children ALCAPA Anomalous Left Coronary Artery arising from the Pulmonary Artery Kawasaki Disease Aneurysms Other vasculitides

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Angiogram of Patient with ALCAPA

ALCAPA EKG Showing Ischemic Pattern:

ALCAPA EKG Showing Ischemic Pattern

Electrolyte/Metabolic Abnormalities:

Electrolyte/Metabolic Abnormalities Hyperkalemia Hypocalcemia Hypermagnesemia Hypoxia Metabolic Acidosis

HEMODYNAMIC CHANGES PROGRESSIVE LEFT HEART FAILURE:

HEMODYNAMIC CHANGES PROGRESSIVE LEFT HEART FAILURE Hours

VENTRICULAR FUNCTION CURVES NORMAL AND FAILING LV:

VENTRICULAR FUNCTION CURVES NORMAL AND FAILING LV

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Cardiogenic Shock - Arrhythmias Check pulses: rapid Check EKG SVT

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INFANT IN SHOCK MANAGEMENT OF SVT Stable Unstable Vagal Maneuvers Adenosine 0.05-0.25 mg/kg Adenosine Synchronized Cardioversion: 0.5 J/kg

Cardiogenic Shock High Afterload:

Cardiogenic Shock High Afterload Tamponade: pulsus paradoxus at risk: chronic renal failure, vasculitides Pulmonary hypertension massive PE High or low SVR Septic shock LV failure from chronic hypertension

Signs and Symptoms:

Signs and Symptoms Shocky, but no history of volume loss Vital signs: tachycardia, hypotension Poor perfusion WHEEZING Metabolic acidosis Hypoglycemia Heart size on CXR may be normal

Management ABC’s:

Management ABC’s Airway and breathing Circulation fluid bolus ? inotropic support

What May be Harmful?:

What May be Harmful? Albuterol Diuretics Fluid restriction

CARDIOGENIC SHOCK INOTROPIC AGENTS:

CARDIOGENIC SHOCK INOTROPIC AGENTS Dobutamine Dopamine Epinephrine Milrinone Norepinephrine Digoxin Vasopressin (?) Nesiritide

Management:

Management Tamponade Fluid bolus Increase heart rate Pericardiocentesis SVT Vagal maneuvers Adenosine Cardioversion Correct electrolyte abnormalities

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Previously healthy Acute myocarditis Failure of “medical” therapy IABP or ECMO Adequate support? YES Weaning NO Short term LVAD Donor heart available? YES Transplant NO Implantable LVAD Optimize clinical status: nutrition + rehabilitation Recovery? YES Weaning NO Bridge to transplant or to recovery Adequate RV function? NO YES Inotropes NO RVAD

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CARDIOGENIC SHOCK MECHANICAL SUPPORT ECMO IABP Counterpulsation Ventricular assist devices

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INTRAAORTIC BALLON PUMP COUNTERPULSATION 30-cm balloon attached on a large bore catheter Advanced into aorta until tip is in origin of left subclavian artery Balloon inflated with helium (35-40 mL) at start of diastole when the aortic valve closes Balloon rapidly deflated at the start of ventricular systole just before the aortic valve opens

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Intraaortic balloon pump counterpulsation

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INTRAAORTIC BALLOON PUMP COUNTERPULSATION Mechanics Inflation of balloon increases peak diastolic pressure and displaces blood toward the periphery  MAP and coronary blood flow Deflation of balloon reduces end-diastolic pressure which reduces impedance to flow when the aortic valve opens at the beginning of systole   ventricular afterload and promotes ventricular stroke output

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IABP - CONTRAINDICATIONS Aortic regurgitation Aortic dissection Prosthetic graft in thoracic aorta within 12 months In children: limited by size

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ECMO Sacrifice of carotic artery and jugular vein Reports of showers of emboli with multi-organ infarction Limited time of use Unlike ventricular assist devices, there are no reports of myocardial function improvement/recovery with ECMO

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VENTRICULAR ASSIST DEVICES RVAD, LVAD, BiVAD Nonpulsatile pump Placed in parallel with RV, LV or both ventricles Adjusted to provide total systemic flow of 2-3 L/min/M 2 Complications in 50% of patients: bleeding systemic embolism

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Physiology of Blood Flow with VAD’s