ภาพนิ่ง 1 - thaipedlung.org fileEvidence of myocardial damage • Creatinine kinase–MB isoenzyme (CK-MB) • Lactate dehydrogenase isoenzyme 1 • Troponin I, Troponin

Evidence of myocardial damageEvidence of myocardial damage

• Creatinine kinase–MB isoenzyme (CK-MB)

• Lactate dehydrogenase isoenzyme 1• Troponin I, Troponin T

Cardiac Troponin T: A Marker in the Diagnosis of Acute

Myocarditis in Children• The cutoff point of cTnT level to diagnose acute

myocarditis was 0.052 ng/ml (sensitivity, 71%;

specificity, 86%).

• cTnT level, EF, and LVEDd z score did not predict short-

term outcomes of patients.

• Our data show that cardiac a cTnT level of 0.052 ng/ml

is an appropriate cutoff point for the diagnosis of acute

myocarditis.

Soongswang et al. Pediatr Cardiol 2005; 26 : 45-9

Evidence of etiologic agentsEvidence of etiologic agents

• เพาะเชื้อไวรัสจาก nasopharynx• เพาะเชื้อไวรัสจาก rectal swab • การตรวจ specific viral antibody titer • การตรวจ PCR for virus • การตรวจ viral RNA จากเนื้อเยื่อที่ทํา endomyocardial

biopsy

EchocardiogramEchocardiogram

• Diagnosis• Myocardial function• Follow up

Causes of Causes of myocarditismyocarditis

1. MicroorganismsViral : Adenovirus, Coxsackie virus, Hepatitis C virus,

Human immunodeficiency virus,Influenzae virus

Bacteria : Mycoplasma pneumoniae, Mycobacterium sp., Streptococcal sp., Treponema pallidum

Fungus : Aspergillus sp., Candida sp., Coccidiodes sp., Cryptococcus sp., Histoplasma sp.

Protozoa : Trypanosoma cruzi

Parasitic : Schistosomiasis, Larva migrans

Causes of Causes of myocarditismyocarditis (2)(2)2. Autoimmune diseases

Hypersensitivity : Sulfonamides, Cephalosporins, Diuretics,

Digoxin, Tricyclic antidepressants,Dobutamine

Immunologic syndromes : Churg-Strauss, Inflammatory bowel

disease, Giant cell myocarditis, Diabetes mellitus,

Sarcoidosis, SLE, Thyrotoxicosis,Takayasu’s arteritis,

Wegener’s granulomatosis

3. Toxic substance : Anthracyclines, Cocaine, Interleukin-2

Supportive treatmentSupportive treatmentInotropic agents • Catecholamine

– Dopamine – Dobutamine

• Non-catecholamine - MilrinoneDiuretics - FurosemideAfterload reducing agent

– Sodium nitroprusside– Milrinone

Dopamine • Dopamine acts on the sympathetic nervous

system, producing effects such as increased heart rate and blood pressure.

• Dosage 1-20 μg/Kg/minutes– Low dose 1-2 μg/Kg/minutesStimulate dopamine receptors producing renal,

mesentary, coronary and cerebral vasodilatation– Moderate dose 2-10 μg/Kg/minutesSimulate Beta-adrenergic receptors– High dose > 10 μg/Kg/minutesStimulate Alpha-adrenergic receptors

Dr. Chaisit SangtawesinPediatric Cardiology Unit, Queen Sirikit National Institute of Child Health

Dobutamine

• Direct-acting inotropic agent whose primary activity results from stimulation of the Beta-adrenergic receptors of the heart

• It does not cause the release of endogenous norepinephrine, as does dopamine.


Dobutamine (2)

• The onset of action of dobutamine is within 1 to 2 minutes; however, as much as 10 minutes may be required to obtain the peak effect of a particular infusion rate.

• The plasma half-life of dobutamine in humans is 2 minutes.


Dobutamine (3)

• The effective infusion rate of dobutaminevaries widely from patient to patient, and titration is always necessary.

• Dobutamine- induced increases in cardiac output and systemic pressure are generally seen, in any given patient, at lower infusion rates than those that cause substantial tachycardia


Dobutamine (4)

• Dobutamine has been shown to increase cardiac output and systemic pressure in pediatric patients of every age group.

.


Milrinone

• Phosphodiesterase III inhibitor

• Potentiates the effect of cyclic adenosine monophosphate (cAMP)

• Enhances relaxation of the left ventricle by increasing Ca2+-ATPase activity on the cardiac sarcoplasmic reticulum


Milrinone (2)

• Positive inotropic effects• Vasodilating effects • Minimal chronotropic effects• Once was considered only when

conventional treatment with vasodilators and diuretics has proven insufficient because of the potentially fatal adverse effects of milrinone, including ventricular arrhythmias.

Milrinone (3)

• The half-life is prolonged (2.5 hrs). This can result in a prolonged weaning and possible adverse outcomes from stopping this medication rapidly.


Digitalis

• An increase of force of contraction via inhibition of the Na+/K+ ATPase pump, a different mechanism from that of catecholamines

• Delayed onset, long half-life, low therapeutic index


Intravenous immune globulinIntravenous immune globulin• There is insufficient data from methodologically

strong studies to recommend routine use of

IVGG for acute myocarditis. Future randomized

studies that take into account the etiology of

acute myocarditis will be required to determine

the efficacy of IVGG

BMC Cardiovasc Disord. 2005 Jun 2;5(1):12

Intravenous immune globulinIntravenous immune globulin• Evidence from one trial does not support the use of IVIG

for the management of adults with presumed viral

myocarditis. There are no randomized paediatric trials.

Further studies of the pathophysiology of this entity

would lead to improved diagnostic criteria which would

facilitate future research.

Cochrane Database Syst Rev. 2005 Jan 25;(1):CD004370

Clinical courseClinical course

After he is stabilized with inotrope, diuretic, vasodilator.

One day later, he is getting worse with irritable, dyspnea, tachypnea,mottling skin, poor peripheral pulse

PE: PR 145/m, RR 50/m, BP 70/45 mmHg, cap refill 4 sec.

H: tachycardia

L: medium crepitation both sides

Liver 4 cm>RCM

What is his problem now ?

How to approach him ?

ตารางที่ 2 Categorize the clinical condition by type and severity

Type Severity

Respiratory - Upper airway obstruction

- Lower airway obstruction

- Lung tissue (parenchymal) disease

- Disordered control of breathing

- Respiratory distress

- Respiratory failure

Circulatory - Hypovolemic shock

- Distributive shock

- Cardiogenic shock

- Obstructive shock

- Compensated shock

- Hypotensive shock

Introduction

• Shock is a syndrome that results from inadequate oxygen delivery to meet metabolic demands

• DO2 < VO2

O2 delivery < O2 consumption

• Untreated this leads to metabolic acidosis, organ dysfunction and death

Classification of Shock

• COMPENSATED– blood flow is normal or increased and may be

maldistributed; vital organ function is maintained

• UNCOMPENSATED– microvascular perfusion is compromised;

significant reductions in effective circulating volume

• IRREVERSIBLE– inadequate perfusion of vital organs; irreparable

damage; death cannot be prevented

C.O. = Stroke volume x Heart rate• Stroke volume:

– Preload– Myocardial contractility– Afterload:

• systemic and pulmonary resistance• blood viscosity

• Heart Rate– Bradycardia– Sustained tachycardia

Differential Diagnosis of Shock I

• Hypovolemic– Hemorrhage– Serum/Plasma loss– Drugs

• Distributive– Analphylactic– Neurogenic– Septic

• Cardiogenic– Myocardial– Dysrrhythmia– CHD-(duct

dependant)• Obstructive

– Pneumo, Tamponade, Dissection

• Dissociative– Heat, CO, Cyanide– Endocrine

Differential Diagnosis of Shock II

• Precise etiologic classification may be delayed

• Immediate treatment is essential• Absolute or relative hypovolemia is

usually present• The size of the cardiac silhouette on

plain film can be used to estimate the need for volume replacement.

Hemodynamic Variables in Different Shock States

↑ or ↔↑↓↓↑↑↓↓Septic: Late↓↓↔ Or ↓↓↓↓↑↑↑Septic: Early

↔ Or ↓↔ Or ↓↔ Or ↓↓↓↓↑↑Distributive↑↑↑↑↔ Or ↓↑↓Obstructive↑↑↑↑↔ Or ↓↑↑↑↓↓Cardiogenic↓↓↓↓↓↓↔ Or ↓↑↑HypovolemicCVPWedgeMAPSVRCO

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

EvaluationEvaluation• Regardless of the cause: ABC’s

– First assess airway patency, ventilation, then circulatory system

• Respiratory Performance– Respiratory rate and pattern, work of

breathing, oxygenation (color), level of alertness

• Circulation– Heart rate, BP, perfusion, and pulses, liver

size– CVP monitoring may be helpful

EvaluationEvaluation• Early Signs of Shock

– sinus tachycardia– delayed capillary refill– fussy, irritable

• Late Signs of Shock– bradycardia– altered mental status (lethargy, coma)– hypotonia, decreased DTR’s– Cheyne-Stokes breathing– hypotension is a very late sign – Lower limit of SBP = 70 + (2 x age in

years)

Cardiovascular Assessment• Heart Rate

– Too high: 180 bpm for infants, 160 bpm for children >1year old

• Blood Pressure– Lower limit of SBP

= 70 + (2 x age in years)

• Peripheral Pulses– Present/Absent– Strength

(diminished, normal, bounding)

• Skin Perfusion– Capillary refill time– Temperature– Color– Mottling

• CNS Perfusion– Recognition of

parents– Reaction to pain– Muscle tone– Pupil size

• Renal Perfusion– UOP >1cc/kg/hr

ManagementManagementAirway management

– Always provide supplemental oxygen– Endotracheal intubation and controlled

ventilation is suggested if respiratory failure or airway compromise is likely• elective is safer and less difficult• decrease negative intrathoracic pressure • improved oxygenation and O2 delivery

and decreased O2 consumption• can hyperventilate if necessary

ManagementManagementCirculation

– Based on presumed etiology – Rapid restoration of intravascular

volume• PIV-if unstable you have 60-90 seconds• I.O. if less than 4-6 years old• Central venous catheter• Use isotonic fluid: NS, LR, or 5% albumin• PRBC’s to replace blood loss or if still

unstable after 60cc/kg of crystalloid – anemia is poorly tolerated in the stressed,

hypoxic, hemodynamically unstable patient

Management : GoalGoal–– Improve cardiac outputImprove cardiac output::::

Correct Correct dysrhymiasdysrhymiasOptimize preloadOptimize preloadImprove contractilityImprove contractilityReduce Reduce afterloadafterload

–– Minimize cardiac work:Minimize cardiac work:Maintain normal temperatureMaintain normal temperatureSedation, Minimize painSedation, Minimize painIntubation and mechanical ventilationIntubation and mechanical ventilationCorrect anemiaCorrect anemia

PATHOPHYSIOLOGY OF MYOCARDITISTHE DOMINO EFFECT

Viral Infection

Inflammation and Injury

Decreased Myocardial Contractility

Heart Enlarges: ↑ LVEDV

↓ Cardiac Output

↑ Sympathetic Tone

CHF

↑ LAP

Pulm.edema

Scarring

Dysrhythmias

Management;Management; HemodynamicHemodynamic statusstatus•• Be alert forBe alert for

ectopy,tachyarrhythmias,bradyarrythmias,AV blocks– Adenosine and defribrilator available (SVT)– Administer, evaluate, and titrate antiarrhythmics– Maintain pacemaker (tranthoracic,trancutaneous)

• Monitor tissue perfusion– Asses pulse quality, capilary refil, skin temp&color, urine

output, mental status, Continually monitor arterial BP– Alert for fluctuations in BP or hypotention– Administer, evaluate, and titrate Inotropic/Vasoactive IV

Management;Management; HemodynamicHemodynamic statusstatus

• Monitor central venous pressure– Use distal port– Monitor at least hourly– Assess for change after fluid bolus/diuretic rx– Recognize variables that affect CVP e.g

PEEP, RV dysfunction, etc.– Monitor trends > actual numbers– Monitor for complications; infection, clot,

thrombus

ManagementManagement

• Prevention of complicationshospital acquired infection

• Family support

Intravenous antiarrhythmic agents

•• AdenosinAdenosine– 0.05-0.1 mg/kg rapid IV bolus– Repeat to a max of 0.3 mg/kg total– Can give 12 mg max for child who wt > 50 kg

•• Action:Action: slow conduction time through AV node, interrpt reentry pathways

• Adverse: arrhythmias, bradycardia, heart block, hypotension


• Amiodarone– Loading 1 mg/kg IV over 5-10 min, can repeat 5 times– Continuous IV at 10-15 mg/kg/day

•• Action:Action: inhibits adrenergic stimulationDecrease AV node conduction & sinus function

• Adverse: bradycardia, heart block, sinus arrest, paroxysmal ventricular tachycardia, hypotensioncongestive heart failure


• Lidocaine– Loading 1 mg/kg IV followed by continuous

infusion of 20-50 ug/kg/min •• Action:Action: suppress automaticity of the

conducting system• Adverse: arrhythmias, bradycardia, heart

block, hypotension, seizures

CARDIOGENIC SHOCKMECHANICAL SUPPORT

• ECMO

• IABP Counterpulsation

• Ventricular assist devices

Documents

ภาพนิ่ง 1 - thaipedlung.org fileEvidence of myocardial damage • Creatinine kinase–MB isoenzyme (CK-MB) • Lactate dehydrogenase isoenzyme 1 • Troponin I, Troponin