Pediatric Cardiac Emergencies. Infant Cardiac Disease Leading to ER Presentation ä Congenital ä...

Pediatric Cardiac EmergenciesPediatric Cardiac Emergencies

Infant Cardiac Disease Leading to ER PresentationInfant Cardiac Disease Leading to ER Presentation

CongenitalCongenital

AcquiredAcquired CardiomyopathyCardiomyopathy Myocarditis (usually with CHF)Myocarditis (usually with CHF) DysrhythmiasDysrhythmias

Heart Failure- Definition:Heart Failure- Definition:

A state in which the heart cannot provide A state in which the heart cannot provide sufficient cardiac output to satisfy the sufficient cardiac output to satisfy the metabolic needs of the bodymetabolic needs of the body

It is commonly termed congestive heart It is commonly termed congestive heart failure (CHF) since symptoms of increase failure (CHF) since symptoms of increase venous pressure are often prominent venous pressure are often prominent

CHF - PresentationCHF - Presentation

infants: irritable, poor feeding (early infants: irritable, poor feeding (early fatigue), failure to thrive, respiratory fatigue), failure to thrive, respiratory symptomssymptoms

always consider in patients with respiratory always consider in patients with respiratory symptoms symptoms often misdiagnosed as respiratory illness / often misdiagnosed as respiratory illness /

infectioninfection

CHF - EtiologyCHF - Etiology

Increased PreloadIncreased Preload L to R shunts (VSD, PDA, AV fistula)L to R shunts (VSD, PDA, AV fistula) severe anemiasevere anemia

Increased AfterloadIncreased Afterload HTNHTN Congenital (aortic stenosis, coarctation of aorta)Congenital (aortic stenosis, coarctation of aorta)

Decreased ContractilityDecreased Contractility myocarditis, pericarditis with tamponademyocarditis, pericarditis with tamponade cardiomyopathy (dilated or hypertrophic)cardiomyopathy (dilated or hypertrophic) Kawasaki syndrome (early phase)Kawasaki syndrome (early phase) metabolic: electrolyte, hypothyroidmetabolic: electrolyte, hypothyroid myocardial contusionmyocardial contusion toxins: dig, calcium channel blockers, beta blockerstoxins: dig, calcium channel blockers, beta blockers

Dysrhythmia Dysrhythmia

CHF - EtiologyCHF - Etiology

presents immediately at birthpresents immediately at birth anemia, acidosis, hypoxia, hypoglycemia, anemia, acidosis, hypoxia, hypoglycemia,

hypocalcemia, sepsishypocalcemia, sepsis presents at 1 day (congenital)presents at 1 day (congenital)

PDA in premature infantsPDA in premature infants presents in first month (congenital) presents in first month (congenital)

HPLV, aortic stenosis, coarctation, VSD presents later HPLV, aortic stenosis, coarctation, VSD presents later presents later (acquired)presents later (acquired)

myocarditis, cardiomyopathy (dilated or hypertrophic), myocarditis, cardiomyopathy (dilated or hypertrophic), SVT, severe anemia, rheumatic feverSVT, severe anemia, rheumatic fever

Etiology Etiology

It is a common end point for many It is a common end point for many diseases of cardiovascular systemdiseases of cardiovascular system

It can be caused by :It can be caused by : --Inappropriate work load Inappropriate work load ((volume or pressure volume or pressure

overload)overload)

--Restricted fillingRestricted filling --Myocyte lossMyocyte loss

by S. Solimanby S. Soliman

Causes of left ventricular failureCauses of left ventricular failure

• • Volume over loadVolume over load: : Regurgitate valveRegurgitate valve

High output statusHigh output status

•• Pressure overload:Pressure overload: Systemic hypertensionSystemic hypertension

Outflow obstructionOutflow obstruction

•• Loss of muscles:Loss of muscles: Post MI, Chronic ischemiaPost MI, Chronic ischemia

Connective tissue diseasesConnective tissue diseases

Infection, Poisons Infection, Poisons (alcohol,cobalt,Doxorubicin)(alcohol,cobalt,Doxorubicin)

• • Restricted Filling:Restricted Filling: Pericardial diseases, Restrictive Pericardial diseases, Restrictive

cardiomyopathy, tachyarrhythmiacardiomyopathy, tachyarrhythmia


PathophysiologyPathophysiology

1.1. Hemodynamic changesHemodynamic changes

2.2. Neurohormonal changesNeurohormonal changes

3.3. Cellular changesCellular changes


Hemodynamic changes Hemodynamic changes

From hemodynamic stand point HF can be From hemodynamic stand point HF can be secondary to systolic dysfunction or secondary to systolic dysfunction or

diastolic dysfunctiondiastolic dysfunction


Neurohormonal changesNeurohormonal changes

N/H changesN/H changes Favorable effectFavorable effect Unfavor. effectUnfavor. effect

Sympathetic activitySympathetic activity HR ,HR , contractility, contractility,

vasoconst. vasoconst. V return, V return,

fillingfilling

Arteriolar constriction Arteriolar constriction After load After load workload workload

OO22 consumption consumption

Renin-Angiotensin – Renin-Angiotensin –

Aldosterone Aldosterone

Salt & water retentionSalt & water retention VR VR Vasoconstriction Vasoconstriction after loadafter load

VasopressinVasopressin Same effectSame effect Same effectSame effect

interleukins &TNFinterleukins &TNF May have roles in myocyte May have roles in myocyte hypertrophy hypertrophy

ApoptosisApoptosis

EndothelinEndothelinVasoconstrictionVasoconstriction VR VR After loadAfter load


Cellular changesCellular changes

Changes in CaChanges in Ca+2+2 handling. handling.

Changes in adrenergic receptors:Changes in adrenergic receptors:

•• Slight Slight in in αα11 receptors receptors

• • ββ11 receptors desensitization receptors desensitization followed by down regulation followed by down regulation

Changes in contractile proteinsChanges in contractile proteins

Program cell death (Program cell death (ApoptosisApoptosis))

Increase amount of fibrous tissueIncrease amount of fibrous tissue


SymptomsSymptoms

• • Shortness of breathShortness of breath, Orthopnea, , Orthopnea, paroxysmal nocturnal dyspneaparoxysmal nocturnal dyspnea

• • Low cardiac output symptomsLow cardiac output symptoms

• • Abdominal symptoms:Abdominal symptoms: Anorexia,nausea,Anorexia,nausea,

abdominal fullness,abdominal fullness, painpain


Physical SignsPhysical Signs

1.1. High diastolic BP & occasional decrease High diastolic BP & occasional decrease in systolic BP (decapitated BP)in systolic BP (decapitated BP)

2.2. JVDJVD

3.3. RalesRales (Inspiratory)(Inspiratory)

4.4. Displaced and sustained apical impulsesDisplaced and sustained apical impulses

5.5. Third heart sound – Third heart sound – low pitched sound that is low pitched sound that is heard during rapid filling of ventricleheard during rapid filling of ventricle


Physical signs (cont.)Physical signs (cont.)

Mechanism of SMechanism of S3 3 sudden deceleration of blood sudden deceleration of blood

as elastic limits of the ventricles are as elastic limits of the ventricles are

reachedreached

Vibration of the ventricular wall by blood Vibration of the ventricular wall by blood

fillingfilling

Common in childrenCommon in children


Physical signs (cont.)Physical signs (cont.)

Fourth heart Sound (S4)

- Usually at the end of diastole

- Exact mechanism is not known

Could be due to contraction of

atrium against stiff ventricle

Pale, cold sweaty skin


Framingham Criteria for Dx of Heart FailureFramingham Criteria for Dx of Heart Failure

Major Criteria:Major Criteria: PNDPND- paroxysmal nocturnal dyspneaparoxysmal nocturnal dyspnea JVDJVD- jugular venous distention- jugular venous distention RalesRales CardiomegalyCardiomegaly Acute Pulmonary EdemaAcute Pulmonary Edema SS3 3 GallopGallop

Positive hepatic Jugular reflexPositive hepatic Jugular reflex ↑ ↑ venous pressure > 16 cm Hvenous pressure > 16 cm H22OO


Dx of Heart Failure (cont.)Dx of Heart Failure (cont.)

Minor CriteriaMinor Criteria

LL edema,LL edema,

Night cough Night cough

Dyspnea on exertionDyspnea on exertion

HepatomegalyHepatomegaly

Pleural effusionPleural effusion ↓ ↓ vital capacity by 1/3 of normalvital capacity by 1/3 of normal

Tachycardia 120 bpmTachycardia 120 bpm

Weight loss 4.5 kg over 5 days managementWeight loss 4.5 kg over 5 days management


Forms of Heart FailureForms of Heart Failure

Systolic & DiastolicSystolic & Diastolic High Output Failure High Output Failure

Pregnancy, anemia, thyrotoxisis, A/V fistula, Beriberi, Pregnancy, anemia, thyrotoxisis, A/V fistula, Beriberi,

Low Output FailureLow Output Failure AcuteAcute

large MI, aortic valve dysfunctionlarge MI, aortic valve dysfunction ChronicChronic


Forms of heart failure ( cont.)

Forms of heart failure ( cont.)

Right vs Left sided heart failure:Right vs Left sided heart failure:

Right sided heart failure :Right sided heart failure : Most common cause is left sided failureMost common cause is left sided failure

Other causes included : Pulmonary embolismsOther causes included : Pulmonary embolisms

Other causes of pulmonary htn.Other causes of pulmonary htn.

RV infarctionRV infarction

MSMS

Usually presents with: LL edema, ascitesUsually presents with: LL edema, ascites

hepatic congestionhepatic congestion

cardiac cirrhosis (on the long run) cardiac cirrhosis (on the long run)


Left ventricular failureLeft ventricular failure

- respiratory discomfort, vary with respiratory discomfort, vary with position,stress and activity, associated with position,stress and activity, associated with physical signs of disturbances in the lungsphysical signs of disturbances in the lungs

- Dyspnea during modest exertion- usually Dyspnea during modest exertion- usually the first symptoms of left heart failure, the first symptoms of left heart failure, associated with increased rate of breathingassociated with increased rate of breathing

- OrtopneaOrtopnea- CoughCough

Left ventricular failureLeft ventricular failure

On examination:On examination:

-patient: pale and sweaty, cold hands because of -patient: pale and sweaty, cold hands because of periferal vasoconstrictionperiferal vasoconstriction

- rapid heart raterapid heart rate- Gallop rhythmGallop rhythm- Murmur of mitral insufficiencyMurmur of mitral insufficiency- Rales on auscultation of the lungsRales on auscultation of the lungs

( interstitial edema and fluid)( interstitial edema and fluid)

Right Ventricular FailureRight Ventricular Failure

-neck veins distention-neck veins distention-hepatomegaly, splenomegaly-hepatomegaly, splenomegaly-congestion and edema of the gastrointestinal tract, -congestion and edema of the gastrointestinal tract,

anorexia,nausea, vomitinganorexia,nausea, vomiting- weight loss, failure to gain weight,malnutritionweight loss, failure to gain weight,malnutrition- Murmur or tricuspid insufficiencyMurmur or tricuspid insufficiency- HydrothoraxHydrothorax- Pericardial effusionPericardial effusion- Irritability,restlessnessIrritability,restlessness- oliguriaoliguria

Differential diagnosis Differential diagnosis

Pericardial diseasesPericardial diseases Liver diseasesLiver diseases Nephrotic syndromeNephrotic syndrome Protein losing enteropathyProtein losing enteropathy


Laboratory Findings Laboratory Findings

AnemiaAnemia Hyperthyroid Hyperthyroid Chronic renal insuffiency, electrolytes Chronic renal insuffiency, electrolytes

abnormalityabnormality Pre-renal azotemiaPre-renal azotemia HemochromatosisHemochromatosis


ElectrocardiogramElectrocardiogram

Old MI or recent MIOld MI or recent MI ArrhythmiaArrhythmia Some forms of Cardiomyopathy are tachycardia Some forms of Cardiomyopathy are tachycardia

related related LBBBLBBB→→may help in managementmay help in management


Chest X-rayChest X-ray

Size and shape of heartSize and shape of heart Evidence of pulmonary venous congestion Evidence of pulmonary venous congestion

(dilated or upper lobe veins (dilated or upper lobe veins → perivascular → perivascular edema)edema)

Pleural effusionPleural effusion


EchocardiogramEchocardiogram

Function of both ventriclesFunction of both ventricles Wall motion abnormality that may signify CADWall motion abnormality that may signify CAD Valvular abnormalityValvular abnormality Intra-cardiac shuntsIntra-cardiac shunts


Cardiac CatheterizationCardiac Catheterization

When CAD or valvular is suspectedWhen CAD or valvular is suspected

If heart transplant is indicatedIf heart transplant is indicated


TREATMENTTREATMENT

Correction of reversible causesCorrection of reversible causes IschemiaIschemia Valvular heart diseaseValvular heart disease Thyrotoxicosis and other high output statusThyrotoxicosis and other high output status ShuntsShunts ArrhythmiaArrhythmia

A fib, flutter, A fib, flutter, permanent junctional reciprocating tachycardiapermanent junctional reciprocating tachycardia

Medications Medications Ca channel blockers, some antiarrhythmics Ca channel blockers, some antiarrhythmics


Diet and ActivityDiet and Activity

Salt restrictionSalt restriction Fluid restrictionFluid restriction Daily weight (tailor therapy)Daily weight (tailor therapy) Gradual exertion programsGradual exertion programs


Diuretic TherapyDiuretic Therapy

The most effective symptomatic reliefThe most effective symptomatic relief Mild symptomsMild symptoms

HCTZHCTZ ChlorthalidoneChlorthalidone MetolazoneMetolazone Block Na reabsorbtion in loop of henle and Block Na reabsorbtion in loop of henle and

distal convoluted tubulesdistal convoluted tubules Thiazides are ineffective with GFR < 30 --/minThiazides are ineffective with GFR < 30 --/min


Diuretics (cont.)Diuretics (cont.)

Side EffectsSide Effects Pre-renal azotemia Pre-renal azotemia Skin rashesSkin rashes NeutropeniaNeutropenia ThrombocytopeniaThrombocytopenia HyperglycemiaHyperglycemia ↑ ↑ Uric AcidUric Acid Hepatic dysfunctionHepatic dysfunction


Diuretics (cont.)Diuretics (cont.)

More severe heart failure More severe heart failure → loop → loop diureticsdiuretics FurosemideFurosemide 1-3 mg/kg m.c. 1-3 mg/kg m.c.Mechanism ofMechanism of actionaction: : Inhibit chloride reabsortion in ascending limb of Inhibit chloride reabsortion in ascending limb of

loop of Henle results in natriuresis, kaliuresis and metabolic alkalosisloop of Henle results in natriuresis, kaliuresis and metabolic alkalosis

Adverse reaction:Adverse reaction:

pre-renal azotemiapre-renal azotemia

HypokalemiaHypokalemia

Skin rashSkin rash

ototoxicityototoxicityby S. Solimanby S. Soliman

K+ Sparing AgentsK+ Sparing Agents

Triamterene & amilorideTriamterene & amiloride – – acts on distal tubules to acts on distal tubules to ↓ K ↓ K secretionsecretion

SpironolactoneSpironolactone (Aldosterone inhibitor) (Aldosterone inhibitor)

recent evidence suggests that it may improve survival in recent evidence suggests that it may improve survival in CHF patients due to the effect on renin-angiotensin-CHF patients due to the effect on renin-angiotensin-aldosterone system with subsequent effect on myocardial aldosterone system with subsequent effect on myocardial remodeling and fibrosisremodeling and fibrosis


Inhibitors of renin-angiotensin- aldosterone system

Inhibitors of renin-angiotensin- aldosterone system

Renin-angiotensin-aldosterone systemRenin-angiotensin-aldosterone system is activation is activation early in the course of heart failure and plays an early in the course of heart failure and plays an

important roleimportant role in the progression of the syndromein the progression of the syndrome

Angiotensin converting enzyme inhibitorsAngiotensin converting enzyme inhibitors Angiotensin receptors blockersAngiotensin receptors blockers SpironolactoneSpironolactone


Angiotensin Converting Enzyme Inhibitors

Angiotensin Converting Enzyme Inhibitors

They block the R-A-A system by inhibiting the They block the R-A-A system by inhibiting the conversion of angiotensin I to angiotensin II conversion of angiotensin I to angiotensin II → → vasodilation and ↓ Na retentionvasodilation and ↓ Na retention

↓ ↓ Bradykinin degradation ↑ its Bradykinin degradation ↑ its levellevel → ↑ PG → ↑ PG secretion & nitric oxidesecretion & nitric oxide

Ace Inhibitors were found to improve survival in Ace Inhibitors were found to improve survival in CHF patientsCHF patients Delay onset & progression of HF in pts with Delay onset & progression of HF in pts with

asymptomatic LV dysfunctionasymptomatic LV dysfunction ↓ ↓ cardiac remodelingcardiac remodeling


Side effects of ACE inhibitorsSide effects of ACE inhibitors

AngioedemaAngioedema HypotensionHypotension Renal insuffiencyRenal insuffiency RashRash coughcough


Angiotensin II receptor blockers

Angiotensin II receptor blockers

Has comparable effect to ACE IHas comparable effect to ACE I

Can be used in certain conditions when ACE I are Can be used in certain conditions when ACE I are contraindicated (angioneurotic edema, cough)contraindicated (angioneurotic edema, cough)


Digitalis Glycosides (Digoxin, Digitoxin)Digitalis Glycosides (Digoxin, Digitoxin)

The role of digitalis has declined somewhat The role of digitalis has declined somewhat because of safety concernbecause of safety concern

Recent studies have shown that digitals does not Recent studies have shown that digitals does not affect mortality in CHF patients but causes affect mortality in CHF patients but causes significant significant Reduction in hospitalizationReduction in hospitalization Reduction in symptoms of HFReduction in symptoms of HF


Digitalis (cont.)Mechanism of ActionDigitalis (cont.)Mechanism of Action

+ve inotropic effect by +ve inotropic effect by ↑ intracellular Ca & ↑ intracellular Ca & enhancing actin-myosin cross bride formation enhancing actin-myosin cross bride formation (binds to the Na-K ATPase → inhibits Na pump (binds to the Na-K ATPase → inhibits Na pump → ↑ intracellular Na → ↑ Na-Ca exchange→ ↑ intracellular Na → ↑ Na-Ca exchange

Vagotonic effectVagotonic effect Arrhythmogenic effectArrhythmogenic effect


Digitalis ToxicityDigitalis Toxicity

Narrow therapeutic to toxic ratioNarrow therapeutic to toxic ratio

Non cardiac manifestationsNon cardiac manifestations

Anorexia,Anorexia,

Nausea, vomiting,Nausea, vomiting,

Headache, Headache,

Xanthopsia sotoma, Xanthopsia sotoma,

DisorientationDisorientation


Digitalis ToxicityDigitalis Toxicity

Cardiac manifestationsCardiac manifestations Sinus bradycardia and arrestSinus bradycardia and arrest A/V block (usually 2A/V block (usually 2ndnd degree) degree) Atrial tachycardia with A/V BlockAtrial tachycardia with A/V Block Development of junctional rhythm in patients with a fibDevelopment of junctional rhythm in patients with a fib PVC’s, VT/ V fib (bi-directional VT)PVC’s, VT/ V fib (bi-directional VT)


Digitalis ToxicityTreatment

Digitalis ToxicityTreatment

Hold the medicationsHold the medications ObservationObservation In case of A/V block or severe bradycardia In case of A/V block or severe bradycardia → →

atropine followed by temporary PM if neededatropine followed by temporary PM if needed In life threatening arrhythmia → digoxin-specific In life threatening arrhythmia → digoxin-specific

fab antibodiesfab antibodies Lidocaine and phenytoin could be used – try to Lidocaine and phenytoin could be used – try to

avoid D/C cardioversion in non life threatening avoid D/C cardioversion in non life threatening arrhythmiaarrhythmia


β Blockersβ Blockers

Has been traditionally contraindicated in pts with CHF

Now they are the main stay in treatment on CHF & may be the only medication that shows substantial improvement in LV function

In addition to improved LV function multiple studies show improved survival

The only contraindication is severe decompensated CHF


VasodilatorsVasodilators

Reduction of afterload by arteriolar vasodilatation (hydralazin) reduce LVEDP, O2

consumption,improve myocardial perfusion, stroke volume and COP

Reduction of preload By venous dilation

( Nitrate) ↓ the venous return ↓ the load on both ventricles.

Usually the maximum benefit is achieved by using agents with both action.


Positive inotropic agentsPositive inotropic agents

These are the drugs that improve myocardial These are the drugs that improve myocardial contractility (contractility (β adrenergic agonists, dopaminergic β adrenergic agonists, dopaminergic

agents, phosphodiesterase inhibitors),agents, phosphodiesterase inhibitors),

dopamine, dobutamine, milrinone, amrinonedopamine, dobutamine, milrinone, amrinone Several studies showed ↑ mortality with oral Several studies showed ↑ mortality with oral

inotropic agentsinotropic agents So the only use for them now is in acute sittings as So the only use for them now is in acute sittings as

cardiogenic shockcardiogenic shock


Anticoagulation (coumadine)Anticoagulation (coumadine)

Atrial fibrillationAtrial fibrillation

H/o embolic episodesH/o embolic episodes

Left ventricular apical thrombusLeft ventricular apical thrombus


AntiarrhythmicsAntiarrhythmics

Most common cause of SCD in these patients is Most common cause of SCD in these patients is ventricular tachyarrhythmiaventricular tachyarrhythmia

Patients with h/o sustained VT or SCD Patients with h/o sustained VT or SCD → ICD → ICD implantimplant


Antiarrhythmics (cont.)Antiarrhythmics (cont.)

Patients with non sustained ventricular tachycardiaPatients with non sustained ventricular tachycardia Correction of electrolytes and acid base imbalanceCorrection of electrolytes and acid base imbalance In patients with ischemic cardiomyopathy → ICD In patients with ischemic cardiomyopathy → ICD

implant is the option after r/o acute ischemia as the implant is the option after r/o acute ischemia as the causecause

In patients wit non ischemic cardiomyopathy In patients wit non ischemic cardiomyopathy management is not clearmanagement is not clear

Amiodarone may have a role in this group of patientsAmiodarone may have a role in this group of patients


New MethodsNew Methods

Implantable ventricular assist devicesImplantable ventricular assist devices

Biventricular pacingBiventricular pacing (only in patient (only in patient with LBBB & CHF)with LBBB & CHF)

Artificial HeartArtificial Heartby S. Solimanby S. Soliman

Nursing Interventions - CHFNursing Interventions - CHF

Decrease energy expenditure Frequent rest periods Small, frequent feedings Minimize crying Prevent cold stress

Provide nutrition Use soft nipple Gavage feeding if needed

Nursing Interventions - CHFNursing Interventions - CHF

Monitor fluid status I & O, specific gravity Daily weight

Provide adequate rest, position for comfort Prevent infections Promote growth & development Reduce respiratory distress

DigoxinDigoxin

Check dosage with another RN Give 1 hour before feeding or 2 hours after

feeding Give at 12 hour intervals Take apical pulse for 1 minute

Hold if HR <90 in infants or<70 in children Monitor serum potassium levels Monitor for toxicity: vomiting, nausea,

bradycardia, lethargy

MyocarditisMyocarditis

leading cause of dilated cardiomyopathy and one leading cause of dilated cardiomyopathy and one of the most common causes of CHF in childrenof the most common causes of CHF in children

etiology: idiopathic, viral, bacterial, parasiticetiology: idiopathic, viral, bacterial, parasitic hallmark is CHFhallmark is CHF failure to respond to bronchodilators in wheezing failure to respond to bronchodilators in wheezing

childchild treatment includes inotropes, afterload reduction, treatment includes inotropes, afterload reduction,

diuretics, antibiotics, antiviralsdiuretics, antibiotics, antivirals

PericarditisPericarditis

sharp stabbing precordial painsharp stabbing precordial pain worse with supine and better leaning worse with supine and better leaning

forwardforward no sensory innervation of the pericardiumno sensory innervation of the pericardium

pain referred from diaphragmatic and pleural pain referred from diaphragmatic and pleural irritationirritation

EtiologyEtiology

infectiousinfectious viralviral bacterialbacterial TBTB fungal fungal parasiticparasitic

Connective tissueConnective tissue RARA Rheumatic feverRheumatic fever SLESLE

Metabolic / EndocrineMetabolic / Endocrine uremiauremia hypothyroidhypothyroid

Hematology / OncologyHematology / Oncology bleeding diathesisbleeding diathesis malignancymalignancy

TraumaTrauma IatrogenicIatrogenic

PericarditisPericarditis

usually a benign courseusually a benign course virulent bacteria (H. flu, E. coli) can cause virulent bacteria (H. flu, E. coli) can cause

constrictive pericarditis and subsequent constrictive pericarditis and subsequent tamponade – may need urgent tamponade – may need urgent pericardiocentesispericardiocentesis

uncomplicated pericarditis usually responds uncomplicated pericarditis usually responds to rest and anti-inflammatoriesto rest and anti-inflammatories

Chest PainChest Pain

4% of children will have a cardiac origin4% of children will have a cardiac origin remainder: MSK, pulmonic (asthma, remainder: MSK, pulmonic (asthma,

bronchitis, pneumonia), GIbronchitis, pneumonia), GI Cardiac causes: myocarditis, pericarditis, Cardiac causes: myocarditis, pericarditis,

structural abnormalities such as congenital structural abnormalities such as congenital heart disease or hypertrophic heart disease or hypertrophic cardiomyopathycardiomyopathy

SyncopeSyncope

20-50% of adolescents experience at least one 20-50% of adolescents experience at least one episode of syncopeepisode of syncope most cases benignmost cases benign

PathophysiologyPathophysiology vascularvascular orthostatic, hypovolemiaorthostatic, hypovolemia neurally mediatedneurally mediated hypoxia: PE, CNS depression from OD, COhypoxia: PE, CNS depression from OD, CO cardiaccardiac

Cardiac SyncopeCardiac Syncope

DysrhythmiasDysrhythmias tachytachy bradybrady

Outflow obstructionOutflow obstruction Myocardial DysfunctionMyocardial Dysfunction

cardiac syncope often precedes future cardiac syncope often precedes future sudden cardiac deathsudden cardiac death

Sudden Cardiac DeathSudden Cardiac Death

EtiologyEtiology myocarditismyocarditis cardiomyopathy (hypertrophic)cardiomyopathy (hypertrophic) cyanotic and noncyanotic congenital heart diseasecyanotic and noncyanotic congenital heart disease valvular heart diseasevalvular heart disease congenital complete heart blockcongenital complete heart block WPWWPW long QT syndromelong QT syndrome Marfan syndromeMarfan syndrome coronary artery diseasecoronary artery disease anomalous coronary arteriesanomalous coronary arteries

Risk Factors for Serious Cause of SyncopeRisk Factors for Serious Cause of Syncope

history of cardiac disease in patienthistory of cardiac disease in patient FH of sudden death, cardiac disease, or deafnessFH of sudden death, cardiac disease, or deafness recurrent episodesrecurrent episodes recumbent episoderecumbent episode exertionalexertional prolonged loss of consciousnessprolonged loss of consciousness associated chest pain or palpitationsassociated chest pain or palpitations medications that can alter cardiac conductionmedications that can alter cardiac conduction

What to look for in the Department: EKG

What to look for in the Department: EKG

Long QT syndromeLong QT syndrome congenital or acquiredcongenital or acquired get paroxysmal v tach with torsades de pointesget paroxysmal v tach with torsades de pointes congenital long QT associated with hypertrophic congenital long QT associated with hypertrophic

cardiomyopathycardiomyopathy long QT defined as corrected QT longer than 0.44 slong QT defined as corrected QT longer than 0.44 s T wave alternans sometimes presentT wave alternans sometimes present can have normal ECG in the departmentcan have normal ECG in the department two clinical syndromes not associated with structural two clinical syndromes not associated with structural

heart disease: Romano-Ward and Jervell-Lange-Nielsenheart disease: Romano-Ward and Jervell-Lange-Nielsen

Other dysrhythmiasOther dysrhythmias

WPW and other SVT’sWPW and other SVT’s AV block AV block

usually acquired, rarely congenitalusually acquired, rarely congenital Sick sinus syndromeSick sinus syndrome

Other structural cardiac diseasesOther structural cardiac diseases

dilated cardiomyopathydilated cardiomyopathy usually secondary to myocarditisusually secondary to myocarditis syncope and death secondary to ventricular dysrhythmias or severe syncope and death secondary to ventricular dysrhythmias or severe

myocardial dysfunctionmyocardial dysfunction arrhythmogenic RV dysplasiaarrhythmogenic RV dysplasia congenital cyanotic and non-cyanotic heart diseasecongenital cyanotic and non-cyanotic heart disease valvular diseasesvalvular diseases

aortic stenosisaortic stenosis coronary artery anomaliescoronary artery anomalies

exertional syncope or sudden deathexertional syncope or sudden death aberrant artery passes between aorta and pulmonary arteryaberrant artery passes between aorta and pulmonary artery

Definition- cardiomyopathyDefinition- cardiomyopathy

““A primary disorder of the heart muscle that A primary disorder of the heart muscle that causes abnormal myocardial performance causes abnormal myocardial performance and is not the result of disease or and is not the result of disease or dysfunction of other cardiac structures … dysfunction of other cardiac structures … myocardial infarction, systemic myocardial infarction, systemic hypertension, valvular stenosis or hypertension, valvular stenosis or regurgitation”regurgitation”

Cardiomyopathy-definitionCardiomyopathy-definition

According to World Health Organisation According to World Health Organisation and International Society and Cardiology and International Society and Cardiology Federation (WHO/ISFC) from 1996, Federation (WHO/ISFC) from 1996, cardiomyopathy is definied as any disease cardiomyopathy is definied as any disease of heartmuscle which is connected with its of heartmuscle which is connected with its disfunctiondisfunction

WHO ClassificationWHO Classification

Unknown causeUnknown cause(primary)(primary) Dilated Dilated HypertrophicHypertrophic RestrictiveRestrictive unclassifiedunclassified

Specific heart muscle Specific heart muscle disease (secondary)disease (secondary) InfectiveInfective MetabolicMetabolic Systemic diseaseSystemic disease HeredofamilialHeredofamilial SensitivitySensitivity ToxicToxic

Br Heart J 1980; 44:672-673

Functional ClassificationFunctional Classification

DilatatedDilatated (DCM) (DCM) ventricular enlargement and syst dysfunctionventricular enlargement and syst dysfunction

HypertrophicHypertrophic ( HCM) ( HCM) inappropriate myocardial hypertrophyinappropriate myocardial hypertrophy

in the absence of HTN or aortic stenosisin the absence of HTN or aortic stenosis RestrictiveRestrictive (infiltrative) (infiltrative)

abnormal filling and diastolic functionabnormal filling and diastolic function

Idiopathic Dilated CardiomyopathyIdiopathic Dilated Cardiomyopathy

IDC - DefinitionIDC - Definition

a disease of unknown etiology that a disease of unknown etiology that principally affects the myocardiumprincipally affects the myocardium

LV dilatation and systolic dysfunctionLV dilatation and systolic dysfunction pathologypathology

increased heart size and weightincreased heart size and weight ventricular dilatation, normal wall thicknessventricular dilatation, normal wall thickness heart dysfunction out of portion to fibrosisheart dysfunction out of portion to fibrosis

Incidence and PrognosisIncidence and Prognosis

3-10 cases per 100,0003-10 cases per 100,000 20,000 new cases per year in the U.S.A.20,000 new cases per year in the U.S.A. death from progressive pump failuredeath from progressive pump failure

1-year1-year 25%25%2-year2-year 35-40%35-40%5-year5-year 40-80%40-80%

stabilization observed in 20-50% of patientstabilization observed in 20-50% of patient complete recovery is rarecomplete recovery is rare

Clinical ManifestationsClinical Manifestations

Highest incidence in middle ageHighest incidence in middle age blacks 2x more frequent than whitesblacks 2x more frequent than whites men 3x more frequent than womenmen 3x more frequent than women

symptoms may be gradual in onsetsymptoms may be gradual in onset acute presentation acute presentation

misdiagnosed as viral URI in young adultsmisdiagnosed as viral URI in young adults uncommon to find specific myocardial disease uncommon to find specific myocardial disease

on endomyocardial biopsyon endomyocardial biopsy

History and Physical Examination

History and Physical Examination

Symptoms of heart failureSymptoms of heart failure pulmonary congestion (left HF)pulmonary congestion (left HF)

dyspnea (rest, exertional, nocturnal), dyspnea (rest, exertional, nocturnal), orthpneaorthpnea

systemic congestion (right HF)systemic congestion (right HF)edema, nausea, abdominal pain, nocturiaedema, nausea, abdominal pain, nocturia

low cardiac outputlow cardiac outputfatigue and weaknessfatigue and weakness

hypotension, tachycardia, tachypnea, JVDhypotension, tachycardia, tachypnea, JVD

Cardiac ImagingCardiac Imaging

Chest radiogramChest radiogram ElectrocardiogramElectrocardiogram 24-hour ambulatory ECG (Holter)24-hour ambulatory ECG (Holter)

lightheadedness, palpitation, syncopelightheadedness, palpitation, syncope Two-dimensional echocardiogramTwo-dimensional echocardiogram Radionuclide ventriculographyRadionuclide ventriculography Cardiac catheterizationCardiac catheterization

age >40, ischemic history, high risk profile, abnormal age >40, ischemic history, high risk profile, abnormal ECGECG

Clinical Indications for Endomyocardial BiopsyClinical Indications for Endomyocardial Biopsy

DefiniteDefinite monitoring of cardiac allograft rejectionmonitoring of cardiac allograft rejection monitoring of anthracycline cardiotoxicitymonitoring of anthracycline cardiotoxicity

PossiblePossible detection and monitoring of myocarditisdetection and monitoring of myocarditis diagnosis of secondary cardiomyopathiesdiagnosis of secondary cardiomyopathies differentiation between restrictive and differentiation between restrictive and

constrictive heart diseaseconstrictive heart disease

Management of DCMManagement of DCM

Limit activity based on functional statusLimit activity based on functional status salt restriction of a 2-g Nasalt restriction of a 2-g Na++ (5g NaCl) diet (5g NaCl) diet fluid restriction for significant low Na+fluid restriction for significant low Na+ initiate medical therapyinitiate medical therapy

ACE inhibitors, diureticsACE inhibitors, diuretics digoxin, carvediloldigoxin, carvedilol hydralazine / nitrate combinationhydralazine / nitrate combination

Management of DCMManagement of DCM

consider adding ß-blocking agents if consider adding ß-blocking agents if symptoms persistssymptoms persists

anticoagulation for EF <30%, history of anticoagulation for EF <30%, history of thromboemoli, presence of mural thrombithromboemoli, presence of mural thrombi

intravenous dopamine, dobutamine and/or intravenous dopamine, dobutamine and/or phosphodiesterase inhibitorsphosphodiesterase inhibitors

cardiac transplantationcardiac transplantation

Hypertrophic CardiomyopathyHypertrophic Cardiomyopathy

Hypertrophic CardiomyopathyHypertrophic Cardiomyopathy

First described by the French and Germans around First described by the French and Germans around 19001900

uncommon with occurrence of 0.02 to 0.2%uncommon with occurrence of 0.02 to 0.2% a hypertrophied and non-dilated left ventricle in a hypertrophied and non-dilated left ventricle in

the absence of another disease the absence of another disease small LV cavity, asymmetrical septal small LV cavity, asymmetrical septal

hypertrophy (ASH), systolic anterior hypertrophy (ASH), systolic anterior motion of the mitral valve leaflet (SAM)motion of the mitral valve leaflet (SAM)

65% 35%

10%

www.kanter.com/hcm

Clinical ManifestationClinical Manifestation

Asymptomatic, echocardiographic findingAsymptomatic, echocardiographic finding SymptomaticSymptomatic

dyspnea in 90%dyspnea in 90% angina pectoris in 75%angina pectoris in 75% fatigue, pre-syncope, syncopefatigue, pre-syncope, syncope

risk of SCD in children and adolescents risk of SCD in children and adolescents palpitation, PND, CHF, dizziness less frequentpalpitation, PND, CHF, dizziness less frequent

Natural HistoryNatural History

annual mortality 3% in referral centersannual mortality 3% in referral centersprobably closer to 1% for all patientsprobably closer to 1% for all patients

risk of SCD higher in children risk of SCD higher in children may be as high as 6% per yearmay be as high as 6% per yearmajority have progressive hypertrophymajority have progressive hypertrophy

clinical deterioration usually is slowclinical deterioration usually is slow progression to DCM occurs in 10-15%progression to DCM occurs in 10-15%

Risk Factors for SCDRisk Factors for SCD

Young age (<30 years)Young age (<30 years) ““Malignant” family history of sudden deathMalignant” family history of sudden death Gene mutations prone to SCD (ex. Arg403Gln)Gene mutations prone to SCD (ex. Arg403Gln) Aborted sudden cardiac deathAborted sudden cardiac death Sustained VT or SVTSustained VT or SVT Recurrent syncope in the youngRecurrent syncope in the young Nonsustained VT (Holter Monitoring)Nonsustained VT (Holter Monitoring) Brady arrhythmias (occult conduction disease)Brady arrhythmias (occult conduction disease)

Br Heart J 1994; 72:S13

ManagementManagement

beta-adrenergic blockersbeta-adrenergic blockers calcium antagonistcalcium antagonist disopyramidedisopyramide amiodarone, sotololamiodarone, sotolol DDD pacingDDD pacing myotomy-myectomymyotomy-myectomy plication of the anterior mitral leafletplication of the anterior mitral leaflet

Restrictive CardiomyopathyRestrictive Cardiomyopathy

Restrictive CardiomyopathiesRestrictive Cardiomyopathies

Hallmark: abnormal diastolic functionHallmark: abnormal diastolic function rigid ventricular wall with impaired rigid ventricular wall with impaired

ventricular fillingventricular filling bear some functional resemblance to bear some functional resemblance to

constrictive pericarditisconstrictive pericarditis importance lies in its differentiation from importance lies in its differentiation from

operable constrictive pericarditisoperable constrictive pericarditis

Exclusion “Guidelines”Exclusion “Guidelines”

LV end-diastolic dimensions LV end-diastolic dimensions 7 cm 7 cm Myocardial wall thickness Myocardial wall thickness 1.7 cm 1.7 cm LV end-diastolic volume LV end-diastolic volume 150 mL/m2 150 mL/m2 LV ejection fraction < 20%LV ejection fraction < 20%

ClassificationClassification

IdiopathicIdiopathic MyocardialMyocardial

1. Noninfiltrative1. Noninfiltrative IdiopathicIdiopathic SclerodermaScleroderma

2. Infiltrative2. Infiltrative AmyloidAmyloid SarcoidSarcoid Gaucher diseaseGaucher disease Hurler diseaseHurler disease

3. Storage Disease3. Storage Disease HemochromatosisHemochromatosis Fabry diseaseFabry disease Glycogen storageGlycogen storage

EndomyocardialEndomyocardial endomyocardial fibrosisendomyocardial fibrosis Hyperesinophilic syndHyperesinophilic synd CarcinoidCarcinoid metastatic malignanciesmetastatic malignancies radiation, anthracyclineradiation, anthracycline

Clinical ManifestationsClinical Manifestations

Symptoms of right and left heart failureSymptoms of right and left heart failure Jugular Venous Pulse Jugular Venous Pulse

prominent prominent xx and and yy descents descents Echo-DopplerEcho-Doppler

abnormal mitral inflow patternabnormal mitral inflow pattern prominent E wave (rapid diastolic filling)prominent E wave (rapid diastolic filling) reduced deceleration time (reduced deceleration time ( LA pressure) LA pressure)

Basic Life SupportBasic Life SupportBasic Life SupportBasic Life Support

Cardiopulmonary ArrestCardiopulmonary Arrest

Cardiac arrestCardiac arrest is the sudden loss of cardiac output, is the sudden loss of cardiac output, which is potentially reversible with prompt which is potentially reversible with prompt restoration of circulation and oxygen delivery. restoration of circulation and oxygen delivery.

Sudden cardiac deathSudden cardiac death and and cardiac arrestcardiac arrest are not are not synonymous. Sudden cardiac death is unexpected synonymous. Sudden cardiac death is unexpected death within 1 hour of symptom onset because of a death within 1 hour of symptom onset because of a primarily cardiac cause in a victim with or without primarily cardiac cause in a victim with or without previously diagnosed heart disease. previously diagnosed heart disease.

Pathophysiology of CPAPathophysiology of CPA

CPA causes hypoxia, respiratory and metabolic acidosisCPA causes hypoxia, respiratory and metabolic acidosis

cell death appears to be mediated by substances cell death appears to be mediated by substances

released from anoxic cell membranes released from anoxic cell membranes

agents associated with brain and heart injury are free agents associated with brain and heart injury are free

iron, hydroxyl radicals, calciumiron, hydroxyl radicals, calcium

CPA for as little as 5 minutes may cause permanent CPA for as little as 5 minutes may cause permanent

brain injury or deathbrain injury or death

The Most Common Causes of Pediatric The Most Common Causes of Pediatric CPACPAThe Most Common Causes of Pediatric The Most Common Causes of Pediatric CPACPA

infantsinfants SIDS (40%)SIDS (40%) respiratory diseasesrespiratory diseases airway obstructionairway obstruction sepsissepsis neurological diseasesneurological diseases metabolic abnormalitiesmetabolic abnormalities

chidren chidren injuryinjury

Pediatric CPAPediatric CPA

the epidemiology of pediatric CPA is different from that the epidemiology of pediatric CPA is different from that

of adultsof adults

sudden, primary cardiac arrest is raresudden, primary cardiac arrest is rare

ventricular fibrillation has been reported in less than 10% ventricular fibrillation has been reported in less than 10%

(more likely in children with complex congenital heart (more likely in children with complex congenital heart

disease)disease)

respiratory insufficiency is the more common causerespiratory insufficiency is the more common cause

50% of all children who require CPR are infants50% of all children who require CPR are infants

Out-of-Hospital CPAOut-of-Hospital CPAOut-of-Hospital CPAOut-of-Hospital CPA

Out-of-hospital primary cardiac failure with Out-of-hospital primary cardiac failure with cardiopulmonary arrest (CPA) is unusual in cardiopulmonary arrest (CPA) is unusual in children. children.

It may occur in children with chronic diseases It may occur in children with chronic diseases cardiomyopathycardiomyopathy myocarditis myocarditis congenital heart diseases.congenital heart diseases.It occur around the home, where children are under It occur around the home, where children are under

the supervision of parents. the supervision of parents. Parents of children at high risk should be educated in Parents of children at high risk should be educated in

BLS.BLS.

In-Hospital CPAIn-Hospital CPAIn-Hospital CPAIn-Hospital CPA

Primary cardiopulmonary arrest is often in Primary cardiopulmonary arrest is often in hospitalised children hospitalised children

after cardiac surgery after cardiac surgery with rare arrhythmia caused by with rare arrhythmia caused by

cardiac catheterization or angiographycardiac catheterization or angiography general anesthesiageneral anesthesia antiarrhythmic drug administrationantiarrhythmic drug administration

Respiratory Causes of Pediatric Cardiopulmonary ArrestRespiratory Causes of Pediatric Cardiopulmonary Arrest

Upper airway obstructionUpper airway obstruction Lower airway Lower airway obstructionobstruction

- croup- croup - asthma- asthma- foreign body- foreign body - bronchiolitis- bronchiolitis- strangulation- strangulation - foreign body- foreign body- inhalation injury- inhalation injury - inhalation - inhalation

injuryinjury

Intrinsic lung conditionsIntrinsic lung conditions- pneumonia- pneumonia- drowning- drowning- chest trauma- chest trauma

Cardiovascular Causes of Pediatric Cardiopulmonary ArrestCardiovascular Causes of Pediatric Cardiopulmonary ArrestHypovolemiaHypovolemia DysrrhythmiasDysrrhythmias

- traumatrauma - open heart surgery- open heart surgery

- burns- burns - cardiac catheterizationcardiac catheterization- gastroenteritis- gastroenteritis - coronary angiography- coronary angiography

SepsisSepsis - - general anesthesiageneral anesthesia

Cardiogenic shockCardiogenic shock - prolonged QT syndrom- prolonged QT syndrom

- congenital heart diseases- congenital heart diseases IntoxicationIntoxication- cardiomyopathycardiomyopathy- myocarditismyocarditis- post-open heart surgery- post-open heart surgery

Basic Life SupportBasic Life Support

Strictly defined, Strictly defined, basic life supportbasic life support (BLS) is the initial (BLS) is the initial

phase of emergency cardiac care, encompassing phase of emergency cardiac care, encompassing

recognition of recognition of cardiac arrestcardiac arrest and delivery of rescue and delivery of rescue

breathing (ventilation) and chest compressions breathing (ventilation) and chest compressions

(circulation). (circulation).

Advanced Life SupportAdvanced Life Support

Advanced life supportAdvanced life support (ACLS) includes BLS, ECG (ACLS) includes BLS, ECG

monitoring, rhythm identification, and restoration monitoring, rhythm identification, and restoration

of hemodynamic stability through intubation, of hemodynamic stability through intubation,

defibrillation, and pharmacologic therapy. defibrillation, and pharmacologic therapy.

Cardiopulmonary resuscitation effectively restores Cardiopulmonary resuscitation effectively restores

hemodynamic stability, return of spontaneous hemodynamic stability, return of spontaneous

circulation (ROSC), in 40% to 60% of arrests.circulation (ROSC), in 40% to 60% of arrests.

Modern CRPModern CRP

Modern CPR began in 1960 with the landmark study by Modern CPR began in 1960 with the landmark study by

Kouwenhoven which reported combining closed chest Kouwenhoven which reported combining closed chest

compression, mouth-to-mouth breathing, and external compression, mouth-to-mouth breathing, and external

defibrillation. As they explained it, their algorithm was defibrillation. As they explained it, their algorithm was

remarkably easy to perform: remarkably easy to perform:

""Anyone, anywhere, can now initiate cardiac resuscitative Anyone, anywhere, can now initiate cardiac resuscitative

procedures. All that is needed are two handsprocedures. All that is needed are two hands." ."

Modern CPRModern CPR

Cardiac arrest outcomes will be most improved with public Cardiac arrest outcomes will be most improved with public

education and earlier initiation of CPR, both Basic Life Support education and earlier initiation of CPR, both Basic Life Support

and Advanced Life Support, notably defibrillation.and Advanced Life Support, notably defibrillation.

After unresponsiveness, lack of pulse, and apnea are confirmed in After unresponsiveness, lack of pulse, and apnea are confirmed in

unmonitored cardiac arrests, the initial management consists ofunmonitored cardiac arrests, the initial management consists of

BLSBLS

closed-chest compressionsclosed-chest compressions

artificial ventilation. artificial ventilation.

Circulation: The Cardiac Pump The Cardiac Pump

TheoryTheory Circulation: The Cardiac Pump The Cardiac Pump

TheoryTheory

The mechanism by which closed-chest compressions The mechanism by which closed-chest compressions

increase forward cardiac output remains increase forward cardiac output remains

controversial. controversial.

The traditional cardiac pump theory states the heart is The traditional cardiac pump theory states the heart is

massaged and blood forced out by massaged and blood forced out by direct direct

compressioncompression between the sternum and spine. between the sternum and spine.

Circulation: The Thoracic Pump The Thoracic Pump TheoryTheory Circulation: The Thoracic Pump The Thoracic Pump TheoryTheory The thoracic pump theory suggests that forward blood The thoracic pump theory suggests that forward blood

flow increases through a passive cardiac conduit by a flow increases through a passive cardiac conduit by a

general general increase in intrathoracic pressureincrease in intrathoracic pressure transmitted transmitted

to the cardiac chambers and the intrathoracic to the cardiac chambers and the intrathoracic

portion of the great vessels. Because of intact venous portion of the great vessels. Because of intact venous

valves, the pressure generated during compression is valves, the pressure generated during compression is

not transmitted to the periphery, forcing blood to not transmitted to the periphery, forcing blood to

flow from the arteries to the veins.flow from the arteries to the veins.

The ABCs of Cardiopulmonary ResuscitationThe ABCs of Cardiopulmonary Resuscitation

AAirwayirway BBreathingreathing CCirculationirculation

The ABCs of CPR - ResponsivenessThe ABCs of CPR - Responsiveness

Quickly assess the presence or extent of injury and Quickly assess the presence or extent of injury and determine whether the child is conscious. determine whether the child is conscious.

The level of responsiveness is determined by tapping The level of responsiveness is determined by tapping the child and speaking loudly to elicit a response. the child and speaking loudly to elicit a response.

Carefully look, listen, and feel the pulse to determine Carefully look, listen, and feel the pulse to determine that a cardiopulmonary arrest has occurred.that a cardiopulmonary arrest has occurred.

Call for help once CPA is diagnosed.Call for help once CPA is diagnosed.

The ABCs of CPR - AirwayThe ABCs of CPR - Airway

Open the airway. Use the Open the airway. Use the head-tilt/chin-lift head-tilt/chin-lift

maneuvermaneuver, avoiding hyperextension of the neck. , avoiding hyperextension of the neck.

Too vigorous head-tilt may occlude the trachea or Too vigorous head-tilt may occlude the trachea or

injure the cervical spine. In infants, large head may injure the cervical spine. In infants, large head may

flex the neck and compromise air exchange.flex the neck and compromise air exchange.

If spinal injury is suspected, use a If spinal injury is suspected, use a jaw-thrustjaw-thrust

instead of head-tilt.instead of head-tilt.

Suction may be needed to clear secretions, blood, Suction may be needed to clear secretions, blood,

or foreign bodies from the airway.or foreign bodies from the airway.

Foreign-Body Airway ObstructionForeign-Body Airway Obstruction

the infant: the infant: back blows back blows chest thrustschest thrusts

the child: the Heimlich maneuverthe child: the Heimlich maneuver abdominal thrusts with victim standing or sitting abdominal thrusts with victim standing or sitting

(conscious)(conscious) abdominal thrusts with victim laying or sitting abdominal thrusts with victim laying or sitting

(conscious (conscious or unconscious)or unconscious)

Foreign-Body Airway ObstructionForeign-Body Airway Obstruction

If the airway remains obstructed attempt to evacuate a If the airway remains obstructed attempt to evacuate a possible aspirated foreign body.possible aspirated foreign body.

For infants give 5 sharp For infants give 5 sharp blows to the backblows to the back with the heel with the heel of the hand between securely held shoulder blades. of the hand between securely held shoulder blades. Then, deliver 5 Then, deliver 5 chest thrustschest thrusts to the mid-sternum. to the mid-sternum.

For children deliver 5 rapid subdiaphragmatic For children deliver 5 rapid subdiaphragmatic abdominal thrustabdominal thrusts using the heel of the hand (modifed s using the heel of the hand (modifed Heimlich maneuverHeimlich maneuver) with the patient supine.) with the patient supine.

If airway patency isn’t established, repeat the sequence. If airway patency isn’t established, repeat the sequence. If 2 rapid series of maneuvers fail, perform immediate If 2 rapid series of maneuvers fail, perform immediate direct laryngoscopy to inspect the obstructed area.direct laryngoscopy to inspect the obstructed area.

The ABCs of CPR - Breathing1The ABCs of CPR - Breathing1

Assessment of breathing Assessment of breathing look for a rise and fall of the chest and abdomen, look for a rise and fall of the chest and abdomen,

listen for exhaled air, and feel for exhaled air flow at listen for exhaled air, and feel for exhaled air flow at the mouth or the palmthe mouth or the palm

Rescue breathing Rescue breathing if no spontaneous breathing is detected, begin if no spontaneous breathing is detected, begin mouth-mouth-

to-mouthto-mouth or or mouth-to-nose-and-mouth mouth-to-nose-and-mouth oror bag-valve- bag-valve-maskmask ventilation ventilation

provide 2 slow breaths, pausing after the first one to provide 2 slow breaths, pausing after the first one to take a breath to maximize oxygen content and take a breath to maximize oxygen content and minimize COminimize CO2 2 concentration in the delivered breathsconcentration in the delivered breaths

The ABCs of CPR - Breathing2The ABCs of CPR - Breathing2

rescue breaths are the most important support for rescue breaths are the most important support for

a nonbreathing infant or childa nonbreathing infant or child

the pressure and volume of ventilation should be the pressure and volume of ventilation should be

sufficient to cause the chest to risesufficient to cause the chest to rise

rapidly performed rescue breathing may cause rapidly performed rescue breathing may cause

gastric distention, which elevating the diaphragm gastric distention, which elevating the diaphragm

and decreasing lung volumeand decreasing lung volume

The ABCs of CPR - Circulation1The ABCs of CPR - Circulation1

Assessment of circulationAssessment of circulation

ineffective cardiac contraction will result in the absence of ineffective cardiac contraction will result in the absence of

a palpable pulse in a large central arterya palpable pulse in a large central artery

in children older than 1 yr, the in children older than 1 yr, the carotid arterycarotid artery , on the side , on the side

of the neck, is the most accessible central artery to palpateof the neck, is the most accessible central artery to palpate

in infants palpation of the in infants palpation of the brachial arterybrachial artery is recommended, is recommended,

due to the short, chubby neckdue to the short, chubby neck

the the femoral arteryfemoral artery is often used by health care is often used by health care

professionalsprofessionals

The ABCs of CPR - Circulation2The ABCs of CPR - Circulation2

Chest compressionsChest compressions

serial rhythmic compressions of the chest circulate serial rhythmic compressions of the chest circulate

blood to the vital organs to keep them viable until blood to the vital organs to keep them viable until

advanced life support (ALS) care can be providedadvanced life support (ALS) care can be provided

chest compressions must always be accompanied by chest compressions must always be accompanied by

ventilation ventilation

the child should be supine on a hard, flat surfacethe child should be supine on a hard, flat surface

for an infant the hard surface can be rescuer’s hand or for an infant the hard surface can be rescuer’s hand or

forearmforearm

The ABCs of CPR - Coordination of Compressions and Rescue BreathingThe ABCs of CPR - Coordination of Compressions and Rescue Breathing external chest compression must always be external chest compression must always be

accompanied by rescue breathingaccompanied by rescue breathing at the end of every fifth compression, a pause of 1 to 1.5 at the end of every fifth compression, a pause of 1 to 1.5

sec should be allowed for a ventilationsec should be allowed for a ventilation in infant and child the 5:1 compression-ventilation in infant and child the 5:1 compression-ventilation

ratio is maintained for both one and two rescuers ratio is maintained for both one and two rescuers the infant and child should be reassessed after 20 cycles the infant and child should be reassessed after 20 cycles

of compression and ventilation (apr. 1 min) and every of compression and ventilation (apr. 1 min) and every few minutes thereafterfew minutes thereafter

Normal Pacemaker Rates at Various AgesNormal Pacemaker Rates at Various Ages

0 - 1 month 0 - 1 month 100 - 180 bpm100 - 180 bpm 1 1 yearyear 110 - 180 bpm110 - 180 bpm 5 5 yearsyears 60 - 120 bpm60 - 120 bpm 10 10 yearsyears 55 - 110 bpm55 - 110 bpm adultadult 50 - 100 bpm50 - 100 bpm

Advanced Life SupportAdvanced Life SupportAdvanced Life SupportAdvanced Life Support

Medication Administration1 Medication Administration1

venous administration (IV) is the preferred route for drug venous administration (IV) is the preferred route for drug

delivery during advanced life support delivery during advanced life support

in neonatal resuscitation the umbilical vein is more easily in neonatal resuscitation the umbilical vein is more easily

cannulated than scalp or peripheral veinscannulated than scalp or peripheral veins

in older infants and children, peripheral access is usually in older infants and children, peripheral access is usually

more easily established than central accessmore easily established than central access

all doses should be followed by a 5 ml normal saline flush all doses should be followed by a 5 ml normal saline flush

to help move the drug more rapidly into the central to help move the drug more rapidly into the central

circulationcirculation

Medication Administration2Medication Administration2

in patients less than 6 yrs of age, an intraosseous (IO) needle in patients less than 6 yrs of age, an intraosseous (IO) needle

may be usedmay be used

all resuscitation medications, including catecholamines, may all resuscitation medications, including catecholamines, may

be administered into the bone marrowbe administered into the bone marrow

intramuscular (IM) and sublingual (SL) routes are not intramuscular (IM) and sublingual (SL) routes are not

recommended due to delayed drug deliveryrecommended due to delayed drug delivery

intracardiac injection is not recommended due to the risks of intracardiac injection is not recommended due to the risks of

hemopericardium and vessel injury; questionable drug hemopericardium and vessel injury; questionable drug

absorptionabsorption

Medication Administration3Medication Administration3

some medications may be given endotracheally (ET) during some medications may be given endotracheally (ET) during

advanced life support if IV or IO access is unavailableadvanced life support if IV or IO access is unavailable

the dose should be diluted in 3 to 5 ml of normal saline the dose should be diluted in 3 to 5 ml of normal saline

(1 to 2 ml for neonatal resuscitation)(1 to 2 ml for neonatal resuscitation)

catheter inserted below the end of the endotracheal tube catheter inserted below the end of the endotracheal tube

each dose should be followed by several positive-pressure each dose should be followed by several positive-pressure

ventilations using a hand resuscitation bag to ensure drug ventilations using a hand resuscitation bag to ensure drug

deposition into the lungsdeposition into the lungs

Epinephrine1Epinephrine1

epinephrine is the most frequently used resuscitation epinephrine is the most frequently used resuscitation medication in infants and childrenmedication in infants and children

alpha-adrenergic effectsalpha-adrenergic effects cause an intense vasoconstriction, cause an intense vasoconstriction, increases systemic vascular resistance, improves coronary increases systemic vascular resistance, improves coronary blood flowblood flow

reduction in blood flow to renal, mucosal, and dermal reduction in blood flow to renal, mucosal, and dermal vascular beds, preserving blood flow to more critical vascular beds, preserving blood flow to more critical organsorgans

beta-adrenergic effectsbeta-adrenergic effects cause an increase in cardiac cause an increase in cardiac contractility and heart rate, while relaxing smooth musclecontractility and heart rate, while relaxing smooth muscle


epinephrine is used for cardiac arrest, asystole, symptomatic epinephrine is used for cardiac arrest, asystole, symptomatic

bradycardia, and hypotension unrelated to volume depletionbradycardia, and hypotension unrelated to volume depletion

it can be administered every 3 to 5 minutes as neededit can be administered every 3 to 5 minutes as needed

in neonatal resuscitation - 0.01 to 0.03 mg/kg in neonatal resuscitation - 0.01 to 0.03 mg/kg

(0.1 to 0.3 ml/kg of the 1:10,000 solution) IV or ET(0.1 to 0.3 ml/kg of the 1:10,000 solution) IV or ET

in the newborn higher doses are not recommended due to in the newborn higher doses are not recommended due to

risk of intracranial hemorrhage and hypertensionrisk of intracranial hemorrhage and hypertension

in pediatric resuscitation, the recommended initial dose of in pediatric resuscitation, the recommended initial dose of

epinephrine is 0.01 mg/kg (0.1 ml/kg of the 1:10,000 solution) epinephrine is 0.01 mg/kg (0.1 ml/kg of the 1:10,000 solution)

IV for bradycardia and cardiac arrestIV for bradycardia and cardiac arrest


if pulseless arrest persists, the dose may be increased to 0.1 if pulseless arrest persists, the dose may be increased to 0.1 mg/kg (0.1 ml/kg of the 1:1000 solutionmg/kg (0.1 ml/kg of the 1:1000 solution

this is the same dose used for endotracheal administration (ET)this is the same dose used for endotracheal administration (ET) patients with continued hypotension, epinephrine may be given patients with continued hypotension, epinephrine may be given

as a continuous infusion (drip)as a continuous infusion (drip) starting dose is 2 mcg/kg/min, with the infusion rate then starting dose is 2 mcg/kg/min, with the infusion rate then

reduced to maintain the desired response, usually to 0.1 to 1 reduced to maintain the desired response, usually to 0.1 to 1 mcg/kg/min. mcg/kg/min.

infusion of doses greater than 5 mcg/kg/min may produce infusion of doses greater than 5 mcg/kg/min may produce profound vasoconstriction at the site of administrationprofound vasoconstriction at the site of administration

AcidosisAcidosis mixed metabolic and respiratory acidosis is common during mixed metabolic and respiratory acidosis is common during

cardiopulmonary arrest as a result of anaerobic metabolism cardiopulmonary arrest as a result of anaerobic metabolism

and carbon dioxide retentionand carbon dioxide retention

acidosis may cause a decrease in myocardial contractility, acidosis may cause a decrease in myocardial contractility,

lowering of blood pressure, and a blunting of the response to lowering of blood pressure, and a blunting of the response to

catecholamines catecholamines

optimal method to reverse this situation is to provide optimal method to reverse this situation is to provide

adequate ventilation (excretion of COadequate ventilation (excretion of CO22) and systemic ) and systemic

perfusionperfusion

sodium bicarbonate is reserved for sodium bicarbonate is reserved for severe metabolic acidosissevere metabolic acidosis

and only when ventilatory support can be assuredand only when ventilatory support can be assured

Sodium Bicarbonate1 - Paradoxical AcidosisSodium Bicarbonate1 - Paradoxical Acidosis bicarbonate infusion has the potential to induce bicarbonate infusion has the potential to induce

paradoxical intracellular and central nervous system paradoxical intracellular and central nervous system

acidosisacidosis

it combines with protons (Hit combines with protons (H++) to produce CO) to produce CO22 and water and water

COCO2 2 is freely diffusable into myocytes and the is freely diffusable into myocytes and the

subarachnoid space where it combines with water to subarachnoid space where it combines with water to

produce free hydrogen ions (COproduce free hydrogen ions (CO22 + H + H22O = HO = H+ + + HCO+ HCO33--))

Sodium Bicarbonate2Sodium Bicarbonate2

standard dose is 1 to 2 mEq/kg IV or IOstandard dose is 1 to 2 mEq/kg IV or IO additional doses (0.5 mEq/kg) should be guided by additional doses (0.5 mEq/kg) should be guided by

assessment of laboratory valuesassessment of laboratory values standard solutions of 8.4% (1 mEq/ml) sodium bicarbonate standard solutions of 8.4% (1 mEq/ml) sodium bicarbonate

are very hyperosmolar (2,000 mOsm/L) and should be used are very hyperosmolar (2,000 mOsm/L) and should be used with cautionwith caution

in neonates, only the 4.2% (0.5 mEq/ml) solution should be in neonates, only the 4.2% (0.5 mEq/ml) solution should be used to avoid increasing the risk of intraventricular used to avoid increasing the risk of intraventricular hemorrhagehemorrhage

rate of administration should be no greater than 1 rate of administration should be no greater than 1 mEq/kg/minmEq/kg/min

Sodium Bicarbonate3Sodium Bicarbonate3

sodium bicarbonate should not be given sodium bicarbonate should not be given

endotracheallyendotracheally

- - it can cause substantial tissue injury it can cause substantial tissue injury

it should not be mixed with other medications it should not be mixed with other medications

-- precipitation of calcium and inactivation of precipitation of calcium and inactivation of

catecholamines may occur if they are mixed with catecholamines may occur if they are mixed with

sodium bicarbonatesodium bicarbonate

Atropine - indicationsAtropine - indications

treatment of symptomatic bradycardia, as a treatment of symptomatic bradycardia, as a second-line therapy after epinephrinesecond-line therapy after epinephrine

bradycardia as the result of increased vagal tone bradycardia as the result of increased vagal tone (such as during intubation) (such as during intubation)

bradycardia as the result of documented bradycardia as the result of documented atrioventricular blockatrioventricular block

AtropineAtropine

in children, the dose of atropine is 0.02 mg/kg in children, the dose of atropine is 0.02 mg/kg

IV,ET or IO, with a minimum dose of 0.1 mg to IV,ET or IO, with a minimum dose of 0.1 mg to

avoid paradoxical bradycardiaavoid paradoxical bradycardia

the recommended maximum single dose is 0.5 mg the recommended maximum single dose is 0.5 mg

for a child and 1 mg for an adolescent or adultfor a child and 1 mg for an adolescent or adult

this dose may be repeated once, if no response is this dose may be repeated once, if no response is

seen within 5 minutesseen within 5 minutes

Naloxone - indicationsNaloxone - indications

pure antagonist which reverses the effects of opioids pure antagonist which reverses the effects of opioids

such as morphine and fentanylsuch as morphine and fentanyl

in resuscitations, it is used to reverse the respiratory in resuscitations, it is used to reverse the respiratory

and central nervous system depression and and central nervous system depression and

hypertension caused by administration of opioids hypertension caused by administration of opioids

naloxone is also indicated for severe respiratory naloxone is also indicated for severe respiratory

depression in neonates whose mothers received opioids depression in neonates whose mothers received opioids

within four hours of deliverywithin four hours of delivery

NaloxoneNaloxone naloxone acts within 2 to 3 minutes and has a duration of naloxone acts within 2 to 3 minutes and has a duration of

30 to 60 minutes30 to 60 minutes dose for total reversal is 0.1 mg/kg for infants and children dose for total reversal is 0.1 mg/kg for infants and children

up to 5 years of age or 20 kg body weightup to 5 years of age or 20 kg body weight children over 5 years or 20 kg should receive a standard 2 children over 5 years or 20 kg should receive a standard 2

mg dosemg dose smaller doses may be used if only partial opioid reversal is smaller doses may be used if only partial opioid reversal is

desireddesired naloxone may be administered by rapid IV push, IO, or ETnaloxone may be administered by rapid IV push, IO, or ET intramuscular or subcutaneous administration may result intramuscular or subcutaneous administration may result

in erratic absorption and reduced efficacyin erratic absorption and reduced efficacy

Calcium chlorideCalcium chloride

calcium enhance cardiac contractility and increase calcium enhance cardiac contractility and increase systemic vascular resistancesystemic vascular resistance

calcium administration is recommended calcium administration is recommended only in cases ofonly in cases of hypocalcemia, hyperkalemia, hypermagnesemia, and hypocalcemia, hyperkalemia, hypermagnesemia, and calcium channel blocker overdosecalcium channel blocker overdose

dose of calcium chloride is 0.2 to 0.25 ml/kg of a 10% dose of calcium chloride is 0.2 to 0.25 ml/kg of a 10% solution, to provide 5 to 7 mg/kg elemental calcium (20 solution, to provide 5 to 7 mg/kg elemental calcium (20 to 25 mg/kg calcium salt)to 25 mg/kg calcium salt)

this dose should be infused at a rate this dose should be infused at a rate no fasterno faster than 100 than 100 mg/min and may be repeated one time - rapid infusion mg/min and may be repeated one time - rapid infusion may result in bradycardia or asystolemay result in bradycardia or asystole

Dopamine - indicationsDopamine - indications

patients who remain hypotensive or poorly perfused patients who remain hypotensive or poorly perfused

after initial resuscitationafter initial resuscitation

dopamine acts at a variety of receptorsdopamine acts at a variety of receptors

dopaminergicdopaminergic 2 to 5 mcg/kg/min2 to 5 mcg/kg/min

beta-adrenergicbeta-adrenergic above 5 mcg/kg/minabove 5 mcg/kg/min

alpha-adrenergicalpha-adrenergic 10 to 20 mcg/kg/min10 to 20 mcg/kg/min

DopamineDopamine

low doses, 2 to 5 mcg/kg/min, dopamine causing increased low doses, 2 to 5 mcg/kg/min, dopamine causing increased renal, coronary, splanchnic, and cerebral blood flowrenal, coronary, splanchnic, and cerebral blood flow

above 5 mcg/kg/min, dopamine stimulates beta-adrenergic above 5 mcg/kg/min, dopamine stimulates beta-adrenergic receptors and increases release of norepinephrine, receptors and increases release of norepinephrine, producing an increase in cardiac contractilityproducing an increase in cardiac contractility

in the range of 10 to 20 mcg/kg/min, dopamine begins to in the range of 10 to 20 mcg/kg/min, dopamine begins to act at alpha-adrenergic receptors, producing act at alpha-adrenergic receptors, producing vasoconstriction and significant tachycardiavasoconstriction and significant tachycardia

because of its rapid elimination, dopamine can only be because of its rapid elimination, dopamine can only be administered as a administered as a continuous infusioncontinuous infusion

DobutamineDobutamine

dobutamine stimulates beta-adrenergic receptors and dobutamine stimulates beta-adrenergic receptors and

produces a positive inotropic responseproduces a positive inotropic response

it does not act on dopaminergic or alpha-adrenergic it does not act on dopaminergic or alpha-adrenergic

receptorsreceptors

dobutamine produces a mild vasodilatationdobutamine produces a mild vasodilatation

it is recommended in cases of cardiogenic or septic shock it is recommended in cases of cardiogenic or septic shock

when the patient is not already hypotensivewhen the patient is not already hypotensive

dobutamine is typically started at a dose of 5 mcg/kg/min and dobutamine is typically started at a dose of 5 mcg/kg/min and

titrated to achieve the desired blood pressure responsetitrated to achieve the desired blood pressure response

AdenosineAdenosine

adenosine is a pharmacologic alternative to defibrillation adenosine is a pharmacologic alternative to defibrillation

in patients with supraventricular tachycardiain patients with supraventricular tachycardia

produces a transient block of the atrioventricular nodeproduces a transient block of the atrioventricular node

its short elimination half-life (approximately 9 seconds) its short elimination half-life (approximately 9 seconds)

makes it a safe medication, but also makes it difficult to makes it a safe medication, but also makes it difficult to

get adequate drug concentrations at the site of actionget adequate drug concentrations at the site of action

dose for infants and children is 0.1 to 0.2 mg/kg dose for infants and children is 0.1 to 0.2 mg/kg

administered by rapid IV push, followed immediately by a administered by rapid IV push, followed immediately by a

2 to 3 ml normal saline flush (maximum dose is 12 mg)2 to 3 ml normal saline flush (maximum dose is 12 mg)

LidocaineLidocaine

lidocaine is used to control ventricular tachycardia or lidocaine is used to control ventricular tachycardia or

fibrillationfibrillation

recommended method of administration is a 1 mg/kg recommended method of administration is a 1 mg/kg

bolus loading dose, followed by a continuous infusion of bolus loading dose, followed by a continuous infusion of

20 to 50 mcg/kg/min20 to 50 mcg/kg/min the dosage should be reduced in children with low the dosage should be reduced in children with low

cardiac output or reduced hepatic blood flow or cardiac output or reduced hepatic blood flow or function to avoid lidocaine accumulationfunction to avoid lidocaine accumulation

signs of toxicity include drowsiness, confusion, tremors, signs of toxicity include drowsiness, confusion, tremors, and seizures.and seizures.

Pediatric Cardiac Emergencies. Infant Cardiac Disease Leading to ER Presentation ä Congenital ä...

Documents

Transcript of Pediatric Cardiac Emergencies. Infant Cardiac Disease Leading to ER Presentation ä Congenital ä...