Pediatric Cardiac Emergencies

Pediatric Cardiac Emergencies

Infant Cardiac Disease Leading to ER Presentation
Congenital Acquired Cardiomyopathy Myocarditis (usually with CHF) Dysrhythmias

Heart Failure- Definition:
A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body It is commonly termed congestive heart failure (CHF) since symptoms of increase venous pressure are often prominent neonatal myocardium is stiff and unable to increase contractility – must increase HR to get increased CO. With increased hr’s get decreased diastolic filling – therefore infants have a reduced cardiac reserve – limited ability to handle pressure or volume overloads

CHF - Presentation infants: irritable, poor feeding (early fatigue), failure to thrive, respiratory symptoms always consider in patients with respiratory symptoms often misdiagnosed as respiratory illness / infection typical physical exam and CXR findings symptoms and signs of increased pulmonary venous pressure and respiratory infection overlap -fever, runny nose, stridor, vomiting suggest infection -dyspnea during feeding, slow feeding, tachypnea, dyspnea suggest elevated pulmonary venous pressures Feeding is how infants exert themselves – symptoms during feeding are equivalent to SOBOE

CHF - Etiology Increased Preload Increased Afterload
L to R shunts (VSD, PDA, AV fistula) severe anemia Increased Afterload HTN Congenital (aortic stenosis, coarctation of aorta) Decreased Contractility myocarditis, pericarditis with tamponade cardiomyopathy (dilated or hypertrophic) Kawasaki syndrome (early phase) metabolic: electrolyte, hypothyroid myocardial contusion toxins: dig, calcium channel blockers, beta blockers Dysrhythmia

CHF - Etiology presents immediately at birth
anemia, acidosis, hypoxia, hypoglycemia, hypocalcemia, sepsis presents at 1 day (congenital) PDA in premature infants presents in first month (congenital) HPLV, aortic stenosis, coarctation, VSD presents later presents later (acquired) myocarditis, cardiomyopathy (dilated or hypertrophic), SVT, severe anemia, rheumatic fever Tintinalli

Etiology It is a common end point for many diseases of cardiovascular system It can be caused by : -Inappropriate work load (volume or pressure overload) -Restricted filling -Myocyte loss by S. Soliman

Causes of left ventricular failure
• Volume over load: Regurgitate valve High output status • Pressure overload: Systemic hypertension Outflow obstruction • Loss of muscles: Post MI, Chronic ischemia Connective tissue diseases Infection, Poisons (alcohol,cobalt,Doxorubicin) • Restricted Filling: Pericardial diseases, Restrictive cardiomyopathy, tachyarrhythmia by S. Soliman

Pathophysiology Hemodynamic changes Neurohormonal changes
Cellular changes by S. Soliman

diastolic dysfunction
Hemodynamic changes From hemodynamic stand point HF can be secondary to systolic dysfunction or diastolic dysfunction by S. Soliman

Neurohormonal changes
N/H changes Favorable effect Unfavor. effect  Sympathetic activity  HR , contractility, vasoconst.   V return,  filling Arteriolar constriction  After load  workload  O2 consumption  Renin-Angiotensin – Aldosterone Salt & water retention VR Vasoconstriction   after load  Vasopressin Same effect  interleukins &TNF May have roles in myocyte hypertrophy Apoptosis Endothelin Vasoconstriction VR  After load by S. Soliman

Cellular changes • Slight  in α1 receptors
 Changes in Ca+2 handling.  Changes in adrenergic receptors: • Slight  in α1 receptors • β1 receptors desensitization  followed by down regulation  Changes in contractile proteins  Program cell death (Apoptosis)  Increase amount of fibrous tissue by S. Soliman

Symptoms • Shortness of breath, Orthopnea, paroxysmal nocturnal dyspnea • Low cardiac output symptoms • Abdominal symptoms: Anorexia,nausea, abdominal fullness, pain by S. Soliman

Physical Signs High diastolic BP & occasional decrease in systolic BP (decapitated BP) JVD Rales (Inspiratory) Displaced and sustained apical impulses Third heart sound – low pitched sound that is heard during rapid filling of ventricle by S. Soliman

Physical signs (cont.) Mechanism of S3 sudden deceleration of blood
as elastic limits of the ventricles are reached Vibration of the ventricular wall by blood filling Common in children by S. Soliman

Physical signs (cont.) - Usually at the end of diastole
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 by S. Soliman

Framingham Criteria for Dx of Heart Failure
Major Criteria: PND- paroxysmal nocturnal dyspnea JVD- jugular venous distention Rales Cardiomegaly Acute Pulmonary Edema S3 Gallop Positive hepatic Jugular reflex ↑ venous pressure > 16 cm H2O by S. Soliman

Dx of Heart Failure (cont.)
Minor Criteria LL edema, Night cough Dyspnea on exertion Hepatomegaly Pleural effusion ↓ vital capacity by 1/3 of normal Tachycardia 120 bpm Weight loss 4.5 kg over 5 days management by S. Soliman

Forms of Heart Failure Systolic & Diastolic High Output Failure
Pregnancy, anemia, thyrotoxisis, A/V fistula, Beriberi, Low Output Failure Acute large MI, aortic valve dysfunction Chronic by S. Soliman

Forms of heart failure ( cont.)
Right vs Left sided heart failure: Right sided heart failure : Most common cause is left sided failure Other causes included : Pulmonary embolisms Other causes of pulmonary htn. RV infarction MS Usually presents with: LL edema, ascites hepatic congestion cardiac cirrhosis (on the long run) by S. Soliman

Left ventricular failure
respiratory discomfort, vary with position,stress and activity, associated with physical signs of disturbances in the lungs Dyspnea during modest exertion- usually the first symptoms of left heart failure, associated with increased rate of breathing Ortopnea Cough

Left ventricular failure
On examination: -patient: pale and sweaty, cold hands because of periferal vasoconstriction rapid heart rate Gallop rhythm Murmur of mitral insufficiency Rales on auscultation of the lungs ( interstitial edema and fluid)

Right Ventricular Failure
-neck veins distention -hepatomegaly, splenomegaly -congestion and edema of the gastrointestinal tract, anorexia,nausea, vomiting weight loss, failure to gain weight,malnutrition Murmur or tricuspid insufficiency Hydrothorax Pericardial effusion Irritability,restlessness oliguria

Differential diagnosis
Pericardial diseases Liver diseases Nephrotic syndrome Protein losing enteropathy by S. Soliman

Laboratory Findings Anemia Hyperthyroid
Chronic renal insuffiency, electrolytes abnormality Pre-renal azotemia Hemochromatosis by S. Soliman

Electrocardiogram Old MI or recent MI Arrhythmia
Some forms of Cardiomyopathy are tachycardia related LBBB→may help in management by S. Soliman

Chest X-ray Size and shape of heart
Evidence of pulmonary venous congestion (dilated or upper lobe veins → perivascular edema) Pleural effusion by S. Soliman

Echocardiogram Function of both ventricles
Wall motion abnormality that may signify CAD Valvular abnormality Intra-cardiac shunts by S. Soliman

Cardiac Catheterization
When CAD or valvular is suspected If heart transplant is indicated by S. Soliman

TREATMENT Correction of reversible causes Ischemia
Valvular heart disease Thyrotoxicosis and other high output status Shunts Arrhythmia A fib, flutter, permanent junctional reciprocating tachycardia Medications Ca channel blockers, some antiarrhythmics by S. Soliman

Diet and Activity Salt restriction Fluid restriction
Daily weight (tailor therapy) Gradual exertion programs by S. Soliman

Diuretic Therapy The most effective symptomatic relief Mild symptoms
HCTZ Chlorthalidone Metolazone Block Na reabsorbtion in loop of henle and distal convoluted tubules Thiazides are ineffective with GFR < 30 --/min by S. Soliman

Diuretics (cont.) Side Effects Pre-renal azotemia Skin rashes
Neutropenia Thrombocytopenia Hyperglycemia ↑ Uric Acid Hepatic dysfunction by S. Soliman

Diuretics (cont.) More severe heart failure → loop diuretics
Furosemide 1-3 mg/kg m.c. Mechanism of action: Inhibit chloride reabsortion in ascending limb of loop of Henle results in natriuresis, kaliuresis and metabolic alkalosis Adverse reaction: pre-renal azotemia Hypokalemia Skin rash ototoxicity by S. Soliman

K+ Sparing Agents Triamterene & amiloride – acts on distal tubules to ↓ K secretion Spironolactone (Aldosterone inhibitor) recent evidence suggests that it may improve survival in CHF patients due to the effect on renin-angiotensin-aldosterone system with subsequent effect on myocardial remodeling and fibrosis by S. Soliman

Inhibitors of renin-angiotensin- aldosterone system
Renin-angiotensin-aldosterone system is activation early in the course of heart failure and plays an important role in the progression of the syndrome Angiotensin converting enzyme inhibitors Angiotensin receptors blockers Spironolactone by S. Soliman

Angiotensin Converting Enzyme Inhibitors
They block the R-A-A system by inhibiting the conversion of angiotensin I to angiotensin II → vasodilation and ↓ Na retention ↓ Bradykinin degradation ↑ its level → ↑ PG secretion & nitric oxide Ace Inhibitors were found to improve survival in CHF patients Delay onset & progression of HF in pts with asymptomatic LV dysfunction ↓ cardiac remodeling by S. Soliman

Side effects of ACE inhibitors
Angioedema Hypotension Renal insuffiency Rash cough by S. Soliman

Angiotensin II receptor blockers
Has comparable effect to ACE I Can be used in certain conditions when ACE I are contraindicated (angioneurotic edema, cough) by S. Soliman

Digitalis Glycosides (Digoxin, Digitoxin)
The role of digitalis has declined somewhat because of safety concern Recent studies have shown that digitals does not affect mortality in CHF patients but causes significant Reduction in hospitalization Reduction in symptoms of HF by S. Soliman

Digitalis (cont.) Mechanism of Action
+ve inotropic effect by ↑ intracellular Ca & enhancing actin-myosin cross bride formation (binds to the Na-K ATPase → inhibits Na pump → ↑ intracellular Na → ↑ Na-Ca exchange Vagotonic effect Arrhythmogenic effect by S. Soliman

Digitalis Toxicity Narrow therapeutic to toxic ratio
Non cardiac manifestations Anorexia, Nausea, vomiting, Headache, Xanthopsia sotoma, Disorientation by S. Soliman

Digitalis Toxicity Cardiac manifestations Sinus bradycardia and arrest
A/V block (usually 2nd degree) Atrial tachycardia with A/V Block Development of junctional rhythm in patients with a fib PVC’s, VT/ V fib (bi-directional VT) by S. Soliman

Digitalis Toxicity Treatment
Hold the medications Observation In case of A/V block or severe bradycardia → atropine followed by temporary PM if needed In life threatening arrhythmia → digoxin-specific fab antibodies Lidocaine and phenytoin could be used – try to avoid D/C cardioversion in non life threatening arrhythmia by S. Soliman

β 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 by S. Soliman

Vasodilators 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. by S. Soliman

Positive inotropic agents
These are the drugs that improve myocardial contractility (β adrenergic agonists, dopaminergic agents, phosphodiesterase inhibitors), dopamine, dobutamine, milrinone, amrinone Several studies showed ↑ mortality with oral inotropic agents So the only use for them now is in acute sittings as cardiogenic shock by S. Soliman

Anticoagulation (coumadine)
Atrial fibrillation H/o embolic episodes Left ventricular apical thrombus by S. Soliman

Antiarrhythmics Most common cause of SCD in these patients is ventricular tachyarrhythmia Patients with h/o sustained VT or SCD → ICD implant by S. Soliman

Antiarrhythmics (cont.)
Patients with non sustained ventricular tachycardia Correction of electrolytes and acid base imbalance In patients with ischemic cardiomyopathy → ICD implant is the option after r/o acute ischemia as the cause In patients wit non ischemic cardiomyopathy management is not clear Amiodarone may have a role in this group of patients by S. Soliman

New Methods Implantable ventricular assist devices
Biventricular pacing (only in patient with LBBB & CHF) Artificial Heart by S. Soliman

Nursing 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 - CHF
Monitor fluid status I & O, specific gravity Daily weight Provide adequate rest, position for comfort Prevent infections Promote growth & development Reduce respiratory distress

Digoxin 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

Myocarditis leading cause of dilated cardiomyopathy and one of the most common causes of CHF in children etiology: idiopathic, viral, bacterial, parasitic hallmark is CHF failure to respond to bronchodilators in wheezing child treatment includes inotropes, afterload reduction, diuretics, antibiotics, antivirals viral causes include: coxsackie, echovirus, mumps, influenza, varicella, Epstein-Barr, HIV bacterial causes include: corynebacterium, Lyme disease, E. coli, Haemophilus influenzae other clues to myocarditis include fever, muscle tenderness, exposure to known toxins or etiologic agents

Pericarditis sharp stabbing precordial pain
worse with supine and better leaning forward no sensory innervation of the pericardium pain referred from diaphragmatic and pleural irritation

Etiology infectious Connective tissue Metabolic / Endocrine
viral bacterial TB fungal parasitic Connective tissue RA Rheumatic fever SLE Metabolic / Endocrine uremia hypothyroid Hematology / Oncology bleeding diathesis malignancy Trauma Iatrogenic

Pericarditis usually a benign course
virulent bacteria (H. flu, E. coli) can cause constrictive pericarditis and subsequent tamponade – may need urgent pericardiocentesis uncomplicated pericarditis usually responds to rest and anti-inflammatories pericaridocentesis with an 18G over the needle catheter is indicated in the emerg dept. if an infant with large heart becomes rapidly unstable with loss of pulse

Chest Pain 4% of children will have a cardiac origin
remainder: MSK, pulmonic (asthma, bronchitis, pneumonia), GI Cardiac causes: myocarditis, pericarditis, structural abnormalities such as congenital heart disease or hypertrophic cardiomyopathy

Syncope 20-50% of adolescents experience at least one episode of syncope most cases benign Pathophysiology vascular orthostatic, hypovolemia neurally mediated hypoxia: PE, CNS depression from OD, CO cardiac Tintinalli

Cardiac Syncope Dysrhythmias Outflow obstruction
tachy brady Outflow obstruction Myocardial Dysfunction cardiac syncope often precedes future sudden cardiac death 25% of children suffering sudden death have history of syncope (percentage may be higher in those patients with a sudden cardiac death) History syncope during exertion increased likelihood of serious etiology FH of structural heart disease, dysrhythmias, sudden death Physical when trying to rule this out pay particular attention to the CV exam: palpation of cardiac impulse, auscultation of heart, evaluation of peripheral pulses; orthostatic measurements

Sudden Cardiac Death Etiology myocarditis
cardiomyopathy (hypertrophic) cyanotic and noncyanotic congenital heart disease valvular heart disease congenital complete heart block WPW long QT syndrome Marfan syndrome coronary artery disease anomalous coronary arteries most common cause of sudden cardiac death in athletes is hypertrophic cardiomyopathy and aberrant coronary arteries - can also have all the other causes commotio cordis

Risk Factors for Serious Cause of Syncope
history of cardiac disease in patient FH of sudden death, cardiac disease, or deafness recurrent episodes recumbent episode exertional prolonged loss of consciousness associated chest pain or palpitations medications that can alter cardiac conduction

What to look for in the Department: EKG
Long QT syndrome congenital or acquired get paroxysmal v tach with torsades de pointes congenital long QT associated with hypertrophic cardiomyopathy long QT defined as corrected QT longer than 0.44 s T wave alternans sometimes present can have normal ECG in the department two clinical syndromes not associated with structural heart disease: Romano-Ward and Jervell-Lange-Nielsen Romano-Ward: autosomal dominant condition not associated with deafness Jervell-Lange-Nielsen – autosomal recessive disease associated with deafness mortality from untreated congenital long QT syndrome is 50%

Other dysrhythmias WPW and other SVT’s AV block Sick sinus syndrome
usually acquired, rarely congenital Sick sinus syndrome

Other structural cardiac diseases
dilated cardiomyopathy usually secondary to myocarditis syncope and death secondary to ventricular dysrhythmias or severe myocardial dysfunction arrhythmogenic RV dysplasia congenital cyanotic and non-cyanotic heart disease valvular diseases aortic stenosis coronary artery anomalies exertional syncope or sudden death aberrant artery passes between aorta and pulmonary artery

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

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

WHO Classification Unknown cause (primary)
Dilated Hypertrophic Restrictive unclassified Specific heart muscle disease (secondary) Infective Metabolic Systemic disease Heredofamilial Sensitivity Toxic Br Heart J 1980; 44:

Functional Classification
Dilatated (DCM) ventricular enlargement and syst dysfunction Hypertrophic ( HCM) inappropriate myocardial hypertrophy in the absence of HTN or aortic stenosis Restrictive (infiltrative) abnormal filling and diastolic function

Idiopathic Dilated Cardiomyopathy

IDC - Definition a disease of unknown etiology that principally affects the myocardium LV dilatation and systolic dysfunction pathology increased heart size and weight ventricular dilatation, normal wall thickness heart dysfunction out of portion to fibrosis

Incidence and Prognosis
3-10 cases per 100,000 20,000 new cases per year in the U.S.A. death from progressive pump failure 1-year 25% 2-year % 5-year % stabilization observed in 20-50% of patient complete recovery is rare

Clinical Manifestations
Highest incidence in middle age blacks 2x more frequent than whites men 3x more frequent than women symptoms may be gradual in onset acute presentation misdiagnosed as viral URI in young adults uncommon to find specific myocardial disease on endomyocardial biopsy

History and Physical Examination
Symptoms of heart failure pulmonary congestion (left HF) dyspnea (rest, exertional, nocturnal), orthpnea systemic congestion (right HF) edema, nausea, abdominal pain, nocturia low cardiac output fatigue and weakness hypotension, tachycardia, tachypnea, JVD

Cardiac Imaging Chest radiogram Electrocardiogram
24-hour ambulatory ECG (Holter) lightheadedness, palpitation, syncope Two-dimensional echocardiogram Radionuclide ventriculography Cardiac catheterization age >40, ischemic history, high risk profile, abnormal ECG

Clinical Indications for Endomyocardial Biopsy
Definite monitoring of cardiac allograft rejection monitoring of anthracycline cardiotoxicity Possible detection and monitoring of myocarditis diagnosis of secondary cardiomyopathies differentiation between restrictive and constrictive heart disease

Management of DCM Limit activity based on functional status
salt restriction of a 2-g Na+ (5g NaCl) diet fluid restriction for significant low Na+ initiate medical therapy ACE inhibitors, diuretics digoxin, carvedilol hydralazine / nitrate combination

Management of DCM consider adding ß-blocking agents if symptoms persists anticoagulation for EF <30%, history of thromboemoli, presence of mural thrombi intravenous dopamine, dobutamine and/or phosphodiesterase inhibitors cardiac transplantation

Hypertrophic Cardiomyopathy

Hypertrophic Cardiomyopathy
First described by the French and Germans around 1900 uncommon with occurrence of 0.02 to 0.2% a hypertrophied and non-dilated left ventricle in the absence of another disease small LV cavity, asymmetrical septal hypertrophy (ASH), systolic anterior motion of the mitral valve leaflet (SAM)

65% 35% 10%

Clinical Manifestation
Asymptomatic, echocardiographic finding Symptomatic dyspnea in 90% angina pectoris in 75% fatigue, pre-syncope, syncope  risk of SCD in children and adolescents palpitation, PND, CHF, dizziness less frequent

Natural History annual mortality 3% in referral centers probably closer to 1% for all patients risk of SCD higher in children may be as high as 6% per year majority have progressive hypertrophy clinical deterioration usually is slow progression to DCM occurs in 10-15%

Risk Factors for SCD Young age (<30 years)
“Malignant” family history of sudden death Gene mutations prone to SCD (ex. Arg403Gln) Aborted sudden cardiac death Sustained VT or SVT Recurrent syncope in the young Nonsustained VT (Holter Monitoring) Brady arrhythmias (occult conduction disease) Br Heart J 1994; 72:S13

Management beta-adrenergic blockers calcium antagonist disopyramide
amiodarone, sotolol DDD pacing myotomy-myectomy plication of the anterior mitral leaflet

Restrictive Cardiomyopathy

Restrictive Cardiomyopathies
Hallmark: abnormal diastolic function rigid ventricular wall with impaired ventricular filling bear some functional resemblance to constrictive pericarditis importance lies in its differentiation from operable constrictive pericarditis

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

Classification Idiopathic Myocardial 1. Noninfiltrative Scleroderma
Amyloid Sarcoid Gaucher disease Hurler disease 3. Storage Disease Hemochromatosis Fabry disease Glycogen storage Endomyocardial endomyocardial fibrosis Hyperesinophilic synd Carcinoid metastatic malignancies radiation, anthracycline

Clinical Manifestations
Symptoms of right and left heart failure Jugular Venous Pulse prominent x and y descents Echo-Doppler abnormal mitral inflow pattern prominent E wave (rapid diastolic filling) reduced deceleration time ( LA pressure)

Basic Life Support

Cardiopulmonary Arrest
Cardiac arrest is the sudden loss of cardiac output, which is potentially reversible with prompt restoration of circulation and oxygen delivery. Sudden cardiac death and cardiac arrest are not synonymous. Sudden cardiac death is unexpected death within 1 hour of symptom onset because of a primarily cardiac cause in a victim with or without previously diagnosed heart disease.

Pathophysiology of CPA
CPA causes hypoxia, respiratory and metabolic acidosis cell death appears to be mediated by substances released from anoxic cell membranes agents associated with brain and heart injury are free iron, hydroxyl radicals, calcium CPA for as little as 5 minutes may cause permanent brain injury or death

The Most Common Causes of Pediatric CPA
infants SIDS (40%) respiratory diseases airway obstruction sepsis neurological diseases metabolic abnormalities chidren injury

Pediatric CPA the epidemiology of pediatric CPA is different from that of adults sudden, primary cardiac arrest is rare ventricular fibrillation has been reported in less than 10% (more likely in children with complex congenital heart disease) respiratory insufficiency is the more common cause 50% of all children who require CPR are infants

Out-of-Hospital CPA Out-of-hospital primary cardiac failure with cardiopulmonary arrest (CPA) is unusual in children. It may occur in children with chronic diseases cardiomyopathy myocarditis congenital heart diseases. It occur around the home, where children are under the supervision of parents. Parents of children at high risk should be educated in BLS.

In-Hospital CPA Primary cardiopulmonary arrest is often in hospitalised children after cardiac surgery with rare arrhythmia caused by cardiac catheterization or angiography general anesthesia antiarrhythmic drug administration

Respiratory Causes of Pediatric Cardiopulmonary Arrest
Upper airway obstruction Lower airway obstruction - croup - asthma - foreign body - bronchiolitis - strangulation - foreign body - inhalation injury - inhalation injury Intrinsic lung conditions - pneumonia - drowning - chest trauma

Cardiovascular Causes of Pediatric Cardiopulmonary Arrest
Hypovolemia Dysrrhythmias - trauma open heart surgery - burns cardiac catheterization - gastroenteritis - coronary angiography Sepsis general anesthesia Cardiogenic shock - prolonged QT syndrom - congenital heart diseases Intoxication - cardiomyopathy - myocarditis - post-open heart surgery

Basic Life Support Strictly defined, basic life support (BLS) is the initial phase of emergency cardiac care, encompassing recognition of cardiac arrest and delivery of rescue breathing (ventilation) and chest compressions (circulation).

Advanced Life Support Advanced life support (ACLS) includes BLS, ECG monitoring, rhythm identification, and restoration of hemodynamic stability through intubation, defibrillation, and pharmacologic therapy. Cardiopulmonary resuscitation effectively restores hemodynamic stability, return of spontaneous circulation (ROSC), in 40% to 60% of arrests.

Modern CRP Modern CPR began in 1960 with the landmark study by Kouwenhoven which reported combining closed chest compression, mouth-to-mouth breathing, and external defibrillation. As they explained it, their algorithm was remarkably easy to perform: "Anyone, anywhere, can now initiate cardiac resuscitative procedures. All that is needed are two hands."

Modern CPR Cardiac arrest outcomes will be most improved with public education and earlier initiation of CPR, both Basic Life Support and Advanced Life Support, notably defibrillation. After unresponsiveness, lack of pulse, and apnea are confirmed in unmonitored cardiac arrests, the initial management consists of BLS closed-chest compressions artificial ventilation.

Circulation: The Cardiac Pump Theory
The mechanism by which closed-chest compressions increase forward cardiac output remains controversial. The traditional cardiac pump theory states the heart is massaged and blood forced out by direct compression between the sternum and spine.

Circulation: The Thoracic Pump Theory
The thoracic pump theory suggests that forward blood flow increases through a passive cardiac conduit by a general increase in intrathoracic pressure transmitted to the cardiac chambers and the intrathoracic portion of the great vessels. Because of intact venous valves, the pressure generated during compression is not transmitted to the periphery, forcing blood to flow from the arteries to the veins.

The ABCs of Cardiopulmonary Resuscitation
Airway Breathing Circulation

The ABCs of CPR - Responsiveness
Quickly assess the presence or extent of injury and determine whether the child is conscious. The level of responsiveness is determined by tapping the child and speaking loudly to elicit a response. Carefully look, listen, and feel the pulse to determine that a cardiopulmonary arrest has occurred. Call for help once CPA is diagnosed.

The ABCs of CPR - Airway Open the airway. Use the head-tilt/chin-lift maneuver, avoiding hyperextension of the neck. Too vigorous head-tilt may occlude the trachea or injure the cervical spine. In infants, large head may flex the neck and compromise air exchange. If spinal injury is suspected, use a jaw-thrust instead of head-tilt. Suction may be needed to clear secretions, blood, or foreign bodies from the airway.

Foreign-Body Airway Obstruction
the infant: back blows chest thrusts the child: the Heimlich maneuver abdominal thrusts with victim standing or sitting (conscious) abdominal thrusts with victim laying or sitting (conscious or unconscious)

Foreign-Body Airway Obstruction
If the airway remains obstructed attempt to evacuate a possible aspirated foreign body. For infants give 5 sharp blows to the back with the heel of the hand between securely held shoulder blades. Then, deliver 5 chest thrusts to the mid-sternum. For children deliver 5 rapid subdiaphragmatic abdominal thrusts using the heel of the hand (modifed Heimlich maneuver) with the patient supine. If airway patency isn’t established, repeat the sequence. If 2 rapid series of maneuvers fail, perform immediate direct laryngoscopy to inspect the obstructed area.

The ABCs of CPR - Breathing1
Assessment of breathing look for a rise and fall of the chest and abdomen, listen for exhaled air, and feel for exhaled air flow at the mouth or the palm Rescue breathing if no spontaneous breathing is detected, begin mouth-to-mouth or mouth-to-nose-and-mouth or bag-valve-mask ventilation provide 2 slow breaths, pausing after the first one to take a breath to maximize oxygen content and minimize CO2 concentration in the delivered breaths

The ABCs of CPR - Breathing2
rescue breaths are the most important support for a nonbreathing infant or child the pressure and volume of ventilation should be sufficient to cause the chest to rise rapidly performed rescue breathing may cause gastric distention, which elevating the diaphragm and decreasing lung volume

The ABCs of CPR - Circulation1
Assessment of circulation ineffective cardiac contraction will result in the absence of a palpable pulse in a large central artery in children older than 1 yr, the carotid artery , on the side of the neck, is the most accessible central artery to palpate in infants palpation of the brachial artery is recommended, due to the short, chubby neck the femoral artery is often used by health care professionals

The ABCs of CPR - Circulation2
Chest compressions serial rhythmic compressions of the chest circulate blood to the vital organs to keep them viable until advanced life support (ALS) care can be provided chest compressions must always be accompanied by ventilation the child should be supine on a hard, flat surface for an infant the hard surface can be rescuer’s hand or forearm

The ABCs of CPR - Coordination of Compressions and Rescue Breathing
external chest compression must always be accompanied by rescue breathing at the end of every fifth compression, a pause of 1 to 1.5 sec should be allowed for a ventilation in infant and child the 5:1 compression-ventilation ratio is maintained for both one and two rescuers the infant and child should be reassessed after 20 cycles of compression and ventilation (apr. 1 min) and every few minutes thereafter

Normal Pacemaker Rates at Various Ages
0 - 1 month bpm 1 year bpm 5 years bpm 10 years bpm adult bpm

Advanced Life Support

Medication Administration1
venous administration (IV) is the preferred route for drug delivery during advanced life support in neonatal resuscitation the umbilical vein is more easily cannulated than scalp or peripheral veins in older infants and children, peripheral access is usually more easily established than central access all doses should be followed by a 5 ml normal saline flush to help move the drug more rapidly into the central circulation

in patients less than 6 yrs of age, an intraosseous (IO) needle may be used all resuscitation medications, including catecholamines, may be administered into the bone marrow intramuscular (IM) and sublingual (SL) routes are not recommended due to delayed drug delivery intracardiac injection is not recommended due to the risks of hemopericardium and vessel injury; questionable drug absorption

some medications may be given endotracheally (ET) during advanced life support if IV or IO access is unavailable the dose should be diluted in 3 to 5 ml of normal saline (1 to 2 ml for neonatal resuscitation) catheter inserted below the end of the endotracheal tube each dose should be followed by several positive-pressure ventilations using a hand resuscitation bag to ensure drug deposition into the lungs

Epinephrine1 epinephrine is the most frequently used resuscitation medication in infants and children alpha-adrenergic effects cause an intense vasoconstriction, increases systemic vascular resistance, improves coronary blood flow reduction in blood flow to renal, mucosal, and dermal vascular beds, preserving blood flow to more critical organs beta-adrenergic effects cause an increase in cardiac contractility and heart rate, while relaxing smooth muscle

Epinephrine2 epinephrine is used for cardiac arrest, asystole, symptomatic bradycardia, and hypotension unrelated to volume depletion it can be administered every 3 to 5 minutes as needed in neonatal resuscitation to 0.03 mg/kg (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 risk of intracranial hemorrhage and hypertension in pediatric resuscitation, the recommended initial dose of epinephrine is 0.01 mg/kg (0.1 ml/kg of the 1:10,000 solution) IV for bradycardia and cardiac arrest

Epinephrine3 if pulseless arrest persists, the dose may be increased to 0.1 mg/kg (0.1 ml/kg of the 1:1000 solution this is the same dose used for endotracheal administration (ET) patients with continued hypotension, epinephrine may be given as a continuous infusion (drip) starting dose is 2 mcg/kg/min, with the infusion rate then reduced to maintain the desired response, usually to 0.1 to 1 mcg/kg/min. infusion of doses greater than 5 mcg/kg/min may produce profound vasoconstriction at the site of administration

Acidosis mixed metabolic and respiratory acidosis is common during cardiopulmonary arrest as a result of anaerobic metabolism and carbon dioxide retention acidosis may cause a decrease in myocardial contractility, lowering of blood pressure, and a blunting of the response to catecholamines optimal method to reverse this situation is to provide adequate ventilation (excretion of CO2) and systemic perfusion sodium bicarbonate is reserved for severe metabolic acidosis and only when ventilatory support can be assured

Sodium Bicarbonate1 - Paradoxical Acidosis
bicarbonate infusion has the potential to induce paradoxical intracellular and central nervous system acidosis it combines with protons (H+) to produce CO2 and water CO2 is freely diffusable into myocytes and the subarachnoid space where it combines with water to produce free hydrogen ions (CO2 + H2O = H+ + HCO3-)

Sodium Bicarbonate2 standard dose is 1 to 2 mEq/kg IV or IO
additional doses (0.5 mEq/kg) should be guided by assessment of laboratory values standard solutions of 8.4% (1 mEq/ml) sodium bicarbonate are very hyperosmolar (2,000 mOsm/L) and should be used with caution in neonates, only the 4.2% (0.5 mEq/ml) solution should be used to avoid increasing the risk of intraventricular hemorrhage rate of administration should be no greater than 1 mEq/kg/min

Sodium Bicarbonate3 sodium bicarbonate should not be given endotracheally - it can cause substantial tissue injury it should not be mixed with other medications - precipitation of calcium and inactivation of catecholamines may occur if they are mixed with sodium bicarbonate

Atropine - indications
treatment of symptomatic bradycardia, as a second-line therapy after epinephrine bradycardia as the result of increased vagal tone (such as during intubation) bradycardia as the result of documented atrioventricular block

Atropine in children, the dose of atropine is 0.02 mg/kg IV,ET or IO, with a minimum dose of 0.1 mg to avoid paradoxical bradycardia the recommended maximum single dose is 0.5 mg for a child and 1 mg for an adolescent or adult this dose may be repeated once, if no response is seen within 5 minutes

Naloxone - indications
pure antagonist which reverses the effects of opioids such as morphine and fentanyl in resuscitations, it is used to reverse the respiratory and central nervous system depression and hypertension caused by administration of opioids naloxone is also indicated for severe respiratory depression in neonates whose mothers received opioids within four hours of delivery

Naloxone naloxone acts within 2 to 3 minutes and has a duration of 30 to 60 minutes dose for total reversal is 0.1 mg/kg for infants and children up to 5 years of age or 20 kg body weight children over 5 years or 20 kg should receive a standard 2 mg dose smaller doses may be used if only partial opioid reversal is desired naloxone may be administered by rapid IV push, IO, or ET intramuscular or subcutaneous administration may result in erratic absorption and reduced efficacy

Calcium chloride calcium enhance cardiac contractility and increase systemic vascular resistance calcium administration is recommended only in cases of hypocalcemia, hyperkalemia, hypermagnesemia, and calcium channel blocker overdose 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 to 25 mg/kg calcium salt) this dose should be infused at a rate no faster than 100 mg/min and may be repeated one time - rapid infusion may result in bradycardia or asystole

Dopamine - indications
patients who remain hypotensive or poorly perfused after initial resuscitation dopamine acts at a variety of receptors dopaminergic 2 to 5 mcg/kg/min beta-adrenergic above 5 mcg/kg/min alpha-adrenergic 10 to 20 mcg/kg/min

Dopamine low doses, 2 to 5 mcg/kg/min, dopamine causing increased renal, coronary, splanchnic, and cerebral blood flow above 5 mcg/kg/min, dopamine stimulates beta-adrenergic receptors and increases release of norepinephrine, producing an increase in cardiac contractility in the range of 10 to 20 mcg/kg/min, dopamine begins to act at alpha-adrenergic receptors, producing vasoconstriction and significant tachycardia because of its rapid elimination, dopamine can only be administered as a continuous infusion

Dobutamine dobutamine stimulates beta-adrenergic receptors and produces a positive inotropic response it does not act on dopaminergic or alpha-adrenergic receptors dobutamine produces a mild vasodilatation it is recommended in cases of cardiogenic or septic shock when the patient is not already hypotensive dobutamine is typically started at a dose of 5 mcg/kg/min and titrated to achieve the desired blood pressure response

Adenosine adenosine is a pharmacologic alternative to defibrillation in patients with supraventricular tachycardia produces a transient block of the atrioventricular node its short elimination half-life (approximately 9 seconds) makes it a safe medication, but also makes it difficult to get adequate drug concentrations at the site of action dose for infants and children is 0.1 to 0.2 mg/kg administered by rapid IV push, followed immediately by a 2 to 3 ml normal saline flush (maximum dose is 12 mg)

Lidocaine lidocaine is used to control ventricular tachycardia or fibrillation recommended method of administration is a 1 mg/kg bolus loading dose, followed by a continuous infusion of 20 to 50 mcg/kg/min the dosage should be reduced in children with low cardiac output or reduced hepatic blood flow or function to avoid lidocaine accumulation signs of toxicity include drowsiness, confusion, tremors, and seizures.

Pediatric Cardiac Emergencies

Similar presentations

Presentation on theme: "Pediatric Cardiac Emergencies"— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

Pediatric Cardiac Emergencies

Similar presentations

Presentation on theme: "Pediatric Cardiac Emergencies"— Presentation transcript:

Similar presentations

About project

Feedback