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Heart failure in children
This document discusses congestive cardiac failure in children. It defines congestive cardiac failure as a state of systemic and pulmonary congestion resulting from impaired ability of the ventricle to fill or eject blood. The most common causes in children are congenital heart defects and cardiomyopathy. Symptoms vary by age but can include poor feeding, tachypnea, coughing, and fatigue. Diagnosis involves history, physical exam assessing vital signs, heart sounds and edema, as well as tests like echocardiogram, ECG and chest x-ray. Management depends on whether the failure is acute or chronic, and involves diuretics, inotropes, oxygen, surgery or catheter interventions, and long-term therapy based
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Heart failure in children
- 1. Congestive Cardiac Failure DrFahad Fayyaz Butt Pediatric Resident
- 2. Definition A state ofsystemic and pulmonary congestion resulting from impairment in the ability of the ventricle to fill and/or eject blood
- 3. Epidemiology • USA: 11,000to 14,000 hospitalizations related to heart failure annually in American children • Age: Most common age at presentation is during infancy • Etiology: Most common cause is Congenital Heart Defects then Cardiomyopathy
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- 6. Chronic Heart Failure Neurohumoral Mechanism SNS HRContractility RAA Na & H20 Retention Apoptosis Fibroblast and collagen replacement Cardiac Dilation Further Systolic Dysfunction Cardiac Oxygen demand Cardiac Remodeling Acute Heart Failure
- 7. Pathophysiology Pressure Overload Volume overload Ventricular Dysfunction Increased Afterload Reduced cardiac output Pulmonaryand venous congestion Increased Preload Increased fluid in heart Pulmonary and venous congestion Systolic dysfunction Reduced cardiac output Pulmonary and venous congestion
- 8. Causes of Heartfailure in infants and children By pathophysiology Pressure Overload • Left sided • Right sided Volume Overload • CHD: Left to right shunting • Valvular insufficiency • Fluid overload Ventricular dysfunction • No structural defects: • Cardiomyopathy • Myocarditis • Arrhythmia • Drug/toxin • Infarction • Structural defects: CHD: post surgical(burn-out?)
- 9. Condition Causes Ventricular Dysfunction Structurally normalCongenital Malformations Cardiac Non cardiac Volume overload Left to right shunting Valvular defects Pressure overload Left sided Right sided
- 10. Symptoms Infant Younger childrenOlder children • Tachypnea • Poor feeding : FTT Cachexia • Diet diaphoresis Often mistaken for: Reflux Asthma • Recurrent coughing • Easy fatigability • Abdominal and vomiting Often mistaken for Asthma Gastritis • Abdominal pain • Recurrent vomiting • Wheezing cough • Chest pain, Syncope & palpitations
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- 12. CHF according toage group Birth One week One month Polycythemia, Anemia, Hypocalcemia Pressure Overload: (DDL) Aortic stenosis Coartation of aorta, Hypoplastic left heart syndrome Volume Overload: VSD , AVSD Truncus arteriosus Others: Respiratory illness, Sepsis, Alcapa
- 13. • Dilated Cardiomyopathy: Myocarditis • Arrhythmia: SVT, CHB • Unrepaired Structural Heart disease: ASD, VSD • Hypothyroidism • Chemotherapeutics • Metabolic: BMD, DMD, MPS Children to adolescents CHF according to age group
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- 17. Normal range forHR and RR Age group Respiratory rate Heart rate Median (1st-99th percentile) Median (1st-99th percentile) 0 to 3 months 43 (25-66) 143 (107-181); term newborn at birth: 127 (90-164) 3 to 6 months 41 (24-64) 140 (104-175) 6 to 9 months 39 (23-61) 134 (98-168) 9 to 12 months 37 (22-58) 128 (93-161) 12 to 18 months 35 (21-53) 123 (88-156) 18 to 24 months 31 (19-46) 116 (82-149) 2 to 3 years 28 (18-38) 110 (76-142) 3 to 4 years 25 (17-33) 104 (70-136) 4 to 6 years 23 (17-29) 98 (65-131) 6 to 8 years 21 (16-27) 91 (59-123) 8 to 12 years 19 (14-25) 84 (52-115) 12 to 15 years 18 (12-23) 78 (47-108) 15 to 18 years 16 (11-22) 73 (43-104) Data from: Fleming S, Thompson M, Stevens R, et al. Normal ranges of heart rate and respiratory rate in children from birth to 18 years of age: a systematic review of observational studies. Lancet 2011; 377:1011.
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- 19. • Thrill: • vibratorysensation felt on the skin overlying an area of turbulence and indicates a loud heart murmur • Impulse: • Precordial impulses are pulsations originating from the heart or great vessels that are visible or palpable on the anterior chest wall.
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- 23. Abnormal Heart sounds Systolic Diastolic ContinuousGallops Clicks Murmurs
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- 25. Timing Systolic Diastolic Continuousmurmur Stenotic Semilunar valves Pulmonary stenosis Aortic stenosis Regurgitant Atrioventricular valves Tricuspid Regurgitation Mitral Regurgitation Ventricular septal defects Regurgitant Semilunar valves Pulmonary Regurgitation Aortic Regurgitation Stenotic Atrioventricular valves Tricuspid stenosis Mitral stenosis Patent ductus arteriosus Aortopulmonary window
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- 28. Pathologic Murmur Features Findings Signsand symptoms: SOB, cyanosis Auscultation Grade 3 and above murmur Diastolic murmur Abnormal Heart sounds: gallop Pulse Abnormal strong or weak pulses
- 29. Differential Diagnosis • RespiratoryDistress: • Neonate: Diaphragmatic hernia, Meconium aspiration • Older infants and children: Pneumonia , Bronchiolitis, Asthma • Shock: • Sepsis, hypovolemia • Failure to thrive: • Cystic fibrosis, Celiac disease • Edema: • Renal Failure Chronic Acute
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- 32. CHF with Rightatrial enlargement
- 33. 8 year oldwith shortness of breath Pericardial effusion
- 34. 10 month oldwith feeding related dyspnea and syncopal episodes, family history of heart diseases
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- 36. Maternal rubella, 1month old with SOB Patent ductus arteriosus
- 37. 5 month oldwith feeding diaphoresis with maternal lupus ECG Third degree Heart block
- 38. 8month old withlethargy and poor feeding Supraventricular tachycardia
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- 40. STAGING Stage Definition ExamplesTherapy A Patients with increased risk of developing HF, but with normal cardiac function and chamber size •Exposure to cardiotoxic agents •Family history of heritable cardiomyopathy •Univentricular heart •Congenitally corrected transposition of the great arteries None B Patients with abnormal cardiac morphology or function, with no symptoms of HF, past or present •Aortic insufficiency with LV enlargement •History of anthracycline exposure with decreased LV systolic function •ACE inhibitor for patients with systemic ventricular dysfunction C Patients with structural or functional heart disease, and past or current symptoms of HF •Symptomatic cardiomyopathy •Congenital heart defect with ventricular pump dysfunction •ACE inhibitor and an aldosterone antagonist; oral diuretic therapy as needed for fluid overload; low-dose digoxin if needed for additional symptom relief •After a few weeks of stability, a beta blocker is added in patients with persistent LV dilation and dysfunction D Patients with end-stage HF requiring specialized interventions •Marked symptoms at rest despite maximal medical therapy •Pharmacologic therapy consists of intravenous diuretics and/or inotropes •Other interventions may include positive pressure ventilation, cardiac resynchronization therapy, mechanical circulatory support, and heart transplantation
- 41. Management Congestive Heart Failure Acute Older child Neonateor young infant chronic
- 42. • Special casebecause: • Ductal-Dependant lesions • 100% oxygen and PaO2 do not go above 150 mm Hg • Alprostadil Acute CHF in neonates and Young infants
- 43. Acute CHF Acute CHF NormalMAP with normal perfusion Diuretics Milrinone Elevated MAP with poor perfusion Milrinone Dopamine Normal MAP with poor perfusion Dopamine Epinephrine Mechanical Ventilation ECMO
- 44. Intervention in chronic/stableCHF Structural Heart Disease Ventricular pump dysfunction • Left to right shunts • Outflow tract obstructions • Surgical or catheter based intervention • Ventricular Systolic dysfunction • Therapy is based on stages of HF
- 45. Stages & Therapyof CHF in pediatrics Stages Define Examples Therapy A Normal ECHO But increased risk Family history Using cardiotoxic therapies None B Abnormal ECHO with no symptoms ASD Using cardiotoxic therapies ACE inh C Abnormal ECHO with symptoms In past or present Dilated cardiomyopahties Add spironolactone And/or Beta blocker Symptomatic: Diuretics or Digoxin D End stage Heart failure: intractable symptoms Eisenmenger IV inotropes & diuretics Mechanical Support Heart transplant International Society for Heart and Lung Transplantation: Practice guidelines for management of heart failure in children
- 46. Goal in ChronicCHF Relieve symptoms Slow disease progression Nutritional support Exercise and physical activity Reduce comorbidities
Editor's Notes
- #4 Age: 90% of cases below <1 years Etiology (AAP defines them as riskfactors) : 65% of cases of CHF due to CHD if it’s a structurally normal heart then Cardiomyopathy 27% is most common reason. 60-90% % are due to dilated cardiomyopathy, hypertrophic cardiomyopathy (HCM) accounted for 25 to 40 percent, left ventricular noncompaction accounted for 9 percent, restrictive or other types of cardiomyopathy accounted for approximately 3 percent.
- #6 Ventricular dysfunction : I should be able to lift 5 pound weight and I am not Pressure or volume overload means I am lifting 1000 pound and I just cant, heart muscle can be initially normal but maybe dysfunctional later.
- #8 Volume: Preload/EDVEDP: initially the heart overcomes the preload by increasing the contractility but if preload becomes too large it dilates the ventricle ultimately reduces contractility Pressure: Afterload/ obstruction i.e Stenosis distal to the ventricles or increased TPR reduces cardiac output Increased afterload: in severe cases only as in mild ,chronic case (initially heart compensates by increasing contractility but only later decompensates) In adults you would imagine Pressure overload essential HTN Hypertrophic , Volume AI or MI Dilated , but that’s not the case with kids, where symptoms sudden and severe , occurring far before culminating in any of those dysmorphologies In cases when initial presenting signs and symptoms are severe and result in immediate seeking of medical care and appropriate management the sequel of heart failure can be avoided which is cardiac remodeling, but as is the case with dilated cardiomyopathies idiopathic and myocarditis
- #9 CHD is likely the predominant underlying aetiology of heart failure in children worldwide CM : 1.13–1.24 cases per 100,000 < 1 year of age cause: 85% idiopathic , myocarditis (15%), Dilated cardiomyopathy 0.57–0.76 per 100,000 is the most common cardiomyopathy diagnosed in childhood . 71% of children with dilated cardiomyopathy present with heart failure, compared with only 13% of those with hypertrophic cardiomyopathy. RCM: 0.03 cases per 100,000 children Volume over load: CHD (65%): PDA, AVSD, VSD, Aortopulmonary window, Valve: MR ( IE, RHD,MVP) , AR bicuspid aortic valves and following catheter-based intervention for valvar aortic stenosis , Fluid overload: Oliguric Renal failure Pressure overload: . Depending on severity and chronicity, pressure overload may result in either systolic or diastolic dysfunction. AS: Congenital or RHD Bicuspid aortic valve 3.8 in 10,000 live births , COA: congenital, 4 per 10,000 live births Ventricular dysfunction leads to impaired ejection of blood from the ventricle. Unless specified, ventricular dysfunction implies systolic dysfunction (reduced ventricular contractility). Ventricular diastolic dysfunction implies impaired ventricular filling and noncompliance with abnormally steep pressure-volume relationship resulting in high ventricular filling pressures. Although the primary physiologic abnormality in DCM is left ventricular (LV) systolic dysfunction, diastolic dysfunction can occur in more severe cases. In contrast, LV systolic function is usually preserved in children with HCM and restrictive cardiomyopathy; when heart failure occurs in these settings, it is usually due to diastolic dysfunction Inflammation of the myocardium (myocarditis) 1 per 100,000 children is usually due to a viral infection or toxins and chemotherapeutics Infarction: Infants born with anomalous left coronary artery arising from the pulmonary artery (ALCAPA), Coronary vasculitis associated with Kawasaki disease Arrhythmia: Bradycardias: Complete heart block: Maternal lupus( , but sometimes TGA , Tachycardias: Supraventricular 90% and Atrial flutter 9% : Toxins: Anthracyclines: doxorubicin 1.6–2.1% of patients within the first year of therapy., Anticonvulsants: Carbamazepine (AV block) , TCA (Na. Block), Antimalarial Quinine (Na. Block), theophylline (Ventricular tachycardia) Non-cardiac cause: sepsis(SIRS), CKD(long standing hypertension, Fluid overload), BPD( RF and PH), long standing anemia
- #10 Structurally Normal: Cardiomyopathies : Cardiac: Cardiomyopathies : Systolic: Dilated( idiopathic or myocarditis), Diastolic: Hypertrophic(idiopathic) , Restrictive: rare ( pompe, hempchromatosis) …. Non-compaction Acquired: Primary cardiac: Myocarditis (infection, immunological), Arrhythmia (MC of childhood tachyarrhythmia SVT, AF, or bradyarrhtmias such as CHB CHF are especially provoled in conditions of stress, in maternal lupus), rare cause is Kawasaki disease, ALCAPA” The myocardium is perfused by the abnormally arising coronary artery, which has a relatively low perfusion pressure and carries blood with a low oxygen saturation, reflecting the pulmonary artery source resulting in ischemia and failure Non cardiac causes: chronic anemia, sepsis, DKA (patient in ICU), Renal failure, Ventricular pump dysfunction associated with Congenital Malformations are those children who had undergone multiple repair surgeries now decompensates into heart failure such : as those after fontan procedure Left to right shunts: Large VSD, ASD, PDA, Aortopulmonary windows, AVSD Volume Overload: AR in bicuspid aortic valve, MR after repair of AVSD, PR after repair of TOF Left sided: COA, AS …. Right sided: PS ( presents as mainly cyanosis rather than CHF)
- #11 You may get very varied history depending on the age of the patient and its important to ask specific question s that are age appropriate In infants: Common presentation is….. Irritability: chest pain Poor feeding: interrupted feeds, frequently pauses to rest during feeds, takes longer to finish each feed FTT and cachexia Diet diaphoresis: forehead sweating, Tachypnea: may be without much retractions and associated grunting Their in ability to feed adequately results in cachexia…. Younger children : the presentation can be very variable and it can be mistaken for…… Older children: peripheral edema A very late sign of heart failure
- #12 Drugs:., Anticonvulsants: Carbamazepine (AV block) , TCA (Na. Block), Antimalarial Quinine (Na. Block), theophylline (Ventricular tachycardia) Birth history : Antenatal History: Diabetic Polycythemia or AVSD, Abruptio placenta anemia Drug use: Alcohol VSD, Preclampsiaseptal defects , TORCH CHD Natal: Prematurity PDA Postnatal Ventilator use BPDLeft ventricular diastolic dysfunction Past medical history: recurrent chest infection , patient is undergoing cancer treatment receiving cardiotoxic medications, Anthracyclines: doxorubicin 1.6–2.1% of patients within the first year of therapy Developmental: motor delay due to FTT Family history: some CHD are familial such as hypertrophic cardiomyopathies
- #13 Infants: Most of the causes of heart failure is CHD Birth to one week: ebstein anamoly , HLHS If it’s around first week of life around the time of pda closure we are looking at Pressure overload: AS, COA&HLHS which depend on PDA for systemic circulation (both are 4 per 10,000) (looking at the pressure gradients between pulses of upper limb and lower limb which is also around the same time as PDA closes identifies COA) therefore a sense of urgency should prevail at birth and one year of life TA and PA which depend on PDA for oulmonary circulation 1-2 months: we don’t see CHF left to right shunts in first week where the pulmonary resistance is still high and prevents left to right shunting in first week and present only around 1-2 months: VSD, Truncus Arteriosus, tricuspid atresia ALCAPA: because the pulmonary vascular resistance has decreased and thus perfusion pressure from anamolus coronary artery from pulmonary artery resulting in ischemia
- #14 Younger children and adolescents: CM: idiopathic 85% , Acquired: In children its idiopathic and we find something it is 15%, myocarditis, familial, arrhythmia, RHD not in patient population over here, Respiratory chain defects rare, we amy also see DCM in icu secondary to sepsis, long standing hypertension in CKD Hypertrophic CM: although rare ,though to be cause of genetic derangement of cardiac tissue when present can cause ventricular arrhythmia and sudden death,
- #15 Color: Pink ( normal) or Mottled ,Pale ( poor cardiac output, anemia or shock) Blue (urgent and elaborate action as PGE1) Alertness: (Urgency of the condition) Awake and calm, agitated , or lethargic Nutritional status: ( chronicity) Malnourished ( Most children with chronic heart failure) or well nourished Clubbing: Prolonged Hypoxemia ( typically seen in children with Congenital Heart defects) Pitting : indentation 0 no pitting or +4 severe pitting Visible pulsations in Neck: JVD, but especially in older children , it may be normally present but when lying at 30-40 these pulsations signify heart failure Hyperdynamic precordium: A visible apical impulse can be present in left ventricular volume overload lesions that include significant mitral or aortic valve regurgitation or large left-to-right shunts
- #16 Pulse: Central pulses Infants: brachial artery or femoral pulses Older children: Carotid pulse Absence needs immediate intervention Peripheral pulses: Radial pulses and compare both sides and upper and lower extremity: COA, IAA Strength: 0-+4= o being absent , 1 being weak, 4 being bounding ( weak pulse signify low output HF such as dilated cardiomyopathy COA , bounding may signify high out put HF such as AVSD, AR) Regularity: Regular tachycardia: SVT, Irregular and tachycardia: Focal Atrial tachycardia, Irregular bradycardia: CHB Pulsus alterans: Alternating strong and weak pulses: signs of failing myocardium Pulsus paradoxus: diminishing of pulses on inspiration Tactile Temperature: if they feel overall warm and dry may be normal, cool & clamy extremities : poor perfusion ( impending shock) Capillary refill time: >3Sec is delayed and indicates poor perfusion( increased TPR in acute compensation) and >5 Sec may require immediate intervention Edema: it is a very late sign of heart failure ,abdominal distention or ascites in younger children or Pedal edema in older children Along with hepatomegaly
- #17 Severity of illness: HR: via pulse or auscultation..15 to 30 seconds and multiply , to know the HR for age (While tachycardia can be a sign of cardiac cause but can also be due to crying, fever or pain , on the other hand Bradycardia can be ominous sign of CV collapse or can be sign of young child with Complete heart block, Hx: Maternal SLE, Long QT syndrome, Structural Heart defect: ASD ) Blood pressure: Systolic/diastolic/ MAP : size and placement is very important, although can be placed on any extremity The cuff should be placed on the arm with the centre of the bladder over the brachial artery. A cuff bladder that encircles close to 80% of the upper arm circumference and cover 80% of upper extremity it will reduce the risk of cuff error significantly. Too small : high BP, Too big : low BP If you need to repeat the BP you should wait one minute to give the vessels a chance to refill. If the BP readings are above the expected level for age and height the BP measurement should be repeated three times, leaving at least one minute between readings or taken manually as automated tend to be higher Newborn or young infants: take four limb BP or pre and post ductal BP: systolic BP >10mm of hg is significant Hypotension is late sign in shock, Blood pressure can be normal in CHF early on Tachypnea: Most common finding in patient with pulmonary congestion , take into account the normal range for age Oxygen saturation: pulmonary congestion due to HF can lead to diminished oxygen saturation preductal and post ductal oxygen evaluated later SpO2 difference >3 percent between the upper and lower extremities (on three measurements, each separated by one hour) pulmonary hypertension but also COA or interrupted aortic arch Reverse differential cyanosis: is a rare finding that may occur in patients with transposition of the great arteries associated with either coarctation or pulmonary hypertension
- #19 Respiratory: You may find it clear in infants older children Rales bilaterally or wheezing GIT: younger children: abdominal distention and ascites and older children pedal edema(late sign), Hepatomegaly ( Acute or severe CHF)
- #20 Impulse literally means force, force that acts to lift your hand
- #21 apical impulse :Inspection and palpation , palpated using the tips of the middle and index fingers and is usually located in the fourth or fifth intercostal space, if laterally displaced then: Signifies dilated left ventricle (dilated cardiomyopathy) , left ventricular volume overload lesions that include significant mitral or aortic valve regurgitation or large left-to-right shunts Parasternal impulse/ heave: Inspection and palpation The right ventricular impulse is palpated by placing the hand along the left sternal border Signifies: right ventricular hypertension (eg, large ventricular septal defect [VSD], large PDA) or right ventricular volume overload (ASD) Palpation: Thrill: systolic and diastolic thrill, though diastolic is uncommon, thrill represents the tactile component of a loud murmur (grade IV or higher), location and timing of a thrill aid in diagnosis
- #24 Heart murmurs are produced as a result of turbulent flow of blood strong enough to produce audible noise. It can benign , it can be made through entirely structurally normal heart or heart with defects
- #25 A third heart sound occurs in early diastole during the rapid filling phase and is best heard with the bell of the stethoscope Signifying: volume overload Heard over Apex: Left ventricle, LLSB: Right ventricle A fourth heart sound is always a pathologic finding. S4 occurs in late diastole during the atrial contraction phase Signifies: Non compliance of ventricle as in restrictive cardiomyopathy or myocardial ischemia or hypertrophy of ventricle Heard Over Apex
- #27 Left upper sternal border AV stenosis: such AS , as long as there is enough CO. Right upper sternal border, Right upper sternal Border: Pulmonic murmur: such as PS Apex Mitral Murmur: such as MR, MS Left lower sternal border: VSD, TR, innocent murmur
- #28 Chest of a child is small murmur can resonate so easily anywhere moreover, Murmur have to transmit from the heart to skin to diaphragm to air column to ear drum , lot of places where it can be lost or distorted Some cardiologist would go with loud or not loud , systolic from diastolic They would forego the quality , pitch, radiation, shape, blowing and rumbling
- #31 Labs: CBC: Anemia and infection( WBCs, HGB) CRP: Can differentiate between myocarditis and idiopathic dilated cardiomyopathy LFT,RFT: elevated LFTs to investigate for liver involvement in case of right heart failure, RFT , look for elevated creatinine as renal failure may be the contributing factor for exacerbating the preexisting HF Lactate: may be elevated due to poor perfusion and hypoxia Blood culture: Especially neonate to rule out sepsis as a cause for illness, aslo in case of suspicion of IE Serum chemistries, Hyponatremia may be seen with severe HF Calcium: hypocalcaemia may cause difficult to control CHF BNP:level >500 pg/mL is indicative for heart failure in children BNP levels can help discriminate between cardiac disease and noncardiac causes of HF symptoms (eg, pulmonary disease) Left-to-right shunting defects (eg, atrial or ventricular septal defects, patent ductus arteriosus), BNP levels correlate with the degree of shunting Troponin: Cardiac troponin I and troponin T are sensitive biomarkers for myocyte injury. Cardiac troponin concentrations usually begin to rise two to three hours after the onset of acute MI. The serum or plasma troponin must be above “the 99th percentile of the upper reference limit (URL)” for the normal range of the assay being used. Other: TFTs, ESR, anti-ANA (SLE), antistreptolysins (RHD) CXR: AP Chest radiography is helpful to assess for cardiomegaly and pulmonary congestion, and monitor the effectiveness of HF treatment. ECG: In some cases, the ECG may point toward an underlying cause, arrhythmia as a cause for symptoms ECHO: assess cardiac function and establishes whether the child has a structurally normal heart or underlying structural congenital heart disease, MRI: altered geometry, patients with myocardial inflammation and intrinsic cardiac muscle disease, myocardial fibrosis, intrinsic cardiac muscle disease Other : cardiac catheterization: coronary arteries: Kawasaki disease, ALCAPA
- #32 Heart: size, when possible chambers Lungs: Pulmonary vasculature and congestion Bony abnormalities Airway
- #33 This is a rheumatic heart disease with right atrial enlargement
- #35 Note cardiomegaly with normal pulmonary vasculature, this is a case of hypertrophic cardiomyopathy with outflow obstruction and normal systolic function
- #36 Reduced pulmonary vasculature after wards
- #37 Increased pulmonary vasculature and fullness of left upper mediastinium
- #38 CHB: P wave and QRS wave are independent but regular/fixed rate
- #39 SVT: 2 year old with SOB <1 year >220/min >1 y>180/min, no p wave , non variable
- #40 Not useful for evaluating Heart failure which is a clinical diagnosis After Accounting for variations by age and body size Anatomy: Congenital heart defects Valves: stenosis , regurgitation, function: rt, and lt. Sizes: chamber size and wall thickness Pericardium: effusions
- #41 Categorization of the stage and severity of the patient's HF is important for monitoring the disease progression and guiding management decisions Stage A B C D, more of classification from academic standpoint??
- #42 Acute/ Decompensated: acute dyspnea, increased effort, and /or hypotension crackles and gallop on auscultation, Chronic/Compensated: Chronic or Stable Congestive Heart Failure Neonate or infant: ductal-dependant lesions, HLHS, COA, alprostadil in initial management , when these ductal depdant lesions cant be ruled out , for example you are giving 100% oxygen PaO2 doesn’t go above >150mm Hg , femoral pulses
- #43 Ductal dependant: transposition of great vessels, HLHS, Pulmonary atresia where the only ay oxygenation to occur is via duct which is closing
- #44 Current therapy for acute heart failure focuses on Improving myocardial performance with inotropic agents, adjustments to afterload and preload, Volume/preload overloaded Afterload overloaded Weak myocardium
- #45 VSD: Surgical closure AS: balloon valvulotomy Systolic dysfunction: Dilated cardiomyopathy
- #46 ECHO: function or structure Mechanical support : Ventilation, ECMO
- #47 Chronic stable CHF Relieve symptoms: Surgery and/or just Medications: digoxins relieve symptoms Slow disease progression: ACE , Spironolactone, Beta blockers Nutrition: Children with HF often have increased caloric needs due to an increased metabolic demand, >150kcal/kg/day Nasogastric or gastrostomy tube feeds may be required. In addition, salt and fluid restriction Exercise: if the child is old enough to cooperate, typically beginning around age 6 or 7 years Reduce comorbidities:Anemia, active infection, HTN, Obesity, Renal failure, hypocalcemia, thromboembolism