OS 213: Circulation and Respiration

LEC 20: CONGESTIVE HEART FAILURE IN CHILDREN

Exam # 1 | Dr. Connie Sison | August 1, 2012
OUTLINE
Introduction
Pathophysiology of Heart Failure
A. Dangerous Compensatory Mechanisms
Clinical Manifestations
Diagnosing Heart Failure in Children
A.
History of Newborn and Infants
B.
History of Children and Young Adults
C.
Physical Examination
D. Heart Failure Classification in Children
E.
Causes of Heart Failure in Children
Management and Treatment
A.
Non-Pharmacologic
B.
Surgical
C.
Pharmacologic
Summary

Note: We did not include the x-ray frames and pictures shown in the lecture since they were the same as those used in lecture 09
(Overview of Heart Diseases in Children). Please refer to the pictures under the Congestive Heart Failure section of the said
transcription. Thank you.

I. INTRODUCTION
Congestive Heart Failure
ULTIMATE GOAL: RECOGNIZE and initially treat a CHILD in HEART FAILURE (HF)
A clinical syndrome in which the heart is unable to pump enough blood to meet its needs, to dispose of venous
return adequately, or a combination of the two
Definition: inadequate oxygen delivery by the heart or circulatory system to meet the demands of the body

II. PATHOPHYSIOLOGY OF HEART FAILURE

Figure 1. Factors affecting Oxygen delivery. Hb = hemoglobin, CO = cardiac ouput, HR = heart rate
Recall: Cardiac output (CO) is the volume of blood being pumped by the heart, in particular by a left (LV) or right
ventricle (RV) in 1 min.; also, CO is the combined sum of output from the RV and the output from LV during systole.
(on the average, CO for male = 5 L/min, CO for female = 4.5 L/min) . (2014)
Supposing Cardiac output okay but child anemic, oxygen delivery still inadequate High Output Cardiac Failure
CO depends on Heart Rate (HR) and Stroke Volume (CO = HR x SV). Stroke volume (SV), which is the volume
of blood pumped from one ventricle of the heart with each beat, depends on preload, contractility and afterload.
o Preload end-diastolic volume (EDV) - degree to which the ventricles are stretched prior to contracting
o Contractility (especially of the LV) inotropy - intrinsic ability of the heart to contract independent of preload
and afterload; how intense the ventricle can propel blood
o Afterload - resistance to which the LV contracts; measure the tension produced by LV in order to contract lower
afterload higher stroke vol higher CO; reflection of PVR
o SV = EDV ESV [ESV = end-systolic volume]
o Ejection fraction = SV/EDV; Ejection fraction is the fraction of blood pumped out of ventricles with each
heartbeat.
In heart failure, the problem lies in the cardiac output. If CO is compromised (i.e. when there is a shunt), heart may
fail to deliver enough blood.
o Nice to know: Cardiovascular disease can be associated with increased CO as occurs during infection and sepsis,
or decreased CO, as in cardiomyopathy and heart failure (2014)
A. Dangerous compensatory mechanisms
When there is a decrease in the oxygen delivery by the heart (CO), PHYSIOLOGIC COMPENSATORY
MECHANISMS come into play to make sure that vital organs get enough oxygen (i.e. augment O 2 delivery).
o Neurohumoral responses
Sympathetic Nervous System Stimulation causing increased cardiac rate and contractility
Renin-angiotensin-aldosterone system: can be activated by beta-1 receptors to produce Angiotensin II
Other Mediators; Arginine Vasopressin (AVP) = antidiuretic hormone (ADH )

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OS 213: Circulation and Respiration

LEC 20: CONGESTIVE HEART FAILURE IN CHILDREN
Exam # 1 | Dr. Connie Sison | August 1, 2012

Figure 2. Neurohormonal Responses w/c compensate for decreased CO.

overcompensations; may not be good for the heart and may lead to heart failure
Increased Preload (remember Frank-Starling mechanism)
o Salt and water retention (expansion of extracellular volume)
o Redistribution of renal flow
o Sympathetic stimulation
o Aldosterone
o AVP/ADH
o possibly, heart will dilate
Increased Cardiac Rate and Contractility
o By means of sympathetic Stimulation
o alpha-1 receptor activation peripheral vasoconstrict
o beta -1 tachycardia, arrhythmia, salt and water retention (Via Juxtaglomerular (JG) cells)
Increased Afterload
o Increased in peripheral vascular resistance
o Sympathetic stimulation
o Angiotensin II (potent vasoconstrictor)
o AVP/ADH
Myocardial hypertrophy/LV remodeling: ultimately associated w/ alterations in cellular & subcellular phenotype
(necrosis, fibrosis) reducing contractility
o Increased in peripheral vascular resistance

Catecholamine
Aldosterone
Angiotensin II

III. CLINICAL MANIFESTATIONS

Increased Preload (and inability of heart to deal with increased preload)
o Pulmonary Congestion
Tachypnea, Dyspnea, Orthopnea

o Systemic Congestion heart cannot dispose of venous return properly

Hepatomegaly (chronic passive congestion), Bipedal Edema

o Pallor
Increased Sympathetic Stimulation
o Tachycardia
o Diaphoresis (excessive sweating)
o Arrhythmia
Increased Afterload
o Vasoconstriction cold extremities because of peripheral vasoconstriction brain heart kidney priority, warmth
means good perfusion less severe heart failure
To perfuse distal organs

o Cold extremities (due to peripheral vasoconstriction)

o Pallor
Hallmark of Heart Failure
Decreased O2 delivery (signs and symptoms) EASY FATIGABILITY (intermittency of feeding)
Feed hingal tigil 1-2 hours before volume of milk is consumed sign of easy fatigueability

SHOCK death

IV. DIAGNOSING HEART FAILURE IN CHILDREN

A. History Taking in Newborn and Infants
Birth and Maternal History
o possible predisposition to congenital causes of HF
Intermittent feeding

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OS 213: Circulation and Respiration

LEC 20: CONGESTIVE HEART FAILURE IN CHILDREN
Exam # 1 | Dr. Connie Sison | August 1, 2012

o feeding may be labored or impossible due to rapid breathing (i.e. in pulmonary congestion)
o slow or poor feeding
Normally, an infant can consume milk equivalent to [age of baby in months + 1] ounces of milk in less than 30
minutes every 2 to 3 hours) [1 oz = 30 ml]
o Easy fatigability (poor eating less energy)
Diaphoresis
o Due to the stimulation of sympathetic NS
o Can be observed especially during feeding
o Excessive sweating even on cool and temperate environments (confirm this with the childs parents; environment
might just really be warm)
o More evident on the forehead
Poor weight gain or weight loss
o body needs more energy to enhance cardiac output
Relative to the other child in the same stage of development
o Refer to growth charts
Repeated respiratory tract infection/chronic cough
o More than 8 instances per year sign of HF
o possible compression of lymphatic drainage bronchial airways due to enlarged PA
Agitation & unusual irritability
o Perfusion of the brain is compromised
o Irritability due to organic cause: rapid breathing; childs does not feed not well

B. History Taking in Children and Young Adults

Exercise intolerance/easy fatigability (hallmark of CHF)
o ask the usual activities, compare it to his/her peers
Tachypnea, shortness of breath, Dyspnea pulmonary congestions
Abdominal pain or distention (e.g. Hepatomegaly, Splenomegaly)
Orthopnea & Paroxysmal Nocturnal Dyspnea (in older children)
o Venous return higher in supine position
o (heart cannot cope with increased preload) pressure reflected back to lungs pulmonary congestion
Chronic cough
Puffy eyelids, swollen feet
o not as common in children (but note that edema in infants is mostly in the back due to supine position) as in older
adults
o points to renal in etiology especially in children (2014)

C. Physical Examination
General Survey
Failure to thrive (FTT)
o Evaluated either by a low weight for the child's age, or by a low rate of increase in the weight
Wasting or acute malnutrition
o Caused by an extremely low energy intake, nutrient losses due toinfection, or a combination of the two
Chromosomal syndromes
o In infants w/ Downs Syndrome, 50% may have cardiac problems, most of w/c have CAVSD (Complete AtrioVentricular Septal Defect)
o Edwards syndrome (Trisomy 18) 98% will have congenital heart disease
o So due to such statistics, it is recommended to have a 2D echo in such cases even if no abnormalities were heard
in ausculation
Color: pale, cyanotic (can help narrow down possible CHDs), jaundiced (i.e. in liver congestion)
Anxious/irritable compromised oxygen to the brain
Signs Diaphoresis - sweat on the forehead sympathetic activation
Signs of Cardiorespiratory distress
o Dyspnea, Shortness of breath, Tachypnea
o Subcostal Retractions = Harrisons groove (make sure to note its presence or absence in routine PE) which
indicates poor lung compliance. But this can also be sings of asthma and pneumonia
Vital Signs
Sinus tachycardia results in decreased cardiac output
o Sustained CR > 220 /min infants
o Sustained CR > 150/min older children
CR = cardiac rate

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OS 213: Circulation and Respiration

LEC 20: CONGESTIVE HEART FAILURE IN CHILDREN
Exam # 1 | Dr. Connie Sison | August 1, 2012
Consider Supraventricular Tachycardia

o Abnormal increase in HR HF
o There are instances when tachycardia is the cause of HF arryhtmia causing HF
o Results in decreased cardiac output
Diastolic filling time decreased in tachycardia decreased stroke volume
Decreased preload

Hypotension
o May lead to shock
Tachypnea
o Pediatric Respiratory Rates (RR)
Table 1. Normal breath rates per pediatric age group
Age
Rate (breaths/min)
Infant
(birth1
3060
yr)
Toddler (13 yrs)
2440
Preschooler (36
2234
yrs)
School-age (612
2440
yrs)
Adolescent (12
1216
18 yrs)
o It is normal for infant to have a RR of 60 breaths/min. Adults with the same RR are already tachypneic.
Cardiac Examination
Precordial activity (possible LVH)
Prominent S3 poor ventricular compliance (Kentucky gallop vs. S4 Tennessee)
Heart murmurs
Lung Examination
Look for signs of pulmonary congestion (compromised oxygenation and ventilation)
o Tachypnea and subcostal retractions
o Labored respiratory effort
o Nasal flaring
use of accessory muscles of respiration

o Grunting

in an attempt to keep the alveoli open (2014)

increase end alveolar pressure

o Hacking cough
bronchial mucosal edema

o Rales or crackles

clicking, rattling, or crackling noises

unusual in infants;
may suggest concurrent pneumonia
(bibasal rales because of gravity)

o Wheezing

continuous, coarse, whistling sound

congestion of airway due to pulmonary edema
not exclusive to asthma; can be also cardiac in etiology; but all who have asthma have wheezing
wheezing despite giving beta-agonists = most probably cardiac in origin

Abdominal Examination
Hepatomegaly
Ascites (accumulation of fluid in the peritoneal cavity)
Splenomegaly
o PE: dullness to percussion over Traube's space
o NOT associated with CHF but due to hematologic disorders like beta-thalassemia and leukemia
Examination of the Extremities
Cool extremities:
o warm extremities = well-perfused; most probably, heart does well
Peripheral pulse
Capillary refill;
o While legs are raised the legs, blood flow should return in < 2 seconds after blanching
Peripheral edema
o Extremely rare in infants; edema found only in dependent area
o Edema usually due to presence of TR (Tricuspid Regurgitation)
o Systemic congestion-dependent edema in adults

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UPCM 2016 B: XVI, Walang

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OS 213: Circulation and Respiration

LEC 20: CONGESTIVE HEART FAILURE IN CHILDREN
Exam # 1 | Dr. Connie Sison | August 1, 2012
HEENT (Head-Eye-Ear-Nose-Throat) Examination
Neck vein distention/engorgement
Difficult to evaluate, small in children; not too common in infants;
in acquired heart disease
o Constrictive pericarditis
o Pericardial effusion
Facial edema/Puffy eyelids
o Again, usually point to a renal etiology in infants
The three-minute examination for CHF (from 2013)

Take sleeping or resting respiratory rate for ONE FULL MINUTE.

Note the patients general appearance - distress, color, perfusion
Palpate forehead for diaphoresis.
Check capillary refill.
Examine tibial and other areas for edema.
Palpate precordium and assess its activity.
Examine the abdomen for hepatomegaly.
Palpate the pulses right arm and leg pulse simultaneously; carotid pulses
Auscultation:
o Head and abdomen bruits
o Heart murmurs or gallops
o Lungs rales or rhonchi

D. Heart Failure Classification in Children

Difficult
Range of ages and developmental stages
Variety of etiology (myocardial dysfunction, left to right shunt)
Table 2. Ross Classification of Heart Failure in Infants
CLASS I

Presence of structural heart disease but NO limitations or symptoms

CLASS II

Mild tachypnea or diaphoresis with feeding in infants; Dyspnea on exertion in older

children (relative to his/her peers) NO Growth failure;

CLASS III

Marked tachypnea or diaphoresis with feeds or exertion; Prolonged feeding times

Growth failure from CHF;
Symptoms in mild activities combing hair, taking a bath*

CLASS IV

Symptoms at rest with tachypnea, retractions, grunting or diaphoresis

Evaluation of CHF in Children

o Medical history
o Physical examination
o CXR (Chest X-Ray); Echocardiography (2D-Echo); ECG (Electrocardiography)
Heart size ct ratio > 0.55
Cephalization vessels at upper lung recruited to aid circulation and become more evident
o ABG (Arterial blood Gas) when patient is in respiratory diseases; how much ventilation is needed
o Low bicarb low pH metabolic acidosis pO2 pCO2
o CBC (Complete Blood Count); RBS (Random Blood Sugar); Electrolytes
Associated and aggravating factors in CHF in children
o Fever*
o Infection*
o Fluid losses*
o Electrolyte imbalance
o Anemia
o Dysrhythmia/Arrhythmia
*will also manifest tachycardia (HR); address or control these first before addressing HF
E. Causes of Heart Failure in Children

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OS 213: Circulation and Respiration

LEC 20: CONGESTIVE HEART FAILURE IN CHILDREN
Exam # 1 | Dr. Connie Sison | August 1, 2012
At Birth
Structural abnormalities
o Hypoplastic Left Heart Syndrome (HLHS)
o Volume overload lesions
Tricuspid Regurgitation
Pulmonary Regurgitation
Systemic Arteriovenous Fistula
Heart rate abnormalities
o Supraventricular Tachycardia
o Congenital Complete Heart Block
Myocarditis
1st Week of Life
Structural abnormalities
o TGA
o PDA (premature infants)
o HLHS
o TAPVR (Total Anomalous Pulmonary Venous Return; w/ obstruction)
o Critical AS (Aortic Stenosis), Coarctation of Aorta, Interrupted Aortic Arch
o Critical PS (Pulmonary Stenosis)
1st Two Months of Life
Decreased pulmonary vascular resistance (due to increased flow of blood to the lungs) compared to the first weeks
of life)
Structural abnormalities
o Left to Right Shunts
Aortic level shunt (e.g. PDA)
Ventricular level shunt (e.g. VSD)
Atrial level shunt (e.g. TAPVR)
o Left-sided obstructive lesions
o Others: Anomalous origin of LCA (Left Coronary Artery) from PA (Pulmonary Artery)
Pulmonary Abnormalities/Chronic Hypoxia (Right-Heart Failure)
o Increase pulmonary artery pressure; pose a higher resistance to right ventricle
o CNS Hypoventilation
o Upper Airway Obstruction
o Broncho-Pulmonary Dysplasia
Heart Muscle Abnormalities
o Cardiomyopathy/EFE (Endocardial Fibroelastosis)
o Myocarditis
o Pompes diseases
Older Children
Acquired Heart Diseases
o Infective endocarditis
o Rheumatic fever & heart disease (5-15 y.o.)
o Myocarditis
o Cardiomyopathy
o Pericarditis
o Cor pulmonale
Congenital Heart Disease
o Unoperated end stage
o Pulmonary hypertension
o Post-operative heart failure
Others
o Infective endocarditis
o Dysrhythmias
o Systemic hypertension
Anemia

V. MANAGEMENT AND TREATMENT

GOALS:
o Augment oxygen delivery
o Temper physiologic (over)compensations
TYPES:
o Non-Pharmacologic

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OS 213: Circulation and Respiration

LEC 20: CONGESTIVE HEART FAILURE IN CHILDREN
Exam # 1 | Dr. Connie Sison | August 1, 2012
o Surgical
o Pharmacologic

A. Non-Pharmacologic
Bed rest; use high back-rest (or just carry the baby on its back); use cardiac chair
O2; ventilatory support; pulmophysiotherapy
Thermoregulation
Appropriate fluid therapy
Nutritional support calories and K+ supplement
Treat associated problems first: anemia and infection (because these may aggravate the manifestations of Heart
Failure and Heart Failure itself)

B. Surgical
Definitive depends on the type of CHD (e.g. VSD closure, PDA transection/ligation, arterial switch operation)
Palliative done to postpone surgery for 6 months until definitive surgery can be done; a usual occurrence in PGH
due to high costs of definitive surgery; usually costs around 20k only (e.g. pulmonary artery banding, man-made
pulmonic valve stenosis)
C. Pharmacologic
Enhance Oxygen Delivery/Increase Cardiac Output
o Augment Myocardial Contractility (for acute HF)
DIGOXIN/LANOXIN
-AGONISTS: Dobutamine, Dopamine
BIPYRIDINES: Milrinone (an inotrope vasodilator)

Tempre compensatory mechanisms

o Decrease Preload/ Volume Overload

DIURETICS: Furosemide, Spirinolactone

VENOUS DILATORS: Nitroglycerin

o Decrease Afterload

ACE INHIBITORS: Captopril, Enalapril

BIPYRIDINES: Milrinone
ARTERIAL VASODILATORS: Nitroglycerin

o Decrease Catecholamine/Sympathetic Effects

-BLOCKERS: Carvedilol

Prevent progressive cell death and structural deterioration

o ALDOSTERONE ANTAGONISTS
o -BLOCKERS
o ACE INHIBITORS
o ARBs (Angiotensin II Receptor Blockers)
o Substances which cause LV Remodeling and deterioration of the heart

Sympathetic s
Aldosterone
Angiotensin II

VI. SUMMARY
Pathophysiology is basically similar to adult CHF.
Clinical manifestations and treatment are grounded on the same principles as adult CHF.
Diagnosis of CHF is based on History and PE
Diagnosis of cause is based on presentation & age group
Chest x-ray, ECG, & echocardiogram are essential in diagnosis and treatment of CHF.
Medical treatment is geared towards augmenting oxygen delivery, decreasing oxygen demand, and
tempering compensatory mechanisms.
Surgery and/or cardiac catherization intervention is often necessary for definitive treatment.

END OF TRANSCRIPTION
James: Kung may game manuod ng cinemalaya sa Diliman, sabihan niyo ko! Tara, punta tayo!
Marky: Omg, Im scared that Nico will okray our formatting. HEEHEE! AND TO THE TRANS COMM HEAD: HELLO, Queen
Elizabeth shall bear down the Hand of Justice. CHOS. :))
Allie: Trese Pwede, halloo. May alam ba kayong pwedeng pagpa-print-an ng t-shirt natin? Lampas isang taon na eh.
Jejeje. Shameless recommendation, ba: My Body is a Cage Peter Gabriel. Or the Arcade Fire version.

MARKY, JAMES, ALLIE

UPCM 2016 B: XVI, Walang

Kapantay!

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