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OS 213: Circulation and Respiration

LEC 20: CONGESTIVE HEART FAILURE IN CHILDREN


Exam # 1 | Dr. Connie Sison | August 1, 2012
OUTLINE
I. Introduction
II. Pathophysiology of Heart Failure
A. Dangerous Compensatory Mechanisms
III. Clinical Manifestations
IV. 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
V. Management and Treatment
A. Non-Pharmacologic
B. Surgical
C. Pharmacologic
VI. 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.

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 O2 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)

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.

MARKY, JAMES, ALLIE

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

UPCM 2016 B: XVI, Walang Kapantay!

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LEC 0X: CONGESTIVE HEART FAILURE IN CHILDREN

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) SHOCK death
Feed hingal tigil 1-2 hours before volume of milk is consumed
sign of easy fatigueability

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
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 Atrio-Ventricular
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
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 yr)
3060
Toddler (13 yrs)
Preschooler (36 yrs)

2440
2234

School-age (612 yrs)


2440
Adolescent (1218 yrs)
1216
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
oxygenation and ventilation)
o Tachypnea and subcostal retractions
o Labored respiratory effort
o Nasal flaring

(compromised

use of accessory muscles of respiration

MARKY, JAMES, ALLIE

UPCM 2016 B: XVI, Walang Kapantay!

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o Grunting

infants; Dyspnea on exertion in older children


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

in an attempt to keep the alveoli open (2014)


increase end alveolar pressure

o Hacking cough
bronchial mucosal edema

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

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
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

MARKY, JAMES, ALLIE

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
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)

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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

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

V. MANAGEMENT AND TREATMENT


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

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 pagpaprint-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.

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

MARKY, JAMES, ALLIE

UPCM 2016 B: XVI, Walang Kapantay!

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