CONGESTIVE HEART FAILURE
Regente Imperial Lapak, MD, FPPS
October 15, 2014 ; 8:00 – 10:00 AM
Pediatrics 2
CONGESTIVE HEART FAILURE
 A condition in which the heart cannot pump
enough oxygenated blood to meet the needs of
the body's organs. The heart pumps
inefficiently.
CARDIAC OUTPUT
 Defined as the amount of blood that is pumped
by the heart per minute
CARDIAC INDEX (CI)
 The hemodynamic parameter that relates
the cardiac output to thebody surface area
Cardiac output is defined as the
stroke volume x heart rate
Stroke volume is divided into three:
Preload, Afterload, Contractility
A. PRELOAD
 It is the amount of blood that fills the ventricles
during end diastole (VOLUME WORK)
B. AFTERLOAD
 The pressure that the left ventricle must
counteract to pump adequate amount of blood
into the circulation (PRESSURE WORK)
The normal systemic pressure in the aorta is
95mmHg and above. But, if the pressure is
≥140mmHg, then that’s hypertension.
C. CONTRACTILITY
 Inherent capacity of the heart muscle to
contract and relax
HEART RATE
 Number of beats per minute
 Tachyarrhythmia and bradyarrhythmia can lead
to heart failure
The SA node paces the electrical impulses in
the heart and therefore the heart rate.
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Slide notes:
Automaticity is the property of cardiac cells to
generate spontaneous action potentials. Spontaneous
activity is the result of diastolic depolarization caused by a
net inward current during phase 4 of the action potential,
which progressively brings the membrane potential to
threshold. The sinoatrial (SA) node normally displays the
highest intrinsic rate. All other pacemakers are referred to as
subsidiary or latent pacemakers because they take over the
function of initiating excitation of the heart only when the
SA node is unable to generate impulses or when these
impulses fail to propagate. There is a hierarchy of intrinsic
rates of subsidiary pacemakers that have normal
automaticity: atrial pacemakers have faster intrinsic rates
than AV junctional pacemakers, and AV junctional
pacemakers have faster rates than ventricular pacemakers.
In normal sinus rhythm, the SA node initiates
action potentials at 60–100/min that are conducted to
the atrioventricular (AV) node, which coordinates the
sequential contraction of the upper (atrial) and then lower
(ventricular) chambers of the heart. If the SA node fails to
provide action potentials, the AV node can independently
generate action potentials at 40–60 beats per minute.
Subsequent transmission of the action potential to the
ventricles is via specialized heart cells (cardiomyocytes) in
the right and left bundle branches and Purkinje fibers that
spread throughout the ventricles. These conduction cells
contain increased numbers of sodium ion channels and
mitochondria while containing fewer cardiac muscle fibers. If
both the SA and the AV nodes fail to provide an action
potential, the Purkinje fibers or ventricular myocytes can
also produce a coordinated contraction at rates slower than
the AV node.
Although the SA and the AV nodes and Purkinje
fibers can independently initiate and continue action
potentials, which provide heart contractions, the vagal
nerves (parasympathetic nerves causing a decreased SA
node rate and force of contraction) and thoracic nerves T1–4
(sympathetic nerves resulting in increased SA node rate as
well as force of contraction) also convey neurological
influences on heart rate. Hormones/neurotransmitters such
as epinephrine (adrenaline) and dopamine increase heart
rate and/or the amount of blood pumped per contraction
(stroke volume). Epinephrine works via binding to 1-, 2-
, 1 and 2-adrenergic, G-protein-coupled receptors. The
receptor signal transduction includes activation of
phospholipase C to increase production of inositol
phosphates/diacylglycerol, protein kinase C activity, and the
release of Ca2+ (1-/Gq protein). Additionally, there will be
inhibition (2-/Gi protein) or activation (1 and 2-/Gs protein) of
adenylyl cyclase to decrease or increase
cyclic adenosine monophosphate (cAMP) production and
protein kinase A activity, respectively (see Chapter 8 for
review of G-protein activities).
HEART RATES IN NORMAL CHILDREN

AWAKE SLEEPING
AGE MEAN
RATE RATE
Newborn to 3mo. 85 to 205 140 80 to 160
3 mo. to 2 yrs 100 to 190 130 75 to 160
2 yrs to 10 yrs 60 to 140 80 60 to 90
More than 10 yrs 60 to 100 75 50 to 90

PATHOPHYSIOLOGY
 Heart failure is caused by any condition which
reduces the efficiency of the myocardium, or
heart muscle, through damage or overloading.
 Congestive heart failure can affect the right side
of the heart, the left side of the heart, or both
sides.
 When the right side of the heart begins to
function less efficiently, it is unable to pump
much blood forward into the vessels of the
lungs. Because of the congestion in the right
side of the heart, blood flow begins to back
up into the veins. Eventually, swelling
(edema) is noticed in the feet, ankles,
eyelids and abdomen due to fluid retention.
 When the left side of the heart fails, it is
unable to pump blood forward to the body
efficiently. Blood begins to back up into
the vessels in the lungs and the lungs
become stressed. Breathing becomes faster
and more difficult. The body does not receive
enough blood to meet its needs, resulting in
fatigue and poor growth.
 Reduced contractility or force of contraction,
due to overloading of the ventricle.
 In a normal heart, increased filling of the
ventricle results in increased contractility (by
the Frank-Starling’s Law of the Heart) and
thus a rise in cardiac output. In heart failure
this mechanism fails, as the ventricle is loaded
with blood to the point where heart muscle
contraction becomes less efficient. This is due
to reduced ability to cross-link actin and myosin
filaments in over-stretched heart muscle.
FRANK-STARLING’S LAW OF THE HEART
 States that the STROKE VOLUME of the
heart increases in response to an increase
in the volume of blood filling the heart
(end diastolic volume) when all other factors
remain constant
As the amount of blood in the left ventricle
increases, the stroke volume also increases, unless the
volume of blood in the left ventricle exceeds its
capacity. When that happens, there will be heart
failure.
As you increase the volume, there is an increase
in contractility; however, if you overstretch your ventricles,
there will be congestive heart failure and you will have a
decrease in cardiac output. Giving inotropes will lead to
improvement in cardiac output.
The higher the left end-diastolic pressure, the
greater the cardiac output; however, if it is beyond the
capacity of the ventricle, your cardiac index decreases,
leading to congestive heart failure.
Cardiac index (CI) is a haemodynamic parameter that
relates the cardiac output to the body surface area.
REDUCED STROKE VOLUME
 Can be a result of a failure of systole, diastole or
both
 Increased end systolic volume is usually caused
by reduced contractility
 Decreased end diastolic volume results from
impaired ventricular filling – as occurs when the
compliance of the ventricle falls (i.e. when the
walls stiffen)
REDUCED SPARE CAPACITY
 As the heart works harder to meet normal
metabolic demands, the amount that the
cardiac output can increase in times of
increased oxygen demand (e.g. exercise) is
reduced
 This contributes to the exercise intolerance
commonly seen in heart failure
 This translates to the loss of one's cardiac
reserve
 Cardiac reserve: the ability of the
heart to work harder during exercise or
strenuous activity
INCREASED HEART RATE (TACHYCARDIA)
 Stimulated by increased sympathetic activity to
maintain cardiac output
 initially, this helps compensate for heart failure
by maintaining blood pressure and perfusion
 places further strain on the myocardium,
increasing coronary perfusion requirements
 can lead to worsening of ischemic heart disease
 Sympathetic activity may also cause potentially
fatal arrhythmias

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HYPERTROPHY VOLUME OVERLOAD
 An increase in physical size of the myocardium  Great vessel level shunts
 Caused by the terminally differentiated heart  PDA, truncus arteriosus
muscle fibers increasing in size  Aortopulmonary window
 An attempt to improve contractility  Ventricular level shunts
 May contribute to the increased stiffness and  VSD, single ventricle w/o pulmonic
decreased ability to relax during diastole stenosis
 Atrioventricular canal
ENLARGEMENT OF THE VENTRICLES  Arteriovenous fistula
 Contributes to the enlargement and spherical
shape of the failing heart CAUSES OF CONGESTIVE HEART FAILURE
 Increase in ventricular volume also causes a IN INFANTS (UP TO 1 YEAR OLD)
reduction in stroke volume due to mechanical
and contractile inefficiency. VOLUME OVERLOAD
 Great vessel level shunts
CAUSES OF HEART FAILURE IN  PDA, truncus arteriosus,
DIFFERENT AGE GROUPS  Aortopulmonary window
 Ventricular level shunts
 Isolated VSD, VSD, w/ transposition
CAUSES OF HEART FAILURE IN UTERO  VSD w/ tricuspid atresia, Single shunts
 Atrial level shunts
ANEMIA  Total anomalous pulmonary venous
 Hemolytic sec. to RH sensitization return
 Fetal maternal transfusion  Heart muscle abnormalities
 Hypoplastic anemia  Endocardial fibroelastosis, myocarditis,
viral, Kawasaki disease
ARRHYTHMIAS  Glycogen storage disease (Pompe’s)
 Supraventricular tachycardia  Secondary heart failure
 Atrial fibrillation  Renal disease, hypertension,
 Atrial flutter hypothyroidism, sepsis
 Ventricular tachycardia
 Complete heart block CAUSES OF CONGESTIVE HEART FAILURE
IN CHILDHOOD
VOLUME OVERLOAD
 Palliated congenital heart disease
 Atrioventricular valve regurgitation in AV canal
 Atrioventricular valve regurgitation
 Tricuspid regurgitation in Ebstein’s disease
 Rheumatic fever
 Arteriovenous fistula
 Viral myocarditis
MYOCARDITIS  Bacterial endocarditis
 Secondary causes
 Hypertension secondary to
CAUSES OF CONGESTIVE HEART FAILURE
glumerulonephritis
IN NEONATES(UP TO 28 DAYS OLD)  Thyrotoxicosis
 Doxorubicin (Adriamycin)
PRESSURE OVERLOAD cardiomyopathy (treating leukemia)
 Aortic stenosis  Sickle cell anemia
 Coarctation of the aorta  Cor pulmonale 2o to cystic fibrosis
 Hypoplastic left heart syndrome
HEMODYNAMICS OF THE HEART
If the pulses in the lower extremities are
weaker than the upper extremities, then, there is a Remember that the right side of the heart
high index of suspicion that that is a case of receives the unoxygenated blood, which has 75%
COARCTATION OF THE AORTA. The same holds true oxygen, because it came from the systemic circulation.
for the blood pressure. Normally, the lower extremity So the blood enters the right atrium, the right
would have higher blood pressure compared to the ventricle, the main pulmonary artery, then the right
upper extremity. If the reverse is true, then patient and left pulmonary artery, until it reaches the lungs. In
might be suffering from coarctation of the aorta. the alveoli, there will be gas exchange. The carbon
Remember, if the weaker pulse is on the LEFT dioxide will be blown off during expiration, the oxygen
extremity only, then the coarctation is on the LEFT will then diffuse in the blood, go through the
SUBCLAVIAN artery. If it’s on the RIGHT only, then pulmonary vein, and later on enter the left side of the
the coarctation is on the RIGHT SUBCLAVIAN heart. The O2 saturation then becomes about 95%.
ARTERY.

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  Obstruction
 Coarctation of aorta,
aortic stenosis, pulmonary EXCESSIVE AFTERLOAD
stenosis, mitral stenosis
 Hypertension
 Tacyarrhythmias-
ventricular/
EXCESSIVE HEART RATE
supraventricular
tachycardia
 Bradycardia- complete
heart block or sick sinus INADEQUATE HEART RATE
syndrome
 Myocarditis, dilated
cardiomyopathy
 Ischemic or hypoxic cardiac
injury hormonal or
electrolyte disturbances INADEQUATE CONTRACTILITY
(hypothyroidism,
hypocalcemia,
hypoglycemia,
hypomagnesemia)

In left-to-right shunting, ang nahihirapan ay

ang left ventricle because of INCREASED PRELOAD.
The same holds true for VSD, ASD, and PDA.

For cyanotic heart diseases, there is

LA pressure is 4mmHg as compared to the
RA pressure, which is 2mmHg. There is a pressure
gradient of 2mmHg. The pressure in the lungs is the
same as RV pressure, while the pressure in the
aorta is the same as the LV pressure. If the pressure
is above 140mmHg, you are hypertensive.
The presence of a shunt between the
ventricles (VSD) will create a murmur because of
the high pressure difference between the RV and
the LV, while a shunt between the atria (ASD) will
not create a murmur since there is only a slight
difference in pressure between the RA and the LA.
There will only be a systolic ejection murmur in ASD
due to relative pulmonary stenosis; there is volume
overload in the RV. In short, the murmur that you
hear in ASD is NOT due to the left-to-right shunt
itself.
INCREASED PRELOAD because of the shunting of
blood. In TOF, there is difficulty in pumping blood to
the pulmonary circulation; that is why unoxygenated
blood will go through the ASD and eventually the
unoxygenated blood will be ejected from the left
ventricle (they are cyanotic kasi unoxygenated blood
ang humahalo sa systemic circulation). The pressure
from the right ventricle is almost equal to the pressure
in the left ventricle because of the large VSD. A small
VSD (or ASD) will not cause heart failure because it
is simply just small.
Rheumatic heart disease will also cause
INCREASED PRELOAD because of the regurgitation of
blood, causing pooling of the blood.
Obstruction causes EXCESSIVE AFTERLOAD
because there is increased pressure that the left
ventricle will need to overcome to be able to maintain
systemic blood pressure and flow. The same is true
with mitral stenosis, where the atrium will need to
overcome a higher amount of pressure.
Patients who have dilated cardiomyopathy
have a poor prognosis. Treatment for their condition is
heart transplant.

DEFECT/ DISEASE PRIMARY EFFECT

 Left-to-right shunts
 VSD, ASD, PDA, AV canal
 Aortopulmonary window,
absent pulmonary valve
 Cyanotic defects
 Truncus arteriosus, TOGA EXCESSIVE PRELOAD
w/ VSD, total anomalous
pulmonary venous
drainage, hypoplastic left
heart
 Rheumatic heart disease

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VENTRICULAR SEPTAL DEFECT
In physics, we are taught that liquids like
blood flow from a chamber of high pressure to a
chamber of lower pressure. If there is a hole between
the ventricles, aside from the blood that will flow to
the aorta, some of the blood will enter the right
ventricle. This is called Left-to-Right Shunting. When
you auscultate a patient with VSD, you will hear a
murmur (lub-woosh-dub). (Hahaha imagine niyo na
lang yung sound. :D)
AGAIN, if there is interatrial shunting, you
will not hear a sound (murmur) because of the small
pressure difference. The shunting in ASD will not
create a turbulence, while that of a VSD will. The
murmur that you hear in ASD is because of the
pulmonary stenosis and not because of the shunting.
SIGNS AND SYMPTOMS OF
RIGHT SIDED VS LEFT SIDED HEART
FAILURE
SIGNS OF LEFT-SIDED FAILURE
 Tachypnea
 Rales or crackles –suggestive of pulmonary
edema
 Cyanosis – suggestive of severe hypoxemia; a
late sign of extremely severe pulmonary edema
 Laterally displaced apex beat
 Gallop rhythm
 Heart murmurs may indicate the presence of
valvular heart disease, either as a cause (e.g.
aortic stenosis) or as a result (e.g., mitral
regurgitation) of the heart failure
SIGNS OF RIGHT-SIDED FAILURE
 Pitting peripheral edema
 Ascites
 Hepatomegaly (check liver size via percussion!)
 Increased jugular venous pressure
hepatojugular reflux
 Parasternal heave
 compensatory increase in contraction
strength
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Chronic hepatomegaly will have a blunt
edge. Acute hepatomegaly will have a sharp edge.
SIGNS OF BIVENTRICULAR HEART FAILURE
 Dullness of the lung fields on percussion
 Reduced breath sounds at the bases of the
lung
 Suggestive of a pleural effusion
 Check for easy fatigability
SIGNS AND SYMPTOMS
The following are the most common symptoms of CHF.
Each child may experience symptoms differently.
Symptoms may include: visible swelling of the legs,
ankles, eyelids, face and (occasionally) abdomen
 Fast breathing during rest or exercise
 Shortness of breath or labored breathing
 Fatigue
 Need to take frequent rest breaks while playing
with friends
 Nausea
 Abdominal pain, vomiting
 Falling asleep when feeding or becoming too
tired to eat
 Lack of appetite
 Weight gain, even when the appetite is poor
 Failure to thrive
 Cough and congestion in the lungs
 Sweating
EASY FATIGUE
 Primarily caused by decreased cardiac output
 May be worsened by peripheral factors such as
abnormal autoregulation of blood flow to the
extremities and muscle deconditioning
A sign of easy fatigability in infants is
interrupted feeding. In children, they usually present
as feeling tired while playing.
DYSPNEA
 Dyspnea on exertion
VOLUME OVERLOAD
 Dyspnea, particularly sudden onset such as in
uncontrolled hypertension
 Orthopnea in ambulatory patients (ask the
number of pillows used in sleep/sleeping position)
 Paroxysmal nocturnal dyspnea (waking up in
the middle of the night with shortness of breath)
 Peripheral edema
 Weight gain– often be elicited
 Bilateral, dependent edema – may resolve after
a night’s rest
 Systemic venous hypertension – internal jugular
venous pressure level higher than 4 cm above
the sternal angle with patient sitting at a 45-
degree angle
 Moist crackles –transudation of fluid into the
alveoli in both lung bases
  Bronchospasm and associated high-pitched C. BLOOD GASES AND PH
wheezes – bronchial congestion  Quantitate the degree of hypoxemia and/or
 S3 gallop – rapid ventricular diastolic filling metabolic acidemia
 Abdomino-jugular reflux  Mild respiratory acidemia (alveolar edema)
 Hepatomegaly and tenderness– hepatic  Severe HF, pulmonary venous
congestion obstruction (vol. overloading)
 Respiratory alkalosis (interstitial edema)
PULSUS PARADOXUS(PP), also paradoxic pulse  Mild HF
and paradoxical pulse, is an exaggeration of the normal  Metabolic acidemia
variation in the pulse during the inspiratory phase of  Severe compromise of systemic
respiration, in which the pulse becomes weaker as one perfusion
inhales and stronger as one exhales. It is a sign that is  Extremely low oxygen tension
indicative of several conditions including cardiac  Obstruction to pulmonary bloody flow
tamponade, pericarditis, chronic sleep apnea, croup, and  Patients with TGA
obstructive lung disease (e.g. asthma, COPD).  Hemoglobin and hematocrit
 Decreased- severe anemia may worsen
CARDIAC REMODELING CHF(if hemoglobin value is 6)
 Cardiomegaly is also a nonspecific yet common  Increased – twin to twin transfusion,
sign in HF patients. placental transfusion
 Polycythemia – reflects significant
DIAGNOSIS systemic desaturation
 Blood Tests  WBC count
 Serum Na & K  May be seen elevated
 Renal function tests – BUN, Crea  Not necessarily signify
 Liver function tests – SOGT, SGPT, Alk infection
Phos  Leukopenia
 Thyroid function tests - TSH T3 T4  Seen in viral myocarditis
 Complete blood count  Sedimentation rate
 C-reactive protein  Elevated- active inflammatory process
 B-type natriuretic peptide is present
 Cardiac markers  However, in severe congestive heart
 Chest x-ray failure the ESR may be low initially, but
 15 leads ECG once the patient is out of the congestive
 2D Echocardiography heart failure it will shoot up

D. CHEST X-RAY
LABORATORY EXAMINATION
 Presence of enlarged cardiac silhouette which
represents ventricular dilatation and/ or
A. ECHOCARDIOGRAPHY
hypertrophy
 Essential to elaborate cardiac arrhythmias
 Cardiac size may be normal
 Use to assess myocardial function with the
 Early stages of myocarditis
measurement of
 Tachydysrhythmias
 Right and left ventricular dimensions
 Obstruction to pulmonary venous
 Circumferential fiber shortening rate
return
 Ejection fraction/FS (should be 50% and
 Pericardial constriction
above.)
 Presence of pulmonary congestion and
 Systolic time interval
association of inflammatory disease
 Use for pericardial effusion
 Barium instillation is avoided because of the
 The most commonly used parameter in
dangers of aspiration
children is FRACTIONAL SHORTENING (a
single dimensional variable), determined as the
difference between end-systolic and end-
diastolic diameter divided by end-diastolic
diameter. Normal fractional shortening is
between 28% and 40%.

B. ELECTROCARDIOGRAM
 Most useful non-invasive tool in assessing
major intracardiac defect
 Nonspecific T wave changes and alterations in
the ST segment occur
 Increase in the height of P wave
 Myocarditis – low voltage with T wave
abnormalities

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MANAGEMENT AND TREATMENT
Treatment is based on:
 Child's age, overall health and medical history
 Extent of the disease
 Child's tolerance for specific medications
 Procedures or therapies
 Doctor’s expectations on the disease
NYHA HEART FAILURE CLASSIFICATION
 Applicable for patients 6 years old and above only
 Without limitations of physical activity
CLASS I  Ordinary physical activity does not cause
undue fatigue, palpitation, or dyspnea
 Slight limitation of physical activity.
 They are comfortable at rest.
CLASS II
 Ordinary physical activity results in
fatigue, palpitation, or dyspnea
 Marked limitation of physical activity.
 They are comfortable at rest.
CLASS III
 Less than ordinary activity causes
fatigue, palpitation, or dyspnea.
 Inability to carry on any physical activity
without discomfort.
CLASS IV
 Symptoms are present even at rest or
minimal exertion.
TREATMENT
GENERAL MEASURES
 Strict bed rest is rarely necessary except in
extreme cases
 Limit fluid intake – compute base on BSA
 Semi-upright sleeping position – for some older
children
 Avoidance of strenuous sports activities
 Positive pressure ventilation – for pulmonary
edema patients
DIET
 Increasing the number of calories per ounce of
infant formula is beneficial
 Severely ill infants - nasogastric feedings may
be helpful
PHARMACOLOGIC
1. DIURETICS
 Interferes with reabsorption of water and
sodium by the kidneys
 Result: reduction in circulating blood volume 
reduces pulmonary fluid overload and
ventricular filling pressure.
 This is most often used in conjunction with
digitalis therapy in patients with severe
congestive heart failure
FUROSEMIDE
 Most commonly used diuretic in patients with
heart failure
 Inhibits the reabsorption of sodium and chloride
in distal tubules, loop of Henle
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 Initial dose: 1–2 mg/kg,  rapid
diuresis/prompt improvement
 Careful monitoring of electrolytes necessary
due to loss of potassium
 Potassium chloride supplementation usually
required (example: spironolactone)
 Potassium-sparing diuretic spironolactone ( 1-2
mg/kg/day)is given concomitantly.
When giving diurectics, always weigh the
patient everyday to know the extent of decrease in
heart rate due to dieresis.
2. INOTROPES
DIGOXIN/DIGITALIS (INOTROPE)
 The mainstay of heart failure management in
both children and adults
 Many cardiologists will use digitalis as adjunct
to ACE inhibitors and diuretics in patients with
symptomatic heart failure
 Digitalis compounds are potent inhibitors of
cellular Na+/K+-ATPase. This ion transport
system moves sodium ions out of the cell and
brings potassium ions into the cell.
 By inhibiting the Na+/K+-ATPase, cardiac
glycosides cause intracellular sodium
concentration to increase. This then leads to an
accumulation of intracellular calcium via the
+ ++
Na -Ca exchange system. In the heart,
increased intracellular calcium causes more
calcium to be released by the sarcoplasmic
reticulum, thereby making more calcium
available to bind to troponin-C, which increases
contractility (inotropy). Inhibition of the
Na+/K+-ATPase in vascular smooth muscle
causes depolarization, which causes smooth
muscle contraction and vasoconstriction.
THERAPEUTIC USES OF DIGITALIS COMPOUNDS
HEART FAILURE
 ↑ inotropy (contractility)
 ↑ ejection fraction
 ↓ preload (diuretic effect)
 ↓ pulmonary congestion/edema
ARRHYTHMIAS 3. Β-ADRENERGIC AGONISTS (CATHECOLAMINES)
 ↓ AV nodal conduction
(parasympathomimetic effect) Beta 1 RECEPTOR
 ↓ ventricular rate in atrial flutter  Main article: Beta-1 adrenergic receptor
and fibrillation  Specific actions of the β1 receptor include:
 Increase cardiac output, by raising heart rate
ACTION DOSAGE (positive chronotropic effect) and increasing
Premature impulse conduction and increasing contraction
0.02-0.025 mg/kg thus increasing the volume expelled with each
beat (increased ejection fraction).
Neonate (1 month or  Renin release from juxtaglomerular cells.
younger)  Lipolysis in adipose tissue.
Digitalization (PO) 0.03-0.04 mg/kg
(3 doses q 8 hr) a) DOPAMINE
Infant or Child  The pharmacodynamic effects of dopamine, an
0.04-0.06 mg/kg endogenous catecholamine, are complex and
mediated through selective activation of
Adolescent or Adult specific dopaminergic and adrenergic receptors
1.0-1.5 mg in divided doses in a dose dependent manner.
Digitalization (I.V.)  Dopamine improves heart output and may
(Timing of Dosage raise blood pressure. It is a continuous IV
75% of PO dose
variable, depending on infusion. It increases the amount of
clinical indications) norepinephrine activity in the body. Dopamine
is often used to help get rid of edema because
EXERCISE COMPUTATIONS of how it affects receptors in the kidney's blood
Stock dose of Lanoxin elixir is 0.05mg/ml vessels.
1. Compute loading and maintenance dose of  Low dose dopamine (Renal dose)(0.5-2
Digitalis elixir for a 5 years patient with BW of micro g/kg/min) induces intrarenal
10 kg. vasodilatation, augmented renal blood flow,
2. Compute Digitalis elixir (loading dose) for a 5 and inhibition of renal tubular sodium
years patient with BW of 10 kg reabsorption through direct stimulation of
peripheral dopaminergic receptors DA1 and
10 x 0.04 mg = 0.4 divided 4 = 0.1 divided 0.05 DA2.
= 2 ml  Intermediate doses (Cardiac dose) (3-10
micro g/kg/min) favor beta (1)-adrenergic
Maintenance Dose receptor stimulation of the heart and peripheral
10 x 0.04 mg = 0.4 divided 10 = 0.004 divided 0.05 vasoconstriction (increase blood pressure) due
= 0.8 ml to alpha-adrenergic receptor stimulation.

3. Compute loading and maintenance dose (IV) of

In higher doses, there is decreased blood flow
Digitalis for a 3 years patient with BW of 8 kg
to the kidneys.
Stock dose = 0.25 mg/ml

4. Compute loading and maintenance dose (IV) of EFFECTS OF DOPAMINE

Digitalis for a 3 years patient with BW of 8 kg .  Increase cardiac output, by raising heart rate
Stock dose = 0.25 mg/ml (positive chronotropic effect) and increasing
impulse conduction and increasing contraction
Maintenance dose thus increasing the volume expelled with each
8 x 0.04 x 0.70 = 0.224 divided 10 = 0.022 mg beat (increased ejection fraction).
0.022/x =0.25/1= 0.088  At higher does (>10 micro g/kg/min), an
elevated systemic vascular resistance prevails
5. Compute loading and maintenance dose (IV) of and the salutary effect on renal blood flow is
Digitalis for a 3 years patient with BW of 8 kg . diminished or lost.
 In short, DO NOT give a high dose of
Stock dose = 0.25 mg/ml dopamine

Wt x dose x 70% b) DOBUTAMINE

8 x 0.04 x 0.70 = 0.224 divided 4  Dobutamine is a direct-acting agent whose
primary activity results from stimulation of the
= 0.056 mg
β1-adrenoceptors of the heart, increasing
contractility and cardiac output. Since it does
Ratio and proportion
not act on dopamine receptors to induce the
0.056/x = 0.25/1 =0.22 ml
release of norepinephrine (another α1 agonist),

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 dobutamine is less prone to induce
hypertension than is dopamine.
 Dobutamine improves heart function and may
lower blood pressure. It is used as a continuous
IV infusion. It helps the body make more use of
a substance called norepinephrine, which the
body makes on its own. Norepinephrine
stimulates the heart to work harder. Potential
side effects include irregular heart rhythm
(although less than with dopamine), and
increased demand for oxygen by the heart
 Dobutamine is predominantly a β1-adrenergic
agonist, with weak β2 activity, and α1 selective
activity, although it is used clinically in cases of
cardiogenic shock for its β1inotropic effect in
increasing heart contractility and cardiac
output.
 Dobutamine also has mild β2 agonist activity,
which makes it useful as a vasodilator.
DOPAMINE & DOBUTAMINE DRIP (FORMULAS)
If there is no pre-mixed drip, use this guide!
CONCENTRATION DOPAMINE D5W
Single (800) 1 49
Double (1600) 2 48
Triple (2400) 3 47
Quadruple (3200) 4 46
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CONCENTRATION DOPAMINE D5W
Single (1000) 4 46
Double (2000) 8 42
Triple (3000) 12 38
4. PHOSPHODIESTERASE INHIBITORS
 The other main type of inotropes are drugs
called "phosphodiesterase-III inhibitors.". These
drugs make your heart beat more strongly and
also relax your blood vessels.
 Milrinone (Primacor) is the most widely used
drug of this type. Milrinone is usually given by IV
at 0.375 to 0.75 micrograms per kilogram of
body weight per minute.
 If the patient is in critical condition, an IV at 50
micrograms per kilogram of patient body
weight may be used. This has to be done very
carefully in patients with low blood pressure.
Since milrinone does not increase the heart's
oxygen demand, it is preferred over other
inotropes in patients with ischemic
cardiomyopathy. Milrinone is also better for
treating severe CHF episodes in patients taking
beta- blockers.
 Other drugs like Amrinone (Inocor) are not used
much these days because they are more likely
to cause dangerous arrhythmias. Pill forms of
some inotropes have been tried but taking
them on a regular basis increased risk of death
in CHFers. The pill forms don't seem to help
CHFers nearly as much as IV inotropes do
either.
 The cardiostimulatory and vasodilatory actions
of PDE3 inhibitors make them suitable for the
treatment of heart failure.
 Arterial dilation reduces afterload on the failing
ventricle and leads to an increase in stroke
volume and ejection fraction, as well as
increases organ perfusion. Reducing the
afterload leads to a secondary decrease in
preload on the heart that helps to improve the
mechanical efficiency of dilated hearts and to
reduce ventricular wall stress and the oxygen
demands placed on the failing heart.
 The cardiostimulatory effects of these drugs
increase inotropy, which further enhances
stroke volume and ejection fraction.
Tachycardia, however, also results, and this is
not beneficial; therefore, doses are used that
minimize the positive chronotropic actions of
the drug. A baroreceptor reflex, which occurs in
response to hypotension, may contribute to the
tachycardia
MILRINONE
 Used for patients refractory to standard therapy
highly effective in managing low-output state in
children after open heart surgery
 Use this only when all other standard
therapies do not work (aka last resort)
 A selective inhibitor of peak III cyclic adenosine
monophosphate (cAMP) phosphodiesterase
in cardiac and vascular muscle. Inhibition of this
enzyme results in an accumulation of cAMP,
 producing an increase in intracellular ionized
calcium in cardiac muscle which increases
contractile force. Increasing cAMP also
produces relaxation of vascular smooth muscle.
 Also enhances relaxation of the left ventricle by
2+
increasing Ca -ATPase activity on the cardiac
sarcoplasmic reticulum. This increases calcium
ion uptake.
 It has positive inotropic, vasodilating and
minimal chronotropic effects. It is used in the
management of heart failure only when
conventional treatment with vasodilators and
diuretics has proven insufficient. This is due to
the potentially fatal adverse effects of
Milrinone, including ventricular arrhythmias.
 Whereas beneficial hemodynamic effects are
shown (at least short-term), several studies
have shown no or a negative effect on mortality
rates of hospitalized patients receiving
Milrinone.
 One negative side to the use of Milrinone is the
prolonged half-life (1 to 2 hours). This can result
in a prolonged weaning and possible adverse
outcomes from stopping this medication
rapidly.
AFTERLOAD-REDUCING AGENTS (ANGIOTENSIN-
CONVERTING ENZYME [ACE] INHIBITORS)
 May be beneficial usually initiated in an
intensive care setting with proper invasive
monitoring of central venous and arterial blood
pressure.
 Blocks the conversion of angiotensin I to
angiotensin II. They therefore lower arteriolar
resistance and increase venous capacity;
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increase cardiac output and cardiac index,
stroke work and volume, lower renovascular
resistance, and lead to increased natriuresis
(excretion of sodium in the urine).
Premature Neonates Dose
0.1-0.4 mg/kg/day PO divided q6-24h;
Start: 0.01 mg/kg/dose; Max: 2 mg/kg/day;
Neonates Dose
0.1-0.4 mg/kg/day PO divided q6-24h;
Start: 0.05-0.1 mg/kg/dose; Max: 2 mg/kg/day;
Infants Dose
2.5-6 mg/kg/day PO divided q6-12h;
Start: 0.15-0.3 mg/kg/dose; Max: 6 mg/kg/day;
Children Dose
2.5-6 mg/kg/day PO divided q6-12h;
Start: 0.3-0.5 mg/kg/dose or 6.25-12.5 mg/dose; Max: 6
mg/kg/day
Adolescents Dose
25-50 mg PO q6-8h;
Start: 12.5-25 mg PO q8h, incr. 12.5-25 mg/dose q1-2wk;
Max: 450 mg/day
Pediatric doses based on weight should not
exceed adult doses. Because recommendations may
change, these doses should always be double-checked.
Doses may also need to be modified in any patient with
renal or hepatic dysfunction and with significant weight
changes.
REVIEW QUESTIONS. Hope this helps!

1. Preload is to _______ work, while afterload is to ________.

2. The cardiac index (CI) relates cardiac output to _________________.
3. Edema is noted in which side of heart failure?
4. What is the Frank-Starling’s Law of the Heart?
5. Give three causes of heart failure in utero.
6. What are the two types of overload that cause CHF in neonates?
7. Give three causes of CHF in childhood.
8. TRUE or FALSE: The murmur heard in patients with ASD are due to left-to-right shunting.
9. TRUE or FALSE: Small ASDs/VSDs will not cause heart failure.
10. Give signs of left-sided, right-sided and biventricular heart failure (at least two each).
11. In pulsus paradoxus, the pulse becomes _______ during exhalation.
12. What laboratory tests would you use to diagnose CHF?
13. In echocardiography, what is the most commonly used parameter for children?
14. What is the most useful non-invasive tool in assessing major intracardiac defects?
15. Another name for interstitial edema.
16. TRUE or FALSE: Cardiac size is normal during the early stages of myocarditis.
17. Furosemide is the most commonly used diuretic in CHF patients, with a dose of ______.
18. What is the mechanism of action of digoxin? What are its therapeutic uses?
19. How is dopamine administered?
20. TRUE or FALSE: An intermediate dose of dopamine is also known as the renal dose.
21. Between dopamine and dobutamine, which one is less likely to induce hypertension?
22. What is the mechanism of action of milrinone?
23. What is the formula for dopamine and dobutamine drips?

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