Download Cardiac failure in children

Cardiac failure in children
Associated professor
Kantemirova M.G.
Terminology
• To determine the impaired hemodynamic in
modern medical literature are used the
following "identical" terms:
• - Circulatory failure (NC)
• - Heart failure (HF)
• - Congestive cardiac failure (CHF)
It is not a diagnosis. It is a clinical syndrome.
Definition
• Congestive cardiac failure (CHF) - syndrome
that occurs due to excessive hemodynamic
load on the heart, disorders of myocardial
contractile function and / or impaird heart
rate and leads to an inability of the heart to
provide the bloodstream, providing the
metabolic needs of the body.
Types of CCF
• Acute and chronic
• Systolic and diastolic
• Left ventricular (LV) and right ventricular (RV)
Systolic CCF – it is unable to propel blood into
the aorta
Diastolic CCF – it receives inadequate blood into
the ventricular cavities
Mechanisms of heart failure
• Overloading of large volumes of pumped
blood
• Excessive loading resistance ( the presence of
obstacle to pumped blood, overloading by
pressure )
• Direct injury of the myocardium (the
infectious-inflammatory, immuneinflammatory, degenerative, hypoxic,
ischemic)
Peculiarities of the mechanisms of
heart failure in children
• More often than in adults can dominate a RV
CCF
• Characteristic (for CHD) inadequate
distribution of intracardiac venous return
• Tachyarrhythmia as a cause of heart failure
• The combination of heart failure and arterial
hypoxemia (in CHD)
• The relatively high incidence of diastolic
dysfunction
The etiology of heart failure
• Congenital heart disease
• Infectious-inflammatory diseases of the heart (myocarditis,
pericarditis, infectious endocarditis, CMP)
• Idiopathic disease (CMP, primary pulmonary hypertension,
tachyarrhythmias)
• Acquired heart defects (chronic rheumatic heart disease)
• Heart disease in systemic connective tissue disease,
vasculitis.
• Heart disease with genetic syndromes, neuromuscular
diseases, storage diseases, mitochondrial diseases.
• Hypertension.
Models of heart failure
• Cardiorenal model
• Cardiocirculotory (cardiocirculating) model
• Neurohormonal model
• Cytokine model
Cardiorenal model
• 40-60 yrs of 20th century
• Edema - the basis of CCF
• Reduction of systolic function → inability to
transfer the venous flow in adequate cardiac
output → ↑ venous p → worsening of renal
microcirculation → decline in kidney filtration
→ fluid retention
Cardiac glycosides, diuretics +
Cardiocirculotory (cardiocirculating) model
• 60-80 years of 20th century
• Decreased cardiac output → vasoconstriction
→ ↑ cardiac pre-and postloading →
worsening of cardiac function ↑ hypertrophy
and dilatation of the heart chambers →
worsening of peripheral microcirculation
Peripheral vasodilators + non-digitalis
catecholaminic inotropic agents (dopamine,
dobutomine)
Neurohormonal model
• 80-90 years of 20th century
• Violation of neurohumoral regulation in the SAS and RAAS
• Decreased cardiac output → decreased blood pressure →
worsening perfusion of organs and tissues →
•
1.activation of tissue neurohormones
•
2. baroreceptors activation → SAS and RAAS and their
major effectors (I-norepinephrine, epinephrine and II angiotensin II, aldosterone) → ↑ inotropic myocardial
function and vasoconstriction
• I and II mediators activate ADH, TNF, cytokines, endoteline
→ retantion of salt and water → vasoconstriction → cell
proliferation, remodeling of "targets“ organs (heart)
Neurohormonal model
β-blockers, ACE (angiotensin converting enzyme)
inhibitors, angiotensin receptor blockers II,
aldosterone antagonists
• The direct correlation between the activity of
renin, aldosterone and plasma catecholamines
and severity of heart failure.
• The basic system opposes the SAS-effectors and
RAAS -Natriuretic peptides (NP) - atrial (ANP)and
brain (BNP). ↑ BNP and NT-pro BNP is a sign of
CCH
Cytokine model
• Prolonged activation of the SAS and the RAAS →
• ↑ production of inflammatory mediators (TNF, IL,
endoteline) systemic inflammatory response →
remodeling of myocardium and vessel walls
• In response to the destruction of the cell → ↑
production of inflammatory mediators (TNF, IL) a local inflammatory cascade
Steroids? Monoclonal antibodies?
Classification of CHF
• Classification of heart failure by V.H.Vasilenko
N.D. Strazhesko (1935)
• International classification of heart failure of New
York Heart Association (NYNA) (1964, 1973)
• Classification of heart failure in children
byN.A.Belokon (1987)
• Classification of heart failure in children by Ross
R.D. (1987)
• Classification of CCF SSCF (2002)
Classification of CCF (N.D.Strazhesko, V.H.Vasilenko)
Degree
CCF
Ist early
stage
Clinical signs
At rest there is no sign of CCF, dyspnea and tachycardia appear on
Phys.exertion. For its detection functional tests are used ( HR, RR, BP on
.exertion).
II А d.
Dyspnea and tachycardia at rest, become worse with little physical effort. In the
lungs: congestion, on auscultation- dry and fine moist rales, more in the lower
parts. The liver is increased by 1-3 cm, no edema, can be decreased urine
output
II B d.
Much severe symptoms of circulatory disorders of the pulmonary and the
systemic circulation. Dyspnea increases with change of position of the patient
in bed, participation of supporting muscles, orthopnea, cough obsessive with
scanty sputum. Tachycardia combined with arrhytmias. The liver is increased by
3-4 cm or more, in young children - an enlarged spleen. Negative urine output,
edema, ascites, hydrothorax, hydropericardium. Metabolic, acid-base balance
shifts. Violation of the general condition.
III d.
(terminal,
dystrophic)
Irreversible morphological changes in the internal organs, cachexia. Dry skin
with trophic changes. Thirst. Negative urine output. Anasarca.
International classification of heart failure - New York
Heart Association (1964,1973) (Four classes of patients
physical tolerance)
• I. Functional class : ordinary physical activity does not cause
the patient's weakness, dyspnea, palpitations;
• II . Functional class : ordinary physical activity is
accompanied by the patient weakness, dyspnea,
palpitations - already there is a limitation of physical
activity;
• III . Functional class : patients still feel comfortable at rest,
but symptoms such as fatigue, dyspnea, palpitations occur
on exertion less intensive than usual, so there is a
significant limitation of physical activity;
• IV. Functional class: distinct symptoms of heart failure are
already determined at rest, patients are not able to carry
out even minimal physical activity;
Classification of CCF SSCF (2002)
Degree of CCF
I d.
The initial stage of heart
disease. Hemodynamics
is not impared. Latent
heart failure.
Asymptomatic LV
dysfunction.
FC of CCF
I fc
Ordinary physical
activity does not cause
the patient's weakness,
dyspnea, palpitations;
Classification of CCF SSCF (2002)
Degree of CCF
II d.
Symptomatic stage heart
disease. Moderate
hemodynamic instability in
the pulmonary or systemic
circulation. Adaptive
remodeling of the heart
and blood vessels.
FC of CCF
II fc.
Slight limitation of
physical activity: no
symptoms at rest, usual
physical activity is
accompanied by fatigue,
shortness of breath and
palpitations.
Classification of CCF SSCF (2002)
Degree of CCF
III
d.
Severe stage of heart
disease. Hemodynamic
changes in both
circulations expressed
moderately. Nonadaptive
remodeling of the heart
and blood vessels.
FC of CCF
III
fc.
A marked limitation of
physical activity: no
symptoms at rest,
physical activity is a lower
intensity than usually
accompanied by
symptoms CCF
Classification of CCF SSCF (2002)
Degree of CCF
IV
d.
End-stage heart disease.
Pronounced changes in
hemodynamics and
severe (irreversible)
structural changes of
target organs (heart,
lungs, blood vessels,
brain, kidneys). The final
stage of remodeling
FC of CCF
IV fc
Can not do anything
without causing
discomfort, symptoms of
heart failure are present at
rest and increase with
minimal physical activity.
Parameters of physical activity in patients with
various FC of CCF
FC
Distance 6-minute walk(m)
0
≥ 551
I
II
III
IV
426-550
301-425
151-300
≤ 150
Clinical manifestations of ССF
• Decrease in exercise (physical) tolerance
• Delay of physical development
• Dyspnea (orthopnea, tachypnea, dyspnea), participation of the
accessory muscles in breathing
• Wheezing in the lungs , dry and moist rales (lower lateral parts of
the lungs, mainly on the left → over the entire surface of the heart)
• Tachycardia (sometimes bradycardia), cardiomegaly, muffled heart
sounds, gallop rhythm, the murmur of the relative insufficiency of
atrio-ventricular valves
• Hepatomegaly, tenderness to palpation of it, mild spleenomegaly
• Gastrointestinal symptoms (congestion of mesenteric vessels and
congestive gastritis)
• Edema (more common in older children in the second part of a day)
feet → leg → sacrum → face
• Hydrothorax, hydropericardium, ascites
Symptoms of heart failure in infants.
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Insufficient weight gain
Difficulties in feeding
Tachypnea
Coughing and wheezing
Anxiety, fatigue, excessive sweating
Hepatomegaly, moderate splenomegaly
Small volume pulse
Peripheral cyanosis
Swelling of the face
Swelling of the feet
Laboratory and instrumental diagnostics
-ECG (overloading, hypertrophy, deviation of ECA, rhythm and
conduction disturbances, ST-T disorders, symptoms hypokaliemia)
-ECG monitoring
-Radiography in frontal and lateral views (cardiomegaly ; patter of
arterial or venous hypervolemia)
-echocardiography
-Laboratory tests: total blood count, electrolytes, creatinine, glucose,
liver function tests, the natriuretic peptides (BNP, NT-pro BNP),
troponin I or T
-MRI of the heart
-CT angiography of the heart
-radioisotope methods
-Exercise testing (VEM, treadmill test)
-coronary angiography
-Right heart catheterization
-endomyocardial biopsy
Acute pulmonary edema
General principles of treatment CCF IN
CHILDREN
•
•
•
The motor activity.
Diet.
Drug therapy.
The motor activity.
• Strict bed rest
•
at CCF II B - III d.
• Relief-bed rest
• II A d.
• rooms regime at I d of CCF
+Physical therapy and massage
Diet therapy
• I d.-IIA d. CCF - Limiting fatty, fried, smoked, extractive food, salt
• II B-III d CCF - -Limiting fatty, fried, smoked, extractive food, salt and
water
• Recommended products: potatoes, apricots, dried apricots, cheese,
milk
Delete: meat and fish broth, smoked meat, strong tea, coffee,
chocolate
Limited to: beans, cabbage, rye bread
• Infants : the total volume of fluid with feeding - 80% of the age
norm, the frequency of feeding ↑ 1-2 times, milk-formula with
increased calories, periodic infusion of 10-20% glucose, switching to
tube feeding (stable gain at 140 -200 kcal / kg per day) –
• The daily weigh the child
Fluid restriction
• II d. CCF
Fluid volume = the diuresis of previous day.
•
II B d.-III d. CCF - No more than 600-800
ml per day
Temperature conditions in newborns
• To ensure body t 36 ◦ - environment t - 32-34
↑ t - uncontrolled tachycardia, vasodilation, reducing
blood pressure to shock, convulsions
↓ t - peripheral vasoconstriction, increased hypoxia,
acidosis, the risk of respiratory arrest
Principles of drug therapy
Decrease the metabolic needs of the body and myocardium
(regime, food, t ◦)
Effects on blood volume (diuretics, diet)
Neurohormonal modulation (ACE inhibitors, angiotensin
receptor blockers II, aldosterone antagonists, β-blockers,
digoxin)
Effects on pulmonary resistance or peripheral vascular (NO, O2,
vasodilators, ACE inhibitors)
Effects on myocardial contractility (digoxin, β-adrenergic
agonists: dobutamine, dopamine, dopaminergic drugs,
phosphodiesterase inhibitors: amrinone,;cardiocytoprotectors)
Regulation of heart rate (atropine, izadrin, obzidan, amyodoron,
sotalex)
Treatment and prevention of thrombosis and embolism
Drug therapy
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Angiotensin-converting enzyme (ACE) inhibitors
diuretics
Cardiac glycosides, dobutamine, dopamine
Beta-blockers
aldosterone antagonists
Angiotenzine II receptor blockers
Drugs that improve myocardial metabolism and trophic
Antiplatelet, anticoagulant
antiarrhythmics
ACE inhibitors
• Regression of cardiac hypertrophy, miocardiofebrosis, increased heart
chambers
• Reduction of postloading on the heart and increase cardiac output by dilation of
the arterial and venous vessels
• Decrease of the heart rate and antiarrhythmic influence
• Na-uretic and diuretic effect
• Potassium retention
• Reduce the pressure in the atria, the antihypertensive doses reduces systemic
blood pressure
• Reduce the total pulmonary resistance
Absolute contraindications - bilateral renal artery stenosis, angioedema on ACE
inhibitors
Distinct therapeutic effect - not before 3-4 weeks
ACE inhibitors (Basargin E.N.Clinic recommendations for pediatric cardiology
and rheumatology. 2011 p.260)
Diuretics
• I-IIA d. CCF - thiazide: triampur ½ -2 Table. / Day.
Hydrochlorothiazide 1 mg / kg / day. Max. Children 50 mg / day.
• IIA-IIB d. CCF. – Loop diuretics: frusemide - infants
0.5-4 mg / kg / day.
• children 1-12 years of 1-3 mg / kg / day.
• Spironolactone (Veroshpirone):
as a diuretic: 2-4 mg / kg / day. In 2 hours
as neurohumoral control: 0.5-1 mg / kg / day. (control
K and createnine)
Teens: starting dose of 25 mg
Inotropic drugs
• Cardiac glycosides: digoxin (systolic dysfunction and left ventricular
cardiomegaly, neuromodulating low dose)
• In infants and children, the first months of life (not a long history of
heart failure not > 2 weeks). Digitalizing dose 0.03-0.05 mg / kg divided
into 6 (newborns) or 9 intakes, the maintenance dose - 0.01 mg / kg /
day . In 2 doses
• In children with myocardial disease - only digoxin maintenance dose in
case of little effect of ACE inhibitors and diuretics, 0.005-0.01 mg \ kg
in 2 divided doses. Children 10-18 years: digoxin initially 0.25-0.5 mg
per day in in 2 divided doses daily, then 0,0625-0,075 mg 1-2 doses
• In /v digoxin, dissolved in physiological saline solution or 5%-10%
glucose solution (concentration digoxin - 0.05 mg / mL) introduced
slowly (30-60 min., 10-20 min.) doses like orally
Inotropic drugs
β-adrenergic agonists– in a short period of
intensive care:
• Dobutamine 2,5-4-5 mcg / kg / min in in
physiological saline solution or glucose
• Dopamine 3.10 mcg / kg / min
• Amrinone 1 mg / kg, singly, then 10 mg / kg /
min
Β- adreno-blocators(BAB)
• Reduction of cardiac activity
• Improvement of contractile synchronism
• Prevention of toxic effects on the myocardium of catecholamines (inhibit
apoptosis)
• antiarrhythmic effect
• Improvement of myocardial bioenergetics
Bisoprolol, metoprolol, carvedilol (complications in the first days of treatment
- hypotension, bradycardia, worsening of heart failure): BAB together with
previously assigned ACEI + diuretics + digoxin , BAB can be used only without
the need to assign I /v inotropic support; in case of hypotension BAB together
with corticosteroids; beginning with the lowest dose)
• Carvedilol: children - an initial dose of 0.03 mg / kg / day in 2 divided doses
(maximum of 0.2 mg / kg / day.)
• Teenagers: 3.125 mg / day. In 2 divided doses (max 15,625-18,75 mg / day.)
Increase the dose to the initial one time in 7 days
Drug therapy of heart failure
Angiotensin receptorII blockers (in case of intolerance ACE
inhibitors) - losartan children of 6-14 years old beginning with
25 mg/1time a day. Gradually - to 50 mg
Teens - 50 to 100 mg / day.
Antiarrhythmics: amyodorone 5 mg / kg / day., Sotalol with slow
titration – begins with dose 0.3 mg / kg / day. 2 times;
increases to 2 mg / kg / day in 2 divided doses
Antiplatelet agents and anticoagulants
Drugs that enhance trophic condition of myocardium: Neoton, El
carnetine, cytoflavin, mildronat, cytochrome-C