Transcript Clinical Approach & Management Of CHF

CLINICAL APPROACH &
MANAGEMENT OF CHF
DR SARIKA GUPTA (MD,PHD)
ASST. PROFESSOR
DEFINITION
 A clinical syndrome
 Occurs when
 The heart is unable to pump enough blood to the body
to meet its needs
 The heart is unable to dispose of systemic or
pulmonary return adequately
 Or a combination of the two
PATHOPHYSIOLOGY
 Systemic oxygen transport = cardiac output X
systemic oxygen content
 Cardiac output = heart rate X stroke volume
 The primary determinants of stroke volume:
 afterload (pressure work)
 preload (volume work)
 contractility (intrinsic myocardial function)
PATHOPHYSIOLOGY
 The heart can be viewed as a pump with an output
proportional to its filling volume and inversely
proportional to the resistance against which it pumps
PATHOPHYSIOLOGY
 As ventricular end-diastolic volume increases, a
healthy heart increases cardiac output until a
maximum is reached
The increased
stroke volume
obtained in this
manner is due to
stretching of
myocardial fibers
Resulting in
increased wall
tension, elevating
myocardial oxygen
consumption
Cardiac muscle
with compromised
intrinsic
contractility
requires a greater
degree of
dilatation to
produce increased
stroke volume &
does not achieve
the same maximal
cardiac output as
normal myocardium
does
PATHOPHYSIOLOGY
Lesion causing
increased preload
(left-to-right
shunt or valvular
insufficiency)
Cardiac chamber is
already dilated
Little room for
further dilatation
as a means of
augmenting
cardiac output
Lesions that result
in increased
afterload to the
ventricle (aortic or
pulmonic stenosis,
coarctation of the
aorta)
decreases cardiac
performance
PATHOPHYSIOLOGY
 Abnormalities in heart rate: compromise cardiac
output
 Tachyarrhythmias shorten the diastolic time interval
for ventricular filling.
 High-output failure:
 NO basic abnormality in myocardial function
 Cardiac output is greater than normal
 Alterations in the oxygen-carrying capacity of blood
(anemia or hypoxemia) & increased oxygen demands
(secondary to hyperventilation, hyperthyroidism, or
hypermetabolism)
PATHOPHYSIOLOGY
ETIOLOGY
FETAL
Severe anemia (hemolysis, fetal-maternal transfusion,
parvovirus B19–induced anemia, hypoplastic anemia)
Supraventricular tachycardia
Ventricular tachycardia
Complete heart block
Severe Ebstein anomaly or other severe right-sided
lesions
Myocarditis
ETIOLOGY
PREMATURE NEONATE
Fluid overload
Patent ductus arteriosus
Ventricular septal defect
Cor pulmonale (bronchopulmonary dysplasia)
Hypertension
Myocarditis
Genetic cardiomyopathy
ETIOLOGY
FULL-TERM NEONATE
Asphyxial cardiomyopathy
Arteriovenous malformation (vein of Galen, hepatic)
Left-sided obstructive lesions (coarctation of aorta,
hypoplastic left heart syndrome)
Large mixing cardiac defects (single ventricle, truncus
arteriosus)
Myocarditis
Genetic cardiomyopathy
ETIOLOGY
INFANT-TODDLER
Left-to-right cardiac shunts (ventricular septal defect)
Hemangioma (arteriovenous malformation)
Anomalous left coronary artery
Genetic or metabolic cardiomyopathy
Acute hypertension (hemolytic-uremic syndrome)
Supraventricular tachycardia
Kawasaki disease
Myocarditis
ETIOLOGY
CHILD-ADOLESCENT
Rheumatic fever
Acute hypertension (glomerulonephritis)
Myocarditis
Thyrotoxicosis
Hemochromatosis-hemosiderosis
Cancer therapy (radiation, doxorubicin)
Sickle cell anemia
Endocarditis
Cor pulmonale (ILD, cystic fibrosis)
Genetic or metabolic cardiomyopathy
CLINICAL FEATURES
 Depend on the degree of the child's cardiac reserve
 A critically ill infant or child who has exhausted the
compensatory mechanisms- symptomatic at rest
 Other patients may be comfortable when quiet but are
incapable of increasing cardiac output in response to
even mild activity without experiencing significant
symptoms
CLINICAL FEATURES
 History:
 Poor feeding, poor weigh gain, tachypnea (worsening
during feeding), cold sweat on the forehead- CHF in
infants
 Shortness of breath, specially with activities, easy
fatigability, puffy eyelids or swollen feet-older
children
CLINICAL FEATURES
 Examination:
COMPENSATORY RESPONSE
 Tachycardia, gallop rhythm, weak & thready pulses
 Growth failure, perspiration, cold & wet skin
 Cardiomegaly
PULMONARY VENOUS CONGESTION
 Tachypnea
 Dyspnea on exertion
 Orthopnea
 Wheezing & pulmonary crackles
CLINICAL FEATURES
 Examination:
SYSTEMIC VENOUS CONGESTION
 Hepatomegaly
 Puffy eyelids
 Distended neck veins
 Ankle edema
Clinical assessment of jugular venous pressure in
infants may be difficult because of the shortness of
the neck & the difficulty of observing a relaxed state;
palpation of an enlarged liver is a more reliable sign
Edema may be generalized & involves the eyelids &
sacrum & less often the legs and feet
CLINICAL FEATURES
INVESTIGATION
 X-RAY Study:
INVESTIGATION
 X-RAY Study:
INVESTIGATION
 ECG: not helpful
 ECHO:
 Standard technique for assessing ventricular function
 The most commonly used parameter in children is
fractional shortening (impaired LV systolic function)
 Difference between end-systolic & end-diastolic
diameter divided by end-diastolic diameter (N=28%42%)
 Ejection fraction (impaired LV systolic function)
 Enlargement of ventricular chambers
 Doppler tissue imaging (impaired LV systolic & diastolic
function)
INVESTIGATION
 Magnetic resonance angiography
 Cardiac catheterization-evaluation of biopsy specimens
 Decreased arterial oxygen levels; respiratory or
metabolic acidosis
 Hyponatremia
 Serum B-type natriuretic peptide (BNP)
 Cardiac neurohormone released in response to
increased ventricular wall tension
 Elevated in patients with heart failure due to systolic
dysfunction (cardiomyopathy)
 Elevated in children with volume overload (left-toright shunts such as ventricular septal defect)
MANAGEMENT
 PRINCIPAL:
 Elimination of the underlying causes
 Treatment of the precipitating or contributing causes
(infection, anemia, arrhythmias, fever)
 Control of the heart failure state
MANAGEMENT
 Control of the heart failure– GENERAL MEASURES
 Bed rest
 Humidified oxygen
 Adequate calories & fluid
1. Calorie dense food
2. Frequent small feeding
3. Nasogastric feeding
4. Salt restrictions
 Patients with pulmonary edema- positive pressure
ventilation
 Daily weight measurement in hospitalized children
MANAGEMENT
 Control of the heart failure state- Drug therapy
 Inotropic agents
 Diuretics
 Afterload reducing agents
DIURETICS:
 interfere with reabsorption of water & sodium by the
kidneys
 results in a reduction in circulating blood volume
 thereby reduces preload & control pulmonary &
systemic venous congestive symptoms
MANAGEMENT
INOTROPIC AGENTS:
 Rapidly acting Inotropic agents
 Dopamine, dobutamine, isoproterenol, epinephrine &
amrinone
 Additional vasodilator actions
 Used for critically ill infants with CHF, those with
renal dysfunction & postoperative cardiac patients with
CHF
 Digoxin
MANAGEMENT
AFTERLOAD REDUCING AGENTS:
 Arteriolar vasodilator
 Augments cardiac output by acting primarily on the
arteriolar bed
 Reduction of afterload
 Hydralazine
 Venodilators
 Dilate systemic veins & redistribute blood from the
pulmonary to the systemic circuits
 Decrease in pulmonary symptoms
 Nitriglycerine, isosorbide dinitrate
MANAGEMENT
AFTERLOAD REDUCING AGENTS:
 Mixed vasodilator
 Act on both arteriolar & venous beds
 ACE inhibitors, nitroprusside & prazosin
 ACEIs have additional beneficial effects on cardiac
structure & function that may be independent of their
effect on afterload
MANAGEMENT
AFTERLOAD REDUCING AGENTS:
 Afterload reducers: especially useful in children with
heart failure secondary to cardiomyopathy & in
patients with severe mitral or aortic insufficiency
 Effective in patients with heart failure caused by leftto-right shunts
 Not used in the presence of stenotic lesions of the left
ventricular outflow tract because of concern over
coronary perfusion
MANAGEMENT
β-ADRENERGIC BLOCKERS:
 β-Blockers are used for the chronic treatment of
patients with heart failure who were symptomatic
despite being treated with standard anticongestive
drugs
MANAGEMENT
MANAGEMENT