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CHF Concept and Physiology Ikm 6.9.19

This document provides an overview of heart failure in children, including: - The physiology of heart failure related to preload, afterload, and contractility. - The pathophysiology of both systolic and diastolic heart failure in terms of impaired ventricular function. - Compensatory mechanisms the body uses to buffer the fall in cardiac output such as the Frank-Starling mechanism and neurohormonal stimulation. - Precipitating factors that can exacerbate heart failure like infection, anemia, arrhythmias or non-compliance with medications.

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47 views31 pages

CHF Concept and Physiology Ikm 6.9.19

This document provides an overview of heart failure in children, including: - The physiology of heart failure related to preload, afterload, and contractility. - The pathophysiology of both systolic and diastolic heart failure in terms of impaired ventricular function. - Compensatory mechanisms the body uses to buffer the fall in cardiac output such as the Frank-Starling mechanism and neurohormonal stimulation. - Precipitating factors that can exacerbate heart failure like infection, anemia, arrhythmias or non-compliance with medications.

Uploaded by

Afifulichwan
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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Concept and physiology

of heart failure in children


Indah K Murni
Department of Pediatrics
Dr Sardjito Hospital/Universitas Gadjah Mada
Yogyakarta
Curriculum vitae
Indah Kartika Murni
Pati, 8 February 1977

Education:
2013 - 2015: Pediatric cardiologist, the University of Indonesia, Indonesia
2010 - 2013: PhD, the University of Melbourne, Victoria, Australia
2001 - 2005: Pediatrician, Universitas Gadjah Mada, Indonesia
2001 - 2004: Magister of Medicine, Universitas Gadjah Mada, Indonesia
1994 - 2000: Physician, Universitas Gadjah Mada, Indonesia

Courses/fellowship/observership:
2019: Summer school on Pediatric sports and Exercise Medicine, Utrecht, the Netherland
2018: Pediatric Cardiology, Royal Children’s Hospital Melbourne, Victoria, Australia
2017: Cardiac Pathology and Imaging Course, Toronto, Canada
2017: Transcatheter closure of VSD, Taichung, Taiwan
2013: Clinical Research, Evidence Based Medicine and Clinical Decision Making, Antwerp, Belgium
2010: Pediatric Intensive Care Unit, Royal Children’s Hospital Melbourne, Victoria, Australia
Outline
• Physiology
• Pathophysiology
• Compensatory mechanisms
• Precipitating factors
Congestive heart failure
• Congestive heart failure (CHF) occurs when the heart can no
longer meet the metabolic demand of the body at normal
physiologic

• CHF is a clinical syndrome in which:


• The heart is unable to pump enough blood to the body to meet its
needs
• To dispose of venous return adequately
• Or a combination of the two
Determinants of Function in the Heart
Preload
Afterload
• The ventricular wall tension during contraction; the
resistance that must be overcome for the ventricle to
eject its content.
• Often approximated by the systolic ventricular (or
arterial) pressure.
Contractility
Pressure–Volume Loops
The important physiologic concepts
• Stroke volume is a function of preload, afterload, and contractility
• SV rises when there is an increase in preload, a decrease in afterload, or
augmented contractility
• Ventricular end-diastolic volume (pressure) is preload
• The end-diastolic volume is influenced by the chamber’s compliance
• Ventricular end-systolic volume depends on the afterload and
contractility, but not on the preload
Classification of heart failure
• The course of disease:
• Acute heart failure
• Chronic heart failure
• The severity:
• Mild or complete compensation
• Moderate or incomplete compensation
• Severe or decompensation
• The cardiac output:
• Low output: volume and pressure overload, contractility problems
• High-output: heart rate is mainly affected (Anemia, arrythmia, AV fistula)
Classification of heart failure
• The location:
• Left heart failure
• Right heart failure
• Left and right heart failure
• The function:
• Systolic heart failure: myocarditis, hypertension
• Diastolic heart failure: restrictive cardiomyopathy, cardiac
tamponade
PATHOPHYSIOLOGY
• impair ventricular contractility systolic heart failure /
• increase afterload systolic dysfunction

diastolic heart failure /


• impair ventricular relaxation and filling
diastolic dysfunction
Systolic heart failure
• the affected ventricle has a diminished capacity to eject blood
• because of incomplete emptying results in a higher end-diastolic
volume and pressure and the end-systolic volume to remain
elevated
• the persistently elevated LV pressure is transmitted to the LA and
to the pulmonary veins and capillaries  pulmonary congestion
Diastolic failure
• Demonstrate abnormalities of ventricular diastolic function
• Often manifest signs of vascular congestion because the elevated
diastolic pressure is transmitted retrograde to the pulmonary and
systemic veins
Impaired contractility Increased afterload

Dilated Aortic stenosis


cardiomyopathies Hypertension

Systolic dysfunction

Heart failure

Diastolic dysfunction

Impaired diastolic
L-R shunt
Restrictive cardiomyopathy
Tamponade
Right-Sided Heart Failure
• the right ventricle (RV) is a thin and high compliant chamber
• the RV has little difficulty accepting a wide range of filling volumes without
significant changes in its filling pressures
• the most common cause of right-sided heart failure is left-sided heart failure
• when the RV fails, the elevated diastolic pressure is transmitted retrograde to the
RA with subsequent congestion of the systemic veins
• isolated right-heart failure may also influence left-heart function
Causes of Right-Sided Heart Failure
Cardiac causes
• Left-sided heart failure
• Pulmonic valve stenosis
• Right ventricular infarction
Pulmonary parenchymal diseases
• Chronic obstructive pulmonary disease
• Interstitial lung disease (e.g., sarcoidosis)
• Adult respiratory distress syndrome
• Chronic lung infection or bronchiectasis
Pulmonary vascular diseases
• Pulmonary embolism
• Primary pulmonary hypertension
COMPENSATORY MECHANISMS

• The Frank– Starling mechanism


• Neurohormonal stimulation
• Ventricular hypertrophy and remodeling
Ventricular
performance
curve
The Frank– Starling mechanism
Neurohormonal
stimulation
The renin–angiotensin system
Antidiuretic hormone (vasopressin)
• ADH increases intravascular volume because it promotes water
retention in the distal nephron
• The increased intravascular volume serves to augment left ventricular
preload and cardiac output
Chronic neurohormonal alteration
• The increased circulating volume and augmented venous return to
the heart may worsen congestive pulmonary symptoms
• Chronically elevated levels of AII and aldosterone provoke the
production of cytokines, activate macrophages, and stimulate
fibroblasts  fibrosis and adverse remodeling of the failing heart
Natriuretic peptides
• Natural “beneficial” hormones secreted in heart failure in response
to increased intracardiac pressures
• Atrial natriuretic peptide (ANP) is released in response to atrial distention
• B-type natriuretic peptide (BNP) is not detected in normal hearts but is
produced in heart failure
• They result in excretion of sodium and water, vasodilatation,
inhibition of renin secretion, and antagonism of angiotensin II
Ventricular Hypertrophy and Remodeling
• Wall stress is increased in heart failure because of LV dilatation or excessive
afterload
• Chronic chamber dilatation owing to volume overload results in the
myocytes to elongate and enlarges (eccentric hypertrophy)
• Chronic pressure overload results in the wall thickness increases without
proportional chamber dilatation, and wall stress may be reduced
(concentric hypertrophy)
PRECIPITATING FACTORS
• Increased metabolic demands: fever, infection, anemia, tachycardia
• Tachyarrhythmia or excessively slow heart rate
• Increased circulating volume (preload): excessive sodium or fluid, renal
failure
• Conditions that increase afterload: hypertension, pulmonary embolism
• Conditions that impair contractility: negative inotropic, myocardial
ischemia or infarction
• Failure to take anti-failure medications
TAKE HOME MESSAGES
• Physiology
• Ventricular stroke volume is a function of preload, afterload, and contractility
• SV rises when there is an increase in preload, a decrease in afterload, or augmented contractility
• Pathophysiology
• impair ventricular relaxation and filling  diastolic failure
• increase afterload and impair contractility  systolic failure
• Compensatory mechanisms
• buffer the fall in cardiac output and help preserve blood pressure to perfuse vital organs
• Precipitating factors
• should be eliminated
ACKNOWLEDGEMENT
Thank you
[email protected]

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