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Thorough Pathophysiology
dr. T. M. Haykal Putra
Heart Failure
Definition of Heart FailureFrank – Starling Relationship
(Preload-Afterload-Contractility)Cardiac OutputPressure-Volume LoopSystolic & Diastolic DysfunctionNeurohormonal AlterationRemodellingClinical Manifestation
Milestones
Leonard S. LillyInability of the heart to pump blood forward at sufficient
rate to meet the metabolic demands of the body (forward failure)
The ability to do so if the cardiac filling pressures are abnormally high (backward failure)
ESCAn abnormality of cardiac structure or function leading to
failure of the heart to deliver oxygen at a rate commensurate with the requirements of the metabolizing tissue, despite normal filling pressure.
Definition
Basic PhysiologyCardiac Output (CO)
Volume of blood ejected from the ventricle every minute
Stroke Volume (SV) Volume of blood ejected from
the ventricle during systole (every beat)
CO = SV x HR
Cardiac Output
Heart Rate Stroke Volume
Preload Afterload Contractility
If the muscle is passively stretched and then stimulated to contracts The force would be augmentedOptimization of myosin & actin interaction Increased sensitivity of myofilament to calcium
Clinical ImplicationThe larger ventricular volume during diastole, the more
fibers are stretchedGreater force of contraction
Stretch of the muscle ~ Preload
Frank-Starling Relationship (I)
The Force of contraction is directly related to the magnitude of the loadThe force is independent of the muscle length before
contraction (stretch)
Clinical ImplicationThe pressure generated by the ventricle depend on the
load (afterload) againts which the ventricle contracts
Magnitude of the load ~ afterload
Frank-Starling Relationship (II)
Myocardial contractility (inotropic) is independent of initial fiber length (preload) & load against which it contracts (afterload)
Contractility reflects chemical & hormonal influences on cardiac contractionEx. Exposure to cathecolamines
Frank-Starling Relationship (III)
Cardiac Output
CO
HR SV
Preload Afterload Contractility
+ +-
The ventricular wall tension at the end of diastoleThe stretch on the ventricular fiber just before the
contraction“Tekanan pengisian ventrikel”
The more ventricle is filled with blood, the greater the volume ejected
Preload is measured as EDVInfluenced by intravascular volume
Decreased in dehydration or hemorrhageIncreased in hypervolemia or water retention
Preload
The ventricular wall tension during contractionThe resistance that must be overcome for the ventricle to ejectVentricular wall stress that develops during systolic ejection “Tekanan Pengosongan Ventrikel”
Measured as wall stress
Wall stress based on Laplace’s relationship Influenced by pressure load (P) Influenced by increased chamber size (r) Influenced by wall thickness (h)
Afterload
Pressure – Volume Loop
Preload – Afterload
Contractility
Cardiac Output
CO
HR SV
Preload Afterload Contractility
+ +-
1. Systolic Dysfunction Abnormality of ventricular emptying “Reduced Ejection Fraction” (EF<50%)
2. Diastolic disfunction Abnormality of ventricular relaxation (ventricular
filling) “Preserved Ejection Fraction” (EF>50%)
Ejection Fraction(stroke volume)/(end-diastolic volume)
Systolic & Diastolic Dysfunction
Diminished capacity to eject blood because of impaired myocardial contractility or pressure overloadContractilityAfterload
Compensatory mechanismIncreased preloadThe volume remains in the ventricle because of
incomplete emptying result in volume accumulation (increased EDV)
Maintain SV via Frank-Starling mechanism
Systolic Dysfunction
Abnormality of vetricular diastolic function either impaired diastolic relaxation (energy-dependent process) or increased stiffness of the ventricular wallIschemia or passive property of the heart (hypertrophy,
fibrosis, etc.)
Reduced chamber complianceThe ease or difficulty with which the chamber can be
filledVentricular filling is at higher pressure
Diastolic Dysfunction
Frank-Starling MechanismNeurohormonal AlterationRemodelling
Compensatory Mechanism
1. Adrenergic Nervous System2. Renin-Angiotensin-Aldosteron System (RAA system)3. Antidiuretic Hormone (ADH)
To maintain arterial perfusion to vital organs (BP)BP = CO x SVRSVR Systemic Vascular Resistance
Moreover, neurohormonal activation results in salt and water retention Which maximizing SV via Frank-Sarling Mechanism
Neurohormonal Alteration (I)
The fall in CO is sensed as decreased pressure by baroreceptors in the carotid sinus and aortic arch
Signal is transmitted to CV control in the MedullaThe result is diminished parasympathetic tone and
increased sympathetic tone
Effect of sympathetic tone:Increased HRIncreased ventricular contractilityVasoconstriction veins & arteries
Adrenergic Nervous System (I)
Adrenergic Nervous System (II)
Augmented CO Increased HR Increased contractility
Vasoconstriction of veins augments blood return to the
heart which increase preload (frank-starling mechanism)
Vasoconstriction of arteries Increased SVR to maintain BP
BP
SVR CO
HR SV
Preload Afterload Contractility
+ +-
RAA system
Vasopressin is secreted by posterior pituitary through baraoreceptors and angiotensin II
Clinical importanceIncreased Intravascular volume (promotes water
retention in the distal nephron)
ADH
Neurohormonal Alteration (II)
Initially beneficial However, continue activation typicaly proves harmful
Increased circulating volume and augmented venous return increase the afterload Against which the failing LV contracts Will impair SV
Increased metabolic demand Further reduce the performance of the failing heart
Chronically elevated AII & aldosterone provoke the production of cytokines Resulting in remodelling and cellular dysfunction
Neurohormonal Alteration (III)
A sustained increase in wall stress (afterload) along with neurohormonal and cytokine stimulate the development of myocardial hypertrophy and deposition of extracellular matrixIs actually compensatory mechanism to counteract wall
stress
However the hypertrophic wall is stiffDiastolic ventricular pressure will be higherThe pressure will be directed backwards to LA &
pulmonary vasculature
Remodelling (I)
Pressure Directed Backwards
There will be myocite loss, cellular dysfunction & deposition of extracellular matrixApoptosisPhagocytosis without inflammatory responseTriggered by Catecholamines, AII, Cytokines &
mechanical strains
Remodelling (II)
Alteration in MyociteBeta-adrenergic desensitizationHypertrophy
Myocardial ChangesMyocite loss (apoptosis)Matrix degradationMyocardial Fibrosis
Alteration in LV GeometryLV dilationLV wall thinningMV incompetence
Remodelling (III)
Clinical Manifestation (I)DOE (dyspneu on
effort/dyspnea on exertion)Decreased COManifestation of
pulmonary venous congestionTransudation of fluid into
pulmonary interstisial increased greater effort of respiration
Juxtacapillary receptor are stimulated and mediate rapid shallow breathing
OrthopneaLabored breathing while
lying flat and relieved by sitting upright
Assessed by the number of pillow being used during sleeping
Results from redistribution of intravascular volume from abdomen & lower extremities towards the lungs
Clinical Manifestation (II)Paroxysmal Nocturnal
Dyspnea (PND)Severe breathlessness
that awakens the patient from sleep 2 to 3 hours after bed
Results from gradual reabsoprtion into circulation of lower extremity intterstisial edema after lying downSubsequent expansion of
intravascular volume
Weight gainAccumulation of
interstitial fluid
Abdominal dyscomfort Engorged liver and
stretched capsule
Diaphoretic Increased sympathetic
activity
ReferrenceLilly LS. Pathophysiology of heart disease. 5th ed. USA:
Williams & Wilkins; 2011.Libby P, Bonow RO, Mann DL, Zipes DP. Braunwald’s
heart disease. 8th ed. USA: elseviers; 2007.McMurray JV, Adamopoulos S, Anker SD, Auricchio A,
Bohmm M, et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012. European Heart Journal 2012; 33: 1787-1847.
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