Heart as a pump, heart failure & its treatment
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Transcript of Heart as a pump, heart failure & its treatment
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Dr Chirantan MandalDr Kajaree GiriDr Shuvam Roy
Dr Avik Basu
Medical College &Hospital Bengal
88 college street, KolkataWest Bengal
India
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HEART FAILURENORMAL CARDIAC PHYSIOLOGY
Presented by:
KAJAREE GIRI Medical College &Hospital Bengal
88 college street, KolkataWest Bengal
India
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PARAMETERS ON WHICH CARDIAC
PHYSIOLOGY DEPENDS
Preload
Afterload
Heart Rate
Ionotropic State
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PRELOAD
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PRELOAD
• IN THE WHOLE HEART PRELOAD SHOULD CONSTITUTE THE TENSION IN THE WALL AT THE END OF DIASTOLE ( WHICH DETERMINES THE RESTING FIBER LENGTH).
• FOR PRACTICAL PURPOSES THE VENTRICULAR EDV/EDP IS USED TO INDICATE PRELOAD.
• IT AFFECTS HEART PERFORMANCE BY “STARLING’S LAW OF THE HEART”.
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AFTERLOAD
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IONOTROPIC STATE
INFLUENCE OF IONOTROPIC STATE ON LENGTH— TENSION RELATIONSHIP OF CARDIAC MUSCLE.
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IONOTROPIC STATE
INFLUENCE OF CHANGE INIONOTROPIC STATE ON FRANKSTARLINGCURVES.
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FACTORS MODIFYING IONOTROPY IN HEART FAILURE, THERE IS A
DECREASE IN IONOTROPY— FALL IN STROKE VOLUME AND INCREASE IN PRELOAD – DECREASE IN EJECTION FRACTION.
CARDIOMYOPATHY, ARRHYTHMIA – LOSS OF INTRINSIC
IONOTROPY – SYSTOLIC HEART FAILURE.
LEFT VENTRICULAR EDP IF GREATER THAN 20 mm Hg – PULMONARY EDEMA.
CHANGES IN IONOTROPIC STATE IMPORTANT DURING EXERCISE.
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MUSCLE CELL TENSION IS DETERMINED BY:
THE NUMBER OF CROSSBRIDGES FORMATION WHICH IN TURN IS DETERMINED BY THE SARCOMERE LENGTH– MYOFILAMENT OVERLAP (RELATED TO PRELOAD).
THE LOAD AND SHORTENING VELOCITY (RELATED TO AFTERLOAD).
THE RELATIVE ACTIVATION OF THIN FILAMENTS AS DETERMINED BY THE SATURATION OF TROPONIN WITH CALCIUM. (RELATED TO CONTRACTILITY).
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The Length-Tension relationship in muscle forms the basis for Frank-Starling’s Law
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SERIES ELASTIC ELEMENTS
CONTRACTILE COMPONENT
(ACTIVE TENSION)
PARALLEL ELASTIC ELEMENTS
(PASSIVE TENSION)
TOTAL TENSION
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THE L-T RELATIONSHIP OF FROG SKELETAL MUSCLE(IN BLACK)THE L-T RELATIONSHIP OF CAT CARDIAC MUSCLE FOR THE RANGE OF PHYSIOLOGICAL SARCOMERE LENGTH(IN RED).
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FORCE –VELOCITY RELATIONSHIP
•THERE’S AN INVERSE RELATION BETWEEN THE SHORTENING VELOCITY OF FIBRES AND AFTERLOAD.
•INCREASING PRELOAD INCREASES MAXIMAL ISOMETRIC FORCE AND INCREASES SHORTENING VELOCITY AT A GIVEN AFTERLOAD,DOESNOT ALTER Vmax.
•INCREASE IN IONOTROPIC STATE INCREASES BOTH Vmax AND MAXIMAL ISOMETRIC FORCE.
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PRESSURE-VOLUME LOOP
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CO = SV x HR
EF = SV / EDV
SBP
DBP
Pes PRESSURE-VOLUME LOOP
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PR
ESS
UR
E
DIASTOLICPRESSURE CURVE
SYSTOLIC PRESSURE CURVE
PRESSURE-VOLUME LOOP
End Diastolic VolumeEnd Systolic Volume
IsovolumetricPhase
Isotonic (Ejection) Phase
StrokeVolume
Pre-load
After-load
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INDEPENDENT EFFECTS OF PRELOAD
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INDEPENDENT EFFECTS OF AFTERLOAD
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INDEPENDENT EFFECTS OF IONOTROPISM
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PRELOAD AFTERLOAD CONTRACTILITY
MANIPULATING CARDIAC FUNCTION
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INTERDEPENDANT ACTIONS OF PRELOAD AND AFTERLOAD AT CONSTANT IONOTROPY.
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TO SUM IT UP
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WHAT IS HEART FAILURE??
HEART FAILURE OCCURS WHEN THE HEART IS UNABLE TO PUMP BLOOD AT A RATE SUFFICIENT TO MEET THE METABOLIC DEMANDS OF THE BODY OF AN INDIVIDUAL.
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HOW HEART FAILURE OCCURS??
FAILURE OF THE PUMPS.
OBSTRUCTION TO FLOW.
REGURGITANT FLOW.
SHUNTED FLOW THROUGH DEFECTS CONGENITAL OR ACQUIRED.
DISORDER OF CARDIAC CONDUCTION.
RUPTURE OF HEART OR MAJOR VESSELS.
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PRINCIPLES OF TREATING HEART FAILURE:
POSITIVE IONOTROPIC AGENTS LIKE DIGITALIS.
DIURETICS.
VASODILATORS-- a) NITROPRUSSIDE (BOTH ARTERIAL AND VENODILATORS).
b) HYDRALAZINES (ONLY ARTERIAL DILATORS).
c) ACE INHIBITORS.
SPECIFIC THERAPIES AIMED AT
1.HEART BLOCK.
2.SERIOUS VALVULAR LESIONS.
3. CORONARY ARTERY NARROWING.
4. SEVERE HYPERTENSION.
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THANK YOU..
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Cardiac Compensation and Decompensation in Heart Failure
Shuvam Roy4th semester student
Medical College &Hospital Bengal 88 college street, Kolkata
West BengalIndia
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Heart failure
• Definition: failure of heart to pump enough blood to satisfy the needs of body
• Types: I) Acute or chronic II) Unilateral (Left/Right) or Bilateral
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Cardiac compensation
• Compensatory mechanisms maintain adequate CO & tissue perfusion
• Mechanisms:– sympathetic stimulation– fluid retention of kidney– varying degrees of recovery of the heart itself
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Sympathetic stimulation
• Occurs within 30s of acute heart failure• CVS reflexes stimulate sympathetic NS and
inhibit parasympathetic NS • Effects:– Increased strength of heart– Increased mean systemic filling pressure– Maintains pressure for perfusion of vital organs
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CVS reflexes
• Baroreceptor reflex• Chemoreceptor reflex• CNS ischaemic response• Reflexes originating in the heart
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Baroreceptor reflex
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Chemoreceptor reflex
• Aortic & carotid bodies stimulated by hypoxia, local concentration of H + & CO2 impulses travel via vagus and Hering’s nervesstimulation of VMC
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CNS ischaemic response
• VMC is directly stimulated by – increase in local concentration of H+ & CO2
– hypoxia
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Bainbridge reflex
• Increase in atrial pressure stimulates atrial stretch receptors which causes reflex increase in heart rate and myocardial contractility
• Afferent pathway: vagus nerve• Efferent pathway: sympathetic and vagus
nerves
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Fluid retention by the kidneys• Occurs over hours to days• Beneficial when pumping ability of heart is not
very severely damaged• Occurs due to – activation of renin- angiotensin-aldosterone system– Decrease in renal blood flow causes decrease in GFR– Increased aldosterone secretion– Increased ADH secretion
• Effects:– Increase in mean systemic filling pressure – Decreased venous resistance
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Recovery of the heart
• Occurs over weeks to months• Includes– Development of collateral blood supply– Fringe areas outside the infarct zone become
functional– Hypertrophy of functional areas occur– Increased collagen that may reduce dilatation
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Hypertrophy of myocardium• In hemodynamic overload it reduces elevated ventricular
wall stress to normal• In pressure overload, increased systolic pressureincreased systolic
stressparallel addition of new myofibrilswall thickening and consequent concentric hypertrophydecreased systolic stress
• In volume overload, increased diastolic pressureincreased diastolic stressserial
addition of new sarcomeres chamber enlargement and eccentric hypertrophy decreased diastolic pressure
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• If heart recovers sufficiently and if adequate fluid volume has been retained, sympathetic
stimulation gradually abates towards normal
• However, cardiac reserve is reduced.
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Decompensated heart failure
• Occurs when compensatory mechanisms can no longer maintain an adequate tissue perfusion
• The same factors that are responsible for cardiac compensation can exacerbate cardiac decompensation
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Factors behind cardiac decompensation
• Salt & water retention: pulmonary congestion, anasarca
• Vasoconstriction: increases cardiac energy expenditure
• Sympathetic stimulation: increases cardiac energy expenditure
• Hypertrophy:deterioration and death of cardiac myocytes
• Increased collagen: impairs relaxation• Cardiac remodelling
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Progressive oedema• Compensatory mechanisms fail to raise CO high
enough to make kidneys excrete enough water• Detrimental effects of fluid retention- Diagnosed
by progressive pulmonary congestion and anasarca, bubbling rales in lung and dyspnoea.
• Treatment– Cardiotonic drugs like digitalis– Diuretics– Restrict salt and fluid intake
• ANP and BNP delay decompensation by increasing salt and water excretion by kidneys
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• Right or left heart failure does not lead to immediate peripheral oedema as ,initially ,
there is a fall in capillary pressure.
• But peripheral oedema begins after one day or so due to fluid retention by the kidneys
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Acute pulmonary oedema in heart failure
• Left heart failure causes pulmonary congestion and oedema
• Pulmonary oedemadecreased oxygenation of bloodfurther weakening of heart and peripheral vasodilatationincreased venous return due to peripheral vasodilatationmore pulmonary oedema
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• Cardiogenic shock– Low output heart failure– shockfall in arterial pressuredecrease in coronary
blood flowdamage to heart– Vicious cycle– Treatment1. Surgical clot removal with coronary bypass graft2. Fibrinolytics3. Cardiotonic drugs4. Increase blood pressure
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HEART FAILURE
PATHOPHYSIOLOGY AND CLINICAL
MANIFESTATIONS
Presented by: AVIK BASU
Medical College &Hospital Bengal 88 college street, Kolkata
West BengalIndia
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ETIOLOGIES
OF HEART FAILURE
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•Depressed Ejection Fraction (<40%)
1. Coronary Artery Disease
2. Chronic Pressure Overload
3. Chronic Volume Overload
4. Non-ischemic Dilated Cardiomyopathy
5. Disorders of Rate and Rhythm
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•Preserved Ejection Fraction (40-50%)
1. Pathological Hypertrophy
2. Aging
3. Restrictive Cardiomyopathy
4. Fibrosis
5. Endomyocardial Disorders
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•Pulmonary heart disease
1. Cor Pulmonale
2. Pulmonary Vascular Disorders
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•High-output states
1. Metabolic Disorders
2. Excessive Blood-flow Requirements
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FORMS OF
HEART FAILURE
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•PATHOLOGICAL CLASSIFICATION
1. Systolic Heart Failure
2. Diastolic Heart Failure
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•CLINICAL CLASSIFICATION
1. RIGHT-SIDED Heart Failure
2. LEFT-SIDED Heart Failure
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•OTHER CLASSIFICATIONS
1. LOW OUTPUT Heart Failure
2. HIGH OUTPUT Heart Failure
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PATHOGENESIS OF
SYSTOLIC HEART FAILURE
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Activation of Neuro-hormonal Systems in Heart Failure
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MOLECULARBASISOF
SYSTOLIC FAILURE
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The molecular basis of systolic failure involves three components:
• Contractile proteins
• Calcium homeostasis
• Signal transduction pathways
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CHANGES IN CONTRACTILE PROTEINS
• Slowing of cross-bridge cycling rate
• Increased expression of fetal isoform of Troponin-T
• Reduced phosphorylation of Troponin-I
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NORMAL HEART FAILING HEART
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CHANGES IN CALCIUM HOMEOSTASIS
• Prolonged Calcium transient
• Increased threshold for Calcium release from sarcoplasmic reticulum
• Increased diastolic Calcium concentration
• Decreased Calcium reuptake by sarcoplasmic reticulum
• Prolonged action potential
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NORMAL HEART
FAILINGHEART
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CHANGES IN SIGNAL TRANSDUCTION PATHWAYS
• Decreased number of β-adrenoreceptors
• Increased expression of β-adrenoreceptor kinase
• Increased expression of inhibitory G-protein
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NORMAL HEART FAILING HEART
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CHARACTERISTIC OF HEART IN SYSTOLIC FAILURE
• Eccentric left ventricular hypertrophy
• Progressive left ventricular dilatation
• Abnormal left ventricular systolic properties
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PATHOGENESIS
OF DIASTOLIC
HEART FAILURE
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FACTORS REGULATING VENTRICULAR RELAXATION
(1)Systolic Load
(2) Myofibre inactivation
(3) Uniformity of the distribution of load and inactivation over space and time
Left ventricular relaxation is under the ‘Triple Control’ of:
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POTENTIAL MECHANISM FOR DIASTOLIC DYSFUNCTION
• Extramyocardial
• Whole heart
• Extracellular matrix
• Cardiomyocyte
• Myofilaments
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CHANGE IN TITIN ISOFORM
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• Titin protein has two isoforms: (1) N2BA (2) N2B
• N2B isoform is stiffer than N2BA isoform.
• Predominance of N2B isoform in the heart leads to increased stiffness of the ventricles leading to diastolic dysfunctioning.
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CHARACTERISTIC OF HEART IN DIASTOLIC FAILURE
• Concentric left ventricular hypertrophy
• Normal or reduced left ventricular volume
• Concentric remodelling
• Abnormal left ventricular diastolic properties
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PATHOGENESIS
OF LEFT-SIDED
HEART FAILURE
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CAUSES OF LEFT-SIDED HEART FAILURE• Ischemic heart disease
• Hypertension
• Aortic and Mitral valvular disease
• Non-ischemic myocardial disease
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MORPHOLOGICAL CHANGES IN THE
HEART• Hypertrophied and Dilated heart
• Myocardial fibrosis
• Secondary left atrial fibrillation
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CLINICAL MANIFESTATIONS
• Paroxysmal Nocturnal Dyspnoea• Orthopnoea• Pulmonary edema• Cheyne-Stokes respiration• Pre-renal azotemia• Hypoxic Encephalopathy
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PATHOGENESIS
OF RIGHT-SIDED
HEART FAILURE
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CAUSES OF RIGHT-SIDED HEART FAILURE
• Secondary to Left-sided heart failure
• Severe Pulmonary Hypertension
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MORPHOLOGICAL CHANGES IN THE
HEART• Hypertrophied and Dilated right ventricle
• Dilated right atrium
• Bulging of ventricular septum to the left
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CLINICAL MANIFESTATIONS
• Raised Jugular Venous Pressure• Congestive hepatomegaly• Hepato-jugular reflex• Congestive splenomegaly• Pedal & Pre-tibial edema
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LOW-OUTPUT HEART FAILURE
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STAGES OF CARDIOGENIC SHOCK
• Non-progressive/Compensatory phase
• Progressive phase
• Irreversible phase
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HIGH-OUTPUT HEART FAILURE
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CONDITIONS LEADING TO HIGH-OUTPUT HEART FAILURE
• Arterio-venous fistula
• Beriberi
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ARTERIO-VENOUS FISTULA
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OXYGEN LACK THEORY
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BERIBERI
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Treatment of Heart Failure
CHIRANTAN MANDAL 4th semester student
Medical College &Hospital Bengal
88 college street, KolkataWest Bengal
India
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Therapeutic Overview Problems • ↓force of contraction• ↑total peripheral resistance• organ hypoperfusion• Ventricular remodelling• Worsening renal function• ↑ venous pressure with ↓cardiac output• edema• ↓exercise tolerance
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Therapeutic Challenges
• Rapid relieve of symptoms• Prevent Sudden Cardiac
Arrest & ventricular remodeling
• Decongest organs • Diurese• Reverse hemodynamic
abnormalities• Decreased renal perfusion
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Diet and Activity
• Salt restricted diet• Fluid restriction• weight loss• Control Hypertension• Reduce cardiac work• Rest
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Diuretic Therapy• fluid volumes overload ↓• ECF volume ↓• venous return ↓• The most effective symptomatic relief• Four Flavours:– Loop diuretics– Thiazide diuretics– K+-sparing– Carbonic anhydrase inhibitors
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ADH Inhibitors Thiazide
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Loop DiureticCarbonic Anhydrase Inhibitors
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Aldosterone Inhibitors (K+ Sparing Agents )
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• For More severe heart failure → loop diuretics– Furosemide, Bumetanide , TorsemideMechanism of action: Inhibit chloride reabsortion in ascending limb of
loop of Henle results in natriuresis, kaliuresis and metabolic alkalosisAdverse reaction:
pre-renal azotemiaHypokalemiaSkin rashototoxicity
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K+ Sparing Agents Potassium sparing diuretics help in reducing the hypokalemia due to
otherdiuretics.
• Triamterene & amiloride – acts on distal tubules to ↓ K secretion
• Spironolactone (Aldosterone antagonist) it improve survival in CHF patients due to the effect on renin-
angiotensin-aldosterone system with subsequent effect on myocardial remodeling and fibrosis
• Aldosterone inhibition minimize potassium loss, prevent sodium and water retention, endothelial dysfunction and myocardial fibrosis.
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Renin angiotensin system• Baroreceptor mediated activation of the SNS leads to an
increase in renin release and formation of angiotensin II
• Angiotensin II acts through AT1 and AT2 receptors (most of its actions occur through AT1 receptors)
• This causes vasoconstriction and stimulates aldosterone production
• aldosterone may also cause myocardial and vascular fibrosis and baroreceptor dysfunction
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Inhibitors of renin-angiotensin- aldosterone system
– Angiotensin converting enzyme inhibitors– Angiotensin receptors blockers– Spironolactone (Aldosterone antagonist)
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Angiotensin Converting Enzyme (ACE) Inhibitors
• ACE inhibitors improve mortality, morbidity, exercise tolerance, left ventricular ejection fraction.
• Captopril, Lisinopril, Enalapril, Ramipril, Quinapril.
Advantages• Improves symptoms significantly• Improves exercise tolerance• Slows disease progression• ↓ cardiac remodeling• Prolong survival
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Scope for ACE Inhibitors…..
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Angiotensin Converting Enzyme Inhibitors MOA
• They block the R-A-A system by inhibiting the conversion of angiotensin I to angiotensin II → vasodilation and ↓ Na retention
• ↓ Bradykinin degradation ↑ its level → ↑ PG secretion & nitric oxide
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Angiotensin Receptor AT-1 blockers (ARB)
Losartan, Irbesartan, Candesartan
• Competitive antagonists of Angiotensin II (AT-1).
• Has comparable effect to ACE I
• Can be used in certain conditions when ACE I are contraindicated (angioneurotic edema, cough)
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ACE-Inhibitors and ARB effects
• Vasodilation
• Decreased fluid retention (afterload & preload)
• Reduction in aldosterone secretion
• Inhibition of cardiac and vascular remodeling
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Animation
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Inotropes
• Increase force of contraction• All increase intracellular cardiac Ca++
concentration• Eg: – Digitalis (cardiac glycoside)– Dobutamine (β-adrenergic recepter agonist)– Amrinone (PDE inhibitor)
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Digoxin MOA
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increased cytoplasmic calcium is
sequestered by SERCA in the SR for later release
Cardiac glycosides : Digoxin (DIGITALIS) inhibit Na +,K + ATPase, the membrane-bound transporter
increase of intracellular sodium concentration
a relative reduction of
calcium expulsion from
the cell by the
sodium-calcium
Exchanger due to ↑ Na
distinctive increase in Cardiac contractility during systole
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Effects
of Digo
xin on
Electrica
l Properti
es
of Cardiac T
issues
early, brief prolongation of the action potential, followed by shortening
(especially the plateau phase)
The decrease in action potential duration is probably the result of increased
potassium conductance that is caused by increased intracellular calcium
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At higher
conce
ntrations…
…..
inhibition of the Na+ pump and reduced intracellular K+
resting membrane potential is reduced
oscillatory delayed depolarizing afterpotentials appear following normally evoked action potentials
overloading of the intracellular calcium stores and oscillations in the free intracellular calcium ion concentration
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β 1 Agonist
Eg: Dobutamine
Effects:-• ↑ cardiac output • ↓ intraventricular filling pressure• direct stimulation of the SA node to↑heart
rate• ↓peripheral resistance by activating alpha2
receptors vasodilation• Conduction velocity in the AVnode is ↑• refractory period is ↓• Intrinsic contractility is ↑• ejection time is ↓
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β 1 Agonist MoA
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BIPYRIDINES phosphodiesterase 3 inhibitor
• Targets PDE -3 (found in cardiac and smooth muscle)• Inamrinone , milrinone
alter the intracellular movements of calcium
by influencing the sarcoplasmic reticulum
increasing inward
calcium flux in the heart during the
action potential
increase myocardial contractility
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Inhibition of PDE3 Increase in cAMP
increase in contractility
vasodilation
↑ Vascular Permeability leads to ↓ in intravascular fluid Volume
the conversion of inactive protein kinase to active form
Protein kinases are responsible for phosphorylation of Ca channels
increased Ca entry into the cell
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β Blockers
MOA
• Acts primarily by inhibiting the sympathetic nervous system (attenuation of the adverse effects of high concentrations of catecholamines)
• reduced remodeling (inhibition of the mitogenic activity of catecholamines.)
• Increases beta receptor sensitivity
bisoprolol, carvedilol , metoprolol
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β blockers
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• Anti-arrhythmic & Anti-oxidant properties.
• shows substantial improvement in LV function & improved survival
• The only contraindication is severe decompensated CHF
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Vasodilators
• Reduction of afterload by arteriolar vasodilatation (hydralazin) reduce LVEDP, O2 consumption,improve myocardial perfusion, stroke volume and COP
• Reduction of preload By venous dilation ( Nitrate) ↓ the venous return ↓ the load on both
ventricles.
• Usually the maximum benefit is achieved by using agents with both action.
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Vasodilators• Isosorbide dinitrate and hydralazine
also used specially in patients who cannot tolerate ACE inhibitors.
• Amlodipine and prazosin are other vasodilators can be used in CCF.
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Calcium Channel Blockers for VasodialationNisoldipine, Isradipine
bind more effectively to open channels and inactivated channels(inner side of the membrane)
reduces the frequency of opening in response to depolarization
marked decrease in transmembrane calcium current
activation of myosin light chain kinase
Vascular smooth muscle (the most sensitive
long-lasting relaxation
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NITRATES & NITRITESNitroglycerin is denitrated by glutathione S -transferase in smooth
muscle
Free nitrite ion is released, which is then converted to nitric oxide
activation of guanylyl cyclase
increase in cGMP
dephosphorylation of myosin light chains, preventing the interaction of myosin with actin
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Venous dilatorsReduce preloadDirect smooth muscle relaxantsEg: sodium nitropruside
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(BNP)-Niseritide• Brain (B-type) natriuretic peptide (BNP) is secreted
constitutively by ventricular myocytes in response to stretch
• Niseritide = recombinant human BNP
• Naturally occurring atrial natriuretic peptide may vascular permeability may reduce intravascular volume)
• Main Side Effect:- hypotension
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Human BNP binds to the particulate guanylate cyclase receptor of vascular smooth muscle and endothelial
intracellular concentrations (cGMP) ↑
smooth muscle cell relaxation
dilate veins and arteries
systemic and pulmonary vascular resistances ↑
Indirect ↑ in cardiac output and diuresis.
Effective in HF because preload and afterload↓
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• ACE inhibitors are cornerstone in the treatment
• β blockers are used in selected patients (mild/moderate failure)
• Diuretics and digoxin are other drugs useful in CCF in select patients.
Conclusion
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STAGE DISABILITY
Stage A MILD
No symptoms Can perform ordinary activities without any limitations
Stage B MILD
Mild symptoms - occasional swelling Somewhat limited in ability to exercise or do other strenuous activities
Stage C MODERATE
Noticeable limitations in ability to exercise or participate in mildly strenuous activitiesComfortable only at rest
Stage D SEVERE
Unable to do any physical activity without discomfort Some HF symptoms at rest
149
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Heart Failure Treatment Algorithm
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Thank U !