Heart failure

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Definition :

  • Is defined as the & rsquo; inability of the heart to make in normal, blood flow necessary for metabolic and functional needs of the various bodies.
  • This definition includes etiologies, pathophysiological mechanisms and various clinical expressions.
  • It is the & rsquo; terminal culmination of most heart disease, to & rsquo; end of their evolution.
  • The European Cardiology Society believes that the syndrome includes heart failure 2 Characteristics :
  1. Symptoms of & rsquo; heart failure (dyspnea, fatigue, cough, edema of the ankles….)
  2. Objective evidence of & rsquo; systolic dysfunction and / or diastolic resting preferably by echocardiography.

Reminder physiology : Curves volume pressures

The pressure-volume curve at heart level helps to understand the meaning of different ventricular function indices :

The cardiac cycle : 4 phases

Phase 1 The LV diastolic fills up & rsquo; to achieve diastolic volume (VTD).

Phase 2 The mitral valve closes, Aortic valve n & rsquo; is not yet open and VG contracts so as isovolumic, s & rsquo pressure; student without volume change.

Phase 3 The aortic valve s & rsquo; opens, and VG ejects its contents in the & rsquo; aorta and decreases in volume up & rsquo; to achieve end-systolic volume (VTS).

Phase 4 The aortic valve is closed and the mitral valve is not yet open while the LV contraction is complete : isovolumic relaxation phase during which the pressure drop without volume change.

  • The phases 1 and 4 correspond to the ventricular diastole and clues obtained during these two phases provide guidance on ventricular diastolic function.
  • The phases 2 and 3 correspond to ventricular systole and provide systolic function indices.

Factors determining cardiac output :

  • The volume of & rsquo; stroke is under the control of :

+ The pre-load or diastolic volume (VTD) = Load before the contraction of myocardial fibers, VTD or more pre-load increases, more contraction strength is great : This s & rsquo; called the law of Frank -Starling.
+ Afterload or end-systolic volume (VTS) = Obstacle to & rsquo; left ventricular ejection (VG) Wall stress =. It depends on arterial or systemic resistance to VG and lung resistance to the right ventricle (CEO).
+ Myocardial contractility or inotropic = myocardial contraction strength regardless of load conditions. Myocardial contractility is under the control of the sympathetic adrenergic system Ê.

Mechanisms of & rsquo; right heart failure and left :

1- Impaired systolic function :

  • It can be the result of & rsquo; a :

+ intrinsic disease of the heart muscle : cardiomyopathie primitive
+ amputation mass contractile : myocardial infarction

  • It corresponds to a Sun înution contraction force = infarction myocardial contractility
  • This impairment of systolic function = pump function, will entramer downstream ventricle decreased cardiac output and upstream increased filling pressures = diastolic pressure VG TV with impact on pulmonary capillary pressure. This will entramer congestive signs.

2- Volume overload :

  • It is linked to an increase in "pre-load", determined by the filling pressure of the ventricular = increased systemic venous pressure for & rsquo; right atrium and pulmonary venous pressure for & rsquo; left atrium.
  • This volume overload is often associated with valvular regurgitation kind mitral insufficiency, aortic insufficiency, and will lead to ventricular dilatation with increased ventricular end-diastolic volume.

3- Increased afterload :

  • related to higher downstream pressures of the left ventricle or the right ventricle. C & rsquo; is precisely against this post load the myocardial fibers must resist by contracting with a consequent elevation myocardial mass and increasing the ratio thickness relative to the left ventricular diameter, while the systolic function remains long in the normal range.

L & rsquo; increased load post reduced the volume of & rsquo; stroke. Its main causes are :

  • To the left ventricle : l & rsquo; hypertension (HTA), aortic stenosis, cardiomyopathie obstructive.
  • To the right ventricle : pulmonary embolism and & rsquo; pulmonary hypertension.

compensatory mechanisms :

  • The d & rsquo mechanism; homeostasis serves to control and maintain blood pressure and tissue perfusion.
  • If & rsquo; heart failure, there is a decrease in cardiac output with repercussions hypotension and tissue hypoperfusion. This will result in & rsquo; activation of compensatory mechanisms based primarily on the neurohormonal system.
  • They are three in number :

1/ La stimulation neurohormonale :

The sympathetic system is activated, with a triple action :

– l’action chronotrope positive
– l & rsquo; increase in contractile force of myocardial fibers by stimulation of beta-1-adrenergic cardiac receptors.
– arteriolar vasoconstriction at the expense of the skin and kidney, allowing the maintenance of vascular tissues such privileged the brain and myocardium.

L & rsquo; activation of the sympathetic system depends mainly on the involvement of baroreceptors consequence of the drop in blood pressure.

The renin-angiotensin system is activated during outbreaks & rsquo; chronic heart failure.

L & rsquo; renin hypersecretion stimulates the formation of & rsquo; angiotensin I and II leading to vasoconstriction and secretion of adrenal medulla & rsquo; aldosterone responsible for retention of water and sodium and potassium leak.

Atrial natriuretic factors are activated by the distension of the atria for the purpose vasodilating action and natriuretic.

2/ The law of Frank Starling :

  • It is based on the & rsquo; increase in myocardial contractile force under the & rsquo; effect of & rsquo; stretching of sarcomeres in diastole caused by ventricular dilatation.
  • L & rsquo; addicted! WARNING pressi o ns of i ntra -cavitai res co ntribue thereby to hold o u I e increase in diastolic volume ventriculairegauche (VTDVG). The heart gradually expands.

3/ peripheral metabolic adaptation.

Vicious circle of compensatory mechanisms

Vicious circle of compensatory mechanisms

Epidemiology :

Prevalence :

– 1 at 3 % of the general population
– more than 5 % after 75 years

Prognosis :

– mortality 60% to 3 years
– mortality 75% at 5

etiologies :

IC LEFT :

—> mechanical overload :

  • Pression : RAO, HTA, coarctation TO
  • Volume :
  • IM, IAO
  • Shunts (CIV, PCA….)
  • Hyper speed (Anemia, fistule OF, hyperthyroidism…)

—> Alteration infarction :

  • Ischemic heart disease (IDM, Angina)
  • CMD
  • Myocardite, surcharge (hemochromatosis, amylose, Amylose)

—> Gene filling VG : CMH, CM restrictive, RM

IC RIGHT :

—> mechanical overload :

pressure : RP, any condition in PAH

volume : IT, IP, Shunts (CIV, CIA …)

—> Alteration infarction :

IDM VD, CMD, myocardial specific diseases

—> Gene filling the VD : Adiastolie : pericarditis, RT

Diagnosis of & rsquo; abortion :

functional signs +++

* Dyspnea d & rsquo; stress :

  • Are represented by fatigue and dyspnea. The NYHA classification (New York Heart Association) allows & rsquo; specify the & rsquo; importance.
  • Classification de la NYHA +++
  • Classe I : heart disease without limiting the & rsquo; physical activity
  • Class II : heart disease with mild limitation of & rsquo; physical activity (unusual efforts)
  • class III : heart disease with marked limitation of & rsquo; physical activity (usual efforts)
  • class IV : heart disease with symptoms present at rest and preventing any physical activity.

* Dvspnée paroxysmal : Most often with nocturnal orthopnea

– L & rsquo; pulmonaireaigu edema (OAP)

  • Intense dyspnea crisis, distressing,
  • often preceded by tickling laryngeal and cough
  • followed & rsquo; a frothy sputum, dew, salmon.
  • need to stand or s & rsquo; sit, thirst & rsquo; air, sweats.
  • l & rsquo; alveolar flooding leads to & rsquo; auscultation by a rising tide of crackles purposes.
  • tachycardia, cyanose, print.
  • C & rsquo; is a serious accident, requiring urgent and intensive treatment.

– L & rsquo; subacute pulmonary edema is the & rsquo; minor equivalent of & rsquo; acute pulmonary edema.

– other signs : Cough d & rsquo; effort or rest, Asthenia, fatigability in & rsquo; stress, alteration of the General, obnubilation, cognitive signs….

physical signs :

  • L & rsquo; cardiac auscultation shows :

– tachycardia with a particular heart rate 3 time evoking the gallop or diastolic presystolic.

– One can find a sweet breath of & rsquo; mitral insufficiency due to a fault d & rsquo; sealing of the mitral valve.

  • The pulse is often fast.
  • Irregular pulse suggests a complete arrhythmia. A low pulse is of poor prognosis.
  • Low blood pressure is a poor prognosis.
  • L & rsquo; auscultation moist rales search, inspiratory, predominant bases that & rsquo; they are called crackles or crackles under which testify d & rsquo; a bronchiolar-alveolar edema.
  • It can s & rsquo; is often associated pleural effusion on the right side transsudatif.

chest X-ray :

  • cardiomegaly,
  • the signs of pulmonary edema :

– first sign, dilated veins upper lobar, signs of venous redistribution to summits
– interstitial edema, which thickens the interlobular septa (decrease diffuse parenchymal transparency, stries Kerley), and drowning the contours of broncho-vascular axes (large hilum to blurry edges)
– alveolar edema : fleeting. Broad opaque beaches vague limits, predominant in peri-hilar regions and basal, more or less symmetrical. Sometimes prickly appearance in some edema subacute
– pleural, very frequented : blunting d & rsquo; a dead end, élargissement d & rsquo; une ligne scissurale, effusion more or less abundant

L’ECG : reveals

  • a sinus tachycardia
  • left ventricular hypertrophy
  • a left axis deviation
  • rhythm disorders or ventricular extra systole (ESV)
  • a left bundle branch block.

L & rsquo; echocardiography appreciate :

  • analysis of the FE of the LV and diastolic function
  • Search d & rsquo; a working IM and d & rsquo; pathology
  • the impact on the right cavities
  • expansion or & rsquo; hypertrophy of the left cavities

catheterization appreciate :

  • heart function

– a diastolic pressure LV > at 12 mm de Hg
– elevated pulmonary capillary wedge pressure
– decrease in & rsquo; cardiac index < 2, 5 l / mn / m2
– measuring the fraction of & rsquo; LV ejection : often < at 45%

  • and finds a heart etiology
  • coronary search of ischemic etiology

Diagnosis of & rsquo; IVD :

functional signs :

  • The gastric gravity hepatalgia form.

physical signs :

  • These are peripheral congestion with signs :

* heart liver, hepatomegaly sensitive to palpation smooth edge to the lower, mousse
* abdominojugular test (RHJ)
* jugular turgor. The RHJ is to search in a semi-sitting position by performing a moderate pressure of the & rsquo; right hypochondrium.

  • The peripheral edema (OMI) reflect the fluid retention that s & rsquo; objective as weight gain. They predominate in the feet and ankles, they are white, mous, painless and take the bucket.
  • These signs are associated with oliguria.
  • L & rsquo; cardiac examination retrieves palpation sign Harzer which is defined as the perception of VD beats at the metasternum.
  • Signs of the causal heart disease and highlights tachycardia, a burst B2 pulmonary hearth, the sign Carvalho which is defined as the & rsquo; emphasis in inspiration d & rsquo; a systolic murmur at home tricuspid and reflects the & rsquo; tricuspid regurgitation.

chest X-ray :

  • Increase in & rsquo; cardiothoracic index : the projection of the & rsquo; lower right arc reflects the expansion of & rsquo; right atrium (FROM) and convexity with peak above-diaphagmatique of & rsquo; s lower left arch & rsquo; observed in case of & rsquo; right ventricular hypertrophy (HVD) important.
  • a projection of & rsquo was observed; arc left means in case of & rsquo; pulmonary hypertension (Htap).
  • L & rsquo; analysis of lung parenchyma can learn about the & rsquo; etiology of & rsquo; IVD.

ECG :

  • n & rsquo; is not specific to the & rsquo; IVD and can show d & rsquo signs right atrial enlargement (HAD) P waves with monophasic, further above 2.5 mm a D2, D3, VF.
  • Signs of & rsquo; HVD with large R waves in precordial straight and large S waves in precordial left.
  • Deflection ventricular transition to the left and right deflection QRS.

Echo-Doppler of the right cavities :

It is done in the same time as the & rsquo; exploration of the left cavities ; she allows to :

* assessing the dilation of the right cavities
* look for signs of volume overload such a paradoxical movement of the interventricular septum.
* quantify systolic pulmonary artery pressure from the & rsquo; tricuspid regurgitation.

Right heart catheterization :

  • This bloody invasive exploration has given way to the & rsquo; Doppler echocardiography today, however it remains interesting for calculation of pulmonary arterial resistance in particular.

Diagnosis of & rsquo; congestive heart failure :

  • C & rsquo; is & rsquo; ultimate evolution of the & rsquo; abortion.
  • L & rsquo; congestive heart failure meets the signs of & rsquo; right heart failure and left.
  • L & rsquo; clinical associate noise examination of galloping left, groans under crackles d & rsquo; alveolar edema or crackles jugular veins, hepatomegaly and edema of the lower limbs.
  • Dyspnea s & rsquo; & rsquo accompanied; hepatalgia and d & rsquo; oliguria in the & rsquo; lack of diuretic therapy. L & rsquo; evolution and prognostic factors
  • It can not be separated from its etiology and treatment, certain diseases in particular valvular being surgically curable.
  • In most of the left heart, l & rsquo; emergence of & rsquo; abortion marks an evolutionary turning point of the disease +++
  • The therapeutic classes discoveries in recent years such as inhibitors of & rsquo; converting enzyme (IEC) antagonists of receptors I’ angiotensin (NOW), l & rsquo; rational use of beta blocker treatment and anti-aldostérones enabled d & rsquo; improve & rsquo; life expectancy of heart failure.
  • Surgical therapy and instrumental (percutaneous angioplasty) have transformed the prognosis of the most serious forms.

L & rsquo; evolution can be considered as follows :

  • recovery or stabilization in the & rsquo; treatment effect
  • evolutionary episodes related : a patient non-compliance, OAP, accidents thrombo-emboliques, superinfection bronchopulmonary….
  • passages congestive heart failure with onset of signs & rsquo; right heart failure.

Factors decompensation :

  • Deviation salt diet
  • Heart rhythm disorders
  • hypertensive
  • IM aigue pair of cordage rupture or endocarditis
  • Renal failure
  • Increased heart rate : fever, anemia, pregnancy, thyrotoxicose
  • Pulmonary embolism In the terminal stage can be faced with low flow with severe hypotension, renal failure, making the patient dependent positive inotropic drugs.

The poor prognostic factors :

  • clinics : advanced age, comorbidity factors, a stage III-IV NYHA, low blood pressure.
  • The test running 6 minutes.
  • Echocardiographique : the fraction of & rsquo; collapsed ejection
  • Biology : renal failure, Brain Natriuretic Peptide rate (BNP).

Treatment :

Heart failure : vicious circle

Outline of treatment :

  • Treatment of the cause (if possible)
  • lifestyle and dietary rules +++
  • Therapeutic education
  • cardiac rehabilitation
  • Medical treatment
  • electrical treatments (GIVE, Resynchronisation)
  • Devices & rsquo; support VG
  • heart transplant (<65 years)

non-drug treatment of chronic ICT :

  • Treatment of the cause (if possible)
  • lifestyle and dietary rules +++
  • Therapeutic education
  • cardiac rehabilitation

A / treatment of the cause (if possible) :

  • Valvulopathies : replacement and valvular plasty…
  • Ischemic heart disease : bridging, angioplasty
  • Treatment of hypertension.

B / lifestyle and dietary rules +++

  • Weaning definitive smoking
  • Good diabetes control.
  • water restriction 1500 mL / 24 when the patient is symptomatic = Equivalent 6 d & rsquo glasses water
  • salt-free diet :

– Banish the salt shaker from the table
– Cook without salt
– Read labels carefully
– Know the foods high in salt
– Know the equivalent gram of salt
– Beware of hidden sources of sodium : pain, conserves, condiments

C / therapeutic Education :

  • Weighing if possible daily, Before the break fast, bladder empty, on the same balance, without shoes.
  • Weight recorded on a calendar next to the person weighs.
  • If weight gain assess :

– Respect for water restriction and sodium diet
– Noncompliance eventual treatment of the causes of decompensation

  • lifestyle and dietary errors Assessment.
  • Information, education and patient motivation to follow treatment, respect the lifestyle and dietary rules and make physical efforts.

D / Cardiac Rehabilitation :

  • Reconditioning to & rsquo; stress
  • socio reintegration – professional
  • Offer physical activity

E / Medication :

anti renin-angiotensin-aldosterone system drugs :

  • Inhibitors of & rsquo; converting enzyme & rsquo; angiotensin IEC =
  • ATI receptor inhibitors of the & rsquo; angiotensin II = ARBs or "ARBs"
  • Diuretics Spironolactone antialdostéroniques = (Aldactone) or eplerenone (Inspra)

IEC :

names : Triatec®. Coversyl®, Innovace®, Lopril® etc…

Buts : mortality decline, improving quality of life, reduced morbidity in all stages.

Cons-indications : Angioedema. bilateral renal artery stenosis, severe renal impairment, the pregnancy.

Side effects : cough, low blood pressure, renal failure, hyperkaliémie.

recommendations : start with moderate doses, BP monitoring +++, gradual but essential increase doses up & rsquo; to the target dose or maximum.

Recommendations of the & rsquo; ESC :

The IEC are recommended in all patients with LV dysfunction (FE< 45%) with or without symptoms

ACE inhibitors improve survival, symptoms, functional capacity, the LV remodeling, and reduces the number and duration of hospitalizations

ARAII :

names : Cozaar®, Treg®, Aprovel®, Atacand® etc…

Buts : replacing IEC if cough, see combination of the two for the most serious patients.

Cons-indications : bilateral renal artery stenosis, renal failure, pregnancy.

Side effects : low blood pressure, renal failure, hyperkaliémie.

recommendations : Monitoring of renal function and BP +++. Start with moderate doses, gradual but essential increase doses up & rsquo; to the target dose or maximum

Diuretics anti-aldostéroniques :

names : ALDACTONE® (spironolactone), Inspra® (eplerenone)

Buts : diuretic, decrease in mortality and morbidity among the most serious patients. Cons-indications : Severe renal impairment, severe hyperkalemia.

Side effects : gynecomastia, renal failure, hyperkaliémie > 5,5 mmol/l.

recommendations : small doses in & rsquo; chronic heart failure, monitoring serum potassium and renal function.

Diuretics s & rsquo; cove, thiazidiques :

– essential for the symptomatic treatment of & rsquo; IC congestive.

+ rapidly improving dyspnea and increase tolerance to & rsquo; stress (Class I recommendation, level A)

+ Starting Salary

Diuretics s & rsquo; loop or thiazide : Lasilix0, FLUDEX0

Always administered in addition to & rsquo; an IEC (Class I recommendation, level of evidence C).

If GFR < 30 mL/min, avoid thiazides

Beta blockers :

Against long-indicated in the & rsquo; IC due to their negative inotropic effects.

names : Dilchard® (carvedilol), Cardensiel® (bisoprolol), the Seloka® (metoprolol), rash things® (nevibolol).

Buts : decrease in mortality and morbidity, symptom improvement.

Cons-indications : decompensation recent heart, BPCO, severe respiratory failure, severe hypotension, cardiac conduction disorder.

Side effects : especially orthostatic hypotension, bradycardia.

recommendations : start remote processing & rsquo; cardiac decompensation phase, in hospital or in the firm & rsquo; a cardiologist, with small doses that are increased gradually by cardiologist during consultations. Monitoring pulse rate and BP ++ and functional tolerance.

digitalis : digoxin® If severe AF or HF.

Treatment retarder and positive inotropic.

Contraindication : trouble conductif, dyskaliémie, renal failure, aortic stenosis, CMOs, WPW, ventricular tachycardia.

Side effects : nausea, vomiting, headaches, confusion, yellow vision, bradycardia.

Risk of overdose : dosage of digoxinémie, ECG.

Other positive inotropic agents :

  • Frequently used intravenously in case of & rsquo; severe heart failure with pulmonary congestion signs and hypo peripheral perfusion.
  • The most commonly used product is the Dobutamine
  • Problems related to the & rsquo; administration of dobutamine are :

– therapeutic exhaust,
– Accéiération heart rate,
– Induction d & rsquo; severe tachyarrhythmia and / or d & rsquo; myocardial ischemia.

Other vasodilators :

If & rsquo; intolerance to ACE inhibitors and ARBs, we can try the & rsquo; hydralazine association dinitrate & rsquo; isosorbide (Class I recommendation, level of evidence B)(A HeFT I).

nitrates : Can be used as adjuvant treatment of & rsquo; angina or to relieve dyspnea.

calcium channel blockers : The newer calcium channel blockers (félodîpine et amlodipîne), if d & rsquo; hypertension or & rsquo; concomitant angina not controlled by nitrates and BB.

Antithrombotiques :

  • Antiagrégants plaquettaires : secondary prevention in & rsquo; IC d & rsquo; ischemic
  • oral anticoagulants : strongly recommended (Recommendation Class i, level of evidence A) in :

– L & rsquo; IC associated with chronic atrial fibrillation,
– ATCD d & rsquo; thromboembolic events
– Thrombus mobile intra VG

anti-arrhythmic treatment : Cordarone® Only if recent FA or ventricular tachycardia proven.

F/ Resynchronisation cardiaque :

Unsynchronized contraction of the ventricles (asynchronisme interventriculaire) / cardiac resynchronization

Effects of cardiac resynchronization

  • heart function

– Increased LVEF
– Decrease in mitral regurgitation
– Increase filling time LV
– Decrease time of isovolumetric contraction
– Increased dP / dt

  • reverse remodeling

– Decreased LV diastolic volume
– Volume decrease systolic LV

driving practice treatment

Dr H. Foudad's course – Faculty of Constantine