- 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 :
- Symptoms of & rsquo; heart failure (dyspnea, fatigue, cough, edema of the ankles….)
- 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
– 1 at 3 % of the general population
– more than 5 % after 75 years
– mortality 60% to 3 years
– mortality 75% at 5
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)
- 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 :
- 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.
- 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
- 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).
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)
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
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.
- 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 :
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
Dr H. Foudad's course – Faculty of Constantine