Congestive Heart Failure

1. HEARTHEART
FAILUREFAILURE

2. HEART FAILUREHEART FAILURE
In the 1.5 - 2% of the world population shows
signs of congestive heart failure
Prevalence of heart failure in Europe - 2.9 - 3.9%
(60% of them without signs of symptomatic
dysfunction of the left ventricle)
In Ukraine every 3 patients with
cardiovascular disorders diagnosed CHF

3. HEART FAILUREHEART FAILURE
 Inability of the heart to pump an adequateInability of the heart to pump an adequate
amount of blood to the body’s needsamount of blood to the body’s needs
 CONGESTIVE HEART FAILURECONGESTIVE HEART FAILURE – refers to– refers to
the state in which abnormal circulatorythe state in which abnormal circulatory
congestion exists a result of heart failurecongestion exists a result of heart failure
“All the signs of CHF are the consequences of
inadequate force of contraction"

4. Spiral structure and function of the heart and major blood
vessels
 Cardiac muscle is one longCardiac muscle is one long
"piece" muscular tissue, twisted"piece" muscular tissue, twisted
in a swirling at 180 º helix.in a swirling at 180 º helix.
 Activity of the heart comparedActivity of the heart compared
with the tornado - the reductionwith the tornado - the reduction
is carried out "by 180 º spiral"is carried out "by 180 º spiral"
with subsequent ejection ofwith subsequent ejection of
blood into the aorta.blood into the aorta.

5. SponsoredSponsored
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6. The phenomenon of
"GOLDEN CROSSING“ Fibonacci
The phenomenon of "GOLDEN CROSSING" Fibonacci -
consequence of the law of proportionality and a share where
this number equals 0.618
Leonardo da Vinci. "Fibonacci phenomenon observed in nature, painting,
architecture, hydrodynamics" ... and in medicine (blood flow,
electrophysiology of the heart) and other
Diastolic blood pressure (80.4 mm Hg), Pulse pressure (49.5 mm)
Systolic blood pressure (130 mm Hg) Diastolic blood pressure (80 mm)
Systole, 0.371 sec
Diastole, 0.600 sec The thickness of the posterior wall of the left
ventricle in systole, 8.04 mm
The thickness of the posterior wall of the left
ventricle in diastole, 1.30 mm
= 0,618
= 0,618
= 0,618
= 0,618

7. CAUSES OF HEART FAILURE:CAUSES OF HEART FAILURE:
 Final common pathway of many kinds of heartFinal common pathway of many kinds of heart
diseasesdiseases
 Ischemic, alcoholic, restrictive, hypertrophicIschemic, alcoholic, restrictive, hypertrophic
 Optimal treatment requires identification of primary &Optimal treatment requires identification of primary &
secondary factors leading to CHFsecondary factors leading to CHF
 HELPFUL RESULT of dilatation:HELPFUL RESULT of dilatation: increases cardiacincreases cardiac
outputoutput
 HARMFUL RESULT of dilationHARMFUL RESULT of dilation: more wall tension,: more wall tension,
more oxygen is needed to produce any given strokemore oxygen is needed to produce any given stroke
volumevolume

8. 1. The most common cause of heart failure is nosological
coronary heart disease (CHD), which, according to
epidemiological and multicenter studies diagnosed in 60% -
75% of patients.
2. Arterial hypertension (AH)
3. Types (phenotypes) CMP:
HCM (hypertrophic);
DCM (dilated);
ARVD (arrhythmogenic right ventricular dysplasia);
RCMP (restrictive );
Unclassified CMP:
incompact myocardium;
stress-induced (takotsubo);
4. Arrhythmias: - tahysystolic, bradysystolichni.
5. Myocarditis: - viral, bacterial, systemic diseases of
connective tannins.
CAUSES OF HEART FAILURE:CAUSES OF HEART FAILURE:

9. 7. Pericardium Diseases : - exudative pericarditis, hydropericardium,
constrictive pericarditis.
8. Secondary cardiomyopathy: - toxic (including alcohol)
- Medications,
- Endocrine (hyperthyroidism,
hypothyroidism, pheochromocytoma)
9. Pulmonary hypertension: - Primary,
- Secondary (pulmonary heart,
congenital, posttromboembolic).
6. Valve and congenital heart defects:
- aortic, mitral, tricuspid,
pulmonary artery valve.
CAUSES OF HEART FAILURE:CAUSES OF HEART FAILURE:

10. Chronic heart failureChronic heart failure
Pathogenesis-1Pathogenesis-1
«Neurohumoral Theory "- RAAS overactivity
- Real effect of ACE inhibitors - 23% (relative risk of death)
- Significant reduction in the risk of death is observed only in the first 18
months. ACE inhibition, and in the next 30 months the effect is similar to
placebo.
But inhibitorr RAAS not able to cause complete its blockade, which
indicates "incomplete competence" neurohumoral theory (an overactive
RAAS)

11. Myocardial
hypertrophy
Intrahlomerulyar
hypertension
RААS
circulatory
(immediate effects)
TissueTissue
(long-term effects)(long-term effects)
Aldosterone
retention of sodium and water
Vasoconstriction
Arrhythmogenic
effects
kidneyskidneys
Heart
Hypertrophy of
vessels
blood vesselsblood vessels

12. CARDIAC FAILURECARDIAC FAILURE
 VENOUS
PRESSURE
 CARDIAC
OUTPUT
 BLOOD
PRESSURE
 SYMPATHETIC
ACTIVITY
 RENAL
BLOOD FLOW
 RENIN ANGIOTENSIN II
 ALDOSTERONE
 SODIUM RETENTION
 CAPILLARY
FILTRATION
EDEMA

13. proinflammatory
cytokines
-negative inotropic effect
- Cardiac remodeling (irreversible dilatation of cavities,
cardiomyocyte hypertrophy)
- Impaired endothelium-dependent dilation aretriol
- Increased apoptosis of cardiomyocytes and cells of
the peripheral muscles
Pathogenesis-2.Pathogenesis-2.
" SY T O K I N M O D E L '" CHF" SY T O K I N M O D E L '" CHF
proinflammatory cytokines: tumor necrosis factor alpha – TNFa, IL - 1, IL - 6
adhesion molecule (LAM-mikrotsytarna adhesion molecules, ISAM-1 intercellular
adhesion molecules, VSAM_sudynno-cell adhesion molecules
- Antibodies to the vascular wall and myocardium
- Chemokines (proteins that induce migration of monocytes in the myocardium)
- Shock proteins ("stress proteins" or "heat shock proteins"(Heat Shock Proteins,
HSP).
- Components of oxidative stress (NO, free radicals)
- Endothelin 1,2,3.

14. Pathophysiological factors of HF
1.HF due to pressure or volume overload
Ventricular overload can be caused or increased resistance to systolic
ejection of blood (so-called "pressure overload") or elevated diastolic blood
blood volume ("volume overload").
LV pressure overload occurs in hypertension and aortic stenosis.
LV volume overload - for aortic and mitral insufficiency.
Right ventricular pressure overload characteristic for pulmonary
hypertension and pulmonary artery stenosis,
Right ventricular volume overload - for tricuspid insufficiency.
2. Primary lesions of the heart muscle
primary Myocardial CH) observed with coronary artery disease
and myocardial lesions. (DCM, most of myocarditis, secondary
cardiomyopathy).

16. Hypertrophy (LVH). This - adaptive phenomenon, aims to maintain the
ability to initially affected or overwhelmed myocardial develop
sufficient intraventricular pressure in systole by reducing the
workload per unit of its mass.

17. Progression of RemodellingProgression of Remodelling
Regression of RemodellingRegression of Remodelling

18. Types remodeling and left ventricular hypertrophy
Types remodeling and left
ventricular hypertrophy
Characteristic types of
remodeling and hypertrophy
Normal left ventricular geometry ventricular mass index <125h/m2 men
<110h/m2 women
index "wall-radius" = 0.42
Concentric remodeling of the left
ventricle
VMI > 125(g/m2) in the norm; index
"wall-radius'> 0.42
Concentric left ventricular hypertrophy VMI >125g/m2 in men,> 110g/m2
women; Index "wall-radius'> 0.42
Eccentric remodeling of the left
ventricle
VMI >125 g/m2 in men,< 110h/m2
women ; Index "wall-radius‘< 0.42
Eccentric left ventricular hypertrophy VMI ≥125g/m2 in men, ≥ 110g/m2
women; Index "wall-radius‘< 0.42

19. Pathophysiology of Cardiac Performance
FactorFactor MechanismMechanism Therapeutic StrategyTherapeutic Strategy
1. Preload (work or1. Preload (work or
stress the heart faces atstress the heart faces at
the end of diastole)the end of diastole)
increased blood volume andincreased blood volume and
increased venous tone---increased venous tone---
>atrial filling pressure>atrial filling pressure
-salt restriction-salt restriction
-diuretic therapy-diuretic therapy
-venodilator drugs-venodilator drugs
2. Afterload2. Afterload
(resistance against(resistance against
which the heart mustwhich the heart must
pump)pump)
increased sympatheticincreased sympathetic
stimulation & activation ofstimulation & activation of
renin-angiotensin systemrenin-angiotensin system
---> vascular resistance --->---> vascular resistance --->
increased BPincreased BP
- arteriolar vasodilators- arteriolar vasodilators
-decreased angiotensin-decreased angiotensin
II ACE inhibitors)II ACE inhibitors)
3. Contractility3. Contractility decreased myocardialdecreased myocardial
contractilitycontractility
-inotropic drugs-inotropic drugs
(cardiac glycosides)(cardiac glycosides)
4. Heart Rate4. Heart Rate decreased contractility anddecreased contractility and
decreased stroke volumedecreased stroke volume
---> increased HR (via---> increased HR (via
activation ofactivation of
b-adrenoceptors )b-adrenoceptors )
antiarrhythmicantiarrhythmic
therapytherapy
metabolic therapymetabolic therapy

20. Classification of heart failure
On flow
AcuteChronic
By the nature dysfunction
Systolic dysfunction
Without dysfunction LV
(Diastolic dysfunction - Types I,
II, III)
Mixed dysfunction
For advantage destruction
left ventricular
right ventricular
total
For stage process (Strazhesko, VH Vasilenko)
changes in organs
I-Compensated CHF
II Decompensated:
IIA reverse
IIB little reverse
III irreversible heart failure
For tolerability loads
I - IV functional class (for NYHA)

21. CLASSIFICATION:CLASSIFICATION:
 CHRONIC HEART FAILURECHRONIC HEART FAILURE
 Typically observed in patients with dilatedTypically observed in patients with dilated
cardiomyopathy or multivalvular heart diseasescardiomyopathy or multivalvular heart diseases
that develops or progresses slowlythat develops or progresses slowly

22. IHD: diffuse atherosclerosis. Atrial fibrillation, permanent tahysystolic form.IHD: diffuse atherosclerosis. Atrial fibrillation, permanent tahysystolic form.
Chronic congestive heart failure, stage III with systolic left ventricularChronic congestive heart failure, stage III with systolic left ventricular
dysfunction, FC IV NYHA.dysfunction, FC IV NYHA.

23. Classification of heart failure
By the nature dysfunction
 SYSTOLIC DYSFUNCTION:SYSTOLIC DYSFUNCTION:
 Inadequate force is generatedInadequate force is generated
to eject blood normallyto eject blood normally
 Reduce cardiac output, ejectionReduce cardiac output, ejection
fraction (< 45%)fraction (< 45%)
 Typical of acute heart failureTypical of acute heart failure
 Secondary to AMISecondary to AMI
 Responsive to inotropicsResponsive to inotropics
 The diameter of the leftThe diameter of the left
atrium in normal (up to 4atrium in normal (up to 4
cm)cm)
 No signs of stagnation inNo signs of stagnation in
the pulmonary circulation.the pulmonary circulation.
 DIASTOLIC DYSFUNCTIONDIASTOLIC DYSFUNCTION
 Inadequate relaxation toInadequate relaxation to
permit normal fillingpermit normal filling
 Hypertrophy and stiffeningHypertrophy and stiffening
of myocardiumof myocardium
 Cardiac output may beCardiac output may be
reducedreduced
 Ejection fraction is normalEjection fraction is normal
 Do not respond optimally toDo not respond optimally to
inotropic agentsinotropic agents
 diameter of the left atrium isdiameter of the left atrium is
enlarged > 4 cm;enlarged > 4 cm;

24. Criteria for diastolic dysfunction
Normal ejection fraction with increasing diameter of the LA and
the presence of congestion in the lungs;
The degree of diastolic dysfunction:
violation of relaxation - Mild diastolic dysfunction or
Type I DDLV E / A <1
psevdonormalne filling-moderate degree of diastolic dysfunction,
Type II DDLV E / A = 1-2
restrictive filling - heavy degree of diastolic dysfunction,
Type III DDLV, E / A> 2

25. Graphic representation of left ventricular diastolic function was
normal.
V (m / sec) - the rate of filling of the left ventricle due
to Elaxation of his Early diastole (E)
and through the left Atrial systole (A).
Norma E / A = 1.5 -1.6

26. The first type of left ventricular
diastolic dysfunction - impaired
relaxation
(E / A <1.0)
The second type of left ventricular
diastolic dysfunction
psevdonormalnyy (E / A ≈ 1,0).
The third type of left ventricular
diastolic dysfunction -
restrictive (E / A = 2-3).

27. CHRONIC HEART dysfunction = CHF
(MD Strazhesko, V.H.Vasylenko, 1935)
StageI (primary, hidden).
Subjective (shortness of breath, palpitations)
and objective signs of circulation are only an
exercise, alone they are missing.
Stage II .
The presence signs of hemodynamics.
Metabolic disorders and functions of other
organs.
Period A (II A).
Insufficiency of "right" or "left" heart.
Stagnation and dysfunction of other organs
are mild and often find themselves at the end
of the day (or after exercise).
Period B (II B).
Insufficiency of "right" and "left" heart.
Stagnation are more pronounced and are at
rest.
Stage III (final, dystrophic).
Insufficiency of heart. Expressed stagnation,
significant metabolism and functions of other
organs. The presence of irreversible
structural and morphological changes in the
organs.
CHRONIC HEART FAILURE
(New York Heart Association - NYHA,
1964) on the basis of subjective criteria
Functional class 1.
Physical activity is not limited. Ordinary
physical activity does not cause undue
fatigue, palpitation, dyspnea or angina.
Functional Class 2.
Some limitations of physical activity.
At rest very well.
Regular physical activity causes excessive
fatigue, palpitation, dyspnea or angina.
Functional class 3.
A major limitation of physical activity. In the
rest very well. A little exercise causes
excessive fatigue, palpitation, dyspnea or
angina.
Functional Class 4.
Patients unable to bear no physical activity
without worsening health. Subjective
manifestations of heart failure can occur even
at rest.
Any physical activity causes deterioration of
health.

28. The Stages of Heart Failure – NYHAThe Stages of Heart Failure – NYHA
ClassificationClassification
ClassClass Patient SymptomsPatient Symptoms
Class IClass I No limitation of physical activity. Ordinary physical activity
does not cause undue fatigue, palpitation, or dyspnea
(shortness of breath).
Class IIClass II Slight limitation of physical activity. Comfortable at rest, but
ordinary physical activity results in fatigue, palpitation, or
dyspnea.
Class IIIClass III Marked limitation of physical activity. Comfortable at rest,
but less than ordinary activity causes fatigue, palpitation, or
dyspnea.
Class IVClass IV Unable to carry out any physical activity without discomfort.
Symptoms of cardiac insufficiency at rest. If any physical
activity is undertaken, discomfort is increased.

29. Physical tolerance to a 6-minute test
FKFK The distance walkThe distance walk
for 6 min, mfor 6 min, m
Maximum oxygenMaximum oxygen
consumption (ml/ kg-consumption (ml/ kg-
1/m)1/m)
FK IFK I 550- 700550- 700 18,1 – 22,018,1 – 22,0
FK IIFK II 301 – 550301 – 550 14,1 – 18,014,1 – 18,0
FKFK ІІІІІІ 150 – 300150 – 300 10,1 – 14,010,1 – 14,0
FKFK ІVІV << 150150 <<1010
This methodical approach allows us not only to determine the
degree of heart failure and evaluate the state of the functional
reserve of the patient, but also monitor the effectiveness of
treatment and timely correction therapy.

30. Patients with cardiac pathology, which limits their
physical activity. Ordinary physical activity does not
cause undue fatigue, palpitation, dyspnea or angina
(Class I New York classification of functional status of patients)
When instrumental study finds at least one of the
signs:
 Left ventricular ejection fraction <50% but> 40%
Absence of ejection fraction increase with stress –
echocardiography at least 10% or ejection fraction
reduction after exercise
 Signs of left ventricular hypertrophy
Asymptomatic left ventricular dysfunctionAsymptomatic left ventricular dysfunction

31. Objective clinical signs of
congestive heart failure
bilateral peripheral edema,
hepatomegaly;
swelling and pulsation of neck veins,
ascites,
hydrothorax (bilateral or right-
handed);
bilateral wet rhonchuses in the
lungs;
tachypnea;
tahisystoliya;
expansion percussion borders of the
heart;
III (protodiastolichnyy) tons;
IV (presystolichnyy) tons;
accent II tone of the pulmonary
artery;
Subjective symptoms of heart
failure
shortness of breath;
cough on exertion and / or
night;
weakness, "cotton" weak
"wilted" feet and hands
fatigue during exercise;
nycturia; oliguria;
weight loss;
Symptoms of the
gastrointestinal tract, and
CNS.
Clinical symptoms
CHF

32. CLASSIFICATION:CLASSIFICATION:
 ACUTE HEART FAILUREACUTE HEART FAILURE
 Sudden development of a large myocardialSudden development of a large myocardial
infarction or rupture of a cardiac valve in ainfarction or rupture of a cardiac valve in a
patient who previously was entirely well, usuallypatient who previously was entirely well, usually
predominant systolic dysfunctionpredominant systolic dysfunction

33. Acute heart failureAcute heart failure
T.Killip, J.Kimball (1997)
I - no stagnant wheezing, absent additional tone (2-4% mortality) are
dyspnea, tachycardia, BP↑,N
IIa - is choking, tachycardia, rales over less congested part of the
lungs (<50% of the area), not auscultated third tone, BP↑,N (3-5%
mortality)
IIb - are dyspnea, tachycardia, rales stagnant over the lower part of
the lungs (<50% of the area), but there protodiastolichnyy gallop BP↓
(mortality 10-15%)
III - is dyspnea, tachycardia, rales stagnant over most of the lung
(>50%), pulmonary edema is protodiastolichnyy gallop BP↓60-
9040
IV - cardiogenic shock DP< 6020

34. Classification of clinical severity of
acute heart failure at Forrester.
Class I, Group A "warm and dry"
Class II, Group B "warm and humid"
Class III group L "cold and dry"
Class IV, Group C "cold and wet"
Score peripheral blood (tissue perfusion)
and auscultation of the lungs (pulmonary congestion)

35. PULMONARY CONGESTION &PULMONARY CONGESTION &
RESPIRATORY SYMPTOMS:RESPIRATORY SYMPTOMS:
 Result of dilatation & increasing left ventricularResult of dilatation & increasing left ventricular
end diastolic pressureend diastolic pressure, left atrial pressure &, left atrial pressure &
capillary pressurescapillary pressures
 Results to pulmonary vascular congestion &Results to pulmonary vascular congestion &
symptoms associated with cough with bloodsymptoms associated with cough with blood
tinged sputumtinged sputum
EDEMA OF THE BRONCHIAL MUCOSAEDEMA OF THE BRONCHIAL MUCOSA
Increases resistance to airflow producingIncreases resistance to airflow producing
respiratory distress similar to asthma (cardiacrespiratory distress similar to asthma (cardiac
asthma)asthma)

37. I. Acute decompensated heart failure
(de novo or as decompensated CHF): KII / FII
II. Hypertensive AHF: K II-III / FII-III
III. AHF with pulmonary edema: K III / FII,
IVa. Cardiohenyc shock / low cardiac output syndrome:
K III- IV / F-III
IVb. Hard cardiohenyc shock: K IV / F IV
V. AHF with high emissions: KII / F-II.
VI. Acute right ventricular failure: F II-III.
Classification AHF of the European
Society of Intensive Care, 2005

38. PHYSICAL EXAM:PHYSICAL EXAM:
 Jugular venousJugular venous
distentiondistention
 RalesRales
 Pleural effusionPleural effusion
 EdemaEdema
 HepatomegalyHepatomegaly
 AscitesAscites

39. Instrumental diagnosis of heart failure
ECHOCARDIOGRAPHY
Chest radiography
electrocardiography
radionuclide ventriculography
Magnetic resonance imaging
EVALUATION heart rate variability
Tests with exertion
Stress echocardiography with dobutamine
transesophageal Echocardiography
EVALUATION respiratory function
Invasive methods (coronary angiography, LV katetyryzatsiya with
contrast ventriculography).
LABORATORY METHODS (brain natriuretic peptide (BNP, NT-Pro BNR).

41. EHOCARDIOHRAFIYA
Норма
Left ventricular
heart failure
Right ventricular
heart failure

42. CLINICAL MANAGEMENT OFCLINICAL MANAGEMENT OF
CONGESTIVE HEART FAILURECONGESTIVE HEART FAILURE
 OBJECTIVES:OBJECTIVES:
 Increase cardiac contractilityIncrease cardiac contractility
 Decrease preload ( left ventricular pressure)Decrease preload ( left ventricular pressure)
 Decrease afterload (systemic vascular resistance)Decrease afterload (systemic vascular resistance)
 Normalize heart rate and rhythmNormalize heart rate and rhythm

43. Reduce workload of heart
1.Limit activity level reduce weight control hypertension
2. Restrict sodium (low salt diet)
3. Give diuretics (removal of retained salt and water)
4. Give angiotensin-converting enzyme inhibitors
(decreases afterload and retained salt and water)
5. Give digitalis (positive inotropic effect on depressed
heart)
6. Give vasodilators (decreases preload & afterload)

44. DRUGS USED TO TREATDRUGS USED TO TREAT
CONGESTIVE HEART FAILURECONGESTIVE HEART FAILURE
VASODILATORS
-ENALAPRIL
-FOSINOPRIL
-LISINOPRIL
-QUINAPRIL
-HYDRALAZINE
-ISOSORBIDE
SODIUM
NIITROPRUSSIDE
DIURETICS
-BUMETANIDE
-FUROSEMIDE
HYDROCHLOROTHIAZIDE
-METALAZONE
INOTROPIC AGENTS
-DIGOXIN
-DIGITOXIN
-DOBUTAMINE
-AMRINONE
-MILRINONE

45. Pharmacotherapy of heart failure with preserved
systolic function, or diastolic dysfunction.
ACE inhibitors: captopril, enalapril, lisinopril, ramipril,
trandolapril, or prestarium-
B ATIIAR candesartan, valsartan, eprosartan (teveten)
β-blockers: metoprolol succinate (betalok-COP),
bisoprolol, NEBILET, carvedilol (koriol, talliton)
CCA: Verapamil, lerkamen, amlodipine
Diuretics: indap, tryfas - carefully
Metabolic drugs (corvitin, enerhoton) and potassium
preparations (Panangin, ritmokor) and magnesium
(ritmokor, Beres-Magnesium plus B6).

46. Treatment of heart failure with systolicTreatment of heart failure with systolic
dysfunctiondysfunction
 BETABETA
ADRENOCEPTORADRENOCEPTOR
STIMULANTS:STIMULANTS:
 DOBUTAMINEDOBUTAMINE
 Increases cardiac outputIncreases cardiac output
 Decrease in ventricularDecrease in ventricular
filling pressurefilling pressure
 Given parenterallyGiven parenterally
 CONTRAINDICATIONS:CONTRAINDICATIONS:
pheochromocytoma,pheochromocytoma,
tachyarrythmiastachyarrythmias
 ADVERSE EFFECTS:ADVERSE EFFECTS:
precipitation or exacerbationprecipitation or exacerbation
of arrythmiaof arrythmia
 DRUGS WITHOUTDRUGS WITHOUT
POSITIVE INOTROPICPOSITIVE INOTROPIC
EFFECTS USED IN HEARTEFFECTS USED IN HEART
FAILURE:FAILURE:
 DIURETICSDIURETICS
 Reduce salt & waterReduce salt & water
retentionretention  reducereduce
ventricular preloadventricular preload
 Reduction in venousReduction in venous
pressurepressure  reduction ofreduction of
edema & its symptoms,edema & its symptoms,
reduction of cardiac sizereduction of cardiac size 
improved efficiency of pumpimproved efficiency of pump
functionfunction

47. Aldosterone antagonists
Until one recommended in 2002 representatives of the class of drugs - spironolactone
in year 2005 added another selective representative of this class - eplerenone.
In new guidelines extended performance directed small doses
of these drugs (not more than 50 mg / d), to improve the
survival of patients with LV systolic dysfunction, including:
a) in addition to the treatment of ACE inhibitors, ß - blockers
and diuretics in patients with HF III - IV FC in NYHA;
b) as an adjunct to the treatment of ACE inhibitors and ß -
blocker in patients after myocardial infarction, heart failure or
signs of diabetes.
Aldosterone antagonists
Until one recommended in 2002 representatives of the class of drugs - spironolactone
in year 2005 added another selective representative of this class - eplerenone.
In new guidelines extended performance directed small doses
of these drugs (not more than 50 mg / d), to improve the
survival of patients with LV systolic dysfunction, including:
a) in addition to the treatment of ACE inhibitors, ß - blockers
and diuretics in patients with HF III - IV FC in NYHA;
b) as an adjunct to the treatment of ACE inhibitors and ß -
blocker in patients after myocardial infarction, heart failure or
signs of diabetes.
Antithrombotic therapy:Antithrombotic therapy: Aspirin + TiyenopiridynyAspirin + Tiyenopiridyny
(Clopidogrel, Plavyks, Aterokard) or Warfarin(Clopidogrel, Plavyks, Aterokard) or Warfarin

48. Cardiac glycosides ( digoxin).Cardiac glycosides ( digoxin).
Positive inotropic effect of glycosides realized
through blocking ATP cardiomyocytes and blockade of potassium-sodium
pump: inhibition of K + entry into the cell and Na release from cells,
cardiomyocytes increase in the number of ionized Ca + (stimulating its
release from tanks sarkoplazmtyc reticulum),
direct stimulatory effect on actomyosin proteins infarction, energy efficiency
increase the efficiency of myocardial energy compensated heart failure.
Their place in medical practice has not been changed.
They are still shown in patients with atrial fibrillation, regardless of
the severity of symptomatic heart failure and LV dysfunction. They
are used mainly in combination with β-blockers. Appointments
consists of digoxin also recommended for patients with sinus
rhythm, taking ACE inhibitors and β-blockers as a means of
reducing the need for hospitalization.
Their place in medical practice has not been changed.
William
Uizerinh
(1741-1799)

49. EFFECTSEFFECTS glycosidesglycosides IN HEART FAILURE:IN HEART FAILURE:
 Stimulates myocardial contractilityStimulates myocardial contractility
 Improves ventricular emptyingImproves ventricular emptying
 Increase cardiac outputIncrease cardiac output
 Augments ejection fractionAugments ejection fraction
 Promotes diuresisPromotes diuresis
 Reduces elevated diastolic pressure & volume &Reduces elevated diastolic pressure & volume &
systolic volumesystolic volume
 Reduces symptoms resulting from pulmonaryReduces symptoms resulting from pulmonary
vascular congestion & elevated systemic venousvascular congestion & elevated systemic venous
pressurepressure

50. Cardiac glycosides ( digoxin).Cardiac glycosides ( digoxin).
Вільям Уізерінг
(1741-1799)
Dosage:
slow mode degitalization 0.5 mg / d the first 2-3 days,
then 0,125-0,375 mg / d in the absence of renal dysfunction,
if any dose is reduced by 50%.
In elderly dose 0.625 -0.125 mg / d
Do not combine with CORDARONE consists of digoxin, verapamil,
quinidine, which are competitors on stage consists of digoxin withdrawal.
Do not interact with CORDARONE, verapamil, quinidine cardiac glycoside-
digotoksyn (0.3 mg / d - in the first 3 days and at 0, 1 mg / d below).
Signs of glycoside intoxication:
-gastrointestinal (dyspepsia, diarrhea, loss of appetite)
-heart (ventricular extrasystole-bihemeniya, AV-blockade syndrome Salvador
Dali)
-neurological (headache, zapamoroky)
Ophthalmic (rainbow when looking at light) allergic

51. TREATMENT OF DIGITALISTREATMENT OF DIGITALIS
INTOXICATION:INTOXICATION:
 Tachyarrythmias: withdrawal of theTachyarrythmias: withdrawal of the
drug, treatment withdrug, treatment with beta blocker orbeta blocker or
lidocainelidocaine
 Hypokalemia:Hypokalemia: potassiumpotassium
administration by the oral routeadministration by the oral route

52. Digitalis
effect
TREATMENT OF DIGITALIS INTOXICATIONTREATMENT OF DIGITALIS INTOXICATION
1. Cancel cardiac glycoside and prescribe potassium
chloride 1-2 g every 4 h or 40-60 ml of 3% solution of
potassium chloride in 500 ml of 5% glucose solution during
process 2-3 h / in
2. Magnesium sulfate introduce 25% solution 20-40 ml / s.
3. Diphenine 100 mg, 3.4 g / d orally for moderate intoxication
and 125-250 mg / in 2-3 min, with severe intoxication
infusion repeated every 10 min, maintenance dose of 400 mg / d
4. If VTA -lidocaine 1 mg / kg / every 20 minutes or CORDARONE 450 mg / d / v +
per os 600-800 mg.
5. When supraventricular arrhythmias novokainamid 250-500 mg every 4 hours
orally and in severe intoxication 50-100 every 2-3min in in jet.
6. When violations conductivity atropine 0.1% solution to 3 mg / d
7. EDTA / iv.
8. Digoxyn petsyfic antibody / iv.
9. Electro therapy is not recommended, except as a means of last resort.
10. When threatened blockades temporary and therefore permanent
elektrokardiostymulation.

53. ANGIOTENSIN-CONVERTINGANGIOTENSIN-CONVERTING
ENZYME INHIBITORS:ENZYME INHIBITORS:
 Reduce peripheral resistance  reducereduce
afterloadafterload
 Reduce salt & water retention ( by reducing( by reducing
aldosterone secretion)aldosterone secretion)  reduce preloadreduce preload
 Reduce the long term remodelling of theof the
heart vessels ( maybe responsible for theheart vessels ( maybe responsible for the
observed reduction in the mortality &observed reduction in the mortality &
morbidity)morbidity)

54. Asymptomatic
LV Dysfubction
Mild to
moderate CHF
Moderate to
severe CHF
ACE inhibitor Digoxin Digoxin
Beta blocker Diuretics Diuretics
ACE inhibitor ACE inhibitor
Beta blocker Beta blocker
Spironolactone

55. The most significant changes were recommendations for the treatment of
CHF resynchronization therapy.
This resynhronization therapy performed by continuous bi-ventricular
elektrokardiostymulation.
It is indicated for patients with reduced EF,
dyssynhroning ventricular (QRS> 120 ms)
severe heart failure (III-IV functional class to NYHA),
despite optimal medical therapy.
This technology is recommended to reduce the symptoms, the number
of hospitalizations and mortality.
.
The most significant changes were recommendations for the treatment of
CHF resynchronization therapy.
This resynhronization therapy performed by continuous bi-ventricular
elektrokardiostymulation.
It is indicated for patients with reduced EF,
dyssynhroning ventricular (QRS> 120 ms)
severe heart failure (III-IV functional class to NYHA),
despite optimal medical therapy.
This technology is recommended to reduce the symptoms, the number
of hospitalizations and mortality.
.
Treatment of CHF dy resynchronization therapy.
MUSTIC (2002), COMPANION (2004), CA-RE-HF (2005)
meta-analysis of randomized studies resynhronization therapy

56. Application ICD shown to improve survival in patients who
survived cardiac arrest or suffer as a result of sustained
ventricular tachycardias, including these, combined with reduced
EF.
Application ICD shown to improve survival in patients who
survived cardiac arrest or suffer as a result of sustained
ventricular tachycardias, including these, combined with reduced
EF.
Combination and SRI biventrikulyarnoyi electrical indicated in
patients with severe heart failure (III-IV classes of NYHA, EF <35%)
and the duration of the interval QRS> 120 ms in order to reduce their
mortality and hospitalizations (research COMPANION, 2004) in
patients after 40 days of of myocardial infarction treated with optimal
baseline therapy with ACE inhibitors, β-blocker, aldosterone
antagonist, statin.
Combination and SRI biventrikulyarnoyi electrical indicated in
patients with severe heart failure (III-IV classes of NYHA, EF <35%)
and the duration of the interval QRS> 120 ms in order to reduce their
mortality and hospitalizations (research COMPANION, 2004) in
patients after 40 days of of myocardial infarction treated with optimal
baseline therapy with ACE inhibitors, β-blocker, aldosterone
antagonist, statin.
Resynchronization therapy using implanted
Cardioverter - Defibrilator (ICD).

57. Current treatments interventricular
asynhronosti as a cause of heart
failure, bi-ventricular
elektrokardiostymulyatsiyeyu

60. Dilated cardiomyopathy, mitral insufficiency without
and with pacing

61. Heart failure: how to prevent and treat
Non-Non-
pharmacologicalpharmacological
pharmacologicalpharmacological Radical / surgeryRadical / surgery
*Correction lifestyle *
Nutrition
* Eliminating bad habits
* At steady state exercise
training: up to 45
minutes a day "on the
state of health" 3-5 times
/ week
* Physical peace in an
unstable condition
Systolic:Systolic:
ACE inhibitorsACE inhibitors
Inhibitors of receptorInhibitors of receptor
Itypu AnhiotenzynuIIItypu AnhiotenzynuII
DiureticsDiuretics
ß - blockerß - blocker
Cardiac glycosidesCardiac glycosides
Diastolic:Diastolic:
the same, with thethe same, with the
exception of diureticsexception of diuretics
and cardiac glycosidesand cardiac glycosides
heart transplantation
Angioplasty, bypass
surgery
Cardiomyoplasty
Puncture of the
pericardium,
pericardiectomy
Surgical correction of
heart defects, hypertrophic
cardiomyopathy, tumors
Radical removal of
arrhythmias,
radiofrequency catheter
ablation
Elektrokardiostymulation
Apparatus artificial
ventricular**The only radical treatment for heart
transplantation

62. Happy New YearHappy New Year

63. Merry Christmas