Chronic Heart Failure

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ChronicHeart Failure

• Dr. Apor Astrid
• SE Heart Center

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Modern clinical definitionESC guideline
Cardiac dysfunction confirmed (ECG, imaging
modalities)
Typical symptoms and signs of heart failure
Neurohumoral aktivation confirmed (BNP)
Response to heart failure treatment
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Cinical symptoms and signs
fluid retention
dyspnoe
fatigue
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Pathophysiology of heart failure
Heart disease valvular myocardial
coronary arterial Extracardiac disease
affecting the heart
Pump function of the heart?
Temporary effects Pump function is maintained
Long term effects Detrimental cardiac,
Cardiovascular impairment
Compensatory mechanisms
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Adaptation in heart failure
Sympathico- adrenal system
Myocardial remodeling
Frank-Starling mechanism
RAAS
vasopressin
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Adaptation in heart failure
BP CO x SVR BP SV x HR x SVR
Frank-Starling Remodelling SA system
SA system RAAS
SA system
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Frank-Starling mechanism

• Energy of contraction is a function of the muscle
• fiber length
• Optimal length 2.2µm
• Stretching beyond this point may diminish LV
• performance

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Myocardial hypertrophy, remodeling

• ?1 receptor density?
• ?1 receptor coupling?
• Ca excitation-contraction
• coupling?
• Myocardial oxidative
• phosphorilation is abnormal

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Myocardial remodelingObjective to maintain
systolic wall stress? myocyte hypertrophy
(excentric/concentric)

• BUT
• This myocardium is diseased!
• myocyte contraction?
• myocyte apoptosis, necrosis
• increased collagén deposition?
• stiff myocardium!
• MMPs activity?
• split collagen cross-links myocyte
  slippage
• capillary density?

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Ventricular remodelling
LV mass?, size?, shape is altered
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Ventricular remodelling
Excitation-contraction coupling?
Electrical dyssynchrony
Mechanical dyssynchrony
Dysrhythmias !
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DCM
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HCM, HOCM
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Restrictive CMP
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Non-compact CMP
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(No Transcript)
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ARVD
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Sympathetic nervous system is activated
Heart rate? Force of contraction? Dilatation of
coronary arteries
Perif. vascular resistance? Redistribution (renal
blood supply?) Direct cytotoxic
effect Apoptosis? Activation of the RAAS
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Activation of the RAAS
Blood pressure? Perfusion of the juxtaglom.
apparátus?
SA activation Sodium and water retention Vasoconst
riction Aldosterone? ADH (vasopressin)? Myocardial
hypertrophy Myocardial fibrosis Endothel
dysfunction Coagulation?
renin
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Maintenance of perfusion of the vital
organs (vasoconstriction)
Prevention of blood loss restoration of blood
volume (salt water retention)
Preparation to fight (SA?)
Wound healing (scarring fibrosis) Prevent wound
infection (inflammation)
Stop bleeding (hemostasis?) Restoration of lost
RBCs (erythropoesis?)
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Counterregulation BNP

• Stress hormone of myocytes (increased wall
  tension)
• Diuresis, natriuresis
• Vasodilation, blood pressure?
• Sympathetic nervous system activation?
• RAAS activation?
• BNP levels correlate with the severity of heart
  falure

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Clinical symptoms of heart failure dyspnoe

• Pulmonary capillary wedge pressure?
• Fluid retention? lung compliance?
• Skeletal/respiratory muscle myopathy
• Abnormal ergoreflex
• (muscle contraction-hyperventillation)

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Clinical symptoms of heart failure fatigue

• Stroke volume?, cardiac output?
• Skeletal muscle myopathy

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Clinical symptoms of heart failure edema, fluid
retention

• Anasarca
• Hepatomegaly
• Gastrointestinal congestion
• Pulmonary edema

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Etiology of heart failure
Heart failure with Low cardiac
output CHD Hypertension Valve diseases Cardiomyop
athies Arrhythmias Pericardial diseases Drug
toxicity RV failure
Heart failure with high cardiac
output circulatory failure Anaemia Thyrotoxicosi
s AV-fistula Cirrhosis of the liver Paget-disease
Beriberi
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Etiology of heart failure
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Diagnosis of heart failure

• Dyspnoe, orthopnoe, PND
• Oedema, anasarca
• Pulm. congestion on auscultation
• S3, gallop rythm, holosystolic murmur
• Jugular vein distension, hepato-jug. reflux
• Pulsatility of the liver, ascites

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Diagnosis of heart failure

• ECG 12 leads
• Chest X-ray
• Lab tests (hyponatraemia!)
• Biomarkers of HF BNP, proBNP, CRP, troponins
• Echocardiography (systolic/diastolic dysfunction,
  structural heart disease)
• spiroergometry

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Diagnosis of heart failure
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How to judge disease severity, clinical status
and prognosis

• NYHA classification
• Quality of life tests
• 6-minute walking test
• Exercise testing
• Other measurements of
• cardiac function

• Prognostic indices
• HFSS
• SHFM
• Risk of sudden death

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Disease progression in heart failure
Stable, worsening, decompensated
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Classification of stages of heart failure
Stage A At high risk of heart failure Hypertens
ion CHD Diabetes Metabolic sy. Cardiotoxin
Stage B Structural heart disease
without symptoms LV remodeling LV
hypertrophy Valve disease
Stage C Structural heart disease with symptoms
of heart failure
Stage D Refractory heart failure
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Forms of heart failure

• Systolic (-diastolic) dysfunction
• Diastolic HF with preserved systolic function
• HFPEF heart failure with preserved ejection
  fraction
• -presence of signs and symptoms
• of CHF
• -LV EF 45-50
• -evidence of diastolic dysfunction
• (echocardiography)

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Treatment of heart failure
Heart transplantation
Pharmacologic treatment Pozitív
inotropok Digitalis Neurohumorális blokád BB,
ACEi Diureticumok Vasodilatorok Antiarrhythmiás
szerek
Surgical/interventional Revascularisation Valve
replacement Aneurysm resection Surgical
remodeling Stem-cell therapy
Non-pharmacologic treatment Resynchronization
(CRT) ICD IABP Assist device
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Treatment of heart failure
Pharmacologic treatment Pozitív
inotropok Digitalis Neurohumorális blokád BB,
ACEi Diureticumok Vasodilatorok Antiarrhythmiás
szerek
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Objectives of treatment in CHF

• 1, Improve prognosis, reduce mortality
• 2, Improve morbidity relieve symptoms
• - increase exercise capacity
• - reduce fatigue and breathlessness
• - eliminate oedema and fluid retention
• 3, Prevention
• - myocardial damage
• - remodelling
• - reoccurence of symptoms
• - hospitalisation

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Maintenance of perfusion of the vital
organs (vasoconstriction)
Prevention of blood loss restoration of blood
volume (salt water retention)
Preparation to fight (SA?)
Wound healing (scarring fibrosis) Prevent wound
infection (inflammation)
Stop bleeding (hemostasis?) Restoration of lost
RBCs (erythropoesis?)
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Inhibition of NEURO-HUMORAL activation ACE
inhibitors Betablockers Aldosterone
Antagonists Digoxin
Reduction of SVR Hydralazine Nitrate Ca-chan
ell Blockers Diuretics
Elimination of oedema Diuretics
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Inhibition of haemostasis Treatment of
precipitating factors Treatment of
comorbidities Reduce risk factors Treatment of
complications
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Symptomatic heart failure reduced ejection
fraction
ACEi (or ARB) ? Diuretics
Betablockers
Aldosterone anatgonists or ARB
Digoxin, Hydralazine, Nitrate
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ACEi BB start with low dose titrate slowly
Consider side effects interactions renal
function liver function
Dosages should be adjusted to clinical
state (diuretics)
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ACE inhibitors

• symptoms?, prognosis?, mortality?
• remodelling?, myocardial fibrosis?
• starting dose, target dose
• Hypotension
• Hyperlakaemia, renal dysfunction
• Cough
• Angio-oedema

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Betablockers

• symptoms?, prognosis?, mortality?
• remodelling?, dyssynchrony?
• SCD ?, antiarrhythmic effect
• starting dose, target dose
• Hypotension
• Fatigue
• Bradycardia, block
• Reduce dose in case of decompensation

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Aldosterone antagonists

• symptoms?, prognosis?, mortality?
• NYHA III, EFlt35
• Renal dysfunction
• Hyperkalaemia

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Diuretics

• symptoms?, oedema?, prognosis?
• only in case of fluid retention
• RAAS activation?add ACEi or ARB!
• Titrate, combine
• Hyonatraemia, hypokalemia, volume depletion,
  renal dysfunction
• Diuretic resistance

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Patients with acute heart failure frequently
develop chronic heart failure.
Patients with chronic heart failure frequently
decompensate acutely.
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Thank you for your patience!