Heart Failure

Stanko P

© Kristína Repová, MD, PhD.

Institute of Pathophysiology, Faculty of Medicine, Bratislava

• Preload

• Afterload

BLOOD PRESSURE(heart work)

Cardiac Output (CO)

Stroke Volume (SV)

Preload

Blood volume

Venous compliance

Contractility

Afterload

Heart Rate (HR)

Peripheral Resistance (PR)

Vessel length

Vessel diameter

Vasoconstriction

Vasodilation

Vessel wall remodelling

Viscosity of blood

Compliance of large arteries

Epidemiology of HF

◼ Prevalency: 2 - 3 %

◼ after 75 years: 10 -20 %

◼ In younger individuals is more frequent in men

◼ 50 % of patients dies within 4 years

◼ 40 % of patients hospitalized with HF dies or is re-

admitted within 1 year

Pathomechanism of HF

◼ Clinical understanding of HF =

congestive HF

• dyspnoea, edema

• compensatory mechanisms

(hypertrophy)

◼ Pathophysiological understanding

of HF = reduced pefusion of

peripheral tissues

• oliguria, muscle weakness, fatigue,

dyspeptic complaints

Causes of HF

1. Chronic hemodynamic overload

2. Restricted filling of ventricles

3. Myocardial impairment

4. Arrythmias

Causes of HF

1. Chronic hemodynamic overload

◼ Pressure:

◼ Left: hypertension, stenosis and coarctation of aorta

◼ Right: pulmonary hypertension, a. pulmonalis stenosis

◼ Volume:

◼ Mitral, aortic insufficiency, arterio-venous shunts, hyperkinetic

circulation

2. Restricted filling of ventricles

◼ Impaired ventricular dilation

◼ Disorder of the ventricular filling

Causes of HF

3. Myocardial impairment

◼ Ischemic heart disease

◼ Cardiomyopathies

◼ Toxic substances: ethanol, diphtheria, drugs

◼ Endocrinopathies: DM, hyper-/hypo-thyreoidism

4. Arrythmias

◼ Extreme tachyarrhythmia: supraventricular tachycardia,

fibrillation, flutter

◼ Extreme bradycardia: sinus, AV block

Forms of Heart Failure (HF)

◼ Acute

◼ Chronic

◼ Right

◼ Left

◼ Systolic

◼ Diastolic

◼ High-output HF

◼ Low-output HF

◼ Compensated

◼ Decompensated

◼ Forward

◼ Backward

Forward / backward HF

◼ insufficient activity of different

organs (GIT, kidney, liver, brain,

etc.).

◼ Dyspnea

◼ Edema

Dyspnoea

➢ Subjectively perceived sensation of breathlessness

◼ Exertional dyspnea◼ Symptomless during rest

◼ physical activity → Sp. → vasoconstriction → venous return → pulmonary pressure → pulmonary compliance

◼ Orthopnea◼ Dyspnea in horizontal position

◼ blood redistribution from distal parts into the heart

◼ Paroxysmal nocturnal dyspnea◼ horisontal position + PSp. during sleeping → contractility and activity of centre of breathing

Edema

◼ RV HF!

◼ Swelling of ankles, feet

◼ Right hypochondrial pain: liver distension

◼ Abdominal swelling (ascites)

◼ Loss of appetite

◼ Malabsorption: bowel edema

◼ ↑ in weight: fluid retention

Pulmonary edema

➢ Accumulation of excessive amount of fluid in pulmonary

interstice or in alveoli

◼ ↑ hydrostatic pressure in pulmonary capillaries

◼ ↑ permeability of capillary wall

◼ ↓ colloid osmotic pressure in blood (hypoproteinemia)

◼ hypoxemia of the liver … ↓ albumin synthesis

◼ renal hypoperfusion … proteinuria

➢ Breathlessness, cyanosis, breath sounds: crackles,

wheezes, decreased breath sounds at bases (effusions);

expectoration of pink foamy sputum, horror mortis

Fatigue and lethargy

◼ Impaired muscle blood flow

◼ Accumulation of lactate

◼ ↓ cerebral blood flow

◼ Somnolence, sleep disorders, confusion

Dyspeptic syndrome

➢ Insufficient perfusion of digenstive organs

◼ Impairment of digestion, absorption of nutrients

◼ ↓ detoxication function of liver

◼ ↓ proteosynthesis in liver

◼ ↓ pancreas functions

◼ Generalized ↓ of muscular mass

◼ Cardiac cachexia

Cyanosis➢ Blue color of the skin and mucose membranes

◼ ↑ reduced hemoglobin (>50 mg/L)

◼ Peripheral cyanosis

◼ Normal saturation

◼ Vasoconstriction: blood stagnating in tissues: cold, shock, HF

◼ Cold, pale auricles, nose, cheeks, external lips, tips of fingers and toes

◼ Central cyanosis

◼ ↓ saturation

◼ ↑ physical exercise, (inborn) heart defects with right-left shunts, pulmonary diseases, HF

◼ Peripheral vasodilation: warm skin, dilated veins

◼ Cyanotic tongue, palate, internal mucose of lips

◼ Polyglobulia, clubbed fingers

Compensatory mechanisms

Pathologic process

Compensated HF Decompensated HF

Without clinical signs of HF With clinical signs of HF

Compensatory mechanisms

◼Acute

◼Frank-Starling mechanism

◼Catecholamines

◼Chronic

◼Myocardial hypertrophy

Acute compensatory mechanismsFrank-Starling mechanism

◼ ↓ ejection fraction ... ↑ end-diastolic volume in ventricles ...

myocyte stretching ... ↑ sarcomere length ... ↑ troponin C

sensitivity to Ca2+ ... ↑ cross-link actin and myosin filaments

... ↑ contraction ... ↑ stroke volume

◼ Maximal force of contraction: sarcomere length near 2.2 um

◼ > 2.2 um ... ↓ myofilament overlapping (HF)

◼ < 2.2 um ... ↓ troponin C sensitivity to Ca2+

↓ ejection fraction ↑ contraction

Low-output vs. high-output HF

◼ Low-output HF

◼ cardiac output lower than before HF, under effort doesn`t increase sufficiently

◼ CAD, hypertension, dilatative cardiomyopathy, valvular, pericardial diseases

◼ High-output HF

◼ cardiac output during HF is HIGHER than before HF, cannot supply inadequately high requests

◼ Thyreotoxicosis, Paget’s disease, beri-beri, anemia, septicaemia, arteriovenous fistulae

◼ Warm extremities, normal or widened pulse pressure

Acute heart failure (AHF)

◼ Sudden deterioration of cardiac function

◼ Acute compensatory mechanisms set on

◼ Hypotension without edemas, acute onset of

dyspnea, pulmonary edema

◼ LV HF: myocardial infarction, arrythmia, acute

valve dysfunction

◼ RV HF: mitral insufficiency, massive pulmonary

embolism

Chronic heart failure (CHF)

◼ Gradual progressive loss of cardiac function

◼ Partly compensated by regulatory mechanisms that

become maladaptive

◼ Peripheral edemas, BP does not change

◼ LV HF: volume (valvular insufficiency) or pressure

(hypertension, valvular stenosis) overload or heart muscle

disease (MI, cardiomyopathy, myocarditis)

◼ RV HF: precapillary, capillary or postcapillary

pulmonary hypertension -> cor pulmonale or

tricuspidal valvular disease.

Systolic dysfunction

◼ myocardial contractility◼ myocardial damage: ischemia, inflammation, intoxication (ethanol, cocain,

amphetamins), ionic changes

◼ volume overload

◼ afterload◼ preddure overload

◼ stenosis of aortic valve, arterial hypertension

◼ Failure of left ventricle to eject blood in systole→ ventricular volume → ventricular pressure → systolic volume → ventricular hypertrophy

Diastolic dysfunction

◼ Impaired ventricular dilation

◼ hypertrophy, fibrosis

◼ increased resistance during ventricular filling: filling pressure →

pulmonary/venous congestion

◼ exertional dyspnoea

◼ aortic stenosis, hypertension, hypertrophic cardiomyopathy

◼ Disorder of ventricular filling

◼ mitral stenosis, tamponade, constrictive pericarditis, tachyarrhythmias

Systolic dysfunction Diastolic dysfunction

↑ end-diastolic volume

atrium

Left side

Pulmonary edema

Right side

Peripheral edema

Inadequate filling of ventricle

↑ end-diastolic pressure

Inadequate empting of ventricle

◼ Physiologic hypertrophy

◼ Pathologic hypertrophy

Chronic compensatory mechanismsMyocardial hypertrophy

Physiologic hypertrophy◼ ontogenetic development

◼ adaptation to increased physical activity

◼ the intensity and duration of overload do not exceed particular measure

◼ overload develops gradually

◼ function of each mass unit is normal or even increased: ◼ enlargement of the muscle mass

◼ improvement of contractility of each mass unit … ↑ systolic function

◼ the content of connective tissue does not increase … elasticity … diastolic function

Chronic compensatory mechanismsMyocardial hypertrophy

Pathologic hypertrophy

◼ hypertrophy of myocytes (↑ length / width)

◼ volume / pressure overload

◼ hormonal stimulation: NE, Ang II

◼ ↑ non-myocytic cells in myocardium

◼ Endothelial cells … endothelins:

◼ Mitogenic ability … stimulation of growth of smooth muscle

cells of vessels and of fibroblasts

◼ Fibroblasts … ↑ production of collagens … fibrosis

Chronic compensatory mechanismsMyocardial hypertrophy

◼ Concentric hypertrophy

◼ Pressure overload (↑ LV end-diastolic wall stress)

◼ ↑ wall thickness / ventricular volume

◼ ↑ afterload

◼ stenosis, coarctation of aorta, arterial hypertension,

obstructive hypertrophic cardiomyopathy, stenosis of a.

pulmonalis, pulmonary hypertension

◼ hypoperfusion of the subendocardium … worsening of

LV function

◼ expression of stretch-activated genes: Ang II,

endothelin, TNF

Chronic compensatory mechanismsMyocardial hypertrophy

◼ Eccentric hypertrophy

◼ Volume overload (↑ LV end-diastolic volume)

◼ ↓ wall thickness / ventricular volume

◼ LV wall thinning, dilating

◼ ↑ preload

◼ aortic, mitral valve insufficiency, pulmonal, tricuspidal

valve insufficiency, atrial septum defect

Chronic compensatory mechanismsMyocardial hypertrophy

◼ Heart enlargement, ventricular wall is absolutely or relatively thinner

◼ Primary dilation

◼ Acute hemodynamic overload

◼ ventricular wall is absolutely thinner vs. normal

◼ Secundary dilation

◼ Chronic hemodynamic overload ... hypertrofic, but failing heart, exhausted compensatory mechanisms

◼ hypertrophied ventricular wall is getting thinner

Myocardial dilation

Peripheral compensatory mechanisms

◼ Neurohumoral: Sp., PSp. activity, RAAS, ADH, ANP

◼ Blood redistribution → centralization of blood flow

◼ Hormonal: tyroxin, growth hormone, dopamine

◼ oxygen extraction from capillary blood → peripheral cyanosis

◼ red blood cells count

Angiotensinogen

Angiotensin I

Angiotensin II

Aldosteron

fluid, Na+

retention

↑ blood volume

↑ preload

adrenalshypophysis

ADHthirst

systemic

vasoconstriction

↑ afterload

Myocardial,

vascular

hypertrophy

Renin

Angiotensin converting

enzyme (ACE)

Renin-angiotensin-aldosteron system (RAAS)

↑ BP

Fibroblasts Cardiomyocytes Endothelium

Tissue Ang II

cardiomyocyte

hypertrophyproliferation vascular wall

hypertrophy

Myocardial remodeling

Myocardial hypertrophy (volume/pressure overload)

↑ preload ↑ afterload ↑ Sp

Systemic (plasma) Ang II

↑ blood osmolarity ↓ blood volume ↓ BP

ADH from hypothalamus

↑ amount of aquaporines in

collecting tubules

↑ water rearpsorption

↓ blood osmolarity ↑ blood volume

Systemic

vasoconstriction

↑ BP

Antidiuretic hormone (ADH) = Vasopressin

Acute atrial

stretching

ANP secretion from atrial cardiomyocytes

↑ glomerular filtration

↑ Na+ excretion

↓ aldosterone, ADH,

renin

↓ preload

↓ peripheral

resistance

↓ BP

↑ extracellular fluid volume

↑ Na+ income

Chron. Heart failure

Volumexpansion

Natriuresis and diuresis

Atrial natriuretic peptide (ANP)

Adrenalin, noradrenalin, ang. II, aldosterone,

ADH

…

preservation of the perfusion of vital organs on

the expense of increased afterload

…

deterioration of heart failure

Centralization of the circulation

Decompensated HF

◼ Exhausted compensatory mechanisms

◼ Stress reaction:

◼ Catecholamines

◼ RAAS

◼ Adequate perfusion through vital organs (heart, brain, kidneys)

◼ Relative ischemia of peripheral organs (skin, digestive tract, muscles, …)