Transcript Heart failure

Left heart failure and right
heart failure because of
pulmonary disease
Dr. Szathmári Miklós
Semmelweis University
First Department of Medicine
25. Oct. 2011.
Heart failure (HF)- definition
• HF is a clinical syndrome that occurs in patients who because of an inherited or acquired abnormality of heart
structure and/or function - develop a constellation of
clinical symptoms (dyspnea and fatique) and signs
(edema and rales) that lead a poor quality of life, and a
shortened life expectancy.
• Diagnostic criterias:
– Clinical symptoms of HF at rest or by exertion
– Identification of abnormal heart function in rest by objective
imaging tools
– Improvement of the symptoms of HF by adequate therapy
• HF patients are categorized into one of two groups:
– HF with a depressed ejection fraction (<40%)- systolic failure
– HF with a preserved ejection fraction (≥40%) – diastolic failure
Control of cardiac performance
and output
• The stroke volume of the ventricle in the intact
heart depend on three major influences:
– The lenght of the muscle at the onset of contraction
(the preload, surrogate parameter is the
enddiastolic volume of the ventricle,EDV). Within
limits the the stroke volume relates closely the
enddiastolic volume.
– The tension that the muscle is called upon to develop
during contraction (afterload), the load that opposes
shortening, or the tension developed in the ventricular
wall during ejection.
– The contractility of the muscle (the extent and
velocity of shortening at any given preload and
afterload).
Determinants of stroke volume
• Ventricular preload
– Blood volume
– Distribution of blood volume
(body position, intrathoracic
pressure, venous tone, etc.)
– Atrial contraction
• Ventricular afterload
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Systemic vascular resistance
Arterial blood pressure
Elasticity of arterial tree
Ventricular wall tension
• Radius, wall tickness
• Myocardial contractility
– Intramyocardial Ca+
– Cardiac adrenergic nerve
activity
– Circulating catecholamins
– Cardiac rate
– Myocardial ischemia
– Myocardial cell death
– Myocardial fibrosis
– Alteration of sarcomeric and
cytoskeletal proteins
– Ventricular remodeling
– Chronic overexpression of
neurohormones
– Chronic myocardial
hypertrophy
Etiologies of heart failure
Depressed
ejection
fraction
Coronary artery disease ( myocardial infarction or ischemia)
Chronic pressure and volume overload (hypertension, obstructive
valvular disease, regurgitant valvular disease, shunting)
Nonischemic dilated, or idiopathic cardiomyopathy*
Disorders of rate and rhythm (chronic brady- and tachyarrhythmias)
Preserved
ejection
fraction
Primary hypertrophic cardiomyopathy
Secondary hypertrophy (hypertension)
Restrictive cardiomyopathy (infiltrative or storage disease)
Fibrosis
Pulmonary
heart disease
Cor pulmonale
Pulmonary vascular disease
High-output
states
Metabolic disorders (hyperthyroidism, nutritional disorders (beri-beri)
Excessive blood-flow requirements (systemic arteriovenous shunting,
chronic anemia)
*infections, toxins, genetic defects of cytoskeletal proteins
Harrison’s: Principles of Internal Medicine. p.1444. modified
Functional classification of heart
failure (NYHA)
• NYHA functional classification:
– Class I. Without limitation of physical activity.
No symptoms with ordinary exertion (latent
decompensation)
– Class II. Slight limitation of physical activity.
Ordinary activity causes symptoms, fatique,
palpitation, dyspnea, anginal pain.
(subdecompensation)
– Class III. Marked limitation of physical activity.
Less than ordinary activity causes symptoms.
– Class IV. Inability to carry out any physical
activity without discomfort. Symptoms are
present at rest.
Epidemiology of heart failure
• The overall prevalence of HF in the adult population in
developed countries is 2%.Over the age 65 affects 610% of people.
• The overall prevalence of HF is thought to be increasing
(most common cause of hospital admissions), in part
because current therapies of cardiac disorders, such as
myocardial infarction, valvular heart disease, and
arrhythmias, are allowing the patients to survive longer.
• Heart failure is the most common cause of death (In the
USA 300 000 death/yaer)
• Patients with symptoms at rest have a 30-70% annual
mortality rate. Patients with symptoms with moderate
activity have an annual mortality rate of 5-10%
Pathogenesis of heart failure with
depressed ejection fraction
– HF begins after an index event (acute MI, or gradual onset as in
the case of pressure or volume overload) produces an initial
decline in pumping activity (systolic dysfunction). The
compensatory mechanismus are activated, including:
• The adrenerg nervous system
– to increase the myocardial contractility
• The renin-angiotensin-aldosterone system
– for maintaining cardiac output through increased retention of salt and
water
• The activation a molecules (BNP, NO, PGE2, PGI2) and cytokin
system that offset the peripheral vasoconstriction
– In the short term these systems are able to restore
cardiovascular function with the result that the patient remain
asymptomatic.
– However, with time the sustained activation of these systems
can lead to secondary end-organ damage within the ventricle,
with left ventricular remodeling and subsequent cardiac
decompensation.
Left ventricular remodeling
The transition to symptomatic HF is accompanied
by increasing activition of neurohormonal,
adrenergic, and cytokine systems that lead to
series of adaptive changes within the
myocardium, collectively referred to as left
ventricle remodeling. These changes include :
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Myocyte hypertrophy
Alteration in the contractile properties of myocyte
Progressive loss of myocyte through necrosis, apoptosis
β-adrenergic desensitization
Abnormal myocardial energetics and metabolism
Reorganization of extracellular matrix with dissolution of
organized structural collagen weave , replacement with an
interstitial collagen matrix that does not provide structural
support to the myocytes
Pathogenesis of heart failure
with preserved ejection fraction
• Diastolic dysfunction
– Impaired myocardial relaxation, an ATP-dependent
process that is regulated by uptake of cytoplasmatic
Ca2+ into the sarcoplasmatic reticulum
• Reduction in ATP concentration in case of ischemia
• Decreased left ventricle compliance (from hypertrophy or
fibrosis)
• An increase in heart rate disproportionately shortens the time
of diastolic filling, which may lead to elevated left ventricle
filling pressures. Elevated LV end-diastolic filling pressures
results in increases in pulmonar capillary pressures, which
can contribute to the dyspnea
– Increased vascular and ventricular stiffness may be
also important
Left ventricle remodeling on
macrostructural level
• Change of LV geometry from ellipsoid to spherical shape
– an increase of meridional wall stress
• Increase in end-diastolic volume – LV wall thinning.
Together with the increased afterload leads to decreased
stroke volume
• High end-diastolic wall stress leads to
– Hypoperfusion of the subendocardium – worsening of LV
function
– Increased oxidative stress
– Sustained expression of wall-strech-activated genes (AII, TNF)
• Because of increased sphericity the papillary mucles are
pulled apart, resulting in incompetence of the mitral valve
– mitral regurgitation – further hemodynamic overloading
of the ventricle
Mechanical burdens that are engendered by
left ventricle remodeling can be expected to
lead to
• decreased forward cardiac output
• increased left ventricle dilatation
(stretch)
• increased hemodynamic overloading
Different forms of left ventricle overload
Volume (diastolic)
overload
• Increased preload
– Increased afterload
– Aortic stenosis,
• Mitral or aortic
hypertension
regurgitation
– Myocardial hypertrophy
• Left ventricle
with minimal dilatation
dilatation
Pressure (systolic)
overload
Clinical symptoms and physical signs
of the heart failure
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Fatique
Dyspnea
Tachycardy
Cyanosis
Pulmonary congestion
Phlebohypertension
Hepatomegaly
Congestion of the kydney
Other symptoms
Clinical symtoms of the heart failure
• Fatique
– The consequence of low cardiac output, but other noncardiac comorbidities (anemia, musculoskeletal
abnormalities) also contribute to this symptom
• Dyspnea (the most important mechanism is the
pulmonary congestion with accumulation of
interstitial or intraalveolar fluid. Other factors are
reduction in pulmonary compliance, increased
airway resistance, respiratory mucle weackness, and
impaired sensitivity of respiratory center)
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Clinical manifestations:
Effort dyspnea
Dyspnea at rest
Orthopnea: Dyspnea occuring in the recumbant position.
Acute episodic shortness of breath
Cheyne-Stokes respiration
Acute and/or periodic forms of
dyspnea
• Paroxysmal nocturnal
dyspnea
– Acute episodes of severe
shortness of breath and
coughing that occur at night
and awaken the patient from
sleep, usually 1-3 after the
patient retires.
– It manifests by coughing or
wheezing, possible because of
increased pressure in the
bronchial artery leading to
airway compression, along
with with interstitial pulmonary
edema.
– It does not improve in upright
position
– It can be associated with
hypertension, aortic vitium,
dilated cardiomyopathy.
• Cheyne-Stokes respiration
– Caused by diminished
sensitivity of respiratory center
to arterial PCO2.
– In the apneic phase the
patient can be unconscious,
Cyanosis
• Bluish color of the skin and mucous membranes
resulting from an increased quantity of reduced
hemoglobin( exceeds 40 g/l) in the small blood
vessels of those areas.
• It is usually most marked in the lips, nail beds,
ears, and malar eminences
• Central cyanosis can be detected reliably when
arterial O2 saturation has fallen to 85% (in darkskinned persons 75%)
Clinical signs and symptoms of
pulmonary congestion
– Decreased vital capacity of the lung because of
interstitial pulmonary edema
– Central cyanosis (inhibited gas exchange)
– Dyspnea
– Coughing
– Brownish sputum (epithel cells containing
hemosiderin pigments), eventually hemoptysis
– Ronchi, wheezing, crackles
– Accentuated pulmonary component of second heart
sound
– Dilated pulmonary veins on the X-ray
Clinical signs and symptoms of rightsided heart failure
• Gärtner’s sign: The veins of the hand remain dilated by the
elevation of the arm to the level of the left atrium
• Distension of the external jugular vein :elevated jugular
venous pressure.
• Positive abdominojugular reflux: With sustained pressure
on the abdomen the jugular venous pressure becomes
abnormally elevated.
• Hepatomegaly. The enlarged liver is frequently tender.
Jaundice and ascites are late finding in heart failure, results
from impairment of hepatic function secondary to hepatic
congestion and hepatic hypoxia.
• Proteinuria
• Anorexia, nausea, and early satiety associated with
abdominal pain and fullness relates to edema of bowel wall
and/or to the congested liver.
Edema
• Edema: : accumulation of fluid in the
interstitial space. Residual imprint of
fingers following application of pressure.
• Latent edema:(less than 5-6 l fluid retention).
Identification: measurement of body weight in the
morning and in the evening and/or compare the
amount of the urine during the day and during the
night.
• Manifest edema: usually symmetric, and occurs
predominantly in the ankles and pretibial region in
ambulatory patients. In bedridden patients, edema
may be found in the sacral area, and the scrotum.
• Differential diagnosis: varicosity, pes planus, deep
vein thrombosis, and v. cava inferior thrombosis)
Cor pulmonale
• Definition: dilatation and hypertrophy of
the right ventricle in response to diseases
of the pulmonary vasculature and/or lung
parenchyma (pulmonary heart disease)
• Chronic obstructive lung disease and
chronic bronchitis are responsible for
approximately 50% of the cases of cor
pulmonale in developed countries
Etiology of chronic cor pulmonale
• Diseases leading to hypoxic
vasoconstriction
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Chronic bronchitis
COPD
Cystic fibrosis
Chronic hypoventilation
• Obesity
• Neuromuscular diseases
• Chest wall deformities
– Living at high altitudes
• Diseases causing occlusion
of the pulmonary vascular
bed
– Recurrent pulmonary
thromboembolism
– Primary pulmonary
hypertension
– Venoocclusive diasese
– Collagen vascular disease
– Drug-induced lung diasease
• Parenchymal pulmonary
diseases
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Chronic bronchitis
COPD
Bronchiectasis
Idiopathic pulémonary fibrosis
Sarcoidosis
Pneumoconiosis
Pathophysiology of cor pulmonale
Pulmonary disease
Pulmonary hypertension
Alteration in RV
volume overload
Right ventricle dilatation and
hypertrophy
-Exercise
Secondary to
alteration of gas
exchange
-Heart rate
- Hypoxia
-Polycythemia
- Hypercapnia
-Salt and water
retention (low CO)
Right ventricle failure
- Acidosis
Symtoms and signs of cor pulmonale
• Dyspnea - result of the increased work of breathing or
altered respiratory mechanics
• Effort-related syncope – because of the inability of the
RV to deliver blood adequately to left side of the heart
• Abdominal pain and ascites
• Lower extremity edema – secondary to neurohormonal
activation, elevated RV filling pressure, or increased
levels of carbon dioxide and hypoxia, which can lead to
peripheral vasodilatation
• RV heave palpable along the left sternal border or in the
epigastrium
• A systolic pulmonary ejection click to the left of the
upper sternum
• Holosystolic murmur of tricuspidal regurgitation (the
intensity of the murmur increases with inspiration)
• Cyanosis – late finding in cor pulmonale