Left heart failure and right heart failure because of

pulmonary disease

Dr. Szathmári MiklósSemmelweis University

First Department of Medicine25. 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– 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)

Harrison’s: Principles of Internal Medicine. p.1444. modified *infections, toxins, genetic defects of cytoskeletal proteins

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 6-10% 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 :

– 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

Pressure (systolic) overload

– Increased afterload– Aortic stenosis,

hypertension– Myocardial hypertrophy

with minimal dilatation

Volume (diastolic) overload

• Increased preload• Mitral or aortic

regurgitation • Left ventricle

dilatation

Clinical symptoms and physical signs of the heart failure

• 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 non-

cardiac 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) – 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 dark-skinned 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 right-sided 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– 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– Chronic bronchitis– COPD– Bronchiectasis– Idiopathic pulémonary fibrosis– Sarcoidosis– Pneumoconiosis

Pathophysiology of cor pulmonale

Pulmonary disease

Pulmonary hypertension

Right ventricle dilatation and hypertrophy

Right ventricle failure

Secondary to alteration of gas exchange

- Hypoxia

- Hypercapnia

- Acidosis

Alteration in RV volume overload

-Exercise

-Heart rate

-Polycythemia

-Salt and water retention (low CO)

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