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%) – HF with a preserved ejection fraction (≥40%) –

systolic failure 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

limits the the stroke volume relates closely the enddiastolic volume.

– The tension that the muscle is called upon to develop during contraction ( shortening, or the tension developed in the ventricular wall during ejection.

– The

contractility

velocity of shortening at any given preload and afterload).

afterload

). Within ), the load that opposes of the muscle (the extent and

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 Preserved ejection fraction Pulmonary heart disease High-output states 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) Primary hypertrophic cardiomyopathy Secondary hypertrophy (hypertension) Restrictive cardiomyopathy (infiltrative or storage disease) Fibrosis Cor pulmonale Pulmonary vascular disease 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 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 ( with water asymptomatic.

systolic dysfunction

• The adrenerg nervous system – to increase the myocardial contractility • The renin-angiotensin-aldosterone system system that offset the peripheral vasoconstriction

left ventricular remodeling

). The compensatory mechanismus are activated, including: – for maintaining cardiac output through increased retention of salt and • The activation a molecules (BNP, NO, PGE2, PGI2) and cytokin – In the short term these systems are able to restore cardiovascular function with the result that the patient remain – However, with time the sustained activation of these systems can lead to secondary end-organ damage within the ventricle, 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 PCO 2 .

– 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 O 2 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

• • • • • •

G ärtner’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

Alteration in RV volume overload

-

Exercise

-

Heart rate

-

Polycythemia

-

Salt and water retention (low CO)

Pulmonary hypertension Right ventricle dilatation and hypertrophy Right ventricle failure Secondary to alteration of gas exchange - Hypoxia - Hypercapnia - 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

peripheral vasodilatation – secondary to neurohormonal activation, elevated RV filling pressure, or increased levels of carbon dioxide and hypoxia, which can lead to • • •

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 Cyanosis

of tricuspidal regurgitation (the intensity of the murmur increases with inspiration) – late finding in cor pulmonale