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17. Vascular Pathology III. Heart Failure 1 17. Vascular pathology III. Heart failure DISEASES OF THE HEART Content Cardiac hypertrophy and congestive heart failure Cor pulmonale Hypertensive heart disease Ischemic heart disease Valvular diseases Myocardial diseases Congenital heart diseases Diseases of the pericardium Cardiac neoplasms HYPERTROPHY OF THE HEART AND HEART FAILURE Normal values assessed by echocardiography Free wall thickness: RV: 3-4 mm, LV:10-11 mm End-diastolic volume (EDV) 120 ml, end-systolic volume (ESV) 50 ml, stroke volume (SV) 70 ml Weight: women: 300 gs, men: 350 gs Hypertrophy of the heart The cardiac myocytes are permanent cells (not able to enter the cell cycle) and, therefore, are not able to proliferate Increase in work load increase in size and pumping capacity of ventricular myocytes Weight > 400 g Types: concentric or dilative Concentric hypertrophy Pathogenesis An obstruction of outflow in systole (i.e., hypertension, aortic valve stenosis) the LV increases the end-systolic pressure pressure overload concentric remodeling and hypertrophy Morphology Concentric hypertrophy of the LV: small lumen; markedly increased wall thickness (> 20 mm); increased mass (> 500 g) Clinical features of pressure-overloaded LV Symptomless for a long period Pump failure occurs lately Risk of sudden cardiac death Dilative hypertrophy Pathogenesis Aortic/mitral valve incompetence leads to diastolic backflow the regurgitated extra volume of blood is accepted with the dilation of the LV an increased EDV is ejected into the circulation during the next systole (volume overload) excentric remodeling and hypertrophy Morphology Dilative hypertrophy of LV: enlarged lumen, enlarged size, slightly increased wall thickness, increased mass Clinical features of volume-overloaded LV Pump failure occurs relatively early Good response to drugs increasing contractility The overall prognosis is better than that of pressure-overloaded heart Cardiac hypertrophy (HT) culminates in congestive heart failure Hypertension or aortic stenosis-induced pressure overload concentric HT Noncontracting areas in myocardial infarction induce volume overload dilative HT Aortic or mitral incompetence-induced volume overload dilative HT These conditions lead to increased cardiac work increased wall stress increased cell strech progressive dilative hypertrophy decreased contractility (systolic dysfunction) Neurohumoral activation occurs: increased secretion of atrial natriuretic peptide and norepinephrin, activation of the renin-angiotensin-aldosteron system Pump failure, arrhythmias death ARRHYTHMIAS Two types: tachyarrhythmia (>100 beats/minute) and bradyarrhythmia (<60 beats/minute) Dg.: upon ECG features Atrial fibrillation and ventricular tachyarrhythmias have particular importance Atrial fibrillation Pathogenesis Most common arrythmia, due to atrial fibrosis resulting from atrial strech, atrial ischemia, neurohumoral activation, etc.. The electrical signals don't begin in the SA node. Instead, they begin in another part of the atria (300-600/minute) and spread a rapid, disorganized way; only a proportion of the impulses are conducted to the ventricles. The atria and ventricles do not beat in a coordinated way; the ventricles usually beat 100 to 180 times a minute tachyarrhythmia Some risk factors of atrial fibrosis Coronary heart disease, hypertensive heart disease, valvular heart disease 1 17. Vascular pathology III. Heart failure Congestive heart failure per se Hyperthyroidism, alcohol toxicity, etc., Clinical features Can be symptomatic (palpitation [feeling that your heart is beating too hard or too fast, skipping a beat, or fluttering], tachyarrhythmia, dizziness, etc.,) or asymptomatic The pulse at wrist feels irregular and beats may be variable in strength Complications: atrial thrombi, embolism induced-cerebral infarction, heart failure, and syncope [fainting; short loss of consciousness and muscle strength] Treatment Sinus rhythmus can be achieved with antiarrhythmic drugs or electrical cardioversion or catheter-based ablation technologies Anticoagulant therapy to prevent thrombus formation Life-threatening ventricular tachyarrhythmias Sustained ventricular tachycardia (>30 sec) Results in dizziness, syncope, hypotension and cardiac arrest Pulse rate between 120 and 220 beats/minute Emergency electrical cardioversion is often necessary Ventricular fibrillation Very rapid and irregular ventricular activation with no mechanical effect The patient is pulseless and becomes rapidly unconscious, and respiration ceases (cardiac arrest) Treatment: electrical defibrillation CONGESTIVE HEART FAILURE (HF) The myocardium is no longer able to pump sufficient blood to meet the need of the body, even at rest Reduced systolic output (forward failure) is accompanied by inadequate emptying of the heart chambers (backward failure) congestion in the venous circulation Classification The pump failure may involve the left or right ventricle or both; and may be acute or chronic Outcome: most frequent cause of death ACUTE LEFT-SIDED HF Causes • Hypertensive crisis • Acute myocardial infarction • Others Morphology Features of hypertensive heart disease or acute myocardial infarction + pulmonary edema: lungs >1200 gs, congested and wet, airways contain bubbly fluid Clinical features Forward failure (echocardiography: ejection fraction ≤40%): hypoperfusion and dysfunction of major organs Brain - somnolence loss of concioussness Kidney - oliguria Liver - jaundice Gut - trophic erosions/ulcers bleeding Backward failure Pulmonary edema, cardiac dyspnea (shortness of breath) and tachypnea + right HF Outcome Varies, frequently results in death CHRONIC LEFT-SIDED HF Causes • Hypertensive heart disease • Ischemic heart disease • Valvular heart disease: aortic stenosis, aortic incompetence, and mitral incompetence Morphology LV hypertrophy and dilation (wall thickness > 15 mm) Lateral dysplacement of the papillary muscles causing mitral regurgitation Subsequent chronic dilation of the LA + thrombus in the left auricle Brown induration of lungs Clinical features Forward failure physical activity, weakness Backward failure Dyspnea during exercise than at rest, fluid retention, pulmonary edema, later systemic venous edema Mitral regurgitation: systolic murmur!; LA dilation atrial strech chronic atrial fibrillation thrombus in the left auricle danger of systemic thromboembolism Prevention of thrombus formation: anticoagulation Outcome The pump failure in the terminal phase is lethal (New York Heart Association grading for cardiac status; NYHA Grade IV) Frequently, intercurrent upper airway or pulmonary infections (influenza, bronchopneumonia) are the direct cause of death 2 17. Vascular pathology III. Heart failure ACUTE RIGHT-SIDED HF Cause Massive pulmonary thromboembolism: obstruction of >50% of the pulmonary vascular bed Morphology Dilation of the RV plus Acute systemic congestion: passive hyperemia of liver, spleen, kidneys, GI mucosa Outcome Fatal in significant number of cases Prolonged right HF and the liver Hepatic congestion is complicated with necrosis in the centrilobular regions; the necrotic foci undergo sec. hemorrhage due to sinusoidal ruptures: central hemorrhagic necrosis Necroenzymes AST (aspartate aminotransferase) and ALT (alanine aminotransferase) become elevated in the blood CHRONIC RIGHT-SIDED HF Dilation and hypertrophy of the RV in response to chronic pulmonary hypertension Causes 1. Chronic left-sided HF; mitral stenosis 2. Chronic diseases of the lung (chronic cor pulmonale) Obstructive diseases: chronic bronchitis, emphysema, bronchiectasis, + bronchial asthma Restrictive (interstitial) diseases, such as idiopathic pulmonary fibrosis, pneumoconiosis, Boeck sarcoidosis 3. Diseases of the pulmonary artery Recurrent pulmonary thromboembolism Primary pulmonary hypertension 4. Deformities affecting chest movement Pectus carinatum (pigeon’s chest) Pectus excavatum (funnel chest) Kyphoscoliosis (abnormal curvature of the spine in both a coronal and sagittal plane) 5. Neuromuscular diseases affecting respiratory muscles Morphology RV hypertrophy (thickness › 6 mm) + dilation, and manifestations of chronic systemic congestion • Anasarca (pedal and pretibial edema; in bedridden patients: primarily presacral) • Bilateral hydrothorax (500 - 1000 ml) • Hydropericardium (300 - 500 ml) • Ascites • Cyanotic induration of liver, spleen (congestive hepato- and splenomegaly) • Chronic congestion of the gut mucosa Chronic congestion of liver: cyanotic induration fibrotic replacement of the hepatocytes cardiac fibrosis fibrotic septa form pseudolobules cardiac cirrhosis (rare) HYPERTENSIVE HEART DISEASE LV hypertrophy as a response to long-standing systemic arteriolar vasospasm Early phase: concentric hypertrophy of LV: wall thickness > 20 mm; weight > 500 g Late phase: LV hypertrophy + dilation: wall thickness < 20 mm; weight > 550 g Clinical features • Asymptomatic for a long time • Atrial fibrillation is common (results from LA enlargement and strech) • Cause of death in 1/3 of hypertensive patients (congestive HF, sudden death) • Since hypertension aggravates atherosclerosis, patients with hypertensive heart disease also suffer from coexisting ischemic heart disease ISCHEMIC HEART DISEASE (IHD) The most common cause of death in industrialized countries Pathogenesis Reduced coronary blood flow commonly due to coronary atherosclerosis Atherosclerosis causes chronic progressive narrowing of
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