[Music] welcome to this presentation on cardiomyopathy part one cardiomyopathy is the measurable deterioration of The myocardium for any reason usually leading to heart failure common symptoms are shortness of breath and peripheral emia there are three forms of cardiomyopathy dilated cardiomyopathy hypertrophic cardiomyopathy and restrictive cardiomyopathy the most common form is dilated cardiomyopathy this diagram shows the pathological features of dilated cardiopathy which which is a condition in the heart becomes weakened and enlarged and cannot pump blood efficiently this diagram shows the other two forms of cter myopathy hypertrophic is a condition in which a portion of The myocardium is hypertrophied without any obvious cause it is a leaving cause of sudden cardiac death in any age group restrictive cardiomyopathy is a situation in which the walls are so rigid that the heart is restricted from stretching and filling with blood properly restrictive cardiopathy is also the least common of the three types although in many cases no cause is apparent dilated cardiopathy is probably related to damage to The myocardium due to a variety of toxic metabolic or infectious agents its typical pathological change is marked enlargement of all four cardiac Chambers this picture shows the comparison between the normal ventricles and the diseased ventricles dilated cardiopathy represents the final common morphologic outcome of various insults is a combination of cardiomyocyte death associated with my cardiio fibrosis which results in impaired mechanical function according to place's law increased diameter increases wall stress and causes further mechanical disadvantage thus M Carter dysfunction can cause a vicious cycle leading to more myard dysfunction meanwhile dilated ventricles also causes atrial ventricular Val regurgitation which further worsens the hemodynamics similar to heart failure compensator mechanisms will be activated however ultimately they're even more detrimental these compensatory mechanisms include ventricular remodeling which changes the shape and function of the heart in extreme circumstances this mechanism can lead to to synchrony of contraction and medical intervention such as bi ventricular pacing or even a heart transplant is necessary clinical presentation of dilated cardiopathy is similar to that of B ventricular heart failure systolic dysfunction in dilated cardiopathy leads to overfilling wherein blood backs up into the Atria and inflow tracks this ultimately leads to congestion in both the pulmonary and systemic circulations this diagram shows its pathophysiology which is similar to that of B ventric heart failure as for Diagnostic evaluation only echocardiography shows typical morphologic changes for preliminary testing signs of peripheral demia may prompt a physician to order a BNP blood test given that renal function has been termined to be normal BNP is a determinant for heart failure and dilated cardiopathy because elevation of BNP is proportion to how much the ventricles are stretched treatment of dilated cardiopathy is also similar to heart failure the goal of the treatment is to decrease mardio oxygen demand and relieve peripheral emia through diuresis spinal lactone is a weak potassium sparing diuretic which means it doesn't cause potassium to be B from the body it is typically combined with another type of diuretic in order to augment its effects it is important to note that it is it is that crucial to control arrhythmias for patients with dilated cardiopathy as they are usually life-threatening arrhythmias it is also recommended for these patients to plant a cardioverter defibrillator with pacemaking functions these Afflicted patients afflicted by cardiopathy tend to be predisposed to rhythmia such as since chamber overload can be the mechanism of cause for example Atri fibrillation may be induced by irritation of the right atrium through excessive filling also it is important to prevent thrombosis formation within the heart which may further cause stroke or other severe esemicolonr cardiopathy have some degree of left ventricular hypertrophy usually there is asymmetric hypertrophy involving the intraventricular septum and is also seen as asymmetric septal hypertrophy this is in contrast to the concentric hypertrophy seen in conditions that increase after load like aortic stenosis or hypertension mocar hypertrophy and extracellular fibrosis predisposed to left ventricular stiffness and arhythmia this is an image of a heart specimen with hypertrophic cardiopathy pay attention to the asymmetric sepal hypertrophy which may obstruct the outflow tra of the left ventricle in hypertrophic cardiopathy the thickened ventricle first leads to diastolic dysfunction manifested as dmia and exercise intolerance what's more important is that a significant amount of patients demonstrate an obstruction to the outflow of blood from the left ventricle during either rest or under certain conditions this is known as Dynamic outflow obstruction because the degree of obstruction is variable and is dependent on the loading conditions and the contractility of The ventricle this diagram shows Dynamic outflow obstruction during syy and conom mital regurgitation it has been cleared that hypertrophic chyom opathy with Dynamic outflow OB struction shows more significant increment in left atrial and Pulmonary Venus pressure this diagram shows the pathophysiology of hypertropic cardiopathy note that ventricular rhythmia is a leading cause of sudden death the clinical course is variable and symptoms may include dmia and Gina palpitations lightheadedness fatigue Syncopy and even sudden cardiac death often symptoms mimic those of a congestive heart failure though treatment is very different again the definitive diagnostic tool is Echo cardiography hyperopic cardiopathy can man itself itself on the easy as severe left ventricular hypy with strain pattern strain pattern refers to SD segment and t-wave changes that signify chronic L left ventricular overload hypertropic cardiopathy may also manifest itself on the E as B ventricular hypertrophy however this is not as common to see on a 12 lead the primary goal of medication is to relieve symptoms such as chest pain shortness of breath and palpitations beta blockers are considered firstline treatments as they can slow down the heart rate for patients who cannot tolerate beta blockers or do not have good control of symptoms with beta blockers calcium tunnel blockers such as fol can be used anti rythmic drugs like amone and ni disopyramide can be prescribed as well antibiotic prophylaxis is important as they can prevent bacteremia as these patients have increased chance to develop infective endocarditis due to turbulent blood flow through a narrowed outflow track and also mitro regurgitation to remove hypert muscle myomectomy which is a surgical excision of hypertrophied muscle mass can be applied in addition per cutaneous seple ablation with alcohol can be considered the prognosis also includes sudden cardiac death in these conditions that takes us to the end of this presentation on cardiomyopathy part one [Music]