SBM2 Cardiovascular System 8 PDF

SBM2 Cardiovascul ar System 8 JENNIFER RAYBURN, M.D. MTSU PHYSICIAN ASSISTANT STUDIES  Objectives 1. Debate the etiology, pathophysiology, and clinical presentation of heart failure 2. Compare and contrast the etiology, pathophysiology, and clinical presentation of dilated,...

SBM2 Cardiovascul ar System 8 JENNIFER RAYBURN, M.D. MTSU PHYSICIAN ASSISTANT STUDIES  Objectives 1. Debate the etiology, pathophysiology, and clinical presentation of heart failure 2. Compare and contrast the etiology, pathophysiology, and clinical presentation of dilated, hypertrophic obstructive, hypertensive, or valvular hypertrophic, and restrictive cardiomyopathy, and stress induced cardiomyopathy  Heart Failure ▪ Heart failure is present when the heart is unable to pump blood forward at a sufficient rate to meet the metabolic demands of the body or can do so only if cardiac filling pressures are abnormally high. ▪ Results in a clinical syndrome of fatigue, shortness of breath and often volume overload ▪ It may be the final and most severe manifestation of nearly every form of cardiac disease ▪ Prevalence in the United States in 2024 is 6.7 million patients & the number is increasing (aging population & interventions to prolong survival after damaging insults to the myocardium); 64 million cases worldwide ▪ Most commonly results from conditions that impair left ventricular function ▪ Lifetime risk of developing HF per Framingham Heart study was one in five  Types & Definition of Heart Failure ▪ Chronic heart failure may result from a wide variety of cardiovascular insults ▪ 1. Impaired ventricular contractility ▪ 2. Increase in afterload (due to chronic pressure overload) ▪ 3. Impaired ventricular relaxation and filling (diastolic) ▪ Systolic Dysfunction: heart failure that results from an abnormality of ventricular emptying (impaired contractility or excessive afterload) ▪ Diastolic Dysfunction: heart failure that is caused by abnormalities of diastolic relaxation or ventricular filling ▪ Many patients may demonstrate both systolic and diastolic dysfunction ▪ New Terminology: ▪ Heart failure with reduced ejection fraction (HFrEF) which is primarily systolic dysfunction ▪ Heart failure with preserved ejection fraction (HFpEF)which is primarily diastolic dysfunction  Right Heart Failure ▪ Right Sided Heart Failure: RV is quite susceptible to failure in situations that present a sudden increase in afterload (ex. PE). ▪ **The most common cause of R sided heart failure is Left sided heart failure! ▪ Isolated R heart failure is less common and usually reflects increased RV afterload owing to diseases of the lung parenchyma (COPD, severe asthma,etc.) or pulmonary vasculature (pulm htn, PE, etc). ▪ Cor pulmonale: R sided heart failure that results from a primary pulmonary process  Compensatory Mechanisms in Heart Failure ▪ Compensatory mechanisms are called into action in patients with heart failure to buffer the fall in CO and help preserve sufficient blood pressure to perfuse vital organs (for as long as possible). ▪ Adverse consequences of these activations/compensations can include an increase in afterload from excessive vasoconstriction and excess fluid retention, which contribute to peripheral edema and pulmonary congestion  Compensatory Mechanisms in Heart Failure Frank Starling Mechanism ▪ Heart failure caused by impaired LV contractile function causes a downward shift of the ventricular performance curve. At a given preload, stroke volume is decreased compared to normal. ▪ Reduced SV results in incomplete chamber emptying so that the volume of blood that accumulates in the ventricle during diastole is higher than normal. This increased stretch on the myofibers induces a greater SV on subsequent contraction, which helps to empty the enlarged LV and preserve forward CO. ▪ This has its’ limits. In the case of severe HF with marked depression of contractility, the curve may be nearly flat, reducing the augmentation of CO. In this instance, marked elevation of the EDV and pressure may result in pulmonary congestion and edema. Compensatory Mechanisms in Heart Failure Neurohormonal Alterations  Compensatory Mechanisms in Heart Failure Ventricular Hypertrophy and Remodeling ▪ Develop over time in response to ventricular wall stress because of either LV dilation or the need to generate high systolic pressure to overcome excessive afterload. ▪ A sustained increase in wall stress stimulates development of myocardial hypertrophy and deposition of extracellular matrix ▪ However, because of the increased stiffness of the hypertrophied wall, these benefits come at the expense of higher-than-normal diastolic ventricular pressures which are transmitted to the LA and pulmonary vasculature ▪ Type of compensatory hypertrophy depends on if the ventricle is subjected to chronic pressure or chronic volume overload ▪ Eccentric hypertrophy: Chronic chamber dilation owing to volume overload (MR, AR) ▪ Concentric Hypertrophy: Chronic pressure overload (htn, AS) results in synthesis of new sarcomeres in parallel with the old). Wall thickness increases without chamber dilation Factors that might precipitate Heart Failure ▪ Many patients with heart ▪ Increased metabolic demands: Fever, Infection, Anemia, Tachycardia, failure remain Hyperthyroidism, Pregnancy asymptomatic for extended ▪ Increased circulating volume (increased periods either because the preload): Excessive sodium content in diet, Excessive fluid administration, Renal failure impairment is mild or because the cardiac ▪ Conditions that increase afterload: Uncontrolled hypertension, Pulmonary dysfunction is balanced by embolism (increases RV afterload) the compensatory ▪ Conditions that impair contractility: mechanisms discussed Negative inotropic medications, Myocardial ischemia or infarction, Excessive ethanol ingestion ▪ Failure to take prescribed heart failure medications ▪ Excessively slow heart rate Clinical Signs of Heart Failure  Cardiomyopathies ▪ A diverse set of heart muscle disorders that affect myocardial systolic and/or diastolic function. ▪ Three main types based on the anatomic appearance and abnormal physiology of the left ventricle. ▪ 1. Dilated cardiomyopathy: ventricular chamber enlargement (one or both) with impaired systolic contractile function ▪ 2. Hypertrophic cardiomyopathy: abnormally thickened ventricular wall with abnormal diastolic relaxation but usually normal systolic function ▪ 3. Restrictive cardiomyopathy: Abnormally stiffened myocardium leading to impaired diastolic relaxation, but systolic contractile function is typically normal or near normal  Dilated cardiomyopathy (DCM) ▪ Multiple causes (genetic mutations, viral myocarditis, chronic excessive alcohol ingestion, peripartum state, cardiotoxic & antineoplastic agents), Bi deficiency, infiltrative diseases; most are idiopathic (50%) ▪ Genetic abnormalities are the most common identifiable cause of DCM; Autosomal dominant (titin gene 20-25% of patients)  Viral Myocarditis (DCM) ▪ Viral Myocarditis: form of DCM that is inflammatory in nature. ▪ Afflicts young, healthy people ▪ Implicated viruses: Coxsackie group B, parvovirus B19, adenovirus, COVID -19, echovirus, Chagas disease among others ▪ Self limited illness with full recovery (but some patients can progress to a post viral form) ▪ Myocardial destruction and fibrosis result from an immune – mediated injury triggered by viral constituents  Other causes of DCM ▪ Non-infectious causes: Sarcoidosis & giant cell myocarditis ▪ Sarcoidosis: is a multisystem inflammatory disease caused by an immunologic response to an unclear trigger ▪ Cardiac involvement is seen in 25% of patients ▪ Giant cell myocarditis is rare cause ▪ Other connective tissue diseases (SLE) ▪ After immune checkpoint inhibitors ▪ Excessive alcohol consumption: thought that ethanol impairs cellular function by impacting oxidative function, myofilament protein synthesis, cytosolic calcium levels and myocyte apoptosis. ▪ **This type of DCM is potentially reversible with cessation of alcohol consumption. ▪ Cocaine ▪ Chemotherapy (doxorubicin or trastuzumab)  Other causes of DCM ▪ Peripartum cardiomyopathy: heart failure symptoms between the last trimester of pregnancy and up to 6 months postpartum ▪ Stress cardiomyopathy (Takotsubo cardiomyopathy): Apical ballooning syndrome. ▪ Coronary artery disease and valvular heart disease (Ischemic or valvular  Stress (Takotsubo) Cardiomyopathy ▪ Transient regional systolic dysfunction of the left ventricle that can imitate myocardial infarction but is associated with the absence of significant obstructive coronary artery disease or evidence of acute plaque rupture. ▪ A form of non-ischemic dilated cardiomyopathy ▪ Risk Factors: Postmenopausal women exposed to physical or emotional stress (aka broken heart syndrome). Loss of estrogen’s protective effects & increased catecholamines directly injure the myocardium ▪ Pathophysiology: Thought to be multifactorial, including a catecholamine surge during physical or emotional stress, microvascular dysfunction, and coronary artery spasm. ▪ See transient apical ballooning which is a transient regional systolic dysfunction of the left ventricle and systolic apical ballooning appearance.  Pathophysiology of DCM ▪ LV dysfunction and enlargement are most often primary ▪ The hallmark of DCM is left ventricular dilation with decreased contractile function. ▪ With disease progression, the right ventricle may also be involved. ▪ Clinical findings are that of heart failure; pulmonary congestion, dyspnea, orthopnea, PND, ascites peripheral edema  Hypertrophic Cardiomyopathy (HCM) ▪ Prevalence of 1 out of every 500 adults ▪ LVH not caused by chronic pressure overload (like in htn or AS) ▪ Systolic LV contraction is typically normal or vigorous, but the affected muscle is thickened and stiff, resulting in impaired ventricular relaxation and elevated LV filling pressure. ▪ It is the most common cause of sudden death in young patients (due to ventricular arrhythmias) ▪ Arises most often from an autosomal dominant mutation in genes that code for components of the sarcomere (chromosome 14) ▪ Asymmetric hypertrophy of the ventricular septum is most common pathologic finding Pathophysiology of HCM Athlete’s Heart/CV disease ▪ In response to endurance training, there can be physiologic increases in LV wall thickness, cavity size and mass, often referred to as athlete’s heart. ▪ In individuals with athlete’s heart, LVH is generally symmetric, and wall thickness is