SBM2 Cardiovascular System7 PDF

SBM2 Cardiovascul ar System7 JENNIFER RAYBURN, M.D. MTSU PHYSICIAN ASSISTANT STUDIES  Objectives Contrast Criticize Inventory Apply Contrast the Criticize the Inventory the Apply the etiology and etiology, pathophy...

SBM2 Cardiovascul ar System7 JENNIFER RAYBURN, M.D. MTSU PHYSICIAN ASSISTANT STUDIES  Objectives Contrast Criticize Inventory Apply Contrast the Criticize the Inventory the Apply the etiology and etiology, pathophysiolog etiology, clinical pathophysiolog y of acute pathophysiolog presentation of y, and clinical rheumatic y, and clinical acute presentation of fever and presentation of pericarditis, valvular heart rheumatic infective pericardial disease, heart disease endocarditis effusion, and including constrictive aortic, mitral, pericarditis pulmonic, and tricuspid  Anatomy and Function of the Pericardium ▪ Pericardium: Is a two- layered sac that encircles the heart. ▪ Inner serosal layer (visceral pericardium): adheres to the outer wall of the heart and is reflected back on itself , at the level of the great vessels. (aka epicardium) ▪ Outer fibrous layer (parietal pericardium): tough, outer layer of the heart ▪ The pericardium has three functions: ▪ 1. It fixes the heart within the mediastinum and limits its motion ▪ 2. It prevents extreme dilation of the heart during sudden rises of intracardiac volume ▪ 3. It may act as a barrier to limit the spread of infection from the adjacent lungs  Acute Pericarditis ▪ The most common affliction of the pericardium ▪ 2. Noninfectious: ▪ Inflammation of the pericardial layers ▪ Following MI: Early type (first few days after MI) results ▪ from inflammation extending from the epicardial surface of Etiologies of pericarditis: the injured myocardium to the adjacent pericardium; more ▪ common in transmural infarctions; more common in patients 1. Infectious (infection of the endothelium/valves medically treated and not after reperfusion (5%). secondary to colonization during transient or persistent bacteremia): ▪ Late Type (Dressler’s syndrome) can develop 2 weeks to ▪ The most common cause of acute pericarditis is several months following acute infarction; cause unknown; idiopathic!! thought to be autoimmune in origin (antigens to necrotic myocardial cells) ▪ However, most of these episodes have been demonstrated to be caused by viral infections (echovirus or coxsackievirus group A or B, influenza, ▪ Uremic pericarditis: complication of untreated chronic renal varicella, mumps, hepatitis B, infectious mononucleosis, failure and COVID-19). ▪ ▪ Neoplastic pericarditis: metastatic spread or local invasion Pericarditis is also the most common manifestation of cardiovascular disease in patients with HIV/AIDS. of cancer by the lung, breast, or lymphoma ▪ Tuberculous pericarditis is also an important cause of ▪ Radiation induced pericarditis: radiation to the thorax pericarditis in immunocompromised patients (worldwide). ▪ Pericarditis due to connective tissue diseases (SLE, RA, ▪ Nontuberculous Bacterial Pericarditis: progressive systemic sclerosis) immunocompromised, severe burns and malignancies. Pneumococci and Staphylococci ▪ Drug-induced pericarditis: (procainamide, hydralazine, immune checkpoint inhibitors, methyldopa, isoniazid, phenytoin, minoxidil, anthracycline chemo such as doxorubicin)  Acute Pericarditis ▪ Three stages: ▪ 1. Local vasodilation with transudation of protein- poor, cell-free fluid into the pericardial space ▪ 2. Increased vascular permeability with leak of protein into the pericardial space ▪ 3. Leukocyte exudation (neutrophils then mononuclear cells)  Clinical Features of Pericarditis ▪ Chest pain (95%) and fever most frequent symptoms ▪ Severe, retrosternal and left precordial pain (localize to back and ridge of left trapezius due to phrenic nerve irritation) ▪ Sudden onset of sharp, pleuritic pain (aggravated by inspiration and deep coughing) ▪ Anterior chest pain that is positional ( worse when supine and improves with sitting and leaning forward which reduces pressure on the parietal pericardium) ▪ Dyspnea (reluctance of the patient to breathe deeply because of pain)  Pericardial Effusion ▪ Normal pericardial space contains 15-50 mL of pericardial fluid (some books quote 5-15 mL) ▪ Larger volumes of fluid may accumulate in the pericardial space in association with any of the forms of acute pericarditis (malignancy is the most common cause such as lung or breast ) ▪ Non-inflammatory serous effusions can result from: ▪ 1. Conditions that increase capillary permeability (severe hypothyroidism) ▪ 2. Increased capillary hydrostatic pressure (CHF) ▪ 3. Decreased plasma oncotic pressure (cirrhosis or nephrotic syndrome) ▪ 4. Chylous effusions may occur in the presence of lymphatic obstruction of pericardial drainage (neoplasm or TB)  Pathophysiology of Pericardial Effusion ▪ The pericardium is a relatively stiff structure and therefore, the relationship between its’ internal volume and pressure is not linear. ▪ At low volumes (normally present in the pericardium), a small increase in volume leads to only a small rise in pressure ▪ When intrapericardial volume expands beyond a critical level, a dramatic increase in pressure is incited by the non-distensible sac. At that point, even a minor increase in volume can translate into an enormous compressive force on the heart. Clinical Features of Pericardial Effusion ▪ May be asymptomatic ▪ Dull, constant ache in the left side of the chest ▪ Cardiac tamponade ▪ Compressive symptoms of adjacent structures (dysphagia, dyspnea, hoarseness, or hiccups) ▪ Muffled heart sounds ▪ Pericardial friction rub  Cardiac Tamponade Medical Emergency!!! ▪ Pericardial fluid accumulates under high pressure, compresses the cardiac chambers, and severely limits filling of the heart. ▪ Ventricular stroke volume and cardiac output decline potentially leading to hypotension, obstructive shock, and death ▪ Any etiology of acute pericarditis can progress to cardiac tamponade ▪ Most common causes are: neoplastic, post-viral, uremic and hemorrhagic (trauma)  Pathophysiology of Cardiac Tamponade ▪ As a result of the surrounding tense pericardial fluid, the heart is compressed and the diastolic pressure within each chamber becomes elevated and equal to the pericardial pressure ▪ The compromised cardiac chambers cannot accommodate normal venous return ▪ The systemic and pulmonary venous pressures rise ▪ The increase of systemic venous pressure results in signs of right-sided heart failure (jugular venous distension, edema, etc.) ▪ The elevated pulmonary pressure leads to pulmonary congestion ▪ Reduced filling of the ventricles during diastole decreases systolic stroke volume and the cardiac output declines Clinical Features of Cardiac Tamponade https://www.youtube.com/watch?v=UoA8EYfk57I (pulsus paradoxus) ▪ Suspect in any patient with known pericarditis, pericardial effusion or chest trauma that develops signs of systemic vascular congestion and decreased cardiac output ▪ Beck’s Triad: ▪ 1. Jugular venous distention ▪ 2. Systemic Hypotension ▪ 3. “small, quiet heart”/muffled heart sounds (insulating effects of the pericardial fluid) ▪ Sinus tachycardia ▪ Pulsus paradoxus ▪ Profound hypotension (if sudden) or fatigue and peripheral edema (if slow) ▪ Dyspnea and tachypnea ▪ Fatigue and peripheral edema  Constrictive Pericarditis ▪ Loss of pericardial elasticity (thickening, fibrosis, & calcification) leading to restriction of ventricular diastolic filling ▪ Most frequently idiopathic (early 20th century it was often due to TB) ▪ Following an episode of acute pericarditis, any pericardial effusion that has accumulated usually undergoes gradual resorption ▪ However, in constrictive pericarditis, the fluid undergoes organization, with subsequent fusion of the pericardial layers, followed by fibrous scar formation. Some patients develop calcification of the adherent layers and further stiffening of the pericardium. ▪ Pathophysiologic abnormalities occur during diastole; normal filling of the cardiac chambers is inhibited; systemic venous pressure rises, and signs of right-heart failure ensue; reduction of stroke volume and CO leads to lower BP ▪ Clinical Features: develop over months to years; Dyspnea, fatigue, & orthopnea are the most common symptoms; jugular venous distension, hepatomegaly with ascites, peripheral edema, hypotension, reflex tachycardia; early diastolic “knock”; Kussmaul sign  Valvular Heart Disease Mitral Stenosis (MS) ▪ MS refers to a narrowed mitral valve orifice leading to obstruction of flow from the LA to the LV & backflow of blood into the left atrium (LA) ▪ The most common cause is prior rheumatic fever (50-70%) ▪ Other causes: calcification of the mitral annulus that extends onto the leaflets, infective endocarditis,& congenital stenosis of the valve ▪ In a normal heart during diastole, the MV opens and blood flows freely from the LA to the LV ▪ In MS, there is obstruction to blood flow across the valve such that emptying of the LA is impeded and there is an abnormal pressure gradient between the LA and LV. LA pressure increases ▪ Higher LA pressure is transmitted retrograde to the pulmonary circulation (increases pulmonary venous and capillary pressures) and the patient may experience dyspnea and heart failure symptoms ▪ Chronic pressure overload of the LA in MS can lead to LA enlargement  Rheumatic Heart Disease ▪ Acute rheumatic fever (ARF) is an inflammatory condition that primarily affects the heart, skin, and connective tissues. ▪ Arises as a complication of group A beta- hemolytic strep infection ▪ ARF can develop 2-3 weeks after strep pharyngitis and present with chills, fever, fatigue and migratory arthritis. ▪ Involvement of the heart is thought to be a result of autoimmune cross-reactivity between bacteria and cardiac antigens. ▪ Carditis affects all layers of the heart ▪ Chronic rheumatic heart disease is characterized by permanent deformity or impairment of one or more cardiac valves ▪ The symptoms of the valve disease do not manifest until 10-30 years after the ARF has resolved (usually 3rd or 4th decade of life). ▪ RHD primarily affects the mitral valve in almost all cases, aortic valve (20-30%) and rarely the tricuspid valve.  Valvular Disorders Mitral Regurgitation (MR) ▪ Incomplete closure of the mitral valve leading to retrograde blood flow from the LV to the LA during systole. ▪ Caused by disruption of structural integrity of the valve structures (annulus, two leaflets, chordae tendineae, papillary muscles) ▪ Primary MR is due to a structural defect in one or more valve components (most common MVP in US and rheumatic disease in developing countries) ▪ Secondary MR is due to left ventricular enlargement (normal valve structure) ▪ Acute MR: Primary in nature and results from sudden damage to components of the valve apparatus (infarcted papillary muscle from STEMI) ▪ Chronic MR: multiple primary causes (mitral valve prolapse (MVP), rheumatic deformity, congenital, calcified annulus)  Valvular Disorders Mitral Regurgitation (MR) ▪ In MR, a portion of the left ventricular stroke volume is abnormally ejected backward into the low -pressure LA during systole. Therefore, the CO is less than the LV’s total output. ▪ Direct consequences: ▪ 1. Elevation of LA volume and pressure ▪ 2. A reduction of forward CO ▪ 3. Volume related stress on the LV because the regurgitant volume returns to the LV in diastole along with normal pulmonary venous return ▪ To meet the circulatory needs and to eject the additional volume the LV stroke volume must rise ▪ Acute MR: Normal LA size and compliance- high LA pressure – High pulmonary venous pressure – Pulmonary congestion and edema ▪ Chronic MR: Increased LA size and compliance – Relatively normal LA and pulmonary venous pressures, but decreased forward cardiac output  Mitral Valve Prolapse (MVP) ▪ Characterized by abnormal billowing of a portion of one or both mitral leaflets into the LA during ventricular systole and is frequently accompanied by MR ▪ May be inherited as a primary AD disorder or due to connective tissue diseases (Marfan’s or Ehlers-Danlos) ▪ The valve leaflets (posterior leaflet) are enlarged, and the normal dense leaflet structure is replaced with loose, myxomatous connective tissue, mitral annular dilatation, or thickened leaflet tissue ▪ More common in young women (15- 35 yo), about 2-5% population ▪ Most often asymptomatic but can describe chest pain or palpitations due to associated arrhythmias  Valvular Heart Disease Aortic Stenosis (AS) ▪ Three major causes: ▪ 1. Degenerative calcification of a previously normal aortic valve (wear & tear, >70 yo) ▪ 2. Calcification of a congenitally bicuspid valve (