ClinMed 2 Cards 8 2024 PDF

CLINMED 2 CARDS 8 Jennifer Rayburn. M.D MTSU Physician Assistant Studies  OBJECTIVES 2. Distinguish between the epidemiology, 1. Relate the etiology, assessment, and evaluation,...

CLINMED 2 CARDS 8 Jennifer Rayburn. M.D MTSU Physician Assistant Studies  OBJECTIVES 2. Distinguish between the epidemiology, 1. Relate the etiology, assessment, and evaluation, and treatment of both treatment of valvular infective and non- disorders of the heart infective forms of endocarditis  VALVULAR HEART DISEASE (VHD) Either functional or anatomic abnormalities affecting the cardiac valves causing either stenosis or regurgitation when damaged Prevalence is 2.5% in developed countries VHD affects 20 million persons in the U.S. 75% due to valve degeneration and 25% due to rheumatic heart disease (infective endocarditis is also a major cause) In developing countries, rheumatic heart disease is the most common cause of valvular heart disease Can be congenital or acquired and risk increases with age (3-6% over age 65 yrs) Exertional dyspnea is the most common symptom of VHD Other symptoms can include: angina, syncope, palpitations, lower extremity edema, and ascites Essential tests for VHD: Twelve-lead ECG, CXR, and transthoracic ECHO  RISK FACTORS FOR VALVULAR HEART DISEASE (VHD) Congenital Factors: 1. Bicuspid Aortic Valve: A congenital condition where the aortic valve has two leaflets instead of the normal three, which predisposes individuals to aortic stenosis or regurgitation. 2. Congenital Heart Defects: Other structural heart defects can lead to valve dysfunction over time. Acquired Factors: 1. Rheumatic Fever: A history of rheumatic fever, often due to untreated streptococcal infections, can lead to rheumatic heart disease, which primarily affects the mitral valve and sometimes the aortic valve. 2. Infective Endocarditis: Infections of the heart valves caused by bacteria or fungi can result in valve damage or destruction, particularly in individuals with pre-existing valve abnormalities. 3. Age-Related Degeneration: 1. Calcific Aortic Stenosis: Progressive calcification and stiffening of the aortic valve, most common in the elderly. 2. Mitral Annular Calcification: Age-related changes in the mitral valve, often leading to mitral regurgitation.  RISK FACTORS FOR VALVULAR HEART DISEASE (VHD) CONTINUED Cardiovascular Risk Factors: 1. Hypertension: Long-standing high blood pressure can increase the workload on the heart and contribute to conditions such as aortic stenosis or mitral regurgitation. 2. Coronary Artery Disease (CAD): This can affect the blood supply to the valves or the supporting structures of the heart, leading to ischemic mitral regurgitation or aortic insufficiency. Lifestyle-Related Risk Factors: 1. Smoking: Increases the risk of both atherosclerosis and infective endocarditis, indirectly contributing to valve dysfunction. 2. Hyperlipidemia: High cholesterol can accelerate calcification of the aortic valve and exacerbate other cardiovascular conditions that influence valve health. 3. Obesity: Increases the risk of hypertension, diabetes, and CAD, which in turn affect valve function. Other Medical Conditions: 1. Marfan Syndrome or Other Connective Tissue Disorders: These can lead to dilation of the aortic root, affecting the aortic valve and leading to regurgitation. 2. Chronic Kidney Disease: Associated with calcium and phosphate imbalances, leading to valve calcification, particularly in the aortic valve. 3. Autoimmune Disorders: Conditions like lupus and rheumatoid arthritis can cause inflammation that affects the valves, leading to stenosis or regurgitation. 4. Radiation Therapy: Previous radiation exposure to the chest, particularly in cancer treatment, can lead to calcification and fibrosis of the heart valves. STAGES OF VHD  Grading of Heart Murmurs Copyrights apply  VALVULAR HEART DISEASE TIPS ON CARDIAC MURMURS Stenosis: abnormal forward flow of blood through a stenotic valve that should be open. Leads to pressure overload. Typically, a harsh, rumble sound Regurgitation: abnormal backflow of blood through an incompletely closed valve. Lead to volume overload. Typically, a blowing sound Any increase in venous return (supine, squat, leg elevation) will increase the intensity of all murmurs EXCEPT for hypertrophic cardiomyopathy and mitral valve prolapse (MVP) Any decrease in venous return (stand, Valsalva) decreases the intensity of all murmurs EXCEPT for hypertrophic cardiomyopathy and mitral valve prolapse Inspiration increases the intensity of R sided murmurs and decreases the intensity of L sided murmurs (think pulmonary pump) Radiation: Axilla is mitral regurgitation and Carotids is aortic stenosis or pulmonic stenosis Diastolic murmurs: Aortic Regurgitation & Mitral Stenosis Systolic murmurs: Aortic Stenosis & Mitral Regurgitation  MURMURS – WAY TO REMEMBER SYSTOLIC VS. DIASTOLIC ARMS REST (Aortic Regurgitation Systolic Murmurs and Mitral Stenosis are Diastolic murmurs) AS PS HOCM VSD AR PR MR TR MVP MS TS  MURMUR ACCENTUATIONS Aortic murmurs are accentuated with sitting up and leaning forward (AS, AR) Mitral murmurs are accentuated with lying on left side (MS, MR) Increased venous return increases all murmurs except for HCM & MVP Decreased venous return decreases all murmurs except for HCM & MVP Inspiration (increases venous return on the R side) and increases all R sided murmurs (pulmonic and tricuspid) Inspiration (decreases venous return on the L side) and decreases all L sided murmurs (mitral and aortic) Expiration (increases venous return on the L side) and increases all L sided murmurs Expiration (decreases venous return on the R side) and decreases all R sided murmurs Handgrip: increases afterload (compresses arteries of the upper extremity) leading to decreased LV emptying (decreased forward flow and increased backflow): outflow murmurs decrease with handgrip (AS, HCM, MVP) Regurgitant murmurs (AR, MR) increase with handgrip (due to backward flow; MS increases due to increased afterload) Amyl Nitrate: decreases afterload and increases LV emptying thus AS, MVP, HCM increase with amyl nitrate  AORTIC STENOSIS VS. HYPERTROPHIC CARDIOMYOPATHY Both: angina, syncope, systolic murmur. Both murmurs go in the same direction with afterload maneuvers (both increase with amyl nitrate and both decrease with handgrip) HOCM: preload maneuvers that decrease LV volume (Valsalva, standing) will worsen murmur of HOCM but decrease the intensity of AS. Increased LV volume (squatting, leg raise) will decrease the murmur of HOCM but will increase the murmur of AS. HOCM does not radiate to the carotids! CARDIAC AUSCULTATION OF MURMURS HEART MURMURS CHART  AORTIC STENOSIS (AS) Most common cause of valvular heart disease (3% of Murmur: Harsh, low-pitched, Systolic persons >65 yrs) crescendo-decrescendo murmur LV outflow obstruction leads to fixed cardiac output, heard best at the RUSB, radiating to increased afterload, LVH and eventually LV failure the carotids Aov orifice 70 yo), chest irradiation Symptoms: Exertional dyspnea is often the most Decreased murmur intensity: common presenting symptom along with decreased decreased venous return, inspiration, exercise tolerance. handgrip Triad of symptoms: Weak, delayed carotid pulse (pulsus Angina (5 yrs mean survival rate), syncope (3 tardus) , narrow pulse pressure years), and CHF (2 years Single, or soft S2 and possibly S4  AORTIC STENOSIS (AS) HTTPS://WWW.YOUTUBE.COM/WATCH?V=EFQI5DLIB2W (AS MURMUR) Diagnostic Studies: ECHO is test of choice (LVH, thickened or calcified aortic valve; look at valve orifice) Cardiac cath may be used prior to surgery & is definitive diagnostic test. ECG will classically show LVH Management: Surgical repair; aortic valve replacement is the only effective treatment. Indications for surgical repair: symptomatic AS; asymptomatic with severe AS (low EF or area PV) Exception is in IV drug use, the tricuspid valve is the most commonly involved Risk factors: Increased age (>60 yrs), rheumatic heart disease, IV drug use, immunosuppression, prosthetic heart valve; congenital heart disease, diabetes, indwelling IV catheters, implanted cardiac device Four Types: 1. Acute bacterial endocarditis: Infection of normal valves with a virulent organism (S. aureus) 2. Subacute bacterial endocarditis: Indolent infection of abnormal valves with less virulent organisms (S. viridans) 3. IV drug-related endocarditis: Most commonly due to S. aureus (especially MRSA), Pseudomonas, Candida 4. Prosthetic valve endocarditis: Early (within 60days): Staphylococcus epidermidis (most common); Late (after 60 days) resembles native valve endocarditis (S. aureus/MRSA)  INFECTIVE ENDOCARDITIS Organisms/Microbiology Clinical manifestations Staphylococcus aureus: Affects normal valves; Persistent fever is the most common; malaise, most common cause of ACUTE IE; IVDU (MRSA) & fatigue, anorexia, chills prosthetic valve IE New onset of a murmur or worsening of an existing Streptococcus viridans: most common cause of murmur (85%) subacute; affects damaged valves; part of oral flora Osler nodes: painful or tender raised or violaceous (poor dentition/dental procedures/gingivitis) nodules on the pads of the digits and the palms Staphylococcus epidermidis: Most common cause Janeway lesions: painless, erythematous macules of early prosthetic valve endocarditis on the palms and soles Enterococcus: Seen in men >50 yrs with recent Splinter hemorrhages: linear reddish-brown lesions history of GI or GU procedures under the nail bed, petechiae (skin or mucus HACEK organisms (Haemophilus aphrophilus, membranes) Actinobacillus, Cardiobacterium hominis, Eikenella Roth spots: retinal hemorrhages with central corrodens, Kingella kingae): gram negative organisms that are hard to culture; suspect these in clearing patients with endocarditis and negative blood Splenomegaly, septic arterial or pulmonary emboli, cultures glomerulonephritis  INFECTIVE ENDOCARDITIS FINDINGS Splinter Osler Nodes Janeway Lesions Roth Spots hemorrhages  INFECTIVE ENDOCARDITIS Diagnosis (Modified Duke Criteria): Blood cultures (before antibiotics); 3 sets at least one hour apart ECG (prone to arrhythmias); ECHO (TTE first); TEE if TTE non-diagnostic (more sensitive) Must get blood cultures and ECHO to establish Duke criteria! Labs: CBC, ESR, blood cultures Management: Prompt & appropriate antimicrobial therapy (risk factors) Surgery if refractory CHF, persistent of refractory infection, invasive infection prosthetic valve, recurrent systemic emboli, fungal infections Know These!!! INFECTIVE ENDOCARDITIS SURGICAL MANAGEMENT Early surgery is recommended for any of the following: 1.Severe valvular dysfunction resulting in CHF, persistent or refractory infection, invasive infection, prosthetic valve, recurrent systemic emboli; fungal infections 2.Left-sided IE caused by S. aureus, fungal infections, or other highly resistant organisms 3.Associated complications, such as annular or aortic abscess, destructive penetrating lesions, or heart block 4.Persistent bacteremia or fevers lasting longer than 5 to 7 days after onset of appropriate antimicrobial therapy  INFECTIVE ENDOCARDITIS MEDICAL MANAGEMENT Type of Infective Endocarditis Management Native Valve (MRSA) or Unknown Vancomycin or Vancomycin plus either ceftriaxone or gentamycin Native Valve (MSSA) Antistaphylococcal penicillin (nafcillin or oxacillin) plus either ceftriaxone or gentamycin Penicillin allergy: Cefazolin Prosthetic Valve Vancomycin plus gentamycin plus rifampin (rifampin kills Staph that are adherent to foreign material) Fungal Parenteral antifungal: Amphotericin containing product with or without combination therapy (Ampho B plus Flucytosine). This is given for 6 weeks; often will need surgery  ENDOCARDITIS PROPHYLAXIS: KNOW THESE!!!! Procedures for which endocarditis prophylaxis IS recommended: Dental: All dental procedures involving manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa Respiratory: Procedures involving incision or biopsy of the respiratory mucosa, such as tonsillectomy and adenoidectomy, rigid bronchoscopy Other: procedures involving infected skin, skin structures, or musculoskeletal tissue prior to incision and drainage Regimens: Amoxicillin 2 grams 30-60 minutes before the procedures listed or amoxicillin/clavulanate 1000/200 mg Clindamycin 600 mg if penicillin allergic Macrolides, Doxycycline, or Cephalexin other options  NEW MARCH 2021 AHA GUIDELINES STATEMENT IE PROPHYLAXIS DENTAL PROCEDURES “All dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa”  LIBMAN-SACKS ENDOCARDITIS Non-bacterial thrombotic endocarditis (marantic endocarditis) is a non-infectious endocarditis due to sterile platelet thrombi deposition on the affected valve. Most commonly affects the mitral and aortic valves Seen with malignancy, SLE, anti-phospholipid antibody syndrome, rheumatic fever, and other inflammatory conditions Clinical manifestations: Most asymptomatic and afebrile; symptoms due to emboli to the skin, kidney, extremities and spleen Management: Manage the causative condition; may need anticoagulation QUESTIONS????