CV Exam 4

Rhabdomyoma Morphology and clinical features

Most common primary cardiac tumor in children which is associated with tuberous sclerosis Morphology: Gray-white myocardial mass composed of "spider cells" with markedly enlarged myocytes with thin, abundant cytoplasm Clinical Features: Typically discovered because of obstruction of the valvular orifice or cardiac chamber

Describe the development/presentation of pericarditis and the common causes

Presentation: pleuritic chest pain, high fever, pericardial friction rub, ECG abnormalities Tuberculous Pericarditis: most common cause of subacute or chronic purulent pericarditis ∙ Diagnosis: TB (+) in smear of pericardial fluid, Histologic examination (caseating granuloma), PCR Purulent Pericarditis: gross pus in pericardium or microscopic purulence, which can spread from intrathoracic foci (S. pneumoniae), blood (S. Aureus), or extension from subdiaphragmatic suppurative focus (infective endocarditis bacteria, S. Aureus, Salmonella)

Differentiate the following based on physical findings: Patent ductus arteriosus (PDA)

Continuous murmur

Discuss the effects of changes in body position (and Valsalva maneuver) on the auscultatory findings of Mitral valve prolapse (MVP)

Control: patient supine - midsystolic click, late systolic murmur Standing: early systolic click, longer & louder systolic murmur Squatting: late systolic click, shorter & quieter systolic murmur

Understand the various phases of the cardiac cycle (as depicted in the Wiggers cycle)

a. Atrial systole (late ventricular diastole) b. Isovolumic contraction c. Early ventricular systole d. Late ventricular systole e. Isovolumic relaxation f. Early diastole (rapid passive vent. filling) g. Mid diastole (diastasis: (near) cessation of ventricular filling due to equalization of atrial and ventricular pressures)

Define syncope

Temporary loss of consciousness and postural tone due to transient cerebral hypoperfusion, followed by spontaneous recovery

A 28-year-old male IV drug abuser presents with fatigue, fever, ascites, and lower extremity edema. Physical examination reveals: temp 101, HR 110, RR 18, and BP 100/60. His neck veins are distended, with large V waves. A grade 3/6 holosystolic murmur is heard along the lower left sternal border, and the murmur gets louder during inspiration. His lungs are clear to auscultation bilaterally. Abdominal examination reveals ascites, and his lower extremities are edematous bilaterally. 1. What is the most likely cause of his signs and symptoms? A. Endocarditis resulting in aortic stenosis B. Endocarditis resulting in mitral regurgitation C. Endocarditis resulting in pulmonic regurgitation D. Endocarditis resulting in tricuspid regurgitation E. Endocarditis resulting in tricuspid stenosis 2. Which of the following is the most likely causative organism? A. Streococcus pyogenes B. Streptococcus mitior (viridans streptococci) C. Streptococcus bovis (gallolyticus) D. Staphlococcus aureus E. Staphlococcus epidermidis

1. D. Endocarditis resulting in tricuspid regurgitation Holosystolic murmur which is louder during inspiration, + large V-waves 2. D. Staphlococcus aureus The most common cause of endocarditis in IVDU

Describe the development of Non-bacterial thrombotic endocarditis (NBTE) and the progression to infective endocarditis (IE)

1. Damage to heart valve that allows for backflow of blood 2. Bacteria adhere to injured/ inflamed valve surface 3. Bacteria proliferate and disseminate throughout the body which can clog vessels

What are the 3 functions of the pericardium?

1. Fixes heart within the mediastinum, limiting its motion 2. Prevents extreme dilation of the heart during sudden rises in cardiac volume 3. Barrier to spread of infection from adjacent structures

Understand the difference in the two types of artificial valves and discuss the complications.

1. Mechanical Valves: consist of different configurations of rigid non-physiologic material (caged balls, tilting disks, hinged semicircular flaps) 2. Tissue Valves (Bioprostheses): composed of porcine aortic valves or bovine pericardium, or can come from human valves (deceased donors). They are flexible and function similar to natural semilunar valves, however, the collection process renders them nonviable Complications ∙ Thromboembolism: major consideration of mechanical valves due to nonlaminar blood flow creating turbulence and stasis ∙ Structural Deterioration: occurs to virtually all bioprosthetic valves due to calcification and/or tearing ∙ Infective Endocarditis: complication of any valve replacement typically caused by S. epidermidis, S. Aureus, Streptococci, and Fungi

What are the layers of the pericardium?

1. Visceral: inner serosal layer that adheres to the epicardium 2. Parietal: outer fibrous layer

Discuss the calcific stenosis of the bicuspid aortic valve

A bicuspid aortic valve (BAV) is a developmental abnormality, with connection to a loss-of-function mutation in NOTCH1, and heritability on chromosome 18q, 5q, and 13q. It results in two functional cusps which are unequal in size, and the larger cusp having midline raphe resulting from incomplete separation during development. The raphe is a major site of calcific deposits. Typically asymptomatic early in life, producing late complications (i.e.- aortic stenosis/ regurgitation, infective endocarditis, and aortic dilation/ dissection)

Loeffler Endomyocarditis

A type of restrictive cardiomyopathy characterized by a stiffened, poorly-functioning heart due to infiltration of eosinophils resulting in endomyocardial fibrosis and production of large mural thrombi

Predict and be able to identify the heart sounds associated with A. Aortic stenosis B. Aortic regurgitation C. Mitral regurgitation D. Mitral stenosis E. Patent ductus arteriosus

A. Aortic Stenosis: Crescendo-Decrescendo murmur which is present during systole, then disappears during diastole ◦ Heard in the Aortic Area (2nd-3rd intercostal space on the right directly next to the sternum) B. Aortic Regurgitation: Decrescendo murmur heard in early diastole, and fading during late diastole/ systole ◦ Heard just below the pulmonic area (2nd-3rd intercostal space on the left directly next to the sternum) C. Mitral Regurgitation: Uniform murmur throughout systole and not present in diastole ◦ Heard in the mitral area (5th intercostal space midclavicular) D. Mitral Stenosis: Uniform murmur heard in late diastole ◦ Heard in the mitral area (5th intercostal space midclavicular) E. Patent Ductus Arteriosus: Uniform "machine-like murmur" that occurs d/t accessory pathway between the aorta and pulmonary artery heard constantly through systole & diastole

Discuss the natural history of aortic stenosis in terms of symptom onset and median survival

A. Relatively long latent period: asymptomatic, with favorable prognosis (irrespective of degree of stenosis) B. Symptomatic: Angina, Syncope, & CHF symptoms- mortality increases dramatically

A 54-year-old woman presents with dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, edema in the legs and feet, and fatigue. She has no history of angina, other signs of coronary artery disease, hypertension, or valvular disease. Echocardiography reveals cardiomegaly, with four-chamber hypertrophy and dilation. Which of the following is the most likely diagnosis? A. Dilated cardiomyopathy B. Hypertrophic cardiomyopathy C. Myocarditis D. Restrictive cardiomyopathy E. Cardiac tumor

A. Dilated cardiomyopathy Causes four-chamber hypertrophy and dilation

Describe and list the potential causes of: A. Exaggerated pulsus paradoxus B. Beck's triad C. Ewart's sign D. Kussmaul's sign

A. Exaggerated pulsus paradoxus: Increase in RV volume during inspiration, causes an exaggerated shift of the IV septum to the left since increased pericardial pressure increases resistance to outward expansion of the ventricle, causing an exaggerated change in pressure (> 10 mmHg) → Pericardial (cardiac) Tamponade → PE → Asthma → Emphysema B. Beck's triad: Hypotension + JVD + Muffled Heart sounds → Pericardial (cardiac) Tamponade C. Ewart's sign: Dullness to percussion over the angle of the left scapula due to compression of the left lung by the enlarged pericardial sac → Pericardial Effusion D. Kussmaul's sign: Increased in Jugular Venous pressure during inspiration due to increased venous return from negative intrathoracic pressure during inspiration that cannot be accommodated by right heart chambers → Constrictive Pericarditis → Restrictive cardiomyopathy → RV infarct or failure → Acute PE

Right-sided pathologic auscultatory findings A in intensity (loudness) during inspiration, except the B

A. Increase B. Pulmonic Ejection click

Know the major causative agents associated with A. Native valve endocarditis B. Prosthetic valve endocarditis and C. Intravenous drug user (IVDU) endocarditis Describe the virulence mechanisms that are responsible for damage & differentiate between (I) Acute and (II) Subacute presentations and the organisms most closely associated with each

A. Native Valve Endocarditis: ◦ Organisms: AACEK Organisms → Aggregatibacter (Haemophilus) aphrophilus: normal flora of the mouth, slow grower & rare → Aggregatibacter actinomycetecomitans: most common, it is a slow grower (3-6 months), associated with periodontal disease ("tooth killer"), produces significant embolization → Cardiobacterium hominus: characterized by large vegetations & emboli, it is a slow grower (2-5 months) and typically does not produce fever → Eikenella corrodens: characteristic bleach smell, often seen in IV drug users (especially emphetamines) & in those suffering from human bites → Kingella kingae: Oxidase (+), Gram (-) rod that is normal flora of the mouth and often infects children B. Prosthetic Valve Endocarditis: ◦ Organisms: S. Epidermidis (first 60 days), Viridans strep. (after 60 days) C. Intravenous Drug User (IVDU) Endocarditis: Typically effects the right side of the heart, with tricuspid valve being most common ◦ Organisms: Staphylococcus Aureus, Pseudomonas Aeruginosa, & Candida Acute Endocarditis: caused by highly virulent bacteria, it has a rapid onset with fever ◦ Staphylococcus Aureus ◦ Streptococcus Pneumoniae ◦ Streptococcus Pyogenes Subacute Endocarditis: caused by low virulence bacteria, it has a gradual onset, and is associated with congenitally abnormal or diseased valves ◦ Viridans Streptococcus → smaller vegetations on valves with a sequela of dental procedures ◦ AACEK organisms → large friable vegetations with frequent emboli, often requiring valve replacement Symptoms: "FROM JANE" ∙ Fever ∙ Roth spots ∙ Osler nodes → raised, painful lesions on finger or toe pads ∙ Murmur ∙ Janeway lesions → small, painless, erythematous lesions on palms or soles ∙ Anemia ∙ Nail-bed hemorrhage ∙ Emboli

Describe the causes of noninfected vegetations A. Nonbacterial thrombotic endocarditis B. Endocarditis of systemic lupus erythematosus (Libman-Sacks endocarditis)

A. Nonbacterial thrombotic endocarditis: Commonly found in debilitated patients (i.e.- cancer or sepsis), it is characterized by the deposition of small, sterile thrombi on the leaflets of the cardiac valves along the line of closure. Can be the source of systemic emboli that produce significant infarcts in the brain, heart, and elsewhere. B. Endocarditis of systemic lupus erythematosus: Seen in systemic Lupus Erythematosus, it is mitral and tricuspid valvulitis with small, sterile vegetations. Lesions are small, single or multiple, sterile, pink vegetations with a warty (verrucous) appearance, and can be located on the undersurface of AV valves, on the valvular endocardium, on the chords, or on the mural endocardium of the atria or ventricles.

Discuss ventricular interdependence and pulsus paradoxus: A. Under normal circumstances B. In pericardial (cardiac) tamponade C. In constrictive pericarditis

A. Normal Circumstances: Increase in RV volume during inspiration, causes a slight shift of the IV septum to the left, resulting in reduced left ventricular stroke volume during inspiration (< 10mmHg change) B. Pericardial (cardiac) tamponade: Increase in RV volume during inspiration, causes an exaggerated shift of the IV septum to the left since increased pericardial pressure increases resistance to outward expansion of the ventricle, causing an exaggerated change in pressure (> 10 mmHg) C. Constrictive pericarditis: Rigid shell around the heart blunts the transmission of negative intrathoracic pressure to the right side of the heart that normally occurs during inspiration, resulting in absent exaggerated pulsus paradoxus

Describe the microbiological techniques used to make a definitive diagnosis of endocarditis

A. Positive Blood Culture: Persistently positive blood cultures for Typical microorganism for IE (S. Viridans, S. Bovis, HACEK group, S. Aureus) from 2 separate blood cultures which are drawn more than 12 hours apart (subacute) or all 3 or majority of 4 separate blood cultures, with the first and last specimen drawn at least 1 hour apart (acute) → Each collection will have (2) draws - an aerobic + anaerobic B. Coxiella Burnetii: single positive blood culture or antiphase I IgG antibody titer >1:800

A 51-year-old female arrives at the emergency department with complaints of lightheadedness, palpitations, and shortness of breath. Her blood pressure is 100/65 mmHg and her heart rate is 110 beats/min. Auscultation reveals a pansystolic murmur heard at the apex of the heart. In a healthy adult female the cause of this patient's murmur typically is responsible for which of the following cardiovascular events? A. S1 heart sound B. S2 heart sound C. Ejection click D. S3 heart sound E. S4 heart sound

A. S1 heart sound Pansystolic murmur (heard throughout systole) can be caused by mitral regurgitation or aortic stenosis. Heard at the apex of the heart, this means it is a mitral valve problem. Mitral valve contributes to S1.

Compare and contrast the different types of acute pericarditis A. Serous pericarditis B. Fibrinous and serofibrinous pericarditis C. Purulent or suppurative pericarditis D. Hemorrhagic pericarditis E. Caseous pericarditis

A. Serous pericarditis: Parietal pericardial distention cause by serous fluid (pericardial effusion) most commonly caused by noninfectious inflammatory diseases (i.e.- Rheumatic fever, Scleroderma, Tumors, Uremia). May also be brought on by viral infection elsewhere (i.e.- URI, pneumonia) or tumors B. Fibrinous and serofibrinous pericarditis: The most frequent type of pericarditis, it is parietal pericardial distention caused by a mixture of serous fluid and fibrous exudate. Commonly caused by MI, post-infarction syndrome, uremia, chest radiation, rheumatic fever, and trauma or routine cardiac surgery. Produce a loud pericardial friction rub C. Purulent or suppurative pericarditis: Parietal pericardial distention cause by pus (purulent pericarditis) which reflects an active infection due to microbial invasion of the pericardial space. Exudate can range from thin/ cloudy fluid to frank pus. D. Hemorrhagic pericarditis: Parietal pericardial distention cause by blood (hemopericardium) mixed with fibrinous or suppurative effusion commonly caused by the spread of malignant neoplasm to the pericardial space (pericardial tap will reveal neoplastic cells) or in bacterial infections with underlying bleeding or TB. E. Caseous pericarditis: Until proven otherwise, tuberculous in origin, it is caused by direct spread from TB foci within the tracheobronchial nodes

Describe the cause of the following components of the jugular venous waveform: A. a wave B. c wave C. v wave

A. a wave: small rise in right atrial pressure due to right atrial contraction B. c wave: small rise in right atrial pressure as the tricuspid valve closes and bulges toward the right atrium C. v wave: rise in right atrial pressure during ventricular systole, when the tricuspid valve is (supposedly) closed

Differentiate the following based on physical findings: Mitral stenosis (MS)

Almost always a sequela of rheumatic fever Mid-diastolic (pre-diastolic accentuation if sinus rhythm) or holodiastolic murmur if severe; low pitched (rumble) and best heard with the patient in the left lateral recumbent position (heard with the bell of the stethoscope at the cardiac apex) ∙ High pitched (opening snap) may occur after S2, early in diastole which occurs closer to S2 if stenosis worsens ∙ May hear loud, accentuated S1

Differentiate Aortic Stenosis (AS) from Hypertrophic cardiomyopathy (HCM) based upon dynamic auscultatory findings.

AS ∙ Louder: Squatting (or lying from standing), Amyl Nitrite Inhalation ∙ Softer: Standing (from squatting or lying), Valsalva maneuver, or Isometric Handgrip HCM ∙ Louder: Standing (from squatting or lying), Valsalva, or Amyl Nitrite inhalation ∙ Softer: Squatting (or lying from standing), isometric handgrip

Interpret the results of blood cultures for acute and subacute Infective Endocarditis (IE)

Acute Persistently positive blood cultures for Typical microorganism for IE (S. Viridans, S. Bovis, HACEK group, S. Aureus) from all 3 or majority of 4 separate blood cultures, with the first and last specimen drawn at least 1 hour apart (acute) Subacute Persistently positive blood cultures for Typical microorganism for IE (S. Viridans, S. Bovis, HACEK group, S. Aureus) from 2 separate blood cultures which are drawn more than 12 hours apart (subacute)

Compare and contrast the pathophysiology, clinical manifestations and management of acute Mitral Regurgitation (MR), chronic MR, and mitral valve prolapse (MVP).

Acute Mitral Regurgitation ◦ Clinical: Normal LA size & compliance, High LA pressure, High pulmonary venous pressure, Pulmonary congestion & edema, early systolic (crescendo) decrescendo murmur ◦ Management → Medical: diuretics, beta-blockers, nondihydropyridine Ca2+ channel blockers, digoxin, anticoagulation (warfarin or heparin) if a-fib develops → Percutaneous: balloon mitral valvuloplasty (BMV) → Surgery: for severe symptomatic MS in non-candidates for BMV, Mitral valve replacement Chronic Mitral Regurgitation ◦ Clinical: Increased LA size & compliance, more normal LA pressure, more normal pulmonary venous pressure, low forward cardiac output, fatigue & weakness, can exhibit Left heart failure symptoms (dyspnea, orthopnea, Paroxysmal nocturnal dyspnea) or right-heart failure symptoms (peripheral edema, abdominal fullness/discomfort) if severe and LV systolic dysfunction develops, pansystolic murmur that does not get louder during inspiration, S3 ◦ Management → Medical: Vasodilators to treat coexisting HTN or LV systolic dysfunction → Surgery: Mitral Valve repair or replacement Mitral Valve Prolapse ◦ Pathophysiology: bowing of one or both mitral leaflets into the left atrium during systole, typically benign ◦ Clinical: more common in females, common cause of chest discomfort & palpitations, may be associated with atrial or ventricular arrhythmias, mid-systolic click & late systolic murmur, squatting makes click later & murmur shorter/softer, standing (or Valsalva) makes click earlier & murmur longer/ louder ◦ Management: typically benign → Medical: Beta-blockers for chest discomfort or palpitations → Surgery: Mitral Valve repair or replacement

Be familiar with the major etiologies of acquired heart valve disease

Almost always a consequence of a remote or chronic injury of the valve cusps that then presents clinically after many years. The most frequent causes include: A. Aortic Stenosis: calcification and sclerosis of an anatomically normal or congenitally bicuspid aortic valve B. Aortic Insufficiency: dilation of the ascending aorta, often secondary to hypertension and/or aging, Syphillis, Marfan's C. Mitral Stenosis: due to rheumatic heart disease D. Mitral Insufficiency: Myxomatous (tumor) degeneration (mitral valve prolapse)

Be able to locate and identify the location where the auscultation of normal heart sounds takes place and what abnormal sounds are heard there as well

Aortic Area: (S2) 2nd-3rd intercostal space on the right, directly next to the sternum ◦ Abnormal Sounds: Ejection-type murmurs- Aortic stenosis & flow murmur Pulmonic Area: (S2) 2nd-3rd intercostal space on the left, directly next to the sternum ◦ Abnormal Sounds: Ejection-type murmurs- Pulmonic stenosis & flow murmur Tricuspid Area: (S1) 4th-5th intercostal space on the left, directly next to the sternum ◦ Abnormal Sounds: Pansystolic murmurs (Tricuspid regurgitation & VSD) and Mid-to-late diastolic murmurs (Tricuspid stenosis & ASD) Mitral Area: (S1) 4th-5th intercostal space midclavicular line ◦ Abnormal Sounds: Pansystolic murmur (Mitral regurgitation) and Mid-to-late diastolic murmurs (Mitral Stenosis)

What is the most common indication for Transesophageal electrocardiography (TEE)?

Assess for thrombus prior to cardioversion or a mass or in a stroke patient

Identify the most likely cause of syncope: Syncope upon lying, bending, or turning over in bed

Atrial Myxoma (tumor) pressing on mitral apparatus

Differentiate the following based on physical findings: Pericardial friction rub

Auscultatory hallmark of acute pericarditis which can be heard in subacute or chronic pericarditis. May be able to hear classic "triphasic" rub if HR <120 ∙ Systolic (most consistently present), mid-diastolic, + presystolic (never heard in atrial fibrillation) ∙ Scratchy sound in the left lower sternal border ∙ Best heard during full held exhalation

A 43-year-old man presents to his primary care physician because of a long history of slowly developing congestive heart failure. His blood pressure is normal. Coronary artery angiography reveals no vascular disease. No heart murmurs are heard. The white blood cell count, differential, and erythrocyte sedimentation rate are normal. The most likely diagnosis is: A. Carcinoid heart disease B. Cardiomyopathy C. Coarctation of the aorta D. Constrictive pericarditis E. Myocardial infarction

B. Cardiomyopathy

How can you decipher chronic mitral regurgitation (MR) from tricuspid regurgitation (TR)?

Both are Holosystolic (pansystolic) murmur MR- does not get louder with inspiration, will get louder with isometric handgrip TR- gets louder with inspiration

A 35-year-old professor has been running every day for the past 6 months. Which of the following changes during exercise is most likely observed in this individual now vs. 6 months ago? A. A decrease in oxygen uptake in the lungs B. A decrease in oxygen extraction in skeletal muscle C. An increase in oxygen delivery to the skeletal muscle D. A decrease in VO2 Max E. An increase in % of cardiac output to the skin at VO2 Max

C. An increase in oxygen delivery to the skeletal muscle

A 52-year-old female present with a history of gradually increasing fatigue and, more recently, dyspnea on exertion. Physical examination shows blood pressure or 105/85 mmHg, regular pulse of 70, chest clear to auscultation and percussion, elevated jugular venous pressure that increases with inspiration, a loud, high-pitched early diastolic sound (not a murmur), and moderate peripheral edema. The EKG is normal, and a posterior anterior chest film is unremarkable. What is the most likely diagnosis? A. Acute pericarditis B. Cardiac Tamponade C. Constrictive pericarditis D. Pericardial Effusion E. Right ventricular MI

C. Constrictive pericarditis Note Kussmaul's sign (elevated jugular venous pressure that increases with inspiration) and a pericardial knock (a loud, high-pitched early diastolic sound (not a murmur))

A 56-year-old female with fever is found to have blood cultures for Viridans streptococcus in two separate bottles. A transesophageal echocardiogram shows a mobile, oscillating intracardiac mass on the mitral valve. A diligent medical student notes that she does not see any painless or painful bumps on the palms or soles. There were no abnormalities on fundoscopic exam. There were no hemorrhages noted near the nail beds. Regarding the diagnosis of infective endocarditis (IE), this patient: A. Does not have IE B. Has possible IE C. Has definite IE D. Has nonbacterial thrombotic endocarditis E. Has blood cultures that would demonstrate a positive coagulase test

C. Has definite IE Has (2) Major criteria 1. Viridans streptococcus in two separate bottles 2. Echocardiogram shows a mobile, oscillating intracardiac mass on the mitral valve

An 18-year-old male, and star high school quarterback from Firebaugh, CA, is seen by his physician for a routine physical. He mentions that he hopes to someday play for the Buffalo Bills, just like the great Josh Allen. His blood pressure is 118/78 mmHg and his heart rate is 52 beats/min. During this exam the physician auscultates the patient's chest and hears a normal S1, an S2 that splits only during inspiration, and an S3. What is the most likely finding of this examination? A. Atrial-Septal defect B. Congestive heart failure C. Normal findings D. Pulmonary valve stenosis E. Aortic valve stenosis F. Mitral valve regurgitation

C. Normal findings S3 heart sounds can be a normal finding in athletes and pregnant patients; it means that the LV is compliant (accommodates additional volume)

Which of the following organ systems sees an increase in tissue blood flow during exercise? A. Brain B. Renal C. Skin D. Liver E. GI tract

C. Skin Most of the internal organs, will see a decrease in blood flow. The skin sees an increase in blood flow in order for temperature control

A 65-year-old retired female schoolteacher is referred to your care from a rural community hospital because of suspected infective endocarditis, based on persistent fever, a mitral regurgitation murmur and microscopic hematuria. All initial blood cultures were negative at the time of the transfer. Apparently, a neighbor has given the patient an available bottle of antibiotics when she seemed to have developed the "flu." The nursing staff reports multiple guaiac-positive stool specimens shortly after admission. A transthoracic echocardiogram demonstrates vegetations on the mitral valve. A gastroenterology consultant recommends and performs colonoscopy, identifying a circumferential carcinoma in the transverse colon. You predict that her eventually positive blood cultures would demonstrate: A. Streococcus pyogenes B. Streptococcus mitior (viridans streptococci) C. Streptococcus bovis (gallolyticus) D. Staphlococcus aureus E. Staphlococcus epidermidis

C. Streptococcus bovis (gallolyticus) Highly linked to colon cancer

Describe the main mechanisms through which cerebral blood flow is regulated

CO2 is the main component which will change cerebral blood flow. The brain is always using the same amount of energy, and therefore it is not concerned about O2 levels, but rather how much CO2 is produced. The brain is highly dependent on autoregulation, in order to maintain blood flow and perfusion pressure. When there is high pressure, there is constriction in the vessels in the brain, decreasing blood flow. When there is low pressure, there is dilation in the vessels of the brain, increasing blood flow.

Differentiate the following based on physical findings: Pulmonic insufficiency (PI)/ Regurgitation

Can be caused by Pulmonary hypertension, in the absence of pulmonic valve deformity (Graham Steell murmur) or deformity of the pulmonic valve (congenital or acquired) ∙ Graham Steell Murmur: early decrescendo, diastolic murmur that begins with a loud pulmonic component of S2, is high-pitched and "blowing" and which gets louder with inspiration - best heard with the diaphragm of the stethoscope at the 2nd-4th intercostal space on the left sternal border ∙ Due to Valve deformity: mid-diastolic crescendo-decrescendo murmur that begins after the pulmonic component of S2, is low-pitched, and gets louder during inspiration - best heard with the bell of the stethoscope at the 3rd-4th intercostal space on the left sternal border

Explain why cardiac output and heart rate are the most important factors for determining VO2 Max and how that can assist patients as they age

Cardiac output is delivery of oxygen to the tissue. The biggest factor in VO2 max is oxygen delivery and heart rate has the greatest impact on increasing cardiac output

Identify the most likely cause of syncope: Syncope upon head rotation, shaving, or wearing a tight collar

Carotid Sinus Hypersensitivity

Giant Cell Myocarditis

Cause is unknown, it results in widespread inflammatory cellular infiltrate containing Multinucleate giant cells

Aortic Insufficiency (AI) Include causes, Physical findings, natural history, medical treatment & follow-up

Causes: ∙ Congenital: Bicuspid Aortic Valve, VSD ∙ Acquired: Infective (endocarditis), Rheumatic, Degenerative ∙ Aortic Dissection: Trauma, Cystic medial necrosis ∙ Dilation: Systemic HTN, Advanced Age, Cystic medical necrosis Physical Findings A. Chronic AI ∙ May be asymptomatic ∙ Primary Murmur: early diastole, Decrescendo, high-pitched, "blowing", best heard with diaphragm of stethoscope at 3rd intercostal space on the right or left sternal border with patient leaning forward, during held-deep-end exhalation ∙ Associated Murmurs: systolic ejection murmur, Austin Flint murmur (diastolic rumble best heard with bell of stethoscope) ∙ Duroziez Sign: systolic murmur over femoral artery when stethoscope is compressed proximally, and a diastolic murmur over femoral artery when stethoscope is compressed distally → most predictive sign of severe AI ∙ Widened Pulse pressure ∙ Quincke's Pulse: phasic blanching of nail bed ∙ Hill's sign: lower extremity systolic pressure exceeds upper extremity systolic pressure by > 60mmHg ∙ de Musset's sign: head bobbing with each systole B. Acute AI ∙ Hypotension ∙ Tachycardia ∙ Pulmonary Edema ∙ "Classic" findings of chronic AI absent (i.e.- widened PP, Quincke's pulse, Hill's sign) ∙ Diastolic murmur soft and short Natural History: depends on LV size and function & the presence or absence of symptoms; 60% of patients who are asymptomatic with normal LV systolic function will remain asymptomatic at 10 years Medical Treatment A. Chronic AI ∙ Nifedipine: may delay need for aortic valve replacement in asymptomatic patients with severe AI and normal LV systolic function ∙ Other Vasodilators (if HTN is present): ACEi, ARBs, Hydralazine B. Acute AI: prompt surgical intervention is needed for hemodynamically unstable patients, but medical tx while waiting for surgery includes: ∙ IV Positive Inotropic agents ∙ IV Vasodilators ∙ DO NOT use Beta-blockers or Intra-aortic balloon pump → decrease in HR, increases diastole allowing more time for the valve to leak; increase in intra-aortic pressure during diastole will force more blood backwards Follow-Up: Re-evaluate clinically & with a echocardiogram every 6 to 12 months

Identify the causes of and explain brain edema and how it relates to cerebral blood flow changes

Causes: Trauma (hard blow to the head), Hyponatremia Additional fluid in the brain, will increases pressure because the brain cannot expand. This increase in pressure causes a collapse in veins and venules, increasing pressure even more and causing more edema The increase in pressure stimulates baroreceptors to decrease HR in an attempt to lower systemic pressure, and compresses the brainstem, altering breathing patterns Cushing's Triad: (1.) Increased SBP (2.) Decreased HR (3.) Irregular breathing

Differentiate the following based on physical findings: Mitral regurgitation (MR)

Chronic: Holosystolic (pansystolic) murmur, does not get louder during inspiration ∙ Best heard at the cardia apex, sometimes radiating to the left axilla ∙ Gets louder during isometric handgrip, sudden squatting, or vasopressor administration Acute: Early systolic decrescendo murmur

Aortic Stenosis (AS) Include classic symptoms, common physical findings, and definitive therapy

Classic Symptoms: 1. Angina 2. Syncope 3. Heart Failure (SOB, Worsening while laying down or waking up patient, fatigue) Physical Findings: Most common finding is a systolic ejection murmur (SEM) that radiates to the neck ∙ Pulsus parvis et tardus - delayed and diminished carotid upstroke (hear S1 with delay in carotid pulse) ∙ S4 ∙ Systolic ejection sound (click) if bicuspid AV ∙ Diminished or absent A2 (single S2) ∙ Paradoxical splitting of S2 Treatment: Aortic Valve Replacement (surgical)

Borrelia Burgdorferi Include Illness, Clinical Presentation, Lab Tests, Transmission, Diagnosis, & Treatment

Disease: Bacterial Myocarditis, AV nodal block, Lyme carditis Clinical Presentation: Bulls-eye rash Lab Tests ∙ Not seen on gram stain ∙ Spirochete seen on fluorescent microscopy ∙ (+) Warthin-Starry stain Transmission: Ixodes Scapularis tick Diagnosis: ELISA, Western blot Treatment: IV ceftriaxone or PCN, in mild cases oral amoxicillin or doxycycline + temporary pacemaker if needed

A 57-year-old female is seen in the ER after experiencing shortness of breath and chest pain. Her blood pressure is 105/70 mmHg (normal 120/80 mmHg). Upon auscultation the physician hears a normal S1 heart sound and an S2 heart sound that splits only during expiration. Which of the following pathologies does this patient most likely have? A. Right bundle branch block B. Pulmonary valve stenosis C. Atrial-septal defect D. Aortic stenosis E. Mitral stenosis F. Normal finding

D. Aortic stenosis This is paradoxical splitting; a delay in the left side will cause this

A 42-year-old male, that plays football for the least popular team in the NFL, is seen at his cardiologists office. The physician auscultates the patients chest and hears a normal sound between the 2nd and 3rd right interspace of the chest. During which phase of the cardiac cycle is this sound most likely observed? A. Isovolumetric Contraction B. Rapid Ejection C. Reduced Ejection D. Isovolumetric Relaxation E. Rapid Filling F. Reduced Filling

D. Isovolumetric Relaxation The aortic valve gets extremely narrow right before relaxation and this is when you would hear the sound

A 47-year-old accountant died suddenly and unexpectedly while working at his office. The coroner performed an autopsy and discovered a prolapsed mitral valve with ruptured chordae tendinea. Which of the following was the most likely underlying condition that predisposed him to his cardiac problem? A. Coronary Artery Disease B. Hypertension C. Intravenous drug abuse D. Marfan Syndrome E. Tertiary Syphilis

D. Marfan Syndrome Predisposes a patient to mitral valve prolapse

Pericardial Effusion Include Definition, clinical features, & treatment

Definition: Accumulation of an abnormally large amount of fluid in the pericardial space (>50cc) Clinical Features: ∙ Symptoms: asymptomatic, chest discomfort, dyspnea, fatigue ∙ Physical: none, in large effusion- muffled heart sounds, Ewart sign (dullness to percussion of the angle of the left scapula) ∙ EKG: normal, or in large effusions - low voltage + electrical alternans ∙ Chest X-Ray: normal, or if large - globular, symmetric enlargement of the cardiac silhouette ("water bottle" heart) ∙ Echocardiogram: Gold Standard - localized and quantifies the effusion Treatment: ∙ Treat Underlying cause if known ∙ Observe if asymptomatic ∙ Pericardiocentesis

Acute Pericarditis Include definition, common causes, clinical features, treatment, & complications

Definition: Acute inflammation of the pericardium Common Causes: A. Infectious: viral (the most common cause, typically deemed idiopathic due to lack of serologic confirmation), Tuberculosis, Pyogenic Bacteria B. Non-Infectious: Post-MI, Uremia, Neoplastic disease, Radiation induced, connective tissue disease, drug-induced Clinical Features: ∙ Chest Discomfort: sharp, pleuritic, positional ∙ Dyspnea ∙ Fever ∙ Pericardial friction rub: scratchy; the auscultatory hallmark of acute pericarditis ∙ EKG: diffuse, concave-upward ST elevation with PR-segment depression in the same leads-- often seen in aVR Treatment: ∙ Rest ∙ Anti-inflammatory medication: NSAIDs (unless associated with MI), Oral corticosteroids/colchicine for pain refractory to NSAIDs ∙ Analgesia Complications: ∙ Pericardial effusion ∙ Pericardial (cardiac) tamponade ∙ Constrictive pericarditis

Pericardial (cardiac) Tamponade Include Definition, clinical features, & treatment

Definition: Cardiac chamber compression caused by pericardial effusion Clinical Features: ∙ Symptoms: fatigue, dyspnea, confusion/agitation ∙ Physical: Exaggerated pulsus paradoxus, Beck's triad (hypotension/ JVD/ Muffled heart sounds), tachycardia, chest discomfort ∙ EKG: sinus tachycardia ∙ Echocardiogram: Diagnostic ∙ Cardiac Cath: diastolic equalization of pressures (all chambers have same pressure), blunted y-descent on right atrial pressure tracing Treatment: ∙ Definitive: pericardiocentesis ∙ Temporizing Measures: IV fluids, IV inotropes

Restrictive Cardiomyopathy Definition, Etiology, Morphology, Pathophysiology, & Clinical Findings

Definition: Heart disorder in which there is abnormally stiffened myocardium (decreased ventricular compliance) impairing diastolic relaxation with near normal systolic contractile function Etiology: ∙ Non-infiltrative (scleroderma) ∙ Infiltrative (Amyloidosis) ∙ Storage Disease "FAILS to fill" → Fibrosis, Amyloidosis, Iron, Loeffler, Sarcoidosis Morphology: no distinct features; ventricles are normal in size or slightly enlarged, but they are firm/ non-compliant Pathophysiology: ∙ Cardiac Amyloidosis → amyloid deposition in myocardium results in hypertrophy in the absence of HTN and abnormal myocardial texture Clinical Findings: ∙ JVD, Edema, Rales, Hepatomegaly, Ascites, Peripheral Edema ∙ Kussmaul's sign (JVP increases during inspiration d/t RV being unable to accommodate venous return) ∙ Pulsus Paradoxus (>10mmHg decrease in SBP with inspiration in supine position)

Hypertrophic Cardiomyopathy Definition, Pathophysiology, Morphology, Clinical Findings, Diagnostic Studies, & Treatment

Definition: Heart disorder in which there is an abnormally thickened LV wall, impairing diastolic relaxation with intact systolic contractility Pathophysiology: Autosomal dominant disease caused by inappropriate, pathologic hypertrophy resulting from cardiac muscle cell disorganization resulting in increased stiffness ∙ Mutation in any one of several genes for sarcomere proteins (most common in the gene encoding beta-myosin heavy chain) Morphology ∙ Disproportionate thickening of ventricular septum relative to left ventricle free wall (asymmetric septal hypertrophy) ∙ Massive myocyte hypertrophy, with Haphazard disarray of myocytes and interstitial replacement fibrosis Clinical Findings: Hallmark murmur→ *harsh crescendo-decrescendo systolic murmur that will increase with Valsalva (squat to stand)* ∙ Dyspnea ∙ Angina Pectoris ∙ Fatigue ∙ Syncope ∙ One of the most common causes of sudden, otherwise unexplained death in young athletes Diagnostic Studies: ∙ Holter Monitoring (arrhythmias) ∙ Chest radiography (increased cardiac silhouette) Treatment: ∙ Cannot participate in competitive sports or strenuous activities ∙ Amiodarone to reduce arrhythmias ∙ Avoid Alcohol ∙ Verapamil, Beta-blockers, Disopyramide ∙ Refractory to medication: removal of part of the septum, Pacing, Alcohol Septal ablation

Dilated Cardiomyopathy Definition, Etiology, Pathophysiology, Clinical Findings, Morphology, Diagnostic Studies, & Treatment

Definition: Heart disorder in which there is ventricular chamber enlargement, impairing systolic contractile function, typically with concomitant hypertrophy. AKA congestive cardiomyopathy Etiology: Multiple causes, including ∙ **Viral: Enterovirus & Coxsackie B** ∙ Toxins: alcohol, chemotherapy (doxorubicin) ∙ Metabolic: Hyperthyroidism, Hypocalcemia, excess catecholamines ∙ Familial: autosomal dominant or X-linked often creating a mutation in dystrophin (associated with Duchenne & Becker muscular dystrophy) ∙ Childbirth: peripartum cardiomyopathy ∙ Iron overload: most common manifestation of iron excess "ABCCCD - Alcohol abuse, Beri beri (wet), Coxsackie B, Cocaine, Chagas Disease, Doxorubicin" Pathophysiology: Neurohormonal disease which results from an increase in Angiotensin II (RAS) & Norepinephrine (SNS) which will cause abnormalities in regional blood flow and LV remodeling leading to hypertrophy, apoptosis, ischemia, arrhythmias, and fibrosis Clinical Findings: Will have marked chamber enlargement of all chambers ∙ Viral: typically in a *young/healthy patient*, it results in myocyte destruction and most often has full recovery ∙ Dyspnea, easy fatigability, poor exertional capacity, JVD, Pulmonary edema, weight loss, ankle edema, nocturnal dyspnea Morphology: ∙ Most muscle cells are hypertrophied with enlarged nuclei ∙ Interstitial and endocardial fibrosis Diagnostic Studies: ∙ EKG, chest X-ray, Echo ∙ CBC Treatment: ∙ Diuretics → first line for symptomatic CHF which activate neurohormonal responses (postural hypotension, Increased HR, Increased BUN + creatinine) and can induce K+ and Mg2+ loss ∙ *ACEi/ARB* → stop production on Angiotensin II ∙ *Beta-blocker* → antagonize sympathetic neurotransmitters which can result in cardiomyocyte death

Constrictive Pericarditis Include Definition, clinical features, & treatment

Definition: Pericardial scarring leading to restricted diastolic filling of all four cardiac chambers (ventricular filling is spared in early diastole) Clinical Features: ∙ Symptoms: Lower extremity edema, abdominal fullness/discomfort, Fatigue, Dyspnea ∙ Physical: Hepatomegaly, Ascites, Peripheral edema, pericardial "knock" (early diastolic sound caused by abrupt cessation of ventricular filling), JVD, Kussmaul's sign (increased JVP during inspiration) ∙ Chest X-Ray: normal or mildly enlarged cardiac silhouette; pericardial calcification seen in ~50% of patients ∙ Echocardiogram: thickened or calcified pericardium may be seen ∙ Cardiac Cath: diastolic equalization of pressures (all chambers have same pressure), Prominent y-descent on right atrial pressure tracing, "dip and plateau" / "square root sign" pattern in diastole on right and left ventricular pressure tracings Treatment: ∙ Definitive: Pericardiectomy ∙ Symptomatic: Diuretics + Salt Restriction

A 36-year-old female presents with a complaint of palpitations over the last few months. She reports occasional chest discomfort but she denies shortness of breath. Her vital signs re stable, and cardiac auscultation reveals a mid to late systolic click followed by a late systolic murmur. The EKG is read is normal. Which of the following is the most likely diagnosis? A. Aortic regurgitation B. Aortic Stenosis C. Mitral Regurgitation D. Mitral Stenosis E. Mitral Valve Prolapse

E. Mitral Valve Prolapse "midsystolic click with late systolic murmur"

Differentiate the following based on physical findings: Aortic insufficiency (AI)/ Regurgitation

Early diastolic, decrescendo high-pitched, "blowing" murmur that is best heard with the diaphragm of the stethoscope at 3rd left or right sternal border, with the patient leaning forward, during held/deep/end-exhalation ∙ Duroziez sign: systolic murmur over femoral artery when compressed proximally & diastolic murmur over femoral artery when compressed distally (most predictive sign of severe AI) ∙ Widened pulse pressure ∙ Quincke's Pulse: phasic blanching of the nail bed ∙ Hill Sign: popliteal systolic blood pressure exceeds brachial blood pressure by >60 mmHg May also have: ∙ Systolic ejection murmur- due to "high flow" across aortic valve from high stroke volume ∙ Austin Flint murmur- diastolic rumble, best heard with the bell of the stethoscope at the apex

Coxsackie Virus B Include Illness, Transmission, Clinical Presentation, & Mechanism

Enterovirus Illness: Severe myocarditis → most threatening in neonates or Acute benign pericarditis (young adults) Transmission: Fecal-Oral Clinical Presentation: ∙ Myocarditis: Febrile illness with sudden unexplained heart failure (cyanosis, tachycardia, cardiomegaly, hepatomegaly) ∙ Pericarditis: MI-like symptoms with fever Mechanism: binds CAR receptor to enter the cell then translates the viral genome, producing viral protease 2A which will cleave dystrophin decreasing myocyte contractility (similar to Duchenne muscular dystrophy)

Tricuspid Regurgitation (TR) Include Etiology, Symptoms, Physical Findings, Diagnosis, Natural History, & management

Etiology: Usually functional (results from RV enlargement and the leaflets cannot meet), can be due to rheumatic fever or carcinoid syndrome Symptoms: ∙ Right Heart Failure symptoms: peripheral edema, abdominal fullness/ discomfort, fatigue/weakness Physical Findings: ∙ Murmur: pansystolic murmur that gets louder during inspiration (Carvallo's sign) often best heard along lower left sternal border ∙ Classic Triad (severe): Carvallo's, Pulsatile JVD, Pulsatile liver Diagnosis: ∙ EKG: characteristics of RV enlargement ∙ Chest X-ray: right atrial enlargement, RV enlargement ∙ Echocardiogram: Diagnostic ∙ Cardiac Catheterization: Large V-waves in the right atrial pressure waveform Natural History: Prognosis depends on the underlying cause; generally well-tolerated Management: ∙ Medical: Diuretics (for right heart failure symptoms) ∙ Surgery: Tricuspid Valves repair or replacement for severe cases or refractory to diuretics

Mitral Stenosis (MS) Include Etiology, Symptoms, Physical Findings, Diagnosis, Natural History, & management

Etiology: Rheumatic fever (>99%), Other (<1%, calcification, congenital, endocarditis) Symptoms: ∙ Dyspnea ∙ Fatigue ∙ Right-Heart Failure (peripheral edema, JVD, ascites, hepatomegaly) ∙ Hemoptysis ∙ Hoarseness → recurrent laryngeal nerve compression by an enlarged left atrium or pulmonary artery Physical Findings: ∙ Murmur: mild diastolic low-pitched (rumble); if severe may be holodiastolic ∙ Opening snap ∙ Loud S1 Diagnosis: ∙ EKG: left atrial abnormality, Right ventricular hypertrophy ∙ Chest X-ray: left atrial enlargement, pulmonary vascular redistribution, right ventricular enlargement, pulmonary artery prominence ∙ Echocardiogram: diagnostic ∙ Cardiac Catheterization: define coronary artery anatomy prior to surgery Natural History: ∙ 10-year survival without treatment: >80% if asymptomatic, 50-60% once symptoms develop ∙ Mean survival <3 years once pulmonary HTN develops Management: ∙ Medical: diuretics, beta-blockers, nondihydropyridine Ca2+ channel blockers, digoxin, anticoagulation (warfarin or heparin) if a-fib develops ∙ Percutaneous: balloon mitral valvuloplasty (BMV) ∙ Surgery: for severe symptomatic MS in non-candidates for BMV, Mitral valve replacement

Mitral Regurgitation (MR) Include Etiology, Symptoms, Physical Findings, Diagnosis, Natural History, & management

Etiology: structural or functional abnormalities of ∙ Mitral Annulus (ring): calcification (elderly), Dilation ∙ Valve Leaflets: Myxomatous degeneration, Rheumatic fever, endocarditis, HOCM ∙ Chordae Tendineae: endocarditis, spontaneous rupture ∙ Papillary Muscles: MI Symptoms: ∙ Fatigue & Weakness ∙ Left heart failure symptoms (dyspnea, orthopnea, Paroxysmal nocturnal dyspnea) ∙ Right-heart failure symptoms (peripheral edema, abdominal fullness/discomfort) Physical Findings: ∙ Increased LA size & compliance ∙ Low forward cardiac output ∙ Pansystolic murmur that does not get louder during inspiration ∙ S3 Diagnosis: ∙ EKG: Left atrial abnormality, LVH ∙ Chest X-ray: pulmonary edema, LV & LA enlargement ∙ Echocardiogram: Diagnostic ∙ Cardiac Catheterization: Evaluation of coronary arteries (for ischemia) Natural History: Prognosis dependent on underlying cause Management: ∙ Medical: Vasodilators to treat coexisting HTN or LV systolic dysfunction ∙ Surgery: Mitral Valve repair or replacement

Viridans Streptococci Include examples, Illness, Lab Tests, & Virulence Factors

Examples ∙ Streptococcus Mutans ∙ Streptococcus Sanguinis Illness: Subacute infective endocarditis → smaller vegetations on valves with a sequela of dental procedures Lab Tests ∙ Gram (+) ∙ Alpha Hemolytic ∙ Optochin resistant ∙ Bile esculin (+) ∙ Normal flora of the: oropharynx, GI tract, GU tract Virulence Factors ∙ Dextrans: bind fibrin-platelet aggregates on damaged heart valves

Differentiate the following based on physical findings: Atrial septal defect (ASD)

Fixed splitting of the 2nd heart sound (splitting of S2 during inspiration and expiration)

Vaccinia Virus Inoculation

Follows small pox vaccination, and causes myocarditis or myocarditis with associated pericarditis

Identify the most likely cause of syncope: Syncope preceded by pain in the oropharynx, tonsillar fossa, or tongue

Glossopharyngeal Neuralgia

Describe the placement of grafts to optimize long term patency rates

Grafts from the internal mammary artery (IMA) are shown to have 95% patency after 10 years → used on the LAD since this is what covers the largest area of myocardium Grafts form the saphenous vein are shown to have 50% patency after 10 years → used for RCA

Differentiate the following based on physical findings: Tricuspid regurgitation (TR)

Holosystolic (pansystolic) murmur (like chronic MR) ∙ Carvallo's sign: louder during inspiration ∙ Classic triad in severe TR: Carvallo's sign, Pulsatile JVD, Pulsatile liver

Differentiate the following based on physical findings: Ventricular septal defect (VSD)

Holosystolic (pansystolic) murmur (like chronic MR) ∙ Does not get louder during inspiration ∙ Best heard at the lower left sternal border ∙ Often is harsh in quality

Discuss chronic (healed) pericarditis and be familiar with adhesive Mediastinopericarditis and constrictive pericarditis

Healed pericarditis may produce plaque-like fibrous thickening of the serosal membrane or thin adhesions or it can produce fibrosis in the form of mesh-like stringy adhesions that obliterate the pericardial sac Adhesive Mediastinopericarditis: may follow infectious pericarditis, cardiac surgery, or mediastinal irradiation. It results in obliteration of the pericardial sac and adherence of the external aspect of the parietal layer to the surrounding structures which strains cardiac function. This results in increased workload of the heart which can lead to cardiac hypertrophy and dilation. Characteristic clinical findings include systolic retraction of the rib cage and diaphragm and pulsus paradoxus Constrictive Pericarditis: heart becomes encased in a dense, fibrous or fibrocalcific scar which limits its diastolic expansion and cardiac output- including to increased systemic demands. Clinically, there is muffled heart sounds, elevated jugular venous pressure, and peripheral edema. This required surgical resection of the shell.

infective endocarditis (IE) Identify individuals at high risk, common signs and symptoms, peripheral stigmata, and complications

High Risk: ∙ Age >60 ∙ Males ∙ IV Drug Users ∙ Poor dental health ∙ Pre-existing structural abnormalities/ valvular disease ∙ History of IE Signs and Symptoms: ∙ Fever is most sensitive ∙ Murmur is most reliable ∙ Chills ∙ Anorexia ∙ Dyspnea ∙ Weight loss Peripheral Stigmata: "FROM JANE" ∙ Petechiae: most frequently found on the conjunctivae, palate, buccal mucosa, and upper extremities ∙ Splinter hemorrhages: 1-2 mm brown streaks under the nails (of greater significance when seen in proximal nail bed) ∙ Osler nodes: small, tender nodules usually found on the finger and toe pads ∙ Janeway lesions: painless, flat (macular), blanching discolorations located on the palms and soles ∙ Roth spots: retinal hemorrhages with pale centers ∙ Mycotic Aneurysm: results from embolic seeding of vasa vasorum of arteries; weaken vessel wall leading to dilatation and possible rupture ∙ Clubbing: of the fingers Complications: ∙ Heart Failure ∙ Conduction disturbances (AV block) ∙ Myocardial/ valve ring abscess ∙ Septic embolism/ immune complex deposition

Staphylococcus aureus Include Illness, Lab Tests, & Virulence Factors

Illness: Acute Infective Endocarditis (IE) → commonly in IV drug users Lab Tests ∙ Gram (+) ∙ Beta-hemolytic ∙ Catalase (+) ∙ Coagulase (+) ∙ Mannitol salt (+)/ferments ∙ FISH (+) Virulence Factors: ∙ Teichoic acid: binds fibronectin, inhibiting antibody-mediated clearance ∙ Protein A: binds Fc-IgG inhibiting complement and phagocytosis

Corynebacterium Diphtheriae Include Illness, Clinical Presentation, Mechanism, Diagnosis, & Treatment

Illness: Bacterial Myocarditis Clinical Presentation ∙ Bull-neck ∙ Gray-white membrane on back of the throat Mechanism: Gram (+) rod that produces a toxin that binds myocyte receptor, ribosylates elongation factor 2 (EP2) thus stopping protein synthesis and killing the cell Diagnosis: ∙ (+) culture from respiratory tract → gray to black colonies on blood agar, Loeffler's serum, or blood tellurite agar ∙ Positive toxin assay → Elek assay Treatment: Antitoxin, Antibiotics

Trypanosoma Cruzi Include Illness, Clinical Presentation, Transmission, Diagnosis, & Treatment

Illness: Chagas Disease, Parasitic Acute Myocarditis Clinical Presentation: ∙ Acute: mild non-specific symptoms (malaise, fever, hepatosplenomegaly), eyelid swelling, chagoma (skin abscess) ∙ Chronic: no signs or symptoms, lasts indefinitely in absence of treatment "Children, Chagoma, Cardiac, Cruzi" Transmission: Trypansoma Cruzi Parasite → takes blood meal and deposits contaminated feces during it ∙ Congenital, blood transfusion, organ transplant, consumption of contaminated food or drink ∙ Parasites will multiply in myocytes and result in cell lysis Diagnosis ∙ Acute: thick and think blood films, PCR ∙ Chronic: serology Treatment: Benznidazole, Nifurtimox

Coxiella Burnetii Include Illness, transmission, clinical presentation, lab tests, & treatment

Illness: Culture (-) Endocarditis Transmission • Inhalation of aerosols from cattle/sheep amniotic fluid → seen most commonly in farmers & veterinarians Clinical Presentation • Night sweats • Fatigue • SOB • Weight Loss • Swelling of limbs Lab Tests • Weakly Gram (-) • Intracellular organisms • Phase (I) Variant (+) Treatment • Must diagnose and treat early + long term: 18-24 months of doxycycline • Without treatment, it is fatal

Parvovirus B19 Include Illness, Transmission, Clinical Presentation, & Diagnosis

Illness: Erythema Infectiosum, Fifth disease → can lead to myocarditis Transmission: respiratory droplets Clinical: Fever followed by "Lacey" rash (immune response), typically 4-15 years old ∙ 2 stages 1. Febrile Stage: infectious stage 2. Symptomatic stage: immune mediated Diagnosis: PCR of serum

Human Herpes Virus 6 (HHV6) Include Illness, Transmission, & Clinical Presentation

Illness: Roseola, 6th disease, Exanthem subitum → remains latent in salivary glands + bone marrow, which can activate later and cause MS, chronic fatigue syndrome, fibromyalgia, and myocarditis later on Transmission: Saliva Clinical: Abrupt onset of high fever (103-104), with "morbilliform" (bumpy) rash appearing after the fever on the trunk and face then spreading to the extremities (caused by infected T-cells or activation of delayed hypersensitivity T-cells in skin)

Staphylococcus Epidermidis Include Illness, Lab Tests, & Virulence Factors

Illness: Subacute Infective Endocarditis (IE) → commonly in prosthetic valves/ devices (i.e.- pacemakers, catheters) Lab Test ∙ Gram (+) ∙ Catalase (+) ∙ Urease (+) ∙ Coagulase (-) ∙ Mannitol Salt (-) Virulence Factors: ∙ Biofilm: prosthetics coated with collagen/ fibrinogen/ fibronectin serves as a receptor which allows for binding. S. Epidermidis then produces an extracellular polysaccharide matrix (slime capsule) that interferes with the immune response and serves as a barrier to antibiotics

Enterococcus Include Illness & lab tests

Illness: Subacute Infective endocarditis → found in older males after GU manipulation or young women after obstetric procedures Lab Tests ∙ Gram (+) ∙ Bile esculin (+) ∙ (+) growth on 6.5% NaCl ∙ PYR (+) ∙ Catalase (-)

Describe the relative amount of coronary blood flow and the phasic nature of the blood flow in both the right and left ventricle. Explain why coronary blood flow is different in systole and diastole.

In systole, the aortic valve is open and the leaflets push against the sinus where the RCA and LCA come off of, decreasing blood flow to the heart Once the valve shuts, in diastole, the sinus can fill and blood is able to rush through the RCA and LCA. The reflective wave from the closure of the aortic valve (increase in aortic pressure) allows blood to be pushed into the aortic sinuses and subsequently the coronary arteries Since right ventricular pressure is much lower than the left ventricle, blood flow isn't blocked as much through the RCA during systole, but only partially blocked by covering of the aortic sinuses

List the indications and contraindications for aortic valve replacement (AVR) surgery for aortic stenosis/aortic regurgitation

Indications ∙ Symptomatic severe Aortic stenosis (i.e.- CHF, Syncope, Angina) ∙ Severe Aortic Stenosis with Left ventricular systolic dysfunction (LV ejection fraction <50% regardless of symptoms) Contraindications ∙ Mechanical valves- GI/ cerebral bleeding because these types of valves require anticoagulation

Myocarditis Include etiology, pathogenesis, morphologic & clinical features

Inflammation or injury to the myocardium Etiology: ∙ Infection: Coxsackie A and B, Enteroviruses, Cytomegalovirus, HIV, Influenza ∙ Immune-mediated: Rheumatic fever, drug hypersensitivity (Methyldopa, Sulfonamides) Morphology: Diffuse mononuclear, Lymphocytic infiltrate Clinical Features: Broad clinical spectrum ∙ Asymptomatic ∙ Fatigue, dyspnea, palpitations, fever, mimic acute MI

Discuss arrhythmogenic right ventricular cardiomyopathy

Inherited disease of the myocardium that causes right ventricular failure with rhythm disturbances and sudden death Morphology: right ventricular wall is severely thinned with loss of myocytes, and extensive fatty infiltration & fibrosis

Describe how coronary blood flow is controlled. Identify both local control elements and nervous system control and explain which is more powerful

Local: Always over-rides nervous system control. Blood flow is regulated almost entirely by the demand for oxygen. Without oxygen there is a huge increase in CO2 which increases blood flow to the heart Nervous system: Increase in sympathetic discharge increases HR and attempts to constrict the coronary arteries, but the increase in HR increases oxygen demand which is overcome by local control

Interpret history and physical results using the Modified Duke Criteria for diagnosing Infective Endocarditis (IE)

Major Criteria A. (2) separate positive blood cultures with microorganism(s) typical for infective endocarditis (S. Viridans, S. Bovis, HACEK group, S. Aureus) or a single positive blood culture for Coxiella Burnetii B. Echocardiographic evidence of involvement: typical valvular lesion (vegetation, abscess or new partial dehiscence of prosthetic valve) C. New Valvular regurgitation Minor Criteria A. Predisposition (heart condition or IVDU) B. Temperature > 38.0°C ( > 100.4°F) C. Vascular Phenomenon: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, Intracranial hemorrhage, conjunctival hemorrhage, Janeway lesions D. Immunological phenomenon: glomerulonephritis, Osler nodes, Roth spots, Rheumatoid factor E. Microbiologic Evidence: positive blood culture but not meeting a major criterion, or serologic evidence of active infection with organisms consistent with infective endocarditis Definite IE ∙ 2 Major criteria (blood culture + echo) ∙ 1 Major criteria + 3 minor criteria ∙ 5 minor criteria Possible IE ∙ 1 major criteria + 1 minor criteria ∙ 3 minor criteria Rejection Criteria ∙ Resolution with antibiotic therapy < 4 days

Differentiate between major and minor Jones criteria and how to use them to diagnose rheumatic fever

Major Criteria ∙ Carditis and valvulitis → Pancarditis & damage to valves d/t M-protein mimicry with myosin ∙ Arthritis (usually polyarthritis predominantly involving large joints) → migratory involving knees, ankles, elbows, wrists, commonly involving >6 joints and subsiding within 4 weeks ∙ Central nervous system involvement → Sydenham Chorea - jerking movements that stop with sleep ∙ Subcutaneous nodules → painless, firm nodules associated with severe carditis ∙ Erythema Marginatum → Serpiginous rash that intermittently appears and disappears, is nonpruritic/nonpainful/pink or faint red on the trunks/limbs but not face Minor Criteria ∙ Arthralgia ∙ Fever ∙ Elevated acute phase reactants (ESR, CRP) ∙ Prolonged PR interval on EKG Rheumatic Fever 1. Evidence of recent Group A beta-hemolytic strep (GABHS) infection 2. Two major manifestations or one major & two minor manifestations

Differentiate the following based on physical findings: Pericardial tamponade

May present with Beck's Triad 1. Hypotension 2. JVD (or high CVP) 3. Muffled or distant heart sounds Exaggerated pulsus paradoxus is a classic physical sign: >10mmHg drop in systolic atrial pressure during inspiration Kussmaul Sign may occasionally be present: Increased JVP (distention) during inspiration

List the changes to Mean arterial pressure, cardiac output, heart rate, stroke volume, peripheral resistance and oxygen consumption that occur during exercise

Mean Arterial Pressure: Slight increase (dramatic increase in SBP, slight increase in DBP) Cardiac Output: Dramatic Increase Heart Rate: Dramatic Increase Stroke Volume: Slight increase Peripheral Resistance: Decreases (more skeletal muscle than other organs, thereby vasodilation wins out) Oxygen Consumption: Dramatic increase

Infective endocarditis Include morphologic features, pathogenesis, and clinical features

Microbial infection of the heart valves or the mural endocardium that leads to the formation of vegetations composed of thrombotic debris and organisms, often associated with destruction of the underlying cardiac tissues. Fungi and other classes of organisms can be involves, but most infections are bacterial (bacterial endocarditis) in nature. Morphology: Vegetations on the heart valves which are friable, bulky, and potentially destructive lesions that contain fibrin, inflammatory cells, and bacteria or other organisms. Occasionally can erode into the underlying myocardium and produce and abscess. Pathogenesis: Can be predisposed by factors that cause microorganisms to seed into the blood stream (i.e.- infection elsewhere, dental or surgical procedure, contaminated needle) ∙ Acute: infection of a previously normal heart valve by a highly virulent organism (i.e.- Staphylococcus Aureus) that rapidly produced necrotizing and destructive lesions ∙ Subacute: infection by organisms with lower virulence (i.e.- Viridans Streptococci) of previously damaged or otherwise abnormal valves that cause insidious infections of deformed valves with overall less destruction Clinical Findings: Rapid onset with fever, chills, weakness, lack of energy, and weight loss. Murmurs are present in 90% of patients with left sided involvement

Differentiate the following based on physical findings: Tricuspid stenosis (TS)

Mid-diastolic (pre-diastolic accentuation if sinus rhythm) or holodiastolic murmur if severe; low pitched (rumble) and best heard along the lower left sternal border ∙ Louder with inspiration Most commonly caused by rheumatic fever, but can be caused by carcinoid syndrome, anorectic diet, or medications

Differentiate the following based on physical findings: Mitral valve prolapse (MVP)

Midsystolic click, late systolic murmur Control: patient supine - midsystolic click, late systolic murmur Standing: early systolic click, longer & louder systolic murmur Squatting: late systolic click, shorter & quieter systolic murmur

Myxoma Morphology and clinical features

Most common primary tumor of adult heart which commonly arises in the atria (left more than right) Morphology: Can form a globular hard mass with hemorrhage or a soft translucent gelatinous appearance; Abundant amorphous extracellular matrix composed of mucopolysaccharide ground substance with scattered multinucleated myxoma cells (abnormal vessel-like formation) Clinical Features: Can cause a ball-valve obstruction which results in "plop" sound

Mitral valve prolapse Include the morphology, pathogenesis, clinical findings, and Treatment

Most commonly found in females 20-40 years old, it is when one or both mitral valve leaflets are "floppy" and prolapse (balloon back) into the left atrium during systole. Morphology ∙ Gross: Interchordal ballooning (hooding) of mitral leaflets; the leaflets will appear enlarged, redundant, thick, and rubbery and the associated cords may be elongated, thinned, or even rupture ∙ Microscopic: Marked thickening of the spongiosa layer with deposition of mucoid material (myxomatous degeneration) with reduction of the collagenous fibrosa layer Pathogenesis: Etiology for weakening of the valve leaflets is typically unknown, but rarely, it can be associated with connective tissue disorders (i.e.- Marfan's) Clinical Findings: Most often found incidentally on physical examination, but in a small minority of individuals it can lead to serious complications ∙ Chest pain mimicking angina (not exertional in nature) ∙ Dyspnea ∙ Infective endocarditis, Mitral insufficiency (with possible chordal rupture), Stroke, Arrhythmias, Sudden cardiac death Treatment: Mitral Valve repair or replacement

Mitral annular calcification Include morphology and clinical findings

Most commonly seen in women >60 years and individuals with mitral valve prolapse, it is due to the deposition of hydroxyapatite (calcium) on the mitral valve Morphology: Irregular, stony hard, occasionally ulcerated nodules at the base of the leaflets ∙ On radiograph, can be seen as ring-like opacities Clinical Features: Does not effect valvular function, but can lead to ∙ Regurgitation → interfering with physiologic contraction of the valve ring ∙ Stenosis → impairs opening of the mitral leaflets ∙ Arrhythmias & Sudden death → penetration of calcium deposits, impinging on AV conduction system Since the calcific nodules also provide a site of thrombus formation: ∙ Increased risk of embolic stroke ∙ Increased risk of infective endocarditis

2D Echocardiography

Multiple ultrasonic beams used to depict anatomic relationships and define movement of cardiac structures relative to one another. Diagnose atrial myxoma

Describe how valvular lesions can lead to turbulent flow within the heart and how turbulent flow causes heart murmurs.

Murmurs are caused by narrowing of a valve that shouldn't occur during that time, leading to turbulent flow This can be due to stenosis, increased flow through normal structures, ejection into dilated chambers, regurgitation across an incompetent valve, or abnormal shunting of blood from one vascular chamber to a lower pressure chamber (i.e.-VSD)

Identify the most likely cause of syncope: Syncope occurs during prolonged standing, in a warm environment, or shortly after severe pain, unpleasant sight, sound or odor

Neurocardiogenic Syncope

Identify the most likely cause of syncope: Syncope during or immediately following exertion

Obstructive cardiac problem (i.e.- aortic stenosis, mitral stenosis, PE, coronary artery disease, pulmonary HTN, congenital long QT syndrome, neurocardiogenic syncope)

Identify the most likely cause of syncope: Syncope upon standing

Orthostatic Hypotension

Myocarditis of Chagas Disease

Parasitization of scattered myofibers by trypanosomes Will result in myofibril necrosis

Understand the basic views of transthoracic echocardiography (TTE)

Parasternal: probe put next to the sternum on the left Apical: put near the apex of the heart, midclavicular line on left

Explain normal (physiological) splitting of the second heart sound, and paradoxical splitting of the second heart sound and list its potential causes

Physiology Splitting: Best heard at the 3rd intercostal space left sternal border; Inspiration will create a negative pressure in the thoracic cavity which is transferred to the pulmonary artery, this will pull blood from the heart towards the lungs and as a result, it takes longer for pulmonary arterial pressure to exceed right ventricular pressure. As a result, there is a "splitting" of the S2 heart sound because the aortic valve is able to close before the pulmonic valve closes (A2 before P2). During expiration, there is positive pressure in the thoracic cavity which stops the pulling of blood from the heart to the lungs, allowing for the pulmonic and aortic valves to close at the same time, leading to the disappearance of the splitting of the S2 heart sound. ◦ "Fixed Splitting": (A2 before P2) Present during inspiration and expiration; auscultatory hallmark of atrial septal defect (ASD) Paradoxical Splitting: Splitting of the S2 heart sound that occurs during expiration, when the pulmonic valve closes before the aortic valve (P2 before A2) and then disappears during inspiration ◦ Potential Causes: Aortic stenosis, Left bundle branch block, Hypertrophic obstructive cardiomyopathy (HOCM), right ventricular pacemaker, right ventricular ectopic beats, systemic HTN (rarely)

What are the major causes of pericarditis?

Primary pericarditis is unusual, and almost always of viral origin. The other major causes include: A. Infectious agents: Viruses, pyogenic bacteria, TB, fungi, parasites B. Immunologically Mediated: Rheumatic fever, Lupus, scleroderma, post MI, drug hypersensitivity C. Miscellaneous: Uremia, Neoplasia, Trauma, Radiation

Lipoma Morphology and clinical features

Primary tumor of the adult heart with is a localized, well-circumscribed, benign tumor that can arise anywhere in the heart but is most often located in the left ventricle, right atrium, or atrium septum Morphology: Fat infiltrate Clinical Features: Can be asymptomatic, create ball-valve obstruction ("plop" sound), or arrhythmias

Papillary Fibroelastoma

Primary tumor of the heart which are typically located on the cardiac valves and have the potential to embolize Morphology: Hair-like projections covered by surface endothelium, surrounding a core of myxoid connective tissue with abundant mucopolysaccharide matrix & elastic fibers

Discuss the basic principles of ultrasound production in diagnostic echocardiography

Produced by Mechanical, Longitudinal waves (particles move in the same direction as the wave) at a rate > 20,000 Hz/sec

What are the pros and cons of Echocardiography?

Pros ∙ Safe/ Non-invasive ∙ Portable ∙ Relatively Inexpensive Cons ∙ Operator Dependent (need sonographer & interpreter) ∙ Patient Dependent (inhibited by obesity, barrel chest/ COPD, Kyphoscoliosis)

Rheumatic heart disease Include morphologic features, pathogenesis, and clinical features

Rheumatic Fever (RF) is an acute immunologically mediated, multisystem inflammatory disease which classically occurs a few weeks after an episode of group A Streptococcal pharyngitis. Acute rheumatic carditis is common in active RF, and over time can progress to chronic rheumatic heart disease (RHD) which mainly manifests as valvular abnormalities. Morphology ∙ Gross: Fibroid necrosis of the endocardium with verrucae (vegetations). Irregular thickening (MacCallum plaques) of the left atrium. Leaflet thickening, commissural fusion and shortening, & thickening and fusion of tendinous cords. The mitral valve is virtually almost always involved (mitral stenosis) in which calcification and fibrous bridging across the valvular commissures creases a "fish mouth" or "buttonhole" stenosis. ∙ Microscopic: Aschoff bodies (distinct lesions in the heart) composed of T-lymphocytes, plasma cells, and activated macrophages (abundant cytoplasm & central round-to-ovoid nuclei) Pathogenesis: Host immune response to group A streptococcal antigens, cross-react with host proteins, including heart tissue by a combination of antibody and T-cell mediated reactions Clinical Findings: The only cause of mitral stenosis, there is also a constellation of other findings ∙ Migratory polyarthritis of the large joints ∙ Pancarditis ∙ Subcutaneous nodules ∙ Erythema marginatum of the skin ∙ Sydenham chorea- neurologic disorder with involuntary rapid purposeless movements

Describe the cardiac disease that is associated with rheumatologic disorders

Rheumatologic Disorders include: rheumatoid arthritis, systemic sclerosis, ankylosing spondylitis, and psoriatic arthritis The most common cardiac finding is fibrinous pericarditis which can progress to fibrous thickening of the visceral and parietal pericardium and dense adhesions. Rheumatoid valvulitis can lead to marked fibrous thickening and secondary calcification of the aortic valve cusps, producing changes resembling those of chronic rheumatic valvular disease

Identify and describe the normal and pathological causes of the first, second, third, and fourth (S1, S2, S3, and S4) heart sounds.

S1: The first heart sound; heard at the end of diastole, just before systole ◦ Normal: Heard during isovolumetric contraction; Produced by Tricuspid & Bicuspid (Mitral) Valve closure ◦ Pathologic: → Louder (accentuated) - 1. Shortened PR interval 2. Mild mitral stenosis 3. High cardiac output states or tachycardia (i.e.- exercise) → Softer (Diminished) - 1. Lengthened PR interval (1st degree AV block) 2. Mitral Regurgitation 3. Severe Mitral Stenosis 4. "Stiff" left ventricle (i.e.- LVH due to systemic HTN) S2: The second heart sound; heard at the end of systole, just prior to diastole ◦ Normal: During isovolumetric relaxation; Produced by Aortic and Pulmonic valve closure ◦ Pathologic: → Paradoxical Split: occurs during expiration and disappears during inspiration; commonly d/t LBBB or Aortic stenosis → Fixed Split: Present during inspiration and expiration; due to ASD S3: "Ventricular gallop"- sounds like Ken-tucky; caused by tensing of the chordae tendineae during rapid filling and expansion of the ventricle and has a low frequency (dull "thud") ◦ Normal: Pregnancy, Athletes, & children→ in which compliant left ventricles are normal ◦ Pathologic: Occurs in early to mid diastole (1/3 way through), during rapid left ventricular filling; due to a very compliant left ventricle → Sign of ventricular dilation → Heard at the apex of the heart (lower left sternal border/ xiphoid) S4: "Atrial Gallop" - sounds like Tennes-see; caused by the atrium vigorously contracting against a stiffened ventricle (resulting from reduced ventricular compliance) ◦ Normal: N/A- common in the elderly ◦ Pathologic: Occurs in late diastole, during active left ventricular filling; due to a non-compliant left ventricle → Sign of diastolic CHF → Heard at the apex of the heart (lower left sternal border/ xiphoid)

Tako-Tsubo Syndrome

Seen most commonly in females in the 5th-6th decade of life which is associated with psychological and physiologic stressors (robbery, break-up, suicide attempt) and results in Reversible LV apical ballooning/ dysfunction without CAD On EKG mimic anterior wall MI and patient has elevated cardiac markers, but angiogram is normal

Identify the most likely cause of syncope: Syncope followed by confusion / slow recovery

Seizure

Identify the most likely cause of syncope: Syncope occurs during or immediately after micturition, cough, swallowing, or defecation

Situational Syncope (reflex-mediated)

What is the most common Coagulase negative staphylococcus involved in native valve endocarditis?

Staphylococcus lugdunensis

Describe the differences between static and dynamic exercise.

Static Exercise: (i.e.- strength exercise) Causes constant contraction of the muscles, and subsequently occlusion of blood flow leading to rapid fatigue of the fibers Dynamic Exercise: (i.e.- running) Pulsatile contractions of the muscle; during relaxation of the muscle, there will be increased blood flow to the muscle

Identify the most likely cause of syncope: Syncope upon arm exercise

Subclavian Steal Syndrome

Compare and contrast epicardial and subendocardial coronary blood flow

Subendocardial tissue is the most prone to ischemic events due to compression of penetrating vessels during systole and thus higher metabolic demands than epicardial tissue with reduced blood flow during systole

Streptococcus Bovis Include Illness & lab tests

Subspecies of Streptococcus Gallolyticus Illness: Subacute Infective endocarditis → normal flora of GI tract, associated with colon cancer + large vegetations Lab Tests ∙ Gram (+) ∙ Bile esculin (+) ∙ No growth on 6.5% NaCl ∙ PYR (-) ∙ Catalase (-) ∙ Hemolysis (-)

Describe how tissue blood flow is controlled by sympathetic discharge and local metabolites. Explain what happens when both are present.

Sympathetic Discharge: Increased HR/ contractility/ cardiac output and vasoconstriction (outweighed by local metabolites in active tissue) in non-essential organs Local Metabolites: (i.e.- CO2, H+, K+, & adenosine) Vasodilation in active skeletal muscles Both: In the skeletal muscles during exercise, local metabolites will outweigh sympathetic discharge for 0.5-2 hours, leading to vasodilation in localized vascular beds

Carcinoid heart disease Include morphologic features, pathogenesis, and Clinical Findings

Systemic disorder marked by flushing, diarrhea, dermatitis, and bronchoconstriction that is caused by bioactive compounds such as serotonin released by carcinoid tumors. Cardiac lesions occur once there is a massive hepatic metastatic burden Morphology: Distinct, glistening white intimal plaque-like thickening of the endocardial surface of the cardiac chambers of valve-leaflets Pathogenesis: Cardiac lesions which develop due to carcinoid tumors that release serotonin, kallikrein, bradykinin, histamine, prostaglandins, and tachykinins

Differentiate the causes of systolic cardiac murmurs from diastolic cardiac murmurs, and be able to grade them.

Systolic Cardiac Murmur: Begins with or after S1 and at or before S2; causes = "MR PASS" ◦ Mitral Regurgitation ◦ Pulmonary & Aortic stenosis 6 grades - based on loudness/ intensity of murmur → Grade 1: Very faint, not usually heard during the first few seconds of listening, no palpable thrill → Grade 2: Faint, but heard immediately, no palpable thrill → Grade 3: Easily heard, no palpable thrill → Grade 4: Easily heard, and associated with a palpable thrill → Grade 5: Very loud, associated with a palpable thrill, audible with only one edge of the stethoscope on the chest → Grade 6: Way loud, associated with a palpable thrill, audible with the stethoscope removed slightly from contact with the chest Diastolic Cardiac Murmur: Begins with or after S2 and ends before the next S1; causes = "Diastolic ARMS" ◦ Aortic Regurgitation ◦ Mitral Stenosis 4 grades - based on loudness/ intensity of murmur → Grade 1: Very faint, not usually heard during the first few seconds of listening → Grade 2: Faint, but heard immediately → Grade 3: Easily heard → Grade 4: Very loud

Differentiate the following based on physical findings: Pulmonic stenosis (PS)

Systolic Crescendo-Decrescendo ejection murmur ("midsystolic") ∙ Increases during inspiration, best heard at the 2nd left sternal border, and does not radiate to the carotids ∙ If ejection sound (click) is present (congenital PS), it gets softer during inspiration

Differentiate the following based on physical findings: Hypertrophic cardiomyopathy (HCM)

Systolic Crescendo-Decrescendo ejection murmur ("midsystolic") ∙ Squatting or isometric handgrip or lying from standing: click occurs later, murmur is shorter and often softer ∙ Standing, Valsalva, or Amyl Nitrite inhalation: click occurs earlier, murmur is longer and often louder

Differentiate the following based on physical findings: Aortic stenosis (AS)

Systolic Crescendo-Decrescendo ejection murmur ("midsystolic"), best heard at the 2nd right sternal border and radiating to the carotids, may have diminished & delayed carotid upstroke (don't feel beat in carotid at same time you hear S1) ∙ If murmur peaks early in systole, stenosis is not severe ∙ Squatting or lying from standing or Amyl Nitrite Inhalation: murmur gets louder ∙ Standing from squatting or lying, Valsalva maneuver, or Isometric Handgrip: murmur gets softer Congenital: bicuspid aortic valve ∙ Aortic ejection sound (click) is the auscultatory hallmark Acquired: Rheumatic fever, Senile Fibrocalcific

Describe the classic auscultatory finding associated with bicuspid aortic valve

Systolic ejection murmur (SEM) that radiates to the neck along with a systolic ejection sound (click)

Identify the functional anatomy of cerebral blood flow and explain the importance of the blood brain barrier

The brain will contain pial arteries which are branching/ distributing arteries which will penetrate arterioles and give rise to cerebral capillaries. They also exhibit myogenic responses meaning that as pressure increases, vessels constrict and as pressure decreases, vessels dilate. Since blood cannot pass the blood brain barrier, the surface must be highly vascularized

Explain the cause of death following coronary occlusion

The cardiomyocytes have a very high level of oxygen demand and cannot sustain long periods of hypoxia (minutes to hours) Normally, cardiac muscle is supplied with much more oxygen (5x) than is needed-- this allows for a large reduction in flow without death. However, when there is a large occlusion, eventually this overcomes the supply of oxygen.

Calcific aortic stenosis Include morphology, clinical features, & treatment

The most common of all valvular abnormalities, it is typically the consequence of age-associated "wear and tear" likely due to recurrent chronic injury (i.e.- hyperlipidemia, HTN, inflammation, etc.). Chronic injury leads to valvular degeneration and the deposition of hydroxyapatite (calcium) Morphology: mounded calcified masses within the aortic cusps that will protrude through the outflow surfaces into the sinuses, preventing cusp opening Clinical Features: Typically comes to clinical attention in the 7th-9th decades of life (bicuspid in the 5th-8th decades) ∙ Obstruction of left ventricular flow leads to increased pressures (>200mmHg) and hypertrophy which tends to be ischemic → angina pectoris ∙ Systolic & diastolic myocardial function impaired → CHF The onset of symptoms (angina, CHF, syncope) is a sign of cardiac decomposition and if left untreated, most patients die within 5 years of developing angina, 3 years of developing syncope, and 2 years of CHF onset Treatment: Surgical valve replacement

M-mode echocardiography

The oldest imaging form that provides data from 1 ultrasonic beam ("Ice pick view") Will give measurements of wall thickness and timing of valve movements

Name the diagnostic test of choice for a patient suspected of having neurocardiogenic syncope

Tilt-table test in order to produce the Bezold-Jarisch Reflex

Explain how exercise alters tissue blood flow, cardiac output, and vascular resistance.

Tissue Blood Flow: Increase to muscular organs (skeletal & cardiac) and decreases to non-essential organs (i.e.- GI, kidneys) Cardiac Output: Greatly increases Vascular Resistance: Dilation to organs with increased activity, contraction to organs with decreased activity

Identify the molecular components that contribute to muscle fatigue

Type I Fibers: slow fibers with less force but unfused tetanic force (pulsatile) meaning they don't fatigue (endurance fibers) Type II Fibers: Fast fibers with more force, but fatigue quickly (strength fibers) Fatigue comes from different things: A. Muscle Fatigue: Excess H+, K+, Lactic acid, and CO2 will cause fatigue of the muscle B. CNS Fatigue: As the muscles work, they turn to glycogenolysis and anaerobic respiration which produce ammonia and lactate, effecting the CNS Immediate energy: ATP & Phosphocreatine - lasts 30 sec to 1 min Nonoxidative energy: breakdown of glycogen to glucose - lasts 3-4 minutes Oxidative energy: oxidation of glucose and fatty acids to create ATP - can last indefinitely

Endomyocardial Fibrosis

Type of restrictive cardiomyopathy in children in young adults (Africa and the tropics) which results in dense fibrosis of the endocardium and subendocardium from apex to AV valves Reduced volume and compliance of affected chambers

Interpret the morphology of hypersensitivity myocarditis

Typically caused by drugs (Sulfonamides, methyldopa, penicillin) Will have Interstitial infiltrate in myocardium composed of lymphocytes, macrophages, and a high proportion of eosinophils

Doppler Echocardiography Include the difference between pulsed, continuous, and color

Used to diagnose aortic stenosis and valvular disease Will determine differences in frequency between sound waves and their echoes to measure the velocity of a moving object Pulsed: Measured velocity at a specific site → good for low gradients (Mitral valve inflow) Continuous: Measures velocity along entire line (range ambiguity) → Good for high gradients (aortic stenosis, mitral regurgitation) Color Doppler: can be used to diagnose regurgitative flow (red in coming towards the doppler, and blue is going away)

Define VO2 Max and explain how is it altered by aerobic exercise and aging.

VO2 Max: the maximum rate of oxygen uptake and use during exercise; it is dependent upon how much oxygen can be taken in, how much oxygen can be delivered to the tissue (this is the biggest factor), and how much oxygen the tissue can take out of the blood Aerobic Exercise: helps to sustain a higher VO2 max Aging: The ability to deliver oxygen is reduced with age, thereby decreasing VO2 max

Identify the most likely cause of syncope: Syncope preceded by vertigo, visual disturbance, hemifacial or perioral numbness, dysarthria or ataxia

Vertebrobasilar Insufficiency TIA/ Migraine/ / Subclavian Steal Syndrome

Discuss post-op atrial fibrillation

Very common, even if using Beta-blocker prophylaxis Increased risk with increased age, COPD, and DM Treatment: Beta-blocker (metoprolol), Diltiazem, Amiodarone, if lasting >48 hours anticoagulation 80% will revert to sinus rhythm in 24 hours

Discuss the utilization trends/referral patterns for cardiac rehab

~12.5 million Americans are eligible for cardiac rehabilitation, on average only 15% of these candidates received cardiac rehabilitation Females and seniors are referred at a lower rate than males and working age patients

Have an appreciation for major disease processes for which echocardiography is helpful for diagnosis

• Evaluate shortness of breath/DOE • Evaluate heart failure • Evaluate murmurs • Evaluate arrhythmias • Evaluate hypotension/shock of unclear etiology

List the indications for surgical intervention for infective endocarditis (IE)

• Heart failure due to valvular dysfunction • Myocardial/ valve ring abscess • Persistent bacteremia despite appropriate antimicrobial therapy • Recurrent embolic events despite appropriate antimicrobial therapy • Presence of large vegetations (>10mm) • Prosthetic valve dehiscence Emergency surgery: • Acute aortic insufficiency with early closure of the mitral valve • Rupture of sinus of Valsalva into right-heart chamber • Rupture of sinus of Valsalva into pericardium

Identify individuals who require antibiotic prophylaxis prior to procedures that are likely to result in bacteremia

• Prosthetic valves • Previous infective endocarditis (IE) • Congenital heart disease: Unrepaired cyanotic lesions, Repaired congenital heart disease with residual defects, & Completely repaired defects for the first six months • Cardiac transplant patients with valvulopathy

Diastolic murmurs occur in what pathologies?

∙ Aortic Regurgitation/ Insufficiency ∙ Pulmonic Regurgitation/ Insufficiency ∙ Mitral Stenosis ∙ Tricuspid Stenosis

Systolic ejection murmurs (crescendo-Decrescendo) occur in what pathologies?

∙ Aortic Stenosis ∙ Pulmonic Stenosis ∙ Hypertrophic Cardiomyopathy

What are the patient benefits from participating in cardiac rehabilitation?

∙ Cardiopulmonary: increase systolic & diastolic function ∙ Vascular system: increase compliance, endothelial function, & angiogenesis ∙ Musculoskeletal system: increase strength, size, & density ∙ Metabolic/ Endocrine System: increase glycemic control and lipid normalization ∙ Subcellular: changes cellular proteins

List the indications for aortic valve replacement (AVR) surgery for Aortic Insufficiency and apply them to clinical scenarios

∙ Decline in LV systolic function: Rule of 55 (LVEF <55%) ∙ Increase in LV size: rule of 55 (end-systolic dimension >55mm) or LV end-diastolic dimension >75mm ∙ Symptom Development: significant fatigue, worsening exercise tolerance, heart failure

What are the risk factors associated with CAD?

∙ Family History ∙ Tobacco Use ∙ HTN ∙ Dyslipidemia ∙ Diabetes ∙ Obesity ∙ Sedentary Lifestyle

State the minimum diagnostic workup for every patient with syncope

∙ History & Physical ∙ 12-lead EKG

List the risk factors for mortality and morbidity in CABG

∙ Increased Age ∙ Renal Insufficiency ∙ Peripheral Vascular Disease ∙ COPD ∙ Prior Open heart surgery ∙ LV Dysfunction ∙ Recent MI (<90 days)

Describe the virulence factors of Streptococcus pyogenes and their contribution to disease

∙ M-protein: binds fibrinogen and other plasma proteins, IgG, & complement regulatory factors → Contains C-repeat regions (A to C = pharyngeal, D to E = impetigo) ∙ Hyaluronidase: facilitates spread ∙ Streptococcal Inhibition of complement (SIC): inactivates MAC ∙ Streptolysin O (SLO): activates other cell types which contribute to ischemic destruction of tissue → Antibodies are formed against this (ASO titer) which peaks 4-5 weeks following infection ∙ Streptokinase A and B: Cleave plasminogen leading to cleaving fibrin and fibrinogen, lysing clots and facilitating spread

Discuss the relative incidences of the various causes of syncope

∙ Neurological/ Cerebrovascular (<10%): can be caused by seizures, migraines, TIA, Vertebrobasilar insufficiency, Arnold-Chiari malformation, concussion, & cerebral syncope ∙ Metabolic (<5%): can be caused by hypoglycemia, hypoxia, hyperventilation (hypocapnea), or drug/alcohol intoxication ∙ Psychiatric (up to 25% of unexplained syncopal episodes): can be caused by hysterical faint, panic disorder, or anxiety disorder ∙ Cardiovascular (50-60%): can be cause by electrical cardiac problems (i.e.- bradyarrhythmia or tachyarrhythmia), mechanical cardiac problems (aortic stenosis, hypertrophic cardiomyopathy, mitral stenosis, thrombus, prosthetic valve malfunction, pulmonic stenosis, tetralogy of Fallot, PE, Pulmonary HTN, MI, coronary spasm, pericardial tamponade, aortic dissection) or vascular problem (reflex-mediated → neurocardiogenic/ carotid sinus hypersensitivity/ situational/ glossopharyngeal neuralgia (preceded by pain in oropharynx/tonsillar fossa/tongue), anatomic → subclavian steal syndrome, orthostatic → > 20mmHg drop in SBP or > 10mmHg drop in DBP within 3 minutes of standing)

Analyze the cardiac effects of noncardiac neoplasms

∙ Pericardial spread → effusion or mass effect (can restrict filling) ∙ Myocardial metastases → clinically silent, nonspecific ∙ Bronchogenic carcinoma, malignant lymphoma → infiltrate mediastinum causing encasement, compression, invasion of SVC with obstruction of blood coming from head and upper extremities (SVC syndrome) ∙ Renal cell carcinoma → invades renal vein, travel up IVC into right atrium, blocking venous return

Describe the laboratory diagnostic tests used to identify S. pyogenes and to diagnose rheumatic fever

∙ Rapid Strep Test: antigen based, positive test requires no further work-up, negative result requires throat culture ∙ Beta-hemolytic on blood agar, Bacitracin Sensitive, PYR positive ∙ ASO titer (lasts 4-5 weeks), Anti-DNAse B antibodies (lasts 6-9months post infection), Streptokinase antibodies, Anti-hyaluronidase antibodies

List the indications for coronary artery bypass surgery (CABG)

∙ Refractory to medical therapy ∙ Triple vessel disease (especially with LV dysfunction) ∙ >50% left main coronary artery occlusion ∙ Two vessel disease with >75% occlusion of the LAD

Holosystolic (pansystolic) murmurs occur in what pathologies?

∙ Tricuspid Regurgitation ∙ Mitral Regurgitation ∙ Ventricular septal defect (VSD)