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CPD 2 > week 3- CV 3 > Flashcards

week 3- CV 3 Flashcards

1
Q

• What is Bundle Branch/Fascicular Blocks?

A

o No conduction past Bundle of His on one side or interruption in a hemifascicle of the bundle
o Often asx
o RBBB usu in otherwise healthy people, and in anterior MI, PE
o LBBB usu dt a structural heart d/o
o EKG: 2 R wave peaks b/c blocked ventricle is excited by delayed spread thru ventricular muscle. Hemiblocks have modest QRS widening.
o mb wide S2 split

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2
Q

• What causes valve dzs? How are they diagnosed?

A

o congenital defects, infective endocarditis, syphilis, carcinoid, sclerosis, myxomatous degeneration, calcification, other heart dz
o Best dx w echo, st catheterization

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3
Q

• What is aortic regurgitation?

A

o incompetent aortic valve → retrograde flow from aorta into LV in diastole
o Dt idiopathic valve degeneration, RF, myxoma, endocarditis, congenital bicuspid valve, syphilis, CT or rheumatologic dos. mb VSD in children
o → LVH and dilation

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4
Q

• What are ssx of aortic regurgitation? Auscultation? Dx?

A

o Asx or DOE, fatigue, syncope, chest pain and ultimately arrhythmias, frank CHF or cardiogenic shock
o Ausc: High pitched decrescendo diastolic murmur; Loudest at 3rd-4th left ICS. Heard best w pt leaning forward, hold expiration.
o Dx: Hx, PE, confirmed w Doppler Echo

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5
Q

• What is aortic stenosis?

A

o Narrow valve obstructs blood flow from LV to ascending aorta in systole
o Causes: Congenital bicuspid valve (most common), RF, or aging
o Classic sxs: syncope, angina and DOE, arrhythmias
o Auscultation: Loud rough systolic crescendo-decrescendo murmur at upper left sternal border, when pt leans forward radiates to right clavicle and neck w thrill
o Dx: Clinical, then Echo w Doppler to quantify degree of stenosis

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6
Q

• What is mitral valve prolapse?

A

o Billowing of mitral valve leaflets into LA in systole
o Causes: idiopathic myxomatous degeneration. mb transient in pregnancy or severe dehydration. Seen in CT d/os
o Sxs: Usu asx. Sxs with high adrenergic tone. mb chest pain, palpitations, arrhythmias, dyspnea, fatigue, orthostatic hypotension, May result in MR
o Ausc: Late systolic murmur and midsystolic click
o Dx: echo, Holter, or ECG to see any assoc arrhythmias

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7
Q

• What is mitral valve regurgitation? Ssx?

A

o Incompetent mitral valve causes flow from LV into LA in systole
o Common caused by RF, IE, papillary muscle damage, ruptured chordae tendinae, LV dilation, annular dilation.
o M>F
o May co-exist with MS or MVP
o Ssx: w progression, eventual LVH/LAH → fatigue, dyspnea, LV failure
o Ausc: blowing holosystolic murmur best heard at apex, pt in LLD

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8
Q

• How is mitral valve regurgitation diagnosed? Tx?

A

o Dx: echo. ECG, CXR (esp if acute) to see if pulmonary edema, chamber hypertrophy or assoc arrhythmias
o Catheterization usu only if surgery required to repair/ replace valve
o Tx: only if severe and symptomatic. Natural therapies to strengthen CT and improve valve function always recommended

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9
Q

• What is mitral stenosis?

A

o Narrowed orifice dt calcification, impeding blood flow from LA to LV
o Most common cause is RF
o Can result in PH, AFib, thromboebolism
o Sxs: when severe, DOE, FOE, tachycardia, fever, arrhythmia, w reduced CO. PND develops, and pulmonary edema.
o Ausc: opening snap, diastolic murmur, loud S1.
o Dx: echo. Notched or wide P waves on ECG dt LAH

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10
Q

• What is Pulmonic regurgitation?

A

o Incompetent pulmonic valve → blood flow from pulm artery into RV in diastole
o Cause: pulm artery dilation w PH
o Sxs: Usu asx, or if severe, signs of RCHF.
o Ausc: high pitched diastolic murmur, upper left sternal border
o Dx: echo. mb RV enlargement on ECG, PH on CXR

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11
Q

• What is pulmonic stenosis?

A

o Narrow pulmonic outflow tract obstructs blood flow from RV to pulm artery in systole
o Usu congenital, affects mostly children
o Ssx:: Usu asx, then mb syncope, angina, dyspnea.
o Mb RVH. RV heave or thrill
o Ausc: Wide S2 split (prolonged pulmonic ejection), mb early systolic click. Harsh crescendo-decrescendo murmur at left 2nd parasternal ICS w no radiation, louder w inspiration.
o Dx: Echo. ECG may show RVH or RBBB

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12
Q

• What is tricuspid regurgitation?

A

o Insufficient tricuspid valve causes blood flow from RV to RA in systole
o Causes: 1st or 2nd to Afib or RV dilation
o Usu asx. May lead to RV and RA enlargement, JVD, HM, ascites, signs of RCHF
o Ausc: pansystolic blowing murmur loudest on inspiration, best heard at R&L lower sternal border
o Dx: Echo. ECG may show RV overload signs with tall peaked P waves in RAH

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13
Q

• What is tricuspid stenosis?

A

o Narrow tricuspid orifice obstructs blood flow from RA to RV
o Cause: RF but mb congenital
o Ssx: Seen w mitral stenosis and tricuspid regurg, sxs of RCHF, w HTN/edema
o Ausc: short, scratchy diastolic, ↑ w inspiration. Heard best in lower R&L parasternal borders

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14
Q

• What are the types of endocarditis?

A

o Infective (IE)
o Subacute bacterial (SBE)
o Acute bacterial (ABE)
o Non-infective

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15
Q

• What is infective endocarditis?

A

o infection of endocardium, usu w bacteria or fungi
o Predisposing factors: abnormality of endocardium, microorganisms in blood stream
o Specifically, congenital heart defects, rheumatic valve dz, bicuspid or calcified aortic valves, MVP, HCM
o Strep viridans cause 50% of community-acquired native valve IE that isn’t from IV drug use. Cutaneous abscess, UTI, implanted device, drug injection site, catheter site, dental origin. Strep and Staph cause 80-90% of cases.
o 80-90% on left side of heart
o IV drug users have higher incidence of right sided IE (30-70%)

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16
Q

• What are consequences of IE?

A

o myocardial abscess, conduction abnormalities, sudden valve regurg, heart failure, death.
o Systemic problems: dt embolization of infective material (lung, kidneys, spleen, CNS)

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17
Q

• What are the abx prophylaxis guidelines for IE?

A

o Prosthetic valve replacements or repairs
o Previous IE
o Certain types of congenital heart dz
o Cardiac transplant recipients w valvulopathy

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18
Q

• What are ssx of IE?

A

o Suspect when: fever w no obvious infectious source, w heart murmur, (+) blood cultures in pts w/ valve dz, IV drug users
o Right sided: cough, chest pain, hemoptysis w septic pulmonary emboli. TC murmur common

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19
Q

• How is IE diagnosed?

A

o Hx & PE
o Tests: 3 serial blood cultures in 24 hr period (mb neg if Abx were given)
o Echo
o mb anemia; hi WBC, ESR, CRP

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20
Q

• what is subacute bacterial endocarditis (SBE)?

A

o usu dt strep, less often Staph
o Insidious onset
o Sxs: Vague: lo fever, night sweats, fatigability, malaise, weight loss, arthralgias, valve insufficiency
o PE: normal, or pallor, fever, change in existing murmur, new murmur, tachycardia. Petechiae, st Osler’s nodes on digits, Roth spots in eye, Janeway lesions, splinter hemorrhages on nails. 35% show CNS effects: TIA, stroke, encephalopathy

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21
Q

• What is acute bacterial endocarditis (ABE)?

A

o Usu dt strep and Staph
o Abrupt development and rapid progression
o mb dt fungi after valve replacement surgery
o Sxs: Fever, toxic appearance, heart murmur; ssx like SBE, but more rapid

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22
Q

• What is non-infective endocarditis?

A

o sterile plt and fibrin thrombi on cardiac valves, and adjacent endocardium in response to trauma, circulating immune complexes, vasculitis, hypercoagulable state.
o Etio: catheter injury to valves, SLE immune complexes, anti-phospholipid syndrome
o Sxs generally of underlying do
o Dx: Echo (vegetations) and blood cultures (-)

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23
Q

• What is pericarditis? Etio? Results?

A

o Inflammation of pericardium, often w effusion
o Etio: Idiopathic, mb dt infection, MI, trauma, tumor, metabolic do
o Mb acute or chronic (> 6mos).
o May result in Cardiac tamponade

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24
Q

• What is constrictive pericarditis? Ssx?

A

o uncommon, unknown etio
o Dt thickening and stiffening pericardium
o Early sxs: mb JVD, HM, early S2 on inspiration. Then, dyspnea, orthopnea, mb severe fatigue

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25
Q

• What are ssx of acute pericarditis?

A

o chest pain, pericardial friction rub, st w dyspnea, 1st sign mb tamponade
o hypotension, shock or pulm edema.
o Pain, like ischemia, may radiate similarly
o Worse w thoracic motion, cough, breathing
o Better sitting up, leaning forward
o Fever, chills, weakness

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26
Q

• What are ssx of pericardial effusion with pericarditis? Cardiac tamponade?

A

o PE: Muffled heart sounds, pericardial rub, mb decreased breath sound and crackles
o CT: like cardiogenic shock, ↓CO, lo arterial pressure, tachycardia, dyspnea. BP may fall, pulse may disappear (pulsus paradoxus). Muffled heart sounds

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27
Q

• How is pericarditis diagnosed? Pericardial effusion?

A

o P: ECG, Elevated ST (no pathologic Q waves as in MI). Echo shows pericardial effusion or thickened pericardium. Hx and PE. Hi WBC and ESR
o PE: CXR enlarged cardiac silhouette, ECG ↓QRS voltage, alternating voltages of P, QRS, T waves (dt variations in cardiac position)

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28
Q

• How are tamponade and constrictive pericarditis diagnosed?

A

o T: Low voltage or electrical alternans on ECG, echo if time. Otherwise, immediate pericardiocentesis for dx and Tx.
o CP: ECG non-specific, low QRS voltage, abn T waves. Afib or flutter in 1/3 of pts. CXR pericardial calcification. Echo non specific, elevated filling pressures. Catheterization confirms abn hemodynamics

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29
Q

• What are aneurysms? Congenital?

A

o Abn dilated artery dt weakened arterial wall
o any artery, often abdominal and thoracic aorta
o Congenital: intracranial arteries, called berry aneurysms, assoc w other abnormalities of arteries causing subarachnoid hemorrhage

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30
Q

• What is an abdominal aortic aneurysm (AAA)? Causes and risk factors?

A

o 3/4 of AA. M:F 3:1
o Diameter > 3 cm. mb lined w thrombi.
o Risk: Atherosclerosis, smoking, HTN, older age (70-80), FHx, Caucasian, male

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31
Q

• What are sxs of AAA? PE? Tests?

A

o Sxs: Usu asx. Or deep, boring back or abdominal pain.
o PE may reveal pulsatile mass in abdomen or bruit
o Testing: US or CT to dx.

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32
Q

• What are thoracic aneurysms?

A

o same causes as AAA, more symptomatic.
o 1/4 of AA. M=F
o may dissect, compress adjacent structures, leak, rupture, or cause thromboembolism.

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33
Q

• What are ssx of TAA?

A

o chest or back pain, cough, dyspnea, dysphagia, hoarseness
o Hemoptysis, Thromboembolism may cause stroke, abd pain, extremity pain
o May see Horner’s (dt compression of sympathetic ganglia), tracheal deviation

34
Q

• How is TAA diagnosed? Px?

A

o Dx: Hx and PE, CXR (often first found incidentally on CXR), CTA or MRA. TEE (transesophageal echo) shows ascending, but not descending aorta.
o Px: enlarge ~5mm/yr. Tend to rupture at 6-7cm. non-tx mortality 65% at 1 yr and 20% at 5 yrs. universally fatal if ruptured

35
Q

• What are aortic branch aneurysms?

A

o much less common than AAA or TAA
o Same risk factors. Sxs vary
o Most not dx’d before rupture, but mb seen incidentally on x-ray if calcified

36
Q

• What is an aortic dissection? Predisposition? Prevalence? Complications?

A

o Surging blood thru tear in aortic intima w separation of intima and media → false lumen. Vessels may rupture.
o risk factors for atherosclerosis (cocaine, smoking, HTN, dyslipidemia), CT dos (acquired and congenital), iatrogenic, trauma. >2/3 related to atherosclerosis
o Highest risk pts: African-Americans, men, elderly, HTN
o Present in 1-3% of autopsies
o Comp: compromised blood supply to tributary arteries, aortic valve dilation and regurg, heart failure, fatal rupture of aorta

37
Q

• What are ssx of aortic dissection?

A

o usu sudden severe pain, sharp, may mimic MI, syncope, cardiac tamponade
o Pulses may wax and wane. Limb BPs may differ by >30 mmHg
o Aortic regurg murmur in 50% w proximal dissection, and rarely, heart failure

38
Q

• How is aortic dissection diagnosed?

A

o Consider in any pt w chest pain, thoracic back pain, unexplained syncope, abdominal pain, stroke, acute-onset HF, esp if pulses and BPs unequal
o CXR (wide mediastinal shadow). ECG (not diagnostic)
o If CXR suggests AD: TEE, CTA or MRA done immediately
o CK-MB and Troponin differentiate from MI. anemia, hi WBC, LDH
o If suspect AD, consult cardiothoracic surgeon immediately!

39
Q

• What is px of AD?

A

o Up to 80% survival w timely surgical repair

o w/o tx mortality 1-3%/hr in first 24 hrs, 30% at 1 wk, 80% at 2 wks, 90% at 1 yr

40
Q

• what is aortitis? Cause, sxs, dx?

A

o Inflamed aorta, may → aneurysm or ischemia
o Common causes: CT dos and infections (syphillis, IE, fungal)
o Sxs and dx differ depending on etio

41
Q

• What is abdominal aortic branch occlusion? Ssx?

A

o Dt atherosclerosis, fibromuscular dysplasia, other conditions that produce ssx of ischemia or infarction.
o Ssx: pain, organ failure, necrosis; depends on location; dt ischemia

42
Q

• What are the peripheral arterial d/os?

A 
o	Acrocyanosis
o	Erythromelalgia
o	Fibromuscular dysplasia
o	Peripheral arterial aneurysms
o	PAD/PVD
o	Raynaud’s
o	Thromboangiitis obliterans
43
Q

• What is acrocyanosis? Ssx?

A

o Persistent, painless, symmetric cyanosis of hands, feet, face, dt vasospasm of small vessels of skin in response to cold.
o F>M, mostly hands. risk factors: cold climate, low BMI, outdoor occupation. More prevalent in young ppl
o Not assoc w atherosclerosis
o not easily reversible (like Raynaud’s), but will eventually
o Ssx: affected area persistently cold, bluish, sweats profusely, may swell
o check for central cyanosis; if present, look for causes of hypoxia

44
Q

• what is erythromelalgia?

A

o paroxysmal vasodilation of small arteries in feet, hands,less common face, ears, knees
o Rare, very distressing
o Mb primary (idiopathic) or secondary (MPDs, HTN, venous insufficiency, DM, SLE, RA, LS, gout, spinal cord dos, or MS)

45
Q

• What are ssx of erythromelalgia? Dx? Ddx?

A

o Ssx: Burning pain, heat, redness in feet, hands; mins to hrs. Trigger: warmth, relieved by cold/ice. range from mild to severe
o Dx: Hx and PE. Tests to determine causes (CBC)
o DDX: post-traumatic reflex dystrophies, shoulder-hand syndrome, peripheral neuropathy, causalgia, Fabry’s dz (X-linked lysosomal storage dz), cellulitis

46
Q

• What is fibromuscular dysplasia?

A

o heterogenous group of non-atherosclerotic, non-inflammatory arterial changes, causing some degree of vascular stenosis, occlusion, or aneurysm.
o Cause unknown, mb genetic, smoking mb risk factor. more common in ppl with certain CT dos
o More common in women 40-60.
o Medial dysplasia most common type. Alternating thick and thin collagen ridges along media or by extensive collagen deposition in outer half (perimedial dysplasia)
o usu affects renal arteries, carotids, intracranial arteries, less often intra-abdominal and external iliac arteries.

47
Q

• What are ssx of fibromuscular dysplasia? Dx?

A

o Ssx: Usu asx, mb claudication depending on location. MB dec femoral pulses, secondary HTN, TIA, stroke, aneurysms, abdominal pain
o Dx: Angiogram, beaded appearance in medial dysplasia, or concentric band or long smooth narrowing in other forms

48
Q

• What is peripheral arterial aneurysm?

A

o abn dilations of peripheral arteries dt weak arterial wall
o 70% are popliteal, 20% iliofemoral, often w abdominal aneurysms
o M:F (20:1), avg 65
o Common causes: atherosclerosis, popliteal a entrapment, septic emboli

49
Q

• What are ssx of peripheral arterial aneurysm? Dx? Px?

A

o Ssx: usu asx. If dt thromboemboli or rupture, mb painful, cold, pale, pulseless extremities. Mb large pulsatile artery if popliteal.
o Dx: US, MRA, CT
o Px: low risk of rupture.

50
Q

• What is peripheral arterial dz (peripheral vascular disease, PVD)?

A

o Atherosclerosis → lower limb ischemia
o 12% of ppl in US, M>F
o Risk factors same as atherosclerosis
o Severity of pain depends on degree of occlusion and collateral circulation, O2 needs of tissues

51
Q

• What are ssx of PVD? PE?

A

o Sxs: pain on exertion relieved by rest (intermittent claudication), numbness, tingling, in severe cases ulceration
o PE: pulses mb reduced or absent in foot, severely ischemic feet are cold, blue, painful, numb. Usu no edema
o Eventually → ulcers, esp after local trauma. mb painful unless also have peripheral neuropathy

52
Q

• How is PVD diagnosed?

A

o Ankle-brachial index <0.90. Start w bilateral ankle and arm systolic BP (can use Doppler probe if unable to palpate pulse) to get ratio of ankle to arm systolic BP
o Doppler US
o Angiography can localize extent of stenosis or occlusion (can also do MRA, CTA)
o Also (risk factors): lipid levels, CRP-hs, homocysteine, fibrinogen, BT

53
Q

• What is Raynaud’s Phenomenon/Dz? Ssx?

A

o Vasospasm esp in digits, nose, w intermittent reversible pallor, redness, cyanosis of skin
o mb 1st (>80%) or 2nd to other systemic conditions: CT dz, endocrine, hematologic, vascular, neurologic dos, drug use, neoplasms, infections, trauma
o Prevalence: 3-5%, F>M
o Ssx: attacks of vasospasm; dt cold, emotion. Pain, paresthesias. May progress to ischemia, esp in 2nd dz
o Warming helps, restores coloration

54
Q

• How is raynaud’s diagnosed?

A

o Primary: 30 at onset, severe painful attacks mb unilateral, ischemic lesions, hx and PE suggest underlying do, nail fold capillaroscopy shows enlarged and tortuous capillaries, abn ESR and AI blood tests
o There are associations bw Raynaud’s and migraine, variant angina, PH, suggesting common pathway

55
Q

• What is thromboangiitis obliterans?

A

o Aka Buerger’s dz; type of PVD aggravated by tobacco

o Produces segmental inflammation in small and medium-sized arteries. If acute may → occlusive thrombi

56
Q

• What are the peripheral venous and lymphatic d/os?

A 
o	DVT
o	Chronic venous insufficiency and postphlebitic syndrome
o	Superficial Venous Thrombosis
o	Varicose veins
o	Idiopathic telangectasias
o	AV fistula
o	Lymphedema
57
Q

• What is DVT? risk factors?

A

o Blood clot in deep vein of extremity (usu calf or thigh) or pelvis
o Risk: > 60yo, smoking (and 2nd), HF, Virchow’s triad, immobile, catheters, limb trauma, obesity, malignancy, nephrotic syndrome, OCP/HRT (hormones), prego, prior DVT, sickle cell, recent surgery

58
Q

• What are ssx of DVT? PE?

A

o Ssx: usu → venous insufficiencymb asx or pain over area w edema, erythema, superficial vein prominence, stasis pigmentation (blue vein), dermatitis, mb ulcer. Most concerning complication is PE.
o PE: mb pain on deep leg palpation, erythema, pitting edema. Check calf circumference, if >3 cm difference, suspect DVT
o Mb positive Homan’s sign, but not sensitive or specific (calf pain on hard dorsiflexion, knee ext)
o Mb hard cord palpated over vein in popliteal fossa or femoral triangle

59
Q

• How is DVT diagnosed?

A

o US w/ Doppler: sees venous lumen, impaired venous flow
o D-dimer (less likely w/o elevation)
o Fibrinogen, BT: throughout tx

60
Q

• What is ddx of DVT?

A

o venous insufficiency, superficial phlebitis, lymphatic obstruction, cellulitis, ruptured Baker’s cyst, muscle or tendon tears.

61
Q

• What is Chronic venous insufficiency and postphlebitic syndrome? Cause and risks?

A

o impaired venous return → tissue edema, inflammation, hypoxia
o etio: DVT, valve insufficiency, ↓muscular contraction, venous HTN
o Risk: trauma, obesity, older age

62
Q

• What are ssx of Chronic venous insufficiency and postphlebitic syndrome? Dx?

A

o Mb asx, but always causes signs
o Sense of fullness, heaviness, aching, cramps, tiredness, paresthesias in legs
o Usu worse standing/walking, relieved by rest and elevation.
o No change → varicose veins → stasis dermatitis → mb ulceration
o Mb Edema, unilateral (BL more likely dt systemic do)
o Dx: Hx and PE. US to exclude DVT

63
Q

• What is Superficial Venous Thrombosis?

A

o clot in superficial vein of extremity
o usu dt IV catheter in arm, or varicose veins in leg
o Can arise over hrs-days
o usu self limited in few weeks

64
Q

• what is found on PE for superficial venous thrombosis? Dx?

A

o PE: palpated as linear indurated cord, mb local inflammation
o Mb tenderness, erythema, mottling, warmth; may look like lymphedema
o Dx: Hx and PE

65
Q

• What are varicose veins?

A

o dilated superficial veins in legs
o dt congenitally absent or incompetent valves of veins
o FHx often positive
o Start out taut → visibly dilated

66
Q

• What are ssx of varicose veins? PE?

A

o Ssx: not dependent on size; aching, fatigue, sense of heat, all better elevation
o PE: Assess when pt is standing; Check for diabetic neuropathy, ulcerations
o Look for other sources of the pain: hip, knee, lumbar problems, arthritis
o check for arterial insufficiency and intermittent claudication

67
Q

• how are varicose veins diagnosed? Complications?

A

o Dx: obvious on PE.
o Comp: edema, eczema, pigmentation, painful ulcers (uncommon)
o Mb thin walled blowouts of affected vessels

68
Q

• What are Idiopathic telangiectasias?

A

o fine, dilated intracutaneous veins
o Usu asx, st burning pain
o Clinically insignificant, often unsightly to pt

69
Q

• What is an Arteriovenous fistula?

A

o abn communication bw artery and vein
o congenital or acquired via trauma or erosion of aneurysm into vein.
o → arterial or venous insufficiency, ulceration with emboli, ischemia
o swollen, warm, distended, pulsating superficial veins
o thrill palpable over fistula

70
Q

• what is lymphedema? Tx?

A

o excess lymph fluid and swelling of subQ tissues dt destruction, obstruction, hypoplasia of lymph vessels
o Tx: compression stockings, increasing circulation

71
Q

• What are the 2 types of lymphedema?

A 
o	primary (hypoplasia): uncommon, but F>M, mb congenital
o	Secondary: dt surgery, trauma, radiation therapy, tumors, infection, chronic venous insufficiency (mild)
72
Q

• What are ssx of lymphedema? Stages?

A

o Aching, heaviness, fullness, swelling; worse heat, prolonged dependency
o usu unilateral, painless
o Stages: pitting edema → non-pitting, chronic soft-tissue inflammation, early fibrosis → irreversible edema, skin changes (hyperkeratosis, hyperpigmentation, verrucae, fungal infections)

73
Q

• What are complications of lymphedema? How is it diagnosed?

A

o lymphangitis dt bacterial infiltration thru cracks in skin dt fungal infxn. Limb feels red and hot, with red streaks from point of entry.
o Dx: Obvious via PE

74
Q

• What is sudden cardiac death in athletes?

A

o 1/200,000 apparently healthy young athletes
o abrupt-onset V-fib, die suddenly. M:F 9:1
o usu dt undetected HCM
o Screening: PM and FHx, PE, mb ECG or Echo

75
Q

• What is Athletic Heart Syndrome?

A

o Many cardiac changes in ppl who train > 1 hr most days
o Intensive training → physiologic adaptations
o ↑LV pressure and volume, ↑LV muscle mass, chamber size
o ↑CO, lower resting HR and longer filling times

76
Q

• What are ssx of athletic heart syndrome? Dx? Px?

A

o Asx; bradycardia, laterally displaced PMI, ejection murmur, additional heart sounds
o Dx: ECG, Echo, exercise stress testing
o Px: unknown if benign or not

77
Q

• What are the 3 types of cardiac tumors?

A

o Benign primary
o Malignant primary
o Metastatic

78
Q

• What are benign primary cardiac tumrors?

A

o 50% myxoma; F>M
o Usu LA, pedunculated, prolapse thru mitral
o If friable, inc risk embolism

79
Q

• What are Malignant primary cardiac tumors?

A

o Sarcomas (most common), pericardial mesothelioma, primary lymphoma
o avg 41
o Usu start in RA, involve pericardium
o mb →obstruction, tamponade, metastases to lung

80
Q

• What do metastatic cardiac tumors come from? Ssx? Dx?

A

o Usu from lung, breast, soft tissue sarcoma, renal CA
o Ssx: like heart failure signs, stroke, CAD depending on location, size, friability
o Dx: usu delayed since signs look like other dos. Echo, bx. TEE for atrial tumors.
o anemia, hi WBC, ESR, CRP. ECG atrial enlargement, CXR calcifications

CPD 2 (10 decks)

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