Download AORTIC ANEURYSMS AND DISSECTION Aorta is about 1 inch or 2

AORTIC ANEURYSMS AND DISSECTION
Aorta is about 1 inch or 2 cm in diameter
Aortic Aneurysm - atherosclerosis
A. Patho/Causes
a. Abnormal localized dilation of aorta usually
btwn the renal arteries and iliac bifrication
b. Risk increases w age; rare before age 50; usually 65-70 yo
c. AAA are much more common in MEN
d. Atherosclerotic weakening of aortic wall
e. Predisposing factors: trauma, HTN, vasculitis, smoking, FHx
f. Syphilis and c.t. abnormalities (Marfan’s dz) assoc w AA but may involve lower aorta
B. History/PE
a. Usually asymptomatic; found on incidental xray or abdominal exam
b. Sense of “fullness”
c. If pain, located in hypogastrium and lower back; “throbbing”
d. Pulsatile mass on abdominal exam
e. Hoarseness or dry cough
i. Pressure of aneurysm on nerve controlling vocal cords
f. Sx suggesting expansion and impending rupture:
i. Sudden onset pain in back or lower abdomen, radiating to groin, butt, legs
ii. Grey Turner’s sign (ecchymoses on back and flanks)
iii. Cullen’s sign (ecchymoses around umbilicus)
g. Rupture of AA
i. TRIAD: abdominal pain, hypotension and palpable pulsatile abdominal mass
ii. Cardiovascular collapse
iii. Syncope or near-syncope; 2* to sudden hemorrhage
iv. N,V
C. Dx
a. US ** TOC – to evaluate both location and size of aneurysm; 100% sensitive
D. Tx
b. CT scan – only in hemodynamically stable pts, “candy cane”
c. Abdominal radiographs – calcifications of the dilated segment; cannot r/o
a. DEPENDS ON SIZE OF ANEURYSM
i. >5 cm in diameter or symptomatic = surgical resection with synthetic graft
ii. <5cm – periodic imaging to follow growth; no “safe size” even small can rupture
b. Ruptured AAAs: emergency surgical repair is indicated. All these pts are unstable.
Aortic Dissection - HTN
A. Patho/Causes
a. Risk Factors: Longstanding systemic HTN (70%); Trauma, c.t. dz (Marfan’s, EhlersDanlos syndrome); Bicuspid aortic valve; Coarctation of the aorta; third trimester preg
b. Transverse tear in intima of a vessel = blood enters media creating a false lumen and
hematoma propagates longitudinally
c. More common in MEN; btwn ages 40-60
d. Stanford classification or DeBakey system
i. Type A (proximal) – ascending aorta (includes retrograde extension from
descending aorta
ii. Type B (distal) – limited to descending aorta
B. History/PE
a. Severe tearing/ripping/stabbing pain in anterior back of the chest - interscapular region
i. Anterior chest pain is MC with proximal dissection (A)
ii. Interscapular back pain is MC with distal dissection (B)
b. Diaphoresis, usually hypertensive (some hypo – pericardial tamponade, hypovolemia
blood loss, acute MI); pulse/BP asymmetry btwn limbs
c. aortic regurg esp w proximal dissections
d. neuro Sx (hemiplegia, hemianesthesia) due to obstruction of carotid artery (aortic
arch or spinal arteries)
C. Dx
a. CXR =WIDENED MEDIASTINUM > 8 mm on AP view
b. Transesophageal echocardiogram (TEE) very high sensitivity and specificity it is
noninvasive and can be performed at bedside
i. Very accurate and ideal in unstable pt bc bedside
c. CT and MRI – more time
i. CT aortic angiography is GOLD STANDARD
d. Dx is very difficult to make bc classic clinical findings often are not apparent. The use
of thrombolytics in aortic dissection pts who have mistaken dx of acute MI can have
fatal consequences!!!!
D. Tx
a. Medical therapy IMMEDIATELY
i. IV BB to lower HR and dec force of LV ejection
ii. IV sodium nitroprusside to lower systolic BP < 120
b. Type A (proximal) – surgical management
c. Type B (distal) – medical management
Coarctation of Aorta
A. Patho/Causes
a. Associated with Turner’s syndrome in women
b. Narrowing/constriction of aorta, usually at origin of left subclavian artery near
ligamentum arteriosum, which leads to obstruction btwn proximal and distal aorta =
increased LV afterload
B. History/PE
a. HTN in upper extremities with hypotension in lower extremities
b. Well developed upper body with underdeveloped lower half
c. Midsystolic murmur heard best over the back
d. HA, cold extremities, claudication with exercise and leg fatigue
C. Dx
a. EKG = LVH
b. CXR = notching of the ribs, “figure 3” appearance due to indentation of aorta at site of
coarctation with dilation before and after stenosis
D. Cx
a. Severe HTN, ruptured cerebral aneurysms, infx endocarditis, aortic dissection
E. Tx
a. Surgical decompression
b. Percutaneous balloon angioplasty
INFECTIVE ENDOCARDITIS
A. Patho/Causes
a. Transient bacteremia – seeding of heart valves
i. infx of endocardial surface
ii. Usually involves cusps of the valves
iii. Greatest risk 6 months following valve replacement
iv. Indwelling catheters
v. PMHx rheumatic fever or valvular dysfunction
b. Acute endocarditis
i. MCC staphylococcus aureus (virulent)
ii. on normal heart valve
iii. untreated can be fatal in 6 wks
c. Subacute endocarditis
i. Virulent organisms – streptococcus viridians and enterococcus
ii. On damaged heart valves
iii. Takes longer than 6 wks to cause death
d. Organisms
i. Native valve endocarditis (acute and subacute)
1. Acute
a. staph. Aureus, virulent
b. normal valve
2. Subacute
a. Strept. Viridians(alpha hemolytic) and enterococcus
b. Damaged valve
i. HACEK organisms
1. Haemophilus, actinobacillus, cardiobacterium,
eikenella, kingella
3. Tx: PCN G + gentamicin
ii. Prosthetic valve endocarditis (early and late)
1. Early
a. Staph aureus MCC of early onset endocarditis
b. Sx w/in 60 days of surgery = Staph. epidermidis
2. Late
a. onset Sx 60 days after surgery = alpha hem streptococci
3. Tx: Vancomycin + gentamicin
a. Can also add Rifampin
iii. Endocarditis associated with IVDA
1. RIGHT SIDED ENDOCARDITIS – tricuspid valve
2. Staph aureus MCC
3. Tx: nafcillin + gentamicin
a. Vancomycin + gentamicin if MRSA
B. History/PE
a. FAME: fever, anemia (splenomegaly), murmur (new onset), emboli (systemic)
b. Constitutional Sx are MC (fever, fatigue, wt loss)
c. Specific embolic signs:
i. focal neuro deficits (embolic stroke)
ii. petechiae
iii. Roth spots (retinal hemorrhages)
iv. splinter hemorrhages (fingerbeds)
v. Osler’s nodes (distal finger tips)
C. Dx
a. 3 sets of blood cultures are highly sensitive
b. TEE is sensitive but not specific for cardiac valve vegetations
c. Always suspect endocarditis in a pt w a new heart murmur and unexplained fever
d. Duke’s Criteria
Major
 Sustained bacteremia of organism known to cause I.E.
 Endocardial involvement
o Echo (veg, abscess, valve perforation, prosthetic dehiscense)
o New valvular regurgitation
Minor
 Predisposing condition
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D. Cx
E. Tx


o Abnormal valve or abnormal risk of bacteremia
Fever
Vascular phenomena
o Septal arterial or pulmonary emboli, mycotic aneurysm, intracranial
hemorrhage, Janeway lesions
Immune phenomena
o Glomerulonephritis, Osler’s nodes, Roth spots, rheumatoid factor
Positive blood cultures – not major criteria
Positive echo – not major criteria
a. Cardiac failure, myocardial abscess, organ damage from showered emboli,
glomerulonephritis arterial emboli and infarcts, infectious emboli, inflammatory and
immune disorders, CHF, abscess, pericarditis, myocarditis, ruptured valve, arrhythmia
and immune-complex glomerulonephritis.
b. Always fatal if left untreated
a. Tx CHF
b. Empiric IV Abx
i. PCN G + gentamicin = DOC (coverage of streptococci)
ii. Nafcillin + gentamicin = DOC IVDA (methicillin-sensitive staph)
1. Resistant = vancomycin
iii. Prosthetic valves = rifampin + vancomicin or gentamicin
c. Parenteral ABx based on 3 blood cultures
d. Negative cultures but high suspicion = PCN or vancomycin plus AMG until organism is
isolated
e. Prophylaxis (amoxicillin) of high risk pts before invasive procedures, dental
f. valve replacement surgery PRN
Signs of PERICarditis
 Pulsus paradoxus, EKG changes, Rub, increased JVP, chest pain
PERICARDIAL DISEASE
Causes = CARDIAC RIND
 Collagen vasc dz, aortic dissection, radiation, drugs, infx, acute renal f, cardiac MI, rheumatic
fever, injury, neoplasms, Dressler’s syndrome
 Inflammation over a period of time results in calcium deposits
Acute Pericarditis
A. Patho/Causes
a. May be isolated finding or secondary to an underlying disorder or generalized dz
b. Idiopathic (probably viral) – usually preceded by recent flulike illness or URI or GI Sx.
c. Infectious (echovirus, coxsackievirus, HIV, hep A or B); bacterial (TB); fungal;
toxoplasmosis
d. Acute MI (first 24 hrs after MI
e. Dressler’s syndrome – wks to months after MI or open heart surgery
i. 2ndary pericarditis
1. Persistent low grade fever, pleuritic chest pain, pericardial friction rub
and pericardial effusion
2. Autoimmure inflammatory reaction to myocardial neo-antigens
ii. Tx:
1. NSAIDs (ASA) or steroids (rare cases)
2. Usually self limited
3. Recurrence is common
f.
B.
C.
D.
E.
Uremia; collagen vasc dz; neoplasm; drug-induced lupus (procainamide, hydralazine);;
post-surgery; amyloidosis; radiation
g. Most pts recover within 1-3 wks
History/PE
a. Pleuritic chest pain – associated with breathing
i. Positional aggravated by lying supine, coughing, swallowing and deep insp
ii. pain is relieved by sitting up and leaning forward
iii. localized to retrosternal and left precordial regions and radiates to trapezius
ridge and neck
b. Pericardial friction rub – hears best w exp and pt sitting up
c. EKG changes
d. Pericardial effusion (w or w/out tamponade)
e. Fever and nonproductive cough
Dx
a. EKG shows:
i. ST elevation and PR depression ** specific for AP
ii. ST segment returns to normal
iii. T wave inverts and then returns to normal
b. Echocardiogram if pericarditis with effusion is suspected
Tx
a. Usually self limited; resolves in 2-6 wks
b. Treat underlying cause
c. NSAIDS – mainstay therapy
d. Glucocorticoids for pain but avoided if possible
Cx
a. Pericardial effusion
b. Cardiac tamponade – 15%
c. Recurrence or refractory cases
i. Pericardial window
ii. Pericardiectomy
Constrictive Pericarditis
A. Patho/Causes
a. Fibrosis scarring of the pericardium leads to rigidity and thickening of the
pericardium, with obliteration of the pericardial cavity
i. Restricts diastolic filling; limit defined by stiff pericardium
ii. In contrast, ventricular filling is impeded throughout diastole in cardiac
tamponade)
b. Diastolic dysfunction – early D: rapid filling; late D: halted filling
c. Idiopathic, but probably previous pericarditis
d. Uremia, radiation therapy, TB, chronic P eff, tumor, ct, prior surgery
B. History/PE
a. Pts appear very ill
i. JVD
ii. Kussmaul’s sign – JVD (venous pressure) fails to dec during inspiration
iii. Pericardial knock – abrupt cessation of ventricular filling
iv. Ascites
C. Dx
D. Tx
v. Dependent edema
b. Early: Systemic venous pressure increases
i. Edema, ascites, hepatic congestion --- always r/o constrictive pericarditis
c. Late: elevation of L-sided intracardiac pressures:
i. Pulmonary congestion: cough, DOE, orthopnea
a. EKG- low QRS, generalized T wave flattening or inversion, LA abnormalities
i. Atrial fibrillation
b. Echo *** TOC
c. CT, MRI – thickened pericardium
d. Cardiac catheterization – elevated and equal diastolic pressures in all chambers
a. Surgical: complete resection of the pericardium is definitive therapy and is indicated in
many pts. It has a significant mortality rate though.
Pericardial Effusion – if it develops rapidly, it could lead to cardiac tamponade
A. Patho/Causes
a. Any cause of acute pericarditis that can lead to exudation of fluid into pericardial space
b. Can occur with ascities and pleural effusion in salt and water retention states such as
CHF, cirrhosis and nephritic syndrome
B. History/PE
a. Muffled heart sounds, soft PMI, dullness at left lung base, sometimes pericardial frc rub
C. Dx
a. Echo *** TOC; can show as little as 20 mL
b. CXR – enlarged cardiac silhouette; “water bottle” appearance
i. Enlarged heart with pulmonary vasculature
c. EKG
i. Low QRS voltages and T wave flattening; electrican alternans = massive
d. CT or MRI
e. Pericardial fluid analysis – clarify cause of effusion
D. Tx
a. Depends if pt is hemodynamically stable
b. Pericadiocentesis is not indicated unless there is evidence of cardiac tamponade.
c. Monitor with echo and small pericardial effusion should resolve w/in 1-2wks
Pericardial Tamponade
A. Patho/Causes
a. Rate of fluid accumulation, not the amount
i. 200 mL of fluid develops rapidly = tamponade
ii. 2 L can accum slowly – heart can adapt and stretch
b. Pericardial effusion that impairs diastolic filling of the heart
c. Pressures of RV, LV, RA, LA, pulm art and pericardium equalize during diastole
i. Ventricular filling is impaired during diastole
ii. Decreased stroke volume and decreased CO
d. Penetrating trauma to thorax (gunshot, stab wounds)
e. Iatrogenic: central line, pacemaker, pericardiocentesis)
f. Pericarditis: idiopathic, neoplastic or uremic
g. Post MI with free-wall rupture
B. History/PE
a. Elevated jugular venous pressure is the most common finding
b. Narrowed pulse pressure (due to dec stroke volume)
C. Dx
D. Tx
c. Pulsus paradoxus
i. Dec in art pressure (femoral or carotid pulse) during inspiration
d. Tachypnea, tachycardia and hypotension with onset of cardiogenic shock
e. Beck’s Triad
i. Hypotension
ii. Muffled heart sounds
iii. JVD
a. Echo
b. CXR – clear lung fields
c. EKG – electrical alternans: alteration of QRS complex amplitude or axis between beats
i. Due to pendular swinging of heart; it is a motion artifact; not diagnostic tho
d. Cardiac catheterization – equalization of all pressures in all chambers of the heart
i. Shows elevated right atrial pressure with loss of the y descent
a. Nonhemorrhagic tamponade
i. Hemodynamically stable pt:
1. monitor echo, EKG, CXR
2. If renal failure, dialysis is more helpful than pericardiocentesis
ii. Pt is not hemodynamically stable
1. Pericardiocentesis not indicated
2. Fluid challenge
b. Hemorrhagic tamponade secondary to trauma
i. Emergent surgery is indicated to repair the injury
ii. Pericardiocentesis is only a temporizing measure and is not definitive treatment
iii. Surgery should not be delayed to perform pericardiocentesis
1. Compare and contrast the clinical manifestations and pathophysiology of restrictive pericarditis vs.
restrictive cardiomyopathy.
(1) Restrictive pericarditis – infiltrates to pericardium (outside heart)
(a) Easily remove pericardium
(2) Restrictive cardiomyopathy – infiltrates within heart muscle
(i) Amyloidosis, sarcoidosis, fibrosis, endocarditis, carcinoid, hemochromatosis
(b) Pericarditis frequently accompanies myocarditis
(c) Heart failure without blockage of coronary arteries, cardiac enzymes may be up
(d) Dx: Echo; Myocardial biopsy = gold standard
(e) Tx: supportive but poor prognosis