S3 vessels

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S3 vessels
2010-10-10 00:53:56
aneurysms HTN PE

Aneurysm, HTN, PE, DVT, coronary
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  1. AAA major complication
  2. AAA indication for Intervention/Type
    • -Elective – 5.0 - 5.5 cm diameter
    • -Emergency – Rupture or impending rupture

    • -Open
    • -Endovascular
  3. Prevelance of AAA
    • 8x more common in men
    • 50% have popliteal or femoral aneurysm
    • 20% first oreder relatives with aneurysm
  4. Natural History of Ruptured AAA
    • 50% die before reaching hospital
    • 25% of those reaching hospital alive, die before surgery
    • 50% of those who undergo surgery survive
    • 80% mortality overall
  5. Most common peripheral aneurysm
    Popliteal aneurysm
  6. Popliteal aneurysm common problems
    Distal embolization and thrombosis
  7. Popliteal Aneurysm Indication for Intervention
    • Elective: > 2 cm diameter in relatively healthy patient
    • Emergency: acute ischemia (thrombosis)
  8. Visceral Aneurysms
    • -Splenic
    • -Renal
    • -Hepatic

    • -Indications for Intervention
    • Elective-- size > 2 cm (Usually found incidentally by CT)
    • Emergency-- Rupture (usually splenic)
    • Hypertension from compression of renal aneurysm on renal artery
  9. Splenic Artery Aneurysms
    • Most common visceral artery aneurysm
    • Third most common intra-abdominal aneurysm
    • Appear and are likely to rupture in multiparous women
    • 4:1 female-to-male ratio
    • Majority are calcified and all are saccular
  10. Splenic artery aneurysm presentation
    • Most asymptomatic and are picked up incidentally
    • LUQ discomfort
    • “Double rupture phenomenon”
    • Free rupture
  11. Indications and Techniques for Treatment of splenic artery aneurysm
    • -Size > 2cm
    • -Symptoms/signs of rupture or impending rupture

    • -Surgical ligation/exclusion
    • -Splenectomy for distal location
    • -Trans-catheter embolization
  12. Aortic Dissection: typical patient/presentation
    • Male
    • 60’s – 70’s
    • Increased BP

    • Chest Pain
    • Anterior (Type A)
    • Posterior (Type B)
    • A,B - Stanford; 1,2,3 - Debakey
  13. Complications of Aortic Dissection
    • Rupture
    • -Pericardial tamponade
    • -Hemomediastinum
    • -Hemothorax (usually left-sided)
    • Occlusion of Aortic Branch Vessels
    • -Carotid (stroke)
    • -Coronary (myocardial infarction)
    • -Splanchnic (organ infarction)
    • -Renal (acute renal failure)
    • -Iliac, brachiocephalic, subclavian (limb ischemia)
    • Distortion of Aortic Annulus
    • -Aortic regurgitation
  14. Aortic dissection treatment
    • Type A
    • -Surgery

    • Type B
    • -Medical (decrease BP)
    • -Intervention for branch complications (open/endovascular)
  15. Stent-Graft Repair of Aortic Dissection
    • Patency of false lumen is a risk factor for progression of chronic dissection to aneurysmal dilatation
    • Induce false lumen thrombosis by sealing the aortic tear with an aortic endograft
    • Redirects flow into the true lumen
    • Treats malperfusion syndromes caused by dynamic obstruction and minimizes aneurysmal degeneration of the outer wall of FL
  16. Arterial Occlusion
    • Thrombotic (atherosclerotic--PVD)
    • Embolic
    • Macroembolic (heart)
    • Microembolic (proximal artery)
    • Vasculitis
  17. The pathology of PVD =
    • =CAD
    • Same risk factors
    • 40% of PVD patients have CAD
  18. Risk Factors for PVD
    • Smoking
    • Diabetes mellitus
    • Genetics
    • Hypertension
    • Hyperlipidemia
    • Radiation
  19. Thrombotic (PVD) Sites
    • Lower extremity arteries
    • Carotid arteries
    • Visceral arteries
    • -Renal
    • -Mesenteric
  20. Site of Peripheral Embolization (Macroembolic)
    Femoral bifurcation 40%
  21. Sources of Peripheral Emboli
    • Cardiogenic 80%
    • -Atrial Fibrillation 50%
    • -Myocardial 25%
    • 10% noncardiac
    • 10% idiopathic
  22. Atheroembolic (Microembolic) Targets
    • Feet/toes (“blue toe” syndrome)
    • Hands/finger tips
    • Brain
  23. Acute Limb or Visceral Ischemia
    • Thrombotic (PVD) or embolic
    • Sudden complete occlusion of artery
    • Common to all: PAIN
  24. Acute Limb or Visceral Ischemia
    Specific to lower extremities
    • Low ankle-brachial index
    • 5 P’s
    • -Pallor
    • -Pulseless
    • -Paralysis
    • -Pain
    • -Paresthesias
  25. Chronic Ischemia
    • Thrombotic (PVD)– long-standing
    • Legs
    • -Claudication
    • -Rest pain
    • -Tissue loss
    • Bowel
    • -Post-prandial pain
    • Kidney
    • -Hypertension
    • -Loss of parenchyma
  26. Treatment for Macroemboli
    • Embolectomy
    • Treat underlying heart problem
    • Anticoagulation
  27. Treatment for PVD (and Microemboli)
    • Open Surgery
    • -Bypass
    • -Endarterectomy
    • Endovascular
    • -Angioplasty
    • -Atherectomy
    • -Stent
  28. Indications for Carotid Endarterectomy (CEA)
    • Hemispheric TIA or amaurosis fugax with a > 70% stenosis
    • Completed stroke with an excellent recovery and a > 70% stenosis
    • Asymptomatic stenosis of > 80% in a “good risk” patient
  29. HTN numbers
    • Treatment of HTN is the most common reason for office visits of non-pregnant adults to physicians in the United States and for use of prescription drugs
    • Normal blood pressure: systolic <120 mmHg and diastolic <80 mmHg
    • Prehypertension: systolic 120-139 mmHg or diastolic 80-89 mmHg
    • Hypertension:
    • --Stage 1: systolic 140-159 mmHg or diastolic 90-99 mmHg
    • --Stage 2: systolic ≥160 or diastolic ≥100 mmHg
  30. Secondary HTN causes
    • Alcohol
    • Aortic coarctation
    • Renal disease
    • Renal artery stenosis
    • Pheochromocytoma
    • Primary aldosteronism
    • Cushing’s syndrome
    • Sleep apnea
    • Thyroid dysfunction
    • Hypercalcemia
    • Drugs
    • -Oral contraceptives
    • -NSAID’s
    • -Cocaine
  31. Hypertensive Emergencies
    • Acute, life threatening episodes of severe HTN with end organ damage (CNS, CVS, renal)
    • Most commonly in patients with h/o uncontrolled HTN, non compliance
    • BP usually >180/120
  32. How hyptertensive emergencies may clinically present
    • Cerebral infarction
    • Pulmonary edema, CHF
    • Encephalopathy
    • ICH
    • Aortic dissection
    • Eclampsia
  33. Hypertensive Urgencies
    • Severe HTN without end organ damage or symptoms, other than headache
    • BP usually >180/120
    • Most commonly in patients with h/o uncontrolled HTN, non compliance
  34. Chronic Consequences of HTN
    Direct Cardiac: Congestive heart failure, Ischemic heart disease, Atrial fibrillation

    Non Cardiac: Cerebrovascular, Renal
  35. Congestive Heart Failure and HTN
    After age 40, the lifetime risk of developing CHF was 2X as high in subjects with a blood pressure ≥160/100 mmHg compared to <140/90 mmHg

    HTN directly leads to left ventricular hypertrophy
  36. __________ is the most common underlying disorder in patients with AF
    Hypertensive heart disease
  37. Risk Factors PE
    • Immobility
    • Increasing age
    • Surgery (pelvic)
    • Trauma
    • Malignancy
    • Pregnancy
    • Central venous catheters
    • Hyperhomocystinemia
    • Estrogenic meds (BCP)
    • Inherited thrombophilias
    • Increased blood viscosity (Sickle cell, polycythemia, Multiple Myeloma etc)
  38. Pathophysiology of PE
    • Abnormal pulmonary gas exchange
    • Pulmonary hypertension
    • Right ventricular failure
    • Cardiogenic Shock
    • Atelectasis
  39. Clinical Presentations of PE
    • Acute unexplained dyspnea
    • Pulmonary hemorrhage/infarction
    • Acute cor pulmonale / cardiogenic shock / syncope / sudden death
    • S/S of DVT – unilateral thigh or calf engorgement

    • Arterial hypoxemia / respiratory alkalosis
    • Dyspnea / hypoxemia not responsive to bronchodilator therapy
    • Fever
    • Unexplained atelectasis or pleural based infiltrate
    • Sudden increase in pulmonary pressures
    • Sudden increase in CVP and decresed organ perfusion
    • Unexplained tachypnea / tachycardia
  40. Diagnostic tools for PE
    • CXR – rarely helpful, can point to other diagnoses (# rib, CHF, pneumonia)
    • ECG – classic – deep S in I, Q in lead III, inverted t in lead III (S1Q3T3)
    • D- Dimer – negative predictive value better than positive
    • Imaging: V/Q scan, CT angiography, pulmonary angiography
  41. D-dimer for PE
    • negative D-Dimer in setting of pre-test low or moderate probability rules out PE
    • High rate of false positives
  42. Ventilation Perfusion Scan
    • Mismatched V/Q abnormalities
    • -A normal scan within days of event reliably rules out PE
    • -A perfectly unmatched defect is highly suggestive (>90%) of PE
    • Matched abnormalities
    • -indeterminate
  43. Proposed Diagnostic Work-up
    • Unlikely -> dimer -> negative no
    • Positive dimer or likely PE -> Chest CTA/V/Q scan --> positive treat, negative no
    • Equivocal--> Ultrasoudn DVT, consider angiogram
  44. Massive PE and Acute MI
    Both: Chest pain, shock, dyspnea

    In Massive PE: RV heave, Incr P2, Rt S3, neck vein distension, clear lungs

    In AMI: No heave, muffled heart sounds, S3 and S4, crackles (pulmonary edema)
  45. Treatment: Massive PE
    • Anticoagulate
    • Increase Preload (fluid)
    • CPR * compressions can dislodge or disrupt clot
    • Inotropic support
    • Consider thrombolytic therapy (rTPA)
    • Mechanical strategies
  46. Mechanical Strategies for PE
    • IVC filter
    • Recurrence despite anticoagulation
    • When anticoagulation is contraindicated
    • Patients with PE at high mortality risk if recurrent
    • Surgical or catheter embolectomy
    • Limited utility – patients are unstable and sick
    • Most improve by the time it is considered
  47. Pathophysiology of Venous Disease 2 Factors:
    • Deep venous thrombosis (DVT)
    • Valvular incompetence (reflux) - trauma, dilation with age, thrombus causes scar
  48. Acute DVT – Clinical Presentation
    • Pain
    • Edema
    • Erythema
    • Tenderness
    • Fever
    • Prominent superficial veins
    • Pain with passive dorsiflextion of foot (Homans’ sign)
    • Peripheral cyanosis
    • Massive pitting edema and blanching (phlegmasia cerulea albans)
    • Painful blue leg (phlegmasia cerulea dolens)
  49. Acute DVT - Diagnosis
    • Lab: D-dimer
    • Imaging:
    • -Duplex ultrasound
    • -Venography
    • -Magnetic resonance venography
    • -Computed tomographic venography
  50. Treatment of acute DVT
    • Anticoagulation
    • Inferior vena cava (IVC) filter if anticoagulation contraindicated
    • Thrombolysis with tissue plasminogen activator (tPA) if DVT is severe and disabling in young patient
    • Compression therapy (elastic stockings) to prevent long-term skin complications of chronic venous insufficiency
  51. Sequelae of venous thromboembolic disease
    • Pulmonary embolism
    • Pulmonary hypertension after PE
    • Death from PE
    • Post-thrombotic syndrome (chronic venous insufficiency - varicose veins, edena, skin changes, ulceration)
  52. Types of superficial thrombophlebitis
    • ST with varicose veins
    • Traumatic
    • Septic/suppurative
    • Migratory thrombophlebitis (Trousseau’s syndrome)
    • SSV thrombophlebitis
    • Upper extremity
  53. Superficial thrombo treatment
    • Antibiotics
    • NSAIDs
    • Warm compresses
    • Anticoagulation
    • Limb elevation
  54. Superficial Thrombophlebitis
    Thrombosis, inflammation, and possibly infection of a superficial vein

    Signs/symptoms: Erythema, Tenderness, Palpable cord
  55. Superior Vena Cava (SVC) Syndrome
    • Venous congestion of head and neck secondary to central venous obstruction
    • Signs/Symptoms – facial swelling, plethora, cough, dyspnea, stridor

    • Intraluminal fibrosis - benign (TB, hypercoaguable, syphilis, defib, pacemaker, catheter
    • or
    • External compression - 80% malignant, also benign

    Stent placement
  56. Lymphatic Diseases
    • Lymphedema
    • Interstitial accumulation of lymph due to impaired drainage
  57. Lymphedema: Primary v Secondary
    • •Classification of lymphedema based on etiology, age of onset, and
    • inheritance

    • •Primary lymphedema
    • –Congenital (onset less than 1 year of age)
    • •Nonfamilial
    • •Familial (Milroy’s disease)
    • –Lymphedema praecox (onset from 1-35 years of age)
    • •Nonfamilial
    • •Familial (Meige’s disease)
    • –Lymphedema tarda (onset after 35 years of age)
    • •Secondary lymphedema
    • –Filariasis
    • –Lymph node excision/radiation
    • –Tumor invasion
    • –Infection
    • –Trauma
  58. Lymphedema Signs, Complications, Treatment
    • •Signs/symptoms
    • –Edema
    • –Skin changes
    • •Peau d’orange
    • •Lichenification
    • •Ulcerations rare (unlike venous stasis)
    • •Complications
    • –Infection (lymphangiitis)
    • –Malnutrition
    • –Immunodeficiency
    • –Malignancy (Stewart-Treves)
    • •Treatment
    • –Sequential mechanical compression
  59. most important risk factor for coronary artery disease
  60. HTN prevalence was highest among
    non-Hispanic blacks
  61. Coronary Artery Disease risk factor:
    High sensitivity C-reactive protein
    • •HsCRP adds prognostic information at all levels of LDL cholesterol and at all levels of risk, as determined by the Framingham Risk Score
    • •In clinical terms, absolute vascular risk is higher in individuals with elevated hsCRP levels and low levels of LDL cholesterol than in those with elevated LDL cholesterol but low levels of hsCRP
  62. Coronary artery disease risk factor - Homocystein
    • marker of inflammation
    • Hiperhomocysteinemia patients present with endothelial dysfunction, accelerated oxidation of LDL cholesterol, impairment of flow-mediated endothelium-derived relaxing factor with subsequent reduction in arterial vasodilation, platelet activation and oxidative stress
  63. Coronary artery disease risk factor:
    •Markers of fibrinolytic function - t-PA
    • Impaired fibrinolysis can result from an imbalance between the clot dissolving enzymes t-PA or urokinase-type plasminogen activator and their endogenous inhibitors, primarily PAI-1
    • A consistent series of prospective studies has linked abnormalities of fibrinolysis to increased risk of arterial thrombosis
  64. Coronary artery disease risk factor:
    •Other markers of inflammation
    Lipoprotein (a)
    The close homology between Lp(a) and plasminogen has raised the possibility that this lipoprotein may inhibit endogenous fibrinolysis by competing with plasminogen binding on the endothelium
  65. Acute MI presentation
    • Same as angina: Retrosternal chest pressure, burning or heaviness; radiating occasionally to neck, jaw, epigastrium, shoulders, or left arm.
    • Sudden onset, usually lasting 30 minutes or longer. Often associated with shortness of breath, weakness, nausea and vomiting.
  66. Pericarditis presentation
    • Sharp, pleuritic pain aggravated by changes in position; highly variable duration
    • Pericardial friction rub
  67. Pulmonary embolism presentation
    • Sudden onset of dyspnea and pain, usually pleuritic with pulmonary infarction
    • Dyspnea, tachypnea, tachycardia, and signs of right heart failure
  68. Pulmonary HTN presentation
    • Substernal chest pressure, exacerbated by exertion.
    • Pain associated with dyspnea and signs of pulmonary hypertension.
  69. Spontaneous Pneumothorax
    • Burning discomfort in midline with dyspnea.
    • Abrupt onset of dyspnea and pain.
  70. Pleuritis/Pneumonia
    • Pleuritic pain, usually brief, over involved area.
    • Pain pleuritic and lateral to midline, associated with dyspnea.
  71. Creatine Kinase (CK): Serum CK often increases within ____ hours after the onset of STEMI, declines to normal within day ____
    • 4 to 8 hours after the onset of STEMI
    • declines to normal within day 2 or 3
  72. Myoglobin and MI
    • •Released from injured myocardial cells
    • •Peak levels are reached 1 to 4 hours after the onset of MI
    • •Poorly specific
    • •Should be supplemented by troponins (cTnI or cTnT)
  73. Troponins:
    •cTnT and cTnI:
    • Start to rise by 3 hours after the onset of chest pain
    • Elevations of cTnI may persist for 7 to 10 days after MI
    • Elevations of cTnT may persist for up to 10 to 14 days
    • Very useful for late diagnosis of MI
    The definition of acute coronary syndrome (ACS) includes unstable angina (UA), non-ST segment elevation myocardial infarction (non-STEMI), and ST segment myocardial infarction (STEMI). However, in practice, ACS is used to indicate UA and non-STEMI
  75. Accute Coronary Syndrome Cause
    • ACS is result of a mismatch between myocardial oxygen supply and demand
    • Occasionally, this is due to anemia, hyperthyroidism, infection, tachyarrhythmias, or valvular heart disease
    • MOST COMMON CAUSE of change from stable CAD to ACS is disruption or fissuring of a vulnerable atherosclerotic plaque; this is followed by platelet-mediated thrombosis and vasoconstriction with or without elevation of cardiac markers
  76. Almost all MIs result from
    coronary atherosclerosis, with thrombosis
  77. Plaque fissuring and disruption
    • Plaques prone to disruption overexpress metalloproteinase enzymes
    • Plaque disruption can be produced by stresses induced by intraluminal pressure, coronary vasomotor tone, tachycardia and disruption of nutrient vessels
    • BP, HR, blood viscosity, t-PA, PAI-1, cortisol and epinephrine in high levels may cause plaque disruption
    • •Coronary embolism: endocarditis, mural thrombi, prosthetic valves, neoplasms
    • •Inflammatory processes:
    • •Infections- viral (Echo, Coxsackie), syphilitic aortitis
    • •Takayasu arteritis
    • •Necrotizing arteritis
    • •Polyarteritis nodosa
    • •Kawasaki disease

    • •SLE
    • •Radiation
    • •Amyloidosis
    • •Hurler syndrome
    • •Homocystinuria
    • •Cocaine abuse
  79. STEMI chest symptoms
    • Rales audible in patients with LV failure
    • Diffuse wheezing can be present in patients with severe LV dysfunction
    • Cough with hemoptysis suggesting pulmonary embolism with infarction can also occur
  80. STEMI heart sounds
    • First sound frequently muffled and occasionally inaudible after the infarct
    • Patients with marked ventricular dysfunction and/LBBB may have splitting of S2
    • S4 almost universally present in patients with STEMI, limited diagnostic value, S3 reflects severe LV dysfunction
  81. STEMI murmur
    • •Systolic murmurs are commonly audible, generally result from MR secondary to papillary muscle dysfunction
    • •An apical holosystolic murmur with a thrill may represent rupture of papillary muscle
    • •In the rupture of the IV septum are similar but murmur and thrill are more prominent in the left sternal border
    • •The systolic murmur of tricuspid regurgitation is also heard along the left sternal border (intensified by inspiration)
  82. STEMI Friction rub
    • May be heard in patients with STEMI
    • Probably more common than reported
    • Most commonly noted on second to third day after MI
    • In patients with STEMI and friction rub may have a pericardial effusion
    • Dressler syndrome: Post-infarction pericarditis (up to 3 months after MI)
  83. •World Health Organization (WHO) criteria for MI diagnosis:
    • History of ischemic-type chest discomfort
    • Evolutionary changes on serial ECG traces
    • Rise and fall in serum cardiac markers