Tachycardia, Venous disease, Arterial disease Flashcards
(237 cards)
1
Q
Tachycardia is defined as what?
A
HR >100bpm
2
Q
What is narrow complex tachycardia?
A
Sinus tachycardia, supraventricular tachycardia, AFIB, aflutter
3
Q
What is wide complex tachycardia?
A
Ventricular tachycardia (Torsade de Pointe), ventricular fibrillation
4
Q
Etiologies of sinus tachycardia (sinus rhythm >100bpm)
A
Exercise, anxiety, pain, exposure to stimulants (caffeine), volume depletion (dehydration or sepsis/SIRS), anemia, hypoxia, hyperthyroidism, PE, pericarditis
5
Q
What are some symptoms of sinus tachycardia?
A
Asymptomatic, heart palpitations, SOB (especially with exertion)
6
Q
Symptoms of sinus tachycardia in pts with heart disease (CAD)
A
Heart palpitations, SOB, chest discomfort, lightheadedness, fatigue
7
Q
How do you treat sinus tachycardia?
A
Treat underlying cause
8
Q
If pt has sinus tachycardia from dehydration, treat how?
A
IV fluid
9
Q
If patient has sinus tachycardia due to pain how do you treat it?
A
Pain meds
10
Q
If patient has sinus tachycardia from a PE, how do you treat?
A
Anticoagulation therapy
11
Q
How do you treat sinus tachycardia if its from sepsis?
A
Treat the source-Abx
12
Q
How do you treat sinus tachycardia if its from anxiety?
A
Consider anxiolytics
13
Q
Supraventricular tachycardia
A
Regular, rapid rhythm, narrow complex (originates above the ventricle), no discernible p waves
14
Q
What are some examples of supraventricular tachycardia?
A
Atrioventricular nodal reentry tachycardia (AVNRT)
Othodromic AV reciprocating tachycardia (AVRT)
Junction all tachycardia (originating at AV node)
15
Q
Symptoms of SVT
A
sudden onset racing heart (palpitations), lightheadedness, pre-syncope, syncope, SOB, anxiety, if underlying heart disease: chest pain or pressure
16
Q
SVT
A
Begins suddenly and ends suddenly, often self-limiting
17
Q
Management of persistent SVT for unstable pts
A
Vagal maneuvers, then in unsuccessful immediate DC cardioversion
18
Q
Management of persistent SVT for a stable pt
A
Vagal maneuvers, carotid massage, Adenosine, CCB or BB
19
Q
What is the dosing for Adenosine (persistent SVT)
A
Initially dose 6mg IVP, then 12mg IVP, then 12mg IVP
20
Q
What do you do with patients who have frequent attacks of SVT?
A
Consult EP -> confirm aberrant pathway -> radiofrequency catheter ablation
21
Q
What is a direct current (DC) cardioversion
A
Medical procedure converting cardiac arrhythmias to NSR using electricity
22
Q
How does DC cardioversion work?
A
Two electrode pads are placed on pt (chest and back), the cardioverter delivers a shock which causes momentary depolarization of most cardiac cells allowing the sinus node to resume normal pacemakers activity
23
Q
Sustained ventricular tachycardia
A
Life threatening, fast wide complex rhythm, frequently associated with syncope
24
Q
What is the usual rate for sustained ventricular tachycardia?
A
160-240bpm with a duration of atleast 20 seconds
25
What is sustained ventricular tachycardia a frequent complication of?
MI and dilated CMP
26
Symptoms of sustained ventricular tachycardia
Heart palpitations, lightheadedness, chest pain, SOB, diaphoresis (drenching sweat), near syncope or syncope, sustained LOC, pulseless electrical activity (death)
27
Treatment of acute ventricular tachycardia if pulseless
CPR, Defibrillation, epinephrine
28
What is the treatment of acute ventricular tachycardia is the pulse is present?
If it causes hypotension, HF, myocardial ischemia-> synchronized DC cardioversion
If pt stable ->Amiodarone
ICDs
29
If patient is stable and has acute ventricular tachycardia, what is the treatment?
Amiodarone 150mg IV bolus followed by continuous infusion
30
What is triggered by hypokalemia, hypomagnesemia, and drugs that prolong the QTc?
Torsades de pointes (type of VTACH)
31
What abxs prolong QTc?
Macrolides: Azithromycin, Quinolones: Levofloxacin, Ciprofloxacin
32
Which antidepressants cause prolong QTc?
Citalopram, Tricyclics antidepressants
33
What other drug classes cause prolongation of QTc?
Antipsychotics
34
What is the treatment of Torsades if pt is unstable?
Prompt defibrillation
35
What is the treatment of Torsades if the pt is stable?
First Line: IV Magnesium
| Temporary transvenous overdrive pacing if no response to magnesium
36
Ventricular fibrillation is often associated with what?
Severe CAD and caused by acute MI (ACS)
37
Characteristics of ventricular fibrillation
Sudden death can be initial manifestation of coronary disease in 20% pts, patients are pulseless and unresponsive
38
Patients are pulseless and unresponsive to what type of tachycardia?
Ventricular fibrillation
39
What are some causes of ventricular fibrillation?
MI, HF, hypoxemia or hyercapnia, hypotension/shock, electrolyte imbalances, stimulants (drugs, caffeine), often preceded by VTACH
40
What is ventricular fibrillation often preceded by?
VTACH
41
What conditions are associated with ventricular fibrillation?
LVH, HOCM, CHF, aortic stenosis (AS), Brugada syndrome
42
What is the treatment of ventricular fibrillation?
CPR, defibrillation, if pulse is regained-> consider coronary ateriography to view and treat CAD
43
What can be used for long term management of ventricular fibrillation?
Implantable cardioverter-defibrillator
44
What is another name for a coronary arteriography?
Cardiac catheterization
45
What types of venous thromboembolisms can occur?
DVT, superficial thrombophlebitis, and phlebitis
46
What are examples of chronic venous disorders?
Varicose veins, chronic venous insufficiency (CVI)
47
What are examples of the deep veins in the UE?
Subclavian, axillary, brachial, ulnar, radial, interosseous veins
48
What are the superficial veins of the UE?
Cephalic, basilic, median cubical, accessory cephalic
49
What are the superficial LE veins?
Greater saphenous, lesser saphenous, non-saphenous
50
What are the deep LE veins?
Iliac, common femoral, deep femoral, femoral, popliteal, deep calf
51
Where can DVTs take place?
Upper extremity vein thrombosis (UEDVT)
Proximal vein thrombosis
Distal Erin thrombosis
52
What veins are effected in proximal vein thrombosis?
Popliteal, femoral, or iliac veins
53
Where would a distal vein thrombosis take place?
In calf veins
54
What is lymphedema?
Local fluid retention, lymph or tissue swelling
55
Phlebitis
Inflammation of vein, red and warm
56
What makes up Virchow’s triad?
Stasis, Endothelial trauma, Hypercoagulable state
57
What are some anatomical risk factors for venous thromboembolism?
Mae-Turner syndrome, IVC abnormalities
58
Half of pts with DVT will have what?
Long-term complications
59
What are some risk factors for venous thromboembolism?
Previous VTE, malignancy, surgery, trauma, pregnancy, drugs, immobilization, recent hospitalization, anti phospholipid antibodies, CVD risk factors
60
What is anti phospholipid antibodies associated with?
Associated with Lupus, the body makes antibodies against phospholipids.
61
What cardiovascular risk factors are risk factors for VTE?
Obesity, *smoking* age
62
What are some hereditary risk factors for VTE?
Factor 5 Leiden mutation, prothrombin gene mutation, protein S and C deficiency, anti-thrombin deficiency, dysfibrinogenemia
63
What can cause thrombophlebitis?
Same risk factors for VTE, peripheral IV catheter placement
64
What types of embolizations are you at risk for with VTE?
Pulmonary embolism, stroke or arterial embolism (PFO or ASD)
65
What is PFO?
Patent foramen ovale, there is a hole in the atria and a clot can easily cross from venous to arterial side
66
What is the most severe type of DVT?
Phlegmasia Cerulea Dolens, get significant pain, swelling, and the leg becomes blue and cyanotic
67
What can be seen in postphlebitic syndrome?
Swelling, pain, discoloration, scaling
68
What is a thrombus extension?
A superior venous thromboembolism that is close to deep system. Need to follow it closely
69
Classic DVT symptoms
Pain, swelling, erythema *severity varies
70
Superficial thrombophlebitis symptoms
Pain at site of superficial veins, erythema, warmth
Can see it and palpate effected vein!
71
PE findings of thrombophlebitis
Palpable tender superficial veins, erythema and warmth in surrounding area, minimal swelling at site; no significant extremity edema
72
DVT PE findings
Unilaterally LE edema or increase in diameter, calf or thigh tenderness, warmth, erythema, palpable cord, superficial venous dilation, tenderness along vein course, skin necrosis or livedo reticularis
73
What is livedo reticularis?
DVT finding; when the skin has a lacy modeled appearance to it
74
Phlegmasia Cerulea Dolens Si/Sx/PE findings
Sudden severe leg pain* swelling, edema, firm (not soft to palpate), cyanosis, venous gangrene, compartment syndrome, arterial compromise
75
What is Phlegmasia Cerulea Dolens followed by?
Circulatory collapse and shock, surgical emergency! Risk of limb and life loss
76
Differential diagnoses for VTE
Superficial thrombophlebitis, muscle strain, tear, twisting injury to leg, lymphangitis or lymph obstruction, Baker’s cyst, cellulitis, knee abnormality, Unknown etiology of edema
77
What diagnostic studies are used for VTE?
Risk assessment tool (well’s score for DVT), D-dimer, compression ultrasonography, venous duplex imaging (serial imaging), contract venography
78
What is the diagnostic study of choice for VTE?
Compression ultrasound
79
Wells Score <1 risk for DVT
5%
80
Wells Score 1-2 risk for DVT
17%
81
Wells score >2 risk for DVT
53%
82
What is a D-dimer?
Degradation product of cross-linked fibrin, sensitive test (82-95%) but not specific (40-68%)
83
When can a D-dimer be elevated?
In states of inflammation
84
When is D-dimer used for DVT diagnosis?
Only use it in low probability patients when ruling out DVT
85
What does venous ultrasonography rely on?
Loss of vein compressibility, thrombus can be directly visualized
86
What is a venography?
Contrast venography, MR, CT or venogram
| Not commonly performed for DVT diagnosis, end of the line test
87
What else can be used to rule out a DVT?
Venous duplex
88
If pt is at a low risk of VTE diagnosis,
Negative D-dimer: rules out DVT
Positive D-dimer: obtain compression US
89
If pt has a moderate risk of VTE:
Positive compression US: Positive for DVT
| Negative compression US: repeat in 1 week
If repeat -, rules out DVT
90
If pt has a high risk for VTE
Positive compression US: positive for DVT
Negative compression US: venography
Negative venography: rules out DVT
91
What is the treatment for superficial thrombophlebitis?
Local heat: warm compresses
Nonsteroidal anti-inflammatories
Remove catheter if in place
92
What is the treatment for superficial thrombophlebitis if its an axial vein near proximal junction?
Example:” saphenofemoral junction
May require serial ultrasound imaging to keep an eye on
93
How long will it take for inflammation to subside for superficial thrombophlebitis?
1-2 weeks; firm cord may remain longer
94
What is the treatment for DVT?
Monitor!
Anticoagulation**
Thrombolysis or thrombectomy
IVC filter placement: limited indications
Compression therapy: compression stocking
95
What anticoags are used for DVT treatment?
IV heparin bridge to Warfarin (bridge for 5-7 days)
*SUBQ LMWH or Fondaparinux and bridge to Warfarin
Oral anticoags: Pradaxa, Xarelto*, Eliquis
96
What oral anticoags are used for DVT?
Pradaxa, Xarelto, Eliquis
97
What is the duration of anticoag therapy for DVT?
If it was a provoked DVT with transient risk factor” 3-12 mos
If unprovoked, recurrent, or provoked with persistent risk factors: indefinitely
98
If DVT occurs in a calf vein, and its asymptomatic, what’s the treatment?
Observation serial US weekly for 2+weeks, if thrombus extension or si: anticoagulate
99
If DVT occurs in calf vein and is symptomatic, what is the treatment?
Anticoags
100
If the DVT is in a proximal vein, what is the treatment?
Anticoags
101
What are the indications for IVC filter treatment (DVT)?
1. Active bleeding precludes anticoags
2. Recurrent venous thrombosis despite intensive anticoags
3. High risk pts who are next candidates for fibrinolysis
102
What are some complications of IVC filters for DVT?
Caval thrombosis, double the DVT rate, migration of filter (can go to RA)
103
Indications for evaluation for a VTE
Unprovoked VTE in age <50yrs, unprovoked VTE w/ family he, recurrent VTE, thrombosis in unusual vascular bed (portal, hepatic, mesenteric), H1 of Warfarin skin necrosis
104
Monitoring for complications of DVT
May need serial venous duplex studies, periodic PE, educate pt of si/sx of complications!
105
Monitoring for complications of anticoagulants
Warfarin: PT/INR 2-3
LMWH, Factor Xa and DTI: no lab monitoring
Educate pt on si/sx of bleeding
106
VTE mechanical prophylaxis
Early mobilization, pneumatic compression stockings, graduated compression stockings
107
VTE medication prophylaxis
LMWH: Lovenox, Fragmin 40 units/day
Low dose unfractionated heparin
Fondaparinux (Arixtra)
108
VTE summary
Assess likelihood prior to ordering D-dimer vs imaging, proved treatmetn immediately with SUBQ heparin, LMWH, or Fondaparinux, Warfarin treatment 3-12 mos vs indefinite
109
Upper extremity DVT
Not as common, anatomic/mechanical obstruction or stenosis
110
Causes of UE DVT
Catheter related thrombosis, Paget-Schroetter syndrome, Thoracic outlet syndrome, tumor
111
When should someone with an UE DVT see a vascular surgeon?
Always!
112
What is Paget-Schroetter syndrome?
Effort induced thrombosis. Young men with repetitive motions over and over again (practicing violin) can cause clavicular impingement
113
What is thoracic outlet syndrome?
Area between 1st rib and clavicle is compressed, depresses the subclavian vein
114
Chronic venous disorders
Includes the full spectrum or morphological and functional abnormalities of venous system
115
Chronic venous disease
Morphological or functional abnormalities (venous valvular incompetence) are present of long duration and manifested as si and or sx indicating the need for treatment and/or further investigations
116
Chronic venous insufficiency or Venous Stasis Disease
Pts with chronic venous disease who display more advanced clinical signs, such as significant edema, skin changes, or ulceration
117
Vein A&P
Thin walled, distensible, collect blood from tissue and return it to the heart, low pressure system
118
What does the venous system rely on?
The pumping action of skeletal muscles to move blood forward
AND
Venous valve to prevent retrograde flow
119
Chronic venous disease pathophys
Inadequate muscle pump function, incompetent venous valves (reflux), elevated venous pressure
120
Chronic venous insufficiency pathophys
Venous blood pools in deep veins, tissue congestion/edema -> tissue ischemia and tissue nutritional impairment
Causes necrosis or SUBQ fat, skin atrophy
121
What causes the brown pigmentation in chronic venous insufficiency?
Hemosiderin deposits from breakdown of RBCs
122
Telangiectasia develops in how many adults
50-66%
123
Varicose veins develop in how many adults
10-30%
124
Chronic venous insufficiency prevalence
0.2-5%
125
What is telangiectasia?
Dilated small superficial veins, most prevalent chronic venous disease
F>M
126
What are varicose veins?
Dilated, tortuous superficial veins (>3mm in size)
127
What vein is mostly involved in varicose veins?
Greater saphenous vein and its tributaries
128
What are some severe symptoms of chronic venous disease/insufficiency
Edema, skin changes, ulceration, recurrent and chronic nature, commonly associated with chronic venous reflux
129
Risk factors for chronic venous disease
Advancing age, family he, ligamentous laxity (hernia, flat feet), prolonged standing, increased BMI, smoking, sedentary lifestyle, LE trauma, prior venous thrombosis, pregnancy
130
Chronic venous disease progression
Appears related to extent of venous valvular incompetence
131
Chronic venous disease clinical signs
Leg pain or “aching” and fatigue, leg heaviness, leg swelling, skin tightness, muscle cramps, skin irritation or itching, non-healing wounds, skin discoloration and thickening, bleeding from varicosity or spider vein
132
When do the clinical signs of chronic venous disease seem to be the worst?
At the end of the day or after standing for a prolonged time
133
Chronic venous disease PE findings
Pitting edema, edema often spares the floor or has NO dorsal pedal hump* venous dilation, skin changes, lipodermastosclerosis, skin discoloration, ulceration
134
What is lipodermastosclerosis?
Fibrosis dermatitis of SUBQ tissue, seen in chronic venous disease
135
What types of venous dilation will be seen on PE of chronic venous disease?
Varicose veins or telangiectasia
136
Dilated small superficial veins
Telangiectasia
137
Chronic venous insufficiency PE findings
Edema, skin changes: stasis dermatitis, brawny discoloration, liposclerosis, ulceration
138
What can be seen with stasis dermatitis?
Pruritus, hemosiderin deposition, erythema, scaling
139
Venous ulcers found in chronic venous insufficiency look like what?
At or above the ankle, can be deeper, irregular borders, surrounding induration, base red in color, drainage can be significant
140
What diagnostic studies can be used for varicose veins?
Venous duplex (ultrasound)
141
What are we evaluating for when using an ultrasound on varicose veins?
Venous reflux in greater saphenous vein and in deep system
| Retrograde flow > than 0.5 second duration is positive
142
How do you make the diagnosis of chronic venous disease?
Presence of typical symptoms, possible presence of dilated superficial veins, presence of skin changes, edema, or ulcers, confirmation with venous duplex study
143
What is the treatment for chronic venous disease?
*compression therapy* leg elevation, exercise, skin care
144
How much compression do the compression stockings apply?
20-30 mmHg of compression
145
Compression wraps
ACE wraps are NOT adequate, use a multilayer wrap or a Unna boot
146
What would be initial conservative management for chronic venous disease?
Stasis dermatitis: respond to dermatologic agents (steroid therapy)
Venous ulceration: compression therapy and wound care (specialist)
147
When should antibiotics be used for chronic venous disease?
With cellulitis or an infected ulcer
148
Systemic antibiotics should be used for chronic venous disease when
Local heat and tenderness, increasing erythema of the surrounding skin, lymphangitis (red streaks traversing up the limb), rapid increase in size of ulcer, fever
149
Indications for surgical intervention- chronic venous disease
Failure of conservative therapy, bleeding from varicosities or telangiectasias, phlebitis or thrombosis or superficial veins
150
What are the ablation techniques for chronic venous disease?
Chemical, mechanical and thermal endovenous ablation
151
Sclerotherapy
Inject sclerosis get agent into varicosed vein, obliterate/permanent fibrosis of involved veins
152
Chemical ablation/sclerotherapy indications
Small veins <4mm diameter
153
Risks and f/u with sclerotherapy
Phlebitis, tissue necrosis, infection are risks involved
| Follow with compression
154
Mechanical ablation of varicose veins
Phlebectomy or ligation, stripping rarely performed
155
What are the two types of thermal ablation?
1. Endovenous laser ablation (ELA)
| 2. Radiofrequency ablation (RFA)
156
When should saphenous vein ablation be considered?
If GSV reflux with normal deep system
| -has high success and low complications
157
What are the risks for a saphenous vein ablation?
Ecchymosis, discomfort, superficial phlebitis, nerve damage, skin burns, DVT, PE
158
When should you refer someone with chronic venous disease to vascular?
Significant saphenous vein reflux, open wounds: should be dealt with by specialists, or if cosmetic concerns
159
Prognosis of chronic venous disease
Varicose veins: surgical correction of reflux 85-90% 5 year success rate
Chronic venous insufficiency: often recurrent complications, noncompliance with compression stocking use
160
Is the lymphatic system low or high pressure?
Low pressure
161
What is lymphatic flow facilitated by?
Vessel contraction, skeletal muscle contraction and unidirectional vale’s
162
Lymphedema
Interstitial Collection of protein-rich fluid due to disruption of lymphatic flow
163
Etiology of lymphedema
1. Congenital malformation
2. Damage to lymphatic vessels/lymph nodes
- reduction of number of available channels
- obstruction of available lymphatic channels
164
Primary lymphedema
Congenital developmental abnormalities
165
Secondary lymphedema
Inflammatory or mechanical obstruction
166
Congenital lymphedema is what age group?
Birth to 2 years old
167
Lymphedema praecox
Onset during puberty or pregnancy prior to age 35
168
Lymphedema tarda
Onset after age 35
169
What is the most common cause worldwide of lymphedema?
Filariasis due to infection by the nematode Wuchereria Bancrofti
170
Most common cause of lymphedema in developed world?
Malignancy or treatment for malignancy
171
Risk factors for lymphedema?
Cancer and cancer treatment* hereditary syndromes (Turners, Noonan syndromes), older age, obesity, inflammatory discovers, arthritis, infeciton
172
Extremity swelling si/sx of lymphedema
Usually insidious, may affect only portion of limb initially, may include corresponding quadrant of trunk, non-pitting, often involves dorsal foot, often unilaterally
173
Si/sx of lymphedema
Aching, pain, or discomfort of the limb, heaviness or tightness of limb, skin changes, restricted ROM
174
Lymphedema PE findings
Non-pitting edema, squaring of toes, *dorsal pedis hump* exaggerated skin folds near ankle
175
Advanced PE findings of lymphedema
Woody appearance, dermal thickening, skin hyperkeratotic, acanthosis and verrucous overgrowth
176
What is the Stemmer sign?
Thickened skin fold at base of 2nd toe or 2nd finger
| Positive sign: inability to lift skin of affected limb
177
Diagnostic studies for lymphedema
Lymphoscintigraphy: flow of fluid from skin to lymph nodes, CT, MRI/MR lymphography, ultrasound to rule out DVT or identify mass
178
In endemic areas with lymphedema, what do you test for?
Filarial infection, circulation filarial antigen (CFA), blood smears, PCR, antifilarial antibody tests, detect worms on ultrasound
179
Findings suggestive of lymphedema
Localized edema, slow and progressive swelling, hx of cancer treatment or trauma, absences of generalized edema, cutaneous and SUBQ thickening, non-pitting edema
180
Diagnosis essentials for lymphedema
Painless persistent edema of one or both lower extremities: primary in young women
Pitting or non-pitting edema without ulceration, varicosities, or stasis pigmentation
181
Lymphedema treatment
*compression* intermittent elevation, good hygiene
182
Prognosis of lymphedema
No cure, long-term prognosis: avoidance of recurrent cellulitis, associated conditions
183
Tunica externa
Adventitia, connective tissue
184
Tunica media
Thickest layer, elastic fiber, connective tissue, and vascular smooth muscle
185
Tunica intima
Thinnest layer, simple squamous endothelial cells
186
Layers of artery from out to in
Tunica: adventitia, media, intima
187
What are the 3 types of aneurysms?
Fusiform, saccular, pseudoaneurysm
188
Fusiform aneurysm
Affects entire circumference of segment of vessel
189
Saccular aneurysm
Involves only a portion of the circumference resulting in outpouching of wall
190
Psuedoaneurysm
Intimal and medial layers of artery are disrupted, tailgated segment is lined by adventitia only (occasionally clot)
191
Aortic aneurysm etiology
Degenerative diseases (cystic medial necrosis), atherosclerosis, inherited or developmental diseases, infections (syphilis), vasculitis (Takayasu’s arteritis, trauma
192
What is cystic medial necrosis?
Degeneration of collage and elastic fibers, effects the proximal aorta, causing circumferential weakness and dilation
193
What type of inherited or developmental diseases put you at risk for a aortic aneurysm?
Marfan syndrome, Ehlers-Danlos syndrome, family hx
194
What types of aneurysms does cystic medial necrosis cause?
Fusiform aneurysms
195
Marfan syndrome
Connective tissue disorder, autosomal dominant, broad range of clinical severity, long extremities with joint laxity
196
Ehlers-Danlos Syndrome
Genetic disorder of connective tissue, causes skin hyperextensibility, joint hyper mobility, and tissue fragility
197
Locations of thoracic aortic aneurysms
Ascending aortic aneurysm: 60%
Aortic arch: 10%
Descending aorta: 40%
Thoracoabdominal: 10%
198
Thoracic aortic aneurysms
Less common than AAA, cystic medial necrosis is most common with ascension aortic aneurysms
199
What is most common with aneurysms of the aortic arch and descending thoracic aorta?
Atherosclerosis
200
Epidemiology of thoracic aortic aneurysms
6th and 7th decade, males 2-4x more likely, >60% have HTN, 20-25% with large thoracic AA also have AAA
201
CXR for Thoracic AA
May be first test to suggest diagnosis*
| Wide mediastinum, tracheal deviation
202
Symptoms of TAA
Often asymptomatic, chest back flank or abdominal pain, cold foot, HF from aortic root dilation, ascending and arch aneurysm can erode into mediastinum
203
What symptoms can be seen if the TAA erodes into the mediastinum?
Hoarseness, wheezing, cough, hemoptysis, dysphasia
204
PE of TAA
Usually normal, if beginning to rupture: tachycardia hypotension
Rarely hoarseness, wheezing, rarely sings of HF; decreased breath sounds at lung bases, crackles with pulmonary auscultation, LE swelling
205
Imaging options for diagnosis of TAA
Echocardiography: proximal ascending aorta and descending thoracic aorta, CT scan, MRI less commonly used
206
Treatment fo TAA
B-adrenergic blockers particularly with Marfan Syndrome, control HTN with ACEI/ARBs
207
When is surgery an indication for TAA?
>5.5cm ascending TAA
| >6.5cm descending TAA
208
What is endovascular repair of a TAA?
Placement of a stent graft
209
AAA
Definition: >3cm, concern for rupture when >5cm
210
Risk factors in development of AAA
Advancing age, male, cigarette smoking, HTN, hyperdyslipidemia, Caucasian, family Hx, presence of other aneurysms, atherosclerosis
211
Symptoms of AAA
Most asymptomatic; abdominal back flank or groin pain, sudden cold or blue distal extremities
212
PE of an AAA
Rarely palpable one xam, pulsating abdominal mass suggests rupture, if ruptured: distention and tenderness, ecchymosis can occur if ruptured
213
Cullen’s sign and Grey Turner’s sign
Ecchymosis that occurs if an AAA ruptures
214
Screening pts who are at risk for AAA
Abdominal ultrasound, men 65-74 with hx of smoking, siblings or offspring of persons with AAA, individuals with thoracic aortic or peripheral arterial aneurysms
215
Diagnostic of choice for AAA
Abdominal ultrasound
216
Treatment for AAA
Surveillance until >5-5.5cm
| Open vs endovascular repair
217
What decides if the surgery for AAA will be open vs endovascular?
Anatomy and comorbidities
218
Aortic dissection etiology
Tear in the aortic intima, blood dissects into the media, intima separates from the surrounding media, false lumen in created and circulation in the affected are can become disrupted
219
Aortic dissection risk factors?
*systemic HTN* atherosclerosis, aortic aneurysm, inflammatory disease, collagen disorders, biscuit aortic valve, aortic coarctation
220
Aortic dissection signs and symptoms
*severe sharp or tearing chest pain in posterior chest or back, sudden onset radiating into anterior chest or neck*
HTN, wide pulse pressure* abdominal pain, syncope, peripheral pulses may be diminished or unequal
221
Other si/sx of aortic dissection
Hemiplegia or paralysis or LEs, diastolic murmur May develop (aortic regurg), HF, cardiac tamponade, intestinal ischemia, limb ischemia
222
Si/sx of dissection occurs in the ascending aorta
Acute aortic valve regurg, Acute MI, cardiac tamponade, hemothroax and exsanguination, variation in SBP between arms, neurologic deficits, stroke, Horner syndrome, vocal cord paralysis
223
Si/sx of dissecting aorta if its in descending aorta
Chest or back pain, abrupt onset of pain, migration pain, HTN, hypotension/shock, pulse deficit, spinal cord ischemia, ischemic peripheral neuropathy
224
Diagnostic studies for aortic dissection
No blood testing, just imaging!
225
Imaging studies for aortic dissection: identify the presence and associated features
Involvement of ascending aorta, extent of dissection, sites of entry and reentry, thrombus in false lumen, branch vessel or CA involvement, aortic valve regurg, PE
226
Imaging studies for aortic dissection
Chest radiograph, echocardiogram, CT commonly used, MRI, aortography
227
Essentials of diagnosis for aortic dissection
Sudden searing chest pain w/radiation to back, abdomen or neck in HTN pt, widened mediastinum on chest radiograph, pulse discrepancy in extremities, acute aortic regurg can develop
228
What is the standford classification of aortic dissection?
Type A: ascending aorta
| Type b: descending, distal to left subclavian
229
DeBakey aortic dissection classification
Type 1: ascending aorta, aortic arch, descending
Type 2: only ascending
Type 3: only descending
230
Treatment of aortic dissection
Considered surgical emergencies
231
Initial management for aortic dissection
HR and BP monitoring, pain reliever with IV morphine, reduction of SBP with BB, ICU level care
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What are they types of surgical management for aortic dissection?
Endovascular repair and open surgical repair
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Long term management and follow up for aortic dissection
1. Medical therapy: minimize aortic wall shear stress
2. Serial Imaging
3. Reoperation when indicated
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What medical therapy is used for long term management of aortic dissection?
Lifelong BB, goals BP less than 120/80, avoid strenuous activity
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How often should imaging be done for someone with aortic dissection?
3 6 and 12 months, then ever 1-2 years
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When is reoperation indicated for aortic dissection?
Extension or recurrence of the dissection, aneurysm formation, leakage at anastomoses or stent sites
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Prognosis of aortic dissection
Mortality untreated type A: 1% per hour for 72 hours, over 90% at 3mos
Untreated complicated type B: high mortality
