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Clin Med 2 > Tachycardia, Venous disease, Arterial disease > Flashcards

Tachycardia, Venous disease, Arterial disease Flashcards

1
Q

Tachycardia is defined as what?

A

HR >100bpm

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2
Q

What is narrow complex tachycardia?

A

Sinus tachycardia, supraventricular tachycardia, AFIB, aflutter

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3
Q

What is wide complex tachycardia?

A

Ventricular tachycardia (Torsade de Pointe), ventricular fibrillation

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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

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5
Q

What are some symptoms of sinus tachycardia?

A

Asymptomatic, heart palpitations, SOB (especially with exertion)

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6
Q

Symptoms of sinus tachycardia in pts with heart disease (CAD)

A

Heart palpitations, SOB, chest discomfort, lightheadedness, fatigue

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7
Q

How do you treat sinus tachycardia?

A

Treat underlying cause

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8
Q

If pt has sinus tachycardia from dehydration, treat how?

A

IV fluid

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9
Q

If patient has sinus tachycardia due to pain how do you treat it?

A

Pain meds

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10
Q

If patient has sinus tachycardia from a PE, how do you treat?

A

Anticoagulation therapy

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11
Q

How do you treat sinus tachycardia if its from sepsis?

A

Treat the source-Abx

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12
Q

How do you treat sinus tachycardia if its from anxiety?

A

Consider anxiolytics

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13
Q

Supraventricular tachycardia

A

Regular, rapid rhythm, narrow complex (originates above the ventricle), no discernible p waves

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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)

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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

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16
Q

SVT

A

Begins suddenly and ends suddenly, often self-limiting

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17
Q

Management of persistent SVT for unstable pts

A

Vagal maneuvers, then in unsuccessful immediate DC cardioversion

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18
Q

Management of persistent SVT for a stable pt

A

Vagal maneuvers, carotid massage, Adenosine, CCB or BB

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19
Q

What is the dosing for Adenosine (persistent SVT)

A

Initially dose 6mg IVP, then 12mg IVP, then 12mg IVP

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20
Q

What do you do with patients who have frequent attacks of SVT?

A

Consult EP -> confirm aberrant pathway -> radiofrequency catheter ablation

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21
Q

What is a direct current (DC) cardioversion

A

Medical procedure converting cardiac arrhythmias to NSR using electricity

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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

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23
Q

Sustained ventricular tachycardia

A

Life threatening, fast wide complex rhythm, frequently associated with syncope

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24
Q

What is the usual rate for sustained ventricular tachycardia?

A

160-240bpm with a duration of atleast 20 seconds

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25
Q

What is sustained ventricular tachycardia a frequent complication of?

A

MI and dilated CMP

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26
Q

Symptoms of sustained ventricular tachycardia

A

Heart palpitations, lightheadedness, chest pain, SOB, diaphoresis (drenching sweat), near syncope or syncope, sustained LOC, pulseless electrical activity (death)

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27
Q

Treatment of acute ventricular tachycardia if pulseless

A

CPR, Defibrillation, epinephrine

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28
Q

What is the treatment of acute ventricular tachycardia is the pulse is present?

A

If it causes hypotension, HF, myocardial ischemia-> synchronized DC cardioversion
If pt stable ->Amiodarone
ICDs

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29
Q

If patient is stable and has acute ventricular tachycardia, what is the treatment?

A

Amiodarone 150mg IV bolus followed by continuous infusion

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30
Q

What is triggered by hypokalemia, hypomagnesemia, and drugs that prolong the QTc?

A

Torsades de pointes (type of VTACH)

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31
Q

What abxs prolong QTc?

A

Macrolides: Azithromycin, Quinolones: Levofloxacin, Ciprofloxacin

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32
Q

Which antidepressants cause prolong QTc?

A

Citalopram, Tricyclics antidepressants

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33
Q

What other drug classes cause prolongation of QTc?

A

Antipsychotics

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34
Q

What is the treatment of Torsades if pt is unstable?

A

Prompt defibrillation

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35
Q

What is the treatment of Torsades if the pt is stable?

A

First Line: IV Magnesium

Temporary transvenous overdrive pacing if no response to magnesium

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36
Q

Ventricular fibrillation is often associated with what?

A

Severe CAD and caused by acute MI (ACS)

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37
Q

Characteristics of ventricular fibrillation

A

Sudden death can be initial manifestation of coronary disease in 20% pts, patients are pulseless and unresponsive

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38
Q

Patients are pulseless and unresponsive to what type of tachycardia?

A

Ventricular fibrillation

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39
Q

What are some causes of ventricular fibrillation?

A

MI, HF, hypoxemia or hyercapnia, hypotension/shock, electrolyte imbalances, stimulants (drugs, caffeine), often preceded by VTACH

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40
Q

What is ventricular fibrillation often preceded by?

A

VTACH

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41
Q

What conditions are associated with ventricular fibrillation?

A

LVH, HOCM, CHF, aortic stenosis (AS), Brugada syndrome

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42
Q

What is the treatment of ventricular fibrillation?

A

CPR, defibrillation, if pulse is regained-> consider coronary ateriography to view and treat CAD

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43
Q

What can be used for long term management of ventricular fibrillation?

A

Implantable cardioverter-defibrillator

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44
Q

What is another name for a coronary arteriography?

A

Cardiac catheterization

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45
Q

What types of venous thromboembolisms can occur?

A

DVT, superficial thrombophlebitis, and phlebitis

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46
Q

What are examples of chronic venous disorders?

A

Varicose veins, chronic venous insufficiency (CVI)

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47
Q

What are examples of the deep veins in the UE?

A

Subclavian, axillary, brachial, ulnar, radial, interosseous veins

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48
Q

What are the superficial veins of the UE?

A

Cephalic, basilic, median cubical, accessory cephalic

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49
Q

What are the superficial LE veins?

A

Greater saphenous, lesser saphenous, non-saphenous

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50
Q

What are the deep LE veins?

A

Iliac, common femoral, deep femoral, femoral, popliteal, deep calf

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51
Q

Where can DVTs take place?

A

Upper extremity vein thrombosis (UEDVT)
Proximal vein thrombosis
Distal Erin thrombosis

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52
Q

What veins are effected in proximal vein thrombosis?

A

Popliteal, femoral, or iliac veins

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53
Q

Where would a distal vein thrombosis take place?

A

In calf veins

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54
Q

What is lymphedema?

A

Local fluid retention, lymph or tissue swelling

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55
Q

Phlebitis

A

Inflammation of vein, red and warm

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56
Q

What makes up Virchow’s triad?

A

Stasis, Endothelial trauma, Hypercoagulable state

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57
Q

What are some anatomical risk factors for venous thromboembolism?

A

Mae-Turner syndrome, IVC abnormalities

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58
Q

Half of pts with DVT will have what?

A

Long-term complications

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59
Q

What are some risk factors for venous thromboembolism?

A

Previous VTE, malignancy, surgery, trauma, pregnancy, drugs, immobilization, recent hospitalization, anti phospholipid antibodies, CVD risk factors

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60
Q

What is anti phospholipid antibodies associated with?

A

Associated with Lupus, the body makes antibodies against phospholipids.

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61
Q

What cardiovascular risk factors are risk factors for VTE?

A

Obesity, smoking age

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62
Q

What are some hereditary risk factors for VTE?

A

Factor 5 Leiden mutation, prothrombin gene mutation, protein S and C deficiency, anti-thrombin deficiency, dysfibrinogenemia

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63
Q

What can cause thrombophlebitis?

A

Same risk factors for VTE, peripheral IV catheter placement

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64
Q

What types of embolizations are you at risk for with VTE?

A

Pulmonary embolism, stroke or arterial embolism (PFO or ASD)

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65
Q

What is PFO?

A

Patent foramen ovale, there is a hole in the atria and a clot can easily cross from venous to arterial side

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66
Q

What is the most severe type of DVT?

A

Phlegmasia Cerulea Dolens, get significant pain, swelling, and the leg becomes blue and cyanotic

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67
Q

What can be seen in postphlebitic syndrome?

A

Swelling, pain, discoloration, scaling

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68
Q

What is a thrombus extension?

A

A superior venous thromboembolism that is close to deep system. Need to follow it closely

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69
Q

Classic DVT symptoms

A

Pain, swelling, erythema *severity varies

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70
Q

Superficial thrombophlebitis symptoms

A

Pain at site of superficial veins, erythema, warmth

Can see it and palpate effected vein!

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71
Q

PE findings of thrombophlebitis

A

Palpable tender superficial veins, erythema and warmth in surrounding area, minimal swelling at site; no significant extremity edema

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72
Q

DVT PE findings

A

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

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73
Q

What is livedo reticularis?

A

DVT finding; when the skin has a lacy modeled appearance to it

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74
Q

Phlegmasia Cerulea Dolens Si/Sx/PE findings

A

Sudden severe leg pain* swelling, edema, firm (not soft to palpate), cyanosis, venous gangrene, compartment syndrome, arterial compromise

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75
Q

What is Phlegmasia Cerulea Dolens followed by?

A

Circulatory collapse and shock, surgical emergency! Risk of limb and life loss

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76
Q

Differential diagnoses for VTE

A

Superficial thrombophlebitis, muscle strain, tear, twisting injury to leg, lymphangitis or lymph obstruction, Baker’s cyst, cellulitis, knee abnormality, Unknown etiology of edema

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77
Q

What diagnostic studies are used for VTE?

A

Risk assessment tool (well’s score for DVT), D-dimer, compression ultrasonography, venous duplex imaging (serial imaging), contract venography

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78
Q

What is the diagnostic study of choice for VTE?

A

Compression ultrasound

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79
Q

Wells Score <1 risk for DVT

A

5%

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80
Q

Wells Score 1-2 risk for DVT

A

17%

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81
Q

Wells score >2 risk for DVT

A

53%

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82
Q

What is a D-dimer?

A

Degradation product of cross-linked fibrin, sensitive test (82-95%) but not specific (40-68%)

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83
Q

When can a D-dimer be elevated?

A

In states of inflammation

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84
Q

When is D-dimer used for DVT diagnosis?

A

Only use it in low probability patients when ruling out DVT

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85
Q

What does venous ultrasonography rely on?

A

Loss of vein compressibility, thrombus can be directly visualized

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86
Q

What is a venography?

A

Contrast venography, MR, CT or venogram

Not commonly performed for DVT diagnosis, end of the line test

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87
Q

What else can be used to rule out a DVT?

A

Venous duplex

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88
Q

If pt is at a low risk of VTE diagnosis,

A

Negative D-dimer: rules out DVT

Positive D-dimer: obtain compression US

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89
Q

If pt has a moderate risk of VTE:

A

Positive compression US: Positive for DVT

Negative compression US: repeat in 1 week
If repeat -, rules out DVT

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90
Q

If pt has a high risk for VTE

A

Positive compression US: positive for DVT

Negative compression US: venography

Negative venography: rules out DVT

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91
Q

What is the treatment for superficial thrombophlebitis?

A

Local heat: warm compresses
Nonsteroidal anti-inflammatories
Remove catheter if in place

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92
Q

What is the treatment for superficial thrombophlebitis if its an axial vein near proximal junction?

A

Example:” saphenofemoral junction

May require serial ultrasound imaging to keep an eye on

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93
Q

How long will it take for inflammation to subside for superficial thrombophlebitis?

A

1-2 weeks; firm cord may remain longer

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94
Q

What is the treatment for DVT?

A

Monitor!
Anticoagulation**
Thrombolysis or thrombectomy
IVC filter placement: limited indications
Compression therapy: compression stocking

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95
Q

What anticoags are used for DVT treatment?

A

IV heparin bridge to Warfarin (bridge for 5-7 days)

*SUBQ LMWH or Fondaparinux and bridge to Warfarin

Oral anticoags: Pradaxa, Xarelto*, Eliquis

96
Q

What oral anticoags are used for DVT?

A

Pradaxa, Xarelto, Eliquis

97
Q

What is the duration of anticoag therapy for DVT?

A

If it was a provoked DVT with transient risk factor” 3-12 mos

If unprovoked, recurrent, or provoked with persistent risk factors: indefinitely

98
Q

If DVT occurs in a calf vein, and its asymptomatic, what’s the treatment?

A

Observation serial US weekly for 2+weeks, if thrombus extension or si: anticoagulate

99
Q

If DVT occurs in calf vein and is symptomatic, what is the treatment?

A

Anticoags

100
Q

If the DVT is in a proximal vein, what is the treatment?

A

Anticoags

101
Q

What are the indications for IVC filter treatment (DVT)?

A
  1. Active bleeding precludes anticoags
  2. Recurrent venous thrombosis despite intensive anticoags
  3. High risk pts who are next candidates for fibrinolysis
102
Q

What are some complications of IVC filters for DVT?

A

Caval thrombosis, double the DVT rate, migration of filter (can go to RA)

103
Q

Indications for evaluation for a VTE

A

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
Q

Monitoring for complications of DVT

A

May need serial venous duplex studies, periodic PE, educate pt of si/sx of complications!

105
Q

Monitoring for complications of anticoagulants

A

Warfarin: PT/INR 2-3
LMWH, Factor Xa and DTI: no lab monitoring
Educate pt on si/sx of bleeding

106
Q

VTE mechanical prophylaxis

A

Early mobilization, pneumatic compression stockings, graduated compression stockings

107
Q

VTE medication prophylaxis

A

LMWH: Lovenox, Fragmin 40 units/day
Low dose unfractionated heparin
Fondaparinux (Arixtra)

108
Q

VTE summary

A

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
Q

Upper extremity DVT

A

Not as common, anatomic/mechanical obstruction or stenosis

110
Q

Causes of UE DVT

A

Catheter related thrombosis, Paget-Schroetter syndrome, Thoracic outlet syndrome, tumor

111
Q

When should someone with an UE DVT see a vascular surgeon?

A

Always!

112
Q

What is Paget-Schroetter syndrome?

A

Effort induced thrombosis. Young men with repetitive motions over and over again (practicing violin) can cause clavicular impingement

113
Q

What is thoracic outlet syndrome?

A

Area between 1st rib and clavicle is compressed, depresses the subclavian vein

114
Q

Chronic venous disorders

A

Includes the full spectrum or morphological and functional abnormalities of venous system

115
Q

Chronic venous disease

A

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
Q

Chronic venous insufficiency or Venous Stasis Disease

A

Pts with chronic venous disease who display more advanced clinical signs, such as significant edema, skin changes, or ulceration

117
Q

Vein A&P

A

Thin walled, distensible, collect blood from tissue and return it to the heart, low pressure system

118
Q

What does the venous system rely on?

A

The pumping action of skeletal muscles to move blood forward
AND
Venous valve to prevent retrograde flow

119
Q

Chronic venous disease pathophys

A

Inadequate muscle pump function, incompetent venous valves (reflux), elevated venous pressure

120
Q

Chronic venous insufficiency pathophys

A

Venous blood pools in deep veins, tissue congestion/edema -> tissue ischemia and tissue nutritional impairment
Causes necrosis or SUBQ fat, skin atrophy

121
Q

What causes the brown pigmentation in chronic venous insufficiency?

A

Hemosiderin deposits from breakdown of RBCs

122
Q

Telangiectasia develops in how many adults

A

50-66%

123
Q

Varicose veins develop in how many adults

A

10-30%

124
Q

Chronic venous insufficiency prevalence

A

0.2-5%

125
Q

What is telangiectasia?

A

Dilated small superficial veins, most prevalent chronic venous disease
F>M

126
Q

What are varicose veins?

A

Dilated, tortuous superficial veins (>3mm in size)

127
Q

What vein is mostly involved in varicose veins?

A

Greater saphenous vein and its tributaries

128
Q

What are some severe symptoms of chronic venous disease/insufficiency

A

Edema, skin changes, ulceration, recurrent and chronic nature, commonly associated with chronic venous reflux

129
Q

Risk factors for chronic venous disease

A

Advancing age, family he, ligamentous laxity (hernia, flat feet), prolonged standing, increased BMI, smoking, sedentary lifestyle, LE trauma, prior venous thrombosis, pregnancy

130
Q

Chronic venous disease progression

A

Appears related to extent of venous valvular incompetence

131
Q

Chronic venous disease clinical signs

A

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
Q

When do the clinical signs of chronic venous disease seem to be the worst?

A

At the end of the day or after standing for a prolonged time

133
Q

Chronic venous disease PE findings

A

Pitting edema, edema often spares the floor or has NO dorsal pedal hump* venous dilation, skin changes, lipodermastosclerosis, skin discoloration, ulceration

134
Q

What is lipodermastosclerosis?

A

Fibrosis dermatitis of SUBQ tissue, seen in chronic venous disease

135
Q

What types of venous dilation will be seen on PE of chronic venous disease?

A

Varicose veins or telangiectasia

136
Q

Dilated small superficial veins

A

Telangiectasia

137
Q

Chronic venous insufficiency PE findings

A

Edema, skin changes: stasis dermatitis, brawny discoloration, liposclerosis, ulceration

138
Q

What can be seen with stasis dermatitis?

A

Pruritus, hemosiderin deposition, erythema, scaling

139
Q

Venous ulcers found in chronic venous insufficiency look like what?

A

At or above the ankle, can be deeper, irregular borders, surrounding induration, base red in color, drainage can be significant

140
Q

What diagnostic studies can be used for varicose veins?

A

Venous duplex (ultrasound)

141
Q

What are we evaluating for when using an ultrasound on varicose veins?

A

Venous reflux in greater saphenous vein and in deep system

Retrograde flow > than 0.5 second duration is positive

142
Q

How do you make the diagnosis of chronic venous disease?

A

Presence of typical symptoms, possible presence of dilated superficial veins, presence of skin changes, edema, or ulcers, confirmation with venous duplex study

143
Q

What is the treatment for chronic venous disease?

A

compression therapy leg elevation, exercise, skin care

144
Q

How much compression do the compression stockings apply?

A

20-30 mmHg of compression

145
Q

Compression wraps

A

ACE wraps are NOT adequate, use a multilayer wrap or a Unna boot

146
Q

What would be initial conservative management for chronic venous disease?

A

Stasis dermatitis: respond to dermatologic agents (steroid therapy)
Venous ulceration: compression therapy and wound care (specialist)

147
Q

When should antibiotics be used for chronic venous disease?

A

With cellulitis or an infected ulcer

148
Q

Systemic antibiotics should be used for chronic venous disease when

A

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
Q

Indications for surgical intervention- chronic venous disease

A

Failure of conservative therapy, bleeding from varicosities or telangiectasias, phlebitis or thrombosis or superficial veins

150
Q

What are the ablation techniques for chronic venous disease?

A

Chemical, mechanical and thermal endovenous ablation

151
Q

Sclerotherapy

A

Inject sclerosis get agent into varicosed vein, obliterate/permanent fibrosis of involved veins

152
Q

Chemical ablation/sclerotherapy indications

A

Small veins <4mm diameter

153
Q

Risks and f/u with sclerotherapy

A

Phlebitis, tissue necrosis, infection are risks involved

Follow with compression

154
Q

Mechanical ablation of varicose veins

A

Phlebectomy or ligation, stripping rarely performed

155
Q

What are the two types of thermal ablation?

A
  1. Endovenous laser ablation (ELA)

2. Radiofrequency ablation (RFA)

156
Q

When should saphenous vein ablation be considered?

A

If GSV reflux with normal deep system

-has high success and low complications

157
Q

What are the risks for a saphenous vein ablation?

A

Ecchymosis, discomfort, superficial phlebitis, nerve damage, skin burns, DVT, PE

158
Q

When should you refer someone with chronic venous disease to vascular?

A

Significant saphenous vein reflux, open wounds: should be dealt with by specialists, or if cosmetic concerns

159
Q

Prognosis of chronic venous disease

A

Varicose veins: surgical correction of reflux 85-90% 5 year success rate
Chronic venous insufficiency: often recurrent complications, noncompliance with compression stocking use

160
Q

Is the lymphatic system low or high pressure?

A

Low pressure

161
Q

What is lymphatic flow facilitated by?

A

Vessel contraction, skeletal muscle contraction and unidirectional vale’s

162
Q

Lymphedema

A

Interstitial Collection of protein-rich fluid due to disruption of lymphatic flow

163
Q

Etiology of lymphedema

A
  1. Congenital malformation
  2. Damage to lymphatic vessels/lymph nodes
    - reduction of number of available channels
    - obstruction of available lymphatic channels
164
Q

Primary lymphedema

A

Congenital developmental abnormalities

165
Q

Secondary lymphedema

A

Inflammatory or mechanical obstruction

166
Q

Congenital lymphedema is what age group?

A

Birth to 2 years old

167
Q

Lymphedema praecox

A

Onset during puberty or pregnancy prior to age 35

168
Q

Lymphedema tarda

A

Onset after age 35

169
Q

What is the most common cause worldwide of lymphedema?

A

Filariasis due to infection by the nematode Wuchereria Bancrofti

170
Q

Most common cause of lymphedema in developed world?

A

Malignancy or treatment for malignancy

171
Q

Risk factors for lymphedema?

A

Cancer and cancer treatment* hereditary syndromes (Turners, Noonan syndromes), older age, obesity, inflammatory discovers, arthritis, infeciton

172
Q

Extremity swelling si/sx of lymphedema

A

Usually insidious, may affect only portion of limb initially, may include corresponding quadrant of trunk, non-pitting, often involves dorsal foot, often unilaterally

173
Q

Si/sx of lymphedema

A

Aching, pain, or discomfort of the limb, heaviness or tightness of limb, skin changes, restricted ROM

174
Q

Lymphedema PE findings

A

Non-pitting edema, squaring of toes, dorsal pedis hump exaggerated skin folds near ankle

175
Q

Advanced PE findings of lymphedema

A

Woody appearance, dermal thickening, skin hyperkeratotic, acanthosis and verrucous overgrowth

176
Q

What is the Stemmer sign?

A

Thickened skin fold at base of 2nd toe or 2nd finger

Positive sign: inability to lift skin of affected limb

177
Q

Diagnostic studies for lymphedema

A

Lymphoscintigraphy: flow of fluid from skin to lymph nodes, CT, MRI/MR lymphography, ultrasound to rule out DVT or identify mass

178
Q

In endemic areas with lymphedema, what do you test for?

A

Filarial infection, circulation filarial antigen (CFA), blood smears, PCR, antifilarial antibody tests, detect worms on ultrasound

179
Q

Findings suggestive of lymphedema

A

Localized edema, slow and progressive swelling, hx of cancer treatment or trauma, absences of generalized edema, cutaneous and SUBQ thickening, non-pitting edema

180
Q

Diagnosis essentials for lymphedema

A

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
Q

Lymphedema treatment

A

compression intermittent elevation, good hygiene

182
Q

Prognosis of lymphedema

A

No cure, long-term prognosis: avoidance of recurrent cellulitis, associated conditions

183
Q

Tunica externa

A

Adventitia, connective tissue

184
Q

Tunica media

A

Thickest layer, elastic fiber, connective tissue, and vascular smooth muscle

185
Q

Tunica intima

A

Thinnest layer, simple squamous endothelial cells

186
Q

Layers of artery from out to in

A

Tunica: adventitia, media, intima

187
Q

What are the 3 types of aneurysms?

A

Fusiform, saccular, pseudoaneurysm

188
Q

Fusiform aneurysm

A

Affects entire circumference of segment of vessel

189
Q

Saccular aneurysm

A

Involves only a portion of the circumference resulting in outpouching of wall

190
Q

Psuedoaneurysm

A

Intimal and medial layers of artery are disrupted, tailgated segment is lined by adventitia only (occasionally clot)

191
Q

Aortic aneurysm etiology

A

Degenerative diseases (cystic medial necrosis), atherosclerosis, inherited or developmental diseases, infections (syphilis), vasculitis (Takayasu’s arteritis, trauma

192
Q

What is cystic medial necrosis?

A

Degeneration of collage and elastic fibers, effects the proximal aorta, causing circumferential weakness and dilation

193
Q

What type of inherited or developmental diseases put you at risk for a aortic aneurysm?

A

Marfan syndrome, Ehlers-Danlos syndrome, family hx

194
Q

What types of aneurysms does cystic medial necrosis cause?

A

Fusiform aneurysms

195
Q

Marfan syndrome

A

Connective tissue disorder, autosomal dominant, broad range of clinical severity, long extremities with joint laxity

196
Q

Ehlers-Danlos Syndrome

A

Genetic disorder of connective tissue, causes skin hyperextensibility, joint hyper mobility, and tissue fragility

197
Q

Locations of thoracic aortic aneurysms

A

Ascending aortic aneurysm: 60%
Aortic arch: 10%
Descending aorta: 40%
Thoracoabdominal: 10%

198
Q

Thoracic aortic aneurysms

A

Less common than AAA, cystic medial necrosis is most common with ascension aortic aneurysms

199
Q

What is most common with aneurysms of the aortic arch and descending thoracic aorta?

A

Atherosclerosis

200
Q

Epidemiology of thoracic aortic aneurysms

A

6th and 7th decade, males 2-4x more likely, >60% have HTN, 20-25% with large thoracic AA also have AAA

201
Q

CXR for Thoracic AA

A

May be first test to suggest diagnosis*

Wide mediastinum, tracheal deviation

202
Q

Symptoms of TAA

A

Often asymptomatic, chest back flank or abdominal pain, cold foot, HF from aortic root dilation, ascending and arch aneurysm can erode into mediastinum

203
Q

What symptoms can be seen if the TAA erodes into the mediastinum?

A

Hoarseness, wheezing, cough, hemoptysis, dysphasia

204
Q

PE of TAA

A

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
Q

Imaging options for diagnosis of TAA

A

Echocardiography: proximal ascending aorta and descending thoracic aorta, CT scan, MRI less commonly used

206
Q

Treatment fo TAA

A

B-adrenergic blockers particularly with Marfan Syndrome, control HTN with ACEI/ARBs

207
Q

When is surgery an indication for TAA?

A

> 5.5cm ascending TAA

>6.5cm descending TAA

208
Q

What is endovascular repair of a TAA?

A

Placement of a stent graft

209
Q

AAA

A

Definition: >3cm, concern for rupture when >5cm

210
Q

Risk factors in development of AAA

A

Advancing age, male, cigarette smoking, HTN, hyperdyslipidemia, Caucasian, family Hx, presence of other aneurysms, atherosclerosis

211
Q

Symptoms of AAA

A

Most asymptomatic; abdominal back flank or groin pain, sudden cold or blue distal extremities

212
Q

PE of an AAA

A

Rarely palpable one xam, pulsating abdominal mass suggests rupture, if ruptured: distention and tenderness, ecchymosis can occur if ruptured

213
Q

Cullen’s sign and Grey Turner’s sign

A

Ecchymosis that occurs if an AAA ruptures

214
Q

Screening pts who are at risk for AAA

A

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
Q

Diagnostic of choice for AAA

A

Abdominal ultrasound

216
Q

Treatment for AAA

A

Surveillance until >5-5.5cm

Open vs endovascular repair

217
Q

What decides if the surgery for AAA will be open vs endovascular?

A

Anatomy and comorbidities

218
Q

Aortic dissection etiology

A

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
Q

Aortic dissection risk factors?

A

systemic HTN atherosclerosis, aortic aneurysm, inflammatory disease, collagen disorders, biscuit aortic valve, aortic coarctation

220
Q

Aortic dissection signs and symptoms

A

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
Q

Other si/sx of aortic dissection

A

Hemiplegia or paralysis or LEs, diastolic murmur May develop (aortic regurg), HF, cardiac tamponade, intestinal ischemia, limb ischemia

222
Q

Si/sx of dissection occurs in the ascending aorta

A

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
Q

Si/sx of dissecting aorta if its in descending aorta

A

Chest or back pain, abrupt onset of pain, migration pain, HTN, hypotension/shock, pulse deficit, spinal cord ischemia, ischemic peripheral neuropathy

224
Q

Diagnostic studies for aortic dissection

A

No blood testing, just imaging!

225
Q

Imaging studies for aortic dissection: identify the presence and associated features

A

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
Q

Imaging studies for aortic dissection

A

Chest radiograph, echocardiogram, CT commonly used, MRI, aortography

227
Q

Essentials of diagnosis for aortic dissection

A

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
Q

What is the standford classification of aortic dissection?

A

Type A: ascending aorta

Type b: descending, distal to left subclavian

229
Q

DeBakey aortic dissection classification

A

Type 1: ascending aorta, aortic arch, descending
Type 2: only ascending
Type 3: only descending

230
Q

Treatment of aortic dissection

A

Considered surgical emergencies

231
Q

Initial management for aortic dissection

A

HR and BP monitoring, pain reliever with IV morphine, reduction of SBP with BB, ICU level care

232
Q

What are they types of surgical management for aortic dissection?

A

Endovascular repair and open surgical repair

233
Q

Long term management and follow up for aortic dissection

A
  1. Medical therapy: minimize aortic wall shear stress
  2. Serial Imaging
  3. Reoperation when indicated
234
Q

What medical therapy is used for long term management of aortic dissection?

A

Lifelong BB, goals BP less than 120/80, avoid strenuous activity

235
Q

How often should imaging be done for someone with aortic dissection?

A

3 6 and 12 months, then ever 1-2 years

236
Q

When is reoperation indicated for aortic dissection?

A

Extension or recurrence of the dissection, aneurysm formation, leakage at anastomoses or stent sites

237
Q

Prognosis of aortic dissection

A

Mortality untreated type A: 1% per hour for 72 hours, over 90% at 3mos
Untreated complicated type B: high mortality

Clin Med 2 (4 decks)

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