Aortic dissection et al

Question 1

Aortic dissection: what it is and isnt

Answer 1

NOT an aneurysm

IS a result of a false lumen between intima and media of arterial wall

Question 2

Classification of aortic dissection

Answer 2

Type A: affects ascending aorta and arch –> requires emergency surgery

Type B: begins in the descending aorta –> might be treatable with conservative management

Question 3

Aortic dissection: acute to chronic

Answer 3

symptom onset:
acute = first 14 days
subacute = 14-90 days
chronic = more than 90 days

Question 4

Etiology/pathophysiology of aortic dissection

Answer 4

Nontraumatic aortic dissection
-due to weakened elastic fibers in arterial wall
-chronic htn hastens the process
-tear in inner layer allows blood to surge between inner and middle layer
-rupture through outside wall can cause death

As heart contracts, each systolic pulsation increases the pressure on the damaged area, making it worse
-may occlude major branches of aorta –> cut off blood supply to brain, abdominal organs, kidneys, spinal cord, and extremeties

False lumen may remain patent, become thrombosed, or rejoin true lumen

Question 5

Aortic dissection: who does it affect?

Answer 5

men more than women
-if women have it, they’re usually old, with HF, coma, or altered mental status

HTN = biggest risk factor
-others: afe, aortic disease, atherosclerosis, blunt trauma, tobacco, cocaine/meth, congenital heart disease, CT disease, fam history, previous heart surgery, and pregnancy

Question 6

Clinical manifestation of aortic dissection Type A and B

Answer 6

Acute type A
-abrupt onset of severe anterior chest pain or back pain

Acute type B
-back, abdomen, or leg pain

*A and B can overlap
*pain described as “sharp”, “ripping”, “tearing”, “stabbing”, “worst ever”

Question 7

Dissection pain vs MI pain

Answer 7

-MI pain is more gradual w/ increased intensity
-dissection pain follows the path of the rip
-old ppl might not experience the intense pain –> vague symptoms and hypotension
-sometimes painless

Question 8

Aortic dissection manifestations specific to aortic arch involvement

Answer 8

-Neurologic deficits
-disruption of blood flow in coronary arteries and aortic valve insufficiency
-if subclavian artery is involved, BP and arterial pulses are dif in arms
-can advance to descending aorta, decreasing tissue perfusion to abdominal organs and lower extremeties

Question 9

Aortic dissection complications

Answer 9

Cardiac tamponade
-severe, life-threatening complication of acute ascending aorta dissection
-happens when blood escapes from dissection into pericardial sac

Aorta may rupture, resulting in hemorrhage in mediastinal, pleural, or abdominal cavities –> exsanguination and death

Occlusion of arterial supply to vital organs: spinal cord, kidneys, abdominal organs

Question 10

manifestations of cardiac tamponade

Answer 10

hypotension
narrowed pulse pressure
distended neck veins
muffled heart souds
pulsus paradoxus

Question 11

Aortic dissection diagnostic studies

Answer 11

H&P
ECG
Chest xray
CT
MRI
TEE

Question 12

Immediate goals for aortic dissection in ICU

Answer 12

HR and BP control
-decrease BP and myocardial contractility to diminish pulsatile forces w/in aorta
-IV B-blocker to get HR below 60 or SBP100-110 –> can also try CCBs

Morphine for pain

Question 13

Conservative therapy for acute or chronic Type B w/o complications

Answer 13

pain relief
HR and BP control
CVD risk factor modification
close surveilance with CT or MRI

Question 14

Endovascular dissection repair

Answer 14

Thoracic endovascular aortic repair TEVAR
-standart to treat acute and chronic type B aortic dissections with complications
-similar to EVAR, but fewer post-op complications
-may have lumbar drain

Question 15

surgical therapy for acute Type A aortic dissection

Answer 15

-emergency surgery (50% mortality)
-considered when drug therapy is ineffective or when complications of aortic dissection are present
-surgery is delayed to allow edema to decrease and permit clotting of blood

Involves resection of aortic segment and replacement with synthetic graft

Causes of death during surgery: aortic rupture, mesenteric ischemia, MI, sepsis, stroke, or multi-organ failure

Question 16

Preop aortic dissection

Answer 16

Semi Fowlers position and quiet enviro to decrease HR and BP
Anxiety and pain –> opioids and sedatives
Titrate IV antihypertensive agents
Continuous BP and ECG monitoring
VS every 2-3 mins (note changes in peripheral pulses)
Monitor for increaseing pain/restlessness/anxiety

Question 17

Postop aortic dissection

Answer 17

*same as for aneurysm

Discharge teaching
-long-term HR and BP control
-Antihypertensive drug and side effects as well as BBs and ACE-is
-regular follow up with CT or MRI

if pain returns or symptoms progress, seek immediate help

Question 18

Phlebitis

Answer 18

acute inflammation of the walls of small cannulated veins of hand or arm (related to IV catheter) –> rarely infectious

Manifests: pain, tenderness, warmth, erythema, swelling, and palpable cord

Risks: irritation from catheter, infusion of irritating drugs, and catheter location at area of flexion

Treatment:
-elevate extremety for edema
-NSAIDs and warm, moist heat for pain/inflammation

Question 19

Venous thrombosis

Answer 19

-most common venous disorder
-formation of a thrombus with vein inflammation
-can be superficial (saphenous) or deep veins (iliac or femoral)
-VTE = DVT to pulmonary embolism

Question 20

Venous thrombosis Etiology

Answer 20

Virchow’s triad
-venous stasis
-damage to endothelium
-hypercoagulability of blood

Question 21

Venous stases: VTE

Answer 21

-dysfunctional valves
-inactive extremety muscles

At risk if:
-obese
-pregnant
-chronic HF or afib
-traveling on long trips w/o exercise
prolonged surgery
-prolonged immobility

Question 22

endothelial damage: VTE

Answer 22

stimulates platelet activation and starts coagulation cascade which predisposes patient to thrombus development

Direct damage
-surgery, burns, IV catheter, trauma, prior VTE

Indirect damage
-chemotherapy, diabetes, sepsis

Question 23

Hypercoagulability of blood: VTE

Answer 23

Occurs with many disorders:
-anemia and polycythemia
-cancr
-nephrotic syndrome
-high homocysteine levels
-coagulation disorders
-sepsis
-drugs: corticosteroids or estrogens
-smoking

Question 24

Who has high risk of hypercoagulability

Answer 24

Women who:
-use tobacco (smoking increases plasma fibrinogen, homocysteine levels, and activates intrinsic coagulation pathway)
-are childbearing age and take E contraceptives
-are postmenopausal and take oral hormone therapy
-are over 35
-have fam history of VTE

Question 25

Pathophysiology of VTE

Answer 25

clot formation occurs when localized platelet aggregation and fibrin entrap RBCs, WBCs, and more platelets Clot gets larer and has a "tail" that blocks the lumen of the vein partial blockage = endothelial cells cover thrombus and stop growth; lysis or adherence w/in 5-7 days detached thrombus results in embolus -travels thru venous system to R side of heart and lodges in pulmonary circulation --> becomes PE -turbulet bloodflow = major factor in embolization

Question 26

Superficial vein thrombosis

Answer 26

more common in legs Manifestations -palpable, firm, cordlike vein -itchy, painful, red, warm -mild fever, leukocytosis Diagnosis: ultrasound Treatment if under 5 cm and not near junction -oral NSAIDs -graduated compression stockings -warm compresses -elevate limb above heart -mild exercise

Question 27

Manifestation of DVT

Answer 27

-in arms or legs, pelvis, vena cava, and pulmonary system Lower extremety -unilateral edema -pain, tenderness with palpatation -dialted superficial veins -full sensation in thigh or calf -paresthesias -red and warm -fever over 100.4

Question 28

manifestations of VTE in IVC and SVC

Answer 28

IVC -legs edematous and cyanotic SVC -similar symptoms of arms, neck, back, and face

Question 29

VTE diagnosis

Answer 29

assessment, D-dimer, and/or ultrasound

Question 30

VTE complications

Answer 30

Serious: -PE -chronic thromboembolic pulmonary htn -postthrombotic syndrome -phlegmasia cerula dolens

Question 31

PTS what is it? symptoms?

Answer 31

-8-70% of VTE patients -chronic inflammation and venous htn --> damage to vein walls and valves, venous valve reflux, and persistent venous obstruction Symptoms -pain, aching, fatigue, heaviness, swollen sensation, cramps, pruritus, tingling, paresthesia, pain with exercise, venous claudication

Question 32

PTS manifestations

Answer 32

edema, spider veins, venous dilation, redness, cyanosis, increased pigmentation, eczema, pain during compression, white scar tissue, lipodermatosclerosis venous ulceration with severe PTS signs may occur in a few months or years

Question 33

PTS risk factors

Answer 33

-persistant leg symptoms for more than 1 month after VTE -VTE: proximal location, extensive or recurrent -residual thrombus -other: obesity, old age, poor INR control, tobacco use, increased D-dimer, increased inflammatory markers, varicose veins, and asymptomatic VTE

Question 34

VTE diagnostic studies

Answer 34

Blood: ACT, aPTT, INR, bleeding time, Hgb, Hct, platelet count, D-dimer, fibrin monomer complex Noninvasive venous: venous compression ultrasound, duplex ultrasound Invasive venous: CT venography, MR venography, contrast venography

Question 35

Prevention and prophylaxis for VTE

Answer 35

VTE prophylaxis is a core measure of high-quality health care in high-risk hospitalized patients Early, aggressive mobilization -walk 4-6x a day; flex joints every 2-4 hrs; oob Graduated compression stockings -use with anticoagulants -don't use if VTE already exists Intermittent compression devices -use with compression stockings (again, not if VTE exists) Anticoagulants -vit K antagonists, thrombin inhibitors, Factor Xa inhibitors

Question 36

Vit K antagonists

Answer 36

Warfarin -inhibits vit K-dependent coagulation factors II, VII, IX, and X and anticoagulant prots C and S -for long term or extended anticoagulation -takes 48-72 hrs to be effective --> overlap with parenteral anticoagulant for 5 days -monitor INR -Antidote = vit K Don't give with antiplatelets or NSAIDs AVOID VIT K Genetics may alter response

Question 37

Thrombin INDIRECT inhibitors

Answer 37

UH (heparin) and LMWH -affects intrinsic plasma antithrombin coagulation pathway; inhibits thrombin mediated conversion of fibrinogen to fibrin Prophylaxis = subcutaneous Existing VTE = continuous IV --> monitor aPTT Heparin -side effect = osteoporosis and heparin induced thrombocytopenia LMWH (enoxaparin) -more predictable with longer half life and fewer bleeding complications -antidote = protamine

Question 38

DIRECT thrombin inhibitors

Answer 38

Hirudin derivative - bivalirudin (angiomax) -binds with thrombin and inhibits function -continuous IV Synthetic (argatroban) -hinders thrombin Both -indications: patient with or at risk for HIT having percutaneous coronary intervention -monitor aPTT or ACT -no antidote Dabigatran (pradaxa) = oral -indications: VTE prevention after elective joint replacement, for stroke prevention in nonvalvular atrial fibrillation, and as a treatment for VTE -antidote: idarucizumab -advantages over warfarin = rapid onset, no monitoring, few drug-food interactions, decreased risk of bleeding, predictable response

Question 39

Factor Xa inhibitors

Answer 39

Rapid anticoagulation -VTE prophylaxis and treatment -Fondaparinux (subq) is contraindicated for renal disease -Rivaroxaba, apixaban, edoxaban = oral -monitoring ot required but can use anti-Xa assays -Andexant Alfa reverses rivaroxaban and apixaban

Question 40

Anticoagulant therapy for VTE prophylaxis

Answer 40

Hospitalized, non bleeding patiet -UH, LMWH, or fondaparinux Low risk VTE = none Moderate risk = UH or LMWH -general, GYN, or urologic surgery High risk = UH or LMWH -trauma, abdominal or pelvic surgery for cancer, or orthopedic surgery

Question 41

anticoagulant therapy for VTE treatment

Answer 41

Initial: LMWH, UH, or oral Factor Xa or VKA INR - maintain 2-3 (VKA therapy) Continue 3 or more months Co morbidities, complex issues, or very large VTE requires hospitalization -IV UH initially

Question 42

Thrombolytic therapy for VTE treatemet

Answer 42

Thrombolytic drug (tPA or urokinase) administered via catheter to dissolve clots, reduce acute symptoms, improve deep venous flow, reduce valvular reflux, and decrease PTS Indication: patient with low risk of bleeding and has acute, extensive, symptomatic, proximal VTE Must have systemic anticoagulation before, during, and after thrombolysis

Question 43

Surgical and interventional radiology therapies

Answer 43

Surgeries 1. Open venous thrombectomy -incision into vein to remove clot 2. Inferior Vena Cava interruption devices -filters placed via right femoral or jugular veins to trap clots without impeding blood flow

Question 44

Inferior vena cava interruption device

Answer 44

recommended for acute PE or proximal VTE of leg with active bleeding or if anticoagulation contraindicated or ineffective Complications: air embolism, improper placement, filter migration, perforation of vena cava with retroperitoneal bleeding, clogged filter

Question 45

Percutaneous endovascular interventional radiology procedures for VTE

Answer 45

Mechanical thrombectomy Pharmacomechanical devices Post-thrombus extraction angioplasty stenting ***can be used with catheter-directed thrombolytic therapy

Question 46

Nursing care for VTE

Answer 46

maintain catheter systems monitor for bleeding, embolization, and impaired perfusion teach VTE prevention

Question 47

Acute care for VTE

Answer 47

Focus on prevention of thrombi and reduction of inflammation Titrate drug doses and administer reversal agents a needed monitor and reduce risk of bleeding bed rest at first; then early ambulation and physical activity

Question 48

Ambulatory care for VTE

Answer 48

Avoid risk factors -smoking, hormone therapy, travel, prolonged sitting Drug side effects and routine blood tests and medic alert ID -avoid falls -apply pressure to bleeding sites for 10-15 mins -no ASA or NSAIDs -limit alcohol If taking warfarin, eat vit K Call EMS if -bleeding -headache, chest pain, stomach pain, palpitations, dyspnea, mental status changes -inform HCP and dentist of anticoagulation

Question 49

Varicose veins

Answer 49

Dilated greater than 3 mm, tortuous superficial veins -Primary = weakness of vein walls -Secondary = direct injury, previous VTE, or excessive dilation -Congenital = chromosomal defects -Reticular = flat, less tortuous, blue-green -Telangiectasias = spider veins less than 1 mm

Question 50

Varicose veins etiology and pathophysiology

Answer 50

Superficial veins in legs become dilated and tortuous from retrograde blood flow and increased venous pressure Risk factors -fam history of venous problems, female, tobacco use, aging, obesity, multiparity, history of VTE, venous obstruction, phlebitis, leg injury, prolonged sitting or standing

Question 51

manifestations of varicoe veins

Answer 51

heavy, achy feeling or pain after prolonged standing or sitting --> relieved by walking or limb elevation -also: pressure, itchy, burning, tingling, throbbing, or cramp-like sensation Complications -Superficial venous thrombosis -Also: rupture of varicosities results in bleeding and skin ulcerations

Question 52

varicose veins diagnosis and conservative treatment

Answer 52

Diagnosis -examination -duplex ultrasound Conservative treatment -ret with limb elevation -graduated compression stockings -leg strengthening exercises -weight loss

Question 53

Drug therapy for varicose veins

Answer 53

Venoactive drugs -antioxidants from plant extracts stimulate release of chems to strengthen the circulation and reduce inflammation and edema Not FDA approved; available OTC and as herbal or dietary supplements -micronized purified flavonoid fraction -rutosides -proanthocyanidins (apples and grapes) -ruscus

Question 54

Varicose vein surgeries

Answer 54

Sclerotherapy - ablates vein by direct injection of sclerosis agent -complications: residual pigmentation, matting, thrombophlebitis, and ulcers -wear compression stocking and limit travel Transcutaneous laser therapy or high-intensity pulsed light therapy -complications: pain, blistering, hyperpigmentation and superficial erosions Endovenous ablation = radiofrequency or laser therapy -complications: bruising, burns, hyperpigmentation, infection, paresthesia, superficial or deep vein thrombosis, PE -graduated compression stockings

Question 55

Interventional and surgical therapies

Answer 55

Traditional: ligation of vein and branches Ambulatory phlebectomy Transilluminated powered phlebectomy -complications: bleeding, bruising, and infection

Question 56

postop varicose veins

Answer 56

deep breathing neuro assessment -evaluate legs graduated compression stockings --> remove every 8 hrs for a while

Question 57

Chronic venous insufficiency

Answer 57

abnormalities of venous system including edema, skin changesm and venous leg ulcers

Question 58

CVI etiology and pathophysiology

Answer 58

-orimary varicose veins and PTS Ambulatory venous htn -serous fluid and RBC leak results in edema and chronic inflamatory changes -hemosiderin = brown skin discoloration -skin is hard, thick, and contracted

Question 59

manifestations of CVI

Answer 59

lower leg is brown, leathery, and edematous eczema with itching and scratching Venous ulcers

Question 60

Caring for venous ulcers

Answer 60

moist environment for wound adequate protein, vit A/C, and zinc keep diabetes in check monitor for infection

Question 61

drugs for ulcers

Answer 61

pentoxifylline or micronized flavonoid fraction