Aortic dissection et al Flashcards
Aortic dissection: what it is and isnt
NOT an aneurysm
IS a result of a false lumen between intima and media of arterial wall
Classification of aortic dissection
Type A: affects ascending aorta and arch –> requires emergency surgery
Type B: begins in the descending aorta –> might be treatable with conservative management
Aortic dissection: acute to chronic
symptom onset:
acute = first 14 days
subacute = 14-90 days
chronic = more than 90 days
Etiology/pathophysiology of aortic dissection
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
Aortic dissection: who does it affect?
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
Clinical manifestation of aortic dissection Type A and B
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”
Dissection pain vs MI pain
-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
Aortic dissection manifestations specific to aortic arch involvement
-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
Aortic dissection complications
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
manifestations of cardiac tamponade
hypotension
narrowed pulse pressure
distended neck veins
muffled heart souds
pulsus paradoxus
Aortic dissection diagnostic studies
H&P
ECG
Chest xray
CT
MRI
TEE
Immediate goals for aortic dissection in ICU
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
Conservative therapy for acute or chronic Type B w/o complications
pain relief
HR and BP control
CVD risk factor modification
close surveilance with CT or MRI
Endovascular dissection repair
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
surgical therapy for acute Type A aortic dissection
-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
Preop aortic dissection
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
Postop aortic dissection
*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
Phlebitis
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
Venous thrombosis
-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
Venous thrombosis Etiology
Virchow’s triad
-venous stasis
-damage to endothelium
-hypercoagulability of blood
Venous stases: VTE
-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
endothelial damage: VTE
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
Hypercoagulability of blood: VTE
Occurs with many disorders:
-anemia and polycythemia
-cancr
-nephrotic syndrome
-high homocysteine levels
-coagulation disorders
-sepsis
-drugs: corticosteroids or estrogens
-smoking
Who has high risk of hypercoagulability
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
Pathophysiology of VTE
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
Superficial vein thrombosis
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
Manifestation of DVT
-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
manifestations of VTE in IVC and SVC
IVC
-legs edematous and cyanotic
SVC
-similar symptoms of arms, neck, back, and face
VTE diagnosis
assessment, D-dimer, and/or ultrasound
VTE complications
Serious:
-PE
-chronic thromboembolic pulmonary htn
-postthrombotic syndrome
-phlegmasia cerula dolens
PTS
what is it?
symptoms?
-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
PTS manifestations
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
PTS risk factors
-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
VTE diagnostic studies
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
Prevention and prophylaxis for VTE
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
Vit K antagonists
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
Thrombin INDIRECT inhibitors
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
DIRECT thrombin inhibitors
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
Factor Xa inhibitors
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
Anticoagulant therapy for VTE prophylaxis
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
anticoagulant therapy for VTE treatment
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
Thrombolytic therapy for VTE treatemet
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
Surgical and interventional radiology therapies
Surgeries
1. Open venous thrombectomy
-incision into vein to remove clot
- Inferior Vena Cava interruption devices
-filters placed via right femoral or jugular veins to trap clots without impeding blood flow
Inferior vena cava interruption device
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
Percutaneous endovascular interventional radiology procedures for VTE
Mechanical thrombectomy
Pharmacomechanical devices
Post-thrombus extraction
angioplasty
stenting
***can be used with catheter-directed thrombolytic therapy
Nursing care for VTE
maintain catheter systems
monitor for bleeding, embolization, and impaired perfusion
teach VTE prevention
Acute care for VTE
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
Ambulatory care for VTE
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
Varicose veins
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
Varicose veins etiology and pathophysiology
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
manifestations of varicoe veins
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
varicose veins diagnosis and conservative treatment
Diagnosis
-examination
-duplex ultrasound
Conservative treatment
-ret with limb elevation
-graduated compression stockings
-leg strengthening exercises
-weight loss
Drug therapy for varicose veins
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
Varicose vein surgeries
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
Interventional and surgical therapies
Traditional: ligation of vein and branches
Ambulatory phlebectomy
Transilluminated powered phlebectomy
-complications: bleeding, bruising, and infection
postop varicose veins
deep breathing
neuro assessment
-evaluate legs
graduated compression stockings –> remove every 8 hrs for a while
Chronic venous insufficiency
abnormalities of venous system including edema, skin changesm and venous leg ulcers
CVI etiology and pathophysiology
-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
manifestations of CVI
lower leg is brown, leathery, and edematous
eczema with itching and scratching
Venous ulcers
Caring for venous ulcers
moist environment for wound
adequate protein, vit A/C, and zinc
keep diabetes in check
monitor for infection
drugs for ulcers
pentoxifylline or micronized flavonoid fraction
