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
