AAA size
normal = 2 cm
AAA= 50% larger, aprox 4 cm
> 5.5cm = sx
common AAA sites
- below renal*
- above renal
- involve aorta and iliac
- abd-thoracic
what causes AAA?
- degeneration of elastin and collagen fibers
- loss of smooth muscle fibers,
- thinning of the medial layer
- loss of structural integrity
- dilation of affected area
diagnose
- US, CT, CT angio
why do you cross clamp for sx?
to prevent plaque traveling
advantages of Endovascular AAA
- local/general anesthesia
- avoids risks of open and cross clamping,
- shorter hosp stay and less pain
Post-op issues of AAA Hemodynamic:
- CAD, dyrhythmias, CHF (watch ST, cardiac function and perfusion = Preload, minimize workload, Sand S of ACS and MI
- fluid overload: weight gain or loss. Gain = increase to myocardial O2 demand. increases preload
- Fluid overload with CAD can = MI, angina, HF, resp failure…
Post-op AAA renal complications
- hypoperfusion from emboli or hypotension, cross clamping
- assess thrombosis
assess the 5 P’s - limbs vaible- perfusion, pulses, necrosis
Post-op AAA GI
- colon ischemia, ischemic colitis, paralytic ilius, BS return 48 hrs
- d/t occlusive disease or emboli, decreased CO or colonic distension
post-op AAA other bad stuff
- hemorrhage
- resp probs
- inj to ureters/bowel
- paraplegia d/t spinal chord ischemia
what is normal EF
50-70%
what is important to control post-op***
HTN- keep 140/90 ish
Afterload reduction: manage fluid intake and overload, meds
recognize and reverse causes if able
when do we see HTN
peri-op drugs
CC illness contribute factor
co-morbidity
SNS response to CC illness (pain, anxiety, altered mentality)
Reverse: shivering, inadequate vent/hypercarbia, bladder distension
what meds do you give for HTN henodynamic instability
- Labetalol
- hydralazine
- nitroprusside
How to manage fluid overload
- chest, edema, abd distension
- CVP, BP, abd pressure
- fluid: intake, feeds, weight
- BW: BUN, Cr, lytes, hgb, hct
what is shock
acute widespread process of impaired tissue perfusion that results in cellular, metabolic and hemodynamic alterations
change in determinants of CO–> hemodynamic instability–> shock
what are the types of shock?***
- hypovolemic
- cardiogenic
- distributive
- obstructive
what is the best take away re shock?
early detection is key
Hypovolemic P, A, C
preload**- decreased inadequate circulating vol
AL- increased
con- decreased
HR: inc, CO: DEc
cardiogenic P, A, C
Preload- increased d/t blood collecting in vena cava
AL- increased
cont**- decreased poor contractility
HR :inc, CO: dec
distributive P, A, C
preload- decreased
AL**- decreased vascular tone disrupted
Cont- decreased
CO: inc, norm, or dec
compensatory mechanisms in shock
SNS
- Neural- Baroreceptors stretch
- increase HR, contract, vasoconstrict - Hormonal- RAAS
- Angio–> ADH retain H20 and Na
- ACTH –> glycogenesis and catecholamines to increase compensatory mechanisms - Chemical- low PaO2 and high PaCO2
RAAS does what?
- vasoconstriction and increased circulating vol
chemical comp mechanisms
- triggered by hypoxemia and hypercapnia
- = increased RR and Vt
