hemodynamic instability Flashcards
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
what happens when comp mechanisms fail and tissue perfusion becomes inadequate?
- cells switch to anaerobic metabolism and lactic acidosis occurs
- increased permeability results in fluid shifting out of vascular space
- clinical signs of poor end-organ perfusion occur in all body systems
obstructive shock
outflow obstructed = high afterload, deceased preload, decreased CO and BP
interventions for shock
- recognize, prevent, intervene early and evaluate effectiveness
Important assess parameters
- hemodynamic status
- tissue perfusion
- cellular oxygenation
what do you assess in shock and what are the metabolic indicators
- MAP, DBP, PP, HR, EOP
- ScvO2, OER, lactate, pH and base deficit
hypotonic sol
fluid goes into intracellular space
hypertonic sol
fluid goes into intracellular space
What to note about NS…
It is acidic. If PT is acidic might want to change
= hyperchloremic acidosis
RL
has electrolytes
crystalloid- isotonic
D5W
hypotonic
SE: cerebral edema
What is TRICC
transfusion requirements in CC
restrictive group: Hgb < 70
liberal group: Hgb <100
