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CICU flash

CICU falsh

QuestionAnswer
alpha1 receptor causes vascular mscl contraction
alpha2 receptor causes (2) decreased sympathetic, decreased insulin
beta1 adrenergic receptor causes (3) increased HR & contractility, increased renin
beta2 adrenergic receptor causes (6) vasodilation, increased HR & contractility, bronchodilation, gluconeogenesis, incrsd ocular pressure!! (so careful in glaucoma)
muscarinic receptors effect on heart decreased HR and contractility
H1 receptor causes (4) contraction bronchioles, incrsd nasal and bronchial secretions, pruritis, pain
H2 receptor causes (1) increased gastric acid secretion
3 classes of GERD/PUD meds and exs PPIs (-azole, ie protonix/propanazole), H2 antagonist (-itidine, ie ranitidine), PGE analogs (misoprostol)
tx for glaucoma by Rx classes and their mech of action (5) a-agonist: decrs aq humor synthesis; b-blocker: decrs aq humor sxn; diuretic: decrs aq humor sxn; cholinomimetics: incrs outflow contracting ciliary; prostaglandin: incrs outflow
tx of glaucoma Rx names and classes a-agonist: epi, brimonidine; b-blocker: timolol; diuretic: acetazolamide; cholinomimetics: pilocarpine (use in emergency), physostigmine; prostaglandin: latanoprost
receptors epinephrine works on a1, a2, b1, b2; but at low doses selective for b1
receptors NE work on a1, a2>b1
dopamine and its effects at different doses 2-5ug/kg/min=renal dose, D1 dilating renals and coronaries;5-10ug/kg/min=also inotropic and chronotropic from b1 receptor activation; incrs CO and BP; 10-20ug/kg/min=pressor dose, causes vasoconstriction, incrs SVR, incrs BP through a1 but hurt kidneys
clonidine, alpha methyl dopa receptor works on and effect alpha2 central acting, decreases sympathetic; good for HTN esp in renal dz (won't decrs BF to kidneys)
affect of NE on SBP, DBP, MAP via which receptors; HR NE affects a1>b2 (net vasoconstriction); causes increase in MAP, increase in SBP and less of increase in DBP so incrsd pulse pressure and reflex brady cardia
2 receptors that counteract blood vessel contraction alpha1 causes contraction, beta2 causes dilation [so if Rx like NE incrses a1>b2 net incrs in contraction]
affect of epi on SBP, DBP, MAP via which receptors; HR incrs alpha1 causes incrs SBP, incrs beta2 causes decrs DBP, MAP unchanged, HR incrses from b1
formula for A-a gradient FiO2*713 - PaO2 - (PaCO2/.8)
nl CO 4-8L/min
nml cardiac index 2.8-4.2
nl MAP 70-100
calculation MAP (SBP-DBP)/3 + DBP
calculation SVR (MAP - CVP)*80 / CO
cut offs for acute respir insuffic PO2<60 on 0.5FiO2 or PCO2>50
cut off ARDS PaO2/FiO2 <200
extubation criteria (5) negative inspiratory force >25; TV >5ml/kg; vital capacity 10-15ml/kg; RR<24/min; ABG ok
weaning failure criteria (4) SBP increases by 20 or to over 160; change in HR by 20% (up or down), or to >140; arrhythmias develop or become more frequent;ABG: PaO2<60 or SaO2<90%; or PCO2>50
causes of shunt (4) Alveolar collapse; Intra-alveolar filling, ie PNA, pul edema; Intracardiac shunt; Vascular shunt within lungs
causes of V/Q mismatch (4) airway dz (asthma, COPD), ILD, alveolar dz, pul vascular dz
how evaluate incrs A-a gradient? What are underlying etiologies for ea? if correctable w O2=V/Q mismatch, if not then its shunt
overall evaluation of hypoxemia 1) if PaCO2 high and A-a nml then its hypoventilation only, if A-a incrsd then also shunt or V/Q mismatch; 2) if PaCO2 nml and A-a nml then low inspired PO2, if A-a high then V/Q mismatch or shunt
shifting Hb curve and effects hypothermia and alkalosis move to L and decrsd delivery to tissues, acidosis moves to R and incrsd delivery to tissues
how incrs oxygenation for someone on vent (4) increase Mean airway pressure by: incrs PEEP, i/e ratio, TV/PIP, and FiO2
target values ABG PaO2>80 (SaO2>95%); PaCO2 32-48; pH 7.32-7.48
what set on BiPAP, how determine TV set inspir and expir pressure (can also have b/u RR); TV is determine by diff in PEEP and PIP
describe PSV, when does pressure given stop; when is this setting used pressure given when breath initiated (PEEP can also be added); pressure given until flow is 25% of peak; often used for weaning
what are settings for volume controlled vent (5) TV, RR, PEEP, inspiratory flow rate (determine i-time), FiO2
what are settings for pressure controlled vent (5) inspiratory pressure, RR, PEEP, i: e ratio, FiO2
when can start weaning (5) chest tube<50ml/hr; SBP 100-120; HR<120 no arrhythm; CI>2.2; ABG ok
how can hi PEEP be bad for cardiac decrses venous return and incrses PVR->decrsd RV output, reducing LV EDV and CO
MC reason to fail vent weaning? Causes overall and 5 specific? hypercarbia from not being able to sustain work of breathing; from incrsd vent demands, incrs CO2 production and O2 demands; sepsis, carbs, incrsd dead space (COPD), decrsd lung compliance; incrsd lung resistance
what's nml SvO2 on Swan-Ganz nml >65%
Hct needs to be maintained grtr >22-24% (note hemodilution s/p CPB)
nml PCWP 5-12mmHg
at what PCWP worried abt pul edema if >20mmHg
when might PCWP overestimate LVEDP mitral stenosis or high PEEP
when might PCWP underestimate LVEDP decrease LV compliance
2 choices for colloid fluids, and advantages/disadv 5% albumin and hetastarch; hetastarch will last longer but should be limited to 20ml/kg/day to minimize adverse effects on coag or if signif mediastinal bleeding
nml RA Pressure 3-8mmHg
nml LA pressure 5-12mmHg
PA pressure (SBP, DBP) 15-30/ 5-12
nml RV P (SBP/DBP) 15-30/3-8
nml LVSP, LVEDP 90-140/ 5-12
nml Ao pressures (sys, dias) 90-140/60-90
Created by: ehstephns on 2010-10-24



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