CICU falsh
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| alpha1 receptor causes | vascular mscl contraction
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| alpha2 receptor causes (2) | decreased sympathetic, decreased insulin
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| beta1 adrenergic receptor causes (3) | increased HR & contractility, increased renin
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| beta2 adrenergic receptor causes (6) | vasodilation, increased HR & contractility, bronchodilation, gluconeogenesis, incrsd ocular pressure!! (so careful in glaucoma)
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| muscarinic receptors effect on heart | decreased HR and contractility
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| H1 receptor causes (4) | contraction bronchioles, incrsd nasal and bronchial secretions, pruritis, pain
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| H2 receptor causes (1) | increased gastric acid secretion
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| 3 classes of GERD/PUD meds and exs | PPIs (-azole, ie protonix/propanazole), H2 antagonist (-itidine, ie ranitidine), PGE analogs (misoprostol)
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| 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
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| tx of glaucoma Rx names and classes | a-agonist: epi, brimonidine; b-blocker: timolol; diuretic: acetazolamide; cholinomimetics: pilocarpine (use in emergency), physostigmine; prostaglandin: latanoprost
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| receptors epinephrine works on | a1, a2, b1, b2; but at low doses selective for b1
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| receptors NE work on | a1, a2>b1
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| 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
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| 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)
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| 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
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| 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]
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| 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
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| formula for A-a gradient | FiO2*713 - PaO2 - (PaCO2/.8)
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| nl CO | 4-8L/min
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| nml cardiac index | 2.8-4.2
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| nl MAP | 70-100
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| calculation MAP | (SBP-DBP)/3 + DBP
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| calculation SVR | (MAP - CVP)*80 / CO
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| cut offs for acute respir insuffic | PO2<60 on 0.5FiO2 or PCO2>50
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| cut off ARDS | PaO2/FiO2 <200
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| extubation criteria (5) | negative inspiratory force >25; TV >5ml/kg; vital capacity 10-15ml/kg; RR<24/min; ABG ok
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| 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
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| causes of shunt (4) | Alveolar collapse; Intra-alveolar filling, ie PNA, pul edema; Intracardiac shunt; Vascular shunt within lungs
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| causes of V/Q mismatch (4) | airway dz (asthma, COPD), ILD, alveolar dz, pul vascular dz
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| how evaluate incrs A-a gradient? What are underlying etiologies for ea? | if correctable w O2=V/Q mismatch, if not then its shunt
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| 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
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| 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
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| how incrs oxygenation for someone on vent (4) | increase Mean airway pressure by: incrs PEEP, i/e ratio, TV/PIP, and FiO2
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| target values ABG | PaO2>80 (SaO2>95%); PaCO2 32-48; pH 7.32-7.48
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| 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
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| 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
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| what are settings for volume controlled vent (5) | TV, RR, PEEP, inspiratory flow rate (determine i-time), FiO2
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| what are settings for pressure controlled vent (5) | inspiratory pressure, RR, PEEP, i: e ratio, FiO2
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| when can start weaning (5) | chest tube<50ml/hr; SBP 100-120; HR<120 no arrhythm; CI>2.2; ABG ok
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| how can hi PEEP be bad for cardiac | decrses venous return and incrses PVR->decrsd RV output, reducing LV EDV and CO
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| 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
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| what's nml SvO2 on Swan-Ganz | nml >65%
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| Hct needs to be maintained | grtr >22-24% (note hemodilution s/p CPB)
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| nml PCWP | 5-12mmHg
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| at what PCWP worried abt pul edema | if >20mmHg
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| when might PCWP overestimate LVEDP | mitral stenosis or high PEEP
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| when might PCWP underestimate LVEDP | decrease LV compliance
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| 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
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| nml RA Pressure | 3-8mmHg
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| nml LA pressure | 5-12mmHg
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| PA pressure (SBP, DBP) | 15-30/ 5-12
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| nml RV P (SBP/DBP) | 15-30/3-8
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| nml LVSP, LVEDP | 90-140/ 5-12
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| nml Ao pressures (sys, dias) | 90-140/60-90
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