Comprehensive CRNA Interview Review Accurate responses are given.

Comprehensive CRNA Interview Review Accurate responses are given. Comprehensive CRNA Interview Review Norepinephrine Mechanism of Action (MOA) A1, A2, B1 agonist. Primary agent used in distributive shock because it's ability to recruit venous volume and augment preload, while increasing arterial tone, and increasing cardiac output. Alpha one causing peripheral smooth muscle contraction. (low dose venous, high dose venous and arterial). Alpha 2 adrenoreceptor agonism actually antagonizes the release of norepinephrine in the CNS, but these receptors are less present in peripheral vasculature and thus, their anti-hypertensive effects are overtaken by A1 agonism. These alpha effects can increase SVR and thereby increase cardiac workload, decrease cardiac output, and increase coronary perfusion pressure. The slight B1 agonism increases inotropy and chonotropy sufficiently to overcome these A1 effects and result in a fairly "pure" vasopressor. Increasing contraction of the heart and increasing AV nodal conduction. **First line agent in septic shock Epinephrine MOA A1 A2 B1 - Stimulate Heart Rate through SA node, increase conduction through AV node. Increase contractility to ATRIAL and VENTRICULAR cardiac muscle. B2 - Smooth muscle relaxation. Resulting in dilation of the bronchial tree, coronary arterial dilation. Also plays a role in insulin and glucagon secretion in the pancreas. Also increases cardiac inotropy/chonotropy B3 - Increase lypolysis and thermogenesis in brown adipose tissue. **Cardiogenic shock or other shock states with a cardiac component. Adjunctive therapy in severe septic shock IVP in cardiac arrest to augment CPP IVP while introducing PPV/intubation Precedex MOA Dexmetatomadine is an alpha 2 adrenoreceptor agonist that acts both on the presynaptic neuron and postsynaptic neuron. Inihibiting norepinephrine release pre-synaptically reduces/halts the transmission of pain, while postsynaptically acts to reduce sympathetic tone. The combination of these effects is anesthesia with analgesia and anxiolysis. loading dose is 1 mg/kg while gtt is .2-1.5 mg/kg/hr **This agent is often used for patients who would not tolerate a precipitous drop in their sympathetic tone, for those patients in severe alcohol withdrawal. propofol MOA Propofol is a lypophylic general anesthetic unlike any drugs of the class benodiazapen, barbituate, or A2 agonist. Its mechanism is proposed to be a GABA (inhibitory neurotransmitter) agonist causing global CNS depression Dosing for procedural sedation of .1-.5 mg/kg as a loading dose with repeat doses. gtt titration ranging from 10-60 mcg/kg/min **Anesthetic Sedation for mechanically ventilated ICU patients Procedural sedation Phenylephrine MOA Pure Alpha adrenergic receptor agonist. Causing increase in SVR through systemic arterial vasoconstriction. This also causes a dose dependent increase in systolic and diastolic blood pressure and thereby decreasing cardiac output, especially in patients with heart failure. 40-100 mcg IVP for hypotension during anesthesia Titrated as a drip from .5-9 mcg/kg/min **used rarely as adjuncitve therapy for patients in septic shock. Used more often in vasodilatory shock states such as neurogenic shock/ shock from epidural/spinal blocks. vasopressin MOA arganine/vasopressin receptor agonist causing potent increase in SVR through 2 different MOA. 1) regulate extracellular fluid volume acting on renal collecting ducts and distal convoluted tubule to increase water permeability via v2 receptors 2)Sodium re-absorption across the ascending loop of HENLe. 3)Binding to V1 receptors on vascular smooth muscle, causing vasoconstriction. Normal concentrations of the drug are below it's vasoactive range, nevertheless in severe hypovolemic shock, AVP increases do contribute to increase in SVR. 1.8 u/hr **used as adjunctive therapy in septic shock. Can be used as a first line agent in a pulmonary hypertensive patient in shock states. Ketamine MOA NMDA receptor antagonist blocking glutamate and thus introducing a cateleptic/dissociative (which is dose dependent) state. N-Methyl-D-Aspartate is a receptor in the CNS responsible for conduction of action potentials associated with memory. Antagonizing these receptors does not allow for the transmission of these signals. .1-.5 mg/kg IVP analgesia 1-5 mg/kg IVP dissociation (procedural) 15-90 mcg/kg/min or 1-6 mg/min for maintenence of anesthesia. Care is to be taken as to not induce a subdissociative like state. DSI/RSI/RSA adjunct analgesic in opiate dependent patients. Nicardapine MOA Voltage sensitive calcium channels regulate the influx and release of calcium in response to action potential and depolarizing signals. Nicardapine inhibits the influx of calcium through these channels thus affecting calcium concentrations. This inhibition results in vasodilation more specific to coronary and cerebral vessels. This vasodilation decreases SVR and opens up the afterload of the heart, increases oxygen delivery and blood flow during vasospastic states, regulates blood pressure during hypertensive emergencies and post transplantation where goal blood pressures need to be tightly met. Has little affect on SA/AV nodal conduction velocity. Begin infusion at 5 mg/hr and titrate by 2.5 every 5-15 minutes for goal blood pressure. Clavidipine MOA Inhibiting influx of Calcium in L-type calcium channels in arterial smooth muscle to decrease SVR. Begin gtt at 1-2 mg/hr. Double dose every 90 seconds for goal blood pressure. Note: that for every 1-2 mg/hr increase in dose, a 2-4 mmHg drop in the systolic blood pressure should be seen. Midazolam enhances GABA effects at GABA-a receptor site producing sedative/hypnotic/anxiolitic/anti- Note: this drug is not used for ICU sedation - increasing the occurence of ICU associated delerium. But can be used for procedural sedation/alcoholic withdrawal states. IVP 1-2.5 mg over 2 min with a 2 min waiting period in between dosing. Generally not exceeding 5 mg IVP. How do you wean a patient from the ventilator Weaning is done on a low-stretch protocol at our ICU. Readiness testing for extubatio includes the following -Fi02<40% -Cause of RF has improved/resolved -PEEP <5 -patient is hemodynamically stable -patient has a cuff leak -patient has a mental status that allows for handling of secretions and protection of one's own airway. Patient can lift head off of pillow -patient is calm/comfortably breathing. RSBi<105 where RSBi = RR/Fi02 .. Ie 20/.4 -MIP more negative than -30 -Acid Base is neutral -Can the patient cough on command? What is End tidal c02? It is the partial pressure of c02 in an exhaled breath -verifying ETT placement -provides instant feedback on the patients ventilatory ( how effective c02 is being eliminated by pulmonary system) - Provides instant feedback on perfusion (how effective c02 is being transported through vascular system) -Provides instant feedback on metabolism (how effective cells are generating c02 Quantitative - waveform with numbers Qualitative- is color change Why do you want to be a CRNA -Independence and autonomy in my specialization. With increased responsibility and reward. -ability to manage airway and hemodynamics. With advanced techniques/medications. To feel calm and collected as a leader in this responsibility. To improve patient outcomes by implimenting best practice. -to become a trauma anesthetist/resusitationist - Through my shadowing I have come to enjoy the profession -to be able to have and support a large family while mantaining my style of living and hobbies that I love. -I want membership in a small/elite profession Why will you do well in the program work ethic - farm hand, school, societies, work drive - ability to navigate difficult life situations up to this point and will be able to employ techniques that I have already used to overcome challneges integrity - I have a strong moral compass, I am someone that you can trust, someone who will ask for help when needed, can be an example in difficult situations. emotional intelligence - ability to use others emotions coupled with my own to achieve a common goal. I am self aware, kind, and willing to be part of something bigger than myself. What is your greatest weakness ... As a member of a small and elite profession, what obligations will you have, if any, toward this profession? ...Advocacy - state and federal ...Time and financial help ... Continual research/publications ... educating the future ... Please explain the difference between SA02 and PA02? ... Tell me everything you know about hemoglobin.. Oxygen carrying capacity 4-02 sites present in PRBCs Protein Product on Bone marrow and erythropoetin from kidney Necessary to mantian perfusion/ scv02 oxyhhbg dissociation curve 13.5-17.5 men 12-15 female oxyhomglobin dissociation curve. What is a shift to the R and the L. What causes these shifts? defines different partial pressures of oxygen required to saturate the hgb molecule Usually defined as p50 (or a certain partial pressure required for 50% hgb saturation A shift to the right (reduced affinity) means that a high partial pressure of oxygen is required to mantain the same saturation. -increased temp -increased 2-3DPG -increased H+ ion (acidosis) A shift to the left means that a hgb molecule will mantain saturation with a smaller Pa02. - decreased temp - decreased 2-3 dpg - decreased H+ ion (alkalosis) Q: Tell me about a time when you had to manage a difficult clinical situation. ... Q: Tell me about a time when you were working with someone who wasn't pulling their weight, and they had a different value system than yours. How did you deal with this person? ... Q: Tell me about a time when you failed. What happened, and how did you recover? Final panel interview for critical care internship - didn't make it. Interview with CICU at the University of Utah wanted more experience. Capstone at shock trauma I had kept in touch but needed to prove myself with experience as this was my final goal as RN. Worked through SLRMC ICU to IMC ICU to reach my goal after having failed. Being patient is not being passive. It is working deligently toward your goals with a hope that your hard work will pay off in the end. Q: Tell me about a time when you had an ethical dilemma at work. What did you do? The process of death and dying... Think of one.. Q: Tell me about a time when you felt it was you against everyone else. You thought you were right and that everyone else was wrong. What did you do? ... Q: How do you handle stress? ... Tell us about your work experience.** ... Q: How do you describe success? I tend to view success incrementally. As someone who is invigorated by new, complex challenges, I never want to find myself in a situation where I feel like there is nothing left to learn or achieve. Bryan Goals! integrate didactic information and clinical data plan and administer a safe and physiologic anesthetic across the lifespan - evidence based translate research evidence to evaluate outcomes The student will demonstrate interprofessional and intraprofessional leadership. Q: Do you foresee any barriers to your education? (finances, time commitments) ... What does a CRNA do Physical assessment - risks to anesthetic administration, risks to procedures. Development of anesthestic management and plan. Anesthetic should be individualized to patient assessment, organ fuction, laborartory values. gathering necessary equipment acting on thoughts concerning assessment (follow up diagnostic tests/labs) Pre-operative teaching/expectations/development of patient relationship Initial anesthetic administration/manmagement of hemodynamics initially, continual assessment and communication with providers. Monitoring vital signs every 3-5 minutes, charting accordingly. Line placement, intubation, spinal/regional nerve blocks/ epidural administration. maintenence of anesthesia, hemodynamics, continued communication with team, diagnostic studys and other management necessary. Volatile/inhaled anesthetic, intravenous anesthetic,e ct. Resolution of anesthetic in timely manner and post operative evaluation and assessment. Following patient back to specific care unit and hand off. Q: What questions do you have for us?** ... If you saw one of your fellow students or colleagues using drugs outside of work/classroom, what would you do? If it was a question of patient safety, I would immediately confront the collegue concerning this problem. I think this would often depend on the situation, for many people would have a risk of self-harm, or harm of others when confronted with this problem Need to further investigate.. What relationship do I have with this person In what setting did it take place? What is the chain of authority like? If you had to pick a topic for a master's thesis or doctoral dissertation, what might it be? Ketamine facilitated Rapid Sequence Awake intubation Trauma Resusitation - damage control resucitation Use of TEG or ROTEM in MTP Ventilation in ARDS like the use of driving pressure Who (within the field) has influenced you the most? What do you consider the biggest issue facing the profession today? Next 5/10 years? Scott weingart - ED critical care in NY state Richard Dutton - R. Adams Cowley Shock Trauma Center - trauma anesthesiologist Rich Levitan - ED physician and airway guru Reubon Strayer - EM physician and Airway What is your strongest trait that will help you in your academic/professional career.** ... What is your most important weakness that you will struggle with, if any, toward this profession? ... What do you know about XYZ School and our program? ... What if in clinical someone told you were taping your IV wrong. What would you do? ... Tell me one of your greatest accomplishments? And at your last job? ... Give an example of where you showed leadership. ... Give an example of community service. ... Give an example of when you worked on a team. Calcium Channel Blocker Overdose Coding x 3 ` Calcium Insulin High Dose Glucogon Drip 3 pressors Push dose epi Vomit/Aspiration/Ards Paralytic Sedation CRRT Give me an example of your problem solving. Exploring ways to more quickly and effectively evaluate fluid responsiveness End Tidal CO2 with PLR/fluid bolus challenege This problem solving occurs with evaluating fluid/volume responsiveness What have you done to develop or change in the last few years?. Change is not a passive process. Constant effort. Tranforme as a nurse and team member. -Develop a greater sense of self awareness and emotional intelligence. -Develop a strong humility -Desire to be observant, to ask be extensively curious as to the "why" -Set goals for self-improvement sipiritally, emotionally, physically, and in all aspects of nursing. -These goals include advance certifications, daily study of up to date techniques, evaluation of progress, and making specific detailed plans. -Not taking myself to seriously and enjoying the journey as much as the result. Do you work well under pressure? Give an example. Trauma Gun shot wound to face/abdomen Hypovolemic shock, young. Trauma resusitation. MTP+fentanyl Calcium How do you think you will fit into the program? ... What do you want written on your tombstone? Humble, Hardworking, Father, and Bryan Graduate What will you do if you don't get into the program? Continue to apply Normal ranges for the following RAP CVP PAP PAWP SVR PVR EF RAP 2-6 CVP 3-8 PAP 20-30/8-15 MEAN <20 PAWP 6-12 (know that to optimize pre-load may mean higher than normal SVR 900-1400 PVR 50-150 EF >50% How do you calculate SVR <(MAP-RAP)x80 > / CO Where are dopaminergic receptors located? What does their stimulation result in? Renal, coronoary, cerebral, and mesenteric - vasodilation Beta 1 stimulation results in.. Inotropy Chonotropy Dromotropy - increased conduction velocity Dopamine MOA, dosing, uses Dubutamine MOA, dosing, uses Dose 2- 20 mcg/kg/min 2-5 mcg/kg/min = dopaminergic stimulation 5-10 mcg/kg/min = beta 1 stimulation 10-20 mcg/kg/min predominant Alpha stimulation Dubutamine 2-20 mcg/kg/min primarily B1 - Chonotropy/inotropy - B2 and A1 adenergic agonist - B2 being slightly more prevalent than A1 resulting in a more vasodilatory effect. Dobutamine 2-20 mcg/kg/min "inodilator" Beta 1 stimuation and vasodilation due to it's major metabolite 3-0 methyldobutamine. Methyldobutamine is an inhibitor of alpha adrenoreceptors. Milrinone .25-1 mcg/kg/min phosphodiasterase III inhibitor does not achieve positive inotropic afects through SNS stimulation. This in turn results in increased cAMP and subsequently, increased CA ion influx into cardiac muscle cells. Increased CA in cardiac cells results in increased force of contraction. In the vascular system, cAMP accumulation results in decreased CA ion influx resulting in vasodilation. Due to the lack of SNS stimulation dysrrhythmias are less common than with other inotropes Tell me about the anesthesia profession CRNAs serve in public sector, military OR, ambulatory surgical centers, physican offices, VA, maternity, military, rural anesthetic collaborative groups, free-lancing 50,000-60,000 CRNAs (50,000 in aana) - 1800's 43 million anesthetics/yr 25% more cost effective than 1:4 anesthesiologist/crna ratio.. 110% more cost effective than 1:1 supervision. How do you stay up to date in your practice I am not one to Go through and read a complete medical journal. I study by disease process, by resusitation technique ect. Monthly AACN Journals New England Journal of Medicine SMACC/FOAM/podcasts EMcrit EMwrap Trauma Cast R ER cast From the head of the bed Deranged Phys Uptodate Life in the fast lane Pulseless Vfib/Vtach Immediate initiation of CPR SHOCK 2 minutes CPR (IV/IO access) SHOCK 2 minutes CPR (EPI every 3-5 minutes), advanced airway, etC02) SHOCK 2 minutes CPR (amiodarone 300 mg bolus followed by 150 mg IV) TREAT REVERSIBLE CAUSES H and T Hypoxia hypovolemia Hydrogen Ion Acidosis Hyopglycemia Hypo/hyperkalemia hypothermia Tension Pneumo Tamponade Coronary/pulmonary thrombosis Toxins asystole/PEA CPR (IV/IO access, Epinephrine every 3-5 minutes, advanced airway etC02) SHOCK if SHOCKABLE CPR TREAT REVERSIBLE CAUSES Balloon pump inflates during Beginning of diastole Balloon pump deflates during End of diastole/beginning of systole Balloon pump results in a decrease in End diastolic blood pressure and after load which decreases myocardial o2 demand and improves systemic perfusion during systole Balloon inflation is triggered by what r wave What does balloon pump increase Diastolic BP Where does balloon pump sit Proximal descending aorta What kind of air is in the balloon pump The balloon is inflated with helium, an inert gas that is easily absorbed into the bloodstream in case of rupture summary of IABP At the start of diastole, the balloon inflates, augmenting coronary perfusion At the beginning of systole, the balloon deflates; blood is ejected from the left ventricle, increasing the cardiac output by as much as 40 percent and decreasing the left ventricular stroke work and myocardial oxygen requirements. In this manner, the balloon supports the heart indirectly. Contraindications for IABP It is contraindicated in patients with aortic regurgitation because it worsens the magnitude of regurgitation. IABP insertion should not be attempted in case of suspected or known aortic dissection because inadvertent balloon placement in the false lumen may result in extension of the dissection or even aortic rupture Depolarizing paralytic Example succinylcholine -Binds to nicotinic ach refeptor and opens the Na channel = Na diffuse down gradient into cell and action potential occurs = keeps mm paralyzed because it sits on the receptor longer than ach -fast on fast off, can't reverse it, don't use in renal failure, can cause hyperkalemia Can cause malignant hyperthermia- treatment dantrolene- direct muscle relaxant Non-depolarizing paralytic Act on nicotinic ach receptor but does not open up Na channel. Just block ach from binding = no jolt = mm can't contract Example rocc/vec Reversal is neostigmine--- interferes with breakdown of ach and indirectly stimulates nicotinic and muscarinic receptors edrophonium severe heads CO2 causes vasodilation- use rate to adjust it: ICP <20 33-38 ICP>30 32-35 * use end tidal c02 monitor and calibrate with abg Can't blow off TOO much CO2 because of ischemia therapeutic Na- 145-155 q6h sodium, osmo Na osmo no >315-320 to avoid acute renal failure CPP= map-icp (drive map up to increase CPP, and use adequate sedation) 3% saline draws fluid out of edemetous cerebral tissue due to high sodium and low h20 (creates an osmotic gradient) BUT watch for hyperchloremic acidosis (Cl in the 120s) switch to sodium acetate-- use q6h abg's to monitor --- 250mL over 20m and then 1mL/kg/hour normal icp >10, severe >40 severe head parameters HOB elevated, head/neck midline temp<100 >97 BG <150 CPP >60 ICP <30 CO2 30-38 call midwest within 1 hour gcs <8 intubate Massive blood transfusions TEG? Thromboelastography -Tranexamic acid 1g/100mL NS over 10m followed by 1g over 8h -cooler 1: 4u group O Leuko reduced PRBC, 4u plasma Recheck CBC, K, ICal, PT/PTT, fibrinogen, ddimer, 1st TEG or repeat TEG? -cooler 2: one Platelet pack to be given first, 4u PRBC, 4u thawed plasma -pcc (prothrombin complex concentrate)- combo of clotting factors and protein C and S. may be given if there is evidence or anti coagulation therapy What is TXA Tranexamic acid -Antifibrinolytic agent- inhibits fibrinolysis thus inhibiting the breakdown of the fibrin making up the clots and helps reduce bleeding -cannot be administered more than three hours after the injury. Unclear why What affect does administering PRBC have on calcium levels -hypocalcemia can be caused due to 3g sodium citrate in PRBC. Sodium citrate binds to ionized calcium -The healthy adult liver will metabolize 3 g citrate every five minutes. Transfusions at rates higher than one unit every five minutes or impaired liver function may lead to citrate toxicity and hypocalcemia What effect does administering PRBC have on potassium levels Hyperkalemia The plasma potassium concentration of stored blood increases during storage and may be over 30 mmol per liter hyperkalemia is generally not a problem unless very large amounts of blood are given quickly epidural hematoma blood accumulates between skull and dura- can be a surgical emergency because it's an arterial bleed subdural hematoma blood accumulates between dura and arachnoid can be treated with surgical evacuation, burr hole, drain placement subarachnoid hematoma blood between dura and pia medical management usually not surgical intraparenchymal hematoma blood accumulates within brain tissue, medical management non-surgical brain edema absence of sulci, ventricles shift seen at times craniectomy/ventriculostomy surgical intervention SIRS HR >90, RR>20, TEMP>38 OR <36, WBC >12 OR <4 OR >10% IMMATURE NEUTROPHILS SEPSIS >2 SIRS CRITERIA + INFECTION 3 hour bundle for sepsis lactate level, blood cultures before antibiotic, broad spectrum abx, map >65, lactate repeat labs until <2 6 hour bundle sepsis pressors to keep map >65, CVP goal 8-12, scvos >70, repeat lactate every 2-3 h until <2 what is sepsis wide spread inflammation triggered by cytokines- TNF, alpha IL2, alpha IL6m in response to infection. usually gram + can result in organ damage and blood clotting septic shock: decreased BP, increased CR(>2), increased Lactic a, AMS procalcitonin is marker for bacterial infection -you know your antibiotics are working if there is a decrease by 50% in procalcitonin in 24h TRALI- transfusion related acute lung injury usually within 6h of blood transfusion dyspnea, tachypnea, fever, cyanosis, hypotension, RR distress, volume overload, pulmonary crackles with no signs of congestive heart failure, cxray wll show bilat pulm edema unassociated w HF --occurs due to donor antibodies vs. reciptient leukocytes (more specifically, neutrophils),, they release cytokines which dilate capillaries making them permeable so they cant move 02 or co2 and are less compliant treat with o2 or vent in severe cases DIC- DISSEMINATED INTRAVASCULAR COAGULATION in dic the processes of coagulation and fibrinolyis sare dysregulated and the result is widespread clotting with resultant bleeding -TF is abundant in lung, tissues, placenta- develops in extensive traumas -TF binds with factor VIIa which activates factor IX, X, IXa, Xa= common coag pathway= formation of thrombin/fibrin -excess thrombin = excess coagulation cascade= cleaves fibrinogen= clots -excess thrombin= conversion plasminogen to plasmin = fibrinolysis. breakdown of clots= excess FDPs= powerful anticoag-hemmorrhage excess plasmin activates complement and kinin systems=shock symptoms and increased vascular permeability HIT heparin induced thrombocytopenia qquired allergy to heparin antibodies produced to heparin (IGG antibodies) that attack heparin and thrombocytes platelet count drops by 50% usually within 4-10 days of heparin administration treat: stop heparin, admin non-heparin anticoagm(ie: direct thrombin inhibitor like angiomax), admin platelets if needed LMW heparin decreases odds of HIT SIADH -too much ADH- produced in the hypothalamus stored in the pituitary -makes you hold onto H2O equals low sodium and Low osmolarity decreased urine output -causes head trauma surgeries cancer chemo..lots -major complication is seizures dilutional hyponatremia leads to fluid shift into the brain cells -treatment treat the cause fluid resuscitation 3% sodium if you have to DI -lose too much H2O 6 to 24 L per day high sodium high Osmo decreased ADH increased urine output -major complication hypovolemia leading to shock -treatment: give ADH, give fluids, monitor urine specific gravity, monitor EKG for ischemia (ADH equals vasoconstriction) hypo-osmolar IVF DKA -blood glucose 400 to 900 do not produce insulin -4-6 L fluid loss -acidosis body breaks down fat as energy equals ketones -kussmal respirations to breathe off CO2 -IVF (NS) to start + insulin GTT -when blood glucose is less than 250 switch IVF to half normal saline with D5 to keep from blood glucose dropping too fast which would cause cerebral edema -imperative to check and give potassium due to state of acidosis pushing potassium out of the cell -when you fix DKA K goes back into the cell equals hypokalemia equals death HHNK hyperglycemic hyperosmolar non-ketoic coma -Blood glucose L fluid loss -do produce insulin -95% mortality rate due to cerebral dehydration equals looks like a neuro problem -no acidosis because insulin prevent breakdown of fat as energy -treat with IV fluids and insulin albumin may be necessary - Free water replacement High-pressure alarm on the ventilator Kinks, H2O in the circuit, high mucus, bronchospasm, coughing Low-pressure alarms on the ventilator Decrease in lung pressure, increase in patient demand for oxygen due to agitation, pain, discomfort, change in lung compliance, patient disconnect, improper inflation of the cuff, loose circuit ARDS -Lungs not properly moving air in and out of blood due to major injury or extreme inflammation somewhere in the body which damages small blood vessel's including those in the lungs (can be direct or indirect) -Direct: Smoke, aspiration, pneumonia, near drowning -indirect: sepsis, blood transfusion, heart - lung bypass, pancreatitis, car accident, hit to the head or chest -leaky capillaries cause ARDS directly= alveolar injury or indirectly= capillary injury -pulmonary edema causes hypercapnia and hypoxemia -decreased alveolar compliance = increased work of breathing and decreased tidal volume= hypercapnia How to treat ARDS -Low volume, low pressure, minimal ventilation = minimize sheer force ( changing pressure/volume ) -want a negative pressure in the lungs at end of ventilation (low plateau pressure) -peep pushes fluid out of the lungs and back into the circulation -diuretics, proning, inhaled nitric oxide -NO dilates veins and healthy Alveoli only which increases oxygenation Oxyhemoglobin dissociation curve -How our blood carries and releases oxygen -The relationship between the partial pressure of oxygen and the oxygen saturation Oxyhemoglobin dissociation curve Shift to the right Caused by high temp, low pH, high PCO2, high DPG production Less affinity for O2 Oxyhemoglobin dissociation curve Shift to the left Caused by high pH, low temp, low PCO2, fatal hemoglobin, low DPG production Greater affinity for o2 pH and potassium Inverse relationship Change in pH by 0.1= increase in K by 0.6 pH. K. 7.45. 4.5 7.35. 5.1 7.25. 5.7 7.15. 6.3 Types of shock Distributive: Anaphylactic, septic, neurogenic Hypovolemic, cardiogenic Neurogenic shock -loss of vasomotor tone causing the parasympathetic nervous system them to dominate leading to massive vasodilation and bradycardia. Cardiac output decreased due to lack of preload and slow heart rate -caused by trauma at or above T6 -treatment: fill the tank and give alpha and beta stimulation -drug of choice phenylephrine Pulmonary shunting Blood that does not get any gas exchange at the alveolar level -can be caused by nipride, Edema, heart failure, severe pneumonia, bronchitis, mucous How to calculate tidal volume 6mL/kg ideal body weight Renin-angiotensin-aldosterone system and HF RASS is increased in patients with heart failure, and its maladaptive mechanisms may lead to adverse affects such as cardiac remodeling and sympathetic activation. Core measures for acute MI -12 lead ECG within 10 minutes -For ST elevation door to needle within 30 minutes (fibrinilytic therapy) or door to balloon (heart cath) within 90 minutes -smoking cessation, aspirin, Statin, beta blocker, ACE or ARB Precedex Alpha 2 agonist Stimulation of a2 inhibits release of norepinephrine Helps with alcohol withdrawal because alcohol withdrawal has excitatory effect on adrenergic system Propofol Like all general anesthetics, is poorly understood. However, propofol is thought to produce its sedative/anesthetic effects by the positive modulation of the inhibitory function of the neurotransmitter GABA through the ligand-gated GABAa receptors. Normal Urine Specific Gravity 1.003-1.030 Normal hemoglobin female 12-16 g/dL Normal hemoglobin male 14-17 g/dL Normal PT time 11-13 seconds Normal PTT 25-35 seconds Normal arterial HCO3 HCO3 22 - 26 mEq/L Normal: • Magnesium (Mg) 1.5 - 2.4 mEq/L Plasma osmolality 280 mOsm/L. Tricuspid valve auscultation location left side of sternum (medially) 5th intercostal space (between ribs 5-6) Mitral valve auscultation location left side of sternum (laterally) 5th intercostal space. (between ribs 5-6) Heart ausculatation pneumonic All Patients Take Medication Cardiac output equation and normal value heart rate x stroke volume. 4-8 L/min P wave represents depolarization of the atrium QRS complex represents depolarization of the ventricles. Q wave represents depolarization of the septum. ST segment represents contraction of the ventricles. T wave represents the ventricles are repolarizing. pulse pressure systolic BP - diastolic BP stroke volume equation End systolic volume - end diastolic volume SVR [(MAP - CVP) / CO] X 80 Sinoatrial Node Impulse-generating group of cells positioned on the wall of the right atrium, he "natural pacemaker" of the heart, ntrinsic firing rate is 60-100/min. atrioventricular node Group of modified cardiac muscle cells that delays action potentials between the atrial and ventricular chambers, intrinsic firing rate is 40-60/min. Normal pressure range Right atrium 1-8 mmHg Normal pressure range Right ventricle 15-30 systolic /0-8 mmHg diastolic Normal pressure range Left atrium 2-12 mmHg Normal pressure range Left ventricle 100-135 systolic /0-12 mmHg diastolic First heart sound (lub) closure of the tricuspid/mitral AV valves. Second heart sound (dub) closure of the semilunar (pulmonic/aortic) valves Frank-Starling Law of the Heart An increase in ventricular filling, increases preload which results in an increase in stroke volume. Normal stroke volume 60-90 mL Ejection Fraction equation ((EDV-ESV)/EDV)x100 or (SV/EDV)x100 Mean Arterial Pressure equation [Systolic + (2 x Diastolic) ] / 3 Cardiac index equation CO / body surface area Normal cardiac index 2.5 - 4.0 L/min/m2 Body surface area calculation square root of (Weight x height / 3600) Normal central venous pressure 3-8 mmHg Normal PAWP 6-12 mmHg Right bundle branch block V1: broad R wave and rSR. V6:qRS with broad S wave Left bundle branch block, causes, and EKG changes *wide QRS, V1 loss of septal R wave, V6 wide Q wave, inverted r Wave*. first degree heart block PR > 0.20 second degree AV block type 1 Prolongation of the PR until QRS drops. second degree AV block type 2 Intermittent non conductive P waves with no progressive prolongation of PR interval Third degree heart block Regular R-R and P-R, the AV node is not synchronized with the SA node A fib oscillating irregular baseline, no P waves, irregular R-R intervals A flutter Flutter waves, is sawtooth shape, with regular R to R intervals. Vtach rate 110-250, if monomorphic, beats have same configuration, if polymorphic, ventricular beats have changing configuration. Ventricular fibrillation irregular, random waveform, wandering baseline with no clearly identifiable p or qrs. Beta-l (B1) adrenergic receptors, where, and what do they do Located in the kidney, heart, and adipose tissue, produce an increase in heart rate and myocardial contractility. Results in increase in heart rate, AV conduction, heart contractility and renin release Beta-2 (B2) adrenergic receptors, where and what they do Located in smooth muscle and in glandular tissue. Causes inhibition of smooth muscle, dilation of blood vessels of skeletal muscle, glycogenolysis, gluconeogenesis, venous vasodilation, bronchodilation, increased lung secretions, insulin release, and Uterine relaxation Alpha-l adrenergic receptors, where and what they do found peripherally in numerous tissues. Stimulation causes vascular smooth muscle contraction, dilates pupil, increased heart contraction, arterial vasoconstriction, venous vasoconstriction, release of RBC from spleen, decrease renin, increased glucagon, uterus contraction Alpha-2 adrenergic receptors, where and what they do Located in sympathetic postganglionic neurons, peripheral tissues, and in the brainstem. Decreased insulin release, increased platelet aggregation, slight sedation, slight analgesia (spinal cord mediated) Effects of Hyperkalemia on the heart increases the excitability of the heart Cranial nerve (I) Olfactory - Transmission of the sense of smell. Cranial nerve (II) Optic - Vision Cranial nerve (III) Oculomotor - Adduction of eye, innervation of the medial rectus muscle, and pupil size. Cranial nerve (IV) Trochlear - Eye movement Cranial nerve (V) Trigeminal - Chewing (muscles involved in mastication) and sensory of the face. Cranial nerve (VI) Abducens - Abduction of eye and innervation of the lateral rectus muscle Cranial nerve (VII) Facial - Innervation of the facial muscles and taste (anterior 2/3 of the tongue). Cranial nerve (VIII) Acoustic - Balance Cranial nerve (IX) Glossopharyngeal - Taste (posterior 1/3 of the tongue) and sending of afferent impulses from the carotid body and carotid sinus to the brain. Cranial nerve (X) Vagus - Decreases heart rate and is involved in motor control of larynx and pharynx. Cranial nerve (XI) Accessory - Movement of the head and shoulders. Cranial nerve (XII) Hypoglossal - Tongue movement, smile. Circle of Willis Allows collateral blood flow in the event that a vessel becomes occluded. It is made up of the right internal carotid, the left internal carotid and basilar artery Cushing's Triad a reflex increase in mean arterial blood pressure a reflex decrease in heart rate irregular respirations. Cerebral Steal blood vessels in the non-ischemic portion of the brain dilate resulting in a decrease in blood flow to the ischemic areas. This can occur with administration of a vasodilator such as nitroprusside, or if a patient is hypoventilated resulting in a build up of CO2 in the blood. Inverse Steal Hyperventilation causes blood vessels in non-ischemic part of the brain to constrict diverting blood to the ischemic areas of the brain. How many vertebrae are there 33 7 cervical 12 thoracic 5 lumbar 5 sacral 4 coccygeal conus medullaris the lower end of the spinal cord. Cervical Plexus Group of nerves that make up the back of the head, the neck and the shoulders, made up of nerves originating from C1, C2, C3, C4, and C5. brachial plexus Made up of nerves originating from C5-C8 & T1 and control the hand, wrist, elbow, and sts of the: Musculocutaneous nerve Axillary nerve Radial nerve Median nerve Ulnar nerve Glutamate The most common excitatory amino acid neuro transmitter in the CNS. Barbiturates block this neurotransmitter. Acetylcholine responsible for Skeletal muscle contraction. Neuromuscular blockers block this neurotransmitter. Glycine An amino acid neurotransmitter that is involved with many motor and sensory pathways. In the spinal cord it is inhibitory in nature and results in a decrease in action potentials. GABA The major inhibitory neurotransmitter in the central nervous system. Benzodiapines (Midazolam, Lorazepam, Diazepam) work by mimicking the action of GABA. Nurse Anesthetist use these medication to induce a sedative/amnestic state in the patient. Pulmonary artery: systolic and diastolic pressure, causes of increases and decreases of pressure systolic pressure of 15-25 mm- Hg, diastolic of 8-15 mm-Hg. Increases in pressures are seen with volume overload, LV failure, mitral stenosis, and cardiac tamponade. Decreases in pressure indicate hypovolemia. vital capacity The maximum volume of air that can be exhaled after taking the deepest breath possible How to estimate PaO2 and PAO2 multiplying percent O2 in the inspired gas mixture by 5, or by 6 for alveolar. Expiratory Reserve Volume (ERV) and normal value 1.5 Liter, the amount of air that you can breathe out after the normal expiratory volume. vital capacity calculation VC = IRV + ERV + VT vital capacity= inspiratory reserve volume + expiratory reserve volume + tidal volume minute ventilation, normal, meaning, equation 6 L and represents the amount of air breathed in over one minute. Minute Ventilation = respiratory rate x tidal volume. Factors that Cause Leftward Shift of oxyhemoglobin dissociation, and effect the amount of O2 carried by hemoglobin is increased in affinity. (unloading is more difficult) - Decreased temperature - Increased pH (decreased H+ concentration) - Decreased PCO2 - Decreased concentration of 2,3- diphosphoglycerate (2,3-DPG) - Fetal hemoglobin (HbF) - Carboxyhemoglobin Methemoglobin Factors that Cause rightward Shift of oxyhemoglobin dissociation, and effect. the amount of O2 carried by hemoglobin is reduced/lower affinity. (unloading is facilitated) Increased temperature - Decreased pH (increased H+ concentration) - Increased PCO2 - Increased concentration of (2,3-DPG) - Sickle cell (HbS) Hering-Breuer reflex a protective mechanism for preventing over inflation of the lungs. The vagus nerve carries the afferent (sensory) information for this reflex. FEV1 reflects the forced expiratory volume in one second. This gives you a volume corresponding to how much gas was expired over first second of expiration. FVC Forced vital capacity is the volume of gas that can be exhaled during a forced expiration. FEV1/FVC ratio useful in distinguishing between Obstructive and Restrictive diseases (Ex. COPD vs Pulmonary fibrosis). ≥ 0.7 (70%). s/s PE Chest pain, Dyspnea, Decreased end tidal CO2, Elevated central venous pressure, Tachycardia, decreased cardiac output, increased dead space ventilation, bronchoconstriction Laplace's law For alveoli with normal surfactant, tension will increase with increases in radius. Since alveolar wall tension increases in proportion to increases in radius, the pressure within the alveolus doesn't change. explains why small alveoli do not empty into large alveoli in normal lung. In ARDS, smaller alveoli empty into larger alveoli causing atelectasis because of surfactant depletion. Alveolar Pressure change of pressure that facilitates the movement of air, goes back and forth from -1 to +1 cm H2O . When alveolar pressure is -1 cm H2O, and pressure outside the body is 0 cm H2O, air begins to move into the lungs. alveolar pressure is negative during inspiration and positive during expiration. The Bohr effect refers to the shift in oxyhemoglobin dissociation curve in response to an increase or decrease in PC02. Haldane effect Changes in the blood (PaO2) can influence the blood CO2 dissociation curve. increased PaO2 causes shifts down and to the right (less likely to pick up CO2, and more likely to let go). If PaO2 decreases, curve shifts up and to the left (meaning more likely to pick up CO2 and less likely to let go). What percent of cardiac output goes to the kidneys? About 25% of cardiac output, which is about 1.25 liters/min, is pumped through the kidneys each minute. proximal tubule Reabsorbs majority of the filtered fluids and dissolved substances (67%). Osmotic diuretics hinder this process. Reabsorption of bicarbonate allows kidneys to balance pH. Glomerular filtration rate definition and normal value Amount of blood passing through the glomerulus each minute. normal GFR is 125 ml/min Decreased GFR: Significant hypotension • Hemorrhage • Hypovolemia • Aging • Renal failure. Increased GFR: • Diuretics • Diabetic Ketoacidosis • Diabetes Insipidus • Hypertension The loop of Henle Establishes and maintains an osmotic gradient in the medulla of the kidney. This osmotic gradient is important in the regulation of water balance. The fluid leaving the loop of Henle is hypo-osmotic. diabetes insipidus s/s and treatment Very high urine output (10-15 liters/day), High serum osmolarity (> 145 mEq/L), Low urine osmolarity (< 1.010), Hypotension, Tachycardia, Excessive thirst. Treatment: Administer IV pitressin (synthetic ADH), Fluid replacement, Correct electrolyte imbalances Aldosterone Regulates extracellular fluid volume and blood pressure. Aldosterone is produced in the zona glomerulosa of the adrenal cortex, and acts primarily the collecting duct of the kidney. Increases the rate of sodium reabsorption and potassium secretion. Renin produced in the kidneys and converts angiotensinogen into angiotensin 1. Angiotensin converting enzyme (ACE) Produced in the lungs. Converts angiotensin 1 into angiotensin 2. Angiotensin 2 causes release of aldosterone from the zona glomerulosa of the adrenal cortex. Hyperkalemia (evidenced by? IV fluids to avoid) Results from the kidneys inability to excrete potassium and is the most serious electrolyte abnormality. Avoid lactated Ringer's (contains 4 mEq/L of potassium). Evidenced by: prolonged P-R interval, widened QRS complex, and peaked T waves. Posterior Pituitary (Neurohypophisis) Produces ‣ Antidiuretic hormone (ADH): regulates the body's retention of water ‣ Oxytocin: stimulates milk production in pregnant women - increased uterine contraction Anterior Pituitary (Adenohypophysis) Produces Growth Hormone (GH), which stimulates growth & cell reproduction; as well as Adrenocorticotropic hormone (ACTH), which in response to biological stress, increases production and release of corticosteroids (cortisol) Cushing's syndrome body is exposed to high levels of the hormone cortisol for a long period of time. Caused by Adrenal tumors and Oral corticosteroid medication. Signs/Symptoms: • Breakdown of tissue and muscle mass • Bone loss • Purple stretch marks on the skin • Fatty hump between your shoulders • Rounded face Treatment: • Lower the body's cortisol levels (reduce dose of oral corticosteroids) • Surgery (remove adrenal tumor) Addison's disease (patho, causes, s/s, treatment) Body's adrenal glands produce insufficient amounts of cortisol and aldosterone. Causes: Genetic predisposition, Adrenal cancer, Pituitary tumor or infection Signs/Symptoms: Inability to handle stress, Hypotension, Dehydration, Darkening of the skin, Hyperkalemia, Mild acidosis Treatment: Corticosteroid replacement Conn's Disease condition characterized by the excessive production of a hormone called aldosterone by the adrenal gland. Causes: Adrenal tumor located in the zona glomerulosa, Enlargement of the adrenal glands Signs/Symptoms: Increased sodium and water retention, Hypokalemia, Weak muscles, Metabolic alkalosis, Headache, Hypertension Treatment: Lowering blood pressure, Reducing water retention, Surgery to remove adrenal tumor hypothalamic-Pituitary thyroid axis The hypothalamus excrete Thyrotropin releasing hormone (TRH), which stimulates the posterior pituitary Gland and the anterior pituitary gland then releases Thyroid stimulating hormone (TSH), which stimulates the Thyroid to excrete Thyroid hormone (Thyroxine/T4). Grave's disease autoimmune disease, antibodies attack the circulating thyroid hormones. People that take in a lot of iodine are at risk. Signs/Symptoms: Increased sweating and intolerance to heat, Weight loss, diarrhea, muscle weakness, mental disorders, & muscle tremors, High level of TSH and low levels of T3 & T4. Treatment: Antithyroid drugs, Propylthiourocil (PTU), Surgery (Removal of thyroid), Radioisotope therapy Normal ICP 7<20 Normal CPP >60 Hyperparathyroidism Caused by Parathyroid adenoma or Chronically low calcium states (chronic renal failure). s/s: High serum calcium levels (> 10.5 mg/dl), S/S of high calcium: (rare) Weakness, Fatigue, and Muscle pain Hypoparathyroidism Caused by Surgical removal or damage to the parathyroid glands. s/s: Low serum calcium levels (< 6.5 mg/dl), S/S of low calcium: Chvostek's Sign (tapping on facial nerve produces tetany of the facial muscles), Trousseau's Sign (placing a blood pressure cuff around the arm will produce a muscle spasm of the forearm and wrist.) and bronchospasms What does % concentration mean? grams/100 ml or move one decimal to the right, and it is mg/mL. What does 1:1,000 mean? 1:1,000 means (1 gram/1,000ml) of solution 1:100,000 concentration of epinephrine is equal to how many mcg/ml? You can convert various concentrations to mcg/ ml by dividing the denominator into 1,000,000. (1,000,000 ÷ 100,000 = 10) 1:100,000 = 10 mcg/ml How do you convert a patient's weight in pounds to kilograms? kilograms = lbs / 2.2 Ideal Body Weight (IBW) definition and calculation for men and women expected weight that a healthy person should be based on gender and height. Male = height (cm) - 100 Female = height (cm) - 105 Conversion of inches to cm 2.54 cm per inch BMI = body weight (kg) / height2 (m) Convert degrees Fahrenheit (F) to degrees Celsius (C)? C = (F - 32) x (5/9) convert degrees Celsius (C) to degrees Fahrenheit (F)? F = (C x 9/5) + 32 Dalton's Law of Partial Pressures states that: The total pressure in a mixture of gases is equal to the sum of the pressures of the individual gases. *We can calculate the partial pressure of a gas by knowing it's % concentration and the total pressure of the mixture.* Phenylephrine Neosynephrine, rate 40-60 mcg/min. Alpha 1 and minimal Alpha 2. Isoproterenol Isuprel, rate 2-20 mcg/min Activates Beta 1 and Beta 2 Used to treat shock, cardiac arrest and anaphylaxis Dobutamine Dobutrex, rate 2-20 mcg/kg/min. Minimally activates Alpha 1 receptors and fully activates Beta 1 receptors. used to treat heart failure and low cardiac output. Epinephrine Adrenalin, rate 0.05-0.1 mcg/kg/min. Activates alpha 1 most, less so Beta 1 and Beta 2, and Alpha 2 least. Norepinephrine Levophed, rate 0.05-0.5 mcg/kg/min. Primarily activates alpha 1, less so Alpha 2 and less so, Beta 1. Dopamine Inotropin, rate 2-20 mcg /kg/min. Activates alpha 1 alpha 2 and beta 1 equally and beta 2 less. Uses include cardiogenic shock, sepsis, cardiac surgery, and hypotension unresponsive to fluid administration. Ephedrine dose 5-10 mg IVP. Activates Alpha 1 and 2 , more strongly than Beta 1 and 2 indirect acting sympathomimetic most effective when treating postural hypotension and asthma Albuterol Ventolin. Dose Aerosolized. Activates Beta 2 , and Beta 1 minimally. ABG pH range 7.35 - 7.45 ABG pCO2 range 35-45 mmHg ABG HCO3 range 22 - 26 mmol/kg ABG Base Excess -2 to 2 ABG PO2 80 - 100 mmHg ABG SaO2 (SpO2) 95-99% on RA Respiratory Acidosis pH < 7.35 PaCO2 > 45 (Primary) HCO3 > 26 (Secondary) Metabolic Acidosis pH < 7.35 HCO3 < 22 (Primary) PaCO2 < 35 (Secondary) Respiratory Alkalosis pH > 7.45 PaCO2 < 35 (Primary) HCO3 < 22 (Secondary) Metabolic Alkalosis pH > 7.45 HCO3 > 26 (Primary) PaCO2 > 45 (Secondary) PaCO2 is a ____, controlled by the _____ Acid Lungs Respiratory parameter - rapid change HCO3 is a ____, controlled by the _____ Base Kidneys Metabolic parameter - slow change Anion Gap Normal 5 - 15 mEq/L Difference between positive and negative anions - increase in gap correlates with metabolic acidosis (Na + K) - (Cl + HCO3) Problems Associated with an Increase in Anion Gap Ketoacidosis Uremia Salicylate intoxication Methanol Alcoholic ketosis Unmeasured osmoles: ethylene glycol, paraldehyde Lactic acidosis: shock, hypoxemia Problems Associated with a Normal Anion Gap Saline Infusions (hyperchloremic acidosis) TPN Diarrhea Ammonium chloride Acute renal failure, sometimes chronic (These are less common - normal anion gap metabolic acidosis) Normal SVR 800 - 1200 SVR Calculation ((MAP - CVP) / CO) x 80 Cardiac Output Calculation CO = HR x SV CO Normal Range 4 - 8 L/min Nicardipine Class - Antihypertensive MOA - Ca Ion Influx Inhibitor or Ca Channel Blocker - slows the transmembrane influx of Ca ions into cardiac muscles and smooth muscle without changing serum calcium concentrations - selective to vascular smooth muscle than cardiac muscle - reduces afterload more - with little or no negative inotropic effect (unless in pts with severe LV dysfunction - leading to worsened failure) (Contraction of heart and smooth muscles dependent on extracellular Ca ion moving into muscle cells through specific ion channels) - liver metabolism mainly Hydralazine Class - Antihypertensive MOA - Unknown - Direct vasodilation of smooth muscle (arteries and arterioles) - decrease SVR and afterload - Reflex tachycardia (baroreceptor reflex) - liver metabolism, kidney excretion Labatalol MOA - mix A1, and B1 and B2 adrenergic receptor blocker Metoprolol MOA - selective B1 receptor blocker Esmolol Class II antiarrhythmic MOA - cardio-selective B1 blocker with rapid onset and short DOA Activation of these receptors cause stimulatory responses Alpha 1 Beta 1 Activation of these receptors cause inhibitory responses Alpha 2 Beta 2 Beta 3 Alpha 1 Receptors - More responsive to Norepi than Epi - Activation causes vasoconstriction - Abundant in vascular smooth muscle - GI & urinary sphincters - dilator muscle of the iris (reducing tone enlarges the pupils) - arrector pili muscle of the hair follicles (reducing tone causes hair to stand on end) Alpha 2 Receptors - Secretary terminals of some postsynaptic adrenergic neurons - negative feedback mechanism on Norepi secretion Beta 1 Receptors - cardiac pacemakers (increase rate) - myocardium (increase force of contraction) - salivary gland ducts - eccrine and apocrine sweat glands Beta 2 & 3 Receptors RELAXATION (Tx Asthma and premature labor) When stimulated by Epi or Norepi - inverse response - Smooth muscle (muscle tone relaxation) in GI tract - Urinary bladder (B3) - Skeletal muscle arteries (enhance blood flow when epi is present) - Bronchial tree (enhance blood flow when epi is present) - Some coronary vessels Dopamine - stimulating B1 receptor (increase HR and contractility) at 5 - 10 mcg/kg/min - minor B2 stimulation related to peripheral vasodilation (at low doses) - higher dosing (10 - 20 mcg/kg/min) can stimulat alpha receptors leading to vasoconstriction and increase in BP - used in tx of septic or cardiogenic shock - neurotransmitter in the brain - inhibits norepi release and acts as vasodilator - increase Na secretion and UO in the kidneys Dobutamine - Stimulates B1 receptor (increase heart rate and contractility) - has less B2 stimulation (vasodilation) - tx heart failure and cardiogenic shock - can further lower SVR therefore not used in tx of septic shock Initial defect in septic shock drop in SVR (vasoconstrictor recommended) Epinephrine (Adrenaline) vs. Norepinephrine Epi - increases HR, cardiac output but not really BP (Primarily B1 stimulation) - B2 - drops SVR - bronchodilator (B2) - mydriatics (B2) - A1 & A2 - Vasoconstrictor at higher concentrations Norepi - transient increase in HR and inotropy (B1) - later decreases due to baroreflex - A1 & A2 - Increases CO and SVR (SBP) - NO B2 stimulation Precedex vs. Propofol ... Benzos & Opioids ... Anesthetic Gases ... Paralytic and Reversal Agents ... Brain Stem Reflexes ... Cranial Nerves ... Oxyhemoglobin Dissociation Curve ... SIADH & DI ... Vasopressin ... Neosynephrine ... Normal PAP 20/8 to 30/15 Mean < 20 Normal PAOP 8-12 mmHg (varies depending on LV function) Normal PVR 50 - 250 Normal ICP & CPP ICP 5 - 15 mmHg CPP 70-80 mmHg Shock States and Hemodynamics ... PA Artery Wave ... Coagulation Cascade ... ACLS concepts*** ... PEA without a pulse ... Nitroprusside & Nipride ... Milronone ... Alpha 1 intracellular mechanism G(q)-coupled secondary messenger system that leads to phospholipase C (PLC) activation, which causes an increase in both inositol triphosphate (IP3) and calcium, which then activates Protein Kinase C, which then phosphorylates numerous other enzymes and regulates ion channels Alpha 2 intracellular mechanism G(i)-coupled secondary messenger system that causes an INHIBITION of adenylate cyclase and hence a decrease in cAMP, ultimately leading to a decrease in protein kinase A (PKA), and decreased cellular activity Beta 1 intracellular mechanism G(s)-coupled secondary messenger system that causes activation of adenylate cyclase which catalyzes the formation of cAMP from ATP. This rise in cAMP leads to an increase in intracellular protein kinase A (PKA), leading to a variety of intracellular events Beta-2 intracellular mechanism G(s)-coupled secondary messenger system that causes activation of adenylate cyclase which catalyzes the formation of cAMP from ATP. This rise in cAMP leads to an increase in intracellular protein kinase A (PKA), leading to a variety of intracellular events General opioid intracellular mechanism G(i) coupled secondary messenger system that prevents conversion of ATP to cAMP. This prevents the influx of Ca2+, hyperpolarizing cells The G(I) protein also prevents K+ from entering, further hyperpolarizing the cell Ultimately, the hyperpolarization leads to decreased excitability This hyper polarization is desired, because it leads to DECREASED released of (inhibitory) GABA in the ANTINOCICEPTIVE pathway in the periaqueductal gray region General benzodiazepine intracellular mechanism Benzodiazepines binds to allosteric sites on GABA receptors. When they do, they cause a conformational change of the receptor which greatly increases the AFFINITY for GABA on the receptor. This increased affinity causes an increase in the FREQUENCY of the opening of the chloride ion channel, leading to hyper polarization across the membrane d/t influx of chloride, decreasing the chance that an AP will occur Dexmedetomidine intracellular mechanism Dexmedetomidine binds to alpha-2 receptors in the locus coeruleum. This area is responsible for the stress response -- it sends inhibitory signals (via GABA) to the ventrolateral pre optic nucleus, which, when activated, typically causes sleep. When alpha-2 receptors are activated (see intracellular mechanism of alpha-2 receptors), GABA release from the locus coeruleum is inhibited, hence the VLPO becomes more activated, leading to a sleep-like state Propofol intracellular mechanism Very similar to benzodiazepines, except instead of increasing the FREQUENCY of Cl- channel opening, it slows its closing time It may also act as a sodium channel blocker It may also have effects on the endocannabinoid system Ketamine intracellular mechanism NMDA receptor antagonist Typically when NMDA receptors are agonized by NMDA (glutamate subtype), there is an influx of positive ions, leading to depolarization Ketamine blocks NMDA from binding, hence this cation influx can't happen, leading to a cessation of APs Pentobarbital/barbiturate intracellular mechanism Very similar to benzodiazepines/propofol, except it increases the DURATION that Cl- channels are open, which makes GABA much more efficient Can be direct agonists of GABA binding sites at sufficiently high doses May also act as glutamate antagonist Vecuronium intracellular mechanism Aminosteroid non-depolarizing neuromuscular blocking agent Vec is a competitive antagonist of nicotinic cholinergic receptors at the motor end plate. Normally, an AP transverses the nerve, which causes an influx of calcium at presynaptic voltage-dependent ion channels, which then release ACh into the synaptic cleft via exocytosis. Once ACh binds to nicotinic ACh receptors on the motor end plate, the cells see a Na+ influx, leading to depolarization, contraction of myofibril and ultimately muscle. Rocuronium intracellular mechanism Same as Vec Cisatracurium intracellular mechanism Tetrahydroisoquinolinium non-depolarizing NM blocking agent Same mechanism as vec/roc, but slightly different chemical base (based on atracurium rather than pancuronium) Dopamine intracellular mechanism DA1/DA receptors, primarily in the kidneys, catalyzes ATP into cAMP via adenylate cyclase, which decreases the activity of the Na+/H+ exchanger (typically causes H+ efflux and Na+ influx, hence retention of water. Stopping this process leads to more extracellular Na+, taking water/urine with it) This cAMP also modulates phopholipase C and other protein kinases Receptors also found in coronary, cerebral, and mesenteric systems, which actually cause arterial vasodilation Milrinone intracellular mechanism Phophodiesterase 3 inhibitor Phophodiesterase typically breaks down bonds in cAMP/cGMP, thereby stopping their intracellular effects. By inhibiting phosphodiesterase, milrinone allows cAMP/cGMP dependent pathways to function longer. Wtih heart cells, cAMP leads to pKA activation, which allows the contractile machinery of cardiac cells to work effectively cAMP in this case also allows an increase of Ca2+ into the cell, also leading to increased myocardial contractility Lastly, increased cAMP in vascular tissue leads to vasodilation Fentanyl: Dosing Onset Duration Half-life Metabolism/elimination AE/contraindications Dosing: 0.5-3 mcg/kg/hr gtt; same bolus (start ~ 1 mcg/kg) Onset: rapid Duration: 30-60 minutes Half-life: alpha - 6-7 minutes; beta - ~6 hours (wide variability) Metabolism: CYP 3A4 Elimination: primarily renal (active metabolites and some unchanged) AE: muscle rigidity in thoracic/abdominal muscles Contraindications: COPD/asthma Hydromorphone Dosing Onset Duration Half-life Metabolism/elimination AE/contraindications Dosing: 0.01-0.04 mg/kg/hr (can increase if HDS and/or for palliative care) Onset: rapid (peak within 0.5-1 hour) Duration: 4-5 hours Half life: (beta) ~2.3 hours Metabolism: hepatic glucuronidation Elimination: renal, as a glucuronide conjugate AE: use caution with renal patients as this can increase it's half life Morphine Dosing Onset Duration Half-life Metabolism/elimination AE/contraindications Dosing: 0.05-0.1 mg/kg (bolus) Onset: rapid (within 5 minutes) Duration: 3-7 hours Half-life: ~ 2 hours Metabolism: hepatic glucuronidation (one metabolite is active, M6G) Elimination: renal, 10% biliary Naloxone dosing and administration 0.1 mg/kg for under 20 kgs; 2 mg for > 20 kg; repeat q2-q3 PRN Infuse over ~1-2 minutes to reduce the risk of emesis Lorazepam Dosing Onset Duration Half-life Metabolism Excretion AE/Contraindications Dosing: 0.05-0.1 mg/kg Onset: 1-5 minutes Duration: ~4 hours; variable with a dose-dependent relationship Half-life: ~10-20 hours Metabolism: hepatic glucuronidation Excretion: renal AE: same as other benzos Midazolam Dosing Onset Duration Half-life Metabolism/excretion AE/contraindications Dosing: 0.01-0.08 mg/kg bolus 0.06-0.24 mg/kg/hr gtt Onset: rapid; 1-5 minutes Duration: 1-6 hours (dose dependent) Half-life: alpha - 6-20 minutes; beta - 1-6 hours (on the longer side for peds) Metabolism: CYP 3A4 to some active/inactive metabolites, which then undergo hepatic glucuronidation Excretion: renal AE/contraindication: same as other benzos Flumazenil dosing and administration 0.01 mg/kg with max dose of 0.2 mg over 15 seconds; repeat after 45 seconds, then every minute with a max of 5 doses (1 mg max) Dexmedetomidine Dosing Onset Duration Half-life Metabolism Excretion AE/contraindications Dosing: 0.2-1 mcg/kg/hr (may use loading dose of 1 mcg/kg over 10 minutes) Onset: 30 minutes (can be decreased with a loading dose) Duration: 4 hours Half-life: alpha - 6 minutes; beta - 2 hours Metabolism: CYP 450 system to active/inactive metabolites, then glucuronidation Excretion: renal AE: bradycardia, hypotension, hypertension at high doses Contraindications: do not use for greater than 24 hours Propofol Dosing Onset Duration Half-life Metabolism/excretion AE/contraindications Dosing: 1-3.5 mg/kg bolus; 5-50 mcg/kg/min gtt Onset: rapid (15-30 seconds) Duration: 5-10 minutes Half life: alpha - 2-8 minutes; beta - 2-24 hours Metabolism: liver glucuronidation Excretion: renal and hepatic AE: arrhythmia, hypotension, apnea, seizure, PROPOFOL INFUSION SYNDROME (heart failure, rhabdo, metabolic acidosis, renal failure, hepatomegaly) Ketamine Dosing Onset Duration Half-life Metabolism/excretion AE/contraindications Dosing: 0.5-2 mg/kg bolus; 5-20 mcg/kg/min (titrate to effect) Onset: ~30 seconds - 5 minutes Duration: < 1 hour (typically 5-10 minutes) Half-life: alpha - 10-15 minutes; beta - 2.5 hours Metabolism: CYP 3A4 Excretion: renal AE: hypertension, bronchospasm, psych reactions (hallucinations, psychosis, etc), muscle spasms Contraindications: increased ICP Pentobarbital Dosing Onset Duration Half-life Metabolism Excretion AE/contraindications Dosing: 10-15 mg/kg over 30 minutes (bolus for induction); 1-4 mg/kg/hr (gtt) Onset: 3-5 minutes Duration: 3-4 hours Half-life: 15-50 hours Metabolism: CYP 450 system, several isoforms + glucuronidation Excretion: renal AE: hypotension!!!! + bradycardia Vecuronium Dosing Onset Duration Half-life Metabolism Elimination AE/contraindications Dosing: 0.1 mg/kg Onset: ~2 minutes Duration: 25-40 minutes Half-life: 65-70 minutes Metabolism: not fully understood Excretion: mostly fecal; some renal (as unchanged drug and metabolites) AE: muscle weakness after prolonged use Contraindications: pts taking quinine/quinidine Vec/Roc/Nimbex reversal Cholinesterase inhibitor such as neostigmine, along with an antimuscarinic like atropine or glycopyrrolate to block adverse muscarinic effects Rocuronium Dosing Onset Duration Half-life Metabolism/elimination AE/contraindications Dosing: 0.6 mg/kg Onset: faster than vec, but slower than succ, typically < 1 minute Duration: 20-30 minutes (shorter than vec) Half-life: 1.5-2.5 hours Epinephrine Dosing Indications Onset Duration Half-life Metabolism/excretion AE 0.03-1 mcg/kg/min (gtt) 0.01 mg/kg (CODE) Indications: COLD shock Onset: rapid Duration: seconds/minutes Half-life: 2-3 minutes Metabolism: COMT and MAO at receptor site AE: tachycardia, arrhythmias, hypertension, shakiness, anxiety Norepinephrine Dosing Indications Onset Duration Half-life Metabolism/excreti