CRNA Interview Prep, crna school, crna notes, crna student, crna study guide, Study Guides, Projects, Research of Nursing

Download CRNA Interview Prep, crna school, crna notes, crna student, crna study guide and more Study Guides, Projects, Research Nursing in PDF only on Docsity! Interview Questions: Why do you want to be a CRNA? Discuss a mistake you made and how you resolved it tell us about yourself. ask you about a "challenging" case you have had What do you see as your role? What would you do if you received a bad review that you felt was untrue? How do you deal with problems, stressful situations, being critiqued, and confrontations What are your strengths/weaknesses? Why did you choose this program? What do you know about this program? What would you do if you didn't get in? What would you do if you saw a fellow student with drugs? (They went into a complete scenario with the "fellow student" even being threatening.) What are your career plans? How do you relax if you're feeling stressed? *How do you handle stress What are your two most important achievements as a nurse? Why did you choose this career field over other advanced practice fields? *why not NP? Why not MD? What attributes make you suitable for this career field? Why should we choose you over other prospective applicants? tell us about what preparations you and your family has done to prepare for the rigors of crna school? how prepared are you to be a novice again? how well do you handle criticism? How do you plan on supporting yourself while in school since you won't be able to work? Do you have any questions for us? What did you do this morning before coming to the interview? How I handled a tough scenario with a colleague. What I would do if I had a disagreement with an anesthesiologist and how I would handle it. *What would you do if a senior anesthetist threatened you? What don't you like about your job What about your experience makes you believe you would like to be a CRNA: What is your support system like: Drugs and pathophys: Beta 1 receptor -> heart, increase HR, contractility, conduction velocity Beta 2 - blood vessels -> dilate Alpha 1 - vasoconstriction Alpha 2 - inhibit norepi release Alpha adrenergic receptors are linked to Gq-proteins that activate smooth muscle contraction through the IP3 signal transduction pathway. Gq-proteins in vascular smooth muscle are coupled to α1-adrenoceptors (bind to norepinephrine), ETA receptors (bind to endothelin-1), AT1 receptors (bind to angiotensin II), V1 receptors (bind to vasopressin), and muscarinic (M3) receptors. Two signal transduction pathways are linked to Gq-proteins: phospholipase C pathway (forms inositol triphosphate, IP3) and Rho-kinase pathway. IP3 pathway stimulates SR release of calcium and activates protein kinase C (PK-C) via formation of diacylglycerol (DAG), which stimulates contraction. The Rho-kinase pathway (not shown in figure) inhibits myosin light chain phosphatase, which enhances contraction. Vasopressin - polypeptide act on V1, V2, V3 receptor. V1 receptor stimulate vascular smooth muscle contraction. V2 receptor act on renal collecting tubule to produce water retention. V3 receptor act in CNS and modulate corticotropin secretion. c/f splanchnic hypoperfusion Dose range: 0.5-4 units/hr Dopamine - stimulate postjunctional dopaminergic receptors in renal, mesenteric, and coronary arterial beds to produce vasodilation 0.5-1 mcg/kg/min dilate renal arteries and increase UOP 2-5 mcg/kg/min beta stimulation 5-10 mcg/kg/min alpha and beta >10 mcg/kg/min predominant alpha stimulation Isoproterenol - beta1 and beta2 agonist (no alpha). Increase HR, contractility, and dilate both venous and arterial vessels. More chronotropy and vasodilation than dobutamine. Dobutamine - selective B1 agonist. Minimal increase in HR, positive inotrope, increase CO, some decrease in systemic and pulm vascular resistance (decrease in afterload and preload). Can cause hypotension or sometimes hypertension (inhibit reuptake of norepi) Dose range: 2-10 mcg/kg/min Milrinone - Phosphodiesterase inhibitor. Increased inotropy and lusitropy (myocardial relaxation). Improve RV function by decreasing pulmonary vasc resistance. Also has vasodilatory effect (hypotension). Relative lack of significant tachyarrhythmias. Amrinone can cause thrombocytopenia May transiently restore beta-adrenergic fxn by decreasing cAMP breakdown -> stimulate cardiac ca+ channels to increased Ca+ concentration as well as potentiating action of administered beta-adrenergic agonists. Cyclic-AMP is broken down by an enzyme called cAMP-dependent phosphodiesterase (PDE). The isoform of this enzyme that is targeted by currently used clinical drugs is the type 3 form (PDE3). Inhibition of this enzyme prevents cAMP breakdown and thereby increases its intracellular concentration. This increases cardiac inotropy, chronotropy and dromotropy. Unlike cardiac muscle, increased cAMP in smooth muscle causes relaxation. The reason for this is that cAMP normally inhibits myosin light chain kinase, the enzyme that is responsible for phosphorylating smooth muscle myosin and causing contraction. Increased cAMP activate protein kinase -> phosphorylate proteins in the sarcoplasmic reticulum/sarcolemma -> increase Ca+ influx via Ca+ channels, amplifying effects of Ca+ on contractile elements. Improve diastolic relaxation (lusitropy) by stimulating reuptake of Ca+ into the SR Loading dose: 50 mcg/kg IV over 10 minutes. Maintenance infusion: 0.2 to 0.8 mcg/kg/min. Decrease preload, decrease afterload, decrease BP, increase contractility Beta blocker - antihypertensive, antianginal, antiarrhythmic Beta-1 blockade produce negative inotropic and chronotropic effect, decrease CO and myocardial oxygen requirement. Beta blocker can cause AV block. Can decrease sign of hypoglycemia. Can interfere with K+ movement. Beta-2 blockade cause bronchoconstriction and peripheral vasoconstriction; inhibit insulin release and glycogenolyis. Metoprolol - selective beta-1 blocker. Risk for bradycardia, bronchospasm, conduction blockade, fatigue Esmolol - 50-300 mcg/kg/min. Cardioselective beta-1 blocker Carvedilol - selective alpha-1 and nonselective beta blocking agent. Used for HTN and HF Labetalol - nonselective beta blocker, has selective alpha-1 blocking. Potent antiHTN Alpha-1 blockade cause vasodilation, treat HTN. risk for postural hypotension, tachycardia Prazosin - selective alpha-1 Phentolamine - nonselective alpha blocker Alpha-2 agonist - decrease sympathetic output. Decrease CO, SVR, and BP. Clonidine -> treat HTN, sedative properties. risk for postural hypotension, sedation, rebound HTN Anticholinergic - atropine, scopolamine, glycopyrrolate (cannot cross BBB), ipratropium bromide (bronchodilation). Blocks muscarinic cholinergic receptors. Acetylcholine - synthesize within the presynaptic neuronal mitochondria by esterification of acetyl coenzyme A and choline by enzyme choline acetyltransferase. Metabolized by acetylcholinesterase. Nitroglycerin (venous, arterial if >1mcg/kg/min) and sodium nitroprusside (arterial) - prodrug that converts to NO in vascular endothelium -> stimulate production of cGMP -> decrease cellular Ca+ -> vascular smooth muscle relaxation Nitroglycerin requires intact endothelial enzymatic activity. Nitroprusside nonenzymatically degrade into NO and cyanide. Nitrate reduce coronary artery spasm, dilation of coronary arteries, venodilaion reduce venous return/ventricular filling pressure, NO inhibit platelet formation Nitroglycerin 10-200 mcg/min Nitroprusside 0.5-10 mcg/kg/min Hydralazine - relax smooth muscle, dilation arterioles, decreasing diastolic > systolic. Risk for reflex tachycardia CCB - verapamil, diltiazem, nifedipine. Risk for Conduction blockade, bradycardia Nicardipine - short acting selective Ca+ channel blocker, act on arteriolar bed. More selective coronary vasodilation than systemic. Reduction in afterload, increased stroke volume, and increase coronary blood flow Clevidipine - CCB. ultra short acting arteriolar vasodilator, have little effect on myocardial contractility. Metabolize by plasma esterases. Half-life 2 min. Reduce afterload w/o affecting cardiac filling pressure. Fenoldopam - vasodilator via dopamine-1 receptor agonist. Selective for renal and splanchnic vasculature. Can cause significant hypotension Renin-angiotensin-aldosterone system Kidney release renin -> convert angiotensinogen to angiotensin I -> Angiotensin converting enzyme (ACE) converts Angiotensin I to angiontensin II Angiotensin II cause release of aldosterone/ADH and is vasoconstrictor. Reabsorption of Na+ and water. ACE inhibitor - captopril, enalapril, lisinopril. anti-HTN Risk for Cough, angioedema, fluid retention, reflex tachycardia, hyperkalemia, renal dysfxn Angiotensin receptor antagonist - losartan. Anti-HTN Risk for Hypotension, renal failure, hyperkalemia Hydrochlorothiazide - thiazide diuretics. anti-HTN. Risk for hypokalemia, hyponatremia, hyperglycemia, hypomag, hypercal. control hypertension in part by inhibiting reabsorption of sodium (Na+) and chloride (Cl−) ions from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive Na+-Cl− symporter. ... Thiazide diuretics also increase calcium reabsorption at the distal tubule. Angiotensin II -> direct vasoconstriction, aldosterone and ADH release Methylene blue -> Nitric oxide stimulates increase of cyclic GMP, promotes smooth muscle vasodilation by reducing the amount of calcium there is within the cytosol. When there is diminished calcium within the cytosol, actin and myosin cannot interact and contraction cannot occur. Calcium channel blockade also reduces the amount of calcium in the cytosol. Methylene blue, by contrast, lowers cGMP by two mechanisms. Firstly, MB directly inhibits the production of nitric oxide via nitric oxide synthase [NOS]. Secondly, MB blocks the generation of cGMP from GTP by inhibiting the iron heme moiety of soluble guanylate cyclase [sGC], the enzyme which turns GTP into cGMP [see figure 1]. Nesiritide - Human BNP binds to the particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells, leading to increased intracellular concentrations of guanosine 3'5'-cyclic monophosphate (cGMP) and smooth muscle cell relaxation. Cyclic GMP serves as a second messenger to dilate veins and arteries. Nesiritide administration leads to a rapid and balanced vasodilatory effect, which results in a significant decrease in right and left ventricular filling pressures and systemic vascular resistance and at the same time in an increase in stroke volume and cardiac output without a change in heart rate. These early hemodynamic changes result in a rapid improvement in symptoms of heart failure. In addition, nesiritide lowers aldosterone, catecholamines, and endothelin-1 levels and its effect on the kidney leads to an increased natriuresis and diuresis without effect on serum potassium or renal function. Indications for central venous catheters - guiding fluid therapy, IV access when PIV insufficient, evaluating cardiac functions Zero arterial line/CVP to phlebostatic axis (an imaginary line from the fourth intercostal space at the sternum and finding its intersection with an imaginary line drawn down the center of the chest below the axillae.) Underdamping - Essentially, the fluid-filled system has a certain "natural frequency" of resonance. The major determinant of this natural frequency is the length of the tubing: the longer the tubing, the lower the natural frequency. The patient's pulse oscillation is usually a fairly low frequency phenomenon, and as the tubing length increases, the natural frequency approaches the patient's pulse wave frequency. The system then resonates, amplifying the signal. Thus, the longer the tubing, the more resonance in the system, and consequently the system will be underdamped. Overdamping - Air bubbles, long tubing, or compliant tubing – all of these absorb some of the force of the pulse wave decreasing the amplitude of the oscillations. This is one of the reasons normal IV tubing is not used to set up an arterial line transducer kit: the IV tubing is too soft and compliant; the elasticity of the plastic would absorb much of the pulse wave. Damping results in a slurred waveform with overestimation of the diastolic and underestimation of systolic; however the MAP value is usually preserved. In contrast, a kinked or clogged art line will see MAP systolic and diastolic all trending towards zero. Prothrombin time: 12-15 sec PTT: 60-90 sec aPTT: 25-38 sec ACT: 70-120 sec INR < 2 platelet : 150K to 400K No swan-ganz if prosthetic TV or PV Cardiogenic shock - give O2/intubate. Treat cause (reperfusion for acute MI w/ PCI or CABG, pericardiocentesis for cardiac tamponade, thrombolytic and anticoag for pulm embolus, surgery, decompression for tension pneumo) - Inotrope (dobutamine) - Decrease preload (diuretics or nitroglycerin) - Decrease afterload (arterio vasodilation like nitroprusside) - Mechanical support (Impella, IABP, VADs) ICP - 5-15 mm Hg. - Elevated ICP from increased brain volume, increased CSF volume, increased blood volume - Hypoxemia, hypercapnia, acidosis -> vasodilation -> increase blood volume Heart block 1st degree - long PR, all P waves followed by QRS. no treatment unless symptomatic (pacing, atropine) 2nd degree Type 1 - progressive lengthening of PR until a P is not followed by a QRS, then repeats. no treatment unless symptomatic (pacing, atropine) 2nd degree Type 2 - fixed PR interval, some QRS not conducted. Treat with pacing, atropine if symptomatic 3rd degree - AV dissociation. Treat with pacing Sinus brady - treat if symptomatic. Atropine, pacing Afib - rate control w/ beta blocker or CCB, amiodarone. Cardiovert if duration < 48 hrs. Anticoagulation. Overdrive pacing. ablation/MAZE Junctional escape rhythm -> do not suppress. Give atropine or pacing Junctional tachycardia - treat cause, vagal stimulation, adenosine, amio, B-blocker, CCB Causes of asystole: H: hypovolemia, hypoxemia, H+ (acidosis), hyperkalemia, hypoglycemia, hypothermia, T: toxins, tamponade, tension pneumothorax, thrombosis (coronary, pulm), trauma Cardiogenic shock - tachycardic, hypotension, tachypnea, crackles, peripheral edema, oliguric. CO/CI decreased, RAP/PAP/PAOP increased. SVR increased. SaO2, SvO2 decreased. Hypovolemic shock - flat neck veins, tachycardic, hypotension, tachypnea, oliguric. CO/CI decreased, RAP/PAP/PAOP decreased. SVR increased. SvO2 decreased. Septic shock - tachycardic, hypotension, tachypnea. Initially warm/moist/flushed skin. CO/CI increase initially then decrease. RAP/PAP/PAOP decreased. SVR decrease. SvO2 increase initially then decrease. SIRS criteria - Temp >38°C (100.4°F) or < 36°C (96.8°F) Heart rate > 90 Respiratory rate > 20 or PaCO₂ < 32 mm Hg WBC > 12,000/mm³, < 4,000/mm³, or > 10% bands Sepsis Criteria (SIRS + Source of Infection) Suspected or present source of infection Severe Sepsis Criteria (Organ Dysfunction, Hypotension, or Hypoperfusion) Lactic acidosis ( >4 mmol/L (36 mg/dL) ), SBP <90 or SBP drop ≥ 40 mm Hg of normal Septic Shock Criteria Severe sepsis with hypotension, despite adequate fluid resuscitation Multiple Organ Dysfunction Syndrome Criteria Evidence of ≥ 2 organs failing Peak airway pressure is measured at the airway opening (Pao) and is routinely displayed by mechanical ventilators. It represents the total pressure needed to push a volume of gas into the Airway pressure release ventilation is similar to PCIRV – instead of being a variation of PCV in which the I:E ratio is reversed, APRV is a variation of CPAP that releases pressure temporarily on exhalation. This unique mode of ventilation results in higher average airway pressures. Patients are able to spontaneously ventilate at both low and high pressures, although typically most (or all) ventilation occurs at the high pressure. In the absence of attempted breaths, APRV and PCIRV are identical. As in PCIRV, hemodynamic compromise is a concern in APRV. Additionally, APRV typically requires increased sedation Dual Modes Pressure Regulated Volume Control (PRVC) A volume target backup is added to a pressure assist-control mode ● Inverse Ratio Ventilation Inverse Ratio Ventilation (IRV) is a subset of PCV in which inflation time is prolonged (In IRV, 1:1, 2:1, or 3:1 may be use. Normal I:E is 1:3). This lowers peak airway pressures but increases mean airway pressures. The result may be improved oxygenation but at the expense of compromised venous return and cardiac output, thus it is not clear that this mode of ventilation leads to improved survival. IRV’s major indication is in patients with ARDS with refractory hypoxemia or hypercapnia in other modes of ventilation Swan-ganz insertion - preceded by insertion of venous introducer into IJ (low risk of pneumothorax), subclavian, or fem vein. Swan is threaded through the introducer into place with CVP catheter tip in the SVC and the PAC tip in a pulm arteriole. Cardiac pressures: RAP 2-5 mm Hg RVP 15-30/0-8 mm Hg PAP 15-30/5-15 mm Hg; PAS reflects Righ side after load, PAD reflects Left side preload PAOP 8-12 mm Hg PAd usually 2-4 mm Hg greater than PAOP SvO2 60-80% SVR 800-1200 = 80 x (MAP-CVP)/CO PVR 50-150 LAP 6-12 mm Hg CO 4-8 L/min CI 2.5-4.5 L/min/m2 If the SVR is elevated, arterial vasodilator like nitroprusside may be used, ACE inhibitor or ARB To lower PVR -> oxygen, pulm vasodilator If the SVR is diminished, a vasoconstrictor such as norepinephrine, dopamine, vasopressin or neosynephrine may be used to treat hypotension To decrease preload -> venodilator, diuretics, ACE inhibitors/ARB Interpretation of ABG ● Respiratory alkalosis: high pH, low CO2 ● Respiratory acidosis: low pH, high CO2 ● Metabolic acidosis: low pH, low HCO3- ● Metabolic alkalosis: high pH, high HCO3- ● Compensated respiratory acidosis: normal pH, high CO2 ● Compensated metabolic acidosis: normal pH, low HCO3- ● Compensated respiratory alkalosis: normal pH, low CO2 ● Compensated metabolic alkalosis: normal pH, high HCO3- Complication of blood transfusions - Febrile nonhemolytic reactions - treat /w tylenol Chill-rigor reactions The most serious complications, which have very high mortality rates, are Acute hemolytic reaction (AHTR) due to ABO incompatibility - Dyspnea, fever, chills, facial flushing, and severe pain may occur, especially in the lumbar area. Shock may develop, causing a rapid, feeble pulse; cold, clammy skin; low blood pressure; and nausea and vomiting. Jaundice may follow acute hemolysis. The goal of initial therapy is to achieve and maintain adequate blood pressure and renal blood flow with IV 0.9% saline and furosemide Graft-vs-host disease (GVHD) Transfusion-associated circulatory overload - The high osmotic load of blood products draws volume into the intravascular space over the course of hours, RBCs should be infused slowly. Typical treatment is with a diuretic like lasix Transfusion-related acute lung injury (TRALI) - caused by anti-HLA and/or antigranulocyte antibodies in donor plasma that agglutinate and degranulate recipient granulocytes within the lung. Acute respiratory symptoms develop, and chest x-ray has a characteristic pattern of noncardiogenic pulmonary edema. Using blood donated by men reduces the risk of this reaction. Supportive care, O2, fluids, pressors. Avoid diuresis. Other complications include Allergic reactions - If an allergic reaction occurs, the transfusion is stopped. An antihistamine (eg, diphenhydramine 50 mg IV) usually controls mild urticaria and itching, and transfusion may be resumed. However, a moderate allergic reaction (generalized urticaria or mild bronchospasm) also requires hydrocortisone (100 to 200 mg IV), and a severe anaphylactic reaction requires additional treatment with epinephrine 0.5 mL of 1:1000 solution sc and 0.9% saline IV along with investigation by the blood bank. Altered oxygen affinity Delayed hemolytic transfusion reaction Infections Post-transfusion purpura The most common symptoms are chills, rigor, fever, dyspnea, light-headedness, urticaria, itching, and flank pain. If any of these symptoms (other than localized urticaria and itching) fibrin) -> promote clotting/slows down bleeding Heparin mechanism of action: Heparin binds to the enzyme inhibitor antithrombin III (AT), causing a conformational change that results in its activation through an increase in the flexibility of its reactive site loop.[36] The activated AT then inactivates thrombin, factor Xa and other proteases. For thrombin inhibition, however, thrombin must also bind to the heparin polymer at a site proximal to the pentasaccharide. The highly negative charge density of heparin contributes to its very strong electrostatic interaction with thrombin.[21] The formation of a ternary complex between AT, thrombin, and heparin results in the inactivation of thrombin. What to give for malignant hyperthermia - dantrolene CABG vasospasm treat with nitroglycerin/ isosorbide/ nitroprusside, CCB like nicardipine, or milrinone Impella - Left ventricular assistive device (RP for RV support). For heart failure and cardiogenic shock. Pull blood from LV and expel into the ascending aorta IABP - provides temporary support for the heart's left ventricle by mechanically displacing blood within the aorta. In normal inflation-deflation timing, balloon inflation occurs at the onset of diastole, after aortic valve closure; deflation occurs during isovolumetric contraction, just before the aortic valve opens. In a properly timed waveform, as shown, the inflation point lies at or slightly above the dicrotic notch. Both inflation and deflation cause a sharp V shape. Peak diastolic pressure exceeds peak systolic pressure; peak systolic pressure exceeds assisted peak systolic pressure. ACT goal 160-180. Monitor for limb ischemia, bleeding, hemolysis. HM II/ Heartware - Left ventricular assistive device, moves blood from ventricle to aorta via a motor. ECMO Protamine sulfate reactions -> In Type I reactions, there is significant hypotension following Protamine administration and is likely secondary to histamine release. Type II reactions are mainly allergic and can be further divided into true anaphylactic (Type IIA) and anaphylactoid type reactions (early IIB and delayed IIC). APH following Protamine is classified as a Type III reaction. APH is diagnosed clinically when a sudden rise in pulmonary artery pressure and associated RV failure and hypotension is noted shortly after protamine administration. Bicuspid aortic valve - A BAV may not be completely effective at stopping blood from leaking back into the heart. This leakage is called aortic regurgitation. The aortic valve may also become stiff and not open up. This is called aortic stenosis, which causes the heart to pump harder than usual to get blood through the valve. Ross procedure - a cardiac surgery operation where a diseased aortic valve is replaced with the person's own pulmonary valve. A pulmonary allograft (valve taken from a cadaver) is then used to replace the patient's own pulmonary valve. Pulmonary autograft replacement of the aortic valve is the operation of choice in infants and children ACLS Algorithms: AHA ACLS Adult Cardiac Arrest Algorithm Shout for Help/Activate Emergency Response Start CPR ‘Give Oxygen Attach Monitor/Defibrillator y Shock CPR 2minutes/5 cydes Obtain IV/IO access I Rhythm shockable? Made tele 1rd CM * CPR 2 minutes/S cycles ’ Shock Obtain IW/lO access Epinephrine every 3-5 min Consider advanced airway CPR 2 minutes/5 cycles Epinephrine every 3-5 min Consider advanced airway. Yes 2 capnography Rhythm shockable? Rhythm shockable? ’ Shock CPR 2 minutes/S cycles Amiodarone Treat reversible causes No * CPR 2minutes/5 cycles Treat reversible causes IV/10 Drugs Dosages: Epinephrine: img Amiodarone: 1 dose 300mg Ifne signs of return of spontaneous circulation {ROSC) go to 2° dose 150mg IfROSC, go to Post- © 2016 Jeffery Media Productions Coie eo AHA ACLS Acute Coronary Syndrome Algorithm ‘Symptoms Indicate possible Ischemia or infarction EMS and Prehospital Care © Must be performed immediately ‘© Must be performed in less than 10 minutes Immediate ED Assessment & Treatment: © Provide nitroglycerine sublingual or spray @ 12 Lead ECG (if not done pre-hospital) Perform brief, targeted hx. & physical exam obtal @ Obtain vital signs; 02 sat © Review fibrinolytic checklist. Check @ Oxygen if 02 sat < 90%; 4L then titrate ccontraindications © Provide Aspirin 160-325mg © Obtain cardiac marker levels, electrolyte, and Provide nitroglycerine sublingual or spray ‘coagulation tests. © Establish IV & give Morphine if needed Portable chest x-ray (<30 min.) Read ECG ‘= Start appropriate therapies: Heparin, Elevated Troponin or Possible admission: monitor serial NTG, B-blockers high-risk patient ECG and cardiac markers. * Reperfusion Therapy STAT Signs for invasive therapy? Consider non-invasive testing like Continued chest discomfort treadmill or thallium stress test. Continued ST deviation Unstable hemodynamics Heart Failure Ventricular Tachycardia ‘Adjunctive Therapies Nitroglycerine (IV/PO) Heparin (IM/IV) Possibly: B-blockers Possibly: Clopidogrel Possibly: Glycoprotein lib/Iila inhibitor { Vv Goal for stent placement or balloon Admit to monitored bed inflation should be within 90 + Continue ASA, heparin, and other minutes indicated therapies. ACE Inhibitors/ARB + Statin Therapy + Expert consultation to assess ‘cardiac risk factors Q. Goal for fibrinolysis should be 30 minutes © 2017 Jeffery Media Productions  AHA ACLS Adult Suspected Stroke Algorithm ID Stroke Signs and Symptoms -—- Activate EMS Dee ae Important Interventions at Hospital Arrival Interventions should eccur_within 10 rminutes of arrival, Neurological Assessment & Stroke Team Evaluation Interventions should eccur within 25 nninutes of arrival. y Head CT scan completed in 25 minutes: and read within 45 minutes No Head Bleed Head Bleed Possible ischemic Stroke ‘Conmate Neurologist: [ibrinolytie Therapy Options/Exclusions ea Begin stroke-or hemorrhage pathway of stroke protocal. © 2026 setiery techs Productions