Critical Care Meds in the Emergency Department

Transcription

1 Critical Care Meds in the Emergency Department Kyle Rupp DO, MBA Medical Director Emergency Services CHI Health Good Samaritan Objectives Identify and describe use of medications used in blood pressure control in the Emergency Room Identify and describe use of medications used in traumatic and non-traumatic brain injuries. 1

2 Blood Pressure Too much? Not enough Mean Arterial Pressure (MAP) Systolic (1/3) + Diastolic (2/3) = MAP 2

3 Blood Pressure Too much Hypertension affects approximately 30% of the U.S. population 1 to 6% of all ED patient will present with severe hypertension 1/3 ½ will have end-organ damage Risk factors for development of hypertensive crisis include: Obesity Cigarette smoking Older age Hypertension Chronic hypertension Asymptomatic hypertension Hypertensive urgency Hypertensive emergency 3

4 Asymptomatic Hypertension Class Systolic Diastolic Normal <120 And <80 Elevated Blood Pressure And <80 Stage Or Stage 2 >140 Or >90 JNC-8 Changes: - Patients >60 y/o threshold has increased from <140/90 to <150/90 - Patients with diabetes mellitus (any age) <140/90 Asymptomatic Hypertension Clinical Features None Evaluation Urine pregnancy (consider preeclampsia Routine screening for acute target organ injury is NOT required (Level C) Suggested algorithm <120 diastolic No screening ED workup > home with outpatient treatment >210 systolic or > diastolic chemistry for acute renal failure 4

5 Asymptomatic Hypertension Routine ED medical intervention is NOT required (level C), may consider initiating or increasing outpatient therapy for long-term control Outpatient HTN meds First line without comorbidities HCTZ 12.5mg (not in CKD, get chemistry) First line DM and/or proteinuria ACEi/ARB Lisinopril (get chemistry) CAD, CHF Beta-blocker Amlodipine for anyone, except people with LE edema Diltiazem for proteinuria in people unable to tolerate ACEi Lasix CHF and/or lower extremity edema Hypertensive Urgency Profound elevations in pressure without acute target organ dysfunction 180/120 mm Hg (arbitrary number) Historically often cited as indication for rapid pharmacologic intervention No clear clinical benefits of such treatment exists and risk can occur from precipitous drops in blood pressure Better seen as a form of severe hypertension with prompt therapy using oral agents is the best path, seeking reduction in blood pressure over days to weeks. 5

6 Hypertensive Emergency Acute elevation of blood pressure associated with end-organ damage Brain, heart, aorta, kidneys, or eyes Aortic dissection, pulmonary edema, myocardia infarction, renal failure, preeclampsia, HELLP syndrome, eclampsia, retinopathy, encephalopathy, subarachnoid hemorrhage, intracranial hemorrhage, ischemic stroke, sympathetic crisis. Hypertensive Emergency Management is based on diagnosis Establish a target range Goal is to minimize end-organ damage while avoiding hypoperfusion of cerebral, coronary, and renovascular beds 6

7 Case 1 65/M Pale, diaphoretic Chest pain Radiates to his back Sudden onset 1h prior Sharp Started center of chest now in lower chest BP 200/130 HR 100 Aortic Dissection Therapeutic goal Systolic pressure between 100 and 140 mm Hg And heart rate 60 bpm Medications Esmolol IV bolus then gtt Labetalol gtt Nicardipine gtt (after β-blocker) Nitroprusside gtt (after β-blocker) 7

8 Esmolol Cardioselective Beta adrenergic receptor blocker Dosage Loading mcg/kg infused over 1-3 minutes (max repeat x 4) Maintenance 50mcg/kg/min (max 300 mcg/kg/min) Ultra-short-acting (Onset 60s, duration minutes) Avoid in bradycardia, cardiogenic shock Caution in Asthma, COPD, CHF 70/F Acute SHOB Crackles BP 230/130 8

9 Acute Hypertensive Pulmonary Edema Therapy goals Reduce BP by 20-30%; diuresis through vasodilation; symptomatic relief BiPAP Nitroglycerin high dose Start 100mcg/min titrate to 400mcg/min for load, then 100mcg/min gtt titrate up Consider sublingual nitro while waiting for drip Usually fluid deplete consider diuretics carefully Nitroglycerin Potent venodilator. Reduces BP by reducing preload and cardiac output. Decreases coronary vasospasm and cardiac workload. Dosage Sublingual 0.4 mg Infusion start 5mcg/min increase q3-5min unless AHPE Avoid compromised cerebral and renal perfusion Avoid with phosphodiesterase 5 inhibitors May cause hypotension with reflex tachycardia 9

10 Case 3 50/M Chest pain Out shoveling snow Diaphoresis Elephant sitting on my chest BP 220/100 Acute Myocardial Infarction Therapy Goals Reduce ischemia; avoid 25% reduction of MAP Nitroglycerin Not with phosphodietsterase inhibitors 24 hours (tadalafil 48 hours) Metoprolol or Labetalol IV bolus Not in CHF or low-output states 10

11 Labetalol Combined selective α1-adrenergic and nonselective β-adrenergic receptor blocker Effect in 2-5 min, peak 15 min, duration 2-4 hours Renal, cerebral, coronary blood flow maintained Avoid bradycardia, heart block, uncompensated cardiac failure, bronchospasm and in patients receiving IV verapamil or diltiazem Caution pt with liver impairment, asthma, COPD, elderly Case 4 BP 220/130 HR

12 Acute Sympathetic Crisis Therapy Goals Reduce excessive sympathetic drive and symptomatic relief Medications Benzodiazepine Nitroglycerine Phentolamine Nicardipine IVF Phentolamine α1 and α2-adrenergic blocking agent Effective for pheochromoctoma and hypercatecholaminergic-induced hypertension Avoid Myocardial infarction Cerebrovascular spasm, cerebrovascular occlusion have occurred after administration 12

13 Case 5 65 BP 230/125 Decreased urinartion Acute Renal Failure Therapy Goals Reduce BP by no more than 20% acutely Medications Nicardipine gtt Labetalol Clevipine gtt Fenoldopam gtt Avoid nitroprusside (renal metabolism) 13

14 Fenoldopam Dopamine 1 receptor agonist Onset 5 min, peak 15 min, duration min. Metabolized by liver. Improves creatinine clearance, urine flow, sodium excretion. Caution causes reflex tachycardia, flushing, dizziness, vomiting, sulfa allergy Infusion: start 0.1mcg/kg/min titrate every 15 min (0.1 to 1.6 mcg/kg/min) Case 6 70/F Nursing home resident AMS Lethargic Headache BP 243/134 14

15 Hypertensive Encephalopathy Therapy Goals Decrease MAP 20-25% in first hour Medications Avoid Nitroglycerin as may worsen cerebral autoregulation Nicardipine gtt Labetalol gtt Fenoldopam gtt Clevipine gtt Nicardipine 2 nd gen dihydropyridine calcium channel blocker with vascular selectivity for cerebral and coronary arteries. Onset 5-10 min, duration 1-4 hours Start at 5 mg/h, increase q15min by 2.5 mg/h to max 15 mg/h 15

16 Clevidipine Dihydropyridine calcium channel blocker Very rapid onset and offset, 1 min Reduces BP without affecting cardiac filling pressures Metabolism independent of kidney or liver May produce systemic hypotension and reflex tachycardia Avoid in allergies to soy or eggs Dosage Infusion at 1-2 mg/h titrate by doubling (max 21 mg/h) Case 7 25/F G1P0 25 weeks pregnant BP 175/115 Seizure 16

17 Severe preeclampsia, HELLP syndrome, Eclampsia Therapy Goals <160/110 mm Hg Medications (MgSO4 to treat and prevent seizures) Labetalol bolus Nifedipine PO Hydralazine Hydralazine Direct arteriolar vasodilator Little to no effect on venous circulation Caution coronary disease, dissection Hypotensive response is less predictable than other parenteral agents Primarily limited to pregnant women Reduction in utero-placental blood flow has been reported IV bolus dose 10 mg (max 20mg) Onset minutes lasts 2-4 hours 17

18 Case 8 47/F Sudden onset Worst headache Thunderclap Subarachnoid Hemorrhage Therapy Goals Not clear SBP <160 mm Hg or MAP <130 mm Hg to prevent rebleeding Some Neurosurgeons may prefer therapeutic HTN to treat vasospasm Avoid hypotension to preserve cerebral perfusion Medications Control pain and provide sedation Labetalol IV gtt Nicardipine IV gtt Esmolol IV bolus, then gtt 18

19 Case 9 80/F Altered mental status Neurological changes BP 245/145 Intracranial Hemorrhage Therapy Goals Systolic mmhg lower to systolic 140 mmhg Systolic > 220 mmhg lower to mmhg Medications Labetalol IV bolus, or continuous gtt Nicardipine IV gtt Esmolol IV bolus then gtt 19

20 Case 10 80/F Altered mental status Neurological changes BP 245/145 Acute Ischemic stroke Therapy Goals Fibrinolytic therapy planned treat if >185/110 mm Hg Tx if >220/120 mm Hg on 3 rd of three measurements, 15 min apart Medications Labetalol IV bonus or gtt Nitroglycerin paste Nicardipine gtt 20

21 Blood Pressure Too much? Not enough Shock inadequate perfusion of the tissues Cardiogenic Obstructive Distributive Hypovolemic 21

22 Critical Perfusion Pressures MAP Kidneys MAP 65 Heart MAP 50 Brain (dogs) MAP 35 Cardiovascular collapse Vasopressor Induce vasoconstriction and elevate MAP Goals Critical perfusion pressures Increase venous return Avoid gut ischemia and flow reduction Indicated for decrease of >30 mmhg from baseline systolic BP or MAP <60 mmhg 22

23 Shock Cardiogenic Obstructive Distributive Hypovolemic Distributive Shock Severe peripheral vasodilation Sepsis Anaphylaxis Neurogenic shock Toxicologic Adrenal crisis 23

24 Sepsis Life threatening organ dysfunction caused by a dysregulated host response to infection Sepsis Pressors indicated if MAP<65 despite adequate IVF or if contraindicated Norephinephrine (5-20 mcg/min) 1 st line Vasopressin (0.03 units/minute fixed dose) 2 nd line Epinephrine (1-20 mcg/min) 2 nd line Dopamine - Usually No Phenylephrine Usually No Dobutamine (2-20 mcg/kg/min) Milrinone 24

25 Norepinephrine Αlpha-1 and β-1 adrenergic receptor agonist Potent vasoconstriction and modest increase in cardiac output Preferred vasopressor for the treatment of septic shock Can do it peripherally, not long term (need central line)?weight based dosing? Vasopressin Antidiuretic hormone Helpful in vasodilatory shock Primarily used as a second-line agent in refractory cases Dose 0.03 units/min Rebound hypotension common 25

26 Epinephrine Potent β-1 adrenergic receptor activity and moderate β-2 and α-1 Low dose increase cardiac output and variable effects on the MAP Higher dose - α-1 dominate, increased SVR and increased CO First line treatment in anaphylaxis Second line agent in septic shock Disadvantages dysrhythmias and splanchnic vasoconstriction Dopamine Second-line alternative to norepinephrine in patient with absolute or relative bradycardia 1-2 mcg/kg/min dopamine-1 receptors 0 selective vasodilation renal, mesenteric, cerebral, and coronary beds 5-10 mcg/kg/min - β-1 increases CO mild alpha >10 mcg/kg/min α increased SVR 26

27 Phenylephrine (Neo-Synephrine) Pure α agonist Vasoconstriction with minimal cardiac inotropy or chronotropy Useful in hyperdynamic sepsis, neurologic disorders, anesthesia-induced hypotension Disadvantage May decrease stroke volume Angiotensin II ATHOS-3 trial FDA Approval?underpowered (N=166)? Benefits outweigh the risks Pro-inflammatory effects Pro-coagulant effects, increase risk of DVT/PE Inhibition of ATII improved survival in animal model of sepsis Hasn t been show to improve outcome other than minor increase in BP Rationale similar to vasopressin 27

28 Angiotensin II Cardiogenic Shock Myocardial infarction Pump failure, acute mitral regurg, VSD, free-wall rupture RV infarction Decreased forward flow Sepsis, rate related (brady, tachy), myocarditis, contusion, cardiomyopathy Mechanical obstruction to forward flow Aortic stenosis, HOCM, Mitral stenosis, pericardial effusion LV regurgitation Chordal rupture, aortic regurg 28

29 Cardiogenic Shock Leading cause of death in patient with ACS who reach the hospital alive Exam Signs of CHF (JVD, pulmonary edema, S3) Murmur End organ hypoperfusion cool/mottled extremities, weak pulses, AMS, decreased UOP Cardiogenic Shock Management Aim for MAP >65 Consider etiologies and treat specific one if present,?ivf Increase inotropy Dobutamine +/- norepinephrine or dopamine Consider milrinone or β-blocker reversal Consider calcium chloride 1g Transfusion if Hgb <10 Intubation? Definitive treatment/intra-aortic balloon pump 29

30 Dobutamine Cardiac effect Strong β1 agonist + inotrope + chronotrope, weak β2 agonist + weak vasodilation Indicated in decompensated systolic HF Initial 3-5 mcg/kg/min, Max 5-15 mcg/kg/min (200) Milrinone Phosphodiesterase inhibitor Inotropic and vasodilatory actions Similar to dobutamine but lower incidence of dysthythmias Most often used to treat patients with impaired cardiac function and medically refractory heart failure 30

31 Obstructive Shock Hypotension associated with distended neck veins Without fluid overload or reduced preload May be combined with coexisting cardiogenic shock Obstructive Shock Treatment Reverse the etiology Cardiac tamponade Pulmonary embolism Aortic stenosis Tension pneumothorax Air embolism Restrictive cardiomyopathy 31

32 Hypovolemic Shock Severe dehydration Hemorrhagic shock Traumatic Non-traumatic Severe Dehydration 32

33 Hemorrhagic Shock Goals of management 1. Find and stop the bleeding 2. Rapidly restore blood volume 3. Maintain functional blood composition (i.e. hemostasis, ph, oxygen carrying capacity, oncotic pressure and biochemistry) Locations of Possible Life-Threatening Bleeding External Internal Thoracic cavity Peritoneal cavity Retroperitoneal space (i.e. pelvic fracture) Femur fracture 33

34 Massive Transfusion Protocol >10 units of blood products within 24 hour period Focus on balanced resuscitation with clotting factors (FFP) and platelets PROPPR trial 1:1:1 vs 1:1:2 (no difference in mortality 1 to 30 days) 1:1:1 less death due to exsanguination in 1 st day ABC score and TASH score Massive Transfusion Protocol Example: 6 units Packed Red Blood Cells (cross matched if available) 6 units of Fresh Frozen Plasma (allow 20 minutes to thaw) 1 unit Platelets 34

35 Massive Transfusion Protocol Example: 6 units Packed Red Blood Cells (cross matched if available) 6 units of Fresh Frozen Plasma (allow 20 minutes to thaw) 1 unit Platelets Consider Tranexamic Acid (TXA) Tranexamic Acid (TXA) Antifibronolytic agent CRASH-2 32% reduction in mortality when given within 1 hour Indication: signs of significant hemorrhage who present within three hours of injury Contraindication: Greater than 3 hours, previous DVT or PE 35

36 Hypotension in Traumatic Brain Injury MAP above 85 mmhg (80) or a systolic blood pressure above 120 mmhg (90) Isolated head injuries rarely produce hypotension If fluid and blood not effective use vasopressors Norepinephrine Considerations Hypertonic saline? Benefit through osmotic movement of intestinal fluids into vascular compartment Modulation of inflammatory response to injury Varied results Colloids Increase intravascular volume Maintain plasma oncotic pressure Did not improve mortality or morbidity in trauma1 36

37 Developing Management of Hemorrhage in Adult Trauma Hemostatic agents Recombinant factor VIIa Red blood cell substitutes Thank you Primary reference Tintinalli 8 th edition Uptodate.com Emcrit.org Please see notes in powerpoint Contact: kylerupp@catholichealth.net 37