Presentation on theme: "Hypertensive Emergencies"— Presentation transcript:
1Hypertensive Emergencies Alyssa Morris, R3March 5, 2009Thanks to Dr Gant!
2Definitions Hypertensive Emergency Acute, life threatening, usually a BP> 180/120Target organ damageHypertensive UrgencyAsymptomatic, severe HTN, usually >180/120NO target organ damageThese are not absolute numbers- nb to treat the patient and not the number
4Components of BP BP= CO x SVR CO= HR x SV Think of the components as: CO= heartBP= arteriesSVR= arterioles- Other systems impact these factors. The RAAS system and the ANS play a role.
5CPP=MAP-ICP-throughout the normal range of BP, cerebral blood flow is maintained by fluctuation in the vascular tone of the cerebral resistance vessels (which are have ability to constrict to prevent too much pressure). So they dilate to increase flow at the bottom of curve and then constrict to prevent to much flow in the upper portion of the curve.- In patients with HTN, cerebral autoregulation is reset at a higher levelLower part of curve, you won’t perfuse brainIn upper part of brain you can get brain edema because previously constricted vessels reach a critical level and then suddenly dilate, leading to leakage of fluid thru BBB
6Secondary causes of HTN Conn’s is primary hyperaldosteronism: increase aldo leads to increase Na therefore increase volume- RAS- bilateral increases RAAS but can’t filter voume like you can with unilateral , therefore, bilat is volume HTN and unilat is constriction HTN- mineralcorticoids increase Na retention- catecholamines increase vasoconstriction
8Hypertensive Encephalopathy Uncommon syndromeAcute and reversibleResults from an abrupt, sustained rise of BP that exceeds the limits of cerebral autoregulation of the small resistance arteries in the brainArises from “breakthrough” hyperperfusion and leakage of fluid thru BBB
10Clinical Presentation Severe h/aDrowsinessALOCVomittingSeizuresFocal neuro deficitsBlindnessFocal neuro do not follow a specific territory or anatomic pattern
11Tx Various recommendations 25% over 3-4hrs 10% in first hour, 15% in next 2-3 hours*will not be able to perfuse brain if you drop it too fast or too much-various recommendations but basically 25% over 3-4 hoursEMR suggested 10% in first hour, then 15% in next 2-3 hours- will not be able to perfuse brain b/c will drop off curve and then get ischemia
12CPP=MAP-ICP-throughout the normal range of BP, cerebral blood flow is maintained by fluctuation in the vascular tone of the cerebral resistance vessels (which are have ability to constrict to prevent too much pressure). So they dilate to increase flow at the bottom of curve and then constrict to prevent to much flow in the upper portion of the curve.- In patients with HTN, cerebral autoregulation is reset at a higher levelLower part of curve, you won’t perfuse brainIn upper part of brain you can get brain edema because previously constricted vessels reach a critical level and then suddenly dilate, leading to leakage of fluid thru BBB
14Nitroprusside Potent smooth muscle relaxing agent Reduces both preload and afterloadRate of onset rapid, duration very shortAlso a cerebral vasodilatorCan increase ICP secondary to increased cerebral blood flowUnstable in UV light, therefore wrapped in tinfoilInfusion at ug/kg/min -then increase by 0.5mcg/kg/minMax of 10 mcg/kg/minThis is an excellent choice in hypertensive crisis for these reasons- b/c of reduction in preload by venous dilation, the CO often improves if CHF or bad LV fxn is present- can get hypotension and get a reflex tachycardia as a result
15Nitroglycerine Activates guanylate cyclase Accumulation of cGMP Sequestration of Ca into SRRelaxation of Vascular smooth muscleDose dependentLow dose: venodilator (preload)High dose: veno and arteriodilator (afterload)Therefore, usually reduce BP by reducing preload and COStart with 10-20ug/min infusionTitrate up 5-10ug/minQ3-5minDoses as high as ug/min may be needed for maximal antihypertensive effect- reduction in preload and CO might not be desirable in pts with poor cerebral and renal perfusion- careful when using it in patients with RV dysfxn to avoid hypotension (preload dependent)- best used in pts with cardiac ischemia or pulmonary edema
16Hydralazine Direct arteriolar vasodilator Used to be used as first line in pregnancy htv emergenciesStarting dose is 5mg IVRepeat doses of 5-10mg IV every 20 mins to maintain desired BPComplications:Marked hypotensionReflex tachycardia (can give angina)Flushing and nauseaH/a- Now using labetolol or nicardipine
17Labetalol Selective α-1 blocker and nonselective β-blocker α:β blockade ratio between 1:3 and 1:7Not a significant drop in CO like other βBDoes not affect cerebral blood flow or renal fxnBP starts to fall in 5-10m, max effect at 30mHow much do you guys give?
18Esmolol Selective β-1 blocker Very short acting Elimination ½ life of 9 minutesNo intrinsic sympathomimetic activity-b/c the half life is 9 mins, you get substantial recovery from B blockade in mins
19Phentolamine α-blocking agent Used for the Mx of catecholamine-induced HTV crisisMAOI, Pheo, CocaineImmediate effectEffect lasts up to 15 mins1-5mg IV bolusesMAOI- pheoCocaine
20CASE 2Head CT demonstrates multiple, bilateral, patchy foci of hypoattenuatin within subcortical white matter in the occipital regions- MR shows hyperintensity within the subcortical white matter of the bilateral occipital and anterior parietal lobes.
21PRES Posterior reversible encephalopathy syndrome Pathophysiology Cerebral vasospasm leading to cytotoxic edemaVasodilattion leading to vasogenic edema- again, disorder of cerebral autoregulation with two theories.
22CASE 3 - What kind of stroke is this? L MCA - Given this, would you treat the blood pressure? (200/110)
23HTN Mx in Ischemic Stroke Consensus guidelines published in the journal of stroke.Stroke. 2007;38:
24- Want to monitor BP after giving TPA as well. Same goals.
25HTN Mx in Ischemic Stroke HTN common in 1st hours after strokeSBP>160 found in 60% pts with acute ischemic strokeFor every 10mmHg raise >180, risk of neurologic deterioration increases by 40% and risk of poor outcome by 23%In these patients, htn is usually the physiologic response to the stroke itself and is not the immediate cause- can try to reduce modifiable factors that could be contributing to the htn
26HTN Mx in Ischemic Stroke Theoretical reasons for lowering BP in strokeDecrease formation of brain edemaLessening risk of hemorrhagic transformation of infarctionPreventing further vascular damageForestalling early recurrent strokeBUT remember aggressive tx of BP may lead to neurologic worsening by decreasing perfusion pressure to ischemic areas of brain
27CPP=MAP-ICP-Do not want to get them too low or won’t perfuse brain and the penumbra is depending on flow to deliver O2 and reduce the ischemic area
28CASE 4 - What kind of stroke is this? L MCA - Given this, would you treat the blood pressure? (200/110)
29HTN Mx in Ischemic Stroke A lot of studies showing harm with reduction of BPMost pts have a decrease in BP a few hours post- stroke w/o interventionOliveira-Filho et al. Neurology. 2003;61:Found >90% pts had a decrease in SBP by 28% in 24hrs post-stroke with no interventionOutside TPA window- DO NOT want to decrease pressure to much b/c penumbra dependant on perfusion pressure
30Consensus Statement“ emergency administration of antihypertensive agents should be withheld unless DBP>120 and SBP>220”“reasonable goal to decrease blood pressure by % within 24 hours”This is a case-by-case decisionMore research needs to be done-typically recommend labetalol 10mg IV over 1-2 minutes with rpt doses as needed unless there is a contraindication to BB then use nicardipine infusion- Stated that the CHIPPS trial might be able to give more evidence
33HTN Mx in Hemorrhagic Stroke Primary rational for reducing BP is to avoid hemorrhagic expansion from potential sites of bleedingBP is correlated with increased ICP and volume of hemorrhageDifficult to determine whether increased BP is a cause of hemorrhage growth or an effect of increased volumes of ICH and increased ICP
34HTN Mx in Hemorrhagic Stroke Summary of studiesIsolated SBP<210 is not clearly related to hemorrhagic expansion or neurologic worseningDecrease in MAP by 15% does not result in decreased CBFBaseline BP was not associated with growth of ICH in largest prospective studyHemorrhage enlargement occurs more frequently in pts with increased SBP but it is not clear if this is an effect of increased growth of ICH with associated increase in ICP or a contributing cause to the growth of ICHEvidence supports maintaining CPP >60mmHgWE DON’T KNOW
35Not a strong stand on the subject - State that much more research needs to be done and could be answered by the ATACH study and the INTERACT study.
36HTN Bleeds Where do you get HTN bleeds in the brain? Cerebellum Pons Basal gangliaThalamus- Areas in brain affected by chronic htn are the perforating arteries which serve these areas-what about BP in the setting of hemorrhagic stroke??
37Case 4With nipride can get increased SV and a reflex tachycardia so you want to avoid it first- go by R arm b/c flap flapping over is falsely lowering L arm BP- remember to check leg BP if arms normal and you are thinking about dissection- want to reduce shear force and pulse pressure- Use a BB to reduce BP (labetalol or esmolol) for a goal of SBP<110 or- if becoming too brady, can switch to nipride because you have sufficiently BB her and will blunt reflex tachycardia and
38HTN Mx in Ao DissectionRemember to check BP in legs if you are thinking dissection b/c the flap can give you falsely low BP in armsWant to avoid shear stress and wide pulse pressuresReduce the LV ejection forceGoal is to get SBP but just do what you canUse labetalol or esmololCan use nipride after have sufficiently BB b/c will blunt the reflex tachycardia and increased SV
39Case 6- Discuss who would treat an urgency with risk factors and who would not
40Drug Summary Nitroprusside Nitro Labetalol 0.25-0.5ug/kg/min Inc by 0.5ug/kg/min quicklyNitro10-20ug/minInc by 5-10ug/min Q3-10minLabetalol10-20mg IV Q5-10minInfusion at 1-2mg/min