HYPERTENSION MANAGEMENT IN - EMCREG-International
HYPERTENSION MANAGEMENT IN - EMCREG-International HYPERTENSION MANAGEMENT IN - EMCREG-International
ADVANCING THE STANDARD OF CARE:Cardiovascular and Neurovascular EmergenciesAt levels of perfusionless than 20 ml/100g/min, neuronalcell membranesbecome impaired withresulting neurologicaldysfunction.dysfunction. 1 Despite this impairment,if blood flow is eventually restored, thistissue is largely salvageable. At levelsof blood flow below 10 ml/100 g/min,the neuronal tissue rapidly becomesirreversibly damaged. In the no-flowstate, neuronal death begins within afew minutes. Thus, any attempts toalter neurovascular physiology mustbe performed with the principle ofmaintaining adequate cerebral bloodflow to maintain tissue viability.Without superimposed pathology, thetwo principal factors that affect thevolume of cerebral blood flow are thecerebral perfusion pressure (CPP) andthe brain’s autoregulatory system.Cerebral perfusion pressure is the meanarterial pressure (MAP) minus either theintracerebral pressure (ICP) or the centralvenous pressure (CVP), whichever ishigher.CPP = MAP – (ICP or CVP, whichever is greater)The native autoregulatory system refersto the brain’s ability to keep the cerebralblood flow at a relatively constantlevel over a wide range of CPP. This isaccomplished by varying the resistance inthe pre-capillary arterioles. 2 Notably thismechanism is functional over a very widerange of CPP (Figure 1). 2 Also note inthis figure that a second curve depicts theautoregulatory curve “shifted” to the right.This curve represents the autoregulatoryrange of the patient with significantunderlying hypertension. For chronicallyhypertensive patients, the native systemwill require higher pressures to achievethe same degree of cerebral blood flowthan the non-hypertensive individual. 3In the setting of neurovascularemergencies, multiple deleterious effectscan ensue. First, the brain’s ability tocontinue normal autoregulation canbecome compromised. This can occurdue to CPP being outside of the rangewhere autoregulation can be maintained.Figure 1. Auto regulation and blood flow in patients with and withoutchronic hypertension. Adapted with permission from Powers.Neurology 1993;43(1):461-7.62w w w . e m c r e g . o r g
HYPERTENSION MANAGEMENT INACUTE NEUROVASCULAR EMERGENCIESWhen CPP is below the limits ofautoregulation, ischemic damage canensue. When CPP is above the upper limit,then autoregulatory breakthrough occurswhich leads to increased intracranialblood volume, increased intracranialpressure and vasogenic edema.In addition, the underlying pathology canhave a significant impact on the cerebralblood flow. In the setting of an acuteischemic stroke, an arterial occlusioncompromises flow to the region at risk tovarying degrees depending on collateralcirculation and the degree of occlusion.For intracerebral hemorrhage (ICH), thehematoma behaves as any mass lesionand causes an acute increase in ICP, thusdecreasing CPP unless the MAP is alsoincreased. It is also hypothesized that inthe region immediately surrounding thehematoma the blood flow is compromiseddue to local physical effects of the masslesion. For subarachnoid hemorrhage(SAH) the extravascular blood can raiseICP and can also cause arterial spasmleading to increased vascular resistance,thereby compromising flow. Thus eachof the individual types of neurovascularemergencies has their own uniquepotential to alter blood flow.Many factors, therefore, may influencethe variable that is most important– the cerebral blood flow. In practiceas emergency physicians, however, it isthe systemic blood pressure over whichclinicians have the greatest control andtherefore it is often the primary therapeutictarget. What must be considered is howtreatment of the systemic blood pressurewill alter the truly important variable,the cerebral blood flow, when treatingpatients.w w w . e m c r e g . o r gAcute Ischemic StrokeAs discussed, the high metabolic demandof brain tissue makes it quite susceptibleto ischemia. In the setting of acuteischemic stroke the duration and extentof ischemia will determine the ultimatefate of the affected area of brain tissue.As shown in Figure 2, there is a clearrelationship between duration of ischemiaand level of residual blood flow that willdifferentiate tissue that is salvageable andthat which will die.To further demonstrate the need forcareful use of blood pressure medicationin neurological emergencies, Figure 3illustrates the effect of blood flow on thedegree of injury that can be expected inmarginally perfused tissue. The centrallylocated black curve is adapted from Zivinwho characterized neuronal injury overtime in the setting of ischemia. The redand blue curves demonstrate the changeResidual Cerebral Blood Flowml 100g -1 min -1 30252015105Normal neuronal functionReversible neuronal dysfunctionNeuronal death12Duration of Transient IschemiaFigure 2. Degree of blood flow reduction and durationeffect tissue outcome. Adapted with permission from Powers.Neurology 1993;43(1):461-7.In the setting of acuteischemic stroke theduration and extent ofischemia will determinethe ultimate fate of theaffectedarea of brain tissue.63
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<strong>HYPERTENSION</strong> <strong>MANAGEMENT</strong> <strong>IN</strong>ACUTE NEUROVASCULAR EMERGENCIESWhen CPP is below the limits ofautoregulation, ischemic damage canensue. When CPP is above the upper limit,then autoregulatory breakthrough occurswhich leads to increased intracranialblood volume, increased intracranialpressure and vasogenic edema.In addition, the underlying pathology canhave a significant impact on the cerebralblood flow. In the setting of an acuteischemic stroke, an arterial occlusioncompromises flow to the region at risk tovarying degrees depending on collateralcirculation and the degree of occlusion.For intracerebral hemorrhage (ICH), thehematoma behaves as any mass lesionand causes an acute increase in ICP, thusdecreasing CPP unless the MAP is alsoincreased. It is also hypothesized that inthe region immediately surrounding thehematoma the blood flow is compromiseddue to local physical effects of the masslesion. For subarachnoid hemorrhage(SAH) the extravascular blood can raiseICP and can also cause arterial spasmleading to increased vascular resistance,thereby compromising flow. Thus eachof the individual types of neurovascularemergencies has their own uniquepotential to alter blood flow.Many factors, therefore, may influencethe variable that is most important– the cerebral blood flow. In practiceas emergency physicians, however, it isthe systemic blood pressure over whichclinicians have the greatest control andtherefore it is often the primary therapeutictarget. What must be considered is howtreatment of the systemic blood pressurewill alter the truly important variable,the cerebral blood flow, when treatingpatients.w w w . e m c r e g . o r gAcute Ischemic StrokeAs discussed, the high metabolic demandof brain tissue makes it quite susceptibleto ischemia. In the setting of acuteischemic stroke the duration and extentof ischemia will determine the ultimatefate of the affected area of brain tissue.As shown in Figure 2, there is a clearrelationship between duration of ischemiaand level of residual blood flow that willdifferentiate tissue that is salvageable andthat which will die.To further demonstrate the need forcareful use of blood pressure medicationin neurological emergencies, Figure 3illustrates the effect of blood flow on thedegree of injury that can be expected inmarginally perfused tissue. The centrallylocated black curve is adapted from Zivinwho characterized neuronal injury overtime in the setting of ischemia. The redand blue curves demonstrate the changeResidual Cerebral Blood Flowml 100g -1 min -1 30252015105Normal neuronal functionReversible neuronal dysfunctionNeuronal death12Duration of Transient IschemiaFigure 2. Degree of blood flow reduction and durationeffect tissue outcome. Adapted with permission from Powers.Neurology 1993;43(1):461-7.In the setting of acuteischemic stroke theduration and extent ofischemia will determinethe ultimate fate of theaffectedarea of brain tissue.63
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