New Understandings/ New Opportunities Learning Objectives Show why - - PowerPoint PPT Presentation

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New Understandings/ New Opportunities Learning Objectives Show why - - PowerPoint PPT Presentation

Reassessing the Definition and Treatment of Severe Hypertension New Understandings/ New Opportunities Learning Objectives Show why the current definitions of severe HTN are 1. wrong and suggest changes Provide a working understanding


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Reassessing the Definition and Treatment of Severe Hypertension

New Understandings/ New Opportunities

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Learning Objectives

1. Show why the current definitions of severe HTN are wrong and suggest changes 2. Provide a ‘working’ understanding of the microcirculation 3. Briefly introduce old and newly acquired technologies for measuring the microcirculation 4. Convince you that this is important to you as a Cardiologist caring for the vascular health of your patients

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ASSESSMENT OF SEVERE HYPERTENSION

  • 1. How high is the BP (> 180/120 mmHg)?
  • 2. Is there evidence of critical vascular damage in

vital organs?

AMI Pulmonary edema Hemorrhagic Stroke Hypertensive encephalopathy Dissecting aneurism Acute renal failure

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PRES (RPLE)

(Posterior Reversible Encephalopathy Syndrome)

Cardinal Sx: H/A, altered LOC, seizures (generalized or focal, usually multiple including status epilepticus and can be non convulsive), focal neurological sx, particularly visual disturbances. PRES is 2- fold more common in females. Diagnosis: Clinical features + early Neuroimaging. Seen on MRI with T2 Diffusion weighted/FLAIR and DWI is the gold standard. The posterior circulation is almost always involved, but can include anterior circulation and brainstem. Also, do an EEG. ??? OCT-SD Prognosis: Potentially reversible with recognition and aggressive use

  • f antihypertensive agents and anticonvulsants. However, can

progress to ischemia/hemorrhage with permanent deficits and even death if not and treated promptly and appropriately.

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BERNOULLI’S PRINCIPLE (conservation of energy)

MAP = 100 Pc = 25

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AUTOREGULATION OF CEREBRAL BLOOD FLOW

Mean Arterial Pressure (mmHg) CBF

60 120

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STARLING EQUATION

(the convective movement of water and

small solutes across membranes)

Pfiltration = Ptransudation - Poncotic

= (Pcap - Pinterst) - (Ocap - Ointerst)

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P

AReg NonReg

P/R=±F P/ ± R=F Pc ± Fc ± Pc  Fc 

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F

AReg NonReg

P/R=±F P/ ± R=F Pc  Fc  Pc  Fc  Pc ± Fc ±

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Re-setting of CEREBRAL AUTOREGULATION Time Course of this is Minutes, Up to an Hour

Mean Arterial Pressure (mmHg) CBF

60 120

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AUTOREGULATION of a very abnormal Cerebral Circulation

Mean Arterial Pressure (mmHg) CBF

60 120 230

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149 HTN MAP PRES MAP Baseline Delta MAP Median Delta MAP Mean 147 100 37 38 95% CI 143-150 93-106 31-45 BP equiv 205/118 (200-209/114-121) from an  baseline BP

Systematic Review of All Cohort Studies and Case Reports of Hypertensive PRES 2005-2011

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C+Tx C+Tx C+Tx CisP

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Loss of AUTOREGULATION of Cerebral Blood Flow

Mean Arterial Pressure (mmHg) CBF

105 60 90 120

{15mmHg}

70

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Reported Associations with PRES

Hypertension, sudden and severe, or not severe but significantly elevated above baseline BP Eclampsia Immunosuppressive Rx (cyclosporine, tacrolimus/sirolimus, steroids) Cytotoxic agents (cyclophosphamide, cisplatin and Pl analogues) Acute or chronic renal failure Alpha interferon, IgG, antiretroviral Rx, VEGEF inhibitors (bevacizumab) Post Vaccination for measles Lupus and other CTD TTP/HUS Erythropoetin Blood transfusions Acute Intermittent Porphyria HIV Sepsis BM transplant Hypercalcemia/hyperparathyroidism Contrast agents Stimulant abuse

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149 HTN MAP PRES MAP Baseline Delta MAP Median Delta MAP Mean 147 100 37 38 95% CI 143-150 93-106 31-45 BP Equiv 205/118 (200-209/114-121) from a (N) baseline BP 37 Low BP MAP PRES MAP Baseline Delta MAP Median Delta MAP Mean 98 94 3 2 95%CI 87-103 89-99

  • 8-14

BP Equiv 139/77 (131-146/73-82); baseline 5 mmHg lower

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ASSESSMENT OF SEVERE HYPERTENSION

  • 1. Is there evidence of critical organ damage?
  • 2. Has there been a blood pressure elevation high

enough and long enough to account for that

  • rgan injury?
  • 3. What was the patient’s baseline BP in the days
  • r weeks prior to the event?
  • 4. Has the BP been poorly controlled for any

length of time in the past?

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TOD for Dx of a Hypertensive Emergency

Major Criteria Supporting Evidence

Hypertensive encephalopathy/PRES Proteinuria/microalbuminuria Acute stroke - ischemic or hemorrhagic Pressure natriuresis Acute coronary syndrome Elevated urate Acute LV dysfunction/pulmonary edema Thrombocytopenia Acute aortic dissection Schistocytosis Acute renal failure Elevated LDH Pregnancy + symptoms of PRES Coagulopathy Pregnancy + HELLP syndrome Fx impairment of any other organ Pregnancy + capillary leak ( BP not req’d) Significant troponin leak Intractable bleeding Pmax, PWD, repolarzn abn on ECG Syndromes of catecholamine excess

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A Severe BP Rise Should be Defined:

a) In all patients, as a persistent rise in MAP of greater than 30-45 mmHg over baseline MAP, or if baseline MAP is not known, above an MAP of 90 mmHg developing over the course of several hours to days, or a rise in MAP of 40- 60 mmHg lasting longer than 1 hour. b) In patients with sepsis/SIRS or those receiving immune modulating or cytotoxic chemotherapy that potentially impair cerebral autoregulation and/or vascular permiability, BP elevations less than these levels may similarly cause a hypertensive emergency.

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c) Patients with poorly controlled hypertension with BPs above 180/120 for a period of time greater than 3 to 6 months are likely to possess adaptive structural changes in their heart and systemic vasculature that support a higher BP. These people are at particular risk of ischemic injury if the BP is rapidly lowered below autoregulatory

  • limits. Thus, severe, poorly controlled hypertension is

also a Hypertensive Emergency

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Long Term Outcome of Patients After a Hypertensive Microvascular Event

MacDonald et al. Am Heart J 2008; 156:91830

Meta-analysis of 5 case control and 10 cohort studies 116,175 eclamptics, 2,259, 576 controls, age < 56 yr OR of subsequent CVD including MI, stroke & CV mortality 2-fold. Also showed an increasing graded risk for  severity

Bellamy et al. BMJ; doi:10.1136/bmj.39335.385301.BE

Meta-analysis of all prospective and retrospective studies 198,252 eclamptics, 3,488,160 controls, weighted mean f/u 14.7 yr OR for IHD, stroke and VTE 1.8-2.2; overall mortality 1.5 Absolute risk of IHD was 4% at 11.7yrs

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DEMENTiA

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How Can We Assess Whether the Microcirculation is in Trouble?

EEG, MRI Microalbuminuria Pressure Natriuresis, Uric acid INR, VWF, platelet cts, schistocytosis, lactate

P-wave dispersion, repolarization abns on the ECG, CMR

Ach- or other endothelial-mediated vasomotion Studies of the retinal microvasculature OCT-SD

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Hughes AD et al. J Hypertension 2006;24:889-94

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