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Hypertension in icu ppt
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Hypertension in icu ppt



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  • 2. DEFINITIONSHYPERTENSIVE EMERGENCY BP elevation is associated with ongoing neurological, myocardial, hematological or renal TARGET ORGAN DISEASE (TOD)HYPERTENSIVE URGENCY - potential for TOD is great & likely to occur if BP is not controlled. - occurs on chronic stable complication . Stable angina . Old MI . CCF,CRF . TIA,old CVA
  • 3. DEFINITIONSACCELERATED HYPERTENSION - keith wagener barker retinopathy grade 3 (constriction,sclerosis+hemorrhages,exudates) - may be urgency or emergency - presence of exudate more worrisome
  • 4. DEFINITIONS• MALIGNANT HYPERTENSION - KWB grade 4 retino + papilledema (neuroretinopathy) - Always an emergency
  • 5. MALIGNANT HYPERTENSION….MALIGNANT HYPERTENSION - Increased BP + neuroretinopathy - Fundus : flame shaped hemmorhags, cotton wool spots, papilledma - Assoc with : encephalopathy, LV failure, micro angio hemolytic anemia, renal fibrinoid necrosis with endarteritis. Risk factors : 30-50ys, male, smoking
  • 6. MALIGNANT HYPERTENSION….Renal failure is most common cause of death(fibrinoid necrosis+prolif endarteritis) espc if assoc with glomerulonephritis.Recovery predicted if combined length of both kidneys >20.2cm & highly unlikely if <14.2 cm.Presenting creatinine >4.5 - dialysisTreatment-sod nitroprusside (0.3microg/kg/min) also-labetolol, nicardipine,fenoldopam
  • 7. BP CLASSIFICATION(Chobanian et al/JNC 7) sys(mm Hg) dias(mm Hg)NORMAL <120 & <80Pre Htn 120-139 or 80-89Stage I Htn 140-159 or 90-99Stage II Htn ≥160 or ≥100Iso sys Htn ≥140 &<90
  • 8. MANIFESTATIONS OF TARGET ORGAN DISEASE LARGE VESSELS Aneurysmal dilations , Acc atheroscl., Aortic dissection CARDIAC Acute - pulm edema , MI Chronic - LVH , CAD CEREBROVASCULAR Intracereb bleed, TIA, seizures, mental status change, stroke RENAL Hematuria, azotemia, Cr>1.5, proteinuria>1+ RETINOPATHY Papilledema, Hemorrhages, Exudates, Arterial nicking
  • 9. PATHOPHYSIOLOGY Increased SVR Damage to endothelial lining Leakage of plasmaFibrinoid necrosis of arterioles(histo hallmark) Local edema & sclerosis Ischemia of brain ,heart, kidneys
  • 10. PATHOPHYSIOLOGYPatients with antecedent Htn can tolerate higher fluctuations due to shift of autoreg threshold.Patients with no antecedent Htn – organ specific changes occur with DBP>100.Most sensitive vascular bed is CEREBRAL.
  • 11. INITIAL EVALUATION Cardinal points in history- - TOD symptoms (most imp) - prior Htn - Medical Renal Disease - medicine with compliance - cocaine, amphetamine-Htn from any cause may enter emergent phase.-Usually occurs on background of essential hypertn.- Imp secondary causes- renovascular(fibromuscular dys- plasia/atheresclerosis) - chronic GN - reflux nephropathy - analgesic nephropathy
  • 12. SYMPTOMS OF HYPERTENSIVE CRISIS MC is - headache (usually worse in morning) - visual (scotoma, diplopia, hemianopia, blindness) - neuro (focal deficits, stroke, TIA, somnolence) - ischemic chest pain - renal (polyuria, nocturia, hematuria) - back pain (aortic aneurysm) - nausea ,vomiting - wt loss.PATIENTS OFTEN HAVE INTRAVASCULAR VOLUME DEPLETION.
  • 13. EXAMINATION• Verify BP recordings in diffn position(if possible)• Fundus exam – arterio thickng, Incr light reflex, vascular tortuosity, AV nicking retinal hemmorhages, lipid leakage (hard exudates) nerve ischemia, papilledema (cotton wool spots)• ABDOMEN masses(PCKD),bruits(aneuyrsm)
  • 14. ANCILLARY TESTSSr Na, K, bicarb, BUN, Cr, CBC (with P/S for schitocytes)PT/aPTT, tox screen, pregnancy test, ECG, urinanalysisUSUALLY - hypoNa and matabolic alkalosis - incr BUN, Cr - proteinuria, hematuria - marked proteinuria suggets GN
  • 15. PSUDOHYPERTENSIONOverestimation of true BP due to stiff arteryOSLERS MANOEUVRE. : inflate BP cuff to greater than brachial systolic, a palpable radial artery but pulseless.Seen in - atherosclerosis, - monckebergs medial calcification, - metastatic calcification(ESRD)
  • 16. TREATMENTInitial therapy should terminate ongoing TOD, not return of BP to normal.Generalized goal : decrease MAP by 20-25% within one hour f/b decr to ~160/100 by 2-6 hrs and towards normal over 1-2 daysEXCPTNS : . ischemic stroke . aortic dissection . active unstable angina or CCF• More gradual reduction in elderly with carotid stenosis .
  • 17. SPECIFIC HYPERTENSIVE CRISIS 1 . PULMONARY EDEMA a) with preserved systolic function(LVH)- - abrupt increase in afterload with poor diastolic relaxation leads to pulmn HTN and edema. - Treatment is with Na-nitropru (it prefrnn dilates resistance vessels) - less emergnt condn – ACEI/CCB
  • 18. PULMONARY EDEMA…B) with poor systolic functionMYOCARDIAL ISCHAEMIA -nitroglycerine is preferred(dilates collaterals)MYOCARDIAL INFARCTION - sedn/pain control - DBP>100 - nitroglycr - early β-blockade
  • 19. SPECIFIC HYPERTENSIVE CRISIS2) AORTIC DISSECTIONBP lowered rapidly to lowest clinically acceptable levelAgents used lobet or esmolol, later on nitropru addedAlternative agent-trimetaphan
  • 20. SPECIFIC HYPERTENSIVE CRISIS3) HYPERTENSIVE ENCEPHALOPATHYWhen high perfusion pressure overwhelms cerebral autoregulation.Can lead to blindness, seizures, coma, gradually worsening headache.Pathologically-cerebral edema, petechial hemorrhg, microinfarcts.Immed Neuroimagng - to rule out ischemic stroke/hemorrhageHallmark is improvement in 12-24 hrs of BP redn.
  • 21. HTN ENCEPH…Treatment short acting parenteral agents used.MAP should decrease by 15-20% over 2-3 hrs.D/d : cerebral infarct, ICH/SAH, subdural hematoma, brain tumor, seizures, vasculitis/meningoenceph.
  • 22. HTN ENCEPH…DIFFN POINTS : 1) Focal neurological deficit is unusual without cerebral bleed2) Papilledema is almost always assoc with Htn enceph3) Mental staus improves by 24-48hrs-delayed in CNS bleed4) Brain dysfunction develops by 12-24 hrs in Htn but more acutely with ischemic stroke/bleed.
  • 23. HTN ENCEPHAL..Posterior leukencephalopathy syn.- reversible vasogenic subcortical edema without infarct MRI – white matter edema in post cerebral hemispheres
  • 24. ISCHEMIC STROKEFor every 10 mmHg incr in pressure >180 a 40% incr in worsening neurological status.Area of stunned but viable tissue(ischemic penumbra)may need higher perfusion pressures, so ASA/AHA-recommends (after excluding pain, nausea, full bladder, hypoxia, incr ICP)BP redn. If sys>220 or dias > 120Also, for thrombolysis BP<185/110.And post reperfusion use lobet or nicardipine for sys>180 or dias>105 & Na nitro for sys >230
  • 25. ISCHEMIC STROKELatest studies recommend modest reduction of BP (10-27mmHg) improved outcomes but effect waned with increasing age ,so,avoid >10% sudden drop
  • 26. SUBARACHNOID HEMORRHAGESAH incr ICP & decr cerebral perfusion causing global ischemiaInduces intense vasospasm in neighbouring vessels (4- 12 days) after initial bleed.Goal-dec 20-25% of MAP over 6-12 hrs but not <160/100.If vasospasm occurs later-inc BP with 3H(not proven)Preffred - lobetAvoid- nitrodilatorsNo data to support oral nimodip dec vasospasm.
  • 27. INTRACRANIAL HEMORRHAGEMajor risk factor is Htn.Most rapid decline in BP occurs in first 24 hrs but may remain elavated for 7-10 days (while in ischemic stroke BP dec to normal in 24-48 hrs)AHA/ASA recommends…decrease BP if- Sys>200 or MAP>150, ICP incr suspected –sys>180 or map>130 ICP incr not suspec-target MAP~100 or BP~160/90Preffred agent : lobet
  • 28. HEAD TRAUMAWith trauma comes edemaWith ICP monitoring –target MAP ≥90Prefferd- lobet or nicardipine
  • 29. POST OP PAINEarly-(0-2hrs) : pain, hypoxemia, hypercabia, shivering.Intermed(12-36hrs) : fluid overload, reaction to ET/FOLEYS.
  • 30. PheochromocytomaVery rare cause of hypertensionHeadache,palpitations,Htn,anxiety,abd pain diaphoresisOrthostatic changes in BPParoxsysmal symptomsT/t : i/v phentolamine f/b b-blockade
  • 31. GESTATIONAL HYPERTENSIONAfter 20 wks in normotensive.SBP>140 & DBP>90 on two separate occasions 6 hrs apart.Pre-eclampsia – gestn htn + 300 mg in 24 hrs proteinuriaEclampsia- +seizuresT/t – bed rest & parenteral MgUse (lobet,hydralazine) if SBP>160 or DBP>100
  • 32. ANTIPHOSPHOLIPID Ab SYNDROMEMicrovasculopathy & emboli to renal arteryT/t – Na nitropru/lobet & anticoagn.
  • 33. GBSDysreflexia (bladder/bowel distension below level of lesion trigger massive sympatc discharge)Symptoms – Htn,bradycardia, diaphoresis,headache.T/t – Na nitroprus., phentolamine,lobet
  • 34. RENAL TRANSPLANT RECEPIENTAcute rejectionObstructive uropathy Cyclosporine/steroid.T/t oral CCB
  • 35. NEW ONSET HYPERTENSION IN ICUPainAnxietyHypoxemiaHpercarbiaShiveringVol overloadDiscontinuation syndrome
  • 36. INTRAVENOUS MEDICATIONSSodium nitoprusside : nitric oxide compound -arterio-veno dilator -useful in most Htn crisis dose 0.25mic/kg/min(max 8)C/I – high output cardiac failure, cong optic atrophy.Cyanide toxicity – anemia & liver d/e -acidosis, tachycardia, almond smell, change in mental status.Thiocyanate tox. – renal d/e -psychosis, hypereflexia,seizure,tinnitus -thiocyanate>10 should be avoided.Avoiod infusion>48 hrs.
  • 37. INTRAVENOUS MEDICATIONSNITROGLYCERINE- predom. Veno dilator, decreases preload.Use : cardiac ischemiaDose : 5mic/min(max 100)C/I : incresed ICP, angle closure glaucomaMost useful in cadiac compromise(MI,LV failure,pulm edema),,not recommnded > 48 hrs.
  • 38. INTRAVENOUS MEDICATIONSLABETOLOL : β > α (7 : 1) adrenergic blockadeOnset 2-5 min, durn 3-6 hrsBolus 20 mg (max 300 mg)Infusion 0.5-2mg/min ,used in pregnancy along with hydralazine.Avoid in bronchospasm, bradycardia, CCF, >first degree heart block,
  • 39. INTRAVENOUS MEDICATIONSESMOLOL: cardioselective β1 blockerUsed in aortic dissectionOnset 60 seconds, duration 10-20 min.Infusion 50-300 mic/kg/min.Not dependant on hepatic/renal function
  • 40. INTRAVENOUS MEDICATIONSFENOLDOPAM : post synaptic dopamine agonist. -primarily arterial dilator,rapid onset/offset of effect.Advantageous in kidney d/e, increases renal blood flow,natriuresis.Dose : 0.1 mic/kg/min.C/I : glaucoma,hypotension,,check K+ every 6 hrs
  • 41. INTRAVENOUS MEDICATIONSHYDRALAZINE : direct arteriolar dilator.Used in pregnancy/eclampsiaDose 10 mg every 60 min (max 20 mg)Duration of action 2-4 hrsReflex tachycardia, exacerbates angina,BP lowering response is less predictable(depends on renin&volume status)
  • 42. INTRAVENOUS MEDICATIONSPHENTOLAMINE: α – blockadeUsed primarily in pheochromocytomaDose 5-15 mgAlways f/b β-blockade
  • 43. INTRAVENOUS MEDICATIONSNICARDIPINE : dihydropyridine CCBOnset 10-20 min,duration 1-4 hrDose 5 mg/hr (max 15 mg/hr)Avoid in CCF,cardiac ischemia.CLEVIDIPINE : short acting dihydropyridine CCB.Reduces BP without affecting cardiac filling pressures or reflex tachycardia
  • 44. INTRAVENOUS MEDICATIONSENALAPRILAT : only parenteral ACE-I.Dose 1.25-5 mg every 6 hr.Response not predictable, hyperkalemia in reduced GFR.TRIMETHAPHAN : nondepolarizer ganglionic blocker.Dose : 0.5-5mg/minUsed in aortic dissectionDisadvntges : paralytic ileus, bladder atony, tachyphyl.
  • 45. Thank you