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Acute pressure syndromes

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  • 1. DR.RISHIKESAN K.VSPECIALIST PHYSICIANVENNIYIL MEDICAL CENTRE SHARJAHACUTE PRESSURESYNDROMESFROM THREAT TO THERAPYGIVING ACUTE HYPERTENSION THE HYPER ATTENTION ITDESERVES
  • 2. HTN AFFECTS AT LEAST 1 BILLIONINDIVIDUALS
  • 3. DEFINITIONSHypertensive crisis, is somewhat of a generic term andmost clinicians break this into 2 categories.The first category is referred to as hypertensiveemergency. This is a severe elevation of BP, defined as>180/120 mm Hg, and it is complicated by target-organdysfunction or damage.Hypertensive urgency means there is a severe elevationin BP but target-organ function remains intact.In terms of severity, pts. who have HE are in worsecondition than those who have hypertensive urgency.
  • 4. HYPERTENSIVE CRISES – OTHER TERMSACCELARATED HYPERTENSIONBP is elevated progressively, at fast pace, with retinalhemorrhage and exudates (Grade III Keith-Wagner-Barker retinopathy ).MALIGNANT HYPERTENSIONSevere elevation BP accompanied with papilledemawhich may be accompanied by encephalopathy ornephropathy.In addition to Grade IV Keith-Wagner-Barkerretinopathy.
  • 5. TARGET ORGAN DAMAGE / DYSFUNCTIONHE includesHypertensive encephalopathy,ICH, AMI, acute LVD with pul. edema,UA, Dissecting aortic aneurysm,In women who are pregnant, eclampsia.In terms of hypertensive urgency, this isstage II HTN, which may present withsevere headache; shortness of breath; epitasis, ornosebleed; or severe anxiety.
  • 6. HOW COMMON IT IS ? IT IS COMMONMost of these patients :• are generally known to have hypertension• are oftentimes noncompliant with treatment• or have been inadequately treated for theirhypertension.• Patients who have had hypertension for 5, 10, or15 years and have never been well controlled areat high risk for these disorders.
  • 7. EPIDEMIOLOGYHow common is this disorder?These numbers are are somewhat suspect. It probably isunderreported.Something on the order of 3% of the patients presenting EDhave hypertensive crisis ie on an annual basis, perhaps 2 to 6out of 100,000 patients coming through EDsOf 500,000 American patients per year who have thisdisorder, about 25% present to the medical section of the ED,and among these, cerebral infarction may occur in up to aquarter, along with other catastrophes like encephalopathyand ICH.
  • 8. URGENCY VS. EMERGENCYIn terms of presentation, there are some differencesbetween HU and HE, but it is not hugely different.People who present with HE tend to be slightly older.Men slightly less commonly have HU; it is fairly equalfor emergency.If you look at the SBP, its important to note that theBP is the same on average: 210 mm Hg.In those in whom it is unknown whether they hadhypertension in the past, urgency is a little morecommon than emergency.
  • 9. PRESENTATIONWe look at the 2 columns onthe right, headache is slightlymore common for pts. Whohave HU compared with HE.Epistaxis is more common.Chest pain, Dyspnoea, ismore common for emergency.Psychomotor agitation ismore common with urgency,and neurological deficit withemergency.
  • 10. RISK FACTORSThe risk factors fordeveloping hypertensivecrises.Having a h/o CRF, a historyof heart failure, knownelevations in SBP and DBP--all of these are basically riskfactors for the developmentof HE.When taking a history, youprobably would want to askabout these things.
  • 11. PATHOGENESISThe pathogenesis of elevations in BP is multifactorial;There is increases in mechanical stress and vascular wall damage which results inincrease in vascular permeability,.There is cell proliferation and activation of the coagulation cascade. Theendothelial cell surface lining of the vascular compartment is damaged, andwhen this is damaged, this leads to endothelial cell dysfunction, which furtherpromotes vasoconstriction and platelet aggregation. There is the release ofvarious vasoconstrictors with this situation.There is activation of the RAAS. Angiotensin II is a very potent vasoconstrictingsubstance, but in addition, it increases the elaboration of cytokines such as IL-6 andNF-kappaB, which is a pro-inflammatory factor.There is white blood cell (WBC) adhesion, as well as proliferation of vascularsmooth muscle cells. NADPH, which generates reactive oxygen species, is alsoincreasedThere is a reduction of NO, which is a protective substance, that leads to vasodilationand inhibition of platelet aggregation, and again, this leads to this inflammatory factor.So this is not a simple situation. There is not a single drug per se that attacksall of these potential targets within the cascade of hypertensive emergency.
  • 12. PATHOGENESIS
  • 13. Vasoactivesubstances VasoactivesubstancesSheer stress ofhigh pressure
  • 14. UNCONTROLLED HYPERTENSION• Hypertensive emergencies encompass a spectrum ofclinical presentations in which uncontrolled BPs lead toprogressive or impending EOD. In these conditions, the BPshould be lowered aggressively over minutes to hours.With the advent of anti hypertensives, the incidence ofhypertensive emergencies has declined from 7% toapproximately 1% of patients with hypertension .• In addition, the 1-year survival rate associated with thiscondition has increased from only 20% (prior to 1950) to asurvival rate of more than 90% with appropriate medicaltreatment.
  • 15. ADAPTIVE VASCULAR CHANGES• A PATIENT WITH CHRONIC HTN IS LIKELY TOHAVE ADAPTIVE VASCULAR CHANGES WHICHPROTECT END ORGANS.• CONVERSELY PTS. WITH NO H/o HTN LACKTHESE PROTECTIONS AND MAY DEVELOP A HEAT A SURPRISINGLY LOW BP (FOR EG. ACUTEGLOMERULONEPHRITIS, ECLAMPSIA INPREGNANACY
  • 16. TREAT THE PATIENT AND NOT THE NUMBER• The fundamental principle in determining thenecessary ED care of the hypertensive patient isthe presence or absence of end-organ dysfunction.Many patients present to the ED with elevated BPs;however, only a small proportion of patients willrequire emergency treatment.• An important point to remember in the managementof the patient with any degree of BP elevation is to"treat the patient and not the number."
  • 17. IF YOU DETERMINE A HU ( NO EVIDENCE OF ENDORGAN DAMAGE )• Rapid reduction can induce cerebral or myocardialischemia• Goal BP, safe level in 6 hrs, 160/110 over 12-24 hrs withconventional oral therapy• Identify the cause and give appropriate TTT.• can give extra or double dose of what the patient isalready on.• Patients can be sent home.• Oral agents may be used in hypertensive urgency, butthey are discouraged in hypertensive emergency.
  • 18. HYPERTENSIVE EMERGENCIES• Admission to a CCU• Hemodynamic monitoring (ECG, CVP and arterial line).• Ensuring proper ventilation, free air way, control of seizures andadequate urinary output are important• The initial goal is to lower the arterial BP by no more than 25%within an hour after the patient is seen and then, if the patient isstable, to titrate the BP to the range of 160/100-110 mm Hgdiastolic within the next 2 to 6 hours.• We do not want to lower the BP in the first 5 minutes.• Avoid excessive reduction, because this can precipitatechanges in blood flow to vital organs, such as the kidney, brain,or coronary arteries
  • 19. WHY NOT ENTERAL OR INTRAMUSCULAROral absorption or absorption through other routes, isnot dependable in this situation.Someone having HE probably does not have normalblood flow to the gut nor the skin; the same would betrue for the muscles.Pts. with HE are volume depleted. They are pumpingblood at the kidney at an accelerated rate, meaninghigh RBF, and essentially pts. are salt and waterdepleted secondary to having very high renal bloodflow.
  • 20. NEUROLOGIC EMERGENCIESRapid BP reduction is indicated in HTNVEencephalopathy, acute ischemic stroke, acuteICH,SAH.In hypertensive encephalopathy, the treatmentguidelines are to reduce the MAP 25% over 8 hours.Labetalol, Nicardipine , Esmolol are the preferredmedications;However, Nitroprusside and Hydralazine should beavoided
  • 21. • What you see here is a so-called U- or J-shaped curve:for DBPs >105 and <70 mmHg, the 90-day death rate ishigher, whereas if thediastolic is in the range of 70to 105 mm Hg, you have thelowest death rate. For SBPthere is a very similarrelationship: having asystolic >220 mm Hg is bad,but having a systolic in therange of 155 to 220 mm Hggives you the best outcome.HTN IS NOT BADIN AIS
  • 22. ACUTE ISCHAEMIC STROKE
  • 23. ICH AND SAH• PREFERRED MEDICATIONS ARE• LABETALOL,NICARDIPINE AND ESMOLOL• IN CASE OF INCREASED ICP• MAINTAIN MAP < 130 mmHg or SBP < 180mmHg FOR THE FIRST 24 HOURS• IF NORMAL ICP MAP <130mmHg OR SBP<160mmHgSAHPREFERRED AGENTS ARE AGAINLABETALOL, NICARDIPNE AND ESMOLOL.MAINTAIN SYS.BP <160 mmHg UNTIL THE ANEURYSM ISTREATED ORCEREBRAL VASOSPASM OCCURS
  • 24. ACUTE CARDIOPULMONARY COMPROMISE
  • 25. NICARDIPINE• Nicardipine is good because• It doesnt depend on renal function or in terms ofliver function for its excretion . It can be given as anIV bolus or constant infusion, and so it is very useful• Dose: 5–15 mg/ hr IV .Onset 5–10 min Duration13–30 min, may exceed 4 hr• AE :Tachycardia, headache, flushing, local phlebitis• Indication : Most HE except acute heart failure;• Caution: coronary ischemia
  • 26. FENOLDOPAM• Fenoldopam mesylate• Dose 0.1–0.3 µg/kg/min as IV infusion. onset of action <5min . Duration 30 min .• AE: Tachycardia, headache, nausea, flushing• Indication Most HEs; Caution with glaucoma• Fenoldopam, I think, is a very expensive alternative drug forthe treatment of hypertensive urgency; again, it must begiven by constant infusion.• There were reportedly advantages in terms of preservingrenal function
  • 27. SNPSodium nitroprusside is a very quick-acting , quickboth in terms of onset and offset.It is good for many situations, but it requires verycareful monitoring, usually within arterial lines, to makesure that you are measuring the true BP.The drug should not be used in pts. who have renalinsufficiency because the metabolic pathway for SNPleads to -CN, and -CN, of course, is very toxic.So in pts. with renal insufficiency, avoid this drug
  • 28. • NOTE THAT DIURETICSARE GENERALLYAVOIDED IN HTNVEEMERGENCIES AS MANYPTS.ARE HYPOVOLEMICDUE TO PRESSUREINDUCED NATRIURESIS.• EXCEPTIONS AREPATIENTS WITH HEARTFAILURE AND ORPULMONARY EDEMADIURETICS
  • 29. BETABLOCKERS , ALPHA BLOCKERS• The adrenergic inhibitors include the beta-blockers labetalol and esmolol andthe alpha-blocker phentolamine• Labetalol is useful in terms of being both an IV bolus with a constant infusionand then potentially a follow-up oral therapy• Esmolol, of course, is ultra-short-acting. It is very useful in critical caresituations in surgery, but certainly not a very useful long-term drug. Adverseeffects apply for all beta-blockers in patients who have bronchospasticdisease, and please note, this means asthma patients, not chronic obstructivepulmonary disease (COPD) patients.• And lastly, phentolamine is a very special-use drug. It specifically blocks thealpha receptor and is particularly useful in situations such aspheochromocytoma, in which the secretion of catecholamines such asepinephrine and norepinephrine are responsible for severe swings inhypertension. This drug is only given IV and is actually somewhat difficult tofind.
  • 30. IV labetalol and hydralazine are considered first-line Rxfor the management of acute-onset, severehypertension in pregnant and postpartum women.Second line alternatives to consider include labetalol ornicardipine by infusion pump .SNP should be reservedfor extreme emergencies and used for the shortestamount of time possible because of concerns aboutcyanide and thiocyanate toxicity and increased ICPwith potential worsening of cerebral edema in themother
  • 31. THAT IS NOT A GOOD IDEA ……….
  • 32. S/L NIFEDIPINEThere are studies for captopril, nifedipine, and prazosin givenorally.These drugs should be avoided. Even though the stuff isout there, it is not really a good idea, especially fornifedipine We had several disasters with sublingualadministration of nifedipine.You poke a hole in the capsule for the immediate-releasenifedipine and you squirt it under the tongue.We had several patients who developed severehypotension and had to be given IV fluids and pressors toget their BP back.
  • 33. CLEVIDIPINEClevidipine, an intravenous CCB, was approved by theFDA in August 2008 for the management of acute,severe hypertension .A 3rd generation DHP CCB that inhibits L-type calciumchannels . A short half life of 1 to 2 minutes, a quickonset of action of 2 to 4 min. and a short duration ofaction of 5 to 15 min.Clevidipine lowers SVR , it has greater effects onarterial vasodilatation
  • 34. CLEVIPREXThe antihypertensive efficacy of intravenous clevidipinewas compared with a placebo in cardiac surgery patientsin 2 randomized, double-blind multicenter studies.• These studies showed that clevidipine was effective inthe treatment of both acute preoperative andpostoperative hypertension.• The antihypertensive efficacy of clevidipine was alsocompared with the efficacies of nitroprusside,nitroglycerin, and nicardipine.• Overall the blood pressure control was similar amongthe 4 treatments.
  • 35. CLEVIDIPINE