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Module 3 chapter 2d

Module 3 chapter 2d. Hypertension and cva. The plan. Introduction Primary prevention of stroke Management of hypertension during acute stoke Secondary prevention Conclusions. Hypertension The leading CVD risk Factor. Contributes to 13% global deaths 1.

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Module 3 chapter 2d

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  1. Module 3 chapter 2d

  2. Hypertension and cva

  3. The plan • Introduction • Primary prevention of stroke • Management of hypertension during acute stoke • Secondary prevention • Conclusions

  4. HypertensionThe leading CVD risk Factor • Contributes to 13% global deaths1 • An increase in the number and severity of risk factors by middle age can affect a person’s remaining lifetime risk for CVD2 • Prevention and control of CVD risk factors are crucial2 Hypertension related deaths 13% http://www.world-heart-federation.org/press/fact-sheets/cardiovascular-disease-risk-factors/ viewed on May 16, 2013, http://hp2010.nhlbihin.net/joinhin/news/professional/hdrisk.asp

  5. HypertensionThe Indian Scenario • > 140 million people have high BP1 • By 2030, it is expected to cross the 214 million1 • Causes more strokes than ACS (34.6% vs 17.9%) • In India, Hypertension is responsible for2 • 57% of all stroke deaths • 24% of all CHD deaths Stroke has higher morbidity, mortality and less treatment options and success when compared to CAD So in hypertension management we must aim at preventing strokes 1. http://www.thehindu.com/sci-tech/health/hypertension-major-contributor-to-avoidable-deaths-in-india-who/article4513904.ece, 2. Journal of Human Hypertension (2004) 18, 73–78

  6. Benefit of Interventions Over 5 Years

  7. The plan • Introduction • Primary prevention of stroke • Management of hypertension during acute stoke • Secondary prevention • Conclusions

  8. Commonly we see.. • Pts. with good BP control suddenly develop CVA • Pts. with long standing high BP don’t develop any vascular event

  9. Mean blood pressure • The average of several readings of systolic or diastolic pressure (expressed as numbers) • Different from mean arterial BP (DBP+1/3 PP) • Derived from many clinical visits, Home BP recordings and ABPM • 7 to 10 or more BP recordings at different clinical visits are needed to get mean blood pressure • Mean BP , thus obtained may be an accurate estimate of usual blood pressure

  10. BP variability • The variation of BP with time • Expressed as Standard Deviation (SD) • Variation may be for beat to beat (ultra short), over 24hrs (Short term) or visit to visit (long term) • Extent of variability is positively related to mean blood pressure

  11. TO PREVENT STROKE • Both mean BP as well as BP variability should be addressed • BP variability is assuming lot of importance in the prevention of stroke • Control of mean BP without achieving reduction in BP variability may not yield benefits

  12. Examples2 patients,5 visits • Patient 1 : 120/130/120/130/120 Mean BP- 620/5 = 124 SD= 5.5 • Patient 2: 150/110/130/140/90 Mean BP – 620/5 =124 SD=24.08 The patient 2 has BP variability although both patients have same mean BP SD :Standard Deviation

  13. BP variability causes and consequences

  14. BP VariabilityEvidences for increased risks Canadian Journal of Cardiology 29 (2013) 557e563

  15. Which drug reduces BP variability

  16. Visit to visit BPV ASCOT TRIAL

  17. Stroke risk and coronary risk expressed by docile of within-visit SBP variability Stroke risk (HR, 95% CI) Number of patients in each docile of within-visit SD SBP Coronary risk (HR, 95% CI)

  18. ALLHAT TRIAL BPV MAP MAP BPV BPV MAP MAP: MEAN BP BPV: BP VARIABILITY REDUCTION OF STROKE WAS THE HIGHEST FOR AMLODIPINE

  19. For primary prevention • The most important aspect of primary prevention of stroke is BP control • Calcium antagonists especially long acting DHPs are powerful drugs to get BP targets • They have additional benefit of reducing BP variability which is emerging as an important risk factor for stroke • Even in combination therapy Calcium antagonists should be tried in 2nd or 3rd step

  20. The plan • Introduction • Primary prevention of stroke • Management of hypertension during acute stoke • Secondary prevention • Conclusions

  21. Early recognition, transport, evaluation and management

  22. BP AND ACUTE STROKE • The risk of high blood pressure in stroke is U-shaped blood pressure during acute stroke should be neither too low nor too high, either in ischemic or in hemorrhagic stroke • However, the treatment of hypertension during acute stroke remains controversial.

  23. Auto regulation When the pressure falls cerebral blood flow (CBF) increases due to fall in resistance.

  24. In ischemic stroke when there is fall in CBF due to occluded artery, CBF has to be maintained By increase in pressure (BP).

  25. But may increase cerebral edema

  26. THE NEW DATA • In spite of the controversy, the evidence that blood pressure in acute stroke should be treated when it is very high, must be treated in some cases, and can be treated safely, is mounting. • The change that has made the greatest difference is the advent of intravenous thrombolytics for acute stroke; • Lowering blood pressure in patients with acute stroke eligible for tissue plasminogen activator to achieve blood pressure below 185 mm Hg systolic and below 110 mm Hg diastolic so that tissue plasminogen activator can be given has become standard therapy

  27. Avoid BP >180/110

  28. ICH

  29. Patients who don’t receive tPA • At this time, the previous recommendation not to lower the blood pressure during the initial 24 hours of acute ischemic stroke unless the blood pressure is >220/120 mm Hg or there is a concomitant specific medical condition that would benefit from blood pressure lowering remains reasonable.

  30. Exceptions • Some conditions, such as myocardial ischemia, aortic dissection, and heart failure, may accompany acute ischemic stroke and may be exacerbated by arterial hypertension. • Whenblood pressure management is indicated for a specific medical condition in the setting of concurrent acute cerebral ischemia, an optimal approach has not been determined. • At present, blood pressure targets are based on best clinical judgment. • A reasonable estimate might be to initially lower the systolic blood pressure by 15% and monitor for neurological deterioration related to the pressure lowering.

  31. Ischemic strokenot eligible for thrombolytic therapy

  32. Intracranial hemorrhage • In both intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH), the approach to blood pressure management must take into account the potential benefits (eg, reducing further bleeding) and risks (eg, reducing cerebral perfusion) of blood pressure lowering.

  33. The difficulty • Reducing the blood pressure in patients with either ICH or SAH may be beneficial by minimizing further bleeding and continued vascular damage . • Patients with an intracranial hemorrhage due to ICH or SAH may have increased intracranial pressure (ICP) due to blood within the cranium. • Cerebral perfusion pressure (CPP) equals MAP minus ICP. Thus, increases in MAP may be the only means to maintain CPP above 60 to 70 mmHg, the level necessary to maintain perfusion . • Measuring intracranial pressure directly allows blood pressure to be reduced as low as possible while still maintaining the cerebral perfusion pressure above the conservative level of 60 mmHg

  34. Guidelines for treatmentICH AND SAH • For patients with SBP >200 mmHg or MAP >150 mmHg, consider aggressive reduction of blood pressure with continuous intravenous infusion of medication accompanied by frequent (every five minutes) blood pressure monitoring • ●For patients with SBP >180 mmHg or MAP >130 mmHg and evidence or suspicion of elevated ICP, consider monitoring ICP and reducing blood pressure using intermittent or continuous intravenous medication to keep cerebral perfusion pressure in the range of 61 to 80 mmHg • ●For patients with SBP >180 mmHg or MAP >130 mmHg and no evidence or suspicion of elevated ICP, consider a modest reduction of blood pressure (eg, target MAP of 110 mmHg or target blood pressure of 160/90 mmHg) using intermittent or continuous intravenous medication, and clinically reexamine the patient every 15 minutes

  35. The agents- B Blockers

  36. The agents – Sodium Nitroprusside

  37. The agents- Calcium Antagonists

  38. New therapy

  39. The plan • Introduction • Primary prevention of stroke • Management of hypertension during acute stoke • Secondary prevention • Conclusions

  40. Importance of BP control • Once the stroke has stabilized, antihypertensive therapy can reduce the rate of recurrent stroke, independent of the baseline blood pressure. • Regardless of the regimen, blood pressure reduction should be gradual.

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