hypertension with bilateral renal artery stensosis


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  • Headache and altered level of con-sciousness are the usual manifestations of hyperten-sive encephalopathy.25,26 Focal neurologic findings,especially lateralizing signs, are uncommon in hyper-tensive encephalopathy, being more suggestive of acerebrovascular accident. Subarachnoid hemorrhageshould be considered in patients with a sudden onsetof a severe headache.
  • Dietary sodium should be reduced tono more than 100 mmol per day (2.4 g of sodi-um).94–
  • Emergencycharacterized bysevere elevations in BP (>180/120 mmHg) compli-cated by evidence of impending or progressive tar-get organ dysfunction (jnc 7)Examplesinclude hypertensive encephalopathy, intracerebralhemorrhage, acute MI, acute left ventricular failure with pulmonary edema, unstable anginapectoris, dissecting aortic aneurysm, or eclampsiaChronic Target Organ Damage (JNC VII)HeartLVHAngina/prior MIPrior coronary revascularizationHeart failureBrainStroke or transient ischemic attackDementiaCKDPeripheral arterial diseaseRetinopathydecompensation of vital organ functionwhereas in children and pregnantwomen, encephalopathy may develop with a DBP ofonly 100 mm Hg.
  • Htnenchephalopathy is vasodilation, edema, and increased intracranial pres-sure. Clinically, patients present with headache, visual changes, nausea, and vomiting. They might complain of transient and migrating nonfocal neurologic deficits, and might progress to seizures and coma.
  • Some patients with hypertensive urgencies maybenefit from treatment with an oral, short-actingagent such as captopril, labetalol, or clonidine followed by several hours of observation.The reason for a stepwise reduction in blood pressure is the fact that patients with chronic hypertension have an altered autoregulation curve. Acute normotension would lead to hypoperfusion in these patients. Those with aortic dissection or pulmonary edema are excepted from the rule of gradual blood pressure reduction. In the presence of these diseases, blood pressure must be reduced rapidly to normal values.Patients with hypertensive urgency should have theirBP reduced within 24 to 48 h, whereas patients with
  • require immediateBP reduction (not necessarily to normal) to pre-vent or limit target organ damage (jnc 7)The initialgoal of therapy in hypertensive emergencies is toreduce mean arterial BP by no more than 25 percent (within minutes to 1 hour), then if stable, to160/100–110 mmHg within the next 2–6 hours.. There are exceptions to the above recommendation—patients with anischemic stroke in which there is no clear evidencefrom clinical trials to support the use of immediate antihypertensive treatment, patients withaortic dissection who should have their SBP lowered to <100 mmHg if tolerated, and patients inwhom BP is lowered to enable the use of thrombolytic agents (see Stroke).return the BP to a level where autoregulation restores normal perfusion pressure to vital organs, not to “nor-mal” BP levels.
  • Those with aortic dissection or pulmonary edema are excepted from the rule of gradual blood pressure reduction. In the presence of these diseases, blood pressure must be reduced rapidly to normal values.Aortic dissection SBP < 100Pulmonary edema rapid decrease required
  • SBP ≥180mmHg or DBP ≥105 mmHg usually necessitatestherapy with intravenous agents to prevent intracerebral bleeding (jnc 7)Aortic dissection 75% die in 2 wks without treatment or 75% survive over 5 yrs with treatment. Left ventricular Force of ejection has to be decreased. Only vasodilator will cause tachycardia and propogation of dissectionThe elevated BP is not a manifes-tation of a hypertensive emergency but rather aprotective physiologic response to maintain cerebralperfusion pressure to the vascular territory affectedby ischemia.
  • Considering the potential for severe toxicity withnitroprusside, this drug should only be used whenother IV antihypertensive agents are not availableand then only in specific clinical circumstances andin patients with normal renal and hepatic function.68The duration of treatment should be as short aspossible, and the infusion rate should not be 2 g/kg/min. An infusion of thiosulfate should be usedin patients receiving higher dosages (4 to 10 g/kg/min) of nitroprusside.7Nitroglycerin reduces BP by reducingpreload and cardiac output; undesirable effects inpatients with compromised cerebral and renal per-fusion Diuretics should beavoided unless specifically indicated for volumeoverload, as occurs in renal parenchymal disease orcoexisting pulmonary edema.
  • Pulmonary edema also start positive pressure ventilation before furosemide. More rapid decrease is permitted but not very severe decrese. More often decrease should be titrated as per symptomsNitroprusside has a rapid onsetof action, and provides both arterial and venous dilation. Heart rate control with β-blockers must be initiated first to avoid reflex tachycardia that will propagate the dis-section. Alternatively, labetalol, with its a -blocking andβ-blocking properties, is a relatively user-friendly option for controlling heart rate and BP simultaneously.); if a thrombolytic is given, reduce BP to 180/105 mm Hg before treatment and 180/100 mm Hg after treatmen
  • hypertension with bilateral renal artery stensosis

    1. 1. Evidence Based management ofHypertensionCase 6
    2. 2.  A 52-year-old man presented to the emergency department with  worsening occipital headache  Confusion 12 hours  numbness and weakness involving the right side of his body  blurry vision. Past medical history  Hypertension  hyperlipidemia..
    3. 3. On physical examination  Blood pressure was 213/134 mm Hg.  Confused.  Papilledema was seen on fundoscopic examination.  motor weakness (4/5) in the right upper extremity.
    4. 4. Laboratory studies revealedfollowing:  serum potassium, 3.1 mEq/L;  blood urea nitrogen, 36 mg/dL; and  serum creatinine, 2.5 mg/dL (baseline creatinine, 1.5 mg/dL).  Electrocardiogram revealed left ventricular hypertrophy by voltage criteria and nonspecific ST-T wave abnormalities in the lateral leads.  Computed tomography scan of the head without contrast revealed diffuse bilateral white matter changes consistent with hypertensive encephalopathy
    5. 5.  Although not specifically addressed in the JNC 7 report, patients with a systolic BP > 179 mm Hg or a diastolic BP > 109 mm Hg are usually considered to be having a “hypertensive crisis”. Crises Emergency Urgency
    6. 6.  The term malignant hypertension has been used to describe a syndrome characterized by elevated BP accompanied by encephalopathy or acute nephropathy. This term, however, has been removed from National and International Blood Pressure Control guidelines and is best referred to as a hypertensive emergency. CHEST / 13 1/6/ JUNE, 2007
    7. 7. Left with 2 terms Hypertensive Emergency Hypertensive Urgency
    8. 8.  Hypertensive emergency (crisis)  severe elevation in blood pressure (> 180/120 mm Hg)  complicated by evidence of impending or progressive target organ dysfunction. Target organ dysfunction (Acute) include Emergency not defined by a  coronary ischemia, specific number, but  disordered cerebral function, rather by evidence of  cerebrovascular events, acute dysfunction in  intracerebral or subarachnoid hemorrhage or  hypertensive encephalopathy. (cerebral edema) cardiovascular,  pulmonary edema, and neurologic, or renal systems  renal failure. The rate of change in blood pressure Dept. of Health and Human Services, National Institutes of Health, Can Fam Physician 2011;57:1137-41 National Heart, Lung, and Blood Institute; 2004. NIH Publication No. 04–5230.
    9. 9. Examples of Hypertensiveemergency hypertensive encephalopathy, Intracerebral hemorrhage, acute MI, acute left ventricular failure with pulmonary edema, unstable angina pectoris, dissecting aortic aneurysm, Eclampsia, HELLP Syndrome Acute renal failure Microangiopathic hemolytic anemia Acute Postoperative Hypertension
    10. 10.  Hypertensive urgency,  severe elevation in blood pressure without progressive target organ dysfunction (>160/110)  Examples  upper levels of stage II hypertension associated with  severe headache,  shortness of breath,  epistaxis, or  severe anxiety. The Seventh Report of the Joint National Committee on Prevention,Detection,Evaluation, and Treatment of High Blood
    11. 11. Pathophysiology Check Activation of Coagulation cascade and standing pro-inflammatory mediators BP Underlying PrecipitatingHypertension Factor
    12. 12. Index case The patient was admitted to the intensive care unit and started on intravenous nitroprusside. Blood pressure decreased to 190/100 mm Hg over the first 3 hours and neurologic symptoms resolved within 5 hours. He was switched to his usual oral regimen on the third day of hospital admission and was discharged home on the fifth day with controlled blood pressure
    13. 13. Management of Urgency Oral antihypertensive agents in an outpatient or observational setting  low doses  incremental doses  Avoid excessive reduction in elderly, patients with PAD/CVD/intracranial disease The initial goal is to reduce blood pressure to 160/110 mm Hg over several hours to days using conventional oral therapy (24-48 hrs) Mean arterial pressure should be reduced by no more than 25% within the first 24 hours using conventional oral therapy.
    14. 14.  Captopril  ACE inhibitor  onset of action 15 to 30 minutes  maximum drop in blood pressure 30 and 90 minutes  25-mg oral dose initially, followed by incremental doses of 50 to 100 mg 90 to 120 minutes later  Significant adverse effects include cough, hypotension, hyperkalemia, angioedema, and renal failure (especially in patients with bilateral renal artery stenosis, in whom it should be avoided).
    15. 15.  Nicardipine  Calcium channel blocker  oral dose is 30 mg,  Repeated every 8 hours until the target blood pressure is achieved.  Onset of action is ½ to 2 hours.  Common adverse reactions include palpitations, flushing, headache, and dizziness Am Heart J 1995;129:917–23
    16. 16.  Labetalol  has mixed α1- and β-adrenergic blocking properties(1:7)  onset of action within 1 to 2 hours  Starting dose is 200 mg orally, which can be repeated every 3 to 4 hours  Common side effects include nausea and dizziness.
    17. 17.  Clonidine  central sympatholytic (α2-adrenergic receptor agonist) agent  onset of action within 15 to 30 minutes  peak effect within 2 to 4 hours  oral regimen is a 0.1 to 0.2 mg loading dose followed by 0.05 to 0.1 mg every hour until target blood pressure is achieved, up to a maximum dose of 0.7 mg.  Common side effects include sedation, dry mouth, and orthostatic hypotension.  Beware of “withdrawl”
    18. 18.  calcium channel blocker Peak effect within 10 to 20 minutes. Short-acting nifedipine is not approved by the US FDA (unpredictable drops in blood pressure and associated risk of stroke) In 1995, an ad hoc panel convened by the National Heart,Lung, and Blood Institute concluded that “short- acting nifedipine should be used with great caution (if at all), especially at higher doses, in the treatment of hypertension.”
    19. 19. Treatment of hypertensiveemergency Use parenteral drugs Continuous monitoring of blood pressure. Reduce the mean arterial pressure by 10% during the first hour and an additional 15% within the next 2 to 3 hours JNC VII  Reduce mean arterial BP by no more than 25 per-cent (within minutes to 1 hour),  then if stable, to 160/100–110 mmHg within the next 2–6 hours.  If tolerated further gradual reductions toward a normal BP can be implemented in the next 24–48 hours More rapid reduction in blood pressure may result in cardiac or renal or cerebrovascular hypo- perfusion.  altered autoregulation curve  Pressure natriuresis may cause volume depletion in patients with hypertensive emergency, and administering vasodilator medications to these patients can lead to precipitous drops in blood pressure. Patients with volume depletion should receive intravenous (IV) saline to restore intravascular volume and shut off the renin-angiotensin-aldosterone system. Elliot WJ. Clinical features and management of selected hypertensive emergencies. J Clin Hypertens (Greenwich) 2004;6:587–92
    20. 20. Exceptions to treatment ofEmergency Aortic dissection Pulmonary edema Stroke Patient requiring thrombolysis
    21. 21.  Hypertension in the setting of an intracerebral bleed  Treat only when blood pressure is more than 180/ 105 mm Hg.(or 200/110)  MBP should be maintained <130 mm Hg Ischemic stroke,  Observe first 1 to 2 hours to determine if it spontaneously decrease s  Only a persistently MAP>130 mm Hg or a SBP> 220 mm Hg or DBP >120, should be carefully treated.  Mean arterial pressure should be lowered by 15% to 20% (10- 15% JNC VII) over 24 hrs  Bring BP <185/110 for thrombolysis. Maintain at <180/105  Labetelol,Sodium Nitroprusside , nicardipine, enalipritat used American Heart association recommendation Adams HP Jr, Adams RJ, Brott T, et al. Guidelines for the early management of patients with ischemic stroke: a scien-tific statement from the Stroke Council of the American Stroke Association. Stroke 2003; 34:1056 –1083 The European Stroke Initiative Executive Committee andthe EUSI Writing Committee. European Stroke Initiativerecommendations for stroke management: update 2003.Cerebrovasc Dis 2003; 16:311–337
    22. 22.  Acute aortic dissection,  IV β-blocker (eg, labetalol or esmolol) followed by a vasodilating agent, classically IV nitroprusside.  lower the SBP to a goal of < 120 mm Hg within 20 minutes (MAP <80).
    23. 23.  Acute stroke with accelerated htn well within accepted range but with concomitant noncerebral acute organ damage . What next? Blood pressure should be reduced carefully beyound the accepted values using emergency guidelines, with careful monitoring of neurological status
    24. 24. Acute Postoperative Hypertension early onset, (within 2 h after surgery) Typically of short duration, (treatment for ≤ 6 hrs) Complications of APH may include hemorrhagic stroke, cerebral ischemia,encephalopathy, myocardial ischemia, myocardial infarction, cardiac arrhythmia, CCF with pulmonary edema, failure of vascular anastomoses, and bleeding at the surgical site Most commonly associated with cardiothoracic, vascular, head and neck, and neurosurgical procedures. Activation of the sympathetic nervous system, increase in afterload, increase in SBP and DBP with or without tachycardia
    25. 25.  Post cardiac surgery, treatment is recommended for a BP > 140/90 or a MAP of > 105 mm Hg. Other conditions the goal may vary Rule out Pain,anxiety, hypothermia with shivering, hypoxemia, hypercarbia, and bladder distension Labetalol, esmolol, nicardipine, and clevidipine have proven effective
    26. 26. Emergencies and urgencies. TheCleveland Clinic diseasemanagement project. 12 Jan2006.
    27. 27. The Seventh Report of the Joint National Committeeon Prevention,Detection,Evaluation, and Treatmentof High Blood Pressure
    28. 28. The current AHA guidelines recommend the use of Labetalol or nicardipine if the SBP is >220 mm Hg or the DBP is from 121 to 140 mm Hg, and nitroprusside for a DBP > 140 mm HgThe diagnosis and management of hypertensive crises.Chest 2000
    29. 29. Take Home Message
    30. 30. 5 patients arrive with identical vital signs: heart rate of 100 beats/min, blood pressure(BP) of 209/105 mm Hg, respiration rate of 20 breaths/min, and temperature of 36.9oC Patient A is a 65-year-old man with nausea,  Intravenous labetalol, bolus or infusion.Target: vomiting, and confusion and papilledema Reduce MAP by 20% to 25% over 2 to 8 hours  Nitroglycerin infusion; intravenous Patient B is a 73-year-old woman with sudden enalaprilat or sublingual captopril. shortness of breath, pink sputum, and heavy Furosemide will work only after adequate chest pain and LVH decrease in preload and afterload  Urgent imaging with simultaneous decrease in Patient C is a 56-year-old man with sharp, BP. Nitroprusside and esmolol infusion; tearing chest and back pain and diastolic labetalol boluses or infusion.Target: Rapidly murmer reduce systolic BP to 110 mm Hg if there is no evidence of hypoperfusion  No treatment.Reduce BP only if it is greater Patient D is a 64-year-old woman with a 6- than 220/120 mm Hg (embolic) or greater hour history of right-sided weakness. NCCT than 180/105 mm Hg (hemorrhagic) no hemorrage. Thrombolysis not contemplated  Restart the medications she was on (Diuretic Patient E is a 51-year-old woman with a mild headache, concerned about her history of and ARB). Ask her to follow up in OPD hypertension.Poorly compliant. LVH +
    31. 31. Thank You