Download Free Medical Hypertensive Emergencies PowerPoint Presentation

Hypertensive Emergencies PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Antihypertensive, which is titled "Hypertensive Emergencies", to know about the categories of hypertension, etiology/pathophysiology, workup, and treatment.

Tags : Antihypertensive, Hypertensive Emergencies, hypertension

Published on : May 25, 2021 | Views : 2435 | Downloads : 5

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

HYPERTENSIVE EMERGENCIES Lakshmi Beeravolu,MD
Slide 2-

Discussion Categories Etiology/pathophysiology History/Physical Workup Treatment
Slide 3-

Case Scenarios A 56 yo CM with no significant PMH presents to the ER with headache,found to have BP 210/110mmHg and papilledema. An 82 yo male with h/o HTN,chronic renal insufficiency presents for a routine physical,found to have BP of 230/130mmHg. A 76 yo female is brought to the ER by the family due to altered mental status.BP is 240/110 mmHg with no focal neuro findings.
Slide 4-

DEFINITIONS Systolic blood pressure >220 and diastolic >120mmHg. Patients with hypertension can be classified into 3 categories based upon their symptoms and the organ systems that are affected at the time of presentation: -HYPERTENSIVE EMERGENCY: also called hypertensive crisis, is severe hypertension with acute impairment of an organ system (e.g., central nervous system [CNS], cardiovascular, renal). In these conditions, the blood pressure (BP) should be lowered aggressively over minutes to hours.Presence of papilledema indicates MALIGNANT HYPERTENSION. -HYPERTENSIVE URGENCY: the BP is a potential risk but has not yet caused acute end-organ damage. These patients require BP control over several days to weeks. -ACCELERATED HYPERTENSION: recent significant increase over baseline blood pressure that is associated with target organ damage. This is usually vascular damage on fundoscopic examination, such as flame-shaped hemorrhages or soft exudates, but without papilledema.
Slide 5-

ETIOLOGY Essential hypertension : Inadequate blood pressure control and noncompliance are common precipitants Renovascular Eclampsia/pre-eclampsia Acute glomerulonephritis Pheochromocytoma Anti-hypertensive withdrawal syndromes Head injuries and CNS trauma Renin-secreting tumors Drug-induced hypertension Burns Vasculitis TTP Idiopathic hypertension Post-op hypertension Coarctation of aorta
Slide 6-

PATHOPHYSIOLOGY NORMAL AUTOREGULATION RISE IN BP ARTERIAL AND ARTERIOLAR CONSTRICTION Normal flow.(flow=P/r) RISE IN BP FAILURE OF VASOCONSTRICTION ENDOTHELIAL DAMAGE (due to shear stress on the wall) AUTOREGULATION FAILURE
Slide 7-

PATHOPHYSIOLOGY BP=PVR*CO(SV*HR) Rate at which MAP rises more important than absolute rise. Acute rise in BP Failure of vasoconstriction Endothelial by autoregulation damage FIBRINOID Activates coagn and Depsn. of proteins/ NECROSIS inflammation fibrinogen in vessel wall RAAS plays an important role in initiating and perpetuating BP rise by causing vasoconstriction and fluid retention.
Slide 8-

CENTRAL NERVOUS SYSTEM CENTRAL NERVOUS SYSTEM: The CNS is affected as the elevated BP overwhelms the normal cerebral autoregulation. Under normal circumstances, with an increase in BP, cerebral arterioles vasoconstrict and cerebral blood flow (CBF) remains constant. During a hypertensive emergency, the elevated BP overwhelms arteriolar control over vasoconstriction and autoregulation of CBF. This results in transudate leak across capillaries and continued arteriolar damage. Subsequent fibrinoid necrosis causes normal autoregulatory mechanisms to fail, leading to clinically apparent papilledema, the sine qua non of malignant hypertension. The end result of loss of autoregulation is hypertensive encephalopathy.
Slide 9-

CARDIOVASCULAR SYSTEM The cardiovascular system is affected as increased cardiac workload leads to cardiac failure; this is accompanied by pulmonary edema, myocardial ischemia, or myocardial infarction.
Slide 10-

RENAL SYSTEM The renal system is impaired when high BP leads to arteriosclerosis, fibrinoid necrosis, and an overall impairment of renal protective autoregulation mechanisms. This may manifest as worsening renal function, hematuria, red blood cell (RBC) cast formation, and/or proteinuria.
Slide 11-

EPIDEMIOLOGY In the US: More than 60 million Americans, about 25-30% of the population, have hypertension. Of these individuals, 70% have mild disease, 20% moderate, and 10% severe hypertension (diastolic BP [DBP] >110 mm Hg). Approximately 1-2% develop a hypertensive emergency with end-organ damage. Mortality/Morbidity: Morbidity and mortality depend on the extent of end-organ damage on presentation and the degree to which BP is controlled subsequently. BP control may prevent progression to end-organ impairment. I yr mortality in untreated pts. >90%.5 yr survival of all presentations is 74%. Race: African Americans have a higher incidence of hypertensive emergencies than Caucasians. Sex: Males are at greater risk of hypertensive emergencies than females. Age:Most commonly in middle-aged people.Peak age:40-50yrs.
Slide 12-

HISTORY Focus on circumstances surrounding hypertension & etiology : -Medications:esp. hypertensive drugs/their compliance,illicit drugs -Duration of hypertension -Duration of current symptoms -Date of LMP -Other medical problems:prior hypertension,thyrotoxicosis,Cushing’s,SLE,renal Focus on complications : -CNS:headaches,blurred vision,wt. loss,nausea,vomiting,weakness,fatigue, confusion and mental status changes. -CVS:symptoms of CHF,angina,dissection,SOB -Renal:hematuria,oliguria.
Slide 13-

PHYSICAL Use an approach based on organ systems to identify signs of end-organ damage -CNS: focal neuro deficits,seizures,stupor,coma, papilledema, hemorrhages, exudates, or evidence of closed-angle glaucoma -CVS:JVD,lung auscultaion for crackles,peripheral edema,extra heart sounds, equal and symmetric BP and pulses bilaterally. -Check for abdominal masses and bruits.
Slide 14-

DIFFERENTIALS Acute Coronary Syndrome Aortic dissection CHF,pulmonary edema Acute Coronary Syndrome Aneurysm, Abdominal Anxiety Congestive Heart Failure and Pulmonary Edema Cushing Syndrome Delirium Tremens Encephalitis Glomerulonephritis, Acute Headache, Cluster Headache, Migraine Headache, Tension Hyperthyroidism, Thyroid Storm, and Graves Disease Myocardial Infarction Pregnancy, Eclampsia Pregnancy, Preeclampsia Stroke, Hemorrhagic Stroke, Ischemic Subarachnoid Hemorrhage Systemic Lupus Erythematosus
Slide 15-

Differential(contd.) Others: -Steroid use -Use of over-the-counter or recreational sympathomimetic drugs -Pheochromocytoma -Acute vasculitis -Serotonin syndrome -Other CNS pathology -Coarctation of the aorta
Slide 16-

Work-up CBC,Chem 8 Urinanalysis:hematuria,proteinuria,RBCs,RBC casts. Toxicology,pregnancy,endocrine causes. Imaging:Chest X-ray,Head CT,Chest CT,aortic angiogram EKG,cardiac enzymes
Slide 17-

TREATMENT Weigh benefits of decreasing BP against risks of decreasing end-organ perfusion. Important steps include: -Appropriately evaluating patients with an elevated BP -Correctly classifying the hypertension -Determining aggressiveness of therapy An important point to remember in the management of the patient with any degree of BP elevation is to "treat the patient and not the number."
Slide 18-

Treatment Initial considerations: Place patient who is not in distress in a quiet room and reevaluate after an initial interview. In one study, 27% of patients with an initial DBP >130 mm Hg had their DBP fall below critical levels after relaxation without specific treatment. Consider the context of the elevated BP (eg, severe pain) Screen for end-organ damage- Patients with end-organ damage usually require admission and rapid lowering of BP using iv meds.Suggested meds depend on the end-organ system damaged. Patients without evidence of end-organ effects may be discharged with follow–up.It is a misconception that a patient should not be discharged from the ER with elevated BP.Giving oral meds such as nifedipine to rapidly lower BP may be dangerous as the BP may have been elevated for sometime and there may be organ hypoperfusion.Acute control has not improved long term mortality and morbidity rates.
Slide 19-

INITIAL STEPS Initial considerations: Place patient who is not in distress in a quiet room and reevaluate after an initial interview. In one study, 27% of patients with an initial DBP >130 mm Hg had their DBP fall below critical levels after relaxation without specific treatment. Consider the context of the elevated BP (eg, severe pain) Screen for end-organ damage- Patients with end-organ damage usually require admission and rapid lowering of BP using iv meds.Suggested meds depend on the end-organ system damaged. Patients without evidence of end-organ effects may be discharged with follow–up.It is a misconception that a patient should not be discharged from the ER with elevated BP. Giving oral meds such as nifedipine to rapidly lower BP may be dangerous as the BP may have been elevated for sometime and there may be organ hypoperfusion.Acute control has not improved long term mortality and morbidity rates.
Slide 20-

DRUGS Once the diagnosis of hypertension is made and end-organ damage confirmed,the BP should be lowered by about 25% of the mean arterial pressure. There are 2 main classes of drugs: -Vasodilators -Adrenergic inhibitors
Slide 21-

VASODILATORS
Slide 22-

ADRENERGIC INHIBITORS
Slide 23-

ORAL DRUGS
Slide 24-

RAPID BP REDUCTION Acute myocardial ischemia:IV NTG,b-blockers,ACE inhibitors. CHF with pulmonary edema:iv NTG,furosemide,morphine Acute aortic dissection:iv nitroprusside+b-blockers or iv trimethaphan+b-blockers. Hypertensive encephalopathy or sub-arachnoid hemorrhage:iv nitroprusside,labetalol or nimodipine. MAO-tyramine interactions with acute hypertension:iv phentolamine.
Slide 25-

SPECIFIC TREATMENT Hypertensive Encephalopathy: Goal is to reduce MAP by not>25% or DBP tp100mmHg in the first hour.Nitroprussi(widely used in past)is a powerful arteriloar dilator,so a rise in ICP may occur.Labetalol,fenoldopam used more now. Intracerebral Hemorrhage: CPP=MAP-ICP.As ICP rises,MAP must rise for perfusion but this raises risk of bleeding from small arteries and arterioles.A prosp. Obs. study in 1997 did not confirm these concerns but it was obscured by early use of anti-hypertensives.Cerebral autoregulation curve in chronic hypertensives may be altered,making them less likely to tolerate aggressive lowering of BP.MAP guidelines:decrease when MAP>130 or SBP>220.Labetalol,esmolol agents of choice. SAH: Nimodipine decreases vasospasm that occurs due to chemical irritation of arteries by blood.Not recommended routinely due to high incidence of hypotension.Cognitive status is a guide.Labetalol,esmolol agents of choice. Acute Ischemic Stroke: High BP can cause hemorrhagic transformation of infarct ,cerebral edema.But,if CPP is low,ischemic penumbra may occur.CPP beyond obstn is low.Distal vessels become dilated with ,loss of autoregulation.A decilne to pre-stroke values in 4 days has been documented often..A Cochrane review examining 65 RCTs with 11,500 pts. Concluded that insufficient data exists to evaluate BP lowering post-stroke.AHA guidelines:BP be reduced only if SBP>220 or DBP>120mmHg.(unless end-organ damage is due to BP).Labetalol,nitroprusside-agents of choice.For thrombolysis,BP<185/110.
Slide 26-

Specific Treatment Aortic dissection: Immediate redn. In BP and mainly,shear stress(change in BP with change in time) is essential to limit the extension of damage as surgery is being considered.Eliminate pain and reduce systolic BP to 100-120 or lowest level that permits perusion.BP redn should proceed with redn.in force of LV contraction. Labetalol or nitroprusside+b-blocker like propranolol agents of choice. MI: NTG,b-blockers,ACE inhibitors. Acute LVF: usually associated with pulm edema and diastolic/systolic dysfx. IV nitroprusside,NTG agents of choice.Titrate until BP controlled and signs of heart failure alleviated. Renal insufficiency: is a cause and effect of high BP.Goal is to prevent further renal damage by maintaining adequate blood flow.Nitroprusside effective.
Slide 27-

COMPLICATIONS CHF Myocardial infarction Renal failure Retinopathy CVA Abrupt lowering of the BP may result in inadequate cerebral or cardiac blood flow leading to stroke or myocardial infarction. PROGNOSIS:Median survival duration is 144 months for all patients presenting to ED with hypertensive emergency. -5 yr survival rate is 74%.
Slide 28-

FOLLOW-UP The Joint National Committee on High Blood Pressure has published a series of recommendations for appropriate follow-up, assuming no end-organ damage. -For a systolic BP 140-159 mm Hg/diastolic 90-99 mm Hg, confirm BP within 2 months. -For systolic BP 160-179 mm Hg/diastolic 100-109 mm Hg, evaluate within a month. - For systolic BP 180-209 mm Hg/diastolic 110-119 mm Hg, evaluate within a week. -For systolic BP greater than 210 mm Hg/diastolic greater than 120 mm Hg, evaluate immediately.
Slide 29-

ppt slide no 29 content not found
Slide 30-

HYPERTENSION(JNC-7class.)
Slide 31-

TRIALS HYPERTENSIVE EMERGENCY:1 RCT HYPERTENSIVE URGENCY:10 RCTS. CONCLUSIONS:-Evidence about effectiveness of antihypertensive agents in people with hypertensive emergencies or hypertensive urgencies is weak. Studies had small sample sizes and were heterogeneous in terms of patients, interventions and outcomes reported. Limited evidence suggests that urapidil is most effective in emergencies. In urgencies, nicardipine; nitroprusside or fenolodopam may be used, but not nifedipine.
Slide 32-

So,………. A 56 yo CM with no significant PMH presents to the ER with headache,found to have BP 210/110mmHg and papilledema. -MALIGNANT HYPERTENSION An 82 yo male with h/o HTN,chronic renal insufficiency presents for a routine physical,found to have BP of 230/130mmHg.-ACCELERATED HYPERTENSION A 76 yo female is brought to the ER by the family due to altered mental status.BP is 240/110 mmHg with no focal neuro findings. –HYPERTENSIVE EMERGENCY