Hypertensive Crises.pptx
- 1. HYPERTENSIVE CRISES Presenter: Awatif Bashir MD (PGY1, IM) Moderator: Semir Abdi MD (Internist)
- 2. OUTLINE OF PRESENTATION oIntroduction oEpidemiology oEtiology oClassification oClinical Picture oDiagnosis oManagement
- 3. HYPERTENSIVE CRISES oDefinition: These are acute, severe elevations in blood pressure that may or may not be associated with end organ damage or dysfunction. oBP Values: oSBP: >180 mmHg oDBP: >120 mmHg oThese can be one of two subsets: oHypertensive Urgency oHypertensive Emergency
- 4. HYPERTENSIVE CRISES oHypertensive Urgency: Severe elevations in Blood pressure without any evidence of end-organ damage oHypertensive Urgency: Severe elevations in Blood pressure with any evidence of end-organ damage
- 5. EPIDEMIOLOGY oApproximately 1% of hypertensive patients may develop a HTN crises in their lifetime. oAnnual Incidence: 1-2100,000 patients oIncidence is higher in African Americans, low SES and in developing countries. oTwice as common in men.
- 7. RISK FACTORS oThere is no single predisposing factor identified to be associated with these conditions. oThe most common ones are: oPoorly controlled HTN oReno-vascular disease oCerebro-Vascular Disease oLow Socioeconomic status oSubstance or alcohol abuse oCigarette smoking oOral Contraceptive Use
- 9. PATHOPHYSIOLOGY oThe underlying mechanism is still not fully understood. oThe transition from mild hypertension or normo-tension to a hypertensive crisis usually is precipitated by an event that leads to an abrupt increase in blood pressure. oThese may include: oCessation of hypertensive medications with potential rebound effects oconsumption of illicit drugs osevere pain oseveral clinical syndromes
- 10. PATHOPHYSIOLOGY oIn most hypertensive crises, the initial rise in blood pressure is secondary to increased systemic vascular resistance. oThe rise in systemic vascular resistance is believed to be caused by humoral vasoconstrictors With the increase in blood pressure, mechanical stress on the arteriolar wall leads to endothelial damage and fibrinous necrosis of the arterioles, this in turn leads to loss of auto-regulatory mechanisms, ischemia, and acute end-organ damage, which prompts further release of vasoconstrictors, thereby initiating a vicious circle
- 11. PATHOPHYSIOLOGY oIt is also linked to 4 distinct mechanisms: oVascular damage: oDue to mechanical stress and vascular damage. oRAAS Activation: oCausing vasoconstriction and Expression of inflammatory cytokines oOxidative stress: oDue to increase in production of reactive oxygen species oEndothelial Dysfunction: oDue to excessive vasoconstriction and coagulation cascade activation
- 12. HYPERTENSIVE EMERGENCIES oHypertensive Encephalopathy oAcute Pulmonary Edema oAcute Myocardial Infraction Angina oAcute Renal Failure oPost-Operative HTN oAcute Aortic Dissection oEclampsia oMalignant Hypertension
- 13. CLINICAL PRESENTATION Hypertensive Urgency: oMostly Completely Asymptomatic oCan Present with: • Headaches • Nausea • Epistaxis • Severe Anxiety oSigns • Elevated BP
- 14. CLINICAL PRESENTATION Hypertensive Emergency: oDepends on the End-Organ Affected: • Chest Pain • Acute Myocardial Infraction • Myocardial IschemiaAngina • Back Pain • Thoracic Aortic Dissection • Dyspnea • Acute Pulmonary Edema • Altered Mentation of FND • Hypertensive Encephalopathy • Cerebrovascular Event
- 16. CLINICAL APPROACH 1. Complete History Taking 2. Physical Examination 3. Investigate for Underlying Organ Damage 4. Management
- 17. HISTORY TAKING • Current Sx like headache, blurred vision, chest pain, back pain, dyspnea, etc. • Any associated symptom • Co-morbid conditions • Duration of HTN and Medication Control, Compliance, Abrupt cessation • Any Illicit Drug use, Smoking, or Alcohol consumption • Any Other medication ex. MOA, SSRI • Any recent head trauma
- 18. PHYSICAL EXAM • Full and Thorough examination is needed • Vital Signs Specially BP (both setting and standing), if peripheral pulses are reduced take lower limb BP as well • General: signs of dehydration (natriuresis occurs in response to rapid BP rise) • CVS: murmurs (aortic insufficiency or ischemic MR). S3 gallop, peripheral edema, raised JVP • Respiratory: Basal Crackles, Tachypnea • Neuro: Altered mental status, FND • Funduscopic: Cotton wool exudates, Hemorrhage, Papilledema
- 19. WORKUP OF PATIENTS Work-up should be done to check for damaged organs and includes: • Complete blood count • Urinalysis (Proteinuria and Hematuria) • Creatinine and BUN • Cardiac Bio-markers • Urine Toxicology • RBS • Liver Function Test • Serum Electrolytes • ECG • Echocardiogram • Chest Radiography • Non-Contrast Head CT • Contrast Induced Chest CT or Transesophageal Echo
- 20. MANAGEMENT o1st ask yourself these 3 question: ois there any end organ damage? oYes: Manage HTN Emergency oNo: Manage HTN Urgency oHow Quickly should BP be reduced? oWhat is the BP Target during that time period? oHow should that Goal be Achieved?
- 21. NO END ORGAN DAMAGE - URGENCY How Quickly Should BP be Reduced? oThe cut-off of lowering BP time is controversial and decision should be taken considering individual risk factors for patients. oHowever, Generally: BP should be reduced gradually over the period of hours to days, to avoid causing ischemic injury and tissue hypo-perfusion to vital organs. What is the Target BP in that Period? oShort-Term Goal: lower BP to <160<100mmHg in first few hours provided that MAP shouldn’t be lowered more then 25% over first 24 hours
- 22. NO END ORGAN DAMAGE - URGENCY How should that goal be achieved? oPreviously the preferred agent was Sublingual or Oral Nefidipine oThat is no longer recommended due to propensity to cause Severe Rebound Hypotension and Organ Ischemia. oCurrent preferred agents Include: oCaptopril oClonidine oLabetalol
- 24. NO END ORGAN DAMAGE - URGENCY In the case of not requiring rapid BP reduction, BP should be reduced over the period of days with specific considerations Pre-Exisitng Hypertension (Options are:) Re-administer previous medication Increase the dose of previous medication or add another agent Add diuretic and adjust sodium intake for patient Un-Treated Hypertension: Gradually reduce BP using one of previously mentioned agents. Evaluate patient's HTN and start new individualized Anti-HTN treatment regimen, considering risk factors, duration of treatment and adverse effects
- 25. END ORGAN DAMAGE - EMERGENCY oOverall Approach: choice of drug, BP goal, and outcome varies based on specific emergency faced oGenerally: MAP should be lowered 10-20% in the first hour and subsequent 5-15% over next 23 hours. oTime Frame: <180120mmHg over first hour o <160110mmHg over next 23 hours
- 26. END ORGAN DAMAGE - EMERGENCY oExceptions to that rule are certain conditions: 1. Acute Ischemic Stroke: BP isn’t lowered unless >185110mmHg if ptn is candidate for reperfusion and >220120mmHg if ptn are not candidates for reperfusion 2. Acute Aortic Dissection: SBP should be rapidly lowered to target of 100-120mmHg within 20 minutes to reduce the shearing force of the aorta 3. Intracerebral Hemorrhage: goal of HTN management in these patient’s is variable and individualized case dependant
- 27. END ORGAN DAMAGE - EMERGENCY oChoice of medication is dependent on the type of emergency encountered. oDuring the first 8-24 hours, BP control should be obtained via Parenteral Drugs. oAfter that period patients should be switched to oral agents with tapering of parenteral agents
- 28. END ORGAN DAMAGE - EMERGENCY oManagement Specific Emergencies should be undertaken as well as BP Control oEx: otPa for Ischemic Stroke Patients oRevascularization for Acute MI patients oDialysis for ESRD patients oManagement Protocol for Acute Heart Failure oSurgery for Acute Aortic Dissection
- 29. HYPERTENSIVE EMERGENCIES oNeurologic Emergencies oIschemic or Hemorrhagic Stroke oHead Injury oHypertensive Encephalopathy oCardiac Emergencies oAcute Heart Failure oAcute Coronary Syndrome oVascular Emergencies oAcute Aortic Dissection oPost Op Hypertension
- 30. HYPERTENSIVE EMERGENCIES oRenal Emergencies oAcute Hypertensive Nephroscelerosis oSympathetic Over activity oAntihypertensive Withdrawal oSerotonin Syndrome oMalignant Hypertension oPheochromocytoma oSevere Autonomic Dysfunction Ex. Guillian Barre Syndrome oPregnancy Emergencies oEclampsia
- 33. FOLLOW UP - URGENCY 1. Observe patient for few hours at hospital to make Ascertain BP Stably improving and that patients remains Asymptomatic 2. Send Home with close monitoring for one week explaining signs of end organ damage 3. Over next weeks to months frequent follow up with dose adjustment of antihypertensive drugs should be commenced to achieve desired pressure goals for individual patients
- 34. FOLLOW UP - EMERGENCY 1. Since Secondary causes are more common in HTN emergencies, patients should be evaluated and treated for secondary causes if present 2. Ensure high quality out-patient follow up and for presenting problems (ex. Dialysis for patients with ESRD) 3. Recurrence and 2nd admission rate is high due to inadequate follow up
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