Hypertensive Crises.pptx

Harrison 20 edition based hypertension crisis with latest guidelines

1. Hypertensive Crises Presenter: Awatif Bashir MD (PGY1 , IM) Moderator: Semir Abdi MD (Internist )

2. Outline of Presentation Introduction Epidemiology Etiology Classification Clinical Picture Diagnosis Management

3. Hypertensive Crises Definition: These are acute, severe elevations in blood pressure that may or may not be associated with end organ damage or dysfunction. BP Values : SBP: >180 mmHg DBP: >120 mmHg These can be one of two subsets: Hypertensive Urgency Hypertensive Emergency

4. Hypertensive Crises Hypertensive Urgency: Severe elevations in Blood pressure without any evidence of end-organ damage Hypertensive Urgency: Severe elevations in Blood pressure with any evidence of end-organ damage

5. epidemiology Approximately 1% of hypertensive patients may develop a HTN crises in their lifetime. Annual Incidence : 1-2\100,000 patients Incidence is higher in African Americans , low SES and in developing countries . Twice as common in men .

6. Risk factors There is no single predisposing factor identified to be associated with these conditions. The most common ones are: Poorly controlled HTN Reno-vascular disease Cerebro -Vascular Disease Low Socioeconomic status Substance or alcohol abuse Cigarette smoking Oral Contraceptive Use

7. pathophysiology The underlying mechanism is still not fully understood. The 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. These may include: C essation of hypertensive medications with potential rebound effects consumption of illicit drugs severe pain several clinical syndromes

8. pathophysiology In most hypertensive crises, the initial rise in blood pressure is secondary to increased systemic vascular resistance. The 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

9. pathophysiology It is also linked to 4 distinct mechanisms: Vascular damage: Due to mechanical stress and vascular damage. RAAS Activation: Causing vasoconstriction and Expression of inflammatory cytokines Oxidative stress: Due to increase in production of reactive oxygen species Endothelial Dysfunction: Due to excessive vasoconstriction and coagulation cascade activation

10. Hypertensive emergencies Hypertensive Encephalopathy Acute Pulmonary Edema Acute Myocardial Infraction\ Angina Acute Renal Failure Post-Operative HTN Acute Aortic Dissection Eclampsia Malignant Hypertension

11. Clinical Presentation Hypertensive Urgency: Mostly Completely Asymptomatic Can Present with: Headaches Nausea Epistaxis Severe Anxiety Signs Elevated BP

12. Clinical Presentation Hypertensive Emergency: Depends on the End-Organ Affected: Chest Pain Acute Myocardial Infraction Myocardial Ischemia\Angina Back Pain Thoracic Aortic Dissection Dyspnea Acute Pulmonary Edema Altered Mentation of FND Hypertensive Encephalopathy Cerebrovascular Event

13. Clinical Approach Complete History Taking Physical Examination Investigate for Underlying Organ Damage Management

14. 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

15. 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

16. 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

17. Management 1 st ask yourself these 3 question: is there any end organ damage? Yes: Manage HTN Emergency No: Manage HTN Urgency How Quickly should BP be reduced? What is th e BP Target during that time period? How should that Goal be Achieved?

18. No End Organ Damage - Urgency How Quickly Should BP be Reduced? The cut-off of lowering BP time is controversial and decision should be taken considering individual risk factors for patients. However, 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? Short-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

19. No End Organ Damage - Urgency How should that goal be achieved? Previously the preferred agent was Sublingual or Oral Nefidipine That is no longer recommended due to propensity to cause S evere R ebound Hypotension and Organ Ischemia. Current preferred agents Include : Captopril Clonidine Labetalol

20. 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

21. End organ damage - emergency Overall Approach: choice of drug, BP goal, and outcome varies based on specific emergency faced Generally: MAP should be lowered 10-20% in the first hour and subsequent 5-15% over next 23 hours. Time Frame: <180\120mmHg over first hour <160\110mmHg over next 23 hours

22. End organ damage - emergency Exceptions to that rule are certain conditions: Acute Ischemic Stroke : BP isn’t lowered unless >185\110mmHg if ptn is candidate for reperfusion and >220\120mmHg if ptn are not candidates for reperfusion Acute Aortic Dissection : SBP should be rapidly lowered to target of 100-120mmHg within 20 minutes to reduce the shearing force of the aorta Intracerebral Hemorrhage: goal of HTN management in these patient’s is variable and individualized case dependant

23. End organ damage - emergency Choice of medication is dependent on the type of emergency encountered. During the first 8-24 hours , BP control should be obtained via Parenteral Drugs . After that period patients should be switched to oral agents with tapering of parenteral agents

24. End organ damage - emergency Management Specifi c Emergencies should be undertaken as well as BP Control Ex: tPa for Ischemic Stroke Patients Revascularization for Acute MI patients Dialysis for ESRD patients Management Protocol for Acute Heart Failure Surgery for Acute Aortic Dissection

25. Hypertensive emergencies Neurologic Emergencies Ischemic or Hemorrhagic Stroke Head Injury Hypertensive Encephalopathy Cardiac Emergencies Acute Heart Failure Acute Coronary Syndrome Vascular Emergencies Acute Aortic Dissection Post Op Hypertension

26. Hypertensive emergencies Renal Emergencies Acute Hypertensive Nephroscelerosis Sympathetic Over activity Antihypertensive Withdrawal Serotonin Syndrome Malignant Hypertension Pheochromocytoma Severe Autonomic Dysfunction Ex. Guillian Barre Syndrome Pregnancy Emergencies Eclampsia

27. Follow up - urgency Observe patient for few hours at hospital to make Ascertain BP Stably improving and that patients remains Asymptomatic Send Home with close monitoring for one week explaining signs of end organ damage Over next weeks to months frequent follow up with dose adjustment of antihypertensive d rugs should be commenced to achieve desired pressure goals for individual patients

28. Follow up - emergency Since Secondary causes are more common in HTN emergencies, patients should be evaluated and treated for secondary causes if present Ensure high quality out-patient follow up and for presenting problems (ex. Dialysis for patients with ESRD) Recurrence and 2 nd admission rate is high due to inadequate follow up

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