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Hypertensive Crisis Halmat M. Jaafar (MSc. Clinical pharmacy)

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Presentation on theme: "Hypertensive Crisis Halmat M. Jaafar (MSc. Clinical pharmacy)"— Presentation transcript:

1 Hypertensive Crisis Halmat M. Jaafar (MSc. Clinical pharmacy)
Hawler Medical University/ College of Pharmacy Department of Pharmacology

2 Outline of this lecture:
What is Heart Hypertensive Crisis? Epidemiology. Classification of Hypertensive Crisis. Causes of Hypertensive Crisis Clinical presentation of Hypertensive Crisis Managment of Hypertensive Crisis

3 What is Hypertensive Crisis?
The term hypertensive crisis is defined as a severe elevation in blood pressure (BP), generally considered to be a diastolic blood pressure greater than 120 mm Hg

4 What is Hypertensive Crisis?
This disorder can be further classified as hypertensive urgency or hypertensive emergency when there is evidence of acutely progressive end-organ damage. If these disorders are not treated promptly, a high rate of morbidity and mortality will occur the 5-year mortality for patients with a history of hypertensive crisis is 26%

5 Epidemiology Epidemiology
Approximately 1% of hypertensive pts. may develop hypertensive crises during their lifetime. Annual incidence of hypertensive emergencies being 1-2 cases/1,00,000 pts. Higher rates have been reported in African Americans, low socioeconomic people, in developing countries. Incidence in men 2 times higher than in women

6 Classification of Hypertensive Crisis

7 Causes of hypertensive emergencies ?
Renovascular Disease Pheochromocytoma Non-adherence to anti-HTN medications (most common) Hyperaldosteronism Anti-hypertensive withdrawal syndromes Head injuries and CNS trauma Post-op hypertension Drug-induced hypertension

8 Causes of hypertensive Urgencies ?
As with hypertensive emergencies ,severe BP elevations may result from inadequate control or poor adherence to current antihypertensive drug regimens. Another cause for patients reaching hypertensive urgency is previous inaccurate BP measurements that underestimate or do not detect increased BP at all (e.g. poor patient technique for self‐monitoring).

9 Causes Hypertensive Urgencies
Causes of hypertensive Urgencies ? Drugs: Non-Narcotic Analgesics : - Non-steroidal anti-inflammatory agents including aspirin - Selective COX-2 inhibitors Sympathomimetic agents: - Decongestants - Diet pills - Cocaine Stimulants: -Methylphenidate, amphetamine.

10 Causes Hypertensive Urgencies
Causes of hypertensive Urgencies ? Lifestyle: - High salt diet, excessive alcohol use. Comorbid Conditions: - Thyroid storm, trauma, renovascular disease, acute ischemic stroke or adrenal dysfunction

11 Clinical Presentation of HC
Emergency Urgency Characterized by severe increase in systolic and/or diastolic blood pressure associated with signs or symptoms of acute end-organ damage. Usually, SBP > 180 mm Hg - DBP > 120 mm Hg Requires an immediate BP reduction in few minutes - hours. Requires an ICU care & IV drugs Elevated BP ( usually systolic > 180 mmHg &/or diastolic > 120 mmHg ) but without evidence of end-organ damage. Usually asymptomatic; severe headache, shortness of breath, epistaxis, severe anxiety. Adequate treatment of these conditions, a BP lowering within 24 hrs by administration of oral drugs. ICU admission is usually not required

12 Clinical Presentation of HC
Emergency Urgency rarely develop in patients without a previous history of hypertension occur in patients with pheochromocytoma or renal vascular disease Cerebral infarctions, encephalopathy and intracranial or subarachnoid hemorrhage. acute heart failure (HF) and pulmonary edema and acute myocardial infarction, unstable angina. Acute dissection, eclampsia. headache (42%) and dizziness (30%). Other symptoms include visual changes, chest discomfort, nausea, epistaxis, fatigue, and psychomotor agitation. Not all patient present with same symptoms 90% of patients had a history of hypertension

13 Acute End-organ Damage
(Complication of HC). Single organ damage in approximately 83%. Two organ damage found in 14%,multiorgan damage in 3 % pts. Most common clinical presentations : - cerebral infarction (24%) - pulmonary oedema (22%) - HTN encephalopathy (16%) - Cong. HF (12%) Less common presentations – IC hemorrhage, Aortic dissection and Eclampsia

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15 MANAGEMENT OF HF

16 MANAGEMENT History Examination Assessment Treatment
The treatment of hypertensive crises must balance preventing further end-organ damage while maintaining tissue perfusion. The initial goal for blood pressure reduction is not to obtain a normal blood pressure. Rapid and aggressive reductions in blood pressure can actually induce cerebral, myocardial, or renal ischemia or infarction if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation. History Examination Assessment Treatment

17 MANAGEMENT HISTORY Duration and degree of pre existing hypertension
Details of antihypertensive therapy Compliance with medications Use of the over counter drugs History of recent operations. History Examination Assessment Treatment

18 MANAGEMENT EXAMINATION

19 ASSESMEN with INVESTIGATION
MANAGEMENT ASSESMEN with INVESTIGATION Lab tests & investigations may be required (e.g. CBC, ECG, urinalysis, renal function; Echo. , consider head imaging if neurological symptoms are present ).

20 Clinical Presentation of HC
Emergency Urgency rarely develop in patients without a previous history of hypertension occur in patients with pheochromocytoma or renal vascular disease Cerebral infarctions, encephalopathy and intracranial or subarachnoid hemorrhage. acute heart failure (HF) and pulmonary edema and acute myocardial infarction, unstable angina. Acute dissection, eclampsia. headache (42%) and dizziness (30%). Other symptoms include visual changes, chest discomfort, nausea, epistaxis, fatigue, and psychomotor agitation. Not all patient present with same symptoms 90% of patients had a history of hypertension

21 MANAGEMENT TREATMENT OF HYPERTENSIVE EMERGENCY GOAL
reduce MAP by no more than 20-25%, DBP to mm Hg within few minutes to 2 hours. More aggressive and rapid BP reduction (Acute Pulmonary edema ,Aortic dissection) More slowly for acute cerebrovascular damages with monitoring of neurological status. Constant infusion of intravenous agents required

22 TREATMENT OF HYPERTENSIVE EMERGENCY
GOAL reduce MAP by no more than 20-25%, DBP to mm Hg within few minutes to 2 hours. More aggressive and rapid BP reduction (Acute Pulmonary edema ,Aortic dissection) More slowly for acute cerebrovascular damages with monitoring of neurological status. Constant infusion of intravenous agents required

23 TREATMENT OF HYPERTENSIVE EMERGENCY
GOAL reduce MAP by no more than 20-25%, DBP to mm Hg within few minutes to 2 hours. More aggressive and rapid BP reduction (Acute Pulmonary edema ,Aortic dissection) More slowly for acute cerebrovascular damages with monitoring of neurological status. Constant infusion of intravenous agents required

24 MANAGEMENT TREATMENT OF HYPERTENSIVE URGENCY GOAL
Overall Goal of Management: reduce SBP by ~ 25% over 24‐48 hours. More conservative BP lowering reduces the risk of potential adverse effects (i.e. perfusion complications worsening incidence of MI, stroke, and death) associated with more aggressive BP lowering if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation . All treatment strategies should consider the patient’s comorbidities and risk of adverse events.

25 MANAGEMENT TREATMENT OF HYPERTENSIVE URGENCY GOAL
Overall Goal of Management: reduce SBP by ~ 25% over 24‐48 hours. More conservative BP lowering reduces the risk of potential adverse effects (i.e. perfusion complications worsening incidence of MI, stroke, and death) associated with more aggressive BP lowering if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation . All treatment strategies should consider the patient’s comorbidities and risk of adverse events.

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