HTN CRISIS SEMINER.pptx
- 1. Hypertensive Crisis Moderator: Dr. Teshome (MD, Assistant Professor of Internal medicine) Presenter: Dr. Hussen (R1) May, 2023 Haramaya University Department of Medicine
- 2. Outlines Introduction Etiology Pathophysiology Clinical Evaluation Management Summery
- 3. Introduction • Hypertension is one of the leading causes of the global burden of disease. • Hypertension doubles the risk of cardiovascular diseases, including coronary heart disease (CHD), congestive heart failure (CHF), ischemic and hemorrhagic stroke, renal failure, and peripheral arterial disease • Overall, approximately 22% of the world's adults are estimated to have hypertension • Sub Saharan Africa has the highest prevalence(40%). • It accounts for loss of 57 million disability adjusted life years (DALYS).
- 4. Intro… oThe likelihood of hypertension increases with age, and among individuals aged ≥60 years, the prevalence is 65.4% o Probably due to the widespread availability of antihypertensive therapy, in the United States, there has been a decline in the numbers of patients presenting with hypertensive crisis. oApproximately 1% of American hypertensive pts may develop hypertensive crisis during their lifetime. oAny primary or secondary hypertension can give rise to a hypertensive crisis, but the most common cause uncontrolled primary hypertension
- 5. Intro… o Epidemiological associations between BP and CV risk are directly related to the height of the blood pressure, beginning at 115/75 mmHg, without evidence of a threshold o Clinically, hypertension may be defined as that level of blood pressure at which the institution of therapy reduces blood pressure–related morbidity and mortality o Hypertension is diagnosed based on the average of two or more seated blood pressure reading Systolic BP > or = 140 mm Hg and Diastolic BP > or = 90 mm Hg at least 6 hours apart.
- 7. Mechanism of hypertension Cardiac output and peripheral resistance are the two determinants of arterial pressure Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment. Peripheral resistance is determined by functional and anatomic changes in small arteries and arterioles
- 8. Blood Pressure Regulation • Many neurohormonal, renal, and vascular mechanisms interact to varying degrees to the mechanism, pathogenesis and progression of the different hemodynamic forms of hypertension • 1. Autonomic Nervous system • With drop in blood pressure sympathetic outflow will increase with the final effect of raising blood pressure by increasing heart rate, myocardial contractility and increasing peripheral vasoconstriction • Change in blood pressure is sensed by baroreceptors in carotid sinus, aortic sinus and heart muscles • In the kidney, activation of α1-adrenergic receptors by norepinephrine increases renal tubular reabsorption of sodium
- 10. 2. Renin-Angiotensin-Aldosterone system: • The renin-angiotensin-aldosterone system contributes to the regulation of arterial pressure primarily via the vasoconstrictor properties of angiotensin II and the sodium-retaining properties of aldosterone. • There are three primary stimuli for renin secretion: • (1) decreased NaCl transport in the distal portion of the thick ascending limb of the loop of Henle that abuts the corresponding afferent arteriole (macula densa), • (2) decreased pressure or stretch within the renal afferent arteriole (baroreceptor mechanism), • (3) sympathetic nervous system stimulation of renin-secreting cells via β1 adrenoreceptors
- 11. RAAS system … • Aldosterone is a potent mineralocorticoid that increases sodium reabsorption by amiloride-sensitive epithelial sodium channels (ENaC) on the apical surface of the principal cells of the renal cortical collecting duct • Electric neutrality is maintained by exchanging sodium for potassium and hydrogen ions • Consequently, increased aldosterone secretion may result in hypokalemia and alkalosis
- 13. 3 .VASCULAR MECHANISMS • In hypertensive patients, decreased vascular compliance and lumen size result from vascular fibrosis lead to increased peripheral resistance • The vascular endothelium synthesizes and releases several vasoactive substances, including nitric oxide, a potent vasodilator. • Endothelium-dependent vasodilation is impaired in hypertensive patients 4 .INTRAVASCULAR VOLUME When NaCl intake exceeds the capacity of the kidney to excrete sodium, vascular volume may initially expand and cardiac output may increase • As arterial pressure increases in response to a high NaCl intake, urinary sodium excretion increases and sodium balance is maintained at the expense of an increase in arterial pressure
- 15. Hypertensive Crises Hypertensive crises are acute severe elevation in blood pressure ( usually > 180/120 mmHg ) that may or may not be associated with end organ dysfunction Based on the degree of end organ damage rather than level of blood pressure alone it has two categories Two subsets Hypertensive Urgency Hypertensive Emergency
- 16. Hypertensive Urgency Hypertensive urgency is suddenly elevated in blood pressure greater than 180/120 with out end organ dysfunction. Usually due to under controlled hypertension. No specific symptoms Need to be reduced over hours to days not over minutes No laboratory evidence of new or worsening target organ damage
- 17. Hypertensive Emergency It is acute severe elevation in blood pressure ( usually > 180/120 mmHg ) associated with impending or progressive organ dysfunction involving neurological, cardiac or renal systems. Require lowering of blood pressure within minutes to hour to prevent morbidity ( not necessarily to normal range ). The clinical presentation and rapidity of BP rises more relevant than the actual level of BP.
- 18. Hypertensive Emergency ... ICU admission usually required Examples of target organ damage associated hypertensive emergency include; Hypertensive encephalopathy Cerebral infarction ( ischemic stroke) Cerebral hemorrhage ( SAH and ICH ) Pulmonary edema Acute congestive heart failure Acute kidney injury Aortic dissection Malignant hypertension: Clinical Syndrome associated with severe abrupt rise in BP (commonly >200/120 mm Hg) , retinopathy ,deteriorating RF with PU, microangiopathic hemolytic anemia and encephalopathy.
- 19. Etiology • Essential hypertension : Inadequate blood pressure control and noncompliance are common precipitants • Renal parenchymal disease • Eclampsia/pre-eclampsia • Pheochromocytoma • Anti-hypertensive withdrawal syndromes • CNS. Guillain Barre Syndrome • Drug-induced hypertension ( cocaine /amphetam/clonidine withdrawal ) • Idiopathic hypertension rapid unexplained rise in BP • Post-op hypertension • Coarctation of aorta
- 20. Pathophysiology • The pathophysiology of hypertensive crises is not completely understood. • With mild-to-moderate elevations in blood pressure, arterial and arteriolar vasoconstriction initially maintains tissue perfusion while preventing increased pressure from being transmitted to more distal vessels. • With severe elevations in blood pressure (i.e., >180/110 mm Hg), this autoregulation fails, and increased pressure in capillaries leads to endothelial damage of the vascular wall, causing fibrinoid necrosis and perivascular edema. Fibrinoid necrosis obliterates the vascular lumen, resulting in organ damage.
- 21. Pathophysiology
- 22. Clinical Assessment Although we consider hypertensive crisis in all patients who present with severely elevated blood pressure ( > 180/120 ) ,regardless of symptoms, quick and focused evaluation is critical in establishing a diagnosis and initial therapy. This include by History Physical examination lab test Imaging
- 23. History A brief and focused history should address the presence of end organ damage, the circumstances surrounding the hypertension, and any identifiable etiology Medical Hx previous diagnosis and treatment chronic illness ( CKD ) Personal Hx smoking alcohol drinking Family Hx DM, cardiac death Pregnancy last menstrual period preeclampsia
- 24. History . . . Specific Hx for end organ damage CVS ( MI ) ; chest pain ,SOB, cough CNS ( stroke ); change in mental status, severe headache, body weakness, blurring vision GUS ( AKI ) ; decreased in urine amount flank pain
- 25. Physical Examination The physical examination should focus on the presence of end organ damage and help with identifying secondary causes of hypertension Confirm elevated BP Proper position, appropriate cuff size Supine and standing and both arms Fundoscopy finding may suggest retinal exudates, hemorrhages, or papilledema which show hypertensive encephalopathy. It is helpful to use an organ system–based approach to identify signs of end- organ damage.
- 26. Focused Physical Examination CNS Focal neurologic finding Seizures Altered mental status Papilledema, hemorrhages, exudates Cardiovascular Evidence of congestive heart failure pulmonary edema Murmur Jugular venous distension Peripheral edema Equal and symmetric blood pressure
- 27. Investigation Lab studies: Electrolytes, urea, and creatinine RBS, CBC ,and urinalysis Imaging studies CXR (chest pain or SOB) Head CT/MRI (abn neurology) Chest CT/Aortic angio (Aortic dissection) 12-lead ECG Other Test Troponin, CK-MB Toxicology Urine HCG Echocardiography
- 28. Management • 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. • At what rate and to what extent should the blood pressure be lowered depend on types of hypertensive crisis and end organ damage
- 29. Management Hypertensive Urgency Gradual lowering of elevated BP with in 24 hours ( reduction of MAP by not more than 25% and DBP to 100 -110 mmHg ) to avoid sudden drop of BP and tissue hypo perfusion Drugs used in these case are Captopril 6.25mg po q6hrs and Clonidine 0.1-0.2mg hourly, up to max 0.8mg in 24 hrs
- 30. Management… Hypertensive emergency o It requires immediate lowering of BP ,admission and intravenous medication. o Initial treatment should reduce MAP by not more than 25 % while maintaining DBP to 100-110mmHg within first few minutes to two hours. oThere are exceptional to this rule : Aortic dissection Acute stroke Preeclampsia o More aggressive and rapid BP reduction (Acute Pulmonary edema ,Aortic dissection) o More slowly for acute cerebrovascular damages with monitoring of neurological status.
- 32. Preferred Parenteral Drugs for Selected Hypertensive Emergencies
- 33. Usual Intravenous Doses of Antihypertensive Agents Used in Hypertensive Emergencies
- 34. Specific Treatment • The specific management depend on the end organ systems that affected by the BP • Hypertensive encephalopathy; defined as acute neurologic syndrome in the setting of severe hypertension in absence of others cause • It is due to increased cerebral perfusion from loss of blood brain barrier integrity, which results in cerebral edema, vasospasm and microhemorrhage formation. • Symptoms include severe headache, nausea, vomiting, visual disturbance, confusion and abnormal body movement. • Signs include disorientation, lethargic, seizure, focal deficits, papilledema and retinopathy.
- 35. Hypertensive encephalopathy • The most common cause is abrupt BP elevation in a chronic hypertension. Other conditions that can predispose a patient to elevated BP and cause the same clinical situation include: AGN, withdrawal from hypertensive drugs, pheochromocytoma, preeclampsia and sympathomimetic agents ( cocaine and amphetamines). • Resolve with reduction in BP. MAP should be reduced by 20 % to DBP of 100 to 110mmHg with in first hour. Suitable drugs in management IV nitroprusside ( DOC ), labetalol, nicardipine and hydralazine.
- 36. Acute Aortic Dissection • Separation of the layers within the aortic wall. The blood driven by pulsatile pressure entering tear in the intima layer results in propagation of dissection . Clinically, patients complain of sudden onset retrosternal or interscapular chest pain that tearing or ripping type. Diagnosis involve clinical and imaging • Anatomic location classified as type A and type B • Type A- Ascending aorta with or without distal aorta involvement • Type B- Only the aortic arch or descending aorta • Type A and life threatening type B are surgical emergency in addition to BP control reduce shear force on damage aorta • Rapidly reduce SBP to 100 -120 mmHg or lowest level that is tolerated with in 5 – 10 munites after achieving HR lower than 60 bpm • Esmolol and nitroprusside are DOC
- 37. Myocardial ischemia/infarction • May be associated with HTN at presentation (usually in a previously HTN pt). • High BP exacerbated by pain and agitation. • IV Nitrates reducing systemic vascular resistance, LV preload, improves coronary perfusion • B blockers may contribute to a fall in BP (reduces myocardial O2 consumption) • BP control mandatory before thrombolysis (BP<180/100 mmHg).
- 38. Acute Pulmonary Edema/Left Ventricular Dysfunction Oxygen (face mask, INO2, intubation • Reduction of LV preload and afterload. • IV nitrate ( nitroglycerin ), loop diuretics. • Others – urapidil, nicardipine,sodium nitroprusside •Ischemic stroke BP elevations can occur in previously hypertensive and in normotensive pts. BP declines to pre stroke values within 3-4 days after an ischemic stroke. Hypertension often transient, physiologic response which resolves spontaneously
- 39. Ischemic stroke…. • Acute treatment of BP elevations is only indicated in limited circumstances • High BP can cause hemorrhagic transformation of infarct ,cerebral edema. But, if CPP is low, ischemic penumbra may occur • Indication for acute treatment include 1. Use of thrombolytic therapy : BP goal before initiating thrombolysis is less than 185/110 mm Hg 2. Other target-organ damage (e.g., aortic dissection, myocardial infarction) : The BP goal is reduction with cautious of 15% (10%– 20%) in the MAP over 24 hours 3. Severe” elevations in BP ( SBP > 220mmHg or DBP >120mmHg ) .
- 40. Acute Hemorrhagic stroke • To prevent rebleeding and reduce edema formation • Reduce SBP to < 180 mmHg over first 24 hrs , if SBP > 220 and Pt with elevated ICP • Reduce SBP to < 160 mmHg over the first few hrs, if the Pt is stable and SBP 150 -220 • Nimodipine, a dihydropyridine calcium blocker,is effective (antagonist effects on cerebrovasospasm). • Preeclampsia : leading cause of maternal and fetal mortality. It defined HTN ( SBP > 140 mmHg and DBP > 90 mmHg on at least two occasion in 4 hrs apart) and Proteinuria( 24 hours collection more than 300 mg ) or HTN and end organ dysfunction with or without proteinuria after 28 wks of gestation or postpartum in previously normotensive woman
- 41. Preeclampsia • Acute severe HTN ( SBP >160 mmHg or DBP >110 mmHg ) and signs/symptoms of end organ dysfunction show severity. • For severe acute HTN, MAP should be decreased by 20%–25% over the first few minutes to hours • Target goal BP is SBP :155-160 mmHg, DBP>105mm Hg.(initiation of Rx) • The target of < or =160/110 mm Hg over the subsequent hours • MgSo4 for seizure prophylaxis • For acute severe BP reduction, it is recommended to use intravenous labetolol or hydralazine, and for chronic severe HTN methyldopa is drug of choice. • Avoid sublingual or oral nifedipine. • Nitroprusside,ACEI – C/I
- 42. Summery
- 43. References • Harrison's principle of internal medicine - 21th Edition • Up to date • 2017 ACC/AHA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults • 2018 ESC/ESH Guidelines for the management of arterial hypertension • 2020 ISH Global Hypertension Practice Guidelines • National NCD guideline
Editor's Notes
- #6: Esc 2018 guideline However, ‘hypertension’ is defined as the level of BP at which the benefits of treatment (either with lifestyle interventions or drugs) unequivocally outweigh the risks of treatment, as documented by clinical trials. ISHH 2020 At each visit take 3 measurements with 1 min between them. Calculate the average of the last 2 measurements. If BP of first reading is <130/85 mm Hg no further measurement is required. Blood pressure of 2–3 office visits ≥140/90 mm Hg indicates hypertension.