Management of hypertension and hypertensive emergencies.pptx

MANAGEMENT OF HYPERTENSION AND

HYPERTENSIVE EMERGENCIESPRESENTERS : Luyimbazi Ivan Omaido Blair AndrewTutor: Dr. Nabunnya Y.

Saturday, April 15, 2023 1

Definition

• Uncontrolled HTN is defined as systolic blood pressure (SBP) ≥140 mm Hg and/or diastolic blood pressure (DBP) ≥90 mm Hg.

• Isolated systolic HTN (ISH) is defined as SBP ≥140 mm Hg and DBP <90 mm Hg, isolated diastolic HTN (IDH) is defined as SBP <140 mm Hg and DBP ≥90 mm Hg, and systolic-diastolic HTN (SDH) is defined as SBP ≥140 mm Hg and DBP ≥90 mm Hg


Epidemiology

• Uncontrolled Hypertension in Uganda: A Comparative Cross-Sectional Study by Geofrey Musinguzi et al, 2014 in 2 districts among 15yr olds and above showed a prevalence of uncontrolled hypertension was 20.2% . The middle aged and older groups had a higher prevalence than the younger subjects(15-34)

• The prevalence of normal blood pressure was 37.6%, pre-hypertension 33.9%, hypertension 28.5% and raised blood pressure 62% among 18yr olds and above: Nuwaha and Musinguzi, 2013


Classification• Based on recommendations of the JNC 7, the

classification of BP (expressed in mm Hg) for adults aged 18 years or older is as follows

•Normal: Systolic lower than 120 mm Hg, diastolic lower than 80 mm Hg

•Prehypertension: Systolic 120-139 mm Hg, diastolic 80-89 mm Hg

•Stage 1: Systolic 140-159 mm Hg, diastolic 90-99 mm Hg

•Stage 2: Systolic 160 mm Hg or greater, diastolic 100 mm Hg or greater


Saturday, April 15, 2023

JNC 8 RECOMMENDATIONS SUMMARY

General population aged ≥60 years, SBP≥150 mm Hg or DBP ≥90 mm Hg and treat to a goal SBP <150 mm Hg and goal DBP <90 mm HgGeneral population <60 years, DBP ≥90 mm Hg or SBP ≥140mmHg and treat to a goal DBP <90 mm Hg or SBP <140mmHgGeneral population aged ≥18 years with chronic kidney disease (CKD), SBP ≥ 140mmHg or DBP ≥ 90mmHg and treat to goal SBP<140mmHg and goal DBP<90 mmHgIn the population aged ≥18 years with diabetes, SBP ≥ 140mmHg or DBP ≥ 90mmHg and treat to a goal SBP <140 mm Hg and goal DBP <85 mm Hg

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RECOMMENDATIONS………

In the general black population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic or CCB. In the population aged ≥18 years with CKD, initial (or add-on) antihypertensive Rx should include an ACEI or ARB to improve kidney outcomes. This applies to all CKD patients with hypertension regardless of race or diabetes status.The main objective of hypertension Rx is to attain and maintain goal BP. If goal BP is not reached within a month of Rx, increase the dose of the initial drug or add a second drug from one of the classes (thiazides, CCB, ACEI, or ARB)

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Cont..

• the JNC 8 recommends treating to 150/90 mm Hg in patients over age 60 years; for everybody else, the goal BP is 140/90

• resistant hypertension: hypertension in which BP is >140/90 mm Hg despite the use of medications from 3 or more drug classes, 1 of which is a thiazide diuretic


Cont..

Hypertension may be • primary, which may develop as a result of environmental or genetic

causes• secondary, which has multiple etiologies, including renal, vascular,

and endocrine causes. Primary or essential hypertension accounts for 90-95% of adult cases,

and secondary hypertension accounts for 2-10% of cases


HTN crises

• Hypertensive crises: a BP of more than 180/120 mm Hg and may be further categorized as

hypertensive emergencies or urgencies.1. Hypertensive emergencies are characterized by evidence of

impending or progressive target organ dysfunction2. hypertensive urgencies are those situations without progressive

target organ dysfunction.


Htn emergency

The most common hypertensive emergency is a rapid unexplained rise in BP in a patient with chronic essential hypertension. Most patients who develop hypertensive emergencies have a history of inadequate hypertensive treatment or an abrupt discontinuation of their medications


Cont..

• In hypertensive emergencies, the BP should be aggressively lowered within minutes to an hour by no more than 25%, and then lowered to 160/100-110 mm Hg within the next 2-6 hours

• Acute end-organ damage in hypertensive emergency include: Neurologic, Cardiovascular, retinal, renal.


Cont..

• Neurologic: hypertensive encephalopathy, intracranial hemorrhage • Cardiovascular: myocardial ischemia/infarction, acute left ventricular

dysfunction, acute pulmonary edema, aortic dissection, unstable angina pectoris

• Other: acute renal failure/insufficiency, retinopathy, eclampsia, microangiopathic hemolytic anemia


Risk factors of htn

• non modifiable–Ethnic-genetic risk (black people)–Age–Gender- family hx

• modifiable–Diabetes–Overweight–Alcohol–Salt intake-Physical inactivity,sedentary lifestyle-stress-cigarette smoking


Pathophysiology of HTN

• Multifactorial• Bp determined by humoral mediators, vascular reactivity, circulating

blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation

• HTN mayb due to genetic predisposition, excess dietary salt intake, and adrenergic tone


Pathophysiology of Hypertension

cardiac output x Peripheral resistance = Blood pressure

Heart Rate Stroke volumex


Pathophysiology of HypertensionThe role of endotheliumand the RAAS cascade

Angiotensinogene

Angiotensin I

Angiotensin II

receptor

Renin

ACE

AT1

AT2

prorenine, catecholamines

Pathway of RAAS in theOrganism (kidney, heart,Vessels) to maintain Fluid volume control,Adjustment of CO and Resistance.If regulation fails, high blood pressure occurs

Pathway of RAAS in theTissues: e.g.

Vessel wall

Competition of receptors:AT1 vasoconstriction AT2 vasodilatation


AT1 AT2

AT1 stimulationleads to:

growth+

vasoconstriction

AT2 stimulationleads to:

differentiation

vasodilatation vasoactivity

Smooth muscle cell growth

Angiotensin II Actions on endothelium and

NO =nitric oxide

modified acc. to Unger T et al 1996

NO

NO inhibition



Pathophysiology of Hypertension: secondary H.

• Renal 2.5-6%• Parenchymal..polycystic kidney disease• Renovascular• Tumors,renin producing• Liddle syndrome

• Endocrine• Thyroid dysfunction (1%)• Adrenal (0,3%)• Carcinoid• Hormones, oral contraceptives, Pheochromocytoma,cushing syndrome,primary aldosteronism

• Aortic coarctation• Pregnancy• Neurogenic (brain tumor, lead, porphyria, sleep apnea)• Acute stress (including surgery)• iv. volume increase• Drugs and toxins –Alcohol,cocaineSome may induce primary hypertension, so that the relationships sometimes are weak



Clinical features

• Referred to as the “silent killer” • Frequently asymptomatic until target organ disease occurs

– Or recognized on routine screening

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Clinical features

• Sx often secondary to target organ disease

• Can include: • Fatigue, reduced activity tolerance• Dizziness• Palpitations, angina• Dyspnea


HTN complications

• Target organ diseases occur most frequently in:• Heart• Brain• Peripheral vasculature • Kidney• Eyes


Complications…

• Hypertensive heart disease• Coronary artery disease• Left ventricular hypertrophy• Heart failure

• Cerebrovascular disease• Stroke

• Peripheral vascular disease• Nephrosclerosis• Retinal damage


Complications…

• Atherosclerosis most common cause of cerebrovascular disease; hypertension major risk factor for cerebral atherosclerosis and stroke

• Atherosclerosis in peripheral blood vessels too; can lead to PVD, aortic aneurysm, aortic dissection

• Hypertension one of leading causes of end-stage renal disease, esp. in African-Americans; some degree of renal dysfunction usual in person with even mild BP elevations

• Retina is only place blood vessels can be directly visualized; if see damage there then indicates damage in brain, heart, & kidney too; Can cause blurring, retinal hemorrhage and blindness


Dx

• History and physical examination• BP measurement in both arms

• Use arm with higher reading for subsequent measurements• BP highest in early morning, lowest at night

In the absence of end-organ damage-mild hypertension dx made after two visits, two weeks apart


Office bp measurement

• Use auscultatory method with a properly calibrated instrument

• Patient seated quietly for 5 min in a chair, feet on the floor, and arm supported at heart level

• Appropriate-sized cuff is necessary to ensure accurate reading

• At least two measurements should be obtained

• Allow at least 1 minute between readings. If one arm higher than other; take BP in higher arm for subsequent measurements


Investigations

• Cbc for hct• Urinalysis• Rft• Lipid profile for total and hdl-

cholesterol,triglycerides• ECG + ECHO

• Thyroid function tests• Renin levels• Vinyl mandelic acid• Radiographic imaging


MANAGEMENT

• The objective of treatment is to reduce risk of complications & improve survival

• Benefits to be weighed against side effects & inconvenience. So it is important to treat the patient as a whole not just blood pressure.

• Treatment involves pharmacotherapy and lifestyle modification measures.


MANAGEMENT

• Who should be treated? — In the absence of end-organ damage, a patient should not be labelled as having hypertension unless: the blood pressure is persistently elevated after two visits, two weeks apart.

• All patients should undergo appropriate nonpharmacologic (lifestyle modification).

• Antihypertensive medications should generally be begun if the systolic pressure is persistently ≥140 mmHg and/or the diastolic pressure is persistently ≥90 mmHg despite attempted nonpharmacologic therapy

• Starting with two drugs should be considered in patients with a baseline BP > 160/100 mmHg.


LIFESTYLE MODIFICATIONSModification Recommendation App. SBP reduction range

Weight reduction Maintain normal body weight (BMI, 18.5 to 24.9 kg/m2)

5-20 mmHg per 10-kg weight loss

Adopt DASH eating plan Consume a diet rich in fruits, vegetables, and low-fat dairy products with a reduced content of saturated and total fat

8 to 14 mmHg

Dietary sodium reduction Reduce dietary sodium intake to no more than 100 mg/day (2.4 g sodium or 6 g sodium chloride)

2 to 8 mmHg

Physical activity Engage in regular aerobic physical activity such as brisk walking (at least 30 minutes per day, most days of the week)

4 to 9 mmHg

Moderation of alcohol consumption

Limit consumption to no more than 2 drinks per day in most men and no more than 1 drink per day in women and lighter-weight persons

2 to 4 mmHg


Lifestyle modification Cont’d

• Patient education — Patient education has been demonstrated to result in improved blood pressure control . In addition to education of patients by their clinicians, blood pressure control may be improved when patients with hypertension hear the personal stories of their peers with hypertension.

• Other — adequate potassium intake, cessation of smoking, and limiting the use of nonsteroidal antiinflammatory drugs.


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2013 ESH/ESC Guidelines for the management of arterial hypertension

The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) - J Hypertension 2013;31:1281-1357

Blood pressure goals in hypertensive patients

SBP, systolic blood pressure; CV, cardiovascular; TIA, transient ischaemic attack; CHD, coronary heart disease; CKD, chronic kidney disease;DBP, diastolic blood pressure.

Recommendations

SBP goal for “most”•Patients at low–moderate CV risk•Patients with diabetes•Consider with previous stroke or TIA•Consider with CHD•Consider with diabetic or non-diabetic CKD

<140 mmHg

SBP goal for elderly•Ages <80 years•Initial SBP ≥160 mmHg

140-150 mmHg

SBP goal for fit elderlyAged <80 years

<140 mmHg

SBP goal for elderly >80 years with SBP•≥160 mmHg

140-150 mmHg

DBP goal for “most” <90 mmHg

DB goal for patients with diabetes <85 mmHg

DRUG TREATMENT

• General efficacy — the amount of blood pressure reduction is the major determinant of reduction in cardiovascular risk in patients with hypertension, not the choice of antihypertensive drug

• Initial monotherapy in uncomplicated hypertension — In the absence of a specific indication: thiazide diuretics, long-acting calcium channel blockers (most often a dihydropyridine such as amlodipine), and ACE inhibitors or angiotensin II receptor blockers. Beta blockers not commonly

• Combination therapy — Single agent therapy may not adequately control the blood pressure, particularly in those whose blood pressure is more than 20/10 mmHg above goal. Has greater blood pressure lowering effect than doubling the dose of a single agent (long-acting ACE I or angiotensin receptor blocker in concert with a long-acting dihydropyridine calcium channel blocker.

• Goal blood pressure for uncomplicated HTN: <140/90 mmHg



DRUG TREATMENTDRUG DOSE TOXICITIES

Thiazide diureticsHydrochlorothiazideChlorthalidone

12.5-50mg P.o od25-100 mg/day p.o.

Hypokalemia, hyperglycemia, hyperuricemia, hyperlipidemia

Loop diuretic:Torsemide

2.5-5mg/day initially increased to 10mg/day po in 4-6 weeks

Hypokalemia, hypovolemia, ototoxicity

ACEICaptoprilLisinoprilRamipril

Captopril 25mg 2-3 times a dayLisinopril 10-40mg/dayramipril 5-10 mg/day

Hyperkalemia; teratogen; cough, first-dose hypotension, rash

ARBsLosartan Valsartan

50-100 mg daily40-160 mg daily

Hyperkalemia; teratogen

CCBsAmlodipineNifedipinediltiazem, verapamil

5-10 mg daily30-90 mg daily200-300 mg daily240 mg daily

Excessive cardiac depression; constipation

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DRUG TREATMENT

DRUG DOSE TOXICITIES

BETA 1 SELECTIVEAtenololMetoprololBisoprolol

50-100 mg daily100-200 mg daily5-10 mg daily

Bradycardia, hypotension

BETA BLOCKERS, ALPHA ACTIVITYLabetalolCarvedilol

200 mg-2.4 g daily in divided doses6.25-25 mg 12-hourly

sexual dysfunction, sedation, sleep disturbances, hypotension, weight gain

VASODILATORSHydralazine

(25-100 mg 12-hourly first-dose and postural hypotension, headache, tachycardia and fluid retention

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HYPERTENSIVE EMERGENCIES

• Defn; Hypertensive emergencies are acute, life-threatening, and usually associated with marked increases in blood pressure , generally ≥180/120 mmHg

• Malignant hypertension is marked hypertension with retinal hemorrhages, exudates, or papilledema.

• Hypertensive encephalopathy refers to the presence of signs of cerebral edema caused by breakthrough hyperperfusion from severe and sudden rises in blood pressure.


MECHANISMS OF VASCULAR INJURY

• With mild to moderate elevations in blood pressure, • damage to the vascular wall. • Disruption of the vascular endothelium then allows plasma constituents

(including fibrinoid material) to enter the vascular wall, thereby narrowing or obliterating the vascular lumen.

• Within the brain, the breakthrough vasodilation from failure of autoregulation leads to the development of cerebral oedema and the clinical picture of hypertensive encephalopathy

• The level at which fibrinoid necrosis occurs is dependent upon the baseline BP


Mechanism…..

• In comparison, hypertensive encephalopathy can be seen at diastolic pressures as low as 100 mmHg in previously normotensive patients with acute hypertension due to preeclampsia or acute glomerulonephritis; patients in whom autoregulation is impaired also may develop hypertensive injury at relatively mild degrees of hypertension



HYPERTENSIVE RETINOPATHY GRADING

Keith Wagener Barker (KWB) GradesGrade 1Arteriolar constriction/attenuation/sclerosis ̀silver wiring` and vascular tortuositiesGrade 2As grade 1 + Irregularly located, tight constrictions Known as `AV nicking` or `AV nipping`Grade 3As grade 2 + Retinal edema, cotton wool spots and flame hemorrhagesGrade 4As grade 3 + swelling of the optic disk (papilloedema) + macular star

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Grade 3 KWB Retinopathy

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GOAL OF THERAPY

• The initial aim of treatment in hypertensive crises is to rapidly lower the diastolic pressure to about 100 to 105 mmHg; this goal should be achieved within two to six hours, with the maximum initial fall in BP not exceeding 25 percent of the presenting value.

• This level of BP control will allow gradual healing of the necrotizing vascular lesions. More aggressive hypotensive therapy is both unnecessary and may reduce the blood pressure below the autoregulatory range, possibly leading to ischemic events (such as stroke or coronary disease).

• Once the BP is controlled, the patient should be switched to oral therapy, with the diastolic pressure being gradually reduced to 85 to 90 mmHg over two to three months.


Parenteral drugs for treatment of hypertensive emergencies

Drug Dose Adverse effects Onset of action

VASODLATORS

Sodium nitroprusside 0.25-10 µg/kg/min as IV infusion

Nausea, vomiting, muscle twitching, sweating, thiocynate and cyanide intoxication

Immediate

Nicardipine hydrochloride

5-15 mg/h IV Tachycardia, headache, flushing, local phlebitis

5-10 min

Clevidipine 1-2 mg/h IV with rapid titration to max of 16 mg/h

Atrial fibrillation, nausea 1-2 min

Fenoldopam mesylate 0.1-0.3 µg/kg per min IV infusion

Tachycardia, headache, nausea, flushing <5 min

Nitroglycerin 5-100 µg/min as IV infusion Headache, vomiting, methemoglobinemia, tolerance with prolonged use.

2-5 min

Hydralazine hydrochloride

20-30 min IM Tachycardia, flushing, headache, vomiting, aggravation of angina

20-30 min IM


Parenteral drugs for treatment of hypertensive emergencies….Drug Dose Adverse effects Onset of action

Andrenergic inhibitorsLabetalol hydrochloride 20-80 mg IV bolus every

10 min0.5-2.0 mg/min IV infusion

Vomiting, scalp tingling, bronchoconstriction, dizziness, nausea, heart block, orthostatic hypotension

5-10 min

Esmolol hydrochloride 250-500 µg/kg/min by infusion; may repeat bolus after 5 min or increase infusion to 300 µg/min

Hypotension, nausea, asthma, first-degree heart block, HF

1-2 min

Phentolamine 5-15 mg IV bolus Tachycardia, flushing, headache

1-2 min




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Management of hypertension and hypertensive emergencies.pptx