Hypertension and Its Management

1. Hypertension and Its Management Dr. SumanChowdhury CMCH Examinee of FCPS

2. Hypertension: • Hypertension is a condition in which arterial BP is chronically elevated.

3. And, What is the upper limit?

4. > 140/90 mmHg

5. For Diabetic Patients:> 130/80mmHg

6. Is it a Sign or Disease? • It is more than a sign • It will not be an exaggeration if we consider it as a disease!

7. Classification

9. The Primary/Essential Hypertension is said to be due to these following mechanisms:

10. Sympathetic nervous system hyperactivity • This is most apparent in younger persons with hypertension, who may exhibit tachycardia and an elevated cardiac output. However, correlations between plasma catecholamines and blood pressure are poor. Insensitivity of the baro-reflexesmay play a role in the genesis of adrenergic hyperactivity. • Abnormal cardiovascular or renal development • The normal cardiovascular system develops so that elasticity of the great arteries is matched to the resistance in the periphery to optimize large vessel pressure waves. In this way, myocardial oxygen consumption is minimized and coronary flow maximized. Elevated blood pressure later in life could arise from abnormal development of aortic elasticity or reduced development of the microvascular network. This has been postulated as the sequence of events in low birth weight infants who have an increased risk of hypertension developing in adulthood. Another hypothesis proposes that the association between low birth weight and hypertension arises from reduced nephron number.

11. Renin–angiotensin system activity • Renin, a proteolytic enzyme, is secreted by cells surrounding glomerular afferent arterioles in response to a number of stimuli, including reduced renal perfusion pressure, diminished intravascular volume, circulating catecholamines, increased sympathetic nervous system activity, increased arteriolar stretch, and hypokalemia. Renin acts on angiotensinogen to cleave off the ten-amino-acid peptide angiotensin I. This peptide is then acted upon by angiotensin-converting enzyme (ACE) to create the eight-amino-acid peptide angiotensin II, a potent vasoconstrictor and stimulant of aldosterone release from the adrenal glands. Despite the role of renin in the regulation of blood pressure, it probably does not play a central role in the pathogenesis of most primary (essential) hypertension; only 10% of patients have high renin activity, whereas 60% have normal levels, and 30% have low levels. Black persons with hypertension and older patients tend to have lower plasma renin activity, which may be associated with expanded intravascular volume.

12. Defect in natriuresis • Normal individuals increase their renal sodium excretion in response to elevations in arterial pressure. In hypertensive patients, this pressure-natriuresis relationship is reset so that maintenance of sodium homeostasis requires increased extracellular fluid volume and higher arterial pressure. • Intracellular sodium and calcium • Intracellular Na+ is elevated in primary (essential) hypertension. An increase in intracellular Na+ may lead to increased intracellular Ca2+ concentration as a result of facilitated exchange and might explain the increase in vascular smooth muscle tone that is characteristic of established hypertension.

13. Though secondary causes are only 5%, the list is not too short!!!!

14. Identifiable causes of Hypertension • Sleep apnea • Drug-induced or drug-related • Chronic kidney disease • Primary aldosteronism • Renovascular disease • Long-term corticosteroid therapy and Cushing syndrome • Pheochromocytoma • Coarctation of the aorta • Thyroid or parathyroid disease

15. Hypertensive Crisis

16. Hypertensive Crisis Hypertensive Urgency Hypertensive Emergency • May be defined as acute and rapidly developing end organ damage with significant hypertension. Here blood Pressure is usually > 220 mm of Hg. • Hypertensive emergencies require substantial reduction of blood pressure within 1 hour to avoid the risk of serious morbidity or death • There is target organ damage. • Hypertensive emergencies are treated in an ICU • BP is progressively (although not abruptly) reduced using a short-acting, titratable IV drug. • Choice of drug and speed and degree of reduction vary somewhat with the target organ involved, but generally a 20 to 25% reduction in MAP over an hour or so is appropriate, with further titration based on symptoms. Then if stable, to 160/100–110 mmHg within the next 2–6 hours. • These include patients with asymptomatic severe hypertension, very high blood pressure diastolic > 120 to 130 mm Hg • There is no target organ damage • BP at these levels often worries the physician; however, acute complications are unlikely, so immediate BP reduction is not required. • Patients should be started on a 2-drug oral combination, and close evaluation (with evaluation of treatment efficacy) should be continued on an outpatient basis.

17. Target Organ damage Cardiac Renal Retinal Organs CNS Acute MI, acute left ventricular failure with pulmonary edema, unstable angina pectoris, dissecting aortic aneurysm Hypertensive nephropathy Hypertensive Retinopathy Grade 4 Disorders Hypertensive Encephalopathy Signs and Symptoms Transient disturbances of speech or vision, paraesthesiae, fits, disorientation, and loss of consciousness, Papilloedema is common A CT scan of the brain often shows haemorrhage in and around the basal ganglia. Chest pain, Dyspnoes, sudden severe pain in back with shock Hematuria,proteinuria,and progressive kidney 'Cotton wool' exudates are associated with retinal ischaemia or infarction, central retinal vein thrombosis

18. In Pregnancy • And also, Disorders Preeclampsia Eclampsia Proteinuria, Edema Preeclampsia + Convulsion Signs and Symptoms

19. Attention!!! • Interesting to note that, in case of Hypertensive encephalopathy, we have to very cautious to exclude stroke of any kind. For which, even an early MRI (T2 weighted) should be done if we are not confident enough after history, and physical (neurological) examination!! • Because, the target and the management plan will be totally changed in case of stroke.

20. Regarding anti Hypertensive in stroke In Haemorrhagic stroke* In ischaemic stroke Intracerebral SAH If thrombolytic therapy is to be used Who are not candidates for thrombolytic therapy Target is SBP> 180mmHg and DBP > 130mmHg Target is MAP > 130mmHg Target is SBP> 185mm Hg and DBP > 110mm Hg Target is SBP> 220mmHg and DBP> 130mmHg

21. Suggested Recommended Guidelines for TreatingElevated Blood Pressure in Spontaneous ICH • If SBP is 200 mm Hg or MAP is 150 mm Hg, then consider aggressive reduction of blood pressure with continuous intravenous infusion, with frequent blood pressure monitoring every 5 minutes • If SBP is 180 mm Hg or MAP is 130 mm Hg and there is evidence of or suspicion of elevated ICP, then consider monitoring ICP and reducing blood pressure using intermittent or continuous intravenous medications to keep cerebral perfusion pressure 60 to 80 mm Hg

23. Management

24. A person with Increased BP Look for Hypertensive Crisis Yes No Urgency Emergency Establish HTN* Call for ICU/HDU Life style Modification Start Oral drugs If not available, manage in Ward If not controlled Drug Rx § e.g. Captopril Add other drugs later if necessary IV drugs with titratable doses Look for compelling indications IV GTN, Hydralazine, Labeteolol Select drugs after excluding compelling Contraindications When the blood pressure has been brought under control, combinations of oral antihypertensive agents can be added as parenteral drugs are tapered off over a period of 2–3 days. Most subsequent regimens should include a diuretic. Look for co-morbid conditions Consider special conditions

25. * Persistent Raised BP: • Measured at past two visits and • Systolic BP or DBP or Both are > 140/90mmHg • § Threshold for offering Drug treatment: • BP > 160/100mmHg, or • Isolated Systolic HTN (Systolic BP> 160 mmHg), or • BP > 140/90mmHg, and • 10 yr CVD risk at list 20 % or • Existing CVD or • Target organ damage

26. Management of Hypertensive urgency

27. General strategies: All patients should be provided a quiet room to rest; this can lead to a fall in BP of 10 to 20 mmHg or more. The approach varies depending on whether the patient has already been treated for hypertension or is untreated. Previously Untreated hypertension Previously treated hypertension Increase the dose of existing antihypertensive medications, or add another agent. Reinstitution of medications in non-adherent patients. Addition of a diuretic, and reinforcement of dietary sodium restriction, in patients who have worsening hypertension due to high sodium intake. In the previously untreated patient, several options are available. The approach should take into consideration: The individual patient's risk with persistence of severe hypertension The likely duration of severe hypertension, Of cerebrovascular or myocardial ischemia with rapid reduction in blood pressure Relatively rapid initial blood pressure reduction (over several hours). We use Oral captopril

28. Following administration of drugs, the patient is observed for a few hours, to ascertain a reduction in blood pressure of 20 to 30 mmHg. Thereafter, a longer acting agent is prescribed and the patient is sent home to follow up within a few days. The drop in blood pressure may take relatively longer with captopril, and may be too large among patients with hemodynamically significant unilateral renal artery stenosis. • Blood pressure reduction over one to two days. There are no data supporting the use of a particular agent in this setting although we generally do not begin therapy with extended release preparations or with a diuretic alone. Depending on the patient, a calcium channel blocker (but not sublingual nifedipine), beta blocker or angiotensin converting enzyme (ACE) inhibitor or receptor blocker can be started, like ramipril10 mg once daily.

29. The choice of agent should take into consideration the type of antihypertensive agent that is most appropriate in the long term (eg, calcium channel blockers and thiazide-like diuretics are preferred over ACE inhibitors and beta blockers as monotherapy in blacks), and underlying conditions that may be favorably or adversely affected by the antihypertensive agent . • Some experts initiate therapy with two agents or a combination agent, one of which is a thiazide diuretic. The rationale is that most patients with blood pressure ≥20/10 mmHg above goal will require two or more antihypertensive agents in order to achieve the goal blood pressure . • It is unlikely that a diuretic in combination with a modest dose of another agent will cause a dangerous reduction in the blood pressure; however, initiation of two agents simultaneously must be done with close blood pressure follow-up, since the full effects of both agents may not occur for a few days, and adverse consequences may ensue if the blood pressure is lowered too quickly. This is particularly true among patients with cerebrovascular disease in whom more cautious blood pressure reduction is warranted.

30. Monitoring and follow-up

31. The patient with severe asymptomatic hypertension is usually managed in the emergency room, since exclusion of acute end-organ damage requires laboratory testing, and the patient may require administration of medications and several hours of observation. However, the patient can often be safely managed in the physician's office if the evaluation and management can be carried out. • The management of a patient who does not have established HTN, follow-up is difficult. Rarely, such patients may require admission. • In addition, patients at high risk for cardiovascular events (e.g, long-standing diabetes, known coronary artery disease or prior stroke), should probably be admitted.

32. Ideally, the patient should be observed for a few hours to ascertain that the blood pressure is stable or improving, and that indeed they are asymptomatic. If so, the patient can be sent home with close follow-up over the subsequent days directed towards evaluation for symptoms related to hypertension or hypotension, and adjustment of medications to achieve the initial blood pressure goal of ≤160/100 mmHg. • In reliable patients who can monitor their blood pressure at home, close phone follow-up may substitute for direct physician visits. If the patient does not have a physician, follow-up may need to be in the emergency room or other acute care setting. • Over the subsequent weeks and months, the dose and selection of medications should be adjusted as needed to achieve the desired blood pressure goals. These issues are discussed elsewhere.

33. Drugs for the Hypertensive Crisis

34. I.V. Drugs for Hypertensive Emergency:

35. Preferred I.V drugs in Selected conditions:

36. Management: • Non pharmacologic therapy: • Lifestyle modification may have an impact on morbidity and mortality. A diet rich in fruits, vegetables, and low-fat dairy foods and low in saturated and total fats (DASH diet) has been shown to lower blood pressure.

38. Pharmacological approach: • Depends mainly on: • Compelling indications • Contraindications • Presence of co-morbid conditions • Some special situations

39. Compelling Indications: • CVD risk+ IHD+ (Previous H/O CVD= ACEi, ARB • Cardiac: • Post MI=ACEi, Aldosterone antagonists • LVF = ARB, Aldosterone antagonists • DM Type 1= ACEi • DM Type = ARB • Older patients+ Isolated Systolic HTN= Thiazide or Thiazide like diuretics • CKD= ARB, ACEi

40. Old Concept New Concept

41. That means, Beta blocker is less favored as an Antihypertensive drug!!

42. Contraindications: • Pregnancy: No ACEi, ARB • Asthma+ COPD= No β Blocker • Young male patient = No β Blocker (Relative) • Significant Renal artery stenosis = ARB, ACEi • Hyperkalaemia = ARB, ACEi

43. Investigations: • For all patients: • Urinalysis for blood, protein and glucose • Blood urea, electrolytes and creatinine • N.B. Hypokalaemic alkalosis may indicate primary hyperaldosteronism but is usually due to diuretic therapy • Blood glucose • Serum total and HDL cholesterol • 12-lead ECG (left ventricular hypertrophy, coronary artery disease)

44. Cont…… • For Selected Patients: • Chest X-ray: to detect cardiomegaly, heart failure, coarctation of the aorta • Ambulatory BP recording: to assess borderline or 'white coat' hypertension • Echocardiogram: to detect or quantify left ventricular hypertrophy • Renal ultrasound: to detect possible renal disease • Renal angiography: to detect or confirm presence of renal artery stenosis • Urinary catecholamines: to detect possible phaeochromocytoma • Urinary cortisol and dexamethasone suppression test: to detect possible Cushing's syndrome • Plasma renin activity and aldosterone: to detect possible primary aldosteronism

45. RESISTANT HYPERTENSION • Resistant hypertension is defined in JNC 7 as the failure to reach blood pressure control in patients who are adherent to full doses of an appropriate three drug regimen (including a diuretic). In this situation, the clinician should first exclude identifiable causes of hypertension, and then carefully explore reasons why the patient might not be at goal blood pressure. • The clinician should pay particular attention to the type of diuretic being used in relation to the patient's kidney function. Aldosterone may play an important role in resistant hypertension and aldosterone receptor blockers can be very useful. If goal blood pressure cannot be achieved following completion of these steps, consultation with a hypertension specialist should be considered.

46. Causes of resistant hypertension • Improper blood pressure measurement • Volume overload and pseudotolerance • Excess sodium intake • Volume retention from kidney disease • Inadequate diuretic therapy • Drug-induced or other causes: • Nonadherence • Inadequate doses • Inappropriate combinations • Nonsteroidal anti-inflammatory drugs; cyclooxygenase-2 inhibitors • Cocaine, amphetamines, other illicit drugs • Sympathomimetics (decongestants, anorectics)

47. Oral contraceptives • Adrenal steroids • Cyclosporine and tacrolimus • Erythropoietin • Licorice (including some chewing tobacco) • Selected over-the-counter dietary supplements and medicines (eg, ephedra, ma huang, bitter orange) • Associated conditions • Obesity • Excess alcohol intake

48. Follow-Up of Patients Receiving Hypertension Therapy • Once antihypertensive drug therapy is initiated, most patients should return for follow up and adjustment of medications at monthly intervals or until the BP goal is reached and laboratory testing limited to tests appropriate for the patient and the medications used. • More frequent visits will be necessary for patients with stage 2 hypertension or with complicating co morbid conditions. Serum potassium and creatinineshould be monitored at least one to two times per year. Yearly monitoring of blood lipids is recommended, and an electrocardiogram should be repeated at 2- to 4-year intervals depending on whether initial abnormalities are present, the presence of coronary risk factors, and age.

49. Optimal target blood pressures during antihypertensive treatment:

50. After BP is at goal and stable, follow up visits can usually be at 3-to 6-month intervals. Co morbidities such as HF, associated diseases such as diabetes, and the need for laboratory tests influence the frequency of visits. Other cardiovascular risk factors should be monitored and treated to their respective goals, and tobacco avoidance must be promoted vigorously. • Low-dose aspirin therapy should be considered only when BP is controlled because of the increased risk of hemorrhagic stroke when the hypertension is not controlled. Pharmacy care programs have been shown to improve compliance with medications. Patients who have had excellent blood pressure control for several years, especially if they have lost weight and initiated favorable lifestyle modifications, should be considered for "step-down" of therapy to determine whether lower doses or discontinuation of medications are feasible.