Hypertension and Peripheral Vascular Disease

1. Hypertension and Peripheral Vascular Disease Terry White, MBA, BSN

2. Hypertension Resting BP consistently >140 systolic or >90 diastolic

3. Epidemiology • 20% of adult population • ~35,000,000 people • 25% do not know they are hypertensive • Twice as frequent in blacks than in whites • 25% of whites and 50% of blacks > 65 y/o

4. Types • Primary (essential) hypertension • Secondary hypertension

5. Primary Hypertension • 85 - 90% of hypertensives • Idiopathic • More common in blacks or with positive family history • Worsened by increased sodium intake, stress, obesity, oral contraceptive use, or tobacco use • Cannot be cured

6. Secondary Hypertension • 10 - 15% of hypertensives • Increased BP secondary to another disease process

7. Secondary Hypertension • Causes: • Renal vascular or parenchymal disease • Adrenal gland disease • Thyroid gland disease • Aortic coarctation • Neurological disorders • Small number curable with surgery

8. Hypertension Pathology • Increased BP  inflammation, sclerosis of arteriolar walls  narrowing of vessels  decreased blood flow to major organs • Left ventricular overwork  hypertrophy, CHF • Nephrosclerosis  renal insufficiency, failure

9. Hypertension Pathology • Coronary atherosclerosis  AMI • Cerebral atherosclerosis  CVA • Aortic atherosclerosis  Aortic aneurysm • Retinal hemorrhage  Blindness

10. Signs/Symptoms • Primary hypertension is asymptomatic until complications develop • Signs/Symptoms are non-specific • Result from target organ involvement • Dizziness, flushed face, headache, fatigue, epistaxis, nervousness are not caused by uncomplicated hypertension.

11. HTN Medical Management • Life style modification • Weight loss • Increased aerobic activity • Reduced sodium intake • Stop smoking • Limit alcohol intake

12. HTN Medical Management • Medications • Diuretics • Beta blockers • Calcium antagonists • Angiotensin converting enzyme inhibitors • Alpha blockers

13. HTN Medical Management Medical management prevents or forestalls all complications Patients must remain on drug therapy to control BP

14. Categories of Hypertension • Hypertensive Emergency (Crisis) • acute  BP with sx/sx of end-organ injury • Hypertensive Urgency • sustained DBP > 115 mm Hg w/o evidence of end-organ injury • Mild Hypertension • DBP > 90 but < 115 mm Hg w/o symptoms • Transient Hypertension • elevated due to an unrelated underlying condition

15. Hypertensive Crisis Acute life-threatening increase in BP Usually exceeds 200/130

16. Hypertensive Crisis • Few Hypertensive Conditions are “Emergencies” • Emergent Hypertensive Conditions include: • encephalopathy (CNS sx/sx) • eclampsia • when associated with • AMI or Unstable angina • Acute renal failure • Intracranial injury • Acute LVF • Aortic dissection

17. Causes • Sudden withdrawal of anti-hypertensives • Increased salt intake • Abnormal renal function • Increase in sympathetic tone • Stress • Drugs • Drug interactions • Monoamine oxidase inhibitors • Toxemia of pregnancy

18. Restlessness, confusion, AMS Vision disturbances Severe headache Nausea, vomiting Seizures Focal neurologic deficits Chest pain Dyspnea Pulmonary edema Signs/Symptoms

19. Hypertensive Crisis Can Cause • CVA • CHF • Pulmonary edema • Angina pectoris • AMI • Aortic dissection

20. Hypertensive Crisis Management • Immediate goal: lower BP in controlled fashion • No more than 30%  in first 30-60 mins • Not appropriate in all settings • Oxygen via NRB • Monitor ECG • IV NS TKO • Drug Therapy • Targeted at simply lowering BP, OR • Targeted at underlying cause

21. Drug Therapy Possibilities • Sodium Nitroprusside (Nipride®) • Potent arterial and venous vasodilator • Vasodilation begins in 1 to 2 minutes • 0.5 g/kg/min by continuous infusion, titrate to effect • increase in increments of 0.5 g/kg/min • 50 mg in 250 cc D5W • Effects easily reversible by stopping drip • Continuous hemodynamic monitoring required • Cover IV bag/tubing to avoid exposure to light • Used primarily when targeting lower BP only

22. Drug Therapy Possibilities • Nitroglycerin • Vasodilator • Nitropaste simplest method • 1 to 2 inches of ointment q 8 hrs • easy to control effect but slow onset • Sublingual NTG is faster route • 0.4 mg SL tab or spray q 5 mins • easy to control but short acting • NTG infusion, 10 - 20 mcg/min • seldom used for hypertensive crisis • Commonly used prehospital when targeting BP lowering only especially in AMI

23. Drug Therapy Possibilities • Nifedipine (Procardia®) • Calcium channel blocker • Peripheral vasodilator • 10 mg Sublingual • Split capsule longitudinally and place contents under tongue or puncture capsule with needle and have patient chew • Used less frequently today! Frequently in past! • Concern for rapid reduction of BP resulting in organ ischemia

24. Drug Therapy Possibilities • Furosemide (Lasix®) • Loop Diuretic • initially acts as peripheral vasodilator • later actions associated with diuresis • 40 mg slow IV or 2X daily dose • most useful in acute episode with CHF or LVF • Often used with other agents such as NTG

25. Drug Therapy Possibilities • Hydrazaline (Apresoline®) • Direct smooth muscle relaxant • relax arterial smooth muscle > venous • 10-20 mg slow IV q 4-6 hrs; initial dose 5 mg for pre-eclampsia/eclampsia • Usually combined with other agents such as beta blockers • concern for reflex sympathetic tone increase • Most useful in pre-eclampsia and eclampsia

26. Drug Therapy Possibilities • Metoprolol (Lopressor®), orLabetalol (Normodyne®) • decrease in heart rate and contractility • Dose • Metoprolol: 5 mg slow IV q 5 mins to total ~15 mg • Labetalol: 10-20 mg slow IV q 10 mins • Metoprolol is selective beta-1 • minimal concern for use in asthma and obstructive airway disease • Labetalol: both alpha & beta blockade • Most useful in AMI and Unstable angina

27. Hypertensive Crisis Management Avoid crashing BP to hypotensive or normotensive levels! Ischemia of vital organs may result!

28. Hypertensive Crisis Management Must assure underlying cause of BP is understood HTN may be helpful to the patient Aggressive treatment of HTN may be harmful What patients may have HTN as a compensatory mechanism?

29. Syncope Sudden, temporary loss of consciousness caused by inadequate cerebral perfusion

30. Vasovagal Syncope • Simple fainting occurring when upright • Increased vagal tone leads to peripheral vasodilation, bradycardia which lead to: • Decreased cardiac output • Decreased cerebral perfusion • Causes • Fright, trauma, pain • Pressure on carotid sinus (tight collar, shaving)

31. Cardiogenic Syncope • Paroxysmal Tachyarrhythmias (atrial or ventricular) • Bradyarrhythmias • Stokes-Adams attack • Valvular disease • especially aortic stenosis • Can occur in any position

32. Postural Syncope Due to decreased BP on standing or sitting up Orthostatic hypotension

33. Postural Syncope • Drugs - usually antihypertensives • Diuretics • Vasodilators • Beta-blockers • Volume depletion • Acute hemorrhage • Vomiting or diarrhea • Excessive diuretic use • Protracted sweating • Neuropathic diseases - diabetes

34. Tussitive Syncope • Coughing • Increased intrathoracic pressure • Decreased venous return • Vagal stimulation • Decreased heart rate

35. Micturation Syncope • Urination • Increased vagal tone • Decreased cardiac output • Frequently associated with • Volume depletion due to EtOH • Vasodilation due to EtOH

36. Syncope History • What were you doing when you fainted? • Did you have any warning symptoms? • Have you fainted before? • Under what circumstances? • Any history of cardiac disease? • Any medications? • Any other past medical history?

37. Syncope Management • Supine position - possibly elevate lower extremities • Do not sit up or move to semi-sitting position quickly • Airway - oxygen via NRB • Loosen tight clothing

38. Syncope Management • Vital signs, Focused Hx & Physical exam • Assess for injuries sustained in fall • Attempt to identify cause • Based on history/physical, Consider: • ECG Monitor • Blood glucose check • Vascular access • Transport for further evaluation

39. Peripheral Vascular Disease Peripheral Atherosclerotic Disease Deep Vein Thrombophlebitis Varicose Veins

40. Peripheral Atherosclerosis • Gradual, progressive disease • Common in diabetics • Thin, shiny skin • Loss of hair on extremities • Ulcers, gangrene may develop

41. Peripheral Atherosclerosis • Intermittent Claudication • Deficient blood supply in exercising muscle • Pain, aching, cramps, weakness • Occurs in calf, thigh, hip, buttocks on walking • Relieved by rest (2 - 5 minutes)

42. Peripheral Atherosclerosis • Acute Arterial Occlusion • Sudden blockage by embolism, plaque, thrombus • Can result from vessel trauma • The 5 Ps of acute occlusion • Pain, worsening over several hours • Pallor, cool to touch • Pulselessness • Paresthesias, loss of sensation • Paralysis

43. Deep Vein Thrombophlebitis • Inflammation of lower extremities, pelvic veins with clot formation • Usually begins with calf veins • Precipitating factors • Injury to venous endothelium • Hypercoagulability • Reduced blood flow (venous stasis)

44. Deep Vein Thrombophlebitis • Signs/Symptoms • May be asymptomatic • Pain, tenderness • Fever, chills, malaise • Edema, warmth, bluish-red color • Pain on ankle dorsiflexion during straight leg lifting (Homan’s sign) • Palpable “cord” in calf • clotted veins

45. Deep Vein Thrombophlebitis May progress to pulmonary embolism!!!

46. Varicose Veins Dilated, elongated, tortuous superficial veins usually in lower extremities

47. Varicose Veins • Causes • Congenital weakness/absence of venous valves • Congenital weakness of venous walls • Diseases of venous system (Deep thrombophlebitis) • Prolonged venostasis (pregnancy, standing)

48. Varicose Veins • Signs/Symptoms • May be asymptomatic • Feeling of fatigue, heaviness • Cramps at night • Orthostatic edema • Ulcer formation

49. Varicose Veins Rupture may cause severe bleeding Control with elevation and direct pressure

50. Aortic Aneurysm Localized abnormal dilation of blood vessel, usually an artery Thoracic Dissecting Abdominal