hypertension and peripheral vascular disease

1. Hypertension and Peripheral Vascular Disease EMS Professions Temple College

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

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!

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

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

51. Thoracic Aortic Aneurysm Usually results from atherosclerosis Weakened aortic wall bows out - lumen distends Most common in males age 50 - 70

52. Thoracic Aortic Aneurysm Sign/Symptoms Dyspnea, Cough Hoarseness/Loss of voice Substernal/back pain or ache Lower extremity weakness/ paresthesias Variation in pulses, BP between extremities

53. Dissecting Aortic Aneurysm Intima tears Column of blood forms false passage, splits tunica media lengthwise Most common in thoracic aorta Most common in blacks, chronic hypertension, Marfan�s syndrome

54. Dissecting Aortic Aneurysm Signs/Symptoms Sudden �ripping� or �tearing� pain anterior chest or between shoulders May extend to shoulders, neck, lower back, and abdomen Rarely radiates to jaw or arms Pallor, diaphoresis, tachycardia, dyspnea

55. Dissecting Aortic Aneurysm Signs/Symptoms Normal or elevated upper extremity BP in �shocky� patient CHF if aortic valve is involved Acute MI if coronary ostia involved Rupture into pericardial space or chest cavity with circulatory collapse

56. Dissecting Aortic Aneurysm Signs/Symptoms CNS symptoms from involvement of head/neck vessel origins Chest pain + neurological deficit = aortic aneurysm

57. Abdominal Aortic Aneurysm Also referred to as �AAA� or �Triple A� Usually results from atherosclerosis White males age 50 - 80

58. Abdominal Aortic Aneurysm Signs/Symptoms Usually asymptomatic until large enough to be palpable as pulsing mass Usually tender to palpation Excruciating lower back pain from pressure on lumbar vertebrae May mimic lumbar disk disease or kidney stone Leaking/rupture may produce vascular collapse and shock Often presents with syncopal episode

59. Abdominal Aortic Aneurysm Signs/Symptoms May result in unequal lower extremity pulses or unilateral paresthesia Urge to defecate caused by retroperitoneal leaking of blood Erosion into duodenum with massive GI bleed

60. Aortic Aneurysm Management ABCs High concentration O2 NRB Assist ventilations if needed Package patient for transport in MAST, inflate if patient becomes hypotensive IVs x 2 with LR enroute Draw labs 12 Lead ECG enroute if time permits

61. Aortic Aneurysm Management If patient hypertensive consider reducing BP Nitropaste Beta blocker Consider analgesia Tolerated best if hypertensive Consider transport to facility with vascular surgery capability

62. Pulmonary Embolism Pathophysiology Pulmonary artery blocked Blood: Does not pass alveoli Does not exchange gases

63. Causes Blood clots = most common cause Virchow�s Triad Venous stasis � bed rest, immobility, casts, CHF Thrombophlebitis � vessel wall damage Hypercoagulability � Birth control pills, especially with smoking

64. Causes Air Amniotic fluid Fat particles Long bone fracture � more quickly splinted, less chance of fat emboli Particulates from substance abuse

65. Signs/Symptoms Small Emboli Dyspnea Tachycardia Tachypnea

66. Signs/Symptoms Larger Emboli Respiratory difficulty Pleuritic pain Pleural rub Coughing Hemoptysis Localized Wheezing

67. Signs/Symptoms Very Large Emboli Respiratory distress Central chest pain Distended neck veins Acute right heart failure Shock Cardiac arrest

68. Signs/Symptoms There are NO findings specific to pulmonary embolism

69. Management Airway Consider intubation early (if does not cause delay) Breathing 100% O2 NRB mask Consider assisting ventilations (if not intubated) Circulation IV x 2, lg bore, NS, TKO May attempt fluid bolus if hypotensive or shock ECG monitor Rapid transport thrombolysis or pulmonectomy may be useful

70. Pulmonary Embolism If the patient is alive when you get to them, that embolus isn�t going to kill them, BUT THE NEXT ONE THEY THROW MIGHT!!!