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Hypertension. Resting BP consistently >140 systolic or >90 diastolic. Epidemiology. 20% of adult population~35,000,000 people25% do not know they are hypertensiveTwice as frequent in blacks than in whites25% of whites and 50% of blacks > 65 y/o. Types. Primary (essential) hypertensionSecondary hypertension.
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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!!!