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Hypertension andPeripheral Vascular Disease
EMS Professions
Temple College
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Hypertension
Resting BP consistently >140
systolic or >90 diastolic
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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
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Types
Primary (essential) hypertension
Secondary hypertension
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Primary Hypertension
85 - 90% of hypertensives
Idiopathic
More common in blacks or with positivefamily history
Worsened by increased sodium intake,
stress, obesity, oral contraceptive use, ortobacco use
Cannot be cured
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Secondary Hypertension
10 - 15% of hypertensives
Increased BP secondary to another
disease process
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Secondary Hypertension
Causes:
Renal vascular or parenchymal disease
Adrenal gland disease Thyroid gland disease
Aortic coarctation
Neurological disorders
Small number curable with surgery
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Hypertension Pathology
Increased BP inflammation, sclerosisof arteriolar walls narrowing of vessels decreased blood flow to major organs
Left ventricular overworkhypertrophy, CHF
Nephrosclerosis renal insufficiency,failure
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Hypertension Pathology
Coronary atherosclerosis AMI Cerebral atherosclerosis CVA Aortic atherosclerosis Aortic
aneurysm
Retinal hemorrhage Blindness
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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.
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HTN Medical Management
Life style modification
Weight loss
Increased aerobic activity
Reduced sodium intake
Stop smoking
Limit alcohol intake
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HTN Medical Management
Medications
Diuretics
Beta blockers
Calcium antagonists
Angiotensin converting enzymeinhibitors
Alpha blockers
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HTN Medical Management
Medical management prevents or
forestalls all complications
Patients must remain on drugtherapy to control BP
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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 ofend-organ injury
Mild Hypertension
DBP > 90 but < 115 mm Hg w/o symptoms Transient Hypertension
elevated due to an unrelated underlyingcondition
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Hypertensive Crisis
Acute life-threatening increase
in BP
Usually exceeds 200/130
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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
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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
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Signs/Symptoms
Restlessness,
confusion, AMS
Vision disturbances
Severe headache
Nausea, vomiting
Seizures
Focal neurologic
deficits
Chest pain
Dyspnea
Pulmonary edema
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Hypertensive Crisis Can Cause
CVA
CHF
Pulmonary edema
Angina pectoris
AMI
Aortic dissection
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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
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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 toeffect increase in increments of 0.5g/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
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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 targetingBP lowering only especially in AMI
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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 patientchew
Used less frequently today! Frequently in past!
Concern for rapid reduction of BP resulting in organischemia
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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
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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 mgfor pre-eclampsia/eclampsia
Usually combined with other agents such asbeta blockers
concern for reflex sympathetic tone increase
Most useful in pre-eclampsia and eclampsia
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Drug Therapy Possibilities
Metoprolol (Lopressor), or
Labetalol (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 obstructiveairway disease
Labetalol: both alpha & beta blockade
Most useful in AMI and Unstable angina
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Hypertensive Crisis Management
Avoid crashing BP to hypotensiveor normotensive levels!
Ischemia of vital organs mayresult!
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Hypertensive Crisis Management
Must assure underlying cause ofBP isunderstood
HTN may be helpful to the patient
Aggressive treatment of HTN may be harmful
What patients may have HTN as acompensatory mechanism?
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Syncope
Sudden, temporary loss of
consciousness caused by
inadequate cerebral perfusion
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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)
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Cardiogenic Syncope
Paroxysmal Tachyarrhythmias (atrial or
ventricular)
Bradyarrhythmias Stokes-Adams attack
Valvular disease
especially aortic stenosis Can occur in any position
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Postural Syncope
Due to decreased BP onstanding or sitting up
Orthostatic hypotension
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Postural Syncope
Drugs - usually antihypertensives
Diuretics
Vasodilators
Beta-blockers
Volume depletion
Acute hemorrhage
Vomiting or diarrhea
Excessive diuretic use
Protracted sweating
Neuropathic diseases - diabetes
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Tussitive Syncope
Coughing
Increased intrathoracic pressure
Decreased venous return
Vagal stimulation
Decreased heart rate
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Micturation Syncope
Urination
Increased vagal tone
Decreased cardiac output
Frequently associated with
Volume depletion due to EtOH Vasodilation due to EtOH
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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?
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Syncope Management
Supine position - possibly elevate lowerextremities
Do not sit up or move to semi-sitting
position quickly Airway - oxygen via NRB
Loosen tight clothing
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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
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Peripheral Vascular Disease
Peripheral Atherosclerotic Disease
Deep Vein Thrombophlebitis
Varicose Veins
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Peripheral Atherosclerosis
Gradual, progressive disease
Common in diabetics
Thin, shiny skin Loss of hair on extremities
Ulcers, gangrene may develop
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Peripheral Atherosclerosis
Intermittent Claudication
Deficient blood supply in exercising
muscle Pain, aching, cramps, weakness
Occurs in calf, thigh, hip, buttocks onwalking
Relieved by rest (2 - 5 minutes)
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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
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Deep Vein Thrombophlebitis
Inflammation of lower extremities, pelvicveins with clot formation
Usually begins with calf veins
Precipitating factors
Injury to venous endothelium
Hypercoagulability
Reduced blood flow (venous stasis)
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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 (Homans sign) Palpable cord in calf
clotted veins
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Deep Vein Thrombophlebitis
May progress to pulmonary
embolism!!!
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Varicose Veins
Dilated, elongated, tortuous
superficial veins usually in
lower extremities
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Varicose Veins
Causes
Congenital weakness/absence ofvenous valves
Congenital weakness of venous walls
Diseases of venous system (Deepthrombophlebitis)
Prolonged venostasis (pregnancy,standing)
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Varicose Veins
Signs/Symptoms
May be asymptomatic
Feeling of fatigue, heaviness Cramps at night
Orthostatic edema
Ulcer formation
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Varicose Veins
Rupture may cause severebleeding
Control with elevation anddirect pressure
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Aortic Aneurysm
Localized abnormal dilation ofblood vessel, usually an artery
Thoracic
Dissecting
Abdominal
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Thoracic Aortic Aneurysm
Usually results from atherosclerosis
Weakened aortic wall bows out -
lumen distends
Most common in males age 50 - 70
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Thoracic Aortic Aneurysm
Sign/Symptoms
Dyspnea, Cough
Hoarseness/Loss of voice
Substernal/back pain or ache
Lower extremity weakness/paresthesias
Variation in pulses, BP betweenextremities
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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, Marfans syndrome
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Dissecting Aortic Aneurysm
Signs/Symptoms
Sudden ripping or tearing pain
anterior chest or between shoulders
May extend to shoulders, neck, lower back, andabdomen
Rarely radiates to jaw or arms
Pallor, diaphoresis, tachycardia,
dyspnea
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Dissecting Aortic Aneurysm
Signs/Symptoms
Normal or elevated upper extremity BPin shocky patient
CHF if aortic valve is involved
Acute MI if coronary ostia involved
Rupture into pericardial space or chest
cavity with circulatory collapse
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Dissecting Aortic Aneurysm
Signs/Symptoms
CNS symptoms from involvement ofhead/neck vessel origins
Chest pain + neurological deficit =aortic aneurysm
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Abdominal Aortic Aneurysm
Also referred to as AAA or
Triple A
Usually results from atherosclerosis
White males age 50 - 80
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Abdominal Aortic Aneurysm
Signs/Symptoms
Usually asymptomatic until large enough to bepalpable as pulsing mass
Usually tender to palpation
Excruciating lower back pain from pressure onlumbar vertebrae
May mimic lumbar disk disease or kidney stone
Leaking/rupture may produce vascularcollapse and shock
Often presents with syncopal episode
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Abdominal Aortic Aneurysm
Signs/Symptoms
May result in unequal lower extremitypulses or unilateral paresthesia
Urge to defecate caused byretroperitoneal leaking of blood
Erosion into duodenum with massive GI
bleed
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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
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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
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Pulmonary Embolism
Pathophysiology
Pulmonary artery blocked
Blood:Does not pass alveoli
Does not exchange gases
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Causes
Blood clots =most common cause
Virchows Triad
Venous stasis bed rest, immobility,casts, CHF
Thrombophlebitis vessel wall damage
Hypercoagulability Birth control pills,
especially with smoking
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Causes
Air
Amniotic fluid
Fat particles
Long bone fracture more quickly
splinted, less chance of fat emboli
Particulates from substance abuse
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Signs/Symptoms
Small Emboli
Dyspnea
Tachycardia
Tachypnea
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Signs/Symptoms
Larger Emboli
Respiratory difficulty
Pleuritic pain
Pleural rub
Coughing
Hemoptysis
Localized Wheezing
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Signs/Symptoms
Very Large Emboli
Respiratory distress
Central chest pain
Distended neck veins
Acute right heart failure
Shock
Cardiac arrest
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Signs/Symptoms
There are NO findings specific
to pulmonary embolism
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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
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Pulmonary Embolism
If the patient is alive when youget to them, that embolus isnt
going to kill them,
BUT THE NEXT ONE THEY
THROW MIGHT!!!
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