Hypertension and
Peripheral Vascular Disease
Terry White, MBA, BSN
Hypertension
Resting BP consistently >140
systolic or >90 diastolic
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

Types
 Primary
(essential) hypertension
 Secondary hypertension
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

Secondary Hypertension
 10
- 15% of hypertensives
 Increased BP secondary to another
disease process
Secondary Hypertension

Causes:
•
•
•
•
•

Renal vascular or parenchymal disease
Adrenal gland disease
Thyroid gland disease
Aortic coarctation
Neurological disorders
Small number curable with surgery
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

Hypertension Pathology
Coronary atherosclerosis  AMI
 Cerebral atherosclerosis  CVA
 Aortic atherosclerosis  Aortic
aneurysm
 Retinal hemorrhage  Blindness

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.
HTN Medical Management

Life style modification
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•
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Weight loss
Increased aerobic activity
Reduced sodium intake
Stop smoking
Limit alcohol intake
HTN Medical Management

Medications
•
•
•
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Diuretics
Beta blockers
Calcium antagonists
Angiotensin converting enzyme
inhibitors
• Alpha blockers
HTN Medical Management
Medical management prevents or
forestalls all complications
Patients must remain on drug
therapy to control BP
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
Hypertensive Crisis
Acute life-threatening increase
in BP
Usually exceeds 200/130
Hypertensive Crisis


Few Hypertensive Conditions are
“Emergencies”
Emergent Hypertensive Conditions include:
• encephalopathy (CNS sx/sx)
• eclampsia
• when associated with
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AMI or Unstable angina
Acute renal failure
Intracranial injury
Acute LVF
Aortic dissection
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
Signs/Symptoms



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Restlessness,
confusion, AMS
Vision disturbances
Severe headache
Nausea, vomiting




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Seizures
Focal neurologic
deficits
Chest pain
Dyspnea
Pulmonary edema
Hypertensive Crisis Can Cause
CVA
 CHF
 Pulmonary edema
 Angina pectoris
 AMI
 Aortic dissection

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
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
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
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
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
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
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 obstructive
airway disease
• Labetalol: both alpha & beta blockade
• Most useful in AMI and Unstable angina
Hypertensive Crisis Management
Avoid crashing BP to hypotensive
or normotensive levels!
Ischemia of vital organs may
result!
Hypertensive Crisis Management
assure underlying cause of BP is
understood
Must
•HTN may be helpful to the patient
•Aggressive treatment of HTN may be harmful
What patients may have HTN as a
compensatory mechanism?
Syncope
Sudden, temporary loss of
consciousness caused by
inadequate cerebral perfusion
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)
Cardiogenic Syncope
Paroxysmal Tachyarrhythmias (atrial or
ventricular)
 Bradyarrhythmias

• Stokes-Adams attack

Valvular disease
• especially aortic stenosis

Can occur in any position
Postural Syncope
Due to decreased BP on
standing or sitting up
Orthostatic hypotension
Postural Syncope

Drugs - usually antihypertensives
• Diuretics
• Vasodilators
• Beta-blockers

Volume depletion
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Acute hemorrhage
Vomiting or diarrhea
Excessive diuretic use
Protracted sweating
Neuropathic diseases - diabetes
Tussitive Syncope
 Coughing
 Increased
intrathoracic pressure
• Decreased venous return
 Vagal
stimulation
• Decreased heart rate
Micturation Syncope
 Urination
 Increased
vagal tone
• Decreased cardiac output
 Frequently
associated with
• Volume depletion due to EtOH
• Vasodilation due to EtOH
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?

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

Syncope Management

Vital signs, Focused Hx & Physical exam
• Assess for injuries sustained in fall
• Attempt to identify cause

Based on history/physical, Consider:
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ECG Monitor
Blood glucose check
Vascular access
Transport for further evaluation
Peripheral Vascular Disease
Peripheral Atherosclerotic Disease
Deep Vein Thrombophlebitis
Varicose Veins
Peripheral Atherosclerosis
Gradual, progressive disease
 Common in diabetics
 Thin, shiny skin
 Loss of hair on extremities
 Ulcers, gangrene may develop

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)
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
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)
Deep Vein Thrombophlebitis

Signs/Symptoms
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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
Deep Vein Thrombophlebitis
May progress to pulmonary
embolism!!!
Varicose Veins
Dilated, elongated, tortuous
superficial veins usually in
lower extremities
Varicose Veins

Causes
• Congenital weakness/absence of
venous valves
• Congenital weakness of venous walls
• Diseases of venous system (Deep
thrombophlebitis)
• Prolonged venostasis (pregnancy,
standing)
Varicose Veins

Signs/Symptoms
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May be asymptomatic
Feeling of fatigue, heaviness
Cramps at night
Orthostatic edema
Ulcer formation
Varicose Veins
Rupture may cause severe
bleeding
Control with elevation and
direct pressure
Aortic Aneurysm
Localized abnormal dilation of
blood vessel, usually an artery
Thoracic
Dissecting
Abdominal
Thoracic Aortic Aneurysm
 Usually
results from atherosclerosis
 Weakened aortic wall bows out lumen distends
 Most common in males age 50 - 70
Thoracic Aortic Aneurysm

Sign/Symptoms
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•
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Dyspnea, Cough
Hoarseness/Loss of voice
Substernal/back pain or ache
Lower extremity weakness/
paresthesias
• Variation in pulses, BP between
extremities
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

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
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
Dissecting Aortic Aneurysm

Signs/Symptoms
• CNS symptoms from involvement of
head/neck vessel origins
• Chest pain + neurological deficit =
aortic aneurysm
Abdominal Aortic Aneurysm
 Also
referred to as “AAA” or
“Triple A”
 Usually results from atherosclerosis
 White males age 50 - 80
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
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
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
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
Pulmonary Embolism
 Pathophysiology
• Pulmonary artery blocked
• Blood:
– Does not pass alveoli
– Does not exchange gases
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
Causes
 Air
 Amniotic
fluid
 Fat particles
• Long bone fracture – more quickly
splinted, less chance of fat emboli
 Particulates
from substance abuse
Signs/Symptoms
 Small
Emboli
• Dyspnea
• Tachycardia
• Tachypnea
Signs/Symptoms
 Larger
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Emboli
Respiratory difficulty
Pleuritic pain
Pleural rub
Coughing
Hemoptysis
Localized Wheezing
Signs/Symptoms
 Very
•
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Large Emboli
Respiratory distress
Central chest pain
Distended neck veins
Acute right heart failure
Shock
Cardiac arrest
Signs/Symptoms
There are NO findings specific
to pulmonary embolism
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
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!!!