Hypertension and Peripheral Vascular Disease

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Hypertension and Peripheral Vascular Disease

• Terry White, MBA, BSN

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Hypertension

• Resting BP consistently gt140 systolic or gt90
  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 gt 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 positive family
  history
• Worsened by increased sodium intake, stress,
  obesity, oral contraceptive use, or tobacco 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, sclerosis of
  arteriolar walls ? narrowing of vessels ?
  decreased blood flow to major organs
• Left ventricular overwork ? hypertrophy, 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 enzyme inhibitors
• Alpha blockers

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HTN Medical Management

• Medical management prevents or forestalls all
  complications
• Patients must remain on drug therapy 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 gt 115 mm Hg w/o evidence of
  end-organ injury
• Mild Hypertension
• DBP gt 90 but lt 115 mm Hg w/o symptoms
• Transient Hypertension
• elevated due to an unrelated underlying condition

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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 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

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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 targeting BP
  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 patient chew
• Used less frequently today! Frequently in past!
• Concern for rapid reduction of BP resulting in
  organ ischemia

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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 gt 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

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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

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Hypertensive Crisis Management

• Avoid crashing BP to hypotensive or normotensive
  levels!
• Ischemia of vital organs may result!

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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?
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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 on standing 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 lower
  extremities
• 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 on walking
• 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, pelvic veins
  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 of venous valves
• Congenital weakness of venous walls
• Diseases of venous system (Deep thrombophlebitis)
• 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 severe bleeding
• Control with elevation and direct pressure

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Aortic Aneurysm

• Localized abnormal dilation of blood 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 between extremities

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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, and
  abdomen
• Rarely radiates to jaw or arms
• Pallor, diaphoresis, tachycardia, dyspnea

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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

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Dissecting Aortic Aneurysm

• Signs/Symptoms
• CNS symptoms from involvement of head/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 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

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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

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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 you get to them,
  that embolus isnt going to kill them,
• BUT THE NEXT ONE THEY THROW MIGHT!!!