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Cardio Block > Peripheral Vascular Disease > Flashcards

Peripheral Vascular Disease Flashcards

1
Q

What are the typical symptoms of acute extremity arterial insufficiency?
Which is the most common presenting symptom?

What is the hierarchy of these symptoms?

A
  1. Pallor
  2. Pain **most common
  3. Poikilithermia (cool)
  4. Pulselessness
  5. Paresthesia
  6. Paralysis (partial or full)

The first 4 have some collateral flow. Paresthesia and paralysis (neurological symptoms are indicative of nerve ischemia and insufficient collateral flow.

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2
Q

What are the 3 main cause of acute arterial insufficiency?

A
  1. atherothrombosis - progressive decrease in flow
  2. arterial embolism (85% from heart, 15% aneurysms)
  3. trauma (blunt, penetrating, iatrogenic)
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3
Q

When there is no collateral flow, how long do you have to restore flow?

A

4-6 hours. After this range, there is bad viability for the limb (high risk of amputation)

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4
Q

Why do some patients present with milder symptoms of acute arterial insufficiency than others?
How will these patients present?

A

They have sufficient collateral circulation to maintain the extremity viability despite the major arterial occlusion. (less volume can go through the collaterals so this is a temporary fix)

They will present with symptoms of chronic extremity arterial insufficiency like past intermittent claudication.

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5
Q

What is a clinical indication that arterial insufficiency has caused ischemia that has progressed to the point of irreversible neurological insult?

A
  1. Persistent pain
  2. acute changes in cutaneous sensation
  3. muscular weakness
  4. paralysis

Most ominous is muscle weakness

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6
Q

What are the 3 presentations of chronic arterial insufficiency?
Which are limb threatening?

A
  1. intermittent claudication- mild to moderate arterial insufficiency- functional disability- not limb threatening
  2. rest pain - severe arterial insufficiency- limb threatening
  3. ischemic tissue loss (gangrene, non-healing ulcers)- severe arterial insufficiency- limb threatening
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7
Q

How is the pain associated with intermittent claudication described?
What body area is affected most?
When does this pain occur?

A

muscular aching/ cramping in the calf, thighs, butt that occurs when walking and is relieved by rest.
It can be consistently reproduced (meaning that if a patient gets this cramp on the third flight of stairs, they will continue to get the same pain every day)

IT NEVER OCCURS AT REST.

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8
Q

A patient experience muscle aching/cramps in his buttocks while laying in bed. What is the most likely cause?

A

Restless leg syndrome or nocturnal cramping.

NOT intermittent claudication, because it is occurring at rest and IC NEVER occurs at rest

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9
Q

What is the pathophysiology of intermittent claudication?

A

Blood flow is adequate to meet the resting metabolic needs of the muscles.
In exercise, the blood flow cannot increase because of the occlusive disease.
This leads to the muscle doing anaerobic glycolysis and generating lactic acid which causes the burning pain

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10
Q

What is the risk of amputation if no intervention is taken for:

  1. intermittent claudication
  2. rest pain
  3. ischemic tissue loss
A
  1. 5% at 5 year
  2. 50% at 1 year
  3. 75% at one year
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11
Q

What are symptoms frequently confused with lower extremity chronic arterial insufficiency and intermittent claudication? How do you differentiate each?

A
  1. osteoarthritis - JOINT as opposed to muscle, variability in pain with exercise, occurs at rest
  2. Lumbar neurospinal compression syndrome- postitional changes, starts immediately with walking
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12
Q

Why is it so important to be able to accurately diagnose ischemic rest pain?

A

It can progress to gangrene and major amputation in high proportions (50%) unless revascularization is undertaken.

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13
Q

How is rest pain described?
Where is the pain?
What aggrevates it and what makes it better?

A

Numb, aching, constant pain that can occur at rest.
“numbness that aches”. can be associated with Paresthesia(burning)
It affects feet, toes, metatarsal heads because rest pain is associated with nerve ischemia and anything downstream will be affected.
It is aggrevated by elevation and is made better with dependency

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14
Q

Why does dependency improve ischemic rest pain?

A

Gravity will slightly increase blood flow to the toes/feet.
The pressure of pressing the foot into the ground will increase venous pressure prolonging RBC time in the capillary.
This allows maximal O2 extraction into the ischemic tissue

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15
Q

What are other disorders that cause pain at rest in the feet that need to be differentiated from ischemic rest pain?

A
  1. Gout - inflamed joint from increased uric acid
  2. peripheral neuropathy- stocking glove, burning pain (alcoholics, diabetics)
  3. metatarsalgia- pain on joint motion
  4. trauma- history, pain on squeezing
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16
Q

How can ischemic rest pain be differentiated from diabetic neuropathy?

A

Both are associated with numbness, but diabetic neuropathy is associated with:

  1. bilateral
  2. soles of feet
  3. stocking glove
  4. hot or burning
  5. NOT aggrevated by elevation or relieved by dependency
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17
Q

What are the signs of chronic arterial insufficiency?

A
  1. absent pulses
  2. decreased hair growth, shiny thin skin, thick nails (dermal appendages)
  3. muscular atrophy
  4. blanches on elevation and dependent rubor (chronic dilation of skin capillaries)
  5. slow venous refill
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18
Q

What is the system used to record the pulse examination?

A 
\+ = normal palpable pulse 
w= weak pulse 
- = no papable pulse
D= non-palpable pulse heard on Doppler
0= not palpable and not heard on Doppler
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19
Q

How do you feel for the femoral pulses?

A

It is difficult in obese patients, but place fingertips in the depths of the groin crease and palpate upward toward inguinal ligament

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20
Q

How do you palpate the popliteal pulses?

A

It is located between the femoral condyles so have the patient flex the knee and relax the extremity.
“strangle the knee” with thumbs on the knee cap and fingers in the popliteal fossa.

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21
Q

How do you palpate the dorsalis pedis pulse?

A

It is lateral to the extensor tendon of the great toe on the bottom of the foot.
Use the pads of index, middle and ring fingers and counterpress with thumbs to increase sensitivity of the fingers. You don’t use finger tips because you might confuse it with your own pulse.

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22
Q

Why is it better to feel for pulses with pads of fingers instead of fingertips or the thumb?

A

Finger tips and thumbs can be confusing because the examiners pulse can be felt too.
Examiner should palpate their own carotid or temporal for comparison.

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23
Q

How should the patients skin temperature be assessed when suspicious of an acute arterial insufficiency?

A

Examiner should use the backs of fingers and palpate both sides because bilateral coldness is indicative of cold weather or anxiety.

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24
Q

When do abdominal aortic aneurysms usually present to the physician? What are the 3 major symptoms they present with? (AAA rupture triad)
Which is the “diagnostic”: feature?

A

They are usually asymptomatic and clinically silent until they rupture at which point, they present with:

  1. pain- sudden onset, sharp, non-cramping, abdomen, flank, lower back
  2. shock (may not be present in initial stages if its not that much blood loss)
  3. pulsating abdominal mass- diagnostic
25
Q

What is the elective mortality for an aortic aneurysm? What is the emergency mortality?

A

Elective 2-3%

Emergency- 50-75%

26
Q

Currently, how are most AAA discovered? How SHOULD they be discovered?

A

They are usually found on MRI, CT, ultrasound for some other procedure.
They should be found on physical exam because they will be palpable

27
Q

How many patients over 60 do AAA affect?

A

1/20

28
Q

Describe the physical exam for palpating AAA.

A

Have the patients lie on their backs with their knees pulled up to relax their abs. Arms should be at their sides.
Stand on the right side and use finger pads of both hands to explore mid-abdomen region around the umbilicus because this is where abdominal aorta usually branches to iliac .

29
Q

95% of AAA are _______ and 30% involve the ___________________.

A

infrarenal; iliac arteries

30
Q

What is the normal diameter of the aorta?

What size should you operate?

A

Normal = 2cm

Operate over 5 (5.5)

31
Q

How should the pulse of an AAA feel?

How is this different from pulsing of a neoplasm or inflammatory mass?

A

Lateral pulsations on each side of the aorta.
If you feel this, follow up with ultrasound and if still nothing, move to CT.

Inflammatory masses and neoplasms will overlie the aorta and will pulse anteriorly and posteriorly.
Because the AAA is expansile in systole, it will pulsate in all directions, including laterally

32
Q

What is the classic presentation for an aortic dissection?

Where do most begin?

A

Most begin in the thoracic aorta just distal to the origin of the left subclavian artery, although it can be anywhere in the aortic arch.
Presents with anterior chest and/or interscapular “tearing” pain

33
Q

What are the 2 most common etiologies for an aortic dissection?

A
  1. Marfan’s or EDS
  2. severe, poorly controlled hypertension (non-compliance, cocaine/meth use)

(can also be pregnancy)

34
Q

What test is diagnostic for an aortic dissection?

A

CTA which can show the “true” and “false” lumen associated with the dissection

35
Q

What are the 2 Stanford classifications of aortic dissection?
What anatomic demarcation determines type?
Are they usually retrograde or anterograde?
Which is usually fatal and requires emergency surgery to correct?

A

Type A are proximal to the left subclavian artery and usually is retrograde (goes toward the ascending aortic arch and heart). It can be fatal and requires emergency surgery.

Type B is distal to the left subclavian artery and extends distally. It is usually more insidious and does not require emergency surgery.

36
Q

What three structures do Type A aortic dissections have a high risk of dissecting into? What are the repercussions of each?

A
  1. coronary sinus- acute left main coronary occlusion and sudden death
  2. aortic valve annulus- acute AR
  3. pericardium- acute cardiac tamponade
37
Q

What surgery is done for type A aortic dissections?

A

cardiopulmonary bypass- the aortic root is replaced just distal to the aortic vale

38
Q

What are the 2 short term risks of type B aortic dissections?

A
  1. malperfusion syndromes- physical obstruction of an aortic branch artery or compression of true lumen
  2. rupture
39
Q

What is a malperfusion syndrome when associated with aortic dissection?
What 3 arteries area most frequently affected?
What would be heard on chest examination ?

A

The dissection physically obstructs an aortic branch or compresses the true lumen so that the true lumen cannot perfuse adjacent organs.

  1. mesenteric - gut ischemia
  2. renal- insufficiency (secondary hypertension)
  3. iliac - leg ischemia

You would hear bruit which indicates turbulent flow in aortic branch vessels

40
Q

What is the most common physical exam finding for an uncomplicated aortic dissection?

A

There will be no exam findings except for the severe elevation in BP that incited the dissection to begin with.

41
Q

What is it important to carefully auscultate the heart when an aortic dissection is suspected?

A

You need to rule out an aortic regurgitation murmur that could be attributed to a retrograde tear into the aortic valve annulus

42
Q

What physical exam finding is present if the aortic dissection compromises flow to the left subclavian artery?
What happens if it compromises iliac artery flow?

A

LS- absent pulses in the left arm

Iliac- absent pulses in the corresponding leg

43
Q

What is the diagnostic test of choice for an aortic dissection?

A
  1. CTA (non-contrast CT does not visualize the true and false lumens)
    if this is not available:
  2. TEE or TTE which can visualize dissections of the thoracic aorta (TEE are inserted in the esophagus adjacent to the descending aorta and posterior to the heart)
44
Q

What do you rely on most for the diagnosis of carotid artery occlusive disease?

A

clinical history - this will help you est. the type and location of cerebral ischemia

45
Q

What can carotid artery occlusive disease lead to?

How can it be prevented?

A
  1. TIA
  2. Stroke

Prevented by carotid endarterectomy

46
Q

What is a transient ischemic attack (TIA)?
How long do they typically last?
Is there permanent neurological damage?
What does an MRI show after a TIA?

A

brief episodes (less than 24hrs) of focal loss of brain function due to ischemia that can be localized to one vascular system (left or right carotid or vertebral systems)

They typically last 2-15 minutes after which they resolve with complete neurological recovery.
Brain imaging shows no evidence of a cerebral infarct.

47
Q

What are the signs and symptoms of a left carotid system TIA?

A
  1. motor dysfunction of right extremities
  2. loss of vision in left eye (amaurosis fugax) and sometimes right
  3. numbness and sensory loss in right extremities
  4. aphasia- language disturbance
48
Q

What signs and symptoms are associated with TIA produced by right carotid occlusive disease?

A
  1. motor dysfunction on left
  2. sensory dysfunction on left
  3. amaurosis fugax on right
  4. only get aphasia if the person is left handed
49
Q

What are the signs and symptoms of a TIA in the vertebral-basilar system?

A

Bilateral symptoms:

  1. motor dysfunction in a combo of upper and lower extremities on left and right
  2. sensory loss on both sides
  3. loss of vision in one or both homonymous visual fields
  4. loss of balance, vertigo, cerebellar problems, double vision
50
Q

What is amaurosis fugax?
How long does it last?
What information is important to gather from the patient?

A

Monocular blindness that occurs during transient interruption to retinal blood flow from an embolic event.

  • lasts seconds to minutes
  • total blindness or “descending curtain shade”

Determine which eye is being effected to narrow the location of the emboli

51
Q

What are the 4 pathophysiologic basis of ischemia with carotid bifurcation plaques?

A
  1. atheroembolism
  2. platelet-fibrin emboli
  3. carotid thrombus
  4. severe stenosis–> reduced flow
52
Q

Why do you take bilateral upper extremity BP in a patient? Differences in left and right above what is considered abnormal?

A

You take bilateral BP to rule out brachiocephalic occlusive disease.
Greater than 15-20 is considered abnormal and be a sign of right or left subclavian artery occlusive disease.

53
Q

What is the most common cause of pulse asymmetry or diminished neck pulses?

A

obesity or short stout necks in muscular ppl

54
Q

Where is the bifurcation of the carotids anatomically?

A

It is usually at the angle of the mandible where the internal carotid dives deep and is no longer palpable.
The neck veins are common carotid/

55
Q

Where is most carotid stenosis located? What should you do in the physical exam to check for this?

A

Most stenosis occurs at the bifurcation of the carotids so you should auscultate at the angle of the mandible to listen for bruits (indicative of turbulent flow through the stenosis)

56
Q

What two situations would cause bruits to be heard in the neck?
What technique allows differentiation?

A
  1. Carotid artery occlusive disease
  2. valvular heart disease

Start listening at the angle of the mandible and move the stethoscope downward along the anterior border of the SCM.
If the bruit gets louder, it is probably valvular.

57
Q

What should you do if you find a carotid bruit?

A

Bruits are non-specific and have a poor correlation between intensity and degree of stenosis.
(very advanced stenosis doesn’t have a bruit)

If the patient has TIA related symptoms order angio, carotid duplex ultrasonography, MRA

58
Q

What is CEA?

Why is it preferable to balloon angiography for a carotid occlusive disease?

A

Carotid endarterectomy where you remove plaque. This is dangerous because the carotid is near a lot of cranial nerves etc.

It is preferred to balloon because this can dislodge emboli and actually cause a TIA/stroke

59
Q

What is a Hollenhorst Plaque?

A

small emboli lodged at bifurcations of retinal artery branches associated with carotid artery occlusive disease

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