PERIPHERAL VASCULAR SYSTEM

I. ANATOMY and VENOUS SYSTEM REVIEW

Arteries & Veins 3 layers tunica media > in arteries flow through a

vessel directly

proportional to the fourth power of the radius

Tunica intima - single continuous lining of endothelial cells- synthesizes regulators of thrombosis

( prostacyclin, plasminogen activator etc), vasoconstrictors ( endothelin) etc.

Tunica media - composed of smooth muscle cells that dilates and contract to accommodate BPTunica adventitia – connective tissue containing nerve fibers

Venous Returna)Skeletal muscle pump

Muscular contraction squeezes adjacent veins milking action

Valves prevent opposite flowb)Respiratory Movements

Diaphragm contraction exerts pressure in abdomen and decrease pressure in thoracic cavity

Blood moves to area of lower pressure in thoraxc) Constriction of veins

Sympathetic stimulation causes contraction of the smooth muscle walls of veins

d)Gravity

• Large/ elastic arteries – aorta, pulmonary, common carotid• Medium sized/ muscular arteries- coronary and renal • Small arteries• Arterioles – where resistance to blood flow occurs primarily

Negative Effects on Venous Returna) Increasd intrathoracic pressureb) PEEP (positive end expiratory pressure) /CPAP

(Continuous Positive Airway Pressure) /BiPAP (Non-invasive respiratory Support)

Arterial Resistance (afterload) a) Blood Pressure = cardiac output x systemic vascular resistance = (stroke volume x heart rate) x systemic vascular resistance

b) Systemic vascular resistance Vasoconstriction- Sympathetic NS effects- Medications (prescription, non-prescription,

recreational)

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PERIPHERAL VESSELSChapter 12: Peripheral Vascular System ( Bate’s 10thed)

Lecturer: Dr. GuzmanDate of lecture: August 26, 2010

Peripheral Vascular System

Subclavian

Axillary

Brachial

Radial

Ulnar

Aorta

Femoral

Iliac

Carotid

Popliteal

Dorsal PedalPosterior Tibial

Innominate

Major Arteries

Peripheral Vascular SystemInternal Jugular

Subclavian

Axillary

Iliac

Femoral

Saphenous

External Jugular

Superior Vena Cava

Inferior Vena Cava

Major Veins

Atheroma - begins in the intima as lipid filled foam cells then form fatty streaksComplex atheroma- thickened asymmetric plaques that narrows lumen of blood vessels

Superficial Venous System System

- RAAS- mechanisms Atherosclerosis –deposition of cholesterol in the

walls of the arteries narrowing/blockage

Peripheral Pulse Sitesa) Temporal - lateral to eye orbitb) Carotid – medial to below angle of jawc) Brachial- medial to biceps tendond) Radial – thumb side of wriste) Ulnar – little finger side of wristf) Femoral- below inguinal ligamentg) Popliteal - behind kneeh) Dorsalis Pedis – top of footi) Posterior Tibial- behind medial malleolus

Perforators Connect superficial to deep veins Locations

- Proximal thigh - Hunterian - Distal thigh - Dodd’s - Knee - Boyd’s

- Ankle/Calf - Cockett’s Incompetent perforators often source of venous stasis

ulcers at medial ankle

A. Normal Venous Anatomy and Function venous system of the lower extremities is a complex

of thin-walled and low-pressure vessels that return blood back to the heart

.Transport of blood is facilitated by1) Low central pressures in the chest cavity promoting

blood return to the heart.2) Active propulsion of blood by muscular contraction in the

calves and thighs functions as a “peripheral heart” 3) Venous valves prevent the backward flow of blood.

3 TYPES OF VEINS OF THE LOWER EXTREMITIES

1) Deep Venous System surrounded by muscular tissue that function as

part of the “peripheral heart” include the gastrocnemius, peroneal and tibial

veins in the calf, the popliteal veins, and the femoral veins in the thigh.

ultimately responsible for most of the venous drainage from the lower extremities.

Through active muscular contraction + normal venous valvular function deep veins provide the only ACTIVE PROPULSION of venous return to the heart

2) Superficial Venous System GREATER SAPHENOUS VEIN ascends along

the inner aspect of the calf and thigh and drains into the femoral vein at the groin, through the saphenofemoral junction.

Major tributaries (branches) include the posterior arch vein in the calf, the posteromedial vein and anterolateral vein in the thigh and the inferior epigastric vein in the groin.

LESSER SAPHENOUS VEIN lies on the posterior aspect of the calf and drains into the popliteal venous system behind the knee, through the saphenopopliteal junction.

May also drain into other venous channels, including the vein of Giacomini, drains into the greater saphenous vein.

3) Perforating Venous System penetrate the fascia and functions to divert

blood from the superficial to the deep venous system.

communicate between the superficial and deep venous systems.

quite variable in their location and prevalence,

normal venous structures even in the absence of venous disease.

. Classically defined perforating veins include the Hunterian and Dodd perforators in the thigh, the Boyd and Cockett perforators in the calf, and a number of perforators in the foot

II. TYPES OF VENOUS DISEASES

Two Major Types

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Deep Venous System

1) Obstruction less common form caused by directly impeding the

return of blood flow to the heart, either due to intrinsic (inside the vein) or extrinsic (outside the vein) blockages.

a) Intrinsic causes primarily of deep venous thrombosis (DVT), or

blood clots, in the major veins of the thighs and/or pelvis.

b) extrinsic obstruction, either actual or “functional” include large pelvic

tumors, morbid obesity, chronic obstructive pulmonary disease (COPD or emphysema)

some types of heart disease such as severe tricuspid valve insufficiency or advanced congestive heart failure

2) Venous insufficiency , or incompetence, more common form it involves a failure of the venous system can be due to a failure of the muscular “peripheral

heart”, but is more frequently due to structural failure of the veins.

Structural failure of veins is either due to a) Secondary venous insufficiency most commonly due to injury from a previous

episode of deep venous thrombosis (DVT),

b) Primary venous insufficiency much more common cause of venous vascular

disease. due to disease of the veins not from an outside

cause weakness and failure of the vein walls and venous valves.

frequently associated with a hereditary pattern of involvement.

In female patients, it may also be associated with multiple pregnancies.

frequently associated with body habitus (obesity), work environment and exercise habits

III. VARICOSE VEINS EXAM

General considerations

2 sets of veins, deep and superficial. " Flow is superficial veins to deep veins. Arise by: calf pumps up, pushing blood out into superficial

veins. Superficial veins then dilate, spreading their own valves apart, so the superficial veins become torturous.

Walking with a pressure tourniquet on leg – competent valves gets better as walk. – incompetent valves between deep and

superficialno effect.

– DVT gets more painful as walk [since exit is blocked].

Can optionally use a Doppler after physical examination.

Management: graduated compression stockings or surgery.

Surgery complications: infection from groin crease, hematoma from strip, scarring, recurrence.

A. History Pain. Possibly hemorrhage or thrombophlebitis. Ask about prior varicose operations and results.

1.) Inspection Pt stands, both legs completely visible. Looking for "dilated, tortuous veins that you will

examine for site of incompetency". Inspect from anterior of thighs to lateral of legs (long

saphenous vein). Inspect back of calves (short saphenous vein). Look for poor skin nutrition:

• Venous ulcers, esp on medial malleolus. • Venous eczema. • Hemosiderin deposition [brown]. • Thin skin.

DDx from femoral hernia, since varicose veins: • Are blue. • Disappear when lie flat. • Show a positive cough impulse.

2.) Palpation Tenderness (thrombophlebitis). Hard (thrombosis). Skin:

• Dermatosclerosis [thick, indurated skin]. • Atrophie blanche [scarred, white skin].

Cough impulse test Pt stands. Doctor’s fingers held over saphenofemoral opening [5

cm below and medial to femoral pulse]. Pt. coughs. If saphenofemoral incompetent, cough makes a fluid

thrill.

Trendelenburg test Evaluate competency of venous valves through

retrograde filling; Test for varicose veins. to find how far up the leg the incompetent valves are.

a) Pt lies flat, leg is elevated to about 90 degreesb) Tie tourniquet around thigh at saphenous opening [5

cm below and medial to femoral pulse] . c) If doctor doesn't have a tourniquet, use 2 fingers

instead. d) Ask Pt to stands , watch for venous filling

Normally the vein should fill from below within 35 seconds with the tourniquet in situ as blood flows though capillary bed into venous system

Rapid filling when saphenous vein is occluded indicate incompetent valves

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Deep Vein Thrombosis venous valves that have been damaged or

destroyed known as the post-phlebitic syndrome associated with venous stasis disease

resulting to changes of the skin at the feet and ankles known as stasis dermatitis

result in open sores, or venous stasis ulcers.

e) Release compression and look for sudden additional venous fillings

Normally there is none, competent valve in the saphenous vein block retrograde flow

INCOMPETENT: sudden gush filling from above when tourniquet is removed incompetent sapheno- femoral valve

When both steps are normal, response is described as negative-negative

Perthes' manoeuvre used to distinguish antegrade flow from retrograde flow

in superficial varicosities. Antegrade flow -- indicator of collateral flow around a deep venous obstruction.

- tourniquet is applied to a varicose leg to compress superficial veins without pressure being applied to the deep vessels. - Patient is then asked to repeatedly stand on tip-toe, activating the calf muscles. - Normally this would empty the varicosities, but in the presence of deep vein obstruction they would paradoxically become congested.

IV. ARTERIAL VESSEL EXAMINATION

A. Grading of peripheral arterial pulse• 4+ - BOUNDING PULSE• 3+ - INCREASED• 2+ - BRISK, EXPECTED• 1+ - DIMINISHED, WEAKER THAN

EXPECTED • 0 - ABSENT, UNABLE TO PALPATE AREAS OF EXAMINATION

Arms Legs Size, Symmetry, Skin color Same Radial, Brachial Pulse Femoral Pulse, Inguinal

o Nodes Epitrochlear nodes Popliteal, Dorsalis pedis,

T Tibial pulse None Perripheral edema ARMS

Inspect both arms- Size, symmetry swelling- Venous pattern- Color of skin and nail beds

Palpate radial pulse- Feel for brachial pulse if arterial

insufficiency( bounding carotid, radial and femoral pulse) is suspect

Feel for epitrocheal nodes

EVALUATING ARTERIAL SUPPLY TO THE HAND Allen Test

Useful to ensure patency of ulnar artery before puncturing radial artery for blood samples

1) Ask patient to make a tight fist, compress both radial and ulnar arteries

2) Ask patient to open the hand in a relaxed position; palm is pale

3) Release pressure over radial artery- the palm and fingers should quickly turn

pink as flow returns

- Delayed flush or no flush indicates partial or complete obstruction of the radial artery

4. Repeat the process, this time removing pressure from the ulnar artery

- Patent ulnar artery, palm flushes within 3-5secs- Return of flow is normally somewhat slower from the ulnar artery, but absence of flush is pathologic.

LEGS Inspects legs from groin/buttocks to feet

- Size, symmetry swelling- Venous pattern- Color of skin and nail beds- Pigmentation, rashes, ulcers

Palpate for superifical inguinal lymph nodes- size, frequency and tenderness

Palpate the femoral, popliteal, dorsalis pedis and posterior tibial pulse- Diminished or absent pulse occlusion

proximally; typically affects all distal pulses- Atherosclerosis most commonly obstructs

circulation of the thigh- Decreased or absent pedal pulses with normal

popliteal and femoral pulses often seen in diabetes mellitus

Note temperature of feet and leg Look for edema/pitting edema

- DVT, extent of edema suggests location of occlusion ( e,g, swollen lower leg/ankle occlusion of popliteal vein)

Inspect saphenous system for varicosities - Ask the patient to stand

B. Palpable Arteries

• Normal pulse pressure: 30 - 40 mm Hg• Wide PP – indications of HPN, AI, PDA, Thyrotoxicosis, AV

Fistula, coarctation of aorta, emotion• Narrow PP - tachycardia, severe AS, ascites, constrictive

pericarditis• Unequal BP in arms - sometimes idiopathic

causes: atherosclerosis of subclavian artery, scalenus anticus syndrome, cervical rib, superior thoracic aperture syndrome, malposition of patient when supine on table after heart surgery

• Diastolic Pressure Sign in AI (Mayne’s Sign) ↓ diastolic BP of ≥ 15 mm Hg when arm is

elevated over the head

C. Arterial Pulses

NORMAL Pulses

Normal Arterial Pulse composed of a swift upstroke to the peak of systolic P,

followed by a secondary smaller upstroke, the Dicrotic wave

Pulsus Bisferiens (Dicrotic Pulse) perceived usually at the carotid artery or by

auscultating the compressed brachial artery normally,

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P produces a knock followed by crescendo-diminuendo systolic bruit ® P abolishes the bruit then the knock dicrotic pulse: double systolic bruit

Duroziez’s sign: systolic - diastolic bruit in free aortic regurgitation, a triple bruit may be

heard

Bounding or Collapsing Pulse (Corrigan Pulse, Water-Hammer Pulse)

may produce pistol - shot sound HPN, thyrotoxicosis, emotional states, AR, PDA,

Arteriovenous fistula

UNEQUAL Pulse - aneurysm, partial obstruction

Arterial Murmur/bruit arterial dilatation, intimal proliferation, arteriosclerotic

plaque, arterial dilatation, arterial aneurysm, congenital arterial constriction

Pistol shot Sound put bell of stethoscope lightly over the artery (femoral)

AR, HPN, thyrotoxicosis, anemia

Duroziez’s Sign compress femoral artery with bell of stethoscope

production of a systolic and a second murmur

AR - also other condition that produce PP

Plateau Pulse (Pulsus Tardus) gradual upstroke, prolonged downstroke, plateaus in

betweenseen in severe AS

Pulsus alternans sign of myocardial weakness with P on cuff: lesser beats ¯ P: beats distinguished from bigeminal rhythm, in

which the intervals between members of a couplet are shorter than between pairs

Pulsus Bigeminus (Coupled Rhythm)

Pulsus Paradoxus normal inspiratory fall of < 10 mm Hg in systolic BP

and accompanying inspiratory fall in venous pressureparadoxical pulse: INSPIRATION: ¯ in arterial BP of ³ 10 mm Hg

- inspiratory venous pressure remains the same orincreases (Kussmaul’s sign)

pericardial effusion, adhesive pericarditis, cardiac tamponade, pulmonary emphysema, severe asthma, para-mediastinal effusion, scleroderma, severe asthma

*** Refer to the 1st handout of CARDIAC PE page 16 for the Table on Abnormalities of Arterial Pulse and Pressure Waves***

V. PERIPHERAL ARTERIAL DISEASE

Peripheral arterial disease (PAD)

clinical disorder in which there is a stenosis or occlusion in the aorta or arteries of the limbs.

Atherosclerosis - leading cause of PAD in patients > 40 years old.

Other causes include thrombosis, embolism, vasculitis, fibromuscular dysplasia, entrapment, cystic adventitial disease, and trauma.

The primary sites of involvement are abdominal aorta and iliac arteries (30% of

symptomatic patients), femoral and popliteal arteries (80–90% of patients), the tibial and peroneal arteries (40–50% of

patients).

Atherosclerotic lesions occur preferentially at arterial branch points, which are sites of

i. increased turbulence,ii. altered shear stress, and iii. intimal injury.

Clinical Evaluation Fewer than 50% of patients with PAD are

symptomatic, although many have a slow or impaired gait. MOST COMMON SYMPTOM: intermittent

claudication,

Symptoms far more common in the lower than in the upper extremities because of the higher incidence of obstructive lesions in the former region.

severe arterial occlusive disease ; resting blood flow cannot accommodate basal nutritional needs of the tissues critical limb ischemia

- Patients will complain of rest pain or a feeling of cold or numbness in the foot and toes.

symptoms frequently occur at night when legs are horizontal

- With severe ischemia, rest pain may be persistent.-

PHYSICAL FINDINGS OF PADa) decreased or absent pulses distal to the obstruction,b) the presence of bruits over the narrowed artery, andc) muscle atrophy.

Increased severity , hair loss, thickened nails, smooth and shiny skin, reduced skin temperature, and pallor or cyanosis are frequent physical signs.

critical limb ischemia, ulcers or gangrene may occur.

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Intermittent claudication, pain, ache, cramp, numbness, or a sense of fatigue in the

muscles; it occurs during exercise and is relieved by rest. site of claudication is distal to the location of the

occlusive lesion example, buttock, hip, and thigh discomfort occur in

patients with aortoiliac disease, whereas calf claudication develops in patients with femoral-popliteal disease

Elevation of the legs and repeated flexing of the calf muscles pallor of the soles of the feet,

-- whereas rubor, secondary to reactive hyperemia, may develop when the legs are dependent.

time required for rubor to develop or for the veins in the foot to fill when the patient's legs are transferred from an elevated to a dependent position is related to the severity of the ischemia and the presence of collateral vessels.

Patients with severe ischemia may develop peripheral edema BECAUSR legs are kept in a dependent position much of the time.

Ischemic neuropathy can result in NUMBNESS and HYPOREFLEXIA

A. Fibromuscular Dysplasia hyperplastic disorder affecting medium-sized and small

arteries. occurs predominantly in females and usually involves

renal and carotid arteries . The histologic classification includes intimal

fibroplasia, medial dysplasia, and adventitial hyperplasia.

B. Thromboangiitis Obliterans (Buerger's disease)

inflammatory occlusive vascular disorder involving small and medium-sized arteries and veins in the distal upper and lower extremities.

develops most frequently in men <40 years. cause of thromboangiitis obliterans is not known, definite relationship to cigarette smoking in patients

with this disorder

clinical features a triad of the ff:: a) claudication of the affected extremity,

- confined to the calves and feet or the forearms and hands because this disorder primarily affects distal vessels

b) Raynaud's phenomenon, and c) migratory superficial vein thrombophlebitis.

severe digital ischemia, trophic nail changes, painful ulcerations, and gangrene may develop at the tips of the fingers or toes.

C. Thoracic Outlet Compression Syndrome symptom complex resulting from compression of the

neurovascular bundle (artery, vein, or nerves) at the thoracic outlet as it courses through the neck and shoulder.

Cervical ribs, abnormalities of the scalenus anticus muscle, proximity of the clavicle to the first rib, or abnormal insertion of the pectoralis minor muscle may compress the subclavian artery, subclavian vein and brachial plexus

thoracic outlet compression syndrome may be divided into arterial, venous, and neurogenic forms.

a) neurogenic thoracic outlet compression - develop shoulder and arm pain, weakness, and paresthesias.

b) arterial compression - experience claudication, Raynaud's phenomenon, and even ischemic tissue loss and gangrene.

c) Venous compression - may cause thrombosis of the subclavian and axillary veins- often associated with effort and referred to as Paget-Schroetter syndrome.

D. Raynaud's Phenomenon

characterized by episodic digital ischemia have sequential development of digital blanching,

cyanosis, and rubor of the fingers or toes following cold exposure and subsequent rewarming.

Emotional stress may also precipitate Raynaud's phenomenon

Classification of Raynaud's Phenomenon• Primary or idiopathic Raynaud's phenomenon:

Raynaud's disease• Secondary Raynaud's phenomenon • Collagen vascular diseases: scleroderma, systemic

lupus erythematosus, rheumatoid arthritis, dermatomyositis, polymyositis

• Arterial occlusive diseases: atherosclerosis of the extremities, thromboangiitis obliterans, acute arterial occlusion, thoracic outlet syndrome

• Pulmonary hypertension • Neurologic disorders: intervertebral disk disease,

syringomyelia, spinal cord tumors, stroke, poliomyelitis, carpal tunnel syndrome

• Blood dyscrasias: cold agglutinins, cryoglobulinemia, cryofibrinogenemia, myeloproliferative disorders, Waldenström's macroglobulinemia

• Trauma: vibration injury, hammer hand syndrome, electric shock, cold injury, typing, piano playing

• Drugs: ergot derivatives, methysergide, -adrenergic receptor blockers, bleomycin, vinblastine, cisplatin •

Raynaud's Disease applied when the secondary causes of Raynaud's

phenomenon have been excluded. patients with Raynaud's phenomenon have Raynaud's

disease. fingers are involved more frequently than the toes.

ARTERIAL ULCERATION typically occurs over the toes, heels, and bony

prominences of the foot. appears “punched out,” well demarcated edges and a

pale, non-granulating, often necrotic base. surrounding skin may exhibit dusky erythema and may

be cool to touch, hairless, thin, and brittle, with a shiny texture.; Gangrene may also occur.

Examination of the arterial system may show a decreased or absent pulse in the dorsalis pedis and posterior tibial arteries.

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DETOX LOUNGE!

- bruits in the proximal leg arteries, indicating the presence of atherosclerosis.

Exhibits reduced capillary refill time. With normal capillary refill, after compression of the

great toe or dorsum of the foot for a few seconds, the skin colour should return to normal in less than two to three seconds.

Delay in return of the normal colour is indicative of vascular compromise.

- delay of more than 10 to 15 seconds in return of colour after raising an ischaemic leg to 45 degrees for one minute (Buerger's test) indicates vascular compromise.

ankle brachial pressure index helps in identifying peripheral vascular disease in the absence of non-compressible vessels resulting from vessel calcification (for example, diabetes) or tissue oedema.

A duplex ( Doppler?) ultrasound scan give info —on arterial occlusion, stenosis, and areas of diffuse and continuous atheromatous disease.

Arteriography - ideal investigation in preoperative planning, allowing direct assessment of the vascular anatomy of the lower limb

ANKLE-BRACHIAL INDEX (ABI) measuring the systolic blood pressure in the brachial

artery and the posterior tibial and/or the dorsalis pedis artery.

. The ABI is the ratio of the ankle systolic pressure to the brachial systolic pressure

RIGHT ABI = highest right avg. ankle pressure ( DP/PT) Highest average arm pressure ( right or left)

LEFT ABI = highest left avg. ankle pressure ( DP/PT) Highest average arm pressure ( right or left)

INTERPRETATION>0.90 ( 0.90-1.30 ) Normal lower extremity blood flow

< 0.89 to > 0.60 Mild PAD< 0.59 to > 0.40 Moderate PAD

< 0.39 Severe PAD

PERIPHERAL CAUSES OF EDEMA

Pitting Edema Chronic Venous

Insufficeincy

Lymphedema

Nature of Edema

Soft Pits on pressure

Soft Pits on pressure; later may become brawny

Soft in early stages then becomes indurated, hard, nonpitting

Skin Thickening

Absent May be present esp. near ankle

Becomes marked

Ulceration Absent Common RarePigmentation Absent Common Absent

Edema of Foot

Present Often present Present including toes

Bilaterality Always Occasionally OftenExamples/ a) ↑ interstitial Chronic Lymph

Mechanism fluid from: legs dependent from prolonged standing;b) CHF c) nephritic syndrome; d) cirrhosis, e) malnutrition

obstruction/ valvular incompetence of deep veins

channels obstructed by tumor, fibrosis, inflammation

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Chronic Arterial Insufficiency

Chronic Venous Insufficeincy

Pain Intermittent claudication progression to pain at rest

Often painful

Mechanism Tissue Ischemia Venous HPNPulses Decreased or absent Normal, difficult to feel

through edemaColor Pale on elevation, dusky

on dependencyNormal or cyanotic on dependency; brown pigmentation chronic

Temperature Cool NormalEdema Absent or mild Present often marked

Skin changes

Trophic changes: thin, shiny, atrophic, loss of hair, nails thickened

Brown pigmentation around ankle, statis dermatitis, thickening of skin

Ulceration Toes or points of trauma on feet

Sides of ankle, esp. medially

Gangrene May develop Does not develop

Let’s review! >>>

Multiple Choice

1. Venous return to the heart is affected by the following exceota. Respiratory movementsb. Gravityc. Skeletal Muscle Pumpd. None of the above

2. Primarily responsible for the active propulsion of venous return to the hearta. Deep veinsb. Perforating veinsc. Superficial veins

3. Ankle-Brachial Index of <0.59 to > 0.40 indicatesa. Mild PADb. Moderate PADc. Severe PAD

4. Clinical features include a triad of claudications involving distal vessels, Raynaud Phenomenonand superficial vein thrombophlebitisa. Fibromuscular Dysplasiab. Buerger’s Diseasec. Raynaud’s Diseased. None of the above

5. Normal pulse pressure isa. 40-60 mmHgb. 60-80 mmHgc. 30-40 mmHgd. 50-70 mmHg

6. This condition exhibits a normal inspiratory fall of ≥10 mm Hg in systolic BP and accompanying inspiratory fall in venous pressurea. Pulsus paradoxusb. Pulsus Bigeminusc. Pulsus Tardusd. Pulsus alternans

7. Wide pulse pressure is indicative of the following excepta. Throtoxicosisb. Coarctation of the aortac. Constrictive pericarditisd. Emotion

8. Negative Trendelenburg test is evident bya. Sudden gush filling of the superficial veins after

tourniquet is removedb. Slow venous filling after tourniquet is removed

9. Grade of +3 in a peripheral arterial pulse is described asa. Boundingb. Increasedc. Brisk, unexpectedd. None of the above

10. Perforator Vein of the Anklea. Hunterianb. Boyd’sc. Dodd’sd. Cockett’s

DISORDER IN THE AMERICAN COURTS

Things people actually said in court, word for word, taken down by court reporters who had the torment of staying calm while these exchanges were actually taking place…

____________________________________ATTORNEY: This myasthenia gravis, does it affect your memory at all?WITNESS: Yes.ATTORNEY: And in what ways does it affect your memory?WITNESS: I forget.ATTORNEY: You forget? Can you give us an example of something you forgot?___________________________________________ATTORNEY: Now doctor, "isn't it true that when a person dies in his sleep, he doesn't know about it until the next morning?"WITNESS: Did you actually pass the bar exam?____________________________________________ ATTORNEY: The youngest son, the twenty-year-old, how old is he?WITNESS: He's twenty, much like your IQ! __________________________________________ATTORNEY: She had three children, right?WITNESS: Yes..ATTORNEY: How many were boys?WITNESS: None.ATTORNEY: Were there any girls?WITNESS: Your Honor, I think I need a different attorney.  Can I get a new attorney?_____________________________________ATTORNEY: How was your first marriage terminated?WITNESS: By death.ATTORNEY: And by whose death was it terminated?WITNESS: Take a guess._____________________________________ATTORNEY: Doctor, how many of your autopsies have you performed on dead people?WITNESS: All of them. The live ones put up too much of a fight.____________________________________And the best for last:ATTORNEY: Doctor, before you performed the autopsy, did you check for a pulse?WITNESS: No.ATTORNEY: Did you check for blood pressure?WITNESS: No.ATTORNEY: Did you check for breathing?WITNESS: No.ATTORNEY: So, then it is possible that the patient was alive when you began the autopsy?WITNESS: No .ATTORNEY: How can you be so sure, Doctor?WITNESS: Because his brain was sitting on my desk in a jar.ATTORNEY: I see, but could the patient have still been alive, nevertheless?WITNESS: Yes, it is possible that he could have been alive

and practicing law. 

☺☺☺

This is going to be my last TRANS for medicine. Hindi dahil ayaw ko na sa MEDICINE o dahil may bitter rivalry kami ni

ziella kay qareem ( isyu!) [ ziella, sayo na si qareem]. It’s simply because I am called for a greater responsibility, haha nagpapaka-superhero. By next sem PEDIA Trans Master na

po ako! Hehe Promoted! BYE MEDICINE… HELLO PEDIA!

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ANSWER

1.D2.A3.B4.B5.C6.A7.D8.B9.B10.D