CVT 100 #8 Physics PP Pathology Flashcards
The usual complication of atherosclerotic obstruction of coronary arteries:
myocardial infarction(heart attack)
Infarct:
tissue death due to ischemia
The usual complication of plaque in carotid arteries:
CVA (stroke)—cerebrovascular infarctiondue to flow restriction and/orembolic activity(brain infarction)
1 killer in the U.S is
M.I. is the #1 killer in the U.S
3 killer in the U.S. is
Stroke is the #3 killer.
Another complication:Aneurysm
Weakening and bulging of the cardiac or arterial wall.
Can be due to infarcted tissue, atherosclerotic degeneration, infection, or congenital weakness.
Aneurysm results when
the wall can no longer provide the tensile strength—the tension— to withstand pressure.
Law of LaPlace:
variables that influence wall tension
T oc P x d
Wall tension oc pressure x diameter
The larger the diameter,
the more tension is required to sustain a given pressure.
Cancel units
dynes x cm —> dynes
——— ——-
cm^2 cm
In the vascular system:
Aorta ____cm
Pressure:____mmHg
Wall tension: _______ dynes/cm
Aorta (2 cm)
Pressure: 100 mmHg
Wall tension: 170,000 dynes/cm
In the vascular system:
Capillary ____ cm
Pressure: ___ mmHg
Wall tension: ____ dynes/cm
Capillary (.0008 cm)
Pressure: 30 mmHg
Wall tension: 16 dynes/cm
Pressure in aorta:_______ times that of capillary
3 or 4 times
Diameter of aorta:_______ times that of capillary
2500 times
Wall tension of aorta:________ times that of capillary
10,000 times
In the body, the mean pressure doesn’t change much—it’s the diameter that changes as the wall weakens, requiring more…
wall tensionto hold things together.(Of course, a hypertensive episode could trigger aneurysm rupture as well…)
T = P * r 100 = 50 x 2 Double the radius: 200 = 50 x 4 Twice as much wall tension needed
Twice as much wall tension needed
Vicious circle:More radius —> more weaknessMore weakness —>
more bulging —> more weakness…etc.(Besides, the more complete form of LaPlace’s equation includes wall thickness, which is reduced with aneurysmal changes.Worse yet.)
Venous side of the circulation has two basic functions:
- Return blood to heart
- Act as reservoir of blood
2/3 to 3/4 of body’s blood is in the venous reservoir at rest
Two functions of the venous reservoir:
- Provide increased flow during exercise
2. Provide volume to the core circulation in the event of severe hemorrhage
Two venous pools:
- Peripheral venous pool
2. Central venous pool(thoracic veins, vena cavae, and RA)
Compliance:
Compliance = ∆ volume
—————-
∆ internal pressure
Ability to expand and contain more volumewith little pressure increase.
Veins are compliant because
of normally semi-collapsed state, not because of elasticity.
Veins can hold much more volume before
pressure increases significantly
Volume up 250% with only0 – 15 mmHg increase in pressure
Veins:
Thin-walled
Less elastin and smooth muscle in the media compared to arteries
Easily collapsed by extrinsic pressure
Work muscles:
Collapse veins, sending bloodback to heart
This increases C.O., sending more nutrients to working muscles
Venous return:
Only about 15 mmHg pressure gradient to move blood back.
Need other sources of energy to get blood back to RA.
Also, must overcome HYDROSTATIC PRESSURE(fluid not moving):
gravity pulling on column of fluid
Potentially about 90 mmHg in standing person
Five mechanisms to aid venous return:
- Venous valve
- Skeletal muscle pump
3. Respiratory pump - Cardiac suction effect
- Vasomotor tone
One-way valves ensure that
blood can move only to heart
Closed by pressure gradient to prevent backflow
Presence of valves breaks upcolumn of fluid
Valves are sparse in femoral/popliteal veins,numerous in calf veins—why?
a
Muscle pump:“Peripheral heart”
Contraction squeezes veins, sending blood toward heart
Relaxation “pulls” blood from muscular veins and superficial veins
Respiratory pump
Inspiration:
Expiration:
Inspiration: lower pressure in thoracic cavity,higher pressure in abdominal cavity
Expiration: higher pressure in thoracic cavity,lower pressure in abdomen
Low intrathoracic pressure on inspiration increases flow from
brachiocephalic and abdominal veins
Lower intra-abdominal pressure on expiration allows flow from
lower extremities to resume
Valsalva maneuver:
Big breath in,hold breath,bear down.
Increases pressure in both thoracic and abdominal cavities, so venous return is slowed or stopped everywhere.
Cardiac suction effect:
Atrioventricular ring pulls down during systole, lowering intra-atrial pressure and encouraging inflow from venae cavae and pulmonary veins
Vasomotor tone:
Physical or emotional stress causes sympathetic nerve changes that cause tensing of venous walls, promoting flow toward heart.
Lower-extremity venous anatomy:
Deep veins (femoral, popliteal, calf)
Superficial veins (greater and lesser saphenous, tributaries)
Perforating veins
LE deep veins:
out of order
Common femoral Superficial femoral Deep femoral (profunda femoris)Popliteal Tibioperoneal trunk Anterior tibial Posterior tibial Peroneal
LE superficial veins:
Great saphenous
Small saphenous
These communicate with deep veins via PERFORATING VEINS, which allow flow only from superficial to deep (see muscle pump)
Venous diseaseAcute vs. chronic
Deep vein thrombosis—important because it can lead to pulmonary embolus(PE)
Virchow’s triad:
- Stasis
- Hypercoagulability
- Vessel wall injury
Stasis:
Blood not moving tends to clot(higher concentration of platelets)
Hypercoagulability:
Some conditions make the blood more likely to clot.(Blood is in continual balance ofclotting vs. not clotting)
Vessel wall injury:
Intima is smooth, tends to repel platelets.Interruption of intimal surface causes platelets to aggregate, which can lead to thrombosis.
DVT is thought to originate often in two places:
- Muscular veins in calf (stasis)
2. Behind valve leaflets(stasis)
Once thrombus gets started, it tends to Typical DVT fills major veinsall the way up to femoral or even iliac veins.
propagate—grow to fill vein lumen,extend along the vein.
Typical DVT fills
major veinsall the way up to femoral or even iliac veins.
Fresh thrombus is more
fragile, poorly adherent to vein wall, more likely to break off and embolize to pulmonary arteries.
DVT symptoms:
SwellingPainAchingWarmth of limbSometimes no symptoms…
Single condition causingchronic venous symptoms:venous hypertensiondue to
- Venous valvular insufficiencyand/or
2. Chronic venous obstruction
Diagnosis of DVT
Now we do venous imagingwith ultrasound
Old way: venous outflow plethysmography(along with CW venous Doppler)
Venous imaging:
Scan in short axis.
Push with probe every 2-3 cm to make walls meet (coapt).
This demonstrates absence of thrombus.
SFA and SFV
Acute thrombus:
Dark intraluminal echoes
Homogeneous echoes
Distension of vein
Poor wall attachment (“tail”)
Chronic thrombus:
Bright intraluminal echoes Heterogeneous echoes Possibly retracted, small lumen Well attached to wall May see recanalization, collaterals Vein may be invisible
Doppler is also part of the venous duplex exam—assess for
normal or abnormal venous flow character.
Doppler is also used to evaluate for
valvular insufficiency:
Try to provoke backflow (reflux)with proximal and distal compression maneuvers.
Plethysmography: recording oflimb volume changes Three types: 1. Pneumoplethysmography 2. Strain gauge 3. Impedance plethysmography
With all three types:Inflate thigh cuff to 50 mmHg to pool blood in the calf veins.Monitor calf blood volume for increase,then for rapid decrease when thigh cuff is deflated.(Capacitance/outflow)
- Pneumo (air cuff):Calf cuff connected to pressure transducerResponds to increase of calf circumference due to pooling of blood
- Strain gauge:Elastic tube with mercury(conductive fluid)Calf circumference increase stretches the strain gauge and increases electrical resistance.
- Impedance:Two electrode bands on calfTiny current runs between the electrodesBlood is a good conductor,so more blood means less impedance(electrical resistance)
