Volume and Pressure

These two systems works opposite of each toehr and pressure is highest in LEFT VENT

Laminar flow- Serum fluid on outside of lumin that is next to a vessel and all other elements are inside=smooth blood flow

Turbulant blood flow- Eleements are bouncing on walls, elements fall out of soulution and into walls, we can sometimes hear this (murmur) Brewy

Pericardium- fiberous sac

Myocardium- heart muscle

Endocardium- membrane lines heart

Large Mitochondria d/t they wrk hard and use up energy

Small er d/t they are not making anything

• Tiny bit of extracelluar calcium moves into cell as AP begins
• This causes SR to open up and allow larger amounts of CA into intercellular and it hooks up with troponin now becoming thick filament
• Actin and myocin hook up causing muslce to contract
• ATP comes on borred to make power stroke causing mycin to let go
• The filament turns away and muscle moves

• isovolumetric contraction- vessels loaded streatches, greater stretch = greater contraction.
• Ventricels are filled with blood and contract
• Push through tricuspid & mitral valve(AV valves)ist heart sound
• Push through semilunar valves into aorta and pulm artery of heart
• blood flows into lungs and aorta

• ventricals relax pressure on pulm and aortic valve stop they close= 2nd heart sound
• blood enters artia flows thru AV valves into ventricals
• Atria contracts forcing blood into ventricals

• Preload- volume work of heart
• Afterload- Pressure wrk of heart
• Contractility
• HR- determs time in diastole and filling time of ventricle and perfusion of arteries
• Rythem- orderly contraction of myocardium

Parasympathetic

Sympathetic

Medulla

Vegus

Slow hrt

ACH

Explain Sympathetic

Thoracic spinal

Sa, AV myocardium

Increase contractions

Norepi

• Ateries-thick muscle layer easy to control- Left Vent is the pump
• Veins depend on valves, no pump, skeletal muscle provide for blood  flow

• autoregulation- needed for 02 and waste removal, vessel dialates to create more blood flow to the area
• Reactive hyperemia- Increase blood flow after lose of blood flow... example fall asleep on ur arm

• Angio genesis/ collateral cirrculation--- created for over the wall hall
• Microcirculation-- Capillary structure-- Interstitum- alot of fluid protien collogen & fiber way to get stuff to cells that are not directly agains a cappilary.

• The more protien the higher densisty= HDL
• The more lipid the lower densisty= LDL

What is the function of HDL?

• Carry CHO from peripheral circluation back to liver

• High HDL can reabsorb cholesterol out of plaque and reverse artherosclerosis
• HDL returns CHO to liver and excretes it in bile rather then using it to form more LDL

• High diet intac
• Genetic- autosomal dominite trate

• defect in lipoprotiens carrier- can't carry them
• Lack CHO receptor in liver- can't hook up in liver
• Defective CHO metabolism- Can't use them

1. Endothial cell injury- d/t turbulant BF
2. Migration of inflmmatry mediators- macrophages move in and engulf LDL
3. Lipid accumulates and smooth muscle cell proliferate- macrophages moved in and enguled as much lipd as they can and turn into  foam cells and now they can't move but keep forming inflam mediators
4. Platelets form a plaque structure over area- collogen trys to heal cap=more turbulant blood flow- vessel eventually rupture- will move down stream and clog a vessel and anything below this popint will no longer have blood flow

Large lipid core

Thin Fibrous Cap- easy to knock off

Fissured cap- bruise

Inflammation CAP

Superficial endotheial erosion- platelet aggregation

You have a women who c/o pain in LLE

why are these things going on?

• Foot cool and Pale
• Reports Often Red/ warm when sitting
• Pain with walking
• Skin on LLE shinner then RLE

• No BF weak pedal pulse
• BF decreased
• Prostoglandins
• Lose fat layer under skin can't maintain tissue

• Risk of clot formation
• treatment- stent graft

Valves become incomplete

loose of muscle tone= worn out

Stasis- Dermatitis- brown looking color to skin d/t rbc break down hemoglobin in tissue

Ulcerations- d/t no blood flow

Thrombophelbitis- clot that gets loose and settles in a vessel= DVT

Causes stasis blood flow, Hyper-reactivity coagulation

Thrombophebitis &

PE

What does BP do?

Systolic?

Diastolic?

Mean Arterial?

Pulse Pressure?

• Reflects rhythmic changes as blood moves through the heart
• Left vent contracts
• Left vent relaxation
• 60 average all pressure together good indicator of good tissue perfusion
• S-D-40 represents general compliance of major vessels if systolic is high indicates artheroscleosis

Neural control- lower pns and medulla cadiovascular center rapid-shorterm regulation

Pheripheral control- Baroreceptors- in carotid and aortic arch respond to pressure changes in SNS heart rate and vasoconstriction

Decreased BP

renin releases angiotensionogen

angiotensis 1 ace in lungs weak

angiootension 2- vasocontrict

aldosterone releases= save sodium excrete K

increases blood volume

angio 2 = increase after load

Released from Post Pituitary when high osmolarity

stops excretion of NA and water increased blood volume= increase bp

Released from over stretched atria

increases NA+ water excretion vasodilation

decreases Preload and afterload= decrease BP

Classification of BP

Normal

Pre

Stage1

Stage 2

120-80

Sp 120-139 or DP 80-89

SP 140-159 0r DP 90-99

SP >160 or DP>100

How does this effect ur BP?

Vasodilation

inhibit angiotension enzyme

calcium blocker

Beta blocker

Decreased stretch of baroreceptor

hypoxemia

First 4 decrease

last 2 increase