Physio_21.txt

Large amount of muscle mass that needs perfused

• 4-5 times normal
• 6-7 times in an athlete

• 3-4 ml/min/100g
• during exercise in an athlete 50-80 ml/min/100g

• during the contraction the pressure of the muscle decreases blood flow
• during tetanic contractions the flow can be almost stopper, the causes rapid weakening of the muscle

• at rest some muscle capillaries have little to no flow
• during exercise dormant capillaries open up to decrease the distance nutrients must travel
• 2-3 fold increase in capillary surface area

• chemical substances
• lack of O2

• without oxygen arterial smooth muscle can not sustain vascular tone
• the lack of oxygen causes the release of vasodilator substances

• adenosine
• only last for 2 hours

• potassium ions
• ATP
• lactic acid
• carbon dioxide

• noreinephrine
• can decrease blood flow to as little as one half to one third normal
• important during shock and times of stress
• maintains a normal arterial pressure

• norepinephrine, vaso constriction
• epinephrine, slight vasodilator due to activation of beta and alpha, slightly more beta

• mass discharge of the sympathetic nervous system
• increase in arterial pressure
• increase in cardiac output

• the heart is stimulated to increase rate and contraction strength.
• most of the peripheral arterials are constricted except those to active muscles. Can account for up to 2L/min extra blood flow to muscles
• The muscle wall of the veins contract, this greatly increases filling pressure by increasing venous return and therefore increases cardiac output.

coronary and cerebral

• vasoconstriction of arterials and small arteries
• increased pumping activity of the heart
• increase in filling pressure and cardiac output
• pressure can become very high if only a few muscles are used since only those muscles become vasodilator
• lower arterial pressure if doing whole body exercise, running swimming, since for vasodialtion is occurring in large masses of muscle

• it increases the force in which blood is moved into the tissue
• The extra pressure stretches the walls of the vessels to allow more flow

increased rate and increased strength of contraction

it must increase

• sympathetic stimulation contracts the veins
• tensing of the abdominal and skeletal muscle compresses internal vessels providing more compression of the capacitive vascular system
• from 7mmhg to 30mmhg

it raises very little because of the greatly increased sympathetic stimulation of the heart

• on the surface
• only the inner 1/10 of a millimeter of endocardium receives nutrition through diffusion

• coronary sinus with a small amount going directly to the right atrium through the anterior veins
• thebesian veins enter the closest chamber

225 ml/min 4-5 % of total CO

coronary blood flow can increase 3-4 fold, the rest of the needed energy comes from the increased efficiency of cardiac energy utilization

• in the left ventricle blood is supplied during diastole and is slowed during systole due to muscle contraction
• the same is true of the right heart but to a much lesser extent, the right ventricle does not contract as strongly

• epicardial, intramuscular branches, subendocardial plexus
• the subendocardial vessels compensate for the lack of flow during systole with there great number

• direct- neurotransmitter stimulation
• indirect- has much more effect, if the sympathetic nervous system increases cardiac out the increase in metabolic products will cause vasodilation even in the presence of norepi, a vasoconstrictor

• alpha is on epicardial
• beta is on intramuscular

the metabolic requirements will over ride the nervous innervation

• fatty acids instead of carbohydrates
• more oxygen is needed for fatty acid metabolism to ATP then with carbs

build up of lactic acid

• first it is metabolized to ADP then to AMP and then to adenosine
• the cellular membrane is permeable to adenosine and it leaves the cell
• Within 30 minutes of severe hypoxia half of the adenosine can be lost from the cell, it can only be produced at 2% an hour in the cell. Because of this after 30 minutes of ischemia relief may be to late

slowly increasing coronary ischemia and weakening of the cardiac muscle

athersclerosis

• genetics
• large cholesterol intake
• sedentary lifestyle

• colesterolo depositino beneath the endothelium that becomes fibrosed and sometimes calcified
• common site is the first few centimeters of a coronary artery

in a person who already has an underlying atherosclerotic coronary disease

• the plaque can cause a thrombus which can then occlude the vessel, this usually occurs where the plaque has broken through the surface and is in direct contact with the blood. Can become an embolus
• The plaque can irritate the smooth muscle of the wall and cause a vaso spasm

• collateral flow
• when an occlusion develops in a large artery the small collateral branches begin to dilate within seconds
• after 24 hours the collateral flow will dilate enough for adequate flow to the muscle, doubling by the second. Can reach normal flow by 1 month
• As the plaque grows this collateral flow will become to little and tissue will die

area of muscle with zero flow or so little it cannot sustain function

• collateral blood begins to seep into the area
• the are becomes overfilled with stagnant blood
• the muscle fibers use oxygen, causing the hemoglobin to become totally de-oxygenated
• the infarct becomes bluish-brown
• the local vessels begin to leak fluid and the area becomes edematous
• cells begin to swell and lose function
• cells die

• 1.3ml/min/100g
• during rest the normal delivery is 8ml/min/100g

• it has extra difficulty obtaining blood flow because of compression of contraction
• this area will be damaged first with compromised blood flow

• decreased cardiac output
• damming of blood in the pulmonary blood vessels, death from pulmonary edema
• fibrillation of the heart
• rupture of the heart

• when the normal portion of the ventricle contracts the ischemic portion of the muscle is forced outward by the intraventricular pressure
• much of the pumping force is dissipated by the bulging of the non functional area

• this is due to lack of blood flow and is called cardiac shock
• usually occurs when 40% of the LV is infarcted
• death in 85% of patients

• no effect for the first couple days
• the blood flow to the kidneys is diminished and the kidneys fail to excrete enough urine
• this will add to the total body fluid and lead to congestive heart failure

• first ten minutes
• one hour after lasting for a few hours

• an acute loss of blood supply to the heart causes depletion of K which increases the amount of extracellular K
• Injury current develops, the ischemic muscle can not fully depolarize after a beat. The outer membrane of these cells is negative and this negativity can spread and depol other section of the heart
• powerful sympathetic reflexes develop after massive infarct
• the weakened muscle will dilate increasing the electrical pathway

• after a few days, the infarcted muscle needs time to degenerate and stretch out before rupturing
• due to systolic stretch

the amount of stretch is assessed every day

compression of the heart from the outside, this blocks the flow of blood into the rt atrium and the pt can die of decreased cardiac output

little to no death can occur, part of the muscle though can become non functional due to inadequate nutrition

• the dead cells are replaced by fibrous scar
• the ischemia will promote the development of a large quantity of fibroblasts
• the scar will contract over the next year
• the normal areas of the heart will hypertrophy to compensate for the muscle loss

the degree of ischemia and the workload of heart muscle

• after MI during excessive exercise the vessels of the healthy tissue will dilate and steal blood supply from the nonfunctional tissue
• this will worsen the ischemic condition and lead to further cell death

• the pumping capacity is permanently diminished
• the normal cardiac reserve at rest is 300-400% so even with a lose of function you can still perform normal activities

• lactic acid
• histamine
• kinins
• proteolitic enzymes

pain felt beneath the sternum when the demand of the heart is greater then the supply

during embryonic life the heart originates in the neck so the heart and arms and neck share the same spinal cord segments for pain fibers

nitroglycerine and nitrates

the metabolic need on the heart