Path Phys Test 3

Front 1

electrocardiogram

Back 1

plotted as voltage vs. time
dipole - equal magnitude but opposite direction

Front 2

dipoles in the heart

Back 2

- ecg measure the net dipole on the OUTSIDE of the myocardial cells.

- this means the peak deflection occurs when an area of myocardium is half depolarized.

Front 3

einthoven triangle

Back 3

- lead 1 - left arm/ right arm
lead 2 - left leg/ right arm
lead 3 - left leg/ left arm

upaward deflection on ecg at a given lead is due to a positive dipole at that lead.

- this allows determination of the mean electrical axis of the heart, which can indicate problems with the conduction system or depolarization and repolaraization of the myocardium.

Front 4

1a 12 lead ECG

Back 4

chest leads - 6 leads, V1- V6
with 3 augmented limb leads

- limb leads indicate cardiac dipole from frontal plane

chest leads indicate dipole from axial plane.

Front 5

components of the ecg

Back 5

- p wave - atreal depolarazation
- qrs - ventricular depolarization
- t wave - ventricular repolarization
- pr interval - time for depolarization to travel from sa node to ventricle, measure of health of av node.

st segment is isoelectric and elevates in MI and depresses in angina.

qrs duration - time needed to depolarize ventricles and its a measure of the conduction system of the heart.

rr interval - indication of vent. rate

PP interval - indication of atrial rate.

Front 6

st segment alterations

Back 6

- angina pectoris - ischemia causes depolarization and that means the apparent baseline on the ecg is actually high (+ chaarge points towards the lead)

- MI - ischemia in MI affects the entire wall
- apparent baseline in MI is lower than true baseline. ST segment appears elevated but it is actually the true baseline.

Front 7

ECG abnormalities

Back 7

- lung QT syndrome -
- usually congenital
- with a prolonged T wave or st segment due to prolonged repolarization
- susceptible to fibrilation and responsible for some cases of sudden cardiac death.

- atrial premature complexes
- early p waves and are present in over half of adults and are usually asymptomatic.

- ventricular premature complexes
- QRS complexes not preceded by a P wave
- present in >60% of normal adults and usually asymptomatic.

Front 8

ECG conduction abnormalities

Back 8

- AV block - first degree - conduction through av slowed (PR interval >.2 secs. all p waves conduct to ventricles

- second degree - incomplete coupling between atria and ventricles; only some p waves are conducted to the ventricles.
- TYpe 1 - PR interval lengthens until conduction fails (almost always in the av node.
- type 2 - PR interval long but constant; every nth ventricular depolarization is missing; almost always in bundle branches

- third degree- no impulse conduction through av node; av dissociation.

Front 9

cardiac function and normal aging

Back 9

- sinus node cells decrease in number
- cal. deposits on valves increase
- left ventricular wall thickness increases

- physiology
- resting heart rate dec.
- max. hr decreases
- max. cardiac output decreases
- pr interval dec.
- vent. relaxatin decreases
- systolic bp increases.

Front 10

q = flow
chang in p = pressure diff. between the ends of a tube. in mm HG
- flow increases as the pressure difference increeases (assuming that resistance is constant
Resistance

Back 10

- flow decreases as the resistance increases

Front 11

determinants of resistance

Back 11

viscosity - property of a fluid that resists the force causing the fluid to flow.
- increased viscosity produces increased resistance

Front 12

hematocrit

Back 12

- percentage of blood volume occupied by red blood cells.
- normal range is 38-54%
- arterioles give most resistance in teh body.

Front 13

viscosity

Back 13

- laminar flow - blood in the center of the vessels tends to flow the fastes - blood flows in concentric layers tha slip past eachother

axial streaming - when flow is slow, red blood cells are distributed throughout the vessel and increase viscosity by rubbing the vessel walls.

- when flow is fast, rbc's move to the center of the vessel, lowering apparent viscosity.

Front 14

determinants of resistance

Back 14

- tube - radius - increased tube radius decreases resistance
- resistance is inversely proportional to teh radius to the 4th power
- doubling the radius decreeases resistance 16X

Front 15

tube length

Back 15

- increased tube length increases resistance.
directly proportional to resistance, double the length and double the resistance.

Front 16

Q = change in pressure (pie) R^4/ 8 viscosity L

Back 16

so flow will increase with increased radius and a change in pressure

it will decrease with change in length.
decrease viscosity and you will increase flow to.

Front 17

arteries

Back 17

- function - passage way from the heart to the tissues
- pressure reservoir to provide driving force for blood during diastole

Front 18

structure from inside to outside of an arteriole

Back 18

- endothelium (tunica intima or interna)
- elastin
- smooth misucle (tunica media)
- conn. tissue - tunica adventitia or externa
- epithelium - serosa

vasa vasorum - blood vessels supplying the outer layers of large arterioles.

Front 19

pulse pressure

Back 19

- systolic pressure - diastolic pressure

- map = diastolic pressure +1/3 pulse pressure

it is not the arithmetic mean of sp and dp, but the average pressure over time, area under the cure divided by thetime interval.

Front 20

prop. of arteries

Back 20

- low resistance (large diameters_
- have elasticity to maintain pressure throughout cardiac cycle.

Front 21

during systole activity at arterioles

Back 21

- during systole, high pressure causes walls of arteries to strectch; 1/3 of stroke volum enters arterioles.

- during diastole - walls of arteries rebound and contin. to push blood toaward arteriols; 2/3 of stroke volume enters arterioles and coronary arteries are perfused.

Front 22

compliance

Back 22

- the ability of the walls to expand and contract
- decrease compliance and you increase systolic pressure (becuase the arteriole walls need to stretch during systole
- decrease diastolic pressure
- increase pulse pressure

Front 23

compliance changes with age

Back 23

- decreases in normal agine and this increases systolic press. and decreases diastolic pressure.

Front 24

MAP

Back 24

MAP = co x svr
where co = cardiac output and svr = systemic vascular resistance

- co = stroke volume x hr

stroke volume - blood volume (which influences preload_ and contractility.

Front 25

arterioles

Back 25

- large arterioles have all 3 layers (intima, media and adventitia)

- small arterioles only have tunica intima surrounded by sm. muscle

- virtually no elastin is present.

Front 26

function of arterioles

Back 26

- primary resistance vessels. -
- note that most of the drop in pressure occurs in arterioles

-

Front 27

svr

Back 27

- R of arteries +R of arterioles + R of capillaries +R of veins.

Front 28

arterioles

Back 28

- control of resistance - symp. vasoconstrictor nerves
- alpha 1 receptors - most abundant in skin and kidney
increased symp. tone = vasoconstriction and decreased symp. tone = vasodilation.

- hormones - epin. causes skeletal muscl dilation via beta 2 r's and constriction to the skin via alpha 1 r's.

angiotensin 2 - vasoconstriciton

arginine vasopressin - vasoconstriction

Front 29

function -

Back 29

maintain perfusion of various autoregulation
- intrinisc ability of an organ to maintain a constant blood flow despite change in perfusion pressure.

differs in diff. tissues - brain, kidneys and heart

- moderate autoregulation - skeletal muscle
- low autoregulation - skin.

mechanisms of autoregulation - myogenic - vasc. sm. muscle contracts when stretched

Front 30

metabolic autoregulation

Back 30

- inc. met. rate vasodilation --> increased blood flow.. allows for more O2 delivery to active tissue (active hyperemia)
- could be due to dec. O2 or ATP intracellularly or increased adenosine, lactic acid, H+, etc. extracellularity.

Front 31

arterioles

Back 31

- endothelial - factors released from endothelial cells diffuse to adjacent smooth musc. cells to produce effects

- NO - vasodilation.

Endothelin - vasoconstriction

Front 32

capillary structure

Back 32

- continuous - low permeability with tight junctions (cns, skin, and muscle)

- fenestrated - moderate permeability, fenestra (exocrine glands, kidney glomeruli and intestinal mucosa)

- discontinuous - high permeability, large intercellular pores (liver) gaps inbetween the cells.

Front 33

properties of capp.

Back 33

- inner diameter - 4-8 micrometers
approx. 10-40 billlion

- total resistance is low because many are in parallel circuits

- precap. sphincters constrict or dilate to regulate flow.

Front 34

function of capps.

Back 34

- exchange of materials
- gases, nutrients and wastes
- water moves through aquaporins
- polar molecules - travel through intercellular pores and fenestrations
- proteins - cross only through large pores

- dist. of ec flued between plasma and interstitial fluid.
- starlings hypothesis

Front 35

starlings hypthesis

Back 35

- the direction and magnitude of the movement of fluid across the capillary wall are determined by the algebraic sum of the hydrostatic and osmotic pressures that exist across the capp. wall.

- interstitial space - ec env. composed of interstitial fluid, collagen, elastin, hyaluronic acid, proteoglycans.

Front 36

capillaries

Back 36

- ultrafiltrate of plasma - fluid moving out and this is basically plasma -
- fluid exchanged across capp. wall; essentially plasma with a low conc. of plasma proteins.

- filtration - movement of flud out of capp.
- absorptin - movement of fluid in capp.

Front 37

pressures involved in capp. flow

Back 37

- blood pressure in capp. is a filtration force

- interstitial fluid hydrostatic pressure - is an absorption force

- plasma (cappilary) osmotic pressure - filtration force

- interstitial oncotic pressure - absorption force

- any force that is interstitial is an absorptive force.

- plasma osmotic pressure is an absorptive force because if the conc. of particles is high in the capp. water will be less likely to flow out right!!

Front 38

net filtration pressure

Back 38

- Pic (bp) + interstitial oncotic pressure - (plasma osmotic pressure+interstitial fluid hydrostatic pressure)

Front 39

cappilaries

Back 39

- physiological/ pathological changes affecting fluid distribution
- arteriolar constriction or dilation
- cinstriction leads to inc. map --> dec. capp. bp --> decreased filtration
- dilation leads to increased capp. bp and increased filtration.

- decreased plasma protein - decreased plasma protein leads to decreased plasma osmotic pressure which leads to more filtration.

Front 40

fuction of veins

Back 40

- blood reservour (about 60% of blood enters here)
- constriction - increased blood return to heart

Front 41

structure of veins

Back 41

- endothelium is tunica intima

less elastin that arteries
- smooth muscle - tunica media
- conn. tissue - tunica adventitia

Front 42

properties of veins

Back 42

- highly distensible -
low resistance
larger veins have valves to aid in blood return to the heart.

Front 43

control of venous return

Back 43

- symp. vasoconstrictor nerves
- NE -- vasoconstriction-- inc. blood return to the heart

- skeletal muscle pump - skeletal muscle contraction compresses adjacent veins

- resp. movements - inspiration -- increased abdominal pressure -- decreased thoracic pressure-- increased venous return to the heart.

effect of changes in venous return -
-- increased venous return -- increased EDV -- increased stroke volume -- increased CO

Front 44

lymphatics

Back 44

- lymphatic capps. - bind ended tubes

- allows fluid to fill in the cells
- note that endothelial cells in the lymphatic bulbs loosely overlap eachother - this allows interstitial fluid to enter.

Front 45

lymphatic return

Back 45

- return of excess fluid
- roughly the entire plasma volume is filtered daily.

- return of filtered protein - defense against disease (immune cells fighting dx)
- defense against disease
- transport of absorbed fat via chylomicrons

Front 46

flow of lymph

Back 46

- spontaneous contraction of lymph bulbs and vessels

- organ movement

- valves - for unidirectional flow.

Front 47

lymphatic problems

Back 47

- blockage of lymph return -- edema

cancer or elephentitis.

Front 48

special circulations

Back 48

- bbb - capps. of the brain and spinal cord have nearly continuous tight junctions between their endothelial cells.
- absence of large pores prevents movement of all but he smallest water soluble molecules.

Front 49

fetal circulation

Back 49

- ductus venosus - bypasses liver

- foramen ovale - from RA to LA bypass pulmonary system

- ductus arteriosus - from pulmonary to aorta.

Front 50

mech. of controlling bp

Back 50

- neural
hormonal
local

Front 51

neural control of bp

Back 51

- spinal cord - conducts symp. imp. that maintain bp

- medulla - generates tonic excitatory signals to maintain bp
- integrates info. from cardio reflexes
- integrates signals from higher cns centers as well as hormones and drugs

- arterioles - inc. symp. activity inc. svr

- veins - high levels of symp. stimulation caused by large dec. in pressure causes venous constriction, which inc. venous return and thus stroke volume.

Front 52

baroreceptors

Back 52

- in carotid sinus and aortic arch
- sensory nerve endings in vessel walls have streteched activated cation channels.

inc. pressure -- stretch -- firing
- neurons profect to medulla; ap firing frequency is proportional to bp.

Front 53

baroreceptor adaptation in hypertension

Back 53

- the baroreceptor reflex will adapt to maintain an elevated setpoint
- in hypertension the baro receptor response is the same at a higher pressure than a normal vessel in normotension.

Front 54

other neural control

Back 54

- chemoreceptors in aortic bodies, carotid bodies and medulla
- inc. perchlorate dec. phosphate and decreased pg -- peripheral vc, inc. heart rate-- increased stroke volume.

- pain receptors - moderate pain --> inc. symp. stimulation --> inc. co, inc. svr
- deep, severe pain --> dec. symp. stimulation --> dec. co, dec. SVR

chemoreceptors in the vent. myocardium - serotonin, bradykinin, prostaglandins in coronary arteries --> dec. MAP

- higher CNS centers - fight or flight

- vasovagal syncope - dec. symp an inc. pns tone

- exercise - redistribution of blood flow leads to increase CO

Front 55

hormonal control of bp - atrial natriuretic peptide

Back 55

- regulates sodium excretion in the urine, produced by atrial myocardial cells.

- if you get atrial stretch atrial natriuretic peptide
- vasodilation
- adrenal cortex - dec. aldosterone and dec. at 2

Front 56

control of BP
- pressure diuresis

Back 56

- increased MAP inc. salt and water excretion
- modulated by neural and hormonal mechanisms.

Front 57

short term control of bp

Back 57

- primarily controlled by baroreceptor reflex
- neural and hormonal mech. regulating vascular tone and co

Front 58

long term control

Back 58

- blood volume regulation via salt and water excretion by the kidneys

- regulation of vascular tone

- erythropoeitin - hormone released by the kidneys that stimulates formation of erythrocytes when hamotocrit is low.

Front 59

risk factors for developing as

Back 59

age - lder age
- untreated hypertension -
- cigarrete smoking
- elevated serum cholesterol - ldl
- diabetes - esecially type 2
- exercise / obesity - obese people have higher bp, high ldl. high blood sugar which affects diabetes

Front 60

early atheroma is reversible.

Back 60

-

Front 61

Mi usually preceded by AP

Back 61

20-30% are silent
- typical symptoms include crushing pain that isn't relieved by taking nitro.

these are 65% of heart attacks.

Front 62

etiology of cardiovascular disease

Back 62

- nearly all patients have as to some degree.
- ischemic necrosis could be precipitated by a thrombus or atheroma or coronary artery spasm

myocardium can withstand total ischemia for 20-30 mins.

Front 63

usual location for blockage of as in the coronary arteries is 1 or 2 cm. from their origin off the aorta.

Back 63

right coronary artery is the post. part
- left circumflex is the lateral part
- ant. descending is the ant. part.

-

Front 64

microscopic events of an mi as it heals to scar tissue

Back 64

- acute infl.
- chronic infl. monocytes and macrophage digest and clear the necrotic tissues
- body fills spac with granulation tissue

- scar tissue follows after a few months.

Front 65

mis are dx by clinical findings and

Back 65

vary abnormal ecg findings
- lab evaluations- a number of cellular enzymes are released during myocardial death
- cardiac muscle creatine kinase and Lactic dehydrogenase.

Front 66

new screening tests for patients with MI

Back 66

- protein called troponin can be used to id if its an MI or not.

Front 67

few major complications of an MI

Back 67

- cardiac tamponade - the granulation tissue is weak and if it breaks open it will cause instant death

- mural thrombus formation - left ventricle thrombus formation that may break free and cause a stroke or pulmonary ischmia

- rupture of papillary muscle causing mitral valve to fail.

- another MI

Front 68

sudden cardiac death

Back 68

- also considered a heart attack, often have a history of symptoms

Front 69

tiology of scd

Back 69

- coronary artery as, NO Ischemic necrosis
- death occurs less than one hour after onset of acute symptoms
- 40% of heart attacks.

- lethal ventricular arrhythmia is caused by MI that greatly reduces cardiac output, resulting in death

- death occurs before myocardium can develop a necrosis.

patients can be revived without necrosis forming..

Front 70

rheumatic fever

Back 70

- preceded by a streptococcal pharyngitis
- rheumatic heart is one complication of RF
- only 1% of untreated strep infections go on to become rhd

Front 71

major immunologic problem of RHD - c

Back 71

cross reactive antibodies that bind to heart tissue.

Front 72

main lesions of RF

Back 72

- migratory arthritis (rf licks the joints and bites the heart)

- pancarditis - inflamation of the 3 layers of the heart

Front 73

major heart problems caused by RF are known as rheumatic heart disease

Back 73

- endocardial infl. causes scarring of the aortic and mitral valves resulting in valves that don't open properly.

- results in stenosis and insufficiency.

- scarring produces rough surface which will harbor bacteria. -- infective endocarditis.

- aschoff's body - microscopic structure of a rhd patient in the myocardium