physiology test 4

what is the driving force for blood pressure?

-ventricular contraction -during ventricular diastole, the semilunar valves shut and the elastic arteriole walls will recoil: driving pressure wave

upstream pacemaker list from 1st to last

1) SA node 2) AV node 3) AV bundle 4) bundle branches

resistance in arterioles how is it influenced

R is proportional to 1/r^4 1) local control: usually first level of control to meet the immediate metabolic needs of the tissue (i.e paracrine control) 2) sympathetic control: regulate blood distribution for the homeostasis (i.e. temperature regulation) 3) hormonal control (i.e. angiotensin) act directly on arterioles or by influencing sympathetic control

What is velocity dependent on?

Velocity is dependent on flow rate -flow rate: volume of blood that passes a given point per unit time -velocity: this is how far a fixed amount of blood travels per unit time v=Q/A

capillary exchange

capillaries are within .1mm of tissue cells -density is directly proportional to metabolic activity -capillary diameter is only large enough for passage of one RBC at a time

myogenic contraction

cardiac muscle cells dont need nerve innervation to contract -signal is from within BUT it can be influenced by ANS innervation -signal comes from autorhythmtic cells (aka pacemakers) -smaller and fewer than other myocardial contractile cells -lack sarcomeres-no contraction -hearts own myogenic pacemaker is 100bpm

sympathetic stimulation

catecholamines (epinephrine/rorepinephrine) -bind to B1 adrenergic receptors (w/ a cAMP second messenger) increases ion flow through both Ca++ and If channels -speeds up the PP

blood distribution to the tissues

dependent on the metabolic needs of that tissue -resting muscle receive about 20% cardiac output -working get about 85%

what does arterial blood pressure reflect?

driving force for blood flow -ventricular pressure during systole is the same as arterial blood pressure

phase 3

early ventricular contraction -depolarization wave moves down the internodal conducting system towards apex -ventricles contract from the bottom -AV valves shut- associated with the first heart sound ("lub") -semilunar valves are also shut at this time and therefore blood stays in the ventricle: known as isovolumic contraction

What is an ECG

electrocardiogram, shows hearts electrical activity -Einthoven's triangle: electrodes placed on both arms and left leg

how does atherosclerosis happen?

endothelial cells line arteries will transport LDL into extracellular space where is accumulates -macrophages will then ingest the cholesterol (become foam cells) -these will release cytokines-cause SMC division (lesion) -as it continues it will eventually develop into large plaques and harden with collagen

Resistance

caused by friction and resistance in vessels -increase in resistance, flow will decrease -determined by: >vessel radius >tube length >fluid viscosity

pericytes

cells surrounding the capillaries -contribute to tightness characteristic of capillaries -i.e. blood brain barrier

What does flow depend on?

change in pressure

low-density lipoprotein (LDL)

cholesterol combines with protein to be soluble BAD PROTEIN -leads to development of atherosclerosis

hypertention

chronically elevated blood pressure >130-140/80-90 mmHG -90% hereditary (primary) -10% from underlying problem (fluid retension from endocrine disorder

what factors influence MAP?

map is a balance between flow into the arteries and out of the arteries >flow into the aorta is the same as cardiac output -flow out of the arteries is influenced by peripheral resistance of the arterioles *MAP is poportional to CO*R arterioles

what are the heart chambers divided by?

septum -prevents blood from mixing

what is a portal system?

special circuit of circulation that starts and ends in a capillary bed: -intestine to liver -kidney -brain

ECG interpretation

p wave to p wave tells us heart rate -ST segment depression can indicate myocardial ischemia

how is varied distribution of blood to tissues possible?

parallel arrangement: blood flow through all the arterioles at the same time is equal to cardiac output -flow can be shunted and redirected

how is the volume of blood for each contraction calculated?

stroke volume: amount of blood pumped by one ventricle during a contraction: EDV-ESV

capillary flow velocity

the smaller the vessel area, the higher the flow velocity (if rate is constant) -capillary flow rate is LOW and so is velocity

where is cardiovascular disease common?

the south

what is myogenic autoregulation?

vascular smooth muscle can respond to increased stretch in the vessel wall -will cause constriction -resistance increases/flow decreases -mechanically gated Ca++ channels open, allowing for Ca++ to enter the cell

phase 4

ventricular ejection -ventricles continue to contract forcing open the semilunar valves -blood is forced out of the ventricles and into the arteries

phase 5

ventricular relaxation -ventricular pressure decreases below that of arterial pressure -the resulting backflow fills the cups of the semilunar valves (remember their structure) -this will cause the semilunar valves to shut >second heart sound- "dub" >isovolumic relaxation

baroreceptor reflex

(carotid artery) -heart rate increases -force of contraction increases -vessels constrict -normal BP and cardiac output return to normal within 2 heart beats

re-active hyperemia

(caused by paracrines) -blood flow is blocked at a certain tissue (low o2, high co2) -local hypoxia produces NO -co2 and NO act as vasodilators -blood flow is increased

capillary hydrostatic pressure

-32mm Hg at arteriole end and decreases to 15mm Hg at venous end -hydrostatic pressure of fluid is very low (basically 0) -filtration: 32-0 at arteriole end

parasympathetic stimulation

-ACh will bind to muscarinic cholinergic receptors -K+ permeadbility increases: hyperpolarizes the cell lowering the beginning of the pacemaker potential -Ca++ permeability decreases -slows PP

What are factors that influence stroke volume?

-SV is directly related to the force of contraction -affected by LENGTH of muscle fiber prior to contraction: dependent on the amount of blood in the ventricle -CONTRACTILITY: intrinsic ability for the cardiac muscle to contract at any given length

edema

-accumulation of fluid in interstitial space (swelling) -results form an alteration in capillary exchange (filtration>absorption) -can occur as result of inadequate lymph drainage (obstruction) -elephantiasis

calcium entry and excitation contraction coupling

-action potential moves across the sarcolemma and into the t-tubule -opens voltage-gated L-type Ca++ on the cell membrane -Ca++ enters causing RyR-2 (heart isoform) on the SR to open -Ca++ induced Ca++ release (Ca++ spark) -several Ca++ sparks= Ca++ signal -Ca++ binds troponin (contractile mechanism same as skeletal muscle)

how do we regulate BP when blood volume changes?

-adjusting small increase in blood volume is regulated by the kidneys -both renal and cardiovascular system work to restore a loss of blood volume (dehydration, hemorrhage) -kidneys can only conserve blood volume -cardiovascular compensation includes sympathetic nervous stimulation *distribution of blood between arterial and venous sides helps maintain arterial pressure

what is the purpose of the internodal conducting system?

-allows for rapid transduction of the signal -SA node will also spread the action potential to the adjacent contractilw cells >they will depolarize and contract BUT transduction is slower

how is the heart contraction coordinated?

-an electrical signal -all individual cells need to depolarize in coordination -AP generated in the sinoatrial node (right atrium) -wave of depolarization spreads over the internodal pathway and the atrioventricular node -depolarization moves into the ventricles to the Purkinje fibers via the atrioventricular bundle and left/right bundle branches

venules and veins

-blood flow is convergent -venules converge into veins they become larger in diameter -veins> arteries; hold more than half of the blood in our bodies (volume reservoir) -walls are thinner with less elastic: readily expand with blood

blood oxygenation

-blood flowing into heart is "deoxygenated" (still has some O2) -deoxygenated blood is darker red and is pumped from the right side of the heart to the lungs (by pulmonary circulation) -oxygenated blood is pumped from the left side of the heart to the rest of the body (by systemic circulation)

what is the order of the heart contracting?

-both atria contract at the same time followed by the ventricles -ventricles will contract from the bottom and upward -connective tissue rings surrounding the 4 heart valves serve as insertion and origin for cardiac muscle -ventricular contraction will pull the apex and base together

arteries and arterioles

-carry blood away from the heart -thick smooth muscle layer a lot of connective tissue >makes these vessels very stiff -flow is described as divergent into smaller vessels *as the size of the vessel shrinks the walls become more muscular and less elastic

sympathetic innervation

-causes vasoconstriction -catecholamines (epi and norepi and dopamine) act on adrenergic receptors -squeezes more blood into the heart: increases stroke volume

fenestrated capillary

-contain large pores allowing passage of large volumes of fluid -kidneys and intestines

sphygmomanometry

-cuff pressure exceeds atrial pressure -cuff pressure is gradually released: blood flow is reestablished (Korotkoff sound) -cuff pressure no longer is compressing the artery --Korotkoff sound disappears (diastolic pressure)

Heart Rate can be influenced by the autonomic nervous system

-determined by speed of pacemaker potential: changes ion permeability in the autorhythmic cells -under influence autonomic nerve innervation -to speed up rate: decrease parasympathetic > increase sympathetic - to slow heart: increase parasympathetic pathway

angiogenesis

-development of new blood vessels -necessary for normal development -occurs during wound healing and uterine lining growth and in response to endurance training -controlled by cytokines and growth factors >stimulate (mitogens): VEGF and FGF _inhibit: angiostatin and endostatin

Why is it necessary to direct the signal through the AV node and not the atria

-dont want the ventricles contracting first -would prevent blood from being pushed out the tops of the ventricles and into the arteries -internodal system spreads the signal to the apex **bottom ventricles contract first

when do you want angiogenesis to stop?

-during malignant tumors

blood in our vessels exert two pressure components

-dynamic (hydraulic pressure) -lateral (hydrostatic pressure) *when a fluid moves through a system it will lose pressure through friction and hydraulic pressure

how can cardiac muscle contraction be graded?

-each fiber has the ability to vary amount of force it generates -proportional to: > # of active crossbridges >amount of Ca++ in cytosol > more Ca++, more troponin bound >more actin and myosin cross bridges can form

continuous capillary

-endothelial cells are connected to one another via leaky junctions -most common; found in muscle, connective tissue, neural tissue (i.e. blood brain barrier)

sympathetic control of the vasculature

-epinephrine binds to alpha receptors for vasoconstriction -will have higher affinity for beta2-receptros -smooth muscle in heart, liver, skeletal muscles -result in vasodilation -important in flight or fight response

length-tension relationship

-force proportional to sarcomere length: longer (optimum) the more force created -ventricle wall stretches as it fills with more blood (preload) the stronger the force of contraction

what makes up the cardiovascular system?

-heart -blood: formed elements and plasma -vaculature: arteries, arterioles, capillaries, venules, veins

how is hypertension a risk factor for atherosclerosis

-high BP-> damage the vascular endothelium--promotes plaque formation -high BP will also put excess strain on the heart

blood pressure facts

-highest in arteries and lowest in veins -aortic pressure around 120 mm Hg during systole and 80 mm Hg during diastole

what factors influence capillary filtration/absorption balance?

-increase in capillary hydrostatic pressure -decrease plasma protein concentration

afterload

-load that ventricle has to overcome during contraction -determined by: arterial blood pressure and EDV -associated with many cardiovascular pathologies: >loss of aortic compliance >systemic hypertension >may result in left ventricular hypertrophy

anatomy of the heart

-located in thoracic cavity -apex angles down and towards the left/base upsidown cone shaped -surrounded by the pericardium -four chambers: >right atrium (blue) >right ventricle (blue) >left atrium >left ventricle

how is exchange accomplished?

-movement between endothelial cells (paracellular) -through the cells (endothelial transport) -large solutes and proteins require vesicles: transcytosis

describe blood vessels

-multilayers: inner most layer is a thin ;ayer of endothelial cell -endothelium: secrete paracrines: >regulate diamerter (blood pressure regulation) >vessel growth >absorption of materials -connective tissue and smooth muscle surround the endothelium >circular layer of vascular smooth muscle for vasoconstriction and vasodilation >maintain muscle tone (partial contraction at all times) >depends on Ca++ entry from extracellular fluid

what controls contractility?

-nervous -endocrine -inotropic agents: >positive effects: norepinephrine on beta-1-receptors >will cause an increase in Ca++

How do you change pressure in a liquid without changing the volume?

-occurs when the walls of the contrainer contract: ventricular walls during systole -increases pressure until liquid has a place to go (like semilunar valves during heart contraction) : "driving pressure"

how are myocardial autorhythmic cells able to generate action potentials?

-pacemaker potential -starts at -60mV and slowly moves towards threshold

myocardial action potentials in diff phases

-phase 4: resting potential: -90mV -phase 0 : depolarization- voltage-gated Na+ channels open and Na+ enters -phase 1: initial repolarization- K+ begins to leave via K+ channels -phase 2: plateau-slow voltage-gated Ca++ channels finally open after initial depolarization; some fast K+ will shut -phase 3: rapid repolarization- slow voltage-gated K+ channels are open; resting potential is reestablished

what allows our blood to flow through our vasculature

-pressure gradient -down a pressure gradient -highest pressure occurs in aorta due to LV contraction -pressure will continually decrease throughout the circulation: lowest in vena cava

what is pulse

-pressure in vessel wall as blood is forced through during ventricular systole -decrease over distance due to resistance: disappears at the capillaries -pulse pressure indicative of strength of the pressure wave, pulse pressure= systolic - diastolic

what are arteries referred to as? what are veins referred to as?

-pressure reservoir -volume reservoir

heart rate and exercise fatigue

-resting heart rate rises -max heart rate declines -due to the fatigue of the nervous system (loss of nervous influence over the heart)

semi lunar valves

-same principle as AV valves -each has three cauplike leaflets that "snap" shut -do not need connective tendons as seen in the AV valves

cardiac muscle relaxation

-similar to skeletal muscle -Ca++ pumped back into SR via action of Ca++ ATPase-Ca++ is also pumped out of the cell via Na+ Ca++ exchanger

capillaries

-site of exchange between the blood and the interstitial fluid -lack smooth muscle and fibrous/elastic connective tissue: facilitates exchange -single endothelial layer supported by a basement membrane

stable vs. vulnerable plaques

-stable: not likely to be a problem -vulnerable: have thin fibrous caps prone to break which can cause a BLOOD CLOT -macrophages in plaque may release enzymes that convert this stable plaque into a vulnerable one

cardiac muscle make up

-striated -smaller muscles than skeletal but similar besides having single nucleus -intercalated disks -T-tubules are larger and branch within -sarcoplasmic reticulum is smaller Ca++ comes from outside cell -mitochondria occupy 1/3 of cell volume

atrioventricular valves

-thin flaps of tissue joined at their base to a ring of connective tissue -flaps connect to chordae tendineae (ventricular side) -chordae tendineae then go on to attach to papillary muscles of the ventricle >these muscles provide stability (dont actively open or close)

which variable in resistance has the most influence?

-vasoconstriction and vasodilation has a large effect on the resistance in that particular vessel

venous contraction/compression

-veins are squeezed by our contracting skeletal muscles -pushes blood forward -EDV increases and therefore stroke volume

venous valves and varicose veins

-venous blood must flow against gravity -internal one-way valves aid in this -varicose veins: >faulty valves >blood pools >may be hereditary >other common risk factors include: female, pregnancy, obesity, meopause

what factors affect venous return?

-venous contraction/compression -abdominal and thoracic pressure changes (due to breathing) -sympathetic nervous innervation

what are the two sets of heart valves?

>antrioventricular (AV) valves: between atria and ventricles: -tricuspid valve (between right atrium and right ventricle) -bicuspid valve: between left atrium and left ventricle >semilunar valves: between the ventricles and arteries: -pulmonary valve (between the right ventricle and pulmonary artery) -aortic valve (between left ventricle and the aorta)

how ECG works...

ECG is recorded from one lead at a time to record a cardiac cycle -p wave: atrial depolarization -QRS: ventricular depolarization -T wave: ventricular repolarization *PQ: atrial contraction *ST: ventricular contraction

functions of cardio vascular system

MAIN: transport materials -nutrients, water and gases to body tissues -materials from cell to cell within the body -waste products/metabolites that cells eliminate

What happens to MAP is CO remains the same, but arteriole resistance increases

MAP increases -happens in hypertension

what is needed to vascular transport?

OXYGEN -if flow to brain is stopped for 5-10 seconds will lose consciousness, brain damage after 5min

high-density lipoprotein (HDL)

a cholesterol combines with this lipoprotein to make it soluble (GOOD PROTEIN)

orthostatic hypotension

arterial drop in BP because of standing up causing blood to pool in extremities -triggers baroreceptor

how does hypertension lead to LVH

as map increases the cardiac muscle must work harder to maintain SV and CO -left ventricle will adapt in size and strength -eventually leads to left ventricular dysfunction (failure) *pulmonary edema, congestive heart failure

pacemaker potentials

at -60mV I(f) channels are open > permeable to both Na+ and K+ >Na+ influx> K+ efflux which causes a gradual depolarization -as the membrane potential becomes more positive I(f) channels shut and Ca++ channels open -Ca++ enters and causes the action potential -Ca++ channels shut at the peak of the AP while at the same time slow K+ channels have finally opened -K+ efflux leads to repolarization

phase 2

atrial systole -final 20% of ventricular filling is accomplished

bulk flow

balance between filtration (flowing out of capillaries) and absorption (fluid flowing into capillaries) -depends on hydrostatic and osmotic pressure >net filtration at arteriole end >net absorption at venous end

stroke volume and venous return

blood returning from systemic or pulmonary veins will ultimately end up in our ventricles: EDV determined by venous return

lymphatic system function

fluid restored by taking it out of interstitial fluid and put back into the plasma

paracrines

function in local control over vascular smooth muscle contraction -i.e. o2, co2, NO increase aerobic metabolism--decrease o2, increase co2--paracrine action--vasodilation

Pressure volume curve

graphical representation of the cardiac cycle with respect to pressure and volume in left ventricle -X-axis: volume -y-axis: pressure *review graph*

atherosclerosis

hardening of arteries -inflammatory process -fatty deposits form inside the arterial blood vessel -cause of almost 1/3 deaths in US

phase 1 of cardiac cycle

heart is at rest, -atrial and ventricular diastole -atria rill with blood -AV valves open and blood will fill into ventricles (gravity)

pressure changes

inspiration increases pressure in thoracic cavity -more blood drawn into thoracic cavity increasing venous return: called respiratory pump

contractility

intrinsic ability of a cardiac muscle fiber to contract at any given length

what do valves in the veins do?

keep blood moving in one direction

what is MAP?

mean arterial pressure -single value to represent the driving pressure in our vessels MAP= diastolic pressure+ 1/3 (systolic-diastolic)

cardiac output definition

measure of cardiac performance -blood volume pumped by one ventricle in a given period of time -normally the same in both ventricles, if one decreases the other will pool

pericarditis

results from friction rub of pericardium on heart

blood flow through the body

right side (blue) left side (red) average cardiac output is 5L/min

how is capillary osmotic pressure determined?

solute concentration (proteins) -more proteins in plasma than interstitial fluid -net flow determines by hydrostatic pressure gradient minus the colloid osmotic gradient

frank-starling law

stroke volume is proportional to EDV (good indicator of preload)

what is myogenic tone of arterioles maintained by?

tonic release of norepinephrine -binds to alpha adrenergic receptors to cause vasoconstriction

what is vascular smooth muscle controlled by?

tonic sympathetic innervation

cardiac output

total blood flow through the entire system

What is the AV node delay?

transmission through the AV node is slower (1/20th the speed) than the rest of the internodal system -allows for atria to complete contraction before ventricular contraction *upstream pacemaker set the rate