Cardiovascular system - Lectures 13-14 Flashcards
cardiovascular system consists of (3)
- heart
- blood vessels
- blood
5 blood vessels
arteries –> arterioles –> capillaries –> veinules –> veins
arteries vs veins –> main function differentce?
- arteries: blood vessels leaving heart
- veins: blood vessels arriving to heart
what system joins 2 capillary beds in series?
portal system
hear:
- ______ divides heart into 2 halves
- _______ receives blood returning to heart
- ________ pumps blood out of heart
- septum divides
- atrium receives
- ventricules pump
plasma vs serum
- plasma: blood sample into anticoagulant tube –> no clot –> plasma contains all clotting factors + hormones/electrolytes/glucose…
- serum: blood sample without coagulant –> blood will clot –> liquid after = serum –> serum = plasma without clotting factors (fibrinogen
blood circulation starting from superior/inferior vena cava
- systemic vs pulmonary
PULMONARY CIRCULATION
- superior/inferior vena cava (deox blood) –> right atrium –> right ventricle –> pulmonary trunk/arteries (containing deox blood) –> lungs –> pulmonary veins (ox blood) –> left atrium
SYSTEMIC CIRCULATION:
- left atrium –> left ventricle –> aorta –> ascending arteries or abdominal aorta –> trunk/digestive system / kidneys / pelvis and legs / arms / head&brain –> capillaries –> ascending veins –> superior/inferior vena cava
- why does blood flow?
- from where to where
- because liquid moves from high to low pressure regions
- blood flows out of heart (highest pressure into closed loop of vessels (lower pressure)
- what are the 2 things that affect blood flow? proportional or inversely proportional?
- what is the formula?
- pressure gradient (delta P) –> difference in pressure btw 2 regions –> higher the pressure gradient, greater the fluid flow = proportional
- resistance –> higher the resistance, lower the fluid flow (inversely proportional)
- R proportional to deltaP/R
the pressure of a fluid in motion decreases/increases with distance
- pressure is increased/lost as blood moves through vessels (because of what?)
- which cavity in heart has highest vs lowest pressure?
- decreases with distance
- pressure is lost due to friction
- L ventricule has highest
- R atrium has lowest
what is hydrostatic pressure?
pressure exerted by a fluid not in motion –> exerted in all directions
contraction of heart creates _________ without changing _________ of blood
- blood leaves heart to vessels –> called ________ __________
- if blood vessels dilate, blood pressure increase/decrease?
- if blood vessels constrict, BP increase/decrease?
- pressure without changing volume of blood
- driving pressure
- dilate –> BP decreases
- constrict –> BP increases
do volume changes affect blood pressure in cardiovascular system?
yes!
which blood vessels have highest pressure? vs which have lowest?
put in order of highest to lowest
aorta (around 93 mmHg) –> arteries –> arterioles –> capillaries –> venules –> veins –> venae cavae (almost 0 mmHg)
What is Poiseuille’s law?
- resistance is proportional/inversely proportional to what? (3) –> relationship?
R = 8Ln/pi*r^4
- proportional to length of blood vessel (increase length = increase resistance
- proportional to viscosity (n) or thickness of blood (increase viscosity = increase resistance)
- inversely proportional to radius to the fourth power (= MOST IMPORTANT ASPECT!) –> increase radius = decrease resistance
flow vs velocity of flow? definition + formula
- flow/flow rate = volume of blood that passes a given point in system per unit of time –> flow = deltaP/ Resistance
- velocity of flow = distance a fixed volume of blood travels in a given period of time –> v = flow rate / cross-sectional area of tube
**flow rate of capillary and artery can be the same, but velocity won’t be bc of cross-sectional area
what is mean arterial pressure (MAP)? (2)
- proportional to what?
- primary driving force for blood force
- pressure reserved in arteries during heart relaxation
- MAP proportional to cardiac output (CO) x peripheral resistance (PR)
heart is made up mostly of which connective tissue? + encased in what?
mostly in myocardium
- encased in pericardium
paired atria vs paired ventricles –> which one are:
- thin-walled vs thick-walled
- upper vs lower chambers
PAIRED ATRIA:
- thin walled
- upper chambers
PAIRED VENTRICLES:
- thick walled
- lower chambers
what serves as origin and insertion for cardiac muscles?
connective tissue rings
- heart = size of a _______
- located under _______
- protected by (2)
- weight heavier in (2)
- base vs apex of heart location
- size of a fist
- under sternum
- protected by sternum and rib structures
- in males and athletes (bc more contractile proteins in muscle cells)
- base = top! vs apex = bottom, pointing towards left side
muscle of the heart is ________ like an ______ –> why?
twisted like an 8
- can squeeze out more blood during contraction (ie wringing out water from a towel)
- what artery/vein feeds heart itself?
- _________ occupy the bulk of the heart
- arteries and veins all attach to the _______ of the heart
- coronary artery and veins –> for blood circulation within the heart –> cardia muscles need E/blood + get rid of waste
- ventricles occupy bulk
- base of heart! (top)
- what are the 2 AV valves? how many cusps?
- how to keep AV valves closed?
- right AV = trisuspid –> 3 cusps
- left AV = bicuspid –> 2 cusps
- cusps linked to connective tissue/strings called chordae tendineae –> linked to papillary muscles. if pressure in ventricle is high, papillary muscle pull chordae tendinae to close valve so no blood goes into atrium
similarities and differences between cardiac and skeletal muscles
- intercalated disks?
- amount of nucleus
- branched?
- longer/shorter?
- striations?
- troponin/tropomyosin?
- contraction system
- SR?
- T-tubules?
- Ca2+ storage
- mitochondria?
DIFFERENCES:
cardiac:
- intercalated disks (desmosomes hold cell together + gap junctions!)
- mostly 1 nucleus
- branched muscle
- shorter than skeletal
- not much Ca2+ storage
- mitochondria occupy 1/3 of cell volume
SIMILARITIES:
- striations
- has troponin/tropomyosin, actin, myosin, sarcomeres
- same contraction system
- SR (although SR of cardiac not super well developed)
- T-tubules (but cardiac t-tubules are larger and branch)
Atrioventricular/AV valves:
- between what and what?
- _______ _____ prevent eversion during ventricular contraction –> attached to valve flaps from _________ muscles
Semilunar valves:
- between what and what
- name of 2 valves
AV VALVES:
- between atria and ventricules
- chordae tendineae –> from papillary muscles
SEMILUNAR VALVES:
- between ventricles and arteries
- aortic valve + pulmonary valve
what circulation supplies blood to heart?
coronary circulation!
valves open or close depending on ___A______
- if _____A_____ is high in left atrium and low in left ventricle –> valve opens or closes?
VS inverse?
- pressure!
- if pressure high in atrium and low in ventricle –> valve opens!
- if pressure low in atrium and high in ventricle (ie during ventricular contraction)–> valve closes
how do semilunar valves open/close?
- when are they open/closed?
- unique shape/structure allows to block backflow –> don’t need chordae tendineae and papillary muscles
- closed when high pressure in atrium and low pressure in ventricle
- open when low pressure atrium and high pressure ventricle (during ventricular contraction)
from where to coronary arteries branch out from?
- left vs right coronary arteries –> branch into what?
- from the aorta!
LEFT: - circumflex branch (goes around)
- anterior interventricular branch (goes down towards apex)
RIGHT: - circumflex branch (goes around)
- posterior interventricular branch (goes down the back of the heart)
- cardiac muscle cells contract without ____________
- what are the 2 types of cardiac cells?
- one of them = 1% of cardiac cells –> function? + 2 charac
- other one = 99% –> describe
- without innervation!
AUTORHYTHMIC CELLS (pacemakers) - fct: signal for contraction! –> generate AP so behave like neurons (although are still muscle cells bc have actin and myosin)
- smaller and fewer contractile fibers compared to contractile cells
- do not have organized sarcomeres
CONTRACTILE CELLS: - striated fibers organized into sarcomeres
intercalated disks contain ______ that transfer _____ from cell to cell, and contain _____ ______ that allow _________ signals to pass rapidly from cell to cell
- desmosomes
- transfer force
- gap junctions
- allow electrical signals
- AP starts with the heart _________ cells
- how is calcium released? (3)
- calcium binds to __________
- ________ cycle as in skeletal muscle
- relaxation calcium removed from cytoplasm (2 ways)
- pacemaker/autorhythmic cells
- a) voltage gated L-type Ca2+ channels in cell membrane open
b) ryanodine receptors (RyR) open in SR in response to inflow of Ca2+ (called calcium spark) –> Ca2+ induced Ca2+ release!
c) summed sparks create a Ca2+ signal - binds to troponin
- crossbridge cycle
- into SR with Ca2+ ATPase AND out of cell through Na+/Ca2+ exchanger (NCX) (Na+ gradient is maintained by Na+/K+ ATPase
cardiac muscle contraction very similar to skeletal muscle contraction
- what’s main difference?
for cardiac, most Ca2+ comes from extracellular fluid (and not SR like skeletal)
cardiac muscle contraction can be ________
- force generated is proportional to number of what? –> determined by what?
- what also affects force of contraction?
- graded!
- proportional to number of active crossbridges
- determined by how much calcium bound to troponin (more Ca2+ = more crossbridges = more contraction)
- sarcomere length
how is cardiac CONTRACTILE cell action potential different than normal AP?
describe 5 phases (0 to 4)
- Na+ channels open (increase PNa+ –> depolarization just like neuron due to Na+ inflow
- Na+ channels close = top of line (decrease PNa+) = initial repolarization
- Ca2+ channels open (from ECF) + fast K+ channels close (decrease PK and increase PCa) –> plateau! = very unique
- long AP due to Ca2+ inflow –> sustains refractory period and prevents tetanus - Ca2+ channels close + slow K+ channels open (decrease PCa and increase PK) –> line goes down = repid repolarization du to K+ outflow
- resting potential
benefits of cardiac AP (with a plateau) –> 2
- have additional Ca2+ flow
- much longer AP = much longer refractory period (lasts as long as the entire muscle twitch)
cardiac muscle can’t have accumulation of summation of muscle contractions (________) –> because of what?
tetanus
- bc much longer refractory period
Action potential in cardiac AUTORHYTHMIC CELLS
- 4 steps!
- pacemaker potential = unstable bc have funny channels/HCN/If channels –> can open both Na+ (get in) and K+ (get out) channels
- mostly Na+ gets in –> membrane potential increase = depolarization - depolarization causes voltage gated Ca2+ channels to open and get into cell = further depolarization –> reaches threshold –> causes AP –> AP caused by Ca2+!! not Na+
- If channels close = decrease Na+ inflow - at threshold, 2nd type of voltage gated Ca2+ channels open = steep deloparization
- rising part of AP = Ca2+ in - At peak, Ca+ channels close + slow voltage gated potassium channels open –> K+ out = repolarization + hyperpolarization –> pacemaker potential returns to lowest point
____A___ signals coordinate heart contraction
- internodal pathway form which node to which node –> routes the direction of ____A_____ signals so the heart contracts from ______ to ______
- _______ fibers transmit signals down what? to _____ and _____bundle branches
- electric signals
- from sinoatrial node (SA) to atrioventricular node (AV)
- direction of electric signals –> contract from apex to base bundle branches
- Purkinje fibers –> down atrioventricular bundle (AV bundle or bundle of His) to left and right buundle branches
what sets the pace of the heartbeat?
- at how much?
- what can act as pacemakers under some conditions? (2)
- how to make sure atrium and ventricles won’t contract at same time?
- SA node! –> like a train where all the cars will be moving at the speed of the fastest car (SA node)
- at 70 bpm
- AV node (50 bpm) and Purkinje fibers (25-40 bpm) –> if problem with SA node, AV node can take over
- AV node delay!
which type of cardiac muscles have a plateau?
contractile cells!
where is SA node located?
between R atrium and superior vena cavae
5 steps for conduction system of the heart
- SA node depolarizes
- electrical activity goes rapidly to AV node via internodal pathway
- depolarization spreads more slowly across atria. conduction slows through AV node
- depolarization moves rapidly through ventricular conducting system to the apex of the heart
- depolarization wave spreads upward from the apex
how to quickly spread electric signals from SA node? (2)
- signals transfer through gap junctions
- intermodal pathways
what does the electrocardiogram show?
- same as action potential?
show the summed electrical activity generated by all the cells of the heart
- no!
3 waves of ECG + 2 segments
WAVES:
- P wave: depolarization of atria
- QRS complex: wave of ventricular depolarization + atrial repolarization (downward curve of Q ish)
- T wave: repolarization of ventricle
SEGMENTS:
- P-R segment : AV node delay
- T-P segment: ventricular and atrial relaxation
diastole vs systole?
- diastole: cardiac muscle relaxes
- systole: cardiac muscle contracts
describe the 5 phases of cardiac cycle
- heart at rest: atrial and ventricular diastole –> atria are filling with blood from vein + AV valves open –> ventricles fill at 80%
- completion of ventricular filling: atrial systole –> atrial contract –> drives last of 20% blood volume into ventricles
- End-diastolic volume (EDV): volume in ventricle at end of ventricular relaxation - early ventricular contraction: close AV valves + semilunar valves closed + no blood in or out = isovolumic ventricular contraction –> increase pressure due to ventricular muscle contraction
- concurrent atrial diastole: atria relax and blood flows in atria - heart pumps: ventricular ejection: pressure in ventricles > arteries pressure = semilunar valves open –> blood ejected in arteries
- End-systolic volume: volume in ventricle at the end of ventricular contraction - isovolumic ventricular relaxation: arterial blood flows back to heart, semilunar valves are closed, ventricular muscles relax and pressure drops (still higher than atrial pressure), no blood exits or enters
- semilunar valves close
- AV valves open when ventricular pressure drops below atrial pressure
What is EDV vs ESV vs isovolumic ventricular contraction?
- End-diastolic volume (EDV): blood volume in ventricle at end of ventricular relaxation –> highest volume in ventricle
- End-systolic volume (ESV): blood volume in ventricle at end of ventricular contraction
- Isovolumic ventricular contraction: no blood in or out
what is cardiac output?
- how to calculate?
cardiac output = how much blood pumped out by 1 ventricule per minutes
- measure of cardiac performance
- CO = stroke volume x heart rate
- average = 5L/min
what is stroke volume?
- How to calculate stroke volume?
- how much blood pumped out per heart beat
- volume of blood before contraction minus volume of blood after contraction
- SV = EDV - ESV
- average: 70 mL for 70kg man at rest
name the 5 phases of cardiac cycle
- atrial and ventricular diastole
- atrial systole
- isovolumic ventricular contraction
- ventricular systole
- isovolumic ventricular diastole: early ventricular diastole + late ventricular diastole
- Atrium & ventricle: systole or diastole?
- AV valves & semilunar valve: open or close?
1. atrial and ventricular diastole
2. atrial systole
3. isovolumic ventricular contraction
4. ventricular systole
5. isovolumic ventricular diastole
ATRIUM:
- D –> S –> D –> D –> D
VENTRICLE:
- D –> D –> S –> S –> D
AV VALVE:
- O –> O –> C –> C –> C/O
SL VALVE:
- C –> C –> C/O –> O –> C
Autonomic division modulates heart rate
- PSNS: decrease/increase HR? How? (2) + what neurotransmitter on what receptors?
- SNS: decrease/increase HR? How? (2) + what neurotransmitter on what receptors?
- tonic control: what dominates?
PSNS:
- decrease heart rate by making it longer to reach threshold
1. K+ permeability increases: pacemaker potential begins at lower value
2. Ca2+ permeability decreases: slows rate of pacemaker depolarization
- Ach on muscarinic receptors of autorhythmic cells
SNS:
- increase HR
1. b1 adrenergic receptors on authorhythmic cells
2. Na+ & Ca2+ permeatbility increases –> increases rate of pacemaker depolarization
- NE on b1-receptors of autorhythmic cells
TONIC CONTROL: normally dominated by parasympathetic activity
what is contractability?
intrinsic ability of a cardiac muscle fiber to contract at any given fiber length
Length-tension relationship:
- determined by ________ of blood at beginning/end of contraction
- degree of stretch is called _______
- increase length = increase/decrease contractile force
- volume of blood at beginning of contraction!
- preload
- increase length = increase contractile force (different than for skeletal muscle where you had to be at optimal length)
Frank-Starling law of the heart:
- stroke volume is proportional to ___A__
- ___A___ is determined by what? which is affected by (3)
- proportional to End-diastolic volume (EDV)
- EDV determined by veinous return
1. skeletal muscle pump
2. respiratory pump (helps blood go back to heart)
3. sympathetic innervation of veins
the force/tension created by a striated muscle is directly related to the _______ _______ of the sarcomere
starting length
- any chemical that affects contractility is an _______ agent
increase or decrease contractibility?: - positive _____A_____ (4)
- negative _____A_____
- inotropic agent! –> inotropic effect
POSITIVE INOTROPES: - increase contractibility
- epinephrine (80%) + norepinephrine (20%) + digitalis + catecholamines increase Ca2+ storage with phospholamban
NEGATIVE INOTROPES: - decrease contractibility
- what is afterload? –> what (2) determine afterload?
- what is ejection fraction? formula?
AFTERLOAD:
- combined load of EDV and arterial resistance during ventricular contraction
- determined by EDV and arterial blood pressure
EJECTION FRACTION:
- percentage of EDV ejected with one contraction
- stroke volume / EDV
how can catecholamines (hormones) increase cardiac contraction? (2 pathways)
NE and E –> bind to b1 receptors –> activate cAMP
1. phosphorylation of voltage gated Ca2+ channels –> open time increases –> increase Ca2+ entry from ECF –> more forceful contraction
2. phorphorylation of phospholamban (membrane protein) –> increase Ca2+ ATPase on SR –> increase Ca2+ stores in SR –> increase Ca2+ released –> more forceful contraction!!
* increase Ca2+ ATPase on SR will also make Ca2+ removed faster from cytosol = shortens Ca-troponin binding time = shorter duration contraction
