cardiovascular system Flashcards
sympathetic
neurons:
neurotransmitters:
post-ganglionic neuron receptors:
target organ receptors:
arise from:
synapse location:
aka:
neurons:
- short pre-ganglionic
- long post-ganglionic
neurotransmitters:
- pre-ganglionic neurons release ACh
- post-ganglionic neurons release NE
post-ganglionic neuron receptors: nicotinic cholinergic receptors
target organ receptors: adrenergic receptors
arise from: thoracic & lumbar region of spine
synapse location: paravertebral ganglia aligned next to spinal cord
aka: thoracolumbar region
parasympathetic
neurons:
neurotransmitters:
post-ganglionic neuron receptors:
target organ receptors:
arise from:
synapse location:
aka:
neurons:
- long pre-ganglionic
- short post-ganglionic
neurotransmitters: both pre & post-ganglionic neurons release ACh
post-ganglionic neuron receptors: nicotinic cholinergic
target organ receptors: muscarinic cholinergic
arise from: brain stem or sacral lumbar region of spinal cord
synapse location:: ganglia in target organs
aka: craniosacral region
afferent pathways
gather/sense info from visceral organs
- aka autonomic afferents
- also subject to input from higher cortical regions
- ↑ in 1 pathway automatically associated w/ ↓ in other
parasympathetic afferents
- CPU in brain stem
- synapse in brain stem
sympathetic afferents
- CPU in para-vertebral ganglia
- synapse in spinal cord
pressure
pressures = force/area
- arterial (adj): related to elastic arteries
-
arteioles = major resistance vessels
- CO determiens bf into arteries but arterioles determine bf out
- systolic/diastolic BP = arterial BP measured in elastic arteries (not ventricular)
- SBP measured when ventricles eject blood into aorta (arteries)
- DBP measured when ventricles are relaxed
- pressure drops as blood flows through the system
CO
CO = HR x SV (mL/min)
- flow out of heart determined by HR & SV
- dependent on:
- radius (main determinant) ➔ flow = r4
- length
- viscosity: dehydration & ↑ RBC count
direction & polarization:
Na
Ca
K
Na in = depolarizing
Ca in = depolarizing
K out = repolarizing
cardiac myocyte AP
phase 0: rapid depolarization
- activation of v-gated channels:
- normal Na channels
- transient Ca channels open but not active
- L-type Ca channels open but not active
- IK-rapid & IK-slow channels open but not active
- IK-T.O. channels open but not active
peak: majority of Na channels inactivate
phase 1: brief incomplete repolarization
- IK-T.O. transient channels active ➔ K efflux
- ICl-T.O.-2 channels active ➔ Cl influx
phase 2: plateau ➔ still depolarized but slowly repolarizing
- L-type Ca channels fully active ➔ Ca influx = depolarizing
- IK-rapid & IK-slow channels fully active ➔ K efflux = repolarizing
transition point: inactivated L-type Ca channels
phase 3: complete repolarization
- IK-rapid & IK-slow channels maximally active
- IK-1 channels always open ➔ background K efflux
phase 4: RMP ➔ IK-1 channels ➔ background K efflux
0: rapid depolarization
- Na channels open ➔ Na influx fast
- L-type Ca channels & transient Ca channels, I_K-rapid & I_K-slow channels also open but not maximally activated
1: brief incomplete repolarization
- Na channels inactivate
- K effliux & Cl influx
- IK-T.O. & ICl-T.O.-2 channels active
2: plateau phase
- K efflux & Ca influx slow
- IK-rapid & IK-slow channels maximally active
- L-type Ca channels maximmaly active
3: complete repolarization
- L-type Ca channels close
- IK-rapid & IK-slow channels remain maximally active
- IK-1 channels ➔ background K efflux
4: RMP
- IK-rapid & I_K-slow channels close
- IK-1 channels remain open
pacemaker cell AP
- excitable autorhythmic cells only ➔ AP changes shape as soon as exits cells
- slow to rise
- maximum diastolic potential (MDP) = −60 mV
phase 4: slow depolarization to threshold
- “funny channel” IF = HCN channel activated during repolarization (phase 3) ➔ Na influx
- critical for autorhythmicity
- inactivated with depolarization ➞ why we need ICa-T
- transient Ca current: I_Ca-T channel activated by depolarization
phase 0: depolarization carried by Ca influx
- L-type Ca channel maximally active
- NCX = Na-Ca Exchanger ➔ removes Ca from intracellular fluid allowing Na influx & depolarizes cells (most active towards end of phase 0)
peak: L-type Ca channels innactivate
phase 3: IK-rapid & IK-slow open when depolarized
- as MP moves towards MDP: both shut down
AV node
atrioventricular node
- in RA (next to R AV valve)
- causes AV nodal delay ➔ ensures atria contract completely & finish ventricular diastole before ventricular systole
- atria always beat before ventricles
- atrial myocytes contract simultaneously
- AN region: slows down AP
- N region: 0.05 m/s (slowest - almost stopped)
- NH region: AP speeds up
ECG
recorded cardiac electrical activity on surface of skin
- segments: time regions between waveforms
- interval: segments + 1-2 waveforms
- P wave: atrial depolarization
- QRS complex: ventricular depolarization (atrial repolarization masked)
- T wave: ventricular repolarization
- PR segment no electrical activity ➔ AV nodal delay: 100 m/s
- PR interval: period of atrial depolarization & delay
-
QT interval: represents ventricular depolarization & repolarization
- ~360-390 msec in men
- ~370-420 msec in women
conductive pathways
- SA (sinoatrial node): primary pacemaker
- interatrial pathway: SA ➔ LA (1 m/s)
- internodal pathway: SA ➔ AV (1 m/s)
- bundle of His & purkinje fibers ➔ ventricles (2-3 m/s)
first degree AV block
- slowing of conduction through the AV node
- PR segment lengthens to ~300 ms (normally 100)
- symptoms: asymptomatic, tiredness, feeling out of sorts, lightheadded, dizzy
- causes: AV nodal infx, heart blockage ➔ ischemia: ↓ bf to cardiac tissues, ↑↑ PNS output
- not usually fatal
- always has QRS complex
first degree heart block
- slowed conduction through AV node
- PR segment lenthens
- asymptomatic, tiredness, feeling out of sorts, lightheaded, dizzy
- causes: AV nodal infx, ischemia, ↑↑ PNS activity
- not usually fatal
- always has QRS complexes
second degree AV block
- skip a ventricular beat
- incomplete coupling of the atria to the ventricles
- missing QRS complex
- no pattern or set # of skips
- when ventricles do depolarize, it happens w/in a given PR segment after atria
- causes: chest trauma, AV nodal disease, bacterial carditis, strong coughing/sneezing
- can lead to sudden cardiac death
- symptoms: tired, dizzy, syncope, usually asymptomatic
2nd degree heart block
- skip a ventricular beat
- incomplete coupling of the atria to the ventricles
- missing QRS complex
- no pattern or set # of skips
- when ventricles do depolarize, it happens w/in a given PR segment after atria
- causes: chest trauma, AV nodal disease, bacterial carditis, strong coughing/sneezing
- can lead to sudden cardiac death
- symptoms: tired, dizzy, syncope, usually asymptomatic
third degree AV block
- no relationship btwn atrial rhythmicity & ventricle rhythmicity
- SA node fires normally but ventricles fire at a different slower given rate
- ventricles are driven by ectopic pacemaker @ slower rate: 40 bpm
- symptoms: tiredness, syncope, foggy brain
- does not usually result in sudden cardiac death
- causes: trauma, cardiac disease
3rd degree heart block
- no relationship btwn atrial rhythmicity & ventricle rhythmicity
- SA node fires normally but ventricles fire at a different slower given rate
- ventricles are driven by ectopic pacemaker @ slower rate: 40 bpm
- symptoms: tiredness, syncope, foggy brain
- does not usually result in sudden cardiac death
- causes: trauma, cardiac disease
long QT syndrome
ventricular myocytes fire AP that are not coordinated in time w/ other ventricular myocytes
- prolonged QT interval (~500+ ms)
- cells still conducting when Na-activation gets get activated
- no blood is ejected
- v-gated channels may still be able to activate as normal
- can result in cardiac arrest & sudden death
- symptoms: fatigue, foggy brain, syncope
- results in ventricular fibrillation
- caused by problems with repolarization
- LQTS #1 & LQTS #5: I_K-slow channel loss of fx
- LQTS #2: I_K-rapid channel loss of fx
- LQTS #3: v-gated Na channel gain of fx activated during absolute refractory period ➞ QT looks normal-shorter than normal on ECG
-
tx:
- β-adrenergic receptor blockers ➞ causes fatigue
- implanted defibrillators
- sympathectomy: cutting sympathetic input ➞ last resort
ventricular fibrillation
torsades de pointes: ventricular myocytes contracting indiv
cardiac myoctes
- strength
- communication
-
desmosomes: strength jxs
- structures in 2 plasma membranes w/ extremely strong linking fibers
- need extra strength b/c of contracting adjacent cells
- gap jxs: electrical pathway for AP to spread to adjacent cells (@ 1 m/s)
valves & walls
atrioventricular (AV) valves prevent backwards flow from ventricles to atria
- tricuspid in R
- bicuspid in L
semilunar valves prevent backwards flow from pulmonary veins & aorta to ventricles
- pulmonary semilunar in R
- aortic semilunar in L
chordae tendineae: fibers attaching AV valves to papillary muscles in ventricle walls
trabeculae carneae: columns of ventricular myocytes w/ deep invaginations that allow separation of blood flow
blood flows in series
vena cava ➔ RA ➔ RV ➔ pulmonary truk➔ L & R pulmonary arteries ➔ pulmonary capillaries ➔ L & R pulmonary veins ➔ LA ➔ LV ➔ aorta ➔ arterioles ➔ capillaries ➔ veins ➔ vena cava
cardiac muscle excitation & contraction coupling
- myocytes are excited to thresholdd by pacemaker AP
- AP travels down T-tubules immediately adjacent to SR
- dihydropyridine receptor (DHPR): v-gated channe in t-tubule membrane activated by depolarization causes Ca influx
- AP & Ca influx activates ryanodine receptors (RYR) in SR ➞ more ca influx
- Ca influx inducers further activation of DHPR
-
Ca induced Ca release (CACR): elevated intracellular Ca activates ryanodine receptors
- I_K-rapid & I_K-slow maintain MP
- Ca interacts w/ regulatory proteins on thin filament
- tropomyosin blocks myosin binding site on thin filament
- stabiilzed in place by troponin w/ 3 subunits
- troponin I binds to actin & inhibits contraction
- troponin T binds to tropomyosin
- troponin C binds to Ca
relaxation of cardiac myocytes
- repolarization (phase 3)
- closed L-type Ca channels
- removes Ca from cytosol
-
NCX: Na-Ca exchanger ➔ 1 Ca out for 3 Na in
- uses 2º active transport: ATP-ase pumps 3 Na out, leaving intracellular space negatively charged
- activated by reduced intracellular [Ca]
- 3 Na enter to fill void ➔ Ca exits cells via counter-current
- SERCA pump: replenish SR Ca store: intracellular Ca ➔ SR
- PM Ca pump: intracelluar Ca ➔ ECF
- Na-K ATP-ase: pumps 3 Na out to 1 K in
-
NCX: Na-Ca exchanger ➔ 1 Ca out for 3 Na in
cardiac pressure volume loop:
1: semilunar valves close
2: diastole
3: isovolumetric relaxation
4: ventricular filling
5: AV valves open
6: end-systolic volume
7: end-diastolic volume
8: atria contract
9: systole
10: AV vavlves close
11: isovolumetric contraction
12: semilunar valves open
13: ventricular emptying
end-diastolic volume
V remaining in blood after complete filling
- determines how much blood is ejected in 1 heartbeat
- ~135 mL in non-diseased resting state
isovolumetric contraction
AV & semilunar valves closed ∴ volume stays the same
- points C-D
- start of systole
isovolumetric relaxation
semilunar & AV valves closed ∴ volume stays the same
- points F-A
- start of diastole
end-systolic volume
V remaining in ventricles after complete ejection
- ~65 mL in non-diseased resting state
stroke volume
SV = EDV - ESV ≈ 70 mL
contractile force vs resting length
↑ EDV due to ↑ venous return → ↑ developed force
- resting length = EDV → already at max force with perfect overlap
mechanisms:
- maybe as we ↑ EDV we ↑ # of cross-bridges
- ↑ EDV (stretching walls of ventricle) ↑ geometric advantage: distance between thick & thin filaments decreases as the sarcomere is stretched ➔ as sarcomeres lengthen, they get smaller in diameter → develops force
- ↑ Ca affinity to troponin-C: stretch of muscle ↑ affinity of troponin-C to Ca → greater amount of time Tn-C is bound to Ca allows greater crossbridge cycling → greater force (depends on [Ca] & affinity)
frank-starling rule of the heart
as EDV ↑, ventricular force ↑
- ↑ venous return → ↑ EDV
- increased Ca sensitivity occurs at longer muscle fiber lengths
- more EDV = more preload = more SV = more forceful contractions
- preload: volume in ventricles (=EDV)
-
afterload = back-pressure in the elastic arteries keeping semilunar valves closed (bad)
-
hypertension: afterload increases
- genearlly aortic/systemic
- must raise pressure in ventricles higher before can open semilunar valves & get normal ejection fraction
- extra work for heart
- > 140/90 (could be normal SP & still hypertensive if >90 DP
- prehypertensive: 130-140/81-90
-
hypertension: afterload increases
pathways in the CV system
- pulmonary circylation+ RA + RV dives bf to lungs for gas exchange (≈ 10-12% total blood volume)
- systemic circulation+ LA + LV: drives bf to tissues
- arteries/arterioles carry blood away from the heart
- capillaries = exchange vessels
- veins & venules carry blood towards the heart
Ca induced Ca release (CACR)
elevated intracellular Ca activates dihydropyridine receptors (DHPR)
vessel layers
tunica adventitia/externa: outermost layer
- strong connective tissue, collagen, elastin, & fibroblasts to help create overall structure
- anchors vessels’s w/in tissue
- proportion of thickness varies btwn vessel type (proportionally larger in veins than arteries)
tunica media: smooth muscle cells & connective tissue
- could be continuous in a distinct layer or discontinuous
- changes diameter of vessel
- missing in capillaries
tunica intima/interna: endothelium
- sometimes can find elastin or connective tissue
vasovasorum: “blood vessels of the blood vessels” ➔ large vessels (aorta/vena cava) require own vessels to supply blood
elastic arteries
fill w/ blood, stretch (storing potential energy), & recoil ➔ squeezes blood ➔ ↑ pressure
- pressure reservoir allows us to drive bf during diastole
- has all 3 tissue layers
-
mean arterial pressure (MAP): driving force for bf from arteries ➞ capillaries
- homeostatically regulated but parameters can shift after years of consistency
- MAP = 1/3 SP + 2/3 DP or MAP = DP + 1/3 (SP−DP)
- 1/3 the time spent in systole & 2/3 spent in diastole
- arteries ≈ 15% total blood volume
muscular arteries
distribution arteries: directs blood to certain regions
- changes proportion of bf allocated
- downstream of elastic arteries
- smaller than elastic arteries
arterioles
major resistance vessels
- vasoconstrict in response to ↑ SNS input
- vasodilate in response to ↓ SNS input & signal factors (local metabolites)
- varying number of tissue layers
- larger arterioles hav eall 3 layers w/ continuous SM
- smaller arterioles have discontinuous bands of SM
- avg diameter ~30 microns
capillaries
exchange vessels
- thin wall, only endothelial cells ➔ facilitates gas exchange
- no tunica media or tunica externa/advantitia
- pores in wall allow water-sol mol + ions + bigger mol through
- slow bf through capillaries
- arranged in beds
-
bg is regulated by sphincters
- closed by ↑ SNS activity
- precapillary sphincters = SM rings slightly up-stream of capillary beds
- metaarterioles: alternate pathways from arterioles straight to veins to bypass capillaries (ex: skin)
- capillaries ≈ 5-7% total blood volume
1. continuous capillaries: impervious to maintain unique ECF composition (i.e. brain, testes) ➔ things must be transported in regulated manner
2. fenestrated capillaries: big holes/perforations
3. sinusoid capillary: vert large pore size facilitates movement of large mol (i.e. bone marrow, spleen, liver)
metaarterioles
alternate pathways from arterioles straight to veins to bypass capillaries (ex: skin)
venules
- receive blood from capillaries
- connect to veins
veins
dynamically store blood
- receive blood from venules
- no elastin
- connective tissue
- very thin walls
- all 3 layers
- low P to drain capillaries & venules ➞ disadvantaged in venous return
- venous valves in large veins prevent backwards flow
- 60-66% total blood volume
A: HCN channels open ➔ Na influx = depolarization
B: maximum diastolic potential (MDP)
C:
- T-type Ca channels open ➔ Ca influx = depolarizing
- HCN channels close with depolarization
D: L-type Ca channels open ➔ Ca influx = depolarizing
E:
- IK-rapid & IK-slow channels open when depolarized
- L-type Ca channels inactivate
F: IK-rapid & IK-slow channels inactivate
G: HCX active
what is the function of funny current via HCN channels?
it induces slow depolarization of the pacemaker potential during phase 4
what is homeostatically regulated by CV system?
- mean arterial pressure (MAP)
- total body water content
why don’t the elastic arteries function in exchange
blood flow is pulsatile & fast flow cannot efficiently exchange material with tissues
what is the driving force acting on blood moving it through the arteries?
mean arterial pressure (MAP)
what is the equilibrium potential due to
passive ion flux across a membrane
function of desmosomes
trnasfer force between contracting cardiac cells
an intercalated disc contains:
desmosomes & gap junctions
what is the function of cardiac papillary muscle contraction
helps prevent the AV valves from everting into atria during ventricular systole
where in the conducting pathways of the heart, does the pacemaking action potential slow down?
the AN region of the AV node
what is the physiologic significance of cardiac muscle refractory period?
the refractory period allows the ventricles to completely fill during diastole
what occurs during the (left) ventricular ejection phase of the cardiac cycle?
ventricular pressure exceeds aortic pressure
what drives blood flow through systemic circulation during diastole
elastic arteries recoil
