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
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
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
metaarterioles
alternate pathways from arterioles straight to veins to bypass capillaries (ex: skin)
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
