PHYS: CVS Flashcards
1
Q
2 circulations in the CVS and what are their pressures?
A
- systemic (left): between organs and heart (high pressure - 95mmHg)
- pulmonary (right): between lungs and heart (low pressure - 15mmHg)
2
Q
describe the TYPE of flow in the systemic and pulmonary circuits
A
- in series with each other: blood goes through one then the other, amt of blood in each circuit is equal per unit time
- pulmonary: blood flows in parallel within the lungs
- systemic: blood is shared amongst organs based on needs (parallel)
3
Q
how does blood flow through vessels?
A
- needs a pressure gradient, will flow from high to low pressure
- NB it is the DIFFERENCE in pressure, not the actual number, that is important
4
Q
2 types of blood flow thru a vessel
A
- laminar: smooth, silent
- turbulent: swirling, noisy, may occur if flow is restricted
5
Q
which 3 factors influence resistance to blood flow?
A
- vessel length
- vessel diameter (blood flow increases in proportion to the 4th power of the radius of the vessel e.g. a 2x increase in radius will cause a 16x increase in flow) - MOST IMPORTANT
- viscosity of blood (based on haematocrit, measured relative to water)
6
Q
what is haematocrit and what is it for males and females?
A
- % volume of blood occupied by RBC (increases w/ doping)
- males have slightly higher haematocrit = more Hb = can carry more oxygen
7
Q
formula for blood flow
A
- flow = pressure gradient/resistance
8
Q
3 components of intercalated discs
A
- gap junctions: electrical connections via flow of ions
- desmosomes: mechanical connections
- fascia adherens: physical adhesion
9
Q
cardiac conduction system
A
- SA node: pacemaker cells that spontaneously generate APs
- internodal pathways connect SA node and AV node
- Bachman’s bundle carries signals from R atrium to L atrium
- AV node
- bundle of his (septum) + L/R bundle branches
- Purkinje fibres
10
Q
why is there slower conduction at the AV node and how is this achieved?
A
- allows sufficient delay for chambers to fill w/ blood b/n atrial and ventricular contraction
- less gap junctions b/n cardiomyocytes @ the AV node
11
Q
how do we record membrane potential?
A
- place a micro electrode inside and outside an SA node cell
- difference b/n ECF and ICF voltage is the membrane potential
12
Q
what is maximum diastolic potential?
A
- lowest membrane potential reached in a cardiac AP (occurs @ diastole)
13
Q
concentrations of Na+, Ca2+, K+ inside vs outside the cell
A
- Na+ and Ca2+ are greater outside the cell
- K+ is greater inside the cell
14
Q
difference b/n cardiac and pacemaker APs
A
- cardiac: stable RMP in between APs, MORE negative maximum diastolic potential (-90mV) , plateau phase @ max potential, NON-SPONTANEOUS
- pacemaker: no stable RMP, LESS negative maximum diastolic potential (-65mV) , no plateau phase @ max potential, SPONTANEOUS
15
Q
stages of a cardiomyocyte action potential
A
- PHASE 4: stable RMP maintained due to relative conc of Na+, Ca2+, K+
- PHASE 0: depol (upstroke) - FAST Na+ channels open = Na+ influx
- PHASE 1 + 2: then to repolarise, K+ channels open for K+ efflux, however L-type Ca2+ channels open in opposition = Ca2+ influx = plateau = elongates AP for ventricular filling
- PHASE 3: repol (downstroke) - Ca2+ channels close = K+ repolarisation force to overpower = K+ efflux = back to RMP (phase 4)
16
Q
stages of the pacemaker (funny) potential
A
- slow depol due to influx of Na+ as it tries to fix the RMP but these are also open too long > reaches threshold
- actual depol: Ca2+ influx via T-type then L-type channels
- repolarisation: K+ efflux to return to RMP but stay open too long (cycle repeats)
17
Q
why can the heart contract spontaneously?
A
- in pacemaker APs: repolarisation of SA node kicks off the next depolarisation > continuous cycle
18
Q
why is the SA node the pacemaker and what happens if it’s damaged?
A
- b/c it generates the most action potentials per min (60-100 bpm)
- if this is damaged the AV node will take over (40-60 bpm)
- if this is damaged, SA node will still beat normally (60-100 bpm) but then purkinje fibres will take over for ventricles (20-40 bpm) > diff rates
- DIFFERENT FROM ECTOPIC BEATS
19
Q
what happens if there is a spontaneous generation of an impulse in another region of the heart? why can this occur?
A
- called ectopic focus
- another component will generate lots of action potentials = fastest = takes over as the primary pacemaker
- e.g. due to electrolyte imbalances, ischaemia, AMI etc
20
Q
changes in HR for fit ppl
A
- decreased resting HR
- goes back to resting HR faster
- max HR not altered (decreases w/ age)
21
Q
how is heart rate maintained @ rest vs during exercise?
A
- normally: by parasympathetic stimulation
- exercise: increased by reducing parasympathetic and increasing sympathetic input to SA node
22
Q
conduction rate of SA node, AV node, purkinje fibres
A
- SA node: 60-100bpm
- AV node: 40-60bpm
- Purkinje fibres: 20-40bpm
23
Q
quadriplegic, sedentary, heart transplant thing
A
- quadriplegic = parasympathetic only, no sympathetic = slower resting HR b/c parasymp dominates and can’t reach max HR of 200
- sedentary = normal autonomic innervation
- transplant recipient = no autonomic innervation = higher resting HR b/c no parasympathetic to slow it down
24
Q
frank starling law
A
- increased EDV = increased stretch of cardiomyocytes = more optimal overlap of actin and myosin = increased force of contraction = increased SV/CO
25
how is blood flow to tissues continuous despite intermittent flow thru aorta?
- 2/3 of blood from each pump goes to stretch artery walls and 1/3 flows straight thru (systole)
- when aortic valve closes during diastole, artery walls recoil and the remaining 2/3 flows thru (diastole)
26
how to calculate pulse pressure and mean arterial pressure
- PP: SBP-DBP
- MAP: DBP + 1/3(PP) OR 2/3(DBP) + 1/3(SBP) OR
CO x TPR
27
dichrotic notch
- small dip in BP due to closing of aortic valve, just after systole
28
how does taking BP work with reference to the brachial artery?
- when we inflate the cuff it compresses the brachial artery = no flow
- when we slowly deflate, the artery is partially open = turbulent flow
- flow becomes laminar
29
cutoff for hyper and hypotension
- HTN: consistently above 140/90
- hypotension: consistently below 100/60
30
main difference in function for arteries vs arterioles
- arteries = pressure reservoir
- arterioles = vasoconstriction or dilation to certain areas based on physiological need
31
metabolic control of arterioles
- arterioles vasodilate in response to increased levels of CO2/H+/K+ etc = increased blood flow
- mostly in skeletal and cardiac muscle
- active hyperaemia
32
myogenic mechanism (autoregulation)
- arterial stretch causes vasoconstriction of downstream arterioles = decreased blood flow
- allows organs to maintain constant blood flow despite upstream changes in arterial pressure
33
2 local methods of control for arterioles
- myogenic mechanism
- metabolic control
34
autonomic innervation of arterioles
- mostly sympathetic only (no parasympathetic apart from genitals)
- NA acts on a1 receptors to cause vasoconstriction = decrease in blood flow to GIT/other organs
35
hormones which act on arterioles
- adrenaline - acts on a1 receptors to cause vasoconstriction to less important organs OR acts on B2 receptors to cause vasodilation to important organs
- angiotensin II and ADH - vasoconstriction
- ANP - vasodilation
36
at rest, are most capillaries open or closed?
- usually closed via precapillary sphincters
- during exercise they open to allow more blood flow
37
normal capillary refill time
- <2 seconds
38
2 major forces driving and opposing capillary filtration and how do we calculate net filtration pressure?
- hydrostatic pressure/blood pressure - DRIVES filtration OUT of capillaries, mostly @ arteriolar end
- plasma osmotic (colloidal/oncotic) pressure - plasma proteins = OPPOSES filtration out of capillaries. mostly @ venular end
- net filtration pressure = hydrostatic - osmotic pressure
39
where does all lymph fluid drain into?
- subclavian vein via thoracic duct
40
4 causes of oedema
- increased hydrostatic pressure/blood pressure (more filtration OUT of capillaries and excess tissue fluid) e.g. HTN or heart failure
- decreased osmotic pressure e.g. thru malnutrition, liver disease, kidney disease
- lymphatic drainage issues e.g. L/N tumour
- capillary permeability issues e.g. inflammation/histamine
41
3 mechanisms which impact venous return
- pressure gradient b/n veins and R atrium (sympathetic action causes stiffening of walls = less compliance = increased pressure)
- skeletal muscle pump
- respiratory pump: decreased pressure in thorax during inspiration = increased pressure in abdomen
42
implication of increased venous return
- increased increased venous return = increased EDV = increased force of ventricular contraction = increased SV = increased CO = increased MAP
43
what is orthostatic hypotension and how does it occur
- defined as when SBP drops by more than 20mmHg, diastolic drops by more than 10mmHg
- stand up quickly = pooling of blood in lower extremities = decreased venous return = decrease EDV, SV and thus CO = rapid drop in MAP
44
what is total peripheral resistance (TPR?)
- sum of vascular resistance of all tissues, altered by constriction or dilation of arterioles
45
baroreceptor reflex in response to LOW pressure
- low blood pressure = decreased stretch of artery walls = decreased AP firing of baroreceptors (aortic arch and carotid sinus)
- leads to sympathetic activation (4 ways):
- SA node increases HR
- ventricles increase SV
- veins constrict and decrease compliance = INITIAL increased venous pressure = increased venous return and EDV
- arterioles constrict = increased TPR
- to increase BP back to WNL
46
5 phases of cardiac cycle
- passive filling of ventricles from atria (80%) since atrial pressure > ventricular pressure (AV open, SL closed)
- atrial systole (20%) - AV open, SL closed
- isovolumetric contraction - ventricles contract but no blood leaves b/c all valves closed = increase in pressure to surpass pressure in aorta/PT
- ventricular ejection - when ventricular pressure surpasses pressure in aorta/PT, SL valves open to allow blood to leave heart
- isovolumetric relaxation - ventricles relax but no blood enters b/c all valves closed = decrease in pressure to be less than atria - cycle repeats
47
why does head-up tilt reduce cardiac output?
- blood pools in veins in lower body
48
compliance formula
- C = (V-V0) / P
- C = compliance
- V = volume
- V0 = min volume required to fill vessel before pressure can increase
- P = pressure
49
how to calculate hydrostatic or colloid pressure
- (hydrostatic or colloid) pressure in capillary - interstitial pressure
50
how does atherosclerosis form
- LDL cholesterol taken up into vascular walls and oxidised
- attracts monocytes > differentiate into macrophages > phagocytose lipids to form foam cells
- inflammatory cytokines released which further attracts immune cells inc B/T cells
- smooth muscle cells migrate to endothelium, forming a fibrous cap to stabilise underlying lipid core
51
3 serum markers of atherosclerosis
- C-reactive protein
- amyloid A
- fibrinogen
52
2 types of atherosclerosis
- stable: thick fibrous cap, thin lipid core, unlikely to rupture, causes stable angina or asymptomatic
- unstable: thin fibrous cap, large lipid core, prone to rupture, causes thrombus/ischaemia = unstable angina/AMI
53
why is angiography not good for identifying unstable plaque?
- can't determine what is happening in wall, only in lumen
54
endothelium derived relaxing factor (EDRF): how is it produced and what does it do?
- nitric oxide (NO)
- produced by endothelium in response to ACh and shear stress (blood flow)
- Ca2+ enters endothelial cells, activating eNOS which converts L-Arginine precursor into NO
- NO diffuses into smooth muscle cells = triggers increase of cGMP = decreased Ca2+ = smooth muscle relaxes (vasodilation)
- if endothelium is damaged = vasoconstriction = increased BP
55
3 factors that cause relaxation of smooth muscle and what type of vessels do they act on?
- EDRF: endothelium derived relaxing factor (large vessels)
- PGI2: prostacyclin (large vessels)
- EDHF: endothelium derived hyperpolarising factor (smaller vessels) > smooth muscle can't contract > vasodilation
56
oxidative stress
- LDL in blood taken up into endothelium and oxidised = creates radicals
- radical binds to NO = less NO to vasodilate arteries = vasoconstriction
- leads to cycle of chronic hypertension > atherogenesis + endothelial dysfunction
57
what leads to an increase in constricting factors
- oxidative stress leads to upregulation of ang II, TxA2, ET-1 (endothelin-1) > vasoconstrictive agents
58
endothelin-1
- both vasoconstrictor and vasodilator
- usually inhibited by NO = when there is less NO due to oxidative stress, vasoconstrictive function dominates
59
first signs of endothelial dysfunction
- HTN
- hypercholesterolaemia
60
prostacyclin vs thromboxane
- physiological antagonists of each other
- both derived from arachidonic acid, produced by COX-1
- prostacyclin (anti-platelet): decreased intracellular Ca2+ = smooth muscle relaxation = vasodilation
- thromboxane (pro-platelet): increased intracellular Ca2+ = smooth muscle contraction = vasoconstriction
61
IL-1B
- what is it produced by
- when is it produced
- what does it do
- produced by inflammasomes in response to cholesterol, neutrophil extracellular traps (NETs) and ischaemia
- promotes atherosclerosis through increasing smooth muscle proliferation, macrophage activation, vascular inflammation, and endothelial dysfunction
