CARDIO Flashcards

1
Q

Describe the general structure of a cardiac myocyte..

A

type of straited muscle fibre

complex arrangement with branched structure whereby adjacent cells are linked by intercalated discs and gap junctions - to support quick ionic diffusion and spread of AP.

elongated structure - 100um x 20um

single nucleus centrally located

many mitochondria - aerobic respiration

membrane - invaginations T tubules - spread AP to centre of cell, increase S.A for ion channels

Sarcoplasmic reticulum for calcium storage - ryanodine receptors and SERCA to coordinate release and re-uptake.

associated with dense capillary bed - aerobic respiration

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2
Q

difference between cardiac and skeletal muscle

A

cardiac - more mitochondria, gap junctions, denser capillary bed , single nucleus

skeletal - multinucleated, triad T tubule with SR, ryanodine 1 receptors

both straited

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3
Q

explain the macroscopic arrangement of cardiac muscle that adapts it to function…

A

looped and helical overlapping muscle structure arranged to contract and expel blood in correct direction e.g. ventricles up into arteries.

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4
Q

what is the function of the intercalated disc?

A

provides electrical and metabolic continuity between myocytes

gap junctions = connexons = pore = fast spread of AP to allow coordinated contraction

structural integrity provided by desmosome junction complex - anchoring of cytoskeleton of 2 cells - increases strength during contraction

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5
Q

describe the structure of a sarcomere..

A

this is the contractile unit of a muscle cell.

consists of thick and thin filaments containing myosin and actin respectively

M line in the middle
bound by 2 Z lines

thin filament consists of actin (protein polymer) strands. Encircling this is tropomyosin and troponin complex of T,I and C.

thick filament consists of myosin filaments and their heads.

many organised in parallel and connected to cytoskeleton of the cell. means that during contraction when actin is pulled across myosin, the sarcomere shortens and this is transmitted throughout the whole cell, shortening the muscle fibre.

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6
Q

what is the function of troponin

A

troponin consists of 3 subunits - T, I and C
this is involved in sensing Ca within myocyte as a result of AP and moving tropomyosin away from actin-myosin binding site on actin.
hence plays a role in excitation- contraction couple

Troponin C bind Ca
Troponin T binds tropomyosin
I - unclear role.

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7
Q

what receptors exist in the heart?

A

adrenoceptors - B1 predominantely (B2 on coronaries)
muscarinic receptors - M2

others
glucagon GPCR Gs
Adenosine
histamine receptors - chronotropy and ionotropy
dopamine receptors - coronary vasculature (D1)

non-receptors but may be targetted by drugs = L type Ca channels,

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8
Q

describe the cardiac cycle…

A

divided into diastole and systole - usually 2/3 of the time spent in diastole, although this shortens with increased HR
which are further divided into 5 stages.

DIASTOLE
* isovolumetric relaxation - immediately after systole i.e. dicrotic notch position. all valves closed, atrial fill.
* ventricular filling phase - AV valve opens, SL closed. atria emptying into ventricles.

SYSTOLE
* atrial contraction - remaining 20% atria empty
* isovolumetric contraction - both valves closed, pressure builds up.
* ejection phase - SL valves open , blood ejected into aorta, initially rapid, then slows

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9
Q

draw a pressure - time curve to describe valvular changes and events during cardiac cycle…

A

1 - atrial systole (AV are open)
2 - AV valves close
3 - Isovolumetric contraction - rapid rise in ventricular pressure
4 - SL valves open + rapid ejection- continued rise in ventricular pressure but starts to curve round. aortic pressure rises as blood ejected out.
5 - reduced ejection
6 - SL close + isovolumetric relaxation - back flow in aortic - dicrotic notch
7 - rapid filing, AV open

important to label axis - x axis -0.2ms at start of contraction to 0.5ms at the end. cycle in total 0.8ms
pressures in aorta = 120/80
LA = 8-10mmJg
LV = 120- 0mmHg
start by drawing ventricular curve first, then aortic, then atrial.

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10
Q

what are the pressures of the right side of the heart…

A

RA = 0 to 4mmHg
RV = 25/0mmHg
Pulmoanry artery 25/10mmHg

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11
Q

draw a volume time curve for LV

A

1 - atrial sysole - remaining 20% enters
2 - isovolumetric contraction - no change in volume
3 - ejection phase - drop in volume
4 - isovolumetric relaxation
5 - diastole and filling phase

volume from 50 to 130
thus SV 80ml
time = 0.8ms in total
contraction = 0.2-0.5 ms

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12
Q

describe the JVP waveform

A

a = atrial contraction
c = tricuspid valve closes and isovolumetric contraction bulges tricuspid upwards
x descent = ejection phase, draws blood out, pulling heart and atria down
v wave = atrial filling against closed tricuspid
y descent = tricuspid valve opens and atria empty

pressure 4-12mmHg
normal JVP max around 8-12mmHg
time 0.8ms

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13
Q

describe the changes in the aortic pressure graph

A

pressure ranges 80-120mmHg
aortic valve opens at end of isovolumetric contraction and begining of ejection phase
blood ejected into aorta - increases pressure.
eventually aortic pressure extends ventricle
delay in closure of the valve since kinetic energy of blood driving it forwards
eventually back flow and closure of SL valve - dicrotic notch as it causes elastic recoil from stretch of this back flow.
aortic pressures gradually drop until next contraction, as blood leaves aorta to systemic circulation.

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14
Q

what do the different heart sounds correspond to?

A

1 = AV valve closure
2 = SL valve closure

slight splitting in inspiration - left side closes before right due to negative thoracic pressure, holding right side open for longer.

other heart sounds
3rd = blood flow in ventricular filling due to tensing of chordae tendinae. normal in children, athletes
4th = blood hitting a stiff ventricle in atrial systole- pathological - HTN, aortic stenosis.

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15
Q

when might a 3rd heart sound be pathological?

A

dilated ventricle e.g. congestive HF

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16
Q

where are heart sounds heard?

A

aortic = 2nd intercostal space, right side sternum, radiates to carotids
pulmonary = 2nd intercostal, left side
tricuspid = 4th intercostal, left side
mitral = apex = 5th intercostal mid clav line

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17
Q

what causes pathological splitting of heart sounds?

A

normally split in inspiration where left side closes first.

may be reversed e.g. systemic HTN, aortic stenosis, aortic regurgitation
may be exagerated e.g. mitral regurg, pulmonary stenosis, pulmonary artery HTN

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18
Q

what are the effects of HR on the cardiac cycle

A

shortening of diastole
some shortening of systole

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19
Q

draw and explain a pressure -volume loop

A

volume on x
pressure on y

1= ESV - around 50ml
2 = ventricular filling phase
3 = EDV = 130 ml
4 = isovolumetric contraction
5 = ejection phase - SV 80ml
6 = isovolumetric relaxation

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20
Q

how is venticular stroke work calculared?

A

pressure x volume
i.e. area inside curve

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21
Q
A
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22
Q

describe the end diastolic and end systolic pressure volume relationship…

A

as EDV increases, i.e. increased preload, further stretch of myocytes and SV increases. results in a wider PV loop

can plot the EDV vs pressure on a graph ..
can see gradual increase in EDV without significant increase in pressure and this allows for SV to be matched. eventually theres a sharp rise. The steeper the gradient, the less compliant the heart, i.e. HTN, cardiomyopathy

for ESV curve - as volume in heart at end of systole increases, so does pressure. the steeper this relationship, the better the contractility i.e. a good heart will remain maximally contracted at end of systole and increase pressure, whereas weak heart will stretch with added volume, reducing efficiency of contraction.

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23
Q

draw P-V curve for increased preload, afterload and contractility …

A

Ea represents afterload
the curve sits between these lines

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24
Q

what happens to PV loop in IHD

A

IHD will result in areas that bulge out with contraction due to scarring.
hence not a straight curve - will be slanted to the left

also loss of diastolic function - hence the EDV curve more steep
loss of ionotrophy - ESV curve shallower
overall reduced SV

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25
draw pressure volume loop for right ventricle
much lower pressures similar volumes
26
describe the cardiac action potential..
300ms long consists of 4 phases at rest potential is -90mV peak of AP = +30mV threshold = -65mV phase 0 - VG Na channels open phase 1 - VG Na close, VG K open Phase 2 - VG L type Ca channels open, Ca into cell. fasciliates contraction, porolongs depolarisation preventing another AP and tetany phase 3 - VG Ca close, K stay open, repolarisation phase 4 - resting membrane potential
27
why is tetany in cardiac AP not possible
due to phase 2 of AP, calcium influx prolongs AP increases period of refractory period, preventing another AP firing.
28
what are the pacemaker cells and where are they found
pacemaker cells are specialised cells capable of initiating periodic action potentials they are found at SAN, AVN and also within purkinje system and bundles of his. they have a baseline potential that is slowly depolarising until threshold is reached and AP is triggered. this cycle repeats, providing regular action potentials that transmit throughout myocardium. SAN has fastest discharge rate and thus sets the HR
29
describe the pacemaker potential..
3 phases at its lowest -60mV, peak AP +30mV phase 4 - baseline, slow depolarisation. HCN channels allow inwards Na 'funny' current. (T type Ca also play a role) phase 0 - when threshold is reached around -45mV, L type Ca channels open and Ca influx and peak AP. phase 3 - repolarisation. closure of Ca channels, VG K open and bring potential back to -60mV
30
describe key differences between cardiac and pacemaker potentials
4 phases vs 3 phases. i.e. no phase 2 in pacemaker the upstroke of AP is goverened by fast VG Na in cardiac, whereas slower L type Ca in pacemaker (less steep upstoke) baseline always depolarising, never stable in pacemaker - due to funny current HCN channels -90mV vs -60mV resting threshold -45mV vs -65mV
31
what are the resting rates of pacemaker cells?
SAN - 100-120bpm (lowered due to vagal tone) AVN - 60bpm bundle of his = 50bpm purkinje = 30-40bpm
32
how does the cardiac conduction system ensure synchronised contraction?
fast coordinated transmission SAN to AVN via 3 bundles - including bachman bundle. bachman bundle also takes depolarisation from right side to left side. slight delay at AVN allows atria systole to preceed ventricular systole. rapid spread down bundle of his - left and right bundles (left split into anterior and posterior) from apex upwards via purkinje fibres synchronised muscle contraction due to gap jucntions spiralling of fibres - corret direction from apex up ensures out of aorta / PA.
33
define cardiac output..
amount of volume ejected from the heart per unit time normally 5L/min can vary in times of stress / exercise or with position e.g. supine/standing or preganncy calculated by SV x HR SV normally around 80ml HR normally around 60bpm
34
how is cardiac output regulated..
**CO = HR x SV** each of these can be regulated by intrinsic and extrinsic factors to manipulate CO. SV in turn can be broken down into pre-load, contractility and afterload. **HR ** - main factor influencing CO - intrinsic control - set by SAN at around 100-120bpm. also brainbridge effect - tachycardia due to atrial stretch to match increased HR with increased preload. - influenced by external factors - vagus nerve (mAChR), catecholamines (B1) **Preload ** intrinsic - frank starling: increased preload, increases stretch and contractile strength, increases SV extrinsic - RAAS, ANP **contractility:** extrinsic - catecholamines (ionotropes), glucagon, dopamine. negative ionotropes (drugs - BB, CaCB) intrinsic - bowditch effect - increased HR results in build up of Ca ions and contractility ANREP effect - increased contractility with increased afterload. **Afterload ** usually determined by SVR - sympathetic NS (alpha receptors) **Control of this regulation** sensors --> control centre --> effectors sensors = baroreceptors, myocytes stretch receptors i.e. improve contractility, release ANP control - medulla oblongata effectors - parasymp, sympathetic, catecholamines, ANP , RAAS
35
outline the intrinsic and extrinsic methods of controlling cardiac output?
Cardiac output is determined by SV and HR. These can be in turn influenced in a number of ways INTRINSIC. * frank starling - improved contractility * afterload - usually increase in afterload, reduces CO. however intrinsic methods help to overcome this e.g.... * Anrep affect - increased afterload increases contractility * brainbridge reflex - increased HR in response to atrial stretch (i.e. preload) - although this uses ANS and vagus nerve * bowditch effect - an increased HR, causes Ca ions to build up intracellularly, increases CO EXTRINSIC * neural - ANS * hormonal - catecholamines, glucagon * metabolic
36
what is the anrep effect, bainbridge effect and bowditch effect
ANREP = increased afterload, causes increase in contractility to overcome this bowditch effect = increased HR results in build up of Ca ions - improves contractility bainbridge effect = preload causes atrial stretch - impulses sent via the myelinated veno-atrial baroceptors via vagus nerve to medulla which triggers increase in HR to accompany this
37
describe the frank starling curve...
describes the intrinsic mechanism whereby SV and contractility increase with preload as preload e.g. EDV increases, there is thought to be a stretch in myocytes which improves their tension and contractility and thus increases SV this can occur up to a point and then there is overstretch, any further increase will result in drop in SV and reduced efficiency. in failing heart this is seen earlier - the myocytes are already maximally stretched.
38
What is la place's law... how can this be used to model tension in the heart
la place law describes the relationsip between tension and pressure in a sphere or tube in a sphere Tension = PR /2h where P = pressure, r = radius , h = wall thickness thus in a hypertrophied heart where the thickness increases, tension is reduced. in a dilated heart where radius is increased, the tension is increased.
39
what is meant by ventriculo-artrial coupling or cardiovascular coupling?
the function of ventricle will effect MAP / SVR the SVR and MAP will inturn effect ventricular function (afterload) Ees = ventricular elastance - i.e. contractility. the less they stretch with volume, the better, more tension created for contraction i.e. steeper the curve Ea = arterial elastance/ afterload - the steeper this is, the poorer the compliance of arterial system and increased afterload. in optimal health Ees = 2x Ea
40
what are baroreceptors, how do they function to maintain CO?
mechanoceptors respond to stretch and BP signal to medulla oblongata to maintain BP via negative feedback loop. 2 main types of baroceptors * high pressure - carotid sinus, aortic arch * low pressure - veno-atrial baroreceptors (myelinated), non myelinated baroreceptors found in ventricles and artia and pulmonary arteries and coronary artery baroceptors. main baroreceptor reflex carotid sinus baroreceptor = glossopharyngeal nerve aortic arch = vagus nerve both travel to NTS in medulla oblongata parasympathetic and sympathetic outputs - HR, SVR, contractility
41
what are the central areas involved in coordinating cardiac output.
main relay centre that processes inputs and regulates outputs via ANS is the NTS within medulla oblongata. recieves inputs via peripheral afferents - baroceptors but also other central areas - hypothalamus, cortex, limbic system, midbrain allows CO to be altered with fear, anticipation and other situations.
42
the NTS is a vagal nuclei, how does this link to activation of sympathetic NS?
activated via rostal ventrolateral medulla which activates appropriate sympathetic chain.
43
how do sympathetic nerve afferents effect heart function?
preganglionic sympathetic fibres originate from the rostral ventrolateral medulla (RVLM) these travel to the paravertebral sympathetic chain the post ganglionic fibres of the sympathetic come from T1-T4 NA released at B1 receptors = chronotrophy and ionotrophy sympathetic NS also causes stimulation of adrenals and systemic catecholamines - adrenaline has higher affinity for B1
44
how does activation of B1 receptor result in chronotrophy and ionotrophy?
B1 = GPCR = Gs Increase in adenyl cyclase activity ATP --> cAMP cAMP activates PKA PKA phosphorylates... L type Ca channels - more Ca, ionotrophy HCN channels - increased rate of depolarisation of pacemaker.
45
what is lusitrophy
the ability of myocytes to relax after contraction. adrenergic stimulation causes increased lusitrophy as well as ionotrophy. this helps with relaxation and hence filing time to improve cardiac function. occurs via phosphorylation of SERCA (increased reuptake) and troponin
46
outline the hormonal control of cardiac function..
RAAS ANP and BNP catecholamines - ionotropy/chronotropy, also change SVR and afterload. thyroid hormones dopamine
47
what is the renin angiotensin aldosterone system (RAAS)?
when BP is low/ hypovolaemia triggers renin release from walls of afferent arterioles renin is a proteolytic enzyme that cleaves angiotensinogen AT2 inhibits renin release - negative feedback. aldosterone - increases ENAC, Na/H and NA/K ATPase
48
what is the juxtamedullary apparatus?
consists of afferent arterioles in close contact with macula densa (part of the DCT) which coordinate the RAAS. as less sodium delivered to DCT, signals to the afferent arterioles to release renin. afferent arterioles are also responsive to stretch (low pressure) and B1 stimulation.
49
what is the role of ANP and BNP
atrial naturietic peptide and brain natrietic peptide. released from atrial and ventricles respectively cause natereisis and water loss in response to stretch ANP inhibits Na reabsorption at collecting duct, aldosterone and renin release. also improves blood flow through vasa recta to reduce osmotic gradient in medulla.
50
draw a graph to show effect of chronotropy on cardiac pacemaker potential
gradient of funny current depolarisation is increased in sympathetic stimulation and decreased in parasympathetic
51
how do parasympathetic afferents effect cardiac function?
originates from NTS and cardiac plexus M2 muscarinic Ach R Gi results in reduced cAMP, PKA reduced phosphorylation of HCN channels and funny current - therefore slows depolarisation also reduced phos of K+ channels results in K+ efflux and hyperpolarisation little effect on ionotropy
52
what vasopressin receptors do you know?
3 types V1 = Gq - found on vasculature - vasoconstriction V2 = Gs = found in collecting duct of kidneys - water retention V3 = Gq - in hypothalamus - linked to ACTH release.
53
vasopressin is invovled in both osmoregulation and BP management. how do these roles effect someone who is bleeding but has low osmolarity (i.e.) less dilute blood)
ADH is released in response to increased osmolarity over normal range to tightly control osmotic pressure of the blood ADH is only released in response to blood volume loss when this is significantly low. then the stimulus for ADH release outweighs that of osmolartiy. i,e, low blood volume and osmolarity are both stimuli for ADH release with different thresholds
54
describe the metabolic regulation of cardiac function...
metabolic factors affecting CO include electrolytes, acidosis, hypoxia, temperature electrolytes - risk of arrythmias hypocalcaemia - reduces contractility and CO. prolongs QTc hypercalcaemia - the opposite and can reduce QTc hyperK - makes cardiac tissue more excitable - risk of VF/VT acidosis - reduces contractility temp - initially increase HR and contraction and then exhausts.
55
increasing HR increases CO, up to a certain point, what is the limit?
>150bpm, starts to reduce filling time in diastole. luisitrophy helps with this bowditch effect helps with this i.e. increased HR, more Ca, stronger contractions.
56
what is the equation for MAP?
MAP = CO x SVR V= IR MAP - CVP = CO x SVR MAP can also be calculated 1/3 systolic + 2/3 diastolic.
57
where is biggest pressure drop seen in circulation?
from arteries to arterioles smaller radius - so increase in resistance so need a big pressure drop for flow to remain constant
58
which vessels are resistance vessels and which the capacitance vessels?
resistance = arterioles capacitance = veins
59
discuss the regulation of blood pressure...
MAP = CO x SVR CO = HR x SV can be further be divided into intrinsci and extrinsic SVR - intrinsic methods * myogenic control - stretch of vessels with increased BP results in recoil + vasoconstriction from increased smooth muscle fibre tension, to maintain constant flow. autoregulation. * chemical vasodilators/vasocontrictors- nitric oxide main vasodilator, endothelin main vasoconstrictor. * reactive hyperaemia - local metabolites cause vasodilation to match flow to demand. e.g. hypoxia, H+ , adenosine SVR - extrinsic methods * alpha 1 receptors - NA sympathetic NS, circulating catecholamines * V1 - vasopressin * D1 - dopamine * RAAS - increased blood volume HR and SV - many intrinsic and extrinsic mechanism
60
how does nitric oxide cause vasodilation?
NO released from endothelium in response to stretch binds guanyl cyclase causes increase in GTP to cGMP activation of PKG PKG phosphorylates MLCP smooth muscle relaxation
61
what peripheral factors activate the sympathetic NS to cause vasoconstriction?
baroreceptors high CO2, hypoxia - via chemoreceptors pain pathway
62
describe the valsalva manoeuvre and changes seen in BP..
this occurs when patient expires against closed glottis. increasing intrathoracic presssure phase 1 = initially increase in BP as aorta is squeezed phase 2a =then drop because reduced venous return and hence CO phase 2b = then increased back to normal - secondary to baroreceptor response , tachycardia + vasoconstriciton phase 3 = then pressure is released and drop in BP as pressure on aorta released phase 4 = then increase in BP and overshoot due to improved venous return and CO and continued baroreceptor response
63
describe the physiological changes that accompany standing?
standing - gravity causes blood to pool in large veins of legs. baroreceptor reflex tachycardia - increase CO vasoconstrcition - increase SVR hence MAP = CO x SVR so MAP maintained.
64
what are the physiological responses to blood loss..
can be divided into short term, medium and later responses... ACUTE: hypovolaemia - reduced blood pressure - baroreceptor response, increased SVR and CO to compensate. activation of sympathetic also causes vasoconstriction in certain vascular beds but dilation in others to divert blood to vital organs. venoconstriction helps maintain preload. MEDIUM activation of RAAS - fluid retention ADH release - when very hypovolaemic reduced ANP/ BNP LONGER TERM EPO --> erythopoeisis and RBC production liver makes more albumin
65
what are the different classes of hypovolaemia?
4 stages of hypovolaemic shock class 1 = 10% blood loss (500ml), normal HR/ BP etc class 2 = 20% (1L) , tachycardia (100-120), orthostatic hypotension, urine output starts to drop under 30ml/hr. cool and pale class 3 = 30% (1.5L) = tachycardia 120-140, BP under 100 systolic, cool pale, UO under 20ml/hr class 4 = 40% (2L) = 140bpm +, less than 80mmHg, UO nil, peripheral cyanosis
66
why may tachypnoea be seen in haemorrhage
vasoconstriciton - can reduce blood flow to areas - anaerobic resp - acidosis - chemoreceptors - tachypnoea
67
draw a graph to show how CO, HR, CVP and BP change with % blood loss
CO - increase initially, then drops as preload drops CVP - remains steady and then starts to drop BP - remains steady unitl 20% then drops HR - increases with % loss.
68
how do clinical signs of shock differ in 18yr old vs 80 yr old?
18yr old good baroreceptor reflex and ANS so will compensate for longer. may not see much change in BP until late stages elderly show signs of decompensaiton earlier - poorer neurology, cardiac function and also B blockers/ ACE i
69
what cardiovascular changes are seen with different types of shock...
4 types of shock cardiogenic shock - vasoconstriction so pale peripheries, low CO (raised JVP) hypovolaemic - high CO and high SVR. if preload falls so may CO. distributive - e.g. sepsis or anaphylaxis - low SVR, warm red peripheries, high CO to compensate. if preload falls, CO could also fall obstructive - low CO, high SVR
70
describe the general structure of a vessel..
tunica intima - squamous cell endothelium + BM tunica media - elastic fibres, muscle fibres tunica adventitia - connective tissue, sometimes vasculature. relatively amounts of each depends on function e.g. arteiroles have a lot of smooth muscle in tunica media
71
describe the difference in structure of a artery, vein and capillary
arteries have thicker walls, more muscle and elastic tissue. i.e. prominent tunica media arterioles - a lot of smooth muscle to regulate vasoconstriction and flow veins also have valves, large lumen = capacitance vessels., relatively thin walls. extensive adventitia capillaries - one cell thick walls, large S.A collectively
72
why is it important arteries are compliant
stretch and recoil - to maintain flow and reduce but maintain BP non-compliant would result in HTN and loss of pressure
73
what happens to blood flow from aorta to capillaries
flow collectively remains the same because all connected however velocity is reduced due to dividing of vasculature into smaller vessels with collectively larger diameter time for gas exchange
74
what determines the blood flow through a vessel?
hagen poiseulle law resistance therefore is the 8nl/πr^4
75
can you explain how splitting of the vasculature into smaller braches lowers the resistance..
resistance of vessels in parallel will drop this is because their cross sectional area collectively is larger so resistance is lower.
76
what is the difference between flow and velocity?
flow = volume of fluid passing a point per unit time = L/s velocity = distance a particle travels per unit time = m/s flow = velocity x cross sectional area.
77
what different types of capillaries do you know?
capillaries can be classified by their structure and degree of permeability continous = tight junctions between endothelial cells. limits movement of substances across. seen in BBB, connective tissue, muscle. fenestrated = small gaps between endothelial cells, allows some movement - GIT, Bowmans capsule sinusoidal = large spaces between endothelial cells, allows proteins and even small cells to pass =e.g. liver and spleen.
78
what are the functions of the vascular endothelium
delivery of substances to tissue via diffusion smooth surface promotes laminar flow regulating BP and maintaining flow - autoregulation - reactive hyperaemia responds to tissue injury to promote haemostasis
79
what are the functions of the peripheral circulation?
delivery of O2 + glucose to tissues removal of CO2 under extrinsic control to help maintain BP by regulation of SVR role in thermoregulation through alteration of SVR hormonal transport for communication inflammation and infection - changes to vascular permeability to support this haemostasis
80
what factors can effect the viscosity of blood
haemocrit platelet count dehydration temperature - the higher , less viscous vessel diameter
81
describe the structure of a capillary and its adaptation to function..
function to allow diffusion of substance between blood and tissue ficks law = conc difference x S.A / distance hence single cell - squamous endothelium - reduces distance many capillaries - reduces distance, increases S.A blood flow - maintains Conc gradient low velocity due to drop in resistance therefore time for gas exhange
82
what factors determine the formation of tissue fluid ...
starlings forces of filtration is a model that helps determine amount of tissue fluid formation based on oncotic pressures and hydrostatic pressures of tissue and capillary at arterial end hydrostatic pressure is highest = 36mmHG at venous end around 10mmHg oncotic pressure remains constant around 24mmHg therefore net driving force out initially and then in.
83
what is the glycolayx model?
now thought that there is a glycolayx between tissue and capillaries ECM making oncotic pressure less significant unless this breaks down. in sepsis glycolayx thought to break down which leads to fluid shifts - colloids can get into institium
84
describe the arrangement of a capillary bed and how flow through it can be regulated?
arterioles give rise to meta-arterioles which have pre-capillary sphinchters allowing for regulation of flow through capillary bed. if the sphinchters are contracted, blood will be diverted from capillary bed and go to veins. local factors such as adenosine, H+ can regulate opening/ closing of these sphinchters to match flow to demand.
85
what is meant by the colloid osmotic pressure?
the osmotic pressure exerted by plasma proteins - this is a force drawing water into the capillaries
86
what is the gibbs donan effect
plasma proteins exert both an osmotic pressure and electrostatic pressure from their positive charge. this electrostatic attraction = gibs donan effect
87
what are the causes of increased interstitial fluid
increased capillary hydrostatic pressure - vasodilation, fluid overload, venous obstruction reduced capillary oncotic pressure - low albumin (malnutrition, liver disease, nephrotic syndrome) increased capillary permeability - i.e. low reflection coefficient. e.g. inflammation, injury
88
what factors affect exchange across a capillary...
DIFFUSION: fick law - SA, Distrance, conc difference grahams MW lipid solubility FASCILATED DIFFUSION carrier proteins channels etc ACTIVE TRANSPORT SYSTEMS PINOCYTOSIS BULK FLOW - solutes are dragged with water
89
describe the structure of the lymphatic system..
blind ended tubules - lined in endothelium carry excessive tissue fluid from interstitum and return it back to the circulation at the thoracic duct. majority of the lymph drains into thoracic duct on left side= lower body and left upper body the right upper half of body drains into right lymphatic duct these empty into brachiocephalic veins larger lymphatic vessels have valves
90
how do the lymphatic vessels function to drain tissue fluid?
negative pressure within vasculature from constant emptying at the thoracic duct into the circulation also traction as vessel wall are anchored open by collagen this draws fluid in from the tissues via a pressure gradient also a peristalsis effect as larger vessels have smooth muscle negative intrathoracic pressure in inspiration also helps
91
contents of lymph
excess tissue fluid - water and ions and glucose lymphocytes chylomicrons - from gut
92
what is the role of lymphatics in immune response
transports antigen presenting cells and lymphocytes to help activate adaptive immune response has lymph nodes where lymphocytes reside
93
what is the structure of the thoracic duct..
45cm long duct found in abdomen and drains into left side branchiocephalic vein drains around 75% of all lymph
94
what happens if lymph drainage is abnormal?
accumulation of tissue fluid may be congenital = primary lymph oedema e.g. milroys disease - autosomal dominant or acquired -e.g. blockage by tumour, lymph resection from surgery , radiation, infections
95
describe the regulation of blood flow to the skin
heavily controlled extrinsically by sympathetic NS thermoregulaiton maintain MAP for vital organs less dependant on autoregulation/ reactive hyperaemia
96
describe the regulation of coronary circulation..
blood flow through coronaries at rest =250ml/min 8-10ml/100g 02 consumption this can increase to 1250ml/min in exercise to meet increased O2 demand. occurs via intrinsic and extrinsic mechanisms intrinsic * nitric oxide - vasodilation * adenosine, hypoxia and acidosis - vasodilation * increased CO --> sheer stress --> releases NO extrinsic * sympathetic NS - B2 * adrenaline - B2 - vasodilation * also have alpha 1 however these have little effect/ overriden compared to the rest
97
describe the structure of pulmonary vasculature..
Pulmoanry artery divides into left and right PA which supply each lung many divisions supplying segmental arteries and eventually capillaries for gas exchange. then feed into pulmonary veins - 2 on left and 2 onf right (superior and inferior)
98
how does pulmonary vasculature compare to systemic?
lower resistance lower pressure thinner walls with less smooth muscle highly compliant - i.e. stretch with changes in CO and hence no increase in pressure. protects from pulmonary oedema respond differently to metabolites hypoxic VASOCONSTRICTION and vasoconstriction to hypercarbia
99
what are the bronchial arteries?
part of systemic circulation supply oxygenated blood to tracheobronchial tree as far as terminal bronchioles. originate from thoracic aorta drain into the - azygous vein on right --> RA - pulmonary vein on left --> LA (shunt)
100
how does pulmonary artery pressures change with increased CO?
highely compliant system so not much change in pressure with CO. achieved through drop in PVR as CO increases. this drop in PVR occurs via 2 mechanisms * distensible vessels * recruitment of underfilled beds V= IR hence if I increases, R reduces to maintain P. graph shows how a MPAP of around 15mmHg is maintain through drop in PVR up to a limit. after this MPAP will rise.
101
draw a graph to describe the change in PVR with volume of lung..
FRC is at its optimum volumes less than this, compresses vessels, smaller diameter, more resistance volumes higher - stretches vessels - increase length - more resistance.
102
what factors affect pulmonary vascular resistance?
pulmonary artery pressure * increased pressure, distends vessels, opens bed, reduces resistance lung volumes * FRC is optimum, below and above this volume, PVR increases hypoxic pulmonary vasoconstriction * hypoxia causes vasoconstriction and increased resistance. * chronically can lead to pulmonary HTN metabolites/hormones * increased by high CO2, acidosis, catecholamines, serotonin, thromboxane * reduced by NO and prostacyclin
103
what is the equation for PVR
can be derived from v=IR 80x (MPAP - PCWP) / CO = PVR in dyns/s/cm5 dynes·seconds per centimeter to the fifth power Left atrial pressure= Pulmonary capillary wedge pressure
104
describe the physiological changes that occur with exercise..
during exercise muscles contract and relax which requires a lot of ATP. hence they need a lot of O2 and glucose for aerobic respiration to support this. CVS and Resp and metabolic changes support this. SYMPATHETIC NS * anticipation activates this, then from acidosis/ CO2 production via chemoreceptors, and muscle afferents (proprioception) * activation of sympathetic NS through cortex * tachycardia, anxiety, increased blood flow to muscle * all via release of catecholamines * B1 on heart - increase CO * A1 on vasculature - diverts blood to vital organs (vasoconstriction of gut and kidneys) * B2 in muscle vasculature and coronarys + respiratory smooth muscle CVS: via HR and SV * contraction of muscles improves venous return and preload - CO * venoconstriction - improves preload * improved contractility from B1 * improved HR from B1 * overal CO from 5L/min to 25L/min RESPIRATORY * increase MV - increased PaCO2 via chemoreceptors - via RR and TV * 5L /min to 100L/min * also joint proprioception feed to resp centre * increased pulmonary blood flow from increase CO. hence V:Q matching. LOCAL EFFECTS * reactive hyperaemia - opens up skeletal muscle beds - relaxation of pre-capillary sphinchters. THERMOREGULATION: * vasodilation of skin capallaries * sweating - latent heat GLYCOLYSIS/ GLUCOGENOLYSIS * goverened by catecholamine
105
how much does muscle blood flow increase in exercise?
1L/min to 22L/min
106
how much can CO increase in exercise
5L/min to 25L/min
107
how much can MV increase in exercise?
5L/min to 100L/min
108
how does O2 consumption change in exercise?
250ml/min O2 to 5L/min
109
what system limits intensity of exercise?
CVS not respiratory - blood fully saturates at lungs.
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how does blood pressure change with exercise?
slight increase - increase in CO but drop in SVR due to vasodilation in skin and muscle. widened pulse pressure systolic increases more than diastolic slight increase in mean pulmonary artery pressure too.
111
draw a graph to show changes to minute volume with intensity of exercise
112
draw a graph to show changes to SV with intensity of exercise
113
what happens once exercise stops - is O2 still required?
after exercise O2 consumption remains high - this is known as O2 debt (also known as excess post exercise O2 consumption) split into 2 phases 1. Alactacid phase - ATP and phosphocreatine are replenished and myoglobin O2 and glycogen stores 2. lactacid phase - conversion of lactate back to pyruvate via cori cycle O2 debt comes from the beginning of exercise when there is a lag behind supply mechanisms matching demands. then a steady state is reached.
114
what is the lactate threshold?
during exercise lactate is produced and removed there is usually a slight steady rise rise until a point where there is a sudden increase = this is the lactate threshold results in fatigue
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how does energy sources change during exercise?
CHO initially then fats CHO if high intensity Fats in low intensity known as cross over concept
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what is meant by VO2 max?
O2 consumption increases linearly with intensity up to a max = VO2 max this is the max capacity for O2 delivery during exercise and will limit any further intensity measured in ml 02/ kg/ min can be a measure of fitness
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what factors can influence VO2 max?
Cardiac - SV - endurance improves this and hence CO pulmonary factors are not usually the limit unless at altitude or pathological lungs. O2 carrying capacity of blood doesnt usually limit, however EPO can increase this - taken by athletes skeletal muscle capillary density - not usually limit. but increases with training.
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which substrates are available to muscles to power contraction..
ATP - stores only last a few seconds phosphocreatine can supply some energy - lasts 7 seconds glycolysis - 2ATP oxidative phosphorylation - 36 ATP B oxidation of fats + oxidatice phosphorylation
119
why might heat stroke occur in exercise?
heat is produced from contracting muscles and from respiration mechanisms to loose heat to maintain body temp - vasodilation and sweating. latent heat of vapourisation however if ambient temp is hot or humid climate this is limit and could result in heat stroke. this presents as confusion, hyperthermic and can result in anhidrosis (inability to sweat)
120
how is heat stroke managed
cooling - ice water, cold IV fluids extracorporeal circuits with heat exchnage gastric levage with cold fluid.
121
what is meant by muscle fatigue?
muscles have a limit to the ability to generate force. it is a protective mechanism preventing damage and apoptosis thought to be due to inhibition of enzymes by lactic acid or intracellular K+ OR exhaustion of glycogen stores with prolonged exercise.
122
what is the difference between dynamic and static exercise?
dynamic = rhythmic contraction and relaxing e.g. running static = contraction against a force but do not length/ shorten e.g. weight lighting differences are that in dynamic exercise the capillary beds vasodilate and there is a drop in SVR in static exercise there is compression of the capillary beds and an increase in SVR - effects diastolic pressure less of increase in HR in static exercise.
123
what is the difference between SV and Ejection fraction?
SV = amount ejected per heat beat in mls. usually 70-80ml ejection fraction is the proportion of blood ejected compared to end diastolic volume. normally 55-70%
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what proportion does atrial systole account for EDV?
under resting condition 10-20% of EDV and hence SV however as diastole reduces with increased HR , this becomes more significant e.g. exercise 40%.
125
what is the problem of anaesthesia in someone with aortic stenosis
in aortic stenosis - increased afterload. the heart relies on this high pressure in aorta to maintain coronary blood flow MAP = SVR x CO. CO in AS is fixed, therefore drop in SVR can affect BP more so than normal heart drop in SVR with anaesthesia can reduce coronary filling time and drop BP significantly should try to avoid changes to SVR as best possible. avoid spinals due to drop in SVR avoid tachycardia - poor filling of coronaries and allows time for slower systolic ejection
126
what considerations are made for someone with mitral stenosis in anaesthesia?
avoid pulmonary HTN - e.g. hypoxia, hypercarbia avoid tachycardia - gives time for slower ejection
127
what considerations are made for anaesthesia in aortic regurgitation?
maintain contractility lower SVR will help maintain forward flow higher heart rate will reduce regurgitation fraction - avoid slow HR
128
what are the roles of calcium in the heart?
pacemaker potential - phase 0 prolongs cardiac AP - phase 2 , prevents tetany, gives time for contraction and ejection contraction - via troponin
129
what does an ECG measure?
potentials from skin surface as a result of rhythmic changes in potentials due to AP within cardiac muscle. the synchronised depolarisations and repolarisations seen in cardiac muscle is recorded as a compound potential at the skin surface measures both magnitude and direction
130
how is an ECG interpretted?
rate = 60/( R -R interval ) if regular. otherwise count no. of Rs in 10s and x 6 rhythm - regular or irregular P wave - should be around 0.12s PR - 120 to 200ms - start of P to start of R followed by QRS - less than 120ms ST - depression / elevation T wave - inversion / tall QT interval - from start of Q to end of T
131
how many ms is each small square and large square on the ECG?
small square = 0.04s large 0.2s
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how is QT interval corrected?
QT interval in seconds / root RR in seconds
133
normal cardiac axis? how is this calculated
-30 degrees to +90degrees e.g. avL = -30 avF = +90 look at 2 perpendicular leads e.g. lead I and aVF. difference in height of QRS in both leads. if these are equal then axis lies 50% between then and hence is around 45 degrees - normal lead 2 should have the bigges QRS in a normal axis
134
causes of left and right axis deviation?
RAD - RBBB, RVH, P.E LAD - LBBB, LV hypertrophy
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what is an arrhythmia?
abnormal rhythm of heart can be categorised by location of origin or pattern. may be an intrinic problem or extrinsic
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what are the mechanisms for arrhythmias?
**increased automaticity** - e.g. sinus tachy - hyperthyroidism **abnormal automaticity** e.g. spontaneous activity from abnormal location e.g. ventricles in VT may occur from ischaemic injured area **re-entry loops**e.g. accessory pathway - WPW **triggered activity**e.g. depolarisation in the repolarisation phase - may trigger another AP e.g. torsades or other electrolyte imbalances.
137
describe the abnormalities of the SAN
sinus bradycardia - external e.g. excess vagal activity, B blcokers, hypothyroid, MI sinus tachycardia - external e.g. catecholamines, antimuscarnics (glycopyrolate) sick sinus syndrome - dysfunctioning may have tachy/brady syndrome or intermittent AF - due to fibrosis
138
what is re-entry phenomena?
WPW - provides accessory pathway - can go down AVN and back up bundle of kent. ischaemia can result in an area that doesnt allow normal direction of depolarisation but allows other direction and then looping can occur
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what ecg changes are seen in WPW?
short PR delta wave due to path down bundle of kent
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what is AF and atrial flutter?
AF = uncoordinated fibrilation of atrial muscles. no synchronised depolarisations or contraction. hence loss of P wave, loss of atrial systole. random transmission via AVN gives irregularly irregular ventricular rate atrial flutter = atrial arrhythmia caused by re-entry loop within atria causing repeated atrial depolarisations and contractions. intermittently get through AVN hence 2:1 or 3:1 pattern. saw tooth pattern seen.
141
outline the different degrees of heart block..
HB conduction defect of the AVN first degree - slow so prolonged PR - can be normal in atheltes second degree - type 1 = prolongs each time and eventually skips second degree type 2 = same length but only transmits set amount e.g. 2:1 or 3:1. third degree/ complete = random / no transmission - ventricular rate 30-40bpm
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what are the causes of Heart block?
MI / myocarditis and fibrosis athletes and type 1 electrical/drugs - b blockers, digoxin
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what is a bundle branch block
2 bundle branches - left and right left divided into anterior and posterior fascicle. if any blocked changes normal conduction pathway e.g. if RBBB - travels down left, left ventricle depolarises and then to right. hence get wide QRS
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classify the tachyarrhythmias
broad or narrow broad = VT narrow * irregular - fast AF * regular - sinus tachy, Supraventricular tachycardia
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what are the key features of VT?
wide complex tachy rate >120bpm may see fusion / capture beats - where some normal conduction via AVN is getting through may be monomorphic or polymorphic = torsardes
146
tell me about torsade de pointe
lifethreatening arrhythmia polymorphic VT caused by prolongation of QT seen with a number of electrolyte derrangements or drug OD e.g. TCA, low K, low Mg
147
what is VF
cardiac arrhtyhmia not compatible with life one of the 4 rhtyhms treated in cardiac arrest ventricles are fibriliating, no synchronisation hence no output
148
ECG changes in MI
hyperacute - Tall T - release of K+ causes exagerated repolarisation ST elevation - full thickness thrombosis ST depression - partial / ischaemia T inversion Q wave - late sign - due to scarring
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describe the pathogenesis of an MI
atherosclerosis HTN/ smoking/ hyperlipidaemia can damage endothelium. LDL deposits in tunica intima macrophases engulf and become foam cells plaques develop - stenosis can rupture and thrombose
150
risk factors for MI
modifiable - HTN, smoking, obesity , diabetes non-modifiable - age, male , FHx
151
can you state some normal ECG varients?
first degree HB R wave progression - increased R wave in V1-V5 R wave negative in V1,2, avR
152
what is a pacemaker device?
medical device that can sense electrical activity and respond to this by either inhibiting or triggering activity in atria or ventricles to maintain normal rhythm. e.g. delivers current to myocardium to maintain rhythm and output may be permanent or temporary may be internal or external may be single or dual chamber
153
what are the indications for pacemakers?
Mobitz II complete heart block symptomatic bradycardia acute anterior MI NOT inferior MIs
154
how is tranvenous temporary pacing performed?
central line Xray to check position manipulate the current theshold and sensitivity until good rhythm stitch securely in place
155
what types of pacing leads do you know?
epicardial = outside of heart e.g. subcut endocardial = via central line into ventricle
156
what is checked at a pacemaker check?
threshold sensing / sensitivity current output correct mode battery life
157
complications of pacemaker insertion?
infection, bleeding, displacement microshocks pain - may feel small electrocutions ICD - can deliver shocks incorrectly
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what is the disadvantage of transcutaneous pacing over transvenous?
more impedance for current path therefore higher current needs to be used can result in msucle contractions that can be uncomfortable may be harder to capture and sense electrical activity
159
what are the functions of an ICD?
internal cardiac defibrilator senses lifethreatening rhtyhms and delivers a shock indicated for those with * previous VF, * VT and structural heart disease * ejection fraction less than 35% post MI with VT * syncope with ECG changes
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what are the components of an ICD?
sensing electrodes microprocessor pulse generator/ current battery
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what are the intraoperative risks associated with pacemakers?
burns * route for current to pass via diathermy and high current density - burn , damage to pacemaker interference * may pick up electrical activity and think its the heart and deliver a shock/ alter rhythm of pacemaker e.g. diathermy or shivering to avoid this deactivate ICD and add defib pads for pacemakers use bipolar diathermy
162
what is cardiac tamponade - causes, clinical signs, treatment?
fluid collection between visceral and parietal layers of pericardium can result in pericardial effusion. vessel injury between these layers or the fibrous pericardium can result in blood between these layers. the fibrous pericardium is tough and non-extensible in tamponade the fluid/blood build up and exerts pressure onto the heart - reduces contraction and CO medical emergency becks triad - raised JVP, low BP, muffled heart sounds. may be caused by trauam, infection, malignancy pericardiocentesis is necesesry - 5th intercostal space, mid clav line, 20degrees up. USS guidance.
163
how is cardiac work calculated?
cardiac work = stroke work + pressure work stroke work = area inside PV loop pressure work = the work done to contract heart against the arteries of the heart e..g higher in HTN cardiac work will correspond to myocardial O2 consumption
164
draw PV loop for right ventricle
stroke work is less pressures are less classically triangular same stroke volume
165
describe what happens to PV loop in systolic heart failure
reduced contractility so Ees gradient reduced (ESPVR= end systolic pressure volume relationship). reduced SV higher EDV and ESV e.g. dilated heart
166
describe what happens to the LV loop in diastolic heart failure?
e.g. stiff hypertrophied ventricle impaired filling now LV less compliant so End diastolic PV relationship altered - steeper gradient less compliant reduced SV
167
which arteries are elastic vs muscular?
elastic - more proximal e.g. aorta - need to expand in systole and recoil in diastole to dampen pulsatile flow muscular - more medium sized arteries and arterioles - used to regulate flow by sympathetic NS
168
what factors are involved in vasodilation/ constriction?
intrinsic * myogenic (via NO or mechanoreceptors) - autoreg * local metabolites - match flow to demand - NO, CO2 adenosine, H+, endothelin, thromboxane - also vasoconstriction with bleeding. extrinsic * neural - ANS - B2 and A1 * hormononal - catecholamines, dopamine, ADH, histamine
169
is the parasympathetic NS invovled in vasoconstriction/ dilation
not normally apart from in penis - vasodilation with erection
170
typical resistance of systemic and pulmnonary system?
pulmonary 160dyns.s.cm5 systemic 1600dys.s.cm5
171
how does the arterial waveform morphology change with position in body?
172
what is the windkessel effect?
expansion of elastic arteries to accomodate the volume without increasing pressure. store this as elastic potential energy in diastole can recoil to convert potential energy to kinetic energy i.e. maintain forward flow in diastole known as windkessel effect. converts sinusoidal pressure to more continuous flow
173
how do starlings forces of filtration differ in lungs?
pressure in arterial system is much lower so doesnt get filtration otherwise would have pulmonary oedema
174
timings for each phase of cardiac AP? what parts of ecg do they correspond to?
overall 300ms phase 0 and 1 = 1-2ms - QRS phase 2 = 200ms - ST phase 3= 50ms - T wave
175
when is the refractory period of Cardiac AP?
absolute - inactivated VG Na channels - starts in phase 0 up to 1/3 of phase 3 = around 200ms. much longer than neurons relative - from phase 3 to some of phase 4
176
define cardiac failure? how is it classified
the inability of the heart to provide sufficient CO to meet the tissue demands it may effect both or one ventricle it can be classified as... high output - CO normal or high but demands are increased e.g. thyrotoxicosis low output - tissue demand normal but low CO or systolic/ diastolic or by cause e.g. structure, metabolic or by severity - new york heart association classification
177
what is the difference between diastolic and systolic HF?
systolic - pump function is reduced i.e. worse contractility. reduced ejection fraction. e.g. dilated heart or damaged myocytes cant produce contractile strength. diastolic - ventricular compliance reduced e.g. hypertrophy, restrictive cardiomyopathy or restrictive post MI. impaired filling, less space so less SV. ejection fraction may be normal
178
what is meant by compensated HF?
ventricular function impaired but CO maintained due to compensatory methods. e.g. sympathetic stimulation - increase contractility and rate expansion of blood volume via RAAS to improve LVEDV and SV. as disease progresses it decompensates
179
what are the clinical consequences of decompensated HF?
LV -pulmonary oedema - eventually pulmonary HTN and Right failure - fatigue muscles, renal failure (reduced output) RV - venous congestion- ankle oedema, ascites, hepatomegaly
180
how does the oxygen extraction ratio of the heart compare to other organs?
oxygen extraction ratio = ratio of consumption to delivery. in heart around 60% higher than other organs e.g. liver 50%, kidney 15%
181
what is meant by acute coronary syndrome?
range of conditions whereby the oxygen supply to myocardium doesnt meet demand and results in ischaemia NSTEMI STEMI unstable angina
182
who is at risk of a silent MI?
elderly diabetic heart transplant
183
ecg changes in MI
ST elevation ST depression T wave inversions LBBB
184
diagnosing MI
clinical ecg biochemical - troponins ECHO - regional wall motion abnormalities
185
what are the 5 types of MI
type 1 - primary coronary event type 2 - ischaemia due to increased demand or poor supply e.g. sepsis , anaemia , rate related type 3 - cardiac death suggestive of MI type 4 - asscoated with percutaneous intervention type 5 - associated with cardiac surgery
186
what factors effect coronary blood flow?
autoregulation - maintians flow over range of BP reactive hyperaemia - adenosine heart rate - occurs in diastole mostly ANS - B2 disease - atherosclerosis
187
normal variations of coronary ciruclation
mostly right dominance - i.e. RCA supplies SAN some have co-dominance in 15% left dominance - whereby the posterior interventricular branch is a branch of circumflex and not RCA
188
what are complications of cardiac ischaemia?
ROS - arrhtyhmias, remodelling scar tissue - ectopic activity, poor conduction, poor contraction valve dysfunction - papillary muscles
189
what is ischaemic preconditioning?
protective mechanism post MI to prevent further damage consequent of reperfusion biochemical changes
190
which drugs affect coronary blood flow?
Nitrates - vasodilation B blockers CaCB pottasium channel activators - nicorandil statins and anti platelet
191
normal cardiac index?
CO/ BSA easier to compare in people of different sizes normal = 3-3.5L/min/m2
192
define shock
circulatory failure whereby there is inability to deliver O2 to tissues adequately 4 types - cardiogenic, distributive, obstructive (tamponade , Pneumothorax or embolus), hypovolaemic
193
why is maintaining BP important?
organs depend on adequate MAP for perfusion e.g. CPP = MAP - ICP/CVP important organs can autoregulate but only within a certain MAP range
194
what abnormalities can be seen in valsalva?
phase 2b - no reflex tachy, hence hypotension phase 4 - no overshoot, no reflex bradycardia
195
what is meant by the square wave response of the valsalva
may occur with HF whereby patients have chronically raised sympathetic outflow MAP remains high because drop in venous return doesnt effect it as it was already at max compliance before i.e. beyond the top end of starling curve however squeezing of aorta does increase MAP
196
what are the clinical uses of valsalva?
termination of SVT - vagal stimulation diagnose murmur - increase left sided mumurs e.g aortic stenosis checking bleeding intraop by increasing venous pressure
197
roles of venous system?
capacitance vessels - hold volume / store blood venous return to the heart - determine preload and hence effect CO carry deoxygenated blood back to heart for oxygenation - completes the circuit pulmonary veins - carry oxygenated blod.
198
what factors determine venous return to the heart?
valves venous pressure abdo throacic pump - i.e. ventilation and abdominal pressure cardiac pump muscular pump
199
value for normal CVP? causes of increase?
2-8mmHg increased in congestive heart failure, hypervolaemia, constrictive pericarditis, PEEP. venous thrombosis
200
patterns of JVP in different conditions
complete HB - cannon a waves - assynchronous contraction of atria and ventricles together. tricuspid regurg - large c and v waves, large x descend AF - loss of a
201
what are the determinants of O2 supply and demand..
O2 supply - coronary perfusion time + O2 content of the blood e.g. HR, coronary vasodilation, diseased coronarys, Hb, sats O2 demand HR, contractility - i.e. how fast and hard the fibres are contracting , wall stress e.g. afterload and preload,