CARDIO Flashcards
Describe the general structure of a cardiac myocyte..
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
difference between cardiac and skeletal muscle
cardiac - more mitochondria, gap junctions, denser capillary bed , single nucleus
skeletal - multinucleated, triad T tubule with SR, ryanodine 1 receptors
both straited
explain the macroscopic arrangement of cardiac muscle that adapts it to function…
looped and helical overlapping muscle structure arranged to contract and expel blood in correct direction e.g. ventricles up into arteries.
what is the function of the intercalated disc?
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
describe the structure of a sarcomere..
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.
what is the function of troponin
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.
what receptors exist in the heart?
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,
describe the cardiac cycle…
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
draw a pressure - time curve to describe valvular changes and events during cardiac cycle…
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.
what are the pressures of the right side of the heart…
RA = 0 to 4mmHg
RV = 25/0mmHg
Pulmoanry artery 25/10mmHg
draw a volume time curve for LV
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
describe the JVP waveform
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
describe the changes in the aortic pressure graph
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.
what do the different heart sounds correspond to?
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.
when might a 3rd heart sound be pathological?
dilated ventricle e.g. congestive HF
where are heart sounds heard?
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
what causes pathological splitting of heart sounds?
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
what are the effects of HR on the cardiac cycle
shortening of diastole
some shortening of systole
draw and explain a pressure -volume loop
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
how is venticular stroke work calculared?
pressure x volume
i.e. area inside curve
describe the end diastolic and end systolic pressure volume relationship…
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.
draw P-V curve for increased preload, afterload and contractility …
Ea represents afterload
the curve sits between these lines
what happens to PV loop in IHD
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
draw pressure volume loop for right ventricle
much lower pressures
similar volumes
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
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.
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
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
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
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
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.
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
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
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
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
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.
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.
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
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
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.
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.
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
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.
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
outline the hormonal control of cardiac function..
RAAS
ANP and BNP
catecholamines - ionotropy/chronotropy, also change SVR and afterload.
thyroid hormones
dopamine
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
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.
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.
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
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
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.
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
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.
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.
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.
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
which vessels are resistance vessels and which the capacitance vessels?
resistance = arterioles
capacitance = veins
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
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
what peripheral factors activate the sympathetic NS to cause vasoconstriction?
baroreceptors
high CO2, hypoxia - via chemoreceptors
pain pathway
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
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.
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
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
why may tachypnoea be seen in haemorrhage
vasoconstriciton - can reduce blood flow to areas - anaerobic resp - acidosis - chemoreceptors - tachypnoea
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.
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
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
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
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
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
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
what determines the blood flow through a vessel?
hagen poiseulle law
resistance therefore is the 8nl/πr^4
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.
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.
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.
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
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
what factors can effect the viscosity of blood
haemocrit
platelet count
dehydration
temperature - the higher , less viscous
vessel diameter
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
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.
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
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.
what is meant by the colloid osmotic pressure?
the osmotic pressure exerted by plasma proteins - this is a force drawing water into the capillaries
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
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
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
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
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
contents of lymph
excess tissue fluid - water and ions and glucose
lymphocytes
chylomicrons - from gut
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
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
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
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
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
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)
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
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)
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.
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.
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
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
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
how much does muscle blood flow increase in exercise?
1L/min to 22L/min
how much can CO increase in exercise
5L/min to 25L/min
how much can MV increase in exercise?
5L/min to 100L/min
how does O2 consumption change in exercise?
250ml/min O2
to 5L/min
what system limits intensity of exercise?
CVS
not respiratory - blood fully saturates at lungs.
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.
draw a graph to show changes to minute volume with intensity of exercise
draw a graph to show changes to SV with intensity of exercise
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.
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
how does energy sources change during exercise?
CHO initially
then fats
CHO if high intensity
Fats in low intensity
known as cross over concept
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
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.
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
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)
how is heat stroke managed
cooling - ice water, cold IV fluids
extracorporeal circuits with heat exchnage
gastric levage with cold fluid.
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.
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.
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%
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%.
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
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
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
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
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
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
how many ms is each small square and large square on the ECG?
small square = 0.04s
large 0.2s
how is QT interval corrected?
QT interval in seconds / root RR in seconds
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
causes of left and right axis deviation?
RAD - RBBB, RVH, P.E
LAD - LBBB, LV hypertrophy
what is an arrhythmia?
abnormal rhythm of heart
can be categorised by location of origin or pattern.
may be an intrinic problem or extrinsic
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 loopse.g. accessory pathway - WPW
triggered activitye.g. depolarisation in the repolarisation phase - may trigger another AP e.g. torsades or other electrolyte imbalances.
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
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
what ecg changes are seen in WPW?
short PR
delta wave
due to path down bundle of kent
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.
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
what are the causes of Heart block?
MI / myocarditis and fibrosis
athletes and type 1
electrical/drugs - b blockers, digoxin
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
classify the tachyarrhythmias
broad or narrow
broad = VT
narrow
* irregular - fast AF
* regular - sinus tachy, Supraventricular tachycardia
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
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
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
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
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
risk factors for MI
modifiable - HTN, smoking, obesity , diabetes
non-modifiable - age, male , FHx
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
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
what are the indications for pacemakers?
Mobitz II
complete heart block
symptomatic bradycardia
acute anterior MI
NOT inferior MIs
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
what types of pacing leads do you know?
epicardial = outside of heart e.g. subcut
endocardial = via central line into ventricle
what is checked at a pacemaker check?
threshold
sensing / sensitivity
current output
correct mode
battery life
complications of pacemaker insertion?
infection, bleeding, displacement
microshocks
pain - may feel small electrocutions
ICD - can deliver shocks incorrectly
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
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
what are the components of an ICD?
sensing electrodes
microprocessor
pulse generator/ current
battery
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
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.
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
draw PV loop for right ventricle
stroke work is less
pressures are less
classically triangular
same stroke volume
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
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
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
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
is the parasympathetic NS invovled in vasoconstriction/ dilation
not normally
apart from in penis - vasodilation with erection
typical resistance of systemic and pulmnonary system?
pulmonary 160dyns.s.cm5
systemic 1600dys.s.cm5
how does the arterial waveform morphology change with position in body?
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
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
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
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
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
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
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
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
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%
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
who is at risk of a silent MI?
elderly
diabetic
heart transplant
ecg changes in MI
ST elevation
ST depression
T wave inversions
LBBB
diagnosing MI
clinical
ecg
biochemical - troponins
ECHO - regional wall motion abnormalities
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
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
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
what are complications of cardiac ischaemia?
ROS - arrhtyhmias, remodelling
scar tissue - ectopic activity, poor conduction, poor contraction
valve dysfunction - papillary muscles
what is ischaemic preconditioning?
protective mechanism post MI to prevent further damage
consequent of reperfusion
biochemical changes
which drugs affect coronary blood flow?
Nitrates - vasodilation
B blockers
CaCB
pottasium channel activators - nicorandil
statins and anti platelet
normal cardiac index?
CO/ BSA
easier to compare in people of different sizes
normal = 3-3.5L/min/m2
define shock
circulatory failure
whereby there is inability to deliver O2 to tissues adequately
4 types - cardiogenic, distributive, obstructive (tamponade , Pneumothorax or embolus), hypovolaemic
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
what abnormalities can be seen in valsalva?
phase 2b - no reflex tachy, hence hypotension
phase 4 - no overshoot, no reflex bradycardia
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
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
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.
what factors determine venous return to the heart?
valves
venous pressure
abdo throacic pump - i.e. ventilation and abdominal pressure
cardiac pump
muscular pump
value for normal CVP? causes of increase?
2-8mmHg
increased in congestive heart failure, hypervolaemia, constrictive pericarditis, PEEP. venous thrombosis
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
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,
