cardio Flashcards
what level are the t tubules
z line
what are ryanodine receptors
calcium release channels on the sarcoplasmic reticulum
they move calcium
where are L type calcium channels located
on the wall of a t tubule
also known as DPHR
ryanodine receptors
they cluster and open in unison to activate to produce aa large signal
the events of cardiac excitation coupling
1- action potential arrives at t tubule
2-depolarises t-tubule
3- opens L type calcium channel
4- calcium released and binds to ryanodine receptor on SR
5-calcium released from SR
6- increase in calcium conc in cytoplasm
7- calcium can bind to troponin-C –> cross bridge formation
where are calcium release sites located
Z line
how does the heart ensure uniform contraction
1-calcium doesn’t have to move very far to get to middle of myofilament
2-all parts of the cell shorten at the same time
troponin complex
C- binds to calcium ions
I- binds to actin- inhibits the binding of myosin to actin
T- binds to tropomyosin
presence of Ca2+ to thin and thick filaments
1-Ca2+ binds to troponin C
2- troponin C binds more strongly to troponin I
3- troponin I no longer binds to actin
4- tropomyosin moves further into the groove of actin
5- the troponin complex swings out of the way
6- the actin-myosin binding site is uncovered, myosin cross-bridges can now bind to actin
removal of Ca2+
1- ATP dependent Ca2+ pump- back into SR
2-Na+/Ca2+ exchanger- uses Na+ chemical gradient
–>3 Na for 1 Ca2+- diff charge so may create current
3- sarcolemmal Ca2+ ATPase- uses energy to push Ca2+ up conc gradient
systole
contraction
diastole
relaxation
cardiac output
amount of blood pumped out of a ventricle in 1 minute
=HRxSV
stroke volume
volume ejected from 1 ejected in a single cardiac cycle
=EDV-ESV
End diastolic volume
volume of blood before contraction
End systolic volume
volume of blood left in ventricle after contraction
Ejection fraction
percentage of blood the ventricle can empty in 1 minute
=SV/EDV
heart failure
when the ejection fraction is below 40%
preload
the volume load on the ventricles before ventricular contraction
–>determined by EDV
after load
the pressure in the artery against which the ventricle is pumping
for the left ventricle it represents diastolic pressure- 80mmHg
Frank-Starling law of the heart
as the degree of stretch on the heart increases so does the force of contraction
Inotropic state
related to the degree of activation of the contractile proteins by Ca2+
factors that influence inotropic state
1- Action potential- increase in plateau length- increase Ca2+ influx
2- external ion concentration
a- increasing external Ca2+
b- lower external Na+- slows Na+/Ca2+ exchange- Ca2+ accumulates inside
3-force frequency relationship
increase stimulation frequency- more Ca2+ entry
sympathetic stimulation increase force of contraction
1- noradrenaline binds to B1 receptors in membrane
2-activated GTP binding protein Gs
3- the alpha subunit activated adenylate cyclase
4-increase cAMP production from ATP
5- activated protein kinase A
6- this affects function of different proteins
pKA phosphorylation
1- L type calcium channel- Increases calcium influx so more released from SR
2-ryanodine receptor- increases sensitivity to calcium- more released from SR
3-phosholamban- This interferes with the mechanism which takes away calcium
ATPase that sits on sarcoplasmic reticulum is normally inhibited
PKA can phosphorylate phospholamban so unleashes ATPase making it better at retaining calcium in calcium store—>more calcium in SR so more can be released
4- troponin– decreased sensitivity to Ca2+ so quicker relaxation- better filling of ventricles
catecholamines
increase the inotropic state- greater filling of ventricles so increased stroke volume
chronotropic effect
how it affects the heart
sympathetic on pacemaker potential
1- makes funny current stronger- slow depolarisation is faster- reaches threshold faster
2-decreases permeability to potassium- membrane potential doesn’t go as negative
3- increased L type Ca2+ current- faster upstroke
isovolumic contraction
volume doesn’t change but there is an increase in pressure due to mitral valve closing
isovolumic relaxation
no change in volume but there is a reduction in pressure
what circulatory tube regulates blood pressure
arterioles
echocardiography
maps the positions of the chambers of the ventricles
MRI
3D imaging- can track the change of the ventricular wall during the cardiac cycle
how does the ventricular wall change during contraction
1- isovolumetric contraction- myocytes shorten and swell sidewas
2- laminar- slide past each other and become more perpendicular to plane of ventricular wall
cellular basis of heart failure
1-increased stiffness- collagen and microtubules
2-changes in action potential
3-negative inotropic state
dysrhythmia/ arrhythmia
disturbance of cardiac rhythm
drug treatment for dysrhythmia
class 1- sodium channel blockers- upstroke of non-pacemaker class 2- beta blockers- L type calcium current- upstroke of pacemaker, plateau of non-pacemaker and funny current class 3- potassium channel blockers- depolarisation class 4- calcium channel blockers- upstroke of pacemaker and plateau in non-pacemaker
Sympathetic stimulation increases funny current and L type calcium current enhances:
early after depolarisation
Increased automaticity
Delayed after depolarisation
ischaemia
restriction in blood supply to tissues
example of 1a drug
quinidine
example of 1b drug
lidocaine
example of 1c drug
flecainide
class 1b drug
used to treat ischaemia as the channels are likely to be inactive
prevents a premature beat
example of class 2 drug
propranolol and atenolol
example of class 3 drug
sotalol and amiodarone
example of class 4 drug
verapamil and dilitizaem
aims for treating heart failure
- relieve symptoms
- improve exercise tolerance
- reduce mortality
in heart failure why do you feel breathless?
ventricular filling pressure is high for stroke volume
in heart failure why do you feel fatigue and unable to exercise
as aortic pressure increases, stroke volume decreases
how do beta blockers help heart failure
1- address the change in autonomic balance- reduce sympathetic
2- reduce hypertrophy
3-stimulates vasodilation
4-reduce dysrhythmia
examples of ACE inhibitors
captopril and ramipril
collaterals
connect systems derived from the major arteries
stable angina
- partial occlusion of a coronary artery
- pain when exercising
- intermittent symptoms with constant severity
where is the heart located
2nd-5th rib
papillary muscles
contract and pull on the chord terndinae to prevent the valves from exerting into the atria
fibroblasts
contribute to extraceullar matrix
provide mechanical support
endothelial cells
lining of blood vessels
smooth muscle cells
in coronary arteries and cells
conduction cells
generation and passing of electrical impulses
cardiomyocytes
form the contractile apparatus of atria and ventricles
roles of intercalated disc
mechanical coupling
electrical coupling
net electrochemical driving force
difference between membrane potential of the cell and the equilibrium potential for a given ion
what does high conc of KCl do?
sodium channels will be inactivated, paralyses muscles and stops cardiomyocytes from contracting
where are the bipolar leads in an ECG placed
left leg, left arm, right arm
what are the layers of a vessel
tunica adventitia- connective tissue
tunica media- smooth muscle and elastin
tunica intima- squamous endothelium
what is darcys law?
the flow is proportional to the pressure difference between 2 points
what is Bernoulli’s theory?
the pressure difference between points A and B is proportional to the difference in mechanical energy between A and B
what is compliance?
change in volume per unit change in distending pressure
distending pressure= pressure inside-pressure outside
autoregulation
intrinsic adjustment of flow to a tissue so that flow meets local requirements
3 roles of lymphatic system
1- transports interstitial fluid back into the vascular system
2- transports fats from small intestine to the blood
3- lymphocytes play a role in immunological defences
baroreceptors
monitor blood pressure
arterial- short term
cardiopulmonary- long term
chemoreceptors
monitor the chemical composition of the blood
2 hypotheses for exercise
1- central command- cerebral cortex
2- peripheral reflex- proprioceptor inputs from joints and muscles
active hyperaemia
leads to increase in blood flow due to increase in metabolic demands
role of cutaneous blood supply
1- heat exchanger for thermoregulation
2- supply of nutrients to cells
3- blood reservoir
how the skin responds to heat
1- hypothalamus- reduced vasomotor tone- vasodilation
2- sweat- production of bradykinin- stimulates endothelial cells to release NO- vasodilation
how the skin responds to cold
1- superficial vessels constrict strongly
2-blood bypasses capillaries, via AV shunts, to vital organs
3-skin may appear rosy- blood may be trapped in superficial vessels following rapid vasoconstriction
minute ventilation
the total amount of air flowing into or out of the respiratory system per minute
forced vital capacity
total volume of air expired after a maximal inspiration and forced exhale
forced expiatory volume in 1 second
the volume of air expired in first second after maximum exhalation
decreasing affinity for oxygen
goes to the right- favours unloading- capillaries
increasing affinity for oxygen
goes to the left- favours loading- lungs
how does increasing temperature affect O2 affinity
it decreases the affinity so the graph goes to the right and O2 is unloaded
how does the decreasing the pH affect O2 affinity
it decreases the affinity so the graph goes to the right
aerobic- increase in CO2
anaerobic- increase in lactic acid
how does increasing CO2 conc affect O2 affinity
increasing CO2 favours O2 unloading as CO2 has a lower affinity for Hb than O2 so will bind more and therefore unloading O2
bohr effect
2,3 DPG
in hypoxia and anaemia promotes O2 unloading
what happens to carbon dioxide in an erythrocyte?
1- converted into HCO3- and H+ by carbonic anhydrase
2- HCO3- leaves the cell and binds to Na and this is used to transport CO2 to the lungs
3- Cl- enters the cell to equal the charges–>chloride shift
4- the H+ is buffered by Hb- favours O2 unloading
Haldane effect
increases the rate of CO2 elimination
O2 conc is increased and this favours unloading of CO2 from Hb
what is hypoxemia
it is where PaO2 is abnormally low
what is shunted blood?
when the blood enters the left ventricle without going through the ventilated areas of the lung so diluting the O2 conc in the left ventricle
what are the chemoreceptors located on the ventral surface of the medulla called and what do they do?
central chemoreceptors
minute by minute control of ventilation
how do central chemoreceptors work?
H+ cannot cross BBB
CO2 cross BBB, carbonic anhydrase converts it into H+ and HCO3-
the chemoreceptors then respond to the rise in H+
inputs then go to respiratory control centres in the pons and medulla
where are peripheral chemoreceptors located
carotid and aortic bodies
O2 sensing in carotid bodes
1- decrease in O2 inactivates membrane K+ channels, reducing K+ influx
2- depolarises the cell, activating Ca2+ channels
3- influx of Ca2+ and release of neurotransmitter (dopamine)
4- NT binds to receptors on afferent and causes a depolarisation and increase in action potential frequency
causes of metabolic acidosis
diarrhoea
exercise
abnormal fat absorption
renal failure
causes of metabolic alkalosis
vomiting
