Cardiac Impulse Flashcards
where in the body are the electrical signal which control the heart stimulated
within the heart
is the heart capable of beating in the absence of external stimuli
yes
what is autorhythmicity
heart’s ability to beat in the absence of external stimuli
where does excitation of the cells normally originate
pacemaker cells in the sino-atrial node
what does the cluster of specialised cells in the SA node initiate
heart beat
where is SA node located
upper right atrium, close to where the superior vena cava enters the right atrium
does the SA node normally drive the pace for the ENTIRE heart
yes
what is sinus-rhythm
when a heart is controlled by the sino-atrial node
describe the stability of the cells in the SA not
not stable as do not have a resting membrane potential- slowly drift towards depolarisation
what potential do cells in the SA node exhibit
spontaneous pacemaker potential
does the spontaneous pacemaker potential create action potential? explain answer
yes- spontaneous pacemaker potential takes the membrane potential to a threshold to generate an action potential
in pacemaker cells in the permeability to K+ always constant
no- changes between action potentials
define pacemaker potential
the slow depolarisation of membrane potential to a threshold
what physiological factors contribute to pacemaker potential
decreased K+ efflux (slowing of accumulation of pos ions leads to depolarisation), Na+ and K+ influx, transient Ca++ influx
what is the funny channel
Na+ and K+ influx
via which type of channels does Ca++ influx
T-type Ca++ channels
what does potassium efflux at normal rate trigger
hyper polarisation
what happens when a pacemaker cells reaches its threshold
cell enters rising phase of action potential
what is the threshold for a pacemaker cell
-40mV
what is the rising phase of the action potential
depolarisation caused by activation of long lasting- influx of Ca++ via L-type Ca++ channels
what follows the rising action potential
falling phase of action potential
what is the falling phase of action potential
re-polarisation caused by inactivation of L-type Ca++ channels and activation of K+ channels (decreased Ca++ influx, increased K+ efflux)
does action potential have to spread to all cardiac muscle
yes
how does action potential travel from the sino-atrial node to the atrioventricular node
cell to cell conduction
describe the anatomy of the atrioventricular node
starts as bundle of specialised cardiac cells (bundle of his), then separates into left and right branches, then further into purkinje fibres
how does the current flow from cell to cell
via gap junctions- desmosome
where does cell-to-cell spread of excitation carry action potential across whole heart
from SA to AV, from SA through both atria, within ventricles
why can action potential travel through a gap junction
as it has lower resistance
what is the AV node
small bundle of specialised cardiac cells
where is the AV node located
at the base of the right atrium, just above the junction of atria and ventricles
how does the AV node connect the artia and ventricles
ONLY point of contact between atria and ventricles- action potential can only go through AV node and not fibrous ring separating chambers
describe the the specialised AV node cells
small in diameter- slow conduction velocity
what other types of pathways all conduction from SA node to the AV node
internodal pathways
why is conduction delayed in the AV node
allows atrial systole (contraction) to precede ventricular systole
what allows rapid spread of action potential to the ventricles
bundle of his, its branches and the network of Purkinje fibres
how does action potential spread within the ventricular muscle
cell-to-cell conduction
is the action potential in contractile cardiac muscles cells the same as pacemaker cells
no v different
describe the resting membrane potential of atrial and ventricular myocytes
remains at -90mV until the cell in excited
what happens to the action potential of a cardiac myocyte when it is excited
enters rising phase of action potential- depolarisation caused by fast Na+ influx
what effect does the rising phase of a mycotyes action potential have on membrane potential
rapidly reverses it to +20mV
what is the rising phase of action potential in contractile cardiac muscles cells known as
phase 0
phases of ventricular muscle action potential; summarise phase 0
fast Na+ influx
phases of ventricular muscle action potential; summarise phase 1
closure of Na+ channels and transient K+ efflux
phases of ventricular muscle action potential; summarise phase 2
mainly Ca++ influx
phases of ventricular muscle action potential; summarise phase 3
closure of Ca++ channels and K+ efflux
phases of ventricular muscle action potential; summarise phase 4
resting membrane potential
what phase of ventricular muscle action potential is the plateau phase
phase 2
describe the plateau phase of ventricular muscle action potential
when membrane potential is maintained near the peak of action potential for a few hundred milliseconds
what is the plateau phase mainly due to
influx of Ca++ through L-type Ca++ channels
what happens after the plateau phase
the falling phase of action potential- re-polarisation
what causes the falling phase of ventricular muscle action potential
(re-polarisation) caused by inactivation of Ca++ channels and activation of K+ channels
what does the falling phase of ventricular muscle action potential result in
k+ efflux
what part of the nervous system influences heart rate
autonomic nervous system
how does sympathetic stimulation affect heart rate
sympathetic stimulation increases heart heart
how does parasympathetic stimulation affect heart rate
decreases heart rate
what is the parasympathetic supply to the heart
vagus nerve
what is the vagal tone
vagus nerve exerts continuous influence on the SA node under resting conditions
what is the dominate influence on the SA under normal resting conditions
vagal tone
what does the vagal tone do to the heart rate
slows it from the intrinsic heart rate (approx 100bpm) to a normal heart rate (approx 70bpm)
what can intrinsic heart rate also be known as
tachycardia
what is a normal resting heart rate
between 60 and 100 BPM
What is bradycardia
a heart rate less than 60 BPM
what is tachycardia
heart rate more than 100 BPM
Does the vagus nerve supply both nodes
yes
what does vagal stimulation do to heart rate
slows it
what does vagal stimulation do to AV nodal delay
increases it
what is the neurotransmitter of the vagus nerve and what does it act through
acetyle choline, muscarinic M2 receptors
what is atropine
competitive inhibitor of acetylcholine
when is atropine used
in extreme bradycardia to speed up the heart
what is the effect of vagal stimulation on pacemaker potentials
cell hyperpolarises- longer to reach threshold= slope of pacemake potential decreases + frequency of AP decreases= negative chronotropic effect
what is a negative chronotropic effect
anything that slows HR- e.g. parasympathetic stimulation
what do the cardiac sympathetic nerves supply
SA node, AV node, myocardium
what effect does sympathetic stimulation have on HR
increases HR
what effect does sympathetic stimulation have on AV nodal delay
decreases it
what else does sympathetic stimulation affect in the heart
force of contraction- increases it
what is the neurotransmitter of the sympathetic nervous system and what does it act through
noradrenaline, acting through Beta1 adrenoceptors
what effect does noradrenaline have on the potential of pacemaker cells
slope of pacemaker potential increases, reaches threshold quicker, frequency of action potentials increases= positive chronotropic effect
what effect does noradrenaline have on pacemaker cell K+ influx
decreases
what effect does acetyl-choline have on pacemaker cell K+ influx
increases it
what effect does acetyl-choline have on pacemaker cell Na+ and Ca++ influx
decreases it
what effect does noradrenaline have on pacemaker cell Na+ and Ca++ influx
increases it
what is an ECG
record of depolarisation and re-polarisation cycle of cardiac muscle obtain from electrical current that move across heart and can be detected on skin surface
where do you attach lead one in an ECG
RA (right arm) to Left arm (LA)
where do you attach lead two in an ECG
RA to LL (left Leg)
where do you attach lead three in an ECG
left arm to left leg
which limb is earthed
right leg
what does P mean in an ECG
atrial depolarisation
what does QRS complex mean in an ECG
ventricular depolarisation (masks atrial repolarisation)
what does T mean in an ECG
ventricular repolarisation
what does PR interval mean in an ECG
largely AV node display
what does ST segment mean in an ECG
ventricular systole
what does TP interval mean in an ECG
diastole
what is the area between two cardiac cells called
intercalated disc
describe arrangement of cardiac muscle
striated
what causes striation
regular arrangement of contractile proteins
are there neuromuscular junctions in the cardiac muscle, explain answer
no as capable of generating own action potential
what is the function of desmosomes within the intercalated discs
provide mechanical adhesion between adjacent cells and ensure tension developed by one cell is transmitted to the next
what is a myofibril
contractile units of muscle- many eithin each muscle fibre
describe the components of myofibrils
alternating segments of thick (myosin) and thin (actin) protein filaments
what causes the darker appearance of muscle
the myosin (thick filaments)
what are sarcomeres
functional unit of the tissue- what actin and myosin are arranged into
what produces muscle tension
sliding of actin filaments on myocin filaments
what is force generation dependant on
ATP-dependant interactionbetween thick (myosin) and thin (actin) filaments. cannot happen in absence of ATP and calcium
is ATP required for both contraction and relaxation
yes
describe the route of ATP in muscle contraction
attaches to myosin head. splits in ADP and Pi creating energised myosin head. depending on presence of Ca2+ myosin enters either resting (absent) or binding (present) state. ATP released as myosin binds and myosin slides along actin.
why is there no cross bride binding in a relaxed muscle fibre
as the binding site on actin is physically covered by the troponin-tropomyosin complex
what does the binding of actin and myosin trigger
power stroke that pulls
thin filament inward during contraction
what allows crossbridges to form in an excited muscle fibre
Ca2+ binds with troponin, pulling troponin-tropomyosin complex aside to expose cross bridge binding site
where in the calcium release from
sarcoplasmic reticulum (SR)
in cardiac muscle what is the release of Ca++ from SR dependant on
presence of extra-cellular Ca++
where is most of the Ca++ in a resting muscle cell
most outwith cell, intracellular Ca++ stored within SR
what happens to the calcium concentration during the plateau phase of ventricular muscle action potential
Ca++ influx through L- type Ca++ channels into cardiac myoctyes
what does the calcium influx during the plateau phase also stimulate
release of more calcium from SR (CICR)
what does the high intracellular calcium combined activate
contractile machinery (stimulates formation of cross bridges)
what happened to Ca++ after action potential passes
Ca++ re-sequestered in SR by Ca++-ATPase and the heart muscle relaxes
what does the long refractory period in ventricular muscle action and tension prevent
tetanic contraction
does skeletal muscle have the same refractory period
no
what is a refractory period
period following an action potential in which it is not possible to produce another action potential
what phase helps create refractory period
plateau
describe the Na+ channels during the plateau phase
in depolarised closed state
describe the K+ channels during the descending phase of the action potential
open, cannot be depolarised
what is stroke volume
the volume of blood ejected by each ventricle per heart beat
when is stroke volume ejected
contraction of ventricular muscle
how is stroke volume calculated
end diastolic volume (EDV) - end systolic volume (ESV)
what is stroke volume regulated by
intrinsic and extrinsic mechanisms
where do intrinsic mechanisms originate from
within the heart muscle (organ) itself
where do extrinsic mechanisms originate from
nervous and hormal control
where does the right side of the heart eject its stroke volume into
PA
where does the left side of the heart eject its stroke volume into
the aorta
what are changes in stroke volume brought about by
diastolic length of myocardial fibres
what is the diastolic length of the myocardial fibres determined by
volume of blood within each ventricle- end diastolic volume
what determines cardiac preload
end diastolic volume
what determines end diastolic volume
venous return to the heart
what does the frank starling law describe
relationship between venous return, end diastolic volume and stroke volume
describe the frank starling law
the more the ventricle is filled with blood during diastole (END DIASTOLIC VOLUME), the greater the volume of ejected blood will be during the resulting systolic contraction (STROKE VOLUME)
when is maximum force generated by a muscle
when fibres are a optimum length
what does the stretch of muscle fibres also increase the affinity for
Ca++
in skeletal muscle when are the fibres at optimum
when at rest
in cardiac muscle when are the fibres at optimum
achieved by stretching the muscle
if a venous return to right atrium increases what happens to the EDV of the right ventricle
increases (increased SV into pulmonary artery)
what happens to the EDV of left ventricle when venous return to left atrium from pulmonary vein increases
increases (increased SV into aorta)
what is afterload
the resistance into which heart is pumping
what happens at first if after load is increased and why
EDV increases as heart unable to eject full SV
what happens if increased afterload continues to exist (e.g. untreated hypertension)
eventually ventricular muscle mass increases (ventricular hypertrophy) to overcome resistance
what does the frank-starling mechanism do to compensate for decreased stroke volume
increased force of contraction
what does sympathetic stimulation do to force of contraction
increases it
what is a positive inotropic effect
increased force of contraction
does noradrenaline have a pos or neg inotropic effect
pos
what does noradrenaline do to left ventricular pressure
increases
what effect does sympathetic stimulation of ventricular contraction have on calcium
activates Ca++ channels- greater Ca++ influx
what mediates the effect of sympathetic stimulation on ventricular contraction
cAMP
what happens to the rate of left ventricular pressure change during stole when under sympathetic stimulation
increases, happens quicker, faster contraction, faster heart rate
what happens to rate of ventricular relaxation (and therefore duration of diastole) when under sympathetic stimulation
increases, reduced rate
what happens to the frank starling curve when ventricular contraction under symp stim
shifted to the right
what effects do positive and negative inotropic agents have on the frank staling curve
pos= shifts to left neg= shifts to right
what inotropic effect will heart failure have on the frank staling curve
shift to right as smaller stroke volume
what effect does vagal stimulation have on ventricular contraction and why
major influence on rate, not force of contraction- as very little innervation on ventricles so has little effect on SV
what releases adrenaline and noradrenaline (hormones) and what effect do they have
adrenal medulla- inotropic and chronotropic effect
what is cardiac output
volume of blood pumped by each ventricle per minute
how is cardiac output calculated
SV x HR
what is the normal resting CO
5 litres per minute
