UNIT 4 REVISION Flashcards
left shift
decreased temp
decreased H+
CO
right shift
reduced affinity
oncreased temp
ioncreased H+
somatic sensory
- Receptor
- Afferent
- Ventral/Dorsal ramus
- Spinal nerve
- Dorsal root
- Spinal cord
- Synapse in the dorsal horn of grey matter
- Neurotransmitter: acetylcholine
somatic motor
- Ventral horn of grey matter
- Efferent
- Ventral root
- Spinal nerve
- Dorsal/ ventral ramus
- Synapse at the effector
- Neurotransmitter: acetylcholine
sympathetic efferent
thoracolumbar outflow
- Preganglionic sympathetic fibre in the lateral horn of grey matter
- Ventral root
- Mixed spinal nerve
- White ramus of communicans (myelinated)
- Synapse in the sympathetic ganglion
- Meets the post ganglionic fibre
- Post ganglionic passes through the grey ramus of communicans (not myelinated)
- Target tissue
- Neurotransmitter: in presynaptic it is acetylcholine and in post it is noradrenaline
parasympathetic efferent
craniosacral outflow
- Efferent through the ventral horn of grey matter
- Ventral root
- Spinal nerve
- Dorsal/ventral ramus
- Synapse in the ganglion before the target tissue
- Neurotransmitter: acetylcholine
where do splanchnic nerves synapse
pre vertebral ganglia
p wave
atrial depolarisaiton
pr interval
time taken for electrical activity to move between atria and the ventricles
QRS
depolarisation of the ventricles
ST segment
isoelectric line
time between depolarisation and repolarisation of the ventricles
T wave
ventricular repolarisation
RR interval
peak of one r wave to peak of next R wave
QT complex
ventricles to depolarise then repolarise
passive ventricular filling
pressure in ventricles lower than in atrai
tricuspid opens
ventricles passively fill with blood
atrial ejection
atria contract
rest of blood to the ventricles
semilunar close as pressure higher in arteries than ventricles
isovolumic contraction
ventricles contract
tension building
pressure higher in ventricles than atria
AV slam shut
pressure not high enough to open aortic and puilmonary
ventircular ejection
pressire in ventricles higher than arteries
aoritc and pulmonary valves open
isovolumetric ventricular repolarisation
ventricles astart to relax
pressure lower in the ventricles than the arteries
aortic and pulmonary valves slam shut
ventricular pressure higher than the atria
AV valves still shut
isotonic contraction
same tension, length changes
isometric contraciton
same length, tension changes, occurs if load is too heavy to move
length tension relaitonship
- Cardiac muscle will only operate on the ascending limb of the curve
- As cardiac muscle is stiffer than skeletal
- Preload for left ventricle is EDV
- Afterload is the aortic pressure
frank starling relationship
- Volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole
stroke volume
volume of blood ejected on each beat, EDV- ESV, roughly 70ml
ejection fraction
fraction of the EDV ejected in one storke volume, storke volume divided by EDV
cardiac output
total volume ejected by the ventricle per unit time, equal to venous return
what factors affect storke volume
prelaod
contractility and afterload
preload and SV
`- Changes in stroke volume occur following changes in resting ventricular muscle fibre length (preload)
- Mechanism intrinsic to the heart
contractility and SV
- Inotropic effect
- Changes in stroke volume without changes in resting ventricular muscle fibre length (no change in preload)
- Mechanism extrinsic to the heart
afterload and SV
- Changes in aortic pressure
absolute refractory
- closure of inactivation gates of sodium channel in response to depolarisation
- gates closed position until cell is depolarised back to resting membrane potential and Na+ have recovered to closed but available state
relative refractory
- action potential can be elicited
- only if a greater than usual depolarisation current
- higher K+ conductance than is present at rest
- membrane potential is closer to K+ equilibrium potential
- more inwards current needed to bring membrane to threshold for next action potential to be initiated
ion currnt
occurs when there is movement of an ion across the cell membrane
when will ions move across the cell membrane
when there is 1. driving force on the ion
2. membrane has conductance to the ion
cardiac action potential
Phase 0: upstroke, rapid depolarisation, Na+ influx
Phase 1: initial repolarisation, Na+ influx stops, K+ efflux
Phase 2: plateau, stable depolarisation, Ca2+ influx via L-type calcium channels, k+ efflux
Phase 3: repolarisation, Ca2+ influx stops, K+ efflux
Phase 4: resting membrane potential, close but not equal to K+ equilibrium potential
SAN action potentia
Phase 0: upstroke, rapid depolarisation, Ca2+ influx
Phase 3: repolarisation, Ca2+ influx stops and K+ efflux
Phase 4: influx of Na+ through funny channels which is turned on by repolarisation from previous AP, gradient restored
features of SAN actrion potentials
Features of SAN action potentials:
1. automaticity: spontaneous AP generation without neural input
2. unstable resting potential
3. no sustained plateau
chronotropic effects
effects on autonomic nervous system on the heart rate , increase is sympathetic
dromotropic effects
: effects on the autonomic nervous system on conduction velocity, increase is the increase in conduction velocity through AV node
inotropism
intrinsic ability of myocardial cells to develop force at a given muscle length, increase will increase contractility
amount of Ca2+ depends on what
- size of inward Ca2+ current
- amount of Ca2+ previously stored in the SR for release
phases of ventricular pressure volume loops
isovolumetric contraction is 1 to 2
ventricular ejection is 2 to 3
isovolumetric relxation is 3 to 4
ventircular fillng is 4 to 1
diastolic pressure
pressure during ventricular relaxation, lowest pressure
systolic pressure
: highest pressure, pressure after the blood has been ejected
dicrotic notch
when aortic valve closes, brief period of retrograde flow towards valve, briefly decreasing aortic pressure below systolic
pulse pressure
difference between diastolic and systolic
mean arterial pressure
Pa, average pressure over complete cardiac cycle, DP + 1/3 pulse pressure, 70-100 mmHg
blood floq
Q= different in pressure / resistance
total peripheral resistance
resistance of entire systemic vasculature (TPR) or systemic vascular resistance (SVR)
R a 1/r4 (remember this!)
baroreceptors
carotid sinus
aortic arch
carotid sinus baroreceptors
glossopharyngeal
nucleus tractus solitarus
cardiac decelerator
parasympathetic
SAN
aortic arch baroreceptors
vagus
nucleus tractus solitarus
decreases careidac acceleratory and vasoconstriction
increases SAN, contractility, arterioles and venous vasodilation
carotid sinus massage
- Massage carotid sinus distends the barorecpetors
- Increases vagal outflow to the heart
- Slows SA firing and AV conduction
- AVN conducts fewer action potentials through ventricles
- Less QRS complexes, ventricular rate slows from dangerously high rates
diving reflex
- Cold water stimulates the sensory receptors of the trigeminal nerve and receptors in the nasopharynx and oropharynx
- Resulting in:
1. Apnoea
2. Bradycardia
3. Peripheral vasoconstriction
procedure of valsalva manoeuvre
- Inhale deeply and then hold the breath.
- Imagine that the chest and stomach muscles are very tight and bear down as though straining to initiate a bowel movement.
- Hold this position for a short time, usually about 10 seconds.
- Breathe out forcibly to release the breath rapidly.
- Resume normal breathing
physiology of valsalva
- Increased intrathoracic pressure increases blood flow from the pulmonary circulation into the left atrium. This increases left ventricular EDV and SV. There is also compression of the aorta, increasing blood pressure.
- High intrathoracic pressure impedes venous return, decreasing SV and therefore also blood pressure. During this period, there is a baroreceptor-mediated increase in heart rate.
- When the manoeuvre is released, compression on the aorta is stopped and left ventricular filling pressures are reduced temporarily as the pulmonary vessels re-expand. This causes a drop in blood pressure.
- VR is restored, increasing cardiac filling pressures and SV. This increases BP, resulting in a baroreceptor reflex-mediated bradycardia and subsequent fall in BP to normal levels.
