physiology Flashcards
where is the SA node found
in the right atrium close to where the SVC enters it
what rhythm is a heart controlled by the SA node said to be in
sinus rhythm
what type of potential to the cells in the SA node exhibit
spontaneous pacemaker potential
what does the pacemaker potential do
takes the membrane potential to a threshold to generate an action potential in the SA node
waht is the pacemaker potential due to
decrease in K efflux
funny current (Na and K influx)
transient Ca influx
describe the ion movement during the phases of the SA node cell AP
note Ca influx via L type Calcium channels during depolarisation
describe the spread of conduction through the heart
SA node initiates an impulse that is conducted to atrial muscle fibres causing them to contract. impulse spread to AVN by myogenic (cell to cell) conduction
bundle of His
left and right branches in muscular interventricular septum
branches ramify into subendocardial branches (Purkinje fibres) which extend into the walls of the respective ventricles
how does excitation spread through cells in the heart
gap junctions- these are protein channels which form low resistance electrical communication pathways between neighbouring myocytes
- across the atria via cell to cell conduction
- there are some internodal pathways between SAN and AVN
- within ventricles
describe the structure of a gap junction
the desmosomes provide mechanial adhesion
what is the only point of electrical contact between the atria and ventricles
AV node
where is the AV node located
base of the RA
why is conduction delayed in the AV node
to allow atrial systole to precede ventricular systole
describe the phases of venticular muscle AP
what is the resting mp?
where does the CNX supply in the heart
vagal stimulation
SA and AV node
vagal stimulation slows heart rate and increases AV nodal delay - negative chronotropic effect
on an ECG this causes decreased slope of pacemaker potential
vagal tone
CNX exerts a continuous influence on the SAN under resting conditions - this dominates and slows the intrinsic HR from 100bpm to around 70bpm in resting conditions
neurotransmitter for parasympathetic supply to the heart
neurotransmitter is ACh through M2 receptors
atropine
inhibitor of ACh - used in severe bradycardia
cardiac sympathetic nerves
- where do they supply
- effect
- neurotransmitter
as they supply the SAN, AVN and myocardium, they have a positive inotropc effect (force) and chronotropic effect (rate)
slope of pacemaker potential increases
neurotransmitter is noradrenaline through ß1 receptors
what is the sarcolemma
the cell membrane of a striated muscle fibre cell
outline actin and myosin crossbridge action
ATP is broken down into ADP and Pi on myosin – myosin extends and can attach to binding sites on actin to form cross bridges.
Power stroke – myosin pulls the actin towards the M-line shortening the sarcomere.
ADP and Pi are released during power stroke.
Myosin remains attached to actin until ATP binds again – contract again or relax.
rigor complex
ATP is needed for contraction and relaxation
a rigor complex is formed when the myosin head is bent and bound to actin
- this explains rigor mortis after death
- muscle cramps may be due to development of rigor complex due to lack of ATP or inability to remove calcium
describe the action of tropomyosin and troponin
when muscle is relaxed tropomyosin blocks the cross bridge binding sites on actin
when Ca levels are high enough, Ca ions bind to troponin which displaces tropomyosin exposing myosin binding sites on actin
muscle contraction
Ca++ ions stored in sarcoplasmic reticulum and are released in response to signals from the nervous system to contract.
Neurotransmitter molecules released from neurone and bind to receptors which depolarises the muscle fibre membrane, electrical impulse travels down T tubules and opens Ca stores in sarcoplasmic reticulum.
These travel to myofibrils – muscle contraction
what does long refractory period prevent and what is the significance of this
generation of tetanic contraction
excessive heart rate provides insufficient time for cardiac filling, problems with insufficient oxygen and blood etc
how is the refractory period generated in ventricular cells and AP
ventricular: during the plateau phase the Na channels are closed
AP: during the descending phase the K channels are open and so membrane cant be depolarised
define SV and its regulation
volume of blood ejected by each ventricle per heart beat
= EDV - ESV
changes in SV are brought about by changes in the diastolic length of the myofibrils - this is determined by the volume of blood within each ventricle by the end of diastole (EDV) = cardiac preload
the EDV is determined by the venous return to the heart
when is maximal force generated by myofibrils
at optimal fibre length
what does the frank starling law state
the larger the VR, the larger the EDV and the larger the SV
what effect does stretch have on the affinity of troponin for Ca++
increases it
in skeletal muscle when is the optimal fibre length
at resting muscle length - maximum overlap of actin and myosin filaments
define afterload
the resistance into which the heart is pumping
how does the frank starling mechanism compensate for increased afterload causing decreased SV
with increased afterload, at first the heart won’t be able to eject full SV, so EDV increases
this causes FS mechanism to increase the force of contraction and SV
what happens in longterm causes of increased afterload
eg untreated hypertension
eventually the ventricular muscle mass increases (hypertrophy) to overcome the resistance
how do inotropes increase force of contraction
activate Ca channels resulting in greater Ca influx - this causes the peak venticular pressure to rise, and the rate of pressure change during systole to increase - thus reducing the duration of systole
(inotropic and chronotropic)
rate of ventricular relaxation also increases, reducing the duration of diastoe
what mediates the positive inotropic effect that sympathetic stimulation has on the heart
cAMP - controls Na and Ca influx
how does sympathetic stimulation affected the Frank Starling Curve
shifts it to the left
what effect does a rise in peak ventricular pressure have on the contractility of the heart at a given EDV
increases it
how does heart failure effect the curve
shift to right
what is the resting CO in adults
5l per minute
what is the ligamentum arteriosus
remnant of the fetal shunt ( ductus arteriosus)
a persistent ductus arteriosus produces a machine like murmur
what are the principles of valves
AV valves are open when atrial pressure exceeds ventricular pressure
semilunar valves are open when ventricular pressure exceeds aortic/pulmonary pressure
passive filling and atrial contraction
pressure in atria and ventricles is close to 0, AV valves are open so venous return flows into the ventricles - 80% passive filling
atrial depolarisation (P wave), atria contract and pressure increases forcing the remaining blood into the ventricles
as AC completes, the pressure in the atria falls and the valves shutl producing the first heart sound - S1 (LUB)
this signifies the beginning of ventricular systole
normal EDV in resting adult
around 130ml
isovolumetric ventricular contraction
early systole, for a short time all the valves are shut and the ventricles depolarize and contract, increasing pressure in the ventricles without a change in volume
the increase in ventricular pressure is sharp
this happens until the pressure in ventricles exceeds that in pulmonary artery/aorta and the semilunar valves open - ventricular ejection
ventricular repolarization occurs, the ventricles relax, pressure falls and the semilunar valves shut - S2 (DUB). this signifies the end of systole
what are the normal values for SV, EDV and ESV
SV = EDV -ESV
70 = 135-60ml
dicrotic notch
coincides with aortic valve closure, caused by the valve vibration
Isovolumetric Ventricular relaxation
Tension falls in ventricles in a closed volume, until ventricular pressure falls below that of atrial, and AV valves open to start cycle again
heart sounds
- S1 (LUB) is caused by the tricuspid and mitral valves closing and signifies the beginning of systole
- S2 (DUB) is caused by the closure of aortic and pulmonary valves and signifies the beginning of diastole
how does arterial pressure not fall to 0 during diastole?
i do not know
explain JVP
it is a biphasic pulse along the sternocleidomastoid
when the pressure in the RA increases, a pressure is exerted outwards onto the IJV
- a wave signifies increase in atrial pressure due to atrial contraction
- c wave signifies increase in atrial pressure due to bulging of tricusped valve into atrium during ventricular contraction
- v wave signifies increase in atrial pressure due to atrial filling, it releases as the AV valve opens
define BP
the outwards pressure that is exerted by the blood on blood vessel walls
Kortkoff sounds
- no sound is heard above systolic pressure eg 120/80*
1. heard at peak systolic pressure
2-3: intermittent sounds heard between 80 and 120
4: muffled sound heard at minimunm/diastolic pressure
5: no sound heard below diastolic (80) as the flow is laminar
* diastolic pressure is measured at the 5th sound as this is more reproducible*
what drives the blood around the systemic circulation
pressure gradient between aorta and right atrium
define MAP
the average arterial blood pressure during a single cardiac cycle
as D is twice as long as S:
MAP = (2xDP + SP) / 3
normal range of MAP
and minimum MAP to perfuse
70-105mmHg
60mmHg
define cardiac output
volume of blood pumped by each ventricle per minute
explain the effect of the sympathetic nervous system on MAP
baroreceptor reflex
Short term regulation of MAP
- the baroreceptors are pressure sensors, they are located in the carotid sinus (carotid ones - CNIX) and aortic area (aortic ones - CNX)
- send signals to medulla via CN
- if there is a drop in BP (eg standing up), they will detect the decrease in tension and stop firing, this allows uninhibited symapthetic activity on the heart
- if there is an increase in BP, they will be stretched and fire, inhibiting sympathetic activity and increasing vagal tone on the heart
- have the ability to reset, eg after one day of increased BP
when does postural hypotension occur
failure of baroreceptor to respond to gravitational shifts in blood (which decrease venous return to heart)
how much of total body fluid is intracellular and extracellular
2/3 intracellular
1/3 extracellular
explain RAAS
note, aldosterone causes sodium retention, and water follows
what is the rate limiting step for RAAS
renin production
activation of RAAS
- renal artery hypotension caused by systemic hypotension
- stimulation of renal sympathetic nerves
- decreased sodium concentration in renal tubular fluid (sensed by macula densa in kidney tubules)
role of ANP
released in response to atrial distension in hypervolaemic states:
- excretion of salt and water in the kidneys, therefore reducing blood volume and pressure
- vasodilation
- decrease renin release - counter regulate RAAS
how many amino acids does ANP have
28
what is ADH secretion stimulated by
dec extracellular fluid or inc extracellular fluid osmolarity (detected by osmoreceptors in the brain near they hypothalamus)
what is the normal osmorality of extracellular fluid
280 mili osmoles
when is ADH important
hypovolaemic shock
what are the major resistance vessels
arterioles
what contains most of blood volume during rest
veins - they are capacitance vessels
resistance to flow equation
vasomotor tone of vascular smooth muscle
blood vessels are partially constricted at rest - tonic discharge of sympathetic nerves, resulting in continuous noradrenaline release, acting on alpha receptors
which smooth muscles have significant parasympathetic innervation
penis and clitoris
describe the organ specific effect of adrenaline and its advantages
- acting on alpha receptors in skin, gut and kidney arterioles, causes vasoconstriction
- acting on ß2 receptors in cardiac and skeletal muscle causes vasodilation
- this allows for the strategic distribution of blood eg during exercise
simply, what comprises extrinsic control of vascular smooth muscles
nerves and hormones
which chemical factors cause vasodilatation and metabolic hyperaemia
- Decreased local PO2
- Increased local PCO2
- Increased local [H+] (decreased pH)
- Increased extra-cellular [K+]
- Increased osmolality of ECF
- Adenosine release (from ATP)
bradykinin
an inflammatory mediator that causes vasodilatation
it is increased by ACE inhibitors, and causes a dry cough
formation of NO
- it is continuously produced by the vascular endothelium from the amino acid L-arginine through the enzymatic action of NOS
- acts in the smooth muscle
nitric oxide
NO is a potent vasodilator - activates the formation of cGMP in the smooth muscle cells which signals smooth msucle relaxalation
- shear stress on vascular endothelium as a result of increased flow, causes calcium release which activates NOS
- chemical stimuli can stimulate NO formation
what do serotonin, thromboaxane A2 and leukotrienes cause
vasocontriction
endothelin
vasoconstrictor released from endothelial cells
sheer stress
dilatation of arterioles causes sheer stress in the arteries upstream to make them dilate - increases blood flow to metabolically active tissues
can local control of TPR override extrinsic control?
yes, it responds to immediate demands of particular tissues, can overide the nerves that control these tissues
how is blood flow to skeletal and cardiac muscles increased during exercise
local hyperaemia overcomes vasomotor drive, resulting in vasodilatation
what happens to pulse pressure during exercise
- decrease in SVR during exercises increases the flow to tissues and increases VR
- this increase CO and systolic BP
- diastolic BP is decrease because TPR decreases
define shock
- abnormality of the circulatory system resulting in inaequate tissue perfusion and oxygenation
- this results in anaerobic metabolism, and accumulation of metabolic waste products
cardiogenic shock
sustained hypotension caused by decreased cardiac contracility
how does a tension pneumothorax cause obstructive shock
increased intrathoracic pressure results in decreased venous return (increased resistance in vena cava)
how does neurogenic shock casue inadeqaute tissue perfusion
loss of sympathetic tone, leading to massive venous and arterial vasodilatation
vasoactive shock
release of vasoactive mediators - massive venous and arterial vasodilatation
increased capillary permeability
during haemorrhagic shock, up to which point can compensatory mechanisms maintain blood pressure
up to 30% blood loss
what are capillaries formed from
a single layer of endothelial cells
what is interstitial fluid
component of the extracellular fluid (70%) that surrounds cells in the body - go between blood and body cells
describe the functions of capillaries
- allow rapid exchange of gases, water and solutes with interstitial fluid
- delivery of nutrients and O2 to cells
- removal of metabolites from cells
how is blood flow to capillaries determined
- the contractile state of terminal arterioles regualte regional blood flow to the capillary bed in most tissues
- precapillary sphincters regulate the flow in a few tissues
describe the blood flow through CB
very slow to allow for adequate time for exchange
name a tissue that has precapillary sphincters
mesentery
how do lipid soluble and water soluble substances pass throughcapillary wall
- lipid soluble pass through endothelial cells
- water soluble pass through water filled pores
- large molecules generally cannot cross the capillary wall eg plasma proteins
starling forces
the forces involved in transcapillary fluid flow
define NFP
(PC + πi) - (pC + πi)
what do starling forces favour at the arteriolar and venular end
favour filtration at the arteriolar end and reabsorption at the venular end
what happens to excess fluid
it is returned to the circulation via lymphatics as lymph
how are the lungs generally kept dry
- they need to be to facilitate gas exchange
- pulmonary resistance is 9x less than systemic
- they have a low capillary hydrostatic pressure and a high capillary osmotic pressure - minimise fluid loss into interstitium
- efficient lymphatic drainage removes any filtered fluid thus preventing accumulation of interstitial fuid
define oedema
accumulation of fluid in the interstitial space
decribe the effect of pulmonary oedema on gas exchange
increases the diffusion distance, compromising gas exchange
name 4 causes of oedema
- raised capillary pressure
- reduced osmotic pressure
- malnutrition, protein malabsorption, hepatic failure
- lymphatic insufficiency
- changes in capillary permeability
- eg inflammation, histamine increases leakage of protein
what can filariasis cause
elephantiasis
