Physiology Flashcards
1) Origin & conduction of cardiac impulse Cards 1-44 2) force generation by heat 45 - 96 3) cardiac cycle 97-130 4) control of arterial blood pressure 131-204 5) integration of cardiovascular mechanism 205-271
how is the heart controlled?
electrically controlled
where are the electrical signals which control the heart generated?
from WITHIN the heart itself
what is auto-rhythmicity?
when the heart is capable of beating rhythmically in the ABSENCE OF EXTERNAL STIMULI
where does excitation of the heart originate from?
pacemaker cells in the SINO-ATRIAL NODE
where is the SA node located?
and where is it close to?
Located;
= upper right atrium
Close to;
= where the superior vena cava enters the right atrium
what sets the pace for the entire heart?
the SA node
what is sinus rhythm?
a heart controlled by SA node.
True or False.
Cells inn the SA node have a stable resting membrane potential?
FALSE.
they have NO stable resting membrane potential
what potential do pacemaker cells in the SA node generate?
spontaneous pacemaker potential
how is an action potential generated?
1) spontaneous pacemaker potential takes membrane potential to a threshold
2) each time threshold is reached, action potential is generated
True or False.
In pacemaker cells, permeability to K+ doesn’t remain constant between action potentials.
True
what is the pacemaker potential?
the slow DEPOLARISATION of a membrane potential to a threshold
what is the pacemaker potential due to? (3)
1) decrease in K+ efflux
2) Na+ & K+ influx
3) transient Ca2+ influx
what is the rising phase of the action potential known as?
depolarisation
what is the rising phase of the action potential (i.e. depolarisation) caused by?
= influx of Ca2+ (due to activation of long lasting L-type Ca2+ channels)
what is the falling phase of the action potential known as?
re-polarisation
what is the falling phase of the action potential caused by?
1) inactivation of L-type Ca2+ channels
2) activation of K+ channels, causing K+ efflux
how does cardiac excitation spread across the heart through cell-cell conduction?
via gap junctions
what is the route taken for excitation to spread to ventricles? (5)
1) SA node
2) AV node
3) bundle of His
4) Purkinje fibres
5) ventricles
what is the AV node comprised of?
small bundles of specialised cardiac cells
where is the AV node located?
at base of the right atrium just above atria & ventricles
where is the AV node the ONLY point of electrical contact between?
are AV node cells large and slow to conduct? true/false
between atria & ventricles.
False.
Small & slow to conduct
why is conduction delayed at AV node?
to allow atria systole (contraction) to precede ventricular systole
what does the resting membrane potential remain at until the cell is excited?
-90mV
what causes the rising phase of the action potential in atrial & ventricular myocytes?
fast influx of Na+
what does the fast influx of Na+ reverse the membrane potential to?
+20mV
ventricular muscle action potential - Phase 0
fast Na+ influx = depolarisation, membrane potential from -90mV to +20mV
ventricular muscle action potential - Phase 1
Closure of Na+ channels
Transient K+ efflux
ventricular muscle action potential - Phase 2
Ca2+ influx
ventricular muscle action potential - Phase 3
Closure of Ca2+ channels
opening of K+ channels allow K+ efflux
causing re-polarisation of membrane back to -90mV
ventricular muscle action potential - Phase 4
resting membrane potential
what is the plateau phase of the action potential?
what is it mainly due to?
= when the membrane potential is maintained near the peak of action potential
= mainly due to influx of Ca2+
what is the heart rate mainly influenced by?
autonomic nervous systeem
what effect does sympathetic & parasympathetic stimulation have on heart rate?
sympathetic = increases HR parasympathetic = decreases HR
what nerve exerts a continuous influence on th e SA node under resting conditions?
vagus nerve
what does the vagal tone do to the intrinsic heart rate?
it slows the intrinsic heart rate from 100-70bpm
what is norma resting HR?
60-100BPM
what is bradycardia?
less than 60BPM
what is tachycardia?
more than 100BPM
what is a parasympathetic neurotransmitter & what does it act through?
= acetylcholine
= acting through muscarinic M2 receptors
what is a competitive inhibitor of acetylcholine and when is it used?
= atropine
= used in extreme bradycardia to speed up the heart
what areas do the cardiac sympathetic nerves supply?
supplies SA node, AV node & myocardium
what is a sympathetic neurotransmitter & what does it act through?
= noradrenaline
= acting through B1 adreenoceptor
describe how sympathetic & parasympathetic nerve supply effects the slope of pacemaker potential & AV node delay?
sympathetic
= increases slope
AV node delay
= decreases
Parasympathetic
= decreases slope
AV node delay
= increases
what term describes the appearance of cardiac muscles?
striated
how is the striation of cardiac muscles caused?
by regular arrangement of contractile protein
True or False.
there is no neuromuscular junctions in the cardiac muscle.
true.
what electrically couples the cardiac myocytes?
gap junctions
what are gap junctions?
what function do gap junctions have?
= they are protein channels
Function
= the form low resistant electrical communication between neighbouring myocytes
what is the All-or-none Law of the heart?
= gap junctions ensure that each electrical excitation reaches all the cardiac myocytes
where are desmosomes located?
they are within the inter-calated discs.
what do desmosomes do?
and what do desmosomes ensure?
= they provide mechanical adhesions between adjacent cardiac cells
= ensuring tension developed by one cell is transmitted to the next
what does each muscle cell contain?
MYOFIBRILS
what do myofibrils do?
they are the contractile units of muscle
what are myofibrils composed of?
alternating segments of thin & thick segments
1) actin
= thin
= light appearance
2) myosin
= thick
darker appearance
within each myofribil, what are actin & myosin arranged into?
they are arranged into a sarcomere
how is muscle tension produced?
by the sliding action of actin filaments & myosin filaments
what is required for contraction & relaxation of cardiac muscle?
ATP is required
what is required tis witch on cross bridge formation/contraction?
Ca2+
where is the Ca2+ released from?
the sarcoplasmic reticulum
in cardiac muscles, what is the release of Ca2+ dependent on?
on the presence of extra-cellular Ca2+
how does excitation of cardiac cells cause contraction?
what factors increase the affinity of troponin for Ca2+?
When relaxed;
- no cross bridge binding as binding site on action for myosin is covered by toponin-tropomyosin complex
When excited;
- Ca2+ binds with troponin, causing a conformational change, pulling the T&T complex aside, exposing the myosin binding sites on actin
Factor
= stretch of cardiac muscles
how does excitation of cardiac cells cause contraction?
what factors increase the affinity of troponin for Ca2+?
When relaxed;
- no cross bridge binding as binding site on action for myosin is covered by toponin-tropomyosin complex
When excited;
- Ca2+ binds with troponin, causing a conformational change, pulling the T&T complex aside, exposing the myosin binding sites on actin
Factor
= stretch of cardiac muscles
what is the refractory period?
a period following an action potential in which is NOT possible to produce another action potential
what phases of ventricular muscle action potential are within the refractory period?
1) plateau phase
2) re-polarisation (descending phase)
during thee plateau phase, describe the state of Na+ channels?
Na+ channels are in the depolarised closed state, not available for opening
during the descending phase of action potential, describe the state of K+ channels?
K+ channel red open & membrane can’t be depolarised
why is a longer refractory period beneficial?
protects the heart as it prevents the generation of TETANIC CONTRACTIONS in cardiac muscle
what is stroke volume?
volume of blood ejected by each ventricle per heart beat
what is End diastolic volume (EEDV) & End systolic volume (ESV)?
EDV
= volume of blood accumulated when heart is at the end of the relaxed phase
ESV
= volume of blood accumulated when the heart is at the end of the contraction phase
what is the relationship between stroke volume, ESV & EDV?
SV = EDV - ESV
what 2 mechanisms regulate stroke volume?
1) intrinsic (within heart itself)
2) extrinsic (nervous & hormonal control)
intrinsically, how are changes in stroke volume bright about?
by changes in diastolic length/diastolic stretch of myocardial fibres.
how are changes in diastolic length/stretch determined?
determined by EDV
how is end diastolic volume determined?
by venous return to the heart
what does the frank-starling mechanism or starlings law of heat describe?
= the relationship between;
- venous return
- end diastolic volume
- stroke volume
what is the relationship between EDV, stroke volume & venous return?
the More the ventricle is filled with blood during diastole (EDV), the greater the volume blood will be ejected when it contracts (stroke volume)
when is optimal length in cardiac muscle achieved?
when is optimal length in skeletal muscle achieved?
cardiac muscle
= when muscle is stretched
skeletal muscle
= when muscle is resting
how is stroke volume of right & let ventricle matched?
- if venous return to right atrium increases, then EDV of right ventricle increases
- if venous return to left atrium (from pulmonary vein) increases, EDV of left ventricle increases
what is after load?
What tis preload?
after load
= the resistance into which the heart is pumping into after contraction
Pre load
= volume of blood in each ventricle before contraction
when is extra load imposed?
after the heart has contracted
what effect does an increased after load have?
- at first, heart is unable to eject full stroke volume so EDV increases
- if the increased after loads continues to exist, then v ventricular mass (hypertrophy) increases to overcome the resistance
what 2 things do extrinsic control of stroke volume involve?
1) nerves
2) hormones
what nerve fibre supplies the ventricular muscle?
sympathetic nerve fibres
what is a neurotransmitter for sympathetic division?
noradrenaline
what does sympathetic stimulation do to the force of contraction?
increases force of contraction
what is the increased force of contraction known as?
positive INOTROPIC effect
what is a positive chonotropic effect?
increase in heart rate
how does noradrenaline increase the force of contraction?
- activates Ca2+ channels
- greater Ca2+ influx
- cAMP mediated
what effect does sympathetic stimulation have on frank starling curve?
curve is shifted to the left
how does parasympathetic nerves effect ventricular contraction?
has very little innervation on ventricle by vagus
- not much influence on force of contraction
which hormone would give an inotropic & chronotopric effect, beside noradrenaline?
adrenaline
where is adrenaline secreted from?
adrenal gland in the medulla
what is cardiac output?
volume of blood pumped by each ventricle per minute
what is the relationship between CO, SV and heart rate?
CO = SV x HR
what is the rest CO in an healthy adult?
5L
when do heart valves produce a sound?
when they shut
do heart valves normally produce a sound when they open?
yes/no
NO
what is the flow of blood across the heart?
SVC - RA - (flows through tricuspid valve) - RV - Pulmonary Valve - Pa -PVein - LA - (flows through Mitral valve) - LV - AV - A
what triggers the recurring cardiac cycle of atrial & ventricular contractions & relaxations?
- the orderly depolarisation/re-polarisation
what is the cardiac cycle?
all the events occurring from begging of one heart beat to beginning of next heart beat
describe the heart in diastole?
heart ventricles = relaxed = fill with blood
describe the heart in systole?
hert ventricles = contract
= pump blood into the aorta (LV) and pulmonary artery (RV)
what are the names of the 4 heart valves?
1) tricuspid
2) mitral (bicuspid)
3) pulmonary
4) aortic
AtrioVentricular valves
= tricuspid
= mitral
SemiLuminar valves
= pulmonary
= aortic
what are the 5 main events in the cardiac cycle?
1) passive filling
2) atrial contraction
3) iso-volumetric ventricular contraction
4) ventricular ejection
5) iso-volumetric ventricular relaxation
what allows passive filling?
pressure in atria & ventricles to be close to zero
what valves open to allow venous return flow into the ventricles?
the AV valves
= tricuspid & mitral
what does the aortic pressure need to be to allow passive filling?
what state should the aortic valves be in?
aortic pressure = 80mmHg
Aortic valve = closed
what side of the heat has a higher pressure?
left
what percentage of the ventricles becomes full by passive filling?
80% of the ventricles
what does the P-wave in the ECG signal?
atrial depolarisation
when does the atria contract in the ECG?
between P wave & QRS
what completes the end diastolic volume (130mmHg in resting normal adults)?
atrial contraction
when does ventricular contraction start in the ECG?
starts after the QRS (signals ventricular depolarisation)
what causes the AV valves to shut?
when the ventricular pressure exceeds atrial pressure
what causes the first heart sounds?
AV valve shutting
describe iso-volumetric contraction after AV valve shutting?
- sine AV valve is shut
- no blood can enter or leave the ventricle
- tension rises around a closed volume
- causing ventricular pressure to rise steeply
when does the aortic/pulmonary valve open causing ventricular ejection?
when ventricular pressure exceeds aorta/pulmonary artery pressure
what does the T wave on the ECG signal?
ventricular re-polarisation
what happens to the ventricles after the T wave?
ventricles relax & pressure starts to fall
what happens to the aortic/pulmonary valves when the ventricular pressure falls below aortic/pulmonary pressure?
the SL valves shut
what produces the second heart sound (DUB)?
closure of SL valves after ventricular ejection
what does the valve vibration produce in aortic pressure curve?
dicrotic notch
what does closure of SL valves signal the start of?
iso-volumetric ventricular relaxation
what happens to the AV valves during iso-volumetric ventricular relaxation?
AV valves are shut, causing tension to fall around a closed volume
when do the AV valves re-open?
when ventricular pressure falls below atrial pressure
what does the first heart sound signal the beginning of?
systole
what does the second heart sound signal the beginning of?
diastole
what is blood pressure?
the outwards pressure exerted by blood on blood vessel walls
what is systolic BP?
what is a normal systolic BP?
= pressure exerted by blood on walls of aorta & systemic arteries when heart contracts
= < 140mmHg
what is diastolic BP?
what is a normal diastolic BP?
= pressure exerted by blood on walls of aorta & systemic arteries when heart relaxes
= < 90mmHg
what is hypertension?
= high blood pressure
= 140/90mmHg or higher
= daytime average 135/85mmHg
what is pulse pressure?
what is the pulse pressure normally?
= difference between systolic & diastolic bp
= normally 30-50mmHg
how would you describe the flow of blood in normal arteries?
laminar
is laminar flow audible through. a stethoscope?
no
if external pressure is applied, what would you hear if the pressure;
1) exceeds the systolic BP
2) is kept between the systolic & diastolic
1) exceeds systolic
= artery is blocked
= no sound is head
2) kept between
= turbulent airflow
= audible
when is the first sound heard?
= peak systolic pressure
what are the intermittent sounds due to?
due to turbulent spurts of flow cyclically exceeding cuff pressure
when is the last sound heard?
at minimum diastolic pressure
why is no sound heard thereafter?
due to un-interupted smooth, laminar flow
what is the mean arterial blood pressure (MAP)?
average arterial blood pressure during a single cardiac cycle (involving contraction relaxation)
which is longer - systolic or diastolic?
diastolic (relaxation) is TWICE AS LONG as the systolic (contraction)
what 2 ways can you calculate MAP?
1) MAP = [(2 x diastolic) + systolic] / 3
2) MAP = diastolic + 1/3rd pulse pressure
what is normal MAP?
70-105mmHg
= 60mmHg is needed to perfuse vital organs
why does MAP need to be regulated within narrow ranges? (2)
1) to ensure pressure is high enough to perfuse vital organs
2) to ensure pressure is not too high to damage blood vessels or place stain on heart
how do you calculate cardiac output?
CO = stroke volume x heart rate
what is the difference between stroke volume & cardiac output?
Stroke volume
= volume of blood pumped by each ventricle PER BEAT
Cardiac output
= volume of blood pumped by each ventricle PER MINUTE
what is systemic vascular resistance?
sum of resistance of all vasculature in systemic circulation
what is another way of calculating MAP?
MAP = cardiac output x systemic vascular resistance
what is the main resistant vessel?
arterioles
what function do baroreceptors have in regulating mean arterial blood pressure?
they are PRESSURE SENSORS
where is the control centre to regulated mean arterial blood pressure?
medulla
name 2 areas which can act as effectors?
1) heart
= heart rate & stroke volume
2) blood vessels
= systemic vascular resistance
are baroreceptors act short term or long term the regulating MAP?
SHORT term
what happens when a person suddenly stands up from lying position?
1) venous return heart decreases
2) MAP decreases
3) reduces rate of firing from baroreceptors
4) vagal tone to heart decreases & sympathetic tone increases
= increasing HR & SV
5) sympathetic constrictor tone increases
= increasing SVR
6) sympathetic constrictor tone to veins increases venous return to heart
7) rapid correction of transient fall in MAP
what is postural hypotension?
results from failure of baroreceptors to respond to gravitational shifts in blood when moving from horizontal to vertical
risk factors fo getting postural hypotension?
1) age
2) medications
3) certain diseases
4) reduced intravascular volume
5) prolonged bed rest
when is a positive result of postural hypotension indicted?
when there is a drop, within 3minutes of standing from lying in;
1) systolic BP of 20mmHg (with or without symptoms)
2) diastolic BP of 10mmHg (with symptoms)
what are symptoms of postural hypotension?
= cerebral hypo-perfusion;
- dizziness
- blurred vision
- faitness
- falls
- light headedness
how can blood volume & MAP be controlled?
by controlling extracellular fluid volume
what does total body fluid consist of?
= intracellular fluid (2/3rd)
= extracellular fluid (1/3rd)
what does extracellular fluid volume (ECFV) consist of?
= plasma volume + interstitial fluid volume
what is interstitial fluid volume?
fluid that bathes the cell & acts as the go between the blood & body cells
what happens if plasma volume falls?
= compensatory mechanisms shift fluid from interstitial compartment to plasma compartment
what 2 factors affect extracellular fluid volume?
1) water excess or deficit
2) Na+ excess or deficit
what are hormones role in regulating extracellular fluid volume?
regulates water & salt balance
what 3 hormones regulate extracellular fluid volume?
1) renin angiotensin aldosterone system (RAAS)
2) natriuretic peptides (NPs)
3) anti-diuretic hormone (arginine vasopressin) - ADH
what is the role of RAAS?
= regulates plasma volume and SVR and hence regulates MAP
what are the 3 components of RAAS?
1) renin
2) angiotensin
3) aldosterone
where is renin released?
from the kidneys
what does release of renin stimulate?
formation of angiotensin I in the blood from angiotensinogen
where is angiotensinogen produced?
by the liver
what converts angiotensin I into angiotensin II?
angiotensin converting enzyme (ACE)
what produces ACE?
pulmonary vascular endothelium
what are 4 things angiotensin II stimulates?
1) release of aldosterone from adrenal cortex
2) systemic vasoconstriction
3) increases SVR
4) stimulates thirst & ADH release (increasing plasma volume)
what is aldosterone and what does it do?
= a steroid hormone
= acting on the kidneys to increase Na and water retention
= increasing plasma volume
what is the rate limiting step for RAAS?
rening secretion
what is RAAS regulated by?
mechanisms which stimulate renin release from juxtaglomerular apparatus in the kidneys
what are 3 mechanisms which stimulate renin release from juxtaglomerular apparatus inn the kidneys?
1) renal artery hypotension (caused by systemic hypotension = decreased BP)
2) stimulation of renal sympathetic nerves
3) decreased Na+ in renal tubular fluid, sensed by macula dense
what are natriuretic peptides?
= peptide hormone
what synthesises NPs?
= heart (also Brian & other organs)
what stimulates the release of NPs?
released in response to cardiac distension or neurohormonal stimuli
what do NPs cause? (4)
1) excretion of salt & water in kidneys
2) decreases renin release
3) vasodilation
4) counter-regulatory system for RAAS
what are the 2 types of NPs released by the heart?
1) atrial natriuretic peptide (ANP)
2) Brian-type natriuretic peptide (BNP)
describe ANP - its components, location & course of action?
Components;
= 28 amino acid peptide
Location
= synthesised & store day atrial muscle cells (atrial myocytes)
Course of action
= released in response to atria distension
describe BNP - its components & where it is synthesised?
Components;
- 32 amino acid peptide
Synthesised
= produced in heart, ventricles, brain & other organs
describe the production of BNP?
1) first as prepro-BNP
2) cleaved to pro-BNP
3) finally as BNP
what is the N-temrinal piece of pro-BNP called?
NT pro BNP
what 2 things can be measured in patients with suspected heart failure?
1) serum BNP
2) NT - pro BNP
what is another name for anti-diuretic hormones (ADH)?
vasopressin
what is ADH & how is it made?
= peptide hormone
= derived from pre-hormone precursor
= synthesised in the hypothalamus
where is ADH stored?
posterior pituitary
what 2 things stimulate section of ADH?
1) reduced extra-cellular fluid volume
2) increased extra-cellular fluid osmolality
what does plasma osmolality indicate?
relative solute-water balance
what is ADH release stimulated by?
increased plasma osmolality
where does ADH act & how?
= acts in kidney tubules to increase re-absorption of water
what would the absorption of water cause?
increase extracellular & plasma volume & hence cardiac output & blood pressure
how does ADH act on blood vessels?
causes vasoconstriction
= increasing SVR & BP
when does vasoconstriction effect on ADH become important?
in hypovolaemic shock (e.g. haemorrhage)
RECAP QUESTIONS
True/false
Higher the blood pressure, the greater the firing of baroreceptors?
true
which CN do the carotid baroreceptors fire through?
CN IX
which CN do the aortic baroreceptors fire through?
CN X
what are the 4 blood vessel components of the CV system?
1) arteries
2) arterioles
3) capillaries
4) veins
in what direction do arteries carry the blood?
carry blood from heart to tissues
what are the capillaries the main site for?
site for gas, nutrient & water exchange between blood & tissue
which blood vessel holds the most amount of blood volume at rest?
veins
why are veins known as the capacitance vessels?
as they contain the most blood volume during rest
in what direction do veins carry the blood?
carry blood from tissues to the heart
what is the main regulator or Heart rate?
autonomic nervous system
what 3 things regulate stroke volume?
1) pre-load
2) myocardial contractility
3) after-load
what is systemic vascular resistance regulated by?
vascular smooth muscles
what consequence does contraction and relaxation of vascular smooth muscles have on SVR and MAP?
Contraction
= increases systemic vascular resistance and increases MAP
Relaxation
= decreases Systemic vascular resistance & decreases MAP
what is resistance to blood flow directly proportional to? (2)
1) blood viscosity (thickness)
2) length of blood vessels
what is resistance to blood flow inversely proportional to? (1)
[radius of blood vessel] ^ 4
how is resistance to blood flow mainly controlled?
through changes in radius of arterioles (vessels)
what 2 things are involved in the extrinsic control of vascular smooth muscle cells?
1) nerves
2) hormonal
what nerve fibres supply vascular smooth muscle cells? and as a result what neurotransmitter is involved and what does this neurotransmitter act on?
supplied by the sympathetic division
Neurotransmitter;
= noradrenaline
= acting on Alpha receptors
what is meant by VASOMOTOR TONE?
= vascular smooth muscles are partially constricted at rest
what causes vasomotor tone?
= by the tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline
what effect will increased and decreased sympathetic discharge have on vasomotor tone?
INCREASED sympathetic discharge;
= will INCREASE VASOMOTOR TONE
= resulting in vasoconstriction
DECREASED sympathetic discharge;
= will DECREASE VASOMOTOR TONE
= resulting in vasodilation
True/false
There is NO parasympathetic innervation of arterial smooth muscles.
False.
- as there is in the penis & clitoris
adrenaline acting on the alpha receptors causes what?
vasoconstriction
adrenaline acting on the beta2 receptors causes what?
vasodilation
where do Alpha receptors predominate?
in skin, gut and kidney arterioles
where are beta2 receptors predominant?
in cardiac & skeletal muscle arterioles
what does the location of the alpha and Beta receptors help with?
strategic redistribution of blood (e.g. during exercise)
what is the effect of angiotensin II on vascular smooth muscle?
vasoconstriction
what other hormone causes vasoconstriction?
anti-diuretic hormone
hormones angiotensin II and anti-diuretic hormone, when are they important in the control of blood pressure?
in the intermediate control of BP
what function do intrinsic controls have on vascular snit muscles?
they match blood flow of different tissues to their metabolic needs
Yes/No
Can intrinsic controls override extrinsic control when controlling vascular smooth muscles?
Yes - intrinsic controls can override extrinsic control.
what word describes vasodilation in metabolic terms?
Metabolic Hyperaemia
what does the local PO2 and PCO2 need to be to cause vasodilation in arteriole smooth muscles?
Vasodilation caused by
= decrease local PO2
= increase local PCO2
what does the local [H+] and extra-cellular K+ need to be to cause vasodilation in arteriole smooth muscles?
Vasodilation caused by
= increase local [H+]
= increased extra-cellular K+
what does the osmolality of ECF and adenosine release need to be to cause vasodilation in arteriole smooth muscles?
Vasodilation caused by
= increases osmolality of ECF
= adenosine release (from ATP)
when might local humeral agents be released?
in response to tissue injury or inflammation
name 3 examples of humoral agents which cause vasodilation of arteriolar smooth muscle.
1) histamine
2) bradykinin
3) nitric oxide
where is nitric oxide continuously produced by and from what?
Produced by = vascular endothelium
= from the amino acid L-arginine
what enzyme allows continuous productions of nitric oxide?
nitric oxide synthase (NOS)
what is nitric oxide important in the regulation and maintenance of?
regulation of blood flow & maintenance of vascular health
what effect does shear stress on vascular endothelium have on nitric oxide production?
- shear stress on vascular endothelium
- causes release of calcium in vascular endothelial cells
- subsequent activation of NOS
True/False
Chemical stimuli can also induce NO formation?
True
= it is receptor stimulated formation
where does nitric oxide diffuse from and into?
Once it has diffused into its target, what does it do?
from = vascular endothelium into = adjacent smooth muscle cell
Where it activates formation of cGMP that acts as a second messenger for signalling smooth muscle relaxation.
name 3 examples of humoral agents that cause vasoconstriction of arteriolar smooth muscle.
1) serotonin
2) thromboxane A2
3) leukotrienes
4) endothelin
what can cause endothelial damage/dysfunction?
1) high blood pressure
2) high cholesterol
3) diabetes
4) smoking
what effect do endothelial produced vasodilators have on thrombosis, inflammation and oxidants?
Vasodilators Anti; = thrombosis = inflammatory = oxidants
what effect do endothelial produced vasoconstrictors have on thrombosis, inflammation and oxidants?
Vasoconstrictors: Pro; = thrombosis = inflammation = oxidants
what temperature cause vasodilation and what temperature causes vasoconstriction?
Vasodilation = warmth
Vasoconstriction = cold
describe myogenic response to stretch?
- if MAP rises, resistance vessels constrict to limit flow
- if MAP falls, resistant vessels dilate to increase flow
= important in brain & kidneys
describe the frank-starling curve, specifically the effect of end diastolic volume and stroke volume.
as you increase end diastolic volume, stroke volume also increases until maximal force is generated at optimum fibre length.
what 4 factors increases venous return to the heart?
1) increase veno-motor tone
2) increased blood volume
3) increased skeletal muscle pump
4) increased respiratory pump
what effect does an increased venous return have on atrial pressure, EDV and stroke volume?
increases;
- atrial pressure
- EDV
- stroke volume
what is venomotor tone?
the degree of tension in the muscle coat of a vein that determines the shape of the vein
what nerve fibre supplies venous smooth muscles?
sympathetic nerve fibres
what does stimulation of these nerve fibres cause venous smooth muscles to do?
causes the venous smooth muscles to constrict
what effect does increased venomotor tone have on venous return, SV and MAP?
Increased venomotor tone…
Increases venous return, SV & MAP
describe what happens to the intra-thoracic pressure, intra-abdominnal pressure and thus pressure gradient for venous return during INSPIRATION.
Doing inspiration
- intra-thoracic pressure decreases
- intra-abdominal pressure increases
= increasing pressure gradient for venous return creating a suction effect that moves blood from veins towards heart
what does the increased pressure gradient for venous return do to depth & rate of breathing?
increases rate and depth of breathing
Where do the large veins in limbs lie between?
lie between skeletal muscles
what does contraction of these muscles aid?
aids venous return
what is present in the heart to ensure one-way flow of blood?
valves
During exercise, what does sympathetic stimulation do to Heart rate, stroke volume and CO?
increases all of them
how does the blood flow change to kidney and gut during exercise after the sympathetic vasomotor stimulation?
REDUCES blood flow to kidneys & gut due to vasoconstriction
How does blood flow change in skeletal and cardiac muscles during exercise?
increases due to vasodilation
what causes vasodilation in skeletal and cardiac muscles during exercise? (i.e. what over-rides sympathetic effects)
metabolic hyperaemia
what effect does this have on blood pressure?
- increases systolic BP (due to increased CO)
- decreases diastolic BP (due to metabolic hyperaemia decreasing SVR)
= pulse pressure increases
how does sympathetic stimulation increase heart rate?
- in relation to SA node & AV node delay..
increases heart rate by increasing firing rate of SA node and decreases AV node delay
what does regular aerobic exercise do to blood pressure?
helps reduce blood pressure
name chronic cardiovascular responses to regulate exercise..
1) reduction in sympathetic tone & noradrenaline levels
2) increased parasympathetic tone to heart
3) cardiac remodelling
4) reduction in plasma renin levels
5) improved endothelial function, increased vasodilators, decreased vasoconstrictors
6) decreased arterial stiffening
