Cardiac circulation control Flashcards
What is a cardiac reflex
◦ “Reflex loops between the heart and central nervous system” which regulate heart rate and peripheral vascular resistance to maintain physiologic homeostasis
List the cardiac reflexes
4B’s 2C’s and a ROD
Bainbridge
Baroreceptor
Bezold Jarish
Barcroft Edholm
Chemoreceptor
Cushing
Respiratory sinus arrhythmia
Oculocardiac
Diving
What is the most important cardiac reflex
Baroreceptor
What are the 5 domains you need to consider for every reflex and every endocrine system
Sensor
Afferent
Processor
Efferent
Effector
Barorecepotr reflex
◦ Sensors: mechanoreceptors detect pressure (carotid sinus and aortic arch)
◦ Afferent: vagus and glossopharyngeal nerves
◦ Processor: nucleus of the solitary tract and nucleus ambiguus (vasomotor centre)in medulla oblongata
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: increased HR and BP (via SVR + increased stroke volume/cardiac output) in response to a fall in BP
Bainbridge reflex
◦ Afferent: vagus (atrial stretch) - increase in central venous pressure triggers low pressure mechanoreceptors in great veins and RA
◦ Processor: nucleus of the solitary tract and the caudal ventral medulla
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: increased RA pressure produces an increased heart rate;
Chemoreceptor reflex
◦ Afferent: carotid / aortic chemoreceptors (low PaO2 and/or high PaCO2) - in the context o response to MAP this will only occur under extreme hypotension
◦ Processor: nucleus of the solitary tract and nucleus ambiguus
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: bradycardia and hypertension in response to hypoxia
‣ (also secondary tachycardia from Bainbridge and Hering-Breuer reflexes)
Cushings reflex
◦ Afferent: mechanosensors in the rostral medulla?
◦ Processor: rostral ventrolateral medulla
◦ Efferent: sympathetic fibres to the heart and peripheral smooth muscle
◦ Effect: hypertension and baroreflex-mediated bradycardia
Bezold Jarish reflex
◦ Afferent: vagus (mechanical/chemical sttimuli to the cardiac chambers - ventricular) C fibres
◦ Processor: nucleus of the solitary tract
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: hypotension, coronary artery dilation and bradycardia
Oculocardiac reflex
◦ Afferent: trigeminal nerve (pressure to the globe of the eye)
◦ Processor: sensory nucleus of CN V; nucleus of the solitary tract
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: vagal bradycardia, systemic vasoconstriction, cerebral vasodilation
Diving reflex
◦ Afferent: trigeminal nerve (cold temperature; pressure of immersion)
‣ Processor: sensory nucleus of CN V; nucleus of the solitary tract
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: vagal bradycardia, systemic vasoconstriction, cerebral vasodilation
Barcroft Edholm reflex
◦ Afferent: emotional distress, hypovolaemia
◦ Processor: unknown
◦ Efferent: vagus nerve and sympathetic chain
◦ Effect: bradycardia, systemic vasodilation, hypotension
Respiratory sinus arrhtyhmia
◦ Afferent: central respiratory pacemaker
◦ Processor: nucleus ambiguus
◦ Efferent: vagus nerve, via the cardiac ganglion
◦ Effect: cyclical increase of heart rate during inspiration
What type of receptor is a baroreceptor? How are they activated?
- Baroreceptors are mechanoreceptors which respond to stretch stimuli.
- This strecth deforms mechanically sensitive sodium channels (DEG/ENaC, degenerin/epithelial sodium channels)
- With sufficient stimulus, sodium current increases to the point where the membrane potential reaches the threshold of local voltage-gated sodium channels, and generates a propagating action potential
Where are baroreceptors located
- Arterial baroreceptors (“high pressure baroreceptors”) are located at the junction of the intima and media of the aortic arch and carotid sinuses
◦ stretch sensitive mechanoreceptors
◦ Carotid sinus - small neurovascular structure in the adventitia in the dilated portion of the common carotid artery (carotid bulb) at its bifurcation. Not to be confused with the carotid body which is a PaO2/PaCO2 sesning chemoreceptor at the same location at the bifurcation of the vessels
◦ sinus senses stretch, and body senses breathing
◦ Aortic arch - medio-adventitial junction mainly confined to a saddle shaped area between the brchiocephalic trunk and the origin of the left subclavian
What layer of the vessel are baroreceptors in
- Arterial baroreceptors (“high pressure baroreceptors”) are located at the junction of the intima and media of the aortic arch and carotid sinuses
◦ stretch sensitive mechanoreceptors
◦ Carotid sinus - small neurovascular structure in the adventitia in the dilated portion of the common carotid artery (carotid bulb) at its bifurcation. Not to be confused with the carotid body which is a PaO2/PaCO2 sesning chemoreceptor at the same location at the bifurcation of the vessels
◦ sinus senses stretch, and body senses breathing
◦ Aortic arch - medio-adventitial junction mainly confined to a saddle shaped area between the brchiocephalic trunk and the origin of the left subclavian
Where is the carotid baroreceptor
- Arterial baroreceptors (“high pressure baroreceptors”) are located at the junction of the intima and media of the aortic arch and carotid sinuses
◦ stretch sensitive mechanoreceptors
◦ Carotid sinus - small neurovascular structure in the adventitia in the dilated portion of the common carotid artery (carotid bulb) at its bifurcation. Not to be confused with the carotid body which is a PaO2/PaCO2 sesning chemoreceptor at the same location at the bifurcation of the vessels
◦ sinus senses stretch, and body senses breathing
◦ Aortic arch - medio-adventitial junction mainly confined to a saddle shaped area between the brchiocephalic trunk and the origin of the left subclavian
Where is aortic baroreceptor
- Arterial baroreceptors (“high pressure baroreceptors”) are located at the junction of the intima and media of the aortic arch and carotid sinuses
◦ stretch sensitive mechanoreceptors
◦ Carotid sinus - small neurovascular structure in the adventitia in the dilated portion of the common carotid artery (carotid bulb) at its bifurcation. Not to be confused with the carotid body which is a PaO2/PaCO2 sesning chemoreceptor at the same location at the bifurcation of the vessels
◦ sinus senses stretch, and body senses breathing
◦ Aortic arch - medio-adventitial junction mainly confined to a saddle shaped area between the brchiocephalic trunk and the origin of the left subclavian
How does the baroreceptor receptor respond to changes in BP –> how does it convey the change to the controller
- Increased blood pressure (increased stretch, increased receptor firing rate)
- Decreased blood pressure (decreased receptor firing rate)
How does the carotid baroreceptor get to the central controller
- From the carotid sinus: carotid sinus nerve, a branch of the glossopharyngeal nerve - courses anteromedially to the internal carotid artery and joins the body of the glosspharngeal nerve at the base of the skull where its cell bodies lie in the petrosal ganglion
◦ Carotid sinus receptors are innervated by the sinus nerve of Hering, which is a branch of the glossopharyngeal nerve
How does the aortic baroreceptor get back to the central controller
- From the aortic arch: aortic nerve, a branch of the vagus nerve - cell bodies also in the petrosal ganglion which is in the jugular foramen where the nerves then synapse with NTS
- Both of these nerves travel through the jugular foramen to enter the medulla
◦ Both myelinated (A) and unmyelinated (C) fibres - fast response and baseline slower regulation
What is the processor of the baroreflex?
Nucleus of the solitary tract
* Sensory interneurons in the posteiror medulla (caudal ventrolateral medulla)
* Roles
◦ ANS
◦ Taste information - mediating cough and gag
◦ Middle ear - tympanic branch of CN9
What does the NTS do?
Nucleus of the solitary tract
* Sensory interneurons in the posteiror medulla (caudal ventrolateral medulla)
* Roles
◦ ANS
◦ Taste information - mediating cough and gag
◦ Middle ear - tympanic branch of CN9
What connections does the NTS have?
◦ Excitatory glutamate-mediated neurotransmission to the nucleus ambiguus translates the afferent signal into increased vagal activity
◦ GABA-ergic inhibitory neurons of the caudal ventral medulla translate the afferent signal into the inhibition of the rostral ventrolateral medulla (vasomotor centre - constant tonic output), which coordinates sympathetic tone
◦ Effrent fibres to the hypothalamus help coordinate the humoural response to changes in blood pressure.
Where is the PSNS 1st order neurons coming from?
◦ Excitatory glutamate-mediated neurotransmission to the nucleus ambiguus translates the afferent signal into increased vagal activity
◦ GABA-ergic inhibitory neurons of the caudal ventral medulla translate the afferent signal into the inhibition of the rostral ventrolateral medulla (vasomotor centre - constant tonic output), which coordinates sympathetic tone
◦ Effrent fibres to the hypothalamus help coordinate the humoural response to changes in blood pressure.
Where is the SNS first order neurons coming from?
◦ Excitatory glutamate-mediated neurotransmission to the nucleus ambiguus translates the afferent signal into increased vagal activity
◦ GABA-ergic inhibitory neurons of the caudal ventral medulla translate the afferent signal into the inhibition of the rostral ventrolateral medulla (vasomotor centre - constant tonic output), which coordinates sympathetic tone
◦ Effrent fibres to the hypothalamus help coordinate the humoural response to changes in blood pressure.
What are the efferent nerves to the heart? What supplies the SA node? What supplies the AV node
- Sympathetic fibres to the heart and peripheral resistance vessels
- Vagal efferents to the cardiac ganglion (heart rate)
Effector: Myocardium, SA and AV nodes, vascular smooth muscle - The right vagus does the SA node and the left vagus does the AV node, with enough overlap that the loss of a vagus does not produce total parasympathetic denervation. PSNS more important in HR control
Describe how circulating volume changes SV, CO and HR using a graph
In response to arterial hypotension:
◦ Decreased receptor discharge rate
◦ Thus, decreased vagal and disinhibited sympathetic efferents
◦ Thus, systemic vasoconstriction and tachycardia
* In response to arterial hypertension:
◦ Increased receptor discharge rate
◦ Thus, increased vagal and inhibited sympathetic efferents
◦ Thus, systemic vasodilation and bradycardia
How long does a baroreceptor response take?
0.5 - 1 seconds
What is the first and fastest response of the baroreceptor reflex
Increased or decreased HR due to PSNS or vagal supply - rapid effect of vagal on HR is through inward rectifying potassium channels
cAMP system is slower
When is the baroreceptor response active?
Constantly, constant tonic activty
Immediate and proportionate response to changes
What is the minimum value for change for baroreceptor firing change
Depends on the baseline state - more sensitive at the higher and lower range of pressures and depends on abruptness of change
Which baroreceptor is more sensitive to hypotension?
Carotid
Which baroreceptor is more sensitive to hypertension
Aortic
How is firing of baroreceptors related to change in pressure?
Generally proportional within the normal ranges however has hysteresis
- Assymmetry: the firing rate has a hysteresis, i.e. it increases exponentially with increasing carotid sinus pressure, but also plateaus at very high pressures. the steepest part of the response seems to be around the normal systolic pressure range, i.e. 100-140 mmHg.
Describe how mechanosensors sense stretch
- Stretch activates sodium current which then reaches membrane potential threshold for voltage gated channels –> action potential
◦ The more stretch the more frequently the receptors fire
What is a stronger stimulus - Bainbridge or baroreflex
Baroreflex
Bainbridge reflex
- Stimulus - pressure/stretch (increased CVP) - sensitive to a volume change of 5-10% in either direction
- Sensors - stretch sensitive low pressure mechanoreceptors in atria, great veins and pulmonary arteries (type B receptors)
◦ Type A receptors - activated by changes in atrial wall tension during systole
◦ Type B - diastolic low pressure receptors - Afferent: vagus triggers low pressure mechanoreceptors in great veins and RA
- Processor: nucleus of the solitary tract and the caudal ventral medulla
- Efferent: vagus nerve (cardiac ganglion) and sympathetic chain
- Effect: increased RA pressure produces an increased heart rate;
What happens with increased RA pressure as an isolated phenomena
INcreased Bainbridge reflex firing –> tachycardia
What are the two mechanoreceptor subtypes in the Bainbridge reflex
- Stimulus - pressure/stretch (increased CVP) - sensitive to a volume change of 5-10% in either direction
- Sensors - stretch sensitive low pressure mechanoreceptors in atria, great veins and pulmonary arteries (type B receptors)
◦ Type A receptors - activated by changes in atrial wall tension during systole
◦ Type B - diastolic low pressure receptors - Afferent: vagus triggers low pressure mechanoreceptors in great veins and RA
- Processor: nucleus of the solitary tract and the caudal ventral medulla
- Efferent: vagus nerve (cardiac ganglion) and sympathetic chain
- Effect: increased RA pressure produces an increased heart rate;
How is the chemoreceptor involved in BP control?
- Regional hypoxia is one of the metabolic stimuli for local vasodilation - systemic hypoxia causes systemic peripheral vasoconstriction
- Afferent: carotid body glomus (Glossopharyngeal) / aortic body glomus (aortic tract of vagus) chemoreceptors (low PaO2 and/or high PaCO2) - in the context o response to MAP this will only occur under extreme hypotension
- Processor: nucleus of the solitary tract and nucleus ambiguus
- Efferent: vagus nerve and sympathetic chain
◦ To the SA node, AV node and vascular smooth muscle
What is the effector response to chemoreceptor triggering cardiovascularly
- Effect:
◦ Primary effects
‣ Vagal - bradycardia
‣ Symapthetic effects - hypertension (tachycardia often absent)
◦ Secondary effects
‣ Increased preload due to increased ventilation –> Bainbridge reflex increasing HR
‣ Activation of pulmonary stretch receptors and thus activation of the Hering Breuer reflex increasing HR
‣ Due to significant hypertension tachycardia is often not marked due Baroreceptors
Where is the receptor for the cushings reflex
mechanosensors in the rostral medulla?/cerebral meduallary vasomotor centre ischameia
Cushings relfex
- Stimulus - ICP or cerebral ischaemia
- Sensors - mechanosensors in the rostral medulla?/cerebral meduallary vasomotor centre ischameia
- Afferent nerves - fibres from the medullary mechanosensitive areas to sympathetic ganglia, descending inhibitory control from cerebral hemispheres to medullary vasomotor centre
- Processor: rostral ventrolateral medulla
- Efferent: sympathetic fibres to the heart and peripheral smooth muscle
- Effect: hypertension and tachycardia –> baroreflex-mediated bradycardia
Where is the vasomotor centre
Rostral ventrolateral medulla
Bezold Jarish reflex is triggered by
vagus (mechanical/chemical sttimuli to the cardiac chambers - ventricular) C fibres
◦ Responds to ventricular or atrial stretch; as well as chemical ATP/capsacin/snake venoms
◦ Loss of stretch decreases firing rat eof C fibre mediated vagal afferent limb, and increased stretch stimulates the reflex
What processes the Bezold Jarish reflex? What does it result in?
- Processor: nucleus of the solitary tract
- Efferent: vagus nerve and sympathetic chain
- Effect: hypotension, coronary artery dilation and bradycardia
- Its physiological role is implicated in haemorrhage or profound hypovolaemia where the vasoconstriction is greater than would purely be seen from barorecepetors and is thought to be due to decreased reflex
Oculocardiac reflex triggered by?
- Stimulus - pressure to the globe of the eye or traction on eye muscles
- Sensor - mechanosensitive stretch receptors in the facial muscles, especially periorbital muscles, and in the globe of the eye
What does oculocardiac reflex result in?
- Afferent: trigeminal nerve - long and short ciliary nerves
- Processor: sensory nucleus of CN V; nucleus of the solitary tract
- Efferent: vagus nerve and sympathetic chain
- Effect: vagal bradycardia, systemic vasoconstriction, cerebral vasodilation
Diving reflex triggered by?
- Stimulus: trigeminal nerve sensory distribution
◦ Pressure to the globe of the eye, or traction on the eye muscles
◦ Pain in the trigeminal nerve distribution
◦ Temperature (cold)
◦ Chemical stimulus of the anterior ethmoidal nerve (noxious) - Sensors: Pain, temperature, chemical and mechanosensitive stretch receptors in the trigeminal nerve distribution
What is the processor fo the diving reflex?
- Processor:
◦ Nucleus of the solitary tract: vagal response
◦ Rostral medulla: sympathetic response
◦ Ventral medulla: apnoea
What is the effect of the diving reflex
- Effects:
◦ Vagal: bradycardia
◦ Sympathetic: cerebral vasodilation, systemic vasoconstriction
◦ Respiratory: apnoea
◦ The net effect is to prevent aspiration and to maximise the blood flow to the central nervous system at the expense of the skin, muscle and splanchnic organs.
What is the vasovagal reflex called
Barcroft Edholm
Why is the Barcroft Edholm reflex thought to exist?
◦ Clotting hypothesis - protective reflex for slowing of circulation in response to haemorrhage allowing permissive hypotension ti minimise blood loss and maximise clot formation
Neurocardiogenic syncope triggers
◦ For “true” vasovagal syncope:
‣ Emotional distress
‣ Orthostatic changes (decreased preload with changes in posture)
◦ For “situational” neurocardigenic syncope:
‣ Micturition
‣ Increased intrathoracic pressure:
‣ Defaecation
‣ Cough, sneeze, laughter, playing a brass instrument
‣ Following exercise
‣ “Carotid sinus syndrome”
What is the afferent, sensor and processor of the vasovagal response?
ensors: Central (descending) as well as peripheral
◦ Mechanoreceptors located in the wall of the left ventricle, the aorta, atria and the pulmonary trunk
◦ Numerous other strecth receptors, eg. splanchnic, bowel,
* Afferent nerves: Unknown! Presumably, both central nervous system and peripheral sensory nerves are involved
* Processor: Unknown! Presumably at some stage the nucleus of the solitary tract and the nucleus ambiguus are involved.
What is the efferent response to vasovagal (4)
- Efferent nerves:
◦ Vagus nerve, via the cardiac ganglion
◦ Sympathetic nervous system - Effector: SA node, AV node, peripheral smooth muscle
- Effects:
◦ Vagal: bradycardia
◦ Sympathetic: systemic vasodilation (mainly muscles)
◦ Vasovagal syncope is thought to have four distint phases:
‣ phase 1: early stabilization (by normal baroreceptor reflex)
‣ phase 2: circulatory instability (baroreflex vasoconstriction)
‣ phase 3: terminal hypotension (bradycardia, cerebral hypoperfusion, systemic vasodilation)
‣ phase 4: recovery
4 phases of vasovagal syncope
- Efferent nerves:
◦ Vagus nerve, via the cardiac ganglion
◦ Sympathetic nervous system - Effector: SA node, AV node, peripheral smooth muscle
- Effects:
◦ Vagal: bradycardia
◦ Sympathetic: systemic vasodilation (mainly muscles)
◦ Vasovagal syncope is thought to have four distint phases:
‣ phase 1: early stabilization (by normal baroreceptor reflex)
‣ phase 2: circulatory instability (baroreflex vasoconstriction)
‣ phase 3: terminal hypotension (bradycardia, cerebral hypoperfusion, systemic vasodilation)
‣ phase 4: recovery
Respiratory sinus arrhythmia is mediated by? Why does it occur?
the normal variation in HR which occurs cyclically in response to normal respiration
* It is not mediated by the Bainbridge reflex instead it is through interaction between medullary respiratory and cardiac centres
* Its role is to potentially increase pulmonary circulation efficiency during inspiration by maximising blood flow across the exchange surface
Describe the respiratory sinus arrhythmia pathway
- Stimulus: presumably, the Pre-Bötzinger complex (“respiratory pacemaker”)
- Sensors: none (unless you count respiratory control chemoreceptors)
- Afferent: central respiratory pacemaker - Pre Botzinger complex - interneurons between it and the nucleus ambiguus
- Processor: nucleus ambiguus
- Efferent: vagus nerve, via the cardiac ganglion
- Effect: cyclical increase of heart rate during inspiration
What is the vasomotor centre
Medullary centres controling SA node rate and peripehral muscle tone
What afferent supply goes to vasomotor centres
- Afferents include:
◦ carotid sinus and aortic arch baroreceptors
◦ “low pressure” baroreceptors in the atria
◦ Cerebral hemispheres, thalami and hypothalamus
How are pacemaker cells rapidly slowed by the vagus
- Efferents release acetylcholine at the pacemaker cells, which opens a ligand-gated potassium channel and hyperpolarises the pacemaker cells
- These effects are more rapid than those of sympathetic regulation
What is the main parasympathetic structure in the medulla?
◦ Nucleus ambiguues contains preganglionic vagal neurons (PSNS) –> Sends efferent fibres to the cardiac ganglia via the vagus nerve –> Cardiac ganglia are near the SA node, AV node, and in the atria
‣ Release of acetylcholine activates Ik ACh channels (ligand gated pottasium channel - hyperpolarises the membrane through K out of the cell and delays the rate of depolarisation)
◦ Involved in the Baroreflex, Bainbridge reflex, Barccroft-Edholm reflex and vasovagal syncope mechanisms
What is the regulator of the nucleus ambiguues and the rostral ventrolateral medullary SNS group?
NTS
Where does vasomotor SNS output come from?
- Rostral ventrolateral medulla (RVLM)
◦ Glutamate-secreting presympathetic neurons which act as the tonic “pacemarker” of sympathetic cardiovascular control
‣ Tonic activity here dictates baseline vascular smooth muscle tone
‣ RVLM sends descending projections to sympathetic preganglionic neurosn in the thoracic intermediolateral spinal cord
How does 1000ml loss of blood affect the cardiovascular system?
20% circulating volume
Acute –> baroreflex + low pressure volume receptors +/- chemo receptors –> central controller
- Autonomic
1. Decreased vagal
2. Increased sympathetic
Net effect
1. SBP and DBP drop is reduced
2. Tachycardia
3. Reduction in pulse pressure
4. Cardiac output returns to close to normal
- Neurohormonal
1. Renin
2. Vasopressin
3. Catecholamines
4. ANP
Net - reduced urine output and increased Na and water retention
Effect of rate of blood loss
Medium to long term response
How does blood loss trigger a response
- Arterial hypotension causes baroreflex activation + low pressure volume receptors of the right atrium and great veins + if severe (with reduced cardiac output/fall in pH) may also induce chemoreceptor activation peripherally accentuating the response
How does sympathetic system respond to blood loss 6
- Increased PVR
- Redistribution of blood volume away from cutaenous, skin, splanchnic
- Preacpillary vasoconstriction –> autotransferusion
- Venoconstriction mobilising venous capacitance (including liver and lung capacitance vessels)
- Cardiac - tachycardia, increased inotropy and cardiac output
- Stimulation of renin and vasopressin release
What are the 4 main systems that are part of the neurohormonal response to blood loss?
- Renin secretion causes:
◦ Vasoconstriction (by angiotensin)
◦ Increased sodium retention (by aldosterone) leading to increased reabsorption of water
◦ Increased thirst - Vasopressin release causes:
◦ Vasoconstriction (by V1 receptors), augments noradrenaline mediated arteriolar vasoconstriction
◦ Increased water retention (by V2 receptors) - Venous hypotension decreases atrial natriuretic peptide secretion, which causes:
◦ Decreased renal blood flow
◦ Decreased urinary water and sodium excretion - Catecholamines - see above
How does rate of blood loss affect response?
- A more rapid rate of blood loss places increased stress on the cardiovascular system to maintain haemodynamic homeostasis
- Healthy individuals will be better able to compensate for more rapid rates of blood loss by increasing their heart rate and cardiac contractility
- Patients with compromised cardiac function (eg. ischaemic heart disease or heart failure) will have impaired compensatory mechanisms and will not be able to compensate for even relatively slow blood loss
How much does pressure change occur with height in the cardiovascular system
1m difference in height corresponds to 73mmHg difference in pressure
How does posture influence the arterial and veinous tree
Equal pressures exerted, diffferent compliance so has slightly different effects
How does posture influence the arterial tree?
‣ Arterial effects: protected in part by high pressure and muscualraity of the walls, as well as only 15-20%^ of the blood being within the arterial circulation
* Decreased perfusion pressure in superior regions
* Increased perfusion pressure pressure in dependent regions
How much blood is in the arterial circulation at any one time?
15-20%
What % of blood is in the veinous system at any one time?
‣ Venous effects: Thinner more compliant walls, 70% of blood volume
How does posture affect the veinous system
‣ Venous effects: Thinner more compliant walls, 70% of blood volume
* Redistribution of venous blood volume (70% of total) into dependent regions due to high venous capacitance - 10% of BV * Thus, decreased venous return (MSFP is unchanged so the vascular function curve alteration is not exactly as depitcted below)
How is MSFP changed by posture?
It is not
What is a hydrostatic indifference point?
◦ The point inside the static circulatory system where pressure and therefore wall stress remains stable irrespective of the change in position.
‣ Venous
* Potentially a few CM below the diaphragm
* 7+/- 4cm below the 4th intervostal space
‣ Arterial - at the level of the heart
What is the name of the point at which static circulatory pressure is unaltered by position
Hydrostatic indfference point
Where is the venous hydrostatic indifferent point
◦ The point inside the static circulatory system where pressure and therefore wall stress remains stable irrespective of the change in position.
‣ Venous
* Potentially a few CM below the diaphragm
* 7+/- 4cm below the 4th intervostal space
‣ Arterial - at the level of the heart
Where is the arterial hydrostatic indifference point
at the level of the heart
Why is the hydrostatic indiffernt point of value?
It is a point about whihc the baroreceptor position will regulate what blood pressure they detect - so not only does a change in position affect preload it also directly via gravitational potential energy effects wall stretch
Explain the response to standing from a cardiac perspectie
Decreased venous return, increased venous pooling –> decreased cardiac output
Raised hydrostatic indifferent point –> supine to standing lowers the cerebral perfusion pressure by 30mmHg at the carotid and 44mmHg at the midbrain
Baroreceptor reflex activated –> increased HR, delayed increase in peripheral vascular resistance and venous return (muscle contraction of standing does aid somewhat)
Net effects
- Increased BP, increased HR
- Reduced cardiac output and SV
- Reduced cerebral perfusion pressure but stable cerebral perfusion (autoregulation)
Both these factors stimulate the carotid baroreceptors
What is the effect on BP, CO, HR, SVR and cerebral blood flow of supine to seated transition?
- BP increases 0-40%
- Cardiac output reduces by 15%
- HR largely unchanged
- SVR increases by 50-80%
- Cerebral blood flow decreases by 15%
What is the effect on BP, CO, HR, SVR and cerebral blood flow of supine to Trendelenburg
- BP increases 0-40%
- Cardiac output reduces by 15%
- HR largely unchanged
- SVR increases by 50-80%
- Cerebral blood flow decreases by 15%
Trendelenburg - 15-20 degrees head down
* BP increases by 5%
* Cardiac output unchanged
* HR unchanged
* SVR decreases by 5%
* Pulmonary artery wedge pressure increases by 3-4mmHg
* Reduced cerebral perfusion due to poor venous drainage
Transition from supine to Prone causes what changes in the below measures
- BP
- HR,
- Cardiac output
- Stroke volume
- PAWP
Prone positioning - main change comes from compressing abdominal structures because no hydrostatic change but most efforts to prone people try to avoid this
* MAP increased by 3.5%
* Cardiac output decreased by 8.6%
* HR decreased by 10%
* Stroke volume decreased by 8%
* PAWP increased by 3-4mmHg
How does ARDS influence impact of prone positioning
Prone positioning - main change comes from compressing abdominal structures because no hydrostatic change but most efforts to prone people try to avoid this
* MAP increased by 3.5%
* Cardiac output decreased by 8.6%
* HR decreased by 10%
* Stroke volume decreased by 8%
* PAWP increased by 3-4mmHg
In ARDS however prone positoining
* INcreased RV preload if welll filled - if no resistance to venous return from IVC compression
◦ Decreased RV preload due to abdominal compression
* RV afterload
◦ Increased due to high pressure ventilation
◦ Improved if prone positioning improves pulmonary compliance with better recruitment, decreased pulmonary vascular resistance as well as improving oxygenation and ventilation which improves it further
* Increased SVR over time
* Increased or stable cardiac output if
◦ RV afterload was the rate limiting step and is releived
◦ Abdominal organs are compressed improving venous return without increasing venous resistance
* Decreased total cardiac output if:
◦ The RV ends up having no added afterload reduction (i.e. prone position did not have any of it desired effects on oxygenation and lung recruitment)
◦ The abdominal contents is compressed to the point where there is increased resistance to venous return from the lower body
◦ The RV pressures increase due to increased preload and afterload to the point where interventricular interdependence affects left ventricular diastolic filling
Using a cardiac function curve illustrate the impact of exercise
Exercise cardiovascular response consists of 4 main domains
- Local muscle tissue vasodilation
- Increased cardiac output
- Central control
- Haemodynamic variables
How does exercise impact regional muscle blood flow? How?
- This increased demand is met by increasing blood flow to exercising muscle
◦ Increased from 1-4ml/100g/min to 400ml/100g/min - The increase in blood flow is mediated mainly by a regional decrease in vascular resistance
◦ It is accompanied by increasing coronary blood flow, decreasing visceral blood flow and increasing skin blood flow (temperature control) - The mechanisms for this vasodilation are:
◦ Vasoactive substrates, hypoxia and products of muscle metabolism,
‣ eg. CO2, lactate, hydrogen peroxide and potassium ions
‣ Regional decrease in pH produces vasodilation independent of CO2 and lactate
◦ Vasoactive mediators released by the endothelium,
‣ eg. nitric oxide (NO), ATP, adenosine, prostaglandins and endothelium derived hyperpolarisation factors (EDHPF)
◦ β-2 adrenoceptor activation - systemic adrenaline release increases muscle blood flow and increases cardiac output
◦ There is also corresponding vasoconstriction of other vascular beds, redirecting blood flow away from viscera and skin
Cardiac output in exercise can reach?
30L/min
How is cardiac output increased in exercise
Increased HR and increased stroke volume
Increased workload
When in exercise is the peak response of stroke volume?
At 50% maximal workload
After this HR causes too much reduction in diastole and SV declines
What happens to CVP and PCWP during exercise
Increase
How does SBP change in exercise
Increased
How does MAP change in exercise
Increased
◦ Increase in cardiac output greater than the decrease in PVR so MAP rises slightly
How does pulse pressure change with exercise?
- Diastolic blood pressure decreases - despite tachyardia due to drop in PVR
- The pulse pressure widens
How is exercise cardiac output requirements fed back to the body?
◦ Increased muscle activity is sensed by stretch receptors and chemoreceptors in the muscle tissue
◦ Decreased peripheral vascular resistance, translating into decreased blood pressure, is sensed by the baroreflex
◦ The central nervous system itself can generate the afferent signals for exercise-related cardiovascular responses in anticipation of effort
What is a valsalva manouvre?
Expiratory effort against an obstructed airway e.g. closed glottis
What sort of pressure do you achieve with Valsalva manouvre?
+40mmHg
How long does a Valsalva manouvre go on for?
15-20 seconds
How many phases are there to a Valsalva manouvre?
4
Describe phase 1 of Valsalva manoeuvre
- Increased intrathoracic pressure due to voluntary breath hold against closed glottis
- Reduced venous return
- Decreased LV afterload with temporarily increased LV preload leading to increase in cardiac output and BP due to increased SV
- Reflexive decrease in HR immediately
Describe early phase 2 of the Valsalva manouvre? and late phase2
- Decreased venous return to the LV due to decreased RV output –> decreased cardiac output and decreased pulse pressure with reduced SV
- Increasing HR baroreflex mediated
- The baroreflex vasoconstriction to bring BP back up is slightly slower and so there is a little lag and dip in BP
Late phase 2
- Restored cardiac output (increased HR compensating for drop in SV)
- Resotred BP due to sympathetic increase in SVR
Phase 3 of the valsalva manouvre
- Release of breath hold –> drop in intrathoracic pressure and increased venous return to the RH
- Increase in LV afterload, interventricular independence, and reduction in venous return further to the LV with reducing intrathoracic pressure –> BP drops, and HR reflex increase, pulse pressure narrowed
Phase 4 of the Valsalva manouvre
- With increase in RV output LV experiences boost in preload –> persistent increase in contractility and elevated SVR –> increased BP and restored cardiac output
- Reduction in HR with slower resolution of BP and SVR due to delay in SNS action
Draw a line representing MAP and HR during a valsalva manouvre
Septic shock does what to cardiac index
Increeases
Septic shock has what effect on PCWP
Normal or reduced
Septic shock affects CVP how?
Normal or reduced
Septic shock has what effect on PVR
Reduced
Septic shokc has what effect on DO2
Increased
What are the parameters required when dioscussing shock
CI
PCWP
CVP
SVR
DO2
How does cardiogenic shock influence CI
Reduced
How does cardiogenic shock influence PCWP
Increases
How does cardiogenic shock affect CVP
Normal or reduced
How does cardiogenic shock affect PVR
Increases
How does cardiogenic shokc influence DO2
Reduced
How does hypovolaemic shock affect CI
Reduced
How does hypovolaemic shock affect PCWP
Decreases
How does hypovolaemic shock affect CVP
Reduced
How does hyopovolaemic shock affect SVR
Increases
How does hypovolaemic shokc affect DO2
Decreased
How does obstructive shock affect CI
Decreased
How does obstructive shock affect PCWP
Normal or increased
How does obstructive shokc affect CVP
Increases
How does obstructive shock affect SVR
Increases
How does obstructive shock influence DO2
decreases
