Cardiovascular challenges and neural mechanism Flashcards
What causes the central blood volume to decrease?
Hemorrhage, head-up tilt, standing (practical class) Lower body negative pressure, crucifixion
challenge for Cardiovasular system in response to Hemorrage is to : maintain adequate arterial pressure and perfusion of the brain and heart in the face of a falling cardiac output.
What causes the central blood volume to increase?
Blood or plasma transfusion
Head-out water immersion
Lower body positive pressure
what changes the energy/organ blood flow requirement?
- *- Exercise** (challange for CV homeostatis : Exercise: Increased delivery of oxygen and nutrients (via increased blood flow) to exercising muscles.
- *-Diving (**Conservation of oxygen by limiting blood flow to non-essential organs.)
- *Alerting responses**
What is mean arterial pressure?
(MAP) is the average arterial pressure throughout one cardiac cycle, systole, and diastole.
Mean arterial pressure = cardiac output x total peripheral resistance
CO is the amount of blood your heart pumps each minute
CO = SV x HR
What is the relationship of MAP and TPR?
MAP = CO/TPC
total peripheral coductance = 1/TPR
CO = MAP/TPR
TPR= MAP/CO
*Arterial pressure and cardiac output can be measured.
TPR can only be calculated
Equation of organ blood flow
Organ blood flow = MAP/Organ VR
VR = vascular resistance
Organ Blood flow = MAP x Organ vascular conductance
Organ Vascular Conductance = 1/vascular resistance
What mechanism effect cardiac output?
How the pressure changes troughout circulation?
Pressure is pausatile in arteries as they are resposible for distribution of blood to different organs
The blood pressure drops rapidly at arterioles as it regulates the vasculture resistance.
The constriction of arterioles increases resistance, which causes a decrease in blood flow to downstream capillaries and a larger decrease in blood pressure.
Which blood vessels control vascular resistance ?
venous vascular tone does play a big role in the
control of venous return and so cardiac output (Frank-Starling Law)
venous tone is a property of the venous system which reflects the venous resistance and pressure. An increased venous tone caused by venoconstriction leads to an increased net capillary filtration by increasing the venous resistance and venous pressure
Poiseulle’s Equation
The relationship between blood vessel diameter and Resistance /Flow
R = 8nL/r^4
R = resistance
n= viscosity
L = length
r = radius
There’s an inverse relationship between blood flow and resistance
Resistance is nversely proportional to the radius to the fourth power (r4)
Factors that can alter the diameter of resistance vessels?
- Local/metabolic /intrinsic factors
- Nerves (mainly sympathetic)
- Hormones (endocrine, paracrine and autocrine)
- Structural properties (egthickness of smooth muscle)
- Pathology (ega therosclerosis, endothelial damage)
What is Active hyperemia?
Blood flow increases when oxygen consumption increases (increase metabolic activity) of an organ or tissue
Example -the heart
What is Reactive Hyperaemia?
Reactive hyperemia is the transient increase in organ blood flow that occurs following a brief period of ischemia (e.g., arterial occlusion).
Factors Contributing to Active and Reactive Hyperaemia
Carbon dioxide
Hypoxia (low oxygen concentration)
Lactic acid
Reduced pH (acidosis)
Adenosine
Endothelial derived nitric oxide
Autoregulation
• Matching blood flow (and/or pressure) to organ function • Particularly seen in organs requiring tight control of blood flow (eg brain, kidney, heart)
What happens during acute blood loss?
Cardiac output drops
As 2/3 of our total blood volume is in venous side of circulation during acute blood loss the the venous pressure decreases and hence the diastolic ventricular filling (venous retrun) declines and hence SV adn cardiac output decreases, systolic blood pressure drops.
How is blood flow maintained to key organs during acute blood loss ?
Brain, Heart
§ arterioles in these organs do not contrict much during mild
blood loss
§ Regional difference in vascular response
§ Mechanisms?
§ Local (metabolic/myogenic), neural and hormonal
When running the skeletal muscles in the legs .
increase oxygen consumption
Tissue carbon dioxide levels increase
The carbon dioxide acts in a paracrine manner to dilate the skeletal muscle arterioles
If the diameter of the arteriole doubles, flow to the muscle will increase 16 fold (Poiseulle’s Law)
Due to the decrease in total peripheral resistance, arterial pressure will fall.
What happens in the 2 phase response to hemorrhage?
Two phases
§ Phase 1
§ Vasoconstriction
§ Blood pressure maintained
§ Phase 2
§ Vasodilation
§ Blood pressure plummets
Recovery from acute blood loss
- *Restoration of cardiac output to normal levels**
- Fluid shifts into the vascular compartment
- Hormone-induced vasoconstriction
- Reduced salt and fluid output (urine production decrease)
- Increased salt and fluid intake (eating/drinking)
Posture and blood pressure
When standing the venous pressure in toes increases from 5mmHg to 80mmHg due to the effect of gravity and the blood from the upper part of the body (brain) is redistributed to the lower part of the body.
Hence there’s a reduction in blood volume in the chest veins aka acute central hypovalemia.
Cardiovascular response to water immersion
How does the cardiovascular system respond?
§ Compression of veins in the lower body
§ Increased central blood volume
§ Increased venous return
§ Increased cardiac output
Cardiovascular responses to a decrease in central blood volume
The Reduced central blood volume result in: (eg hemorrhage)
- Reduced venous return
- Reduced cardiac output
The compensatory responses…..
- Increased heart rate
- Vasoconstriction (except brain and heart)
- Increased salt appetite & thirst
- Reduced urinary salt and water excretion
- Movement of extracellular fluid volume
into plasma
Cardiovascular responses to increase in central blood volume?
The Increase in central blood voume result in: (eg water immersion)
- Increased venous return
- Increased cardiac output
§ The compensatory response…..
- Vasodilation (except heart and brain)
- Reduced salt and water appetite
- Increased urinary salt and water excretion
- Movement of plasma fluid into the the
extracellular fluid
Cardiovascular responses to exercise
There’s an Increased demand of exercising muscles for oxygen and other nutrients
The cardiovascular system compensatry responses are:
Increased cardiac output
Vasoconstriction in guts, kidney and skin
Vasodilatation in skeletal muscle
Cardiovascular responses to diving
The aim of CV is to Conserve oxygen but maintain blood flow to vital organs
through
Reduced cardiac output
Vasoconstriction every but the brain
Divisions of the autonomic nervous system and how they innervate the cadiovascular system
EFFERENT – effector
Parasympathetic nervous system
mainly heart
Sympathetic nervous system
Heart and blood vessels
AFFERENT - Feedback to neural and hormonal efferent
mechanisms
§ Arterial baroreceptors
§ Arterial chemoreceptors
§ Cardiac baroreceptors and chemoreceptors
§ Other ( eg renal baroreceptors, brain chemoreceptors)
What part of the brain controls cardiovascular activity?
The regulation of the heart and peripheral circulation by the nervous system is accomplished by control centers in the rostral part of medulla
Parasympathetic nerve pathway controlling the CV
The parasymoathtic activity starts at the NTS - nucleus tractus solitarius of the Medulla oblongata which trasmit the information via interneuron to
- *NA - Nucleus ambiguous** and Dorsal Vagal Nucleus (DVN)
- *(cardiohibitory centre).** The nerual information is passed through the preganglionic parasympathetic neurons to Cardiac parasympathetic ganglia. The post ganglonic fiber innervating the
- *Sinoatrial node** slows doewn the HR.
sympathetic nerve pathway controlling the CV
NTS - nucleus tractus solitarius
RVLM (vasoconstrictor centre)
CVLM - caudal ventrolateral medulla (vasodilator centre)
IML - the intermediolateral cell column - located in spinal cord
Sympathetic ganglia
Target organs - SA node, Heart muscle, and blood vessles
What are Some of the afferent inputs regulating cardiovascular function?
Baroreceptors (pressure sensing, stretch sensitive)
§ Aortic Arch and Carotid Sinus (major) *
§ Cardiac (atrial and ventricular) *
Chemoreceptors (oxygen and carbon dioxide)
§ Carotid Sinus*
§ Brain
Others
§ Pulmonary stretch receptors*
§ Trigeminal Afferents (nasopharyngeal)
* First Synapse in Brain is Nucleus Tractus Solitarius (NTS)
True or false?
Baroreceptors are very abundant in the great veins and heart
true
but the Function less well understood than arterial baroreceptors
What are baroreceptors?
Spray-type’ nerve endings in blood vessel walls
§ Respond to stretch
§ Firing increases with increased pressure
§ First synapse in the brain in the nucleus tractus solitarius (NTS)
§ Baroreceptors rapidly ‘reset’
§ Contribute to the short-term (moment to moment) control of
blood pressure
Baroreceptor firing increases when ——— and Baroreceptor firing decreases when ——
events that occur in response to a reduction in central blood
Venous pressure decreases
The pressure driving filling of the heart decreases
End-diastolic volume is reduced
Stroke volume is reduced (due to the Frank-Starling law)
Cardiac output decreases and MAP falls
In response to Crucifixion
Venous pressure decreases
atrial filling pressure decreases
stroke volume decreases
cardiac output decreases
arterial pressure falls
blood flow to the brain decreases
The brain will become hypoxic and the person will faint
the person when they faint will loose consciouness and but flow to the brain will remain low and the cells in the brain will start to die
Neural mechanism -hypoxia
Baroreceptor and chemoreceptor afferent sensory nerves first synapse in the nucleus tractus solitarius
Nociceptors and nasopharnygeal receptors have inputs to the nuclus tractus solitarius and rostral ventrolateral medulla
Higher brain regions have inputs to the NTS and RVLM which can modify the reflex responses arising from the various peripheral sensory receptors
There are seperate descending outputs from the RVLM that can differententially regulate sympathetic outflow to different regional vascular beds
In response to hypoxia chemoreceptors trigger an increase in parasympathetic and sympathetic activity, that results in a reduction in heart rate and an increase in vascular resistance
