Co-ordinated Cardiovascular response-Gravity and Exercise Flashcards
How is gravity involved with CVS?
Description of orthostasis or “standing up” on the CVS due to effect of gravity on venous and arterial blood pressures
Changes in cardiac output, central venous filling, heart rate and arterial pressure in response to changes in posture
Effects on microgravity on the CVS
During orthostasis, how does the CVS change according to gravity?
On standing (orthostasis), the cardiovascular system changes according to the effect of gravity:
1. Blood pressure falls at first- postural hypotension, lack of blood flow to brain- faint
2. Quickly recovers- due to homeostatic mechanisms such as baroreflex
3. Baroreflex integrates three smaller changes by increasing:
Heart rate
Force of contraction
Total peripheral resistance
How does gravity affect blood pressure during orthostasis? (Bernoulli’s law)
How to get arterial blood flow from heart to feet when standing up
Arterial pressure gradient is 95-180 mmHg
How will Darcy’s law work?
Darcy’s work doesn’t really work here but what does work is Bernoulli’s law
Bernoulli’s law:
Blood flow= pressure energy + potential energy + kinetic energy
Increased potential energy at heart level vs. feet + increased kinetic energy of ejected blood
Total energies means blood flow from heart to feet
Why does gravity induce high venous blood pressure?
Gravity induced high venous blood pressures
The high pressure in the venous system at the feet is really due to hydrostatic pressure
Pressure = ρhg
Pressure (P) is higher at the bottom of the tube
Magnitude of pressure depends on the height of the fluid column, the density of the fluid, and gravity
How does orthostasis cause hypotension?
(LOok up to double-check)
- Fall in central venous pressure
- Decreased end-diastolic volume
- Decreased stroke volume
- Decreased cardiac output
- Poor perfusion of brain resulting in dizziness and fainting
What is the reflex response to orthostasis?
- Less stimulation (unloading) of baroreceptors
- Lower afferent fibre activity
- Less NTS switches off inhibitory nerves that go from Caudal ventrolateral medulla (CVLM) to Rostral ventrolateral medulla (RVLM)
- Results in RVLM being more active sending efferent signals to heart and arterioles
- Increased sympathetic drive to SA node and increased HR
Myocardium increased contractility
Vasoconstriction (arterioles, veins) increases TPR
Less vagal parasympathetic activity to SA node via NA, overall increase in blood pressure
What makes postural hypotension worse?
A-adrenergic blockade or generalised sympathetic blockade or other drugs that reduce vascular tone e.g. side effect with calcium channel blockers used to treat hypertension, angina
Varicose veins- impairs venous return
Lack of skeletal muscle activity- due to paralysis or forced inactivity e.g. long term bed rest, soldiers on guard
Reduced circulating blood volume e.g. haemorrhage
Increased core temperature- peripheral vasodilatation, less blood volume available e.g. standing up after bath
What effect does microgravity (space) have on the cardiovascular system?
It doesn’t matter whether you are standing or lying down in microgravity
Redistribution of blood into chest region
Initially:
Blood not pooling in feet, it returns to the heart easily, increases atria/ventricle volume and so preload and cardiac output.
Sensed by cardiac mechanoreceptors leading to a reduction in sympathetic activity
This reduces ADH and increases atrial natriuretic peptide (ANP), there is increased glomelular filtrartion rate (GFR) and reduced RAAS
Overall reduction in blood volume by 20%
Long-term:
Less blood volume
Reduced stress on heart
Heart reduces in muscle mass
General drop in BP
On return to gravity:
Several postural hypotension
Due to much lower blood volume
Smaller heart
Baroreceptor reflex can not compensate
What does exercise have to do with CVS?
Cardiovascular changes and control of blood pressure during exercise
Mechanisms leading to the increased blood supply to exercising muscle rather than other tissues
Implications of different types of exercise
What is the cardiovascular response to exercise?
Integrated by central command in the brain
Just anticipation of exercise will cause some of the changes to be initiated
Once exercise commences there is feedback from the muscles via mechanoreceptors and metaboreceptors
All changes are going to affect sympathetic activity and vagus inhibition
Increase lung oxygen uptake, transport around body and supply to exercising muscle
Increased HR and force of contraction
Control of BP- despite huge changes cardiac output and resistance (protect heart from excessive afterload which will reduce cardiac output)
Selectively target where the oxygen is delivered so co-ordinated dilation/constriction of vascular beds
How is the integration of several small adaptations important?
Integration of several small adaptations create overall large response to exercise
Oxygen uptake by pulmonary circulation can increase 10-15 times during strenuous exercise
This very big change brought about by the integration of three smaller changes
Increases in:
Heart rate- 3x (60bpm to 180bpm)
Stroke volume 1.5x (70ml to 120 ml)
Arteriovenous O2- 3x (gradient + Bohr effect)
3 x 1.5 x 3=13.5 times
How is cardiac output changing during exercise?
There is an increase in CO
As heart rate keeps increasing and stroke volume increased up to a point
If we go too far we start to get an over-stretch of the heart and get a decreased CO. We increase afterload and Starling’s law has that elastic limit
So heart rate takes over by increasing itself
What happens during exercise-induced tachycardia?
Heart Rate (tachycardia):
Brain central command
Ready for exercise and muscle mechanoreceptors (fast feedback to brain on exercise being carried out)
Decreased signal down vagus nerve to SA and AV nodes
Increased sympathetic activity to SA and AV nodes
Maximum HR= 220 - age, approximate increase 65 to 195 (3x)
Overall- Cardiac output increase 4.5x (5 to 22l/min), Heart rate (3x) x Stroke volume (1.5x)
What happens during exercise-induced stroke volume?**************
Stroke volume (ejection):
Sympathetic activity increases stroke volume
Increased end-diastolic volume (filling pressure)
Increases sympathetic activity and calf muscle pump cause venoconstriction which increases venous return/CVP - activates Starling law increasing preload
Faster ejection
Increased sympathetic activation of b1 receptors cause faster ejection (inotropic increase in Ca2+)
Decreased end-systolic volume (increased ejection)
Increased contractility by sympathetic activation of b1 receptors and also increased stretching e.g. Starling’s law
What is happening to the increase in cardiac output?
IDK go back
