Physiology of the Cardiovascular System Flashcards
components of the cardiovascular system diagram
Components of the cardiovascular system:
- cardiopulmonary unit
- left side and right side
- pulmonary artery and vein
- arteries, arterioles, capillaries, venules and veins
- portal systems: hepatic portal system and hypopyseal ( connects hypothalamus with anterior pituitary)
- intra-renal circulation
- intra-cranial circulation
- intra-coronary circulation
Hypophyseal
a system of blood vessels in the microcirculation at the base of the brain, connecting the hypothalamus with the anterior pituitary. Its main function is to quickly transport and exchange hormones between the hypothalamus arcuate nucleus and anterior pituitary gland.
State the 2 overall functions of the cardiovascular system:
- rapid convective transport of substances
- homeostatic control
Overall functions of the cardiovascular system: rapid convective transport of (6): Name three examples.
- O2
- glucose
- amino acids and fatty acids
- vitamins
- water
- waste products of metabolism: CO2, urea, creatine
Overall functions of the cardiovascular system: Homeostatic control:
- hormones
- temperature
Stroke Volume
the volume of blood pumped by the left ventricle per beat
Cardiac Output
stroke volume x heart rate
the volume of blood pumped by the heart per unit time
measured as L/minute
Perfusion
the passage of blood through the circulatory system to the body’s tissues
measured as ml of blood per minute per gram of tissue
Preload (cardiovascular):
- definition
- measured
- denoted
the degree to which the bentricles are filled at the end of diastole, just prior to systolic contraction
measured as end-diastolic volume in mL
denoted by EDV
Contractility (cardiovascular):
- definition
- measured
- denoted
the innate ability of the myocardium to contract
Afterload (cardiovascular):
- definition
- measured
- denoted
the resistance (increases if blood is thicker or vessels is affected) against which the left ventricle must eject the stroke volume from the heart
measured as aortic pressure during systole divided by cardiac output
Compliance (cardiovascular):
- definition
- measured
- denoted
- the ability of a blood vessel to expand and contract with changes in pressure
- measured as unit of volume change per unit of pressure change
- denoted by c
Factors affecting heart rate
Factors affecting Stroke Volume
Factors affecting Cardiac Output
Factors affecting Stroke Volume
Frank-Starling Mechanism
The stroke volume of the heat increases in response to an increase in the volume of blood in the ventricles before contraction, when all other factors remain constant
Frank-Starling Mechanism
Pressure Volume Diagram
Extrinsic Control of circulation:
- autonomic vasomotor nerves:
- sympathetic vasoconstriction
- parasympathetic vasodilation
- sympathetic vasodilation - Renin-Angiotensin- Aldosterone
- Adrenaline
- Anti-diuretic hormone/ arginine
vasopressin - natriuretic peptides
- other hormone control
- sensory nerve vasodilation
Autonomic Nervous System
Autonomic Nervous System and Cardiovascular Control: Parasympathetic Control:
- in the absence of extrinsic control of the heart, the heart beats ate approx 100bpm
- during rest, sleep, the parasympathetic nervous system predominates and decreases the heart rate to a resting rate of 60-75 bmp
Most blood vessels have a constant state of parasympathetic tone.
True or False?
False
Most blood vessels lack parasympathetic innervations and their diameter is regulate by the sympathetic nervous system input, so that they have a constant state of sympathetic tone
What allows vasodilation?
A decrease in sympathetic stimulation or tone that allows vasodilation
At any given time, the effect of the ANS on the heart is the
net balance between the opposing actions of the sympathetic and parasympathetic systems
Functions of sympathetic and parasympathetic receptors in the heart and vessels
Factors that affect heart rate:
- contraction starts in the atria
- autonomic innervation: parasympathetic decreases your heart rate in sleep
- hormones:
Factors affecting stoke volume by affecting preload:
- venous return
- filling time
- hydration affects venous return/ if fainted you lift a persons legs up
- preload affects end diastolic volume (EDV) and end systolic volume (ESV)
Stroke volume equation
SV = EDV-ESV
stroke volume = end diastolic volume - end systolic volume
Factors affecting stroke volume by affecting contractility:
- autonomic innervation: tone of cardiac muscles, how hard and fast contraction occurs (max strong vol, with min ESV)
- hormones: affects speed and force of contraction
- contractility affects end systolic volume ESV
- high contractility decreases ESV and hence increases SV
Factors affecting stroke volume by affecting afterload:
- vasoconstriction or vasodilatation
- affects vol of blood leaving
- if peripheral vasodilation, then heart sees vessels need to be filled so squeezes harder during systole so decreases ESV
- if vasoconstriction or blockage in circulation there is a high resistance so increases work heart has to do
- afterload affects end systolic volume ESV
How will a faster filling time and increased venous return affect stroke volume?
Increases end diastolic volume EDV
increases stroke volume
How will a high intracellular calcium ion concentration affect stroke volume?
- high contractility
- decreases end systolic volume ESV
- increases stroke volume
ionotropy definition and affect on heart
an agent that alters the force or energy of muscular contractions
positive, increases heart contractility and hence stroke volume
Chronotropy definition and affect on heart
something that changes the heart rate and rhythm by affecting the electrical conduction system
positive means heart rate increased
Dronotropy definition and affect on heart
something that affect the speed of action potential conduction in the AV node
positive increase conduction of cardiac action potential, so shortens duration of systole and therefore increases the heart rate
Add table
insert
—- expression of alpha 1 receptors in myocytes
low
stimulation causes ionotropic, chronotropic, dronotropic increase
—– expression of alpha 2 receptors in cardiac myocoytes
no alpha 1 in cardiac myocytes
main affect of alpha receptor stimulation on cardiovascular system?
vascular smooth muscle
vasoconstriction
beta 1 adrenergic receptors are found in the heart and in vascular smooth muscle
True or False?
False
Only in heart not vascular smooth muscle
beta 1 activation in the heart causes
increase in inotropic, chronotropic and dromotropy
beta 2 adrenergic receptors found in
beta 2 receptors are expressed in mainly in vascular smooth muscle, skeletal muscle and coronary circulation
low expression in cardiac myococytes which cause ionotropy, chronotropy aand dromotropy when stimulated
vasodilation increases blood perfusion
the parasympathetic nervous system inhibits ionotropy, chronotropy and dronotropy by (receptor and neurotransmitter) (found abundantly where in heart)
ach binidng to M2
nodal and atrial tissue
slows heart rate till it reaches normal sinus rhythm by slowing the rate of depolarisation and reducing conduction velocity through the atrioventricular node
reduces contractility of atrial cardiac myocytes and hence reduces overall cardiac output of the heart
renin angiotensin aldosterone system
Where is renin mainly released from?
juxtaglomerular cells in the afferent arteriole of the renal glomerulus
Renin release stimulated by
- sympathetic nervous activation (through beta 1 adrenoreceptors)
- renal artery hypotension (due to systemic hypotension or renal artery stenosis)
- decreased sodium delivery to the distal tubules of the kidney sensed by cells in the macula densa
Renin release causes
angiotensinogen to be cleaved to form angiotensin 1
Conversion of angiotensin 1 to angiotensin 2
- vascular endothelium (especially in the lungs) contains Angiotensin Converting Enzyme (ACE), which cleaves Angiotensin 1 into Angiotensin 2
- Angiotensin 2 is the most active peptide in RAAS and there are two identified Angiotensin 2 receptors
- type 1 receptors cause vasoconstriction, cell proliferation, inflammatory responses, blood coagulation and extracellular matrix remodelling
- type 2 receptors counteract these effects
The effects of angiotensin 2 and the cardiovascular system
- constricts resistance vessels thereby increasing Systemic vascular resistance and arterial pressure
- stimulates sodium transport (reabsorption) at several renal tubular sites, thereby increasing sodium and water retention by the body
- acts on the adrenal cortex to release aldosterone
- stimulates the release of vasopressin (ASH( from the posterior pituitary
- stimulates thirst
- facilitates noradrenanline release from the sympathetic nerve endings and inhibits its reuptake
- stimulates cardiac hypertrophy and vascular hypertrophy
aldosterone
- angiotensin 2 acts on the adrenal gland to stimulate the release of aldosterone
- aldosterone affects the final part of electroly and water absorption within the nephron before excretion in the urine
- increases the amount of sodium reabsorbed from the distal tubule and the collecting duct of the kidney
- increases the amount of water reabsorbed in turn
- only affects 3% of the total water absoprtion
- aldosterone acts synergistically with ADH to cause an increase in the amount of water taken up through the nephron, therefore increasing blood pressure
adrenaline affect on cardiovascular system
- the adrenal medulla is the exception to typical sympathetic fiber arrangement
- preganglionic fibers terminate on chromaffin cells in the adrenal medulla that release both adrenaline and noreadrenaline
- stimulates all the major adrenergic receptors
- at low concentrations is beta 2 selsctive and causes vasodilation
- at higher concentrations stimulates other adrenergic receptors causing vasoconstriction and increases heart rate and contractility
- also causes renal arteriole vasoconstriction, reducing blood flow to glomeruli and nephrons
ADH
- released during hypovolaemic shock
- synthesis in the hypothalamus and released from the posterior pituitary gland
- released in response to a reduction in plasma volume and an increase in plasma osmolarity
- in the CVS it acts via V1 receptors to cause arteriolar vasoconstriction
- in the kidney acts via V2 recepptors to cause increases in the amount of water reabsorbed from the renal tubules
Natriuretic peptides released by the heart
- 2 natriuretic peptides released by the hear:
- atrial natriuretic peptide (ANP)
- brain natriuretic peptide (BNP)
- produced stored and released by atrial myocytes mainly in response to trial distention
- act to increase renal sodium excretion in response to increased stretching of atria due to increased atrial blood volume
