integration of cardiovascular mechanisms Flashcards
what factors influence stroke volume?
- preload
- myocardial contractibility
- afterload
what can you regulate to regulate mean arterial blood pressure (MAP)?
regulate heart rate, stroke volume and systemic vascular resistance
what regulates systemic vascular resistance?
smooth muscles
what is the main site of SVR?
arterioles
what effect does vasoconstriction have on stroke volume (SV) resistance and mean arterial blood pressure (MAP)?
vasoconstriction = increase SV & increases MAP
what are 2 categories of mechanisms that control vascular smooth muscle?
- intrinsic
- extrinsic
what is relationship between resistance to blood flow, blood viscosity, length of blood vessel and radius of blood vessel?
resistance to blood flow is directly proportional to blood viscosity & length of blood vessel
- it’s inversely proportional to radius of blood vessel to power of 4
= this shows that minor change to radius has massive impact on flow
what is resistance to blood flow mainly controlled by?
controlled by vascular smooth muscle through changes in radius of arterioles
what are examples of extrinsic control of vascular smooth muscle?
nerves (like baroreceptor reflex, sympathetic = noradrenaline) & hormones (adrenaline, angiotensin II, antidiuretic hormone)
what nervous system mostly supplies vascular smooth muscles?
sympathetic nerve fibres = noradrenaline on alpha receptors
(There is no significant parasympathetic innervation of arterial smooth muscles)
what is vasomotor tone?
when blood vessels are partially restricted at rest
what causes vasomotor tone?
tonic (continuous) discharge of sympathetic nerves = continuous release of noradrenaline
what effect does
a) increase sympathetic discharge
b) decrease sympathetic discharge
have on vascular smooth muscles?
a) increase the vasomotor tone resulting in vasoconstriction
b) decrease the vasomotor tone resulting in vasodilatation
what is effect of adrenaline on vascular smooth muscle?
effect of adrenaline = organ specific! depends predominantly on type of receptor
- adrenaline (not same as noradrenaline - adrenaline = hormone!) from adrenal medulla
what effect does adrenaline binding to
a) alpha receptor?
b) beta 2 receptor?
a) vasoconstrictors (alpha receptors often at skin)
b) vasodilation & bronchodilation
where are alpha receptors predominant?
skin, gut or kidney arterioles
where are beta 2 receptors predominant?
cardiac & skeletal muscles arterioles
what effect does angiotensin II have on vascular smooth muscle?
vasoconstriction
what effect does antidiuretic hormone have on vascular smooth muscle?
vasoconstriction
how is intrinsic control and metabolic processes related?
- intrinsic control matches blood flow of different tissues to their metabolic need
which one out of intrinsic/extrinsic can override the other?
intrinsic can OVERRIDE extrinsic control mechanisms
what factors are involved in intrinsic control?
- chemical (local metabolites & local humoral agents)
- physical factors (temperature, myogenic response, sheer stress)
how do local metabolites affect vascular smooth muscle?
= they’re a type of chemical intrinsic control
- local metabolic changes within an organ influences the contraction of arteriolar smooth muscles
- increased blood flow to metabolically active tissue
what factors cause relaxation resulting in vasodilation & metabolic hyperaemia?
- decreased local pO2 (oxygen partial pressure)
- increased local pCO2 (CO2 partial pressure)
- increased local H+ (decrease pH)
- increased extracellular K+
- adenosine release (from ATP)
what is metabolic hyperaemia?
the process by which the body adjusts blood flow to meet the metabolic needs of its different tissues in health and disease (usually more blood than normal going to specific organ)
what are examples of local humoral agents that cause vasodilation?
humoral agents= chemical intrinsic control
- histamine
- bradykinin
- NO
when are local humoral agents released?
in response to tissue injury or inflammation
what is mechanism of nitric oxide (NO)?
NO diffuses from the vascular endothelium into the adjacent smooth muscle cells where it activates the formation of cGMP that serves as a second messenger for signalling smooth muscle relaxation
when is nitric oxide produced?
continuous = continuously produced by the vascular endothelium from the amino acid L-arginine through enzymatic action of Nitric Oxide Synthase (NOS)
flow dependent = Shear stress on vascular endothelium, as a result of increased flow, causes release of calcium in vascular endothelial cells and the subsequent activation of NOS
Chemical stimuli = receptor stimulated NO formation – many vasoactive substances act through stimulation of NO formation
what are some examples of humoral agents that cause vasoconstriction?
humoral agent = chemical intrinsic control
- serotonin
- Thromboxane A2
- Leukotrienes
- Endothelin
what is endothelin?
potent vasoconstrictor released from endothelial cells. Its production is stimulated by various agents which cause vasoconstriction
(type of humoral chemical intrinsic control)
what are endothelial produced
a) vasodilators
b) vasoconstrictors
properties?
a) Endothelial produced vasodilators are anti-thrombotic, anti-inflammatory, anti-oxidants
b) Endothelial produced vasoconstrictors are pro-thrombotic,pro-inflammatory, pro-oxidants
what effect does temperature have on vascular smooth muscle?
Cold - causes vasoconstriction
Warmth - causes vasodilatation
what is myogenic response to stretch?
= help keep flow constant in face of changing blood pressure
Important in tissues like brain and kidneys – helps with regulation of local blood flow:
- If MAP rises resistance vessels automatically constrict to limit flow
- If MAP falls resistance vessels automatically dilate to increase flow
what is sheer stress effect on vascular smooth muscle?
sheer stress = increased blood flow
Dilation of arterioles causes sheer stress in the arteries upstream to make them dilate. This increases blood flow to metabolically active tissues
what is relationship between end diastolic volume and stroke volume?
increased end diastolic volume = increased stroke volume as more stretch = more contraction according to Frank Starling curve
what factors increase venous return?
- increased venomotor tone
- increased blood volume
- increased respiratory pump
- increased skeletal muscle pump
what does increased venous return lead to?
increased end diastolic volume = increased stroke volume (Frank-starling)
where contains most of blood volume under resting conditions?
the veins are capacitance vessels that contain most of blood volume under resting conditions
what nerve fibres supply venous smooth muscles?
sympathetic - stimulation = contraction
why is blood driven to RA in veins?
on account of venous valves (prevent backflow)
what is respiratory pump? and what effect does that have on venous return?
- during inspiration, intrathoracic pressure decreases and intra-abdominal pressure increases
- This increases pressure gradient for VENOUS RETURN and creates a suction effects that moves blood from veins towards the heart
- Increasing rate and depth of breathing increases VENOUS return to heart
what is skeletal muscle pump? and what effect does it have on venous return?
- Large veins in limbs lie between skeletal muscles
- Contraction of muscles aids venous return
- One-way venous valves allow blood to move forward towards the heart
- Muscle Activity increases VENOUS RETURN to heart
what is cardiovascular response to exercise?
- sympathetic vasomotor nerves reduce blood flow to kidneys & gut by vasoconstriction
- metabolic hyperaemia overcomes vasomotor tone to increase blood to skeletal & cardiac muscle = vasodilation
- also adrenaline acting on beta 2 causes bronchodilation and vasodilation to skeletal & cardiac
what is effect on CO and BP in exercise?
- this increase in CO increases systolic BP - metabolic hyperaemia & adrenaline decrease SVR and decrease diastolic blood pressure (so widened pulse pressure →increase as reflects force of each heartbeat & decrease in resistance in diastole)
- systolic bp increase but diastolic mostly remains the same in exercise
what is chronic cardiovascular response to exercise (of exercise a lot)?
- regular aerobic exercise helps reduce blood pressure (mechanism not fully understood - likely to be multifactorial)
- reduction in sympathetic tone & noradrenaline levels
- increased parasympathetic tone to the heart
- cardiac remodeling
- reduction in plasma renin levels (rate limiting step in RAAS)
- improved endothelial function = increased vasodilators and decreased vasoconstrictors
- decreased arterial stiffening
