Cardiovascular mechanisms Flashcards by Louise Emerson

what are capillaries the site of

Exchange of gas, nutrients and water between blood and tissues

How well did you know this?

Not at all

Perfectly

what blood vessels contain majority of blood volume during rest

veins

How well did you know this?

Not at all

Perfectly

what is afterload

the stress in the wall of the left ventricle during ejection or the end load against which the heart contracts to eject blood

How well did you know this?

Not at all

Perfectly

how is MAP calculated using CO

CO x SVR

How well did you know this?

Not at all

Perfectly

how is SVR regulated

by vascular smooth muscles in blood vessels

How well did you know this?

Not at all

Perfectly

vasocontriction of vascular smooth muscle causes what

increases MAP and SVR

How well did you know this?

Not at all

Perfectly

vasodilation of vascular smooth muscle causes what

decreases SVR and MAP

How well did you know this?

Not at all

Perfectly

what are vascular smooth muscles controlled by

extrinsic and intrinsic mechanisms

How well did you know this?

Not at all

Perfectly

where through pathway of blood through circulation is the biggest drop in pressure

when blood travels from arterioles to capillaries

How well did you know this?

Not at all

Perfectly

what is resistance to blood flow directly proportional to

blood viscosity and length of blood vessel

How well did you know this?

Not at all

Perfectly

what is resistance to blood flow indirectly proportional to

the radius of blood vessel to the power 4

How well did you know this?

Not at all

Perfectly

what is the resistance to blood flow mainly controlled by

via vascular smooth muscle through changes in the radius of arterioles

How well did you know this?

Not at all

Perfectly

what nerves supply vascular smooth muscles

sympathetic nerve fibres

How well did you know this?

Not at all

Perfectly

what is the neurotransmitter for sympathetic nerve fibres and what receptors do they act on

noradrenaline, alpha receptors

How well did you know this?

Not at all

Perfectly

what is the vasomotor tone

due to continuous release of noradrenaline vascular smooth muscles are partially constricted at rest

How well did you know this?

Not at all

Perfectly

what does increased sympathetic discharge cause

increases the vasomotor tone

How well did you know this?

Not at all

Perfectly

where is vasculature innervated with parasympathetic nerve fibres

penis and clitoris only

How well did you know this?

Not at all

Perfectly

what does adrenaline acting on alpha receptors do

causes vasoconstriction

How well did you know this?

Not at all

Perfectly

what does adrenaline acting on beta 2 receptors do

causes vasodilatation

How well did you know this?

Not at all

Perfectly

when are alpha receptors predominant

skin, gut and kidney arterioles

How well did you know this?

Not at all

Perfectly

where are B2 receptors predominant

cardiac and skeletal muscle arterioles

How well did you know this?

Not at all

Perfectly

what do B2 receptors in muscle arterioles help to achieve

strategic redistribution of blood e.g. during exercise

How well did you know this?

Not at all

Perfectly

what are two other hormones that affect vascular smooth muscle (and what do they do)

Angiotensin II: causes vasoconstriction

Antidiuretic hormone (vasopressin): causes vasoconstriction

How well did you know this?

Not at all

Perfectly

what are Angiotensin II and Antidiuretic hormone (vasopressin) important in controlling

the intermediate control of blood pressure

How well did you know this?

Not at all

Perfectly

what do the intrinsic control mechanisms of VSM match to what

the blood flow of their tissue to their metabolic needs

what can the extrinsic control mechanisms over-ride

extrinsic control mechanisms

what do intrinsic control mechanisms include

LOCAL chemical and physical factors

what is the main way local blood flow is controlled

local intrinsic control mechanisms

what can local metabolic changes within an organ influence

the contraction of arteriolar smooth muscles

name the local metabolic factors causing relaxation of arteriolar smooth muscles (6)

Decreased local PO2 Increased local PCO2 Increased local [H+] (decreased pH) Increased extra-cellular [K+] Increased osmolality of ECF Adenosine release (from ATP)

what does relaxation of arteriolar smooth muscles result in

vasodilatation and metabolic hyperaemia

what us hyperaemia

excess of blood in a vessel

In addition to metabolites what other local chemicals released within an organ influence the contraction of arterial and arteriolar smooth muscles

local humoral agents

what can the release of local humoral agents be caused by

tissue injury or inflammation

give three examples of local humoral agents that cause relaxation of ASM

Histamine Bradykinin Nitric Oxide (NO)

describe the release if NO

continuously released by endothelial cells of arteries and arterioles

what are local humoral agents classed as as a mechanisms

intrinsic control mechanisms of VSM (chemical)

how is NO produced

by the vascular endothelium from the amino acid L-arginine through enzymatic action of Nitric Oxide Synthase (NOS)

what is the role of NO

is a potent vasodilator which is important in the regulation of blood flow and maintenance of vascular health

what is the duration of life of NO

few seconds

what causes the release of calcium in vascular endothelial cells and what does this cause (WHAT IS THIS CALLED)

FLOW DEPENDANT NO FORMATION Shear stress on vascular endothelium, as a result of increased flow- subsequent activation of NOS (which will produce NO from L-arginine )

what is receptor stimulated NO formation

when chemical stimuli induce NO formation

describe the path of NO

diffuses from endothelium into the adjacent smooth muscle cells

what does NO do when in smooth muscle cells

activates the formation of cGMP that serves as a second messenger for signalling smooth muscle relaxation

give four examples of humoral agents which cause contraction of arteriolar smooth muscles resulting in VASOCONSTRICTION

Serotonin Thromboxane A2 Leukotrienes Endothelin

describe endothelin

is a potent vasoconstrictor released from endothelial cells

what is the production of endothelin caused by

various agents which cause vasoconstriction

what can damage endothelium

high blood pressure, high cholesterol, diabetes and smoking

describe endothelial produced vasodilators

anti-thrombotic, anti-inflammatory, anti-oxidants

describe endothelial produced vasoconstrictors

are pro-thrombotic, pro-inflammatory, pro-oxidants

what are the three physical control mechanisms of VSM

temperature, myogenic response, sheer stress

what does myogenic response stop

changes in blood affecting the brain and the kidneys

describe the action of myogenic response if MAP increases

resistance vessels automatically constrict to limit flow

describe the action of myogenic response if MAP falls

resistance vessels automatically dilate to increase flow

what creates sheer stress and what does it cause

Dilatation of arterioles causes sheer stress in the arteries upstream to make them dilate. This increases blood flow to metabolically active tissues

what is the autoregulation of cerebral blood flow

myogenic response

what else is cerebral blood flow controlled by

Sympathetic nerve stimulation

what four factors increase venous return

increased; venomotor tone, skeletal muscle pump, blood volume, respiratory pump

what pressure does increased venous return increase

atrial pressure

how does increased venous return affect EDV

increases it

how does increased venous return affect SV

increases it (starling curve)

describe the respiratory pump

Descend of diaphragm when breathing increases abdominal pressure and decreases intrathoracic pressure which decreases pressure in RA which creates a bigger pressure gradient therefore increasing venous return

what type of vessels are veins

capacitance vessels

what nerve fibres are venous smooth muscles supplied with

sympathetic

what does increased venomotor tone lead to (3)

increased; | venous return, SV and MAP

what does invrease vasomotor tone do (2)

increased; | SVR and MAP

how does skeletal muscle activity affect venous return and how

increased activity increases venous return as large veins in limbs lie between muscle which pump blood when they constrict

what affects blood volume (2)

fluid shifts across capillaries and salt & water balance

what happens to sympathetic nerve activity during exercise

increases

what happens to HR and SV during exercise

increases

what is the action of sympathetic vasomotor nerves during exercise

reduce flow to kidneys & gut - vasoconstriction

what overcomes vasomotor drive in skeletal and cardiac muscle during exercise and casuing what

metabolic hyperaemia, vasodilation

in proportion to what during exercise does blood flow increase

metabolic activity

what do the increases in CO during exercise do to systolic BP

increase it

what does the metabolic hyperaemia do to SVR and DBP

decreases them

why does DBP decrease during exercie

as muscle bed big tissue so has lot of vasodilatation

what is the effect of sympathetic stimulation on the heart

increases HR by increasing SA node firing and decreasing nodal delay and increases force of contraction

what does sympathetic stimulation do to the slope of pacemaker potential

decreases it, positive chronotropic effect

what is the effect of sympathetic nerve stimulation on ventricular contraction

Peak ventricular pressure rises - contractility of heart at a given EDV rises

what is the effect of sympathetic nerve stimulation on the frank starling curve

shifted to the left

what does regular aerobic exercise help to reduce

what might chronic cardiovascular responses to regular exercise include (6)

Reduction in sympathetic tone and noradrenalile levels Increased parasympathetic tone to the heart Cardiac remodeling Reduction in plasma renin levels, reduces BP Improved endothelial function: more vasodilators less vasoconstrictors less arterial stiffening- therefore decrease BP