regulation of the cardiovasuclar system

EDV, and what is it determined by

end diastolic volume

determined by ventricular diastole duration and venous pressure

ESV and what is it determined by

end systolic volume

determined by arterial blood pressure and force of ventricular contraction

SV

stroke volume

volume of blood ejected in one beat

calculate sv from edv and esv

SV=EDV-ESV

caridac output

volume of blood pumpled into the aorta per unit time

sv x hr

venous return

volume of blood that comes back to the right atrium per unit time.

equal to cardiac output in hearts with normal function

determinants of cardiac output

preload- degree of cardiomyocyte stretch just prior to contraction

afterload- back pressure exerted by arterial blood

contractability- contraction strength at a given muscle length

how is hr regulated

• vagus nerve (parasympathetic) innervates SA and AV nodes, small amount to atria

• Adrenergic fibres (sympathetic) innervate SA and AV nodes, atria and ventricles

• Heart rate of resting mammal is inherent to pacemaker (SA node)

• At rest parasympathetic (vagus) effects predominate

• HR can be increased by decreasing vagal tone or increasing sympathetic tone

innervation of para and sympathetic

• which neurotransmitter and which antagonists

• parasympathetic vagal innervation- ACh release slows HR. Muscarinic receptor antagonists increase HR

• sympathetic innervation- NAd release accelerates HR . Beta adrenoceptor antagonists slow HR.

what does release of NAd from sympathetic effect

open more slow sodium channels

effect of release of ACh from parasympathetic

open more potassium channels (hyperpolarisation) opposing the slow sodium channels

effect of sypathetic and parasympathetic innervation on the AV node

• para inceases AV refractory period and decreases AV conduction

• sympatheic decreases AV refroactory and increase AV conduction

how is contractility regulated

• what type of innervation is it influenced by

• what do atrial myocytes respond to

• influenced by autonomic innervation

• atrial myocytes respond to both sympathetic simulation (beta1)  and parasympathetic simukation (M2)

• ventricuar myocytes are not directly responsive to parasympathetic simulation but have beta1 receptprs

factors influencing venous return

• displacement of blood from peripheral to central vein (sympathetic vasoconstrictor fibres) increases venous return and increases stroke volume

• lower limb skeletal muscle activity promotes blood transfer back to the heart so raises CVP and stroke volume

• thoracic pump, on inspiration intrathoracic pressure is negative and abdominal pressure is positive- pressure gradient favours venous return

what is the frank starling law

• stroke volume of the left ventricle will increase as left ventricular volume increases due to myofibre length, dictated by left ventricle EDV or EDP

• if venous return (central venous pressure) increases there is a greater lv-edp (stretch/preload) and a stronger contraction (stroke volume) in the next beat

• non linear

• increasing venous return increases volume of blood entering during diastole

• so increased end diastolic volume increases strength of subsequent systole

• flow rate into and out of heart equalised

preload

• initial stretch of cardiomyocytes before contraction caused by vol of blood filling ventricles following diastole

• dictated by filling pressure of heart

afterload

• what is it

• what is this determined by and what is that proportional to

• resistance the heart overcomes to pump blood out the ventricles to body

• pressure against at which the heart ejects

• determined by peripheral resistance which is proportional to arterial pressure

effect of reduced afterload

• increased stroke volume

• reduces end diastolic pressure

effect of increased afterload

• reduecd stroke volume

• increases end diastolic pressure

positive inotropic effect

increase strenght of heart contractions

can maintain stroke volume after increased afterload

reflex responses during haemorrhage

• stroke volume decreases

• heart rate increases

• cardiac outpit decreases

• total peripheral resistance increase

• mean arterial pressure decreases then returns

what is increased blood flow during exercise caused by

local hypoxia and adenosine

what happens during exercise

• increased muscle blood flow

• capillafy recruitment

• massive sympathetic discharge

  • direct effects on heart plus generalised vasoconstriction

  • increased venous return, sv and thus co

• release from abdominal venous reservoirs

• vasodilation in cardiac muscle and later in skin (heat dissipation)

• vasoconstriction in inactive tissues (splanchic, renal)

• skeletal muscle metaboloreceptors K+ and lactate sensors

  • exercise pressor response (tachycardia plus positive tropism)