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Flashcards in Dixon Heart, circulation, and hypertension Deck (26):

describe the cardiac cycle

diastole: ventricles relax and refill
systole: ventricles contract and eject blood


describe general anatomy parts of the heart

left and right atriums
left and right ventricles
left: pulmonary artery, and pulmonary veins

right: aorta and vena cava


what is the cardiac output ?

stroke volume (ml/beat) x heart rate (beats/min)


how does the heart pump blood?

electrical excitation spreads from sinoatrial node (SA node) across the left and right atria
electrical signal reaches Atrioventricular node
AV node: spreads to bundle of his and to purkinje fibres up the left and right ventricle


describe the parts of the electrocardiogram:
P wave
PR interval/segment
QRS complex
ST segment
T wave
Qt interval
TP interval

P wave: atrial depolarisation

PR interval/segment: AV nodal delay

QRS complex: ventricular depolarisation

ST segment: time when ventricles are contracting

T wave: ventricular repolarisation

Qt interval: period of depolarisation and repolarisation of ventricle

TP interval: ventricles are relaxing and filling


how is cardiac input regulated

heart rate is defined by SA node

stroke volume is defined by left ventricular myocytes


what is heart rate and stroke volume regulated by?

autonomic regulation: parasympathetic and sympathetic NS

hormonal regulation

activation of sensory receptors (baroreceptors)

stroke volume: preload (how stretched walls of ventricles are before contraction takes place) and afterload (atrial blood pressure of blood)


heart rate is determined by pacemaker slope of SA node action potential. what does the SNS and PNS do to it?

SNS: increases heart rate (steep slope on graph)

PNS: decreases heart rate (shallow slope on graph)


how does the parasympathetic regulate the heart

dominates at rest
main effect is on heart rate - slows down rate of AP firing from SA node (negative chronotropic effect)

slows down rate of AP conduction through AV node

ACh activates muscarinic M2 ACh receptors coupled to K(ACh) channels = leading to increased K+ efflux from cells

hyperpolarisation: reduced excitability


how does the sympathetic regulate the heart

dominates during exercise/stress
effects stroke volume and heart rate
noradrenaline activates B1 adrenoceptors
1) increased heart rate (positive chronotropic effect) = SA node
2) increase force of myocardial contraction (positive inotropic effect) location = left ventricular myocytes


what are the effects mediated by the sympathetic nervous system on receptors

activation of b1 adrenoceptors on ventricular myocytes increases:
cyclic AMP synthesis
probability of voltage sensitive Ca2+ channels opening
heigh of Ca2+ plateau in ventricular myocyte action potential
= increased force of contraction (+ve inotropic effect)

activation of b1 receptors on SA node cells increases:
cyclic AMP synthesis
size of inward Na+ and Ca2+ currents
steepends pacemaker slope (reaches threshold more quickly)
= increased heart rate (+ve chronotropic effect)


what are the effects mediated by the parasympathetic nervous system on receptors

muscarinic ACh receptors in heart are M2 = open K+ channels and inhibit Ca2+ channel opening
reduces pacemaker slope on SA node action potentials
= reduced heart rate (-ve chronotropic effect)


what receptors detect changes in blood pressure

found in common carotid artery and aortic arch


what is the baroreceptor reflex in response to a fall in Blood pressure

decreased BP
decreased frequency of impulses sent to brain
decreases parasympathetic outflow and increases sympathetic outflow
=increased CO
= increased BP


how is stroke volume stregulated by preload, contractibility and afterload?

length of muscle fibres - preload (preload is determined by end of diastolic volume) adds to stroke volume

force of contraction - contractility adds to SV

arterial blood pressure - afterload (higher afterload = more inhibitory effect it has on SV) takes away stroke volume


discuss how preload regulates stroke volume

initial myocardial length is determined by END-DIASTOLIC VOLUME (EDV)
The EDV determines the PRELOAD
The EDV determines how stretched the muscle fibres’ are

greater length of resting muscle fibres = greater contraction of muscle

greater EDV = greater stretch = greater contraction = greater SV


what is starling's law

more a muscle is stretched before it begins to contract = greater the force of subsequent contraction


discuss how contractility regulates stroke volume

performance of heart at a given preload and afterload

it is increased by inotropic agents.
Noradrenaline and adrenaline increase stroke volume and contractility


discuss how afterload regulates stroke volume

systemic arterial pressure against which systolic ejection must occur

increased arterial BP = decrease in stroke volume


discuss changes in ventricular and aortic pressures

blood is only ejected from the heart when the pressure in the left ventricle (red line in graph) exceeds pressure in the aorta (blue line in graph)
if all remains unchanged = increase in arterial pressure will reduce cardiac output and increase cardiac work


what is total peripheral resistance?

resistance of entire vasculature to blood flow as arterioles smooth muscle contracts - the radius is reduced and resistance increases
contraction of smooth muscle controlled by receptors


what receptors control the contraction of vascular smooth muscle

receptors on vascular smooth muscle cells e.g. adrenoreceptors

receptors on endothelial cells e.g. receptors for ACh, and that sense shear stress


discuss the effects and activation of alpha1 adrenoceptors on vascular smooth muscle cells

alpha1 adrenoceptors - major determinant of blood pressure.

Widely distributed (of particular importance on vascular smooth muscle of pre-capillary arterioles)

Activated by noradrenaline released from sympathetic nerve endings (and by adrenaline from adrenal medulla via blood i.e. hormonal)

Stimulation of these receptors causes contraction = increases resistance

antagonists will reduce reistance e.g. antihypertensive agents


discuss the effects and activation of beta2 adrenoceptors on vascular smooth muscle cells

acivated by noradrenaline/adrenaline
activation causes relaxation and decreased resistance

however it has a more restricted distribution than alpha1 adrenoceptors so =
little influence over total peripheral resistance

b2 adrenoceptor antagonists will increase resistance i.e. they will be hypertensive agents


discuss the indirect mode of action on vsm contraction (receptors on endothelial cells)

endothelial cells release endothelium-derived relaxing factors i.e. nitric oxide = major EDRF

EDRF diffuses to VSM and causes vasodilatation (decrease TPR)

lots of receptors on endothelial cells increase EDRF release - ACh, ADP, receptors that sense shear stress


adrenalines effects on vascular constriction

released from adrenal medulla (stress - fight or flight)

potent vasoconstrictor at alpha1 receptors on VSM = increases BP

activates beta2 receptors in skeletal muscle -
important for fight or flight response
results in diversion of blood flow to important tissue (increase to skeletal muscle, decrease to GI)