LIFE1032: CARDIAC FUNCTION AND

CONTROL OF BLOOD PRESSURE

Prof Jeanette Woolard

Professor, Cardiovascular Physiology and
Pharmacology
School of Life Sciences

[email protected]
Created with BioRender.com
COMPARISON OF SKELETAL MUSCLE AND
CARDIAC MUSCLE

Skeletal Muscle Cardiac Muscle

 Muscle cells made up of  Similar to skeletal muscle in terms
sarcomeres that contain thick of composition and function
filaments (composed of myosin)  DIFFERENT in terms of how cells
and thin filaments (composed of interact
actin)
 Cardiac muscle acts like a
 Shortening of sarcomere occurs
syncytium – a single, multi-
via sliding filament mechanism, nucleated cell formed from many
where actin filaments slide along fused cells
adjacent myosin filaments
 A wave of depolarisation is
followed by atrial and ventricular
contraction
 CARDIAC EXCITATION

 The heart can

generate its
own rhythm:
 1% cardiac
cells – with
pacemaker
activity (auto-
rhythmic cells)
 99% cardiac
cells –
contractile
function
 SA NODE: NATURAL PACEMAKER OF THE
HEART

 Sinoatrial (SA) node is approximately 8 mm long and 2 mm thick

 It is a specialised region in the right atrial wall at the junction between
the superior vena cava and the right atrium
 Cells within the SA node normally fire very FAST; generate heart beat
 Do not have a resting potential; transmembrane potential ‘less
negative’ than in ventricular cardiomyocytes

 Phases:
 Phase 0: upstroke of action potential is less steep than myocyte
 Phase 3: Plateau is not sustained
 Phase 4: Membrane potential deviates from K+ equilibrium potential
 3

ACTION
POTENTIAL
0
OF SA
NODE CELL
4

 Slow depolarisation: Na+ influx (slow),

Ca2+ influx; reduced K+ efflux
 Rapid depolarisation: Ca2+ influx
 Repolarisation: K+ efflux
 ACTION
POTENTIAL
OF
VENTRICULA
R CELL

 No pacemaker potential: Cells remain essentially at rest (-

90mV) until excited by electrical activity propagated from
the pacemaker
 Rapid depolarisation: Na+ influx
 Plateau phase: Ca2+ influx
 Repolarisation: K+ efflux
 CARDIAC EXCITATION
 Needs to be efficient and co-
ordinated
 action potentials generated at
SA node
 rapid excitation through both
atria
 excitation reaches AV node
where conduction is SLOW
allows atria to contract and
empty blood into ventricles
 excitation spreads rapidly down the bundle of His & Purkinje
fibres to ensure almost simultaneous activation of ventricular
cells  efficient, co-ordinated pump
 CARDIAC EXCITATION

 Can be recorded from the surface of the

body with an electrocardiogram (ECG)
 Four events, but only 3 are visible:
1. Atrial depolarisation (P wave)
2. Ventricular depolarisation (QRS complex)
 Masks atrial repolarisation

3. Ventricular repolarisation (T wave)

Please see Xerte package on

cardiovascular measurements for more
details! This will be considered more
closely in the CV practical
 CARDIAC CONTRACTION
1. Atrial systole:
 A-V valves open and atria empty blood into ventricles
 Atrial excitation and contraction should be complete before onset of
ventricular contraction

2. Ventricular systole:
 Part 1: Ventricles contract  rise in pressure closes A-V valve
 Part 2: Pressure in ventricle rises above aortic pressure  aortic valve
opens and blood is ejected from heart

3. Ventricular diastole
 Part 1: Pressure in ventricles falls below aortic pressure  aortic valve
closes
 Part 2: Pressure in ventricles falls below atrial pressure  A-V valve
opens and filling begins
 CARDIAC FUNCTION
Cardiac output = Heart rate X Stroke volume
(litres / min) (beats/min) (ml/beat)
 At rest: 5 litres/min ~ 70 beats/min
X 70 ml/beat

 During exercise: 22 litres/min ~ 200 beats/min X 110 ml/beat

 Therefore, control of CARDIAC OUTPUT depends on:

 Factors affecting HEART RATE
 Factors affecting STROKE VOLUME

It is worth noting that increasing only heart rate may impair filling time,
reducing stroke volume
 STROKE VOLUME INFLUENCE BY SEVERAL
FACTORS
1. End Diastolic Volume (preload):
 Resting cardiac muscle stretched prior to contraction
 Venous tone, blood volume, posture, intrathoracic pressure

2. Aortic pressure (afterload):

 Pressure against which the heart must work to eject blood during systole
 Aortic stiffness, peripheral resistance, blood volume

3. Contractility:
 Strength and vigour of the heart's contraction (myocardial fibres) during systole,
at a given preload and afterload
 Increased by sympathetic nerve stimulation and circulating catecholamines,
calcium, positive inotropic drugs (Sympathetic  noradrenaline  β1-
adrenoceptors)
 Decreased by hypoxia, acidosis, infarction
 HEART RATE INFLUENCE BY SEVERAL
FACTORS

1. Intrinsic rate: heart can initiate its own heart beat in the absence of
any nervous or hormonal control
 Pacemaker (sino-atrial node)
 Conduction (atrio-ventricular node)

2. Influenced by:
 Sympathetic nervous system  noradrenaline  β1-adrenoceptors

Leads to increase in heart rate

 Parasympathetic  acetylcholine  muscarinic receptors

Leads to decrease in heart rate

 Hormones – e.g. adrenaline acting on β-adrenoceptors to cause an increase in
heart rate
 Extra/intracellular ions – e.g. K+
Arterial pressure (mmHg)
120 Systolic pressure Notch
caused by
Pulse closure of
pressure aortic
Mean valve
pressure
93

80 Diastolic pressure
systole diastole
Time (msec)

SYSTOLE - heart contracting (highest pressure)

 Systolic blood pressure ~ 120 mmHg

DIASTOLE - heart relaxing (pressure falls to lowest level)

 Diastolic blood pressure ~ 80 mmHg
 CONTROL OF BLOOD PRESSURE (BP)
Systolic Blood Pressure (SBP): Force the heart exerts on the walls of
the arteries every time it beats (~120 mmHg)
 Determined by:
 Stroke volume (StV)  increases in StV will increase in SBP
 Aortic elasticity  decreases in elasticity will also increase SBP

Diastolic Blood Pressure (DBP): Pressure within the arteries during the
period when the heart is not beating, as heart fills with blood (~80 mmHg)
 Determined by:
 Peripheral resistance (TPR)  increases in TPR, increase DBP
 Aortic elasticity  decreases in elasticity will decrease DBP
 Heart rate (HR)  decreases in HR will decrease DBP
MEASUREMENTS OF MEAN BLOOD PRESSURE
(BP)

Stroke volume (Stv) = End diastolic volume (EDV)

1
– End
systolic volume (ESV)
2 Cardiac output (CO) = Stroke volume (Stv) x Heart rate (HR)

3 Pulse pressure = Systolic BP – Diastolic BP

4 Mean BP = Diastolic BP + 1/3 Pulse pressure

5 Flow (cardiac output) = Mean

BP

Mean BP drives flow

Total peripheral resistance
FACTORS AFFECTING PERIPHERAL
RESISTANCE

Resistance = Pressure difference

Flow
 Changes in vessel radius have the greatest influence on
resistance; flow is inversely related to resistance

 Vasoconstriction  Decrease in diameter  increased resistance

 Vasodilatation  Increase in diameter  decreased resistance

 Left ventricular end systolic volume 110 ml
Left ventricular end diastolic volume 160 ml
Left ventricular end diastolic pressure 30 mmHg
Systemic arterial systolic blood pressure 140 mmHg
Systemic arterial diastolic blood pressure 80 mmHg
Heart rate 100 beats/min

1) What is the stroke volume?

 Stv = EDV-ESV = 160 ml–110 ml = 50 ml

2) Calculate the cardiac output:

 CO = Stv X HR = 50 ml/beat X 100 beats/min = 5000ml/min = 5L/min

3) What is the systemic mean BP?

 PP = SBP - DBP= 140 mmHg – 80 mmHg = 60 mmHg
 Mean BP = DBP + (1/3) PP = 80 mmHg + (1/3) 60 mmHg = 100 mmHg

4) Calculate the total peripheral resistance:

 TPR = Mean BP/CO = 100 mmHg / 5 L = 20 resistance units (mmHg/L/min)
 Mean BP = CO X TPR

 Systemic circulation:
 Mean BP (also called mean arterial pressure; MAP) ~ 100 mmHg
 Cardiac output (CO) ~ 5 litres/min
 Total peripheral resistance (TPR) ~ 20 Units (mmHg/litre/min)

 Pulmonary circulation:
 Mean BP (also called mean arterial pressure; MAP) ~ 10 mmHg
 Cardiac output (CO; right heart) ~ 5 litres/min
 Pulmonary vascular resistance ~ 2 Units (mmHg/litre/min)
 WHY IS CONTROL OF BLOOD PRESSURE
IMPORTANT?

 Arterial blood pressure is the driving force for the provision

of blood to tissues
 Too low  inadequate supply of oxygen and nutrients to
tissues
 Too high  Excessive strain on the heart and increased risk
of vascular damage

 In order to effectively control blood pressure, we need:

 Effector mechanisms  autonomic nervous system
 Pressure sensors  baroreceptors
EFFECTOR MECHANISMS: AUTONOMIC
CONTROL OF BLOOD PRESSURE

 Heart
 Parasympathetic (acetylcholine, muscarinic receptors, decrease
HR)
 Sympathetic (noradrenaline, β1- adrenoceptors, increase HR and
force)

 Vasculature (arterioles)
 Sympathetic  noradrenaline  α1, α2 - adrenoceptors cause
vasoconstriction
 Sympathetic  noradrenaline  β2- adrenoceptors cause
vasodilatation
 EFFECTOR MECHANISMS

 Arterioles are innervated by

the sympathetic nervous
system. In the peripheral
vasculature:
 Noradrenaline  α1-adrenoceptors
 vasoconstriction
 Noradrenaline  β2-adrenoceptors
 vasodilatation
Generally, sympathetic
stimulation leads to
vasoconstriction and increased
total peripheral resistance
(TPR)
 EFFECTOR MECHANISMS: PRESSURE
SENSORS (BARORECEPTORS)
 Located in the walls of major arteries (carotids and aorta; arterial
baroreceptors) and the heart/pulmonary blood vessels
(cardiopulmonary baroreceptors) where they sense changes in
transmural pressure (stretch)

FALL IN BLOOD PRESSURE (supine  standing)

Sensed by baroreceptors (decrease venous return, CO, MAP)
Afferent input to CNS cardiovascular centres
Information centrally integrated
Efferent output via autonomic nervous system
Increased sympathetic drive to heart and blood vessels
Increase in HR, StV (therefore CO) and TPR
RISE IN BLOOD PRESSURE TOWARDS NORMAL
Baroreceptor Central
Reflex Integration
LEARNING OBJECTIVES 1:

State State the essential properties of myocardial pacemaker cells

Draw a diagram of an action potential as would be recorded from

Draw a pacemaker cell in the sinoatrial node or classical ‘ventricular’
cell and describe its ionic basis

Describe briefly the sequence of events by which excitation

Describe spreads from the sinoatrial node through the heart

Define the terms cardiac output, heart rate and stroke volume and
Define give approximate values for these in man

State the influence of venous return on cardiac output and explain

State how preload, afterload and contractility may affect cardiac output
LEARNING OBJECTIVES 2:

Define the terms systolic blood pressure, diastolic pressure, pulse

Define pressure and mean blood pressure

Understand Understand factors that affect total peripheral resistance

Describe the effector mechanisms involved in autonomic control

Describe of the circulation, and list receptor subtypes involved

State the influences of pressure sensors (baroreceptors) and

State central integration on overall regulation of blood pressure

Draw a box and arrow diagram illustrating the arterial

Draw baroreceptor reflex