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ECG and Blood Pressure Control

Sport and Exercise Science Lecture on BP control and recap on ECG
by

Alan Richardson

on 29 November 2016

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Transcript of ECG and Blood Pressure Control

How and why do we control blood pressure?
Dr Alan Richardson
Vein
Artery
Atherosclerosis
Plaque build up around the vascular walls

Become rigid – reduced distensibility and contractility.

Endothelial function – Reduced nitric oxide release.

All increase total peripheral resistance (TPR)

Blood Flow
Blood Flow = Δpressure / resistance

Vasoconstriction: radius of the vessel decreases, decreasing blood flow

Vasodilation: radius of the vessel increases, increasing blood flow

Capilliarisation
Increased Haemoglobin Mass
Increased Red Blood Cell Count
Greater Viscosity
Slower Blood Movement
Total Peripheral Resistance

X

Cardiac Output
Blood Pressure
?
Vasodilation
Vasoconstriction
Local Factors
Venous Return
Body Position
pH
Hypoxia
Altitude
Catecholamines
Angiotensin
Health
Artherosclerosis
Nitric Oxide
Kinins
Prostaglandins
Vascular Distensibility
TPR
Q
Sodium
Blood Volume
Cell Mass
Plasma Volume
Cardiac Function
Contractility
Heart Rate
Stroke volume
(Related to Venous return)
Cardiac Volume
Cardiac Efficiency
Hormones
ADH
ANP
?
EXERCISE
Resistance Exercise
Aerobic Exercise
Peak Systolic
Peak Diastolic
Smaller muscle mass of upper body (localised blood flow)

Change in breathing patterns = changes in intrathoracic pressure

Muscle mass constricts vessels increasing TPR

Recovery?
Due to pooling of blood in visceral organs or lower limbs and post exercise vasodilation.

Supports use of exercise as a non-pharmacological treatment for hypertension

BP decreases after submaximal exercise to less than
pre-exercise values for both normotensive and
hypertensive people

If resting = 120mmHg, post exercise will be ~110mmHg and
stabilises at 120mmHg after 12 hours

WHY?
Consider the changes in blood pressure for both aerobic and resistance activity.
What are the key differences? What mechanisms cause the changes?......


Aerobic: High systolic, small change in diastolic.

Resistance: Large increase in both values

Causes
Aerobic: Large cardiac output = Increased systolic,
Minor vasoconstriction with ex induced sympathetic neural tone, although muscles release some vasodilators – so diastolic relatively unchanged

Causes
Resistance:
Localised blood flow
Upper body work induces greater BP due to smaller muscle mass of upper body
and the need to stabilise the body.
Breathing patterns are altered increasing the intrathoracic pressure (valsalva maneuver)
= Increased TPR.

What factors influence each of these?
Transportation
Temperature regulation
Acid–base (pH) balance

Localised Blood Flow
Stimuli to increase local blood flow

Metabolic factors
increased oxygen demand
increases in metabolic by-products
inflammatory chemicals

Endothelium released factors
Nitric oxide
Prostaglandins
Endothelium-derived hyperpolarization factors (EDHF)

Myogenic responses

Neural vasoconstriction

Read about cardiac morphology

Consider what morphological changes you would undergo in your sport.

What negatives are their to cardiac morphology?

We will be discussing next week
Directed Study
Neural Stimulation of the Cardiac
A 54yr old gentlemen has a stroke volume of 49ml/bt and an end systolic volume of 53ml. What is the gentlemen’s ejection fraction?

At maximal exercise his EDV can reach 131ml and his ESV can reach 43ml. What is his maximal predicted cardiac output?

SV = EDV – ESV
49ml/bt = ? – 53ml
EDV = 102ml
EJ = (SV / EDV) *100
EJ = (49 / 102) *100
EJ = 48%

SV = EDV – ESV
88ml/bt = 131 - 43
SV * HR (220 - age) = Q
2. 88ml/bt * 166bt/min = 14.6L/min

ECG
Sinus Rhythm
Sinus Tachycardia
Atrial Flutter
Ventricular Fibrillation
Premature Ventricular Complex
ST Depression
Asystole
Atrial Fibrillation
Neural Activation
Climate
Endothelial Function
Capilliarisation
Activity
Muscular Contractions
Viscosity
Activity
Full transcript