Transcript Cardiovascular System & Disease

Course Contents
Section 1
Exercise and the cardiovascular system
1.1
Structure and function of the cardiovascular system
1.2
Pathology of cardiovascular diseases (CVD)
1.3
Role of exercise in prevention and treatment of CVD
Section 2
Exercise and Metabolism
2.1
Energy
2.2
Body composition & Weight Control
2.3
Diabetes Mellitus
2.4
Osteoporosis
BHF Survey, 2007
Scottish Stats
Deaths from CHD
The CVS is subject to disease processes e.g.
Atherosclerosis & hypertension are disease processes that
lead to the development of :
Structure/ Function of CVS

2 parts:
Pump
 Vessels

Heart
Heart external
view

Double pump
Right side – pumps to lungs (pulmonary
circulation)
BICUSPID
 Left side – pumps to body (systemic
(mitral)
circulation
VALVE
 Left
side > right side
TRICUSPID
VALVE
 Heart
Valves prevent backflow of blood
 Coronary arteries supply heart muscle with
blood (food & oxygen)

SEMILUNAR VALVE
Heart & Blood Supply
Pulmonary artery – deoxygenated blood
 Pulmonary
N.B.
Hepatic Portal vein
Vein – oxygenated
 Coronary
arteries
– heart.
supply heart
does not return
blood to

 Coronary veins – drain into the right atrium
Supplies
liver with products of digestion.
Aorta
- blood
body
(from L. ventricle)
Important
in firstto
pass
metabolism
 Vena cava
(sup./toxins
inf.)to -bedrain
(into
– allowing
broken body
down before
systemic circulation
R atrium)

Heart Beat

Heart beat is endogenous (continues to beat if
removed from body)


Rhythmical contraction of muscles
Under nervous/ hormonal control


Influence strength & frequency of contraction
Heart beat originates in SinoAtrial node



Max. rate limited (refractory period)
AV node collects signal and initiates ventricular
contraction via Bindle of His after a short delay.
In disease, arrythmia can develop in damaged tissue


Extra heart beat can occur initiated by damaged tissue
Heart beat signal propagated through heart by bundle
of His (atria – ventricles), & Purkinje fibres (nerves
through muscle tissue)
Heart Sounds

Stethoscope
Listen to heart sounds
 Lub dub (closing of valves)

Lub – closure of AV valves
 Dub – closure of semilunar valves


Diagnostic of valvular disease

Leaky – indistinct lub/ dub
Heart & ECG

ECG is a record of the electrical signals
producing the heart beat


ECG= ElectroCardioGram
Used diagnostically to show heart
problems
Cardiac Cycle

DIASTOLE (relaxed phase)

Venous filling of atria


Atria distend
Some passive flow into ventricles

SYSTOLE (contractile phase)

SA initiates atrial contraction
Blood expelled from atria into ventricles
Bundle of His conducts excitation to
ventricles/ propagated rapidly by Purkinje
fibres
Ventricle contracts expels blood into arteries
Contraction ends, relaxes (refractory period)




Blood Vessels
Arteries
 Must withstand high pressure



Thick walled
Mainly elastic fibres near heart



Arteries more distant from heart less elastic fibres/
more muscle (under nervous control)


Stretch to absorb pressure of blood expelled by heart
At diastole stretched arteries relax so maintain blood
flow (120/80 mmHg)
Muscles regulate blood flow into capillary beds
Arteries lead to arterioles

Can have pre-capillary sphincters to completely close
blood flow e.g to skin in cold
Blood Vessels

Capillaries
Wall single cell thick
 Allows exchange of soluble substances
 No cell more than few cell widths from a
capillary
 Diffusion rapid over these short distances

Blood vessels

Veins
Less muscle/ elastic fibre than arteries
 Floppy
 Low pressure in vein – requires valves to
stop backflow
 Muscle pumping in calves helps venous
return (Economy Class Syndrome)

Blood Pressure
High arterial blood pressure (80-120
mmHg (systolic/ diastolic)
 Rapid fall in BP in arterioles/ capillaries
 Very low BP in veins

Blood Pressure

BP quoted as Systolic / diastolic
Measure with a sphygmomanometer
 Block all blood flow
 Slowly release pressure
 Systoliic BP = pressure when sound of
artery closing (snap) is heard
 Diastolic BP = pressure when all noises
stop

Summary of Structure
Cardiovascular Disease

Coronary Heart disease
Angina pectoris
Myocardial infarction
CVD s
Cerebrovascular disease
Stroke (cerebrovascular
accident (CVA))
Cardiovascular disease
pathology

Two major pathological processes lead to
CVD

Atherosclerosis


Narrowing & hardening of arteries (claudication/ angina)
Damage to endothelium
– promotes blood clot formation
 blocking arteries – thrombosis/ embolism

Hypertension

Prolonged, elevated blood pressure
– Primary – no known cause
– Secondary – caused by pathology
 Kidney disease
 Phaeochromacytoma (excess epinephrine produced)
Atherosclerosis

Typically starts in childhood, progresses in
adulthood.
 Damage to the arterial wall caused by e.g.




elevated levels of cholesterol and triglyceride in
the blood
high blood pressure.
tobacco smoke
diabetes
Atherosclerosis

Fat accumulates under inner lining of arteries



As disease progresses, fibrous material / calcium/
lipids (inc. cholesterol) accumulates (atheroma)
Bulges into lumen of vessel
Starts to reduce diameter of artery



Restricts blood flow
Reduces elasticity of arterial wall
Can lead to high blood pressure
Atherosclerosis

Progression accelerated by:






High blood cholesterol (especially LDL or "bad"
cholesterol over 100 mg/dL)
Cigarette smoking and exposure to tobacco
smoke
High blood pressure
Diabetes mellitus
Obesity
Physical inactivity
Cholesterol & CVD

Cholesterol – steroid
– Cell membranes, hormones, bile salts
Most cholesterol in blood is synthesised by liver
 Dietary cholesterol acts to suppress liver biosynthesis


Dietary cholesterol NOT important risk factor for
CVD (overall cholesterol should be less than
200mg/dl)
Saturated fats (animal) are used by liver to
produce cholesterol
 High dietary saturated fat INCREASES blood
cholesterol levels!!

Cholesterol & CVD

Cholesterol – insoluble in blood


Transported attached to a protein LIPOPROTEIN
Two types of LIPOPROTEIN


HDL – High density lipoprotein
LDL – Low density lipoprotein

HDL – transports cholesterol to liver for destruction

LDL – transports cholesterol to body cells for
deposition
GOOD
BAD

In abnormal circumstances LDL will deposit cholesterol in
arteries
Cholesterol & CVD

LDL (bad) – 60-70% blood cholesterol


As LDL increases risk of atherosclerosis
increases
HDL (good) – 20-30% blood cholesterol

AS HDL increases risk of atherosclerosis
decreases
Risk of CHD is predicted from HDL:LDL ratio
 High HDL (40mg/dl or more):LDL is GOOD
 Exercise, low fat diet, not smoking improve
HDL:LDL ratio

Atherosclerosis – Heart - AP

Narrowing of coronary arteries leads to
ischaemia (inadequate blood flow)


Pain - angina pectoris (AP) due to ischaemia in
heart muscle
AP only during exertion of heart (when O2 needs
are high)



Glycerol trinitrite tablets release Nitric oxide (dilates
blood vessels)
Angioplasty/ Stents
Bypass surgery
Atherosclerosis – Embolism

Clots


thrombus-attached
embolus-travelling
Embolus/ thrombus can cause blood supply to a
region of the heart muscle (myocardium) to
become blocked, causing myocardial infarction
 Thrombosis/ embolus may occur in cerebral artery
– stroke (cerebrovascular accident-CVA)
 or lungs pulmonary embolus

Myocardial Infarction

Myocardial infarction – MI (death of heart tissue)

Caused by a sudden blockage to a coronary artery.





Due thrombosis/ embolis
Atherosclerosis (may cause angina symptoms) leads to increased
likelihood that thombosis will occur.
Causes pain (15 min) in arm, neck, jaw; nausea.
If large artery blocked – collapse, sudden death
Tissue dies forming a scar, can cause:



Heart failure (weak pumping action)
Arrythmia, irregular contraction
Cardiac arrest – ventricular fibrillation
Hypertension
Persistently high resting blood pressure
e.g. diastolic >90mmHg (normal
120/80; high 140/90)
 Often caused by atherosclerosis leading
to narrowing of arteries or loss of
elasticity


Risk factor for majority of CVDs (incl. CHD)
Hypertension – risk factors





Diet (high salt
(Na+), high fat)
 Nicotine (vasoconstrictor)
Smoking
Obesity
Genetic
predisposition
Stress
Risk Factors for CVD- SQA

Modifiable


Diet, Smoking, Activity, Obesity
Non modifiable

Age, Gender, Race, Heredity
Risk factors Summary
What other factors contribute to heart disease risk?
•Diabetes•The
mellitus
—heart disease in people who drink
risk of
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andseriously
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is defined
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the
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likely
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develop
heart
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and stroke
Physical
inactivity
•Aboutounces
three-quarters
of
people spirits
with diabetes
of some form of
(fl oz)
ofother
80-proof
(such asdie
bourbon,
even
if
they
have
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risk
factors.
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moderate-to-vigorous
physical
activity helps
prevent
heart
heart
or
blood
vessel gin,
disease.
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1
fl
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blood
pressure
High
cholesterol
and blood
blood
vessel
disease.
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weight
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the
heart's
work.
Itworkload,
also raises
blood
oz
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12
fl
oz
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beer.
It's
not
recommended
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blood
pressure
increases
the
heart's
causing
As
blood
cholesterol
rises,
so does
risk
of coronary
heart
The
more
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and
blood
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and
that
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that
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the
heart
to
thicken
and
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stiffer.
disease. Physical activity can help control blood cholesterol, diabetes and
lowers
HDL
("good")
cholesterol
levels.
increase
the
amount
they
drink.
Tobacco
It
also
smoke
increases
your
risk
of
stroke,
heart attack,
kidney failure
When
other
highpressure
blood pressure
and
tobacco
obesity,
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in some
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and
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may have
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losing
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person's
level
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by age,
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•
Exposure to other people's smoke increases the risk of heart
disease even for nonsmokers.
Exercise & CVS

Cardiovascular system (CVS) delivers oxygen
& nutrients to body tissues, removes wastes


During exercises more O2 & nutrients required by
exercising tissues (muscles), wastes removed
Exercise effects Cardiovascular system
function


Cardiac output increased
Circulation redistributed to important tissues
Cardiac Output
Cardiac output (C.O.) = volume of
blood pumped per min. by the heart
 Regulated by:

– Heart rate (H.R.)
– Stroke volume (S.V.)

C.O. = H.R. x S.V.
Exercise effects on Heart
Exercise causes HR & SV to increase i.e.
CO
 Meets needs of muscles

Athlete’s Heart


Regular exercises strengthens heart muscle
Ventricular mass (echocardiography) increases (210-300g)
 Force of contraction , more blood expelled per beat (SV )

Ventricular volume also increases (100-180ml) (SV )
 Consequently HR at rest of a trained athlete 
 (Bjorn Borg – 32bpm, Miguel Induraine, 29bpm)

CO of trained heart increased so more O2 and food
delivered at max. HR

Therefore max. level of activity greater
Redistribution of Blood flow
During exercise blood flow directed
away from non-essential needs (gut,
kidney)
 Redirected to heart, muscles, skin
(cooling)
 Vasodilation/ vasoconstriction of
supplies to these tissues.

Exercise & Blood Pressure

Cardiac Output increased (HR/ SV)


Tends to increase BP
Vasodilation of blood supply to muscles
Increases volume of vascular system
 Peripheral vascular resistance reduced
 Tends to reduce BP

Overall slight increase in BP
 Systolic increase > diastolic

Exercise & Hypertension
Regular exercise, produces long term,
moderate fall in BP
 Offsets age related hardening of arteries
 Acutely, a fall in BP is also found following
exercise.

Role of exercise
- in preventing CVD

Decreases a number of risk factors:







HDL , LDL 
Resting HR 
Arterial blood pressure 
Body fat  (i.e. obesity )
Reduces development of atheroma
Reduces stress
Moderate exercise 3-5 times per week lasting
more than 20mins
Exercise testing - Introduction
Monitor recovery from MI
 Monitor improvement in athletic training
programme

Measure aerobic capacity
 Assess performance of respiratory and
cardiovascular systems in delivering oxygen

Exercise testing - Principles
Oxygen required by body to work
 Maximum work rate – determined by body’s
ability to deliver oxygen to body




VO2max – maximal oxygen uptake
Higher the VO2max, the greater the aerobic fitness
Measure by exercising to exhaustion and
directly measure O2 uptake and CO2 ouput
Exercise testing – Direct Method

Treadmill/ bicycle ergometer
Using online gas analysis
 Progressively increase workload until no
further increase in O2 consumption
 i.e. exercise to exhaustion
 Oxygen consumption at that point =
VO2max


Suitable for fit people
Exercise testing – Indirect
Method

Shuttle test
Run between two cones (20m apart)
 Rate determined by a tape (beep)
 Subject continues until they can’t maintain
pace


Number of completed shuttles can be
used to predict VO2max
Exercise Testing – Sub maximal






If exercise to exhaustion clinically contraindicated
Submaximal testing used
Patient O2 consumption measured at various
levels of work intensity (submaximal)
Graph of O2 consumption vs. HR plotted
Theoretical max. HR calculated (220-age)
Graph extrapolated to estimate theoretical
max. O2 consumption
Exercise Testing – Sub maximal

Assumptions:


Direct relation between HR and O2 consumption
and intensity of exercise
Sources of error:

HR affected by other factors:
– Emotion
– Temperature
– Anxiety

Predicted HR may be inaccurate for a given
individual
Exercise Stress Testing
Used to diagnose heart abnormality
only present under stressed conditions
 Bruce Protocol

Treadmill speed/gradient increased
incrementally
 Exercise to exhaustion


ECG can be monitored to evaluate
effect of exercise on heart