ANATOMY AND PHYSIOLOGY OF REPRODUCTIVE SYSTEM.pptx
Hepc01 cv system 2012
1. HEPC01HEPC01
Sport & ExerciseSport & Exercise
Physiology & AnatomyPhysiology & Anatomy
The Cardiovascular SystemThe Cardiovascular System
To get the full experience of this
lecture please download this FREE
app
You will also need a QR code reader app
2. Respiratory recapRespiratory recap
Describe the passage of air through the
respiratory system
How is gas breathed in and out mechanically?
What factors affect the rate that we
breath at?
What is FVC?
What happens if you hold your breath whilst
exercising?
3. Aims/ObjectivesAims/Objectives
The components of CV system
Factors that affect the Heart’s output
How blood is transported around the body
Blood pressure and response
Electrical activity of the heart
Regulation of the heart’s activity
Some responses to activity
5. Major Cardiovascular Functions
Delivery (O2 and nutrients)
Removal (CO2 waste products)
Transportation (Hormones)
Maintenance (Body temperature, pH)
Prevention (Infection—immune function)
What are the functions?
9. Atrioventricular (AV)Atrioventricular (AV)
valvesvalves
Separate theSeparate the
atria from theatria from the
ventriclesventricles
– bicuspid (mitral)bicuspid (mitral)
valve – left sidevalve – left side
– tricuspid valve –tricuspid valve –
right sideright side
anterior
10. Semilunar valvesSemilunar valves
Pulmonary
semilunar valves
Aortic semilunar
valves
Things that can go wrong
– Incompetent – does’nt
close correctly
– Stenosis – hardened,
even calcified, and does
not close correctly
13. Factors Affecting SVFactors Affecting SV
3 most important factors:3 most important factors:
–Preload
–ContractilityContractility
–AfterloadAfterload
amount ventricles are stretchedamount ventricles are stretched
by contained bloodby contained blood
cardiac cell contractile forcecardiac cell contractile force
due to factors other than EDVdue to factors other than EDV
back pressure exerted byback pressure exerted by
blood in the large arteries leaving the heartblood in the large arteries leaving the heart
14.
15. The Blood VesselsThe Blood Vessels
ARTERY
VEIN
CAPILLARY
Aorta Arteries Arterioles
Capillaries
Capillaries Venules Veins
Vena Cava (S or I)
16. Arterial systemArterial system
High pressureHigh pressure
tubes, conduct Otubes, conduct O22
rich bloodrich blood
Composed of layersComposed of layers
of connective tissueof connective tissue
and smooth muscleand smooth muscle
Thick walls so noThick walls so no
gas exchangegas exchange
occursoccurs
AortaAorta
ArteriolesArterioles
CapillariesCapillaries
ARTERY
20. Blood pressureBlood pressure
Surge of blood enters aorta with eachSurge of blood enters aorta with each
contractioncontraction
Peripheral vessels do not allow run off asPeripheral vessels do not allow run off as
rapidly as it is ejected from heartrapidly as it is ejected from heart
Therefore a portion is stored in aortaTherefore a portion is stored in aorta
This creates pressure down arterial system toThis creates pressure down arterial system to
remote branches (pulse)remote branches (pulse)
21. Arterial blood pressureArterial blood pressure
BP = force exerted by blood againstBP = force exerted by blood against
arterial wallsarterial walls
– How much blood is pumpedHow much blood is pumped
– Resistance to blood flowResistance to blood flow
SphygmomanometerSphygmomanometer
Normal - 120 mmHgNormal - 120 mmHg
8080
Systolic / diastolicSystolic / diastolic
25. HypertensionHypertension
<120/<80 – normal<120/<80 – normal
140-159 / 90-99 – Stage 1 hypertension140-159 / 90-99 – Stage 1 hypertension
160 or higher / 100 or higher – Stage 2160 or higher / 100 or higher – Stage 2
Absolute contraindicaction -Absolute contraindicaction -
26.
27. Mean Arterial PressureMean Arterial Pressure
DBP +PP (pulse pressure)DBP +PP (pulse pressure)
The pressure the arteries wouldThe pressure the arteries would
sustain if blood flow was constantsustain if blood flow was constant
See alsoSee also Rate-Pressure ProductRate-Pressure Product
The workload of the myocardiumThe workload of the myocardium
SBPxHR/100SBPxHR/100
Angina…Angina…
29. Electrical ActivityElectrical Activity
SA node generates impulse; atrial excitation begins
Impulse delayed at AV node, then passed to ventricles
Enters AV bundle branches, excitation begins at apex
Purkinje Fibres spread throughout vent. (speed x6)
37. Cardiac ArrhythmiaCardiac Arrhythmia
4) Ventricular tachycardia4) Ventricular tachycardia
– 3 or more premature contractions can3 or more premature contractions can
lead to ventricular fibrillationlead to ventricular fibrillation
– Heart cannot pump bloodHeart cannot pump blood
– Cause of most cardiac deathsCause of most cardiac deaths
– CPRCPR
38. Cardiovascular responseCardiovascular response
to exerciseto exercise
Anticipatory Heart Rate
The brain releases chemicals when you think you are
about to exercise. This increases HR before any
physical activity is performed.
Redirection of blood flow
Vasodilation
Vasoconstriction
Increase in heart rate in line with intensity
What would the maximum HR be?
Short Term changes are seen when exercise is being
performed.
39. Blood Flow Changes During Exercise inBlood Flow Changes During Exercise in
cmcm33
/min/min
40. Short term response to exercise –Short term response to exercise –
Blood PressureBlood Pressure
250mmHg!!
115mmHg!!
+20mmHg!!
44. Review of the Aims/ObjectivesReview of the Aims/Objectives
The components of CV systemThe components of CV system
Factors that affect the Heart’s outputFactors that affect the Heart’s output
How blood is transported around the bodyHow blood is transported around the body
Blood pressure and responseBlood pressure and response
Electrical activity of the heartElectrical activity of the heart
Regulation of the heart’s activityRegulation of the heart’s activity
Some responses to activitySome responses to activity
The Frank-Starling law of the heart (also known as Starling's law or the Frank-Starling mechanism ) states that the greater the volume of blood entering the heart during diastole (end-diastolic volume), the greater the volume of blood ejected during systolic contraction (stroke volume). This means that as the heart fills with more blood than usual, the force of the muscular contractions will increase; this is a result of an increase of the load experienced by each muscle fibre due to the extraneous blood entering the heart. This stretching of the muscle fibres increases the affinity of troponin C for Calcium, causing a greater number of cross-bridges to form within the muscle fibres; this increases the contractile force of the cardiac muscle. The force that any single muscle fiber generates is proportional to the initial sarcomere length (known as preload), and the stretch on the individual fibers is related to the end-diastolic volume of the ventricle. In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometers, a length which is rarely exceeded in the normal heart. Initial lengths larger or smaller than this optimal value will decrease the force the muscle can achieve. For larger sarcomere lengths, this is the result of less overlap of the thin and thick filaments; for smaller sarcomere lengths, the cause is the decreased sensitivity for calcium by the myofilaments. This can be seen most dramatically in the case of premature ventricular contraction. The premature ventricular contraction causes early emptying of the left ventricle (LV) into the aorta. Since the next ventricular contraction will come at its regular time, the filling time for the LV increases, causing an increased LV end-diastolic volume. Because of the Frank-Starling law, the next ventricular contraction will be more forceful, causing the ejection of the larger than normal volume of blood, and bringing the LV end-systolic volume back to baseline. For example, during vasoconstriction the end diastolic volume (EDV) will increase due to an increase in TPR(Total Peripheral Resistance) (increased TPR causes a decrease in the stroke volume which means that more blood will be left in the ventricle upon contraction - an increased end systolic volume (ESV). ESV + normal venous return will increase the end diastolic volume). Increased EDV causes the streching of the venticular myocardial cells which in turn use more force when contracting. Cardiac output will then increase according to the Frank-Starling graph. The above is true of healthy myocardium. In the failing heart, the more the myocardium is dilated, the weaker it can pump, as it then reverts to Laplace's law.
65% of blood at rest held in veins. Capacitance vessels. Venous Pooling Varicose veins.
At rest only 1 in 30-40 capillaries are open. Refer to decreased peripheral resistance Nitric Oxide released when vessels stretched . This in turn dilates blood vessels. Muscle tissue – 0.01mm diameter / 2000/3000 capillaries/m 2 Heart Muscle more dense. No cell more than 0.008mm from capillary
Platelets are important in healing injuries. Extension activity – discuss haemophilia.
DBP stays the same during exercise… It measures peripheral resistance…diameters of blood vessels dilate during exercise which counters the increase in heart rte…if up vessesl are not dilating