Cardiac Rehabilitation Flashcards
Health definition
a state of complete physcial, mental and social well being not just the absence of disease or illness
effect of fitness on mortality rate
higher levels of fitness = lower mortailty rate
effect of being unfit and becoming fit
increases mortality slightly
effects of being fit and becoming unfit
mortality increase
effect of being unfit and staying unfit
hgihest mortality level
every 1 MET increase in areobic fitness = ?% decline in mortality
10-15% decline
when are the greatest health benefits achived
A. sedentary to mod
b. mod to high
A. when increasing PA from sedentary to moderate
each 10mins of MVPA results in a ?% decrease mortaility risk
10%
each 150mins of MVPA results in a ?% decrease mortaility risk
30-40%
each 750mins of MVPA results in a ?% decrease mortaility risk
50%
PA reduces relative risk of dementia by ?%
30%
PA reduces relative risk of depression by ?%
30%
PA reduces relative risk of T2D by ?%
40%
PA reduces relative risk of CVD by ?%
35%
PA reduces relative risk of all-cause mortailty by ?%
30%
questions to ask when assessing PA
medical history medications PA levels - current and historic likes/dislikes lifestyle/employment motivations
stroke volume equation
SV = preload - afterload
preload def
the amount of blood in the ventricles before contraction
end diastolic volume
afterload def
amount of blood in the ventricles after contraction
end systolic volume
ejection fraction equation
EDV-ESV/EDV x100 or SV/EDV
shortening fraction def
how much the chambre reduces in size at rest
35%
factors affecting HR
PNS
SNS
adrealine
factors affecting preload
ventricle size
venous return
ventricular plasticity
factors affecting afterload
contractility
systematic vascular resistance
effect of PNS and SNS on HR
PNS decrease, from 100 to 0
SNS increase, from 100+
effect of SNS on contractility
increases
limiting factor of heart hypertrophy
pericardium
what is the frank starling mechanism
increased stretching of the myocardial will increase strength of contractions
cardiac muscle properties
same length-tension properties to skeletal
operates well below optimum length
typical blood volume in adults
5L
distribution of blood during rest
5000ml liver - 27% kidneys 22% brain 14% (700ml) heart 4% muscle 20%
distrbution of blood during exercise
25,000ml
how much blood resides in veins during rest
2/3s
70%
vasodilators
increased NO K+ Co2 lactate prostaglandins bradykinis
vasoconstrictors
increased SNS activity relases NE
factors that increase venous return during exercise
increased SNS activity
constriction of venous smooth muslce
venoconstraiction
muscle contraction
how much of the blood is shunted through venoconstricition
20%
explain venous return pumps
high pressure during contraction
low pressure during relaxation
creates a vaccum sucking blood towards heart
what is ventricular rotation
due to the order the heart contracts from the elcetrical signal the heart twists as it contracts
atrial twists clockwise
ventricles - anticlockwise
effect of ventricular rotation
helps faciliate blood ejection
means it moves over a gretaer distance so recolis further allwoing more blood to enter
what is the respirtatory venous pump
pressure increases in the thorax during expiration - blood returns to heart
low pressure during inspiration creates a vaccum sucking blood towards heart
factors which affect afterload
any that impede ejection of blood
- volume of blood in the arterial contraction
- pressure in the aorta at onset of ejection (DAP)
- compliance of aorta
- size of pulmonary/aorta lumen
at what blood pressure does Q decrease
approx 150mmHg
effect of increase afterload
SV reduces in the acute phase
preload increases (to restore SV)
reduced velocity of contraction and ejection in acute phase
markes rise in myocaridal O2 consumption
Mechanoreceptors
detect stretch and contraction
faciliate reflex
signal to brain to alter HR
Metaboreceptors
chemical activation of the afferent receptors in interstitum of the muscle
type IV unmyleinated afferent receptor
what are metaboreceptors sensitive to
increased
- lactacte
- prostaglandins
- phosopahte
Baroreceptors
detect changes in BP
in walls of carotid sinus and aortic arch
sense arterial pressure
stretched activated
Baroflex for decreased BP
baroreceptor stimulated cardioacceleratory centre inhibited cardioinhibitory centre stimulated vasomotor centres = decreased Q and vasodilation
chemoreceptors
detect changes in levels of O2 and CO2
located in walls of carotid sinus and aortic arch
bainbridge reflex
increased cardiac filling elicts tachycardia
increase right atrium filling from increase venous return
stretch receptors in rigth atrium and vena cava stretched
increased firing to brain
increased HR and SV
effect of tachycardia on diasolic time
decreases diastolic time
what is the endothelium
inner most layer of artery
permable barrier that allows through flow of nutritents and metabolic end products
what does the endothelium produce /release
produces growth factor
releases platlets aggregation, clotting and anti-clotting substances
process of atherosclerosis
damage to endotehlium
damage monocytes adhere to endothelium become macrophages secrete growth factor and vasocontraction substances infitraion of LDL casues inflammation LDL oxidised caused
process of atherosclerosis
what do marcophages secrete
growth factor and vasocontraction substances
what does the infiltraion of LDL into the intima cause
inflammation
what does LDL release when its oxidises
leukocyte adhesion molecules
what happend when LDL taken up by macropahges
macrophages become foam cells
what do vascular cell adhesion molecules cause endothelium to become
becomes sticky rather than smooth
what adhere and attract to VCAM
platlets
monocytes
lymphocytes
what do t cells release and whats the effect
release growth factors
cause proliferartion and attract smooth muscle cells
what are fatty plaques filled with
cholestrol laden particles platlets calcium lymphocytes, macrophages abnormally spreading smooth muscle cells connective tissue cells
what reduces plaque stability
inflammatory response
- increase inflammatory cytokines
- release protease
- release prothrombotic and procoagulant factors
effect of protease
weaken collagen
effect of prothrombotic and procoagulant factors
cause a clot when plaque ruptures
what damages the endothelial layer
normal microvasuclar wear and tear viral attack high BP turbulent flow free radicals carbon monoxide elevated blood glucose and lipids
stenosis
narrowing of arteries
