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purposes of the cardiorespiratory system
transport O2 and nutrients to tissues
removal of CO2 wastes from tissues
regulation of body temperature
two major adjustments of blood flow during exercise
increased cardiac output
redistribution of blood flow
path of blood
vena cavae —> right atrium —> right AV (tricuspid) valve —> right ventricle —> pulmonary valve —> pulmonary arteries —> lungs —> pulmonary veins —> left atrium —> left AV (bicuspid) valve —> left ventricle —> aortic valve —> aorta —> systemic circulation
chordae tendinae
fibrous cords that anchor the AV valve to the ventricle walls and keep them from flipping backwards when the ventricle contracts
heart
organ that creates pressure to pump blood
does not create flow, creates PRESSURE
pulmonary circuit
right side of the heart
pumps deoxygenated blood to the lungs via pulmonary arteries
returns oxygenated blood to the left side of the heart via pulmonary veins
systemic circuit
left side of the heart
pumps oxygenated blood to the whole body via arteries
returns deoxygenated blood to the right side of the heart via veins
order of heart mechanisms
AV valves open —> ventricles fill passively —> atrial contraction (or kick) —> ventricular contraction —> aortic/pulmonary valves open —> ejection through the pulmonary artery/aorta
electrical event —> mechanical event —> pressure change —> volume change
myocardial infarction
when a part of the heart’s wall dies
myocardial ischemia
when a part of the heart’s wall is not getting enough oxygen due to lack of blood flow and could lead to a myocardial infarction
endocardium
innermost layer of the heart
-it’s made up of simple squamous cells and it’s what lines the atria and ventricles
myocardium
thick, middle later of the heart made up of cardiac myocytes
-blood vessels are found here
pericardium
outermost layer of the heart and it has 3 layers of its own
-the middle layer is the pericardial cavity and it contains fluid that allows for friction-free beating of the heart
-outermost layer is fibrous, fatty, and is strongly attached to the great vessels, sternum and diaphragm
cardiac muscle (myocardium)
type of muscle that only has one fiber type and it similar to type I muscle fibers
has high capillary density
high number of mitochondria
striated
only one nucleus per cell
small, short, branched
continuous, involuntary rhythmic contractions
calcium-induced calcium release with calcium coming from sarcoplasmic reticulum and from outside the cell
no satellite cells present
ventricular systole
contraction phase
ejection of blood in pulmonary and systemic circulation (~2/3 blood is ejected from ventricles per beat)
pressure in ventricles rises
semilunar valves open when ventricular P > aortic P
is shorter during exercise
ventricular diastole
relaxation phase
filling with blood from atria
pressure in ventricles is low
AV valves open when ventricular P < atrial P
takes longer than systole when you’re at rest
is shorter during exercise
average aortic bp
120/80 mmHg
pressure the heart must pump against to eject blood
“afterload”
heart sounds
“lub” sound: closing of AV valves
“dub” sound: closing of aortic and pulmonary semilunar valves
isovolumetric relaxation
occurs in early diastole and all gates are closed here
stroke volume
the amount of blood ejected from the ventricle
SV=EDV-ESV
SV=CO/HR
end-diastolic volume (EDV)
volume of blood left at the end of ventricular filling
preload
end-systolic volume (ESV)
volume of blood left in the ventricle after contraction
atrial kick
the atrial contraction that gives ventricular filling an extra boost
c wave
the bump that follows the atrial kick in the Wigger’s diagram
is due to the AV valves bulging into the atria
v wave
the final point before the AV valve opens again and the ventricles begin to fill in the Wigger’s diagram
aortic valve shutting causes this bump in the aortic pressure line
cardiac output
the amount of blood your heart pumps per minute
CO = HR * SV
P wave
part on an ECG that denotes when the blood moves from the atria into the ventricles (so it’s part of diastole)
lasts 0.8 seconds
represents the depolarization of the atria
QRS complex
part of the ECG that…
represents ventricular depolarization
causes ventricular contraction
leads to AV valve shutting
leads to aortic valve opening
transitions into phase 2 (isovolumetric contraction, then ejection)
typically 0.06 to 0.1 seconds
polarization, depolarization, to even stronger repolarization
T wave
part of the ECG that denotes when blood moves from vena cavae to atria
early diastole
ventricular repolarization
potassium is leaving the cells here
pulse pressure
difference between systolic and diastolic pressure and it’s the amount of pressure the heart is generating with each beat
PP=SBP- DBP
mean arterial pressure (MAP)
average pressure in the arteries
determinants of MAP
cardiac output
total vascular resistance
chronotropy
the effect that change’s the heart’s rate of contraction, influencing how quickly the SA node fires and thus how many beats occur per minute
preload
end diastolic pressure and degree of stretch of cardiac muscle cells before they contract
increased in hypervolemia, regurgitation of cardiac valves, heart failure
afterload
resistance left ventricle must overcome to circulate blood
increased in hypertension and vasoconstriction
when it increases, it increases cardiac workload
hypertension increases afterload, which results in increased ESV and reduced stroke volume
Frank-Starling law
fundamental principle that the heart pumps harder when it’s filled with more blood
cause cardiac muscle exhibits a length-tension relationship
stroke volume increases when there is an increase in venous return
what increases venous return
venoconstriction via SNS
skeletal muscle pump
respiratory pump (changes in thoracic pressure pull blood toward heart)
cardiac output is increased by
increase in heart rate (increase in sympathetic adrenergic activity and decrease in parasympathetic activity)
increase in stroke volume (increase in central venous pressure, increase in inotropy, increase in lusitropy)
MAP and PP increased by
CO increases more than SVR decreases
Increase in stroke volume increases PP
CVP maintained by
venous constriction (increase in sympathetic adrenergic activity)
muscle pump activity
abdominothoracic pump
SVR decreased by
metabolic vasodilation in active muscle and heart
skin vasodilation
preload increased by
increase in EDV
increase in plasma volume
afterload decreased by
decrease in the arteriolar constriction in muscles, increasing maximal muscle blood flow with no change in mean arterial blood pressure
so ventricle ends up working less hard
maximal stroke volume increased by
increase in preload
increase in contractility
decrease in afterload
phase 1
ventricular filling (mid-to-late diastole)
accompanied by atrial contraction
phase 2a
isovolumetric contraction phase
start of ventricular systole
phase 2b
ventricular ejection phase
pressure in the LV exceeds pressure in the LA and aorta
begins with aortic valve opening
blood flows from the LV into the aorta
volume in the LV decreases
phase 3
isovolumetric relaxation
early diastole
what decreases BP to its set point
decrease in SNS activity
systemic vasodilation
physiological determinants of MAP
MAP = CO(SVR)
clinical determinants of MAP
MAP = DBP + 1/3(SBP-DBP)
respiratory pump
increased volume during inhalation decreases pressure in the thoracic cavity, pulling blood back to the heart
this increases venous return, which increases stroke volume
what increases stroke volume during exercise
increased contractility (increases ejection power, so more blood is pumped out)
increased skeletal muscle contractions (increases venous return/preload)
increased breathing rate (respiratory pump mechanism increases venous return)
increased venoconstriction
how afterload is affected by exercise
there ends up being an increase in this in the left ventricle because more pressure is needed to pump the increased preload into the aorta
positive inotropic agents
increased calcium influx due to increased sympathetic stimulation
hormones like thyroxine, glucagon, and epinephrine
negative inotropic agents
acidosis
increased extracellular potassium
calcium channel blockers
central command
initial signal to “drive” cardiovascular system comes from higher brain centers
due to centrally generated motor signals
in regards to BP central control
exercise pressor reflex
neural feedback system that increases heart rate, blood pressure, and breathing during physical activity
involved muscle chemoreceptors and muscle proprioceptors
metaboreflex
¤Chemicals released from contraction stimulate chemoreceptors
¤Stimulation of chemoreceptors send afferent information to the medullary CV centers via group IV afferent nerves.
¤This causes a “shift” in MAP control: baroreflex resetting
mechanoreflex
¤Mechanical deformation (movement) from contracting/moving limbs stimulate mechanoreceptors
¤Stimulation of mechanoreceptors send afferent information to the medullary CV centers via group III afferent nerves
¤This causes a “shift” in MAP control: baroreflex resetting
relationship between resistance and vessel radius
halving the radius of a blood vessel increases the resistance 16 fold
doubling the radius of a blood vessel decreases the resistance 16 fold
what produces minimum SVR during exercise
exercising on a hot day
exercising the whole body
exercising at a high intensity
aerobically trained heart
left ventricle is larger primarily due to eccentric hypertrophy
LV can fill more and contract more efficiently
stroke volume is increased
eccentric hypertrophy
when more sarcomeres are added in series to the heart wall due to volume overload that occurs during aerobic training
changing of MAP at onset of exercise
central command
mechanical
metabolic (things like calcium)
autonomic (SNS)
humoral (hormones)