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CV overall function
Transport
pulmonary circuit
pumps deoxygenated blood to the lungs
Systemic circuit
pumps oxygenated blood from the lungs to the body
True or false: Right and left sides MUST each pump equal volumes per unit time
True
Blood flow through heart
Inferior and superior vena cavae
Right atrium
Tricuspid valve
Right ventricle
Pulmonary semilunar valve
Pulmonary arteries
Lungs
Pulmonary veins
Left atrium
Bicuspid (mitral) valve
Left ventricle
Aortic semilunar valve
Aorta
Epicardium
outer, connective tissue, protection
Myocardium
middle, muscular layer, thick layer
Endocardium
inner, endothelium overlaying a thin connective layer
Septum
muscular wall separating L & R halves of heart
Pericardium
triple layer bag that surrounds & protects heart (reduces friction)
Heart valves
purpose is to prevent back flow of blood, ensuring one-way blood flow, They open and close passively with pressure of blood against them
AV Valves
thin walls, open when P in atria is higher than ventricles, close w/ retrograde P of blood against valves
Chordae tendinae and Papillary muscles
prevent AV valves from reopening during ventricular contraction and causing leakage of blood into atria
SL Valves
thicker walls, open and close when ventricular pressures exceed arterial pressures, close as blood flows backwards and fills cusps, no chordae tendinae or papillary muscles
Lub sound
the closing of the two atrioventricular valves
Dub sound
the closing of semilunar valves
3 classes of cardiac muscle
Atrial contractile
Ventricular contractile
Specialized conductive
Myocardium characteristics
striated, sarcomere, and crossbridge cycle all the same as skeletal muscles
Intercalated Disks
join adjacent muscle cells together
Desmosomes
adhering junctions
Gap junctions
diffusion of ions between fibers with very little electrical resistance (almost free flow)
Major importance of syncytial arrangement
1 impulse spreads to all fibers in syncytium to contract as a unit
2 syncytia
atrial and ventricular
Autoconduction
no need for innervation, creates own AP, no fiber type differences, fibers are highly oxidative
Autoconduction + Syncytial arrangement
= Autorhythimicity
What allows us to autoconduct?
Pacemaker potentials or funny currents
What causes plateau in AP?
Opening of L type Ca++ channels, decreased membrane permeability to K+, delays repolarization
Significance of refractory periods
they prevent tetany (involuntary contraction of muscles)
Increased extracellular Ca++ levels
enhance contraction
Decreased extracellular Ca++ levels
inhibit contraction
SA Node
sinus rhythm
SA Node - pacemaker
greatest permeability to Na+
AV Node pause duration and purposes
delays delivery of signal to ventricles by 0.13 s, allowing time for ventricular filling & AV valve closure
Net effects of specialized ventricular conduction system
allows simultaneous contraction of all parts of ventricles (6x normal ventricular fiber conduction speed)
Ventricular conductive system:
Bundle of His (AV bundle)
Bundle Branches (R & L)
Purkinje fibers
Chronotropic regulation
regulates heart rate
Inotropic regulation
regulates contractive force
Frank-starling Mechanism
increase in venous return, increase stretch on cardiac fibers, increase recoil upon contraction, increase contractive force
PNS
vagus nerve, ACh
Increase in K+ permeability
hyperpolarizes membrane, decrease HR
Vagal tone
normal parasympathetic stimulation to control HR at rest
Decrease in Ca++ entering through L type channels
decrease permeability, decrease force
E/NE
released due to SNS stimulation, effects same as SNS
Heart regulation - body temp
Increase BT, increase membrane permeability to Na+ & Ca++, increase HR & contractive force
Proprioceptors
increase HR at exercise onset
Baroreceptors
stretch/pressure receptors in aorta and carotids
Decreased BP
SNS stimulation
Increased BP
PNS stimulation
Chemoreceptors
sensitive to chemical concentrations in blood; located in aorta and carotids
Decreased O2, increased CO2 &/or decreased pH
SNS stimulation
P-wave
atrial depolarization
QRS complex
ventricular depolarization
T-Wave
ventricular repolarization
Diastole
phase of cardiac cycle when myocardium relaxed
Systole
phase of cardiac cycle when myocardium contracted
Atrial diastole
pressure ~ 0 mmHg, 70% of blood enters ventricles passively
Atrial systole
last 30% filling (atrial kick), atria primer pumps for ventricles, closing of AV valves ends
Ventricular Systole
Ventricular contraction increases pressure until semilunar valves open
Isovolumetric contraction
valves closed, builds pressure
Afterload
resistance against which left ventricle pumps
Isovolumetric relaxation
valves closed again, most of our drop in pressure
ESV
blood remaining in LV at end of ventricular systole, amount remaining after contraction
Ventricular diastole
1st ⅓ rapid filling (70%)
2nd ⅓ - not much
Last ⅓ - atrial systole (30%) atrial kick
EDV
volume of blood in left ventricle at end of ventricular diastole
Preload
load to which a muscle is subjected before shortening (initiates frank starling)
Stroke Volume
volume of blood pumped from LV with each beat
SV formula
SV = EDV - ESV
Ejection Fraction
proportion of blood pumped out of LV w/ each beat, 60-70% at rest, 80-90% when exercising
EF formula
EF = SV / EDV
Cardiac Output (Q)
volume of blood pumped per unit time (per minute), 5 L/min at rest, 25 L/min while exercising
Q formula
Q = HR x SV
Vascular system 3 wall layers
Itima, media, adventita
Itima
inner, contacts blood, single layer endothelial cells w/ thin basement membrane
Media
middle, smooth muscle
Adventita
outer, connective tissue
Arteries Function
carry blood away from heart
Arteries characteristics
thick, elastic, high pressure
Veins function
return blood to the heart
Veins characteristics
thin walls, low pressure
Precapillary sphincter
controls blood flow into capillaries
Capillaries
1 cell thick vessels for gas exchange
Unidirectional valves
prevent back flow and aid venous return
SBP
highest BP within vascular system, generated during cardiac systole
DBP
lowest BP within vascular system, generated during cardiac diastole
BF distribution
at rest, 64% of blood is in veins
Venous reservoir
veins store blood and can constrict to increase venous return
BF from submax to max exercise
decrease BF to skin, compromise heat dissipation in favor of muscle contraction
Microvascular regulation
adjusting smooth muscle tone in vessel walls, especially arterioles at precapillary sphincter
Acute control
changes in local concentrations of substances that act as vasodilators or vasoconstrictors
Long-term control
production of vascular growth factors that cause angiogenesis
Oxygen effect
high oxygen - vasoconstriction
low oxygen - vasodilation
Endothelin
Released when endothelium damaged
Powerful vasoconstriction
prevents excessive blood loss in affected artery
Increase SNS stimulation
constricts vessels further, increase arterial pressure
Decrease SNS stimulation
relieves some constriction, vessels dilate, decrease arterial pressure
SNS stimulation to veins
causes venoconstriction, increase venous return
Vasomotor tone
SNS continuously transmits frequent impulses to blood vessels, it keeps vessels in state of moderate constriction to maintain adequate BP
Blood Volume Components
plasma 55%, RBC 45%, WBC/PLatelets < 1%
Plasma
55-60% of total blood volume
90% water w/ dissolved proteins (7%) & nutrients, electrolytes, hormones, antibodies, and waste (3%)
Hematocrit
% of total blood volume that consists of formed elements or RBCs