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Circulation and respiration (Circulation (Cardiovascular system (anatomy…
Circulation and respiration
Circulation
Hematology and Oncology
Cardiovascular system
anatomy and physiology
four-chambered heart
circuitry
left-heart CO = right-heart CO
direction of blood flow
hemodynamics
vascular components
arteries
arterioles
capillaries
venules
veins
blood flow and blood flow velocity
velocity of blood flow (v = Q/A)
blood flow
Q = pressure gradient / R
CO = MAP - right atrial pressure / TPR
resistances in parallel or in series
R = (8)(blood viscosity)(length) / (pi)(blood vessel radius)^4
capacitance (compliance)
C = V / P
blood vessel pressure profiles
arterial pressure, venous pressure, and atrial pressure
arterial pressure
systolic pressure
diastolic pressure
pulse pressure
venous pressure
atrial pressure
cardiac electrophysiology
ECG
P wave (atrial depolarization)
PR interval (AV nodal conduction, initial ventricular depolarization)
Heart block: sympathetic nervous system stimulation (+) decreases AV nodal conduction and increases PR interval
QRS complex (ventricular depolarization)
QT interval (ventricular depolarization and repolarization)
ST segment (isoelectric, ventricular depolarization)
T wave (ventricular repolarization)
cardiac APs
ventricles, atria, and the Purkinje system: stable resting potential (-90 mV)
Phase 0 (AP upstroke)
transient increase in Na+ conductance --> INWARD Na+ current (INa)
Phase 1 (initial repolarization)
chemical and electrical gradients favor K+ ions out of the cell due to decreased Na+ conductance
Phase 2 (AP plateau)
transient increase in Ca2+ conductance --> INWARD Ca2+ current (ICa)
Phase 3 (repolarization)
high K+ conductance --> large OUTWARD K+ current (Ik)
Phase 4 (resting membrane potential, -90 mV)
equal INWARD and OUTWARD currents (Ik1) --> membrane potential approaches K+ equilibrium potential
SA node and AV node
SA node AP: unstable resting potential
Phase 0 (AP upstroke)
INWARD Ca2+ current (Ica)
Phase 3 (repolarization)
increased K+ conductance --> OUTWARD K+ current (Ik)
Phase 4 ("automaticity", slow depolarization)
increased Na+ conductance --> INWARD Na+ current (If)
AV node AP: stable resting potential (-90 mV)
Phase 0 (AP upstroke)
INWARD Ca2+ current (Ica)
conduction velocity and excitability
conduction velocity
depends on
fastest
Purkinje system
slowest
AV node (PR interval on ECG), allows time for ventricular filling before ventricular contraction
definition
excitability
definition
refractory periods
Absolute refractory period (ARP)
Effective refractory period (ERP)
Relative refractory period (RRP)
ANS effects on HR and conduction velocity
inotropic effects, chronotropic effects, and dromotropic effects
parasympathetic effects on HR and conduction velocity
sympathetic effects on HR and conduction velocity
cardiac muscle and cardiac output (CO)
myocardiac cell structure
sarcomere
intercalated disks
gap junctions
mitochondria
T tubules
sarcoplasmic reticulum (SR)
excitation-contraction coupling steps (7)
AP spreads from cell membrane into T tubules
During AP plateau, Ca2+ conductance increases and Ca2+ enters cell from extracellular fluid (inward Ca2+ current) through L-type Ca2+ channels (dihydropyridine receptors)
Ca2+ entry triggers release of even more Ca2+ from SR (Ca2+ -induced Ca2+ release) through Ca2+ release channels (ryanodine receptors)
Intracellular [Ca2+] increases
Ca2+ binds to troponin C, and tropomyosin is moved out of the way, removing the inhibition of actin and myosin binding
Actin and myosin bind, the thick and thin filaments slide past each other, and the myocardial cell contracts. The magnitude of the tension that develops is proportional to the intracellular [Ca2+] .
Relaxation occurs when Ca2+ is reaccumulated by the SR by an active Ca2+ -ATPase pump.
contractability (inotropism)
definition
related to
estimated by
factors and agents that increase contractility (positive inotropism)
factors and agents that decrease contractility (negative inotropism)
ventricular Length-tension relationship and Pressure-volume loops
Length-tension relationship in the ventricles: analogous to relationship in skeletal muscle
Afterload (aortic pressure or pulmonary artery pressure), related to left ventricle and right ventricle
Frank-Starling relationship and the effect of positive and negative inotropic agents
SV or CO vs. Right atrial pressure or EDV
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left ventricle (aortic pressure)
decrease aortic pressure
increase aortic pressure
right ventricle (pulmonary artery pressure)
increase pulmonary artery pressure
decrease pulmonary artery pressure
definition
Preload (end-diastolic volume, EDV), related to right atrial pressure
right atrial pressure (end-diastolic volume, EDV)
decrease venous return
increase venous return
Sarcomere length
determines maximum number of cross-bridges that can form between actin and myosin and maximum tension, or force of contraction
Velocity of contraction at a fixed muscle length
maximal contractile velocity
decreased by
Frank-Starling relationship
based on
decribes
mechanism that matches
Changes in contractility shift the Frank-Starling curve.
increases in contractility
decreases in contractility
Ventricular pressure-volume loops
Definition: Combined systolic and diastolic pressure curves
Example: Single left ventricular cycle of contraction, ejection, relaxation, and refilling
Steps and changes in the cycle (4), left ventricular PV loop
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cardiac and vascular function curves
Simultaneous plots of cardiac output (CO) and venous return as a function of right atrial pressure or end-diastolic volume (EDV).
Cardiac function (CO) curve: CO as a function of EDV; Frank-Starling relationship for the ventricle
Vascular function (venous return) curve: Relationship between blood flow through the vascular system (or venous return) and right atrial pressure.
Mean systemic pressure
Increase mean systemic pressure (2): shift vascular function curve right
Decrease mean systemic pressure (2): shift vascular function curve left
Slope of venous return curve
Resistance of arterioles, or Total peripheral resistance (TPR)
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Combined cardiac output (CO) and venous return curves
Superimosed curves predict direction and magnitude of changes in CO and the corresponding values of right atrial pressure.
Point of intersection: Equilibrium, or steady-state, point Equilibrium occurs when CO equals venous return.
Changes that effect both curves, the CO curve, and the venous return curve
Both curves: Changes in TPR change both the cardiac output (CO) and the venous return curves simultaneously; however, right atrial pressure remains unchanged.
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Venous return curve only: Changes in blood volume (BV) or venous capacitance change the venous return curve.
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Cardiac output (CO) curve only: Inotropic agents change the CO curve.
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stroke volume (SV), cardiac output (CO), and ejection fraction
Stroke volume (SV): SV = End-diastolic volume - End-systolic volume
Cardiac Output (CO): CO = SV x HR
Ejection fraction is the fraction of the end-diastolic volume (EDV) ejected in each stroke volume (SV), is related to contractility, and is normally 0.55 (55%).
Ejection fraction = SV / EDV
stroke work
Stroke work is the work the heart performs on each beat, equal to pressure x volume.
Fatty acids are the primary energy source for stroke work.
Stroke work = Aortic pressure x Stroke volume
cardiac oxygen (O2) consumption
Directly related to the amount of tension developed by the ventricles.
Increased by:
Increased afterload (increased aortic pressure)
Increased size of heart (Laplace's law states that tension is proportional to the radius of a sphere.)
Increased contractility
Increased HR
measurement of cardiac output (CO) by Fick principle
Cardiac output (CO) = O2 consumption / [O2]pulmonary vein - [O2]pulmonary artery
O2 consumption for the whole body is measured (mL/min).
Pulmonary vein [O2] is measured in systemic arterial blood (mL O2/mL of blood).
Pulmonary artery [O2] is measured in systemic mixed venous blood (mL O2/mL of blood).
cardiac cycle
atrial systole
isovolumetric ventricular contraction
rapid ventricular ejection
reduced ventricular ejection
isovolumetric ventricular relaxation
rapid ventricular filling
reduced ventricular filling (diastasis)
regulation of arterial pressure
baroreceptor reflex
renin-angiotensin-aldosterone system
other regulations of arterial blood pressure
microcirculation and lymph
structure of capillary beds
passage of substances across capillary wall
fluid exchange across capillaries and nitric oxide (NO)
special circulations
local (intrinsic) control of blood flow
hormonal (extrinsic) control of blood flow
coronary circulation and cerebral circulation
skeletal muscle and skin
Integrative functions of the CV system: Gravity, Exercise, Hemorrhage
changes in gravitational forces
excercise
hemorrhage
Respiration