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106 Cards in this Set
- Front
- Back
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What two components is blood made out of? |
Cellular & fluid components |
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What % is the cellular component? |
45% |
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What % is the fluid component? |
55% |
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What makes up the cellular component? |
RBC's WBC's Platelets |
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What makes up the fluid component? |
Plasma Volume |
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Characteristics of cardiac muscle |
Striated
Troponin- 3 proteins that is integral for muscle contraction Tropomysin- protein found in cell cytokines
Myogenic contraction- contraction initated my myogenic cell itself, not an outside nerve.
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Depolarization |
Contraction of heart cells |
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Repolarization |
Resting or filling of heart cells |
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Resting potential |
? |
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Action potential |
? |
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Excitation-contraction coupling |
Action potential triggers release of Ca++
Muscle fibers contract
Tropomysin blocks myosin binding sites (muscle fiber relaxes)
Ca++ transported back |
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Pacemaker/autorhymic cells |
2 areas of concentration
SA node (upper RA, near SVC)
AV node (near TV in IAS)
Parasympatheic and sympathetic nerves
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Function of conduction fibers |
move the action potentials faster |
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Excitation-contraction pathway |
electrical activity spreads like a wave
contraction follows
propagation of this impulse is "excitation-contraction coupling" |
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Excitation-contraction pathway |
Action potential (SA node) Action potential are conducted to atrial muscle Action potential spread through atria to the AV node (conduction slows slightly) Action potentials travel rapidly through the conduction system to the apex of the heart (ventricles) Action potentials spread upward through the ventricular muscle Eventually the heart returns to the resting state, remaining there until another potential is generated in the SA Node |
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P-wave |
Atrial depolarization |
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QRS complex |
ventricular depolarization |
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T-wave |
Repolarization of ventricles |
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Systole takes up what percent of the cardiac cycel |
35% |
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Diastole takes up what percent of the cardiac cycle |
65% |
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Why does isovolumetric relaxation occur? |
because pressure is too low to keep semilunar valves open but too high to allow AV valves to open - so all valves are closed |
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What happens in early diastole? |
ventricular myocardium is relaxing
Isovolumetric period |
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What happens in mid-late diastole? |
Blood is returning to heart b/c atria are relaxed
Semilunar valves are closed, ventricular pressure is more than pressure in aorta and pulmonary arteries |
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What happens in late diastole? |
Atria contract
Blood is actively pushed into ventricles |
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What happens in the beginning of systole? |
Ventricles contract
(when ventricular pressure is more than atrial pressure, AV valves close)
Semilunar valves are closed b/c ventricular pressure still not high enough to open them
This phase ends when semilunars open b/c ventricular pressure is less than pressure in AO/Pulmonary arteries |
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What happens in the remainder of systole/end of systole? (not beginning) |
Ventricular pressure peaks and then decreases
Blood leaves ventricles, go to semilunars
Ventricular volume is being decreased
When ventricular pressure falls below the AO and Pulmonary A's, the semilunars close which ends ejection (& systole)- This beings diastole again |
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End-diastolic volume (EDV) |
Volume of blood in the ventricle at end-diastole
NL- 145ml |
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End-systolic volume (ESV) |
Volume of blood in the ventricle at end-systole NL-65ml |
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Stroke volume (SV) |
Amount of blood ejected during each heartbeat
SV= EDV-ESV
NL- 70-100 ml/beat |
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Cardiac Output (CO) |
Amount of blood circulating in the body per minute
CO= SV x HR
NL- 4-8 liters/min |
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Cardiac index (CI) |
Cardiac output adjusted by body surface area
NL- 2.4-4.2 liters/min/m2
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Body surface area |
Height x weight
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Abnormal shock in regards to CI |
less than 2.0 liters/min/m2 |
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Fractional shortening (FS) |
Percentage of left ventricular shortening during systole
NL- 28-44% |
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Ejection Fraction (EF) |
Percentage of blood that is ejected with every heartbeat
EF%= EDV - ESV/EDV x 100
NL- 55-75% |
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Preload (end-diastolic pressure) |
End-diastole volume is primary determine by preload
The end-diastolic pressure places tension (load) on the myocardium before it begins to contract
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Preload = |
Preload= end-diastolic volume = SV |
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Afterload |
tension developed by the ventricular myocardium just prior to ventricular ejection |
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What exactly happens in after load? |
The ventricle is pushing blood out into the system of arteries (which have a pressure within them)
Arterial pressure places a load on the myocardium after contraction starts
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Left ventricle after load is determined by? |
Determined by pressure in aorta during the ejection period |
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Volume depletion? |
Volume depletion = decreased preload
Examples are hemorrhage, dehydration |
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Factors affecting preload |
Total blood volume
Filling time
Atrial Pressure
Distribution of blood
Atrial Contraction |
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Filling time depends on what? |
HR |
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Atrial pressure is determined by? |
determined by venous return and the force of atrial contraction |
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Distribution of blood can be effected by? |
Body posture Intrathoracic pressure Intrapericardial pressure Venous tone
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Atrial contraction |
Vigorous and appropriately time atrial contractions augments preload
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Atrial contraction is responsible for ? |
1/4 of the stroke volume (SV) |
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Factors affecting afterload |
aortic pressure
flow resistance of aortic valve
dispensability of vessel
peripheral vascular resistance
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Increased arterial pressure usually = |
decreased stroke volume |
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Intracardiac pressures- differences |
systemic artery pressure is 5-6 times more than pulmonary arteries |
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Intracardiac pressures- similarites |
Volume of blood is basically the same
CO may be slightly higher
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Cardiac maneuvers in intracardiac pressures |
Increases/decreases venous return/heart rate and therefore increases/decreases SV &CO
Examples are valsavla, amyl nitrate, position of body |
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Valsalva |
Causes positive intrathoracic pressure which diminishes venous return to that cardiac output and arterial pressure falls
Heart rate increases and constricts arterioles |
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Amyl nitrate |
Vasodilation
Decreased filling of the LV |
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What is force-velocity relationship? |
increased force (after load) encountered by a cardiac cell causes a decrease in velocity of contraction |
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What is Frank Starling's law of the heart? |
When the rate at which blood flows into the heart from the veins (venous return) changes, the heart automatically adjusts its output to match the inflow |
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Starling effect
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Increased EDV= increased force of ventricular contraction = increased SV & CO
Decreased EDV= decreased force of ventricular contraction = decreased SV & CO
Increased EDV= increased length of muscle fibers of ventricular myocardium; this increased length/stretch = Increased force of contraction |
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Frank Starlings law of heart, the heart regulates what? |
the heart regulates its size, (if more in than out, the heart would stretch and become enlarged) |
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Interval-strength relationship |
Length of time between muscular contractions and the resultant effects on the heart's after load
Less time involved in diastolic filling, the less distending the ventricles become, and therefore, the myocardial stretch
Frank starling law- the less myocardial fiber stretch, weaker force of contraction |
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How do valves open and close? |
due to pressure differences in the chambers
All valves open and close passively
Close when a backward pressure gradient pushes blood backward
Open when a forward pressure gradient forces blood forward |
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How do semilunar valves open/close? |
Open when the pressure in the ventricles exceed the pressure in the great vessels (PA & AO)
Close when the pressure in the great vessels exceed the pressure in the ventricles
requires a strong back flow for closure |
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How do atrioventricular valves open/close? |
Open when the pressure in the atria exceeds the pressure in the ventricles
Require very small back flow for closure |
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Difference in how semilunar and atrioventricular valves close? |
High pressures in the arteries at end-systole cause the semilunar valves to snap shut
Atrioventricular valves close in a much softer way |
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Why is the velocity of forward blood greater through semilunar than AV? |
due to smaller openings |
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Which set of valves have more "wear and tear" & why? |
There is more "wear and tear" on the edges of the semilunar valves due to rapid closure and rapid ejection |
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Which set of valves are supported by chordae? |
Atrioventricular are supported by chordae
Semilunar are not
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What is the function of the chordae? |
to pull the leaflets inward toward the ventricles to prevent bulging into the atria during ventricular systole |
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What are some control mechanisms that affect the heart/cardiac cycle? |
Local control
CNS
Chemical and hormonal control
Biochemicals that allow for vessel constriction or dilation |
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What are some examples of local control? |
rate of tissue metabolism
role of metabolism on amount of vasodilator each tissue releases |
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Examples of CNS control on heart? |
Vasomotor nerve fibers regulate vessel diameter and function by release of norepinephrine or epinephrine (hormones) |
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Examples of chemical or hormonal control on heart? |
Thyroid hormones
insulin
glucagon |
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Examples of biochemicals on heart? |
Angiotensin II
Epinephrine
Kinis
Histamines |
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Parasympathetic NS |
Decrease heart rate Decrease conduction through AV node Decreases contractility (atrial) |
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Sympathetic NS |
Increases heart rate Increases conduction through AV node Increases contractility |
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What is hemodynamics? |
Blood movement
The physical laws that govern the flow of blood in the heart and vascular system
In echo, we quantify this blood movement or hemodynamic flow, by using doppler to make measurements |
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What are some clinical applications of volumetric flow calculations? |
Assess SV & CO Quantificaiton of regurgitant volumes and regurgitant fractions Calculation of valve areas Calculation of intracardiac shunt ratios |
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Volumetric flow is bases upon what principle? |
Hydraulic principle
Q= V x CSA
This all works provided that the CSA is fixed and the velocity is constant
In our hearts, CSA is not fixed & velocity is not constant
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In the heart (& blood vessels) is the CSA fixed? Is the velocity constant? |
NO |
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Are velocities in the heart constant?
Why? |
NO,
in the heart blood flow is pulsatile so the velocities are changing |
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In the cardiovascular system, does the CSA stay the same? |
NO, i.e. different valve orifices/lumen (AV is different from TV)
Blood vessels are different sizes- like a larger river with a system of tributaries and streams |
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What is CSA equal to? |
CSA = 0.785 x D^2
Normal Diameter: Mitral annulus (3-3.5 cm) LVOT (2.0 cm) Aortic annulus (1.8-2.2cm) |
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Volume = |
Volume = CSA x D |
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How can we determine the CSA of valves? |
When considering that blood is moving through different sized valves, we can determine the CSA of the valves
Area (cm2) = 0.785 D2 (cm)
Area (cm2) = pie/4 (ab) (cm) |
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What is Velocity time integral (VTI)? |
the measurement of the distance that a column of blood travels with each hear beat |
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How is VTI determined? |
determined when we trace the area under the Doppler curve |
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What does the area under the Doppler curve represent? |
The area under the Doppler curve represents the distance the "column" of blood travels with each heart beat. So VTI is sometimes called "stroke distance" |
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The concept of what is happening in the heart is comparable to ? |
The concept of what is happening in the heart is comparable to determining the volume of fluid in a cylinder
VOLUME = CSA x D |
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SV = ? |
SV = CSA x VTI |
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How can the velocities by underestimated (pitfalls of VTI and CSA measurements)? |
If there is a large angle of incidence between the ultrasound beam and blood flow, then the velocities will be underestimated |
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How can the distance not be accurately quantified (pitfalls of VTI & CSA measurements)? |
If area under the Doppler curve is incorrectly traced, the distance will not be accurately quantified |
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Volumetric flow depends upon ? |
Volumetric flow depends upon the CSA of the valves. Accurate CSA measures depend upon accurate measurements of the diameters across valve orficies/annulues |
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What are some possible ways to get poor CSA? |
Diameter measured during the wrong phase in cardiac cycle
Measures of annulus are inconsitent |
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What is the continuity principle based on? |
Based on conservation of mass (assuming there is no loss of flow)
What comes in, must go out!
This is important when talking about stenosis or a physical narrowing of a valve- think about putting your finger over a wave hose- same amount of water has to get through a smaller area |
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Continuity principle, what is Q? |
Q is volumetric flow rate
If we conserve the volume of flow in an area of stenosis- something has to happen to offset the decreased CSA of the valve
Q1=Q2
CSA1 x V1 = CSA2 x V2 |
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Continuity principle
How can you determine the area of a narrowed orifice? (due to stenosis or whatever) |
Stroke volume method- CSA1 x VTI1 = CSA2 x VTI2
OR |
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Where to measure for pulmonic stenosis? |
VTI of PV
RVOT diameter |
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Where to measure for tricuspid stenosis? |
VTI of TV
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Where to measure for aortic stenosis? |
LVOT diameter
VTI of AV
VTI of LVOT |
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Where to measure for mitral stenosis? |
VTI of MV
MV annulus |
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Pitfalls of measurements of continuity principle |
Error in diameter measurements will result in erroneous CSA
Erroneous peak velocities and/or VTI measurements |
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What does the "simplified bernoulli equation" do? |
helps us determine pressure gradients
Lots goes into the actual bernoulli equation (i.e., pressure differences, vessel resistance) we use a simplified version
Based upon conservation of energy (in the absence of any applied forces)
Energy in= energy out |
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Bernoulli equation- In an area of narrowing (stenosis), the velocity at the narrowing must ____? |
In an area of narrowing, the velocity at the narrowing must increase to maintain energy
So if there is a narrowing- Proximal to the narrowing, P is higher b/c C is lower
At the narrowing, P decrease b/c V has to increase |
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Velocity and pressure are? |
inversely porportional or related |
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Peak velocity (Vpeak) |
the highest point of the Doppler curve; represents the highest velocity of RBC's traveling through that point |
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What is deceleration time (DT)? |
the time it takes to decerlerate/decrease velocity of flow |
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What is planimetry? |
a tracing of the stenotic valve orifice to assess valve area
AV & MV Done in PSAX Measure at leaflet tips Can be difficult if calcification (lots of it) Very operator dependent Errors can significantly affect the quantification of MVA or AVA |
