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What are conduit vessels?: Large arteries whose dimensions do not change. They are innervated by sympathetic nerves.
What is a normal MAP?: ~100 mmHg
Describe resistance vessels. What are they? What are some functions (2)?: *small arteries and arterioles
*diameter <300 microns
*able to change dimensions, which changes resistance
*fxns: change flow to tissues; regulate MAP through peripheral resistance
What are exchange vessels? What are their characteristics? What is their fxn?: *capillaries
*no contraction or dilation - no smooth muscle, no innervation
*fxn: control diffusion between blood and tissue
Where is the majority of the blood volume held?: 60-70% is held in the capacitance vessels (large veins)
Give the avg. pressure at the following places: conduit vessels resistance vessles exchange vessels venules, sm. veins capacitance vessels primary veins: conduit vessels = 100mmHg
resistance vessles = 95 mmHg
exchange vessels = 25 mmHg
venules, sm. veins = 15 mmHg
capacitance vessels = 10 mmHg
primary veins = 1-3 mmHg
What is the equation for flow through a vessel?: Q = P/R
What is the equation for MAP?: MAP = CO x SVR
What is the equation for CO? What is CO? What is normal?: *CO = HR x SV
*the volume of blood pumped per minute
*5 L/min
List the 7 stages of the cardiac cycle.: 1. atrial systole
2. isovolumetric contraction
3. rapid ejection
4. reduced ejection
5. isovolumetric relaxation
6. rapid filling
7. reduced filling
What cause S1 heart sound?: The closure of the mitral and tricuspid valves.
What causes the S2 heart sound?: The closure of the aortic and pulmonic vlaves.
What is LVEDV? What is its normal value? How is this achieved?: *left vent. end diastolic volume
*140cc
*10-15% from atrial contraction, the rest due to passive filling
What is LVESV? What is its normal value?: *left. vent. end systolic volume
*volume of blood in LV at isovolumetric relaxation
*60-65cc
How is the ejection fraction calculated? What is normal?: *EF = SV/EDV
*nl = 60% (55-75%)
How can SV be calculated? Normal value?: *SV = LVEDV - LVESV
*75cc
Which opens first, the pulmonic or the aortic valve? Why?: *pulmonic
*there is less pressure that must be overcome
Which closes first, the pulmonic or the aortic valve? Why?: *aortic
*there is greater pressure in the aorta than the pulmonary trunk
How would a right bundle branch block affect the heart sounds? Why?: *T will be delayed from S1
*P will be delayed from S2
*this is because depol. of the RV is delayed in this defect
How does a ventricular septal defect affect heart sounds? Why?: *A is early in S2
*P is delayed in S2
*the defect causes blood to flow from the LV to the RV...the larger volume of blood in the RV takes longer to eject (hence delayed P)...the smaller vol. of blood in the LV takes less time to eject
What causes S3? When in the cardiac cycle might it be heard?: *low frequency vibration and tensing of chordae tendinae
*occurs early in diastole
What causes S4? When in the cardiac cycle might it be heard?: *forceful ejection of blood from atria causes turbulence
*occurs at the end of diastole
What are the three significant waves of the venous pulse?: *a - atrial contraction
*c - ventricular contraction
*v - venous filling
What kind of timing differences are there btwn the LV and RV?: The LV begins to contract and to relax before the RV.
What can a S4 atrial gallop ("tennessee") be a sign of?: LV hypertrophy
What are murmurs? What causes them (in general)?: *Abnormal sounds during silent periods
*caused by unexpected turbulence
When can systolic murmurs be heard? Name three things that can cause them.: *between S1 and S2
*aortic stenosis, mitral regurgitation, ventricular septal defect
When can diastolic murmurs be heard? Name two possible causes.: *Between S2 and S1
*mitral or tricuspid stenosis, semilunar regurgitation
What three things influence SV?: PL, AL, & CTY
Define PL. How is it largely determined?: *the amt of stretch, tension, or force experienced by the LV after diastole but before systole
*ventricular filling
Are PL and force of contraction directly or inversely related?: Directly.
How does an increase in PL cause a more forceful contraction?: *increased stretching leads to more efficient interaxn between thick and thin filaments in the cardiac myocytes
Name two clinically significant indices of preload and their normal values.: *LVEDV - 140cc
*LVEDP - 6mmHg
How are PL and SV related?: They are directly related - an increase in PL causes an increase in SV.
How might an increase in CVP affect PL? There are 4 steps.: 1.Incr CVP = incr right heart P
2.Incr R heart P = Incr pulm P
3.Incr pulm P = Incr LA P
4.Incr LA P = Incr filling of LV
filling of LV = PL
How might a decrease in CVP affect PL? Run through the cycle.: It will decrease PL
What are the three primary determinants of CVP?: 1.Tot blood vol
2.Venous tone
3.body position
How does body position affect CVP?: Rising from a supine pposition to a standing position will cause a decrease in CVP.
How would a primary decrease in SV affect CVP? Why would this happen? How might it be partially corrected?: *A dec in SV would increase CVP
*pulm P incr due to pooling in the LV and this backlog is reflected in incr CVP
*there is an incr in PL due to the pooling, which increases SV some
How can AL be defined?: The "load" (i.e. pressure) the LV must work against to open the aortic valve and eject its SV.
How does an incr in AL affect SV? Why?: *SV decreases
*as the P the LV must work against incr, a larger part of systole must be spent in isovol contraction generating this P and there is less time to eject blood
What is the primary index of AL?: *diastolic arterial blood pressure
*HTN = incr AL
What is the cellular basis for the effect of AL?: The bigger the load to contract against, the slower the formation of crossbridges.
Besides an incr in arterial P, what is something else that can cause an incr in AL?: Aortic stenosis
How can CTY be defined?: The contractile force generated at a given AL and PL.
How do changes in PL and AL affect CTY?: *They don't - CTY is "load independent".
*CTY is the instrinsic ability of the heart to contract at given conditions
What does an incr in CTY do to SV?: Causes an incr in SV, they are directly related
What is the primary determinant of CTY?: Ca++ kinetics: how fast [Ca] reaches its peak and how fast it is resolved.
What effect does B-1 stim have on CTY? Explain: *it increases CTY
*B-1 stim = incr cAMP = incr [Ca] = incr CTY
How would hypoxia or ischemia affect CTY? Explain: *CTY decreases
*smaller peak of [Ca] and reduced pumping efficiency
How can physical training incr CTY?: It would change the composition of myosin ATPase to the faster isoforms
Under what circumstances does [ATP] affect CTY?: Only during extreme ischemia
What effect do catecholamines have on CTY?: Increase
What effect does thyroid hormone have on CTY?: Increase, through an increase in cAMP which then increases Ca++
Name two drugs that increase CTY.: Caffeine and digitalis
How is an increase in CTY reflected on the pressure loop graph?: Aortic valve closure occurs at a higher LVP and a lower LVV
Why would a patient in heart failure be treated with an inotropic drug?: It would increase CTY and raise SV w/o causing the rise in LVEDP that occurs when the body tries to compensate by increasing PL.
What is a slow mechanism the body uses to correct reduced SV during heart failure.: Fluid retention leads to increased blood volume and increased CVP. This increases PL and thus SV.
Give the normal ranges and max values for: HR SV CO: HR = 70-150bpm (max = 200)
SV = 75 - 150cc (max = 180)
CO = 5-25L/min (max = 35)
What can cause an increase in the "a" wave of venous pressure?: Tricuspid stenosis.
What can cause an increase in the "c" and "v" waves of venous pressure?: Tricuspid insufficiency.
The "c" can also be increased in IV septal defects.
Absence of the "a" wave in venous pressure can be caused by what?: Atrial flutter or fibrillation.

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