Cardiovascular Physiology 1

Circulatory system as a circuit

systemic circuit

pulmonic circuit

Physical characteristics of blood

hematocrit

blood viscosity 1:
  increases with ↑ hematocrit or vasoconstriction
  decreases with ↑ flow velocity or vessel diameter < 300 μm

hematocrit

3× water at normal hematocrit, 10× at 70

in small vessels

Fahraeus-Lindqvist effect

↓ η when RBCs line up (vessel diameter < 300 μm)

rouleaux formation

vessel clogging

↑ η when RBCs fill capillaries (vessel diameter < 20 μm)

plasma

about 7% protein

albumins

globulins

fibrinogen

Blood flow

Ohm’s law 2

Q = ΔP/R

laminar flow

parabolic velocity profile

turbulent flow

additional details on turbulent flow from Guyton’s Physiology

measurement of flow

ml/min

Blood pressure

an account of pressure measurement written in 1733

standard units

mm Hg

1 mm Hg ≈ 1 Torr

1 pascal ≡ 1 N/m2

1 atm = 760 Torr = 101.325 kPa = 29.92 in Hg

1 mm Hg = 1.36 cm H2O

estimates of mean pressure

MAP = DAP + 1/3 APP, where APP = SAP - DAP

MAP = SAP × DAP

Resistance to blood flow

R = ΔP/Q

1 PRU = (1 mm Hg)/(1 ml/sec)

R (in dyne sec/cm5) = (1333 mm Hg)/(ml/sec)

systemic vascular resistance

idealized:  RA = 3 mm Hg, AoS = 113 mm Hg, AoD = 67 mm Hg

pressures during the cardiac cycle

total pulmonary resistance

idealized:  LA = 8 mm Hg, PAS = 25 mm Hg, PAD = 10 mm Hg

Conductance

measure of blood flow for a given ΔP

conductance = 1/R

effect of vascular diameter

conductance ∝ diameter4

Poiseuille's law

expresses the relationship of all factors in total blood flow 3

mean velocity v = (ΔPr2)/(8ηl)

Q = vπr2

substitute v, and Q = ( πΔPr4)/(8ηl)

solve for R

resistance of vessels in series:  Rtotal = R1 + R2 + R3 + ...

resistance in parallel:  start with conductances

Ctotal = C1 + C2 + C3 + ...

Vascular distensibility

distensibility = (increase in volume)/((increase in pressure)×(original volume))

veins vs. arteries

Vascular compliance

compliance = (increase in volume)/(increase in pressure)

note that a vessel with a greater original volume will be more compliant

Cardiac cycle

systole and diastole

relationship of the ECG 4 to the cardiac cycle

labeled image of normal sinus rhythm ECG

[ http://en.wikipedia.org/wiki/Image:SinusRhythmLabels.svg ]

cardiac cycle events

cardiac cycle events occuring in the left ventricle

[ This file is licensed under the Creative Commons Attribution ShareAlike 2.5 License. ]

ventricles as pumps

ventricular filling

diastasis

isovolumic contraction

period of ejection

isovolumic relaxation

stroke volume output

role of preload and afterload

Cardiac output

cardiac index

metabolism and exercise

Question:
Why does one’s fitness level not have a direct correlation to cardiac output? The formula for cardiac output is CO=HR×SVO, so if you have a 55 kg marathoner whose resting heart rate is 50 bpm and a 140 kg extremely unfit person, whose resting heart rate is 85, does that not mean that the marathoner’s heart functions more efficiently with less effort? In other words does the 140 kg–unfit person’s heart have to work harder to accomplish the same task?

One’s fitness (whatever that means) influences how one achieves a given cardiac output. CO=HR×SVO, as you noted, but there are many ways to get to CO. The reason the athlete’s HR is only 50 bpm at rest is because her SVO is 100 ml/beat, whereas the couch potato has a HR of 85 bpm at rest because his SVO is only 59 ml/beat. Why the difference? There are many things that contribute to SVO; for the athlete, contractility is undoubtedly better (as a result of her conditioning) and SVR (systemic vascular resistance) is markedly decreased (again, her conditioning, resulting in a lower BP) so the EDV is increased. While both the athlete and couch potato have the same CO at rest, the difference shows up if they were to compete in an athletic event:  She might be able to increase her SVO to 200 ml/beat with a HR of 150 bpm (achieving a CO of 30.0 l/min), whereas he will get his HR up to 180 bpm but only be able to increase the SVO to 120 ml/beat, a CO of only [!] 21.6 l/min. So, at the extreme, fitness does affect CO, but not at rest. This is why the totally diseased heart with an EF (ejection fraction) of only 20% can still maintain a CO of 5.0 l/min.
Explanation of previous statement:  EF measures the percentage of SVO/EDV. So, if one has a SVO of 80 ml/beat and an EDV of 100 ml, then the EF is 80% [that’s very good for a human; cats have an EF of about 95%!]. If the patient has an EDV of 300 ml and an EF of 20% [possible in a very diseased heart], then a HR of 83 bpm will achieve a CO of 5.0 l/min.

age

Regulation of cardiac output

control of cardiac output by venous return

permissive role of heart

sympathetic stimulation

role of total peripheral resistance

Questions for thought
1.   Describe the effects of sympathetic and parasympathetic stimulation on the heart.
2.   Describe the roles of the sinoatrial and atrioventricular nodes in the cardiac cycle.
3.   Karen is taking the medication verapamil, a drug belonging to a class called calcium-channel blockers. What effect should this have on Karen’s stroke volume output?
4.   Describe the significance of Poiseuille’s law.
5.   Draw and label a normal ECG pattern. Explain the significance of each deflection.
6.   Define blood pressure. Differentiate between systolic and diastolic pressures. Give a formula for calculating the mean blood pressure.
7.   Nicole the neonate needs surgery—she was born with a condition called transposition of the great vessels, in which the aorta arises from the R ventricle, and the pulmonary trunk arises from the L ventricle. Describe the physiological consequences of such a defect. What is her prognosis without surgery?

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