Physiology Flashcards
How do you calculate MAP?
Diastolic pressure + 1/3 pulse pressure (systolic-diastolic)=MAP
This value is not an average and will fall closer to the diastolic value because 2/3 of the time you are in diastole.
How do you calculate HR and where do you get the information you need?
1 beat/cycle length which can be determined by looking at the R-R interval on an EKG. This maybe in msec, but must be converted to bpm.
What is the ejection fraction commonly used to estimate?
Contractility/inotropic effect. If you keep EDV constant but have an increase in SV this translates to a greater ejection fraction, which is the result of Ca2+ entry into the muscle leading to a positive inotropic effect/contraction.
What are the two equations for MAP? How can your body affect change to MAP? If you have a lot of atherosclerosis leading to arteriosclerosis how will this affect MAP?
MAP=diastolic + 1/3 Pulse Pressure (systolic-diastolic)
MAP=CO x TPR
MAP-RAP=CO x TPR (usually Right Atrial Pressure is close to zero and is omitted from calculation, but as it rises the MAP will fall).
If you want to change MAP you need to vary one of these variables.
CO=HR x SV; HR is regulated by Autonomic nervous system via B1 receptors on the heart and parasympathetic input from the vagus nerve on the SA and AV nodes; which can be manipulated with drugs or vagal maneuvers. SV is affected by inotrophy and the sympathetics.
Artherosclerotic plaques can narrow vessels and a decrease in the radius of a vessel has a large impact on resistance and thus TPR. If this leads to arteriosclerosis (stiff non compliant vessels) this will increase TPR and thus MAP.
What is the equation for velocity? How does velocity of blood in the arteries compare to that of the capillaries? What is the purpose of this in the body?
V=Q/A velocity=flow/area
As area decreases (capillaries) velocity increases.
Comparing Total Cross-sectional area though, capillaries have the largest area in the body, so relative to other vessels the RBC velocity is the smallest.
What is the primary regulator of blood flow in the body? How is this accomplished and what system oversees this regulatin?
Blood vessel diameter
alpha 1 receptors cause vasoconstriction when acted upon by the sympathetics via NE.
If you stand up and then feel faint what does this tell you about the auto-regulation system of the brain in response to variations in bp?
That your bp has fallen below the range in which blood flow is auto-regulated in the brain (approx: 60-140mmHg). The flow of blood in the brain is usually maintained at a steady rate unless blood pressure moves outside this range.
When you stand up after lying down what happens to each of these variables and why: SV, CO, HR, bp, and TPR? How does the body compensate for each of these changes?
SV-decreases due to decreased venous return leading to decreased EDV.
CO-decreases as it is directly related to SV in the equation CO=SV x HR. Comp- carotid sinus baroreceptors (sensitive to hypotension) will generated a sympathetic response in the NTS: The cardiac accelerator region will increase HR (SA node) and contractility (increase SV and thus CO), and the vasoconstriction region will affect arteries and veins via alpha1 receptors using NE (returning more blood to the heart).
HR- increase is a compensation.
bp-drops (both systolic and diastolic) MAP=CO x TPR. Decreased CO means decreased bp.
TPR- increase as a compensation (described above) to protect against hypotension and syncope.
Compensation- normally a decrease in CO and an increase in TPR should offset each other and lead to a relatively even bp (helping to prevent large variation).
Which of the following would have an effect on EDV? You can choose 1 or more than one answer. A) Exersise B) Standing up C) Digestion D) Laying Down
B and D
Standing up will decrease venous return and thus decrease EDV, laying down will do the opposite. EDV is affected by the venous system.
Exercise will shunt blood to areas of decreased resistance that are in need of O2 such as the skeletal muscle or cardiac muscle. Blood will shunt from the GI or renal systems to do this, because they aren’t needed during exersise. In order for this shunting to be effective it should be obvious that this is arteriole (oxygen rich) blood. This will not affect EDV.
What is the Fick equation; explain each component
CO=VO2/[O2]sa-[O2]pa
VO2=Total oxygen consumption
sa-systemic artery which approximates the O2 concentration in the pulmonary veins.
pa-pulmonary arterys
Central venous pressure estimates what? Pulmonary capillary wedge pressure estimates what?
central venous pressure (CVP) estimates Right atrial pressure (RAP)
Pulmonary capillary wedge pressure (PCWP) estimates Left atrial pressure (LAP)
When someone is in hypovolemic shock why is their skin pale and cold?
Blood is being shunted away from less important organs to more vital ones to keep the body alive.
What role do vasodilators in the kidneys play when someone is in hypovolemic shock? How could aspirin affect the role of these vasodilators?
With decreased bp due to blood loss the body will shunt blood from less vital organ to more vital ones (vasoconstriction). If you loose too much blood the body might start depriving vital organs of blood including the kidney. Local vasodilators like Prostaglandins, NO, bradykinin and dopamine will act in a protective way to stop vasoconstriction in the kidney which could lead to renal failure.
Aspirin is a COX inhibitor and can inhibit these protective prostaglandins, which would be detrimental in this instance.
dopamine is a vasodilator most places in the body; name the exceptions where it acts as a vasoconstrictor
muscle and cutaneous regions
How does aldosterone influence K+ levels in the kidney?
Aldosterone acts on principle cells in the collecting duct to increase Na+ reabsorption, and increase K+ excretion into the urine. The sodium rich principle cells then drive ATP in the cell to increase the rate of the Na+ K+ pumps. This drives Na+ into the blood and water follows. The reason for the hypokalemia that results is from K+ entering the principle cells to drive the pump and then being kicked out immediately into the urine.
How do single kidney problems have systemic effects, how can one kidney affect the other?
Lets say the left kidney has a lot of atherosclerotic plaque leading to arteriosclerosis of the renal artery. This sends the signal to the left kidney that the body has low bp when in reality it does not. This kidney will compensate through the RAAS system to increase systemic bp (via renin etc). The right kidney will then react to this increase in bp to lower bp (inhibiting renin etc). This can cause problems through out the body.
This would be a good time to use an ACE inhibitor (or some other pharmacologic treatmetn) to stop renin secreted from the left kidney from increasing bp.
Your patient too an unknown drug which somehow lowered their blood pressure but you’re not sure how. It doesn’t seem to be affecting the sympathetic regulation of the heart or vasculature, but has increased the CVP. How might this drug be working; explain?
A) beta blocker acting to increase HR without adequate blood volume
B) diuretic increasing fluid retention
C) anti-diuretic increased CVP thus lowering MAP
D) atropine to speed up the heart without adequate volume
C-anti-diuretic: increasing fluid retention, increase CVP, this is equivalent to increasing RAP which is factored into MAP when the value increases enough. MAP-RAP=CO x TPR.
You have a patient with a MPAP of 52mmHg and a MAP of 120mmHg with a standard CO of 5L. Calculate their TPR and PVR. Which should be larger? Does this example meet this expectation?
PVR=MPAP/CO 52mmHg/5L=10.4mmHg/L
TPR=MAP/CO 120mmHg/5L=24mmHg/L
TPR>PVR which is the case here.
Viscosity can be increased or decreased in the blood via what type of changes?
Increased polycythemia (increased RBC), or increase in protein
Decreased- anemia (may increase turbulence and murmurs)
During exersise how are EF, EDV, SV and CO affected?
EDV is constant, SV increases (increases CO) and thus EF increases according to the equation below.
EF=SV/EDV
Use the darcey equation (ohms) to calculate resistance through the coronary arteries using the following information. Q= 5%, Pv= 0.12ml O2/ml blood, Pa= 0.22 ml O2/ml blood.
R=change in Pressure (Pa-Pv)/Q (flow)
Q=5% of CO which is typically 5L/min = 250ml
Pv=0.12
Pa=0.22
(0.22ml O2/ml blood-0.12 ml O2/ml blood)/250ml=4x 10-4
What’s the difference between velocity and flow?
Velocity is about speed and direction
Flow is specific to volume.
If an artery is narrowed the flow decreases and the velocity increases. assuming total energy is conserved on both sides.
How do thoracic pressure and skeletal muscle pumps affect blood flow to the heart when you walk?
Decreased thoracic pressure from breathing deeply increase venous return to the heart.
Skeletal muscle contraction in the calves increases pressure in the veins and b/c of one way valves blood can only move forward (up to the heart).
The combination of these actions decreases venous pressure and more blood flows across the capillary beds from the arteriole side, and circulation improves.
Which is the greatest factor in increasing CO during exercise?
- SV
- HR
- VO2
- HR
Pulse pressure can increase dramatically when you exercise what is the greatest factor in this change?
SV
PP=systolic-diastolic
The SV is directly related to systolic pressure and it will increase while diastolic will slightly decrease.
If your patient had a heart transplant what system do they rely on to increase their HR?
Adrenal glands, b/c autonomic innervation to the heart is lost.
What are the four major controls of blood volume in our bodies?
RAAS
SNS
ADH/AVP
ANP
