Download Cardio60-Intro

Cardio #60
Tuesday 1/21/03 10 AM
Dr. Smith
Kyle Hendrix
Proscribe: Kevin Stancoven
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Will post any corrections
Introduction to Cardiovascular System
The written test next Monday will be at 10 AM.
The week will focus on anatomy, histology, and some physiology. There will be a few test questions from
this lecture. This lecture is an introduction to the cardiac system. The coming weeks will go further into
detail.
1.
2.
3.
4.
Flow through the circuit
a. Heart → Arterial tree → Capillaries → Venous tree → Heart
i. Heart is a pump
ii. Cardiac system is set up to protect the brain by supplying the correct amount,
content, etc… of blood to the brain
b. Systemic vs. pulmonary vs. coronary circuits
i. Pulmonary circulation comes from right side of heart
ii. System circulation comes from left side of heart & goes to all systems in body
1. Vascular resistance = systemic vascular resistance
iii. Coronary circulation supplies heart muscle
1. Comes off aorta
c. Right side vs. left side
i. Output/flow (output from right & left side is normally equal)
ii. Pressures
1. Pressure in right side of heart is less than left side
iii. Resistance
1. Ohms law: Pressure = Flow x Resistance
2. Vascular resistance in pulmonary (right side) circuit is lower than
systemic (left side) resistance
d. Coronary circuit
i. Will have full lecture later
ii. Important diseases with coronary problems
This graph shows the blood distribution throughout the body
a. Shows all three circuits listed above
b. Blood to GI system, skin, kidneys
This is “Wigger’s Diagram”
a. Shows sequence of events in cardiac cycle
b. P & QRS wave described below
Cardiac function
a. Electrical event precedes mechanical event (will talk in detail tomorrow & next week)
i. SA node in right atria (pacemaker)
ii. P wave is wave of depolarization of atria
iii. QRS is depolarization of ventricles
iv. Mechanical event → muscles contract, cause increase in ventricular pressure
b. Electrical activity through the heart
i. Delay of wave at AV node
ii. Max heart rate is around 200 bpm (3 beats/second)
c. Diastole vs. systole
i. Diastole – relaxation stage
ii. Systole – contraction stage
d. Preload
5.
6.
7.
i. Similar to concept of stretching a skeletal muscle will cause an increase in the
force of contraction
ii. Preload – load prior to contraction (how much volume in chamber before
contraction)
1. AKA “end diastole” volume of ventricles the greatest
2. Causes greater stretch and greater stroke volume
e. Starling’s Law of the heart
i. Frank-Starling mechanism
ii. More volume in heart, the harder the contract force (stroke volume)
f. Venous return
i. Amount of blood that returns to heart
ii. Dictates Starling’s Law because venous return is the amount of blood that will
fill the heart
g. Afterload
i. What the heart has to pump against
ii. How much force has to overcome and generated when the heart contracts
iii. Clinically important in blood pressure and vascular resistance of systemic
circulation
1. Increase vascular resistance will increase afterload
h. Contractility
i. How hard the heart is contracting
ii. Independent of preload
i. Cardiac output = HR x SV
i. Increased contractility will increase stroke volume
j. Ohm’s Law: ΔP = CO x R
i. Cardiac output inversely related to resistance
ii. CO up, R goes down
k. Control of cardiac function
i. Hormones, nerves
Dr. Smith found this in a new book
a. We may want to use this as an overview of cardiac cycle
Circulation
a. Arteries
i. High pressure conduit
1. Blood pressure is measurement of arterial pressure
2. Helps direct blood to where it should be going
3. Need pressure difference for blood to flow
ii. Vasoconstriction & vasodilation
b. Capillaries
i. Exchange of nutrients & metabolites
c. Veins
i. Conduit of return to heart
1. Low pressure
ii. High capacitance (compliance)
1. Accept blood
d. Venous return
i. Ohm’s Law: ΔP = Q x R (Q=Flow)
ii. Poiseuille’s Law: Flow = ΔP x r4/η
1. Used better to use when describing single vessel
2. Flow dependent on pressure gradient and radius of vessel
3. Control of flow mainly through increasing/decreasing radius
4. η = viscosity (doesn’t change much)
Normal values (don’t need to know many values)
a. Aortic systolic & diastolic pressures
i. Systemic pressures
ii. Will discuss normal ranges later
b.
LV end-diastolic & end-systolic pressure
i. Peak systolic pressure is normally equivalent to aortic pressure
ii. End-diastolic pressure in ventricles is very low (basically 0)
c. Left atrial pressure
i. During relaxtion, tracts left ventricle pressure
d. Pulmonary capillary wedge pressure
i. Measured by Schwann-Gans catheter (spelling?)
ii. Pressure in pulmonary circuit is almost identical to left atrium
iii. Measure left ventricular end-diastolic pressure (Preload)
e. Heart rate
f. Cardiac output
i. 5L/min
g. Stroke volume
h. Venous pressure
i. Low
8. Cardiovascular control
a. Regional
i. Local control
1. Level of heart
2. Blood vessels control mediated by metabolism
a. If a tissue is activated, vasodilation occurs, and blood flow
increases (vasodilation = decrease resistance)
ii. Cardiac output distribution
b. Neural
i. Reflex
ii. ANS
iii. Sensors
c. Hormonal
i. Circulating
9. Link a Disease
a. Coronary circulation
Ischemia/MI/CAD (clot)
b. Systole/diastole of the heart
Heart Failure
c. Cardiac output
Heart Failure (low output)
d. Arterial pressure
Hypertension
e. Vascular resistance
Hypertension
f. Preload
Syncope (decreased preload)
g. Afterload
Hypertrophy
i. Chronic hypertrophy may cause hypertension
h. Conduction
Arrhythmias
i. Venous system
Syncope
j. Venous return
Syncope
10. Function: Delivery System
a. Delivery nutrients such as O2, Glucose, etc…
b. Discard CO2 at the lungs
c. “Take out the trash”… Take toxins to the liver and kidneys
d. When heart rate increases, the cardiac cycle length (time between heart beats) will
decrease.
e. Stroke volume = EDV – ESV. Assuming no changes in other variables, if for a given
heartbeat the SV is increased, then the ESV will be less.
f. Which is greater, end-diastolic volume or end-systolic volume? EDV
g. Venous return is = to cardiac output
h. An acute increase in which of the following will increase cardiac output
i. Contractility
ii. Venous return
iii. Afterload (will decrease cardiac output)
iv. Heart rate
v. Stroke volume
vi. Infusion of 1L of whole blood
i. An increase in contractility of the heart would be expected to increase stoke volume
j. Assuming no change in contractility, a decrease in cardiac cycle length will result in a
decrease in stroke volume (less filling of heart)
k. During exercise producing an increased HR from 60 to 150 bpm. You would predict that
the delay through the AV node to be decrease
l. Applying Ohm’s Law, if BP decreases the neural response to compensate would be to:
i. Increase systemic vascular resistance
ii. Increase heart rate
iii. Increase stroke volume
m. During exercise, the skeletal muscle would cause a local effect (due to increased
metabolism) to increase blood flow by vasodilation
n. During intense exercise, the working muscle is profoundly vasodilated causing systemic
vascular resistance (SVR) to decrease and potentially cause BP to decrease
o. To prevent hypotension, there is concomitant vasoconstriction in the renal and splanchnic
(GI) blood vessels
p. Nitropursside causes systemic vasodilation, this will cause a reflex response to increase
systemic vascular resistance (Ohm’s Law)