Cardio #60 Tuesday 1/21/03 10 AM Will post any corrections Dr. Smith Kyle Hendrix Proscribe: Kevin Stancoven Page 1 of

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. 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 2. This graph shows the blood distribution throughout the body a. Shows all three circuits listed above b. Blood to GI system, skin, kidneys 3. This is “Wigger’s Diagram” a. Shows sequence of events in cardiac cycle b. P & QRS wave described below 4. 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 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 5. Dr. Smith found this in a new book a. We may want to use this as an overview of cardiac cycle 6. 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) 7. 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)