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.the-aps.org/education/MedPhysObj/medcor.htm In some case, the order of the topics and the objectives have been modify
Understand the principles underlying cardiac output measurements made using a) The Fick’s method and b) indicator dilution methods using a Swan-Ganz catheter Calculate CO by using Fick’s method Understand the concept of “mean systemic pressure”, its normal value, and how various factors can alter its value. Construct a vascular function curve. Identify on the curve the normal central venous pressure and mean circulatory pressure. Predict how the curve is altered by a) changes in resistance to venous return and b) changes in blood volume or vascular compartment size. Define venous return. Understand the concept of “resistance to venous return” and know that factors determine its value theoretically, what factors are most important in practice, and how various interventions would change the resistance to venous return. Know how cardiac function (output) curves are generated and how actors which cause hyper effective or hypo effective changes (contractility) in the heart can alter the shape of cardiac function curve. Use a combined cardiac output / venous return graph to predict how interventions such as hemorrhage, increase in preload, acute and chronic heart failure, autonomic stimulation or ihibition, and exercise will affect cardiac output and right atrial pressure. Predict how physiological compensatory changes would alter acute changes.
Cardiac output (CO)
Is the volume of blood pumped into the aorta each minute by the left ventricle. For a 70kg man normal values are HR=70/min and SV=70ml, giving a cardiac output of about 5litre/min. . CO can be increased to 20 l/min depending on the body’s demand for O2. A. The cardiac index is the cardiac output per square meter of body surface area, normal 2 values range from 2.5-4.0 litre/min/m . Body surface area normalizes for different shapes, heights and weights. Tables are available that estimate body surface area from weight and height. An average surface area is 1.73 square 2 meters (m ). Therefore a person with an average cardiac output of 5 l/min would have a Cardiac 2 2 Index of: 5 l/min ÷ 1.73 m = 2.89 l/min/m . II. 1. 2. 3. 4. 1. Methods of measuring the Cardiac Output Fick’s principle Dye dilution Thermodilution Doppler techniques The Fick’s Method
Flow can be measured by adding (or removing) a substance to the liquid as it passes through the tube. Blood is pumped from the venous system through the lungs to the arterial system. In the lungs, O2 is taken up into the blood stream. The total uptake of O2 by the lung per minute has to be equal to the product of the pulmonary blood flow per min. and the difference in O2 concentration in pulmonary venous and pulmonary arterial blood. The O2 uptake can be measured by spirometry. Arterial and venous O2 concentrations can be measured by withdrawing and analyzing blood from both vessels. Therefore: Cardiac Output = O2 consumption/min ÷ (aO2 - vO2)
A known quantity of a dye is injected into the right atrium via catheter. A measured quantity of an indicator (dye) is injected into a large central vein or into the right side of the heart through a catheter. Arterial blood is continuously drown and passes through a photosensitive device that measures the dye concentration. The resulting curve measures dye concentration as a function of time.
The area under the dye-dilution curve can be calculated and approximates the average concentration of dye over time. Knowing the quantity of dye injected, the cardiac output can be determined by: Cardiac output = Quantity of dye injected ÷ area under the curve
The procedure is the same, but blood temperature is measured instead of dye color. A cold dextrose solution (2.5-10 ml) is injected through one part (proximal opening) of a double lumen catheter which is positioned near right atrium and a small thermistor attached to catheter tip lies in pulmonary artery and measures the profile of temperature change with time. The degree of change in the temperature is inversely proportional to the cardiac output. Then: Increased blood flow (and CO) = Minimal temperature change Decreased blood flow (and CO) = Pronounced temperature change Plotting this temperature change against the time it took for the cooler fluid to reach the thermistor gives us a thermo dilution curve, a computer built into the monitor calculates and integrates the area under the thermo dilution curve, and gives a digital readout of the cardiac output in L/min 4. Doppler techniques
Is a non-invasive technique. The machines transmit an ultrasonic vibration into the body and record the change in the frequency of the signal that is reflected off the red blood cells, so Doppler techniques measure velocity, not flow. The flow could be obtained by integrating the signal over the cross-sectional area of the vessel. The velocity of blood in the ascending aorta may be measured using the Doppler effect. The length of a column of blood passing through the aorta in unit time is estimated and then multiplied by the cross-sectional area of the aorta to give stroke volume.
Central venous pressure (CVP) monitoring
The central venous pressure (CVP) measures the filling pressure of the right ventricular (RV); it gives an estimate of the intravascular volume status and is an interplay of the (1) circulating blood volume (2) venous tone and (3) right ventricular function.
Waveforms in CVP
The normal CVP waveform consists of three upwards deflections (a, c, & v waves) and two downward defections (x and y descents). These waves are produced as follows:
1. The ‘a’ wave is produced by right atrial contraction and occurs just after the P wave on the ECG. 2. The ‘c’ wave occurs due to isovolumic ventricular contraction forcing the tricuspid valve to bulge upward into the right atrium. (RA) 3. The pressure within the RA then decreases as the tricuspid valve is pulled away from the atrium during right ventricular ejection, forming the X descent. 4. The RA continues to fill during late ventricular systole, forming the V wave. 5. The Y descent occurs when the tricuspid valve opens and blood from the RA empties rapidly into the RV during early diastole.(1 B. Pulmonary artery and pulmonary capillary wedge pressure monitoring
The pulmonary artery catheter (PAC) help to monitoring the pulmonary artery (PA) pressure, pulmonary capillary wedge pressure (PCWP) as well as central venous pressure (CVP). The PCWP under most circumstances provides an accurate estimate of the diastolic filling (preload) of the left heart.
Factors that influence RAP:
Atrial contraction Intrapleural pressure Posture Blood volume Intrinsic venous tone Sympathetic neural tone to veins Venous pump (exercise IV. Venous return must equal cardiac output.
Over time cardiac output and venous return must be equal for each ventricle, although transient differences can occur. Changes in posture, such as lying down, can briefly increase venous return. The resulting change in the preload should increase cardiac output. But the vascular system is a closed circuit, blood pumped from the heart returns to the heart, therefore, venous return must equal cardiac output over time. V. Determinants of Cardiac Output
CO is the product of heart rate (HR) and stroke volume (SV): CO = HR x SV A. Heart rate: is determined by the rate of spontaneous depolarization at the sinoatrial node and is modified by the autonomic nervous system. The vagus nerve acts on muscarinic receptors to slow the heart, whereas the cardiac sympathetic fibers stimulate beta-adrenergic receptors and increase heart rate. B. Stroke volume is determined by three main factors: preload, afterload and contractility. 1. Preload: is the ventricular volume at the end of diastole. An increased preload leads to an increased stroke volume. Preload is mainly dependent on the return of venous blood from the body. Venous return is influenced by changes in position, intra-thoracic pressure, blood volume and the balance of constriction and dilatation (tone) in the venous system. As the EDV (end-diastolic volume) increases and stretches the muscle fiber, the energy of contraction and stroke volume increase, until a point of over-stretching when stroke volume may actually decrease, as in the failing heart. Cardiac output will also increase or decrease in parallel with stroke volume if there is no change in heart rate. 2. Afterload: is the resistance to ventricular ejection. This is caused by the resistance to flow in the systemic circulation and is the systemic vascular resistance. The resistance is determined by the diameter of the arterioles and pre-capillary sphincters; the narrower or more constricted, the higher the resistance. The level of systemic vascular resistance (total peripheral resistance TPR) is controlled by the sympathetic system which controls the tone of the muscle in the wall of the arteriole, and hence the diameter. 3. Contractility describes the ability of the myocardium to contract in the absence of any changes in preload or afterload. In other words, it is the "power" of the cardiac muscle. The
most important influence on contractility is the sympathetic nervous system. Norepinephrine stimulate Beta-1 adrenergic receptors, and contractility increases. VI. Vascular function curves
State the relationship of right atrial pressure (RAP) and venous return (VR). When graphed the independent variable is the CO, and the dependent variable is the CVP. A. The major determinant of venous return
1. Is the systemic filling pressure . This is the difference between peripheral venous pressure and right atrial pressure (Right atrial pressure is typically ~ 2 mmHg with a mean systemic filling pressure of 7 mmHg. At this pressure difference (7 - 2) and the low resistance of the venous system, venous return is approximately 5 l/min. 2. Blood transfusion or retention of salt and water results in an increase of Pcm, then would increase the pressure difference and increase venous return Hemorrhage would reduce peripheral venous pressure and reduce venous return for a given right atrial pressure. The vascular function curves by effect of changing circulatory volume are parallel to each other.
The cardiac function curves. The Frank–Starling Principle :
This principle illustrates the relationship between cardiac output (CO) and left ventricular end diastolic volume (LVEDV), or the relationship between stroke volume and right atrial pressure. The relationship between LVEDV and SV is known as Starling's law of the heart, which states that the energy of contraction of the muscle is related/proportional to the initial length of the muscle fiber (left graph) A. An increase in LVEDV (preload) The ventricular fiber length is also increased, resulting in an increased tension of the muscle.
An increase in preload (going from point A to B or from C to D in the graph at the right) will increase the cardiac output until very high end diastolic volumes are reached. At this point cardiac output will not increase with any further increase in preload, and may even decrease after a certain preload is reached.
B. Change in contractility Any increase or decrease in the contractility of the cardiac muscle for a given end diastolic volume will act to shift the curve up or down, respectively. (see graph at the left)The curves show how the heart performs at different states of contractility, ranging from the normal heart to one in cardiogenic shock. This is a condition where the heart is so damaged by disease that cardiac output is unable to maintain tissue perfusion. Also shown are increasing levels of physical activity which require a corresponding increase
D. Afterload Relationship between stroke volume and afterload. A series of curves illustrates the effects of increasing afterload on systemic vascular resistance. As afterload increases, the patient moves to a lower curve, with a lower stroke volume for the same ventricular enddiastolic volume (preload).
Interaction of Cardiac and Vascular Function Curves:
Simultaneous plots of cardiac output and venous return as a function of end diastolic volume (or right atrial pressure. A Cardiac Function Curve: This is simply the Frank-Starling curve for the ventricle showing the relationship of cardiac output as a function of end diastolic volume. B. Venous Return Curve. This is the relationship between blood flow in the vascular system (venous return) and right atrial pressure. C. Mean Systemic Pressure This is the point where the venous return curve intersects the X axis. The mean systemic pressure reflects the right atrial pressure when there is ‘no flow’ in the system. At this point the pressure is equal throughout the circulatory system.
This is the steady-state where the two curves intersect; it reflects the point where cardiac output is equal to venous return. E. Factors that affect CO Cardiac output can increase or decrease by altering the Frank-Starling curve, the venous return curve, or both; some predictions can be made by examining how the curves shift as the variables change. 1. Inotropic Changes: Contractility is determined by various autonomic mechanisms and certain drugs (such as digitalis). Inotropic changes will alter the slope of the cardiac curve up or down (as discussed above). a. Positive inotropic agents, such as digoxin or sympathetic stimulation, will increase contractility and therefore increase the cardiac output. This new equilibrium point now reflects an increased CO and a lower RAP (more blood is now being ejected from the heart with each beat). b. Negative inotropic agents have the opposite effect, decreasing contractility and CO, and increasing RAP. 2. Total Peripheral Resistance Changes: TPR is determined by the resistance of the arterioles. Changes in TPR will change the slope of both the cardiac function curve and the venous return curve. a. An increase in TPR (left side graph) will cause blood to be retained on the arterial side of circulation and will increase the aortic pressure against which the heart must pump. This will act to shift both slopes downward. As a result of this simultaneous change, both the cardiac output and the venous return are decreased, however the right atrial pressure remains the same . b. A decrease in TPR (not shown) will allow more blood to flow to the venous side of circulation and will lower the aortic pressure against which the heart must pump. This will shift both slopes upward. Both cardiac output and venous return will be simultaneously increased; again, right atrial pressure will remain the same 3. Exercise. Cardiac output will change to match changing metabolic demands of the body. The outputs of both ventricles must be identical, and also equal the venous return of blood from the body.
During exercise the cardiac output and venous return are balanced. Blood vessels dilate in exercising muscle groups because of increased metabolism, and blood flow increases. This increases venous return and right ventricular preload. More blood is delivered to the left ventricle and cardiac output increases. Associated with exercise there is an increase in sympathetic activity that will lead to an increased contractility and heart rate, further increasing cardiac output to meet tissue requirements.
Role of Heart Rate (HR) in control of cardiac output (CO) Changes in HR alters:
1. Preload An increase in HR decreases diastolic time 2. Afterload An increase in HR alter CO, and changes in CO alter BP 3. Contractility an increase in HR increases net Calcium influx/min –Rate induced regulationB. Graph analysis
The graph to the right shows the effect of changes in HR on CO when the rate of the atrium is paced and gradually increases. 1. A change in HR from 50 to100 causes a decrease in SV but an increase in CO 2. A change in HR from HR 100-200 causes a decrease in SV but CO remains practically constant 3. A change in HR from HR 200 to 250 causes a decrease in SV and a drastic decrease in CO
CONGESTIVE HEART FAILURE A. Definition: Impaired contractility of the myocardium that is not able to provide adequate blood flow to the meet the needs of the tissues. Below figures show that in a patient with heart failure, the chronically low blood pressure causes the kidney to retain fluid in an attempt to restore it. Because contractility is impaired, fluid retention can not restore the cardiac output. Venous pressure increases (venous congestion) with the consequent edema formation (increased capillary filtration)
Acute heart failure (HF)
Sudden coronary occlusion No change in blood volume Cardiac function curve shift downward, and the equilibrium point is where it intersects the normal vascular function curve Change from equilibrium point A to point B (moderate HF) or from A to C (acute HF) C. Chronic heart failure
Hypertension, ischemic heart disease Increase in blood volume because of kidney retention Change from the equilibrium point A to point D (moderate HF) or from A to E (severe HF) D. Signs and symptoms:
Fatigue Low exercise tolerance Venous congestion and edema Dyspnea Reduced ejection fraction E. Compensations
Fluid retention raises venous pressure Healthy chamber pumps blood into the weak chamber. Failure is often on only one side of the heart. Thus the healthy chamber can greatly raise the venous pressure of the affected chamber even without fluid retention. Often seen in acute infarction of the left ventricle where pulmonary edema occurs. F. Causes of hypertrophy/failure
1. Pressure overload causes concentric hypertrophy where the ventricle remodels inwardly causing low lumen volume and thick wall. Caused by hypertension or outflow track obstruction. 2. Volume overload leads to eccentric hypertrophy. The heart remodels outwardly to give a large lumen volume and a thin wall. Caused by regurgitant aortic valve or AV fistulas.