logging in or signing up Cardiac output aSGuest59024 Download Post to : URL : Related Presentations : Let's Connect Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 4621 Category: Education License: All Rights Reserved Like it (3) Dislike it (0) Added: August 06, 2010 This Presentation is Public Favorites: 4 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript CARDIAC OUTPUT : CARDIAC OUTPUT By Umadevi.K.N II MD Dept of Kriya Shareera Slide 2: Quantity of blood pumped into aorta each minute by the heart Male - 5.6 lit/min Female - 4.9 lit/min Slide 8: CO = SV x HR Factors affecting CO : Factors affecting CO Venous return Force of contraction Heart rate Peripheral resistance Slide 10: Stroke volume is the amount of blood pushed out of the heart upon contraction. End-diastolic volume is the amount of blood that fills in the heart after relaxation and just before the next contraction. End-diastolic pressure (preload) is the pressure present before a contraction. It indicates the extent of cardiac muscle stretching and determines the force at which the blood can be pushed out during contraction. Myocardial contractility is the the ability of the heart muscle to push out blood upon contraction. It is essentially the strength of the heart muscle to produce force. Systolic aortic pressure is the pressure of the blood that is pushed out of the heart which will be at its greatest immediately after the blood leaves the heart and enters the aorta. Stroke volume and systolic aortic pressure is a combination of end-diastolic volume, end-diastolic pressure and myocardial contractility. If any of the above factors are affected or impaired, the cardiac output can be reduced. This means that the sufficient blood will not be circulated throughout the body at a pressure that will maintain a healthy circulation and perfusion. Windkessel Effect The aorta is elastic and will stretch as high pressure blood leaves the heart. The recoil of the aorta will then play a further role is keeping the blood flowing at the correct pressure – this prevents excessively high pressure of blood leaving the heart and maintains a sufficient pressure to return blood to the heart. This is known as the “Windkessel Effect”. Starling’s Law of Heart This law states that in a healthy heart with normal cardiac output, the amount of blood that is pumped out of the heart (stroke volume) should return in full (end diastolic volume). The greater the volume of blood that leaves the heart, the greater the volume that will return and vice versa. If less blood returns that what was pushed out, then the cardiac output will decrease. This is an important concept to understand in order to identify the type of heart failure and identify the cause of reduced cardiac output. Slide 11: Maintaining and regulating cardiac output, which is usually proportional to the tissues' need for oxygen and other nutrients, is one of the circulatory system's most intricate functions. Measurement of cardiac output makes possible an evaluation of respiratory exchange, i.e., the delivery of oxygen to the tissuesThe cardiac output represents the volume of blood that is delivered to the body, and is therefore an important factor in the determination of the effectiveness of the heart to deliver blood to the rest of the body, (i.e., determining heart failure, inadequate circulation, etc). Slide 13: Windkessel Effect The aorta is elastic and will stretch as high pressure blood leaves the heart. The recoil of the aorta will then play a further role is keeping the blood flowing at the correct pressure – this prevents excessively high pressure of blood leaving the heart and maintains a sufficient pressure to return blood to the heart. This is known as the “Windkessel Effect”. Starling’s Law of Heart This law states that in a healthy heart with normal cardiac output, the amount of blood that is pumped out of the heart (stroke volume) should return in full (end diastolic volume). The greater the volume of blood that leaves the heart, the greater the volume that will return and vice versa. If less blood returns that what was pushed out, then the cardiac output will decrease. This is an important concept to understand in order to identify the type of heart failure and identify the cause of reduced cardiac output. Factors affecting venous return : Factors affecting venous return Respiratory pump Muscular pump Gravity Venous pressure Sympathetic tone Slide 16: Causes of abnormal cardiac outpu . • High cardiac output is almost always caused by reduced total peripheral resistance. • Low cardiac output is caused by (1) decreased ability of the heart to pump (severe infarction, valvular disease, cardiac damage, cardiac metabolic derangements); and (2) decreased venous return (decreased blood volume, acute venous dilatation, obstruction of large veins). Circulatory shock – decrease of cardiac output below an adequate level Slide 17: Sufficient cardiac output is necessary to deliver adequate supplies of oxygen and nutrients (glucose) to the tissues. This translates to the conclusion that cardiac output is directly related to energy production. Low cardiac output will reduce energy levels. For example, if your cardiac output fell to 3500 ml (about 2/3 of normal) your oxygen - and hence your energy supply - would be decreased as well. Your brain with 1/3 less energy may be less sharp, confused or even unconscious. Your muscles with 1/3 less energy would feel weaker. In contrast, high cardiac output satisfies periods of high energy demand. Rate of flow to tissues depends on tissue needs (i.e. it depends on Total Peripheral Resistance). Therefore, cardiac output is proportional to the energy requirements of the tissues. Slide 18: FRANK STARLING LAW Force of ventricular contraction is directly proportional to initial length of muscle fibers. Pre Load is directly proportional to End Diastolic Volume. (End Diastolic Volume is the amount of blood remaining in ventricles at the end of diastole). Greater is preload; more is length of muscle fibers. EDV is increased by greater venous return. Therefore more is pre load more is force of myocardial contraction. Frank – Starling Principle : Frank – Starling Principle This principle illustrates the relationship between cardiac output and left ventricular end diastolic volume (or the relationship between stroke volume and right atrial pressure.) Frank – Starling Principle : Frank – Starling Principle The Frank Starling principle is based on the length-tension relationship within the ventricle. If ventricular end diastolic volume (preload) is increased, it follows that the ventricular fiber length is also increased, resulting in an increased ‘tension’ of the muscle. Cardiac output is directly related to venous return, the most important determining factor is preload. The contraction and therefore stroke volume in response to changes in venous return is called the Frank-Starling mechanism (or Starling's Law of the heart). Slide 21: Starling's Law describes the relationship between end-diastolic volume and stroke volume. It states that the heart will pump out whatever volume is delivered to it. If the end-diastolic volume doubles then stroke volume will double. Slide 22: 22 Frank-Starling Law Of The Heart The heart normally pumps the blood returned to it Therefore, the more blood that is returned to the heart (venous return) the higher the EDV and therefore the higher the stroke volume. The extent of cardiac filling is referred to as the “preload” It is called the preload, because it is the work load imposed on the heart before contraction even begins Preload : Preload afterload : afterload Slide 26: 26 Slide 27: 27 Slide 28: 28 Slide 29: Increased Sympathetic Stimulation - Increased sympathetic stimulation (due to fright, anger, etc.) increases the heart rate. It also increases stroke volume by increasing contractility, which results in more complete ejection of blood from the heart (lower ESV). • Increased Parasympathetic Stimulation - Parasympathetic activity increases after a crisis has passed. This reduces heart rate and stroke volume from their high levels, bringing cardiac output back to normal. • Increased Venous Return - Cardiac muscle fibers are stretched by increased blood volume returning to the heart (increased venous return and EDV). Increased stretch results in greater force of contraction, which increases stroke volume. • Slow Heart Rate - Slow heart rate allows for more time for ventricular filling, increasing EDV and therefore stroke volume. • Extremely Fast Heart Rate - Extremely rapid heart rate results in low venous return and therefore decreased stroke volume. • Exercise - Exercise activates the sympathetic nervous system, increasing heart rate, contractility, and stroke volume. Both the higher heart rate and squeezing action of skeletal muscles on veins increase venous return, contributing to increased stroke volume. • Sudden Drop in Blood Pressure - A sudden drop in blood pressure results in low venous return and therefore decreased stroke volume. However heart rate increased due to sympathetic activity, and normal cardiac output is maintained. • Rising Blood Pressure - Rising blood pressure reduces sympathetic activity, decreasing heart rate. High blood pressure also increases arterial pressure which ventricles must overcome before semilunar valves open, increasing ESV and decreasing stroke volume. Reduced cardiac output helps bring blood pressure down to normal levels. • Sudden Drop in Blood Volume - A sudden drop in blood volume (eg. due to severe blood loss) results in low venous return and therefore decreased stroke volume. Sympathetic activity increases heart rate, maintaining cardiac output. • Excess Calcium - Excess calcium can lead to spastic heart contractions, an undesirable condition. Calcium also increases stroke volume by enhancing contractility. Slide 30: Heart Rate Sympathetic stimulation increases heart rate, parasymp reduces. HR must remain within a range to acheive adequate perfusion. Cardiac output falls if heart rate is too slow or too fast. Slowing heart rate beyond a limit has little effect on stroke volume because most ventricular filling occurs in early diastole anyway, so the extra time at the end adds little. Very rapid heart rate impinges on filling time, decreasing stroke volume, and hence cardiac output. So extreme brady or tachy require correction (pharacological or electrical). Slide 31: Afterload If output reseistance is high, a standard contraction will force out less blood than normal. Starling's law remedies this problem. Higher output resistance overwhelms one beat forcing some blood to remain in the ventricle; thus, for the next beat the ventricle will be extra full, so next beat will be more forceful. Afterload: Afterload is the tension (or the arterial pressure) against which the ventricle must contract. If arterial pressure increases, afterload also increases. Afterload for the left ventricle is determined by aortic pressure, afterload for the right ventricle is determined by pulmonary artery pressure Preload is the degree to which cardiac muscle cells are stretched by the blood entering the heart chambers. According to the Frank-Starling law of the heart, the more the chamber is stretched, the greater the force of its contraction. Because end-diastole volume (EDV) is a measure of how much blood enters the ventricles, the EDV is an indicator of ventricle preload. Preload is the muscle length prior to contractility, and it is dependent of ventricular filling (or end diastolic volume.) This value is related to right atrial pressure. The most important determining factor for preload is venous return. Slide 32: Afterload is a measure of the pressure that must be generated by the ventricles to force the semilunar valves open. The greater the afterload, the smaller the stroke volume. Arteriosclerosis (narrowing of the arteries) and high blood pressure increase afterload and reduce stroke volume. Afterload is basically the pressure against which the left ventricle has to push the blood from it to the aorta, so if that pressure decreases, it'll be easier for the blood to be pushed thru it, which is the stroke volume. Hope this helps! Slide 33: The total amount of blood flow circulating through the heart, lungs and all the tissues of the body represents the cardiac output. Most individual tissues determine their own flow in proportion to their metabolic rate. The skin is a notable exception where the priority is thermal rather than metabolic. Renal blood flow and metabolic rate are related but plasma flow determines metabolic rate rather than metabolic rate determining blood flow. 1 Brain, heart, skeletal muscle and the splanchnic area all vary their blood flows according to local tissue metabolic rate. Summation of peripheral blood flows constitutes venous return and hence cardiac output. Cardiac output is therefore, largely, determined by the metabolic rate of the peripheral tissues; the heart ‘from a flow standpoint, plays a “permissive” role and does not regulate its own output’. 2 This peripheral tissue, largely metabolic, determination of cardiac output has been known for many years. 3,4 Determinants of Cardiac Output (CO) : Determinants of Cardiac Output (CO) Preload Heart Rate Afterload Contractility Cardiac Output Stroke Volume Definitions : Definitions Preload amount of stretch on the ventricular myocardium prior to contraction Afterload the arterial pressure (or some other measure of the force) that a ventricle must overcome while it contracts during ejection impedance to ventricular ejection Definitions : Definitions Contractility myocardium’s intrinsic ability to efficiently contract and empty the ventricle (independent of preload & afterload) Slide 37: Preload = ventricular filling or volume Determinants of Cardiac Output- Preload Slide 38: Preload approximated by measuring: 1. Central venous pressure (CVP) = right atrial pressure. 2. Pulmonary capillary diastolic wedge pressure (PCWP) = LVEDP Parameters: 1. CVP 3mm Hg (normal range 1 - 5) 2. PCWP 9mm Hg (normal range 2 - 13) Determinants of Cardiac Output - Preload Frank-Starling Mechanism of the Heart : Frank-Starling Mechanism of the Heart The intrinsic ability of the heart to adapt to changing volumes of inflowing blood Frank-Starling Law : Frank-Starling Law What goes into the heart comes out. Increased heart volume stretches muscles and causes stronger contraction. Stretch increases heart rate as well. Direct effect on sino-atrial node Bainbridge reflex (through the brain) Slide 41: Frank-Starling law of the heart Intrinsic variation as EDV increases, so does force of contraction (increased stretch) Increased peripheral resistance Increased EDV Increased stretch Next contraction is stronger Process is highly adjustable Slide 44: the Frank - Starling mechanism of the heart: Left ventricle (LV) function curve, or Frank - Starling curve (1914): Normal range of the LVEDP, 5-6 mmHg Optimal initial preload, 15-20 mmHg (Sarcomere, 2.0 – 2.2 µm When the LVEDP > 20 mmHg, LV work is maintained at almost the same level, does not change with the increase of LVEDP Mechanism Concept of heterometric regulation Factors determining the preload (LVEDP) : Factors determining the preload (LVEDP) Period of the ventricle diastole (filling) – heart rate Speed of the venous return (difference between the venous pressure and atrial pressure) Importance of the heterometeric regulation : Importance of the heterometeric regulation In general, heterometric regulation plays only a short-time role, such as during the body posture change, artery pressure increase, unbalance of ventricular outputs. In other conditions, such as exercise, cardiac output is mainly regulated by homometric regulation. Slide 47: Determinants of Cardiac Output - Afterload Slide 48: Short time change of the arterial pressure Transit arterial pressure rise isovolumetric contraction phase become longer period of ejection shorter stroke volume less more blood left in the ventricle left LVEDP increase through heterometeric regulation stroke volume return to normal in next beat. Slide 49: Contractility (neural and humoral regulation) Sympathetic nerve (norepinephrine) or the epinephrine and norepinephrine (adrenal gland) enhance the strength and the velocity of the cardiac contraction. The change of myocardial property is independent of the preload. We call it the contractility. Importance: exert a long – time influence on the cardiac output. Determinants of Cardiac Output - Contractility Definitions : Definitions Contractility myocardium’s intrinsic ability to efficiently contract and empty the ventricle (independent of preload & afterload) Action of Sympathetic Stimulation : Action of Sympathetic Stimulation Sympathetic nerve stimulation increases cardiac contractility. At rest the heart is under sympathetic tone. Noradrenaline enhances calcium entry into cardiac cells. Parasympathetic stimulation has little affect on contractility due to the innervation pattern of the heart. Slide 52: Normal range of the heart rate 60 – 100 beats/min Within physiological limit?, the higher the heart rate, the more blood that the heart pump. Determinants of Cardiac Output - The heart rate Slide 53: Cardiac Output Regulation Slide 11.19 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 11.7 Cardiac index : Cardiac index Amount of blood pumped out of ventricle per minute per square meter of body surface area Q/BSA f blood pumped out of ventricle per minute per s3lit/min/m2 of body surface area CI varies with age, peaking at around 8 years. Cardiac reserve : Cardiac reserve Maximum amount of blood that can be pumped out by the heart above normal value The ratio between the maximum and resting cardiac output of an individual is the cardiac reserve It reflects the ability of the heart to adapt the change of environment (internal or external) blood that can be pumped out by the heart above normal value is called cardiac reserve Expressed in percentage Young healthy adult – 300 - 400% Old age - 200-250% Variations in Cardiac Output : Variations in Cardiac Output Physiological variations 1. Age: In children CO is less →less blood volume. Cardiac index is more than adults because of less body surface area. 2. Sex: Females CO less → cardiac index is more because of less body surface area. Regulators of the Heart: Factors Influencing Stroke Volume : Regulators of the Heart: Factors Influencing Stroke Volume Figure 14-31: Factors that affect cardiac output Frank-Starling Law : Frank-Starling Law What goes into the heart comes out. Increased heart volume stretches muscles and causes stronger contraction. Stretch increases heart rate as well. Direct effect on sino-atrial node Bainbridge reflex (through the brain) Frank Starling Law of the Heart : Frank Starling Law of the Heart The more cardiac muscle is stretched within physiological limits, the more forcibly it will contract. Rubber band analogy Increasing volumes of blood in ventricles increase the stretch & thus the force generated by ventricular wall contraction. Greater stretch means more blood volume is pumped out, up to physical limits. Frank Starling Law of the Heart : Frank Starling Law of the Heart Increased blood volume = increased stretch of myocardium = Increased force to pump blood out. Effects of Sympathetic Stimulation : Effects of Sympathetic Stimulation Increases contractility of the heart. Decreases volume by contracting the veins. Increases filling pressure Increases resistance Hypereffective Heart : Hypereffective Heart Effected by: Nervous excitation. Cardiac Hypertrophy Exercise – Marathon runners may get 30 to 40 L/min Aortic Valve Stenosis Hypoeffective Heart : Hypoeffective Heart Valvular disease Increased output pressure Congential heart disease Myocarditis Cardiac anoxia Toxicity Disease States Lowering Total Peripheral Resistance : Disease States Lowering Total Peripheral Resistance Beriberi: insufficient thiamine – tissues starve because they cannot use nutrients. AV fistula: e.g. for dialysis. Hyperthyroidism: Reduced resistance caused by increased metabolism Anemia (lack of RBCs): effects viscosity and transport of O2 to the tissues. Disease States Lowering Cardiac Output : Disease States Lowering Cardiac Output Heart attack, valvular disease, myocarditis, cardiac tamponade, shock. Shock: Nutritional deficiency of tissues. Decreased venous return caused by: Reduced blood volume Venous dilitation (increased circulatory volume) Venous obstruction Changes in Intrapleural Pressure : Changes in Intrapleural Pressure Generally shift the cardiac output curve in proportion to pressure change (breathing, Valsalva maneuver). Cardiac Tamponade (filling of pericardial sac with fluid) lowers rate of change of CO with right atrial pressure Heart Pericardial Sac 15 L/min Determinants of Venous Return : Determinants of Venous Return Mean systemic filling pressure Right Atrial Pressure Resistance to Flow Pressure change is slight. Thus, small increase in RA Pressure causes dramatic reduction in venous return. (mean systemic filling pressure). Disease States Lowering Total Peripheral Resistance : Disease States Lowering Total Peripheral Resistance Beriberi: insufficient thiamine – tissues starve because they cannot use nutrients. AV fistula: e.g. for dialysis. Hyperthyroidism: Reduced resistance caused by increased metabolism Anemia (lack of RBCs): effects viscosity and transport of O2 to the tissues. Disease States Lowering Cardiac Output : Disease States Lowering Cardiac Output Heart attack, valvular disease, myocarditis, cardiac tamponade, shock. Shock: Nutritional deficiency of tissues. Decreased venous return caused by: Reduced blood volume Venous dilitation (increased circulatory volume) Venous obstruction Filling Pressure : Filling Pressure Mean Circulatory: The pressure within the circulatory system when all flow is stopped (e.g. by stopping the heart). Mean Systemic: Pressure when flow is stopped by clamping large veins. The two are close numerically. Measurement of CO : Measurement of CO Electromagnetic/ultrasonic (transit time) flow meter. Oxygen Fick method: CO = (Rate of O2 absorbed by lungs) [O2]la - [O2]rv Indicator dilution method: Inject cold saline (or dye) into RA, measure temperature (or concentration) in aorta. You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.