Heart Rate, Stroke Volume, and Cardiac Output PDF

HEART RATE, STROKE VOLUME AND CARDIAC OUTPUT AND ITS REGULATION 1  HEART RATE The number of times the heart beats per minute. Normal heart rate is 72/minute but ranges between 60 to 100 per minute....

HEART RATE, STROKE VOLUME AND CARDIAC OUTPUT AND ITS REGULATION 1  HEART RATE The number of times the heart beats per minute. Normal heart rate is 72/minute but ranges between 60 to 100 per minute. 2  REGULATION OF HEART RATE 1. Nervous 2. Hormonal 3 NERVOUS The nervous regulation of heart rate consists of three components: 1. Cardiac or Vasomotor center 2. Motor (efferent) nerve fibers to the heart 3. Sensory (afferent) nerve fibers from the heart 4  Cardiac or Vasomotor center Vasomotor center is bilaterally situated in the reticular formation of medulla oblongata and lower part of pons. Vasomotor center is formed by three areas: 1. Vasoconstrictor area or cardioaccelerator center: pressor area 2. Vasodilator area or cardioinhibitory center: depressor area 3. Sensory area: receives afferent impulse from the heart to the nucleus of tractus solitaries. These cardiac centers send impulses to the heart via the autonomic nervous system. 5 Nervous regulation cont’d The accelerator center sends impulses along the sympathetic nerve fibers which cause increase in heart rate & force of contraction. The inhibitory center sends parasympathetic impulses along the vagus nerve which cause decrease in heart rate. 6 Stimuli for the cardiac centers 1. Changes in blood pressure: Baroreceptors (pressoreceptors) located in the carotid sinuses and aortic sinus detect changes in blood pressure 2. Changes in oxygen level of the blood: Chemoreceptors located in the carotid bodies and aortic body detect changes in the oxygen content of the blood. The sensory nerves for the carotid receptors are the glossopharyngeal (9th cranial) nerves. The sensory nerves for the aortic arch receptors are the vagus (10th cranial) nerves. 7 8  A drop in blood pressure is detected by the baroreceptors in the carotid sinuses. This drop causes fewer impulses to be generated by the baroreceptors. The impulses travel along the glossopharyngeal nerves to the medulla. The decrease in frequency of impulses stimulate the accelerator center. The accelerator center generates impulses that are carried by sympathetic nerves to the SA node, AV node and ventricular myocardium to cause increase in heart rate and force of contraction. This leads to an increase in blood pressure. When blood pressure is increased above normal, the heart receives parasympathetic impulses from the inhibitory center along the vagus nerves to the SA node & AV node which then slow the heart rate to normal. 9 Decrease in oxygen content of the blood This is sensed by chemoreceptors in the aortic body which generate impulses. These impulses are carried by the vagus nerves to the accelerator center in the medulla. The accelerator center then sends sympathetic impulses to the heart muscles to increase the heart rate and force of contraction to circulate more oxygen to correct the hypoxia. 10  HORMONAL REGULATION In stressful conditions, the adrenal medulla secretes epinephrine. Epinephrine increase the heart rate and force of contraction. This helps to increase blood supply to tissues in need of more oxygen. 11 12  APPLIED PHYSIOLOGY 1. TACHYCARDIA Tachycardia is the increase in heart rate above 100/minute. Physiology Causes: Newborn or Childhood, Anxiety, Exercise, Pregnancy (especially during labor) Pathology Causes: Anaemia, Hyperthyroidism, Valvular heart disease, Cardiomyopathy, Hypoxia, Fever, Drugs (e.g catecholamines). 2. BRADYCARDIA Bradycardia is the decrease in heart rate below 60/minute. Physiology Causes: During Sleep, Athletes Pathology Causes: Heart Failure, Congenital heart disease, hypothyroidism, hypothermia, Raised intracranial pressure, Drugs (Antiarrhythmic drugs, calcium channel blockers, beta blockers). 13 STROKE VOLUME 14  STROKE VOLUME The amount of blood pumped out of each ventricle per beat is called stroke volume (SV). 70 ml. The output of the heart per unit time (minute) is called cardiac output. Cardiac Out put= Stroke Volume x Hear Rate [70 mL x 72 beats / min= 5040 ml. Approx] Cardiac Index: There is a correlation between resting cardiac output and body surface area. The output per minute per square meter of body surface is called cardiac index. Averages 3.2 L. 15  Stroke volume is also defined as the difference between the ventricular End Diastolic Volume [EDV] and the End Systolic Volume [ ESV]. SV = EDV -ESV EDV is the filled volume of ventricle prior to contraction ESV is the residual volume of blood remaining in the ventricle after ejection. The EDV is about 120 ml of blood and the ESV about 50 ml of blood. The difference in these two volumes 70 ml represents the SV. Factor that alters either the EDV or the ESV will change SV. Example: Increase in EDV increases SV, whereas an increase in ESV decreases SV. 16  When the heart contracts strongly, the end-systolic volume can be decreased to as little as 10 to 20 milliliters. Conversely, when large amounts of blood flow into the ventricles during diastole, the ventricular end diastolic volumes can become as great as 150 to 180 milliliters in healthy heart. By both increasing the end-diastolic volume and decreasing the end- systolic volume, the stroke volume output can be increased. 17  Preload affect the SV through the increase in venous return to the heart, increases the filled volume (EDV) of the ventricle, which stretches the muscle fibers thereby increasing their preload. This leads to an increase in the force of ventricular contraction. Afterload is related to the pressure that the ventricle generate to eject blood into the aorta. Changes in afterload affect the ability of the ventricle to eject blood and thereby alter ESV and SV. increase in afterload, increase aortic pressure, decreases SV, and causes ESV to increase. 18 19  Factor No change Sleep Moderate changes in environmental temperature Increase Anxiety and excitement (50–100%) Eating (30%) Exercise (up to 700%) High environmental temperature Pregnancy Epinephrine Decrease Sitting or standing from lying position (20–30%) Rapid arrhythmias, Heart disease PRESSURE VOLUME LOOP 22 There are only three ways that the body regulates stroke volume from minute-to -minute: Filling pressure (preload) Aortic pressure (afterload) Contractility 23 PRESSURE VOLUME LOOP The ejection loop 24 PRESSURE VOLUME LOOP Changing filling pressure changes stroke volume only by changing LVEDV This could be an example of transfusion Lowering LVEDP has the opposite effect (hemorrhage) 25 Lowering the aortic pressure causes the ventricle to empty more completely. The stroke volume increases by an amount equal to the fall in LVESV. LVEDV is not affected. Raising aortic pressure has the opposite effect 26 PRESSURE VOLUME LOOP Increasing contractility decreases LVESV and thus increases stroke volume. LVEDV is not affected. Heart failure has the opposite effect 27 PRESSURE VOLUME LOOP 28 The real ejection loop has a rounded top since the blood pressure increases during ejection (auxotonic beat) 29 Decreased compliance occurs only in disease and is not a physiological regulator 30  Hypertrophy Normal Dilation 31  Hypertrophy results Hypertroph y from increased afterload over several months. Normal Dilation results from Dilation persistently elevated preload over several days. 32  Hypertrophy results Hypertroph y from increased afterload over several months. Normal Dilation results from Dilation persistently elevated preload over several days. Fiber slippage at the desmosomes will occur before the fibers will extend beyond Lo 33  Hypertrophy results from increased work load over several Hypertroph months.
y Increased mass Dilation results from Normal persistently elevated Dilation preload over several days.
Same mass The large chamber diameter and thin wall puts the dilated heart at a mechanical disadvantage. 34 Notice that stroke volume change in a reciprocal manner. Stroke Work = P x Vol As P goes up V naturally goes down so their product remains constant. Stroke work should be independent of any change in blood pressure. 35 If aortic pressure is held constant stroke volume increases with contractility. Stroke volume goes down as aortic pressure goes up. Since stroke volume changes reciprocally with aortic pressure their product (stroke work) is relatively independent of aortic pressure 36 How can we measure contractility in the patient? Ejection fraction = (LVEDV-LVESV) / LVEDV The fraction of the ventricular contents at end diastole that is ejected. 37 How can we measure contractility in the patient? Ejection fraction = (LVEDV-LVESV) / LVEDV A normal ejection fraction should be above 0.50. Ejection fractions of 0.30-0.50 are of concern. Values below 0.30 carry a poor prognosis. 38 How can we measure contractility in the patient? Ejection fraction = (LVEDV-LVESV) / LVEDV Can be easily measured by X-ray Nuclear techniques Echo 50-60 normal 35-49 concern ↑CO 51  2 factors that ↑ heart pumping when the vol is ↑ed are 1. Frank Starling Mechanism - Major 2. (R) Atrial wall stretch => direct ↑ HR by 10-20%. 52 Heart Rate Heart Rate: Cardiac output is directly proportional to heart rate provided, the other three factors remain constant. 53  Peripheral Resistance Peripheral resistance is the resistance offered to blood flow at the peripheral blood vessels. Peripheral resistance is the resistance or load against which the heart has to pump the blood. So, the cardiac output is inversely proportional to peripheral resistance. Resistance is offered at arterioles so, the arterioles are called resistant vessels. In the body, maximum peripheral resistance is offered at the splanchnic region 54 CO & Total Peripheral Resistance(TPR) CO = Arterial Presure TPR Long term changes of TPR only (no other functions of the circulation change), the CO changes quantitavely in opposite direction 55 Measurement of CO 56 In animals Direct method 1. Cardiometer 2. Flow meter a) Electromagnetic flow meter b) Mechanical flow meter 57 In humans Indirect methods 1. Direct/O2 Fick method 2. Indicator dilution method 3. Doppler + echocardiography 58 Direct Fick Method Described by Adolph Fick in 1870. Fick’s principle states that the amount of a substance taken up by an organ (or the whole body) or given out in a unit time is equal to the arterial level of the substance minus the venous level(A-V difference), multiplied by blood flow. It can be used to determine cardiac output by measuring the amount of oxygen consumed(or carbon di oxide given out) by the body in a given period divided by the A-V difference across the lungs. Advantage: accurate. Disadvantage: invasive(catheter is inserted through patient’s vein). 59 Indicator dilution technique A known amount of a dye or radioactive isotope is injected into an arm vein and the concentration of the indicator in serial samples of arterial blood is determined. The output of the heart is equal to the amount of indicator injected divided by its average concentration in arterial blood after a single circulation through the heart. The log of the indicator concentration in serial arterial samples is plotted against time as concentration rises, falls and rises again as indicator re- circulates. Advantage: accurate. Disadvantage: invasive (involves injection of marker substance). 60 Thermodilution cont’d The temperature change is inversely proportional to the amount of blood flowing through the pulmonary artery(i.e. the extent to which the cold saline is diluted by the blood). Advantages of thermodilution 1. The saline is completely innocuous. 2. The cold is dissipated in the tissues so, re-circulation is not a problem. 3. The catheter can also be used to determine hemodynamic pressures and collect mixed venous blood. 4. Accurate. 61  Doppler technique + echocardiography To measure velocity and volume of flow through valves. Clinical usefulness: evaluating & planning therapy in patients with valvular lesions. Echocardiography is a non-invasive technique in which pulses of ultrasonic waves at a frequency of 2.25MHz are emitted from a transducer/receiver. Waves are reflected back from various parts of the heart. Reflections occur wherever acoustic impedance changes. A recording of the echoes displayed against time on an oscilloscope provides a record of the movements of the ventricular wall, septum and valves during the cardiac cycle. 62 Doppler echo cont’d Advantages: provides information about structure and movement of valves and chambers. Disadvantage: less accurate & requires well-trained operator. 63 Others Ultrasonic Doppler transducer technique Ballistocardiography 64  HYPEREFFECTIVE AND HYPOEFFECTIVE HEART Cardiac output curves for the normal heart and for hypoeffective and hypereffective hearts. Point A on the normal cardiac output curve denotes resting cardiac output (5 L/min at a right atrial pressure of 0 mmHg). Several other curves are also depicted for hearts that are not pumping normally. The uppermost curves are for hypereffective hearts that are pumping better than normal and the lowermost curves are for Figure 1.0 hypoeffective hearts that are pumping at levels below normal. 65  The figure 1.0 above depicts cardiac output curves for the normal heart and for hypoeffective and hypereffective hearts at increasing levels of right atrial pressure. Point A on the normal cardiac output curve denotes resting cardiac output (5L/min at a right atrial pressure of 0 mmHg). It is important to note that the plateau level for this normal cardiac output curve is about 13L/min, which is 2.5 times normal cardiac output. This means that the normal heart, functioning without special stimulation, can pump an amount of blood 2.5 times the normal amount before the heart becomes a limiting factor in the control of cardiac output. Several other curves are also denoted in Figure 1.0 for hearts that are not pumping normally. Predictably, the changes in cardiac output that arise from the need to meet different physiological conditions can be produced by changes in heart rate or stroke volume or both. 66  Factors That Can Cause Hypereffective Heart They are (1) Nervous stimulation and (2) Hypertrophy of the heart muscle. 1.) Nervous stimulation: The combination of sympathetic stimulation and parasympathetic inhibition does two things to increase the pumping effectiveness of the heart: 1. It greatly increases the heart rate—sometimes, in young people, from the normal level of 72 beats/min up to 180 to 200 beats/min—and 2. It increases the strength of heart contraction (which is called increased “contractility”) to twice its normal strength. Combining these two effects, maximal nervous excitation of the heart can raise the plateau level of the cardiac output curve to almost twice the plateau of the normal curve, as shown by the 25-liter level of the uppermost curve in Figure 1 above. 67  2. Hypertrophy of the heart muscle: Increased Pumping Effectiveness Caused by Heart Hypertrophy. A long-term increased workload, but not so much excess load that it damages the heart, causes the heart muscle to increase in mass and contractile strength in the same way that heavy exercise causes skeletal muscles to hypertrophy. For instance, it is common for the hearts of marathon runners to be increased in mass by 50 to 75 per cent. This increases the plateau level of the cardiac output curve, sometimes 60 to 100 percent, and therefore allows the heart to pump much greater than usual amounts of cardiac output. When combines the nervous excitation of the heart and hypertrophy, which occurs in marathon runners, the total effect can allow the heart to pump as much 30 to 40 L/min, this increased level of pumping is one of the most important factors in determining the runner’s running time. 68  Factors That Cause a Hypoeffective Heart Any factor that decreases the heart’s ability to pump blood causes hypoeffectivity. Some of the factors that can do this are the following: Coronary artery blockage, causing a “heart attack” Inhibition of nervous excitation of the heart Pathological factors that cause abnormal heart rhythm or rate of heartbeat Valvular heart disease Increased arterial pressure against which the heart must pump, such as in hypertension Congenital heart disease Myocarditis Cardiac hypoxia 69 THANK YOU 70