Diese Präsentation wurde erfolgreich gemeldet.
Wir verwenden Ihre LinkedIn Profilangaben und Informationen zu Ihren Aktivitäten, um Anzeigen zu personalisieren und Ihnen relevantere Inhalte anzuzeigen. Sie können Ihre Anzeigeneinstellungen jederzeit ändern.
Nächste SlideShare
×

# Cardiac output by Dr. Amruta Nitin Kumbhar Assistant Professor, Dept. of Physiology, DYPMC,KOP

2.352 Aufrufe

Veröffentlicht am

Deﬁnition of cardiac output and related terms
Measurement of cardiac output
Variations in cardiac output
Regulation of cardiac output
Cardiac output control mechanisms
Role of heart rate in control of cardiac output
Integrated control of cardiac output
Heart–lung preparation

Veröffentlicht in: Gesundheit & Medizin
• Full Name
Comment goes here.

Are you sure you want to Yes No

### Cardiac output by Dr. Amruta Nitin Kumbhar Assistant Professor, Dept. of Physiology, DYPMC,KOP

1. 1. Cardiac output Dr. Amruta Nitin Kumbhar Assistant Professor Dept. Of Physiology
2. 2. SLOs 1. Deﬁnition of cardiac output and related terms 2. Measurement of cardiac output 3. Variations in cardiac output 4. Regulation of cardiac output 5. Cardiac output control mechanisms 6. Role of heart rate in control of cardiac output 7. Integrated control of cardiac output 8. Heart–lung preparation
3. 3. CARDIAC OUTPUT  Cardiac output is defined as amount of blood pumped out of each ventricle per minute.  Cardiac output is expressed in two forms,  1)stroke volume  2) minute volume Unit – liter (ml) / min
4. 4.  CO = SV x HR  cardiac output = stroke volume X heart rate (ml/minute) (ml/beat) (beats/min)  a.Average heart rate = 70 bpm  b.Average stroke volume = 70−80 ml/beat  c.Average cardiac output = 5000 ml/minute  Cardiac output varies widely with the level of activity of the body.  CO = SV x HR  Cardiac index is the cardiac output expressed in relation to the body surface area.  The normal cardiac index is about 3.2 L/min/m2.
5. 5. Distribution of the cardiac output  Of the total cardiac output, about 75% is distributed to the vital organs of the body and rest of 25% to the skeletal muscle, other organs of the body and skin.
6. 6. Regulation of cardiac output 1. Control of HR or Extrinsic autoregulation 2. Control of SV or Intrinsic autoregulation All the conditions that affect either heart rate or stroke volume or both will produce variations in the cardiac output
7. 7. Stretching of myocardium (i.e. extent of preload) determines
8. 8. Stretching of myocardium(i.e. extent of preload) Increased by Decreased by 1. Increase in total blood volume Decrease in total blood volume 2. Atrial contraction (aid ventricular filling) Increase in intrapericardial pressure 3. Increase pumping action of skeletal muscle Decrease in ventricular compliance 4. Increase venous tone Body position 5. Decrease in intra thoracic pressure (during inspiration) increase in intra thoracic pressure (during expiration)
9. 9. Interaction between the factors that regulate cardiac output and arterial pressure
10. 10. Control of heart rate or extrinsic autoregulation  Primarily govern by cardiac innervation  Cardiac centres located in medulla (vasomotor centre, VMC and cardiac vagal centre, CVC)
11. 11. Control of stroke volume or intrinsic autoregulation 1. Heterometric regulation 2. Homometric regulation
12. 12. Heterometric regulation  Force of contraction of myocardium is dependent upon its pre-load and afterload  Pre-load : is the degree to which the myocardium is stretched before it contracts  After- load is the resistance against which the ventricles pump the blood
13. 13. Heterometric regulation Homometric regulation 1.Hetero means different; metric means measure. Therefore, here change in myocardial contractility varies with initial length of cardiac muscle fibers. Thus within physiological limits, force of ventricular contraction is directly proportional to the initial length of muscle fibres 1.Homo means same; therefore here change in myocardial contractility is independent of the resting length of cardiac muscle fibers 2. This effect is independent of cardiac innervation 2. This effect is dependent on cardiac innervation. Eg. i. Sympathetic stimulation increases and ii. Parasympathetic stimulation decreases myocardial contractility
14. 14.  The relationship between extent of pre-load and the total tension developed in cardiac muscle is given by length- tension relationship (Frank – Starling law)  Extent of pre-load is directly proportional to the End- diastolic Volume(EDV) i.e. amount of blood remaining in ventricles at the end of diastole.  Any factor which increases venous return (VR) i.e. volume of blood returning to heart will increase ‘EDV’  More is ‘EDV’, more will be stretching of the myocardium, i.e initial length of cardiac muscle fiber ; and more will be the force of contraction of myocardium
15. 15. Factors affecting venous return 1. Thoracic pump or respiratory pump 2. Cardiac pump 3. Muscle pump 4. Total blood volume 5. Capacity of venous system 6. Body position 7. Ventricular compliance (distensibility)
16. 16. Thoracic pump or respiratory pump  Normal intrathoracic pressure at the end of expiration is subatmospheric, (-2 mm Hg)  During inspiration: i. Intra- thoracic pressure decreases to -5mm Hg causing less pressure over larger veins and arteries; ii. Descent of diaphragm, increases intra-abdominal pressure to squeeze blood out of the abdomen
17. 17. Cardiac pump i. Vis-a-tergo i.e force from behind which drives the blood forward ‘VR’ depends on vis-a-tergo i.e. forward push from behind i.e propelling force which is imparted by: a) The contraction of heart to the blood during its passage through the heart b) Elastic recoil of arterial wall, blood enters the venules with an appreciable pressure higher than that of right atrium(RA). The flow of blood in the veins is therefore towards the heart ii. Vis-a-fronte i.e. force acting from the front to attract blood in the veins towards the heart. It is exerted by contraction of the ventricles and has 2 components – a) Ventricular systolic suction- b) Ventricular diastolic suction-
18. 18. Muscle pump  Rhythmic contraction of skeletal muscles, venous segments are squeezed and the rise of pressure forces the blood towards the heart  Venous valves prevents back flow  As soon as muscle relax the depleted segments are promptly refilled from the more peripheral channels and also from superficial veins vai their valved communicating channels
19. 19. Total blood volume  Increase in total blood volume increases , while decrease in total volume decreases VR
20. 20. Capacity of venous system  Veins are capacitance vessels  Increase sympathetic activity , increases venous tone, thus increase VR
21. 21. Body position  In standing position , peripheral pooling occurs and VR decreases
22. 22. Ventricular compliance  Following MI ventricular compliance decreases thus decreases VR
23. 23. Homometric regulation  Here, myocardial contractility increases without an increase in initial length of cardiac muscle fiber  Increase myocardial contractility : 1. Ventricles able to do more work per stroke at a given EDP 2. Venrticles develop tension more rapidly 3. Myocardial fibers shorten quickly 4. Ejection of blood is faster 5. Duration of myocardial contraction is brief 6. Rate of ventricular relaxation is faster
24. 24. Factors affecting myocardial contractility Increased Decreased Catecholamines MI Sympathetic stimulation Parasympathetic activity Digitalis, glucagon, caffeine, theophylline Intrinsic myocardial depression Hypoxia, hypercapnia,acidosis barbiturates, overdose of anaesthetic agents,
25. 25. INTEGRATED CONTROL OF CARDIAC OUTPUT
26. 26. ROLE OF HEART RATE IN CONTROL OF CARDIAC OUTPUT
27. 27. Clinical significance of Frank–Starling mechanism  For small, momentary adjustments necessary for keeping the outputs of two ventricles equal  Maintenance of constant stroke volume when the peripheral resistance is increased is carried out by intrinsic mechanism  Intrinsic control mechanism serves as a life-saving device in a cardiac failure.
28. 28. MEASUREMENT OF CARDIAC OUTPUT 1. Methods based on Fick’s principle 2. Indicator or dye dilution method 3. Thermodilution method 4. Method employing inhalation of inert gases 5. Physical methods such as –  Doppler technique echocardiography –  Ballistocardiography
29. 29. METHODS BASED ON FICK’S PRINCIPLE  Fick’s principle  The Fick’s principle states that the amount of a substance taken up by an organ (or by the whole body) per unit of time is equal to the arterial level of the substance (A) minus the venous level (V) times the blood flow (F), i.e. Q = (A − V) F or F = Q (A − V)  This principle can be of course, only in situations in which the arterial blood is the sole source of the substance taken up.  In this method ,cardiac output is determined by measuring the pulmonary blood flow.  Pulmonary blood flow/min = right ventricular output.  Right ventricular output = left ventricular output (cardiac output).
30. 30. Measurement of pulmonary blood flow  by measuring the amount of O2 taken by the blood from the lungs,  O2 concentration of the venous blood from pulmonary artery (PAO2) and  O2 concentration of the arterial blood from the pulmonary vein (PVO2).  Amount of O2 uptake/min is determined with the help of a spirometer,  PAO2 is measured from the venous blood sample taken from the pulmonary artery directly with the help of a cardiac catheter.  PVO2, because of practical difficulty in taking sample from pulmonary vein, is measured from the arterial blood sample taken from any peripheral artery,  e.g. brachial artery (the O2 content of all the major arteries is same as that of pulmonary veins).
31. 31.  Amount of O2 taken by the lungs/min Pulmonary blood flow = PVO2 − PAO2 O2 taken up by the lungs/min  Cardiac output = PVO2 − PAO2
32. 32.  If O2 uptake is 250 mL/min. PVO2 is 19 mL/ 100 mL and PAO2 is 14 mL/100 mL, then calculate cardiac output
33. 33. Disadvantages of Fick’s principle 1. It is an invasive technique, so there are risks of infection and haemorrhage. 2. The cardiac output estimated may be somewhat higher than normal as the patient becomes conscious of the whole technique. 3. A fatal complication like ventricular fibrillation may occur if the indwelling catheter irritates the ventricular walls, especially when the cardiac output is being measured during heavy exercise.
34. 34. INDICATOR OR DYE DILUTION METHOD  In this method, a known amount of the dye is injected into a large vein or preferably into the right atrium by cardiac catheterization.  By its passage through heart and pulmonary circulation it will be evenly distributed in the blood stream.  Its mean concentration during the first passage through an artery can be determined from the successive samples of blood taken from the artery.  The blood flow in litres/min (F) is given by the following formula: Q  F = Ct F = Blood flow in litres/min, Q = Quantity of the dye injected, C = Mean concentration of dye and t = Time duration in second of the first passage of dye through the artery.
35. 35. Prerequisites for an ideal indicator 1. It should be non-toxic. 2. It must mix evenly in the blood. 3. It should be relatively easy to measure its concentration. 4. It should not alter the cardiac output or haemodynamics of blood flow. 5. Either it must not be changed by the body during mixing period or the amount changed must be known. 6. The dye commonly used in humans for determining the cardiac output is Evans blue (T-1824) or radioactive isotopes.
36. 36.  Calculation of cardiac output-  Q  Cardiac output=  ct  Q= 5mg  C=1.5mg/L  t=40sec 5x60  Cardiac output=  1.5 x 40
37. 37. THERMODILUTION METHOD  Principle: It is also an indicator dilution technique in which instead of a dye, ‘cold saline’ is used as an indicator.  The cardiac output is measured by determining the resultant change in the blood temperature in the pulmonary artery. 1. A known volume of sterile cold saline is then injected into the inferior vena cava. 2. Temperature of the blood entering the heart from the inferior vena cava and that of the blood leaving the heart via pulmonary artery is determined by the thermistors. 3. The cardiac output is then measured from the values of temperature by applying the principle of indicator dilution technique.
38. 38. PHYSICAL METHODS Echocardiography  Echocardiography refers to the ultrasonic evaluation of cardiac functions.  It is a noninvasive technique that does not involve injections or insertion of a catheter.  It involves B-scan ultrasound at a frequency of 2.25 MHz using a transducer which also acts as a receiver of the reflected waves.  The recording of the echoes displayed against time on an oscilloscope provides a record of: 1. The movement of the ventricular wall and septum, and valves during the cardiac cycle. 2. When combined with the Doppler techniques, echocardiography can be used to measure velocity and volume of flow through the valves. 3. It is particularly useful in evaluating end-diastolic volume (EDV), end-systolic volume, CO and valvular defects.
39. 39. VARIATIONS IN CARDIAC OUTPUT  PHYSIOLOGICAL CAUSES OF VARIATIONS IN CARDIAC OUTPUT 1. Age- Because of less body surface area the children have more cardiac index than adults. 2. Sex- Since the body surface area is less in females so they have more cardiac index than the males. 3. Diurnal variation- In the early morning cardiac output is low which increases in the day time depending upon the basal condition of the individual. 4. Environmental temperature- Moderate change in the environmental temperature does not cause any change in cardiac output. A high environmental temperature is associated with an increase in the cardiac output. 5. Anxiety and excitement are reported to increase the cardiac output by 50–100%.
40. 40. PHYSIOLOGICAL CAUSES OF VARIATIONS IN CARDIAC OUTPUT 6. Eating is associated with an increase in cardiac output approximately by 30%. 7. Exercise may increase the cardiac output up to 700% depending upon the vigorousness of exercise. 8. Pregnancy- An increase in cardiac output to the tune of 45–60% is reported during the later months of the pregnancy. 9. High altitude- The cardiac output is increased at a high altitude due to release of adrenaline as a consequence to hypoxia. 10. Posture change - Sitting or standing from lying down position may decrease the cardiac output by 20–30% because of pooling of blood in the lower limbs.
41. 41. PATHOLOGICAL CAUSES OF VARIATIONS IN CARDIAC OUTPUT  Increase in cardiac output : 1. Fever, due to increased oxidative processes 2. Anaemia, due to hypoxia 3. Hyperthyroidism, due to increased metabolism
42. 42. Decrease in cardiac output 1. Rapid arrhythmias, 2. Congestive cardiac failure, 3. Cardiac shock, 4. Incomplete heart block, 5. Haemorrhage and 6. Hypothyroidism
43. 43. References 1. Text book of medical physiology Indu Khurana 2. Text book of Physiology, Gyuton 2nd south Asian Edition 3. Text book of Physiology, Ganong 4. Comprehensive Text book of Physiology, G.K.Pal vol.I 5. Internet source