Cardiac Output & Venous Return Regulation Lec9 PDF

Cardiac Output & Venous Return and its Regulation














Dr. Fatima Abid



Objectives Define heart rate, stroke volume, venous return and cardiac output. Regulation of cardiac output and its determinants Explain the Starling’s l...

Cardiac Output & Venous Return and its Regulation














Dr. Fatima Abid



Objectives Define heart rate, stroke volume, venous return and cardiac output. Regulation of cardiac output and its determinants Explain the Starling’s law of the heart. Physiological variations in cardiac output Nervous regulation Cardiac output (CO) CO is the volume of blood ejected from the left ventricle (or the right ventricle) into the aorta (or pulmonary trunk) each minute. CO equals the stroke volume (SV) multiplied by heart rate (HR) CO = SV X HR SV volume of blood ejected by the ventricle during each contraction HR number of heart beats per minute. CO = SV X HR = 70 ml/beat X 75 beats/minute = 5.25 L/min Cardiac Output cont. CO may  to meet demands During exercise CO can increase to 20-25 L/ min  Minute volume Amount of blood pumped out by each ventricle in one minute Routine practice in medicine is cardiac output means minute volume  Cardiac Terminology
End diastolic volume (EDV): blood in the ventricles at the end of diastole. Ejection fraction: fraction of EDV that is ejected (%), used to measure heart efficiency. End systolic volume (ESV): blood that remains in the ventricle at the end of systole. Preload: the degree of stretch on the heart before it contracts. Afterload: the pressure that must be exceeded before ejection of blood from the ventricles can occur.  DISTRIBUTION OF CARDIAC OUTPUT The whole amount of blood pumped out by right vent goes to lungs but the blood pumped by left vent is distributed to different parts of body Distribution to particular region depends upon the metabolic activities of the region  DISTRIBUTION OF CARDIAC OUTPUT Liver 1500 ml 30 % Kidneys 1300 ml 26 % Sk muscles 900 ml 18 % Brain 800 ml 16 % Skin, bones & GIT 300 ml 6% Heart 200 ml 4% Total 5000 ml 100 % The heart which pumps the blood to all the organs, receive least amount of blood  DETERMINANTS OF CARDIAC OUTPUT Cardiac output is maintained or determined by four factors 1. Venous return 2. Force of contraction 3. Heart rate 4. Peripheral resistance Regulation of cardiac output CO= SV x HR Depends on the regulation of SV and HR Regulation of stroke volume THREE factors regulate SV: 1. Preload (EDV) Venous Return 2. Contractility 3. Afterload 1. Preload: effect of stretching Frank-Starling (F-S) law of the heart:  Within limits, the more the heart fills during diastole (preload – stretching), the greater the force of contraction during systole.  the preload is proportional to EDV, the greater the EDV, the more forcefull the next “The heart will pump what it receives” contraction - Starling’s law of the heart Preload cont. Two factors determine EDV: 1. Duration of ventricular diastole (HR) Ventricular filling occur during diastole Tachycardia ( HR) diastole duration ventricular filling end diastolic volume CO 2. Venous return (volume of blood flowing back to the heart through systemic veins)  CONTROL OF CARDIAC OUTPUT BY VENOUS RETURN
ROLE OF THE FRANK-STARLING MECHANISM OF THE HEART
This law states: “ When increased quantities of blood flow into the heart, the increased blood stretches the walls of the hear t chambers. As a result of the stretch, the cardiac muscle contracts with increased force, and this empties the extra blood that has entered from the systemic circulation”. 14  FRANK-STARLING MECHANISM “within physiological limits, the heart pumps all the blood it receives without allowing excessive damming of blood in the veins” Increased Venous return Increased cardiomyocyte contractility Increased stroke volume  VENOUS RETURN It is the amount of blood which is returned to heart from different parts of body Cardiac output is directly proportional to venous return provided the force of contraction, heart rate and peripheral resistance remain constant Cardiac Output (CO)=Venous Return (VR) Venous Return derives Cardiac Output  VENOUS RETURN Depends upon five factors 1. Respiratory pump 2. Muscle pump 3. Gravity 4. Venous pressure 5. Sympathetic tone  1. Respiratory pump It is the activity that helps return of blood back to heart during inspiration, also called abdominothoracic pump During inspiration thoracic cavity expand and makes the intrathoracic pressure more negative It increases the diameter of inferior vena cava resulting in increase in venous return Same time the descent of diaphragm increase the intra abdominal pressure which compresses the abdominal veins and pushes the blood upward towards the heart and venous return is increased  2. Muscle pump It is the muscular activity that helps return of the blood back to heart During muscular activities, the veins are compressed or squeezed, due to presence of valve into the veins, during compression the blood is moved toward the heart When muscular activity increases, the venous return is more  3. Gravity Gravitational force reduces the venous return When person stands for the longer period, gravity causes pooling of blood in the legs, which is called venous pooling Due to venous pooling, the amount of blood returning to heart decreases  4. Venous pressure The venous pressure in the venules is 12- 18 mm Hg In smaller and larger veins the pressure gradually decreases, in inferior and superior vena cava pressure falls to 5.5 mm Hg It is 4.5 at the junction between vena cavae and right atrium Pressure in right atrium is still low, it falls to zero during atrial diastole The pressure gradient at every part of venous tree helps as a driving force for venous return  5. Sympathetic tone Venous return is aided by sympathetic or vasomotor tone also It causes constriction of venules Venoconstriction pushes the blood towards heart 2. Contractility Contractility: strength of contraction at any given preload +ve inotropism:  contractility Include: - sympathetic stimulation - Hormones; adrenaline and noradrenaline -ve inotropism:  contractility May result from: - inhibition of the sympathetic system - anoxia - acidosis 3. Afterload pressure in pulmonary tract is a bout 20 mm.Hg and in the aorta is about 80 mm Hg. This pressure must be overcome before the semilunar valves open. Depend on: Elasticity of large arteries Peripheral resistance of arterioles An  in afterload  SV more blood remains in ventricle at end of systole (ESV) Conditions that  afterload include: Hypertension Narrowing of arteries by atherosclerosis Regulation of heart rate Several factors, the most important are 1. Nervous factors 2. Chemical factors 3. Others  CARDIOVASCULAR SYSTEM REGULATION CARDIOVASCULAR CENTER Nervous system regulation of heart originate in the cardiovascular center in medulla oblongata This region of the brain stem receives input from variety of sensory receptors and from higher brain centers, such as limbic system and cerebral cortex The cardiovascular center then directs appropriate output by increasing or decrea sing the frequency of nerve im pulses in both sym pa thetic a nd parasympathetic branches of ANS Autonomic regulation of HR  AUTONOMIC ACTIVITY Sympathetic stimulation Positive inotropic effect Increases HR and SV Releases NE Dominant during exercise and stress Parasympathetic stimulation Negative inotropic effect Decreases HR and SV Releases Ach Dominant at rest Chemical regulation of HR 1. Hormones:  Adrenaline and noradrenaline (adrenal medulla) HR &  contractility Adrenal medulla stimulated by:  exercise  stress  excitement  Thyroid hormones  HR & Contractility Hyperthyroidism tachycardia 2. Cations   Na+ & K+  HR & Contractility  Ca2+  HR & Contractility Other factors in HR regulation  Age: Newborn HR ~120 beats/min Old people may also develop  HR  Gender: Adult females higher HR than males  Exercise: Athletic bradycardia (60 or under) (more efficient heart)  Body temperature (BT):  BT (fever or exercise)  HR BT  HR & contractility  CARDIAC OUTPUT
PHYSIOLOGICAL VARIATIONS Age The cardiac output is regulated throughout life almost directly in proportion to the overall bodily metabolic activity. In children cardiac output is less because of less blood vol. Sex In females cardiac output is less Diurnal variation Cardiac output is low in early morning and increase in day time. It depend upon the basal conditions of individuals  CARDIAC OUTPUT
PHYSIOLOGICAL VARIATIONS Environmental temperature Increase in temperature above 30 Celsius, raise the cardiac output Emotional conditions Anxiety and excitement increases cardiac output 50 to 100 % through the release of catecholamine which increases the heart rate and force of contraction After meals During the first one hour after taking meals cardiac output increases Exercise It increases during exercise due to increase in heart rate  CARDIAC OUTPUT
PHYSIOLOGICAL VARIATIONS High altitude Increases because of increase in secretion of adrenaline due to hypoxia Posture Changing from recumbent to upright position the cardiac output decreases Pregnancy During the later months of pregnancy the cardiac output increases by 40 % Sleep Slightly decreased  CARDIAC OUTPUT
PATHOLOGICAL VARIATIONS Cardiac output increases in 1. Fever due to increase oxidative processes 2. Anemia due to hypoxia 3. Hyperthyroidism due to increase basal metabolic rate  CARDIAC OUTPUT
PATHOLOGICAL VARIATIONS Cardiac output decreases in 1. Hypothyroidism due to decrease BMR 2. Atrial fibrillation due of incomplete filling 3. Myocardial ischemia due to defective pumping action of heart 4. Congestive Cardiac Failure(CCF) due of weak contraction of heart 5. Shock due to poor pumping and circulation 6. Heamorrhage due of decrease blood volume SUMMARY