Cardiac Output - Lecture Notes PDF

CARDIAC OUTPUT Curriculum: Phase 1/Semester 3/CVS/Session 5 Lecturer: teacher Dr. Shahlaa chabuk khazaal Degrees: MSc/Ph.D. Phsiology At each beat The stroke volume is pushed into the A ARTERIES low resistance vessels with a high pressure in them arterial pressure must rise high enough to drive...

CARDIAC OUTPUT Curriculum: Phase 1/Semester 3/CVS/Session 5 Lecturer: teacher Dr. Shahlaa chabuk khazaal Degrees: MSc/Ph.D. Phsiology At each beat The stroke volume is pushed into the A ARTERIES low resistance vessels with a high pressure in them arterial pressure must rise high enough to drive the cardiac output through the resistance of the arterioles PULSATILE FLOW The heart ejects blood intermittently in systole blood flows into arteries in diastole it does not IF TOTAL PERIPHERAL RESISTANCE CHANGES if TPR falls and CO does not change – arterial pressure will fall – venous pressure will rise if TPR rises and CO does not change – arterial pressure will rise – venous pressure will fall IF CARDIAC OUTPUT CHANGES if CO rises and TPR does not change – arterial pressure will rise – venous pressure will fall if CO falls and TPR does not change – arterial pressure will fall – venous pressure will rise CHANGES IN DEMAND FOR BLOOD TPR is inversely proportional to the body’s need for blood if metabolism changes, TPR will change and generate ‘signals’ in the form of changes in arterial and venous pressure. EXAMPLE if we eat a meal the gut needs more blood local vasodilators dilate arterioles total peripheral resistance falls if CO does not change, arterial pressure will fall and DEMAND-LED PUMPING if the body needs more blood, the heart needs to pump more to meet the ‘demand’ demand is expressed as changes in arterial and venous pressure Signals to the heart if the heart responds to falls in arterial pressure and rises in venous pressure by pumping more blood CONTROL OF CARDIAC OUTPUT cardiac output is the product of – stroke volume – heart rate both arterial and venous pressures affect both STROKE VOLUME Control of stroke Is interaction of volume stroke volume is the: the difference between Preload – end diastolic volume Inotropic state – end systolic volume Afterload heart fills in diastole VENTRICULAR FILLING The ventricle fills until the walls stretch enough to produce an intraventricular pressure equal to venous pressure.PRESSURE AND VENTRICULAR FILLING VENOUS The higher the venous pressure the more the heart fills in diastole relationship between venous pressure and ventricular volume known as the ventricular compliance curve END DIASTOLIC VOLUME AND FORCE OF CONTRACTION like all muscle, if ventricular muscle is stretched before contracting it contracts harder Starlings STARLINGS LAW law of the heart the more the heart fills the harder it contracts (up to a limit) the harder it contracts the bigger the stroke volume rises in venous pressure automatically lead to MYOCARDIAL CONTRACTILITY INOTROPIC STATE Being affected by sympathetic or vagal nerves activity, drugs,receptors etc… Stimulation of the sympathetic nerves cause an increase of myocardial contractility “+ve inotropic effect” Stimulation of the vagal nerve causes decrease of myocardial contractility “-ve inotropic effect END SYSTOLIC VOLUME - how much the ventricle empties depends on – how hard it contracts – how hard it is to eject blood Force of contraction determined by – end diastolic volume (Starlings Law) – contractility contractility increased by sympathetic DIFFICULTY OF EJECTING BLOOD ‘aortic impedance’ depends mainly on TPR the harder it is to eject blood the higher the pressure rises in the arteries End systolic volume the easier it is to eject blood, the more comes out in systole so, if arterial pressure falls end systolic volume will fall and stroke volume rise DIRECT EFFECTS OF ARTERIAL AND VENOUS PRESSURES ON STROKE VOLUME if venous pressure rises – stroke volume will rise if arterial pressure falls – stroke volume will rise CONTROL OF HEART RATE autonomic outflow to the heart controlled by signals from baroreceptors carotid sinus senses arterial pressure sends signals to medulla which controls the heart Falls in arterial pressure increase heart rate by – reducing parasympathetic activity – increasing sympathetic activity increase contractility by – increasing sympathetic activity COMPENSATORY MECHANISMS: NEUROHORMONAL ACTIVATION – VASOPRESSIN Decreased systemic blood pressure Central baroreceptors Stimulation of Increased systemic blood hypothalamus, which pressure produces vasopressin for release by pituitary gland Release of vasopressin by Vasoconstriction pituitary gland SO, IN SUMMARY …falls in arterial pressure increase cardiac output via: increase stroke volume (sympathetic activity and direct effect) – increase heart rate …Rises in venous pressure: sensed in right atrium lead to reduced parasympathetic activity and so a rise in heart rate: the ‘Bainbridge reflex’ – increase stroke volume (Starlings Law) – increase heart rate