RAK Cardiac Output PDF

Prof. Tarig Hakim Merghani RAKCOMS- RAKMHSU  Objectives  Define cardiac output and its significance in cardiovascular physiology.  Describe the factors affecting stroke volume and heart rate in cardiac output regulation.  Analyze the mechanisms that regulate venous return and cardiac outp...

Prof. Tarig Hakim Merghani RAKCOMS- RAKMHSU  Objectives  Define cardiac output and its significance in cardiovascular physiology.  Describe the factors affecting stroke volume and heart rate in cardiac output regulation.  Analyze the mechanisms that regulate venous return and cardiac output in health and disease  The cardiac output (COP) Definition: The volume of blood ejected by each ventricle per minute. TEbloodgeted by each ventricle per minute The cardiac output (COP) smm It equals the venous return = 5 L/min (In a young healthy male under resting conditions)  Cardiac index= COP/ Surface Area D of f  Normally= 2.5 to 4 L/min/m2  Allows comparisons Imprisons  The cardiac output (COP) Normal value is affected by: Age Gender Physical activity is affected Value of COI Activity gender physical by Age  Control of the cardiac output COP=Heart rate (HR) x Stroke volume (SV) Increase/ decrease in HR &/or SV = Increase/ decrease in the COP howto call.tt COI Heart rate X strock volume HR HR SU COP SU cop HR  The heart rate =The number of heart beats per minute 60-100 beats/minute. > 100 is tachycardia < 60 is bradycardia Any factor that increases or decreases the HR is described as having +ve or –ve on chronotropic effect chamelect  Normal heart rate varies with: D Age: HR decreases with age Gender: HR of females> males Sleep: of HR decreases during sleep a Training: In athletes the HR is slowed stem  Normal heart rate varies with: Neural factors 50 Symp. Increases HR Parasymp decreases HR - O Chemoreceptors increase HR Baroreceptors decrease HR Bainbridge effect increases HR  Normal heart rate varies with: Hormones: Thyroid & catecholamines in increase HRp Physical factors: Fever or high temperature increases HR Drugs: Beta agonists & anticholinergics (muscarinic blockers) increase HR  The heart rate Very high rate = less time for cardiac filling = reduction of the stroke volume and the COP. time for cardiac less HR filling stroch volume  The stroke volume Definition: Volume of blood ejected by each ventricle each beat. F =End diastolic volume – End systolic volume End systolic End diastolic = 70 ml 70m  The stroke volume End diastolic volume (EDV): Is determined by the venous return. End diastolic volume EV is determined by the venous return  End diastolic End systolic volume volume The stroke volume is determined is determined by venone by cardiac return contractility End systolic volume (ESV): Is determined by cardiac contraction (contractility). Any factor that increases or decreases the contractility is described as having +ve or –ve inotropic effect idiot  Stroke volume varies with: - Age: SV increases with age Gender: SV of males> females Sleep: SV decreases during sleep e - Training: SV is higher in athletes  Stroke volume varies with: Neural factors: Sympathetic increases SV I Parasymp has no direct effect Chemoreceptors increase SV Baroreceptors decrease SV has no direct effect Parasympathec in stock value  Stroke volume varies with: D Hormones: Thyroid Hs & catecholamines increase SV Physical factors: Fever or high F temperature increases SV is  The ejection fraction (EF) II SV/EDV x 100% of 5 EF = 70/ 120 = about 65 %  A sensitive indicator of myocardial contractility EF decreases in heart failure eggiffmf.at  Lnd diactors The preload = Tension before contraction Represented by the EDV (i.e., by the venous return) Tension before contraction is called preload Represented by EDI veneration  The preload The Frank-Starling Law: (within certain limits, the force of muscle contraction is directly proportional to the initial length of its muscle fibers)  preload The preload EDI The initial length of ventricular fibers is determined by the preload (= EDV) so Increase in venous return ieai.am the venousreturn = Increase in EDV e = Increase in preload (more stretch) = increase in stroke volume initial length of ventricular inVenous the return.ca fibers is determined by a strokevolume EYou  The preload What happens if the preload remains high for long time? Chronic increase in preload leads = Cardiac muscle dilatation = Weakness= Heart failure.  The after load = The resistance in aortic or pulmonary artery (against ejection) after load or in Aortic The resistance Againstejection pulmonaryartery  The after load Examples of high after load: Hypertension Aortic valve stenosis Wh affert Exampu Hypertension stenos Aortic valve Measurement of the cardiac output Indirect methods (like indicator dilution technique, Fick principle and thermodilution method) Direct methods (using E electromagnetic or ultrasonic flow- meter devices). Hamilton dye dilution method Q amount of a dye is injected in an arm vein; then serial arterial samples are obtained from a peripheral artery to measure the dye concentration (C) during certain time (t) COP = (Q x 60) / (C x t) Hamilton dye dilution method  Fick principle Used for measurement of blood flow to organs It states, “The amount of a substance consumed (or added) by an organ in a given time equals the arterial-venous difference in concentration times the blood flow to the organ”. Fick principle In summary: Q = [A] - [V] x Blood flow to the organ Or Blood flow= Q/[A]- [V] Fick principle If the lungs are taken as an organ, their blood flow = the cardiac output from the right ventricle The substance consumed (actually added) by the lungs is oxygen. Fick principle Oxygen added by the lungs = 250 ml oxygen/ min, measured by spirometer. Fick principle Oxygen concentration in the pulmonary artery = 150 ml oxygen/L (the blood sample should be taken from the pulmonary artery by cardiac catheterization) Fick principle Oxygen concentration in the pulmonary vein = 200 ml oxygen/L (The blood sample can be taken from any peripheral artery). Fick principle By applying the above values to the formula: COP = Q / [A] – [V] COP = 250 ml oxygen/min / [50 ml oxygen/L] = 5 L/min Venous Return  The blood that returns back to the heart.  = 5 L/min (in adult male at rest) venous Return what is head back to the that return The blood  vein Venous Return Artery Capillan  Pressure gradient:  Arteries> capillaries > veins. will reduce Bleading  Blood Volume venous return t  Bleeding reduces venous return. the blood that returnback to theheart  Venomotor Tone: i  Venoconstriction increases venous return.  Venodilation I decreases venous return i r Venous Return  Muscle Pump:  Contraction of skeletal muscles pushes blood toward the heart (why?)  Respiratory Pump:  Inspiration enhances venous return.  Expiration decreases venous return. during venous Return Expiration Inspiration Increasevenous thatvfen.net  return venous Return Gravity Venous Return saying  Gravity: standing densevenous Return Increase  Standing: decreases venous return venove Rem  Lying down: increases venous return.  Valvular lesions/ Pericardial effusion  Decrease venous return. 1E.EE venue on decrease