Factors affecting cardiac output

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Presentation transcript:

Factors affecting cardiac output DR S.PARTHASARATHY MD., DA., DNB., DIP. DIAB. PhD, FICA, IDRA, Diploma in software based statistics

Volume ejected by left ventricle to the aorta and thus to the rest of the body Cardiac output is the amount of blood the heart pumps in 1 minute

Male 5 – 6 litres / minute Females – 4 – 4.75 litres / minute may be less Children 350 ml/ kg/ minute – birth 150 – 200 ml/ kg / minute after one week Cardiac index – 3 – 3.2 litres/min/m2

Basically Cardiac output = heart rate * stroke volume 70/ minute * 70ml/ cycle = 4900 ml = approx 5 litres / minute

Permissive role of the heart The Frank-Starling relationship is an intrinsic property of myocardium by which stretching of the myocardial sarcomere results in enhanced myocardial performance for subsequent contractions 13 – 15 litres/ minute Permissive role

Starling law or the catapult theory Permissive role is increased in exercise & Athletes Decreased in heart diseases Starling law or the catapult theory

Catapult Stretch End diastolic fibre length – true preload LV compliance , volume Mitral valve Atrial contractility Pulmonary hypertension Pulmonary stenosis RV and RA changes CVP !!!! – preload

During times of physiologic stress, cardiac output will increase to ensure adequate tissue perfusion. Fick’s principle illustrates this notion in equation form: CO = VO2/ (a – v O2 difference) where VO2 represents oxygen use by tissue and a-V O2 is the difference in oxygen content of arterial and venous blood

What factors affect stroke volume Cardiac output = stroke volume * heart rate Preload Contractility Afterload

Preload – tailwind pushing the cycle Speed of the bicycle - Venous return

Preload is equal to the ventricular wall stress at end-diastole. It is determined by ventricular EDV, end-diastolic pressure (EDP), and wall thickness

Preload --take it as venous return !! Blood Volume Elasticity of heart – if it decreases , the heart loses its capacity to fill easily !! Valves in small veins Muscle pump : leg muscles contract – squeezed blood to the heart Gravity – Intrapericardial pressure Respiratory pump RAP – usually close to ZERO

Mean systemic filling pressure Pressure in all parts of the systemic circulation when blood flow is stopped and the blood is redistributed to all the vessels 7 mmHg Ultimate pressure that puts blood to the right atrium venous return = Psf – RAP

Venous return may decrease Bleeding Obstruction of large veins Sudden dilation of veins

Force of cardiac contraction (contractility) Clearly, if the cyclist flexes his/her muscles a little and pushes harder on the pedals, then the bicycle will move faster. This can be equated to an increased contractility of the heart muscle, resulting in increased cardiac output

Afterload Afterload can be considered either as the stress imposed on the ventricular wall during systole or as the arterial impedance to the ejection of SV. σ ∝ P×r /h - ( law of laplace) σ = ventricular wall stress P = ventricular pressure r = ventricular radius h = wall thickness Hypertension Aortic stenosis

Heart rate cardiac conduction system, central nervous system, autonomic nervous system Cycle fastens – moves faster but after some time it fatigues to go down under Around 175/ minute

As the long-distance cyclist will know, prolonged strenuous exercise can lead to high tissue oxygen demands, which can later result in impaired muscle contraction and poor performance. Continuous prolonged inotropes !! ??

How does it feel to cycle down hill ?? This is what vasodilators do to decrease afterload !!

Push the pedal faster Also make the road less bumpy and smooth !! Sometimes we need both Inodilators like milrinone Inotropy and vasodilation

ANS, myocardial disease Blood volume muscle pump Resp pump gravity Valves

Thank you all