
Cardiac Output
Learn about cardiac output and stroke volume - two crucial factors affecting cardiovascular health. Explore how heart rate, force of contraction, and blood volume influence cardiac output, and how variables like end diastolic volume and contractility regulate stroke volume. Discover the key factors impacting heart health and blood circulation.
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Presentation Transcript
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
CO = SV x HR CO cardiac output = stroke volume X heart rat (ml/minute) (ml/beat) rate (ml/minute) (ml/beat) = SV x HR cardiac output = stroke volume X heart e (beats/min) (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.
FACTORS EFFECTING CARDIAC OUTPUT Heart rate When heart rate increases ,cardiac output also increases.Any factor which changes heart rate will also changes cardiac output. Force of contraction of heart When the force of contraction of the heart increases, stroke volume will increase. Therefore cardiac output will increase. Blood volume When blood volume increases cardiac output increases. Venous return
STROKE VOLUME Stroke volume ( SV ) is the volume of blood pumped out of each ventricle per beat or contraction . As the stroke volume increases the cardiac output also increases. Stroke Volume depends upon 1. End diastolic Volume 2. Contractility SV = EDV ESV
The generally equal, both being approximately 70 ml in a healthy 70 kg man. stroke volumes for each ventricle are Men, on average, have higher stroke volumes than women due to the larger size of their hearts.
REGULATION OF STROKE VOLUME Regulated by three variables: a.End diastolic volume (EDV): volume of blood in the ventricles at the end of diastole. 1)Sometimes called preload 2)Stroke volume increases with increased EDV. b.Total peripheral resistance: Frictional resistance in the arteries. 1)Inversely related to stroke volume 2)Called after load
c.Contractility: strength of ventricular contraction 1)Stroke volume increases with contractility. Ejection fraction (EF) percentage of the EDV that is ejected per cardiac cycle. Stroke volume = EDV ESV EF% = (SV / EDV) x 100 Normal ejection fraction is about 50-65%.
VENOUS RETURN End diastolic volume is controlled by factors that affect venous return: a.Total blood volume b.Venous pressure (driving force for blood return) Veins have high compliance stretch more at a given pressure than arteries (veins have thinner walls). Veins are capacitance vessels 2/3 of the total blood volume is in veins. They hold more blood than arteries but maintain lower pressure.
FACTORS IN VENOUS RETURN a.Pressure difference between arteries and veins (about 10mm Hg) b.Pressure difference in venous system - highest pressure in venules vs. lowest pressure in vena cava into the right atrium . c.Sympathetic nerve activity to stimulate smooth muscle contraction and lower compliance d.Pressure difference between abdominal and thoracic cavities (respiration) e. Blood volume
Physiological variations of cardiac output Age:Cardiac output is more in adults than in children because blood volume is more. Gender: cardiac output is more in male than females. Altitude:cardiac output increases at high altitude places. Pregnancy:cardiac pregnancy Exercise:cardiac exercise Emotion:cardiac output emotional expressions. output increases during output increases during increases during
PATHOLOGICAL VARIATION OF CARDIAC OUTPUT Pathological increase: Hyperthyroidism Fever Pathological decrease: Hypothyroidism Hypovolumia Haemorrhage Myocardial infarction
MEASURING CARDIAC OUTPUT 1. The Fick principle 2. Dilution methods 3. Pulmonary artery thermo dilution (trans- right-heart Thermo dilution) 4. Doppler ultrasound method 5. Impedance cardiography
RELATIONSHIP WITH BP As Cardiac output is made up of heart rate and stroke volume - at rest these are relatively constant. With exercise the heart beats faster - more blood is pumped out with each beat contributing to a rise in BP. Changes in the volume of blood within the cardiovascular system will also affect Bp.
A person was severely dehydrated or lost a large quantity of blood through a wound, there would be less blood for the heart to pump, thereby reducing cardiac output and BP. For a typical, fit young person, the cardiac output might go up to about 20 litres/min at the peak of exercise. For a world-class athlete in an endurance sport, the maximum cardiac output might be around 35 litres/min.
REGULATION OF CARDIAC OUTPUT It means maintaining a constant cardiac output around 5 litres/min under normal conditions and adjusting the cardiac output as per the physiological demands. It has to be regulated to have an optimum cardiovascular efficiency.
MECHANISM OF REGULATION 1)By venous return: Force of contraction of a muscle fibre is proportional to its initial length .It is known as Starling s law of muscle contraction.
Role Of Frank-Starling Mechanism Frank-Starling Law: It states that Within physiologic limits, the heart pumps all the blood that returns to it by the way of veins. Increased Venous Return Cardiac muscles stretches to greater length Ventricular muscle contracts with greater force Increased Cardiac Output
2)By nervous system: Autonomic nervous system takes a role in the regulation of cardiac output. Whenever sympathetic increases e.g. ; during emotions, exercise etc,it will stimulate both SA node as well as ventricular myocardium. This will increase both heart rate as well as force of contraction of muscles or stroke volume .This will inturn increase cardiac output. If parasympathetic activity increases as during sleep, it will inhibit SA node, it will decrease heart rate, this will inturn decrease cardiac output. major nervous activity
3)Hormonal regulation of cardiac output: Whenever adrenaline level in the blood increases it will stimulate SA node and ventricular myocardium. This will increase both heart rate and stroke volume. This will inturn increase cardiac output.
LIMITATIONS FOR THE CARDIAC OUTPUT There are definite limits to the amount of blood that the heart can pump, which is expressed quantitatively in the form of cardiac output curves. Normal: The plateau level of this normal cardiac output curve is about 13 L/min. Hypo effective: The lowermost curves are for hypo effective hearts that are pumping at levels below normal.Hypoeffective heart plateau 5 L/min Hyper effective: The uppermost curves are for Hyper effective hearts that are pumping better than normal. Hyper effective heart plateau 20 L/min
HYPO EFFECTIVE HEART In this the heart is pumping at a very slow rate and the cardiac output decreases. Factors that can cause hypo - effectivity are following: 1. IncreasedArterial Pressure 2. Inhibition of Nervous excitation 3.Abnormal Heart Rhythm 4. CoronaryArtery Blockage 5. Valvular Heart Disease 6. Congenital Heart Disease 7. Myocarditis 8. Cardiac Hypoxia
HYPEREFFECTIVE HEART In this the heart is pumping at a high rate and the cardiac output increases. Two type of factors can make the heart a better pump than normal: 1. Nervous Stimulation: It involves Sympathetic stimulation and Parasympathetic Inhibition. 2. Hypertrophy of The Heart Muscles: It involves the increased mass and contractile strength due to exercise and causing hypertrophy which allows increased cardiac
PATHOLOGICALLY HIGH OR LOW CADIAC OUTPUT In healthy humans, the average Cardiac Outputs are surprisingly constant from one person to another. However multiple clinical abnormalities can cause either high or low cardiac outputs.
HIGH CARDIAC OUTPUT High cardiac output is mostly caused by reduced total peripheral Resistance. Following are some of the conditions that can decrease the Peripheral Resistance and at the same time increase the Cardiac Output to above the normal. 1. Beriberi 2. Arteriovenous Fistula 3.Hyperthyroidism 4.Anaemia
LOW CARDIAC OUTPUT There are two factors that cause Low Cardiac Output: A. Abnormalities that cause the Venous Return to fall too low B. Abnormalities that cause pumping effectiveness of the Heart to fall too
Reference Text book of physiology-DrAP Krishna Essentials of medical physiology,2ndedition by K. Sembulingam and Prema Sembulingam