Cardiac Cycle, Cardiac Output presentation
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The document outlines the cardiac cycle, detailing its stages including atrial diastole, atrial systole, ventricular systole, and ventricular diastole, along with the regulation of cardiac output which is determined by stroke volume and heart rate. It highlights the roles of the sino-atrial node and atrio-ventricular node in initiating heart contractions and maintaining rhythm. Furthermore, it discusses factors affecting cardiac output, such as blood volume, contractility, and variations due to physiological and pathological conditions.
Cardiac Cycle, Cardiac Output presentation
- 1. Cardiac Cycle, Cardiac Output Blood Pressure Monnaf M. Sc. OTAT
- 2. Definition • Cardiac cycle is the complete cycle of events in the heart from the beginning of one heart beat to the beginning of the next • Cardiac muscle differs from all other muscles of the body • It is myogenic • Heart muscle has its own built in mechanism for bringing about: contraction & relaxation
- 3. Mechanism • Heart muscle cells cannot contract by their own natural rhythms • So, cardiac cycle is initiated in a specialized patch of muscle Found in the right atrium called the sino-atrial node (SAN) Located near the opening of vena cava Consists of a small number of cardiac muscle fibres and few nerve endings Stimulus for contraction of the heart is originated in the SAN
- 4. Mechanism • However, there is a band of fibres between the atria and ventricles which does not conduct the excitation wave of the SAN • The only route through is via a patch of conducting fibres Called the atrio-ventricular node (AVN) situated in the septum
- 5. Mechanism • AVN picks up excitation wave as it spreads across the atria and passes it on to a bunch of conducting fibres called the Purkinje tissue • This transmits the excitation wave rapidly down to the base of the septum and then to the walls of the ventricles • Thus, causing the cardiac muscle in these walls to contract. Squeezing blood upwards and into arteries.
- 6. Stage 1 - Atrial diastole • Bicuspid and tricuspid valves are closed • Muscles in the atria relaxes and the pressure decreases while volume increases inside • Blood returns to the heart under low pressure in the veins and enters the two atria • The vena cava carry deoxygenated blood to the right atrium • The pulmonary veins carry oxygenated blood to the left atrium
- 7. Stage 2 - Atrial systole • It is the time when the heart is filled with blood • The muscle in the atrial walls contracts with the help of SAN • The pressure increases and the atrio- ventricular valves open so the blood found in atria is forced into the ventricles • Blood from atria does not go back into the pulmonary veins or the vena cava because of the semilunar valves which prevent backflow
- 8. Stage 3 - Ventricular systole • 0.1 second after the contraction of the atria, the ventricles also contract • Thick muscular walls of the ventricles squeeze inwards on the blood, increasing pressure and pushing it out of the heart • As pressure in ventricles become greater than that in atria, the atrio-ventricular valves shut, preventing backflow to the atria • Instead, blood rushes upwards into the aorta and the pulmonary artery, pushing open the semilunar valves
- 9. Stage 4 - Ventricular diastole • Here, the muscles relaxes • As this happens, pressure in ventricles drops • The high-pressure blood which has just been pushed into the arteries would flow back into the ventricles • But, this is prevented by the presence of the semilunar valves which snap shut as the blood fills their cusps
- 10. 4 stages of cardiac cycle
- 11. 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
- 12. CO = SV x HR cardiac output = stroke volume X heart rate (ml/minute) (ml/beat) (beats/min) Average heart rate = 70 bpmb. Average stroke volume = 70-80 ml/beat Average cardiac output = 5000 ml/minute Cardiac output varies widely with the level of activity of the body.
- 13. • 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
- 14. 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
- 15. • The stroke volumes for each ventricle are generally equal, both being approximately 70 ml in a healthy 70 kg man. • Men, on average, have higher stroke volumes than women due to the larger size of their hearts.
- 16. 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. 3) Inversely related to stroke volume 2) Called after load
- 17. 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%.
- 18. VENOUS RETURN • End diastolic volume is controlled by factors that affect venous return: a. Total blood volumeb. b. Venous pressure (driving force for blood return) • Veins have high compliance - stretch more at a given pressure than arteries (veins havethinner 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.
- 19. 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 complianced. d. Pressure difference between abdominal and thoracic cavities (respiration) e. Blood volume
- 20. 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 output increases during pregnancy • Exercise : cardiac output increases during exercise • Emotion : cardiac output increases during emotional expressions.
- 21. PATHOLOGICAL VARIATION OF CARDIAC OUTPUT Pathological increase: • Hyperthyroidism • Fever Pathological decrease: • Hypothyroidism • Hypovolumia • Haemorrhage • Myocardial infarction
- 22. 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
- 23. 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.
- 24. • 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.
- 25. 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.