Biological Sciences
Cardiac Cycle
The cardiac cycle refers to the sequence of events that occur during one heartbeat. It includes the contraction (systole) and relaxation (diastole) of the heart chambers, leading to the pumping of blood throughout the body. The cardiac cycle is essential for maintaining blood circulation and delivering oxygen and nutrients to tissues.
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eBook - PDFCrash Course Cardiovascular System Updated Edition - E-Book
Crash Course Cardiovascular System Updated Edition - E-Book
- Jonathan Evans, Daniel Horton-Szar(Authors)
- 2015(Publication Date)
- Mosby Ltd.(Publisher)
The Cardiac Cycle and control of cardiac output 4 Objectives You should be able to: • Describe the stages of the ventricular cycle and the pressure/volume changes that take place. • Describe the stages of the atrial cycle and the corresponding changes in the jugular venous pressure. • Describe the normal and added heart sounds. • Understand what a murmur is and why they occur. • Describe the common causes, haemodynamic changes, symptoms and signs of common valvular abnormalities. • Understand the principles and common indications for echocardiography. • Understand the definition and significance of preload, afterload and contractility. • Understand the physiological and pharmacological factors that affect contractility. • Describe Starling’s law of the heart and its implications. THE Cardiac Cycle The Cardiac Cycle is the sequence of pressure and volume changes that take place during cardiac activity (Figs 4.1 and 4.2). At a resting heart rate of approximately 70 beats per minute (bpm), the Cardiac Cycle lasts 0.85 sec- onds. This is divided into diastole, which lasts 0.6 s and systole, which lasts 0.25 s. When considering the Cardiac Cycle, it is useful to remember that: • Blood flows down a pressure gradient. • The state of a valve is dependent on the pressure gradient across it. The ventricular cycle The ventricular cycle consists of four phases. The duration and order of each of these phases is shown in Fig. 4.2. 1. Ventricular filling (diastole) The atria and ventricles are all relaxed initially, and there is passive filling of the atria and ventricles as a result of central venous pressure and pulmonary venous pressure (right and left side respectively). The volume increases until a neutral ventricular volume is reached. Further filling makes the ventricle distend, causing ventricular pressure to rise. This passive ventricular filling will stop when ventricular pressure reaches central venous/ pulmonary venous pressure.
eBook - PDF- Gerard J. Tortora, Bryan H. Derrickson(Authors)
- 2018(Publication Date)
- Wiley(Publisher)
2. The movement of blood through the heart is controlled by the opening and closing of the valves and the contraction and relaxation of the myocardium. 3. Coronary (cardiac) circulation delivers oxygenated blood to the myocar- dium and removes carbon dioxide from it. 4. Deoxygenated blood returns to the right atrium via the coronary sinus. 15.3 Conduction System of the Heart 1. The conduction system consists of specialized cardiac muscle tissue that generates and distributes action potentials. 2. Components of this system are the sinoatrial (SA) node (natural pace- maker), atrioventricular (AV) node, atrioventricular (AV) bundle (bundle of His), bundle branches, and Purkinje fibers. 15.4 Electrocardiogram 1. The record of electrical changes during each Cardiac Cycle is referred to as an electrocardiogram (ECG). 2. A normal ECG consists of a P wave (depolarization of atria), QRS complex (onset of ventricular depolarization), and T wave (ventricular repolarization). 3. The ECG is used to diagnose abnormal cardiac rhythms and conduction patterns. 15.5 The Cardiac Cycle 1. A Cardiac Cycle consists of systole (contraction) and diastole (relaxation) of the chambers of the heart. 2. The phases of the Cardiac Cycle are (a) the relaxation period, (b) atrial systole, and (c) ventricular systole. 3. A complete Cardiac Cycle takes 0.8 sec at an average heartbeat of 75 beats per minute. 4. The first heart sound (lubb) represents the closing of the atrioventricular valves. The second sound (dupp) represents the closing of semilunar valves. 15.6 Cardiac Output 1. Cardiac output (CO) is the amount of blood ejected by the left ventricle into the aorta each minute: CO = stroke volume × beats per minute. 2. Stroke volume (SV) is the amount of blood ejected by a ventricle during ventricular systole. It is related to stretch on the heart before it contracts, forcefulness of contraction, and the amount of pressure required to eject blood from the ventricles.
eBook - PDF- Gerard J. Tortora, Bryan H. Derrickson(Authors)
- 2016(Publication Date)
- Wiley(Publisher)
The major part of ventricular filling occurs just after the AV valves open. Blood that has been flowing into and building up in the atria during ventricular systole then rushes rapidly into the ventricles. At the end of the relaxation period, the ventricles are about three- quarters full. The P wave appears in the ECG, signaling the start of another Cardiac Cycle. 20.4 The Cardiac Cycle OBJECTIVES • Describe the pressure and volume changes that occur during a Cardiac Cycle. • Relate the timing of heart sounds to the ECG waves and pressure changes during systole and diastole. A single Cardiac Cycle includes all of the events associated with one heartbeat. Thus, a Cardiac Cycle consists of systole and diastole of the atria plus systole and diastole of the ventricles. Pressure and Volume Changes during the Cardiac Cycle In each Cardiac Cycle, the atria and ventricles alternately contract and relax, forcing blood from areas of higher pressure to areas of lower pressure. As a chamber of the heart contracts, blood pressure within it increases. Figure 20.14 shows the relationship between the heart’s electrical signals (ECG) and changes in atrial pressure, ventricular pressure, aortic pressure, and ventricular volume during the Cardiac Cycle. The pressures given in the figure apply to the left side of the heart; pressures on the right side are considerably lower. Each ventricle, however, expels the same volume of blood per beat, and the same pattern exists for both pumping chambers. When heart rate is 75 beats/ min, a Cardiac Cycle lasts 0.8 sec. To examine and correlate the events taking place during a Cardiac Cycle, we will begin with atrial systole. Atrial Systole During atrial systole, which lasts about 0.1 sec, the atria are contracting. At the same time, the ventricles are relaxed. 1 Depolarization of the SA node causes atrial depolarization, marked by the P wave in the ECG.
- Gerard J. Tortora, Bryan H. Derrickson, Brendan Burkett, Gregory Peoples, Danielle Dye, Julie Cooke, Tara Diversi, Mark McKean, Simon Summers, Flavia Di Pietro, Alex Engel, Michael Macartney, Hayley Green(Authors)
- 2021(Publication Date)
- Wiley(Publisher)
As a chamber of the heart contracts, blood pressure within it increases. Figure 20.14 shows the relationship between the heart’s electrical signals (ECG) and changes in atrial pressure, ventricular pressure, aortic pressure, and ventricular volume during the Cardiac Cycle. The pressures given in the figure apply to the left side of the heart; pressures on the right side are considerably lower. Each ventricle, however, expels the same volume of blood per beat, and the same pattern exists for both pumping chambers. When heart rate is 75 beats/min, a Cardiac Cycle lasts 0.8 sec. To examine and correlate the events taking place during a Cardiac Cycle, we will begin with atrial systole. Atrial systole During atrial systole, which lasts about 0.1 sec, the atria are contracting. At the same time, the ventricles are relaxed. 1 Depolarisation of the SA node causes atrial depolarisation, marked by the P wave in the ECG. 2 Atrial depolarisation causes atrial systole. As the atria contract, they exert pressure on the blood within, which forces blood through the open AV valves into the ventricles. 3 Atrial systole contributes a final 25 mL of blood to the volume already in each ventricle (about 105 mL). The end of atrial systole is also the end of ventricular diastole (relaxation). Thus, each ventricle contains about 130 mL at the end of its relaxation period (diastole). This blood volume is called the end-diastolic volume (EDV). 4 The QRS complex in the ECG marks the onset of ventricular depolarisation. Ventricular systole During ventricular systole, which lasts about 0.3 sec, the ventricles are contracting. At the same time, the atria are relaxed in atrial diastole. 5 Ventricular depolarisation causes ventricular systole. As ventricular systole begins, pressure rises inside the ventricles and pushes blood up against the atrioventricular (AV) valves, forcing them shut. For about 0.05 seconds, both the SL (semilunar) and AV valves are closed.
eBook - PDF- Gerard J. Tortora, Bryan H. Derrickson(Authors)
- 2020(Publication Date)
- Wiley(Publisher)
(a) ECG. (b) Changes in left atrial pressure (green line), left ventricular pressure (blue line), and aortic pressure (red line) as they relate to the opening and closing of heart valves. (c) Heart sounds. (d) Changes in left ventricular volume. (e) Phases of the Cardiac Cycle. A Cardiac Cycle is composed of all of the events associated with one heartbeat. Q How much blood remains in each ventricle at the end of ventricular diastole in a resting person? What is this volume called? 20.4 The Cardiac Cycle 751 relationship between the heart’s electrical signals (ECG) and changes in atrial pressure, ventricular pressure, aortic pressure, and ventricular volume during the Cardiac Cycle. The pressures given in the figure apply to the left side of the heart; pressures on the right side are considerably lower. Each ventricle, how- ever, expels the same volume of blood per beat, and the same pattern exists for both pumping chambers. When heart rate is 75 beats/min, a Cardiac Cycle lasts 0.8 sec. To examine and correlate the events taking place during a Cardiac Cycle, we will begin with atrial systole. Atrial Systole During atrial systole, which lasts about 0.1 sec, the atria are contracting. At the same time, the ventri- cles are relaxed. 1 Depolarization of the SA node causes atrial depolarization, marked by the P wave in the ECG. 2 Atrial depolarization causes atrial systole. As the atria contract, they exert pressure on the blood within, which forces blood through the open AV valves into the ventricles. 3 Atrial systole contributes a final 25 mL of blood to the volume already in each ventricle (about 105 mL). The end of atrial systole is also the end of ventricular diastole (relaxation). Thus, each ventricle contains about 130 mL at the end of its relaxation period (diastole). This blood volume is called the end-diastolic volume (EDV). 4 The QRS complex in the ECG marks the onset of ventricular depolarization.
eBook - PDF- Bryan H. Derrickson(Author)
- 2019(Publication Date)
- Wiley(Publisher)
Atrial Contraction Atrial depolarization causes atrial systole. While the atria are in systole, the ventricles remain in diastole. As the atria contract, atrial pressure increases (step 4 in Figure 14.19) and more blood is forced through the open AV valves into the ventricles. Atrial contraction contributes a final 25 mL of blood to the volume already in each ventricle (about 105 mL). The end of atrial systole is also the end of ventricu- lar diastole (relaxation). Thus, each ventricle contains about 524 CHAPTER 14 The Cardiovascular System: The Heart Question How much blood remains in each ventricle at the end of ventricular diastole in a resting person? What is this volume called? A Cardiac Cycle includes all of the events associated with a single heartbeat. FIGURE 14.19 Cardiac Cycle. (a) ECG. (b) Changes in left atrial pressure (green line), left ventricular pressure (blue line), and aortic pressure (red line) as they relate to the opening and closing of heart valves. (c) Heart sounds. (d) Changes in left ventricular volume. (e) Phases of the Cardiac Cycle. 0 20 40 60 80 100 120 (b) Pressure (mmHg) (c) Heart sounds (a) ECG Aortic valve opens (d) Volume in ventricle (mL) 130 60 0 Atrial contraction Ventricular ejection Isovolumetric ventricular contraction Isovolumetric ventricular relaxation (e) Phases of the Cardiac Cycle End-systolic volume Stroke volume S1 S2 End-diastolic volume Bicuspid valve closes Bicuspid valve opens Aortic valve closes Dicrotic wave Left atrial pressure Aortic pressure Left ventricular pressure P R Q S T Passive ventricular filling 3 6 10 2 8 11 12 1 7 4 13 5 9 14.5 Cardiac Output 525 14.5 Cardiac Output Objectives • Define cardiac output. • Describe the factors that regulate stroke volume. • Discuss the factors that regulate heart rate. Although the heart has autorhythmic fibers that enable it to beat independently, its operation is governed by events occur- ring throughout the body.
eBook - ePub- Thomas Foster, Jasmine Shen, Shreelata T Datta, Philip Xiu, Shreelata T Datta, Philip Xiu(Authors)
- 2018(Publication Date)
- Elsevier(Publisher)
Table 2.1 ). At a resting heart rate of approximately 75 bpm, the Cardiac Cycle lasts 0.80 s. This is divided into diastole and systole, which last approximately 0.53 s and 0.27 s respectively. When considering the Cardiac Cycle, it is useful to remember that:- • Blood flows down a pressure gradient.
- • The position of a valve is dependent on the pressure gradient across it.
Fig. 2.8 Pressure–volume cycle of left ventricle. The most significant pressure changes occur within the ventricles during the isovolumetric stages.Table 2.1 Summary table of the stages of the Cardiac CycleDiastole Systole Diastole Stage Ventricular filling Isovolumetric contraction Ejection Isovolumetric relaxation Atrioventricular (AV) valves Open Closed Closed Closed Arterial valves Closed Closed Open Closed Ventricular pressure Falls then slowly rises Rapid rise Rises then slowly falls Rapid fall Ventricular volume Increases Constant Decreases Constant Note: changes at fixed volume are referred to as isovolumetric and precede the later contraction or dilation of the ventricles .The ventricular cycle
The ventricular cycle consists of four phases. The duration and order of each of these phases is shown in Table 2.1 .- 1. Ventricular filling (diastole). The atria and ventricles are initially relaxed, with passive filling occurring due to central venous pressure (CVP) and pulmonary venous pressure. Filling distends the ventricle, causing pressure to rise. Passive ventricular filling stops when ventricular pressure reaches pulmonary venous pressure. Contraction of the atria further increases the filling of the ventricles. This accounts for about 15%–20% of ventricular filling at rest but is more important during exercise as the time for passive ventricular filling is reduced. The volume of blood in the ventricle at the end of diastole is termed the end-diastolic volume (EDV).
Clinical NoteThe ‘atrial kick’ is absent in people with atrial fibrillation due to ineffective atrial contraction. This has little effect on cardiac output at rest.- 2. Isovolumetric contraction (systole). Ventricular contraction increases ventricular pressure. As ventricular pressure rises above atrial pressure, the atrioventricular valves close early in systole. This creates a closed chamber as all valves are closed. Ventricular contraction continues, causing a rapid rise in ventricular pressure. No blood is ejected from the ventricles because aortic/pulmonary pressure is greater than that in the ventricles, keeping the aortic and pulmonary valves closed.
eBook - PDFFundamentals of Critical Care
A Textbook for Nursing and Healthcare Students
- Ian Peate, Barry Hill(Authors)
- 2022(Publication Date)
- Wiley-Blackwell(Publisher)
Relaxation period Ventricular systole Atrial systole 2 3 1 Figure 18.7 The Cardiac Cycle. Heart Rate (HR) × Stroke Volume (SV) = Cardiac Output (CO) 70 bpm × 70 mls = 4.9 L/min Figure 18.8 Cardiac output. 238 Chapter 18 Cardiac physiology Cardiac output can increase significantly to meet meta- bolic demands by altering both heart rate and stroke volume with some athletes able to increase their cardiac output to over 30 l/min. Cardiac output is intrinsically linked with blood pressure which can be defined as the pressure blood exerts on the walls of the arteries and is influenced by cardiac output, blood viscosity and systemic vascular resistance (SVR), the degree of vasoconstriction in the circulation. Regulation of heart rate The regulation of heart rate allows cardiac output to match metabolic demand and respond to physiological stressors such as hypovolemia. Remember, the sinoatrial node is autorhythmic and left to its own devices would depolarise 80–100 times per minute. This intrinsic heart rate, however, can be influenced by both neurological and biochemical mechanisms. Neural regulation is controlled by the cardiovascular centre, part of autonomic nervous system found within the brain stem. This centre receives information from various tissues including baroreceptors in the major vessels (aorta and carotid) which detect blood pressure, proprioceptors in skeletal muscle and even the limbic system which accounts for the effect of emotional states, such as fear, on heart rate. Sympathetic neurones which project from the cardiovascu- lar centre via the spinal cord to the cardiac conduction system and the myocardium increase heart rate (and cardiac contractility) by releasing the neurotransmitter, norepi- nephrine which stimulates Beta one adrenoreceptors (β 1 ) (see Table 18.1).
eBook - PDFThe Cardiovascular System
Physiology, Diagnostics and Clinical Implications
- David C. Gaze(Author)
- 2012(Publication Date)
- IntechOpen(Publisher)
10. May 2011 3. Conclusion Cardiac Cycle phase analysis method allows tracking any changes of hemodynamics and functions of the cardiovascular system. It can be used to identify the original cause of pathologies and to efficiently monitor the treatment progress. 4. References [1] Rudenko, M.; Voronova, O. & Zernov. V. Innovation in cardiology. A new diagnostic standard establishing criteria of quantitative & qualitative evaluation of main parameters of the cardiac & cardiovascular system according to ECG and RHEO based on Cardiac Cycle phase analysis (for concurrent single-channel recording of cardiac signals from ascending aorta). http://precedings.nature.com/documents/3667/version/1/html [2] Leontieva I. & Sukhorukov V. The implications of metabolic disorders in the genesis of cardiac myopathia and possible use of L-carnitine for therapeutic correction. . Saint Petersburg. Manuscript -2006. [3] Vasilenko V. Kh., Feldman S. B., Khotrov N.N., Miocardyodistrophia. - Moscow. Medicine. – 1989. -272. [4] Kushakovsky M.S. Metabolic cardiac diseases. Saint Petersburg. Manuscript -2000. 128. 11 Application of Computational Intelligence Techniques for Cardiovascular Diagnostics C. Nataraj, A. Jalali and P. Ghorbanian Department of Mechanical Engineering, Villanova University, Villanova, Pennsylvania, USA 1. Introduction Cardiovascular disease, including heart disease and stroke, remains the leading cause of death around the world. Yet, most heart attacks and strokes could be prevented if it were possible to provide an easy and reliable method of monitoring and diagnostics. In particular, the early detection of abnormalities in the function of the heart, called arrhythmias, could be valuable for clinicians. Hemodynamic instability is most commonly associated with abnormal or unstable blood pressure (BP), especially hypotension, or more broadly associated with inadequate global or regional perfusion.
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