{"id":4775,"date":"2025-08-25T00:04:04","date_gmt":"2025-08-25T04:04:04","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&p=4775"},"modified":"2025-12-13T17:53:48","modified_gmt":"2025-12-13T22:53:48","slug":"cardiac-output-and-factors-affecting-heart-function","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/cardiac-output-and-factors-affecting-heart-function\/","title":{"raw":"7p6 Cardiac Output and Factors Affecting Heart Function","rendered":"7p6 Cardiac Output and Factors Affecting Heart Function"},"content":{"raw":"

What is Cardiac Output (CO)?<\/strong><\/h2>\r\n

Definition:<\/strong><\/h1>\r\n
    \r\n \t
  • The\u00a0amount of blood ejected<\/strong>\u00a0by each ventricle\u00a0per minute<\/strong>.<\/li>\r\n \t
  • Abbreviations:\u00a0CO<\/strong>\u00a0or\u00a0Q<\/strong>.<\/li>\r\n<\/ul>\r\n

    Formula:<\/strong><\/h1>\r\n
      \r\n \t
    • Cardiac Output = Stroke Volume \u00d7 Heart Rate<\/strong><\/li>\r\n \t
    • Stroke Volume:<\/strong> Volume of blood pumped out of the ventricle with each contraction (beat).\u00a0 Stroke Volume is also called Ejection Volume).<\/li>\r\n \t
    • Heart Rate:<\/strong>\u00a0Number of contractions per minute.<\/li>\r\n \t
    • Normal Values for Healthy Adult:\r\n
        \r\n \t
      • Heart Rate<\/strong> at Rest:<\/strong> approximately 70 beats per minute<\/li>\r\n \t
      • Stroke Volume<\/strong> at Rest:<\/strong> approximately 70mL per beat<\/li>\r\n \t
      • Resulting Cardiac Output<\/strong> at Rest=<\/strong> HR x SV = 70 x 70 = 4900 mL per minute = 4.9L per minute<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n

        Key Terms:<\/strong><\/h1>\r\n
          \r\n \t
        1. Preload:<\/strong><\/li>\r\n<\/ol>\r\n
            \r\n \t
          • The\u00a0initial stretching<\/strong>\u00a0of cardiac myocytes before contraction.<\/li>\r\n \t
          • Measured as\u00a0venous return<\/strong>\u00a0\u2014 the blood volume arriving in the right atrium via superior and inferior vena cava.<\/li>\r\n<\/ul>\r\n
              \r\n \t
            1. Afterload:<\/strong><\/li>\r\n<\/ol>\r\n
                \r\n \t
              • The\u00a0force or resistance<\/strong>\u00a0the ventricle must overcome to eject blood into the aorta.<\/li>\r\n \t
              • Primarily determined by\u00a0peripheral resistance<\/strong>\u00a0in blood vessels.<\/li>\r\n \t
              • Increased afterload<\/strong> (e.g., constricted aorta) strains the heart, making it work harder.<\/li>\r\n \t
              • Decreased afterload<\/strong>\u00a0(e.g., dilated arteries) eases the workload.<\/span><\/li>\r\n<\/ul>\r\n

                Pressure and Blood Flow:<\/strong><\/h1>\r\n
                  \r\n \t
                • Blood flows from\u00a0high pressure<\/strong>\u00a0to\u00a0low pressure<\/strong>.<\/li>\r\n \t
                • Pressure is highest in the\u00a0left ventricle<\/strong>\u00a0(~93 mm Hg) during systole.<\/li>\r\n \t
                • Pressure drops through the circulatory system:\r\n
                    \r\n \t
                  • Aorta:<\/strong>\u00a0~120 mm Hg systolic.<\/li>\r\n \t
                  • Capillaries:<\/strong>\u00a0~35 mm Hg.<\/li>\r\n \t
                  • Venous system:<\/strong>\u00a018 mm Hg before returning to the right atrium (2 mm Hg).<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                  • Blood flow is driven by this pressure gradient against gravity, with the\u00a0right ventricle<\/strong>\u00a0generating ~12 mm Hg for pulmonary circulation.<\/li>\r\n<\/ul>\r\n

                    Influences on Cardiac Output:<\/strong><\/h1>\r\n
                      \r\n \t
                    1. Heart Rate:<\/strong><\/li>\r\n<\/ol>\r\n
                        \r\n \t
                      • Controlled by the\u00a0medulla oblongata<\/strong>\u00a0via sympathetic and parasympathetic pathways.<\/li>\r\n \t
                      • Sympathetic stimulation:<\/strong>\r\n
                          \r\n \t
                        • Releases\u00a0epinephrine<\/strong>\u00a0onto\u00a0beta-1 adrenergic receptors<\/strong>\u00a0on the SA node.<\/li>\r\n \t
                        • Speeds up depolarization, increasing heart rate and contraction force (fight or flight<\/strong>).<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                        • Parasympathetic stimulation:<\/strong>\r\n
                            \r\n \t
                          • Via\u00a0vagus nerve<\/strong>, releases\u00a0acetylcholine<\/strong>\u00a0onto SA node.<\/li>\r\n \t
                          • Opens\u00a0potassium channels<\/strong>, hyperpolarizing heart cells, slowing heart rate (rest and digest<\/strong>).<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n
                              \r\n \t
                            1. Stroke Volume:<\/strong><\/li>\r\n<\/ol>\r\n
                                \r\n \t
                              • Starling's Law:<\/strong>\r\n
                                  \r\n \t
                                • Increased\u00a0venous return<\/strong>\u00a0leads to greater\u00a0end-diastolic volume<\/strong>\u00a0(preload) and hence increased stroke volume.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                                • Contractility:<\/strong>\r\n
                                    \r\n \t
                                  • Sympathetic stimulation increases force of contraction, ejecting more blood.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                                  • Afterload:<\/strong>\r\n
                                      \r\n \t
                                    • Increased resistance decreases stroke volume as the heart faces more opposition during ejection.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n

                                      Venous Return & Blood Flow Against Gravity<\/strong><\/h1>\r\nVenous Return Support:<\/strong>\r\n
                                        \r\n \t
                                      1. Respiratory Pump:<\/strong>\r\n
                                          \r\n \t
                                        • During inhalation, thoracic volume increases, decreasing pressure in veins (like the inferior vena cava), helping \"suck\" blood back to the heart.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                                        • Skeletal Muscle Pump:<\/strong>\r\n
                                            \r\n \t
                                          • Muscle contractions compress veins; valves prevent backflow, assisting blood return.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                                          • Valves:<\/strong>\r\n
                                              \r\n \t
                                            • Ensure unidirectional blood flow toward the heart, especially important in lower limbs.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ol>\r\n

                                              Summary:<\/strong><\/h1>\r\nCardiac output depends on heart rate and stroke volume, both influenced by neural, hormonal, and mechanical factors. Venous return, blood resistance, and external muscle activity all contribute to maintaining effective circulation. Proper regulation ensures tissues receive adequate oxygen and nutrients, especially during stress or activity.","rendered":"

                                              What is Cardiac Output (CO)?<\/strong><\/h2>\n

                                              Definition:<\/strong><\/h1>\n
                                                \n
                                              • The\u00a0amount of blood ejected<\/strong>\u00a0by each ventricle\u00a0per minute<\/strong>.<\/li>\n
                                              • Abbreviations:\u00a0CO<\/strong>\u00a0or\u00a0Q<\/strong>.<\/li>\n<\/ul>\n

                                                Formula:<\/strong><\/h1>\n
                                                  \n
                                                • Cardiac Output = Stroke Volume \u00d7 Heart Rate<\/strong><\/li>\n
                                                • Stroke Volume:<\/strong> Volume of blood pumped out of the ventricle with each contraction (beat).\u00a0 Stroke Volume is also called Ejection Volume).<\/li>\n
                                                • Heart Rate:<\/strong>\u00a0Number of contractions per minute.<\/li>\n
                                                • Normal Values for Healthy Adult:\n
                                                    \n
                                                  • Heart Rate<\/strong> at Rest:<\/strong> approximately 70 beats per minute<\/li>\n
                                                  • Stroke Volume<\/strong> at Rest:<\/strong> approximately 70mL per beat<\/li>\n
                                                  • Resulting Cardiac Output<\/strong> at Rest=<\/strong> HR x SV = 70 x 70 = 4900 mL per minute = 4.9L per minute<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n

                                                    Key Terms:<\/strong><\/h1>\n
                                                      \n
                                                    1. Preload:<\/strong><\/li>\n<\/ol>\n
                                                        \n
                                                      • The\u00a0initial stretching<\/strong>\u00a0of cardiac myocytes before contraction.<\/li>\n
                                                      • Measured as\u00a0venous return<\/strong>\u00a0\u2014 the blood volume arriving in the right atrium via superior and inferior vena cava.<\/li>\n<\/ul>\n
                                                          \n
                                                        1. Afterload:<\/strong><\/li>\n<\/ol>\n
                                                            \n
                                                          • The\u00a0force or resistance<\/strong>\u00a0the ventricle must overcome to eject blood into the aorta.<\/li>\n
                                                          • Primarily determined by\u00a0peripheral resistance<\/strong>\u00a0in blood vessels.<\/li>\n
                                                          • Increased afterload<\/strong> (e.g., constricted aorta) strains the heart, making it work harder.<\/li>\n
                                                          • Decreased afterload<\/strong>\u00a0(e.g., dilated arteries) eases the workload.<\/span><\/li>\n<\/ul>\n

                                                            Pressure and Blood Flow:<\/strong><\/h1>\n
                                                              \n
                                                            • Blood flows from\u00a0high pressure<\/strong>\u00a0to\u00a0low pressure<\/strong>.<\/li>\n
                                                            • Pressure is highest in the\u00a0left ventricle<\/strong>\u00a0(~93 mm Hg) during systole.<\/li>\n
                                                            • Pressure drops through the circulatory system:\n
                                                                \n
                                                              • Aorta:<\/strong>\u00a0~120 mm Hg systolic.<\/li>\n
                                                              • Capillaries:<\/strong>\u00a0~35 mm Hg.<\/li>\n
                                                              • Venous system:<\/strong>\u00a018 mm Hg before returning to the right atrium (2 mm Hg).<\/li>\n<\/ul>\n<\/li>\n
                                                              • Blood flow is driven by this pressure gradient against gravity, with the\u00a0right ventricle<\/strong>\u00a0generating ~12 mm Hg for pulmonary circulation.<\/li>\n<\/ul>\n

                                                                Influences on Cardiac Output:<\/strong><\/h1>\n
                                                                  \n
                                                                1. Heart Rate:<\/strong><\/li>\n<\/ol>\n
                                                                    \n
                                                                  • Controlled by the\u00a0medulla oblongata<\/strong>\u00a0via sympathetic and parasympathetic pathways.<\/li>\n
                                                                  • Sympathetic stimulation:<\/strong>\n
                                                                      \n
                                                                    • Releases\u00a0epinephrine<\/strong>\u00a0onto\u00a0beta-1 adrenergic receptors<\/strong>\u00a0on the SA node.<\/li>\n
                                                                    • Speeds up depolarization, increasing heart rate and contraction force (fight or flight<\/strong>).<\/li>\n<\/ul>\n<\/li>\n
                                                                    • Parasympathetic stimulation:<\/strong>\n
                                                                        \n
                                                                      • Via\u00a0vagus nerve<\/strong>, releases\u00a0acetylcholine<\/strong>\u00a0onto SA node.<\/li>\n
                                                                      • Opens\u00a0potassium channels<\/strong>, hyperpolarizing heart cells, slowing heart rate (rest and digest<\/strong>).<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n
                                                                          \n
                                                                        1. Stroke Volume:<\/strong><\/li>\n<\/ol>\n
                                                                            \n
                                                                          • Starling’s Law:<\/strong>\n
                                                                              \n
                                                                            • Increased\u00a0venous return<\/strong>\u00a0leads to greater\u00a0end-diastolic volume<\/strong>\u00a0(preload) and hence increased stroke volume.<\/li>\n<\/ul>\n<\/li>\n
                                                                            • Contractility:<\/strong>\n
                                                                                \n
                                                                              • Sympathetic stimulation increases force of contraction, ejecting more blood.<\/li>\n<\/ul>\n<\/li>\n
                                                                              • Afterload:<\/strong>\n
                                                                                  \n
                                                                                • Increased resistance decreases stroke volume as the heart faces more opposition during ejection.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n

                                                                                  Venous Return & Blood Flow Against Gravity<\/strong><\/h1>\n

                                                                                  Venous Return Support:<\/strong><\/p>\n

                                                                                    \n
                                                                                  1. Respiratory Pump:<\/strong>\n
                                                                                      \n
                                                                                    • During inhalation, thoracic volume increases, decreasing pressure in veins (like the inferior vena cava), helping “suck” blood back to the heart.<\/li>\n<\/ul>\n<\/li>\n
                                                                                    • Skeletal Muscle Pump:<\/strong>\n
                                                                                        \n
                                                                                      • Muscle contractions compress veins; valves prevent backflow, assisting blood return.<\/li>\n<\/ul>\n<\/li>\n
                                                                                      • Valves:<\/strong>\n
                                                                                          \n
                                                                                        • Ensure unidirectional blood flow toward the heart, especially important in lower limbs.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n

                                                                                          Summary:<\/strong><\/h1>\n

                                                                                          Cardiac output depends on heart rate and stroke volume, both influenced by neural, hormonal, and mechanical factors. Venous return, blood resistance, and external muscle activity all contribute to maintaining effective circulation. Proper regulation ensures tissues receive adequate oxygen and nutrients, especially during stress or activity.<\/p>\n","protected":false},"author":1370,"menu_order":12,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-4775","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":55,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4775","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":7,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4775\/revisions"}],"predecessor-version":[{"id":5283,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4775\/revisions\/5283"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/55"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4775\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=4775"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=4775"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=4775"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=4775"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}