1. Adequate cardiac output is necessary in order to supply oxygen and other nutrients to all body tissues. Cardiac output is influenced by stroke volume and heart rate. Factors affecting the stroke volume include PRELOAD, CONTRACTILITY, and AFTERLOAD.
In the following conditions, indicate what factor/s influence the cardiac output: PRELOAD, CONTRACTILITY, AFTERLOAD, HEART RATE. Explain why the factor/s affects cardiac output in 1 to 2 sentences.
a. High blood pressure:
Increased blood volume or high blood pressure (which can be thought of as the initial stimulus) stimulates sympathetic nervous activity. The increased venous return increases end-diastolic volume and preload and the increased force of contraction ejects the increased end-diastolic volume, leading to an increased stroke volume, increased cardiac output, and an increased mean arterial pressure.
b. Massive bleeding:
Massive bleeding or hemorrhage leads to a decreased venous return, which leads to a decreased stroke volume and cardiac output. With that, the decrease in cardiac output observed physiologically in people under hypovolemic shock (hemorrhaging) is due to the reduced preload, contractility, and afterload as decreased preload decreases stroke volume by altering the force of contraction of the cardiac muscle.
c. The drug dopamine:
The drug dopamine produces positive chronotropic and inotropic effects on the myocardium, leading to an increase in contractility and cardiac output. This increase in cardiac output due to secretion of dopamine is caused by the increased force of contraction (contractility), which increases stroke volume and, together with the increased heart rate, the cardiac output.
d. Running a sprint:
Increased cardiac output due to running a sprint (or exercise) is caused by the factors preload and contractility. Increased venous return due to the aforementioned activity increases end-diastolic volume and preload, which leads to an increased force of contraction needed to eject the end-diastolic volume, all leading to an increase in stroke volume and cardiac output.
e. Hyperthyroidism with increased secretion of thyroid hormones:
Hyperthyroidism, which consists of an increase in thyroid hormones such as thyroxine, leads to an increase in cardiac output due to an increase in heart rate and contractility (increased contractile force of cardiac muscle). The increased force of contraction decreases end-systolic volume, which increases stroke volume, and both the increased stroke volume and heart rate increases the cardiac output together.
f. Massive myocardial infarction (cardiac tissue death):
Massive myocardial infarction, the decreased or complete cessation of blood flow to the heart, leads to reduced cardiac output. The reduced cardiac output due to myocardial infarction or cardiac tissue death is caused by decreased contractility and, in return, increased afterload, which also causes widespread proliferation of diffuse fibrosis across the ventricle.
g. Hypothermia:
A reduction of core temperature (hypothermia) results in reflex adrenergic vasoconstriction of the skin and increased cardiac output. This is mainly due to the increased force of contraction (contractility), which, in turn, increases the stroke volume, leading to increased cardiac output.
h. Emotional distress:
Emotional distress leads to an increase in cardiac output due to increased contractility. Increased sympathetic stimulation (simultaneous with increased epinephrine and norepinephrine secretion as stimulated by emotions) leads to an increased heart rate and contractility, both of which increase stroke volume and, ultimately, cardiac output.
References:
Hanna, J. N., McN Hill, P., & Sinclair, J. D. (1975). Human cardiorespiratory responses to acute cold exposure. Clinical and experimental pharmacology & physiology, 2(3), 229–238. https://doi.org/10.1111/j.1440-1681.1975.tb03028.x
Marieb, E., & Hoehn, K. (2018). Human Anatomy & Physiology (11th ed.). Pearson.
McDonough, K. H., Giaimo, M., Quinn, M., & Miller, H. (1999). Intrinsic myocardial function in hemorrhagic shock. Shock (Augusta, Ga.), 11(3), 205–210. https://doi.org/10.1097/00024382-199903000-00009
Motloch, L. J., Ishikawa, K., Xie, C., Hu, J., Aguero, J., Fish, K. M., Hajjar, R. J., & Akar, F. G. (2017). Increased afterload following myocardial infarction promotes conduction-dependent arrhythmias that are unmasked by hypokalemia. JACC. Basic to translational science, 2(3), 258–269. https://doi.org/10.1016/j.jacbts.2017.02.002
Nall, R. M. (2022, August 2). Heart Failure and Cardiac Output: Understanding Preload and Afterload. Healthline. https://www.healthline.com/health/heart-failure/preload-and-afterload-in-heart-failure
Peate, I., & Nair, M. (2016). Fundamentals of Anatomy and Physiology: For Nursing and Healthcare Students (2nd ed.). Wiley-Blackwell.
Tortora, G. J., & Derrickson, B. H. (2020). Principles of Anatomy and Physiology (16th ed.). Wiley.
VanPutte, C. L., Russo, A. F., Regan, J. L., Seeley, R. R., Stephens, T., & Tate, P. (2019). ISE Seeley’s Anatomy & Physiology. McGraw-Hill Education.