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
-High blood pressure or hypertension increases the afterload (the pressure needed to open the semilunar valve), often leading to a decline in stroke volume (Bruss & Raja, 2022).
b. Massive bleeding
-To compensate for the massive blood loss, the heart rate increases with the signal from the sympathetic nervous system. Since there is less blood being pumped by the heart, the arterial pressure, stroke volume (with less afterload), and overall cardiac output also decrease (Gupta & Fahim, 2005).
c. The drug dopamine
-As dopamine levels increase, the cardiac output and heart rate increase while the peripheral resistance and pulmonary artery pressure decrease. In lower doses of dopamine, there is a slight increase in stroke volume, but in higher doses, the stroke volume and blood pressure no longer accompany the increase in heart rate (Schönborn et al., 1976).
d. Running a sprint
-In exercises such as sprint running, there is an increase in cardiac output to a large extent due to an increase in heart rate brought about by the heightened sympathetic activity, and to a lesser extent due to a slight increase in stroke volume. For the stroke volume, the contractility of the ventricles increases through the signals of the sympathetic nerves to the myocardium, while the preload also increases due to the increase of end-diastolic volume as explained by the Frank-Sterling mechanism (McGilll Physiology Virtual Lab, n.d.).
e. Hyperthyroidism with increased secretion of thyroid hormones
-The manifestations of hyperthyroidism are increases in heart rate, stroke volume, and ejection fraction. Preload rises and the elevated heart rate increases the cardiac output, while the decline in systemic vascular resistance results in a decreased afterload and an overall increase in stroke volume (Osuna et al., 2017).
f. Massive myocardial infarction (cardiac tissue death)
-Acute myocardial infarction more commonly known as heart attack is characterized by a compromised myocardial contractility resulting from muscle hypoxia or low oxygen supply to muscles and cardiac cell death or necrosis. This is then followed by a sudden decline in arterial blood pressure and lower cardiac output (Khalid & Dhakam, 2008).
g. Hypothermia
-Hypothermia or low body temperature is marked by a significant drop in heart rate and a notable rise in stroke volume, with no noticeable changes in overall cardiac output (Brooks et al., 1984). In stroke volume, the cool temperatures lead to an increase in preload in terms of central venous pressure and pulmonary capillary wedge pressure, and an increase in afterload due to a rise in mean arterial pressure (Wilson & Crandall, 2011).
h. Emotional distress
-During periods of emotional or mental stress, the body releases the hormone adrenaline which triggers a rise in heart rate and blood pressure. This is then accompanied by a decline in stroke volume and cardiac output resulting from poor blood circulation (Henley et al., 2018).
REFERENCES:
Brooks, D. P., Chapman, B. J., & Munday, K. A. (1984). The effect of hypothermia on the cardiovascular system and the pressor actions of angiotensin II. Journal of Thermal Biology, 9(4), 243-246
Bruss, Z. S., & Raja, A. (2022). Stroke volume physiology. Stat Pearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK547686/#:~:text=An%20increase%20in%20afterload%2C%20for,preload%20or%20decreasing%20the%20afterload.
Gupta, R.K., & Fahim, M. (2005). Regulation of cardiovascular functions during acute blood loss. Indian Journal of Physiology and Pharmacology, 49(2), 213–219. https://pubmed.ncbi.nlm.nih.gov/16170991/
Henley, B. C., Shokouhi, M., Mahajan, A. Y., Inan, O. T., & Hajjar, I. (2018). Cardiovascular response to mental stress in mild cognitive impairment and its association with cerebral perfusion. Journal of Alzheimer's Disease, 63(2), 645–654. https://doi.org/10.3233/JAD-180036
Khalid, L., & Dhakam, S. H. (2008). A review of cardiogenic shock in acute myocardial infarction. Current Cardiology Reviews, 4(1), 34–40. https://doi.org/10.2174/157340308783565456
McGilll Physiology Virtual Lab (n.d.). Exercise physiology: Cardio/CNS contribution. http://www.medicine.mcgill.ca/physio/vlab/exercise/cardio_cns.htm
Osuna, P. M., Udovcic, M., & Sharma, M. D. (2017). Hyperthyroidism and the heart. Methodist DeBakey Cardiovascular Journal, 13(2), 60–63. https://doi.org/10.14797/mdcj-13-2-60
Schönborn, H., Prellwitz, W., Schuster, H. P., & Johannes, K. J. (1976). Untersuchungen zur Beeinflussung von Hämodynamik, Mikrozirkulation und Nierenfunktion durch Dopamin bei Schlafmittelvergiftungen [The influence of dopamine on hemodynamics, microcirculation and renal function in patients with hypnotic drug intoxication (author's transl)]. Klinische Wochenschrift, 54(12), 549–559. https://doi.org/10.1007/BF01619570
Wilson, T. E., & Crandall, C. G. (2011). Effect of thermal stress on cardiac function. Exercise and Sport Sciences Reviews, 39(1), 12–17. https://doi.org/10.1097/JES.0b013e318201eed6