Page 115 - Alaska A & P Primer

19.3 Cardiac Cycle
19.5 Development of the Heart
19.3 OBJECTIVES
1. Summarize the events of the cardiac cycle
19.5 OBJECTIVES
1. Relate fetal heart structures to adult counterparts
The period of time that begins with contraction of the atria and ends with ventricular re- laxation is known as the cardiac cycle. The period of contraction that the heart undergoes while it pumps blood into circulation is called systole. The period of relaxation that occurs as the chambers fill with blood is called diastole. Both the atria and ventricles undergo sys- tole and diastole, and it is essential that these components be carefully regulated and coor- dinated to ensure blood is pumped efficiently to the body.
19.4 Cardiac Physiology
The autorhythmicity inherent in cardiac cells keeps the heart beating at a regular pace; however, the heart is regulated by and responds to outside influences as well. Neural and endocrine controls are vital to the regulation of cardiac function. In addition, the heart is sensitive to several environmental factors, including electrolytes.
Cardiac output (CO) is a measurement of the amount of blood pumped by each ventricle in one minute. To calculate this value, multiply stroke volume (SV), the amount of blood pumped by each ventricle, by heart rate (HR), in contractions per minute (or beats per minute, bpm). It can be represented mathematically by the following equation:
CO = HR X SV
SV is normally measured using an echocardiogram to record EDV(end diastolic volume) and ESV (end systolic volume), and calculating the difference: SV = EDV – ESV. SV can also be measured using a specialized catheter, but this is an invasive procedure and far more dangerous to the patient. A mean SV for a resting 70-kg (150-lb) individual would be approximately 70 mL. There are several important variables, including size of the heart, physical and mental condition of the individual, sex, contractility, duration.
The heart is the first organ to form and become functional, emphasizing the importance of transport of material to and from the developing infant. It originates about day 18 or 19 from the mesoderm and begins beating and pumping blood about day 21 or 22. It forms from the cardiogenic region near the head and is visible as a prominent heart bulge on the surface of the embryo.
Repair and Replacement of the Heart
Damaged cardiac muscle cells have extremely limited abilities to repair themselves or to replace dead cells via mitosis. Recent evidence indicates that at least some stem cells re- main within the heart that continue to divide and at least potentially replace these dead cells. However, newly formed or repaired cells are rarely as functional as the original cells, and cardiac function is reduced. In the event of a heart attack or MI, dead cells are often replaced by patches of scar tissue. Autopsies performed on individuals who had success- fully received heart transplants show some proliferation of original cells. If researchers
can unlock the mechanism that generates new cells and restore full mitotic capabilities to heart muscle, the prognosis for heart attack survivors will be greatly enhanced. To date, myocardial cells produced within the patient (in situ) by cardiac stem cells seem to be non- functional, although those grown in Petri dishes (in vitro) do beat. Perhaps soon this mys- tery will be solved, and new advances in treatment will be commonplace.
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Listen to Heart Sounds:
http://www.littmann.ca/wps/portal/3M/en_CA/3M-Littmann-CA/stethoscope/littmann
-learning-institute/heart-lung-sounds/heart-sounds/
19.4 OBJECTIVES
1. Describe heart rate to cardiac output
Heart: Broken Heart Syndrome
Extreme stress from such life events as the death of a loved one, an emotional break up, loss of income, or foreclosure of a home may lead to a condition commonly referred to as broken heart syndrome. This condition may also be calledTakotsubo cardiomyopathy, tran sient apical ballooning syndrome, apical ballooning cardiomyopathy, stress-induced car- diomyopathy, Gebrochenes-Herz syndrome, and stress cardiomyopathy. The recognized effects on the heart include congestive heart failure due to a profound weakening of the myocardium not related to lack of oxygen. This may lead to acute heart failure, lethal ar- rhythmias, or even the rupture of a ventricle. The exact etiology is not known, but several factors have been suggested, including transient vasospasm, dysfunction of the cardiac capillaries, or thickening of the myocardium—particularly in the left ventricle—that may lead to the critical circulation of blood to this region. While many patients survive the ini- tial acute event with treatment to restore normal function, there is a strong correlation with death. Careful statistical analysis by the Cass Business School, a prestigious institu- tion located in London, published in 2008, revealed that within one year of the death of a loved one, women are more than twice as likely to die and males are six times as likely to die as would otherwise be expected.
This content is available for free at https://cnx.org/content/col11496/1.7
State of Alaska EMS Education Primer - 2016
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