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The Heart CH 20

QuestionAnswer
location in thoracic cavity in mediastenum; in pericardium sack
fribrous perdicardium tough outer layer; prevents over distention; anchor
serous pericardium thin inner layer; simple squamous epithelium
heart wall epicardium= smooth outermyocardium= middle layer w/cardiac muslce for heart contractingendocardium= smooth inner
pectinate muscles muscluar ridges in auricles and right atrial wall
trabecular carnae muscular ridges on inside of ventricles
coronary artery exit aorta just superior to where it exits heart
tricuspid valve on right side
bicuspid/mitral valve on left side
SA node pacemaker; generate spontaneous APs, medial to opening of superior vena cavae
AV node APs conducted slower to ensure ventricles recieve signal to contract after atria have contracted
AV bundle pass thru hole in cardiac skeleton to reach interventricular septum
bundle branches extend beneath endocardium to L & R ventricles apices
purkinje fibers conduct APs to ventricular muscle cells; contain gap junctions
P wave depolarization of atrial myocardium, signals onset of atrial contraction
QRS complex ventricular depolarization, signals onset of ventricular contraction and repolarization of atria
T wave repolarization of ventricles
systole period of isovolumic contraction; ventricle muscles contract & AV valves closes
diastole period of isovolumic relaxation; ventric pressure falls rapidly; pulm trunk/aorta pressure > ventricles; elastic recoil causes blood to flow towards ventricles and semilunar valves close
end diastolic volume amt of blood left after previous distole when atria emptied into ventricles (120-130 ml blood)
period of ejection when pressure in ventricles is greater than pressure in pulm trunk/aorta, the semilunar valves are opened and blood ejects from ventricles; left ventricle has more than right
end systolic volume amt of blood left after period of ejection (50-60 ml)
passive ventricular filling while ventricles were in systole, atrials filled with blood; atrial pressure >ventricular, AV valves open and blood flows into ventricles (70% of filling)
active ventricular filling depol of SA node causes APs to spread over atrias (P wave) & atria contract, which completes filling; this type unnecessary when at rest
lubb sound AV vales and surrounding fluid vibrate as valves close at beginning of systole
dupp sound closure of semilunar valves at beginning of distole
Mean Arterial Pressure CO x PR
stroke volume (sv) amt of blood pumped during each heartbeat
heart rate (hr) # times heart beats per minute
cardiac reserve difference between CO at rest and maximum CO
CO amt of blood pumped by heart per minute; SV xHR
PR total resistance against which blood must be pumped
intrinsic regulation results from normal functional characteristics of heart
preload amt of stretch of ventricular walls
starlings law the greater the preload the greater the force of the contraction
afterload pressure contracting muslce have to produce to overcome pressure in aorta and move blood into aorta
extrinsic regulation involves neural and hormonal control
sympathetic stimulation supplied by cardiac nerves; innervate SA & AV nodes, coronary vessels and atrial and ventricular myocardium. Increases heart rate and force of contraction. Increased heart rate-> increased cardiac output; lower end systolic volume bc of greater force;
parasympathetic stimulation supplied by vagus nerve, decreases heart rate; acetycholine hyperpolarizes heart
hormonal control epinephrine and norepinephrine released my adrenal medulla in response to high physical activity or stress
homeostasis of heart baroreceptors monitor blood pressure and send info to medulla oblongata. low oxygen levels causes increase heart rate and BP so more oxygen can be delivered. heart rate increases when body temp increase.
Created by: 619572525