packet 3 Flashcards
Action potentials of all active cells can be detected and recorded
EKG
atrial depolarization
* muscle contraction signal
P wave
conduction time from atrial to ventricular excitation
P to Q interval
ventricular depolarization
*stronger action potential
QRS complex
ventricular repolarization
T wave
At 75 beats/min, one cycle requires 0.8 sec.
End diastolic volume (EDV)
End systolic volume (ESV)
Stroke Volume (SV)
one cardiac cycle
volume in ventricle at end of diastole, about 130ml
end diastolic volume
volume in ventricle at end of systole, about 60ml
end systolic volume
the volume ejected per beat from each ventricle, about 70ml
SV = EDV - ESV
stroke volume
brief period when volume in ventricles does not change– ventricles relax, pressure drops and AV valves open
Isovolumetric relaxation
as blood flows from full atria
diastasis: as blood flows from atria in smaller volume
atrial systole pushes final 20-25 ml blood into ventricle
Ventricular filling
ventricular systole
isovolumetric contraction
ventricular ejection: as SL valves open and blood is ejected
ventricular systole
erratic heartbeat, uncoordinated contractions
fibrillation
interference with AV node erratic, incomplete atrial contractions. Often secondary to other heart problem, and rarely life-threatening.
Treatment: drug/electro-cardioconversion; anti-coagulants
Symptoms: none, palpitations, fainting, nausea, chest pain; can lead to stroke and congestive heart failure.
atrial fibrillation
erratic, incomplete ventricular contractions. Immediately life-threatening due to lack of somatic, pulmonary, and cardiac circulation; often secondary to other heart disease.
Symptoms: sudden collapse; death often first “symptom.”
Treatment: electric cardioconversion, then treat underlying issue
ventricular fibrillation
rapid (especially ventricular) heartbeat.
Symptoms: range from faintness, short-of-breath to sudden death, depending location and cause.
Treatment: drug or electric cardioconversion, then treat underlying issue
Tachycardia
slows heartbeat
bradycardia
Blood pressure in aorta is 120mm Hg
Blood pressure in pulmonary trunk is 30mm Hg
Differences in ventricle wall thickness allows heart to push the same amount of blood with more force from the left ventricle
The volume of blood ejected from each ventricle is 70ml (stroke volume)
ventricular pressures
mL blood pumped/min
= mL blood/beat x beat/min
cardiac output
70mL/beat x 75 beat/min = 5.25L
(thus blood moves through body 1x/min!)
normal CO
regulate stroke volume by allowing more blood in the ventricle and/or stronger contractions). Upper limit = size of ventricle and time allowed to fill.
more blood/beat
increase heart rate). Upper limit = need to reinitiate beat (refractory period)
more beats/min
Nervous system control
Sensors
sympathetic NS
Parasympatheitc NS
limbic system, baroreceptors, chemoreceptors, proprioreceptors. Feed into medulla’s cardiovascular center (medulla). Control through ANS.
sensors
nerves connect with SA & AV nodes and myocardium. HORMONE? increases rate of autorhythmic SA firing and uptake of Ca++ ( contractility) by all muscle cells.
sympathetic NS
nerves (CN???) connect with SA & AV nodes and myocardium of atria. Decreases rate of autorhythmic firing with ACh.
parasympathetic NS
What controls heart rate and blood pressure
Nervous system
endocrine system
cation control
metabolic control
Adrenal medulla (responding to hypothalamus) releases epinephrine and norepinephrine = increase of autorhythmic rate and contractility.
endocrine system
Increased K+ prevents action potential
Increased Na+ blocks Ca++ entry
Increased Ca++ boost contractility, rate
cation control
Increased H+ (acidosis) or OH– decrease heart rate.
metabolic control
