Heart./Exercise Physiology Review Flashcards
Diastole
Relaxation phase during which the ventricles fill with blood
AV valves open
Aortic and pulmonic valves closed
Systole
Contraction phase during which ventricles expel blood
AV valves closed
Aortic and pulmonic valves open
Intrinsic Control of the Cardiac Cycle
Autorythmaticity
Sinoatrial Node
Atrioventricular Node
Purkinje Fibers
Authorhytmaticity
ability to initiate impulse for contraction at regular intervals
Sinoatrial Node
Pacemaker of the heart
Atrioventricular Node
Delays impulse by 1/10 of second, allowing atria to contract before ventricles
Purkinje Fibers
Rapidly spread the impulse to contract throughout the ventricles
P wave
atrial depolarization
QRS complex
Ventricular depolarization and atrial repolarization
T wave
ventricular repolarization
Myocardial Ischemia
ST- segment depression
Pressure During Diastole
Pressure is low
Atria fill with blood because the AV valves are open when the ventricular pressure is less than the atrial pressure
Pressure During Systole
Pressure in ventricles rises and blood is ejected into the pulmonary and systemic circulation
Semilunar valves are open when ventricular P is greater than atrial P
LUB sound
closing of the AV valves
DUB sound
closing of the aortic and pulmonary valves
Cardiac Output (Q)
= HR x SV
Stroke Volume controlled by …
end diastolic volume, after load, contractility
Extrinsic Regulation of Heart Rate
PNS via valgus nerve
SNS via cardiac accelerator nerves
Low resting HR dude to Parasympathetic tone
Increase in HR at onset of exercise
Valgus Nerve
Slows HR by inhibiting SA and AV node
Cardiac Accelerator Nerves
Increases HR by stimulating SA and AV Node
Baroreceptors
carotid artery/ aortic arch
sense pressure changes by responding to changes in the tension of the ventricular wall I
If BP is high: send signal to medulla oblongata to increase PNA, decrese SNA, decrease HR (and SV, TPR) thus reduced BP
Preload/EDV
volume of blood in the ventricles at the end of diastole
Aortic BP/afterload
pressure the heart must pump against to eject blood (Mean Arterial Pressure)
The tension developed in the wall of the left ventricle during ejection
Contractility
strength of the ventricular contraction
enhanced by circulating epinephrine and norepinephrine and also direct sympathetic stimulation of heart
Frank-Starling Mechanism
Greater EDV results in a more forceful contraction (Due to stretch of ventricles)
Dependent of venous return
Increase venous return
Increase by venoconstriction, skeletal muscle pump and respiratory pump,
Skeletal Muscle Pump
rhythmic skeletal muscle contractions force blood in the extremities toward the heart
one-way valves in veins prevent backflow of blood
Respiratory Pump
changes in thoracic pressure pull blood toward the heart
High afterload
decrease in stroke volume, requires greater force generation by the myocardium to eject blood into the aorta
Increased contractility
results in higher stroke volume
- circulating epinephrine and norepinephrine
- direct sympathetic stimulation of the heart
Increase Stroke Volume
Increase EDV
Decrease Afterload
Increase Contractility
Determinants of mean arterial pressure
cardiac output, total vascular resistance ( TVR or TPR)
ABP= CO xTPR
Short term regulation of ABP
sympathetic nervous system to heart and vasculature
baroreceptors in aorta and carotid arteries
increase in BP= decrease SNS activity= Normal BP
decreased BP =increased SNS activity=normal BP
Long term regulation of BP
kidneys via the blood volume control
TPR
regulated by vasodilation or vasoconstriction
vasodilation
decreased resistance, decreased BP
nitric oxide
vasoconstriction
increased resistance, increased BP
Norepinephrine
Blood pressure eqx
BP= Q x TPR
To increase HR
increase SNA
Decrease PNA
Increase TPR
Increase SNA and Decrease the radius
