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CO

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imissyou419's version from 2017-01-31 04:32

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Question Answer
CO = HR x SV, amount of blood pumped by ventricles in 1 min (at rest it is 5L/min), matched to O2 demands
Total blood volume5L
Under resting conditions, which organ has the most blood flow?liver (it is largest organ)
SNS vs PNS in terms of distribution to SA and AV node effect on ventricular muscleSNS are distributed to SA and AV node has a stronger representation to ventricular muscle,
PNS are distributed to SA and AV node have small (indirect) effect on ventricular muscle
Effect of PNS on HR1. ↓ HR (negative chronotropic response) by ↓SA node activity.
2. ↓AP conduction through AV node.
3. ↓ force of contraction (negative ionotropic effect);
Ach binding to Muscarinic (M2) receptor on the SA node ↑ K+ permeability -> hyperpolarizes cell, ↓ Ca2+ permeability (& possibly Na+);
Decrease pre-potential & ↓ AP conduction velocity through AV node
Effect of SNS on HR1. ↑ HR (positive chronotropic response).
2. ↑ AP conduction rate through AV node.
3. ↑ force of cardiac contraction (positive inotropic effect);
NE binds to Beta 1 adrenergic receptor on SA node which ↑ Na+ (funny channel) permeability, ↑ Ca2+ (slow L-type channel) permeability;
therefore SA node: ↑ slope of pre-potential, AV node: ↓ conducting time between atria and ventricles
For HR < 100 bpmactivate PNS "vagal tone"
For HR = 100 bpmno ANS (intrinsic rate set by SA node)
For HR > 100 bpmactivate SNS
Hr max =220 - age
Stroke volume = EDV - ESV
Effect of SNS on SVNE bind to beta-adrenergic receptor in contractile cells, increases Ca2+ entry (slow L-type Ca2+ channels), ↑ force of contraction, ↑ SV, ↑ CO (extracellular Ca2+ can directly bind to troponin + cause Ca2+ induced Ca2+ release),

Ach bind to nicotinic (N2) receptor on adrenal medulla and release E (80%), NE (20%), these hormones act on B1-adrenergic receptors which ↑ HR (SA node), ↑ contractility of heart (due to Ca2+ entry), ↑ SV, ↑CO
Patients with heart transplants increase CO with no ANS innervation to heart how?through sympathetic stimulation of adrenal medulla and release of E and NE into circulation (↑ HR, ↑SV), through muscle pump (↑ venous return = ↑ SV)
Effect of PNS on SVleft vagal nerve innervate left ventricles, ↓ Ca2+ (slow L-type channels) into contractile cells, ↓ force of contraction, ↓ SV (and by removing all SNS activity)
How does preload affect SVextent of filling of the heart before contractions,
↑ EDV = ↑ preload (↑ length of ventricular muscle fibers/stretch muscle fibers, which generate more force due to maximal overlap of actin and myosin + stretch sensitive Ca2+ channels (↑ extracellular Ca2+ entry), stretching ↑ troponin's affinity for Ca2+), ↑ force of contraction, ↑ SV.
Frank-Starling Law of the Heart"The greater the diastole volume, the greater quantity pumped during systole"
How is EDV increased by? (3 mechanisms for ↑ venous return)1. muscle pump: rhythmic contraction & relaxation of skeletal muscles pump blood back to heart, ↑ venous return, ↑ EDV, ↑ SV, ↑CO.
2. Respiratory pump: ↓ pressure in chest cavity, pull blood back to heart.
3. ANS: SNS causes slight VENOconstriction
How does afterload affect SVResistance against which ventricles pump blood (pressure in aorta during systole is afterload encountered by left ventricle.
Ventricles need time to generate more pressure to exceed aortic pressure so ejection phase is shorter therefore ↓ SV (↑ESV)
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