Cardiovascular Muscle and Heart Function

Presentation Transcript

Cardiovascular Muscle and Heart Function Cardiac muscle strands are striated – sarcomere is the utilitarian unit Fibers are extended; interface with each other at intercalated plates . The circles contain a few crevice intersections Nuclei are halfway found Abundant mitochondria SR is less plenteous than in skeletal muscle, however more prominent in thickness than smooth muscle Sarcolemma has particular particle channels that skeletal muscle does not – voltage-gated Ca2+ channels Fibers are not tied down at closures; takes into consideration more prominent sarcomere shortening and stretching

How are cardiovascular compressions begun? Cardiovascular conduction framework Specialized muscle cells "pace" whatever remains of the heart; cells contain less actin and myosin, are thin and pale minutely Sinoatrial (SA) hub; pace of around 65 bpm Internodal pathways interface SA hub to atrioventricular (AV) hub AV hub could go about as an auxiliary pacemaker; autorhythmic at around 55 bpm Bundle of His Left and right package branches Purkinje strands; additionally autorhythmic at around 45 bpm ALL CONDUCTION FIBERS CONNECTED TO MUSCLE FIBERS THROUGH GAP JUNCTIONS IN THE INTERCALATED Disks

Why are filaments of the leading framework autorhythmic ? I f channels How does the depolarization in these cells influence heart muscle cells? Superimpose changes in the muscle cell's film potential on this diagram Membrane capability of SA nodal cells

Changes in particle focuses in a heart muscle fiber taking after depolarization What causes the muscle resting layer potential to change at first? What might occur with a skeletal muscle now?

The recalcitrant period is short in skeletal muscle, however long in heart muscle. This implies skeletal muscle can experience summation and lockjaw, by means of rehashed incitement Cardiac muscle CAN NOT aggregate activity possibilities or withdrawals and can't be tetanized

Autonomic sensory system balances the recurrence of depolarization of pacemaker Sympathetic incitement (neurotransmitter = ); ties to b 1 receptors on the SA nodal layers Parasympathetic incitement (neurotransmitter = ); ties to muscarinic receptors on nodal films; expands conductivity of K+ and reductions conductivity of Ca2+ How do these neurotransmitters get these outcomes?

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ECG looks at how depolarization occasions happen in the heart If a wavefront of depolarization goes towards the anode connected to the + input terminal of the ECG enhancer and far from the cathode appended to the - terminal, a positive avoidance will result.  If the waveform ventures far from the + terminal lead towards the - terminal, a negative going redirection will be seen.  If the waveform is going in a heading opposite to the line joining the locales where the two leads are set, no diversion or a biphasic redirection will be created.

The electrical action of the heart starts in the sino-atrial node.  The drive then quickly spreads through the correct chamber to the atrioventricular node.  (It likewise spreads through the atrial muscle specifically from the correct chamber to one side atrium.)  This produces the P-wave The principal zone of the ventricular muscle to be initiated is the interventricular septum, which enacts from left to right.  This creates the Q-wave Next the majority of the muscle of both ventricles gets actuated, with the endocardial surface being actuated before the epicardial surface. This produces the R-wave A couple of little ranges of the ventricles are enacted at a somewhat late stage.  This creates the S-wave Finally, the ventricular muscle repolarizes. This produces the T-wave

Since the bearing of atrial depolarization is precisely parallel to the hub of lead II (which is from RA to LL), a positive diversion (P wave) would bring about that lead. Since the ventricular muscle is significantly thicker in the left than in the correct ventricle, the summated depolarization of the two ventricles is downwards and toward the left leg:   this produces again a positive redirection (R-wave) in lead II, since the depolarization vector is in an indistinguishable course from the lead II hub. Septal depolarization moves from left to right, the depolarization vector is coordinated towards the - terminal of lead II (RA), and accordingly a negative diversion (Q-wave) is created.

Arhythmias can be distinguished with an ECG draw the others Normal Bradycardia Tachycardia Atrial fibrillation Ventricular fibrillation Compounds that expansion or diminishing rate are called chronotropic operators Compounts that increment or decline compel of withdrawal are called inotropic specialists

Cardiac Cycle http://www.physiology.wisc.edu/phys335/Cycle_11-14-99.swf

100 50 Atrial volume (ml)

Cardiac Output = Q = volume of blood launched out from the heart every moment What might I need to know to have the capacity to figure out what the cardiovascular yield is very still? What is the stroke volume? What decides the stroke volume? How might I modify heart yield?

What causes this expansion in stroke volume?