Copyright © 2010 Pearson Education, Inc. Marieb Chapter 18 Part B: The Heart.

Copyright © 2010 Pearson Education, Inc.

Marieb Chapter 18 Part B: The Heart


Cardiac Muscle Contraction

• About 1% of cardiac cells have automaticity—(are self-excitable)

• Depolarization of the heart is rhythmic and spontaneous (autorhythmic)

• The other 99% are contractile cells, responsible for the muscle contraction

• Gap junctions ensure the heart contracts as a unit

• Long absolute refractory period (250 ms); muscle fibers can’t go into sustained contraction with no relaxation

Copyright © 2010 Pearson Education, Inc. Figure 18.12

Absoluterefractoryperiod

Tensiondevelopment(contraction)

Plateau

Actionpotential

Time (ms)

1

2

3

Depolarization isdue to Na+ influx throughvoltage-gated Na+

channels. A positivefeedback cycle rapidlyopens many Na+

channels, reversing themembrane potential.Channel closing endsthis phase.

Plateau phase isdue to Ca2+ influx throughCa2+ channels. Thiskeeps the cell depolarized.

Repolarization is due to Ca2+ channels closing and K+ channels opening. This allows K+ efflux, which brings the membranepotential back to itsresting voltage.

1

2

3

Tensi

on (

g)

Mem

bra

ne p

ote

nti

al (m

V)

Action Potential in CONTRACTILE Myocardium

The streets!


Heart Physiology: Electrical Events

• Intrinsic cardiac conduction system

• A network of specialized non-contractile (autorhythmic) muscle cells that start and spread impulses to cause depolarization and contraction of the heart

• The freeways! (contractile cells are the streets!)

• Have unstable resting potentials (pacemaker potentials) due to open Na+ channels


1 2 3 Pacemaker potentialThis slow depolarization is due to both opening of Na+

channels and closing of K+

channels. Notice that the membrane potential is never a flat line.

Depolarization Depolarization is due to Ca2+ influx through Ca2+ channels.

Repolarization is due to Ca2+ channels closing and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its most negative voltage.

Actionpotential

Threshold

Pacemakerpotential

1 1

2 2

3

Action Potential in Conduction System Cells


Heart Physiology: Sequence of Excitation

1. Sinoatrial (SA) node (pacemaker)

• Beats about 75 times/minute (called the sinus rhythm)

• If the vagus is cut, the rate is 100 times per minute (bpm)

• Depolarizes faster than any other part of the myocardium

2. Atrioventricular (AV) node

• Delays impulses approximately 0.1 second; gives the atria _____________________

• Depolarizes at 40 - 60 times per minute in absence of SA node input

• Is this fast enough to stay alive?



3. Atrioventricular (AV) bundle (bundle of His)

• Only electrical connection between the atria and ventricles

• Fibrous skeleton (fibrous trigone) stops ventricular impulses from re-entering the atria

4. Right and left bundle branches

• Two pathways in the interventricular septum that carry the impulses toward the apex of the heart



5. Purkinje fibers

• End in the apex and ventricular walls

• AV bundle and Purkinje fibers depolarize only 30 times per minute in absence of AV node input

• Is this fast enough to keep you alive?

Copyright © 2010 Pearson Education, Inc. Figure 18.14a

(a) Anatomy of the intrinsic conduction system showing the sequence of electrical excitation

Internodal pathway

Superior vena cavaRight atrium

Left atrium

Purkinje fibers

Inter-ventricularseptum

1 The sinoatrial (SA) node (pacemaker)generates impulses.

2 The impulsespause (0.1 s) at theatrioventricular(AV) node. The atrioventricular(AV) bundleconnects the atriato the ventricles.4 The bundle branches conduct the impulses through the interventricular septum.

3

The Purkinje fibersdepolarize the contractilecells of both ventricles.

5


Homeostatic Imbalances

• Defects in the conduction system may cause:

1. Arrhythmias/dysrhythmias: irregular heart rhythms

2. Uncoordinated atrial and ventricular contractions (out of sync)

3. Fibrillation: rapid, irregular contractions; useless for pumping blood



• Defective SA node may result in:

• Ectopic focus: abnormal pacemaker somewhere else takes over

• If the AV node takes over, the rate will be 40-60 bpm

• Defective AV node may result in:

• Partial or total heart block

• Few or no impulses from SA node reach the ventricles

• See P waves but they don’t always cause QRST tracings


Extrinsic Innervation of the Heart and Blood Vessels

• Heart beat is modified by the ANS

• Three cardiac/vascular centers are located in the medulla oblongata

• Cardioacceleratory center (CAC) innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons

• Cardioinhibitory center (CIC) inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves

• A vasomotor center (VMC) is also in the medulla; it uses sympathetic fibers to signal blood vessels


Thoracic spinal cord

The vagus nerve (parasympathetic) decreases heart rate.

Cardioinhibitory center

Cardioacceleratorycenter

Sympathetic cardiacnerves increase heart rateand force of contraction.

Medulla oblongata

Sympathetic trunk ganglion

Dorsal motor nucleus of vagus

Sympathetic trunk

AV node

SA nodeParasympathetic fibersSympathetic fibersInterneurons

The VMC is not shown in this image


ANS Effects on HR


Electrocardiography

• Electrocardiogram (ECG or EKG): a composite of all the action potentials generated by all cardiac cells at a given time

• THIS IS NOT AN OSCILLOSCOPE TRACING!!!!!

• Three waves

1. P wave: depolarization of SA node

2. QRS complex: ventricular depolarization

3. T wave: ventricular repolarization

See the next two figures…


Sinoatrialnode

Atrioventricularnode

Atrialdepolarization

QRS complex

Ventriculardepolarization

Ventricularrepolarization

P-QInterval

S-TSegment

Q-TInterval


ECG

Copyright © 2010 Pearson Education, Inc. Figure 18.17, step 3

Atrial depolarization, initiated bythe SA node, causes the P wave.

P

R

T

QS

SA node

AV node

With atrial depolarization complete,the impulse is delayed at the AV node.

Ventricular depolarization beginsat apex, causing the QRS complex.Atrial repolarization occurs.

P

R

T

QS

P

R

T

QS

Depolarization

Repolarization

1

2

3

Copyright © 2010 Pearson Education, Inc. Figure 18.17, step 6

Ventricular depolarization iscomplete.

Ventricular repolarization beginsat apex, causing the T wave.

Ventricular repolarization iscomplete.

P

R

T

QS

P

R

T

QS

P

R

T

QS

Depolarization

Repolarization

4

5

6


Sample ECG Printout


(a) Normal sinus rhythm.

(c) Second-degree heart block. Some P waves are not conducted through the AV node; hence more P than QRS waves are seen. In this tracing, the ratio of P waves to QRS waves is mostly 2:1.

(d) Ventricular fibrillation. These chaotic, grossly irregular ECG deflections are seen in acute heart attack and electrical shock.

(b) Junctional rhythm. The SA node is nonfunctional, P waves are absent, and heart is paced by the AV node at 40 - 60 beats/min.


Holter Monitors


Pacemakers


Heart Sounds• Two sounds (lub - dup) associated with closing of

heart valves

• First sound (lub) occurs as AV valves close and signifies beginning of systole

• Second sound (dup) occurs when SL valves close at the beginning of ventricular diastole

• Heart murmurs: abnormal heart sounds occur due to:

• valve problems (mostly)

• hole in a septum

• heart chamber irregularity


Heart Murmurs

• Here is a good heart sounds website:

• http://www.wilkes.med.ucla.edu/intro.html


Mechanical Events: The Cardiac Cycle

• Cardiac cycle: all events associated with blood flow through the heart during one complete cycle, from heartbeat to heartbeat

• Systole—contraction

• Diastole—relaxation

• The atria and the ventricles contract at different times and are sometimes both relaxed at the same time


Phases of the Cardiac Cycle – Pressure Rules!

1. Ventricular filling —takes place in mid-to-late diastole

• AV valves are open; SL valves are closed

• 80% of blood passively flows into ventricles (Drips!)

• Then atrial systole delivers the remaining 20%

• End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole


Phases of the Cardiac Cycle

2. Ventricular systole

• Atria relax and ventricles begin to contract

• Rising ventricular pressure results in closing of AV valves

• Isovolumetric contraction phase (all valves are closed)

• In the ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the SL valves open

• End systolic volume (ESV): volume of blood remaining in each ventricle


Phases of the Cardiac Cycle

3. Isovolumetric relaxation occurs in early diastole

• Ventricles relax; pressure decreases

• Backflow of blood in aorta and pulmonary trunk closes SL valves and recoil causes the dicrotic notch (a brief rise in aortic pressure)


1 2a 2b 3

Atrioventricular valves

Aortic and pulmonary valves

Open OpenClosed

Closed ClosedOpen

Phase

ESV

Left atriumRight atrium

Left ventricle

Right ventricle

Ventricularfilling

Atrialcontraction

Ventricular filling(mid-to-late diastole)

Ventricular systole(atria in diastole)

Isovolumetriccontraction phase

Ventricularejection phase

Early diastole

Isovolumetricrelaxation

Ventricularfilling

11 2a 2b 3

Electrocardiogram

Left heart

P

1st 2nd

QRSP

Heart sounds

Atrial systole

Dicrotic notch

Left ventricle

Left atrium

EDV

SV

Aorta

T

Ventr

icula

rvolu

me (

ml)

Pre

ssu

re (

mm

Hg

)


Cardiac Output (CO)

• Volume of blood pumped by each ventricle in one minute

• CO = heart rate (HR) x stroke volume (SV)

• HR = number of beats per minute

• SV = volume of blood pumped out by a ventricle with each beat


Cardiac Output (CO)• At rest:

• CO (ml/min) = HR (75 beats/min) SV (70 ml/beat)

= 5.25 L/min

• Maximal CO is 4–5 times resting CO in nonathletic people

• Maximal CO may reach 35 L/min in trained athletes

• What’s the resting CO in athletes?


Cardiac Output (CO)

•Why do athletes have a low HR? (bradycardia)


Regulation of Stroke Volume

• SV = EDV – ESV

• Three main factors affect SV

• Preload (how much blood is there)

• Contractility (what the symp NS does)

• Afterload (how constricted or “plugged up“ are your systemic vessels?)



• Preload: degree of stretch of cardiac muscle cells before they contract (Frank-Starling law of the heart)

• Cardiac muscle exhibits a length-tension relationship

• At rest, cardiac muscle cells are shorter than optimal length

• Slow heartbeat and exercise increase venous return

• Increased venous return ( ) stretches the ventricles and increases contraction force (SNAP!)

• More ---> more



• Contractility: contractile strength at a given muscle length, independent of muscle stretch and EDV

• Dependent on the activity of the sympathetic NS

• Positive inotropic agents increase contractility

• Specific hormones, ions, drugs (digoxin)

• Negative inotropic agents decrease contractility

• Increased extracellular H + or K+

• Calcium channel blockers



• Afterload: pressure that must be overcome for ventricles to eject blood

• Pulmonary or systemic hypertension increases afterload, resulting in increased ESV and reduced SV

• What else could increase afterload?

• A valve problem


Chemical Regulation of Heart Rate

1. Hormones

• Epinephrine from adrenal medulla enhances heart rate and contractility

• Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine

2. Ions

• Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function


Other Factors that Influence Heart Rate

• Age

• Gender

• Exercise

• Body temperature



• Tachycardia: abnormally fast heart rate (>100 bpm)

• If persistent, may lead to fibrillation

• Bradycardia: heart rate < 60 bpm

• May result in grossly inadequate blood circulation

• May be a desirable result of endurance training


Congestive Heart Failure (CHF)

• Progressive condition where the CO is so low that blood circulation is inadequate to meet tissue needs

• Some possible causes of this condition:

• Coronary atherosclerosis

• Persistent high blood pressure

• Multiple myocardial infarcts

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Copyright © 2010 Pearson Education, Inc. Marieb Chapter 18 Part B: The Heart.

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